Hyper/Hypo Adrenocortistism Flashcards by Corinne Perra

Excessive production of glucocorticoids by the adrenal glands

Hyperadrenocortisim

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What are the three forms of HAC

Pituitary dependent (PDH) 
Adrenocortical neoplasia (AT) 
Iatrogenic

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What is the most common type of HAC?

Pituitary dependent

Accounts for 80-85% of cases

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What type of HAC causes bilateral adrenocortical hyperplasia?

Pituitary dependent

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What type of HAC causes bilateral adrenal atrophy?

Iatrogenic

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What type of HAC has and enlarged adrenal gland with atrophy of the contralateral gland

Adrenocortical tumors (AT)

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Species predisposed to HAC?

Poodles
Boxer 
Dashunds 
Schnauzers 
Boston terriers 
German shepherds

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At what age do you usually see HAC?

Middle aged to old dog, ave 12yrs

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What is not a clinical finding associated with HAC?

PU/PD 
Bilaterally symmetrical alopecia 
Pendulous abdomen 
Seborrhea 
Calcinosis cutis

Seborrhea - associated with hypothyroidism

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What would you expect to find on a CBC, chem panel and UA of a cushings patient

CBC- polycythemia, stress leukogram

Chem- increased ALP, hypercholesterolemia, mildly increase ALT and glucose

UA- decreased specific gravity, proteinuria
USG <1.025

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What may you see on a radiograph of a HAC patient?

Hepatomegaly –corstiol makes the liver larger

Distended bladder- PU/PD

Mineralization
Osteopenia

Metastasis of adrenal tumors

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Would you expect to see an increased BP in cushings patient?

50-80% of patients are hypertensive

Maybe du to PLN

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T/F: baseline cortisol can be normal in cushings dogs

True

Secretion in episodic

Mean daily cortisol is increased but individual measurement can be normal

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What would the urine cortisol: creatinine ratio be in a cushings patient?

Would be increased

Urine cortisol excretion increases with adrenal secretion of cortisol

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T/F: a high urine cortisol: creatinine ratio can be diagnostic for cushings

False

Positive test makes cushings a possibility, but is not diagnostic

However, a negative test makes cushings unlikely

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What is the low dose dexamethasone suppression test?

Dexamethasone inhibits release of ACTH from pituitary

Normal - cortisol suppressed

Cushings- no suppression

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Low Dose Dex suppression test

50% suppression at 4 hrs with lack of suppression at 8hrs.
What is your interpretation?

Pituitary dependent hyperadrenocortisim

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Low Dose Dex suppression test

No suppression at 8hrs or 4hrs.
What is your interpretation?

Cushings

Could be either AT or PDH

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What is the test of choice for iatrogenic cushings?

ACTH stimulation test

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What are the cons of the ACTH stimulation test?

Expensive

Compounded gels are not recommended.

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What is the high dose Dex suppression text?

About 10x dose of LDDST
Cannot be used to diagnose cushings, test to differentiate between PDH and AT

Suppression =PDH
No suppression= inconclusive

Cannot definitely diagnose AT

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What would you use an Endogenous corticotrophin to diagnose?

To differentate between PDH and AT

Cannot be used to diagnose cushings b/c of overlap in ACTH in normal animals and PDH animals

Normal 20-100pg/mL
PDH 40-500pg/mL
AT <20pg/mL

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T/F: ultrasound can be used to differentiate malignant from benign adrenal tumors

False

Can usually only determine malignancy this way if there is invasion of the vena cava or liver metastases

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What test would be the BEST to diagnose cushings in a case with only mild clinical signs or lab abnormalities only

ACTH stim

Also good for

patients with concurrent nonadrenal illness
patients with suspected iatrogenic cushings
patients on phenobarbital

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What test would be BEST to diagnose a cushings case in a patient with severe clinical signs and no evidence of non adrenal illness?

LDDS

What would be the BEST test to diagnose a suspected adrenal tumor?

LDDS

Which test is the BEST at differentiating PDH vs AT HAC, is this the most practical clinically?

Endogenous ACTH. Not most clinically practical because test is expensive and sample required very careful handling. See more often in University setting. Clinically, abdominal radiographs are used to visualize AT

You run LDDS, ACTH stim, Endogenous ACTH and they all come back negative, but the dog has classical cushingoid appearance. What could be the problem with this dog?

Noncortisol hormones and cushings | -> derangement of steroid pathway and overproduction of precursors

If you think a dog has noncortisol cushings, how would you confirm your diagnosis?

