HLD Pharmacology Flashcards
Atorvastatin, Simuvastatin, Rosuvastatin classification
HMG-CoA reductase inhibitors
HMG-CoA reductive inhibitors suffix
–statins
Atorvastatin, Simvastatin, Rosuvastatin MOA
Inhibits HMG-CoA reductase which causes less cholesterol to be made by the liver; LDL and TG decrease and HDL increases
Atorvastatin, Simnuvastatin, Rosuvastatin adverse effects
Myopathy, rhabdomyolysis (can lead to acute kidney failure), mild cramping, some hepatotoxicity
Atorvastatin, Simuvastatin, Rosuvastatin nursing considerations
Can take a couple weeks to get effects, make take with food if GI discomfort, best to take at night (simvastatin, rosuvastin), avoid alcohol
ezetimibe (Zetia) classification
Cholesterol reabsorption inhibitor
ezetimibe (Zetia) MOA
Blocks absorption of cholesterol in jejunum (dietary)
ezetimibe (Zetia) adverse effects
Muscle pain, liver damage
ezetimibe (Zetia) nursing considerations
Usually a second line therapy, the effect is greater when taken with a statin so two meds may be better, watch liver pt
cholesterol
highly insoluble; builds estrogen and testosteron, vitamin D, cortisol, bile acids, skin barrier; essential part of bilayer in all cell membranes
Cholesterol source
25% exogenous (diet); 75% endogenous (HMG-CoA reductase is the prcoess the liver uses to make cholesterol using saturated fat)
Liver’s negative feedback loop
When the liver senses high LDL with LDL receptors, there is decreased HMG-CoA production to decrease cholesterol; when more cholesterol is needed, body makes more receptors to pull more cholesterol out of the blood
kinds of lipoproteins
HDL–the good kind, higher protein content; LDL–the bad kind, leads to plaque, lower protein; VLDL–low protein and contributes to heart disease with LDL
hypercholesterolemia
hyperlipidemia/dyslipidemia; excess cholesterol in the blood
How to diagnose high cholesterol
Few symptoms, screen starting at age 20 every 5 years or in kids at high risk; look at overall cholesterol fasting numbers
Healthy cholesterol levels
Total cholesterol <200mg
HDL >50 or 60
LDL <100
Triglycerides <150
Familial hypercholesterolemia
caused by a defect in LDL receptors in liver cells; liver can’t make LDL receptors well, causing elevated LDL in blood; causes heart problems in kids; diet can’t change the amounts
Risk factors for hyperlipidemia
age, family history, smoking, sedentary, obesity, poor diet, DM
Elevated LDL and cholesterol causes
increased risk of atherosclerosis (decreased ability of BVs to dilate)
arteriosclerosis
thickened/hardened arterial wall that decreases the arteries ability to carry oxygenated blood
How does atherosclerosis form
Injury to epithelial layer on the inner BVs that causes plaque formation–chemicals from smoking, chronic hemodynamic wall stress, hyperglycemia; oxidation of epithelial tissue
C-reactive protein (CRP) and results from it
Marker of systemic inflammation; can be a sign of atherosclerosis; binds to phospholipids on bacterial cell membranes and indicates increased risk of disease state
Erythrocyte sedimentation rate (SED)
Inflammatory marker
How does increased arterial permeability lead to atherosclerosis
Injuries make arteries more susceptible so LDL can bury in; macrophages try to eat lipids, making foam cells that appear as fatty streaks in the walls and make plaques that can expand and impede blood flow
