Small animal endocrinopathies 5 Flashcards

Calcium disorders

1
Q

What are the 2 main differentials for hypercalcaemia in a cat?

A
  • Hypercalcaemia of malignancy

- Idiopathic hypercalcaemia

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2
Q

What is the most common neoplastic cause of hypercalcaemia in cats?

A

Lymphosarcoma

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3
Q

What group of cats is most at risk of idiopathic hypercalcaemia?

A

Young to middle aged

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4
Q

How is idiopathic hypercalcaemia diagnosed?

A

Diagnosis by exclusion, need to rule out everything else

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5
Q

Explain why diagnosis of idiopathic hypercalcaemia can be difficult

A
  • Hypercalcaemia can lead to renal damage (calcium oxalate urolithiasis)
  • Can give the impression that the hypercalcaemia is due to chronic kidney disease
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6
Q

When diagnosing the cause of hypercalcaemia, what are the key factors that need to be considered?

A
  • Calcium and phosphate balance: do different things in different diseases
  • Hormone balance: also varies depending on disease
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7
Q

What conditions would you be suspicious of in a patient with Severely elevated calcium and moderately low phosphorous?

A

Primary hyperparathyroidism and hypercalcaemia of malignancy

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8
Q

What conditions would you be suspicious of in a patient with moderately increased calcium and severely increased phosphorous?

A

Renal failure

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9
Q

What conditions would you be suspicious of in a patient with moderate elevations in calcium and phosphorous?

A

Vitamin D toxicity and Addison’s

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10
Q

What conditions would you be suspicious of in patient with normal to mildly reduced calcium and moderately elevated phosphorous?

A

Nutritional secondary hyperparathyroidism

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11
Q
What condition would you be suspicious of with the following hormonal profile:
Severely elevated PTH
Mild-severely reduced PTHrP
Severely elevated ionised calcium
Severely elevated vit D
A

Primary hyperparathyroidism

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12
Q
What condition would you be suspicious of with the following hormonal profile:
Mild-severely reduced PTH
Severe increase in PTHrP
Severely elevated ionised calcium
Mild - severely decreased vit D
A

Lymphosarcoma

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13
Q
What condition would you be suspicious of with the following hormonal profile:
Severely elevated PTH
Severely elevated PTHrP
Severely reduced ionised calcium
Mild-severely reduced vit D
A

Chronic renal falure

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14
Q
What condition would you be suspicious of with the following hormonal profile:
Mild-severely reduced PTH
Mild-severely elevated PTHrP
Mild-severely elevated ionised calcium
Mild-severely reduced vit D
A

Apocrine gland tumours of the anal sac

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15
Q
What condition would you be suspicious of with the following hormonal profile:
Mild-severely reduced PTH
Mild-severely reduced PTHrP
Mild-severely elevated ionised calcium
Mild-severely elevated vit D
A

Hypervitaminosis D

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16
Q

What condition would you be suspicious of with the following hormonal profile:
Mild-severely reduced PTH
Mild-severely reduced ionised calcium
Mild-severely reduced vit D

A

Hypoparathyroidism

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17
Q

Outline the general management of hypercalcaemia

A
  • May require supportive care until can identify cause
  • Active treatment ifc calcium >4.0mmol/L (16.0 mg/dL)
  • Treatment depends on magnitude of hypercalcaemia, clinical condition of patient, additional factors e.g. most likely differential and cost, presence of complicating factors e.g. azotaemia, abnormal phosphate levels
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18
Q

List the treatment options for hypercalcaemia

A
  • IV fluids (0.9% saline)
  • Diuretics
  • Glucocorticoids
  • Mithromycin
  • Bisphosphonates (pamidronate or zoledronate)
  • Most manageed with fluids, diuretics and steroids
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19
Q

Why is the use of fluids or diuretics beneficial in the treatment of hypercalcaemia?

A

Encourages sodium and calcium loss in the kidney

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20
Q

Why is the use of glucocorticoids beneficial in the treatment of hypercalcaemia?

