Medicine Subspecialties

Before naming a neurological disease, localise the lesion anatomically. Decide whether the syndrome is cortical, subcortical, brainstem, cerebellar, spinal cord, nerve root, peripheral nerve, neuromuscular junction or muscle.

Use onset and tempo first: seconds-minutes suggests vascular/seizure; hours-days inflammatory/infectious/toxic; weeks-months neoplastic/degenerative. Look for cortical signs (aphasia, neglect, seizures), crossed brainstem findings, sensory level, dermatomal or length-dependent patterns, fatigability and proximal myopathy.

Perform mental status, cranial nerves, tone, power, reflexes, plantar responses, sensory modalities, coordination and gait in a fixed sequence. Pattern matters more than isolated weakness.

Select tests after localisation: CT/MRI brain, MRI spine, EEG, CSF, nerve-conduction/EMG or targeted laboratory testing. Avoid shotgun testing before deciding the likely anatomical level.

Treat emergencies before completing localisation: airway compromise, status epilepticus, acute stroke, spinal cord compression, meningitis/encephalitis and impending herniation.

Acute ischemic stroke is sudden focal neurological deficit caused by cerebral arterial occlusion; TIA is transient neurological dysfunction without acute infarction. Modern management is a reperfusion race.

Document last-known-well, focal deficit and NIHSS; check glucose immediately. Posterior circulation stroke may present with diplopia, dysarthria, severe ataxia or acute vestibular syndrome rather than classic FAST symptoms.

ABC first, then focused neurologic examination. Look for stroke mimics but do not delay pathway activation. Dysphagia screening is required before oral intake.

Urgent noncontrast CT excludes haemorrhage; CTA identifies large-vessel occlusion. Advanced CT/MR perfusion can select patients in extended windows. ECG, troponin and vascular/cardiac evaluation follow without delaying reperfusion.

Eligible patients within the thrombolytic window may receive IV tenecteplase or alteplase according to the 2026 AHA/ASA pathway and local protocol; thrombectomy eligibility has expanded for selected LVO patients. Start secondary prevention after mechanism is defined.

Spontaneous ICH is bleeding directly into brain parenchyma, commonly related to hypertension, cerebral amyloid angiopathy, anticoagulation or structural vascular lesions.

Typical presentation is sudden focal deficit, headache, vomiting or declining consciousness. Deep ganglionic/thalamic/pons/cerebellar bleeds suggest hypertensive arteriopathy; lobar bleeds raise amyloid or structural causes.

Assess ABC, GCS, pupils, BP and signs of raised ICP/herniation. Cerebellar ICH can deteriorate rapidly from brainstem compression or obstructive hydrocephalus.

Noncontrast CT confirms location, volume, intraventricular extension and mass effect. CTA is useful in selected patients for vascular cause/spot sign; coagulation and medication history guide reversal.

Reverse anticoagulation urgently when appropriate, manage BP with a smooth protocolised strategy, treat ICP/airway problems and involve neurosurgery early for cerebellar haemorrhage, hydrocephalus or selected surgically accessible lesions.

Aneurysmal SAH is bleeding into the subarachnoid space, usually from a ruptured intracranial aneurysm, and is a neurological emergency because of rebleeding, hydrocephalus and delayed cerebral ischemia.

Classically causes thunderclap headache maximal at onset, often with vomiting, neck stiffness, transient loss of consciousness or focal deficit. Sentinel headaches may precede rupture.

Assess consciousness, pupils and meningism; treat airway or shock first. Avoid diagnostic delay in a convincing thunderclap syndrome.

Urgent noncontrast CT is highly sensitive early. If CT is negative but suspicion remains, further evaluation follows local protocol with LP and/or CTA depending on timing. CTA/angiography identifies aneurysm.

Early neurosurgical/neurointerventional securing of the aneurysm is definitive. Nimodipine reduces poor outcome from delayed cerebral ischemia; manage hydrocephalus, sodium disturbance and complications in a neurocritical setting.

A seizure is a transient event from abnormal excessive neuronal activity; epilepsy is a predisposition to recurrent unprovoked seizures. A first event requires confirmation that it was epileptic and determination of recurrence risk.

Clarify eyewitness description: aura, tonic-clonic movements, eye/head deviation, tongue bite, incontinence, duration and postictal confusion. Differentiate syncope, psychogenic nonepileptic events and metabolic provoked seizures.

Perform full neurologic examination, check injury and identify persistent focal deficit or altered consciousness.

Check glucose and targeted electrolytes/renal/hepatic causes. EEG supports classification and recurrence risk; MRI epilepsy protocol is preferred for structural evaluation when indicated.

Treat an acute provoked cause. Long-term antiseizure therapy after a first unprovoked seizure is individualised according to recurrence risk, structural lesion, epileptiform EEG and patient priorities; WHO notes many patients can achieve seizure freedom with appropriate therapy.

Convulsive status epilepticus is operationally treated when a seizure lasts 5 minutes or recurrent seizures occur without recovery, because spontaneous termination becomes less likely and neuronal/systemic injury rises.

Persistent convulsion, repeated convulsions without awakening or subtle ongoing twitching with impaired consciousness should trigger the status pathway.

ABCDE, lateral positioning when possible, suction/oxygen, monitors, IV/IO access and immediate bedside glucose. Treat hypoglycaemia without delaying antiseizure therapy.

Obtain electrolytes, Ca/Mg, renal/hepatic tests, toxicology or antiseizure levels as indicated; CT, LP and EEG follow stabilisation according to cause.

Give an adequate benzodiazepine first, then a full second-line load such as levetiracetam, valproate or fosphenytoin/phenytoin. Refractory status requires airway control, anaesthetic infusion and EEG-guided ICU care.

Headache assessment begins by distinguishing primary headache from secondary dangerous causes. Migraine is a recurrent neurovascular headache syndrome with or without aura.

Red flags include sudden thunderclap onset, new neurological deficit, fever/meningism, papilloedema, cancer/immunosuppression, pregnancy/postpartum state, head trauma or a new/progressive pattern after age 50.

Perform BP, mental status, cranial nerves, fundoscopy and focal neurologic examination. Typical migraine often has unilateral pulsatile moderate-severe pain with nausea and/or photophobia/phonophobia.

Imaging is not routine for a stable typical primary headache with normal examination; image urgently for red flags. ESR/CRP are relevant when giant cell arteritis is suspected.

Acute migraine treatment uses an NSAID, paracetamol or triptan according to patient factors; antiemetic may be added. Preventive treatment is considered for frequent/disabling attacks, with options including propranolol, topiramate, amitriptyline and CGRP-pathway therapies depending on guideline/availability.

Meningitis is inflammation of the meninges, with acute bacterial meningitis requiring immediate empirical treatment because delay worsens outcome.

Fever, headache, neck stiffness and altered mental status are classic but not always all present. Seizures, focal deficits, shock or petechial rash increase urgency.

ABCDE, sepsis assessment, GCS, meningism and focal neurologic signs. Obtain blood cultures promptly but do not delay antibiotics for CT or LP in an unstable patient.

LP provides opening pressure, cell count, glucose/protein, Gram stain/culture and molecular tests. Brain imaging before LP is reserved for features suggesting mass effect/raised ICP or according to local protocol.

Start empirical IV antibiotics immediately when bacterial meningitis is suspected and add dexamethasone with or just before first antibiotic dose where recommended. Choice depends on age, immune status and local epidemiology. WHO published updated meningitis diagnosis/treatment guidance in 2025.

Encephalitis is brain parenchymal inflammation causing altered mental status plus evidence of CNS inflammation; infectious and autoimmune etiologies are major categories.

Fever, confusion, behaviour change, seizures, focal deficit and memory disturbance are common. Temporal-lobe syndrome should raise HSV encephalitis.

Assess airway, GCS, seizures and raised ICP; document focal signs and movement/psychiatric features that may suggest autoimmune encephalitis.

MRI brain is more sensitive than CT; CSF cell count, protein/glucose and PCR are central. EEG detects nonconvulsive seizures/temporal abnormalities. Autoimmune antibody testing is guided by syndrome.

Start IV acyclovir empirically when HSV encephalitis is possible and do not wait for PCR. Treat seizures and ICP complications. Autoimmune encephalitis requires specialist immunotherapy after infectious causes are appropriately addressed.

Raised ICP results when intracranial volume compensation is exhausted; causes include mass, haemorrhage, hydrocephalus, edema and impaired venous drainage. Herniation threatens brainstem function.

Headache, vomiting, declining consciousness, papilloedema and sixth-nerve palsy may occur. Cushing triad is a late sign. Unilateral dilated pupil with deterioration suggests uncal herniation.

Head elevation, neutral neck, oxygenation/ventilation and frequent GCS/pupil assessment are immediate priorities. Avoid fever, hypotension and hypoxia.

Urgent CT identifies mass effect, hydrocephalus and herniation; MRI/MRV is used selectively. Do not perform LP when a mass lesion/obstructive process is suspected.

Treat the cause. Hypertonic saline or mannitol provides temporary osmotherapy in acute deterioration; neurosurgical decompression/CSF diversion may be definitive. Brief controlled hyperventilation is a rescue bridge for impending herniation, not routine therapy.

Parkinson disease is a progressive neurodegenerative disorder with bradykinesia plus rest tremor and/or rigidity, caused primarily by degeneration of nigrostriatal dopaminergic neurons.

Look for asymmetric onset, rest tremor, rigidity, bradykinesia, reduced arm swing, hypomimia and shuffling gait. Early falls, severe autonomic failure or gaze palsy suggest atypical parkinsonism.

Examine repetitive finger tapping/hand opening, rigidity, tremor, posture, gait and postural stability; assess cognition, mood, swallowing and autonomic symptoms.

Diagnosis is clinical; routine imaging does not diagnose typical PD. MRI is used when atypical features suggest another cause.

Levodopa is the most effective symptomatic therapy. Dopamine agonists and MAO-B inhibitors have roles in selected patients; physiotherapy, exercise, speech/swallow assessment and multidisciplinary care are important. Suspected PD should be referred untreated to a movement-disorder specialist where feasible.

Dementia is acquired cognitive decline severe enough to interfere with independence; Alzheimer disease is the most common neurodegenerative cause.

Alzheimer disease often begins with episodic memory impairment; vascular dementia may be stepwise/executive, Lewy body dementia features fluctuation, visual hallucinations and parkinsonism, and frontotemporal dementia often begins with behaviour/language change.

Assess cognition, ADLs/IADLs, mood, hearing/vision, gait and focal neurology; obtain collateral history. Distinguish delirium, depression and medication effects.

Use a validated cognitive test plus targeted CBC, electrolytes, renal/liver, TSH and B12. Structural brain imaging is generally part of evaluation; specialist biomarkers are used in selected cases.

Provide person-centred care, safety/driving/finance planning and caregiver support. Cholinesterase inhibitors are used in Alzheimer disease and some Lewy body cases; memantine is used in moderate-severe Alzheimer disease. Manage vascular risks.

MS is an immune-mediated inflammatory demyelinating CNS disease characterised by lesions disseminated in space and time.

Typical syndromes include optic neuritis, partial transverse myelitis, internuclear ophthalmoplegia, sensory symptoms and brainstem/cerebellar episodes. Heat may transiently worsen old symptoms.

Examine visual acuity/colour, eye movements, pyramidal signs, sensory level, coordination and gait. Distinguish true relapse from pseudo-relapse due to fever/infection.

MRI brain and spinal cord is central; CSF oligoclonal bands can support diagnosis when criteria are not fulfilled by imaging alone. Exclude important mimics such as NMOSD/MOGAD when phenotype suggests them.

Acute disabling relapse is commonly treated with high-dose corticosteroid. Disease-modifying therapy should be individualised early through a specialist MS service, balancing activity, pregnancy plans, infection risk and monitoring.

GBS is an acute immune-mediated polyradiculoneuropathy, often post-infectious, causing rapidly progressive symmetrical weakness and areflexia with risk of respiratory and autonomic failure.

Weakness typically ascends over days; paresthesias, facial/bulbar weakness and severe neuropathic pain may occur. Autonomic instability can cause BP swings or arrhythmias.

Check reflexes, cranial nerves, swallowing and serial respiratory function (FVC/negative inspiratory force where available). Do not wait for dyspnoea before monitoring breathing.

CSF classically shows albuminocytologic dissociation after the first week; nerve-conduction studies support subtype/diagnosis. Marked CSF pleocytosis suggests an alternative.

Admit and monitor progressing patients. IVIG or plasma exchange are effective disease-modifying treatments; corticosteroids alone are not effective. Early ICU involvement is needed for bulbar weakness, autonomic instability or falling respiratory measures.

MG is an autoimmune postsynaptic neuromuscular-junction disorder producing fluctuating fatigable weakness, commonly from antibodies to acetylcholine receptor or MuSK.

Ptosis/diplopia, dysarthria, dysphagia, neck weakness and proximal limb weakness fluctuate and worsen with activity; sensation and reflexes are generally normal.

Test sustained upgaze, repeated movements and bulbar/respiratory function. Myasthenic crisis is respiratory or bulbar failure requiring ICU care.

AChR/MuSK antibodies and repetitive nerve stimulation or single-fibre EMG support diagnosis. Chest imaging evaluates thymoma.

Pyridostigmine is symptomatic therapy; corticosteroids and steroid-sparing immunotherapy are used for generalised disease. IVIG or plasma exchange is used for crisis or rapid worsening; thymectomy is indicated for thymoma and selected AChR-positive generalised MG.

Peripheral neuropathy is dysfunction of peripheral nerves and is classified by fibre type, distribution, tempo and axonal versus demyelinating pattern.

Distal symmetrical sensory loss/burning with reduced ankle reflexes is common in diabetes. Asymmetry, rapid progression, motor predominance or prominent autonomic features require broader evaluation.

Map sensory loss, reflexes, distal/proximal power, gait and autonomic signs. A stocking-glove pattern suggests length-dependent polyneuropathy.

Check glucose/HbA1c, B12, TSH, renal function, alcohol exposure and selected SPEP/autoimmune/infectious tests. NCS/EMG distinguishes axonal/demyelinating and focal/generalised patterns.

Treat the cause and protect insensate feet. Neuropathic pain can be treated with agents such as duloxetine, gabapentinoids or amitriptyline depending on comorbidity. Rapid or demyelinating presentations need neurology referral.

MND/ALS is progressive degeneration of upper and lower motor neurons causing weakness without a primary sensory deficit.

Mixed UMN and LMN signs in different regions, fasciculations, wasting, spasticity and bulbar dysfunction are typical. Ocular movements and sphincters are relatively preserved until late.

Look for regional spread, tongue fasciculation, brisk reflexes with wasting and respiratory weakness. Ask about orthopnoea, morning headache and weak cough.

EMG supports active/chronic denervation and helps exclude mimics; MRI/labs are used to exclude structural, metabolic or inflammatory alternatives.

Multidisciplinary care is essential. Riluzole modestly prolongs survival; noninvasive ventilation improves symptoms and survival in appropriate patients. Address nutrition, communication, secretion and advance-care planning early.

Myelopathy is spinal cord dysfunction; acute compressive myelopathy is an emergency because neurological recovery depends on rapid diagnosis and decompression.

Weakness below the lesion, sensory level, sphincter dysfunction and UMN signs suggest cord disease. Back pain, cancer, fever or trauma increase concern for compression, epidural abscess or metastasis.

Examine tone, reflexes, plantar responses, sensory level, sacral function and gait; assess for spinal shock in acute severe lesions.

Urgent MRI of the relevant/whole spine is the key investigation for suspected compression. CBC/CRP and cultures are added when infection is possible.

Immobilise if trauma is possible. Urgent neurosurgical/spine evaluation is required for compression. Dexamethasone is commonly used for malignant spinal cord compression while definitive radiotherapy/surgery is arranged, according to oncology protocol.

AFP is acute weakness with reduced tone and reflexes and is a syndrome rather than a diagnosis; causes include GBS, spinal shock, anterior horn disease, neuromuscular-junction disorders, toxins and severe electrolyte abnormalities.

Define onset, symmetry, sensory symptoms, cranial/bulbar involvement, bladder symptoms, fever, diarrhoea, vaccination/travel and toxin exposure.

Check reflexes, sensory level, cranial nerves and respiratory function. Preserved sensation with descending paralysis suggests botulism; ascending areflexic weakness suggests GBS.

Electrolytes, CK, CSF, NCS/EMG and spinal imaging are selected by localisation. Public-health notification/testing is required for suspected poliomyelitis in relevant settings.

Treat respiratory/bulbar failure immediately and manage the cause. Avoid anchoring on GBS when there is a sensory level, marked bowel/bladder involvement or early persistent fever.

Movement disorders are abnormal involuntary movements caused mainly by basal-ganglia/cerebellar network dysfunction. Precise phenomenology comes before etiology.

Rest tremor suggests Parkinsonism; action/postural tremor is typical of essential tremor. Chorea is irregular flowing movement; dystonia is sustained/intermittent patterned twisting posture.

Observe at rest, posture, action and walking. Ask medication exposure, family history, thyroid symptoms and onset/tempo.

Tests are targeted: thyroid function, metabolic/toxic studies, MRI or genetic testing depending on phenotype. Typical essential tremor or PD is often clinical.

Treat the syndrome and cause: propranolol/primidone for essential tremor, dopaminergic therapy for PD, botulinum toxin for focal dystonia, and cause-specific therapy for chorea.

Vertigo is an illusion of movement. The key emergency question is whether acute vestibular syndrome is peripheral or due to posterior circulation stroke.

Peripheral causes often produce intense vertigo/nausea with positional triggers; central causes are more likely with focal neurologic signs, severe gait inability, direction-changing/vertical nystagmus or new deafness.

Examine nystagmus, head impulse, skew and gait. HINTS is appropriate only in continuous acute vestibular syndrome and only when performed by a trained clinician.

MRI is preferred when central cause is suspected; CT is relatively insensitive for posterior fossa ischemia. Hallpike confirms posterior-canal BPPV.

BPPV is treated with canalith repositioning (Epley). Acute central features require immediate stroke pathway. Vestibular suppressants should generally be short-term only.

Cranial neuropathies localise lesions from brainstem nuclei/fascicles to subarachnoid space, cavernous sinus, skull base and peripheral nerve.

A painful pupil-involving third-nerve palsy raises concern for posterior communicating artery aneurysm. Sixth palsy can be a false localising sign of raised ICP. Multiple ocular motor palsies suggest cavernous sinus/orbital apex disease.

Examine pupils, eye position/movements, ptosis, facial sensation/motor, hearing, palate, tongue and long-tract signs.

Imaging depends on pattern: urgent CTA/MRA for suspected aneurysmal third palsy, MRI for brainstem/skull base, and targeted metabolic/inflammatory tests when appropriate.

Treat the cause. Isolated microvascular palsies in diabetes/hypertension often recover, but atypical features, pupil involvement, multiple nerves or progressive course need urgent imaging.

Coma is unarousable unresponsiveness due to bilateral hemispheric dysfunction, reticular activating system injury or diffuse metabolic/toxic disturbance.

Structural causes often produce focal deficits, asymmetric pupils or abnormal posturing; metabolic/toxic coma more often has symmetric findings, though exceptions occur.

ABCDE, GCS, pupils, eye movements, respiratory pattern, tone/reflexes and bedside glucose. Give naloxone when opioid toxicity with respiratory depression is plausible.

Targeted labs include electrolytes, renal/liver, ABG, toxicology and infection studies. Urgent CT brain is typical when structural cause is possible; EEG detects nonconvulsive status. LP follows when CNS infection is suspected and safe.

Treat reversible causes immediately—hypoxia, hypoglycaemia, seizures, shock and poisoning—while protecting airway/ventilation. Do not label coma as intoxication before excluding structural/metabolic emergencies.

Brain tumours cause symptoms through focal tissue dysfunction, seizures, raised ICP, hydrocephalus or endocrine effects; metastases are common in adults.

New focal deficit, new-onset seizure, progressive headache with vomiting/papilloedema, personality change or progressive gait/cognitive decline should raise concern.

Perform complete neurologic exam including fundoscopy. Look for focal deficits, cognitive change and signs of raised ICP.

MRI brain with contrast is preferred for characterisation; CT is used urgently when MRI is unavailable or in emergency deterioration. Histopathology and molecular classification guide definitive diagnosis.

Dexamethasone reduces vasogenic edema around many tumours when symptomatic; antiseizure therapy is used after seizures rather than routinely in all seizure-naïve patients. Neurosurgery, oncology and radiotherapy decisions are multidisciplinary.

Ataxia is impaired coordination from cerebellar, sensory or vestibular dysfunction. The first task is to identify the type and tempo.

Cerebellar ataxia causes wide-based gait, dysmetria, intention tremor and nystagmus; sensory ataxia worsens with eye closure and has impaired proprioception; vestibular ataxia is associated with vertigo.

Test stance/gait, heel-shin, finger-nose, rapid alternating movements, eye movements, proprioception and Romberg sign.

Acute ataxia requires evaluation for posterior circulation stroke, intoxication, infection or metabolic causes; chronic disease prompts MRI, B12/thyroid, alcohol/medication review and selected autoimmune/genetic tests.

Treat cause and use neurorehabilitation. Sudden severe gait ataxia is a stroke presentation until excluded.

Chest pain assessment first separates immediately life-threatening causes—acute coronary syndrome, acute aortic syndrome, pulmonary embolism, tension pneumothorax, oesophageal rupture and pericarditis/tamponade—from common non-cardiac causes.

Characterise onset, site, quality, radiation, duration, exertional relation and associated dyspnoea, diaphoresis, syncope or vomiting. Pressure/heaviness with exertion supports myocardial ischemia, but atypical symptoms do not exclude ACS.

Assess ABC, haemodynamics, pulse symmetry, heart/lung examination and signs of heart failure. Obtain a 12-lead ECG promptly in suspected ACS and repeat if symptoms persist or evolve.

Use serial high-sensitivity troponin with an accepted rapid rule-in/rule-out pathway; add CXR, echo, CT angiography or D-dimer/PE imaging only when the differential indicates them.

Treat instability immediately while pursuing the cause. In suspected ACS use evidence-based antithrombotic/reperfusion pathways; avoid reflex nitrates in hypotension or suspected RV infarction.

ACS is the spectrum of acute myocardial ischemia comprising STEMI and non-ST-elevation ACS; contemporary management integrates ECG, serial high-sensitivity troponin, risk assessment and timely invasive care.

Typical ischemic discomfort may be accompanied by dyspnoea, diaphoresis or nausea; older adults, women and people with diabetes may have less typical presentations.

Look for shock, pulmonary oedema, new murmur, arrhythmia and mechanical complications. Repeat ECGs when the first tracing is nondiagnostic but suspicion remains.

Obtain ECG and serial hs-troponin; bedside echo helps with LV/RV function and complications but should not delay reperfusion in clear STEMI.

Give aspirin unless contraindicated, select additional antiplatelet/anticoagulant therapy according to ACS strategy and bleeding risk, use high-intensity lipid lowering, and pursue reperfusion/invasive management according to STEMI/NSTE-ACS pathway.

STEMI usually reflects acute coronary occlusion causing transmural ischemia and requires immediate reperfusion when the patient is eligible.

Persistent ischemic symptoms with diagnostic ST elevation or an accepted STEMI-equivalent pattern should trigger the reperfusion pathway; do not wait for troponin confirmation.

Assess shock, pulmonary oedema, RV infarction, malignant arrhythmias and new mechanical murmurs. Inferior STEMI with hypotension should prompt right-sided leads.

Serial ECGs and urgent coronary angiography are central. Troponin confirms myocardial injury but must not delay reperfusion.

Primary PCI is preferred when it can be delivered promptly. When timely PCI is unavailable and there is no contraindication, fibrinolysis may be appropriate within the accepted early window followed by transfer/rescue or pharmacoinvasive PCI strategy.

NSTE-ACS results from acute coronary plaque complication without persistent diagnostic ST elevation. NSTEMI has acute troponin-defined myocardial injury; unstable angina has ischemia without biomarker evidence of necrosis.

Symptoms may occur at rest, be new/severe or crescendo. Dynamic ST depression/T-wave change increases likelihood and risk.

Look for ongoing pain, heart failure, hypotension, arrhythmia or recurrent ischemia—features that accelerate invasive management.

Use serial hs-troponin, ECG and validated risk assessment. Echocardiography evaluates function and alternative diagnoses.

Use aspirin plus tailored antithrombotic therapy, intensive lipid lowering and anti-ischemic treatment. Very-high-risk features require immediate invasive evaluation; high-risk NSTEMI generally warrants early angiography.

Chronic coronary syndrome describes stable manifestations of coronary atherosclerotic disease, including exertional angina and patients stabilised after ACS or revascularisation.

Estimate clinical likelihood from symptoms and risk factors. Typical angina is predictable exertional pressure relieved by rest; dyspnoea may be an anginal equivalent.

Examine for hypertension, vascular disease, heart failure and valvular disease; a normal examination is common.

Resting ECG and baseline labs are followed by non-invasive anatomical or functional testing chosen according to likelihood, patient characteristics and local expertise. CT coronary angiography is increasingly central in suitable patients.

Treat lifestyle and risk factors aggressively, use antiplatelet therapy when indicated, intensive LDL lowering, and antianginal therapy such as beta blocker, calcium-channel blocker or nitrates tailored to haemodynamics. Revascularisation is used for prognostic indications or persistent symptoms despite therapy.

Heart failure is a clinical syndrome caused by structural or functional cardiac abnormality leading to elevated filling pressures and/or inadequate cardiac output; classify by EF and clinical stage.

Typical features include exertional dyspnoea, orthopnoea, PND, fatigue and oedema. Search for precipitants such as ischemia, infection, arrhythmia, uncontrolled BP, renal dysfunction and medication nonadherence.

Assess JVP, congestion, perfusion, murmurs, lung crackles and peripheral oedema. Distinguish 'wet/dry' and 'warm/cold' profiles in acute presentations.

BNP/NT-proBNP supports diagnosis; ECG, CXR, renal/electrolytes and echocardiography define cause and phenotype.

For chronic HFrEF, foundational disease-modifying therapy comprises ARNI/ACEI/ARB, evidence-based beta blocker, mineralocorticoid receptor antagonist and SGLT2 inhibitor as tolerated. Diuretics treat congestion; devices/advanced HF referral are selected by phenotype.

Acute cardiogenic pulmonary oedema is rapid accumulation of lung interstitial/alveolar fluid from elevated left-sided filling pressure and can cause life-threatening hypoxaemic respiratory failure.

Severe dyspnoea, orthopnoea, diaphoresis, crackles and sometimes frothy sputum are typical. Blood pressure phenotype strongly guides treatment.

Sit the patient upright, monitor continuously and assess work of breathing, perfusion, JVP, oedema and signs of ACS or acute valve disease.

ECG, CXR, bedside echo, troponin, renal function/electrolytes and natriuretic peptide are selected without delaying stabilisation.

Give oxygen for hypoxaemia and early NIV when appropriate. IV loop diuretic is used for congestion; in markedly hypertensive pulmonary oedema, rapid vasodilation with nitrates can be highly effective when BP permits. Treat the precipitant.

Hypertension is persistent elevation of arterial pressure that increases cardiovascular, cerebrovascular and renal risk. Diagnosis requires accurate measurement and often confirmation outside the clinic.

Most patients are asymptomatic. Assess global cardiovascular risk and look for secondary-cause clues, medication/substance contributors and target-organ damage.

Measure BP correctly in both arms initially; assess BMI, pulses, cardiac examination, bruits and signs of endocrine/renal disease. Check for orthostatic change when relevant.

Use home or ambulatory BP when useful to identify white-coat or masked hypertension. Baseline evaluation includes renal function/electrolytes, glucose/HbA1c, lipids, urinalysis/albuminuria and ECG.

