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Diseases of WBC & Lymph Nodes Pathology-B Lab      Ravi A Patel
M++ Hodgkin’s Disease-Spleen TB- Lymph node Non-Hodgkin’s disease Papillary carcinoma  metastatic to lymph node Multiple Myeloma
What is it ?   – NHL represents a monoclonal proliferation of lymphoid cells and be of B-cell origin(70 %) or T-cell origin(30 %). -- The incidence of this tumour increases with age. -- Clinical treatment depends on the grading(reflection of proliferation rate)- Higher the grade, higher the proliferation rate. Organ involved- Lymph node Extra nodal involvement is common– Bone marrow(more common 60% in low grade than high grade disease), gut, thyroid, lung, skin, testis, Brain and rarely bone. Extra nodal involvement is more common in T-cell disease
Clinical manifestation:- -- Lymph node enlargement which may be associated with systemic upset – weight loss, sweats, fever and itching. -- Compression syndromes may occur– GUT obstruction, ascites, superior vena caval obstruction and spinal cord compression.  -- Hepatosplenomegaly may be present. Diagnosis:-  Routine bone marrow aspiration with trephine(surgical instrument  used to make hole in bone) Immunophenotyping of surface antigen to distinguish T & B cell tumours. Immunoglobulin determination Measurement of uric acid level(some  very aggressive high grade NHLs are associated with very high urate levels, which can precipitate Renal failure when treatment is started) HIV testing(Appropriate only if risk factors are present)
Management:-  Asymptomatic patients may not require therapy. Indication of treatment include marked systemic symptoms, lymphadenopathy(causing discomfort), bone marrow failure or compression syndromes. Low grade NHL – following are the options Radiotherapy- used for localized stage 1 disease  which is rare. Chemotherapy(chlorambucil- most patient respond to this) – Main stay therapy Monoclonal antibody therapy- Rituximab showed improvement in 60% of the patients. Marrow Transplantion High Grade NHL- patients with high grade NHL need treatment at initial presentation Chemotherapy(90 % of the patients need this) mainstay  combination intravenous therapy(Cyclophosphamide, doxorubicin, vincristine& prednisolone) Radiotherapy Monoclonal Antibody therapy-Rituximab(increases the survival rate in combination with the Chemotherapy. Marrow Transplantation
HPO Majority of the Tumour cells Have the  Appearance of Small Round  Lymphocytes. But they are irregular And have cleaved  Nuclear outlines
Prolymphocyte (large cell) With a centrally  Placed nucleolus HPO
LPO Diffuse Nodal  Architecture
It is malignancy of B-cell origin.  Histologic hallmark:- Reed sternberg cells(large malignant cells of B-cell origin)
Clinical Manifestation Painless rubbery lymphadenopathy, usually in the  neck or supraclavicular fossae, may fluctuate in size.. Young patients with Nodular sclerosing may have large Mediastinal mass which are surprisingly asymptomatic but may cause dry cough and some breathlessness. Hepatosplenomegaly may be present. Spread is contiguous from one node to other. Rare extra nodal involvement.
Diagnostic investigation:- Full blood count may be completely normal.Anormochromic,normocytic anaemia may be present together with lymphopenia which is a bad prognosis factor. ESR may be raised Renal function tests are required to ensure function is normal prior to treatment. Liver function test may be abnormal. Chest X-ray may show mediastinal mass CT scan of chest and abdoment to permit staging. Lymph node biopsy. ,[object Object],Treatment options include Radiotherapy, chemotherapy or a combination of both.
WHO pathological classification & incidence of Hogkin lymphoma
HPO Apart  From the RS cells Other cellular  Infiltrates like  Lymphocyte are present
HPO
HPO
LPO
Clinical difference
20x 100x H O D G K I N S N O N H O D G K I N S 40x 40x
What is it ? It is a malignant proliferation of plasma cells. Normal plasma cells are derived from B-cells  and produce immunoglobulins which contain heavy and light chains. Normal immunoglobulins are polyclonal which means that a variety of heavy chains are produced and each may kappa or lamba type. In Myeloma plasma cells produce immunoglobulin of  a single heavy and light chain(monoclonal protein called Paraprotein) In some cases only light chain is produced and this appears in the urine as Bencejonesprotenuria.
Pathology:-  Majority of the malignant plasma cells are present in the bone marrow(although some are also present in circulation) The malignant plasma cells produce cytokines which stimulate osteoclasts and result in net bone absorption. The resulting lytic lesions cause bone pain, fractures and hypercalcemia.
Clinical Manifestation  Bone pain/Fractures due to lytic lesions Spinal cord compression Bony collapse Extradural mass Paraproteinemia Immune paresis Bencejonesprotenuria Renal failure Paraprotein deposition Hypercalcemia Infection Amyloid Amyloid Hyperviscosity- Retinal bleeds,Bruising,heartfailure,cerebral ischemia.
