Lipid Disorders Lecture Powerpoint Flashcards
fuck me jerry
Genetic dyslipidemia
Genetic predisposition to excessive LDL levels regardless of diet and lifestyle often (not due to obesity or other controllable circumstances)
LDL
Low density lipoprotein, a source of vascular disease thru deposition in the form of plaque buildup on vessel walls
HDL
High density lipoprotein, act via reverse transport mechanism of LDL deposition removing plaque buildup and bringing it back to the liver, acting cardioprotective against heart disease
Fatty streak development
Intracellular lipid accumulation in the early stage progression of atherosclerosis, often seen in ages 4-5 in about 50% of patients and indicative of slight increasing endothelial dysfunction (but does not manifest with any clinical symptoms and is clinically “silent”)
Stable plaque vs vulnurable plaque
Stable - a buildup of cholesterol that has fibrous scar tissue forming around it as well as migrating smooth muscle tissues that narrow the lumen of the artery (fibrous plaque)
Vulnurable - occurs in more advanced stages of atherosclerosis, where scar tissue has calcified over and if endothelium is damaged collagen is exposed causing platelets to aggregate and clot forming a thrombus at risk for embolism
Arteriosclerosis
General term for several diseases resulting from hardening of the arteries either by atherosclerosis (plaque deposition) arteriosclerosis (prolonged hypertension, DM), or monckeberg’s arteriosclerosis (Ca2+ deposition in small to med sized arteries)
Atherosclerosis
Most common type of arteriosclerosis and caused by fatty tissue deposition and plaque formation that eventually calcifies over
Leading cause of death in US
Coronary heart disease
Vascular dimentia
A potential consequence of atherosclerosis occlusion resulting in chronic decreased blood flow to the brain, other causes could be acute episodes such as stroke, hypoxia, etc.
Ethnicity and coronary heart disease and theory as to what impacts it
Blacks and hispanics > whites, thought to be due to increased obesity and diabetes levels in these populations
Dyslipidemia definition
Elevated plasma conc. of either total or LDL cholesterol, or low HDL, can be primary (genetic) but can also be secondary
Funduscopic exam for heart disease
One of the only spots in the body we can visualize vessels and potential plaque build up, a staple of work up for heart disease as allows for visualization of dilated or broken vessels as well as fatty streak deposition
Xanthelasma/tendon xanthomas
A condition seen in primary genetic dyslipidemia leading to cutaneous manifestations of cholesterol deposits on the joints and palms (and eyelids lol)
Most common familial hyperlipidemia and what is elevated?
Type IIa, LDL
Most common hyperlipidemia in those with metabolic disorders and what is elevated?
Type IIb, LDL and VLDL
Most common hyperlipidemia in diabetics and what is elevated?
type IV, VLDL
Primary vs secondary dyslipidemia (3 things that can cause secondary elevated LDL)
Primary is genetic, Secondary is due to other underlying conditions such as DM, steroid treatment, and thyroid disease
2 medications that can cause 2ndary elevation of triglyceride or drop in HDL
- B blockers
- thiazide diuretics
Metabolic syndrome
A condition characterized by 3 of the following
- abdominal obesity (>40 inch males and 35 inch in females)
- HDL below 40mg/dL male and 50mg/dL female
- hypertension >130/85mmHg
- elevated fasting glucose to either pre-diabetic (>110mg/dL) or diabetic stage (>125mg/dL)
Fasting lipid profile
A sampling with no food for 12 hours before to measure total cholesterol, LDL-C, HDL, and triglycerides
Before we could request directly measured LDL, had to calculate LDL-C using this formula
LDL-C=TC-HDL-(trig/5)
Apolipoprotein B100 serum lab study and healthy values
Measurement test of secondary marker for LDL measuring a substrate of LDL indicating risk of developing cardiovascular disease, with normal values below 100mg/dL
___LDL particles are more atherogenic than ___ ones
Smaller, larger
Lpa serum lab study
A measurement test that detects levels of lipoprotein a, a component in HDL and LDL in blood, elevated value puts at risk for foam cell development and decreased thrombolysis putting them at higher risk for cardiovascular disease
