5080 - HTN & Hyperlipidemia Flashcards
Exam 1 study guide review
CMA
Cost minimization analysis - compares cost of 2 different interventions where outcomes are not necessarily equal or even measured. Should only be used when outcomes are identical.
Cost minimization analysis
How hospital formularies are developed
CBA
Cost benefit analysis - dollar signs assigned to treatments as well as outcomes. As ratio or an actual dollar amount.
CEA
Cost effectiveness analysis - commonly used. Compares multiple treatments that have different costs.
CUA
Cost utility analysis - takes patient preference into analysis. Often reported as quality adjusted life years.
quality adjusted life years
CUA - cost utility analysis
Medicare PART A
hospital insurance
Medicare PART B
outpatient medical insurance
Medicare PART D
prescription drug plan
Dosage form versus delivery system
Delivery system talks about how the dose form is delivered
Routes of administration
Oral: PO
Parenteral: IV, SC, IM
Sublingual; Inhalation; Rectal; Vaginal; Ocular; Nasal; Transdermal
How many Americans have HTN?
75 million
90% of people over 55 have:
HTN
Primary hypertension:
90% of cases - multifactorial response
Secondar hypertension:
10% of cases - with specific and known direct cause. Most common in renal dysfunction. Also sleep apnea, Cushing’s and other.
Meds can cause HTN specifically:
Stimulants, immunosuppressants, decongestants, high-dose NSAIDs
Uncontrolled HTN can lead to:
MI, stroke, renal failure and death
Measure what doubles cardiovascular risk in HTN:
Every 20/10 reading
MAP is:
1/3 SBP + 2/3 DBP
BP patho is:
Cardiac output + total peripheral resistance
RAAS stands for:
Renin angiotensin aldosterone system
RAAS does what:
effects blood pressure by manipulating sodium., potassium and blood volume
BP 140/90 is:
prehypertension
BP 160/100 is:
stage 1 hypertension
BP >160/100 is:
stage 2 hypertension
Clinical presentation of BP:
Asymptomatic
Risk factors for HTN:
Age, DM, hyperlipidemia, family hx, obesity, inactivity, tobacco use
Lab tests for HTN:
BUN, serum creatinine, fasting lipids, blood glucose, electrolytes, Hb/Hct. Values may be normal, but will help identify other cardiac risk factors or end organ damage
HTN complications:
kidney disease, stroke, CVD, retinopathy, PAD
ACE inhibitors:
Inhibits conversion from angiotensin 1 to angiotensin 2. Also blocks bradykinin which causes cough from ACE inhibitors.
ACE inhibitors are proven to:
Reduce cardiovascular risk as well as chronic kidney disease.
ACE inhibitors are first-line therapy for:
DM, stroke, and post MI
ACE inhibitors can increase which electrolyte:
Potassium
Do not use ACE inhibitors during:
Pregnancy
ARB (angiotensin receptor blockers) are:
Similar to ACE inhibitors by blocking angiotensin 2 regardless of pathway. No cough with ARBs. Generally equivalent to ACE however fewer side effects.
Thiazide diuretics are:
First-line medications for HTN or as a combination. They are preferred.
What is the classifications of: Benezepril, Catopril, Enalapril, Fosinopril, Lisinopril, Moxepril, Periindopril, Quinapril, Ramipril, and Trandolapril?
ACE inhibitors for treating HTN
What are the classifications of: Azilsartan, Candesartan, Eprosartan, Irbesartan, Losartan, Olmesartan, Telmisartan, and Valsartan?
ARBs (angiotensin receptor blockers) for treating HTN
Thiazide diuretics are dosed in:
The morning
Thiazide diuretics adverse events are:
Electrolyte abnormalities and hyperuricemia (high uric acid in the blood)
What is the classification of: Chlorthalidone, Hydrochlorothiazide, Indapamide, Metolazone?
Thiazide diuretics
Calcium channel blockers two classes are:
Dihydropyridines (potent vasodilators) and Non-dihydropyrides (decrease heart-rate and AV node conduction)
Calcium channel blockers work by:
Inhibiting the influx of calcium across the membrane
What is the classification of: Amlodipine, Felodipine, Isradipine, Nicardipine, Nifedipine, and Nisoldipine?
Dihydropyridine calcium channel blockers
What is the classification of: Diltiazem (SR, CD, XT, XR, LA), and Verapamil (SR):
Non-dihydropyridine calcium channel blockers
Adverse effects of non-dihydropyridine calcium channel blockers:
Hypotension, AV block, bradycardia
Drug interactions of non-dihydropyridine calcium channel blockers:
CYP 3A4 inhibitors and grapefruit juice
Loop diuretics are:
Treatment of HTN but NOT first-line tx
What is the classification of: Bumetanide, Furosemide and Torsemide:
Loop diuretics
Adverse events of loop diuretics
Hypokalemia and hypocalcemia
What is the classification of: Amiloride, and Triamterene:
Potassium sparing diuretics (for HTN)
What is the classification of: Eplerenone, Spironolactone:
Aldosterone antagonists (for HTN)
What is the classification of: Atenolol, Meteprolol tartrate/succinate?
