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SA Medicine Endocrine > Hyperadrenocorticism > Flashcards

Hyperadrenocorticism Flashcards

1
Q

HPA Axis

A
  • Remember it and make sure you can draw it out
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2
Q

Hyperadrenocorticism Definition

A
  • Constellation of clinical signs/abnormalities resulting from chronic glucocorticoid exposure
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3
Q

What is the primary cause of Cushing’s if not iatrogenic?

A
  • due to a TUMOR in either
    1. Pituitary gland (PDH)
    2. Adrenal gland(s) (ADH)
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4
Q

Iatrogenic Cushing’s

A
  • Due to exogenous exposure
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5
Q

What type of tumor is most common in dogs with Cushing’s?

A
  • Pituitary (PDH)

- 80-85% of dogs

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6
Q

Are most pituitary tumors in Cushing’s benign or malignant?

A
  • Benign
    85% are <1cm microadenomas
  • > 1 cm would be a macroadenoma
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7
Q

What breed size (small/toy vs medium/large) is more likely to have a PDH?

A
  • 75% of small and toy breeds have PDH

- <20kg

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8
Q

What percentage of dogs will have an adrenal dependent Cushing’s?

A
  • 15%
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9
Q

What is the breakdown for benign adenoma vs carcinoma in adrenal dependent Cushing’s?

A
  • 50/50 for benign adenomas vs carcinomas
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10
Q

Breed distribution for adrenal dependent hyperadrenocorticism

A
  • Affects large breed dogs more frequently (50% > 20kg)

- MORE LIKELY to have a adrenal than a shih tzu, but most common is still pituitary dependent in large breeds

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11
Q

Typical age in Cushing’s

A
  • Tend to be middle to older age
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12
Q

Typical sex in Cushing’s

A
  • Predisposition towards females
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13
Q

Most common presenting complaints in Cushing’s

A
  • PU/PD
  • Polyphagia
  • Panting
  • Dermatologic problems (e.g. alopecia)**
  • Secondary infections (e.g. UTI)
  • Respiratory
  • Musculoskeletal
  • General
  • Macroadenoma (neurologic)
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14
Q

Dermatologic Manifestations of Cushing’s

A
  • Calcinosis cutis**
  • Truncal alopecia (common signs)**
  • Symmetrical, non-pruritic unless secondary infection
  • Thin skin
  • Recurrent pyodermas
  • Adult onset demodicosis
  • Cutaneous hyperpigmentation
  • Difficulty of skin wounds to heal
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15
Q

Calcinosis Cutis

A
  • Deposits of calcium in the skin

- Firm plaques that may be ulcerated or irritated

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16
Q

What is the most common presenting complaint for hyperadrenocorticism?

A
  • PU/PD (80-91% of cases)

- May no longer be housebroken

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17
Q

What is the pathophysiology of PU/PD in Cushing’s?

A
  • Blocks action of ADH at the collecting tubules
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18
Q

What should you do with the urine sample for Cushing’s?

A
  • CULTURE THE URINE

- (1) Dilute urine and (2) Poor immune response predispose to UTI

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19
Q

What is the most common musculoskeletal complaint with Cushing’s?

A
  • > 80% of cases have abdominal distention

- Fat redistribution, increased liver size, weakness of abdominal muscles

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20
Q

Other musculoskeletal signs with Cushing’s

A
  • Generalized weakness
  • Muscle wasting (protein catabolism)
  • Collagen breakdown
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21
Q

Respiratory signs of Cushing’s

A
  • Panting (diaphragm is weakened and liver is enlarged)

- If severe dyspnea seen, suspect pulmonary thromboembolism (PTE) (hypercoagulable from the clots)

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22
Q

Other fairly common clinical signs with Cushing’s?

