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Gastrointestinal System Step 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

H2 blockers names

A

cimetidine
Ranitidine
famotidine
nizatidine

Take H2 blockers before you dine.
“Table for 2”

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2
Q

Adverse Effects of H2 blockers

A

Cimetidine:
potent inhibitor of P450
Has antiandrogenics effects
can cross BBB (confusion, headaches) and placenta

Both cimetidine and ranitidine lower reanl excretion of creatinine

Other H2 blockers are relatively free of these effects.

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3
Q

MOA of PPIs vs H2 blockers

A

IRREversible block of H/K ATPase in stomach parietal cells (vs H2 reversible)
They also have longer t1/2 compared to H2

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4
Q

Adverse Effects of PPIs

A
  1. higher risk of C difficile infection
  2. –//— of pneumonia
  3. lower serum Mg with long term use
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5
Q

Antacid use adverse effects and effects to the physiology of the body

A

Can affect absorption,bioavailability, urinary excretion of other drugs by altering gastric pH or delaying gastric emptying.
All can use hypokalemia.

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6
Q

Aluminum hydroxide use SE

A

Constipation and hypophosphatemia
Proximal Muscle weakness
Osteodystrophy
Seizures

aluMINIMIMUM amount of feces

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7
Q

Calcium carbonate SE

A

Hypercalcemia(milk alkali syndrome)
rebound acid high
It can chelate and lower effectiveness of other drugs(eg tetracyclines)

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8
Q

Magnesium Hydroxide SE

A

Diarrhea
Hyporeflexia
Hypotension
Cardiac Arrest

Mg2= Must Go Two the bathroom

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9
Q

Bismuth, Sucralfate MOA

A

Bind to ulcer, provide physical protection and allow Hco3- to reestablish pH gradient in mucous layer

Require acidic environment(not given with ppis etc)

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10
Q

Misoprostol MOA

A

PGE1 analogue:

Increase production and secretion of gastric mucous
and
decrease acid production

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11
Q

Clinical uses of Misoprostol

A
  1. Prevention of NSAID induced peptic ulcers

2. Off-label for induction of labour(rippens cervix)

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12
Q

Misoprostol CI

A

Avoid in women of childbearing potential

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13
Q

Misoprostol AE

A

Diarrhea

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14
Q

Octreotide MOA

A

Long acting somatostatin analogue

Inhibits secretion of various splachnic vasodilatory hormones

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15
Q

Octreotide Clinical Uses

A

Acute variceal bleeds
acromegaly
VIPoma\carcinoid tumours

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16
Q

Octreotide AE

A

Nausea
Cramps
Steatohrea
Increased risk of cholelithiasis

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17
Q

MOA of cholelithiasis with ocreotide use

A

Inhibition of CCK

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18
Q

Sulfasalazine MOA

A

Combination of

  1. sulfapyridine(antibacterial)
  2. 5-aminosalycilate acid(anti-inflammatory)

Activated by colonic bacteria

It is also a DMARD for RA
MOA:
1.SP lowers B cell functions
2.5ASA possibly inhibits COX

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19
Q

Why shouldn’t you give sulfasalazine to a patient with Crohn and no colonic involvement?

A

Sulfasalazine gets avtivated by colonic bacteria and works there.
Give it to someone with colonic participation or UC

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20
Q

Sulfasalazine AE

A

Malaise
Nausea
Sulfonamide Toxicity (G6PD)
Reversible oligospermia

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21
Q

Loperamide MOA

A

agonist at m-opioid receptors, slows gut motiity.

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22
Q

Can you get addicted to loperamide?

A

No, low CNS penetration

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23
Q

Loperamide Clinical use

A

Diarrhea

24
Q

Loperamide AE

A

Constipation

Nausea

25
Q

Ondasetron MOA

A

5HT3 antagonist –> lower vagal stimulatin

Powerful central antiemetic

26
Q

Ondasetron Clinical Uses

A

postop

chemo

27
Q

Ondasetron AE

A

Headache
Constipation
long QT
Serotonin Syndrome

28
Q

Metoclopramide MOA

A

D2 receptor antagonist
Increases resting tone, contractility, LES tone, motility, promotes gastric emptying

does NOT influence colon transport time

29
Q

Metoclopramide Clinical Uses

A

Diabetic and postsurgery gastroparesis
Antiemetic
Persistent GERD

30
Q

Metoclopramide AE

A

Parkinsonian Effects, Tardive Dyskinesia

Restlessness, drowsiness,fatigue, depression, diarrhea

31
Q

Metoclopramide Drug Interactions

A

digoxin

diabetic agents

32
Q

Metoclopramide CI

A

Small bowel obstruction

Parkinson

33
Q

Orlistat MOA

A

Inhibits gastric and pancreatic lipase

–>

lowers breakdown and absorption of FA

34
Q

Orlistat clinical use

A

Weight loss

35
Q

Orlistat AE

A

Steatorrhea

Deacreased absorption of ADEK

36
Q

Laxatives I

A

constipation

patients on opiates

37
Q

Laxatives categories

A
  1. Bulk-forming
  2. Osmotic laxatives
  3. Stimulants
  4. Emolients
38
Q

Bulk Forming laxatives names

A

Psyllium

Methylcellulose

39
Q

Bulk Forming laxatives MOA

A

soluble fibers, draw water into gut lumen–> promote peristalsis

40
Q

Bulk forming laxatives AE

A

Bloating

41
Q

Osmotic laxatives names

A

Magnesium hydroxide
Magnesium citrate
polyethylene glycol
lactulose

42
Q

Osmotic laxatives MOA

A

Provide osmotic load to draw water into gut lumen

43
Q

Why is lactulose a different osmotic laxative?

A

Gut flora degrade it into metabolites(lactic acid, acetic acid) that promoted nitrogen excretion as NH4

Hepatic Encephalopathy

44
Q

Osmotic Laxatives AE

A

Diarrhea

Dehydration

45
Q

People category that may abuse osmotic laxatives

A

Bulimia nervosa

46
Q

Stimulant laxatives names

A

Senna

47
Q

Stimulant laxatives MOA

A

Enteric Nerve stimulation–> colonic contraction

48
Q

Stimulant laxatives AE

A

Diarrhea

Melanosis Coli

49
Q

Emollient laxatives names

A

docusate

50
Q

Emollient laxatives MOA

A

Osmotic draw into lumen–>

increased water absorption of stool

51
Q

Emollient laxatives SE

A

Diarrhea

52
Q

Aprepitant MOA

A

Substance P antagonist

Blocks NK1 receptors in brain

53
Q

Aprepitant clinical uses

A

Antemetic for chemo induced nausea and vomiting

54
Q 
Emesis antagonists
(Which categories of receptors do I block for antiemetic effect)
A

5HT3–> setrons
D2–> prochloperazine, metoclopramide
M1–>diphenhydramine,meclizine,promethazine
NK1..> aprepitants

55
Q

CB1 receptor agonists

A

cannabinoids

Gastrointestinal System Step 1 (5 decks)

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