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sam dr green > hyperadrenocorticotism > Flashcards

hyperadrenocorticotism Flashcards

1
Q

etiology for hyperadrenocorticotism

A
  • Bilateral adrenocortical hyperplasia (80-85%)
    • ACTH secreting adenoma of pars distalis
    • PDH –Pituitary Dependent Hyperadrenocorticism
  • Adrenocortical neoplasia (15-20%)
    • ADH –Adrenal Dependent Hyperadrenocorticism
  • Iatrogenic
    • Exogenous steroids
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2
Q

causes of pituitary dependent hyperadrenocortism

A
  • Microadenoma
    • Most (85%) pituitary tumors are microadenomas
    • < 1 cm in diameter
    • Clinical signs are due to excessive ACTH production
  • Macroadenoma
    • Up to 15% of pituitary tumors may be macroadenomas
    • > 1 cm in diameter
    • Clinical signs are due to excessive ACTH production AND signs associated with mass effects of tumor
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3
Q

eitiology for adrenal dependent hyperadrenacorticotism

A

50% are benign (adenoma)
50% are malignant (adenocarcinoma)
Often large, more invasive (vena cava)
Can potentially metastasize (lungs, liver, etc.)
More common in large breed dogs

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4
Q

signalment for hyperadrenocortism

A
  • Middle-aged to older dogs
  • Most are > 9 years of age
  • No strong sex predilection
  • Any breed or mixed breed dogs
  • PDH -often affects smaller dogs
  • ADH –often affects larger dogs (exception: PDH in Boxers)
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5
Q

history for hyperadrenocorcotism

A
  • Generally considered “healthy” by the owner
  • Clinical signs due to effects of excess glucocorticoids
    • Gluconeogenic
    • Lipolytic
    • Protein catabolic
    • Anti-inflammatory
    • Immunosuppressive
  • The P’s
    • Polyuria and polydipsia (80% of cases)
    • Polyphagia (90% of cases)
    • Panting
  • Decreased exercise tolerance

Lethargy

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6
Q

what do u feel on pe of a hyperadrenocorticotism dog

A
  • Abdominal enlargement (80%)
    • Muscle weakness
    • Hepatomegaly
    • Hepatocyte vacuolation due to glycogen accumulation
  • Almost all have some dermatologic signs
    • Bilaterally symmetric truncal alopecia
    • Thin, dry, scaling skin
    • Hyperpigmentation
    • Easy bruising (e.g. after venipuncture)
      Comedones
    • Calcinosis cutis
      • Calcium deposition in the dermis
      • Uncommon but very suggestive of hyperadrenocorticism
      • Pyoderma
      • Increased susceptibility to infection
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7
Q

other findings of hyperadrenocorcocotism

A
  • Hypertension (> 50% of cases)
  • Poor wound healing
  • Pulmonary thromboembolism
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8
Q

cbc findings of hyperadrenocorcocotism

A
  • Stress leukogram
    • Leukocytosis due to neutrophilia
    • Monocytosis
    • Lymphopenia, eosinopenia (80% of cases)
  • Mild to moderate erythrocytosis
  • Thrombocytosis (cause unknown)
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9
Q

chemistry profile for hyperadrenococotism

A
  • Mild hyperglycemia (50% of cases)
    • Glucocorticoids increase hepatic gluconeogenesis and decrease peripheral uptake of glucose
  • Increased ALP (90% of cases)
    • CIALP unique to the dog
    • Sensitive but not specific
  • Hypercholesterolemia (75% of cases)
  • Increased ALT –mild to moderate (50% of cases)
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10
Q

urinalysis findings of hyperadrenocoticotism

A
  • Low urine specific gravity (80% of cases)
    • < 1.015 to 1.020
  • Bacteriuria in 50% of cases but pyuria < 20% of cases
  • Avoid catheterization for urine collection
    • Increased risk of infection; use cystocentesis
  • Proteinuria (can have mildly increased UPC)
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11
Q

abdominal rads findings for hyperadrenocorticotism

A
  • Hepatomegaly (80-90% of cases)
  • Enlarged bladder (due to polyuria)
  • Approximately 50% of adrenocortical tumors calcified
  • Increased risk of calcium-containing urinary calculi (calcium oxalate or calcium phosphate)
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12
Q

discuss resting cortisol levels as a dx for hyperadrenocorticotism

A
  • Not valuable because many dogs with hyperadrenocorticism have normal cortisol concentrations at any given moment due to the episodic secretion of ACTH
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13
Q

screening tests for hyperadrenocoticotism

A
  • ACTH Stimulation Test
  • Low Dose Dexamethasone Suppression Test (LDDST)
  • Urine Cortisol/Creatinine Ratio (UCCR)
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14
Q

