Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Pharm B Test 1 > Flashcards

Pharm B Test 1 Flashcards

1
Q

What cells release histamine?

A

Mast cells and basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Does histamine cross the BBB?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of response is activated when histamine binds to its receptors?

A

Antigen-antibody response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

H1 receptor activation causes what muscles to contract?

A

Smooth muscles in the respiratory and GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Main effects from H2 receptor activation

A

1) Increased GI secretion of H+

2) Increased HR and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Effects of H3 receptor activation

A

DECREASED histamine synthesis and release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Respiratory effect from histamine release

A

Constriction of bronchial smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

GI effects from histamine release

A

Increased gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dermal effects of histamine release

A

Flare and wheal response (hives)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Histamine is a mediator of what immunological reaction?

A

Type I hypersensitivity reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which histamine receptor can be activated even with low concentrations of histamine?

A

H1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does H1 activation affect the AV node?

A

Decreased AV node conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does H1 activation affect the coronary arteries?

A

Causes them to vasoconstrict

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which histamine receptor creates an aspiration risk when activated?

A

H2 - due to the increased gastric H+ secretion in the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Activation of which histamine receptor causes a catecholamine release?

A

H2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does H2 receptor activation affect the coronary arteries?

A

Causes them to vasodilate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which negative side effects from histamine release are blocked by histamine antagonists?

A

Edema and pruritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which negative side effect of histamine release is NOT blocked by histamine antagonists?

A

Hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Other than H1 receptors, what other receptors are activated by 1st generation H1 blockers?

A
  • Muscarinic
  • Serotonin
  • Alpha
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Do 1st generation H1 blockers cross the BBB?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which generation of H1 blockers becomes non-competitive at higher doses?

A

Second generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Do 2nd generation H1 blockers cause sedation?

A

Maybe some - but MUCH less than first generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Examples of 1st generation H1 blockers (3)

A
  • Diphenhydramine (Benadryl)
  • Dramamine
  • Promethazine (Phenergan)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does Dramamine work?

A

It crosses the BBB and works on the auditory vestibular area of the brain to inhibit motion induced N/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Examples of 2nd generation H1 blockers (2)

A
  • Loratadine (Claratin)

- Fexofenadine (Allegra)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Negative side effect of 2nd generation H1 blockers

A

QT prolongation at high doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical uses of H1 blockers

A
  • Rhinoconjunctivitis
  • Bronchospasm (prophylactic treatment)
  • Allergic reactions
  • Motion sickness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Function of H2 blockers

A

Inhibit gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Examples of H2 blockers (4)

A
  • Cimetidine (Tagamet)
  • Ranitidine (Zantac)
  • Famotidine (Pepcid)
  • Nizatidine (Axid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

List potency of H2 blockers from least to most potent

A

Cimetidine (1) –> Ranitidine=Nizatidine (10) –> Famotidine (Pepcid) (50)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the only H2 blocker administered intravenously?

A

Famotidine (Pepcid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pharmacokinetics of H2 blockers

A

Rapid oral absorption with extensive first-pass metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do H2 blockers affect the brain and placenta?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

In which patients should you consider decreasing the dose of H2 blockers?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Clinical uses of H2 blockers

A
  • Treatment of duodenal ulcers
  • Allergy prophylaxis (contrast dye)
  • Pre-op medication for aspiration prophylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Negative side effects of H2 blockers

A
  • Diarrhea (most common)
  • Headache
  • Susceptibility to H. pyloria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Risk factors for side effects of H2 blockers

A
  • Chronic users of H2 blockers

- Elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does Cimetidine (H2 blocker) affect the metabolism of other drugs?

A

It inhibits the cytochrome p450 system so it can cause a prolonged response to drugs that are metabolized by p450

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the concern with having a long term epidural in a patient on chronic Cimetidine?

A

We would worry about LAST because lidocaine is metabolized by cytochrome p450 which is inhibited by Cimetidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is Cromolyn?

A

A mast cell stabilizer that works in the lungs to inhibit antigen induced release of histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How is Cromolyn administered?

