Pharm B Test 1 Flashcards
1
Q
What cells release histamine?
A
Mast cells and basophils
2
Q
Does histamine cross the BBB?
A
No
3
Q
What type of response is activated when histamine binds to its receptors?
A
Antigen-antibody response
4
Q
H1 receptor activation causes what muscles to contract?
A
Smooth muscles in the respiratory and GI tract
5
Q
Negative side effects of H1 receptor activation
A
1) Pruritis
2) Sneezing
3) Nitric oxide release by vasculature, causing hypotension
4) Hives
5) Leaky capillaries
6
Q
Main effects from H2 receptor activation
A
1) Increased GI secretion of H+
2) Increased HR and contractility
7
Q
Effects of H3 receptor activation
A
DECREASED histamine synthesis and release
8
Q
Cardiovascular effects from histamine release
A
1) Decreased blood pressure (due to nitric oxide and increased capillary permeability)
2) Increased heart rate and contractility
3) Increased capillary permeability
9
Q
Respiratory effect from histamine release
A
Constriction of bronchial smooth muscle
10
Q
GI effects from histamine release
A
Increased gastric acid secretion
11
Q
Dermal effects of histamine release
A
Flare and wheal response (hives)
12
Q
Histamine is a mediator of what immunological reaction?
A
Type I hypersensitivity reaction
13
Q
Which histamine receptor can be activated even with low concentrations of histamine?
A
H1
14
Q
How does H1 activation affect the AV node?
A
Decreased AV node conduction
15
Q
How does H1 activation affect the coronary arteries?
A
Causes them to vasoconstrict
16
Q
Which histamine receptor creates an aspiration risk when activated?
A
H2 - due to the increased gastric H+ secretion in the stomach
17
Q
Activation of which histamine receptor causes a catecholamine release?
A
H2
18
Q
How does H2 receptor activation affect the coronary arteries?
A
Causes them to vasodilate
19
Q
Which negative side effects from histamine release are blocked by histamine antagonists?
A
Edema and pruritis
20
Q
Which negative side effect of histamine release is NOT blocked by histamine antagonists?
A
Hypotension
21
Q
How do histamine receptor antagonists inhibit histamine effects?
A
They competitively block the activation of receptors, but do not block the release of histamine
22
Q
Other than H1 receptors, what other receptors are activated by 1st generation H1 blockers?
A
- Muscarinic
- Serotonin
- Alpha
23
Q
Do 1st generation H1 blockers cross the BBB?
A
Yes
24
Q
Negative side effects of 1st generation H1 blockers
A
1) Sedation
2) Dry mouth
3) Blurred vison
4) Urinary retention
5) Impotence
6) Tachycardia
7) Dysrhythmias
25
Which generation of H1 blockers becomes non-competitive at higher doses?
Second generation
26
Do 2nd generation H1 blockers cause sedation?
Maybe some - but MUCH less than first generation
27
Examples of 1st generation H1 blockers (3)
- Diphenhydramine (Benadryl)
- Dramamine
- Promethazine (Phenergan)
28
How does Dramamine work?
It crosses the BBB and works on the auditory vestibular area of the brain to inhibit motion induced N/V
29
Examples of 2nd generation H1 blockers (2)
- Loratadine (Claratin)
| - Fexofenadine (Allegra)
30
Negative side effect of 2nd generation H1 blockers
QT prolongation at high doses
31
Clinical uses of H1 blockers
- Rhinoconjunctivitis
- Bronchospasm (prophylactic treatment)
- Allergic reactions
- Motion sickness
32
Function of H2 blockers
Inhibit gastric acid secretion
33
Examples of H2 blockers (4)
- Cimetidine (Tagamet)
- Ranitidine (Zantac)
- Famotidine (Pepcid)
- Nizatidine (Axid)
34
List potency of H2 blockers from least to most potent
Cimetidine (1) --> Ranitidine=Nizatidine (10) --> Famotidine (Pepcid) (50)
35
What is the only H2 blocker administered intravenously?
Famotidine (Pepcid)
36
Pharmacokinetics of H2 blockers
Rapid oral absorption with extensive first-pass metabolism
37
How do H2 blockers affect the brain and placenta?
