Endocrinology - Cushings 2

Question 1

How do you differentiate AT from PDH?

Answer 1

Diagnostic imaging, LDDST, HDDST, and endogenous ACTH concentrations

Question 2

If you have a pituitary microadenoma, what does it secrete and how will the adrenal glands look?

Answer 2

It causes bilateral adrenomegaly due to excessive ACTH

Question 3

Why is an ultrasound only a differentiating test for PDH?

Answer 3

Because adrenals with PDH can be a normal size

Question 4

What do functional adrenal tumors do?

Answer 4

They secrete cortisol independent of pituitary control

Question 5

Why is CT/MRI not a reliable differentiating test between FAT and PDH?

Answer 5

It can find a macroadenoma, but cannot differentiate all microadenomas from normal so it is not a reliable differentiating test

Question 6

How do dogs react to a HDDST if they have a FAT?

Answer 6

There is not cortisol suppression

Question 7

How do dogs react to a HDDST if they have PDH?

Answer 7

75% of dogs with PDH will suppress it at the 4 and/or 8 hour measurement

Question 8

What is the disadvantage to a HDDST test?

Answer 8

It can never confirm the presence of a FAT

Question 9

How do dogs with PDH react to endogenous ACTH?

Answer 9

They should have elevated ACTH levels

Question 10

How do dogs with FAT react to endogenous ACTH?

Answer 10

They should have decreased levels due to negative feedback

Question 11

How do you treat an adrenal tumor?

Answer 11

Surgery

Question 12

What complications are associated with removal of an adrenal tumor?

Answer 12

Hemorrhage, thromboembolism, pancreatitis, arrhythmias, and hypoadrenocorticism

Question 13

How do you medically treat PDH?

Answer 13

Trilostane (FDA approved) or Mitotane

Question 14

How does Trilostane work?

Answer 14

It blocks the steriodogenesis pathway therefore inhibits cortisol production

Question 15

What is the recommended dosage of Trilostane?

Answer 15

1 mg/kg BID PO - Low dose protocol

Question 16

What adverse effects are associate with Trilostane?

Answer 16

Possible adrenal necrosis, vomiting, diarrhea, hyperkalemia, and Addison’s disease

Question 17

Trilstane is effective in ______% of patients.

Answer 17

> 90% .

Question 18

How quickly will PU/PD/PP improve once Trilostane is started?

Answer 18

within 4 weeks

Question 19

How quickly will skin improve once Trilostane has been started?

Answer 19

within 3 months

Question 20

How do you monitor effectiveness of Trilostane? When should you?

Answer 20

Via ACTH stimulation 4-6 hours post pill administration

Question 21

After you start Trilostane, when should you do your first ACTH stimulation and why?

Answer 21

At 10-14 days to make sure the patient isn’t Addisonian - don’t change dose unless cortisol is too low

Question 22

After the initial ACTH stim, when do you want to do the next ones?

Answer 22

At 30 days, then every 10-14 days until controlled, and then at 30 days, 90 days, and every 3 months thereafter

Question 23

What is the goal level for ACTH stimulation in patients treating for Trilostane?

Answer 23

To have the pre and post ACTH cortisol concentration between 1 and 5 micrograms/dl

Question 24

What is the prognosis for dogs with Trilostane therapy?

Answer 24

Good - median survival with PDH is almost 2 years, and with AT is around 14 months

Question 25

What type of drug is Mitotane and what does it do?

Answer 25

It is an adrenocorticolytic that causes Zona fasciculata and reticularis necrosis

Question 26

When do you want to do a recheck for a patient that has begun Mitotane therapy?

Answer 26

Recheck in 8 days or when appetitie decreases

Question 27

What should be done at the recheck appointment in a patient that is getting Mitotane therapy?

Answer 27

Perform an ACTH stimulation test and repeat every 7-10 days until adequate suppression

Question 28

What are the potential adverse effects associated with Mitotane therapy?

Answer 28

Vomiting, diarrhea, inappetance, lethargym depression, adrenocorticol necrosis, and unmask concurrent diseases such as allergies, arthritis, and UTIs

Question 29

What are the non-medical options for PDH treatment?

Answer 29

Surgical removal of pituitary mass, radiation therapy, and a bilateral adrenalectomy

Question 30

What are the major complications of not treating hyperadrenocorticism?

Answer 30

Hypertension, hypercoagulability, calcium oxalate urinary stones, gallbladder mucocele, and infections

Question 31

What is secondary adrenocortical insufficiency also known as?

Answer 31

Iatrogenic Cushing’s

Question 32

What is iatrogenic Cushing’s?

Answer 32

Glucocorticoid therapy resulting in clinical HAC due to suppression of the HPA axis

Question 33

What clinical signs are associated with Iatrogenic Cushing’s?

Answer 33

PU/PD, polyphagia, panting, cutaneous changes, and labwork consistent with HAC

Question 34

What happens when the glucocorticoids suppress the HPA axis?

Answer 34

They decrease CRH release from the hypothalamus, decrease ACTH release from the pituitary, and cause atrophy of the zona fasciculata

Question 35

What determines the effectiveness of glucocorticoids?

Answer 35

Relative potency, formulation, dose, and duration

Question 36

If you remove glucocorticoids in an iatrogenic Cushing’s patient, what clinical signs may they show?

Answer 36

Signs similar to atypical adrenocortical insufficiency - collapse, weakness, and depression

Question 37

True or False: There are electrolyte disturbances in patients with iatrogenic HAC.

Answer 37

FALSE

Question 38

How do you diagnose iatrogenic HAC?

Answer 38

History of glucocorticoid administration, physical findings, and ACTH stimulation test

Question 39

What will an ACTH stimulation test show in patients with iatrogenic HAC?

Answer 39

a suppressed adrenal response similar to primary hypoadrenocorticism

Question 40

How do you treat iatrogenic HAC?

Answer 40

Remove the source of glucocorticoid but make sure to taper the dose if a patient has been on glucocorticoids for a long period