Combine lifestyle measures with pharmacotherapy according to BP and cardiovascular risk. Common first-line classes include ACEI/ARB, dihydropyridine CCB and thiazide/thiazide-like diuretic; combinations are frequently required.

Hypertensive emergency is severe BP elevation with acute hypertension-mediated organ damage; the emergency is the organ injury, not the BP number alone.

Presentations include encephalopathy, ICH, ACS, acute pulmonary oedema, acute aortic syndrome, AKI or pregnancy-related emergencies.

Assess neurologic status, fundoscopy, heart failure, pulse deficits and perfusion. Identify the affected organ before choosing the drug and BP target.

ECG, troponin, renal tests, urinalysis and targeted CT/echo are guided by symptoms. Do not delay treatment when clear acute organ injury is present.

Use titratable IV therapy in a monitored setting. The speed and magnitude of BP reduction are syndrome-specific—acute aortic syndrome, ICH, ischemic stroke and pre-eclampsia require different targets.

AF is a supraventricular arrhythmia with disorganised atrial activation and an irregularly irregular ventricular response; management addresses symptoms, stroke prevention and risk-factor modification.

Patients may have palpitations, dyspnoea, fatigue, chest discomfort or be asymptomatic. Determine onset, triggers and associated HF, thyroid disease, alcohol, obesity and sleep apnoea.

Assess haemodynamic stability first. ECG shows absent organised P waves and irregular RR intervals.

Check ECG, electrolytes, thyroid function and echocardiography; evaluate thromboembolic risk and bleeding modifiers.

Unstable AF requires urgent synchronised cardioversion. Stable patients need rate or rhythm strategy based on symptoms/comorbidity, and anticoagulation according to validated thromboembolic risk rather than AF pattern alone. Early rhythm control/ablation is increasingly important in selected patients.

Paroxysmal SVT commonly reflects AVNRT or AVRT and presents as a regular narrow-complex tachycardia with abrupt onset and termination.

Typical symptoms are sudden palpitations, light-headedness, dyspnoea or chest discomfort. Ask about pre-excitation/WPW and prior ECGs.

First decide stable versus unstable and regular versus irregular; obtain a 12-lead ECG if this does not delay urgent therapy.

For stable regular narrow-complex SVT, use vagal manoeuvres then adenosine when appropriate. Unstable tachycardia requires synchronised cardioversion.

Recurrent symptomatic AVNRT/AVRT is often definitively treated by catheter ablation. Avoid AV-nodal blockers in pre-excited AF because they may accelerate conduction through the accessory pathway.

VT is a ventricular-origin tachyarrhythmia, often associated with structural heart disease or prior MI, and may deteriorate to ventricular fibrillation.

Wide-complex regular tachycardia should be presumed VT in an adult with structural heart disease until proved otherwise.

Assess pulse and haemodynamic stability immediately. Look for AV dissociation, capture/fusion beats and prior scar disease.

Obtain ECG, electrolytes and ischemia evaluation; echo assesses structural disease. Do not delay cardioversion in instability.

Pulseless VT is treated with defibrillation and cardiac-arrest protocol. Unstable VT with a pulse requires synchronised cardioversion. Stable monomorphic VT may receive an appropriate IV antiarrhythmic and expert evaluation; recurrent scar VT may need ICD/ablation.

Clinically important bradycardia may arise from sinus-node dysfunction or AV conduction disease and becomes urgent when it causes hypotension, ischemia, heart failure or altered mental status.

Symptoms include syncope/presyncope, fatigue, dyspnoea or chest discomfort. Review beta blockers, non-DHP CCBs, digoxin, ischemia and electrolyte causes.

Assess perfusion and identify Mobitz II or complete heart block. Inferior MI often causes nodal block; anterior MI with new high-grade block is more ominous.

Use 12-lead ECG, electrolytes, medication review and ischemia evaluation; ambulatory monitoring is useful for intermittent symptoms.

For symptomatic unstable bradycardia, atropine may be attempted while preparing transcutaneous/transvenous pacing and/or chronotropic infusion when needed. Persistent high-grade AV block often requires permanent pacing after reversible causes are addressed.

Syncope is transient loss of consciousness from global cerebral hypoperfusion with rapid onset, short duration and spontaneous recovery.

Classify as reflex/vasovagal, orthostatic or cardiac. Exertional syncope, supine syncope, palpitations before collapse, structural heart disease or family history of sudden death are red flags.

Perform orthostatic BP, cardiac and neurologic examination. A postictal state or prolonged confusion argues against simple syncope.

Every unexplained syncope needs an ECG. Further testing—echo, rhythm monitoring, exercise testing or tilt testing—is driven by risk and suspected mechanism.

Treat the cause. High-risk suspected cardiac syncope warrants monitored evaluation; low-risk vasovagal syncope is managed with education, hydration, trigger avoidance and selected counter-pressure strategies.

AS is obstruction at the aortic valve, most commonly calcific in older adults or bicuspid-valve related in younger patients.

Classic advanced symptoms are exertional dyspnoea, angina and syncope. A harsh ejection systolic murmur radiating to the carotids and delayed low-volume pulse are typical.

Assess carotid upstroke, pulse pressure, murmur, S2 and signs of LV failure.

Echo defines valve velocity/gradient, valve area and LV function. Discordant low-flow/low-gradient disease may require stress echo or CT calcium assessment.

Severe symptomatic AS generally requires valve replacement; TAVI versus surgery is individualised by age, anatomy, life expectancy and procedural risk.

MS is obstruction to LV inflow, classically rheumatic, causing elevated left atrial pressure, pulmonary hypertension and AF.

Dyspnoea, orthopnoea, haemoptysis and palpitations are common. Auscultation may reveal loud S1, opening snap and low-pitched mid-diastolic rumble at the apex.

Assess AF, pulmonary hypertension, right-heart failure and embolic signs.

Echo measures valve area, gradient, morphology, pulmonary pressure and LA thrombus risk; TOE is important before balloon commissurotomy when thrombus must be excluded.

Diuretics relieve congestion and rate control helps AF. Anticoagulate AF when indicated. Percutaneous mitral commissurotomy is preferred for suitable severe symptomatic rheumatic MS without contraindicating morphology/thrombus/regurgitation.

MR is systolic backflow from LV to LA and may be primary from valve apparatus disease or secondary from LV/atrial remodelling.

Chronic MR causes exertional dyspnoea and fatigue; acute severe MR can cause pulmonary oedema and shock with a relatively soft murmur.

Look for displaced hyperdynamic apex and pansystolic apical murmur radiating toward axilla, plus congestion or AF.

Echo defines mechanism, severity, LV/LA size and pulmonary pressure; TOE is useful for repair planning and transcatheter assessment.

Treat acute severe MR as an emergency with haemodynamic support and urgent surgical/interventional assessment. Chronic severe primary MR is preferably repaired when symptomatic or when LV/other guideline triggers emerge; secondary MR requires optimisation of HF therapy first.

AR is diastolic backflow from aorta to LV caused by valve disease or aortic-root pathology, producing chronic LV volume overload.

Chronic severe AR may cause exertional dyspnoea and forceful heartbeat; acute AR may present with pulmonary oedema and shock.

Typical chronic findings include wide pulse pressure, bounding pulse and early diastolic decrescendo murmur along the left sternal border.

Echo assesses severity, LV dimensions/function and aortic root; CT/CMR is useful when aortopathy or discordant measurements are present.

Treat hypertension appropriately in chronic AR. Severe symptomatic AR or severe AR with LV dysfunction/dilatation meeting guideline thresholds requires valve surgery; acute severe AR usually requires urgent surgery.

IE is microbial infection of endocardial surfaces, usually valves, causing destructive lesions and systemic embolic/immunologic complications.

Think of persistent fever with murmur, embolic phenomena, prosthetic valve/device, prior IE or injection-drug exposure.

Examine for HF, new regurgitant murmur, neurologic deficit, splenic/renal emboli and peripheral stigmata, although classic signs are often absent.

Obtain multiple blood-culture sets before antibiotics when the patient is stable enough; TTE is first-line and TOE has greater sensitivity, especially with prosthetic valves/devices. Apply contemporary diagnostic criteria.

Start pathogen-directed IV antibiotics after cultures; unstable sepsis may require immediate empiric therapy after cultures are drawn. Early Heart Team/surgical evaluation is needed for HF, uncontrolled infection, abscess or selected embolic-risk lesions.

Acute pericarditis is inflammatory pericardial disease; effusion is fluid accumulation and becomes tamponade when intrapericardial pressure impairs cardiac filling.

Pericarditic pain is sharp, pleuritic and improved by sitting forward. ECG may show diffuse ST elevation/PR depression. Tamponade causes dyspnoea, tachycardia and hypotension.

Listen for a friction rub and assess JVP, pulsus paradoxus and shock. Beck's triad is insensitive and often incomplete.

Echo assesses effusion and haemodynamic compromise. In pericarditis evaluate inflammatory markers and targeted cause; troponin elevation suggests myopericardial involvement.

Uncomplicated idiopathic/viral pericarditis is usually treated with an NSAID/aspirin plus colchicine when appropriate. Tamponade requires urgent drainage; large/recurrent or specific-cause effusions need targeted management.

Cardiomyopathies are myocardial disorders including dilated, hypertrophic, arrhythmogenic and restrictive phenotypes; modern classification integrates phenotype, genetics and acquired causes.

Presentation ranges from asymptomatic disease to HF, arrhythmia, thromboembolism or sudden cardiac death. Family history is crucial.

Assess HF phenotype, murmurs, arrhythmia and extracardiac clues such as neuropathy or systemic infiltration.

ECG and echo are first-line; CMR provides tissue characterisation. Genetic counselling/testing and family screening are important in selected inherited disease.

Treat phenotype-specific HF/arrhythmia and prevent sudden death using validated risk markers. HCM management includes symptom control and selected septal reduction/myosin inhibition; infiltrative disease requires cause-specific therapy.

Pulmonary hypertension is elevated pulmonary arterial pressure from heterogeneous causes; classification into groups 1–5 is essential because treatment differs substantially.

Progressive exertional dyspnoea, fatigue, chest discomfort and syncope are common; advanced disease causes right-heart failure.

Look for loud P2, RV heave, TR murmur, raised JVP, hepatomegaly and oedema.

Echo estimates probability and right-heart effects, but right-heart catheterisation is required to confirm and haemodynamically classify PH when specific therapy is contemplated. Evaluate lung disease, left-heart disease and chronic thromboembolism.

Treat the underlying group. PAH requires specialist risk-stratified combination therapy; CTEPH should be assessed for pulmonary endarterectomy or balloon angioplasty. Routine PAH drugs are not appropriate for most group 2/3 PH.

Cardiogenic shock is critical end-organ hypoperfusion due to cardiac pump failure, commonly after acute MI but also from mechanical complications, myocarditis, severe valve disease or arrhythmia.

Hypotension may coexist with cool extremities, altered mentation, oliguria, rising lactate and pulmonary/systemic congestion; some patients maintain BP early despite hypoperfusion.

Assess ABC, perfusion, JVP, lungs, murmurs and rhythm. Mechanical complications after MI must be actively sought.

ECG, serial lactate, renal/liver tests, troponin and immediate bedside echo are central; coronary angiography is urgent when ACS is suspected.

Provide oxygen/ventilatory support, cautious fluids only when appropriate, norepinephrine commonly for severe hypotension and an inotrope when low output persists. In MI-related shock, urgent culprit-vessel revascularisation is central; mechanical circulatory support is selected case-by-case.

Systematic ECG interpretation prevents missed rhythm, conduction and ischemic abnormalities. Always interpret the tracing in clinical context and compare with prior ECGs.

Use a fixed sequence: calibration → rate → rhythm → axis → P waves → PR → QRS → R-wave progression → ST segments → T waves → QT.

Localise ischemia by contiguous leads: inferior II/III/aVF; anterior V1–V4; lateral I/aVL/V5–V6. Reciprocal change increases specificity.

Repeat ECGs during ongoing symptoms and use posterior/right-sided leads when posterior or RV infarction is suspected.

ECG findings guide emergency reperfusion and arrhythmia management, but absence of classic ST elevation does not exclude acute coronary occlusion or NSTEMI.

Cardiovascular prevention targets cumulative atherosclerotic risk through smoking cessation, BP control, lipid lowering, diabetes management, exercise, diet and weight management.

Estimate global risk and distinguish primary from secondary prevention. Established ASCVD automatically places patients in a high-risk prevention pathway.

Assess BP, BMI/waist, peripheral vascular signs and lifestyle factors; ask family history of premature ASCVD.

Measure lipid profile and diabetes markers; consider Lp(a) at least once in adulthood where available and use coronary calcium selectively when risk remains uncertain.

Use high-intensity statin therapy for established ASCVD unless contraindicated, adding ezetimibe and/or a PCSK9-directed agent when LDL reduction remains inadequate according to risk-based targets. Aspirin is standard in many secondary-prevention settings but not routine primary prevention.

Dyspnoea is the subjective sensation of uncomfortable breathing. First distinguish acute life-threatening disease from chronic cardiopulmonary, metabolic, neuromuscular and functional causes.

Clarify onset, progression, exertional threshold, orthopnoea/PND, cough, wheeze, fever, pleuritic pain, haemoptysis and exposure history. Sudden dyspnoea suggests PE, pneumothorax, acute pulmonary oedema or airway obstruction.

Assess respiratory rate, work of breathing, SpO2, mental status, airway, chest symmetry, breath sounds, crackles/wheeze, JVP and perfusion. Inability to speak, exhaustion or altered sensorium indicates impending failure.

Use ECG/CXR and targeted blood tests early; ABG/VBG, ultrasound, D-dimer/CTPA, echo, spirometry or CT are selected according to physiology and pre-test probability.

Stabilise airway, breathing and circulation first; oxygen is titrated to an appropriate saturation target and ventilatory support is escalated when needed. Definitive treatment follows the identified cause.

Respiratory failure occurs when the respiratory system cannot maintain adequate oxygenation and/or carbon-dioxide elimination. Type 1 is predominantly hypoxaemic; type 2 includes hypercapnia.

Look for severe dyspnoea, tachypnoea, accessory-muscle use, cyanosis, agitation followed by drowsiness, inability to speak and exhaustion. Hypercapnia may cause headache, confusion and asterixis.

Assess airway patency, respiratory pattern, SpO2, consciousness, haemodynamics and signs pointing to COPD/asthma, pneumonia, oedema, neuromuscular weakness or CNS depression.

ABG defines oxygenation, ventilation and acid-base status. CXR, ECG, ultrasound and cause-directed testing should proceed without delaying support.

Treat the cause while titrating oxygen. Use HFNC/NIV in appropriate phenotypes and intubate when airway protection, refractory hypoxaemia, severe acidosis, exhaustion or haemodynamic instability makes non-invasive support unsafe or unsuccessful.

ABG analysis integrates pH, PaCO2, bicarbonate and oxygenation to identify acid-base and respiratory abnormalities.

Use a fixed sequence: pH → primary respiratory/metabolic process → expected compensation → anion gap when relevant → assess for mixed disorder → evaluate oxygenation.

Interpret the ABG alongside respiratory rate, ventilatory support, haemodynamics and clinical context; numbers without context can mislead.

Calculate expected compensation using standard rules, and assess PaO2/FiO2 or A–a relationships when hypoxaemia needs characterisation.

Management targets the underlying disorder rather than 'correcting the ABG' in isolation. Ventilator changes should follow whether the problem is oxygenation, ventilation or both.

CAP is an acute infection of lung parenchyma acquired outside hospital or early after admission, ranging from mild outpatient illness to severe sepsis and respiratory failure.

Fever, cough, sputum, pleuritic pain and dyspnoea are typical but elderly patients may present with confusion or functional decline.

Assess oxygenation, respiratory rate, BP, mental status, focal crackles/bronchial breathing and sepsis. Severity tools such as CURB-65 or PSI support but do not replace clinical judgement.

Chest imaging confirms infiltrate when diagnosis is uncertain or hospitalisation is considered. Obtain cultures and targeted microbiology in severe disease or when resistant/unusual pathogens are plausible.

Start empiric antibiotics according to severity, comorbidity, local resistance and recent antibiotic exposure, then de-escalate to microbiology. Provide oxygen/fluids judiciously and treat sepsis/complications.

HAP develops ≥48 hours after admission and VAP generally ≥48 hours after endotracheal intubation; both require attention to local antimicrobial resistance.

New/progressive infiltrate plus fever, purulent secretions, leukocytosis/leukopenia and worsening oxygenation raises suspicion, but no single feature is diagnostic.

Assess sepsis, ventilator requirements, secretion burden and alternate sources. Review prior antibiotics, colonisation and local antibiogram.

Obtain respiratory cultures and blood cultures when appropriate before antibiotics if this does not delay treatment. Imaging and clinical trajectory help distinguish pneumonia from atelectasis/oedema.

Use empiric therapy based on MDR risk and local susceptibility, then narrow promptly. Prevention includes hand hygiene, minimising sedation/intubation duration, head elevation and evidence-based ventilator bundles.

Pulmonary TB is infection with Mycobacterium tuberculosis transmitted through airborne droplet nuclei and may cause cavitary, infiltrative or disseminated disease.

Chronic cough, fever, night sweats, weight loss and haemoptysis are classic, but presentation varies with immunity and disease burden.

Assess nutrition, lymph nodes, chest findings and extrapulmonary disease; institute airborne precautions when infectious pulmonary TB is suspected.

Use sputum molecular testing as an initial diagnostic tool where available, with smear/culture and drug-susceptibility testing according to programme guidance. Chest imaging supports but does not prove TB.

Treat drug-susceptible or drug-resistant TB according to current national/WHO regimens, ensure adherence and public-health notification/contact evaluation.

Asthma is a heterogeneous disease characterised by variable respiratory symptoms and variable expiratory airflow limitation, usually with chronic airway inflammation.

Episodic wheeze, dyspnoea, chest tightness and cough vary over time and intensity and may be triggered by viral infection, allergens, exercise, smoke or occupational exposure.

Examination may be normal between attacks. During exacerbation assess speech, respiratory rate, accessory muscles, SpO2, air entry and signs of exhaustion.

Demonstrate variable airflow limitation with spirometry/bronchodilator response, peak-flow variability or other accepted objective testing when possible.

Current GINA strategy favours ICS-containing treatment for all adults/adolescents rather than SABA-only therapy. Acute exacerbations require rapid bronchodilation, systemic corticosteroid when indicated, oxygen and escalation for severe disease.

Acute severe asthma is a potentially fatal exacerbation with marked airflow obstruction; deterioration can occur despite initially impressive wheeze.

Inability to complete sentences, marked tachypnoea, accessory-muscle use, hypoxaemia and reduced peak flow indicate severity. Silent chest, exhaustion, confusion or bradycardia are ominous.

Assess continuously for air entry, respiratory effort, SpO2, pulse and mental state. Avoid sedatives.

PEF helps grade severity when feasible; ABG is indicated in severe/life-threatening disease. Rising or normalising PaCO2 despite distress suggests ventilatory failure.

Give repeated inhaled short-acting beta2 agonist, add ipratropium in severe attacks, systemic corticosteroid early and controlled oxygen. IV magnesium is used in selected severe cases; intubation requires experienced airway/ventilator management.

COPD is persistent respiratory symptoms and airflow limitation from airway/alveolar abnormalities, commonly related to tobacco or biomass exposure.

Progressive exertional dyspnoea, chronic cough and sputum are typical. Ask smoking/biomass exposure, exacerbation frequency, exercise tolerance and comorbidity.

Look for prolonged expiration, reduced breath sounds, hyperinflation and advanced signs of pulmonary hypertension/cachexia, although examination can be normal early.

Post-bronchodilator spirometry confirms persistent airflow obstruction. Assess symptoms, exacerbation history, eosinophils where relevant and imaging when alternate/additional pathology is suspected.

Smoking cessation, vaccination, pulmonary rehabilitation and inhaled long-acting bronchodilators are core. Add ICS selectively, especially with exacerbations and eosinophilic features; reassess inhaler technique and adherence.

AECOPD is acute worsening of dyspnoea and/or cough/sputum beyond usual variation, often triggered by infection or environmental exposure.

Assess increased breathlessness, sputum volume/purulence, wheeze and alternative diagnoses such as pneumonia, HF, PE or pneumothorax.

Check work of breathing, SpO2, mental state, air entry and signs of cor pulmonale. Drowsiness may indicate hypercapnic encephalopathy.

ABG is important in severe exacerbation or suspected hypercapnia; CXR and ECG help identify complications/alternatives.

Use controlled oxygen—commonly targeting 88–92% when at risk of hypercapnic respiratory failure—short-acting bronchodilators and a short systemic corticosteroid course. Antibiotics are selected for likely bacterial exacerbation; NIV is first-line ventilatory support for appropriate acute hypercapnic acidosis.

Bronchiectasis is permanent abnormal bronchial dilatation associated with impaired mucociliary clearance, chronic infection and airway inflammation.

Chronic productive cough, recurrent infections, purulent sputum and haemoptysis are common. Ask childhood infections, TB, immune disease, ABPA and aspiration.

Coarse crackles, wheeze and clubbing may occur. Assess exacerbation severity and haemoptysis.

High-resolution CT confirms bronchial dilatation. Send sputum cultures, including evaluation for Pseudomonas and mycobacteria when appropriate, and investigate underlying cause.

Airway-clearance techniques, exercise, vaccination and culture-directed antibiotics are central. Long-term macrolide or inhaled antibiotic strategies are specialist options in selected frequently exacerbating patients.

ILD comprises diffuse parenchymal disorders causing varying combinations of inflammation and fibrosis, restrictive physiology and impaired gas exchange.

Progressive exertional dyspnoea and dry cough are typical. Ask connective-tissue symptoms, drugs, occupational/environmental exposures and family history.

Fine bibasal 'Velcro' crackles and clubbing suggest fibrotic ILD; examine for connective-tissue disease.

HRCT pattern is pivotal; PFT commonly shows restriction with reduced DLCO. Autoimmune serology, exposure evaluation, BAL or biopsy is selected in multidisciplinary assessment.

Management depends on subtype: remove offending exposure/drug, treat inflammatory disease when appropriate, and use antifibrotic therapy for IPF and selected progressive pulmonary fibrosis phenotypes. Provide oxygen/rehabilitation/transplant referral as indicated.

IPF is a chronic progressive fibrosing interstitial pneumonia of unknown cause occurring primarily in older adults and associated with a usual interstitial pneumonia pattern.

Progressive exertional dyspnoea and dry cough develop over months to years; exposures and connective-tissue disease must be excluded.

Bibasal fine inspiratory crackles and finger clubbing are common.

HRCT showing definite UIP can establish diagnosis in the correct context without surgical biopsy. PFT and DLCO track physiological impairment.

Antifibrotic therapy with nintedanib or pirfenidone slows functional decline; pulmonary rehabilitation, oxygen when indicated, vaccination and early transplant consideration are important.

Pleural effusion is abnormal fluid accumulation in the pleural space caused by systemic hydrostatic/oncotic imbalance or local pleural disease.

Dyspnoea, pleuritic pain and cough occur depending on size and cause. Common causes include HF, infection, malignancy and TB.

Large effusions cause reduced expansion, stony dull percussion and diminished breath sounds.

CXR/ultrasound confirms fluid. Diagnostic thoracentesis is indicated for most new unexplained effusions; Light's criteria classify exudate versus transudate. Cell count, pH, glucose, microbiology, cytology and ADA are selected by context.

Treat the cause. Complicated parapneumonic effusion/empyema requires drainage plus antibiotics; recurrent malignant effusion may require indwelling catheter or pleurodesis.

Pneumothorax is air in the pleural space causing partial or complete lung collapse; tension physiology occurs when intrathoracic pressure compromises venous return and circulation.

Sudden unilateral pleuritic pain and dyspnoea are typical. Secondary pneumothorax occurs with underlying lung disease and may be poorly tolerated.

Reduced unilateral breath sounds and hyperresonance support diagnosis. Hypotension, severe distress and obstructive shock suggest tension pneumothorax.

Stable patients are confirmed with CXR or ultrasound. Do not delay decompression for imaging when tension pneumothorax is clinically evident.

Management depends on symptoms, size, physiology and primary versus secondary disease, ranging from observation to aspiration or chest drainage. Tension pneumothorax requires immediate decompression followed by definitive pleural drainage.

Parapneumonic effusions accompany pneumonia; complicated effusions and empyema reflect pleural infection and frequently require drainage.

Persistent fever, pleuritic pain or sepsis despite pneumonia treatment should raise suspicion.

Look for reduced breath sounds/dullness and ongoing systemic toxicity.

Ultrasound identifies loculation and guides aspiration. Pleural pus, positive culture, or low pleural pH in the appropriate context supports drainage; CT helps define complex disease.

Give appropriate antibiotics and drain infected pleural fluid. Intrapleural enzyme therapy or surgery is considered when loculated infection fails adequate tube drainage.

PE is obstruction of pulmonary arteries, usually by venous thromboembolism, with severity determined primarily by haemodynamic and RV consequences.

Acute dyspnoea, pleuritic pain, tachycardia, syncope or haemoptysis are common but nonspecific. Assess provoking factors and VTE history.

Check haemodynamics, SpO2 and signs of DVT/RV strain. Shock defines a high-risk presentation.

Use validated clinical probability first. D-dimer can exclude PE in appropriate low/intermediate-risk patients; CTPA is standard imaging, with V/Q scanning useful in selected patients. Echo helps in unstable PE.

Start anticoagulation when indicated and bleeding risk permits. High-risk PE with shock may require systemic thrombolysis or catheter/surgical reperfusion; stable patients are risk-stratified for anticoagulation and disposition.

Pulmonary hypertension has multiple causes; cor pulmonale describes right-ventricular structural/functional change caused by pulmonary disease or pulmonary vascular pathology.

Progressive exertional dyspnoea, fatigue and syncope suggest PH; advanced disease produces oedema and abdominal distension.

Look for loud P2, RV heave, raised JVP, TR murmur, hepatomegaly and peripheral oedema.

Echo estimates probability and RV effects; right-heart catheterisation confirms haemodynamics when needed. Determine whether disease is due to left heart, lung/hypoxia, thromboembolism or PAH.

Treat the underlying group, correct hypoxaemia and manage volume overload. PAH-targeted drugs require specialist classification; CTEPH requires operability assessment.

ARDS is acute diffuse inflammatory lung injury causing increased permeability pulmonary oedema, bilateral opacities and hypoxaemia not fully explained by cardiac failure.

Common triggers include pneumonia, sepsis, aspiration, pancreatitis and major trauma. Respiratory distress and escalating oxygen need develop within days of the insult.

Assess oxygenation, work of breathing, haemodynamics and precipitating sepsis/organ failure.

Diagnosis uses timing, bilateral imaging and oxygenation criteria under appropriate PEEP/CPAP; bedside echo helps assess cardiac contribution.

Treat the cause and use lung-protective ventilation with low tidal volume based on predicted body weight, limitation of plateau/driving pressure, appropriate PEEP, and prone positioning for severe ARDS. Use conservative fluid strategy after shock is controlled.

NIV provides positive-pressure ventilatory support without an artificial airway; HFNO provides heated humidified high-flow oxygen with modest positive airway and dead-space washout effects.

NIV is particularly effective in acute hypercapnic COPD exacerbation and acute cardiogenic pulmonary oedema. HFNO is useful in selected acute hypoxaemic respiratory failure.

Assess consciousness, secretion handling, facial fit, work of breathing, gas exchange and haemodynamic stability. Failure signs require early reassessment.

ABG and continuous clinical monitoring determine response. Improvement in pH, respiratory rate and effort within the early hours supports NIV success.

Choose support according to physiology, use appropriate interface/settings and reassess frequently. Do not persist with NIV/HFNO when there is worsening shock, inability to protect airway or refractory failure requiring intubation.

