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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 4: GI Pharmacology > Flashcards

Exam 4: GI Pharmacology Flashcards

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1
Q

Histamine is stored in:

A

Vesicles of mast cells and circulating basophils

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2
Q

Histamine is released in response to:

A

Antigen/antibody reactions and certain drugs

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3
Q

Histamine is synthesized by:

A

Decarboxylation of histadine

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4
Q

Roles of histamine:

A

Inflammatory mediator
Regulation of gastric acid secretion
Regulation of neurotransmission

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5
Q

Histamine receptors:

A

H1, H2, H3

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6
Q

Histamine and the BBB:

A

Does not cross BBB, no CNS effects

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7
Q

H1 and H2 antagonists function by:

A

Blocking the response to histamine, not the actual release

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8
Q

Sites/effects (5) of H1 receptor activation:

A

Lungs: bronchoconstriction/↑ airway resistance
Vascular smooth muscle: dilation/hypotension/erythema
Vascular endothelium: ↑ capillary permeability/edema
Peripheral nerves: sensitization/itching, pain, sneezing
Heart: slows AV node conduction/↓ HR

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9
Q

Sites/effects (4) of H2 receptor activation:

A

Airways: relaxation of bronchial smooth muscle
Coronary vasculature: vasodilation
Heart: + inotrope/chronotrope
Stomach: activates proton pump of parietal cells to ↑ H+

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10
Q

Sites/effects of H3 receptor activation:

A

Heart and presynaptic, postganglionic SNS fibers

Inhibits synthesis/release of histamine (inhibitory receptor!)

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11
Q

Effect of H2 antagonists on H3 receptors:

A

Cross-antagonizes H3 receptors, which promotes histamine release

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12
Q

Anesthetic consideration with H2 blockers:

A

If given alongside histamine-releasing drugs, can cause ↑ histamine release d/t H3 antagonism

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13
Q

Structure of histamine receptors:

A

Seven-transmembrane GPCRs

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14
Q

First generation H1 antagonists:

A

Sedating; activate muscarinic, serotonin, and α receptors

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15
Q

Second generation H1 antagonists:

A

Non-drowsy; less CNS effects

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16
Q

Indications for H1 antagonists:

A 
Rhinitis
Conjunctivitis
Urticaria
Pruritis
Motion sickness
Chemotherapy N/V
Insomnia
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17
Q

Ineffective uses for H1 antagonists:

A

Systemic anaphylaxis

Asthma

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18
Q

Characteristics of first-generation H1 antagonists:

A

Lipophilic

Neutral at physiologic pH (cross the BBB!)

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19
Q

Examples of first-generation H1 antagonists:

A 
Diphenhydramine
Hydroxyzine
Chlorpheniramine
Promethazine
Doxepin
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20
Q

Characteristics of second-generation H1 antagonists:

A

Albumin binding

Ionized at physiologic pH (do not cross BBB)

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21
Q

Examples of second-generation H1 antagonists:

A 
Loratidine
Desloratidine
Acrivastine
Fexofenadine
Cetirizine
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22
Q

PK of H1 antagonists:

A 
Well-absorbed
Cmax: 2-3 hours
Protein binding: 78-99%
Metabolism: CYP450
E1/2t: variable (2-24 hrs)
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23
Q

A/E of H1 antagonists:

A

CNS toxicity/sedation
QT interval prolongation
Anticholinergic effects

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24
Q

MoA of H2 antagonists:

A

Competitive antagonism of H2 receptors to suppress gastic acid secretion via ↓cAMP

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25
Q

Examples of H2 antagonists:

A

Cimetidine (least potent)
Nizatidine
Ranitidine
Famotidine (most potent)

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26
Q

Effect of H2 antagonists on gastric emptying/tone:

A

None

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27
Q

Prophylactic dosing of cimetidine before GA induction:

A

300mg PO/IV 1-2 hours prior

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28
Q

Prophylactic dosing of famotidine before GA induction:

A

20-40 mg PO or 20 mg IV am of surgery

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29
Q

Prophylactic dosing of ranitidine before GA induction:

A

150 mg PO or 50 mg IV

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30
Q

Indications for H2 antagonists:

A

GERD
Duodenal ulcer disease
Chemoprophylaxis pre-GA

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31
Q

Effect of H2 antagonists on gastric pH and volume:

A

NO effect on pH of gastric fluid already present

Unpredictable effect on volume

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32
Q

Chemoprophylaxis for patients allergic to contrast dyes:

A

H1 and H2 blocker combined

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33
Q

PK of H2 antagonists:

A

Rapid absorption and extensive first-pass effect
Cmax: 1-3 hrs (oral)
Protein binding: 13-35%
E1/2t: 1.5 - 4 hrs

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34
Q

H2 antagonists and the BBB:

A

All cross the BBB!

