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git mod > acid peptic ulcer disease drugs > Flashcards

acid peptic ulcer disease drugs Flashcards

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1
Q

cells in cardia that secrete mucus

A

foveolar cells

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2
Q

fundus and body of stomach contains _ cells?

A

parietal and enterochromaffin-like cells

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3
Q

antrum and pyloric part of stomach contains what cells?

A

G-cells

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4
Q

receptors on parietal cells

A
  1. m3 r for ach
  2. h2 r for histamine
    3.cck r for gastrin
    inhibiton
  3. sst-r for somatostatin
    5.pge2 r for prostaglandin
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5
Q

stomach expansion activates - leading to release of ach

A

vagus nerve

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6
Q

g cells activated by - and releases

A

partially digested protein, gastrin

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7
Q

+ of enterochromaffin cells by- and they release-

A

gastrin and ach, histamine

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8
Q

mechanism of hcl production

A
  1. activationof m3, cck2,h2 r lead to co2 and h20 being converted to
  2. h ions and hco3 by carbonic anhydrase
  3. h ions pumped out into the lumen along with cl
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9
Q

moa of ppi

A

forms covalent disulfide bonds with h/k ATPase irreversibly (effect last till these pumps regenerate)

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10
Q

ppi’s 3 oral medications?

A

omeprazole
lansoprazole
dexlansoprazole

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11
Q

ppi’s iv medication?

A

pantoprazole
esomeprazole

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12
Q

ppi’s are - line of treatment for reducing -

A

1st, acid secretion

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13
Q

indications for ppi

A

Gastroesophageal reflux disease
Peptic ulcer disease
zollinger-ellison syndrome
H pylori-associated ulcers(weak antibacterial effect)
NSAID-associated ulcers
Prevention of rebleeding from peptic ulcers
Nonulcer dyspepsia
Prevention of stress-related mucosal bleeding
Gastrinoma and other hypersecretory conditions

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14
Q

days for ppis to reduce acid secretion

A

3-4 days

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15
Q

se of ppis

A
  1. gi disturbances like nausea, abdominal pain, diarhea
  2. nutritional def (bec the acid is needed for digestion)- ivxm- iron, vb12, calcium, magensium
  3. ecl hyperplasia
  4. respiratory(pnemonia) and enteric infection (no acid so loss of protective effect)
  5. headaches, rashes, osteoporosis
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16
Q

ppis reduce absoption of

A
  1. digoxin
    2.ketocanozole
  2. atazanavir
    4.itraconazole
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17
Q

omeprazole and esomeprazole impair metabolism of

A

warfarin, diazepam, phneytoin

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18
Q

omeprazole inhibits liver enzyme that reduce activation of

A

antiplatelet drug- clopidogrel

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19
Q

h2 r antagonist moa

A

competetively bind to h2 receptors.
reduce mainly noctural acid secretion as well as food-stimulated acid secretion.

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20
Q

h2 antagonsist works within - hr of ingestion

A

1 hour

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21
Q

h2 antagonists names

A

cimetidine, ranitidine, famotidine, and nizatidine.

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22
Q

h2 antagonists indications?

A

peptic ulcers,
prevention of ulcers and stress ulcers, gastroesophageal reflux disease (GERD)
Zollinger-Ellison syndrome,

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23
Q

se of h2 antagonists

A

headache, fatigue, myalgias, diarrhea, and constipation
mental status changes in renal/hepatic dysfunction patients

24
Q

cimetidine (inhibitor of p450) red the rate of elimination of - drugs

A

benzodiazepines or warfarin,

25
Q

cimetidine se and why?

A
  1. gynecomastia , impotence
  2. galactorrhea
    it inhibits the dht conversion to testosterone, inhibits metabolism of estradiol, increases serum prolactin levels
  3. crosses bbb so confusion and dizziness
26
Q

cimetidine and ranitidine increases serum-

A

serum creatinine

27
Q

preferred h2 antagonist in preg and lactation

A
  1. ranitidine
  2. famotidine
28
Q

antimuscarinic agent?

