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Emily: Pharm 2 > Quiz 1: Vasoconstrictors and DIrect Vasodilators > Flashcards

Quiz 1: Vasoconstrictors and DIrect Vasodilators Flashcards

1
Q

How is Norepinephrine made?

A
  1. Dompamine enters the synaptic vessel
  2. Dopamine beta Hyroxylase converts dopamine to Norepiniphrine .
  3. An action potential releases NE from the synaptic vessel.
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2
Q

Termination of Norepinephrine is done by:

A
  • reuptake
  • Dilution by diffusion
  • Metabolim: Monamine Oxidae (MAO) and catechol-o0methyltranserase
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3
Q

List the Adrenergic receptors for the Sympathetic Nervous System?

A
  • Alpha 1: Periphery
  • Alpha 2: Central
  • Beta 1: heart
  • Beta 2: other smooth muscle
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4
Q

List the sympathetic nervous system Alpha 1 (Receptor) Postsynaptic effect on the body?

A
  • Increase intracellular calcium
    -Smooth muscle contraction
    -Peripheral vasoconstriction
    -Bronchoconstriction
    -Inhibits Insulin secretion
    Stimulate glycogenolysis and gluconeogenesis
    -Mydriasis
    -GI relaxatioin
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5
Q

List the sympathetic nervous system Alpha 2 (Receptor) Postsynaptic effect on the body?

A

PRESYNAPTIC IN THE PNS

  • Decreases entry of calcium into the cell
  • Limits the release of norepinephrine

POSTSYNAPTIC IN THE CNS

  • Sedation
  • Decreased sympathetic outflow
  • Decreased BP
  • Platelet aggregation
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6
Q

List the sympathetic nervous system Beta 1 (Receptor) Postsynaptic effect on the body?

A

INCREASE

  • Heart Rate
  • Conduction velocity
  • myocardial contractility
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7
Q

List the sympathetic nervous system Beta 2 (Receptor) Postsynaptic effect on the body?

A
  • Smooth muscle relaxation
  • Peripheral vasodilitation
  • Decrease in B/P
  • Bronchodilitation
  • Increases insulin secreation
  • Increases glycogenolysis and gluconeogenesis
  • Decreases GI mobility
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8
Q

What is the Sympathetic Nervous System?

A
  • Thoracolumar origin (T1-T12)
  • Preganglia near spinal cord
  • Postganglia secret norpinephrine ->adrenergic fibers
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9
Q

What is the Parasympathetic Nervous System?

A
  • Craniosacral origin 3, 5, 7, 10
  • Preganglia near organs of innervation
  • Postganglia secret acetylcholine (Ach) -> Cholinergic fibers
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10
Q

T/F: Acetylcholine activates both arms of the SNS.

A

TRUE

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11
Q

What creates acetylcholine?

A
  • Choline + Acetyl CoA
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12
Q

What deactivates acetylcholine?

A
  • Acetylcholinesterse
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13
Q

What are the cholinergic receptors?

A
  • Nicotinic

- Muscarinic

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14
Q

_______ _________ : extended exposure to agonists reduces the number, but not their response. Results in tachyphylaxis.

A
  • Down regulation
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15
Q

_______ ______ : chronic depletion of catecholamine or use of antagonists increases the number of receptors, but not their sensitivity. May account for withdrawal syndrome with beta blockers.

A
  • Up regulation
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16
Q

Describe receptor Uncoupline?

A
  • Occurs rapidly

- Inability of the receptor to bind G protein ( alter the function of the receptor)

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17
Q

Describe receptor Sequestration?

A
  • Occurs more slowly

- Movement of receptors from the cell surface to intracellular compartments

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18
Q

Describe receptors downregulation on a cell?

A
  • Prolonged process

- Movement of receptors from the cell surface to intracellular compartments, but then DESTROYED

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19
Q

What is pheochromocytoma?

A

-Uncontrolled release of catacolamines via a adrenal tumor which causes SNS stimulation.

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20
Q

T/F: a Catecholamine can be either a neurotransmitter or a hormone.

A

TRUE

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21
Q

What receptor does a catecholamine work on?

A

-Adrenergic receptor

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22
Q

What is a sympathomimetic?

A

-Compound that resemble catecholamines except that hydroxyl groups are not present in both the 3 and 4 posetions of the Benzene ring.

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23
Q

How are sympathomimetic classified?

