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

Exam 4: GI Pharmacology Flashcards

(108 cards)

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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
Examples of H2 antagonists:
Cimetidine (least potent) Nizatidine Ranitidine Famotidine (most potent)
26
Effect of H2 antagonists on gastric emptying/tone:
None
27
Prophylactic dosing of cimetidine before GA induction:
300mg PO/IV 1-2 hours prior
28
Prophylactic dosing of famotidine before GA induction:
20-40 mg PO or 20 mg IV am of surgery
29
Prophylactic dosing of ranitidine before GA induction:
150 mg PO or 50 mg IV
30
Indications for H2 antagonists:
GERD Duodenal ulcer disease Chemoprophylaxis pre-GA
31
Effect of H2 antagonists on gastric pH and volume:
NO effect on pH of gastric fluid already present | Unpredictable effect on volume
32
Chemoprophylaxis for patients allergic to contrast dyes:
H1 and H2 blocker combined
33
PK of H2 antagonists:
Rapid absorption and extensive first-pass effect Cmax: 1-3 hrs (oral) Protein binding: 13-35% E1/2t: 1.5 - 4 hrs
34
H2 antagonists and the BBB:
All cross the BBB!
35
Clearance of H2 antagonists:
Nizatidine: renal | Cimetidine, ranitidine, famotidine: hepatic
36
Clearance of H2 antagonists:
Nizatidine: renal | Cimetidine, ranitidine, famotidine: hepatic
37
IV administration of H2 antagonists:
Rapid administration causes bradycardia and hypotension! Cimetidine & ranitidine over 15-30 minutes Famotidine over 2 minutes
38
Hepatic A/E of H2 antagonists:
Transient elevation in LFTs | Decreases metabolism of hepatic extraction drugs
39
Cimetidine slows metabolism of these drugs:
``` Lidocaine Diazepam Theophylline Propranolol Phenobarb Warfarin Phenytoin ``` Lift the LiD and use TP when you PeWP
40
Three risk factors for PUD:
H. pylori NSAID use Smoking
41
Three goals of PUD therapy:
Reduce gastric acidity Enhance mucosal defenses Eliminate H. pylori
42
Drug classes (4) used to inhibit/neutrailize gastric acid secretion in PUD:
H2 antagonists PPIs Anticholinergics Antacids
43
Drug classes (3) used to protect the gastric mucosa in PUD:
Sucralfate Colloidal bismuth Prostaglandins
44
Drug class used to eradicate H. pylori in PUD:
Antibiotics
45
MoA of PPIs:
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
Examples of PPIs:
All of the -prazoles
47
PK of PPIs:
Rapidly absorbed E1/2t: short Hepatically metabolized Crosses the placenta
48
A/E of PPIs:
``` Headache GI disturbance Nausea Enteric infections Long-term unknown: carcinoid tumor? ```
49
Indications for PPIs:
PUD w/ H. pylori Hemorrhagic ulcers PUD in patient needing NSAIDs
50
Clotting and pH:
Clot formation impaired in acidic environments; PPIs help ulcers clot and heal
51
Example of anticholinergic used for acid reduction:
Dicyclomine
52
Efficacy of dicyclomine:
Less effective than H2 blockers/PPIs
53
MoA of anticholinergics for acid control:
Decrease PSNS production of acid/gastrin-mediated acid production
54
Structure of sucralfate:
Salt of sucrose sulfate and aluminum hydroxide
55
MoA of sucralfate:
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
A/E of sucralfate:
Constipation; little systemic absorption
57
Disadvantages of sucralfate:
Large tablets, frequent administration
58
Drug interactions with sucralfate:
Binds to drugs and impairs their function
59
Colloidal bismuth as PUD therapy:
Coating agent; forms barrier to protect mucosa Stimulates mucosal bicarb and PGE2 Impedes H. pylori growth
60
Misoprostol as PUD therapy:
Prostaglandin analogue that prevents NSAID-induced ulcers Can cause abdo discomfort, diarrhea; contraindicated in pregnancy
61
Triple therapy for H. pylori:
Amoxicillin Clarithromycin PPI
62
Quadruple therapy for H. pylori:
Tetracycline Metronidazole PPI Bismuth
63
Types of antacids:
Aluminum hydroxide Magnesium hydroxide Sodium bicarbonate Calcium carbonate
