Endocrinology > Lipids > Flashcards

Lipids Flashcards

(47 cards)

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1
Q

Cholesterol is found in all human cell membranes except:

A

RBC

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2
Q

Whats the name of proteins found on the surface of lipoproteins?

A

Apolipoproteins

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3
Q

What are some functions of apolipoproteins?

A
  1. Maintain structure
  2. Acts as ligands
  3. Act as co-factors
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4
Q

List some of the apolipoproteins and their functions:

A
  1. Apo A-1: protein for HDL
  2. Apo B-100: protein for VLDL, IDL, LDL, Lp(a_ and receptor ligand
  3. Apo C-II: lipoprotein lipase activator (found in chylomicrons)
  4. component of Lp(a), and plasminogen antagonist
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5
Q

What is the relevance of lipoprotein (a)?

A

A marker for CVD and has the apolipoprotein a

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6
Q

Sources of TAGs?

A

Liver synthesis and diet

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7
Q

List primary dyslipidemia disorders:

A
  • mixed dyslipidemia
  • familial hypertriglycerides
  • lipoprotein lipase deficiency
  • Apo C-II deficiency
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8
Q

List acquired conditions that lead to dyslipidemia:

A
  • diabetes mellitus
  • nephrotic syndrome
  • hypothyroidism
  • Alcohol
  • Drugs (Estrogen, thiazides, b-blocker, corticosteroids, cyclosporine, HAART)
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9
Q

Is HDL-C or LDL-C predictor of CHD?

A

HDL-C

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10
Q

Functions of HDL?

A
  • reverse transport of cholesterol
  • prevents LDL oxidation (this is more atherogenic)
  • inhibits endothelial cell adhesion molecules and platelet aggregation
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11
Q

What is dyslipidemia?

A

high cholesterol and/or elevated TAGs, or low HDL

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12
Q

True or False: primary dyslipidemia is a genetically determined?

A

True

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13
Q

What things will lead to consider a primary dylipidemia?

A
  • anyone with, or family history of, premature onset coronary heart disease or stroke: Men <55, Women <65
  • markedly total elevated cholesterol (>6.5-7.0 mmol/L, normal < 5.2)
  • triglycerides (>4.0 mmol/L, normal < 1.4)
  • very low HDL (< ~ 0.7 mmol/L, normal >0.9).
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14
Q

What is considered for atherosclerosis risks (major risks)?

A
  1. Age: Men >45; Women >55
  2. Elevated cholesterol level, esp. low density lipoprotein cholesterol (LDL-C)
  3. Low levels of high density lipoprotein cholesterol (HDL-C)
  4. Family history of premature atherosclerosis: first degree male relative <55, female relative <65
  5. Hypertension (high blood pressure) (even if controlled with medication)
  6. Diabetes
  7. Smoking: One or more cigarettes daily
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15
Q

What are some factors associated with increased atherosclerosis risks?

A 
Obesity / Metabolic Syndrome
Sedentary lifestyle
High stress levels
Elevated Triglycerides
Elevated Lp (a)
Elevated C-reactive protein
Elevated Homocysteine
Elevated Fibrinogen
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16
Q

True or False: Lifestyle changes (more PA, and low fat diet) is enough to maintain genetic dyslipidemia in check?

A

False: can only lower by 20%

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17
Q

List the CV risk calculators:

A
  • Framingham

- Reynolds Risk Score (adss CRP level - marker of inflammation in vasculaure)

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18
Q

Who do we screen for CVD?

A
  • Men and women at or over 40 yrs (or postmenopausal); and higher risk groups (FN and South Asians)
  • smoker, hiv, showing signs of atherosclerosis, hypertensive disease of pregnancy
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19
Q

How do we screen for CVD?

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A
  • history, physical
  • lipid panel (TC, LDL-C, HDL-C,, TG)
  • non-HDL
  • glucose
  • eGFR

non-fasting lipids are acceptable now

20
Q

What is the aim for statin treatment?

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A

LDL-C less than 2mmol/L or greater than 50% reduction, or ApoB less than 0.8g/L or non-HDL-C less than 2.6 mmol/L

21
Q

List the classes of lipid lowering drugs:

Study These Flashcards
A
  1. Statins - HMG CoA reductase inhibitors
  2. Cholesterol absorption inhibitors
  3. Bile acid sequestrants
  4. Fibrates
  5. Nicotinic acids
  6. PCSK9 inhibitors
22
Q

Give an example of cholesterol absorption inhibitor and its effects:

Study These Flashcards
A

Ezetimide

Lowers LDL up to 18-25% and more if synergistically used with statins

23
Q

What happens to cholesterol and fatty acids in enterocytes?