Mechanical ventilation supports oxygenation and ventilation while the underlying disease recovers; settings should minimise ventilator-induced lung injury.

Separate oxygenation problems from ventilation problems. FiO2/PEEP mainly influence oxygenation, while minute ventilation (rate × effective tidal volume) strongly influences PaCO2.

Monitor synchrony, airway pressures, exhaled tidal volume, SpO2, haemodynamics and sedation needs.

Use ABG plus ventilator waveforms/pressures. Plateau pressure reflects alveolar pressure during an inspiratory hold; high peak with normal plateau suggests increased airway resistance.

Use lung-protective tidal volumes when indicated, appropriate PEEP, avoid excessive pressures, and adjust rate/volume to pH and PaCO2 goals. Daily readiness for liberation should be assessed.

Liberation from ventilation requires improvement of the original illness, adequate oxygenation, haemodynamic stability and ability to sustain spontaneous breathing and protect the airway.

Assess mental status, cough, secretion burden and respiratory muscle capacity; identify reversible barriers such as fluid overload, electrolyte disturbance or oversedation.

Perform a spontaneous breathing trial when readiness criteria are met and monitor distress, tachypnoea, gas exchange and haemodynamics.

RSBI may support assessment but should not replace clinical judgement. Evaluate airway protection and, in selected high-risk patients, post-extubation support strategy.

Extubate after successful SBT when airway protection is adequate. Prophylactic NIV or HFNO may reduce reintubation in selected high-risk groups; failed extubation should not be managed with prolonged ineffective support.

OSA is recurrent upper-airway collapse during sleep causing intermittent hypoxaemia, arousals and sleep fragmentation.

Loud snoring, witnessed apnoea, nocturnal choking and daytime sleepiness are common; obesity, resistant hypertension and AF increase suspicion.

Assess BMI, neck/upper-airway features and cardiometabolic comorbidity.

Diagnosis is established with sleep testing—polysomnography or appropriate home testing depending on patient complexity. AHI/REI quantifies event frequency.

Weight management and risk-factor modification are important. CPAP is standard effective therapy for symptomatic/moderate-severe OSA; mandibular advancement devices and selected surgical approaches are alternatives in suitable patients.

Lung cancer is broadly classified into non-small-cell and small-cell carcinoma; treatment depends on histology, stage, molecular alterations and patient fitness.

Persistent cough, haemoptysis, weight loss, chest pain or recurrent focal pneumonia warrant evaluation; apical tumours may cause shoulder pain/Horner syndrome.

Look for lymphadenopathy, clubbing, pleural effusion, SVC obstruction and metastatic or paraneoplastic features.

Contrast CT defines anatomy; obtain tissue by the safest high-yield route (bronchoscopy, EBUS, percutaneous or metastatic site). PET-CT/brain imaging and molecular/PD-L1 testing guide staging and therapy.

Early NSCLC may be treated surgically or with definitive radiation; locally advanced/metastatic disease uses combinations of systemic therapy, targeted therapy, immunotherapy and radiation according to tumour biology. SCLC generally requires systemic therapy with stage-directed radiation.

Haemoptysis is expectoration of blood originating below the vocal cords; severity is determined more by airway compromise and physiological effect than by an exact volume threshold.

Differentiate true haemoptysis from epistaxis/oropharyngeal bleeding and haematemesis. Common causes include infection/TB, bronchiectasis, malignancy and vascular disease.

Assess airway, respiratory distress, haemodynamics and side of bleeding if known. Massive bleeding threatens life mainly through asphyxiation.

CXR is initial imaging in many stable patients; CT angiography localises cause/bronchial vessels and bronchoscopy is important for airway control, localisation or endobronchial disease.

Stabilise airway and circulation, reverse correctable coagulopathy, position the bleeding lung dependent when the side is known, and treat the cause. Bronchial artery embolisation is a key therapy for significant/recurrent bleeding; surgery is selected for specific failures/causes.

Dysphagia is difficulty in swallowing and should first be localised to oropharyngeal versus oesophageal dysfunction. Progressive mechanical dysphagia requires exclusion of malignancy or stricture.

Oropharyngeal disease causes difficulty initiating a swallow, coughing, choking or nasal regurgitation. Oesophageal dysphagia is perceived after swallowing; solids first suggests obstruction, whereas solids and liquids from onset suggest a motility disorder.

Assess oral cavity, cranial nerves, bulbar function, neck nodes and nutritional status. Alarm features include weight loss, bleeding, anaemia, odynophagia and rapidly progressive symptoms.

Upper GI endoscopy is central for structural oesophageal disease and permits biopsy. Barium studies help selected structural/motility problems; high-resolution manometry defines oesophageal motility disorders.

Protect the airway and nutrition when swallowing is unsafe. Treatment is cause-specific—dilation/acid suppression for selected strictures, cancer pathways for malignancy, and targeted therapy for motility disease.

Gastro-oesophageal reflux disease results when reflux of gastric contents causes troublesome symptoms and/or complications, commonly due to impaired antireflux barrier function.

Typical symptoms are heartburn and acid regurgitation. Dysphagia, GI bleeding, anaemia, persistent vomiting and weight loss are alarm features requiring investigation.

Physical examination is often normal; assess obesity, medication contributors and signs suggesting alternative cardiac or abdominal disease.

Typical uncomplicated GERD may be managed empirically. Endoscopy is indicated for alarm symptoms, refractory disease or Barrett's risk assessment; ambulatory reflux monitoring helps when diagnosis remains uncertain.

Weight reduction when appropriate, avoiding individually relevant triggers and optimised proton-pump inhibitor therapy are mainstays. Antireflux surgery/endoscopic options are reserved for selected objectively confirmed disease.

PUD is mucosal ulceration of stomach or duodenum, most commonly related to Helicobacter pylori or NSAID exposure.

Epigastric pain or dyspepsia is common, but ulcers may first present with bleeding or perforation. Ask NSAIDs, antiplatelets, anticoagulants and prior H. pylori treatment.

Look for pallor, haemodynamic instability, peritonism or features of gastric outlet obstruction when complicated.

Test for H. pylori using validated non-invasive or biopsy-based methods depending on context. Endoscopy is indicated for alarm features, bleeding and selected age/risk groups; gastric ulcers generally require biopsy assessment.

Eradicate H. pylori and confirm cure using an appropriate test after therapy. Stop unnecessary NSAIDs and use PPI healing therapy; complicated ulcers require endoscopic, radiologic or surgical management.

H. pylori is a chronic gastric infection associated with peptic ulcer disease, gastric adenocarcinoma and gastric MALT lymphoma.

Many patients are asymptomatic; presentations include dyspepsia or ulcer complications. Previous antibiotic/macrolide exposure influences regimen choice.

Examination is usually nonspecific unless complications are present.

Urea breath test and stool antigen are useful non-invasive tests; biopsy testing is used during indicated endoscopy. PPIs and recent antibiotics can reduce test sensitivity and require appropriate withholding intervals.

Use an effective locally appropriate eradication regimen based on resistance patterns and prior antibiotic exposure; contemporary practice increasingly favours bismuth-based quadruple therapy where clarithromycin resistance is a concern. Confirm eradication after treatment.

UGIB originates proximal to the ligament of Treitz and commonly results from peptic ulcer disease, varices, erosive disease or mucosal tears.

Haematemesis, coffee-ground vomiting or melaena are typical; brisk UGIB may produce haematochezia. Syncope and shock indicate major blood loss.

Prioritise airway, haemodynamics and perfusion. Examine for chronic liver disease and abdominal tenderness; calculate a validated risk score such as Glasgow-Blatchford when appropriate.

Check CBC, urea/creatinine, coagulation, liver tests and group/crossmatch. Upper endoscopy provides diagnosis and therapy after initial resuscitation.

Use restrictive transfusion principles in most patients while individualising for shock/cardiac disease. Give IV PPI for suspected non-variceal high-risk bleeding pathways; suspected variceal bleeding requires vasoactive therapy plus antibiotics and urgent endoscopic haemostasis.

LGIB usually arises from colon or rectum; diverticular bleeding, angioectasia, colitis, neoplasia and anorectal disease are common causes.

Haematochezia is typical. Ask pain, diarrhoea, weight loss, anticoagulants and prior diverticular disease. Massive UGIB can also present with bright red rectal bleeding.

Assess haemodynamics, abdominal tenderness, rectal findings and signs of chronic liver or vascular disease.

CBC and crossmatch are initial tests. Colonoscopy is important after stabilisation and bowel preparation; CT angiography is particularly useful in significant ongoing bleeding and can guide embolisation.

Resuscitate and correct clinically important anticoagulation when appropriate. Treat the identified lesion endoscopically, radiologically or surgically according to bleeding severity and source.

Acute diarrhoea is usually infectious and self-limited, but severity depends on dehydration, systemic toxicity, host vulnerability and invasive disease.

Characterise duration, stool frequency, blood, fever, vomiting, travel, food/water exposure, antibiotics, hospitalisation and immunosuppression.

Assess hydration, BP, pulse, mental status, abdominal tenderness and peritonism.

Most uncomplicated cases need no testing. Stool studies are targeted to severe, bloody, persistent, outbreak-associated, immunocompromised or healthcare-associated disease.

Oral rehydration is the cornerstone; IV fluids are used for severe dehydration. Antibiotics are reserved for selected syndromes/pathogens because unnecessary therapy can cause harm.

Chronic diarrhoea lasting more than about four weeks may be watery, fatty or inflammatory and requires a structured evaluation.

Ask nocturnal symptoms, weight loss, blood, steatorrhoea, medications, travel, diet and relation to fasting. Functional diarrhoea/IBS is common but alarm features require organic evaluation.

Assess nutritional status, anaemia, thyroid signs, oral ulcers, skin/joint findings and abdominal masses.

Initial tests commonly include CBC, inflammatory markers, coeliac serology and selected stool tests. Faecal calprotectin helps distinguish inflammatory bowel disease from functional disease in appropriate patients; colonoscopy/biopsy is guided by risk.

Treat the identified cause and correct fluid/nutritional deficits. Avoid repeatedly prescribing empirical antimicrobials without an indication.

IBS is a disorder of gut-brain interaction characterised by recurrent abdominal pain related to defecation and/or change in stool frequency or form without explanatory structural disease.

Classify constipation-predominant, diarrhoea-predominant, mixed or unclassified patterns. Alarm features include bleeding, weight loss, anaemia, nocturnal symptoms and relevant family history.

Examination is usually normal; look for signs that suggest inflammatory, malignant, endocrine or malabsorptive disease.

Use a positive symptom-based diagnosis after appropriate limited evaluation rather than exhaustive exclusion. Coeliac testing and inflammatory markers/calprotectin are useful in selected diarrhoeal presentations.

Education, dietary/lifestyle strategies and soluble fibre are useful. Low-FODMAP dietary therapy should ideally be supervised; pharmacological treatment targets predominant bowel pattern and pain.

IBD comprises Crohn's disease and ulcerative colitis, chronic immune-mediated intestinal disorders with relapsing inflammation and important extraintestinal manifestations.

UC classically causes bloody diarrhoea and urgency with continuous colonic disease; Crohn's may cause pain, diarrhoea, weight loss, strictures, fistulae and segmental disease anywhere in the GI tract.

Assess nutrition, abdominal tenderness/mass, perianal disease, oral ulcers, joints, skin and eyes.

Use CBC/CRP, faecal calprotectin, stool infection testing and ileocolonoscopy with biopsies; cross-sectional enterography assesses small bowel and penetrating Crohn's disease.

Therapy is severity- and phenotype-based, using 5-ASA principally in UC, corticosteroids for induction rather than maintenance, and immunomodulator/biologic/small-molecule therapies for appropriate moderate-severe disease. Surgery is curative for colitis in UC but not Crohn's disease.

UC is chronic mucosal inflammation beginning in the rectum and extending proximally in a continuous pattern through the colon.

Bloody diarrhoea, urgency and tenesmus are typical. Severe attacks may produce fever, tachycardia, anaemia and colonic dilatation.

Assess hydration, abdominal tenderness/distension and extraintestinal features. Avoid unnecessary repeated rectal examinations in acute severe colitis.

Stool testing excludes infection; flexible sigmoidoscopy with limited insufflation and biopsy is useful in severe attacks. Abdominal imaging evaluates toxic megacolon.

Mild-moderate disease often uses oral/topical mesalamine according to extent. Acute severe UC requires hospital care, IV corticosteroids, thromboprophylaxis and early surgical involvement; steroid non-response prompts rescue biologic/calcineurin therapy or colectomy.

Crohn's disease is transmural, segmental inflammation that may affect any GI segment and can cause stricturing, penetrating and perianal complications.

Abdominal pain, chronic diarrhoea and weight loss are common; perianal fistula/abscess may be a major clue.

Assess nutritional status, abdominal mass/tenderness, perianal disease and extraintestinal manifestations.

Ileocolonoscopy with biopsy plus MR/CT enterography defines disease extent and complications. Faecal calprotectin supports assessment of intestinal inflammation.

Corticosteroids can induce remission but are not maintenance therapy. Immunomodulators, biologics and small molecules are chosen by severity/phenotype. Drain abscesses and involve surgery for obstruction, fistula complications or refractory disease.

Coeliac disease is an immune-mediated enteropathy triggered by gluten in genetically susceptible individuals and may present with intestinal or extraintestinal disease.

Diarrhoea, bloating and weight loss are classic, but iron-deficiency anaemia, osteoporosis, infertility, dermatitis herpetiformis or abnormal liver tests may dominate.

Assess nutritional deficiency, oral ulcers, dermatitis and growth/weight status.

Test tissue-transglutaminase IgA with total IgA while the patient is consuming gluten. Duodenal biopsy confirms diagnosis in most adults; IgG-based testing is used when IgA deficient.

Use a lifelong strict gluten-free diet with dietitian support and correct deficiencies. Assess response and associated autoimmune/nutritional complications.

Malabsorption results from impaired digestion, mucosal absorption or nutrient transport and may cause global or selective deficiencies.

Steatorrhoea, weight loss, bloating, diarrhoea, anaemia and bone disease suggest malabsorption. Causes include coeliac disease, pancreatic insufficiency, small-bowel disease/resection and cholestatic disorders.

Look for wasting, oedema, glossitis, bruising, neuropathy and signs of the underlying systemic disorder.

Use targeted CBC, iron/B12/folate, albumin, calcium/vitamin studies and disease-specific tests. Stool fat/pancreatic elastase, coeliac testing, imaging or endoscopy are selected by suspected mechanism.

Treat the cause and replace deficient macro- and micronutrients. Pancreatic enzyme replacement is used for exocrine pancreatic insufficiency.

Acute pancreatitis is acute pancreatic inflammation diagnosed when at least two of three are present: characteristic pain, pancreatic enzymes >3× upper limit, or characteristic imaging.

Severe persistent epigastric pain radiating to the back with nausea/vomiting is typical. Gallstones and alcohol are common causes; also consider hypertriglyceridaemia, drugs and procedures.

Assess haemodynamics, volume status, hypoxaemia and organ failure rather than relying on enzyme magnitude.

Check lipase, liver tests, triglycerides/calcium when indicated and ultrasound for gallstones. CT is not routinely required immediately when diagnosis is clear; use it for uncertainty or complications/non-improvement.

Use early goal-directed isotonic crystalloid resuscitation without fluid overload, adequate analgesia and early oral/enteral feeding as tolerated. ERCP is urgent for pancreatitis with cholangitis or persistent biliary obstruction; antibiotics are not routine for sterile necrosis.

Chronic pancreatitis is progressive fibro-inflammatory pancreatic disease causing recurrent/chronic pain, exocrine insufficiency and eventually diabetes.

Recurrent epigastric pain, weight loss and steatorrhoea are common; alcohol, smoking, genetic and obstructive causes should be assessed.

Look for malnutrition, vitamin deficiency and diabetes; examination may be unremarkable between attacks.

CT/MRCP/EUS demonstrate calcification, ductal abnormalities and structural disease. Faecal elastase supports exocrine insufficiency assessment.

Stop alcohol and smoking, optimise nutrition, use pancreatic enzyme replacement for exocrine insufficiency and manage diabetes. Endoscopic or surgical therapy is considered for obstructive pain/complications.

Pancreatic ductal adenocarcinoma is an aggressive malignancy often diagnosed late because early symptoms are nonspecific.

Progressive painless jaundice, weight loss, epigastric/back pain and new or worsening diabetes are important clues; migratory thrombophlebitis may occur.

Assess jaundice, cachexia, palpable gallbladder, nodes and metastatic disease.

Pancreas-protocol contrast CT is central for staging/resectability. EUS-guided tissue acquisition is commonly used when histology is required; CA 19-9 supports monitoring but is not a population screening test.

Potentially resectable disease requires multidisciplinary surgical-oncology assessment, often with perioperative systemic therapy. Unresectable disease receives systemic/palliative therapy and biliary drainage when clinically indicated.

Acute mesenteric ischaemia is sudden inadequate intestinal perfusion from arterial embolism/thrombosis, venous thrombosis or non-occlusive hypoperfusion and is time-critical.

Severe acute abdominal pain disproportionate to early physical findings is classic. AF, atherosclerosis, shock and hypercoagulability are key risk contexts.

Early examination may be deceptively mild; peritonitis indicates advanced bowel infarction.

CT angiography should be obtained urgently when suspected and should not be delayed solely because of renal concerns when the diagnosis is life-threatening. Lactate may be normal early.

Resuscitate, give broad-spectrum antibiotics and anticoagulate when appropriate; urgent vascular/surgical revascularisation and resection of nonviable bowel are central.

Chronic mesenteric ischaemia is usually atherosclerotic reduction of mesenteric blood flow producing demand-related intestinal ischaemia after meals.

Postprandial abdominal pain beginning predictably after eating, food fear and unintentional weight loss form the classic syndrome.

Examination may show vascular disease/bruits but can be largely normal; significant weight loss is an important clue.

CT angiography is a preferred anatomical test; duplex ultrasound or MR angiography may be alternatives in selected patients.

Revascularisation is the definitive treatment for symptomatic disease, commonly using an endovascular-first strategy when anatomy is suitable, alongside aggressive atherosclerotic risk reduction.

Intestinal obstruction prevents normal passage of bowel contents and may be mechanical or functional; strangulation threatens bowel viability.

Colicky pain, vomiting, distension and obstipation are typical. Adhesions and hernias are common small-bowel causes; malignancy is important in large-bowel obstruction.

Assess dehydration, scars, hernias, distension and bowel sounds. Continuous pain, fever, tachycardia, peritonism or metabolic acidosis raises concern for ischaemia/perforation.

CT abdomen with contrast usually defines level, cause and complications. Labs assess dehydration, renal injury and electrolyte disturbance.

Keep NPO, decompress with NG tube when indicated, give IV fluids/electrolyte correction and obtain early surgical review. Strangulation, perforation, closed-loop obstruction or unresolved complete obstruction requires urgent intervention.

Constipation includes infrequent stools, hard stools, excessive straining, incomplete evacuation or difficult defecation and may be primary or secondary.

Review diet, mobility, medications, endocrine/metabolic disease and alarm symptoms such as bleeding, anaemia, weight loss or new late-onset change.

Perform abdominal and, when appropriate, digital rectal examination to assess impaction, mass and pelvic-floor dysfunction.

Most patients need limited tests; colon evaluation is indicated by age-appropriate screening or alarm features. Refractory disease may require transit and anorectal physiological testing.

Increase appropriate fibre/fluids/activity, remove contributors and use osmotic laxatives such as polyethylene glycol when needed. Refractory pelvic-floor dyssynergia responds to biofeedback rather than simply escalating laxatives.

Colorectal cancer commonly develops through adenoma-carcinoma or serrated pathways and is preventable/curable when detected early.

Rectal bleeding, iron-deficiency anaemia, altered bowel habit, weight loss or obstruction are important presentations; right-sided cancers may present primarily with anaemia.

Assess pallor, abdominal/rectal mass, hepatomegaly and nodes.

Colonoscopy with biopsy establishes diagnosis. CT stages chest/abdomen/pelvis; rectal cancer requires dedicated pelvic MRI, and CEA is useful for surveillance rather than screening diagnosis.

Treatment is stage- and site-specific using surgery, systemic therapy and for rectal cancer selected radiotherapy/neoadjuvant strategies. Population screening reduces mortality.

Colonic diverticulosis is common and often asymptomatic; diverticulitis occurs when a diverticulum becomes inflamed, sometimes complicated by abscess, fistula, obstruction or perforation.

Acute left lower-quadrant pain, fever and altered bowel habit are typical in left-sided disease; location varies with anatomy/population.

Assess focal tenderness, peritonism and systemic toxicity.

CT abdomen confirms diagnosis and detects complications in uncertain or significant presentations. Colonoscopy is avoided during acute severe inflammation but may be indicated after recovery depending on prior evaluation and course.

Uncomplicated disease is often managed conservatively; antibiotics are selective rather than automatic in immunocompetent mild uncomplicated cases. Abscess, perforation or sepsis may require drainage or surgery.

C. difficile causes antibiotic-associated colitis through toxin production, ranging from mild diarrhoea to fulminant colitis and toxic megacolon.

New significant diarrhoea after antibiotics or healthcare exposure is typical; recurrence is common.

Assess dehydration, abdominal distension/tenderness, ileus, fever and shock. Severe ileus may paradoxically reduce stool output.

Test only unformed stool from symptomatic patients using an accepted multistep toxin/NAAT strategy. Leukocytosis, creatinine and imaging help grade severe/fulminant disease.

Stop unnecessary inciting antibiotics and treat with recommended first-line therapy such as fidaxomicin or oral vancomycin according to episode/severity and availability. Fulminant disease needs high-dose enteral vancomycin-based therapy, IV metronidazole and early surgical input; recurrent disease may benefit from microbiota-based strategies.

Colorectal polyps include conventional adenomas and serrated lesions with differing malignant potential; screening aims to detect cancer early and remove precursors.

Most polyps are asymptomatic. Risk rises with age, family history, hereditary syndromes and prior advanced polyps.

Physical examination usually contributes little to screening but helps when symptomatic disease is present.

Screening options include stool-based tests and structural examinations such as colonoscopy; the appropriate starting age and interval depend on guideline, risk and test. Post-polypectomy surveillance is based on number, size and histology.

Remove premalignant polyps endoscopically when feasible and ensure appropriate surveillance. High-risk hereditary patterns require genetic assessment and intensified screening.

Jaundice is visible bilirubin accumulation and should be approached by determining whether hyperbilirubinaemia is predominantly unconjugated or conjugated and whether the process is prehepatic, hepatocellular or cholestatic.

Ask onset, fever, abdominal pain, pruritus, pale stool, dark urine, weight loss, alcohol, drugs, transfusion/travel and haemolytic symptoms. Painless progressive jaundice with weight loss suggests malignant obstruction; fever with RUQ pain suggests cholangitis.

Assess pallor, fever, scratch marks, hepatosplenomegaly, ascites, chronic liver stigmata, palpable gallbladder and encephalopathy.

Fractionated bilirubin, AST/ALT, ALP/GGT, albumin and INR establish the biochemical pattern and synthetic function. Ultrasound is first-line when obstruction is possible; MRCP/CT/EUS/ERCP are selected subsequently.

Treat the cause rather than bilirubin itself. Urgent biliary drainage is required for obstructive jaundice complicated by cholangitis; acute liver failure requires specialist/transfer assessment.

Liver tests reflect different processes: aminotransferases indicate hepatocellular injury, ALP/GGT cholestasis, while albumin and INR better reflect hepatic synthetic function.

Interpret magnitude, pattern and time course rather than labelling any abnormality 'liver failure'. AST/ALT ratio and medication/alcohol/metabolic context can narrow the differential but are not diagnostic alone.

Look for jaundice, chronic liver disease, volume overload and encephalopathy; compare abnormalities with clinical severity.

Calculate an R ratio when drug-induced liver injury is considered: (ALT/ULN)/(ALP/ULN). Repeat/expand testing based on persistence and pattern; ultrasound is useful for cholestasis.

Stop potential hepatotoxins when appropriate and investigate viral, metabolic, autoimmune, vascular or obstructive causes according to the pattern.

Acute hepatitis is recent hepatocellular inflammation/injury from viral infection, drugs/toxins, ischemia, autoimmune disease or other causes.

Malaise, anorexia, nausea, RUQ discomfort, dark urine and jaundice may occur, but some cases are asymptomatic. Ask specifically about paracetamol, herbal products and viral exposures.

Assess haemodynamics, mental status, jaundice, liver size and signs of chronicity. Encephalopathy indicates severe dysfunction.

Check AST/ALT, bilirubin, INR, glucose and cause-directed viral/autoimmune/toxicology tests. Very high aminotransferases suggest ischemic, toxic or severe viral injury among key differentials.

Most viral hepatitis is supportive, while specific causes require targeted therapy. Monitor INR, glucose and mental status closely; evolving acute liver failure needs urgent transplant-centre discussion.

Acute liver failure is acute severe hepatic dysfunction with coagulopathy and hepatic encephalopathy in a patient without pre-existing cirrhosis, with timing definitions varying by framework.

Early nausea/jaundice can rapidly progress to confusion, cerebral oedema, hypoglycaemia, lactic acidosis, renal failure and shock.

Serially assess encephalopathy grade, pupils/neurology, haemodynamics, volume status and infection while avoiding unnecessary stimulation in advanced cerebral oedema risk.

Urgently obtain INR, glucose, lactate, renal/electrolytes, arterial/venous gas and aetiology tests including paracetamol level where relevant. Use prognostic criteria and early transplant-centre consultation.

Give cause-specific treatment such as N-acetylcysteine for paracetamol toxicity and often selected non-paracetamol ALF, meticulous ICU supportive care, glucose management and cerebral-oedema precautions. Do not delay transplant referral.

Cirrhosis is advanced hepatic fibrosis with architectural distortion and portal hypertension; clinical course is divided into compensated and decompensated disease.

Compensation may be silent. Ascites, variceal bleeding, encephalopathy or jaundice mark decompensation and substantially worsen prognosis.

Look for sarcopenia, spider naevi, palmar erythema, splenomegaly, ascites, oedema, asterixis and endocrine stigmata.

Determine cause and severity using CBC, liver/renal tests, INR, ultrasound and non-invasive fibrosis assessment. Child-Pugh and MELD-based scores provide complementary prognostic information.

Treat the aetiology, prevent decompensation, vaccinate appropriately, optimise nutrition, screen for HCC and varices/clinically significant portal hypertension, and refer for transplant assessment after decompensation or other appropriate triggers.

Portal hypertension is elevated pressure within the portal venous system, most commonly from cirrhosis; clinically significant portal hypertension drives varices and decompensation.

Patients may develop splenomegaly, thrombocytopenia, ascites, varices and portosystemic collaterals.

Assess spleen size, ascites, abdominal-wall collaterals and signs of decompensation.

Endoscopy or validated non-invasive pathways identify patients needing variceal prophylaxis. Doppler ultrasound evaluates portal flow and thrombosis; HVPG is the reference haemodynamic measurement in specialised settings.

Non-selective beta blockers—particularly carvedilol in appropriate compensated cirrhosis—or endoscopic strategies are used according to variceal/CSPH status. Treat the underlying liver disease and avoid unnecessary portal-pressure-provoking insults.

Ascites is pathological peritoneal fluid accumulation, most often from portal hypertension with renal sodium retention in cirrhosis.

Increasing abdominal girth, early satiety, dyspnoea and oedema are typical. New or worsening ascites can signal infection, renal dysfunction or malignancy.

Assess shifting dullness, oedema, JVP and signs of infection/encephalopathy.

Perform diagnostic paracentesis for new-onset ascites and in hospitalised cirrhotics with ascites when clinically indicated. SAAG ≥1.1 g/dL supports portal hypertension; cell count/culture detects SBP.

