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SA DX & TX II > Exam 4 - Hyperadrenocorticism > Flashcards

Exam 4 - Hyperadrenocorticism Flashcards

1
Q

T/F: for hypercortisolism, in regards to chronic exposure to glucocorticoids, exogenous exposure includes topical medications

A

true

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2
Q

in a normal dog, how is cortisol release controlled by the HPA axis?

A

in a normal dog, cortisol is only released when ordered by ACTH

ACTH release is determined by CRH from the hypothalamus

cortisol exerts a negative feedback on CRH (powerful) & ACTH (modest) release

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3
Q

what part of the adrenal gland releases cortisol? what do the other parts of the adrenal gland produce?

A

zona fasciculata - produces cortisol & corticosterone

adrenal cortex
1. zona glomerulosa - produces aldosterone (superficial layer - mineralocorticoids)
2. zona fasciculata - cortisol (middle)
3. zona reticularis - androgens/sex hormones (deep)

adrenal medulla - catecholamines (epinephrine & norepinephrine)

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4
Q

what are the 2 forms of spontaneous hypercortisolism? which is more common?

A
  1. pituitary-dependent hypercortisolism, MORE COMMON
  2. functional adrenal cortical tumor
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5
Q

what dogs are commonly affected by PDH?

A

mini poodles, dachshunds, beagles, bostons - middle aged to older dogs

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6
Q

what is the pathogenesis of PDH?

A

underlying cause is a secretion of ACTH by anterior pituitary tumor that is usually an adenoma & <1 cm in diameter

chronic adrenal stimulation from excessive ACTH release results in bilateral adrenal enlargement

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7
Q

what is the most common form of hypercortisolism?

A

PDH - >85% of cases, especially in small dogs

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8
Q

what is the pathogenesis of adrenal tumor hypercortisolism?

A

can either be malignant or benign tumor - 50/50 shot (malignant tumors are very aggressive)

endogenous ACTH release is very low due to negative feedback from the excessive cortisol release from the tumor

the contralateral adrenal tumor becomes atrophied

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9
Q

what dogs are affected by functional adrenal cortical tumors causing hypercortisolism?

A

<15% of cases

dogs > 20kgs - GSD predisposed

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10
Q

what is the most common clinical sign seen in animals with hypercortisolism? why do they have it?

A

PU/PD!

polyuria - due to compromised secretion of ADH & the impairment of the action of ADH on the collecting ducts

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11
Q

T/F: hypercortisolism is the most common cause of hyposthenuria

A

true

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12
Q

does a urine specific gravity > 1.030 make hypercortisolism likely or unlikely? why?

A

unlikely - there is compromised secretion of ADH & impairment of ADH/s actions on the collect ducts!

urine is often < 1.015 or hyposthenuric

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13
Q

why do we see increased thirst & hunger in animals with hypercortisolism?

A

increased thirst - secondary to the increased obligatory water loss in the urine

increased hunger - chronic glucocorticoid release stimulates the release of ghrelin from the stomach (hunger hormone) & ghrelin antagonizes insulin production from the beta cells of the endocrine pancreas

insulin antagonism results in compromised feelings of satiety & chronic hunger

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14
Q

what respiratory signs are seen in animals with hypercortisolism?

A

panting is common due to changes in pulmonary perfusion

pickwickian syndrome due to fat deposits in the thoracic cavity

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15
Q

what dermatological signs are seen in animals with hypercortisolism?

A

truncal alopecia, thinning of the dermis, secondary pyoderma, skin fragility in cats, comedomes

calcinosis cutis in dogs - classic for hypercortisolism but uncommon

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16
Q

why do we see abdominal distension in animals with hypercortisolism?

A

increased intra-abdominal fat, hepatomegaly, loss of abdominal muscle strength

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17
Q

T/F: in dogs with hypercortisolism, the lowest point of the abdomen is often the liver

A

true

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18
Q

what reproductive signs are seen in animals with hypercortisolism?

A

anestrus in females

testicular atrophy in males

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19
Q

what musculoskeletal changes are seen in animals with hypercortisolism?

A

loss of abdominal muscles causes pot belly appearance

‘barrel on sticks’

stretching of the carpal & tarsal ligaments

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20
Q

what consequences are seen as a result of hypercortisolism?

A

chronic infections - pyoderma/UTIs

poor healing post-injury or surgery

hypertension, proteinuria, pulmonary thromboembolism, decrepitude, & poor quality of life

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21
Q

what is seen upon physical exam that lends suspicion to a diagnosis of hypercortisolism?

A

old/decrepit animal

skin changes

abdominal distension/pot belly look

bruising

poor musculature & hyperextension of the ligaments especially in the carpus

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22
Q

what are the 3 reasons in which you may pursue a workup for hypercortisolism?

