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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
what are sympathomimetics
- 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
what are indirect-acting sympathomimetics and what do they do
- synthetic non-catecholamines - release endogenous NE from postganglionic sympathetic nerve endings
27
what are direct acting sympathomimetics
- catecholamines and synthetic non-catecholamines
28
sympathomimetics are derived from
B phenylethylamine
29
composition of catecholamines
- presence of hydroxyl groups in the 3rd and 4th position of the benzene ring of hte B phenylethylamine creates a catachol
30
inhibition of the reuptake of catecholamines
- inhibition of the reuptake mechanism produces a greater potentiation of effects of epinephrine that inhibition of either enzyme
31
metabolism of synthetic non-catecholamines
- 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
sulfoconjugation reactions
- participate in the metabolism of catecholamines and phenylephrine - SULT1A3/ SULT1A4 polymorphisms primarily effect phenylephrine metabolism
33
vasoconstrictors effects on the body
- increase arterial resistance and afterload & increase venous return - reflex changes: decreased HR, conduction, contractility
34
time frame for end-organ damage with decreased MAP
MAP < 65 mmHg for 13-28 min MAP < 50 mmHg for 1 min
35
natural catecholamines
- dopamine - NE - epi
36
epinephrine receptors
- stimulates Alpha-1, Beta-1, Beta-2 - most potent for Alpha-1
37
indirect effects of epinephrine
- increases lipolysis, glycogenolysis, inhibits insulin - decreases renal BF even in the absence of changes in BP - stimulates the release of renin indirectly
38
low dose effects of epi (1-2 mcg / min)
- stimulates beta-2 - net effect is decreased SVR
39
intermediate dose effect of epinephrine (4 mcg/min)
- stimulate beta-1 - increased HR, contractility, and CO - increased automaticity (dysrrhythmias)
40
high dose epi effects (>10 mcg/ min)
- stimulates alpha-1 - potent vasoconstrictor (no effect on cerebral arteries) - used to maintain myocardial and cerebral perfusion - reflex bradycardia can occur
41
racemic epi
- mixture of levo- dextrorotatory isomers that constrict edematous mucosa - lasts 30-60 min
42
side effects of epi
- hyperglycemia, mydriasis, platelet aggregation, sweating, headache, tremor, nausea, arrhythmias
43
norepinephrine effects on body
- increases BP by adjusting SVR - increases systolic, diastolic, MAP - vasoconstricts renal, mesenteric, cutaneous vascular beds - may decrease renal blood flow (oliguria) - mesenteric infarct
44
norepi receptors
- primarily alpha-1 - beta-1 is overshadowed by by alpha-1
45
CO and norepi
- CO increases at low doses - CO may decrease at high doses due to increased afterload and baroreceptor mediated reflex bradycardia
46
dopamine effects at different doses
- low dose causes NE to be released - high doses effects alpha receptors
47
ephedrine receptors
- synthetic catecholamine - works on alpha-1 and beta - tachyphylaxis can occur
48
ephedrine effects to body
- principle action increased myocardial contractility - venoconstriction > arteriolar = increased preload w/ increased HR, and increased myocardial contractility = increased CO, increasing BP
49
ephedrine effects in in other parts of the body
- increases uterine blood flow - bronchial smooth muscle relaxant
50
phenylephrine effects
- synthetic non-catecholamine - alpha-1 - increases preload > afterload - increases pressure without changing CO - ok in pregnant pts
51
side effects of phenylephrine
- reflex brady - decreases renal and splanchnic blood flow - increases pulmonary artery resistance and pressure - no dysrrhythmias as a direct effect
52
vasopressin primary use
- 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
V1 receptors
- arterial constriction - increases sensitivity of baroreceptor in aortic arch = increased HR = increased BP - angiotensin is the primary working molecule
54
V2 receptors
- in renal collecting ducts - increases the permeability of cell membranes resulting in reabsorption of water - AQP2 pulls the fluid back into circulation
55
advantages of vasopressin over epi
- 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
oxytocin effects and uses
- increases Ca++ in the myometrium, increasing strength of contraction - oxytocin receptors increase during pregnancy - used to increase uterine contractions and reduce postpartum hemorrhage
57
oxytocin effects on mother
- 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
oxytocin effects on baby
- bradycardia, PVC, arrythmias - permanent brain damage - death - seizures - low apgar at 5 min - jaundice - retinal hemorrhage
59
drug interactions with vasoconstrictors
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
cocaine and vasoconstrictors
- 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
what to give for extravasation
- phentolamine (alpha 1 and 2 antagonist) - peripheral vasodilator - 5-10 mg around the site of extravasation

Pharm 2 (10 decks)

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