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Clin Med2- Hematology > Leukemias and Lymphomas > Flashcards

Leukemias and Lymphomas Flashcards

1
Q

what is leukemia

A

cancer of the bone marrow

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2
Q

what is primarily involved in leukemias

A

WBC - “leuk” for leukocytes
overgrowth of immature or abnormal cells leading to suppression of normal cells/cell growth

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3
Q

what are the classifications of leukemias

A

Myeloid vs. Lymphoid
acute vs. crhonic

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4
Q

what is the presentation of acute leukemias

A

all ages, more likely in kids
sudden onset
rapid course
symptoms present (bleeding, infections, anemia)
high % of blasts
variable WBC count
Anemia
thrombocytopenia
minimal lympadenopathy
minimal splenomegaly
goal of treatment is to cure (chemo, BMT)

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5
Q

what is the presentation of chronic Leukemias

A

older age of onset, less likely in kids
insidious onset
prolonged course
often asymptomatic
higher % of mature cells
increased WBC count
minimal anemia
minimal thrombocytopenia
lympadenopathy
splenomegaly
treatment goal is to slow disease progression, normalize cell counts - less often curative

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6
Q

what are the primary types of leukemia

A

Acute myeloid leukemia (AML)
Chronic Myeloid leukemia (CML)
Acute lymphocytic leukemia (ALL)
Chronic Lymphocytic Leukemia (CLL)

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7
Q

what is the epidemiology of AML

A

no significant predilection for gender or race
median age of diagnosis: 68
- rarely diagnosed under age 60
- makes up of 80% of acute leukemia in adults

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8
Q

what is the pathophysiology of AML

A

exact etiology unknown - many sporadic genetic mutations identified
environmental exposures increase risk

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9
Q

what environmental exposures increase risk for AML

A

Benzene exposure (fires, fuels, cigarette smoke, plastics/resins, dyes/detergents, pesticides)
Radiation exposure
Exposure to alkylating agents or topoisomerase inhibitors - antineoplastic agents

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10
Q

what is the presentation of AML

A

non specific symptoms less than 3 months in duration
fatigue (most common)
anorexia
weight loss
fever
weakness
dyspnea on exertion (DOE)
cough
HA
bone pain
unexplained infections
sweating (night sweats)
bruising/easy bleeding (epistaxis)

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11
Q

what is the diagnostic lab for for AML

A

variable WBC count - depends on disease stage (Blasts >20%)
Low neutrophil count
thrombocytopenia (low platelet count)
Anemia (decreased reticulocyte count - bone marrow failure)

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12
Q

what are the diagnostics for AML

A

Blasts >20% OR + genetic testing required for diagnosis
definitive dx with BM biopsy

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13
Q

what is the histological presentation of AML

A

AUER RODS- pathognomonic for AML if present - crystallized cytoplasmic inclusion granules

cytoplasmic granules on peroxidase stain
immature nuclei

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14
Q

what is the treatment of AML

A

Goal is complete remission
Induction treatment: combination chemotherapy
Post remission treatment: BMT is more effective
-preferred for anyone age <75 or who has an HLA compatible donor
-if patient is low risk can consider continuing cytarabine

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15
Q

what are the supportive treatment measures of AML

A

platelet transfusions
PRBC’s
Prophylaxis with neutropenia
Prompt broad-spectrum abx if febrile

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16
Q

what is the prognosis of AML

A

overall 5 year survival rate of 28.7%

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17
Q

what makes the prognosis for AML worse

A

Older age - tx toxicities, more likely to have resistant disease
prior hematologic disease (myelodysplastic syndromes)
prior environmental exposures (benzene, radiation, etc)
certain genetic profiles
shorter time between remission and relapse

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18
Q

What is the epidemiology of CML

A

15% of all cases of leukemias
more common M>F
no significant predilection for race
median age at diagnosis: 65
- rare under age 40

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19
Q

what is the pathophysiology of CML

A

not hereditary
exception radiation, not related to environmental exposure (peak dx 5-10 years after radiation)
90% secondary to chromosomal translocation: 9:22
Bcr-abl gene (PHILADELPHIA CHROMOSOME)

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20
Q

What does the Bcr-abl gene result in

A

hyperactive tyrosine kinase
also interferes with the JAK/STAT pathway to produce resistance to apoptosis

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21
Q

what is the presentation of CML

A

most patient identified on routine screenings
patients without healthcare may be symptomatic with non-specific symptoms: fatigue, weight loss, abd pain, blood clots, evidence of bleeding, bone pain