A

Via inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is Cromolyn used clinically?

A

As prophylaxis for bronchial asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

MOA of proton pump inhibitors

A

Inhibits proton pumps in the stomach and cause prolonged inhibition of gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Examples of proton pump inhibitors (3)

A

1) Omeprazole (Prilosec)
2) Protonix
3) Prevacid (Lansoprazole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

When should proton pump inhibitors be administered as a pre-op medication?

A

At least 3 hours prior to surgery because it only works prophylactically, does not treat what is already in the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Gastric effects of proton pump inhibitors

A
  • Can increase gastric fluid pH (since it inhibits H+ release)
  • Can decrease gastric fluid volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where in the body is serotonin found?

A

1) Enterchromaffin cells of GI tract (90%)
2) CNS
3) Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which serotonin receptor causes gastrokinetic effects?

A

5-HT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Which serotonin receptor causes drug-induced N/V?

A

5-HT3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Which serotonin receptor causes cerebral vasoconstriction?

A

5-HT1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Common 5HT1 agonist and its clinical use

A

Sumatriptan - used to improve migraine and cluster headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Where is serotonin receptor 5-HT3 located?

A

In the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Examples of 5-HT3 antagonists

A
  • Ondansetron
  • Tropisetron
  • Dolasetron
  • Granisetron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Side effects of Zofran

A
  • Headache
  • Diarrhea
  • Increased liver enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Action of antacids

A

Bind H+ ions in the gut to neutralize the acidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Do antacids need to be administered prophylactically?

A

No - they work on what is already in the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Trade name of the antacid Sodium Bicarbonate

A

Tums

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What can be caused by an excess of sodium bicarbonate (Tums)?

A

Alkalosis which can affect the absorption of other drugs in the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Trade name of the antacid Magnesium Hydroxide

A

Milk of Magnesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What can be caused by high doses of Magnesium Hydroxide

A

Hypermagnesemia which can cause muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Which antacid can cause acid rebound

A

Calcium Carbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Side effects of Calcium Carbonate (antacid) with chronic use

A
  • Metabolic alkalosis

- Hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Side effects of Aluminum Hydroxide (antacid)

A
  • Phosphate depletion

- Decreased gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Which non-particulate antacid is given pre-op to neutralize stomach acid?

A

Bicitra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is Sucralfate?

A

Anti-ulcer drug that coats the stomach to protect it from acid and its used to treat duodenal or gastric ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Function of Prokinetics

A

Increase gastric emptying thus decreasing the volume in the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Clinically useful Prokinetics (4)

A
  • Metoclopramide (Reglan)
  • Domperiodone
  • Cisapride
  • Erythromycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Clinical effects of Metoclopramide (Reglan)

A
  • Increased gastric emptying
  • Increases lower esophageal tone
  • Relaxes pylorus and duodenum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Metoclopramide (Reglan) is an antagonist to which neurotransmitter? What side effects stem from this?

A

Dopamine antagonist - may cause sedation, agitation, dysphoria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Metoclopramide (Reglan) is completely contraindicated in which patients?

A

Patients with Parkinson’s – because it is a dopamine antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Pharmacokinetics of Metoclopramide (Reglan)

A
  • Oral absorption

- Renal elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Clinical uses of Metoclopramide (Reglan)

A
  • Antiemetic
  • Gastroparesis therapy
  • GERD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What patients need Metoclopramide (Reglan) prior to surgery?

A
  • Full stomach
  • Trauma
  • Obese
  • Diabetic
  • Parturient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What patients should not be given Metoclopramide (Reglan)?

A
  • Parkinsons
  • Patients with SBO
  • Patients with acute gut injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Most common side effects of Metoclopramide (Reglan)

A
  • Dry mouth
  • Abdominal cramping
  • Dysrhythmias
  • Extrapyramidal effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Rare side effects of Metoclopramide (Reglan)

A
  • Hirsuitism (excessive hairiness)

- Maculopapular rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Pituitary side effects of Metoclopramide (Reglan) due to prolactin association

A
  • Breast enlargement

- Menstrual irregularities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Clinical effects of Domperidone (Motilyium)

A
  • Stimulates peristalsis
  • Increases LES tone
  • Increases gastric emptying
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Which prokinetic is safe for patients with Parkinson’s?

