CO1 Hemolymphatic Flashcards
Hemolymphatic System: What is it?
- Hematopoietic cells
- Where they are derived & where they develop
- Routes they travel & sites they work
- Myeloid tissues = bone marrow & the circulating cells derived there (RBCs, neutrophils, eosinophils, basophils, mast cells, platelets)
- Lymphoid tissues = lymph nodes, spleen, thymus, circulating lymphocytes, Bursa of Fabricius
hematopoietic cell lines
pluripotent stem cell becomes:
1. myeloid stem cell
> macrophage
> neutrophil
> eosinophil
> basophil
> mast cell
> platelets
> erythrocyte
2. lymphoid stem cell
- T lymphocyte
- B lymphocyte
> plasma cell
primary lymphoid organs
- Bone Marrow
- Thymus
secondary lymphoid organs
- Lymph nodes
- Tonsils
- Spleen
- Mucosa-associated lymphoid tissue (MALT)
bone marrow function
= Major hematopoietic organ in adults
= Major site for B-cell development throughout life
Where does hematopoiesis occur?
Yolk-sac
– Embryo: shifts to liver & spleen in fetus
Liver & Spleen
– Fetus: shifts to bone marrow prior to birth
– Mature: Extramedullary hematopoiesis (EMH)
Bone Marrow
– Young: all marrow spaces
– Mature: marrow spaces of the axial bones, proximal humerus and femur
reasons for bone marrow hyperplasia
Increased demand
– Loss of RBCs/platelets
> Hemorrhage, Hemolytic anemia etc.
– Inflammatory stimulus
> Liver abscess, Pneumonia etc.
when do we see myelopthisis
(bone marrow replacement)
– Myelofibrosis, Chronic Leukemia etc.
when do we see serous atrophy of fat in bone marrow
– Cachexia, Starvation
* Fat is metabolized, bone marrow reticular cells produce a mucoid substance
gross pathology of bone neoplasia vs osteomyelitis? what about bone marrow activiation?
osteomyelitis - craters with pus
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neoplasia / osteosarcoma - lack of support / weakness, new bone added to outside
> activated endosteal bone marrow to clean necrosis
what is the structure and function of the thymus?
- Differentiation, selection, & maturation of T-cells
– T-cell receptor (TCR) rearrangement
– Positive selection (MHC binding)
– Negative selection (self-reactive)
<><> - 3 Zones:
1. Subcapsular: T-cells from bone marrow enter thymus
2. Cortex: positive/negative selection + TCR rearrangement
3. Medulla: negative selection
- What % of T-cells exit the Thymus?
2%
Two main cell types of the thymus:
- Lymphocytes
- Epithelial cells (Hassall’s corpuscles)
thymus location and appearance
- intrathoracic mediastinum, cranial to the heart and ventral to the trachea
- pink, lobulated
What is the term used to describe the normal physiologic change in the thymus with age?
thymic involution (replacement of thymus with adipocytes)
- begins after puberty / sexual maturity
reasons for a smaller thymus
- Involution (physiological NOT pathological)
- Inadequate Nutrition
- Stress (glucocorticoids)
- Infectious Agents (viruses)
- Intoxicants (lead, mercury)
- Medical Tx (radiation, chemotherapy)
- Aplasia (SCID)
reasons for a large thymus (diffuse and focal)
Diffuse:
- variation (physiological NOT pathological)
- Hyperplasia (repeated immunization)
Focal/Localized:
- Cysts (persist during involution or acquired)
- Neoplasia (thymoma*) > associated with paraneoplastic syndromes
Thymic Hemorrhage
* Important features of signalment/history? (3)
- age
- access, eg. to anticoagulants
- automobile??
Ddx for thymic hemorrhage
I. Idiopathic hemorrhage
II. Anticoagulant toxicity (rodenticide)
III. Traumatic hemorrhage
ante and post mortem diagnostic tests for thymic hemorrhage
- Antemortem (CBC, clotting times)
- Postmortem (stomach content…freeze it)
Signalment: canine, 11 mos, CM
Spontaneous Idiopathic Thymic Hemorrhage
– Proposed pathogenesis:
– This is a diagnosis of:
- Thymic involution → thin walled vessels no longer have structural support from adjacent parenchyma → (minor trauma?, sudden increase in BP?) → hemorrhage
– This is a diagnosis of: exclusion
prepubescent dog with thymic hemorrhage - histologic findings?
– absence of evidence of thymic involution (pre-onset of sexual maturation)
– extensive hemorrhage
pathogenesis of rodenticide toxicity causing thymic hemorrhage
- Ingestion of anticoagulant rodenticide → vitamin K deficiency → clotting factors consumed without replacement → hemorrhage
Spontaneous Idiopathic Thymic Hemorrhage
- Rule outs? how? requires what?
R/O: Trauma, anticoagulant rodenticide
– History
– Physical examination
– Clotting times
– Examination of ingesta
– Toxicological screening for anticoagulant rodenticides
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* Required: Currently undergoing thymic involution
– Signalment: begins at 6-12 mos depending on the breed
thymic neoplasia
- is it common
- diffuse or localized? types?
- paraneoplastic syndromes?
- Uncommon
- Thymoma (& thymic carcinoma) = localized
- lymphoma = diffuse
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dogs: myasthenia gravis
cats: exfoliative dermatitis
Myasthenia Gravis 2° to Thymoma
- pathogenesis
– Thymoma → develop autoantibodies against thymic myoid cells (which have acetylcholine receptors=AChR) → antibodies in systemic circulation → bind to AChRs on postsynaptic membrane at the neuromuscular junctions → preventing ACh binding ∴ preventing muscle contraction → muscle weakness
<><>
> look at eyes, esophagus - first places to seeit
cell types in the stroma of the spleen
1) Endothelium
2) Smooth muscle cells
3) Fibroblasts
cell types in the white pulp of the spleen? function?
Cell types:
1) Lymphocytes
2) Histiocytes (Dendritic Cells)
Function:
1) Adaptive immune function
cell types in the red pulp of the spleen? function?
Cell types:
1) Erythrocytes
2) Histiocytes (Macrophages)
Function:
1) Innate immune function
2) Storage
3) EMH
what can cause bloody nodules in the spleen?
- neoplasia
- hematoma
- nodular hyperplasia
- infarct
what causes not-bloody nodules in the spleen?
- Neoplasia
- Abscess/Granuloma
- Nodular Hyperplasia
- Infarct
- Siderotic Plaques
what could cause extra / multiple normal spleens?
- Ectopic
- Fracture
- Splenosis
what could cause a congested spleen?
- Acute Septicemia
- Barbiturates
- Volvulus/Torsion
- Infectious Disease
- Acute IMHA
what could cause a meaty spleen?
- Neoplasia
- Phagocytosis
- Storage Material
- Bacteremia/Abscess
- Granuloma, EMH
what colour is nodular hyperplasia?
red, white, or both
