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23 spring: pharm > test 1: lecture 13 > Flashcards

test 1: lecture 13 Flashcards

1
Q

⍺1 adrenergic agonists will cause — in the heart

A

nothing, no ⍺1 receptors in the heart

phenylephrine (Neo-Synephrine), oxymetazoline (Dristan), tetrahydrozoline (Visine)

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2
Q

what are some ⍺1 adrenergic agonists

A

phenylephrine (Neo-Synephrine), oxymetazoline (Dristan), tetrahydrozoline (Visine)

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3
Q

what will ⍺1 adrenergic agnosists due to vasculature

A

vasoconstriction

this will trigger vagal effect and bradycardia

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4
Q

phenylephrine (Neo-Synephrine) is used for —
tetrahydrozoline (Visine) is used for —

A

nasal decongestant
eye redness

both are ⍺1 adrenergic agonists that cause vasocontriction and then vagal reflex

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5
Q

Activation of presynaptic α2 receptor causes —

A

decreased NE release from neurons

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6
Q

clonidine (catapres) is a —

A

⍺2 adrenergic agonist → causes hypotension

binds to presynaptic ⍺2 receptor and causes decrease in NE release

will also attach to autoreceptors within the CNS, that will decrease SYM outflow to periphery

Also stimulate postsynaptic α2 receptors in periphery on VSMC → vasoconstriction

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7
Q

what are two ⍺2 adrenergic agonists?

A

clonidine
xylazine

cause decreased NE release, decreased SYM outflow in the brain, cause vasoconstriction on vascular smooth muscle cells

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8
Q

Postsynaptic α2 receptor activation on VSMC in certain vascular beds result in — and a potential increase in —

A

vasoconstriction
BP

clonidine(catapres) and xlyazine (rompun) are ⍺2 adrenergic agonists

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9
Q

biphasic response of ⍺2 adrenergic agnoists

A

brief initial pressor (hypertensive) effect that is gradually reverses to hypotension

2B postsynaptic ⍺2 receptors on VSMC cause inital vasoconstriction→HTN

2A ⍺2 activation in the CNS reduces SYM tone causing low BP

2A ⍺2 activation of the presynaptic receptor located on peripheral sympathetic nerve terminals innervating vascular smooth muscle augments vasodilation

drug used to treat HTN

clonidine (catapres)

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10
Q

xylazine

A

⍺2 agonist that causes sedation and analgesia

because it binds to a2 receptors in the brain

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11
Q

what is rebound hypertension from a2 agonists

A

a2 on nerve stops NE release, smooth muscle cell increases receptors looking for NE, when you stop drug the extra receptors lead to bigger response

= vasoconstriction

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12
Q

rebound effect of a1 agonists

A

nasal spray

chronic use of a1 agonist, will cause decrease in a1 receptors. if you stop drug quickly, normal amount of NE will be released but there is now lower # of a1 receptors. This leads to leaky vessels and nasal congestion

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13
Q

nonselective B adrenergic agonists (B1/2) are used for —

A

B>a receptors
B1=B2

CHF → B1 increases cardiac contractility and CO

B2 activation causes brochodilation, used to treat asthma

isoproterenol (isuprel)

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14
Q

isoproterenol (isuprel) is a —

A

Nonselective β Adrenergic Agonists (β1/2)

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15
Q

isoproterenol (Isuprel) is used to treat

A

CHF: B1 activation causes increased cardiac contractility and increased CO

asthma: B2 activation leads to bronchodilation

B1/2 have B>a, with B1=B2

Nonselective β Adrenergic Agonists (β1/2)

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16
Q

B1 agonist is used to treat

A

short term CHF

increases force of cardiac contraction but does not effect HR

dobutamine (dobutrex)

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17
Q

dobutamine (dobutrex) is what type of drug

A

B1 adrenergic agonist

increases force of cardiac contraction but has minimal effect on HR

treatment of short term CHF

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18
Q

— are b2 adrenergic agonists

A

albuterol (Salbutamol)
Metaproterenol

B2>B1 at low dose

β2-stimulation ↑ bronchodilation and other smooth muscle relaxation

prevent premature labor by relaxing uterine smooth muscle

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19
Q

albuterol is used for

A

β2 Adrenergic Agonists

B2>B1 at low dose

β2-stimulation increased bronchodilation and other smooth muscle relaxation

Also used to prevent premature labor by relaxing uterine smooth muscle

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20
Q

if you give high dose albuterol what will happen

A

spillover to B1 receptors

albuterol is a B2 agonist that causes bronchodilation and other smooth muscle relaxation

