Saturday, August 21, 2010

Serum Bilirubin

Serum Bilirubin

Introduction

      Spectrophotometric determinations of serum bilirubin in clinical laboratory measures two pigment fractions: (1) The water soluble conjugated fraction that gives a direct reaction with diazo reagent and consist largely of conjugated bilirubin. (2) The lipid soluble indirect – reaction fraction that represents primarily unconjugated bilirubin.

Indications

Differential diagnosis of disease of hepatobiliary system and pancreas and other

Causes of jaundice.

 

Normal levels

Total bilirubin

Direct bilirubin

   0.1 – 1.2 mg/dL

  0.03 – 0.5 mg/dL

 

Increased in

Direct (conjugated) Bilirubin in

20 -40% of total: more suggestive of hepatic than posthepatic jaundice, 40 -60% of total: occur in either hepatic or posthepatic; > 50% of total: more suggestive of posthepatic than hepatic jaundice; total serum bilirubin > 40mg/dl indicates hepatocellular rather than extrahepatic obstruction.

Conditions

·        Hereditary disorders (e.g. Dubin Johnson syndrome, Rotor's syndrome)

·        Biliary duct obstruction (extra and intrahepatic)

·         Hepatic cellular damage (viral, toxic, alcohol/ drug related)

·        Infiltration, space – occupying lesions (e.g. metastatic tumor, abscess, granulomas)

  Increased unconjugated (indirect) bilirubin in

Increased bilirubin production; hemolytic diseases (e.g. hemoglobinopathies, RBC enzyme deficiencies, disseminated intravascular coagulation (DIC), autoimmune hemolysis); ineffective erythropoiesis; blood transfusions; hematomas; hereditary disorders (e.g. Gilbert's disease, Crigler – Najjar syndrome); drugs causing hemolysis.

Tuesday, August 17, 2010

Uric Acid

1.      Uric Acid

 

Introduction

Uric acid levels are very labile and show day to day and seasonal variation in same person, also increased by emotional stress, total fasting, increased body weight, uric acid levels that do not correlate with the severity of kidney damage; urea and Creatinine are better.

Indications

Monitor chemotherapeutic treatment of neoplasms to avoid renal urate deposition with possible renal failure; monitor treatment of gout.  

 

Normal Levels

           Males

            Females

         1 –3 years

    4.0 – 8.6 mg/dL

        3 – 5.9 mg/dL

         1. 8 -5

Increased in

Renal failure; gout and also in 25% of relatives of patients of gout; asymptomatic hyperuricemia; leukemia, multiple myeloma, malignancies, lymphoma and other disseminated neoplasm and cancer chemotherapy; hemolytic and sickle cell anemia; toxemia of pregnancy; psoriasis (1/3 cases); drug use (barbiturates, methyl alcohol, salicylates, thiazides, furosemide, mitomycin, levodopa, phenytoin sodium); metabolic acidosis; diet (high protein, weight reduced diet). 

 

Others von Gierke's disease, lead poisoning, Down's syndrome, polycystic kidney disease, atherosclerosis and hypertension (serum uric acid is increased in 80% of patients with elevated serum triglycerides).

Decreased in

Drugs (adrenocorticotropic hormone [ ACTH], high dose salicylates, probenecid, cortisone); Wilson's disease, Fanconi's syndrome, celiac disease, xanthuria

Creatinine

Creatinine

Introduction

Serum Creatinine is the most specific and sensitive indicator of renal disease. Use of BUN and Creatinine levels together is more informative in renal disorders.

      

Normal Range

    Male

        Female

         Fetal

  Pregnancy

 0.7 - 1.4 mg/dL

  0.6 – 1.1 mg/dL

   0.4 – 0.9 mg/dL

0.4 – 0.6 mg/dL

 

Indications

       Diagnosis of renal insufficiency

 

Increased in

Diet [ingestion of Creatinine (roast meat); prerenal azotemia; postrenal azotemia; impaired kidney function, 50% of renal function is needed to increase serum Creatinine from 1.0 – 2.0mg/dl. Therefore, not sensitive to mild – to moderate renal injury.

