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Clin Lab > Cardio labs > Flashcards

Cardio labs Flashcards

1
Q

vascular disease

A

all organs and tissue are potential targets of injury in vascular disease

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2
Q

blood vessel diseases

A

-Atherosclerosis
-HTN
-Vasculitis (inflammation)- autoimmune, infection -> can cause stroke (w/o any common risk factors!)
-Aneurysms
-Tumors- increase vascular supply to grow
-DVT
-PE
-Stroke

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3
Q

atherosclerosis

A

-Labs to identify cause of atherosclerosis
-Lipids
-Ingestion of saturated fats & cholesterol
-Primary Lipid disorders- intake, genetics
-Secondary Lipid disorders- pancreas issues

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4
Q

atherosclerosis: lipid profile

A

-8-12hr fast for blood draw
-Total Cholesterol - >200 (high)
-LDL- >200 (high) -> friedwald formula or direct assay
-HDL- you want it > 40
-Triglycerides- >190 (high)

-numbers diff by age, risk factors, gender

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5
Q

lifestyle modifications: elevated LDL

A

-exercise
-smoking cessation
-target BMI
-diet

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6
Q

screening and managing hyperlipidemia chart

A

-hormone and steroids are known to elevate cholesterol
-if yes, do lipid panel and/or repeat lipid panel
-then, follow AHA chart

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7
Q

total cholesterol

A

-non specific
-is good cholesterol elevated?
-is bad cholesterol elevated?
-you never just look at this value

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8
Q

TG elevated chart

A
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9
Q

framingham score

A

-gold standard cardiovascular risk
-memorize it
-HDL is the only protective factor -> reduces risk of atherosclerotic disease

-Total Cholesterol
-HDL
-Age
-Gender
-Smoking
-HTN
-DM

-procram score- includes family hx

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10
Q

clinical picture flow chart

A

-clinical ASCVD- CAD, MI, PAD, cerebral vascular disease, carotid disease, renal artery stenosis
-primary prevention- preventing the first event
-secondary prevention- preventing a second even from happening
-know this chart

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11
Q

statin ADR

A

-muscle cramps
-elevated LFTs- 6 weeks lipid levels, and LFTs
-statins attack endogenous LDL- genetic cholesterol
-ezetimibe stops LDL absorption

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12
Q

info about lipid values

A

-HDL- low levels represent a cardiac risk factor
->60 HDL reduces cardiac risk
-total cholesterol- HDL+LDL+VLDL+IDL+Lp
-triglycerides- elevated in hypothyroidism, nephrotic syndrome, liver disease, metabolic disorder, pancreatitis*, toxemia

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13
Q

C-reactive protein

A

-Persistent inflammatory process
-Increased risk of cardiovascular events
-<1.0 mg/L low risk, 1-3 mg/L intermediate, >3.0 mg/L high risk.
-Used to classify those patients who are at borderline CV risk
-is this due to vasculitis?

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14
Q

metabolic syndrome

A

-Series of risk factors for cardiovascular disease ( MI, CVA, DM), kidney dysfunction,
-40% of US pts over 60 years of age!
-May not have any physical symptoms

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15
Q

metabolic syndrome criteria

A

->= 3 of the following:
-impaired glucose tolerance (pre-diabetes)- fasting plasma glucose >=100 or A1c 5.6-6.4
-abdominal obesity
-hypertriglyceridemia- >=150 or on on meds for it
-low levels of HDL- <40 (men), <50 (women), or on meds for it
-HTN- >130/85, or on meds for it

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16
Q

dx criteria for familial/genetic hypercholesterolemia

A

-acrus cornealis- black ring around eye

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17
Q

assessment of CV risk

A

-Smoking,
-Hypertension
-DM
-Obesity
-Physical inactivity
-Family History of coronary disease

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18
Q

HTN

A

-in US up to 50% of adults have HTN
-microvascular damage
-chronic HTN can affect GFR / kidney function
-correctable causes of HTN:
-obesity
-tobacco
-Na intake
-ETOH
-oral contraceptives
-NSAIDS

-secondary:
-renal artery stenosis
-pheocromocytoma
-hyperadlosteronism
-hypothyroidism