ACTH stimulation test

A
  • Normal resting cortisol
    • 1-5 μg/dL; normal post-ACTH cortisol: 5-22 μg/dL
  • Dogs with hyperadrenocorticism
    • Exaggerated response to ACTH
    • Post-ACTH cortisol > 22 μg/dL)
  • Very sensitive (approximately 95%)
  • Reasonably specific (approximately 90%)
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15
Q

advantages of ACTH stimulation test

A
  • Cheaper than LDDST and takes less time
  • Only test to identify iatrogenic hyperadrenocorticism
  • Test of choice to monitor dogs being treated with mitotane or trilostane
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16
Q

disadvantages of ACTH stimulation test

A

Stress of non-adrenal illness can cause abnormal test results

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17
Q

how does LDDST test work

A
  • Measure plasma cortisol before and 4 and 8 hours after 0.01 mg/kg/IV dexamethasone
  • Normal dogs
    • Plasma cortisol decreases to < 1.4 μg/dL 4 and 8 hours after dexamethasone
  • Failure to suppress suggests Cushing’s syndrome
  • Very sensitive (approximately 95%)
  • Not very specific (approximately 70%)
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18
Q

adv. of urine cortisol/crea. ratio

A

Easy (have owners get free catch from dog at home)

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19
Q

disadvantages of urine cortisol/creat. ratio

A
  • Extremely low specificity (20-40%) despite very high sensitivity (> 90%)
  • Used primarily when you don’t think the animal has Cushing’s and you want to quickly rule it out
  • Not helpful at all in ruling in Cushing’s
    • If positive, must perform ACTH stim or LDDST
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20
Q

PDH vs. ADH……does it really matter?

A

PDH vs. ADH……does it really matter?

21
Q

disadvantages of HDDST

A
  • Previously used as a discriminatory test
  • Based on principle that a high dose (0.1 mg/kg/IV) of dexamethasone would suppress cortisol in dogs with PDH but not ADH
  • Unfortunately, 40-50% of dogs with PDH also fail to suppress with HDDST
  • Thus suppression indicates PDH but NO conclusion can be drawn if dog fails to suppress
22
Q

disadvantages of radioimmnoassay in ACTH

A
  • Previously used as a discriminatory test
  • Based on principle that a high dose (0.1 mg/kg/IV) of dexamethasone would suppress cortisol in dogs with PDH but not ADH
  • Unfortunately, 40-50% of dogs with PDH also fail to suppress with HDDST
  • Thus suppression indicates PDH but NO conclusion can be drawn if dog fails to suppress
23
Q

what would u see on US in a patient with PDH vs ADH

A
  • Most practical test
  • PDH
    • Bilateral symmetrical enlargement
    • Glands retain their normal “peanut” shape
    • Normal echogenicity
  • ADH
    • Unilateral enlargement with distortion of shape
24
Q

words of wisdom for abd. Us in hyperadrenocorticotism

A
  • Don’t use as a screening test
    • Dogs with non-adrenal illness can have enlarged adrenal glands
    • Dogs with hyperadrenocorticism may have normal adrenal glands
  • Not all identified adrenal masses are functional (e.g. non-functional adenoma, pheochromocytoma)
  • Contralateral adrenal gland in dogs with ADH is not necessarily small on ultrasound examination as might be expected
25
Q

guiding principles for tx hypeadrenocoticotism

A
  • DO NOTtreat a dog with hyperadrenocorticism that has NO clinical signs
  • In other words…..no clinical signs…..NO TX!!!
  • High ALP does NOTequal hyperadrenocorticism
  • Hyperadrenocorticism is a CLINICAL diagnosis!!!!!
26
Q

discuss adv. and disd. of unilateral adrenalectomy in the tx of adh

A
  • Preoperative thoracic radiographs to rule out metastatic disease
  • Very difficult (best left to specialist surgeons)
  • High risk of thromboembolism and high mortality 24-48 hours postoperatively
  • Delayed wound healing
  • Contralateral adrenal suppressed
    • Dog must be supported with glucocorticoids intra-and post-operatively
  • Potentially good prognosis (adenoma better than carcinoma)
27
Q

disadvantages of Hypophysectomy

A
  • for pdh
  • Difficult technique
  • Requires specialist surgeon
  • Not routinely performed in dogs in USA
  • Due to loss of pituitary hormones
    • Must replace glucocorticoids, T4, and ADH post-op
    • DI often is transient
    • Lifelong glucocorticoid and T4 support is needed
28
Q