Cardioselective beta blockers (for HTN)
What is the classification of: Nadolol, Propranolol
Nonselective beta blockers (for HTN)
What is the classification of: Carvedilol, Nebivolol:
Mixed alpha and beta blockers (for HTN)
What is the classification of: Doxazosin, Prazosin, Terazosin:
Alpha blockers (for HTN)
What is the classification of: Aliskiren:
Direct renin inhibitors (for HTN)
What is the classification of: Clonidine, Methyldopa:
Central alpha2-agonists (for HTN)
What is the classification of: Reserpine:
Peripheral Adrenergic Antagonists (for HTN)
What is the classification of: Minoxidil, Hydralazine:
Direct arterial vasodilators (for HTN)
Monitor __ for ACE & ARBs:
BP, BUN, Serum Creatinine, Potassium
Monitor __ for Calcium Channel Blockers and Beta Blockers:
BP, HR
Monitor __ for diuretics:
BP, BUN, Serum Creatinine, Potassium, Magnesium, Sodium - and uric acid for thiazides
Nonpharmacological therapy for HTN:
Weight loses, sodium restriction, limit alcohol, increase physical activity, smoking cessation
Compelling indications for HTN therapy are:
Heart failure with reduced ejection fraction; post MI; Coronary artery disease; DM; Chronic kidney disease; stroke
Chylomicrons, VLDL, LDL, HDL are:
Lipoproteins
Atherogenic development causes/is evidenced by:
Angina, MI, arrhythmias, stroke and PAD
Cytokine recruitment and plaque formation is cause by:
Inflammatory cascade promoted by LDL on the artery wall
Laboratory tests for hyperlipidemia:
TC, LDL, Triglycerides, HDL, CRP, ApoB
Assess these risk factors: ___ every ___ years in patients __ to __ years old.
1: Medical history, physical exam, fasting lipid panel, ASCVD risk. 2: 4- years. 3: 20-79 years old
Target lab values for cholesterol: Total: HDL: LDL: Triglycerides:
Total: <200 mg/dL
HDL: >= 60 mg/dL
LDL: <100 mg/dL
Triglycerides: <150 mg/dL
HMG-CoA Reductase Inhibitors are:
Statins
What statin intensity of:
Atorvastatin 80mg
Rosuvastatin 40mg
High intensity LDL >=50%
What statin intensity of: Atorvastatin 20mg Rosuvastatin 10mg Simvastatin 20-40mg Pravastatin 80mg Lovastatin 80mg Pitavastatin 4mg
Moderate intensity LDL 30-50%
What statin intensity of: Fluvastatin 10-20mg Lovastatin 20mg Pitavastatin 10-20mg Simvastatin 10mg
Low intensity LDL <30%
Statin metabolism for Lovastatin, Simvastatin and
Atorvastatin:
CYP 3A4
Statin metabolism for Fluvastatin and Rosuvastatin:
CYP 2C9
Statin metabolism for Pitavastatin:
UGT1A3
Statin metabolism for Pravastatin:
Not oxidized
Adverse events of statin medications for hyperlipidemia:
Rhabdomyolysis (death of muscle fibers = muscle injury), elevated serum transaminase, PREGNANCY CATEGORY X
Clinical controversies with statin medications:
Cancer, diabetes and cognition
Statin myopathy is __ and how to reverse:
Myopathy, myalgia (muscle pain), myositis (muscle inflammation), rhabdomyopathy - so alway measure baseline CK before initiating - to reverse adverse effects, DC offending agent.
Ezetimibe (Zetia) is:
Cholesterol absorption inhibitor by blocking NPC1L1. Used as second line agent. It lacks the morbidity or mortality benefit in cardiovascular disease. Reduces LDL by 19% as single agent.
What classification is: Fenofibrate, Gemfibrozil:
Fibrate medication that reduces triglycerides by 50%, reduces CVD mortality, provides small increase in HDL.
When is Fenofibrate or Gemfibrozil used:
When triglycerides are >500 mg/dL to treat cholesterol
Adverse events of Fibrates:
Myalgias, renal insufficiency
Drug interactions of Fibrates:
Warfarin (INR concerns) and with Gemfibrozil, statins.
What classification is: Cholestyramine, Colestipol, Colesevela,:
Bile acid sequestrates. Usually have high adverse drug reactions in GI and high drug interaction profiles.
What is a second line agent that can increase HDL and decrease TGs:
Niacin, by reducing hepatic synthesis of VLDL and decreases hepatic removal of HDL.
Adverse effects of Niacin:
flushing, itching, hepatotoxicity, concern for pre-existing gout and DM
What OTC with primary use to treat hypertriglyceridemia and reduce CAD risk:
Omega-3 fatty acids
What adverse event concern with Omega-3 fatty acids:
Alter INR
Nonpharmacological interventions for hyperlipidemia:
Dietary counseling, reduce saturated fats, increase fiber, weight control, physical activity
Treatment goal of hyperlipidemia therapy:
Prevention of ASCVD using fixed dose statin therapy (in moderate to high)
