GIT (Acid-Peptic Diseases) Flashcards

1
Q

Drugs used for peptic acid disease

A

Proton Pump Inhibitors
Antacids
Mucosal protective agents
H2 Blockers
Antibiotics

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2
Q

Motility promoters

A

Motilin agonists, antidiarrheals, Dopamine antagonists, laxatives,

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3
Q

Drugs for irritable bowel disease

A

Chloride Channel activators, antispasmodics, serotonin inhibitors

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4
Q

Drugs for inflammatory bowel disease

A

Corticosteroids immunosuppresants, anti-tnf drugs, 5-asa drugs

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5
Q

Other agents

A

Pancreatic lipase, Antidiarrheal ursodiol, laxatives

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6
Q

antiemetics

A

neurkinin receptor, cannabinoids, corticosteroids, antimuscarinic, h1 blockers, d2 blockers, 5 ht3 blockers

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7
Q

Acid– peptic disease includes:

A

Gastroesophageal Reflux
Peptic ulcer (gastric or duodenal)
Stress related injury

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8
Q

Gastroesophageal Reflux refers to

A

Heart burn

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9
Q

Heart burn occurs when acid rise to the

A

esophagus

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10
Q

T/F: The location of HB and Angina are the same and
but the pain felt are different

A

T

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11
Q

heat sensation rising

A

Heartburn

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12
Q

suffocating/ crushing feeling

A

Angina

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13
Q

The higher the stress, the ________(higher/lower) the secretion of
acid

A

higher

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14
Q

Acid-Peptic Disease is the mucosal erosion or ulceration due to the caustic effect of ______, ______, and ______

A

acid, pepsin and bile

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15
Q

Peptic ulcer may also be dueto the presence of

A

Helicobacter pyroli

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16
Q

Prolong use of NSAIDs can lead to formation of ______

A

gastric
ulcer

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17
Q

Simplest drug used in acid peptic disease

A

ANTACID

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18
Q

ANTACIDs are ______ bases that react with the gastric HCl

A

weak bases

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19
Q

Principal mechanism of Antacid

A

reduction of the intragastric
acidity

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20
Q

For Antacids, a single dose of _______ mEq of antacid given _______ after meal
effectively neutralizes gastric acid for up to __________

A

156; 1 hour; 2 hours

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21
Q

Antacids may affect the absorption of other medications by __________ or ________

A

binding
the drug or altering the intragastric pH

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22
Q

Baking soda, Alka seltzer

A

SODIUM BICARBONATE

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23
Q

SODIUM BICARBONATE produces

A

CO2 and NaCl

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24
Q

In Sodium bicarbonate, unreacted alkali is readily absorbed which could lead to
_______________

A

metabolic alkalosis

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25
Q

exacerbate fluid retention

A

Sodium chloride

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26
Q

ADR of NaHCO3

A

○ Flatulence
○ Bloating
○ Belching

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27
Q

Tums

A

CaCO3

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28
Q

Less soluble and reacts slowly than sodium bicarbonate

A

CaCO3

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29
Q

CaCO3 forms

A

CaCl2 and CO2

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30
Q

Excessive dose of CaCO3 could lead to

A

hypercalcemia, renal
insufficiency and metabolic alkalosis

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31
Q

MgOH/AlOH reacts slowly to

A

HCl

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32
Q

Unabsorbed magnesium salt may cause

A

osmotic diarrhea

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33
Q

Unabsorbed aluminum salt

A

constipation

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34
Q

Commonly administered together to minimize impact on
bowel function

A

MgOH/AlOH

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35
Q

MgOH/AlOH is absorbed and excreted by the __________ thus should not be
taken in long term by patients with __________

A

kidney; renal insufficiency

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36
Q

-tidine drugs

A

HISTAMINE 2 RECEPTOR ANTAGONIST

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37
Q

Introduced in the 1970s

A

H2 antagonist

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38
Q

H2 antagonist drugs

A

Cimetidine, Ranitidine, Famotidine and Nizatidine

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39
Q

blocks histamine at the H2 receptor gastric parietal cells

A

H2 antagonist

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40
Q

H2 antagonists are rapidly absorbed from the

A

intestine

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41
Q

Mainstay drug in APD

A

H2 antagonist

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42
Q

Inhibits stomach acid production, especially at night

A

H2 antagonist

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43
Q

H2 antagonists that undergo first pass
hepatic resulting to a bioavailability of approximately 50%