A

Cisapride because it does not work on dopamine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Glucocorticoid and dose used as an antiemetic

A

4mg dexamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What butyrophenone + dopamine antagonist is used as an antiemetic? What is the dose?

A

0.625mg Droperidol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Black box warning for Droperidol

A

QT prolongation leading to Torsades de Pointes at high doses of 12-25mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Anticholinergic used as a pre-op antiemetic

A

Scopolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

NK1 antagonist given orally in pre-op for PONV

A

Aprepitant (Emend)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Dose of Reglan (Metoclopramide)

A

10mg (0.15mg/kg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

MOA of thiazide diuretics

A

Inhibit Na+ and Cl- reabsorption at Ascending Loop of Henle, so it increases the excretion of these ions from the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What metabolic condition can be caused from thiazide diuretics?

A

Metabolic alkalosis – because Na+ can still get reabsorbed at the collecting duct in exchange for K+ and H+ secretion from the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What ion imbalance can be caused by thiazide diuretics?

A

Hypokalemia (due to Na+/K+ exchange at collecting duct)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Which thiazide diuretic is a first line treatment for hypertension?

A

Hydrochlorothiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Clinical uses for thiazide diuretics

A
  • Essential HTN
  • Heart failure
  • Diabetes Insipidus
  • Hypercalcemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What causes thiazides’ antihypertensive effects

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Metabolic side effect of thiazides

A

Hypokalemic, hypochloremic metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

General side effects of thiazides

A
  • Cardiac dysrhythmias
  • Hypovolemia
  • Orthostatic hypotension
  • Hyperglycemia
  • Hyperuricemia
  • Renal/hepatic failure
  • Allergic reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Patients with what allergy are at risk for an allergic reaction to thiazides?

A

Sulfa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

How do loop diuretics work

A

Inhibit reabsorption of many ions in the medullary portion of the ascending loop of Henle (K+, Ca2+, Mg2+, Na+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Examples of loop diuretics

A
  • Furosemide (Lasix)

- Ethacrynic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Clinical uses of loop diuretics

A
  • Mobilization of edema (CHF, pulmonary edema)
  • Treatment of ICP
  • Differential diagnosis of oliguria (low urine output)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What metabolic syndrome can be caused by loop diuretics?

A

Hypokalemic metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Side effects of loop diuretics

A
  • Hypokalemia
  • Increased chance of digitalis toxicity
  • Hyperuicemia
  • Aminoglycoside toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Loop diuretics can potentiate the effects of what class of drugs due to the decrease in Ca2+ concentration?

A

Neuromuscular blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Loop diuretics can cause toxicity from what antibiotic?

A

Gentamycin (aminoglycoside)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Loop diuretics have cross reactivity with what other drugs

A

Sulfa drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is the major osmotic diuretic currently used?

A

Mannitol

108
Q

Characteristics of osmotic diuretics (mannitol)

A

They are freely filterable at the glomerulus and undergo limited reabsorption - “pharmacologically inert”

109
Q

MOA of osmotic diuretics (mannitol)

A

Prevent water reabsorption at proximal tubule and descending loop of Henle by increasing the osmolarity of renal tubular fluid and plasma

110
Q

Clinical uses of osmotic diuretics

A
  • 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
Q

Dose of mannitol used to treat increased ICP

A

0.25-1g/kg bolus

112
Q

How is mannitol usually supplied

A

20%

113
Q

How should mannitol be administered?

A

Slowly to avoid rapid shifts in volume and demyelination

114
Q

What patients should you NOT give mannitol to?

