Unit 4 Lipids Flashcards

His LDL is elevated. Look at his Total Cholesterol value, it’s probably above 200, but might not be, because his HDL is likely low. <19 mg/dL is really really low, but it’s not out
of the realm of possibility.

Optimal: <115 mg/dL
High Risk: >150 mg/dL

Optimal: <170 mg/dL
High Risk:>200 mg/dL

Optimal: >40 (♂ male) >50 (♀ female) mg/dL
High Risk:<35 mg/dL

Optimal: <110 mg/dL
High Risk: >160 mg/dL

Answer: Usually, it takes decades of living on this earth for fatty plaques and fibrous plaques to develop. We can accelerate the formation of atherosclerosis by eating diets high in saturated fats. If we desire to have the opposite effect, we can eat a mostly vegetarian diet (defined as eating meat <2 times per week) and exercise 2-3 times per week for 30 minutes which will lead to optimal cardiovascular health. Of course, there are some pathologies which can promote atherosclerotic development quicker, but we’re just talking about
run-of-the-mill atherosclerosis here.

Answer:
Elevated. Likely this is because alcohol commonly causes pancreatitis, which then released a ton of triglycerides and caused the hypertriglyceridemia. This is an example where the etiology of the hypertriglyceridemia can be discovered, that does NOT always happen though.

Answer:
A mutation in the gene that regulates either the receptor or the utilization of
internalized LDL particles in the peripheral cells. Mammalian cells are required to
have cholesterol in their cell membranes, so our cells must produce their own
cholesterol because they can’t take it in from the outside world.

Answer:
> 500 mg/dL

Answer:
HDL-C

Answer:
The correct answer is B) Acute Pancreatitis. Remember, hypertriglyceridemia can cause acute pancreatitis when the level goes above 500 mg/dL. HDL is the good cholesterol, so there really isn’t a time when we would need to decrease the HDL only.

The correct answer is D) LDL Receptor. This patient likely has Familial Hypercholesterolemia (FH), an uncommon, but commonly tested cholesterol abnormality. The patients don’t have the proper genes to use the LDL particles (i.e. they can’t bring them into their cells). Because of this, the blood level of LDL remains extremely high. These patients can have their first heart attack as teenagers. There are several mutations which will cause this but just know that this is caused by an inability for the body to take in the LDL molecule into their cells and use it.

Answer:
The correct answer is Patient C. This patient has hypobetalipoproteinemia, which is seen by the genetic deletion of apo-B which associates itself with LDL-C. This deletion does not allow for the LDL receptors to recognize the LDL particle with the apo-B wrapped around it.
Patient A has Familial Hypercholesterolemia.

Patient B has hypoalphalipoproteinemia.

Patient D has Primary Hypertriglyceridemia.

Answer:
Provide the body with tons and tons of energy

lipids that are absorbed from the diet and contain Apo B48

chylomicrons travelling to the liver in the lymphatics that are newly created from
the absorbed micelles in the intestinal cells and contain Apo B-100

Triglycerides packaged by the liver into VLDL for circulation around the body
and contain Apo B-100

Cholesterol and Fatty Acids being transported from the peripheral tissues for excretion in the bile and contain Apo A-I and Apo A-II

- Apo B-48

Note: Chylomicrons are large triglyceride-rich lipoproteins produced in enterocytes from dietary lipids—namely, fatty acids, and cholesterol. Chylomicrons are composed of a main central lipid core that consists primarily of triglycerides, however like other lipoproteins, they carry esterified cholesterol and phospholipids.

- Apo B-100, Apo A-I, Apo C-II, Apo E

stands for very low density lipoprotein. Lipoproteins are made up of cholesterol , triglycerides, and proteins. They move cholesterol, triglycerides, and other lipids (fats) to around the body. VLDL is one of the three main types of lipoproteins. VLDL contains the highest amount of triglycerides.

Apo B-100, Apo-E

- Apo B-100

LDL (low-density lipoprotein) cholesterol, sometimes called “bad” cholesterol, makes up most of your body's cholesterol. High levels of LDL cholesterol raise your risk for heart disease and stroke.

