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Pathology > Chapter 6 ( WBC Disorders ) > Flashcards

Chapter 6 ( WBC Disorders ) Flashcards

1
Q

Causes and ttt of neutropenia ?

A

1- drug toxicity ( chemotherapy with alkylating agents )
2- sever infection ( gram negative sepsis )

GM-CSF and G-CSF may be used to boost granulocyte production to decrease risk of infection

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2
Q

Causes of lymphopenia ?

A

Immunodeficiency
High cortisol state
Autoimmune destruction (SLE)
Whole body radiation

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3
Q

Causes of neutrophilic leucocytosis ?

A

Bacterial infection or tissue necrosis ( increase release of marginated pool and bone marrow neutrophils including immature forms ( shift to the left )

High cortisol state release marginated pool of neutrophils

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4
Q

Causes of monocytosis ?

A

Chronic inflammatory state ( autoimmune and infectious )

Malignancy

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5
Q

Causes of eosinophilia ?

A

Allergic reactions ( type I hypersensitivity )
Parasitic infections
Hodgkin lymphoma

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6
Q

Causes of basophilia ?

A

CML

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7
Q

Causes pf lymphocytic leucocytosis ?

A 
Viral infections ( T lymphocytes undergo hyperplasia ) 
Bordetella pertussis infection ( this bacteria produce lymphocytosis promoting factor which prevents lymphocytes from leaving blood to enter lymph nodes )
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8
Q

EBV affects which organs ?

A

1- oropharynx resulting in pharyngitis
2- liver resulting in hepatitis and hepatomegaly
3- B cells

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9
Q

What does reactive CD8+ T cells response EBV lead to ?

A

1- generalized lymphadenopathy ( T cell hyperplasia in lymph nodes paracortex )
2- splenomegaly ( T cell hyperplasia in periarterial lymphatic sheath )
3- high WBC count with atypical lymphocytes ( reactive CD8+ T cells )

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10
Q

Mechanism of monospot test ?

A

Detects IgM antibodies that cross react with horse or sheep RBCs ( heterophile antibodies )
Turns positive after 1 week of infection

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11
Q

What a negative monospot test suggests in case of IM ?

A

CMV as a possible cause for IM

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12
Q

Definitive diagnosis of IM ?

A

By serologic testing for the EBV viral capsid antigen

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13
Q

Complications of IM ?

A

Splenic rupture
Rash if exposed to ampicillin
Dormancy of virus in B cells increases the risk for both Recurrence and B cell Lymphoma especially if immunodeficiency develops

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14
Q

Acute leukemia ?

A

Accumulation of > 20% blasts in the bone marrow

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15
Q

Blast appearance ?

A

Large immature cells with punched out nucleoli

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16
Q

Histological characteristic of lymphoblasts ?

A

Positive nuclear staining for TdT ( DNA polymerase )

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17
Q

Which part of the population has increased risk for acute lymphoblastic leukemia ?

A

Children associated with down syndrome ( after the age of 5 years )

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18
Q

Character of B-ALL ?

A

Lymphoblasts that express CD10 , CD19 , CD20

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19
Q

Excellent response to chemotherapy in B-ALL requires what ?

A

Prophylaxis to scrotum and CSF

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20
Q

Prognosis of B-ALL based on what ? Explain .

A

On cytogenetic abnormalities :
1- t(12;21) has a good prognosis ( seen in children )

2- t(9;22) has a poor prognosis ( seen in adults ) ( Ph+ ALL)

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21
Q

Character of T-ALL ?

A

Lymphoblasts that express markers ranging from CD2 to CD8

The blasts don’t express CD10

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22
Q

Presentation of T-ALL ?

A

Usually in teenagers as mediastinal mass ( thymic mass ) thats why its called acute lymphoblastic lymphoma

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23
Q

Histological characteristic of Myeloblasts ?

A

Positive cytoplasmic staining for myeloperoxidase

Crystal aggregates of MPO may be seen as Auer rods

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24
Q

Which part of the population has increased risk of developing AML ?

A

Older adults ( 50-60 years )