Decreased in

Pregnancy – normal value is 0.4 – 0.6 mg/dL. > 0.8mg/Dl is abnormal and should alert clinician to further diagnostic evaluation.

Blood Urea Nitrogen (BUN)

1.      Blood Urea Nitrogen (BUN)

 

Introduction

 

BUN correlates with uremic symptoms better than serum creatinine.

 

Normal Range

Adults: 7 –20mg/dL

Neonate: 5 –18 mg/dL

6 –8 mg/dL: associated with over hydration states

50 – 150mg/dL: implies serious impairment of renal function

150 –250mg/DL: is conclusive evidence of severely impaired glomerular function.

 

Indications

Differential diagnosis of various renal disorders; evidence of hemorrhage in Gl tract; assessment of patients requiring nutritional support in excess of catabolism (e.g. burns, cancer).

Increased in

Impaired kidney function; prerenal azotemia – ant case of reduced renal blood flow; congestive heart failure; salt and water depletion (vomiting, diarrhea, sweating); shock; postrenal azotemia – any obstruction of urinary tract (increased blood urea nitrogen [BUN] / Creatinine ratio); hemorrhage into Gl tract; AMI; stress.

Decreased in

Diuresis (e.g. with overhydration, often associated with low protein catabolism); severe liver damage (drug poisoning, hepatitis, other); increased utilization of protein for synthesis (late pregnancy, infancy, acromegaly, malnutrition ); diet (low protein and high carbohydrate, impaired absorption, malnutrition); nephritic syndrome; syndrome of inappropriate antidiuretic hormone secretion ( SIADH). 

Triglycerides (80% in VLDL 15% in LDL)

1.      Triglycerides (80% in VLDL 15% in LDL)

Introduction

Triglyceride levels are not strong predictors of atherosclerosis or CAD and may not be an independent risk factor. Triglyceride levels are inversely related to HDL cholesterol levels.

Normal Range

                                                 20 –170mg/dL

Classification

 

 

 

Normal Range

    Borderline

       High

  Very high

< 150mg/dL

  150 – 199mg/dL

 200 – 499mg/dL

> 500mg/dL

 

Increased in

Genetic hyperlipidemias (e.g. Lipoprotein lipase deficiency, apo C..II deficiency, familial Triglyceridemia, dysbetalipoproteinemia); secondary hyperlipidemias (gout, pancreatitis, acute illness (e.g. in AMI rises to peak in 3 weeks and increase may persist for 1 year); drug use (e.g. thiazides, steroids, amiodarone, interferon).

Decreased in

Abetalipoproteinemia; malnutrition; vigorous exercise; drugs (e.g. ascorbic acid, clofibrate, phenformin, metformin, progestins).  

LDL (Low Density Lipoprotein) cholesterol (Lipid Profile)

1.      LDL (Low Density Lipoprotein) cholesterol

Introduction

LDL levels are directly related to risk fill CAD

 

Indication

Assess risk and decide treatment for CAD

 

Normal Levels

 

      No coronary heart disease (CHD) and < 2 risk factors < 160mg/dL

 

No CHD but > 2 risk factors < 130mg/dL

 

Presence of CHD < 100mg/dL

Increased in

Familial hypercholesterolemia and combined hyperlipidemia; diabetes mellitus (DM) and hypothyroidism; chronic renal failure; diet high in cholesterol and total and saturated fat;

Pregnancy; cholesteryl ester storage disease; drug use (e.g. anabolic, steroids, beta – blockers, progestins, carbamazepine).

Decreased in

Severe illness; abetalipoproteinemia; some laboratories also various ratios; total cholestero/HDL ratio – low risk: 3.3 – 4.4, average risk: 4.4 – 7.1, moderate risk: 7.1 – 11.0, high risk > 11.0.