- Apo A-I, Apo A-II, Apo C-II, Apo E

HDL (high-density lipoprotein) cholesterol, sometimes called “good” cholesterol, absorbs cholesterol in the blood and carries it back to the liver. The liver then flushes it from the body. High levels of HDL cholesterol can lower your risk for heart disease and stroke.

Answer: Apo B-100

This would be expected. An HDL value elevated above the LDL value is what happens in athletes that eat mostly fruits and vegetables and little meat. This is the most optimal circumstance for this man’s cardiovascular health. Of note, estrogen causes HDL-C to be increased so the reference range for women is about 10 mg/dL higher than the range for men. A higher HDL level confers better cardiovascular health for premenopausal women. This advantage disappears after menopause and the cardiovascular risks for females become equal to that of males.

This is a three-step method which produces hydrogen peroxide and a color change from cholesterols.

120 mg/dL

Lipids serve as

1.Energy Storage

2.Membrane Structure

3.Cell Signaling Molecules

Lipids are insoluble in water

1.Triglycerides

2.Phospholipids

1.Sphingomyelin

2.Glycosphingolipids

1.Vitamins A, E, K

apolipoproteins

contain an alkyl chain WITHOUT a double bond.

note:

There is no more room to stick any more hydrogen on that chain It is “saturated” with hydrogen

- contain an alkyl chain WITH a double bond

There is room to stick more hydrogen on that chain It is “unsaturated” with hydrogen

1.Cholesterol

2.Steroid hormones

3.Bile acids

4.Vitamin D

it's absorbed from Diet

it's produced by the Liver

Chylomicrons and HDL-C - associated with getting lipids into the blood

Chylomicrons, to be shipped from the intestines to the liver

= LDL-C, to be shipped to the periphery and deposited in blood vessels, liver, and muscle...high levels are correlated with risk of myocardial infarction

Chylomicrons, HDL-C, and VLDL-C - only found in the extremes of lipid concentrations in lipoproteins (e.g. very high and very low), involved in transfer for the endogenous cholesterol pathway

Chylomicrons and HDL-C (there are others, but these are the important ones to understand) To help me remember, E stands for Exogenous

to maintain an equilibrium of cholesterol

glycerol forming esters

A mutation in the LDL-R gene that regulates either the receptor or the utilization of internalized LDL particles in the peripheral cells. Mammalian cells are required to have cholesterol in their cell membranes, so our cells must produce their own cholesterol because they can’t take it in from the outside world.

Hyperthyroidism

Hepatic Failure

Malnutrition / Anemia

Starvation / Anorexia

Abetalipoproteinemia

Hypertriglyceridemia can cause Acute Pancreatitis and Acute Pancreatitis can cause hypertriglyceridemia

Can occur because of Acute Alcoholism

High fat meal (lipemic specimens)

Hereditary hypertriglyceridemia

An independent and very significant risk factor for Coronary Artery Disease (CAD)

Physiologic role is undefined, but an association with CAD has been identified

Bilirubin significantly decreases all enzymatic cholesterol assays

• Cigarette smoking
• BP ≥140/90
• HDL <40 mg/dL
• Family history of coronary heart disease
• Age ≥45 men ≥55 women

The higher CAD risk, the lower the LDL goal

LDL cholesterol goal: <100 mg/dL

Initiate lifestyle changes: >100 mg/dL

Consider drug therapy: >100 mg/dL

LDL cholesterol goal: <130 mg/dL

Initiate lifestyle changes: >130 mg/dL

Consider drug therapy: >160 mg/dL

LDL cholesterol goal: <160 mg/dL

Initiate lifestyle changes: >160 mg/dL

Consider drug therapy: >190 mg/dL

HDL-C <40 mg/dL

Age >45(men) >55(women)

Family History of Coronary Artery Disease

Blood Pressure >140/90

Diabetes

Cigarette smoking

Low

High. Because they’re flowing right through without being absorbed.