Restrict dietary sodium moderately and use spironolactone with/without furosemide according to setting. Large-volume paracentesis requires albumin replacement when substantial volumes are removed. Refractory ascites prompts TIPS/transplant consideration.

SBP is infection of ascitic fluid without a surgically treatable intra-abdominal source and is a major complication of cirrhosis.

Fever, abdominal pain, encephalopathy, hypotension or renal deterioration may occur, but SBP can be clinically subtle.

Assess sepsis, abdominal tenderness, mental status and perfusion.

Ascitic PMN count ≥250 cells/mm³ establishes the treatment threshold. Inoculate ascitic fluid into blood-culture bottles at bedside to improve yield; evaluate for secondary peritonitis when features are atypical.

Start appropriate empiric antibiotics promptly and give IV albumin in recommended high-risk SBP settings to reduce renal failure/mortality. Secondary prophylaxis is indicated after recovery; selected high-risk patients receive primary prophylaxis.

Hepatic encephalopathy is potentially reversible brain dysfunction from liver insufficiency and/or portosystemic shunting, commonly precipitated by infection, GI bleeding, constipation, renal dysfunction or sedatives.

Features range from subtle cognitive change and sleep reversal to asterixis, disorientation, somnolence and coma.

Grade mental status, assess airway and search actively for precipitating infection, bleeding, dehydration, electrolyte disturbance and drug exposure.

HE is a clinical diagnosis; ammonia level alone neither confirms nor grades it reliably. Investigate precipitants and consider neuroimaging when focal signs or alternative diagnoses exist.

Treat the precipitant and use lactulose titrated to regular soft stools for overt HE; rifaximin reduces recurrence in appropriate patients. Protect the airway in advanced encephalopathy.

Acute variceal haemorrhage is a portal-hypertension emergency with high early rebleeding and mortality risk.

Haematemesis/melaena in cirrhosis should be considered variceal until assessed. Shock, encephalopathy and aspiration risk worsen prognosis.

Resuscitate ABCs, assess perfusion and mental status, and avoid excessive crystalloid/transfusion that can increase portal pressure.

Check CBC, INR, renal/liver tests and crossmatch. Endoscopy should follow stabilisation, generally urgently within the recommended early window.

Start vasoactive therapy such as terlipressin or octreotide and prophylactic antibiotics as soon as variceal bleeding is suspected. Endoscopic band ligation is standard for oesophageal varices; high-risk failure may require early/pre-emptive TIPS or rescue TIPS.

HRS-AKI is functional renal failure in advanced cirrhosis driven by severe circulatory dysfunction and renal vasoconstriction after other causes of AKI are excluded.

Rising creatinine, oliguria and decompensated ascites are common; infection or excessive diuresis may precipitate deterioration.

Assess volume status, sepsis, nephrotoxins, bleeding and shock; distinguish from hypovolaemia and intrinsic renal injury.

Evaluate creatinine trend, urine findings and ultrasound as appropriate. Diagnosis requires cirrhosis/ascites and exclusion of shock, nephrotoxins and significant structural kidney disease after appropriate volume assessment.

Stop nephrotoxins/adjust diuretics, treat precipitating infection and give albumin during diagnostic/therapeutic volume expansion when indicated. Vasoconstrictor therapy—terlipressin where available, or norepinephrine in appropriate ICU settings—plus albumin is used; transplant is definitive.

Hyponatraemia in advanced cirrhosis is usually dilutional, caused by impaired free-water excretion from non-osmotic vasopressin release and circulatory dysfunction.

It often accompanies ascites and severe portal hypertension and is associated with worse prognosis; severe acute falls may cause neurological symptoms.

Assess extracellular volume, mental status and precipitating diuretic use, GI loss, infection or renal dysfunction.

Confirm hypotonic hyponatraemia and exclude hyperglycaemia/pseudohyponatraemia. Interpret urine studies cautiously in patients receiving diuretics.

Treat the precipitant, review diuretics and potassium, and restrict free water in selected significant hypervolaemic hyponatraemia. Hypertonic saline is reserved for severe symptomatic cases with careful correction limits.

Alcohol-associated liver disease ranges from steatosis to alcohol-associated hepatitis and cirrhosis; sustained abstinence is the most important disease-modifying intervention.

Ask quantity, pattern, duration and last intake nonjudgmentally. Jaundice, fever, tender hepatomegaly and recent heavy alcohol use suggest alcohol-associated hepatitis.

Assess nutrition, withdrawal risk, chronic liver signs, infection and encephalopathy.

AST is often greater than ALT but usually not in the thousands. Exclude viral/drug/obstructive causes and assess severity with validated scores in suspected severe hepatitis.

Provide alcohol cessation treatment, thiamine and nutritional support. Selected severe alcohol-associated hepatitis may receive corticosteroids after excluding contraindications/infection and assessing response; transplant evaluation is appropriate in carefully selected severe disease.

MASLD is hepatic steatosis associated with cardiometabolic risk and ranges from simple steatosis to steatohepatitis, fibrosis and cirrhosis.

Most patients are asymptomatic; obesity, type 2 diabetes, dyslipidaemia and hypertension are common. Cardiovascular disease is a major competing cause of death.

Assess BMI/waist, BP and signs of advanced liver disease while evaluating metabolic comorbidity.

Ultrasound may detect steatosis but does not stage fibrosis well. Use non-invasive fibrosis pathways such as FIB-4 followed by elastography/second-line testing when indicated; biopsy is reserved for selected diagnostic/staging questions.

Weight reduction through diet and exercise is foundational; optimise diabetes, lipids and BP. Patients with significant fibrosis require specialist surveillance and selected disease-directed pharmacotherapy according to current approvals/guidance.

Chronic HBV infection is persistent hepatitis B surface antigen/infection with variable viral replication, inflammation and risk of cirrhosis/HCC.

Patients are often asymptomatic until advanced disease. Assess family history, perinatal origin, immunosuppression, pregnancy and coinfections.

Look for chronic liver disease and extrahepatic manifestations, although examination may be normal.

Interpret HBsAg, anti-HBc, HBeAg/anti-HBe, HBV DNA, ALT and fibrosis together. Screen for HIV/HCV/HDV as appropriate and perform HCC surveillance in risk groups.

Treat patients meeting virologic, biochemical, fibrosis/cirrhosis or special-situation criteria with potent high-barrier nucleos(t)ide analogues such as tenofovir or entecavir. Monitor untreated patients because disease phase can change.

HCV is a blood-borne RNA virus that can cause chronic hepatitis, cirrhosis, HCC and extrahepatic disease; modern direct-acting antivirals cure most infections.

Often asymptomatic; ask transfusions/unsafe injections, injection drug use, dialysis and other blood exposures.

Assess fibrosis/chronic liver disease and extrahepatic features such as cryoglobulinaemic disease.

Positive anti-HCV indicates exposure and must be followed by HCV RNA to diagnose current infection. Stage fibrosis and assess HBV/HIV interactions before treatment.

Use guideline-recommended pangenotypic direct-acting antiviral regimens for most patients, with regimen/duration adapted to cirrhosis, prior treatment and renal/drug-interaction considerations. Confirm sustained virologic response after therapy.

Autoimmune hepatitis is immune-mediated hepatocellular inflammation characterised by compatible biochemistry, autoantibodies, elevated IgG and typical histology after excluding competing causes.

Presentation ranges from incidental transaminitis to acute hepatitis or cirrhosis; other autoimmune disorders may coexist.

Assess jaundice, hepatomegaly and chronic liver signs; examination may be normal.

Check ANA, SMA and other relevant antibodies, serum IgG and exclude viral/drug/metabolic disease. Liver biopsy is important for diagnosis and activity assessment.

Induction commonly uses corticosteroid-based therapy, often with azathioprine as steroid-sparing maintenance when appropriate. Monitor biochemical remission and treatment toxicity.

PBC is autoimmune destruction of small intrahepatic bile ducts causing chronic cholestasis, predominantly in middle-aged women.

Fatigue and pruritus are common; patients may be detected by isolated cholestatic liver tests.

Look for scratch marks, xanthelasma, hepatosplenomegaly and associated autoimmune disease.

Persistent ALP elevation with antimitochondrial antibody usually establishes diagnosis in the correct setting; imaging excludes extrahepatic obstruction. Biopsy is reserved for atypical/overlap cases.

Ursodeoxycholic acid is first-line disease-modifying therapy. Inadequate biochemical response prompts second-line specialist therapy; treat pruritus, bone disease and fat-soluble vitamin issues.

PSC is chronic fibro-inflammatory disease of intra- and/or extrahepatic bile ducts causing multifocal strictures and increased cholangiocarcinoma risk, strongly associated with IBD.

Patients may have pruritus, fatigue, cholangitis or incidental cholestatic tests. Many have ulcerative colitis.

Assess jaundice, hepatosplenomegaly and signs of IBD or cholangitis.

MRCP is the preferred non-invasive diagnostic imaging test showing multifocal stricturing/beading. ERCP is reserved mainly for therapeutic intervention or sampling of concerning strictures.

No medical therapy reliably reverses established PSC. Manage dominant/relevant strictures and cholangitis, perform cancer/IBD surveillance according to specialist guidance and refer for transplant when advanced.

Wilson disease is autosomal-recessive ATP7B dysfunction causing impaired biliary copper excretion and toxic copper accumulation, particularly in liver and brain.

Young patients may present with hepatitis, cirrhosis, haemolysis, movement disorder, psychiatric change or acute liver failure.

Look for Kayser–Fleischer rings, tremor/dystonia and chronic liver signs; rings may be absent in isolated hepatic disease.

Use serum ceruloplasmin, 24-hour urinary copper, slit-lamp examination and, when needed, hepatic copper/genetic testing in combination—no single test is perfect.

Use copper chelation (e.g., penicillamine or trientine) or zinc according to phenotype and specialist guidance, with lifelong monitoring. Acute liver failure or advanced decompensation may require transplant.

Hereditary haemochromatosis causes excessive intestinal iron absorption and progressive tissue iron deposition, most commonly from HFE-related disease in susceptible populations.

Fatigue, arthralgia, diabetes, liver disease, skin pigmentation and cardiomyopathy may occur, though screening often detects disease earlier.

Assess hepatomegaly, joint disease and endocrine/cardiac manifestations.

Transferrin saturation is an early screening marker; ferritin estimates iron burden but rises with inflammation. HFE testing and fibrosis assessment follow in appropriate patients.

Regular phlebotomy is first-line for iron overload when tolerated. Treat organ complications and provide HCC surveillance for patients with cirrhosis/advanced fibrosis.

DILI is liver injury attributable to a medication, herbal or dietary supplement and is a diagnosis requiring careful temporal and competing-cause assessment.

Presentation ranges from asymptomatic enzyme elevation to hepatitis, cholestasis or acute liver failure. Obtain a complete timeline of prescription, OTC and herbal agents.

Assess jaundice, rash, fever, eosinophilic/systemic features and liver failure.

Classify hepatocellular, cholestatic or mixed injury using the R ratio; exclude viral, autoimmune, ischemic and obstructive causes. Rechallenge is generally avoided.

Stop the suspected agent when clinically appropriate and provide supportive/cause-specific therapy; N-acetylcysteine is essential in paracetamol toxicity. Severe injury requires specialist and possible transplant-centre evaluation.

HCC most often arises in cirrhosis or chronic HBV and is managed according to tumour burden, liver function and performance status.

Early HCC is usually asymptomatic; later disease may cause pain, weight loss or sudden decompensation in a previously stable cirrhotic patient.

Assess liver reserve, portal hypertension, ascites and performance status.

At-risk patients undergo surveillance, commonly ultrasound with or without AFP every six months depending on guideline. Characteristic multiphasic CT/MRI enhancement can diagnose HCC non-invasively in appropriate high-risk patients.

Potentially curative options include resection, ablation and transplantation in selected early disease. Locoregional and systemic therapies are used according to stage and liver reserve within multidisciplinary care.

Budd–Chiari syndrome is hepatic venous outflow obstruction from hepatic veins to the IVC, usually thrombotic and often associated with an underlying prothrombotic disorder.

Abdominal pain, hepatomegaly and ascites form the classic triad; presentation ranges from acute liver failure to chronic portal hypertension.

Assess tender hepatomegaly, ascites and signs of portal hypertension.

Doppler ultrasound is first-line; CT/MRI confirms anatomy. Investigate myeloproliferative neoplasm, antiphospholipid syndrome and other thrombophilias.

Anticoagulate unless contraindicated and treat the underlying prothrombotic state. Use a step-up approach with angioplasty/stenting, TIPS and transplantation for persistent or advanced disease.

Liver transplantation replaces a failing liver and is definitive therapy for selected decompensated cirrhosis, acute liver failure, HCC and certain metabolic/cholestatic disorders.

Referral should occur before irreversible multiorgan deterioration. Recurrent decompensation, rising MELD-based risk, refractory ascites, HRS or HCC within transplant pathways are important triggers.

Assess frailty, nutrition, cardiopulmonary fitness, infection, malignancy and psychosocial/adherence factors.

Evaluation defines disease severity, contraindications, vascular anatomy and comorbidity. Allocation systems vary by region and use urgency/benefit frameworks.

Optimise nutrition, complications and vaccination while awaiting transplant. After transplantation, lifelong immunosuppression and surveillance for rejection, infection, metabolic disease and malignancy are required.

AKI is an abrupt fall in kidney function identified by a rise in serum creatinine and/or reduced urine output. Classify causes as prerenal, intrinsic renal or postrenal while assessing severity and complications.

Ask about volume loss, sepsis, hypotension, nephrotoxins, contrast, urinary obstruction, systemic disease and baseline renal function. Oliguria is important but non-oliguric AKI is common.

Assess haemodynamics, volume status, JVP, oedema, bladder distension, rash, joints and systemic clues. Look immediately for pulmonary oedema, encephalopathy and arrhythmia.

Trend creatinine and urine output; obtain urinalysis with microscopy, electrolytes and ultrasound when obstruction is plausible. Urine sediment can distinguish tubular, glomerular and interstitial patterns.

Restore perfusion when deficient, stop nephrotoxins, treat sepsis/obstruction and adjust drug doses. Dialysis is indicated for refractory life-threatening electrolyte, acid-base, volume or uraemic complications rather than a creatinine number alone.

CKD is abnormal kidney structure or function present for at least three months with health implications. It is staged by cause, GFR category and albuminuria category.

Patients may remain asymptomatic until advanced disease. Ask diabetes, hypertension, cardiovascular disease, nephrotoxins, family history and urinary abnormalities.

Assess BP, volume status, vascular disease, neuropathy, anaemia and signs of systemic or hereditary renal disease.

Use eGFR and urine albumin-to-creatinine ratio together for risk stratification. Evaluate electrolytes, bicarbonate, CBC, mineral-bone parameters and renal ultrasound according to stage/cause.

Treat the cause, control BP, use ACEI/ARB for appropriate albuminuric disease and SGLT2 inhibitors in eligible CKD, manage cardiovascular risk and avoid nephrotoxins. Refer for advanced CKD, rapid progression or uncertain diagnosis.

Proteinuria is excess urinary protein; albuminuria is particularly important as a marker of glomerular injury and cardiovascular/renal risk.

Ask diabetes, hypertension, oedema, systemic autoimmune disease, infection and drugs. Transient proteinuria can occur with fever, exercise or acute illness.

Check BP, oedema and systemic signs of glomerular or vascular disease.

Quantify with spot urine ACR for albumin and PCR when broader protein quantification is needed. Confirm persistent abnormality and examine urine sediment; nephrotic-range proteinuria requires evaluation of cause.

Treat the underlying disorder and optimise BP. ACEI/ARB and SGLT2-based kidney-protective therapy are used in appropriate albuminuric CKD; significant unexplained proteinuria may require nephrology review/biopsy.

Haematuria may be glomerular or non-glomerular and can represent renal inflammation, stones, infection or urinary tract malignancy.

Ask visible versus microscopic blood, dysuria, colic, clots, exercise, anticoagulation and systemic symptoms. Cola-coloured urine without clots favours glomerular bleeding.

Assess BP, oedema, abdominal/flank mass, rash and systemic disease.

Urinalysis with microscopy is pivotal: dysmorphic RBCs and RBC casts suggest glomerular bleeding. Quantify protein and assess renal function; urologic imaging/cystoscopy is guided by age and malignancy risk.

Treat the cause. Glomerular haematuria with proteinuria, reduced GFR or hypertension needs nephrologic evaluation; visible unexplained haematuria often requires urologic assessment.

Nephritic syndrome reflects inflammatory glomerular injury causing haematuria, variable proteinuria, reduced GFR, hypertension and salt retention.

Patients may develop cola-coloured urine, oliguria, oedema and hypertension following infection or with systemic autoimmune/vasculitic symptoms.

Assess BP, volume overload, rash, arthritis, pulmonary haemorrhage and infection clues.

Urine shows dysmorphic RBCs/RBC casts. Check creatinine, complement, ANA, ANCA, anti-GBM and infection-related studies as indicated; renal biopsy is often decisive.

Control BP/volume and treat the specific glomerulonephritis. Rapidly progressive disease requires urgent nephrology input and cause-specific immunosuppression/plasma exchange in selected conditions.

Nephrotic syndrome consists of heavy proteinuria, hypoalbuminaemia, oedema and often hyperlipidaemia, with increased thrombotic and infectious risk.

Progressive oedema and frothy urine are common. Ask diabetes, autoimmune disease, malignancy, infection and implicated drugs.

Assess generalised oedema, ascites, BP, thrombosis and signs of secondary disease.

Quantify proteinuria, serum albumin/lipids and renal function; evaluate secondary causes and perform renal biopsy when indicated by age/context.

Use sodium restriction and diuretics for oedema, kidney-protective antiproteinuric therapy and disease-specific treatment. Anticoagulation is individualised by thrombosis versus bleeding risk.

RPGN is a clinical syndrome of rapidly declining renal function with nephritic urine sediment, usually associated histologically with crescentic glomerulonephritis.

Symptoms may include haematuria, oliguria and systemic vasculitic features; pulmonary haemorrhage suggests pulmonary-renal syndrome.

Look for volume overload, purpura, sinus/ENT disease, neuropathy and respiratory bleeding.

Urgently check ANCA, anti-GBM, complements, ANA and infection testing as appropriate, while arranging renal biopsy. Do not delay critical therapy in a strongly suspected life-threatening syndrome.

Treatment depends on cause and commonly requires high-dose glucocorticoid plus additional immunosuppression; plasma exchange has specific indications such as anti-GBM disease and selected severe scenarios.

Diabetic kidney disease is CKD attributable to diabetes, typically manifested by persistent albuminuria and/or reduced eGFR and carrying high cardiovascular risk.

Usually asymptomatic initially. Review glycaemic history, BP, retinopathy, cardiovascular disease and medication use.

Assess BP, oedema, peripheral vascular disease and diabetic complications.

Measure eGFR and urine ACR at recommended intervals. Atypical features—active sediment, abrupt GFR loss or very rapid proteinuria—should prompt consideration of non-diabetic kidney disease.

Optimise glucose and BP, use ACEI/ARB for hypertension with albuminuria, SGLT2 inhibitor in eligible patients and finerenone in selected persistent albuminuric type 2 diabetes; manage lipids and cardiovascular risk.

Chronic hypertension can cause and accelerate CKD through vascular and glomerular injury; kidney disease can in turn worsen hypertension.

Often silent until CKD is established. Resistant or abrupt hypertension should raise suspicion of secondary renal/renovascular disease.

Measure BP accurately, assess volume status, bruits, retinopathy and vascular disease.

Use creatinine/eGFR, urine ACR and urinalysis; ultrasound and renovascular testing are selected when clinical clues justify them.

Achieve guideline-appropriate BP control with lifestyle and pharmacotherapy. ACEI/ARB is particularly useful with albuminuria; avoid dual renin-angiotensin blockade.

Acute tubular injury is a common intrinsic cause of AKI due to ischemic or nephrotoxic tubular damage.

Typical settings include prolonged hypotension/sepsis, major surgery, pigment injury and nephrotoxins. Creatinine may continue to rise after the initiating insult.

Assess volume/perfusion and signs of the precipitating illness rather than assuming persistent hypovolaemia.

Urine microscopy may show granular 'muddy brown' casts and tubular epithelial cells. Fractional indices can support but are unreliable in several clinical contexts.

Correct the precipitant, optimise haemodynamics, avoid further nephrotoxicity and manage complications. Repeated fluid loading is harmful once adequate perfusion is restored.

AIN is inflammatory injury of the renal interstitium, most often drug-induced but also related to infection or autoimmune disease.

AKI develops after exposure to drugs such as antibiotics, PPIs or NSAIDs; fever, rash and eosinophilia form a classic but uncommon triad.

Look for rash, fever, arthralgia and signs of the underlying systemic disorder.

Urinalysis may show pyuria, WBC casts, haematuria and mild-moderate proteinuria. Eosinophiluria is neither sensitive nor specific; biopsy is used when diagnosis is uncertain or severe.

Stop the offending agent promptly and provide supportive care. Corticosteroids are considered in selected biopsy-supported or strongly suspected persistent cases after infection is excluded.

RTA comprises disorders of renal acid handling causing normal-anion-gap metabolic acidosis with relatively preserved GFR.

Distal type 1 may cause stones/hypokalaemia; proximal type 2 causes bicarbonate wasting; type 4 is associated with hypoaldosteronism and hyperkalaemia.

Assess volume, muscle weakness, stones and features of autoimmune disease or diabetes.

Confirm normal-gap acidosis, assess potassium and urine pH/urinary ammonium surrogates in context. Exclude diarrhoeal bicarbonate loss.

Treat the underlying cause and provide alkali replacement in types 1/2. Type 4 management focuses on hyperkalaemia, medication review and selected alkali/diuretic/mineralocorticoid strategies.

Hyperkalaemia is potentially life-threatening because elevated extracellular potassium alters cardiac conduction and neuromuscular function.

Symptoms may be absent or include weakness/palpitations. Ask CKD, RAAS blockers, potassium-sparing drugs, tissue breakdown and acidosis.

Assess haemodynamics, muscle weakness and obtain ECG promptly in significant hyperkalaemia.

Repeat a potentially haemolysed sample when clinically safe, but do not delay treatment for severe hyperkalaemia. ECG can progress from peaked T waves to QRS widening/sine-wave, yet may be deceptively normal.

With ECG toxicity or severe hyperkalaemia, stabilise myocardium with IV calcium, shift potassium intracellularly with insulin-glucose and beta2 agonist, and remove potassium using diuretics, binders or dialysis according to context.

Hypokalaemia results from reduced intake, intracellular shift or—most commonly—renal/GI losses and can cause arrhythmia and muscle weakness.

Ask vomiting, diarrhoea, diuretics, laxatives, insulin/beta-agonists and hypertension suggesting mineralocorticoid excess.

Assess weakness, ileus and rhythm disturbance.

Check magnesium, acid-base status and urinary potassium when the cause is unclear. ECG may show ST depression, T-wave flattening and U waves.

Replace potassium orally when feasible; use monitored IV replacement for severe/symptomatic cases. Correct magnesium deficiency because it can make hypokalaemia refractory.

Hyponatraemia is excess water relative to sodium and should first be classified by measured serum osmolality and then by volume/ADH physiology.

Neurologic symptoms depend on severity and speed of onset, ranging from nausea/headache to seizures and coma.

Assess volume status, neurological state and medication/endocrine contributors.

Confirm hypotonicity, then use urine osmolality and urine sodium in context; exclude hyperglycaemia and consider adrenal/thyroid disease where appropriate.

Severe symptomatic hyponatraemia requires controlled hypertonic saline boluses with frequent sodium monitoring. Chronic cases are treated according to cause while avoiding overcorrection; desmopressin may be used to control an excessive correction trajectory.

Hypernatraemia represents a relative water deficit and usually reflects impaired access to water, excessive water loss or, less often, sodium gain.

Thirst, weakness, confusion, seizures or coma may occur; vulnerable elderly, neurologically impaired and critically ill patients are at greatest risk.

Assess volume status, mental state, urine output and access to water.

Measure serum/urine osmolality and urine volume to distinguish renal from extrarenal water loss and evaluate diabetes insipidus. Estimate free-water deficit as a guide, not a substitute for serial measurements.

Restore circulation first with isotonic fluid if shocked, then replace free water gradually and treat ongoing losses. Chronic hypernatraemia should generally be corrected cautiously with frequent sodium checks.

Metabolic acidosis is a primary reduction in bicarbonate and is classified into high-anion-gap and normal-anion-gap disorders.

Causes of high-gap acidosis include lactate, ketoacids, renal failure and toxins; normal-gap causes include GI bicarbonate loss and RTA.

Assess perfusion, respiratory compensation, toxin clues and underlying sepsis/renal disease.

Calculate anion gap corrected for albumin and use expected respiratory compensation to detect mixed disorders. Lactate, ketones, renal tests and toxicology are targeted to cause.

Treat the cause and restore perfusion. Bicarbonate is reserved for selected severe acidemia or specific indications rather than routine correction of every low bicarbonate.

Metabolic alkalosis is a primary rise in bicarbonate maintained by chloride depletion, volume contraction, potassium deficiency, mineralocorticoid excess or impaired renal bicarbonate excretion.

Vomiting, nasogastric loss and diuretics are common causes. Hypertension with hypokalaemia suggests mineralocorticoid excess.

Assess volume status, BP and signs of gastric losses or endocrine disease.

Urine chloride helps distinguish chloride-responsive from chloride-resistant alkalosis, interpreted with recent diuretic exposure.

Correct the cause, potassium and chloride deficits. Saline is effective in appropriate chloride-responsive volume-depleted states; mineralocorticoid-driven disease requires specific therapy.

Kidney stones cause urinary obstruction and renal colic; calcium oxalate is the commonest composition, but uric acid, struvite and cystine stones have distinct associations.

Severe colicky flank pain radiating to groin, nausea and haematuria are typical. Fever with obstruction is a urologic emergency.

Assess fever, haemodynamics, CVA tenderness and signs of sepsis.

Non-contrast CT is highly sensitive; ultrasound is preferred in pregnancy and useful for hydronephrosis. Recurrent/high-risk stone formers need metabolic evaluation including stone analysis and 24-hour urine studies.

Provide analgesia and hydration to euvolaemia; selected ureteric stones may receive medical expulsive therapy. Infected obstruction requires urgent drainage plus antibiotics. Prevention is tailored to stone type, with adequate fluid intake foundational.

UTI ranges from lower urinary infection to pyelonephritis involving renal parenchyma; complicated infection is shaped by host and structural factors.

Dysuria/frequency suggest cystitis; fever, flank pain, nausea and systemic illness suggest pyelonephritis.

Assess sepsis, CVA tenderness, hydration and obstruction risk.

Urinalysis supports diagnosis and urine culture is important in pyelonephritis/complicated infection. Imaging is indicated for obstruction, stones, severe sepsis or failure to improve.

Choose antibiotics based on syndrome, local resistance, prior cultures and renal function. Severe pyelonephritis needs systemic therapy; drain an infected obstructed collecting system urgently.

Autosomal dominant polycystic kidney disease is an inherited cystic disorder causing progressive CKD and extrarenal manifestations.

Hypertension, flank pain, haematuria, stones and cyst infection may occur; ask family history of kidney failure and intracranial aneurysm.

Assess BP, abdominal masses and valvular/cardiovascular findings.

Ultrasound or cross-sectional imaging establishes diagnosis using age/family-context criteria. Risk stratification can use kidney volume/genotype and clinical progression.

Control BP, manage CKD complications and counsel on inheritance. Tolvaptan can slow progression in selected adults at risk of rapid progression; aneurysm screening is targeted to risk rather than universal.

Kidney replacement therapy supports solute, acid-base and volume control when native renal function is inadequate; modalities include intermittent haemodialysis, continuous therapies and peritoneal dialysis.

