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129 Cards in this Set
- Front
- Back
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What are the 4 anatomic sites that control BP and how do they affect BP?
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HEART: cardiac output= rate & contractility
VENULES: Stroke volume- constriction increases preload ARTERIOLES: svr- constriction increases resistance KIDNEY: regulates blood volume and affects CO |
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3 BP regulatory systems:
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Baroreflex: high BP increases baroreceptor firing and decreases sympathetic NS
RAAS: Low BP, kidney releases renin, increase angiotensin 2 increases vasoconstriction, increase aldosterone and increase NA and water retention Local hormones: NO, endothelin 1 control vascular resistance |
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Diuretic subclasses
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thiazide
loop K sparing |
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Sympatholytics subclasses
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CNS blockers
Ganglionic blockers alpha 1 antagonists Beta antagonist |
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Vasodilator subclasses
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Calcium channel blockers
minoxidil hydralazine sodium nitroprusside |
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RAAS system blockers subclasses
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ACE inhibitors
Angiotensin II receptor type 1 blockers Renin inhibitor |
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Section of nephron where MOST NA+ is reabsorbed?
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Proximal convoluting tubule
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What section of kidney does each class of diuretic work on?
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Thiazide: Distal convoluting tubule
Loop: thick ascending limb or loop of Henle K sparing: upper collecting duct Carbonic anhydrase: Proximal convoluting tubule |
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MOA each class of diuretic?
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Loop: inhibit Na-K-Cl cotransporter in TAL
Thiazide: inhibit Na-Cl transporter in DCT K sparing: aldosterone antagonist or inhibit Na transport Carbonic anhydrase inhibitors: inhibit CA in PCT |
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Acetazolamide
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Carbonic anhydrase inhibitor for GLAUCOMA
(Not diuretic bc low efficacy, compensatory reabsorption later in kidney) |
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Furosemide
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sulfonamide loop diuretic
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bumetanide
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sulfonamide loop diuretic
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torsemide
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sulfonamide loop diuretic
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ethacrynic acid
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non-sulfonamide loop diuretic
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Which diuretic increases Ca and Mg excretion?
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Loop
also increases renal blood flow by increasing renal synthesis of prostaglandins |
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Therapeutic indication for loop
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acute pulmonary edema/ HF
anion OD acute renal failure |
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Side effects Loop
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hypokalemia
allergic reaction ototoxicity Mg depletion |
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Chlorthalidone
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thiazide
slowly absorbed longer duration |
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MOA Thiazide
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inhibit Na+Cl- transport in DCT
inhibit carbonic anhydrase enhance Ca reabsorption |
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Thiazide therapeutic indications
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hypertension
heart failure |
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Thiazide side effects
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hypokalemia
increase digitalis toxicity hyperlipidemia allergic reactions (sulfonamide group) |
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Spironolactone
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K sparing diuretic
competitive aldosterone antagonist |
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eplerenone
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K sparing diuretic
competitive aldosterone antagonist |
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Triamterene
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K sparing diuretic
Na transport inhibitor in apical membrane of collecting tubule |
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Amiloride
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K sparing diuretic
Na transport inhibitor in apical membrane of collecting tubule |
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Therapeutic use of K sparing diuretic
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Help maintain serum K level in combo w/ other diuretic
Heart failure: aldosterone antagonists |
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K sparing diuretic side effects and contraindications
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hyperkalemia
caution beta blockers and ACE inhibitor also increase K+ Contraindicated in renal dysfunction |
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4 classes of sympatholytic agents
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Centrally acting symph agents: block sympathetic activity in brain
Ganglion blocking agents: not used. block nicotinic receptors Neurotransmitter depleting agent: reduce NE release Adrenoceptor antagonists: block alpha or beta receptors |
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Centrally acting Sympatholytic Agents
MOA Therapeutic indication Side effects |
MOA: decrease sympathetic outflow from CNS by presynanptic alpha 2 agonist- less NE release decreases HR, contractility and vascular tone
INDICATION: HTN (not 1st line) Side effects: sedation, depression, fluid retention |
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Why is fluid retention a side effect of Central sympatholytic agents?
