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Pharm 4 > Upper GI > Flashcards

Upper GI Flashcards

1
Q

Non-pharmacologic therapy for peptic ulcer disease

A

stop smoking, avoid alcohol and NSAIDs and ASA, avoid irritating foods

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2
Q

General options for pharmacologic therapy for PUD

A

Eradicate H. pylori, antacids, H2-blockers, PPIs, sucralfate, bismuth subsalicylate, prokinetic agents, misoprostol

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3
Q

Drugs for H. pylori

A

clartithro + amox or metro + PPI for 14d
or tetra + metro + PPI + bismuth subsalicylate for 14d
or amox + PPI x5d then clarithro + tinidazole x5d

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4
Q

MOA of antacids

A

quickly neutralize HCl for symptomatic relief of dyspepsia or GERD; does NOT heal erosions

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5
Q

sodium bicarbonate

A

antacid for PUD; baking soda

ADR: systemic absorption –> Na overload, metabolic alkalosis

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6
Q

calcium carbonate

A

antacid for PUD

ADR: constipation, acid rebound, hypercalcemia, milk-alkali syndrome (HA, nausea, calcium stones)

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7
Q

aluminum hydroxide

A

antacid for PUD, very little absorption, used with MgOH to balance GI sx (Mylanta, Maalox)
ADR: constipation, phosphate binding, aluminum absorption

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8
Q

magnesium hydroxide

A

antacid for PUD, very little absorption, used with AlOH

ADR: diarrhea, Mg accumulation in renal disease

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9
Q

MOA of H2-blockers

A

dose-dependent inhibition of gastric acid secretion by blocking H2-R on parietal cells; mostly basal/fasting HCl production; slower onset but longer duration than antacids

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10
Q

Uses of H2-blockers

A

Low doses for heartburn

Higher doses for GERD, PUD

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11
Q

ADR of H2-blockers

A

generally well-tolerated
high dose -> confusion, delirium, HA, lethargy in elderly
tolerance with repeated use
rebound acid hyper secretion after abrupt discontinuation
pregnancy category B

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12
Q

cimetidine

A

H2-blocker with shortest duration
ADR: high potential for drug intxn, mod-strong inh of CYP 2C9, 2D6, 3A4
*Avoid in elderly and if on multiple drugs

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13
Q

ranitidine

A

H2-blocker

intermediate duration, BID

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14
Q

famotidine

A

H2-blocker

longest duration of action, BID or at bedtime

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15
Q

MOA of PPIs

A

bind irreversibly to Na/K ATPase in parietal cells, blocking secretion of HCl
*more complete acid suppression than H2-blockers to relieve sx and heal ulcers more quickly

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16
Q

Use of PPIs

A

GERD and PUD

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17
Q

Metabolism of PPIs

A

prodrug converted when pH trapped in parietal cells
unstable in gastric acid
delayed onset of action, short T1/2

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18
Q

ADR of PPIs

A

Short-term: minor HA, constipation, diarrhea, abd pain
Drug intx: inh CYP 2C19 -> dec effect clopidogrel, inc level phenytoin, loss of efficacy of bisphosphonates, reduced abs of itraconazole, PIs
Long-term: inc risk fx, C. diff, CAP, B12-def, hypo-Mg
*Abrupt withdrawal after 3 months = hyper secretion of HCl

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19
Q

omeprazole

A

PPI

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20
Q

esomeprazole

A

PPI

also IV

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21
Q

lansoprazole

A

PPI

also liquid for NG tube

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22
Q

pantoprazole

A

PPI

also IV; preferred PPI in hospitals

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23
Q

MOA of sucralfate

A

AlOH complex of sucrose
at low pH binds damaged and ulcerated tissue = physical barrier to prevent injury
*ineffective with H2-blockers or PPI d/t inc pH

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24
Q

ADR of sucralfate

A

can bind and prevent absorption of drugs like digoxin, quinolone, levothyroxine, phenytoin, warfarin

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25
Q

ADR of bismuth subsalicylate

A

at pH 3.5, reacts with HCl -> bismuth oxychloride (not abs) and salicylic acid (abs) -> salicylate poisoning like ASA
bismuth sulfate turns tongue and stool black temporarily

26
Q

MOA bismuth subsalicylate

A

inhibits pepsin & antimicrobial against H. pylori

27
Q

GERD pathophysiology

A

reflux of gastric acid, pepsin, bile acids, pancreatic enzymes into esophagus -> inflammation and complication (directly related to exposure time to acid)

