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54 Cards in this Set
- Front
- Back
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TYPE OF HTN |
Essential (primary) Secondary (pheochromocytoma, renal disease, Cushings, hyperaldosteronism) Medications Resistant HTN |
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FACTORS AFFECTING PRIMARY HTN |
genetics, cardiac output, sodium regulation, RAAS, sympathetic over-activity, peripheral resistance, obesity, inactivity, insulin resistance, K+/Mg+ depletion, chronic moderate ETOH, smoking, caffeine |
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DESIRED OUTCOMES OF CONTROLLING HTN |
-Reduce risk of CVD and end-organ damage -Targeting a specific BP (140/90, 150/90 if >65 y/o) -Pharm tx should be adjunct to non-pharm tx -TLC--DASH diet, reduced Na+ intake, exercise, achieve/maintain IBW, limit ETOH, smoking cessation |
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THIAZIDE DIURETICS (Chlorthalidone--Hygroton, indapamide--Lozol, HCTZ, metolazone--Zaroxolyn) |
Most commonly prescribed (one of two best choices in AA w/ HTN) Act in DCT Inhibit Na+ and Cl- reabsorption K+ and Mg+ excretion enhanced Reduced excretion of Ca++ and uric acid Has better outcome with HF than ACE or CCB Adverse effects: hyponatremia, hypokalemia, hypomagnesemia, HYPERCALCEMIA, hyperlipidemia, hyperglycemia, hyperuricemia; decrease in efficacy of anticoagulants and gout meds; increased risk of toxicity of lithium, digoxin, quinidine, & anti arrhythmic agents. NSAIDs reduce efficacy; limited benefit in advanced renal impairment |
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LOOP DIURETICS (Furosemide--Lasix, bumetanide--Bumex, torsemide (Demedex), etharynic acid) |
Act in thick ascending loop of Henle (site where over 65% of Na+ filtered) Diuretic effect more potent than other diuretic subtypes. Adverse effects: hyponatremia, hypokalemia, hypomagnesemia, HYPOCALCEMIA, hypotension, hyperglycemia, hyperuricemia; cardia arrhythmia potential.
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OTHER DIURETICS |
Aldosterone inhibitor: spironolactone, eplerenone exchange inhibitors: triamterene, amiloride Used to offset K+ loss by other diuretics. Increased risk of hyperkalemia, esp. with ACE or renal insufficiency |
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BETA BLOCKERS |
Not 1st line MOA: modulation of renin, reduction in CO/HR, negative inotropic/chronotropic effects Well established role in pt's with HTN w/ CHF, post MI, & high coronary artery disease risk Vasodilatory properties (alpha1 receptor blockade, L-argininine/nitric oxide induced release from endothelial cells (Bystolic) Reduce peripheral resistance On initiation--bradycardia, heart block, s/sx heart failure Abrupt DC--precipitating factor for development of ischemic syndromes, so taper
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BETA BLOCKERS--ADVERSE EFFECTS |
hypotension, syncope, bronchospasm/dyspnea, fatigue, electrolyte imbalance, depression may mask s/sx of hypoglycemia strong caution with HR <60 bpm and respiratory diseases |
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BETA BLOCKERS--MEDICATIONS |
Cardioselective--atenolol (Tenormin), bisoprolol (Zebeta), metoprolol (Lopressor, Toprol XL), esmolol (brevibloc) Non-cardioselective--nadolol (Corgard), nevbivolol (Bystolic), propranolol (Inderal), timolol (Blocardren), pindolol, carteolol, penbutolol Mixed alpha and beta blocker--carvedilolol (Coreg), labetalol (Trandate) |
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CALCIUM CHANNEL BLOCKERS Nondihydropyridine agents Verapamil, diltiazem |
MOA--electrophysiological effects, negative chronotropic/inotropic effects, effectively block cardiac conduction. Valuable in Afib, HTN Adverse effects--bradycardia, heart block, constipation DO NOT CAUSE REFLEX TACH |
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CALCIUM CHANNEL BLOCKERS Dihydropyridine agents amlodipine (Norvasc), felodipine (Plendil), isradipine (Dyna Circ SR), nicardipine (Cardene), niphedipine (Adalat), Procardia, nisoldipine (Sular) |
MOA--no utility in managing atrial dysrhythmias, coronary vasodilating properties Adverse effects--Edema, constipation, reflex tach. **Particularly useful in AA w/ HTN |
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ACE INHIBITORS |
May use 1st line for HTN and in CKD Indications: heart failure, post MI, CKD (not renal failure), recurrent stroke prevention, diabetes |