A

Patients with CHF

115
Q

Side effects of osmotic diuretics

A
  • Pulmonary edema
  • Hypovolemia
  • Electrolyte imbalance
  • Plasma hyperosmolarity
116
Q

Examples of K+ sparing diuretics

A
  • Triamterene

- Amiloride

117
Q

MOA of K+ sparing diuretics

A
  • Inhibit Na+ influx in the luminal membrane

- Inhibit Na+ reabsorption and prevent K+ secretion in collecting tubules

118
Q

Clinical uses of K+ sparing diuretics

A

Used when Lasix and other diuretics cause hypokalemia

119
Q

Side effects of K+ sparing diuretics

A

Hyperkalemia

120
Q

Aldosterone antagonist used as a diuretic

A

Spironolactone

121
Q

Clinical uses for aldosterone antagonists (Spironolactone)

A

Hypertension

122
Q

Side effects of aldosterone antagonists (Spironolactone)

A
  • Hyponatremia

- Hyperkalemia

123
Q

MOA of Spironolactone

A

Inhibits NaCl reabsorption in cortical portion of collecting tubule

124
Q

Carbonic anhydrase inhibitor used as a diuretic

A

Acetazolamide (Diamox)

125
Q

MOA of Acetazolamide (CA inhibitor)

A

Inhibits reabsorption of sodium bicarb at the proximal tubule

126
Q

Side effects of Acetazolamide (CA inhibitor)

A
  • Hyperchloremic metabolic acidosis

- Potassium wasting

127
Q

Clinical uses for Acetazolamide (CA inhibitor)

A
  • Altitude sickness (decreases pH of CSF and stimulates hyperventilation)
  • Eye cases (stimulates hyperventilation and decreases CBF)
128
Q

Urea works as which type of diuretic

A

Osmotic diuretic

129
Q

2 main components of blood pressure

A

1) Cardiac output

2) Systemic vascular resistance

130
Q

How do inotropes work to increase blood pressure

A

Improve contractility thus increase cardiac output

131
Q

How do vasopressors work to increase blood pressure

A

Increase SVR

132
Q

Basic physiology of heart muscle contraction

A

Calcium binds to troponin which causes tropomyosin to shift and allows myosin to interact with actin and form a cross-bridge

133
Q

Basic physiology of calcium release in myocytes

A

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
Q

What regulates the release of Ca2+ from the sarcoplasmic reticulum

A

Ryanodine receptors located on non-voltage dependent Ca2+ channels

135
Q

What pumps calcium back into the sarcoplasmic reticulum during relaxation

A

ATPase

136
Q

What pumps Ca2+ out of the cell

A

Na/K+ ATPase and Na+/Ca2+ exchange

137
Q

What is inotropy dependent on

A

The quantity of intracellular Ca2+ in the cell

138
Q

What is chronotropy dependent on

A

The rate of Ca2+ delivery

139
Q

What is lusitropy dependent on

A

The rate of removal of Ca2+

140
Q

What molecule is an important second messenger for calcium release

A

Cyclic AMP

141
Q

Which classes of medications increase contractility by increasing cAMP

A
  • Beta agonists (stimulate adenylate cyclase)

- Phosphodiesterase inhibitors (prevent cAMP breakdown)

142
Q

What are our primary drug choices for activating beta receptors (beta agonists)

A

Catecholamines…(DINE)

  • Dobutamine
  • Isoproteronol
  • Norepi
  • Epi
143
Q

CV effects of B1 activation

A
  • Increased chronotropy

- Increased inotropy

144
Q

CV effects of B2 activation

A
  • Smooth muscle vasodilation (bronchial, vessels)

- Increased inotropy

145
Q

What is the strongest beta agonist available with virtually no alpha effects

A

Isoproteronol

146
Q

Which adrenergic receptor inhibits norepinephrine release

A

Alpha 2

147
Q

Adrenergic receptors activated by norepi

A

A1, B1

148
Q

Infusion rate for norepi in mcg/min

A

1-20mcg/min

149
Q

Adrenergic receptors activated by dopamine

A

A1, B1, B2

150
Q

Infusion rate for dopamine in mcg/kg/min

A

2-20mcg/kg/min

151
Q

Adrenergic receptors activated by epinephrine

A

A1, B1, B2

152
Q

Infusion rate for epinephrine in mcg/min

A

1-20mcg/min

153
Q

Adrenergic receptors activated by dobutamine

A

B1, B2, A1

154
Q

Infusion rate of dobutamine in mcg/kg/min

A

2-10mcg/kg/min

155
Q

Adverse effects of norepinephrine

A

Can decrease cardiac output because of the intense vasoconstriction caused by a1 activation

