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GI > Pharm 23 Objectives > Flashcards

Pharm 23 Objectives Flashcards

1
Q

Describe the physiology of the protective gastric mucosal layer

A

secreted by gastric mucosal cells, protective layer.

blood flow vitally maintains mucosal barrier

tight junctions –> relatively impermeable to acid

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2
Q

Describe the physiology of the protective gastric epithelium

A

Epithelial regeneration - rapid cell turnover

The epithelium of the mouth and stomach –> most frequently replaced cells in the body

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3
Q

Prostaglandins effects on gastric acidity

A

Inhibit gastric acid secretion by the parietal cell

Enhance mucosal defense mechanisms (bicarb)

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4
Q

Misoprostol MOA

A

Synthetic PGE1 analog

Inhibits basal and nocturnal gastric acid secretion via direct action on parietal cell

Stimulates mucosal protectant effect

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5
Q

What pregnancy category does Misoprostol fall under?

A

Category X

can cause miscarriage, uterine contraction, and teratogenic.

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6
Q

Indication for Misoprostol?

A

Indicated for NSAID induced gastric ulcer prophylaxis

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7
Q

ASES of Misoprostol?

A

Diarrhea, dose-dependent abdominal pain, headache, flatulence, n/v

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8
Q

List and compare measures to prevent GI ulcers in patients who take NSAIDs long term

A

Find an alternative to systemic NSAIDs

Add Misoprostol or PPI to and NSAID (reduce risk for GI bleed)

Choose a COX-2 selective NSAID

Reduce direct irritation of the GI mucosa (ie. DR tabs and prodrugs)

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9
Q

What is the role of gastrin that stimulates parietal cell acid secretion?

A

Released in response to stomach distension and Ach

Increases intracellular calcium levels in parietal cells

Acids in the stomach is a negative feedback on gastrin release

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10
Q

What is the role of pepsin that stimulates parietal cell acid secretion?

A

Most active at pH 2.0

Becomes progressively less active at higher pH

Irreversibly inactive at pH of 8

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11
Q

What is the role of acetylcholine that stimulates parietal cell acid secretion?

A

Released in response to amino acids in foods and stomach distention

Increase intracellular calcium levels in parietal cells

The most potent stimulator of pepsinogen secretion from chief cells

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12
Q

What is the role of Histamine that stimulates parietal cell acid secretion?

A

Release of histamine is stimulated by Ach and gastrin

The most potent stimulator of gastric acid secretin

Receptor = Gs protein linked —> increase cAMP

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13
Q

What is the role of H+/K+-ATPase that stimulates parietal cell acid secretion?

A

Stimulated via protein kinases

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14
Q

MOA of antacids

A

Increases pH

Inactivated pepsin (at least temporarily)

Bind bile salts

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15
Q

Adverse effects of antacids?

A

Diarrhea, constipation, acid-base disruption and excessive sodium intake, drug interactions that can result in treatment failures:
- mostly chelation issues, which prevents absorption of both drug and mineral

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16
Q

Clinical use/effectiveness of antacids?

A

Rapid onset and short duration of action

Rapid relief

OTC and inexpensive

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17
Q

Molecular formula of calcium carbonate

A

CaCO3

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18
Q

Molecular formula of magnesium hydroxide

A

Mg(OH)2

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19
Q

Molecular formula of sodium bicarbonate?

A

NaHCO3

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20
Q

Mg(OH)2 is frequently added to what?

A

Calcium or aluminum to be constipation neutral

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21
Q

H2 receptor antagonist (H2RA) drug names?

A

Ranitidine

Famotidine

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22
Q

H2 receptor antagonist (H2RA) efficacy?

A

Strongest stimulator of parietal cell

Reduce total volume of gastric juice –> decreasing pepsin secretion

1st line for GERD

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23
Q

H2 receptor antagonist (H2RA) FDA indications?

A

Duodenal ulcer disease

Erosive esophagitis

Gastric hypersecretion

Gastric ulcer

GERD

H. pylori gastrointestinal tract infection, Indigestion

Zollinger-Ellison syndrome

Night time symptoms

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24
Q

H2 receptor antagonist (H2RA) pharmacokinetics?

A

First mass metabolism –> reduces bioavailability 30-60%

Do cross the BB

Are excreted in breast milk

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25
Q

H2 receptor antagonist (H2RA) onset of action?

