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hiv homiez > Hematologic Malignancies COPY > Flashcards

Hematologic Malignancies COPY Flashcards

1
Q

Cancer and Treatment

A

Local=surgery
Regional=Radiation
Systemic=chemotherapy

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2
Q

Hematological Cancers

A

Cancer of the blood; no solid tumor
-TNM grading system does not apply and surgery is not an option

Divided into two major types:

  • leukemia
  • lymphoma + myeloma
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3
Q

Symptoms of Hematological cancer

A

Can present with multiple symptoms or none at all
-tumor compression, invasion, or destruction of surrounding tissues causes symptoms–> cancer located in GI tract

Systems:

  • N/V
  • constipation
  • diarrhea
  • bloody stools
  • abdominal pain
  • early satiety

unexplained weight loss=more universal

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4
Q

7 Signs of Cancer

A 
C: change in bladder or bowel habits 
A: A sore that doesnt heal 
U: unusual bleeding or discharge
T: thickening or lump in breast or elsewhere 
I: indigestion or trouble swallowing 
O: obvious change in wart or mole 
N: nagging cough or hoarseness

**seek doctor

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5
Q

Heme Malignancy

-Symptoms

A

“tumors” are uncommon

Symptoms:

  • elevated/decreased blood counts (RBC, WBC, platelets)
  • coagulopathies
  • swollen lymph nodes
  • B-symptoms: fevers, night sweats, and weight loss
  • splenomegaly
  • malaise

diverse and not easily identified on symptoms alone

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6
Q

Blood: Function

A

1) Transport: oxygen, carbon dioxide
- nutrients
- waste
- hormones
- ions/electrolytes

2) Protection:
- WBC
- antibodies
- platelets

3) Regulation
- body temperature
- pH
- water balance

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7
Q

Hematopoiesis: Bone Marrow

A

richly innervated, highly vascularized spongey tissue

- flat and long bones, trabecular (cancellous) bone,

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8
Q

Lymph Node Biopsies

A

whole node, fine needle aspirate, core

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9
Q

Bone marrow biopsy + aspirate

A

commonly used to examine cells for identification of various heme disorders + malignancies

  • smear: direct visual examination of cells
  • fluorescence in situ hybridization (FISH): chromosomal changes
  • karyotype testing: chromosome map (arrangement, size, shape, number)
  • flow cytometry: identification of cells; quantitative analysis
    - immunophenotyping: fluorescent antibody labeled cells
  • immunohistochemistry (IHC): utilizes antibodies that bind to certain antigens/cell surface markers to stain protein + make visible under microscope
  • polymerase chain reaction (PCR): amplification + detection of DNA segments
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10
Q

Hematologic Malignancies

A
  • Essential Thrombocythemia (ET): platelets abnormal
  • Polycythemia Vera (PV): red blood cells (abnormal)
  • Myelofibrosis (MF): collagen and reticulin fibers (fibrosis)
  • Myelodysplastic Syndromes (MDS): immature blood cells
  • Acute Myelogenous Leukemia (AML): immature white cells
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11
Q

Leukemia

A

produce poorly differentiated cells; derived from disruption in hematopoiesis

  • involved cells may have features of any phase of myelocytic or lymphocytic maturation depending on hematopoiesis maturation
  • can develop at any stage, any cell line
  • uncontrolled production of precursor WBC that cannot mature but can proliferate
  • survival advantage over normal cells “crowding out” phenomenon of normal cells in marrow
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12
Q
  • Common Myeloid Progenitor
  • Common lymphoid progenitor

Presentation

Diagnosis

A
  • Acute myelogenous leukemia (AML), chronic myelogenous leukemia (CML)
  • Acute lymphoblastic leukemia (ALL), chronic lymphoblastic leukemia (CLL)
  • fatigue, weight loss, anemia, thrombocytopenia, leukopenia OR leukocytosis, splenomegaly, hepatomegaly
  • CBC, bone marrow aspirate + biopsy, molecular testing for FMS-like tyrosine kinase 3 (FLT3), nucelophosmin (NPM1)
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13
Q

Genetic alterations in leukemias

A
  • activation of protooncogene to signal increased proliferation
  • loss of differentiation signals
  • loss of tumor suppressor genes (P53)
  • loss of apoptotic signals
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14
Q

Potential chromosomal alterations

A
  • numerical (duplication/deletion)
  • inversion (exchange of genetic info within)
  • translocation (between)
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15
Q