156
Q

Adverse effect of epinephrine

A

Arrythmogenic

157
Q

Adverse effect of dopamine

A

Largely increase acting, causes the release of norepi

158
Q

Adverse effect of dobutamine

A

Tachycardia

159
Q

Adverse effects of isoproterenol

A
  • Significant tachycardia
  • Arrhythmias
  • Decreased SVR
160
Q

Function of phosphodiesterases (PDEs)

A

Breakdown cyclic nucleotides cAMP and cGMP

161
Q

Function/location of PDE1

A

Smooth muscle cells, regulate proliferation in vascular tissue

162
Q

Location of PDE3

A
  • CV system and platelets

- Adipose/liver (type B)

163
Q

Function/location of PDE4

A

Inflammatory cells, may play a role in COPD/arthritis

164
Q

Location of PDE5

A

Corpus cavernosum of penis

165
Q

Which PDE family is activated by insulin

A

PDE3

166
Q

MOA of phosphodiesterase 3 inhibitors in cardiac myocytes

A

Increase cAMP thus increasing Ca2+ and contractility

167
Q

MOA of phosphodiesterase 3 inhibitors in vascular tissues

A

Increase cGMP which causes smooth muscle relaxation - decreasing SVR and PA pressures

168
Q

Common PDE III inhibitors

A
  • Amrinone
  • Milrinone
  • Enoximone
169
Q

Loading dose of Amrinone

A

1mg/kg

170
Q

Infusion rate of Amrinone

A

2-10mcg/kg/min

171
Q

Loading dose of Milrinone

A

0.05mg/kg

172
Q

Onset time for a loading dose of Milrinone

A

5 minutes

173
Q

Duration of a loading dose of Milrinone

A

30 minutes

174
Q

Infusion rate for Milrinone

A

0.5mcg/kg/min

175
Q

Onset time for an infusion of Milrinone

A

About an hour

176
Q

Loading dose of Enoximone

A

0.5mg/kg

177
Q

Infusion rate of Enoximone

A

10mcg/kg/min

178
Q

1st line inotrope

A

Norepinephrine

179
Q

Which class of vasopressors don’t use the CNS?

A

Non-catecholamine non-sympathathomimetics

180
Q

What is the second messenger for alpha activation on vasculature?

A

IP3

181
Q

Activation of alpha1 receptors result in what?

A

Increase in Ca2+ and smooth muscle contraction in systemic and pulmonary vasculature

182
Q

List the catecholamines in order of greatest to least alpha1 activation

A

Norepi, dopamine=epi, dobutamine (isoproteronol has none)

183
Q

How can you alter the doses of catecholamines to get a greater alpha effect?

A

Increase the doses

184
Q

Examples of non-catecholamine sympathomimetics that are pure, direct acting alpha agonists

A
  • Phenylephrine

- Methoxamine

185
Q

Onset of phenylephrine

A

30 seconds

186
Q

Duration of phenylephrine

A

2-3 minutes

187
Q

Infusion rate of phenylephrine in mcg/min

A

25-100

188
Q

Bolus dose of Methoxamine

A

5-10mg

189
Q

Onset of Methoxamine

A

1 minute

190
Q

Duration of Methoxamine

A

5-10 minutes

191
Q

MOA of ephedrine

A

Indirect acting, causes release of NE from neurons and has a little beta activation

192
Q

What liver enzyme inactivates ephedrine

A

MAO

193
Q

Why will patients in heart failure not be affected by ephedrine

A

Because they are catecholamine depleted

194
Q

What prescribed medications can cause an exaggerated effect of ephedrine?

A

MAO inhibitors for depression because the ephedrine won’t be inactivated

195
Q

Which vasopressor has minimal effect on uterine vascular resistance?

