Blood andIts Components
(Part - 2)
By: Dr. Arun Panwar
WHITEBLOOD CELLS
Leucocytes (WBC’s)
Functions
• Neutrophils: Phagocytosis of Organisms
• Eosinophils: Combat the effect of histamine in
allergic reactions, kill parasitic worms.
• Basophils: Release heparin, histamine and
serotonin in allergic reactions that promote
overall inflammatory response.
• Monocytes: Phagocytosis( after transforming
into macrophages)
• Lymphocyte: Mediate immune responses
Classification
• 1. Granulocytes-with granules
– Neutrophils,
– Eosinophils and
– Basophils
• 2. Agranulocytes-without granules.
– Monocytes and
– Lymphocytes
Normal range of WBC
Blood and its components Part 2
Blood and its components Part 2
Blood and its components Part 2
Blood and its components Part 2
Blood and its components Part 2
Blood and its components Part 2
Neutrophils
NEUTROPHILS
ļ‚§ Their main function is to
recognise, ingest and destroy
foreign particles and
microorganisms.
ļ‚§ Everyday 1011
neutrophils
enter the circulation.
ļ‚§ They spend 6-10 hours in the
circulation before being
removed, mostly by the spleen
ļ‚§ Alternatively, they pass into
the inflammatory process or
undergo apoptotic cell death
and phagocytosis by
macrophages.
• Size : 10- 14 µ diameter
• Nucleus: Usually multilobed
• Cytoplasm : Fine pink granules
Neutrophilia
Depression
Exercise
lactation
pregnancy
Infections, especially bacterial
Acute haemorrhage,
Burn, trauma, shock
Leukemia
Stress, Smoking
Neutropenia
Typhoid,
paratyphoid
HIV infection
Aplastic anemia
Hypersplenism
Viruses: Measles,
Influenza
Marrow infiltration
Sepsis
Drugs That Induce Neutropenia
Eosinophils
red, have
• Size : 10- 14 µ diameter
• Nucleus : purple, bilobed
• Cytoplasm : acidophilic
• Granules : coarse, bright
lysozymes
– Major basic proteins (MBP)
– Eosinophil peroxidase
– Eosinophilic cationic proteins (ECP)-
neurotoxin
Life span : 7-12 days
Normal Eosinophil arrowed with normal
neutrophil.
Eosinophilia:
• Allergic conditions: Bronchial
asthma, urticaria
• Parasitic infections: Ascariasis,
filariasis,
• Pulmonary eosinophilia
• Addison’s disease
• Langerhan’s cell histiocytoses
Eosionopenia:
• Cushing’s syndrome
• Aplastic Anemia
• Steroid therapy
Eosinophils from a case
of Hypereosinophilic
syndrome
Hypereosinophlic syndrome
• Persistent elevation of the eosinophil count
(>1.5x109
) of uncertain cause for more
than 6 months.
• Treatment initially with steroids and then with
cytotoxic drugs if these fail.
Basophils
• Size
• Nucleus
: 8-10 µ diameter
: bilobed, Sshaped
lenty,
• Cytoplasm : basophilic,granular
• Granules : coarse, purple/ blue,p
Secrete:
– Histamine
– Tryptase
– Esoniphil chemotactic factor
of anaphylaxis (ECF-A)
• Life span : 12-15days
• Functions :
- produce hypersensitivity reaction like
allergy and anaphylaxsis
-- mild phagocytosis
Basophilia
Chicken pox
Small pox
Polycythemia
Iron deficiency
Chronicmyeloid
leukemia
Basopenia
•Steroid therapy
•Cushing’s
syndrome
•Hyperthyroidism
Monocytes
: 14- 18 µ diameter (largest)
: pale , round/kidney shaped
• Size
• Nucleus
• Cytoplasm : termed agranular but fine
pale blue granules are present
• Life span : 48-72 hrs in blood & 3
months in tissues.
