CO3 Hemolymphatic Flashcards
Components of the hemolymphatic system:
- Thymus
- Spleen
- Bone marrow
- Lymph nodes
- All cells in blood:
Granulocytes, lymphocytes, red blood cells, platelets, monocytes, etc.
Conditions affecting the hemolymphatic system
- Hypoplasia or atrophy (= immunodeficiency)
- Hyperplasia (= immune reactivity)
- Inflammation (lymphadenitis)
- Infection
- Neoplasia
X-linked SCID in dogs- example of hypoplasia of the hemolymphatic system
- what occurs?
Naïve helper T- lymphocyte meets antigen
> production of cytokines to “help” B lymphocytes become plasma cells, and cytotoxic lymphocytes become “killer” cells
(IL2, 4, 7, 9, 15)
> product is cytotoxic lymphocytes and plasma cells
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In X-linked SCID in dogs, the helper T-cell is not able to signal to B-cells and cytotoxic lymphocytes, so they do not differentiate into full-grown immune cells
> a mutation that impairs cytokine signals that are necessary for lymphocytes to respond to antigens
How would a dog with SCID present clinically?
-puppy
- opportunistic infections
- gender (male more likely)
- undetectable lymph nodes
What lab tests would confirm SCID in a dog?
- lymphopenic - no puppy should have this
- low globulins
difference between a normal lymph node and one from a dog with SCID?
- no lymphocytes in SCID
> undetectable lymph nodes
SCID in horse - how does this arise?
The condition is due to inability to recombine genes necessary to generate functional receptors on lymphocytes
> As a result, affected animals have neither the ability to produce antibodies (B lymphocytes) nor the ability to kill virus-infected cells (CD8+ cytotoxic T cells) nor can they generate helper cytokines (CD4+ helper T cells)
is lymphoid hypoplasia common in animals?
no - lack of lymphocytes is incompatible with life
types of reactive lymphoid hyperplasia
= the immune system hard at work!
* follicular hyperplasia - B cells
* paracortical hyperplasia - T cells
* sinus histiocytosis - macrophages, et al.
> In general, all elements occur simultaneously
gross clinical finding for reactice lymphoid hyperplasia
palpably enlarged lymph nodes
what is cloncal expansion, and how does it result in an enlarged lymph node
A very active immune response often manifests with palpably enlarged lymph nodes due to B cell activity (follicular hyperplasia), T cell activity (parafollicular hyperplasia) and/or macrophage hyperplasia (sinus histiocytosis). In general, all elements occur simultaneously, and a lymph node is enlarged because antigen-specific cells divide (hyperplasia) and are larger than resting lymphocytes (hypertrophy). This process is called clonal expansion, and results in enlargement of the node
is the causative organism necessarily present in a reactive lymph node? what about neutrophils and eosinophils?
In reactive lymphoid hyperplasia the causative organism may not present in the lymph node, but rather microbial components have been phagocytosed by macrophages at tissue sites, and are being presented as processed antigens to lymphocytes in the lymph node. Thus, “primary” inflammatory cells such as neutrophils or eosinophils may not be present in enlarged lymph nodes.
Cytologic examination of a lymph node aspirate in reactive lymphoid hyperplasia yields what?
Cytologic examination of a lymph node aspirate does not yield architectural information, but rather a somewhat “haphazard” mixture of cells from various sites within the node. Since the follicles comprise the majority of a hyperplastic node, plasma cells (mature B cells) are typically prominent. Thus, the picture of lymphoid hyperplasia consists of a mixture of cells with small resting lymphocytes, large lymphoblasts, plasma cells, and macrophages. Long- standing lymphoid hyperplasia may result in the formation of Russell bodies (immunoglobulin accumulated in the endoplasmic reticulum of plasma cells).
Splenomegaly due to lymphoid hyperplasia occurs in what type of infections?
systemic infections, in particular those that have a blood-borne phase
causes for spleen enlargement other than blood-borne systemic infection
extramedullary hematopoiesis, congestion, neoplasia, or excessive phagocytic activity (i.e. immune hemolytic anemia).