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91 Cards in this Set
- Front
- Back
Describe the cortisol feedback loop
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ACTH
-secreted from where |
-pituitary
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ACTH
-secretion influenced by |
Feeding
Physiologic/environmental stress: -Pain -Trauma -Pyrogens -Cold exposure -Surgery |
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Canine cushings
-forms |
-Pituitary dependent hyperadrenocorticism
-Adrenal dependent hyperadrenocorticism |
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Canine Cushing
-most common form |
-Pituitary dependent
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PDH
-mechanism of action |
-pituitary tumor overproduces ACTH
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PDH
-etiology |
-microadenoma (no CNS signs)
-macroadenoma (possible CNS signs) |
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PDH
-majority of cases |
-microadenoma
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PDH
-distinguishing from ADH |
-bilateral adrenal hyperplasia due to excess ACTH not allowing for neg. feedback
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Adrenal Dependent Hyperplasia
-characterized by |
-autonomous production of cortisol (and possibly other steroids)
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ADH
-causes |
-Adenoma (benign)
-Carcinoma (malignant) --> matastasis via vena cave |
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ADH
-common findings |
-unilateral adrenal hyperplasia with contralateral hypotrophy
-neg. feedback still works --excessive cortisol production inhibiting ACTH ---contralateral adrenal hypotrophies because unneeded |
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Canine Hyperadrenocorticism
-signalment |
Cushingoid dog
-10-11 yrs but can be younger -PDH common in smaller dogs |
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HAC
-clinical signs |
-feel and act well (generally)
-PU/PD**** -normal to increased appetite -panting and restless at night -Cushingoid body type |
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Cushingoid Body Type
-describe |
-pendulous/distended abdomen (organomegaly, gravity weight on organs)
-muscle wasting -thin coat -multiple dermatologic lesions (thin skin, comedones) |
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Cushingoid dog
-characteristic skin lesions |
-non-pruritic
-bilateral alopecia -truncal distribution |
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HAC
-reason for PU/PD |
-glucocorticoids interfere with ADH
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HAC
-reason for polyphagia |
-glucocorticoids have a direst stimulatory effect on appetite
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HAC
-associated clinical abnormalities |
-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 |
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HAC
-reproductive signs |
-androgen-dependent perianal adenoma in neutered dogs****
-dec. in testicular androgen production in males -anestrus in females |
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HAC
-minimum data base |
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 |
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HAC
-reason for stress leukogram |
-circulating cortisol
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HAC
-reason for elevated ALP |
-glucocorticoid induced isoenzyme (dog)
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HAC
-reason for elevated ALT |
-hepatic necrosis
-glycogen accumulation in hepatocytes |
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HAC
-why is low urine specific gravity very common? |
-cortisol produces a nephrogenic diabetes insipidus
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HAC
-why should a urine culture be performed regardless of urine sediment? |
-immunosuppression from cortisol --> inactive sediment with active infection
-cystic calculi from inc. in calcium excretion |
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HAC
-common blood pressure finding |
-hypertensive
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HAC
-radiographic diagnosis |
Support but can't confirm
-hepatomegaly -adrenal tumor (not common) -focal calcification -lung mineralization -metastatic lesions |
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HAC
-why is definitive diagnosis difficult? |
-no single test is perfect
-hypercortisolemia occurs during non-adrenal illness |
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Reasons why signs may be compatible with HAC but diagnostics are inconsistent
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-presumptive HAC diagnosis is incorrect
-overproduction of another steroid is cause of signs |
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HAC
-2 step diagnostic approach |
-Screening tests
-Differentiating tests |
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HAC
-purpose of screening tests |
-confirm adrenal hypersecretion
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HAC
-Screening tests |
-urine cortisol:creatinine ratio (UCCR)
-low dose dexamethasone suppression test (LDDST) -ACTH stimulation test -Combination of ACTH stim test and LDDST test |
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HAC
-purpose od differentiating tests |
-distinguish between PDH and ADH
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HAC
-differentiating tests |
-Adrenal ultrasound
-endogenous ACTH -High dose dexamethasone suppression test (HDDST) |
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HAC
-primary differentiating test |
-Adrenal Ultrasound
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Urinary Cortisol:Creatinine Ratio
-best used for? --why? |
-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 |
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Urinary Cortisol:Creatinine Ratio
-benefit of use |
-can have the urine collected at home when the dog is not stressed
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LDDST
-why use? |
-effective screening test (high sensitivity)
-can be a differentiating test |
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LDDST
-interpretation |
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 |
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LDDST
-false positives caused by |
-stress
-nonadrenal illness |
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HAC
-ACTH stimulation test use |
-if non adrenal illness is suspected
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ACTH
-causes of false positives |
-stress
-nonadrenal illness |
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ACTH stimulation test
-problem |
-can't distinguish PDH for AT
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HAC
-use of a differentiation test when? |
-after HAC has been confirmed using a screening test
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High Dose Dexamethasone Suppression Test (HDDST)
-interpretation |
-suppressed --> PDH
-No suppression --> ADH occasionally PDH will not suppress |
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HDDST
-why can't you run without the screening test first? |
-PDH gets suppressed to basal levels (normal) so normal and PDH would not be able to be separated.
