Hyperadrenocorticism Flashcards

1
Q

OBJ: Understand adrenal gland functional anatomy and regulation

A
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2
Q

OBJ: Know the common clinical signs of hyperadrenocorticism (HAC)

A
  • PU/PD
  • normal to increased appetite
  • panting, restless, anxiety
  • Cushingoid body type
    • pendulous distended abdomen
    • muscle wasting
    • thin coat
    • multiple dermatologic lesions
      • thin skin
      • comedones
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3
Q

OBJ: Understand the two most common types of HAC (PDH and ADH)

A
  • Pituitary Dependent Hyperadrenocorticism
    • Pituitary
    • Adenoma
    • 85% of cases
    • bilateral enlargement of adrenal size due to hyperplasia
  • Adrenal Dependent Hyperadrenocorticism
    • adrenal gland
    • adenoma or adenocarcinoma
    • 15% of cases
    • Unilateral enlargement
      • contralateral atrophy
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4
Q

OBJ: Understand common screening and differentiating test for HAC

A
  • Screening
    • UCCR
    • LDDST
    • ACTH
  • Differentiating
    • Adrenal US
    • Endogenous ACTH measurement
    • HDDST
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5
Q

OBJ: Know treatment options for PDH and ADH

A
  • PDH
    • hypophysectomy
    • Medical management
      • anti-adrenal therapy
      • pituitary therapy
    • Radiation
  • ADH
    *
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6
Q

OBJ: Review/Understand Pertinent aspects of feline HAC

A
  • PDH
    • hypophysectomy
    • Medical management
      • anti-adrenal therapy
      • pituitary therapy
    • Radiation
  • ADH
    • Adrenalectomy
    • Anti-adrenal therapy
      • Trilostane
      • Lysodren
      • Ketoconazole
      • Anipryl
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7
Q

How is cortisol secretion regulated?

A
  • Regulated through the Hypothalamic Pituitary Adrenal Axis (HPAA)
    • See Image
  • ACTH secretion is pulsatile
    • Influenced by:
      • Feeding
      • Physiologic / environmental stress
        • Pain
        • Trauma
        • Hypoxia
        • Pyrogens
        • Cold exposure
        • Surgery
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8
Q

What is the difference between PDH and ADH?

A
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9
Q

What is the common signalment of hyperadrenocorticism in dogs?

A
  • Any breed
  • Median age of diagnosis is 10-11yr
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10
Q

What are the clinical signs of Hyperadrenocorticism?

A
  • Dogs with HAC generally feel and act well
  • PU/PD - almost all dogs with HAC
  • Appetite normal to increased
  • Panting, restlessness, anxiety
  • ‘Cushingoid’ body type
    • pendulous and distended abdomen
    • muscle wasting
    • thin coat
    • multiple dermatologic lesions
    • thin skin
    • comedones
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11
Q

What neurologic signs are common in hyperadrenocorticism dogs?

A
  • signs caused by macroadenoma (10-15% PDH cases)
  • Anorexia
  • behavioral changes
  • disorientation
  • blindness
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12
Q

What Cardiovascular effects are common in hyperadrenocorticism dogs?

A
  • Hypertension
  • Thromboembolism (hypercoagulable)
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13
Q

What musculoskeletal problems are common in hyperadrenocorticism dogs?

A
  • Poor body condition
  • muscle loss
  • cruciate rupture
  • myopathy
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14
Q

What reproductive signs are common in hyperadrenocorticism dogs?

A
  • decrease in testicular androgen production in males
  • Anestrus in females
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15
Q

What findings are common on diagnostic imaging in dogs with hyperadrenocorticism

A
  • Hepatomegaly
  • Adrenal tumor
  • Focal calcification
  • Lung mineralization
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16
Q

What CBC findings are common in hyperadrenocorticism dogs?

A
  • Anemia is uncommon
  • Stress leukogram - neutrophilia, lymphopenia
  • Thrombocytosis
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17
Q

What Serum Chemistry findings are common in hyperadrenocorticism dogs?