A

Cimetidine, Ranitidine and Famotidine

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44
Q

H2 antagonist that has little first pass metabolism

A

Nizatidine

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45
Q

H2 antagonist is cleared bya combination of__________, __________, ____________

A

a combination of hepatic metabolism,
glomerular filtration and renal tubular secretion

46
Q

H2 antagonist reduces acid secretion stimulated by histamine as well as ___________, and _________ agents by 2 mechanisms

A

gastrin and cholinomimetic

47
Q

2 mechanisms involved in the reduction of acid secretion by H2 Antagonist

-Histamine release from ________ by ________ stimulation blocked from binding to the parietal cell H2 receptor

-____________of the parietal cell by gastrin or acetylcholine has a ____________ on acid secretion in the presence of H2 receptor blockade

A

-Histamine release from ECL cells by gastrin or vagal stimulation blocked from binding to the parietal cell H2 receptor

-Direct stimulation of the parietal cell by gastrin or acetylcholine has a diminished effect on acid secretion in the presence of H2 receptor blockade

48
Q

When given in usual prescription doses, all inhibit 60 – 70
% of total 24-hour acid secretion.

A

H2 Antagonist

49
Q

Clinical uses of H2 Antagonists

A

○ GERD
○ PUD
○ Non-ulcer dyspepsia
○ prevention of bleeding from stress-related gastritis

50
Q

T/F: H2 Antagonists are extremely safe drugs

A

T

51
Q

T/F: H2 Antagonists rarely causes ADR

A

T - Occur in less than 3%: diarrhea, headache, fatigue,
myalgias and constipation

52
Q

this may increase
the risk of nosocomial pneumonia in critically ill patients

A

IV H2 blocker of PPI

53
Q

All except _________ inhibit gastric first pass metabolism
of ethanol, especially in women

A

famotidine

54
Q

Cimetidine inhibits binding of ____________ to androgen
receptor, inhibits metabolism of _________ and increase
___________ levels

A

dihydrotestosterone; estradiol; serum prolactin levels

55
Q

Long term or high dose may cause impotence

A

Cimetidine

56
Q

impotence in men

A

Gynecomastia

57
Q

impotence in women

A

Galactorrhea

58
Q

CIMETIDINE interferes with several important ________________________
drug metabolism pathway

A

hepatic cytochrome P450

59
Q

Half-lives of drugs metabolized by the pathways may be
prolonged

A

CIMETIDINE

60
Q

Compete with creatinine and certain drugs for renal
tubular secretion

A

CIMETIDINE

61
Q

-prazole drugs

A

PROTON PUMP INHIBITOR (PPI)

62
Q

PROTON PUMP INHIBITOR (PPI) DRUGS

A

Omepazole, Esomeprazole, Lansoprazole, Dexlansoprazole,
Rabeprazole and Pantoprazole

63
Q

PPI is a substituted ___________ that resembles H2 antagonist

A

benzimidazole

64
Q

to protect the acid labile prodrug
formulated for delayed release as acid resistant, enteric
coated capsule or tablet

A

Inactivate prodrug

65
Q

T/F: PPI must be inactivated to protect the acid labile prodrug
formulated for delayed release as acid resistant, enteric
coated capsule or tablet

A

T

66
Q

T/F: PPI drugs are mostly modified release

A

T

67
Q

Lipophilic weak base (pKa 4 to 5), and after intestinal
absorption, diffuses readily across lipid membrane into
acidified compartment

A

PPI

68
Q

Irreversibly inactivate the H+/K+ ATPase pump

A

PPI

69
Q

Rapidly metabolized PPI may require ______________ to have an
effect

A

3 – 4 days

70
Q

PPI must be administered with food or without food?

A

Without food

71
Q

inhibits both fasting and meal stimulated secretion
because they block the final common pathway of acid
secretion

A

PPI

72
Q

Preferred to use than H2 blockers

A

PPI

73
Q

at Standard doses, inhibits 90 to 98% of 24-hour acid
secretion

A

PPI

74
Q

Chronic treatment for hypergastrinemia

A

PPI

75
Q

Minor reduction in _______
occur during proton pump inhibition

A

oral cyanocobalamin absorption

76
Q

May cause Respiratory and enteric infection

A

PPI

77
Q

T/F: Decreased gastric acidity may alter absorption of drug
which intragastric acidity affect drug bioavailability

