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Medicine II > malignancies > Flashcards

malignancies Flashcards

1
Q

acute leukemia

Onset
Cell Type
Survival
Treatment

A

Rapid
Immature
Fatal if untreated
Aggressive chemotherapy

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2
Q

chronic leukemia

Onset
Cell Type
Survival
Treatment

A

Gradual
More mature
Long survival
Observation, chemotherapy or targeted agents

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3
Q

CM and PE of AML

A

67 yo

week history of fatigue as well as shortness of breath with exertion, low grade fever.

Physical exam shows gingival hyperplasia, petechiae over her arms.

splenomegaly

CNS-HA confusion TIA
PULM: respiratory distress

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4
Q

MC Acute form of leukemia in adults (80% of cases].

A

AML

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5
Q

AML labs

A

Profound anemia, thrombocytopenia
neutropenia
WBC>100,000

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6
Q

DX of AML

A

BONE MARROW
&>20% blasts.*

favorable or unfavorable dx for determination of need of stem cell transplant

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7
Q

Two types of AML

A

iv. Primary AML: arises de novo (new)
v. Secondary AML: Leukemia that develop from previous hematologic disorders or from previous chemotherapy for other cancers

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8
Q

tx of AML

A

Supportive care w/ transfusions

Chemotherapy - induction chemotherapy followed by consolidation chemotherapy

ATRA/Arsenic for AML-M3 subtype (causes DIC, bleeding complications)

Stem cell transplant

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9
Q

MC form of acute leukemia in children

A

Acute lymphoblastic leukemia

representing 80% of acute leukemia in children and 20% in adults

Highest incidence is 3-7 years

second rise around 40

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10
Q

CM of acute lymphoblastic leukemia seen as a result of bone marrow failure

A

Profound anemia (pallor, lethargy, dyspnea)

Neutropenia (FEVER MC SX, malaise, infxns of mouth, throat)

Thrombocytopenia (bruising, bleeding gums)

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11
Q

other than sxs of bone marrow failure what else do we see associated with CM of acute lymphoblastic leukemia

A

organi filtration
o Tender bones, LAD, splenomegaly, hepatomegaly in 20% of pts

o CNS involvement in 6%
headache, stiff neck, visual changes, vomiting. CNS & testes MC site for METS.

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12
Q

Work up for acute lymphoblastic anemia

A

Work up
Decreased or increased WBC

Peripheral blast

Elevated LDH, uric acid

Bone marrow blast present

Lumbar puncture

CXR may have enlarged mediastinal mass

CXR may have enlarged mediastinal mass

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13
Q

what is acute lymphocytic leukemia

A

Malignancy of lymphoid stem cells/BLASTS in bone marrow <=>lymph nodes, spleen, liver, other organs.

can be B cells T cells or non B/T

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14
Q

Pancytopenia seen with leukemia is the result of

A

crowding out from hyperproliferation of blasts

loss of RBC= anemia
loss of platelets= thombocytopenia and purpura
neutropenia= infx and fever

spilling of blasts = increase in WBC

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15
Q

differentiating blasts on a smear

A

they are huge and have low cytoplasm

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16
Q

How do you differentiate ALL from AML

A

How do you differentiate ALL from AML

TDT

Terminal deoxynucleotidyl transferase = ALL
“ ↑ LDH & uric acid
“ Peripheral blast
“ CXR – may have mediastinal mass

myeloperxidase or aeur rod

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17
Q

most common subtype of ALL

A

BALL

C10
C19
C20

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18
Q

would you see CNS directed tx for ALL or AML

A

ALL

this is to prevent and treat CNS dz

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19
Q

genetically modified T cells

A

Allogeneic transplant

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20
Q

Allogeneic transplant Imatinib

indicated for

A

philadephia chromosome positive ALL, primary refractory or early relapsed dz

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21
Q

with this chronic leukemia you have cells dividing too quickly

A

cml

both result in cytopenia

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22
Q

With this chronic leukemia you have cells not dying when they should be

A

CLL

both result in cytopenia

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23
Q

CML most common cause

A

translocation of philadelphia
T 9;22

BCR-ABL Oncogene

  1. Stem cell disorder
  2. Characterized bymyeloproliferation
  3. Well-described clinical course

22 is philadelphia

forces continual divisions or premature leukocytes

causes spill over into the blood
splenomegaly

can progress and accelerate in blast crisis

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24
Q

Dx hallmark of CML

A

= leukocytosis w/ WBC 50K

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25
Q

CM

A

Male to female ratio 1.4 to 1

Most frequently b/w ages 40 to 60, but may occur at any age

Symptoms related to hypermetabolism: (weight loss, anorexia, night sweats)

