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CPR II Pharm > Adrenergic Drugs > Flashcards

Adrenergic Drugs Flashcards

1
Q

Direct-acting Adrenomimetic Classes

A
  • Alpha agonists
  • Mixed alpha and beta agonists
  • Beta agonists
  • Dopamine agonists
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2
Q

Alpha agonists

A
  • Phenylephine

- Clonidine

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3
Q

Mixed alpha and beta agonists

A
  • NE

- Epi

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4
Q

Beta agonists

A
  • Dobutamine
  • Isopreterenol
  • Albuterol
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5
Q

Dopamine agonists

A
  • Dopamine
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6
Q

Indirect adrenominetics classes

A
  • inhibitors of MAO
  • inhibitors of reuptake of DA and NE
  • Reverse NE and DA uptake mechanisms and increase their release
  • Releasing agent and direct adrenergic receptor agonist
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7
Q

Inhibitor of re-uptake of DA and NE

A
  • Cocaine
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8
Q

Inhibitors of MAO

A
  • Phenelzine

- Selegiline

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9
Q

Reverse NE and DA uptake mechanisms

A
  • Amphetamines
  • Methylphrnidate
  • Tyramine (byproduct of tyrosine metabolism, not a drug)
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10
Q

Releasing agent and a direct adrenergic receptor agonist

A
  • Ephedrine
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11
Q

Direct acting antiandrenergic drug classes

A
  • alpha adrenergic antagonists
  • mixed blockers
  • beta adrenergic antagonists
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12
Q

Non-selective receptor antagonists

A
  • Phentolamine (reversible, competitive)

- Phenoxybenzamine (non-competitive, irreversible)

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13
Q

Alpha 1 selective antagonists

A
  • Prazosin
  • Tamsulosin
  • Doxazosin
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14
Q

Mixed antagonists (blockers)

A
  • Labetalol
  • Carvedilol
  • both are alpha and beta 1 antogonists
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15
Q

Beta 1 and Beta 2 blockers (nonselective)

A
  • Propranolol
  • Pindolol
  • Nadolol
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16
Q

B1 selective blockers

A
  • Metoprolol
  • Betaxolol
  • Acebutolol
  • Atenolol
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17
Q

Indirect acting antiandrenergic drug groups

A
  • NE release inhibitor

- inhibitor of tyrosine hydroxylase

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18
Q

NE release inhibitor

A
  • Guanethudine (indirect)
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19
Q

Inhibitor of tyrosine hydroxylase

A

Metyrosine (indirect)

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20
Q

Alpha 1 G protein and effects

A

Gq - Increase IP3 and DAG

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21
Q

Alpha 2 G protein and effects

A

Gi - decrease cAMP

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22
Q

Beta type G protein and effects

A

Gs - increase cAMP

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23
Q

Dopamine type G proteins

A
  • D1 and D5 - Gs - increase cAMP

- D2 - D4 - Gi - decrease cAMP

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24
Q

Epinephrine

A
  • a1 = a2; B1 = B2
  • Effects on cardiac function (B1)
  • – increase HR
  • – Increase force of contraction
  • – increase conduction velocity at AV node
  • Effects on vascular tone (B2 and a1)
  • – increases systolic BP
  • – may decrease diastolic BP and TPVR
  • Effects on respiratory system
  • – relaxed bronchial muscle (b2)
  • – decreased bronchial secretion and congestion within bronchial mucosa (a1)
  • Skeletal muscle
  • – muscle tremor (B2)
  • – increase K uptake by skeletal muscle (B2)
  • elevates blood glucose levels
  • – enhances liver gluconeogenesis and glycogenolysis (B2)
  • increases free fatty levels in blood (B)
  • increases renin release (B1)
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25
Q

Norepinephrine

A
  • a1 = a2; B1&raquo_space; B2
  • cardiac stimulant but reduces HR
  • pontent vasoconstrictor
  • Lacks B2 agonist effects
  • Increases PVR and BP
  • Role of baroreflex
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26
Q