A
  • By their selectivity for stimulating the alpha and/or beta receptor.
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24
Q

Indirect acting sympathomimetics are:

A
  • Synthetic non-catecholamines

- release endogenous neurotransmitter NE from postganglionic sympathetic nerve endings

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25
Q

Direct-acting sympathomimetics are:

A

-Catecholammines and synthetic non-catecholamines

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26
Q

All sympathomimetic are derived from ______.

A

-B phenylethylamine

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27
Q

Presence of ______ groups on the 3 and 4 postion of the benzene ring of the B phenylethylamine creates a CATACHOL.

A
  • hydroxyl
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28
Q

Pharmacological effects of sympathomimetics for vasoconsticition effect:

A

-cutaneous and renal circulations

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29
Q

Pharmacological effects of sympathomimetics for vasodilation effect:

A

-skeletal muscle

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30
Q

Pharmacological effects of sympathomimetics for respiratory effect the lungs in what way?

A

-bronchodilation

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31
Q

Pharmacological effects of sympathomimetics for cardiac stimulation effect:

A
  • Increased heart rate
  • Increased myocardial contractility
  • Vulnerability to dysrhythmias
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32
Q

Pharmacological effects of sympathomimetics for hepatic effect:

A

-glycogenolysis

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33
Q

Pharmacological effects of sympathomimetics modulate what hormones:

A
  • insulin
  • renin
  • pituitary
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34
Q

Pharmacological effects of sympathomimetics for the CNS is:

A

Stimulation

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35
Q

T/F: The only time a vaopressor should be used is when the patient’s blood pressure must be increased immediately to avoid pressure dependent reduction in organ perfusion with subsequent ischemia.

A

TRUE

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36
Q

The pharmacologic response caused by a sympathomimetic is related to the _____ of the alpha and beta adrenergic receptors in the tissues.

A

-density

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37
Q

T/F: There is a direct relationship between the concentration of available sympathomimetic and the number of receptors.

A

FALSE (There is an inverse….)

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38
Q

What enzymes are responsible for inactivating the drugs containing the 3,4 dihydroxybenzene (catecholamines) structure?

A
  • Monoamine oxidase (MAO)

- Catechol-o-transferase (COMT)

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39
Q

T/F: Administration of catecholamines is effective through oral, SQ, or IV routes.

A

FALSE (….effective through SQ and IV routes.)

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40
Q

Where are monoamine oxidase (MAO) primarily found?

A
  • liver
  • Kidnerys,
  • GI tract
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41
Q

What is the best way for administration of Epi.

A
  • SQ

- IV

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42
Q

What is the best way for administration of Dopa. or Norepi.

A

-IV

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43
Q

Metabolism of synthetic noncatecholamines would be:

A
  • lack the 3 hydroxyl group
  • Metabolism is often SLOWER that that of catechos
  • Inhibition of MAO may prolong their duration of action.
  • Patients on MAO inhibitors may manifest exaggerated responses when treated with synthetic non-catecholamines.
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44
Q

Metabolism of a synthetic non-catecholamine is metabolized by ______ and not by _______.enzymes.

A
  • MAO

- COMT

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45
Q

Vasoconstrictors increase aterial _____ and ____ as well increase venous ______.

A
  • resistence
  • afterload
  • return
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46
Q

What would be some reflex changes seen with vasoconstrictors?

A

DECREASE

  • Heart Rate
  • conduction
  • contractility
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47
Q

What noncardiac effects are seen with vasoconstictors?

A
  • Bronchodilate
  • Glycogenolysis
  • Insulin, renin, pituitary hormone
  • CNS stimulation
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48
Q

What would be the indication for a vasconstrictor?

A

-Decrease in arterial resistance

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49
Q

After administering a proper dose of a vasoconstrictor iatrogenic affects can be seen in the patient. What would be the proper action?

A

-All is well….Iatrogenic means the results of administering the vasoconstrictor

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50
Q

What would be contraindications/complications for using vasoconstrictor:

A
  • Worsen LV failure
  • exacerbate RV failure
  • Decrease renal blood flow
  • Can mak hypovolemia
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51
Q

What would be the three natural catecholamines?

A
  • Epinephrine
  • Norepinephrine
  • Dopamine
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52
Q

Epinephrine stimulate what receptors?

