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D&T:1 > WBC Pathology > Flashcards

WBC Pathology Flashcards

1
Q

Follicular Lymphoma

A

Differentiated from follicular hyperplasia by:

Disrupted architecture

Lack of a mantle zone w/ polarity

No dark/light zones w/ tangible body macros

Reverse bcl2 staining

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2
Q

Paracortical hyperplasia

A

Enhanced growth of the T-cell region due to stimulation via infection, drugs (Dilantin), and even dermatopathic lymphadenopathy

-Must correlate w/ clinical findings and TCR rearrangement studies

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3
Q

Sinus histiocytosis

A

Numerous macrophages within the lymph sinuses thought to be the response to malignant cells

-Will be prominent in nodes draining cancer

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4
Q

Nonspecific lymphadenitis

A

Follicular hyperplasia that occurs due to the drainage of infections; results in large, tender nodes

-Can be acute or chronic; common in kids

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5
Q

Precursor-B cell ALL

A

Clinical: Abrupt stormy onset, BONE PAIN (marrow involvement), possible CNS symptoms

Immunophenotype: CD19, CD22, CD10 (+), TdT (+)

Cytogenetics: Can involve t(12;21) mutating ETV6 and RUNX1 genes or t(9;22) mutating BCR-ABL

Treatment: Aggressive chemo including CNS prophylaxis
(Very successful in children; adults can sometimes not handle the chemo)

*Monitor to ensure there is no detection of MDR

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6
Q

Precursor T-cell ALL

A

Clinical: Abrupt stormy onset, Bone pain, CNS sx, MEDIASTINAL MASS

Diagnosis: MPO(-), disruption of normal architecture
*CD34, TdT, CD1a, CD2, CD5, CD7 (+)

*NOTCH1 mutations seen in 70%

Prognosis: Aggressive chemo and CNS prophylaxis

*Detection of MRD is assoc. w/ bad outcome

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7
Q

CLL/ASL

A

Clinical: Generalized lymhadenopathy w/ hypogammaglobulinemia (infxns)

Diagnosis: Smudge cells on PS, Increased small and mature lymphs that are hyperclumped,

(SLL)-lymphoid aggregates in BM and white/red pulp in spleen/liver

* Pale areas on lymph node can be indicative
* CD19, CD5, CD23, CD20-dim, surface light chain restricted-dim

Prognosis=> Most pts. die of other problems

**Progression to Richter Syndrome possible

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8
Q

Follicular Lymphoma

A

Clinical: Painless lymphadenopathy, mimics normal architecture

Diagnosis: LN has a nodular pattern w/ lack of an asymmetric mantle zone; liver shows “portal tracks”

* CD10, 19, 20, surface light chain restriction
* t(14;18) =>> bcl2 and bcl6 overexpression

Prognosis: Chemotherapy is ineffective but disease is indolent
–transformation to DLBCL occurs later

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9
Q

Bcl2

A

Inhibits apoptosis via the mitochondrial pathway

-Normally shut off to allow for normal lymphocyte maturation

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10
Q

Bcl6

A

Encodes for a DNA zinc finger that is normally required for normal germinal center regulation

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11
Q

Mantle Cell Lymphoma

A

Clinical: Painless lymphadenopathy, lymphomatoid polyposis, BM involvement

Diagnosis: CD5, CD19, CD20, BRIGHT surface light chain

* t(11;14) =>>Increased cyclin D1 expression and increased G1-S phase transition 
* Tumor cells can resemble that of normal mantle cells

Prognosis: Retuximab and Chemo; possible BM transplant in adolescents
*Most pts. relapse or die of organ failure in 3 yrs

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12
Q

Marginal Zone Lymphoma (nothing special)

A

Clinical: Assoc. w/ hyperinflammatory states (Hashimotos, Sjogrens); can regress if these states are controlled; cells can resemble normal marginal zone cells

Diagnosis: Pleomorphic population of plasmacytoid and monocytoid B-cells w/ destructive infiltration of host tissue