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ACE INHIBITORS--ADVERSE EFFECTS |
Persistent dry cough Angioedema hyperkalemia (anticipate moderate elevations) decreased renal function (afferent/efferent renal artery tone changes) hypotension blood dyscrasias **CONTRAINDICATED IN PREGNANCY** |
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ACE INHIBITORS--MEDICATIONS |
benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), fosinopril (Monopril), lisinopril (Zestril), Moexipril (Univasc), perindopril (Aceon), quinapril (Accupril), ramipril (Altace), trandolopril (Mavik) |
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ANGIOTENSIN RECEPTOR BLOCKERS |
One of 1st line for HTN and one of two for CKD and HTN effectiveness enhanced when combined with diuretics Well tolerated alternatives to ACE Useful with DMII and LVH Adverse effects--hyperkalemia, decreased renal function, angioedema, hypotension **CONTRAINDICATED IN PREGNANCY** |
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ANGIOTENSIN RECEPTOR BLOCKERS--MEDS |
candesartan (atacand), eprosartan (Tevetan), irbesartan (Avapro), losartan (Cozaar), olmesartan (Benicar), telmisartan (Micardis), valsartan (Diovan) |
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RENIN BLOCKERS |
Blocks renin effects (blocks A-I and A-II) effective alone or with HCTZ Adverse effects--angioedema, hypotension, hyperkalemia
Aliskiren (Tekturna) |
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ALPHA BLOCKERS |
Alpha blockers: Doxazosin (Cardura), terazosin (Hytrin), prazosin (Minipress)
Not first line (use for add-on therapy)
used in pts with BPH
ADE--syncope, dizziness, palpitations
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CENTRALLY ACTING AGENTS |
Centrally acting agents (no evidence JNC8) clonidine, methyldopa, guanfacine, guanabenz
reduce sympathetic outflow, enhance parasympathetic activity
ADE--orthostasis, sedation, dry mouth, visual disturbance |
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HYPERTENSIVE CRISIS |
Severe elevation in BP with potentially life-threatening target organ damage
SEND TO ER . . . WILL BE ADMITTED AND TREATED INPATIENT. |
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HYPERTENSIVE URGENCY |
Severe elevation in BP WITHOUT evidence of acute or life threatening end organ damage
Send to ER where they will be treated with an oral short acting med (captopril, clonidine, labetalol); observation in ED; DC on oral meds; f/u outpatient w/in 24 hours.
**Avoid short acting CCB (Procardia) d/t increased risk of MI and stroke. |
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DEVELOPMENT OF CAD |
Begins with LDL migration into vascular sub epithelial space, retained by binding to proteoglycans
LDL becomes oxidized; promotes uptake of monocytes/macrophages, which promotes further LDL uptake--vicious cycle. |
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FOUR STATIN BENEFIT GROUPS |
ASCVD
Elevations of LDL to 190 mg/dl
40-75 y/o w/ DM, LDL 70-189, no ASCVD
No ASCVD or DM 40-75 y/o with est. 10 yr ASDVD risk of 7.5 or above
(also may treat in carotid stenosis) |
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INTENSITY OF STATIN EFFECT |
ASCVD--<75 y/o high; >75 y/o moderate
LDL >/= 190 mg/dl high
DM--moderate unless ASCVD risk >/=7.5, then high
ASCVD risk >/=7.5 (age 40-75) high |
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STATINS |
Medication of choice to treat high LDL Inhibit conversion of HMG-CoA to L-mevalonic acid and subsequently cholesterol Lower LDL 25-62% Moderately reduce triglycerides and modestly raise HDL LDL receptor up-regulation primary MOA |
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STATINS: PLEIOTROPIC EFFECTS |
Reduce inflammation-decrease CRP
Reduce lipoprotein oxidation
Enhance endothelial synthesis of nitric oxide
Inhibit thromboses |
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STATINS: AVAILABLE AGENTS |
Moderate to high intensity--Rosuvastatin (Crestor), Atorvastatin (Lipitor)
Low to moderate intensity--simvastatin (Zocor), pitavastain (Livalo), pravastatin (Pravachol), lovastatin (Mevacor, Altoprev), Fluvastatin (Lescol) |
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STATINS: ADVERSE EFFECTS |
Increased LFTs--monitor at baseline, then no more unless clinically indicated. LFTs and CPKs as indicated by symptoms.
