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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?

25
How does niacin work?
- inhibits lipolysis in adipose tissue - fewer FAs taken back to liver - fever VLDL produced/released due to less TGs
26
What are the side effect of niacin?
``` 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
Name 2 fibric acid derivatives/fibrates.
gemfibrozil | fenofibrate
28
What is the mechanism of fibrates?
increases VLDL clearance by increasing LP lipase activity
29
What are the side effects of fibrates?
MAJOR - flu-like (muscle cramps, tenderness, stiff, weak) - increased risk of myopathy when combine with statins
30
What are 3 ways to decrease cholesterol?
``` 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
Name 2 bile acid binding resins. | What do they do?
- cholestyramin and colestipol - decrease cholesterol levels by decreasing reabsorption of bile acids - only used when LDL levels are elevated
32
How do bile acid binding resins work?
- 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
What are the side effects of bile acid binding resins?
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
Name 2 HMG-CoA reductase inhibitors. | What do they do?
- lovastatin, simvastatin (the "statins") - decrease LDL levels - modest HDL increase
35
How do statins work?
- 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
What are the side effects of statins?
``` - 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
What is P-gp? | What happens if this is inhibited?
- 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
What must you monitor if a patient is on a statin?
- liver enzymes --> looking for possible liver failure | - watch for myopathy (muscle weakness & myalgia)
39
What secondary benefits contribute to the name "super statins"?
- 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
Name a cholesterol absorption inhibitor. | What does it do?
- ezetimibe - inhibits dietary and biliary cho. absorption - works at intestinal brush border (doesn't affect TGs or fat soluble vitamins)
41
How do cholesterol absorption inhibitors work?
- 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
what other lipid lowering drug are cholesterol absorption inhibitors usually combined with?
- statins | - combo allows lower doses of statins and a greater elevations of transamidases
43
What are the side effects of ezetimibe?
- myalgia - hepatits - rhabdomyolysis (death of muscle fibers with release of their contents into bloodstream) - acute pancreatitis
44
What is the main mechanism of statins?
decrease of LDLs
45
What is the main mechanism of fibrates?
decrease triacylglycerides and increase HDLs
46
what is the main mechanism of niacin?
decrease triacylglycerides and increase HDLs
47
What is the main mechanism of bile acid sequestrants?
decrease LDLs
48
What is the main mechanism of cholesterol absorption inhibitors?
to decrease LDLs
49
Why is the combo of bile acid binding resins and HMG-CoA inhibitors a good combo?
- 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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