**Starts off as a reactive polyclonal reaction to inflammation, acquires mutations or t(11;18) to express MALT1 or BCL10 that will not respond to extrinsic signaling =»lymphoproliferation

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13
Q

Causes of lymphadenopathy

A

AI disorders- Sjogrens, SLE

Iatrogenic- Drugs, silicone

Infection

Malignancy

Sarcoidosis

Dermatopathic lymphadenopathy

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14
Q

Lymphoplasmocytic Leukemia

A

Resembles SLL only most neoplastic cells are plasma cells; secretes monoclonal IgM =»Waldenstrom’s Macroglobulinemia

-Cryoglobulinemai, visual/neurologic symptoms

  • Involves a mutation in the MYD88 gene
    • promotes the growth and survival of tumor cells

-Plasmapharesis alleviates symptoms

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15
Q

Hairy Cell Leukemia

A

Clinical: Monocytopenia, splenomegaly; *assoc. w/ mutations in BRAF

Diagnosis: Diffuse, fried eggs in the BM; dry tap of BM; red pulp involvement w/ obliteration of the white pulp
*CD11c/CD25/CD103 (+) =»CHARACTERISTIC

Prognosis: Indolent course; use chemo w/ BRAF inhibitors

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16
Q

Multiple Myeloma

A

Pathophysiology: MUST CONTAIN

  1. M-protein in blood/urine
  2. Monoclonal plasma cells
  3. End organ damage

Clinical: Weakness (anemia), recurrent infxn, polyuria (hypercalcemia), renal failure (BJ protein), amyloidosis

* Labs: BJ protein in urine; increased IgG or IgA; anemia; Rouleux and "Blue smear" on peripheral blood slide 
    - Bony, lytic lesions on x-rays of bone
  • Caused by translocations involving IgH, del17p, and rearrangements involving MYC
    • Increased IL-6 also increases the activity of osteoclasts

Treatment: Chemo and stem cell transplant may prolong life but not cure

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17
Q

MGUS

A

“Monoclonal Gammopathy of Unknown Significance”

-Most common cause of monoclonal gammopathy that must be monitored (BJ protein and serum protein M levels) to ensure it doesn’t progress to MM

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18
Q

Plasmacytoma

A

Soft tissue clonal plasma cell masses that commonly collect on the spine (bone site) or lung/oropharynx (soft tissue site)

-Can progress to MM; treat w/ localized radiation

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19
Q

Diffuse Large B-Cell Lymphoma

A

Clinical: B-grade symptoms w/ rapidly forming mass; BM involvement later

Diagnosis: Diffuse disruption of BM architecture by large lymphocytes; mitotically active and have indistinct cell borders
*No pathognomic cell markers, just CD10, 19, surface light chain
*Can have bcl2, bcl6, or myc8 gene rearrangement
=»DLBCL w/ two of these is much more aggressive

Treatment: R-CHOP works pretty well; fatal if untreated tho

*Can occur in IC pts. where it is assoc. w/ EBV infection

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20
Q

Burkitt Lymphoma

A

Clinical: 30% of childhood NHL; usually extranodal w/ mandibular mass and abdominal masses
=»can lead to Tumor Lysis Syndrome
*Assoc. w/ EBV infections in endemic areas

Diagnosis: “Starry Sky” appearance of BM (macros eating dead cells); infiltrate of medium sized cells w/ basophilic cytoplasm; high mitotic activity

  • typically has translocation of MYC protein allowing for increased glycolysis by the tumor
    * Is bcl2, CD34, and Tdt (-) because the cells are MATURE

***ASSOC. W/ t (8;14)

Treatment: Responds well to systemic chemotherapy as well as intrathecal administration

21
Q

Tumor Lysis Syndrome

A

Rapid cell turnover and death causes the release of uric acid, K+, and Ca2+

=»Medical emergency requiring hydration, binding of electrolytes, and hemodialysis