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compensatory response: body senses decrease BP and activates RAAS to increase fluid retention
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Clonidine
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alpha 2 agonist
Centrally acting sympatholytic agent Do not stop suddenly |
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Guanabenz
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alpha 2 agonist
Centrally acting sympatholytic agent Do not stop suddenly |
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Guanfacine
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alpha 2 agonist
Centrally acting sympatholytic agent Do not stop suddenly |
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methyldopa
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alpha 2 agonist
Centrally acting sympatholytic agent prodrug |
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Guanethidine
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NT depleting agent: inhibits release of NE by displacing NE from vesicles
Last line agent- for severe HTN causes postural/orthostatic hypotension DOES NOT CROSS BBB |
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Reserpine
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NT depleting agent: inhibits release of NE by blocking DA transport into vesicles
Last line agent- for mild/moderate HTN causes sedation and depression DOES CROSS BBB |
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Alpha antagonist side effects
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dizziness, nasal congestion, HA
orthostatic hypotension reflex tachycardia (baroreceptor) fluid retention |
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Prazosin
terazosin doxazosin trimazosin |
Selective alpha 1 antagonists
Less tachycardia |
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Phentolamine
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non-selective alpha antagonist
more tachycardia |
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Phenoxybenamine
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non-selective alpha antagonist
more tachycardia |
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Beta blockers
MOA 3 types |
Block NE and Epi from binding to beta receptors
Non-selective: beta 1 &2 cardioselective: beta 1 vasodilation: beta & alpha blocker |
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Beta receptor action when stimulated in heart vs. blood vessels
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Heart: beta 1 & 2 cause contraction
Blood vessels: beta 2 causes relaxation Beta blockers generally have more activity in heart |
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Beta blockers cardiovascular effects
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decrease HR & contractility
decrease conduction velocity mild vasocontriction Decrease SVR in long term thru decreased renin excretion in kidney |
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Beta blockers therapeutic indications
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HTN
angina and MI arrhythmias congestive heart failure |
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Beta blockers side effects
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hypotension
bradycardia AV block bronchoconstriction Changes lipids: increase TG and decrease HDL use cautiously in diabetics: may mask tachycardia hypglycemic warning sign |
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Beta blocker contraindication
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bradycardia
AV block asthma (?) esp non selective |
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Propanolol
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non-selective beta blocker
lipid soluble, crosses BBB |
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Esmolol
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cardioselective (beta 1) beta blocker
ultra short acting |
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Nadolol
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non-selective beta blocker
long acting and water soluble |
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Sotolol
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non-selective beta blocker
blocks K+ channels ?? |
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Labetalol
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alpha and beta blocking beta blocker
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Pindolol
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non-selective beta blocker
partial agonist |
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acebutolol
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cardioselective (beta 1) beta blocker
partial agonist |
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penbutolol
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non-selective beta blocker
partial agonist |
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Calcium channel blockers
MOA |
blocks Ca entry into cell by binding to alpha1 subunit of L type Ca channels in vascular smooth muscle or cardiac muscle
HEART Less Ca = decreased contraction strength also less frequent SA node firing VSM Less Ca= less MLCK = less constriction |
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Cardiovascular effects of calcium channel blockers
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decrease contractility
decrease heart rate decrease conduction velocity smooth muscle relaxation |
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differences between dihydropyridine and non-dihydropyridine calcium channel blockers
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dihydropyridine: more vascular selective
non-dihyropyridine: more cardiac selective |
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nifedipine
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dihydropyridine CCB
rapid onset and short action reflex increase in cardiac function |
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nicardipine
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dihydropyridine CCB
rapid onset and short action reflex increase in cardiac function |
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felodipine
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dihydropyridine CCB
slow release, long action less adverse effects |
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isradipine
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dihydropyridine CCB
slow release, long action less adverse effects |
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nitrendipine
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dihydropyridine CCB
less cardioselectivity |
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amlodipine
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dihydropyridine CCB
less cardioselectivity |
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lercanidipine
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dihydropyridine CCB
broad therapeutic indications (HF/MI) |
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lacidipine
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dihydropyridine CCB
broad therapeutic indications (HF/MI) |
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Verapamil
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NON-dihydropyridine CCB
more cardiac selective |
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Diltiazem
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NON-dihydropyridine CCB
both cardiac and vascular selective |
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CCB therapeutic indications
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HTN
Angina: non-DHPs or longer acting DHPs Arrhythmia: non-DHPs |
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CCB side effects
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flushing, HA hypotension
edema: compensatory baroreceptor/RAAS response reflex tachycardia (vascular selective CCB): compensatory baroreceptor/ RAAS bradycardia, impaired electrical and depressed contractility (cardiac selective) |
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Potassium channel openers
MOA Side effects Indications |
MOA: opens K+ channels is VSM which closes Ca channels leading to vasodilation
Side Effects: reflex cardiac function, tachycardia, edema Indications: refractory and severe HTN |
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Minoxidil
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K+ channel opener
dilates arterioles not veins stimulates hair growth |
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Diazoxide
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K+ channel opener
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Pinacidil
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K+ channel opener
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Hydralazine
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direct vasodilator
for severe HTN or heart failure Side effects: reflex tachycardia HA, dizzinness, flushing |
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Organic nitrates
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release NO after enzymatic reaction and causes vasodilation
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Sodium nitroprusside
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spontaneously releases NO causing vasodilation (increases cGMP)
Dilates both arteries and veins for HTN emergency and severe heart failure Side effects: HA, flushing, reflex tachycardia, cyanide toxicity |
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ACE Inhibitors MOA and effects
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block angiotensin 2 formation:
dilates arteries and veins- VASODILATION decrease aldosterone- BLOOD VOLUME decrease NE release- SYMPATHETIC ACTIVITY increases bradykinin (cough) |
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ACE inhibitor therapeutic uses
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HTN
Heart failure post- myocardial infarction |
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ACE inhibitor side effects
Contraindications |
dry cough
hypotension hyperkalemia Contraindication: pregnancy |
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What HTN drug classes cause increase in lipids?
