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Pharmacology > Sympathomimetic Agents > Flashcards

Sympathomimetic Agents Flashcards

1
Q

Alpha1 adrenergic Receptors

A

GPCR Gq -> activation of PLC/IP3/DAG pathway

alpha1A/B/D subtypes

found on postsynaptic membranes - predominantly in vascular beds of skin and splanchnic vessels, bladder, a pregnant uterus, prostate and iris muscle.

action is contraction of smooth muscle - i.e. like piloerector muscles

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2
Q

which adrenergic receptor activates the G-alpha-s Adenylyl cyclase protein and which inhibits?

A

beta receptors activate AC causing an increase of IC cAMP

Alpha2 receptors inhibit AC leading to the opposite effect

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3
Q

alpha2 adrenergic receptors

A

alpha2A/B/C subtypes

found in adrenergic and cholinergic nerve terminals, some vascular smooth muscle, fat cells, pre-synaptic and post-synaptic CNS neurons and platelets/leukocytes.

Acts via Gi GPCR pathway to inhibit adenylyl cyclase activity and neurotransmitter release

in some sites also activates PLC/MAPK pathways - smooth muscle

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4
Q

Beta adernergic receptors

A

all subtypes - beta1/2/3 - increase activity of adenylyl cyclase

effects - increases HR and heart contractility, stimulates smooth muscle relaxation and enhances secretion of insulin

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5
Q

Beta1 Receptors

A

found predominately in heart but also juxtaglomerular cells of kidney (activates renin-angiotensin-aldosterone pathway to increase BP)

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6
Q

Beta2 Receptors

A

found on smooth muscle and pre-/post-synaptic membranes.

Causes smooth muscle relaxation, vasodilation in skeletal muscle, bronchodilation, relaxation of uterine smooth muscle, and decreases motility of the GI tract.

enhances insulin secretions

causes platelet aggregation

found on presynaptic neurons -> release of neurotransmitters (function as auto or heteroreceptors)

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7
Q

Beta3 receptors

A

On postsynaptic membrane

predominately on adipocytes causing breakdown of TAGs and thermiogenesis

also causes relaxation of detrusor muscle

has a higher affinity for NE than for Epi

resistant to antagonist - propranolol

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8
Q

Dopamine

A

a central neurotransmitter that regulates rewards, emotion, cognition, memory, and motor activity

circulating DA in periphery mainly binds D1 receptors

two main receptor types - D1 and D5 and D2/3/4

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9
Q

Dopamine Receptors

A

D1 and D5 Receptors - GsPCR increases adenylyl cyclase, increases cAMP
(causes vasodilation in renal, coronary, mesenteric and cerebrovascular arteries)

D2, D3, and D4 Receptors - GiPCRs decrease activity of adenylyl cyclase causes the activation of hyperpolarizing K+ channels and inhibition of Ca++ channels
(modulates neurotransmission of CNS)

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10
Q

indirect-acting adrenergic agonists

A

amphetamine and tyramine are releasing agents

cocaine is an uptake inhibitor

selegiline is an MOA inhibitor

entacapone is an COMT inhibitor

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11
Q

what is the mixed-acting adrenergic agonist?

A

ephedrine - alpha1/2, beta1/2 and releasing agent.

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12
Q

epinephrine - what are it’s pharmacokinetics?

A

methylated amino-group enhances beta2 activity

exhibits a dose dependent response

Has equal affinity for Beta 1 and 2 receptors, slightly less affinity for alpha 1 and 2

A - given subcutaneous, intramuscular, IV and inhalation. D - does not cross BBB, M- degraded by MAO and COMT. E - excreted in urine. Onset is rapid, slowest being subcutaneous 5-10 minutes

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13
Q

epinephrine - what are it’s pharmacokinetics?

