pathology of hematopoiteic system Flashcards

1
Q

hematopoiesis

A

-process of how blood cells are made
-made in:
embryo: yolk sac
fetus: liver, spleen, bone marrow, lymph nodes
neonates: bone marrow of long/ flat bones, red marrow.
adults: bone marrow in all regions of flat/long bones. see yellow marrow.
-extra-medullary hematopoieses EMH due to need.

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2
Q

basic concepts of hematopoiesis

A
  • Bone marrow is located in multiple sites but responds as a single tissue
  • Samples can be taken from any bone with red marrow:
  • Proximal femur, iliac crest, proximal humerus of dogs and cats
  • Sternum of horses
  • Proximal rib of cattle
  • Aspirates and core biopsies
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3
Q

pathology of bone marrow and blood cell

A

-end result depends on which type of cell damaged.
* Multipotent stem cells = multiple cell lines affected
* Committed stem cells = one or more lines affected
* Differentiated cells = one cell type affected.
-alterations are reflected in peripheral blood. decreased cell lines=cytopenias, anemias
increases in cell lines= cytoses and philias.
-in the bone marrow, changes are reflected as increased or
decreased cellularity the changes in red hematopoetic tissue (red marrow) to adipose tissue (yellow marrow)

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4
Q

bone marrow and blood cells degeneration and necrosis

A

-hematopoietic tissues are highly active and susceptible to insults.
-radiation/ toxins and drugs. viral agents. immune mediated or idiopathic causes.

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5
Q

bone marrow inflammation

A

-osteomyelitis: * Inflammation of the bone (osteitis)
and the medullary cavity (myelitis).

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6
Q

bone marrow hypoplasia/ aplasia

A

-decreased proliferative activity
-more yellow, white marrow than red
causes: bone marrow suppression (estrogen, chronic renal disease)
-lack of nutrients (iron, B12, folate)
-endocrine disorders (hypothyroidism)

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7
Q

bone marrow hyperplasia

A

-proliferative response more red replaces yellow
-response to increased peripheral demand or hypodunction of blood cells.
–Erythroid hyperplasia ➝ response to anemia
–Megakaryocytic hyperplasia ➝ response to ↓ platelets
-myloid hyperplasia (neutrophilia, esoniphilia, monocytosis) from bacterial infections, parasites, chronic infections.

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8
Q

bone marrow atrophy

A

-serous atrophy of fat
* Gelatinous transformation of fat within the marrow. Due to cachexia. (severe stage of emaciation) due to cancer ect.

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9
Q

hematopoietic neoplasia

A
  • Affect primarily:
  • Bone marrow
  • The circulating blood (leukemia)
  • Lymphoid tissue (lymph nodes, spleen, thymus, etc)
    -divided into lymphoproliferative and myeloproliferative diseases:
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10
Q

lymphoproliferative diseases

A

-neoplastic disorders of lymphocytes (t, b NK cells)
-lymphoma (in bone marrow/blood)
-lymphoid leukemia (neoplastic lymphocytes in tissues/organs)
-plasma cell tumors

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11
Q

Myeloproliferative
Disease

A

-histocytic neoplasia
-myloid leukemia
-mast cell tumors

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12
Q

canine lymphoma

A

-most common canine hematopoitic neoplasia
-older or middle ages animals
-85% habe multicentric lymphoma
-enlarged lymph nodes with firbosis
-organomegly
-thickening of tubular organs
-hypercalcemia of malignancy sometimes seen.

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13
Q

types of lymphomas

A
  • Alimentary (tubed organs, intestines)
    > multicentric
    > thymic (lung)
    -cutaneous (skin)
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14
Q

feline lymphomas

A

-most common malignant neoplasia of cats
-Alimentary > multicentric
> thymic > miscellaneous
forms
* Leukemia and bone
marrow involvement are
common
-path: feline leukemia virus FeLV. 10-20% cats.
* FeLV is associated with mediastinal and multicentric T cell lymphoma
* Young cats!

