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Here is a complete, detailed explanation of every topic on your exam paper:
1st Terminal Examination — General Medicine: Complete Topic Guide
QUESTION 1 — MCQ EXPLANATIONS
Q1. Lactic Acidosis — Drug: Metformin ✅
Answer: b. Metformin
Metformin is a biguanide used in Type 2 Diabetes. It inhibits mitochondrial complex I, impairing oxidative phosphorylation and forcing cells to rely on anaerobic glycolysis, producing excess lactate. The resulting metformin-associated lactic acidosis (MALA) carries up to 50% mortality.
- Mechanism: Impairs hepatic lactate clearance + increases pyruvate-to-lactate conversion
- Risk factors: Renal impairment (drug accumulates), sepsis, hepatic failure, contrast dye use, alcohol
- Features: Nausea, vomiting, abdominal pain, hypotension, altered mental status, pH <7.35, lactate >5 mmol/L
- Treatment: Stop metformin, IV fluids, bicarbonate, hemodialysis (removes drug effectively)
Other options: Pioglitazone (causes fluid retention/heart failure), Voglibose (alpha-glucosidase inhibitor, causes flatulence), Sitagliptin (DPP-4 inhibitor, causes nasopharyngitis) — none cause lactic acidosis.
Q2. Most Common Cause of Cushing's Disease — Pituitary Adenoma ✅
Answer: b. Pituitary adenoma
| Cause | Notes |
|---|---|
| Exogenous steroids | Most common cause of Cushing's Syndrome overall |
| Pituitary adenoma (ACTH-secreting) | Most common cause of Cushing's Disease (endogenous) — ~70% |
| Ectopic ACTH | Small cell lung cancer, carcinoid — ~15% |
| Adrenocortical adenoma | Autonomous cortisol secretion — rare |
Key distinction: Cushing's Disease specifically = pituitary adenoma → excess ACTH → bilateral adrenal hyperplasia → excess cortisol.
Features: Central obesity, moon face, buffalo hump, purple striae, proximal myopathy, hypertension, hyperglycemia, osteoporosis, hirsutism.
Diagnosis: 24-hr urine free cortisol → overnight dexamethasone suppression test → CRH stimulation → MRI pituitary.
Treatment: Transsphenoidal surgery.
Q3. Which is NOT used as an Analgesic — Ivabradine ✅
Answer: Ivabradine
- Diclofenac: NSAID — inhibits COX-1 and COX-2, used for pain and inflammation
- Tramadol: Weak opioid agonist + serotonin/norepinephrine reuptake inhibitor — used for moderate pain
- Naproxen: NSAID — used for pain, fever, arthritis
Ivabradine: A selective funny channel (I_f) inhibitor in the SA node — used for stable angina and heart failure (rate control). It has NO analgesic properties.
Q4. Non-Modifiable Risk Factor — Race ✅
Answer: Race
| Modifiable | Non-Modifiable |
|---|---|
| Weight ✓ | Race ✗ |
| Smoking ✓ | Age |
| Alcoholism ✓ | Sex/Gender |
| Family history | |
| Genetics |
Race is determined genetically and cannot be changed. It is a non-modifiable risk factor for diseases like hypertension, diabetes, and cardiovascular disease (e.g., African Americans have higher rates of hypertension).
Q5. NOT a Part of Light's Criteria — c. Pleural fluid LDH >0.6 ✅
Answer: c. Pleural fluid/serum LDH >0.6
Light's Criteria (1972) — an exudate if ANY ONE is present:
- Pleural fluid protein / serum protein > 0.5
- Pleural fluid LDH / serum LDH > 0.6
- Pleural fluid LDH > 2/3 of the upper limit of normal serum LDH
Option (c) says "PF LDH >0.6" — this is incorrect because the ratio PF LDH/serum LDH >0.6 is the criterion, not PF LDH alone being >0.6. So (c) is the incorrect/non-existent criterion.
If ANY of Light's criteria is met → exudate (think infection, malignancy, TB).
If NONE met → transudate (think heart failure, cirrhosis, nephrotic syndrome).
Q6. Relative Bradycardia — All of the Above ✅
Answer: All of the above (Typhoid fever, Q fever, Leptospirosis)
Relative bradycardia (Faget's sign) = Heart rate does not rise proportionally to the degree of fever (pulse-temperature dissociation). Normally, each 1°C rise in temperature → ~10 bpm rise in heart rate.
