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3. Sys Path 2 > ENDOCRINOLOGY- The pituitary-adrenal axis > Flashcards

ENDOCRINOLOGY- The pituitary-adrenal axis Flashcards

1
Q

screening vs confirmatory test sn, sp
- examples for hyperadrenocorticism

A

Screening:
High sensitivity at the expense of specificity
> i.e. steroid-induced ALP for hyperadrenocorticism
<><>
Confirmatory tests:
High specificity at the expense of sensitivity
> i.e. ACTH stimulation test for hypoadrenocorticism

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2
Q

precision vs accuracy

A
  • precise means all at the same spot, but may not reflect reality
  • accurate means it is close to the true value
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3
Q

endocrine assays coefficient of variation
- how accurate and precise?

A

Endocrine assays generally have a coefficient of variation (CV) of 10 –15% = not necessarily very precise or accurate (CV = SD/mean x 100)

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4
Q

Recommendations to maximize test performance:

A

i. Use the same laboratory for all your endocrine assays.
ii. Submit 0, 4 and 8 hour samples together to the same lab.
iii. Adhere to laboratory guidelines for sample preparation.

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5
Q

what evidence do we need to diagnose an endocrine disorder? one test?

A

Weight of evidence:
Expert scientific judgment to assess, review and integrate all of the results to form a meaningful conclusion.
- A single test is often insufficient to diagnose a lifelong endocrine disorder.

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6
Q

Common veterinary pituitary and adrenal endocrine diseases

A
  • Canine hyperadrenocorticism
  • Canine hypoadrenocorticism
  • (Equine hyperadrenocorticism = pars pituitary intermedia dysfunction=PPID)
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7
Q

Corticotropin (adrenocortico- trophic hormone, ACTH)
- action
- control

A
  • Action: Stimulation of adrenal steroid synthesis and secretion
  • Control: Serum cortisol, hypothalamic corticotrophin releasing hormone (CRH)
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8
Q

Thyrotropin (= thyroid stimulating hormone, TSH)
- action
- control

A
  • Action: Stimulation of thyroxine synthesis and release
  • Control: Serum thyroxine, hypothalamic thyrotropin releasing hormone (TRH)
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9
Q

adrenal gland zones, and what they do

A
  • z. glomerulosa: aldosterone
  • z. fasciculata: Corticosteroids
  • z. reticularis: androgens
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10
Q

Canine hyperadrenocorticism
- cushings syndrome vs cushings disease

A

Terms derived from the human literature but commonly used in veterinary medicine:
<><>
Cushing’s syndrome =
- clinical and chemical abnormalities associated with chronic high cortisol concentration in blood
<><>
Cushing’s disease =
- excess cortisol secretion secondary to pituitary adenoma (human medicine)

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11
Q
  • Canine hyperadrenocorticism is generally of what origin?
  • what is a less common origin?
  • what is another possibility when we see high cortisol, and its effect on the adrenals?
A
  1. Pituitary tumor producing ACTH (~85% of dogs)
    > pituitary adenoma resulting in 2nd degree adrenal hyperplasia (overstimulation)
    > bilateral
    <><>
  2. Adrenal tumor: ~15%
    > Adrenal tumor producing cortisol
    > unilateral (generally)
    <><>
  3. Iatrogenic overdose with corticosteroids
    > Hypoplastic adrenal glands
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12
Q

diagnostic approach to endocrine disease

A
  • Endocrine diagnoses are rarely “black and white” = weight of all evidence
  • Clinical signs, history and other laboratory findings are very important.
  • Important to be confident in the diagnosis since long-term and/or drastic therapy!
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13
Q

Diagnostic approach
- what gives us clinical suspicion of hyperadrenocorticism?
> history
> physical appearance
> hematology
> biochem
> urinalysis

A

a. History: depression, PU/PD, polyphagia
b. Physical appearance: pot-bellied, thin skin, poor wound healing, hair loss
c. Hematology: “stress” leukogram
d. Biochemistry: Steroid-induced ALP, increases
in other liver enzyme activities, cholesterol
e. Urinalysis: isothenuria or low specific gravity, mild proteinuria

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14
Q

screening tests for hyperadrenocorticism

A

a. Steroid–induced ALP
b. Urinary cortisol/creatinine ratio

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15
Q

Screening tests for HAC: Steroid–induced ALP
- how does it work?
- properties? what does it tell us?