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15
Q

bovine lymphoma forms

A

-ezonitc bovine lymphoma
* Sporadic Bovine Lymphoma
* Calf form
* Juvenile form / Thymic form
* Cutaneous form

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16
Q

Enzootic bovine lymphoma

A

-adult cattle
* Bovine leukemia virus (retrovirus)
* 30% of infected cattle → persistent lymphocytosis
* < 5% of infected cattle → lymphoma
* Multicentric lymphoma of B cell origin.
-more common in dairy
-transmission by arthropods, breeding, tagging.
-lesions in heart, abomasum, uterus and spinal canal.

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17
Q

Sporadic bovine lymphoma

A

-Not associated with a viral infection!
-Affects young animals, 3 forms:
1 calf form: young, symmetrical lymphadenopathy. leukemia. kidney, liver, spleen. (multicenteric)
2: juveiline form= thymic form: mediastinal mass.
3 cutaneous form: 2-3 yr old. plagues or nodular raised skin lesions which leads to systemic. survive 12-18 months.

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18
Q

porcine lymphoma

A

-most common neoplasm of pigs
-multicenteric
-often less than 1 yr, more in females
-heriditory form (large white pigs)

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19
Q

reaction of bone to injury and disease

A
  1. Two processes usually occur together
    * removal of damaged bone
    * resorption or lysis
    * production of new bone.
  2. Injury to the periosteum (and
    endosteum) will usually be
    followed by new bone production.
    -bone density will change is response to use wolffs law.
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20
Q

fractures and path (on exam)

A
  • physical discontinuity in a bone
    resulting in instability and pain
  • A normal bone fractures due to excessive
    force → traumatic fracture
  • An abnormal bone fractures under normal
    force → pathologic fracture
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21
Q

fracture repair 5 phases

A

1 - inflammation and injury. tearing of perio and endostium, rupture of BV. growth factors
2- organization of the hematoma
3- callus formation external and internal callus
4- callus remodeling
5- callus modeling

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22
Q

fracture repair phase 1

A

Phase 1 – Injury and inflammation
* tearing of the periosteum & endosteum
* rupture of blood vessels of the bone
* surrounding soft tissue injury
 hematoma
 ischemia
inflammation-> growth factors

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23
Q

fracture repair phase 2

A

Organization of the hematoma
* activation of undifferentiated
mesenchymal (stem) cells
* neovascularization

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24
Q

fracture repair phase 3

A

-Callus formation: external and internal callus
-distant to the fracture gap
* ‘favorable’ environment BS is still intact, lots of O2 so osteoblasts → woven bone
-near the fracture gap
* ‘poor’ environment
* fibroblasts & chondroblasts
* cartilage is later replaced via endochondral ossification
-begins 24 hr
-36 hours for bone production
-can see callus on xray at 2 weeks
-time varies with age, health, nutrition ect.

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25
Q

fracture phase 4

A

-callus remodeling
* woven bone replaced by lamellar bone
* compact bone formed in cortex
* cancellous bone in metaphysis / diaphysis
-during callus remodeling bone marrow may be filled with bone

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26
Q

fracture phase 5

A

Callus modeling
* Restoration of bone to its original form & function
* Months to years

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27
Q

nonunion/ delayed union/ malunion

A

-nonunion: failure a fractured bone to heal
-delayed: longer/slower than normal healing time of a bone. lack of progress after 3 months and healing after 6 months.
-malunion: healing which results in deformity

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28
Q

Complications of Fracture Repair

A
  • inadequate blood supply
  • instability
  • infection
  • fragments of necrotic bone or soft tissue
  • other underlying disease
  • pathologic fracture
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29
Q

Disorders Associated with the Physis

A
  1. Physeal / growth plate fractures
    * Salter-Harris fractures
  2. Growth retardation lattices
  3. Growth arrest lines
  4. Premature closure
  5. Osteochondrosis / osteochondritis
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30
Q