A
  • Polyphagia (90% or more of cases)
  • Lethargy
  • Diabetes mellitus
  • Obesity (if weight loss occurs, suspect diabetes mellitus or macroadenoma)
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23
Q

Macroadenoma signs

A
  • Neurologic signs
  • Inappetance/anorexia (most common)*
  • Dullness (most common)*
  • Disorientation
  • Circling
  • Ataxia
  • Behavior Changes
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24
Q

Common changes on CBC for Cushing’s

A
  • Stress leukogram

- Thrombocytosis (not well understood)

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25
Q

Biochemistry panel common changes for Cushing’s

A
  • Increased ALP (moderate to marked)
  • Increased ALT (mild - swollen hepatocytes swell and accumulate glycogen; crowd other cells and either cause hypoxia or bile damage )
  • Increased cholesterol (variable)
  • Elevated fasting blood glucose (mild)
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26
Q

What are the most common findings on chemistry in Cushing’s?

A
  • Increased ALP and cholesterol are most constant findings and seen in >90% of dogs with Cushing’s
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27
Q

Urinalysis changes with Cushing’s and Pathophysiology

A
  • Isothenuria (1.007-1.012 due to cortisol interfering with ADH at the distal tubules)
  • Proteinuria (due to glomerular scerlosis)
  • Urinary tract infections common (should perform culture and sensitivity even with quiet sediment)
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28
Q

Most common findings on abdominal films with Cushing’s disease

A
  • Hepatomegaly
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29
Q

Potential findings on thoracic films in patients with Cushing’s

A
  • Rarely, metastasis from adrenal adenocarcinoma
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30
Q

What tests are involved in ruling Cushing’s in or out?

A
  1. Urine cortisol to creatinine ratio
  2. ACTH stimulation test
  3. Low dose dexamethasone suppression test
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31
Q

Pros of urine cortisol/creatinine ratio

A
  • Easy to perform
  • inexpensive
  • high sensitivity (75-100%)
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32
Q

Cons of urine cortisol/creatinine ratio

A
  • Can’t be performed during hospital visit

- Not specific (<20%)

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33
Q

Urine C/C Ratio test protocol

A
  • have owner bring first morning urine as the stress of the visit to the hospital will increase cortisol
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34
Q

Interpretation of a positive UCCR test

A
  • Could be Cushing’s, but could be a number of other diseases that aren’t Cushing’s either
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35
Q

Interpretation of a negative UCCR test

A
  • Probably not Cushing’s
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36
Q

ACTH stim test principle

A
  • Evaluates maximal stimulation of adrenocortical reserve
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37
Q

Speed of ACTH stim test

A

Fast (1 hr)

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38
Q

Sensitivity of ACTH stim test

A
  • Good (60-85%)
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39
Q

Specificity of ACTH stim test

A
  • Good (85-90%)

- Less affected by non-adrenal illness

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40
Q

What is the disease that only the ACTH stim test can test for?

A
  • Iatrogenic Cushing’s
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41
Q

Price of ACTH stim test

A

Expensive

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42
Q

Can ACTH stim test differentiate between PDH and ADH?

A
  • No
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43
Q

Post cortisol value >21 µg/dL in ACTH Stim Test

A
  • generally considered diagnostic in an animal with appropriate clinical signs and no concurrent illness
  • SUPPORTIVE
44
Q

ACTH Stim test with PDH

A
  • Tumor producing high amounts of ACTH
  • Consistently high ACTH has the adrenal glands ramped up and producing more cortisol than normal dogs
  • Give ACTH: adrenal glands respond by releasing all of the cortisol that they have saved up
  • In most dogs, cortisol levels will increase beyond the reference ranges
45
Q

ACTH stim test with ADH

A
  • Adrenal tumor cells produce cortisol erratically and are not necessarily responsive to exogenous ACTH
  • Cortisol may be elevated with an adrenal tumor but a normal result does not rule out ADH
46
Q

Iatrogenic Cushing’s result

A
  • Cushing’s like signs and blood abnormalities due to administration of exogenous steroids
  • Atrophy of the adrenal glands leading to lack of endogenous steroid production
  • Inability of adrenal glands to respond to ACTH
  • Your ACTH stim test would be low
  • It should look like <2 and <2 µg/dL for both pre-and post
47
Q

Low dose Dexamethasone Suppression test Normal individual

A
  • Dexamethasone suppresses ACTH and decreases cortisol release from adrenals
48
Q

Price of LDDST

A
  • less than ACTH
49
Q

Sensitivity of LDDST

A
  • Good (90-95%)
50
Q

Specificity of LDDST

A
  • Fair (50%)

- More affected by non-adrenal illness

51
Q

Can LDDST differentiate between PDH and ADH?

