Hyperadrenocorticism

Question 1

____________ is released from the paraventricular nucleus of the hypothalamus.

Answer 1

corticotrophin-releasing hormone (CRH)

Question 2

__________ is released from the pars distalis of the anterior pituitary and is derived from proopiomelanocortin (POMC).

Answer 2

adrenocorticotrophic hormone (ACTH)

Question 3

CRH is released from the _______ nucleus of the hypothalamus.

Answer 3

paraventricular

Question 4

ACTH is released from the ______ _______ of the anterior pituitary and is derived from ___________________.

Answer 4

pars distalis; proopiomelanocortin (POMC)

Question 5

______% of HAC are pituitary dependent.

Answer 5

70-85%

Question 6

________ are the most common cause of pituitary-dependent HAC.

Answer 6

microacdenomas; macroadenomas (>1cm) = rare

Question 7

____% of HAC are adrenal-depndent.

Answer 7

15-30%

Question 8

Adrenal-dependent HAC are 50% _____ and 50% ______.

Answer 8

carcinomas, adenomas; most common in large breeds

Question 9

HAC is more common in ______ (2x more common).

Answer 9

females

Question 10

What are more common breeds to develop HAC?

Answer 10

bichon frise, schnauzer, terriers, boxers, dachshunds, poodles

Question 11

PU/PD is the most common clinical signs of HAC. cortisol –> ______ +/- central ______ ______.

Answer 11

nephrogenic, DI; 25-70% PP, 50% obese, 30-75% alopecia (follicular atrophy)

Question 12

Macroadenomas associated with pituitary dependent HAC can results in ________ signs of _________.

Answer 12

neurologic; dullness, seizures, circling, CN deficits

Question 13

Clin path findings with HAC?

Answer 13

stress leukogram (neutrophilia, eosinopenia, lymphopenia, thrombocytosis, monocytosis), elevated ALP (+/- other ELE); ALP corticosteroid-induced/glycogen accumulation

Question 14

Cortisol excess in HAC increases _______ and ________ antagonism, which leads to mild hyperglycemia in 20-60% of case. Cortisol excess also leads to increases in _______, which leads to hyperlipidemia in 50-90% cases (increased _________ and __________).

Answer 14

gluconeogenesis, insulin, lipolysis, cholesterol, triglycerides

Question 15

Dogs with HAC can also have secondary __________________ (increased ______, normal calcium, high-normal ________)

Answer 15

hyperparathyroidism, PTH, phosphorus

Question 16

HAC can result in increased _______ activity, which leads to hypertension.

Answer 16

RAAS; 30-85% cases

Question 17

Hyperlipemia (cortisol excess –> increased lipolysis) can increase risk of developing ________ and _________ __________.

Answer 17

pancreatitis, gallbladder mucoceles

Question 18

HAC can result in _______ resistance, which increases risk of developing ____________.

Answer 18

insulin, DM and DKA

Question 19

In cats, HAC is most commonly _________, with _____ being the most common complaint.

Answer 19

iatrogenic (exogenous steroids), DM; pituitary > adrenal, alopecia and fragile skin 30% cases

Question 20

LDDS has a sensitivity of _______% and specificity of _______% in dogs.

Answer 20

~95%, ~50-70%

Question 21

ACTH stim has a sensitivity of _____% and specificity of ____ in dogs

Answer 21

~90% PDH and 60% ADH; 60-90%

Question 22

UCCR (urine cortisol:creatinine ratio) is used to rule out HAC and has a sensitivity of _____% in dogs.

Answer 22

> 90%; specificity >95% for healthy dogs, but 20-25% dogs with non-adrenal illness.

Question 23

Trilostane is a synthetic steroid analogue that acts
as a competitive inhibitor of ______________, which catalyzes adrenocortical conversion of ___________ to______________.

Answer 23

3-beta-hydroxysteroid dehydrogenase (3-beta-HSD), pregnenolone, progesterone

Question 24

What protein showed promise for differentiating well-controlled from undercontrolled dogs with HAC?

Answer 24

Haptoglobin

Question 25

Trilostane can result in _______ _______ and rarely _______ ________.

Answer 25

adrenal hyperplasia, adrenal necrosis

Question 26

Risk of permanent hypoadrenocorticism with treatment of HAC is ______%

Answer 26

~5%

Question 27

MST for PDH is ________.

Answer 27

~2-3 years. trilostane may results in longer survival than mitotane

Question 28

MST for medical management of ADH is _________.

Answer 28

9-12 months. similar survival with trilostane and mitotane

Question 29

MST for surgical treatment of ADH is _______, though ______% peri-operative mortality rate.

Answer 29

2 years. 5-10%