A

Ephedrine

196
Q

What is the main non-sympathomimetic vasopressor

A

Vasopressin

197
Q

MOA of vasopressin

A

Activates V1 receptors which increases Ca2+ and causes smooth muscle contraction

198
Q

Effect of vasopressin receptor V2 activation

A

Increased water permeability at the kidneys and increased urination

199
Q

Effect of vasopressin receptor V3 activation

A

Increased ACTH release via actions at the pituitary gland

200
Q

How do the levels of AVP change over time in patients in sepsis and on CPB

A

Onset causes AVP levels to rise by 2-3x then as time goes on, levels drop to 1/3 of the normal levels

201
Q

Infusion rate of vasopressin in units/hr

A

4-6 units/hr

202
Q

Side effects of vasopressin

A

Side effects are related to intense vasoconstriction

1) Myocardial ischemia
2) Decreased cardiac output
3) Mesenteric ischemia
4) Digital necrosis

203
Q

Vasopressin is thought to have less of an effect on which vasculature area? How would this be clinically relevant?

A

Thought to have less of an effect on pulmonary vasculature, could be beneficial in patients with pulmonary hypertension

204
Q

What are “calcium mobilizers”?

A

Drugs that cause an increase in Ca2+ influx leading to increased contractility (i.e. catecholamines and PDE inhibitors)

205
Q

What are “calcium sensitizers”

A

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
Q

Advantages of calcium sensitizers

A
  • Less arrythmogenic

- Don’t increase O2 consumption

207
Q

Current Ca2+ sensitizers available

A
  • Pimobendan

- Levosimendan

208
Q

Clinical use of Pimobendan

A

Oral Ca2+ sensitizer used for long term treatment of CHF

209
Q

MOA of Levosimendan

A

Binds to troponin C and stabilizes the troponin/Ca2+ conformational change

210
Q

What drug is used as a rescue measure due to its role in treating refractory vasodilatation

A

Methylene blue

211
Q

Under what circumstances may methylene blue be used to treat refractory dilatation

A
  • MAP below 50mmHg

- Norepi infusion over 35mcg/min

212
Q

MOA of methylene blue for treatment of refractory vasodilatation

A

Decreases cGMP which leads to less vasodilation

213
Q

Bolus dose of methylene blue

A

1.5-2mg/kg

214
Q

How should methylene blue be administered

A

Given over 10-60 minutes

215
Q

Side effects of methylene blue

A
  • Transient decrease in SpO2 monitoring

- Mild skin/urine discoloration

216
Q

What can result from high doses of methylene blue

A
  • Hyperbilirubinemia

- Hemolytic anemia

217
Q

Top 5 patient risk factors for PONV

A
  1. Female
  2. History of PONV
  3. Non-smoker
  4. Motion sickness
  5. Age under 50
218
Q

Top 4 surgical risk factors for PONV

A
  1. Cholecystectomy
  2. Laparoscopic procedures
  3. Gynecologic
  4. Long length of procedure
219
Q

Prophylactic PONV agents to consider prior to surgery

A

1) Transdermal scopolamine
2) NK-1 antagonists
3) Midazolam

220
Q

What is the priming dose contained in the layer closest to the skin of the scopolamine patch

A

140mcg

221
Q

Onset time of the scopolamine patch

A

2-4 hours

222
Q

Side effects of scopolamine patch

A
  • Visual disturbances
  • Dry mouth
  • Confusion
223
Q

NK-1 antagonists used for PONV

A
  • Aprepitant
  • Rolapitant
  • Casopitant
224
Q

What drug may be useful for patients who have complained of getting sick once they get home from their surgery

A

Aprepitant because it has a long 9-13 hour half life

225
Q

Dose of Aprepitant comparable to 4mg Zofran

A

40mg

226
Q

In which patients should you use caution when considering Aprepitant?

A

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
Q

Patients on hormonal birth control should use back-up birth control for how long after taking Aprepitant?

