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Neurology 2 > Adrenergic Drugs > Flashcards

Adrenergic Drugs Flashcards

1
Q

Alpha-1 pathway

A

Gq - PLC, IP3/DAG, Ca++/CaM, PKC, Ras, Raf, Mek, Erk

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2
Q

Beta/gamma subunit activity in Gq

A

PI-3 kinase, AKT

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3
Q

Alpha-2 pathway

A

Gi - Adenylyl cyclase inhibition, less cAMP, less PKA

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4
Q

Beta pathway

A

Gs - Adenylyl cyclase, cAMP, PKA (catalytic subunits)

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5
Q

Vascular smooth muscle

A

Alpha-1: Vasoconstriction

Beta-2: Vasodilation

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6
Q

Pupil

A

Alpha-1

Dilation

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7
Q

Hair

A

Alpha-1

Erects hair

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8
Q

Prostate

A

Alpha-1

Contraction

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9
Q

Heart

A

Alpha-1: Contraction

Beta-1: Contraction

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10
Q

Adrenergic and cholinergic nerve terminals (pre-synaptic)

A

Alpha-2: Inhibits transmitter release (auto-regulation)

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11
Q

Fat cells

A

Alpha-2: Inhibits lipid release

Beta-3: Activates lipid release

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12
Q

Smooth muscle (respiratory, uterine)

A

Beta-2: relaxation

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13
Q

Skeletal muscle

A

Beta-2: Potassium uptake

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14
Q

Liver

A

Beta-2: Glycogenolysis (activate glucose release)

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15
Q

Bladder

A

Beta-3: Relax detrusor

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16
Q

Renal blood vessels

A

D1: Dilation

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17
Q

Nerve endings

A

D2: Modulates transmitter release

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18
Q

Direct-acting adrenergic drug clases

A

Agonsts, antagonists

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19
Q

Indirect-acting adrenergic drug function

A

Altering NE at receptor location

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20
Q

Cocaine

A

Indirect agonist

Re-uptake inhibitor for DA and NE

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21
Q

Selegiline, Phenelzine

A

Indirect agonist

MAO inhibitors

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22
Q

Ephedrine

A

Mixed-acting agonist

NE release + receptor agonist

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23
Q

Amphetamines, Methylphenidate (Ritalin)

A

Indirect agonist

Reverse NE and DA uptake, increased release

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24
Q

Alpha direct agonist drugs

A

Phenylephrine
Methoxamine
Clonidine

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25
Q

Mixed alpha/beta direct agonist drugs

A

NE, Epinephrine

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26
Q

Beta direct agonist drugs

A

Dobutamine
Isoproterenol
Terbutaline
Albuterol

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27
Q

Dopamine direct agonist drugs

A

Dopamine

Fenoldopam

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28
Q

Alpha-1 > alpha-2 direct agonists

A

Phenylephrine

Methoxamine

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29
Q

Alpha-2 > alpha-1 direct agonists

A

Clonidine, methylnorepinephrine

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30
Q

NE vs Epinephrine

A 
NE = Both alpha's, Beta-1
Epi = Both alpha's, both beta's
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31
Q

Beta-1 > beta-2 direct agonist

A

Dobutamine

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32
Q

Beta-2 > beta-1 direct agonists

A

Albuterol, terbutaline, ritodrine

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33
Q

Isoproterenol

A

Both beta’s equal

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34
Q

Fenoldopam

A

D1

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35
Q

Overall effect of an adrendergic drug is based on what things?

A
  1. Receptors expressed at a tissue
  2. Receptor selectivity of drug
  3. Intrinsic activity of drug
  4. Compensatory reflexes
  5. Tolerance and tachyphylaxis development
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36
Q

Tachyphylaxis

A

Sudden decrease in response to drug after administration

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37
Q

Drug tolerance

A

Progressively reduced response to drug over time

38
Q

Epinephrine effects

A
  1. Increased heart fxn (beta-1)
  2. Constant arterial pressure (beta-2 + alpha-1)
  3. Bronchial relaxation (beta-2)
  4. Decreased bronchial secretion (alpha-1)
  5. Muscle tremor and hypokalemia (beta-2)
  6. Elevated blood glucose (beta-2 and alpha-2)
  7. Elevated blood FA’s (beta’s)
39
Q

Norepinephrine effects

A

NOT beta-2…

  1. Increased heart fxn (beta-1)
  2. Vasoconstriction –> increased BP (alpha-1)
40
Q

NE does NOT do what?

A

Bronchodilation or vasodilation

41
Q

Dopamine effects at normal dose

A
  1. Renal, cerebral, mesenteric, coronary vasodilation (D1)

2. Suppressed NE release (D2)

42
Q

Dopamine effect at higher doses

A
  1. Beta-1 activation in heart

4. Alpha-1 vasoconstriction

43
Q

Phenylephrine effects

A

Alpha-1 direct agonist…

  1. Myadriasis (pupillary dilation) and decongestant
  2. Severe BP elevation (vasoconstriction)
44
Q

Phenylephrine + baroreflex

A

HR sharp drop following BP elevation

45
Q

Clonidine effects

A

Alpha-2 direct agonist (vasomotor center of brainstem)

- Decreased sympathetics (blocked NE release)
      a. Reduced BP (blocked NE = blocked alpha-1)
      b. Bradycardia (blocked NE = blocked beta-1)
46
Q

Clonidine local application

A

Vasoconstriction????

