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Hematology > Hematologic Malignancies > Flashcards

Hematologic Malignancies Flashcards

1
Q

Types of Heme Malignancies

A

Leukemia

Lymphoma

Myeloma

Myelodysplastic Syndrome

Myeloproliferative Disorder

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2
Q

What is leukemia?

A

cancer of the blood and bone marrow characterized by the uncontrolled accumulation of malignant white blood cells

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3
Q

Leukemia

Acute vs. Chronic

A

Acute

  • block in differentiation of immature WBC
  • rapid course
  • death within days to weeks if untreated

Chronic

  • excess proliferation of more mature WBCs
  • indolent course
  • may survive for years even if untreated
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4
Q

Leukemia

Signs and Symptoms

A

Can be asymptomatic to sudden, severe illness

Initally presentation is often non-specific

  • fatigue
  • infection (recurrent, persistent)
  • mild bleeding symptoms (bruising, epistaxis)
    • these patients will generally get bounced around before getting their final dx

Abnormal CBC

  • pancytopenia
  • marked leukocytosis
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5
Q

Leukemia

Diagnosis

A

Get it done ASAP!

Detail H&P

Labs: CBC, renal and liver function, coags, peripheral blood immunophenotyping

Bone marrow aspirate and biopsy (within 24hrs)

Imaging studies as directed by H&P

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6
Q

Classification of Leukemia

A

Myeloid vs. Lymphoid

  • from which stem cell arises from
  • determines treatment options

Acute vs. Chronic

  • determines urgency of treatment
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7
Q

Leukemia

Risk Factors

A

**In most cases, the cause is unknown **

AML

  • Radiation exposure
  • Chemotherapy
  • Benzene
  • Tobacco smoke
  • Genetic disorders - Down and Fanconi anemia
  • Preexisting MDS

ALL

  • Radiation exposure
  • Viral infection - EBV, HTLV-1
  • Genetic disorders - Down

**CML **

  • Radiation exposure

**CLL **

  • Race/genetics (white males >70)
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8
Q

Secondary Leukemia

Causes

A

Arises from pre-existing MDS/MPD or following exposure to radiation or chemotherapy

Latent period approximately 5 years

Almost always myeloid, and usually preceded by dysplastic changes in all 3 cell lines

Abnormalities in multiple chromosomes and complex karyotypes common

Prognosis is worse than for de novo AML

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9
Q

Leukemia

Age that it affects

A

Bimodal distrubition - >20, <65 MC

Older pts more likely to die from leukemia

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10
Q

Leukemia

Treatment

A
  • Little role for surgery or radiation
  • Chemo is the main treatment modality
  • Stem cell transplant
  • Prognosis varies widely
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11
Q

Leukemia

Treatment and Prognosis of Each Type

A

ALL

  • MC in kids; highly curable with chemo
  • Adults: less common, nasty, usually requires transplant to cure

AML

  • uncommon in kids
  • several subtypes so prognosis is variable

Generally, tx - induction, consolidation, maintenance

CLL

  • Not seen in kids, common in elderly
  • Don’t treat until sxs develop
  • Goal is to control disease with chemo, true cure unlikely

CML

  • very uncommon in kids
  • chronic, accelerated, adn blast crisis phases
  • up to 70% cure if transplanted in chronic phase
  • Philadelphia chromosome: Gleevec and other TKIs block faulty protein that signals cells to grow out of control
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12
Q

Leukemia

Histology

A

Bone marrow - Increase in cellularity

AML - Auer rods (clusters of granules) on peripheral blood smears

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13
Q

Lymphadenopathy

A

Palpable lymph nodes - cervical, supraclavicular, axillary, inguinal

What they feel like

  • soft, tender, mobile = infx/inflammation
  • firm, rubbery, mobile, non-tender = lymphoma
  • hard, fixed, non-tender = carcinoma

Localized Lymphadenopathy:

  • Infection - bacterial or viral
  • Lymphoma - Hodgkin/NHL
  • Carcinoma (metastatic)

Generalized Lymphadenopapthy

  • Infection - bacterial, viral, fungal
  • Inflammatory - sarcoid, SLE
  • Leukemia
  • Lymphoma
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14
Q

What is Lymphoma?

A

CA of lymphoid tissues, malignant cell is the lymphocyte

Malignant lymphocytes accumulate in the lymph nodes, spleen, liver, and bone marrow

Malignant lymphocytes can also circulate in the blood and resemble leukemia

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15
Q

Lymphoma

Classification

A

Hodgkin’s Disease

  • Relatively uncommon
  • Primarily affects young adults
  • High cure rates

Non-Hodgkin Lymphoma (NHL)

  • Common
  • Low grade typically affects older adults
  • High grade (less common) affects kids, but responds better to chemo
  • Wide variation in prognosis, tx success

Both have different subtypes depending on histology

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16
Q

Lymphoma

Signs and Symptoms

A

Ranges from asymptomatic to sudden, severe illness

Fatigue, weight loss, fever, night sweats

Lymphadenopathy (localized or generalized)

Enlarged liver and / or spleen

Skin lesions, pruritis

GI bleeding, obstruction - when lymphoma is near GI tract

Lymphocytosis

17
Q

Lymphoma

Diagnosis

A

Detailed H&P

Labs: CBC, renal and liver ftn, coags, LDH, peripheral blood immunophenotyping (flow cytometry used in staging)

Imaging: CT, MRI, PET from head to toe to determine what is affected (usually more than one region)

Biopsy: lymph node (want entire node to accurately dx/stage) - surgical procedure; bone marrow, skin lesion, GI tract, liver depending on what is involved

