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Pharmacology > adrenergic agonists and antagonists > Flashcards

adrenergic agonists and antagonists Flashcards

1
Q

Epinephrine

A

Agonist
Receptor- alpha and Beta 2
Low dose beta effects
high dose alpha effects

Indications/ effects- high doses, potent vasopression, increase in blood pressure (systolic more than diastolic. positive chornoropic and inotropic effects ( beta 1), vasoconstriction(alpha1) increase in cardiac output and increase in O2 demand from heart

  • bronchodilation (Beta2)
  • relaxation GI smooth muscle with contracted sphincters( alpha1)
  • relaxed detrusor ( Beta2)
  • Metabolic hyperglycemia due to increase in glycogenolysis and glucagon release (Beta2). There is a net inhibition of insulin secretion(alpha2) while beta 2 enhances secretion)
  • increase in lipolysis through Beta2(increase incAMp and HSL)

DOC for patients in anaphylactic shock- cardiac arrest, asthma(combined with local anesthetics to increase duratino) glaucoma ( decreased production of aqueous humor)

Pharmacokinetics- rapid onset, brief duration, administered IV in emergences. can also be administered SC, ET tube, inhalation, and topically on eye.

Adverse/contra ( CNS disturbances) restlessness, fear, apprehension, headache, tremor(secondary effects outside the CNS), ICH due to increased BP, Cardiac arrhythmias, especially in patients on digitalis, pulmoary edema

synthesized from tyrosine in the adrenal medulla.

  • it is a polar molecule and doesn’t cross CNS
  • metabolized by COMT and MAO into VMA and meanephrime
  • hyperthyroid may enhance CV actions likely due to upregulation of receptors
  • cocaine prevents reuptake
  • beta blockers cause predominate alpha effects such as incerease in TPR and BP
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2
Q

NE

A

alpha and Beta1 more than Beta 2- agonist

Indications/effects-Vasoconstriction (alpha 1)- increased PVR which causes increased systolic and diastolic pressure along wiht mean areterila pressure
-bradycardia due to decreased sympathetic outflow following the baroreceptor response (indirect effect throughM2). induces hyperglycemia(less potent than epi)

-Limited therapeutic vaule but can treat shock, but dopamine is better due to preservation of renal blood flow.

Adverse/contra- may cause kidney shutdown

Baroreceptor reflex counteracts local action which can be blcoked by pretreatment with atropine reveals direct effect of tachycardia

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3
Q

Dopamine

A

Dopamine, alpha, beta agonist

Effects/indications
-central regulator of movement
-CVS: low doses vasodilate through D1 receptor (cAMP) especially at renal, mesenteric and coronary
- ionotropic effect at intermediat concentration (beta1) and increasing release of NE
-increase in Systolic BP
-High concentration- alpha1 mediated vasoconstriction,
DOCfor cardiogenic and hypovolemic shot. it increases GFR, renal blood flow and Na excretion which preserves renal function.

Pharmacokinetics:Ineffective when given orally due to metabolism by MAO and COMT

Adverse/contra: overdose causes sympathomimetic symptoms
-can cause nausea, HTN and arrhythmia but it is short lived due to rapid metabolism to HVA

doesn’t cross BBB

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4
Q

Fenoldopam

A

D1 agonist- Peripheral vasodilation- used in short term management of HTN

give continuosly via IV not bolus

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5
Q

Isoproterenol

A

drect acting beta1,2 agonist

effects/indications
CVS- increases CO through rate and force of contraction, used in AV block or cardiac arrest. decrease in TPR due to no alpha 1 opposing it.
-slight increase in Systolic blood pressure, decrease in mean arterial pressure and diastolic blood pressure, tachycardia

pharmacokinects. most reliable when given parenterally or inhaled

similar adverse effects compared to epi

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6
Q

Dobutamine

A

direct acting beta 1 agonist

used in acute managment of congestive heartfailure. increases contractility. increase in cardiac output with little change in heart rate. O2 demands of the myocardium are not significantly affected. it gives it an advantage over other sympathomimetics.

