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SBL Test 1 > Chapter 13 > Flashcards

Chapter 13 Flashcards

1
Q

HSC differentiate into what?

A
  1. Myeloid-derived cells
  2. Lymphoid-derived cells
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2
Q

Myeloid-derived cells

A

(MMEG)

  1. Monocytes (=> MO and DC)
  2. Megakaryocytes (=> platelets)
  3. Erythrocytes
  4. Granulocytes
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3
Q

Lymphoid – derived cells

A
  1. Lymphocytes (T-cells, B-cells, plasma cells)
  2. NK cells
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4
Q

Describe development of HSC and blood cells

A

(Young Liver Synthesizes Blood: Yolk sac, liver, spleen, BM)

  1. 3rd week of development:
    1. Shortly in yolk sac, then definitively in mesoderm of intraembryonic aorta/gonads/mesonephros region
  2. 3rd month of embryogenesis:
    1. Migrate to liver
      1. Liver = main site of BC formation until shortly before birth.
  3. 4th month of embryogenesis:
    1. Migrate to bone marrow
  4. By birth:
    1. BM in ENTIRE skeleton = haematopoietically active
    2. Liver hematopoiesis ↓ ↓ ↓
  5. After puberty:
    1. ONLY BM in AXIAL skeleton = haematopoietically active
      1. BM biopsies in adults are taken from PSIS.
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5
Q

Leukoerythroblastosis

A

processes that distort architecture of BM (cancer, granulomatous disese) è release of immature precursors into blood. Results in:

  1. Left-shift: increase release of immature neutrophil precursor cells into the blood
  • MCC = bacterial Infection
  • Example: Acute inflammation may cause a increase in neutrophils in bloo

2. Leukoerythroblastic reaction: left shift that in involves the release of immature RBC. Cause =

    1. Physiologic cause seen in anemia
    1. Response of bone marrow to fibrosis or a tumor taking up space
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6
Q

NOTE: [IMP]

  • cytosis = _____ ↑↑↑ in cell line
  • Example = _____
  • emia = _____ ↑↑↑ in cell line
  • Example = ______
A

NOTE: [IMP]

  • cytosis = reactive ↑↑↑ in cell line
  • Example = Lymphocytosis
  • emia = neoplastic ↑↑↑ in cell line
  • Example = Leukemia
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7
Q

NL adults =____ fat: hematopoietic element ratio

A

1:1

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8
Q

__________ states = ↓ ↓ ↓ # of fat cells

__________ states = ↑↑↑ # of fat cells

A
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9
Q

Granulocytes

A
  1. Neutrophil
  2. Basophil
  3. Eosinophil
  4. Mast cell
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10
Q

*80% of lymphocytes in peripheral blood are what?

A

T-cells

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11
Q

What is Leukmoid reaction?

A

Leukocytosis d/t reactive states (inflammation/stress) causes an

  • ↑↑↑ release of immature granulocytes/neutrophils =>
  • ↑↑↑ LAP (leukocyte alkaline phosphatase
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12
Q

Leukmoid reaction mimics ______.

A

Myeloid leukemia

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13
Q

Leukemia = ____ LAP

A

Leukemia = NL LAP

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14
Q
  • Neutropenia = _____ cells/mm3
  • Agranulocytosis = _____ cells/mm3
A
  • Neutropenia = < 1500 cells/mm3
  • Agranulocytosis = < 500 cells/mm3
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15
Q

Causes of neutropenia

A

Neutropenia is caused by:

1. Inadequate or ineffective granulopoiesis (4 mechanisms):

  • Suppress HSCs (Ex: Aplastic anemia, infiltrative marrow disorders); Patient will also [granulocytopenia + anemia + thrombocytopenia)
  • Suppress committed granulocytic precursors due to drugs ***
  • Diseases that cause ineffective hematopoiesis (Ex: Megaloblastic anemia, Myelodysplastic syndromes)
  • Congenital conditions that cause defects that impair differentiation of granulocytes (Kostmann Syndrome)

2. Rapid destruction or sequestration of neutrophils in periphery

  • Immunologically mediated (AI disorder or drugs)
  • Splenomegaly: Large spleen causes sequestration of neutrophils and modest neutropenia. Pts will have [neutropenia + anemia + thrombocytopenia]
  • Increased peripheral utilization (bacterial/fungal/rickettsial infection)
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16
Q

Suppression of HSC will cause what symptoms?

