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Anaemia
Reduction in the Hb concentration below the
lower limit of normal range with respect to age,
gender and race of an individual
Always associated with
pallor (pale)
CAUSES OF ANAEMIA
Insufficient number of RBCs
RBC number < 5 X 106/ µl blood
Haemorrhagic anaemia
Results from blood loss
Haemolytic anaemia
Results from RBC rupture, or lyse, prematurely
Aplastic anaemia
↓↓ production of RBCs in the bone marrow
Tumors, drugs & chemicals, x-rays
CAUSES OF ANAEMIA
Low haemoglobin content
Hb concentration < 11 – 12 g/dL blood
Hb molecules are normal, but Hb content in
RBC < normal
Megaloblastic anaemia
Microcytic anaemia
CAUSES OF ANAEMIA
Low haemoglobin content
Megaloblastic anaemia
Results from deficiency of vitamin B12 &/or folic
acid
Pernicious anaemia
Normal RBC
POLYCYTHAEMIA
Hb concentration > 16 – 18 g/dL or RBC number
> 8 x 106 /µL blood
Cancer of the bone marrow causing ↑ production
of RBCs – polycythaemia vera (primary
polycythaemia)
Conditions causing hypoxia (through EPO) –
secondary polycythaemia:
Natives living in high altitudes
Heart disease
Lung disease
ERYTHROCYTE SENDIMENTATION RATE
(ESR)
When blood to which an anticoagulant has been
added is allowed to stand in narrow tube, the
RBCs form a pile of aggregates (rouleaux)
Rouleaux gradually sediment leaving a clear
zone of plasma above
The length (mm) of the column of clear plasma
after one hour is the measure of ESR
Normal ESR values:
Male: 3 – 5 mm
Female: 4 – 7 mm
FACTORS AFFECTING ESR
Types of Percentage
Cells / µL
WBC Distribution
Neutrophils 3000 – 6000 60 – 70 %
Chemotaxis
Attracted to chemicals from pathogens or damaged tissues
Amoeboid movement
Allows leukocytes to move through tissues
Diapedesis
Leave capillaries by squeezing themselves between
endothelia cells and enter tissues
Phagocytosis
Remove pathogens and cell debris by engulfing them
CHARACTERISTICS OF LEUKOCYTES
GRANULOCYTES
Nuclei segmented into several lobes of varying
shapes
Cytoplasm contains an abundance of membrane-
enclosed granules
3 types:
Neutrophil
Eosinophil
Basophil
Life span:
<12 hours in transit in the blood before entering tissues
3 – 4 days in tissues
GRANULOCYTES
Neutrophil
Lobed nucleus (3 – 6)
Purplish granules
Number ↑ (neutrophilia) in acute
bacterial infections
First WBCs that react to
inflammatory responses triggered
by bacterial infection
Destroy bacteria by phagocytosis
GRANULOCYTES
Eosinophil Bilobed, purplish nucleus
Dark pink granules (contain
histamine, serotonin)
Number ↑ (eusinophilia) during
allergic diseases (asthma, hay fever,
food allergy), skin diseases &
parasitic infestations (worms)
Inactivate inflammation-inducing
mediators released from mast cells
during allergic reactions
GRANULOCYTES
Basophil
Bilobed nucleus
Dark blue granules (contain
histamine, serotonin, heparin)
Release histamine with IgE
antibody signal
Number ↑ (basophilia) in
inflammatory & allergic
reactions
AGRANULOCYTES
Single, large, non-segmented nucleus
Few granules
2 types:
Monocytes
Lymphocytes
AGRANULOCYTES
Monocytes
Life span: months - years
Dark blue-purple , kidney shape
nucleus; gray-blue cytoplasm
Digests bacteria, antigen & old or
damaged cells by phagocytosis
Leave the blood after 1 – 2 days &
enter tissues to become
macrophages
Number ↑ (monocytosis) in chronic
infections (tuberculosis, syphilis,
malaria)
AGRANULOCYTES
Lymphocytes
Life span:100 – 300 days
Spherical dark purple-blue nucleus; pale
blue cytoplasm
Body immunity
Protection against bacterial & viral
infections
B Lymphocytes
Produce antibodies against different antigens
T Lymphocytes
Respond against virus infected cells & tumor
cells
Release chemicals that destroy the victim
cells
LEUCOCYTE DESTRUCTION
Leukopaenia
Abnormally low WBC count
HIV infection, radiation therapy,
chemotherapy, glucocorticoids
LEUKOCYTES DISORDERS
Leukocytosis
An increase in the number of leukocytes over
the upper limits
A modest leukocytosis is normal during an
infection
Extreme leukocytosis generally indicates
leukaemia
LEUKOCYTES DISORDERS
Leukaemia
Cancerous conditions involving WBCs
Two general types
myelogenous leukaemia
Cancerous production of young myelogenous cells in the bone
marrow
lymphocytic leukaemia
Cancerous production of lymphoid cells, usually beginning in a
lymph node or other lymphocytic tissue
Acute and chronic leukaemia
THROMBOCYTES / PLATELETS
Small non-nucleated cells (2 – 4 m
in diameter)
Irregularly shaped; stained dark
purple
Granules contain serotonin, ADP,