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22
Q

what is the physical exam findings for CML

A

splenomegaly
hepatomegaly
myphadenopathy

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23
Q

what are the laboratory findings for CML workup

A

primary leukocytosis
WBC > 50,000
presence of band cells/’left shift’
increased ANC/neutrophil %
often with thrombocytosis
+/- anemia (1/3 of pts)

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24
Q

what is the definitive diagnostic test for CML

A

BM biopsy - hypercellular marrow, preponderance of myeloid cells, large immature granulocytes

Genetic testing - t(9:22) on FISH/PCR

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25
Q

what is the treatment for CML

A

first line = tyrosine kinase inhibitors (TKIs) - imatinib (gleevec), dasatinib, hilotinib, bosutinib - chronic treatment: goal is complete cytogenic response after 12 months

BMT - considered curative, but TKIs superseded as first line

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26
Q

what is the prognosis of CML

A

all will predictably develop resistance/progression
accelerated phase: 70% 4 year survival rate
Blastic phase identified by >30% blasts

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27
Q

how are progressions of CML identified

A

leukocytosis resistant to treatment
worsening anemia
fever and B symptoms
increase number of blasts/basophils

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28
Q

What is the epidemiology of ALL

A

M = W
more common in hispanic and caucasian patients
median age at diagnosis: 17
most common malignancy in kids

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29
Q

what is the pathophysiology of ALL

A

drives from T or B cells:
- 75-85% B cell types; T cell type has worse prognosis
etiology unknown: several associated mutations
increased risk with exposure to radiation/chemicals/chemotherapy - risk less than AML
children with down syndrome have 20x increased risk for developing ALL

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30
Q

what is the presentation of ALL

A

similar to AML
Non-specific symptoms less than 3 months in duration: fever (most common), fatigue/lethargy, bone pain (more common than AML), anorexia, weight loss, weakness, dyspnea on exertion(DOE), cough, HA, unexplained infections, sweating, bruising/ easy bleeding

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31
Q

what is shown on the PE for ALL

A

Pallor, petechiae, ecchymosis are most common fdindings
hepatomegaly, splenomegaly and lymphadenopathy more common than AML
+/- anterior mediastinal mass (cough, dyspnea, orthopnea, stridor, cyanosis, dysphagia, edema, syncope, elevated ICP)

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32
Q

what are the laboratory findings for ALL

A

leukocyte count normal or evelated
90% of pts will have blasts
elevated # eosinophils
anemia
neutropenia
thrombocytopenia

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33
Q

what is the presentation of ALL

A

more likely to have other metabolic derangements
- elevated LDH - marker or ‘tumor burden’
- elevated serum uric acid - increase purine metabolism
-elevated BUN/creatinine/phosphorus - kidney involvement
- hypercalcemia - bone infiltration, parathyroid-hormone like proteins

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34
Q

what is the definitive diagnostic test for ALL

A

BMB
hypercellular marrow, preponderacne of lymphoblasts, large immature lymphocytes

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35
Q

what are adjunctive tests used for ALL diagnosis

A

imaging - pts should be screened with CXR - r/o anterior mediastinal mass
CSF analysis - looking for blasts in CSF, r/o lymphoblastic infiltration

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36
Q

what is responsible for the production and maturation of T-lymphocytes

A

thymus

37
Q

what is the treatment of ALL

A

goal is remission
induction therapy: multi-agent chemotherapy
intensification/consolidation therapy: another round of same or different multi-agent chemotherapy
continuation therapy: lower dose treatment for additional 2-3 years, longer for boys then girls
+/- intrathecal chemotherapy - indicated if CNS involvement

38
Q

what is the prognosis of ALL

A

better in kids than adults:98% remission in kids
- 90% 5 year survival rare, close to 90% cure rates, 50% 5 year survival rate in adults

39
Q

what makes a poorer prognosis for ALL

A

primarily T cell ALL
increased age (>35, worse >60)
males
Leukocyte count <50
certain genetic profiles
longer time to response after initiation of treatment

40
Q

what time period of remission of ALL typically indicates a cure

A

10 or more years of remission = cure

41
Q

what is the CLL epidemiology

A

M>F
caucasians > other ethnicities
median age at diagnosis: 70
- 90% > 50 yo

42
Q

what is the pathophysiology of CLL

A

malignancy of B lymphocytes
etiology unclear: risk increased with + FH of leukemia, lymphoma or myeloma - no specific genes identified
NOT associated with radation

43
Q

what increases your risk factors for CLL

A

farmers
hairdressers
history of HCV infection
AGENT ORANGE EXPOSURE (Vietnam vets)**

44
Q

what is the presentation of CLL

A

primarily identified by asymptomatic screening/incidental finding
non-specific symptoms: fatigue, lymphadenopathy, recurrent infections, fever, weight loss, night sweats, symptoms from anemia