A

[granulocytopenia + anemia + thrombocytopenia]

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17
Q

Presentation of neutropenia

A
  1. Fever
  2. Malaise
  3. Chills
  4. Weakness and fatigue
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18
Q

Histology of neutropenia

A

Hypocellularity OR hypercellularity in BM

  1. Hypo = agents that suppres/destroy granulocytic precursors
  2. Hyper = excessive destruction of cells in periphery or neutropenia that cause ineffective granulopoiesis = megaloblastic anemia and myelodysplastic)
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19
Q

MCC of agranulocytosis

A

Drug toxicity

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20
Q

Complications of agranulocytosis

A

↑↑↑ susceptibility to:

  1. Bacterial infections
  2. Fungal infections (Candida and Aspergillus)
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21
Q

Presentation of agranulocytosis

A
  1. ^ same sx^
  2. Death in hours - days
  3. If patient develops infection: Ulcerating necrotizing lesions in the oral cavity (gingiva, floor of mouth, buccal mucosa, pharynx)
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22
Q

Lymphopenia = _____ (adults)

Lymphopenia = _____ (children)

A
  • Lymphopenia = < 1500 (adults)
  • Lymphopenia = < 3000 (children)
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23
Q

What is the process of neutrophil migration that occurs in Neutrophila (Neutrophilic Leukocytosis)?

A

MO release IL1 (endogenous pyrogen = fever) & TNF-a => ↑↑↑ synthesis of endothelial adhesion molecules (allow neutrophils to NTR). Neutrophil exit BS => tissue via 4 steps

Rolling

  1. ↑↑↑ in E/P selectin on endothelial cells
  2. Selectin ligand on PMNs bind to E/P selectins

Crawling (tight binding):

  1. LPS or C5a stimulate expression of integrin on PMNs
  2. Integrin binds to ICAM on endothelium

Transmigration

  1. Neutrophils bind PECAM-1 between endothelial cells

Migration to site via C5a and IL8

↓↓↓ CD16 and Fc receptors

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24
Q

Eosinophilic Leukocytosis (Eosinophilia) is due to?

A
  1. Allergic reaction (Type 1 Hypersensitivity reaction)
  2. Parasite infections
  3. Hodgkin’s/Non-Hodgkin’s Lymphoma
  4. Drug reactions
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25
Q

Pathogenesis of INC eosinophils

A

Th2 => ↑↑↑ IL-5 => ↑↑↑ IgE => ↑↑↑ eosinophils

26
Q

Basophilic Leukocytosis (Basophilia) is due to

A

Rare, except in Myeloproliferative diseases (CML = Chronic Myeloid Leukemia)

27
Q

Pathogenesis of Basophilia

A

Basophils are located in blood stream.

  1. Bind to Fc portion of IgE Ab.
  2. IgE molecules crosslink => degranulation
  3. Release of histamine (vasodilation) and enzymes (peroxidases and hydrolases)
28
Q

Monocytosis (INC in MO) is due to?

A
  1. Chronic bacterial infections (TB)
  2. Bacterial endocarditis
  3. Malaria
  4. Protozoa infections
  5. AI: SLE
  6. IBD
29
Q

MO/DC are made in ________, as _______.

How do they develop?

A
  1. MO/DC are produced in bone marrow as monocytes.
  2. 3 days later, monocytes NTR tissue => become MO or DC.
  3. Name depends on which tissue they’re located
30
Q
  • MO in liver => ______ cells
  • MO in brain => ______ cells
  • MO in bone => _______
A
  • MO in liver => Kupfer cells
  • MO in brain => Microglial cells
  • MO in bone => Osteoclasts
31
Q

Functions of monocytes

A
  1. Phagocytosis
  2. Makes cytokine (Key = IL-1 and TNF-a)
  3. Present antigens
32
Q

Lymphocytosis often accompanies _______.

