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Small Animal Final Year > Canine hyperadrenocorticism > Flashcards

Canine hyperadrenocorticism Flashcards

1
Q

What controls glucocorticoid release?

A
  1. Within the hypothalamus there are neurones called the “paraventricular nuclei”
  2. These synthesise and release corticotrophin releasing hormone, or CRH
  3. CRH travels via the pituitary portal blood system to the pars distalis in the anterior pituitary
  4. Here it causes cells called corticotrophin cells to make and release ACTH
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2
Q

What do different parts of the adrenal cortex make?

A
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3
Q

Show how important cholesterol is in making adrenal cortex hormones?

A
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4
Q

What is Hyperadrenocorticism characterised by?

A
  • HAC is a condition that can develop in all domestic species and is characterised by the excessive production of steroid hormones, especially glucocorticoids, from the adrenal cortex
  • Clinical signs therefore relate to abnormal circulating concentrations of steroid hormones
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5
Q

What two forms of hyperadrenocorticism are there?

A
  • Can be either spontaneous or iatrogenic
  • Spontaneous disease has two forms:
    • Pituitary-dependent (PDH) 80-90% cases excess ACTH secretion and bilateral adrenal hyperplasia
    • Adrenal-dependent (ADH) 10-20% cases

50% Adenomas 50% carcinomas

Independent of pituitary control - Low ACTH

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6
Q

What causes pituitary dependent hyperadrenocorticism?

A
  • Accounts for 80-90% of spontaneous cases
  • Microadenomas are <10mm diameter and probably account for approx 80% of cases (in a small number of pit independent dogs tumour can get worse with treatment as the supression of the excess cortisol is removed and micro develop to macro extremely rare but something to bear in mind.
  • Macroadenomas are >10mm diameter, slow growing and do not always produce neurological signs
  • Can arise from the pars distalis (70%) or the pars intermedia (30%)
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7
Q

How do the adrenal glands appear with pituitary dependent hyperadrenocorticism?

A
  • Excessive ACTH causes bilateral adrenal hyperplasia and excess cortisol production
  • Normal negative feedback mechanisms fail
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8
Q

How do the adrenal glands appear in adrenal dependent hyperadrenocorticism?

A
  • Unilateral adrenal enlargement with atrophy of contralateral side
  • 50% carcinomas and 50% adenomas
  • Independent of pituitary control
  • ACTH concentration low or undetectable
  • Accounts for <20% of cases
  • Generally more common in larger breeds
  • Cortisol production independent of ACTH control
  • Can be difficult histologically to distinguish adenoma from carcinoma
  • Unilateral tumour causes atrophy of contralateral gland
  • Approx 50% will be partly calcified, regardless of tumour type ( can see mineralisiation/caclification on ultrasound or radiograph)
  • Rare, bilateral tumours have been reported
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9
Q

What is the signalment for adrenal dependent and pituitary dependent hyperadrenocorticism?

A
  • ADH (adrenal dependent) generally seen in older dogs (median 11-12 years) whilst PDH seen in middle-aged dogs (median 7-9 years)
  • SMALL BREEDS: Poodles, Dachshunds and small Terriers predisposed to PDH (pituitary dependent)
  • Larger breed dogs appear more at risk for ADH (50% of cases seen in breeds over 20kg)
  • No sex predisposition for PDH. Females slightly more at risk for ADH (60-65%)
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10
Q

What are the clinical signs of hyperadrenocorticism?

A
  • PU/PD (MOST)
  • Abdominal enlargement
  • Polyphagic (based around antagonims of insulin)
  • Hepatomegaly
  • Muscle wasting/weakness
  • Lethargy/exercise intolerance / panting
  • Skin changes
  • Alopecia
  • Reproductive changes
  • Calcinosis cutis
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11
Q

Describe some of the skin changes seen with HAC?

A
  • Skin is thin and inelastic. Remains tented.
  • Prominent vessels. Epigastric vessels etc..
  • Comedomes caused by follicular plugging
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12
Q

What clinical signs are NOT usually associated with ‘simple’ HAC?

A
  • Vomiting
  • Diarrhoea
  • Pruritus (steroids is treatment for this so would not see in cushings as there is an excess of steroids, e.g dog with atopic dermatitis develops cushings and pruritis goes away then starts cushings treatment and pruritis comes back)
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13
Q

How is hyperadrenocorticism diagnosed?

A
  • FIRSTLY NEED HIGH INDEX OF SUSPICION
  • Get good Hx
  • Perform thorough clinical examination
  • Blood test investigations
    • Biochemistry
    • Complete blood count (CBC)
  • Urinalysis
  • Imaging
  • Specific diagnostic tests
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14
Q

What biochemical abnormalities are observed with HAC?