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35
Q

Clearance of H2 antagonists:

A

Nizatidine: renal

Cimetidine, ranitidine, famotidine: hepatic

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36
Q

Clearance of H2 antagonists:

A

Nizatidine: renal

Cimetidine, ranitidine, famotidine: hepatic

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37
Q

IV administration of H2 antagonists:

A

Rapid administration causes bradycardia and hypotension!

Cimetidine & ranitidine over 15-30 minutes
Famotidine over 2 minutes

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38
Q

Hepatic A/E of H2 antagonists:

A

Transient elevation in LFTs

Decreases metabolism of hepatic extraction drugs

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39
Q

Cimetidine slows metabolism of these drugs:

A 
Lidocaine
Diazepam
Theophylline
Propranolol
Phenobarb
Warfarin
Phenytoin

Lift the LiD and use TP when you PeWP

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40
Q

Three risk factors for PUD:

A

H. pylori
NSAID use
Smoking

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41
Q

Three goals of PUD therapy:

A

Reduce gastric acidity
Enhance mucosal defenses
Eliminate H. pylori

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42
Q

Drug classes (4) used to inhibit/neutrailize gastric acid secretion in PUD:

A

H2 antagonists
PPIs
Anticholinergics
Antacids

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43
Q

Drug classes (3) used to protect the gastric mucosa in PUD:

A

Sucralfate
Colloidal bismuth
Prostaglandins

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44
Q

Drug class used to eradicate H. pylori in PUD:

A

Antibiotics

45
Q

MoA of PPIs:

A

Block the K+/H+/ATPase (proton pump) leading to a total shutdown of acid release

Prodrug converted to active drug in parietal cell; forms covalent bond with proton pump

46
Q

Examples of PPIs:

A

All of the -prazoles

47
Q

PK of PPIs:

A

Rapidly absorbed
E1/2t: short
Hepatically metabolized
Crosses the placenta

48
Q

A/E of PPIs:

A 
Headache
GI disturbance
Nausea
Enteric infections
Long-term unknown: carcinoid tumor?
49
Q

Indications for PPIs:

A

PUD w/ H. pylori
Hemorrhagic ulcers
PUD in patient needing NSAIDs

50
Q

Clotting and pH:

A

Clot formation impaired in acidic environments; PPIs help ulcers clot and heal

51
Q

Example of anticholinergic used for acid reduction:

A

Dicyclomine

52
Q

Efficacy of dicyclomine:

A

Less effective than H2 blockers/PPIs

53
Q

MoA of anticholinergics for acid control:

A

Decrease PSNS production of acid/gastrin-mediated acid production

54
Q

Structure of sucralfate:

A

Salt of sucrose sulfate and aluminum hydroxide

55
Q

MoA of sucralfate:

A

Forms a viscous gel that binds to (+) proteins (albumin/fibrinogen) thus sticking to areas of ulceration and protecting it

Does NOT alter pH; affords symptomatic relief

56
Q

A/E of sucralfate:

A

Constipation; little systemic absorption

57
Q

Disadvantages of sucralfate:

A

Large tablets, frequent administration

58
Q

Drug interactions with sucralfate:

A

Binds to drugs and impairs their function

59
Q

Colloidal bismuth as PUD therapy:

A

Coating agent; forms barrier to protect mucosa

Stimulates mucosal bicarb and PGE2

Impedes H. pylori growth

60
Q

Misoprostol as PUD therapy:

A

Prostaglandin analogue that prevents NSAID-induced ulcers

Can cause abdo discomfort, diarrhea; contraindicated in pregnancy

61
Q

Triple therapy for H. pylori:

A

Amoxicillin
Clarithromycin
PPI

62
Q

Quadruple therapy for H. pylori:

A

Tetracycline
Metronidazole
PPI
Bismuth

63
Q

Types of antacids:

A

Aluminum hydroxide
Magnesium hydroxide
Sodium bicarbonate
Calcium carbonate

64
Q

Antacids increase gastric pH to:

A

> 5

65
Q

Effects of antacids on ulcers:

A

↑ rate of ulcer healing, duodenal ulcer pain relief

66
Q

A/Es of antacids:

A

Constipation
Diarrhea
Electrolyte abnormalities

67
Q

PK of bicitra:

A

Onset: rapid
pH: 8.4 (unpleasant taste)

68
Q

Dosing of bicitra:

A

15-30ml PO 15-30 minutes pre-op

69
Q

Dosing of bicitra:

A

15-30ml PO 15-30 minutes pre-op

70
Q

Disadvantage of bicitra:

A

Increases intragastric volume

71
Q

Effects of prokinetic drugs:

