🩺 MBBS FINALS - Medicine

a) Etiology, risk factors and clinical features
Etiology: Autoimmune Hashimoto thyroiditis is the commonest cause in iodine-sufficient regions. Other causes include iodine deficiency/excess, thyroidectomy or radioiodine therapy, drugs such as amiodarone/lithium, infiltrative disease, congenital thyroid disorders and post-thyroiditis states.
Risk factors: Female sex, increasing age, family/personal history of autoimmune disease, previous neck irradiation or thyroid surgery, postpartum state and drugs affecting thyroid function.
Clinical features: Fatigue, somnolence, weight gain despite reduced appetite, cold intolerance, constipation, dry/coarse skin, hair loss, hoarse voice, myalgia/cramps, menstrual disturbance/infertility, depression or cognitive slowing. Examination may show bradycardia, cool dry skin, periorbital puffiness, non-pitting myxedema, delayed ankle-jerk relaxation and, in Hashimoto disease, goiter.

b) Diagnostic evaluation
Primary hypothyroidism: TSH elevated with free T4 low. Subclinical hypothyroidism: TSH elevated with free T4 normal. Anti-TPO antibody supports autoimmune thyroiditis. Baseline CBC, sodium, lipid profile, glucose, liver enzymes and CK may identify consequences/alternatives. ECG may show sinus bradycardia/low voltage. Ultrasound is not routinely required unless goiter/nodule is present.

c) Management and follow-up
Treat with oral levothyroxine, usually once daily on an empty stomach. Young otherwise healthy adults can generally start near full replacement (~1.6 microgram/kg/day), while elderly patients or those with ischemic heart disease should start low and titrate slowly. Recheck TSH about 6-8 weeks after starting or changing dose, then every 6-12 months once stable. Aim for TSH in the reference range, assess adherence and interactions (iron, calcium, antacids, some foods), and adjust dose in pregnancy. Myxedema coma requires emergency IV thyroid hormone, glucocorticoid coverage until adrenal insufficiency is excluded, supportive care and treatment of precipitating cause.

Urinary loss of anticoagulant proteins such as antithrombin III and proteins C/S, increased hepatic synthesis of procoagulant factors and fibrinogen, platelet hyperreactivity, hemoconcentration from diuresis/intravascular depletion and reduced fibrinolysis together produce a hypercoagulable state. Renal-vein thrombosis and venous thromboembolism are important complications.

High extracellular potassium reduces the resting membrane potential, initially increasing excitability but then inactivating fast sodium channels and slowing conduction. ECG progression may include peaked T waves, PR prolongation, loss of P waves, QRS widening, sine-wave pattern and ventricular fibrillation/asystole.

Elevated LV end-diastolic and left atrial pressures raise pulmonary venous/capillary hydrostatic pressure, causing interstitial and alveolar transudation. Dependent basal lung regions are affected early. During inspiration, reopening of fluid-lined small airways/alveoli produces fine basal crackles.

Iron deficiency limits heme and hemoglobin synthesis. Erythroblasts undergo extra cell divisions before reaching an adequate intracellular hemoglobin concentration, producing smaller cells (microcytosis). Reduced hemoglobin concentration gives increased central pallor (hypochromia).

Excess ADH causes water retention and dilutional hyponatremia. The mild extracellular-volume expansion suppresses renin/aldosterone and promotes natriuresis, allowing sodium and water excretion until near-euvolemia is restored. Thus there is excess total body water without overt edema in most patients.

Treat as an emergency. Assess ABCs, vital signs, oxygen saturation, hemodynamic stability, heart failure and complications; obtain focused history (onset, contraindications to reperfusion/antithrombotics) and repeat 12-lead ECG. Establish IV access, monitor rhythm, send troponin, CBC, renal function, glucose and electrolytes without delaying reperfusion. Give aspirin loading plus an appropriate P2Y12 inhibitor and anticoagulation according to reperfusion strategy. Give sublingual/IV nitrates if pain/ischemia persists and there is no hypotension, RV infarction or PDE-5 inhibitor use; use analgesia judiciously. Oxygen only if hypoxemic/respiratory distress. High-intensity statin should be started. Primary PCI is preferred when promptly available; otherwise fibrinolysis is considered within the appropriate time window if no contraindication, followed by transfer for angiography. Inferior STEMI should prompt right-sided leads if RV infarction suspected and careful avoidance of preload-reducing drugs in hypotension.

Diagnosis is clinical: fever/systemic symptoms plus urinary symptoms and flank/CVA tenderness. Perform urinalysis for pyuria, leukocyte esterase/nitrite and send urine culture before antibiotics if possible. Check pregnancy status where relevant, CBC, renal function and blood cultures if septic/severely ill. Imaging is not routinely required in uncomplicated disease; ultrasound/CT is indicated for obstruction, stone, atypical course, severe illness or failure to improve. Start appropriate empirical antibiotics based on local resistance and severity, then tailor to culture. Give oral fluids/analgesia/antipyretics if stable; admit for IV antibiotics and fluids if vomiting, sepsis, pregnancy, obstruction, major comorbidity or inability to take oral therapy. Urgent urologic drainage is required for infected obstruction.

Assess severity of distension, dyspnea, edema, encephalopathy, infection, GI bleed and renal dysfunction. Examine JVP, abdomen, hernias and signs of chronic liver disease. Do CBC, LFT/INR, renal function/electrolytes and ultrasound. Diagnostic paracentesis is indicated in new-onset ascites and in hospitalized/decompensated patients, with cell count/differential, albumin and total protein; PMN ≥250/mm3 supports spontaneous bacterial peritonitis. Restrict dietary sodium; avoid NSAIDs and nephrotoxic drugs. Use spironolactone with or without furosemide while monitoring weight, creatinine, sodium and potassium. Large-volume paracentesis is used for tense/refractory ascites with albumin replacement when large volumes are removed. Treat SBP promptly, consider prophylaxis when indicated, assess for TIPS in selected refractory cases, and refer appropriate decompensated patients for liver-transplant evaluation.

