Al-Mehdi: Gastric Acid Pharmacology

Question 1

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

Answer 1

H. pylori infection

Question 2

H. pylori infection of corpus (body) leads to

Answer 2

gastric cancer

Question 3

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

Answer 3

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

Question 4

H. pylori infection of antrum leads to

Answer 4

peptic ulcer (in duodenum)

Question 5

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

Answer 5

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

Question 6

a2
EP3
SST2
M2
type of G receptor

Answer 6

Gi

Question 7

H2 type of G receptor

Answer 7

Gs (cAMP)

Question 8

H1
a1
M1
M3
CCK2
type of G receptor

Answer 8

Gq (Ca2+)

Question 9

5-HT3 receptor

Answer 9

Ca2+ influx

Question 10

how is H+ brought into lumen from parietal cell

Answer 10

H+/K+ ATPase

Question 11

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

Answer 11

HCO3/Cl exchanger

Question 12

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

Answer 12

increased

Question 13

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

Answer 13

decreased

Question 14

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

Answer 14

increased

Question 15

where does gastrin travel when it is released by G cell

Answer 15

into blood then to parietal cell

Question 16

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

Answer 16

decreased

Question 17

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

Answer 17

increased

Question 18

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

Answer 18

increases

Question 19

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

Answer 19

stimulates

Question 20

somatostatin blocks ____ and ___ secretion

Answer 20

gastrin and histamine

Question 21

vagus (M2:Gi) blocks _____ secretion

Answer 21

somatostatin

Question 22

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

Answer 22

increase

Question 23

cells specific to body (corpus) of gut

Answer 23

parietal
chief

Question 24

cell specific to antrum of gut

Answer 24

G cell

Question 25

surface mucosal cell (foveolar cell) hyperplasia

Answer 25

Menetrier Disease

Question 26

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

Answer 26

increase in TGF-alpha

Question 27

hypoproteinemia parietal cell loss (achlorhydria) giant gastric rugae

Answer 27

Menetrier Disease

Question 28

to Rx Menetrier disease

Answer 28

Cetuximab Trastuzumab

Question 29

2 main causes of peptic ulcer disease

Answer 29

H. pylori and NSAID use

Question 30

gastrin producing tumor's primary location

Answer 30

duodenum

Question 31

gastrin producing tumor

Answer 31

gastrinoma

Question 32

to dx peptic ulcer disease

Answer 32

H pylori test (stool, urea); endoscopy

Question 33

to Rx peptic ulcer disease

Answer 33

PPI H2 blockers Ab's (for H. pylori)

Question 34

-prazoles

Answer 34

PPIs

Question 35

PGE2 analog used for peptic ulcer disease

Answer 35

Misoprostol

Question 36

PPI that inhibits CYP2C19

Answer 36

Omeprazole

Question 37

PPIs can lead to what -emia

Answer 37

hypergastrinemia

Question 38

best treatment for GERD

Answer 38

PPI

Question 39

are PPIs safe during pregnancy

Answer 39

yes

Question 40

K+ competitive acid blocker used for peptic ulcer disease

Answer 40

VONOPRAZAN

Question 41

H2-blockers

Answer 41

-TIDINEs

Question 42

reduces acid secretion and binds to EP3 (Gi)

Answer 42

PGE2

Question 42

these 2 H2 blockers have no significant avidity for CYP450 enzymes

Answer 42

FAMOTIDINE NIZATIDINE

Question 43

agonist for EP3 (Gi)

Answer 43

MISOPROSTOL

Question 44

mucosal defense agent CI in pregnancy

Answer 44

MISOPROSTOL

Question 45

SE of SUCRALFATE

Answer 45

bezoar formation

Question 46

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

Answer 46

diarrhea

Question 47

SE of CaCO3 (calcium carbonate) antacid

Answer 47

constipation

Question 48

CaCO3 can lead to ______ in CKD

Answer 48

hypercalcemia

Question 49

triple therapy for H. pylori infection without macrolide resistance

Answer 49

PPI clarithromycin amoxicillin

Question 50

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

Answer 50

Metronidazole

Question 51

quadruple therapy for H. pylori infection

Answer 51

PPI tetracycline metronidazole bismuth

Question 52

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

Answer 52

ulcer bleeding or perforation

Question 53

pathogenesis of peptic ulcers w/ NSAIDs

Answer 53

PGE2 depletion (barrier loss) direct toxicity ischemia

Question 54

what parts of the gut does H. pylori affect

Answer 54

corpus antrum

Question 55

what part of the gut do NSAIDs affect

Answer 55

the whole gut

Question 56

Rx NSAID ulcer

Answer 56

stop NSAIDs PPI

Question 57

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

Answer 57

Celecoxib acetominophen

Question 58

______ is tolerable in patients w/ peptic ulcers or asthma

Answer 58

acetaminophen

Question 59

inhibits COX 3 in brain

Answer 59

acetaminophen