GI Flashcards

1
Q

Where are lipids absorbed?

A

in the jejunum

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2
Q

What is a common cause of Zenker diverticulum?

A

Cricopharyngeal dysfunction: diminished relaxation of pharyngeal mm. during swallowing → ↑P → protrusion of mucosa through muscular layer → false diverticulum

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3
Q

What are the symptoms of cricopharyngeal dysfunction?

A

High dysphagia: difficulty swallowing felt at throat, coughing, choking, occassionally nasal regurgitation

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4
Q

What causes achalasia?

A

degenerative changes of the myenteric plexus

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5
Q

How do you test for malabsorption

A
  1. Sudan III stool stain checks for fat in stool
  2. Quantitative analysis confirms diagnosis (>7 g/day of excreted fat = malabsorption)
  3. Investigate cause using endoscopy, barium studies, etc..
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6
Q

Name the part of the duodenum where most duodenal ulcers occur. What are the risks involved with an anterior and a posterior ulcer in this location?

A

most ulcers occur in the duodenal bulb, right after the stomach; most are anterior → risk of perforation; poster → risk of hemorrhage of gastroduodenal artery

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7
Q

What causes the ↓ stool pH in lactose intolerance?

A

bacterial fermentation of lactose → short-chain FAs and excess H+

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8
Q

What happens to the stool osmolar gap in lactose deficient patients?

A

↑ due to poorly absorbable substances (including fermentation products)

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9
Q

Explain the pathogenesis of hepatic encephalopathy

A

Often triggered by GI bleeding in cirrhotic pt→ ↑ absorption of ammonia (NH4) → NH4 affects brain in two ways:

  1. ↑ action of glutamine synthase (glutamate → glutamine) →
    (a) ↑ glutamine → astrocyte hyperosmolar swelling and mitochondrial dysfunction, and
    (b) ↓ glutamate → ↓ ability to excite neurons
  2. ↑ action of glutamate dehydrogenase (NH4 + α-ketoglutarate → glutamate) → ↓ α-ketoglutarate (a Kreb’s cycle intermediate) → impaired energy metabolism
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10
Q

What is the chemical name for lactose?

Hint: think about what two sugars make the molecule and what links them

A

Galactosyl β-1, 4-glucose

1, 4-glycosidic linkage b/w glucose and galactose

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11
Q

What are the two important histological morphologies of polyps? Which indicates malignancy?

A

tuberous vs. villous (=villainous = malignant)

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12
Q

Failure of what structure to obliterate → Meckel’s diverticulum? Is it a true or false diverticulum?

A

Omphalomesenteric (vitalline duct); true, meaning it has all wall layers

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13
Q

What are the 3 unique characteristics of ulcerative colitis (to differentiate from Chron’s)?

A
  1. the rectum is always involved
  2. inflamm. is limited to mucosa and submucosa only
  3. mucosal damage is continuous (no areas of normal mucosa b/w affected segments)
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14
Q

What are the 3 unique characteristics of Chron’s?

A
  1. transmural inflammation
  2. non-caseating granulomas
  3. perianal fistulae
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15
Q

What are conditions that occur in association with an imperforate anus?

A
  1. Most commonly, fistulas: urorectal, urovesical, or urovaginal → meconium may discharge from the urethra or vagina
  2. In up to 50% of pts: Renal agenesis, hypospadias, epispadias, bladder extrophy
  3. Less common: VACTERL syndrome (vertebral defects, anal atresia, cardiac abnormalities, tracheoesophageal fistula, esophageal atresia, renal abnormalities, limb abnormalities
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16
Q

Contrast the mechanism of gastric vs. duodenal ulceration caused by H. pylori

A

H. pylori lives in the antrum mucus layer, causing inflammation →

  1. Destruction of somatostatin-producing antral cells (mech. unclear) → ↑ acidity → duodenal ulcer
  2. Destruction of gastric mucosa → ↓ defense against acid → gastric ulcer (does not require ↑ acidity, just ↓ defense)
17
Q

What finding on liver function is diagnostic for alcoholic hepatitis? What are 2 other findings which can be indicative of chronic alcohol use

A

AST:ALT ratio > 2; ↑ gamma-glutamyltransferase (GGT) and macrocytosis (due to folate or B12 deficiency or direct EtOH induced BM toxicity)

18
Q

What causes WDHA and how can this condition be treated?

A

VIPoma - (WDHA = watery diarrhea, hypokalemia, achlorhydria)
VIP causes:
1. ↑ chloride (and bicarb) release from pancreas → loss of H2O, Na+, K+ → diarrhea and hypokalemia
2. ↓ gastric acid secretion → achlorhydria
Somatostatin inhibits release of VIP

19
Q

What are organisms commonly isolated from intraabdominal infections?

A

E. coli and B. fragilis (most common)
Enterococci
Streptococci

20
Q

Which is deeper in the glands of the stomach: parietal cells or chief cells?

A

chief cells (secrete pepsinogen)

21
Q

What esophageal condition can mimic unstable angina?

A

DES - diffuse esophageal spasm; (DES patients have to have a cardiac workup to r/o cardiac cause of pain)

22
Q

What are the steps in the colorectal cancer sequence?

A
  1. APC inactivation → hyperproliferative state → polyp
  2. Methylation abnormalities and COX-2 over-expression
  3. K-RAS activation → size ↑ in polyp
  4. DCC and p53 inactivation → large adenomatous polyp to adenocarcinoma transformation
23
Q

What disease is characterized by PAS-positive granules in macrophages at the lamina propria and steatorrhea?

A

Whipple’s disease; note that the granules will be resistant to diastase and the macrophages will also have rod-shaped bacilli

24
Q

How are gallstones and osteomalacia related?

A

gallstones can lead to malabsorption of fat soluble vitamins, including vit D. → impaired Ca2+, PO4 uptake & mineralization of bone

25
Q

What is biliary sludge and what causes its formation?

A

gallbladder hypomotility → bile ppt → biliary sludge, which contains cholesterol monohydrate crystals, calcium bilirubinate, and mucus; this is a precursor to stone formation

26
Q

What do brown and black gallstones indicate?

A
brown = biliary tract infection
black = intravascular hemolysis
27
Q

What disease is characterized by antimitochondrial antibodies, lymphocytic infiltrate and granulomas around bile ducts?

A

primary biliary cirrhosis

28
Q

What does ↑ HBeAg signify?

A

active viral replication and thus high transmissibility (it is a core protein like HBcAg), especially when there is no Anti-HBeAg

29
Q

What can cause HCC without causing cirrhosis first? Why?

A

HBV – it is not vert cytotoxic, but integrates into host genome and acts as an oncogene; most people who get it have no symptoms and become immune after fighting it off

30
Q

What causes the spider angiomata in alcoholic cirrhosis?

A

hyperestrinism

31
Q

What is the triad of late-stage hemochromatosis? What is the worst complication?

A

aka “bronze diabetes”
1. hyperpigmentation (esp. in sun-exposed areas)
2. diabetes mellitus
3. pigment cirrhosis with hepatomegaly
Could progress to hepatocellular carcinoma

32
Q

What lab test should follow a moderately elevated alkaline phosphatase of unclear etiology? Why?

A

gamma-glutamyl transpeptidase (GGTP) because it is not present in bone, so can help distinguish if ↑ ALP is hepatic or bony in origin

33
Q

What is Gilbert syndrome?

A

reduced UDP-glucuronyl transfereases → ↑ unconjugated billirubin → jaundice after trigger s.a. hemolysis, fasting, physical exertion, febrile illness, stress, or fatigue