- Typhoid fever (Salmonella typhi): Classic teaching — bradycardia despite high fever
- Q fever (Coxiella burnetii): Intracellular organism causing relative bradycardia
- Leptospirosis (Leptospira): Can cause pulse-temperature dissociation
Other causes: Brucellosis, Legionella, drug fever, yellow fever, malaria.
Mechanism: These organisms or their toxins directly suppress the sinoatrial node, offsetting the normal sympathetic-mediated tachycardia of fever.
Q7. NOT a Part of CHA₂DS₂-VASc Score — c. Duration ✅
Answer: c. Duration
CHA₂DS₂-VASc is used to estimate stroke risk in non-valvular atrial fibrillation and guide anticoagulation.
| Letter | Risk Factor | Points |
|---|---|---|
| C | Congestive heart failure | 1 |
| H | Hypertension | 1 |
| A₂ | Age ≥ 75 | 2 |
| D | Diabetes mellitus | 1 |
| S₂ | Stroke/TIA/thromboembolism | 2 |
| V | Vascular disease | 1 |
| A | Age 65–74 | 1 |
| Sc | Sex category (female) | 1 |
Duration of AF is NOT included. Maximum score = 9. Score ≥2 in males, ≥3 in females → anticoagulate.
Q8. SAAG Ratio is Measured in — Ascitic fluid ✅
Answer: Ascitic fluid
SAAG = Serum Albumin − Ascitic Fluid Albumin
| SAAG | Implies | Causes |
|---|---|---|
| ≥ 1.1 g/dL | Portal hypertension | Cirrhosis, heart failure, Budd-Chiari, portal vein thrombosis |
| < 1.1 g/dL | Non-portal | Peritoneal carcinomatosis, TB peritonitis, nephrotic syndrome, pancreatitis |
SAAG is calculated from ascitic fluid obtained by paracentesis, not from CSF, urine, or pleural fluid.
Q9. SGLT2 Inhibitor — Dapagliflozin ✅
Answer: Dapagliflozin
SGLT2 (Sodium-Glucose Cotransporter 2) inhibitors block glucose reabsorption in the proximal tubule → glucosuria → lowered blood glucose.
| Drug | Class |
|---|---|
| Dapagliflozin | SGLT2 inhibitor ✅ |
| Empagliflozin | SGLT2 inhibitor |
| Canagliflozin | SGLT2 inhibitor |
| Glimepiride | Sulfonylurea |
| Pioglitazone | Thiazolidinedione |
| Voglibose | Alpha-glucosidase inhibitor |
Benefits beyond glucose: Cardiovascular protection, heart failure reduction (reduced hospitalizations), renoprotection. Side effects: Genital mycotic infections, UTIs, DKA (euglycemic), Fournier's gangrene (rare).
Q10. Joint Spared in Rheumatoid Arthritis — DIP ✅
Answer: DIP (Distal Interphalangeal joint)
RA characteristically affects:
- PIP (Proximal Interphalangeal) ✓ — affected
- MCP (Metacarpophalangeal) ✓ — affected
- Wrist ✓ — affected
- DIP (Distal Interphalangeal) ✗ — SPARED in RA
DIP joints are typically affected in Osteoarthritis (Heberden's nodes) and Psoriatic arthritis. RA is a symmetrical, additive, peripheral polyarthritis that spares DIPs.
QUESTION 2 — Cardiomyopathy
Definition
Cardiomyopathy is a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually exhibit inappropriate ventricular hypertrophy or dilatation, leading to heart failure, arrhythmias, and sudden cardiac death, often in the absence of coronary artery disease, hypertension, or valvular disease.