High Density Lipoprotein (HDL) Cholesterol (Lipid Profile)

1.      High Density Lipoprotein (HDL) Cholesterol

Introduction

Levels of HDL are inversely related to risk of CAD. For every mg/dL decreased in HDL, risk of CAD increase by 2 -3%

 

Indications

Assessment of risk of CAD

 

Diagnosis of various lipoproteinemia

 

Normal Levels

          Men

         Women

   > 40mg/dL

  > 50mg/dL

 

Increased in (60mg/Dl is negative risk factor for CAD)

 

Vigorous exercise; moderate consumption of alcohol; Increased clearance of triglyceride (VLDL), Familial lipid disorders with protection against atherosclerosis (illustrates importance of measuring HDL to evaluate hypercholesterolemia); 1 in 20 adults with mild increased total cholesterol levels (240 – 300mg/dL) secondary to increased HDL ( > 70mg/dL); Hypobetalipoproteinemia.

 

Decreased in (< 32mg/dL in men, < 38mg/dL in women)

Stress and recent illness (e.g. acute myocardial infarction [AMI], stroke, surgery, trauma); starvation, non fasting sample; obesity and lack of exercise; cigarette smoking; DM, hypo – and hyper – thyroidism; acute and chronic liver disease; genetic disorders; familial hypoalphalipoproteinemia.

Total Serum Cholesterol (Lipid Profile)

ToTotal Serum Cholesterol

Indications

Monitoring for increased risk factor for coronary artery disease(CAD); Screening for primary and secondary hyperlipidemias; Monitoring of treatment for hyperlipidemias.

 

Normal range

Adults: 130 –20mg/dL

Fetal: 32 – 76mg/dL

Increased in

Hyperlipoproteinemias; cholesteryl  ester storage disease; biliary obstruction (stone, carcinoma, cirrhosis); von Gierke's disease; hypothyroidism; nephrosis (due to chronic nephritis, amyloidosis, renal vein thrombosis, systemic lupus erythematosus [ SLE]; Pancreatic disease, diabetes mellitus.

Decreased in

Severe liver cell damage (due to chemicals, drugs, hepatitis); hyperthyroidism; malnutrition; infection and inflammation; drugs.

Oral Glucose Tolerance Test (OGTT)

Oral Glucose Tolerance Test (OGTT)

      Introduction

OGTT is done after overnight fasting for 10 –16 hrs. Certain drugs should be stopped several weeks before the test (e.g. oral diuretics, 0.Cs phenytoin). Loading dose of glucose [adults = 75gms, for children 1.75gm/kg (of ideal body weight in obese children but never > 75gms). Pregnancy = 100gms] is consumed in 5 mins. Blood sample drawn at fasting, 30, 60, 90, 120 mins.

Indications

OGTT should be reserved principally for patients with '' borderline'' fasting plasma glucose levels ( i.e. fasting range 110 – 140 mg/dL).

All pregnant women should be tested for gestational diabetes with a 50gms dose at 24 – 28 weeks of pregnancy; if result abnormal, OGTT should be performed after pregnancy.

Increased tolerance in 

Pancreatic is let cell hyperplasia or tumor, poor absorption from gastrointestinal (Gl) tract in intestinal disease (e.g. steatorrhea, sprue, colic disease), hypothyroidism Addison's disease, liver disease, hypopituitarism.

 Decreased tolerance in   

Diabetes mellitus- For diagnosis of diabetes in nonpregnant adults, at least two values of OGTT should be increased (or fasting serum glucose > 140mg/dL on more than one occasion and other causes of transient glucose intolerance must be ruled out.

                Other causes of decreased tolerance are hyperthyroidism, hyperlipidemia, steroid effect, Cushing's effect, administration of adrenocorticotropic hormone (ACTH) or steroids, pregnancy.

Drugs like indomethacin, various neuroactive drugs (phenothiazines, tricyclics, lithium, haloperidol), heparin.

Blood Glucose

Blood Glucose

Indications

Diagnosis of diabetes mellitus [defined by World Health Organization (WHO) as unequivocal increase of fasting serum (or plasma) glucose > 126 mg/dl on more than one occasion or any glucose level  > 200mg/dL]; Control of Diabetes Mellitus; Diagnosis of hyperglycemia. 

