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OMS II BECOM Exam 1 > Pathology White cell disorders I - Zaloga > Flashcards

Pathology White cell disorders I - Zaloga Flashcards

1
Q

myeloid tissues

A
  • include bone marrow and derived cells

- bone marrow is “house” for all progenitor cells

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2
Q

lymphoid tissues

A

-include thymus, spleen, lymph nodes, MALT and resident cells

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3
Q

where does primary hematopoiesis occur?

A

-bone marrow and thymus**

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4
Q

where does secondary hematopoiesis occur?

A

-spleen, lymph nodes, tonsils, peyer’s patch

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5
Q

HSC vs. multipotent progenitors

A
  1. HSC - pluripotent, can develop into any mature cell, self renewal, no surface markers (cannot identify), used in transplants
  2. multipotent progenitor - go down a cell lineage (terminal differentiated), less self renewal, higher proliferation
    - differentiation driven by cytokines/growth factors
    - increase division as cell matures –> change in surface markers
    - unregulated clonal expansion with hematopoietic tumors
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6
Q

what does G-CSF and IL-5 do?

A
  • G-CSF –> stimulate granulocyte precursors

- IL-5 –> stimulate eosinophilia

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7
Q

sinusoids

A

-where formed elements enter the blood from the marrow

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8
Q

marrow morphology

A
  • myeloid cells (granulocytes) paratrebecular
  • RBCs surround Macs to get Fe
  • megakaryocytes surround next to sinusoids to release platelets

leukoerythroblastosis –> immature precursors released into blood

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9
Q

leukopenia

A
  • low WBC count
  • neutropenia most common**
  • lymphopenia less common (in HIV, steroids, autoimmune, viral infections)
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10
Q

proliferative disorders

A
  • expansion of leukocytes
    1. reactive - has inflammation/infection
    2. neoplastic - no inflammation, just proliferation forming tumor
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11
Q

neutropenia aka agranulocytosis

A
  • risk of hematologic disease or increased risk for infection**
  • see ulcerating lesions of mucous membranes from bacterial/fungal infection
  • risk for deep fungal infections by candida and aspergillum
  • massive organism growth, little leukocyte response
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12
Q

levels of neutropenia**

A

Mild: 1.0-1.5×109 neutrophils/L
Moderate: 0.5-0.9×109 neutrophils/L
Severe: <0.5×109 neutrophils/L

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13
Q

downey cells**

A
  • activated lymphocytes reacting EBV, CMV**

- atypical lymphocytes

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14
Q

causes of neutropenia

A
  1. ineffective/inadequate erythropoiesis
    - suppression of HSC
    - drug suppression of precursors –> drug toxicity most common cause** (chemo, alkylating agents, sulfonamides, pmenothiazines) –> high risk of infection**
    - ineffective hematopoiesis from megaloblastic anemia –> apoptosis
    - inherited gene defects that impair granulocyte proliferation
    - increased destruction or sequestration –> from severe infection or splenomegaly**
    - increased destruction of neutrophils –> hyper cellular marrow*
    - agranulocytosis (from overwhelming infection) –> hypocellular marrow*
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15
Q

reactive proliferations of WBC –> leukocytosis

A
  • increase in WBC count
  • inflammation, infection, hypoxia increase release from storage pool
  • exercise and catecholamines increase demargination (break off of vessel walls)
  • cortisol decreases extravasation into tissues
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16
Q

neutrophilic leukocytosis causes

A
  • infection, inflammation most important**
  • acute infection –> increase neutrophil production via TNF from Macs (also increase other cells from bone marrow via cytokines)
17
Q

leukocytosis types**

A
  1. Neutrophilia: Acute bacterial infection, sterile inflammation (ex. tissue necrosis)
  2. Eosinophilia: Allergy, parasites, drug reaction, certain malignancies (Hodgkin)**, autoimmune disorders
  3. Basophilia: Rare, indicates myeloproliferative disease (ex. CML)**
  4. Monocytosis: Chronic infections (ex. tuberculosis)**, rickettsiosis, malaria, autoimmune disorder
  5. Lymphocytosis: Accompanies monocytosis, associated with chronic immune stimulation (ex, tuberculosis), viral** infections
18
Q

sepsis or sever inflammatory disorders

A

-changes in neutrophils: toxic granulations, dohle bodies** (ER in neutrophils showing overwhelming infection)

19
Q

left shift

A
  • increased production of immature neutrophils (band cells) due to infection
  • bone marrow working harder to release more granulocytes
20
Q

reactive vs. neoplastic leukocytosis

A
  1. reactive: severe infections where granulocytes mimic myeloid leukemia (leukemoid rxn)
    - LAP (leukocyte alkaline phosphatase) elevated due to infection
  2. neoplastic: acute viral infections where many lymphocytes resemble neoplastic cells
    - LAP low bc there is no infection
21
Q

lymphadenitis: reactive proliferations of lymph nodes

A
  1. B cells: bone marrow –> primary lymphoid follicle in lymph nodes
    - T cell stimulation from antigen produces secondary lymphoid follicle with germinal center where B cells create high affinity antibodies
    - plasma cells release antibodies
  2. T cells: thymus –> paracortex of lymph node
  3. macrophages in medulla
22
Q

acute nonspecific lymphadenitis

A
  • nodes enlarged, painful, and suppurative
  • draining sinuses of teeth or tonsils**
  • due to systemic viral infections
  • large reactive germinal centers
  • histiocytes travel to where neutrophils destroyed pyogenic bacteria –> apoptosis/necrosis –> macrophages clean up debris
  • lots of neutrophils, Macs, and necrosis –> not neoplastic process**
23
Q

chronic nonspecific lymphadenitis

A
  • nontender, slowly enlarging nodes
  • in inguinal and axillary nodes**
  • follicular hyperplasia with humoral response (by any antigen or bacteria)**
  • polarized germinal center: centroblasts in dark zone (develop high affinity antibodies), centrocytes in light zone**
  • DCs present antigens to B cells in germinal center, macrophages phagocytose B cells that can’t make high affinity antibodies
  • favors reactive hyperplasia, not neoplastic process
  • paracortical hyperplasia from stimuli that trigger T cell mediated response like acute viral infection (ex. mono from EBV)** –> expanded T cell zone, less follicular hyperplasia
  • sinus histiocytosis: increase cells lining sinusoids like Macs and endothelial cells –> used to drain cancers (ex. breast cancer)**
24
Q

hemophagocytic lymphohistiocytosis (HLH)

A
  • aka macrophage activation syndrome** (also activate CD8 T cells)
  • triggered by infection, EBV most common**
  • lead to cytopenias and systemic inflammation
  • phagocytize cells and suppress hematopoiesis with cytokine storm (shock like syndrome)
  • familial forms and mutations –> cannot form cytotoxic granules –> febrile and hepatosplenomegaly
  • may see hepatitis, DIC, multi organ failure, shock, death
25
Q

myeloid neoplasms - originate in bone marrow

A
  1. Acute myeloid leukemias –> myeloid progenitor cells accumulate in marrow
  2. Myelodysplastic syndromes –> inef­fective hematopoiesis and peripheral cytopenias
  3. Chronic myeloproliferative disorders –> increased production of one or more terminally differentiated myeloid elements
26
Q

leukemia vs lymphoma

A
  1. leukemia: blood cells or bone marrow –> affect spleen or liver when entering circulation
  2. lymphoma: cancer in lymph nodes –> cannot enter circulation
27
Q

lymphoid neoplasms - tumors of B,T, NK origin

A

-stop normal maturation –> uncontrolled proliferation

28
Q

chromosomal mutations leading to neoplastic proliferation

A
  • oncoproteins block normal maturation, activate pro-growth, and protect from apoptosis
  • mutations in transcription regulators enhance self-renewal of tumor cells (MLL translocation, PML-RARA fusion gene)
    • tyrosine kinase –> + RAS, PI3K/AKT, MAPK –> pro growth
  • BCL2 translocation –> inhibit apoptosis
  • Neoplasia from the proto-oncogenes being turned on (due to errors in antigen receptor gene) and releasing their products
  • MYC (protooncogen) and BCL6 (TF for transcription repression) activated in germinal center B cell lymphomas
29
Q

lymphotrophic viruses and associated lymphomas**

A
  1. HTLV1 –> adult T cell leukemia/lymphoma (ATLL)
  2. EBV –> Burkitt lymphoma, Hodgkins lymphoma, B-cell lymphoma with T-cell immunodeficiency, NK-cell lymphoma
  3. HHV-8 (Kaposi sarcoma, malignant effusion B-cell lymphoma)
30
Q

agents that cause chronic inflammation –> lymphoid hyperplasia and neoplasia

A
  1. H. pylori –> gastric B cell lymphoma
  2. gluten sensitive enteropathy –> intestinal T cell lymphoma
  3. smoking –> AML

OMS II BECOM Exam 1 (30 decks)

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