A
  • Elevated liver enzymes (ALP > ALT)
    • ALP - GC induced isoenzyme
    • ALT - vacuolar hepatopathy
  • Hypercholesterolemia
  • Hyperglycemia (mild)
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18
Q

What urinalysis findings are common in hyperadrenocorticism dogs?

A
  • Low urine specific gravity <1.020
  • Proteinuria
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19
Q

How is hyperadrenocorticism diagnosted?

A
  • 2 step approach
    • Screening tests - confirm adrenal hypersecretion
      • Urine cortisol:creatinine ratio (UCCR)
      • Low does dexamethasone suppression test (LDDST)
      • ACTH stimulation test
    • Differentiating tests - distinguish PDH and ADH
      • Adrenal US (or other dx imaging)
      • endogenous ACTH measurement
      • High dose dexamethasone suppression test (HDDST)
20
Q

What do the results of a Urine Cortisol : Creatinine Ratio (UCCR) test mean?

A
  • Dogs with HAC have elevated urine cortisol:creatinine ratio
  • normal results rule out HAC - high specificity
  • Abnormal result require confirmation with another screening test
21
Q

What do the results of a Low Dose Dexamethasone Suppression Test (LDDS) mean?

A
  • Effective screening test
  • can be a differentiating test
  • dogs with HAC have elevated 8-hr cortisol
  • Stress / Nonadrenal illness = False +
22
Q

What do the results of a ACTH stimulation Test mean?

A
  • Generally considered more Specific than LDDS
  • Dogs with HAC have elevated post-ACTH cortisol
  • Cannot distinguish between PDH and AT
23
Q

What Hyperadrenocorticism screening test is a good choice if non-adrenal illness is suspected?

A

ACTH Stimulation test

24
Q

What do the results of a High Dose Dexamethasone Suppression Test (HDDST) mean?

A
  • Suppression = PDH
    • 70% of PDH cases suppress - can differentiate from AT
    • 30% of PDH cases do not suppress
  • No Suppression = AT
25
Q

What doe the results of an Endogenous ACTH Test (eACTH) mean?

A
  • Low = AT
  • High = PDH
  • Diagnostic in >80% of dogs (>95% when re-tested)
26
Q

Compare and contrast Hyperadrenocorticism tests

A
27
Q

What imaging techniques are useful for diagnosing PDH?

A
  • CT, MRI, and US
    • Pituitary tumor (macroadenoma or smaller)
      • only 50% of PDH have detectable ass
    • Bilateral adrenal hypertrophy (uniform / nodular)
      • normal and abnormal glands overlap in size
28
Q

What imaging techniques are useful for diagnosing ADH?

A
  • US, CT
    • Unilateral adrenal enlargement (usually nodular change)
    • Atrophy of contra-lateral gland
    • Not every adrenal mass is functional - possible misdiagnosis if functional testing is not done
29
Q

What are the treatment options for PDH?

A
  • Hypophysectomy
    • Surgical
      • removal/destruction of adenoma
      • Difficult
  • Medical Management
    • Anti-adrenal therapy
    • Pituitary Therapy
  • Radiation
    • Reserved for macroadenoma
    • Slows tumor growth
    • less effect on abnormal hormone production
30
Q

What is an Adrenalectomy?

A
  • Preferred treatment for ADH
  • Pre-op imaging - asses metastasis and local invasion
  • May require pre-surgical stabilization
  • Peri- and post-operative complications
    • Hemorrhage
    • Thromboembolism
    • Adrenal insufficiency
  • Prognosis
    • good is tumor is benign and easily removed
    • malignant tumors = less favorable prognosis
31
Q

What medications are available to treat hyperadrenocorticism?

A
  • Trilostane
  • Lysodren
  • Ketoconazole
  • Anipryl
32
Q

How does Trilostane work to treat HAC?

A
  • Inhibits synthesis for adrenal cortical steroids
  • Reversible inhibitor of 3B-hydroxysteroid dehydrogenase
33
Q

What is the dose of Trilostane? Adverse effects?