Phenylephrine

A
  • alpha agonist; a1
  • effective mydriatic and decongestant
  • severe vasoconstriction, BP elevation and severe bradycardia
  • role of baroreflex in the response to phenylephrine
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27
Q

Clonidine

A
  • selective a2 agonist
  • central effect on a2 receptors in lower brainstem area
  • – decreasing sympathetoc outflow
  • – reduction in BP
  • – bradycardia
  • local application produces vasoconstriction
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28
Q

Isoproterenol

A
  • B agonist; B1 = B2
  • nonselective
  • positive inotropic and chronotropic action, increases CO (B1)
  • vasodilator, decreases arterial pressure (B2)
  • causes bronchodilation (B2)
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29
Q

Dobutamine

A
  • Beta agonist; B1 > B2, a1
  • selective B1 agonist
  • (-) isomer is agonist; (+) isomer is antagonist (of a1)
  • potent inotropic action
  • less prominent chronotropic action compared to isoproterenol
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30
Q

Albuterol

A
  • selective B2 agonist

- cause bronchodilation and relaxation of the uterus

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31
Q

Dopamine

A
  • D1 = D2
  • D1 stimulation causes vasodilation
  • activation of presynaptic D2 suppresses NE release
  • activate B1 in heart at higher doses
  • at even higher doses, stimulates vascular a1 AR to cause vasoconstriction
32
Q

Indirect adrenergic agonist properties

A
  • usually more lipophilic compounds

- easily penetrate BBB

33
Q

Amphetamine , methamphetamine

A
  • marked stimulant effect on mood and alertness
  • decrease appetite
  • drugs of abuse
34
Q

Methylphenidate

A
  • used in children with ADHD

- has abuse potential

35
Q

Cocaine

A
  • inhibits transmitter reuptake at adrenergic synapses
  • peripheral and intense central action
  • local anesthetic properties
  • heavily abused drug
36
Q

Ephedrine

A
  • releases stored catecholamines w/ some direct action
  • long duration of action
  • nonselecive
  • mild stimulant
  • clinical use
  • – nasal decongestant
  • – increases BP
  • – stress incontinence in women
37
Q

Phenelzine, Selegiline

A
  • inhibitors of MAO
  • increase NE stores in CNS
  • antidepressant action
38
Q

Tyramine

A
  • product of tyrosine metabolism found in cheese, cured meats, smoked and pickled fish
  • releases stored NE from presynaptic terminals (if given parenterally)
  • is metabolized by MAO in live
  • may lead to increase in BP in patients taking MAO inhibitors
39
Q

Which adrenergic agonist used to increase BP

A
  • hypotensive emergencies
  • – NE
  • – Phenylephrine
  • Chronic hypertension
  • – ephedrine
  • cardiogenic shock
  • – dopamine
  • – dobutamine
40
Q

Heart Failure

A
  • short term use of dobutamine in acute HF

- dopamine in congestive severe HF w/ reduced renal perfusion

41
Q

Hypertension drug

A

Alpha 2 agonists for long term treatment

42
Q

Emergency therapy for complete AV block and cardiac arrest

A
  • Epi

- Isoproterenol

43
Q

Narcolepsy Drugs

A
  • amphetamines

- methyphenidate

44
Q

ADHD drug

A
  • methylphenidate
45
Q

Obesity drug

A
  • ephedrine

- amphetamines

46
Q

Decongestion of mucous membranes

A
  • phenyephrine

- ephedrine

47
Q

Examination of retina (mydriasis)

A
  • phenylephrine
48
Q

Glaucoma

A
  • alpha-2 selective agonists
49
Q

GU applications

A
  • ephedrine for urinary incontinence
50
Q

CV adverse effects of adrenergic agonists

A
  • elevation of BP
  • Increased cardiac work may precipitate myocardial ischemia and heart failure
  • sinus tachycardia and serious ventricular arrhythmias, may induce sudden cardiac death
51
Q

Central nervous system toxicity

A
  • insomnia
  • lack of appetite
  • anxiety, restlessness
  • psychoses
  • convulsions and hemorrhagic stroke (cocaine)
52
Q

