Clinic-Gastritis Flashcards

1
Q

gastritis vs gastropathy

A

gastritis = inflammation of gastric mucosa; gastropathy = damage without significant inflammation

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2
Q

clinical presentation for gastritis

A

dyspepsia (“boring” pain), N/V, do not correlate with pathology!

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3
Q

erosive gastritis is also known as?

A

reactive gastropathy

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4
Q

major etiologies of gastritis

A

DRUGS=Aspirin/NSAIDs/meds is a BIG one; INFECTION=h pylori, viral; INFLAMM=”non-specific”, eosinophilic

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5
Q

complications of atrophic gastritis (autoimmune)

A

achlorhydria leads to hypergastrinemia and gastric carcinoids; decreased IF leads to macrocytic “pernicious” anemia (impaired absorption of B12)

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6
Q

Menetrier’s disease results in hypertrophy of ____, leading to increased ____ and loss of ____ from the blood

A

gastric folds/rugae; mucus production; protein (severe hypoproteinemia)

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7
Q

symptoms of menetrier’s dz

A

abdominal pain, N/V, diarrhea, weight loss, anemia

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8
Q

who get’s menetrier’s dz

A

rare, more common in men

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9
Q

what is an ulcer?

A

a defect in mucosal surface penetrating through the muscularis mucosa

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10
Q

the number of uncomplicated gastric ulcers has ____ since 1970; the number of hemorrhagic gastric ulcers has ____ since 1970

A

decreased; increased (NSAID use)

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11
Q

peptic ulcer disease is due to an imbalance between?

A

aggressive and defensive factors in the GI tract

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12
Q

name 5 defensive factors in the stomach/duodenum

A

mucus barrier, bicarb secretion, prostaglandins, cellular resistance, mucosal blood flow

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13
Q

name 5 aggressive factors that degrade the stomach’s defenses

A

H. pylori, NSAIDs, gastric acid, alcohol, smoking

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14
Q

gastroduodenal mucus is ___% water; degraded by ___; slows diffusion of ____; secretes ____

A

95%; pepsin; H+; bicarb

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15
Q

what do prostaglandins do?

A

stimulate mucus and bicarb production; reduce acid secretion

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16
Q

celebrex is selective for inhibition of?

A

COX-2 only (does not cause ulcers)

17
Q

name three components of cellular defense

A

tight junctions, mucosal restitution (reforms barrier through small cell breakage), regeneration (larger cell breaks)

18
Q

mucosal restitution occurs by ____, while regeneration requires _____

A

migration, cell division

19
Q

more than 50% of mucosa is vulnerable when ____ in reduced

A

mucosal blood flow

20
Q

uncomplicated PUD presents with?

A

epigastric pain, nonspecific GI issues (nausea, bloating, fullness), or asymptomatic

21
Q

a bleeding ulcer presents with?

A

melena, hematemesis, hematochezia if brisk

22
Q

a perforated ulcer presents with?

A

toxic appearance/shock, peritoneal signs

23
Q

an obstruction presents with?

A

vomiting, succussion splash

24
Q

dx of PUD is usually through what two tests

A

endoscopy, barium enema with radiography

25
Q

tx of uncomplicated PUD (2-4 things)

A

acid reduction with PPI, eradication of H pylori, reduce/stop NSAIDs, stop smoking

26
Q

tx of bleeding ulcer

A

endoscopic therapy (ablation?)

27
Q

tx of perforated ulcer

A

surgery to px peritonitis, sepsis, shock, and death

28
Q

tx of obstruction

A

nasogastric suction, dilation/surgery

29
Q

Zollinger-Ellison occurs when there is a ____, often in the ____,____, or _____ leading to hypersecretion of _____

A

gastrinoma; pancreas, pituitary, or parathyroid; gastrin

30
Q

patients with Zollinger-Ellison syndrome have what three major symptoms?

A

refractory peptic ulcers, GERD, and steatorrhea (inactiv of pancreatic enzymes)

31
Q

a serum gastrin greater than ____ is diagnostic for ZES, but it can be confirmed with a _____ test

A

1000; secretin stimulation

32
Q

how is a gastrinoma localized?

A

somatostatin receptor scintigraphy, endosonography, more than 90% in the gastrinoma triangle

33
Q

name two causes of hypergastrinemia with high gastric acid

A

ZES, gastric outlet obstruction

34
Q

name two causes of hypergastrinemia with low gastric acid

A

PPI use, pernicious anemia

35
Q

where does ZES usually metastasize?

A

LN, liver