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Pharmacology > GI: PUD, GERD > Flashcards

GI: PUD, GERD Flashcards

1
Q

what dz are we talking about for “acid-peptic dz”

A

GERD
Gastric/duodenal ulcers
non-ulcer dyspepsia
stress related gastritis

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2
Q

causes of PUD

A
  1. infection w/ gram- HP **
  2. use of NSAIDs **
  3. increase HCL secretion
  4. inadequate mucosal defense against gastric acid
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3
Q

list the tx approaches for PUD

A
  1. eradicate HP (ABX)
  2. reduce secretion of gastric acid (PPIs, H2 recp)
  3. Provide agents that protect gastric mucosa from damage (prostaglandins, antimuscarinics, antacids, mucosal protective agents)
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4
Q

pneumonic for tx PUD

A

Acid.. decrease it
Protect…gastric mucosa
Eradicate HP if tests +

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5
Q

6 agents used for PUD

A 
H2 rec antags 
PPI 
Antacids 
Prostaglandins 
Mucosal protectors 
anti-microbials
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6
Q

List the H2 receptor antagonists

*ending?

A

-tidine

Cimetidine
Famotidine
nizatidine
ranitidine

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7
Q

what stimulates gastric acid secretion? (3)

A

ACH
histamine
Gastrin

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8
Q

MOA for H2 blockers

A
  1. competitively block binding of histamine to the H2 receptor (NOT H1****)–>reduces H+ being secreted into stomach
  2. inhibit basal, food stimulated and nocturnal secretion of gastric acid
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9
Q

explain what happens after ACH histamine and gastrin bind to stomach receptors

A
  1. stimulation of H+/K+-ATP proton pump–>secretes H+ in exchange for K+–>goes into the stomach lumen
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10
Q

Percent that H2’s reduce gastric acid

A

70%

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11
Q

direct and indirect pathways for H2 rec antags

A

DIRECT: ACH, gastrin and histamine stimulate parietal cell–trigger release of H+ into stomach lumen

INDIRECT: ACH and gastrin also stimulate enterochromaffin-like cells (ECL)–>result in secretion of histamine–>then histmaine also acts on parietal cell

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12
Q

indications for H2 receptor antags

A

PUD (w/o HP)
stress ulcers
GERD

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13
Q

Pharmkinetics for H2 receptor antags

  • abs
  • excretion
  • T1/2
  • peak time
A

well absorbed
peaks in 1-3 hours
short half life
excreted by kidneys

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14
Q

time of day to take H2 antags

A

at night or in fasting state

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15
Q

NSAID induced ulcers–PPI or H2 blockers work best? why

A

PPI

*helps heal and prevent future ulcers better than H2

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16
Q

high or low tolerance for H2 recep blockers

A

High **

so it is common for s/s to return after a few days of tx

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17
Q

Cimetidine:

-drug to drug rxns high or low? and why

A

HIGH since it is CYP450 isoenzyme inhibitor

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18
Q

what drugs interact heavily with Cimetidine (10)

A

INCREASES levels of:

  • warfarin
  • TCAs
  • Lidocaine
  • CCBs
  • quinidine
  • oral sulfonylureas
  • phenytoin
  • theophylline
  • benzos
  • BBs (metroprolol and prorp)
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19
Q

Famotidine routes of admin

A

IV or PO

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20
Q

which H2 blocker was removed by FDA in 2020 and why

A

Ranitidine
*low levels of nitrosamine impurity was found

Nizatadine also removed by FDA

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21
Q

H2 rec antags and ketoconazole

WHY?

A

Concomittant use can reduce effectiveness of ketoconazole

*for ketoconazole to work— it needs to be in an acidic envi and H2 blockers reduce the acidic envir

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22
Q

Absorption of H2 rec blockers is reduced or increased by __% when given with ____?

A

REDUCED
10-20%
Antacids

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23
Q

do H2 blockers go into Breast milk?

A

yes

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24
Q

do H2 blockers cross placenta?

A

yes

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25
Q

SE of Cimetidine

A

endocrine SE due to its antiandrogen effects:

  • gynecomastia
  • impotence
  • Galactorrhea

CNS:
-confusion, AMS (usually with older or after IV admin) MORE so than Famotidine

inhibits CYP450 so it interfers with a lot of drugs***

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26
Q

which H2 rec blocker is assoc with causing the most SE?

A

Cimetidine

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27
Q

how long does it take for tolerance to develop with cimetidine?

A

days

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28
Q

PPIs list of drugs

*ending?

