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344 > Dyslipidemia Screening and Assessment > Flashcards

Dyslipidemia Screening and Assessment Flashcards

1
Q

• Dyslipidemia defintion
• Abnormal ____ in the blood
• Elevation of _____ lipoprotein(s) or reduced ____
4 main category

A

fats
≥1, HDL‐C

  • Low‐density lipoprotein (LDL‐C) = “bad” cholesterol
  • High‐density lipoprotein (HDL‐C) = “good” cholesterol
  • Total cholesterol (TC) = all lipoproteins
  • Triglycerides (TG)
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2
Q

interchangeable terms to dyslipidemia

A
  • Hyperlipidemia (hypercholesterolemia)
  • Hypertriglyceridemia
  • Isolated hyperlipidemia/dyslipidemia
  • Mixed hyperlipidemia/dyslipidemia
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3
Q

primary vs secondary dyslipidemia

A
  • Primary = genetic cause
  • Known as familial hypercholesterolemia (FH)
  • Most common cause in children
  • Secondary = other causes
  • Most common cause in adults
  • Sedentary lifestyle
  • Excessive dietary intake of fat or EtOH
  • Diseases (hypothyroidism, kidney/liver disease)
  • Cigarette smoking
  • Drugs
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4
Q

what is familial hypercholesterolemia (FH)?

A
  • Autosomal dominant genetic disorder
  • High LDL‐C level  premature CVD
  • Normal: 2‐5 mmol/L
  • Heterozygous (1/500): 5‐13 mmol/L
  • Homozygous (1/1,000,000): >13 mmol/L
  • Require aggressive treatment:
  • Pharmacologic (e.g., statins)
  • Non‐pharmacologic (LDL‐C apheresis)
  • Goal: 50% reduction in LDL‐C
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5
Q

how might homozygous FH present?

A 
young age
Deposits of cholesterol leading to bumps
Right coronary artery
No vessel for left, blocked off right side
At 5 years old
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6
Q

Drugs Causes of Dyslipidemia

A
  • Amiodarone
  • β‐blockers (non‐ISA)
  • Carbamazepine
  • Clozapine
  • Corticosteroids
  • Cyclosporine
  • Loop diuretics
  • Oral contraceptives
  • Olanzapine
  • Phenobarbital
  • Phenytoin
  • Protease inhibitors
  • Retinoids
  • Thiazide diuretics
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7
Q

Pathophysiology

CAD Coronary artery disease

A
  • Positive association between high TC or LDL‐C and CAD
  • Inverse association between high HDL‐C and lower risk of CAD/atherosclerosis regression
  • Relationship between TG and CAD has not been established
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8
Q

Signs and Symptoms

A
  • Most patients are asymptomatic
  • Possible signs:
  • Xanthoma/xanthelasma (skin condition in which certain fats build up under the surface of the skin)
  • Corneal arcus (arcus senilis) ( gray or white arc visible above and below the outer part of the cornea)
  • Carotid bruits (a vascular sound usually heard with a stethoscope over the carotid artery because of turbulent, non-laminar blood flow through a stenotic are)
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9
Q

Who to Screen

A

• Men ≥40 and Women ≥40 or postmenopausal
• Consider earlier screening in high‐risk ethnic populations (e.g., South
Asians, First Nations)
• Clinical evidence of atherosclerosis
• Abdominal aortic aneurysm (AAA)
• Diabetes mellitus (DM)
• Arterial HTN
• Current cigarette smoker
• Stigmata of dyslipidemia (corneal arcus, xanthelasma, xanthoma)
• FamHx of premature CVD (1° relative)
-=->Men <55 or women <65 years of age
• FamHx of dyslipidemia
• CKD (eGFR <60 mL/min/1.73 m2 or ACR ≥3 mg/mmol)
• Obeseity (BMI >30 kg/m2)
• Inflammatory diseases (e.g., rheumatoid arthritis, systemic lupus erythematosus)
• HIV infection
• Erectile dysfunction
• Chronic obstructive pulmonary disease (COPD)
• History of hypertensive disorder of pregnancy [gestational diabetes mellitus (GDM), pre‐term birth (PTB), stillbirth, low birthweight, placental abruption/infarction]

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10
Q

Risk Factors for Atherosclerotic Cardiovascular Disease

modifiable

A

HTN, smoking, dyslipidemia, diabetes, obesity, alcohol misuse, unhealthy diet, phys inactivity, pscyhosocial factors

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11
Q

Risk Factors for Atherosclerotic Cardiovascular Disease

nonmodifiable

A

genetic, race/ethnicity, gender, aging

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12
Q

Risk Assessment

what is FRS used in practice to determine?

A

Framingham Risk Score (FRS)
• Risk prediction tool
• Weights the relative contributions of all of the CVD risk factors a patient
possesses
• Estimates 10‐year risk of total CVD = CAD, stroke, PAD, heart failure
• Reported as a percentage

  • Used in practice to determine:
  • Risk level
  • Treatment recommendation
  • Therapeutic target
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13
Q

Primary vs Secondary Prevention

when to use FRS?