A

Parameters elevated:

  • ALP (usually marked) in around 90% cases (glucorticoid enduced iso enzyme)
  • ALT (mild-moderate)
  • Cholesterol (high)
  • Bile acids (mild-moderate) (grey zone)
  • Fasting glucose (mild hyperglycaemia)

Parameters reduced

  • Urea (BUN) (due to pu/pd)
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15
Q

What complete blood count changes may be observed with HAC?

A

CBC Changes (stress leucogram)

  • Lymphopenia (low lymphocytes)
  • Eosinopaenia (low eosinophils)
  • Neutrophilia (high neutrophils)
  • Monocytosis (high monocytes)
  • Erythrocytosis
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16
Q

What changes in urinalysis may be seen with HAC?

A
  • Urine specific gravity (USG) often <1.015 but can be hyposthenuric (<1.008)
  • UP:UC >1.0 in 50% of dogs. Often associated with systemic hypertension
  • Evidence of urinary tract infection – diagnosis can be difficult, as action of steroids => few inflammatory cells present
17
Q

What radiographic changes can be observed with HAC?

A

Abdominal radiographs

  • Good contrast
  • Hepatomegaly
  • Pot-bellied appearance
  • Calcinosis cutis
  • Distended bladder

Thoracic radiographs

  • Tracheal and bronchial wall mineralisation
  • Pulmonary metastasis
  • Osteoporosis
18
Q

What are the ultrasonographic findings of HAC?

A
  • Approximate normal size = 12-33mm x 3-7mm
  • Hyperplastic adrenals are larger but have a normal echogenicity
  • Thickness >7.5mm for the left gland considered sensitive
  • Compare size of both glands
19
Q

What should be considered when doing screening tests for HAC?

A
  • Only perform tests in animals with consistent history and clinical signs
  • No tests are 100% accurate! – at least one positive screening test should be achieved before embarking on treatment
20
Q

Options for screening for HAC?

A

Options include:

  1. Urinary cortisol:creatinine ratio
  2. ACTH stimulation test
  3. Low dose dexamethasone suppression (LDDS) test
  4. 17 alpha-OH progesterone)
21
Q

How does the Urinary cortisol: creatinine ratio work to detect HAC?

A
  • Easy to perform
  • Owner collects a urine sample in the morning at home
  • A low ratio make HAC extremely unlikely i.e. highly sensitive (c. 100%)
  • A high ratio means the animal could have HAC, but it is also elevated in many other diseases i.e. low specificity
  • Therefore good screening test to RULE OUT the disease
  • Do not make diagnosis on this test alone.
22
Q

How does the ACTH stimulation test detect HAC?

A
  • Quick and easy to perform
  • Fairly high sensitivity
  • Approx 85% of PDH
  • >50% of ADH
  • So Don’t exclude HAC if negative
  • Best specificity of screening tests
  • =relatively few false positives
  • Specificity relates to the test’s ability to exclude a condition correctly
  • (High specificity for confirmatory test)
  • Protocol:
  • Starve overnight
  • Collect heparin sample time 0
  • Inject synthetic ACTH (Synacthen) i.v
  • Collect second sample 30-60 minutes later into heparin tube again
  • Normal result:
  • Pre-stim <200 nmol/l; post stim < 600 nmol/l
  • ‘Positive’ result:
  • Post stimulation > 600 nmol/l
23
Q

How does a Low Dose dexamethasone suppression test (LDDS) screen for HAC?

A
  • More sensitive test – should detect nearly 90-95% of PDH and most ADH cases
  • Therefore good test to choose if highly suspicious of HAC
  • Lower specificity=more false positives
  • Requires prolonged hospital stay and sampling
  • Sensitivity relates to the test’s ability to identify a condition correctly
  • Protocol:
    • Starve overnight
    • Collect baseline heparin sample
    • Inject 0.01mg/kg dexamethasone i.v
    • Collect heparin samples at 3 and 8 hours
  • Normal animals will suppress to <50% basal by 3 hours and remain suppressed
  • ‘Positive result’ = cortisol > 50 nmol/l at 8 hours
  • Limited use at differentiating PDH from ADH
24
Q

How does 17 alpha-OH progesterone help to screen for HAC?

A

17 alpha-OH progesterone is something we could measure for diagnosis.

25
Q

How should screening tests be used when suspicion of HAC is made?