     

Normal Range

       Fasting

       Post prandial (2hrs)

       

  60 – 100mg/dL

      < 140 mg/dL

     

      Higher levels seen in

Diabetes Mellitus including: hemochromatosis, Cushing's syndrome; acromegaly and gigantism, Increased circulating epinephrine due to – adrenaline injection, pheochromocytoma, stress, acute and chronic pancreatitis, effect of drugs like (corticosteroids, estrogens, alcohol, phenytoin, thiazides.)

Lower levels seen in

Pancreatic disorders (e.g. Islet cell tumor, Pancreatitis, glucagons deficiency); extrapancreatic tumors (e.g. carcinoma of adrenal gland and stomach, fibrosarcoma); hepatic disease (e.g. hepatitis, poisoning, cirrhosis, primary or metastatic tumor); endocrine disorders (hypopituitarism, Addison's disease, hypothyroidism); functional disturbances (e.g. postgastrectomy, gastroenterostomy, autonomic nervous system disorders); pediatric anomalies (e.g. prematurity, infant of diabetic mother); enzyme disease (e.g. von Gierke's disease, galactosemia, fructose intolerance others like malnutrition, alcoholism, exogenous, insulin or oral hypoglycemics).  

Activated Partial Thromboplastin Time(aPTT)

Activated Partial Thromboplastin Time(aPTT)

 

Introduction

aPTT is the best screening test for disorders of coagulation; it is abnormal in 90% of patients with coagulation disorders. Screens for all coagulation factors that contribute to thrombin except factor VII and XII. The test may not detect mild clotting defects which seldom cause significant bleeding.

 

Normal range

25 – 38 seconds

Indications and Interpretation

Monitor heparin therapy; Screen for hemophilia A and B,

Prolonged by

Defect in following factors: I, II, V, VIII, IX, X, XI, XII; Presence of specific inhibitors of clotting factors (most frequently antibody against factor VIII, in 15% of patients with hemophilia); heparin, warfarin and lupus anticoagulant.

Normal in

 Thrombocytopenia, Platelet dysfunction, Von Willebrand's disease, isolated defects of factor VII.

Prothrombin Time(PT)

Prothrombin Time(PT)

Normal range

      11 –16 seconds

      Indication

Control of long – term oral anticoagulant therapy with coumarins and indanedione derivatives; evaluation of liver functions( PT is the most useful test of impaired liver synthesis of prothrombin complex factors[ factor II, VII, IX, Protein C & S]; evaluation of coagulation disorders- screen for abnormality of factors involved in extrinsic pathway (factor V, VII, IX, Prothrombin, fibrinogen). Should be used with a PTT.

Prolonged by defect in

Factor I, II, V, VII and X

Prolonged in

In adequate vitamin K in diet, premature infants, newborns of vitamin K deficient mothers, poor fat absorption (obstructive jaundice, colitis, steatorrhea), severe liver damage (hepatitis, poisoning), anticoagulant drugs, familial hypoprothrombinemia. 

Coagulation Time/ Clotting Time (CT)

Coagulation Time/ Clotting Time (CT)

Normal range

 6 –17 minutes (glass tube),

Indications and Interpretations         

Former routine method for control of heparin therapy but now replaced by a partial thromboplastin time(PTT) as it is not a reliable screening test for bleeding conditions because it is not sensitive enough to detect mild conditions but only detects severe ones; normal coagulation time does not rule out a coagulation defect; routine preoperative bleeding and coagulation time are of  little value for preoperative screening.

Prolonged in

Severe deficiency (< 6%) or any known plasma clotting factors except factor XII and factor VII, afibrinogenemia and presence of circulating anticoagulant (including heparin).

Normal in

Thrombocytopenia, deficiency of factor VII, von Willebrand's disease, and mild coagulation defects due to any causes.

Bleeding Time (BT)

Bleeding Time (BT)

 

Normal Range

3 – 9.5 minutes

Indications and Interpretations         

·        BT is functional test of primary hemostasis

·        BT is single screening test for platelet functional or structural disorders, acquired (e.g. uremia) or congenital

·        Normal BT without suggestive history usually excludes platelet dysfunction. However, a normal BT does not rule out significant defect; with clinical suspicion platelet aggregation should be performed

·        To work up for coagulation disorders in patients, having history of excess bleeding even with normal platelet count.

