Lipids in heart disease Flashcards

1
Q

Why are lipids needed in the body

A
  • Importatn in constituent of the cell membranes
  • helps in the absorption of fat soluble vitamins
  • maintains membrane fluidity
  • acts as a thermal insulator adn cellular metabolic regulator
  • hormone synthesis - steroid synthesis
  • organ padding
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2
Q

What are the fat soluble vitamins

A

A
B
E
K

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3
Q

What enzyme do statins inhibit

A
  • HMG CoA reductase
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4
Q

What do statins lower

A
  • Cholestrol level
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5
Q

What is cholestrol important for

A
  • Vitamin D syntehsis
  • steroids
  • bile salts
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6
Q

What are modifiable cardiovascualr risk factors

A
  • smoking
  • high cholestrol
  • hypertension
  • high blood glucose
  • obesity
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7
Q

What are the unmodifiable risk factros for cardiovascular disease

A
  • Age
  • gender
  • family history
  • ethinicty
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8
Q

The smaller the molecule

A

the smaller the moelcule the easier it is to penetrate between the endoithelial cells and go into the endothelium
- therefore easy for LDl molecules to get in adn less easy for VLDL adn IDL

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9
Q

Describe how LDLs, HDLs and chylomicrons work together

A
  • Chylomicrons transport fat from the itnestinal mucsoa to the liver
  • in the liver some of the chylomicrons release triglycerides and some cholestrol and become low density lipoproteins (LDL)
  • LDL then carries fat and cholestrol to the bodys cells
  • High density lipoproteins (HDL) Ccarr fat and cholestrol back to the liver for excretion
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10
Q

What is the difference between HDL and LDL

A
  • LDL then carries fat and cholestrol to the bodys cells

- High density lipoproteins (HDL) Ccarr fat and cholestrol back to the liver for excretion

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11
Q

What are the two types of hyperlipidaemias

A

Primary

Secondary (more common)

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12
Q

What are causes of secondary hyperlipidaemia

A
∗ Diet
∗ Alcohol
∗ Hypothyroidism
∗ Nephrotic syndrome
∗ Anorexia nervosa
∗ Obstructive liver disease
∗ Obesity
∗ Diabetes mellitus
∗ Pregnancy
∗ Acute hepatitis
∗ Systemic lupus erythematousus
∗ Drugi nduced-Thiazides, B-blockers, anti retroviral drugs, anti-depressants
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13
Q

What do you look for in a fasting lipid profile

A
∗ Serum total cholesterol 
∗ Serum LDL-cholesterol
∗ Serum (fasting) triglyceride 
∗ Serum HDL cholesterol
∗ Cholesterol-HDL ratio
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14
Q

What is the friedewald formula

A

The Friedewald formula (FF) is an estimation of LDL-c level that uses the following levels of

  • total cholesterol (TC),
  • triglycerides (TG)
  • high-density lipoprotein cholesterol (HDL-c):

LDL-c (mg/dL) = TC (mg/dL) − HDL-c (mg/dL) − TG (mg/dL)/5 [6, 11–13].

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15
Q

What levels do you use in the Friedewald formula (FF)

A
  • total cholesterol (TC),
  • triglycerides (TG)
  • high-density lipoprotein cholesterol (HDL-c):

LDL-c (mg/dL) = TC (mg/dL) − HDL-c (mg/dL) − TG (mg/dL)/5 [6, 11–13].

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16
Q

What does the serum look like if you have high triglyceride

A

serum looks white

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17
Q

What can happen with high triglyercide

A

acute pancretitis

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18
Q

What causes primary hyperlipidaemia

A

genetic

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19
Q

Name a type of primary hyperlipidaemia

A
  • Familial Hypercholesterolemia (FH)
  • familial combined hyperlipideaemia
  • dysbetalipoproteinemia
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20
Q

What happens in Familial Hypercholesterolemia (FH)

A
  • Codominant genetic disorder, occurs in
    heterozygous form
  • Mutation in LDL receptor, resulting in elevated levels of LDL at birth and throughout life
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21
Q

What are pateints with Familial Hypercholesterolemia (FH) at risk of

A
  • Atheroscloeris
  • tendon xanthomas (75% of patients)
  • tuberous xanthomas
  • xathelasmas of eyes
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22
Q

what is the genetics of familial combined hyperlipidaemia

A
  • Autosomal dominant
23
Q

What is there increased secretion of in familial combined hyperlipidaemia

A
  • Increased secretions of VLDLs
24
Q

What happens in dysbetalipoproteinemia

A

Results in apo E2, a binding-defective form of apoE (which usually plays important role in catabolism of chylomicron and VLDL)

25
Q

What can dysbetalipoproteinemia cause an increase risk of

A
  • atherosclerosis
  • peripheral vascualr disease
  • tuberous xanthomas
  • striae palmaris
26
Q

What are the two sources of cholestrol

A
  • diet

- liver synthesises cholestrol

27
Q

What happens if the body is deficient or resistant in lipoprotein lipase

A

increases amount of chylomicron leading to increased cholestrol in ciruclation

28
Q

What is the genetics of Familial Hypercholesterolemia (FH)

