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Internal Medicine/ Ettinger > Canine Hyperadrenocorticism > Flashcards

Canine Hyperadrenocorticism Flashcards

1
Q

What is the key enzyme that is present in the zone fasciculata and reticularis that is not present in the glomerulosa that synthesis cortisol?

A

17-alpha-hydroxylase

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2
Q

What are the 2 form of canine hyperadrenocorticism? Which form is more common?

A

Pituitary vs adrenal dependent
PDH is more common (80-85%) & 90% have a detectable pituitary tumour

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3
Q

Other than CRH, what else can stimulate ACTH secretion?

A
  • dopamine
  • cytokines (IL-1, IL-6, TNF-alpha)
  • leptin
  • AVP
  • Angiotensin II
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4
Q

What inhibits CRH secretion?

A
  • glucocorticoids (negative feedback loop) = dominant one
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5
Q

What are the 2 theories of PDH in dogs?

A
  1. Hypothalamic theory (not widely accepted)
    - excessive CRH secretion and vasopressin + defective cortisol receptor
  2. Pituitary (monoclonal) - accepted and supported
    - single somatic mutation of a corticotroph leading to tumour
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6
Q

Can cytology ddx between adrenal adenoma vs carcinoma?

A

No

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7
Q

What are some features that would be more consistent with an adrenal carcinoma?

A
  • > 2cm
  • vascular invasion
  • broken through the capsule
  • down regulation of ACTH receptor
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8
Q

What are some common urinary signs of dogs with hyperadrenocorticism?

A
  • PU/PD
  • UTI
  • overflow incontinence
    Steroid can interfere with ADH, leading to PU
    The dilute urine, urine retention and immunosuppression = increased risk of UTI
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9
Q

What are some common non-urinary signs of dogs with hyperadrenocorticism?

A
  • polyphagia
  • 5-10% develop diabetes mellitus
  • pot-bellied appearance –> combination of weakened muscle, hepatomegaly and large urinary bladder, redistribution of peripheral fat to mesentery
  • muscle weakness = catabolic effect of glucocorticoids
  • excessive panting –> decreased pulmonary compliance, pulmonary hypertension, respiratory muscle weakness, or direct effect of glucocorticoids on the respiration centre
  • pulmonary thromboembolism = rare complication
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10
Q

What are some CNS of dogs with hyperadrenocorticism?

A

Due to pituitary macroadenoma (10-25% dogs with PDH)
- most common signs = moderate to severe lethargy
- others: aimless wandering, decrease appetite/ anorexia, stupor, circling, ataxia, change in behaviour, seizures

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11
Q

What are some uncommon signs of dogs with hyperadrenocorticism?

A
  • Cushing’s psuedomyotonia –> stiff gait, dog “hops”
  • ligament laxity (plantigrade stance)
  • facial nerve paralysis, anestrus, testicle atrophy, thromboembolism due to hypercoagulopathy (FAT can invade in the phrenicoabdominal vein, caudal vena cava, or both)
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12
Q

What are some common physical exam abnormalities noted for dogs with hyperadrenocorticism?

A

Common:
- pot belly
- bilateral symmetrical alopecia
- thin skin, hyperpigmentation
- comedone
- pyoderma

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13
Q

What’s the pathogenesis of calcinosis cutis?

A

Calcinosis cutis = irregular plagues in/under skin. Mostly in the dorsal neck/ midline, ventral abdomen, inguinal regions or temporalis region
- due to gluconeogenic and protein catabolic mechanisms of glucocorticoids –> rearrangement of protein structures –> formation of organic matrix that attracts and binds Ca2+, forming apatite crystals

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14
Q

How does HAC effect sexually intact dogs?

A

Less common signs
- testicular atrophy and anestrous
- due to glucocorticoid negative feedback on the synthesis and secretion of FSH and LH

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15
Q

Can HAC dogs be acutely ill?

