Lipids Flashcards
1
Q
Functions of Triglycerides
A
• Energy storage*
• Insulating and protecting organs
• Cellular membrane fluidity
• Fat soluble vitamin transport
2
Q
Cholesterol is a component of: (5)
A
-Bile acids
-Progesterone
-Vitamin D
-Glucocorticoids
-Minerocorticoids
3
Q
Function of cholesterol
A
Cell membrane fluidity
4
Q
Sources of cholesterol
A
• De novo: endogenous (70-80%)-liver
• Diet
5
Q
Cholesterol is eliminated through conversion by:
A
The liver to salts of bile acids
6
Q
ApoB
A
Atherogenic: Chylomicrons, VLDL, IDL, LDL (“Bad”), Lp (A)
7
Q
ApoA
A
Cardioprotective-HDL (“good”)
8
Q
Main component of chylomicrons
A
Triglycerides
9
Q
Chylomicrons are:
A
Exogenous: 12 hours to clear circulation
10
Q
VLDL are the predominant carrier of:
A
Blood triglycerides
11
Q
VLDLs are:
A
Endogenous*
12
Q
IDLs are formed after:
A
Removal of some triglycerides from VLDL
13
Q
LDLS are formed after:
A
Removal of triglycerides from IDL
14
Q
LDLs carry:
A
Cholesterol to be deposited into tissues
15
Q
Lp(a)
A
• LDL particle with additional lipoprotein attachment
• Highly heritable*, tend to be stable over time
16
Q
Components of LDL
A
-45% cholesterol, 10% triglycerides, 20% phosphates, 25% protein
17
Q
HDL is synthesized by:
A
Liver and small intestines
18
Q
HDLs carry a higher percentage of:
A
Protein
(50% protein, 1-5% triglycerides, 15% cholesterol, 30% phospholipid)
19
Q
Total Cholesterol: Desirable Level
A
125-200 mg/dL
20
Q
LDLc Levels
A
<100: Optimal*
100-129: Near Optimal*
130-159: Borderline high*
160-189: high
>190: Very High
21
Q
HDLc: Desirable Levels
A
• Men: >40 mg/dL
• Women: >46 mg/dL
22
Q
HDLc tends to have an inverse relationship with:
A
Triglycerides
23
Q
TC: HDL Ratio provides insight into balance between:
A
Atherogenic and cardioprotective lipoproteins
24
Q
TC:HDL Radio: Average Risk
A
• 5:1 (males)
• 4.5:1 (females)
-3:1 (Ideal Ratio)
25
Non-HDL Cholesterol =
TC-HDLc
26
Non-HDL Cholesterol includes cholesterol carried by: (4)
VLDL, IDL, LDL, Lp(a)
27
Non-HDL Cholesterol: Desirable Level
LDL target + 30 mg/dL
28
Triglycerides: Desirable Level
Desirable: <150 mg/dL
29
HLP IIa: Description
Excessive LDL-c in circulation and excessive deposition in peripheral tissue
30
HLP IIa: Serum Cholesterol
500-1200mg/dL
31
HLP IIa: Signs/Symptoms
• Xanthelasmas
• Tendon and tuberous xanthomas*
• Arcus juvenilis
• Arterial bruit
• Claudication
• Accelerated atherosclerosis
32
HLPIIa: Lab Findings
**Serum cholesterol increased
• Homozygous – 500-1200 mg/dL
• Heterozygous – 250-500 mg/dL
• Triglycerides normal
• **Increased LDL (>190mg/dL)
33
HLP IV: Description
• Genetic problem causing decreased elimination of VLDL
34
HLP IV: Signs/Symptoms
-Obesity
-Lipemia retinalis
-Atherosclerosis
-Hepatosplenomegaly
-Possible pancreatitis* (esp if notable increase in triglycerides (>500))
35
HLP IV: Lab Findings
• **Increased triglycerides: 250-500mg/dL
• Normal cholesterol
• Normal LDL
• *Decreased HD
36
Hyperelphalipoproteinemia
• Elevated HDL cholesterol (80-100+)
37
Secondary Causes of Dyslipidemia
38
Diabetes Mellitus
Increased production of VLDL->Increased TGs/Decreased HDL
-Increased LDLc
-Increased TC
39
Hypothyroidism
-Increased LDL
-Increased TC
-Increased TGs
-Decreased HDLs
40
Chronic Liver Disease (2)
-Increased TGs
-Decreased HDL
41
Obstructive Liver Disease
-Cholelithiasis (gallstone-colicky pain)
-Increased LDL
-Increased TC: 400-500 (acute)/700-800 (chronic)
-Increased TGs
-Decreased HDL
42
Pregnancy
-Increased TGs (3rd trimester)
-Increased LDL
-Increased TC
-Decreased HDL
43
PCOS
-Increased TG
-Decreased HDL
-Increased LDL
-Increased TC
44
Certain Medications
-Oral contraceptives
-Corticosteroids
-Diuretics
45
• Lipid panel abnormalities tend to be _____ than those seen with genetic abnormalities
Milder
46
Ranges indicative of lifestyle factors
• Total cholesterol: 200-250
• LDLc: 100-190;
• Triglycerides: 150-250\
-HDL: Exercise, inverse of TGs
47
Causes of Hypocholesterolemia
-Chronic liver disease,
-Hyperthyroidism,
-Anemia
-MMMs (Malignancy, malnutrition, malabsorption)