Types of Cardiomyopathy
1. Dilated Cardiomyopathy (DCM)
- Most common type (~60% of cases)
- Dilatation of all 4 chambers, predominantly left ventricle, with systolic dysfunction (↓EF)
- Causes: Idiopathic, viral myocarditis (Coxsackie B), alcohol, peripartum, drugs (doxorubicin), genetic
- Features: Progressive dyspnea, orthopnea, S3 gallop, pulmonary congestion, mitral regurgitation
- ECG: LBBB, atrial fibrillation
- Echo: Dilated LV, EF <40%, global hypokinesia
2. Hypertrophic Cardiomyopathy (HCM)
- Genetic, autosomal dominant — mutations in sarcomeric proteins (β-myosin heavy chain most common)
- Asymmetric septal hypertrophy, diastolic dysfunction, dynamic LVOTO
- Most common cause of sudden cardiac death in young athletes
3. Restrictive Cardiomyopathy (RCM)
- Rigid, non-compliant ventricles; impaired diastolic filling; systolic function relatively preserved
- Causes: Amyloidosis (most common), sarcoidosis, hemochromatosis, endomyocardial fibrosis, radiation
- Features mimic constrictive pericarditis — elevated JVP, Kussmaul's sign
- Echo: Biatrial enlargement, small stiff ventricles, "granular sparkling" in amyloidosis
4. Arrhythmogenic Cardiomyopathy (ARVC)
- Fibro-fatty replacement of right ventricular myocardium
- Presents with VT (LBBB morphology), syncope, SCD in young adults
- ECG: Epsilon wave, T-wave inversions V1–V3
- Genetic: Desmosomal protein mutations (plakophilin-2)
5. Takotsubo (Stress) Cardiomyopathy
- Transient apical ballooning of LV triggered by emotional/physical stress
- Mimics MI but coronaries are normal
- Mainly post-menopausal women; usually reversible
Hypertrophic Cardiomyopathy (HCM) — In Detail
Genetics: Autosomal dominant. Mutations in sarcomeric genes — β-myosin heavy chain (MYH7, ~35%), myosin-binding protein C (MYBPC3, ~25%), troponin T (TNNT2), troponin I. Penetrance is variable.
Pathophysiology:
- Asymmetric hypertrophy, especially of the interventricular septum
- Abnormal disarray of cardiomyocytes (myofibrillar disarray)
- Diastolic dysfunction: Stiff hypertrophied walls → impaired filling → raised filling pressures
- Dynamic Left Ventricular Outflow Tract Obstruction (LVOTO): Hypertrophied septum + Systolic Anterior Motion (SAM) of mitral valve leaflet → obstruction worsens with:
- Decreased preload (dehydration, Valsalva, standing)
- Decreased afterload (vasodilators)
- Increased contractility (exercise, digoxin)
Clinical Features:
- Dyspnea (most common) — diastolic dysfunction → pulmonary congestion
- Angina — increased O₂ demand + microvascular ischemia
- Syncope/pre-syncope — LVOTO during exertion
- Sudden cardiac death — due to ventricular arrhythmias (most common cause of SCD in athletes <35 yrs)
- Palpitations — AF, VT
Examination:
- Jerky carotid pulse (rapid upstroke)
- Double apical impulse
- Systolic ejection murmur at LLSE — increases with Valsalva/standing (↓preload → ↑obstruction); decreases with squatting (↑preload → ↓obstruction)
- Mitral regurgitation murmur (due to SAM)
Investigations:
- ECG: LVH, deep Q waves (pseudo-infarct pattern) in lateral leads, ST changes
- Echocardiography (gold standard): Septal thickness ≥15 mm (or ≥13 mm with family history), SAM of mitral valve, LVOT gradient >30 mmHg at rest or >50 mmHg with provocation
- Cardiac MRI: Best for myocardial fibrosis (late gadolinium enhancement)
- Genetic testing: Identifies mutations; family screening recommended
Management:
- Beta-blockers (metoprolol) — first line; reduce heart rate, improve diastolic filling
- Non-dihydropyridine CCBs (verapamil) — if beta-blockers not tolerated
- Disopyramide — negative inotrope for LVOTO
- Mavacamten — novel myosin inhibitor (FDA approved 2022) for obstructive HCM
- AVOID: Nitrates, digoxin, dihydropyridine CCBs, ACE inhibitors in LVOTO (worsen obstruction)
- ICD — for SCD prevention in high-risk patients (VT, syncope, massive LVH, family history of SCD)
- Septal reduction: Surgical myectomy or alcohol septal ablation for refractory obstructive HCM
- Anticoagulation — for concurrent atrial fibrillation
QUESTION 3 — Short Notes (4 marks each)
a. Management of Heart Failure
Acute (Decompensated) Heart Failure:
- Position: Sit upright
- IV Furosemide (loop diuretic) — first line for congestion/fluid overload
- IV Nitrates — vasodilation, reduce preload (if SBP >90)
- Oxygen — target SpO₂ >94%; NIV (CPAP/BiPAP) for pulmonary edema
- Morphine — reduces anxiety/preload (use cautiously)
- Identify and treat precipitant (infection, AF, MI, non-compliance)
Chronic HF with Reduced EF (HFrEF) — "Foundational Four":
| Drug | Benefit |
|---|---|
| ACE inhibitor/ARB/ARNi (e.g., sacubitril-valsartan) | ↓ mortality, ↓ remodeling |
| Beta-blocker (carvedilol, metoprolol, bisoprolol) | ↓ mortality, ↓ HR |
| MRA (spironolactone, eplerenone) | ↓ mortality, ↓ fibrosis |
| SGLT2 inhibitor (dapagliflozin, empagliflozin) | ↓ HF hospitalizations, ↓ CV death |
Additional:
- Diuretics for symptom relief
- Ivabradine — if HR >70 despite beta-blockers, in sinus rhythm
- Digoxin — reduces HF hospitalizations (not mortality)
- ICD/CRT — for EF <35% with LBBB
b. Portal Hypertension
Definition: Portal venous pressure >12 mmHg (normal 5–10 mmHg); clinically significant when HVPG (Hepatic Venous Pressure Gradient) ≥10 mmHg.