A

methylated amino-group enhances beta2 activity

exhibits a dose dependent response

Has equal affinity for Beta 1 and 2 receptors, slightly less affinity for alpha 1 and 2. Acts preferentially on Beta2 receptors

A - given subcutaneous, intramuscular, IV and inhalation. D - does not cross BBB, M- degraded by MAO and COMT. E - excreted in urine. Onset is rapid, slowest being subcutaneous 5-10 minutes

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14
Q

How does epinephrine cause an increase in systolic blood pressure?

A

skeletal muscle is rich in beta2 receptors

epinephrine acts directly on cardiac tissue to increase heart rate and strength of ventricular contraction

causes alpha receptor mediated vasoconstriction in much of the bodies smooth muscle, precapillary vessels of the skin, mucosa, kidney and the mesentery and veins.

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15
Q

How does epinephrine cause a decrease in diastolic BP?

A

By activation of Beta2 receptors in skeletal muscle vasculature inducing vasodilation which decreases peripheral resistance. The decrease in peripheral resistance decreases diastolic blood pressure

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16
Q

epinephrines cardiac, respiratory, metabolic, CNS effects, effect on peripheral circulation and effect on BP?

A

Cardiac: increases HR, stroke volume, cardiac output and coronary blood flow. Can cause arrhythmia (Beta1)

Respiratory:
bronchodilation (Beta2)

BP: increases systolic pressure, decreased diastolic pressure, mean pressure is only slightly elevated, mean pulmonary pressure is elevated.

Metabolic: increases oxygen consumption, blood glucose, and lactic acid. Decreases plasma K+

peripheral circulation: decreased or unchanged TPR, slight increase of cerebral blood flow, increase in skeletal muscle flow and decrease in cutaneous and renal blood flow

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17
Q

effect of epinephrine at physiologic concentrations - slow IV infusion

A

beta2 mediated enhanced blood flow to skeletal muscles which decreases peripheral resistance and diastolic BP

Beta1 mediated increased HR, stroke volume, cardiac output and heart work

typically not much change in MAP

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18
Q

epinephrine at intermediate rates

A

causes alpha mediated vasoconstriction in skeletal muscles as well

theres a compensatory reflex that can counter the epinephrine caused increase in heart rate

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19
Q

rapid infusion of epinephrine

A

a high concentration of epinephrine causes the alpha receptor effects to be predominate.

TPR is increased, HR and heart contractility is increased.

systolic and diastolic blood pressure is increased

reflex homeostatic decreases HR

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20
Q

epinephrines cardiac, respiratory, metabolic, CNS effects, effect on peripheral circulation and effect on BP?

A

Cardiac: increases HR, stroke volume, cardiac output and coronary blood flow. Can cause arrhythmia (Beta1)

Respiratory:
bronchodilation (Beta2)

BP: increases systolic pressure, decreased diastolic pressure, mean pressure is only slightly elevated, mean pulmonary pressure is elevated.

Metabolic: increases oxygen consumption, blood glucose, and lactic acid. Decreases plasma K+

peripheral circulation: decreased or unchanged TPR, slight increase of cerebral blood flow, increase in skeletal muscle flow and decrease in cutaneous and renal blood flow

CNS - increases respiration and subjective sensations: causes anxiety - headache, restlessness, apprehension, tremor and palpitations.

21
Q

what are the therapeutic uses of epinephrine? What are the adverse affects?

A

drug of choice for anaphylactic shock

can be used for vasoconstriction with local anesthetics

bronchodilation in acute asthmatic episodes

used to as a cardiopulmonary resuscitation during MI

can be used as a topical hemostat - stop bleeding.

adverse effects - restlessness, apprehension, throbbing headache, tremor, palpitations, premature ventricular contractions, arrhythmias, angina and a very large dose as cause cerebral hemorrhage because of a sharp increase in BP

22
Q

what are the contraindications of using epinephrine?

A

cardiac dilatation or coronary insufficiency because of oxygen consumption

cardiogenic shock because of increased myocardial oxygen demand

hypertension - because of pressor effects and cardiac stimulation

organic brain damage because of increased cerebral pressure

hypersensitivity

23
Q

what are the drug interactions of epinephrine?

