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Pharmacology > Acid-Peptic Disorders > Flashcards

Acid-Peptic Disorders Flashcards

1
Q

Which receptors are found on parietal cells and stimulate HCl secretion?

A
  1. Gastrin (CCK-B)
  2. Histamine (H2)
  3. Ach (M3 muscarinic)
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2
Q

What is MOA of gastrin, Ach, and histamine?

A

When they bind there receptor on parietal cells, they:

  1. increase cytosolic calcium
  2. stimulate protein kinases
  3. stimulate acid secretion from a H/K ATPase (proton pump)
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3
Q

T/F If you block the H/K ATPase you can’t make HCl

A

TRUE

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4
Q

T/F If you block the histamine/H2 or gastrin receptor/CCK-B you can still make HCl

A

TRUE

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5
Q

What are the two classes of drug tx in acid secretion?

A
  1. reduce intragastric acidity

2. promote mucosal defense

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6
Q

Name the three drug classes that reduce intragastric acidity?

A
  1. Antacids-TUMS, Mylanta, Alkaseltzer
  2. H2 blockers -Cimetidine, Ranitidine
  3. Proton Pump Inhibitors (PPI) (Prilosec, Protonix)
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7
Q

What is the clinical use of antacids?

A

heart burn and dyspepsia

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8
Q

How do antacids work?

A

they are weak bases that react with HCl to form salt and water
-single dose of 156 mEq given 1 hr after a meal effectively neutralizes gastric acid for up to 2 hours

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9
Q

T/F Antacids work better for duodenal ulcers?

A

TRUE

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10
Q

What is MOA of sodium bicarbonate?

A

reacts with HCl to make CO2 and NaCl

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11
Q

What are the ADE of sodium bicarbonate? (3)

A

Ex. Baking soda, Alka seltzer

  • CO2 causes belching and gastric distention
  • metabolic alkalosis
  • NaCl absorption may exacerbate fluid retention in pts with CHF, HTN, and renal insufficiency
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12
Q

What is MOA of calcium carbonate?

A

Ex. TUMS, OS-Cal

-less soluble and reacts more slowly with HCl to form CO2 and CaCl2

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13
Q

What are ADE of calcium carbonate?

A
  • bleching
  • metabolic alkalosis
  • excessive doses of either NaHCO3 or calcium carbonate with dairy products can cause hypercalcemia, milk-akali syndrome
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14
Q

T/F calcium carbonate antacid can be taken by pregnant women

A

TRUE

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15
Q

What is MOA for Mg-hydroxide?

A

reacts slowly to make MgCl and water

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16
Q

What is MOA for Al-hydroxide?

A

reacts slowly to make AlCl and water

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17
Q

What are ADE of Al-hydroxide and Mg-hydroxide?

A
  • absorbed Mg salts can cause osmotic diarrhea

- Aluminum salts can cause constipation

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18
Q

Who should avoid taking Al-hydroxide and Mg-hydroxide?

A

-patients with renal issues due to the fact that Mg and Al are excreted in the kidney

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19
Q

T/F Al-hydroxide and Mg-hydroxide are administered together to balance between diarrhea and constipation

A

TRUE

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20
Q

What side effects are not caused by Al-hydroxide and Mg-hydroxide?

A

belching/no gas

metabolic alkalosis

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21
Q

Name 4 drug interactions with antacids?

A
  1. Tetracycline
  2. Fluoroquinilone
  3. Itraconazole
  4. Iron
    * should not be given within 2 hours of dose with the above meds
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22
Q

What are pharmockinetics of H2 receptor blockers?

A
  • rapidly absorbed by intestine

- first pass hepatic metabolism -cimetidine, ranitidine, and famotidine

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23
Q

Name 4 H2-receptor antagonist? Which is most effective?

A
  1. Cimetidine
    2 Ranitidine
  2. Famotidine-most effective
  3. Nizatidine
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24
Q

What is MOA of H2-receptor antagonist?

A
  • block H2 receptor on parietal cells
  • suppress meal stimulated acid secretion in a linear, dose dependent manner
  • highly selective: don’t bind H1 or H3
  • exception: cimetidine binds H1, ranitidine binds H1 as well but not as much as cimetidine
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25
Q

What is MOA of H2-receptor antagonist?continued…

A
  • volume of gastric acid decreased
  • pepsin concentration reduced
  • in presence of H2-antagonist, gastrin and Ach have diminished effect on acid secretion
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26
Q

Which H2 antagonist is the most potent?

A

Famotidine >Ranitdine, Nizatidine> Cimetidine

27
Q

What is the difference between OTC H2 blockers and Rx H2 blockers?

A

RX H2 blockers maintain greater than 50% acid inhibition for 10 hours while OTC is less than 6 hrs

28
Q

What is the cinical use of H2-Receptor antagonist?

A

GERD
peptic ulcer disease
Nonulcer dyspepsia
prevention of bleeding from stress related gastritis

29
Q

What is ADE of H2-Receptor antagonist?

A

diarrhea, HA, fatigue myalgias,

  • in elderly with renal or liver issues : mental status changes ( hallucinations, agitation)
  • RELATIVELY SAFE
30
Q

What is the unique ADE of cimetidine?

A
  • blocks dihydorestrogen from binding to androgen receptors, blocks estradiol and increases serum prolactin levels
  • gynecomastia in men and glactorrhea in women
  • secreted in breast milk and crossess the placenta-limit use in pregnancy
31
Q

What are drug interactions with H2-Receptor antagonist?