Functions :
-2nd
line of defense
-Are phagocytic
-Secrete IL-1
MONOCYTES
Monocytopenia:
• Aplastic anemia
• Septicemia
Monocystosis:
• Acute monocystic leukemia
• Hodgkin’s disease
• Malaria
• Glucocorticoid therapy
Lymphocytes
• Can be classified in two ways
– Based on size:
a) large : 10-12 µ
b) small : 7-10 µ
– Based on function:
a) T Lymphocytes
b) B Lymphocytes
• Life span : ½-1 day
Small lymphocyte
Large lymphocyte
• Normal Lymphocyte count is 20 – 40% of total
leucocytes
• Absolute cunt is 500 – 800 per cu mm of blood
Functionally lymphocytes are divided into:
• B cells: mediate humoral or antibody
mediated immunity
• T cells: mediate cellular or cell mediated
immunity
• NK cells: mediate natural and nonspecific
immunity
• Small Lymphocytes:
• Constitute- 20 – 50% of total lymphocytes
• Cell are 6 – 9 um in diameter
• Nucleus: Ovoid or Kidney shaped
• Large Lymphocytes:
• Constitute: 50 – 80% of total lymphocytes
• Size: 10 – 15 um in diameter
• Nucleus: Oval and eccentrically placed
Causes for Lymphocytosis:
• Acute lymphocytic leukemia
• Chronic lymphocytic leukemia
• Infectious mononucleosis
• Tuberculosis
• Postsplenectomy
Lymphocytopenia:
• AIDS
• Aplastic anemia
• Hepatitis
• Glucocorticoid therapy
Pathological Variations
Blood and its components Part 2
Blood and its components Part 2
Leukemia
ā–Ŗ It is malignant neoplasia of hemopoetic
cells in which there is abnormal
proliferation of leucocytes and their
precursors.
ā–Ŗ Due to impaired differentiation,
regulation and programmed cell death
ā–Ŗ Immature WBCs in the circulating blood
ā–Ŗ Increased susceptibility to infection &
bleeding
Classification:
• Based on clinical behaviour: Acute/ Chronic
• Based on primary hematopoietic cell line:
Myeloid /Lymphoid
Four principal diagnostic categories:
• Acute myelogenous leukemia
• Acute lymphocytic leukemia
• Chronic myelogenous leukemia
• Chronic lymphocytic leukemia
WHOclassification of Acute Leukemia
69
AcuteLeukemia
• There is a failure of cell maturation in acute
leukemia.
• Proliferation of cells which do not mature
leads to an accumulation of primitive cells
which take up more and more marrow
space at the expense of normal
haematopoietic elements.
• Acute lymphoblastic leukemia (ALL) is 4
time more common in children than in
adults.
• Clinical features are similar to those of
bone marrow failure.
Chronic Leukemia
• Chronic myeloid leukemia accounts for 20% of
all cases.
• Between 30 – 60 years of age
• Outstanding physical sign :
• CML- splenomegaly, lymphadenopathy (rare)
• Marked elevation of leucocyte count
• CLL- Lymphadenopathy, splenomagaly (rare)
• Mild
Blood and its components Part 2
ClinicalFeatures
• Anaemia – weakness and lethargy
• Leucopenia – infections
• Thrombocytopenia – purpura and
bleeding
• Bone and joint pain may occur
• Lymphadenoapthy and
hepatosplenomegaly are frequent
• CNS presentation is rare at though
common at late stages of the disease.
Management
– Remission Induction:
Last for 28 days
3-4 Drugs( Vincristine, Prednisone, L-asparaginase)
– CNS Preventive therapy/Prophylaxis
CNS – site for leukemic infiltrates
Chemotherapeutic Drugs – Cross BBB
Intrathecal injection - Methotrexate
– Maintenance
Suppress leukemic growth- Cont. admin Methotrexate & 6-
mercaptopurine
Summary
• WAYS TO MAINTAIN YOUR WBC’S:
• Avoid sugar and keep sweet stuff to a minimum. Sugar
prevents white blood cells from being their strongest
• Eliminate unhealthy fats. Polyunsaturated fats in
vegetable oils such as corn, safflower, and sunflower oil
are deterrents to a healthy immune system .
• Drink plenty of water to boost the immune system as
well as flush out.
• Avoid stress and try to relax. Stress is rightly called the
silent killer and too much stress invariably leads to a
lowered immune system.
• Leukemoid reaction
• A leukemoid reaction is an increase in the
white blood cell count, which can
mimic leukemia. The reaction is actually due
to an infection or another disease and is not a
sign of cancer.