64
Antacids increase gastric pH to:
> 5
65
Effects of antacids on ulcers:
↑ rate of ulcer healing, duodenal ulcer pain relief
66
A/Es of antacids:
Constipation Diarrhea Electrolyte abnormalities
67
PK of bicitra:
Onset: rapid pH: 8.4 (unpleasant taste)
68
Dosing of bicitra:
15-30ml PO 15-30 minutes pre-op
69
Dosing of bicitra:
15-30ml PO 15-30 minutes pre-op
70
Disadvantage of bicitra:
Increases intragastric volume
71
Effects of prokinetic drugs:
Increases LES tone Accelerates rate of gastric emptying Enhances peristalsis
72
MoA of metoclopramide:
Dopamine antagonist; achieves post-synaptic release of ACh
73
Effects of metoclopramide on stomach:
Kinetic only; pH unchanged ↑ LES tone ↑ gastric/small bowel motility Relaxation of pylorus/duodenum
74
Antagonist for metoclopramide:
Atropine/glyco
75
A/E of metoclopramide:
EPS effects | Prolactin secretion
76
Mechanism of anti-emesis effect of metoclopramide:
Blocks dopamine stimulation of CRTZ
77
PK of metoclopramide:
``` Rapid absorption Onset (IV): 3-5 min Cmax: 40 - 120 min E1/2t: 2 - 4 hrs 40% excreted unchanged renally ```
78
Indications for metoclopramide:
``` ↓ gastric volume Antiemetic Tx of gastroparesis Symptom tx for GERD ? lactation ```
79
Pre-op dosing of metoclopramide:
10 - 20mg IV over 3-5 min 15-30 min pre-induction Fast administration → cramping
80
PONV dosing of metoclopramide:
0.15 mg/kg IV
81
A/E of metoclopramide:
``` Cramping Cardiac dysrhythmias Sedation Dry mouth Dystonic EPS ↑ sedation with CNS depressants May inhibit plasma cholinesterases Akathesia ```
82
Contraindications for metoclopramide:
``` Parkinson's Bowel obstruction Pheochromocytoma Seizure d/o Phenothiazines (promethazine etc) ```
83
Examples of extrapyramidal symptoms:
Oculogyric crisis Trismus Torticollis Akathesia
84
Role of serotonin in the gut:
90% in enterochromaffin cells n the gut; carry pain/nausea impulses
85
Synthesis of serotonin:
5-Hydroxytryptamine (5HT) synthesized from tryptophan
86
Examples of 5HT3 antagonists:
Ondansetron Granisetron Dolasetron Tropisetron
87
MoA of 5HT3 antagonists:
Selective antagonism at GI vagal afferent and CRTZ receptors
88
Types of N/V best suited to 5HT3 antagonist use:
Chemo PONV Hyperemesis gravidarum
89
A/E of 5HT3 antagonists:
Headache with rapid IV push Dysrhythmias Slow clearance in liver disease
90
Dosing of ondansetron:
Adults: 4 - 8mg IV Peds: 0.05 - 0.15 mg/kg IV (up to 4mg)
91
Dosing of granisetron:
Adults: 0.01 - 0.04 mg/kg
92
Dosing of dolasetron:
Adults: 12.5 mg IV
93
Dosing of tropisetron:
5 mg
94
Dosing of dexamethasone for PONV:
4 - 10mg IV
95
Examples of phenothiazines:
Prochlorperzine (Compazine) | Promethazine (Phenergan)
96
MoA of phenothiazines:
Interaction with dopaminergic receptors in CRTZ
97
PK of promethazine:
Onset: 5min Duration: 4 - 6hr E1/2t: 9 - 16hr Hepatic metabolism
98
Contraindications for phenothiazines:
99
Indications for phenothiazines:
Blood transfusion rxn Allergic rxn Sedation PONV
100
Incidence and timing of neurolept malignant syndrome:
0.5 - 1% of patients taking phenothiazines 24 - 72 hrs after dose Usually young men
101
Presentation of neurolept malignant syndrome:
``` Tachy Dysrthymias BP alterations LOC alterations MH-like: muscle rigidity, hyperthermia, rhabdo, ANS instability ```
102
Tx of neurolept malignant syndrome:
Amantadine and Dantrolene
103
MH vs. NMS:
NDMR will produce flaccid paralysis in NMS but not in MH
104
Example of butyrophenones:
Droperidol
105
MoA of droperidol:
Inhibitis dopaminergic receptors in CRTZ
106
Dosage of droperidol:
0.625 - 1.25 mg IV
107
A/E of droperidol:
``` ↓ BP Peripheral α blockade EPS Akathesia Dysphoria ```
108
Droperidol is black boxed due to:
QT prolongation, torsades

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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