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Gastrointestinal > PUD and other GI disorders > Flashcards

PUD and other GI disorders Flashcards

1
Q

gastrin and acetylcholine signal thru

A

Gq pathways-calcium induced acid secretion

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2
Q

Somatostain and PG’s signal thru

A

Gi signalling pathwaays-cAMP pathways- ATP/PKA mediated acid secretion

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3
Q

histamine signals thru

A

Gs signalling pathways-cAMP/ATP/PKA mediated acid secretion

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4
Q

NSAIDS cause ulcers because

A

COX2 is protective-loss of PG’s takes away a natural inhibitor of acid secretion-tips the balance in favor of more acid secretion with less ways to counteract it

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5
Q

gastric acid output in gastric ulcers

A

strangely-normal amount or reduced

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6
Q

gastric acid output for duodenal ulcers

A

high amounts of gastirc acid output–> esopecially at night

*this is the location of ulcers that dominates in the US

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7
Q

primary factors that cause GERD

A 
increased tRLES's
less saliva
altered mucosal resistance
delayed gastric emptying
esophageal dysrythmia?theres a few more but can only remember 4 right now
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8
Q

commonest cause of ulcers

A

H pylori

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9
Q

virulence factors for H pylori

A
  1. flagella
  2. adhesins
  3. CagA
  4. LPS
  5. UREASE-makes their local environment less acidic–they are trophic for mucosal neck cells within glands
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10
Q

Dx of H pylori

A

Blood antigen test ( well tell if currently or if ever been infected)
urea breath test-active infection

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11
Q

Ulcer disease DDX

A
  1. always consider H. pylori and everyone with it gets treated
  2. if negative for h pylori-consider NSAIDS
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12
Q

Gastroduodenal ulcer causes

A
  1. H pylori
  2. NSAIDS
  3. Gastrinoma
  4. Other
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13
Q

IN the US- H pylori-induced ulcer most likely to show up in

A

dudodenum-92% of duo-ulcers are due to H pylori

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14
Q

G cells present in

A

antrum

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15
Q

oxyntic cells present in

A

body of stomach

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16
Q

IN the US, in people who make a large amount of acid….H pylori usually infects what part of the stomach

A

the antrum–less acidic environment

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17
Q

if the stomach is making less acid…

A

H pyloris can infect the corporal (oxyntic) areas-> more likley to cause atrophy in this area

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18
Q

regimine for H pylori infection (not penicillin allergic)

A
  1. PPI + clarithromycin + amoxicillin
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19
Q

regimine for H pylori is penicillin allergic

A
  1. PPI + clarithromycin + metronidazole
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20
Q

quad regimin for H pylori

A

> PPI or H2RA + bismuth + metronidazole + tetracyline

*with no subs

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21
Q

if a patient fails initial therapy with clarithromycin involved either from compliance or from lack of efficacy

A

change the regimen-new one cannot include clarithromycin- the resident strain is considered to be resistant

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22
Q

theory behind antacid

A

weak bases + strong acids yield salt water and CO2

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23
Q

aluminum and calcium antacids cause

A

constipation

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24
Q

magnesium compounds cause

A

diarrhea

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25
Q

antacids effciacy

A

neutralize acid-short term effect–BUT DO NOT HEAL UNDERLYING CAUSE

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26
Q

antacids and pepsinogen

A

pepsinogen inactive at pH above 4–normal antacids are effective at inhibting pepsinogen activation
*h2ra’s are not-the inadequately rais pH

27
Q

dosing for antacids

A

1 hour and 3 hours after a meal and before bed

28
Q

do not take antacids with

A

other drugs-can effect their absroption/efficacy

*take 1-2 hours before other drugs

29
Q

the only immediate release PPI

A

IROMC-NAhc03

30
Q

H1 receptor involed in

A

urticaria and angiedema

31
Q

H2 receptor active in

A

pareital cells in the gut which cause secertion of H

32
Q

profile for H2RA’s

A

reduce both volume and H conecntratioon
good at inhibiting BASAL gastric acid secetion-so really only effective at night
*really only good at inhibiting food stimulated acid sec
*do not raise gastirc pH adequateley to inhibit the activation of pepsinogen
*outperformed vastly by PPI’s for PUD and H pylori-worse at mitigating and preventing ulcers
*all OTC with similar effectiveness and varied potency
*less convenient dosing and shorter half lives than PPI’s

33
Q

SIde effects generally rare and mild–> however, do not (cimetedine-tagamet) take with

A

theophylline
warfarin
phenytoin
*narrow therapeutic window

34
Q

the major CYP inhibitor H2AR

A

cimetidine-tagamet

35
Q

purifed enantiomers of PPI’s

A

esomeprazole-all R ismers or omperazole

dexanzoprole? L isomers of one of them i dont rememebr

36
Q

MOA for PPI’s

*remember-short half lives but the effect are seen long after drug is gone from plasma-thus they are amenaable to once daily dosing

A

ORAL PRODRUG taken up gradually in the neutral environment INTESTINES (most are entericaly coated and thus absorption is sporadic)–travel in the blood stream-> trophic for parietal cells-> cross the basolateral membrane-are protonated–>travel to apical/lumen border and are sulfated?–> then form a cystein-Sh bond with the H/K ATPase–>permanently inhibit–>cell must code for an entirely new pump

37
Q

PPI metabolized to a much less extent than others by CYP450

A

rabeprozole

38
Q

food and PPI’s

A

since PPI’s are trophic for pareital cells-> food intake causes Parietal cells to make more acid and icnreases the efficacy of the drug to inhibit the pump
>more acitve the pump is the better it takes up the drug
>this is an added benefit that the H2Ar’s do not have

39
Q

dosing of PPI’s

A

once daily-(can be twice but not FDA approved)
-take in morning on empty stomach
>eat 1 hour later

40
Q

end result of PPI’s

A

Achlorydia-ALL ALL ALL gastric acid secretion is blocked

41
Q

inidcations for PPI’s

A

ZE syndrome-short term

  • refractory ulcer
  • GERD
  • single daily dose safe and effective for over 2 years
42
Q

how does Bismuth (cytoprotective agent) work?

A

increases HCO3-secretion
inhibits pepsin (Antacids and PPI’s indirectly inhibit pepsin by preventing it from being activated due to an adequatley elevated gastric pH)
-inhbits h PYLORI?

43
Q

name the cytoprotective agents

A

bismuth
sucralfate
Misoprostol-PGE1

44
Q

Sucralfate MOA

A

forms sticky, viscous gel that adheres to gastric epithelial cells protecting them from acid and pepsin

45
Q

only agent in treatment of PUD that requirec an acidic pH for maximal activity

A

sucralfate

46
Q

when do you give sucralfate

A

one hor before bed to promot gastric healing

*remember this is when the stomach is at basal acid levels

47
Q

used in chronicaly bed ridden patients

example PPI or H2RA induced pneumonia

A

sucralfate-used acid envirnoment

-ther drugs which induce alkalinization allow bacteria to creeeeeeeeep in

48
Q

Misoprostol-PGE1 MOA

A

increases HCO3 production and mucus production

49
Q

side effect of misoprostol

A

DIarrhea in 40%-usually intolerable

50
Q

primarily used in tx of ulcers in pt.’s who MUST use NSAIDS

A

misoprostol

51
Q

if clarithromycin and azithromycin resistance is suspected add

A

furazolindone

52
Q

postural and dietary management of GERD

A 
decrease gastic size (smaller meal)
weight loss
bed elevation
low fat diet-to increase gastric emptying
avoid coffee, mints-these relax LES
53
Q

H2AR’s only indicated in

A

mild-infrequent GERD

54
Q

2 classes to treat gerd

A

Prokinetics

Antisecretory drugs

55
Q

prokinetic drugs aim to

A

improve LES tone and competence
enhance esophageal clearance
hasten gastric emptying

56
Q

Prokinetics

A

Metoclopramide-Reglan
Domperidone
Cisapride-not available in US–then why did you fucking put it on here doosher

57
Q

dopaminergic signalling..

A

inhibits contraction of gastric smooth muscle

-domperidone and metoclopramide aim to inhibit dopaminergic signalling-thus are prokinetic

58
Q

Metocloprimide MOA

A

Dopa (D3R) antagonist-SM agonist
Seritonin (5HT4R) agonist-increases SM contraction-prokinetic
Seritonin (5HT3R) antagonist-inhibits the inhibition-prokinetic

59
Q

cisapride moa

A

pure 5HT4R agonist-prokinetic

60
Q

main side effect of Dromperidone and MAINLY METOCLOPRIMIDE

A

Tardive Dyskinesia-(from the dopa antagonism)

61
Q

never give metocloprimide for longer than

A

1-2 weeks

62
Q

do all GERD patients make excess acid

*we give them to decrease acid for relief of symptoms and to allow healing

A

no=only 16%
*h pylori patients make a shit ton of acid though because when the bug infect the cells in the antrum=it causes distrbances and they make a lot of gastrin–gastrin has tropic effects on parietal cells-thus H pylori patients have increased number of parietal cells on average

63
Q

effects of PPI’s and H2AR on esophageal peristalsin, LES tone, gastric emptying

A

NONE

Gastrointestinal (9 decks)

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