·        Normal in all other disorders of coagulation except von Willebrand's disease deficiency and some cases of very low plasma fibrinogen.

·        May be useful to monitor treatment of active hemorrhage in patients with prolonged BT due to uremia, Von Willebrand's disease, congenital platelet function abnormalities or severe anemia.

·        No value in performing BT if platelet count < 100,000/cumm as BT is usually prolonged. Prolonged BT with platelet count > 100, 000/cumm usually indicates impaired platelet function (e.g. due to aspirin) or von Willebrand's disease.   

·        Even with a prolonged BT, blood loss does not exceed that of patients with normal BT. Prolonged BT does not necessarily cause increased bleeding.

·        BT increased out of proportion to platelet count suggests von Willebrand's disease or qualitative platelet defect.

Usually prolonged in 

Thrombocytopenia: Platelet count < 100,00/cumm and usually < 80,000/cumm before BT becomes abnormal and < 40,000/cumm before abnormality becomes pronounced.


Platelet function disorders

Hereditary: Von Willebrand's disease, deficient release of platelet glycoproteins, gray platelet syndrome, hereditary hemorrhagic telangiectasia

Acquired: Drugs (aspirin, non- steroidal anti-inflammatory drugs [ NSAIDs], antimicrobials, anticoagulants, anesthetic, calcium channel blockers, β – blockers, phenothiazine, antidepressants), uremia, fibrin degradation products (e.g. disseminated intravascular coagulation [DIC], liver disease, fibrinolytic therapy, immune thrombocytopenias, myeloproliferative disease, vascular disorders, amyloidosis, viral infections, scurvy.

Usually normal in

Hemophilia, severe hereditary hypoprothrombinemia or hypofibrinogenemia.

Erythrocyte Sedimentation Rate (ESR)

Erythrocyte Sedimentation Rate (ESR)

Introduction

ESR is the rate at which RBC's settle down when blood, to which anticoagulant is added, is allowed to stand in a narrow tube for one hour expressed in millimeters of clear plasma at the end of 1st hour. Sedimentation rate depends on various factors like; rouleaux formation (Rouleaux formation is directly proportional to concentration of fibrinogen and globulin in plasma. It is retarded by albumin); viscosity of plasma (ESR decreases if viscosity increases); ratio of cells to plasma (decreased ratio leads to increase Rouleaux formation); nature of anticoagulant used.

 

 

                                      Normal Range (mm in 1 hr)

        Westergren

                       Wintrobe's            

 Males

   Females

 Males

Females

 Children

Newborns

 0 –13

    0 –20

  0 –10

 0 -15

 0 – 13

0 -2

 

Increased in

Tissue damage or inflammation, anemia, any toxic or infective condition (acut or chronic), malignancies, nephrosis, physiological increase in females, pregnancy increase in temperature.

            Decreased in

Polycythemia, leukemia, hypofibrinogenemia, pernicious anemia, congestive heart failure (CHF), Protein shock (e.g. burns, severe allergic reactions), physiological decrease in newborns, decrease in temperature.

Reticulocyte Count (RC)

Reticulocyte Count (RC)

Introduction

The reticulocyte count is a fairly accurate reflection of erythropoietic activity therefore their number increases whenever red blood cells (RBCs) are being rapidly manufactured.

Normal Range

Adults: 0.5 – 1.85 % of erythrocytes, absolute count – 29,000 – 87, 000/cu.mm.

Newborn: 2.5 – 6.5 %, falls to adult range by second week of life.

Indications

·        Diagnosis of inffective erythropoiesis or decreased RBC formation

·        Increase indicates effective RBC production used as: Index of therapeutic response to iron, folate or vitamin B12 therapy and blood loss; monitor treatment response after bone marrow suppression and transplantation; monitor response to erythropoietin therapy.

Increased in

 After blood loss or increased RBC destruction, after iron therapy, after specific therapy for megaloblastic anemia and other hematologic conditions like polycythemia, metastatic carcinoma in bone marrow.

