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PHS 931 > Block 1 Lecture 6 -- Adrenergics > Flashcards

Block 1 Lecture 6 -- Adrenergics Flashcards

1
Q

Describe NT affinity for alpha receptors.

A

EPI ~ NE&raquo_space; ISO

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2
Q

Describe NT affinity for beta receptors.

A

ISO > EPI > NE

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3
Q

Where are alpha1 receptors located?

A

vascular, glandular smooth muscle

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4
Q

Where are alpha2 receptors located?

A

presynaptic nerve terminals

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5
Q

Where are beta1 receptors located?

A

cardiac muscle

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6
Q

Where are beta2 receptors located?

A
    • vascular, bronchiole smooth muscle
    • skeletal muscle
    • liver
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7
Q

Where are beta-3 receptors located?

A

adipose

bladder smooth muscle

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8
Q

What type of GPCR is alpha-1?

A

Gq

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9
Q

What type of GPCR is alpha-2?

A

Gi

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10
Q

What type of GPCR are the beta receptors?

A

Gs

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11
Q

alpha-1 agonists cause:

A

contraction of vascular and glandular smooth muscle

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12
Q

alpha-2 agonists cause:

A

decreased NE release from pre-synaptic nerve terminals

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13
Q

beta-1 agonists cause:

A

increased HR + FOC in cardiac muscle

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14
Q

beta-2 agonists cause:

A
    • relaxation of vascular and bronchiole smooth muscle
    • glycogenolysis in skeletal muscle
    • glycogenolysis + gluconeogenesis in the liver
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15
Q

beta-3 agonsits cause:

A
    • lipolysis in adipose

- - relaxation of bladder smooth muscle

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16
Q

What do G-alpha-s GPCRs do?

A

activate adenylyl cyclase

    • ++ cAMP
    • ++ Ca
    • ++ PKA, phosphorylation
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17
Q

What do G-alpha-i GPCRs do?

A

inhibits adenylyl cyclase

    • (–) cAMP
    • (++) K efflux
    • (–) Ca channels
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18
Q

What do G-alpha-q GPCRs do?

A

activates PLC-beta

    • PIP2 –> IP3 + DAG
    • IP3 causes Ca release from ER into cytosol
    • DAG activates PKC
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19
Q

What are the G protein receptor subtypes?

A

alpha-s
alpha-i
alpha-q

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20
Q

What do sympatholytics do?

A

block synthesis of catecholamines

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21
Q

What is the class and MoA of carbidopa?

A

Sympatholytic

    • inhibits DOPA-decarboxylase in the periphery (prevents L-DOPA dose wasting)
    • does not cross BBB (DA does not x either, but L-DOPA does)
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22
Q

What do sympathomimetic drugs do?

A

increase the activity of the SNS

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23
Q

How do indirect-acting sympathomimetics have effect?

A

increase [NT] in cleft

1) reuptake transporter inhibitors
2) block catabolism (MAOIs)
3) increase presynaptic NE and DA release

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24
Q

How does Atomoxetine work?

A

indirect-acting sympathomimetic (reuptake blocker)

    • NET blocker
    • nonstimulant for ADHD
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25
Q

How does Methylphenidate work?

A
    • indirect-acting sympathomimetic (reuptake blocker)

- - NET, DAT blocker

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26
Q

What makes a drug a stimulant?

A

blocking DAT (increasing DA)

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27
Q

How does Phentermine work?

A

indirect-acting sympathomimetic

    • increases NE/DA release
    • appetite-modulatory hypothalamic effect
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28
Q

When is Phentermine used?

A

short-term obesity treatment (less than 1 mo.)

– Topiramate added due to subjective evidence of weight loss in epileptics

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29
Q

What are ADRs of Phentermine?

A

1) HTN
2) tachycardia
3) palpitations
4) H/A
5) insomnia

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30
Q

What are C/Is of Phentermine?