A
  • Alpha 1
  • Beta 1
  • Beta 2
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53
Q

T/F: Epinephrine is the most potent activator of Alpha 1 receptor.

A

TRUE

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54
Q

What does epinephrine increase?

A
  • lipolysis,

- glycogenolysis

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55
Q

What does epinephrine decrease?

A

insulin

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56
Q

T/F: Epinephrine will still decrease renal blood flow even in the ABSENCE of changes in the systemic BP.

A

TRUE

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57
Q

Epinephrine stimulates renin release which is a ____ effect.

A

-indirect

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58
Q

A low dose of epinephrine of 1-2 mcg/min will:

A

-stimulate alpha 1 receptor at the skin, mucosa, and hepatorenal system WHILE beta 2 receptors are stimulated in the muscle

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59
Q

During a low dose of epi (1-2 mcg/min) does the MAP remain the same?

A

YES

60
Q

Giving an intermediate does of epinephrine (4 mcg/min) will cause:

A

INCREASE (BETA 1)

  • Heart rate
  • Contractility
  • Cardiac output
61
Q

T/F: An intermediate does of epinephrine may lead to dysrhythmias (PVC) in sensitized myocardium.

A

TRUE

62
Q

High dose of epinephrine (10 mcg/min) would cause:

A

-vasoconstriction of cutaneous, splanchnic and renal vascular beds.

63
Q

T/F: Epinephrine at high doses has no effect on cerebral arterioles.

A

TRUE

64
Q

What reflex could be seen with high doses of epinephrine?

A

-Bradycardia

65
Q

What is Racemic Epinephrine made up of:

A
  • Levo

- dextrorotatory isomers

66
Q

T/F: Norepinephrine effect beta more than it does alpha.

A

FALSE

67
Q

Norepinephrine is a potent vasoconstrictor of the _______, ___________, and ___________ vascular beds.

A
  • renal
  • mesenteric
  • cutaneous
68
Q

What refractory can be seen with norepinephrine?

A
  • HYPOTENSION

- (bradycardia)

69
Q

At high does why may C.O. be decreased?

A
  • Increased afterload

- baroreceptor-mediated reflex bradycardia

70
Q

T/F: Dopamine effects both the alpha and beta receptors.

A

TRUE

71
Q

Dopamine over 5 mcg/kg/min causes ______ to be released.

A

-noriepinephrine

72
Q

Dopamine at 10 mcg/kg/min _____ effects start to predominate.

A

Alpha

73
Q

T/F: Dopamine has NO effect on pulmonary status.

A

TRUE

74
Q

What CNS effects will be seen with dopamine:

A 
INCREASE 
-mania
DECREASE
-Schizophrenia, ADHD, PG
-prolactiv secretion
-D2 inhibition
75
Q

What monitors will be needed with dopamine:

A

-BP, HR, MAP, urine output, mental status

76
Q

T/F: Ephedrine is an endogenous catecholamine.

A

FALSE (…..is a synthetic noncatecholamine.)

77
Q

Ephredrine principle effect is stimulating the releases of _________

A

-noriepinephrine

78
Q

Ephredrine principle mechanism is increased ______ ________.

A

-myocardial contractility

79
Q

Ephedrine causes _________ greater than ________ constriction increases _______ and with ________ heart rate and myocardial __________, INCREASES CARDIAC OUTPUT (beta 1 receptor)

A
  • venoconstriction
  • arteriolar
  • preload
  • Increased
  • contractility
80
Q

T/F: Ephedrine preserves/increases uterine blood flow.

A

TRUE

81
Q

Ephedrine is a _______ smooth muscle relaxant.

A

bronchial

82
Q

Ephedrine compared to epinephrine has a ____ BP response, but a ______ duration.

A

-less

longer

83
Q

What are some side effects of ephedrine.

A
  • HTN,
  • insomnia,
  • urinary retention,
  • headache,
  • weakness,
  • tremor,
  • palpitation,
  • psychosis
84
Q

Phenylephrine is a _______ ____ catecholamine.

A

-synthetic non

85
Q

Phenylephrine is a increases _____ more than _______.

A
  • Preload

- afterload

86
Q

T/F: Phenylephrine has a small beta 1 effect.

A

TRUE

87
Q

What are other uses of phenylephrine.

A
  • drug induced priapism
  • mydriatic agent
  • nasal decongestant
88
Q

Phenylephrine causes reflex ________.

