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Neuro II Exam 2 > Adrenergic Drugs > Flashcards

Adrenergic Drugs Flashcards

1
Q

What do adrenergic drugs do?

A

Modulate adrenergic transmission and primarily control function of sympathetic nervous system

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2
Q

Contrast adrenomimetics vs sympatholytics

A
  • Adrenomimetics/sympathomimetics/drugs activating adrenergic transmission: mimic or promote effects of norepinephrin/epinephrine/dopamine at adrenergic receptors in sympathetic NS
  • Sympatholytics/antiadrenergic/drugs inhibiting adrenergic transmission: prevent effects of norepinephrine/epinephrine/dopamine at adrenergic receptors in sympathetic NS
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3
Q

Describe types of adrenergic receptors

A 
Alpha1: Gq: Increase IP3, DAG
Alpha2: Gi: decrease cAMP
Beta: Gs: increase cAMP
D1 and D5: Gs: Increase cAMP
D2-4: Gi: decrease cAMP
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4
Q

Describe alpha1 receptor activation, tissue, and actions

A

IP3 leads to increase in cytosolic Ca2+.
DAG activates PKC

Most vascular smooth muscle = contraction
Pupillary dilator muslce = contraction (dilates)
Pilomotor smooth muscle = erects hair
Prostate = contraction
Heart = increases force of contraction

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5
Q

Describe alpha2 receptor activation, tissue, and actions

A

Decrease in cAMP and inhibition of PKA

Postsynaptic CNS neurons = multiple actions
Platelets = aggregation
Adrenergic and cholinergic nerve terminals = inhibits transmitter release
Some vascular smooth muscle = contraction
Fat cells = inhibits lipolysis

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6
Q

Beta receptor activation?

A

Accumulation of cAMP

Activation of PKA

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7
Q

Beta1 tissue and actions

A

Heart, juxtaglomerular cells = increases force and rate of contraction. Increases renin release

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8
Q

Beta2 tissue and actions

A

Respiratory, uterine, vascular smooth muscle = relaxation
Skeletal muscle = promote potassium uptake
Liver = activates glycogenolysis

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9
Q

Beta3 tissue and actions

A

Bladder = relaxes detrusor muscle

Fat cells = activates glycogenolysis

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10
Q

D1 and D2 tissue and actions

A 
D1 = smooth muscle = dilates renal blood vessels
D2 = nerve endings = modulates transmitter release
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11
Q

Compare direct-acting adrenergic drugs with indirect-acting

A

Direct-acting: interaction with adrenergic receptors: agonists and antagonists

Indirect-acting: increase or reduce concentration of NE at target receptors

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12
Q

List alpha agonist drugs and receptor affinities

A

Phenylephrine, methoxamine: a1>a2»>B

Clonidine: a2>a1»>B

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13
Q

List mixed alpha and beta agonists and receptor affinities

A

Norepinephrine: a1=a2; B1»B2
Epinephrine: a1=a2; B1 = B2

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14
Q

List beta agonists and receptor affinities

A

Dobutamine: b1>b2»>a
Isoproterenol: b1 = b2»>a
Albuterol, terbutaline: b2»b1»>a

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15
Q

List dopamine agonists and receptor affinities

A

Dopamine: D1 = D2»b»a
Fenoldopam: D1»D2

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16
Q

Describe epinephrine effects on cardiac function

A

Beta1
Increases force of contraction: positive inotropic effect
Increases heart rate
Increases conduction velocity at AV node

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17
Q

Epinephrine effects on vascular tone

A

Beta2 and alpha1
Increases systolic BP
May decrease diastolic BP and total peripheral vascular resistance
Mean arterial pressure often remains unchanged
Significant differences in receptor types found in vascular beds
-skin vessels and mucous membranes: mostly alpha1
-skeletal muscle: alpha1 and beta2
-renal, cerebral: D1 and alpha1

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18
Q

Epinephrine effects on respiratory system

A

Relaxes bronchial muscle: beta2

Decreases bronchial secretion and congestion within bronchial mucosa: alpha1

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19
Q

Epinephrine effects on skeletal muscle, blood glucose, free fatty acids, renin

A

Skeletal muscle
causes muscle tremor: b2
Increases K+ uptake by skeletal muscle: b2
-promotes hypokalemia and decreases K+ excretion by kidneys

Elevates blood glucose levels

  • enhances liver glycogenolysis: b2
  • inhibits insulin release: a2

Increases free fatty acid levels in blood: beta
Increases renin release: b1

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20
Q

Describe norepinephrine effects

A

A1=a2; B1»B2
Potent cardiac stimulant but reduces heart rate
Potent vasoconstrictor
Lacks B2 agonist effects: no bronchodilation and vasodilation
Increases peripheral vascular resistance and blood pressure
Role of baroreflex

