blood biochemistry

1. Princy Francis M
IInd Yr MSc (N)
JMCON

2. SENSITIVITY AND
SPECIFICITY
Specificity :
It is the ability of the test to correctly identify those without
the disease (true negative rate)
 Sensitivity
It is the ability of a test to correctly identify those with the
disease (true positive rate)

3. CARDIAC MARKERS
A diagnostic profile for acute MI.
Injured cells interstitial spaces lymphatic/
coronary circulation blood

4. CREATINE KINASE
The first enzyme level to increase in MI
Creatine- phosphate + ADP -----→ Creatine + ATP
2 polypeptide chains- B and M
 3 forms: CK-MM, CK-MB and CK-BB.
Increase after 6 hours, reaches a peak level in 24- 30
hours and returns to normal level in 2-4 days

5. TIMING OF APPEARANCE AND DISAPPEARANCE
OF COMMONLY USED CARDIAC MARKERS AND
ENZYMES IN RELATION TO ONSET OF CARDIAC
SYMPTOMSMarker/ Enzyme Starts to rise (Hrs) Peak (Hrs) Return to normal (Days)
AST 8 24 -48 4
CK 4-6 24 3 -4
CK-MB 4 18 2
LDH 24 72 8- 9
Myoglobin 2 -4 8 – 12 1 – 2
Troponin I 4- 6 10- 24 4
Troponin T 4- 6 10- 24 10

6. MYOGLOBIN
An early marker of MI
It is a heme protein with a small molecular weight.
It increase within 1 – 3 hrs after the onset MI, peaks in 4-
12 hrs and return to normal in 24 hrs.
Myoglobin elevations can also occur in patients with renal
or musculoskeletal disease.
Negative results are helpful in ruling out an early
diagnosis of MI.

7. TROPONINS
 Troponins are contractile proteins
 3 troponins : Troponin C , Troponin I, Troponin T
 Necrosis – I and T released.
 Troponin T and I are proteins found only in cardiac muscle.
 Elevated serum troponin T and I concentrations can be detected within 3 – 4 hrs,
they peak in 4 – 24 hrs and remain elevated for 1- 3 weeks.
 Reference Range
Troponin I: 0.0- 0.05 ng/mL
Troponin T: <0.01 µg/L

8. LACTATE
DEHYDROGENASE
 LDH catalyzes the reversible conversion of pyruvic acid and lactic acid.
 In AMI, serum activity rises within 12-24 hours, attain peak at 48 hours,
reaching about 1000 IU/L and returns gradually to normal from 8th to 14th day.
 The appearance of more LD1 than LD2, also called ‘flipped pattern’, is typical of
cardiac muscle damage but is non- specific since it also is associated with RBC
cell haemolysis or megaloblastic anaemia.
 The ‘flipped pattern’ pattern, in which LD1 > LD2, lasts up to 3-4 days after the
heart attack

9. Test Sensitivity (%) Specificity (%)
AST increased 89 -97 48 -88
CK increased 69 – 99 68 -84
CK-MB increased 79- 80 96
LDH increased 87 88
Myoglobin 92 94
Troponin I 90 – 100 83 - 96
Troponin T 93 85

10. LIPID PROFILE
 Cholesterol, triglycerides and lipoproteins are measured to evaluate a persons risk of
developing atherosclerotic disease.
 Cholesterol and triglycerides are transported in the blood by combining with protein
molecules to form lipoproteins.
 The lipoproteins are referred to as low density lipoproteins (LDL) and high density
lipoproteins (HDL).
 The risk of CAD increases as the ratio of LDL to HDL or the ratio of total cholesterol
(LDL + HDL ) to HDL increases.
 cholesterol levels remain relatively constant over 24 hrs, the blood specimen for the lipid
profile should be obtained after a 12 hour fast.

11. CHOLESTEROL LEVEL (<
200MG/DL)
 Cholesterol is a lipid required for hormone synthesis and cell
membrane formation.
 It is found in large quantities in brain and nerve tissue.
 Factors that contribute to variations in cholesterol levels include
age, gender, diet, exercise patterns, genetics, menopause, tobacco
use and stress levels.