A

Yes!
- severe lethargy, weakness, pale mucus membranes, pain
- may be due to rupture of the adrenal mass

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16
Q

What are some CBC changes typically noted for dogs with HAC?

A
  • lymphopenia
  • eosinopenia (bone marrow sequestration)
  • monocytosis, neutrophilia (steroid-enhanced capillary margination)
  • thrombocytosis, mild erythrocytosis (direct bone marrow stimulation or ventilation response)
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17
Q

What are is the common biochem change for dogs with HAC?

A

Most common (85-95%) = marked increase in ALP
- ALT: mild to moderate increase
- Cholesterol/ triglycerides: mild to moderate increase, seen in > 50% of HAC dogs

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18
Q

How does HAC influence blood sugar level?

A
  • mild hyperglycemia: due to the gluconeogenic nature, and decreased peripheral glucose utilization by interfering insulin action at a cellular level (receptor/ post receptor) level
  • abdominal fat and adipokines also play a role in insulin resistance
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19
Q

How does HAC influence other biochemical parameters?

A
  • BUN decreased in 30-50% of dogs, due to diuresis
  • phosphorus and calcium can also be decreased due to increased urinary excretion –> secondary hyperparathyroidism possible
  • Azotemia = uncommon
  • bile acids may be elevated in up to 30% of patients
20
Q

How does HAC influence coagulation?

A

dogs with HAC = hypercoagulable
- increases in pro-coagulants (II, V, VII, IX, X, XII) and decreased antithrombin
- TEG changes
- shortened PT, higher fibrinogen concentration

21
Q

What kind of U/A changes are noted with HAC?

A
  • low USG, commonly < 1.012
  • proteinuria, UPCR 1-6, >0.5 in 70%; >1 in 45%
  • UTI, occult possible, should culture
22
Q

How does HAC influence thyroid function test?

A
  • can be low (T4, fT4)
  • due to hypothalamic-pituitary suppression from excessive corticosteroids
23
Q

What changes on CXR can be noted for dogs with HAC?

A
  • want to rule out metastatic disease
  • look for PTE (alveolar infiltrates)
  • commonly have interstitial lung pattern
  • sometimes mineralized bronchi/ tracheal rings
24
Q

What changes on abdominal radiographs can be noted for dogs with HAC?

A
  • enlarged liver and bladder
  • dystrophic mineralization
  • mineralization of adrenal nodule does not correlate to malignancy
25
Q

What are some common AUS findings for dogs with pituitary dependent hyperadrenocorticism?

A

in PDH
- adrenal glands should be bilaterally enlarged –> size (breed dependent)
- signs of metastasis
- can use ultrasound to assess vascular invasion
- can also look for sequelae of HAC – gallbladder mucocele, uroliths
- 25% PDH will have normal adrenal glands
- adenomegaly does not equal HAC

26
Q

What are some common AUS findings for dogs with functional adrenal tumour?

A

in FAT
- single gland is enlarged, irregular, invading/ compressing on adjacent structures
- ddx: pheochromocytoma, aldosteronoma, metastatic mass, non-functional adrenal tumour

27
Q

What’s the utilities of CT/MRI for dogs with HAC?

A

Use if PDH is suspected - macroadenoma = >1cm pituitary gland
- based on neurological signs (66% will have a pituitary tumour)
- but >70% of dogs with PDH won’t have neurological signs
- CT can miss 56% of dogs with PDH (ie normal pituitary size)

28
Q

What’s the utilities of CT/MRI for the abdmomen?

A
  • can identify adrenal incidentaloma (most are non-function, benign)
  • CT/MRI are both good –> assess vascular invasion, tissue invasion, metastasis
29
Q

What’s the utilities of urine cortisol to creatinine ratio (UCCR) test for dogs suspected of having HAC?

A
  • high sensitivity, low specificity
  • good for ruling out HAC
  • if >100 (normal <10), 90% = PDH
30
Q

What’s the utilities of ACTH stim for dogs suspected of having HAC?

