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PHARM 2 > Vasoconstrictors > Flashcards

Vasoconstrictors Flashcards

1
Q

The sympathetic nervous system originates from where?

A

Thoracolumbar origin (T1-L2)

Preganglia near spinal cord

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2
Q

Postganglia adrenergic fibers secrete what?

A

Norepinephrine

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3
Q

How is norepinephrine synthesized?

A

Dopamine enters the synaptic vessel

Dopamine beta hyroxylase converts dopamine to NE

An action potential releases NE from the synaptic vessel

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4
Q

What 4 things cause the signal termination of release of NE?

A

Reuptake: recycling and putting back where it came from

Dilution by diffusion

Metabolism: Monamine oxidase (MAO) and catechol-o-methyltranserase (COMT)

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5
Q

What are the 4 adrenergic receptors?

A

Alpha 1: periphery (helps us in fight or flight response)

Alpha 2: central (negative feedback loop in response to agonist)

Beta 1: heart

Beta 2: other smooth muscle

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6
Q

Activation of Alpha 1 postsynaptic receptor causes:

A
  • Activation increases intracellular calcium
  • smooth muscle contraction
  • peripheral vasoconstriction
  • bronchoconstriction
  • inhibits insulin secretion
  • stimulates glycogenolysis and gluconeogenesis
  • mydriasis
  • GI relaxation
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7
Q

Stimulation of Alpha-2 receptors causes what -

Presynaptic in PNS

Postsynaptic in CNS

A

Presynaptic in PNS: decreases entry of calcium into the cell. Limits the release of norepinephrine

Postsynaptic in CNS: sedation, decreased sympathetic outflow, decreased BP, platelet aggregation

negative feedback loop

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8
Q

Stimulation of beta 1 post-synaptic receptor causes what?

A

Increased HR
Increased conduction velocity
Increased myocardial contractility

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9
Q

Stimulation of Beta 2 postsynaptic receptor causes what?

A 
Smooth muscle relaxation
Peripheral vasodilation
Decreases BP
Bronchodilation
Increases insulin secretion
Increases glucogenolysis and gluconeogenesis
Decreases GI mobility
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10
Q

The parasympathetic nervous system originates from where?

A

Craniosacral origin (III, V, VII, X)

Preganglia near organs of innervation

Postganglia secrete acetylcholine (ACh) —> cholinergic fibers

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11
Q

Acetylcholine activates which arms of the ANS?

A

Both

SNS and PNS

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12
Q

What makes up acetylcholine?

A

Choline + acetyl CoA

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13
Q

ACh is deactivated by what

A

Acetylcholinesterase

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14
Q

Acetylcholine has a __________ mediated action potential

A

Calcium

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15
Q

What are the 2 cholinergic receptors?

A

Nicotinic

Muscarinic

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16
Q

SNS stimulation of GI tract does what?

PNS stimulation of GI tract does what?

A

SNS: decreases motility secretions, sphincter contraction

PNS: increases motility, secretions, sphincter relaxation

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17
Q

SNS stimulation of coronary arteries does what?

A

Alpha: constriction

Beta: relaxation

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18
Q

SNS of skeletal muscle arterioles

A

Alpha: constriction
Beta: relaxation

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19
Q

Down regulation of effector cell receptors happens why?

A

Extended exposure to agonists reduces the number, but not their response. Results on tachyphyaxis

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20
Q

Up regulation of effector cell receptors is caused by what?

A

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

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21
Q

T/F receptor uncoupling occurs gradually over time

A

False

Occurs rapidly

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22
Q

This is the movement of receptors from the cell surface to intracellular compartments.

Occurs more slowly

A

Sequestration

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23
Q

This is the movement of receptors from the cell surface to intracellular compartments, but then destroyed

A

Downregulation

Prolonged process

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24
Q

This refers to residual basal activity of the autonomic system

A

Tone

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25
Q

What is pheochromocytoma?

A

Uncontrolled release of catecholamines due to an adrenal gland tumor - constant SNS stimulation

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26
Q

These are both neurotransmitters and hormones, and act on adrenergic receptors.

A

Catecholamines

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27
Q

Norepinephrine is primarily a ____________ and epinephrine is primary a __________

A

NE: neurotransmitter

Epi; hormone

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28
Q

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

A

Sympathomimetics

Mimic SNS

They are classified according to their selectivity for stimulating alpha and/or beta receptors

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29
Q

What are indirect-acting sympathomimetics?