Ultra sensitive CRP and homocystine serum lab studies
Measurement test that detects non specific marker of inflammation that could be indicating increased inflammation of vessels and heart putting patient at risk for heart attack, but could also be due to any number of inflammatory conditions or infection
CPK serum lab studies
Measures CPK in blood stream, a biproduct of muscle tissue breakdown, elevated in conditions such as rhabdomyolysis or heart disease and administered prior to starting lipid lowering therapy
Screening guidelines for hyperlipidemia
- fasting lipid profile in all pediatric patients age 9-13 (2 readings 13 weeks apart)
- screen adults if not screened as child starting at initial visit
- high risk repeat screening at 25-30 for males or 30-35 for females
- if low risk (serum lipid profile) then repeat screening at 35 for males 45 for females
- screen every 5 years of sooner if change in clinical status
Dyslipidemia/cardiovascular disease lifestyle modifications that should be recommended to patients(2)
- low fat, low cholesterol diet
- 30 min of sustained aerobic exercise daily
Bile acid sequestrants
Dyslipidemia pharmacologic treatment option minimally effective and act only on gut absorption, used in kids or pregnancy
HMG co-reductase inhibitors (statins)
Dyslipidemia/hypertriglyceridemia pharmacologic treatment option to lower LDL production in liver, can cause rhabdo or liver dysfunciton in some rare cases, and require LFT and TSH monitoring while on medication as well as baseline CPK
Ezetimibe (zetia)
Dyslipidemia pharmacologic treatment option that systemically blocks cholesterol absorption at the bowel, can cause abdominal pain or diarrhea, and requires LFT and CPK monitoring while on medication
Fibrates
Hypertriglyceridemia pharmacologic treatment option that inhibits triglyceride synthesis and stimulates catabolism of triglyceride lipoproteins, can cause abdominal pain or diarrhea or pancreatitis, requires LFT and pancreatic enzymes monitoring while on medication
Statin therapy intensity indications
Low intensity - dietary changes to decrease LDL-C by <30%
Moderate intensity - those who don’t already have a vascular event or diabetes but need therapy to lower LDL-C by 30-50%
High intensity - those with history of vascular event or diabetes and need to lower LDL-C by >50%
LDL >190 indicates a need for…
….high intensity dosing therapy
Statin therapy in children
Often considered if there is family history of dyslipidemia or co-morbidities such as congenital heart disease or diabetes, considered if patient fails lifestyle modifications
Statin therapy and pregnancy
Contraindicated!!! can be replaced with less effective bile acid sequestrant
Patients with triglycerides greater than ___mg/dL are at risk for developing ___ and therefore require ____ therapy if triglycerides exceed ___mg/dL
1000mg/dL, Spontanous pancreatitis, fibrate, 500
Lipid definition
Combination of cholesterol and triglycerides carried i lipoproteins thru the blood, produced in the liver and obtained thru diet
Thrombus
A blood clot that forms in a vessel reducing flow thru the vessel and has a risk of embolism
Embolism
Anything, but most often a piece of a thrombus that has broken free, that travels thru the blood stream and occludes a vessel further downstream
Monckeberg’s arteriosclerosis
Degenerative poorly understood condition where Ca2+ deposition causes arteriosclerosis separate from any other atherosclerosis that might be occurring in the body
Lifestyle factors that contribute to increased triglycerides and decreased HDL (4)
- DM
- lack of exercise
- alcohol
- renal insufficiency or B blockers/thiazide diuretics
Framingham study shows risk of recurrent MI is ___x greater in women and ___x greater in men whose cholesterol levels are greater than ___mg/dL
9, 4, 275
Hyperlipidemia primary prevention guidelines
-Calculate CVD risk model and if greater than 7.5% may discuss options of starting statin therapy with patient (which sees 20-30% reduction in risk depending on pros and cons as the patient sees fit
Hyperlipidemia secondary prevention guidelines
-begin statin therapy independent of baseline LDL levels, if patients do not acheive <70 mg/dL LDL (monitored every six weeks) then maximize statin therapy and consider adding a second agent (Ezetimibe)