Classification by Site:
- Prehepatic: Portal vein thrombosis, splenic vein thrombosis
- Intrahepatic (sinusoidal): Cirrhosis (most common worldwide), schistosomiasis
- Posthepatic: Budd-Chiari syndrome, right heart failure, constrictive pericarditis
Pathophysiology: Cirrhosis → sinusoidal fibrosis → ↑resistance → ↑portal pressure → splanchnic vasodilation → hyperdynamic circulation → further ↑portal flow.
Complications & Management:
| Complication | Treatment |
|---|---|
| Esophageal varices | Non-selective β-blockers (propranolol/carvedilol); TIPS; EVL (Endoscopic variceal ligation) |
| Acute variceal bleed | IV terlipressin + antibiotics + urgent EVL; Sengstaken tube if uncontrolled |
| Ascites | Salt restriction, spironolactone ± furosemide, LVP (large volume paracentesis) for tense ascites |
| SBP | IV ceftriaxone/cefotaxime; prophylaxis with norfloxacin |
| Hepatic encephalopathy | Lactulose, rifaximin |
| Hepatorenal syndrome | Terlipressin + albumin |
c. Addison's Disease (Primary Adrenal Insufficiency)
Definition: Destruction/dysfunction of the adrenal cortex leading to deficiency of cortisol, aldosterone, and androgens.
Causes:
- Autoimmune (most common in developed world — ~80%) — anti-21-hydroxylase antibodies
- Tuberculosis (most common worldwide)
- Bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome — meningococcal sepsis)
- HIV, metastases, sarcoidosis
Clinical Features:
- Hyperpigmentation (buccal mucosa, skin creases, scars) — due to excess ACTH/MSH
- Fatigue, weakness
- Postural hypotension
- Weight loss, anorexia, nausea
- Salt craving
- Hyponatremia, hyperkalemia, hypoglycemia
- Addisonian Crisis: Acute collapse, severe hypotension, vomiting, hypoglycemia → medical emergency
Diagnosis:
- Short Synacthen Test (gold standard): 250 mcg synacthen IM/IV → cortisol <550 nmol/L at 30–60 min = inadequate response
- ↑ACTH (in primary), ↓cortisol, ↓aldosterone, ↑renin
- Autoantibodies (anti-21-hydroxylase)
Treatment:
- Hydrocortisone (cortisol replacement): 15–25 mg/day in divided doses (morning: afternoon = 2:1)
- Fludrocortisone (mineralocorticoid replacement): 100–200 mcg/day
- DHEA — in women for well-being/libido
- Sick day rules: Double/triple dose during illness
- Adrenal crisis: IV hydrocortisone 100 mg stat + IV saline + dextrose
d. Trigeminal Autonomic Cephalalgias (TACs)
Definition: A group of primary headache disorders characterized by strictly unilateral trigeminal pain with prominent ipsilateral cranial autonomic features.
