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clinical pathology > Endocrine: Adrenal Glands > Flashcards

Endocrine: Adrenal Glands Flashcards

1
Q

What are the 3 layers of the adrenal cortex and what do they produce? What does the medulla produce?

A
  1. zona glomerulosa - RAAS produces aldosterone, which causes the retention of Na+ in exchange for K+ and H+
  2. zona fasciculata - glucocorticoids
  3. zona reticularis - androgens and estrogens

epinephrine and norepinephrine

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2
Q

What hormone from the pituitary affects the adrenal glands? What 4 reactions is it responsible for?

A

ACHT = cortisol secretion

  1. fat redistribution
  2. protein catabolism
  3. gluconeogenesis and insulin antagonism
  4. anti-inflammatory or immunosuppression
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3
Q

What is the hypothalamic-pituitary-adrenal axis?

A

corticotropin-releasing hormone (CRH) from the hypothalamus causes the pituitary to secrete ACTH, which acts on the adrenal gland, causing cortisol release from the zona fasciulata

  • high cortisol levels have a negative feedback on CRH and ACTH production
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4
Q

What is canine hyperadrenocorticism? What are the 3 forms?

A

Cushing’s —> persistent cortisol secretion in episodic exaggeration secretion or mild continuously increased secretion

  1. pituitary-dependent hyperadrenocorticism (85%)
  2. functional adrenal tumors (15%)
  3. iatrogenic
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5
Q

How do pituitary tumors cause hyperadrenocorticism?

A

bilateral adrenal hypertrophy increases production and secretion of cortisol

  • negative feedback works on the hypothalamus, but the pituitary continues secreted ACTH
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6
Q

How do adrenocortical tumors cause hyperadrenocorticism?

A

adrenal tumor itself produces constant cortisol and the contralateral gland becomes atrophied

  • constant negative feedback occurs, resulting in only a small amount of ACTH to be secreted
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7
Q

What causes iatrogenic hyperadrenocorticism?

A

long-term glucocorticoid therapy causes constant negative feedback, with only a small amount of ACTH to be produced and results in 2 atrophied glands

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8
Q

What are the 5 most common breeds affected by canine hyperadrenocorticism?

A
  1. Poodles
  2. German Shepherds
  3. Dachshunds
  4. Labs
  5. Terriers
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9
Q

What age is most affected by canine hyperadrenocorticism? What are the most common clinical signs?

A

middle-aged to older, uncommon in those <6 y/o (slowly progressive)

  • PU/PD
  • polyphagia
  • potbellied appearance/pendulous abdomen due to hepatomegaly and decreased abdominal muscle strength
  • muscle weakness
  • alopecia +/- calcinosis cutis
  • pruritus
  • thin skin with hyperpigmentation, pyoderma, and seborrhea
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10
Q

What 3 signs on CBC indicate canine hyperadrenocorticism?

A
  1. mild erythrocytosis
  2. STRESS LEUKOGRAM: neutrophilia, lymphopenia, monocytosis, eosinopenia
  3. thrombocytosis
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11
Q

What are the 3 most important indications on biochemical profiles of canine hyperadrenocorticism? What else is seen?

A
  1. increased ALP
  2. increased ALT
  3. increased cholesterol
  • increased fasting glucose (glucocorticoids induce insulin resistance, causing increased insulin with normal to increased glucose)
  • normal to increased insulin
  • abnormal bile acids
  • decreased BUN
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12
Q

What are the 2 most common findings on urinalysis in canine hyperadrenocorticism?

A
  1. low USG (1.004-1.020)
  2. UTI with or without neutrophils - increased risk to pyelonephritis and renal failure
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13
Q

Why is it important to differentiate pituitary-dependent and primary adrenal tumors causes of hyperadrenocorticism?

A

treatment is different for each:

  • pituitary-dependent HAC = medically managed
  • adrenal tumors = Sx
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14
Q

How are screening, confirmatory/diagnostic, and differentiating tests used in diagnosing hyperadrenocorticism?

