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USMLE Pathoma > WBC Pathoma > Flashcards

WBC Pathoma Flashcards

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
Q

Adult T-Cell Leukemia/Lymphoma (ATLL)

Pathology:

Symptoms/Signs

A

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

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26
Q

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

A

Adult T-Cell Leukemia/Lymphoma (ATLL)

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27
Q

Mycosis Fungoides

Pathology/Symptoms:

Lab findings:

A

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

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28
Q

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

A

Mycosis Fungoides

29
Q

Sezary Syndrome

Pathology:

Lab findings:

A

Path:
Blood involvement of neoplastic cells from mycosis fungoides

Labs:
Sezary cells with cerebriform nuclei seen on blood smear

30
Q

Path:
Blood involvement of neoplastic cells from mycosis fungoides

Labs:
Sezary cells with cerebriform nuclei seen on blood smear

A

Sezary Syndrome

31
Q

Chronic Myeloid Leukemia (CML)

Pathology:

Symptoms/Signs:

Treatments:

Complication:

A

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
Q

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

A

Chronic Myeloid Leukemia (CML)

33
Q

CML vs. Leukemoid Reaction

A

CML is differentiated from leukemoid reaction by negative leukocyte alkaline phosphatase (LAP) stain, increased basophils, and presence of t(9;22)

34
Q

Polycythemia Vera (PV)

Pathology:

Symptoms/Signs:

Lab findings:

Treatments:

A

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
Q

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)

A

Polycythemia Vera (PV)

36
Q

_______ due to high altitude or lung disease, Sao2 is low, and
EPO is increased.

A

reactive polycythemia

37
Q

________ a due to ectopic EPO production from renal cell
carcinoma, EPO is high, and Sao2 is normal

A

reactive polycythemia

38
Q

Essential Thrombocythemia (ET)

Pathology:

Symptoms/Signs:

A

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
Q

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

A

Essential Thrombocythemia (ET)

40
Q

Myelofibrosis

Pathology:

Symptoms/Signs:

“Muscly SEaLs”

A

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
Q

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

A

Myelofibrosis

42
Q

Lymphadenopathy (LAD)

Pathology:
- Painful vs Painless

A

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
Q

Follicular hyperplasia (B-cell region) seen in conditions like

A

rheumatoid arthritis and early HIV infection

44
Q

Paracortex hyperplasia (T-cell region) seen in viral infections, such as

A

infectious mononucleosis (EBV)

45
Q

Follicular Lymphoma

Pathology:

Symptoms/Signs:

Treatments:

A

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
Q

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

A

Follicular Lymphoma

47
Q

Mantle Cell Lymphoma

Pathology:

A

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
Q

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

A

Mantle Cell Lymphoma

49
Q

Marginal Zone Lymphoma

Pathology:

A

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
Q

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

A

Marginal Zone Lymphoma

51
Q

Burkitt Lymphoma

Pathology:

Symptoms/Signs:

Lab findings:

A

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
Q

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

A

Burkitt Lymphoma

53
Q

Diffuse Large B-Cell Lymphoma

Pathology:

A

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
Q

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

A

Diffuse Large B-Cell Lymphoma

55
Q

Reed-Sternberg Cells in Hodgkin Lymphoma

Pathology:

Lab findings:

A

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
Q

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

A

Reed-Sternberg Cells in Hodgkin Lymphoma

57
Q

Hodgkin Lymphoma Subtypes

Pathology:

A

Path:
Reactive inflammatory cells form bulk of tumor and define classification subtypes: nodular sclerosis, lymphocyte-rich, mixed cellularity, lymphocyte-depleted

58
Q

Multiple Myeloma

Pathology:

Symptoms/Signs:

Lab findings:

A

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
Q

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

A

Multiple Myeloma

60
Q

Monoclonal Gammopathy of Undetermined Significance (MGUS)

Pathology:

A

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
Q

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

A

Monoclonal Gammopathy of Undetermined Significance (MGUS)

62
Q

Waldenstrom Macroglobulinemia

Pathology:

Symptoms/Signs:

Lab findings:

Treatments:

A

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
Q

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

A

Waldenstrom Macroglobulinemia

64
Q

Letterer-Siwe Disease

Pathology:

Symptoms/Signs:

Complications:

A

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
Q

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

A

Letterer-Siwe Disease

66
Q

Eosinophilic Granuloma

Pathology:

Symptoms/Signs:

Lab findings:

A

Path:
Eosinophilic Granuloma

Signs:
In adolescents: pathologic fracture, no skin involvement

Labs:
Langerhans cells with eosinophils

67
Q

Path:
Eosinophilic Granuloma

Signs:
In adolescents: pathologic fracture, no skin involvement

Labs:
Langerhans cells with eosinophils

A

Eosinophilic Granuloma

68
Q

Hand-Schuller-Christian Disease

Pathology:

Symptoms/Signs:

A

Path:
Malignant proliferation of Langerhans cells

Signs:
In children: scalp rash, lytic skull defects, diabetes insipidus, exophthalmos

69
Q

Path:
Malignant proliferation of Langerhans cells

Signs:
In children: scalp rash, lytic skull defects, diabetes insipidus, exophthalmos

A

Hand-Schuller-Christian Disease

USMLE Pathoma (20 decks)

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