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Gastroenterology Flashcards

1
Q

________ in saliva helps neutralize the acid in gastric reflux

A

bicarbonate

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2
Q

LES maintains tonic (sustained) contraction and relaxes through ___________ to allow the passage of food into the stomach

A

parasympathetic, vagal stimuli

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3
Q

The LES is a smooth muscle. What drugs could inhibit (or antagonize) the tonic contraction of this muscle?

A

Dihydropyridine CCBs

can cause relaxation of LES –> reflux of food

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4
Q

What do parietal cells do?

A

secreted HCl, which:

1) helps prevent microbial foodborne illnesses
2) activates certain enzymes
3) secretes IF –> allows body to absorb Vit B12

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5
Q

Antacids MOA

A

acid buffer, luminal side

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6
Q

Antacids pharmcokinetics

A

1) onset: immediate (< 5 min)
2) DOA: short (20-30 min) - limited to activity only while w/in stomach

**food can prolong DOA, potentially up to 3-hr

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7
Q

Which antacid is preferred?

A

they are generally interchangeable when doses appropriately

*just because a majority of OTC contain Calcium carbonates, does not make it a superior agent

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8
Q

What age group are OTC antacids indicated for?

A

> /= 12 y/o

calcium is approved for infants

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9
Q

What is/are the calcium carbonate antacid(s)?

A

Tums
Maalox (tabs)
Alka-Mints

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10
Q

What is/are the magnesium hydroxide antacid(s)?

A

Milk of Magnesia

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11
Q

What is/are the sodium bicarbonate antacid(s)?

A

Alka-Seltzer

original formula also contained 325mg aspirin

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12
Q

What is/are the bismuth subsalicylate antacid(s)?

A

Pepto-Bismol

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13
Q

What is/are the mixed antacid(s)?

A

Rolaids
Maalox (liquid)
Gaviscon
Mylanta

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14
Q

caution should be used when using antacids with medications that ______

A

can chelate

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15
Q

Calcium carbonate ADRs

A
  • Ca++ may cause constipation/flatulence

- about 10% of Ca++ is absorbed into blood

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16
Q

Magnesium hydroxide ADRs

A
  • Mg++ may cause diarrhea

- about 20% is absorbed into blood

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17
Q

Sodium bicarbonate ADRs

A
  • forms NaCl

- may not be great for pt. on sodium-restrictive diets

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18
Q

Bismuth subsalicylate ADRs

A
  • dark stools (an unnecessary pt. panic)
  • tongue discoloration
  • hearing loss
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19
Q

Aluminum hydroxide ADRs

A

some Al is absorbed and can accumulate –> altered mental statues (esp. in CKD)

**generally avoided

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20
Q

Natural product interactions of antacids

A

Lilly of the Valley and Strophanthus

*Both have major interactions w/ Ca++ and moderate interactions with aluminum hydroxide and bismuth subsalicylate

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21
Q

Which antacid can cause constipation?

A

calcium carbonate (Tums, Maalox tabs, Alka-Mints)

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22
Q

Which antacid can cause diarrhea?

A

magnesium hydroxide (milk of magnesia)

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23
Q

Histamine_2 Receptor Antagonists (H2RA) MOA

A

selective, competitive blockage of type 2 histamine receptors on basolateral side of parietal cells –> prevents stimulation of proton pump w/out blocking it directly

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24
Q

Histamine_2 Receptor Antagonists (H2RA) pharmacokinetics

A

1) onset: 30-45 min

2) DOA: 4-10 hr

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25
Q

Which Histamine_2 Receptor Antagonists (H2RA) is preferred?

A

products are considered interchangeable

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26
Q

What are the main Histamine_2 Receptor Antagonists (H2RA) drugs?

A

Famotidine (Pepcid)
Ranitidine (Zantac)
Cimetidine (Tagamet HB)
Nizatidine (Axid AR)

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27
Q

How long should pt. take antacids for?

A

= 2 wks OTC

therapy can be indefinite

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28
Q

How long should pt. take Histamine_2 Receptor Antagonists (H2RA) for?

A

< 2x/day for = 2 wks OTC

therapy can be indefinite under supervision

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29
Q

Histamine_2 Receptor Antagonists (H2RA) ADRs

A
  • anti-androgenic (reversible gynecomastia, rarely impotence w/ cimetidine)
  • arrhythmias (IV)
  • HA
  • dizziness
  • GI disturbance
  • tachyphylaxis (taking for more than a couple days can lead to tolerance and reduced effectiveness…should only taken prn)
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30
Q

Which Histamine_2 Receptor Antagonists (H2RA) is rarely used b/c it has lots of s/e and many drug interactions?

A

Cimetidine

**it is a CYP450 inhibitor

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31
Q

Histamine_2 Receptor Antagonists (H2RA) natural product interactions

A
  • Caffeine (cimetidine)
  • Hypericum (ranitidine and cimetidine
  • many other moderate interactions
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32
Q

Dose of Histamine_2 Receptor Antagonists (H2RA) needs to be reduced in people with _________

A

renal disease

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33
Q

Proton Pump Inhibitors (PPI) MOA

A

selective, irreversible H/K/ATPase inhibition on luminal side of parietal cells

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34
Q

Proton Pump Inhibitors (PPI) pharmacokinetics

A

1) onset: 2-3 hr
2) DOA: 24 hr**
3) T1/2: 1 hr (except tenatoprazole is 8-9hr)
4) acid-labile medication so 50% decrease in bioavailability if taken with food (recommended to take qd 30 min before breakfast)
5) Takes up to 1-4 days for full effect of drug when initiating tx
6) Drugs become MORE bioavailable and absorption INCR. with repeat dosing
7) Metabolism: CYP2C19 and CYP3A4 (hepatic impairment and old age decr. clearance)

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35
Q

Proton Pump Inhibitors (PPI) drugs

A 
Omeprazole (Prilosec)
Esomeprazole (Nexium)
Lansoprazole (Prevacid) 
Pantoprazole (Protonix) 
Rabeprazole (Aciphex)
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36
Q

How long should a patient take PPIs for?

A

< 1x/day for = 2 wks OTC

therapy can be indefinite and up to bid under supervision

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37
Q

Which PPI can be taken with food?

A

Dexlansoprazole

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38
Q

How long does it take for secretory activity to return after stopping PPIs?

A

3-5 days

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39
Q

Proton Pump Inhibitors (PPI) ADRs

A
  • Mg++ depletion (monitor levels)
  • osteoporosis (dietary Ca++ absorption requires acidic environment)
  • Clostridium difficile infx
  • community acquired pneumonia
  • HA
  • dizziness
  • GI disturbance
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40
Q

Proton Pump Inhibitors (PPI) natural product interactions

A
  • Grapefruit
  • Hypericum

many other moderate interactions

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41
Q

Are PPIs or H2RAs better at immediate sx relief?

A

H2RAs

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42
Q

Which site of action do PPIs and H2RAs have in common?

A

Parietal cells

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43
Q

Lactose intolerance is very common in

A

Black (90%) and Asian (75%) populations

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44
Q

Lactose is a disaccharide composed of

A

glucose + galactose

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45
Q

Do probiotics help with lactose intolerance?

A

questionable

May improve bloating w/ lactase deficiency

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46
Q

Simethicone (Gas-X, Mylicon Infant’s drops) MOA

A

inert silicone polymer, “de-foaming” agent –> reduces surface tension of gas bubbles –> relieves gas

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47
Q

Simethicone pharmacokinetics

A

1) Not absorbed

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48
Q

Simethicone drug interactions

A

can bind to thyroid products (e.g. levothyroxine) and decr. absorption of thyroid med

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49
Q

Activated charcoal MOA

A

highly absorptive charcoal; possible adsorbent effects –> gas relief

**this product is charcoal plus w/ simethicone)

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50
Q

Activated charcoal pharmacokinetics

A

1) not absorbed

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51
Q

Activated charcoal drug interactions

A

may significantly impact absorption of medications

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52
Q

Alpha-Galactoside (Beano, Gaz away) MOA

A

mold-derived enzyme, cleaves oligosaccharides before reaching colonic bacteria

recommended for gas prevention with high-fiber diets

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53
Q

Alpha-Galactoside (Beano, Gaz away) cautions

A

avoid with DM and galactosemia

No known drug interactions

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54
Q

Pt. with flatulence would like OTC to relieve gas sx. Pt. has DM and would like to avoid a product that could interfere w/ absorption of medications. He has not food restrictions/intolerances. What drug should he try?

A

Simethicone

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55
Q

What is the recommended supplementation for lactose intolerance?