They can cross both the brain and placenta but they're aren't H2 receptors in the brain so there is little effect, and the baby is not harmed by H2 blockers
38
In which patients should you consider decreasing the dose of H2 blockers?
- Renal dysfunction because some H2 blockers are excreted by the kidneys
- Elderly because they have decreased blood flow to the liver and increased volume of distribution
39
Clinical uses of H2 blockers
- Treatment of duodenal ulcers
- Allergy prophylaxis (contrast dye)
- Pre-op medication for aspiration prophylaxis
40
Negative side effects of H2 blockers
- Diarrhea (most common)
- Headache
- Susceptibility to H. pyloria
41
Risk factors for side effects of H2 blockers
- Chronic users of H2 blockers
| - Elderly
42
How does Cimetidine (H2 blocker) affect the metabolism of other drugs?
It inhibits the cytochrome p450 system so it can cause a prolonged response to drugs that are metabolized by p450
43
What is the concern with having a long term epidural in a patient on chronic Cimetidine?
We would worry about LAST because lidocaine is metabolized by cytochrome p450 which is inhibited by Cimetidine
44
What is Cromolyn?
A mast cell stabilizer that works in the lungs to inhibit antigen induced release of histamine
45
How is Cromolyn administered?
Via inhalation
46
How is Cromolyn used clinically?
As prophylaxis for bronchial asthma
47
MOA of proton pump inhibitors
Inhibits proton pumps in the stomach and cause prolonged inhibition of gastric acid secretion
48
Examples of proton pump inhibitors (3)
1) Omeprazole (Prilosec)
2) Protonix
3) Prevacid (Lansoprazole)
49
When should proton pump inhibitors be administered as a pre-op medication?
At least 3 hours prior to surgery because it only works prophylactically, does not treat what is already in the stomach
50
Gastric effects of proton pump inhibitors
- Can increase gastric fluid pH (since it inhibits H+ release)
- Can decrease gastric fluid volume
51
Where in the body is serotonin found?
1) Enterchromaffin cells of GI tract (90%)
2) CNS
3) Platelets
52
Which serotonin receptor causes gastrokinetic effects?
5-HT4
53
Which serotonin receptor causes drug-induced N/V?
5-HT3
54
Which serotonin receptor causes cerebral vasoconstriction?
5-HT1
55
Common 5HT1 agonist and its clinical use
Sumatriptan - used to improve migraine and cluster headaches
56
Where is serotonin receptor 5-HT3 located?
In the brain
57
Examples of 5-HT3 antagonists
- Ondansetron
- Tropisetron
- Dolasetron
- Granisetron
58
Side effects of Zofran
- Headache
- Diarrhea
- Increased liver enzymes
59
Action of antacids
Bind H+ ions in the gut to neutralize the acidity
60
Do antacids need to be administered prophylactically?
No - they work on what is already in the gut
61
Trade name of the antacid Sodium Bicarbonate
Tums
62
What can be caused by an excess of sodium bicarbonate (Tums)?
Alkalosis which can affect the absorption of other drugs in the gut
63
Trade name of the antacid Magnesium Hydroxide
Milk of Magnesia
64
What can be caused by high doses of Magnesium Hydroxide
Hypermagnesemia which can cause muscle weakness
65
Which antacid can cause acid rebound
Calcium Carbonate
66
Side effects of Calcium Carbonate (antacid) with chronic use
- Metabolic alkalosis
| - Hypercalcemia
67
Side effects of Aluminum Hydroxide (antacid)
- Phosphate depletion
| - Decreased gastric emptying
68
Which non-particulate antacid is given pre-op to neutralize stomach acid?
Bicitra
69
What is Sucralfate?
Anti-ulcer drug that coats the stomach to protect it from acid and its used to treat duodenal or gastric ulcers
70
Function of Prokinetics
Increase gastric emptying thus decreasing the volume in the stomach
71
Clinically useful Prokinetics (4)
- Metoclopramide (Reglan)
- Domperiodone
- Cisapride
- Erythromycin
72
Clinical effects of Metoclopramide (Reglan)
- Increased gastric emptying
- Increases lower esophageal tone
- Relaxes pylorus and duodenum
73
Metoclopramide (Reglan) is an antagonist to which neurotransmitter? What side effects stem from this?