12. TRIGLYCERIDES
 Normal range is 100 – 200mg/dL
 It composed of free fatty acids and glycerol, are stored in the adipose
tissue and are a source of energy.
 Triglycerides levels increase after meals and are affected by stress.
Diabetes, alcohol use and obesity can elevate triglycerides level.
 These levels have a direct correlation with LDL and an inverse one with
HDL.

13. LIPOPROTEINS (CONJUGATED
PROTEINS)
Chylomicrons
VLDL
LDL
HDL

14.  LDL is rich in cholesteryl esters, mainly transports cholesterol and its
esters from hepatocytes to extrahepatic tissues.
 In CAD or Diabetes, the primary goal of lipid management is reduction of
LDL level to < 70 mg/dL
 Friedewald formula : LDL = total Cholesterol – HDL - ( Triglycerides/ 5)

15.  Normal level in men is 35 – 70mg/dL; in women 35 – 85mg/dl
 It have a protective action. They transport cholesterol away from the tissue
and cells of the arterial wall to the liver for excretion.
 In patients with CAD, a secondary goal of lipid management is the increase
of HDL levels to more than 40 mg/dL.
 HDL removes excess cholesterol from tissues and routes into the liver for
reprocessing or removal

16. Chylomicrons
 Transport mainly TG from either food or synthesized in enterocytes,
also small amount of Phospholipid, cholesteryl esters and fat-soluble
vitamins from the intestine to liver, adipose tissues and muscles.
VLDL
 Transport mainly endogenous TG, synthesized in hepatocytes, from
liver to extrahepatic tissues, mainly adipose tissues for storage.

17. A modified form of LDL
High lipo(a) level inhibit plasmin formation by attracting the
plasminogen activators and blocking their action.
If patients have elevated levels of Lipo(a), their blood tends
to clot.

18.  Because of structural similarity to plasminogen, lipo(a)
interferes with the fibrinolysis by competing with plasminogen
activation, plasmin generation and fibrinolysis.
 This promotes the deposition of cholesterol as atherosclerotic
plaques.

19.  Enzyme immunoassay (PLAC test) is done to measure the level of
Lp -PLA2.
 Elevated levels of Lp -PLA2 are associated with vascular
inflammation and increased risk for CAD.
 Normal 131 – 376 ng/ml (men) and 120 – 342 ng/ml ( female).
 Lipoprotein associated phospholipase A2 , also known as platelet
activating factor acetylhydrolase.

20. Ceramides are transported through the blood by
lipoproteins and are associated with atherosclerosis.
Three specific ceramides have been linked to plaque
buildup in the arteries and insulin resistance.
Elevated levels indicates a higher risk of cardiovascular
disease within one to five years.

21.  Cardiac natriuretic peptide is part of the neurohormonal system that participates
in cardiovascular homeostasis.
 Three natriuretic peptides – type A and B originate in cardiac myocyte and type C
originates in the endothelial and renal epithelial cells.

22.  BNP is a neurohormone that helps regulate BP and fluid volume.
 It is primarily secreted from the ventricles in the response to increased
preload with resulting elevated ventricular pressure.
 The level of BNP in the blood increases as the ventricular walls expand
from increased pressure.
 BNP can elevated in number of conditions like pulmonary embolus, MI
and ventricular hypertrophy.
 A BNP level greater than 100 pg/mL is suggestive of HF.

23.  Atrial myocardium secretes ANP when stretched.
 In response to high cardiac filling response specialized
myocytes in atria secretes ANP.
 ANP increases excretion of salt and water from renal tubules.
 It also has a small vasodilation effect.

24.  High- sensitivity assay for C- reactive protein is a venous blood test
that measures the level of CRP.
 A protein produced by the liver in response to systemic
inflammation.
 Inflammation play an important role in the development and
progression of atherosclerosis.
 People with high levels of CRP (3mg/dL) are having greater risk for
CVD.

