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Summer pharm 4 > Acid/Peptic > Flashcards

Acid/Peptic Flashcards

1
Q

How do acid/peptic disorders develop

A

Mucosal erosions or ulcerations arise when the caustic effects of aggressors (acid, pepsin, bile) overwhelm he defensive factors of the GI mucosa

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2
Q

What normally regenerates GI mucosa after injury

A

Mucus and bicarb secretion
prostaglandins
blood flow

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3
Q

What causes peptic ulcers

A

MC: H pylori

NSAIDs

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4
Q

What are the two classes of peptic disease fighting agents

A

agents that reduce intragastric acidity

agents that promote mucosal defense

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5
Q

What contributes to acid secretion

A

Gastrin from antral G cells, Ach from postganglionic nerves, and Histamine bind receptors (CCK-B, H2, M3) on parietal cells
Binding causes increase in calcium which stimulates protein kinase which stimulates acid secretion from H/K ATPase (proton pump)

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6
Q

Do the three receptors work together

A

They are all on the same cell (parietal cell) but if you block any of the three, they are not dependent on each other
If you block one specific one, you don’t necessarily block the acid stimulation from the others

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7
Q

What agents reduce intragastric acidity

A

Antacids
H2 blockers
PPI

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8
Q

What are antacids

A

Non-Rx meds for intermittent heartburn and dyspepsia
They are weak bases that react with gastric HCl to form a CO2 and NaCl= less acidity
Give 1 hour after a meal to neutralize gastric acid for up to 2 hours

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9
Q

What are some antacids

A

sodium bicarb: Baking soda, Alka seltzer
Calcium carbonate: tums, Os-Cal
Mag hydroxide
Aluminum hydroxide

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10
Q

ADE of Sodium bicarb antacids are

A

CO2 gastric distention and belching
Unreacted alkali is absorbed and can cause metabolic alkalosis if high dose in renal insufficiency
NaCl absorption enhances fluid retention if w/ HF, HTN, or renal insufficiency

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11
Q

What is the MOA of Calcium carbonate

A

Less soluble and reacts more slowly w/ HCl to form CO2 and CaCl

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12
Q

ADE of calcium carbonate are

A

belching
metabolic alkalosis
Excess sodium bicarb or calcium carb w/ calcium dairy= hypercalcemia, renal insufficiency, metabolic alkalosis (milk-alkali syndrome)

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13
Q

What is the MOA of mag/aluminum hydroxide

A

React slowly with Hcl to form mag chloride or aluminum chloride and water
No gas! does not cause belching
Metabolic alkalosis is not common

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14
Q

ADE of mag/aluminum hydroxide are

A

Osmotic diarrhea (unabsorbed mag)
Constipation (aluminum salts)
-Commonly used with Gelusil, Maalox, and Mylanta to minimize impact on bowel

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15
Q

Who should not take mag/aluminum hydroxide antacids

A

Renal insufficiency patients, because both are absorbed and excreted by the kidneys

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16
Q

Never give antacids w/in 2 hours of giving these meds (mag, alu, and Ca interfere with them)

A

Tetracyclines
Fluoroquinolones
Itraconazole
Iron

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17
Q

How do antacids affect other drugs

A

They can affect absorption of other meds by binding drug and:
reducing absorption -or- increasing pH so solubility of drug is altered

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18
Q

What are the H2 blockers

A

Cimetidine- least potent
Ranitidine (zantac)
Famotidine (pepcid)- most potent
Nizatidine

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19
Q

What is the PK of H2 blockers

A

Rapidly absorbed from intestine

First pass hepatic metabolism (all except nizatidine)

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20
Q

Do you have to dose adjust H2 blockers

A

Yes in mod-severe renal insufficiency (and hepatic)

Elderly 2/2 reduction in volume distribution and drug clearance

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21
Q

What is the MOA of H2 blockers

A

Competitively inhibit H2 receptors (not H1 or 3)
Suppress acid secretion
Reduce volume of gastric secretion and concentration of pepsin
Reduce acid secretion stimulated by histamine, gastrin, and cholinomimetic agents
Block histamine release from ECL gells
Diminish direct stimulation of parietal cell to release gastrin or ACh

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22
Q

When should you give an H2 blocker

A

before bed! This is when the most acid is produced

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23
Q

Is Rx H2 blocker better than OTC?

