lymphomas Flashcards

1
Q

most lymphomas arise from where

A

85% of lymphomas arise from B-cells whereas 10-15% arise from T-cells.

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2
Q

Germinal B center > any mutation here leads to

A

follicular lymphoma,
diffuse large B cell lymphoma
hodgkin’s lymphoma

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3
Q

Each subtype originates from a specific place in the lymph node, so let’s see what’s the structure of lymp node

A

1- Capsule
2- Lymph and blood vessels
3- Cortex >has follicles

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4
Q

Mantle zone > naïve mature B cells, any mutation that happens here=

A

mantle zone lymphoma

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5
Q

what is a diagnostic method for lymphomas

A

Lymph node excisional biopsy (NOT FNA)

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6
Q

where does hodgkin lymphoma arise from

A

germinal center of B cells

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7
Q

what CD is found in hodgkin

A

Cd 15,30 characteristic of reed sternberg cell

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8
Q

what age is in hodgkin

A

Bimodal age distribution — 15 to 30 years old and >50 of age

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9
Q

four subtypes in hodgkin according to histology

A

o Lymphocyte predominance (5%) — few Reed-Sternberg cells & many B-cells- best prognosis

o Nodular sclerosis (70%) — more in women: bands of collagen envelope Reed- Sternberg cells
o Mixed cellularity (25%) — large numbers of Reed-Sternberg cells in a pleomorphic background

o Lymphocytic depletion (<1%) — worst prognosis

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10
Q

ann arbor staging system 4 stages

A

• Stage 1: Single LN region

• Stage 2: Two or more LN regions on the same side of diaphragm, above or below the diaphragm

• Stage 3: LN regions both above and below diaphragm
• Stage 4: Widespread involvement of one or more organs (liver, spleen, bone marrow, lung) +/- LN involvement

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11
Q

Ex: Patient with one group of LN and constitutional symptoms = stage ?

A

1B

Suffix A: No symptoms
Suffix B: Constitutional: fever, weight loss, night sweats (worse prognosis)

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12
Q

signs anf symptoms of hodgkin lymphoma

A

• Painless cervical lymphadenopathy —most common presentation

• Supraclavicular, cervical, axillary, mediastinal lymph nodes — spreads by continuity from one to adjacent. Has rubbery consistency on examination.

• +/- hepatosplenomegaly, B symptoms (fever, night sweats,and weight loss), pruritis, and cough (secondary to mediastinal involvement)

• less commonly, alcohol related pain at site of LN.

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13
Q

main risk factors of hodgkin

A

• HIV, EBV, infectious mononucleosis (CD15, CD30)
• Benzene (also RF for acute leukemia)

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14
Q

in biopsy what is seen in hodgkin

A

Reed Sternberg on LN biopsy (binucleate or multinucleate malignant B-lymphocytes)

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15
Q

tx of hodgkin

A

• Stage 1A and 2A: Local radiation + small course of chemo
•Stage 3 and 4: (or any B-symptoms): Chemo ABVD
o A = Adriamycin (doxorubicin)
o B = Bleomycin
o V = Vinblastine
o D = Dacarbazine

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16
Q

non hodgkin lymphoma

A

a group of blood cancers that originate from lymphocytes (B cells or T cells) in the lymphatic system. It is more common than Hodgkin lymphoma and has many subtypes, ranging from slow-growing (indolent) to aggressive.

17
Q

risk factors of non hodgkin

A

• Older age (Most common in 60s-70s)
• Weakened immune system (HIV/AIDS, organ transplant, autoimmune diseases)
• Viral infections (EBV, HTLV-1, Hepatitis C)
• Chronic inflammation or infections (H. pylori → MALT lymphoma)
• Exposure to chemicals (pesticides, herbicides, chemotherapy, radiation)

18
Q

symptoms of non hodgkin

A

Mnemonic: “B-Symptoms + Lymph Nodes”
1. Painless swollen lymph nodes (neck, armpits, groin)
2. B-Symptoms (Seen in aggressive cases)less common than in hodgkin
• Fever (>38°C/100.4°F)
• Drenching night sweats
• Unintentional weight loss (>10% in 6 months)

19
Q

Extranodal involvement is more common than Hodgkin:

A

o Hepatosplenomegaly, abdominal pain or fullness
o BM infiltration: anemia, infections, bleeding
o Skin (in T-cell): mycosis fungoides, Sezary syndrome

