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Flashcards in Upper GI Deck (61):
1

Non-pharmacologic therapy for peptic ulcer disease

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

2

General options for pharmacologic therapy for PUD

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

3

Drugs for H. pylori

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

4

MOA of antacids

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

5

sodium bicarbonate

antacid for PUD; baking soda
ADR: systemic absorption --> Na overload, metabolic alkalosis

6

calcium carbonate

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

7

aluminum hydroxide

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

8

magnesium hydroxide

antacid for PUD, very little absorption, used with AlOH
ADR: diarrhea, Mg accumulation in renal disease

9

MOA of H2-blockers

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

10

Uses of H2-blockers

Low doses for heartburn
Higher doses for GERD, PUD

11

ADR of H2-blockers

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

12

cimetidine

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

13

ranitidine

H2-blocker
intermediate duration, BID

14

famotidine

H2-blocker
longest duration of action, BID or at bedtime

15

MOA of PPIs

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

16

Use of PPIs

GERD and PUD

17

Metabolism of PPIs

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

18

ADR of PPIs

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

19

omeprazole

PPI

20

esomeprazole

PPI
also IV

21

lansoprazole

PPI
also liquid for NG tube

22

pantoprazole

PPI
also IV; preferred PPI in hospitals

23

MOA of sucralfate

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

24

ADR of sucralfate

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

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