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
How is hyperAC treated in ferrets?
Surgery Mitotant Ketoconazole Trilostane
26
How is hyperAC prevented in ferrets?
Sterilse with GnRH agonist implants rather than castration e.g. deslorelin
27
What causes hypoAC?
I-M adrenocorticolysis Increased ACTH > adrenal haemhorrage Both lead to decreased cortisol and aldosterone
28
What is atypical hypoAC?
HypoAC with no electrolyte imbalances
29
Outline the signalment of hypoAC
young-middle aged dog F > M Poodles, bearded collies, leonburgers, retrieves
30
What are the clinical signs of acute hypoAC?
Hypovolaemia Shock Tachy/bradycardia Underperfusion
31
Which clinical signs are most easily recognised with acute hypoAC?
Combination of bradycardia with hypovolaemic shock
32
What are the clinical signs of non-acute hypoAC?
``` Waxing and waning signs Lethargy, depression Weakness Inappetence V/D Melaena +/- bradycardia ```
33
What's the diagnostic problem with non-acute hypoAC?
Non-specific GIT and neuromuscular clinical signs > difficult to recognise
34
What clinical pathology results indicate hypoAC?
``` Mild-mod anaemia Hypoproteinaemia Eosinophilia Azotaemia HypoNA HyperK HyperCa ```
35
Which organs are rich in mast cells? What is a sign of inflammation in these organs?
Gut Resp Uterus Eosinophilia
36
How does hypoAC cause hypercalcaemia?
No one knows!
37
Can hypoNa combined with hyperK diagnose hypoAC?
No - is suggestive in typical patients - doesn't occur in atypical patients
38
What are the risks of misdiagnosing hypoAC?
Exacerbation of already comprised organs Periods of inappropriate medication + ADR Once on medication, can make further investigation v hard to analyse
39
How can diagnosed of hypoAC be confirmed?
ACTH stim test | HypoAC > subnormal levels of cortisol before and after ACTH stimulation
40
What are the dis/advantages of the ACTH stim test?
+ very high sensitivity and specficity of hypoAC - any glucocorticoid tx can interfere
41
How is acute hypoAC treated?
0.9% NaCL 7-8ml/kg/hr Hydrocortisone sodium succinate
42
When can hydrocortisone sodium succinate first be given to treat acute hypoAC?
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
How does the glucocorticoid and mineralocorticoid balance differ when treating acute and non-acute hypoAC?
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
How is non-acute hypoAC treated?
``` Deoxycortisterone pivalate (DOCP) - 1st in cascasde Fludrocortisone Cortisone acetate Prednisolone Dietary changes ```
45
What must be administered alongside DOCP when treating non-acute hypoAC?
Is 100% mineralocorticoid > needs glucocorticoid supplementation e.g pred
46
What is the glucocorticoid activity of pred, dexamethasone, DOCP and fludrocortisone compared to cortisol?
P - 5x D - 30x DOCP - 0x F - 15x
47
Does fludrocortisone required glucocorticoid supplementation?
Almost enough glucocorticoid - supplement with lead potent glucocorticoid (cortisone acetate)
48
How is hypoAC treatment monitored?
Clinical response Leukogram Na and K levels
49
What is the glucocorticoid of choice in small dogs and why?
Cortisone acetate - less risk of accidental overdose