Dopamine antagonist - may cause sedation, agitation, dysphoria
74
Metoclopramide (Reglan) is completely contraindicated in which patients?
Patients with Parkinson's -- because it is a dopamine antagonist
75
Pharmacokinetics of Metoclopramide (Reglan)
- Oral absorption
| - Renal elimination
76
Clinical uses of Metoclopramide (Reglan)
- Antiemetic
- Gastroparesis therapy
- GERD
77
What patients need Metoclopramide (Reglan) prior to surgery?
- Full stomach
- Trauma
- Obese
- Diabetic
- Parturient
78
What patients should not be given Metoclopramide (Reglan)?
- Parkinsons
- Patients with SBO
- Patients with acute gut injury
79
Most common side effects of Metoclopramide (Reglan)
- Dry mouth
- Abdominal cramping
- Dysrhythmias
- Extrapyramidal effects
80
Rare side effects of Metoclopramide (Reglan)
- Hirsuitism (excessive hairiness)
| - Maculopapular rash
81
Pituitary side effects of Metoclopramide (Reglan) due to prolactin association
- Breast enlargement
| - Menstrual irregularities
82
Clinical effects of Domperidone (Motilyium)
- Stimulates peristalsis
- Increases LES tone
- Increases gastric emptying
83
Which prokinetic is safe for patients with Parkinson's?
Cisapride because it does not work on dopamine receptors
84
Glucocorticoid and dose used as an antiemetic
4mg dexamethasone
85
What butyrophenone + dopamine antagonist is used as an antiemetic? What is the dose?
0.625mg Droperidol
86
Black box warning for Droperidol
QT prolongation leading to Torsades de Pointes at high doses of 12-25mg
87
Anticholinergic used as a pre-op antiemetic
Scopolamine
88
NK1 antagonist given orally in pre-op for PONV
Aprepitant (Emend)
89
Dose of Reglan (Metoclopramide)
10mg (0.15mg/kg)
90
MOA of thiazide diuretics
Inhibit Na+ and Cl- reabsorption at Ascending Loop of Henle, so it increases the excretion of these ions from the body
91
What metabolic condition can be caused from thiazide diuretics?
Metabolic alkalosis -- because Na+ can still get reabsorbed at the collecting duct in exchange for K+ and H+ secretion from the body
92
What ion imbalance can be caused by thiazide diuretics?
Hypokalemia (due to Na+/K+ exchange at collecting duct)
93
Which thiazide diuretic is a first line treatment for hypertension?
Hydrochlorothiazide
94
Clinical uses for thiazide diuretics
- Essential HTN
- Heart failure
- Diabetes Insipidus
- Hypercalcemia
95
What causes thiazides' antihypertensive effects
- Initially they cause a decrease in extracellular fluid volume, which causes a decrease in cardiac output
- Long term, they cause peripheral vasodilation due to prostaglandin
96
Metabolic side effect of thiazides
Hypokalemic, hypochloremic metabolic alkalosis
97
General side effects of thiazides
- Cardiac dysrhythmias
- Hypovolemia
- Orthostatic hypotension
- Hyperglycemia
- Hyperuricemia
- Renal/hepatic failure
- Allergic reactions
98
Patients with what allergy are at risk for an allergic reaction to thiazides?
Sulfa
99
How do loop diuretics work
Inhibit reabsorption of many ions in the medullary portion of the ascending loop of Henle (K+, Ca2+, Mg2+, Na+)
100
Examples of loop diuretics
- Furosemide (Lasix)
| - Ethacrynic acid
101
Clinical uses of loop diuretics
- Mobilization of edema (CHF, pulmonary edema)
- Treatment of ICP
- Differential diagnosis of oliguria (low urine output)
102
What metabolic syndrome can be caused by loop diuretics?
