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MI Internal Medicine > Leukemia and lymphoma > Flashcards

Leukemia and lymphoma Flashcards

1
Q

Major concerns with leukemic patient falling ill suddenly

A
  1. Infection
  2. Bleeding
  3. Hyperviscocity
  4. Tumor lysis
  5. Disseminated intravascular coagulation: malignancy, sepsis, trauma, obstetric

Non-specific confusion

a. Take blood culture
b. exclude hypoglycemia
c. UEC, LFT, Ca, clotting screen
d. Consider CNS bleeding->CT/MRI

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2
Q

Neutropenic regimen

A
  1. Close liason with microbiologist and hematologist
  2. Full barrier nursing. Hand washing.
  3. Avoid IM injections->infected hematoma
  4. Look for infection->mouth, axilla, perineum, IV site. Take swabs
  5. Check: FBC, PLTs, INR, UEC, LFTs
  6. Take cultures, urine, sputum, stool
  7. CXR
  8. Wash perineum after defecation
  9. Oral hygeine
  10. TPR obs 4 hourly
  11. High calorie diet
  12. Vases with roses pose a pseudomonas risk
  13. Antibiotics: if febrile >38/toxic= septicemia, piperacillin+tazobactam + ceftriaxone
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3
Q

What is tumor lysis syndrome, electrolyte changes, risk+, prevention

A
  1. Massive cell destruction= hyperkalemia, hyperuricemia, renal impairment
  2. Risk + if +LDH, +Cr, +urate, +WCC
  3. Prevention with high fluids, allopurinol pre cytotoxics
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4
Q

Management of DIC

A
  1. Identify cause

2. Replace PLTS, cryoprecipitate (replacing fibrinogen), FFP to replace coagulation

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5
Q

What is ALL, associations and epidemioloy, CNS

A
  1. Malignancy of lymphoid, either T/B cell
  2. Arrested maturation, proliferation of Blast cells
  3. Most commonly malignancy of childhood, rare in adults
  4. CNS involvement is common
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6
Q

Classification systems in ALL

A
  1. Morphological: L1, 2, 3
  2. Immunological: Precursor B, T ALL, B ALL
  3. Cytogenetic: Philaedelphia has poor prognosis
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7
Q

Signs and symptoms of ALL

A 
1. Marrow failure=
Anemia
Bleeding 
Infection
2. Infiltration
Hepato/splenomegaly
Lymphadenopathy
Orchidoplexy
CNS->CN palsies, menningism
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8
Q

Common infections in ALL

A
  1. Mouth
  2. Skin
  3. Perianal
  4. Lung
  5. Pneumocystis
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9
Q

Investigations in ALL

A
  1. FBC, peripheral blood smear w/ blasts, +WCC
  2. CT/CXR for mediastinal
  3. LP for CNS involvement
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10
Q

Management of ALL

A
  1. Educate and motivate
  2. Supportive
    Transfusions, IV fluids, allopurinol
    Hickman line for IV access
  3. Infections: neutropenia regime. IV antibiotics->co-trimoxazole to prevent Pneumocystsis, antivirals, antifungals
  4. Chemotherapy
    National trials
    a. Remission induction
    b. Consolidation
    c. CNS prophylaxis
    d. Maintenance for 2 years
  5. Bone marrow transplant
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11
Q

Where is relapse common in ALL

A
  1. Blood

2. Testes

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12
Q

Prognosis: cure rates, poor prognostics

A
  1. 70-90% cure in children, 40% in adults
  2. Prognostics
    Male
    Adult
    Philadelphia: BCR:ABL translocation of 9:22
    CNS
    Anemic
    +WCC
    Minimal residual disease
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13
Q

What is AML, incidence, asssociations

A
  1. Acute myeloid leukemia
  2. Most common leukemia in adults
  3. Associated with radiation, MDS, Downs syndrome
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14
Q

Morphological classification of AML

A
  1. AML with recurrent genetic abnormalities
  2. AML with multi-lineage dysplasia
  3. AML therapy related
  4. AML other
  5. Acute leukemia of ambiguous lineage
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15
Q

Is CNS involvement in AML, what about gums

A
  1. CNS involvement is rare

2. Finding of gum hypertrophy

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16
Q

What findings on smear is diagnostic of AML

A

Auer rods

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17
Q

How is AML diagnosed

A
  1. Immunophenotyping, molecular methods

2. Cytogenetic analysis

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18
Q

Pitfalls in AML complication recognition

A
  1. AML itself causes fever
  2. Common organisms present oddly
  3. Few antibodies are made
  4. Rare organisms (fungi)
19
Q

Treatment for AML

A
  1. Supportive as for ALL
  2. Chemotherapy
  3. Bone marrow transplant
20
Q

Prognosis in AML

A
  1. 60% long term survival
21
Q

What is CML, epidemiology, Philadelphia chromosome, symptoms

A
  1. Proliferation of myeloid cells, 15% leukemia
  2. Most common in 40-60, rare in childhood
  3. Ph xsome most common abnormality
  4. Fatigue, weight loss, gout, fever, sweats, bleeding, abdominal discomfort
22
Q