Autonomic features (same side as pain):
- Lacrimation, conjunctival injection
- Ptosis, miosis (Horner-like)
- Nasal congestion/rhinorrhea
- Eyelid edema, facial sweating
Types:
| Type | Duration | Frequency | Key Feature |
|---|---|---|---|
| Cluster Headache | 15 min–3 hrs | 1–8/day | Excruciating periorbital pain; "alarm clock" headache; circadian pattern; restlessness |
| Paroxysmal Hemicrania | 2–30 min | >5/day | Responds dramatically to indomethacin |
| SUNCT/SUNA | 5–240 sec | Up to 200/day | Shortest duration; triggered by touch |
| Hemicrania Continua | Continuous | Continuous | Responds to indomethacin |
Cluster Headache Management:
- Acute: 100% high-flow O₂ (first line), subcutaneous sumatriptan
- Prophylaxis: Verapamil (drug of choice), lithium, short-course steroids
Mechanism: Involves the trigeminovascular system and hypothalamic activation (posterior hypothalamus — hence "hypothalamic headaches"). PET scans show hypothalamic activation during cluster attacks.
e. Iron Deficiency Anemia
Definition: Microcytic, hypochromic anemia due to depleted iron stores.
Causes:
- Blood loss: Menorrhagia (women), GI bleed (men/post-menopausal women — rule out colon cancer/peptic ulcer)
- Inadequate intake: Vegetarian diet, malnutrition
- Malabsorption: Celiac disease, post-gastrectomy, H. pylori infection
- Increased demand: Pregnancy, infancy
Stages:
- Iron depletion (↓ferritin, normal Hb)
- Iron-deficient erythropoiesis (↓serum iron, ↑TIBC, ↑transferrin, normal Hb)
- Iron deficiency anemia (↓Hb, microcytic hypochromic RBCs)
Clinical Features:
- Fatigue, pallor, dyspnea on exertion
- Koilonychia (spoon-shaped nails)
- Angular stomatitis, glossitis
- Pica (craving for ice/clay)
- Plummer-Vinson syndrome: IDA + dysphagia + esophageal web (post-cricoid)
Investigations:
- ↓Hb, ↓MCV (<80 fL), ↓MCH
- Blood film: Microcytic, hypochromic, pencil cells, target cells
- ↓Serum ferritin (most sensitive store indicator; but acute-phase reactant)
- ↓Serum iron, ↑TIBC (↑Transferrin)
- ↓Transferrin saturation (<20%)
Treatment:
- Oral ferrous sulfate 200 mg TDS — take with vitamin C (enhances absorption); avoid tea/calcium
- Duration: 3 months to replenish stores after Hb normalizes
- IV iron (ferric carboxymaltose) if oral not tolerated/malabsorption
- Blood transfusion if severely symptomatic or pre-operative
- Treat the underlying cause
QUESTION 4 — Short Answers (2 marks each)
a. ACR/EULAR 2010 Criteria for Rheumatoid Arthritis
Used for classification (not diagnosis). Score ≥6/10 = definite RA.
| Domain | Score |
|---|---|
| Joint involvement | |
| 1 medium-large joint | 0 |
| 2–10 medium-large joints | 1 |
| 1–3 small joints | 2 |
| 4–10 small joints | 3 |
| >10 joints (at least 1 small) | 5 |
| Serology | |
| Negative RF and anti-CCP | 0 |
| Low positive RF or anti-CCP | 2 |
| High positive RF or anti-CCP | 3 |
| Acute phase reactants | |
| Normal CRP and ESR | 0 |
| Abnormal CRP or ESR | 1 |
| Duration of symptoms | |
| <6 weeks | 0 |
| ≥6 weeks | 1 |
Prerequisite: At least 1 joint with definite clinical synovitis + synovitis not explained by another disease.
