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Step 1 > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

Aflatoxins

A

aspergillus

HCC

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2
Q

vinyl chloride

A

liver

angiosarcoma

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3
Q

carbon tetrachlordie

A

liver

centrilobular necrosis, fatty change

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4
Q

nitrosamines

A

smoked foods

gastric cancer

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5
Q

arsenic

A

cutaneous squamous cell

liver angiosarcoma

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6
Q

naphthalene dyes

A

bladder transitional cell carcinoma

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7
Q

Alkylating agents

A

leukemia

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8
Q

Psammoma bodies

A 
laminated, concentric calcific spherules
Papillary adenocarcinoma of thyroid
Serous papillary cystadenocarcinoma of ovary
Meningioma
Mesothelioma
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9
Q

CEA

A

CRC, pancreatic

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10
Q

CA 19-9

A

pancreatic

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11
Q

CA 125

A

Ovarian

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12
Q

Mycosis fungoides

A

Chronic T cell leukemia
CD4+
Pautrier microabscesses (skin)
–> sezary syndrome (blood) – cerebroform nuclei

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13
Q

CLL

A 
chronic lymphoid leukemia  Small lymphocytic lymphoma (when in LNs)
Naive B Cells
60+
CD5, CD20
Smudge cells
hypo-IgG  AIHA (bad IgG)
Can --> DLBCL (p/w enlarging spleen)
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14
Q

Hairy cell

A 
chronic lymphoid leukemia
Mature B Cells
TRAP +
Red pulp of spleen, no LAD, dry BM tap
Tx: 2-CDA (cladribine) -- adenosine deaminase inhibitor
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15
Q

ATLL

A 
Adult T cell Leukemia/Lymphoma
HTLV-1
Japan, Caribbean
Rash, HSM, LAD
Lytic Bone Lesions **
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16
Q

CML

A 
30-60yrs
Granulocytes, basophils* (vs leukemoid)
t(9; 22) -- BCR-abl
Tx: imatinib
chronic phase: large spleen
Accelerating phase: enlarging spleen. can transform to AML or ALL (b/c mutx in HSCs, not myeloblasts)
LAP (-) (or v low) vs leukemoid rxn
17
Q

PV

A 
RBCs
JAK2
hyperurecemia/gout
thrombosis, itching, hyperviscosity
can --> acute leukemia
Tx: phlebotomy, hydroxyurea
18
Q

ET

A 
PLTs
JAK2
incr bleeding or incr thrombosis
no hyperuricemia/gout
no transformation
19
Q

Myelofibrosis

A 
megakaryocytes
JAK2
incr PDGF --> myelofibrosis
extra-medullary hematopoesis
infection, thrombosis, bleeding
leuko-erythroblastic smear, tear drop cells
20
Q

Acute monocytc AML

A

AML: BM blasts >20%. Can arise from myelodysplasia. MPO+. 55yrs
subset of AML with gum involvement

21
Q

Acute megakaryoblastic AML

A

AML: BM blasts >20%. Can arise from myelodysplasia. 55yrs
MPO -
Down’s before 5

22
Q

APML (M3)

A 
AML: BM blasts >20%. Can arise from myelodysplasia. MPO+. 55yrs
t(15;17) --> RAR disruption
Auer rods
DIC!
Tx: ATRA
23
Q

B ALL

A 
ALL: tdt+, Down's after 5
CD 19, 20, 10
Tx: Chemo with ppx to brain, scrotum
t (12;21) = kids, good prognosis
t (9;22) (Phil) = adults, poor prognosis
24
Q

T ALL

A 
ALL: tdt+, Down's after 5
CD2 - CD8 +
no CD10
Thymic mass
Teenager
25
Q

DLBCL

A 
large cell lymphoma
CD20+
Older adults, sometimes kids
diffuse sheets of cells
sporadic vs transformed
clinically aggressive
26
Q

Burkitt’s

A 
intermediate B Cell lymphoma
CD20
Adolescents/young adults
EBV
African --> jaw
sporadic --> abdomen
c-myc* (varied translocations eg t (8; 14))
Starry-sky (due to apoptosis from rapid cell growth
27
Q

Marginal zone

A

small B cell lymphoma
CD20
2/2 chronic inflammation
Hashimoto’s, Sjogren’s –> parotid. H Pylori –> MALT

28
Q

Small lymphocytic lymphoma

A

CLL involving LNs

29
Q

Follicular lymphoma

A 
small B cell
CD20
late adulthood
LAD --> lots of follicles
t(14; 18) = IgH- bcl2
Can --> DLBCL
vs reactive: bcl2+, loss of architecture, monoclonal, no tingible body MPhages
Tx: CTX or rituximab
30
Q

Mantle cell

A

small B cell lymphoma
CD20
t(11;14) = IgH - Cyclin D (G1/S phase)

31
Q

Hodgkin’s lymphoma

A

Bimodal: young adults; > 55yo
rare neoplastic cells (R-S)
CD15, CD30
CD20 (-) (Although it is B cell lymphoma)
cytokine production –> B Sx, reactive infiltrate, fibrosis
localized, contiguous vs multiple peripheral
50% EBV

32
Q

Nodular sclerosing

A

hodgkin’s subtype
cervical, mediastinal with broad fibrosis
young female

33
Q

Lymphocyte rich

A

hodgkin’s subtype

best prognosis

34
Q

lymphocyte depleted

A

hodgkin’s subtype
worst prognosis
elderly/HIV

35
Q

Mixed hodgkin’s

A

Eosinophils! 2/2 IL-5

Can have peripheral eosinophilia

36
Q

Waldenstrom’s

A

B cell lymphoma producing IgM
Generalized LAD, incr serum protein with M spike 2/2 IgM (not IgG or A, as in MM)
Hyperviscosity –> bleeding, stroke, retinal hemorrhage, NO lytic bone lesions (vs MM)
Tx: pheresis

37
Q

Langerhans cell histiocytosis

A

Proliferative d/o of dendritic cells from monocyte lineage
Kids
Lytic bone lesions and rash
S-100 and CD1a
“tennis rackets” on EM (looks like C Tetani spore)

38
Q

multiple myeloma

A

IgG > IgA
Incr IL-6, osteoclast activating factor –> clast stimulation via RANK
infection (most common cause of death)
AL amyloidosis, reulauex formation
Bence Jones, myeloma kidney
M spike on SPEP
“punched out” lesions =/= ratty lesions of Paget’s

Step 1 (15 decks)

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