Cardiovascular Labs Flashcards

1
Q

LDH1

A

heart and RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

LDH5

A

muscle and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CPK

A

is elevated in first 24 hours and goes away after three days

  • most important in ddx recurrent MI, would see a secondary spike in CPK

(troponin would remain elevated for ten days)

CPK-MM = muscle
CPK-MB - heart
CPK-BB = brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

troponin

A

early leakage seen in MI, stays elevated for 5-10 days

  • higher sensitivity tests now available
  • Cardiac muscle contains specific cTnI and cTnT isoforms. Most cTn is bound, but a small amount is free in the cytosol. The initial rise of cTn after myocyte damage is thought to be release of the unbound cytosolic cTn. This is followed by more prolonged appearance of troponin from damage to the myofilament structures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how do you ddx reinfarction?

A

elevated levels of CK-MB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what things needed to ddx an MI?

A

elevated/falling troponin I or T

EKG changes including new onset of LBBB

chest pain

echocardiogram showing wall motion abnormality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

other things that could elevated troponin?

A

MI, pericarditis, myocarditis, PE, sepsis, LVH, CHF, CKD, DM

thus need more than just troponin elevtaion to ddx MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hsCRP

A

best for testing for CAD

  • released by hepatocytes under influence of IL6 and TNFalpha
  • if elevated more than 3 mg/L = worse prognosis for stable CHD
  • best level of hsCRP <1 mg/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are mediators released in inflammation?

A
  • IL1, IL6 and TNF go to liver
  • liver releases:
    1. fibrinogen (activation of coagulation system)
    2. Serum amyloid A
    3. CRP
    4. C3
    5. Haptoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

homocysteine

A

associated with vascular injury, ASHD, coagulation, and venous thromboembol- ism, but less important than cholesterol, DM, smoking, and HTN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how to calculate LDL-C levels?

A

LDL-C = total-C – [VLDL-C (1/5 trig) + HDL-C]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how to calculate Non-HDL-C levels?

A

Non-HDL-C = total C – HDL-C = cholesterol in LDL

** this is a better measurement of risk than just LDL-C alone***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PLAQ test

A

Lipoprotein Phospholipase A2.
A lipoprotein associated, macrophage secreted enzyme.
Elevated levels lead to increased MI and stroke.
Cleaves oxidized fatty acids from LDL-C.
Levels decreased by statins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

best supporting test for ddx of CVD?

A

cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

best marker for severity of CHF?

A

serum sodium

  • high serum sodium is poor prognosis for CHF
  • see hypotonic hypervolemic hyponatremia with urinary sodium less than 10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

best cardiac marker to exclude CHF?

A

NT-pro BNP levels are low

17
Q

BNP

NT proBNP?

A

if pt. comes in complaining of SOB, can use these levels, if low, to rule out CHF and to look towards resp issues

Greater than 400 pg/mL = possible CHF.

Less than 100 pg/mL = no CHF.

  • NT-proBNP levels are more specific (<400 excludes CHF)
18
Q

look at slide 41 and memorize!

A

do it now

19
Q

steps of lipid metabolism?

A
  • chylomicrons from diet come in and are broken up by Apo B48, ApoE, ApoCII.
  • once chylomicron is broken down the liver can take up the remant and its excreted as VLDL
  • VLDL is made into LDL-R by ApoB100 and Apo E3/E3 and is stored in the liver
  • if don’t have ApoB48 –> results in high levels of triglycerides and creamy blood
20
Q

hyperlipoproteinemia IIa?

A
  • have defective LDL receptor or defective Apo B100 ligand, which results in LDL not being taken up into the liver or fat cells
  • see high cholesterol levels with high LDL-C levels
    • pt. presents with high levels LDL, corneal arcus, tendinous xanthomata, premature CAD, aortic stenosis
  • ** strong family hx
21
Q

hyperliporpteouemia IIb?

A

= “familial combined hyperlipidemia”

  • liver is putting out too much ApoB100 and too much VLDL
  • results in high levels of triglycerides and high cholesterol (though not even)
  • see NO Xanthomas,
  • often seen in diabetics
  • most common cause of lactescent plasma and primary hyperlipidemia
22
Q

hyperlipoproteinemia III?

A
  • due to defective inherited Apo E3/E3 (instead have E2/E2)
  • see equal amounts of cholesterol and triglycerides
    _“dysbetalipoproteinemia = E2/E2
  • see weird xanthoma rash on hands and elbows
23
Q

what are markers of CHD?

A

coronary heart disease stratification = Identify CHD equivalents (DM, TIA, PAD, AAA, 10-year risk of CHD > 20%). If present, the cholesterol goal is HDL-C < 100 mg/dL, with an optional goal of < 70 mg/dL

age, total cholesterol, smoking, HDL cholesterol, BP.
also considered to evaluate risk