Haemopoetic system

Haemopoetic system – By Prof.Dr.R.R.Deshpande
Uploaded on 24 June 17
This PPT is a part of First BAMS .Syllabus of Sharir Kriya .Paper 2 & Part B. Point 1 . Haemopoetic system
.This PPT contains ---
Composition & functions of blood & blood cells ,Haemopoiesis (stages & development of RBCs, & WBCs & platelets) , composition & functions of bone marrow ,structure , types & functions of haemoglobin , mechanism of blood clotting , anticoagulants , physiological basis of blood groups , plasma proteins , introduction to Anaemia & jaundice .
Mobile – 922 68 10 630
Web site – www.ayurvedicfriend.com

1. Haemopoetic System
•Presented By –
Prof.Dr.R.R.Deshpande
(M.D in Ayurvdic
Medicine & M.D. in
Ayurvedic Physiology)
•www.ayurvedicfriend.co
m
•Mobile – 922 68 10 630
•professordeshpande@
gmail.com
6/24/2017 Prof.Dr.R.R.Deshpande 1

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Sharir Kriya -- Paper 2 –
Part B –Point 1
•Presented By –
•Prof.Dr.R.R.Deshpande (M.D in Ayurvdic
Medicine & M.D. in Ayurvedic Physiology)
•www.ayurvedicfriend.com
•Mobile – 922 68 10 630
•[email protected]

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Sharir Kriya Text Books

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Sharir Kriya Hand Book –
1
st
to last year BAMS
•Best for Fast Revision
•Paper 1,Paper 2
•Practicals
•Instruments
•Histology
•IMP Schlok
•All basics of
Dodha,Dhatu & Mala

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Sharikriya Paper Practical Book
•As per Very New
Syllabus formed By
CCIM IN 2012
•Ayurvedic Practicals
like Prakruti,sara,Agni
•Modern
Haematological
Practicals
•CNS & CVS
Examination

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Clinical Examination
•Systemic Examination
of 8 systems
•Ayurvedic Srotas
Examination
•Clinical significance of
Lab Tests &
Radiology,USG,2D
Echo

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Sharir Kriya Paper 1
•Book in English
•Total CCIM Syllabus
covered
•Chaukhamba Sanskrit
Pratisthan Publication
•Popular Nationwide &
In Germany also
•Dosha & Prakruti

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Sharir Kriya Paper 2
•Book in English
•Total CCIM Syllabus
covered
•Chaukhamba Sanskrit
Pratisthan Publication
•Popular Nationwide &
In Germany also
•Dhatu,Mala

9. 6/24/2017 Prof.Dr.R.R.Deshpande 9
Prof.Dr.Deshpande’s
Popular Links on Internet
•Just Start Internet on Desk top or Lap top
or on your mobile . Copy Following Link &
Paste as Web address –URL
•http://www.youtube.com/user/deshpande1
959
•http://www.slideshare.net/rajendra9a/
•http://www.mixcloud.com/jamdadey/
6/24/2017 Prof.Dr.R.R.Deshpande 9

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Prof.Dr.Deshpande’s
Popular Links on Internet
•Just Start Internet on Desk top or Lap top
or on your mobile . Copy Following Link &
Paste as Web address –URL
•http://professordeshpande.blogspot.in
•http://professordrdeshpande.blogspot.in/
•http://www.mixcloud.com/rajendra-
deshpande
•https://soundcloud.com/professor-
deshpande
6/24/2017 Prof.Dr.R.R.Deshpande 10

11. Contents of this PPT
•Composition & functions of blood & blood
cells
•Haemopoiesis (stages & development of
RBCs, & WBCs & platelets)
•Composition & functions of bone marrow
•Structure , types & functions of
Haemoglobin
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of.Dr.R.R.Deshpande
11

12. Contents of this PPT
•Mechanism of blood clotting
•Anticoagulants
•Physiological basis of blood groups
•
•Plasma proteins
•Introduction to Anaemia & jaundice
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Blood
•Definition - The red body fluid that flows through
all the vessels, except the lymph vessel is called
blood
• Blood is a viscous fluid. It is thicker than water
• Blood may be described as a tissue, in which
there is intercellular substance, known as
plasma & formed elements, the R.B.C.s,
W.B.C.s & platelets, suspended in the plasma.

14. Haemopoesis
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15. Blood cells
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1) Red blood corpuscles (Erythrocytes)
•Mature RBC is a circular,
biconcave, non - nucleated disc.
•The edges are rounded & thicker
than the centre (Hence, central
portion appears to have a lighter
shade)

17. 1) Red blood corpuscles (Erythrocytes)
•Under the microscope a single red
cell seems to have a light brown /
yellowish colour
•But when seen in bulk, R. B. C.s
appear to be red
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Composition of R. B. C.
•i) Water - 60 - 70 %
•ii) Solid - 30 - 40 % - Haemoglobin (29 %)
•Other proteins (1 %)
•Diameter of R. B. C. - varies form 5.5 to
8.8 microns.
•Mean diameter of R. B. C. - 7.2 microns.

19. RBC - Morphology
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Important
•1) The small size & the great number
of red cells are having significance,
because ---
•This makes available surface area
very large & thus facilitates rapid
exchange of gases & other materials
between the cells & the plasma.

