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Pharmacology > Lipid Disorders > Flashcards

Lipid Disorders Flashcards

1
Q

Cholesterol is primarily derived from what?

A

LDL’s

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2
Q

What is atherosclerosis?

A
  • abnormal deposition of cholesterol in the arteries
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3
Q

VLDL’s are the endogenous forms of ____

A

cholesterols

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4
Q

Describe triglycerides?

A
  • primarily chylomicrons, VLDLs as well

- increase pancreatitis

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5
Q

What are some of the other key factors in deposition on artery walls?

A
  • smoking
  • hypertension
  • diabetes
  • genetic factors
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6
Q

What is the LDL involvement in the generation of atherosclerosis?

A
  • LDL’s make their way inside the artery, and from here are able to produce oxidizing products (are able to oxidize)
  • from here, they cannot move out of the artery, have to stay here inside the artery
  • they send out signals to attract monocytes into the intima
  • monocytes are transformed into macrophages and are very efficient into taking up LDL
  • increase in the level of foam cells, where cholesterol can be taken up- these foam cells developing a core that allows plaques to form on the artery wall, and these plaques can get so big that they can cause blockage
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7
Q

What is the action of HDL?

A
  • takes cholesterol from the peripheral circulation and takes them back into the proteins that of to the liver
  • allows the cholesterol from being excreted into the bile from the liver
  • HDL cannot cause the build up of the plaque- it can go into the lymphatic vessels because it is so small, but because LDL is so big it cannot move from inside the arteries to the lymph vessels
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8
Q

What would be recommend to a patient that has no risk factors and has only slightly elevated cholesterol?

A
  • no medication intervention , do NOT give drugs
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9
Q

What are the potential sites to decrease cholesterol?

A
  1. decreasing GI uptake
    - decreasing dietary intake
    - decreasing reabsorption of bile acids
    - decreasing reabsorption of cholesterol
  2. decreasing LDL levels
    - decreasing VLDL
    - increasing LDL receptors
  3. decreasing endogenous cholesterol synthesis
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10
Q

What are the non-pharmacological treatment options for lowering cholesterol?

A
  • can increase dietary fibre

- adding in omega 3 fatty acids- will use a reduction in LDL cholesterol levels

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11
Q

What are HMG-CoA reductase inhibitors also known as?

A

statins

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12
Q

Statins are known as the first choice for most patients with a risk for what?

A

coronary heart disease

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13
Q

What do statins do?

A
  • decrease LDL levels
  • also decrease triglyceride levels
  • patients with a coronary artery disease - decreased cardiac morbidity, mortality, reduced incidence of stroke
  • benefits seen with initial high or normal cholesterol
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14
Q

What is the mechanism of statins?

A
  • inhibit HMG-CoA reductase, the rate limiting step of cholesterol synthesis
  • compensatory increase in LDL receptors
  • best if given in the evening- diurnal pattern of cholesterol synthesis
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15
Q

What are the adverse effects of statins?

A
  • well tolerate but contraindicated in pregnancy
  • myalgia, muscle weakness
  • may increase with cyclosporin, fibrates or niacin
  • monitor creatine kinase levels
  • increase in plasma aminotransferase >3x in ,2% (symptomatic hepatitis is rare)
  • first pass metabolism- CYP3A4 (avoid inhibitors like grapefruits with some statins)
  • renal dysfunciton, behavioural and cognitive, diabetes, neuropathy
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16
Q

What is the effect that grapefruit will have on the availability of stains in the body?

A

there is an INHIBITION of the enzyme (CYP3A4) that metabolizes statins, causing an increase in the amount go medication that is in the body
- the concentration of the statin is increased

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17
Q

Which statins in particular are affected by grapefruit juice?

A
  • atorvastatin and simvastatin
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18
Q

Ezetimibe belongs to what class?

A

cholesterol absorption inhibitors

19
Q

Ezetimibe causes inhibition of both ___ and ____ cholesterol absorption

A

dietary and biliary

work at the intestinal brush border

20
Q

What is the specific protein that ezetimibe works on?

A
  • it inhibits a cholesterol transport protein that is known as NPC1L1
21
Q

Ezetimibe lowers cholesterol by _____ when used alone, but you can get reflex increase in cholesterol ____

A

15-20%

- synthesis

22
Q

What is the one dangerous part of potentially combining ezetimibe with a statin?

A

possible greater elevations of transaminases compared to just using statins alone (does allow a lower dose of statin to be used however)

23
Q

What are the adverse effects associated with using ezetimibe?

A
  • myalgia, hepatitis, rhabdomyolysis, acute pancreatitis
24
Q

What are the examines of bile acid binding resins?

A
  • cholestyramine (Questran), colestipol (Colestid), colesevelum
25
Q

What are tile acid binding resins useful for?

A
  • useful in mild to moderate elevated LDL levels

- effective with statins or nicotinic acid in high LDL levels

26
Q

Are bile acid binding resins absorbed by the gut?

A
  • no, they are not (they are anion exchange resins)
27
Q

What is the mechanism of action of bile acid binding resins?

A
  • binds bile acids in the intestinal lumen - prevents reabsorption (normally 95% reabsorbed)
  • to produce new bile acids, the liver must do what?
  • > take up cholesterol (increase LDL receptors and/or synthesize de novo cholesterol)
28
Q

What are the most common adverse effects associated with bile acid binding resins?

A
  • may increase LDL levels
  • decrease absorption of fat soluble vitamins (vitamin K deficiency is a problem)
  • nausea, constipation and bloating
  • unpleasant taste and texture
  • absorption of drugs is altered (positive, negative and neutral) eg. digitalis, thiazides, warfarin and aspirin
29
Q

Why is ezetimibe beneficial to use with a statin?

A
  • additively lower the level of cholesterol
  • ezetimibe decreases cholesterol uptake in the gut, but compensatory increase in cholesterol synthesis in the liver
  • HMG-CoA reductase inhibitors blocks the increased synthesis in the liver
30
Q

What are some of the reasons that there is such a failure to achieve the LDL target concentrations?

A
  • poor adherence to the treatment
  • high baseline LDL-concentrations
  • high cholesterol diet
  • high cholesterol absorption
  • variable statin release
  • inability to tolerate (higher dose) statins
31
Q

What are the newest therapies used to lower lipids?

A
  • targeting the LDL receptor for degradation
  • inject human monoclonal antibodies to PCSK9 to increase LDL receptors on the liver
  • known as evolocumab
32
Q

What is the role o PCSK9 in the regulation of LDL receptor expression

A
  • LDL particle binds to the LDL receptor in the absence of the PCSKp complex
  • LDL receptor recirculates back to the surface
  • more LDL receptor on the surface of the liver which will allow the liver to pull in more of the LDL and metabolize it
  • this receptor is primarily found on the liver, BUT you can still see muscle weakness with this therapy
33
Q

What are the potential sites to decrease triglycerides?

A
  • decrease dietary triglycerides
  • increase lipoprotein lipase activity
  • decrease VLDL secretion from the liver
34
Q

What is the non-pharmacological approach in decreasing lipids?

A
  • decreasing dietary TG’s

- increasing dietary fibre - increasing soluble and insoluble fibre

35
Q

What are the other uses of dietary fibre?

A
  • increases bulk of the stool
  • good for constipation
  • decreases colonic cancer
36
Q

In fenofibrate and gemfibrozil (fibrates) the incidence of death from coronary heart disease, non-fatal MI and stroke was decreased, but what was NOT altered?

A
  • LDL levels were unaltered
37
Q

Vibrates may ____ triglycerides and may _____ HDL

A

decrease

increase

38
Q

What is the mechanism of fibrate action?

A
  • increased VLDL clearance (increase lipoprotein lipase activity)
  • decreased VLDL secretion
39
Q

What are the adverse effects of fibrates?

A
  • flu-like: muscle cramps, tenderness, stiff, weak
    • increased myopathy when combined with statins
  • avoid in hepatic or renal dysfunction
  • may potentiate oral anticoagulants and hypoglycaemia agents
  • increases cyclosporine clearance - transplant rejection?
  • use with caution if increased risk of biliary tract disease (women, obese patients, First Nation)
40
Q

Generally describe niacin?

A
  • water soluble vitamin B3 (nicotinic acid) - NOT nicotinamide
  • low dose can increase HDL levels (most effective)
  • higher dose - decreases VLDL levels - decreases triglycerides and may therefore may decrease LDL levels
41
Q

What effect does niacin have on men with a previous MI?

A
  • decreases the incidence of a non-fatal MI and at 9 years a decreases mortality rate
42
Q

What is the mechanism that nicotinic acid has action at?

A
  • decreased hepatic VLDL production - activated Niacin receptors in adipocytes -> decrease in cAMP -> decreases TG hydrolysis -> less fatty acid in circulation to be taken up by the liver and converted to TG and then secreted as VLDL
  • increased VLDL clearance (increase lipoprotein lipase activity)
  • effective at decreasing triglycerides and increasing high density lipoproteins
43
Q

What are the common adverse effects of niacin use?

A
  • limited because it is poorly tolerated
  • skin flushing and pruritus
    (acute and aspirin blunts)
  • exacerbation of peptic ulcers
  • may increase aminotransferase or alkaline phosphatase (monitor liver function regularly for hepatotoxicity)
  • can lead to glucose intolerance

Pharmacology (23 decks)

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