Axel Patho Lymphoma

Etiolog

Exposure to toxic chemicals o Factory workers o Black hair dye

Risk factors

Idiopathic

Stress Genetic: family history of Lymphoma

Acquisition of self sufficiency growth signal

Disregard normal regulation of cell proliferation

Loss capacity for apoptosis

Circumvent programmed limitations to proliferate

Previous infections o Human T Lymphocytic Virus Type 1 o Epstein Barr virus Medical condition that compromise the immune system: o Patient who undergone tonsillectomy o HIV o Patient with Immunosuppressive therapy o Inherited immunodeficiency

Loss of sensitivity of anti-growth signal

Escape replicative senescence

Avoiding differentiation

Genetically unstable

Mutation inactivates tumor suppressor genes

Mutation inactivates DNA repair gene

Increase mutation rate

Increase growth of oncogenes

Damage DNA Alteration of genetic expression of the cell

Night sweats

Fever

Increase metabolic rate

Changes in the molecular structure of DNA

Chills

Presence of proliferating atypical Reed Sternberg cell in the Lymph Node

Increase body temperature

R-S cells counteracts

Continuous Inflammatory process Continuous activation of lymphoid markers or immune response markers

Production of Cell lines of RS cells L1236 KMCH2

Due to obvious neoplastic growth

CD15 Mediates phagocytosis & chemotaxis

CD25 Activation of T&B lymphocytes

CD30 Increase tumor necrosis factors Regulates Apoptosis

CD40 Co stimulatory protein Enhance release of chemical mediators

CD71 Recognizes Transferin receptor Regulates transport of iron into proliferating cells (Macrophages, B lymphocytes etc.)

BLOCK this mechanism

Cysteinyl Leukotrines Receptor

Slowly progressive defect in humoral and cell-mediated immunity Continuous exhaustion and depletion of normal functioning lymphocytes Weakened immune system Increase proliferation of opportunistic microorganisms  Cough  Diarrhea

Decrease oxygen perfusion

Weakness

Unbalanced/uncontrolled proliferation of multiple cytokines Altered cytokines function in Hematopoiesis

CancerCachexic Syndrome

Uncontrolled decrease stimulation of BM Pluripotent cell and Progenitor cells

 Unexplain ed loss of wt.  Muscle atrophy  weakness

Clonal cytogenetic abnormality of p53 Decrease anticancer mechanism

Altered or Disruption in Hematopoietic process

Mutation and clonal immunoglobulin rearrangements

Release more blocking factors that coat the neoplastic cells (RS cell) Increase resistance of R-S cells to any immune response action

Increase neoplastic growth

Anemia Lymphadenopathy

Increase tumor size

Easy fatigability Swelling/Enlargement of the Lymphnode

Altered Lymphnode function

Lymphatic drainage obstruction

Decrease ability filter and cleanse Lymph

Contributes to bacterial, unusual fungal, viral and protozoal infections

Stagnation of lymph in the interstitial space

Occurrence of fluid shifting

Edema

Bacteremia

Sepsis

DEATH

Acquisition of ability to invade neighboring tissue

Penetrate lymphatic vessels

Enter circulation

Cross the basal lamina and endothelial lining of the vessel Exit circulation

Establish a new cellular colony at distant sites

Infiltration to body organs

Metastatic cells enhance angiogenic signals

Angiogenesis

Deprivation of nourishment to normal cells

Cell death

Metastatic cell overtakes

Infiltrated organs Bone Marrow

Depressed BM activity Altered Hematopoetic function Pancytopenia

Spleen

Liver

Decrease spleen function

Decrease liver function

Decrease ability to store platelets

Unable to conjugate indirect Bilirubin

Decrease mechanical filtration

Systemic absorption

Decrease ability to remove unwanted materials and old RBC Decrease anti infection mechanism

Accumulation in the skin Jaundice

Pruritus