21. Important
•2) The absence of nucleus is
also beneficial –
• Because it gives biconcave
shape & also makes room for
more haemoglobin
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Development of R. B. C.s
•i) In the embryo
•Develop form the area vasculosa of the yolk sac.
At first the cells are nucleated. From the middle
of the foetal life the nucleated cells disappear
form the peripheral circulation.
•ii) From the middle foetal life to about a
month before birth
•The liver & spleen are the main sites of R. B. C.
formation

23. Erythropoesis
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24. Site of Erythropoesis
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Development of R. B. C.s
•iii) After birth
•The bone marrow is the main site of
erythrogenesis.
•At first all bones take part but by 20th
year almost all the long bones
become filled up with inactive yellow
marrow & stop R. B. C. formation.

26. Development of R. B. C.s
•Only the & continue to form R. upper ends
of femur & humerus contain red marrow
B.C.s.
•The vertebrae, the ribs & the flat bones
produce R.B.C. throughout the life.
•Span of life - The average span is 120
days in man.
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Bone Marrow
•Bone marrow is the flexible
tissue, found inside the bones
• Haemopoesis process takes
place in the bone marrow

28. Bone Marrow
•Bone marrow is also important as a
part of lymphatic system, by
producing lymphocytes
•Lymphocytes , support immune
system
•Bone marrow occupies 4% of total
body mass
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29. Bone Marrow
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Types of bone marrow
•1) Red bone marrow - which
consist of Haemopoetic tissue
•2) Yellow bone marrow - this is
made up of flat cells

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Red Bone Marrow
•R.B.C.s W.B.C.s & platelets arise
in red bone marrow
• At birth all bone marrow is red
•As age advances, more & more is
converted to yellow type

32. Red Bone Marrow
•Then after the age of 20, red marrow
is found in ---
• Flat bones like pelvis, sternum,
cranium, Ribs, vertebrae, scapulae
• In spongy material at the epiphyseal
ends of long bones like femur &
humerus
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Yellow Bone Marrow
•This is found in hollow interior, of
the middle portion, of long bones
• In case of severe blood loss,
body can convert yellow marrow
back to red marrow, to increase
blood cell production.

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Stroma
•This is not directly involved in the
function of haemopoesis
•
•Though stroma is not active as
parenchymal red marrow, it is
directly helping haemopoesis

35. Stroma
•Stroma generates colony
stimulating factors, which help
haemopoesis
• Stroma has following types of
cells: fibroblast, osteoblast,
macrophages etc
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Bone marrow
•Bone Marrow Barrier
•Blood vessels of the bone marrow constitute a
barrier, which stop immature blood cell from
leaving the bone marrow.
•Mesenchymal stem cells
•They are also called as marrow stromal cells.
These are multi potent stem cells, which can be
differentiated into different types of blood cells.

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Bone marrow
•Red Marrow Parenchyma
•Examples of some cells are ---
•Myeloblast
•Neutrophilic myelocyte
•Megakaryocyte
•Reticular cells

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Diseases of Bone Marrow
•Normal bone marrow can be damaged by ----
Aplastic anaemia, cancer like multiple myeloma,
infection like T.B.
•Bone marrow is damaged due to --- radiation,
chemotherapy, side effect of drugs
•
•To diagnose diseases of bone marrow, biopsy or
bone marrow aspiration is done by hollow
needle putting into crest of ilium under GA or LA

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Diseases of Bone Marrow
•As part of treatment, sometimes bone marrow
transplant is done. (Haemopoetic stem cells are
removed from a person & infused into another
person i.e. called as allogenic or sometimes into
same person i.e. called as autologus)
•
•Another option is to administer certain drugs,
which stimulate the release of stem cells from
the bone marrow

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Fate of R.B.C.s
•Cells grow senile.
•Change their shape & size.
•Throw out processes.
•Cells are called as poikilocytes.
Breakdown of cells release
haemoglobin.

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Normal R. B. C. count
•i) Adult male - 5 million / c. mm
•ii) Adult females –
• 4.5 million / c. mm
•iii) Infants - 6 - 7 million / c. mm
•iv) Foetus - 7 - 8 million / c. mm

42. RBC Number
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43. RBC – Size & Shape
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Fate of Haemoglobin

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RBC Count -Physiological variations
•i) Diurnal variation - Lowest in sleep,
•maximum in the evening.
•ii) Muscular exercise - Temporarily
rise in count.
•iii) Altitude - At higher altitude -count ↑
•iv) High external temperature -count ↑

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Functions of R.B.C.
•i) Respiratory - R.B.C. carry O2 &
CO2
•ii) Maintain the viscosity of blood

•iii) Maintain acid - base balance
•iv) Maintain ion balance.

47. Function of RBC
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Haemoglobin
•Red pigment of blood is called as
haemoglobin. It is a chromoprotein.
•It consists of following 2 parts -
•a) Simple protein (Colourless)
(Globin) - 96 %
•b) Iron containing coloured pigment
(Haem) - 4 %

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Structure of Haemoglobin
•Hemoglobin has a quaternary
structure characteristic of many
multi-subunit globular proteins
• Most of the amino acids in
hemoglobin form alpha helixes,
connected by short non-helical
segments

50. Structure of Haemoglobin
•Hydrogen bonds stabilize the helical
sections inside this protein, causing
attractions within the molecule, folding
each polypeptide chain into a specific
shape
•Hemoglobin's quaternary structure
comes from its 4 subunits in roughly a
tetrahedral arrangement.
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Structure of Haemoglobin
•The hemoglobin molecule is an
assembly of 4 globular protein
subunits
•Each subunit is composed of a
protein chain tightly associated
with a non-protein heme group

52. Structure of Haemoglobin
•Each protein chain arranges into a
set of alpha-helix structural
segments connected together in
a globin fold arrangement
•This folding pattern contains a
pocket that strongly binds the
heme group
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Structure of Haemoglobin
•A heme group consists of an iron
(Fe) ion held in a heterocyclic
ring, known as a porphyrin
•This porphyrin ring consists of 4
pyrrole molecules cyclically linked
together with the iron ion bound in
the centre

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Structure of Haemoglobin
•The iron ion, which is the site of
oxygen binding, coordinates with the
4 nitrogens in the center of the ring,
which all lie in one plane.
•The iron is bound strongly to the
globular protein via theimidazole
ring of F8 histidine residue below the
porphyrin ring.