A
  • Autosomal dominant
29
Q

What is a high risk of Familial Hypercholesterolemia (FH)

A
  • high risk of premature CHD - have to identify those with FH
  • early treatment leads to a near normal life expectancy
  • over 50% risk of CHD in men by age 50 and at least 30 % risk in women by age 60
30
Q

What criteria can you use to diagnose FH

A
  • Simon Broome criterai
31
Q

who should you consider FH in

A

Consider FH in all adults with total cholesterol greater than 7.5 mmol/l

32
Q

all patients with possible FH should be referred to

A

A specialist lipid clinic to…

  • confirm diagnosis
  • intiate cascade testing
  • treat
33
Q

What are the normal cholestrol ranges

A
  • total cholestrol more than 5 is high
  • LDL choelstrol more than 3 is high
  • HDL high is better
34
Q

What should definite FH in adults have (Simon broom critera)

A

Total cholesterol >7.5 and LDL-C > 4.9
AND tendon xanthomata or evidence of these in 1st or 2nd degree relative
OR
An identified genetic mutation for FH

35
Q

What should you diagnose possible FH in adult with (Simon broom critera)

A

Total cholesterol > 7.5 and LDL-C > 4.9 and at least one of the following :
1) Family history premature CHD i.e.
MI aged < 60yrs in 1st deg relative or
< 50yrs in 2nd deg relative
2) Family history raised total cholesterol in 1st or 2nd deg relative (> 7.5 in adult OR > 6.7 in child)

36
Q

What can you see in the patients that shows you have high cholestrol

A
  • Subcutaenous tissue nodules
  • athermatous plawues
  • fibrous tissue formation
  • eruptuive xanthomata = small itchy nodules, VLDL/chylomicron associated
  • Tuberous xanthomata - yellow plaques over elbows and knees, IDL induced
  • xanthelasma - periorbital skin depositis - LDL assocaition
  • tendons - xanthomata
  • cornea acrus - under age of 40
37
Q

what is the Q risk

A
  • it is a cardiovascular risk that is calculated by taking in smoking history, cholestrol level, blood pressure
  • more than 10% tend to be started on treatment if lifestyle changes do not help
38
Q

What is primary prevention for people at risk of developing hyperlipidemia

A

At risk people
- statin to lower lipids

People without risk factors
- Statins used in asymptomatic men with LDL cholesterol levels persistently above 5 mmol/L despite dietary change

39
Q

When is statins used for primary prevention for hyperlipidaemia

A
  • Used in asymptomatic individuals with type 2 diabetes

Used in people with two or more of

  • positive family history of cardiovascular disease
  • albuminuria
  • hypertension
  • smoking
40
Q

What is secondary prevention for hyperlipidaemia

A
  • Statins for any patient with macrovascular disease, TIA, or stroke
41
Q

What drugs can cause hyperlipidaemia

A
  • oral contraceptives

- retinoids, thiazide diuretics, corticosteroids, beta blockers, anti-retrovirals

42
Q

Who do you screen for hyperlipidaemia

A
  • family history of hyperlipidaemia
  • corneal arcus less than 50 years old
  • Xanthomata or Xanthelasmata
43
Q

What are xanthomata

A

these are yellow lipid deposits that can be eruptive or tuberous plaques on elbows and knees or planar on palmar creases

  • these are diagnostic of hyperlipidaemia
  • can also be in tendons
44
Q

What is mixed hyperlipdiameia

A
  • this is an increase in both LDL and triglycerides
45
Q

What causes mixed hyperlipidaemia

A
  • type 2 diabetes
  • metabolic syndrome
  • alcohol abuse
  • chronic renal failure
46
Q

What is Xanthelasmata

A
  • these are lipid laden yellow plaques that congregate around the lids or just below the eyes
  • these signify hyperlipidaemia
47
Q

What is the most widely used drug to treat hyperlipidameia

A

Statins

48
Q

How does statins work

A
  • Inhibit HMG-CoA reductase

- this decreases cholesterols synthesis in the liver

49
Q

Name the adverse effects of statins

A
  • Rhabdomyolysis
  • muscle aches
  • don’t drink grapefruit juice with simvastatin
50
Q

What lifestyle advice should be given with someone with hyperlipidaemia

A
  • BMI of 20-25
  • mediterranean diet - increase fruit, veg, fish, unsaturated fats, decreased red meat
  • increase exercise
51
Q

Name the 1st line therapy for hyperlipdiaemia

A
  • Atrovastatin 20mg at night for primary prevention and 80mg for secondary prevention and primary prevention to those with kidney disease
  • Can use simvastatin 40mg as an alternative
52
Q

What is the 2nd line therapy for hyperlipidaemia

A
  • Ezetimibe - cholesterol absorption inhibitor

- used in statin intolerance or combination with statins to achieve target reduction

53
Q

Name the 3rd line therapy for hyperlipidemia

A
  • Allirocumab - monoclonal antibody against PCSK9 - reduces hepatocyte LDL receptor expression
  • effective in reducing LDL - expensive and needs to be given by injection every 2 weeks