Gastric Disorders Flashcards

1
Q

2 disorders that cause injury of gastric mucosa are ________
disorder that causes injury of esophageal mucosa is ____________

A

injury of gastric mucosa: gastritis/peptic ulcer disease (PUD)
injury of esophageal mucosa: GERD

*these are separate diseases, they do NOT cause each other!

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2
Q

parietal cells of the gastric lumen secrete HCl and ____

A

Intrinsic Factor, which protects vitamin B12 in acid environment

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3
Q

prostoglandins help do what in the gut?

A

protect mucus lining

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4
Q

what is the difference between gastritis and peptic ulcer disease and gastropathy

A

Gastritis is superficial inflammation of gastric mucosa with mucosal injury
Ulcer is penetration of the mucosa
Gastropathy: mucosal injury without inflammation

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5
Q

most common cause of gastritis + other causes. common clinical presentation

A
#1 is H. pylori, other causes = NSAIDS, ASA, acute stress, alcohol
CP = most commonly AS
if sxs, epigastric pain, often described as “gnawing” and other similar sxs as PUD (vs acidic, burning, reflux pain like GERD)
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6
Q

Gastric vs. duodenal ulcer pain response to food is …?

A

gastric usually pain with eating and duodenal is pain after eating

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7
Q

hematemesis, melena suggest ______

A

hemorrhage, GI bleed

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8
Q

any alarm signs need what for Dx ?

A

Urgent endoscopy in these patients to rule out perforation, gastric cancer or obstruction

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9
Q

non-alarm sign but not getting better? …what will you do?

A

now is a good time to endoscope

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10
Q

barium sticks to _____ or ______

A

ulcerated or inflamed tissue (makes it a good Dx test for these)

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11
Q

what is the CLO test?

A

Campylobacter-like organism (CLO) test: Tissue biopsy and test for urease activity

*-Campylobactor is a Hpylori-like organism, these hydrolyze (split) the urea so that its detection means positive for these

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12
Q

EGD endoscopy assesses _______, _______ and _______

A

bleeding, reflux and dysphagia

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13
Q

erosive gastritis vs NSAID gastritis on EGD?

A

erosive: looks like mucosal inflammation
NSAID: “shotgun” pattern - little black spots of NSAIDs seen

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14
Q

what is atrophic gastritis and where does it normally occur?

A

chronic inflammation of the gastric mucosa with loss of the gastric glandular cells and replacement by intestinal-type epithelium and fibrous tissue.
-decrease in glandular cells = loss of secretory mucosa
normally occurs in fundus and body

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15
Q

atrophic gastritis may be related to _____, _____ or _______

A

alcohol, Hpylori, or Vit B12 deficiency (from decrease in intrinsic factor)

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16
Q

atrophic gastritis may progress to _____

A

adenocarinoma (b/c it is a chronic inflammation issue)

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17
Q

Xray of bowel perforation shows what?

A

FREE AIR UNDER DIAPHRAGM

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18
Q

why can’t we use barium contrast if there is a possible bowel perforation? what can we use instead?

A

barium will stay in the gastric cavity for a while

- use water-soluble gastrograffin instead!

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19
Q

what is a vagotomy and why does it work for gastritis/PUD?

A

removal of vagus nerve branch (to get rid of the Ach input that is causing the gastritis/PUD)

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20
Q

heliobacter pylori formerly known as ________

A

campylobacter

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21
Q

H. Pylori: colonizes….

hydrolyzes…

A

Colonizes gastric type mucosa. Is extremely sensitive to acid
Hydrolyzes urea to create a neutral pH for itself

22
Q

how is H pylori transmitted?

A

close human contact through oral-oral in industrialized world and fecal-oral in developing world, we think

23
Q

H. Pylori is NOT related to _____ or ______

A

Is NOT related to nonulcer dyspepsia or GERD

24
Q

what three tests will test for active H. pylori infection?

A

Non-invasive tests:
1). urea breath testing: 13C labeling of orally digesting urea and checking the lungs for excretion (as 13CO2)
2). stool antigen test
Invasive test is endoscopic tests where you take a biopsy sample and test it for H. pylori
*can use all three of these tests to confirm eradication after tx but stool antigen/urea breath prob more common

25
Q

Standard Txt for H pylori?

A
Quadruple therapy is best
PPI
Tetracycline
Flagyl
Bismuth subsalicylate
for 14 days
26
Q

PPIs for H pylori, you must dose with what?

