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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
Q

what are the clinically important actions of useful ergot alkaloids? what are they?

A

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)
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26
Q

what is ergonovine used for?

A

oxytocic to control post-partum bleeding as alpha-agonist

27
Q

what is ergotamine used for?

A

acute migraine control as alpha-agonist

28
Q

what is bromocriptine used for?

A

ergot alkaloid

  • hyperprolactenemia - decrease PRL from pituitary (D2 agonist)
  • Parkinsonism - D agonist
29
Q

what are common side effects of alpha adrenergic agonists?

A
  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
Q

what are a2 agonists primarily used for?

A

central control of BP via nucleus tractus solitarus

-decrease central sympathetic output, thus decrease BP to treat HTN

31
Q

what are examples of a2 agonists?

A
  1. clonidine

2. alpha-methyldopa (prodrug)

32
Q

what is clonidine used for?

A

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
Q

what are B1 agonists mainly used for? examples?

A

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
Q

what are B1 agonists mainly used for? examples?

A
  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
Q

what are side effects of beta adrenergic agonists?

A
  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
Q

what notable adrenergic agonist is used as a stimulant?

A

amphetamine

  • treats narcolepsy and hyperkinesis (ADHD)
  • increases release of NE
37
Q

what notable adrenergic agonist is used as a diet aid?

A

phenylephrine

38
Q

what are first generation beta blockers?

A

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
Q

what are second generation beta blockers?

A

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
Q

what are third generation beta blockers?

A

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
Q

what are uses of beta blockers/

A
  1. HTN
  2. cardiac arrythmias
  3. angina pectoris
  4. glaucoma
  5. migraine
  6. stage fright
  7. heart failure
42
Q

how do beta blockers treat HTN?

A

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
Q

how do beta blockers treat cardiac arrhtymias?

A

stabilize rate through B1 receptor block

44
Q

how do beta blockers treat angina pectoris?

A

decrease myocardial work and O2 demand

45
Q

how do beta blockers treat glaucoma?

A

only timolol - decrease secretion of aqueous humor from ciliary process

46
Q

how do beta blockers treat migraine?

A

unknown mechanism

  • much used for prophylaxis (not acute attack)
  • may prevent B2 dilation of cranial vessels
47
Q

how do beta blockers treat stage fright/anxiety?

A

may prevent the tachycardia feedback cycle

48
Q

how do beta blockers treat heart failure?

A

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
Q

what are major effects of B1 blockers? what is a caution?

A

cardiac depression

  • if central effect: fatigue
  • nausea, vomiting, diarrhea, sexual dysfunction common
  • do NOT withdraw abruptly
50
Q

what are major effects of B2 blockers?

A

bronchoconstriction

-may precipitate asthmatic attack

51
Q

what is phentolamine?

A

nonselective a-receptor antagonist (a1/2)

-imidazoline derivatives

52
Q

what is phenoxybenzamine?

A

nonselective a-receptor antagonist (a1/2)

  • nitrogen mustard compound that forms covalent bond with receptor
  • haloalkylamine derivative
53
Q

what is prazosin?

A

selective a1 antagonist

  • part of a family with other -zosins
  • quinazoline derivative
54
Q

what is the major application of alpha-antagonists?

A
  1. HTN
  2. peripheral vascular disease
  3. pheochromocytoma
  4. shock
  5. BPH
55
Q

how does one treat peripheral vascular disease?

A

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
Q

what alpha blocker treats pheochromocytoma?

A

phenoxybenzamine

  • also give fluids b/c vessel volume increases dramatically
  • may also add beta-blocker
57
Q

how do alpha blockers treat shock?

A

breaks profound vasoconstriction and improves perfusion

58
Q

how do alpha blockers treat BPH?

A

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
Q

what are side effects of sympathetic blocking drugs?

A

alpha: postural hypotension, nasal stuffiness, and inhibition of ejaculation
beta1: erectile dysfunction, bradycardia
B2: bronchoconstriction, metabolic alterations
CNS: drowsy/dizzy

60
Q

what are neuron-blocking drugs?

A

block synthesis, packaging, release, and reuptake of nt

  • little clinical use, and many serious side effects
  • rare uses are HTN and inoperable pheochromocytoma
61
Q

what is alpha-methyltyrosine?

A

neuron blocking drug that manages inoperable pheochromocytoma
-inhibits synthesis of NE

62
Q

what is reserpine?

A

neuron blocking drug that was an older hypertensive

-blocks vesicles from filling with E or NE, preventing NE or E release

63
Q

what is guanethidine?

A

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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