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• History of RBC• Function• Shape and size• Concentration• Production• Pathologies- polycythemia• aneamia

RED BLOOD CELL

HISTORY:- Dutch biologist Jan Swammerdam in 1658 Anton van Leeuwenhoek in 1674 In 1901, Karl Landsteiner- BLOOD GROUP

The oldest intact red blood cells ever discovered were found in Ötzi the Iceman, a natural mummy of a man who died around 3255 BC. These cells were discovered in May 2012.

FUNCTIONS

Shape and Size of Red Blood Cells

Concentration of Red Blood Cells in the Blood

Hb RBC (SI unit) USA UNITMales 13-18g/dL (4.0-5.5)x 1012/L 4.0-5.2 x

106 /mm3

Females 11.5-16.5g/dL (3.5-5.0)x 1012/L 3.5-5.0x 106 /mm3

Neonates 17-20g/dL (6.0-7.0)x 1012/L 6.0-7.0 x 106 /mm3

Erythropoiesis is the process by which the origin, development and maturation of erythrocytes occur

PRODUCTION OF RED BLOOD CELLS

IN EARLY WEEK OF EMBRYONIC LIFE- DURING SECOND TRIMESTER OF GESTATION- AFTER BIRTH- AFTER 20 YEARS:-

GENESIS of Red Blood Cells

ProerythroblastStem cell Early

erythroblast

Intermediate erythroblast Reticulocyte RBC

POLYCYTHEMIA VERA-myeloproliferative disorder-excessive proliferation of erythroid elements-RBC 6 to 12 million/cubic mm with a hemoglobin concentration of 18 to 24 g/Dl-increased blood viscosity and thrombosis-clinical picture of ruddy cyanosis is seen on the face and extremities

Clinical Manifestations

TREATMENT

Myelosuppresive drugs like hydroxyurea can be used

SECONDARY POLYCYTHEMIA: ERYTHROCYTOSIS

• increase in erythropoietin production to compensate for hypoxia

• High altitudes• Chronic pulmonary disease

APPARENT POLYCYTHEMIA

• increased hemoglobin concentration and packed-cell volume

• normal RBC mass

ANEAMIA

decrease in the normal amount of circulating hemoglobin

Anemia may be defined as reduction of hemoglobin concentration per unit volume of blood below the lower limit of normal range for age & sex of the individual

CLASSIFICATION OF ANEAMIA

Common symptoms

With dry mouth

1: Clinical features:-

What can be the cause??

Complete blood picture• cells are microcytic and hypochromic• hemoglobin value is less • low serum iron concentrations • ferritin levels are markedly reduced.• high serum iron-binding capacity• absence of stainable iron in the bone marrow

• The physician must perform a thorough search for the source of bleeding, including using radiologic surveys of the gastrointestinal tract, sigmoidoscopy, a gynecologic examination, and a complete menstrual and dietary history.

diagnosis

DAILY REQUIREMENT OF IRON

treatment• -ferrous sulphate 200 mg three times daily• -Alternative preparations include ferrous

gluconate and ferrous fumarate.• -Iron sorbitol injection is a complex of iron, • -sorbitol and citric acid• 10-20 deep intramuscular injections are given

over two to three weeks.

Clinical features

- ATROPIC ORAL MUCOSA

- ATROPIC MUCOSA OF PHARYNX , UPPER ESOPHAGUS.

- SPASM IN THROAT

- FOOD STICKING IN THROAT

- DYSPHAGIA

• First described by Plummer and Vinson• Plummer-Vinson syndrome is potentially

serious because pharyngeal and intraoral carcinoma are more common in these patients.