A

1) HTN
2) CVD
3) hyperthyroidism
4) glaucoma
5) MAOIs
6) drug abusers

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31
Q

How does amphetamine work?

A

indirect-acting sympathomimetic

    • increases presynaptic DA/NE release
    • reverses DAT by acting on VMAT to increase cytoplasmic DA
    • D-amphetamine also weak MAOI
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32
Q

What is amphetamine used for?

A

ADHD
narcolepsy
short-term appetite suppression

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33
Q

How does modafinil work?

A

same as amphetamines…
indirect-acting sympathomimetic
– increases presynaptic DA/NE release
– reverses DAT by acting on VMAT to increase cytoplasmic DA
– more selective for DA neurons in HT areas

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34
Q

What is modafinil used for?

A

1) narcolepsy
2) shift-work sleep disorder
others…
MS, cognition, anti-depressant, ADHD, bipolar, meth/cocaine addiction

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35
Q

What are ADRs of modafinil?

A

dermatological

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36
Q

What is the MoA of pseudoephedrine?

A

sympathomimetic: indirect + direct agonist
- - displaces NE + DA from vesicles in CNS and PNS
- - direct-acting agonist for alpha/beta adrenergic receptors
- - not degraded by MAO/COMT

37
Q

What is the half-life of pseudoephedrine relative to NE?

A

10x longer

38
Q

What are the effects of pseudoephedrine?

A

1) relax bronchiole sm
2) vasoconstriction for nasal/pulmonary
3) anorexigenic
4) thermogenesis
5) HR, FOC, TPR

39
Q

What are ADRs of pseudoephedrine?

A

1) thermogenic effects worse with exercise

40
Q

What are C/I’s of pseudoephedrine?

A

1) CVD/HTN, obesity, MAOIs
2) overuse = HTN crisis, arrhythmias, death
3) hyperthyroidism (increased beta1 receptors…CV thyrotoxicosis)

41
Q

What is the MoA of phenylephrine?

A

alpha-1 agonist

    • mydriatic (dilation) and nasal decongestant
    • 1% nasal, 10% ophth solns
42
Q

What are other uses of alpha-1 agonists?

A

1) idiopathic orthostatic hypotension
2) alpha-1 mediated vasoconstriction for surgery (less anesthetic and blood loss)
3) allergy (decreases mediators like histamine)
4) stress incontinence

43
Q

Describe relative potency of NE and phenylephrine?

A

Phenylephrine less potent but longer t1/2

44
Q

What is the MoA of doxazosin/terazosin?

A

alpha-1 antagonist; 1000x more selective for a1 than a2, but non-selective among a1’s
– decrease TPR by blocking a1a, a1c on vsm

45
Q

What are uses of doxazosin/terazosin?

A

BPH
HTN
CHF
pheochromocytoma

46
Q

What is the MoA of Tamsulosin?

A

alpha-1 antagonist selective for a1a of trigone muscle in bladder

47
Q

What are ADRs specific to tamsulosin?

A

associated with intra-operative floppy iris syndrome during surgery

48
Q

What are ADRs of alpha-1 antagonists?

A

1) orthostatic hypotension
2) nocturia
3) stuffy/runny nose

49
Q

What are C/I’s of alpha-1 antagonists?

A

prostatic carcinoma

50
Q

What is the MoA of clonidine?

A

selective alpha2 agonist

– reduces sympathetic CNS outflow (major) and local sympathetic outflow (minor)

51
Q

What is clonidine used for?

A

HTN secondary to increased CNS SNS outflow (withdrawal)

– ADHD (sleep), migraine prophylaxis, neuropathic pain, smoking cessation, PMS, PTSD

52
Q

What are ADRs of Clonidine?

A

sedation
hypotension
bradycardia
dry mouth

53
Q

How is clonidine supplied?

A

oral or TD patch

54
Q

How does albuterol work?

A

beta2 agonist

55
Q

What is albuterol used for?

A

acute bronchospasm

    • rapid onset, short acting
    • over use = status asthmaticus (PD tolerance)
56
Q

What is the MoA for Mirabegron?

