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P1 Spring - Pharm Sci > adrenergic quiz > Flashcards

adrenergic quiz Flashcards

1
Q

2 main adrenergic neurotransmitters

A

epi and NE

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2
Q

Epi is syn and stored in the

A

adrenal medulla (making it a neurohormone)

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3
Q

Epi has a different response at different levels meaning it is

A

concentration dependent

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4
Q

Epi at low concentrations

A

has predominant beta effects more than alpha

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5
Q

Epi at high concentrations

A

engages beta and alpha receptors at the same degree

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6
Q

in the heart, Epi

A

increases HR, FOC, SV, CO, BP

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7
Q

in the lungs, Epi

A

bronchodilation occurs

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8
Q

in the vasculature, Epi

A

low concentrations = beta = vasodilation (decrease TPR)

high concentrations = alpha engaged = constriction (increase TPR)

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9
Q

is epi appropriate for asthma attack

A

yes B2 engaged = bronchodilation

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10
Q

epi with an anesthetic

A

vasoconstriction; anesthetic is kept localized; good for prolonged procedures

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11
Q

NE is synthesized and stored

A

sympathetic post ganglionic neuron

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12
Q

NE targets which receptors

A

beta1, alpha1, alpha2

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13
Q

NE at the heart

A

increases HR, FOC, CO

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14
Q

NE at the lungs

A

no clinical observation is observed

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15
Q

NE in the vasculature

A

vasoconstriction (alpha1)

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16
Q

Dopamine is syn and stored in the terminal of the

A

sympathetic postganglionic neuron

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17
Q

DA targets which receptors at different concentrations meaning it is

A

D1, beta1, alpha1; concentration dependent

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18
Q

at low concentrations DA

A

has the highest affinity (lowest kd); leads to vasodilation of gut and renal by lowering TPR; good for maintaining good kidney function

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19
Q

at mild concentrations DA

A

engages B1 receptors as well as D1; leads to vasodilation, increasing HR and CO

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20
Q

at high concentrations DA

A

engages alpha1 (B1 and D1 also); it causes vasoconstriction, increasing TPR, CO; it can be effected by vagal response

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21
Q

at the kidney DA

A

increases RBF and increases GFR (only at low doses due to D1)

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22
Q

at the heart DA

A

increases HR, FOC, (through B1 engagement at mid to high conc)

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23
Q

at the vasculature

A

decreases TPR (some due to D1) increases TPR (alpha1 engagement)

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24
Q

therapeutic uses for dopamine

A

shock, hypotension, poor tissue perfusion, low CO

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25
Q

sympathomimetics

A

synthetic receptor agonists mimic the actions of catecholamines

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26
Q

alpha 1 receptor agonists

A

phenylephrine
naphazoline
oxymetazoline
tetrahydrozoline

topical, decongestants, vasoconstrictors in cornea

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27
Q

alpha 2 receptor agonists

A

clonidine
guanfacine
methyldopa

activate alpha 2 and therefore decrease SNS outflow
decrease HR, TPR, BP
upregulation of peripheral B1 and alpha1

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28
Q

beta 1 agonists

A

dobutamine

IV only; preserves CO; increases HR and FOC; decompensated heart failure; low CO = risk to vital organs; can only use for 3 days due to downregulation

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29
Q

Beta 2 agonists

A

albuterol (SABA)
terbutaline
salmeterol (LABA)

good for bronchodilation; good for patients with asthma

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30
Q

isoproterenol

A

non selective B1 and B2 agonist

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31
Q

beta blockers are used to treat

A

hypertension, chronic angina, heart failure

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32
Q

in treating hypertension and chronic angina, beta blockers work to

A

decrease CO, FOC, HR; block the effects of NE on the heart; improve blood flow and decrease oxygen

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33
Q

beta 1 antagonists also effect the RAA system

A

block the beta 1 receptors on the JG cells of the kidney which are responsible for the activation of the RAA pathway

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34
Q

cardioselective beta blockers are more selective for

A

B1 than B2

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35
Q

why would these agents be favored over non selective

A

they specifically block B1 more than B2 good for patients that have COPD or asthma or diabetes

diabetes blocking B2 would lead to decreased insulin secretion and decreases tissue sensitivity to insulin

36
Q

nonselective B blockers increase the change of developing

A

type 2 diabetes

37
Q

ISA

A

intrinsic sympathomimetic activity; partial agonist

38
Q

agents with ISA include

A

pindolol, acebutolol, labetalol

bind to the receptor and have the same ability to turn it on but not to the same ability; could be used to reduce the degree of bradycardia or limit the effect on lipid profile

39
Q

Labetalol has ISA at beta 2 receptors

A

will cause B2 stimulation and vasodialate reducing TPR and reducing BP; nonselective; don’t want to mess with B2 still full agonist to open airways is always better

40
Q

carvedilol

A

blocks alpha 1, blocks L type CC, anti-oxidant

vasodilation, decreased HR, limited oxidative damaged seen in heart failure

41
Q

nebivolol

A

increased NO production in vasculature

causes vasodilation; maybe B3

42
Q

labetalol

A

B1 antagonist; B2 ISA; alpha1 blocked

affects glucuronidation pathway; gives vasodilation, happens on JG cells good at lowering BP

