Lab Med Flashcards

1
Q

Acute MI

A

imbalance b/w myocardial O2 supply (ischemia) and demand, resulting in injury to and the eventual death of myocytes

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2
Q

myocardial necrosis is most often associated with what?

A
  • a thrombotic occlusion superimposed on coronary atherosclerosis
  • the process of plaque rupture and thrombosis is one of the ways in which coronary atherosclerosis progresses
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3
Q

STEMI

A

-total occlusion of coronary blood flow = ST elevation

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4
Q

NSTEMI

A

partial occlusion of coronary blood flow = no ST elevation (could show ischemia as ST depression)

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5
Q

What does the absence of blood flow lead to?

A
  • cardias muscle tissue death

- spilling cardiac biomarkers into the circulatory system

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6
Q

How often is the initial EKG diagnostic for AMI?

A

-about 30% of patients

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7
Q

When is troponin testing most useful?

A

when patients are having nondiagnostic EKG tracings

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8
Q

Troponin (cTnI or cTnT)

A

cardiac regulatory proteins specific to the myocardium that control the Ca++-mediated interaction b/w action and myosin

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9
Q

Troponin is the perferred test for the diagnosis of what?

A

ACS

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10
Q

troponin establishes the diagnosis of what?

A

irreversible myocardial necrosis, even when EKG changes are non diagnostic

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11
Q

What is important to know about an elevated troponin?

A

several distinct pathologies may cause it to be elevated, not all of them involve myocyte necrosis

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12
Q

How is NSTEMI strictly defined in terms of lab values?

A

-a rise and fall in serum biomarkers (usually troponin) exceeding the 99th percentile of a normal reference population

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13
Q

Time it takes for troponin levels to rise

A
  • 3-6 hrs after onset of ischemic symptoms

- can be delayed from 8-12 hrs

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14
Q

Why is it important to know that troponin levels could be delayed in rising?

A

need to get serial troponin levels

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15
Q

Why is troponin most useful in NSTEMI

A

CK-MB and myoglobin are not useful in the diagnosis of ACS w/ mild ischemia w/o necrosis

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16
Q

CK-MB is more relevant to use with what condition?

A

STEMI

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17
Q

CK-MB levels time to rise

A

-3-4 hrs after onset of myocardial injury

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18
Q

myoglobin

A
  • early marker for myocardial necrosis

- increases 2 hrs after onset of necrosis

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19
Q

What is the recommendation for when a pt has negative biomarkers w/i 6 hrs of onset of sx?

A

remeasure 8-12 hrs after onset

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20
Q

What other reasons could CK-MB be elevated?

A
  • MANY (not listing all from lecture)
  • necrosis or inflammation of cardiac muscle
  • necrosis, inflammation or acute atrophy of striated muscle
  • endocrine disorders
  • some infections
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21
Q

explain why CK-MB detects muscle problems

A

-CK (creatine kinase) is an enzyme that controls energy flow within muscle cells

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22
Q

in addition to everything listed that can cause CK-MB to increase, what can cause CK to increase?

A

she emphasized rhabdomyolysis but there are many more

23
Q

additional sxs of CHF

A
  • 2-3+ bipedal edema

- b/l diffuse course rales on ausculation

24
Q

BNP (brain natriuretic peptide)

A

-a hormone secreted by myocytes in the left ventricle in response to pressure overload/myocyte stretch

25
Q

what effects does BNP cause

A
  • diuretic
  • natriuretic
  • vascular smooth muscle relaxation
26
Q

In what conditions can BNP be increased?

A
  • heart failure
  • left vent. dysfunction
  • renal impairment
  • CAD
  • valvular dz
  • arrhythmias
  • brain injury
  • anemia
  • sepsis/shock
27
Q

What is BNP used for?

A
  • screening and diagnosis of CHF

- prognosis of heart failure

28
Q

what is the correlation of BNP and prognosis of heart failure?

A

the higher the BNP, the worse the outcome (same in AMI)

29
Q

D-dimer is a test to rule out what?

A
  • aortic dissection
  • PE
  • DVT
30
Q

D-dimer ELISA use for PE

A

in pts w/ low pretest probability:

-can rule out PE if it is negative (high NPV)

31
Q

when is d-dimer ELISA not helpful?

A
  • if positive (low PPV)

- if pretest probability is intermediate or high

32
Q

PT (prothrombin time)

A

-assesses the coagulation activity of the extrinsic and common coagulation pathways

33
Q

PTT (partial thromboplastin)

A

-thromboplastin is potent activator of coag system

34
Q

Use of PT/INR and PTT

A
  • eval of clotting disorders
  • eval of liver function
  • monitor long term oral anticoag therapy (coumadin)
35
Q

what is the preferred reporting to monintor pts on vit. K antagonist therapy?

A
  • INR

- (in all other cases PT)

36
Q

market prolongation of the PT in liver dz indicates?

A

advanced dz

37
Q

market elevation of INR in pts using vit. K antagonists is a marker of what?

A

excessive anticoagulation

38
Q

INR below 2 reflects what?

A

insuffiecient anticoagulation

39
Q

In what 2 circumstances is combined abnormal PT and PTT found?

A
  1. medical: admin of oral anticoags, DIC, liver dz, vit. K deficiency, massive transfusions
  2. coag factor abnormalities
40
Q

What all is included in a lipid panel?

A
  • total cholesterol
  • LDL
  • HDL
  • triglycerides
41
Q

cholesterol

A
  • steroid carried in the bloodstream as a lipoprotein
  • necessary for cell membrane functioning
  • precursor to bile acids, progesterone, vit. D, estrogens, glucocorticoids and mineralocorticoids
42
Q

total cholesterol level

A

-desirable level that puts a person at a lower risk of coronary heart dz

43
Q

LDL

A
  • produced in the metabolism of VLDL
  • carry cholesterol in the bloodstream from the liver to the peripheral tissues
  • “bad cholesterol”
44
Q

LDL levels are associated w/ what?

A
  • atherosclerosis

- coronary heart dz

45
Q

LDL is increased in what conditions?

A
  • familial hypercholesterolemia
  • nephrotic syndrome
  • hepatic dz or obstruction
  • chronic renal failure
  • DM
  • hyperlipidemia
46
Q

LDL is decreased in what conditions?

A
  • a-betalipoproteinemia
  • hyperthyroidism
  • tangier dz
  • hypolipoproteinemia
  • chronic anemia
  • Apo C-II deficiency
  • hyperlipidemia type I
47
Q

when do you measure LDL values?

A

fasting

48
Q

What extrinsic factors could reduce LDL?

A
  • stress
  • recent illness
  • estrogens
49
Q

What extrinsic factors could increase LDL?

A
  • cigs
  • HTN
  • fam hx
50
Q

HDL

A
  • produced by liver
  • carries cholesterol in the blood from tissues to the liver (reverse transport)
  • “good cholesterol”
51
Q

how are HDL levels related to CHD

A
  • inversely

- it is an independent risk factor

52
Q

concentrations of HDL and triglycerides associated w/ certain disorders

A
  • 250-500: peripheral vascular dz
  • > 500: panreatitis risk
  • > 1000: hyperlipidemia
  • > 5000: eruptive xanthoma, corneal arcus, lipemia retinalis, enlarged liver and spleen
53
Q

triglycerides

A
  • form of fat and major source of energy for the body
  • stored in adipose
  • move via blood from gut to adipose
  • play important role in metabolism and transport
54
Q

review

A

case study at end of lecture