19
Q

vasculitis

A

-inflammation of the blood vessel wall
-decrease blood flow -> necrosis of tissue
-antineutrophil cytoplasmic antibody, ANCA
-vessel bx

-primary- no cause
-secondary- infection (HIV, Hep B, Hep C,) and autoimmune (lupus, RA)

20
Q

dx of vasculitis

A

-Presence of characteristics of particular clinical findings
-Inflammation within particular size blood vessels
-Labs:
-ANCA antibiodies IgG (dont need to know this)
-Elevated erythrocyte sedimentation rate, ESR
-C-reactive protein
-End organ damage
-antineutrophil cytoplasmic antibody, ANA

21
Q

types of vasculitis

A

-Giant Cell Arteritis
-Takayasu Arteritis
-Polyarteritis nodosa
-Kawasaki disease
-Granulomatous polyaniitis “Wegener’s”
-Eosinophilic granulomatous polyangiitis -“Churg-Strauss Syndrome”
-Microscopic polyangiitis
-Henoch-Schonlein Purura
-Cryoglobulinemic vasculitis
-Cutaneous leukocytoclastic angitis

22
Q

vasculitis sx

A

-mottled, lacey, palpable purpura
-livedo reticularis
-fever, headache, wt loss
-joint pain
-GI- bloody stool, ab pain
-heart- MI, HTN
-stroke- if pt comes in with suspected stroke -> and the c-reactive protein, ANA, ERS -> suspect vasculitis
-eye- reduced visual acuity
-nose bleeds
-lungs- bloody cough, infiltrates
-kidneys- glomerular nephritis

23
Q

DVT/PE

A

-D-Dimer:
-Cross linked fibrin generation
-Elevated in setting of DVT/PE however not specific!
-Can help to rule out only

-Hypercoagulable state?

24
Q

stroke

A

-Atherosclerotic disease
-Antiphospholipid syndrome
-Prothrombotic condition
-No diagnostic lab for stoke, no organ marker
-Hypercoagulable work up
-Anti-platelet therapy
-ischemic stroke- blood supply cut off
-hemorrhagic- lack of blood flow due to hemorrhage

25
Q

acute coronary syndrome event flow chart (low risk)

A

-ischemic chest pain- STEMI, NSTEMI, unstable angina

26
Q

overview of approach to pts with suspected MI in ER chart

A
27
Q

TIMI score

A

The TIMI Risk Score for UA/NSTEMI estimates mortality for patients with unstable angina and non-ST elevation myocardial infarction (MI).

28
Q

HEART score- chest pain

A

-0-3- low risk
-4-6- intermediate
->7- high risk

29
Q

likelihood of acute coronary syndrome secondary to coronary heart disease in pts without ST segment elevation

A
30
Q

short term risk of death or nonfatal myocardial infarction (MI) in pts with unstable angina/NSTEMI

A
31
Q

cardiac biomarkers

A

-MI:
-cardiac troponin
-serial rise in troponin
-elevation for days after MI
-all other biomarkers of nonspecific and not helpful

32
Q

troponin

A

-Only marker used to diagnosis a Myocardial Infarction!
-Normal value is <0.01 ng/ml
-Released within 2-4 hrs, peaks 10-24 hrs, drops within 1-2 weeks
-Can calculate size or evolving MI
-Used in conjunction with clinical signs
-dont need to know numbers
-cardiac troponin I and cardiac troponin T
-high sensitivity troponin assays have cut off that is 99th precentile of cardiac disease-free reference population

33
Q

other causes for troponin elevation

A

-cardiac surgery
-cocain- vasospasms
-PE, stroke
-hemorrhage

34
Q

other markers

A

-Poor Specificity because of wide tissue distribution:
-Aspartate Aminotransaminase (AST)
-Creatine phosphokinase (CK)
-CK-MB
-Myoglobin
-Total lactate dehydrogenase (LDH)

35
Q

CK and CK-MB

A

-Creatine kinase (CK) and its MB isoenzyme (CK-MB) -> most commonly used serologic tests for dx of MI prior to troponin
-not really used anymore
-Many institutions no longer offer CK-MB testing.
-some use CK-MB for detection of early reinfarction, although not guideline recommended
-Elevations in total serum CK lack specificity for myocardial damage, which improves with measurement of the MB fraction.
-normal range of CK also varies considerably; a twofold or greater increase in the CK concentration is required for dx
-criterion can be problematic in older individuals who, because of their lower muscle mass, may have low baseline serum total CK and, during MI, may have elevated serum CK-MB with values of total CK that rise but remain within the normal range -> For these reasons, total CK has not been used in the diagnosis of myocardial damage for years.