• Patients with symptoms of this syndrome should be followed up at short intervals and checked for the development of lesions that raise the suspicion of malignancy.

treatment

• IRON THERAPY HELPS

HEMOLYTIC ANEAMIA

extracorpusc

ular

intracorpuscular

diagnosis• -decreased hemoglobin, increased reticulocytes.• Coombs test directLooks for immunoglobulin &/or complement of

surface of red blood cell (normally neither found on RBC surface)• Coombs reagent - combination of anti-human immunoglobulin & anti-human

complement• Mixed with patient’s red cells; if immunoglobulin or complement are on surface,

Coombs reagent will link cells together and cause agglutination of RBCs• INDIRECT coomb• Looks for anti-red blood cell antibodies in the patient’s serum, using a panel of

red cells with known surface antigens• Combine patient’s serum with cells from a panel of RBC’s with known antigens• Add Coombs’ reagent to this mixture• If anti-RBC antigens are in serum, agglutination occurs

Clinical features

• pallor of nails bed, sclera , skin , soft palate , tongue .

• Produces jaundice due to hyperbilirubineamia

Hemolysis due to:-

Paroxysmal nocturnal hemoglobinuriadefect is an acquired clonal stem cell disorder that results in abnormal sensitivity of the RBC membrane to lysis by complement.

Glucose 6 phosphate dehydrogenase deficiency

Lack of G6PD leads to hemolysis during oxidative stress

• Due to hemolysis hb can be reduced by 3-4g/dl

• Drugs that induce hemolysis should be avoided such as dapsone,phenacetin.

c/f

Glossitis , Glossodynia

red beefy tongue

Dysphagia and taste change

Burning mouth

Dysphagia , taste aberrations

c/f

cause

Lab finding

macrocytic normochromic red cells MCV increasedMCH increasedshape of the red cells variespresence of megaloblastic marrow changesSchilling test is used

Causes of B12 deficiency

42

B12 deficiency

Inadequate intake

Increased need

Impaired absorption

Lack of IF

Malabsorption

Gastrectomy

Perniciousanaemia

treatment

administration of parenteral cyanocobalamin1000 μg/day for 1 week, then 1000 μg/week for 1 month, followed by 1000 μg/month for life

Clinical feature

Lab findings

• low serum assays of folic acid• macrocytic normochromic red cells • MCV increased• MCH increased• shape of the red cells varies• presence of megaloblastic marrow changes

Treatment

5mg per day for 3 weeks sufficient

c/f

Absent or hypoplastic thumbMental and sexual retardation

Causes of aplastic

Aplastic aneamia

• Caused by bone marrow failure.

• Fanconi aneamia:- IS INHERITED APLASTIC ANEAMIA

Lab findings

• Sickle shaped cell• Hemoglobin electrophoresis is less expensive,

more accurate, and more definitive in the diagnosis of sickle cell disease as it detects hemoglobin S.

• chipmunk facies.”• Frontal bossing, maxillary hypertrophy,

depression of nasal bridge , Malocclusion of teeth

PARAVERTEBRAL MASSES:• Broad expansion of ribs at vertebral

attachmentPATHOLOGICAL FRACTURES:• Cortical thinning• Increased porosity of long bones DELAYED PNEUMATISATION OF SINUSES

X ray skull:

“ hair on end” appearance

or“crew-cut” appearance

• The skin color becomes ashen-gray due to the combination of pallor, jaundice, and hemosiderosis.

• Patients also present with cardiomegaly, hepatomegaly, and splenomegaly

Lab findings• Hemolytic anemia with hypochromic microcytic• red blood cells that vary in size and shape • increased amounts of fetal hemoglobin

• Prenatal diagnosis of thalassemia is facilitated by deoxyribonucleic acid(DNA) analysis of amniotic fluid cells, and it plays an important role in genetic counseling.

References:--DAVIDSONS- GENERAL MEDICINE 20TH EDITION-ABC OF CLINICAL HAEMATOLOGY- 2ND EDITION-GUYTON – TEXT BOOK OF MEDICAL PHYSIOLOGY 11TH EDITION-WILLIAMS HEAMATOLOGY- 7TH EDITION-BURKETS – TEXT BOOK OF ORAL MEDICINE – 7TH EDITION

NEXT SEMINAR

• BY DR.CHINTAN SAVANI

PATHOPHYSIOLOGY OF WHITE BLOOD CELLS