Medical Adrenalectomy

A
  • for PDH
  • Intentional over dosage of mitotane to completely destroy adrenal glands
  • Hypoadrenocorticism is created
    • Dog must be supported with glucocorticoids and mineralocorticoids for life
  • Indications
    • Extremely refractory cases of PDH
29
Q

discuss ketakonazole in the txment of PDH

A
  • Anti-fungal drug
  • Inhibits biosynthesis of steroids
  • Adverse effects
    • Anorexia, increased liver enzymes, icterus
  • NOTrecommended for routine treatment of hyperadrenocorticism
30
Q

discuss mitotanein txment of PDH

A
  • Lysodren®
  • Most common treatment for PDH in USA
  • Selective necrosis of zona fasiculata, zona reticularis
  • Dogs with ADH are refractory to tx
31
Q

discuss induction of mitotane

A
  • Mitotane -PDH
  • Induction
  • Owner must monitor appetite and water intake carefully to identify endpoint
  • Stop treatment if decreased appetite or water intake and return for ACTH stimulation test
  • Stop after 10-14 days regardless (maybe even 7 days?)
    • Repeat ACTH stimulation test
32
Q

discuss mitotane toxicity

A
  • Direct toxicity of mitotane
    • Anorexia, vomiting, diarrhea, lethargy, weakness
    • Must be differentiated from development of actual hypoadrenocorticism by ACTH stimulation if these signs develop
  • Mitotane-induced hypoadrenocorticism may be transient or permanent
33
Q

successful induction of mitotane

A
  • Both pre-and post-ACTH cortisol concentrations should be 1-5 μg/dL
  • Decreased responsiveness of adrenal glands to ACTH
  • Most importantly: control of clinical signs
34
Q

what should u do If post-ACTH cortisol > 5 μg/dL after mitotane induction

A
  • Administer mitotane for an additional 3-5 days
  • “Mini-induction”
  • Repeat ACTH to determine that both pre-and post-ACTH cortisol concentrations are 1-5 μg/dL
35
Q

discuss mitotane maintainance

A
  • in PH we keep on adjusting the drug
  • Relapses are not unusual and require “mini-inductions” of 3-5 days of mitotane followed by return to maintenance
36
Q

response of dogs to mitotane tx

A
  • Overall good clinical response to mitotane
  • 80% of dogs with PDH respond well
  • Survival of 2 years or more (geriatric dogs)
37
Q

advantages of trilostane tx

A
  • Can be used for both PDH and ADH
  • drug of choice if u decide nt to send the dog to sx wen they hav adrenal mass
  • no induction dose
38
Q

px with trilostane tx

A
  • Good clinical response in 80% of treated dogs with survival times of 2-3 years
  • Control of biochemical abnormalities (e.g., ALP, cholesterol) is less reliable than control of clinical signs (e.g. PU, PD, polyphagia)
39
Q

advantages of trilostane

A
  • Well-tolerated
  • Useful in dogs with other serious medical problems
  • Effects are reversible
  • No induction phase
40
Q

disad. of trilostane

A
  • Expensive
  • Rare cases of adrenal necrosis
41
Q

disad. of raditherapy for PDH

A
  • Only available at selected institutions
  • May see substantial reduction in size of pituitary tumor but only transient resolution of clinical signs
  • Usually recommended for tumors > 7 mm
  • So-called “macroadenomas” are ≥ 10 mm
42
Q

complications for hypercorticotism tx

A

Hypertension
Proteinuria (related to hypertension or PLN or both?)
Thromboembolism
Susceptibility to infections (e.g., UTI)
Urolithiasis (e.g., calcium oxalate, calcium phosphate)
Concurrent diabetes mellitus in 5% of dogs with hyperadrenocorticism

43
Q

px for PDH

A

Depends on size and rate of growth of pituitary tumor

44
Q

px for ADH

A
  • Depends on local invasion or distant metastasis
  • Adenomas have better prognosis than carcinomas
45
Q

px for hyperadrenocorticotism

A
  • With treatment, clinical signs regress in 3-5 months
  • Polyphagia, polydipsia, polyuria within 10 days
  • Muscle strength returns and abdominal distension improves within weeks
  • Improvement in hair coat and resolution of hypertension and proteinuria over months (some don’t resolve?)
  • Improvement in biochemistry (e.g. SAP, cholesterol) over months
46
Q

hyperadrenocorticosm in cats

A
  • Rare but increasingly reported
  • Older cats
  • Usually presented for DM that is difficult to control
  • Insulin resistant DM
  • Fragile, thin skin!!!
  • Weakness, weight loss, polyuria, polydipsia
  • PU/PD due to concurrent DM
  • Glucocorticoids do NOT usually cause PU/PD in cat
  • Ocular abnormalities (mydriasis, blindness, retinal detachment) associated with hypertension
47
Q

lab findings for hyperadrenocorticotism in cats

A

Hypokalemia, hypernatremia, metabolic alkalosis, increased creatine kinase (due to hypokalemic myopathy), dilute urine
Very high aldosterone (> 1000 pg/L; normal, 200-400 pg/L)
Caused by aldosterone-secreting adrenal adenoma or adenocarcinoma

48
Q

tx and px for hyperthyroidism in cats

A
  • Tumors identified on abdominal ultrasound (1-3 cm diameter)
  • Surgical removal is difficult (adherence to caudal vena cava) but treatment of choice for adenomas
  • Palliative management
    • Spironolactone (aldosterone antagonist)
    • Potassium supplementation
    • Long-term survival (up to 3 years) reported

sam dr green (10 decks)

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