A

In dogs, corticosteroids consistently induce production of an isoenzyme of ALP, which can be readily measured in serum
* High sensitivity and low specificity
* Many non-adrenal illnesses also cause increased ALP activity
* Magnitude of increase not related to disease severity

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16
Q

Screening tests for HAC: Urinary cortisol/creatinine ratio
- how do we do it?
- rationale?
- interpretation?
- cautions?

A
  • collect morning urine sample (ideally at home)
  • measure cortisol and creatinine concentration in urine
  • calculate cortisol/creatinine ratio
    <><><>
    Rationale:
  • Dogs with hyperadrenocorticism excrete more cortisol over the course of 24 hours than healthy dogs.
  • Urine cortisol concentration is “normalized” to the urine creatinine concentration
    <><><>
    Interpretation:
  • Healthy dogs have urinary cortisol/creatinine <10x10-6
    <><>
    Caution:
    1. Sick or stressed dogs have increased urine cortisol.
    2. Not interpretable if renal disease (changes creatinine excretion).
    3. Test has high negative predictive value and good sensitivity.
    4. Should not be used alone for establishing diagnosis.
17
Q

Confirmatory tests for hyperadrenocorticism

A

a. Low dose (0.01 mg/kg) dexamethasone suppression.
b. ACTH stimulation test (Cortrosyn)

18
Q

Low dose (0.01 mg/kg) dexamethasone suppression.
- what is this test?
- rationale?
- interpretation

A

Measure plasma cortisol at 0, 3 or 4, and 8 hours.
<><><>
Rationale:
1. In healthy dogs administering a low dose of dexamethasone profoundly suppresses ACTH secretion and therefore cortisol secretion by the adrenal glands.
2. In dogs with pituitary tumors there is partial or variable suppression from exogenous dexamethasone.
3. Almost all adrenal tumors secrete cortisol autonomously and are unresponsive to exogenous dexamethasone.
<><><>
Interpretation:
1. Healthy dogs suppress to <40 nmol/L for 8 hours.
2. More than 90% of dogs with hyperadrenocorticism have >40nmol/L cortisol at 8 hours.
3. Not a reliable test for confirming HAC in cats.
(4. The cortisol concentration at 4 hours aids in distinguishing between pituitary and adrenal tumors.)

19
Q

ACTH stimulation test (Cortrosyn)
- what is this?
- rationale?
- interpretation
- cautions

A

Inject ACTH IV. Measure plasma cortisol concentration at 1 hr (dog) and at 1⁄2 hr and 1 hr (cat).
<><><>
Rationale:
- Dogs with hyperplastic adrenal glands or adrenal tumors have an exaggerated response to ACTH compared to healthy dogs.
<><><>
Interpretation
1. Healthy dogs: cortisol concentration will be between 250 and 600 nmol/L
2. About 85% of dogs with pituitary tumors have an exaggerated response (>600 nmol/L)
3. About 60% of dogs with adrenal tumors hyper-respond.
<><><>
Caution
* Some dogs with hyperadrenocorticism (~10%) will have normal test results.
* The test does not distinguish between pituitary or adrenal origin.
* Very stressed/sick dogs may also have an exaggerated response (big adrenal glands!)
* Dogs with iatrogenic disease do not respond.

20
Q

Distinguish pituitary tumor from adrenal tumor
- tests

A

a. Low dose dexamethasone suppression
b. High dose dexamethasone suppression test
c. Endogenous ACTH concentration

21
Q

Distinguish pituitary tumor from adrenal tumor
- Low dose dexamethasone suppression
> what do we do
> interpretation

A

0.01 mg/kg dexamethasone –> 0, 4, 8 hr blood samples
<><>
Interpretation
- Healthy dogs suppress endogenous cortisol production to <40 nmol/L at 4 and 8 hours.
Dogs with pituitary tumors:
1. Suppress endogenous cortisol production to <40 nmol/L at 4 hours and/or
2. Suppress to less than 50% of the baseline cortisol value at 4 hours and/or at 8 hours
3. They usually “escape” suppression at 8 hours.

22
Q

Distinguish pituitary tumor from adrenal tumor
- High dose dexamethasone suppression
> what we do
> rationale
> interpretation

A

Administer 0.1 mg/kg (or 1 mg/kg). Measure plasma cortisol concentration at 0, 4 and 8 hours.
<><><>
Rationale:
- Adrenal tumors secrete cortisol entirely independent of negative feedback mechanisms, while secretion of ACTH by pituitary tumors can be suppressed by high doses of exogenous corticosteroid.
<><><>
Interpretation:
- Healthy dogs suppress plasma cortisol levels to <40 nmol/L at 4 or 8 hours. Dogs with pituitary tumors have 4 hr cortisol <40 nmol/L, or either the 4 or 8 hour cortisol suppressed by greater than 1⁄2 the baseline concentration
- Cortisol levels are not suppressed in dogs with adrenal tumors. The majority (~70%) of dogs with pituitary tumors suppress endogenous cortisol production in response to high dose dexamethasone administration.

23
Q

Distinguish pituitary tumor from adrenal tumor
- Endogenous ACTH concentration
> what we do
> rationale
> interpretation

A

Measure ACTH (labile)
<><>
Rationale:
- Once hyperadrenocorticism is confirmed, the plasma ACTH concentration may distinguish pituitary from adrenal tumors.
<><>
Interpretation
- Healthy dogs have ACTH concentrations between 7 and 40 pmol/L.
- Dogs with pituitary tumors have normal or increased endogenous ACTH concentrations.
- Dogs with adrenal tumors have low normal or decreased endogenous ACTH concentrations.

24
Q

hyperadrenocorticism in cats
- how common? usual etiology?
- clinical presentation is related to what
- nature of the disease
- signs, lab values

A
  • Uncommon in cats, almost always due to pituitary adenoma
  • Clinical presentation most closely linked to insulin resistance and therefore diabetes mellitus
  • Fragile skin, debilitating disease
  • Hyperglycemia, glucosuria, increase ALT
25
Q

hyperadrenocorticism diagnostic steps in cats

A
  1. Dexamethasone suppression test (0.1 mg/kg): sample blood for cortisol at 0, 4, 6, and 8 hrs.
    Many cats with poorly controlled diabetes will not suppress adequately
  2. Plasma ACTH concentration: only very high values are useful
  3. Urinary cortisol/creatinine ratio: good for screening
  4. Cortrosyn injection and sample at 0, 1⁄2 and 1 hr
26
Q

Hyperadrenocorticism in horses
- nature of the disease?
- age of onset
- association
- pathogenesis

A

(Pituitary pars intermedia dysfunction = PPID)
* Common condition of aged horses
* Associated with pituitary hyperplasia and neoplasia
* Mainly over-production of pro-opiomelanocortin (POMC) = precursor to ACTH, MSH, endorphin, lipotropin, and others
* Overproduction of all peptides is associated with clinical picture
<><><>
* Lack of dopamine production by hypothalamus > hyperplasia/ hypertrophy/
neoplasm of the pars intermedia of the pituitary gland
* Neurodegenerative disease
* Clinical disease from excess PI hormones
<><>
loss of neurons from hypothalamus > decreased dopamine levels > increased growth of cells of pars intermedia (portion of pituitary gland) > increased hormone levels

27
Q

Clinical findings - PPID

A
  • Hirsutism
  • Hyperhidrosis
  • Hyperglycemia
  • Glucosuria
  • Polyuria
  • Polyphagia
  • Polydipsia
  • “pot-bellied”
28
Q

EMS and PPID have what clinical findings in horses that overlap?

A
  • abnormal fat deposits
  • hyperinsulinemia
  • (high risk of) laminitis
  • PU/PD
  • exercise intolerance
  • infertility
  • abnormal sweating
29
Q

PPID treatment

A

Pergolide = dopamine agonist

30
Q

PPID confirmatory test

A

Endogenous ACTH concentration is reasonably useful:
- Healthy horses 54 –115 pmol/L
- HAC horses 74 – 1719 pmol/L
<><>
Horses normally have higher ACTH concentration in the fall than at other times of the year.

31
Q

Hyperadrenocorticism in ferrets
- etiology? what do we see?
- Dx?

A
  • typically not associated with high cortisol concentrations or pituitary tumors
  • adrenal hyperplasia ~45%, adrenal tumors ~55%
  • classic clinical signs due to sex hormone overproduction
  • Diagnosis: imaging, measure full panel of sex hormones

3. Sys Path 2 (47 decks)

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