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ACVIM: SAIM Specialty boards study 2023 > Endocrine: Hyper and hypoadrenocorticism, adrenal tumors > Flashcards

Endocrine: Hyper and hypoadrenocorticism, adrenal tumors Flashcards

1
Q

Name 4 stimulators of hypothalamic corticotropin-releasing hormone (CRH) release

A

Inflammatory cytokines (IL-1, IL-6, TNFalpha), leptin, dopamine, angiotensin II

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2
Q

What is the precursor molecule to ACTH?

A

Pro-opiomelanocortin (POMC)

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3
Q

Synthesis of most adrenal steroids is mediated by what enzymes?

A

Cytochrome P450 oxygenase enzymes

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4
Q

Where in the adrenal gland are mineralocorticoids formed?

A

Outer zona glomerulosa

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5
Q

Where in the adrenal gland are glucocorticoids formed?

A

The middle zona fasciculata and the inner zona reticularis

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6
Q

What enzyme is deficient in the outer zona glomerulosa, causing this region to be unable to synthesize glucocorticoids?

A

17-alpha-hydroxylase

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7
Q

80-85% of dogs with HAC have what form of the disease?

A

PDH

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8
Q

Where in the pituitary gland do tumors causing PDH arise?

A

70% - Pars distalis
30% - Pars intermedia

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9
Q

Ectopic ACTH secretion can occur from what tissues?

A

Carcinomas - small cell lung carcinoma most common in humans, pancreatic carcinoma described in a GSD

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10
Q

What are the effects of glucocorticoids on protein and lipid metabolism?

A

Protein catabolic, lipolytic

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11
Q

Why do glucocorticoids lead to polyuria?

A
  • Increased GFR
  • Inhibition of ADH at the renal tubular level, leading to a decrease in water reabsorption
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12
Q

Why do glucocorticoids lead to panting?

A
  • Decreased pulmonary compliance
  • Respiratory muscle weakness
  • Direct effects of cortisol on the respiratory center
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13
Q

What cranial nerve can be affected by HAC?

A

Unilateral or bilateral facial nerve paralysis can occur

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14
Q

Describe Cushing’s pseudomyotonia

A

A myopathy characterized by persistent, active muscle contraction after cessation of voluntary effort - usually affects the pelvic limbs and causes a stiff gait

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15
Q

How is Cushing’s pseudomyotonia diagnosed?

A
  • Electromyography - myotonic, bizarre and high frequency discharges are noted
  • Biopsy: non-inflammatory, degenerative myopathy
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16
Q

Describe how calcinosis cutis forms

A

Cortisol leads to the rearrangement of molecular protein structures and formation of an organic matrix that attracts and binds calcium, forming apatite crystals in the skin

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17
Q

What are the effects of HAC in intact dogs? Why?

A
  • Testicular atrophy and anestrus
  • Cortisol’s negative feedback to the pituitary gland leads to decreased synthesis and secretion of LH and FSH
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18
Q

Describe why a stress leukogram forms

A
  • Lymphopenia due to steroid lympholysis
  • Eosinopenia due to bone marrow sequestration
  • Neutrophilia/monocytosis due to steroid-enhanced capillary demargination
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19
Q

How do glucocorticoids lead to hyperglycemia?

A
  • Increase hepatic gluconeogenesis
  • Interfere with insulin at the cellular level (receptor defects)
  • Suppress gene expression of insulin signal molecules in the cell (post-receptor defects)
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20
Q

A pituitary tumor of what size is considered a macroadenoma?

A

> 1cm

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21
Q

What is the sensitivity and specificity of UCCR? What is it useful for?

A
  • Sensitivity is nearly 100%, but specificity is terrible (20-77%)
  • Great for ruling OUT HAC (normal result makes HAC very unlikely), but further testing is warranted if it is normal
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22
Q

To avoid the effects of stress, when should a UCCR be collected?

A

At home, at least 2 days after a vet visit or other stressful event

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23
Q

What is the test of choice for identifying iatrogenic Cushing’s? What would the result look like?

A

ACTH stimulation test - there would be no response (stimulation) to ACTH, resulting in a low concentration of cortisol pre and post

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24
Q

Dogs with naturally occurring HAC may have what response to an ACTH stimulation test?

A

A normal or exaggerated response

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25
Q

What is the sensitivity and specificity of an ACTH stimulation test for diagnosing HAC?

A
  • Sensitivity: 85% for PDH but only 60% for FAT
  • Specificity: 90%
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26
Q

What is the sensitivity and specificity of LDDST for diagnosing HAC?

A

Sensitivity 90-95%
Specificity as low as 40-50% in populations with non-adrenal illness - do no test ill dogs and do not diagnose based solely on LDDST

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27
Q

What drug can interfere with a LDDST?

A

Phenobarbital

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28
Q

What pattern on a LDDST is consistent with PDH? How often does this occur?

