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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
ADR of bismuth subsalicylate
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
MOA bismuth subsalicylate
inhibits pepsin & antimicrobial against H. pylori
27
GERD pathophysiology
reflux of gastric acid, pepsin, bile acids, pancreatic enzymes into esophagus -> inflammation and complication (directly related to exposure time to acid)
28
managing GERD non-pharmacologically
weight loss, elevate head of bed, avoid meals 2-3 hours before bedtime
29
when and how to treat GERD pharmacologically
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
receptors in vomiting center of brain
5HT3-R, D2, M
31
pathway of pharynx -> vomiting
pharynx -> STN -> VC
32
pathway of blood-borne emetics -> vomiting
BB emetics -> stomach/ small int (5HT3, D2, NK1, opioid-R) -> chemoreceptor trigger zone and nuc/tract solitarius -> VC
33
pathway of inner ear -> vomiting
inner ear -> cerebellum (M, H1) -> VC
34
other pathways to cause vomiting
other -> higher centers (NK1, cannabinoid-R) -> VC
35
What is NK1 receptor
neurokinin-R stimulated by substance P when exposed to chemo, radiation, morphine, nicotine
36
treating n/v for viral infection, excessive food or EtOH intake, motion sickness
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
treating n/v in pregnancy
``` 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
treating n/v if mild-mod
monitor hydration OTC anti-emetic oral rehydration therapy (as in food poisoning)
39
types of prescription meds for n/v
D2 antagonists, 5HT3 antagonists, anti-ACh, anxiolytics, synthetic cannabinoids, dexamethasone, subsance P/NK-1-R antagonists
40
types of D2 antagonists
phenothiazines and metoclopramide
41
prochlorperazine
phenothiazine D2-blocker
42
promethazine
phenothiazine D2-blocker
43
MOA and use of phenothiazines
block D2-R at CTZ level of brain | common for PONV (not as good as 5HT3-blockers)
44
ADR of phenothiazines
hypotension, sedation, extrapyramidal reactions (acute dystonias)
45
metoclopramide
blocks D2 at CTZ level in brain | in high doses, blocks 5HT3-R at GI level
46
ondansetron
5HT3-blocker for n/v
47
granisetron, dolasetron
5HT3-blocker for n/v | half life 4-8 hours
48
palonosetron
5HT3-blocker for n/v | IV only; T1/2 40 hours
49
when specifically to give 5HT3-blockers
before chemo drug exposure
50
scopolamine
anti-ACh transdermal patch for n/v d/t motion sickness
51
lorazepam
benzodiazepine; anxiolytic for n/v | used for anticipatory n/v prior to chemo
52
dronabinol, nabilone
synthetic cannabinoids similar to THC for chemo-induced n/v | ADR: orthostasis, psychomimetic reactions, high abuse potential
53
dexamethasone
GC for n/v | enhances activity of 5HT3-blockers and metoclopramide
54
MOA and ADR substance P/NK-1-R antagonists
used in combo with 5HT3-blocker and dexamethasone for highly emetogenic chemotherapy ADR: metabolized by and mod inh of CYP 3A4
55
aprepitant, fosaprepitant
substance P/NK-1-R antagonists
56
treatment of acute esophageal varices bleeding
vitamin K (if elevated INR, common in liver failure), octreotide IV for up to 5d, sclerotherapy
57
MOA octreotide
somatostatin analogue, potent vasoconstrictor, reduces portal and collateral blood flow
58
MOA sclerotherapy
inject sclerosing agent like 11.5% NaCl into vein under fiberoptic esophagascope to occlude vein w/i 5 minutes
59
prophylaxis/ rebleeding prevention for esophageal varices
beta blockers and isosorbide dinitrate
60
MOA of beta-blockers for esophageal varices
reduces portal vein pressure by decreasing HR (B1 blocked) and splanchnic blood flow (B2 vasodilation blocked)
61
MOA of isosorbide dinitrate
decrease portal pressure by selective venodilation in splanchnic circulation

Pharm 4 (8 decks)

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