Med I - Canine Hyperadrenocorticism

Front 1

Describe the cortisol feedback loop

Back 1

Front 2

ACTH
-secreted from where

Back 2

-pituitary

Front 3

ACTH
-secretion influenced by

Back 3

Feeding

Physiologic/environmental stress:
-Pain
-Trauma
-Pyrogens
-Cold exposure
-Surgery

Front 4

Canine cushings
-forms

Back 4

-Pituitary dependent hyperadrenocorticism
-Adrenal dependent hyperadrenocorticism

Front 5

Canine Cushing
-most common form

Back 5

-Pituitary dependent

Front 6

PDH
-mechanism of action

Back 6

-pituitary tumor overproduces ACTH

Front 7

PDH
-etiology

Back 7

-microadenoma (no CNS signs)
-macroadenoma (possible CNS signs)

Front 8

PDH
-majority of cases

Back 8

-microadenoma

Front 9

PDH
-distinguishing from ADH

Back 9

-bilateral adrenal hyperplasia due to excess ACTH not allowing for neg. feedback

Front 10

Adrenal Dependent Hyperplasia
-characterized by

Back 10

-autonomous production of cortisol (and possibly other steroids)

Front 11

ADH
-causes

Back 11

-Adenoma (benign)
-Carcinoma (malignant) --> matastasis via vena cave

Front 12

ADH
-common findings

Back 12

-unilateral adrenal hyperplasia with contralateral hypotrophy

-neg. feedback still works
--excessive cortisol production inhibiting ACTH
---contralateral adrenal hypotrophies because unneeded

Front 13

Canine Hyperadrenocorticism
-signalment

Back 13

Cushingoid dog
-10-11 yrs but can be younger
-PDH common in smaller dogs

Front 14

HAC
-clinical signs

Back 14

-feel and act well (generally)
-PU/PD****
-normal to increased appetite
-panting and restless at night
-Cushingoid body type

Front 15

Cushingoid Body Type
-describe

Back 15

-pendulous/distended abdomen (organomegaly, gravity weight on organs)
-muscle wasting
-thin coat
-multiple dermatologic lesions (thin skin, comedones)

Front 16

Cushingoid dog
-characteristic skin lesions

Back 16

-non-pruritic
-bilateral alopecia
-truncal distribution

Front 17

HAC
-reason for PU/PD

Back 17

-glucocorticoids interfere with ADH

Front 18

HAC
-reason for polyphagia

Back 18

-glucocorticoids have a direst stimulatory effect on appetite

Front 19

HAC
-associated clinical abnormalities

Back 19

-chronic, recurrent infections (urinary, respiratory, oral, skin)
-neurologic signs (anorexia, behavioral change, disorientation, blindness)
-musculoskeletal problems (poor BCS, muscle loss, cruciate rupture)
-cardiovascular effects (hypertension)
-reproductive signs

Front 20

HAC
-reproductive signs

Back 20

-androgen-dependent perianal adenoma in neutered dogs****
-dec. in testicular androgen production in males
-anestrus in females

Front 21

HAC
-minimum data base

Back 21

CBC
-stress leukogram
-marked thrombocytosis

Serum chemistry
-Elevated liver enzymes (ALP>ALT)
-Hypercholesterolemia
-Hyperglycemia

Urinalysis
-Low urine specific gravity <1.020
-Proteinuria

Urine culture - recommended
Blood Pressure - recommended

Front 22

HAC
-reason for stress leukogram

Back 22

-circulating cortisol

Front 23

HAC
-reason for elevated ALP

Back 23

-glucocorticoid induced isoenzyme (dog)

Front 24

HAC
-reason for elevated ALT

Back 24

-hepatic necrosis
-glycogen accumulation in hepatocytes

Front 25

HAC
-why is low urine specific gravity very common?

Back 25

-cortisol produces a nephrogenic diabetes insipidus

Front 26

HAC
-why should a urine culture be performed regardless of urine sediment?

Back 26

-immunosuppression from cortisol --> inactive sediment with active infection
-cystic calculi from inc. in calcium excretion

Front 27

HAC
-common blood pressure finding

Back 27

-hypertensive

Front 28

HAC
-radiographic diagnosis

Back 28

Support but can't confirm

-hepatomegaly
-adrenal tumor (not common)
-focal calcification
-lung mineralization
-metastatic lesions

Front 29

HAC
-why is definitive diagnosis difficult?

