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Pharmacology II - Emily Britton > Vasoconstrictors - Pharm 2 > Flashcards

Vasoconstrictors - Pharm 2 Flashcards

1
Q

Stimulation of presynaptic Alpha-2 receptors results in _________ of NE release from the nerve ending

A

inhibition

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2
Q

SNS has a thoracolumbar origin of ___ to ___

A

T1-L2

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3
Q

Preganglia are near the _____ ______

A

spinal cord

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4
Q

Postganglia secete ________ which act on ______ fibers

A

norepinephrine / adrenergic

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5
Q

NOREPINEPHRINE: Dopamine enters the ________ vessel. Dopamine beta hydoxylase converts dopamine to _________. An _____ _______ releases NE from the synaptic vessel.

A

synaptic / norepinephrine / action potential

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6
Q

Norepinephrine signal termination is accomplished by what?

A

Reuptake, dilution by diffusion, Metabolism by MOA and COMT

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7
Q

Most of norepi is being recycled and some of norepinephrine is being _____ down

A

broken

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8
Q

Alpha-1

A

periphery

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9
Q

Beta-1

A

heart

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10
Q

Beta-2

A

periphery

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11
Q

Alpha-2

A

central

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12
Q

When norepinephrine is binds with beta-1 G-proteins cause ________ changes. Review slide 8

A

confomrational

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13
Q

Review slide 9 for alpha 1 and 2 with norepi

A

Review slide 9

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14
Q

Alpha-1 Postsynaptic receptor

A

Activation increases intracellular calcium, smooth muscle contraction, periphereral vasoconstriction, Bronchoconstriction, inhibits insulin secretion, stimulates glycogenolysis and gluconeogenesis, mydriasis, GI relaxation

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15
Q

Alpha-2 receptors: Presynaptic in the PNS

A

decreases entry of calcium into the cell AND limits the release of norepinpehrine

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16
Q

Alpha-2 receptors: Postsynaptic in the CNS

A

sedation, decreased sympathetic outflow, decreased BP, platelet aggregation

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17
Q

Beta-1 Postsynaptic receptor

A

increases HR, increases conduction velocity, increases myocardial contractility

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18
Q

Beta-2 postsynaptic receptor

A

stimulation leads to smooth muscle relaxation, peripheral vasodilation, decreases BP, bronchodilation, increases insulin secretion, increases glycogenolysis and gluconeogensis, decreases GI mobility

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19
Q

PNS is CRANIOSACRAL origin. Which CN?

A

III, V, VII, X

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20
Q

The PNS is preganglia near _______ or innervation

A

organs

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21
Q

PNS postganglia secrete _______ and act on _______ fibers

A

acetylcholine / cholinergic

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22
Q

Acetylcholine activates both arms of the _______

A

ANS

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23
Q

Review slide 15

A

acetylcholine and calcium mediated action potential

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24
Q

SNS stimulation of the heart results in

A

increased HR, increased conduction velocity, increased automacity, increased contractility

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25
Q

SNS stimulation of the bronchial smooth muscle results in

A

relaxation

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26
Q

SNS stimulation of the GI tract results in

A

decreased motility, decreased secretion, sphincter contraction

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27
Q

SNS stimulation of the gallbladder results in

A

relaxation

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28
Q

SNS stimulation of the urinary bladder results in

A

smooth muscle relaxation and spincger contraction

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29
Q

SNS timulatioin of the uterus and ureters

A

contraction

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30
Q

SNS stimulation of the eye

A

mydriasiss

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31
Q

SNS stimulation of the Liver

A

glycogenolysis and gluconeogensis

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32
Q

SNS stimulation of the pancreas

A

Decreased beta cell secretion (decreased insulin)

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33
Q

SNS stimulation of the salivary glands

A

increased secretion

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34
Q

SNS stimulation of Sweat glands

A

increase

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35
Q

PNS stimulation of heart

A

Decreased HR, decreased conduction velocity, slight decrease in contractility

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36
Q

PNS stimulation of the bronchial smooth muscle

A

contraction (resting state)

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37
Q

PNS stimulation of the GI tract

A

Increased motility, increased secretion, sphinter relaxation

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38
Q

PNS stimulation of the galllbadder

A

contraction

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39
Q

PNS stimulation of the urinary bladder

A

smooth muscle contraction, spincter relaxation

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40
Q

PNS stimulation of the uterus

A

variable

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41
Q

PNS stimulation of the ureter

A

relaxatioin

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42
Q

PNS stimulation of the eye

A

miosis

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43
Q

PNS stimulation of the liver

A

glycogen synthesis

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44
Q

PNS stimulation of the salivary gland

A

marked increase in secretion

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45
Q

PNS stimulation of sweat glands

A

increases

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46
Q

Extended exposure to agonists reduces the number, but not their response. Results in tachyphylaxis.

A

down regulation

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47
Q

Chronic depletion of catecholamines 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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48
Q

OCCURS RAPIDLY. Inability of the receptor to bind G protein (alter the function of the receptor)

A

Receptor uncoupling

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49
Q

OCCURS more SLOWLY. Movement of receptors from the cell surface to intracellular compartments.

A

Sequestration

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50
Q

Rapidly diminishing response to successive doses of a drug, rendering it less effective. The effect is common with drugs acting on the nervous system

A

Tachyphylaxis

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51
Q

T/F There is a residual basal activity of the ANS

A

TRUE

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52
Q

Uncontrolled release of catecholamines due to an adrenal gland tumor that results in constant SNS stimulation

A

pheochromocytoma

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53
Q

Catecholamines are considered both _______ and _________

A

neurotransmitters and hormones

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54
Q

Catecholamines act on _______ receptors

A

adrenergic

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55
Q

Catecholamines have both the ____ and ____ group

A

catechol and amine

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56
Q

Sympathomimetics, which means they mimic the SNS, they do not all have to be _________.

A

catecholamines

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57
Q

Sympathomimetics are classified according to their selectivity for stimulating ____ and/or _____ receptors

A

alpha / beta

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58
Q

INDIRECT-ACTING sympathomimetics are considered synthetic ___________. They work by causing release of endogenous neurotransmitter _________ from ______sympathetic nerve endings

A

non-catecholamines / norepinephrine / postganglionic

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59
Q

DIRECT-ACTING sympathomimetics are ________ and ________

A

catecholamines and synthetic non-catecholamines

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60
Q

All sympathomimetics are derived from __________

A

B-phenylethylamine

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61
Q

Presence of hydroxyl groups on the 3 and 4 position of the benzene ring of the B-phenylethylamine creates a catachol. Drugs with this composition are _______

A

catecholamines

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62
Q

Sympathomimetics are most often used as _____ ________ to improve cardiac contractility OR ________ to elevate blood pressure from unacceptable low levels.

A

positive inotrope / vasopressor

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63
Q

The only time a vasopressor should be used is when the patient’s blood pressure must be increased __________ to avoid pressure-dependent reductions in organ perfusion with subsequent ischemia

A

immediately

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64
Q

Other uses for sympathomimetics

A

treatment of brnochospasm in the asthmatic patient, management of anaphylaxis, addition to local anesthetic to slow systemic absorption of local anesthetic from site of infiltration or injection

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65
Q

Metabolism of Catecholamines: All drugs containing the 3,4 dihydroxybenzen (catecholamines) structure are rapidly inactivated by ____ and ______

A

MAO and COMT

66
Q

Monamine oxidase (MAO) is an enzyme present in liver, kidneys, GI tract that ________ oxidative deamination

A

catalyzes

67
Q

Catechol-o-transferase (COMT) ________ the hydroxyl group of catecholamines

A

methylates

68
Q

Reupatake of catecholamines: Inhibition of this uptake mechanism produces a greater potentiation of effects of ________ than does inhibition of either enzyme (MAO or COMT)

A

Epinephrine

69
Q

Non-catecholamines are only metabolized by ______

A

MAO

70
Q

Synthetic non-catecholamines are not involved in _______

A

reuptake

71
Q

Metabolism of non-catecholamines: Since they lack a 3-hydroxyl group they are not metabolized by ______. They are dependent on _______ for metabolism. Metabolism is often _______ than that of catechols. Therefore, inhibition of MAO may PROLONG their DOA. Patients on MAO inhibitors may manifest exaggerated responses when treated with SYNTHETIC NON-CATECHOLAMINES

A

COMT / MAO / Slower

72
Q

T/F Parkinson’s patients may be on MAOB inhibitors and PTSD patients as well may be on TCAs which are MAO inhibitors so may have exaggerated responses to synthetic non-catecholamines

A

TRUE

73
Q

Reflex changes from vasoconstrictors

A

decreasede HR, Decreased conduction, occasionally decreased contractility

74
Q

If the heart feels like it is pumping against a high pressure, you may see a reflex of _______

A

decreased HR

75
Q

Vasoconstrictors non-cardiac effects

A

bronchodilate, glycogenolysis, insulin, renin, pituitary hormone, CNS stimulation

76
Q

Risk of end organ damage and mortality increases with time. So MAP <65 when can we see end organ damage?

A

13-28 minutes

77
Q

MAP <50 for how long will usually result in end organ damage?

A

1 minute

78
Q

Other indications for vasoconstrictors include anaphylactic shock, intracardiac __ to ___ shunts, and hypovolemia after adequate fluids

A

R to L

79
Q

Vasoconstrictors contraindications / complications

A

Can worsen LV faliure, Can exacerbate RV failure, can decrease renal blood flow, can mask hypovolemia

80
Q

Natural catecholamines

A

epi, norepi, dopamine

81
Q

Epinephrine is a natural catecholamine that stimulates what?

A

alpha-1, beta-1, beta-2 receptors

82
Q

Most potent activator of Alpha-1 receptors and is 2-10x more potent than norepi

A

epinephrine

83
Q

______ has the most potential for side effects because it stimulates everything

A

epi

84
Q

T/F Norepinephrine at any dose stimulates alpha-1

A

TRUE

85
Q

Epinephrine ______ lipolysis and glycogenolysis, and _______ secretion of insulin

A

increases / inhhibits

86
Q

Epi decreases renal blood flow even in the absence of changes in ________. It is a potent renal vasoconstrictor which relates to it’s _____ effect. It also stimulates _____ release (indirect effect)

A

systemic BP / alpha-1 / renin

87
Q

Low dose Epi (1-2 mcg/min)

A

stimulate alpha-1 receptors in the skin, mucosa, and hepatorenal system while Beta-2 receptors are stimulated in skeletal muscle.

88
Q

Low dose Epi (1-2 mcg/min), Beta-2 effects in peripheral vasculature _________. The net effect is decreased SVR and distribution of blood to skeletal muscle. MAP essentially ______

A

predominates / stays the same

89
Q

Intermediate dose epi (4mcg/min)

A

BETA-1 / increases HR and contractility and increases CO. Increased automacity may lead to dysrrhythmias

90
Q

High dose epi (>10mcg/min)

A

ALPHA-1

91
Q

_____ is the most potent activator of alpha-1 receptors. At high doses (>10mcg/min) it is a potent vasoconstrictor including cutaneous, splanchninc and renal vascular beds. No significant effect on _____ ______. Used to maintain myocardial and cerebral perfusion. _______ bradycardia can occur

A

epi / cerebral arterioles / reflex

92
Q

Only __ to __% of anything inhaled actually makes it into the lungs and subsequentally the blood stream

A

12 to 15%

93
Q

Racemic epi is a mixture of levo- and dextrorotary isomers that constrict edematous mucosa. It is used to treat severe _____ and post extubation or traumatic airway ______.

A

croup / edema

94
Q

Racemic epi treatment lasts ___ to ____ and should observe the patient for ___ after treatment to watch for rebound

A

30 to 60 min / 2 hours

95
Q

Epinephrine side effects

A

hyperglycemia, mydriasis, platelet aggregation, sweating, headache, tremor, nausea, arrhythmias

96
Q

With epinephrine there are no CNS effects noticed with initial doses but tremors, shakiness, and jitters after _________ use.

A

prolonged

97
Q

Looks and smells like EPI, but it’s really beta-1 light, get improved CO, improved contractility, and maintain conduction velocity, but not a significant change in HR

A

Norepinephrine

98
Q

Endogenous catecholamine that is responsible for maintaining BP by adjusting the SVR. It Increases systolic, diastolic and MAP.

A

Norepinephrine

99
Q

Norepinephrine is a potent vasoconstrictor or renal, mesenteric and cutaneous vascular beds. Ths vasoconstriction may _______ renal blood flow and cause _______. May lead to mesenteric ______. Peripheral hypoperfusion can lead to _______ of digits.

A

decrease / oliguria / infact / gangrene

100
Q

Norepi alpha and beta effects

A

primarily alpha-1 Agonist | Beta-1 effects are overshadowed by its Alpha-1 effects | Beta-2 effets are minimal to none

101
Q

With norepi, CO may increase at ____ doses. _______ doses may decrease CO because of increased afterload and baroreceptor-mediated reflex bradycardia and could result in refractory hypotension

A

low / high

102
Q

T/F there are case reports of tachyphylaxis with norepinephrine when used for a long time

A

TRUE

103
Q

T/F Norepi has more metabolic effects than epi

A

FALSE, It has LESS metabolic effects than epi and they are only seen at larger doses

104
Q

Review slides 60-63

A

Cardiac effects of Epi vs. norepi

105
Q

Dopamine: Beta and Alpha receptor effects (10-20 mcg/kg/min)

A

At doses over 5 mcg/kg/min causes NE to be released contributing to cardiac stimulation (precursor). At doses over 10 mcg/kg/min ALPHA effects start to predominate.

106
Q

With Dopamine, at doses of >20 mcg/kg/min, it is mainly ______ receptor effects

A

alpha

107
Q

Dopamine has no effect on ________ status. Dopamine given IV does not cross the ______. Increased mania, decreased schizophrenia, ADHD, and PD, so monitor mental status

A

pulmonary / BBB

108
Q

Synthetic noncatecholamine with direct and indirect actions. Principle effect is indirect. It works on both alpha-1 and beta receptors.

A

ephedrine

109
Q

With epehdrine, ______ stimulatioin may evoke arrhythmia, particularly in a sensitized myocardium.

A

beta

110
Q

Ephedrine relies primarily on _______ for metabolism.

A

MAO

111
Q

Alpha-1 effects of ephedrine is coming from the release of ______ from storage vessicles in the CNS

A

Norepi

112
Q

The principle mechanism of ephedrine is increased _______ ______

A

myocardial contractility

113
Q

Epehedrine causes _________ greater than ___________ constriction which increases preload and with increased HR and myocardial contractility, it increases CO (beta-1 receptor action). IT INCREASES SBP AND DBP as a result.

A

venoconstriction / arteriolar constriction

114
Q

With ephedrine, _________ can occur. Can start having negative feedback at alpha-2 receptors and will stop the release of _________.

A

Tachyphalxis / norepinephrine

115
Q

Ephedrine preserves or _______________ uterine blood flow

A

increases

116
Q

Ephedrine is also a bronchial smooth muscle _______

A

relaxant

117
Q

Ephedrine dose is 2.5-25 mg IV. What is the onset and duration?

A

onset 1 min | Duration: 5-10 min

118
Q

PO dose of ephedrine

A

25-50 mg PO or IM

119
Q

Ephedrine is like ________, but BP response is less intense and lasts LONGER

A

epi

120
Q

E-meds are everything

A

epi and ephedrine hit everything

121
Q

Side effects of epehedrine

A

HTN, insomnia, urinary retention, headache, weakness, tremor, palpitations, psychosis

122
Q

Synthetic non-catecholamine that is a direct alpha-1 agonist

A

phenylephrine

123
Q

Increases PVR when CO is adequate

A

phenylephrine

124
Q

May be used to improve coronary perfusion pressure without chronotropic side effects

A

phenylephrine

125
Q

T/F Phenylephrine is ok to use in pregnant patients

A

TRUE

126
Q

Other uses for phenylephrine

A

drug induced priapism, mydriatic agent, nasal decongestant

127
Q

Phenylephrine causes a reflex _______. Decreases renal and _______ blood flow. Increases ________ artery resistance and pressure. NO DYSRRHYTHMIAS as a direct effect.

A

bradycardia / splanchnic / pulmonary

128
Q

Phenylephrine dose, onset, duration, infusion

A

dose: 50-100 mcg bolus or drip | onset: 1-2 min | duration: 5-10 min | infusion: 10-20 mcg/min

129
Q

Phenylephrine is like ________ but less potent and longer lasting

A

norepinephrine

130
Q

Onset of epi and norepi is _________ while onset of ephedrine and phenylephrine is ______.

A

immediate / 1-3 min

131
Q

Duration of epi and norepi is ______ while ephedrine is_____ and phenylephrine is ________

A

5-15 min / 15-20 min / 10-20 min

132
Q

Review slide 76

A

chart comparison of catecholamines

133
Q

Arginine vasopressin is formerly known as

A

ADH

134
Q

Posterior pituitary hormones

A

AVP (arginine vasopressin), DDAVP, Oxytocin

135
Q

Review potency on slide 79

A

Appears DDAVP is most potent

136
Q

Vasopressin has vasopressor effects as well as _____ effect

A

antidiuretic

137
Q

Vasopressin stimulates V1a receptors causing intense _______ ________

A

arterial vasoconstriction

138
Q

Vasopressin in the renal collecting ducts increases the permeabilty of cell memranes resulting in the passive reabsorption of water which is the ____ effect

A

V2

139
Q

Used to PRESERVE cardiocirculatory homeostasis in patients with advanced vasodilitory shock

A

vasopressin

140
Q

Patients who have failed of resistant to conventional vasopressor therapy may benefit from _________

A

vasopressin

141
Q

Unlike catecholamines, effects of arginine vasopressin are preserved during _____ and severe ______

A

hypoxia and severe acidosis

142
Q

Studies mention that when someone is acidotic and hypoxic, __________ still works so consider using it first

A

vasopressin

143
Q

In animal studies, vasopressin is associated with

A

better blood flow to vital organs, bettery delivery of cerebral oxygen, better chance of resuscitation and better neurologic outcome HOWEVER, human data is lacking

144
Q

Catecholamines may not work well in an acidic environment associated with ____

A

CPR

145
Q

EPI increases myocardial oxygen consumption which can contribute to risk of developing post-resuscitation _____ and arrhythmias

A

MI

146
Q

Vasopressin is at least effective as ____, may have fewer adverse side effects than ____, and therefore is a reasonable alternative to _____ in the treatment of cardiac arrest

A

Epi / epi / epi

147
Q

Cardiac dysrhythmias from vasoconstrictors is usually from _____ stiimulation

A

beta

148
Q

Pure alpha agonsists can activate _______ and possible decrease CO

A

baroreceptor reflex-mediated bradycardia

149
Q

Antihypertensives may decrease the pressor response to _______ acting drugs OR enhance the response to _______ acting drugs (denervation hypersensitivity)

A

indirect / direct

150
Q

TCAs and MAOIs increase the availability of endogenous __________. Exaggerated response with ______ acting agents.

A

norepi / indirect

151
Q

With TCAs and MAOIs interacations with vasoconstrictors will be worse in the first 14-21 days of therapy and then a ________ __________ of receptors occurs.

A

down regulation

152
Q

With someone on TCAs and MAOIs what vasoconstrictors would you use?

A

It’s okay for them to continue their meds but you would use a DIRECT acting drugs at a DECREASED dose

153
Q

_______ is the primary way we get rid of our catecholamines.

A

reuptake

154
Q

Make sure you use combo agents with both alpha and beta blockade for someone with cocaine use. What are examples of these drugs?

A

coreg and labetolol

155
Q

Cocaine facts

A

interferes with reuptake of catecholamines. Both exogenous and endogenous catecholamines exhibit enhanced effects. Produces central and peripheral sympathetic stimulation, resulting in vasoconstriction, tachycardia, and potentially and arrhythmias. Acute toxicity may best be mananged with adrenergic blockade (labetolol with alpha and beta effects)

156
Q

How long before surgery should ephedrine or pseudoephedrine be stopped

A

at least 24 hrs prior to surgery

157
Q

Treatment for extravasation

A

phentolamine

158
Q

Alpha 1 and 2 agonist. It is a peripheral vasodialtor that treats skin necrosis secondary to norepi, epi and dopamine.

A

phentolamine

159
Q

Giapreza AKA

A

Angiotensin II

160
Q

Increases blood pressure in adults with septic shock or other distributive shock who do not adequately respond to available therapies.

A

Giapreza

161
Q

Increases aldosterone and causes to hold on to fluids and increases BP. Used when failing norepi, vasopressin, and full of fluids. However this is a last resort and can cause >10% chance of DVT, arterial thrombosis, and prophylactic treatment for blood clots should be used.

A

Giapreza

Pharmacology II - Emily Britton (5 decks)

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