b. Difference Between Bacterial and Tubercular Meningitis
| Feature | Bacterial Meningitis | TB Meningitis |
|---|---|---|
| Onset | Acute (hours–days) | Subacute/chronic (weeks–months) |
| CSF appearance | Turbid/purulent | Clear/fibrinous ("cobweb clot") |
| CSF pressure | Raised | Raised |
| Cell type | Neutrophils (>1000/µL) | Lymphocytes (100–500/µL) |
| Protein | ↑↑ (>100 mg/dL) | ↑ (100–500 mg/dL) |
| Glucose | Very low (<40 mg/dL) | Low (<45 mg/dL) |
| CSF:Serum glucose | <0.3 | <0.5 |
| Gram stain/Culture | Positive in 60–80% | ZN stain; AFB culture (weeks); GeneXpert MTB |
| Organisms | S. pneumoniae, N. meningitidis, Listeria | M. tuberculosis |
| Treatment | IV Ceftriaxone + Dexamethasone | RHEZ (Rifampicin, INH, Ethambutol, Pyrazinamide) × 2 months, then RH × 10 months |
| Mortality if untreated | ~100% | ~100% |
c. Drugs for Diabetes Mellitus
| Class | Drug | Mechanism | Key Feature |
|---|---|---|---|
| Biguanide | Metformin | ↓Hepatic gluconeogenesis | First line T2DM; weight neutral |
| Sulfonylurea | Glimepiride, Glibenclamide | ↑Insulin secretion (β-cell) | Risk of hypoglycemia + weight gain |
| DPP-4 inhibitor | Sitagliptin, Vildagliptin | Prolongs GLP-1 → ↑insulin | Weight neutral, no hypoglycemia |
| GLP-1 agonist | Semaglutide, Liraglutide | ↑Insulin, ↓glucagon | Weight loss, CV benefit |
| SGLT2 inhibitor | Dapagliflozin, Empagliflozin | ↑Urinary glucose excretion | Weight loss, CV + renal benefit |
| Thiazolidinedione | Pioglitazone | ↑Insulin sensitivity (PPAR-γ) | Weight gain, fluid retention |
| Alpha-glucosidase inhibitor | Voglibose, Acarbose | ↓Carbohydrate absorption | GI side effects |
| Insulin | Regular, NPH, Glargine | Direct glucose uptake | T1DM essential; T2DM step-up |
d. Autoimmune Hepatitis (AIH)
Definition: Chronic inflammatory liver disease of unknown etiology, characterized by hepatocyte necrosis, elevated transaminases, hypergammaglobulinemia, and autoantibodies.
Types:
- Type 1 (most common): Anti-smooth muscle antibody (ASMA), Anti-ANA; affects all ages
- Type 2: Anti-LKM1 (anti-liver-kidney microsomal Ab); children/young women
- Type 3: Anti-SLA (soluble liver antigen)
Clinical Features: Fatigue, jaundice, hepatomegaly, amenorrhea; may present as acute liver failure; associated with other autoimmune diseases (thyroiditis, celiac, IBD).
Diagnosis (Simplified Criteria):
- ANA/ASMA ≥1:40 — 1 point each
- IgG >ULN — 1 point; >1.1× ULN — 2 points
- Liver histology: Compatible — 1 point; Typical — 2 points
- Absence of viral hepatitis
- Score ≥6 = probable AIH; ≥7 = definite AIH
Treatment:
- Induction: Prednisolone 40–60 mg/day
- Maintenance: Azathioprine (reduces steroid dose), taper over 18–24 months
- Liver transplantation for end-stage disease
e. Acute Pancreatitis
Definition: Acute inflammatory process of the pancreas with variable involvement of peripancreatic tissue and distant organs.
Causes (GET SMASHED):
Gallstones (40–50%) | Ethanol (30–35%) | Trauma | Steroids | Mumps/viruses | Autoimmune | Scorpion/snake venom | Hyperlipidemia/Hypercalcemia/Hypothermia | ERCP | Drugs (azathioprine, furosemide, valproate)
Pathophysiology: Premature activation of trypsinogen → trypsin → autodigestion of pancreas → acinar cell necrosis → inflammatory cascade → SIRS/MODS.
Clinical Features: Severe epigastric pain radiating to the back, nausea/vomiting, fever. Grey-Turner sign (flank bruising), Cullen's sign (periumbilical bruising) — indicate hemorrhagic pancreatitis.
Investigations:
- Serum amylase >3× upper limit of normal (rises in 2–12 hrs, peaks at 24 hrs)
- Serum lipase (more sensitive and specific, remains elevated longer)
- ↑WBC, ↑CRP (marker of severity), ↑glucose, ↓calcium
- CECT abdomen (contrast CT) — gold standard for severity, shows necrosis
Severity (Ranson's Criteria / Atlanta Classification):
- Mild: No organ failure, no local complications
- Moderately severe: Transient organ failure (<48 hrs) OR local complications
- Severe: Persistent organ failure (>48 hrs)
Management:
- Aggressive IV fluid resuscitation (Ringer's lactate preferred)
- Analgesia (IV tramadol/pethidine; morphine traditionally avoided)
- Nil by mouth initially; early enteral nutrition (nasojejunal feeding) is preferred over TPN
- Antibiotics only if infected necrosis (meropenem)
- ERCP if gallstone pancreatitis with cholangitis
- Cholecystectomy during same admission after mild biliary pancreatitis
- Monitor for complications: Pseudocyst, abscess, ARDS, AKI, DIC
This covers every question and sub-topic from both pages of your exam paper. Let me know if you need any topic expanded further or summarized into flashcard format.
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