Drugs for Hyperlipidemia

Question 1

athherosclerosis

Answer 1

• 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)
  =>

Question 2

hyperlipidemia

Answer 2

high levels of fat particles in blood

Question 3

blood lipids

Answer 3

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

Question 4

lipoproteins

Answer 4

tiny particles that contain lipids (cholesterol, phospholipids, triglycerides) and proteins

Transport blood lipids and are measured as “cholesterol”

Question 5

HDL

Answer 5

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

Question 6

LDL

Answer 6

low density = bad!

• contain highest amount of cholesterol
• sticks to arterial walls and contributes to cholesterol build up
• high levels of LDL is dangerous

Question 7

VLDL

Answer 7

very low density

• extra “light” b/c carry mainly triglycerides
• usually not measured

Question 8

hyperlipidemia

Answer 8

total cholesterol = high
LDL = high
HDL = low
Triglycerides = high

Question 9

causes of hyperlipidemia

Answer 9

Autosomal dominant disorder

• xanthomas (skin) = lipid deposit in skin
• may experience MI < 40

Bad dietary habits

Metabolic diseases
- DM, alcoholism, obesity, liver disease

Question 10

Risk factors for hyperlipidemia

Answer 10

1. age = men>45, women>55
2. family history
3. HTN
4. smoking
5. low HDL (<40)

Question 11

Treatment for hyperlipidemia

Answer 11

Therapeutic Lifestyle Changes (TLC) diet
- non-drug measures: diet, exercise, weight control, stop smoking

Drug therapy - lipid lowering agents

Question 12

At risk and healthy levels of LDL

Answer 12

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

Question 13

good levels of HDL

Answer 13

protective level = > 60

dangerous (low) level = < 40

Question 14

when give drugs for hyperlipidemia

Answer 14

• 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

Question 15

drugs for hyperlipidemia

Answer 15

1. statins (HMG-CoA reductase inhibitors)
   - most effective
   - lowers LDL
2. bile acid sequestrant
3. Niacin (nicotinic acid)

Question 16

MOA of statins (HMG-CoA reductase inhibitors)

Answer 16

1. block HMG-CoA reductase (enzyme that makes cholestoral in the liver) => ↓ synthesis of LDL in the liver => ↓ LDL cholestoral
2. stabilize cholesterol-filled plaque in artery walls
3. calm inflammation
4. ↓ progression of CAD

Question 17

statins (HMG-CoA reductase inhibitors)

Answer 17

• statin = lipid ↓ agent

Atorvastatin (Lipitor)
Lovastatin (Mevacor)
Pravastatin (Pravachol)
Simvastatin (Zocor

Question 18

statins (HMG-CoA reductase inhibitors)

Route / when / interactions?

Answer 18

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

Question 19

statins (HMG-CoA reductase inhibitors): side effects

Answer 19

• 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

Question 20

NIs and Pt Education - Statins

Answer 20

1. “pepsi pee” - myoglobinuria
2. call Dr. w/muscle pain
3. restrict fatty diet
4. liver damage - if jaundice, call - treat w/lots of fluids

Question 21

Bile acid sequestrants (bile acid-binding resins) - how they work

Answer 21

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

Question 22

Examples of Bile acid sequestrants (bile acid-binding resins)

Answer 22

coles -

Colesevelam (Welchol)
Cholestyramine (Questran)
Colestipol (Colestid)

Question 23

Bile acid sequestrants (bile acid-binding resins) - side effects

Answer 23

• 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

Question 24

Nicotinic acid (Niacin) - what does it do?

Answer 24

• part of a Vit B complex (B3)
• ⇡HDL by 30%
• ↓ LDL chol, triglycerides, VLDL
• most effective when used w/a statin

Question 25

Nicotinic acid (Niacin) - side effects

Answer 25

• flushing (very red face) - nearly all pts.
• pruritus (itching)
• orthostatic hypotension (from flushing)
• hepatotoxicity
• hyperuricemia - give “Allopurinol” if ⇡uric acid

Question 26

Nicotinic acid (Niacin) - NI

Answer 26

• 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

Question 27

Hyperlipidemia and children

Answer 27

• 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)