Lipid Profile Flashcards

1
Q

Major lipids present in plasma?

A

fatty acids, triglycerides, cholesterol and phospholipids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Atherosclerosis?

A
  • Atherosclerosis is associated with elevated plasma concentrations of lipids; cholesterol in particular
  • characterized by development of abnormalities calledlesionsin walls ofarteries
  • These lesions may lead to narrowing of the arterial walls due to buildup ofatheromatous plaques
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Complications of atherosclerosis?

A

it can result incoronary artery disease,stroke,peripheral artery disease, orkidney disorders, depending on which body parts(s) the affected arteries are located in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Lipid transport?

A

Lipids are carried in the bloodstream by complexes called lipoproteins. Lipids are not soluble in plasma/water. Therefore, they are transported in micelle-like complexes composed of phospholipids, cholesterol and protein on the outside with cholesteryl esters and TGs on the inside.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Classes of lipoproteins?

A

chylomicrons, VLDL (mainly TGs), LDL (mainly cholesterol) and HDL (mainly phospholipid).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Significance of a lipid profile?

A

The lipid profile test is a combination of tests conducted together to check for any risks of coronary heart disease (CHD), or as a preventive measure to check any risks depending on factors like eating habits, diet, stress, exercise and life-style related

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lipid profile contains?

A

Triglyceride (TG) levels
Total cholesterol
High density lipoprotein (HDL)- cholesterol
Low density lipoprotein (LDL)- cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Whos should get a lipid profile?

A

People with known vascular disease and those at increased risk.
CAD, cerebrovascular and peripheral vascular disease risk
FHx of premature CAD- CAD occurring at age <60 years, hyperlipidaemia
DM, HTN
Patients with clinical features of hyperlipidemia- corneal arcus etc
Patients with lipaemic plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors needing a lipid profile?

A

abnormal cholesterol levels, elevated levels ofinflammatory biomarkers, high blood pressure,diabetes,smoking(both active andpassive smoking),obesity, genetic factors, family history, lifestyle habits, and an unhealthy die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lipid profile test procedure?

A

Clean the site with an antiseptic and use a tourniquet
With a needle and syringe, draw 5 mls of blood
The test is done on serum; therefore, blood is allowed to clot and separate by centrifugation.
Pretest: 12 hour fast prior to sample collection, patient should follow their normal diet 1week before test. No alcohol 24-48 hours prior to test.
However, in emergency situations e.g. patient presenting with MI, it can be a non-fasting lipid profile with caveat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are triglycerides?

A

Triglyceride (TG) is an ester derived from glycerol and free fatty acids. Glycerol backbone with FAs attached by ester bonds.
TGs are the main constituent of body fat in humans and other vertebrates, as well as vegetable fat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of increased TGs?

A

Levels increase from eating extra calories- esp. carbs, alcohol etc Exogenous source: Diet. Endogenous: Liver & tissue storage
High levels are associated with heart disease, blood vessel disease, fatty liver disease, pancreatitis, diabetes, kidney diseases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Increased TGs?

A

Hyperlipoproteinemia, liver disease, alcoholism, nephrotic syndrome, renal disease, hypothyroidism, poorly controlled DM, pancreatitis, glycogen storage disease (Von Gierke’s disease), MI (elevated levels may persist for several months after MI), Gout, Werner’s syndrome, Down’s syndrome and Anorexia nervosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Decreased TGs?

A

Congenital alpha beta lipoproteinaemia, malnutrition, malabsorption syndromes, hyperthyroidism, brain infarction and chronic obstructive lung disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Serum TGs?

A

Hypertriglyceridemia increases the risk for pancreatitis
Hypertriglyceridemia is associated with the following clinical findings: eruptive xanthoma, lipema retinalis, hepatomegaly, splenomegaly, depressed HDL-C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lipemia retinalis?

A

is an eye condition caused by elevated levels oftriglyceridesin the blood, a condition known ashypertriglyceridemia, or due tolipoprotein lipase deficiency(chylomicronemia).In this condition, theretinal arteries and veins, and occasionally the entirefundus, exhibit acreamy-white to salmon-red discoloration

17
Q

Cholesterol?