A
  1. owner has a complaint that suggests hypercortisolism - urinating in the house, stealing food, etc
  2. clinical impression - exam room diagnosis, patient is overtly cushingoid
  3. medical issues suggest hypercortisolism - recurrent infections (skin, uti), hypertension, proteinuria, thromboembolism, & uncontrolled diabetes mellitus with insulin resistance
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23
Q

what is the most consistent finding on biochemistry of dogs with hypercortisolism?

A

elevated ALP - almost 100%

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24
Q

what changes are often seen on CBC in animals with hypercortisolism?

A

hematocrit often increased

WBC usually elevated - classic stress leukogram

increased platelets

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25
Q

what changes are often seen on chemistry panels in animals with hypercortisolism?

A

elevated ALP, cholesterol, phosphorus (30% of cases in dogs), BUN may be low, & may have mild elevations in ALT

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26
Q

urinary tract infections are common in animals with hypercortisolism, but the sediment is often unexciting - why?

A

the urine is so dilute & the animal is immunosuppressed

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27
Q

what is commonly seen on urine analysis of patients with hypercortisolism?

A

low USG, often <1.015

UTIs are common

proteinuria is common

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28
Q

what are the steps you should take when deciding to work up a patient for hypercortisolism?

A
  1. have sound reasoning for considering this diagnosis
  2. make sure routine diagnostics support hypercortisolism & exclude other causes of clinical signs
  3. perform a confirmatory test - establish they do have it
  4. perform a differentiating test after the screening test - determine if it is PDH or an adrenal tumor
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29
Q

what 3 tests are commonly used for confirmatory tests for hypercortisolism?

A
  1. ACTH stimulation test
  2. low dose dexamethasone test
  3. urine cortisol:creatinine ratio
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30
Q

T/F: it is not uncommon to need to run 2 tests to be able to diagnose hypercortisolism

A

true

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31
Q

what are some examples of reasons you may get a false positive on an ACTH stimulation test?

A

patient has a chronic illness will have appropriate adrenal hyperplasia, so you will get an exaggerated response

patient has a severe, acute/life-threatening illness, so you will see an exaggerated response

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32
Q

what are some examples of ACTH stimulation test results in a dog with a functioning adrenal tumor?

A

can be exaggerated & consistent with a diagnosis of hypercortisolism

can be normal

can be flat line

these patients have unpredictable responses

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33
Q

what test is used regularly for monitoring patients being treated for hyperadrenocorticism?

A

ACTH stim test

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34
Q

how is an ACTH stim test done in dogs?

A

patient is fasted prior to testing

baseline sample is taken & checked for hemolysis/lipemia

1 ug/kg of cosyntropin is given IV or 5 ug/kg is given IM

collect serum sample 60 minutes after the injection

35
Q

how are ACTH stim tests interpreted?

A

normal dogs will be between 7-17 ug/dL

post-ACTH stim cortisol > 22ug/dL indicates HAC in a dog

36
Q

what are flat line results for ACTH stim tests? why may you get a flatline result for an ACTH stim test in a dog with all the signs of HAC?

A

pre & post samples are <5 ug/dL

could be iatrogenic disease or could be an adrenal tumor

37
Q

what is the preferred test for diagnosing HAC in cats? what test is not preferred?

A

LDDST

ACTH stim - not reliable!

38
Q

how is an LDDST stim test done in dogs?

A

patient is fasted prior to testing

baseline sample is taken & checked for hemolysis/lipemia - serum/plasma promptly spun & separated before refrigeration

dexamethasone injected IV - dogs 0.01 mg/kg (diluted with saline) & cats 0.1 mg/kg

collect 2nd blood sample 4 hours later

collect 3rd blood sample 8 hours later

39
Q

how should a LDDST be interpreted? what do the results indicate?

A

look at the 8 hour value first - if < 1.4 ug/dl, indicates suppression of the axis, so suppression at 8 hours indicates normal function

if > 1.4 ug/dl, indicates axis dysfunction (supports either adrenal tumor or PDH), so you need to look at the 4 hour value

if 4 hour value is < 1.4 ug/dl or <50% baseline - PDH

some tumors are transiently inhibited, but don’t assume a dog has an adrenal tumor if there is no suppression

40
Q

why may you get a false positive on a urine cortisol: creatinine ratio? how do you counteract this?

A

stress drives up result & so does non-adrenal disease

any condition that causes pu/pd will cause false results

collect morning urine at home to avoid any stressors!!

41
Q

what is the purpose of doing a urine cortisol: urine creatinine for testing for hypercortisolism? what are the benefits of using this test? what are the disadvantages?

A

amount of cortisol in the urine reflects the amount in the blood - elevated UCCR is consistent with hypercortisolism

benefits - very sensitive test with a high negative predictive value, so a normal result essentially rules it out

disadvantages - positive result is of little use because the test lacks specificity & there is not enough evidence to confirm the disease

42
Q

when would a urine cortisol: urine creatinine ratio test be an ideal test to use for a patient?