A

Lactaid (lactase enzyme)

**take at FIRST bite of lactose containing food

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56
Q

___________ laxatives are preferred if there is any concern for intestinal obstruction or if rapid onset is required

A

rectally administered

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57
Q

Senna (Senokot, Ex-Lax) classification

A

stimulant laxative

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58
Q

Senna (Senokot, Ex-Lax) MOA

A

anthraquinone –> direct action on intestinal mucosa or nerve plexus –> stimulates peristaltic activity

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59
Q

Senna (Senokot, Ex-Lax) pharmacokinetics

A

1) Onset: 6-24 hr

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60
Q

How long should pt. use Senna (Senokot, Ex-Lax) for?

A

less than 1 wk OTC

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61
Q

Senna (Senokot, Ex-Lax) ADRs

A

cramps, N/V, diarrhea, melanosis coli

**AVOID with actual/possible bowel obstruction

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62
Q

Senna (Senokot, Ex-Lax) natural products interactions

A
  • Jalap (electrolyte/fluid depletion)

- Oleander (incr. risk of cardiac glycoside toxicity d/t K+ depletion

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63
Q

Bisacodyl (Dulcolax) class

A

Stimulant laxative

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64
Q

Bisacodyl (Dulcolax) MOA

A

directly irritates sm. mm. in intestine –> stimulates peristalsis

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65
Q

Bisacodyl (Dulcolax) pharmacokinetics

A

1) onset: 6-12 hr (oral); < 60 min suppository; < 20 min enema
2) minimal absorption (< 5%)

66
Q

Bisacodyl (Dulcolax) ADRs

A

cramps, diarrhea, N/V, electrolyte disturbances, local irritation

**AVOID with actual/possible bowel obstruction

67
Q

Bisacodyl (Dulcolax) natural product interactions

A
  • Jalap (electrolyte/fluid depletion)

- Oleander (incr. risk of cardiac glycoside toxicity d/t K+ depletion

68
Q

Polyethylene Glycol 3350 Electrolyte Sol’n (Miralax) class

A

osmotic (electrolyte) laxative

69
Q

Polyethylene Glycol 3350 Electrolyte Sol’n (Miralax) MOA

A

osmotic water retention in stool and incr. stool frequency

**AVOID w/ actual/possible bowel obstruction

70
Q

Polyethylene Glycol 3350 Electrolyte Sol’n (Miralax) pharmacokinetics

A

1) onset = 24-96 hr

2) minimal absorption

71
Q

How long should a pt. use Bisacodyl (Dulcolax)?

A

< 1 week OTC

72
Q

How long should a pt. use Polyethylene Glycol 3350 Electrolyte Sol’n (Miralax)?

A

< 1 week OTC

73
Q

Polyethylene Glycol 3350 Electrolyte Sol’n (Miralax) ADRs

A

cramps, diarrhea, urticaria

74
Q

Magnesium Citrate class

A

osmotic (electrolyte) laxatives

75
Q

Magnesium Citrate MOA

A

osmotic retention of fluid in bowel

**AVOID with actual/potential bowel obstruction

76
Q

Magnesium Citrate pharmacokinetics

A

1) onset = 30-60min

2) up to 30% absorbed

77
Q

How long should pt. take Magnesium Citrate?

A

< 1 wk OTC

78
Q

Magnesium Citrate ADRs

A

cramps, diarrhea, flatulence

magnesium toxicity early signs = hypotn, N/V, facial flushing, retention or urin, ileus, depression, lethargy

magnesium toxicity later signs = mm. weaknes, difficulty breathing, extreme hypotn, irregular heartbeat, cardiac arrest

**risk of magnesium toxicity incr. w/ renal failure

79
Q

Magnesium Citrate natural product interactions

A

magnesium chelation and various moderate interactions

overall, osmotic lax are less likely to cz electrolyte abnormalities than stimulant lax

80
Q

Docusate (Colace) class

A

bowel softener

81
Q

Docusate (Colace) MOA

A

dioctyl dosium sulfosuccinate reduces surface tension of oil-water interface of the stool –> enhances incorporation of water and fat into stool

may also stimulate the secretion of water and electrolytes on contact w/ the mucosa

82
Q

Docusate (Colace) pharmacokinetics

A

1) onset: 12-72 hr (oral); 2-15 min (rectal)

2) absorbed and excreted into bile

83
Q

Docusate (Colace) ADRs

A

throat irritation (liquid formulation)

84
Q

Docusate (Colace) natural product interactions

A

many moderate, may incr. absorption of various oral agents, including mineral oil (avoid combination)

theoretical concern that docusate salts can emulsify mineral oil, leading to systemic absorption and toxicity

85
Q

A patient already taking senna could add which other agent(s) (with a different mechanism) for help with persistent constipation?