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Structure of Haemoglobin
•Even though carbon dioxide is carried by
hemoglobin, it does not compete with
oxygen for the iron-binding positions,
but it is actually bound to the protein
chains of the structure.
•The iron ion may be either in the Fe2+ or
in the Fe3+ state, but ferrihemoglobin
(methemoglobin) (Fe3+) cannot bind
oxygen.

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Structure of Haemoglobin
•In adult humans, the most common
hemoglobin type is a tetramer (which
contains 4 subunit proteins) called
hemoglobin A, consisting of 2 α &
2 β subunits non-covalently bound,
each made of 141 & 146 amino acid
residues, respectively

57. Structure of Haemoglobin
•This is denoted as α2 β2.
•The subunits are structurally similar &
about the same size.
•Each subunit has a molecular weight
of about 17,000 daltons, for a total
molecular weight of the tetramer of
about 64,000 daltons (64,458 g/mol).
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Structure of Haemoglobin
•In human infants, the
hemoglobin molecule is made
up of 2 α chains & 2 γ chains
•The gamma chains are gradually
replaced by β chains as the infant
grows

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Hb Types in humans
•Hemoglobin variants are a part of
the normal embryonic & fetal
development
•But pathologic mutant forms of
hemoglobin are also seen caused
by variations in genetics

60. Hb Types in humans
•Some well-known hemoglobin
variants such as sickle-cell anemia
are responsible for diseases, & are
considered hemoglobinopathies
•Other variants cause no detectable
pathology, & are thus considered non-
pathological variant
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Hb Types in humans
•In the embryo - Gower 1 & Gower 2
•Hemoglobin Portland (ζ2γ2).
•In the fetus - Hemoglobin F (α2γ2)
•In adults -- Hemoglobin A (α2β2) - The
most common with a normal amount over
95%

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Hb Types in humans
•Hemoglobin A2 (α2δ2) - δ chain synthesis
begins late in the third trimester & in
adults, it has a normal range of 1.5-3.5%
•Hemoglobin F (α2γ2) - In adults
Hemoglobin F is restricted to a limited
population of red cells called F-cells.
However, the level of Hb F can be
elevated in persons with sickle-cell
disease & beta-thalassemia.

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Variant forms which cause disease
•Hemoglobin H (β4) - A variant form of
hemoglobin, formed by a tetramer of β
chains, which may be present in variants
of α thalassemia
•Hemoglobin Barts (γ4) - A variant form of
hemoglobin, formed by a tetramer of γ
chains, which may be present in variants
of α thalassemia

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Variant forms which cause disease
•Hemoglobin S (α2βS2) - A variant
form of hemoglobin found in people
with sickle cell disease
•There is a variation in the β-chain
gene, causing a change in the
properties of hemoglobin, which
results in sickling of red blood cells

65. Variant forms which cause disease
•Hemoglobin C (α2βC2) - Another variant
due to a variation in the β-chain gene. This
variant causes a mild chronic hemolytic
anemia.
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Variant forms which cause disease
•Hemoglobin E (α2βE2) - Another
variant due to a variation in the β-
chain gene. This variant causes a
mild chronic hemolytic anemia
•Hemoglobin AS - A heterozygous
form causing Sickle cell trait with one
adult gene & one sickle cell disease
gene

67. Variant forms which cause disease
•Hemoglobin SC disease –
•A compound heterozygous form
with one sickle gene & another
encoding Hemoglobin C
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Formation of Hb
•Factors necessary for the synthesis of Hb -
•i) First class proteins - Diet containing milk, lean
meat, fish, poultry eggs, nuts, legumes, beans &
pulses
•ii) Metals - Iron - Daily 12 mgm, copper,
manganese & cobalt
•iii) Porphyrins
•iv) Endocrine - Thyroxine
•v) Vitamins - C & B12

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Hb
•Normal value of Hb - 14.5 gm %
•Function of Hb
•i) Essential for O2 carriage & CO2
transport
•ii) Maintain acid base balance.
•iii) Various pigments of urine, stool, bile etc.
are formed from it

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WBC Classification

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Physiological variation in WBC count
•i) Dinural variation - Morning & after rest ↓,
•Midday ↑ highest in the evening
•ii) Muscular exercise - Count ↑
•iii) After meal - Count ↑
•iv) Excitement - Count ↑
•v) Age - New born - 20,000 / cmm
•During infancy & childhood - Lymphocytes 40 -
50 %
•vi) Pregnancy, at full term - Count ↑

72. Blood cells
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73. PBS – Eosinophil
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74. Types of WBCs
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i) Neutrophilia
•Acute infections like Boils, Abscess,
Tonsillitis, Cellulitis, Meningitis,
Pneumonitis, Appendicitis
•Non infective conditions like Haemorrhage,
burn, Trauma (Surgical operations),
myeloid leukaemia, coronary thrombosis,
Intoxication due to drugs.