A
  • Synthetic non-catecholamines
  • Release endogenous neurotransmitter NE from postganglionic sympathetic nerve endings

*ephedrine is an example

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30
Q

What are direct-acting sympathomimetics?

A

Catecholamines and synthetic non-catecholamines

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31
Q

T/F: Sympathomimetics can be both naturally occurring and synthetic.

A

True

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32
Q

T/F: All catecholamines are sympathomimetics

A

True

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33
Q

T/F: All sympathomimetics are catecholamines

A

FALSE

Not all sympathomimetics are catecholamines

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34
Q

What are the 2 most common uses for sympathomimetics?

A
  • positive Inotrope to improve cardiac contractility

- vasopressor to elevate BP from unacceptable levels

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35
Q

T/F: vasopressors are first line treatment for low BP

A

FALSE

They are a last resort

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36
Q

What are 3 other uses of sympathomimetics?

A
  1. Treatment of bronchospasm in the asthmatic pt
  2. Management of anaphylaxis
  3. Addition to LA to slow systemic absorption of LA from site of infiltration or injection
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37
Q

What influences the response evoked by the sympathomimetics?

A

The anatomical distribution of alpha and beta adrenergic receptors

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38
Q

Does NE have significant or minimal effects on airway resistance?

A

Minimal

Adrenergic receptors in bronchial smooth muscle are mostly beta-2 and thus not stimulated by this catecholamine

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39
Q

What are 2 potent bronchodilators as a result of their ability to activate beta-2 receptors?

A

Epinephrine

Isoproterenol

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40
Q

What 2 enzymes metabolize catecholamines?

A 
Monoamine oxidase (MAO)
-enzyme present in liver, kidneys, GI tract that catalyze oxidative deamination

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

**if its a catecholamine its metabolized by both, if its not a catecholamine its just metabolized by MAO

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41
Q

Does inhibition of the reuptake mechanism or inhibition of MAO and COMT cause a greater potentiation of epinephrine

A

Reuptake mechanism

42
Q

The reuptake mechanism causes ________ presence of unchanged catecholamines in urine

A

Minimal

43
Q

T/F: oral administration of catecholamines is effective

A

FALSE

Metabolism of these compounds in GI mucosa and liver before reaching systemic circulation

44
Q

Acceptable routes of administration of epi

A

Sub-Q

IV

45
Q

Routes of administration for dopamine

A

IV

46
Q

Synthetic non-catecholamines are dependent on what for metabolism?

A

MAO

Not metabolized by COMT bc lack a 3-hydroxyl group

47
Q

Which is faster, metabolism of catechols or non-catechols?

A

Catechols is faster than non-catechols

48
Q

Pts on MAO inhibitors may manifest ________ responses when treated with synthetic non-catecholamines

A

Exaggerated

49
Q

What are 2 hemodynamic effects of vasoconstrictors?

A
  • increase arterial resistance and afterload (increase SVR and usually MAP)
  • increase venous return (increase preload and CO)
50
Q

What are some reflex changes that can occur with vasoconstrictors?

A

Decreased HR
Decreased conduction
Occasionally decreased contractility

51
Q

What are 4 non-cardiac effects of vasoconstrictors?

A
  • Bronchodilate
  • Glycogenolysis
  • Insulin, renin, pituitary hormone
  • CNS stimulation (low lipid solubility)
52
Q

What are indications of use of vasoconstrictors?

A

Decreased arterial resistance (hypotension)

  • iatrogenic
  • physiologic

CPR

  • restore perfusion pressure to vital organs
  • used in conjunction of other appropriate cardiac drugs

Other indicators

  • anaphylactic shock
  • iatracardiac R —> L shunts
  • hypovolemia
53
Q

According to study in Anesthesiology - risk of end organ damage and mortality increase with time

  • MAP <65 for ______________ minutes
  • MAP <50 for ______________ minutes
A

MAP <65 for 13-28 minutes

MAP <50 for 1 minute

54
Q

What are 4 contraindications/compilations of vasoconstrictors?

A

Can worse LV failure

Can exacerbate RV failure

Can decrease renal blood flow

Can mask hypovolemia

55
Q

What are the 3 natural catecholamines?

A

Epinephrine

Norepinephrine

Dopamine

56
Q

Epi stimulates what receptors?

