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’.
Prognosis - EMP
o Soft tissue form better px than SBP = solitary bone plasmacytoma
o Non-cutaneous, non-oral sites carry worse prognoses
o SOP may MM
Contrast MM in dogs versus cats
Both fairly similar in presentation signs.
DOG – 8-9 yo, IgG and IgG equally common, radiographs more likely visible bone disease, 30% thrombocytopaenic, hyperCa can occur but also in cats, enlarged liver and spleen, bone (latter two are CS specific to dogs)
CATS – less common, 12-14, possible male predisposition, no evidence that FeLV, FIV or FIP related, 80% IgG and 20% IgA, more likely to have heart murmur/ cardiomegaly, skeletal lesions rare, 50% thrombocytopaenic, dogs respond better (cat MST 137 d). Tend to get Bence Jones proteinuria more commonly than dogs. Only about 30 cases have ever been reported though. Main CS anaemia.
What is the biggest immunoglobulin? Clinical significance?
- IgM
- . If this is present more serious glomerular disease as nephritis (d/t size of globulin – a macroglobulin). Syndrome = ‘Wadestroms macroglobinuria’.
Give an overview of Histoplasma capsulatum
- worldwide
- Endemic - US (Mississippi, Ohio River Valleys)
- Fungus found in soil containing bird and bat manure
- Oval or round (2-4 micrometers diameter within macrophages)
- Basophilic centre surrounded by clear area caused by shrinkage from fixation
Transmission - Histoplasma capsulatum
- Aerosol contamination of respiratory tract (commonly)
* Primary site of infection: lungs, thoracic LNs, or GIT
Presentation - Histoplasma capsulatum
• CS vary and are non-specific (many different organs involved)
• Chronic GI signs, especially large intestinal diarrhoea, usually most obvious in dog, often progress to small intestinal diarrhoea
• Many dogs have a protracted course of weight loss to emaciation, chronic cough, poor coat, persistent diarrhoea, fever, anaemia, hepatomegaly/splenomegaly, lymphadenopathy, nasopharyngeal and GI
ulceration
• Fever (non-respondant to antibiotics)
• Acute histoplasmosis may be fatal after 2-5 weeks
CBC - histoplasma
• Normocytic, normochromic non-regenerative anaemia
(blood loss, inflammation, marrow infiltration)
• Thrombocytopenia (Platelets sequestered in spleen or liver
• Neutrophilia or neutropaenia
• Eosinophilia or eosinopaenia
• Monocytosis
• Chronic cats may show no blood abnormalities!
UA - histoplasma
usually normal
Biochem - histoplasma
- Hypoalbuminemia common in cats and dogs (blood loss, decreased synthesis due to inflammation, protein losing enteropathy)
- Hyperglobulinemia in cats and dogs (inflammation)
- Increased ALT, ALP and bilirubin (hepatic involvement)
Why is a fungal culture not recommended to dx Histoplasma?
risk to staff
Serology - histoplasma
- Test for Abs but many false negatives/positives
- Testing for Ag: Quantitative antigen ELISA is used in humans on urine, serum, and CSF but - limited research into canine and feline use thus far
Treatment - histoplasma
- Itraconazole 10 mg/kg/day for 60-130 days is the treatment of choice for disseminated histoplasmosis in dogs and cats. Oral suspension or IV if oral impossible
- Ketoconazole, 10–15 mg/kg, bid for 4–6 mo, may be effective in early or mild cases in dogs.
- Consider corticosteroids (pred 2mg/kg every 12-24 hours) if significant airway obstruc-tion from enlarged lymph nodes or lung inflammation