A

Peak [ ] in serum in 1-3 hrs

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26
Q

H2 receptor antagonist (H2RA) drug interactions?

A

Cimetidine - gynecomastia, heart rate changes (brady (MC) or tachy)

Nizatidine - insomnia, somnolence, anemia

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27
Q

H2 receptor antagonist (H2RA) common ASEs?

A 
Headache
Diarrhea
N/V
Constipation
Vertigo/dizziness
Fatigue
Confusion
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28
Q

H2 receptor antagonist (H2RA) severe ASEs?

A

Organ impairment/toxicity:

- hepatic, cardiac, pancreatic, renal

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29
Q

H+/K+ ATPase (PPI) efficacy?

A

More effective and longer lasting effects than H2RAs/antacids.

Suppress daytime, nocturnal, and meal stimulated acid secretion

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30
Q

H+/K+ ATPase (PPI) FDA indications?

A

Erosive esophagitis

GERD

Duodenal ulcer

H. Pylori

31
Q

H+/K+ ATPase (PPI) pharmacokinetics?

A

Short half lives

metabolize by the liver by CYP2C19 and CYP3A4 to inactive metabolites

32
Q

H+/K+ ATPase (PPI) onset of action?

A

0.6 - 1.9 hrs

33
Q

H+/K+ ATPase (PPI) drug interactions?

A

Ketoconazole

Amphetamines

Citalopram

Clopidogrel

34
Q

PPI + ketoconazole causes?

A

May impair the GI absorption of ketoconazole leading to loss of therapeutic effect.

(drink coke if need to take the two together)

35
Q

PPI + Amphetamines causes?

A

Increases the absorption of amphetamine

36
Q

PPI + citalopram causes?

A

Citalopram tox: serotonin syndrome, QT prolongation.

37
Q

PPI + clopidogrel causes?

A

PPI may decrease serum [ ] of the active metabolites of clopidogrel.

38
Q

H+/K+ ATPase (PPI) ASEs?

A

“GI” side effects

HA

Hypomagnesemia (long term use)

Gastric atophy

Iron and B12 deficiencies

Hypersensitivity rxn: immunologic, dermatologic, hematologic, hepatic manifestation.

39
Q

H+/K+ ATPase (PPI) appropriate duration?

A

2 wks, 4wks, up to 8-12 wks

- lowest effective dose for the shortest duration possible.

40
Q

What is hypergastrinemia caused by a PPI?

A

High gastrin [ ] in the blood.

- cellular and hormonal changes that increase gastric acid secretion capacity.

41
Q

Sucralfate MOA?

A

Reacts with HCl

Adherent, paste-like substance, an acid buffer

Binds electrostatically to proteins on ulcer surface (protective barrier)

42
Q

Sucralfate proper dosing?

A

1 gram QID on empty stomach for 4 weeks

Acid neutralizers should not be taken within one-half hour before or after administration

Avoid H2RAs, fluroquinolones, tetracyclines, or digoxin within 2 hours before administration

43
Q

Sucralfate ASEs?

A

Potential aluminum toxicity with long term use, esp. in patient with kidney dysfunction

Hypophosphatemia

Flatulence

HA

44
Q

Safe and effective therapeutic treatment of PUD w/ H pylori?

A

MC = the PPI-based 3-Drug Regimen - first choice if local resistance is low.

3 Drugs = 1 Acid Reducer + 2 Antibiotics

  • Amoxicillin, clarithromycin, lansoprazole
  • Amoxicillin, clarithromycin, omeprazole

Pts w/ penicillin allergy: used metronidazole over amox.

45
Q

Safe and effective therapeutic treatment of PUD w/ dyspesia?

A

Acid suppression: Antacids, H2RAs, PPIs

46
Q

Safe and effective therapeutic treatment of PUD w/ GERD phase 1?

A

phase 1:

- OTC antacids, H2RA, or PPI x2 wks

47
Q

Define what a “prokinetic” drug would do?

A

increases GI transit rates

48
Q

Describe the relative lack of availability of “prokinetic” agents within the U.S.

A

Reported CV deaths

49
Q

Metoclopramide MOA

A

Promotes motility in upper GI tract, sensitizes tissues to ACh action w/o stimulation of gastric secretions.

