Gastrointestinal Flashcards

1
Q

What are true diverticuli (e.g. Meckel’s, the appendix) and pseudodiverticuli (e.g. Zenker’s esophageal, diverticulosis) composed of?

A

True diverticuli contain mucosal, submucosal, muscularis and serosal layers (all the parts of the intestinal wall). Pseudodiverticuli only have mucosal, submucosal and serosal layers (lack a muscular layer).

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2
Q

Compared to sporadic colorectal carcinoma, colitis-associated (particularly UC) carcinoma has what features?

A

Affects younger patients, progresses from flat and non-polypiod dysplasia, histologically appears mucinous and/or has signet ring morphology, develops early p53 mutations and late APC gene mutations (opposite in sporadic), be distributed within the proximal colon (especially in Crohn’s disease), and be mulitfocal in nature.

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3
Q

What is carcinoembryonic antigen (CEA) used for in relation to colon cancer?

A

It is used to monitor for colon cancer recurrence (baseline serum values are taken before treatment).

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4
Q

What is the cause of gynecomastia, spider angiomas, and testicular atrophy in the setting of liver cirrhosis?

A

Hyperestrinism, likely due to increase adrenal production of androstenedione with aromatization to estrone and eventual conversion to estradiol.

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5
Q

What complication of opioid analgesics, such as morphine, causes right upper quadrant pain?

A

Sphincter of Oddi spasm (due to smooth muscle contraction). Although uncommon, this can lead to biliary colic.

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6
Q

What is the significance of an elevated 𝛾-Glutamyl transferase (GGT) lab value?

A

It is a diagnostic marker for liver disease. Chronic elevations are often seen in chronic viral hepatitis. It may also be used to detect biliary tract disease, similar to alkaline phosphate (getting both values can help to verify biliary tract disease).

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7
Q

What are Mallory bodies?

A

Cytoplasmic inclusions in hepatocytes, most often associated with alcoholic liver disease. They may also be found in Wilson’s disease, primary biliary cirrhosis, non-alcoholic cirrhosis, hepatocellular carcinoma, and morbid obesity.

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8
Q

What is the most common benign liver tumor?

A

Cavernous hemangioma. It presents around 30-50 years of age. Thought to be congenital malformations that enlarge by ectasia (dilation), not hyperplasia or hypertrophy. They are well-circumscribed masses of spongy consistency. Microscopically, these tumors consist of cavernous, blood-filled vascular spaces of variable size lined by a single epithelial layer. Most patients are asymptomatic, although some present with abdominal pain and right upper quadrant fullness. Excellent prognosis.

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9
Q

What are the affects of VIPoma tumors?

A

Excessive vasoactive intestinal peptide (VIP) secretion from pancreatic islet cells results in watery diarrhea, hypokalemia, and achlorhydria (WDHA) syndrome (pancreatic cholera). VIP stimulates pancreatic bicarb and chloride secretion, and its binding to intestinal epithelial cells leads to adenylate cyclase activation and increased cAMP production, causing sodium, chloride, and water secretion into the bowel. It can be treated with somatostatin (octreotide).

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10
Q

What is the preferred diagnostic study (e.g. colonoscopy, abdominal x-ray, barium enema, etc.) to look for toxic megacolon in the setting of ulcerative colitis.

A

Abdominal x-ray (can show colonic dilation). Patients with abdominal pain/distention, bloody diarrhea, fever, and signs of shock in the setting of UC likely have toxic megacolon. Barium enema and colonoscopy are contraindicated in patients suspected of toxic megacolon due to risk for bowel perforation.

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11
Q

What is the most useful initial test for confirming carcinoid syndrome?

A

Elevation of the serotonin metabolite 5-hyroxyindoleacetic acid (5-HIAA) in a 24-hour urine sample.

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12
Q

What is the mechanism of fat accumulation in the liver in the setting of alcoholic fatty liver?

A

Decreased free fatty acid oxidation secondary to excess NADH production by the 2 major alcohol metabolism enzymes: alcohol dehydrogenase and aldehyde dehydrogenase.

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13
Q

What is the cause of brown pigment stones, and what enzyme plays a role in their pathogenesis?

A

Infection of the biliary tract (e.g. E. coli, Ascaris lumbricoides, Clonorchis sinensis), which results in the release of beta-glucuronidase by injured hepatocytes and bacteria. This enzyme hyrdolyzes bilirubin glucuronides and increases the amount of unconjugated bilirubin.