A
  • A “V” pattern - suppression at 4 hours with a higher cortisol concentration at 8 hours confirms PDH
  • Serum cortisol concentration at 4 or 8 hours that has decreased to <50% of baseline but is still >1mcg/dL is also most likely PDH
  • 65% of dogs with PDH will have one of these findings
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29
Q

How can the HDDST be used to discriminate PDH from FAT?

A

High doses of dexamethasone can overcome resistance to suppression in most PDH cases, but FAT cases will still fail to suppress
- If cortisol drops to <1.4, it’s diagnostic for PDH
- BUT 35% of PDH will still fail to suppress, so failure to suppress is not diagnostic for FAT

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30
Q

What is a potential side effect of both trilostane and mitotane on the pituitary gland?

A

Both decrease plasma cortisol => increased ACTH secretion, which can enhance pituitary tumor growth

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31
Q

What is the mechanism of action of trilostane?

A
  • Synthetic steroid analogue
  • Acts as a competitive inhibitor of the enzyme 3-beta-hydroxysteroid dehydrogenase (3-beta-HSD), which catalyzes the conversion of pregnenolone to progesterone
  • Blocks synthesis of cortisol and to a lesser extent aldosterone
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32
Q

When monitoring trilostane therapy, what time should an ACTH stimulation test be performed?

A

Peak: 2-3 hours post-pill
Trough: just before the next dose

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33
Q

Should mitotane be given with or without food?

A

With - fat soluble drug

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34
Q

Cats with adrenocortical tumors secreting what hormone may mimic signs of HAC?

A

Progesterone

35
Q

Unlike dogs, cats with HAC do not exhibit what clinical signs?

A

PU/PD - unless diabetic or CKD

36
Q

What Na:K ratios can be used for ruling out hypoadrenocorticism or raising suspicion for it?

A

<24 = hypoadrenocorticism is likely
>27 or 28 = hypoadrenocorticism is very unlikely

37
Q

Why do 60% of dogs with hypoadrenocorticism display a metabolic acidosis?

A

Aldosterone facilitates urine H+ ion excretion

38
Q

When monitoring DOCP, Na and K should be checked 14 days after administration. If the Na:K ratio is above 32 at day 14, what can be done at the next administration?

A

Reduce dose by 10%

39
Q

When monitoring DOCP, if the Na:K ratio is above 32 at day 25, what can be done?

A

Wait at least 5 days to give the next injection

40
Q

What other pituitary hormone can be increased in dogs with untreated hypoadrenocorticism? How long does it take to normalize after treatment?

A

TSH - can take up to 4 months to normalize
Careful when diagnosing hypothyroidism in new Addisonians

41
Q

In one study, what was the median duration of action of DOCP and how frequently did dogs require dosing?

A

Median duration: 62 days
Median dosing interval: 58 days

42
Q

How does age impact DOCP dosing?

A

Young animals and growing animals require higher doses of DOCP compared to older dogs

43
Q

The labeled starting dose of DOCP is 2.2mg/kg. In one study, what dose could be used instead?

A

One study: A starting dose of 1.5mg/kg was effective in the majority of dogs. Many dogs needed lower doses (1.1mg/kg median) to maintain an injection interval of 28-30 days
Another study: 1.1mg/kg was effective

44
Q

Describe the urine electrolyte changes in dogs with hypoadrenocorticism

A

Urine Na:K ratio is twofold higher, median fractional excretion of sodium is fourfold greater compared to controls

However, too much overlap exists with controls to be diagnostically useful

45
Q

What UCCR cut off value yielded a 100% sensitivity and 97% specificity for diagnosing hypoadrenocorticism?

A

<1.4 in the Italian study

46
Q

Describe changes in calcium homeostasis in dogs with HAC

A

Dogs with HAC had increased urinary fractional excretion of Ca, higher serum PTH concentrations, but no change in iCa or calcitriol

47
Q

What percent of dogs develop systemic hypertension during the first year of treatment for HAC, despite control of clinical signs?

A

1/3 - always check a BP on HAC dogs

48
Q

What dose of cosyntropin is needed for the diagnosis of HAC? For monitoring treatment?

A

For diagnosis, 5 ug/kg is still needed
For monitoring treatment or diagnosing hypoadrenocorticism, 1ug/kg can be used

49
Q

What test should not be used as a sole monitoring tool for treatment of HAC with trilostane?

A

Baseline cortisol

50
Q

Dogs with PDH and a gallbladder mucocele had higher circulating concentrations of what hormone?

A

Leptin

51
Q

What percent of dogs with HAC are hypertensive?

A

82% - 46% had severe hypertension

52
Q

Hypertension was common among HAC dogs with what other abnormalities?

A

Thrombocytosis (all dogs had hypertension)
Lower median potassium
UPC >0.5

53
Q

What percent of dogs are alive 4 weeks post-hypophysectomy? What percent are in remission from HAC?

A

91% alive
Of those, 92% in remission

54
Q

What percent of dogs developed recurrence of HAC after hypophysectomy and when?

