Clinic-Gastritis Flashcards Preview

Gastrointestinal > Clinic-Gastritis > Flashcards

Flashcards in Clinic-Gastritis Deck (35):
1

gastritis vs gastropathy

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

2

clinical presentation for gastritis

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

3

erosive gastritis is also known as?

reactive gastropathy

4

major etiologies of gastritis

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

5

complications of atrophic gastritis (autoimmune)

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

6

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

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

7

symptoms of menetrier's dz

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

8

who get's menetrier's dz

rare, more common in men

9

what is an ulcer?

a defect in mucosal surface penetrating through the muscularis mucosa

10

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

decreased; increased (NSAID use)

11

peptic ulcer disease is due to an imbalance between?

aggressive and defensive factors in the GI tract

12

name 5 defensive factors in the stomach/duodenum

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

13

name 5 aggressive factors that degrade the stomach's defenses

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

14

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

95%; pepsin; H+; bicarb

15

what do prostaglandins do?

stimulate mucus and bicarb production; reduce acid secretion

16

celebrex is selective for inhibition of?

COX-2 only (does not cause ulcers)

17

name three components of cellular defense

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

18

mucosal restitution occurs by ____, while regeneration requires _____

migration, cell division

19

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

mucosal blood flow

20

uncomplicated PUD presents with?

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

21

a bleeding ulcer presents with?

melena, hematemesis, hematochezia if brisk

22

a perforated ulcer presents with?

toxic appearance/shock, peritoneal signs

23

an obstruction presents with?

vomiting, succussion splash

24

dx of PUD is usually through what two tests

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