von Willebrand factor, fibrinogen
Produced in bone marrow from
special cells called megakaryocytes
150- 400 x 103 /µL blood
Life span: 7 – 14 days
Destroyed in the spleen and liver
FORMATION OF PLATELETS
Thrombopoiesis
FUNCTIONS OF PLATELETS
Prevents bleeding
Coagulation of blood
HAEMOSTASIS
4 mechanisms involved:
Vasoconstriction (vascular spasms)
Formation of platelet plug
Formation of blood clot
Permanent repair and fibrinolysis
VASCULAR SPASMS
First response to vascular injury
Vasoconstriction of injured vessel due to
contraction of smooth muscle in the wall
of vessel
Triggered by
Local myogenic reflexes (direct injury to
vascular smooth muscle)
Reflexes initiated by local pain receptors
Vasoconstrictors (serotonin, thromboxane A2)
released by endothelial cells & platelets
Instantly reduces the flow of blood from the ruptured
vessel
FORMATION OF PLATELET PLUG
Injury to a vessel disrupts the endothelium
& exposes the tissue collagen molecules
Platelets adhere to collagen via von
Willebrand factor (vWF)
Binding of platelets to collagen triggers the
platelets to release ADP & serotonin –
platelet activation
Platelet activation causes new platelets to
adhere to the old ones – platelet
aggregation
Platelet aggregation rapidly creates a
platelet plug inside the vessel
Adhesion of platelet induces synthesis of
thromboxane A2 – which further stimulate
platelet activation & aggregation, and
vasoconstriction
FORMATION OF PLATELET PLUG
FORMATION OF PLATELET PLUG
Formation of
(Active factor XII) prothrombin
activator
Factor XII
Coagulation
Ca2+
BLOOD COAGULATION
Prothrombin
activator
Haemostasis
PERMANENT REPAIR & FIBRINOLYSIS
Contraction of platelet trapped within the clot
shrinks the fibrin mesh
Draws the edges of the damaged vessel together
Serum is squeezed from the clot
(serum: plasma without clotting factors)
Platelet-derived growth factor (PDGF) –
stimulates fibroblast migration & fibrous tissue
growth → Scar
The clot is gradually dissolved away (fibrinolysis)
FIBRINOLYSIS
Dissolution of blood clots
Brought about by a proteolytic enzyme – plasmin
Plasmin digests fibrin into soluble fibrin fragments,
thereby dissolve the clot
Plasminogen activators
Plasminogen Plasmin
Soluble fibrin
Fibrin
fragments
BLOOD CLOTTING DISORDERS
Haemophilia
Genetically
inherited clotting insufficiency
Haemophilia A
Classic haemophilia (85 %)
An abnormality or deficiency of Factor VIII
Haemophilia C
Very rare
A deficiency of Factor XI
BLOOD CLOTTING DISORDERS
Haemorrhagic disorders that due to
liver disease
deficiency of coagulation factors that are
synthesised in the liver (Factors I,II, V, VII, IX and
X)
Vitamin K deficiency
Synthesis of Factors II (prothrombin),VII, IX and X
are reduced
Vitamin K is required as coenzyme for synthesis of
these factors
BLOOD CLOTTING DISORDERS
Thrombosis
Formation of clots (thrombus) inside the blood
vessel
Causes of thrombosis
Roughed endothelial surface of a vessel
caused by arteriosclerosis, infection, or
trauma
Blood flow is sluggish and allows activated
coagulation factors to accumulate
Emboli- freely flowing clots in the blood
stream to other organs and cause damage
ANTICOAGULANT AGENTS
Agents that prevent clotting of blood
In vitro and in vivo
Heparin
Naturally occurring anticoagulant
Facilitates the action of antithrombin → inactivates
thrombin and other proteases involved in blood
clotting
Found in the granules of basophils and mast cells
Used in vitro and in vivo
ANTICOAGULANT AGENTS
Chelating agents
Citrate,
oxalate, flouride, EDTA
Combine with plasma Ca2+ & form insoluble
complexes
Used in vitro only
Agents that inhibit the action of vitamin K
Coumarin derivatives: warfarin, dicumarol
Clinically used in vivo only as drug for treatment of
thrombosis
Arvin (extract from venom of Malayan viper)
Depletes fibrinogen by forming imperfect fibrin which
is removed by macrophages (defribrination)
BLEEDING TIME
A medical test done on someone to assess their
platelet function
The time it takes for bleeding to stop (as thus the
time it takes for a platelet plug to form) is measured
Normal value: 2 – 9 min
Bleeding time ↑ when:
Thrombocytopenia (platelet difficiency)
Disseminated intravascular coagulation
(DIC)
CLOTTING TIME
DONOR RECIPIENT
O
A B AB
Antigen (anti-A,
(anti-B) (anti-A) (-)
anti-B)
A (A) X √ X √
B (B) X X √ √
AB (A,B) X X X √
O (-) √ √ √ √
BLOOD GROUP ABO SYSTEM
Universal donor
Universal recipient
RHESUS SYSTEM
Rh negative individuals:
Plasma does not contain antibodies to
antigen D
4. Rh+ transfusion
(2nd time after 4 – 6 months)