A

30 days

228
Q

Dosing range of midazolam useful for PONV

A

0.05-0.075mg/kg

229
Q

Regional anesthesia is __ times less likely to cause PONV than general anesthesia

A

9

230
Q

There is a very very low risk of PONV when using nitrous for less than…

A

1 hour

231
Q

PONV is very likely when running nitrous for longer than…

A

2 hours

232
Q

When have opioids been found to increase risk of PONV?

A

When it is given post-operatively

233
Q

Why is IV acetaminophen thought to decrease PONV?

A

It reduces pain scores which decreases chance of PONV

234
Q

When must IV acetaminophen be administered to reduce the incidence of PONV?

A

Intra-operatively or immediately post-operatively

235
Q

There is evidence that 8mg of Zofran may be useful for which patients

A

Patients with a history of PONV

236
Q

Dose of Granisetron equivalent to 4mg Zofran

A

0.3-3mg IV

237
Q

MOA of Palonosetron

A

Allosteric binder that changes the conformation of the receptor so serotonin cannot bind

238
Q

Dose of Palonosetron for PONV

A

0.075mg IV

239
Q

Current recommended dose of Decadron for PONV

A

4-5mg

240
Q

Only case found to benefit from 8mg of Decadron for PONV

A

Lap chole

241
Q

Disadvantages of high doses of Decadron

A
  • Suppression of HPA axis

- Increased chance of wound infection

242
Q

What dose of Metoclopramide is equivalent to 4mg of Zofran to treat early nausea

A

25-30mg

243
Q

What dose of Metoclopramide is equivalent to 4mg of Zofran to treat late nausea

A

50mg

244
Q

Risk of giving 25-50mg of Metoclopramide

A

Extrapyramidal symptoms

245
Q

Recommendations for PONV prophylaxis for low risk patients with 0 risk factors

A

No prophylaxis

246
Q

Recommendations for PONV prophylaxis for medium risk patients with 1 risk factor

A

1 PONV agent

247
Q

Recommendations for PONV prophylaxis for moderate risk patients with 2-3 risk factors

A

2-3 PONV agents

248
Q

Recommendations for PONV prophylaxis for high patients with 4+ risk factors

A

3-4 agents +/- TIVA

249
Q

MOA of Droperidol/Haldol as PONV agents

A

Anti-dopaminergic action at the chemoreceptor trigger zone

250
Q

How should Droperidol be administered for PONV treatment

A

0.625-1.25mg at the end of surgery

251
Q

Black box warning for Droperidol

A

QT prolongation and serious arrhythmias (e.g. Torsades)

252
Q

It is strongly advised that your patient must have what test before having Droperidol?

A

12 lead ECG

253
Q

Guidelines for ECG monitoring after administration of Droperidol

A

ECG monitoring for 2-3 hours after administration

254
Q

Dose giving Zofran and Droperidol together have additive effects on the risk of QT prolongation?

A

No

255
Q

Dose of Haloperidol for PONV prophylaxis and rescue

A

0.5-2mg IM or IV

256
Q

Risk of Haloperidol at a 4mg dose

A

Extrapyramidal symptoms

257
Q

Dose of Dimenhydrinate (Dramamine) for PONV

A

1mg/kg IV

258
Q

Side effects of Promethazine at higher doses

A
  • Confusion
  • Sedation
  • Akasthesia
  • Tardive dyskinesia
259
Q

Rare but morbid side effects of Promethazine

A
  • Neuroleptic Malignant Syndrome
  • Tissue necrosis
  • Seizures
260
Q

2 black box warnings for Promethazine

A
  • Tissue necrosis

- Don’t give to patients under 2 years old due to respiratory depression

261
Q

Dose of Promethazine for PONV

A

6.25mg IV

262
Q

Dose of propofol as rescue PONV drug

A

20mg doses

263
Q

Dose of benadryl as rescue PONV drug

A

6.25-12.5mg IV

264
Q

Dose of Haldol as rescue PONV drug

A

1mg IV

265
Q

Dose of Zofran as PONV rescue drug

A

1mg IV

266
Q

Dose of Droperidol as PONV rescue drug

A

0.625mg IV

Pharmacology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions