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G.I & Nutrition > Pharm: Acid Peptic Drugs > Flashcards

Pharm: Acid Peptic Drugs Flashcards

1
Q

T/F PUD can involve any of the upper GI organs

A

T

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2
Q

Which cell layer is involved in PUD

A

PUD includes inflammatory mucosal disorders of the upper GI tract

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3
Q

What kind of receptor is the histamine receptor in the fundus of the stomach?

A

H2

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4
Q

What kind of receptor is the acetylcholine receptor in the fundus of the stomach?

A

M3

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5
Q

What activates the H+/K+ ATPase in the parietal cell?

A

increase in cAMP and intracellular Ca2+

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6
Q

Does the H+/K+ ATPase in the parietal cell use energy?

A

yes

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7
Q

What other cells support the HCl secretory function of parietal cells?

A

neighboring enterochromaffin like cells have receptors for ACh and gastrin and secrete histamine when stimulated.

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8
Q

Which excitatory input is not regulated by negative feedback at the level of the parietal cell in gastric acid secretion?

A

ACh

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9
Q

Which cells secrete pepsin

A

gastric chief cells

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10
Q

Above what pH is pepsin inactivated?

A

4

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11
Q

Above what pH is pepsin IRREVERSIBLY inactivated?

A

6 –> means new enzyme has to be synthesized

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12
Q

T/F pepsin will be inactivated by anything that increases the gastric pH

A

T

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13
Q

T/F bile can be damaging to the GI lining in the absence of acid.

A

T

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14
Q

What usually prevents reflux of bile into the stomach and esophagus?

A

pylorus and LES

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15
Q

Bile gastritis is a consequence of surgery in what kind of patient?

A

in patients in whom the anatomy of the pylorus has been disrupted (pyloroplasty)

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16
Q

What environmental factor enhances acid secretion and lowers LES pressure?

A

caffeine

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17
Q

What environmental factor is directly toxic to upper GI organs?

A

alcohol

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18
Q

What environmental factor may increase acid secretion but does not impair mucosal protective factors?

A

tobacco

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19
Q

What areas of the GI tract secret bicarbonate?

A

stomach, duodenal surface epithelia, mucus neck cells, Brunner’s glands

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20
Q

Which prostaglandins enhance cytoprotective mechanisms, increase bicarbonate secretion, increase mucous thickness, and increase mucosal blood flow in the GI tract?

A

PGE 1 and 2

21
Q

What structural element in the GI tract ensures mucosal integrity against back diffusion of H+?

A

tight junctions between gastric cells

22
Q

What is the target of PPIs?

A

H+/K+ ATPase

23
Q

What is the target of H2receptor antagonist?

A

Rs histamine receptor

24
Q

How are H2RA’s metabolized?

A

hepatic p450

25
Q

How are H2RA’s excreted?

A

renally

26
Q

How are H2RA’s dosed?

A

continuous dosing for a gastric pH of 4

27
Q

How do H2RA’s work?

A

blocks H2 to limit H+ secretion –> elevated pH inactivates pepsin

28
Q

How quickly are H2RA’s absorbed and onset?

A

rapid absorption and quick onset

29
Q

What are the primary drug interactions of H2RAs?

A
  1. cimetidine binds to p450 and increases levels of warfarin, phenytoin, diazepam
  2. ranitidine binds less avidly, famotidine and nizatidine do not bind the p450 systme
30
Q

How do PPI’s work?

A

irreversibly block H+/K+ ATPase in the final common pathway and reduce acid secretion by parietal cells in lumen

31
Q

What kind of receptor function do H2RAs have?

A

competitive antagonist

32
Q

Of PPIs and H2RAs, which is more effective?

A

PPIs have more effect and longer lasting effect on acid secretion

33
Q

How are PPIs delivered?

A

prodrugs with acid resistant coating

34
Q

Where is the outer layer of PPIs dissolved?

A

small intestine –> alkaline environment

35
Q

T/F lipophilic prodrug of PPI is inactive at neutral/alkaline pH

A

true

36
Q

How is PPI prodrug absorbed?

A

blood stream

37
Q

What happens to PPIs at the level of the parietal cell?

A

cross membrane, protonated, concentrated, sulphonated, binds to atpase

38
Q

Plasma half life of PPIs like omebrazole?

A

1-2 hours but duration of action is 24-36 hours because of the capsule –> highly effective with single dose inhibiting ~65% of acid secretion

39
Q

PPI side effects

A
  1. high level of gastrin production interferes with negative feedback loop and may cause gastric carcinoid tumors (in rats)
  2. long term use reduces calcium absorption and reduced osteoclast acid production = hip fx risk
  3. increased respiratory infections from changed bacteria in GI tract
40
Q

weak bases that neutralize HCl to form a salt and H2O are called ____

A

antacids

41
Q

Antacid adverse effects depend on ____

A

the specific ion–> but they all have chalky tastes and may affect the absorption of other drugs, specifically tetracyclines

42
Q

Adverse effects of antacids: Mg

A

diarrhea, muscle weakness –> Mg accumulation can cause renal failure

43
Q

Adverse effects of antacids: AL

A

constipation, binds phosphate (protects against renal failure) –> may contribute to osteomalacia

44
Q

Adverse effects of antacids: Ca (TUMS)

A

rebound acid secretion, nephrocalcinosis (“milk alkali syndrome”)

45
Q

Tx of H pylori

A

triple/quadruple regimens:

  1. clarithromycin, amoxiccilin ppi
  2. clarithomycin, metranidazole, ppi
  3. levofloxacin, metronidazole, ppi, bisumuth
46
Q

Misoprostol GI effects

A

primary prevention of GU in NSAID users, decrease hemorrhage risk if already using NSAID –> use limited by GI side effects of bloating and diarrhea + abortifacient effect

47
Q

Sucralfate MOA

A

binds to GI mucosa and stimulates mucous, bicarbonate and PGE2 production/secretion –> increases resistance to pepsin

  • not absorbed, no direct effect on acid production

basically coats your tummy and makes you feel better

48
Q

Misoprostol GI effects

A

primary prevention of GU in NSAID users, decrease hemorrhage risk if already using NSAID –> use limited by GI side effects of bloating and diarrhea + abortifacient effect

49
Q

Sucralfate MOA

A

binds to GI mucosa and stimulates mucous, bicarbonate and PGE2 production/secretion –> increases resistance to pepsin

  • not absorbed, no direct effect on acid production

basically coats your tummy and makes you feel better

G.I & Nutrition (43 decks)

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