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CMPP > Lipid Disorders > Flashcards

Lipid Disorders Flashcards

1
Q

What three things are cholesterol needed for

A

Cell membranes steroids vitD

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2
Q

What is the goal of fats

A

To get to the liver for synthesis storage and export

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3
Q

What makes it harder for fat to make it to the liver

A

The fact that they are hydrophobic I need it lipoprotein’s to take them there

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4
Q

Where are triglycerides broken down

A

In the intestine

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5
Q

What are triglycerides broken down into

A

Glycerides and fatty acid’s

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6
Q

What breaks triglycerides down

A

Pancreatic enzymes that are activated by bile acids

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7
Q

How are triglycerides broken down

A

They are rearrange and cholesterol is Esterfied and then join forces to form a chylomicron this chylomicron goes through the lymphatic system and eventually gets into

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8
Q

What are proteins that aid in metabolism

A

C proteins aka c Apolipoprotein’s

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9
Q

What is a cofactor for lipoprotein lipase

A

C-II

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10
Q

Order of increasing density of lipoprotein’s and decreasing amount of lipid caring capacity

A

Chylomicrons VLDL IDL LDL HDL

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11
Q

What form to carry fat from the intestine

A

Chylomicrons

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12
Q

Where is VLDL made

A

In the liver

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13
Q

What increases VLDL formation

A

Increased fatty acids to the liver

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14
Q

Where does the VLDL transport triglycerides and cholesterol to

A

Adipose tissue for storage and other tissue for fuel

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15
Q

What does removal of triglycerides produce

A

IDL and LDL

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16
Q

What are for stimulators a VLDL release

A

Obesity
increase in calories
ethanol
estrogen

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17
Q

How did fatty acids get delivered to the periphery

A

Hydrolysis of triglycerides in VLDL

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18
Q

What causes an increase of storage of fat

A

Increased lpl when is regulated by insulin

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19
Q

What preevent storage of fat

A

Starvation because it decreases LPL

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20
Q

What does LPL stand for

A

Lipoprotein lipase

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21
Q

Where are chylomicron Reminence taken up by

A

The liver

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22
Q

What helps to store cholesterol and the tissues

A

LDL

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23
Q

Where does catabolism of LDL take place

A

The liver

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24
Q

What happens as a product of LDL catabolism

A

Free cholesterol is made

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25
Q

What down regulates the HGM co-a reductase

A

Free cholesterol

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26
Q

What is the rate limiting step of cholesterol synthesis

A

HGM co-a reductase

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27
Q

Where does LDL catabolism take place

A

The liver

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28
Q

Where is HDL made

A

In the liver and intestines

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29
Q

What is scavenges cholesterol and returns it to the liver for excretion via bile salts

A

HDL

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30
Q

What is HDL able to accept

A

Free cholesterol and phospholipids from broken down chylomicrons and VLDL’s

31
Q

What enzyme is employed by HDL

A

LCAT

32
Q

What does LCAT stand for

A

Lecithin cholesterol acetyltransferase

33
Q

Where is LCAT produced

A

The liver

34
Q

What did patients with liver disease have an increase in

A

Free cholesterol

35
Q

What can HDL donate when it is broken downI

A

C proteins for VLDL’s and chylomicrons

36
Q

What delivers cholesterol to the adrenal glands and gonads for stereo genesis

A

HDL

37
Q

How much ingested cholesterol is actually absorbed

A

One third at typical dietary intake

38
Q

What happens to the most of cholesterol that is turned in the bile acid and secreted into the intestine

A

It is reabsorbed

39
Q

Two reasons why you should fast for cholesterol

A

Chylomicrons can be present in the blood up to 10 hours after a meal and this. Maybe prolonged of alcohol is consumed

40
Q

4 risk factors for hyperlipidemia

A

Hypertension
smoking
family history
siblings in the 40s with CAD

41
Q

Four components of the lipid panel

A

Total cholesterol HDL LDL triglycerides

42
Q

Who is high-risk for hyperlipidemia and should be tested

A

Men at 25 and women at 35+ one risk factor

43
Q

Who is low risk for hyperlipidemia and should be tested

A

Men at 35 women at 45

44
Q

Equation for total cholesterol

A

HDL plus LDL plus VLDL

45
Q

How do you calculate VLDL

A

Triglycerides divided by five

46
Q

What should total cholesterol levels be under

A

200

47
Q

What is an inherited disorder of overproduction of VLDL

A

Familial hyperlipidemia

48
Q

How do you treat hyperlipidemia when it is familial

A

Dietary restriction and lipid lowering agents

49
Q

What is the inheritance of familial hypercholesterolemia

A

Autosomal dominant

50
Q

What if three populations have a higher incidence of familial hypercholesterolemia

A

French-Canadians
Africans
Ashkenazi Jews

51
Q

What is the problem and familial hypercholesterolemia

A

There is a mutation and LDL receptor gene and hepato- sites and cells are able to have an LDL reuptake

52
Q

Levels of LDL cholesterol and triglycerides in familial hypercholesterolemia

A

LDL increase between 260 and 400
cholesterol above 300
triglycerides normal

53
Q

Clinical hallmark of familial hypercholesterolemia

A

Tendon xanthomas typically the Achilles patellar extensor tendons of the hands

54
Q

What is the primary treatment of familial hypercholesterolemia

A

Statins

55
Q

What treatment is used in combination with statins for familial hypercholesterolemia

A

Niacin
bile acid sequestrants
Exetimibe

56
Q

What is the inheritance of familial hypertriglyceridemia

A

Autosomal dominant

57
Q

2 lab findings of familial hypertriglyceridemia

A

Moderate triglyceride elevation

moderate cholesterol elevation

58
Q

Two problems in familial hypertriglyceridemia

A

Increase in VLDL production and a decrease in VLDL catabolism

59
Q

Triad of diagnosis of familial hypertriglyceridemia

A

Triglyceride between 250 and 1000
cholesterol less than 250
decrease in HDL

60
Q

What is the rate limiting step of cholesterol synthesis in the liver

A

HMG co-a reductase

61
Q

What happens when you decrease cholesterol production

A

Increase his LDL receptors on the hepatocytes

62
Q

What happens when you increase receptors on the hepatocytes for LDL

A

More LDL is reabsorbed from the blood

63
Q

Two medications and their brands for the first line treatment of high cholesterol

A

Atorvastatin Lipitor
pravastatin Pravacho
HMG co a reductase

64
Q

What is the mechanism of action of bile acid sequestration

A

Binds to the bile acids in the intestinal tract cholesterol is converted to bile acids bile acids are excreted into the intestine to aid digestion and are reabsorbed

65
Q

2 bile acid sequestration drugs

A

Cholestyramine (questran)

Colesevalam (welchol)

66
Q

Two unknown MOA second line treatments for high cholesterol

A

GemfibroZil (lopid)

Niacin

67
Q

Side effects of cholestyramine

A

Constipation

68
Q

Side effect of Niacin

A

Flushing

69
Q

What drug fights cholesterol in the intestines before it gets to the bloodstream

A

Ezetimibe (zetia)

70
Q

What is good to mix zetia with for increased cv benefit

A

Statins

71
Q

Does the AHA recommend a specific number for LDL

A

No

72
Q

What two things does LDL reduction lower the risk of

A

Stroke and MI

73
Q

What three things are fats made of

A

Cholesterol triglycerides phospholipids

CMPP (17 decks)

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