Myopathy & Rhabdo--monitor at baseline and when symptoms dictate; DC if CK >10 x ULN |
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CHOLESTEROL ABSORPTION INHIBITOR |
Ezetimbe (Zetia)--used as adjunctive therapy w/ statin--blocks biliary and dietary cholesterol absorption; reduces liver cholesterol stores, up regulation of LDL receptors, decreasing serum cholesterol.
ADE: fatigue, diarrhea, GI upset, myalgias |
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BILE ACID SEQUESTRANTS |
Adjunct to statin--additional lowering of LDL
Highly charged resins--bind to bile acids, excreted in feces
Meds--cholestyramine (Questran, Prevalite), colestipol (Colestid), colesevelam (Welchol) |
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BILE ACID SEQUESTRANTS--ADE |
GI problems, bloating, flatulence, constipation (have pt increase fluid intake)
May interfere with absorption of other meds, so take it at separate time
Welchol not well tested with other meds, separate by at least 4 hours
Some evidence suggests BAS may decrease HgbA1c |
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NIACIN |
Shown to reduce CHD events and progression of atherosclerosis when combined with statin
Consider Zetia or BAS first
Reduces LDL by 5-25%, triglycerides 20-50%; increases HDL by 15-35%.
Start low dose to avoid flushing; can raise BS and uric acid level. |
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FIBRATES |
Most effective triglyceride lowering med (used primarily in pts with elevated triglycerides and low HDL)
MOA: Stimulate function of lipoprotein lipase
Decrease triglyceride levels by 20-50%; increase HDL levels by 9-30%
Generally well tolerated; AR--GI upset, flatulence, abd pain, dyspepsia, fatigue; myopathies (esp when combined with statin)
Available meds: fenofibrate (Tricor, Triglide), gemfibrozil (Lopid), fenofibric acid (Trilipix) |
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OMEGA 3 FATTY ACIDS |
Useful for pts with high triglycerides despite diet, ETOH restriction, & fibrate therapy
MOA: May stimulate PPAR-a and reduce Apo B-100 secretion
30-50% reduction, may require high doses
Antiarrhythmic and anti-platelet aggregation properties (probably accounts for decrease in sudden death) |
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COMBOS FOR HYPERLIPIDEMIA |
Additional reductions in LDL--statin + ezetimimbe, statin + BAS (if statin in tolerant, ezetimibe + BAS)
Mixed dyslipidemia--statin + zetia or statin + fibrate
Very high triglycerides--statin + fibrate, statin + fish oil, fibrate + fish oil |
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HEART FAILURE |
Inability of the heart to pump enough blood to meet blood flow and metabolic demands of body.
High output--demands outpace CO; normal heart Low output--Low CO d/t impaired cardiac function
Classification--ischemic (70%), non-ischemic Most common causes--HTN, CAD, MI, dilated cardiomyopathy. |
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HEART FAILURE--CAUSES |
Systolic dysfunction--decreased contractility, evidenced by decreased EF Diastolic dysfunction--restriction in ventricular filling--EF is preserved--HTN plays major role, causing LVH.
Compensatory mech--increased sympathetic tone (increased preload-volume, vasoconstriction, tachycardia--increases myocardial O2 demand, increased contractility)--makes situation worse. |
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HEART FAILURE--TREATMENT |
Address risk factors--treat HTN, smoking cessation, treat lipid disorders, optimize DM tx, exercise, no excessive ETOH, salt reduction (not restriction)
Pharmacology--Diuretics (thiazide-maintenance, loop-exacerbation), ACE or ARB, beta blocker (esp if recent MI), aldosterone antagonist (monitor K+), hydralazine/nitrates (esp AA in failure), digoxin (later stages) |
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HEART FAILURE--OTHER THINGS TO KNOW |
Avoid TZD's (DM meds, cause fluid retention), Metformin (lactic acidosis), CCB (negative inotrope), NSAIDs (fluid retention).