Hypokalemic metabolic alkalosis
103
Side effects of loop diuretics
- Hypokalemia
- Increased chance of digitalis toxicity
- Hyperuicemia
- Aminoglycoside toxicity
104
Loop diuretics can potentiate the effects of what class of drugs due to the decrease in Ca2+ concentration?
Neuromuscular blockers
105
Loop diuretics can cause toxicity from what antibiotic?
Gentamycin (aminoglycoside)
106
Loop diuretics have cross reactivity with what other drugs
Sulfa drugs
107
What is the major osmotic diuretic currently used?
Mannitol
108
Characteristics of osmotic diuretics (mannitol)
They are freely filterable at the glomerulus and undergo limited reabsorption - "pharmacologically inert"
109
MOA of osmotic diuretics (mannitol)
Prevent water reabsorption at proximal tubule and descending loop of Henle by increasing the osmolarity of renal tubular fluid and plasma
110
Clinical uses of osmotic diuretics
- Prophylaxis against renal failure
- Given before clamping of major vessels in cardiac surgeries such as AAA for renal protection
- Differential diagnosis of oliguria
- Treatment of increased ICP
- Reduction in intraocular pressure (glaucoma)
111
Dose of mannitol used to treat increased ICP
0.25-1g/kg bolus
112
How is mannitol usually supplied
20%
113
How should mannitol be administered?
Slowly to avoid rapid shifts in volume and demyelination
114
What patients should you NOT give mannitol to?
Patients with CHF
115
Side effects of osmotic diuretics
- Pulmonary edema
- Hypovolemia
- Electrolyte imbalance
- Plasma hyperosmolarity
116
Examples of K+ sparing diuretics
- Triamterene
| - Amiloride
117
MOA of K+ sparing diuretics
- Inhibit Na+ influx in the luminal membrane
| - Inhibit Na+ reabsorption and prevent K+ secretion in collecting tubules
118
Clinical uses of K+ sparing diuretics
Used when Lasix and other diuretics cause hypokalemia
119
Side effects of K+ sparing diuretics
Hyperkalemia
120
Aldosterone antagonist used as a diuretic
Spironolactone
121
Clinical uses for aldosterone antagonists (Spironolactone)
Hypertension
122
Side effects of aldosterone antagonists (Spironolactone)
- Hyponatremia
| - Hyperkalemia
123
MOA of Spironolactone
Inhibits NaCl reabsorption in cortical portion of collecting tubule
124
Carbonic anhydrase inhibitor used as a diuretic
Acetazolamide (Diamox)
125
MOA of Acetazolamide (CA inhibitor)
Inhibits reabsorption of sodium bicarb at the proximal tubule
126
Side effects of Acetazolamide (CA inhibitor)
- Hyperchloremic metabolic acidosis
| - Potassium wasting
127
Clinical uses for Acetazolamide (CA inhibitor)
- Altitude sickness (decreases pH of CSF and stimulates hyperventilation)
- Eye cases (stimulates hyperventilation and decreases CBF)
128
Urea works as which type of diuretic
Osmotic diuretic
129
2 main components of blood pressure
1) Cardiac output
| 2) Systemic vascular resistance
130
How do inotropes work to increase blood pressure
Improve contractility thus increase cardiac output
131
How do vasopressors work to increase blood pressure
Increase SVR
132
Basic physiology of heart muscle contraction
Calcium binds to troponin which causes tropomyosin to shift and allows myosin to interact with actin and form a cross-bridge
133
Basic physiology of calcium release in myocytes
Action potential travels down the cell and down into T-tubules. This causes a small amount of Ca2+ to enter the sarcoplasmic reticulum which leads to a large release of Ca2+ from the SR
134
What regulates the release of Ca2+ from the sarcoplasmic reticulum
Ryanodine receptors located on non-voltage dependent Ca2+ channels
135
What pumps calcium back into the sarcoplasmic reticulum during relaxation
