GI DRugs Flashcards

1
Q

A PGE1 analog Increase ?production and secretion of gastric mucous barrier, Decrease ?acid production.

A

Misoprostol

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2
Q

Uses of Misoprostol?

A

Prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production);

maintenance of a PDA.

Also used off-label for induction of labor (ripens cervix).

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3
Q

What can we use for acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors.

What is the mechanism of action?

Side effects?

A

Octreotide

Long-acting somatostatin analog; inhibits actions of many splanchnic vasoconstriction hormones.

Nausea, cramps, steatorrhea.

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4
Q

When would we prescribe antacids?

What are some contraindications?

How do antacids affect pH

A

Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.

All can cause hypokalemia.
Overuse can also cause the following problems.

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5
Q

Antacid that causes constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures

A

Aluminum hydroxide: Aluminimum amount of feces.

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6
Q

Antacid that causes Hypercalcemia, rebound acid ?Increase

Side: Can chelate and ? effectiveness of other drugs (e.g., tetracycline).

A

Calcium carbonate

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7
Q

Antacid that causes Diarrhea, hyporeflexia, hypotension, cardiac arrest

A

Magnesium hydroxide

Mg = Must go to the bathroom.

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8
Q

Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose.

These are all examples of?

What is their mechanism?

When do we px them?

A

Osmotic laxitives

MOA: Provide osmotic load to draw water into the GI lumen.

Constipation.
Lactulose also treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+.

Diarrhea, dehydration; may be abused by bulimics.

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9
Q

also treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+.

A

Lactulose

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10
Q

What would we Px to people with UC or Crohns that needs to be activated by gut bacteria to work?

What is it’s MOA?

A

Sulfasalazine

combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria.

Sides: Malaise, nausea, sulfonamide toxicity, reversible oligospermia.

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11
Q

When would we Px Sulfasalazine?

What is it’s MOA?

A

Use for UC or Crohns

A combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria

Sides: Malaise, nausea, sulfonamide toxicity, reversible oligospermia.

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12
Q

5-HT3 antagonist;? DECREASES vagal stimulation. Powerful central-acting antiemetic.

Used post op and to prevent vomiting

A

Ondansetron

Headache, constipation, QT interval prolongation.

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13
Q

When Would we prescribe Orlistat?

What it it’s MOA?

A

Orlistat

Inhibits gastric and pancreatic lipase–> DECRASES ??breakdown and absorption of dietary fats.

Sides: Steatorrhea,?absorption of fat-soluble vitamins.

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14
Q

Drug used for Diabetic and postsurgery gastroparesis, antiemetic.

Contraindicated in pts with short bowel or parkinsons.

What’s it’s MOA

A

Metoclopramide

D2 receptor antagonist.? INCREASES resting tone, contractility, LES tone, motility. Does not influence colon transport time.

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15
Q

Side effects of Metoclopromide

When would we px it?

MOA?

A

Side: ?parkinsonian effects, tardive dyskinesia. Restlessness, drowsiness, fatigue, depression, diarrhea. Drug in_teraction with digoxin and diabetic agent_s. Contraindicated in patients with small bowel obstruction or Parkinson disease (due to D1-receptor blockade).

Uses: Diabetic and postsurgery gastroparesis, antiemetic.

Mechanism: D2 receptor antagonist. INCREASE ?resting tone, contractility, LES tone, motility. Does not influence colon transport time.

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