Effects of Alpha antagonists on CV system

A
  • decreased PVR and BP
  • postural hypotension
  • reflex tachycardia
53
Q

Effects of Alpha antagonists on GU system

A
  • relaxation of sm muscle in prostate

- decreased resistance to the flow of urine

54
Q

Effects of Alpha antagonists on the eye

A
  • relaxation of pupillary dilator muscle - miosis
55
Q

Pheochromocytoma treatment

A
  • antag
  • phentolamine
  • phenoxybenzamine
56
Q

Chronic (essential) hypertension treatment

A
  • antag
  • Prozosin, Doxasin (a1 selective)
  • – work well in moderate hypertension
  • – generally well tolerated
57
Q

Erectile dysfunction treatment

A
  • combination of phentolamine and papaverine
58
Q

BPH treatment

A
  • Tamsulosin
  • – greater affinity for a1A
  • Prozosin and doxazosim are also effective but will cause more pronounced drop in BP
59
Q

Adverse Effects of alpha antagonists

A
  • seen less with a1 selective
  • postural hypotension
  • tachycardia
  • retention of fluid and salt
  • impaired ejaculation
  • nasal stiffness
60
Q

B blocker antagonists

A
  • Atenolol
  • Nadolol
  • Propranolol
  • Betaxolol
61
Q

B blocker partial agonists

A
  • acebutolol
  • Lebetalol
  • Pindolol
62
Q

B blocker inverse agonists

A
  • Carvedilol

- Metoprolol

63
Q

Full agonists

A
  • fully activate receptors
  • produce maximal pharmacological effect when all receptors occupied
  • maximal intrinsic activity
64
Q

Partial agonists

A
  • partially activate upon binding
  • produce sub-maximal effect
  • intrinsic efficacy varies depending on drug
65
Q

Inverse agonists

A
  • decrease receptor signaling
  • decrease response at receptors with significant level of constitutive receptor activity
  • intrinsic activity present and related to inhibition of receptor function
66
Q

Antagonists

A
  • do not activate the receptor upon binding
  • no effect is agonist is not present
  • no intrinsic activity
67
Q

Effects of B-blocker on CV

A 
Heart 
- negative inotropic and chronotropic effect
- slow AV node conduction 
Blood vessels 
- initially - rise in PVR
- chronic - decrease in PVR
RAS
- inhibit renin release
68
Q

Effects of B-blocker on respiratory system

A
  • increase airway resistance
69
Q

Effects of B-blocker on Eye

A
  • reduce production of aqueous humor - reduce intracular pressure
70
Q

Metabolic Effects of B-blocker

A
  • inhibit lipolysis
  • increase VLDL and decrease HDL
  • inhibit glycogenolysis and glugoneogenesis in the liver
71
Q

Clinical uses of Beta blockers

A
  • hypertension (both b and mixed blockers)
  • angina pectoris
  • MI
  • cardiac arrhythmias
  • heart failure
  • glaucoma
  • hyperthyroidism (propranolol)
72
Q

CNS B-blocker adverse effects

A
  • sedation
  • sleep disturbances
  • depression
  • switch to more hydrophilic drug
73
Q

Respiratory B-blocker adverse effects

A
  • increased airway resistance
  • trigger bronchospasm and asthma attack in susceptible people
  • switch to B1 selective
74
Q

CV B-blocker adverse effects

A
  • depression of HR, cardiac contractibility and excitability

- exacerbation of peripheral vascular disease

75
Q

Lipid profile B-blocker adverse effects

A
  • chronic use - increase VLDL, decrease HDL
  • seen with both selective and non-selective
  • switch to partial agonist
76
Q

Hypoglycemic episodes B-blocker adverse effects

A
  • switch to B1 selective

- more on slide 49

77
Q

Abrupt discontinuation of B blocker therapy

A
  • increased numbers and responsiveness of receptors to endogenous agonists
  • enhanced cardiac stimulation and arrhythmias

CPR II Pharm (4 decks)

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