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61 Cards in this Set
- Front
- Back
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Epinephrine
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*Heart (β1): ↑automaticity, ↑HR, ↑conduction velocity, ↑CO (β1 stimulated ↑ in contractility + relaxation in blood vessels due to β2 stimulation @ therapeutic dose), ↑O2 consumption, ↓efficiency
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*BP (β2 & α1): ↓ @ low [ ] via β2 dilation, ↑ as [ ] ↑ & α1 receptors become occupied; If both receptors occupied – α1 response predominates; @ low [ ] MBP is often ↓, @ high [ ] MBP is ↑
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*Respiratory tract (β2 & α1): bronchioles dilated via β2 – most prominent when bronchial muscle is constricted due to drugs/disease; secretions ↓ via α1
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Metabolism: ↑ glycogen breakdown (β2); ↓ glycogen synthesis (α1); ↓ insulin secretion (α2), ↑ free fatty acids (β3)
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Norepinephrine
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*Heart(β1): direct effects; same as epi
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*BP (α1): ↑ systolic, diastolic and mean
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*Cardiac Output: no change or slightly ↓ due to α1 mediated constriction of blood vessels
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*Metabolism; ↓ glycogen synthase activity via α1
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Isoproterenol
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*Heart (β1) – direct effects same as epi
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BP (β2): ↓BP
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Respiratory Tract (β2): relaxes bronchi
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Dopamine
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*Receptors activated (DA, β1, β2, α1 @ ↑ [ ])
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Heart (β1): HR ↑
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BP: ↓ by DA receptor activation in renal/mesenteric beds; ↓ by β2 receptor activation; ↑ by ↑↑↑ [ ] by α1 receptor activation
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Dobutamine
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*Heart (β1*) – greater inotropic (contractility) than chronotropic (rate) effects; ↑↑ [ ] may also ↑ automaticity
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*BP: ↑ [ ] can ↑ BP via α1
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Phenylephrine
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*Non-catecholamine α stimulators are NOT metabolized by COMT
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Ephedrine
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Clonidine
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*Brain: α2 @ receptors sites block sympathetic output – postsynaptic
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α-Methyldopa
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*Periphery: α2 act @ presynaptic receptors to inhibit NE release
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Terbutaline
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Albuterol
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Amphetamine
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*Displaces NE from terminal à sympathomimetic effects
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*Substrate for NET and ↑ synaptic NE via facilitated exchange diffusion
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Methylphenidate
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Prazosin
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*Block α1 receptors only
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*α1 blockade: ↓BP, get reflex tachycardia
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Phenoxybezamine
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*Block α1 receptors only
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*Duration of action ~24 hrs
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*Must synthesize new receptor to recover α1 effect
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Phentolamine
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*Block α1 and α2 receptors
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*α1 blockade ↓ BP
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*α2 blockade prevents feedback inhibition by released NE, causing more NE to be released onto β receptors in heart, producing even GREATER TACHYCARDIA than w/ a selective blocker
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Propanolol
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*Blocks β1 and β2
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*Cardiac effects: ↓ HR due to β1 block; ↓ CO (more pronounced during exercise); ↓ conduction velocity, myocardial O2 demand, & spontaneous rate of depolarization
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*Vascular & BP Effects: β2 may ↑ TPR slightly; ↓ plasma rennin due to β1 block; net effect BP ↓
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*Metabolic Effects: no effect on plasma glucose in normal, but does slow recovery from hypoglycemia in diabetics (less of a problem w/ β selectives); ↑ plasma [ ] of triglycerides (VLDL) and ↓ [ ] HDL
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*Respiratory Tract (β2 block): airway resistance ↑; can be life threatening in asthmatics
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Atenolol
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*Cardiac effects: similar to non-selective β blockers
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Esmolol
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*Less danger of respiratory side effects than w/ non-selective
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Timolol
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*At ↑ [ ] à NO β blocker is really “selective”
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(nonselective)
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Caffeine
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*CNS: all cortical areas are sensitize; ↑ [ ] sensitize the respiratory areas to CO2 & ↑ respiratory rate
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*CV: ↑ HR and ↑ contractility; systemic BV dilate; TPR ↓ (looks like β2 stimulation); cerebral blood vessels constricted; net effect à BP ↑ because caffeine releases catecholamines
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Theophylline
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*Respiratory tract: bronchi relaxed
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Guanethidine
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Enters via NET, uncouples AP from Ca++ entry, and stabilizes vesicular membrane; stops NE from being stored; ↓BP
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Reserpine
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Enters the terminal (lipid soluble), stabilizes vesicular membrane, causing depletion of NE over time; stops NE from being stored
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Tyramine
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Cause displacement of NE from terminal à sypathomimetic effects
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*normally metabolized by monamine oxidase in the gut
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*In CNS metabolized to octopamine which is stored in vesicles causing displacement of NE
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Cocaine
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*Blocks NET à ↑ synaptic NE
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Imipramine
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*Blocks NET à ↑ synaptic NE
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Atomoxetine
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*Blocks NET à ↑ synaptic NE
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(selective NE reuptake inhibitor)
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