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Endocrine > Pituitary Adrenal Disorders > Flashcards

Pituitary Adrenal Disorders Flashcards

1
Q

What causes hyperadrenocorticism?

A

Pituitary increases in ACTH
Functional neoplasia of adrenal cortex
Iatrogenic

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2
Q

What are the signs of hyperadrenocorticism in a patients history?

A 
PU/PD
Anoestrus F
Normal/increase appetite 
\+/- exercise intolerance
\+/- abdo distension, panting
\+/- coat changes. alopecia
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3
Q

What are the clinical signs of hyperadrenocorticism?

A 
Panting
Muscle weakness/atrophy
Hepatomegaly
Testicular atrophy
Dermal changes
Depressed mentation
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4
Q

Why does testicular atrophy and vulval/mammary hypertrophy occur with hyperadrenocorticism?

A

Testosterone production is inhibited by increased levels of cortisol

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5
Q

What dermal changes indicative about hyperadrenocorticism?

A

Chronic

  • Symmetrical alopecia
  • Hyperpigmentation
  • Hyperkeratosis
  • Comedones
  • Calcinosis cutis
  • Reccuring infections
  • Thin skin
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6
Q

Outline the clinical presentation of hyperadrenocorticism in…

a. dogs
b. cats

A

a. PUPD, panting, inactive <20kg

b. DM thats hard to manage, plantigrade stance

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7
Q

What clinical pathology results are expected with hyperadrenocorticism?

A
  • Eosinopaenia
  • Lymphocytopaenia
  • Raised ALP and ALT
    + ALP > ALT
  • Hyper cholesterolaemia
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8
Q

How is hyperadrenocorticism diagnosed?

A

Stress leukogram, ALP > ALT

Increased cortisol:creatinine in urine

ACTH stim

LDDST

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9
Q

What level of post-ACTH cortisol is extremely diagnostic of hyperadrenocorticism? What level is poorly diagnostic and required further testing?

A

> 1000nmol/l

500-700nmol/l

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10
Q

Outline the ACTH stim test

A

Measure plasma cortisol at 0h and 1h after administration of synthetic ACTH

Normal animal –> 300-600nmol/L

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11
Q

Outline the LDDST…

A

Measure plasma cortisol levels at 0, 4 and 8h after administering dexamethasone (0.01mg/kg IV)

Normal animal –> 4 and 8h <20nmol/L

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12
Q

What would you expect to see at the readings of a LDDST in a hyperAC patient?

A

Continued high levels of cortisol at all readings

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13
Q

A LDDST test present to you with a high reading at basal, low reading at 4hr and an increased reading at 8 hr. What does this indicate?

A

PDH dependent hyperAC
Animal is stressed at 0h
Disease e.g. pancreatitis

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14
Q

How are PDH and ADH hyperAC differentiated?

A

LDDST test results
Adrenal US
>2 basal plasma ACTH levels

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15
Q

How are PDH and ADH hyperAC treated?

A

PDH

  1. trilostane
  2. mitotant
  3. surgery

ADH

  1. surgery
  2. trilostane
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16
Q

How does trilostane work? How effective is it in dogs?

A

Inhibits enzymes involved in synthesis of cortisol > increased ACTH > adrenal haemorrhage

75% effective

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17
Q

Describe the US appearance of adrenal glands post-trilostane treatment

A

Cortical hyperlucency

Fluid accumulation

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18
Q

What are the possible complication of trilostane treatment?

A

Ineffective

HypoAC

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19
Q

How does mitotane work?

A

Direct cytotoxicity to zona fasciculata and reticularis

Increased ACTH > adrenal haemorrhage > general adrenocorticol destruction

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20
Q

How is mitotane dosed?

A

Induction - 25mg/kg BID for 5-7 days

Maintenance - 25mg/kg once weekly

21
Q

What endocrinopathies can affect ferrets?

A

Adrenal gland disease
Insulinomas
DM

22
Q

Outline the signalment of hyperAC in ferrets…

A

Middle - older age
Normal pituitary gland
Hyperplasia, adeno or adenocarincoma of adrenal gland

23
Q

Outline the pathogenesis of hyperAC in ferrets…

A

Neutering increased GnRH levels > increased LH and FSH > over expression of LH receptis in adrenal cortex > increased adrenocorticoid production

24
Q

What are the clinical signs of hyperAC in ferrets?