Indications arise from clinical complications rather than an isolated urea/creatinine value.

Assess refractory pulmonary oedema, uraemic complications, haemodynamic stability and vascular/peritoneal access considerations.

Use the classic emergency framework: refractory Acidosis, dangerous Electrolyte disturbance, selected Intoxications, refractory fluid Overload and symptomatic Uraemia, while integrating overall trajectory.

Choose modality according to haemodynamics, neurological status, catabolic burden, resources and patient goals. Chronic modality choice should use shared decision-making and transplant planning.

Haemodialysis can cause intradialytic hypotension, cramps, arrhythmia, access problems, infection and dialysis disequilibrium, alongside long-term cardiovascular complications.

Symptoms during dialysis—dizziness, nausea, chest pain, dyspnoea or headache—require immediate physiological assessment rather than assumption of a benign reaction.

Check BP, rhythm, volume status and vascular access for bleeding/infection.

Review ultrafiltration rate, electrolytes, ECG and access function; blood cultures are needed when catheter-related infection is suspected.

Treat the specific complication: reduce ultrafiltration and support BP for intradialytic hypotension, manage electrolyte/rhythm abnormalities and treat access infection urgently. Prevent excessive interdialytic weight gain and inappropriate ultrafiltration rates.

CKD-MBD is a systemic disorder of mineral metabolism involving phosphate, calcium, PTH, vitamin D, bone turnover and vascular calcification.

It is often asymptomatic until advanced disease; fractures, bone pain and vascular calcification reflect late consequences.

Assess skeletal symptoms, vascular disease and signs of severe secondary hyperparathyroidism.

Monitor calcium, phosphate, PTH and alkaline phosphatase according to CKD stage and trends; interpret values together rather than targeting a single laboratory number.

Manage phosphate burden, dietary intake and binders when indicated; use vitamin D compounds or calcimimetics selectively based on stage and PTH pattern. Avoid hypercalcaemia and unnecessary calcium loading.

CKD anaemia is mainly caused by inadequate erythropoietin production, with iron deficiency, inflammation, blood loss and nutrient deficiency frequently contributing.

Fatigue, reduced exercise tolerance and dyspnoea are common but nonspecific.

Assess pallor, bleeding, nutritional status and volume overload.

Check CBC, reticulocyte context, ferritin and transferrin saturation; exclude iron, B12/folate deficiency and occult blood loss before attributing anaemia solely to CKD.

Replete iron when deficient and consider erythropoiesis-stimulating therapy in appropriate patients after individual risk-benefit assessment. Avoid targeting a normal haemoglobin with high ESA doses.

Diabetes mellitus is chronic hyperglycaemia caused by impaired insulin secretion, insulin action or both. Correct classification matters because type 1 diabetes requires lifelong insulin whereas type 2 diabetes is managed according to metabolic and cardiorenal phenotype.

Ask polyuria, polydipsia, weight loss, recurrent infection, visual symptoms, medications and family history. Rapid weight loss, ketosis or presentation at a young age raises concern for insulin deficiency.

Assess BMI/waist, BP, hydration, acanthosis, feet, peripheral pulses and neuropathy. Look for autoimmune disease when type 1 diabetes is suspected.

Diagnosis uses validated plasma glucose or HbA1c criteria, with repeat confirmation when unequivocal hyperglycaemia is absent. Check renal function, urine albumin, lipids and complications; C-peptide/autoantibodies help when diabetes type is uncertain.

Individualise glycaemic targets. Combine nutrition, activity and weight management with glucose-lowering therapy; select SGLT2 inhibitors and/or GLP-1 receptor agonist therapy when cardiorenal or weight benefits are important, and use insulin whenever clinically required.

Type 1 diabetes results from autoimmune beta-cell destruction causing absolute insulin deficiency and a lifelong risk of ketosis.

Polyuria, polydipsia, weight loss and fatigue may progress to DKA. Autoimmune thyroid or coeliac disease can coexist.

Assess hydration, weight, injection sites, glucose-monitoring practices and complications; look for signs of ketosis during acute illness.

Plasma glucose/HbA1c establish diabetes. Islet autoantibodies support autoimmune type 1 disease; C-peptide helps assess endogenous insulin when classification is uncertain.

Use physiologic basal-bolus insulin or pump therapy with carbohydrate education and glucose monitoring/CGM. Teach hypoglycaemia treatment, ketone testing and sick-day rules; insulin must not be stopped during illness.

Type 2 diabetes is characterised by insulin resistance with progressive beta-cell dysfunction and is strongly associated with obesity, metabolic dysfunction and cardiovascular-kidney disease.

Many patients are asymptomatic; others have osmotic symptoms or present through complications. Review diet, activity, weight trajectory and cardiovascular/renal disease.

Assess adiposity, BP, acanthosis, feet, pulses and evidence of microvascular or macrovascular complications.

Use glucose/HbA1c for diagnosis and monitor kidney function, albuminuria, lipids, retinal and foot status. Consider alternative diabetes types when phenotype is atypical.

Lifestyle and weight management remain foundational. Metformin is widely used when appropriate, but therapy should prioritise agents with proven cardiovascular, kidney or weight benefits when those indications exist; insulin is appropriate for severe symptomatic hyperglycaemia or marked insulin deficiency.

DKA is an acute insulin-deficient state causing hyperglycaemia, ketonaemia and metabolic acidosis; euglycaemic DKA can occur, particularly with SGLT2 inhibitors.

Polyuria, vomiting, abdominal pain, dehydration and Kussmaul breathing are typical; altered consciousness suggests severe disease or another process.

Assess ABCs, perfusion, mental status, volume depletion and precipitating infection, infarction or insulin omission.

Measure glucose, electrolytes, venous/arterial pH, bicarbonate and blood beta-hydroxybutyrate when available. Correct sodium interpretation and serial potassium monitoring are essential.

Give isotonic fluid, IV insulin and potassium according to level/urine output; add dextrose once glucose falls so insulin can continue until ketoacidosis resolves. Treat the precipitant and transition to subcutaneous insulin with overlap.

HHS is severe hyperglycaemia with hyperosmolality and profound dehydration, usually with little or no significant ketoacidosis.

Evolution is often slower than DKA, with polyuria followed by marked dehydration, weakness and neurological dysfunction.

Assess volume depletion, haemodynamics and mental status carefully; search for infection, MI, stroke and medication triggers.

Measure glucose, electrolytes, osmolality, renal function and ketones. Corrected sodium and effective osmolality guide fluid/electrolyte management.

Fluid replacement is the initial priority, followed by potassium-guided insulin therapy and gradual correction of osmolality. Prevent overly rapid osmotic shifts and treat the precipitating illness.

Hypoglycaemia is clinically important low glucose, especially in insulin- or secretagogue-treated diabetes. Severe hypoglycaemia is defined by need for assistance rather than a glucose threshold alone.

Autonomic symptoms include sweating, tremor and palpitations; neuroglycopenia causes confusion, behavioural change, seizure or coma.

Assess airway and consciousness immediately and look for insulin/sulfonylurea exposure, alcohol, renal failure or sepsis.

Confirm glucose when possible without delaying treatment. In recurrent unexplained episodes, obtain critical-sample glucose, insulin, C-peptide and related studies during hypoglycaemia.

Give oral fast carbohydrate if conscious and able to swallow; severe episodes require IV glucose or glucagon when IV access is unavailable. Identify the cause and adjust therapy to prevent recurrence.

Chronic hyperglycaemia damages retinal, renal and peripheral/autonomic neural microvasculature; risk is strongly influenced by duration, glycaemic exposure and BP.

Ask visual change, sensory loss, neuropathic pain, autonomic symptoms and kidney disease. Complications may be asymptomatic until advanced.

Perform foot/neurologic assessment, BP and appropriate eye surveillance; inspect for ulcers and loss of protective sensation.

Screen urine ACR/eGFR and perform guideline-based retinal assessment. Neuropathy is primarily clinical after excluding important mimics.

Optimise glycaemia and BP, use kidney-protective therapy where indicated, manage lipids/smoking and provide foot care. Treat painful neuropathy symptomatically while protecting insensate feet.

Hypothyroidism is deficient thyroid hormone action, most commonly primary autoimmune thyroid failure in iodine-sufficient settings.

Fatigue, cold intolerance, constipation, weight gain, dry skin and menstrual disturbance are common but nonspecific.

Look for bradycardia, delayed reflex relaxation, dry/coarse skin, goitre or prior thyroid surgery/radiation.

Primary hypothyroidism typically shows elevated TSH with low free T4; subclinical disease has elevated TSH with normal free T4. Central hypothyroidism requires free T4-based interpretation because TSH may be misleading.

Levothyroxine is standard therapy, dosed according to age, weight, cardiac status and severity, with TSH-guided titration in primary disease. Separate dosing from interfering iron/calcium when possible.

Thyrotoxicosis is excess thyroid-hormone action; hyperthyroidism specifically implies increased thyroid hormone synthesis, as in Graves disease or toxic nodular disease.

Weight loss, heat intolerance, tremor, palpitations and frequent stools are common. Graves may cause eye disease and diffuse goitre.

Assess pulse/rhythm, tremor, goitre/nodules, eye signs, proximal weakness and heart failure.

Low TSH with elevated free T4 and/or T3 confirms overt thyrotoxicosis. TSH-receptor antibodies and radionuclide uptake/imaging distinguish Graves, toxic nodules and thyroiditis when needed.

Beta blockade controls adrenergic symptoms. Antithyroid drugs, radioactive iodine or surgery treat hyperthyroidism according to cause and patient factors; thyroiditis generally does not benefit from antithyroid synthesis inhibitors.

Thyroid storm is life-threatening decompensated thyrotoxicosis with systemic dysfunction, commonly triggered by infection, surgery or interruption of treatment.

High fever, marked tachycardia/AF, agitation/delirium, vomiting/diarrhoea, heart failure and hepatic dysfunction are characteristic.

Assess ABCs, temperature, rhythm, heart failure, volume status and CNS dysfunction.

Diagnosis is clinical; thyroid hormone concentrations may not be dramatically higher than uncomplicated thyrotoxicosis. Search aggressively for a precipitant.

Use ICU supportive care, beta blockade when haemodynamically appropriate, thionamide to block synthesis, iodine after thionamide to block release, and glucocorticoid; treat the precipitating illness.

Most thyroid nodules are benign; evaluation aims to identify clinically significant thyroid cancer and autonomous hormone production without unnecessary biopsy.

Ask growth, dysphagia, voice change, radiation exposure and family history of thyroid cancer syndromes.

Assess size, fixation, cervical nodes and compressive signs.

Measure TSH and perform high-quality ultrasound risk stratification. A suppressed TSH may prompt radionuclide scanning; FNA decisions depend on ultrasound pattern and nodule size rather than size alone.

Observe low-risk nodules with appropriate surveillance; suspicious cytology/molecular profiles are managed surgically or by specialist pathways. Hyperfunctioning nodules are treated according to thyrotoxicosis strategy.

Primary adrenal insufficiency is failure of the adrenal cortex causing cortisol deficiency and usually aldosterone deficiency; autoimmune adrenalitis is a major cause.

Fatigue, weight loss, postural dizziness, abdominal symptoms and salt craving are common. Hyperpigmentation reflects elevated ACTH.

Assess hypotension/orthostasis, dehydration and pigmentation of creases/scars/mucosa.

Low morning cortisol with elevated ACTH raises suspicion; ACTH stimulation testing confirms many cases. Hyponatraemia, hyperkalaemia and elevated renin may support mineralocorticoid deficiency.

Replace glucocorticoid and, in primary disease, mineralocorticoid as needed. Teach stress dosing, emergency steroid use and medical-alert identification.

Adrenal crisis is acute life-threatening cortisol deficiency causing shock and metabolic disturbance, often precipitated by infection, surgery or abrupt steroid withdrawal.

Vomiting, abdominal pain, weakness, hypotension, confusion, fever and hypoglycaemia may occur.

Assess ABCs, shock, dehydration and the precipitating illness.

Draw cortisol/ACTH if this does not delay therapy; check glucose and electrolytes. Treatment must never await confirmatory testing when crisis is suspected.

Give immediate parenteral hydrocortisone and rapid isotonic saline, adding dextrose for hypoglycaemia as required; treat the precipitant.

Cushing syndrome is chronic pathological glucocorticoid excess; exogenous corticosteroid exposure is the commonest overall cause.

Progressive central adiposity, proximal weakness, easy bruising, wide purple striae, diabetes, hypertension, osteoporosis and mood change are suggestive.

Look for facial plethora, supraclavicular fullness, thin skin, bruising, myopathy and infection risk.

First exclude exogenous steroids. Screen endogenous disease with validated tests such as overnight dexamethasone suppression, late-night salivary cortisol or 24-hour urinary free cortisol; ACTH then guides localisation.

Treat the source—pituitary, adrenal or ectopic—usually with surgery when feasible; medical cortisol-lowering therapy is used in selected persistent, severe or inoperable disease.

Primary aldosteronism is autonomous aldosterone production causing sodium retention, hypertension and potassium wasting; it is a common potentially treatable cause of secondary hypertension.

Suspect resistant hypertension, hypertension with spontaneous/diuretic-induced hypokalaemia, adrenal incidentaloma or relevant family history.

Assess BP and consequences of chronic hypertension; many patients are normokalaemic.

Screen with aldosterone-renin ratio under appropriate conditions and medication interpretation. Confirmatory testing and adrenal CT/adrenal-vein sampling are used to distinguish unilateral from bilateral disease when surgery is considered.

Unilateral disease is often treated with adrenalectomy; bilateral disease is treated with mineralocorticoid receptor antagonists such as spironolactone or eplerenone.

PPGLs are catecholamine-producing neuroendocrine tumours arising from adrenal medulla or extra-adrenal paraganglia and may be hereditary.

Episodic headache, sweating and palpitations with paroxysmal or sustained hypertension are classic but not universal.

Assess BP including episodic patterns and look for features of associated genetic syndromes.

Measure plasma free or urinary fractionated metanephrines under appropriate sampling conditions. Localise with CT/MRI after biochemical evidence; genetic evaluation is important in many patients.

Definitive therapy is surgical when appropriate, preceded by adequate alpha blockade and volume preparation. Beta blockade, if needed, is introduced only after alpha blockade.

Pituitary adenomas may cause hormone hypersecretion, hypopituitarism or mass effect; clinically important functional types include prolactin-, GH- and ACTH-secreting tumours.

Ask headache, visual loss, galactorrhoea, menstrual/sexual dysfunction and features of acromegaly or Cushing disease.

Assess visual fields, cranial nerves and phenotype of hormone excess/deficiency.

Obtain pituitary hormone profile and dedicated MRI. Formal visual-field testing is required when the lesion approaches/compresses the optic chiasm.

Treatment depends on subtype: dopamine agonists are first-line for most prolactinomas; transsphenoidal surgery is first-line for many other symptomatic/functional adenomas, with medical/radiation options as needed.

Acromegaly is chronic GH excess after epiphyseal closure, usually from a pituitary somatotroph adenoma, producing elevated IGF-1 and multisystem morbidity.

Progressive enlargement of hands/feet, coarse facial features, sweating, headache, sleep apnoea, diabetes and arthropathy are common.

Look for prognathism, widened interdental spacing, macroglossia, large hands and visual-field defects.

Screen with age-adjusted IGF-1; confirm inappropriate GH suppression with oral glucose testing when required and perform pituitary MRI after biochemical diagnosis.

Transsphenoidal surgery is preferred for resectable pituitary disease. Somatostatin receptor ligands, pegvisomant or other medical therapy and radiotherapy are used for persistent disease.

Hyperprolactinaemia may result from prolactinoma, medications, hypothyroidism, pregnancy, renal disease or pituitary stalk interruption.

Women may have galactorrhoea, amenorrhoea and infertility; men often present with sexual dysfunction or mass effects.

Assess visual fields when a macroadenoma is possible and look for hypothyroidism or medication causes.

Confirm prolactin, exclude pregnancy where relevant, review drugs and TSH, and obtain pituitary MRI when persistent unexplained elevation is significant. Consider macroprolactin and the assay hook effect in selected discordant cases.

Dopamine agonists—especially cabergoline—are first-line for most symptomatic prolactinomas and often shrink the tumour dramatically.

Diabetes insipidus causes excretion of large volumes of dilute urine due to deficient vasopressin secretion (central) or renal resistance (nephrogenic).

Polyuria, polydipsia and nocturia are typical; hypernatraemia develops when water access is impaired.

Assess hydration, mental status and true urine volume; distinguish polyuria from urinary frequency.

Confirm hypotonic polyuria with paired serum/urine osmolality. Water-deprivation/desmopressin testing or copeptin-based pathways distinguish central DI, nephrogenic DI and primary polydipsia under specialist supervision.

Central DI is treated with desmopressin and adequate water access. Nephrogenic DI requires cause removal where possible, dietary solute reduction and selected thiazide/amiloride strategies.

SIADH is inappropriate antidiuretic hormone effect causing euvolaemic hypotonic hyponatraemia with inappropriately concentrated urine after exclusion of endocrine, renal and volume-related causes.

Symptoms reflect hyponatraemia severity and chronicity; causes include CNS/pulmonary disease, malignancy and many drugs.

Patients are clinically euvolaemic without substantial oedema or dehydration.

Confirm hypotonic hyponatraemia, urine osmolality >100 mOsm/kg and an inappropriately elevated urine sodium in context, while excluding adrenal insufficiency, severe hypothyroidism, renal failure and diuretic confounding.

Treat the cause and restrict fluid in many chronic cases; increase solute or use other specialist therapies when refractory. Severe symptomatic hyponatraemia requires controlled hypertonic saline regardless of cause.

Primary hyperparathyroidism is autonomous PTH secretion, usually from a single adenoma, producing hypercalcaemia and skeletal/renal effects.

Many patients are asymptomatic; stones, osteoporosis, constipation, neurocognitive symptoms and polyuria may occur.

Assess hydration, skeletal complications and nephrolithiasis history.

Confirm repeatedly elevated calcium corrected for albumin or ionised calcium with inappropriately high/non-suppressed PTH. Check renal function, vitamin D, urinary calcium and bone density; distinguish familial hypocalciuric hypercalcaemia when relevant.

Parathyroidectomy is definitive and recommended for symptomatic disease and patients meeting guideline criteria. Monitor selected mild asymptomatic disease when surgery is not undertaken.

Hypocalcaemia may result from hypoparathyroidism, vitamin D deficiency, CKD, pancreatitis or severe illness; acute falls increase neuromuscular excitability.

Perioral tingling, cramps, carpopedal spasm, seizures and prolonged QT may occur.

Assess Chvostek/Trousseau signs cautiously, airway spasm, tetany and postsurgical neck history.

Confirm corrected or ionised calcium and check magnesium, phosphate, PTH, vitamin D and renal function to determine mechanism.

Severe symptomatic hypocalcaemia requires monitored IV calcium; chronic hypoparathyroidism is managed with oral calcium and active vitamin D, while correcting magnesium and avoiding hypercalciuria.

Osteoporosis is skeletal fragility characterised by reduced bone strength and increased fracture risk; hip and vertebral fractures carry major morbidity.

Often silent until a fragility fracture. Assess menopause/age, glucocorticoids, low body weight, smoking, alcohol and secondary endocrine causes.

Measure height, kyphosis and fall risk; examine for secondary causes.

DXA T-score ≤−2.5 defines osteoporosis in appropriate postmenopausal women/older men, while a hip/vertebral fragility fracture can establish high risk regardless of BMD. FRAX supports risk estimation.

Ensure adequate calcium/vitamin D, resistance/weight-bearing activity and fall prevention. Use antiresorptive or anabolic therapy according to fracture risk, renal function and prior fractures, with planned reassessment rather than indefinite unreviewed treatment.

Obesity is a chronic relapsing disease of excess adiposity that increases diabetes, cardiovascular, sleep, hepatic and musculoskeletal risk; management should focus on health outcomes rather than appearance.

Assess weight trajectory, diet, activity, sleep, medications and complications. Endocrine causes are uncommon but should be tested when clinical features suggest them.

Measure BMI and waist where useful, BP and signs of metabolic complications; avoid attributing every symptom to body weight.

Screen for diabetes, dyslipidaemia, MASLD, OSA and other complications according to risk. Routine broad endocrine panels are unnecessary without clinical clues.

Use structured nutrition, physical activity, behavioural support and complication management. Evidence-based anti-obesity pharmacotherapy—including incretin-based agents where appropriate—and metabolic/bariatric surgery are effective options for eligible patients.

Classify polyarthritis by inflammatory versus non-inflammatory pattern, acute versus chronic onset, symmetry, joint distribution and extra-articular features.

Inflammatory disease causes prolonged morning stiffness, swelling and improvement with activity. Viral/crystal disease may be acute; chronic symmetric small-joint synovitis suggests RA.

Confirm true synovitis and examine skin, nails, eyes, entheses, dactylitis and systemic clues.

CBC and ESR/CRP are useful initial tests; RF/anti-CCP, ANA and infection testing should be phenotype-directed. Aspirate any acutely hot swollen joint when infection or crystals are possible.

Treat the cause and refer persistent inflammatory arthritis early because timely DMARD therapy prevents irreversible structural damage.

RA is a systemic autoimmune inflammatory synovitis capable of progressive erosive joint damage and extra-articular disease.

Typical disease is symmetric MCP, PIP and wrist polyarthritis with prolonged morning stiffness; DIP joints are usually spared.

Assess synovitis, deformity, nodules, tendon disease and cervical spine; examine lungs and eyes and assess cardiovascular risk.

Anti-CCP is relatively specific and prognostically useful; RF is less specific. ESR/CRP and imaging help assess activity and damage.

Start a DMARD early, commonly methotrexate when appropriate, using a treat-to-target strategy. Escalate to biologic or targeted DMARD therapy when control remains inadequate.

SLE is a heterogeneous autoimmune disease involving skin, joints, kidneys, blood, nervous system and other organs through autoantibody-mediated inflammation.

Photosensitivity, oral ulcers, non-erosive arthritis, cytopenias, serositis and renal or neurological disease occur in variable combinations.

Examine skin/scalp, oral cavity, joints, BP/oedema, cardiopulmonary and neurological systems.

ANA is sensitive but nonspecific. Anti-dsDNA, anti-Sm, complement, CBC, creatinine and urinalysis/protein quantify organ involvement and activity.

Hydroxychloroquine is foundational for most patients unless contraindicated. Organ-threatening disease requires appropriate immunosuppression while minimising cumulative glucocorticoid exposure.

Lupus nephritis is immune-complex glomerular disease in SLE and a major determinant of renal prognosis.

Proteinuria, haematuria, hypertension or declining renal function may occur, but clinically important nephritis can initially be subtle.

Assess BP, oedema, volume status and other evidence of active SLE.

Serial urinalysis, urine protein, creatinine, complements and anti-dsDNA are important; kidney biopsy usually defines histologic class when significant renal involvement is suspected.

Use renoprotective therapy plus class- and severity-directed immunosuppression, followed by maintenance therapy after response.

Axial spondyloarthritis is inflammatory disease predominantly affecting sacroiliac joints and spine and may occur before radiographic sacroiliitis is visible.

Inflammatory back pain usually begins young, improves with exercise and may cause night pain. Uveitis, psoriasis, IBD and enthesitis are important clues.

Assess spinal mobility, sacroiliac region, entheses, dactylitis, skin/nails and eyes.

HLA-B27 supports but does not diagnose disease. MRI can demonstrate active sacroiliitis before structural radiographic change; CRP can be normal.

Exercise and physiotherapy are central. NSAIDs are initial drug therapy; persistent active axial disease may require biologic or targeted treatment.

Ankylosing spondylitis is radiographic axial spondyloarthritis with established structural sacroiliac disease and potential spinal ankylosis.

Inflammatory low-back/buttock pain, morning stiffness and reduced spinal mobility are typical; anterior uveitis is a classic extra-articular manifestation.

Measure spinal movement and chest expansion and examine hips, entheses and eyes.

Pelvic radiographs demonstrate established sacroiliitis; MRI can identify active inflammation. HLA-B27 and CRP are supportive rather than definitive.

Regular exercise/postural physiotherapy and NSAIDs are first-line; persistent active disease warrants appropriate biologic or targeted therapy.

Psoriatic arthritis can involve peripheral joints, spine, entheses and digits in association with psoriasis.

Patterns include asymmetric oligoarthritis, symmetric polyarthritis, DIP disease and axial disease. Dactylitis is highly characteristic.

Search scalp, umbilicus and gluteal cleft for psoriasis; inspect nails for pitting or onycholysis and examine entheses.

Diagnosis is clinical with imaging support; inflammatory markers may be normal and RF can occasionally be positive.

Select therapy according to dominant musculoskeletal and skin domains; conventional DMARDs help peripheral arthritis while biologic/targeted agents treat more significant disease.

Reactive arthritis is sterile inflammatory arthritis occurring after certain gastrointestinal or genitourinary infections.

Acute asymmetric lower-limb oligoarthritis with enthesitis may follow diarrhoea or urethritis; conjunctivitis/uveitis and mucocutaneous lesions can coexist.

Examine joints, entheses, eyes, skin and oral/genital mucosa.

There is no single diagnostic test. Investigate relevant triggering infection when indicated and aspirate a hot joint to exclude septic/crystal disease.

Treat persistent active infection when present; NSAIDs are first-line for arthritis, with intra-articular steroids or DMARDs for persistent disease.

Gout is inflammatory arthritis caused by deposition of monosodium urate crystals from sustained hyperuricaemia.

Abrupt severe monoarthritis, especially first-MTP podagra, peaks within hours; recurrent disease may cause tophi and polyarthritis.

Look for intensely inflamed joints and tophi on ears, elbows, fingers and toes.

Synovial fluid showing needle-shaped strongly negatively birefringent crystals confirms gout. Serum urate can be normal during a flare.

Treat flares with NSAID, colchicine or glucocorticoid according to comorbidity. Long-term urate-lowering therapy, usually allopurinol, is titrated to target when indicated.

CPPD results from calcium pyrophosphate crystal deposition and can mimic gout, OA or chronic inflammatory arthritis.

Acute CPP crystal arthritis often affects the knee or wrist in older adults.

Assess the involved joint and consider metabolic associations in younger or atypical patients.

Synovial fluid shows rhomboid weakly positively birefringent crystals; radiographs may show chondrocalcinosis.

Acute attacks are treated with NSAIDs, colchicine or corticosteroids as appropriate; unlike gout, no established crystal-depleting therapy exists.

Septic arthritis is joint infection and a medical emergency because cartilage destruction and systemic sepsis may evolve rapidly.

Acute painful monoarthritis with fever is classic, but systemic features may be muted in elderly or immunosuppressed patients.

Look for effusion, warmth and markedly painful passive movement and search for skin, bloodstream or prosthetic-joint sources.

Urgent arthrocentesis for cell count, Gram stain, culture and crystals is essential; obtain blood cultures when appropriate.

Start empiric antibiotics promptly after cultures when feasible and arrange drainage/source control with specialist input.

PMR is an inflammatory syndrome in adults over 50 causing bilateral shoulder and often hip-girdle pain and stiffness without primary muscle injury.

Prominent morning stiffness and difficulty dressing or rising are typical; always ask for symptoms of giant-cell arteritis.

Shoulder/hip movement is pain-limited, but objective muscle power is preserved; assess temporal arteries and vision.

ESR/CRP are usually raised and CK is generally normal. Ultrasound may demonstrate bursitis or tenosynovitis.

Low-dose glucocorticoid typically gives substantial improvement; taper gradually and consider steroid-sparing therapy in relapsing disease.

GCA is granulomatous large- and medium-vessel vasculitis in adults over 50 with risk of irreversible visual loss.

New headache, scalp tenderness, jaw claudication and visual symptoms are key clues; PMR frequently coexists.