Acute Leukemias

A

most common malignancies in children, leading cause of cancer-related death in patients <20 years

Both AML + ALL

  • arise from single leukemia cell: acquires from additional mutations
  • fail to maintain balance of proliferation + differentiation –> myeloblasts/ lymphoblasts proliferate uncontrollably)
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16
Q

Acute Leukemia Causes

A

infection, genetic factors: strongest association to development of acute leukemias
- drugs: alkylating agents, anthracyclines
- genetic conditions
- chemical exposure: benzene, pesticides
- ionizing radiation
- viruses: Epstein-Barr, human T-lymphoctye virus
= social habits: cigarette smoking, maternal ethanol/marijuana use

MOST cases diagnosed do not have a cause identified

17
Q

Acute Myeloid Leukemia

A

Rapidly progressing leukemia; can be fatal if not treated rapidly

Improper maturation; not differentiated

  • arise from pluripotent stem cell
    • older patients: arises from stem/early progenitor cell
    • younger patients: differentiated cell becomes malignant (different forms of resistance)

Secondary leukemias: prolonged “preleukemic phase” of hypoproduction/abnormal maturation

18
Q

Chronic Myeloid Leukemia

A

indolent leukemia from immature granulocytes in marrow and circulation

50% are asymptomatic at time of diagnosis (chronic phase-CP)
-accelerated phase: progressive myeloid maturation arrest (increased blasts), exacerbation of symptoms

HALLMARK SIGN: Philadelphia chromosome-translocation of chromosomes 9 + 22

Targeted therapy: inhibit BCR-ABL by competitively interfering with ATP-binding site

19
Q

Lymphocytic Leukemias: Acute Lymphocytic (ALL)

A

Rapidly progressive, derived from lymphoblasts; more common in adults

Classified according to B-cell or T-cell lineage, includes cytogenetic abnormalities (immunophenotyping)

Philadelphia chromosome: different role than CML; targeted therapies not effective

20
Q

Lymphocytic Leukemia: Chronic Lymphocytic (CLL)

A

Most common leukemia in US

Neoplasm of more mature, but nonfunctioning B-cells, lymphocytes may not be morphologically different

  • Same underlying disease as lymphocytic non-bodkin lymphoma
  • Chromosome 17 short arm deletion: p53 silencing –> more proliferation + maturation of cells

Signs+Symptoms: anemia, thrombocytopenia, lymphadenopathy, splenomegaly, hepatomegaly, fatigue, weight loss

21
Q

Lymphoma

A

Diverse group of neoplasms characterized by proliferation of malignant lymphocytes in the lymphoid system; most common heme malignancy in US
- Germinal center = site of differentiation for B-cells in the lymph nodes

Non-Hodgin lymphoma: ~85%
-B or T cell; indolent or aggressive

22
Q

Hodgkin Lymphoma

A

Most curable form; affects patients in 20-30s + after age 50

Signs + Symptoms:
-fatigue, pruritis, lymphadenopathy, B symptoms (fever, night sweats, weight. loss)

Clonal malignant lymphoid disease of transformed B-lymphocytes: Reed-Sternberg cells
-found in an inflammatory microenvironment

Infectious Associations: immunosuppression (congenital, organ transplant, HIV infection)

23
Q

Non Hodgkin Lymphoma

A

Heterogenous group of lymphoproliferative disorders

Causes: genetic disease, environmental exposure, infection
Smoking does NOT have strong association

24
Q

Non - Hodgkin Lymphoma

  • Indolent
  • Aggressive
  • Very Aggressive
A

Indolent: small cell lymphocytic, follicular, marginal zone

  • untreated survival: years
  • curable: no
  • treat? defer (asymptomatic)

Aggressive: diffuse large B-cell, mantle cell

  • untreated survival: months
  • curable: possible
  • treat? yes

Very Aggressive: Burkett’s

  • untreated: weeks
  • curable: possible
  • treat? yes
25
Q

Multiple Myeloma

A

Malignant plasma cells (differentiated B cells)

  • overproduction of monoclonal paraprotein
  • plasmacytosis
  • M protein: abnormal, ineffective antibodies

Microenvironment promotes further expansion of myeloma clones, disease progression, resistance to therapy

Signs + Symptoms: CRAB

  • Calcium elevation
  • Renal insufficiency
  • Anemia
  • Bone lesions/pain

Diagnosis: bone marrow biopsy with >10% plasma cells, M-protein spike (urine or plasma); Swiss cheese type lesions

hiv homiez (8 decks)

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