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DIG: Biweekly 1 > Al-Mehdi: Gastric Acid Pharmacology > Flashcards

Al-Mehdi: Gastric Acid Pharmacology Flashcards

1
Q

duodenal and gastric ulcer
gastric cancer
(both a consequence of….)

A

H. pylori infection

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2
Q

H. pylori infection of corpus (body) leads to

A

gastric cancer

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3
Q

4 steps leading to gastric cancer from H. pylori infection:

A
  1. decreased acid secretion (dead parietal cell)
  2. bacterial proliferation
  3. nitrite production in antrum
  4. gastric cancer
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4
Q

H. pylori infection of antrum leads to

A

peptic ulcer (in duodenum)

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5
Q

5 steps leading to peptic ulcer from H. pylori infection:

A
  1. depletion of somatostatin
  2. increased gastrin
  3. increased acid secretion
  4. gastric metaplasia
  5. H. pylori colonizes and ulcer forms
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6
Q

a2
EP3
SST2
M2
type of G receptor

A

Gi

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7
Q

H2 type of G receptor

A

Gs (cAMP)

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8
Q

H1
a1
M1
M3
CCK2
type of G receptor

A

Gq (Ca2+)

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9
Q

5-HT3 receptor

A

Ca2+ influx

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10
Q

how is H+ brought into lumen from parietal cell

A

H+/K+ ATPase

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11
Q

how is Cl- brought into lumen to form acid (HCl) from parietal cell

A

HCO3/Cl exchanger

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12
Q

membrane H+, K+ ATPase abundance is ______ by Vagus (Ach,M3:Gq)

A

increased

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13
Q

membrane H+, K+ ATPase abundance is _____ by PGE2 (EP3:Gi)

A

decreased

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14
Q

membrane H+, K+ ATPase abundance is _____ by G cell gastrin (CCK2:Gq)

A

increased

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15
Q

where does gastrin travel when it is released by G cell

A

into blood then to parietal cell

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16
Q

membrane H+, K+ ATPase abundance is ____ by D cell somatostatin (SST2:Gi)

A

decreased

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17
Q

membrane H+, K+ ATPase abundance is ____ by ECL cell histamine (H2:Gs)

A

increased

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18
Q

gastrin (CCK2:Gq) also _____histamine secretion by ECL cell

A

increases

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19
Q

vagus (M1:Gq) also _____ histamine secretion by the ECL cell

A

stimulates

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20
Q

somatostatin blocks ____ and ___ secretion

A

gastrin and histamine

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21
Q

vagus (M2:Gi) blocks _____ secretion

A

somatostatin

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22
Q

Vagus releases GRP to ____ gastrin secretion via bombesin (BB2:Gq)

A

increase

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23
Q

cells specific to body (corpus) of gut

A

parietal
chief

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24
Q

cell specific to antrum of gut

A

G cell

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25
Q

surface mucosal cell (foveolar cell) hyperplasia

A

Menetrier Disease

26
Q

increase in _____ causes HER1 activation (human EGFR1)—hyperplasia

A

increase in TGF-alpha

27
Q

hypoproteinemia
parietal cell loss (achlorhydria)
giant gastric rugae

A

Menetrier Disease

28
Q

to Rx Menetrier disease

A

Cetuximab
Trastuzumab

29
Q

2 main causes of peptic ulcer disease

A

H. pylori and NSAID use

30
Q

gastrin producing tumor’s primary location

A

duodenum

31
Q

gastrin producing tumor

A

gastrinoma

32
Q

to dx peptic ulcer disease

A

H pylori test (stool, urea); endoscopy

33
Q

to Rx peptic ulcer disease

A

PPI
H2 blockers
Ab’s (for H. pylori)

34
Q

-prazoles

A

PPIs

35
Q

PGE2 analog used for peptic ulcer disease

A

Misoprostol

36
Q

PPI that inhibits CYP2C19

A

Omeprazole

37
Q

PPIs can lead to what -emia

A

hypergastrinemia

38
Q

best treatment for GERD

A

PPI

39
Q

are PPIs safe during pregnancy

A

yes

40
Q

K+ competitive acid blocker used for peptic ulcer disease

A

VONOPRAZAN

41
Q

H2-blockers

A

-TIDINEs

42
Q

reduces acid secretion and binds to EP3 (Gi)

A

PGE2

42
Q

these 2 H2 blockers have no significant avidity for CYP450 enzymes

A

FAMOTIDINE
NIZATIDINE

43
Q

agonist for EP3 (Gi)

A

MISOPROSTOL

44
Q

mucosal defense agent CI in pregnancy

A

MISOPROSTOL

45
Q

SE of SUCRALFATE

A

bezoar formation

46
Q

side effect of Mg(OH)2 (magnesium dihydroxide) antacid

A

diarrhea

47
Q

SE of CaCO3 (calcium carbonate) antacid

A

constipation

48
Q

CaCO3 can lead to ______ in CKD

A

hypercalcemia

49
Q

triple therapy for H. pylori infection without macrolide resistance

A

PPI
clarithromycin
amoxicillin

50
Q

if patient with H. pylori infection is allergic to penicillin, what can you substitute amoxicillin with

A

Metronidazole

51
Q

quadruple therapy for H. pylori infection

A

PPI
tetracycline
metronidazole
bismuth

52
Q

chronic NSAID users can present with ___ or ____ without prior ulcer symptoms

A

ulcer bleeding or perforation

53
Q

pathogenesis of peptic ulcers w/ NSAIDs

A

PGE2 depletion (barrier loss)
direct toxicity
ischemia

54
Q

what parts of the gut does H. pylori affect

A

corpus
antrum

55
Q

what part of the gut do NSAIDs affect

A

the whole gut

56
Q

Rx NSAID ulcer

A

stop NSAIDs
PPI

57
Q

in patients with gastritis/ulcer/ or asthma, what drugs to use for pain

A

Celecoxib
acetominophen

58
Q

______ is tolerable in patients w/ peptic ulcers or asthma

A

acetaminophen

59
Q

inhibits COX 3 in brain

A

acetaminophen

DIG: Biweekly 1 (11 decks)

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