Acid/Peptic Flashcards Preview

Summer pharm 4 > Acid/Peptic > Flashcards

Flashcards in Acid/Peptic Deck (63):
1

How do acid/peptic disorders develop

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

2

What normally regenerates GI mucosa after injury

Mucus and bicarb secretion
prostaglandins
blood flow

3

What causes peptic ulcers

MC: H pylori
NSAIDs

4

What are the two classes of peptic disease fighting agents

agents that reduce intragastric acidity
agents that promote mucosal defense

5

What contributes to acid secretion

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)

6

Do the three receptors work together

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

7

What agents reduce intragastric acidity

Antacids
H2 blockers
PPI

8

What are antacids

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

9

What are some antacids

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

10

ADE of Sodium bicarb antacids are

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

11

What is the MOA of Calcium carbonate

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

12

ADE of calcium carbonate are

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

13

What is the MOA of mag/aluminum hydroxide

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

14

ADE of mag/aluminum hydroxide are

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

15

Who should not take mag/aluminum hydroxide antacids

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

16

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

Tetracyclines
Fluoroquinolones
Itraconazole
Iron

17

How do antacids affect other drugs

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

18

What are the H2 blockers

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

19

What is the PK of H2 blockers

Rapidly absorbed from intestine
First pass hepatic metabolism (all except nizatidine)

20

Do you have to dose adjust H2 blockers

Yes in mod-severe renal insufficiency (and hepatic)
Elderly 2/2 reduction in volume distribution and drug clearance

21

What is the MOA of H2 blockers

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

22

When should you give an H2 blocker

before bed! This is when the most acid is produced

23

Is Rx H2 blocker better than OTC?

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

24

What disorders benefit from H2 blockers

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

25

ADE of H2 blockers are

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)

26

Can pregnant women take H2 blockers

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

27

What is specific about Cimetidine

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

What do H2 blockers interact with

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

What are the PPI

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

30

What is the PK of PPI's

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

What decreases bioavailability of drug

food! by about 50%
So, give PPI 30-60 min before meal (MC breakfast)

32

What do PPI's block

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

33

How long are PPI active

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

34

Do you need to adjust PPI doses

Yes, in patients with severe liver impairment

35

Where are H/K ATPase pumps found

ONLY on parietal cells

36

What is acid suppression from a PPI dependent on

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

37

PPI's can be used for

GERD
PUD
NUD
prevention of stress related mucosal bleeding
Gastrinoma

38

What are ADE of PPI's

*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

What happens to Gastrin when you give a PPI

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

40

What do PPI's interact with

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

41

If you are taking clopidogrel what PPI do you prefer

Pantoprazole
Rabeprazole

42

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

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

What are the mucosal protective agents

Sucralfate
Prostaglandin analogs
Bismuth

44

What is Sucralfate

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

What is Sucralfate used for

Prevent stress related bleeding

46

What are ADE of Sucralfate

Constipation (aluminum=constipation!)
*Do not use prolonged if w/ renal insufficiency

47

What does Sucralfate interact with

other meds; can bind and impair their absorption

48

What does the GI mucosa produce

Prontaglandins! Mainly E and F

49

What is a prostaglandin analog

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

50

Do you need to adjust dose of misoprostol in renal insufficiency

NO!!!

51

How does Misoprostol work

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

What are the clinical uses for Misoprostol

Reduces incidence of NSAID induced ulcers

53

ADE of Misoprostol are

Diarrhea, abdominal cramping
Stimulates uterine contraction; NO IN PREGNANCY

54

What are the two bismuth compounds available

Bismuth subsalicylateL non-Rx
Bismuth subcitrate potassium: Rx drug w/ flagyl&tetracycline

55

What happens to Bismuth subsalicylate in the body

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

How do Bismuth compounds work

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

What are clinical uses of bismuth compounds

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

58

ADE of bismuth compounds are

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

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

CBC, electrolytes, renal and liver function tests

60

What do you have to monitor with Misoprostol

PREGNANCY! make sure they arent
Also, Serum phosphate

61

When would you treat a patient with H. Pylori

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

62

What are controversial indications to treating H Pylori

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

63

What are other regimens used for H Pylori

PPI + Clarithromycin + Amoxicillin/Flagyl
PPI + Bismuth + Tetracycline + Flagyl