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Pharm2 S.Horvath > Vasoconstrictors > Flashcards

Vasoconstrictors Flashcards

1
Q

where does the SNS originate?

A

Thoracolumbar T1-L2

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2
Q

what converts dopamine to norepinephrine ?

A

dopamine beta hyroxylase

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3
Q

norepinephrine is metabolized by ___ and ___

A

MAO and COMT (monamine oxidase and catecholo-methyltranseraese

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4
Q

what are the 4 adrenergic receptors

A

alpha 1&2, beta 1&2

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5
Q

alpha 1 Is located in the ___

A

periphery

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6
Q

alpha 2 is located ___

A

centrally (negative feedback like precedex)

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7
Q

beta-1 is located in the ___

A

heart

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8
Q

beta-2 is located in the ___

A

smooth muscle (some beta 2 can be on the heart)

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9
Q

T/F Even though Beta1 and Beta2 share g-protein type mechanism and the end result is increasing cyclic AMP, the end product is different

A

TRUE . beta1: contraction. beta2: vasodilation

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10
Q

T/F Alpha-1 leads to bronchodilation

A

FALSE- bronchoconstriction - no good!

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11
Q

Alpha 1 inhibits or promotes insulin secretion?

A

inhibits

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12
Q

Alpha 1 causes smooth muscle ____

A

contraction

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13
Q

Alpha 1 receptor is PRE or POST synaptic?

A

post

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14
Q

Alpha1 causes peripheral vaso____

A

constriction

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15
Q

what is Alpha 1’s relationship to glucose

A

stimulates glycogenolysis and gluconeogenesis - by inhibiting insulin, there is more glucose in the blood to use, more ATP, more energy

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16
Q

Alpha 1 effect on pupils?

A

mydriasis. pupil dilation - open up the eyes more so you can see surroundings

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17
Q

Alpha 1 causes GI contraction or relaxation ?

A

relaxation

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18
Q

Alpha 2 is pre or post synaptic?

A

PREsynaptic in the PNS, POSTsynaptic in the CNS

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19
Q

Alpha 2 MOA in PNS

A

post-synaptic - decreases entry of CA into the cell, limits the release of nor-epi

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20
Q

alpha 2 MOA in the CNS

A

sedation, decreased sympathetic outflow, decreased BP, platelet aggregation

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21
Q

BETA1 receptor is ____synaptic

A

POST

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22
Q

what does Beta1 do to HR, conduction velocity, and myocardial contractility ?

A

Increases.

Beta1–more complete and faster heartbeat to get more blood out into the circulation faster

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23
Q

BETA2 is ____synaptic

A

post

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24
Q

beta 2 stimulation leads to smooth muscle contraction or relaxation?

A

relaxation

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25
Q

beta 2 leads to peripheral vasoconstriction or vasodilation?

A

vasodilation.

think: more of a surface area in the periphery for o2 exchange

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26
Q

T/F Beta 2 receptor decreases BP

A

TRUE

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27
Q

Beta2 causes broncho____

A

dilation

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28
Q

Beta 2 ___ insulin secretion, but also ____ glycogenolysis and gluconeogenesis

A

increases.

seems counter intuitive but does both

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29
Q

Beta 2 ____ GI motility

A

decreases

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30
Q

The PNS has a ____ origin.

A

craniosacral (III, V VII, X)

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31
Q

PNS - preganglia near _____

A

organs of innervation

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32
Q

PNS - postganglia secrete _____

A

Ach

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33
Q

T/F acetylcholine activates both arms of the ANS

A

TRUE

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34
Q

acetylcholine participates in a ____ ____ action potential

A

calcium mediated

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35
Q

Cholinergic receptors can be ___ or ____

A

nicotinic, muscarinic

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36
Q

SNS affects on urinary bladder: smooth muscle ____, sphincter ____

A

relaxation, contraction

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37
Q

SNS affects on urinary bladder: smooth muscle ____, sphincter ____

A

contraction, relaxation

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38
Q

SNS cause bronchial smooth muscle ___, while PNS causes bronchial smooth muscle ____

A

relaxation, contraction

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39
Q

SNS stim causes gallbladder ____, while PNS causes ____

A

relaxation, contraction

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40
Q

PNS affects on GI tract - motility and sphincter

A

increases motility, secretion, sphincter relaxation

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41
Q

PNS stim causes ___ of the eye

A

miosis (constriction)

42
Q

T/F both SNS stim and PNS stim increase salivary secretions, but PNS has a marked increase

A

TRUE

43
Q

SNS stim causes ___ beta cell secretion

A

decreased - (fight/flight)

44
Q

T/F PNS stim causes glycogen synthesis

A

true (rest/digest)

45
Q

T/F SNS stim of beta causes constriction of coronary arterioles

A

FALSE.

stim of ALPHA causes constriction of coronary arterioles

stim of BETA causes relaxation of coronary arterioles

same idea with skeletal muscle arterioles.

46
Q

T/F PNS stim causes relaxation of : coronary arterioles, skin and mucous arterioles, and skeletal muscle arterioles , and pulmonary arterioles.

A

TRUE

47
Q

T/F SNS stim causes constriction of all the arterioles, except when beta is stimulated.

A

TRUE

48
Q

Down regulation is a reduction in the ____ of receptors

A

number.

Reduces the number, but not their response.

when you’re using an agonist for a very long time, overstimulating the receptors, eventually your body realizes something is wrong so it will begin to break down and remove your receptors.

49
Q

T/F Up regulation results in tachyphylaxis

A

FALSE

down regulation results in tachyphylaxis.

50
Q

Chronic depletion of catecholamines or use of antagonists increases the number of receptors, but not their sensitivity… otherwise known as?

A

up regulation

51
Q

T/F Up-regulation may account for withdrawal syndrome with beta blockers

A

TRUE

52
Q

what is receptor uncoupling?

A

inability of the receptor to bind G protein (alters the function of the receptor)

occurs rapidly (minutes to hours)

53
Q

movement of receptors from the cell surface to intracellular compartments is

A

sequestration

occurs more slowly (couple of days)

54
Q

the movement of receptors from the cell surface to intracellular compartments, but then destroyed = _____

A

downregulation

prolonged process (weeks to months)

55
Q

what results in uncontrolled release of catecholamines due to an adrenal gland tumor?

A

pheochromocytoma

56
Q

catecholamines can be either ___ or ____

A

neurotransmitters and hormones

57
Q

T/F All catecholamines are sympathomimetics but not all sympathomimetics are catecholamines

A

TRUE

58
Q

what are compounds that resemble catecholamines except that hydroxyl groups are not present in both the 3 and 4 positions of the benzene ring

A

sympathomimetics

59
Q

all sympathomimetics are derived from ____

A

B phenylethylamine (ring)

60
Q

T/F Presence of hydroxyl groups on the 3 and 4 position of the benzene ring of the B phenylethylamine creates a catachol

A

TRUE

61
Q

sympathomimetics ___ skeletal muscle

A

dilate

62
Q

T/F sympathomimetics increase vulnerability to dysrhythmias

A

TRUE

63
Q

sympathomimetics have what effect hepatically?

A

glycogenolysis (glucose going up bc glycogen is broken down into glucose)

64
Q

sympathomimetics cause CNS ____

A

stimulation

65
Q

the only time a vasopressor should be used is when….

A

the patient’s BP must be increased immediately to avoid pressure-dependent reductions in organ perfusion with subsequent ischemia

66
Q

T/F sympathomimetics are used as additive to LA to slow systemic absorption of LA from site of infiltration or injection

A

TRUE

67
Q

The ____ of alpha and beta receptors influences the response evoked by the sympathomimetic

A

anatomical distribution.

(the primary action at the organ has to do with the amount of that type of receptor that is there, and what the affinity for that receptor is.

68
Q

T/F norepinephrine has minimal effects on airway resistance because adrenergic receptors in bronchial smooth muscle are mostly beta-2 and thus not stimulated by catecholamine.

A

TRUE

69
Q

T/F Epi and isoproterenol are potent bronchodilators as a result of their ability to activate beta2 receptors

A

TRUE

70
Q

where is MAO located?

A

Monoamine oxidase in an enzyme present in liver, kidneys, GI tract that catalyzes oxidative deamination

71
Q

COMT methylates the _____ of catecholamines

A

hydroxyl group

72
Q

If it’s a catecholamine its metabolized by ___, if its non-catecholamine its just ____`

A

both, MAO

73
Q

T/F inhibition of the reuptake of catecholamines produces a greater potentiation of effects of epinephrine than does inhibition of either enzyme.

A

TRUE

74
Q

how is completeness of the reuptake mechanism and metabolism evidenced?

A

presence of unchanged catecholamines in the urine

75
Q

why are PO catecholamines ineffective

A

because of metabolism of these compounds by enzymes in the GI mucosa and liver before reaching the systemic circulation

76
Q

what routes can epi be given

A

sq, IV

77
Q

what routes can dopamine and norepi be given

A

IV

78
Q

T/F patients on MAO inhibitors may manifest reduced responses when treated with synthetic non-catecholamines

A

FALSE - exaggerated responses

79
Q

what are the reflexive changes of vasoconstrictors

A

decreased HR, decreased conduction, occasionally decreased contractility

80
Q

vasoconstrictors broncho____

A

dilate

81
Q

T/F non cardiac effects of vasoconstrictors include glycogenolysis and CNS stimulation

A

true

82
Q

risk of end organ damage with a MAP <65 occurs after how long

A

13-28min

83
Q

risk of end organ damage with a map <50 occurs after how long

A

1 min

84
Q

vasoconstrictors contraindications:

A

can worsen LV failure, can exacerbate RV failure, can decrease RBF, can mask hypovolemia

85
Q

what are the 3 natural catecholamines

A

epi, norepi , dopamine

86
Q

what receptors does epi stimulate

A

alpha 2, beta 1, beta 2

87
Q

what drug is the most potent activator of alpha1?

A

epi. 2-10x more potent than NE

88
Q

epi ____ blood sugar

A

increase

89
Q

epi ____ secretion of insulin (promotes or inhibits?)

A

inhibits

90
Q

epi ___ lipolysis

A

increases

91
Q

epi __ glycogenolysis

A

increases

92
Q

how does epi decrease renal blood flow?

A

potent renal vasoconstrictor (alpha-1 effect)

stimulates renin release

93
Q

what effects do low dose EPI have? (1-2mcg/min)

A

beta 2 in peripheral vasculature predominates- the net effect is decreased SVR and distribution of blood to skeletal muscle.

map remains essentially the same

94
Q

what effects do intermediate dose epi have? (4mcg/min)

A

beta1

increased HR and contractility and increased C.O.

increased automaticity (may lead to dysrrhythmias)

95
Q

what effects do high doses of epi have (>10mcg/min)

A

alpha 1

at this point A1 overrides any B1 effects and you can see slight reflect bradycardia, bradyarrthmia.

potent vasoconstrictor including cutaneous, splanchnic and real vascular beds. (no significant effect on cerebral arterioles)

used to maintain myocardial and cerebral perfusion.

reflex brady can occur

96
Q

racemic epi is a mixture of ___ and ___ that constrict edematous mucousa

A

levo and dextrorotatory isomers that constrict edematous mucousa

97
Q

what effect does epi have on coagulation

A

platelet aggregation

98
Q

what does epi do to pupils

A

dilate - mydriasis

99
Q

norepinephrine is primarily an ___ agonistt

A

alpha 1

100
Q

T/F both epi and norepinephrine have the potential to interact with all the receptors, but norepinephrine does not interact with all the receptors. these drugs have different affinities to for the same receptors

A

TRUE

norepinephrine is primarily an alpha-1 agonist

beta-1 effects are overshadowed by its alpha 1 effects

beta 2 effects are minimal

101
Q

at higher doses of norepinephrine, what happens to cardiac output?

A

decrease. because of increased afterload and baroreceptor-mediated reflex bradycardia.

explains refractory hypotension

102
Q

T/F norepinephrine has greater metabolic effects than epi

A

false. LESS

they both share the property of creation of glucose and liberation of glucose (glycogenolysis and gluconeogensis). but when you dont have the beta2 effect you might lose some of those metabolic effects (not gone just lesser than)

Pharm2 S.Horvath (13 decks)

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