• Blood counts often return to normal when
the underlying condition is treated.
• Tuberculosis
• Infectious mononucleosis
• In aleukemic leukemia, increased number of
white blood cells is not detected in a blood
test.
• It is a rare type of leukemia. This type of
leukemia can also be lymphocytic, monocytic,
or myelogenous.
• Hairy cell leukemia is a rare, slow-growing cancer
of the blood in which your bone marrow makes
too many B cells (lymphocytes).
• These excess B cells are abnormal and look
"hairy" under a microscope. As the number of
leukemia cells increases, fewer healthy white
blood cells, red blood cells and platelets are
produced.
• Hairy cell leukemia affects more men than
women, and it occurs most commonly in middle-
aged or older adults.
• Etiology of leukemia:
• Involves a combination of genetic and environmental
factors.
• Leukemia cells acquire mutations in their DNA that
cause them to grow abnormally and lose functions of
typical white blood cells.
• One type of change in the cells' DNA that is common in
leukemias is known as a chromosome translocation. In
this process, a portion of one chromosome breaks off
and attaches to a different chromosome.
• Translocation seen in almost all cases of CML and in
sometimes in other types of leukemia is an exchange
of DNA between chromosomes 9 and 22, which leads
to what is known as the Philadelphia chromosome.
This creates an oncogene (cancer-promoting gene)
known as BCR-ABL.
• A condition known as Li-Fraumeni syndrome is characterized by an
inherited mutation in a tumor suppressor gene known as TP53,
and individuals with this condition have an increased risk of
leukemia and other cancers.
• Other hereditary conditions that can increase the risk of developing
leukemia include Down syndrome, neurofibromatosis type 1, ataxia
telangiectasia, and Noonan syndrome.
• Exposure to radiation is known to increase the risk of developing
AML, CML, or ALL. Increases in leukemia were observed in people
surviving atomic bombs. Radiation therapy for cancer can also
increase the risk of leukemia.
• Exposure to certain chemicals, including benzene (used commonly
in the chemical industry), increases the risk of leukemia. Cigarette
smoking is known to increase the risk of developing AML.
• Blood disorders known as myelodysplastic
syndromes confer an increased risk of
developing AML.
• Human T-cell leukemia virus type 1 (HTLV-1)
is a virus that causes a rare type of leukemia.
• Certain chemotherapy drugs for cancer can
increase the risk for AML or ALL.
Lazy leukocyte syndrome
• Characterized by
• recurrent infections,
• stomatitis,
• a low neutrophil count, and
• impaired neutrophil motility,2-5 a
• Etiology: mutations in actin-interacting protein 1 (Aip1)
• Lazy leukocyte syndrome is a severe neutropenia with associated
abnormal neutrophil motility.
• The marked increase in neutrophil actin filament content, failure of
these cells to form a normal polar structures with lamellipodia at
the front, and the marked slowing of cell motility in response to
chemoattractants.
• Mechanisms listed below may be involved in
mediating the effects of dietary fat on immune
Response (IR):
• Serum lipoproteins. Both the concentration and
composition of dietary fat (fatty acids as well
cholesterol) can alter serum lipoprotein profile, which
influences the activity of the immune cells.
• Low-density lipoproteins (LDL) inhibited lymphocyte
and neutrophil functions, while high-density
lipoproteins (HDL) enhanced neutrophil chemotaxis
and phagocytosis.
• One of the mechanisms by which LDL inhibits
lymphocyte and monocyte functions is through apolipo
proteins B and E (apo B and E).
• The primary issue with Poly Unsaturated Fatty Acids is that they are highly
unstable.
• All fats have a temperature with which they oxidize (i.e. become unstable,
go rancid, become toxic).
• For PUFAs that temperature is very low. An easy way to remember this is
that UNsaturated fats are UNstable and Saturated fats are Stable.
• Unstable fats are prone to oxidation. Oxidation lead to free radicals.
• Free radicals lead to cellular damage in body that can manifest both
internally in the form of damaged organs/glands and externally in the
form of rapidly aging skin.
• During processing, many of these "seed" oils are exposed to high heat
(imagine trying to extract oil from a grape seed), which can often make the
oils unstable. In addition, these oils may be exposed to high heat during
travel which can also lead to a damaged and unstable product.
