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Fundamentals 3- Heme > Clinical and Therapeutic Aspects of Leukemia and Lymphoma > Flashcards

Clinical and Therapeutic Aspects of Leukemia and Lymphoma Flashcards

1
Q

What are the six most common presentations of acute leukemia?

A
  1. anemia
  2. thrombocytopenia
  3. neutropenia
  4. leukostasis
  5. Tumor lysis syndrome
  6. DIC
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2
Q

Leukemias are malignancies caused by excessive proliferation with the _______________________. Therefore, _______ accumulate and lead to __________________.

A

Excessive proliferation with the inability to differentiate.
Blasts accumulate and lead to bone marrow failure

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3
Q

In acute leukemias, what happens to the WBC count?
What does the differential of WBC show?
What will blood chemistries reveal?

A

1/3 have high WBC, 1/3 normal, 1/3 low WBC
The differential shows blasts with low neutrophils.
Platelets and RBC are also low.
The blood chemistry will show hyperurecimia due to increased breakdown of malignant cell components

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4
Q

What are common symptoms of anemia?

A

fatigue
pallor
dyspnea
tachycardia

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5
Q

What are common symptoms of thrombocytopenia?

A

bleeding, bruising, petechiae

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6
Q

What are the common symptoms of neutropenia?

A

fever, infection

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7
Q

What is leukostasis?

What leukemia is it commonly associated with?

A

When blasts clog the vasculature in the CNS or lungs

Occurs especially in AML when blasts are >100,000/microliter

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8
Q

What is tumor lysis syndrome?

If it is severe, what 4 things can occur?

A

It is when there is a massive release of blast contents: uric acid, phosphate, K+

Severe tumor lysis syndrome causes:

  1. uric acid neuropathy
  2. renal failure
  3. life threatening acidosis
  4. hyperkalemia
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9
Q

What is disseminated intravascular coagulation?
What is the manifestation?
What leukemia is it associated with?

A

When procoagulants are released from blasts and initiate clotting cascade, which creates an imbalance with the fibrinolytic cascade.
Coagulation factors, fibrinogen and platelets are used up.

It manifests with severe bleeding.
It is common in APML.

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10
Q

What are the four things that are reviewed to make a diagnosis of leukemia?

A
  1. morphology of the cells in the periphery and marrow
  2. flow cytometry
  3. cytogenetics
  4. molecular tests
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11
Q

What are the 3 worst acute leukemias?

A
  1. Secondary AML (post therapy or as a result of MDS)
  2. Philadelphia + ALL
  3. Elderly AML
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12
Q

What are the acute leukemias with the best prognosis?

A
  1. Children with ALL

2. APML

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13
Q

What are the 4 major AML drugs?

A
  1. Cytarabine
  2. High dose cytarabine
  3. ATRA aka tretinoin (for APML)
  4. Anthracyclines (doxorubicin/bleomycin)
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14
Q

What are the 6 drugs used for ALL?

A
  1. vincristine
  2. corticosteroids
  3. anthracyclines
  4. asparaginase
  5. methotrexate
  6. others
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15
Q

What are the 5 “supportive care” treatments for leukemia?

A
  1. allopurinol- decrease uric acid
  2. transfusions- help get mature cells
  3. Heme growth factors- speed recovery of cell count
  4. antibiotics
  5. leukaphoresis- to bring down WBC in patients with leukostasis
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16
Q

What is the most aggressive treatment available for acute leukemia?
What is the pro and con of using it?

A

Allogenic bone marrow transplantation
Pro: curative potential
Con: very toxic, GVHD, radiation and chemo prior to receiving the donor cells

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17
Q

What are the 4 phases of treatment for acute leukemia?
Which are used for AML? ALL?

How long does treatment last?

A
  1. Induction - both
  2. Consolidation-both
  3. Maintenance - ALL
  4. Bone marrow transplant- severe cases of either

Treatment lasts months to 3 years

18
Q

What is the goal of the induction phase of acute leukemia treatment?

A

Remission which is reducing the number of leukemia cells from the large number at presentation to undetectable by routine means

19
Q

After attaining remission, some cancer cells stull are present. What phase of treatment eliminates these additional cells?

A

Consolidation. (and maintenance for ALL)

20
Q

What treatment is needed for severe ALL in addition to the bone marrow transplant?

A

CNS prophylaxis (intrathecal injection of chemo) because ALL has a high incidence of CNS involvement

21
Q

What is used to treat APML?

22
Q

What is the translocation associated with APML? What is the mechanism by which it causes leukemia?
What is used to treate APML?

