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Pharmacology > Lipids > Flashcards

Lipids Flashcards

1
Q

what is atherosclerosis

A

deposition of cholesterol in arteries

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2
Q

what are the risk factors in deposition?

A

smoking
hypertension
diabetes mellitus
genetic factors

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3
Q

what is cholesterol mainly composed of?

A

LDLs

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4
Q

What ages create a higher risk for coronary heart?

A

men >45

women >55

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5
Q

what blood pressure values creates a risk factor for CHD?

A

> 140/90

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6
Q

are low HDL-C levels a risk for CHD? What are their values?

A

yes

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7
Q

what is the difference between a thrombus and an embolus?

A

thrombus is adhered to the inner wall of the artery

Emboli are thrombus that have been dislodged and are now floating through the circulation

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8
Q

what could happen if a thrombus detached from the carotid artery wall?

A

the emboli could become lodged in the brain capillaries –> stroke

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9
Q

what could happen if a thrombus detached for the coronary artery wall?

A

could get lodged in the coronary capillaries –> heart attack

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10
Q

triacylglycerols and cholesterol can flow freely in the blood. True or false?

A

False

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11
Q

What is a chylomicron?

A
  • carrier of dietary lipids in blood to liver

- triglyceride rich, some cholesterol

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12
Q

What are VLDLs?

A
  • very low density lipoproteins
  • carrier of lipids from liver to periphery in blood
  • triglyceride rich, some cholesterol
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13
Q

What are LDLs?

A
  • low density lipoproteins
  • BAD cholesterol
  • carrier of cholesterol from liver in blood
  • want these levels to low
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14
Q

What are HDLs?

A
  • high density lipoproteins
  • GOOD cholesterol
  • scavenge cholesterol from artery wall
  • want these levels to be higher
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15
Q

What is indicated if you have high levels of chylomicrons?

A

you have triglycerides floating around in your blood

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16
Q

What organ has the ability to make its own cholesterol if levels are low?

A

the liver

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17
Q

What is the purpose of bile salts?

A

to break down large fat molecules into smaller ones

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18
Q

What are LDL receptor and where are they found?

A

receptor that monitor for bad cholesterol

- found on the liver

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19
Q

What is LP lipase? What is its function?

A
  • lipoprotein lipase
  • found in capillaries
  • takes triglycerides and turns them into free FAs
  • cholesterol is left behind
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20
Q

Where do the free FAs go after LP lipase metabolism?

A

into adipose tissue and muscle

21
Q

Which structure does LP lipase mainly target. Why?

A
  • chylomicrons and VLDLs

- because these are the carrier of triglycerides

22
Q

what are 3 ways to decrease triglycericides?

A
  • decrease dietary TGs
  • increase LP lipase activity
  • decrease VLDL secretion from liver
23
Q

Which drugs are used to increase LP lipase activity

A
  • gemfibrozil

- niacin

24
Q

what drug decreases VLDL secretion?

A
  • niacin
25
Q

How does niacin work?

A
  • inhibits lipolysis in adipose tissue
  • fewer FAs taken back to liver
  • fever VLDL produced/released due to less TGs
26
Q

What are the side effect of niacin?

A 
Serious 
- increased liver enzymes in blood
- hyperglycemia
Short term
- skin flushing and pruritis (ASA will prevent this)
caution
- could exacerbate peptic ulcers
Minor
- dry eyes
- blurred vision
- fatigue
- GI distress
27
Q

Name 2 fibric acid derivatives/fibrates.

A

gemfibrozil

fenofibrate

28
Q

What is the mechanism of fibrates?

A

increases VLDL clearance by increasing LP lipase activity

29
Q

What are the side effects of fibrates?

A

MAJOR

  • flu-like (muscle cramps, tenderness, stiff, weak)
  • increased risk of myopathy when combine with statins
30
Q

What are 3 ways to decrease cholesterol?

A 
Decrease GI uptake
- decrease dietary uptake
- decrease reabsorption of bile acids 
- decrease absorption of cholesterol
Decrease LDL levels
- decrease VLDLs
- LDL receptors
Decrease endogenous cholesterol synthesis
31
Q

Name 2 bile acid binding resins.

