Hyperlipidemia Flashcards
Where does the majority of cholesterol come from and what is the second most common source?
the majority is made in the liver
some comes from diet
Important facts about familial Hypercholesterolemia
monogenic
hetero 2x
homo 8x the normal value of LDL
treat with statin
important facts about polygenic hypercholesterolemia
multiple genes involved
increased LDL levels
premature onset of CHD
treat with statin
important facts about familial combined hyperlipidemia
polygenic
wide variety of lipid abnormalities
treat with statin
some causes of secondary hyperlipidemia
diabetes excessive alcohol smoking obesity hypothyroidism chronic renal disease liver disease medications
at what point is HDL a risk factor and when is it a negative risk factor
HDL is less than 40 is a risk factor
HDL is greater than or equal to 60 is a negative risk factor
What does a fasting lipid panel consist of and how long should you fast
total cholesterol, triglycerides, LDL, and HDL
Total cholesterol = HDL + LDL + (triaglycerides/5)
12 hours
Lipid profile desireable, borderline, high risk
Cholesterol
<200, 200-239, 240
Lipid profile desireable, borderline, high risk
Triaglycerides
<150, 150-199, 200-499
Lipid profile desireable, borderline, high risk
HDL Cholesterol
60, 35-45, <35
Lipid profile desireable, borderline, high risk
LDL Cholesterol
60-130, 130-159, 160-189
cholesterol filled, soft, yellow plaques that appear in various places
plane xanthomas
yellow-orange nodules often located over knees and elbows
can also be in the tendons
associated with familial hypercholesterolemia
tuberous xanthoma
crops of small red-yellow papules with abrupt onset
extensor surfaces and buttocks most common areas
caused by elevated triglycerides often > 1500 mg/dL
may indicate familial HDL
eruptive xanthomas
white grey ring around the cornea
common in pts over 40 without elevated lipids
corneal arcus
diet approaches to stop hypertension DASH diet
rich in fruits and vegetables
moderate in low-fat dairy products
low in animal protein
low sodium
exercise benefits
can increase HDL
3-4 session/week 40 min mod-vigorous
Statins mechanism of action
- inhibit HMG-CoA reductase a rate limiting step in cholesterol synth
- increases production of LDL receptors
- receptors bind LDL and VLDL
- LDL and VLDL enter liver and are digested
Statin contraindications
absolute: active liver disease, pregnancy
Use with caution: concomitant use of CYP3A4 inhibitors and various drugs, chronic kidney/liver disease
how often should lipid panel be taken during statin therapy
every 4-12 weeks after initiation or dose adjustment and then repeat every 3-12 months as needed
Bile acid sequestrants aka Resins mechanism and facts
bind bile acids in the intestine
Decrease LDL by upto 24%
act synergistically with statins
SAFE DURING PREGNANCY
adverse effects of resins
constipation
gas
may affect warfarin or vitamin absorption
can INCREASE triglycerides
contras of resins
absolute: Triaglycerides > 400
relative: Triglycerides >200
Nicotinic acid (Niacin) uses
reduces production of LDL
increases HDL
may reduce triglycerides
adverse effects of nicotinic acid
flushing
pruritis
liver damage monitor LFTs
safety concern when used with statin
contraindications of nicotinic acid
absolute: active liver disease
relative: hyperuricemia, hyperglycemia, unstable angina
not used during pregnancy
purpose of fibric acid derivatives (gemfibrozil, fenofibrate, bezafibrate)
lower triglycerides up to 50%
raising HDL up to 25%
useful with elevated triglycerides
not used in pregnancy
adverse effects of fibric acid derivatives
gallstones
hepatitis
myositis
contras of fibric acid derivatives
absolute: severe hepatic or renal disease, preexisiting gallstones, taking simvastatin
relative: other statin use, concurrent warfarin use
ezetimibe mechanism
blocks intestinal absorption of dietary and biliary cholesterol via transporter
ezetimibe contraindications
use with a statin in active liver disease pregnancy
PCSK9 inhibitor important notes
can reduce LDL levels as much as 70%
expensive
requires injections
4 statin benefit groups
- Individuals with ASCVD (secondary prevention)
acute coronary syndromes, history of MI, symptomatic peripheral artery disease, stroke or TIA
Primary prevention:
- individuals with LDL greater than or equal to 190
- individuals with diabetes aged 40-75 years with LDL greater than or equal to 70
- individuals without ASCVD or diabetes with LDL 70-189 and estimated 10 year ASCVD risk greater than or equal to 7.5%