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14
Q

What are the GI symptoms associated with lead poisoning?

A

Constipation, abdominal pain, and decreased vitamin D metabolism

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15
Q

Nutritional supplementation with what is required following a Billroth II gastrojejunostomies (attachment of gastric body to the jejunum, bypassing the gastric antrum and duodenum)?

A

Iron (primarily absorbed in the duodenum and proximal jejunum, procedure also decreases gastric acid production from the antrum and acid helps with iron absorption).
Patients may also experience malabsorption of B12, folate, fat-soluble vitamins (especially D), and calcium.

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16
Q

What vitamin deficiencies may be seen in patients with a terminal ileum resection?

A

Vitamins A, E, D, K (due to loss of absorption of bile acids and thus fat), and B12.

Patients may experience increased bleeding and bruising from vitamin K deficiencies.

17
Q

What cell type is found ectopically in Meckel diverticula?

A

Gastric tissue. This is why 99mTc-pertechnetate scans light up these diverticula along with the stomach (and bladder as the chemical accumulates). The radioisotope has an affinity for parietal cells.

18
Q

How does increased serum secretin affect acid production in the setting of Zollinger-Ellison syndrome?

A

Although under normal conditions secretin causes increased pancreatic bicarbonate secretion and inhibits gastrin release from normal gastric G cells, gastrinomas have abnormal adenylate cyclase activation in response to secretin. This stimulates gastrin release from gastrinomas. Thus, secretin administration can be used to differentiate ZES from other causes of hypergastrinemia (e.g. atrophic gastritis).

19
Q

Serum concentrations of what vitamins are increased in the setting of small intestinal bacterial overgrowth?

A

Vitamin K and folate (produced by bacteria).

20
Q

Are villous or tubular adenomas of the colon more likely to undergo malignant transformation?

A

Villous

21
Q

What is Peutz-Jeghers syndrome?

A

AD syndrome. Numerous hamartomas throughout the GI tract, along with hyperpigmented mouth, lips, hands, and genitalia. Associated with an increased risk of breast and GI cancers (e.g. colorectal, stomach, small bowel, pancreatic).

22
Q

What is the definition of a gastric erosion vs a gastric ulcer?

A

A gastric erosion does not fully extend through the muscularis mucosa (i.e. limited to the mucosal layer). Ulcers penetrate the mucosal layer and extend into the submucosal layers.

23
Q

What are the symptoms of a glucagonoma?

A

Necrolytic migratory erythema (erythematous papules/plaques on face, perineum, extremities; lesions enlarge and coalesce, leaving a bronze-colored, central induration area with peripheral blistering and scaling), diabetes mellitus, and gastrointestinal symptoms (diarrhea, anorexia, abdominal pain). Diagnosed by markedly elevated glucagon levels.

24
Q

What are some differences between right-sided (e.g. ascending colon) and left-sided (e.g. rectosigmoid colon) colon cancers?

A

Right: tend to be large, bulky masses that protrude into the lumen. More likely to bleed so more likely to cause iron deficiency anemia (usually occult bleeding).
Left: tend to be smaller and often infiltrate the wall of the colon, encircling it and narrowing the lumen. This causes obstruction, altered bowel habits, abdominal distention, and nausea and vomiting.

25
Q

What is the Sudan III stain?

A

Tests for the presence of fat within stool (looking for steatorrhea)

26
Q

What is the cause of the esophageal dysmotility in CREST syndrome?

A

Atrophy and fibrous replacement of the muscularis in the lower esophagus.

27
Q

How many calories come from a gram of protein, carbs, and fat?

A

Carbs and protein: 4 calories/gram

Fat: 9 calories/gram

28
Q

What is the underlying mechanism of a Zenker diverticulum?

A

Cricopharyngeal motor dysfunction during swallowing (increased oropharyngeal intraluminal pressure eventually results in herniation of the pharyngeal mucosa through a zone of muscle weakness [false diverticulum] in the posterior hypopharynx [Killian triangle]).

29
Q

What are the two watershed areas of the colon?

A

The splenic flexure and the rectosigmoid junction

30
Q

What is the cause of achalasia?

A

Distal esophageal aperistalsis (lack of peristalsis) and a hypertensive lower esophageal sphincter that is unable to relax.