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Summer 3 > Lymphomas > Flashcards

Lymphomas Flashcards

1
Q

What are the lymphocytes

A

T cells: most of the lymphocytes, mature in thymus
B cells: mature in marrow, go into circulation
NK cells

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2
Q

What are the primary lymphatic organs

A 
Where B and T cells mature and differentiate 
Bone marrow (b cells) Thymus (t cells)
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3
Q

What are secondary lymphatic organs

A

Where mature antigen specific B and T cells interact with each other
where APC that recognize antigens mount a response
Spleen, lymph nodes, tonsils, MALT

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4
Q

What are NK cells

A

Sniff out cancer cells all the time

Live for 40-60 years

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5
Q

What is your primary vs secondary response

A

Primary: IgM
Secondary: IgG

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6
Q

What causes lymphomas

A

Arise from any step of maturation-
Antigen exposure from EBV or HL
Chronic irritation in extra nodal marginal zone
Random mutations (BCL6)

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7
Q

What is Non-hodgkins lymphoma

A 
has a lot of sub-types 
range from indolent to very aggressive 
Painless LAD* 
Fever, night sweats, weight loss 
Classification based on biology and cytology
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8
Q

What is Hodgkins lymphoma

A

Bimodal (20’s and 50’s)
Reed sternberg cells
Painless LAD
fever, weight loss, night sweats, generalized pruritis

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9
Q

What is the NHL staging system (or any lymphoma?)

A 
I: one node 
II: two nodes, same side of diaphragm
III: crosses diaphragm 
IV: in BM or liver 
Type A: absence of B Sx 
Type B: fever, night sweats, weight loss
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10
Q

NHL labs may show

A 
CBC: abnormal 
CMP: normal 
LDH: elevated 
Beta 2 microglobulin: often elevated 
Uric acid: elevated
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11
Q

Where can NHL arise form

A

T cells: cutaneous or peripheral lymphoma

B cells: diffuse large B cell, follicular, mantle cell

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12
Q

How do you diagnose NHL

A 
CT to check for nodes 
PET/CT check biologic activity 
BM Bx (BM involvement?) 
LP (meningeal involvement?) 
*must Bx nodes to find out type of lymphoma
Skin Bx for cutaneous T cell lymphoma
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13
Q

How does Cutaneous T cell lymphoma present

A

Scaly psoriasis-like rash that dos not clear with steroids or vitamin D analogs

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14
Q

How do you treat NHL

A

Watchful approach: good for low grade, elderly, little node involvement- Follow w/ CT and PET
Chemo low grade (after watchful): CVP! cyclophosphamide, vincristine, prednisone
Chemo high grade: CHOP +/- rituxan (cyclophosphamide, doxyrubicin, oncovin, prednisone)- and local radiation
Very high risk: Autologous SCT as soon as MF possible

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15
Q

What is the prognosis of NHL

A

Indolent: 6-8 years (can progress to aggressive)

Elderly, high LDH, high stage, poor performance: worse

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16
Q

What is Hodgkin’s disease

A

May be caused by EBV* outbreak
presents with fever, night sweats, wt loss, painless LAD (nodes hurt after drinking EtOH*)
Get a CBC and EBV titer to r/o mono

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17
Q

When can you use the watchful waiting approach

A

ONLY if elderly, or like about to die

18
Q

How do you treat Hodgkins lymphoma

A

Radiation: early stage or bulky disease

Standard Chemo: AVBD (adriamycin, bleomycin, vinblastin, dacarbazine)

19
Q

What is the prognosis of hodgkins lymphoma

A

Ia-IIa: 10 year is 80%

IIIb-IV: 5 yr is 50%

20
Q

How exactly do you implement Hodgkins Tx in different stages

A

I/IIA: ABVD x 6 cycles (or 2-4 cycles w/ IFR)
I/IIB: involved field radiation (IFR) or extended field radiation (EFR)
III-IV: ABVD x 6-8 cycles, IFR. Autologous SCT if relapsed. Bretuximab if relapse after SCT

21
Q

Patients with hodgkins are at increased risk for

A 
other lymphomas 
Leukemia 
gastric CA 
lung CA
breast CA (esp in women 30-35); radiation to chest has same risk as BRCA mutation
22
Q

If a patient presents with AKI, keep this in mind on your DDx

A

Multiple myeloma!
in MM kidney disease may be 2/2 hypercalcemia or accumulation of gammaglobulins (specific light chains on immunoglobulins)

23
Q

What is multiple myeloma

A

Plasma cells increase abnormally from a single clone; cells don’t need to be triggered by an antigen to mature
Cells expand causing anemia, bone pain, kidney disease