A

Alpha 1
Beta 1
Beta 2

most potent activator of alpha 1 receptors. 2-10x more potent than NE

EPI = everything

57
Q

What are some uses of epinephrine?

A

Asthma, anaphylaxis, cardiac arrest, bleeding, and prolong regional anesthesia

58
Q

Does epi increase or decrease lipolysis and glycogenolysis?

A

Increases

It also inhibits the secretion of insulin.

Can see increase in BG due to the stress of surgery

59
Q

What does epinephrine do to renal blood flow?

A

It decreases renal blood flow even in the absence of changes in systemic BP

  • potent renal vasoconstrictor (alpha-1 effect)
  • stimulates renin release (indirect effect)
60
Q

What happens with low doses of epi (1-2 mcg/min)?

A

Primarily beta-2 effects

-stimulates alpha-1 receptors in the skin, mucosa, and hepatorenal system while bets-2 receptors are stimulated in skeletal muscle

  • Beta-2 effects in peripheral vasculature predominate
    • net effect is decreased SVR and distribution of blood to skeletal muscle
    • MAP remains essentially the same
61
Q

What happens with intermediate doses (4 mcg/min) of epinephrine?

A

Primarily beta-1 effects

Increased HR and contractility and increased CO

Increased automaticity - may lead to dysrhythmias

62
Q

What happens with high doses (>10 mcg/min) of epinephrine?

A

Primarily alpha-1 effects.

Potent vasoconstrictor including cutaneous, splanchnic and renal vascular beds (no significant effect on cerebral arterioles)

Used to maintain myocardial and cerebral perfusion

Reflex bradycardia can occur

63
Q

What is the most potent activator of alpha-1 receptors?

A

Epinephrine

64
Q

This is a mixture of levo- and dextrorotatory isomer that constrict edematous mucosa.

What is it used to treat?

A

Racemic epinephrine

Used to treat sever croup and post-extubation or traumatic airway edema

*treatment lasts 30-60 minutes. Observe for 2 hours after treatment to watch for rebound

65
Q

What are side effects of epinephrine?

A

No CNS effects
Hyperglycemia, mydriasis, platelet aggregation, sweating, HA, tremor, nausea, arrhythmias

*monitor BG, RR, O2 sats, HR, and BP

66
Q

This is an endogenous catecholamine responsible for maintaining BP by adjusting SVR.

A

Norepinephrine

Increases systolic, diastolic, and mean arterial pressure

67
Q

T/F: Norepinephrine is a potent vasoconstrictor of renal, mesenteric, and cutaneous vascular beds

A

TRUE

  • may decrease renal blood flow and cause oliguria
  • may lead to mesenteric infarct
  • peripheral hypoperfusion can lead to gangrene of digits
68
Q

How does norepinephrine effect the alpha and beta receptors?

A

Primarily and alpha-1 agonist

Beta-1 effects are overshadowed by its alpha-1 effects

Beta-2 effects are minimal

69
Q

How does norepinephrine affect CO?

A

CO may increase at low doses.

Higher doses CO may decrease because of increased afterload and baroreceptor-mediated reflex bradycardia

May see refractory hypotension

70
Q

T/F: Norepinephrine has more metabolic effects than epinephrine

A

FALSE

LESS metabolic effects than epi

71
Q

This endogenous catecholamine has similar effects as epi - different doses affect different receptors.

A

Dopamine

72
Q

Is ephedrine a catecholamine?

A

No. It’s a synthetic noncatecholamine

73
Q

Is ephedrine direct or indirect acting?

A

Principle effect is indirect - causes release of norepi from vessels.

74
Q

What receptors does ephedrine work on?

A

Alpha-1 and beta receptors.

75
Q

Ephedrine’s principle mechanism is to increase myocardial contractility. How does this occur?

A

Venoconstriction is greater than arteriolar constriction —> increases preload and with an increased HR and myocardial contractility, increases CO (beta-1 receptor action)

-increases SBP and DBP as a result

76
Q

Can tachyphylaxis occur with ephedrine?

A

YES

77
Q

How does ephedrine affect uterine blood flow and bronchial smooth muscle

A

It preserves or increased uterine blood flow

Bronchial smooth muscle relaxant

78
Q

Side effects of ephedrine

A

HTN, insomnia, urinary retention, HA, weakness, tremor, palpating, psychosis

*monitor BP, pulse, UO, and mental status

79
Q

T/F: phenylephrine is a synthetic catecholamine

A

FALSE

It’s a synthetic non-catecholamine

80
Q

Phenylephrine affects what receptors?