A
  • If you have a low suspicion, trying to rule out HAC using an urine cortisol:creatinine ratio
  • Many vets opt for the ACTH stimulation test first. If clearly positive and clinical and other findings fit, treat
  • If the ACTH is negative but you are suspicious of the disease, perform a LDDS test. If positive treat. If negative consider other DDX
  • With equivocal results, consider re-testing later before treatment
  • LDDS. High sensitivity: Sensitivity relates to the test’s ability to identify a condition correctly
  • ACTH: High specificity: Specificity relates to the test’s ability to exclude a condition correctly
26
Q

Does it matter that we differentiate between PDH and ADH?

A
  • Yes!
  • The Tx of choice for ADH is adrenalectomy, although of course there are many reasons why this is frequently not performed
  • Dogs with ADH are normally more resistant to medical management, so it is important to make owners aware of this
  • Therefore the prognosis for PDH is normally better than for ADH
  • If you diagnose a pituitary macroadenoma, you may want to monitor for neurological signs (and warn the owner)
27
Q
A
28
Q

What can be used to differentiated between PDH and ADH?

A
  • Endogenous ACTH concentration
  • Abdominal ultrasound
29
Q

How is the Endogenous ACTH concentration used to differentiate between ADH and PDH?

A

Endogenous ACTH concentration (no point as diagnosis of HAC alone using acth as it is pulsitile and you may measure at the wrong point)

  • This is a very labile hormone, so this test is difficult to perform in general practice
  • Higher in PDH
  • Lower in ADH
30
Q

How is abdominal ultrasound used to distinguish between ADH and PDH?

A
  • Measure the dimensions of the adrenal glands
  • In PDH, one would expend adrenal glands that are approximately equal in size. Although hypertrophied glands would be expected, this is not always the case
  • In ADH, one adrenal gland should be enlarged and the other atrophied (due to negative feedback on the ‘normal’ gland)
31
Q

Why should the HDDS test not be used to distinguish between PDH and ADH?

A
  • This is still used by some people to distinguish PDH from ADH
  • Theory is that in PDH a high dose of dexamethasone should inhibit pituitary ACTH secretion, through –ve feedback, so suppress cortisol
  • Adrenocortical tumours are autonomous and thus cortisol is not suppressed
  • HOWEVER, 25-30% of PDH cases fail to suppress with HDDS
  • THEREFORE, NO LONGER A RECOMMENDED TEST
32
Q

How should you discuss treatment of HAC with an owner?

A
  • Most dogs with HAC are happy and some owners may be reluctant to treat their dogs
  • Tx should be recommended however, as untreated HAC dogs are at risk of:
    • UTI
    • Glomerulonephropathies
    • Hypertension
    • Thromboembolic disease
    • Diabetes mellitus because of IR effects of glucocorticoids
  • Dogs with HAC have a high incidence of urinary tract and skin infections, so at the very least these should be treated
  • Well treated and monitored cases of HAC can live for over 5 years if well controlled
33
Q

What is the treatment of ADH?

A
  • Surgery is the choice for ADH
  • Advanced imaging often used prior to surgery to check for local invasion and metastatic disease
  • Complication rate can be high
  • Not a day one skill!
  • Consider referral
34
Q

How can HAC be medically managed?

A
  • Trilostane (“Vetoryl”) is the licenced drug
    • Licenced
    • Competitively inhibits 3-ß hydroxysteroid dehydrogenase, thereby decreasing steroid production
    • Effects on cortisol production are reversible
    • Lower risk of side-effects as duration of activity not thought to be prolonged
  • Response to treatment seen in attached picture

Furthermore:

  • Mitotane occasionally used (unlicensed)
35
Q

What are the potential complications associated with trilostane use?

A

Signs of hypoadrenocorticism (anorexia, vomiting, diarrhoea) with overdosage

Steroid withdrawal

Monitoring

  • Recheck 10-14 days after initiating or changing treatment
  • History, clinical examination and an ACTH stimulation check
  • Perform ACTH stimulation test at 4-6 hours post medication
36
Q

What is the prognosis for HAC?

A
  • Well managed cases can live for several years
  • The median survival time for animals treated with trilostane was 662 days (range 8-1,971) and for mitotane it was 708 days (range 33-1,399)
  • 30kg dog requires 120mg/day at a cost of approximately £3-4. Also costs of monitoring
  • Surgery. One off cost in the region of £3-5k
37
Q

Summarise HAC?

A
  • Canine HAC is a relatively common disease esp in middle aged to older small breed dogs
  • Most cases have PU/PD. GI signs are not seen
  • Biochemistry usually demonstrates increased ALP
  • A diagnosis should always be suspected based on HX and PE before one of the confirmatory tests are performed
  • Ultrasound examination of the adrenals can be useful
  • Be aware of false negative and positive results of the ACTH and LDDS tests
  • Trilostane is the licensed treatment. Monitoring is required
  • Dogs can survive when treated although there are cost implications

Small Animal Final Year (317 decks)

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