25.  Homocysteine, an aminoacid, is linked to the development of atherosclerosis
because it can damage the endothelial lining of arteries and promote thrombus
formation.
 An elevated blood level of homocysteine indicate a high risk for CAD, stroke and
peripheral vascular disease.
 A 12 hr fast is necessary before drawing a blood sample for an accurate serum
measurement.
 Genetic factors and a diet low in folate, vit B6 and Vit B12 are associated with
elevated homocysteine level. Test results are interpreted as optimal (<12mcmol/L),
borderline(12 – 15mcmol/L) and high risk (> 15mcmol/L).

26. Interpretation
Optimal (<12mcmol/L)
Borderline(12 – 15mcmol/L)
High risk (> 15mcmol/L).

27.  This is an intracellular enzyme involved in amino acid metabolism.
 An increased level indicates necrosis or disease in the tissues.
 aspartate + alpha-ketoglutarate ↔ oxaloacetate + Glutamate.
 Concentration of the enzyme is very high in myocardium.
 In AMI, serum activity rises sharply within the first 12 hours, with
a peak level at 24 hours or over and return to normal within 3-5
days.

28. G-GTP catalyzes the transfer of the ϒ-glutamyl group from
one peptide to another peptide or to an amino acid.
increase in serum ϒ-glutamyl transpeptidase in acute
myocardial infarction.
The peak activity is between 7th and 11th day and lasts as
long as a month

29.  A small amount is found in human heart muscle.
 Serum enzyme activity rises within 6 hours of MI and persists
for whole of first week.
 It helps in early diagnosis of MI even when ECG failed to
reveal.
 The reference range : 0.12-0.76 PU/ml

30.  Cholinesterases are enzymes which hydrolyze esters of choline to give
choline and acid
Raised activity is found within 12 hours or even as early as 3 hours found
in some cases.
 A sensitive index for determination of cellular necrosis in myocardium.

31.  2 types:
1. True cholinesterase: It is responsible for destruction
of acetyl choline at the neuromuscular junction and is found
in nerve tissues and RB cells.
2. Pseudo cholinesterase: It is found in various
tissues such as heart muscle and liver.

32. 1. Sodium (135 – 145 mEq/L)
 Hyponatremia can be caused by heart failure and administration of
thiazide diuretics.

33.  It plays a major role in cardiac electrophysiologic function.
 Severe Hyperkalemia will slow cardiac impulse conduction, producing
changes in ECG, suppress conduction until cardiac arrest occurs. Heart
block , life threatening ventricular dysrhythmia , asystole occurs.
 Hypokalemia makes cardiac muscle irritable, increasing the risk of
premature atrial or ventricular contractions that can trigger ventricular
tachycardia, which can progress to fibrillation and death.
 Potassium level in cardiac patients are maintained above 4mEq/L

34.  Hypermagnesemia. causes impaired cardiac conduction and contractibility
produce bradycardia and hypotension and can progress to heart block and a full
cardiac arrest.
 Hypomagnesaemia increases cardiac muscle irritability and the potential for
atrial or ventricular dysrhythmias, especially in patients with a recent MI.
 This is especially important in patients recovering from an acute MI.

35.  It involved in contracting cardiac and smooth muscle, generating cardiac
impulses, mediating cardiac pacemaker function and forming bones and teeth.
 Hypocalcemia develop cardiac symptoms, including life threatening ventricular
dysrhythmias, heart failure.
 Hypercalcemia cardiovascular effects include hypertension and conduction
abnormalities that can progress varying degree of heart block and to cardiac
arrest.
 Hypercalcemia indicates digitalis toxicity.