Back 29

-no single test is perfect
-hypercortisolemia occurs during non-adrenal illness

Front 30

Reasons why signs may be compatible with HAC but diagnostics are inconsistent

Back 30

-presumptive HAC diagnosis is incorrect
-overproduction of another steroid is cause of signs

Front 31

HAC
-2 step diagnostic approach

Back 31

-Screening tests
-Differentiating tests

Front 32

HAC
-purpose of screening tests

Back 32

-confirm adrenal hypersecretion

Front 33

HAC
-Screening tests

Back 33

-urine cortisol:creatinine ratio (UCCR)
-low dose dexamethasone suppression test (LDDST)
-ACTH stimulation test
-Combination of ACTH stim test and LDDST test

Front 34

HAC
-purpose od differentiating tests

Back 34

-distinguish between PDH and ADH

Front 35

HAC
-differentiating tests

Back 35

-Adrenal ultrasound
-endogenous ACTH
-High dose dexamethasone suppression test (HDDST)

Front 36

HAC
-primary differentiating test

Back 36

-Adrenal Ultrasound

Front 37

Urinary Cortisol:Creatinine Ratio
-best used for?
--why?

Back 37

-determining if a dog does not have HAC

-sensitivity = almost 100%
--high serum cortisol results in a proportionately high amount excreted in the urine
--neg. results rule out HAC

Front 38

Urinary Cortisol:Creatinine Ratio
-benefit of use

Back 38

-can have the urine collected at home when the dog is not stressed

Front 39

LDDST
-why use?

Back 39

-effective screening test (high sensitivity)
-can be a differentiating test

Front 40

LDDST
-interpretation

Back 40

Normal
-suppression of plasma cortisol at 4 and 8 hrs

HAC
-no suppression at 4 or 8 hrs
-PDH --> can be decreased at 4 hrs but escape at 8 hrs

Front 41

LDDST
-false positives caused by

Back 41

-stress
-nonadrenal illness

Front 42

HAC
-ACTH stimulation test use

Back 42

-if non adrenal illness is suspected

Front 43

ACTH
-causes of false positives

Back 43

-stress
-nonadrenal illness

Front 44

ACTH stimulation test
-problem

Back 44

-can't distinguish PDH for AT

Front 45

HAC
-use of a differentiation test when?

Back 45

-after HAC has been confirmed using a screening test

Front 46

High Dose Dexamethasone Suppression Test (HDDST)
-interpretation

Back 46

-suppressed --> PDH
-No suppression --> ADH

occasionally PDH will not suppress

Front 47

HDDST
-why can't you run without the screening test first?

Back 47

-PDH gets suppressed to basal levels (normal) so normal and PDH would not be able to be separated.

Front 48

Endogenous ACTH test
-advantages

Back 48

Can positively differentiate
-PDH = normal to high ACTH
-ADH = low to non-detectable ACTH

Front 49

Endogenous ACTH test
-disadvantages

Back 49

-difficult to measure
-special sample handling required for accurate measurement

Front 50

Abdominal ultrasound
-PDH findings

Back 50

-bilateral adrenal hypertrophy
-normal and hypertrophied glands overlap in size
-cut off of 7.4 mm diameter

Front 51

Abdominal ultrasound
-ADH findings

Back 51

-unilateral adrenal enlargement
-nodular change
-atrophy of the contralateral gland
-possible misdiagnosis because not every adrenal mass is functional

Front 52

CT scan
-use in HAC

Back 52

-diagnose adrenal tumors

Front 53

CT scan
-findings

Back 53

-pituitary tumors when a macroadenoma is present

Front 54

MRI
-use in HAC

Back 54

-visualization of small pituitary tumors

Front 55

HAC
-factors affecting treatment

Back 55

-HAC is a clinical syndrome (not usually life threatening)
-Treatment is not benign
-can be expensive to treat

Front 56

PDH
-treatment of choice

Back 56

Medical management
-Mitotane
-Trilostane

Front 57

PDH
-Mitotane effect

Back 57

-induce adrenal cortical necrosis

Front 58

PDH
-effect of trilostane

Back 58

-inhibit steroid synthesis

Front 59

PDH
-"other" options for treatment

Back 59

-radiation for pituitary microadenoma
-Surgery = hypophysectomy

Front 60

Trilostane
-trade name

Back 60

-Vetoryl

Front 61

Trilostane
-MOA

Back 61

-inhibitor of 3beta hydroxysteroid dehydrogenase (reversible)

