NEET SS Gastroenterology (DM) Syllabus

What are the Rome IV criteria for diagnosing irritable bowel syndrome?

Recurrent abdominal pain at least 1 day/week in the last 3 months, associated with two or more of: related to defecation, change in stool frequency, or change in stool form (onset at least 6 months prior).

What are the alarm/red-flag features in suspected IBS that mandate further workup?

Age of onset >50, rectal bleeding/melena, nocturnal symptoms, weight loss, anemia, family history of colorectal cancer/IBD, and abnormal inflammatory markers.

Which medications are used for IBS-with-constipation versus IBS-with-diarrhea?

IBS-C: lubiprostone, linaclotide, plecanatide, PEG. IBS-D: loperamide, rifaximin, eluxadoline, alosetron (5-HT3 antagonist).

What is the most common cause of acute lower GI bleeding in adults, and the most common cause of massive lower GI bleeding in the elderly?

Diverticulosis is the most common cause overall; angiodysplasia and diverticulosis are the most common causes of massive lower GI bleeding in the elderly.

What is the recommended colorectal cancer screening interval for average-risk individuals by colonoscopy, and starting age?

Colonoscopy every 10 years starting at age 45 (or 50), with shorter intervals if adenomatous polyps are found.

Describe the adenoma-carcinoma sequence in colorectal cancer.

Normal mucosa -> APC mutation (adenoma initiation) -> KRAS activation (growth) -> loss of DCC/SMAD -> TP53 mutation (carcinoma). Stepwise accumulation of mutations over ~10 years.

What genetic syndrome causes Lynch syndrome (HNPCC) and what is the screening tool?

Germline mutations in DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2) causing microsatellite instability. Amsterdam II criteria and Bethesda guidelines guide testing.

What are the revised Atlanta criteria for diagnosing acute pancreatitis (2 of 3 required)?

(1) Characteristic epigastric pain radiating to the back; (2) serum amylase/lipase >3x upper limit of normal; (3) characteristic imaging findings (CT/MRI/US).

What are the two most common causes of acute pancreatitis worldwide?

Gallstones (most common) and alcohol. (Mnemonic: I GET SMASHED.)

What is the BISAP score and what parameters make it up?

A bedside severity score for acute pancreatitis (1 point each): BUN >25, Impaired mental status, SIRS, Age >60, Pleural effusion. Score >=3 predicts higher mortality.

When and how should infected pancreatic necrosis be managed?

Suspect after 7-10 days with clinical deterioration; confirm by gas on CT or FNA. Treat with antibiotics and delayed (>4 weeks) minimally invasive 'step-up' debridement (percutaneous drainage then necrosectomy).

What are the classic features and the most common cause of chronic pancreatitis?

Triad: pancreatic calcification, steatorrhea, and diabetes mellitus. Most common cause is chronic alcohol use; in children, cystic fibrosis.

What enzyme supplementation and vitamins are needed in pancreatic exocrine insufficiency?

Pancreatic enzyme replacement therapy (lipase) with meals, plus fat-soluble vitamin supplementation (A, D, E, K).

What is Charcot's triad and Reynolds' pentad in acute cholangitis?

Charcot's triad: fever, RUQ pain, jaundice. Reynolds' pentad adds hypotension and altered mental status, indicating suppurative cholangitis.

What is the imaging test of choice for diagnosing acute cholecystitis and the classic finding?

Ultrasound is first-line (gallstones, wall thickening >3 mm, pericholecystic fluid, sonographic Murphy's sign); HIDA scan is most sensitive (non-visualization of gallbladder).

What is primary sclerosing cholangitis, its imaging hallmark, and disease association?

Chronic fibrosing inflammation of intra/extrahepatic bile ducts; MRCP shows multifocal strictures with a 'beaded' appearance. Strongly associated with ulcerative colitis and risk of cholangiocarcinoma.

What antibody and demographic characterize primary biliary cholangitis?

Anti-mitochondrial antibody (AMA) positive in ~95%; typically affects middle-aged women with pruritus and fatigue. First-line treatment is ursodeoxycholic acid.

What serologic markers indicate acute Hepatitis B infection versus immunity from vaccination?

Acute HBV: HBsAg+, IgM anti-HBc+. Vaccine immunity: anti-HBs+ only (HBsAg-, anti-HBc-). Natural immunity: anti-HBs+ and anti-HBc+.

Which hepatitis viruses are transmitted enterically (fecal-oral) and which are most likely to cause chronic infection?

Fecal-oral: Hepatitis A and E. Chronicity: Hepatitis C (most likely, ~75-85%), and Hepatitis B/D (parenteral).

Why is Hepatitis E especially dangerous in pregnant women?

Hepatitis E carries a high risk of fulminant hepatic failure with mortality up to 20-25%, particularly in the third trimester.

What is the first-line treatment goal and regimen class for chronic Hepatitis C today?

Direct-acting antivirals (DAAs, e.g., sofosbuvir-based combinations) for 8-12 weeks; the goal is sustained virologic response (SVR, undetectable RNA 12 weeks post-treatment = cure).

What is the Child-Pugh classification based on, and what does it predict?

Bilirubin, albumin, INR/prothrombin time, ascites, and encephalopathy. It predicts cirrhosis severity and surgical mortality (Class A, B, C).

What is the MELD score used for and its components?

Model for End-stage Liver Disease prioritizes liver transplant allocation; based on serum bilirubin, INR, creatinine (and sodium in MELD-Na).

How is the diagnosis of spontaneous bacterial peritonitis (SBP) made and treated?

Ascitic fluid PMN count >=250 cells/mm3; treat with IV third-generation cephalosporin (cefotaxime) and IV albumin. Prophylaxis with norfloxacin in high-risk patients.

What is the serum-ascites albumin gradient (SAAG) and what does a value >=1.1 g/dL indicate?

SAAG = serum albumin minus ascitic albumin. >=1.1 g/dL indicates portal hypertension (cirrhosis, heart failure); <1.1 g/dL suggests non-portal causes (malignancy, TB, nephrotic syndrome).

What is the diagnostic criteria and characteristic finding of hepatorenal syndrome?

Renal failure in advanced cirrhosis/ascites with no other cause; characterized by very low urine sodium (<10 mEq/L), absence of significant proteinuria, and lack of response to volume expansion.

What is the laboratory and physical hallmark of Wilson's disease?

Low serum ceruloplasmin, high urinary copper, and Kayser-Fleischer rings (corneal copper deposits). Treated with chelators (penicillamine/trientine) and zinc.

What is the classic triad and gene defect of hereditary hemochromatosis?

Triad: cirrhosis, diabetes ('bronze diabetes'), and skin pigmentation due to iron overload. Caused by HFE gene C282Y mutation; high transferrin saturation and ferritin. Treated with phlebotomy.

What antibodies characterize Type 1 versus Type 2 autoimmune hepatitis?

Type 1 (adults): ANA and anti-smooth muscle antibody (ASMA). Type 2 (children): anti-LKM-1 and anti-liver cytosol antibodies. Both treated with corticosteroids +/- azathioprine.

What is the King's College Criteria used for in acute liver failure?

It identifies patients with acute liver failure who need urgent liver transplantation. For acetaminophen toxicity: arterial pH <7.3, OR the triad of INR >6.5, creatinine >3.4 mg/dL, and grade III/IV encephalopathy.

What grading system is used for hepatic encephalopathy and what is the first-line treatment?

West Haven criteria (Grade I-IV based on consciousness/asterixis). First-line treatment is lactulose (lowers ammonia) plus rifaximin; identify and treat precipitants.