A

when you think that hypercortisolism is very unlikely & you just want to rule it out

43
Q

when are differentiating tests not necessary for patients with confirmed hypercortisolism?

A

if the patient was suppressed at 4 hours on the LDDST - this result is diagnostic for PDH

not necessary if surgery is not an option due to financial or other issues

44
Q

what is the purpose of using differentiating tests for patients with hypercortisolism?

A

you do it after a screening test has confirmed hypercortisolism - need to differentiate between an adrenal tumor & PDH

45
Q

what changes are seen on ultrasound with PDH? what about adrenal tumors? what is the disadvantage of using ultrasound as a differentiating test?

A

PDH - fairly symmetrical bilateral adrenal gland enlargement (some nodular changes may be seen)

adrenal tumor - one large gland & may not atrophied other gland, need to check for invasion into surrounding structures & mets to nodes/liver

ultrasound is highly operator & equipment dependent

46
Q

when may abdominal radiographs be beneficial as a differentiating test for hypercortisolism?

A

useful in large dogs (high risk for adrenal tumors if > 20 kg) - if access to ultrasound is limited

47
Q

T/F: calcification on abdominal radiographs of the adrenal glands indicates malignancy

A

false

48
Q

what are the benefits of using abdominal radiographs as a differentiating test for hypercortisolism?

A

may reveal an adrenal tumor

50% are calcified & visible on a lateral view

49
Q

when may you use an endogenous ACTH measurement as a differentiating test for hypercortisolism?

A

used to differentiate between adrenal tumors & PDH if the ultrasound scan is equivocal or unavailable

50
Q

what results are expected on an endogenous acth measurement for a patient with PDH?

A

elevated or normal acth levels - many dogs with PDH have results in the normal range

ongoing secretion of ACTH in a dog with hypercortisolism means PDH!!!

51
Q

what results are expected on an endogenous acth measurement for a patient with an adrenal tumor causing hypercortisolism?

A

very low to undetectable amounts of endogenous acth

52
Q

T/F: HDDST are not commonly used any more because other tests are safer & more reliable

A

true

53
Q

when may radiation therapy be useful for a patient with hypercortisolism?

A

patients with large tumors & associated neurologic issues which improves medical control but doesn’t replace it! often palliative for the pituitary

54
Q

what some concurrent issues that commonly occur alongside hypercortisolism that must be treated?

A

infections, proteinuria, & hypertension

may need to start clopidogrel to reduce the risk of pulmonary hypertension

55
Q

what is the current standard therapeutic approach for PDH? how does it work?

A

medical therapy - reduces cortisol release by the adrenal glands therefore controlling the signs of hypercortisolism, but doesn’t address the actual cause (may cause neuro signs if the pituitary tumor becomes too large)

56
Q

what is the mechanism of action of vetoryl? what is it licensed for use in?

A

reversible enzyme inhibitor - inhibits the 3b-hydroxysteroid dehydrogenase that is essential for the synthesis of cortisol from cholesterol that has some effect on aldosterone & other adrenal cortical hormones

dogs with PDH & adrenal tumors - life long dosing required

57
Q

how long does trilostane last in most dogs? how should it be given?

A

18 hours - effect is dose dependent & wears off when the drug is cleared

orally administered with food in the morning

58
Q

T/F: regular monitoring is required with trilostane therapy for achieving the desired effect

A

true

59
Q

what is the recommended dosing protocol used for trilostane?

A

2-3 mg/kg total daily starting dose - SID (unless diabetic, do BID)

round down to the nearest capsule size - dose must be adjusted to limit cortisol synthesis but not stop it entirely

60
Q

what tests are used to monitor effects of trilostane in patients with hypercortisolism?

A

ACTH stim test - started 4 hours post dosing

baseline cortisol - collect 4 hours post dosing

pre-trilostane protocol - collected immediately before the next dose is given

client questionnaire/patient assessment - no cortisol measured at all if the dog is doing well

61
Q

what recheck schedule is used for monitoring trilostane?

A

recheck visit 2 weeks after starting

recheck 2-4 weeks later

recheck 3 months later

recheck every 4-6 months long term

62
Q

what should be included in your recheck plan for cushing’s patients managed with trilostane?

A

physical exam & status updates

owner questionnaire - ask about thirst, hunger, energy levels

serum chemistry panel with lytes - first recheck & after dose increases, mostly interested in potassium (indicates suppression of aldosterone - must decrease dose)

ACTH stim test - always do one if the dog is unwell!!!

63
Q

if you have a cushing’s patient present with some issues after starting trilostane that you run an acth stimulation test on, what would a cortisol result of < 0.7 ug/dl indicate?

A

need to stop trilostane!!!!!

do not restart trilostane unless the patient has signs of cushings again

64
Q

if you have a cushing’s patient present with some issues after starting trilostane that you run an acth stimulation test on, what would a cortisol result between 0.7-2.0 ug/dl indicate?

A

need to stop trilostane for 48 hours & restart it at 50% of the previous dose

65
Q

if you have a cushing’s patient present managed with trilostane present for a recheck with no issues that you run an acth stimulation test on, what would a cortisol result between 2.0-7.0 ug/dl indicate?

A

continue your present dose

66
Q

if you have a cushing’s patient present managed with trilostane present for a recheck for signs of pu/pd that you run an acth stimulation test on, what would a cortisol result > 7.0 ug/dl indicate?

A

consider a 25-50% increase in dose if patient is showing signs of cushings

67
Q

what is the most important factor in deciding about dose adjustment in patients with hypercortisolism?

A

clinical status of the patient!!! does the patient seem cushingoid? does it seem ill?

68
Q

when presented with an ill dog managed with trilostane for cushings, what should you do after stopping trilostane?

A

check electrolytes to rule out adrenal necrosis

do an acth stim test to assess adrenal function

69
Q

what are the risks of using trilostane for managing cushingoid dogs?

A

can cause hypoadrenocorticism - either transient or permanent adrenal gland necrosis

70
Q

how do you treat a dog with transient hypocortisolemia from trilostane therapy?

A

dog will improve as soon as the drug is stopped

give pred at 0.5 mg/kg daily for 2 days

restart trilostane at a lower dose

71
Q

how do you treat a dog with permanent adrenal necrosis from trilostane therapy?

A

unexplained idiosyncratic drug reaction - dogs will need life long supplementation with pred & DOCP

72
Q

what are the mechanisms of action of ketoconazole & l-deprenyl for treating hypercortisolism?

A

ketoconazole - reversible inhibition of cholesterol synthesis (not very effective)

l-deprenyl - monoamine oxidase inhibitor, thought to affect acth release through modification of dopamine events (not effective)

73
Q

what is the mechanism of action of mitotane? what are the downfalls of using this drugs?

A

causes necrosis of the adrenal cortex, especially the zona fasciculata

has a lag period between dose administration & full effect, so you need very careful monitoring & thorough client education, side effects & overdose are common

maintenance dose is only given when adrenal function is adequately controlled

74
Q

what is the treatment of choice for adrenal tumors?

A

surgery - for adenomas & non-metastatic adenocarcinomas

75
Q

what are the risks of surgery for patients with adrenal tumors? what does management look like after surgical removal of the tumor?

A

risk of infection, thrombosis - try to control cushings with trilostane to improve morbidity

patient will be hypocortisolemic as soon as the tumor is removed!!!!! temporary steroid support is needed with a tapering dose - other gland should regain function with in 4-6 weeks

76
Q

when is medical therapy indicated for patients with adrenal tumors?

A

poor surgical candidates & dogs with metastatic disease - drug of choice is trilostane as mitotane is of little use because tumors are often quite resistant to its effects

77
Q

what is the general background of hypercortisolism in cats?

A

much less common in cats compared to dogs - strongly associated with diabetes mellitus (doesn’t have to be diabetic cat, but very likely)

most likely due to PDH but can have adrenal tumors

some cats with adrenal tumors has signs of sex hormone production - aggression, spraying, etc

78
Q

what are the clinical signs seen in cats with hypercortisolism?

A

very different than dogs - unlikely to be pu/pd unless concurrently diabetic

eats well, but not ravenous

skin issues are common - fragility is a classic finding, patchy/poor hair growth, & ventral alopecoa

79
Q

what is seen on physical exam of a cat with hypercortisolism?

A

muscle weakness, plantigrade stance due to ligament weakness, mild abdominal distension, skin changes (thin skin on ventrum, poor hair coat, skin fragility), & folded ear tips (uncommon but essentially pathognomonic!!! more often seen in iatrogenic cases)

80
Q

what lab changes are seen in cats with hypercortisolism?

A

variable hyperglycemia - often diabetic or borderline diabetic

hypercholesterolemia

rest of chemistry panel relatively normal - no increase in ALP

cbc often normal

urine often > 1.030 +/- proteinuria

81
Q

what is the dose used for LDDST in cats?

A

0.1 mg/kg IV!! dose is different than the one we give dogs

82
Q

how do we differentiate between PDH & adrenal tumors in cats causing hypercortisolism?

A

abdominal ultrasound

can also measure endogenous acth

83
Q

what treatment is used for cats with hypercortisolism?

A

often a challenge - remove adrenal in cat with an adrenal tumor

try trilostane in a cat with PDH - 10-30 mg once daily, dose adjusted based on acth stim test

radiation or hypophysectomy should be considered

SA DX & TX II (62 decks)

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