Diseases of the myeloid and lymphoid system

Cards (16)

  • What are the myeloid systems?
    Cells:
    • Granulocytes (neutrophils, eosinophils, mast cells ect..)
    • Moncytes
    • Macrophages
    • Erythrocytes
    • Thrombocytes
    • Other (e.g. dendritic cells)
    Tissue:
    • Bone marrow
  • What are the lymphoid systems?
    Cells:
    • Lymphocytes
    Tissues:
    • Lymph nodes
    • Thymus
    • Spleen
    • Other (e.g. Peyer’s patches).
  • Common stimuli of the myeloid and lymphoids
    Physiologic leukocytoasis (fight or flight)
    • Epinephrine
    Physiological stress (stress leukogram)
    • Corticosteroid (including exogenous)
    Iatrogenic antigenic stimulation (vaccines)
    Inflammation
    Infection
    Parasites/ foreign bodies.
  • Examples of non-neoplastic disorders
    Tissues:
    • Lymph nodes - Hyperplasia lymphadenitis
    • Spleen - Torsion
    • Thymus - Haemorrhage infarction
    Lymphatics:
    • Major lymphatic vessels - Chylous effusions
    • Intestinal lacteals - lymphangiectasia
  • What is chyle?
    A mixture of lymph and chylomicrons
    Chylomicrons = lipids absorbed from intestine - transported via lymphatics.
    Chylous effusions may result from rupture (e.g. trauma) or obstruction (e.g. neoplasia) of thoracic duct or other major lymphatic vessel.
    • Often idiopathic, site of leak not always detected.
    Both effusions (thoracic, abdominal) are rare.
  • Chylothorax and chyloabdomen
    Chylothorax is usually a bilateral pleural effusion.
    Chylous effusion = chyle
    • Previously classified as modified transudate (progressing to exudate as inflammatory cells react to its presence).
    • Lipid will interfere with refractometry.
    Treatment may involve ligation of the thoracic duct.
  • What is lymphangiectasia
    Lacteals dilation
    Pathophysiology - intestinal lymphatics dilate and lose chyle into the lumen - protein losing enteropathy.
    Aetiology (in most common idiopathic)
    • Congenital - may be inherited
    • Acquired obstruction - e.g. neoplasia
    Thought to be more common in dogs; rare in cats.
    May be managed with low-fat diet +/- immunosuppressive (e.g. prednisolone)
  • approach to the investigation of lymphangiectasia?
    History:
    • Gastrointestinal signs
    • Weight loss
    • Diarrhoea (chronic)
    • Vomiting
    Physical exam:
    • May present with poor body condition
    • Ascites
    Biochemistry:
    • Parameters suggestive of PLE (e.g. hypoalbuminaemia)
    • Hypocholesterolaemia (component of chyle).
    Haematology:
    • Lymphopaenia (loss of chyle)
    Imaging:
    • Ultrasound (Hyperchoic lacteals)
    Biopsy:
    • Consider endoscopic vs surgical
  • Examples of myeloid neoplasia
    Myeloid leukaemia:
    • Acute (immature cells)
    • Chronic (differentiated cells)
    • Polycythaemia Vera (erythrocytes)
    Myeloid cells
    • Mast cell tumour
    • Histiocytoma (Langerhans cells = macrophages)
    • Transmissible veneral tumour (TVT) (believed to be histiocytic).
  • Myeloid neoplasia - transmissible venereal tumour
    Infectious tumour:
    • Usually transmitted during mating
    • Beleived to be histiocytic in origin
    Not endemic in the UK
    • May see more with increased number of imported dogs.
    Can respond well to chemotherapy (e.g. vincristine).
  • Myeloid neoplasia - Histiocytoma
    Common neoplasm in small animal practice
    Young dogs (<2 years)
    Classically benign
    Can regress independently over several weeks
    But use caution when advising clients
    • Mast cell tumour can look a lot like Histiocytoma.
  • Myeloid neoplasia - mast cell tumour
    Mast cell are a form of granulocyte
    • may be normal to see them in reactive lymph nodes.
    Malignant transformation - MCT
    • Usually older dogs but any age at risk.
    MCTs usually present as skin masses
    • Common - up to 20% of all canine skin tumours.
    • Cytoligy very sensitive - FNA of suspected skin masses recommended.
    • Some breeds more susceptible: boxers, labradors, golden retriever's, Staffordshire bull terriers, Boston terriers, pugs.
  • What’s so bad about MCTs?
    Variable grades:
    • Lower grades may be managed by excision and monitoring.
    • Higher grades may spread to lymph nodes, liver, spleen, bone marrow - importance of staging.
    Locally invasive:
    • For high grade, recommendations of 3cm margins and 1-2 fascia plane deep to tumour.
    • Revisional surgery may be required.
    Risk of degranulation:
    • Mass histamine release can produce anaphylaxis.
    • Many sources recommend H1 blockers (e.g. chlorphenamine) if tumour likely to be damaged during biopsy or surgery.
  • How do we grade MCTs?
    Two grading systems in common use
    • Grading in histopathology (not fine needle aspirate).
    Evaluation of proliferative activity per high power field:
    • Mitotic index
    • Multinucleated cells
    • Atypical nuclei (shape and size)
    • Guided by anisokaryosis
  • MCTs in cats
    Cutaneous form:
    • If well differentiated may act benign
    Visceral form - poorer prognosis
    • Spleen, LN, liver
    • Intestine may be diffuse
    No grading system currently available
    Association between mitotic index and survival time.
  • Plasmacytomas
    Extramedullary plasmacytoma - skin, oral cavity, colon/rectal mucosa, solitary osseus (rare).
    Usually benign (but can be locally invasive)
    • Complete excision of solitary lesion should be curative.
    • Cutaneous plasmacytosis (multiple skin tumours) more aggressive.
    Rare in cats.