GI Flashcards

(33 cards)

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
What is biliary sludge and what causes its formation?
gallbladder hypomotility → bile ppt → biliary sludge, which contains cholesterol monohydrate crystals, calcium bilirubinate, and mucus; this is a precursor to stone formation
26
What do brown and black gallstones indicate?
``` brown = biliary tract infection black = intravascular hemolysis ```
27
What disease is characterized by antimitochondrial antibodies, lymphocytic infiltrate and granulomas around bile ducts?
primary biliary cirrhosis
28
What does ↑ HBeAg signify?
active viral replication and thus high transmissibility (it is a core protein like HBcAg), especially when there is no Anti-HBeAg
29
What can cause HCC without causing cirrhosis first? Why?
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
What causes the spider angiomata in alcoholic cirrhosis?
hyperestrinism
31
What is the triad of late-stage hemochromatosis? What is the worst complication?
aka "bronze diabetes" 1. hyperpigmentation (esp. in sun-exposed areas) 2. diabetes mellitus 3. pigment cirrhosis with hepatomegaly Could progress to hepatocellular carcinoma
32
What lab test should follow a moderately elevated alkaline phosphatase of unclear etiology? Why?
gamma-glutamyl transpeptidase (GGTP) because it is not present in bone, so can help distinguish if ↑ ALP is hepatic or bony in origin
33
What is Gilbert syndrome?
reduced UDP-glucuronyl transfereases → ↑ unconjugated billirubin → jaundice after trigger s.a. hemolysis, fasting, physical exertion, febrile illness, stress, or fatigue