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Clin Med II > dyslipidemia and CAD > Flashcards

dyslipidemia and CAD Flashcards

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1
Q

role of TG

A
  • metabolic fuel
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2
Q

role of phospholipids

A
  • metabolic fuel
  • lipoproteins
  • blood clotting
  • myelin sheath
  • cell membranes
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3
Q

role of cholesterol

A
  • plasma membranes
  • bile salts
  • steroid hormones
  • other specialized molecules
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4
Q

lipoproteins

A
  • fat carrying proteins that encapsulate and transport cholesterol and TG through blood
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5
Q

apoprotein

A
  • any protein that binds with lipid to form a lipoprotein

- precursor to LDL and HDL

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6
Q

chylomicrons

A
  • carry exogenous TG and cholesterol
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7
Q

VLDL

A
  • carry endogenous TG (mainly) and cholesterol
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8
Q

LDL

A
  • “bad cholesterol”

- carries cholesterol to cells

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9
Q

HDL

A
  • “good cholesterol”

- carries cholesterol from cells

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10
Q

main source of exogenous cholesterol

A
  • diet

- mainly animal sources

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11
Q

main source of endogenous cholesterol

A
  • produced from liver and cells lining the GIT
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12
Q

liver and cholesterol metabolism

A
  • adjusted via pos and neg feedback loops
  • results in relatively stable plasma cholesterol lev
  • *very difficult to change serum levels with diet alone
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13
Q

what are the ways in which LDL is removed from circulation

A
  • receptor dependent

- non-receptor dependent macrophages

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14
Q

receptor dependent LDL removal

A
  • binds to cell surface receptors -> endocytosis

- LDL degraded -> cholesterol released into cytoplasm and excreted

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15
Q

non-receptor dependent LDL removal

A
  • ingestion of phagocytic monocytes
  • macrophage uptake of LDL in arterial wall -> accumulation of insoluble cholesterol ester -> foam cells -> atherosclerosis
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16
Q

dyslipidemia values

A
  • LDL > 160
  • HDL < 40
  • TG > 150
  • all three are independent risk factors for CAD
  • ratio of LDL to HDL is important risk factor
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17
Q

what level of HDL is protective

A
  • HDL > 60
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18
Q

how do we measure LDL

A
  • indirectly via friedwald equation

- LDL = total cholesterol - HDL- TG

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19
Q

primary dyslipidemia

A
  • intrinsic causes- familial autosomal dominant mutations
  • over production or impaired removal
  • strongly linked to premature CAD
  • > 200 LDL receptor mutations
  • xanthomas, high LDL, FHx
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20
Q

secondary causes of dyslipidemia

A
  • generally modifiable risk factors
  • DM2
  • obesity
  • drugs
  • cigarettes
  • excessive alcohol
  • cholestatic liver disease
  • nephrotic syndrome or chronic renal failure
  • hypothyroidism
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21
Q

who should be screened for dyslipidemia

A
  • men > 35, women > 45
  • men > 25 or women > 35 with CV risk factors
  • pts with diabetes
  • pts with first degree relative with premature CAD
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22
Q