43
Q

nearly all B blockers are eliminated by

A

the liver 2D6

44
Q

which B blockers are eliminated by the kidney

A

nadolol and atenolol and 50% of bisopropol

45
Q

esmolol

A

has a half life of 10 minutes; metabolized by gut (plasma) esterases; shorter half life = quicker response; given IV

46
Q

nadolol has a half life of ___

A

24 hours; making it the longest for a B blocker

47
Q

most hepatically cleared have a half life of

A

4-6 hours

48
Q

atenolol has a half life of

A

12 hours

49
Q

4 diff types of adverse effects associated with B blockers

A

lipids CNS sexual dysfunction, hypoglycemia

50
Q

lipid adverse effect

A

increased LDL, increased VLDL; decreased HDL

wouldn’t use this medication on statin therapy

51
Q

glaucoma

A

role of beta receptors on aqueous humor production

52
Q

thyrotoxicosis

A

thyroid hormone increases the expression of beta receptors

increase production of thyroid hormone by way of B1

53
Q

tremor

A

activation of B2 receptors can cause tremors; trigger for excess symp activity

54
Q

migraine

A

beta blockers; mechanism is unknown; effective in preventing migraines

55
Q

alpha blockers are primarily used in the treatment of

A

BPH and hypertension (not as good as others)

56
Q

the least selective of alpha antagonists

A 
phent, PB2
outside vasculature
decreases blood to tissues 
necrosis occurs
give an IV of alpha blocker around site where it occurs
57
Q

the first alpha 1 selective antagonists ___ led to the development of ___ and ___

A

prazonsin; terozosin and doxazosin

58
Q

alpha 1 antagonist use in treating BPH

A

decrease growth and contraction of prostatic tissues

59
Q

the different types of alpha 1 receptor subtypes include

A

A, B, D

60
Q

the most predominant subtype in the prostate is the

A

alpha 1 a

61
Q

the most predominant alpha 1 receptor subtype in the vasculature is

A

B and D

62
Q

what counseling would you give to someone on an alpha 1 antagonist

A

get up slowly; take a bedtime; due to orthostatic hypotension (dilates arterioles and effects venous tone)

63
Q

what is an ADR associated with tamsulosin

A

floppy iris syndrome

alpha 1 A receptors are located on the dilator muscles of the iris and it can lead to atrophy of the muscle

64
Q

which neurons use ACh

A

parasymp, nicotinic, muscarinic, neuromuscular

65
Q

cholinergic

A

any system affected by or involving ACh

66
Q

M3

A

“secretory” (SLUD)
any muscle
contraction including smooth muscle
circulatory muscles in the eye constrict

67
Q

M2

A

“cardiac”
decrease HR
slows SA node
slows down AV node

68
Q

M1

A

cholinergic pathways
Alzheimer’s; circuits involved in memory and cognition
neural receptor

69
Q

muscarinic agonist would lead to what

A

increased SLUD and decreased HR

70
Q

muscarinic agonists would treat

A

tachycardia, dry mouth, constipation, glaucoma

71
Q

muscarinic antagonists would lead to

A

decreased SLUD and increased HR

72
Q

muscarinic antagonists would treat

A

urinary urgency
eye surgery
IBS (type D)

73
Q

nicotinic receptors

A

ligand gated Na+ ion channels

74
Q

nicotinic receptors are found in (2)

A

autonomic ganglia

neuromuscular junction

75
Q

autonomic ganglia

A

Ng

parasymp or symp

76
Q

neuromuscular junction

A

some selective nicotinic
Nm
could paralyze someone with a nicotinic blocker

77
Q

AChE

A

where ACh is released, this enzyme is present, highest turnover rate of all enzymes

78
Q

lack of AChE

A

lack of breakdown of ACh
increase SLUD
decrease HR
in brain = increase cholinergic activity (treatment of Alz)

79
Q

ACh antagonist could treat

A

COPD/asthma

80
Q

quaternary ammonium compound is (in ACh and choline)

A

unable to get into the CNS

unable to cross BBB

81
Q

rotamers

A

rotational conformers of norepinephrine
play a role in which receptors are activated
beta 1, alpha 1, and alpha 2
can twist to activate all three receptors despite it being 1 molecule

82
Q

Receptors use __ to define a ligand binding site

A

side chains of AA

83
Q

interactions of drugs with ligand binding site (3)

A
  1. H bonds - one of the polar groups needs an H to donate to form the H bond
  2. ionic bond - very strong (not as covalent) can help hold drugs in receptor active site
  3. van der waals - hydrophobic interactions; lipid or nonpolar areas of a molecule interacting with non polar
84
Q

affinity (B2 adrenergic agonists)

A

want a highly potent agent / low dose

85
Q

activation (B2 adrenergic agonists)

A

full or partial agonist

86
Q

lipophilicity (B2 adrenergic agonists)

A

does play a role in B2 receptor selectivity and for some of the long acting beta 2 agonists (LABA)

P1 Spring - Pharm Sci (9 decks)

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