Assess temporal arteries, vision, pulses and BP in both arms.

ESR/CRP support diagnosis. Temporal-artery ultrasound or biopsy and large-vessel imaging are chosen according to presentation and expertise.

Begin high-dose glucocorticoid immediately when visual-threatening disease is suspected; do not delay treatment for biopsy. Steroid-sparing therapy such as tocilizumab is appropriate in selected cases.

Takayasu arteritis is granulomatous inflammation of the aorta and major branches, typically affecting younger women.

Constitutional inflammation may precede limb claudication, dizziness, pulse deficits or renovascular hypertension.

Compare bilateral arm BP, palpate pulses and listen for vascular bruits.

CTA, MRA or PET-based imaging defines vessel inflammation and stenotic disease; inflammatory markers may not perfectly track activity.

Glucocorticoids plus steroid-sparing immunosuppression treat active disease; revascularisation is preferably performed when inflammation is controlled.

AAV includes GPA, MPA and EGPA and causes pauci-immune small-vessel inflammation with potentially life-threatening renal and pulmonary disease.

ENT disease, pulmonary nodules or haemorrhage, rapidly progressive GN, neuropathy and purpura are key patterns; asthma/eosinophilia suggest EGPA.

Examine ENT tract, lungs, skin and peripheral nerves and assess renal involvement.

Urinalysis, creatinine, PR3/MPO-ANCA and imaging guide diagnosis; tissue biopsy is preferred when feasible and safe.

Organ-threatening disease requires remission induction using glucocorticoid-sparing regimens with rituximab or cyclophosphamide-based therapy followed by maintenance.

Behçet disease is variable-vessel inflammatory disease characterised by recurrent mucosal ulceration and systemic ocular, vascular, skin, joint or neurologic involvement.

Recurrent oral ulcers are common; genital ulcers, uveitis, erythema-nodosum-like lesions and thrombosis are major clues.

Examine oral/genital mucosa, skin, eyes and vascular/neurologic systems.

Diagnosis is clinical; no diagnostic autoantibody exists. Pathergy can provide supportive evidence in some populations.

Therapy is organ-directed, from colchicine for selected mucocutaneous/joint disease to immunosuppressive or biologic therapy for major-organ disease.

Systemic sclerosis is autoimmune vasculopathy with progressive fibrosis of skin and internal organs, broadly classified as limited or diffuse cutaneous disease.

Raynaud phenomenon commonly precedes skin thickening; reflux, ILD, pulmonary hypertension and renal crisis are important complications.

Assess skin thickening, digital ulcers, telangiectasia, BP and cardiopulmonary findings.

ANA is common; anticentromere and anti-topoisomerase I help phenotype risk. Screen appropriately for ILD and pulmonary hypertension.

Management is organ-specific using vasodilators, reflux therapy, immunomodulatory/antifibrotic approaches for selected ILD and PAH-directed treatment.

Scleroderma renal crisis is abrupt renal vascular injury in systemic sclerosis causing accelerated hypertension and AKI.

New severe hypertension, headache, visual symptoms, dyspnoea or rapidly rising creatinine are typical; microangiopathic haemolysis may occur.

Measure BP urgently and assess volume, cardiac and neurological complications.

Check creatinine, urinalysis, CBC, smear, platelets and haemolysis markers; biopsy is not routinely needed in a classic presentation.

Start an ACE inhibitor immediately, often rapidly titratable captopril, and escalate treatment appropriately; dialysis may be temporary in some patients.

Sjögren syndrome is systemic autoimmune disease targeting exocrine glands and may also involve nerves, lungs, kidneys and blood.

Dry eyes, dry mouth, dental caries and parotid enlargement are typical; fatigue, arthritis, neuropathy or RTA may occur.

Inspect oral dryness, dentition, salivary glands, eyes, joints, nodes and purpura.

Anti-Ro/SSA is important; objective ocular/salivary tests and minor salivary-gland biopsy are used when needed.

Use tear/saliva replacement, secretagogues when appropriate and meticulous dental care; systemic immunomodulation is reserved for significant extraglandular disease.

Inflammatory myopathies are immune-mediated muscle diseases including dermatomyositis, necrotising myopathy and antisynthetase syndromes.

Symmetric proximal weakness causes difficulty climbing stairs, rising or lifting arms; dysphagia, ILD and characteristic rashes may occur.

Test objective proximal power and inspect for heliotrope rash, Gottron papules and mechanic's hands.

CK, myositis antibodies, MRI/EMG and muscle or skin biopsy help define phenotype; assess malignancy risk in appropriate dermatomyositis patients.

Glucocorticoids with steroid-sparing immunosuppression are commonly used; severe/refractory disease may require IVIG or biologic strategies.

APS is an autoimmune thrombophilia defined by characteristic thrombosis and/or pregnancy morbidity with persistent antiphospholipid antibodies.

Venous or arterial thrombosis, recurrent pregnancy loss and placental complications are important presentations.

Assess thrombosis, livedo and associated autoimmune disease, especially SLE.

Test lupus anticoagulant, anticardiolipin and anti-beta2-glycoprotein I antibodies; persistence at least 12 weeks apart is required for classification.

Many thrombotic APS patients require long-term anticoagulation, commonly a vitamin K antagonist in high-risk disease; pregnancy therapy is phenotype-directed.

Fibromyalgia is a chronic nociplastic pain disorder with widespread pain, fatigue, sleep disturbance and cognitive symptoms without inflammatory tissue damage.

Persistent widespread pain commonly coexists with non-restorative sleep, headache, IBS or mood symptoms.

Diffuse tenderness may occur, but synovitis and objective inflammatory weakness are absent.

Diagnosis is clinical; extensive autoimmune testing is unnecessary without red flags, though targeted tests can exclude important mimics.

Education, graded aerobic/resistance activity, sleep optimisation and psychological strategies are foundational; selected neuromodulatory medicines may help.

Osteoarthritis is whole-joint degenerative disease involving cartilage, subchondral bone and synovium, commonly affecting knees, hips, hands and spine.

Pain is typically activity-related with brief morning stiffness; advanced disease causes functional limitation.

Look for crepitus, bony enlargement, restricted movement and Heberden/Bouchard nodes without prominent inflammatory synovitis.

Diagnosis is usually clinical; weight-bearing radiographs demonstrate joint-space narrowing, osteophytes and sclerosis when imaging is needed.

Exercise, weight management when relevant, education and topical/oral analgesic strategies are first-line; joint replacement is considered for severe refractory functional disease.

Raynaud phenomenon is episodic digital vasospasm triggered by cold or stress and may be primary or secondary to connective-tissue disease.

Attacks cause sharply demarcated colour change with numbness or pain; ulcers or tissue injury suggest secondary disease.

Inspect digits for ulcers, pits and sclerodactyly and assess nailfold capillaries and pulses.

Primary disease usually requires limited testing; ANA and nailfold capillaroscopy are useful when systemic sclerosis or another connective-tissue disease is suspected.

Keep warm, stop smoking and avoid vasoconstrictors; dihydropyridine calcium-channel blockers are first-line medication, while critical digital ischaemia requires urgent specialist therapy.

Sarcoidosis is a multisystem granulomatous disorder that may cause arthritis, periarthritis and erythema nodosum.

Löfgren syndrome combines acute ankle periarthritis/arthritis, erythema nodosum and bilateral hilar lymphadenopathy and often has a favourable course.

Examine ankles, skin, eyes, nodes and respiratory system.

Chest imaging is central; biopsy showing non-caseating granulomas supports diagnosis after excluding infectious and other granulomatous causes. Serum ACE is not diagnostic.

Many acute musculoskeletal cases respond to NSAIDs/supportive care; persistent or organ-threatening disease may require glucocorticoids and steroid-sparing therapy.

Anaemia is a reduction in haemoglobin below the appropriate reference range. A practical diagnostic approach begins with MCV and reticulocyte response, then integrates morphology and clinical context.

Ask bleeding, diet, drugs, chronic disease, renal disease, jaundice, transfusions and family history. Symptoms include fatigue, dyspnoea, palpitations and reduced exercise tolerance.

Assess pallor, tachycardia, flow murmur, jaundice, glossitis, koilonychia, lymph nodes and hepatosplenomegaly. Look specifically for the source of blood loss.

Start with CBC, RBC indices, reticulocyte count and peripheral smear. Ferritin/iron profile, B12/folate, renal/liver tests and haemolysis studies are selected according to the pattern.

Treat the underlying cause rather than haemoglobin alone. Transfusion is reserved for clinically significant anaemia according to symptoms, haemodynamics, comorbidity and severity.

Iron deficiency causes impaired haem synthesis and typically produces microcytic hypochromic anaemia; chronic blood loss is a major cause in adults.

Fatigue, pica, restless legs and exertional symptoms may occur. Ask menstrual and gastrointestinal blood loss, diet, pregnancy and malabsorption.

Look for pallor, koilonychia, angular cheilitis and glossitis, while actively searching for evidence of the cause.

Low ferritin is highly supportive; transferrin saturation falls and TIBC often rises. In inflammation, ferritin can be misleadingly normal or elevated.

Replace iron orally when feasible or intravenously when absorption, tolerance, severity or ongoing loss warrants it. Investigate unexplained iron deficiency, especially in adult men and postmenopausal women, for occult GI blood loss.

Megaloblastic anaemia results from impaired DNA synthesis, most commonly vitamin B12 or folate deficiency, producing ineffective haematopoiesis and macro-ovalocytes.

B12 deficiency may cause neuropathy, gait disturbance and cognitive symptoms; folate deficiency does not produce the classic neurological syndrome.

Look for pallor, glossitis, jaundice and neurological signs such as impaired vibration/proprioception.

CBC may show macrocytosis and pancytopenia; smear shows macro-ovalocytes and hypersegmented neutrophils. Measure B12/folate and investigate pernicious anaemia or malabsorption where appropriate.

Replace the deficient vitamin and treat the cause. If B12 deficiency is possible, do not give folate alone before adequately addressing B12 because haematologic improvement can mask ongoing neurological injury.

Inflammation increases hepcidin, restricting iron availability and reducing erythropoiesis, producing anaemia of inflammation that is often normocytic but can become microcytic.

Symptoms usually reflect both anaemia and the underlying infection, inflammatory disease, malignancy or chronic systemic illness.

Examination is directed toward the underlying inflammatory condition and severity of anaemia.

Serum iron and transferrin saturation are low, while ferritin is usually normal or elevated and TIBC tends to be low or normal. Mixed iron deficiency is common and may complicate interpretation.

Treat the underlying disease. Iron or erythropoiesis-stimulating therapy is used only in selected settings such as documented deficiency or specific CKD/oncology indications.

Haemolysis is premature RBC destruction and may be intravascular or extravascular, inherited or acquired.

Patients may have jaundice, dark urine, anaemia symptoms, gallstones or episodic crises triggered by infection or drugs.

Look for pallor, jaundice and splenomegaly and assess for thrombosis or underlying systemic disease.

Typical laboratory pattern is reticulocytosis, elevated LDH and indirect bilirubin with low haptoglobin. Smear morphology and direct antiglobulin testing help determine cause.

Treat the specific mechanism and provide supportive folate/transfusion when required. Severe immune haemolysis may require glucocorticoids and additional immunomodulatory therapy.

AIHA is antibody-mediated RBC destruction and is classified broadly into warm-antibody and cold-antibody disease.

Warm AIHA may be idiopathic or associated with autoimmune disease, lymphoid malignancy or drugs; cold disease can cause acrocyanosis and cold-triggered symptoms.

Assess jaundice, splenomegaly and evidence of autoimmune, infectious or lymphoproliferative disease.

Haemolysis markers establish RBC destruction and the direct antiglobulin test identifies immunoglobulin/complement coating patterns.

Warm AIHA is commonly treated initially with glucocorticoids, with rituximab or other therapy for refractory/relapsing disease. Cold agglutinin disease management includes cold avoidance and targeted therapy when clinically significant.

G6PD deficiency is an X-linked enzymatic defect that reduces RBC protection against oxidative stress and can cause episodic intravascular haemolysis.

Haemolysis may follow infection, fava beans or oxidant drugs, with jaundice and dark urine developing abruptly.

During a crisis assess pallor, jaundice, haemodynamics and renal complications.

Smear may show bite cells and blister cells; Heinz bodies require supravital staining. G6PD testing can be falsely normal during acute haemolysis because older deficient cells have already been destroyed.

Stop the oxidant trigger, treat infection and provide supportive care/transfusion when needed. Counsel patients regarding avoidable oxidant exposures.

Hereditary spherocytosis is an inherited RBC membrane disorder causing poorly deformable spherocytes and chronic extravascular haemolysis.

Anaemia, jaundice, splenomegaly and pigment gallstones vary in severity; parvovirus B19 can precipitate aplastic crisis.

Look for jaundice and splenomegaly and assess growth in younger patients.

CBC may show increased MCHC; smear demonstrates spherocytes. EMA-binding flow cytometry is a useful confirmatory test; DAT is negative, helping distinguish it from warm AIHA.

Folate support is used in chronic haemolysis. Splenectomy is reserved for selected moderate/severe disease after appropriate vaccination and counselling; it improves haemolysis but does not correct the membrane defect.

Sickle cell disease is caused by pathogenic haemoglobin S polymerisation under deoxygenated conditions, producing chronic haemolysis and recurrent vaso-occlusion.

Pain crises, acute chest syndrome, stroke, splenic dysfunction, infection and chronic organ injury are major manifestations.

Assess pain, oxygenation, hydration and signs of acute chest syndrome, stroke, infection or splenic sequestration during acute illness.

Diagnosis is established by haemoglobin analysis such as HPLC/electrophoresis. CBC/reticulocytes and organ-specific tests assess complications.

Acute crises require rapid analgesia, hydration to euvolaemia and treatment of the precipitant; transfusion is used for specific indications. Hydroxyurea reduces vaso-occlusive complications, while curative options include selected transplantation and newer gene-based therapies.

Thalassaemias are inherited disorders of alpha- or beta-globin synthesis causing microcytosis with variable ineffective erythropoiesis and haemolysis.

Severe beta-thalassaemia presents early with transfusion dependence, growth failure and skeletal expansion; trait is often asymptomatic.

Look for pallor, jaundice, hepatosplenomegaly and skeletal changes in severe disease.

CBC shows marked microcytosis; smear may show target cells. Iron studies prevent misdiagnosis as iron deficiency, and haemoglobin analysis/genetic testing defines subtype.

Trait usually needs no treatment. Transfusion-dependent disease requires regular transfusion, iron-chelation monitoring and complication surveillance; haematopoietic stem-cell transplantation can be curative in selected patients.

Aplastic anaemia is bone-marrow failure causing pancytopenia with a hypocellular marrow in the absence of malignant infiltration or major fibrosis.

Fatigue, infection and mucosal/skin bleeding reflect anaemia, neutropenia and thrombocytopenia. Splenomegaly is usually absent.

Assess pallor, fever/infection and bleeding; significant lymphadenopathy or splenomegaly suggests an alternative diagnosis.

CBC shows pancytopenia with low reticulocytes. Bone-marrow biopsy demonstrates hypocellularity; evaluate drugs/toxins, viral causes, PNH clone and inherited marrow-failure syndromes where relevant.

Severe disease requires specialist therapy with stem-cell transplantation in suitable patients or immunosuppressive therapy such as antithymocyte globulin plus ciclosporin with thrombopoietin-receptor agonist strategies in appropriate settings.

Pancytopenia is reduction of RBCs, WBCs and platelets and results from reduced marrow production, marrow replacement, ineffective haematopoiesis or peripheral sequestration/destruction.

Ask drugs, toxins, infection, nutritional deficiency, weight loss, fever, bleeding and liver disease.

Assess pallor, petechiae, fever, lymphadenopathy and hepatosplenomegaly.

CBC with reticulocyte count and peripheral smear are foundational. B12/folate, liver tests, infection studies and bone-marrow examination are selected according to clues.

Stabilise severe infection, bleeding or symptomatic anaemia while establishing the cause; definitive treatment ranges from vitamin replacement to malignancy or marrow-failure therapy.

AML is a clonal myeloid malignancy characterised by accumulation of blasts that suppress normal haematopoiesis; genetic subtype strongly influences prognosis and therapy.

Fatigue, infection, bleeding and bruising are common; leukostasis can cause respiratory or neurological emergencies in marked hyperleukocytosis.

Assess pallor, fever, bleeding, hepatosplenomegaly and signs of leukostasis or tumour lysis.

CBC/smear may show circulating blasts and Auer rods. Bone marrow with flow cytometry, cytogenetic and molecular testing establishes diagnosis and risk classification.

Treatment is subtype-, age- and fitness-directed using intensive or lower-intensity regimens, followed by consolidation and selected transplantation. Acute promyelocytic leukaemia requires immediate ATRA when suspected because coagulopathy can be fatal.

ALL is a malignant proliferation of lymphoid precursors and is the commonest childhood acute leukaemia, though adults are also affected.

Marrow failure causes fatigue, fever and bleeding; bone pain, lymphadenopathy, hepatosplenomegaly and CNS/testicular involvement can occur.

Assess nodes, liver/spleen, neurological signs and bleeding/infection.

Diagnosis uses marrow morphology and flow cytometry, with cytogenetic/molecular testing such as BCR::ABL1 where relevant; CSF assessment is incorporated into treatment pathways.

Multi-agent chemotherapy includes induction, consolidation/intensification, CNS-directed therapy and maintenance, with targeted agents and transplantation in selected genetic/risk groups.

CML is a myeloproliferative neoplasm driven by the BCR::ABL1 fusion tyrosine kinase from the Philadelphia chromosome.

Many patients are diagnosed incidentally with leukocytosis; fatigue, weight loss, night sweats and splenic discomfort may occur.

Splenomegaly is common; assess constitutional symptoms and signs of progression.

CBC shows granulocytic leukocytosis with a full spectrum of myeloid maturation and often basophilia. Demonstration of BCR::ABL1 by molecular/cytogenetic testing confirms diagnosis.

Tyrosine kinase inhibitors are standard therapy and produce deep durable responses in most chronic-phase patients; quantitative molecular monitoring guides response and treatment decisions.

CLL is a clonal mature B-cell lymphoproliferative disorder, commonly discovered as persistent lymphocytosis in older adults.

Patients may be asymptomatic or have lymphadenopathy, infections, constitutional symptoms, autoimmune cytopenias or splenomegaly.

Assess lymph-node regions, liver/spleen and infection or anaemia/thrombocytopenia signs.

Persistent clonal B-cell lymphocytosis is demonstrated by flow cytometry; FISH/molecular markers including TP53 status influence treatment selection.

Asymptomatic early disease is usually observed rather than treated. Symptomatic/progressive disease is treated with modern targeted agents such as BTK- or BCL2-directed regimens according to patient and molecular factors.

Hodgkin lymphoma is a lymphoid malignancy characterised in classical forms by Hodgkin/Reed-Sternberg cells in an inflammatory background.

Painless lymphadenopathy, often cervical or mediastinal, may be accompanied by fever, drenching night sweats and weight loss.

Examine all nodal regions and assess hepatosplenomegaly; document B symptoms.

Excisional or adequate core-node biopsy establishes diagnosis. PET/CT is central to staging and response assessment; routine extensive marrow biopsy is often unnecessary when PET staging is adequate.

Combination chemotherapy with or without radiotherapy is stage- and risk-adapted, increasingly using PET-guided strategies and novel agents in selected disease.

NHL comprises diverse B-, T- and NK-cell malignancies ranging from indolent to highly aggressive disease.

Persistent painless lymphadenopathy, B symptoms or extranodal disease may occur; presentation varies greatly by subtype.

Assess nodal stations, liver/spleen, extranodal sites and performance status.

Tissue biopsy with morphology, immunophenotyping and genetic studies is essential; PET/CT or CT staging depends on histology.

Treatment is subtype-specific, ranging from observation for selected indolent lymphomas to immunochemotherapy, targeted therapy, cellular therapy or transplantation for aggressive/refractory disease.

Multiple myeloma is a clonal plasma-cell malignancy producing monoclonal immunoglobulin and organ damage or defined myeloma biomarkers.

Bone pain, fractures, fatigue, recurrent infection and renal dysfunction are common.

Assess pallor, skeletal tenderness, neurological compression signs and volume status in hypercalcaemia/renal injury.

Use CBC, calcium, creatinine, serum/urine monoclonal protein studies, serum free light chains, marrow examination and whole-body imaging. CRAB features and myeloma-defining biomarkers establish treatment-requiring disease.

Modern combinations use proteasome inhibitors, immunomodulatory agents, monoclonal antibodies and steroids, with autologous transplantation for eligible patients and bone-protective/supportive care.

MGUS is an asymptomatic monoclonal gammopathy without myeloma-defining organ damage and carries a lifelong risk of progression to plasma-cell or lymphoid malignancy.

It is usually discovered incidentally; symptoms suggesting anaemia, bone disease, neuropathy or renal injury require evaluation for a related disorder rather than simple MGUS.

Examination focuses on signs of myeloma, lymphoma, neuropathy or organ involvement.

Characterise M-protein, immunoglobulin type and serum free-light-chain ratio and assess CBC, calcium and renal function; further marrow/imaging depends on risk and clinical findings.

MGUS itself requires no anti-plasma-cell therapy. Risk-stratified long-term surveillance is used to detect progression.

ITP is an acquired immune-mediated thrombocytopenia caused by increased platelet destruction and impaired production, diagnosed after excluding other causes.

Petechiae, purpura, epistaxis or menorrhagia may occur; many patients are asymptomatic despite low counts.

Assess mucocutaneous bleeding and look for lymphadenopathy or hepatosplenomegaly, which may suggest another diagnosis.

CBC typically shows isolated thrombocytopenia and smear excludes clumping, schistocytes and marrow disorders. Routine antiplatelet-antibody testing is generally not useful.

Observation is appropriate for selected patients without significant bleeding. Corticosteroids or IVIG are used when treatment is required; thrombopoietin-receptor agonists, rituximab or splenectomy are options for persistent disease.

TTP is a thrombotic microangiopathy caused by severe ADAMTS13 deficiency, usually autoimmune, producing platelet-rich microvascular thrombosis.

Thrombocytopenia and microangiopathic haemolytic anaemia are central; neurological, renal, cardiac or fever manifestations vary and the classic pentad is uncommon.

Assess neurological status, bleeding, renal/cardiac involvement and haemodynamic stability.

Smear shows schistocytes with haemolysis markers and thrombocytopenia. Send ADAMTS13 activity/inhibitor testing, but treatment must not wait when clinical probability is high.

Urgent plasma exchange plus glucocorticoids and caplacizumab is standard in acquired immune TTP, with rituximab commonly used to suppress autoantibody production.

DIC is systemic pathologic coagulation activation causing consumption of platelets/coagulation factors, microvascular thrombosis and bleeding, usually secondary to severe illness.

Bleeding from lines/wounds, purpura and organ dysfunction occur in sepsis, trauma, obstetric catastrophe or malignancy.

Assess bleeding, shock, acral ischaemia and the underlying trigger.

Typical findings include thrombocytopenia, prolonged PT, elevated D-dimer/fibrin degradation products and falling fibrinogen, interpreted as serial trends in clinical context.

Rapid treatment of the underlying cause is fundamental. Blood components are used for clinically significant bleeding or procedures according to laboratory deficits rather than simply normalising tests.

Haemophilia A and B are inherited deficiencies of factor VIII and IX respectively, causing impaired secondary haemostasis and deep-tissue bleeding.

Haemarthroses, muscle haematomas and prolonged bleeding after procedures are characteristic; severe disease presents early.

Assess joint swelling, chronic arthropathy and occult deep bleeding; intracranial bleeding is a medical emergency.

Isolated prolonged aPTT with normal PT suggests an intrinsic-pathway defect; factor assays establish diagnosis and severity. Mixing studies help distinguish deficiency from inhibitor.

Treat bleeding and provide prophylaxis with factor replacement or modern non-factor therapies according to haemophilia type and inhibitor status. Avoid unnecessary IM injections and platelet-impairing drugs.

VTE includes deep-vein thrombosis and pulmonary embolism and results from interactions among stasis, endothelial injury and hypercoagulability.

DVT causes unilateral swelling/pain; PE may cause dyspnoea, pleuritic pain, syncope or shock. Clinical probability should guide testing.

Assess haemodynamics and oxygenation first in suspected PE; examine legs for asymmetric swelling and risk factors such as cancer, surgery or immobility.

Use validated pretest probability with D-dimer in appropriate low/intermediate-risk patients and compression ultrasound or CT pulmonary angiography when indicated.

Anticoagulation is the mainstay, with duration determined by provoking factors, recurrence and bleeding risk. Haemodynamically unstable high-risk PE may require systemic thrombolysis or catheter/surgical reperfusion.

Cancer evaluation begins by defining the presenting syndrome, identifying red flags, establishing tissue diagnosis and determining disease extent before treatment.

Unexplained weight loss, persistent mass, abnormal bleeding, progressive dysphagia, change in bowel habit, persistent cough, pathological fracture or unexplained organ dysfunction warrant structured evaluation.

Perform complete general examination including performance status, nutrition, lymph nodes and organ-specific examination; look for metastatic signs such as hepatomegaly, bone tenderness or neurological deficits.

Use targeted imaging and laboratory tests based on the suspected primary. Histopathology is usually essential; immunohistochemistry and molecular testing refine tumour origin and actionable biology.

Stabilise emergencies first, obtain adequate tissue, stage accurately and discuss confirmed malignancy in a multidisciplinary setting. Avoid empiric anticancer therapy before diagnosis except in selected oncologic emergencies.

Staging describes anatomical disease burden and is fundamental to prognosis and treatment intent; performance status estimates functional reserve and tolerance of therapy.

Localised disease may be potentially curable with local therapy, while metastatic disease usually requires systemic treatment, though oligometastatic exceptions exist.

Document ECOG performance status, weight loss, frailty and organ function rather than relying on chronological age alone.

TNM staging is used for many solid tumours, while tumour-specific systems exist for others. CT, MRI, PET/CT and pathological staging are selected according to cancer type.

Treatment decisions integrate stage, biology, performance status, comorbidity and patient goals. Re-stage at clinically meaningful points rather than ordering indiscriminate imaging.

Cytotoxic chemotherapy preferentially damages rapidly dividing cells and is used in curative, adjuvant, neoadjuvant or palliative settings, often in combinations to improve efficacy and reduce resistance.

Toxicities commonly involve marrow, gastrointestinal mucosa, hair follicles and reproductive tissues, while individual drugs have characteristic organ toxicities.

Assess performance status, infection, hydration, neuropathy and treatment-specific toxicities before each cycle.

CBC, renal and hepatic function guide dosing. Baseline cardiac, pulmonary or other testing is obtained when the regimen has predictable organ toxicity.

Use protocol-based dosing, antiemetic prophylaxis and supportive care. Dose modification depends on toxicity, organ function and treatment intent; extravasation precautions are mandatory for vesicants.

Targeted therapies inhibit molecular drivers or signalling pathways that are disproportionately important to cancer cells and require appropriate biomarker selection for many indications.

Responses can be dramatic in oncogene-addicted tumours, but acquired resistance commonly develops through secondary mutations or bypass pathways.

Examine for treatment-specific effects such as rash, hypertension, diarrhoea, cardiac dysfunction or hepatotoxicity depending on the agent.

Molecular profiling may use PCR, FISH, immunohistochemistry or next-generation sequencing. The detected alteration must be clinically actionable in that tumour context.

Match validated biomarkers to approved/evidence-based therapy and monitor for characteristic toxicity and resistance. Re-biopsy or circulating tumour DNA may help at progression in selected cancers.

Immune checkpoint inhibitors restore antitumour T-cell activity by blocking inhibitory pathways such as PD-1/PD-L1 or CTLA-4, producing durable responses in selected cancers.

