Pituitary Endocrinopathies Flashcards
Clinical consequences of pituitary disorders and the corresponding clinical signs
- intracranial effects directly
- intracranial effects indirectly
- ^ endocrine activity if functional
- v endocrine activity if non-functional
> NEURO signs d/t intracranial dysfunction (seizures, mentation, under-responsive, behaviour) likely mild, may be normal and symmetrical d/t central location of pituitary
> alterations BW size or growth (appetite changes)
> alterations cycling, fertility or libido
> PUPD (behavioural or hormonal)
Give 3 egs of altered endocrine function with pituitary disorders
- hypersomatotropism
- hyposomatotropism
- diabetes insipidus
> not likely related to size of lesion
Outline pathogenesis of hypersomatotropism
- autonomous growth hormone production
-> IGF1 production
-> tissue proliferation and insulin resistance
~ dogs - growth hormone produced by MAMMARY TISSUE
- d/t ^ progestin activity/exposure
~ cats - growth hormone producing pituitary tumour
Hx and CS of hypersomatotropism in dogs
- Hx progestin administration or intact females (or ovarian remnant/tumour after spay)
- thick set facial features
- ^ interdental spaces
- insulin resistance (can lead to diabetes melitus(?put insipidus before))
- possibly PUPD (osmotic diuresis)
- Usually associated with dysmenorrhea (abnormal cycling)
- unless dogs develop DM may not be recognisable
- difficult to control DM
Is hypersomatotropism common in dogs?
Very rare esp where most animals are neutered
How has hypersomatotropism in the cat changed recently
- more common than dogs
- under noticed potentially (study at RVC found lots of acromegalic cats with only sign difficult to manage diabetic,
What do cats nearly always have with hypersomatotropism
Diabetes mellitis (hard to control)
How can hypersomatotropism be dx in cats in general practice?
IGF1 levels >1000 nmol/l
fGH not measurable commercially
What is needed for the liver to produce IGF1?
Insulin somewhere in the system
- so in newly diabetic cats IGF1 may be low d/t lack of insulin
Clinical characteristics of feline hypersomatotropism
- PUPD ^ appetite
- prognathism, ^ body size, organomegaly
- insulin resistance
- clinically significant glucose intolerance
- more common than is perceived!! UNderdiagnosed
- more variable prevalence, consistency and severity of clinical signs than originally repored
Diagnostic characteristics of feline hypersomatotropism
- fasting blood glucose 12-39mmol/l
- fructosamine 440-733umol/l
- insulin doses 0.5-8
- IGF values variable
- serum fGH >10ng/ml
Tx feline hypersomatotropism
>radio tx -£3-5000 d/t repeated anaesthesia - efficacy variable > aggressive insulin Tx - long term instability > hypophyectomy - replacement hormone Tx required > pasireotide injections - multireceptor somatotroph antagonist
What should make you consider hypersomatotropism in cats
Uncontrollable diabetic
When may serum IGF1 be falsely elevated?
Cats on insulin esp high dose
What type of diagnostic imaging is best for pituitary masses?
- CT
Hx and clinical signs of hyposomatotropism
- smaller animal but with proportional stature
- non-chondrodystrophic condition (so don’t look funny)
- immature hair coat
- persistent oestrus/anoestrus
- males often infertile
- normal life expectancy
- usually only present as puppies
Pathogenesis of hyposomatotropism
- LHX3 defec
- ACTH upstream of defect so unaffected
- FSH, LH, TSH, PRL downstream but still UNAFFECTED
- GH only one affected
Diagnostic AIDS for hyposomatotropism
- serum IGF1 estimation or GH
- radiography persistent epiphyseal plates
2 reasons for true PUPD
- wants to drink more
1 PD - needs to drink more
Renal dysfunction - structural or functional
What endocrine controls body water? HOW?
> Vasopressin
- Rs activate cytoplasmic aquaporin to move to tubular luminal membrane
- allows tubular water resorption
- water moves extracellularly (down conc gradient)
- endothelial cell V-Rs (vWF and factor VIII do something???)
What is central diabetes insipidus?
Absolute vasopressin deficiency
- 1* pituitary probelm
What is nephrogenic/renal diabetes insipidus?
Vasopressin resistance
- 1* renal problem or metabolic dysfunction -> renal dysfunction
Hx and clinical signs with central diabetes insipidus?
- marked unrelenting PUPD
- > 200ml/kg/d
- otherwise unremarkable
Logical approach to a potential central diabetes insipidus case
- R/o primary polydipsia (hospitalise and observe behaviour changes)
> Diagnostics: - USG
Outline water deprivation test and desmopressin response test protocol
> water dep - patient must become dehydrated - objective criteria (eg. 5% reduction in body weight, ^ PCB TSP, ^ sodium, ^ urea etc.) - may take up to 72hrs > if inability demonstrated administer desmopressin - IM (or IV) 2-10ugm per animal - response within 2-12hrs - expect USG >1.020 within 4 hrs - allow limited water (50-100ml/kg/day)
Tx central diabetes insipidus?
- conjunctivally administered desmopressin
- 1-4drops per patient
- q12-24hrs
- adjust dose down depending on patient