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thiazides
beta blockers |
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Which drug HTN drug classes cause reflex tachycardia?
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-CCB
-K+ channel blockers -sodium nitroprusside -alpha 1 blockers -hydralazine |
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Captopril
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sulfhydryl ACE inhibitor
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Enalapril
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non-sulfhydryl ACE inhibitor
COO- |
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Ramipril
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non-sulfhydryl ACE inhibitor
COO- |
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Perindopril
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non-sulfhydryl ACE inhibitor
COO- |
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Lisinopril
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non-sulfhydryl ACE inhibitor
COO- |
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Benazepril
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non-sulfhydryl ACE inhibitor
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Fosinopril
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non-sulfhydryl ACE inhibitor
POO- |
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Angiotensin 2 Receptor blocker
MOA Indication Side effects |
blocks type 1 angiotensin 2 receptors
HTN, CHF, post MI Side effects: hyperkalemia contraindicated in pregnancy stronger &more specific than ACE-Is |
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Saralasin
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peptide IV ARB
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Losartan
Valsartan Candesartan Eprosartan Irbesartan Telmisartan |
ARBS
Candesartan is strongest and longest |
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Aliskiren
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Renin inhibitor
side effects: hyperkalemia, allergy |
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If pt has elevated BP for first time, when should follow up be to measure BP for second time?
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1-2 months
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3 benefits to lowering BP
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reduce:
stroke MI heart failure |
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Rx drugs that can increase BP?
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Adrenal steroids
anorectics bupropion calcinuerin inhibitors decongestants estrogens MOA Inhibitors NSAIDS thyroid hormons venlafaxine erthropoiesis stimulators anti VEGF agents |
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TOD
organs signs |
HEART: LVH, angina, MI, HF, stents
BRAIN: stroke, transient ischemic attack EYES: hemorrhage, papilledema KIDNEY- GFR <60, protein in urine PERIPHERAL ARTERIES: absent pulse, intermittent claudication |
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3 Goals for HTN therapy JNC 7
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-Reduce CVD and renal morbidity/mortality
-Treat to goal BP: <140/90 OR <130/80 DM or CKD -Achieve SBP goal esp for pts >50 yrs old |
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AHA HTN treatment recommendations
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-General: <140/90
-Most complications: <130/80 (DM, CKD, CAD, stroke and framinghouse >10%) -Left ventricle dysfunction (HF): <120/80 |
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CVD Risk factors (9)
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-HTN
-Smoking -Obesity - physical inactivity -dyslipidemia -diabetes -protein in urine or GFR <60 -old age (55men, 65 women) -Family history of premature CVD |
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Compelling indications/ comorbid conditions (6)
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-heart failure/ left ventricular dysfunction
-post myocardial infarction -diabetes -chronic kidney disease -recurrent stroke prevention -coronary disease/ high cardiovascular risk (angina, framinghouse >10%) |
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TLC
Therapeutic lifestyle changes |
Weight reduction
DASH diet (fruit, veggies, low fat dairy, high K+, Ca2+) reduce Na intake exercise moderate alcohol (2drinks/day men 1/day women) stop smoking (none for > 1month) |
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1st line HTN agents (JNC 7)
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Thiazide diuretic
beta blockers ACE-I/ARB/ Renin inhibitor CCB |
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Last line
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alpha blockers
central alpha 2 agonists reserpine vasodilators |
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ALLHAT primary and secondary outcomes and results
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Primary: Fatal CHD or MI
-ACE-I and CCB NOT better than thiazide -Thiazide better than alpha blockers Secondary: Heart failure, stroke, angina -Thiazide better than CCB and ACE-I |
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Thiazide doses
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HCTZ or chlorthalidone: Start at 6.25-12.5mg
50mg MAX |
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When titrating drug doses, how often to increase dose?
