23. Hyperadrenocorticism Flashcards
Signalment?
Signalment: Rare In the cat, common In dogs
Pathophysiology?
Pathophyslology:
./” Elevated cortisol levels
./ Pituitary-dependent hyperadrenocortlclsm (PDH): 85%
> Excessive production of ACTH from a tumour In the pituitary gland, leads to bilateral adrenal gland
cortex hyperplasia
./ Functional adrenal tumour or adrenal dependant hyperadrenocortlclsm (AOH): 15%
> Secretion of excess quantities of cortisol, due to adrenal gland adenomas or adenocarc!nomas,
results in atrophy of uninvolved gland
> Adenomas are benign, adenocarclnomas are mallgnant (poor prognosis)
./ Iatrogenic:
> Long lerm use or long acting corticosteroids
Clinical signs?
Clinical signs:
./ Polyurla, polydlpsla, polyphagla, pot-betlled (due to hepatomegaly and muscle wasting)
./ Panting (muscle wasting), acute dyspnoea and hypoxia caused by a pulmonary thromboembollsm
./ Lethargy and weakness due to muscle wasting, can cause cruclate ligament ruptures
./ Skin and hair coat changes:
> Alopecla bflaterat and symmetrical, hyperpigmentation
> Thin skin, able to see blood vessels more easy and calclnosis culls
> Predisposes to recurrent and chronic bacterial infections (skin/urinary tract)
./ Neurological signs from pituitary tumours causing compression or Increased intracranlal pressure
Diagnosis?
Diagnosis:
./ Haematology, biochemistry and urinalysfs:
> Stress leukogram (neutrophilla, monocytosis, lymphopenla and eoslnopenia)
> Elevated ALP (can be very high, with no concurrent hyperbllfrublnemia) and ALT (usually mild),
hypercholeslerolaemla, hyperllpldaemla, hyperglycaemia:
Steroid lsoenzyme can also be Increased by diabetes mellltus, hepatic disease, pancreatitis,
congestive heart failure and malignancies
> Dilute urine,+/· bacteria (culture urine regardless),+/· protelnurla, Increased risk of calcium urolllhs
./ Diabetes mellltus and hyperadrenocorticlsm:
> Difficult to diagnose hyperadrenocortlclsm In a dog with diabetes
> Adrenal screening tests are affected by non-adrenal illness, test only after stablllslng diabetes
Screening tests?
Screening tests (to positively diagnose hyperadrenocorticfsm):
./ Low*Dose Oexamethasone Suppression Test (LDDST):
> Testing for hyperadrenocortfclsm should be delayed If the dog Is ill as LDDST is affected by nonadrenal illness (false positives), or use the ACTH stimulation test
> Best screening test, very sensllfve (85-95%) but less specific (50-70%)
> Can differenllate between PDH and ADH In some cases
> Protocol:
* Collect blood for a resting cortisol level (8 and 10am)
Administering dexamethasone 0.01 mg/kg IV
Collect 4 and 8 hours post Injection
> Interpretation:
Normally the pituitary-adrenal axis Js suppressed by exogenous dexamethasone
Cort/sol levels >30nmoVL at 8 hours post dex~methasone .. hyperadrenocortlolsm
* Cortisol levels <50% or <40nmoVL at 4 hours post dexamethasone = PDH
o Seen in 20% of cases, if no suppression at 4 hours then still could be PDH
ACTH stimulation response test?
ACTH stfmulatlon responH test:
> Less sensitive (80%) but highest specificity (80-90%)
> USED if concurrenl illness (not as affected by non-adrenal illness) and also to monitor the
response to treatment
> Protocol:
Synthetic ACTH (tetracosactrin, Synaclhen ®)
Collect blood for a resting cortlsol levet
Inject 5ug/kg of ACTH IM or IV, or 1 vial for large dog or½: a vial for a small dog
Collect a second blood sample 1-hour later
» Interpretation:
Normal dogs: 2-3-fotd increase in cortlsOI compared to restlng levels
1 hour cortisol level: ,·
o >550nmoVL = hyperadrenocortlclsm {ldeatly >600nmoVL)
o 400-600 “Grey zone” = false positive results may occur
* Reduced response:
o Adrenocortlcal atrophy= hypoadrenocorticlsm
,1 Urinary Cortisol: Creatlnlne Ratio:
> Normal urinary cortlsol:creatinine ratio = NOT hyperadrenocortlcism
Discrimination test?
Discrimination test
- To distinguish the various causes of the disease
I ..
‘·,,; ./ Ultrasonography:
. > If bilateral enlargement - likely PDH but 20% of PDH can have no enlargement
,:, If unilateral enlargement and atrophy of the other gland –likely ADH
[·.:
‘
v Hlgh*Oose Dexamethasone Suppression Teat:
> Same protocol as LDDST except administer 0.1 mg/kg:
* Suppressed cortisol concentration at 1 hour”’ POH
Failure to supprejls cortisol concen1ratlon at 1 hour= AOH
Treatment?
Treatment:
1 Pituitary gependent hypprgdrenocort[clsm;
J ./ Mltotane:
» Potent adrenocortlcolytfc action
I l > Beware patients with pre-exisling diabetes as may need ~o reduce lnsulln dosage
: ,1 Induction phase:
. 1 > Mltotane at 50mg/kg dally (Into two doses) given with food
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> Dlspeiise predn!solone if accldently overdose occurs
> Start maintenance dose when indicators of ·end-point of therapy” therapy have occurred:
Water consumption <60mVkg/day QB
Reduction In appetite occurs QB
Vomiting, diarrhoea or listlessness
> Perfonn an ACTH stimulation test:
If both pre and post-ACTH cortisol levels are < 30nmoVI then = “end-point of therapy” -+ start
maintenance phase
v Maintenance phase:
), <IO days to reach end-point of therapy start maintenance dosage of 25 mg/kg weekly
> > 10 days to reach “end-point of therapy” start maintenance dosage of 50 mg/kg weekly
) Divide weekly dose Into two to four treatments per weak
) Clinlcal signs may take up to 6 months to abate
./ Relapses during maintenance phase:
) Restart Induction phase - mltotane 50mg/kglday (divided)
) Then Increase the weekly maintenance dose by 25·50% to prevent future relapse when “endpoints of therapy” have occurred,
./ Hypoadrenocorticlsm during maintenance phase:
» Clinical signs of overdose/Iatrogenic hypoadrenocorticism: Anorexia, vomiting, lethargy, weakness,
ataxia
) Perform ACTH stlmulallon test
, Treat with short-term prednisolone 0.25 - 0.5 mg/kg SID, then reduce the weekly maintenance
dose by 25-50%
./ Monitoring:
) Water Intake
) Re-examination and undergo ACTH stimulatlon tests every 3 months
Treatment 2?
