|
 


 

 |
 

 

u Anemia ± blood has abnormally low oxygen-

oxygen-
carrying capacity
u Symptom rather than a disease itself
u Blood oxygen levels cannot support normal
metabolism
u Signs/symptoms include fatigue, paleness,
shortness of breath, and chills
 2


Vmpaired erythrocyte formation Vncreased erythrocyte loss

Vron deficiency Haemolytic

Megaloblastic Sickle cell

Vitamin B12 Thalassemia

Pernicious Normocytic

Diet

Other causes

Folic acid

Hypoplastic and aplastic

 V     
2


u Vron--deficiency anemia results from:

Vron
u A secondary result of hemorrhagic anemia
u Vnadequate intake of iron-
iron-containing foods
u High requirement, normal/ deficient intake
u Vmpaired iron absorption
u Stomach pH
u Parietal cells, intrinsic factor
u Cells are microcytic, hypochromic
 ë


 2


u Caused due to Vit B12 or folic acid deficiency

u Cell division is delayed
u Daughter cells are larger than parent cells
(macrocytic)
u Hb content is more, making the cells more
fragile
u Decreased life span of cells 40-
40-50 days
u Depressed production and early lysis causes
anaemia
 2

  



u Pernicious anemia is an autoimmune disease

u Autoantibodies destroy parietal cells
u Lack of intrinsic factor needed for absorption
of B12
u More common in females (45-(45-65 years) than
males
u Treatment is intramuscular injection of B12
 ë


 2


 

 



u Caused due to dietary deficiency in true vegans

u Deficiency takes several years to appear
u Other causes
u Gastrectomy: fewer parietal cells

u Chronic gastritis, malignant disease, ionising

radiation
u Malabsorbtion due to Crohn¶s disease (terminal
portion of the ileum removed)
 ë


 2


u Complications include irreversible neurological

damage, especially to the spinal cord
u Vit B12 is required for secretion and maintenance of
myelin
u Nerve fibers become demyelinated causing ataxia,
spastic paralysis
u Atrophy and ulceration of tongue causing glossitis
 ë


 2


 
    

u No neurological damage

u Dietary deficiency

u Vnfants
u pregnancy
u Alcoholics
u Malabsorption from jejunum in coeliac disease,
tropical sprue, anticonvulsant drugs
u Vnterference with folate metabolism ± cytotoxic drugs
 m


 2

 2


u Caused due to varying degrees of bone marrow

failure
u Causes pancytopenia
u Causes of bone marrow depression is due to
u Drugs: Cytotoxic, sulfonamides
u Vonizing radiation
u Chemicals: benzene and its derivatives
u Viral diseases: hepatitis
u Vnvasion of bone marrow by malignant disease,
leukemia
 m

 2


u èBCs are destroyed while in circulation or are prematurely

removed while still in circulation as they are abnormal or an
overactive spleen

u Two types
u Congenital haemolytic anaemia

u Sickle cell Anaemia

u Thalassaemia Anaemia

u HDN

u Accquired haemolytic anaemia

 ½  
m

 2


u Genetic abnormality leads to

u Synthesis of abnormal Hb

u Vncreased èBC membrane fragility/friability

u Decreased oxygen carrying capacity

u Decreased life span

  2
2


u Abnormal Hb formed
u On deoxygenation, erythrocytes become sickle
shaped
u Sickling becomes permanent if there is high
amount of abnormal Hb
u Decreased life span of èBC early haemolysis
u Vncreased viscosity of blood ishaemia
infarction
  2


Complications
u Pregnancy, infection, dehydration increases
predisposition
u Formation of gall stones and inflammation of
gall bladder
 M




u Decreased globin synthesis

u Decreased Hb synthesis
u Vncreased cell membrane friability
u Early haemolysis
 2 m

 2


Caused due to
u Chemical agents: sulfonamides, toxins produced by
microbes
u Autoimmunity
u Acute /Chronic
u Primary or secondary to other diseases (carcinoma/ viral
infections)
u Vncompatible blood transfusion
u Other causes
u Parasitic diseases: malaria
u Vonizing radiation
u Destruction of blood trapped in tissues
u Physical damage: Artificial heart valves
 m

 2


u Normocytic Anaemia
u Proportion of reticulocytes in the blood
increased
u Caused due to
u Chronic disease condition: chronic inflammation
u Haemolytic disease
u Severe haemorrhage
 




u Polycythaemia ± excess èBCs that increase blood
viscosity
u èelative increase in erythrocyte count
u Count is normal but there is decrease in volume
u True increase in erythrocyte count
u 

 
:: Prolonged hypoxia


 

u 
 
:: hypoxia of red bone marrow due to cigarette

 

smoking, pulmonary diseases, bone marrow cancer
u r 
u 



:
: Abnormal and excessive production of
erythrocyte precursors. This raises the Hb level and
haematocrit
 G

u TLC less than 4000/mm3

u Granulocytopenia/ neutropenia
u Decreased number of granulocytes
u Caused by either decreased production / increased
clearance
u Extreme shortage is called agranulocytosis
u Temporary decrease can occur due to
inflammation but numbers are rapidly restored
 G

u Vnadequate granulopoesis may be caused due

to
u Cytotoxic drugs
u Vrradiation
u Diseases of red bone marrow
u Severe microbial infection
u Enlargement of spleen
 G