Pharmacokinetics: can build up a tolerance with long term use

racemic mixture: negative is an alpha 1 and weak Beta 1 agonist, positive is an alpha 1 antagonist and a potent beta 1 agonist which makes it a selective beta agonist.

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7
Q

Terbutaline

A

direct acting beta 2 agonist

bronchodilator, used for emergency treatmetn of status asthmatics, reduces uterine contractions in premature labor.

resorcinol ring is no metabolized by COMT giving it a longer duration . Oral, inhalation or SC

Selectively is lost at high concentrations, used in treatment of asthma without having effects on heart

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8
Q

Albuterol

A

direct acting beta 1 agonist

Selectively is lost at high concentrations, used in treatment of asthma without having effects on heart

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9
Q

Salmetrol/Formeterol

A

beta 2 direct acting agnoist

bronchodilator- long acting not used for prompt relief of bronchospasm

slow onset, but prolonged action (12 hours) after inhalation

Selectively is lost at high concentrations, used in treatment of asthma without having effects on heart

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10
Q

Phenylephrine

A

Direct acting alpha 1 agonist
causes peripheral vasoconstriction

indications/effects
Vasoconstrictor: ↑ SBP and DBP
Nasal decongestant 
Mydriasis
Tx of supraventricular tachycardia

oral or topical.
NO direct effect on heart, but does cause reflex bradycardia after parenteral administration

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11
Q

Clonidine

A

alpha2 direct acting partial agonist. activation of CENTRAL ALPHA 2 RECEPTORS which suppresses sympathetic outflow

antihypertensive

Acute rise in BP due to transient vasoconstriction when given IV, but not when given orally

Adverse/Contra: Centrally acting antiadrenergic drugs:Sedation, mental lassitude, impaired concentration

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12
Q

Methyldopa

A

direct acting alpha 2 agonist

Indications/effects
Metabolized to α-methylnorepinephrine which causes effects similar to clonidine: ↓ TPR and BP… prodrug
DOC in pregnant patients with HTN [safety]

adverse/contra:Centrally acting antiadrenergic drugs:Sedation, mental lassitude, impaired concentration

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13
Q

Brimonidine

A

direct acting alpha 2 agonist

↓ aqueous humor production along with increased outflow
↓ intraocular pressure in glaucoma

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14
Q

Amphetamine

A

Indirect acting adrenergic agonist

Displaces catechol from storage vesicle
Weak inhibitor of MAO
Blocks catechol reuptake

↑ BP through α1 and β effects
Central stimulatory action: alertness, ↓ fatigue & appetite, insomnia,
Tx of depression, narcolepsy and appetite suppression [in the past]

adverse/contra:Fatigue and depression following stimulation

Releasing Agents
Potentiate actions of endogenous NE by causing release from presynaptic vesicles

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15
Q

Methylphenidate

A

indirect acting adrenergic agonist,
structural analog of amphetamine,
used in treatment of ADHD in children

Releasing Agents
Potentiate actions of endogenous NE by causing release from presynaptic vesicles

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16
Q

Tyramine

A

Not clinically useful, but is found in fermented foods [cheese and wine]
Byproduct of tyrosine metabolism, normally oxidized by MAO

Serious vasopressor episodes in patients on MAO-I’s after release of NE

Releasing Agents
Potentiate actions of endogenous NE by causing release from presynaptic vesicles

17
Q

Cocaine

A

Drug acting presynaptically on DAT, SERT, NET receptor

Blocks dopamine [major effect], serotonin and NE transporters → potentiation and prolonged effects

Sympathomimetic
Therapeutic use: blockage of voltage gated Na+ channels → local anesthetic

Intense euphoria from blockage of dopamine reuptake in the limbic system

Monoamine reuptake inhibitors

18
Q

Atomoxetine

A

Drug acting presynaptically on NET receptor

Selective NET inhibitor
Tx of ADHD

Monoamine reuptake inhibitors

19
Q

Ephedrine

A

alpha and beta mixed acting agonist

INDICATIONS EFFECTS:
Vasoconstriction and cardiac stimulation → ↑ BP
Bronchodilation [prophylactic Tx of asthma because it is slower onset and less potent than epi or isoproterenol]
Synergistic effect with Anti-AChE in treatment of myasthenia gravis
Mild CNS stimulation [alertness] and increased athletic performance