A

Yes, maintains greater than 50% acid inhibition x 10 hours whereas OTC provides only 6 hours of relief

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24
Q

What disorders benefit from H2 blockers

A

GERD
PUD
NUD (non-ulcer dyspepsia)
Prevention of bleeding from stress related gastritis

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25
Q

ADE of H2 blockers are

A

diarrhea, HA, fatigue, myalgias, constipation- BUT
These occur in <3% of patients! H2 blockers are VERY safe
-Nosocomial PNA in critically ill pt
Mental status changes: confusion, hallucinations, agitation (IV or pt in ICU)

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26
Q

Can pregnant women take H2 blockers

A

They cross the placenta and are secreted into breast milk so ONLY give if absolutely necessary

27
Q

What is specific about Cimetidine

A

Inhibits binding of DHT to androgen receptors= inhibits estradiol metabolism & increases serum prolactin
Can cause gynecomastia or impotence in men or galactorrhea in women

28
Q

What do H2 blockers interact with

A

Cimetidine: inhibits hepatic CYP450 pathways
Ranitidine: binds 4-10 times less avidly than cimetidine to CYP450
Nizatidine and Famotidine don’t really interact with CYP450

29
Q

What are the PPI

A 
Omeprazole (prilosec) 
Esomeprazole (nexium) 
Lansoprazole (prevacid) 
Dexlansoprazole 
Rabeprazole 
Pantoprazole (protonix)
30
Q

What is the PK of PPI’s

A

They are inactive acid labile prodrugs; PO are delayed release and acid resistant (enteric coated) while prodrugs rapidly become protonated within canaliculus
*Rapid first pass hepatic metabolism
(really no renal clearance)

31
Q

What decreases bioavailability of drug

A

food! by about 50%

So, give PPI 30-60 min before meal (MC breakfast)

32
Q

What do PPI’s block

A

They inactivate actively secreting pumps, but do NOT have effects on inactive or dormant pumps

33
Q

How long are PPI active

A

They inhibit acid for up to 24 hours (irreversible inactivation of PP)- it takes 18 hours for synthesis of new proton pump molecules

34
Q

Do you need to adjust PPI doses

A

Yes, in patients with severe liver impairment

35
Q

Where are H/K ATPase pumps found

A

ONLY on parietal cells

36
Q

What is acid suppression from a PPI dependent on

A

irreversible inactivation of proton pump, not the PK of different agents

37
Q

PPI’s can be used for

A 
GERD 
PUD 
NUD 
prevention of stress related mucosal bleeding 
Gastrinoma
38
Q

What are ADE of PPI’s

A

Diarrhea, decreased B12 release from food, HA, abd pain
Promotes absorption of iron, calcium, magnesium (monitor bone density and give calcium supplements)
Increased risk of infections, nosocomial PNA, C. Diff

39
Q

What happens to Gastrin when you give a PPI

A

Increases 2x

transient rebound acid hypersecretion for 2-4 weeks (dyspepsia, heartburn)

40
Q

What do PPI’s interact with

A

Decrease absorption of: Ketoconazole, digoxin
Reduce activation of: Clopidogrel
Omeprazole inhibits warfarin
Rabeprazole and Pantoprazole have no specific drug interactions

41
Q

If you are taking clopidogrel what PPI do you prefer

A

Pantoprazole

Rabeprazole

42
Q

How does the gastroduodenal mucosa protect itself from acid/pepsin effects

A

Mucus and epithelial tight junctions restrict back diffusion of acid/pepsin
Blood flow carries bicarb and nutrients to surface cells
Prostaglandins stimulate mucus, bicarb and blood flow

