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N929 Pharmacology > Exam 2 Week 2 Cardiovascular Drugs > Flashcards

Exam 2 Week 2 Cardiovascular Drugs Flashcards

1
Q

Central Nervous System NT

A 
epinephrine
norepinephrine
dopamine
serotonin
gamma aminobutyric acid
acetylcholine
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2
Q

Natural Catecholamine Agonists

A

Epi
NE
dopamine

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3
Q

Synthetic Catecholamine Agonist

A

isoproterenol

dobutamine

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4
Q

Order of potency for alpha receptors

A

NE>E>Iso

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5
Q

Order of Potency for Beta Receptors

A

Iso>E>NE

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6
Q

Alpha 1 Receptor Physiology (location and effect)

A

Post-synaptically found in the vasculature, heart, glands and gut
Activation causes vasoconstriction and relaxation of the GI tract

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7
Q

Alpha 2 Receptor Physiology (Location and Effect)

Pre

A

Pre-synaptic

  • Found in peripheral vascular smooth muscle, coronaries and brain
  • Activation causes inhibition of NE release and inhibition of sympathetic outflow leading to decrease BP and decrease HR
  • inhibition of CNS activity
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8
Q

Alpha 2 Receptor Physiology (Location and Effect)

Post

A

found in: coronaries, CNS

activation causes constriction and sedation and analgesia

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9
Q

Beta 1 Receptor Physiology (Location and Effect)

A

found in: myocardium, SA node, ventricular conduction system, coronaries, kidney
Activations causes: increase in inotropy, chronotropy, myocardial conduction, velocity, coronary relaxation and renin release

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10
Q

Beta 2 Receptor Physiology (Location and Effect)

A

Found in: Vascular, bronchial, and uterine smooth muscle, smooth muscle in the skin, myocardium, coronaries, kidneys, gi tract
Activation causes: vasodilation, bronchodilation, uterine relaxation, gluconeogensis, insulin release, potassium uptake by the cells

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11
Q

Synthetic Non Catecholamines

A

Ephedrine (Direct and Indirect)

Phenylephrine (Direct)

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12
Q

Pharmacologic Targets of HTN: Local regulators

A

endothelin antagonist
nitroprusside
ACEi
ARB

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13
Q

Pharmacologic Targets of HTN: Circulating regulators

A

Alpha 1 antagonists
alpha 2 agoinst
ACEi
ARB

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14
Q

Pharmacologic Targets of HTN: Na/H20 Retention

A

Diuretics
ACEi
ARB

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15
Q

Pharmacologic Targets of HTN: Venous Tone

A

alpha 1 antagonist
ARB
ACEi
Nitroprusside

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16
Q

Pharmacologic Targets of HTN: HR

A

Beta antagonist

CCB

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17
Q

What are the effects of most anesthetics?

A

myocardial depressant and vasodilators

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18
Q

Alpha 1 of most vascular smooth muscle (blood vessels, sphincters & bronchi) cause

A

contraction

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19
Q

Alpha 1 receptors of Iris (radial muscle) causes

A

contraction (dilates pupils= mydriasis)

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20
Q

Alpha 1 receptors of pilomotor smooth muscle causes

A

erect hair

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21
Q

alpha 1 receptors of prostate and uterus causes

A

contraction

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22
Q

alpha 1 receptors of the heart causes

A

increase force of contraction (B1 more impt)

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23
Q

Alpha 2 receptors of platelets cause

A

aggregation

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24
Q

Alpha 2 receptors of the adrenrgic & cholinergic nerve terminals (presynaptic)

A

inhibit transmitter release (decrease BP and decrease HR)

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25
Q

Alpha 2 receptors of vascular smooth muscle cause

A

contraction (post synaptic) OR dilation (pre-synaptic, CNS)

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26
Q

Alpha 2 receptors of the GI tract causes

A

relaxation (presynaptic)

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27
Q

Alpha 2 receptors of the CNS cause

A

sedation and analgesia via decrease SNS outflow from brain stem

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28
Q

Beta 1 receptors on kidney and heart cause

A

increase force and rate of contraction
chronotropy, inotropy
stimulation of renin release

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29
Q

Beta 2 receptors on respiratory, uterine, vascular, GI, GU (visceral smooth muscle) causes