Physeal or growth plate fractures

A
  • Physis is composed of cartilage
  • Weak compared to bone
  • More easily injured / fractured
  • Physis is site of growth
  • injury can affect growth
    capital femoral physeal fracture in cats-common in young under 2 yr overweight neutered males.
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31
Q

Salter-Harris classification scheme for physeal fractures

A

S – straight across
(separated or slipped)
A – above (or away from joint)
L – lower (into joint)
T -through everything all together
E -through everything all together
R – rammed (ruined / crushed)

32
Q

Growth retardation lattices

A
  • Thin lines to wide bands of osteosclerosis
    in the metaphysis, parallel to the physis
  • GRL are due to impaired osteoclastic
    activity and retention of 1° spongiosa
  • Typically detected in aborted, stillborn, or
    neonatal animals
  • Look for the underlying cause
33
Q

Premature closure

A
  • Partial (or focal)
  • alters shape
  • Complete (or diffuse)
  • short bones
  • Many causes
  • trauma, vitamin A toxicity, Mn
    deficiency, radiation, other
     congenital spinal stenosis
34
Q

Osteochondrosis

A

“The focal or multifocal failure (or delay)
of endochondral ossification resulting in
localized thickening of hyaline cartilage.”
Physis or articular surface
* articular-epiphyseal (AE) complex
* Not as stable a bone
* Subject to injury

35
Q

plasma cell tumors

A
  1. Cutaneous Plasmacytoma
    * Common skin masses in dogs
    * Surgical excision is usually curative
  2. Extramedullary Plasmacytoma
    * Arising at sites other than BM / skin
    * Often affect the GI tract
    * More aggressive, may metastasize to
    the lymph nodes
36
Q

Multiple Myeloma

A

-plasma cell tumor
-dogs> cats
* Malignant tumour of plasma cell
origin arising in the bone marrow
* Neoplastic (clonal) plasma cells
secrete immunoglobulin leading to
hypergammaglobulinemia

36
Q

Multiple myeloma clinical signs

A

Clinical diagnosis of multiple myeloma is based on finding 2 - 3 + of the
following features:
* Increased plasma cells in bone marrow
* Punched out lesions on radiographs
* Monoclonal gammopathy
* Hypercalcemia
* Light chain (Bence-Jones) proteinuria

37
Q

Lymph node metastasis

A
  • Common with carcinomas, melanomas, mast cell tumors…
  • May see lymph node enlargement
  • Variable effacement of normal architecture.
38
Q

Thymus – Structure and function

A
  • Structure
    – Composed of epithelial tissue and lymphoid tissue
    – Lobulated and split into cortical and medullary areas
  • Function
    – Proliferation & maturation of T cells
39
Q

thymus diseases

A

-thymic aplasia/hypoplasia from congenital immunodeficeincy
-lymphocytolysis, thymic atrophy: can lead to acquired immunodeficiency from malnutrition, drugs, infections.
-thymic hemmorage/ hematoma

40
Q

thymic hemorrhage

A
  • In dogs, sudden death is occasionally seen due to hypovolemic shock
    resulting from massive
    thymic/mediastinal hemorrhage
  • Several implicated causes: trauma, ruptured aorta, anticoagulant rodenticide
41
Q

thymus primary neoplasm feautures

A
  • Space occupying mass in
    cranial mediastinum
  • Dyspnea
  • 2 main differentials (thymic lymphona, or thymoma)
42
Q

thymic lymphona

A

Neoplastic proliferation of
T-lymphocytes
-Often younger animals (cats,
calves, and dogs)
Malignant behavior

43
Q

Thymoma

A

-Neoplastic proliferation of
Epithelial cells
-Dogs, sheep, goats
-Slow growing, encapsulated

44
Q

spleen structure and function

A

-red pulp: sinusoids, spenic cords= filter blood. RBC storage and hematopoieses
-white pulp: T cells, B cells= immune response.