Warfarin dose has to be reduced, INR will be higher w/ acute heart failure |
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DETERMINANTS OF MYOCARDIAL O2 DEMAND |
Heart rate
Wall stress (preload & afterload)
Contractility |
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RAAS |
Renin-angiotensin-aldosterone system 1. kidneys release renin in response to low blood volume 2. renin in bloodstream converts angiotensin to angiotensin I 3. angiotensin converting enzyme converts angiotensin I to angiotensin II 4. angiotensin II causes vasoconstriction, increased BP 5. also causes release of aldosterone from adrenal cortex 6. aldosterone acts on distal tubules and collecting ducts 7. increases reabsorption of H2O leading to Na+ retention and K+ excretion |
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ISCHEMIA |
Two factors happen simultaneously: 1. ambient factors increase MVO2 demand (exercise, stress); increased demand 2. circumstances decrease O2 supply (atherosclerotic arteries impair O2 transport); decreased supply |
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CHRONIC STABLE ANGINA: Drug therapy goals |
Relieve acute pain
Prevent progression of CHD (controlling HTN & lipids)
Improve functional capacity |
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CHRONIC STABLE ANGINA: Lifestyle changes |
Smoking cessation
Maintain normal weight
Low fat/low carb diet (low carb better)
Regular aerobic exercise |
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CHRONIC STABLE ANGINA: #1 pharm intervention |
NITRATES--halt acute attack, prevent predictable episodes, chronic treatment
Cause dilation of veins and arteries, decrease venous return to the heart=decreased preload=decreased workload |
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CHRONIC STABLE ANGINA: #1 pharm intervention-cont'd |
RAPID ACTING NITRATES provide relief in 1-5 minutes forms--sublingual (nitrostat), spray (Nitromist, Nitrolingual
dosage--0.3, 0.4, 0.6 mg per dose Call EMS IF PAIN NOT RELIEVED AFTER 1ST DOSE
**can cause hypotension, tell them to sit down** |
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CHRONIC STABLE ANGINA: #1 pharm intervention-cont'd |
LONG ACTING NITRATES Used for chronic prophylaxis, maintain vasodilation and decreased workload
forms-isosorbide dinitrate (Dilatrate SR), isosorbide mononitrate (Imdur), transdermal (Nitro-Dur)
**can develop tolerance, prevent by 10-12 hour nitrate free period per day** |
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CHRONIC STABLE ANGINA: #2 pharm intervention |
BETA BLOCKERS Indications: complementary effects when used with nitrates; benefits for exertional angina
Decrease MVO2 and consumption by antagonizing adrenergic receptors
Contraindications: preexisting brady, acute decompensated HF, reactive airway disease
ADE: slowing of nodal conduction, avoid abrupt w/d (reflex tach), drowsiness, depression |
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CHRONIC STABLE ANGINA: #2 pharm intervention--cont'd |
SELECTIVITY
Cardioselective-atenolol (Tenormin), metoprolol tartrate (Lopressor), metoprolol succinate (Toprol XL)
Nonselective-propranolol (Inderal)--causes bronchospasm with increased doses |
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CHRONIC STABLE ANGINA: #3 pharm intervention |
CCB Indications-vasospastic angina (Prinzmetal's), exert vasodilation & depress HR/contractility
MOA-blocks Ca++ entrance into smooth muscle cells; decrease muscle contraction=vasodilation Smooth muscles in arteries > veins; no reduction in preload. |
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CHRONIC STABLE ANGINA: #3 pharm intervention--cont'd |
NONDIHYDROPYRIDINE (decreases HR) suppresses contractility, reduces heart rate, causes reduction in O2 demand
Diltiazem-suppresses contractility, decreased HR, decrease O2 demand
Verapamil-decreases rate of AV node conduction
Also used with arrhythmias |
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CHRONIC STABLE ANGINA: #3 pharm intervention--cont'd |
DIHYDROPYRIDINE (does not decrease HR) does not alter conduction provides dilation of coronary and peripheral arteries
nifedipine (1st gen) amlodipine (2nd gen)
SE: leg edema, fatigue, flushing, dizziness, headache, gingival hyperplasia
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CHRONIC STABLE ANGINA: #3 pharm intervention--cont'd |
CCB Contraindications
preexisting LV dysfunction heart block sick sinus syndrome hypotension CHF |
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CHRONIC STABLE ANGINA: #4 pharm intervention |
ANTIPLATELETS Indications-all patients with acute or chronic angina; primary and secondary prevention of CVD |