A

Yes

52
Q

Length of LDDST

A
  • 8 hrs
53
Q

LDDST and Iatrogenic Cushing’s

A
  • Cannot diagnose it
54
Q

Protocol for LDDST

A
  • Check baseline cortisol
  • Administer dexamethasone
  • Check cortisol at 4 hours and 8 hours post
  • 8 hr time point is used for diagnosis of Cushing’s; 4 hr time point is used for differentiation
55
Q

Result if LDDST is >1.4µg/dL at 8 hr time point?

A
  • This is consistent with Cushing’s

- overwhelming your negative feedback

56
Q

LDDST PDH response

A
  • Tumor cells may briefly suppress in response to dexamethasone (4 hr)
  • They will then usually recover and go back to their ways and return to producing large amounts of ACTH (8 hours)
  • This is called an escape
57
Q

ACTH stim and LDDST diagrams *(Just a reminder, not an actual flash card)

A
  • This is your reminder to look at the diagrams for the tests because they are quite helpful!
58
Q

LDDST ADH response

A
  • Producing cortisol erratically independent of pituitary
  • High amount of cortisol produced by the tumor causes negative feedback on the pituitary thus little ACTH is produced
  • Cortisol will stay high with no suppression at any time point
59
Q

LDDST Interpretation with suppression 4 hrs and escape at 8 hrs?

A
  • Diagnostic for PDH

- 65% of dogs with PDH will show this pattern

60
Q

LDDST Interpretation with lack of suppression at 4 hrs

A
  • Does not differentiate between PDH and ADH

- Need further differentiating tests

61
Q

HDDST (High Dose Dexamethasone Suppression) Procedure

A
  • Same as LDDST only with a higher dexamethasone dose
62
Q

Purpose of HDDST

A
  • More likely to show the suppression and escape pattern for PDH than LDDST
  • Still need LDDST as a screening test
63
Q

HDDST pattern with PDH

A
  • Suppression at 4 hours and escape at 8 hrs

- 75% of PDH will show this

64
Q

HDDST pattern with ADH

A
  • Never suppress
65
Q

Interpretation of HDDST test without suppression?

A
  • Does not differentiate between PDH and ADH

- Further differentiating tests needed

66
Q

Ability of Endogenous ACTH test to diagnose:

  1. ) ADH
  2. ) PDH
A
  1. ) Can diagnose ADH

2. ) Cannot diagnose PDH

67
Q

Speed of Endogenous ACTH

A
  • Send out test - delayed results
68
Q

Endogenous ACTH Sample Handling

A
  • Special sample handling required to prevent false results
69
Q

Endogenous ACTH results with adrenal tumor

A
  • ACTH suppressed due to negative feedback so levels are low
  • Poor sample handling can lead to rapid degradation of ACTH in blood which can falsely lower
70
Q

Endogenous ACTH results with pituitary tumor

A
  • Secretion of ACTH is variable, but ACTH usually normal or high
71
Q

Further testing to support Hyperadrenocorticism

A
  • Abdominal ultrasound
72
Q

Abdominal ultrasound benefits for Cushing’s

A
  • Superior to radiographs
  • Evaluate size and shape of both adrenals
  • Helps to differentiate between PDH and adrenal tumors, as well as evaluate for metastasis
  • Evaluate liver and look for causes of cholestasis
73
Q

What imaging is recommended in cases of PDH?

A
  • CT/MRI

- Evaluate pituitary tumor and look for macroadenoma

74
Q

What imaging is recommended if owners want to pursue adrenalectomy for ADH?