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Every 2-4 weeks
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Main risk of combination therapy?
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orthostatic hypotension
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Low Potency Neurolpetics
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Chlorpromazine, Thioridazine
1. More anticholinergic side effects than Extrapyramidal 2. Chlorpromazine: Corneal Deposits 3. Thioridazine: retinal deposits |
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Which drug class has biggest decrease in BP with dose increase?
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CCB
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Which drug class has least side effects with increase dose?
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ACE-I
ARB |
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When to follow up?
Controlled HTN Uncontrolled HTN |
3-6 months if TOD, bad adherance
6-12 if normal Uncontrolled: 2-4 weeks to avoid clinical inertia |
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Most common causes of resistant hypertension? (3)
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non-adherence
secondary HTN (overactive adrenal glands) Fluid retention (esp from kidney failure) |
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Define hypertensive emergency and urgency
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Urgency: BP >=180/120 (or 110)
Emergency: BP AND evidence target organ damage. But any TOD is emergency |
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Risk factors for HTN crisis
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Non-compliance (80% of ER visits)
access to healthcare illicit drug use pre-eclampsia pheochromocytoma |
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Hypertensive urgency
Goals Plan Setting Follow up |
Safely & gradually reduce BP to JNC stage 1 over 24-48 hours
Oral meds preferred ER or Dr. office. monitor BP &HR every 15-30 mins appointment with PCP in 1-2 days |
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Hypertensive emergency goals
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Decrease mean arterial pressure by 25% within 1 hour
Decrease BP to 160/100 within 2-6 hours (if stable) Decrease BP to goal over next 24-48 hours (if stable) |
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Hypertensive emergency
setting plan follow up |
Inpatient (ICU)
continuous cardiac monitoring IV meds: sodium nitroprusside, fenoldopam, labetalol, esmolol, nicardipine, clevidipine Must transition to oral meds before discharge See PCP in 1-2 days |
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Drugs causing hypokalemia and MOA
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loop and thiazide diuretics
-reabsorbs Na+ by exchanging K+ -Less volume increases aldosterone increases K+ excretion Beta agonists, insulin, sorbitol, polystyrene sulfonate, laxatives, antibiotics, digoxin |
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drugs causing hyperkalemia
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ACE-I, ARB, (decrease aldosterone)K+ sparing diuretics, aldosterone antagonists, beta blockers
prostaglandin inhibitors, digoxin, trimethoprim |
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signs, symptoms and labs for hypokalemia
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cramping, weakness, muscle pain
EKG: ST depression, T wave inversion, U wave elevation Arrhythmias Serum K+: <3.5 mEg/L Mild 3-3.5 Moderate 2.5-3 Severe <2.5 |
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signs, symptoms and labs for hyperkalemia
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heart palpitations, skipped heartbeat
EKC: peak T wave loss of P wave Flaccid paralysis Serum K+:>5.5 mEq/L Mild 5.5-6 Moderate 6-6.9 Severe >7 |
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Drugs to treat hyperkalemia
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loop diuretics (eliminate)
insulin + dextrose (shift) albuterol (shift) sodium bicarbonate (shift) dialysis (eliminate) sodium polysterene sulfonate (eliminate) |
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Hyponatremia
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most common electrolyte abnomality
Serum Na+<135mEq/L |
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Standard therapy for LV dysfunction
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Diuretic w/ ACE inhibitor
then add Beta blocker Add-on: ARB or aldosterone antag |
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Standard therapy for recurrent stroke prevention
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Diuretic w/ ACE inhibitor
OR ARB |
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Standard therapy for post MI
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beta blocker
then add ACE-I or ARB add-on: aldosterone antag |
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Standard therapy for diabetes
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ACE inhibitor
OR ARB Add-on: diuretic then beta blocker or CCB |
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Standard therapy for coronary disease
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Beta blocker
then add ACE-I or ARB Add-on: CCB, diuretic |
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Standard therapy for chronic kidney disease
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ACE-I
OR ARB |
