The document provides an overview of leukemia and lymphoma, detailing types, symptoms, causes, risk factors, diagnostic methods, and treatments. Leukemia is classified into acute and chronic forms based on the maturity of white blood cells involved, while lymphoma includes Hodgkin's and non-Hodgkin's variants. Treatment options vary but commonly include chemotherapy, radiation, and targeted therapies, with specific management strategies based on the leukemia or lymphoma type.

1. PRESENTED BY
Ved prakash panda
M.PHARM(PHARMACOLOGY)

2. CONTENT
 INTRODUCTION
 TYPES
 SYMPTOMS
 CAUSES
 RISK FACTORS
 DIAGNOSTIC METHODS
 TREATMENTS

3. INTRODUCTION
 Leukemia is a group of cancers that usually begin in
the bone marrow and result in high numbers of white
blood cells.
 These white blood cells are not fully developed and are
called blasts or leukemia cells.
 Clinically and pathologically, leukemia is subdivided
into a variety of large groups.
 The first division is between its ACUTE and
CHRONIC forms.

4. Acute leukemia
 Acute leukemia is characterized by a rapid increase in
the number of immature blood cells.
 The crowding that results from such cells makes the
bone marrow unable to produce healthy blood cells.
 Immediate treatment required because of the rapid
progression and accumulation of the malignant cells.
 Most common form of leukemia in children.

5. CHRONIC LEUKEMIA
 It is characterized by the excessive buildup of relatively
mature, but still abnormal, white blood cells.
 Typically taking months or years to progress, the cells
are produced at a much higher rate than normal,
resulting in many abnormal white blood cells.
 Chronic leukemia are monitored for sometimes before
treatment to ensure maximum effectiveness of
therapy.
 Mostly occurs in older people, but can occur in any age
group.

6. SUBDIVISION OF LEUKEMIA
 The diseases are subdivided according to which kind
of blood cell is affected.
 This divides leukemias into lymphoblastic or
lymphocytic leukemias and myeloid or
myelogenous leukemias.
 In lymphoblastic or lymphocytic leukemias, the
cancerous change takes place in a type of marrow cell
that normally goes on to form lymphocytes.
 Most lymphocytic leukemias involve a specific subtype
of lymphocyte, the B-cell.

7.  In myeloid or myelogenous leukemias, the
cancerous change takes place in a type of marrow cell
that normally goes on to form red blood cells, some
other types of white cells, and platelets.
 There are some types of subcategories like hairy cell
leukemia(subset of chronic lymphocytic leukemia), T-
cell prolymphocytic leukemia(very Rare and
aggressive), large granular lymphocytic
leukemia(involve either T-cells or Nk cells, adult T-cell
leukemia (caused by human T- lymphotropic virus),
clonal eosinophilias (mutation in hematopoietic
stem cells).

8. MAJOR TYPES OF LEUKEMIA.
 Acute lymphoblastic leukemia.
 Acute myeloid leukemia.
 Chronic lymphocytic leukemia.
 Chronic myeloid leukemia.

9. ACUTE LYMPHOBLASTIC LEUKEMIA
 Most common type of leukemia in young children.
 It also affects adults, especially those 65 and older.
 Standard treatment involve chemotherapy and
radiotherapy.
 The survival rate vary by age : 85% in children and 50%
in adults.

10. CHRONIC LYMPHOCYTIC LEUKEMIA
 Most often affects adults over the age of 55.
 Sometimes occurs in younger adults, but it almost
never affects children.
 Two-third of affected people are men.
 It is incurable , but there are many effective
treatments.
 The five year survival rate is 75%.

11. ACUTE MYELOGENOUS LEUKEMIA
 It occurs more commonly in adults than in children,
and are more commonly in men than women.
 It is treated with chemotherapy.
 The five year survival rate is 40%.

12. CHRONIC MYELOGENOUS
LEUKEMIA
 It occurs mainly in adults; a very small number of
children also develop this disease.
 It is treated with imatinib (Gleevec in United states,
Gluivec in Europe).
 The five year survival rate is 90%.

13. SYMPTOMS
 Bleeding.
 Bruising.
 Feeling tired.
 Fever.
 Increased risk of infections.
 Pale skin.
 An enlarged spleen.

14. CAUSES
 Mutation in the DNA: can trigger leukemia by activating
oncogenes or deactivating tumor suppressor gene.
 Inherited: genetic predisposition towards leukemia.
Demonstrated by family histories and twin studies.
 Viruses : human T-lymphotropic virus causes adult T-cell
leukemia.
 Radiation: Large doses of Sr-90 emission from nuclear
reactors, increases the risk of bone cancer and leukemia in
animals and in people.
 Non-ionizing radiation: High levels of extremely low
frequency magnetic field energy might cause cases of
childhood leukemia.

15. RISK FACTORS
 Smoking.
 Family history.
 Ionizing radiation.
 Some chemicals.
 Prior chemotherapy.
 Down syndrome.

16. PATHOPHYSIOLOGY
 Sometimes an immature blast cell have two gene
mutations which prevent it from maturing into a
specialized blood cell and cause it to multiply out of
control.
 These immature blast cells crowd the bone marrow
and impair the ability of the to make healthy blood
cells.

