Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medicine II > malignancies > Flashcards

malignancies Flashcards

(77 cards)

Start Studying
1
Q

acute leukemia

Onset
Cell Type
Survival
Treatment

A

Rapid
Immature
Fatal if untreated
Aggressive chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

chronic leukemia

Onset
Cell Type
Survival
Treatment

A

Gradual
More mature
Long survival
Observation, chemotherapy or targeted agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AML labs

A

Profound anemia, thrombocytopenia
neutropenia
WBC>100,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DX of AML

A

BONE MARROW
&>20% blasts.*

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

differentiating blasts on a smear

A

they are huge and have low cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

most common subtype of ALL

A

BALL

C10
C19
C20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

would you see CNS directed tx for ALL or AML

A

ALL

this is to prevent and treat CNS dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

genetically modified T cells

A

Allogeneic transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Allogeneic transplant Imatinib

indicated for

A

philadephia chromosome positive ALL, primary refractory or early relapsed dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

with this chronic leukemia you have cells dividing too quickly

A

cml

both result in cytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

CLL

both result in cytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Dx hallmark of CML

A

= leukocytosis w/ WBC 50K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
CM
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
26
BCR-ABL causes CML how
turns on tyrosine kinases and leads to build up of premature leukocytes more to liver and spleen causing swelling
27
lab dxs for CML
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
28
tx of CML
" Tyrosine kinase inhibitors " Chemotherapy " Interferon " Stem cell transplant -
29
when would we use stem cell transplant for CML
in imatinib failure
30
how do you monitor for pt undergoing tx for CL
check CBC reguarly 6mo Bone marrow biopsy then monitor every three moneths with peripheral blood PCR for BCR-Abl
31
MC type of CLL and when do we see it
B cell Chronic lymphocytic leukemia iv. Peak incidence age 60 to 80 MC in western world
32
tx for CLL
Indolent disease, many patients never need chemotherapy Treat if symptomatic: organomegaly, hemolysis, bone marrow suppression' " Chemotherapy (FCR Therapy - best frontline regimen
33
specific dx for CLL
isolated lymphocytosis w/ leukocytosis > 20K Smudge cells
34
Uncommon B cell lymphoproliferative disorder With a higher prevalence in males
hairy cell leukemia
35
CM of hairy cell leukemia
Peak incidence 40-60 years Clinical presentation: infections, anemia or splenomegaly Lymphadenopathy is very UNCOMMON Pancytopenia is usual
36
tx for Hairy cell
2 CDA or pentostatin | achieve response in >80% patients.
37
tx for non-hodkins
R-CHOP therapy = MC regimen
38
standard dx for lymphoma
biopsy of lymp nodes
39
non-hodkin's lym,phoma dx
Excisional Lymph node biopsy CBC, CMP, LDH, Uric acid, Serum protein electrophoresis CT, CXR for staging Bone marrow biopsy
40
most common non-hodgkin's lymphoma
B cell lymphoma (lymph tumor) comprises 85% of cases T cell and NK cell together comprises 15% of cases.
41
sxs of non-hodgkin's
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
reed-sternberg cell is associated with
non-hodgkin
43
describe non-hodkin lymphoma
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
MC form of NHL
indolent follicular lymphoma mean survival is 10 years
45
NHL associated with elevated IgM
Lymphoplasmacytoid lymphoma
46
Second MC type of NHL
Diffuse large B cell lymphoma this one is aggressive
47
2. R-EPOCH
high risk NHL treatment that requires hospitalization
48
types of t cell NHL
Peripheral T cell lymphoma Angiioimmunoblastic lymphadenopathy Mycosis fungoides- causes patches on the skin Sezary syndrome
49
when would you use radiation tx for NHL
consider for stage DLBCL
50
sxs of HL
" Can present at any age: peak incidence in young adults " Mediastinal involvement in 6-11% " Constitutional symptoms can be prominent
51
types of HL
nodular sclerosis mixed cellularity lymphocyte depleted, lymphocyte rich Nodular lymphocyte predominant
52
tx of HL
Treatment " Chemotherapy " Radiation " Both Late effects of Hodgkin's disease and treatment can include secondary lung cancer, myelodysplasia, cardiac disease.
53
Multiple myeloma
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
B sxs with HL indicate
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
CM on early HL
firm, non-tender, freely mobile(especially supra clavicular, cervical &mediastinal) .Alcohol may induce lymph node pain.* Hepatosplenomegaly.
56
CD15+, CD30+. "owl-eye appearance" both characteristic of
HL
57
Cancer associated with proliferation of a single clone of plasma cells*
multiple myeloma increase in monoclonal Ab Especially IgG or IgA
58
CM of multiple myeloma
``` Bone pain Recurrent infx Elevated Ca Anemia Kidney failure ```
59
only heme malignancy associated with bone destruction
multiple myeloma
60
dx of multiple myeloma
``` 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
what bone changes might we see in a pt with multiple myeloma
Skull Radiographs: “punched-out"Ivtic lesions. * Bone scans NOT helpful!
62
tx of multiple myeloma
supportive Autologous stem cell transplant definitive treatment. tPreceded by chemotherapy ex. Thalidomide or alkylating agents ex. Melphalan). Bisphosphonates for bony destruction.
63
Myeloproliferative disorder
Bone marrow disorder characterized by clonal proliferation of one or more hematopoietic components in the bone marrow.
64
three types of myeloproliferative disorder
1. Polycythemia Vera 2. Essential thrombocynthemia 3. myelofibrosis
65
Polycythemia Vera
primarily seen as the increase in RBC but also seen as increase in WBC and platelets
66
Polycythemia sxs
Headache, pruritus, facial plethora, splenomegaly, HTN. Gout can be a result of elevated uric acid. pruritus associated with hot bath
67
tx of polycythemia
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
hallmark of essential Thrombocynthemia
Sustained increase in platelet count
69
what labs do we see with Thrombocynthemia
ii. Hematocrit is normal iii. Half of patient has JAK-2 mutation o JAK-2 mutation o ↑ Megakaryocytes
70
complications of Thrombocynthemia
iv. Clinical complications: thrombosis and hemorrhage
71
erythormelagia, up to 40% has splenomegaly
polycythemia
72
Polycythemia
o JAK2 mutation o ↓ EPO increased Hct in the absence of hypoxia
73
sustained increase in platelet count is characteristic of this myeloproliferative disorder
essential thrombocytopenia
74
what would you expect to see in the bone marrow of a pt with essential thrombocytopenia
bone marrow shows increase megakaryocytes
75
excess production of RBCs is characteristics of which myeloproliferative what age gorup do we normally see hthis in
polycythemia 50-60yr median survival 10 years
76
clinical sxs of polycythemia
HA, pruritis faical plethora HTN gout as a result of elevated uric acird
77
what would be the tx for a pt with myeloproliferative d/o
phlebotomoy to maintain <45 PO hdyrea can be used thombocytosis indterferon alternative to hydrea

Medicine II (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions