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68 Cards in this Set

  • Front
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Sympathomimetic

Mimic sympathetic NS

Sympathetic responses

Increase heart rate, force of contraction, velocity of electricity, peripheral vasoconstriction, BP


Decrease blood flow to kidneys


Breakdown stored resources increasing glucose


Ischaemia = necrotic tissue

Adrenergic receptors bind to

Epi norepinephrine dopamine

Adrenergic receptors promote the release of _____ and reuptake of _______. Also inhibit inactivation. Inhibit MAO

Norepinephrine

MAO

monoamine oxidase

Catecholamines

IV, brief, not BBB


Ex: epi, norepinephrine, and dobutamine

Noncatecholimines

Oral, long, cross BBB


Ex: ephedrine, albuterol, phenylephrine, terbutaline

Epi effects

A 1 2 and B 1 2

Norepinephrine effects

A 1 2 and B 1

Dopamine effects

A 1 B 1 and dopamine

Dobutamine effects

B 1

Ephedrine effects

A 1 2 and B 1 2

Phenylephrine effects

A 1

Terbutaline effects

B 2

Albuterol effects

B 2

Alpha 1 receptor activation

Vasoconstriction (elevated BP and nasal decongestion)


Adjunct to local anesthesia bc vessels will constrict to prevent toxicity and keep it in the local area


Mydriasis

Mydriasis

Dilation of pupils

Adverse effects of alpha 1 activation

Hypertension, necrosis, reflex bradycardia (elevated BP triggers baroreceptors and HR declines)

Alpha 2 receptor activation

Minimal peripheral effects


Primarily CNS effects


Activate presynaptic neurons- reduce sympathetic stimulation of CVS and reduce pain response

Where are adrenergic drugs working

In peripheral NS not CNS

Beta 1 receptor activation

Stimulates the heart


Cardiac arrest (restart arrested heart, positive inotrope by increasing force contraction, increase conduction of SC block)

Adverse effects of beta 1 activation

Altered rate or rhythm, angina pectoris, MI by increasing the workload of heart

Beta 2 receptor activation

Bronchodilation asthma pre term labor


Uterine smooth muscle contraction can slow labor

Adverse effects of beta 2 receptor activation

Tremor- skeletal muscle stimulation


Hyperglycemia- promotes breakdown of glycogen to glucose

Dopamine receptor activation peripheral

Dopamine is only neurotransmitter


Peripheral receptors in kidney (dilate renal bv, protect kidney- shock, increase urine output)

Adrenergic agonist- epi

Everything from anaphlactic shock to nasal decongestant alpha 1


All adrenergic receptors


Cardiac, vascular, pulmonary effects


Varied concentration and administration routes: IV, SC, topical, inhalation, intracardiac, intraspinal

What intensified the effects of epi

TriC antidepressants and MAO inhibitors

Epi A 1

delay absorption of local anesthetics, control superficial bleeding, reduce nasal congestion, increase BP, and dilate pupils

Epi B 1

Cardiac stimulation, overcome AV block, and start a stopped heart

Epi B 2

Bronchodilation

Norepinephrine/levophed

A 1 and B 1 (BP and heart rate)


Easily and quickly broken down


Only given IV drip no pb


Strong A 1 less B 1


Constant monitoring

What is the drug of choice for lie threatening hypotension

Norepinephrine/levophed

Dobutamine/dobutrex (mule)

B 1 specific - increase force of heart


Positive inotropic effect


Improve CO in heart failure


Effectiveness of drug needs to be balanced with patients condition (MI may be extended if workload increases)

What prolongs and intensifies the effect of dobutamine

MAO inhibitors and TriC antidepressants

Dopamine/intropin

Dose dependant


Low doses- increase renal perfusion and urinary output, d-receptors


High doses- vasoconstrict A 1, increase HR B 1 (decreases BP bc warm and vessels dilate)


Balance with patient status- don't overwork heart, tachydysrythmias, tissue ischwmia, peripheral necrosis

Beta 2 drug

Albuterol/ventolin

Albuterol/ventolin

Asthma- mediated bronchodilation


Side effect is tremor and tachycardia with large doses that effect B 1


Not beta selective

What is the drug of choice to delay preterm labor

Terbutalene/brethine

Ephedrine noncatecholimine MOST USED

Activates A 1 2 and B 1 2 directly


Acts directly and increases norepinephrine release


Nasal decongestion A 1 but when inhaled there is intense rebound, if taken oral there are a lot of side effects (HTN, dysthymias, angina, hyperglycemia, insomnia)


Narcolepsy A 2 receptors to brain

Phenylephrine/neo-synephrine

A 1


Nasal decongestion- orally and topically, BP side effects, less rebound than ephedrine and epi


Parenteral increases BP (post op)

Amphetamines

Agonist increases symp


Increase release and slow reuptake of norepinephrine and dopamine


CNS- euphoria PNS-cardiovascular (appetite suppressant, narcolepsy, ADHD)

Amphetamines ephedrine pseudoephedrine

Nasal congestion, weight loss, cardiac events and stroke (f>m) BANNED in OTC products, used to make meth

Adrenergic antagonists

Drugs that inhibit the sympathetic

Alpha blockade

Used for essential hypertension


Benign prostatic hyperplasia (relax smooth muscle in prostate)


Pheochromocytoma- catecholamine secreting tumor (adrenal medulla)


Raynaud's disease- peripheral vasospasms


When overdose on a 1 agonist

Alpha 1 blockers

Prazosin/minipress


Vasodilation, htn


Ortho static hypotension


1st dose effect is really bad


Reflex tachycardia


Nasal congestion


Inhibition of ejaculation


Sodium retention

A 1 blockers

Tamsulosin/flomax BPH


Selective so not so many side effects


Specific to bladder neck prostate and urethra


NOT USED FOR HTN


can cause impotence


Allow urine to flow easy

Impotence

Occurs when a man can't get or keep an erection firm enough for sexual intercourse

Phentolamine/regitine

A 1 and 2


Cause vasodilation to save tissues


Prevent necrosis with extravasation of vasoconstriction (dopa/ levo)

What is a BP controller but not reducer

Beta blocker

Beta blocker

Therapeutic effects


REDUCE CARDIAC WORKLOAD


reduce heart rate, force of contraction, velocity of impulse conduction

Beta block therapeutic uses

Angina pectoris, htn, dysthymias (tachy), MI, heart failure, migraine, hyperthyroidism, stage fright, Pheochromocytoma

Beta blockade adverse effects

Bradycardia, reduced CO, precipitation of heart failure, AV heart block, bronchoconstriction, peripheral vasoconstriction, inhibition of glycogenolysis, rebound cardiac excitation (body will load up with epi)

Never give beta blockers to these people because they will have a heart attack

AV heart block people

Common beta blockers


Nonselective


Selective


Alpha 1 and beta 1 and 2

Propranolol/inderal (give when wheezing effect BP) nadolol/corgard


Metoprolol/lopresson toprol and atenolol/tenormin (long acting)


Carvedilol/coreg (IV) and labetalol/normodyne/trandate (effect heart rate and BP

lol=

Beta blocker

Indirect acting anti-adrenergic

Act centrally alpha 2 agonists

Indirect-acting anti-adrenergic


Therapeutic uses and adverse effects


GLOBAL RESPONSE NOT SPECIFIC

Central acting, decrease sympathetic response- slow heart rate, decrease metabolic response (glucose), decrease BP


Bradycardia, hypotension, hypoglycemia

Indirect anti-adrenergic agents


Alpha 2- agonist

Reserpine (rauwolfia serpenina)- stops the formation and release of NE, used for hypotension but has severe CNS effects:


Deep depression, sedation, indifference to environment


Cardiovascular and GI effects

Indirect adrenergic agents


Alpha 2 agonist

Clonidine/catapres- central acting, reduces activation of adrenergic system


Primary indication HTN need to decrease BP, symp response, 2nd relief for Cancer (menopause flushing, withdrawal from opioids/nicotine, tourettes)


Oral or transdermal

Adrenergic drugs effect receptors by changing the release of

Norepinephrine

What is known as the big guns

Catecholamines

Dobutamine is very

Selective

Vascular decongestion doesn't get rid of

Secretions, vessels so wide that when you constrict them you feel better

Alpha 2 decreases

Symp response and treat pain caused by popcorn

Beta 1 will restart

Hart and support weak heart

Beta 2 will increase

BS

Dopamine will dilate

Renal bv, protect in shock ->fluid left the vascular space

Why we are giving epi. IV vs inhale

Your about to die or prevent asthma attack