36.  It helps to maintain electrical neutrality and act as an acid base
buffer.
Anion Gap (12mEq/L)
 The anion gap measures the normal balance between positive and
negative electrolytes in the serum.
 It describes the relationship between serum sodium (a cation) and
bicarbonate and chloride (anions). A normal anion gap is.
 Anion Gap = sodium + potassium – (bicarbonate + chloride) = 10 –
12 mEq/L

37. Serum osmolality reflects the osmotic property of the blood.
It determines the whether water excess or deficit occurs.
Serum osmolality = (2 x sodium) + (glucose / 18) + (BUN /1.8) =
280 – 300mOsm/kg.

38.  To assess renal function, although creatine is a more sensitive
measure.
 BUN reflects reduced renal perfusion from decreased cardiac output.
 Renal impairment is detected by an increase in elevated BUN and
creatinine.
BUN : 10- 20 mg/dL
Creatinine : 0.7 – 1.4 mg/dL.

39.  Routinely performed before cardiac catheterization, cardiac surgery and
electrophysiology studies.
 Partial Thromboplastin Time (PTT) and Activated partial Thromboplastin Time
(aPTT)
 Prothrombin time (PT)
 International Normalized Ratio
 Platelets
 Activated Coagulation Time
 Fibrinogen level
 Protein C and protein S

40.  PTT or aPTT measures the activity of the intrinsic pathway and is
used to assess the effects of unfractioned heparin.
 PTT measures deficiencies in all factors except factor VII and XIII
 aPTT measures all coagulation factors except platelet factor III,
factor XIII and factor VII.
 A therapeutic range is 1.5- 2.5 times baseline values.

41. Adjustment of heparin dose is required for aPTT<50 sec
(increase dose) or > 100s (decrease dose).
The blood is usually drawn 30 – 60 mts before the next
dose of heparin.
The PTT and aPTT are prolonged in heparin
administration, congenital clotting factor deficiencies,
cirrhosis of liver, Vit K deficiency, DIC and drugs like
Antihistamines, ascorbic acid, Chlorpromazine and
salicylates

42.  PT measures the extrinsic pathway activity
 It is used to monitor the level of anticoagulation with warfarin.
 Prothrombin is synthesized in liver.
Decreased PT
 Thrombophlebitis, MI and pulmonary embolus.
 Medications that reduce PT include digitalis, diuretics, diphenhydramine and
metaproterenol.

43. Prolonged PT
Heart failure, vit k deficiency , liver disease, bile duct
obstruction, DIC , massive blood transfusion, salicylate
intoxification and alcohol use.
 Drugs that prolong PT include some antibiotics,
allopurinol , cimetidine, warfarin, heparin, quinidine and
aspirin

44. It provides a standard method for reporting PT levels and
eliminate the variation of PT results from different
laboratories.
The INR rather than PT alone is used to monitor the
effectiveness of warfarin.
The therapeutic range of INR is 2 – 3.5.

45.  Platelets are first line protection against bleeding.
 Once activated by blood vessel wall injury or rupture of atherosclerotic
plaque, platelets undergo chemical changes that form a thrombus.
 Medication inhibit platelet function including aspirin, clopidogrel and
intravenous glycoprotein IIb/IIIa inhibitors, epitifitamide and
tirofiban.

46.  The time it takes whole blood to clot reflects the activity of the
intrinsic clotting mechanism.
 It is used during cardiac surgery and cardiac catheterization to
monitor heparinization.
 During extracorporeal heparin therapy , the ACT is kept at 4-6
times the baseline value.
 The use of ACT rather than aPTT to monitor heparin therapy in
patients with unstable angina or acute MI may result in much
steadier levels of anticoagulation and prevent ischemic recurrence

47.  Fibrinogen is a plasma protein synthesized by the liver.
 This test measures the conversion of fibrinogen to fibrin by thrombin.
 Elevated in acute infections, collagen disease, inflammatory disease and
hepatitis.
 Decreased levels are seen in severe liver disease, DIC, Leukemia, cardiac
surgery, fibrinolytic disorders and obstretric complications.
 Streptokinase therapy lower the fibrinogen level to < 100mg/dL, Urokinase
minimally decrease fibrinogen whereas tissue plasminogen activator
therapy doesnot reduce fibrinogen.

