Dyslipidemia Flashcards
Describe the process of plaque formation
High levels of LDL will lead to LDL being absorbed by vessel. Once in vessel LDL becomes oxidized.
Oxidized LDL will be consumed by macrophage. Macrophage cannot breakdown LDL so it is becomes foam cell.
What happens to foam cells, what can they lead to
The foam cell is a macrophage that cannot breakdown the LDL. Foam cells will cause increased cytokine release, whereby more macrophages consume LDL and become foam cells as well.
*feed forward mechanism
Triglycerides function
Primary fat storage. Stored triglycerides can be catabolized into free fatty acids and used for energy during fasting/between meals.
What happens when fatty acid tails are cleaved
They are cleaved into acetyl coa.
Acetyl coa goes to liver and becomes glucose.
*becomes ketoacids in type 1 uncontrolled diabetes
How does Acetyl coa convert to cholesterol
Acetyl coa converts to hmg coa. With the catalyst hmg coa reductase becomes mevalonate. Further downstream becomes cholesterol.
List the different types of Lipoproteins
Chylomicrons, VLDL, LDL, HDL
Describe chylomicrons and why they can alter lab tests
Chylomicrons are dietary fats. These can increase cholesterol levels in lab tests therefore lab tests should be drawn while fasting.
Explain VLDL production and conversion
VLDL is produced in the liver (endogenous pathway)
Discuss statins MOA
Statins block hmg coa reductase decreasing fatty acid tails (from triglycerides) conversion to cholesterol
Statin side effect
Muscle pain, can be debilitating.
Asian population cannot tolerate statins.
Niacin MOA
Niacin blocks production of cholesterol carrier protein. Increasing cholesterol excretion in bile.
Niacin main side effect
Flushing d/t cutaneous vasodilation
Fibrates
Break down lipids including triglycerides. When lipids are low liver decreases VLDL production.
Inhibitors of intestinal Sterol absorption MOA and example
Zetia (ezetimibe)
Blocks NPC1L1 transporter.
Ezetimibe toxicity
Hepatotoxocity possible arterial wall thickening
