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Pharm > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

Test 4

1
Q

Define dyslipidemia

A

High cholesterol
Pathologic level of lipids in the bloodstream

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2
Q

What is the leading cause of death in the US?

A

Atherosclerosis

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3
Q

What is Atherosclerosis?

A

Lipid deposits in coronary arteries which can lead to an ischemic event (MI, stroke)

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4
Q

Describe the process of atherogenesis

A
  1. Low-density lipoprotein (LDL) - cholesterol-carrier molecule produced in liver and distributes cholesterol throughout the body
  2. Excessive LDL leads to increased cholesterol molecules deposited under endothelial lining of the intima of arteries (connective tissue) → WBCs migrate into area and converge into Macrophages
  3. Macrophages are pro-inflammatory and are able to recognize cholesterol via CD36 and SR-A receptors → Macrophages swallow up the cholesterol → ROS, SO, HP, metalloproteinase and other pro-inflammatory markers are released → LDL is oxidized and becomes antigenic
  4. Oxidized LDL can reenter blood stream → antibodies produced against it enter the area and form immune complexes → elevates immune response even more→ calcification of destroyed cells
  5. Macrophages can’t break down cholesterol b/c unable to break steroid ring ; it can be turned into bile acids so the cholesterol builds up inside macrophages more and more and are called foam cell (spongy large appearance) → cholesterol begins to crystallize in foam cell → foam cell ruptures → calcified necrotic plaque formed in vessel
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5
Q

What are all the types of lipids?

A

Free fatty acids
phospholipids
cholesterol
triglycerides
Glycolipids
prostaglandins

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6
Q

Increasing triglycerides _______ risk for metabolic syndrome

A

increases

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7
Q

Describe Triglyceride

A

glycerol ester combined with free fatty acids

form adipose tissue/fat
majority neutral fats

used as energy during fasting or between meals

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8
Q

What is the main storage form of fat in humans?

A

triglyerides

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9
Q

A cholesterol is a _____ molecule

A

sterol

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10
Q

What is cholesterol a precursor to?

A

steroid hormones
cell membranes
vitamin D
bile salts

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11
Q

Describe a choleterol structure

A

3-6 carbon rings with a -OH tail attached to a 5 carbon ring

adding side chains through metabolism & enzymes changes the molecule

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12
Q

How do we get cholesterol?

A
  1. diet
  2. de novo synthesis: liver makes cholesterol
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13
Q

T/F: diet alone can fix high cholesterol

A

F

only 20% of cholesterol comes from diet
need medications

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14
Q

What is the precursor & enzyme for cholesterol?

A

HMG-CoA
HMG-CoA reductase

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15
Q

What does HMG-CoA convert to? What enzyme is needed for this?

A

Mevalonate

HMG-CoA reducatase

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16
Q

Where is cholesterol made?

A

Liver

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17
Q

Describe lipoproteins

A

Circulate in the bloodstream & carry cholesterol/lipids in a shell bc they are not water soluble

Consist of “apolipoprotein” outer shell that is proteins & lipids mixed together to make it more water soluble in blood.

Shell that carries lipids through blood

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18
Q

What are the 4 types of lipoproteins?

A
  1. Chylomicron (Highest fat, lowest protein)
    -Formed in GI; final in liver
    -carry triglycerides & cholesterol
  2. VLDL
    -secreted by liver; travel to peripheries
    -converts to LDL
  3. LDL - Primary circulating in body
    -produced from liver; excess in arteries
    -“Bad cholesterol” associated w/ CAD
  4. HDL (lowest fat, highest protein)
    -produced in liver
    -“Good cholesterol”
    -scavenger of cholesterol from cells & other lipoproteins & takes them back to liver to be excreted in bile
    -Decreased levels associated w/ atherosclerosis
19
Q

What is the good cholesterol and why?

A

HDL - high density lipoprotein

Scavenges bad cholesterol & takes it back to the liver to be excreted in bile

20
Q

Describe the difference between triglycerides and cholesterol

A

Cholesterol: Sterol molecule and important for a number of precursor molecules needed within cell

triglycerides: Majority of neutral fats and consists of glycerol esters combined with fatty acids

21
Q

What is the lab test associated with cholesterol? what are the most important values on there?

A

Lipid profile

Total cholesterol & LDL/HDL ratio

22
Q

What is the normal LDL/HDL cholesterol ratio? If this ratio is increased, what does this mean? Give an example.