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Endogenous ACTH test
-advantages |
Can positively differentiate
-PDH = normal to high ACTH -ADH = low to non-detectable ACTH |
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Endogenous ACTH test
-disadvantages |
-difficult to measure
-special sample handling required for accurate measurement |
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Abdominal ultrasound
-PDH findings |
-bilateral adrenal hypertrophy
-normal and hypertrophied glands overlap in size -cut off of 7.4 mm diameter |
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Abdominal ultrasound
-ADH findings |
-unilateral adrenal enlargement
-nodular change -atrophy of the contralateral gland -possible misdiagnosis because not every adrenal mass is functional |
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CT scan
-use in HAC |
-diagnose adrenal tumors
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CT scan
-findings |
-pituitary tumors when a macroadenoma is present
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MRI
-use in HAC |
-visualization of small pituitary tumors
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HAC
-factors affecting treatment |
-HAC is a clinical syndrome (not usually life threatening)
-Treatment is not benign -can be expensive to treat |
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PDH
-treatment of choice |
Medical management
-Mitotane -Trilostane |
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PDH
-Mitotane effect |
-induce adrenal cortical necrosis
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PDH
-effect of trilostane |
-inhibit steroid synthesis
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PDH
-"other" options for treatment |
-radiation for pituitary microadenoma
-Surgery = hypophysectomy |
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Trilostane
-trade name |
-Vetoryl
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Trilostane
-MOA |
-inhibitor of 3beta hydroxysteroid dehydrogenase (reversible)
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Trilostane
-monitored vie |
-ACTH stimulation
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Trilostane
-efficacious in what species |
dogs
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Trilostane
-adverse effects |
-vomiting, diarrhea, lethargy
-rare hypoadrenocorticism -acute fatal reaction (adrenal necrosis) |
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Lysodren
-aka |
-Mitotane
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Lysodren therapy
-induction phase |
"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 |
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Lysodren therapy
-maintenance phase |
-standard dose divided into 2 doses given on 2 days of the week (M, W)
-continue indefinitely with periodic monitoring |
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Lysodren therapy
-ideal response |
-controlled addisonian
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Only useful test that monitors adrenocortical reserve
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-ACTH stimulation
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Flat Stim Test
-describe |
-test to see if animal is a controlled addisonian
-basal level of cortisol is normal and it is not stimulated by ACT'H |
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Ketoconazole
-MOA |
-reversible inhibition of adrenal steroidgenesis
-not used clinically |
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ADH
-methods of treatment |
-Surgical
-Medical |
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ADH
-treatment of choice |
-surgical
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ADH
-surgery |
-unilateral adrenalectomy
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ADH
-when is unilateral adrenalectomy the preferred treatment? |
-no evidence of metastasis or local invasion
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Unilateral adrenalectomy
-perioperative and postoperative complications |
-hemorrhage, thromboembolism
-adrenal insufficiency, organ failure |
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Unilateral adrenalectomy
-prognosis |
-good if tumor benign
-malignant tumors are less favorable |
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ADH
-medical treatment options |
-Trilostane
-Lysodren |
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ADH
-drug approved for medical treatment |
-Trilostane
-but no efficacy reported |
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ADH
-Lysodren function |
-necrosis of the adrenal cortex
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ADH
-Lysodren efficacy |
-may have an effect on metastatic lesions
-requires a long induction phase and higher maintenance dose |
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PDH
-prognosis |
Fair
-average = 2.5 yrs, but hesitate to use becomes some dogs can live fine with Cushings |
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ADH
-prognosis |
-Benign adrenal tumors --> good
-Malignant tumors --> guarded to grave |
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Feline Hyperadrenocorticism
-cause |
-usually PDH
-uncommon to rare |
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Feline hyperadrenocorticism
-signalment |
-middle aged and older
-female -insulin resistance and diabetes mellitus |
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Feline HAC
-clinical signs |
-PU, PD, Polyphagia
-Diabetes that's difficult to regulate -Weight loss/failure to gain weight -lethargy -skin fragility, alopecia, failure to groom, pendulous abdomen |
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Feline HAC
-minimum data base |
CBC
-no consistent abnormalities Serum chem -hyperglycemia -ALP & ALT not increased Urinalysis -low specific gravity -glucosuria |
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Feline HAC
-diagnosis |
2 step diagnosis
-screening tests (ACTH stim, LDDST, Urine cortisol : Creatinine Ratio) -differentiating tests (HDDST, Abdominal US, Endogenous ACTH levels) |
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Feline HAC
-treatment |
ADH
-surgery if not metastatic PDH (controversy in treatment of choice) -surgery (bilateral adrenalectomy) -hypophysectomy -radiation -medical |
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Feline PDH
-medical treatment |
-Mitotane: cats resistant
-Trilostane: limited info for use in cats -Ketoconazole: cats more resistant |
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Feline HAC
-prognosis |
-guarded to poor
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