 Decreased in   

Ineffective erythropoiesis or decreased RBC formation (severe autoimmune type  of hemolytic disease, megaloblastic disorders), alcoholism, myxedema.

Wednesday, August 11, 2010

Abnormally shaped RBCs Spiculated

Abnormally shaped RBCs

Spiculated –
Acanthocytes (abetalipoproteinemia, post – splenectomy, fulminating liver disease); Burr cells (stomach cancer, GI bleeding, uremia); Bite cells (hemolysis due to drugs); RBC fragmentation (cytotoxic chemotherapy, autoimmune hemolytic anemia, deficiency anemias, acute leukemia, inherited structural abnormality of RBC membrane protein spectrin).

Abnormally shaped RBCs Elongated

Abnormally shaped RBCs
Elongated –
Elliptocytes (hereditary, microcytic anemia); ovalocytes (megaloblastic anemia); teardrop cells (spent polycythemia. myelofibrosis. Thalassemia); Sickle cells (sickle cell disorders); HbC crystalloids (HbC trait or disease). Acute alcoholism); Target cells (HbC disease or trait, HbD, HbE, HbS, thalassemia, iron deficiency anemia, liver disease, post – splenectomy).

Abnormally shaped RBCs Round

Abnormally shaped RBCs

Round – Macrocytes (increased erythropoiesis); round macrocytes (liver disease, hypothyroidism, alcoholism); macro – ovalocytes (megaloblastic anemia, cancer chemotherapy, myelodysplastic syndromes); microcytes (hypochromic anemias), spherocytes (hereditary spherocytosis, recent blood transfusion); stomatocytes (hereditary stomatocytosis, acute alcoholism); target cells (HBC disease or trait, HbD, HbE, HbS, thalassemia, iron deficiency anemia, liver disease, post splenectomy).

Peripheral Blood Smear (PS)

Peripheral Blood Smear(PS) - RBCs

Indications

Peripheral smear is done for typing anemia, to confirm red blood cells (RBC) indices or indicate leukemia or other conditions,


RBC inclusions

Basophilic or polychromatophilic macrocytes ( < 15 in healthy persons, increased in erythropoiesis due to hemorrhage or hemolysis); microcytes with stippling (thalassemia, lead poisoning); Cabot's rings (severe hemolytic anemias, pernicious anemia [ PA]); Howell – Jolly bodies(megaloblastic anemia, thalassemia, hyposplenism, splenectomy); Pappenheimer bodies (Sideroblastic anemia, thalassemia, lead poisoning, pyridoxine unresponsive or responsive anemias); Heinz bodies (congenital G – 6 PD deficiency, drug induced hemolytic anemias); Plasmodium trophozoites(malaria); reticulocyte.

Thrombocytopenia (Decreased Platelet Count )

Thrombocytopenia in

Bone marrow depression, hypersplenism, viral infections (especially in dengue fever), drug hypersensitivity, antiplatelet antibodies (lgG and lgM), increased platelet consumption in thrombotic thrombocytopenia (TTP), disseminated intravascular coagulation (DIC) and septicemia.

Thrombocytosis (Increased Platelet Count )

Thrombocytosis in

After administration of epinephrine due to splenic contraction or after splenectomy, trauma (e.g. surgery, injury, childbirth) and stress.

Platelet Count (PC)

 Platelet Count (PC)

 

Normal Range

1,50,000 – 3, 50,000/cu.mm.

Causes of eosinophilia (> 250/cu.mm. diurnal variation with highest levels in morning)

Causes of eosinophilia (> 250/cu.mm. diurnal variation with highest levels in morning)

Allergic diseases (bronchial asthma, hay fever, urticaria, allergic rhinitis);

Parasitic infestations, mycoses, scarlet lever, erythema multiforme systemic lupus erythematous, rheumatoid arthritis, skin diseases (e.g.pemphigus).

Causes of monocytosis ( > 10% of differential absolute count > 500/cu.mm.)

Causes of monocytosis ( > 10% of differential absolute count  > 500/cu.mm.)