A

SCREENING = identifies animals that POTENTIALLY have a disease for further assessment with more specific tests

C/D = used in animals with positive screening tests to differentiate between animals with disease and those that have other diseases with similar clinical signs/lab results

DIFF = discriminates between pituitary-dependent HAC and adrenal tumors

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15
Q

What screening, confirmatory/diagnostic, and differentiating tests are used to diagnose hyperadrenocorticism?

A

SCREENING = ALP activity, urine cortisol:creatinine ratio

C/D = low dose dexamethasone suppression test*, ACTH stimulation test

DIFF = low dose dexamethasone suppression test, endogenous ACTH measurement, imaging, high dose dexamethasone suppression test

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16
Q

How are ALP levels used to screen for hyperadrenocorticism? What are 2 problems associated?

A

ALP is frequently high in HAC (>90%), so dogs with high sALP are moved along for further testing, since dogs with normal ALP are highly unlikely of having HAC

  1. exogenous glucocorticoids increase ALP
  2. non-adrenal diseases may also cause ALP increases
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17
Q

How does urine cortisol:creatinine ration screen for hyperadrenocorticism? What is a major problem associated?

A

high sensitivity, low specificity - HAC is unlikely in dogs with normal UCCR, so HAC can be ruled out

increased value is NOT specific for HAC, since the ratio can be increased in stressed dogs with non-adrenal disease

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18
Q

How should healthy dogs react to low dose dexamethasone suppression test?

A
  • inject synthetic glucocorticoid
  • this causes negative feedback on the pituitary, resulting in less secretion of ACTH
  • less ACTH = less cortisol and serum cortisol levels should decrease
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19
Q

How do dogs with hyperadrenocorticism react to low dose dexamethasone suppression test?

A

PITUITARY TUMOR = autonomous secretion of ACTH results in maintenance of cortisol production despite glucocorticoid (may be suppressed with testing)

ADRENAL TUMOR = autonomous secretion of cortisol and will NEVER be suppressed

20
Q

What is the protocol for low dose dexamethasone suppression tests?

A
  • take baseline blood sample for cortisol
  • inject 0.01 mg/kg of dexamethasone
  • obtain samples at 4 hr and 8 hr post-injection
21
Q

What are the expected results for healthy dogs and those with hyperadrenocorticism following low dose dexamethasone suppression?

A

HEALTHY - adrenal cortisol secretion will be decreased

HAC - >90% of the time, cortisol secretion will not be decreased

22
Q

What is a pro and con to low dose dexamethasone suppression?

A

PRO - can distinguish between adrenal and pituitary origin

CON - takes 8 hrs to perform

23
Q

What are the 2 major ways to interpret low dose dexamethasone suppression?

A
  1. 8 hr result = CONFIRMATORY —> decreased = normal; increased = HAC
  2. 4 hr result = DIFFERENTIATING —> increased = PDH or AT, further testing needed; decreased = PDH (no further testing needed)
24
Q

LDDST, 8 hr result:

A
  • normal dogs = suppression
  • HAC dogs = no suppression
25
Q

How should a healthy dog respond to ACTH stimulation test? How is it done?

A

increased adrenal cortisol secretion causes an increase in serum cortisol

  • obtain baseline plasma cortisol
  • inject 0.25 mg/kg of synthetic ACTH or 2.2 IU/kg of ACTH gel
  • measure plasma cortisol 1 hr post-administration
26
Q

What are the pros and cons to using the ACTH stimulation test?

A

PROS - quick, economical, easy to perform, only test that identified iatrogenic HAC, if used in patients with concurrent non-adrenal disease, it is less likely to be positive

CONS - does not differentiate between PDH and AT

27
Q

How do normal dogs, those with HAC (PDH, AT), and iatrogenic HAC react to the ACTH stimulation test?

A

NORMAL - predictable range of serum cortisol secretion (4-20)

HAC - ACTH = hypersecretion of cortisol (>20)

IATROGENIC = flat line, no change between pre and post ACTH administration

28
Q

When does PDH suppression at 4 hours with low dose dexamethasone suppression occur?

A

(if you’re lucky!)

  • cortisol in <50% baseline value
  • cortisol is less than <1.5 µg/dL
29
Q

How does high dose dexamethasone suppression test compare to LDDST? What is it best at differentiating?

