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Pharm 2 > week 1 vasoconstrictors > Flashcards

week 1 vasoconstrictors Flashcards

1
Q

Parasympathetic receptor/ transmitter pathway

A

pre-ganglionic neuron releases acetylcholine > nicotinic receptor causing post-ganglionic neurons to release acetylcholine > muscarinic receptor

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2
Q

sympathetic receptor/ transmitter pathway

A

pre-ganglionic neuron releases acetylcholine > nicotinic receptor causing post-ganglionic receptor release norepi which binds to adrenergic receptor

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3
Q

Sympathetic nervous system nerve location

A
  • thoracolumbar origin (T1-L2)
  • preganglia near spinal cord
  • postganglia secrete norepi
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4
Q

what converts dopamine to NE

A

dopamine beta hydroxylase

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5
Q

how NE is formed

A
  • dopamine enters the synaptic vessel
  • dopamine beta hydroxylase converts dopamine to NE
  • an action potential releases NE from the synaptic vessel
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6
Q

what happens to NE when the signal is terminated

A
  • reuptake
  • dilution by diffusion
  • metabolism
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7
Q

what metabolizes NE and catecholamines

A
  • monamine oxidase (MAO)
  • catechol-o-methyltransferase (COMT)
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8
Q

receptors and their location of effect

A
  • alpha 1: peripheral
  • alpha 2: cnetral
  • beta 1: heart
  • beta 2: smooth muscle (lungs)
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9
Q

binding pathway from NE

A

NE binds to B1 and B2 extracellularly causing Gs proteins (2nd messenger) to release adenylyl cyclase which uses ATP to release cAMP to cause contraction

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10
Q

effects from activation of Alpha-1 postsynaptic receptor

A
  • increases in intracellular Ca
  • smooth muscle contraction
  • peripheral vasoconstriction
  • bronchoconstriction
  • inhibits insulin secretion (increases glucose for energy)
  • stimulates glycogenolysis and gluconeogenesis
  • mydriasis
  • GI relaxation
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11
Q

activation of presynaptic alpha 2 receptors (PNS)

A
  • decreases Ca into the cell
  • limits the release of NE
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12
Q

activation of alpha-2 in postsynaptic (CNS)

A
  • sedation
  • decreased sympathetic outflow
  • decreased BP
  • platelet aggregation
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13
Q

beta 1 postsynaptic activation

A
  • increases HR
  • increases conduction velocity
  • increases myocardial contractility
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14
Q

activation of postsynaptic beta-2 receptors

A
  • smooth muscle relaxation
  • peripheral vasodilation
  • decreased BP
  • bronchodilation
  • increases insulin secretion
  • increases glycogenolysis and gluconeogenesis
  • decreases GI mobility
  • many more beta 2 in lungs which overrides alpha 1 constriction
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15
Q

parasympathetic nervous system location

A
  • craniosacral origin (III, VII, IX, X)
  • preganglia near organs of innervation
  • postganglia secrete acetylcholine to cholinergic fibers
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16
Q

effects of acetylcholine

A
  • activates both arms of the autonomic nervous system
  • choline + acetyl CoA = acetylcholine - choline acetyltransferase
  • calcium mediated action potential
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17
Q

what deactivates acetylcholine

A
  • acetylcholinesterase
  • breaks it down to choline and acetate
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18
Q

cholinergic receptors

A
  • nicotinic
  • muscarinic
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19
Q

down regulation

A
  • extended exposure to agonists reduces the number but not their response = tachyphylaxis
  • movement of receptors from the cell surface to intracellular compartments, but then destroyed
  • prolonged process
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20
Q

up regulation

A
  • chronic depletion of catecholamines or agonists increases the number of receptors but not their sensitivity
  • may account for withdraw syndrome with beta blockers
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21
Q

receptor uncoupling

A
  • occurs rapidly
  • inability of the receptor to bind to G protein (alter the function of the receptor)
  • desensitization
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22
Q

sequestration

A
  • occurs more slowly (desensitization)
  • movement of the receptors from the cell surface to intracellular compartments
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23
Q

tone

A
  • residual basal activity of the autonomic nervous system
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24
Q

what are catecholamines and where do they act

A
  • both neurotransmitters and hormones
  • act on adrenergic receptors
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25
Q

what are sympathomimetics

A
  • compounds that resemble catecholamines except hydroxyl groups are not present in the 3 and 4 positions of the benzene ring
  • classified according to their selectivity for receptors (alpha or beta)
  • all catecholamines are sympathomimetic but not all sympathomimetics are catecholamines
26
Q

what are indirect-acting sympathomimetics and what do they do

A
  • synthetic non-catecholamines
  • release endogenous NE from postganglionic sympathetic nerve endings
27
Q

what are direct acting sympathomimetics

A
  • catecholamines and synthetic non-catecholamines
28
Q

sympathomimetics are derived from

A

B phenylethylamine

29
Q

composition of catecholamines

A
  • presence of hydroxyl groups in the 3rd and 4th position of the benzene ring of hte B phenylethylamine creates a catachol
30
Q

inhibition of the reuptake of catecholamines

A
  • inhibition of the reuptake mechanism produces a greater potentiation of effects of epinephrine that inhibition of either enzyme
31
Q

metabolism of synthetic non-catecholamines

A
  • lack a 3-hydroxyl group
  • not metabolized by COMT
  • dependent on MAO for metabolism
  • metabolism often slower than catechols
  • pts on MAO inhibitors manifest exaggerated responses
32
Q