A

interacts with anything that has similar effects (agonists to adrenergic receptors) or anything that would block it’s effect

interacts with alpha (counteracts effect of epi) and beta AR (causes unopposed epi actions on alpha1 ARs) antagonists

drugs that cause hypertension, tachycardia or cardiac arrythmias (increases risk of hypertension and arrythmia)

NO reuptake inhibitors

MAO or COMT inhibitors - causes hypertensive crisis

dihydroergotamine - causes extreme hypertension

24
Q

Norepinephrine effects and therapeutic uses

A

Nor-Epi has equal and greatest affinity for alpha receptors and some for beta1 receptors

NorEpi has NO affinity for Beta2 R

NorEpi is a potent vasopressor (a) which increase contractility of the heart and it’s oxygen consumption (B1)

HR is either unchanged or decreased because of homeostatic reflexes

used therapuetically for septic shock and profound hypotension - only after blood volume has been restored (meaning patient has been given fluids)

25
Q

norepinephrine contraindications, adverse effects and drug interactions

A

contraindications - in patients with blood loss: needs restoration of BV

Adverse effects - reduced blood flow to organs puts them at danger for organ failure, arrhythmia. digital ischemia and extravasation at injection site -> blood leakage causes ischemia and can lead to gangrene

26
Q

dopamine pharmacokinetics

A

DA has the highest affinity for D receptors, then beta1 and then alpha.

given by IV infusion with onset in 5 min

DA is inactivated by MAO and COMT with a half life of 5 mins, meaning it’s duration of action is 10 mins.

27
Q

dopamine concentration dependent effects - low dose vs. intermediate dose vs high dose

A

low conc - DA binds D1 receptors in renal, mesenteric and coronary vascular beds causing vasodilation. Net effects include an increase in renal blood flow, GFR and Na+ excretion. Decreased Peripheral vascular resistance

intermediate conc - DA stimulates beta1 R increasing HR and has a inotropic effect (mediated by the releasing of NE from nerve terminal - a side effect of beta1 R stimulation) Increases systolic BP

At high conc DA is a pressor - it activates vascular alpha1 R causing vasoconstriction (this increases peripheral resistance)

28
Q

what are DA therapeutic uses and adverse effects?

A

therapeutic uses are for shock with proper fluid administration, decompensated heart failure (short-term) and postop myocardial depression.

adverse effects in high dose are that of any sympathomimetic - headache, tachy, anginal pain, arrhythmias and hypertension. Also, extravasation at injection site which can cause tissue necrosis

29
Q

isopreterenol

A

potent, nonselective Beta agonist with no affinity for alpha R

causes cardiac chronotropic and inotropic effects increasing cardiac output and increases Oxy comsumption. Also, relaxes bronchus and GI smooth muscle

decrease peripheral vascular resistance, diastolic BP and MAP.

30
Q

therapuetic uses and adverse effects of isopreterenol

A

historically used for bradyarrhythmia, AV block and asthma

adverse effects include headache, tremor, dizziness, palpitations and sinus tachycardia

in patients with underlying coronary or cardiac disease cardiac ischemia and arrythmias can occur

31
Q

dobutamine

A

Beta1 selective agonist

Racemic mixture

(+) has high potency for beta ARs

(-) has potency for alpha 1 but the (+) enantiomer is a alpha1 antagoist so the effects are nulled.

Beta 1 effect predominates

Increases contractility of the heart and cardiac output with less reflex tachycardia (like would be seen with isoproterenol)

Used therapeutically short-term. For cardiac decompensation and for cardiac stress testing in patient who cannot perform the exercise stress test.

Adverse effects - tachyphylaxis, prolonged use (24-72hrs) causes receptor desentization and internalization. Causes Beta1 R induced hypertension, angina, arrhyymia, tachycardia

32
Q

Short acting selective beta2 agonists

A

Metaproterenol
Albuterol
Levalbuterol
Terbutaline

Onset 10 mins. Last 4-6hrs

Routes - oral systemic, inhalation and IV (IV should only be used in emergencies)

Used from brochodilation
Systemically could prolong labor

33
Q

Long acting selective beta2 agonists

A

Formoterol
Indacaterol
Olodaterol
Salmeterol

Last 12hours - these should never be used for an acute bronchial attack because they have a longer onset, 15-19 minutes

Given only by oral inhalation
Metabolized CYP

34
Q

What are the effects and therapeutic uses of selective beta2 agonsts?