45
Q

what is the PE findings for CLL

A

80% have lymphadenopathy - non-tender, non-fixed (Mobile)
50% with splenomegaly or hepatomegaly
+/- bruising, petechiae/purpura
+/- pallor

46
Q

what is the laboratory presentation of CLL

A

sustained lymphocytosis >20,000
lymphocytes on differential
CD19 and CD5 markers on flow cytometry
+/- hypogammaglobulinemia - reduced levels of circulating IgG, IgM and IgA
+/- anemia - normocytic, normochromic, normal Hct
platelet count usually normal

47
Q

how are CLL definitively diagnosed

A

BM biopsy
- lymphocytic infiltration
- usually small, mature lymphocytes
- SMUDGE cells - ruptured CLL cells during slide preparation, presence of larger % Smudge cells - better prognosis

48
Q

what is the classifications of CLL

A

staged based on Rai classification
Stage 0 - Stage IV

49
Q

what is Stage 0 CLL

A

isolated lymphocytosis

50
Q

what is stage I CLL

A

presence of lymphadenopathy

51
Q

what is stage II CLL

A

spleno - or hepatomegaly

52
Q

what is stage III CLL

A

presence of anemia

53
Q

what is stage IV CLL

A

presence of thrombocytopenia

54
Q

what is the treatment of CLL

A

very slowly progressive
first line treatment = observation
- chemo/chemoimmunotherapy offer no significant survival beneift

treatment if symptomatic- first line = bruton tyrosine kinase (BTK) inhibitors - ibrutinib, acalbrutinib

55
Q

what is the prognosis of CLL

A

significantly improved with targeted therapy (BTK inhibitors)
- stage 0-1 = median survival of 10-15 years
- stage II - IV = 2 year survival of 90%

56
Q

what are at risk for developing secondary malignancy with CLL

A

skin - annual derm exams
Breasts - annual mammograms
GU cancer - annual PAP
Prostate - annual PSA, DRE
Colon - colonoscopy every 5 years after age 50

57
Q

what is non-hodgkin lymphoma

A

7th most common cancer (heterogenous group of lymphoproliferative malignancies)
originates in lymph system, lymphoid tissues
M>F
Caucasians > other ethnicities
Median age at dx: 76 (65-74)

58
Q

what is the pathophysiology of non-hodgkin lymphoma

A

malignancy of lymphoid origin - B or T lymphocytes (85% B lymphocyte origin)
oncogene activation or tumor suppressor gene inactivation

59
Q

what are the two types of non-hodgkin lymphoma

A

Burkitt lymphoma: t(8:14) - over expression of c-myc gene; leads to unchecked b-cell proliferation

Follicular lymphoma: t(14: 18) - bcl-2 over-expression; inhibition of apoptosis

60
Q

what is the presentation of non-hodgkin lymphoma

A

primarily present with lymphadenopathy - one or multiple (usually painless, mobiles, rubery)
Often with B symptoms: fever, night sweats(drenching), weight loss
1/3 of pts have extranodal involvement (skin lesions, GI tract, bone marrow, GU tract, thyroid, CNS)

61
Q

what is the laboratory findings of non-hodgkin lymphoma

A

normal lab workup - may see anemia, thrombocytopenia, lympocytosis if BM infiltration
no circulating abnormal lymphocytes or lymphocytosis

62
Q

how is non-hodgkin lympoma definitively diagnosed

A

lymph node biopsy

63
Q

what are the tests that non-hodgkin lymphoma is staged with

A

PET/CT neck, chest and pelvis
BMB
+/- lumbar puncture (r/o CNS infiltration)

64
Q

what is the treatment of non-hodgkin lymphoma

A

mainstay is chemotherapy
Radiation therapy: possible stand alone treatment for some stage 1 and 2 disease
BMT often reserved for relapse that remains responsive to chemotherapy

65
Q

what is the prognosis of Non-hodgkin lymphoma

A

median survival of 10-15 years
all eventually becomes refractory to chemotherapy - transition to more aggressive disease

66
Q

what makes a worse prognosis with non-hodgkin lymphoma

A

age > 60
elevated serum LDH
stage III or IV
> 1 extranodal site
poor baseline functional status

67
Q

what stage of non-hodgkin lymphoma is the most common presentation

A

stage 4: diffuse or disseminated involvement

68
Q

What is Hodgkin lymphoma

A

M>F
no predilection for ethnicity
median age at diagnosis: 39.5
- ave age range 20-34
- more common in young adults (20)
- second peak > age 55