A

pirenzepine(blocks m1 receptor)

29
Q

how long is omeprazole effective for?

A

2-3 days and with continual doses antisecretory effect can last for up to 5 days.

30
Q

antacids moa

A

weak bases that neutralize acidity by binding to h+ions.

31
Q

uses of antacids

A
  1. relieve indigestion
  2. repairs damage done by excess acid to the stomach lining
  3. inhibit pepsin activity
  4. increase tone of the lower esophageal spincter
  5. symptomatic relieve of GERD
32
Q

classification of antacids

A

systemic- sodium bicarbonate, sodium citrate
non-systemic- magnesium hydroxide, al hydrooxide

33
Q

calcium bicarbonate, sodium bicarb se

A

milk-alkali syndrome- metabolic alkalosis, hypercalcemia, renal insuffiency

34
Q

al(oh)2 se

A

contipation
hypophostamenia
proximal muscle weakness
osteoporosis
seizures

35
Q

mg(oh)2 se

A

diarhea—hypotension
hypermagnesemia
hyporeflexia
cardian arrest

36
Q

common se of all antacids

A

hypokalemia
delays gastric empyting

37
Q

antacids dec absorption

A

digoxin , phenytoin,warfarin

38
Q

mg(oh)2 reduce absorption of

A

tetracyline

39
Q

alginate consists of

A

carbonate and alginic acid.

40
Q

moa of alganate

A

form a barrier that floats on top of the acid in stomach.
This barrier helps prevent stomach acid from moving up into esophagus.

41
Q

sulralfate moa?

A
  1. sucrose sulfate-aluminium complex that after polymerization binds to the ulcer, creating a physical barrier that protects the gastrointestinal tract from stomach acid and prevents the degradation of mucus.
  2. promotes bicarb production
42
Q

se of sucralfate?

A

constipation, flatulence, headache, hypophasphatemia, xerostomia

43
Q

prostaglandin analog for nsaid-induced ulcers?

A

misoprostol

44
Q

action of misoprostol

A
  1. acid inhibition
  2. +mucus and bicarb production
  3. enhance mucosal blood flow
45
Q

se of misoprostol

A

diarhea, cramping, abdominal pain,
c.i in pregnancy

46
Q

2 bismuth compouds

A

bismuth subsalicylate
bismuth subcitrate potassium

47
Q

moa of bismuth

A

Bismuth coats ulcers and erosions, creating a protective layer against acid and pepsin.
It may also stimulate prostaglandin, mucus, and bicarbonate secretion.
Bismuth subsalicylate reduces stool frequency and liquidity in acute infectious diarrhea.

48
Q

clinical uses of bismuth

A

nonspecific treatment of dyspepsia
acute diarrhea.
prevention of traveler’s diarrhea
In 4-drug regimens for the eradication of H pylori infection

49
Q

se of bismuth compounds

A
  1. harmless blackening of the stool & tongue.
  2. caution in renal insuff patients
  3. prolonged use–bismuth toxicity–encephalopathy(ataxia, headaches, confusion, seizures)
50
Q

triple therapy for h.pylori?

A

ppi 2x daily
clarithromycin
either amoxillin or metronidazole

51
Q

clarithromyosin moa

A

inhibits bacterial protein synthesis

52
Q

amoxicillin moa

A

inhibition of bacterial cell wall synthesis

53
Q

metronidazole moa

A

inhibit protein syn , fee radical producer—cell death

54
Q

tetracyclin moa

A

inhibit protein synthesis

55
Q

quadriple regimen for h.pylori infection?

A

ppi, bismuth subsalicylate, tetracycline, metronidazole

56
Q

ppi need to give -weeks after triple therapy and why?

A

4-6 weeks, complete ulcer healing

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