A 
Symmetrical alopecia
Vulva enlargement
Pruritus
Urtheral obstruction
Mammary enlargement
25
Q

How is hyperAC treated in ferrets?

A

Surgery
Mitotant
Ketoconazole
Trilostane

26
Q

How is hyperAC prevented in ferrets?

A

Sterilse with GnRH agonist implants rather than castration e.g. deslorelin

27
Q

What causes hypoAC?

A

I-M adrenocorticolysis
Increased ACTH > adrenal haemhorrage

Both lead to decreased cortisol and aldosterone

28
Q

What is atypical hypoAC?

A

HypoAC with no electrolyte imbalances

29
Q

Outline the signalment of hypoAC

A

young-middle aged dog
F > M
Poodles, bearded collies, leonburgers, retrieves

30
Q

What are the clinical signs of acute hypoAC?

A

Hypovolaemia
Shock
Tachy/bradycardia
Underperfusion

31
Q

Which clinical signs are most easily recognised with acute hypoAC?

A

Combination of bradycardia with hypovolaemic shock

32
Q

What are the clinical signs of non-acute hypoAC?

A 
Waxing and waning signs
Lethargy, depression
Weakness
Inappetence 
V/D
Melaena
\+/- bradycardia
33
Q

What’s the diagnostic problem with non-acute hypoAC?

A

Non-specific GIT and neuromuscular clinical signs > difficult to recognise

34
Q

What clinical pathology results indicate hypoAC?

A 
Mild-mod anaemia
Hypoproteinaemia
Eosinophilia
Azotaemia
HypoNA
HyperK
HyperCa
35
Q

Which organs are rich in mast cells? What is a sign of inflammation in these organs?

A

Gut
Resp
Uterus

Eosinophilia

36
Q

How does hypoAC cause hypercalcaemia?

A

No one knows!

37
Q

Can hypoNa combined with hyperK diagnose hypoAC?

A

No

  • is suggestive in typical patients
  • doesn’t occur in atypical patients
38
Q

What are the risks of misdiagnosing hypoAC?

A

Exacerbation of already comprised organs

Periods of inappropriate medication + ADR

Once on medication, can make further investigation v hard to analyse

39
Q

How can diagnosed of hypoAC be confirmed?

A

ACTH stim test

HypoAC > subnormal levels of cortisol before and after ACTH stimulation

40
Q

What are the dis/advantages of the ACTH stim test?

A

+ very high sensitivity and specficity of hypoAC

  • any glucocorticoid tx can interfere
41
Q

How is acute hypoAC treated?

A

0.9% NaCL 7-8ml/kg/hr

Hydrocortisone sodium succinate

42
Q

When can hydrocortisone sodium succinate first be given to treat acute hypoAC?

A

Immediately after 2 ACTH sample.

Any earlier will give false results for ACTH stim

Doesn’t matter if wrong as had a short half life and will be eliminated from body quickly

43
Q

How does the glucocorticoid and mineralocorticoid balance differ when treating acute and non-acute hypoAC?

A

Acute requires supplementation of cortisol which needs 50% gluco and mineralocorticoid

Non-acute requires appropriate balance of gluco and mineralocorticoids that will effectively treat clinical signs

44
Q

How is non-acute hypoAC treated?

A 
Deoxycortisterone pivalate (DOCP) - 1st in cascasde
Fludrocortisone
Cortisone acetate
Prednisolone
Dietary changes
45
Q

What must be administered alongside DOCP when treating non-acute hypoAC?

A

Is 100% mineralocorticoid > needs glucocorticoid supplementation e.g pred

46
Q

What is the glucocorticoid activity of pred, dexamethasone, DOCP and fludrocortisone compared to cortisol?

A

P - 5x
D - 30x
DOCP - 0x
F - 15x

47
Q

Does fludrocortisone required glucocorticoid supplementation?

A

Almost enough glucocorticoid - supplement with lead potent glucocorticoid (cortisone acetate)

48
Q

How is hypoAC treatment monitored?

A

Clinical response
Leukogram
Na and K levels

49
Q

What is the glucocorticoid of choice in small dogs and why?

A

Cortisone acetate - less risk of accidental overdose

Endocrine (10 decks)

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