Front 62

Trilostane
-monitored vie

Back 62

-ACTH stimulation

Front 63

Trilostane
-efficacious in what species

Back 63

dogs

Front 64

Trilostane
-adverse effects

Back 64

-vomiting, diarrhea, lethargy
-rare hypoadrenocorticism
-acute fatal reaction (adrenal necrosis)

Front 65

Lysodren
-aka

Back 65

-Mitotane

Front 66

Lysodren therapy
-induction phase

Back 66

"loading"
-client education important --> contact daily to ensure adequate owner compliance & understanding (monitor food and water intake--> stop giving drug if not eating)
-daily dose
-Goal: ACTH stimulation in desired range

Front 67

Lysodren therapy
-maintenance phase

Back 67

-standard dose divided into 2 doses given on 2 days of the week (M, W)
-continue indefinitely with periodic monitoring

Front 68

Lysodren therapy
-ideal response

Back 68

-controlled addisonian

Front 69

Only useful test that monitors adrenocortical reserve

Back 69

-ACTH stimulation

Front 70

Flat Stim Test
-describe

Back 70

-test to see if animal is a controlled addisonian
-basal level of cortisol is normal and it is not stimulated by ACT'H

Front 71

Ketoconazole
-MOA

Back 71

-reversible inhibition of adrenal steroidgenesis
-not used clinically

Front 72

ADH
-methods of treatment

Back 72

-Surgical
-Medical

Front 73

ADH
-treatment of choice

Back 73

-surgical

Front 74

ADH
-surgery

Back 74

-unilateral adrenalectomy

Front 75

ADH
-when is unilateral adrenalectomy the preferred treatment?

Back 75

-no evidence of metastasis or local invasion

Front 76

Unilateral adrenalectomy
-perioperative and postoperative complications

Back 76

-hemorrhage, thromboembolism
-adrenal insufficiency, organ failure

Front 77

Unilateral adrenalectomy
-prognosis

Back 77

-good if tumor benign
-malignant tumors are less favorable

Front 78

ADH
-medical treatment options

Back 78

-Trilostane
-Lysodren

Front 79

ADH
-drug approved for medical treatment

Back 79

-Trilostane

-but no efficacy reported

Front 80

ADH
-Lysodren function

Back 80

-necrosis of the adrenal cortex

Front 81

ADH
-Lysodren efficacy

Back 81

-may have an effect on metastatic lesions
-requires a long induction phase and higher maintenance dose

Front 82

PDH
-prognosis

Back 82

Fair
-average = 2.5 yrs, but hesitate to use becomes some dogs can live fine with Cushings

Front 83

ADH
-prognosis

Back 83

-Benign adrenal tumors --> good
-Malignant tumors --> guarded to grave

Front 84

Feline Hyperadrenocorticism
-cause

Back 84

-usually PDH

-uncommon to rare

Front 85

Feline hyperadrenocorticism
-signalment

Back 85

-middle aged and older
-female
-insulin resistance and diabetes mellitus

Front 86

Feline HAC
-clinical signs

Back 86

-PU, PD, Polyphagia
-Diabetes that's difficult to regulate
-Weight loss/failure to gain weight
-lethargy

-skin fragility, alopecia, failure to groom, pendulous abdomen

Front 87

Feline HAC
-minimum data base

Back 87

CBC
-no consistent abnormalities

Serum chem
-hyperglycemia
-ALP & ALT not increased

Urinalysis
-low specific gravity
-glucosuria

Front 88

Feline HAC
-diagnosis

Back 88

2 step diagnosis
-screening tests (ACTH stim, LDDST, Urine cortisol : Creatinine Ratio)
-differentiating tests (HDDST, Abdominal US, Endogenous ACTH levels)

Front 89

Feline HAC
-treatment

Back 89

ADH
-surgery if not metastatic

PDH (controversy in treatment of choice)
-surgery (bilateral adrenalectomy)
-hypophysectomy
-radiation
-medical

Front 90

Feline PDH
-medical treatment

Back 90

-Mitotane: cats resistant
-Trilostane: limited info for use in cats
-Ketoconazole: cats more resistant

Front 91

Feline HAC
-prognosis

Back 91

-guarded to poor