A

promotes smooth muscle relaxation

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30
Q

Beta 2 receptors on mast cells cause

A

decrease histamine release

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31
Q

Beta 2 receptors on skeletal muscles

A

potassium uptake, dilation of vascular beds, tremor, increase speed contraction

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32
Q

Beta 2 receptors on liver, pancrease and adrenergic nerve terminals cause

A

glyconeolysis, increase insulin secretion, increase NE release

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33
Q

Beta 3 receptors on fat cells cause

A

activates lipolysis; thermogenesis

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34
Q

Dopamine 1 receptors located on smooth muscle cause

A

dilation of renal, mesenteric, coronary, cerebral blood vessels (post synaptic)

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35
Q

dopamine 2 receptors located on nerve endings cause

A

modulates transmitter release, nausea and vomitting (pre-synaptic)

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36
Q

Alpha adrenergic receptors

A

GPCR

ligands include NE, E and DA

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37
Q

alpha 1 excitatory pathway is

A

increase in Ca leads to increase camodulin activiation, increases actin-myosin interaction causes smooth muscle contraction

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38
Q

Alpha 2 inhibitory pathway includes

A

decrease cAMP decrease NE release

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39
Q

Beta adrenergic receptors

A

B1-B3
GCPRs, G3s
activation of adenyl cyclase, increase cAMP, increase kinase activation and phosphorlyation

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40
Q

Classes of drugs that treat hypertension include

A

sympathetic nervous system
renin-angiotensin-aldosterone system
endothelium derived mediator and/or ion channel modulators

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41
Q

What is a normal BP?

A

less then 120/80

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42
Q

When should someone implement lifestyle modications

A

> 120/80

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43
Q

Treatment Goals (age 18-59)

A

no comorbidites and 60 and older with diabetes and/or chronic kidney disease <140/90

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44
Q

Treatment Goals (age >60)

A

<150/90 with no diabetes or kidney disease

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45
Q

First line therapy for HTN

A

thiazide diuretic unless compelling indication (ie decompensation)

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46
Q

Hypertensive Urgency

A

diastolic BP >120 with evidence of progressive end organ damage

47
Q

Goal of Hypertensive Urgency is

A

decrease DBP to 100-105 within 24 hours (clonidine)

48
Q

Hypertensive Crisis

A

diastolic BP >120 with evidence of EOP

49
Q

Goal of Hypertensive Crisis

A

decrease DBP 100-105 asap (nitroprusside, nitroglycerin, labetalol, fenoldapam)

50
Q

Alpha antagonist

A

bind selectively to alpha receptors and interfere with the ability of catecholamines to cause a response

51
Q

Competitive alpha antagonist

A

phentolamine, prazosin, yohimibine

52
Q

Phenoxybenzamine

A

binds covalently and is tough to overcome

53
Q

Alpha 1 antagonist effects

A

smooth muscle relaxation
decrease PVR
decrease BP

54
Q

Alpha 1 antagonist clinical uses include

A

hypertension

BPH

55
Q

alpha 1»>alpha 2

Alpha antagonist

A

prazosin, terazosin, doxazosin

56
Q

alpha 1>alpha 2

Alpha antagonist

A

phenoxybenzamine

57
Q

Alpha 2= alpha 1

Alpha antagonist

A

phentolamine

58
Q

Alpha 2»>Alpha 1

A

yohimibine, tolazoline

59
Q

Mixed alpha and beta antagonist

A

labetalol and carvedilol

B1=B2 >/or equal to alpha 1 > alpha 2

60
Q

B1>B2

beta antagonist

A

metoprolol, atenolol, esmolol

61
Q

B1=B2

beta antagonist

A

propanolol, nadolol, timolol

62
Q

B2> b1

beta antagonist

A

butoxamine

63
Q

cardiovascular effects of alpha 1 antagonism

A

decrease PVR and lower BP

postural hypotension due to failure of venous vasoconstriction upon standing

64
Q

Cardiovascular effects of alpha 2 antagonism

A

increases NE release from nerve terminals result in tachycardia due to stimulation of beta receptors in the heart

65
Q

Alpha antagonist GU effects

A

blockade in prostate and bladder cause muscle relaxation and ease micturation

66
Q

Additional alpha antagonist effects

A

miosis

increase nasal congestion

67
Q

Phenoxybenzamine

A

binds covalently
alpha 1>alpha 2
decrease SVR, vasodilation
nonselective alpha antagonist
less alpha 2 so less associated with tachycardia with decrease in SVR
PO medication for pre-operative control of blood pressure in patients with pheochromocytoma (0.5-1mg/kg)

68
Q

Pharmacokinetics for Phenoxybenzamine

A

pro-drug with 1 hours onset time
long acting
e1/2 24 hours
used for patients with raynaud disease