A

Direct alpha-1 agonist

  • increases preload > afterload
  • small beta-1 effect

Increases PVR when CO adequate
May be used to improve coronary perfusion pressure with out chronotropic side effects

81
Q

What are some other uses for phenylephrine?

A

Drug induced priapism
Mydriasis agent
Nasal decongestant

82
Q

What are some side effects of phenylephrine?

A

Reflex bradycardia
Decreases renal and splanchnic blood flow
Increases pulmonary artery resistance and pressure

*no dysrrhythmias as a direct effect

83
Q

Which catecholamine is phenylephrine similar to?

A

Like norepinephrine, but less potent and longer lasting

84
Q

What are the 3 posterior pituitary hormones ?

A
  1. Arginine vasopressin (formally known as ADH)
  2. DDAVP (desmopressin)
  3. Oxytocin (pitocin)
85
Q

Place 3 posterior pituitary hormones in order of most to least for their antidiuretic effects, and then their vasopressor effects

A

Antidiuretic: DDAVP > arginine vasopressin > oxytocin

Vasopressor effects: arginine vasopressin > DDAVP > oxytocin

86
Q

Vasopressin stimulates what receptors?

A

V1a: causing intense arterial vasoconstriction

V2: in renal collecting ducts —> increases permeability of cell membranes resulting in the passive reabsorption of water

87
Q

This is used to preserve cardiocirculatory homeostasis in pts with advanced vasodilatory shock

A

Vasopressin

88
Q

T/F: Effects of catecholamines are preserved during hypoxia and severe acidosis

A

FALSE

The effects of arginine vasopressin are preserved during hypoxia and severe acidosis

89
Q

What are 2 advantages of vasopressin over epinephrine?

A
  1. Epi increases myocardial O2 consumption

2. Catecholamines may not work well in an acidic environment associated with CPR

90
Q

T/F: There is significant human data showing the benefit of vasopressin

A

FALSE

Human data lacking

91
Q

3 Benefits of vasopressin shown in animal studies

A
  1. Better blood flow to vital organs
  2. Better delivery of cerebral oxygen
  3. Better chance of resuscitation and better neurologic outcome
92
Q

T/F: vasopressin is at least as effective as Epi, may have fewer adverse effects than Epi, and therefore is a reasonable alternative to Epi in treatment of cardiac arrest.

A

TRUE

93
Q

Name 3 adverse effects/drug interaction of vasoconstrictors

A
  1. Cardiac dysrhythmias (Beta stimulation)
  2. Pure alpha agonists can activate baroreceptor reflex-mediated bradycardia and possible decrease CO
  3. Antihypertensives may decrease the pressor response to indirect acting drugs, or enhance the response to direct acting drugs (denervation hypersensitivity)
94
Q

This class of medications can increase the availability of endogenous norepinephrine

A

Tricyclics antidepressants and MAO Inhibitors

95
Q

You can have an exaggerated response to direct or indirect acting agents when using tricyclic antidepressants and MAO inhibitors

A

INDIRECT

96
Q

The exaggerated response to indirect acting agents while on tricyclic antidepressants and MAOI is worse in the first _______ days of therapy

A

14 - 21

  • Ok to continue these drugs in the perioperative period.
  • Use a decreased dose of direct acting drugs
97
Q

How does cocaine effect the re-uptake of catecholamines?

A

It interferes with it.

Both exogenous and endogenous catecholamines exhibit enhanced effects.

Produces central and peripheral sympathetic stimulation resulting in vasoconstriction, tachycardia, and potentially arrhythmias

98
Q

Cocaine acute toxicity is bestmanaged with what?

A

Adrenergic blockade

Labatelol with both alpha and beta effects

*don’t just give a beta blocker bc alpha stimulation will still be occurring.

99
Q

This weight loss drug may contain ma huang and can cause tachyphylaxis from depletion of endogenous catecholamine stores.

A

Ephedra

100
Q

This medication is given when there is extravasation of IV during administration of vasoconstrictors

A

Phentolamine

Alpha 1 and 2 antagonist

Peripheral vasodilator

Treats skin decors is secondary to NE, dopamine and epi

101
Q

This drug is synthetic human angiotensin II

A

Giapreza

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