Decreases the flow in the esophageal varices causing a reduction in variceal pressure

Dopamine (D2) central and peripheral receptor inhibition w/o antipsychotic or tranquilizing activity

Weak 5-HT3 receptor antagonism

50
Q

Metoclopramide clinical use

A

GERD

Relief of symptoms in adults with acute and recurrent diabetic gastroparesis

Chemotherapy-induced or postoperative nausea/vomiting

MAX 12 wks

51
Q

Metoclopramide ASEs

A

Tardive dyskinesia (BB warning)

Headache, somnolence, fatigue, N/V

52
Q

Production of serotonin?

A

Tryptophan - 5-HTP (5-hydroxytryptophan)
—>
5-HT (5-hydroxytryptamine)

= serotonin

53
Q

Distribution of serotonin?

A

95% in GI tract of the 95%:

  • 90% is in Enterochromaffin cells
  • 10% is in Enteric neurons
54
Q

Metabolism of serotonin through pineal gland?

A 
Serotonin (5-HT)
--->
pineal gland 
---> 
melatonin 
--->
6-sulfaoxymelatonin
55
Q

Metabolism of serotonin through MAO?

A 
Serotonin (5-HT)
--->
MAO 
--->
5-hydroxyindolacetic acid
56
Q

Location of serotonin receptors?

A

Gut has 7 types of receptors

  • Gut: increase tone and facilitate peristalsis
  • CNS
  • PNS
  • Lungs- bronchoconstriction
  • Enteric nerves: bady, hypoTN, nausea.
57
Q

List the drugs that agonize the 5- HT4 receptor?

A

Tegaserod

Prucalopride

58
Q

Describe gastrointestinal therapeutic applications of drugs that act on the agonize the 5- HT4 receptor?

A

Speeds GI transit

Stimulates peristalsis

Improves BM frequency

Soften stool

59
Q

List the drugs that antagonize the 5- HT3 receptor?

A

Alosetron

Ondsanserton

Cilansetron

60
Q

Describe gastrointestinal therapeutic applications of drugs that act on the antagonize the 5- HT3 receptor?

A

Nausea/vomiting

Irritable-bowel (diarrhea predominant)

61
Q

Safe and effective therapeutic treatment of PUD w/ GERD phase 2?

A
  • Rx H2RA (6-12wks)

- Rx PPI (4-8wks) or prokinetic agent if motility disorder.

62
Q

List the 5 primary antiemetic drugs classes

A
  1. 5-HT3 antagonist
  2. Dopamine 2 antagonist
  3. Substance P/Neurokinin-1 antagonist
  4. Antimuscarinics
  5. 1st gen antihistamines
63
Q

5-HT3 antagonist most appropriate clinical uses?

A

Nausea

Vomiting

IBS

64
Q

Dopamine 2 antagonist most appropriate clinical uses?

A

Psychiatric disorders

65
Q

Substance P/Neurokinin-1 antagonist most appropriate clinical uses?

A

Vasodilation

Inflammation

Pain

Mood

Vomiting

66
Q

Antimuscarinics most appropriate clinical uses?

A

Motion sickness (scopolamine patch)

67
Q

1st gen antihistamines most appropriate clinical uses?

A

Motion sickness

Anxiety for flights

68
Q

5-HT3 antagonist ASEs?

A

HA

Constipation

Fever

Diarrhea

Prolonged QT interval

Cardiac arrhythmias

69
Q

Dopamine 2 antagonist ASEs?

A

Extrapyramidal sxs

QT Prolongation

NMS

70
Q

Substance P/Neurokinin-1 antagonist ASEs?

A

Steven johnson syndrome

Diarrhea

Constipation

71
Q

Antimuscarinics ASEs?

A

Dry mouth and skin

Blurred vision

Hot flashes

72
Q

1st gen antihistamines ASEs?

A

Sedation

Fatigue

Dizziness

Anticholinergic side effects (dry mouth, tachy, blurred vision)

73
Q

What drug is used for motion sickness and temporarily as a sleep aid?

A

First generation antihistamines

ie. Dimenhydrinate (Dramamine), promethazine.

74
Q

Name the drug under the class: substance p/neurokinin 1 receptor antagonists?

A

Aprepitant

GI (16 decks)

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