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Clin Med II > dyslipidemia and CAD > Flashcards

dyslipidemia and CAD Flashcards

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
Q

what is the standard of care for lipid lowering agents and why

A
  • 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
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26
Q

how do statins work

A
  • inhibit HMG CoA reductase which is required for biosynthesis of cholesterol
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27
Q

what should you order before starting statin therapy

A
  • fasting lipid panel
  • LFTs
  • CK
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28
Q

benefit groups for statins

A
  • 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
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29
Q

monitoring response to therapy with statins

A
  • 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
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30
Q

what is the best combo agent to use with statins

A
  • ezetimibe
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31
Q

ADRs of statins

A
  • myopathies

- LFT abnormalities- 3X ULN, not common and reversible

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32
Q

myopathies and statins

A
  • 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
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33
Q

treatment for mild-mod muscle sx while on statin

A
  • 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
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34
Q

other causes for elevated CK other than statins

A
  • hypothyroid disease
  • inflammatory myopathies
  • PMR in pts > 50
  • injury or excessive exercise
  • alcohol misuse
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35
Q

increased risk for statin intolerance

A
  • erythromycin
  • cyclosporin
  • HIV tx
  • grapefruit juice
  • combo lipid tx- fibrates and niacin
36
Q

cholesterol absorption inhibitors

A
  • 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
Q

mild-mod hyperTG

A
  • 150-1000 mg/dL

- unclear if tx makes difference for CV outcomes

38
Q

severe hyperTG

A
  • levels over 1000 mg/dL
  • risk of pancreatitis
  • lipemic blood samples
39
Q

tx for hyperTG

A
  • 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
Q

metabolic syndromes

A
  • 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
Q

what is the leading cause of death in adults in US

A
  • CAD
42
Q

pathophys of CAD

A
  • atherosclerosis- thickening of arterial vessel wall

- increased vasc resistance -> progression -> complete occlusion d/t ruptured clot -> MI

43
Q

primary prevention of CAD

A
  • 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
Q

angina pectoris

A
  • chest pain d/t myocardial ischemia

- tightness, squeezing, burning, gas, indigestion or ill characterized

45
Q

anginal equivalent

A
  • sx other than chest discomfort attributable to myocardial ischemia
  • i.e. SOB, dizziness, nausea, fatigue
46
Q

four main risk factors that affect 02 demand

A
  • HR
  • SBP
  • myocardial wall tension or stress
  • myocardial contractility
47
Q

how is myocardial ischemia on EKG represented

A
  • ST depressions
48
Q

stable angina

A
  • asymptomatic at rest

- sx provoked by predictable amount of exertion

49
Q

unstable angina

A
  • sx at rest or sx with less and less exertion
50
Q

sx of chronic stable angina

A
  • 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
Q

physical exam for CAD

A
  • 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
Q

EKG findings in CAD

A
  • 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
Q

stress testing

A
  • best method for dx CAD in conjunction with rest of clinical assessment
  • appropriate for stable angina
  • c/i in unstable angina
54
Q

what is the gold std for CAD dx

A
  • coronary angiography
  • not used often as primary method
  • expensive and invasive
  • does not have physiologic info
55
Q

estimating pre stress test probability of CAD

A
  • classic/ typical angina
  • probable or atypical angina
  • non-anginal or non-ischemic chest pain
  • intermediate pretest probability yield most results on stress test
56
Q

classic/ typical angina

A
  • substernal chest pain
  • typical in quality and duration
  • provoked by exertion/ stress and relieved be rest or NTG
57
Q

probable or atypical angina

A
  • chest pain with 2/3 characteristics of classic
58
Q

non-anginal or non- ischemic ches tpain

A
  • chest pain with one or non of characteristics of classic
59
Q

indications for stress test

A
  • 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
Q

exercise tolerance testing (ETT)

A
  • 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
Q

findings on resting EKG that disqualify a pt from ETT

A
  • ST abnormalities
  • LVH
  • LBBB
  • ventricular paced
  • WPW
62
Q

stress echo

A
  • 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
Q

radionuclide myocardial perfusion imaging

A
  • 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
Q

nuclear medicine PET CT stress test

A
  • very sensitive
  • very expensive
  • best for obese pts
  • not readily avail
65
Q

acute coronary syndrome (ACS)

A
  • unstable angina
  • NSTEMI
  • STEMI
66
Q

sx of ACS

A
  • 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
Q

clinical findings of unstable angina

A
  • ischemic sx suggestive of ACS but no elevated troponins
  • unstable plaque without rupture
  • +/- ST depressions or nonspecific changes
68
Q

clinical findings of NSTEMI

A
  • ischemic sx suggestive of ACS
  • elevated troponins
  • unstable plaque +/- rupture
69
Q

clinical findings of STEMI

A
  • classic presentation

- plaque rupture with complete occlusion

70
Q

initial management of chest pain

A
  • 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
Q

what is the TIMI risk score

A
  • estimates 14 day mortality for pts with unstable angina/ NSTEMI
  • low risk = score 0-2
  • intermed risk= 3-4
  • high risk = 5-7
72
Q

indications for urgent angiography and revascularization

A
  • 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
Q

requirements to be labeled STEMI

A
  • > 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
Q

anterior MI

A
  • V2 V3 V4

- LAD

75
Q

left lateral MI

A
  • I aVL V5 V6

- left circumflex a

76
Q

inferior MI

A
  • II III aVF

- RCA

77
Q

right ventricular MI

A
  • aVR V1

- RCA

78
Q

posterior MI

A
  • ST depression in V2 V3 V4

- RCA

79
Q

goal of tx of STEMI

A
  • 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
Q

fibrinolytic agents

A
  • alteplase
  • reteplase
  • streptokinase
81
Q

antithrombotic agents

A
  • ticagrelor
  • clopidogrel
  • prasugrel
82
Q

management of pts with acute STEMI

A
  • 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
Q

prinzmetal angina

A
  • 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
Q

risk factors/ triggers for prinzmetal angina

A
  • cigarette smoking
  • genetics
  • insulin resistance
  • changes in autonomic activity- HR variability
  • drugs- epi, cocaine, marijuana, alcohol, amphetamines
  • Mg deficiency
85
Q

vasospastic angina vs true STEMI

A
  • 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
Q

management of prinzmetal angina

A
  • 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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