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21
Q

Describe effects of dopamine

A

D1=D2»B1»a1

D1 stimulation causes vasodilation
-high density of D1 receptors in renal, cerebral, mesenteric and coronary vessels

Activation of presynaptic D2: suppresses norepinephrine release

Activates B1 in heart at higher doses

At still higher doses stimulates vascular alpha1 AR to cause vasoconstriction

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22
Q

Effects of phenylephrine

A

Alpha agonist. a1>a2»>B
Not a catecholamine, not inactivated by COMT
-longer duration of action
Effective mydriatic and decongestant
Causes severe vasoconstriction and blood pressure elevation
Role of baroreflex in response to phenylephrine

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23
Q

Effects of Clonidine

A

Selective alpha2 agonist. a2>a1»»b
Central effect on alpha2 receptors in lower brainstem area
-decreasing sympathetic outflow
-reduction in blood pressure
-bradycardia (reduces peripheral vascular resistance, decrease heart rate and cardiac output)

Local application produces vasoconstriction

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24
Q

Effects of isoproterenol

A

B1=B2»>A
Nonselective beta agonist
Positive inotropic and chronotropic action, increases cardiac output: B1
Vasodilator, decreases arterial pressure: B2
Causes bronchodilation: B2

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25
Q

Effects of dobutamine

A

B1>B2, a1
Selective B1 agonist
A1 receptor activity (-)isomer agonist at these receptors, while +isomer is a1 antagonist
Potent inotropic action
Less prominent chronotropic action as compared to isoproterenol

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26
Q

Effects of terbutaline, albuterol

A

B2>B1»>a
Selective B2 agonists
Cause bronchodilation and relaxation of uterus

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27
Q

Describe indirect adrenergic agonists

A

Usually more lipophilic compounds (not catecholamines)

Easily penetrate BBB: have significant central effects: CNS system stimulants

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28
Q

Effects of amphetamine, methamphetamine, methylphenidate

A

Mild alerting effects

Improved attention

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29
Q

Effects of cocaine

A

Inhibits transmitter reuptake at adrenergic synapses
Peripheral and intense central adrenomimetic action
Local anesthetic properties

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30
Q

Effects of ephedrine

A

Releases stored catecholamines with some direct adrenomimetic action
Plant constituent
Non-catechol
-long duration of action
-effective after oral administration
Nonselective: similar to epinephrine in actions
Mild stimulant enter CNS

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31
Q

Effects of tyramine

A

Accumulates in protein-rich foods during fermentation
Readily metabolized by MAO in liver (very high first-pass effect)
If administered parenterally, affords indirect sympathomimetic action caused by release of stored catecholamines (norepinephrine-like effect)

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32
Q

Use of adrenergic agonists on CV conditions to increase blood pressure

A

Hypotensive emergencies: hemorrhagic shock, overdose of antihypertensives, CNS depressants
-Norepinephrine, phenylephrine, methoxamine

Chronic hypotension: ephedrine

Cardiogenic shock (due to massive acute MI): dopamine, dobutamine

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33
Q

Use of adrenergic agonists on CV conditions: heart failure

A

Short-term use of dobutamine in acute HF

Dopamine in congestive severe HF with reduced renal perfusion

34
Q

Use of adrenergic agonists on CV conditions: hypertension

A

Alpha-2 agonists for long-term treatment

Fenoldopam in hypertensive emergencies

35
Q

Use of adrenergic agonists on CV conditions: emergency therapy for complete AV block and cardiac arrest

A

Epinephrine, isoproterenol

36
Q

Use of adrenergic agonists on CV conditions: decongestion of mucous membranes

A

Phenylephrine, ephedrine, pseudoephedrine

37
Q

Use of adrenergic agonists for bronchial asthma

A

Beta-2 selective agonists:

Albuterol, terbutaline

38
Q

Use of adrenergic agonists for anaphylaxis (immediate type 1 allergic reaction characterized by respiratory and CV components)

A

Respiratory component: bronchospasm and upper airway congestion
CV component: severe hypotension, cardiac depression
Ephinephrine: effective at both components

39
Q

Use of adrenergic agonist for ophthalmic applications

A

Exam of retina: induction of mydriasis: phenylephrine

Glaucoma: alpha-2 selective agonists: apraclonidine, brimonidine

40
Q

Use of adrenergic agonist for GU applications

A

Suppression of premature labor: beta-2 agonists: terbutaline
Stress urinary incontinence: ephedrine
Priapism: alpha-1 agonists (phenylephrine) via injection into penis

