Pituitary endocrinopathies - hyper and hyposomatotrophism

Question 1

Clinical consequences of pituitary disorders

Answer 1

• indirect and direct intracranial effects
• increased endocrine activity with variable clinical effects
• decreased endocrine activity with variable clinical effects

Question 2

Clinical problems - pituitary disorders

Answer 2

• neuro signs referable to intracranial dysfunction
• altered body weight and size or growth
• altered cycling, libido and fertility
• PD and PU

Question 3

Intracranial effects of pituitary disorders

Answer 3

• various, non-specific, neuro signs although rarely seizures
• depression, under-responsive to external stimuli, behavioural changes
• non-specifical neuro signs

Question 4

Altered endocrine functions with pituitary problems

Answer 4

• hypersomatotrophism
• hyposomatotrophism
• diabetes insipidus

Question 5

Pathogenesis hyper somatotrophism. How does it differ between dogs and cats?

Answer 5

• autonomous GH production for some reason
• results in increased IG1 production
• increased IGF1 produces: tissue proliferation, insulin resistance (d/t increased IGF1 and GH)
• DOGS: GH producing mammary tissue, usually a result of hyperprogesteronemia
• CATS: GH producing pituitary tumour

Question 6

Hx and CS - hyper somatotrophism

Answer 6

• dogs, entire females or hx of progestin adminisatraion
• ‘thick-set’ facial features
• increased interdental spaces
• insulin resistance
• possibly PD and PU

Question 7

Canine hypersomatotrophism

Answer 7

• v uncommon in populations where females are generally neutered
• usually associated with dysmenorrhea
• unless dogs develop DM may not be easily recognisable
• if dog has DM, their diabetes is difficult to control

Question 8

Feline hypersomatotrophism

Answer 8

• opinions have changed

- now more common than originally thought

Question 9

Clinical characteristics - feline hypersomatotrophism

Answer 9

• PUPD and increased appetite
• prognathism, increased body size, organomegaly
• insulin resistance
• clinically significant glucose intolerance
• far more common than once presumed
• more variable prevalence, consistency and severity of CS than was originally perceived/ reported

Question 10

Tx - feline hypersomatotrophism

Answer 10

• radiotherapy to cats with pituitary tumours
• 10-12 doses thrice weekly for 5 weeks
  £3000-50000
  Tumour size reduced to variable degree
  Variable responses

Question 11

Acromegaly management

Answer 11

• aggressive insulin tx (prepare for long term instability)
• radiotherapy (inconsistent)
• hypophysectomy (rvc only, replacement hormone tx required)
• pasireotide injections (RVC only, multi-receptor somatotroph antagonist)

Question 12

Diagnostic AIDS - feline hypersomatotrophism

Answer 12

• serum IGF1 helpful but can be elevated in cats receiving insulin
• diagnostic imaging CT
• serum fGH is aspirational in 2015

Question 13

Hx and CS hypo somatotrophism

Answer 13

• smaller animal but with relatively proportional stature
• non-chondrodystrophic condition generally
• variably have immature hair coat
• persistent oestrous, males often infertile
• normal life expectancy

Question 14

Dx - hyposomatotrophism

Answer 14

• serum IGF1 estimation (or GH)

- radiographs - persisting epiphyseal plates

Question 15

Tx - hyposomatotrophism

Answer 15

• possible progestin administration
• manage expectations
• care with survival/ life expectancy data

Question 16

2 causes of true PUPD

Answer 16

1. Primary PU

2. Renal dysfunction

Question 17

Pathogenesis - hyposomatotrophism

Answer 17

• adenohypophyseal malformation
• GH deficiency
• corticotrophin deficiency
• gonadotrophi deficiency
• thyrotrophin deficiency
• ADH deficiency

Question 18

Outline vasopressin in its control of body water

Answer 18

• V1, V2, V3 receptors
• V2 activates cytoplasmic aquaporin-2
• results in aquaporin-2 moving to tubular luminal membrane
• allows tubular water resorption
• water moves extra-cellularly down its concentration gradient
• endothelial cell V2-Rs

Question 19

2 types of diabetes insipidus (DI)

Answer 19

• CENTRAL: absolute vasopressin deficiency, primary pituitary problem
• NEPHROGENIC or RENAL: vasopressin ‘resistance’, a primary renal problem or a metabolic problem resulting in renal dysfunction

Question 20

Hx and CS - CDI

Answer 20

• marked and unrelenting PD
• usually > 200ml/kg/day
• naturally concurrent PU
• as there is usually nothing else wrong, frequently the animal is otherwise unremarkable

Question 21

How to investigate CDI

Answer 21

• usually dealing with a well dog that is PD
• numerous diagnostic possibilities
• if truly PD and PU, there are only 2 possible explanations:
  1. ) primary PD (increased urination is appropriate)
  2. ) renal dysfunction (unable to concentrate urine volume normally).
• ACTIONS:
  1. ) hospitalise for 12-24 hours
  2. ) do nothing other than observe water consumption
  3. ) if stops drinking will almost certainly be a primary PD problem
  4. ) if keeps drinking we need to do more

Question 22

Dx - CDI

Answer 22

• expect USG

Question 23

Outline water deprivation test

Answer 23

• patient must become dehydrated
• objective criteria necessary: at least 5% reduction in body wt, increased PCV and TSP
• increased Na or urea
• can take a long time (up to 72 hours)
• once inability has beendemonstrated, we can administer desmopressin
• give IM (or IV): 2-10 microgram /animal
• response within 2-12 hours
• usually USG >1.020 within 4 hours
• allow limited water: 5-100ml/kg/24hours

Question 24

Tx - CDI

Answer 24

• start with conjunctivally administered desmopressin
• usually 1-4 drops per patient
• given every 12-24 hours
• dose adjustments based on response of patient and usually dose can be adjusted down