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GI #1 > PUD & gastritis > Flashcards

PUD & gastritis Flashcards

1
Q

differentiate PUD from gastritis & gastropathy

A
  • Gastritis: precursor to PUD; hard to differentiate; inflammation associated w/ mucosal injury; symptoms jus like PUD
  • PUD: mucosal defect in GI tract exposed to acid and pepsin secretion
  • Gastropathy: epithelial cell damage and regeneration +/- inflammation; secondary to irritants
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2
Q

common causes of gastritis

A

H. pylori
NSAIDs, radiation, allergic, autoimmune, duodenitis

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3
Q

location of GU vs DU?

A

GU in antrum
DU in bulb

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4
Q

how do ulcers development

A
  • buffered surface mucous layer with rapid epithelial turnover or tight junctions
  • deficient protective prostagladins (less bicarb/mucous)
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5
Q

high risk vs low risk NSAIDs

A
  • high risk: feldene/proxicam, ketorolac/toradol, indomethacin
  • low risk: celebrex, under 1500mg/day ibuprofen, etc
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6
Q

who is at risk for NSAID induced PUD (3)

A
  • prior hx of adverse GI event
  • over 60 yo
  • high dose NSAID + steroid or anticoag
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7
Q

differentiate DU from GU

A
  • DU> GU
  • DU always nonmalignant & feels better with eating (weight gain)
  • GU is typically benign but can be malignant; feels worse after eating
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8
Q

ulcers in which location requires repeat endoscopy after acid suppression treatment & documentation & biopsy

A

gastric

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9
Q

describe sx of PUD and 3 associated sx

what is this condition

A

epigastric pain (burning or gnawing) around meals or at night that is relieved by antacids or vomiting
* dyspepsia, hematemesis or melena

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10
Q

where does NSAID vs h.pylori induced ulcers occur? which shows more severe bleeding?

A
  • h. pylori is more in duodenum and superficial; less severe bleeding
  • NSAIDs in deep and in stomach; more severe bleeding and sometimes asymptomatic
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11
Q

list 3 complications of PUD and which is most common?

A

bleeding: most common
gastric outlet obstruction
perforation: top cause of pneumoperitoneum

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12
Q

best initial diagnostic study for perforated peptic ulcer?

A

upright abdominal plain films

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13
Q

morphology of H. pylori

A

spiral gram - rod w/ flagella
secreates urease which converts urea to amonia
produves alkaline environment

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14
Q

diseases associated with PUD– increases risk (3) & hypersecretory ones (2)

A
  • hypersecretory– gastrinoma (zollinger-ellison), MEN-1
  • increased risk–cirrhosis, chronic pulm dz, renal fail
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15
Q

3 PE findings of PUD

A
  • mild epigastric tenderness
  • maybe melena/guaiac + stool
  • peritonitis with perforation
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16
Q

5 diagnostic tools for H. pylori

A
  1. EGD w/ biopsy
  2. rapid urease
  3. urea breath test
  4. stool antigen
  5. serolofy
17
Q

classic triad of sudden severe diffuse abdominal pain, tachycardia, abdominal regidity

A

hallmark of peptic ulcer perforation

18
Q

test that you can do for H.pylori PUD for initial diagnosis + confirmation of eradication?

A

Urea Breath test

19
Q

test that is good for initial diagnosis + confirmation of eradication of h.pylori (4 wks after tx); needs little prep

A

HpSA antigen test

20
Q

which two H.pylori tests can have false negative with PPI, bismuth and abx

A

urea breath test
fecal antigen testing (hpsa)

21
Q

test that can detect IgG antibodies but does NOT determine if its an active H. pylori infection
* useful for those who never got treated or symptomatic pt not using NSAIDs

A

serology

22
Q

which meds should patients be off for stool and both urea based testing? (3)

A

PPI
abx
bismuth (pepto bismol, etc)

use antacids and H2 blockers if symptomatic

23
Q

binds to ulcer base forming a protective coat and has anti-inflammatory and bactericidal properties’; can cause dark stools

A

bismuth subsalicylate (pepto bismol)

24
Q

Selectively block H2 receptors on parietal cells reducing acid secretion
* Used primarily in non-H. Pylori ulcer dz for 6-8 wks

what class? what are SE?

A

H2 blockers
Cimetidine SE: confusion in elderly, impotence +/- gynecomastia, may alter levels of other drugs, may alter renal function requiring lower dose

25
Q

Decreases gastric acid secretion by blocking parietal cell H/K ATP pump
* better for NSAID related PUD
* duration depends on location, etiology, complications

what class? SE?

A

PPI
SE: calcium malabsorption (achlorhydria); low Mg, infection and fracture risk

26
Q

4 medical tx of non-h.pylori PUD

A

OTC neutralizers
H2 blockers
PPI
surgery

27
Q

3 surgical options for PUD

A

Antrectomy with vagotomy
Truncal vagotomy w/ pyloroplasty
Highly selective vagotomy

28
Q

how is H.pylori PUD treated?

A
  • triple therapy x 14 days
  • quadruple therapy
29
Q

triple vs quad therapy

A

PPI + clarithromycin + amoxicillin (sub for metronidazole if PCN allergic)
OR
Bismuth + tetracycline + metronidazole + PPI

30
Q

3 steps in treating NSAID-PUD

A
  1. discontinue NSAIDs if you can, if not reduce dose
  2. Sucralfate or Misoprostol
  3. prophylactic treatment
31
Q

what is given prophylactically for NSAID-PUD and who gets it?

A
  • for high risk ppl taking nonselective NSAIDs
  • Misoprostol 200 mg 4x/day + Iansoprazole 15 or 30 mg daily
32
Q

when do you do PPI IV?

A

complicated ulcers

33
Q

tx duration for complicated DU vs GUvs NSAID induced?

A
  • DU: PPI x 4-8wks
  • GU: PPI x 8-12 wks until EGD confirms healing
  • NSAID induced: PPI x 4-8wks
34
Q

which type of ulcer requires surveillance?

A

GU requires it in 8-12 wks

only done in DU if sx persist

GI #1 (10 decks)

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