Clinic-Gastritis Flashcards

(35 cards)

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
tx of uncomplicated PUD (2-4 things)
acid reduction with PPI, eradication of H pylori, reduce/stop NSAIDs, stop smoking
26
tx of bleeding ulcer
endoscopic therapy (ablation?)
27
tx of perforated ulcer
surgery to px peritonitis, sepsis, shock, and death
28
tx of obstruction
nasogastric suction, dilation/surgery
29
Zollinger-Ellison occurs when there is a ____, often in the ____,____, or _____ leading to hypersecretion of _____
gastrinoma; pancreas, pituitary, or parathyroid; gastrin
30
patients with Zollinger-Ellison syndrome have what three major symptoms?
refractory peptic ulcers, GERD, and steatorrhea (inactiv of pancreatic enzymes)
31
a serum gastrin greater than ____ is diagnostic for ZES, but it can be confirmed with a _____ test
1000; secretin stimulation
32
how is a gastrinoma localized?
somatostatin receptor scintigraphy, endosonography, more than 90% in the gastrinoma triangle
33
name two causes of hypergastrinemia with high gastric acid
ZES, gastric outlet obstruction
34
name two causes of hypergastrinemia with low gastric acid
PPI use, pernicious anemia
35
where does ZES usually metastasize?
LN, liver