Classification
ALL can be classified into 3 types on
morphological criteria (FAB
classification)
L1: most cells are small with little cytoplasm
and indistinct nucleoli.
L2: cells tend to be larger with relatively
more cytoplasm. Nuclei often clefted with
prominent nucleoli.
L3: large blasts with very blue cytoplasm
with prominent vacuoles. These blasts are
like found in Burkitt’s lymphoma.
Thank You 

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Blood and its components Part 2

  • 1. Blood andIts Components (Part - 2) By: Dr. Arun Panwar
  • 4. Functions • Neutrophils: Phagocytosis of Organisms • Eosinophils: Combat the effect of histamine in allergic reactions, kill parasitic worms. • Basophils: Release heparin, histamine and serotonin in allergic reactions that promote overall inflammatory response. • Monocytes: Phagocytosis( after transforming into macrophages) • Lymphocyte: Mediate immune responses
  • 5. Classification • 1. Granulocytes-with granules – Neutrophils, – Eosinophils and – Basophils • 2. Agranulocytes-without granules. – Monocytes and – Lymphocytes
  • 13. Neutrophils NEUTROPHILS ļ‚§ Their main function is to recognise, ingest and destroy foreign particles and microorganisms. ļ‚§ Everyday 1011 neutrophils enter the circulation. ļ‚§ They spend 6-10 hours in the circulation before being removed, mostly by the spleen ļ‚§ Alternatively, they pass into the inflammatory process or undergo apoptotic cell death and phagocytosis by macrophages. • Size : 10- 14 µ diameter • Nucleus: Usually multilobed • Cytoplasm : Fine pink granules
  • 14. Neutrophilia Depression Exercise lactation pregnancy Infections, especially bacterial Acute haemorrhage, Burn, trauma, shock Leukemia Stress, Smoking Neutropenia Typhoid, paratyphoid HIV infection Aplastic anemia Hypersplenism Viruses: Measles, Influenza Marrow infiltration Sepsis
  • 15. Drugs That Induce Neutropenia
  • 16. Eosinophils red, have • Size : 10- 14 µ diameter • Nucleus : purple, bilobed • Cytoplasm : acidophilic • Granules : coarse, bright lysozymes – Major basic proteins (MBP) – Eosinophil peroxidase – Eosinophilic cationic proteins (ECP)- neurotoxin Life span : 7-12 days Normal Eosinophil arrowed with normal neutrophil.
  • 17. Eosinophilia: • Allergic conditions: Bronchial asthma, urticaria • Parasitic infections: Ascariasis, filariasis, • Pulmonary eosinophilia • Addison’s disease • Langerhan’s cell histiocytoses Eosionopenia: • Cushing’s syndrome • Aplastic Anemia • Steroid therapy Eosinophils from a case of Hypereosinophilic syndrome
  • 18. Hypereosinophlic syndrome • Persistent elevation of the eosinophil count (>1.5x109 ) of uncertain cause for more than 6 months. • Treatment initially with steroids and then with cytotoxic drugs if these fail.
