Flashcards in Lipid pathologies Deck (49):
What is the fate of lipids?
Fats that are either absorbed from foods or synthesized by liver
Where are trigs stored?
Triglycerides store energy in adipocytes & muscle cells
What is the role of cholesterol?
constituent of cell membranes, steroids, bile acids
How is cholesterol transported?
Most cholesterol is carried in LDL and HDL
How are most triglycerides transported?
transported in chylomicrons or VLDL
What are the 5 major classes of lipoproteins?
1. Lipoproteins are divided into five major classes, based on density:
B. Very low-density lipoproteins (VLDL)
C. Intermediate-density lipoproteins (IDL)
D. Low-density lipoproteins (LDL)
E. High-density lipoproteins (HDL)
A group of disorders characterized by an excess of serum cholesterol, especially excess LDL-C &/or excess triglycerides
What causes abnormal lipoprotein metabolism? What follows?
1. Defects in lipoprotein synthesis, processing & clearance
2. Accumulation of lipids in plasma & vessel endothelium
3. High LDL & low HDL associated with increased risk for ASHD
What causes primary dyslipidemia/hyperlipoprooteinemia?
1. Gene mutations
2. Familial combined hypercholesterolemia most common primary
A. ↑ Triglycerides & cholesterol & ↓ plasma HDL-C
Are secondary or primary dyslipidemia/hyperlipoprooteinemia?
What are the secondary causes of hyperlipidemia?
2. Glycogen storage diseases
A. Genetic or acquired enzyme defic. disorders
A. Abn. or degenerative conditions of adipose tissue
4. Excessive steroid use
7. Renal Dz
8. Hepatic dysfunction
10. Cushing’s Syndrome
What is isolated hypercholesterolemia?
due mostly to high LDL
What is mixed dyslipidemia?
– high total or LDL cholesterol + high triglycerides
What is isolated hypertriglyceridemia?
What is Low HDL cholesterol?
alone or w/ high total cholesterol or high triglycerides
What is the epidemiology for lipid pathologies?
1. T chol & LDL-C levels are similar in whites and blacks
2. Trig lower & HDL-C levels higher in African-Americans
3. Asian-Indians have the highest risk
4. Chinese have the lowest risk
5. Europeans have intermediate risk
6. Differences in lipid levels can be partly explained by dietary & lifestyle differences
What are the risk factors for lipid disorders?
1. Habitual excessive alcohol use
3. Lack of exercise
4. M > W
5. Ethnic groups adopting a 'western' lifestyle
What is the most typical sxs of lipid pathologies?
1. Typically asymptomatic
A. Incidental diagnosis from routine blood work
What sxs are indicative of lipid pathologies?
A. Yellow plaques on medial aspect of eyelids
2. Arcus (Senilis) Corneae
A. Onset <45 y/o
B. White/gray ring around corneal margin
3. Eruptive xanthomas
A. Subcutaneous nodules along tendons/ligaments
4. GI manifestations
What are the dx studies for lipid pathologies?
1. Screening total cholesterol & HDL (+/- fasting)
When is a fasting lipid profile performed?
1. Abnormal screening test
2. (+) CHD
When does the US Preventive Services Task Forcerecommend screening for lipid pathologies?
1. Based on risk factors, age and sex
A. (+) Risk factors for CAD
Begin: M @ 25 yr
F @ 35 yr
B. (-) Risk factors for CVD
Begin: M @ 35 yr,
F @ 45 yr
What is step one in management of abnormal fasting lipid profile?
Evaluate results of LDL, total & HDL cholesterol levels
What is step two in management of abnormal fasting lipid profile?
1. Identify CHD and CHD risk equivalents
2. Clinical CHD
3. Symptomatic carotid artery disease (TIA/Stroke of carotid source)
What is step three in management of abnormal fasting lipid profile?
1. Evaluate for other major risk factors (other than LDL)
B. Cigarette smoking
C. FH premature CHD
-M < 55 yr
-F < 65 yr
D. Low HDL
-High HDL >60 subtract 1 risk factor
E. Patient age
-M ≥ 45 yr
-F ≥ 55 yr
What is step four in management of abnormal fasting lipid profile?
