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Clin Med2- Hematology > Leukemias and Lymphomas > Flashcards

Leukemias and Lymphomas Flashcards

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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
what is the treatment for CML
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
26
what is the prognosis of CML
all will predictably develop resistance/progression accelerated phase: 70% 4 year survival rate Blastic phase identified by >30% blasts
27
how are progressions of CML identified
leukocytosis resistant to treatment worsening anemia fever and B symptoms increase number of blasts/basophils
28
What is the epidemiology of ALL
M = W more common in hispanic and caucasian patients median age at diagnosis: 17 most common malignancy in kids
29
what is the pathophysiology of ALL
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
30
what is the presentation of ALL
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
31
what is shown on the PE for ALL
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)
32
what are the laboratory findings for ALL
leukocyte count normal or evelated 90% of pts will have blasts elevated # eosinophils anemia neutropenia thrombocytopenia
33
what is the presentation of ALL
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
34
what is the definitive diagnostic test for ALL
BMB hypercellular marrow, preponderacne of lymphoblasts, large immature lymphocytes
35
what are adjunctive tests used for ALL diagnosis
imaging - pts should be screened with CXR - r/o anterior mediastinal mass CSF analysis - looking for blasts in CSF, r/o lymphoblastic infiltration
36
what is responsible for the production and maturation of T-lymphocytes
thymus
37
what is the treatment of ALL
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
what is the prognosis of ALL
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
what makes a poorer prognosis for ALL
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
what time period of remission of ALL typically indicates a cure
10 or more years of remission = cure
41
what is the CLL epidemiology
M>F caucasians > other ethnicities median age at diagnosis: 70 - 90% > 50 yo
42
what is the pathophysiology of CLL
malignancy of B lymphocytes etiology unclear: risk increased with + FH of leukemia, lymphoma or myeloma - no specific genes identified NOT associated with radation
43
what increases your risk factors for CLL
farmers hairdressers history of HCV infection AGENT ORANGE EXPOSURE (Vietnam vets)**
44
what is the presentation of CLL
primarily identified by asymptomatic screening/incidental finding non-specific symptoms: fatigue, lymphadenopathy, recurrent infections, fever, weight loss, night sweats, symptoms from anemia
45
what is the PE findings for CLL
80% have lymphadenopathy - non-tender, non-fixed (Mobile) 50% with splenomegaly or hepatomegaly +/- bruising, petechiae/purpura +/- pallor
46
what is the laboratory presentation of CLL
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
how are CLL definitively diagnosed
BM biopsy - lymphocytic infiltration - usually small, mature lymphocytes - SMUDGE cells - ruptured CLL cells during slide preparation, presence of larger % Smudge cells - better prognosis
48
what is the classifications of CLL
staged based on Rai classification Stage 0 - Stage IV
49
what is Stage 0 CLL
isolated lymphocytosis
50
what is stage I CLL
presence of lymphadenopathy
51
what is stage II CLL
spleno - or hepatomegaly
52
what is stage III CLL
presence of anemia
53
what is stage IV CLL
presence of thrombocytopenia
54
what is the treatment of CLL
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
what is the prognosis of CLL
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
what are at risk for developing secondary malignancy with CLL
skin - annual derm exams Breasts - annual mammograms GU cancer - annual PAP Prostate - annual PSA, DRE Colon - colonoscopy every 5 years after age 50
57
what is non-hodgkin lymphoma
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
what is the pathophysiology of non-hodgkin lymphoma
malignancy of lymphoid origin - B or T lymphocytes (85% B lymphocyte origin) oncogene activation or tumor suppressor gene inactivation
59
what are the two types of non-hodgkin lymphoma
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
what is the presentation of non-hodgkin lymphoma
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
what is the laboratory findings of non-hodgkin lymphoma
normal lab workup - may see anemia, thrombocytopenia, lympocytosis if BM infiltration no circulating abnormal lymphocytes or lymphocytosis
62
how is non-hodgkin lympoma definitively diagnosed
lymph node biopsy
63
what are the tests that non-hodgkin lymphoma is staged with
PET/CT neck, chest and pelvis BMB +/- lumbar puncture (r/o CNS infiltration)
64
what is the treatment of non-hodgkin lymphoma
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
what is the prognosis of Non-hodgkin lymphoma
median survival of 10-15 years all eventually becomes refractory to chemotherapy - transition to more aggressive disease
66
what makes a worse prognosis with non-hodgkin lymphoma
age > 60 elevated serum LDH stage III or IV > 1 extranodal site poor baseline functional status
67
what stage of non-hodgkin lymphoma is the most common presentation
stage 4: diffuse or disseminated involvement
68
What is Hodgkin lymphoma
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
what is the pathophysiology of Hodgkin lymphoma
still a malignancy of lymphoid tissue - B-cell origin genetics less implicated than non-Hodgkin lympoma - but +FH does increase risk
70
what are the risk factors of Hodgkin lymphoma
50% associated with Epstein Barr Virus (EBV) associated with HIV and AIDS
71
What is the presentation of Hodgkin lympoma
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
what are the laboratory findings for Hodgkins lymphoma
presentation same as non-Hodgkin lympoma often normal lab work-up no circulating abnormal lymphocytes or lymphocytosis
73
what is the definative diagnosis for hodgkins lymphoma
lymph node biopsy REED-STERNBERG cells on biopsy (owl eye appearance, symmetric bilobed nucleus)
74
what is the treatment of Hodgkin lymphoma
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
what is the prognosis of hodgkin lymphoma
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
what are poor prognostic factors for hodgkin lymphoma
stage 4 age > 35 male gender lymphocyte deplete WBC count >15,000 Hgb <10 albumin < 4
77
what is multiple myeloma
Males equal to or greater than females age > 40 (avg 65) 2x more likely in AA most common primary bone malignancy
78
What is the pathophysiology of Multiple Myeloma
plasma cell tumor
79
what is the presentation of MM
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
what is the lab work up presentation of MM
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
how is MM diagnosed
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
what is the gold standard diagnostic test for MM
biopsy >60% plasma cells "fried egg appearance"
83
What is the treatment of MM
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
what is the prognosis of MM
median overall survival: 7 years lower risk genotypes + BM transplant: 10 years
85
What is Leukopenia
reduced leukocyte (WBC) count <4300 - neutropenia: ANC <2,000 - lymphopenia: absolute count <1,000 - monocytopenia: absolute count <100 - eosinopenia: aboslute count <50
86
what are the causes of Neutropenia
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
What are the causes of Lymphopenia
acute stressful illness: MI, Pneumonia, sepsis Glucocorticoids lymphoma immunodeficiency syndromes immunosuppressants radiation chronic illness bone marrow failure
88
What are the causes of Monocytopenia
acute stressful illness glucocorticoids aplastic anemia leukemia chemotherapy immunosuppressants
89
what are the causes of Eosinopenia
acute stressful illness glucocorticoids

Clin Med2- Hematology (8 decks)

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