69
Q

what is the pathophysiology of Hodgkin lymphoma

A

still a malignancy of lymphoid tissue - B-cell origin
genetics less implicated than non-Hodgkin lympoma - but +FH does increase risk

70
Q

what are the risk factors of Hodgkin lymphoma

A

50% associated with Epstein Barr Virus (EBV)
associated with HIV and AIDS

71
Q

What is the presentation of Hodgkin lympoma

A

similar to non-hodgkin lympoma:

lymphadenopathy, usually painless, mobile rubbery enlarged nodes
usually arises as single lymph node- contiguous spread - hematogenous spread
generalized pruritus with ETOH ingestion and bathing

72
Q

what are the laboratory findings for Hodgkins lymphoma

A

presentation same as non-Hodgkin lympoma
often normal lab work-up
no circulating abnormal lymphocytes or lymphocytosis

73
Q

what is the definative diagnosis for hodgkins lymphoma

A

lymph node biopsy
REED-STERNBERG cells on biopsy (owl eye appearance, symmetric bilobed nucleus)

74
Q

what is the treatment of Hodgkin lymphoma

A

mainstay of treatment is chemotherapy
stage 1 or 2: short course + radiation
stage 3 or 4: full chemo cycle
BM transplant often reserved for relapse that remains responsive to chemo

75
Q

what is the prognosis of hodgkin lymphoma

A

better than non-hodgkin lymphoma
75% of patients if 0-1 prognostic factors, 55% if 3+ prognostic factors

stage 1 and 2: 10 year survival rate 90%
Stage 3 and 4: 10 year survival rate of 50-60%

76
Q

what are poor prognostic factors for hodgkin lymphoma

A

stage 4
age > 35
male gender
lymphocyte deplete
WBC count >15,000
Hgb <10
albumin < 4

77
Q

what is multiple myeloma

A

Males equal to or greater than females
age > 40 (avg 65)
2x more likely in AA
most common primary bone malignancy

78
Q

What is the pathophysiology of Multiple Myeloma

A

plasma cell tumor

79
Q

what is the presentation of MM

A

many pts are asymptomatic
many identified incidentally via labs
if symptomatic, present with: bone pain(often first symptom - spine, chest, skull), spinal cord compression (numbness, weakness of legs), pathologic fracture (femoral neck or vertebrae)

80
Q

what is the lab work up presentation of MM

A

anemia (characteristic rouleaux formation) - rarely plasma cells on peripheral smear
hypercalcemia (secondary to bone resorption)
renal insufficiency (elevated BUN/creatinine)
Proteinuria - BENCE JONES proteins on urine protein electrophoresis (UPEP) - pathognomonic

81
Q

how is MM diagnosed

A

presence of paraproteins - plasma cells - produce immunoglobulins (antibodies): increase in monoclonal proteins on serum protein electrophoresis (SPEP) - characteristic “M spike”

Lytic lesions on imaging - “moth eaten” ,” punched out appearance”

82
Q

what is the gold standard diagnostic test for MM

A

biopsy
>60% plasma cells
“fried egg appearance”

83
Q

What is the treatment of MM

A

annual surveillance for myeloma ‘precursors’
Frank multiple myeloma - multi-agent chemotherapy +/- radiation for palliation of bone pain/prevention of fx, +/- stem cell transplant, +/- bisphosphonates, +/- immunotherapy, operative fixation of fx/impending fxs

84
Q

what is the prognosis of MM

A

median overall survival: 7 years
lower risk genotypes + BM transplant: 10 years

85
Q

What is Leukopenia

A

reduced leukocyte (WBC) count <4300
- neutropenia: ANC <2,000
- lymphopenia: absolute count <1,000
- monocytopenia: absolute count <100
- eosinopenia: aboslute count <50

86
Q

what are the causes of Neutropenia

A

Drugs: chemotherapy, antiseizure meds, abx, gout meds, immunosuppressants, ETOH, thyroid meds
infections: viral, bacterial, malarial
Nutritional: B12 and folate deficiency
Genetic
Hematologic disease: leukemia, lymphomas, aplastic anemia, etc
Hypersplenism
Autoimmune disease: SLE

87
Q

What are the causes of Lymphopenia

A

acute stressful illness: MI, Pneumonia, sepsis
Glucocorticoids
lymphoma
immunodeficiency syndromes
immunosuppressants
radiation
chronic illness
bone marrow failure

88
Q

What are the causes of Monocytopenia

A

acute stressful illness
glucocorticoids
aplastic anemia
leukemia
chemotherapy
immunosuppressants

89
Q

what are the causes of Eosinopenia

A

acute stressful illness
glucocorticoids

Clin Med2- Hematology (8 decks)

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