Why does it occur?

A

monocytosis

  1. Chronic infections (TB)
  2. Viral infections (HepA, CMV, EBV)
  3. B. Pertussis
33
Q

Primary lymphoid organs = _____________

  • Sites: ________

Secondary lymphoid organs = ______________

  • Sites: ______________
A

Primary lymphoid organs = where lymphocytes are formed

  • Sites: BM and thymus

Secondary lymphoid organs = where mature lymphocytes proliferate

  • Sites: LN, spleen, Peyer’s patches and tonsils
34
Q

Describe layers of LN

A
  1. Cortex, which contains follicles (site of B-cell activation)
    * NL germinal centers contain centroblasts (dark on histology) and centrocytes (light on histology)
  2. Paracortex, which contains T-cells activated by APC and high endothelial venules (vessels that let B/T cells NTR node)
  • Engorged in immune response
  • DiGeorge syndrome = deficiency in T-cells that causes underdeveloped paracortex
  1. Medulla, made up of cavities/sinuses and cords
  • Medullary sinuses/cavities = contain MO = filter lymph and cause phagocytosis
  • Medullary cords = tissues between cavities that contain plasma secreting AB.
35
Q

How are lymphocytes in LN activated to help fight infections?

A
  1. Lymph drains from site of infection.
    1. In lymph, DC picks up antigen via MHC Class I/II and B7.
  2. Lymph NTRs nodes and moves through: cortex => paracortex => medulla.
  3. APC (DC) presents antigen to lymphocytes
    1. LN Cortex:
      1. What happens? Activation of B-cells
      2. How: APC stimulates primary follicles (inactive follicles that contain follicular DCs and quiet B cells) => enlarge => become secondary follicles/ germinal centers (where B cells grow and differentiate, make AB, undergo class switching) => B-cells are activated
    2. LN Paracortex:
      1. What happens? Activation of T-cells
    3. Medulla:
36
Q

What is a lab result to help us differentiate a reactive WBC proliferation (infection) vs. WBC neoplasm?

A

LAP (leukocyte alkaline phosphatase)

  • HIGH in reactive states
  • NL in neoplasms
37
Q

Difference in LN morphology in Acute vs. Chronic Nonspecific Lymphadenitis

A
  1. Acute = enlarged and TENDER
  2. Chronic = NON-tender
38
Q

Histology in Acute Nonspecific Lymphadenitis

A
  1. Large, reactive germinal centers with many mitotic figures
  2. Hyperplasia of endothelial cells that line sinuses
  3. Less severe infections = neutrophils in lymphoid sinuses
  4. Severe infections = entire LN can become necrotic/bag of pus
39
Q

Types and Causes of Chronic Nonspecific Lymphadenitis

A

1. Follicular hyperplasia

  • MOA = activation of humoral immune response (B-cells)
  • Causes = RA, toxoplasmosis, early HIV, B-cell responses

2. Paracortical Hyperplasia

  • MOA = stimulation of T-cells
  • Causes = Acute viral infections (like EBV)

3. Sinus histiocytes (reticular hyperplasia)

  • Non-specific finding, but MC in breast carcinoma.
  • Does NOT mean metastatic cancer, LN are just reacting to cancer.
40
Q

Histology in Chronic Nonspecific Lymphadenitis

A
  1. No acute inflammation
  2. No tissue damage
41
Q

Histology of Follicular Hyperplasia

A
  1. Large germinal centers, surrounded by a collar of small, resting naïve B-cells (mantle zone)
  2. Tingible-body MO = contain nuclear debris of B cells that undergo apoptosis if they cannot make a Ab with high affinity for antigen
42
Q

How can we tell if a process is follicular hyperplasia or follicular lymphoma (neoplastic process)? In reactive LAD,

A
  1. LN architecture is preserved: recognizable light (-cyte) and dark (-blast) zones
  2. Size and shape of LN vary
  3. Tingible-body MO
  4. – BCL2 staining
43
Q

Histology of Paracortical Hyperplasia

A
  1. Immunoblasts (3-4x size of resting and dark staining): activated T-cells
  2. Expansion of T-cell zones (containing immunoblasts), that can encroach on follicles
44
Q

Hemophagocytic Lymphohistiocytosis (MO activating syndrome) is triggered by?