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WBC - Pathology
•ii) Eosinophilia
•Parasitic infections (Helminths, Filaria),
Allergic diseases (Cold, Asthama,
Urticaria), Skin diseases (Scabies,
Eczema)
•iii) Basophilia
•Chronic myeloid Leukaemia

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WBC - Pathology
•iv) Lymphocytosis
•Infections (Whooping cough, Chronic
infections like T.B.), Lymphoid Leukaemia
•v) Monocytosis
•Infections (Malaria, Typhoid), Monocytic
Leukaemia

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Leucopenia - causes
•i) Infections - Influenza, enteric
fever, malaria
•ii) Severe Anaemia
•
•iii) Malnutrition, Starvations,
Debility

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RBC & WBC

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IV) Functions of WBC -Phagocytosis
•What is Phagocytosis ?
•The neutrophils & monocytes engulf
foreign particles & bacteria
• Neutrophils manufacture a trypsin like
enzyme, with which they digest the
bacteria & dead tissue
•So the dead tissue in an inflammatory area
becomes liquefied & "Pus" is formed.

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IV) Functions of WBC
•ii) Antibody formation - Lymphocytes
•Manufacture β & fractions γ of serum
globulin. Immune bodies are associated
with Gamma (γ) Globulin fraction.
•iii) Anti - histamine (Anti - allergic)
function
•Eosinophils are rich in Histamine. They
fight against allergic conditions

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IV) Functions of WBC
•iv) Prevent intravascular
clotting
•Basophils secrete Heparin which
prevents intravascular clotting.

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Blood platelets (Thrombocytes)
•Non - nucleated, round / oval bodies,
having various sizes
•Average size 2.5 micron
•Average life is about 3 days
•Total count 2, 50, 000 to 5, 00, 000/cu.mm
(In 'Purpura', haemorrhage occurs beneath
the skin & mucous membrane & platelet
count is found to be low)

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Functions of Platelets
•i) Initiate blood clotting
•ii) Repair capillary endothelium
•
•iii) Speed up clot retraction
•vi) Helps in haemostatic
mechanism

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Functions of blood
•1) Transport of O2 & CO2
•2) Transport of nutrition
•3) Drainage of waste products to lungs,
kidney, intestine etc
•4) Vehicle media for carrying hormones,
vitamins, other essential chemicals
•5) Maintenance of water balance

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Functions of blood
•6) Maintenance of ion balance
•7) Maintenance of acid base equilibrium
•8) Regulation of body temperature
•9) Helps in the defence mechanism of the
body
•10) Due to coagulation property, guards
against haemorrhagic ill effects

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Haemopoiesis
•The process by which blood cell is formed
is called Haemopoiesis / Haematopoiesis
•Undifferentiated mesenchymal cells in
red bone marrow are transformed into
Haemocytoblasts, immature cells, which
undergo differentiation into 5 types of cells
from which the major types of blood cells
develop

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Haemopoiesis
•i) Proerythroblasts - form mature erythrocytes
•ii) Myeloblasts - from mature Neutrophils,
Eosinophils & Basophils
•
•iii) Megakaryoblasts - form mature thrombocytes
(Platelets)
•iv) Lymphoblasts - form mature Lymphocytes
•
•v) Monoblasts - from mature monocytes

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WBC production
•a) Granular leucocytes produced
in red bone marrow (myeloid
tissue)
•b) Agranular leucocytes are
produced in both myeloid &
lymphoid tissue.

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Haemostasis
•Haemostasis means stoppage of
bleeding
•Usually, haemorrhage in smaller blood
vessels (micro - circulation) stops
automatically
•But extensive haemorrhage from larger
vessels usually requires voluntary
intervention like ligation of blood vessels /
cauterisation etc.

91. Haemostasis
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What is coagulation / clotting ?
•When blood comes out of the body, it
looses its fluidity in a few minutes & a
semisolid jelly is formed
•This phenomenon is called clotting /
coagulation of blood. Coagulation is the
property of plasma alone & not of blood
cells. Platelets do take some part in the
process

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Process of clotting of blood
•Normal clotting time (C. T.) = 3 to 8 min.
•It consists of following 3 steps –
•i) Vascular spasm.
•ii) Platelet plug formation.
•iii) Clotting.

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i) Vascular spasm
•Smoot muscles of blood vessel's walls
contract immediately after damage ---
• This is called as vascular spasm
• It reduces blood loss

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ii) Platelet plug formation
•a) When blood comes out ---
•The platelets come into contact with parts
of a damaged blood vessel --
•This is Platelet adhesion

96. ii) Platelet plug formation
•b) Platelets disintegrate & liberate
Thromboplastin ---
•Certain amount of Thromboplastin is also
derived from the damaged tissues of the
injured part
•This phase is called as platelet release
reaction
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97. 6/24/2017 Prof.Dr.R.R.Deshpande 97
ii) Platelet plug formation
•c) Thromboplastin converts prothrombin
into thrombin with the help of of Ca.
•Thromboplastin + Prothrombin +
Calcium ion ---- Gives --Thrombin
•d) Thrombin interacts with fibrinogen
forming fibrin
•This is the clot
•Thrombin + Fibrinogen = Fibrin (Clot)

98. 6/24/2017 Prof.Dr.R.R.Deshpande 98
What are coagulation factors ?
•Clotting involves various chemicals known
as coagulation factors
•Total 12 factors are as follows -

99. 6/24/2017 Prof.Dr.R.R.Deshpande 99
12 Clotting Factors

100. 6/24/2017 Prof.Dr.R.R.Deshpande 100
Some more details
•i) Fibrinogen
•Globulin in nature, present in plasma
•ii) Prothrombin
•Protein in nature. Present in plasma.
Normal prothrombin time is 12 - 13 sec.
It will be longer in deficiency of factor v / vii.
Prothrombin is manufactured in liver. Vit. K
is essential for the formation.

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Some more details
•iii) Thromboplastin
•Derived form 2 sources - Intrinsic in the
plasma, Extrinsic in the tissues
•iv) Anti haemophilic factor
•In Haemophilia, due to absence of this
factor, breakdown of platelets & liberation
of thromboplastin becomes difficult.

102. 6/24/2017 Prof.Dr.R.R.Deshpande 102
Christmas Factor
•This factor is essential for the formation of
intrinsic thromboplastin
•A disease simulating Haemophilia is
developed due to the absence of this
factor
•This type of disease was first found in a
patient named Christmas & hence the
name.

103. 6/24/2017 Prof.Dr.R.R.Deshpande 103
Factors accelerating coagulation
•Warmth (Cautery)
•Contact with water wettable surface
•
•Inj. vit. K / oral administration of high
doses increases the prothrombin
•Addition of calcium chloride
•Inj. Adrenaline

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What is thrombosis ?
•This is intravascular clotting, which is abnormal
•
•Thrombus is a clot formed inside the blood
vessels. eg. - Coronary thrombosis & cerebral
thrombosis
•Heparin is anticoagulant both in vivo & in vitro
•The first thrombolytic agent, approved to use in
1982 is "Streptokinase (Streptase)"

105. 6/24/2017 Prof.Dr.R.R.Deshpande 105
Blood groups
•Knowledge of blood groups is a
gift of current century
•This has a great practical
significance, especially during
blood transfusion

106. Blood groups
•When the blood of a healthy man (Donor)
is injected into the body of the patient
(Recipient) ---
•If 2 bloods are not compatible,
haemolysis of the donors corpuscles will
take place ---
• Which lead to dangerous effects to the
recipient.
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107. Blood Groups
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108. 6/24/2017 Prof.Dr.R.R.Deshpande 108
Blood groups
•So, compatibility / matching of blood groups is
very essential
•There are, at least, 300 blood group systems,
that can be detected on the surface of RBC
•The 2 major blood group classifications ABO &
RH
•Among the others are the Lewis, Kell, Kidd &
Duffy systems.

109. 6/24/2017 Prof.Dr.R.R.Deshpande 109
Blood groups
•The phenomenon of haemagglutination is due to
interaction between 2 factors Agglutinogens (
Antigens) , present in the corpuscles &
Agglutinins ( Antibody) , present in the
plasma OR serum
• The ABO blood grouping is based on 2
agglutinogens symbolised as A & B. Individuals,
whose erythrocytes manufacture only
agglutinogen or Antigen A are said to be blood
Group A.

110. 6/24/2017 Prof.Dr.R.R.Deshpande 110
Blood groups
•Those who manufacture only agglutinogen
B are type B
•Individuals who manufacture both A & B
are type AB
•Those who manufacture neither are type
"O"

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What is danger in incompatible
blood transfusion (B.T.) ?
•In an incompatible BT, the donated
erythrocytes are attacked by the recipient
agglutinins, causing the blood cells to
agglutinate (clump)
•Agglutinated cells become lodged in
small capillaries throughout the body &
over a period of hours, the cells swell,
rupture & release Hb into the blood.

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What is danger in incompatible
blood transfusion (B.T.) ?
•Such a reaction is called hemolysis.
• eg.- If an individual with type A blood receives a
transfusion of type B blood
•The recipient's blood contains A –Antigen & B
Antibodies.
•The donor's blood contains B Antigens & A –Antibodies
•So, B Antibodies in the recipient's plasma will attack the
B Antigens on the donor's erythrocytes, causing
agglutination & haemolysis.

113. 6/24/2017 Prof.Dr.R.R.Deshpande 113
Table of donor & recipient

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Rh system
•This classification is named because it
was first worked out in the blood of the
Rhesus monkey
• Individuals whose erythrocytes have the
Rh agglutinogens are called as Rh positive
(Rh +)
•Those who do not have Rh agglutinogens
are called as Rh negative (Rh –)

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Utility of blood typing
•1) Blood transfusion
•2) Certain blood diseases
•3) Paternity test
•4) Anthropological studies
•5) Ethnological studies
•6) Identification of blood stains in murder &
other cases

116. 6/24/2017 Prof.Dr.R.R.Deshpande 116
What is erythroblastosis fetalis ?
•If an Rh –ve female is impregnated by an RH +ve male
& the foetus is Rh +ve, foetal Rh +ve agglutinogens may
enter the maternal blood via the placenta during delivery
• Upon exposure to the foetal Rh +ve agglutinogens, the
mother will make anti Rh agglutinins
• If the female becomes pregnant again, her anti Rh -
agglutinins will cross the placenta into the foetal blood
•If the foetus is Rh +ve, haemolytic disease of the
newborn will result, which is called as erythroblastosis
foetalis

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1) Anticoagulant
•An anticoagulant is a substance that prevents
coagulation or clotting of blood
•Such substances found naturally in leeches.
•Anticoagulants can be used as a medication for
thrombotic disorders
• Some anticoagulants are used in medical equipment,
such blood transfusion bags, & renal dialysis equipment
•Anticoagulants reduce blood clotting --- This prevents
deep vein thrombosis, pulmonary embolism,
myocardial infarction & stroke

118. 6/24/2017 Prof.Dr.R.R.Deshpande 118
Coumarins (vitamin K antagonists)
•These oral anticoagulants are derived from
coumarin, which is found in many plants.
• A well known example from this group is
warfarin (coumadin)
• It takes at least 48 to 72 hours for the
anticoagulant effect to develop

119. Coumarins (vitamin K antagonists)
•Where an immediate effect is required,
Heparin Can be used
• These anticoagulants are used to treat
patients with deep-vein thrombosis (DVT),
pulmonary embolism (PE), atrial fibrillation
(AF), & mechanical prosthetic heart valves.
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120. 6/24/2017 Prof.Dr.R.R.Deshpande 120
Heparin
•Heparin is a biological substance,
usually made from pig intestines
• It works by activating anti
thrombin III, which blocks
thrombin from clotting blood

121. 6/24/2017 Prof.Dr.R.R.Deshpande 121
Food & Herbal supplements –
Anti coagulants
•Foods & food supplements with blood-
thinning effects include ----
•Alfalfa, avocado, beer, celery, cranberries,
fish oil, garlic, ginger, ginseng, grapefruit,
green tea, liquorice, niacin, onion, papaya,
pomegranate, soybean, turmeric,
wheatgrass.

122. 6/24/2017 Prof.Dr.R.R.Deshpande 122
General indications- Anti coagulants
•Therapeutic uses of anticoagulants include
---
•Atrial fibrillation, pulmonary embolism,
deep vein thrombosis, venous thrombo-
embolism, congestive heart failure, stroke,
myocardial infarction, & genetic or
acquired hyper -coagulability.

123. 6/24/2017 Prof.Dr.R.R.Deshpande 123
Laboratory use –Anti coagulant
•Laboratory instruments, blood transfusion
bags, & medical & surgical equipment will
get clogged up & become nonoperational if
blood is allowed to clot
•In addition, Bulbs used for laboratory
blood tests will have chemicals added as
Anticoagulant

124. Laboratory use –Anti coagulant
•Like Wintrobe bulb or Fluoride bulb
•But in plain bulb there is no anticoagulant
•Plain bulb is used for collecting blood for
serological Tests like Liver Function Test,
Renal Function Test
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125. 6/24/2017 Prof.Dr.R.R.Deshpande 125
Some examples of Anticoagulants
used in Laboratory
•1) EDTA strongly & irreversibly binds
calcium. It is in a powdered form

•2) Citrate is in liquid form in the tube & is
used for coagulation tests, as well as in
blood transfusion bags. It binds the
calcium, but not as strongly as EDTA

126. 6/24/2017 Prof.Dr.R.R.Deshpande 126
Some examples of Anticoagulants
used in Laboratory
•3) Oxalate has a mechanism similar to
that of citrate
•It is the anticoagulant used in fluoride
oxalate tubes used to determine glucose &
lactate levels.

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Plasma Proteins

128. Plasma Proteins
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129. 6/24/2017 Prof.Dr.R.R.Deshpande 129
3) Introduction to Anaemia
•Anaemia is the condition where there
is decrease in RBC count, Hb & PCV
•This occurs due to decreased
production of RBC, increased
destruction of RBC, excess loss of
blood from the body

130. 6/24/2017 Prof.Dr.R.R.Deshpande 130
Types of Anaemia –
Morphological classification

131. Anaemia & RBCs
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132. Symptoms of Anaemia
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133. 6/24/2017 Prof.Dr.R.R.Deshpande 133
1) Haemorrhagic Anaemia
•Acute haemorrhage causes - sudden loss
of large quantity of blood during accident
•In one day plasma portion of the blood is
replaced
•But replacement of RBCs takes place
within 4 to 6 weeks
•Chronic haemorrhage occurs due to peptic
ulcer, purpura, haemophilia, menorrohagia

134. 1) Haemorrhagic Anaemia
•Iron is lost in the haemorrhage.
•Iron is necessary for the synthesis of
Hb. So loss of iron causes Anaemia .
•Classical haemorrhagic diseases are
Idiopathic thrombocytopenic
purpura or Werlhof’s disease &
haemophilia
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135. 6/24/2017 Prof.Dr.R.R.Deshpande 135
i) Purpura
•Cause is unknown
•Main pathology is Platelet deficiency
•Blood platelet count becomes less
than 40,000/cmm
•Bleeding tome is markedly prolonged
but CT & Prothrombin time are normal

136. 6/24/2017 Prof.Dr.R.R.Deshpande 136
i) Purpura
•This is common in children & young adult
females
•Spontaneous bleeding occurs after
trauma, surgery or dental procedures
•Nature of haemorrhage in skin is like
petechae, purpura or ecchymosis,
epistaxis or bleeding gums, haematuria,
malaena may occur

137. i) Purpura
•Sub conjunctival & retinal haemorrhages
are also common
• Spleen is slightly enlarged & soft
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138. Purpura
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139. 6/24/2017 Prof.Dr.R.R.Deshpande 139
i) Purpura
•During acute phase of bleeding, BT is
given, bed rest is advised
• Heavy dose of Prednisolone
(60mg/day) is given
• If bleeding does not stop within 2
weeks, spleenectomy is done.

140. 6/24/2017 Prof.Dr.R.R.Deshpande 140
ii) Haemophilia
•This is hereditary disorder of
coagulation of blood, due to
deficiency of anti-haemoplilic factor
•This is result in haemorrhagic
tendency
• Here BT is normal but CT is
markedly prolonged

141. 6/24/2017 Prof.Dr.R.R.Deshpande 141
ii) Haemophilia
•Disease is manifest in infancy
•Males are more affected
•Traumatic bleeding is more
common than spontaneous
haemorrhage
•Bleeding is not very profuse but
persist for days or even weeks

142. ii) Haemophilia
•Haemorrhage occurs from nose, mouth,
elementary tract, urinary tract, muscles
& joints
•Cutaneous haemorrhage is rare but
bruises may occur after slight knock
•Recurrent haemorrhage in to joint space is
common
•In adults knee joints are affected
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143. 6/24/2017 Prof.Dr.R.R.Deshpande 143
ii) Haemophilia
•General management includes - Advise to avoid
sports, swimming, cycling
•Planned pre & post operative care,
•Care of dental hygiene.
•During bleeding phase bed rest is necessary
•Fresh BT is given
•Local haemostasis is important like pressure,
immobilisation etc

144. 6/24/2017 Prof.Dr.R.R.Deshpande 144
2) Haemolytic Anaemia
•This occurs due to destruction of RBCs. The
subtypes are Extrinsic & Intrinsic.
•a) Extrinsic haemolytic anaemia - Main causes
are infections like Malaria, septicaemia, side
effects of drugs like penicillin, anti-malarial &
Sulpha drugs, liver failure, renal problems,
spleenomegaly, burn, lead poisoning,
autoimmune diseases like rheumatoid arthritis &
ulcerative colitis

145. 6/24/2017 Prof.Dr.R.R.Deshpande 145
2) Haemolytic Anaemia
•b) Intrinsic haemolytic anaemia
–
• Destruction of RBCs takes place
due to defective RBCs. RBCs
become more fragile & prone for
haemolysis. Classical examples
are as follows →

146. 6/24/2017 Prof.Dr.R.R.Deshpande 146
i) Sickle cell Anaemia
•Also called as Haemoglobin S or
Sickle cell disease
•This is common in Africa
•Occurs due to abnormal
haemoglobin, called ----
•haemoglobin S

147. i) Sickle cell Anaemia
•Here Alpha chains are normal &
Beta chains are abnormal
•RBCs get sickle or crescent
shaped
•They become more fragile &
haemolysis occurs
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148. Sickle Cell Anaemia
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149. 6/24/2017 Prof.Dr.R.R.Deshpande 149
i) Sickle cell Anaemia
•Haemolysed sickle cell aggregate & blocked the
blood vessels
•Infracted small cell in hand & foot results in
varying length in the digits (Hand & Foot
syndrome)
•Clinically patient is presented with severe
Anaemia, Haemolytic Jaundice, weakness, leg
ulcers, thrombotic episodes
•Haemolytic crisis occur from time to time, when
blood transfusion is given

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ii) Thalassaemia or coolie’s Anaemia
•Alpha & beta are 2 subtypes
•This is common in Thailand & in
Mediterranean countries
•This is metabolic fault of RBCs, which
leads to continued production of foetal
haemoglobin
•In normal haemoglobin number of alpha &
beta polypeptide chains is equal.

151. Thalassemia
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152. Thalassemia – Trait
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153. 6/24/2017 Prof.Dr.R.R.Deshpande 153
ii) Thalassaemia or coolie’s Anaemia
•In Thalassaemia, production of these
chains become imbalanced
•In beta type, beta chains are less in
number, absent or abnormal with
excess of alpha chains
• Alpha chains precipitate & cause
defective erythropoesis & haemolysis

154. 6/24/2017 Prof.Dr.R.R.Deshpande 154
ii) Thalassaemia or coolie’s Anaemia
•Clinically patient presents with pallor, anaemia,
haemolytic Jaundice, Splenomegale.
•Crisis occur from time to time.
•In blood examination foetal Hb is found more than
normal.
•X-ray of skull shows “hair on end” appearance.
•X-ray of maxilla & mandible shows “Pepper & salt
effect”. X-ray of metacarpal bones shows increased
trabeculation.
•BT during crisis is the only treatment. Splenectomy is
contraindicated.

155. 6/24/2017 Prof.Dr.R.R.Deshpande 155
3) Nutrition deficiency Anaemia
•a) Iron deficiency anaemia –
•Causes -- Repeated small blood loss in
bleeding piles, menorrhagia, improper
intake of iron, poor absorption of iron from
intestine, increased demands for iron in
conditions like growth, pregnancy,
lactation

156. Anaemia --Koilynochia
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157. Anaemia – Pale Conjunctiva
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158. 6/24/2017 Prof.Dr.R.R.Deshpande 158
Iron deficiency anaemia -Symptoms
•Weakness or fatigue, palpitation,
•Breathlessness on exertion
•Tingling numbness,
•Oedema,
•Loss of appetite,
•Giddiness
•Insomnia.

159. Iron deficiency anaemia - Signs
•Pallor, koilonychia
•Inelastic dry skin, dry scanty hair
•Ankle oedema
•Pulse is collapsing type but rate is increased
•Angular stomatitis, smooth & bald tongue, liver
& spleen are palpable, functional soft systolic
murmur may be present
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160. 6/24/2017 Prof.Dr.R.R.Deshpande 160
b) Protein deficiency anaemia
•Due to protein deficiency, Hb synthesis is
reduced
•PCM = Protein Calorie Malnutrition
•PCM includes – Marasmus & Kwashiorkar

161. 6/24/2017 Prof.Dr.R.R.Deshpande 161
Pernicious anaemia or Addison’s anaemia
•This is inherited constitutional
weakness, where stomach fails to
produce HCL, pepsin, intrinsic
factor
•Due to autoimmune cause
atrophy of gastric mucosa takes
place

162. c) Pernicious anaemia or Addison’s anaemia
•Due to decreased production of
intrinsic factor, vit. B12 is poorly
absorbed
•B12 is the maturation factor for RBCs
•RBCs become larger & immature
(With normal or slightly low Hb)
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163. 6/24/2017 Prof.Dr.R.R.Deshpande 163
c) Pernicious anaemia or Addison’s anaemia
•This anaemia is common in old age & found
more in females
•This is associated with other autoimmune
diseases like of thyroid gland
•IMP feature of this disease is lemon yellow
colour of skin & red sour tongue
•In extreme conditions numbness, tingling,
burning, progressive weakness & ataxia may be
seen

164. 6/24/2017 Prof.Dr.R.R.Deshpande 164
iv) Megaloblastic anaemia
•This is due to deficiency of folic acid
•Here also RBCs are not mature
•RBCs are megaloblastic & hypochromic
•Clinical features are same as Pernicious
Anaemia (neurological disorders may not
develop)

165. 6/24/2017 Prof.Dr.R.R.Deshpande 165
4) Aplastic anaemia
•Here red bone marrow is reduced & replaced
by fatty tissues. There are 2 subtypes - i)
primary or idiopathic & secondary
•Causes of secondary aplastic anaemia are - side
effects of the drugs like chloramphenicol,
arsenic, gold, chlorpropamide etc. repeated
exposure to x-ray, gamma rays or use of
radioactive substances, chronic infection like TB,
viral infections like hepatitis, HIV, terminal stage
of renal failure

166. 6/24/2017 Prof.Dr.R.R.Deshpande 166
4) Aplastic anaemia
•Blood examination shows pancytopenia
•RBCs are normocytic normochromic
•Bone marrow examination shows absence
of red bone marrow & many fat cells
•Prognosis is bad & patient may die within
9 months

167. 5) Anaemia in chronic diseases
•This is caused by disturbance in Iron
metabolism or resistance to erytrhopoetin
action
•This anaemia develops after few months
of occurrence of disease
•Common causes are rheumatoid
arthritis, TB, CRF, Hodgkin’s disease,
cancer of lung & breast
6/24/2017 Prof.Dr.R.R.Deshpande 167

168. 4) Introduction to Jaundice
•Jaundice is yellow coloration of skin,
mucus membrane ---
•Due to increase serum bilirubin level
(Normal- 0.5 to 1.5mg/100ml)
•When Bilirubin value is greater
than 2mg/100ml, it is called as
Jaundice.
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169. 3 types of Jaundice
•1) Preheaatic / Haemolytic
•2) Hepatic / Hepatocellular
•3) Post hepatic / obstructive
6/24/2017 Prof.Dr.R.R.Deshpande 169

170. Causes of Jaundice
6/24/2017 Prof.Dr.R.R.Deshpande 170

171. 1) Hemolytic Jaundice
•This occurs due to excessive
destruction of RBCs
•Un conjugated or indirect
bilirubin level in the blood
increases
•Urobilinogen, stercobilinogen
increases
6/24/2017 Prof.Dr.R.R.Deshpande 171

172. 1) Hemolytic Jaundice
•Van den bergh reaction is indirect
positive
•Liver functions are normal
•Blood shows Anaemia,
reticulocytosis, abnormal RBCs
•Plasma albumin & globulin are normal
•Haemorrhagic tendency is absent
6/24/2017 Prof.Dr.R.R.Deshpande 172

173. 1) Hemolytic Jaundice - Causes
•Hb abnormalities like Sickle cell Anaemia
or Thalassemia
•Malaria
•Hypersplenism
•Autoimmune diseases
•Burn
•Side effect of drugs
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174. 2) Hepatic Jaundice
•This occurs due to damage of hepatic cells
•Conjugated or direct bilirubin level in
the blood increases
•urobilinogen & stercobilinogen decreases
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175. 2) Hepatic Jaundice
•Van Den Bergh reaction is biphasic

•Liver functions are abnormal.
•Blood picture is normal.
•Blood albumin & globulin increases, but
A:G ratio decreases.
•Haemorrhagic tendency is present, due to
lack of Vit. K.
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176. 2) Hepatic Jaundice
•Liver functions are abnormal
•Blood picture is normal
•Blood albumin & globulin
increases, but A:G ratio decreases
•Haemorrhagic tendency is present,
due to lack of Vit. K.
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177. Jaundice --Icterus
6/24/2017 Prof.Dr.R.R.Deshpande 177

178. 2) Hepatic Jaundice --Causes
•Infective hepatitis due to -------
•Virus A
•Alcoholic hepatitis
•Liver cirrhosis
6/24/2017 Prof.Dr.R.R.Deshpande 178

179. 3) Obstructive Jaundice
•This occurs due to obstruction of bile flow
at any level of biliary system
• Blood conjugated Bilirubin increases
• Urobilinogen decreases & absent in
severe obstruction
• Stercobilinogen is absent & hence faeces
are clay colored
6/24/2017 Prof.Dr.R.R.Deshpande 179

180. 3) Obstructive Jaundice
•Van Den Bergh reaction is direct
positive
• Blood picture is normal
• Plasma albumin & globulin are normal
Haemorrhagic tendency is present due to
lack of Vit-K
•Causes - Gallstones or cancer of biliary
system or Pancreas
6/24/2017 Prof.Dr.R.R.Deshpande 180

181. Prof.Dr.R.R.Deshpande
•Sharing of Knowledge
•FOR
•Propagating Ayurved
6/24/2017 181Prof.Dr.R.R.Deshpande