A

Docusate (Colace) - stool softener

mush and push

86
Q

Psyllium (Metamucil) class

A

Bulk laxative

87
Q

Psyllium (Metamucil) MOA

A

soluble fiber, absorbes water in the intestine –> viscous liquid –> promotes peristalsis AND reduces transit time

**AVOID if bowel is obstructed

88
Q

Psyllium (Metamucil) pharmacokinetics

A

1) onset: 12-72 hrs

89
Q

Psyllium (Metamucil) ADRs

A

cramps, respiratory distress (if inhaled in susceptible individuals), constipation (MUST incr. fluid intake as well)

may cause bowl obstruction

90
Q

Psyllium (Metamucil) interactions

A

many moderate

can affect absorption (e.g. digoxin) d/t slowed GI transit

91
Q

_________ are being used to reverse opioid induced constipation in the gut

A

opiate receptor antagonists

naloxone is esp. useful b/c it isn’t absorbed well so it stays in the gut and blocks opiate receptors there (relieving constipation) but it does not really get into the bloodstream so opiates can still act systemically

92
Q

anti-diarrheal meds that are OTC rely on an ______________ mechanism, so there is abuse potential; especially with __________

A

opiate-based

loperamide

93
Q

Loperimide (Immodium) class

A

opiate-like antidiarrheal

94
Q

Loperimide (Immodium) MOA

A

decr. GI motility by effects on the circular and longitudinal mm.

reduced GI secretions produced by opiod receptor binding effects in the intestinal mucosa

95
Q

Loperimide (Immodium) pharmacokinetics

A

1) onset: < 1 hr

2) poorly absorbed (when absorbed, metabolism via hepatic oxidative N-demethylation)

96
Q

Loperimide (Immodium) ADRs

A

dizziness, cramps, nausea, toxic megacolon and rashes (rare), **pro-arrhythmic cz QTC prolongation (high doses and in combination)

**At high doses leads dependence and abuse

97
Q

Loperimide (Immodium) natural product interactions

A

1) Henbane (additive anticholinergic effects)
2) Scopolia (additive anticholinergic effects)
3) Hypericum (induction of PgP)

98
Q

Diphenoxylate and Atropine (Lomotil) class

A

opioid-like antidiarrheal

**This is a controlled substance

99
Q

Diphenoxylate and Atropine (Lomotil) MOA

A

opiate receptor agonist (stimulates mu receptors) –> inhibits excessive GI motility and GI propulsion

100
Q

Diphenoxylate and Atropine (Lomotil) pharmacokinetics

A

1) onset: 45-60min

2) extensively absorbed (hydrolyzed to active diphenoxylic acid)

101
Q

OTC preparations of __________ contain a subtherapeutic amt of atropine to discourage abuse

A

Diphenoxylate and Atropine (Lomotil)

102
Q

Diphenoxylate and Atropine (Lomotil) ADRs

A

many anti-cholinergic s/e d/t atropine (inhibited SLUD and dry skin) and CNS depressant effects

103
Q

Diphenoxylate and Atropine (Lomotil) natural product interactions

A

1) Henbane (additive anticholinergic effects)

2) Scopolia (additive anticholinergic effects)

104
Q

Lamotil and Imodium exert their anti-diarrheal effects based on what similar mechanism?

A

reducing GI motility (and also acting on opioid receptors)

105
Q

What are the primary drug categories used to tx IBD?

A

1) Corticosteroids/Glucocorticoids
2) Aminosalicylates (5-ASA)
3) Immunosuppressants/Biologics
4) Antibiotics

106
Q

Prednisone/prednisolone class

A

corticosteroid (includes both glucocorticoid and mineralcorticoid)

107
Q

Prednisone/prednisolone MOA

A

1) modulates protein synthesis –> reduced migration of polymorphonuclear leukocytes and fibroblasts
2) reverses capillary permeability and lysosomal stabilization –> controls inflammation
3) immunosuppression

**use for IBD is limited to acute flares or salvage therapy

108
Q

Prednisone/prednisolone pharmacokinetics

A

1) onset: days-weeks

2) DOA: 12-18 hr

109
Q

Budesonide (Entocort EC) class

A

glucocorticoid

110
Q

Budesonide (Entocort EC) MOA

A

synthesis –> reduced migration of polymorphonuclear leukocytes and fibroblasts

2) reverses capillary permeability andlysosomal stabilization –> controls inflammation
3) immunosuppression
4) **Release mechanism of enteric-coated tablets (Uceris) and capsules (Entocort) delay release until pH > 5.5