ATPase
136
What pumps Ca2+ out of the cell
Na/K+ ATPase and Na+/Ca2+ exchange
137
What is inotropy dependent on
The quantity of intracellular Ca2+ in the cell
138
What is chronotropy dependent on
The rate of Ca2+ delivery
139
What is lusitropy dependent on
The rate of removal of Ca2+
140
What molecule is an important second messenger for calcium release
Cyclic AMP
141
Which classes of medications increase contractility by increasing cAMP
- Beta agonists (stimulate adenylate cyclase)
| - Phosphodiesterase inhibitors (prevent cAMP breakdown)
142
What are our primary drug choices for activating beta receptors (beta agonists)
Catecholamines...(DINE)
- Dobutamine
- Isoproteronol
- Norepi
- Epi
143
CV effects of B1 activation
- Increased chronotropy
| - Increased inotropy
144
CV effects of B2 activation
- Smooth muscle vasodilation (bronchial, vessels)
| - Increased inotropy
145
What is the strongest beta agonist available with virtually no alpha effects
Isoproteronol
146
Which adrenergic receptor inhibits norepinephrine release
Alpha 2
147
Adrenergic receptors activated by norepi
A1, B1
148
Infusion rate for norepi in mcg/min
1-20mcg/min
149
Adrenergic receptors activated by dopamine
A1, B1, B2
150
Infusion rate for dopamine in mcg/kg/min
2-20mcg/kg/min
151
Adrenergic receptors activated by epinephrine
A1, B1, B2
152
Infusion rate for epinephrine in mcg/min
1-20mcg/min
153
Adrenergic receptors activated by dobutamine
B1, B2, A1
154
Infusion rate of dobutamine in mcg/kg/min
2-10mcg/kg/min
155
Adverse effects of norepinephrine
Can decrease cardiac output because of the intense vasoconstriction caused by a1 activation
156
Adverse effect of epinephrine
Arrythmogenic
157
Adverse effect of dopamine
Largely increase acting, causes the release of norepi
158
Adverse effect of dobutamine
Tachycardia
159
Adverse effects of isoproterenol
- Significant tachycardia
- Arrhythmias
- Decreased SVR
160
Function of phosphodiesterases (PDEs)
Breakdown cyclic nucleotides cAMP and cGMP
161
Function/location of PDE1
Smooth muscle cells, regulate proliferation in vascular tissue
162
Location of PDE3
- CV system and platelets
| - Adipose/liver (type B)
163
Function/location of PDE4
Inflammatory cells, may play a role in COPD/arthritis
164
Location of PDE5
Corpus cavernosum of penis
165
Which PDE family is activated by insulin
PDE3
166
MOA of phosphodiesterase 3 inhibitors in cardiac myocytes
Increase cAMP thus increasing Ca2+ and contractility
167
MOA of phosphodiesterase 3 inhibitors in vascular tissues
Increase cGMP which causes smooth muscle relaxation - decreasing SVR and PA pressures
168
Common PDE III inhibitors
- Amrinone
- Milrinone
- Enoximone
169
Loading dose of Amrinone
1mg/kg
170
Infusion rate of Amrinone
2-10mcg/kg/min
171
Loading dose of Milrinone
0.05mg/kg
172
Onset time for a loading dose of Milrinone
5 minutes
173
Duration of a loading dose of Milrinone
30 minutes
174
Infusion rate for Milrinone
0.5mcg/kg/min
175
Onset time for an infusion of Milrinone
About an hour
176
Loading dose of Enoximone
0.5mg/kg
177
Infusion rate of Enoximone
10mcg/kg/min
178
1st line inotrope
Norepinephrine
179
Which class of vasopressors don't use the CNS?
Non-catecholamine non-sympathathomimetics
180
What is the second messenger for alpha activation on vasculature?
IP3
181
Activation of alpha1 receptors result in what?
Increase in Ca2+ and smooth muscle contraction in systemic and pulmonary vasculature
182
List the catecholamines in order of greatest to least alpha1 activation
Norepi, dopamine=epi, dobutamine (isoproteronol has none)
183
How can you alter the doses of catecholamines to get a greater alpha effect?
