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Endocrine > Hyperadrenocorticism > Flashcards

Hyperadrenocorticism Flashcards

1
Q

What is the definition of HAC?

A

clinical problem brought about by sub-acute over exposure to glucocorticoids

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2
Q

What proportion of naturally occurring HAC is a) pituitary dependant b) adrenal dependant

A

a) PDH = 85-90% b) ADH = 10-15%

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3
Q

What is the main cause of iatrogenic HAC?

A

Chronically administered UNDER dosing of glucocorticoids

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4
Q

What proportion have PUPD?

A

85-90%

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5
Q

What proportion have excellent appetite?

A

80% If not polyphagic probably has something else going on as well

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6
Q

What proportion have exercise intolerance?

A

About 60%

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7
Q

What proportion have abdominal distension?

A

About 50% due to hepatomegaly and abdominal weakness

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8
Q

What proportion have coat changes?

A

About 50%

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9
Q

What proportion have alpecia and hyperpigmentation?

A

About 35%

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10
Q

What proportion of intact females have anoestrus?

A

90%

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11
Q

What are the most common clinical signs associated with hyperadrenocorticism?

A

Panting, muscle weakness and atrophy, hepatomegaly & abdo distension, increased abdominal fat deposition, testicular atrophy, vulval enlargement, dermal changes, altered mentation

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12
Q

What are the dermal changes which can be present with HAC?

A

Hyperpigmentation Symmetrical alopecia Hyperkeratosis Non-pruritic Comedones Possibly calcinosis cutis

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13
Q

Where are the two most common sites for infection in HAC dogs?

A

UTI and skin

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14
Q

Is PUPD in HAC patients normally primary PU or primary PD?

A

Primary PD - psychogenic

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15
Q

What are the five reasons that you can have PUPD? (generally, not just in HAC)

A

Primary PD Structural renal disease (loss of nephrons) Something stopping nephrons working (eg countercurrent) Osmotic diuresis Something interfering with ADH

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16
Q

Where does the alopecia tend to occur?

A

Mostly over the trunk

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17
Q

What’s this?

A

Calcinosis cutis

Calcium phosphate deposition in the skin

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18
Q

Why do HAC dogs tend to pant?

A

Muscle weakness and increased abdominal volume means that to maintain minute volume need to increase rate and decrease tidal volume

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19
Q

Why are HAC dogs more prone to throwing blood clots?

A

Prolonged GC exposure = hypercoagulability

(thrombocytosis)

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20
Q

What clinpath findings might you expect?

A

Eosinopenis, lymhocytopenia

Increased ALP, increased ALT (ALP more increased than ALT in dogs)

Hypercholesterolaemia

Increased thrombocyte count

Low USG possibly

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21
Q

Why do cats with HAC normally present?

A

difficult to manage Diabetes

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22
Q

What size of dog normally gets HAC?

A

<20kg

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23
Q

Primary PD can be water deprived as doesn’t need to drink, what should you rule out in HAC patients before taking away their water?

A

UTI

Endotoxins interfere with urine concentration

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24
Q

What are the two dynamic tests that you can do to test for HAC?

A

Low dose Dexamethasone suppression test

ACTH stimulation test

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25
Q

When might you have an abnormal Dex suppresiion test in a non HAC animal?

A

General illness-Need increased cortisol so adrenal acting above normal

26
Q

How do you perform an ACTH stim test?

A

Measure plasma cortisol at 0 hrs and 1hr

Give 5ugm/kg of tetraosactrin IV or 250UMG/dog

27
Q

What would be the normal plasma cortisol level post ACTH stim?

A

300-600 nmol/L

28
Q

Beyond 1000nmol/L we can say that..

A

Animal almost definitely has HAC, below this si a grey area and some animals may even have within normal range but have HAC

29
Q

Can you use an ACTH stim test to decide whether it is PDH or ADH?

A

No

30
Q

How do you perform a LDDST?

A

Measure plasma cortisol at 0,4 and 8h

Dose of 0.01mg/kg dexamethasone given IV

Expect supppression at 4h AND 8h

31
Q

What level of cortisols should be expected if the result of the LDDST is normal?

A

<20nmol/L

32
Q

Can you use a LDDST to decide whether PDH or ADH?

A

Yes to a degree, initial suppression then increased at 8h is PDH. 70-80% of PDH cases have this pattern

Supressed at 4h and 8h could be ADH or the remaining 20-30% of PDH cases

33
Q

What is the SHOP stimulation test?

A

17-OH progesterone levels taken before and after ACTH

Inadequate precision to be worth your time

34
Q

What might you expect to see on adrenal ultrasonography if it is ADH?