Diagnostic investigation Diagnosis of Myeloma requires one of the following criteria Increased malignant plasma cells in the bone marrow Serum and/or urinary paraprotein Skeletal lesions.
Management If patients are asymptomatic treatment may not be required. If symptomatic then measures below should be considered. Immediate support High fluid intake to treat renal impairment and hypercalcemia Analgesia for Bone pain Allopurinol to prevent urate nephropathy Chemotherapy Radiotherapy Marrow transplantation
HPO
HPO
HPO
HPO
LPO
HPO
HPO
Papillary carcinoma is the most common of the malignant thyroid tumours and accounts for 90%  of the irradiation induced thyroid cancer. It may be multifocal and spread to regional lymph nodes. Origin of Tumour:- Follicular cells of Thyroid gland
Papillary Carcinoma metastatic to lymph node From Thyroid gland Lyphoid follicle with germinal center It metastasize evenly
Manifestation Cervical lymphadenopathy With/without thyroid enlargement Diagnosis- Palpable lymph nodes Lymph node biopsy Isotope scanning may be required. Management- usually by  total thyroidectomy
HPO Characterically Orphan annie Nuclei..
Orphan Annie- Nuclei HPO
HPO Psamomma Body
HPO
HPO
HPO
Lymphadenitis is the most frequent form of extra pulmonary  tuberculosis usually occuring in the cervical region(“ Scrofula”) HIV patients always demostrate multifocal disease, systemic symptoms and either pulmonary or other organ involvement due to active tuberculosis. It may take upto 3 year time from initial infection for TB of Lymph nodes, GIT, bones and joints.
Clinical Manifestation Mostly Scrofula(Lymphadenitis of cervical lymph nodes) followed by axillary and inguinal. Nodes are usually painless General observation Weight loss, night sweats and fever. Diagnosis Tuberculin test is strongly positive in these patients. Tissue biopsy  Management-  4 drug therapy Isoniazid, Rifampin, Ethambutol, Pyrizinamide
LPO Granuloma
LPO Granuloma
HPO
HPO
HPO
HPO
Reference Davidson’s Principles and Practice of Medicine Robbins- Basic Pathology
Thanking to the entire Universe Beautiful  Aurora

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Diseases Of Wbc

  • 1. Diseases of WBC & Lymph Nodes Pathology-B Lab Ravi A Patel
  • 2. M++ Hodgkin’s Disease-Spleen TB- Lymph node Non-Hodgkin’s disease Papillary carcinoma metastatic to lymph node Multiple Myeloma
  • 3. What is it ? – NHL represents a monoclonal proliferation of lymphoid cells and be of B-cell origin(70 %) or T-cell origin(30 %). -- The incidence of this tumour increases with age. -- Clinical treatment depends on the grading(reflection of proliferation rate)- Higher the grade, higher the proliferation rate. Organ involved- Lymph node Extra nodal involvement is common– Bone marrow(more common 60% in low grade than high grade disease), gut, thyroid, lung, skin, testis, Brain and rarely bone. Extra nodal involvement is more common in T-cell disease
  • 4. Clinical manifestation:- -- Lymph node enlargement which may be associated with systemic upset – weight loss, sweats, fever and itching. -- Compression syndromes may occur– GUT obstruction, ascites, superior vena caval obstruction and spinal cord compression. -- Hepatosplenomegaly may be present. Diagnosis:- Routine bone marrow aspiration with trephine(surgical instrument used to make hole in bone) Immunophenotyping of surface antigen to distinguish T & B cell tumours. Immunoglobulin determination Measurement of uric acid level(some very aggressive high grade NHLs are associated with very high urate levels, which can precipitate Renal failure when treatment is started) HIV testing(Appropriate only if risk factors are present)
  • 5. Management:- Asymptomatic patients may not require therapy. Indication of treatment include marked systemic symptoms, lymphadenopathy(causing discomfort), bone marrow failure or compression syndromes. Low grade NHL – following are the options Radiotherapy- used for localized stage 1 disease which is rare. Chemotherapy(chlorambucil- most patient respond to this) – Main stay therapy Monoclonal antibody therapy- Rituximab showed improvement in 60% of the patients. Marrow Transplantion High Grade NHL- patients with high grade NHL need treatment at initial presentation Chemotherapy(90 % of the patients need this) mainstay combination intravenous therapy(Cyclophosphamide, doxorubicin, vincristine& prednisolone) Radiotherapy Monoclonal Antibody therapy-Rituximab(increases the survival rate in combination with the Chemotherapy. Marrow Transplantation
  • 6. HPO Majority of the Tumour cells Have the Appearance of Small Round Lymphocytes. But they are irregular And have cleaved Nuclear outlines
  • 7. Prolymphocyte (large cell) With a centrally Placed nucleolus HPO
  • 8. LPO Diffuse Nodal Architecture
  • 9. It is malignancy of B-cell origin. Histologic hallmark:- Reed sternberg cells(large malignant cells of B-cell origin)
  • 10. Clinical Manifestation Painless rubbery lymphadenopathy, usually in the neck or supraclavicular fossae, may fluctuate in size.. Young patients with Nodular sclerosing may have large Mediastinal mass which are surprisingly asymptomatic but may cause dry cough and some breathlessness. Hepatosplenomegaly may be present. Spread is contiguous from one node to other. Rare extra nodal involvement.
