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Nayla Foundations > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

What is hyperlipidemia

A

elevation of total cholesterol AND triglycerides, the two main types of lipids

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2
Q

What do cholesterol and triglycerides do

A

Chol: helps form steroid hormones and bile acids
Tg: transfer energy from food to skeletal muscle/adipose

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3
Q

What are lipoproteins

A

how lipids are transported. That contain apoproteins and can be:
Low density (more TG)
High density (more APOPROTEIN)
-VLDL, IDL, LDL, HDL, and chylomicrons

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4
Q

What is the process of lipid transport (VLDL/LDL)

A

Liver uses TG and CHO to make VLDL
VLDL transfers TG to cells. less TG= becomes LDL
LDL provides Chol to cells
Excess LDL taken up by liver, cholesterol excreted into bile

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5
Q

Where is HDL made

A

liver and intestine

helps apoprotein transport by taking CHOL from the cells and bring to liver or other lipoproteins

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6
Q

What preventions exist for CVD

A

Primary: preventing HLD without risk for disease/diet
Secondary: preventing progression and managing disease

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7
Q

What is primary dyslipidemia

A

Genetic abnormality of cholesterol metabolism

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8
Q

What is secondary dyslipidemia

A

Dz develops secondary to:
DM, excess alcohol, hypothyroid, cholestatic liver dz, renal dz, smoking, obesity
Meds (OCP, thiazide, BB, atypical antipsychotics, protease inhibitors (HIV))

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9
Q

What do most clinics measure

A

Total Chol (LDL, VLDL, HDL)
Tg
HDL
—-More difficult to measure VLDL and LDL so measure based on the above measurements

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10
Q

How can you tell what VLDL contains when calculating a lipid fraction

A

VLDL have 5x more Tg than chol

VLDL cholesterol= TG/5

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11
Q

How can you calculate LDL cholesterol

A

Total cholesterol- HDL cholesterol- TG/5

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12
Q

What are stipulations to calculating lipid levels

A

Pt must be fasting to give lowest TG

Tg level should be <400-500 (best LDL est. if TG <200)

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13
Q

What is ASVCD

A

When fatty materials collect in arterial walls and hardens over time
LDL can no longer put cholesterol into cells so it starts accumulating into plaques

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14
Q

What disorders can lead to ASCVD

A 
Abnormal cholesterol metabolism disorders (genetic, insulin resistance, organ dysfunction) 
Lifestyle factors (sat and trans-fat, obesity, smoking, high BP)
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15
Q

How does plaque formation occur

A

small dense LDL enters and sticks to artery wall, triggering cascade
LDL is oxidized, attracting macrophages
Endothelial dysfunction
Vasoconstriction
–Usually not symptomatic (angina) until obstructive to blood flow

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16
Q

What can plaque rupture lead to

A

they are free to travel and can lodge in:
coronary arteries (MI)
brain (CVA/TIA)

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17
Q

What are the CVD risk factors

A

Non-modifiable (age, sex, race, FHx, etc.)

Modifiable (smoking, weight, diet, HTN, renal dz, low HDL)

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18
Q

What CVD risk factor calculators exist

A

Framingham risk score (what is the chance they will have a cardiac incident in the next 10 years) Non-DM
ACC/AHA risk score (what is the chance they will develop HD or stroke in the next 10 years)

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19
Q

What can lowering cholesterol reduce

A

Morbidity and mortality in men and women, middle aged and older

20
Q

How does LDL reduction affect risk

A

1% LDL reduction= 1-1.5% CV risk reduction

2-3% HDL increase= 2-4% CV risk reduction

21
Q

What evidence of CVD or secondary causes of HLD could you see on PE

A 
elevated BP, BMI, waist circumference
Xanthomas, rashes
Corneal arcus, lipemia retinalis, AV nicking
Adventitious sounds in lungs 
PMI, extra heart sounds
hepatomegaly, kidney mass, bruits
edema, PAD, diabetic foot
abnormal DTR
22
Q

How do most HLD patients present

A

asymptomatic!