A

T

78
Q

All PPI are metabolized by

A

hepatic P450 cytochrome

79
Q

T/F: Because of its short half-lives PPI interaction are rare

A

T

80
Q

PPI that inhibits metabolism of warfarin,
diazepam and phenytoin

A

Omeprazole

81
Q

PPI that decreases metabolism of diazepam

A

Esomeprazole

82
Q

PPI that enhances clearance of theophylline

A

Lansoprazole

83
Q

PPI that has no significant drug
interaction

A

Rabeprazole and Pantoprazole

84
Q

important in
stimulating mucus and bicarbonate secretion and mucosal
blood flow

A

Mucosal prostaglandins

85
Q

MUCOSAL PROTECTIVE AGENTs

A

Sucralfate
Misoprostol
Bismuth Compound

86
Q

Salt of sucrose complexed to sulfurated aluminum
hydroxide

A

SUCRALFATE

87
Q

In water or acidic solution, it forms a viscous, tenacious
paste that binds selectively to ulcer or erosion for up to 6
hours

A

SUCRALFATE

88
Q

Is sucralfate soluble or poorly soluble

A

Poorly soluble molecule

89
Q

binds to injured tissue in the stomach

A

Sucralfate

90
Q

(Sucralfate) Negatively charged sucrose binds to the positively charged
protein in the base of ulcer or erosion, forming a ___________________ that resist further caustic damage and stimulates
mucosal prostaglandin and bicarbonate secretion

A

physical
barrier

91
Q

Sucralfate must be taken _____ times daily

A

4 times daily

92
Q

Prostaglandin E1 (PGE1) analogue

A

MISPROSTOL

93
Q

Increased mucosal protection inhibit acid secretion

A

MISOPROSTOL

94
Q

Oral administration is rapidly absorbed and metabolized to
free acid

A

MISOPROSTOL

95
Q

Serum T1/2 : <30 minutes hence may be administered 3 – 4
times

A

MISOPROSTOL

96
Q

Misoprostol is excreted in the

A

urine

97
Q

T/F: Misoprostol has acid inhibitory and mucosal protective properties

A

T

98
Q

Reduce ulcer in NSAID users

A

Misoprostol

99
Q

Bismuth subsalicylate and Bismuth subcitrate potassium

A

BISMUTH COMPOUND

100
Q

Coats ulcers and erosions, creating a protective layer
against acid and pepsin

A

BISMUTH COMPOUND

101
Q

May also stimulate prostaglandin, mucus and bicarbonate
secretion

A

BISMUTH COMPOUND

102
Q

Bismuth compound may also stimulate ______, _______, and __________ secretion

A

prostaglandin, mucus and bicarbonate
secretion

103
Q

reduces stool frequency and liquidity in acute
infectious diarrhea, due to salicylate inhibition of
intestinal prostaglandin and chloride secretion

A

Bismuth subsalicylate

104
Q

Bismuth subsalicylate reduces stool frequency and liquidity in acute
infectious diarrhea, due to ____________ inhibition of
intestinal _________ and _________ secretion

A

salicylate; prostaglandin and chloride

105
Q

Bismuth subsalicylate reduces _________ and __________ in acute
infectious diarrhea, due to salicylate inhibition of
intestinal prostaglandin and chloride secretion

A

stool frequency and liquidity

106
Q

Direct antimicrobial effec

A

BISMUTH COMPOUND

107
Q

Causes a black tongue and black stool

A

BISMUTH COMPOUND

108
Q

Widely used by patients for the nonspecific treatment of
dyspepsia and acute diarrhea

A

BISMUTH COMPOUND

109
Q

Also used for the prevention of Traveller’s diarrhea

A

BISMUTH COMPOUND

110
Q

Used in 4-drug regimen for the eradiacation of H. pylori

A

BISMUTH COMPOUND

111
Q

4-drug regimen for the eradiacation of H. pylori:
○ PPI BID
■ Bismuth Subsalicylate (2 tab; _ mg)
■ Tetracycline( ________mg)
■ Metronidazole ( mg) times daily for

○ PPI BID
■ Bismuth Subcitrate mg
■ Metronidazole mg
■ Tetracycline mg, taken times daily for
days

A

○ PPI BID
■ Bismuth Subsalicylate (2 tab; 262 mg)
■ Tetracycline(250 to 500 mg)
■ Metronidazole (500 mg) four times daily for 10 to
14 days

○ PPI BID
■ Bismuth Subcitrate 140 mg
■ Metronidazole 125 mg
■ Tetracycline 125 mg, taken four times daily for 10
days