20
Q

types of non hodgkin lymphoma

A
  1. B-Cell Lymphomas (Most Common, ~85%)
    • Diffuse Large B-Cell Lymphoma (DLBCL) → Most common, aggressive
    • Follicular Lymphoma → Slow-growing, indolent
    • Burkitt Lymphoma → Highly aggressive, associated with EBV
    • Mantle Cell Lymphoma → Rare, aggressive
    • Marginal Zone Lymphoma (MALT lymphoma) → Linked to chronic infections (e.g., H. pylori in the stomach)
21
Q

tx of of NHL indolent

A

• Watchful waiting (if asymptomatic)
• Rituximab (Anti-CD20 antibody) ± Chemotherapy
• Radiation therapy (for localized disease)

22
Q

tx of Aggressive NHL (e.g., DLBCL, Burkitt)

A

Chemotherapy (CHOP regimen)
• Cyclophosphamide
• Hydroxydaunorubicin (Doxorubicin)
• Oncovin (Vincristine)
• Prednisone
• Rituximab (Anti-CD20, for B-cell NHL)

Stem cell transplant (for refractory or relapsed cases)

23
Q

what type of non hodgkin lymphoma is associated with EBV presents with a mass in jaw and GI involvement and mmostly in childhood most aggressive

A

burkitts lymphoma

24
Q

histology of burkitts lymphoma

A

starry night appearance

25
what is tumor lysis syndrome
occurs when a large number of cancer cells die rapidly, releasing their intracellular contents into the bloodstream. This overwhelms the kidneys and leads to dangerous electrolyte imbalances. "PUCK” → ↑ Phosphate, ↑ Uric acid, ↑ Calcium (binds to phosphate, but free calcium ↓), ↑ Kalemia (potassium).
26
multiple meloma main features
CRAB: hyperCalcemia Renal failure Anemia Bone pain
27
skeletal manifestations in multiple myeloma
o Bone pain due to osteolytic lesions, fractures and vertebral collapse o Pathological fractures o Loss of height secondary to vertebral collapse
28
multiple myeloma cancer of what
Cancer of plasma cells → Overproduction of M-protein.
29
most common antibodies in multiple myeloma
IgG (57%) IgA (21%) light chain only (18%)
30
in multiple myeloma the patient will have expansion and proliferation of “ MONICLONAL” plasma cells that secrete same type of antibodies. Other types of antibodies will not be secreted. So there’s decrease in totalantibody production, this decrease is called
hypogammaglobulinemia
31
most common cause of deatg in MM
up to 70% of patients die of infection
32
peripheral blood smear would show what in MM
RBCs in rouleaux formation (stacking of RBCs like coins) > hyperglobulinemia causes the RBCs to stick together
33
diagnosis of MM blood tests
1. Blood Tests • Serum protein electrophoresis (SPEP) → Detects M-protein (monoclonal spike) • Immunofixation Electrophoresis (IFE) → Identifies M-protein subtype (IgG, IgA most common) • Serum Free Light Chains (FLC) → Detects abnormal κ (kappa) or λ (lambda) light chains
34
urine tests on MM
Urine Protein Electrophoresis (UPEP) → Detects Bence Jones proteins (light chains)
35
tx of MM
1. Initial Therapy (For Fit Patients) • Triplet Therapy: • Bortezomib (Proteasome inhibitor) • Lenalidomide (Immunomodulator) • Dexamethasone (Steroid) • Stem Cell Transplant (For eligible patients under 70-75 years)
36
what is WALDENSTROM MACROGLOBULINEMIA
Excess IgM (macroglobulin) → Causes hyperviscosity, anemia, and immune suppression.
37
Symptoms of Waldenström Macroglobulinemia
1. Hyperviscosity Syndrome (Thick Blood) → Classic Feature! • Blurry vision (retinal vein dilation, hemorrhages) • Headaches, dizziness, confusion • Nosebleeds, easy bruising 2. Bone Marrow Failure (Due to Cancer Cell Infiltration) • Anemia → Fatigue, weakness, pallor • Low platelets (Thrombocytopenia) → Bleeding tendency 3. Enlarged Organs (Lymph Nodes, Spleen, Liver) • Painless swollen lymph nodes • Hepatosplenomegaly (big liver/spleen) 4. Neuropathy (IgM-related nerve damage) • Numbness, tingling, burning pain in hands/feet 5. Cryoglobulinemia (Cold-Sensitive Proteins) • Raynaud’s phenomenon (fingers turn white/blue in cold) • Skin ulcers, joint pain 6. Infections (Weak Immune System) • Frequent bacterial infections
38
diagnosis of WM SPEP
Serum Protein Electrophoresis (SPEP) & Immunofixation → Detects IgM monoclonal spike
39
what determines prognosis in WM
Beta-2 microglobulin