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Small Animal Medicine > Canine Pituitary & Adrenal Diseases > Flashcards

Canine Pituitary & Adrenal Diseases Flashcards

1
Q

What are the 2 forms of naturally occurring Cushing’s syndrome? Which one is most common?

A
  1. ACTH-dependent - pituitary hypercorticism, commonly caused by a tumor (PDH)**
  2. ACTH-independent - adrenal hypercorticism, commonly caused by a tumor (ADH)
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2
Q

What is the most common cause of iatrogenic Cushing’s syndrome?

A

exogenous excess of cortisol, commonly caused by too high doses or chronic glucocorticoid administration

  • betamethasone
  • dexamethasone
  • prednisone
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3
Q

What are the 2 pituitary tumors that cause Cushing’s syndrome? Which one is most common?

A
  1. microadenoma**
  2. macroadenoma - >1 cm, large enough to cause neurological signs
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4
Q

What are the chances that adrenal tumors that cause Cushing’s are benign vs. malignant?

A

50/50

  • malignant tends to invade vessels and metastasize (surgical removal!)
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5
Q

What is the most common signalment of dogs with Cushing’s syndrome?

A

middle-aged to older Poodles, Dachshunds, Beagles, Boxers, Boston Terriers, and Bichons

  • no sex predisposition
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6
Q

What are the 5 signs associated with the classic Cushingoid dog?

A
  1. PU/PD - cortisol decreases ADH action at kidneys
  2. polyphagia
  3. panting
  4. potbelly appearance - hepatomegaly + weak abdominal muscles (muscle weakness = exercist intolerance)
  5. alopecia
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7
Q

What are the most common cutaneous manifestations of Cushing’s?

A
  • hyperpigmentation
  • thin skin
  • rat tail
  • comedones
  • bruising
  • calcinosis cutis
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8
Q

What are 2 additional signs of Cushing’s?

A
  1. hepatomegaly
  2. recurrent infections
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9
Q

How is the cardiovascular system affected by Cushing’s?

A
  • hypertension
  • hypercoagulability (PTE, not as common)
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10
Q

Most common signs of Cushing’s:

A
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11
Q

What findings are commonly seen on CBC, biochem, and UA in Cushingoid dogs?

A

increased cortisol = stress leukogram (neutrophilia, lymphopenia)

increased ALP caused by isoenzyme production (C-ALP) in 90% of dogs

concentration varies, byt hyposthenuria is common + proteinuria

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12
Q

What is the difference between screening and differentiation adrenal testing for Cushing’s?

A

SCREENING - presence of hyperadrenocorticism (yes/no)

DIFFERENTIATION - type of hyperadrenocorticism (PDH/can’t tell)

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13
Q

What 3 adrenal tests are used for Cushing’s?

A
  1. LDDST
  2. ACTH stimulation
  3. urine cortisol:creatinine ratio
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14
Q

How is LDDST performed?

A
  • take a pre cortisol sample
  • give dexamethasone injection
  • measure cortisol at 4 and 8 hrs later
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15
Q

What is the sensitivity and specificity of LDDST like?

A

sensitivity = ~95% (great at screening)

specificity = low - false positive associated with non-adrenal illness

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16
Q

What is expected in normal and Cushingoid dogs in response to LDDST?

A

NORMAL - dexamethasone injection should suppress ACTH secretion from the pituitary and a decrease in cortisol by 8 hrs

CUSHINGOID - dexamethasone has no effect on the pituitary or adrenal gland because the tumors will continue to secrete ACTH and cortisol, causing high cortisol level by 8 hrs

17
Q

How is the LDDST interpreted?

A

8 hr sample confirms hyperadrenocorticism - if high, Cushing is present; if suppressed, there is no hyperadrenocorticism

can differentiate PDH:
- suppressed at 4 hrs
- 4 or 8 hr results are <50% baseline, indicating relative suppression

18
Q

Is this patient Cushingoid? Can it be differentiated?

A

YES - 8 hr sample is above RI

YES, PDH - 4 hr sample is not suppressed, but 4 and 8 hr samples are <50% of baseline = relative suppression

19
Q

Is this patient Cushingoid? Can it be differentiated?

A

NO - 8 hr sample within RI

20
Q

Is this patient Cushingoid? Can it be differentiated?

A

YES - 8 hr sample is above RI

YES, PDH - 4 hr sample is suppressed

21
Q

How is an ACTH stimulation test performed?

A
  • collect a pre cortisol sample
  • inject ACTH (Cortrosyn) and take a sample 1 hr later (elevated if Cushingoid)
22
Q

In what 4 ways does the ACTH stim test compare to LDDST?

A

85% sensitivity and specificity

  1. 15% of Cushingoid dogs will not have high cortisol, if signs are there, perform a LDDST
  2. higher specificity makes it less affected by non-adrenal illness
  3. only test able to diagnose iatrogenic and spontaneous hyperadrenocorticism (cannot differentiate other types)
  4. only takes an hour, better for a time crunch
23
Q

How do normal dogs react to ACTH stim test? PDH? ADH? Iatrogenic?