Splenomegaly is often present
Anemia
Bruising, epistaxis from platelet dysfunction

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26
Q

BCR-ABL causes CML how

A

turns on tyrosine kinases and leads to build up of premature leukocytes

more to liver and spleen causing swelling

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27
Q

lab dxs for CML

A

Lab work up

Increased WBC: usually >50K, usually see a complete spectrum of myeloid cells
Increased basophils
Normocytic anemia
Platelet may be increased, normal or decreased

Bone marrow is hypercellular
PH chromosome positive

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28
Q

tx of CML

A

” Tyrosine kinase inhibitors
“ Chemotherapy
“ Interferon
“ Stem cell transplant -

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29
Q

when would we use stem cell transplant for CML

A

in imatinib failure

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30
Q

how do you monitor for pt undergoing tx for CL

A

check CBC reguarly
6mo Bone marrow biopsy

then monitor every three moneths with peripheral blood PCR for BCR-Abl

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31
Q

MC type of CLL and when do we see it

A

B cell Chronic lymphocytic leukemia

iv. Peak incidence age 60 to 80

MC in western world

32
Q

tx for CLL

A

Indolent disease, many patients never need chemotherapy

Treat if symptomatic: organomegaly, hemolysis, bone marrow suppression’
“ Chemotherapy (FCR Therapy - best frontline regimen

33
Q

specific dx for CLL

A

isolated lymphocytosis w/ leukocytosis > 20K

Smudge cells
34
Q

Uncommon B cell lymphoproliferative disorder With a higher prevalence in males

A

hairy cell leukemia

35
Q

CM of hairy cell leukemia

A

Peak incidence 40-60 years

Clinical presentation: infections, anemia or splenomegaly

Lymphadenopathy is very UNCOMMON

Pancytopenia is usual

36
Q

tx for Hairy cell

A

2 CDA or pentostatin

achieve response in >80% patients.

37
Q

tx for non-hodkins

A

R-CHOP therapy = MC regimen

38
Q

standard dx for lymphoma

A

biopsy of lymp nodes

39
Q

non-hodkin’s lym,phoma dx

A

Excisional Lymph node biopsy

CBC, CMP, LDH, Uric acid, Serum protein electrophoresis

CT, CXR for staging

Bone marrow biopsy

40
Q

most common non-hodgkin’s lymphoma

A

B cell lymphoma (lymph tumor) comprises 85% of cases

T cell and NK cell together comprises 15% of cases.

41
Q

sxs of non-hodgkin’s

A

Lymphadenopathy: Asymmetric painless enlargement of lymph nodes

Constitutional symptoms: fever, night sweats, weight loss. Oropharyngeal involvement in 5-10%

Infections

with extra-nodal involvement:

BO, anemia, weakness (spinal cord)

42
Q

reed-sternberg cell is associated with

A

non-hodgkin

43
Q

describe non-hodkin lymphoma

A

genetic mutation leads to lymphomas

can be nodal or extra-nodal

if extranodal can cause GI (MC) BO
cause pancytopenia in the bone marrow

or spinal cord compression

44
Q

MC form of NHL

A

indolent follicular lymphoma

mean survival is 10 years

45
Q

NHL associated with elevated IgM

A

Lymphoplasmacytoid lymphoma

46
Q

Second MC type of NHL

A

Diffuse large B cell lymphoma

this one is aggressive

47
Q
  1. R-EPOCH
A

high risk NHL treatment that requires hospitalization

48
Q

types of t cell NHL

A

Peripheral T cell lymphoma

Angiioimmunoblastic

lymphadenopathy

Mycosis fungoides- causes patches on the skin

Sezary syndrome

49
Q

when would you use radiation tx for NHL

A

consider for stage DLBCL

50
Q

sxs of HL

A

” Can present at any age: peak incidence in young adults
“ Mediastinal involvement in 6-11%
“ Constitutional symptoms can be prominent

51
Q

types of HL

A

nodular sclerosis
mixed cellularity
lymphocyte depleted, lymphocyte rich
Nodular lymphocyte predominant

52
Q

tx of HL

A

Treatment
“ Chemotherapy
“ Radiation
“ Both

Late effects of Hodgkin’s disease and treatment can include secondary lung cancer, myelodysplasia, cardiac disease.