sulfoconjugation reactions

A
  • participate in the metabolism of catecholamines and phenylephrine
  • SULT1A3/ SULT1A4 polymorphisms primarily effect phenylephrine metabolism
33
Q

vasoconstrictors effects on the body

A
  • increase arterial resistance and afterload & increase venous return
  • reflex changes: decreased HR, conduction, contractility
34
Q

time frame for end-organ damage with decreased MAP

A

MAP < 65 mmHg for 13-28 min
MAP < 50 mmHg for 1 min

35
Q

natural catecholamines

A
  • dopamine
  • NE
  • epi
36
Q

epinephrine receptors

A
  • stimulates Alpha-1, Beta-1, Beta-2
  • most potent for Alpha-1
37
Q

indirect effects of epinephrine

A
  • increases lipolysis, glycogenolysis, inhibits insulin
  • decreases renal BF even in the absence of changes in BP
  • stimulates the release of renin indirectly
38
Q

low dose effects of epi (1-2 mcg / min)

A
  • stimulates beta-2
  • net effect is decreased SVR
39
Q

intermediate dose effect of epinephrine (4 mcg/min)

A
  • stimulate beta-1
  • increased HR, contractility, and CO
  • increased automaticity (dysrrhythmias)
40
Q

high dose epi effects (>10 mcg/ min)

A
  • stimulates alpha-1
  • potent vasoconstrictor (no effect on cerebral arteries)
  • used to maintain myocardial and cerebral perfusion
  • reflex bradycardia can occur
41
Q

racemic epi

A
  • mixture of levo- dextrorotatory isomers that constrict edematous mucosa
  • lasts 30-60 min
42
Q

side effects of epi

A
  • hyperglycemia, mydriasis, platelet aggregation, sweating, headache, tremor, nausea, arrhythmias
43
Q

norepinephrine effects on body

A
  • increases BP by adjusting SVR
  • increases systolic, diastolic, MAP
  • vasoconstricts renal, mesenteric, cutaneous vascular beds
  • may decrease renal blood flow (oliguria)
  • mesenteric infarct
44
Q

norepi receptors

A
  • primarily alpha-1
  • beta-1 is overshadowed by by alpha-1
45
Q

CO and norepi

A
  • CO increases at low doses
  • CO may decrease at high doses due to increased afterload and baroreceptor mediated reflex bradycardia
46
Q

dopamine effects at different doses

A
  • low dose causes NE to be released
  • high doses effects alpha receptors
47
Q

ephedrine receptors

A
  • synthetic catecholamine
  • works on alpha-1 and beta
  • tachyphylaxis can occur
48
Q

ephedrine effects to body

A
  • principle action increased myocardial contractility
  • venoconstriction > arteriolar = increased preload w/ increased HR, and increased myocardial contractility = increased CO, increasing BP
49
Q

ephedrine effects in in other parts of the body

A
  • increases uterine blood flow
  • bronchial smooth muscle relaxant
50
Q

phenylephrine effects

A
  • synthetic non-catecholamine
  • alpha-1
  • increases preload > afterload
  • increases pressure without changing CO
  • ok in pregnant pts
51
Q

side effects of phenylephrine

A
  • reflex brady
  • decreases renal and splanchnic blood flow
  • increases pulmonary artery resistance and pressure
  • no dysrrhythmias as a direct effect
52
Q

vasopressin primary use

A
  • preserve cardiocirculatory homeostasis in patients with advanced vasodilatory shock
  • pts who failed conventional vasopressor therapy
  • pts with adverse effects of vasopressors
  • unlike catecholamines, effects of vasopressin are preserved during hypoxia and severe acidosis
53
Q

V1 receptors

A
  • arterial constriction
  • increases sensitivity of baroreceptor in aortic arch = increased HR = increased BP
  • angiotensin is the primary working molecule
54
Q

V2 receptors

A
  • in renal collecting ducts
  • increases the permeability of cell membranes resulting in reabsorption of water
  • AQP2 pulls the fluid back into circulation
55
Q

advantages of vasopressin over epi

A
  • epi increases myocardial O2 consumption (risk of MI and arrythmias)
  • vasopressin has not direct effect on HR reducing myocardial O2 consumption
  • vasopressin works in an acidic environment
56
Q

oxytocin effects and uses

A
  • increases Ca++ in the myometrium, increasing strength of contraction
  • oxytocin receptors increase during pregnancy
  • used to increase uterine contractions and reduce postpartum hemorrhage
57
Q

oxytocin effects on mother

A
  • HTN
  • N/V
  • bleeding
  • pelvic hematoma
  • arrythmias, PVC’s
  • uterine rupture in high doses
    ***severe water intoxication + seizures and coma with 24 hour infusion - possible death
58
Q

oxytocin effects on baby

A
  • bradycardia, PVC, arrythmias
  • permanent brain damage
  • death
  • seizures
  • low apgar at 5 min
  • jaundice
  • retinal hemorrhage
59
Q

drug interactions with vasoconstrictors

A

tricyclic antidepressants and MAO inhibitors
- cause increased endogenous NE
- worse in the first 14-21 days and then down regulation occurs
- okay to use these drugs pre-op (use decreased dose of pressor)

60
Q

cocaine and vasoconstrictors

A
  • interferes with re-uptake of catecholamines (enhanced effects)
  • cocaine produces vasoconstriction and tachycardia
  • acute toxicity may be managed with lebatolol (has both alpha and beta effects)
61
Q

what to give for extravasation

A
  • phentolamine (alpha 1 and 2 antagonist)
  • peripheral vasodilator
  • 5-10 mg around the site of extravasation

Pharm 2 (10 decks)

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