A

Cholesterol is a type of fat found in our blood.
It is produced by our body and is ingested from the foods we eat (animal products)
It is made by the liver and is also used by the liver to make bile which helps in the digestion of foods.
Cholesterol is also needed to make certain hormones and to produce vitamin D.
High cholesterol is a significant risk factor for atherosclerosis and coronary arterial occlusion.

18
Q

Normal cholesterol?

A
19
Q

Post cholesteral test?

A

Post test: Cholesterol levels > 200mg/dl should be re-tested, and the results averaged. If the two results differ by >10%, a third test should be done.

20
Q

Management for high cholesterol?

A

If hypercholesterolaemia has been established, the diet should be lower in animal fats and replace saturated fats with unsaturated fats.

Eat more fruits, vegetables and whole grains

At least 6 months of diet before initiating cholesterol lowering drug therapy.

21
Q

Saturated vs unsaturated fats?

A

Unsaturated fats: Nuts, plant oils, fish like salmon/tuna, avocado, olives etc
Saturated: fatty beef, pork, poultry with skin, dairy etc

22
Q

Elevated cholesterol?

A

Hyper-lipoprtoteinemia, cholestasis, hepatocellular disease, nephrotic syndrome, Chronic renal failure, hypothyroidism, poorly controlled DM, alcoholism, glycogen storage disease, obesity, diet high in Cholesterol

23
Q

Decreased cholesterol?

A

Severe hepatocellular disease, malabsorption syndrome, malnutrition, hyperthyroidism, chronic anaemias, conditions of acute illness, severe burns, mental retardation

24
Q

High density lipoprotein cholesterol?

A

HDL-C is a class of lipoproteins produced by the liver and the intestines.
It is composed of phospholipids and one or two apolipoproteins.
It plays a role in the metabolism of the other lipoproteins and in cholesterol transport from the peripheral tissues to the liver.

25
Q

Values for HDL cholesterol?

A
26
Q

Low denisty lipoprotein cholesterol?

A

They are formed from VLDL in the blood circulation and transport cholesterol from liver to other tissues.
The higher the number of LDL particles, the higher is the risk for CAD.
LDL can build up on the walls of the arteries and make them narrower. The fatty deposits form plaques that lines the arteries and may cause blockages. This build up is atherosclerosis.

27
Q

Values of LDL-C?

A
28
Q

Positive risk factors?

A
29
Q

Negative risk factors?

A
30
Q

Types of hyperlipedemia?

A

Common primary hyperlipidaemia- elevated LDL only. 70%
Familial primary hyperlipidaemia: multiple phenotypes exist
Secondary hyperlipidaemia: causes include Cushing’s syndrome, hypothyroidism. Nephrotic syndrome, cholestasis. LDL elevated. Treat cause first.
Mixed hyperlipidaemia: Elevated LDL and TGs. Caused by T2DM, metabolic syndrome, alcohol abuse and CRF.

31
Q

Management?

A

Identify familial or 2° hyperlipidaemias, as TX may differ.

Give lifestyle advice; aim for BMI of 20–25; encourage a Mediterranean-style diet—more fruit, vegetables, fish, unsaturated fats; and less red meat; more exercise.

32
Q

Primary and secondary management?

A

Top tx priority are those with known CVD (there is no need to calculate their risk: ipso facto they already have high risk).
Second tx priority is primary prevention in patients with chronic kidney disease or type-1 diabetes, and those with a 10-yr risk of CVD >10%, irrespective of baseline lipid levelsP

33
Q

Pharmacological treatment?
1st line

A

1st-line therapy: Atorvastatin 20mg PO at night, for primary prevention, and 80mg for secondary prevention and primary prevention in those with kidney disease.

34
Q

2nd line pharmacological treatment?

A

2nd-line therapy: Ezetimibe—a cholesterol absorption inhibitor, may be used in statin intolerance or combination with statins to achieve target reduction.

35
Q

3rd line pharmacological treatment?

A

3rd-line therapy: Alirocumab—a monoclonal antibody against PCSK9 (acts to reduce hepatocyte LDL receptor expression).

36
Q

Other pharmacological treatments?

A

Others: fibrates, eg bezafibrate (useful in mixed hyperlipidaemias); anion exchange resins, eg colestyramine; nicotinic acid (increases HDL; reduces LDL; SE: severe flushes; aspirin 300mg ½h pre-dose helps this).