However, can have xanthomatous tendons, corneal arcus, lipemia retinals, xanthelasma, eruptive xanthomas

23
Q

What are the NCEPP ATP III guidelines for treating ASCVD

A
  1. Obtain fasting lipid profile (9-12 hours) LDL, HDL, total chol
  2. ID CHD risk equivalents (CAD, PAD, AAA, DM)
  3. Presence of major risk factors (smoking, HTN, HDL <40, FHx premature HD, men >45, women >55)
  4. Use framingham for 10 year risk (>20% if w/ CHD risk equivalent) (10-20% if 2+RF) (<10% if 0-1 RF)
  5. Determine risk category (CHD risk equivalent, LDL <70) (2+ RF, LDL <100) (0-1 RF, LDL <160)
  6. Initiate TLC if LDL above goal (can reduce LDL 25-30%)
  7. Add drug therapy if LDL still above goal after 3 mo.
  8. ID (3+ RF) and treat metabolic syndrome
  9. Treat elevated Tg and low HDL
24
Q

What is the ATP III classification for lipids

A

LDL: optimal <100 (If with CAD, <70)
Total chol: desirable <200
HDL: low <40 (low women <50)

(step 9 says normal Tg are <150)

25
Q

What factors make up TLC

A

AHA low fat diet (<30% kcal from fat, sat fat <7%)
Diet chol. intake <200 mg
Increase soluble fiber (10-25 g)
Add plant stanols
Aggressive weight management
Increase phys activity (30 min most days)

26
Q

What are Metabolic Syndrome RF

A 
Abdominal obesity (men >40, women >35)
TG >150
Low HDL (men <40, women <50)
High BP (>130/85)
Impaired fasting glucose (>100mg)
27
Q

How can you treat elevated TG and low HDL (step 9)

A

TG: add nicotinic acid/fibrate to lower VLDL
If >200, statin therapy the add non-statins
HDL: exercise, increase MONOUNSATURATED fats, smoking cessation, mod EtOH intake (1-2xday)

28
Q

What are the ACC/AHA guidelines on screening

A

Adults 21+
Every 5 years for low risk
More often if close to therapeutic threshold

29
Q

Who does the ACC/AHA say SHOULD be treated with statins

A

Anyone with ASCVD
Adults with LDL >190 (extreme)
40-75 y/o w/ DM or LDL 70-189
40-79 y/o w/ 10 year risk >7.5%

30
Q

What are the ACC/AHA HIGH intensity treatment recommendations

A

anyone with ASCVD
Adults w/ LDL >190
** treat w/ Atorvastatin (40/80) or Rosuvastatin (20/40)
Should reduce LDL 50% in 3 mo.

31
Q

What are the ACC/AHA treatment recommendations for DM patients

A

Moderate intensity statin (30-50% LDL reduction)
-Atorvastatin 10-20
Simvastatin 20-40
Pravastatin 40

32
Q

What are the ACC/AHA treatment recommendations for its with LDL >70

A

Moderate-high intensity statin

33
Q

What are HMG CoA reductase inhibitors

A 
Statins;
Inhibit cholesterol formation
Reduce mortality
Best dosed at night (when chol. is made) 
**LDL decrease 20-55%
34
Q

Who are Statins contraindicated in

A

Pregnancy/BF
Liver dz
High TG

35
Q

What are side effects of Statins

A

Myalgia/Rhabdo
Hepatotoxicity (measure LFT/CK)
DM risk

36
Q

What are cholesterol absorption inhibitors

A

-Ezetimibe-
decrease absorption of cholesterol in SMALL INTESTINE
**LDL decrease 15-20%

37
Q

What are contraindications to cholesterol absorption inhibitors

A

Caution hepatic impairment

DON’T USE with fibrates

38
Q

What are fabric acid derivatives

A

-Fenofibrate, Gemfibrozil-
Reduce synthesis/increase breakdown of VLDL
**Use if TG >500 (TG decrease 40%)

39
Q

What are contraindications for fibrins

A

Don’t use with statins (increased rhabdo risk)

40
Q

What does Niacin (B3) do

A

Reduced VLDL production
Short or long acting (long better)
**HDL increase 25-35%
-Flushing

41
Q

What are contraindications for Niacin

A

Pregnancy, BF, liver dz, PUD

Caution Gout, DM

42
Q

What are Bile acid binding resins

A

-Colestipol, Cholestyramine, Colesevelam
bind bile acids in INTESTINE so liver makes more bile (uses chol to make bile acid)
**SAFE IN PREGNANCY!!
Decrease LDL 15-25% (may increase TG)

43
Q

What are bile acid binding resin contraindications

A

GI obstruction
HTG
Pancreatitis

44
Q

What are PCSK9 inhibitors

A

-Alirocumab, Evolocumab-
block PCSK9 so LDL receptors are NOT degraded and can bind more LDL
**LDL decrease 50-60%
Good for non-tolerance of statins, but $$

45
Q

What is familial hypercholesterolemia

A

LDL receptors absent/dysfunctional
Homozygotes start as kids
Heterozygotes start in 30’s

46
Q

What is familial hyperchylomicronemia

A

Lipoprotein lipase abnormality that allows periphery to take up TG from chylomicron and VLDL
Causes HIGH TG

Nayla Foundations (18 decks)

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