A

Nizatidine and Famotidine: no drug interactions
Ranitidine: binds cytochrome P450 but less sttrongly when compared to cimetidine
CImetidine: interferes with P450, CYP3A4, CYP1A2, CYP2D6-alot of liver enzymes!

32
Q

Name 6 PPI?

A 
Omperazole-favorite
Esomeprazole
Lansoprazole
Dexlansoprazole 
Rabeprazole 
Pantoprazole
33
Q

Which PPI has the shortest 1/2 life?

A

Omeprazole> Esomeprazole> Lansoprazole Dexlansoprazole, Pantoprazole, Rabeprazole
(ordered from shortest half life to longest)

34
Q

T/F PPI are formulated as acid resistant enteric coated capsules to avoid rapid destruction within the gastric lumen

A

True

35
Q

T/F Bioavailability of PPI’s s decreased by 50% with food

A

TRUE

36
Q

When should you take PPI?

A

30-60 min before a meal

37
Q

What is MOA of PPI’s?

A

block the final common pathway of acid secretion (H/K ATPase in parietal cells)
-PPI’s work only when the pump is active and have no effect when the pump is not working

38
Q

T/F PPI’s inhibit acid secretion for up to 24 hrs and irreversibly inactivates the proton pump

A

TRUE

39
Q

PK of PPI’s

A
  • high hepatic first pass effect
  • neglibele renal clerance
  • dose reduction in patienst with liver issues
40
Q

T/F PPI’s affect acid supression based on irreversible inactivation of the proton pump rather than the PK of different agents

A

TRUE

41
Q

What is clinical use of PPI?

A 
GERD
PUD
Non ulcer dyspepsia 
prevention of stress related mucosal bleeding 
Gastrinoma or hypersecretory conditions
42
Q

What are ADE of PPI’s?

A
  • c. diff, diarrhea
  • issues with dissolving and or absorbing B-12, iron, ca, Mg
  • increased risk for development of salmonella, shigella, e. cloi, capmpylobacter
  • gastrin levels rise 2 fold ( from hyperplasia of ECLcells) thi can cause rebound acid hypersecretion with increased heartburn-taper PPI’s off to avoid this
43
Q

What are drug interactions with PPI?

A

decreased absorption of ketaconazole, digoxin, itraconazole
omperazole blocks metabolism of warfarin diazepam, and phenytoin
esomeprazole: decreases metabolism of diazepam
lansoprazole: clears theophylline faster

44
Q

Which PPI has no drug interactions?

A

Rabeprazole

45
Q

T/F PPI do not block efficacy of clopidogrel

A

TRUE

46
Q

What should you monitor if pt is taking PPI’s?

A
  • bone scan/bone health

- stool-c. diff

47
Q

Name 3 mucosal protective agents?

A

sulcrafate
prostaglandin analogs
bismuth

48
Q

How is stomach mucosa protected?

A
  • Mucus and epithelial cell-cell tight junctions restrict back diffusion of acid and pepsin
  • Blood flow carries bicarbonate and vital nutrients to surface cells
  • Mucosal prostaglandins appear to be important in stimulating mucus and bicarbonate secretion and mucosal blood flow
49
Q

What is sulcralfate? MOA

A

sucrose bound to sufated AlOH

  • neg charged sulcrafate binds pos charges in ulcer surface, creates a paste that covers the ulcers and protects it from caustic damage
  • Stimulates mucosal prostaglandin and bicarbonate secretion
50
Q

What is the use of sulcrafate?

A

-used for stress related bleeds

51
Q

What are ADE of sulcrafate?

A

constipation due to the aluminum salt

dont use in renal insufficiency

52
Q

What is a prostaganidn analog?

A

Misoprostol

53
Q

GI mucosa synthesize what prostaglanids?

A

PGE E and F

54
Q

What is MOA of Misoprostol?

A
  1. stimulates mucous and bicarbonate secretion
  2. binds prostaglandin receptor and reduces histamine induced cAMP which then reduces acid secretion
    * both protective ad acid inhibitory effects
  3. stimulate uterine contraction, electrolyte and fluid secretion and intestinal motility
55
Q

What is the clinicl use of Misoprostol?

A

Misoprostol reduces the incidence of NSAID-induced ulcers to less than 3% and the incidence of ulcer complications by 50%

56
Q

What are ADE of misoprotsol?

A
  • stimulates uterine contractions-don’t use in pregnancy or women of child bearing age unless they are on BC
  • diarrhea, cramping, abdominal pain
57
Q

What are 2 bismuth compounds?

A

Bismuth subsalicylate: OTC bismuth and salicylate

Bismuth subcitrate potassium: contains metro, tetra for tx of h.pylori, RX

58
Q

PK of bismuth?

A
  • Bismuth subsalicylate undergoes rapid dissociation within the stomach, allowing absorption of salicylate
  • Over 99% of the bismuth appears in the stool
  • Salicylate (like aspirin) is readily absorbed and excreted in the urine
59
Q

What is MOA of bismuth?

A
  • MOA not known
  • coats ulcers
  • releases prostaglandins, mucous, and bicarb
  • direct antimicrobial effects
60
Q

What is special about bismuth subsalicylate?

A

Reduces stool frequency and liquidity in acute infectious diarrhea

61
Q

T/F Bismuth compounds have direct antimicrobial activity against H pylori

A

True

62
Q

What is the clinical use of Bismuth?

A

prevent traveler’s diarrhea
H. pylori
acute diarrhea
dyspepsia

63
Q

ADE of Bismuth?

A

black stool and tongue
salicylate toxicity
avoid in renal issues
Bismuth toxicity: brain issues, encephalopathy

Pharmacology (47 decks)

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