PK:
NOT a catecholamine → poor substrate for COMT and MAO → longer duration of action
Excellent oral absorption, enters CNS

Eliminated unchanged in urine

ADVERSE/CONTRA: herbal supp, banned due to life threatening CV reactions

Induces release of NE and activates adrenergic receptors

Use declining due to better drugs with fewer side effects

20
Q

Pseudoephedrine

A

alpha and beta mixed acting agonist

Nasal decongestant with an H1 histamine antagonist

21
Q

alpha 1 antagonists

A

Primary effect on blood pressure: vasculature is under tonic sympathetic control so blockade of these receptors reduces tone and decreases TPR

Epinephrine Reversal: all α-blockers inhibit Epi induced vasoconstriction, but not the β effect of vasodilation → ↓ BP in response to Epi in the presence of phenoxybenzamine [NE is only diminished]

Selective α1 blockers can cause dizziness, lack of energy, nasal decongestant, HA, drowsiness, orthostatic hypotension; tendency to retain Na+ and fluid → give with a diuretic

22
Q

phenoxybenzamine

A

Nonselective α

Alkylation irreversibly blocks receptor

Slightly α1 selective
Also blocks H1, M and 5-HT receptors; inhibits NET

EFFECTS:
-CVS: prevents vasoconstriction of peripheral blood vessels →
reflex tachycardia
-Presynaptic α2 block → ↑ CO

INDICATIONS

  • Pheochromocytoma [DOC]: blocks effects of excess catecholamines [may require a β blocker to control tachycardia after α blockade is established]
  • Historically used to lower BP, but was unsuccessful [block presynaptic α2]
ADVERSE:
Postural hypotension
Nasal stuffiness
Nausea and vomiting
Inhibit ejaculation

CONTRA-in pt’s with decreased coronary perfusion due to reflex tachycardia

23
Q

Phentolamine

A

Nonselective α

Reversible α blocker
Serotonin blocker
Muscarinic, H1 and H2 agonist

INDICATIONS:

  • Dx & control hypertensive episodes of pheochromocytoma
  • Prevents dermal necrosis when NE extravasates
  • Antihypertensive in stimulant OD, sudden withdrawal of sympatholytics [clonidine], interaction between MAO-Is and tyramine

ADVERSE
Postural hypotension –baroreceptor reflex and α2 blockade on cardiac nerves
Arrhythmia & angina

CONTRAINDICATED in pt’s with decreased coronary perfusion

24
Q

Prazosin

A

Selective α1 -
Useful in treatment of HTN

↓ TPR through relaxation of arterial and venous smooth muscle

EFFECTS:
↓ BP without reflex tachycardia […α2]
↓ LDL/TAG, ↑ HDL
I-mproves urinary blood flow

INDICATIONS:

  • Suppress sympathetic outflow from CNS
  • Tx of HTN, BPH

ADVERSE

  • Not the DOC for primary HTN
  • First dose effect may cause exaggerated hypotensive response and syncope [adjust 1st dose ¼ of normal]
25
Q

Terazosin/doxazosin

A

Selective α1 -
Useful in treatment of HTN

Structural analog of prazosin → longer t1/2 → Less frequent dosing
the rest is the same as prozosin

26
Q

Tamsulosin

A

Selective α1 -
Useful in treatment of HTN

ADVERSE

  • Not the DOC for primary HTN
  • First dose effect may cause exaggerated hypotensive response and syncope [adjust 1st dose ¼ of normal]
27
Q

Yohimbine

A

α2 blocker → indirect adrenergic agonist

Effects;↑ NE release → ↑ BP

Tx of erectile dysfunction, but has been replaced by PDE-5 inhibitors

Can reverse effects of α2 agonists i.e. clonidine [bad]

