lipids

LDL

bad cholesterol, buildup can get oxidized, inflammed, and plaque forms causing atherosclerosis

HDL

good cholesterol, removes it from arteries

low amount increases risk of cad

high triglycerides can cause

pancreatitis and increase CV risk

what makes cholesterol

liver

what carries triglycerides from liver to tissues

VLDL, and turns into LDL after release of TG

what increases LDL

high saturated and trans fats

thyroid hormone

reduces LDL

insulin

increases TG storage, decreases lipolysis, decreases circulating TG

cortisol

increases lipolysis and hepatic VLDL, increasing TG and LDL

normal LDL

< 100 mg/dL

normal HDL

> 60 mg/dL

normal TG value

< 150 mg/dL

normal total cholesterol

< 200 mg/dL

familial hypercholesterolemia

inherited defect in LDL clearance, increased LDL from birth

polygenic risk

multiple genes, increased LDL or TGs

who has earlier ASCVD risk

men

low risk ASCVD

< 3%

borderline risk ASCVD

3-5%

intermediate risk ASCVD

5-10%

high risk ASCVD

> 10%

lipoprotein A

genetically determined risk factor, measure at least once in adulthood

elevated: > 125 nmol/L

apolipoprotein A

reflects the number of atherogenic lipoprotein particles

coronary artery calcium

CT scan that detects calcified coronary plaque

goal LDL for borderline/intermediate primary prevention risk

< 100 mg/dL

high primary prevent risk group goal LDL

< 70 mg/dL

ASCVD - very high risk goal LDL

< 55 mg/dL

what is the first line for dyslipidemia

statins

primary prevention for dyslipidemia

PREVENT ascvd

athersclerosis

chronic inflammation of arterial walls → lipid plaque buildup → narrowed/stiff arteries, decreased blood flow to tissues

pathophysiology of athersclerosis

1. normal artery

2. endothelial injury

3. fatty streak (macrophages take up LDL make foam cells)

4. fibrous plaque (smooth muscle cells and collagen)

5. complicated plaque (plaque ruptures, can block BF)

endpoint of atherosclerosis

reduced bloodflow leading to acute ischemic events (MI, stroke)

complications of atheroscleorsis

CAD, angina

cerebrovascular disease (TIA or stroke)

mesenteric ischemia (abdominal pain, poor digestion, bowel damage)

peripheral artery disease (pain, ulcers, gangrene)

aneursyms

management for atherosclerosis

statins, ezetimibe, PCSK9 inhibitors

hypertriglyceridemia

increased Tg production or less clearance, increased VLDL and chlomicrons

causes of hypertriglyceridemia

obesity/insulin resistance, diabetes, diet/alcohol, hypothyroidism, medications, genetics

risks of hypertriglyceridemia

increased ascvd, pancreatitis

severe TG elevation

fibrates, prescription omega 3s

peripheral artery disease

narrowing or blockage of peripheral arteries due to athersclerosis

s/s of PAD

intermittent claudication, cool extremities, decreased peripheral pulses, shiny skin, slow healing wounds or ulcers

diagnostic testing for PAD

CTA, doppler if needed

management for acute PAD

revascularization, IV fluids, bowel rest, broad spectrum abx, anticoagulation, resect nonviable bowel

management for chronic PAD

risk factor modification, antiplatelets, surgical bypass

aortic aneurysm

permanent, abnormal dilation of the aorta due to weakening of the wall

s/s of aortic aneurysm

deep, constant abdominal or back pain

pulsatile abdomnal mass

hypotension and shcok

diagnostic testing for aortic aneurysm

ultrasound (first line) CTA

complications of aortic aneurysms

rupture, dissection, thrombosis, embolization, compression, end organ ischemia