A

Ratio = LDL / HDL
Normal = 120 / 40
Approxiamtely = 3

If this is increased that means the risk of developing CVD from cholesterol is increased

Ex) Ratio = 240/40 –> 6
Since normal ratio is 3; 6 is 2x more than 3; you are 2x more likely to CVD related to cholesterol

23
Q

What are normal cholesterol levels?

A

Total cholesterol < 200
LDL <130
HDL > 40

24
Q

T/F: if total cholesterol is >200 and LDL is normal, but HDL is high, you most likely won’t get put on a -statin

A

T

25
Q

What is Familial hypercholesterolemia?

A

Genetic disorder that causes increase in LDL

More likely to develop CAD d/t problem regulating LDL

have hyperlipoproteinemias

26
Q

What are some secondary causes of dyslipidemia?

A

DM
Estrogen use
Acromegaly (excess growth hormone produced by pituitary gland)

27
Q

What are diet considerations when trying to lower cholesterol?

A
  • only eat 20% of calories from fat
  • eat more complex cars & fiber
    -lose weight
    -eat more omega-3 fatty acids
28
Q

Besides high cholesterol, what is another reason to be put on a statin?

A

Previous MI
Heart disease

29
Q

Where do most dyslipidemia drugs target?

A

heptatocytes in the liver

30
Q

Drugs: Statins

A

-Statin

Class: Statins
MOA: Block HMG-CoA reductase enzyme -> reduces cholesterol synthesis in the liver

-Reduce LDL (which causes increase in LDL-R) & trigylcerides
-slight increase in HDL

Take with food - increases absorption

Toxicity: elevated liver enzymes
-Muscle pain/weakness that may be severe if so, switch them off this medication
-elevated CK

31
Q

Compare a statin & HMG-CoA reductase enzyme

A

They have similar structures

Statins work as a competitive inhibitor. They binds to HMG–CoA and which prevents HMG-CoA reductase from binding and prevents conversion to cholesterol.

32
Q

Why do LDL receptors increase when LDL decreases?

A

To scavenge LDL from the blood

33
Q

When does cholesterol synthesis happen?

A

At night

34
Q

T/F: Its okay to give statins to pregnant women, breastfeeding women, or children

A

FALSE

IT IS NOT OKAY!!!!!!
THEY NEED THEIR CHOLESTEROL

YOU DO NOT BLOCK CHOLESTEROL IN ANY OF THESE POPULATIONS OF PEOPLE

Do not give them any medication that blocks their cholesterol even outside of statins

35
Q

Drugs: Niacin

A

Vitamin B3

Class: Niacin
MOA: Blocks movement of cholesterol into VLDL lipoproteins

Decreases VLDL/LDL
Increases HDL

Incorporated into NAD (energy producing pathway)

Megadose of 2-6 GRAMS needed

Toxicity: #1 effect = cutaneous vasodilation which is flushing in the face.
- elevated liver enzymes
-pruritis
-GI discomfort

36
Q

What is the 1st lipoprotein that comes from the liver? what is it converted to?

A

VLDL

LDL

37
Q

Drugs: Gemfibrozil

A

-fib-

Class: Fibrates
MOA: Increase lipolysis in the liver through PPAR which decreases lipid production

decreases VLDL & LDL

Toxicity: GI

38
Q

Drugs: Bile acid binding resins

A

Class: Bile acid binding resins

MOA: Large cation exchange resins surround food & prevent binding to cell membrane in intestine
- lipids not absorbed/prevent reabsorption

Need to be used in conjunction

May increase VLDL (not getting in diet so liver wants to produce more)

Granular preparation in liquid
Must be taken with meals

Toxicity: GI

Maybe not give this med to patients who are already have an issue with malabsorption or malnutrition

DO NOT TAKE THIS WITH OTHER MEDS BC OTHER MEDS WONT BE ABSORBED

39
Q

Drugs: Ezetimibe (Zetia)

A

Class: Inhibitor of intestinal sterol absorption
MOA: inhibits NPC1L1 transporter and prevents the uptake of cholesterol in the gut

Reduces LDL

Toxicity: Liver issues? arterial wall thickening?

40
Q

What is the cholesterol transporter in the gut called?

A

NPC1L1

41
Q

The ______ are cells line the GI tract

A

enterocytes

42
Q

Drugs: Evolocumab

A

Class: Monoclonal anitbody
PCSK9 inhibitor

MOA: Bind to PCSK9 (which inhibit LDL-R) to allow more LDL-R to allow statins to work better
Must be taken in conjuction with statins

LDL lowered to <25 mg/dL

43
Q

What is hypocholesterolemia associated with?

A

Cancer
Hemorrhagic stroke
depression
anxiety
preterm birth and low birthweight

Pharm (30 decks)

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