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28 Cards in this Set
- Front
- Back
Pheochromocytoma
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adrenal medulla tumor
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Cushing's disease
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increased adrenal cortex secretion
increased Na+ retention |
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Renal disease
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increases retention of fluid: also renin - angiotension -aldosterone release
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Autonomic modifiers
Non-autonomic inhibitors of smooth muscle of vessels Modifiers of circulatory volume |
What are the 3 broad classes of antihypertensive drugs?
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Autonomic modifiers
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broad class name
affect heart and blood vessel diameter block sympathetic only - either alpha or beta or both Parasympathetic stimulators not used |
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Non-autonomic inhibitors of smooth muscle of vessels
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Dilate blood vessels diameter directly or indirectly, not using neural receptors
(broad class name) |
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Modifiers of circulatory volume
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(broad class name)
direutics brings blood volume down |
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Alpha blockers
Beta blockers Ganglionic blockers Central or central and peripherial sympathetic blockers |
What are the 4 autonomic modifiers?
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Alpha blockers
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mechanism of action
block action of E and NE on receptors - inhibits vasoconstriction |
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Alpha blockers
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Side or toxic effects
postural hypotension (dizziness upon standing including weakness and fainting), reflex tachycardia |
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Beta blockers
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mechanism of action
decreases HR and heart force of contraction, therefore decreases Cardiac output; also inhibits renin release |
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Beta blockers
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Side effects or toxic effects
GI - nausea, vomiting, diarrhea heart - uncommon, but may cause serious cardiac depression; can cause AV block bronchioles - constrict airway |
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asthma
AV block |
What are the contraindications for B-blockers?
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Ganglionic blocker
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This drug is no longer recommended.
(mechanism of action) antinicotinic drug inhibits sympathetic ganglia decreases BP (decrease CO and vasoconstriction) inhibition of parasympathetic ganglia, may increase HR. |
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Ganglionic blocker
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Therapeutically, __________ blockers are as good as many other antihypertensives, BUT too many annoying side effects.
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Beta
Calcium channel |
______ blockers most useful in patients under 40, but patients over 60 do poorly, and respond well to ________ _________ blockers.
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Central blockers
Rauwolfia Alkaloids (resperpine) Monoamine Oxidase inbititors |
What are the different central and peripheral sympathetic blockers called?
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Central blockers
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withdrawl can cause rebound hypertension
do not miss a dose; withdraw slowly - these agents should not be used for initial treatment. Sedation, dry mouth, dizziness occur frequently. |
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Rauwolfia Alkaloids (resperpine)
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What drug was originally used to treat psychoses?
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Rauwolfia Alkaloids (resperpine)
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mechanism of action
depletes Norepi decreases sympathetic effect by decreasing Norepi released in sympathetic centers in the brain as well as in the heart. |
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Rauwolfia Alkaloids (resperpine)
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side effects or toxic effects
(mostly due to CNS and GI tract) CNS - sedative effect, psychic depression GI - (decreases symp. so parasymp. effect seen) increases tone and motility - abdominal cramps and diarrhea, increased gastric secretion. other - nasal congestion |
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cancerous
seminal cancer |
Rauwolfia Alkaloids (resperpine)
Note: Is a correlation btwn use and __________ tumors of adrenal medulla gland, mammary gland and _______ vesicles in rats and mice. However, risks of hypertension are much worse than risks of _______. |
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Rauwolfia Alkaloids (resperpine)
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Contraindications or cautions
patients with depressive episodes gastric ulcers pregnant women (babies born with respiratory problems) |
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Monoamine Oxidase inbititors
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What does MAO stand for?
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increases
NE decreases false transmitter tyrosine |
Monoamine Oxidase inbititors
Mechanism of action In CNS, ________ NE (good antidepressant) MAO is prevented from destroying ____________. In SNS, first increases then _________ NE. The increase is expected with MAO inhibition The decrease is thought to be because of the "______ _________" idea GI enzyme also inhibited which floods peripheral vesicles and receptors with ________ which is much less effective as a transmitter. This is why it works as an antihypertensive. |
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Monoamine Oxidase inbititors
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Side effects or toxic effects
possibly more than any other any hypertensive agent. Acute: 1. CNS stimulation - hallucination, agitation, convulsions 2. hypo or hypertension Chronic: 1. CNS stimulation - tremors, insomnia, nightmares, mood elevation rarelly confusion and hallucinations 2. Inhibition of sympathetic nervous sytem -GI - nausea, constipation (common, but cause unknown) - postural hypotension - decreased sexual function 3. hypertensive crisis may occur |
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Monoamine Oxidase inbititors
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Contraindication or cautions
1. Interactions with food 2. Interactions with drugs 3. Watch for renal and accumulation of the drug |
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increase
cheeses hypertensive suicidal antihistamines 2 failure |
Contraindication or cautions
1. Interactions with food - som foods ________ NE release (aged _______, beer, chianti wine, canned figs) - may bring on _________ crisis (headache, fever, chest pain, death from intracranial bleeding) - depressed patients may use foods as ________ agents 2. Interactions with drugs - caffiene, alcohol, __________ , barbituates, chloralhydrates, other hypnotics, sedatives, tranquilizers and narcotics; i.e. use caution with all drugs - wait up to ____ weeks before switching treatment to a contraindicated drug. 3. Watch for renal _______ and accumulation of the drug |