A
  • Evaluate adrenal glands and tumor for surgical planning
75
Q

Cost of CT/MRI

A

$$$$$

76
Q

Differentials for Adrenal Tumor (4 main ones plus mets)

A
  • Functional adenoma - producing cortisol
  • Nonfunctional adenoma (incidentaloma)
  • Cortical adenocarcinoma (functional or not)
  • Pheochromocytoma - medullary tumor producing catecholamines
  • Other - metastasis (pulmonary, mammary, prostatic, gastric, pancreatic, carcinoma, melanoma, lymphoma, etc.)
77
Q

How can you determine of the adrenal tumor is producing cortisol?

A
  • Endogenous ACTH
  • Measures baseline levels of ACTH being produced by the pituitary gland
  • Should be quite low with ADH
78
Q

Differentiating ADH and PDH and normal dogs with endogenous ACTH

A
  • Minimal overlap between PDH and ADH
  • Significant overlap between PDH and normal
  • Minimal overlap between ADH and normal
79
Q

What are the primary categories of treatment options for PDH?

A
  1. Medical management with drugs
  2. Medical management with irradiation
  3. Surgery
80
Q

What drugs are used for treatment of PDH?

A
  1. Mitotane
  2. Trilostane
  • Selegiline and ketoconazole not recommended anymore
81
Q

What type of surgery is performed to treat PDH?

A
  • Hypophysectomy
82
Q

Mitotane overview

A
  • Chemotherapeutic agent

- Adrenolytic - destroys adrenal tissue

83
Q

Mitotane monitoring

A
  • Monitor with ACTH stim testing
84
Q

Trilostane overview

A
  • Synthetic steroid analog and enzyme inhibitor that prevents formation of cortisol
85
Q

Reversibility of trilostane vs mitotane

A
  • Trilostane is reversible with dose dependent side effects

- Mitotane is not reversible

86
Q

Monitoring for trilostane

A
  • Monitor with ACTH stim testing and electrolytes
87
Q

Radiation for PDH duration of effectiveness

A
  • variable
88
Q

Radiation for PDH onset of effect

A
  • can take awhile

- up to months

89
Q

Radiation for PDH Cost

A
  • Expensive

- 3 weeks ~$3500

90
Q

Radiation for PDH Availability

A

Limited

91
Q

Surgery for PDH

A
  • Hypophysectomy (removing the pituitary)
92
Q

What do you need to supplement if you do a hypophysectomy?

A
  • Other hormones (e.g. thyroid, vasopressin)
93
Q

Availability and cost of hypophysectomy

A
  • HIGHLY technical surgery
  • Very limited availability
  • Very expensive
94
Q

Efficacy of trilostane vs mitotane for PDH

A
  • Similar survival times (14-16 months)
  • No major difference in efficacy
  • Both drugs control clinical signs
95
Q

Adverse effects of trilostane vs mitotane for PDH

A
  • Rate of side effects and severity of side effects may be higher with mitotane
  • Mitotane up to 40%
  • Trilostane up to 63% (usually mild)
96
Q

Trilostane benefits for PDH

A
  • Generally considered more user friendly
97
Q

Mitotane benefits for PDH

A
  • Less expensive overall in most cases

- Requires less frequent dosing

98
Q

Monitoring in trilostane vs mitotane

A
  • Both require significant monitoring especially early on
99
Q

Options of treatment for ADH

A
  • Medical vs surgical
100
Q

Medical treatment for ADH

A
  • Trilostane or Mitotane

- No major difference in efficacy, and both control clinical signs

101
Q

Surgical treatment for ADH

A
  • adrenalectomy

- potential to be curative (whenever possible, they want to go in)

102
Q

Prognosis for Cushing’s: Degree of ALP elevations in terms of severity of disease or response to treatment

A
    • Does not reflect severity
103
Q

Prognosis for Cushing’s: Pituitary microadenoma

A
  • good long term prognosis
104
Q

Prognosis for Cushing’s: Pituitary macroadenoma

A
  • Poor without treatment, can be fair with effective treatment
105
Q

Prognosis for Cushing’s: Adrenal tumors

A
  • Good to poor depending on the type and treatment performed

SA Medicine Endocrine (8 decks)

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