Dyslipidemia - Pathophysiology

Front 1

Risk factors

Back 1

-Genetics
-Physical inactivity
-Dietary
-Smoking
-ETOH
-DM
-hypothyroidism
-Kidney disease

Front 2

Why transport TGs?

Back 2

-Energy Utilization
-Bile acid formation
-Lipid deposition

Front 3

LDL =

Back 3

= TC - [HDL + (TG/5)]
= TC - HDL - (TG/5)
-only accurate if TG < 400 mg/dL

Front 4

Major apoprotein of HDL

Back 4

apoA-1

Front 5

Disorders of Lipoproteins: Primary Dyslipidemia

Back 5

-6 categories based on composition of elevated lipoprotein(s)
-Gene mutation: deficient or defective LDL-receptor --> elevated LDL
-Xanthomas on hands

Front 6

Disorders of Lipoproteins: Hypertriglyceridemia

Back 6

-Worsened by: obesity, physical inactivity, excessive alcohol use
-When elevated > 1000 mg/dL --> increased risk of acute pancreatitis

Front 7

Secondary dyslipidemia - Increased LDL caused by

Back 7

-hypothyroidism
-nephrotic syndrome
-obs. liver disease
-anabolic steroids

Front 8

Secondary dyslipidemia - Increased TG caused by

Back 8

-Alcoholism
-Dm
-hypothyroidism
-bile acid squestrants
-Systemic estrogens
-Systemic retinoids
-Protease inhibitors

Front 9

Secondary dyslipidemia - Decreased HDL caused by

Back 9

-DM
-hyperthyroidism
-hypertriglyceridemia
-tobacco use
-anabolic steroids

Front 10

Atherosclerosis

Back 10

-hardening of the arteries
-formation of fibrofatty lesions in the intimal lining of the medium and large arteries
-types of lesions associated with atherosclerosis: fatty streaks, fibrous atheromatous plaque,complicated lesion

Front 11

Fatty Streaks

Back 11

-Thin, flat, yellow,intimal discolorations that progressively enlarge by becoming thicker and slightly as they grow in length
-Consists of macrophages and smooth muscle cells that become distended with lipids to form foam cells
-Can occur as early as 1st decade of life until 20 years of age

Front 12

Atheromatous plaque

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-Clinical atherosclerosis
Accumulation of intracellular and extracellular lipids
Profileration of vascular smooth muscle
Formation of scar tissue
-Lesions lead to thickening of vessel intima
Core composed of lipids
Covered by fibrous cap of connective tissue and smooth muscle

Front 13

Screening for dyslipidemia

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-Primary: Every 5 years if >= 20 years old and no known CVD or diabetes
-Secondary: Annually if known atherosclerosis or diabetes

Front 14

CVD Risk Factor Assessment

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1. Age: men >= 45, women >=55
2. Family HX of premature CVD: men <= 55, women <= 65
3. Cigarette smoking
4. Hypertension 140/90
5. Low HDL-C <40
-High HDL-C is a NEGATIVE risk factor >60 (subtract 1)

Front 15

Lower risk

Back 15

-Patients with 0-1 risk factors
-10-year risk of CHD is likely <10%
-No Framingham risk score needed

Front 16

Moderate and moderately high risk

Back 16

-Patients with >=2 risk factors and no CVD or risk equivalent
-Calculate 10-year Framingham risk score
Moderate risk if <10%
Moderately high risk if 10-20%

Front 17

High Risk

Back 17

-No Framingham risk score needed
-Patientswith CHD
-CHD risk equivalent
Non-coronary atherosclerotic vascular disease
Diabetes
Patients with >= 2 risk factors and a 10-year Framingham risk score of > 20%

Front 18

Very high risk

Back 18

-No Framingham risk score needed
-Established CVD and 1 of the following criteria
Mutltiplemajor risk factors
Severe and poorly controlled risk factors
Multiple risk factors for metabolic syndrome
Acute coronary syndromes

Front 19

When does TG become your primary goal?

Back 19

>=500 mg/dL
> 1000 mg/dL increased risk of pancreatitis