Immune-related adverse events can affect skin, gut, liver, lungs, endocrine organs, kidneys, heart or nervous system and may occur during or after treatment.

Ask new diarrhoea, dyspnoea, rash, weakness, headache or endocrine symptoms at every visit; grade severity and assess haemodynamic stability.

Investigations are organ-directed and must exclude infection, cancer progression and other drug toxicity. Thyroid, adrenal and hepatic testing is commonly required.

Hold immunotherapy for clinically significant toxicity and use guideline-directed corticosteroids or other immunosuppression according to organ and grade; endocrine deficiencies often require hormone replacement.

Oncologic emergencies arise from tumour burden, metabolic effects or treatment and require simultaneous stabilisation, diagnosis and cancer-specific intervention.

Important syndromes include febrile neutropenia, tumour lysis, hypercalcaemia, spinal cord compression, SVC syndrome, raised intracranial pressure and malignant pericardial effusion.

Use ABC assessment, haemodynamics, neurological examination and focused search for infection, obstruction or metabolic derangement.

Urgent CBC, electrolytes, renal function, calcium and syndrome-directed imaging are obtained without delaying time-critical therapy.

Stabilise first and involve oncology plus relevant specialties early. Treatment may include antibiotics, fluids, steroids, radiotherapy, surgery, drainage or metabolic therapy according to the emergency.

Febrile neutropenia is fever in a patient with significant neutropenia and is treated as a medical emergency because infection may progress rapidly without localising signs.

Fever may be the only manifestation; mucositis, catheter infection, pneumonia, abdominal or perianal infection are important sources.

Assess ABCs and sepsis, inspect oral cavity, skin and vascular lines, and examine lungs/abdomen; avoid traumatic rectal procedures in profound neutropenia.

Obtain CBC, renal/liver tests and blood cultures from appropriate sites before antibiotics if this causes no delay. Imaging is symptom-directed.

Give prompt empiric broad-spectrum antipseudomonal antibiotics according to local resistance patterns. Risk-stratify for inpatient versus carefully selected outpatient therapy and consider G-CSF according to indication.

TLS results from rapid malignant-cell breakdown releasing potassium, phosphate and nucleic acids, causing hyperkalaemia, hyperphosphataemia, hypocalcaemia and uric-acid nephropathy.

It occurs especially in highly proliferative haematologic cancers after therapy but can be spontaneous; arrhythmia, seizure and AKI are major complications.

Assess hydration, urine output, rhythm and neurological status.

Serial potassium, phosphate, calcium, uric acid, creatinine and LDH are essential. Risk is estimated before treatment from tumour type, burden and renal function.

High-risk patients need vigorous monitored hydration and urate-lowering prophylaxis; rasburicase is used in selected high-risk or established hyperuricaemia. Treat electrolyte emergencies and initiate dialysis when indicated.

Cancer can cause hypercalcaemia through PTH-related peptide, osteolytic metastases or calcitriol-mediated mechanisms and severe cases are oncologic emergencies.

Thirst, polyuria, dehydration, constipation, confusion and weakness are typical; severe disease can cause arrhythmia or coma.

Assess volume status, mental state and underlying cancer burden.

Confirm corrected or ionised calcium and assess renal function, phosphate and mechanism when needed. ECG is useful in severe cases.

Begin isotonic IV fluids in significant symptomatic hypercalcaemia, add calcitonin for rapid short-term lowering when severe, and use an antiresorptive such as IV bisphosphonate or denosumab according to renal status and context; treat the cancer.

Metastatic epidural spinal cord compression is an emergency caused by tumour compressing the cord or cauda equina and threatens irreversible paralysis.

New severe back pain, nocturnal pain, radicular symptoms, weakness, sensory change or sphincter dysfunction in a cancer patient are red flags.

Perform urgent motor, sensory, reflex and sphincter examination and document the neurological level.

Urgent MRI of the whole spine is preferred because multiple levels may coexist; do not rely on plain radiography.

Give dexamethasone promptly when malignant cord compression is suspected and arrange urgent multidisciplinary radiotherapy and/or surgical decompression according to stability, radiosensitivity and prognosis.

SVC syndrome results from obstruction of venous return from the head, neck and upper extremities, most commonly from thoracic malignancy.

Facial/neck swelling, dyspnoea, cough, distended chest veins and symptoms worse on bending or lying down are typical; cerebral or airway compromise indicates severity.

Assess airway, stridor, neurological status, facial/upper-limb oedema and collateral veins.

Contrast CT chest usually defines the obstruction and underlying mass. Tissue diagnosis should be obtained before tumour-specific therapy when the patient is stable.

Elevate the head and treat severe airway/cerebral compromise urgently. Endovascular stenting can provide rapid relief; chemotherapy or radiotherapy depends on tumour histology and clinical urgency.

Cancer creates a hypercoagulable state and VTE may arise from tumour biology, immobility, surgery, central lines or systemic therapy.

DVT causes unilateral swelling and pain; PE causes dyspnoea, pleuritic pain, tachycardia, syncope or shock.

Assess haemodynamic stability, oxygenation and bleeding risk, including thrombocytopenia or tumour sites prone to bleeding.

Use standard probability-based imaging pathways, but D-dimer is less specific in cancer. CT pulmonary angiography or compression ultrasonography confirms most events.

Anticoagulate with an evidence-based DOAC or LMWH according to cancer type, interactions, GI/GU bleeding risk, renal function and platelet count; duration is usually extended while cancer remains active if bleeding risk permits.

Cancer pain may be nociceptive, neuropathic or mixed and should be assessed systematically because good analgesia improves function and quality of life.

Characterise site, intensity, breakthrough episodes, neuropathic descriptors, sleep and functional impact and distinguish treatment-related pain.

Examine the painful site and look for pathological fracture, cord compression, infection or other reversible emergencies.

Imaging is targeted when a structural complication is suspected; pain severity itself does not dictate the imaging modality.

Use regular multimodal analgesia matched to severity, including non-opioids, opioids and adjuvant neuropathic agents, with prophylaxis for predictable opioid adverse effects. Palliative radiotherapy or procedures can be highly effective for focal pain.

Chemotherapy-induced nausea and vomiting is predictable according to emetogenic potential and is more effectively prevented than rescued after onset.

Acute symptoms occur within 24 hours, delayed symptoms later, and anticipatory nausea can develop after poorly controlled prior cycles.

Assess hydration, weight, oral intake and alternative causes such as obstruction, brain metastasis, hypercalcaemia or infection.

Laboratory testing is guided by dehydration/electrolyte disturbance and the differential diagnosis rather than routine nausea alone.

Use regimen-matched prophylaxis combining agents such as 5-HT3 antagonists, dexamethasone, NK1 antagonists and olanzapine for highly emetogenic therapy. Provide breakthrough rescue from a different pharmacologic class.

Breast cancer is biologically heterogeneous; systemic treatment is driven by stage and biomarkers including ER, PR and HER2, with genomic assays useful in selected early hormone-receptor-positive disease.

A breast lump, nipple change, skin retraction or axillary node may present; metastatic disease commonly involves bone, liver, lung and brain.

Examine both breasts, regional nodes and signs of metastatic disease and document menopausal/performance status.

Diagnosis requires core biopsy with histology and ER/PR/HER2 testing. Imaging stages disease according to clinical risk; germline testing is indicated for selected hereditary-risk patients.

Early disease uses combinations of surgery, radiotherapy and subtype-directed systemic therapy. Endocrine therapy treats hormone-receptor-positive disease, HER2-targeted therapy treats HER2-positive disease and chemotherapy/immunotherapy are selected by stage and subtype.

Lung cancer is broadly divided into non-small-cell and small-cell cancers; modern NSCLC treatment depends heavily on histology, stage and molecular drivers.

Persistent cough, haemoptysis, weight loss, dyspnoea or metastatic symptoms may occur; some tumours are screen-detected.

Assess performance status, supraclavicular nodes, respiratory findings and metastatic neurological or skeletal signs.

Obtain adequate tissue for histology and biomarker testing. Advanced nonsquamous NSCLC commonly requires broad molecular profiling plus PD-L1; brain imaging and PET/CT are used in appropriate staging.

Early disease is managed with curative local therapy plus perioperative systemic treatment when indicated. Advanced disease uses targeted therapy for actionable drivers or immunotherapy/chemotherapy according to molecular and PD-L1 profile.

Colorectal cancer systemic management depends on stage, tumour sidedness and molecular biology, particularly mismatch-repair status and RAS/BRAF alterations in advanced disease.

Change in bowel habit, rectal bleeding, iron-deficiency anaemia, obstruction or weight loss are common presentations.

Assess abdomen, liver, nodes and rectal findings when appropriate, plus performance/nutritional status.

Colonoscopy with biopsy establishes diagnosis. CT stages disease; CEA is useful for monitoring rather than screening diagnosis. Test MMR/MSI in all colorectal cancers and broader biomarkers in metastatic disease.

Adjuvant chemotherapy is used for stage III and selected high-risk stage II disease. Metastatic treatment uses chemotherapy plus biologic or immunotherapy strategies according to MSI/MMR, RAS/BRAF, sidedness and resectability.

Gastric/GEJ cancers require multidisciplinary staging because treatment varies by resectability, location and biomarkers.

Progressive dyspepsia, early satiety, weight loss, anaemia, vomiting or dysphagia can occur; advanced disease may cause Virchow node or ascites.

Assess nutrition, supraclavicular nodes, abdomen and signs of peritoneal or liver metastasis.

Upper endoscopy with biopsy establishes diagnosis. CT and often staging laparoscopy/EUS are used in potentially curable disease. Advanced adenocarcinoma requires HER2, PD-L1 and mismatch-repair/MSI assessment, with additional biomarkers where relevant.

Resectable disease often uses perioperative systemic therapy plus surgery. Advanced disease receives biomarker-directed combinations including chemotherapy, HER2-targeted therapy or immunotherapy in appropriate patients.

Pancreatic ductal adenocarcinoma is aggressive and often presents late; resectability and performance status are central to treatment selection.

Painless jaundice, weight loss, epigastric/back pain and new or worsening diabetes are common clues.

Assess jaundice, nutrition, performance status, hepatomegaly/ascites and thrombotic complications.

Pancreatic-protocol CT defines resectability. Tissue diagnosis is required before systemic therapy; germline testing and selected tumour molecular profiling are increasingly relevant.

Resectable disease generally requires surgery plus perioperative/adjuvant chemotherapy. Borderline/locally advanced disease often receives systemic therapy first; metastatic disease uses combination chemotherapy in fit patients and biomarker-directed treatment in selected subsets.

Prostate cancer growth is usually androgen-driven; systemic therapy ranges from androgen-deprivation therapy to androgen-receptor pathway inhibitors, chemotherapy and targeted/radioligand treatments.

Localised disease may be asymptomatic; advanced disease often causes bone pain, urinary symptoms or complications of metastases.

Assess performance status, bone pain, neurological deficits suggesting cord compression and treatment-related metabolic/cardiovascular effects.

PSA supports diagnosis/monitoring but histology establishes cancer. Staging uses risk-adapted conventional or PSMA-based imaging; germline and somatic testing are important in advanced disease.

ADT is the backbone of metastatic hormone-sensitive disease and is generally intensified with an androgen-receptor pathway inhibitor and/or docetaxel in appropriate patients. Castration-resistant disease has multiple sequential systemic options.

Epithelial ovarian cancer commonly presents at advanced stage and treatment integrates cytoreductive surgery with platinum-based systemic therapy.

Bloating, early satiety, pelvic/abdominal discomfort and increasing abdominal girth are typical but nonspecific.

Assess ascites, pelvic/abdominal masses, pleural effusion and performance/nutritional status.

Imaging and CA-125 support evaluation but do not replace histology. Germline and tumour BRCA/HRD testing are important because they influence hereditary counselling and maintenance therapy.

Use primary cytoreductive surgery when optimal resection is feasible or neoadjuvant platinum-taxane chemotherapy followed by interval surgery in selected patients. Maintenance PARP inhibitor and/or antiangiogenic therapy is biomarker- and response-directed.

Most mucosal head-and-neck squamous cancers are strongly related to tobacco/alcohol or HPV depending on site; treatment is multidisciplinary and aims to preserve function while achieving control.

Persistent neck node, oral ulcer, dysphagia, odynophagia, hoarseness or unilateral ear pain may be presenting features.

Perform careful oral/oropharyngeal and neck examination and assess airway, nutrition and swallowing.

Biopsy establishes histology; contrast imaging and endoscopic assessment stage disease. HPV/p16 testing is essential for oropharyngeal SCC because of prognostic and staging implications.

Locally advanced disease may require concurrent chemoradiotherapy or surgery plus risk-adapted adjuvant therapy. Recurrent/metastatic disease uses immunotherapy with or without chemotherapy according to PD-L1 and clinical factors.

Clear-cell RCC is a vascular tumour with frequent VHL-pathway biology and is relatively resistant to conventional cytotoxic chemotherapy; modern treatment uses immunotherapy and VEGF-targeted agents.

Haematuria, flank pain and mass are uncommon as a complete triad; many tumours are incidental, while metastatic disease can produce constitutional or paraneoplastic features.

Assess performance status, BP, anaemia, abdominal mass and metastatic symptoms.

Cross-sectional imaging defines stage and resectability. Biopsy is generally required before systemic therapy when histology is not otherwise established.

Localised RCC is primarily surgical or ablative. Advanced clear-cell disease is commonly treated with immune-checkpoint combinations or immunotherapy plus VEGF-targeted therapy; cytoreductive nephrectomy is reserved for selected patients.

Melanoma is an aggressive malignancy in which immune checkpoint inhibition and BRAF/MEK targeted therapy have transformed outcomes in advanced disease.

Changing pigmented lesion, asymmetry, border irregularity, colour variation or growth may prompt diagnosis; metastatic disease can involve almost any organ.

Examine the entire skin and regional nodes and document performance status and neurological symptoms.

Excisional biopsy with Breslow depth and ulceration guides staging. BRAF V600 testing is important in advanced disease and selected high-risk settings; imaging is stage-directed.

Early disease is surgical with sentinel-node assessment when indicated. High-risk resected and metastatic disease may receive checkpoint immunotherapy; BRAF-mutant disease can receive BRAF plus MEK inhibition.

Palliative oncology focuses on symptom relief, communication and quality of life alongside disease-directed therapy and is appropriate from diagnosis of advanced cancer—not only at the end of life.

Common burdens include pain, dyspnoea, nausea, fatigue, anorexia, anxiety, depression and caregiver distress.

Assess symptoms, function, cognition, psychosocial needs and the patient's understanding and priorities.

Investigations should be ordered when results are likely to change symptom management or meaningful treatment decisions, avoiding burdensome low-value testing near end of life.

Integrate specialist palliative care early for advanced disease, clarify treatment intent, manage symptoms proactively and discuss resuscitation and future care according to patient values. Hospice/end-of-life care is introduced when appropriate.

Fever is a regulated rise in body temperature caused by pyrogen-mediated elevation of the hypothalamic set point. The diagnostic approach should distinguish acute self-limited infection from focal infection, systemic inflammatory disease, malignancy and prolonged unexplained fever.

Define duration, pattern, travel, exposures, animal/contact history, medications, immune status and localising symptoms. Weight loss, night sweats, rash, arthralgia or recurrent fever broaden the differential beyond routine infection.

Perform repeated complete examinations because diagnostic signs can evolve. Focus on skin, oral cavity, lymph nodes, heart murmurs, lungs, abdomen, joints and neurological findings.

Initial tests are guided by severity and clues: CBC, renal/liver profile, urinalysis and cultures when indicated. Imaging and serology should be hypothesis-driven. FUO requires systematic reassessment rather than indiscriminate panels.

Stabilise sepsis when present and treat proven or strongly suspected infections. In stable FUO, avoid blind antibiotics or corticosteroids because they can obscure the diagnosis.

Sepsis is life-threatening organ dysfunction caused by a dysregulated response to infection; septic shock represents a high-risk subset with persistent circulatory and metabolic abnormalities.

Fever or hypothermia, altered mentation, tachypnoea, hypotension and oliguria may occur. Elderly or immunosuppressed patients may lack fever.

Assess ABCs, perfusion, capillary refill, mental state, urine output and source. Look for pneumonia, urinary, abdominal, skin, line and CNS infection.

Obtain cultures promptly when this does not substantially delay antimicrobials, measure lactate when indicated and assess organ dysfunction with CBC, renal/liver tests and source-directed imaging.

Give prompt appropriate antimicrobials, IV crystalloid for hypoperfusion and early source control. Norepinephrine is first-line vasopressor for septic shock when hypotension persists despite adequate fluid resuscitation.

Antimicrobial stewardship aims to provide the right drug, dose, route and duration while reducing toxicity, resistance and unnecessary broad-spectrum exposure.

Before prescribing, identify the likely syndrome, severity, probable organisms, prior cultures, recent antibiotics, allergies and local resistance pattern.

Examine for a genuine bacterial focus and distinguish colonisation or contamination from infection.

Obtain high-value cultures before antibiotics when feasible in serious infection. Review microbiology at 48–72 hours and reassess whether antibiotics are still required.

Start empiric therapy proportional to illness severity, then de-escalate to the narrowest effective regimen. Use IV-to-oral switch and shortest evidence-based duration when clinically appropriate.

CAP is acute infection of lung parenchyma acquired outside hospital and ranges from mild outpatient disease to severe pneumonia requiring ICU support.

Cough, fever, sputum, pleuritic pain and dyspnoea are common; older adults may present with confusion or functional decline.

Assess respiratory rate, oxygen saturation, work of breathing, BP and mental state; auscultate for focal crackles or bronchial breathing.

Chest imaging confirms an infiltrate when diagnosis is uncertain or disease is significant. CBC, renal/liver tests, cultures and urinary antigens are reserved according to severity and setting.

Choose empiric antibiotics according to severity, comorbidity and local resistance, then narrow when microbiology is available. Provide oxygen/ventilatory support and treat complications such as empyema.

HAP develops after hospitalisation and VAP after mechanical ventilation, with pathogen risk shaped by local ecology, prior antibiotics and duration of healthcare exposure.

New or worsening respiratory infection is suggested by fever, purulent secretions, worsening oxygenation and a new/progressive infiltrate, but none is individually diagnostic.

Assess oxygenation, ventilator requirements, haemodynamics, secretion burden and alternative causes such as atelectasis, pulmonary oedema or PE.

Obtain respiratory cultures and blood cultures in appropriate severe disease. Imaging supports diagnosis; biomarkers cannot reliably replace clinical assessment.

Start empiric therapy based on severity and local antibiogram, including resistant Gram-negative/MRSA coverage only when indicated. De-escalate using cultures and clinical response and use evidence-based duration.

Tuberculosis is caused by Mycobacterium tuberculosis and most commonly affects lungs but can involve virtually any organ; latent infection is biologically distinct from active disease.

Chronic cough, fever, night sweats, weight loss and haemoptysis suggest pulmonary TB. Extrapulmonary presentations include nodes, pleura, CNS, abdomen, bone and genitourinary disease.

Assess nutritional status, nodes, respiratory findings and extrapulmonary sites; evaluate HIV and other immunosuppressive risks.

Microbiological confirmation is preferred using rapid molecular testing plus smear/culture and drug-susceptibility testing. Imaging supports but does not prove TB.

Drug-susceptible TB requires multidrug therapy using national/programmatic regimens with adherence support. Drug-resistant TB requires resistance-guided expert treatment and public-health measures including infection control/contact evaluation.

HIV causes progressive CD4 T-cell dysfunction if untreated; modern antiretroviral therapy suppresses viral replication and allows near-normal life expectancy for many patients.

Acute HIV may resemble mononucleosis; chronic infection can be asymptomatic or present with weight loss, recurrent infection, mucocutaneous disease or opportunistic illness.

Assess general condition, oral cavity, skin, nodes, neurological system and signs of opportunistic infection or coinfection.

Diagnosis uses recommended HIV antigen/antibody algorithms with supplemental differentiation/nucleic-acid testing when required. Baseline viral load, CD4 count, resistance testing, hepatitis/TB/STI screening and renal/liver assessment guide care.

Start ART promptly for essentially all people with HIV, using a recommended integrase-inhibitor-based regimen in many settings, while managing opportunistic infections and drug interactions.

Opportunistic infections emerge as cellular immunity declines, with risk strongly related to CD4 count, exposure and ART status.

PCP, tuberculosis, cryptococcosis, toxoplasmosis, CMV disease and disseminated mycobacterial/fungal infections produce organ-specific syndromes.

Assess oxygenation, neurological status, fundi when relevant, oral lesions and evidence of disseminated disease.

Use syndrome-directed microbiological/antigen/PCR testing and imaging. CD4 count helps prioritise the differential but does not establish a specific infection.

Treat the identified OI and initiate or optimise ART at the recommended timing for that infection. Provide prophylaxis when CD4/clinical criteria indicate and discontinue appropriately after immune recovery.

Dengue is a mosquito-borne flaviviral infection ranging from uncomplicated febrile illness to severe plasma leakage, bleeding and organ dysfunction.

High fever, severe myalgia, headache, retro-orbital pain and rash are common. Warning signs often emerge around defervescence: abdominal pain, persistent vomiting, mucosal bleeding, lethargy or fluid accumulation.

Assess haemodynamics, capillary refill, bleeding, hepatomegaly and signs of plasma leakage; serial assessment is more valuable than a single snapshot.

CBC commonly shows leukopenia and thrombocytopenia. Rising haematocrit with falling platelets suggests plasma leakage. NS1/NAAT are useful early and serology later according to illness day.

Use careful oral or IV isotonic fluid according to phase and haemodynamics, avoiding both under-resuscitation and fluid overload. Blood products are for significant bleeding rather than platelet count alone.

Malaria is a protozoal infection transmitted by Anopheles mosquitoes; Plasmodium falciparum causes most severe disease, while P. vivax can relapse from hepatic hypnozoites.

Fever, chills, headache and malaise are common; severe malaria may cause altered consciousness, shock, acidosis, severe anaemia, jaundice, AKI or respiratory distress.

Assess mental status, haemodynamics, respiratory status, pallor, jaundice and splenomegaly and look actively for severe-malaria criteria.

Diagnosis requires parasite demonstration by microscopy or rapid diagnostic test. Quantify parasitaemia when possible in falciparum malaria and monitor glucose, renal function and haemoglobin in severe disease.

Uncomplicated malaria is treated with species- and region-appropriate combination therapy. Severe malaria requires urgent IV artesunate followed by complete oral therapy; vivax/ovale radical cure requires assessment for G6PD deficiency before primaquine/tafenoquine.

Enteric fever is systemic infection caused by Salmonella Typhi or Paratyphi, transmitted faeco-orally and increasingly influenced by antimicrobial resistance.

Prolonged fever, headache, abdominal discomfort, constipation or diarrhoea and relative systemic toxicity are typical; complications include intestinal bleeding or perforation.

Assess hydration, abdominal tenderness/distension, hepatosplenomegaly and signs of perforation or encephalopathy.

Blood culture is the preferred diagnostic test early in illness; bone-marrow culture is more sensitive but rarely needed routinely. Widal testing has poor diagnostic specificity and should not be relied upon alone.

Use resistance-informed antibiotics based on local susceptibility and disease severity, with supportive care and prompt surgical evaluation for perforation.

Leptospirosis is a zoonotic spirochaetal infection acquired through contact with urine-contaminated water or soil, especially after flooding or occupational exposure.

Acute fever, severe myalgia—often calves—headache and conjunctival suffusion are characteristic; severe Weil disease causes jaundice, AKI and bleeding.

Look for conjunctival suffusion, jaundice, calf tenderness, haemorrhage and meningism.

PCR is useful early and serology becomes more informative later; CBC, renal/liver tests and urinalysis assess organ involvement.

Mild disease can be treated with appropriate oral antibiotics; severe disease requires IV therapy and organ support, including dialysis or ventilation when needed.

Scrub typhus is caused by Orientia tsutsugamushi and transmitted by chigger mites; rickettsial infections produce systemic endothelial injury and vasculitis-like illness.

Acute undifferentiated fever with headache, myalgia, thrombocytopenia or hepatitis is common; an eschar is highly suggestive but may be absent or hidden.

Search carefully for an eschar in axillae, groin, inframammary areas and skin folds; assess rash, nodes, lungs and CNS.

Serology or molecular testing supports diagnosis where available, but early tests can be negative. Laboratory abnormalities are nonspecific.

Doxycycline is highly effective for most scrub/rickettsial disease; azithromycin is an alternative in selected patients. Severe disease requires organ support.

Japanese encephalitis is a mosquito-borne flavivirus causing inflammatory brain disease and is an important cause within the broader acute encephalitis syndrome in endemic Asia.

Fever followed by altered consciousness, seizures, movement disorder or focal neurological signs suggests encephalitis; severe disease may progress to raised intracranial pressure and respiratory failure.

Assess GCS, airway protection, seizures, focal signs and signs of raised intracranial pressure or brainstem dysfunction.

CSF usually shows a viral inflammatory pattern; JE-specific IgM in CSF/serum supports diagnosis. Neuroimaging may show thalamic/basal ganglia involvement but is not diagnostic alone.

No proven specific antiviral therapy exists for JE; management is meticulous supportive neurocritical care, seizure control, airway/ventilation and management of raised intracranial pressure. Vaccination and mosquito control are preventive.

Acute bacterial meningitis is infection of the meninges and subarachnoid space and can cause rapid neurological injury, shock and death.

Fever, headache, neck stiffness and altered mental state are classic but the complete triad is not always present; seizures or focal deficits may occur.

Assess ABCs, GCS, meningism, focal deficits, papilloedema and sepsis.

Obtain blood cultures and perform lumbar puncture promptly when safe. CT before LP is reserved for selected features suggesting mass effect or markedly increased herniation risk and must not delay antibiotics.

Give immediate age/risk-appropriate IV antibiotics; dexamethasone is given with or just before the first antibiotic dose when indicated, particularly for suspected pneumococcal meningitis. Treat shock and seizures.

HSV encephalitis is a treatable cause of sporadic encephalitis and preferentially affects temporal and frontal lobes.

Fever, altered behaviour, confusion, seizures, aphasia or focal deficits may evolve rapidly.

Assess airway, consciousness, seizures and focal neurological findings.

CSF usually shows lymphocytic pleocytosis and HSV PCR is the key diagnostic test. MRI is more sensitive than CT and often shows temporal-lobe abnormalities; EEG can support evaluation.

Start IV acyclovir immediately when HSV encephalitis is suspected—do not wait for PCR confirmation. Adjust dose for renal function and maintain adequate hydration.

Infective endocarditis is microbial infection of the endocardial surface, usually valves, producing persistent bacteraemia and embolic/immunological complications.

Fever, malaise, new or changing murmur, embolic events or unexplained systemic illness occur; prosthetic valves and injection drug use increase risk.

Examine cardiac murmurs, heart failure, skin/eyes and neurological system and look for embolic or vascular phenomena.

Obtain multiple blood-culture sets before antibiotics in stable patients. Echocardiography is central—TTE first in many cases and TEE when sensitivity must be higher. Diagnostic criteria integrate microbiology and imaging.

Use prolonged pathogen-directed IV or highly bioavailable therapy according to organism and valve context. Early surgical consultation is needed for heart failure, uncontrolled infection, abscess or selected embolic-risk lesions.

SSTIs range from superficial cellulitis and abscess to rapidly destructive necrotising infection; purulent and non-purulent syndromes have different microbiology and management.

Cellulitis causes spreading erythema, warmth and tenderness; abscess produces focal fluctuance. Pain out of proportion, bullae, crepitus or systemic toxicity suggest necrotising infection.

Mark extent, examine for fluctuance, portal of entry and neurovascular compromise and assess systemic toxicity.