69
Q

Phentolamine

A

nonselective alpha antagonist
produces peripheral vasodilation and a decrease in SCR
causes reflex mediated and alpha 2 associated increase in HR and CO

70
Q

Uses of phentolamine

A

intraoperative management of HTN crisis (30-70mcg/kg)
pheochromyocytoma manipulation
autonomic hyper-reflexia
extravascular administration of sympathomimetic agents (2.5-5mg)

71
Q

Prazosin

A

selective alpha1 antagonist
less likely to cause tachycardia
dilates both arterioles and veins

72
Q

Uses of prazosin

A

pre-op prep of patients with pheochromocytoma
(controls BP)
essential HTN (combined with thiazides)
decreasing afterload in patients with heart failure
raynaud phenomenon

73
Q

Yohimibine

A

alpha 2 selective blocker
increases the release of NE from post synaptic neuronu
used with increase orthostatic hypotension, impotence

74
Q

Terazosin and Tamsulosin

A

Taking for BPH
long acting selective alpha 1a particularly effective in prostatic smooth muscle relaxation
vary in elimination times
orthostatic hypotension is biggest concern

75
Q

Beta Blocker in the heart cause

A

bradycardia, decreased contractility, decreased conduction velocity, improves O2 supply and demand balance

76
Q

Beta Blocker in the Airway

A

bronchoconstriction can provoke bronchospasm in patietns with asthma or COPD

77
Q

BB in the BV cause

A

vasoconstriction in skeletal muscles

PVD symptoms increase

78
Q

BB in the Juxtaglomerular cells cause

A

decrease renin release

indirect way of decrease BP

79
Q

BB in the pancreas

A

decrease stimulation of insulin release of epi/NE at B2 and then masked symptoms of hypoglycemia B1

80
Q

MOA of beta adrengeric receptor antagonist

A

selective binding to beta receptors (influence inotropy, chronotropy)
competitive and reversible inhibition- large doses of agonist will completely overcome antagonism
chronic use of associated with increase in the # of receptors (up-regulation)

81
Q

Nonselective BB

A

propanolol, nadalol, timolol, pindolol

82
Q

Cardioselective BB

A

beta 1
metoprolol, atenolol, acebutolol, betaxolol, esmolol
large doses lose sensitivity

83
Q

Clinical Uses of BB

A

treatment of HTN
management of Angina
decrease mortality in treatment of Post MI
used periop and preop for pts at risk for MI
suppression of tachyarrthmias
prevention of excessive sympathetic nervous system activity

84
Q

Relative contraindications of BB

A

pre-existing AV heart block or cardiac failure
reactive airway disease
DM (W/O BS monitoring)
hypovolemia

85
Q

Side effects of BB

A

decrease HR, contractility, BP
exacerbation of PVD (block of B2 vasodilation)
airway resistance
alter carb and fat metabolism, mask hypoglycemia
distribution of extracellular K
interaction of anesthetic (decrease MP with IA)
fatigue, lethergy
N/V/D
reduction in IOP
decreased concentrations of HDL

86
Q

Propanolol Protype

A

nonselective beta blocker
decreases HR and contractility
undergoes extensive 1st pass effect
limited use in anesthesia
concerns with anesthesized pt w/ propanolol:
decrease clearance of amide local anesthestics, decrease pulmonary clearance of fentanyl
Administered with goal HR of 55-60bpm

87
Q

Cardiac Effects of Propanolol

A

decreased HR, contractility, decreased CO
above effects are especially prominent during excerise and sympathetic outflow
blockade of B2 receptors increased PVR, increase Cop vascular resistance
however, due to decreased HR and CO oxygen demand in lowered opposing the above effects
reduction in renin

88
Q

Pharmacokinetics of Propanolol

A

significant first pass effect
oral dose larger then IV dose
Protein bound (90-95%)
metabolized in liver
E1/2t of 2-3 hours (will be increase in low hepatic blood flow states)
decreases clearance of amide LAs due to a decrease in hepatic blood flow inhibiting metabolism in the liver- risk of systemic toxicity of amide local anesthetics

89
Q

Metoprolol

A 
Lopressor
Beta 1 selective (inotropic and chronotropic)
selectivity is dose related
about 60% thru first pass effect
metabolized in liver
E1/2t 3-4 hours
IV form
90
Q

IV propanolol dose

A

0.05mg/kg IV

1-10mg (give slowly 1mg q5mins)

91
Q

Metoprolol Dose

A

PO 50-400mg

IV 1-15mg (max)