Monocytic leukemia, other myeloproliferative disorders, lymphomas, lipid storage diseases, post splenectomy, protozoal and some rickettsial infections, SBE, tuberculosis, brucellosis sarcoidosis, rheumatoid arthritis, systemic lupus erythematosus(SLE).

Causes of basopenia

Causes of basopenia

Hyperthyroidism, pregnancy, irradiation, chemotherapy, glucocorticoid administration, acute phase of infection.

Basophilia (50/cumm or > 1%)

Basophilia (50/cumm or > 1%)

May be first sign of blast crisis or accelerated phase of chronic myelocytic leukemia (CML).

Persistent basophilia may indicate unsuspected myeloproliferative disease.

Causes

Chronic myelogenous leukemia, basophilic leukemia, polycythemia, myeloid metaplasia, Hodgkin's disease, chronic sinusitis and hemolytic anemia.

Causes of lymphocytopenia (Decreased Lymphocytes) (< 1500 in adults, < 3000 in children)

Causes of lymphocytopenia (< 1500 in adults, < 3000 in children)

Increased destruction (chemotherapy or radiation treatment, corticosteroids), 
increased loss via Gl tract (thoracic duct drainage obstruction to intestinal lymphatic duct drainage), 
congestive heart failure, 
decreased production (aplastic anemia, malignancy, AlDS).

Causes of lymphocytosis (Increased Lymphocytes) (> 4000/cumm in adults, > 7200/cumm adolescents, > 9000/cumm in children and infants)

Causes of lymphocytosis (> 4000/cumm in adults, > 7200/cumm adolescents, > 9000/cumm in children and infants)

Infection (Pertusis, infectious, lymphocytosis, infectious hepatitis, cytomegalovirus (CMV) infections, mumps, rubella, varicella, toxoplasmosis, chronic tuberculosis), 

Others like 

thyrotoxicosis,

Addison's disease, 

neutropenia with relative lymphocytosis, 

lymphatic leukemia, 

Crohn's disease, 

ulcerative colitis and 

infancy (normal count 40- 60 %) called relative lymphocytosis.

Causes of Neutropenia (Decreased Neutrophil) (Absolute count < 8000/ cu.mm.)

Causes of Neutropenia (Absolute count < 8000/ cu.mm.)

·        Infections: bacterial (e.g. overwhelming infection, septicemia, typhoid, paratyphoid) viral infections (infectious mononucleosis, hepatitis, influenza, measles, rubella), rickettsia, others (malaria, kala- azar).

·        Infants (normal count 40%).

·        Hodgkin's disease, chronic sinusitis, hemolytic anemia and lonizing radiation

·        Drugs & chemical (antibiotics, analgesics, antithyroids, arsenicals and ionizing radiation

·        Hematopoietic diseases (aleukemic leukemia, aplastic anemia) and splenic sequestration.

·        Autoimmune and isoimmune neotropenias.

·        Immune defects like infertile genetic agranulocytosis.

Causes of Neutrophilia (Increased Neutrophil) (Absolute count > 8000/ cu.mm.)

Causes of Neutrophilia (Absolute count > 8000/ cu.mm.)  

·        Acute infections:

·        Localized (e.g. Pneumonia, meningitis, tonsillitis).

·        Generalized (e.g. acute rheumatic fever, septicemia, cholera).

·        Inflammation (e.g. vasculitis).

·        Intoxications: metabolic (e.g. acidosis, uremia, acute gout); Poisonings (e.g. mercury, epinephrine, black widow spider bite).

·        Acute hemorrhage or hemolysis of red blood cells.

·        Tissue necrosis (e.g. acute myocardial infarction [AMI], burns, gangrene).

·        Physiological (e.g. exercise, Stress, obstetric labor, menstrution).