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25
AML subclassified based on what ?
Cytogenetic abnormalities , lineage of myeloblasts , surface markers
26
Acute promyelocytic leukemia mechanism ? Character ? Ttt ?
Mechanism : t(15;17) translocation of the retinoic acid receptor on chromosome 17 to chromosome 15 , RAR disruption blocks maturation and promyelocytes accumulation Character : contain numerous primary granules ( Auer rods ) that increase risk for DIC Ttt : all trans retinoic acid ( which binds the altered receptor and causes the blasts to mature )
27
Acute moncytic leukemia characters ?
Usually lack MPO | Blasts infiltrate gums
28
Acute megakaryoblastic leukemia characters ?
Lack MPO | Associated with down syndrome ( arises before age of 5 )
29
Presentation pf myelodysplastic syndrome ?
Cytopenias Hypercellular bone marrow Abnormal maturation of cells Increased blasts >20%
30
Mechanism of CLL ?
Neoplastic proliferation of naive B cells that coexpress CD5 , CD20
31
Histologic characters of CLL ?
Increased lymphocytes and smudge cells on blood smear
32
Small lymphocytic lymphoma ?
Involvement of lymph nodes in CLL that leads to generalized lymphadenopathy
33
Complications of CLL ?
Hypogammaglobulinemia ( infections is the most common cause of death ) Autoimmune hemolytic anemia Transformation into diffuse large B cell lymphoma ( marked clinically by an enlarging lymph node or spleen )
34
Richter transformation ?
Transformation of CLL into diffuse large B cell lymphoma
35
Mechanism of hairy cell leukemia ?
Neoplastic proliferation of mature B cells characterized by hairy cytoplasmic processes
36
Histological characteristic of hairy cell leukemia ?
Cells are positive for tartrate-resistant acid phosphatase (TRAP)
37
Clinical features of hairy cell leukemia ?
TRAP disease : 1- B cells Trapped in bone marrow ( marrow fibrosis leading to Dry Tap ) 2- B cells Trapped in red pulp of spleen ( splenomegaly ) 3- No lymphadenopathy as the B cells are Trapped in bone marrow and spleen
38
Drug used in Ttt of hairy cell leukemia ? Its mechanism ?
2-CDA ( Cladribine ) | An adenosine deaminase inhibitor leads to accumulation of adenosine to toxic levels in neoplastic B cells
39
Mechanism of Adult at cell Leukemia/Lymphoma (ATLL) ? Caused virus ? Seen where ?
Neoplastic proliferation of mature CD4 T cells Associated with HTLV-1 Seen in Japan and Caribbean
40
Clinical features of ATLL ?
``` Rash Generalized lymphadenopathy Hepatosplenomegaly Lytic ( punched out ) bone lesions Hypercalcemia ```
41
Mechanism of Mycosis Fungoides ?
Neoplastic proliferation of mature CD4 T cells that infiltrate the skin producing : Rash Plaques Nodules
42
Pautrier microabscesses ?
Aggregates of neoplastic cells in the epidermis seen in Mycosis Fungoides
43
Sezary syndrome ?
Occurs when mature CD4 neoplastic mature T cells spread to involve the blood in Mycosis Fungoides Characterized by Presence of Sezary cells ( lymphocytes with cerebriform nuclei ) on blood smear
44
General complications of myeloproliferative disorders ?
1- increased risk for hyperuricemia and gout due to high turnover of cells 2- progression to marrow fibrosis 3- transformation to acute leukemia
45
Mechanism of chronic myeloid leukemia ?
Neoplastic proliferation of mature myeloid cells specially Granulocytes and their precursors ( Basophils are increased ) Driven by t(9;22) which generates BCR-ABL fusion protein with increased tyrosine kinase activity
46
First line ttt in CML ?
Imatinib , which blocks tyrosine kinase activity
47
To which type of acute leukemia can CML transfer to ?
To both typer since in a pluripotent stem cell 2/3 of cases to AML 1/3 of cases to ALL
48
How is CML distinguished from leukemoid reaction ?
1- negative leukocyte alkaline phosphatase stain (LAP) 2- increased basophils 3- t(9:22)
49
Polythycemia Vera defect ? Clinical symptoms ? Ttt ?
Defect : associated with JAK2 kinase mutation Clinical symptoms : (due to hyperviscosity of blood) Blurry vision and headache Increased risk of venous thrombosis (hepatic vein , portal vein , dural sinus) Flushed face due to congestion Itching ( histamine release from increased mast cells) Ttt: phlebotomy , Hydroxyurea
50
Mechanism of myelofibrosis ?
Neoplastic proliferation of mature myeloid cells especially megakaryoctes Associated with JAK2 kinase mutation ( 50% of cases ) Megakaryocytes produce excess PDGF causing marrow fibrosis
51
Clinical features of myelofibrosis ?
1- splenomegaly 2- Leukoerythroblastic smear ( tear-drop RBCs - nucleated RBCs - immature granulocytes ) 3- increased risk of infection, thrombosis , bleeding
52
Types of lymph nodes enlargement due to inflammation according to the hyperplastic zone ?in Which conditions they occur ?
1- follicular hyperplasia : seen with RA and early stages of HIV infection 2- paracortex hyperplasia : with viral infections as IM 3- hyperplasia of sinus histiocytes : LNs draining tissue with cancer
53
Classification of non-Hodgkin lymphoma according to cell size ?
1- small B cells : follicular lymphoma Mantle cell lymphoma Marginal zone lymphoma Small lymphocytic lymphoma 2- intermediate sized B cells : Burkitt lymphoma 3- large B cells : diffuse large B cell lymphoma