1. If 2+ risk factors (in addition to ↑ LDL) & no CHD or CHD risk equivalents
A. Assess 10yr CHD risk (Framingham tables)
What is step five in management of abnormal fasting lipid profile?
1. Determine risk category using ATP III to
A. Establish LDL goal therapy
B. Determine need for therapeutic lifestyle changes (TLC)
C. Determine level for drug consideration
What is step six in management of abnormal fasting lipid profile?
1. Initiate TLC if LDL above goal
A. Diet low in saturated fats & cholesterol
B. ↑ Soluble fiber
C. Weight reduction
D. ↑ Physical activity
What is step seven in management of abnormal fasting lipid profile?
1. Consider drug therapy
2. See STEP V guidelines
What is step eight in management of abnormal fasting lipid profile?
1. Identify Metabolic Syndrome
A. Abdominal obesity, ↑ triglycerides, ↓ HDL, HTN, Impaired FBS
2. Treat triglycerides/HDL if remains abnormal after 3 mo lifestyle changes
3. Treat underlying metabolic syndrome
A. Weight loss, physical activity
C. ASA if CHD
What is step nine in management of abnormal fasting lipid profile?
Treat elevated triglycerides if present
What are the treatment recommendations for Individuals w/ clinical ASCVD?
receive high-intensity statin therapy (moderate-intensity for those patients >75 years)
What are the treatment recommendations for Individuals w/ primary elevations of LDL–C ≥190 mg/dL?
receive high-intensity statin therapy
What are the treatment recommendations for Individuals 40 to 75 yr w/ DM & LDL-C 70 to 189 mg/dL?
receive at least moderate-intensity statin therapy
What are the treatment recommendations for Individuals 40 to 75 yr w/out clinical ASCVD or DM w/ LDL-C 70 to 189 mg/dL & estimated 10-year ASCVD risk of 7.5% or higher?
receive moderate- or high-intensity statin therapy
What is high intensity statin therapy?
1. daily dose lowers LDL on average by approximately >50%
2. Ex. Atorvastatin (lipitor) 40-80 mg
Rosuvastatin (crestor) 20-40 mg
What is moderate intensity statin therapy?
1. daily dose lowers LDL on average by approximately 30-50%
Atorvastatin (Lipitor) 10–20 mg
Rosuvastatin (Crestor) 5–10 mg
Simvastatin (Zocor) 20–40 mg
Pravastatin (Pravachol) 40–80 mg
What is low intensity statin therapy?
daily dose lowers LDL on average by approximately <30
Simvastatin 10 mg
What is the moa of HMG CoA Reductase Inhibitors statins?
1. Inhibit enzyme used in cholesterol synthesis
2. Upregulate LDL receptors
3. Increase LDL clearance
What are the se of statins?
1. Myositis, myalgias, rhabdomyolysis (risk ↑ when used w/ niacin or fibrate)
2. Elevated LFT’s
What are the statins?
Lovastatin (Mevacor), Atorvastatin (Lipitor), Simvastatin (Zocor) Fluvastatin (Lescol), Pravastatin (Pravachol), rosuvastatin (Crestor)
What is the moa of the bile acid sequestrants?
1. Bind bile acid in intestine preventing reabsorption
2. Lower hepatic cholesterol
When are bile acid sequestrants used?
Used w/ statin or nicotinic acid
What are the bile acid sequestrants?
Cholestyramine (Questran/Light), colestipol (Colestid), colesevelam (Welchol)
What is the moa of nicotinic acid (Vit. B3) What can it be used with?
1. Decreases hepatic LDL/VLDL production
2. Can be used with statins/bile acid sequestrants
3. Niacin, Niaspan
What is the moa and effects of fibric acid?
1. MOA unknown
2. Inhibits trig synthesis & stimulates catabolism of trig-rich lipoproteins
3. ↑ HDL
4. Gemfibrozil (Lopid), fenofibrate (Tricor), finofibric acid (Trilipix)
What is the moa of Ezetimibe (Zetia)?
1. Inhibits cholesterol absorption in small intestine
2. Used alone or w/statin
What homeopathic remedies are available for high cholesterol?
1. Red Yeast Rice
3. Coenzyme Q-10