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Hyperlipidemia Flashcards

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1
Q

Hyperlipidemia

A

Elevated TG & total cholesterol

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2
Q

Cholesterol forms what?

A

Forms steroid hormones/bile acids.

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3
Q

Triglyceride function

A

Transfers energy from food to cells.

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4
Q

Lipoproteins

A

Transfer lipids via apoproteins.
Low density: High TG.
High density: High apoproteins.

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5
Q

Two types of lipids

A

Cholesterol & TG

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6
Q

VLDL physio/pathway

A
  1. Made in liver
  2. VLDL transfers TG to cells
  3. Turns into LDL.
  4. LDL transfers cholesterol to cells
  5. Excess taken by liver & excreted via bile
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7
Q

HDL physio/path

A

Made in liver & intestine.

Collects LDL from plaques & cells and transfers to liver.

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8
Q

CVD (Cardiovascular disease/ASCVD)

A

CHD, Cerebrovascular, Peripheral artery, aortic atherosclerosis, AAA, TAA.

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9
Q

Primary HLD

A

Genetic abnormality due to cholesterol metabolism

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10
Q

Secondary HLD

A

Due to: DM, Alcohol, Renal ds, Cholestatic liver ds, Meds, Obesity/diet/sedentary

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11
Q

Medications causing secondary HLD

A
  1. OCP
  2. Thiazide diuretics
  3. Beta-blockers
  4. Atypical antipsychotics
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12
Q

Components measured

A

Total cholesterol & HDL

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13
Q

VLDL calculation

A

(TG/5)

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14
Q

LDL calculation

A

Total cholesterol-HDL-(TG/5)

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15
Q

LDL estimation incorrect if…

A

TG are above 200

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16
Q

Causes of abnormal cholesterol metabolism

A
  1. Genetic
  2. Insulin Resistance
  3. Organ dysfunction
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17
Q

Plaque formation

A
  1. LDL sticks to artery wall
  2. LDL oxidized (Pro-inflammatory & thrombotic)
  3. Macrophages eat lipids= Foam cells
  4. Endothelial dysfunction
  5. Vasoconstriction leads to exertional angina
  6. Plaque ruptures leads to MI/TIA/CVA
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18
Q

Non-modifiable risk factors

A
  1. M>45, F>55
  2. Male
  3. Premature family hx
    (M<55, F<65, 1st degree)
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19
Q

Modifiable risk factors

A
  1. Dyslipidemia, Low HDL,
  2. HTN
  3. Alcohol/smoking/diet
  4. DM
  5. PAD
  6. Renal ds
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20
Q

Under 65, what % dx/death

A
  1. Dx: 50%

2. Death: 15%

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21
Q

Hard Coronary Framingham risk

A

10 year risk of MI/death

Takes into account: Age, sex, smoke, Cholesterol, HDL, SBP, Tx.

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22
Q

ACC/AHA risk score

A

10 year risk of Heart disease/stroke

Takes into account: same + Race, DBP, Diabetes

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23
Q

High LDL/HDL relationship with ASCVD

A

High LDL high ASCVD
Decrease 1% LDL, Decrease CVD 1-1.5%
High HDL low ASCVD
Increase 2-3% HDL, Decrease CVD 2-4%

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24
Q

Primary vs Secondary prevention

A

Primary: modest benefits
Secondary: Strong benefits (if already had event)