A

27%, median of 555 days

55
Q

What predicted recurrence of HAC in dogs post-hypophysectomy?

A

Higher pituitary height/brain area ratio
Higher pre-operative UCCR

56
Q

In dogs undergoing hypophysectomy, pituitary size correlated with what?

A

Survival time and disease free fractions - prognosticator

57
Q

What percent of adrenal tumors are metastasis from other locations?

A

Dogs: 30%
Cats: 60%

58
Q

Is FNA of the adrenal glands diagnostic?

A

90-100% accurate for distinguishing between cortical and medullary origin, but cannot distinguish between benign and malignant tumors

59
Q

Odds of malignancy are increased if the greatest diameter of the adrenal tumor is larger than what?

A

> 2cm

60
Q

What stimulates aldosterone secretion?

A
  • Directly: increases in serum potassium
  • Indirectly: decreases in blood pressure, which activate RAAS => angiotensin II stimulation of aldosterone secretion
61
Q

What is primary hyperaldosteronism? How does it affect the RAAS system?

A
  • Autonomous aldosterone secretion by adrenocortical cells
  • Increased circulating aldosterone => negative feedback and suppression of renin release
62
Q

What is secondary hyperaldosteronism? What would renin levels be with this condition?

A

Increased aldosterone due to conditions that stimulate RAAS (CKD, CHF) - renin concentrations would be increased

63
Q

What are the clinical signs of feline primary hyperaldosteronism (aldosteronoma)?

A

Related to hypokalemia and hypertension - weakness, tortuous retinal vessels or detachment, heart murmur/arrhythmia due to left ventricular hypertrophy from hypertension

64
Q

Why is hypernatremia uncommon with feline primary hyperaldosteronism?

A

Aldosterone escape occurs - hypernatremia leads to volume expansion and hypertension => pressure induced natriuresis

65
Q

What is the acid/base status of patients with feline primary hyperaldosteronism?

A

Usually metabolic alkalosis - aldosterone results in hydrogen ion excretion

66
Q

Why might a progestin secreting tumor result in clinical signs similar to glucocorticoid excess?

A

Progestins may bind glucocorticoid receptors or displace cortisol from its binding protein, leading to increased serum free cortisol concentrations

67
Q

In dogs, increased serum progestins cause what changes to ACTH release and adrenal size?

A

Suppress ACTH secretion and cause adrenal atrophy (looks like exogenous glucocorticoids)

68
Q

What cells give rise to pheochromocytoma?

A

Chromaffin cells of the adrenal medulla

69
Q

What amino acid are catecholamines synthesized from?

A

Tyrosine

70
Q

What triggers release of catecholamines from the adrenal medulla?

A

Stimulation of the chromaffin cells by acetylcholine from the sympathetic nervous system

71
Q

What is the function of alpha 1 adrenergic receptors?

A

Mydriasis

72
Q

What is the function of alpha 2 adrenergic receptors?

A

Vasoconstriction, decrease in insulin and glucagon secretion, increase in urinary sphincter tone

73
Q

What is the function of beta 1 adrenergic receptors?

A

Increased heart rate and contractility

74
Q

What is the function of beta 2 adrenergic receptors?

A

Vasodilation of skeletal muscle arterioles and coronary arteries, relaxation of bronchial muscles, decreased GI motility, increase in insulin/glucagon secretion, increased lipolysis, relaxation of the detrusor

75
Q

How do pheochromocytomas induce PU/PD?

A

Catecholamines interfere with ADH release in the hypothalamus

76
Q

Are right or left sided adrenal tumors more likely to invade the caudal vena cava?

A

Right

77
Q

Which urine catecholamine test has the highest sensitivity?

A

Urine normetanephrine : creatinine ratio

78
Q

What is the mechanism of action of phenoxybenzamine?

A

Alpha-adrenergic receptor antagonist - binds irreversibly to alpha1 and alpha2-adrenergic receptors

79
Q

How long before surgical removal of a pheochromocytoma should you start pretreating a dog with phenoxybenzamine?

A

2 weeks at least

80
Q

If a patient with a pheochromocytoma is displaying tachyarrhythmias, what drug can be added to help? When should it be added?

A

Beta blocker - atenolol
Only add after phenoxybenzamine is on board, as loss of beta-adrenergic vasodilation leaves alpha-adrenergic stimulation unopposed and can cause a hypertensive crisis

81
Q

Dogs weighing <12kg should have an adrenal thickness less than what? Dogs weighting >12kg?

A

<12kg: <0.62cm
>12kg: <0.72cm

82
Q

What is critical illness-related corticosteroid insufficiency?

A

Inadequate endogenous corticosteroid activity in relation to the severity of a patient’s illness - causes increased mortality in humans

83
Q

Does the use of hydrocortisone improve outcome in patients with suspected critical illness-related corticosteroid insufficiency from septic shock?

A

No, treated patients did worse :(
- Higher mortality, took longer to respond to vasopressors and to maintain BP

ACVIM: SAIM Specialty boards study 2023 (38 decks)

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