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

Gastrointestinal System and Nutrition syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Gastrointestinal System and Nutrition in Physician Assistant National Certifying Examination (PANCE), not a summary of it.

1. 1

   Esophageal and Gastric Disorders

   4 topics

   • Gastroesophageal reflux disease and Barrett esophagus
   • Esophagitis and esophageal motility disorders
     • Achalasia
     • Eosinophilic esophagitis
   • Peptic ulcer disease and H. pylori
     • Testing modalities and eradication therapy
   • Gastritis and gastric cancer
2. 2

   Small and Large Bowel Disease

   5 topics

   • Inflammatory bowel disease
     • Crohn disease versus ulcerative colitis
     • Biologic and immunomodulator therapy
   • Irritable bowel syndrome
   • Celiac disease and malabsorption
   • Diverticular disease and appendicitis
   • Colorectal cancer and screening
3. 3

   Hepatobiliary and Pancreatic Disease

   4 topics

   • Viral and alcoholic hepatitis
     • Hepatitis B and C serology
   • Cirrhosis and portal hypertension
     • Ascites, varices, and encephalopathy
   • Cholelithiasis and cholecystitis
   • Acute and chronic pancreatitis
     • Ranson criteria and lipase interpretation
4. 4

   Acute Abdomen and Anorectal Disorders

   5 topics

   • Bowel obstruction and ileus
   • Mesenteric ischemia
   • GI bleeding (upper and lower)
   • Hemorrhoids, anal fissure, and abscess
   • Hernias
5. 5

   Nutritional and Metabolic Disorders

   4 topics

   • Vitamin and mineral deficiencies
   • Obesity and metabolic syndrome
   • Eating disorders
   • Enteral and parenteral nutrition principles

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

23 of 51 cards from the Gastrointestinal System and Nutrition deck — real questions with worked answers.

1. What is the underlying mechanism and the classic symptom of gastroesophageal reflux disease (GERD)?

   Inappropriate transient relaxation of the lower esophageal sphincter (LES) allows acidic gastric contents to reflux into the esophagus. The classic symptom is retrosternal burning (heartburn/pyrosis), often worse postprandial and when supine.

2. What histologic change defines Barrett esophagus, and why is it clinically important?

   Metaplasia of the normal stratified squamous epithelium to specialized intestinal columnar epithelium with goblet cells, caused by chronic GERD. It is important because it is a premalignant lesion that raises the risk of esophageal adenocarcinoma.

3. What are the alarm/red-flag symptoms in a patient with reflux that warrant prompt upper endoscopy (EGD)?

   Dysphagia, odynophagia, weight loss, GI bleeding/melena/hematemesis, iron-deficiency anemia, persistent vomiting, an epigastric mass, and onset of new symptoms in a patient over 60. These suggest complicated GERD or malignancy.

4. What is the first-line pharmacologic therapy for erosive GERD and Barrett esophagus?

   Proton pump inhibitors (PPIs, e.g., omeprazole), which irreversibly block the gastric H+/K+-ATPase. They provide superior acid suppression and mucosal healing compared with H2-blockers.

5. Contrast infectious esophagitis caused by Candida, HSV, and CMV in terms of endoscopic appearance.

   Candida: yellow-white adherent plaques. HSV: small, well-circumscribed 'punched-out' ulcers. CMV: large, linear/serpiginous, deep ulcers. All are most common in immunocompromised (e.g., HIV) patients.

6. What are the manometric findings and classic barium-swallow appearance of achalasia?

   Manometry shows incomplete LES relaxation, elevated LES resting pressure, and absent (aperistaltic) esophageal body peristalsis. Barium swallow shows a dilated esophagus tapering to a 'bird's beak' at the gastroesophageal junction.

7. How does diffuse esophageal spasm present and appear on barium swallow?

   Intermittent dysphagia and non-cardiac chest pain due to uncoordinated, simultaneous esophageal contractions. Barium swallow shows a 'corkscrew' or 'rosary bead' esophagus.

8. Name the two major causes of peptic ulcer disease and which ulcer type is improved versus worsened by eating.

   H. pylori infection and NSAID use. Duodenal ulcer pain is classically relieved by food (then recurs 2-5 hours later); gastric ulcer pain is classically worsened by food, leading to weight loss.