48
Cardiac Risk Assessment: Pathophysiology
1. Endothelial cell damage (HTN, smoking, hyperglycemia, increased homocystemia..)
2. LDL deposition in tunica intima
3. WBCs enter, release free radicals*
4. LDL oxidized*
5. Positive feedback loop
6. Lipid plaque formed from dead WBCs and smooth mucles that engulfed LDL
7. Lipid plaques become fibrous*
8. Inflammation>plaque instability>plaque rupture*
49
Major Risk Factors
• Smoking
• High blood pressure
• High LDL cholesterol
• Low HDL cholesterol
• Diabetes
• Age: Male (45+)/Female (55+/menopause)
• Premature family history of cardiovascular disease (1st degree): Male (<55)/Female (<65)
50
Risk Enhancing Factors
-Based on 10 year risk profile
• Obesity
• Sedentary
• Diet
• Alcohol
• Stress and psychosocial factors
• Elevated triglycerides
• Metabolic syndrome
51
Risk Enhancing Factors: Other Abnormalities
• Lp(a)
• Hyperhomocystinemia
• Prothrombotic factors (fibrinogen)*
• hsCRP (inflammation)
-Sleep apnea
52
Cluster of metabolic abnormalities->increased risk for:
• Type 2 DM
• Cardiovascular disease
• Stroke
• Fatty liver
• Certain cancers
53
Metabolic Abnormalities
• Intra-abdominal obesity
• Dyslipidemia
• Hypertension
• Insulin resistance (w/ or w/o insulin impaired glucose tolerance)
• Proinflammatory state
• Prothrombotic state
54
Metabolic Syndrome: Epidemiology
• Predominant age: >60 years old
• Male = female
• >1/3 US affected
55
In order to be diagnosed with metabolic syndrome, we need 3+ of the following:
Abdominal obesity
•Waist circumference:
• >40 inches men
• >35 inches women
• TGs >150 mg/dL
Low HDL cholesterol
• Men: <40 mg/dL
• Women: <50 mg/dL
• BP >130/85 mm Hg
• Fasting glucose ≥100 mg/dL but <126 mg/dL (prediabetes)
56
Metabolic Syndrome: Management
• Primary therapeutic goal is to prevent or reduce obesity
• Aggressive lifestyle modification (diet and exercise) considered first line therapy
• Treat lipid and non-lipid risk factors if they persist despite lifestyle changes
57
Metabolic Syndrome: Prognosis
-Increased risk of: Type 2 DM (5x), CAD (3x), Acute myocardial infarct (3x), All-cause mortality (1.5x)
58
A risk assessment primarily includes:
History, physical exam, lipoprotein panel, additional lab testing
59
A lipoprotein panel primarily assesses:
Cardiac risk
60
Most risk assessment still focuses on:
LDL-c, Total Cholesterol, HDL-c
61
CRP measures levels from:
10 mg/L to 10,000 mg/L (general inflammation)
62
Hs-CRO measures levels from
0-10 mg/L (cardio CS/inflammation-endothelial damage
63
Hs-CRP: Levels
-Normal: <0.3mg/L
-Low: <1mg/L
-Average: 1-3mg/L
-High>3mg/L
-General Inflammation: >10mg/L
64
Lipoprotein particle size
Small/dense (more athrogenic), large/pillowy (less athro.
65
AHA Guidelines: Dietary pattens
Mediterranean, DASH, low glycemic index/load, plant-based
66
AHA guidelines: Activity
Activity: About 150 minutes of moderate to vigorous exercise per week (3-4 40-minute sessions)
67
AHA guidelines: Other factors
• Maintaining healthy body weight
• Smoking cessation
• Limiting alcohol use
• Sleep
68
Lipid Panel: What factors must we determine if abnormalities are due to primary causes or secondary
• Biliary obstruction
• Hypothyroidism
• Chronic kidney disease
• Pancreatic disease (diabetes mellitus, chronic pancreatitis)
• Pregnancy
• Certain medications
69
Statin use Guidelines
1. LDL-c >190 (21+ years of age)
2. LDL-c 70-189 in adults 40-75 with diabetes
3. LDL-c 70-189 in adults 40-75 with moderate risk
70
Neutraceuticals
• Red yeast rice: LDL, TC
• Plant sterols and stanols: LDL
• EPA/DHA: Triglycerides
• CoQ10
-Niacin
71
Statin induced myopathy: Symptoms
• Fatigue, muscle pain/tenderness, weakness, tendon pain, nocturnal muscle cramping
• Proximal, generalized, worse with exercise (bilateral)
72
Lower CRP by:
Exercise, alcohol
73
Lower homocysteine
Exercise, B6, folate, B12
74
Risk Assessment: Follow-Up and Monitoring
• Discuss other risk factors: Lp(a), homocysteine, HsCRP
• Rule out pathology as secondary cause: Diabetes, hypothyroid, pregnancy, Ckd, meds
• Recommend dietary lifestyle changes for 6 months
• Retest lipid panel at 6-8 weeks, 3 months, and 6 months
• If pharmaceutical intervention is decided upon:
• Liver enzymes and CPK should be measure before initiation and after several months