22
Q

Peripheral T-Cell Lymphoma

A

Clinical: General lymphadenopathy, eosinophilia

Diagnosis: Large sized malignant cells w/ paracortical effacement; CD34 and TdT (-)

Prognosis: Not good

23
Q

Anaplastic Large Cell Lymphoma

A

Clinical: Extranodal infiltrate w/ BM involvement
*Involves ALK translocation which can be stained w/ immunohistochemistry

Diagnosis: *Hallmark= Large anaplastic cells w/ horseshoe appearing nucleus
*Neoplastic cells congregate around sinuses

Prognosis: Favorable unless you are adult and ALK (-)

24
Q

Adult T-cell Leukemia

A

Clinical: T-cells infected w/ HTLV-1 that presents as generalized lymphadenopathy, skin lesions, and lymphocytosis
*Skin lesions only=favorable prognosis

Diagnosis: Cloverleaf cells; ^**CD4(+)/CD7(-); HTLV-1 (+)

25
Q

Mycosis fungoides/Sezary Syndrome

A

CD4+ tumor in the skin w/ three stages:

  1. Patch
  2. Plaque
  3. Tumor
    * Can spread to blood and progress to Sezary syndrome and will see exfoliative erythema

Diagnosis: Dermal plaque, *Cerebriform nuclear contours in neoplastic cells, Sezary cells in the blood

Prognosis: Indolent; death can occur due to immunodeficiency produced

26
Q

Large Granular Lymphocytic Leukemia

A

STAT3 mutations =» large, GRANULAR lymphocytes

*Can be T-cell or NK cell (NK type is more aggressive)

Clinical: Neutropenia (decreased myeloid growth in the BM
Felty Syndrome
Anemia

27
Q

Felty Syndrome

A

RH arthritis, splenomegaly, and neutropenia

28
Q

Reed-Sternberg Cell

A

Characteristic neoplastic cell of Hodgkin’s Lymphoma; makes up the minority of the cell population

  • derived from the germinal center and can potentially harbor EBV
  • Has appearance of Owl Eyes, Mononuclear, Lacunar (folded due to disruption during fixation), or Popcorn (specific to Nodular Sclerosing HL)

CD15/CD30 (+)

*Except in NSNHL; this will have CD45, B-cell Ag, and Bcl6 (+)

29
Q

Hodgkin’s Lymphoma Staging

A

I- One node region

II- Two node regions

III- Has crossed the diaphragm

IV- Dissemination

30
Q

NSHL

A

Nodular Sclerosing Hodgkin’s Lymphoma - most common subtype

Involves cervical, supraclavicular, mediastinal nodes that have formation of nodules due to sclerosing collagen
-RS lacunar cells present

31
Q

MCHL

A

Mixed Cellularity Hodgkin’s Lymphoma- second most common subtype

  • See diffuse effacement of lymph nodes w/ many RS cells
  • EBV ASSOCIATED
  • Causes eosinophilia
32
Q

Possible causes of suppression of granulocytic precursors

A

Drugs: Phenothiazines, thiouracil, sulfonamides, aminopyrine, and chemotherapy

Infection

Large Granulocytic Lymphocytic Leukemia

-Bone marrow suppression can also be due to aplastic anemia, Kostmann syndrome

33
Q

Consequences of neutropenia

A

(Infections)

  • mucosal ulcers
  • invasive infxns of bladder, kidney, lung
  • sites of infxn show numerous organisms w/ little response
34
Q

AML Morphology

A

Myelocytic: *Auer rods can be present
CD15/CD33/CD34 (+); MPO (+); NSE (-)

Monocytic: CDllb/CD14/HLADR (+); MPO (-); NSE (+)

35
Q

APML

A

Caused by t(15;17) =» PML/RARA; blocks differentiation at the promyelocyte stage

*Can cause DIC; look for schistocytes on PB; WBCs can have Auer rods

Treatment: Anthracycline chemo + ATRA
(All-trans Retinoic Acid/Vitamin A)
*Arsenic can promote degradation of the PML/RARA protein product