A

-bradycardia

89
Q

Phenylephrine _________ renal and splanchnic blood flow

A

decreases

90
Q

Phenylephrine _______ pulmonary artery resistance and pressure.

A

Increases

91
Q

T/F: Phenylephrine has no dysrrhythmias as a direct effect.

A

TRUE

92
Q

Phenylephrine ______ Right to Left shunt in Tetrology of Fallot.

A

REVERSES

93
Q

Unlike catecholamine, effects of arginine vasopressin are _______ during hypoxia and severe acidosis.

A

preserved

94
Q

Vasopressin is used to preserve the ___________ homeostasis in patient with advanced vasodilitory shock.

A

cardiocirculatory

95
Q

Vasopressin advantages over epinephrine are:

A
  • does not increase myocardial oxygen consumption

- may work better in acidic environment patients

96
Q

What causes the cardiac dysrhythmias in vasoconstrictors?

A

Beta Stimulation

97
Q

Pure alpha agonists can _____ baroreceptor reflex-mediated ________ and possible _________ CO.

A
  • activate
  • bradycardia
  • decrease
98
Q

Antihypertensives may _______ the pressor response to indirect acting drugs or _______ the response to direct acting drugs (denervation hypersensistivity)

A
  • decrease

- enhance

99
Q

Cocaine interferes with reuptake of catecholamines. Both exogenous and endogenous catecholamines exhibit ________ effects.

A

enhanced

100
Q

Acute toxicity of cocaine may best be treated with ________ blockade.

A

adrenergic

Labetalol with alpha and beta effects

101
Q

Natural weight loos products may contain “ma huang” which is ______.

A

ephedra

102
Q

T/F: Ephedra contains ephedrine and psuedoephedrine.

A

TRUE

103
Q

How long do you want a person to stop taking “ma huang” before surgery?

A

24 hours

104
Q

T/F: Long term use of “ma huang” (ephedra) results in tachyphylaxis from depletion of endogenous catecholamine stores and may contribute to perioperative hemodynamic instability and cardiovascular collapse.

A

TRUE

105
Q

Phentolamine treats:

A

-Skin necrosis secondary to norepinephrine, dopamine and epinephrine

106
Q

What receptors does phentolamine work on and is it an agonist or antagonist?

A
  • Alpha 1 and 2

- Antagonist

107
Q

What is idiopathic hypertension:

A
  • over activity of the ANS
  • Interaction with the Renin angiotensin system
  • factors related to the sodium homeostasis and intravascular volume
108
Q

What would cause perioperative hypertension:

A
  • inadequaate anesthesia
  • airway manipulation
  • hypercarbia
  • hypoxia
  • medications
  • aortic cross clamp
  • hypervolemia
  • hypothermia
  • pain
109
Q

What pre-existing disease would cause perioperative hypertension:

A
  • pheochromocytoma
  • Hyperthyroid
  • autonomic hyperreflexia
  • malignant hyperthermia
  • intracranial hypertension
  • renal disease
  • poorly controlled hypertension
110
Q

What are the complication of perioperative hypertension?

A
  • CVA
  • MI
  • ischemia
  • LV dysfunction
  • arrhythmias
  • increased suture tension
  • hemorrhage,
  • pulmonary edema
  • cognitive dysfunction
111
Q

What is the primary cause of perioperative hypertension?

A

-Increased sympathetic discharge with systemic vasoconstriction

112
Q

What are the mechanism of action for vasodilators:

A
  • Direct smooth muscle dilatation (Calcium channel blocker and nitrates)
  • Alpha 1 antagonists (prazosin and labetalol)
  • alpha 2 agonists (clonidine and alpha-methyldopa)
  • A.C.E. inhibitors (captopril ad enalapril)
113
Q

What would be the site of action for vasodilators;

A
  • arterial dilators
  • venodilators
  • Balanced vasodilators
114
Q

Pure arterioe dilator causes minimal effect on _____.

A

preload

115
Q

“Pure” venodilators are ___ available. NTG acts primarily on the venous circulation, but also affects ______.

A
  • NOT

- arterioles

116
Q

Balanced vasodilator (SNP) decreases ______ and ________.

A
  • afterload

- preload

117
Q

T/F: Inhaled NO may be only “pure” pulmonary vasodilator.

A

TRUE

118
Q

Prostaglandin E1 (PGE1) is excellent pulmonary ________, but also causes systemic _______ requiring noriepinephrine to maintain systemic B/P.