Bile acids allow us to emulsify and absorb fats from our food

Remember also, that lipids are removed from the body in the bile

Note: This can tip the balance toward lipid deposition

Excessive elimination of cholesterol can lead to gallstone formation

HDL-C, LDL-C, and Triglycerides all increase

However, the HDL-C/LDL-C ratio remains the same

Glucocerebrosidase deficiency

Fats collect in the spleen, liver, kidneys, lungs, brain, and bone marrow

It’s a lipid storage disease, so what do you think it does to fat levels? It increases them!

Symptoms are painless splenomegaly, anemia, or thrombocytopenia and occasionally seizures

Sphingomyelinase deficiency (Memory Trick: Pick your nose with your sphinger)

Autosomal recessive disorder caused by accumulation of lipids in the liver, spleen, bone marrow, lungs, and brain

Neurologic complications include ataxia: can’t walk, eye paralysis, brain degeneration, hypersensitivity to touch

Characteristic cherry-red spot develops in the retina

Alpha galactosidase A deficiency

Deposits fats in the autonomic nervous system, eyes, kidneys, and cardiovascular system

Fabry disease is the only X-linked lipid storage disease, so it primarily affects only Males, Females can be affected though, usually with a milder form

Renal failure is common, so kidney transplants or dialysis are also frequently used

Enzyme replacement can be an effective therapy

Classified as a GM2 gangliosidosis which is usually a storage of fats in nervous tissues

Memory Trick: Tay-Sa(x) Disease = He(x)oseaminidase deficiency

Symptoms include progressive loss of mentation, dementia, sensorineural hearing loss, blindness, and also a cherry red spot on the macula

Typically occurs in young children and death is usually caused by bronchopneumonia

Dextran sulfate with MgCl2 and the Lieberman-Burchard method using acetic anhydride

Enzymatic methods are commonly performed in today’s laboratories

HDL > 60 mg/dL is desired

HDL < 40 is a risk factor for CAD

Total Cholesterol: 140-200 mg/dL (3.6-5.2 mmol/L)

HDL-C: 40-75 mg/dL (1.0-2.0 mmol/L) tip 4 Head, at 75 your Helpless.

LDL-C: 50-130 mg/dL (1.3-3.4 mmol/L) Tip: roman numeral L= 50, 13 in unLucky

Triglycerides: 60-150 mg/dL (0.7-1.7 mmol/L) tip: tri X 20 to 50 times to get right

The correct answer is B) HDL 35 mg/dL and LDL 250 mg/dL. A poor diet is the number one influencing factor on cholesterol in our blood. This is not only mediated by his lack of vegetable consumption, but more importantly, he is over-consuming beef and pork … just like 90% of America. He gets adequate exercise, which increases HDL and decreases LDL. However, his diet overshadows this positive effect on HDL. Answer A) is rare and would be seen in hypoproteinemia and an inability to form the
apolipoproteins. Answer C) is commonly seen in pregnant or recently postpartum females who have a diet rich in saturated fat. Answer D) is not a common plausible
pathology so you don’t need to worry about it. Usually, if HDL is greater than LDL, that is a good thing, but it’s usually pretty close like HDL 60, LDL 40.

The correct answer is C) LDL-C. This is calculated by the Friedewald calculation which requires values for all the other components of the lipid panel. Here is the equation:
LDL-C = Tchol - HDL-C - (TRIG / 5) LDL-C = 201 mg/dL - 38 mg/dL - (298 mg/dL /5) = 123.4 mg/dL

The correct answer is B) B, E. Apo B-100 and Lp(a) are poor markers for health. Apo B-100 is the apolipoprotein that tells the body to take this bag of lipids to the tissues.
Lp(a) is a small particle associated with Apo B-100. Lp(a) is a particle with higher lipid content than LDL-C, is slightly larger, and significantly contributes to the risk for coronary artery disease and strokes.

Serum from a fasting specimen, this is commonly collected in a serum separator tube

Cholesterol oxidase