Routine cultures are unnecessary for uncomplicated cellulitis, whereas pus should be cultured in selected abscesses. Imaging can help when deep infection or gas is suspected but must not delay surgery.

Drain abscesses when indicated and use antibiotics according to syndrome and MRSA risk. Suspected necrotising fasciitis requires immediate surgical exploration/debridement plus broad-spectrum antibiotics.

UTIs range from lower bladder infection to renal parenchymal infection; complicated infection is defined by host or anatomical factors that increase treatment failure.

Dysuria, frequency and urgency suggest cystitis; fever, flank pain, vomiting and systemic illness suggest pyelonephritis.

Assess temperature, hydration, haemodynamics and costovertebral-angle tenderness and look for obstruction or sepsis.

Urinalysis supports diagnosis; urine culture is particularly important in pyelonephritis, recurrent/complicated disease and resistant-risk patients. Imaging is reserved for obstruction, severe disease or failure to improve.

Use syndrome- and resistance-appropriate antibiotics, adjusting to culture. Severe pyelonephritis may need IV therapy; urgent drainage is required when infection coexists with an obstructed collecting system.

C. difficile causes toxin-mediated colitis after disruption of normal intestinal microbiota, commonly following antibiotic or healthcare exposure.

Watery diarrhoea, abdominal pain and fever occur; fulminant disease can cause ileus, toxic megacolon, shock or perforation.

Assess hydration, abdominal tenderness/distension and severity markers; ileus can paradoxically reduce diarrhoea in fulminant disease.

Test only patients with clinically significant unexplained diarrhoea using recommended toxin/NAAT algorithms. Do not test formed stool or use tests of cure routinely.

Stop unnecessary inciting antibiotics and treat with recommended oral therapy such as fidaxomicin or vancomycin according to episode and severity. Fulminant disease requires intensive medical and early surgical input.

HBV is a DNA virus causing acute or chronic hepatitis; chronic infection can lead to cirrhosis and hepatocellular carcinoma even when symptoms are absent.

Acute disease may cause jaundice, malaise and anorexia; chronic HBV is often asymptomatic until advanced liver disease.

Assess jaundice, hepatomegaly and signs of cirrhosis or portal hypertension.

Interpret HBsAg, anti-HBc and anti-HBs systematically. In chronic infection, HBV DNA, ALT, HBeAg status and fibrosis assessment guide treatment; screen for HIV/HCV/HDV as appropriate.

Potent nucleos(t)ide analogues such as tenofovir or entecavir are first-line for many treatment-eligible patients. Prevent transmission with vaccination, perinatal prophylaxis and appropriate contact management.

HCV is an RNA virus that frequently becomes chronic and can cause cirrhosis, hepatocellular carcinoma and extrahepatic disease; modern direct-acting antivirals cure most infections.

Most acute and chronic infections are asymptomatic; fatigue, liver disease or extrahepatic manifestations may prompt testing.

Assess chronic liver disease, portal hypertension and risk exposures including transfusion history and injection drug use.

Anti-HCV indicates exposure but does not prove active infection; HCV RNA confirms current viraemia. Assess fibrosis and HBV/HIV coinfection before treatment.

Use an appropriate pangenotypic direct-acting antiviral regimen based on cirrhosis status, prior therapy, renal function and interactions. Confirm sustained virologic response after therapy.

Rabies is an almost invariably fatal encephalitis once clinical symptoms develop, but appropriate post-exposure prophylaxis is highly effective before disease onset.

Risk follows bites, scratches or mucosal exposure to saliva from a potentially rabid mammal; exposure category and animal epidemiology determine management.

Inspect and document all wounds and exposure sites and assess tetanus status and secondary bacterial infection risk.

Rabies diagnosis is not required before PEP after a credible exposure. Animal observation/testing is incorporated according to species and local public-health guidance.

Immediately wash wounds thoroughly with soap and running water. Give rabies vaccine according to recommended schedule and infiltrate rabies immunoglobulin into/around category III wounds for previously unvaccinated patients, according to national guidance.

Tetanus is caused by tetanospasmin from Clostridium tetani contaminating wounds, producing disinhibition of motor neurons and sustained muscle rigidity/spasms.

Trismus, neck stiffness, dysphagia, risus sardonicus and painful stimulus-induced spasms are characteristic; autonomic instability marks severe disease.

Assess airway, respiratory muscle involvement, rigidity, wound and autonomic instability while minimising unnecessary stimulation.

Diagnosis is clinical; cultures are insensitive and a negative wound culture does not exclude tetanus.

Provide ICU-level supportive care when severe, wound debridement, human tetanus immune globulin, appropriate antimicrobial therapy and spasm/autonomic control. Active vaccination is still required because disease does not confer reliable immunity.

Invasive fungal infections disproportionately affect neutropenic, transplant, critically ill and otherwise immunocompromised patients; Candida and Aspergillus are major pathogens.

Persistent fever despite antibiotics, pulmonary nodules, pleuritic pain, sinus disease, hepatosplenic lesions or bloodstream infection may occur depending on host and fungus.

Assess immune risk, respiratory status, skin, sinuses, lines and organ-specific findings.

Blood cultures detect many candidemias but are insensitive for moulds. CT, fungal biomarkers and tissue microscopy/culture/histopathology are combined according to syndrome.

Therapy depends on organism and host: echinocandins are common initial therapy for candidemia, while voriconazole or other mould-active agents are used for invasive aspergillosis. Remove infected lines when indicated and reverse immunosuppression when feasible.

Hanging and strangulation can produce airway injury, cerebral hypoxia, vascular injury and cervical trauma; apparently stable patients may deteriorate.

Loss of consciousness, neck pain, dysphonia, dysphagia, dyspnoea, seizures or neurological deficits are concerning.

Prioritise airway and cervical-spine precautions; inspect ligature marks, neck swelling, voice change and neurological status.

Pulse oximetry, ABG and trauma-directed imaging are guided by severity. CT/CTA neck is considered when structural or vascular injury is suspected.

Secure a threatened airway early, provide oxygen/ventilation and treat associated trauma, seizures and post-hypoxic complications. Observe significant symptomatic injuries appropriately.

Drowning is respiratory impairment from submersion/immersion; hypoxaemia is the principal mechanism of organ injury.

Cough, dyspnoea, hypoxaemia, altered consciousness or cardiac arrest may follow rescue; respiratory deterioration can evolve after initial improvement.

Assess ABCs, oxygenation, temperature, trauma and neurological status.

Investigations are severity-directed; chest radiography and ABG are useful in symptomatic hypoxaemia, while routine tests are unnecessary in fully asymptomatic patients.

Restore oxygenation and ventilation rapidly, provide lung-protective ventilation when required and treat hypothermia. Prophylactic antibiotics are not routinely indicated unless grossly contaminated water or infection is suspected.

Poisoning management begins with resuscitation, recognition of toxidromes, focused exposure history and selective antidote use rather than exhaustive toxicology screening.

Ask substance, amount, route, time, co-ingestants and intent; altered sensorium, arrhythmia, seizures and respiratory failure indicate severe toxicity.

Use ABCDE assessment and look for pupil size, skin moisture, bowel sounds, temperature and characteristic odours or neuromuscular findings.

ECG and bedside glucose are high-yield early tests. Electrolytes, ABG, paracetamol level and targeted drug levels are selected according to exposure.

Provide supportive care first, use activated charcoal only in selected early protected-airway cases and administer specific antidotes when indicated. Contact a poison centre/toxicology service when available.

Organophosphates inhibit acetylcholinesterase, causing excessive muscarinic, nicotinic and CNS cholinergic activity.

Salivation, lacrimation, bronchorrhoea, vomiting, diarrhoea, miosis, fasciculations, weakness and altered consciousness are typical.

Airway secretions, wheeze, bradycardia, pupils, fasciculations and respiratory muscle strength require repeated assessment.

Diagnosis is primarily clinical; cholinesterase activity can support exposure but should not delay treatment. ABG and ECG assess complications.

Decontaminate safely, suction and oxygenate, give atropine rapidly and titrate to drying of bronchial secretions/adequate ventilation rather than pupil size. Pralidoxime is used according to poisoning severity and local protocols, especially early significant nicotinic toxicity.

Aluminium phosphide releases phosphine gas and can cause profound myocardial depression, vasoplegia, metabolic acidosis and multiorgan failure; no proven specific antidote exists.

Vomiting, abdominal pain, refractory hypotension, arrhythmias and rapidly progressive shock are typical severe manifestations.

Assess airway, perfusion, rhythm, mental status and signs of cardiogenic/vasodilatory shock.

Serial ECG, ABG/lactate, electrolytes, renal/liver function and bedside echocardiography help guide supportive care.

Management is aggressive ICU supportive care with cautious fluids, vasopressors, correction of metabolic/electrolyte abnormalities and organ support; early toxicology/critical-care involvement is essential.

Paracetamol overdose produces a toxic metabolite that depletes glutathione and can cause delayed hepatic necrosis despite initially mild symptoms.

Early nausea or vomiting may be followed by a deceptively well period before hepatic injury develops.

Assess timing, dose, co-ingestants, intent and signs of hepatic failure.

Obtain a timed paracetamol concentration after an acute single ingestion and interpret with the treatment nomogram when applicable. Check ALT/AST, INR, creatinine and glucose in significant or delayed presentations.

Give N-acetylcysteine when the nomogram indicates toxicity, timing/dose is uncertain with significant risk, presentation is delayed, or hepatic injury is present according to protocol.

Salicylates stimulate the respiratory centre and disrupt cellular metabolism, classically causing respiratory alkalosis with an evolving high-anion-gap metabolic acidosis.

Tinnitus, vomiting, tachypnoea, sweating, fever, confusion and pulmonary oedema can occur.

Assess respiratory pattern, temperature, volume status, mental state and glucose availability.

Serial salicylate levels, ABG/VBG, electrolytes, glucose and renal function are essential because severity may worsen despite an early level.

Give activated charcoal when appropriate, correct volume/electrolytes and alkalinise serum/urine with IV sodium bicarbonate in significant toxicity. Haemodialysis is indicated in severe poisoning according to clinical and biochemical criteria.

Toxic alcohol metabolites cause severe metabolic acidosis; methanol particularly injures the optic system while ethylene glycol causes renal and systemic toxicity.

Visual blurring or 'snowfield' vision suggests methanol; intoxication followed by acidosis, hypocalcaemia or AKI suggests ethylene glycol.

Assess mental status, vision, respiratory compensation, haemodynamics and renal findings.

Calculate anion and osmolar gaps while obtaining specific alcohol levels when available. ABG, electrolytes, renal function and calcium are important.

Block alcohol dehydrogenase with fomepizole (or ethanol where appropriate), correct severe acidosis and use haemodialysis for severe toxicity or established criteria. Folate is used in methanol and thiamine/pyridoxine may support ethylene-glycol metabolism.

Carbon monoxide binds haemoglobin and disrupts cellular oxygen utilisation, causing tissue hypoxia despite a potentially normal pulse oximeter reading.

Headache, dizziness, nausea, confusion, syncope, chest pain or seizures occur; multiple affected household members are an important clue.

Assess neurological and cardiac status and consider concomitant smoke-inhalation injury.

Measure carboxyhaemoglobin by co-oximetry; standard pulse oximetry is unreliable. ECG/troponin are appropriate in significant exposure or cardiac symptoms.

Give 100% oxygen promptly and consider hyperbaric oxygen in severe neurological, cardiac, metabolic or pregnancy-related exposure according to specialist criteria.

Snake envenomation can cause neurotoxicity, coagulopathy, haemorrhage, myotoxicity, AKI and local tissue injury depending on species.

Progressive swelling, ptosis, ophthalmoplegia, weakness, bleeding or dark urine indicate systemic envenomation.

Assess ABCs, serial limb swelling, cranial nerves/respiratory power, bleeding and urine output.

Use bedside coagulation testing where validated plus CBC, renal function, coagulation profile and CK/urinalysis according to syndrome.

Immobilise the limb and give appropriate antivenom for systemic envenomation or severe progressive local toxicity according to national protocols. Support ventilation, shock, bleeding and AKI; avoid incision, suction and tight tourniquets.

Hymenoptera stings can cause local reactions or systemic IgE-mediated anaphylaxis with airway, breathing or circulatory compromise.

Urticaria, angioedema, wheeze, stridor, vomiting, dizziness or hypotension can develop rapidly after a sting.

Assess airway, breathing, BP, skin and mental status immediately.

Anaphylaxis is a clinical diagnosis; investigations must not delay treatment. Serum tryptase may support retrospective diagnosis in selected cases.

Give IM adrenaline into the anterolateral thigh promptly and repeat as needed, with airway support, oxygen and IV fluids for shock. Antihistamines are adjuncts for skin symptoms and must not delay adrenaline.

Animal bites require simultaneous wound management, bacterial-infection prevention, tetanus assessment and rabies risk evaluation.

Clarify species, provoked/unprovoked behaviour, ownership/vaccination, availability for observation and exact nature of bite/scratch/saliva exposure.

Inspect depth, neurovascular/tendon injury and high-risk sites such as hands, face and genitals.

Routine wound cultures are unnecessary unless infected. Rabies decisions are exposure- and epidemiology-based rather than dependent on routine laboratory testing.

Immediately wash and irrigate thoroughly. Give tetanus prophylaxis and antibiotics for selected high-risk wounds. Provide rabies vaccine and immunoglobulin according to exposure category, previous vaccination and national guidance.

Scorpion envenomation can produce an autonomic storm with cardiovascular and respiratory complications, particularly in children.

Severe pain is common; sweating, salivation, vomiting, tachycardia, hypertension followed by shock, myocarditis or pulmonary oedema may occur.

Assess haemodynamics, perfusion, respiratory status and signs of autonomic excess.

ECG, glucose, electrolytes and echocardiography are useful in systemic envenomation; cardiac biomarkers may help in severe cases.

Provide analgesia and supportive care. In regions/species where evidence supports it, early prazosin is used for autonomic cardiovascular toxicity; manage pulmonary oedema/shock in an appropriate monitored setting.

Heat stroke is severe heat illness defined by marked hyperthermia with CNS dysfunction and can rapidly cause coagulopathy, hepatic injury, rhabdomyolysis and multiorgan failure.

Confusion, delirium, seizure or coma during heat exposure/exertion is diagnostic territory even if sweating is present.

Measure core temperature and assess neurological status, haemodynamics and signs of organ injury.

CBC, electrolytes, glucose, CK, renal/liver function, coagulation and serial metabolic testing assess complications.

Begin immediate rapid cooling while resuscitating; cold-water immersion is highly effective for exertional heat stroke when feasible. Avoid antipyretics because the hypothalamic set point is not elevated.

Hypothermia is core temperature below 35°C and progressively impairs neurological, respiratory and cardiac function.

Shivering, confusion and ataxia progress to bradycardia, reduced consciousness and malignant arrhythmias in severe cases.

Handle gently, measure core temperature and assess airway, breathing, circulation and associated trauma/exposure.

ECG may show bradyarrhythmias and Osborn waves; check glucose, electrolytes, renal function and contributing conditions.

Remove wet clothing, insulate and use passive or active external/internal rewarming according to severity. Severe unstable hypothermia may require extracorporeal rewarming where available.

Electrical injury can cause arrhythmia, deep tissue burns, rhabdomyolysis and trauma despite limited external skin findings; lightning has distinct high-voltage physiological effects.

Loss of consciousness, chest pain, burns, weakness or trauma may occur.

Assess ABCs, rhythm, entry/exit injuries, neurological deficits, compartment syndrome and associated falls.

ECG is essential in significant exposure; CK, renal function and urine assessment are used when muscle injury is suspected. Imaging is trauma-directed.

Treat life threats, burns and rhabdomyolysis and monitor patients with abnormal ECG, significant symptoms or high-risk exposure. Lightning cardiac arrest warrants aggressive resuscitation.

Alcohol intoxication causes dose-dependent CNS depression but should never be assumed to explain altered consciousness until dangerous mimics are considered.

Ataxia, dysarthria, disinhibition and somnolence occur; severe intoxication can cause aspiration, hypoglycaemia, hypothermia or respiratory depression.

Assess ABCs, GCS, trauma, pupils, focal deficits and temperature.

Check bedside glucose early. Electrolytes, ethanol level, imaging and toxicology are selective based on severity and differential diagnosis.

Support airway and ventilation, correct hypoglycaemia and dehydration appropriately and give thiamine to patients at risk of deficiency, particularly before or with carbohydrate in malnourished patients.

Alcohol withdrawal follows abrupt reduction after sustained heavy use; severe withdrawal can cause seizures and delirium tremens.

Tremor, anxiety, sweating, tachycardia and insomnia may progress to hallucinations, seizures and delirium with autonomic hyperactivity.

Assess orientation, agitation, autonomic signs, hydration and complications including trauma or infection.

Diagnosis is clinical; check glucose, electrolytes including magnesium, liver function and alternative causes of delirium when indicated.

Benzodiazepines are first-line, titrated to severity; give thiamine and correct fluids/electrolytes. Severe delirium requires close monitoring and treatment of coexisting illness.

Opioid toxicity causes a classic triad of CNS depression, respiratory depression and miosis, though pupils may not always be pinpoint.

Slow breathing, cyanosis, reduced consciousness and aspiration are major threats.

Assess ventilation rather than oxygen saturation alone; look for trauma and co-ingestion.

Bedside glucose and ECG are useful; blood gas helps in severe respiratory depression. Routine broad toxicology screens rarely guide immediate management.

Support airway/ventilation and give naloxone titrated to restore adequate breathing, not necessarily full wakefulness. Repeated doses or infusion may be needed for long-acting opioids.

Benzodiazepines typically cause CNS depression with relatively preserved haemodynamics when taken alone, but co-ingestion can make toxicity severe.

Somnolence, dysarthria and ataxia are typical; respiratory depression is more concerning with opioids, alcohol or other sedatives.

Assess airway, ventilation, GCS and signs suggesting mixed overdose.

Check glucose and ECG and investigate co-ingestants according to history. Toxicology screening is usually not required for immediate care.

Supportive care is usually sufficient. Flumazenil is avoided in most undifferentiated overdoses because it can precipitate seizures or withdrawal, especially in dependent patients or proconvulsant co-ingestion.

Strong acids and alkalis can cause oropharyngeal, oesophageal and gastric necrosis with perforation and later strictures.

Drooling, dysphagia, odynophagia, chest/abdominal pain, vomiting or respiratory symptoms indicate significant injury, but absence of oral burns does not exclude oesophageal damage.

Assess airway early and examine mouth, chest and abdomen for perforation or peritonism.

Early upper GI endoscopy is used in selected significant ingestions to grade injury; CT is useful when deep necrosis/perforation is suspected.

Secure a threatened airway, keep significant cases nil by mouth initially and involve gastroenterology/surgery. Do not induce vomiting, neutralise chemically or perform blind gastric lavage.

Hydrocarbons primarily cause chemical pneumonitis after aspiration; systemic toxicity varies by compound.

Coughing, choking, wheeze or hypoxaemia after ingestion suggests aspiration.

Assess respiratory status and oxygen saturation; neurological abnormalities raise concern for specific hydrocarbon toxicity or co-exposure.

Chest radiography is reserved for symptomatic patients or evolving respiratory disease; routine gastric testing has little value.

Support oxygenation and ventilation. Do not induce vomiting or perform routine gastric lavage because aspiration risk outweighs benefit; antibiotics/steroids are not routinely indicated for uncomplicated chemical pneumonitis.

Severe asthma becomes life-threatening when airflow obstruction causes exhaustion, hypoxaemia or rising CO2; a 'silent chest' is ominous.

Severe dyspnoea, inability to speak, agitation then drowsiness, poor air entry or cyanosis indicate critical disease.

Assess work of breathing, speech, mental status, SpO2 and air entry; avoid relying on wheeze intensity alone.

Peak flow is useful when feasible; ABG is indicated in severe or deteriorating disease. A normal or rising PaCO2 in a distressed patient is concerning for fatigue.

Give repeated inhaled short-acting bronchodilator plus ipratropium, systemic corticosteroid, oxygen to target and IV magnesium in severe attacks. Intubate for impending respiratory arrest/exhaustion with an obstructive-lung ventilation strategy.

Aspiration pneumonitis is chemical lung injury from sterile gastric contents, whereas aspiration pneumonia is infection following aspiration of colonised material.

Acute hypoxaemia soon after a witnessed large aspiration favours pneumonitis; delayed fever and infiltrates in a high-risk patient may indicate pneumonia.

Assess oxygenation, airway protection and aspiration risk such as dysphagia or reduced consciousness.

Chest imaging defines infiltrates but cannot reliably distinguish chemical from infectious aspiration by itself.

Supportive care is central for pneumonitis and antibiotics are not automatically required. Treat established aspiration pneumonia according to severity and local microbiology; address swallowing and aspiration prevention.

Altitude illness results from hypobaric hypoxia; AMS can progress to life-threatening HACE or HAPE.

Headache with nausea, dizziness or fatigue after ascent suggests AMS; ataxia/confusion suggests HACE, while dyspnoea at rest, cough and hypoxaemia suggest HAPE.

Assess mental status, gait, respiratory distress and oxygenation.

Diagnosis is clinical; pulse oximetry supports severity and investigations are mainly used to exclude alternatives.

Stop ascent. Descend for severe illness and give supplemental oxygen. Dexamethasone is used for HACE/severe AMS; nifedipine can be used for HAPE when descent/oxygen are limited or as adjunct according to guidance.

Rapid pressure reduction can generate inert-gas bubbles causing musculoskeletal, neurological, pulmonary or vascular injury in divers.

Joint pain, paresthesia, weakness, vertigo, dyspnoea or altered consciousness after diving are concerning; sudden focal neurological symptoms immediately after ascent suggest arterial gas embolism.

Assess ABCs, neurological status and diving profile.

Diagnosis is clinical; imaging may be normal and should not delay recompression when the syndrome is convincing.

Give 100% oxygen, fluids as appropriate and urgent consultation with a hyperbaric/recompression facility. Avoid unnecessary altitude exposure during transport.

High-dose whole-body ionising radiation can damage marrow, gastrointestinal tract, skin and neurovascular systems depending on dose.

Early nausea/vomiting may be followed by a latent period, then cytopenias, infection, bleeding or GI failure.

Assess contamination separately from irradiation, document skin findings and monitor systemic status.

Serial absolute lymphocyte counts and CBC trends help estimate severity; specialised dosimetry is used with radiation experts.

Decontaminate external radioactive material when present, provide supportive care, infection prevention/treatment, blood products and haematopoietic growth-factor strategies according to dose and syndrome.

Cyanide inhibits mitochondrial cytochrome oxidase, producing cellular hypoxia and profound lactic acidosis despite available oxygen.

Rapid collapse, altered consciousness, seizures and cardiovascular failure may occur after smoke inhalation or industrial exposure.

Assess airway, circulation and concomitant carbon-monoxide/smoke injury.

Marked lactate elevation can support suspicion in the right context; treatment should not await cyanide levels in a critically ill patient.

Give high-flow oxygen and an appropriate cyanide antidote such as hydroxocobalamin when severe poisoning is suspected, plus aggressive supportive care.

Methemoglobinaemia oxidises haemoglobin iron so it cannot effectively carry oxygen, producing functional hypoxia.

Cyanosis with headache, dyspnoea, confusion or arrhythmia may follow oxidant drugs/chemicals; pulse oximetry often remains near the mid-80s despite oxygen.

Look for cyanosis disproportionate to respiratory findings and assess neurological/cardiovascular severity.

Co-oximetry confirms methemoglobin level; arterial PaO2 may be normal despite tissue hypoxia, creating a saturation gap.

Stop the oxidant and give oxygen. Methylene blue is used for significant symptomatic disease but requires caution/alternative strategies in G6PD deficiency and certain drug interactions.

Adrenal crisis causes life-threatening cortisol deficiency with hypotension, electrolyte disturbance and impaired stress response, often triggered by infection or abrupt steroid withdrawal.

Weakness, vomiting, abdominal pain, confusion and shock are common; hyperkalaemia is typical in primary adrenal failure but may be absent in secondary disease.

Assess haemodynamics, volume depletion, pigmentation and precipitating illness.

Draw cortisol/ACTH if feasible before treatment, but never delay therapy. Check sodium, potassium, glucose and renal function.

Give immediate IV hydrocortisone and isotonic saline, adding dextrose for hypoglycaemia, while treating the trigger.

Hypoglycaemia is a time-critical cause of neuroglycopenia and autonomic activation and may result from diabetes therapy, critical illness, alcohol, endocrine disease or insulinoma.

Sweating, tremor, palpitations and hunger can progress to confusion, seizure, focal deficits or coma.

Check consciousness and airway and look for medication/exposure clues.

Measure bedside glucose immediately and confirm when appropriate; investigate the cause after reversal in unexplained or recurrent episodes.

Give rapid oral carbohydrate if awake and safe to swallow; use IV dextrose or IM glucagon when severe/unconscious according to access and context, then prevent recurrence with longer-acting carbohydrate or infusion when needed.

Rhabdomyolysis is skeletal-muscle breakdown releasing myoglobin and intracellular electrolytes, risking AKI and hyperkalaemia.

Muscle pain, weakness and dark urine may follow crush injury, seizures, exertion, heat illness, drugs or prolonged immobilisation.

Assess volume status, muscle swelling, compartment syndrome and the precipitating cause.

CK is the key marker; monitor potassium, calcium, phosphate, creatinine and urine. Dipstick positive for blood with few RBCs suggests myoglobinuria.

Treat the cause and give appropriate IV crystalloid to maintain renal perfusion while monitoring for fluid overload. Treat hyperkalaemia urgently and use dialysis for standard indications.

Compartment syndrome is increased pressure within a closed fascial compartment causing muscle and nerve ischaemia and requires urgent decompression.

Severe escalating pain, especially pain with passive stretch, is an early clue; sensory loss, weakness and absent pulses are late findings.

Examine tense swelling, passive-stretch pain and serial neurovascular status.

Diagnosis is primarily clinical; compartment-pressure measurement helps when examination is unreliable or equivocal.

Remove constrictive dressings, keep the limb near heart level and obtain immediate surgical assessment for fasciotomy. Do not delay surgery for imaging.

Mass-casualty triage prioritises limited resources to achieve the greatest overall survival when patient numbers exceed immediate treatment capacity.

Patients are categorised by urgency using rapid assessment of mobility, breathing, perfusion and mental status according to the local triage system.

Perform only rapid life-saving assessments/interventions during primary triage rather than complete individual examinations.

Diagnostics are deferred until after initial categorisation and movement to treatment areas unless immediately life-saving.

Use a predefined incident command and triage framework, reassess categories dynamically and separate contamination/decontamination pathways when relevant.

After return of spontaneous circulation, secondary brain injury, myocardial dysfunction and the precipitating cause determine outcome.

Coma, shock, arrhythmia and respiratory failure are common after ROSC.

Stabilise airway/ventilation, haemodynamics, neurological status and temperature while searching for the arrest cause.

Obtain ECG, blood gas, electrolytes and cause-directed imaging/coronary evaluation. Avoid premature neurological prognostication while confounders remain.

Target appropriate oxygenation and ventilation, maintain perfusion, treat the cause and actively prevent fever; use structured temperature-control strategies in comatose survivors according to current protocols.

Delirium is an acute fluctuating disorder of attention and cognition caused by an underlying physiological disturbance and is especially common in older or critically ill patients.

Inattention, altered arousal, disorganised thinking and fluctuation over hours are characteristic; hypoactive delirium is easily missed.

Assess attention, consciousness, focal neurology, hydration, pain, urinary retention and infection and review medications.

Check glucose, oxygenation and targeted labs; imaging or LP is guided by neurological findings and clinical context.

Treat the cause, optimise sleep/orientation, mobility, hearing/vision and hydration and minimise deliriogenic drugs. Use sedating medication only when severe agitation threatens safety or essential care.