Increase the doses
184
Examples of non-catecholamine sympathomimetics that are pure, direct acting alpha agonists
- Phenylephrine
| - Methoxamine
185
Onset of phenylephrine
30 seconds
186
Duration of phenylephrine
2-3 minutes
187
Infusion rate of phenylephrine in mcg/min
25-100
188
Bolus dose of Methoxamine
5-10mg
189
Onset of Methoxamine
1 minute
190
Duration of Methoxamine
5-10 minutes
191
MOA of ephedrine
Indirect acting, causes release of NE from neurons and has a little beta activation
192
What liver enzyme inactivates ephedrine
MAO
193
Why will patients in heart failure not be affected by ephedrine
Because they are catecholamine depleted
194
What prescribed medications can cause an exaggerated effect of ephedrine?
MAO inhibitors for depression because the ephedrine won't be inactivated
195
Which vasopressor has minimal effect on uterine vascular resistance?
Ephedrine
196
What is the main non-sympathomimetic vasopressor
Vasopressin
197
MOA of vasopressin
Activates V1 receptors which increases Ca2+ and causes smooth muscle contraction
198
Effect of vasopressin receptor V2 activation
Increased water permeability at the kidneys and increased urination
199
Effect of vasopressin receptor V3 activation
Increased ACTH release via actions at the pituitary gland
200
How do the levels of AVP change over time in patients in sepsis and on CPB
Onset causes AVP levels to rise by 2-3x then as time goes on, levels drop to 1/3 of the normal levels
201
Infusion rate of vasopressin in units/hr
4-6 units/hr
202
Side effects of vasopressin
Side effects are related to intense vasoconstriction
1) Myocardial ischemia
2) Decreased cardiac output
3) Mesenteric ischemia
4) Digital necrosis
203
Vasopressin is thought to have less of an effect on which vasculature area? How would this be clinically relevant?
Thought to have less of an effect on pulmonary vasculature, could be beneficial in patients with pulmonary hypertension
204
What are "calcium mobilizers"?
Drugs that cause an increase in Ca2+ influx leading to increased contractility (i.e. catecholamines and PDE inhibitors)
205
What are "calcium sensitizers"
Drugs that work on the interaction of troponin/Ca2+ or the response of myofilaments to Ca2+ binding - don't cause an increase in Ca2+ levels, but decrease the amount of Ca2+ needed to get the desired effect
206
Advantages of calcium sensitizers
- Less arrythmogenic
| - Don't increase O2 consumption
207
Current Ca2+ sensitizers available
- Pimobendan
| - Levosimendan
208
Clinical use of Pimobendan
Oral Ca2+ sensitizer used for long term treatment of CHF
209
MOA of Levosimendan
Binds to troponin C and stabilizes the troponin/Ca2+ conformational change
210
What drug is used as a rescue measure due to its role in treating refractory vasodilatation
Methylene blue
211
Under what circumstances may methylene blue be used to treat refractory dilatation
- MAP below 50mmHg
| - Norepi infusion over 35mcg/min
212
MOA of methylene blue for treatment of refractory vasodilatation
Decreases cGMP which leads to less vasodilation
213
Bolus dose of methylene blue
1.5-2mg/kg
214
How should methylene blue be administered
Given over 10-60 minutes
215
Side effects of methylene blue
- Transient decrease in SpO2 monitoring
| - Mild skin/urine discoloration
216
What can result from high doses of methylene blue
- Hyperbilirubinemia
| - Hemolytic anemia
217
Top 5 patient risk factors for PONV
1. Female
2. History of PONV
3. Non-smoker
4. Motion sickness
5. Age under 50
218
Top 4 surgical risk factors for PONV
1. Cholecystectomy
2. Laparoscopic procedures
3. Gynecologic
4. Long length of procedure
219
Prophylactic PONV agents to consider prior to surgery
1) Transdermal scopolamine
2) NK-1 antagonists
3) Midazolam
220
What is the priming dose contained in the layer closest to the skin of the scopolamine patch
140mcg
221
Onset time of the scopolamine patch
2-4 hours
222
Side effects of scopolamine patch
- Visual disturbances
- Dry mouth
- Confusion
223
NK-1 antagonists used for PONV
- Aprepitant
- Rolapitant
- Casopitant
224
What drug may be useful for patients who have complained of getting sick once they get home from their surgery
Aprepitant because it has a long 9-13 hour half life
225
Dose of Aprepitant comparable to 4mg Zofran
40mg
226
In which patients should you use caution when considering Aprepitant?
