1. The document provides an overview of red blood cells, including their history, functions, production, pathologies like polycythemia and anemia. 2. Red blood cells are biconcave disks that transport oxygen and carbon dioxide throughout the body. They are produced through erythropoiesis in the bone marrow. 3. Polycythemia is an excess of red blood cells and can be primary or secondary. Anemia is a low blood count and has numerous causes like iron deficiency, B12/folate deficiency, blood loss, or hemolytic disorders.

3. content
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History of RBC
Function
Shape and size
Concentration
Production
Pathologies- polycythemia
aneamia

4. 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.

5. FUNCTIONS

6. Shape and Size of Red Blood
Cells

7. Concentration of Red Blood Cells in
the Blood
Hb
RBC (SI unit)
USA UNIT
Males
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

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

9. PRODUCTION OF RED BLOOD
CELLS
IN EARLY WEEK OF EMBRYONIC LIFEDURING SECOND TRIMESTER OF
GESTATIONAFTER BIRTHAFTER 20 YEARS:-

10. GENESIS of Red Blood Cells
Stem cell
Proerythroblast
Early
erythroblast
Intermediate
erythroblast
Reticulocyte
RBC

11. 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

12. Clinical Manifestations

13. TREATMENT
Myelosuppresive drugs like hydroxyurea
can be used

14. SECONDARY POLYCYTHEMIA:
ERYTHROCYTOSIS
• increase in erythropoietin production to
compensate for hypoxia
• High altitudes
• Chronic pulmonary disease

15. APPARENT POLYCYTHEMIA
• increased hemoglobin concentration and
packed-cell volume
• normal RBC mass

17. 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

18. CLASSIFICATION OF
ANEAMIA

22. Common symptoms

23. 1: Clinical features:-
With dry mouth

24. What can be the cause??

25. Complete blood picture
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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.

26. diagnosis

27. DAILY REQUIREMENT OF IRON

29. 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.

30. Clinical features
- ATROPIC ORAL MUCOSA
- ATROPIC MUCOSA OF
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PHARYNX , UPPER
ESOPHAGUS.
SPASM IN THROAT
FOOD STICKING IN
THROAT
DYSPHAGIA

31. • 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.

32. treatment
• IRON THERAPY HELPS

33. HEMOLYTIC ANEAMIA
extracorpuscular
intracorpuscular

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

35. Clinical features
• pallor of nails bed, sclera , skin , soft palate
, tongue .
• Produces jaundice due to hyperbilirubineamia

36. Hemolysis due to:Paroxysmal nocturnal hemoglobinuria
defect 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

37. • Due to hemolysis hb can be reduced by 34g/dl
• Drugs that induce hemolysis should be
avoided such as dapsone,phenacetin.

38. c/f
Glossitis , Glossodynia
red beefy tongue
Dysphagia and taste change
Burning mouth
Dysphagia , taste aberrations

39. c/f

40. cause

41. Lab finding
macrocytic normochromic red cells
MCV increased
MCH increased
shape of the red cells varies
presence of megaloblastic marrow
changes
Schilling test is used

42. Causes of B12 deficiency
Inadequate
intake
Increased need
Malabsorption
B12 deficiency
Impaired
absorption
Gastrectomy
Lack of IF
Pernicious
anaemia
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43. treatment
administration of parenteral
cyanocobalamin
1000 μg/day for 1 week, then
1000 μg/week for 1 month, followed by
1000 μg/month for life

44. Clinical feature

46. Lab findings
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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

48. Treatment
5mg per day for 3 weeks
sufficient

49. c/f
Absent or hypoplastic thumb
Mental and sexual retardation

50. Causes of aplastic

51. Aplastic aneamia
• Caused by bone marrow
failure.
• Fanconi aneamia:IS INHERITED APLASTIC
ANEAMIA

56. 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.

57. • chipmunk facies.”
• Frontal bossing, maxillary
hypertrophy, depression of nasal bridge
, Malocclusion of teeth

58. PARAVERTEBRAL MASSES:
• Broad expansion of ribs at vertebral
attachment
PATHOLOGICAL FRACTURES:
• Cortical thinning
• Increased porosity of long bones
DELAYED PNEUMATISATION OF SINUSES

59. X ray skull:
“ hair on end”
appearance
or
“crew-cut”
appearance

60. • The skin color becomes ashen-gray due to the
combination of pallor, jaundice, and
hemosiderosis.
• Patients also present with
cardiomegaly, hepatomegaly, and
splenomegaly

61. 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.

62. References:-DAVIDSONS- GENERAL MEDICINE
20TH EDITION
-ABC OF CLINICAL HAEMATOLOGY2ND EDITION
-GUYTON – TEXT BOOK OF MEDICAL PHYSIOLOGY
11TH EDITION
-WILLIAMS HEAMATOLOGY- 7TH EDITION
-BURKETS – TEXT BOOK OF ORAL MEDICINE –
7TH EDITION

63. NEXT SEMINAR
• BY DR.CHINTAN SAVANI
PATHOPHYSIOLOGY OF WHITE BLOOD CELLS