A
  • 2 - 4 mg/kg/day (divided BID)
  • Incremental increase as needed
  • Minimal Adverse Effects:
    • Transient vomiting, diarrhea and lethargy
    • Rarely, hypoadrenocorticism may develop
    • Acute adrenal necrosis (rare
34
Q

How can trilostane therapy be monitored for effectiveness?

A
  • ACTH stimulation test
    • 10 - 14 days after starting
    • 2 weeks after dose increase
    • q3 months for the long term
    • Target post-ACTH of 1.45 - 5.4 ug/dl
      • up to 9.1 ug/dl is acceptable if clinical signs are controlled
  • Post-dose cortisol concentration
    • sample 4 - 6 hr post-dose.
    • Cortisol ≥ 1.3 ug/dl excludes excessive suppression
    • ≤ 2.9 excludes grossly inadequate control
  • Pre-dose Cortisol
    • pre-trilostane cortisol of 1.4 - 5 ug/dl correlates with effective control of clinical signs but not with post-ACTH stim cortisol concentrations
35
Q

How does Lysodren work to control HAC?

A
  • “mitotane”
  • Adrenocorticolytic that acts by destruction of functional adrenal tissue
  • Occasionally used as alternative to trilostane
36
Q

How does Ketoconazole work to control HAC?

A
  • Reversible inhibition of adrenal steroidogenesis (primarily glucocorticoids)
37
Q

How does Anipryl control HAC?

A
  • “selegiline’ ‘L-deprenyl’
  • Monoamine oxidase inhibitor (MAO) - reduces ACTH production
38
Q

What is the Prognosis of HAC?

A
  • PDH
    • goal - improved quality of life
    • CNS signs carry guarded prognosis
  • ADH
    • Benign adrenal tumors - good/excellent prognosis if removed
    • Malignant tumors - guarded to poor prognosis due to local tissue invasion
39
Q

Do cats suffer from hyperadrenocorticism?

A
  • Considered uncommon to rare
    • >80% have PDH
      • ~50% have microscopic pituitary tumors
    • Iatrogenic - less common than dogs
    • Differentials include DM and acromegaly
40
Q

What is the common signalment of cats with HAC?

A
  • Middle age or older (average - 10 yr)
  • Higher incidence in females (70%)
  • 80% of cats have insulin resistance and diabetes
41
Q

What are the common clinical signs of Feline HAC?

A
  • PU/PD
  • polyphagia
  • Diabetes that is “difficult to regulate”
  • weight loss / failure to gain weight
  • Lethargy; look ill
  • Skin fragility
  • alopecia
  • failure to groom
  • pendulous abdomen
42
Q

What laboratory findings are common with Feline HAC?

A
  • Limited Database
  • CBC - no consistent abnormalities
  • Serum chemistry
    • hyperglycemia
    • ALP not increased
      • cats lack GC - induced ALP isoform
  • Urinalysis
    • Spec Gravity usually <1.020
    • Glucosuria
43
Q

How is Feline HAC diagnosed?

A
  • Screening test - same as Canine HAC
    • ACTH stimulation test
    • LDDS Test
      • use 0.1 mg/kg (vs 0.01 mg/kg in dog)
    • UCCR
  • Differential testing - same as Canine HAC
    • HDDS test
      • Use 1.0mg/kg (0.1mg/kg in the dogs)
    • Abdominal ultrasound
    • Endogenous ACTH levels
44
Q

What is the treatment for Feline ADH?

A
  • Surgery best option if metastatic disease/invasion absent
45
Q

What is the treatment for Feline PDH?

A
  • Treatment of choice is controversial
  • Surgery - Bilaeteral adrenalectomy
  • Hypophysectomy
  • Radiation Therapy
  • Medical Therapy
    • mitotane - cats more resistant
    • Trilostane - limited information
    • Ketoconazole - cats more resistant
46
Q

What is the prognosis for Feline HAC?

A

guarded to poor