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Endocrinology > Lipids > Flashcards

Lipids Flashcards

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?

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?

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:

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:

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?

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?

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
Q

PCSK9 inhibitors are recommended in adjunct with diet for which group of populations?

A

Those with familial hypercholesterolemia

26
Q

What is the first line treatment for severely high TAGs (hypertriglyceridemia) and how do they work ?

A

Fibrates (or Niacin) : increase oxidation of FAs and HDL production
Lowers TAGs by 20-30%, HDL increase 10-20%

27
Q

What are the side effects of fibrates?

A

Side effects
Myopathy, dyspepsia, gallstones with older agents
Myopathy increased if combined with statins
Contraindicated in patients with severe kidney or liver disease

28
Q

What is the best agent to raise HDL-C?

A

Niacin

29
Q

What are the effects of niacin and how does it work?

A

-reduces HDL catabolism and VLDL creation by reducing mobilization of FAs from peripheral tissues

30
Q

What are the side effects of niacin?

A

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
Q

What are some options for hypercholesterolemia?

A

LDL Apheresis, Liver Transplantation, PCSK9

32
Q

What are some options for hypercholesterolemia?

A

LDL Apheresis (removal of VLDL, IDL, LDL, Lp(a)), Liver Transplantation

33
Q

What is the most common genetic lipid disorder and describe it:

A

Familial Combined Hyperlipidemia:

  • autosomal dom.
  • overprod. of apoB100 –> increased VLDL secretion –> high cholesterol and TAGs in blood
34
Q

What is Familial Hypertriglyceridemia?

A

Uncommon, autosomal dom., increased TAG production with normal choles.

35
Q

What deficiencies could lead to the inability of TAG digestion from chylomicrons (chylomicronemia)?

A
  1. Lipoprotein Lipase deficiency

2. Apo C-II Deficiency

36
Q

Eruptive xanthomata is related to?

A

chylomicronemia

37
Q

What is Remnant Removal Disease (“Dysbetalipoproteinemia”) and an associated physical sign?

A

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
Q

What is Familial Hypercholesterolemia and it is higher which Canadian population?

A
  • 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
Q

What is Familial Ligand-defective ApoB?

A
  • mutation in apoB which leads to defective interaction with ApoB/E receptors
  • more common with European ancestry
  • affects LDL uptake
40
Q

What are the clinical presentations of too much cholesterol (ie. hypercholesterolemia, ligand-defective ApoB)?

A
  • Xanthelasma

- Tendon xanthoma

41
Q

What are secondary causes of low HDL?

A 
Smoking
Diabetes
Obesity
Hypertriglyceridemia
Androgens
Progesterones
ß-blockers
Diuretics
42
Q

What does very severe elevations of choles and TAGs mean?

A

It is the result of genetic and secondary causes, e.g., Familial combined hyperlipidemia plus diabetes

Because secondary causes only raise these mildly

43
Q

What happens in diabetic dyslipidemia?

A
  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
Q

How does hypothyroidism affect lipids?

A

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
Q

What are the two kidney diseases that affect lipids?

A
  1. Uremia: decreased LPL activity

2. Nephrotic syndrome: overproduction of lipoproteins by the liver; decreased LPL activity

46
Q

What do dietary cholesterol and sat. fats do to lipid metabolism?

A

Saturated Fats: suppress hepatic LDL receptors, increasing LDL in plasma; increase substrate for VLDL production by liver

Dietary cholesterol: suppresses hepatic LDL receptors

47
Q

Drugs usually affect which lipid?

A

TAGs

Endocrinology (16 decks)

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