9. List the noninvasive tests used to diagnose H. pylori infection.

   Urea breath test, stool antigen test, and serology (IgG antibody, but cannot distinguish active from past infection). Breath and stool tests confirm active infection and can document eradication.

10. What is standard triple therapy for H. pylori eradication?

    A PPI plus two antibiotics — typically clarithromycin and amoxicillin (or metronidazole if penicillin-allergic) — for 10-14 days. Quadruple therapy (PPI + bismuth + tetracycline + metronidazole) is used where clarithromycin resistance is high.

11. What gastrin-secreting tumor should be suspected with multiple/refractory peptic ulcers, and what is its hallmark lab finding?

    Zollinger-Ellison syndrome (gastrinoma). Hallmark is a markedly elevated fasting serum gastrin level with high gastric acid output; associated with MEN1.

12. Differentiate type A and type B chronic gastritis.

    Type A (autoimmune) affects the fundus/body, involves anti-parietal cell and anti-intrinsic factor antibodies, causes pernicious (vitamin B12-deficiency) anemia. Type B (most common) affects the antrum and is caused by H. pylori (or NSAIDs).

13. What is the most common histologic type of gastric cancer, and what are its two morphologic subtypes?

    Adenocarcinoma. The intestinal type forms glands/bulky masses (linked to H. pylori, diet, atrophic gastritis); the diffuse type infiltrates the wall as signet-ring cells, producing 'linitis plastica' (leather-bottle stomach).

14. Name the classic physical-exam lymph node findings that signal metastatic gastric cancer.

    Virchow node (left supraclavicular), Sister Mary Joseph nodule (periumbilical), and Krukenberg tumor (metastasis to the ovaries from signet-ring cells).

15. Compare Crohn disease and ulcerative colitis by location and depth of involvement.

    Crohn disease: anywhere mouth-to-anus (often terminal ileum), with 'skip lesions' and transmural inflammation. Ulcerative colitis: limited to the colon, starts at the rectum and spreads continuously, with mucosa/submucosa-only inflammation.

16. List characteristic complications that distinguish Crohn disease from ulcerative colitis.

    Crohn: fistulas, strictures, abscesses, perianal disease, 'cobblestoning,' noncaseating granulomas, and 'creeping fat.' UC: continuous friable mucosa, crypt abscesses, toxic megacolon, and higher colorectal cancer risk; associated with primary sclerosing cholangitis.

17. What is the Rome IV-based clinical definition of irritable bowel syndrome (IBS)?

    Recurrent abdominal pain at least 1 day per week (average) in the last 3 months, associated with two or more of: relation to defecation, change in stool frequency, or change in stool form. It is a diagnosis of exclusion with no structural abnormality.

18. What serologic antibodies and small-bowel biopsy findings support a diagnosis of celiac disease?

    Anti-tissue transglutaminase (anti-tTG) IgA (most sensitive/specific) and anti-endomysial IgA antibodies. Duodenal biopsy shows villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis. Testing must be done while on a gluten-containing diet.

19. What pruritic skin condition is pathognomonically associated with celiac disease?

    Dermatitis herpetiformis — symmetric, intensely pruritic papulovesicles on extensor surfaces. It responds to a gluten-free diet (and dapsone).

20. What stool test screens for fat malabsorption, and what vitamin deficiencies result from fat malabsorption?

    Sudan III stain / 72-hour fecal fat quantification for steatorrhea. Fat malabsorption causes deficiency of the fat-soluble vitamins A, D, E, and K (e.g., night blindness, osteomalacia, neuropathy, coagulopathy).

21. Differentiate the pathology of diverticulosis from diverticulitis.

    Diverticulosis: outpouchings of mucosa/submucosa through the colonic wall (most common in sigmoid colon), often asymptomatic but a common cause of painless lower GI bleeding. Diverticulitis: inflammation/microperforation of a diverticulum causing LLQ pain and fever.

22. Why is barium enema and colonoscopy generally avoided during acute diverticulitis, and what imaging is preferred?

    They risk perforation during acute inflammation. CT scan of the abdomen/pelvis with contrast is the preferred imaging to confirm diverticulitis and detect abscess or perforation.

23. Describe the classic migration of pain and key signs in acute appendicitis.

    Periumbilical pain migrating to the right lower quadrant (McBurney point). Signs include Rovsing (LLQ palpation causes RLQ pain), psoas, and obturator signs, plus anorexia, low-grade fever, and leukocytosis.

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