A

Does the patient have CVD?
No –> primary prevention, use FRS
Yes –> secondary prevention, high risk

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14
Q

Secondary Prevention

• Examples of CVD:

A
  • MI or ACS
  • Stable angina or documented CAD by coronary angiogram
  • Previous CABG surgery
  • ACS (myocardial infarction or unstable angina)
  • Stroke, transient ischemic attack [TIA], or carotid
  • PAD, defined as significant claudication (a condition in which cramping pain in the leg is induced by exercise) or ankle‐brachial index (ABI) < 0.90 (calf pain)
  • Abdominal aortic aneurysm (AAA) ‐‐ an abdominal aorta measuring >3.0 cm or previous AAA surgery
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15
Q

High Risk Patients

3 types

A

• Most Patients with DM:
• Any patient ≥40, patients ≥30 with DM for >15 yr or
patients with microvascular complications

• CKD:
• Age >50 yrs and >3 months duration (not a single
measure) with eGFR <60 mL/min/1.73 m2 or ACR >3
mg/mmol

• Familial Hypercholesterolemia (FH):
• LDL‐C >5.0 mmol/L or documented FH (genetic
testing), after excluding all secondary causes

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16
Q

Components of FRS

A 
• Age (yr)
• HDL‐C and TC (but not LDL‐C) (mmol/L)
• Systolic blood pressure (mmHg)
• DM (yes or no)
• Smoking status (yes or no)
Only need to calculate for patients without a statin indicated condition –calculate for all primary prevention patients
17
Q

what are the FRS risk levels?

what is the modified FRS

A

High FRS ≥20% or established CVD
Intermediate FRS 10 – 19%
Low FRS <10%

• Multiply FRS x 2 for any patient with positive FamHx
of premature CVD (referred to as the “modified FRS”)
• positive FamHx = men <55 yrs old or women <65 yrs old in first degree relatives (parents, siblings)

18
Q

Metabolic Syndrome

A 
- aka syndrome X
central obesity, apple central adiposity 
high bp
high tg
lol HDL-cholesterol
insulin resistance'

• No uniform classification system
• Higher risk than individual risk factors alone?
• No clinical trial has investigated the treatment of
patients with metabolic syndrome
• Recommend using FRS for risk assessment not the
metabolic syndrome criteria

19
Q

how to screen, what lab tests?

A

For all:
• History and physical examination
• Standard lipid profile: total cholesterol (TC), low‐density lipoprotein cholesterol
(LDL‐C), high‐density lipoprotein cholesterol (HDL‐C), non‐HDL‐C, triglycerides (TG)
• Fasting plasma glucose (FPG) or glycated hemoglobin (A1c)
• estimated glomerular filtration rate (eGFR)
• Lipoprotein(a) [Lp(a)] – once in a person’s lifetime, with initial screening
Optional:
• Apolipoprotein B (ApoB)
• Urine Albumin to Creatinine ratio (ACR) – should be checked if patient has an
eGFR <60 mL/min/1.73 m2, hypertension, or diabetes.

20
Q

LDL‐C
positioned in clinical trials as a treatment target and is emphasized in worldwide guidelines as the __________

  • the gold standard of LDL‐C measurement has been preparative ultracentrifugation (lab technique), but given its time requirements and expenses, it is _________
  • Friedwald equation – developed in 1972:
A

primary cholesterol target

calculated rather than measured directly

• LDL‐C (mmol/L) = TC ‐ HDL‐C ‐ TG/2.2
inaccuracy at low LDL‐C and/or high TG levels, where errors in estimating VLDL‐C are magnified given its use of a fixed factor of 2.2
This equation cannot be used if TG’s >4.5 mmol/L ‐‐ lab will not give an LDL‐C value
Estimates of accuracy in predicting LDL‐C reported to be ~60%

21
Q

Apolipoprotein B (ApoB)

Each of the atherogenic lipid particles (LDL, Lp(a), IDL, VLDL) contain _______
• serum concentration of Apo B reflects the
total number of these particles in the circulation
• Measuring apo‐ B provides information
about the _________
• Available as routine laboratory value in all
provinces except Ontario

A

1 molecule of ApoB

number and total atherogenicity of the lipid profile

22
Q

Non‐HDL‐C

A

• New alternate target in 2012 guidelines when ApoB was not uniformly available in Canadian labs
• Provides an estimated sum of all atherogenic lipoproteins
• Calculation: TC – HDL‐C
• May be a more practical choice of a lab parameter to evaluate atherogenicity of lipid profile – no additional expense to health care system and routinely
provided on lab report with a lipid panel (or clinician can calculate)

23
Q

We recommend that for any patient with triglycerides > 1.5 mmol/L, _________ be used instead of ________ as the preferred lipid parameter
for screening.

A

non‐HDL‐C or ApoB instead of LDL-C

  • Rationale:
  • above this level of triglyceride, some cholesterol in LDL particles is replaced by triglyceride, which promotes production of more atherogenic small dense LDL particles, and makes the amount of cholesterol in LDL‐C an unreliable reflection of actual LDL particle number
24
Q

TG
Causes of hypertriglycericemia:

• Reducing TG with pharmacologic therapy does what?

A
  • high dietary fat intake
  • excessive EtOH (binge)
  • poor DM control
  • Very high TG associated with pancreatitis
  • recommend specific TG‐lowering treatment to prevent this risk if TG >10 mmol/L
  • Reducing TG with pharmacologic therapy does not reduce CV events
  • Proven by multiple randomized control trials
25
Q

Laboratory Evaluation of Lipids

benbefits of non-fasting lipid evaluation?

A

• Currently, non‐fasting lipid evaluation recommended, unless patient has very elevated TG’s
Patient convenience – no need to go to lab early in the morning and fasting; no
need for retesting if not fasting
• ↓ wait times and reduced early morning patient burden in labs
• Safety – prevention of hypoglycemic episodes in diabetics
• Enhances compliance ‐ avoids delay in screening & follow up tests
• Enhanced predictive value for CVD & mortality of nonfasting lipids
• Identification of high remnants/insulin resistance
• Removal of need to perform fasting blood work generally
• HbA1c is accepted as a diagnostic & follow up test by CDA/ADA that does NOT have to be accompanied by a fasting glucose

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