48.  Protein C with cofactor protein S, is a natural anticoagulant protein
whose function is to degrade activated factor V and VIII.
 Deficiency in either protein C or S can lead to a hypercoagulable state
that may cause venous thrombosis.
 Protein C is a vitamin K dependent and indirectly promotes fibrinolysis.
 Warfarin should be discontinued for atleast 10 days before testing for
protein c or protein S.
 The reference range is approximately 70 -140%

50.  The total number of white and red blood cells and platelets and measures
hemoglobin and hematocrit.
 It is important for evaluating the oxygen carrying capacity of the blood and the
response of the body to invasion by foreign cells such ad bacteria.
 RBC increase in congenital heart disease, severe COPD and polycythemia.

51.  The hematocrit represents the percentage of red blood cells found in
100 mL of whole blood.
 Low hematocrit and hemoglobin level have serious consequences for
patients with cardiovascular disease, such as more frequent angina
episodes or acute MI.
 Hematocrit : Male 42-52%, Female 35- 47%
 Hemoglobin: Male : 13-18g/dL, Female : 12 – 16g/dL

52.  Mean Corpuscular Volume (MCV) : Individual RBC cell size
MCV = Hematocrit (%) x 10 / RBC Count (Millions per mm3)
 Mean Corpuscular Hb : Amount of Hb present in a single cell
MCH = Hemoglobin (g/100mL) x 10 / RBC Count (Millions per mm3)
 Mean Corpuscular Hb Concentration ( MCHC) : The proportion of each cell
occupied by Hb
MCHC = Hemoglobin / Hematocrit

53.  5 types of WBC : neutrophils, eosinophils, basophils, monocytes and lymphocytes.
 Elevated WBC count in the patients with cardiac disease may be caused by MI, bacterial
endocarditis or Dressler syndrome.
 WBC counts are monitored in immunocompromised patients, including patients with heart
transplants, after invasive procedures etc.
 ESR measures the speed at which anticoagulated erythrocytes settle in a long narrow tube.
 Elevated in MI and bacterial endocarditis
 Usually low in heart failure.

54.  Frequently assessed in the patient with cardiac disease.
 Tissue oxygenation, carbondioxide removal and acid base status are
analyzed through the assay of arterial blood gases.
 ABG results guide treatment decisions in ventilated patients,
critically ill, nonventilated patients

55.  Alkaline phosphatase

56.  Alkaline phosphatase is an enzyme released in liver.
 Lipid lowering agents such as bile acid resins, HMG Co- A
reductase inhibitors (Statins) and nicotinic acid can alter alkaline
phosphatase along with liver enzymes.
 Alkaline phosphatase, Alanine aminotransferase(ALT), Aspartate
aminotransferase(AST) is typically measured before initiation of
lipid lowering therapy, every 6- 12 weeks at the start of therapy ,
every 6 – 12 weeks for the first year of therapy and then early 6
months throughout the treatment.

57. It is found predominantly in liver tissue.
The hepatocellular enzyme is released into the blood stream
when there is injury or disease affecting liver parenchyma

58.  It is located in the cell cytoplasm and in the mitochondria.
 The enzyme is widely distributed with high concentration in the
liver, Skeletal muscle, kidney, red blood cells and myocardium.
 AST is elevated with cardiac surgery, cardiac catheterization,
angioplasty, sever angina, acute pulmonary embolus, renal
infarction, acute pancreatitis, musculoskeletal diseases, trauma and
sternous exercises.

59. Epinephrine and norepinephrine are elevated in
pheochromocytoma.
 Pheochromocytoma is a cause of high blood pressure.

60.  Glucose is elevated in chronic renal failure, acute pancreatitis, acute MI, CHF,
extensive surgery and infections.
 Mild hyperglycemia can be expected whenever the patient is under stress.
 Glycated Hemoglobin / HbA1c / Glycosylated Hemoglobin : It provides an index
of a person’s average blood glucose concentration during 2- 3 month period.
 Glysated Serum Protein (GSP) : The degree of glysation of serum proteins
provides an index of glycemic control over a short period of time( 1-2 weeks)
than HbA1c.