Tuesday, August 10, 2010

Differential leukocyte Count (DLC)

Differential leukocyte Count (DLC)
                                               Normal Range
Granulocytes
    Percentage
Agranulocytes
   Percentage
Neutrophils
    54-62 %
 Lymphocytes
    20- 40 %
Eosinophils
     1-4 %
 Monocytes
     3-7 %
Basophils
     < 1 %




Indications
 Support diagnosis of various infections and inflammation; 
diagnosis of myeloproliferative disorders;
neutrophil and band counts may be useful in acute appendicitis and 
neonatal sepsis with moderate sensitivity and specificity

TLC Decreased

Leukopenia in
Some bacterial infections (e.g. typhoid), 
viral or protozoal infection, 
bone marrow depression and 
starvation and 
physiological at night. 

TLC Increased

Leukocytosis in

Any acute/ chronic pyogenic or pyogenic (fever producing) infection, 
leukemias, 
physiological in newborns, 
after exercise, 
in evenings, 
epinephrine injection, 
stress, 
pregnancy, 
menstruation, 
lactation, 
administration of steroids. 

Total leukocyte Count (TLC) Normal Range

Total leukocyte Count (TLC)

Normal Range (leucocytes/cumm)
       Adults
       New born
        1-23 months
4000 – 10,500
9100 – 34,000
6000 – 14,000

Mean Corpuscular Hemoglobin Concentration (MCHC)

Mean Corpuscular Hemoglobin Concentration (MCHC)

Introduction
      MCHC is calculated as Hb divided by Hct.
      
      Normal Range
      32-38 %

      Indications
For laboratory quality control, chiefly because changes occur very late in the course of iron deficiency when anemia is severe and for instrument calibration.

Increased in
Hereditary spherocytosis (MCHC is > 36 gm/dL), infants and newborns, other causes due to automated cell counters are hemolysis, cold agglutinins, lipemia, rouleaux or RBC agglutinates.

Decreased in
Hypochromic anemia (Low MCHC may not occur in iron deficiency anemia when measured with automated instruments), marked leukocytosis (automated cell counter).

Wednesday, August 4, 2010

Mean Corpuscular Hemoglobin (MCH)

Mean Corpuscular Hemoglobin (MCH)

Introduction

MCH is calculated as Hb divided by total RBC count.

Normal range

            Adults – 27-31Pg
            New born – 33- 39Pg

Indications

Limited value in differential diagnosis of anemias; Used for instrument calibration.

Increased in

Macrocytic anemia, infants and newborns, marked leukocytosis( > 50,000/cu.mm),cold agglutinins, in vivo hemolysis, monoclonal proteins in blood, high heparin concentration, lipemia.

Decreased in

Microcytic and normocytic anemias.

Causes of lymphocytosis (> 4000/cumm in adults, > 7200/cumm adolescents, > 9000/cumm in children and infants)

Causes of lymphocytosis (> 4000/cumm in adults, > 7200/cumm adolescents, > 9000/cumm in children and infants)

Infection (Pertusis, infectious, lymphocytosis, infectious hepatitis, cytomegalovirus (CMV) infections, mumps, rubella, varicella, toxoplasmosis, chronic tuberculosis), 

Others like thyrotoxicosis, 

Addison's disease,

neutropenia with relative lymphocytosis, 

lymphatic leukemia, 

Crohn's disease, 

ulcerative colitis and 

infancy (normal count 40- 60 %) called relative lymphocytosis.

Sunday, August 1, 2010

Mean Corpuscular Volume (MCV)

Mean Corpuscular Volume (MCV)

Introduction
MCV is calculated as hematocrit (Hct) divided by RBC count with manual methods measured directly by automated instruments.
 
Normal range
Adults – 78-100Fl
Neonates- 102-115Fl.

Indications
Classification and differential diagnosis of anemia; useful screening test for occult alcoholism

Increased in (MCV > 95fL, Often > 110Fl)
All macrocytic anemias (megaloblastic anemias, Vit. B12’ folate deficiency, sprue, macrocytic anemia of pregnancy, megaloblastic anemia due to alcoholism, liver disease and hypothyroidism), infants and newborns.
 
Decrease in (MCV < 80FL)
Microcytic anemias
Usually hypo chromic (e.g. iron deficiency, pyridoxine – responsive thalassemia,   lead poisoning), chronic disease, abnormal HbC and HbE.