A

Decrease absorption of calcium from intestine, reduce bone resorption of calcium, and enhance calcium excretion from kidneys

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21
Q

Why is the use of bisphosphonates beneficial in the treatment of hypercalcaemia?

A

Inhibit osteoclast resorption of bone (but are not short term drugs)

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22
Q

At what level of hypocalcaemia are clinical signs usuallly detected and what response is required?

A

<1.5mmol/L, treatment must be initiated as quickly as possible - quick deterioration

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23
Q

What are the clinical signs of hypocalcaemia in dogs and cats?

A
  • Focal muscle spasms/fasciculations
  • Ataxia/spasticity
  • Tetany and generalised seizures
  • Nervousness
  • Prolongation of ST segment and QT interval; arrhythmias
  • Prolapse of third eyelid (cats)
24
Q

What is eclampsia?

A

A manifestation of hypocalaemia, aka puerperal tetany

25
Q

Describe the clinical features of eclampsia

A
  • Lactation hypocalcaemia
  • Plasma calcium <1.5mmol/L
  • Most common in small dogs
  • Tetany observed
  • Fever can develop as muscle contraction generates heat
  • Clinical signs depend on rate of decline of serum calcium
  • Most comonly in first 21 days of nursing, but report in last 2 weeks of gestation and up to 45 days post whelping
26
Q

Describe the pathophysiology of eclampsia

A
  • Results from extreme hypocalcaemia in bitches and queens
27
Q

Describe the aetiology of eclampsia

A
  • Loss of calcium into milk and foetal skeleton
  • Poor dietary use of calcium
  • Reduced appetite due to stress of parturition
  • Parathyroid atrophy poor diet/dietary supplements)
  • Hypomagnasaemia
28
Q

Explain the significance of hypomagnasaemia in eclampsia

A
  • Impact on how effectively hypocalcaemia can be treated and its development
  • Cannot measure magnesium in practice but may need to address magnesium concentration to improve calcium uptake and control
29
Q

When are eclampsia cases most likely to be identified and brought into the practice?

A
  • Seizures/tetany often associated with exercise

- Owner may bring in for another reason and have episode while in waiting room

30
Q

Describe the treatment approach to an eclampsia episode

A
  • 10% calcium gluconate SLOW IV
  • Do not adminster with fluids containing bicarb precursors e.g. Hartmann’s
  • 5-15mg/kg IV slow over 10-20 min (equiv. to 0.5-1.5ml/kg), are aiming for calcium above 0.6-0.7mmol/L
  • Continue with CRI 2.5-3.75mg/kg/hr of elemental calcium, then review and address cause
31
Q

What are the presenting features of a dog with pituitary dwarfism?

A
  • Smaller vs litter mates
  • Retention of puppy coat
  • Metabolism may be non-functional
  • Truncal alopecia sparing head and extremities
  • hyperpigmentation
  • Pyoderma
  • Cryptorchidism
  • Persistent oestrus
  • Proportional dwarfism
32
Q

Which breed is predisposed to pituitary dwarfism?

A

GSD

33
Q

What is the difference between proportional and disproportional dwarfism?

A
  • Proportional: small but in proportion

- Disproportionate: shorter stature than appropriate for heads size

34
Q

What diagnostic tests are available to differentiate pituitary dwarfism from other disorders causing stunted growth?

A
  • IgF-1 most easily available

- GHRH/clinidine stimulation tests used in research

35
Q

How does mammary growth hormone relate o the treatment of pituitary dwarfism?

A
  • Current treatment is ingestion of growth hormones
  • In metoestrus, high P4 leads to mammary development, leading to release of mammary growth hormone
  • Instead of GH injections, injections of progesterone could be used which would induce release of GH from mammary glands into circulation
36
Q

What is a common consequence of agromegaly and why?

A

Diabetes mellitus, as growth hormone is a potent insulin antagonist that causes insulin insensitivity

37
Q

What is acromegaly?

A

Disorder of growth hormone excess

38
Q

What are the common causes of acromegaly?