45
Q

siderofibrosis = gamna-gandy bodies

A

-spleen is granular white, yellow deposites in splenic capsule.
-incidental finding maybe due to hemorrhage.
-fibrous tissue, mineral deposits, hematoidin.

46
Q

splenic contraction

A
  • Contraction of the smooth muscle in the capsule/trabeculae
  • Occurs with catecholamine release, shock, acute splenic rupture
  • Gross: Small dry spleen with wrinkling of the capsule
    -can have areas of black looking like infarctions.
47
Q

splenic rupture

A
  • Fairly common
  • Primary - trauma
  • Secondary to splenomegaly,
    splenic neoplasia.
  • Potential sequelae include
    hemoabdomen and splenosis
48
Q

Splenic rupture → splenosis

A

splenosis: seeding of splenic explants on peritoneal surfaces forming accessory spleens.
-small red nodules within the omentum.

49
Q

spleen circulatory disturbances

A

-Active hyperemia (acute systemic infection)
-Passive congestion (vascular pooling shock, barbituate administration, hemolytic anemia
-splenic infarction
-splenic hematoma
-grossly: dark blue or black, oozes blood when cut.

50
Q

Splenic Infarcts

A

-Ischemic necrosis of the spleen
-causes:
1. Vascular damage
2. Hypercoagulable states
3. Splenomegaly (of any cause)
4. Septic emboli

51
Q

splenic hematoma

A
  • Common in dogs
  • Trauma
  • Often associated with nodular hyperplasia or vascular tumours
    -gross: red nodular mass, very large, soft and dark red.
    -use histo to rule out neoplasia
52
Q

acute spenitis ( Multifocal necrotic or suppurative splenitis)

A

-caused by tularemia, or yersenosis (Yersinia pseudotuberculosis).
-gross: miliary white foci in the spleen, may also be in lymph node and liver.

53
Q

Acute splenitis – Septicemic splenitis

A

-causes: African swine fever
* Erysipelas
* Anthrax*
-gross: splenomegaly, dark discoloration, engorged viscous blood.

54
Q

anthrax pathogenesis for septic splenitis events

A

-caused by bacillus anthracis
-ingested spoores or contact
-lymphagitis and lymphadentis
-massive bacteriemia (sepsis) and toxemia
-increased vascular permeability and impaired coagulation
-sudden death
-take blood smear from ear

55
Q

chronic spenitis - granulomatous splenitis

A
  • can be nodular or diffuse.
    -causes: myobacterium avium in chickens.
    -hispoplasmosis in dogs.
56
Q

spleen growth disturbances

A

-Aplasia
-Atrophy
-Benign nodular hyperplasia
-Lymphoid hyperplasia
-Hyperplasia of the monocyte-
macrophage system
-Extramedullary hematopoiesis

57
Q

Lymphoid hyperplasia of spleen

A

-hyperplasia of white pulp
-response to blood-borne chronic antigenic stimulation
-Malignant Catarrhal Fever, Bovine

58
Q

primary splenic neoplasias

A

-Lymphoproliferative diseases:
Lymphoma/Leukemia*
-Myeloproliferative diseases:
-Histiocytic sarcoma*
-Mastocytosis*
-Hemangioma
-Hemangiosarcoma
Others: Fibrosarcoma,
Fibrohistiocytic nodules, etc

59
Q

Splenic hemangioma

A

-benign tumor of endothelial origin
-gross: single, soft, dark red nodular mass
-histology is needed.

60
Q

Splenic hemangiosarcoma

A

-primary neoplasm
-most common malignant tumor of canine spleen
-gross: single to multiple masses, dark red
-leads to splenic rupture, hemaabdomen, peritoneal seeding. common masses in liver.