Signs in CML and investigations

A
  1. +Liver/spleen, anemia, bruising
  2. ++WBC, +BEN, anemia, PLT
  3. +Urate, +B12.
  4. Hypercellular BM
23
Q

Natural history in CML

A
  1. Survival 5-6 years

2. Chronic (months)->accelerated (+sympT, +spleen)->blast transformation

24
Q

Treatment in CML

A
  1. Chemotherapy->Imatinib specific BCR:ABL tyrosine kinase inhibitor
  2. Hydroxycarbamide
  3. Dasatinib
  4. Stem cell transplant
25
Q

What is hallmark of CLL, epidemiology, rai staging

A
  1. Most common leukemia, arrested B cells->+proliferation
  2. Rai stage
    0= Lymphocytosis >13yr survival
    1= +lymphadenopathy 8yr survival
    2= +spleno/hepatomegaly 5yr
    3= +anemia 2 yr survival
    4= +thrombocytopenia 1 yr survival
26
Q

Typical presentation in CLL

A
  1. Asymptomatic
  2. Surprising finding on routine blood tests
  3. Enlarged, non-tender rubbery nodes, +spleen/liver
27
Q

Investigations and complications in CLL

A
  1. +Lymphocytes
  2. Autoimmune hemolysis
  3. Marrow infiltration->anemia, neutropenia, thrombocytopenia

Complications

  1. Autoimmune hemolysis
  2. Marrow failure
  3. +Infection due to hypogammaglobulinemia
28
Q

Management in CLL

A
  1. Fldarabine + cyclophosphamide
  2. Steroids in autoimmune hemolysis
  3. Radiotherapy to relive lymphadenopathy/splenomegaly
  4. Supportive
  5. Stem cell transplant
29
Q

Prognosis in CLL`

A
  1. One third never progress
  2. One third will progress in time
  3. One third are actively progressing
30
Q

What is lymphoma

A
  1. Malignant proliferation of lymphocytes within lymph nodes, but can be in peripheral blood and infiltrate organs
31
Q

Characteristic cell of hodgkins lymphoma

A

Reed-Sternberg

32
Q

Epidemiology of HL and risk associations

A
  1. Young and elderly
  2. More common in males
  3. Risk + if affected sibling, EBV, SLE, post transfusion, Westernisation and obesity
33
Q

Symptoms of HL

A
  1. Enlarged, non tender, rubbery superficial LN->cervical, axillary, inguinal
  2. Weight loss, night sweats, pruritus
  3. Mass effect from mediastinal mass->SVC obstruction/bronchial
  4. Alcohol induced LN pain
34
Q

Signs of HL

A
  1. Weight loss, cachexia

2. Hepato-splenoM

35
Q

Investigations in HL

A
  1. FBC->anemia and low PLT
  2. UEC, LFTs, LDH, Urate (cell turnover)->baseline prior to therapy commencement
  3. ESR ++
  4. CXR->mediastinal mass
  5. PET-CT, LP
  6. Contrast CT N, chest, abdomen/pelvis (for staging)
  7. Excisional LN biopsy
  8. Immunohistochemistry
36
Q

Staging in HL

A
  1. Confined single LN region
  2. 2+ nodal areas on same side of diaphragm
  3. Nodes on both sides of the diaphragm
  4. Spread beyond the LN->liver or bone marrow
37
Q

Management

A 
1. Chemotherapy ABVD
Adriamycin
Bleomycin
Vinblastine
Dacarbazine
2. Radiotherapy
38
Q

General risks in radiotherapy

A
  1. Increased risk of secondary malignancies->solid
  2. IHD
  3. Hypothyroidism
  4. Lung fibrosis
39
Q

Classification of HL

A
  1. Nodular sclerosing
  2. Mixed cellularity
  3. Lymphocyte rich
  4. Lymphocyte depleted
40
Q

Causes of NHL

A
  1. Congenital immunodeficiency
  2. Acquired immunodeficiency
  3. HIV infection
  4. Infection->HTCLV-1, EBV, H pylori
  5. Environmental toxins
41
Q

Is NHL just LN

A

No, can occur at other lymphoid tissue->MALT

42
Q

Signs and symptoms of NHL

A
  1. Nodal disease
  2. Superficial lymphadenopath
  3. Extranodal: oropharynx, skin, bone, gut, CNS, lung
  4. Fever, night sweats, weight loss
  5. Pancytopenia: anemia, infection, bleeding
43
Q

Investigations in NHL

A
  1. FBC->anemia and low PLT
  2. UEC, LFTs, LDH, Urate (cell turnover)->baseline prior to therapy commencement
  3. ESR ++
  4. CXR, LP
  5. PET-CT
  6. Contrast CT N, chest, abdomen/pelvis (for staging)
  7. Excisional LN biopsy
  8. Immunohistochemistry
44
Q

Chemotherapy regime in high grade NHL

A 
RCHOP
Rituximab
Cyclophosphamide
Hydroxydaunorubicin
Vincristin (Oncovin)
Prednisolone

MI Internal Medicine (67 decks)

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