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MSII Pharmacology > Unit 2 - Autonomics V > Flashcards

Unit 2 - Autonomics V Flashcards

1
Q

explain what the difference between direct and indirect adrenergic agonists are

A

direct: “personal” interaction with postsynaptic receptor
indirect: drug causes release of NE (from small cytoplasmic pool, NOT vesicles), which itneracts with postsynaptic receptor

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2
Q

what is tyramine? does it act directly or indirectly?

A

indirect adrenergic agonist

  • IV injection produces BP spike from released NE
  • found in fermented foods
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3
Q

what is tachyphylaxis?

A

acute tolerance to tyramine, such that BP won’t increase anymore
-when small cytoplasmic pool of NE is rapidly used up with repeated tyramine injections

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4
Q

structure-wise, what is selected for direct action?

A

side-chain hydroxy groups, either on chain or on ring

  • one imparts partial direct activity
  • both imparts full direct activity
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5
Q

how is dopamine a direct and indirect acting adrenergic agonist?

A

low dose: direct action of dopamine on D1 receptors
medium dose: direct action on B1 in heart, with some indirect action/NE release
high dose: direct action B1 in heart and a1 in vasculature, indirect action/NE release

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6
Q

what happens in low doses of dopamine?

A

direct action of dopamine on D1 receptors causes vasodilation, thus increases blood flow at renal, mesenteric, cerebral vessels
-lowers BP and increases urine output

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7
Q

what happens in medium doses of dopamine?

A
  • more of what happens at low doses (vasodilation b/c dopamine on D1 receptors)
  • direct action on B1 receptors in heart
  • indirect action/NE release, causing positive inotropic effect
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8
Q

what happens in high doses of dopamine?

A
  • more of what happens at low (vasodilation b/c dopamine on D1 receptors) and medium doses (direct action on B1 in heart, indirect action –> positive inotropic effect)
  • direct action on vascular a1 receptors
  • indirect action/NE release, causing vasoconstriction (including renal, as a1 activation dominates D1 receptor activation)
  • this causes increased BP that negates “low dopamine” effects
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9
Q

what is fenoldopam?

A

synthetic dopamine receptor agonist

  • activates D1 receptors only (no alpha/beta activating properties, doesn’t cause NE release)
  • mainly increases blood flow at renal, mesenteric, and cerebral arteries and lowers BP
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10
Q

when should you use fenoldopam?

A

in hypertensive emergencies

  • very short half life (10 minuets)
  • increases renal perfusion
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11
Q

what happens if you give NE, E, and ISO to dogs with vagal nerves cut?

A

NE: HR (B1) and MAP (a1) increase
E: HR (B1) and MAP (a1 > B2) increases
ISO: HR (B1) increases, MAP (B2) decreases

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12
Q

what happens if you give NE, E, and ISO to dogs with vagal nerves cut, after giving alpha-adrenergic blocking drug?

A

NE: HR (B1) increases, no change in MAP (a1)
E: HR (B1) increases, MAP (B2 > a1) decreases
ISO: HR (B1) increases, MAP (B2) decreases

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13
Q

what happens if you give NE, E, and ISO to dogs with vagal nerves cut, after giving beta-adrenergic blocking drug?

A

NE: no change in HR (B1), MAP increases (a1)
E: no change in HR (B1), MAP increases (a1 > B2)
ISO: no change in HR (B1) or MAP (B2)

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14
Q

what happens if you give NE, E, and ISO to dogs with vagal nerves cut, after giving alpha and beta-adrenergic blockers??

A

no change in anything

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15
Q

in humans, why does giving NE cause increased BP, but decreased HR?

A

reflex bradycardia due to baroreceptor response

-decreases HR to “save” the increased BP

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16
Q

what are the applications for vasoconstrictor actions of a1 agonists?

