Cushing's Disease Flashcards by Jessica Hodson

what are the functions of cortisol

anti-inflammatory and immunosuppressive

increase BG
promote vascular integrity
promote GI mucosal integrity
decrease bone formation
aid in RBC production

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pituitary dependent hypercortisolism (PDH) pathogenesis

pituitary micro or macroadenoma –> secretes ACTH –> overstimulation of adrenals –> bilateral adrenal hyperplasia –> excess cortisol production

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PDH prevalence

most common cause of Cushing’s

most common in small dogs

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PDH etiology

pituitary adenoma

majority are microadenomas

macroadenomas: either >1 cm OR growing out of the sella turcica

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what is a sign that a well managed PDH dog has a pituitary macroadenoma

suddenly beomces inappetent, lethargic, disoriented, blind, etc

recommend workup for space occupying brain lesion (macroadenoma)

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PDH adrenal morphology

bilateral hyperplasia

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PDH ACTH levels

high to normal

(would expect 0 with high cortisol due to negative feedback)

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adrenal dependent hypercortisolism (ADH) pathogenesis

functional adrenal tumor causing excess cortisol production –> suppression of CRH and ACTH from the hypothalamus + pituitary

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ADH prevalence

less common than PDH

more common in large breed dogs

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ADH etiology

adrenal adenoma
adrenal carcinoma

both are equally likely

criteria of malignancy:
1. > 2cm
2. local invasion
3. hemorrhage/necrosis
4. mineralization

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ADH adrenal morphology

unilateral hypertrophy (tumor) + contralateral adrenal atrophy

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ADH ACTH levels

low (should be 0)

caused by negative feedback from excess cortisol production

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iatrogenic cushing’s

exogenous administration of glucocorticoids causes suppression of the HPA axis

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iatrogenic cushing’s adrenal morphology

bilateral atrophy

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iatrogenic cushing’s ACTH levels

low (should be 0)

negative feedback from exogenous glucocorticoids

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most common clinical signs of cushing’s in dogs

PU
PD
PP
panting
potbelly/pendulous abdomen
alopecia

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what are additional signs of cushing’s in dogs

thin skin
weakness (muscle atrophy)
weight redistribution - often perceived as weight gain due to fat deposition in the abdomen w/ appendicular muscle loss

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dermatologic changes associated with cushing’s disease

endocrine alopecia - bilaterally symmetric, truncal, non-pruritic alopecia

hyperpigmentation

calcinosis cutis

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how is a diagnosis of cushing’s typically made

in the exam room - any further testing beyond clinical presentation is done to determine the type of cushing’s

iatrogenic can be ruled out with medication history

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what are good screening tests for cushing’s

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history + PE
minimum database
UCCR
ACTH stimulation test
LDDS test

cbc changes with cushing’s

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stress leukogram
mild polycythemia
mild thrombocytosis

chem changes with cushing’s

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increased ALP (steroid isoenzyme)
mild hyperglycemia
hyperlipidemia (cholesterol + triglycerides)
mild low BUN

UA changes with cushing’s

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iso to hyposthenuria (due to secondary nephrogenic DI)

urine cortisol:creatinine ratio

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good RULE OUT test for cushing’s - can NOT definitively diagnose

ideal to take a sample in a STRESS FREE environment at home (free catch)

acth stimulation test

best used for PDH > ADH if < 2 --> addison's if 2-18 --> unlikely cushing's (can't rule out) if > 20 --> cushing's likely

why does PDH stim higher than ADH on an ACTH stim test

PDH: the ACTH will stimulate two hyperplastic glands to produce even more cortisol ADH: only one adrenal is functional (tumor) and the other is non-productive due to atrophy, so ACTH stimulation will not result in much higher cortisol production

low dose dexamethasone suppression test (LDDS)

best for ADH > PDH take 3 cortisol samples at times 0, 4, and 8 hours after low dose dex administration

how to evaluate LDDS results

1. evaluate the 8 hr sample - if < 1.4 --> normal - if > 1.4 --> consistent w/ Cushing's - use 4 hr sample to determine the type 2. evaluate the 4 hr sample - if < 1.4 --> PDH - if 4 or 8hr is < 50% baseline --> PDH - if > 1.4 --> ADH or PDH

do adrenal tumors suppress during a LDDS test

no - ADH patients will not suppress cortisol production at any time point tumors do NOT respond to negative feedback because ACTH is already low/zero (cannot get any lower) therefore - any signs of suppression at the 4 or 8 hour time point rules out ADH

what tests are primarily used to differentiate ADH from PDH

- endogenous ACTH - abdominal US - HDDS test - CT - MRI

endogenous ACTH test

measures ACTH in the blood must handle sample carefully - difficult test to run if ACTH = 0 --> ADH if ACTH > 0 --> PDH

what imaging is the best and most cost effective option to differentiate ADH and PDH

abdominal US - if bilateral hyperplasia --> PDH - if unilateral hypertrophy w/ contralateral atrophy --> ADH - if bilateral atrophy --> iatrogenic

what is CT used for

pre-adrenalectomy surgical planning assessment for macroadenoma

what is MRI used for

best choice for assessment of pituitary macroadenomas

what are the two medical therapy options for cushings

1. trilostane (vetoryl) 2. mitotane (lysodren)

trilostane (vetoryl) MOA

enzyme inhibitor blocks an enzyme that is involved in converting cholesterol into cortisol in order to decrease cortisol production best for ADH > PDH

trilostane pros

- reversible - many tablet sizes for more accurate dosing (5, 10, 30, 60) - FDA approved in dogs

trilostane cons

- monitoring can only be based on clinical signs, USH, water intake - ACTH stimulation is NOT a reliable indicator of clinical monitoring

mitotane (lysodren) MOA

selective adrenal necrosis of the zona fasciculata + reticularis best for PDH > ADH

mitotane pros

- ACTH stimulation test is VERY helpful for clinical monitoring - highly effective drug for PDH

mitotane cons

- risk of irreversible adrenal necrosis leading to addison's - only ONE tablet size - more difficult to dose - NOT FDA approved for dogs or cats

what are the two surgical options for cushing's and what type are they used for

1. adrenalectomy (ADH) 2. hypophysectomy (PDH)

adrenalectomy

can be laparoscopic for non-invasive tumors must be open laparotomy for invasive tumors - greater risk of hemorrhage and post op complications

complications of adrenalectomy

poor healing risk of pancreatitis post op PTE bilateral adrenalectomy may cause addison's disease

hypophysectomy

transoral approach less common in vet med in the US will require lifelong glucocorticoids + levothyroxine due to lack of all anterior pituitary hormones after removal

when is radiation therapy useful

non resectable adrenal masses pituitary macroadenomas goal: resolve the space occupying effects of masses

differences in cushing's disease in cats compared to dogs

1. no elevated ALP (no steroid isoenzyme in cats) 2. no calcinosis cutis 3. no PU/PD/PP unless concurrent diabetes mellitus

what are the most common consequences of cushing's (or exogenous steroid administration) in cats

1. diabetes mellitus 2. feline skin fragility syndrome

Cushing's Disease Flashcards

(48 cards)