A

They slow uterine contractions, induce bronchodilation, they can suppress leukotienes and histamine release and they enhance mucocilliary function

Therapeutic uses in asthma and COPD - specifically short-acting. Long-acting is used prophalatically or for symptomatic noctornal asthma.

Also for tocolytic - terbutaline which causes relaction of the myometrium and prolongs labor.

35
Q

What are the adverse effects of beta2 selective agonists?

A

Tremor - because of skeletal muscle Beta2 activation

Tachycardia - stimulation of cardiac Beta AR, could be reflex tachycardia as well

Restlessness, apprehension, anxiety - occurs with systemic administration

Metabolic effects include hypokalemia and hyperglycemia

36
Q

alpha1 selective agents

A

phenylephrine
oxymetazoline
midodrine

37
Q

alpha2 selective agents - and the effect?

A

clonidine
methlydopa

acts on GiPCR and decreases central sympathetic tone both by direct action on alpha2 receptors and inhibiting release of NE.

leads to decrease in BP and HR

38
Q

therapeutic uses of phenylephrine

A

phenylephrine is an alpha1 selective agent

it is a vasopressor, temporary nasal decongestant

topical uses are for ocular decongestant, mydriatic, hemostatic agent and hemorrhoids

39
Q

therapeutic uses of clonidine

A

decrease BP by decreasing peripheral resistance and renal vascular resistance and HR – Hypertension

pain management - epidural

ADHD and hot flash treatments

assists with withdrawal syndromes - opiod withdrawal or smoking cessation

40
Q

clonidine adverse effects

A

dry mouth and sedation are most common

also possible is hypotension, bradycardia, sexual dysfunction

Abrupt withdrawal causes rebound hypertension with reflex tachycardia

interacts with beta blockers, beta blockers must be discontinued first

41
Q

methyldopa - drug type and overall effects

A

alpha2 selective agonists

converts into methylnorepinephrine which decrease PVR and BP

42
Q

methlydopa - therapeutic uses

A

used for hypertension, even for hypertension in pregnancy

-has no adverse effects in fetus, maintains blood flow to uterus and does not reduce maternal CO or renal perfusion.

43
Q

methyldopa - adverse effects

A

dry mouth and sedation

orthostatic hypotension

headache, ejaculation disorder, impotence and reduced libido

endocrine effects that cause tremors similar to whats seen in parkinson’s disease, hyperprolactinemia, gynecomastia and galatorrhea

also - rarely, hepatitis, hemolytic or aplastic anemia, drug fever

44
Q

ephedrine

A

mixed action sympathomimetics

increases HR, CO and BP
causes bronchodilation and increases resistance to the outflow of urine - alphaR

therapeutic uses are for spinal anesthesia (induction of hypotension) and nasal congestion

45
Q

ephedrine - indirect and direct actions

A

indirect action - enhance’s NE release from sympathetic neurons

Direct action - agonist for both alpha and beta receptors

46
Q

what are the mech of actions for amphetamine and cocaine?

A

amphetamine blocks/inhibits VMAT which increases the availability of NE
VMAT re-sequesters NE into storage vesicles

cocaine inhibits monoamine reuptake transporters NET, DAT, and SERT

47
Q

what are the therapeutic uses of MAO inhibitors?

A

treatment for depression by inhibiting MAO theres an increase of Epi, NorEpi, Dopamine and serotonin

can cause accumulation of tyramine (from food)

48
Q

what are the therapeutic uses of COMT inhibitors?

A

COMT inhibitors are given along Levadopa to treat parkinson’s disease - causes more sustained levodopa serum level

Pharmacology (23 decks)

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