A

t(15,17) where the translocation results in PML-RARa fusion protein (retinoic acid receptor alpha). The fusion protein binds to DNA and recruits repressors which inhibit transcription of genes needed for differentiation.

ATRA at levels much higher than physiological level bind to the RARa portion of the fusion protein which causes the repressor proteins to be released and allows for the transcription of differentiation genes

23
Q

Lymphomas are cancers of _________.

A

Immune cells that populate lymphoid tissue

24
Q

How do patients present with lymphoma? (potentially 5 things)

A
  1. enlarged lymph nodes that are rubbery (carcinoma would be hard as a rock) and non-tender (infections would be tender)
  2. enlarged liver and spleen
    3 .B symptoms (fever, night sweats, weight loss
  3. SVC syndrome
  4. Tumor lysis syndrome
25
What causes B symptoms?
Cytokines released from lymphoma cells
26
What is SVC syndrome?
When a large mediastinal mass obstructs the SVC blocking blood return from the upper trunk and face causing swelling and engorged blood vessels
27
What lymphoma is frequently associated with tumor lysis syndrome?
aggressive NHL especially Burkitt's lymphoma
28
For a low grade lymphoma, what is the: 1. extent of spread at diagnosis 2. rate of growth 3. response to treatment
1. widespread 2. slow (year or two) 3. excellent, but incurable
29
For an intermediate grade lymphoma, what is the: 1. extent of spread at diagnosis 2. rate of growth 3. response to treatment
1. localized or widespread 2. rapid (weeks) 3. excellent and curable
30
For a high grade lymphoma, what is the: 1. extent of spread at diagnosis 2. rate of growth 3. response to treatment
1. widespread 2. extremely rapid 3. excellent, often curable
31
Describe the four stages of lymphoma using the Ann Arbor staging scale.
``` 1= one group of lymph nodes is involved 2= two groups of lymph nodes on the same side of the diaphragm 3= atleast two groups of lymph nodes on opposite sides of the diaphragm 4= involvement of other organs like liver or bone marrow ```
32
How is staging determined?
1. CT scan | 2. Bone marrow biopsy (*must be excisional because fine needle does not show tissue architecture)
33
What are the 5 strategies of treatment for lymphomas?
1. RAdiation 2. chemotherapy (alkylating agents, anthracycline, vinca alkyloids, corticosteroids) 3. Monoclonal Antibodies (rituximab anti-CD20 or radiolabelled anti-B cell antibody) 4. bone marrow transplant for aggressive lymphoma 5. watch and wait for indolent lymphomas
34
How is Hodgkin's lymphoma treated?
``` Chemotherapy with or without radiation. Early: ABVD regimen (Adriamycin, bleomycin, vinblastine, DTIC) for 4 cycles--> cure rate 85% Advanced lymphoma: ABVD for 6 to 8 cycles--> cure rate 70% ```
35
What is the treatment regimen for Diffuse large B-cell lymphoma?
``` Early 3 cycles of CHOP regimen with or without radiation 1. cyclophosphamide 2. Adriamycin 3. vincristine 4. prednisone ``` Rituximab (anti-CD20) is also given (75% cure) Late: 8 rounds of CHOP with rituximab (40% cure)
36
What is a blast crisis? What cancer is it associated with?
It is associated with CML. Early in CML the cells proliferate excessively but they differentiate to mature cells With time, the transformed stem cells acquire another mutation leading to more malignant, less differentiated cells--> blasts
37
How do patients with CML present?
They are often asymptomatic but history and physical can reveal: 1. fatigue, fullness in abdomen 2. splenomegaly 3. elevated WBC with mature cells 4. elevated platelets 5. elevated uric acid bc of cell turnover
38
What is the morphology of CML? | What is the cytogenetics?
Bone marrow is hypercellular with a preponderance of granulocytic precursors. Phl chromosome t(9,22)
39
What is the traditional treatment for CML? What is the best-risk cure rate and worst-risk cure rate? What is the problem with this treatment?
Allogenic stem cell transplantation 65% cure rate to 35% cure rate. The treatment is very toxic so there is an initial steep decline in survival
40
What is the new treatment option for CML? What are the pros and cons?
Imatinib (Gleevec) competitively inhibits the ATP-binding pocket of bcr-abl so that it can't constitutively activate the tyr kinase. Pro: well tolerated, lasting remission Con: does not cure so must stay on medication, most primitive CML cells are resistant so there is relapse

Fundamentals 3- Heme (19 decks)

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