24
Q

Characteristics of multiple myeloma disease are

A

Clones of plasma cell proliferate
MC 65 y/o
Plasma cells secrete OAF (osteoclast activating factors) that eat the marrow and cause cytopenias, anemias, and bony pain
Immunoglobulins produce hyperviscosity

25
Q

What are plasmacytomas

A

Plasma cells in multiple myeloma that can cause tumors (like her pt that came in with a “tumor” on his clavicle

26
Q

S/Sx of multiplemyeloma are

A

fatigue
bony pain
frequent infections (immunoglobulins decreased 2/2 low plasma cells)- is this like all others are low besides the 1 that is proliferating?
Mucosal bleeding or alterations in mental status (2/2 hyperviscosity)
AKI
Hypercalcemia (Ca 14-15 range)

27
Q

On PE of MM you may see

A 
Hepatosplenomegaly 
LAD* 
retinal vein enlargement 
AKI 
Hypercalcemia
28
Q

Labs for MM may show

A

Anemia!
hypercalcemia, elevated BUN/Cr
**Rouleaux formation (falsely elevated MCV)
M spike on Sr protein electrophoresis!
Immunofixation (monoclonal Ig- all one type! like IgG)
*Bence Jones proteins on urine electrophoresis
Total protein rises + elevated globulin + decreased albumin

29
Q

Example MM lab read

A

Hgb: 9
Hct: 27%
MCV: 89
Total protein: elevated w/ elevated globulin protein
Na+ low (2/2 gammaglobulin levels being high)

30
Q

Ways to diagnose Myeloma are

A 
Increased Serum Immunoglobulins 
Bm Bx* (definitive!)- >20-30% plasma cells 
Rouleaux formation 
Elevated Sr protein, low albumin 
-SPEP
-Immunofixation (shows type) 
-24 hr UPEP (urine) 
-PET scan (check for lytic lesions- esp on skull*)
31
Q

How do you stage multiple myeloma

A 
Depends on organization! International system: 
I: Beta 2 micro and albumin >3.5 
II: neither I or II 
III: Beta2 micro >5.5 
-i dont get it..
32
Q

What is the prognosis of MM

A

10% indolent
15% die in first 3 months of dx
Chronic phase: 2-5 years before terminal phase (BM failure)
46% die in chronic phase (renal failure, sepsis)
26% die in acute terminal phase

33
Q

What is the acute terminal phase of MM

A

They are no longer eligible for treatment so you just do palliative care and wait until they pass

34
Q

Indications to treat multiple myeloma are

A 
CRABI! 
Calcium- rising 
Renal insufficiency 
Anemia 
Bone lytic lesion 
Infections
35
Q

MM treatment is based on

A

high vs intermediate vs low risk

Chromosomes, stage, and presentation (AKI or hypercalcemia)

36
Q

Common MM drug regimens are

A

“-ide” + steroid
Velcade / Revlamid / Thalidomide / Pomolidamide + Decadron
End stage: Kyrpolis- steroids rupture cells
Younger pt: Autologous SCT
Monthly IV Zoledronic acid (bisphosphanate) for lytic lesions
Xgeva (?)
local radiation for plasmacytoma
F/u with nephrology

37
Q

AKI in MM can be due to

A

gammaglobulins getting stuck in tubules, can be reversed (myeloma kidney may need dialysis and plasmapharesis)
Extreme dehydration from hypercalcemia (**Vigorous hydration, zoledronic acid)

38
Q

What are S/Sx of hypercalcemia

A 
stones (calcium stones) 
bones (lytic lesions)
groans (constipation)
moans
physh overtones (confusion)
39
Q

What is MGUS

A

Monoclonal Gammopathy of Undetermined Significance
similar to MM!
Elevated Immunoglobulin on SPEP w/ lytic lesions, increased plasma cells in BM, or light chains in urine (bence jones)
BUT*** some will develop more severe dz- myeloma, amyloidosis, CLL, or lymphoma

40
Q

What is Waldenstrom Macroglobinemia

A

Diseased B cells containing lymphocytic and plasma cell components (AKA- Lymphoplasmacytic lymphoma)
Arise from BM but does NOT cause lytic lesions
Proliferation of IgM (large, macromolecule)
S/Sx are weakness, fatigue, epistaxis, dizziness

41
Q

How can you diagnose Waldenstrom macroglobinemia

A

SPEP: IgM spike***
PE: hepatosplenomegaly, retinal vein occlusion (sausage link)

42
Q

How do you treat Waldenstrom macroglobinemia

A

Emergent electropharesis

Chemo CHOP- Cyclophosphamide, Doxarubicin, Oncovin, Prednisone

Summer 3 (12 decks)

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