41
Q

Use of adrenergic agonist on CNS conditions

A

Narcolepsy (sudden brief sleep attacks): amphetamines, methylphenidate

ADHD (short attention span, learning problems, and hyperkinetic physical behavior): methylphenidate

Obesity (central inhibition of appetite and increased energy expenditure): phentermine, ephedrine, amphetamines

42
Q

Cardiovascular adverse effects of adrenergic agonists

A

Elevation in blood pressure
Increased cardiac work may precipitate myocardial ischemia and heart failure: special attention given to elderly pts and pts with hypertension, coronary artery disease, and chronic heart failure
Sinus tachycardia and serious ventricular arrhythmias
Direct myocardial damage leading to cardiomyopathy
May induce sudden cardiac death

43
Q

Central nervous system toxicity of adrenergic agonists

A

Most of agonist drugs (catecholamines and other polar drugs that do not cross BBB) do not cause CNS toxicity

Amphetamine and amphetamine-like compounds cause: insomnia, lack of appetite, anxiety, restlessness, psychoses (paranoid state, hallucinations)

Cocaine may cause: convulsions, arrhythmias, hemorrhagic stroke

44
Q

Direct vs indirect adrenomimetic drugs at synapse

A

Monoamine oxidase (MAO) inhibitors: Selegiline, phenelzine (indirect)
Reuptake blockers: Cocaine (indirect)
Releasing agents: amphetamines, methylphenidate (indirect)
Mixed acting: ephedrine (direct and indirect)
Adrenergic receptor agonists (direct)

45
Q

Describe common sites of action for antiadrenergic drugs (direct vs indirect)

A

Inhibits NE synthesis: metyrosine (indirect)
Deplete NE: guanethidine (indirect)
Adrenergic receptor antagonists (direct)

46
Q

What are the nonselective alpha receptor antagonists?

A

Phentolamine

Phenoxybenzamine

47
Q

What are the alpha1 receptor selective antagonists?

A 
All end in -osin
Prazosin
Terazosin
Tamsulosin
Doxazosin
Alfuzosin
Silodosin
48
Q

Compare competitive alpha antagonist with irreversible alpha antagonist

A 
Competitive alpha antagonist:
Noncovalent binding to receptor
Shorter acting
Effect antagonized by high concentration of agonist
Ex: phentolamine
Irreversible alpha antagonist:
Covalent binding to a receptor
Longer acting
Effect is not antagonized by alpha agonist
Ex: phenoxybenzamine
49
Q

Alpha antagonist effects on CV system

A

Decreased peripheral vascular resistance and blood pressure
Reflex tachycardia
Postural hypotension

50
Q

Alpha antagonist effects on GU system

A

Relaxation of smooth muscle in prostate

Decreased resistance to flow of urine

51
Q

Alpha antagonist effects on

A

Relaxation of pupillary dilator muscle (miosis)

52
Q

Alpha antagonist effects on pheochromocytoma

A

Tumor of adrenal medulla producing catecholamines
Excess causes tachycardia, arrhythmias, hypertension
Treatment: phentolamine, phenoxybenzamine

53
Q

Alpha antagonist effects on chronic hypertension

A

Prazosin, terazosin, doxazosin: alpha1 selective
Work well in moderate hypertension
Generally well tolerated
Nonselective alpha-blockers not used

54
Q

Alpha antagonist effects on erectile dysfunction

A

Combination of phentolamine and nonspecific vasodilator papaverine (injected into penis)

55
Q

Alpha antagonist effects on benign prostate hyperplasia (BPH) to treat chronic urinary obstruction

A

Tamsulosin
Silodosin
-greater selectivity for alpha1a than alpha1b
-alpha1a most important alpha subtype mediating prostate smooth muscle contraction
-effectively relieves urinary obstruction and pain with little effect on blood pressure
Prazosin, doxazosin, terazosin also effective

56
Q

Adverse effects of alpha antagonists

A

Most significant effects are on CVS
Seen less with alpha1 selective antagonists
Postural hypotension: antagonism of alpha1 in venous smooth muscle
Tachycardia
Retention of fluid and salt
Impaired ejaculation
Nasal stuffiness

57
Q

What are the mixed antagonists?

A

Labetalol (beta and alpha1 antagonist)

Carvedilol (beta and alpha1 antagonist)

58
Q

What are the beta1 and beta2 antagonists?

A

Propranolol
Pindolol
Nadolol
Penbutolol

59
Q

What are the beta1 selective antagonists?

A

Metoprolol
Betaxolol
Acebutolol
Atenolol

60
Q

Which beta-blockers are antagonists, partial agonists, inverse agonists?

A

Antagonists: atenolol, nadolol, propranolol, betaxolol
Partial agonists: acebutolol, labetalol, penbutolol, pindolol
Inverse agonists: carvedilol, metoprolol

61
Q

Effects of beta-blockers on CV system

A 
Heart
Negative inotropic effect
Negative chronotropic effect
Block AV node
-slowed atrioventricular conduction
-increased PR interval

Blood vessels
Initially: rise in peripheral vascular resistance
Chronic use: decrease in PVR (lowers blood pressure in hypertensive individuals)

RAS
Inhibit renin release

62
Q

Effects of beta-blockers on respiratory system

A

Increase in airway resistance

63
Q

Effects of beta-blockers on eye

A

Reduce production of aqueous humor: reduce intraocular pressure

64
Q

Effects of beta-blockers on metabolic effects

A

Inhibit lypolysis
Increase VLDL and decrease HDL, reduce HDL cholesterol/LDL cholesterol ratio
Inhibit glycogenolysis in the liver

65
Q

Effects of beta-blockers on hypertension

A

Antihypertensive effect is delayed

Both beta-blockers and mixed alpha and beta blockers (Labetaolol, alpha1 and beta blocker) are used

66
Q

Effects of beta-blockers on angina pectoris

A

Blocking cardiac beta-receptors decreases cardiac work and reduces oxygen consumption
Beta-blockers reduce the frequency of anginal episodes and improve exercise tolerance

67
Q

Effects of beta-blockers on myocardial infarction

A

Long-term use in postinfarction period: prolong surivival
Timolol, propranolol, metoprolol

Acute phase of myocardial infarction
Contraindications: bradycardia, hypotension, acute heart failure, AV block, active airway disease

68
Q

Effects of beta-blockers on cardiac arrhythmias

A

Effective in ventricular and supraventricular arrhythmias

  • atrial flutter and atrial fibrillation
  • ventricular ectopic beats
69
Q

Effects of beta-blockers on heart failure

A

Effective for treatment of chronic heart failure in selected pts
Metoprolol, bisoprolol, carvedilol
Contraindicated in acute congestive heart failure

70
Q

Effects of beta-blockers on glaucoma

A

Mech involves reduction in production of aqueous humor by ciliary body
Timolol, betaxolol: blockers w/o local anesthetic activity (propranolol not used)

71
Q

Effects of beta-blockers on hyperthyroidism

A

Important aspect: excessive catecholamine action on heart
Thyroid storm: severe form of hyperthyroidism
Tachycardia, supraventricular and ventricular ectopic arrhythmias
Propranolol

72
Q

Adverse effects of beta-blockers on CNS

A

(Switch to more hydrophilic drug)
Sedation
Sleep disturbances
Depression

73
Q

Adverse effects of beta-blockers on respiratory system

A

(Switch to beta-1 selective)
Increase airway resistance
Trigger bronchospasm and asthma attack in susceptible indivduals (chronic asthma, COPD, chronic bronchitis)

74
Q

Adverse effects of beta-blockers on CV system

A

Depression of heart rate, cardiac contractility and excitability (switch to partial agonist)
Exacerbation of peripheral vascular disease (switch to beta1 selective)

75
Q

Adverse effects of beta-blockers on lipid profile

A

(Switch to a partial agonist drug)
Chronic use: increase VLDL and decrease HDL (LDL usually not changed, but ratio HDL/LDL cholesterol decreases)

Seen with both selective and non-selective B-blockers

76
Q

Adverse effects of beta-blockers on hypoglycemic episodes

A

(Switch to beta1-selective)
May delay recovery form insulin-induced hypoglycemia by inhibiting glucose output by liver
Blunt perception of hypoglycemia by these pts (tremor, tachycardia, and nervousness are caused by B-AR activation)
Increased incidence and severity of hypoglycemic episodes in pts with diabetes type 1 on insulin
Much safer in diabetes type 2 pts who usually do not have hypoglycemic reactions

77
Q

Adverse effects of beta-blockers on abrupt discontinuation of beta-blocker therapy

A

Increased risk in pts with ischemic heart disease

Gradually taper beta blocker dosing to prevent sympathetic hyper-responsiveness and potential toxicity

78
Q

What is the norepinephrine release inhibitor?

A

Guanethidine
Taken up by reuptake mech
Replace norepinephrine in vesciles
Causes a gradual depletion of norepinephrine stores
Inhibition of norepinephrine release via local anesthetic properties

79
Q

What is the inhibitor of tyrosine hydroxylase

A

Metyrosine

80
Q

Clinical use of indirect acting antiadrenergic drugs

A

Chronic hypertension: guanethidine

Pheochromocytoma: metyrosine

Neuro II Exam 2 (6 decks)

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