A

You’d expect to possibly see one adrenal enlarged but more importantly, the other adrenal should be SMALLER than normal (<5mm) as no stimulation because ACTH not released due to negative feedback by high levels of circulating cortisol

35
Q

What would you expect from basal plasma ACTH levels in ADH/PDH?

A

Important to take at least 2 ACTH assays as is a finicky tets

ADH-Should be almost no ACTH in the system

PDH-Normal or increased

36
Q

Which adrenal gland is this? Is it normal or abnormal?

A

Left-bean shape

37
Q

Which adrenal gland is this?

A
38
Q

What is this?

A

An adrenal mass

39
Q

What are the two available medical treatments available for PDH?

A

Trilostane

Mitotane

40
Q

Can you do surgical treatment for PDH and ADH?

A

Yes. probably more likely to do surgery on ADH than PDH

41
Q

What does trilostane inhibit?

A

Inhibits 3-B hydroxysteroid dehydrogenase

therefore inhibits steroid production

42
Q
A
43
Q

Which species is Trilostane more effective in, dogs or cats?

A

Dogs

44
Q

Why do some dogs get adrenal necrosis?

A

Trilostane inhibits cortisol synthesis and therefore increases ACTH as lack of negative feedback

ACTH increases adrenocortical blood flow which is a fragile network

Adrenocortical haemorrhage

Necrosis and acute reduction in cortisol production

45
Q

If treating with Trilostanem, do you get a greater degree of adrenal haemorrhage with PDH or ADH?

A

PDH

In ADH pre treatment levels of circulating ACTH are very low so an increase unlikely to be as bad as in PDH when they are normal or increased before treatment

46
Q

Which condition is Trilostane more ‘efficacious’ PDH or ADH?

A

PDH for reason on last slide, more likely to create adrenal necrosis

NB this may be desirable or undesirable

47
Q

Why is it a concern that Trilostane may cause adrenal necrosis?

A

Patient may develop acute hypoadrenocorticism

could have iatrogenic addisonian crisis

48
Q

Why can’t you use urinary cortisol concentrations to assess treatment success in dogs being treated with trilostane?

A

Levels remain elevated because when you treat animals with trilostane, you get an increase in 11-hydroxysteroid dehydrogenase 2, which turns cortisome in to cortisol.

You DO have decreased circulating active cortiSOL which is why clinical signs look better but still have cortisONE in the circulation which is measured in the urine/blood as cortisol

49
Q

What is the minimum dose for trilostane?

A

2-4mg/kg/24h with food

ACTH test 2-4 hrs post dose

don’t underdose

50
Q

What should you do with the proportion of animals (about 25%) who don’t respond satisfactorally in the first instance?

A

Review dose, consider twice daily dosing but NB price and compliance issues

Consider mitotane?

51
Q

How does mitotane work?

A

Reduces cortisol production through direct cytotoxicity to the zona fasciculata and reticularis & generalised adrenocortical destruction via increased ACTH

52
Q

What instructions would you give an owner for the induction dose of mitotane?

A

25mg/kg/12h for 5-7 days

ALWAYS with food

Keep an eye on demeanour and appetite

53
Q

How should you monitor your mitotane treatment at the end of the induction phase?

A

Do an ACTH stimulation 24-36h after the last mitotane

pre and post cortisols should be less than 30nmol/L

54
Q

What is the general dose for maintenance with mitotane?

A

25mg/kg/12h on one day per week

ALWAYS with food

55
Q

How should you check your treatment with mitotane once on maintenance dose?

A

Evaluate with an ACTH stim in the same way as before, 24-36h after the last mitotane

Pre and post cortisols of less than 30nmol/L

56
Q

What should you do if you are maintaining an animal on mitotane and control is lost?

A

restart induction

DON’T use an increased maintenance dose

57
Q

What are the possible side effects of mitotane?

A

Variably reversible GIT signs

Neuropathies - particularly cranial nerve palsies

Unpredictable onset of clinically significant hypoadrenocorticism

58
Q

What is the other option if you cannot achieve control with mitotane OR trilostane?

A

Bilateral adrenalectomy

59
Q

What do you need to do to supplement animals that have had a bilateral adrenalectomy?

A

Hydrocortisone infusion (implement at time of surgery)

Post surgical hydrocortisone infusion with transfer to oral medication

60
Q

Which drug do you have to use first (in the UK) to medically manage HAC?

A

Trilostane-Licensed

61
Q

What oral medication do you give dogs that have had bilateral adrenalectomy?

A

Cortisone acetate or prednisolone

and

Fludrocortisone acetate

62
Q
A

Endocrine (11 decks)

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