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Gen Med: Ednocrine > Lipid pathologies > Flashcards

Lipid pathologies Flashcards

1
Q

What is the fate of lipids?

A

Fats that are either absorbed from foods or synthesized by liver

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2
Q

Where are trigs stored?

A

Triglycerides store energy in adipocytes & muscle cells

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3
Q

What is the role of cholesterol?

A

constituent of cell membranes, steroids, bile acids

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4
Q

How is cholesterol transported?

A

Most cholesterol is carried in LDL and HDL

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5
Q

How are most triglycerides transported?

A

transported in chylomicrons or VLDL

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6
Q

What are the 5 major classes of lipoproteins?

A
  1. Lipoproteins are divided into five major classes, based on density:
    A. Chylomicrons
    B. Very low-density lipoproteins (VLDL)
    C. Intermediate-density lipoproteins (IDL)
    D. Low-density lipoproteins (LDL)
    E. High-density lipoproteins (HDL)
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7
Q

Define hyperlipidemia

A

A group of disorders characterized by an excess of serum cholesterol, especially excess LDL-C &/or excess triglycerides

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8
Q

What causes abnormal lipoprotein metabolism? What follows?

A
  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
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9
Q

What causes primary dyslipidemia/hyperlipoprooteinemia?

A
  1. Gene mutations
  2. Familial combined hypercholesterolemia most common primary
    A. ↑ Triglycerides & cholesterol & ↓ plasma HDL-C
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10
Q

Are secondary or primary dyslipidemia/hyperlipoprooteinemia?

A

Secondary

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11
Q

What are the secondary causes of hyperlipidemia?

A
  1. DM
  2. Glycogen storage diseases
    A. Genetic or acquired enzyme defic. disorders
  3. Lipodystophies
    A. Abn. or degenerative conditions of adipose tissue
  4. Excessive steroid use
  5. ETOH
  6. OCP’s
  7. Renal Dz
  8. Hepatic dysfunction
  9. Hypothyroidism
  10. Cushing’s Syndrome
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12
Q

What is isolated hypercholesterolemia?

A

due mostly to high LDL

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13
Q

What is mixed dyslipidemia?

A

– high total or LDL cholesterol + high triglycerides

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14
Q

What is isolated hypertriglyceridemia?

A

inc trig

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15
Q

What is Low HDL cholesterol?

A

alone or w/ high total cholesterol or high triglycerides

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16
Q

What is the epidemiology for lipid pathologies?

A
  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
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17
Q

What are the risk factors for lipid disorders?

A
  1. Habitual excessive alcohol use
  2. Obesity
  3. Lack of exercise
  4. M > W
  5. Ethnic groups adopting a ‘western’ lifestyle
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18
Q

What is the most typical sxs of lipid pathologies?

A
  1. Typically asymptomatic

A. Incidental diagnosis from routine blood work

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19
Q

What sxs are indicative of lipid pathologies?

A 
1. Xanthelasmas
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
A. Pancreatitis
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20
Q

What are the dx studies for lipid pathologies?

A
  1. Screening total cholesterol & HDL (+/- fasting)
21
Q

When is a fasting lipid profile performed?

A
  1. Abnormal screening test

2. (+) CHD

22
Q

When does the US Preventive Services Task Forcerecommend screening for lipid pathologies?

A 
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
23
Q

What is step one in management of abnormal fasting lipid profile?

A

Evaluate results of LDL, total & HDL cholesterol levels

24
Q

What is step two in management of abnormal fasting lipid profile?

A
  1. Identify CHD and CHD risk equivalents
  2. Clinical CHD
  3. Symptomatic carotid artery disease (TIA/Stroke of carotid source)
  4. PAD
  5. AAA
  6. DM
25
Q

What is step three in management of abnormal fasting lipid profile?

A 
1. Evaluate for other major risk factors (other than LDL)
A. HTN
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
26
Q

What is step four in management of abnormal fasting lipid profile?

A
  1. If 2+ risk factors (in addition to ↑ LDL) & no CHD or CHD risk equivalents
    A. Assess 10yr CHD risk (Framingham tables)
27
Q

What is step five in management of abnormal fasting lipid profile?

A
  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
28
Q

What is step six in management of abnormal fasting lipid profile?