A

same as LDDST, but uses a higher dose of dexamethasone

pituitary HAC is more likely to suppress with high doses of dexamethasone

30
Q

How should the results of HDDST be interpreted?

A
  • 8 hr sample < cut off = pituitary HAC
  • 8 hr sample > cut off = pituitary or adrenal HAC
  • 4 hr sample < cut off = more consistent with pituitary HAC than adrenal HAC
31
Q

About 30% of dogs with pituitary tumors do not suppress with either LDDST or HDDST. What should be done in these cases?

A

measure ACTH or pursue diagnostic imaging

32
Q

How do PDH and AT HAC compare when measuring endogenous ACTH concentration?

A

PDH = intermittently or constantly secrete ACTH = normal or increased ACTH

AT = secrete cortisol independent of ACTH = negative feedback of cortisol on pituitary causes a decreased in ACTH

33
Q

How does iatrogenic hyperadrenocorticism affect the adrenal glands? What are the 3 expected results?

A

bilaterally small adrenals due to negative feedback of the administered corticosteroids on ACTH secretion

  1. baseline cortisol is decreased
  2. minimal to no response on ACTH stimulation
  3. endogenous ACTH is decreased
34
Q

What is the most common signalment for Addison’s disease? What breeds have an increased risk?

A

young to middle-aged (>5 y/o) mixed breed female dogs

  • Great Danes
  • Poodles
  • WHWT
35
Q

What are the 2 types of Addison’s disease?

A
  1. PRIMARY = immune-mediated destruction of adrenal cortices*
  2. SECONDARY = destructive lesions in hypothalamus or pituitary results in less ARH or ACTH
36
Q

What 2 hormones are decreased in Addison’s disease? What do clinical signs correlate?

A
  1. aldosterone
  2. cortisol

lack of aldosterone

37
Q

What is an Addisonian crisis?

A

excessive Na+ excretion and K+ retention due to decreased aldosterone causes hyponatremia, resulting in hypovolemia, hypotension, and pre-renal azotemia

38
Q

What are the most common clinical signs in canine hypoadrenocorticism?

A
  • poor appetite/anorexia
  • lethargy/depression
  • vomiting/regurgitation
  • weakness, dehydration
  • shock, collapse
  • bradycardia, weak femoral pulse
  • melena
  • hypothermia
  • painful abdomen
39
Q

What are 2 common findings on CBC due to canine hypoadrenocorticism? What happens following an Addisonian crisis?

A
  1. mild to moderate non-regenerative anemia
  2. erythrocytosis and increased PCV due to dehydration

rehydration can dilute RBCs to life-threatening levels

40
Q

What finding is unique on the leukogram in an Addisonian dog?

A

lack of a stress leukogram

  • sick and stressed animals are expected
41
Q

What are the 3 most common findings on biochemistry with canine hypoadrenocorticism?

A
  1. pre-renal azotemia
  2. increased BUN due to dehydration and GI hemorrhage
  3. hypoglycemia* - resolves within 24-48 hours of glucocorticoid and dextrose treatment
42
Q

What electrolytes should be examined if canine hypoadrenocorticism is suspected? What do they evaluate?

A

EVALUATES ALDOSTERONE —> hyponatremia, hyperkalemia: serum Na:K ration < 27 is suggestive

  • not specific to Addison’s: acute renal failure, pyometra, pyoderma, bacterial pneumonia, parasitism
43
Q

What is the test of choice for diagnosing canine hypoadrenocorticism? What does is evaluate? What result is expected in Addisonian dogs?

A

ACTH stimulation test —> cortisol (plasma ACTH is too variable and unhelpful)

since adrenal cortex is atrophied, there should be no response in cortisol production in response to the synthetic ACTH

44
Q

How is the ACTH stimulation test done? What is diagnostic for Addison’s disease?

A
  • collect baseline cortisol levels
  • inject synthetic ACTH
  • collect cortisol levels 1 hr (dogs) or 30 mins (cats) post-injection

1 hr cortisol < 1.8 µg/dL

45
Q

Hyperadrenocorticism and hypoadrenocorticism responses to diagnostic tests:

A

clinical pathology (33 decks)

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