A
  • vasodilator

- hypotension

119
Q

What is reflex effect of using a vasodilator:

A

increase heart rate

120
Q

What will vasodilators do to the hear arterioles?

A

-cause coronary steal

121
Q

How much artery perfusion to the LEFT VENTRICLE occurs during diastole?

A

70 - 90%

122
Q

T/F: Aortic systole pressure governs perfusion.

A

FALSE (Aortic diastolic….)

123
Q

Nitroglycerin preferentially dilates _______ vessels and ______ more blood toward ischemic zones.

A
  • conductace

- directs

124
Q

What are the vasodilators?

A
  • hydralazine
  • nitroglycerine
  • Sodium nitroprusside
125
Q

Is Hydralazine a direct acting or indirect acting arterial vasodilator.

A

-direct acting

126
Q

What effects does hydralazine have on the cardiovascular system?

A

INCREASES

  • heart rate
  • contractility
  • cardiac output
  • stroke volume
  • renin activity
  • fluid retention
  • MYOCARDIAL OXYGEN DEMAND

DECREASES
-B/P (diastolic > systolic)

127
Q

What type of patient do you want to avoid administering hydralazine to.

A
  • CAD
  • Increased ICP
  • Lupus
128
Q

What are the advantages of hydralazine?

A
  • maintains/increases cerebral blood flow
  • increases CO
  • Increases Stroke volume
129
Q

What are the disadvantages of hydralazine?

A

-Reflex tachy

-

130
Q

Nitroglycerine causes a release of ____ _____ for ___- specific relaxation of the vascular smooth muscle.

A
  • nitric oxide

- non

131
Q

What does nitroglycerine do to the coronary arteries?

A
  • relaxes

- relieves spasms

132
Q

What are some non-cardiac effects of nitroglycerine?

A
  • dilates meningeal vessels
  • Decrease renal blood flow with decrease BP
  • dilates pulmonary vessels
133
Q

Nitroglycerine is metabolized by ___________ nitrate reductase in the ______?

A
  • glutathione

- LIVER

134
Q

A nitrite ion oxidizes Hgb to ___________.

A

methemoglobin

135
Q

Nitroglycerine tolerance in _______ vessels can occur with chronic administration but not in the venous vessels.

A
  • arterial

- venous

136
Q

What are warnings and contraindications for nitroglycerine?

A
  • PDE5 (Viagra, cialis, ravashia)
  • narrow angle glaucoma
  • head trauma, cerebral hemorrhage
  • severe anemia
  • hypotension
137
Q

Does sodium nitroprusside directly or indirectly vasodilate arteries and veins?

A

-DIRECTLY

138
Q

With abrupt discontinuation of sodium nitroprusside can cause ______ _______ and _________.

A
  • reflex
  • tachycardia
  • hypertension
139
Q

Sodium nitroprusside causes a _____ in renal blood flow.

A

Decrease

140
Q

Sodium nitroprusside causes pronounced hypotensive effects with ______ and _______ ________.

A
  • spinal
  • general
  • anesthesia
141
Q

T/F: Sodium Nitroprusside metabolites are active and increase the effects.

A

FALSE (….are not active….)

142
Q

What are some warning and contraindication for sodium nitroprusside?

A
  • congenital optic atrophy
  • hypovolemia
  • compensatory HTN (AV shunting and aortic coarctation)
  • Severe renal/hepatic impairment
143
Q

What type of toxicity could sodium nitroprusside cause:

A

cyanide

144
Q

What is the presentation of cyanide toxicity:

A
  • hypotension
  • blurred vision
  • fatigue
  • metabolic acidosis
  • pink skin
  • absence of reflexes
  • faint heart sounds
145
Q

What are the thiocyanate levels: -

A

-therapuetic 6 - 29
-toxic 35-100
fatal >200

146
Q

What are the advantages of sodium nitroprusside:

A
  • immediate onset
  • short duration
  • reduced myocardial O2 demand
147
Q

What are the disadvantages of sodium nitroprusside:

A
  • reflex tachycardia
  • cyanide toxicity
  • intrapulmonary shunting
  • precipitous drop in BP
  • photodegradation
  • methemoglobinemia
  • coronary steal
  • Enhanced bleeding
  • cerebral vasodilator

Emily: Pharm 2 (11 decks)

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