A 
1. Initiate TLC if LDL above goal
A. Diet low in saturated fats & cholesterol
B. ↑ Soluble fiber
C. Weight reduction
D. ↑ Physical activity
29
Q

What is step seven in management of abnormal fasting lipid profile?

A
  1. Consider drug therapy

2. See STEP V guidelines

30
Q

What is step eight in management of abnormal fasting lipid profile?

A
  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
    B. HTN
    C. ASA if CHD
31
Q

What is step nine in management of abnormal fasting lipid profile?

A

Treat elevated triglycerides if present

32
Q

What are the treatment recommendations for Individuals w/ clinical ASCVD?

A

receive high-intensity statin therapy (moderate-intensity for those patients >75 years)

33
Q

What are the treatment recommendations for Individuals w/ primary elevations of LDL–C ≥190 mg/dL?

A

receive high-intensity statin therapy

34
Q

What are the treatment recommendations for Individuals 40 to 75 yr w/ DM & LDL-C 70 to 189 mg/dL?

A

receive at least moderate-intensity statin therapy

35
Q

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?

A

receive moderate- or high-intensity statin therapy

36
Q

What is high intensity statin therapy?

A
  1. daily dose lowers LDL on average by approximately >50%
  2. Ex. Atorvastatin (lipitor) 40-80 mg
    Rosuvastatin (crestor) 20-40 mg
37
Q

What is moderate intensity statin therapy?

A
  1. daily dose lowers LDL on average by approximately 30-50%
  2. Ex.
    Atorvastatin (Lipitor) 10–20 mg
    Rosuvastatin (Crestor) 5–10 mg
    Simvastatin(Zocor) 20–40 mg
    Pravastatin (Pravachol)40–80 mg
38
Q

What is low intensity statin therapy?

A 
daily dose lowers LDL on average by approximately <30
2. Ex. 
Simvastatin 10 mg
Pravastatin 10-20
Fluvastatin 20-40
39
Q

What is the moa of HMG CoA Reductase Inhibitors statins?

A
  1. Inhibit enzyme used in cholesterol synthesis
  2. Upregulate LDL receptors
  3. Increase LDL clearance
40
Q

What are the se of statins?

A
  1. Myositis, myalgias, rhabdomyolysis (risk ↑ when used w/ niacin or fibrate)
  2. Elevated LFT’s
41
Q

What are the statins?

A

Lovastatin (Mevacor), Atorvastatin (Lipitor), Simvastatin (Zocor) Fluvastatin (Lescol), Pravastatin (Pravachol), rosuvastatin (Crestor)

42
Q

What is the moa of the bile acid sequestrants?

A
  1. Bind bile acid in intestine preventing reabsorption

2. Lower hepatic cholesterol

43
Q

When are bile acid sequestrants used?

A

Used w/ statin or nicotinic acid

Synergistic effect

44
Q

What are the bile acid sequestrants?

A

Cholestyramine (Questran/Light), colestipol (Colestid), colesevelam (Welchol)

45
Q

What is the moa of nicotinic acid (Vit. B3) What can it be used with?

A
  1. Decreases hepatic LDL/VLDL production
  2. Can be used with statins/bile acid sequestrants
  3. Niacin, Niaspan
46
Q

What is the moa and effects of fibric acid?

A
  1. MOA unknown
  2. Inhibits trig synthesis & stimulates catabolism of trig-rich lipoproteins
  3. ↑ HDL
  4. Gemfibrozil (Lopid), fenofibrate (Tricor), finofibric acid (Trilipix)
47
Q

What is the moa of Ezetimibe (Zetia)?

A
  1. Inhibits cholesterol absorption in small intestine

2. Used alone or w/statin

48
Q

What homeopathic remedies are available for high cholesterol?

A
  1. Red Yeast Rice
  2. Psyllium
  3. Coenzyme Q-10
49
Q

What pt education needs to take place?

A
  1. For each 1% reduction in the level of LDL-C, there is a 1% to 1.5% reduction in the risk of major cardiovascular events
  2. Lifestyle modifications
    A. Weight loss, exercise, & dietary changes
    B. Key in long-term management

Gen Med: Ednocrine (8 decks)

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