2.1 Pharm Exam1: Adrenergic Drugs

Front 1

What are the 3 types of adrenergic drugs?

Back 1

direct acting- activates or inactivates receptor

indirect acting- changes release or metabolism of NT

mixed acting- activates/inactivates receptor AND changes release

Front 2

What are the 2 types of direct acting?

Back 2

adrenergic agonists

adrenergic antagonists

Front 3

What are the selective adrenergic agonists?

Back 3

alpha1

alpha2

beta1

beta2

Front 4

What are the catecholamine adrenergic agonists?

Back 4

non-selective: epinephrine (EPI), norepinephrine (NE), isoproterenol (ISO)

selective beta1: dopamine (DA), dobutamine

*highly potent, rapidly inactivated, polar & dont cross BBB

Front 5

What is the advantage of non-catecholamines (phenylephrine & ephedrine)?

Back 5

longer half-lives

(greater CNS side effects bc non-polar)

Front 6

Which catecholamine acts on all receptors (a1, a2, b1. b2)?

Back 6

EPI

Front 7

Which catecholamine acts on a1, a2, & b1?

Back 7

NE

Front 8

Which catecholamine acts on both beta receptors only (B1 & B2)?

Back 8

ISO

Front 9

Both dopamine & dobutamine are selctive for b1, however ________ also acts on D1 & D2

Back 9

DA also acts on dopamine receptors (D1 & D2)

Front 10

List the catecholamines according to alpha affinity (highest to lowest)

Back 10

(highest-->lowest)

EPI--> NE--> ISO

Front 11

List the catecholamines according to beta affinity (highest to lowest)

Back 11

(highest--> lowest)

ISO--> EPI--> NE

Front 12

vasoconstriction*

inc. peri resist*

inc. BP

mydriasis

closes internal bladder sphincter

which adrenoceptor?

Back 12

alpha1

Front 13

vasodilation*

dec. peri resist*

bronchodilation

inc. glycogenolysis

inc. glucagon release

relaxes uterine sm musc

Back 13

beta2

Front 14

tachycardia

inc. lipolysis

inc. myocardial contractility

inc. renin release

Back 14

beta1

Front 15

(AUTO_INHIBITION)

inhibit NE release

inhibit Ach release

inhibit insulin release

Back 15

alpha2

Front 16

Does NE have a higher affinity for alpha or beta1?

Back 16

alpha > beta1

Front 17

Does EPI have a higher affinity for alpha or beta1 or beta2?

Back 17

beta2 > beta 1> alpha

Front 18

Cutaneous blood vessels have alpha receptors ONLY, how will they respond to EPI? NE?

Back 18

EPI- vasoconstriction

NE- vasoconstriction

(both EPI & NE go to alpha & alpha induces vasoconstriction)

Front 19

Skeletal muscle blood vessels have BOTH beta2 & alpha receptors. How will they respond to EPI? NE?

Back 19

EPI- vasodilation

(EPI has a higher affinity to beta2 which vasodilates)

NE- vasoconstriction

(NE does not bind to beta2, thus only alpha will be activated, vasoconstricting)

Front 20

Activation of (alpha/beta) receptors on the vasculature will have a greater impact on baroreflex response

Back 20

alpha

(increases BP alone & via inc resistance & vasoconstriction, thus initiating baroreflex bradycardia & slowing of conduction)

Front 21

(EPI/NE/ISO)

causes;

-initial drop in resistance (via beta2 affinity), followed by an increase & leveling resistance (alpha1)

-tachycardia (beta1), stimulating baroreflex to increase sympathetic tone

Back 21

EPI

Front 22

(EPI/NE/ISO)

causes;

-large increase in peripheral resistance (via unopposed alpha1)

-initial tachycardia (via beta1), stimulating baroreflex to decrease sympathetic tone

Back 22

NE

Front 23

(EPI/NE/ISO)

causes;

-large decrease in peripherial resistance (via unopposed beta2)

-tachycardia (via beta1), stimulating baroreflex to increase sympathetic tone

Back 23

ISO

Front 24

______ cannot be given orally because it will be rapidly inactivated. How is it given so that it has high affinity & potency for adrenergic receptors?

Back 24

EPI

given via IV or inhalation

Front 25

_____ causes;

vetricular arrhythmias

hyperglycemia

reflex bradycardia

tremor

(due to its affect on all 4 receptors some of which are contradictory)

Back 25

EPI

Front 26

What is EPI used as a drug for?

Back 26

asthma

hypersensitivity rxns

cardiac resuscitation

prolong local anesthetic

glaucoma

Front 27

Why shouldn't you use EPI in pts w/ hyperthyroidism, diabetes, or on beta blockers?

Back 27

hyperthyroidism- will increase the likelihood of arythmias

diabetes- increase the likelihood of hyperglycemia

beta blockers- leaves alpha completely unopposed--> dangerous inc. of BP & peripheral resistance & vasoconstriction

Front 28

What are the effects of DA on beta1, D1, & D2 receptors?

Back 28

beta1- increased contractility (+ ionotropy)

D1- vasodilation, natriuresis, & diuresis

D2- interferes w/ NE release

(also a precursor to NE & EPI)

Front 29

Where are D1 & D2 receptors located?

Back 29

D1

- renal & mesenteric vasculature

- renal thick ascending loop & loop of henle (PT)

D2

- presynaptic adrenergic neurons

Front 30

_________ is used to improve cardiac function & renal perfusion ONLY after hypovolemia is corrected w/ fluid replacement

Back 30

DA

(used only in severe cases)

Front 31

_______ is made up of + & - enantiomers, both of which are beta1 agonist

Back 31

dobutamine

(- is alpha1 agonist, + is alpha1 antagonist, effects cancel out)

Front 32

Why is dobutamine used instead of DA?

When is it used?

Back 32

more prominent ionotropic effects on heart

*used short-term after cardiac surgery, MI, CHF to increase CO & SV (contractility) w/o inc HR & BP

Front 33

Q: What kind of drug is preferable for cardiac resuscitation?

alpha1 agonist

beta1 agonist

a & b agonists

beta2 agonist

Back 33

A: beta1 agonist

(inc both HR & contractility)

Front 34

oxymetazoline is a non-selective (alpha/beta) agonist

what is it used for?

Back 34

alpha agonist (a1 & a2)

nasal decongestant- constricts the small arterioles in nasal mucosa

(overuse= damage to mucosa & eventual receptor desensitization)

Front 35

Phenylephrine is a selective (a1/a2) agonist

what is it used for?

Back 35

a1 agonist

primarily for nasal decongestant

(less damaging than oxymetazoline)

also mydriatic (pupil dilates) w/o loss of accomodation, glaucoma, & short-term hypotensive emergencies

Front 36

Phenylephrine use for mydriasis is contraindiacted in ____________

Back 36

narrow/closed angle glaucoma

Front 37

clondine is a selective (a1/a2) agonist

what is it used for?

Back 37

a2 agonist

prevents increase in sympathetic activity & cravings in withdraw patients

Front 38

MAO of clondine

Back 38

partial alpha2 agonist

(primarily acts at presynaptic a2)

-acts on lower brainstem nuclei to decrease sympathetic outflow to heart & vasculature--> decreases BP (crosses BBB)

Front 39

clonidine is given _________ or __________ NOT via IV

Back 39

orally or transdermal patch

(patch reduces CNS side-effects)

(orally for hypotension)

Front 40

Side effects of Clonidine

Back 40

dry mouth

sedation

bradycardia

sexual dysfunction

(= dec. sympathetics, usually diminish after a few wks of use)

(abrupt discontinuation is dangerous= rebound hypertension)

Front 41

apraclondine is a selective (a1/a2) agonist

what is it used for?

Back 41

a2 agonist

primarily used for glaucoma (w/ other timolol & pilocarpine), to dec intraocular pressure

Front 42

MAO of apraclondine

Back 42

(does NOT cross BBB)

vascoconstriction in ciliary epithelium to decrease aqueous humor

Front 43

Albuterol & salmeterol are BOTH selective (beta1/beta2) agonists

What are they used for?

Back 43

beta2 agonists

to treat asthma & COPD

via Bronchodilation

Front 44

(Albuterol/Salmeterol)

Slower onset of action

Longer duration of action

Works better for COPD

Back 44

Salmeterol

(albuterol is faster acting & necessary for acute asthma attacks, usually given both)

Front 45

ritodrine is a selective (beta1/beta2) agonist

What is it used for?

Back 45

beta2 agonist

uterine relaxation, stops premature labor

(IV admin)

(ritodrine = right on time, deliver on time, not early)

Front 46

Why is skeletal muscle tremors a side effect of beta2 agonists (albuterol, salmeterol, & ritodine)?

Back 46

beta2 causes increased glucose release-->

leading to increased insulin-->

insulin increases skeletal muscle uptake of K+-->

hypokalemia--> muscle tremors

Front 47

what are the main types of adrenergic antagonists?

Back 47

non-selective alpha

alpha1 selective

alpha2 selective

non-selective beta

beta1 selective

beta2 selective

Front 48

Phenoxybenzamine & phentolamine are what type of adrenergic antagonists?

Back 48

non-selective alpha antaongists (a1 & a2)

Front 49

Prazosin & Tamsulosin are what type of adrenergic antagonists?

