WBC Pathoma Flashcards
Neutropenia
Pathology:
Causes:
Path:
Decreased circulating neutrophils
Causes:
1) Drugs (Chemo & alkylating agents)
2) Gram -ve sepsis
Path:
Decreased circulating neutrophils
Causes:
1) Drugs (Chemo & alkylating agents)
2) Gram -ve sepsis
Neutropenia
Lymphopenia
Pathology:
Causes:
Path:
Decreased circulating lymphocytes
Causes:
1) DiGeorge syndrome or HIV
2) exogenous corticosteroids or Cushing syndrome
3) SLE
4) Radiation
Path:
Decreased circulating lymphocytes
Causes:
1) DiGeorge syndrome or HIV
2) exogenous corticosteroids or Cushing syndrome
3) SLE
4) Radiation
Lymphopenia
INFECTIOUS MONONUCLEOSIS (IM)
Pathology:
Symptoms/Signs:
Causes:
Labs/Histological findings:
Complications
Path:
lymphocytic leukocytosis with reactive CD8+ T cells
Signs:
1) Pharyngitis
2) Hepatitis & Hepatomegaly
3) Splenomegaly
4) Generalized lymphadenopathy
Causes:
1) EBV (saliva #1)
2) CMV
Labs/Histo:
1) Monospot test detects IgM Abs that cross react with horse/sheep blood aka heterophile Abs(-ve test =CMV)
2) High WBC
Complication:
1) Splenic rupture
2) Rash with amoxicillin
3) Recurrence & B cell lymphoma
Path:
lymphocytic leukocytosis with reactive CD8+ T cells
Signs:
1) Pharyngitis
2) Hepatitis & Hepatomegaly
3) Splenomegaly
4) Generalized lymphadenopathy
Causes:
1) EBV (saliva #1)
2) CMV
Labs/Histo:
1) Monospot test detects IgM Abs that cross react with horse/sheep blood aka heterophile Abs(-ve test =CMV)
2) High WBC
Complication:
1) Splenic rupture
2) Rash with amoxicillin
3) Recurrence & B cell lymphoma
INFECTIOUS MONONUCLEOSIS (IM)
B-ALL
Pathology:
Lab findings:
Prognosis:
Path:
The most common type of ALL (neoplastic accumulation of lymphoblasts in bone marrow)
Labs:
lymphoblasts
(TdT+) that express CD10, CD19, and
CD20
Prognosis:
t(l2;2l) = good prognosis (Children)
t(9;22) = poor prognosis (adults aka philadelphia)
T-ALL
Pathology:
Lab findings:
Prognosis:
Path:
type of ALL (neoplastic accumulation of lymphoblasts in bone marrow) that affects teens as a mediastinal (thymic mass)
Labs:
lymphocytes with (TdT+) CD2 to CDS (e.g., CD3, CD4, CD7)
Path:
The most common type of ALL (neoplastic accumulation of lymphoblasts in bone marrow)
Labs:
lymphoblasts
(TdT+) that express CD10, CD19, and
CD20
Prognosis:
t(l2;2l) = good prognosis (Children)
t(9;22) = poor prognosis (adults aka philadelphia)
B-ALL
Path:
type of ALL (neoplastic accumulation of lymphoblasts in bone marrow) that affects teens as a mediastinal (thymic mass)
Labs:
lymphocytes with (TdT+) CD2 to CDS (e.g., CD3, CD4, CD7)
T-ALL
“Thymic-Teens Accumulate lots of Lymphocytes”
Acute Myeloid Leukemia
Pathology:
Lab findings:
Path:
Neoplastic accumulation of myeloblasts (> 20%) in the bone marrow, usually characterized by MPO staining
Older adults with average age of 50-60 years
Labs:
Auer rods (+ve MPo)
Path:
Neoplastic accumulation of myeloblasts (> 20%) in the bone marrow, usually characterized by MPO staining
Older adults with average age of 50-60 years
Labs:
Auer rods (+ve MPo)
Acute Myeloid Leukemia
Acute Promyelocytic Leukemia (APL)
Pathology:
Treatment:
“APT = Abnormal Promyelocytes & Translocation”
Path:
characterized by t(15;17) translocation leading to abnormal promyelocytes
Treatment with all-trans-retinoic acid (ATRA) to induce maturation and cell death
Path:
characterized by t(15;17) translocation leading to abnormal promyelocytes
Treatment with all-trans-retinoic acid (ATRA) to induce maturation and cell death
Acute Promyelocytic Leukemia (APL)
Acute Monocytic Leukemia:
Path:
proliferation of monoblasts, may infiltrate gums
Path:
proliferation of monoblasts, may infiltrate gums
Acute Monocytic Leukemia:
Acute Megakaryoblastic Leukemia:
proliferation of megakaryoblasts, associated with Down syndrome
proliferation of megakaryoblasts, associated with Down syndrome
Acute Megakaryoblastic Leukemia:
AML from Pre-Existing Dysplasia
Pathology:
Symptoms/Signs:
Complications:
Path: May arise from myelodysplastic syndromes, (exposure alkylating agents or radiotherapy)
Signs:
1) cytopenia’s
2) hypercellular bone marrow
3) abnormal cell maturation
4) increased blasts (< 20%)
Complication
1) Death from infection or bleeding
2) Progression to acute leukemia
Path: May arise from myelodysplastic syndromes, (exposure alkylating agents or radiotherapy)
Signs:
1) cytopenia’s
2) hypercellular bone marrow
3) abnormal cell maturation
4) increased blasts (< 20%)
Complication
1) Death from infection or bleeding
2) Progression to acute leukemia
AML from Pre-Existing Dysplasia
Chronic Lymphocytic Leukemia (CLL)
Pathology:
Symptoms/Signs:
Lab findings:
Complications
Path:
Neoplastic proliferation of CD5 and CD20 co-expressing naive B cells,
Signs:
1) generalized lymphadenopathy (small lymphocytic lymphoma)
Labs:
Blood smear shows increased lymphocytes and smudge cells
Complications:
1)Hypogammaglobulinemia
2) Autoimmune hemolytic anemia
3) Transformation to diffuse large B-cell
lymphoma (Richter transformation) marked by enlargement of lymph node or spleen
Path:
Neoplastic proliferation of CD5 and CD20 co-expressing naive B cells,
Signs:
1) generalized lymphadenopathy (small lymphocytic lymphoma)
Labs:
Blood smear shows increased lymphocytes and smudge cells
Complications:
1)Hypogammaglobulinemia
2) Autoimmune hemolytic anemia
3) Transformation to diffuse large B-cell
lymphoma (Richter transformation) marked by enlargement of lymph node or spleen
Chronic Lymphocytic Leukemia (CLL)
Hairy Cell Leukemia
Pathology:
Symptoms/Signs:
Lab findings
Treatments:
Path:
Neoplastic proliferation of mature B cells with hairy cytoplasmic processes
Signs:
1) splenomegaly
2) “dry tap” on bone marrow aspiration
(NO lymphadenopathy)
Labs:
Cells are TRAP-positive
Treatments:
1) 2-CDA (cladribine)
2) an adenosine deaminase inhibitor (accumulates adenosine to toxic levels in neoplastic cells)
Path:
Neoplastic proliferation of mature B cells with hairy cytoplasmic processes
Signs:
1) splenomegaly
2) “dry tap” on bone marrow aspiration
(NO lymphadenopathy)
Labs:
Cells are TRAP-positive
Treatments:
1) 2-CDA (cladribine)
2) an adenosine deaminase inhibitor (accumulates adenosine to toxic levels in neoplastic cells)
Hairy Cell Leukemia
Adult T-Cell Leukemia/Lymphoma (ATLL)
Pathology:
Symptoms/Signs
Path:
Neoplastic proliferation of mature CD4+ T cells
Associated with HTLV-(Japan and the Caribbean)
Signs:
1) Rash
2) Lymphadenopathy
3) Hepatosplenomegaly,
4) Lytic bone lesions with hypercalcemia
Path:
Neoplastic proliferation of mature CD4+ T cells
Associated with HTLV-(Japan and the Caribbean)
Signs:
1) Rash
2) Lymphadenopathy
3) Hepatosplenomegaly,
4) Lytic bone lesions with hypercalcemia
Adult T-Cell Leukemia/Lymphoma (ATLL)
Mycosis Fungoides
Pathology/Symptoms:
Lab findings:
Pathology/Signs:
Neoplastic proliferation of mature CD4+ T cells in the skin, causing rash, plaques, and nodules
Lab findings:
1) Pautrier micro abscesses (Aggregates of neoplastic cells in the epidermis)
Complication:
Sezary syndrome
Pathology/Signs:
Neoplastic proliferation of mature CD4+ T cells in the skin, causing rash, plaques, and nodules
Lab findings:
1) Pautrier micro abscesses (Aggregates of neoplastic cells in the epidermis)
Complication:
Sezary syndrome
Mycosis Fungoides
Sezary Syndrome
Pathology:
Lab findings:
Path:
Blood involvement of neoplastic cells from mycosis fungoides
Labs:
Sezary cells with cerebriform nuclei seen on blood smear
Path:
Blood involvement of neoplastic cells from mycosis fungoides
Labs:
Sezary cells with cerebriform nuclei seen on blood smear
Sezary Syndrome
Chronic Myeloid Leukemia (CML)
Pathology:
Symptoms/Signs:
Treatments:
Complication:
Path:
Neoplastic proliferation of mature myeloid cells, especially granulocytes, and their precursors with increased basophils
Driven by t(9;22) (Philadelphia chromosome) creating BCR-ABL fusion protein with high tyrosine kinase activity
Signs:
1) Splenomegaly
Treatments:
First-line treatment is imatinib, targeting tyrosine kinase activity
Complication:
1) Can transform to AML or ALL as mutation originates in a pluripotent stem cel
Path:
Neoplastic proliferation of mature myeloid cells, especially granulocytes, and their precursors with increased basophils
Driven by t(9;22) (Philadelphia chromosome) creating BCR-ABL fusion protein with high tyrosine kinase activity
Signs:
1) Splenomegaly
Treatments:
First-line treatment is imatinib, targeting tyrosine kinase activity
Complication:
1) Can transform to AML or ALL as mutation originates in a pluripotent stem cel
Chronic Myeloid Leukemia (CML)
CML vs. Leukemoid Reaction
CML is differentiated from leukemoid reaction by negative leukocyte alkaline phosphatase (LAP) stain, increased basophils, and presence of t(9;22)
Polycythemia Vera (PV)
Pathology:
Symptoms/Signs:
Lab findings:
Treatments:
Path:
Neoplastic proliferation of mature myeloid cells, primarily RBCs with increased granulocytes and platelets. Associated with JAK2 kinase mutation
Signs:
1) blood hyperviscosity
- blurry vision
- headache
- risk of venous thrombosis
-flushed face
- itching after bathing
Labs:
EPO levels are decreased, and Sao2, is normal
Treatment:
1) phlebotomy as first-line
2) hydroxyurea as second-line
(Without treatment, death typically within a year)
Path:
Neoplastic proliferation of mature myeloid cells, primarily RBCs with increased granulocytes and platelets. Associated with JAK2 kinase mutation
Signs:
1) blood hyperviscosity
- blurry vision
- headache
- risk of venous thrombosis
-flushed face
- itching after bathing
Labs:
EPO levels are decreased, and Sao2, is normal
Treatment:
1) phlebotomy as first-line
2) hydroxyurea as second-line
(Without treatment, death typically within a year)
Polycythemia Vera (PV)
_______ due to high altitude or lung disease, Sao2 is low, and
EPO is increased.
reactive polycythemia
________ a due to ectopic EPO production from renal cell
carcinoma, EPO is high, and Sao2 is normal
reactive polycythemia
Essential Thrombocythemia (ET)
Pathology:
Symptoms/Signs:
Path:
Neoplastic proliferation of mature myeloid cells, particularly platelets, with increased RBCs and granulocytes
Associated with JAK2 kinase mutation
Signs:
1) bleeding and/or thrombosis risk, rarely progresses to acute leukemia
Path:
Neoplastic proliferation of mature myeloid cells, particularly platelets, with increased RBCs and granulocytes
Associated with JAK2 kinase mutation
Signs:
1) bleeding and/or thrombosis risk, rarely progresses to acute leukemia
Essential Thrombocythemia (ET)
Myelofibrosis
Pathology:
Symptoms/Signs:
“Muscly SEaLs”
Path:
Neoplastic proliferation of mature myeloid cells, notably megakaryocytes, linked to JAK2 kinase mutation
Megakaryocytes overproduce platelet-derived growth factor (PDGF) leading to marrow fibrosis
Signs:
1) Splenomegaly from extramedullary hematopoiesis,
2) Leucoerythroblastic smear
3) Risks of infection, thrombosis, and bleeding
Path:
Neoplastic proliferation of mature myeloid cells, notably megakaryocytes, linked to JAK2 kinase mutation
Megakaryocytes overproduce platelet-derived growth factor (PDGF) leading to marrow fibrosis
Signs:
1) Splenomegaly from extramedullary hematopoiesis,
2) Leucoerythroblastic smear
3) Risks of infection, thrombosis, and bleeding
Myelofibrosis
Lymphadenopathy (LAD)
Pathology:
- Painful vs Painless
Path:
Enlarged lymph nodes,
1) Painful LAD typically seen in acute lymphadenitis from acute infection
2) Painless LAD can be caused by chronic inflammation, metastatic carcinoma, or lymphoma
Follicular hyperplasia (B-cell region) seen in conditions like
rheumatoid arthritis and early HIV infection
Paracortex hyperplasia (T-cell region) seen in viral infections, such as
infectious mononucleosis (EBV)
Follicular Lymphoma
Pathology:
Symptoms/Signs:
Treatments:
Path:
Neoplastic proliferation of small B cells (CD20+) forming follicle-like nodules
Presents in late adulthood with painless lymphadenopathy
Driven by t(14;18) translocation leading to overexpression of Bcl2 inhibiting apoptosis
Signs:
1) disrupted architecture, absence of tangible body macrophages, Bcl2 expression, and monoclonality
2) Enlarged Lymph nodes
Treatment:
low-dose chemotherapy or rituximab
Path:
Neoplastic proliferation of small B cells (CD20+) forming follicle-like nodules
Presents in late adulthood with painless lymphadenopathy
Driven by t(14;18) translocation leading to overexpression of Bcl2 inhibiting apoptosis
Signs:
1) disrupted architecture, absence of tangible body macrophages, Bcl2 expression, and monoclonality
2) Enlarged Lymph nodes
Treatment:
low-dose chemotherapy or rituximab
Follicular Lymphoma
Mantle Cell Lymphoma
Pathology:
Path:
Neoplastic proliferation of small B cells (CD20+) expanding the mantle zone
Presents in late adulthood with painless lymphadenopathy
Driven by t(11;14) translocation leading to overexpression of cyclin D1 promoting cell cycle transition
Path:
Neoplastic proliferation of small B cells (CD20+) expanding the mantle zone
Presents in late adulthood with painless lymphadenopathy
Driven by t(11;14) translocation leading to overexpression of cyclin D1 promoting cell cycle transition
Mantle Cell Lymphoma
Marginal Zone Lymphoma
Pathology:
Path:
Neoplastic proliferation of small B cells (CD20+) expanding the marginal zone
Associated with inflammatory conditions like Hashimoto thyroiditis, Sjogren syndrome, and H. pylori gastritis
MALToma is marginal zone lymphoma in mucosal sites with potential regression in gastric MALToma with H. pylori treatment
Path:
Neoplastic proliferation of small B cells (CD20+) expanding the marginal zone
Associated with inflammatory conditions like Hashimoto thyroiditis, Sjogren syndrome, and H. pylori gastritis
MALToma is marginal zone lymphoma in mucosal sites with potential regression in gastric MALToma with H. pylori treatment
Marginal Zone Lymphoma
Burkitt Lymphoma
Pathology:
Symptoms/Signs:
Lab findings:
Path:
Neoplastic proliferation of intermediate-sized B cells (CD20+) often with EBV association
Signs:
1) extranodal mass in child or young adult, African form involving the jaw, sporadic form involving the abdomen
Labs:
Driven by c-myc translocations promoting cell growth, with high mitotic index and ‘starry-sky’ appearance on microscopy
Path:
Neoplastic proliferation of intermediate-sized B cells (CD20+) often with EBV association
Signs:
1) extranodal mass in child or young adult, African form involving the jaw, sporadic form involving the abdomen
Labs:
Driven by c-myc translocations promoting cell growth, with high mitotic index and ‘starry-sky’ appearance on microscopy
Burkitt Lymphoma
Diffuse Large B-Cell Lymphoma
Pathology:
Path:
Neoplastic proliferation of large B cells (CD20+) growing diffusely in sheets
it’s clinically aggressive (high-grade)
Arising sporadically or from transformation of low-grade lymphoma like follicular lymphoma
Signs:
1) Enlarging lymph nodes in adulthood
Path:
Neoplastic proliferation of large B cells (CD20+) growing diffusely in sheets
it’s clinically aggressive (high-grade)
Arising sporadically or from transformation of low-grade lymphoma like follicular lymphoma
Signs:
1) Enlarging lymph nodes in adulthood
Diffuse Large B-Cell Lymphoma
Reed-Sternberg Cells in Hodgkin Lymphoma
Pathology:
Lab findings:
Path:
Neoplastic proliferation of Reed-Sternberg cells, large B cells with multilobed nuclei and prominent nucleoli
Labs:
Cells positive for CD15 and CD30, that attract reactive cells like lymphocytes and eosinophils
Path:
Neoplastic proliferation of Reed-Sternberg cells, large B cells with multilobed nuclei and prominent nucleoli
Labs:
Cells positive for CD15 and CD30, that attract reactive cells like lymphocytes and eosinophils
Reed-Sternberg Cells in Hodgkin Lymphoma
Hodgkin Lymphoma Subtypes
Pathology:
Path:
Reactive inflammatory cells form bulk of tumor and define classification subtypes: nodular sclerosis, lymphocyte-rich, mixed cellularity, lymphocyte-depleted
Multiple Myeloma
Pathology:
Symptoms/Signs:
Lab findings:
Path:
Malignant proliferation of plasma cells in bone marrow, most common primary malignant bone tumor
Signs:
1) Bone pain with hypercalcemia
2) Proteinuria with Bence Jones protein in urine (myeloma kidney and renal failure risk)
Labs:
1) High serum IL-6 stimulates plasma cell growth and Ig production
2) Elevated serum protein with M spike on SPEP (monoclonal IgG/IgA)
3) Rouleaux formation of RBCs on blood smear
AL amyloidosis with free light chain deposition in tissues
Path:
Malignant proliferation of plasma cells in bone marrow, most common primary malignant bone tumor
Signs:
1) Bone pain with hypercalcemia
2) Proteinuria with Bence Jones protein in urine (myeloma kidney and renal failure risk)
Labs:
1) High serum IL-6 stimulates plasma cell growth and Ig production
2) Elevated serum protein with M spike on SPEP (monoclonal IgG/IgA)
3) Rouleaux formation of RBCs on blood smear
AL amyloidosis with free light chain deposition in tissues
Multiple Myeloma
Monoclonal Gammopathy of Undetermined Significance (MGUS)
Pathology:
Path:
Increased serum protein with M spike on SPEP, without features of multiple myeloma
Common in elderly (5% of 70-year-olds), 1% develop multiple myeloma yearly
Path:
Increased serum protein with M spike on SPEP, without features of multiple myeloma
Common in elderly (5% of 70-year-olds), 1% develop multiple myeloma yearly
Monoclonal Gammopathy of Undetermined Significance (MGUS)
Waldenstrom Macroglobulinemia
Pathology:
Symptoms/Signs:
Lab findings:
Treatments:
Path:
B-cell lymphoma with monoclonal IgM production
Signs:
1) generalized lymphadenopathy
2) Visual and neurologic deficits
3) Bleeding
Labs:
increased serum protein with IgM M spike
Treatments:
Acute complications treated with plasmapheresis to remove excess IgM
Path:
B-cell lymphoma with monoclonal IgM production
Signs:
1) generalized lymphadenopathy
2) Visual and neurologic deficits
3) Bleeding
Labs:
increased serum protein with IgM M spike
Treatments:
Acute complications treated with plasmapheresis to remove excess IgM
Waldenstrom Macroglobulinemia
Letterer-Siwe Disease
Pathology:
Symptoms/Signs:
Complications:
Path:
Malignant proliferation of Langerhans cells
Signs:
in infants < 2 years: skin rash, cystic skeletal defects
Complications:
Involves multiple organs and can be rapidly fatal
Path:
Malignant proliferation of Langerhans cells
Signs:
in infants < 2 years: skin rash, cystic skeletal defects
Complications:
Involves multiple organs and can be rapidly fatal
Letterer-Siwe Disease
Eosinophilic Granuloma
Pathology:
Symptoms/Signs:
Lab findings:
Path:
Eosinophilic Granuloma
Signs:
In adolescents: pathologic fracture, no skin involvement
Labs:
Langerhans cells with eosinophils
Path:
Eosinophilic Granuloma
Signs:
In adolescents: pathologic fracture, no skin involvement
Labs:
Langerhans cells with eosinophils
Eosinophilic Granuloma
Hand-Schuller-Christian Disease
Pathology:
Symptoms/Signs:
Path:
Malignant proliferation of Langerhans cells
Signs:
In children: scalp rash, lytic skull defects, diabetes insipidus, exophthalmos
Path:
Malignant proliferation of Langerhans cells
Signs:
In children: scalp rash, lytic skull defects, diabetes insipidus, exophthalmos
Hand-Schuller-Christian Disease