43
Q

What are the mucosal protective agents

A

Sucralfate
Prostaglandin analogs
Bismuth

44
Q

What is Sucralfate

A

Salt of sucrose + aluminum hydroxide
In water, it forms a viscous paste that binds ulcers for 6 hours It is negatively charged and proteins on ulcers are + charged)
This physical barrier restricts caustic damage
-ALSO: stimulates mucosal prostaglandin and bicarb secretion

45
Q

What is Sucralfate used for

A

Prevent stress related bleeding

46
Q

What are ADE of Sucralfate

A

Constipation (aluminum=constipation!)

*Do not use prolonged if w/ renal insufficiency

47
Q

What does Sucralfate interact with

A

other meds; can bind and impair their absorption

48
Q

What does the GI mucosa produce

A

Prontaglandins! Mainly E and F

49
Q

What is a prostaglandin analog

A

Misoprostol (PGE1)
Rapidly absorbed, must admin 3-4x day (half life <30 min)
Excreted in urine

50
Q

Do you need to adjust dose of misoprostol in renal insufficiency

A

NO!!!

51
Q

How does Misoprostol work

A

Inhibits acid and protects mucosa
Stimulates mucus and bicarb secretion (= more blood flow)
Binds PG receptor on parietal cells= reduced histamine
Stimulate intestinal electrolyte and fluid secretion, intestinal motility, and uterine contractions

52
Q

What are the clinical uses for Misoprostol

A

Reduces incidence of NSAID induced ulcers

53
Q

ADE of Misoprostol are

A

Diarrhea, abdominal cramping

Stimulates uterine contraction; NO IN PREGNANCY

54
Q

What are the two bismuth compounds available

A

Bismuth subsalicylateL non-Rx

Bismuth subcitrate potassium: Rx drug w/ flagyl&tetracycline

55
Q

What happens to Bismuth subsalicylate in the body

A

Undergoes rapid dissociation in the stomach= absorption of salicylate
99% of bismuth appears in the stool (turns it black or grey) while salicylate is absorbed and excreted in the urine

56
Q

How do Bismuth compounds work

A

Coats ulcers and erosions, protecting from acid and pepsin
Stimulate PG, mucus, and bicarb secretion
Subsalicylate: reduce stool frequency and liquidity in acute infectious diarrhea (inhibits PG and chloride secretion)
Directly antimicrobial against H Pylori and travelers diarrhea

57
Q

What are clinical uses of bismuth compounds

A

Dyspepsia
Acute diarrhea
Subsalicylate: prevent travelers diarrhea
H. Pylori eradication: Used with PPI+Tetracycline+Flagyl x10-14 days (take bismuth 4x daily)

58
Q

ADE of bismuth compounds are

A 
Black stool (harmless) 
Darkening of tongue (harmless) 
High doses= salicylate toxicity
Bismuth toxicity= encephalopathy (ataxia, confusion, HA, seizure)- but not with either of the drugs we learned
59
Q

What do you have to monitor with a PPI and H2 blockers

A

CBC, electrolytes, renal and liver function tests

60
Q

What do you have to monitor with Misoprostol

A

PREGNANCY! make sure they arent

Also, Serum phosphate

61
Q

When would you treat a patient with H. Pylori

A

Gastric/duodenal ulcer
MALT lymphoma
after endoscopic resection of gastric cancer
uninvestigated dyspepsia

62
Q

What are controversial indications to treating H Pylori

A 
NUD 
GERD 
On NSAIDs 
High risk gastric cancer 
Unexplained Fe deficiency anemia
63
Q

What are other regimens used for H Pylori

A

PPI + Clarithromycin + Amoxicillin/Flagyl

PPI + Bismuth + Tetracycline + Flagyl

Summer pharm 4 (14 decks)

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