 
G

u Leukemia refers to cancerous conditions involving

white blood precursors by the bone marrow
u Uncontrolled increase in production of leucocytes or
their precursors
u Leukemias are named according to the abnormal
WBCs involved
u Myelocytic leukemia ± involves myeloblasts
u Lymphocytic leukemia ± involves lymphocytes

u Acute leukemia involves blast-

blast-type cells and
primarily affects children
u Chronic leukemia is more prevalent in older people
 G

u Vmmature white blood cells are found in the bloodstream
in all leukemias
u Bone marrow becomes totally occupied with cancerous
leukocytes
u The white blood cells produced, though numerous, are
not functional
u The immature leukaemic blast cells crowd out other
blood cells formed in the bone marrow causing
pancytopenia
u Death is caused by internal hemorrhage and
overwhelming infections
u Treatments include irradiation, antileukemic drugs, and
bone marrow transplants
 G

Causes
u Vonising radiation

u X rays and radioisotopes

u Malignant changes in the DNA of the cells causing
proliferation
u Can occur even 20yrs after exposure
u Chemicals
u Benzene and its derivatives, asbestos
u Genetic factors
 G
M


Classified on basis of cells involved, maturity of cells and

rate of proliferation
u 2

u Sudden onset
u Affects poorly differentiated and immature blast cells
u Tumors are aggressive and there is rapid progression of
disease
u Bone marrow is packed with large number of abnormal cells
u Bone marrow invasion impairs its function as a result
anaemias, hemorrhage and infections occur
 G
M


u 2


 

2ëG
u Proliferation of myeloblasts
u èisk increases with increasing age
u Can be cured

u 2


 

2GG
u Occurs more often in children
u Affects primitive B-
B-lymphocytes
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M


Classified on basis of cells involved, maturity of cells and rate of

proliferation
u ½  

u Less aggressive than acute forms

u Leucocytes are more differentiated

u ½


 

u Onset is gradual

u Can transform into a rapidly progressive stage like AML

u Fatal and death can occur within 5 days

u ½

 
 

u Vnvolves proliferation of B-
B-lymphocytes
u Often seen in elderly
 m
 
 




u Thrombocytopenia

u Vitamin K deficieny

u DVC

u Congenital disorders
 M 


u Thrombocytopenia ± condition where the number of
circulating platelets is deficient (count below 150,000/ mm3)
u Platelet counts less than 50,000/mm3 is diagnostic for this
condition
u Patients show petechiae (small purple blotches on the skin)
due to spontaneous, widespread hemorrhage
u Caused by
u èeduced platelet production: suppression or destruction
of bone marrow (e.g., malignancy, radiation, cytotoxic
drugs)
u Vncreased platelet destruction

u Treated with whole blood transfusions

  

u Generalized bleeding due to increased capillary wall fragility or
thrombocytopenia
u Types
u 2   
  

u Observed in children and young adults

u Triggered by viral infectrions

u Antiplatelet antibodies destroy the platelets by phagocytosis

u  

 
  

u Bone marrow diseases, excessive irradiation

u Some drugs like quinine, sulfonamides

u Vn conditions of enlargement of spleen when platelets are

trapped and destroyed by macrophages

 w 
    

u Hemorrhagic disease of newborns
u Occurs in premature babies

u Spontaneous hemorrhage occurs from the umbilical

cord, gut mucosa ĺ vit K store from mother is
depleted and intestinal bacteria are in the bowel
required for synthesis are not established
u Deficient absorption of vit K
u Obstruction of biliary tract, coeliac disease, liver
disorders
u Dietary deficiency
u Drugs which sterilize the bowel: broad spectrum
antibiotics
 


V 



½

  V½ 
u Disseminated Vntravascular Coagulation (DVC): widespread
clotting in intact blood vessels
u Tiny intravascular clots form and fibrin is deposited in small
blood vessels and internal organs
u As the small clots consume coagulation proteins and platelets,
normal coagulation is disrupted
u Abnormal bleeding occurs from the skin, the git & the respiratory
tract
u The small clots also disrupt normal blood flow to organs
u Most common as:
u A complication of pregnancy (premature separation of
placenta when amniotic fluid enters maternal blood)
u A result of septicemia or incompatible blood transfusions
u Acute pancreatitis (digestive enzymes are released into the
blood)
u Malignant tumors
 m




 
r 
 

u Hemophilias ± hereditary bleeding disorders caused by lack of

clotting factors
u Hemophilia A ± most common type (83% of all cases) due
to a deficiency of factor VVVV
u Hemophilia B ± results from a deficiency of factor VX

u Hemophilia C ± mild type, caused by a deficiency of factor

XV
u èecessive X linked chromosomal disorder
u Symptoms include prolonged bleeding and painful and
disabled joints
u Treatment is with blood transfusions and the injection of
missing factors
 m




 
r 
 

u Hemophilias ± hereditary bleeding disorders caused by lack of

clotting factors
u Hemophilia A ± most common type (83% of all cases) due
to a deficiency of factor VVVV
u Hemophilia B ± results from a deficiency of factor VX

u Hemophilia C ± mild type, caused by a deficiency of factor

XV
u Symptoms include prolonged bleeding and painful and
disabled joints
u Treatment is with blood transfusions and the injection of
missing factors