A

in response to ACTH, the adrenal gland will produce cortisol within an expected RI

bilaterally enlarged adrenal glands - exaggerated post cortisol levels above RI

doesn’t tend to work as well in these dogs, but unilarerally enlarged adrenal glands - exaggerated post cortisol levels above RI (not seen, do LDDST)

atrophied glands will not secrete cortisol, even if stimulated by ACTH

24
Q

Are these dogs Cushingoid? They all present with signs of Cushing’s and have no other adrenal illness identified.

A
  1. borderline high - likely yes, try a LDDST to be sure
  2. YES - 1 hr sample above RI
  3. YES - iatrogenic!
25
Q

How is a urine cortisol:creatinine ratio performed?

A

collect urine at home, then measure cortisol and creatinine in urine - Cushingoid dogs have excess urinary cortisol excretion

  • high sensitivity, poor specificity (false positives!)
  • able to r/o Cushing’s with low results
26
Q

What imaging can be done to diagnose Cushing’s?

A
  • abdominal ultrasound - expect enlarged adrenals; unilateral (with contralateral atrophy) = ADH, bilateral = PDH
  • CT/MRI - pituitary macroadenoma (neuro signs)
27
Q

What are the 2 medical treatment options for Cushing’s?

A
  1. Trilostane (Vetoryl)* - reversible inhibitor of 3-beta-hydroxysteroid dehydrogenase, which stops cortisol synthesis
  2. Mitotane (Lysodren) - irreversible destruction of zona fasciculata and reticularis, which stops cortisol synthesis
28
Q

How is the dosage of Mitotane developed for Cushingoid dogs?

A

irreversible destruction to adrenal cortex

  • begin with a loading dose
  • wait for decrease in polyphagia and polydipsia, depending on owner observation
  • continue with a maintenance dose to avoid developing Addison’s disease
29
Q

When is surgical management recommended with Cushingoid dogs?

A

as a whole, medical management is safest and most commonly recommended

  • PDH = med > sx
  • ADH = surgical removal of unilateral tumor, avoids malignant metastasis into vena cava (thrombosis, embolism)
30
Q

How is medical treatment of Cushing’s monitored?

A

use ACTH stim test with a goal of 1.5-5 and up to 9 if signs are controlled (with reference to no longer being clinical)

  • 2 week follow-up to ensure hypoadrenocorticism is occuring
  • another 2 week follow-up to see if it is controlled and if dosage changes are required
  • every 4 week follow-ups
  • periodic follow-ups
31
Q

What are the 3 main adverse effects associated with medical treatment of Cushing’s?

A
  1. cortisol deficiency - anorexia, vomiting, diarrhea
  2. aldosterone deficiency - hyponatremia, hyperkalemia, collapse, hypovolemia (decreased Na = decreased water withing ECF)
  3. direct GI effects (cortisol responsible for GIT mucosa health) - anorexia, vomiting diarrhea
32
Q

What is prognosis of PDH Cushing’s like?

A

MICROADENOMA - lifelong medical treatment with good prognosis, median 2 years with death not due to hyperadrenocorticism

MACROADENOMA - fair to good with radiation treatment and better without neurological signs at outset

33
Q

What is prognosis of ADH Cushing’s like?

A

ADENOMA - excellent with surgery

CARCINOMA - fair to poor

34
Q

What is atypical hyperadrenocorticism? How is it diagnosed? Treated?

A

patient has signs consistent with hyperadrenocorticism, but ACTH and LDDST are normal thought to be caused by increased sex hormones

Tennessee panel - ACTH stim with sex hormone measurement

same as typical HAC - Trilostane, monitor with ACTH stim

35
Q

What clinical signs are associated with sex hormone-secreting adrenal tumors?

A
  • as expected estradiol and androgen levels (if testosterone increased in cats = barbs on penis)
  • increased PROGESTERONE = cortisol-like signs - anorexia, vomiting, diarrhea
36
Q

What is the most common presentation, clinical pathology, and treatment used for Cushing’s?

A

panting and alopecia common, fragile skin that does not tear

  • elevated ALP (90%) due to steroid-induced ALP form
  • stress leukogram
  • 10% diabetic

mitotane, trilostane, sx for unilater AT

37
Q

What is the pathophysiology of pituitary dwarfism?

A

deficient pituitary gland causes decrease in GH, TSH, prolactin, and gonadotropins

38
Q

When do clinical signs of pituitary dwarfism appear? What signs are most common?

A

3-5 m/o

  • proportionate dwarfism
  • retention of puppy coat
  • alopecia, hyperpigmentation
  • weakness, ataxia
39
Q

What are 2 ways of diagnosing pituitary dwarfism? How is it treated?

A
  1. genetic test for LHX3 gene (GSDs)
  2. decreased IGF-1 (no tests available in the US for GH)

hormone supplementation - thyroid, GH

Small Animal Medicine (52 decks)

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