A
  1. control hemorrhage
  2. contain local anesthetic
  3. nasal decongestion
  4. allergic/anaphylactic shock
  5. occular pharmacology
  6. hypotension
  7. shock
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17
Q

how do a1 agonists control hemorrhage? what is most commonly used

A

vasoconstriction (superficial surgery)

-use epinephrine

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18
Q

how do a1 agonists contain local anesthetic? what is most commonly used

A

vasoconstriction (superficial surgery)

-use epinephrine

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19
Q

how do a1 agonists cause nasal decongestion? what is most commonly used

A

vasoconstriction decreases swollen mucosa

  • ephedrine*
  • phenylephrine* (Neo-synephrine)
  • phenylpropanolamine
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20
Q

how do a1 agonists help allergies or anaphylactic shock? what is most commonly used

A

epinephrine causes alpha and beta activation

  • a1: vasoconstriction
  • B1: bronchodilation
  • B2: decrease histamine release from mast cells
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21
Q

how do a1 agonists help in ocular pharmacology? what is most commonly used

A

treats glaucoma

  • hydroxyampphetamine releases NE (diagnostic)
  • epinephrine lowers intraocular pressure
  • -dipivalyl epinephrine, DPE is E prodrug
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22
Q

how do a1 agonists treat hypotension? what is most commonly used

A

vasoconstriction

  • especially to support missign adrenal catecholamines
  • often dopamine is used
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23
Q

do a1 agonists treat shock? what is most commonly used

A
  • vasoconstriction occurs already via reflex sympathetic activity, so giving more via a1 agonists might not be helpful
  • vasodilators (alpha-blockers) are actually more effective
  • -increase volume with extra fluids
  • -use dopamine to produce vasodilation by D1 receptors
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24
Q

why shouldn’t you use alpha-agonists to treat shock?