A
  • Pituitary adenoma
  • Metoestrus
  • Pharmacological action
39
Q

Compare the prevalence of pituitary adenoma and progesterone as a cause of acromegaly in the dog

A
  • Pituitary adenoma almost unheard of

- Progestone as a a cause: not uncommon in treated animals and animals in metoestrus

40
Q

Compare the prevalence of pituitary adenoma and progesterone as a cause of acromegaly in the cat

A
  • 15-30% of diabetic cats will have a pituitary adenoma

- Cat mammary tissue keeps GH local, so progesterone is not a cause of acromegaly in cats

41
Q

What is an unusual clinical feature of poor diabetic control in acromegalic cats compared to cats with poor diabetic control for other reasons?

A

Poor diabetic control but despite this they maintain or increase body weight - if was due to something other than acromegaly, would expect weight loss

42
Q

How do dogs and cats differ in the growth hormone response to progesterone?

A
  • In bitches, progesterone stimulates the release of growth hormone from mammary glands, which can then get into systemic circulation
  • In cats, this is not possible and GH remains in mammary tissue
43
Q

What are the treatment options available for a diabetic cat with acromegaly?

A
  • INcreasing insulin dose as required to gain some control (doses of 30-40IU not unheard of)
  • More advanced therapies e.g.: somatostatin (expensive), pituitary surgery, pituitary radiotherapy
44
Q

What is a typical clinical presentation for functional adrenocortical tumours in ferrets?

A
  • > 3yo
  • Hair loss
  • Vulvar swelling
  • Unusual sexual behaviour and aggression
  • Difficulty urinating
  • Lack of energy (lethargy)
  • Muscle atrophy
  • Skin disorders and itching
45
Q

Compare classic hyperadrenocorticism in dogs with the functional adrenal tumours in ferrets

A
  • In ferrets, occurs in oestrus in jills, which will only end if she mates
  • Is due to oestrogen toxicity
  • Main product of ferret adrenal tumour is adrenal androgens rather than cortisol
46
Q

What would be the clinical signs in a dog with an adrenal tumour that produced adrenal androgens rather than cortisol?

A

Very similar to classic hyperadrenocorticism

47
Q

How could you test for a funtional adrenal tumour in ferrets?

A
  • ACTH stimulation tests, but look for 17-hydroxy progesterone, +/- androstendione and oestradiol
48
Q

What is the more common product of a functional adrenal tumour in cats?

A

Aldosterone

49
Q

What biochemical abnormality and consequently the clinical signs of this change are common in functional adrenal tumours of cats?

A
  • If producing aldosterone mainly, expect hypokalaemia

- Polymyopathy muscle wekaness, ventroflexion of neck

50
Q

What are the treatment options for an adrenal tumour in ferrets?

A
  • Surgery

- Desorelin (GnRH supeagonist)

51
Q

What are the treatment options for an adrenal tumour in a dog with progesterone secreting adenoma?

A
  • Surgery

- If not surgery, trolistane (vetoryl): inhibits at lvel of 3hydroxysteroid dehydrogenase

52
Q

What are the treatment options for an aldosteronoma?

A
  • Surgery

- Or spironolactone (prilictone): aldosterone competitor

53
Q

What clinical signs would be expected in a dog with phaechromocytoma?

A
  • High levels of adrenaline leading to PUPD, panting, inconsistent hypertension, collapse, dysrhythmia
54
Q

What are the differentials for a dog presented with PUPD, panting, inconsistent hypertension, collapse, dysrhythmia?

A
  • Phaechromocytoma

- Hyperadrenocorticism

55
Q

What changes on haematology and biochemistry as a consequence of Cushings would need to be corrected prior to anaesthesia and how?

A
  • Stress leukogram may be seen, no effect on anaesthetic
  • High PCV: dehydration, provide fluid therapy
  • High liver enzymes on biochem, but ACP does not affect liver as much as A2A would
  • Kidney parameters and electrolytes may be altered, corrected with fluid therapy
  • Some biochem parameters may indicate acidosis (due to panting), controlled by fluid therapy