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29 Cards in this Set
- Front
- Back
Neurotransmitter released from ganglion
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acetylcholine
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CNS alpha-2 agonists
examples |
clonidine
alphamethyldopa guanabenz |
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sympathetic nerve ending antagonists
example |
reserpine
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beta receptor blockers
examples: |
propranolol
nadolol timolol (and many others) |
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peripheral alpha receptor antagonists
alpha 1- Selective |
prazosin
terazosin doxazosin |
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peripheral alpha receptor antagonists
non selective |
phentolamine
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alpha 1 receptor antagonists
(prazosin) |
Absorbed in the GI tract.
T1/2: 3-4 h Indication: combination therapy of hypertension. |
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why combination therapy with alpha 1 receptor antagonists?
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because it’s a vasodilator, body will try to fight…
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alpha 1 receptor antagonist
MOA |
competitive antagonist
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alpha 1 receptor antagonist
adverse effects orthostatic hypertention |
Extension of drug’s dilator action on veins.
Most common at the initial stages of therapy. |
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Info provided: When a person gets up quickly, blood pools in the veins of the lower extremities. Question: What immediately happens to cardiac output and arterial pressure when a person gets up quickly?
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decreases
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Info provided: A healthy person rapidly (seconds) compensates for an orthostatic fall in cardiac output and arterial pressure.Question: What is the mechanism involved in such compensation?
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baroreceptor reflex
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beta receptor antagonists
propranolol |
Absorbed in the GI tract.
T1/2: 3.5-6 h Indication: therapy for hypertension |
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beta receptor antagonists
adverse effect asystole and cardiac arrest |
May occur due to exacerbation of the bradycardic effect of these drugs, either in patients with AV node dysfunction or in patients taking other bradycardic medications (e.g., Ca2+ channel blockers).
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drug variations
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1) There are selective beta 1-antagonists (e.g., atenolol). They are less likely to precipitate bronchospasm.
2) There are -rec. antagonists (e.g., pindolol) that have intrinsic sympathomimetic activity (ISA). These drugs prevent that endogenous NE activates -receptors (antagonist effect), but they may weakly activate beta-receptors in the absence of NE (partial agonist effect). These drugs are less likely to cause bradycardia and asystole. 3) There are drugs (e.g., labetalol) that act as antagonists on beta 1/2 and alpha 1 receptors. Like giving propranolol and prazosin together. |
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Adrenergic neuron blockers
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Guanethidine
Reserpine |
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adrenergic neuron blockers
guanethidine |
Absorbed in the GI tract.
T1/2: 5 days |
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adrenergic neuron blockers
reserpine |
Absorbed in the GI tract.
T1/2: 1-2 days |
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adrenergic neuron blockers
indication |
Sometimes used as last resort in therapy of hypertension
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guanethidine
adverse effects |
Guanethidine does not cross the blood-brain barrier. Its adverse effects are generally related to blockade of peripheral synapses.
examples: Postural hypotension Diarrhea Delayed ejaculation (sympathetic nervous system) |
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reserpine
adverse effects |
Reserpine crosses the blood-brain barrier. Most severe adverse effects are related to blockade of central synapses.
examples: Sedation Mental depression Parkinson’s-like symptoms |
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CNS acting drugs
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clonidine
methyldopa |
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clonidine
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Absorbed in the GI tract.
T1/2: 8-12 h |
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methyldopa
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Absorbed in the GI tract.
T1/2: 2 h |
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CNS acting drugs
indications |
Usually not first choice in therapy of chronic hypertension, but…
…clonidine is often used in hypertensive crisis. …methyldopa is drug of choice for management of chronic hypertension during pregnancy. |
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CNS acting drugs
adverse effects |
Most severe adverse effects are related to blockade of central synapses.
example Dry mouth Sedation Mental depression ** Parkinson’s symptoms are not there because it doesn’t interfere with the dopamine receptors. |
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What is the mechanism of the anti-hypertensive action of guanethidine?
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It takes the place of norepinephrine in secretory vesicles
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How does prazosin lower blood pressure?
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It reduces peripheral vascular resistance
Decreases renal excretion of sodium Increases cardiac output (Frank Starling) |
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what is Frank Starling?
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states that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume) and vice-versa.
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