Physician Assistant National Certifying Examination (PANCE) Gastrointestinal System and Nutrition Flashcards

24 sample cards from the Gastrointestinal System and Nutrition deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Interpret the hepatitis B serologic pattern: HBsAg positive, anti-HBc IgM positive, HBeAg positive.

   Acute hepatitis B infection with high infectivity. HBsAg = active infection, anti-HBc IgM = recent/acute infection, HBeAg = active viral replication and high transmissibility.

2. What hepatitis B serology indicates immunity from vaccination versus immunity from natural infection?

   Vaccination: anti-HBs positive only. Natural prior infection (resolved): anti-HBs positive AND anti-HBc (total/IgG) positive, with HBsAg negative.

3. What is the characteristic AST:ALT ratio in alcoholic hepatitis, and what is a typical threshold?

   AST is elevated more than ALT, classically an AST:ALT ratio greater than 2:1 ("toast and ratio"). Transaminases are usually only modestly elevated (typically under 300-500 U/L).

4. List the major clinical features of cirrhosis caused by portal hypertension and hepatocellular failure.

   Portal hypertension features: esophageal/gastric varices, caput medusae, splenomegaly, ascites. Liver failure features: jaundice, hypoalbuminemia, coagulopathy, palmar erythema, spider angiomata, gynecomastia, and hepatic encephalopathy (asterixis).

5. What is the serum-ascites albumin gradient (SAAG), and what does a value of $\geq 1.1\ \text{g/dL}$ indicate?

   $$\text{SAAG} = \text{serum albumin} - \text{ascitic fluid albumin}$$ A value $\geq 1.1\ \text{g/dL}$ indicates portal hypertension (e.g., cirrhosis, heart failure); a value $< 1.1\ \text{g/dL}$ suggests non-portal causes (e.g., malignancy, infection, pancreatitis).

6. How is hepatic encephalopathy treated pharmacologically and why?

   Lactulose (acidifies the colon, trapping ammonia as ammonium for excretion) and rifaximin (reduces ammonia-producing gut bacteria). These lower serum ammonia, the suspected neurotoxin.

7. What is the most common type of gallstone, and what are the classic 'risk factor' fs?

   Cholesterol stones (radiolucent) are most common. The classic risks are the 4 Fs: Female, Fat (obesity), Forty (age), and Fertile (multiparity); also rapid weight loss and estrogen use.

8. Differentiate biliary colic from acute cholecystitis.

   Biliary colic: transient RUQ pain from a stone temporarily obstructing the cystic duct, resolving in hours, no fever or leukocytosis. Acute cholecystitis: persistent obstruction causing inflammation with RUQ pain, fever, leukocytosis, and a positive Murphy sign.

9. What is the Murphy sign, and what imaging is first-line for acute cholecystitis?

   Murphy sign: inspiratory arrest during deep RUQ palpation due to pain. First-line imaging is RUQ ultrasound (showing stones, wall thickening >3 mm, pericholecystic fluid); HIDA scan is most sensitive if ultrasound is equivocal.

10. What is Charcot triad and Reynolds pentad, and which condition do they indicate?

    Charcot triad (ascending cholangitis): RUQ pain, fever, and jaundice. Reynolds pentad adds hypotension and altered mental status, indicating suppurative cholangitis and sepsis — a surgical/biliary-decompression emergency.

11. What are the two most common causes of acute pancreatitis, and which lab is most specific?

    Gallstones and alcohol. Serum lipase is more specific and stays elevated longer than amylase. Levels typically rise to more than 3 times the upper limit of normal.

12. Name two physical findings of hemorrhagic pancreatitis.

    Cullen sign (periumbilical ecchymosis) and Grey Turner sign (flank ecchymosis), both indicating retroperitoneal hemorrhage.

13. What is the classic triad of chronic pancreatitis, and what imaging finding is characteristic?

    Calcification, steatorrhea, and diabetes mellitus (from loss of exocrine and endocrine function). Imaging characteristically shows pancreatic calcifications on CT/X-ray. Often caused by chronic alcohol use.

14. Compare the presentation of small bowel obstruction (SBO) versus large bowel obstruction.

    SBO: early bilious vomiting, crampy periumbilical pain, less distension, 'stepladder' air-fluid levels and dilated loops centrally. LBO: more distension, late feculent vomiting, X-ray shows dilated colon peripherally. Adhesions cause most SBO; cancer/volvulus cause most LBO.

15. How does adynamic (paralytic) ileus differ from a mechanical bowel obstruction on exam and imaging?

    Ileus has absent/hypoactive bowel sounds (mechanical obstruction has high-pitched 'tinkling' sounds and visible peristalsis early). Imaging in ileus shows diffuse gas throughout small and large bowel without a transition point. Common after surgery, opioids, or electrolyte abnormalities.

16. What is the classic presentation of acute mesenteric ischemia, and what is the typical exam paradox?

    Sudden severe periumbilical 'pain out of proportion to physical exam findings,' often in a patient with atrial fibrillation (embolic) or atherosclerosis. The abdomen is initially soft/benign despite severe pain. Lactic acidosis is a late, ominous sign.

17. How does chronic mesenteric ischemia ('intestinal angina') present?

    Postprandial abdominal pain beginning 15-30 minutes after eating, leading to 'food fear' and weight loss. It is due to atherosclerotic narrowing of the splanchnic arteries.

18. Differentiate upper from lower GI bleeding by source location and stool/vomit findings.

    Upper GI bleed: proximal to the ligament of Treitz; presents with hematemesis, 'coffee-ground' emesis, and melena (black, tarry stool). Lower GI bleed: distal to the ligament of Treitz; presents with hematochezia (bright red blood per rectum).

19. What lab ratio is often elevated in upper GI bleeding, and why?

    An elevated BUN:creatinine ratio (often greater than 20-30:1) due to absorption/digestion of blood proteins in the small intestine plus prerenal volume depletion.

20. What is the most common cause of massive lower GI bleeding in older adults, and what vascular lesion is a frequent cause?

    Diverticulosis is the most common cause of acute lower GI bleeding. Angiodysplasia (arteriovenous malformations), often in the right colon, is another frequent cause.

21. Differentiate internal from external hemorrhoids by location, innervation, and symptoms.

    Internal hemorrhoids are above the dentate (pectinate) line, are not innervated by somatic nerves (painless), and present with painless bright-red bleeding/prolapse. External hemorrhoids are below the dentate line, somatically innervated (painful), and can thrombose.

22. What is the classic presentation of an anal fissure and its typical location?

    Severe, sharp anal pain during and after defecation with bright-red blood on the toilet paper, often after passing hard stool. Most fissures occur in the posterior midline.

23. Define the difference between a reducible, incarcerated, and strangulated hernia.

    Reducible: contents can be pushed back into the abdomen. Incarcerated: contents are trapped/non-reducible but viable. Strangulated: blood supply is compromised, causing ischemia — a surgical emergency presenting with pain, erythema, and signs of obstruction.

24. Differentiate indirect from direct inguinal hernias by anatomy.

    Indirect inguinal hernia (most common overall) protrudes through the deep inguinal ring, lateral to the inferior epigastric vessels, following the spermatic cord into the scrotum; due to a patent processus vaginalis. Direct hernia protrudes through Hesselbach triangle, medial to the inferior epigastric vessels, from a weak abdominal wall.

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