A

meal! (prior to meal)

27
Q

which are the worst offenders of NSAID-induced- ulcers? which one spares most prostaglandin production (and therefore is less likely a cause of this? )

A

worst: ASA

least offender: Cox2 inhibitors

28
Q

4 part Txt of NSAID ulcer

A
  1. Stop the NSAID; use lowest possible dose for shortest possible time
  2. Give: misoprostol, PPI, H-2 blocker
  3. Switch to acetaminophen/COX-2 specific
  4. Warn patients of the risk, Caution the use of combination products (e.g. Goody or B.C. powders, others)
29
Q

what is zollinger-ellison syndrome? MC site (and others). Common CP or index of suspicion

A

gastrin-secreting neuroendocrine tumor which leads to severe PUD and diarrhea, MC in duodenum (also seen in pancreas, lymph nodes)
CP: pts with severe, multiple, recurrent ulcers + diarrhea

30
Q

how to dx and txt zollinger-ellison syndrome. what is the most common site of metastasis?

A

Dx:
Best screening = elevated fasting gastrin levels (>1000) and confirm this with a secretin test (which causes severe increase in gastrin after administration)
Tx: Surgery to locally resect, if metastatic or unable to resect then med management with lifelong high dose PPIs
*MC site of metastasis is liver and associated lymph nodes

31
Q

what is gastroparesis

A

an autonomic neuropathy (usually mediated in walls of GI). You’re not getting the big contractions that you need for digestion.

32
Q

gastroparesis is common in what pts? what are the signs?

A

DM; early satiety or post-prandial nausea

33
Q

Relapse rates for treated ulcers are ______; suspect ________ if relapse occurs

A

low

NSAIDS/OTC meds

34
Q

how to diagnose and tx gastritis?

A

dx: H. pylori testing, UGD with biopsy is test of choice
tx: eradicate h. pylori with quad therapy if needed, PPI or H2 blocker to suppress acid or prophylaxis for stress gastritis, prevention of cause (like meds)

35
Q

which type of ulcer is more common in PUD? which ulcer type is more likely to progress into malignancy?

A

duodenum more common and often younger pts, while gastric is more likely to become malignant (4% turn to gastric adenocarcinoma) and usually presents in older pts

36
Q

PP behind duodenal vs gastric ulcers. what are the most common causes for PUD?

A

duodenal: increase in aggressive factors (H. Pylori, HCl)
gastric: decrease in protective factors (mucus, bicarbonate, prostaglandins)
* causes SAME as as gastritis: H. pylori (MC), NSAIDS/ASA more likely gastric ulcers, ETOH, smoking, stress PLUS zollinger-ellison syndrome

37
Q

CP for PUD and perforated ulcer

A

dyspepsia (burning, gnawing epigastric pain), N/V, duodenal (pain after eating) vs gastric (pain with eating), bleeding ulcer presents with hematemesis or melena
Perforated ulcer: sudden onset severe abd pain plus peritoneal signs (rebound tenderness, guarding and rigidity)

38
Q

what is the most common cause of GI bleed?

A

PUD

39
Q

how do you dx PUD?

A

UGD with biopsy is TOC (best to diagnose H. pylori infection as well)

40
Q

tx for PUD? what does this depend on?

A

tx depends on H. Pylori status
if +, then tx infection
refractory to medical therapy, can do surgical approaches of vagotomy or Bilroth II (partial gastrectomy)

41
Q

when do you use EGD vs non-invasive tests to diagnose H. pylori?

A

if a patient doesn’t need an EGD (more likely gastritis) then do one of the other two tests first

42
Q

all gastric ulcers need what repeat imaging to confirm healing?

A

repeat EGD, even if AS

43
Q

what is pyloric stenosis, what does it lead to, and it is the MC cause of what in infants?

A

hypertrophy and hyperplasia of pyloric sphincter which causes functional outlet obstruction
MC cause of intestinal obstruction in infants

44
Q

CP and PE for pyloric stenosis

A

CP: non-bilious projectile vomiting especially after feeding, maybe dehydration or weight loss
PE: olive shaped nontender abdominal pass

45
Q

Dx, labs and Tx for pyloric stenosis

A

Dx: US shows enlongated, thickened pylorus (initial test), Upper GI series shows “string sign” (barium passing through thickened pylorus)
Labs: hypokalemic and hypochloremic metabolic alkalosis
Tx: rehydration (IV fluids) and electrolyte repletion first, pyloromyotomy definitive

46
Q

MC type of gastric carcinoma, MC risk factor and others

A

MC type: adenocarcinoma (90%)

H. pylori is biggest RF, also smoking, preserved foods, chronic atrophic gastritis, and NHL

47
Q

CP of gastric carcinoma

A
  • Most are advanced at presentation*

- weight loss and persistent abdominal pain , early satiety, hematemesis/melena

48
Q

how to dx and tc gastric carcinoma

A

dx: EGD with biopsy is initial test of choice
tx: endoscopic resection for early local dz, +/- chemo/radiation

49
Q

which lymph node is commonly enlarged or should be examined if gastric cancer is suspected?

A

left supraclavicular node (virchow’s node)

50
Q

what is the triple therapy tx of H pylori?

A

PPI, clarithromycin, and amoxicillin