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25
Physical exam signs
Xanthomatous tendons (Plaques on knuckles/elbows) Xanthelasma (plaques on eyelids) Corneal arcus Lipemia retinalis (white arteries on retina) Eruptive xanthomas
26
NCEP ATP III 9 steps
1. Fasting lipid panel 2. CHD risk equivalent 3. Major risk factors 4. Framingham risk (if 2+ rf/CHD equiv) >20%=CHD risk equivalent 5. Determine LDL goal dependent on risk category 6.TLC 7. Drug therapy for LDL 8. Metabolic syndrome after 3 mo (ID&treat) 9. Treat TG/HDL
27
Optimal fasting levels
1. Total: less than 200 2. LDL: less than 70 3. HDL: greater than 40, greater than 50 for women
28
CHD equivalent
1. Coronary artery disease 2. Peripheral artery disease 3. AAA 4. Diabetes
29
Major risk factors
1. Smoking 2. HTN 3. HDL <40 4. Family hx premature CAD 5. Men>45, Women>55
30
LDL goals for categories
1. CHD/Equivalent: <70 2. 2+ risk factors: <100 3. 0-1 risk factors: <160
31
TLC & effect on LDL
1. Low fat diet (<30% calories) 2. Cholesterol <200 daily 3. Increase viscous fiber (10-25g) 4. Plant stanols/sterols 5. Weight management Decrease LDL 25-30%
32
When to initiate drug therapy?
After 3 months of TLC, LDL still high
33
Metabolic syndrome (3 of 5)
1. Abdominal obesity (40M, 35W) 2. TG > 150 3. Low HDL 4. Elevated BP 5. Fasting glucose >100
34
TG values
1. Normal: <150 2. Mild hypertrig: 200-499 3. Moderate/Risk for pancreatitis: >500 4. Large risk for pancreatitis: >1000
35
ACC/AHA screening
>21 yo, every 5 years for low to moderate risk | More frequent for high risk
36
ACC/AHA: Who to treat with statin?
1. ASCVD 2. LDL>190 3. Diabetes: age 40-75, LDL >70 4. 10 year risk >7.5%, age 40-75
37
High intensity treatment medication.
1. Atorvastatin 40/80 2. Rosuvastatin 20/40 (Decrease LDL 50%)
38
Who to treat high intensity?
1. ASCVD up to age 75 2. LDL > 190 3. Diabetes, age 40-75, LDL >70, >7.5% risk
39
Moderate intensity treatment medication.
1. Atorvastatin 10-20 2. Simvastatin 20-40 3. Pravastatin 40 (Decrease LDL 30-50%)
40
Who to treat moderate intensity?
1. Age over 75 | 2. 40-75 yo, DM, LDL 70-189, 5-7.5% risk
41
Statin MOA
Decrease rate limiting enzyme for cholesterol formation in cells. HMG-CoA reductase inhibitor.
42
Statin benefits/lipid effects
``` Decrease all cause mortality Decrease MI & CVA LDL 20-55% TG 7-30% HDL 5-15% ```
43
Statin CI
1. Pregnancy/Breastfeeding 2. Liver disease/Unexplained LFT increase (Get baseline LFT) Not effective: TG>400 Most effective: dose at night.
44
Statin side effects
1. Myalgias 2. Rhabdomyolysis/Myopathy (check CK if at risk) 3. Hepatotoxicity (Check baseline LFT) 4. Increase risk for DM
45
Cholesterol absorption inhibitor: MOA
Decrease absorption in intestine. | Increase LDL receptors peripherally.
46
Cholesterol absorption inhibitor: Lipid effects
LDL 15-20%
47
Cholesterol absorption inhibitor: CI
1. With fibrates | 2. Hepatic impairment
48
Fibric acid derivates: MOA & names
Increase VLDL breakdown, decrease synthesis | Gemfibrozil, Fenofibrate
49
Fibric acid derivates: Lipid effects
Drug of choice for TG>500 TG 40% LDL 10-15% HDL 15-20%
50
Fibric acid derivates: Side effects
1. Cholelithiasis 2. Hepatits 3. Myositis
51
Fibric acid derivates: CI
1. Gallbaldder ds 2. Liver ds 3. Caution-Pregnancy & Renal ds 4. With Statin
52
Niacin: MOA
Decrease VLDL production
53
Niacin: Lipid effects
Good for very low HDL/mod high LDL HDL 25-35% LDL 15-25% TG 50%
54
Niacin: Side effects
Flushing | Long acting better tolerated
55
Niacin: CI
1. Pregnancy 2. Liver ds 3. Peptic ulcer 4. Caution: Gout & DM
56
Bile-acid binding resins: MOA/Names
Binds bile acids in intestine. Decreases bile acids in entero-hepatic system. Liver increases bile acid production. Uses up cholesterol. Names: Chole- Cole-
57
Bile-acid binding resins: Lipid effects/who to us it in
LDL 15-25% HDL insig TG little/may increase SAFE in pregnancy Good for mod LDL & normal HDL/TG
58
Bile-acid binding resins: side effects
GI upset/constipation
59
Bile-acid binding resins: CI
1. GI obstruction 2. Hypertriglyceridemia 3. Pancreatitis
60
PCSK9 Inhibitor: MOA
Blocks LDL receptor degradation. | Is a monoclonal ab
61
PCSK9 Inhibitor: Lipid effects, who to use
LDL 50-60% | Good for familial HLD
62
Omega-3 fatty acids benefits
Improves TG, decreases CV, anti-inflammatory
63
Familial hypercholesterolemia
LDL receptor dysfxn/gone 1. Homo: LDL 8X, childhood 2. Hetero: LDL 2X, 30s
64
Familial hyperchylomicronemia
Abnormal lipoprotein lipase (enzyme allows tisue to take TG from VLDL/chylomicrons) Severe TG

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