61
Q

histocytic proliferative disorders

A

-cutaneous histiocytoma: common begin skin mass
-reactive histocytosis
-histocytic sarcoma

62
Q

Histiocytic Sarcoma

A
  • Malignant neoplasia of macrophages
    or dendritic cells
  • Breed predispositions
  • Bernese Mountain dog, Rottweiler,
    Flat-coated Retriever
  • Can be solitary of multiple:
  • Solitary lesions
  • Subsynovium (joints), subcutis
  • Lymph nodes, spleen or liver
  • Multiple lesions
  • Disseminated histiocytic
    sarcoma = Malignant
    histiocytosis
63
Q

mast cell neoplasia

A

-mast cells are in connective tissue but originate in bone marrow.
-common cutaneous mast cell tumors in dogs.
-systemic mastocytosis are visceral mast cell tumors to the hematopoietic system and other organs

64
Q

secondary bone marrow neoplasia

A
  • Results of
    metastasis of
    a tumour
    from a
    distant site to
    the bone
    marrow
  • Can be a
    carcinoma or
    a sarcoma
65
Q

Myelophthisis

A

-Replacement of hematopoietic tissue within
the bone marrow by abnormal tissue.
-fibrosis-> myelofibrosis
-neoplastic cells-> leukemia
-can result in pancytopenia due to competition for space and nutrients.

66
Q

lymph nodes structure and function

A

-filtration of lymph and immune response.
-outer cortex (B cells)
-inner cortex (T cells) and medulla

67
Q

enlarged lymph node differentials

A

-lymphadentitis
-lymhoid hyperplasia
-hyperplasia of monocyte system
-primary or secondary neoplasia

67
Q

Lymphadenopathy

A

-enlargement of the lymph nodes from unknown causes

68
Q

Lymphadenitis

A
  • An inflammatory response to an
    infectious agent within the node
    not reactive hyperplasia which is antigen driven response.
    -acute: the result of a
    regional lymph node
    draining a site of
    infection/inflammation and
    becoming infected
69
Q

Chronic lymphadenitis

A
  • With chronicity the
    lymph nodes
    become large,
    irregular, and firm
    due to fibrosis
    -can then be suppurative or granulatamous.
    -path: could be rhodococcus equi.
70
Q

Equine Strangles

A
  • Streptococcus equi subsp
    equi
  • Inflammation of the URT
    → abscesses in the
    mandibular,
    retropharyngeal and
    parotid LN
  • May fistulate to the
    surface
71
Q

Caseous lymphadenitis

A
  • Chronic suppurative lymphadenitis in sheep & goats
    -caused by Corynebacterium pseudotuberculosis
    -enters via shear wounds, drains in regional LN.
    -* Chronic suppurative
    inflammation, caseous necrosis & fibrosis
  • As lesion progresses →
    characteristic concentric
    laminations
72
Q

Nodular granulomatous lymphadenitis bovine

A

-bovine tuburculosis caused by myobacterium bovis.
-enlargement of lymph nodes with yellow nodules.

73
Q

Diffuse granulomatous lymphadenitis pigs

A

-Postweaning multisystemic wasting syndrome (PMWS):
Porcine Circovirus type 2
-gross enlargement of mesenteric lymph nodes

74
Q

Benign Reactive Hyperplasia of lymph nodes

A
  • Immunological reaction = response to antigen presentation or circulating
    interleukin levels
  • Causes lymph node enlargement
  • Can be localized or generalized
  • Lymph nodes draining site of local infection or vaccination
75
Q

Secondary lymph node neoplasia

A
  • Lymph node metastasis:
  • Common with carcinomas, melanomas, mast cell tumors…
  • May see lymph node enlargement
    One basis of staging tumor malignancy
  • Stage 0: regional node normal
  • Stage 1: regional node enlarged but still freely moveable
  • Stage 2: regional node enlarged and fixed
    Lymph node: Neoplasia
    Secondary lymph node neoplasia