17. DIGNOSTIC METHODS
 BLOOD TEST: Complete blood counts(white blood
cell count increases abnormally).
 LYMPH NODE BIOPSY: Performed to diagnose certain
types of leukemia in certain situations.
 BONE MARROW THERAPY: abnormal cell division in
the bone marrow WBC’s amount continues to
increase.
 X-ray (bones),MRI(Brain),Ultrasound(kidney, spleen,
liver).

18. TREATMENT
 Chemotherapy:
 Acute Lymphoblastic/ Acute Myelogenous: to prevent
leukemic cells from spreading to other sites, particularly
the CNS. Treatment divided in several phases:
• Induction therapy(bone marrow remission)
Adults: predinisone, vincristine, and an anthracycline drug.
Children: prednisone, L- asparginase, and vincristine.
• Consolidation therapy or intensification
therapy(eliminate remaining leukemia cells)
Antimetabolite drugs : methroxate and 6- meracaptopurine.

19. Chronic Lymphocytic leukemia
• Primary chemotherapeutic plan,
 Combination therapy with chlorambucil or cyclophosphamide, plus a
corticosteroid such as prednisone or prednisolone.
• In Resistant cases, single agent treatments with nucleoside drugs
such as fludarabine, pentostatin, orcladribine.
 Chronic Myelogenous
• Standard of care of newly diagnosed patient
 imatinab (Gleevec) therapy
 Hairy Cell
• One week of cladribine( i.v) or 6 months of pentostatin, given every 4
weeks by i.v route.
• Other treatments include rituximab infusion or self- injection with
Interferon- alpha.
 T-cell prolymphocytic leukemia
• Purine Analogues( pentostatin, fludarabine, cladribine)
chlorambucil.
• Combination Therapy ( cyclophosphamide, bleomycin VAPEC-B).
• Alemtuzumab( Campath ), a monoclonal antibody.
 BONE MARROW TRANSPLANTATION .

20. LYMPHOMA

21. INTRODUCTION
 Lymphoma is a group of blood cell tumors that develop
from lymphocytes(a type of white blood cell).
 Lymphoma most often spreads to the lungs, liver, and
brain.
 Lymphoma’s symptoms are like enlarged lymph nodes ,
fever, sweat, itching etc.
 The enlarged lymph nodes are usually painless.
 There are two types of lymphomas:
• Hodgkin’s lymphomas
• Non- hodgkin lymphoma.
 About 90% of lymphomas are non-hodgkin lymphomas.

22. HODGKIN’S LYMPHOMAS
 Hodgkin lymphoma is one of the most common
known types of lymphomas.
 A hodgkin lymphoma is marked by the presence of a
type of cell called the reed-sternberg cell.

23. PATHOPHYSIOLOGY
 The pathophysiology of lymphoma refers to the
process or processes going on inside the body that are
sometimes reflected in the signs and symptoms that
are identified as being indicative of lymphoma.
 For example, swollen, painless lymph nodes are a
symptom of lymphoma. Pathophysiology of
lymphoma with this symptoms is that it becomes this
way when cancerous lymphocytes do not die, as they
are supposed to, but rather proliferate and collect at
the lymph nodes.

24.  in follicular lymphoma, it is very common to find that
a specific gene, known as BCL-2, has undergone
chromosomal rearrangement—in other words, a
structural change has occurred to that gene and is
likely the reason it turned cancerous. As it develops,
the pathophysiology of lymphoma often includes
mutations of certain proteins that encode certain
genes, such as p53 and p16. Since the gene encoded by
p53 is a tumor suppressor gene, a mutation in p53 could
mean that the ability of that gene to suppress tumor
development is compromised.

25. SYMPTOMS
 Enlarged lymph nodes Or lymphadenopathy.
 B symptoms (systemic symptoms)- can be associated
with both Hodgkin lymphoma and non-hodgkin
lymphoma. They consist of :
• Fever
• Night Sweats
• Unintended weight loss
• Itching
• Feeling tired/fatigue.
• Anorexia or loss of appetite.

26. RISK FACTORS
 Risk factors for Hodgkin lymphoma include infection
with,
• Epstein-barr virus.
• History of the disease in the family.
 Risk factors for common types of non-Hodgkin
lymphomas include,
• Autoimmune disease.
• HIV/AIDS.
• Infection with human T- lymphotropic virus.
• Immunosuppresant medications.
• Pesticides.
• Tobacco smoking.

27. DIAGNOSTIC METHOD
 Lymph Node Biopsy.
• A partial or total excision of a lymph node examined under the
microscope.
• This examination reveals the histopathology features that may
indicate lymphoma.
• After lymphoma is diagnosed, a variety of tests may be carried
out to look for specific characteristic of different types of
lymphoma. These includes :
• Immunophenotyping (study the protein expressed by cells).
• Flow cytometry (simultaneous multiparametric analysis of the
physical and chemical characteristics of up to thousands of
particles per second).
• Fluorescence in situ hybridization testing.(to detect and
localize the presence or absence of specific DNA sequences on
chromosomes ).

28. TREATMENT
 Treatment may involve chemotherapy, medication,
radiation therapy and rarely stem-cell transplant.
 Medications
 Chemotherapy,
 Bone marrow stimulant,
 Steroid, and Blood transfusion
 Surgery
 Autotransplantation

29. REFERENCE
 Clinical pharmacy and therapeutics, Roger Walker
 Rang & Dale’s pharmacology
 Essential of medical pharmacology, K D Tripathi
 www.Google.com