A

Increases LES tone
Accelerates rate of gastric emptying
Enhances peristalsis

72
Q

MoA of metoclopramide:

A

Dopamine antagonist; achieves post-synaptic release of ACh

73
Q

Effects of metoclopramide on stomach:

A

Kinetic only; pH unchanged

↑ LES tone
↑ gastric/small bowel motility
Relaxation of pylorus/duodenum

74
Q

Antagonist for metoclopramide:

A

Atropine/glyco

75
Q

A/E of metoclopramide:

A

EPS effects

Prolactin secretion

76
Q

Mechanism of anti-emesis effect of metoclopramide:

A

Blocks dopamine stimulation of CRTZ

77
Q

PK of metoclopramide:

A 
Rapid absorption
Onset (IV): 3-5 min
Cmax: 40 - 120 min
E1/2t: 2 - 4 hrs
40% excreted unchanged renally
78
Q

Indications for metoclopramide:

A 
↓ gastric volume
Antiemetic
Tx of gastroparesis
Symptom tx for GERD
? lactation
79
Q

Pre-op dosing of metoclopramide:

A

10 - 20mg IV over 3-5 min
15-30 min pre-induction

Fast administration → cramping

80
Q

PONV dosing of metoclopramide:

A

0.15 mg/kg IV

81
Q

A/E of metoclopramide:

A 
Cramping
Cardiac dysrhythmias
Sedation
Dry mouth
Dystonic EPS
↑ sedation with CNS depressants
May inhibit plasma cholinesterases
Akathesia
82
Q

Contraindications for metoclopramide:

A 
Parkinson's
Bowel obstruction
Pheochromocytoma
Seizure d/o
Phenothiazines (promethazine etc)
83
Q

Examples of extrapyramidal symptoms:

A

Oculogyric crisis
Trismus
Torticollis
Akathesia

84
Q

Role of serotonin in the gut:

A

90% in enterochromaffin cells n the gut; carry pain/nausea impulses

85
Q

Synthesis of serotonin:

A

5-Hydroxytryptamine (5HT) synthesized from tryptophan

86
Q

Examples of 5HT3 antagonists:

A

Ondansetron
Granisetron
Dolasetron
Tropisetron

87
Q

MoA of 5HT3 antagonists:

A

Selective antagonism at GI vagal afferent and CRTZ receptors

88
Q

Types of N/V best suited to 5HT3 antagonist use:

A

Chemo
PONV
Hyperemesis gravidarum

89
Q

A/E of 5HT3 antagonists:

A

Headache with rapid IV push
Dysrhythmias
Slow clearance in liver disease

90
Q

Dosing of ondansetron:

A

Adults: 4 - 8mg IV
Peds: 0.05 - 0.15 mg/kg IV (up to 4mg)

91
Q

Dosing of granisetron:

A

Adults: 0.01 - 0.04 mg/kg

92
Q

Dosing of dolasetron:

A

Adults: 12.5 mg IV

93
Q

Dosing of tropisetron:

A

5 mg

94
Q

Dosing of dexamethasone for PONV:

A

4 - 10mg IV

95
Q

Examples of phenothiazines:

A

Prochlorperzine (Compazine)

Promethazine (Phenergan)

96
Q

MoA of phenothiazines:

A

Interaction with dopaminergic receptors in CRTZ

97
Q

PK of promethazine:

A

Onset: 5min
Duration: 4 - 6hr
E1/2t: 9 - 16hr
Hepatic metabolism

98
Q

Contraindications for phenothiazines:

A
99
Q

Indications for phenothiazines:

A

Blood transfusion rxn
Allergic rxn
Sedation
PONV

100
Q

Incidence and timing of neurolept malignant syndrome:

A

0.5 - 1% of patients taking phenothiazines
24 - 72 hrs after dose
Usually young men

101
Q

Presentation of neurolept malignant syndrome:

A 
Tachy
Dysrthymias
BP alterations
LOC alterations
MH-like: muscle rigidity, hyperthermia, rhabdo, ANS instability
102
Q

Tx of neurolept malignant syndrome:

A

Amantadine and Dantrolene

103
Q

MH vs. NMS:

A

NDMR will produce flaccid paralysis in NMS but not in MH

104
Q

Example of butyrophenones:

A

Droperidol

105
Q

MoA of droperidol:

A

Inhibitis dopaminergic receptors in CRTZ

106
Q

Dosage of droperidol:

A

0.625 - 1.25 mg IV

107
Q

A/E of droperidol:

A 
↓ BP
Peripheral α blockade
EPS
Akathesia
Dysphoria
108
Q

Droperidol is black boxed due to:

A

QT prolongation, torsades

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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