54
Follicular lymphoma presentation ? Ttt ? Complication ?
Presents in late adulthood with painless lymphadenopathy Ttt : for symptomatic patients : Low dose chemotherapy Rituximab ( annti CD20 antibody ) Important complication : progression to diffuse large B cell lymphoma presents as an enlarging lymph node
55
How is follicular lymphoma distinguished from reactive follicular hyperplasia ?
1- Disruption of normal LN architecture 2- Lack of Tingible body macrophages in germinal centers 3- Bcl2 expression in follicles 4- Monoclonality
56
Marginal cell lymphoma associated with what ?
Chronic inflammatory states as Hashimoto thyroiditis Sjorgen syndrome H pylori gastritis
57
Marginal zone in LN is formed by ?
Post germinal center B cells
58
MALToma ?
Marginal zone lymphoma in mucosal sites | Gastric MALToma may regress with ttt of H pylori
59
Burkitt lymphoma associated with what ? Presentation ?
EBV Presents as an extranodal mass in child or young adults : 1- African form : involves jaw 2- Sporadic form : involves abdomen
60
Histological characteristic of Burkitt lymphoma ?
High mitotic index | Starry-sky appearance on microscope
61
Most common form of NHL ? Prognosis ? Histology appearance ? Presentation ?
Diffuse large B cell lymphoma Clinically aggressive - grows diffusely in sheets Presents in late adulthood as an enlarging LN or an extranodal mass
62
Mechanism of Hodgkin lymphoma ?
Neoplastic proliferation of Reed-Sternberg cells
63
Characters of Reed Sternberg cells ?
Large B cells With multilobed nuclei And prominent nucleoloi ( owl eyed nuclei ) Positive for CD15 and CD30
64
What does RS cells secret ? It action ?
``` Cytokines that lead to : 1- B symptoms ( fever,chills,weight loss,night sweats ) 2- attraction of Reactive lymphocytes Plasma cells Macrophages Eosinophils 3- fibrosis ```
65
Subtypes of Hodgkin lymphoma ?
1- Nodular sclerosis 2- Lymphocyte-rich 3- Mixed cellularity 4- Lymphocyte-depleted
66
Most common subtype of Hodgkin lymphoma ? Presentation ? Histological characters ?
Nodular sclerosis Presents as enlarging cervical or mediastinal LN in a young adult , usually female Histology :LN is divided by bands of sclerosis and RS cells present in lake like spaces ( lacunar cells )
67
Subtype of HL that has the best prognosis ?
Lymphocyte-rich
68
Characteristic of mixed cellularity HL ?
Abundant eosinophils
69
The most aggressive subtype of HL ? Seen in which patients ?
Lymphocyte-depleted | Seen in elderly and HIV positive individuals
70
Mechanism of multiple myeloma ?
Most common primary tumor of bone Due to malignant proliferation of plasma cells in bone marrow , high serum IL-6 maybe present which stimulates plasma cell growth and immunoglobulin production
71
Clinical features of multiple myeloma ?
I BM and RAP 1- bone pain with hypercalcemia ( neoplastic plasma cells activate the RANK receptor on osteoclasts leading to bone destruction ) 2- elevated serum proteins ( M spike on SPEP due to monoclonal IgG or IgA ) 3- increased risk of infection ( monoclonal antibodies lacks antigenic diversity ) 4- Rouleaux formation of RBCs ( increased serum proteins decrease charge between RBCs ) 5- primary AL amyloidosis ( free light chains deposit in tissues ) 6- proteinuria ( free light chains are excreted in urine as Bence Jones proteins , deposition in kidney tubules leads to risk of renal failure ( Myeloma kidney )
72
Monoclonal Gammpathy of Underestimated Significance ( MGUS ) ?
Increased serum proteins with M spike on SPEP but other features of MM are absent Common in elderly , 1 % of patients with MGUS develop MM each year
73
Waldenstorm Macroglobulinemia mechanism ? Clinical features ? Ttt ?
B cell lymphoma with monoclonal IgM production Clinical features : 1-Generalized Lymphadenopathy 2-Increased serum proteins with M spike on SPEP ( due to ⬆️ IgM ) 3-Visual and neurological deficits ( retinal hemorrhage or stroke ) ( IgM causes hyperviscosity ) 4-Bleeding ( viscous proteins results in defective platelet aggregation ) Ttt : plasmapheresis
74
Source and function of Langerhans cells ?
Derived from bone marrow monocytes | Present antigen to naive T cells
75
Langerhans cell histiocytes ?
``` Neoplastic proliferation of Langerhans cells Characteristic Birbeck ( tennis racket ) granules are seen on electron microscopy Cells are CD1a+ and S100+ by immunohistochemistry ```
76
Letterer Siwe disease mechanism ? presentation ?
Malignant proliferation of langerhans cells Skin rash Cystic skeletal defects in an infant < 2 years Multiple organs maybe involved Rapidly fatal
77
Eosinophilic granuloma mechanism ? Presentation ? Histological chacters ?
Benign proliferation of langerhans cells Pathologic fracture in an adolescent Skin is not involved Biopsy :langerhans cells with mixed inflammatory cells including numerous eosinophils
78
Hand-Schuller-Christian disease mechanism ? Presentation ?
``` Malignant proliferation of Langerhans cells LEDS Scalp rash Lytic skull defects Diabetes insipidus Exophthalmos In a child > 3 years ```

Pathology (18 decks)

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