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Bloc F - Defense > Pathology > Flashcards

Pathology Flashcards

1
Q

Differential diagnosis of Reactive lymphadenopathy?

A
  • Infections: bacteria and viruses
  • Immune or connective tissue disorders: rheumatoid arthritis, systemic lupus erythematosus
  • Iatrogenic causes (drugs…)
  • Idiopathic (but often specific pattern): progressive transformation of germinal centers, Kikuchi-Fujimoto lymphadenopathy
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2
Q

Origin of leukemia (derived from which cells)?

A

Mostly myeloid cells and lymphoid cells, less erythroid cells or megakaryocytes

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3
Q

Origin of lymphoma (derived from which cells)?

A

–Precursor B- or T-lymphoblasts

–Mature B- or T- lymphoid cells

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4
Q

Those symptomes are suggestive of what ?

–Effects due to replacement of marrow

  • Anemia: fatigue, weakness, dyspnea
  • Neutropenia: infections
  • Thrombocytopenia: bleeding…
  • Bone pain

–Abdominal pain (splenomegaly)

–Systemic symptoms: fever, night sweats…

A

Leukemia

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5
Q

Those symptoms are suggestive of what?

–Enlarged lymph nodes, mass, pain, bleeding, organ-related symptoms

–Abdominal pain (splenomegaly or other)

–Systemic effects: “B” symptoms (fever, night sweats, weight loss), fatigue…

A

Lymphomas

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6
Q

Diffuse large B-cell lymphoma (DLBCL)?

A

–Aggressive B-cell lymphoma with large cells in a diffuse pattern

–Most common NHL in adults

Immunoprofile

  • CD20+
  • High Ki67 proliferation rate
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7
Q

Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL)?

A
  • Prognosis: indolent
  • Therapy is specific, so need a specific diagnosis!
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8
Q

Follicular lymphoma (FL)?

A
  • Neoplasm of B-cells of germinal center origin: centrocytes + centroblasts in follicular pattern
  • 2nd most common NHL, ~40% in West
  • Grading (correlates with prognosis)

–Low grades 1, 2: ≤ 15 centroblasts per high power field

–High grade, 3A, B: >15 centroblasts/HPF

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9
Q

Plasma cell neoplasms?

A

Diagnosis based on

  1. Clinical: pathological fractures, bone pain, anemia, low immunity, renal failure, hypercalcemia
  2. Radiological: Iifiltration of bone and marrow (always) by neoplastic plasma cells
  3. Pathological findings: paranuclear Golgi, CD138
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10
Q

Mature T- and NK-cell lymphomas’ general features?

A
  • Prognosis generally poorer than B-cell lymphomas, more difficult to treat
  • T-cell markers positive (or loss): CD2, CD3, CD5…
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11
Q

General features of Hodgkin lymphoma?

A

A clinically and pathologically distinctive lymphoma derived from germinal center B-cells composed of a small population of malignant cells, the Reed-Sternberg or other “Hodgkin” cells, admixed with numerous reactive cells

  • Principally a nodal disease
  • Orderly spread by contiguity
  • Often a single group of lymph nodes (esp. cervical)
  • Mesenteric nodes & Waldeyer ring rarely involved
  • Extra-nodal involvement rare
  • Leukemic phase extremely rare
  • Prognosis very good to excellent with Rx
  • Two main types each with distinctive features and immunohistochemical profile
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12
Q

Types of Hodgkin lymphoma (HL)?

A
  1. Nodular lymphocyte predominant: mostly males, age 30-50, cervical, axillary, inguinal nodes
  2. Classical: M ~ F, 15-35 + peak in older persons, cervical, mediastinal, axillary, para-aortic
  3. Nodular sclerosis
  4. Mixed cellularity
  5. Lymphocytes-depleted
  6. Lymphocytes-predominant
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13
Q

Popcorn cells is a pathologic feature of?

A

Nodular lymphocyte predominant HL

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14
Q

Reed-Sternberg cell are a pathological feature of?

A

Classical Hodgkin lymphoma

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15
Q

What are the B cell markers (mature)?

A

CD20, CD19: very specific

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16
Q

T cell markers?

A

–CD3 very specific

–CD4: helper T-cells; CD8: cytotoxic T-cells

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17
Q

BCL6, CD10 are markers for?

A

follicular center cells

18
Q

CD138, k, l light chains are markers of?

A

plasma cells myeloma

19
Q

CD45 is a marker for?

A

lymphoid cells, some myeloid

20
Q

CD8 is a marker for?

A

cytotoxic T-cells

21
Q

CD5 is a marker for?

A

mostly T-cells, but present and diagnostic of some B-cell lymphomas (CLL/SLL, mantle cell)

22
Q

BCL2 is a marker for?

A

anti-apoptotic protein: follicular lymphomas (B-cells)

23
Q

Ki67 is a marker for?

A

proliferation

24
Q

What are the Primary B Cell Deficiencies?

A
  • Agammaglobulinemia (X-linked [XLA], AR)
  • Hyper IgM immunodeficiency (HIGMS)
  • Common variable immunodeficiency (CVID)
  • Selective IgA deficiency
  • Anti-polysaccharide antibody deficiency
  • Transient hypogammaglobulinemia of infancy (THI)
25
Q

What are the Primary T Cell deficiencies?

A
  • Severe combined immunodeficiency (SCID)
  • DiGeorge syndrome
  • Wiskott-Aldrich syndrome
  • Ataxia-Telangiectasia
  • Miscellaneous CID
26
Q

Clinical presentation of XLA?

A
  • Infections begin at 4-6 months when maternal immunity wanes
  • Absent circulating mature B cells
  • All major classes of immunoglobulin affected (IgG, IgM, IgA)
  • No antibody responses to antigen
  • Sino-oto-pulmonary infections with encapsulated bacteria
  • Bacteremia, meningitis, septic arthritis, etc
  • Chronic infections with enteroviruses
27
Q

Clinical presentation of SCID?

A
  • Lymphopenia is an early clue
  • Also severe antibody deficiency
  • Extreme susceptibility to infection since birth to high-grade or low-grade pathogens
  • Protracted diarrhea, failure to thrive
  • Ommen Syndrome: desquamating erythroderma, fever, hepatosplenomegaly, lymphadenopathy, eosinophilia, high IgE, diarrhea, FTT
28
Q

Molecular mechanism of XLA?

A
  • Arrest of B cell development at pre-B cell stage
  • Mutation in btk gene (Bruton tyrosine kinase)
  • Autosomal recessive: µ, Ig-α, λ-5 chains
29
Q

Molecular mechanism of SCID?

A
  • Severe defect in T cell development: EMPTY THYMUS
  • No T cells, +/- B cells or NK cells
  • Many genetic variants: γ-common chain (XL) is the most frequent
30
Q

Treatment od XLA?

A

IVIG: antibody replacement

31
Q

Treatment of SCID?

A

Bone marrow transplant before 1 unless death

32
Q

What are the 2 main classes of HLA?

A
  1. MHC class I aka HLA A, B, C, found on all nucleated cells
  2. MHC class II aka HLA DR, DQ, DP, found on APC
33
Q

What are the 3 structures of the MHC complexe?

A
  1. Class I: 3 different gene sections for the protein that become ONE class I molecule
  2. Class III: contains a lot of the HLA-like proteins & some genes for proteins for other parts of immune system (ex: complement)
  3. Class II: the structure of class II on surface of cell = alpha chain + beta chain

–> Great variability

34
Q

What are the characteristics of HLA?

A
  • Polymorphic: many shapes
  • Polygenic: come from many different genes
  • Linkage disequilibrium: genes are inherited are preferentially in blocks / as a group –> 1/4 match with sibling
  • Co-dominantly expressed: genes on BOTH chromosomes are expressed (ABC from mom + ABC from dad = 6 class I proteins on one cell)
35
Q

What are the HLA tissue typing and their characteristics?

A
  • Serology: gives you the type (gets you 80% out of the way)
  • Genetic: used to better define the allele carried by the patient, ideal tool
  • Functional typing: MLR (mixed lymphocyte rxn), can be evaluated in lab, may be done with patients with previous solid organ transplant
36
Q

What is the limitation with cord blood donner?

A

Higher possibility of FAILURE TO ENGRAFT + repopulating from such a naive pool means time for symptoms to show up is slower (while infection risks are higher because your patient is immunosuppressed)

37
Q

What is the limitation with Haplo-identival transplant?

A

When a parent gives a transplant to their child, there’s an extra HLA-Y: girls into boys OK, boys into girls might be a problem

38
Q

For what type of transplant we don’t have to do HLA match?

A
  • Blood ***but does have to match for ABO
  • Corneal
39
Q

What type of match is essential for kidney grafts and solid organts?

A

Class I

40
Q

What type of match has to be done with bone marrow transplants?

A

Class II

Bloc F - Defense (7 decks)

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