Pituitary Endocrinopathies Flashcards

1
Q

Clinical consequences of pituitary disorders and the corresponding clinical signs

A
  • 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)
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2
Q

Give 3 egs of altered endocrine function with pituitary disorders

A
  • hypersomatotropism
  • hyposomatotropism
  • diabetes insipidus
    > not likely related to size of lesion
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3
Q

Outline pathogenesis of hypersomatotropism

A
  • 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
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4
Q

Hx and CS of hypersomatotropism in dogs

A
  • 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
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5
Q

Is hypersomatotropism common in dogs?

A

Very rare esp where most animals are neutered

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6
Q

How has hypersomatotropism in the cat changed recently

A
  • more common than dogs

- under noticed potentially (study at RVC found lots of acromegalic cats with only sign difficult to manage diabetic,

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7
Q

What do cats nearly always have with hypersomatotropism

A

Diabetes mellitis (hard to control)

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8
Q

How can hypersomatotropism be dx in cats in general practice?

A

IGF1 levels >1000 nmol/l

fGH not measurable commercially

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9
Q

What is needed for the liver to produce IGF1?

A

Insulin somewhere in the system

- so in newly diabetic cats IGF1 may be low d/t lack of insulin

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10
Q

Clinical characteristics of feline hypersomatotropism

A
  • 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
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11
Q

Diagnostic characteristics of feline hypersomatotropism

A
  • fasting blood glucose 12-39mmol/l
  • fructosamine 440-733umol/l
  • insulin doses 0.5-8
  • IGF values variable
  • serum fGH >10ng/ml
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12
Q

Tx feline hypersomatotropism

A
>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
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13
Q

What should make you consider hypersomatotropism in cats

A

Uncontrollable diabetic

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14
Q

When may serum IGF1 be falsely elevated?

A

Cats on insulin esp high dose

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15
Q

What type of diagnostic imaging is best for pituitary masses?

A
  • CT
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16
Q

Hx and clinical signs of hyposomatotropism

A
  • 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
17
Q

Pathogenesis of hyposomatotropism

A
  • LHX3 defec
  • ACTH upstream of defect so unaffected
  • FSH, LH, TSH, PRL downstream but still UNAFFECTED
  • GH only one affected
18
Q

Diagnostic AIDS for hyposomatotropism

A
  • serum IGF1 estimation or GH

- radiography persistent epiphyseal plates

19
Q

2 reasons for true PUPD

A
  • wants to drink more
    1 PD
  • needs to drink more
    Renal dysfunction - structural or functional
20
Q

What endocrine controls body water? HOW?

A

> 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???)
21
Q

What is central diabetes insipidus?

A

Absolute vasopressin deficiency

- 1* pituitary probelm

22
Q

What is nephrogenic/renal diabetes insipidus?

A

Vasopressin resistance

- 1* renal problem or metabolic dysfunction -> renal dysfunction

23
Q

Hx and clinical signs with central diabetes insipidus?

A
  • marked unrelenting PUPD
  • > 200ml/kg/d
  • otherwise unremarkable
24
Q

Logical approach to a potential central diabetes insipidus case

A
  • R/o primary polydipsia (hospitalise and observe behaviour changes)
    > Diagnostics:
  • USG
25
Q

Outline water deprivation test and desmopressin response test protocol

A
> 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)
26
Q

Tx central diabetes insipidus?

A
  • conjunctivally administered desmopressin
  • 1-4drops per patient
  • q12-24hrs
  • adjust dose down depending on patient