36
Q

AML Clinical Features

A

Similar to ALL; bleeding is much more striking

Prognosis: Allogenic BM transplants; prior MDS; del11q23 =» BAD

37
Q

Granulocytic Sarcoma

A

Tissue mass of erythroid blasts w/o BM or PB involvement

=»Treat before it progresses to AML

38
Q

Myelodysplastic Syndrome

A

Clonal stem cell abnormality characterized by ineffective erythropoesis; seen in older pts. a few years post-chemo or idioapathic and presents as pancytopenia

PM: Will see NRBCs w/ ringed sideroblasts and some megakaryocytes
BM: Packed w/ trilineage precuros BUT > BM transplant
Elderly=» Supportive therapy

39
Q

CML

A

Characterized by excess effective hematopoesis; MUST HAVE Philadelphia Chromosome to call it this

*CML disorder is in the pluripotent stem cell; can give rise to multiple erythroid and lymphoid cell lines

40
Q

CML Morphology

A

PB: Leukocytosis w/ left shift; eosinophilia; ⭐️BASOPHILIA

BM: Packed w/ prominent hyperplasia but NO DYSPLASIA; sea-blue histiocytes

Hepatosplenomegaly to to EMH

41
Q

CML Treatment

A

Gleevac (TK inhibitor)
-some resistance occurs w/ altered BCR-ABL protein

*Disease often discovered accidentally; may feel LUQ symptoms due to EMH

42
Q

Polycythemia Vera

A

Caused by a JAK-2 mutation; increased cells of mulitple lineage (mostly RBC) alongside DECREASED EPO

-Has minimal reticulin fibrosis; may cause a dry tap

Clinical: Headache, dizziness, parasthesias (due to increased RBC mass); hyperuricemia (gout); DVT in weird sites (mesenteric/hepatic circulation)

Treatment: Therapeutic phlebotomy; JAK-2 inhibitors

43
Q

Essential Thrombocytosis

A

Caused by JAK-2 mutations; platelet counts of greater than >450K w/ abnormally large platelets in the PB

Diagnosis: Must exclude iron deficiency anemia and reactive thrombocytosis; inflammatory process

Clinical: Erythomelalgia, unusual sites of thrombosis; BM will have large hyperlobated megakaryocytes

Treatment: Indolent; myelosuppressive therapy

44
Q

Primary Myelofibrosis

A

Neoplastic megakarocytes release PDGF and TGF-B =» Proliferation of fibroblasts resulting in increased reticulin and a fibrotic BM =» EMH

Clinical: Early Pre-Fibrotic: Hypercellular marrow w/ cloudy megakaryocytes
Late Fibrotic: Hypocellular marrow w/ fibrosis, NRBCs and teardrop cells due to EMH, osteosclerosis, splenomegaly causing early satiety

45
Q

Hypersplenism

A

Splenomegaly causing pancytopenia due to excess removal of blood products by the spleen

Correct w/ splenectomy

46
Q

Congestive Splenomegaly

A

Intrahepatic: Right heart failure; hepatic cirrhosis

Extrahepatic: Portal vein thrombosis; splenic vein thrombosis

Clinical: Spleen becomes firm w/ increased congestion over time; increased pressure =» intraparenchymal hemorrhage

*Sugar icing occurs due to fibrosis of the outer capsule when it is trying to contain the size of the spleen

47
Q

Splenic Infarct

A

Pale, wedge-shaped, and subcapsular

  • Could be abscess formation if assoc. w/ infective endocarditis
  • Common in splenomegaly
48
Q

Thymic Hyperplasia

A

Appearance of secondary B-follicles usually assoc. w/ Myasthenia Gravis

49
Q

Thymoma

A

Non-hematopoetic neoplasm that is a tumor of the thymic epithelial cells; forms of a small mass in the anterior superior mediastinum (similar to NSHL)

Benign, encapsulated: Medullary

Malignant: Epithelial cells or SCC (lymphoepithelioma-like)

D&T:1 (6 decks)

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