test 1: lecture 13

Question 1

⍺1 adrenergic agonists will cause — in the heart

Answer 1

nothing, no ⍺1 receptors in the heart

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

Question 2

what are some ⍺1 adrenergic agonists

Answer 2

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

Question 3

what will ⍺1 adrenergic agnosists due to vasculature

Answer 3

vasoconstriction

this will trigger vagal effect and bradycardia

Question 4

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

Answer 4

nasal decongestant
eye redness

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

Question 5

Activation of presynaptic α2 receptor causes —

Answer 5

decreased NE release from neurons

Question 6

clonidine (catapres) is a —

Answer 6

⍺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

Question 7

what are two ⍺2 adrenergic agonists?

Answer 7

clonidine
xylazine

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

Question 8

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

Answer 8

vasoconstriction
BP

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

Question 9

biphasic response of ⍺2 adrenergic agnoists

Answer 9

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)

Question 10

xylazine

Answer 10

⍺2 agonist that causes sedation and analgesia

because it binds to a2 receptors in the brain

Question 11

what is rebound hypertension from a2 agonists

Answer 11

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

Question 12

rebound effect of a1 agonists

Answer 12

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

Question 13

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

Answer 13

B>a receptors
B1=B2

CHF → B1 increases cardiac contractility and CO

B2 activation causes brochodilation, used to treat asthma

isoproterenol (isuprel)

Question 14

isoproterenol (isuprel) is a —

Answer 14

Nonselective β Adrenergic Agonists (β1/2)

Question 15

isoproterenol (Isuprel) is used to treat

Answer 15

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)

Question 16

B1 agonist is used to treat

Answer 16

short term CHF

increases force of cardiac contraction but does not effect HR

dobutamine (dobutrex)

Question 17

dobutamine (dobutrex) is what type of drug

Answer 17

B1 adrenergic agonist

increases force of cardiac contraction but has minimal effect on HR

treatment of short term CHF

Question 18

— are b2 adrenergic agonists

Answer 18

albuterol (Salbutamol)
Metaproterenol

B2>B1 at low dose

β2-stimulation ↑ bronchodilation and other smooth muscle relaxation

prevent premature labor by relaxing uterine smooth muscle

Question 19

albuterol is used for

Answer 19

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

Question 20

if you give high dose albuterol what will happen

Answer 20

spillover to B1 receptors

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

Question 21

— is a B3 Adrenergic Agonists

Answer 21

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)

Question 22

myrbetric (mirabegron) is what type of drug

Answer 22

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

Question 23

what does myrbetric(mirabegron) do

Answer 23

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

B3 agonist

Question 24

how does tyramine and amphetamines get into the neuron?

Answer 24

presynaptic plasma membrane transporters

these are indirectly acting synpathomimetics

Question 25

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

Answer 25

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

Question 26

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

Answer 26

inreased release of endrogenous catecholamines **(NE)** ## Footnote tyramine and amphetamine

Question 27

what are three catecholamine reuptake inhibitors

Answer 27

cocaine imipramine (impril) amitryptyline (amitril) allow NE,DA and serotonin to stay in synapse for longer, acts as **antidepressants**

Question 28

how do reuptake inhibitor sympathomimetics work?

Answer 28

allow NE,DA and serotonin to stay in synapse for longer, acts as **antidepressants** cocaine imipramine (impril) amitryptyline (amitril)

Question 29

how do mixed acting sympathomimetics work?

Answer 29

Cause release of endogenous catecholamines and ALSO bind directly to adrenergic receptors **ephedrine** Adverse effect: Potential hypertension and cardiac arrhythmias

Question 30

ephedrine

Answer 30

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

Question 31

sudafed (pseudoephedrine) is a ---

Answer 31

mixed acting sympathomimetic Cause release of endogenous catecholamines and ALSO bind directly to adrenergic receptors can also be used to make **meth**

Question 32

phenylephrine (sudafed-PE)

Answer 32

is a mixed acting sympathomimetic Cause release of endogenous catecholamines and ALSO bind directly to adrenergic receptors can not be used to make meth!

Question 33

what does guanethidine do?

Answer 33

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** ## Footnote Gua**NE**thidine prevents NE (norepinephrine) release

Question 34

bretylium

Answer 34

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

Question 35

clonidine

Answer 35

a2 agonist binds to a2 on presynaptic nerve, which **stops NE release**

Question 36

reserpine

Answer 36

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

Question 37

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

Answer 37

reserpine leads to decreased NE, cause cytoplasmic NE will get broken down by MAO can also decrease EPI in adrenal gland

Question 38

⍺-methyl-DOPA

Answer 38

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

Question 39

--- is a false transmitter release

Answer 39

**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

Question 40

what are two things that block NE synthesis in the cell

Answer 40

α-CH3-p-tyrosine NE at high doses

Question 41

--- inhibits tyrosine hydroxylase enzyme

Answer 41

α-CH3-p-tyrosine

Question 42

--- are MAO inhibitors

Answer 42

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

Question 43

what is cheese syndrome

Answer 43

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**

Question 44

5 uses of a- adrenergic receptor blockage

Answer 44

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

Question 45

--- are irreversible ⍺ receptor blockers

Answer 45

dibenamine phenoxybenzamine

Question 46

phenoxybenzamine and dibenamine are --- and work ---

Answer 46

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

Question 47

--- is a reversible ⍺ receptor blocker

Answer 47

phentolamine (regitin)

Question 48

how does phentolamine (regitin) work

Answer 48

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**

Question 49

prazosin (minipress)

Answer 49

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)

Question 50

tamsulosin (flomax)

Answer 50

selective ⍺1 blocker works on α1A- in urinary tract used to improve urinartion with men you have Benign Prostatic Hyperplasia (BPH) → relaxes muscle

Question 51

yohumbine

Answer 51

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**

Question 52

yohimbine will reverse ---

Answer 52

xylazine-induced sedation yohimbine is a ⍺2 blocker xylazine is a ⍺2 agonist

Question 53

side effects of ⍺ receptor blockage

Answer 53

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

Question 54

beta blockers are used for

Answer 54

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

Question 55

propranolol(inderal)

Answer 55

non selective B blocker B1=B2 **decreases** HR, contractility and CO **Membrane stabilization** effect at high doses large withdrawal and rebound effect

Question 56

propranolol (inderal) withdrawal effect

Answer 56

non-selective B blocker

Question 57

pindolol (calvisken)

Answer 57

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

Question 58

timolol (timoptic)

Answer 58

B blocker nonselective B1=B2 less membrane stabilization used for **wide angle glaucoma**

Question 59

metoprolol (lopressor)

Answer 59

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**

Question 60

butoxamine

Answer 60

selective B2 blocker Selective for blocking smooth muscle relaxation No pronounced cardiac effects (**No β1 action)**

Question 61

side effects of B blocker

Answer 61

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

Question 62

Answer 62

Question 63

Answer 63

Question 64

Answer 64

Question 65

Answer 65