how often do you screen for dyslipidemia

A
  • every 5 years if clearly above threshold

- every 3 years if near threshold

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23
Q

what is considered premature CAD

A
  • before 55 in men

- before 65 in women

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24
Q

lifestyle modifications to treat dyslipidemia

A
  • diet high in vegetables, whole grains, low or nonfat dairy
  • some alcohol
  • low red or processed meats
  • low sugar intake
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25
what is the standard of care for lipid lowering agents and why
- HMG CoA reductase inhibitors - AKA statins - most powerful at lowering LDL, modest HDL increase - only lipid lowering agent shown to improve CV outcomes both short and long term - improves all cause mortality
26
how do statins work
- inhibit HMG CoA reductase which is required for biosynthesis of cholesterol
27
what should you order before starting statin therapy
- fasting lipid panel - LFTs - CK
28
benefit groups for statins
- clinical atherosclerosis CVD - LDL > 190, age > 21 - primary prevention for diabetics: age 40-75, LDL 70-189 - primary prevention for nondiabetics: > 7.5% 10 year ACSVD risk, age 40-75, LDL 70-189
29
monitoring response to therapy with statins
- have pt repeat labs in 4-6 weeks - high intensity tx should see 50% drop in LDL, mod intensity 30-50% - if dont get expected drop then have them return in 1 mo and recheck - if levels still not as anticipated add another agent
30
what is the best combo agent to use with statins
- ezetimibe
31
ADRs of statins
- myopathies | - LFT abnormalities- 3X ULN, not common and reversible
32
myopathies and statins
- myalgia- normal CK - myositis- somewhat elevated CK > 10X ULN - rhabdo- markedly increased CK, pain, very ill - if pt has severe muscle sx or fatigue address possibility of rhabdo via CK, creatinine, UA for myoglobinuria
33
treatment for mild-mod muscle sx while on statin
- d/c statin until sx are evaluated - can decrease dose or switch agent - eval pt for other conditions that might increase risk for muscle sx - if after 2 mo without statin rx and still have sx or elevated CK it is likely not due to stain
34
other causes for elevated CK other than statins
- hypothyroid disease - inflammatory myopathies - PMR in pts > 50 - injury or excessive exercise - alcohol misuse
35
increased risk for statin intolerance
- erythromycin - cyclosporin - HIV tx - grapefruit juice - combo lipid tx- fibrates and niacin
36
cholesterol absorption inhibitors
- agent- ezetimibe - used in combo with statins to further lower LDL - good alt to high dose statin if pt is intolerant - monitor liver function
37
mild-mod hyperTG
- 150-1000 mg/dL | - unclear if tx makes difference for CV outcomes
38
severe hyperTG
- levels over 1000 mg/dL - risk of pancreatitis - lipemic blood samples
39
tx for hyperTG
- focus on metabolic syndrome - weight loss* - aerobic exs- mod intensity for 4 hours a week - avoid sugars - strict glycemic control in diabetics - unclear if any meds make a dif- fish oil, niacin, fibrates
40
metabolic syndromes
- increased risk of atherogenesis, pro-inflammatory state - need 3 of 5 risk factors - glucose intolerance - HTN - dyslipidemia ( TG and HDL sep risk factors) - central obesity- male waist circumference > 40 in., female > 35 in.
41
what is the leading cause of death in adults in US
- CAD
42
pathophys of CAD
- atherosclerosis- thickening of arterial vessel wall | - increased vasc resistance -> progression -> complete occlusion d/t ruptured clot -> MI
43
primary prevention of CAD
- maintain/ achieve ideal weight - PE and healthy diet - no smoking - maintain BP goals at < 140/90 or 130/80 if other known risk factors - glycemic control in diabetes - high risk pts should take ASA daily - small amounts of alcohol consumption
44
angina pectoris
- chest pain d/t myocardial ischemia | - tightness, squeezing, burning, gas, indigestion or ill characterized
45
anginal equivalent
- sx other than chest discomfort attributable to myocardial ischemia - i.e. SOB, dizziness, nausea, fatigue
46
four main risk factors that affect 02 demand
- HR - SBP - myocardial wall tension or stress - myocardial contractility
47
how is myocardial ischemia on EKG represented
- ST depressions
48
stable angina
- asymptomatic at rest | - sx provoked by predictable amount of exertion
49
unstable angina
- sx at rest or sx with less and less exertion
50
sx of chronic stable angina
- chest pain or DOE lasting 5-15 min - predictable and reproducible - d/t flow limiting lesions - relieved by rest or NTG - localized to central or slightly left side of chest - presyncope and fatigue
51
physical exam for CAD
- most often normal - general appearance- central obesity, sweaty, SOB with minimal exertion - vitals- HTN - diminished peripheral pulses- PAD - bruits of carotid, renal, aorta, and femoral aa.
52
EKG findings in CAD
- often normal in early or stable CAD - pathologic Q waves- prev MI - nonspecific St or T wave abnormalities - LVH- d/t long standing HTN - ST elevation during STEMI
53
stress testing
- best method for dx CAD in conjunction with rest of clinical assessment - appropriate for stable angina - c/i in unstable angina
54
what is the gold std for CAD dx
