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34 Cards in this Set
- Front
- Back
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Atherosclerosis |
Plaque build-up on the walls of arteries. Leads to coronary heart disease |
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What percent of cholesterol in the body is synthesized by the liver, in comparison to dietary sources? |
80% |
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The outer shell of lipoproteins is made up of what? What characteristics does this have? |
Phospholipids, they are hydrophilic and soluble in plasma |
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The inner core of lipoproteins is made up of what? What characteristics does this have? |
cholesterol and triglycerides, and they are lipophilic |
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Apolipoproteins |
Embedded in the phospholipid shell. Have three functions: 1. Recognition by other cells which may ingest lipoproteins 2. Activate enzymes that metabolize lipoproteins 3. Increase the structural stability of lipoproteins |
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Apolipoproteins A-I |
transports cholesterol from non-hepatic tissues back to the liver |
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Apolipoproteins B-100 |
transports cholesterol to non-hepatic tissues |
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Very Low Density Lipoproteins (VLDL) |
- Deliver triglycerides from the liver to adipose tissue and muscle cells. - Triglyceride rich core - High VLDL= maybe atherosclerosis - Contain apolipoprotein B-100 |
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Low Density Lipoproteins (LDL) |
- Deliver cholesterol to non-hepatic tissue (ex: muscle) - cholesterol rich core - High LDL= OBVI atherosclerosis - Contain apolipoprotein B-100 - "Bad cholesterol" |
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High Density Lipoprpteins (HDL) |
- Deliver cholesterol from non-hepatic tissue back to the liver - cholesterol rich core - high HDL= LOWER chance of coronary heart disease - multiple apolipoproteins (A-I, A-II, A-IV) - "good cholesterol" |
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How is atherosclerosis initiated? |
Damage to the endothelium |
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How does atherosclerosis occur? |
1. Damage to endothelium 2. LDL accumulates in damaged space, and are oxidized 3. Macrophages ingest oxidized LDL; become larger foam cells 4. Accumulation of foam cells causes ruptured endothelium 5. Fibrous cap is made outside of fatty streak |
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Who is cholesterol screening recommended for? |
Males>40 and females>50 OR -diabetes -heart disease (or family history) -hypertension -central obesity -have smoked -inflammatory or renal diseases |
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Framingham Risk Score (what does it measure, what affects the score) |
Measures cardiovascular risk. Uses 1. Gender 2. Age 3. Total blood cholesterol 4. Smoking status 5. HDL cholesterol 6. Systolic blood pressure |
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Metabolic Syndrome |
When patients have THREE or more of: 1. Central trunk obesity 2. Elevated triglycerides in the blood 3. Low HDL cholesterol 4. Hyperglycemia 5. Hypertension |
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What are the non-drug treatments of LDL cholesterol? |
1. Diet 2. Weight control 3. Exercise 4. Cigarette smoking |
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How do statins work? |
HMG CoA is converted to mevalonic acid by HMG CoA reductase (which eventually becomes cholesterol)(rate-limiting step). Statins inhibit this enzyme, therefore less cholesterol made. ALSO, it causes an upregulation of hepatic LDL receptors, so the liver can remove more cholesterol from the blood. |
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How do statins affect LDL, HDL and blood triglycerides? |
lower LDL increase HDL lower blood triglycerides |
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Primary vs secondary prevention studies: what are they, and which of them do statins help? |
Primary is the prevention of first time occurrence, secondary is to prevent recurrence. Statins help with both!!! |
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Atorvastatin |
- low oral bioavailability -distribution primarily to liver but also spleen, adrenal glands, and skeletal muscle - metabolized by CYP3A4 - eliminated through the bile and into the feces |
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Rosuvastatin |
- low oral bioavailability -distribution primarily to liver but also to skeletal muscle - not extensively metabolized -eliminated through the bile and into feces - 2x higher concentrations in azns!! |
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What are the main adverse effects of statins? |
-Myopathy (muscle injury) - Rhabodomyolysis (rare muscle lysis and severe muscle pain) - hepatotoxicity - potentially teratogenic |
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Rhabodomyolysis (what is it, how is it diagnosed) |
Rare but serious adverse effect of statins. Muscle lysis and severe muscle pain. Diagnosed by seeing if there is a lot of creatine kinase in the blood. |
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How does Nicotinic Acid (Niacin) work? |
Inhibits the hepatic secretion of VLDL particles |
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How does Niacin affect LDL, HDL and blood triglycerides? |
decreases LDL and VLDL (triglycerides), increases HDL |
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What are Niacin's main adverse effects? |
Intense facial flushing, hepatotoxicity, hyperglycemia, skin rash, and increased uric acid levels |
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How do bile acid seqeuestrants work? |
They are positively charged molecules that bind the the negatively charged bile acids in the intestine, preventing reabsorption in the body. Since bile acids usually undergo enterohepatic recycling, this causes an increased demad for bile acid in liver. Liver cells increase the number of LDL receptors because LDL is required for bile acid synthesis. |
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What are the main adverse effects of bile acid sequestrants? |
Constipation and bloating |
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How do cholesterol absorption inhibitors work? |
It inhibits the NPC1L1 transporter, to decrease blood levels of dietary LDL cholestrol in the blood |
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Ezetimibe |
a cholesterol absorption inhibitor |
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What are the main adverse effects of cholesterol absorption inhibitor? |
A compensatory increase in hepatic cholesterol synthesis in the liver |
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Vytorin |
A combination pill of a statin along with ezetimibe. Lowers LDL by up to 60%!! |
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How do fibric acid derivatives (fibrates) work? |
Binds to and activated PPARa, which: 1. increases lipoprotein lipase synthesis (enhances clearance of triglyceride rich lipoproteins) 2. decreases apolipoprotein C-III (increases lipoprotein lipase activity) 3. Increases apolipoprotein A-I and A-II (increases HDL levels) |
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What are the main adverse effects of fibrates? |
- higher risk of gallstones -myopathy -hepatotoxicity (similar to statins, so patients should be monitored if taking both) |
