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GI II Exam I AP > Drugs- Treatment of GERD and PUD (Kinder) > Flashcards

Drugs- Treatment of GERD and PUD (Kinder) Flashcards

1
Q

what 3 things regulate acid secretion from parietal cells

A

i) Neuronal (acetylcholine, ACh), paracrine (histamine), and endocrine (gastrin) factors regulate acid secretion through receptor binding on parietal cells.

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2
Q

Somatostatin

A

produced by antral D cells inhibits gastric acid secretion.

(1) When gastric pH falls below 3, this stimulates SST release which suppresses gastrin in a negative-feedback loop.

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3
Q

what is the role of Prostaglandins and how are they affected by NSAID’s

A

(1) Prostaglandins E2 and I2 inhibit the proton pump by reducing cAMP production (EP3 receptors are GPCRs coupled to Gi on parietal cells).
(2) PGE2 and PGI2 also stimulate production of protective factors (mucus, bicarbonate) by superficial epithelial cells and enhance mucosal blood flow.
(3) Non-steroidal anti-inflammatory drugs (NSAIDs) block PG production resulting in more acid secretion, less mucus and bicarbonate production, and diminished blood flow. Thus, NSAIDs are ulcerogenic and should be avoided or dose reduced in ulcer patients.

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4
Q

what are the causes of GERD

A

transient lower esophageal sphincter relaxation, reduced lower esophageal sphincter tone, delayed gastric emptying, or hormonal changes due to pregnancy.

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5
Q

how do you treat mild intermittnet symtpoms of GERD

A

antacid or H2RA as needed

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6
Q

NERD treatment

A

antacid or H2RA (PPI may be required in more severe symptoms)

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7
Q

Erosive esophagitis treatment

A

PPI for 8 weeks

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8
Q

what are the symptoms of Peptic ulcer disease

A

iii) Symptoms:
burning epigastric pain,
pain occurring after meals or on an empty stomach,
nocturnal pain relieved by food intake (less common symptoms: indigestion, vomiting, heartburn).

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9
Q

what are the alarming symptoms of GERD

A

i) Alarm symptoms: bleeding, anemia, early satiety, unexplained weight loss, progressive dysphagia, recurrent vomiting, family history of GI cancer, previous esophagogastric malignancy.

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10
Q

treatment of duodenal ulcer

A

H2RA or PPI for 4 weeks

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11
Q

gastric ulcer treatment

A

PPI for 8 weeks

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12
Q

what are the 3 agents that reduce gastric acidity

A

PPI’s

H2RA

antacids

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13
Q

what are the agents that promote mucosal defense

A

bismuth compounds

misoprostol

sucralfate

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14
Q

“prazole”

A

Proton pump inhibitors

a) Dexlansoprazole, esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole

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15
Q

MOA of PPI’s

A

: inactive pro-drugs, lipophilic weak bases diffuse readily across lipid membranes into acidified compartments (parietal cell canaliculus) from the alkaline intestinal lumen. Rapidly becomes protonated and undergoes conversion to active form which forms a covalent disulfide bond with H+/K+-ATPase, irreversibly inactivating the enzyme.

inhibits both fasting and meal stimulated acid secretion.

i) Blocks final common pathway of acid secretion – the proton pump
ii) Inhibits 90-98% of 24 hour acid secretion in standard doses

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16
Q

why are PPI’s ideal drugs from PK perspective

A

c) PK: ideal drugs from a PK perspective as they have short serum half-lives, concentrated and activated near site of action, and have a long duration of action.

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17
Q

food impact on PPI’s

A

ii) Bioavailability – decreased ~50% by food, administer on an empty stomach at least 30 minutes before a meal (breakfast).

PPIs only inhibit actively secreting proton pumps so should preferably be given 1 hour before a meal so peak concentration coincides with max activity of proton pump.

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18
Q

when should you dose adjust PPI’s

A

hepatic insufficiency

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19
Q

what is the therapeutic use of PPI’s

A

GERD

PUD

H. pylori infection

NSAId ulcers

stress related mucosal injury

prevention of re-bleeding

Zollinger-ellison syndrome

OTC’s- for heartburn

20
Q

what are the adverse drug reactions of PPI’s

A

i) 1-5% (only slightly increased over placebo): diarrhea, headache, abdominal pain
ii) Increased risk (2-3x) of hospital- and community-acquired Clostridium difficile
iii) Decreased vitamin B12 absorption (potentially leads to subnormal levels with prolonged therapy), modest increased risk of hip fracture, increased risk of nosocomial pneumonia, small increased risk of enteric infections.

21
Q

what are the drug drug interactions of PPI’s

A

i) Decreased gastric acidity may alter drug absorption (ketoconazole, itraconazole, digoxin, atazanavir)
ii) All PPIs metabolized via CYP P450 enzymes (including 2C19 and 3A4) but clinically significant drug interactions are rare due to short half-lives of the PPIs.

22
Q

what does omeprazole interact with

A

(1) Omeprazole may inhibit metabolism of warfarin, diazepam, phenytoin, and others

23
Q

PPI’s and clopidogrel

A

(a) Clopidogrel is a pro-drug which requires activation by CYP2C19. PPIs (especially omeprazole, esomeprazole, lansoprazole, and dexlansoprazole) could reduce clopidogrel activation thus reducing anti-platelet activity. If co-administration is required, pantoprazole or rabeprazole preferred.