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21
Q

— is a B3 Adrenergic Agonists

A

myrbetric (mirabegron)

B3 receptors are in brown fat, β3 receptor stimulation leads to increased lipolysis (fat breakdown)

B3 are also in bladder can be used to treat overactive bladder (OAB)

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22
Q

myrbetric (mirabegron) is what type of drug

A

β3 Adrenergic Agonists

used to treat overactive bladder

Sympathetic action on bladder causes relaxation of detrusor muscle and therefore a decrease in urge to urinate

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23
Q

what does myrbetric(mirabegron) do

A

Sympathetic action on bladder causes relaxation of detrusor muscle and therefore a decrease in urge to urinate

B3 agonist

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24
Q

how does tyramine and amphetamines get into the neuron?

A

presynaptic plasma membrane transporters

these are indirectly acting synpathomimetics

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25
Q

why dont ‘Indirectly acting’ sympathomimetics induce release of EPI from Adrenal gland?

A

indirectly acting symoathomimetics need to be transported into the cell by receptor: they then increase NE release

adrenal gland chromaddin cells do not have a way to reuptake EPI

tyramine and amphetamines are indirectly acting sympathomimetics that cause release of NE in nerve

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26
Q

indirectly acting sympathomimetics will be transported into the nerve terminal and cause

A

inreased release of endrogenous catecholamines (NE)

tyramine and amphetamine

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27
Q

what are three catecholamine reuptake inhibitors

A

cocaine
imipramine (impril)
amitryptyline (amitril)

allow NE,DA and serotonin to stay in synapse for longer, acts as antidepressants

28
Q

how do reuptake inhibitor sympathomimetics work?

A

allow NE,DA and serotonin to stay in synapse for longer, acts as antidepressants

cocaine
imipramine (impril)
amitryptyline (amitril)

29
Q

how do mixed acting sympathomimetics work?

A

Cause release of endogenous catecholamines and ALSO bind directly to adrenergic receptors

ephedrine

Adverse effect: Potential hypertension and cardiac arrhythmias

30
Q

ephedrine

A

mixed acting sympathomimetics

Cause release of endogenous catecholamines and ALSO bind directly to adrenergic receptors

can cause: increase HTN, decreased bladder sphincter incompetence, increased bronchodilation for treatment of asthma

Adverse effect: Potential hypertension and cardiac arrhythmias

31
Q

sudafed (pseudoephedrine) is a —

A

mixed acting sympathomimetic

Cause release of endogenous catecholamines and ALSO bind directly to adrenergic receptors

can also be used to make meth

32
Q

phenylephrine (sudafed-PE)

A

is a mixed acting sympathomimetic

Cause release of endogenous catecholamines and ALSO bind directly to adrenergic receptors

can not be used to make meth!

33
Q

what does guanethidine do?

A

decreases NE release from nerve terminal

guanethidine accumulates and replaces NE in vesicle

High doses cause TRIPHASIC effect
(1) Transient hypertension due to displaced NE
(2) Drop in BP due to decrease NE release
(3) Progressive drop in BP and cardiac output
used an an anti-hypertensive

GuaNEthidine prevents NE (norepinephrine) release

34
Q

bretylium

A

blocks transmitted release by stopping release of NE vesicles

different from guanethidine which accumulates and replaces NE in vesicle

No BBB cross
no affect on EPI release form adrenal medulla cause it needs plasma membrane transporter to get into nerve

35
Q

clonidine

A

a2 agonist

binds to a2 on presynaptic nerve, which stops NE release

36
Q

reserpine

A

Blocks the uptake of DA and NE into synaptic vesicles by VMAT

Does not require transporter to enter cells

may also cause lower EPI in adrenal gland

long acting tranquilizer in horses

37
Q

— blocks DA and NE uptake by VMAT into vesicles and does not need transporter to get into cells

A

reserpine

leads to decreased NE, cause cytoplasmic NE will get broken down by MAO

can also decrease EPI in adrenal gland

38
Q

⍺-methyl-DOPA

A

false transmitter

gets into cell without transporter

cell thinks it is a normal DOPA and turns it into a-methyl-NE and released in the vesicle with normal NE

a-methyl-NE will not bind as strongly to a1 but will also bind to a2 autoreceptors→ decreases release of NE from the cell

a-methyl-dopa will use up the enzymes that usually make NE, will lead to smaller amount of NE released

39
Q

— is a false transmitter release

A

α−methyl-DOPA

gets into cell without transporter

cell thinks it is a normal DOPA and turns it into a-methyl-NE and released in the vesicle with normal NE → a-methyl-dopa will use up the enzymes that usually make NE, will lead to smaller amount of NE released

a-methyl-NE will not bind as strongly to a1 but will also bind to a2 autoreceptors→ decreases release of NE from the cell