- coronary angiography - not used often as primary method - expensive and invasive - does not have physiologic info
55
estimating pre stress test probability of CAD
- classic/ typical angina - probable or atypical angina - non-anginal or non-ischemic chest pain - intermediate pretest probability yield most results on stress test
56
classic/ typical angina
- substernal chest pain - typical in quality and duration - provoked by exertion/ stress and relieved be rest or NTG
57
probable or atypical angina
- chest pain with 2/3 characteristics of classic
58
non-anginal or non- ischemic ches tpain
- chest pain with one or non of characteristics of classic
59
indications for stress test
- intermed pretest probability - pre-op risk assessment for non-cardiac sx - pts with significant change in cardiac sx - after resolution of acute chest pain - prior to angiography to localize lesion
60
exercise tolerance testing (ETT)
- first line for most pts - resting EKG cannot have abnormalities - must be able to exs - low-mod risk CAD - women tend to have more false positives
61
findings on resting EKG that disqualify a pt from ETT
- ST abnormalities - LVH - LBBB - ventricular paced - WPW
62
stress echo
- either exs or pharmacologically induced - echo at rest then after stress - look for stress induced regional wall motion abnormalities to localize lesions - operator dependent
63
radionuclide myocardial perfusion imaging
- either exs or pharmacologically induced - imaging before and after stress - inject radioactive nucleotide - poorly perfused areas of heart do not take up color- localizes lesions - highly sensitive - aka stress myoview or stress MIBI
64
nuclear medicine PET CT stress test
- very sensitive - very expensive - best for obese pts - not readily avail
65
acute coronary syndrome (ACS)
- unstable angina - NSTEMI - STEMI
66
sx of ACS
- severe chest pressure usually in early morning - radiates to L arm, both arms, or jaw - SOB, nausea, diaphoresis, light headedness - lasts > 20 min but < 1 hour - poor exs tol at baseline
67
clinical findings of unstable angina
- ischemic sx suggestive of ACS but no elevated troponins - unstable plaque without rupture - +/- ST depressions or nonspecific changes
68
clinical findings of NSTEMI
- ischemic sx suggestive of ACS - elevated troponins - unstable plaque +/- rupture
69
clinical findings of STEMI
- classic presentation | - plaque rupture with complete occlusion
70
initial management of chest pain
- vitals, EKG, cardiac monitor - O2 if sat < 90% - IV, bloodwork, CXR - H&P - ASA- 325 mg - sublingual NTG q5 min X 3 - morphine for severe pain - beta blockers within 24 hours - anticoag- IV heparin cont infusion - K and Mg
71
what is the TIMI risk score
- estimates 14 day mortality for pts with unstable angina/ NSTEMI - low risk = score 0-2 - intermed risk= 3-4 - high risk = 5-7
72
indications for urgent angiography and revascularization
- hemodynamic instability or cardiogenic shock - severe LV dysfunction or F - recurrent or persistent rest angina despite intensive tx - new or worsening mitral regurg - sustained ventricular arrhythmias
73
requirements to be labeled STEMI
- > 2 mm St elevation in 2 contiguous precordial leads (1.5 in women) - > 1 mm ST elevation in 2 contiguous other leads - new LBBB in setting of acute chest pain is MI until proven otherwise - often see reciprocal changes in opposite leads
74
anterior MI
- V2 V3 V4 | - LAD
75
left lateral MI
- I aVL V5 V6 | - left circumflex a
76
inferior MI
- II III aVF | - RCA
77
right ventricular MI
- aVR V1 | - RCA
78
posterior MI
- ST depression in V2 V3 V4 | - RCA
79
goal of tx of STEMI
- relieve chest pain - correct abnormal hemodynamics - initiate PCI within 90 min (120 min acceptable) - if PCI unavail initiate fibrinolysis - antithrombotic tx to prevent re-thrombosis or acute stent thrombosis - BB to prevent recurrent ischemia and ventricular arrhythmias
80
fibrinolytic agents
- alteplase - reteplase - streptokinase
81
antithrombotic agents
- ticagrelor - clopidogrel - prasugrel
82
management of pts with acute STEMI
- acute triage - activate cath lab -> PCI - fibrinolytics if no PCI - MONA - O2 if sat < 90% - BB - high dose ASA - K and Mg - if pt found to have 3 vessel disease they skip PCI and get CABG
83
prinzmetal angina
- aka vasospastic angina - d/t smooth muscle hyperreactivity - angina sx at rest - often between midnight and early morning - assoc with transient (15 min) ST segment elevation, obstruction and myocardial ischemia - possible MI - triggered by coronary artery vasospasm - usually dont have CAD
84
risk factors/ triggers for prinzmetal angina
- cigarette smoking - genetics - insulin resistance - changes in autonomic activity- HR variability - drugs- epi, cocaine, marijuana, alcohol, amphetamines - Mg deficiency
85
vasospastic angina vs true STEMI
- pts usuall younger with vasospasm - fam hx of prinzmetal - few if any CV risk factors - drug use - repeat EKG in 15 min shows total resolution of ST segments
86
management of prinzmetal angina
- sublingual NTG during episodes - smoking cessation - long acting nitrates and CCB- prevent vasoconstriction and promote dilation - statins - Mg - PCI with stent (rare)

Clin Med II (16 decks)

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