  • 11.
  • 12. WHO pathological classification & incidence of Hogkin lymphoma
  • 13. HPO Apart From the RS cells Other cellular Infiltrates like Lymphocyte are present
  • 14. HPO
  • 15. HPO
  • 16. LPO
  • 18. 20x 100x H O D G K I N S N O N H O D G K I N S 40x 40x
  • 19. What is it ? It is a malignant proliferation of plasma cells. Normal plasma cells are derived from B-cells and produce immunoglobulins which contain heavy and light chains. Normal immunoglobulins are polyclonal which means that a variety of heavy chains are produced and each may kappa or lamba type. In Myeloma plasma cells produce immunoglobulin of a single heavy and light chain(monoclonal protein called Paraprotein) In some cases only light chain is produced and this appears in the urine as Bencejonesprotenuria.
  • 20. Pathology:- Majority of the malignant plasma cells are present in the bone marrow(although some are also present in circulation) The malignant plasma cells produce cytokines which stimulate osteoclasts and result in net bone absorption. The resulting lytic lesions cause bone pain, fractures and hypercalcemia.
  • 21. Clinical Manifestation Bone pain/Fractures due to lytic lesions Spinal cord compression Bony collapse Extradural mass Paraproteinemia Immune paresis Bencejonesprotenuria Renal failure Paraprotein deposition Hypercalcemia Infection Amyloid Amyloid Hyperviscosity- Retinal bleeds,Bruising,heartfailure,cerebral ischemia.
  • 22.
  • 23. Diagnostic investigation Diagnosis of Myeloma requires one of the following criteria Increased malignant plasma cells in the bone marrow Serum and/or urinary paraprotein Skeletal lesions.
  • 24.
  • 25. Management If patients are asymptomatic treatment may not be required. If symptomatic then measures below should be considered. Immediate support High fluid intake to treat renal impairment and hypercalcemia Analgesia for Bone pain Allopurinol to prevent urate nephropathy Chemotherapy Radiotherapy Marrow transplantation
  • 26. HPO
  • 27. HPO
  • 28. HPO
  • 29. HPO
  • 30. LPO
  • 31. HPO
  • 32. HPO
  • 33. Papillary carcinoma is the most common of the malignant thyroid tumours and accounts for 90% of the irradiation induced thyroid cancer. It may be multifocal and spread to regional lymph nodes. Origin of Tumour:- Follicular cells of Thyroid gland
  • 34. Papillary Carcinoma metastatic to lymph node From Thyroid gland Lyphoid follicle with germinal center It metastasize evenly
  • 35. Manifestation Cervical lymphadenopathy With/without thyroid enlargement Diagnosis- Palpable lymph nodes Lymph node biopsy Isotope scanning may be required. Management- usually by total thyroidectomy
  • 36. HPO Characterically Orphan annie Nuclei..
  • 39. HPO
  • 40. HPO
  • 41. HPO
  • 42. Lymphadenitis is the most frequent form of extra pulmonary tuberculosis usually occuring in the cervical region(“ Scrofula”) HIV patients always demostrate multifocal disease, systemic symptoms and either pulmonary or other organ involvement due to active tuberculosis. It may take upto 3 year time from initial infection for TB of Lymph nodes, GIT, bones and joints.
  • 43. Clinical Manifestation Mostly Scrofula(Lymphadenitis of cervical lymph nodes) followed by axillary and inguinal. Nodes are usually painless General observation Weight loss, night sweats and fever. Diagnosis Tuberculin test is strongly positive in these patients. Tissue biopsy Management- 4 drug therapy Isoniazid, Rifampin, Ethambutol, Pyrizinamide
  • 46. HPO
  • 47. HPO
  • 48. HPO
  • 49. HPO
  • 50. Reference Davidson’s Principles and Practice of Medicine Robbins- Basic Pathology
  • 51. Thanking to the entire Universe Beautiful Aurora