40
Q

what are two things that block NE synthesis in the cell

A

α-CH3-p-tyrosine

NE at high doses

41
Q

— inhibits tyrosine hydroxylase enzyme

A

α-CH3-p-tyrosine

42
Q

— are MAO inhibitors

A

pargyline
moclobemide

Used as antidepressant. It blocks degradation of DA and Serotonin in CNS too

43
Q

what is cheese syndrome

A

thyramine is found in cheese and wine, is usually degraded by MAO

if you use antidepressents like pargyline and moclobemide which inhibit MAO, can lead to build up of thyramine

can lead to hypertensive crisis

44
Q

5 uses of a- adrenergic receptor blockage

A

hypertension: decreased a1 vasoconstiction leads to decreased peripheral resistance

CHF: lower arterial pressure improved CO

peripheral vascular disease (raynauds)

benign prostatic hyperplasia: decreases tone of prostate and urethral sphincter allows urinartion

shock: decrease shock mediated vasoconstriction to increase organ perfusion and fluid replacement

45
Q

— are irreversible ⍺ receptor blockers

A

dibenamine
phenoxybenzamine

46
Q

phenoxybenzamine and
dibenamine are — and work —

A

irreversible ⍺ receptor blockers

will bind nonselectively to a1 and a2 and break receptors

will need to wait for body to make new a1 or a2 receptors

47
Q

— is a reversible ⍺ receptor blocker

A

phentolamine (regitin)

48
Q

how does phentolamine (regitin) work

A

reversible ⍺ receptor blocker

a1=a2

if you block a2 autoreceptor that causes increased release of NE, which will trigger B1 in the heart and can lead to tachycardia

49
Q

prazosin (minipress)

A

selective ⍺1 blocker

a1»a2
will block a1= decrease BP

does not affect a2 at low dose so no extra release of NE and no tachycardia (this is what happens with reversible ⍺ receptor blocker, phentolamine (regitin)

50
Q

tamsulosin (flomax)

A

selective ⍺1 blocker

works on α1A- in urinary tract

used to improve urinartion with men you have Benign Prostatic Hyperplasia (BPH) → relaxes muscle

51
Q

yohumbine

A

selective ⍺2 blocker
(only 40:1 a2>a1= high spill over)

will block a2 which causes increase of NE relased

this leads to increased HR and vasocontraction down stream

used to reverse xylazine induced sedation

52
Q

yohimbine will reverse —

A

xylazine-induced sedation

yohimbine is a ⍺2 blocker
xylazine is a ⍺2 agonist

53
Q

side effects of ⍺ receptor blockage

A

Postural Hypotension
* Block of α1 -mediated reflexive vasoconstriction upon standing → venous pooling → syncope

reflexive trachycardia
* a2 block will increase NE and cause tachycardia through B1

nasal stuffiness
* Block sympathetic tone on vessels in the nose leasing to increased in fluid leakage

54
Q

beta blockers are used for

A

Afib
HTN- will decrease BP
Angina:
Anxiolytic: stop tremors and anxiety
glaucoma: decrease production of aqueous humor in the eye

55
Q

propranolol(inderal)

A

non selective B blocker
B1=B2

decreases HR, contractility and CO

Membrane stabilization effect at high doses

large withdrawal and rebound effect

56
Q

propranolol (inderal) withdrawal effect

A

non-selective B blocker

57
Q

pindolol (calvisken)

A

nonselective B blocker

partial agonist: less withdrawal syndrome, less reduction in heart rate, but at high dose will cause increased HR,BP and brochodilation

58
Q

timolol (timoptic)

A

B blocker

nonselective B1=B2
less membrane stabilization

used for wide angle glaucoma

59
Q

metoprolol (lopressor)

A

selective B1 blocker

As potent as propranolol at β1 but 100X less potent at β2 Little effect on adrenergic β2 -mediated effects Cardioselective cause hitting B1 not B2

60
Q

butoxamine

A

selective B2 blocker

Selective for blocking smooth muscle relaxation

No pronounced cardiac effects (No β1 action)

61
Q

side effects of B blocker

A

cardiac failure: in CHF patients

bradycardia from decreased SYM to SA node

Bronchial asthma: cause bronchoconstriction

diabetics using oral hypoglycemics: B2 is needed to release EPI which causes release of glucose from liver, B blocker would cause hypoglycemic shock

62
Q
A
63
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A
64
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65
Q
A

23 spring: pharm (46 decks)

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