Delirium is an acute, fluctuating disturbance of attention and cognition. Confirm with bedside assessment (e.g. 4AT/CAM), determine baseline cognition and assess ABCs, oxygenation, glucose, hydration, pain, urinary retention/constipation and neurological signs. Common precipitants include infection, hypoxemia, medications (sedatives, anticholinergics, opioids), withdrawal, electrolyte/metabolic disturbance, dehydration, organ failure, sleep disruption and unfamiliar environment. Investigations are targeted: CBC, electrolytes, renal/liver function, glucose, oxygenation, urinalysis/culture and imaging when indicated. Treat the underlying cause; provide orientation, clocks/family contact, glasses/hearing aids, sleep hygiene, hydration, nutrition and early mobilization. Avoid restraints and unnecessary sedatives. If severe agitation creates immediate risk, use the lowest effective short course of an antipsychotic after considering QT/prolongation, Parkinsonism/Lewy-body dementia and other contraindications.

Features include weight loss despite appetite, heat intolerance, sweating, palpitations, tremor, anxiety, diarrhea, proximal myopathy, menstrual disturbance, tachycardia/AF, warm moist skin and goiter. Graves disease may cause eye signs and pretibial myxedema. Diagnosis: suppressed TSH with elevated free T4 and/or T3; TSH-receptor antibodies support Graves. Radionuclide uptake or ultrasound is selected when etiology is unclear. Symptom control with a beta-blocker; antithyroid drugs (usually methimazole/carbimazole; PTU in selected pregnancy/thyroid storm settings), radioiodine or surgery depending on cause/patient factors. Monitor thyroid tests and adverse drug effects; manage thyroid storm as an emergency.

Risk factors include age extremes, smoking, alcohol excess, chronic lung/heart/renal/liver disease, diabetes, immunosuppression and aspiration risk. Typical presentation: acute fever, cough, sputum, pleuritic pain, dyspnea, tachypnea, hypoxemia and focal crepitations/bronchial breathing. Confirm with chest radiography where appropriate and assess severity (e.g. CURB-65 plus clinical judgment). Obtain cultures in severe disease. Give timely empiric antibiotics according to local guidelines and severity, oxygen if hypoxemic, fluids, antipyretics and thromboprophylaxis where indicated. Reassess response and complications such as sepsis or pleural infection.

Presentations include hematemesis, coffee-ground vomiting or melena; hematochezia may occur with massive bleeding. Assess ABCs, shock index, orthostatic signs and comorbidity. Establish large-bore IV access, CBC, group/crossmatch, renal/liver tests and coagulation. Resuscitate with crystalloids and blood products using a generally restrictive transfusion strategy unless specific indications. Stop/reverse anticoagulation when appropriate. Give IV PPI in suspected non-variceal bleeding according to local protocol; if varices suspected, start vasoactive therapy and antibiotics. Urgent endoscopy after stabilization allows diagnosis and endoscopic hemostasis. Persistent/recurrent bleeding may require interventional radiology or surgery.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is a subset with profound circulatory/metabolic abnormalities, typically requiring vasopressors to maintain MAP ≥65 mmHg and lactate >2 mmol/L despite adequate volume resuscitation. Recognize infection plus organ dysfunction: altered mentation, hypotension, tachypnea/hypoxemia, oliguria, mottling and raised lactate. Obtain cultures promptly without delaying antibiotics, measure lactate, give early appropriate broad-spectrum antimicrobials, IV balanced crystalloids for hypoperfusion, reassess fluid responsiveness, and start norepinephrine if hypotension persists. Provide source control, oxygen/ventilatory support and organ-specific care.

Use antibiotics only for likely/confirmed bacterial infection; obtain relevant cultures before therapy when this does not delay urgent treatment. Choose the narrowest effective agent based on likely pathogen, local antibiogram, allergy, site penetration, renal/hepatic function and severity. Use correct dose/route and shortest effective duration. Review at 48-72 h: stop if infection unlikely, narrow/de-escalate when cultures allow, switch IV to oral when stable. Avoid duplicate coverage and unnecessary prophylaxis. Stewardship also includes infection prevention, vaccination, hand hygiene, audit-feedback, formulary guidance and surveillance of resistance/consumption.

Assess BMI, waist circumference, weight trajectory, diet/activity, sleep, medications and secondary causes. Screen for complications: diabetes, hypertension, dyslipidemia, NAFLD, OSA, osteoarthritis, GERD, infertility and cardiovascular disease. Management is long-term: individualized calorie deficit with nutritionally balanced diet, regular aerobic plus resistance activity, behavioral strategies, sleep optimization and treatment of comorbidities. Anti-obesity pharmacotherapy can be considered when indicated, alongside lifestyle therapy. Metabolic/bariatric surgery is considered for severe obesity meeting accepted criteria after multidisciplinary assessment.

A structured approach improves clarity and empathy. SPIKES: Setting up the interview; assess Perception; obtain Invitation regarding desired information; give Knowledge in small clear chunks; respond to Emotions with empathy; Strategy and Summary with next steps. BREAKS similarly emphasizes Background/preparation, Rapport, Exploring understanding, Announcing the news, Kindling/responding to emotions and Summarizing/strategy. Ensure privacy, avoid jargon, check understanding, allow silence/questions and document key decisions.