Back 49

alpha1 selective alpha antagonists

Front 50

Phenoxybenzamine

clinical use-

MOA-

Side effects-

Back 50

clinical use- pheochromocytoma (adrenal tumor, inc NE & EPI)

MOA- irreversible alpha antagonist--> decrease peripheral resistance & pre-load

(prevents action of inc NE & EPI on alpha receptors)

side effects- postural/orthostatic hypotension, reflex tachycardia (inc NE release), sexual dysfunction

Front 51

Prazonsin

clinical use-

MOA-

side effects-

Back 51

clinical use- hypertension, CHF, BPH

MOA- blocks alpha1 in vasculature--> dec peripheral resistance & pre-load

suppresses sympathetic outflow from CNS

side effects- postural hypotension & syncope (after 1st dose), water/Na retention, sexual dysfunction

Front 52

Tamsulosin

clinical use-

MAO-

Back 52

clinical use: BPH

MAO: blocks alpha 1 on internal bladder sphincter & prostate= relaxation--> symptomatic relief of inability to urinate caused by BPH (enlargened prostate due to too much DHT)

Front 53

Propranolol, timolol, & sotalol are what type of adrenergic antagonists?

Back 53

non-selective beta antagonists

(1st generation)

Front 54

Labetalol & carveilol are 3rd generation non-selective beta antagonists, what else do they do?

Back 54

also alpha1 antagonists

Front 55

Atenolol (tenormin), esmolol, nebivolol, & metoprolol are what type of adrenergic antagonists?

Back 55

beta1 selective antagonists

(all 2nd generation, EXCEPT nebivolol is 3rd)

Front 56

What are the general clinical uses for beta-blockers (beta-antagonists)?

Back 56

mostly cardio

-MI/angina

-Arrythmias

-CHF

-hypertension

also

-anxiety, glaucoma (timolol)

Front 57

Propranolol

clinical use:

MAO:

Back 57

clinical use: thryotoxicity (HR & arrythmia) & anxiety

MAO: non-specific beta antagonists, blocks sympathetic activation of heart & blocks renin release (thus blocking angiotensin 2)--> overtime dec. per res

Front 58

Timolol

clinical use:

MOA:

Back 58

clinical use: open angle glaucoma

MOA: non-specific beta blocker, reduces IOP by dec. aqueous humor production by ciliary body

Front 59

General side effects of beta blockers

Back 59

-bronchioconstriction (use cautiously in asthma pts)

-arythmias

-sexual dysfunction

-masked hypoglycemia (DONT give to diabetic)

do NOT STOP taking abruptly

Front 60

Labetaolol

clinical uses:

MOA:

Back 60

clinical uses: hypertension/hypertensive emergency

MOA: beta1 antagonist--> reduces HR & contractility, alpha1 antagonist--> reduces peripheral resistance, beta2 agonist--> vasodilation

Front 61

Carvedilol

clinical uses:

MOA:

Back 61

clinical uses: hypertension, CHF

MOA: beta1 antagonist--> reduces HR & contractility, alpha1 antagonist--> reduces peripheral resistance

Front 62

Nebivolol

clinical uses:

MOA:

Back 62

clinical uses: hypertension

MOA: beta1 antagonist--> reduces HR & contractility, increases NO bioavailability

Front 63

What are some of the additional effect of 3rd generation beta blockers?

(labetalol, carvedilol, nebividol)

Back 63

-beta2 agonist & alpha1 antagonist = vasodilation

-antioxidant

-antiproliferative

Front 64

Desoxyn, dexedrine, & ritalin are examples of ______________

Back 64

amphetamines

indirect acting sympathomimetics

Front 65

Amphetamines (desoxyn, dexedrine, ritalin)

clinical uses:

MAO:

side effects:

Back 65

clinical uses: narcolepsy, ADHD, ADD, appetite suppressant (oral admin)

MAO: crosses BBB, inhibits uptake 1 of NT, inhibits MOA, inhibits vesicular transporters--> inc release of dopamine & other biogenic amine

side effects:

general inc in sympathetics

Front 66

Phenelzine, tranylcypromine, & selegilline are examples of _____________

Which one of these is specific?

Back 66

MAOIs

indirect acting sympathomimetics

selegine is MAO-B selective (others are for A & B)

(delay NT degradation)

Front 67

What are Phenelzine & Tranylcypromine used for?

Back 67

tx depression

Front 68

What is selegilline used for?

Back 68

adjunct tx in Parkinson's disease

Front 69

Entacapone & tolcapone are examples of __________

what are they used for?

Back 69

COMT inhibitors

indirect acting sympathomimetics

adjunct tx in Parkinson's disease

(delay NT degradation)

Front 70

Metyrosine & Aldomet are examples of __________

Back 70

indirect acting sympatholytics

Front 71

What is metyrosine used for?

Back 71

pheochromocytoma

(inhibits dopa synthesis, thus inhibits NE & EPI synth)

Front 72

What is Aldomet used for?

Back 72

hypertension in pregnancy

(acts as false precursor, makes methyl NE instead of NE)

Front 73

Ephedrine is an example of ____________

Back 73

mixed acting sympathomimetic

Front 74

ephedrine

clinical use:

MAO:

side effect:

Back 74

clinical use: potent CNS stimulant

MAO: agonist for ALL adrenergic receptors, inc DA & NE release, crosses BBB

side effects: arrhythmias, headache, insomnia, nausea, tremors