1) Hepatic failure patients (Aprepitant is metabolized by CYP450)
2) Patients on hormonal birth control
3) Patients on warfarin
4) Patients on Cisapride, Pimozidine
227
Patients on hormonal birth control should use back-up birth control for how long after taking Aprepitant?
30 days
228
Dosing range of midazolam useful for PONV
0.05-0.075mg/kg
229
Regional anesthesia is __ times less likely to cause PONV than general anesthesia
9
230
There is a very very low risk of PONV when using nitrous for less than...
1 hour
231
PONV is very likely when running nitrous for longer than...
2 hours
232
When have opioids been found to increase risk of PONV?
When it is given post-operatively
233
Why is IV acetaminophen thought to decrease PONV?
It reduces pain scores which decreases chance of PONV
234
When must IV acetaminophen be administered to reduce the incidence of PONV?
Intra-operatively or immediately post-operatively
235
There is evidence that 8mg of Zofran may be useful for which patients
Patients with a history of PONV
236
Dose of Granisetron equivalent to 4mg Zofran
0.3-3mg IV
237
MOA of Palonosetron
Allosteric binder that changes the conformation of the receptor so serotonin cannot bind
238
Dose of Palonosetron for PONV
0.075mg IV
239
Current recommended dose of Decadron for PONV
4-5mg
240
Only case found to benefit from 8mg of Decadron for PONV
Lap chole
241
Disadvantages of high doses of Decadron
- Suppression of HPA axis
| - Increased chance of wound infection
242
What dose of Metoclopramide is equivalent to 4mg of Zofran to treat early nausea
25-30mg
243
What dose of Metoclopramide is equivalent to 4mg of Zofran to treat late nausea
50mg
244
Risk of giving 25-50mg of Metoclopramide
Extrapyramidal symptoms
245
Recommendations for PONV prophylaxis for low risk patients with 0 risk factors
No prophylaxis
246
Recommendations for PONV prophylaxis for medium risk patients with 1 risk factor
1 PONV agent
247
Recommendations for PONV prophylaxis for moderate risk patients with 2-3 risk factors
2-3 PONV agents
248
Recommendations for PONV prophylaxis for high patients with 4+ risk factors
3-4 agents +/- TIVA
249
MOA of Droperidol/Haldol as PONV agents
Anti-dopaminergic action at the chemoreceptor trigger zone
250
How should Droperidol be administered for PONV treatment
0.625-1.25mg at the end of surgery
251
Black box warning for Droperidol
QT prolongation and serious arrhythmias (e.g. Torsades)
252
It is strongly advised that your patient must have what test before having Droperidol?
12 lead ECG
253
Guidelines for ECG monitoring after administration of Droperidol
ECG monitoring for 2-3 hours after administration
254
Dose giving Zofran and Droperidol together have additive effects on the risk of QT prolongation?
No
255
Dose of Haloperidol for PONV prophylaxis and rescue
0.5-2mg IM or IV
256
Risk of Haloperidol at a 4mg dose
Extrapyramidal symptoms
257
Dose of Dimenhydrinate (Dramamine) for PONV
1mg/kg IV
258
Side effects of Promethazine at higher doses
- Confusion
- Sedation
- Akasthesia
- Tardive dyskinesia
259
Rare but morbid side effects of Promethazine
- Neuroleptic Malignant Syndrome
- Tissue necrosis
- Seizures
260
2 black box warnings for Promethazine
- Tissue necrosis
| - Don't give to patients under 2 years old due to respiratory depression
261
Dose of Promethazine for PONV
6.25mg IV
262
Dose of propofol as rescue PONV drug
20mg doses
263
Dose of benadryl as rescue PONV drug
6.25-12.5mg IV
264
Dose of Haldol as rescue PONV drug
1mg IV
265
Dose of Zofran as PONV rescue drug
1mg IV
266
Dose of Droperidol as PONV rescue drug
0.625mg IV