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A

Fatty acids are used to esterify cholesterol with the help ACAT enzyme or used to create TAGs
These molecules are then incorporated in chylomicrons with apoB-48

24
Q

How do bile acid sequestrants work and what are the side effects?

Study These Flashcards
A

Bind and inhibit reabsorption of bile acids and this increases LDL-receptors in liver –> lowers LDL-C (15-30%)

Side effects:

  • increase in TAGs (should not be used for those with hypertriglyceridemia)
  • constipation/upset stomach
25
PCSK9 inhibitors are recommended in adjunct with diet for which group of populations?
Those with familial hypercholesterolemia
26
What is the first line treatment for severely high TAGs (hypertriglyceridemia) and how do they work ?
Fibrates (or Niacin) : increase oxidation of FAs and HDL production Lowers TAGs by 20-30%, HDL increase 10-20%
27
What are the side effects of fibrates?
Side effects Myopathy, dyspepsia, gallstones with older agents Myopathy increased if combined with statins Contraindicated in patients with severe kidney or liver disease
28
What is the best agent to raise HDL-C?
Niacin
29
What are the effects of niacin and how does it work?
-reduces HDL catabolism and VLDL creation by reducing mobilization of FAs from peripheral tissues
30
What are the side effects of niacin?
Side effects Flushing, itch, hepatotoxicity, hyperglycemia, hyperuricemia, upper GI distress Contraindicated in patients with liver disease,gout, peptic ulcer; elevated blood sugar is relative but not absolute contraindication
31
What are some options for hypercholesterolemia?
LDL Apheresis, Liver Transplantation, PCSK9
32
What are some options for hypercholesterolemia?
LDL Apheresis (removal of VLDL, IDL, LDL, Lp(a)), Liver Transplantation
33
What is the most common genetic lipid disorder and describe it:
Familial Combined Hyperlipidemia: - autosomal dom. - overprod. of apoB100 --> increased VLDL secretion --> high cholesterol and TAGs in blood
34
What is Familial Hypertriglyceridemia?
Uncommon, autosomal dom., increased TAG production with normal choles.
35
What deficiencies could lead to the inability of TAG digestion from chylomicrons (chylomicronemia)?
1. Lipoprotein Lipase deficiency | 2. Apo C-II Deficiency
36
Eruptive xanthomata is related to?
chylomicronemia
37
What is Remnant Removal Disease (“Dysbetalipoproteinemia”) and an associated physical sign?
Disorder where there is a mutation on ApoE (E3) protein, which leads to defects in recognition of this protein by LDL-R --> leads to elevated choles. and TAGs Presentation is ApoE mutation and overproduction of VLDL. Palmar xanthomas
38
What is Familial Hypercholesterolemia and it is higher which Canadian population?
- autosomal dom. condition where there is mutation in LDL-R - affects higher in French-Canadians - homozygous have CHD in childhood - heterozygous 30-40s onset
39
What is Familial Ligand-defective ApoB?
- mutation in apoB which leads to defective interaction with ApoB/E receptors - more common with European ancestry - affects LDL uptake
40
What are the clinical presentations of too much cholesterol (ie. hypercholesterolemia, ligand-defective ApoB)?
- Xanthelasma | - Tendon xanthoma
41
What are secondary causes of low HDL?
``` Smoking Diabetes Obesity Hypertriglyceridemia Androgens Progesterones ß-blockers Diuretics ```
42
What does very severe elevations of choles and TAGs mean?
It is the result of genetic and secondary causes, e.g., Familial combined hyperlipidemia plus diabetes Because secondary causes only raise these mildly
43
What happens in diabetic dyslipidemia?
1. Elevated triglycerides - increased intracellular lipolysis, increased free fatty acids for triglyceride synthesis by liver decreased lipoprotein lipase activity in plasma 2. Low HDL-C - decreased lipoprotein lipase activity, decreased synthesis by liver, replacement of HDL cholesterol with triglycerides
44
How does hypothyroidism affect lipids?
reduced LDL receptor number leading to increased plasma LDL; decreased lipoprotein lipase activity leading to increased triglycerides; decreased HDL synthesis by liver (combined dyslipidemia)
45
What are the two kidney diseases that affect lipids?
1. Uremia: decreased LPL activity | 2. Nephrotic syndrome: overproduction of lipoproteins by the liver; decreased LPL activity
46
What do dietary cholesterol and sat. fats do to lipid metabolism?
Saturated Fats: suppress hepatic LDL receptors, increasing LDL in plasma; increase substrate for VLDL production by liver Dietary cholesterol: suppresses hepatic LDL receptors
47
Drugs usually affect which lipid?
TAGs
Endocrinology
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