28
Q

Propranolol

[prototype]

A

β1 & 2 antagonist

MECHANISM:
-CVS: ↓ HR and contractility
↑ TPR [β2]
-Metabolic: ↓ glycogenolysis and glucagon secretion → severe hypoglycemia in pt’s on insulin

Effects/INDICATIONS

  • Used in treatment of:HTN [through ↓ CO, not the DOC]
  • Migraine [blocks vasodilation]
  • Hyperthyroidism
  • Chronic angina [↓ O2 requirement]
  • A-fib, MI [protective]
  • Performance anxiety/stage fright [DOC]
  • Essential tremor

ADVERSE/CONTRA
-Bronchoconstriction →
Contraindicated in patients with COPD or asthma; variant angina
-Impair recovery from hypoglycemia in insulin dependent patients → syncope
Mask signs i.e. tachycardia seen in such episodes
-CNS: sedation, dizziness, lethargy, fatigue, depression

Does not induce postural hypotension because α1 receptors remain active

Reduce HDL and increase LDL and TAGs [block activation of HSL] – β1 selective actually improve the lipid profile

Abrupt withdrawal → HTN

29
Q

Nadalol

A

Beta 1 and 2 blocker

longer duration of action, used in long term treatmetn of angina and HTN

30
Q

TImool

A

used in HTN, prophylaxis for migraine’s glaucoma(open angle)

31
Q

Atenolol/metroprolol

A

beta1 cardioselectiveblocker

Management of HTN in pt’s with impaired pulmonary function or IDDM

Less likely to induce bronchospasm

Long term management of angina; s/p MI reduces mortality

32
Q

Esmolol

A

Beta1 cardioselective blocker

indications/effects:
Useful in controlling arrhythmia [supraventricular or thyrotoxicosis], perioperative HTN, and MI in acutely ill pt’s

Safer in critically ill patients

PK: Ultra short acting: t1/2 is about 10 minutes
Administered IV

33
Q

Labetalol

A

Combined α-1 and β-antagonists

Mechanism:/Effects/indications
Decrease in BP:
α1 → relaxation of arterial smooth muscle
β1 → blocks sympathetic reflex
β2 → sympathomimetic action contributes to vasodilation

PK:
More potent β antagonist
Oral: chronic HTN
IV: emergencies

Adverse Effects:
Orthostatic hypotension and dizziness [α1]

34
Q

Carvedilol

A

Combined α-1 and β-antagonists

Used on pt’s with CHF and HTN
More potent β antagonist
Antioxidant properties

35
Q

Pindolol

A

β partial agonist- beta blocker with intrinsiic sympathomimetic activity helps manage HTN

Causes a smaller reduction in resting HR and BP
Preferred in pt’s with diminished cardiac reserve or propensity to bradycardia

36
Q

α-methyltyrosine

aka: metyrosine

A

Mechanism:Blocks NE [& E] synthesis through competitive inhibition of tyrosine hydroxylase

Indications/Effects:

Used in adjuvant therapy with phenoxybenzamine in treatment of malignant pheochromocytoma [when surgery is not possible]

37
Q

Reserpine:obsolete

A

Irreversible damage to VMAT → ↓ NE and dopamine availability → sympatholytic response

Unable to concentrate and store NE and dopamine in the vesicle → continuous breakdown by MAO
↓ BP and HR

Historical Tx of HTN
PK: Slow onset and long duration

38
Q

Guanethidine

A

Uptake into nerve terminal via NET → storage in vesicle and displacement of NE → NE depletion

Anti-hypertensive that was used in the early 1970’s

Orthostatic HTN and male sexual dysfunction

Also disrupts the release of NE from the nerve terminal

39
Q

Autocoids

A

 Autocoids have diverse physiologic and pharmacologic activities; site of action is near their synthesis and their lifetime is brief
 Formed by decarboxylation of L-histidine
 Most found in mast cells and basophils; also in ECL cells in the fundus of the stomach → activates parietal cells
 Found in the brain as a neurotransmitter

HIstamine agonists

Pharmacology (6 decks)

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