24
Q

H2RA’s (“tidine”)

MOA

A

inhibition at parietal H2 receptors (highly selective) does not affect H1 or H3

blocks histamine released from ECL cells by gastrin or vagal stimulation

25
Q

in what pt’s do you adjust dosing of H2RA’s

A

renal insufficiency and hepatic insufficiency

26
Q

therapeutic uses of H2RA”s

A

especially effective at inhibiting nocturnal acid secretion

control of nocturnal acid secretion is the most important determinant of duodenal ulcer healing thus evening dosing is typical

GERD
PUD
NSAID ulcers (only if the offending NSAID is discontinued, otherwise use PPI)
Stress mucosal injury

27
Q

ADR’s of H2RA’s

A

Diarrhea, headache, fatigue, myalgia (< 3%)

Mental status changes (ICU patients, elderly, renal or hepatic impairment), thrombocytopenia

Nosocomial pneumonia, rare blood dyscrasias, bradycardia/hypotension (rapid IV infusion) so give over longer period of time

28
Q

what are the DDI’s of H2RA’s

A

inteferes with CYP1A2, 2C9, 2D6, 3A4 (Cimetidine&raquo_space;»ranitidine)

drugs with narrow TI (theophylline, warfarin, phenytoin, lidocaine) may result in adverse effects –> increased levels of these drugs

29
Q

what are the antacids used

and MOA

A

sodium bicarb–> CO2 and NaCl
calcium carbonate
magnesium hydroxide/aluminnum hydroxide

MOA:
react with hydrochloric acid to form a salt and water

30
Q

sodium bicarb

creates what when combined with HCL?
what pt’s do you NOT use these in

A

NaCl and CO2
CO2 (distension and belching)
Alkali absorption (metabolic alkalosis)
NaCl absorption (fluid retention)

Caution:
heart failure, HTN, renal insufficiency

31
Q

Calcium carbonate forms what

A

CO and CaCL2

belching
metabolic alkalosis

can lead to hypercalcemia when taken with dairy products

should not take long term for risk of metabolic alkalosis and renal insufficiency

32
Q

what does mag hydroxide form

A

MgCl2 or AlCl3 and H2O

can cause osmotic diarrhea b/c of Mg salts

can cause constipation b/c of Al3+ salts

33
Q

if a pt has a stress ulcer, and has no nasoenteric tube present or has significant ileus what treatment will you use

A

H2RA’s

34
Q

bismuth subsalicylate and bismuth subcitrate potassium

MOA:

A

exact mechanism unknown
Bismuth coats ulcers and erosions; stimulates intestinal prostaglandin, mucus, and bicarbonate secretion
Salicylate (like ASA) inhibits intestinal prostaglandin and chloride secretion- useful in diarrhea

35
Q

what is the therapeutic use of bismuth compounds

A

dyspepsia and acute diarrhea

traveler’s diarrhea

h. pylori

36
Q

ADR’s of bismuth compounds

A

harmless blackening of stool and tongue

salicylate toxicity (high doses)

don’t use in pt’s with influenza, or chickenpox due to risk of Reye’s

avoid in renal impairment

37
Q

misoprostel

A

prostaglandin analog

methyl analog of PGE1
Stimulates mucus and bicarbonate secretion (mucosal protective)
Binds receptors on parietal cell reducing histamine stimulated cAMP production (modest acid inhibition)

does not require dose adjustment in renal failure

38
Q

what are the ADR’s of prostaglandin analogs

A

Diarrhea and cramping abdominal pain (10-20%)

Stimulates uterine contractions (contraindicated in pregnancy)

39
Q

therapeutic use of prostaglandin analogs

A

NSAID induced ulcers

not often used b/c not well tolerated

40
Q

sucralfate

A

mucosal protective agent

Sucrose complexed to sulfated aluminum hydroxide
MOA: exact mechanism unknown
(-)charged sucrose binds (+)charged proteins at base of erosions, forms physical barrier

41
Q

what are the ADR’s of sucralafate

DDI’s?

A

Not absorbed = no side effects
Constipation (2%)

Binds/impairs absorption of other drugs
Separate administration by hours

42
Q

what is the therapeutic use of Sucralafate

A

Stress-related mucosal injury

43
Q

when do you test for H. pylori

A

active PUD

past history of PUD

MALT lymphoma

test and treat strategy for pt’s with uninvestigated dyspepsia –> <55 yrs old,

44
Q

what is the combination therapy treatment for H.pylori

A

PPI + 2-3 antibiotics

Antibiotics
amoxicillin, clarithromycin
metronidazole, tetracyclines

45
Q

what is the recommended initial therapy for pt’s hwo have not received clarithromycin

A

14 day triple therapy

PPI
clarithromycin
amxoicillin or metronidazole

46
Q

14 day quadruple therapy

A

used in pt’s previously treated with macrolide antibiotic or in areas with high rate of clarithromycin or metronidazole resistance

PPI or H2RA
Metronidazole
Tetracycline or doxy
bismuth subsalicylate

GI II Exam I AP (8 decks)

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