CS - difficult cases in gastroenterology Flashcards
Ddx - monoclonal gammopathies
o Lymphoreticular tumours (lymphoma, EMP, chronic and acute lymphocytic leukaemia)
o Chronic infections (e.g. ehrlichiosis, leishmaniasis, FIP)
o MGUS (monoclonal gammopathy of unknown significance)
T/F: you see BM plasmactyosis in myeloma and lymphoma
True
If you believe a dz is undistributed in bone. what do you do?
multiple samples
How commonly is extramedullary plasma cell tumour (EMP) associated with paraneoplastic disease?
rarely
What is Pythium insidiosum?
- an oomycete = an algae
- sort of like a fungus
Species - Pythium insidiosum
horses, dogs, cats
Typical signalment - animals suffering from Pythium insidiosum
- algae freshwater infection therefore hunting/working dogs.
Forms - Pythium insidiosum
- cutaneous
- vascular
- ocular
- GIT
- systemic (typically too late to respond to tx)
CS - Pythium insidiosum
- vague
- vomiting
- wt loss
- anorexia
Lab findings - Pythium insidiosum
• Eosinophilic and granulomatous inflammation
• Mesenteric lymphadenopathy
• Stomach, duodenum and ileocolic junction (possible any part of GIT)
• Not associated with immunosuppression like other fungal dz
++++
Dx - Pythium insidiosum
3 ways:
o Wet mount exam in 10% KOH followed by culturing
o Detect anti-P Abs using serological assays
o Detection of DNA of the infectious agent in the infected tissue by PCR/ se-quencing
Tx - Pythium insidiosum
- SURGICAL EXCISION (best, poor px if excision not possible, sx debridement of skin lesions popular but high recurrence rate)
- MEDICAL: 20% success rate, anti-fungals have reduced efficacy as not true fungus, steroids may decrease inflammation, immunotherapy tx available but low efficacy
Differentiate atypical addison’s from secodary addisons
> Atypical addisons = primary hypoadrenocorticism, normal serum electrolytes (MC levels not affected as doesn’t affect zona glomerulosa)
> Secondary addisons = pituitary gland doesn’t secrete ACTH. Serum electrolytes are also still normal because aldosterone preserved. D/t destruction poutiitary (neoplasia, inflammation, head trauma) or chronic exogenous GCs negative feedback to pituitary.
CS - atypical addisons
- normal serum electrolytes
- decreased post ACTH cortisol
- normal post-ACTH aldosteroine
- increased endogenous ACTH
Lab findings - atypical addisons
- Hypoglycaemia (GCs stimulate glucose production)
- Mild, normocytic, normochromic non-regenerative anaemia
- Absence of stress leukogram
- Hypocholestrolaemia (decreased GIT absorption)
- Hypoalbuminaemia (d/t gut issues)
Dx - atypical addisons
• 1st ACTH stimulation test – confirms hypoadrenocorticism but doesn’t differentiate primary/secondary hypoadrenocorticism
• Dz d/t atypical or secondary hypoadrenocorticism via lack of electrolyte imbalance
• Ddx atypical vs secondary = periodic +++
• ULTRASOUND
• ECG
++++++++++++++++++++++
Tx - atypical addisons - what dose of prednisolone?
o Immunosuppressive dose is 2-4mg/kg BID (other dz)
o Anti-inflammatory dose is 0.5-1mg/kg BID (other dz)
o Physiological dose – this case as replacing body’s GC – 0.1mg/kg/BID. More is usually given to owner so that if they anticipate a stressful event can give 5mg in a day to reduce chance of Addisonian crisis.
What to monitor with atypical addison’s?
electrolyte changes regularly as some atypical addison’s can primary hypoadre-nocorticism (begin to lack MCs) need MC and GC supplementation
What lab findings suggest EMP?
- cytopathology of BM aspirate (in EMP, plasma cell infiltration doesn’t exceed 5% of all nucleated cells. In MM, >20% plasma cells are present)
- Histopath (gastric tumour) : plasma cell neoplasm and primary amyloidosis
- Biochemistry: high TP –> serum electrophoresis –> monoclonal spike in globulin.
- Haematology: check PCV, PLT and WBC to check no BM involvement
- Radiograph: skeletal lytic (‘punched out’) lesions
Features of EMP staging
- Skeletal radiography
- BM aspiration
- Serum protein electrophoresis
Dx - multiple myeloma (MM)
MM requires 2 of the 4 following signs: radiographic lytic ‘punched out’ lesions, Bence-Jones proteinuria (Ig light chains in urine, not part of standard UA panel), monoclonal gammopathy and >20% plasma cells on BM aspirates.
What method allows categorisation of the immunoglobulin class involved in a monoclonal/polyclonal spike?
Immunoelectrophoresis
Tx - EMP
- establish staging before tx (often metastasises)
- GIT protectants (sucralfate and kaolin)
- prednisolone (lyses plasma cells)
- if non-resectable, use chemo or radiotherapy (depends on location)
- chemo: melphalan and cyclophosphamide protocol or melphalan/ prednisolone protocol/
What is good about melphalan/prednisolone protocol?
give orally, at home, less hassle, less invasive. Although px for MM not great, many owners adopt this protocol as ‘nicer’.