A

-prazole **

Esomeprazole 
Iansoprazole 
Omeprazole 
Dexlansoprazole 
Pantoprazole 
Rabeprazole
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29
Q

what class of drugs is Aripiprazole and Brexpiprazole

A

Antipsychotics and NOT PPIs**

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30
Q

MOA for PPIs

A

bind to H+/K+ ATPase proton pump and suppress H+ secretion into the gastric lumen

  • *Irreversible**
  • *membrane bound proton pump is the final step in acid secretion**
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31
Q

PPIs affect on basal and stimulated acid secretion

A

Stops BOTH !

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32
Q

explain chemical composiiton of the PPIs

A
  • prodrugs

* have enteric coating that is acid-resistant so they are not degraded in the gastric acid

33
Q

when is the enteric coating of the PPIs degraded? aka where are they absorbed

A

in the duodenum aka an alkaline environment

*absorbed and transported to the parietal cell

34
Q

what do the active forms of PPI bind to after being asborbed?

A

bind to the H+/K+ ATPase enzyme IRREVERSIBLY–stops the acid production for about 18 hours until new enzyme is resynthesized

35
Q

how long does the effects of PPI generally last for?

A

18 hours—then new ATPase enzyme is synthesized

36
Q

indications for PPIs (6)

A
  • GERD
  • erosive esophagitis
  • active duodenal ulcer
  • pathologic hypersecretory conditions (Zollinger-Ellison)
  • prophylaxsis use to prevent NSAID induced ulcers and stress induced ulcers
  • reduce risk of bleeding from ulcers caused by ASA
  • combined with ABXs for tx of HP
37
Q

*duration of action and first time dosing effects for PPI

A

limited effect with the first dose BUT bc of irreversible binding, they have a PROLONGED effect over time

38
Q

best to give PPIs with full or empty stomach

A

fasting state

39
Q

most effective route of admin for PPIs

A

PO

40
Q

when to administer PPI

A

30 to 60 mis before breakfast or largest meal of the day

41
Q

why do PPIs have a long duration of action?

A

beause of the COVALENT irreversible binding to the H+/K+ ATPase enzyme

42
Q

Metabolism for PPIs

*drug-drug interactions: which ones?

A

P450 enzyme

  • Clopidogrel effectiveness decrease if administerd with Omeprazole and Esomeprazole
  • warfarin, diazepma, phenytoin
  • methotrexate toxicity*
43
Q

increase in _____ with >1 year of use of PPIs

A

fractures

44
Q

SE of PPIs (9)

A
  • increase risk of fx (bc of Ca2+ absoprtion issues)
  • B12 deficiency
  • increase risk of C. Diff and enteric infections
  • diarrhea
  • affects Ca2+ and B12 and magnesium absorption
  • hypomagnesia
  • incr risk of pneumonia
  • HA
  • nausea
45
Q

Esomeprazole has a plasma half-life of a few hours yet suppresses acid secretion for 24 to 48 hours. The reason for this paradox is____?

A

acid suppression continues unitl new H+/K+ ATPase molecules are synthesized

46
Q

antacids

*describe chemical composition

A

weak bases

47
Q

what happens when antacids react with gastric acid

A

form water and salt–>diminishes gastric acidity

48
Q

list the antacids

A

Aluminum hydroxide
Mag hydroxide
Ca Carbonate (tums)
Mag Trisilicate

49
Q

at what ph is pepsin deactivated

A

pH > 4

50
Q

what is pepsin

A

proteolytic enzyme

51
Q

MOA of antacids

A

They are weak bases**

  • react with gastric acid to form salt and water
  • since they raise pH, they also inactivate pepsin
52
Q

take antacids on full or empty stomach

A

FULL aka take antacids AFTER meal

  • delayed gastric emptying with a full stomach
  • so allows more time for the antacids to work–>prolong the duration of action
53
Q

why is sodium bicarbonate not recommended as an antacid?

A

because it produces transient metabolic alkalosis–>producing a high sodium load

54
Q

therapeutic uses for antacids

*what are they not used for?

A
  • symptomatic relief of PUD (but not to treat PUD)
  • heartburn
  • GERD

NOT USED: tx of PUD

55
Q

SE of aluminum hydroxide

A

constipation

56
Q

SE of magneisum hydroxide

A

diarrhea

57
Q

which antacid causes:

  1. diarrhea
  2. constipation
A
  1. mag hydroxide

2. aluminum hydroxide

58
Q

which antacids are combined in OTC preparations and WHY

A

Aluminum and mag hydroxide beause their SE of costipation and diarrhea cancel eachother out

59
Q

antacids + renal impaired patients can lead to?