A

EBV infection

45
Q

Acute Myeloid Leukemia

A

Malignant proliferation of myeloblasts in BM => released into blood suppress NL hematopoeisis

46
Q

Disorders where myeloid progenitors don’t mature correctly => ineffective hematopoeisis => thrombocytopenias

A

Myelodysplastic Syndromes (MDS)

More severe than proliferative

47
Q

Myeloproliferative Disease (MPDs)

A

Proliferation of 1 or more terminally differentiated myeloid elements => IC peripheral blood counts.

Types:

48
Q

Types of Myeloproliferative Diseases

A
  1. CML (Chronic Myeloid Leukemia): ↑ Granulocytes
  2. Polycythemia Vera:↑ RBC
  3. Essential Thrombocytopenia: ↑ Megakaryocytes/platelets
  4. Primary Myelofibrosis
49
Q

What factors influence WBC neoplasia?

A
  1. Chromosomal translocations and other acquired mutations: majority of WBC neoplasms have non-random chromosomal ABNLties
  2. Inherited genetic factors
  3. Viruses
  4. Chronic inflammation
  5. Iatrogenic (chemo)
  6. Smoking
50
Q

HTLV-1 =>

A

Adult T-cell leukemia/lymphoma

51
Q

EBV =>

A

Infects B-cells in the CTX, causing paracortical hyperplasia of T-cells

52
Q

KSHV/HHV8 =>

A

B-cell Lymphoma that presents as a malignant effusion in the pleural cavity

53
Q

HIV => ___

A

B-cell Lymphoma

54
Q

Smoking is a RF for what?

A

AML

55
Q

______ IN PERIPHERAL BLOOD = ALWAYS ABNL

A

-BLASTS

56
Q

Lymphoid neoplasms can present as what?

A

Leukemias or lymphomas, depending on where they originate.

  • Lymphoma = tumor that originates in a lymphoid organ (LN, spleen, etc) OUTSIDE the bone marrow.
  • Leukemia = originates in BM, often leaking into the peripheral blood.
57
Q

Common presentation of Lymphoma

A
  1. Present as a mass
  2. Mostly enlarged, PAINLESS LN (2/3 of NH-lymphoma and all Hodgkins lymphoma)
    1. 1/3 of NH-lymphoma = symptoms depending on which tissue/organ is involved
  3. B-symptoms (cytokines cause systemic symptoms: fevers, chills, night sweats)
58
Q

Types of lymphomas

A
  1. NHL
  2. Hodgkin’s Lymphoma
  3. Plasma cell neoplasias = Most commonly Multiple Myeloma – lytic lesions of bone/secretion of light chains or entire Ig
59
Q

How do Leukemias usually present?

A

Presentation due to BM suppression (tumor cells suppress NL hematopoiesis)

  1. Infection (neutropenia)
  2. Bleeding (thrombocytopenia)
  3. Anemia
60
Q

Rules for lymphoid neoplasms

A
  1. Histology needed to dx
  2. Daughter cells are all monoclonal
  3. Most are B-cell origin (85-90%), even though T-cells are 80% of lymphocytes
  4. Cause immunological dusfunction: assx with immune ABNL and may express mutated Ig
  5. Neoplastic B and T-cells circulate widely, but tend to home to and grow in areas where NL counterparts reside
  6. Differentiation of neoplastic WBC is NOT useful for diagnosis or determine the prognosis.
  7. Staging ONLY useful for Hodgkin’s lymphoma.
61
Q

Why is staging ONLY useful for Hodgekins lymphoma

A
  • HL = spreads in orderly fashion.
  • NHL = spreads widely and unpredictably
62
Q
A

SBL Test 1 (15 decks)

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