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USMLE Pathoma > WBC Pathoma > Flashcards

WBC Pathoma Flashcards

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1
Q

Neutropenia

Pathology:

Causes:

A

Path:
Decreased circulating neutrophils

Causes:
1) Drugs (Chemo & alkylating agents)
2) Gram -ve sepsis

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2
Q

Path:
Decreased circulating neutrophils

Causes:
1) Drugs (Chemo & alkylating agents)
2) Gram -ve sepsis

A

Neutropenia

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3
Q

Lymphopenia

Pathology:

Causes:

A

Path:
Decreased circulating lymphocytes

Causes:
1) DiGeorge syndrome or HIV
2) exogenous corticosteroids or Cushing syndrome
3) SLE
4) Radiation

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4
Q

Path:
Decreased circulating lymphocytes

Causes:
1) DiGeorge syndrome or HIV
2) exogenous corticosteroids or Cushing syndrome
3) SLE
4) Radiation

A

Lymphopenia

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5
Q

INFECTIOUS MONONUCLEOSIS (IM)

Pathology:

Symptoms/Signs:

Causes:

Labs/Histological findings:

Complications

A

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

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6
Q

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

A

INFECTIOUS MONONUCLEOSIS (IM)

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7
Q

B-ALL

Pathology:

Lab findings:

Prognosis:

A

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)

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8
Q

T-ALL

Pathology:

Lab findings:

Prognosis:

A

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)

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9
Q

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)

A

B-ALL

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10
Q

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)

A

T-ALL

“Thymic-Teens Accumulate lots of Lymphocytes”

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11
Q

Acute Myeloid Leukemia

Pathology:

Lab findings:

A

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)

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12
Q

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)

A

Acute Myeloid Leukemia

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13
Q

Acute Promyelocytic Leukemia (APL)

Pathology:

Treatment:

“APT = Abnormal Promyelocytes & Translocation”

A

Path:
characterized by t(15;17) translocation leading to abnormal promyelocytes

Treatment with all-trans-retinoic acid (ATRA) to induce maturation and cell death

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14
Q

Path:
characterized by t(15;17) translocation leading to abnormal promyelocytes

Treatment with all-trans-retinoic acid (ATRA) to induce maturation and cell death

A

Acute Promyelocytic Leukemia (APL)

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15
Q

Acute Monocytic Leukemia:

A

Path:
proliferation of monoblasts, may infiltrate gums

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16
Q

Path:
proliferation of monoblasts, may infiltrate gums

A

Acute Monocytic Leukemia:

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17
Q

Acute Megakaryoblastic Leukemia:

A

proliferation of megakaryoblasts, associated with Down syndrome

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18
Q

proliferation of megakaryoblasts, associated with Down syndrome

A

Acute Megakaryoblastic Leukemia:

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19
Q

AML from Pre-Existing Dysplasia

Pathology:

Symptoms/Signs:

Complications:

A

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

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20
Q

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

A

AML from Pre-Existing Dysplasia

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21
Q

Chronic Lymphocytic Leukemia (CLL)

Pathology:

Symptoms/Signs:

Lab findings:

Complications

A

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

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22
Q

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

A

Chronic Lymphocytic Leukemia (CLL)

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23
Q

Hairy Cell Leukemia

Pathology:

Symptoms/Signs:

Lab findings

Treatments:

A

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)

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24
Q

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)

A

Hairy Cell Leukemia

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25
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
26
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)
27
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
28
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
29
Sezary Syndrome Pathology: Lab findings:
Path: Blood involvement of neoplastic cells from mycosis fungoides Labs: Sezary cells with cerebriform nuclei seen on blood smear
30
Path: Blood involvement of neoplastic cells from mycosis fungoides Labs: Sezary cells with cerebriform nuclei seen on blood smear
Sezary Syndrome
31
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
32
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)
33
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)
34
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)
35
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)
36
_______ due to high altitude or lung disease, Sao2 is low, and EPO is increased.
reactive polycythemia
37
________ a due to ectopic EPO production from renal cell carcinoma, EPO is high, and Sao2 is normal
reactive polycythemia
38
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
39
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)
40
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
41
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
42
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
43
Follicular hyperplasia (B-cell region) seen in conditions like
rheumatoid arthritis and early HIV infection
44
Paracortex hyperplasia (T-cell region) seen in viral infections, such as
infectious mononucleosis (EBV)
45
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
46
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
47
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
48
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
49
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
50
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
51
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
52
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
53
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
54
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
55
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
56
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
57
Hodgkin Lymphoma Subtypes Pathology:
Path: Reactive inflammatory cells form bulk of tumor and define classification subtypes: nodular sclerosis, lymphocyte-rich, mixed cellularity, lymphocyte-depleted
58
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
59
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
60
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
61
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)
62
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
63
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
64
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
65
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
66
Eosinophilic Granuloma Pathology: Symptoms/Signs: Lab findings:
Path: Eosinophilic Granuloma Signs: In adolescents: pathologic fracture, no skin involvement Labs: Langerhans cells with eosinophils
67
Path: Eosinophilic Granuloma Signs: In adolescents: pathologic fracture, no skin involvement Labs: Langerhans cells with eosinophils
Eosinophilic Granuloma
68
Hand-Schuller-Christian Disease Pathology: Symptoms/Signs:
Path: Malignant proliferation of Langerhans cells Signs: In children: scalp rash, lytic skull defects, diabetes insipidus, exophthalmos
69
Path: Malignant proliferation of Langerhans cells Signs: In children: scalp rash, lytic skull defects, diabetes insipidus, exophthalmos
Hand-Schuller-Christian Disease

USMLE Pathoma (20 decks)

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