36
Q

rhabdo

A

-sustained exercise, compartment syndrome, crush injury
-hallmark of rhabdomyolysis is an elevation in CK and other serum muscle enzymes.
-Serum CK levels at presentation are usually at least 5x upper limit of normal, but range from approximately 1500 to over 100,000 international units/L
-The serum CK begins to rise within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hours. A decline is usually seen within three to five days of cessation of muscle injury. CK has a serum half-life of about 1.5 days and declines at a relatively constant rate of about 40 to 50 percent of the previous day’s value. In patients whose CK does not decline as expected, continued muscle injury or the development of a compartment syndrome may be present

37
Q

myoglobin

A

-rhabdo
-Myoglobin is a ubiquitous heme protein that is rapidly released from damaged tissue because of its small size. Its half-life in plasma is in the range of nine minutes. Due to its early appearance in the serum, myoglobin was postulated to be a useful adjunct to either troponin or creatine kinase MB (CK-MB) for the early diagnosis of myocardial infarction (MI)
-With contemporary, highly sensitive cardiac troponin (cTn) assays and the use of the 99th percentile or 10 percent coefficient of variation cut-off, cTn is elevated prior to elevations in myoglobin

38
Q

lactate dehydrogenase

A

-Lactate dehydrogenase (LD, formerly abbreviated LDH) was commonly used in the past in combination with aspartate aminotransferase (AST or SGOT) and creatine kinase MB (CK-MB) to diagnose an acute myocardial infarction (MI).
-LD consists of M (muscle) and H (heart) subunits that give rise to five isoenzymes. The heart primarily contains LD1 and some LD2. Red cells, kidney, stomach, and pancreas are other important sources of LD1. In contrast, LD5 predominates in skeletal muscle and liver.
-LD activity rises to abnormal levels approximately 10 hours after the onset of MI, peaks at 24 to 48 hours, and remains elevated for six to eight days. However, since troponins are more specific than LD and remain elevated for 5 to 10 days, current recommendations suggest that LD no longer has a role in the diagnosis of MI

39
Q

congestive heart failure

A

-only cardiovascular disease with increasing incidence
-leading cause of hospitalizations in pts 65yo and older
-5 mil pts with CHF, 400,000 new cases each year
-5 year mortality 10% mild CHF- 80% end stage disease

40
Q

monitoring CHF

A

-Brain natriuretic peptide, BNP
-Rise from myocardial stress or fluid overload
-Filling pressure defect
-Chronically elevated with acute elevation in setting of volume overload in CHF patients
-Ordering a BNP in patients with shortness of breath can reduce uncertainty of diagnosis
-In the setting of a normal BNP, diagnosis of CHF is highly unlikely.
-Long term monitoring in guiding therapy, monitoring course of disease and risk stratification

41
Q

BNP

A

-5- 1,300 pg/mL
->400 HF with dyspnea
-<100 negative predictive for HF
-Difference by age, sex, BMI
-Elevated in renal failure
-Equivalent to or better predictior than CXR and P/E
-Correlates with NYHA Class
-Patients in the highest 25% have greater mortality at 2 years then those in lowest 25%
-Can not be used with Entresto

42
Q

pro-BNP

A

-Age ranges for HF diagnosis
-<50yo HF @ 450 pg/mL
-50-75 yo @ 900 pg/mL
->75 yo 1800 pg/mL
-Greater prognostic value then BNP (more LF function effect)
-Difference by age, sex, BMI
-Elevated renal failure

43
Q

initial eval of high B-type natriuretic peptide in adults chart

A
44
Q

common triggers of elevated BNP and NT-proBNP

A

Clin Lab (14 decks)

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