(a) Discuss in short the etiology, diagnosis, treatment and complications of cirrhosis of liver. (5+5+5+5=20 marks) (b) A…

Part (a) Cirrhosis of Liver

Etiology: Cirrhosis results from chronic hepatic injury leading to diffuse fibrosis and regenerative nodules. Key etiologies include chronic alcohol abuse, chronic viral hepatitis (Hepatitis B and C), non-alcoholic fatty liver disease (NAFLD/NASH), autoimmune hepatitis, biliary diseases (primary biliary cholangitis, primary sclerosing cholangitis), and metabolic disorders (Wilson's disease, hemochromatosis, alpha-1 antitrypsin deficiency).

Diagnosis: Diagnosis is established through a composite of clinical stigmata (spider angiomas, palmar erythema, jaundice), laboratory findings (thrombocytopenia, elevated PT/INR, hypoalbuminemia, transaminitis), and non-invasive imaging (ultrasound showing nodular liver and portal hypertension; transient elastography/FibroScan). Prognosis is quantified using the Child-Pugh and MELD/MELD-Na scoring systems. Liver biopsy remains the diagnostic gold standard when etiology is uncertain.

Complications: Cirrhosis precipitates portal hypertension leading to esophageal and gastric variceal bleeding, ascites, and splenomegaly. Other major life-threatening sequelae include spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, hepatorenal syndrome (HRS), hepatopulmonary syndrome, and progression to hepatocellular carcinoma (HCC).

Treatment: Management relies on treating the underlying cause (alcohol abstinence, direct-acting antivirals for HCV, nucleoside analogs for HBV, weight loss), lifestyle modifications, and managing complications. Pharmacotherapy includes non-selective beta-blockers (carvedilol, propranolol) or endoscopic band ligation for varices, diuretics (spironolactone and furosemide) for ascites, and lactulose plus rifaximin for encephalopathy. Regular six-monthly ultrasound screening for HCC is mandatory. Liver transplantation offers definitive cure for decompensated end-stage disease.

Part (b) Pediatric Acute Gastroenteritis with Severe Dehydration

(i) Assessment of Severity: According to WHO/IMCI guidelines, the child has Severe Dehydration (Plan C) based on the presence of lethargy and inability to drink, accompanied by sunken eyes and skin pinch retracting very slowly (>2 seconds). This represents a volume deficit exceeding 10% of total body weight (>100 ml/kg, or a weight deficit >1 kg from baseline 10 kg).

(ii) Fluid Management in the First 3 Hours: Initiate immediate intravenous resuscitation using Ringer’s Lactate (or Normal Saline) at 100 ml/kg (1000 ml total for 10 kg) over 3 hours:

• Give 30 ml/kg (300 ml) rapidly over the first 30 minutes.
• Give the remaining 70 ml/kg (700 ml) over the subsequent 2.5 hours. Monitor heart rate, pulse volume, capillary refill, and respiratory rate every 15–30 minutes to ensure hemodynamic recovery and avoid fluid overload.

(iii) Treatment Guidelines Post-3 Hours: Reassess clinical status completely. If signs of severe dehydration persist, repeat the IV fluid regimen. If dehydration is reduced to "Some Dehydration", switch to WHO Plan B (ORS 75 ml/kg over 4 hours). If rehydrated, transition to Plan A. Administer elemental Zinc (20 mg/day orally for 14 days) to promote intestinal epithelial regeneration, resume age-appropriate feeding immediately once awake, and monitor for hypoglycemia, hyper/hyponatremia, and hypokalemia.

(iv) WHO Oral Rehydration Salts (ORS): The WHO reduced-osmolarity formulation (total osmolarity 245 mOsm/L) contains:

• Sodium chloride: 2.6 g/L (Na+: 75 mmol/L, Cl-: 65 mmol/L)
• Glucose, anhydrous: 13.5 g/L (Glucose: 75 mmol/L)
• Potassium chloride: 1.5 g/L (K+: 20 mmol/L)
• Trisodium citrate, dihydrate: 2.9 g/L (Citrate: 10 mmol/L) Preparation: Dissolve the entire contents of one packet in precisely 1 litre of clean drinking water. Stir thoroughly until fully dissolved. Do not add sugar, milk, or boil after mixing; discard unused solution after 24 hours.

Part (c) Psoriatic Arthritis (PsA)

(i) Differential Diagnosis and Distinguishing Features:

• Rheumatoid Arthritis (RA): RA presents with symmetrical, small-joint polyarthritis sparing DIPs, with positive RF and anti-CCP. PsA characteristically involves distal interphalangeal (DIP) joints, exhibits asymmetric oligoarthritis, and is seronegative (RF/anti-CCP negative).
• Ankylosing Spondylitis (AS): AS shows symmetric sacroiliitis with predominant axial involvement; PsA exhibits asymmetric sacroiliitis, prominent peripheral enthesitis, and cutaneous psoriasis.
• Gout: Gout presents as acute monoarthritis with hyperuricemia and birefringent urate crystals; PsA presents with persistent joint inflammation and characteristic "pencil-in-cup" deformities on X-ray.
• Reactive Arthritis: Preceded by genitourinary/enteric infection; PsA features chronic course, dactylitis ("sausage digits"), and psoriatic nail changes (pitting, onycholysis, oil-drop signs).

(ii) Management: Employs a multidisciplinary, treat-to-target strategy addressing both cutaneous and musculoskeletal domains:

• Mild/Peripheral Disease: NSAIDs for symptomatic relief; intra-articular corticosteroid injections for localized synovitis; conventional synthetic DMARDs (Methotrexate, Sulfasalazine, Leflunomide) for persistent peripheral arthritis.
• Moderate-to-Severe / Axial / Refractory Disease: Biologic DMARDs targeting TNF-α (Infliximab, Adalimumab, Etanercept), IL-17 (Secukinumab), or IL-12/23 (Ustekinumab), alongside targeted synthetic DMARDs (JAK inhibitors like Tofacitinib; PDE-4 inhibitor Apremilast). Physical therapy, skin management, and smoking cessation form critical adjuncts.

A systematic approach bridging emergency volume resuscitation, chronic organ-failure staging, and targeted immunomodulatory therapy provides the definitive pathway to optimize clinical outcomes across acute and chronic systemic conditions.