Drugs for Hyperlipidemia Flashcards
athherosclerosis
- LDL deposits cause development
- progressive disease = atheroma (damage to walls cause build up of plaque)
- chronic inflammatory process = injury to intimal lining of arteries by HTN, smoking, hyperlipidemia, DM (diabetes mellitus)
=>
hyperlipidemia
high levels of fat particles in blood
blood lipids
Cholesterol
- waxy fats carried thru bloodstream by lipoproteins
- necessary for normal body fx = production of steroid hormones (glucocorticoid), components of cell membranes
- sources = food and produced by liver
Phospholipids
Triglycerides
lipoproteins
tiny particles that contain lipids (cholesterol, phospholipids, triglycerides) and proteins
Transport blood lipids and are measured as “cholesterol”
HDL
high density = good!
- contain mostly proteins
- synthesized in liver
- protects arteries by removing LDL from plaques
- high HDL level is protective => ↓ risk of CAD
- ↓ level of HDL is dangerous (can be genetic, DM, liver disease
LDL
low density = bad!
- contain highest amount of cholesterol
- sticks to arterial walls and contributes to cholesterol build up
- high levels of LDL is dangerous
VLDL
very low density
- extra “light” b/c carry mainly triglycerides
- usually not measured
hyperlipidemia
total cholesterol = high
LDL = high
HDL = low
Triglycerides = high
causes of hyperlipidemia
Autosomal dominant disorder
- xanthomas (skin) = lipid deposit in skin
- may experience MI < 40
Bad dietary habits
Metabolic diseases
- DM, alcoholism, obesity, liver disease
Risk factors for hyperlipidemia
- age = men>45, women>55
- family history
- HTN
- smoking
- low HDL (<40)
Treatment for hyperlipidemia
Therapeutic Lifestyle Changes (TLC) diet
- non-drug measures: diet, exercise, weight control, stop smoking
Drug therapy - lipid lowering agents
At risk and healthy levels of LDL
CAD equivalents and risks
- LDL goal <100
w/multiple risk factors (>2), but no CHD
- LDL goal < 130
w/0-1 risk factors
- LDL goal < 160
good levels of HDL
protective level = > 60
dangerous (low) level = < 40
when give drugs for hyperlipidemia
- goal is prevention (prophylaxis)
- recommended when diet therapy and lifestyle changes aren’t enough
- pt should continue diet changes while on drug therapy
- for pts w/ S/Sx of CAD, + family history (FH), HTN, DM, smoking
- not for children < 10
drugs for hyperlipidemia
- statins (HMG-CoA reductase inhibitors)
- most effective
- lowers LDL - bile acid sequestrant
- Niacin (nicotinic acid)
MOA of statins (HMG-CoA reductase inhibitors)
- block HMG-CoA reductase (enzyme that makes cholestoral in the liver) => ↓ synthesis of LDL in the liver => ↓ LDL cholestoral
- stabilize cholesterol-filled plaque in artery walls
- calm inflammation
- ↓ progression of CAD
statins (HMG-CoA reductase inhibitors)
- statin = lipid ↓ agent
Atorvastatin (Lipitor)
Lovastatin (Mevacor)
Pravastatin (Pravachol)
Simvastatin (Zocor
statins (HMG-CoA reductase inhibitors)
Route / when / interactions?
PO
Give at bedtime (body produces cholestoral at night)
Metabolized by liver
- if CYP inducer given too => ↓ effect
- if CYP inhibitor given too => ⇡ effect
contraindications: pt w/liver disease due to hepatotoxic; pregnancy category X
statins (HMG-CoA reductase inhibitors): side effects
- generally well tolerated
- mild GI upset
- get baseline LFT, then check periodically
- myopathy (CALL DR. - can damage skeletal muscle)
- Rhabdomyolysis - muscle damage => myoglobinuria => acute kidney failure
NIs and Pt Education - Statins
- “pepsi pee” - myoglobinuria
- call Dr. w/muscle pain
- restrict fatty diet
- liver damage - if jaundice, call - treat w/lots of fluids
Bile acid sequestrants (bile acid-binding resins) - how they work
Bile acids are synthesized from cholesterol in liver
Drug binds bile acids in the intestines => ⇡ excretion of bile acids w/stool => stimulate hepatic synthesis of bile acids from cholesterol => ↓ LDL cholesterol
* given to pts w/liver issues b/c isn’t absorbed
Examples of Bile acid sequestrants (bile acid-binding resins)
coles -
Colesevelam (Welchol)
Cholestyramine (Questran)
Colestipol (Colestid)
Bile acid sequestrants (bile acid-binding resins) - side effects
- mix powder w/ beverages
GI - abdominal fullness, cramps, constipation, flatulence are common - ↓ absorption of other oral drugs
= take other meds 1 hour before or 4 hours afterwards
Nicotinic acid (Niacin) - what does it do?
- part of a Vit B complex (B3)
- ⇡HDL by 30%
- ↓ LDL chol, triglycerides, VLDL
- most effective when used w/a statin
Nicotinic acid (Niacin) - side effects
- flushing (very red face) - nearly all pts.
- pruritus (itching)
- orthostatic hypotension (from flushing)
- hepatotoxicity
- hyperuricemia - give “Allopurinol” if ⇡uric acid
Nicotinic acid (Niacin) - NI
- Caution patient about flushing and orthostatic hypotension
- 1 ASA (aspirin) 30 min before usually ↓ flushing and itching
- start low, gradually increase to reduce flushing
- Should be taken w/meals
Hyperlipidemia and children
- autosomal dominant disorder
- ⇡ risk of CV morbidity and mortality in adults
- 25% of males w/+ FH = fatal CD by 50
- Amer Acad of Pediatrics (2008)
= screening every 3-5 yr beginning at 2 yr
= diet - reduced fat milk at 1 yr
= exercise
= initiate statins a 8 yrs old (minimum)
