33 Antihypertensives
Last updated
Last updated
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antihypertensives work by either decreasing CO or decrease TPR
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do not want to block b2
not really used for hypertension
b1 blockade: general lower BP, including portal system
b2 increase flow to liver, block to decrease flow
carvedilol: clinical trial shows benefit, not because of special receptor
at low sympathetic level, higher activation of beta receptor than sympathetic activity, thus agonist
high level, lower activation of beta receptor than sympathetic, thus blocker
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fatigue, etc: blunt CNS activity
hyperlipidemia not clinically relevant
given because many benefits
diabetics often hypoglycemic because taking insulin
BB cause hypoglycemia and masks symptoms, except sweating (Ach receptors)
decompensated
acute HF: pt with pulmonary edema/sick from HF can get very sick with BB's lowering of CO
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stimulates myocardiocytes at different site
stimulate heart and bypass beta receptors
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tamsulosin very good for BPH
warm autoimmune hemolytic anemia
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pt not taking CCB: arteriole constrict, leading to lower hydrostatic pressure in capillaries
CCB: dilate arteriole, higher hydrostatic pressure
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like b1, slow HR, decrease contractility
inhibits renin, decrease AI production
HCTZ: used often for antihypertensives by inhibit Na absorption
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rapid acting drugs that can be titrated carefully
increased renal perfusion
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diuretic pts: dependent on AII to maintain BP
ACE I block AII
occurs with first dose of ACE I given to diuretic pt
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RAAS blockade leads to malformation
ACE I: decrease AII, renal failure
aldosterone decrease: more K