A

accumulation of Mg, Al, Ca (cations)

–>milk Alkali Syndrome

60
Q

lab findings for milk alkali syndrome

A

hypercalcemia
alkalosis
renal injury

61
Q

Prostaglandin-E

  • where/what produces it
  • function?
A

prod: by gastric mucosa

Funct: inhibits secretion of acid and stimulates secretion of mucus and bicarb

***cytoprotective effect

62
Q

deficiency of prostaglandin can lead to___

A

Peptic ulcers

63
Q

list the prostaglandin drugs

A

Misoprostol

64
Q

Misoprostol

  • drug class
  • MOA
  • indications and contras
  • SE
A

Class: Prostaglandin E1 analog

MOA: inhibits secretion of gastric acid and stimulates secretion of bicarb and mucous

Indications: prevention of NSAID induced gastric ulcers
*good for prophylactic use

Contra: pregnancy bc it can stim contractions and cause miscarriages

SE:

  • MC= diarrhea (dose-related)
  • cramping
  • abdominal pain
65
Q 
which drug class is preferred for prevention of NSAID induced ulcers 
Prostaglandin analogs or PPIs?
A

PPIs

66
Q

what drug classes are known to be cytoprotective ?

A
  1. prostaglandin analogs

2. mucosal protective agents

67
Q

define cytoprotective

A

agents stimulate mucus production and enhance blood flow throughout the lining of the gastrointestinal tract. These agents also work by forming a coating that protects the ulcerated tissue

68
Q

Sucralfate

  • drug class
  • Drug composition
  • MOA
  • indications and not used for?
  • contraindications
  • drug-drug rxns?
  • SEs
A
  • Class: Mucosal Protective Agents
  • Drug Composition: Aluminum Hydroxide + Sulfated Sucrose
  • MOA:
    1. Binds to ions in normal + damaged mucosa–>creating a physical barrier (gel like substance)
    2. Protects ulcer from pepsin and acid– allowing ulcer to heal
    3. DOES NOT affect gastric acid or pepsin secretion
  • indications:
    1. GERD in pregnancy
  1. NOT USED IN: PUD due to PPIs being superior

Contras: none

  • requires acidic environment for activation DO NOT use with PPIs, H2 antags or antacids
  • can bind to other drugs and interfere with their absoprtions

SE: very well tollerated

69
Q

MOA for the class of drugs: Mucosal Protective Agents

A

*MOA: cytoprotective: enhance mucosal protection mechanisms, prevent mucosal injury, reduce inflammation, and heal existing ulcers

70
Q

List the mucosal protective agents

A

Bismuth Subsalicylate and Bismuth Subcitrate

Sucralfate

71
Q

Bismuth Subsalicylate and Bismuth Subcitrate

  • Drug class
  • MOA
  • indication
  • SEs
A

Drug class: Mucosal protective Agent

MOA:

  1. supresses HP via its antimicrobial actions
  2. inhibits pepsin
  3. may increase mucus secretion–to promote ulcer healing via interacting with glycoproteins in necrotic tissue and coats/protects ulcer
  4. No effects on inhibiting or neutralizing acid

Indications:
*part of quad tx for HP eradication

SE:

  • black stool
  • can raise levels of salicylates–>possible toxicity
72
Q

which is superior for GERD and PUD: PPIs or H2

A

PPIs

73
Q

PPIs are superior to H2 rec antags for tx of?

A

acid suppresion in PTs with GERD and PUD

74
Q

which drug class can patient’s develop a tolerance for?

A

H2 rec antagonists

*why their use is limited

75
Q

HP is effectively eradicated via?

A

COMBO of
1. acid-suppressing drugs
2. multiple ABX
10-14 days

76
Q

which patients need ABX?

A

HP infections and PTs with PUD (both duodenal and gastric)

77
Q

List the drugs in the two regimens for tx of PUD with +HP infection
*percent eradication for each

A

FIRST LINE: QUAD THERAPY 91%: bismuth subsalicylate + metronidazole + tetracycline + PPI x14 days

OR

TRIPLE THERAPY 80%: Clarithromycin + amoxicillin (or metronidazole if PCN allg) + PPI X14 days

78
Q

if someone if allergic to Penicllin, which ABX can you give instead
*replace _____ with____?

A

replace amoxicillin for metronidazole in triple therapy

Pharmacology (28 decks)

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