A

b3 agonist

57
Q

What are the uses of Mirabegron?

A

OAB

– especially if comorbid dementia when anticholinergics that cross BBB may be C/I

58
Q

What are the ADRs of Mirabegron?

A

increased HR and BP

also very expensive

59
Q

How is Mirabegron metabolized?

A

CYP3A4 and CYP2D6

moderate inhibitor of 2D6

60
Q

How do beta antagonists differ?

A

1) subtype selectivity
2) ISA (partial agonist?)
3) lipid solubility (x BBB)
4) metabolic pathways

61
Q

Describe ADME of propranolol

A

75% lost to 1st pass
90% bound in plasma
t1/2 = 3 hours

62
Q

How does propranolol work?

A

beta-blocker (b1/cardioselective)

    • competitive antagonist
    • no ISA or alpha affinity
63
Q

How does carvedilol work?

A

beta-blocker

    • competitive antagonist of a1 and b2
    • moderate ISA of b1
64
Q

What are the c/i’s of carvedilol?

A

asthma

65
Q

Which beta blockers are nonselective?

A

propranolol

carvedilol

66
Q

Which beta blockers are selective?

A

metoprolol

nebivolol (bystolic)

67
Q

How does metoprolol work?

A

selective b1 beta blocker

    • no ISA
    • big 1st pack
    • best for asthma pts
68
Q

What is uptake 1?

A

presynaptic/primary

69
Q

What is uptake 2?

A

postsynaptic/astrocytic – secondary

70
Q

What are Uptake 1 transporters?

A
    • NET, DAT, SERT (NE transporter, DA transporter, Serotonin transporter)
    • MAO
71
Q

What are uptake 2 transporters?

A

COMT

72
Q

Describe NT affinity for uptake 1 vs uptake 2?

A

Uptake 1 = NE

Uptake 2 = Epi

73
Q

Where is MAO expressed?

A
    • presynaptic terminals
    • astrocytes
    • gut lining
74
Q

Where is COMT expressed?

A
    • pre- and post-synaptic
    • astrocytes
    • periphery
75
Q

What NTs are broken down by MAO-A?

A

NE, Epi, 5-HT

tyramine

76
Q

Where is NE synthesized in the CNS?

A

locus coeruleus

77
Q

What is tyramine?

A

a toxic dietary substance if absorbed with MAOI

    • found in fermented cheeses, etc.
    • broken down by MAO
78
Q

What NTs are broken down by MAO-B?

A

It’s more selective for DA

79
Q

In what disease might MAOB-I’s be used?

A

PD

80
Q

What is one counseling point for MAO-AI’s?

A

dietary restrictions! (tyramine)

81
Q

What are MAO-AI’s used for?

A

depression

82
Q

How do drugs that increase NE/DA presynaptic release work? (mechanisms)

A

1) alter VMAT fx (reverse direction)
2) displace NE from synaptic vesicles
3) reverse NET/DAT

83
Q

What class of drug is yohimbine?

A

a2 antagonist

84
Q

What are LABAs used for?

A

asthma (not acute) in conjunction with an inhaled steroid

85
Q

What drugs has an increase in sudden death been correlated to?

A

LABAs

only when used for asthma; no issues for COPD

86
Q

What are the uses of beta blockers?

A

1) HTN, angina, arrhythmias, MI, CHF
2) hyperthyroidism
3) migraine prophylaxis
4) acute panic attack/stage fright

87
Q

What are ADRs of beta antagonists?

A

1) bradycardia
2) pulmonary airway resistance
3) cold extremities, rash (vasodilation)
4) hypoglycemia
5) weight gain
6) CNS: fatigue, insomnia, depression, nightmares, fever
7) rebound hypersensitivity

88
Q

What are the effects of rebound hypersensitivity from b-blocker?

A

HTN, angina, MI, fatal arrhythmias

PHS 931 (29 decks)

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