18
Q

Lymphoma

Staging

A

**Stages determine treatment **

  • Stage I: 1 node group
  • Stage II: > 1 node groups, same side of diaphragm
  • Stage III: nodes on both sides of diaphragm
  • Stage IV: marrow or other extranodal side

**Type (A - yes, B - no) determine prognosis **

  • presence of fevers, night sweats, weight loss
19
Q

Lymphoma

Treatment

A

Treatment approach varies depending on age of patient and specific type of lymphoma

  • Surgery - to obtain tissue for diagnosis
  • Chemo and Stem cell transplant (common)
  • Radiation (uncommon)
20
Q

Spectrum of Plasma Cell Disorders

General

A

MGUS – Smoldering Myeloma – Multiple Myeloma

Monoclonal gammopathy - excess production of gamma globulin protein (IgG) by a single clone of B cells/plasma cells

21
Q

Plasma Cell Disorders

MGUS

A

Monoclonal Gammopathy of Underdetermined Significance

Common - occurs in 3% of people >70 y.o.

Plasma cells grow enough that you can monitor its antibody protein in the blood

Will see increased plasma cells on bone marrow biopsy, but no other clinical features of myeloma

Generally benign, but may progress to multiple myeloma (10-20% progress to myeloma, but can take more than 10 years)

No way to prevent the progression, so monitor closely

22
Q

Plasma Cell Disorders

Multiple Myeloma

Etiology, epidemiology, clinical presentation

A

Malignant proliferation of plasma cells

10% of hematologic malignancies, MC >65y.o., MC AA

**Clinical Manifestations: **

  • Monoclonal protein:
    • ppts into kidneys –> renal failure
    • hyperviscosity which can lead to hypoperfusion
    • amyloidosis
  • Lytic Bone Lesions: punched out appearance on x-rays because increased cell turnover
    • Bone pain
    • Pathologic fxs
    • Hypercalcemia –> renal failure
  • Anemia: because less EPO as kidneys fail, bone marrow replaced with plasma cells
  • Infections: antibodies aren’t function so can’t fight infx
23
Q

Plasma Cell Disorders

Multiple Myeloma

Treatment

A

Complete remission more common and durable

  • Higher response rates to chemo - thalidomide as an angiogesis inhibitor
  • Better are doing transplants

Treatment depends on age, etc.

24
Q

Leukemia, Lymphoma, and Myeloma

vs.

MDS and MPN

A

Leukemia, Lymphoma, and Myeloma

  • malignant transformation of mature blood cell or precursor
  • accumulation of malignant cells result in clinical manifestations
  • specific treatments - chemo - can reuslt in cure

MDS, MPN

  • mutation in stem cell or early progenitor –> anything produced from these are malignant
  • results in ineffective hematopoiesis (hypercellular, but dec production) or the overproduction of mature blood cells
  • may transform to AML
  • only curable with transplant
  • generally are slower
25
Q

MDS

A

Myelodisplastic Syndrome

Pathophysiology

  • Heterogeneous group of malignant hematopoietic stem cell disorders
  • Characterized by dysplastic and ineffective blood cell production
  • Clonal process thought to develop from a single mutated stem cell –> any cell that arises from this is abnormal

Epidemiology/RF

  • >65y.o.
  • Benzene, radiation, tobacco, chemo, and genetic factors

Classification - dependent on molecular features in hopes to develop targeted therapies

Clinical Features

  • anemia - transfusion dependent
  • thrombocytopenia - nuisance to life threatening, transfusion dependent
  • leukopenia - dysfunctional neutrophils –> infection
  • transformation to secondary AML may occur after a few months, years, or not at all

**Diagnosis **

  • Ineffective hematopoiesis - hypercellular marrow but low peripheral counts
  • Dysplastic cells on smear and in bone marrow
  • Cytogenetic abnormalities (FISH)
  • Presence of circulating blasts, or increasing numbner of marrow blasts (<20% or AML)

Treatment: sucks - chemo, radiation, etc. Transplant only curative option

26
Q

MPN

Patho, epidemiology

A

Myeloproliferative Neoplasms

Like MDS, MPN is a clonal process from a single mutation stem cell, but are characterized by excessive proliferation of mature blood cells

Median age 60 y.o, but more common in younger individuals

With tx survival for decades is possible

27
Q

MPN

Specific entities

Common features

Complications

A
  • polycythemia vera (p. vera)
  • essential thrombocythemia (ET)
  • chronic myeloid leukemia (CML)
  • primary myelofibrosis (PMF)

Common features:

  • chronic course
  • over production of 1-3 blood cell lines
  • marrow fibrosis, leading to splenomegaly
  • PV, ET, PMF have JAK2 mutation - intracellular signaler that is more sensitive to GF

Complications

  • clonal evolution, transformation to AML
  • thrombosis - venous and arterial, unusual locations
  • marrow fiborsis
28
Q

MPN

Clinical features

Diagnosis

Treatment

A

Symptoms:

  • disabling fatigue
  • pruritis - p. vera
  • splenomegaly
  • hypermetabolic sx (wt loss, fever, night sweats)
  • bone pain
  • erythromelagia (burning sensation in hands/feet with erythema, pallar, or cyanosis, with palpable pulses)
  • neurologic sxs

Diagnosis

  • some diagnosed incidentally (CBC)
  • others present with complications of dramatically elevated blood counts –> clotting

Treatment

  • can’t prevent marrow fibrosis or transformation to AML
  • PV and ET want to control counts to reduce symptoms and prevent thrombotic complications (phlebotomy adn hydroxyurea)
  • CML - Gleevec
  • PMF - JAK2 inhibitor
  • transplant only curative therapy but limited use because of patient age

Hematology (7 decks)

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