  • 19. Basophils • Size • Nucleus : 8-10 µ diameter : bilobed, Sshaped lenty, • Cytoplasm : basophilic,granular • Granules : coarse, purple/ blue,p Secrete: – Histamine – Tryptase – Esoniphil chemotactic factor of anaphylaxis (ECF-A) • Life span : 12-15days
  • 20. • Functions : - produce hypersensitivity reaction like allergy and anaphylaxsis -- mild phagocytosis Basophilia Chicken pox Small pox Polycythemia Iron deficiency Chronicmyeloid leukemia Basopenia •Steroid therapy •Cushing’s syndrome •Hyperthyroidism
  • 21. Monocytes : 14- 18 µ diameter (largest) : pale , round/kidney shaped • Size • Nucleus • Cytoplasm : termed agranular but fine pale blue granules are present • Life span : 48-72 hrs in blood & 3 months in tissues. Functions : -2nd line of defense -Are phagocytic -Secrete IL-1 MONOCYTES
  • 22. Monocytopenia: • Aplastic anemia • Septicemia Monocystosis: • Acute monocystic leukemia • Hodgkin’s disease • Malaria • Glucocorticoid therapy
  • 23. Lymphocytes • Can be classified in two ways – Based on size: a) large : 10-12 µ b) small : 7-10 µ – Based on function: a) T Lymphocytes b) B Lymphocytes • Life span : ½-1 day Small lymphocyte Large lymphocyte
  • 24. • Normal Lymphocyte count is 20 – 40% of total leucocytes • Absolute cunt is 500 – 800 per cu mm of blood Functionally lymphocytes are divided into: • B cells: mediate humoral or antibody mediated immunity • T cells: mediate cellular or cell mediated immunity • NK cells: mediate natural and nonspecific immunity
  • 25. • Small Lymphocytes: • Constitute- 20 – 50% of total lymphocytes • Cell are 6 – 9 um in diameter • Nucleus: Ovoid or Kidney shaped • Large Lymphocytes: • Constitute: 50 – 80% of total lymphocytes • Size: 10 – 15 um in diameter • Nucleus: Oval and eccentrically placed
  • 26. Causes for Lymphocytosis: • Acute lymphocytic leukemia • Chronic lymphocytic leukemia • Infectious mononucleosis • Tuberculosis • Postsplenectomy Lymphocytopenia: • AIDS • Aplastic anemia • Hepatitis • Glucocorticoid therapy
  • 30. Leukemia ā–Ŗ It is malignant neoplasia of hemopoetic cells in which there is abnormal proliferation of leucocytes and their precursors. ā–Ŗ Due to impaired differentiation, regulation and programmed cell death ā–Ŗ Immature WBCs in the circulating blood ā–Ŗ Increased susceptibility to infection & bleeding
  • 31. Classification: • Based on clinical behaviour: Acute/ Chronic • Based on primary hematopoietic cell line: Myeloid /Lymphoid Four principal diagnostic categories: • Acute myelogenous leukemia • Acute lymphocytic leukemia • Chronic myelogenous leukemia • Chronic lymphocytic leukemia
  • 33. AcuteLeukemia • There is a failure of cell maturation in acute leukemia. • Proliferation of cells which do not mature leads to an accumulation of primitive cells which take up more and more marrow space at the expense of normal haematopoietic elements. • Acute lymphoblastic leukemia (ALL) is 4 time more common in children than in adults. • Clinical features are similar to those of bone marrow failure.
  • 34. Chronic Leukemia • Chronic myeloid leukemia accounts for 20% of all cases. • Between 30 – 60 years of age • Outstanding physical sign : • CML- splenomegaly, lymphadenopathy (rare) • Marked elevation of leucocyte count • CLL- Lymphadenopathy, splenomagaly (rare) • Mild
  • 36. ClinicalFeatures • Anaemia – weakness and lethargy • Leucopenia – infections • Thrombocytopenia – purpura and bleeding • Bone and joint pain may occur • Lymphadenoapthy and hepatosplenomegaly are frequent • CNS presentation is rare at though common at late stages of the disease.
  • 37. Management – Remission Induction: Last for 28 days 3-4 Drugs( Vincristine, Prednisone, L-asparaginase) – CNS Preventive therapy/Prophylaxis CNS – site for leukemic infiltrates Chemotherapeutic Drugs – Cross BBB Intrathecal injection - Methotrexate – Maintenance Suppress leukemic growth- Cont. admin Methotrexate & 6- mercaptopurine
  • 38. Summary • WAYS TO MAINTAIN YOUR WBC’S: • Avoid sugar and keep sweet stuff to a minimum. Sugar prevents white blood cells from being their strongest • Eliminate unhealthy fats. Polyunsaturated fats in vegetable oils such as corn, safflower, and sunflower oil are deterrents to a healthy immune system . • Drink plenty of water to boost the immune system as well as flush out. • Avoid stress and try to relax. Stress is rightly called the silent killer and too much stress invariably leads to a lowered immune system.
  • 39. • Leukemoid reaction • A leukemoid reaction is an increase in the white blood cell count, which can mimic leukemia. The reaction is actually due to an infection or another disease and is not a sign of cancer. • Blood counts often return to normal when the underlying condition is treated. • Tuberculosis • Infectious mononucleosis
  • 40. • In aleukemic leukemia, increased number of white blood cells is not detected in a blood test. • It is a rare type of leukemia. This type of leukemia can also be lymphocytic, monocytic, or myelogenous.
  • 41. • Hairy cell leukemia is a rare, slow-growing cancer of the blood in which your bone marrow makes too many B cells (lymphocytes). • These excess B cells are abnormal and look "hairy" under a microscope. As the number of leukemia cells increases, fewer healthy white blood cells, red blood cells and platelets are produced. • Hairy cell leukemia affects more men than women, and it occurs most commonly in middle- aged or older adults.
  • 42. • Etiology of leukemia: • Involves a combination of genetic and environmental factors. • Leukemia cells acquire mutations in their DNA that cause them to grow abnormally and lose functions of typical white blood cells. • One type of change in the cells' DNA that is common in leukemias is known as a chromosome translocation. In this process, a portion of one chromosome breaks off and attaches to a different chromosome. • Translocation seen in almost all cases of CML and in sometimes in other types of leukemia is an exchange of DNA between chromosomes 9 and 22, which leads to what is known as the Philadelphia chromosome. This creates an oncogene (cancer-promoting gene) known as BCR-ABL.
  • 43. • A condition known as Li-Fraumeni syndrome is characterized by an inherited mutation in a tumor suppressor gene known as TP53, and individuals with this condition have an increased risk of leukemia and other cancers. • Other hereditary conditions that can increase the risk of developing leukemia include Down syndrome, neurofibromatosis type 1, ataxia telangiectasia, and Noonan syndrome. • Exposure to radiation is known to increase the risk of developing AML, CML, or ALL. Increases in leukemia were observed in people surviving atomic bombs. Radiation therapy for cancer can also increase the risk of leukemia. • Exposure to certain chemicals, including benzene (used commonly in the chemical industry), increases the risk of leukemia. Cigarette smoking is known to increase the risk of developing AML.
  • 44. • Blood disorders known as myelodysplastic syndromes confer an increased risk of developing AML. • Human T-cell leukemia virus type 1 (HTLV-1) is a virus that causes a rare type of leukemia. • Certain chemotherapy drugs for cancer can increase the risk for AML or ALL.
  • 45. Lazy leukocyte syndrome • Characterized by • recurrent infections, • stomatitis, • a low neutrophil count, and • impaired neutrophil motility,2-5 a • Etiology: mutations in actin-interacting protein 1 (Aip1) • Lazy leukocyte syndrome is a severe neutropenia with associated abnormal neutrophil motility. • The marked increase in neutrophil actin filament content, failure of these cells to form a normal polar structures with lamellipodia at the front, and the marked slowing of cell motility in response to chemoattractants.
  • 46. • Mechanisms listed below may be involved in mediating the effects of dietary fat on immune Response (IR): • Serum lipoproteins. Both the concentration and composition of dietary fat (fatty acids as well cholesterol) can alter serum lipoprotein profile, which influences the activity of the immune cells. • Low-density lipoproteins (LDL) inhibited lymphocyte and neutrophil functions, while high-density lipoproteins (HDL) enhanced neutrophil chemotaxis and phagocytosis. • One of the mechanisms by which LDL inhibits lymphocyte and monocyte functions is through apolipo proteins B and E (apo B and E).
  • 47. • The primary issue with Poly Unsaturated Fatty Acids is that they are highly unstable. • All fats have a temperature with which they oxidize (i.e. become unstable, go rancid, become toxic). • For PUFAs that temperature is very low. An easy way to remember this is that UNsaturated fats are UNstable and Saturated fats are Stable. • Unstable fats are prone to oxidation. Oxidation lead to free radicals. • Free radicals lead to cellular damage in body that can manifest both internally in the form of damaged organs/glands and externally in the form of rapidly aging skin. • During processing, many of these "seed" oils are exposed to high heat (imagine trying to extract oil from a grape seed), which can often make the oils unstable. In addition, these oils may be exposed to high heat during travel which can also lead to a damaged and unstable product.
  • 48. Classification ALL can be classified into 3 types on morphological criteria (FAB classification) L1: most cells are small with little cytoplasm and indistinct nucleoli. L2: cells tend to be larger with relatively more cytoplasm. Nuclei often clefted with prominent nucleoli. L3: large blasts with very blue cytoplasm with prominent vacuoles. These blasts are like found in Burkitt’s lymphoma.