111
Q

Budesonide (Entocort EC) pharmacokinetics

A

1) onset: days - weeks
2) absorption varies, overall minimal absorption (11%)
3) rapid and extensive first-pass (major CYP3A4)
4) Glucocorticoid&raquo_space; mineralcorticoid receptor affinity (15-fold compared to prednisolone)
5) good topical activity w/ low systemic bioavailability

112
Q

Budesonide (Entocort EC) natural product interactions

A

1) Grapefruit (CYP3A4 inhibitor)

2) Hypericum (CYP3A4 inducer)

113
Q

Which corticosteroid(s) cover the duodenum/ jejunum?

A

1) Beclomethasone

2) Prednisone (PO/IV)

114
Q

Which corticosteroid(s) cover the ileum?

A

1) Entocort EC

2) Budesonide

115
Q

Which corticosteroid(s) cover the colon?

A

1) Budesonide

116
Q

Which corticosteroid(s) cover the anus/rectum?

A

1) topical hydrocortisone

2) budesonide

117
Q

Mesalamine class

A

aminosalicylates (5-ASA)

118
Q

Mesalamine MOA

A

1) modulates local chemical mediators of inflammation (anti-inflammatory), esp. leukotrienes
2) free radical scavenger
3) inhibitor of TNF

119
Q

Mesalamine pharmacokinetics

A

1) onset: 3-4 wks
2) absorption varies (baled on dosage form), overall minimal absorption (10%)
3) activity is mostly topical

120
Q

Sulfasalazine class

A

aminosalicylates

121
Q

Sulfasalazine MOA

A

1) **Prodrug of mesalamine (the Azo, N=N, bond is cleaved by colonic bacteria)

122
Q

Sulfasalazine ADRs

A

1) dose dependent: nausea, anorexia, folate deficiency, HA, alopecia
2) dose independent: male infertility, rash, hemolytic anemia, hepatitis, pancreatitis, agranulocytosis

123
Q

Sulfasalazine pharmacokinetics

A

1) onset: 3-4 wks
2) metabolism: intestinal bacteria –> sulfapyridine and 5-ASA –> 5-ASA is poorly absorbed and continues thru GI
3) absorption: sulfasalazine (< 15%); sulfapyridine (60%), 5-ASA (10%)

124
Q

Sulfasalazine metabolism is dependent on

A

NAT (N-acetyltransferase) phenotype

  • 5-ASA is metabolized in colonic mucosa by NAT1
  • sulfapyridine is metabolized in liber by NAT 2
125
Q

Which 5-ASA drug(s) cover the duodenum/jejunum?

A

1) Pentasa (ER caplet)

126
Q

Which 5-ASA drug(s) cover the ileum?

A

1) Asacol (enteric coated tablet)
2) Claversal
3) Salofack

127
Q

Which 5-ASA drug(s) cover the colon?

A

1) Sulfasalazine

2) Osalazine

128
Q

Which 5-ASA drug(s) cover the anus/rectum?

A

1) topical 5-ASA

129
Q

Which folic acid derivative immunosuppressant is MC used in Crohn’s and UC?

A

methotrexate

130
Q

Which purine analog immunosuppressant is MC used in Crohn’s and UC?

A

6-mercaptopurine

131
Q

Azathioprine class

A

purine analog antimetabolite (immunosuppressant)

132
Q

Azathioprine MOA

A

inhibits purine synthesis and DNA replication –> anti-proliferative effect and apoptosis of T-cells

133
Q

Azathioprine pharmacokinetics

A

1) onset: 1-3 mo.
2) absorption 60%
3) pro-drug (imidazolyl derivative) which is converted to active form 6-mercaptopurine

134
Q

Azathioprine has a major interaction with

A

Ethanol (incr. risk for hepatotoxicities)

135
Q

Tumor Necrosis Factor-alpha class

A

monoclonal Abs

immunosuppressant

136
Q

Tumor Necrosis Factor-alpha MOA

A

inhibit TNFa

137
Q

Tumor Necrosis Factor-alpha pharmacokinetics

A

1) onset: 1-2 wks
2) T1/2: 7-12 days
3) DOA: 8-48 wks
4) metabolisms: mononuclear phagocyte system

138
Q

Tumor Necrosis Factor-alpha C/I

A
  • active HepB
  • MS, optic neuritis
  • active serious infx
  • chronic/recurrent infx
  • current neoplasia
  • Hx TB or positive PPD (untx)
  • CHF (class III or IV)
139
Q