61.  Albumin (53%)
 Globulin (15% α, 12% β and 20 % γ )
 Albumin (4 – 5.5 gm/dL) contributes to the balance of osmotic pressure
between blood and tissues. Albumin is reduced in Heart failure because of
hypervolemic dilution.
 Globulins (2 – 3gm/dL) influence osmotic pressure and include
immunoglobulins (antibodies). The α and β globulins tend to decrease with
abnormal liver function. The γ globulins, the body’s antibodies increase with
chronic diseases.

62. Drug Therapeutic Range Toxic level
Amiodarone 1-3.4 µg/mL
Digitoxin 15.g/mL >40 ng/mL
Digoxin 0.5 – 2 µg/mL >4 ng/mL
Diltiazem 100 – 200 ng/mL
Lidocaine 0.5 – 5 µg/mL > 6 µg/mL
Metoprolol 120 – 200 ng/mL
Nifedipine 50 – 100 ng/mL
Phenytoin 10 -20 µg/mL > 18 µg/mL
Procainamide 4. – 8 µg/mL > 10 µg/mL
Propranolol 30 -50 ng/mL
Quinidine 2.5 – 5 µg/mL > 6 µg/mL
Theophylline 10 -20 µg/mL > 20 µg/mL
Verapamil 50-400ng/mL

63.  The cardiac nurse should be aware of any actual or potential
problems related to hematologic abnormalities.
 Explain to patient the purpose of serial sampling (every 6- 8 hr x 3)
in conjunction with serial ECG.
 Myoglobin cleared from the circulation rapidly and most diagnostic
if measured within measured with first 12 hr of onset of chest pain.

64.  Cholesterol levels can be obtained in a non-fasting state, but for
triglyceride levels and lipoproteins, fasting state for at least 12 hr
(except for water) is necessary and no alcohol intake is allowed for
24hr before testing.
 Risk for cardiac disease is assessed by dividing the total cholesterol
level by the HDL level.
 Target values are <5 for men and 4.4 for women.
 Lp-PLA2 levels can be obtained in a non-fasting state.

65.  1. Role and importance of biochemical markers in clinical cardiology.
Mauro Panteghini, European Heart Journal .
 Biochemical markers play a pivotal role in the diagnosis and
management of patients with acute coronary syndrome (ACS), as
witnessed by the incorporation of cardiac troponins into new
international guidelines for patients with ACS and in the re-
definition of myocardial infarction.

66. Despite the success of cardiac troponins, there is still a need
for the development of early markers that can reliably rule
out ACS from the emergency room at presentation and also
detect myocardial ischemia in the absence of irreversible
myocyte injury. Under investigation are two classes of
indicators: markers of early injury/ischemia and markers of
inflammation and coronary plaque instability and
disruption. Finally, with the characterisation of the cardiac
natriuretic peptides, Laboratory Medicine is also assuming a
role in the assessment of cardiac function.

67. 2. Uric acid and cardiovascular risk considered : an update
Rouilope L, Cerezo C, European Society of cardiology.
 A relationship between hyperuricemia and CV disease has been
established since the 1900's. Increased uric acid serum levels are a
common finding in patients with high blood pressure, insulin resistance,
obesity and CV disease. Furthermore, uric acid as a CV risk factor has
been addressed in numerous prospective and cohort studies. In patients
with heart failure there is significant confirmation that elevated uric acid
levels predict an increase in morbidity and mortality both in acute and
chronic heart failure patients.

68.  Recent evidence has emerged in parallel suggesting uric acid is an
inflammatory factor that also plays a role in endothelial dysfunction.
Thus, uric acid can induce proinflammatory changes in the
adipocyte that are similar to those observed in the prediabetic
subject. Finally, most of these trials suggested that uric acid’s
cardiorenal effects are due to its intracellular effects, unlike gout
and stones.

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