Dyslipidemia resident survival guide
Synonyms and keywords: HDL, LDL, VLDL, hyperlipidemia, hypolipidemia, statin

# Overview
Dyslipidemia is a metabolic abnormality that leads to an increase in the plasma concentrations of cholesterol and triglycerides. Lipoprotein abnormalities can be classified on the bases of the pattern of change in the lipoprotein levels, etiology, and the type of lipid that is increased. Dyslipidemia can be caused by endocrine disorders such as hypothyroidism, diabetes mellitus, medications such as protease inhibitors or antihypertensive, anabolic steroid use, cholestasis, and autoimmune disorders. While screening the disease it is important to identify the cardiovascular disease risk factors among patients. Framingham Risk Assessment Tool and Reynolds Risk Score are utilized to screen for CVD risk and follow-up screening varies with the diabetes mellitus status, patient age, and gender. Treatment involves setting the target cholesterol levels of < 200 mg/dL, and LDL-C levels of < 70 mg/dL for very high risk patients OR < 100 mg/dL for all other patients. HDL should be as high as possible. Lifestyle recommendations is the first step in treatment before pharmacotherapy. Pharmacotherapy includes monotherapy such as statins (monitor AST, ALT, and CK); fibrates; niacin; and bile acid sequestrants. Uncontrolled dyslipidemia requires combination therapy. Regular follow up with labs to access drug side effects and monitoring patient health is vital.

# Classification
There are several ways in which lipoprotein abnormalities are classified. Lipoprotein disorders can be classified according to:
- The pattern of change in the lipoprotein levels, described as hyperlipidemia (increase in lipid levels) and hypolipidemia (decrease in lipid levels):  However, this classification is problematic because the lipids and lipoproteins levels in some situation can be elevated in some types of lipoproteins and lipids and decreased in others.
- Phenotype, or the specific type of lipid that is increased, as classified by Fredrickson: This classification is problematic because it does not include abnormalities in the level of HDL.
- Etiology, as primary (genetic) or secondary to another condition: This classification can be problematic because most conditions involve the intersection of genetics and lifestyle issues. However, there are a few well defined genetic conditions that are usually easy to identify.
- Levels of measured lipids (cholesterol and triglycerides), described as hypercholesterolemia and hypocholesterolemia or hypertriglyceridemia and hypotriglyceridemia: This distinction is not specific because it does not reflect the specific lipoprotein(s) that are abnormally high or low.

## Fredrickson Classification of Hyperlipoproteinemia

### Unclassified forms
Non-classified forms are extremely rare:
- Hypo-alpha lipoproteinemia
- Hypo-beta lipoproteinemia (prevalence 0.01-0.1%)

## Classification According to Etiology

## Classification According to Laboratory Results

# Causes
Secondary causes of dyslipidemia may cause either an increase in total-cholesterol & low density lipoprotein-cholesterol (LDL-C) or an increase in total triglycerides & very low density lipoprotein cholesterol (VLDL-C). Common causes are listed below.

## Increase in Total Cholesterol and LDL-C
- Hypothyroidism
- Nephrosis
- Dysgammaglobulinemia (systemic lupus erythematosus, multiple myeloma)
- Cholestatic hepatic diseases due to abnormal lipoproteins (e.g. primary biliary cirrhosis)
- Administration of protease inhibitors (treatment for HIV infection)
- Administration of progestin or anabolic steroids

## Increase in Total Triglycerides and VLDL-C
- Chronic kidney disease
- Type 2 diabetes mellitus
- Obesity
- Excessive alcohol intake, poor diet
- Hypothyroidism
- Administration of anti-hypertensive therapy (thiazide diuretics or B-blockers)
- Administration of corticosteroids, retinoids (depends on the duration of use and type of steroid)
- Severe stress that increases endogenous corticosteroid concentration
- Elevated concentrations of estrogen (administration of oral (not transdermal) estrogen therapy, oral contraceptives, or pregnancy)
- Administration of protease inhibitors (treatment for HIV infection)
To view a comprehensive list of dyslipidemia causes, click here

# Screening
The following algorithm explains the approach to screening for dyslipidemia patients.
Abbreviations: ASA: American society of anesthesiologists; BP: Blood Pressure; CCS: Canadian cardiovascular society; CrCl: Creatinine clearance; CXR:  Chest X-ray; DNI: Do not intubate; DNR: Do not resuscitate; ECG: Electrocardiogram; eGFR: estimated glomerular filtration rate; HR:Heart rate; INR: International normalized ratio; LMWH: Low molecular weight heparin; LV: Left ventricle; LVED: Left ventricular ejection fraction; NOAC: Novel oral anticoagulant; NPO: Nothing per os; PMI: Point of maximal impulse; PT: Prothrombin time; RR: Respiratory rate;  SpO2: Oxygen saturation; T: Temperature; VT: Ventricular tachycardia

# Complete Diagnostic Approach
The algorithm explains the approach to the diagnosis of dyslipidemia.
Boxes in red signify that an urgent management is needed.
Abbreviations: ASA: American society of anesthesiologists; BP: Blood Pressure; CCS: Canadian cardiovascular society; CrCl: Creatinine clearance; CXR:  Chest X-ray; DNI: Do not intubate; DNR: Do not resuscitate; ECG: Electrocardiogram; eGFR: estimated glomerular filtration rate; HR:Heart rate; INR: International normalized ratio; LMWH: Low molecular weight heparin; LV: Left ventricle; LVED: Left ventricular ejection fraction; NOAC: Novel oral anticoagulant; NPO: Nothing per os; PMI: Point of maximal impulse; PT: Prothrombin time; RR: Respiratory rate;  SpO2: Oxygen saturation; T: Temperature; VT: Ventricular tachycardia

# Treatment
The algorithm demonstrates the treatment strategy for patients with confirmed dyslipidemia.

# Do's
- Treat pediatric patients who are older than 8 years of age with either LDL-C > 190 mg/dL or LDL > 160 mg/dL plus any of the following conditions: either  2 CV risk factors even after lifestyle intervention, family history of premature CAD, or overweight/obese/insulin resistance.

# Don'ts
- Do not routinely order homocysteine, uric acid, plasminogen activator inhibitor 1, or other inflammatory markers.
- Do not routinely perform non-invasive measures of atherosclerosis (e.g. carotid intima media thickness).
- Do not treat dyslipidemia among postmenopausal women with hormonal replacement therapy.