Tumor Necrosis Factor-alpha ADRs

A
  • infusion rxn/anaphylaxis
  • infection (TB and HepB re-activation)
  • HA
  • transaminitis
  • N/V
140
Q

Premedication with __________ may be considered to prevent and manage infusion-related rxn to Tumor Necrosis Factor-alpha

A

antihistamines (H1-antag. +/- H2-antag.), acetaminophen, and/or corticosteroids

141
Q

Infliximab (Remicade) class

A

anti-TNFa monoclonal Ab
(immunosuppressant)

xi = chimera (human-mouse)
mab = monoclonal Ab
142
Q

Infliximab (Remicade) MOA

A

chimeric IgGk that binds to both free and membrane bound TNFa

143
Q

Infliximab (Remicade) major interaction

144
Q

Adalimumab (Humira) class

A

anti-TNFa
(immunosuppressant)

lim = immune/immunomodulator 
u = mouse 
mab = monoclonal antibody
145
Q

Adalimumab (Humira) MOA

A

human mAb (IgGk) against TNFa

146
Q

Drugs used for nausea/emesis

A

1) Serotonin (5-HT3) antagonists
2) Dopamine (D2) antagonists/prokinetics
3) Antipsychotics
4) Steroids
5) Cannabinoids
6) Antihistamines

147
Q

Ondanstron class

A

Serotonin (5-HT3) antagonist

148
Q

Ondanstron MOA

A

selectively antagonizes serotonin at 5-HT3-receptors (both peripherally on vagal n. terminals and centrally in chemoreceptor trigger zone)

149
Q

Ondanstron pharmacokinetics

A

1) onset: 30 min
2) DOA: 3-6 hr (prolonged T1/2 w. hepatic impairment)
3) metabolism: 1’ hepatic - hydroxylation, glucuronide, sulfate conjugation, demethylation (involves CYP450 enzymes)

150
Q

Ondanstron ADRs

A
  • CV (QTc prolongation)
  • HA
  • fatigue/malaise
  • diarrhea
  • transient transaminitis
151
Q

Ondanstron natural product interactions

A

1) Grapefruit (CYP3A4 inhibitor)

2) Hypericum (CYP3A4 inducer)

152
Q

If serotonin antagonists prevent/treat nausea…what would you expect SSRIs to do?

A

s/e of nausea

153
Q

Promethazine class

A

dopamine (D2) antagonist

154
Q

Promethazine MOA

A
  • blocks postsynaptic mesolimbic dopaminergic receptors in the brain
  • exhibits a strong alpha-adrenergic blocking effect
  • depresses release of hypothalamic and hypophyseal hormones
155
Q

Promethazine pharmacokinetics

A

1) onset: 20 min (PO, IM) or 5 min (IV)
2) DOA: 4-6 hr
3) metabolism: significant first-pass, hydroxylation via CYP2D6 and N-demethylation via CYP2B6

156
Q

Promethazine ADRs

A
  • CV (arrhythmia, hypotension)
  • dopamine suppression “extrapyramidal” effects (e.g. akathisia, acute dystonia, pseudoparkinsonism, tardive dyskinesia)
  • endocrine (amenorrhea, gynecomastia, hyperglycemia)
157
Q

Promethazine natural product interactions

A

1) Henbane (additive anticholinergic effects)
2) Scopolia (potentiate s/e and ADRs of anticholinergic drugs)

(anticholinergic = anti-SLUD)

158
Q

Metoclopramide class

A

Dopamine (D2) antagonist

159
Q

Metoclopramide MOA

A
  • antagonizes dopamine receptors

- at high doses blocks serotonin receptors in chemoreceptor trigger zone of CNS (antiemetic)

160
Q

Metoclopramide pharmacokinetics

A

1) onset: 30-60 min (PO), 10-15 min (IM), 1-3 min (IV)
2) DOA: 1-2 hr
3) metabolism: extensive absorption, N-demethylation and N-hydroxylation via CYP2D6 and CYP1A2

161
Q

Metoclopramide ADRs

A

relatively few at low doses

at higher doses may see dopamine-suppression “extrapyramidal” effects (e.g. akathisia, acute dystonia, pseudoparkinsonism, tardive dyskinesia)

162
Q

Metoclopramide has effects on which receptors?

A

both D2 receptors and 5-HT4 receptors

Pharmacology (14 decks)

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