What do they do?

A
  • cholestyramin and colestipol
  • decrease cholesterol levels by decreasing reabsorption of bile acids
  • only used when LDL levels are elevated
32
Q

How do bile acid binding resins work?

A
  • bile acids are normally 95% absorbed
  • binding resins prevent this
  • bile acids lost in feces
  • now the body need more bile acid and requires cholesterol to synthesis them
  • liver get cholesterol by making new ones or by uptake through LDL receptors
  • LDL levels will ultimately decrease
33
Q

What are the side effects of bile acid binding resins?

A

MAJOR
- may increase VLDL levels (BAD and we don’t know why it does this)
MINOR
- decrease absorption of fat soluble vits (vitK deficiency is a problem)
- nausea, constipation, bloating
- alters absorption of thiazides, warfarin, aspirin, etc

34
Q

Name 2 HMG-CoA reductase inhibitors.

What do they do?

A
  • lovastatin, simvastatin (the “statins”)
  • decrease LDL levels
  • modest HDL increase
35
Q

How do statins work?

A
  • inhibit rate limiting step of cholesterol synthesis
  • this decreases hepatic cho. levels which increases the expression of hepatic LDL receptor genes
  • this will then increase the uptake of LDLs (and cho.) from the circulation through LDL receptors
36
Q

What are the side effects of statins?

A 
- generally well tolerated
MAJOR
- myopathy (severe myalgia, muscle weakness)
- hepatotoxicity
MINOR
- first pass metabolism
- avoid CYP3A4 inhibitors (grapefruit juice)
- safety unknown in pregnancy --> avoid
37
Q

What is P-gp?

What happens if this is inhibited?

A
  • P-glycoprotein
  • get rids of things our body doesn’t normally encounter (drugs)
  • found in liver and small intestine
  • drugs are attacked by P-gp first then by CYPs to decrease the % of drug that gets in the body
  • if inhibited, drugs get into the body at much higher concentrations
38
Q

What must you monitor if a patient is on a statin?

A
  • liver enzymes –> looking for possible liver failure

- watch for myopathy (muscle weakness & myalgia)

39
Q

What secondary benefits contribute to the name “super statins”?

A
  • may increase bone formation (reduced fractures in elderly)
  • HTN –> may lower BP
  • dementia –> decreased risk of development
  • renal function –> helps preserve it
  • asthma –> in trials for a possible drug
40
Q

Name a cholesterol absorption inhibitor.

What does it do?

A
  • ezetimibe
  • inhibits dietary and biliary cho. absorption
  • works at intestinal brush border (doesn’t affect TGs or fat soluble vitamins)
41
Q

How do cholesterol absorption inhibitors work?

A
  • stops absorption of cho. in the intestine
  • lowers cho. in chylomicrons
  • liver responds with LDL uptake through receptors and cho. synthesis
  • therefore, decreases LDL and cholesterol
42
Q

what other lipid lowering drug are cholesterol absorption inhibitors usually combined with?

A
  • statins

- combo allows lower doses of statins and a greater elevations of transamidases

43
Q

What are the side effects of ezetimibe?

A
  • myalgia
  • hepatits
  • rhabdomyolysis (death of muscle fibers with release of their contents into bloodstream)
  • acute pancreatitis
44
Q

What is the main mechanism of statins?

A

decrease of LDLs

45
Q

What is the main mechanism of fibrates?

A

decrease triacylglycerides and increase HDLs

46
Q

what is the main mechanism of niacin?

A

decrease triacylglycerides and increase HDLs

47
Q

What is the main mechanism of bile acid sequestrants?

A

decrease LDLs

48
Q

What is the main mechanism of cholesterol absorption inhibitors?

A

to decrease LDLs

49
Q

Why is the combo of bile acid binding resins and HMG-CoA inhibitors a good combo?

A
  • have additive effects
  • bile acid sequestrants increase LDL removals but have a compensatory increase in cho. synthesis
  • HMG-CoA inhibitors block this compensatory actions

Pharmacology (5 decks)

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