SBL Test 1 > Chapter 13 > Flashcards

Chapter 13 Flashcards

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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
Pathogenesis of **INC eosinophils**
**Th2** =\> ↑↑↑ **IL-5** =\> ↑↑↑ **IgE** =\> ↑↑↑ **eosinophils**
26
**Basophilic Leukocytosis (Basophilia)** is due to
**Rare**, except in **Myeloproliferative diseases (CML = Chronic Myeloid Leukemia)**
27
Pathogenesis of **Basophilia**
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
**Monocytosis** (INC in **MO**) is due to?
1. **Chronic bacterial infections (TB)** 2. **Bacterial endocarditis** 3. **Malaria** 4. **Protozoa infections** 5. **AI:** SLE 6. **IBD**
29
**MO/DC** are made in \_\_\_\_\_\_\_\_, as \_\_\_\_\_\_\_. How do they develop?
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
* MO in **liver** =\> ______ cells * MO in **brain** =\> ______ cells * MO in **bone** =\> \_\_\_\_\_\_\_
* MO in liver =\> **Kupfer cells** * MO in brain =\> **Microglial cells** * MO in bone =\> **Osteoclasts**
31
Functions of **monocytes**
1. **Phagocytosis** 2. **Makes cytokine** (Key = **IL-1** and **TNF-a**) 3. **Present antigens**
32
**Lymphocytosis** often accompanies \_\_\_\_\_\_\_. Why does it occur?
monocytosis 1. **Chronic infections** (TB) 2. **Viral infections** (HepA, CMV, EBV) 3. **B. Pertussis**
33
**Primary lymphoid organs** = \_\_\_\_\_\_\_\_\_\_\_\_\_ * Sites: \_\_\_\_\_\_\_\_ **Secondary lymphoid organs** = \_\_\_\_\_\_\_\_\_\_\_\_\_\_ * Sites: \_\_\_\_\_\_\_\_\_\_\_\_\_\_
**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
Describe layers of **LN**
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 3. **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
How are **lymphocytes** in LN activated to help fight infections?
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
What is a lab result to help us differentiate a **reactive WBC proliferation (infection)** vs. **WBC neoplasm?**
**LAP** (leukocyte alkaline phosphatase) * HIGH in reactive states * NL in neoplasms
37
Difference in LN morphology in **Acute** vs. **Chronic Nonspecific Lymphadenitis**
1. Acute = enlarged and TENDER 2. Chronic = NON-tender
38
Histology in **Acute Nonspecific Lymphadenitis**
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
Types and Causes of **Chronic Nonspecific Lymphadenitis**
**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
Histology in **Chronic Nonspecific Lymphadenitis**
1. No ac**ute inflammation** 2. **No tissue damage**
41
Histology of **Follicular Hyperplasia**
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
How can we tell if a process is follicular hyperplasia or follicular lymphoma (neoplastic process)? In reactive LAD,
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
Histology of **Paracortical Hyperplasia**
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
Hemophagocytic Lymphohistiocytosis (MO activating syndrome) is triggered by?
**EBV infection**
45
**Acute Myeloid Leukemia**
Malignant proliferation of **myeloblasts in BM** =\> released into blood **suppress NL hematopoeisis**
46
Disorders where myeloid progenitors **don't mature correctly** =\> **ineffective hematopoeisis** =\> **thrombocytopenias**
**Myelodysplastic Syndromes (MDS)** ## Footnote More severe than _proliferative_
47
**Myeloproliferative Disease (MPDs)**
Proliferation of 1 or more terminally differentiated myeloid elements =\> IC peripheral blood counts. Types:
48
Types of **Myeloproliferative Diseases**
1. **CML (Chronic Myeloid Leukemia):** ↑ Granulocytes 2. **Polycythemia Vera**:↑ RBC 3. **Essential Thrombocytopenia:** ↑ Megakaryocytes/platelets 4. **Primary Myelofibrosis**
49
What factors influence **WBC neoplasia?**
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
**HTLV-1** =\>
**Adult T-cell leukemia/lymphoma**
51
**EBV** =\>
Infects **B-cells** in the **CTX**, causing **paracortical hyperplasia of T-cells**
52
**KSHV/HHV8** =\>
**B-cell Lymphoma** that presents as a malignant effusion in the pleural cavity
53
**HIV** =\> \_\_\_
**B-cell Lymphoma**
54
**Smoking** is a RF for what?
**AML**
55
\_\_\_\_\_\_ IN PERIPHERAL BLOOD = ALWAYS ABNL
**-BLASTS**
56
**Lymphoid neoplasms** can present as what?
**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
Common presentation of **Lymphoma**
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
Types of **lymphomas**
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
How do **Leukemias** usually present?
Presentation due to **BM suppression** (tumor cells suppress NL hematopoiesis) 1. **Infection** (neutropenia) 2. **Bleeding** (thrombocytopenia) 3. **Anemia**
60
Rules for **lymphoid** neoplasms
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
Why is staging ONLY useful for **Hodgekins lymphoma**
* **HL** = spreads in orderly fashion. * NHL = spreads widely and unpredictably
62
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