53
Q

Multiple myeloma

A

Neoplastic proliferation characterized by plasma cell accumulation in the bone marrow, the presence of monoclonal protein in the serum and or urine and related tissue damage.

54
Q

B sxs with HL indicate

A

Systemic “B” symptoms (advanced disease)

(cytokines => Pel-Ebstein fever (cyclical fever
that increase & decrease over a period of 1-2 weeks, night sweats), weight loss, anemia, pruritus

55
Q

CM on early HL

A

firm, non-tender, freely mobile(especially supra clavicular, cervical
&mediastinal)
.Alcohol may induce lymph node pain.*
Hepatosplenomegaly.

56
Q

CD15+, CD30+.
“owl-eye appearance”

both characteristic of

A

HL

57
Q

Cancer associated with proliferation of a single clone of plasma cells*

A

multiple myeloma

increase in monoclonal Ab Especially IgG or IgA

58
Q

CM of multiple myeloma

A 
Bone pain
Recurrent infx
Elevated Ca
Anemia
Kidney failure
59
Q

only heme malignancy associated with bone destruction

A

multiple myeloma

60
Q

dx of multiple myeloma

A 
o	CBC → anemia and reouleaux formation 
o	Creatinine
o	↑ Calcium
o	****SPEP: monoclonal M protein spike
 UPEP
--> 	24 hr urine - Bence Jones Protein; Bone marrow biopsy
61
Q

what bone changes might we see in a pt with multiple myeloma

A

Skull Radiographs: “punched-out”Ivtic lesions. * Bone scans NOT helpful!

62
Q

tx of multiple myeloma

A

supportive
Autologous stem cell transplant definitive treatment.

tPreceded by chemotherapy ex.
Thalidomide or alkylating agents ex. Melphalan).

Bisphosphonates for bony destruction.

63
Q

Myeloproliferative disorder

A

Bone marrow disorder characterized by clonal proliferation of one or more hematopoietic components in the bone marrow.

64
Q

three types of myeloproliferative disorder

A
  1. Polycythemia Vera
  2. Essential thrombocynthemia
  3. myelofibrosis
65
Q

Polycythemia Vera

A

primarily seen as the increase in RBC

but also seen as increase in WBC and platelets

66
Q

Polycythemia sxs

A

Headache, pruritus, facial plethora, splenomegaly, HTN. Gout can be a result of elevated uric acid.

pruritus associated with hot bath

67
Q

tx of polycythemia

A

Phlebotomy to maintain hct <45

Hydrea can be used for patients who cannot tolerate phlebotomy, or has progressive splenomegaly, thrombocytosis.

Interferon is another option. It is less convenient than oral hydrea.

Median survival 10-16 years. Transition to myelofibrosis occurs in 30% pts, about 5% progresses to leukemia.

68
Q

hallmark of essential Thrombocynthemia

A

Sustained increase in platelet count

69
Q

what labs do we see with Thrombocynthemia

A

ii. Hematocrit is normal
iii. Half of patient has JAK-2 mutation

o JAK-2 mutation
o ↑ Megakaryocytes

70
Q

complications of Thrombocynthemia

A

iv. Clinical complications: thrombosis and hemorrhage

71
Q

erythormelagia, up to 40% has splenomegaly

A

polycythemia

72
Q

Polycythemia

A

o JAK2 mutation
o ↓ EPO

increased Hct in the absence of hypoxia

73
Q

sustained increase in platelet count is characteristic of this myeloproliferative disorder

A

essential thrombocytopenia

74
Q

what would you expect to see in the bone marrow of a pt with essential thrombocytopenia

A

bone marrow shows increase megakaryocytes

75
Q

excess production of RBCs is characteristics of which myeloproliferative

what age gorup do we normally see hthis in

A

polycythemia

50-60yr

median survival 10 years

76
Q

clinical sxs of polycythemia

A

HA, pruritis
faical plethora
HTN
gout as a result of elevated uric acird

77
Q

what would be the tx for a pt with myeloproliferative d/o

A

phlebotomoy to maintain <45 PO hdyrea can be used

thombocytosis indterferon alternative to hydrea

Medicine II (21 decks)

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