47
Q

Isoproterenol effects

A

Beta (both) direct agonist (inotropic, chronotropic)

- Increased cardiac output (beta-1)
- Decreased BP (beta-2)
- Bronchodilation (beta-2)
48
Q

Dobutamine effects

A

Beta-1 agonist (inotropic)

- Increased heart contractility

49
Q

Isoproterenol vs. dobutamine

A

Isoproterenol = MORE chonotropic action than dobutamine

50
Q

Dobutamine and alpha-1

A

Given as racemic mixture of (+) isomer and (-) isomer, which antagonize alpha-1 and agonize alpha-1, respectively.

Outcome = no changed effect on alpha-1 receptors

51
Q

Terbutaline effects

A

Beta-2 agonist

- Bronchodilation, uterine relaxation

52
Q

Albuterol effects

A

Same as terbutaline

53
Q

Selectivity of indirect-acting drugs

A

Non-selective, all receptors activated by the neurotransmitter are affected

54
Q

Characteristics of indirect-acting agonist drugs

A

Lipophilic, penetrate BBB, CNS STIMULANTS

55
Q

Function of indirect-acting agonists

A

Increase NE in cleft for signaling

56
Q

Amphetamines

A

Increased NE in CNS…

  • Alerting effects
  • Improved attention
57
Q

Cocaine

A

Inhibits transmitter re-uptake at adrenergic synapses

58
Q

Ephedrine

A

Nonselective direct adrenergic agonist (like epinephrine)
Indirect increased release of transmitters (like amphetamines)
Mild CNS stimulant

59
Q

Treating hypotensive emergencies

How?

A

NE, phenylephrine, methoxamine

60
Q

Alpha-1 and alpha-2 antagonists

A

Phentolamine, phenoxybenzamine

61
Q

Alpha-1 antagonists

Commonality?

A

Prazosin, Terazosin, Tamsulosin, Doxazosin, Alfuzosin, Silodosin

ALL END IN “-OSIN”

62
Q

Phentolamine vs. phenoxybenzamine

A

Both alpha1 and alpha2 antagonists…

Phentolamine = competitive
Phenoxybenzamine = irreversible non-competitive
63
Q

Alpha antagonists on CV system

A

Decreased BP (peripheral)
Reflex tachycardia
Postural hypotension

64
Q

Alpha antagonists on GU system

A

Prostate relaxation

Decreased resistance to urine flow

65
Q

Alpha antagonists on eye

A

Pupillary constriction (dilator relaxation)

66
Q

Alpha-1 selective vs. non-selective alpha antagonsits

A 
Alpha-1 = decreased beta activity via alpha-2 activity
Both = increased beta activity (increased heart fxn)
67
Q

Atenolol, Betaxolol

A

Beta-1 antagonist

68
Q

Nadolol, Propranolol

A

Beta antagonist

69
Q

Acebutolol

A

Beta-1 partial agonist

70
Q

Labetalol

A

Beta and alpha-1 partial agonist

71
Q

Penbutolol, Pindolol

A

Beta partial agonist

72
Q

Carvedilol

A

Beta and alpha-1 inverse agonist

73
Q

Metoprolol

A

Beta-1 inverse agonist

74
Q

Beta/beta-1 partial agonists are ______

A

Beta blockers with ISA (intrinsic sympathomimetic activity)

75
Q

Partial agonists produce a ______

Benefit?

Used when?

A

Blunted sympathetic response

Less risk for bradycardia, increased cholesterol, or other beta receptor blockage issues

When full antagonist is not indicated (ex. lowering BP)

76
Q

Beta-blockers on heart

A

Negative inotropic
Negative chronotropic
Block AV node (increased PR interval)

77
Q

Beta-blockers on blood vessels

A

Initial rise in vascular resistance

Chronic - decrease in PVR due to heart effects

78
Q

Beta-blockers on renal system

A

Inhibit renin release (decrease BP)

79
Q

Beta-blockers on respiratory system

A

Increased airway resistance

80
Q

Beta-blockers on eye

A

Reduced aqueous humor production –> lower intraocular pressure

81
Q

Beta blockers on metabolism

A

Inhibit lypolysis
Increase LDL/HDL ratio (bad)
Inhibit glycogenolysis

82
Q

Adverse effects of beta-blockers

A

Sedation/depression (CNS effects)
Bronchospasm/asthma attack (beta-2 blockers)
Hypotension
Increased VLDL, decreased HDL
Hypoglycemic episodes (post-prandial, DM type 1)
Blunted perception of hypoglycemic episodes

83
Q

How to fix sedation/depression from beta-blockers

A

Switch to more hydrophilic drug

84
Q

How to fix bronchospasm from beta-blockers

A

Switch to beta-1 selective

85
Q

How to fix heart slowing from beta-blockers

A

Switch to partial agonist

86
Q

How to fix VLDL increase from beta-blockers

A

Switch to partial agonist

87
Q

How to fix hypoglycemic episodes from beta-blockers

A

Switch to beta-1 selective

88
Q

Abrupt discontinuation of beta-blockers

Why?

A

Sympathetic hyper-response, heart problems

Body increases NE production to try to override beta-blocker, THUS will have extra after quitting drug

89
Q

Guanethidine

Clinical use?

A

NE release inhibitor

Chronic HTN

90
Q

Clonidine

Clinical use?

A

Presynaptic alpha-2 agonist

Chronic HTN

91
Q

Metyrosine

Clinical use?

A

Tyrosine hydroxylase inhibitor (catecholamine production)

Pheochromocytoma

92
Q

MoA of Guanethidine

A

NE release inhibitor…

Taken up by reuptake mechanism
Replaces NE in vesicles
Gradual depletion of NE stores

Neurology 2 (22 decks)

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