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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
What is MOA of H2-receptor antagonist?continued...
- volume of gastric acid decreased - pepsin concentration reduced - in presence of H2-antagonist, gastrin and Ach have diminished effect on acid secretion
26
Which H2 antagonist is the most potent?
Famotidine >Ranitdine, Nizatidine> Cimetidine
27
What is the difference between OTC H2 blockers and Rx H2 blockers?
RX H2 blockers maintain greater than 50% acid inhibition for 10 hours while OTC is less than 6 hrs
28
What is the cinical use of H2-Receptor antagonist?
GERD peptic ulcer disease Nonulcer dyspepsia prevention of bleeding from stress related gastritis
29
What is ADE of H2-Receptor antagonist?
diarrhea, HA, fatigue myalgias, - in elderly with renal or liver issues : mental status changes ( hallucinations, agitation) - RELATIVELY SAFE
30
What is the unique ADE of cimetidine?
- 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
What are drug interactions with H2-Receptor antagonist?
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
Name 6 PPI?
``` Omperazole-favorite Esomeprazole Lansoprazole Dexlansoprazole Rabeprazole Pantoprazole ```
33
Which PPI has the shortest 1/2 life?
Omeprazole> Esomeprazole> Lansoprazole Dexlansoprazole, Pantoprazole, Rabeprazole (ordered from shortest half life to longest)
34
T/F PPI are formulated as acid resistant enteric coated capsules to avoid rapid destruction within the gastric lumen
True
35
T/F Bioavailability of PPI's s decreased by 50% with food
TRUE
36
When should you take PPI?
30-60 min before a meal
37
What is MOA of PPI's?
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
T/F PPI's inhibit acid secretion for up to 24 hrs and irreversibly inactivates the proton pump
TRUE
39
PK of PPI's
- high hepatic first pass effect - neglibele renal clerance - dose reduction in patienst with liver issues
40
T/F PPI's affect acid supression based on irreversible inactivation of the proton pump rather than the PK of different agents
TRUE
41
What is clinical use of PPI?
``` GERD PUD Non ulcer dyspepsia prevention of stress related mucosal bleeding Gastrinoma or hypersecretory conditions ```
42
What are ADE of PPI's?
- 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
What are drug interactions with PPI?
decreased absorption of ketaconazole, digoxin, itraconazole omperazole blocks metabolism of warfarin diazepam, and phenytoin esomeprazole: decreases metabolism of diazepam lansoprazole: clears theophylline faster
44
Which PPI has no drug interactions?
Rabeprazole
45
T/F PPI do not block efficacy of clopidogrel
TRUE
46
What should you monitor if pt is taking PPI's?
- bone scan/bone health | - stool-c. diff
47
Name 3 mucosal protective agents?
sulcrafate prostaglandin analogs bismuth
48
How is stomach mucosa protected?
- 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
What is sulcralfate? MOA
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
What is the use of sulcrafate?
-used for stress related bleeds
51
What are ADE of sulcrafate?
constipation due to the aluminum salt | dont use in renal insufficiency
52
What is a prostaganidn analog?
Misoprostol
53
GI mucosa synthesize what prostaglanids?
PGE E and F
54
What is MOA of Misoprostol?
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
What is the clinicl use of Misoprostol?
Misoprostol reduces the incidence of NSAID-induced ulcers to less than 3% and the incidence of ulcer complications by 50%
56
What are ADE of misoprotsol?
- stimulates uterine contractions-don't use in pregnancy or women of child bearing age unless they are on BC - diarrhea, cramping, abdominal pain
57
What are 2 bismuth compounds?
Bismuth subsalicylate: OTC bismuth and salicylate | Bismuth subcitrate potassium: contains metro, tetra for tx of h.pylori, RX
58
PK of bismuth?
- 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
What is MOA of bismuth?
- MOA not known - coats ulcers - releases prostaglandins, mucous, and bicarb - direct antimicrobial effects
60
What is special about bismuth subsalicylate?
Reduces stool frequency and liquidity in acute infectious diarrhea
61
T/F Bismuth compounds have direct antimicrobial activity against H pylori
True
62
What is the clinical use of Bismuth?
prevent traveler's diarrhea H. pylori acute diarrhea dyspepsia
63
ADE of Bismuth?
black stool and tongue salicylate toxicity avoid in renal issues Bismuth toxicity: brain issues, encephalopathy

Pharmacology (47 decks)

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