28
Q

managing GERD non-pharmacologically

A

weight loss, elevate head of bed, avoid meals 2-3 hours before bedtime

29
Q

when and how to treat GERD pharmacologically

A

occasional or non-erosive esophagitis: antacids or H2-blockers
erosive esophagitis: 8 wk of PPI (before 1st meal); switch PPI or increase dose to BID if partial response

30
Q

receptors in vomiting center of brain

A

5HT3-R, D2, M

31
Q

pathway of pharynx -> vomiting

A

pharynx -> STN -> VC

32
Q

pathway of blood-borne emetics -> vomiting

A

BB emetics -> stomach/ small int (5HT3, D2, NK1, opioid-R) -> chemoreceptor trigger zone and nuc/tract solitarius -> VC

33
Q

pathway of inner ear -> vomiting

A

inner ear -> cerebellum (M, H1) -> VC

34
Q

other pathways to cause vomiting

A

other -> higher centers (NK1, cannabinoid-R) -> VC

35
Q

What is NK1 receptor

A

neurokinin-R stimulated by substance P when exposed to chemo, radiation, morphine, nicotine

36
Q

treating n/v for viral infection, excessive food or EtOH intake, motion sickness

A

No therapy EtOH
OTC for disagreeable food/overeating: antacids, H2-blockers, Pepto-Bismol (bismuth subsalicylate)
OTC for motion sickness: antihistamines (dimenhydramine), anti-ACh (meclizine)

37
Q

treating n/v in pregnancy

A 
avoid food with strong odor, eat smaller more frequent meals
antihistamine Diclegis (doxylamine + pyridoxine [B6]) up to 3x/d (preg cat A, active ingredient in Unisom for sleep)
38
Q

treating n/v if mild-mod

A

monitor hydration
OTC anti-emetic
oral rehydration therapy (as in food poisoning)

39
Q

types of prescription meds for n/v

A

D2 antagonists, 5HT3 antagonists, anti-ACh, anxiolytics, synthetic cannabinoids, dexamethasone, subsance P/NK-1-R antagonists

40
Q

types of D2 antagonists

A

phenothiazines and metoclopramide

41
Q

prochlorperazine

A

phenothiazine D2-blocker

42
Q

promethazine

A

phenothiazine D2-blocker

43
Q

MOA and use of phenothiazines

A

block D2-R at CTZ level of brain

common for PONV (not as good as 5HT3-blockers)

44
Q

ADR of phenothiazines

A

hypotension, sedation, extrapyramidal reactions (acute dystonias)

45
Q

metoclopramide

A

blocks D2 at CTZ level in brain

in high doses, blocks 5HT3-R at GI level

46
Q

ondansetron

A

5HT3-blocker for n/v

47
Q

granisetron, dolasetron

A

5HT3-blocker for n/v

half life 4-8 hours

48
Q

palonosetron

A

5HT3-blocker for n/v

IV only; T1/2 40 hours

49
Q

when specifically to give 5HT3-blockers

A

before chemo drug exposure

50
Q

scopolamine

A

anti-ACh transdermal patch for n/v d/t motion sickness

51
Q

lorazepam

A

benzodiazepine; anxiolytic for n/v

used for anticipatory n/v prior to chemo

52
Q

dronabinol, nabilone

A

synthetic cannabinoids similar to THC for chemo-induced n/v

ADR: orthostasis, psychomimetic reactions, high abuse potential

53
Q

dexamethasone

A

GC for n/v

enhances activity of 5HT3-blockers and metoclopramide

54
Q

MOA and ADR substance P/NK-1-R antagonists

A

used in combo with 5HT3-blocker and dexamethasone for highly emetogenic chemotherapy
ADR: metabolized by and mod inh of CYP 3A4

55
Q

aprepitant, fosaprepitant

A

substance P/NK-1-R antagonists

56
Q

treatment of acute esophageal varices bleeding

A

vitamin K (if elevated INR, common in liver failure), octreotide IV for up to 5d, sclerotherapy

57
Q

MOA octreotide

A

somatostatin analogue, potent vasoconstrictor, reduces portal and collateral blood flow

58
Q

MOA sclerotherapy

A

inject sclerosing agent like 11.5% NaCl into vein under fiberoptic esophagascope to occlude vein w/i 5 minutes

59
Q

prophylaxis/ rebleeding prevention for esophageal varices

A

beta blockers and isosorbide dinitrate

60
Q

MOA of beta-blockers for esophageal varices

A

reduces portal vein pressure by decreasing HR (B1 blocked) and splanchnic blood flow (B2 vasodilation blocked)

61
Q

MOA of isosorbide dinitrate

A

decrease portal pressure by selective venodilation in splanchnic circulation

Pharm 4 (8 decks)

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