A
  • only test to differentiate between true HAC vs iatrogenic HAC
  • less affected by non-adrenal illness
  • does not differentiate between PDH or FAT
  • has 60% sensitivity for FAT, 85% sensitivity for PDH, with overall specificity of 85-90%
  • may be good for dogs with atypical / occult Cushing’s
31
Q

What’s the utilities of low dose dexamethasone suppression test (LDDST) for dogs suspected of having HAC?

A
  • it’s the test of choice
  • sensitivity 90-95% of PDH, virtually 100% for FAT
  • specificity is only 40-50%, esp if patient has non-adrenal illness
  • pre, 4 and 8h post samples
  • if escaped pattern “V” pattern noted at 4th hour = PDH
  • if less than 50% of baseline $ 4h = PDH
  • failure to suppress but >50% of baseline = HAC, but can’t differentiate between PDH and FAT
32
Q

How does UCCR/LDDST combo work?

A

The owner collects urine for 2 consecutive days as baseline @ 8am
- after the 2nd collection, give dexamethasone 0.01mg/kg PO
- collect urine again @ 2 & 4pm
- dogs with HAC would not suppress

33
Q

What are the 3 criteria to qualify for PDH wit LDDST?

A
  1. 4h cortisol < 1.4mcg/dL
  2. 4h cortisol <50% basal
  3. 8h cortisol <50% of basal, but > 1mcg/dL
    - 65% of dogs of PDH will fit one of the 3 criteria
    - none of the dogs with FAT will fit those requirements
34
Q

What’s the utilities of high dose dexamethasone suppression test (HDDST) for dogs suspected of having HAC?

A
  • it’s good for the 10% of patients that failed to suppress on LDDST
  • if that was the case, other differentiating test, such as head imaging or endogenous ACTH test would be better than HDDST
35
Q

How does UCCR/HDDST combo work?

A
  • 3 consecutive morning urine samples
  • dexamethasone 0.1mg/kg PO q8h given right after the 2nd urine sample
  • if baseline UCCR is increased = HAC
  • if 3rd sample is <50% of baseline = PDH
36
Q

What’s the utilities of eACTH for dogs suspected of having HAC?

A
  • should only be used once HAC is confirmed to differentiate between PDH vs FAT
  • eACTH is normal or increased in PDH
  • eACTH is low in FAT or iatrogenic HAC
  • expensive and difficult to process samples
37
Q

How can AUS ddx PDH vs FAT?

A
  • PDH: both adrenal gland will be enlarged
  • however, some can be normal, some can be asymmetrical
  • FAT: usually one enlarged gland
  • examining the smaller gland thickness: <5mm = tumour, > 5mm = hyperplasia
38
Q

How is CT/MRI helpful in HAC dogs?

A
  • CT/MRI cannot replace endocrine testing
  • changes in height will be noted first (expands dorsally)
  • 50-60% of dogs with PDH can be detected on CT
  • 50% of non-neurological dogs with HAC with a pituitary mass identified on MRI
39
Q

How does mitotane work?

A

It inhibits 3-Beta-hydorxysteorid dehydrogenase (3 beta HSD), which is required to convert pregnenolone to progesterone, thus inhibiting cortisol synthesis
- it also inhibits aldosterone (minor)

40
Q

How often should trilostane be givien?

A
  • historically high dose once a day (up to 50mg/kg/day)
  • now, BID should be considered (0.5-1mg/kg BID)
  • BID may have better control and long term outcome
41
Q

How is effectiveness of trilostane monitored?

A

improved in PU and lethargy should be noted in 7-10 days
- derm issues may take longer
- ACTH stim can be done to assess treatment

42
Q

What’s the recurrence rate of trans-sphenoid hypophysecotmy?

A

25%

43
Q

What’s the risk of side effects with mitotane? What are they?

A

60%
- anorexia, weakness, vomiting, diarrhea, and lethargy

44
Q

What’s the best medical treatment for FAT?

A

trilostane

45
Q
A

Internal Medicine/ Ettinger (93 decks)

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