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Pathophysiology - Hematology > Benign Lymphocyte Disorders > Flashcards

Benign Lymphocyte Disorders Flashcards

1
Q

How do you identify a NK cell?

A

Large granular lymphocyte

-> only lymphocyte which will have granules to kill target cell

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2
Q

How is lymphocytosis (not leukocytosis) defined in adults and infants / young children?

A

Adults - >4,000 / microliter

Infants and young children - >9,000 / microliter

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3
Q

How is lymphopenia defined and what is relative lymphocytosis?

A

Lymphopenia - <1,500 / microliter

Relative lymphocytosis - absolute lymphocyte count is normal / near normal despite low WBC count -> makes up a relatively larger percentage

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4
Q

How is leukocytosis vs leukopenia defined?

A

Leukopenia - <5k / ul

Leukocytosis - >10k / ul

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5
Q

A patient has lymphadenopathy AND lymphocytosis. What findings suggest the cause is more likely malignant than benign?

A

> 5 cm lymph node. (very large, anything over 1 cm is abnormal)

SEVERE anemia or thrombocytopenia (viral may be mild)

Older patient or constitutional symptoms

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6
Q

What are the benign acute causes of lymphocytosis / lymphadenopathy (L/L)?

A

Bordetella Pertussis (think of the popcorn spilling in sketchy)

Infectious mononucleosis (reactive lymphocytosis in infectious process)

Infectious Hepatitis

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7
Q

What are the benign chronic causes of lymphocytosis / lymphadenopathy (L/L)?

A

Brucellosis
Tuberculosis
Toxoplasmosis
Secondary and congenital syphilis

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8
Q

What are the malignant disorders which are associated with L/L?

A
  1. Chronic Lymphoid Leukemias
  2. ALL
  3. Leukemic phase of lymphomas
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9
Q

What are the peripheral blood smear features of infectious mononucleosis?

A

Reactive lymphocytes with atypical macrophage-like morphology (can look like blasts)

Red cell hugging - cytoplasm of CD8 reactive T cells will hug RBCs

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10
Q

What establishes diagnosis of IM in a patient? How can you generally tell if an increase in antibodies is benign or malignant?

A

Heterophile IgM antibody

Can tell by running flow cytometry for B cell light chain. If both light chain types are present equally, it’s benign (polyclonal). If one is greatly favored, it’s malignant (monoclonal).

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11
Q

What usually causes IM, who gets it, and what are the clinical symptoms?

A

IM usually caused by EBV, less commonly CMV. Virus infects B cells, and T cells react

Affects young people (kissing disease)

Constitutional symptoms + stiff neck

  • Splenomegaly - T cell hyperplasia in PALS
  • Lymphadenopathy - often generalized, usually in neck (where infection started)
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12
Q

What are the atypical lymphocytes of IM called?

A

Downey cells

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13
Q

What is the risk of treating IM as a bacterial infection and what is the general care we advise?

A

If patient is given ampicillin, they will develop a rash

Only give steroids in very severe symptoms, otherwise just supportive

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14
Q

What are the complications of IM?

A

Splenic rupture

AIHA - due to cold agglutinins

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15
Q

What is definition of localized vs generalized lymphadenopathy?

A

Localized - <3 contiguous lymph node affected

Generalized - >=3 noncontiguous lymph nodes affected

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16
Q

What are the general causes of local lymphadenopathy?

A

Local infection - i.e. pyogenic infection, cat scratch, TB

Lymphomas - HL and NHL

Metastatic carcinomas

17
Q

What are the general causes of generalized lymphadenopathy?

A

Infections

Non-infectious inflammatory processes (sarcoidosis, SLE, RA)

Malignant processes which have spread more

Miscellanous (drug reactions, hyperthyroidism, sinus histiocytosis with massive lymphadenopathy)

18
Q

What are the superficial vs axial lymph nodes?

A

Superficial - accessible by physical exam

Axial - located in chest, abdomen, and pelvis, better seen by imaging. I.e. hilar nodes, para-aortic nodes.

19
Q

How do you know something is abdominal lymphadeopathy on CT and not just a blood vessel or a loop of bowel?

A

You give them both oral and IV contrast with their CT

20
Q

What features of lymphadenopathy lead you to believe its more likely a benign than a malignant process?

A

Rapid onset (days) - except for very aggressive lymphomas

Associated with pain / tenderness (lymphadenitis draining an area of infection)

Soft consistency

21
Q

What would a firm vs a woody / hard lymph node give you suspicion for?

A

Firm - Non-Hodgkin’s lymphoma

Woody hard - metastatic carcinoma

22
Q

What diagnostic workup should be done with isolated lymphadenopathy?

A

CBC with differential
Serology and cultures (for viruses and bacteria)
Flow cytometry if lymphocytes are increased

Lymph node biopsy as a last resort

23
Q

What are the four types of lymph node hyperplasia which can be detected by biopsy?

A

Follicular - stimulation of B cells

Paracortical - T cell hyperplasia

Sinus - expansion of sinus histiocytes

Angiofollicular hyperplasia - “onion skinning appearance”

24
Q

What are the causes of follicular and paracortical hyperplasia of LN?

A

Follicular - bacterial and viral infections, autoimmune diseases like RA (which overproduce Abs)

Paracortical - T cell processes, i.e. drug reaction and infectious mononucleosis

25
Q

What are the causes of sinus and angiofollicular hyperplasia?

A

Sinus:
Sinus histiocytosis with massive lymphadenopathy - Rosai-Dorfman disease

Angiofollicular hyperplasia - Castleman’s disease

26
Q

What are the two types of Castleman’s disease? What is usually associated with second type, and their overall clinical course?

A
  1. Unicentric - localized angiofollicular hyperplasia - indolent, benign course
  2. Multicentric - multicenter angiofollicular hyperplasia -HHV-8-associated, aggressive, lymphoma-like course
27
Q

What pathological subtype of Castleman’s disease is most associated with unifocal castleman’s disease (UCD)? What are its features

A

Hyaline vascular type

  • > onion peel mantle zone
  • > Lollipop appearance - radially penetrating sclerotic vessels
  • > lots of pink, acellular material
28
Q

What pathological subtype of Castleman’s disease is most associated with multifocal castleman’s disease (MCD)? What are its features, and how is it treated?

A

Plasma cell / plasmablastic type - IL-6 driven (cytokine)

  • > Sheets of plasma cells
  • > more aggressive course, treated like myeloma
29
Q

What are the events in the pathogenesis of Castleman’s disease?

A

Viral homologue of IL-6 drives B cell proliferation

Infected B cells localize to mantle zone of LN follicles, and cytokine release contributes to constitutional symptoms

30
Q

What are the treatments for UCD and MCD?

A

UCD - surgical resection

MCD - Rituximab, corticosteroids, antiviral agents

31
Q

What is the definition of splenomegaly?

A

> 14cm span in the mid-clavicular line

32
Q

What are the criteria for hypersplenism and its underlying pathophysiology?

A
  1. Splenomegaly
  2. Reduction of at least one cell line in the blood
  3. Normal bone marrow function

-> spleen is enlarging due to sequestering more WBCs/RBCs

33
Q

What are the indications for splenectomy?

A

Splenic rupture
Chronic immune thrombocytopenia
Hemolytic anemias - hereditary spherocytosis, AIHA, thalassemia major or intermedia
Hypersplenism (in symptomatic patients)

34
Q

What must be done prior to splenectomy?

A

Pneumococcal vaccination at least two weeks before, annual flu shots, and meningococcal vaccine

Pathophysiology - Hematology (14 decks)

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