GI drugs Flashcards

1
Q

What is the MOA of Bismuth?

A

Two MOAs:

1) Disrupts cell wall, prevents adhesion, inhibits urease
2) Coats ulcer, stimulates PGE, Mucus and Bicarb release

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2
Q

What are three regimens for PUD treatment?

A

1) PPI + Amoxacillin followed by Clarithromycin and Tinidazole
2) PPI + Tetracyclin+ metronidazole + ciprofloxacin
3) PPI + Amoxacillin + rifabutin +ciprofloxacin

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3
Q

1st line treatment for GERD?

A

Lifestyle modification

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4
Q

2nd line treatment for GERD?

A

H2 blockers

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5
Q

3rd line treatment for GERD?

A

PPIs, esomeprazone

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6
Q

Name PPIs

A

Esomeprazole/

Omeprazole, Lansoprazole, Pantoprazole, Rabeprazole

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7
Q

What is the MOA of PPIs? (Esomeprazole/

Omeprazole, Lansoprazole, Pantoprazole, Rabeprazole)

A

Irreversibly inhibit H/K ATPase

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8
Q

Name common antacids

A

Aluminum hydroxide, calcium carbonate, magnesium hydroxide, sodium bicarbonate

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9
Q

Name AEs of aluminum hydroxide

A

Constipation, decreased PO4 absorption (osteomalacia)

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10
Q

Name AEs of Magnesium hydroxide

A

Osmotic diarrhea

In pts with renal insufficiency –> hypermagnesemia –> cardiotoxicity

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11
Q

Name AE of calcium carbonate

A

Metabolic alkalosis when systemically absorbed

Hypercalcemia if taken w/ dairy products

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12
Q

Name AEs of sodium bicarbonate

A

Systemically absorbed: metabolic alkalosis, hypercalcemia

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13
Q

What are AEs of PPI use?

A

ECL hyperplasia due to decreased negative feedback of gastrin from somatostatin

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14
Q

What are CCK effects on gastric mucosa?

A

Increased pepsinogen (chief cell), increased somatostatin (D cell)

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15
Q

What are Gastrin effects on Gastric mucosa?

A
Increased acid secretion (direct)
Increased histamine release (ECL cell)
Increased pepsinogen (chief cell)
Increased growht
Decreased somatostatin (D cell)
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16
Q

Name H2 blockers?

A

Cimetidine, Famotidine, Nizatine, Ranitidine

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17
Q

What is the MOA of H2 blockers? (Cimetidine, Famotidine, Nizatine, Ranitidine)

A

competitive H2 antagonists that decrease all forms of gastric acid secretion

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18
Q

What do H2 blockers compete with for elimination?

A

weak bases (i.e. metronidazole)

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19
Q

What are AEs of cimetidine?

A
Inhbitor of CYP450
Androgenic effects (gynecomastia, galactorrhea)
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20
Q

What is the MOA of misoprostol?

A

PGE1 analog

Used to treat NSAID-induced ulcers- reverses action of NSAIDs at ulcer

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21
Q

AEs of misoprostol?

A

Diarrhea and severe nausea

Stimulate uterine contractions (abortafactant)

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22
Q

MOA of sucralfate

A

sucrose sulfate aluminum hydroxide complex that attaches to the basement membrane of the ulcer
May stimulate mucosal PGE and bicarb secretion

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23
Q

What are the pharmacokinetics of sucralfate?

A

Requires an acidic environment to be activated

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24
Q

What are AEs of sucralfate?

A

constipation due to aluminum salt

may bind to other meds decreasing absorption

25
Q

What is the MOA of bismuth subsalicylate?

A

Bismuth: stimulate PG release

Disrupts cell wall, prevents adhesion, inhibits urease

26
Q

AEs of bismuth subsalicylate?

A

Blackening of stool and tongue

High doses of subsalicylate may lead to salicylate toxicity: vomiting, tinnitus, metabolic acidosis/alkalosis

27
Q

MOA of pancrelipase?

A

Enriched extract of hog pancreatic enzymes to supplement a pt’s lack of

28
Q

AE of pancrelipase?

A

Diarrhea, abdominal pain

Hyperuricosuria –> renal stone

29
Q

MOA of orlistat?

A

lipase inhibitor- pancreatic and gastric lipase and phospholipase A2, decreasing digestion and absorption of fat

30
Q

AEs of orlistat?

A

Decreased fat absorption –> increased flatus, fecal urgency

Decreased fat soluble vitamins ADEK

31
Q

MOA of ursodiol?

A

Secondary acid ursodeoxycholic acid, conjugates w/ glycine and taurine in liver decreasing CE in bile decreasing CE gallstones

32
Q

Action of CCK on pancreatic acini

A

Increase enzyme secretion in intestinal phase

Increase growth

33
Q

Action of Gastrin on Pancreatic acini

A

Increase enzyme secretion (gastric phase)

34
Q

What is the MOA of lubipristone?

A

CIC-2 activator, increase Cl excretion, retain H2O in lumen

35
Q

What are AEs of Lubipristone?

A

Increased fetal loss, diarrhea in infants (found in milk)

36
Q

What is the MOA of Linaclotide?

A

GC-C activator, increasing cGMP, activationg CFTR channel

37
Q

What are AEs of linaclotide?

A

Increased maternal death in animals, mortality of juvenile mice

38
Q

What is MOA of Crofelemer?

A

voltage-independent inhibition of CFTR, decreasing Cl- secretion

39
Q

What is AE of crofelemer?

A

Constipation

40
Q

What is MOA of octreotide?

A

Somatostatin analogue, decreases 5HT stimulation, decrease hormone release.

Low dose increases motility, High does decreases motility

41
Q

What are the uses for octreotide?

A

treatment of tumors, severe diarrhea due to dumping syndrome, short bowel syndrome, vagotomy

42
Q

what are AEs of octreotide?

A

Decrease in GI motility, impaired pancreatic secretion

43
Q

What is the use of lactulose?

A

Decreases plasma ammonia levels due to alkalinizing lumen,

also increases H2O retention due to osmotic forces

44
Q

What are the AEs of lactulose?

A

When metabolized by gut bacteria, severe cramps and flatulence

45
Q

What are MOA of sodium phosphate?

A

Increase osmotic pressure in lumen, creating looser stools

46
Q

What are AEs of sodium phosphate?

A

Intracellular volume depletion and electrolyte imbalances

47
Q

What are MOA od cholestyramine and colestipol?

A

Decrease reabsorption of bile salts

48
Q

What are AEs of cholestyramine and colestipol?

A

Bloating, flatulence, constipation, fecal impaction

49
Q

What is MOA of Alosetron?

A

5HT3 antagonist, decreasing motility (decreasing afferent stimulation)

50
Q

What are AE of alosetron?

A

Constipation in 30% of patients

ischemic cholitis.

51
Q

What are MOA of tegaserod and cisapride?

A

Activation of 5HT4 presynaptic receptors, increasing gastric motility

52
Q

what are AEs of tegaserod and cisapride?

A

Arrhythmias, long QT

53
Q

What is the MOA of Diphenoxylate and Loparimide?

A

u-agonists, decrease motility and secretion

54
Q

What are AEs of diphenoxylate and loparimide?

A

Constipation, abdominal cramps, TOXIC MEGACOLON

They can make people high, too

55
Q

What is MOA of Alvimopan, methylnaloxone?

A

u-receptor antagonists; increase gastric motility

56
Q

What are AEs of alvimopam and methynaloxone?

A

Alvimopam: increased risk of MI

57
Q

What is MOA of domperidone and metaclopramide?

A

Inhibits dopamine inhibition, increasing ACh in gut, increasing motility

58
Q

Whar are AEs of domperidone and metaclopramide?

A

Domperidone: Sudden cardiac death

Metoclopramide: dystonia, parkinsonism, tardive dyskinesia

59
Q

How do they decrease the risk of abuse with domperidone?

A

D2 receptor antagonist, Add atropine