A
  1. localized ischemia may occur at infusion site
  2. avoid extravasation
  3. gradually decrease infusion
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25
what are the clinically important actions of useful ergot alkaloids? what are they?
ergotamine and ergonovine are a1 adrenergic and serotonin agonists (enhanced due to hydrogenation of DB in lysergenic acid nucleus) - vasoconstriction - smooth muscle contraction (uterine) - CNS (delirum and confusion)
26
what is ergonovine used for?
oxytocic to control post-partum bleeding as alpha-agonist
27
what is ergotamine used for?
acute migraine control as alpha-agonist
28
what is bromocriptine used for?
ergot alkaloid - hyperprolactenemia - decrease PRL from pituitary (D2 agonist) - Parkinsonism - D agonist
29
what are common side effects of alpha adrenergic agonists?
1. hypertension/headache 2. localized ischemia - a1 (especially with extravasation 3. dramatic fall in BP on rapid withdrawal 4. nervousness, anxiety, insomnia if they cross BBB (not NE or E)
30
what are a2 agonists primarily used for?
central control of BP via nucleus tractus solitarus | -decrease central sympathetic output, thus decrease BP to treat HTN
31
what are examples of a2 agonists?
1. clonidine | 2. alpha-methyldopa (prodrug)
32
what is clonidine used for?
a2 agonist to treat high blood pressure - also prevents withdrawal symptoms from opioids and alcohol - -prevents "super-sympathetic" state - main side effects: sedation and retention of Na and water
33
what are B1 agonists mainly used for? examples?
emergency or short-term treatment of cardiac arrest, AV block, or CHF - epinephrine (B1/2, a1/2), isoproterenol (B1/2), dobutamine (B1 selective) - use dobutamine for "chemical cardiac strength test"
34
what are B1 agonists mainly used for? examples?
1. bronchial asthma: causes bronchial smooth muscle relaxation - effective, but serious cardiac side effects if use E or ISO - use B2-selective terbutaline and albuterol to prevent cardiac side effects 2. uterine smooth muscle relaxation if premature labor - terbutaline 3. opthalmic uses like glaucoma
35
what are side effects of beta adrenergic agonists?
1. cardiac arrhythmia - direct effect from B1 receptor activation - indirect response to lowered BP resulting from B2-receptor mediated vasodilation 2. occasional skeletal muscle tremor with B2-receptor agonists
36
what notable adrenergic agonist is used as a stimulant?
amphetamine - treats narcolepsy and hyperkinesis (ADHD) - increases release of NE
37
what notable adrenergic agonist is used as a diet aid?
phenylephrine
38
what are first generation beta blockers?
both are non-selective - propranolol - gold standard war horse; half life 4 hours - -large differences in plasma levels resulting from large individual differences in bioavailability - timolol; half life 4 hours
39
what are second generation beta blockers?
B1-selective (so that B2 doesn't precipitate asthma attacks) - *metoprolol; half life 4 hours - -less dramatic differences in bioavailability than propranolol - *atenolol; half life 6-8 hours - -least lipid soluble beta-blocker, thus not much in CNS - bisoprolol
40
what are third generation beta blockers?
L and C are non-selective, while B is B1 selective; both have "additional actions" such as a1 receptor antagonism - *Labetalol; treats HTN and lowers TPR with little tachycardia - Carvedilol; treats HTN and heart failure - Betaxolol
41
what are uses of beta blockers/
1. HTN 2. cardiac arrythmias 3. angina pectoris 4. glaucoma 5. migraine 6. stage fright 7. heart failure
42
how do beta blockers treat HTN?
mechanisms not well understood, but several possible contributions: - block renin release from JA - presynaptic B1 receptors enhance NE release - production of NO - block a1 receptors - block Ca entry - open K channels
43
how do beta blockers treat cardiac arrhtymias?
stabilize rate through B1 receptor block
44
how do beta blockers treat angina pectoris?
decrease myocardial work and O2 demand
45
how do beta blockers treat glaucoma?
only timolol - decrease secretion of aqueous humor from ciliary process
46
how do beta blockers treat migraine?
unknown mechanism - much used for prophylaxis (not acute attack) - may prevent B2 dilation of cranial vessels
47
how do beta blockers treat stage fright/anxiety?
may prevent the tachycardia feedback cycle
48
how do beta blockers treat heart failure?
while beta-blockers are contraindicated in patients with heart failure, they are also firth line therapy in such patients -but can only use 2nd or 3rd generation beta-blockers, or else B2 will exacerbate CHF
49
what are major effects of B1 blockers? what is a caution?
cardiac depression - if central effect: fatigue - nausea, vomiting, diarrhea, sexual dysfunction common - do NOT withdraw abruptly
50
what are major effects of B2 blockers?
bronchoconstriction | -may precipitate asthmatic attack
51
what is phentolamine?
nonselective a-receptor antagonist (a1/2) | -imidazoline derivatives
52
what is phenoxybenzamine?
nonselective a-receptor antagonist (a1/2) - nitrogen mustard compound that forms covalent bond with receptor - haloalkylamine derivative
53
what is prazosin?
selective a1 antagonist - part of a family with other -zosins - quinazoline derivative
54
what is the major application of alpha-antagonists?
1. HTN 2. peripheral vascular disease 3. pheochromocytoma 4. shock 5. BPH
55
how does one treat peripheral vascular disease?
with prazosin, phentolamine, or phenoxybenzamine (alpha receptor agonists) -most are chronic occlusive, thus non-responsive, but those that are vasospastic (like Raynauds, frost bite) are responsive
56
what alpha blocker treats pheochromocytoma?
phenoxybenzamine - also give fluids b/c vessel volume increases dramatically - may also add beta-blocker
57
how do alpha blockers treat shock?
breaks profound vasoconstriction and improves perfusion
58
how do alpha blockers treat BPH?
reduce resistance to outflow of urine contributed by trigone muscle of bladder and urethra - give prazosin or other a1-selective blockers - also may give drugs that inhibit conversion of testosterone to DHT
59
what are side effects of sympathetic blocking drugs?
alpha: postural hypotension, nasal stuffiness, and inhibition of ejaculation beta1: erectile dysfunction, bradycardia B2: bronchoconstriction, metabolic alterations CNS: drowsy/dizzy
60
what are neuron-blocking drugs?
block synthesis, packaging, release, and reuptake of nt - little clinical use, and many serious side effects - rare uses are HTN and inoperable pheochromocytoma
61
what is alpha-methyltyrosine?
neuron blocking drug that manages inoperable pheochromocytoma -inhibits synthesis of NE
62
what is reserpine?
neuron blocking drug that was an older hypertensive | -blocks vesicles from filling with E or NE, preventing NE or E release
63
what is guanethidine?
neuron blocking drug that was an older antihypertensive | -prefered substrate fro vesicles, such that no NE or E are packed into vesicles ("shooting blanks")

MSII Pharmacology (43 decks)

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