92
Q

Atenolol

A

most selective beta 1 antagonist and thought to have the least CNS effects
E1/2t is 6-7 hours
not metabolized in liver, excreted via renal system
pts with renal dx, e1/2t increased
advantageous to pt who need beta 2 receptor activity
oral drug for HTN
long lasting antihypertensive effects

93
Q

Esmolol

A

Breviblock
rapid onset and short duration on beta 1 selective blocker
IV only
metabolized by plasma esterase (less than 1% of drug is excreted unchanged in urine)
Poor lipid solubility dose not cross BBB or placenta
rapidly hydrolyzed by plasma esterase
no effect on succinylcholine metabolism or duration of action

94
Q

Esmolol Onset of Action

A

60 seconds

95
Q

Esmolol E1/2t

A

9 minutes

96
Q

Esmolol DOA

A

30 minutes

97
Q

Esmolol Treats

A

useful in treating HTN and tachycardia associated with laryngoscopy
Treats: phenochromocytoma, thyrotoxicosis, thyroid storm

98
Q

Timolol

A

Brimonidine
nonselective beta blocker
used to treat glaucoma
decreases intraocular pressure by decrease produciton of aqeuous humor
eye drops can cause decrease BP, HR and increased airway resistance

99
Q

Nadolol

A

nonselective BB
no significant metabolism (renal/biliay elim)
e1/2t of 20-40 hours take 1x daily

100
Q

Betaxolol

A

cardioselective B1 blocker
E1/2 time is 11-22 hours
single dose daily for HTN
topical used for glaucoma, with less risk of bronchospasm as seen with timolol, so good alternative choice in asthmatics with glaucoma

101
Q

Side effects of Timolol

A

xerostomia, dizziness, weakness

102
Q

Timolol Potential interactions

A 
alpha agonist
beta agonist
amiodarone
cardiac glycosides
CNS depressants
lidocaine
methacholine
MAOis/ SSRIs
quinidine
alcohol
103
Q

Precautions with timolol

A 
bronchospastic disease
DM
glaucoma, angle closure
MGravis
Thyrotoxicosis
hepatic/ renal impairment
pregnancy/ lactation
104
Q

Contraindications of Timolol

A

Hypersensitivity to drug and/or its components
sinus bradycardia
cardiogenic shock
heart failure, uncompensated
heart black, 2nd or 3rd degree (except with pacemarker)
Severe COPD/asthma
MAO inhibitor use with or within 14 days

105
Q

Labetalol

A

combined nonselective antagonist
IV beta to alpha blockade 7:1
PO beta to alpha blockade 3:1
metabolism with conjugation of glcuronic acid; < 5% receovered unchanged in urine
E1/2t of 5-8 hours, prolonged in liver disease not effected by renal dysfunction
maximum drop in BP 5-10 mins after IV administration
decreases systemic BP with attenuated reflex tachycardia (beta 2 blockade)
used to treat intraoperative HTN and hypertensive crisis
can be used in hypotensive technique without an increase in HR
can cause orthostatic hypotension, bronchospasm, heart block , CHF and bradycardia

106
Q

Dose of Labetalol

A

0.1-0.5 mg/kg

usually 5mg at a time for mild hypertension in the OR

107
Q

Centrally acting BP agents MOA

A

reduce sympathetic outflow from vasomotor centers in the brain stem
centrally acting selective partial alpha2 adrenegric agonist

108
Q

Centrally acting BP agents Site of action

A

CNS non adrenergic binding sites and alpha 2 receptor agonism

109
Q

Clinical uses of Centrally acting BP agents

A

hypertension, induce sedation, decrease anesthetic requirements, improve peri-operative hemodynamics, analgesia

110
Q

Clonidine

A

centrally acting agent
results in decreased BP from decreased CO to decrease HR and peripheral resistance
rebound HTN and abrupt cessation

111
Q

Side effects of Clonidine

A 
bradycardia
sedation
xerostomia (dry mouth)
impaired concentration
nightmares
depression
vertigo
EPS
lactation in men
112
Q

Pharmacokinetics of Clonidine

A

available as PO or transdermal patch

50/50 hepatic metabolism and excretion

113
Q

Withdrawal Syndrome of Centrally acting agents

A

occurs with doses >1.2mg/day
occurs 18 hours after acute discontinuation of drug
lasts 24-72 hours
treatment for rectal or transdermal clonidine

114
Q

Sympathomimetics

A 
ephedrine
phenylephrine
vasopressin
epinephrine
NE
dopamine
Dobutamine

N929 Pharmacology (16 decks)

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