Perform ACTH stimulation and assay noncortisol hormones (Eg progestin)

What are the medical therapy treatments for cushings?

``` Mitotane Selegiline Ketoconazole Trilostane Cyprohetadine Bromocriptine ```

What is the MOA of mitotane ?

Destroy zona fasciculata and reticularis of adrenal gland -> permanent atrophy Inhibits cholesterol side chain cleavage.

What is the dosage of mitotane and how would you monitor this therapy?

Starting dose - 50mg/kg/day, divided BID with meals Maintenance - 50mg/kg/week Monitor - ACTH stim within 5-10days then 1 and 3 months after diagnosis

What is the MOA of selegiline

Irreversible inhibitor of monoamine oxidase type B -> restore central dopamine concentration -> decrease the clinical signs of cushings, but does not have any effect on the tumor

Which therapy may be a good option for patients whose owners do not want to used Lysodren due to side effects or the high cost of Trilostane

Selegiline (Anipryl)

When is Anipryl use appropriate?

Patients with mild cushings signs but are negative on lab tests May have a role in patients that test positive for cushings but have no clinical signs Cognitive dysfunction Behavior - pee in the right places

What is the MOA of trilostane?

Competitive inhibitor of 3B-hydroxysteroid dehydrogenase —> inhibit synthesis of steroids (cortisol and aldosterone)

T/F: Mitotane and Trilostane are reversible drug therapies

False Only trilostane is reversible

What drug should you do periodic monitoring of electrolytes because it can cause a hyperkalemia ?

Trilostane

How does ketoconazole treat cushings?

Inhibit steroid biosynthesis -> imidazole antifungal drug EXPENSIVE

What are adverse effects of ketoconazole ?

Excessive glucocorticoids deficiency -> cessation of therapy Vomiting, diarrhea, anorexia, and elevated liver enzymes

What is the MOA of cyprohetadine? How does this treat cushings?

Antiserotonin, anticholinergic, and antihistamine effects Increased serotonin theroeticallly associated with excess pituitary ACTH

What are the non-drug therapies for cushings?

Surgical - transsphenoidal hypophysectomy - very difficult and requried lifelong thyroid pred replacement - bilateral adrenalectomy Radiation therapy

What is the treatment of pituitary macroadenomas ?

Radiation therapy -reduce tumor size and clinical signs. Often still require medical therapy to control cushings disease

What is the treatment f choice for adrenal tumors?

Adrenalectomy - are often vascular and invasive even if benign 50% malignant -> very poor prognosis

How can you reduce risk of thromboembolism post-adrenalectomy

Treatment with dexamethasone, heparin, plasma, and Hetastarch- over first 5 days

What are some complications associated with PDH?

Hypertension, PTE, CNS signs, infections, recurrence of disease, CHF

What are the 5P’s of HAC?

``` Panting PU PD PP Potbelly ```

What is the signalment of hypoadrenocorticism ?

Med to lg breed dogs | Younger

Release of aldosterone from the adrenal gland has what effect?

Increased Na and water reabsorption Increased K secretion into urine Increase blood volume

Aldosterone release from the adrenal gland is stimulated by?

Angiotensin II

Deficiency in aldosterone results in...?

HYPO natermia and chloremia | HYPER kalemia

What are the major regulators of aldosterone secretion?

Plasma K levels and RAAS

Where does aldosterone exert its effect?

DCT and collecting duct -> increase Na reabsorption

What is the signalment of Addison’s disease?

Dog, young to middle aged | F>M

Clinical signs of Addisons?

``` “Ain’t doing right” Waxing and waning Anorexia Lethargy Dehydration Weakness Polyuria ```

What does an addisons crisis appear like?

Collapse, bradycardia, melena

What is “typical” hypoadrenocorticism ?

Deficient in both mineralalocortocoids and glucocorticoids Due to primary lesions - usually immune mediated adrenal gland destruction

What is the normal function of glucocorticoids? What will you see in a deficiency?

Normal fx: increase blood glucose, gluconeogensis, glycogenolysis, muscle/fat catabolism Deficiency: anorexia, lethargy, fasting hypoglycemia

What is atypical hypoadrenocorticism? What are the two causes?

Low glucocorticoids - pituitary lesion so there is not enough ACTH - early in a typical addisons, before it progresses to include mineralocorticoids

What is iatrogenic hypoadrenocorticism ?

Abrupt discontinuation of glucocorticoids without time for the atrophied adrenals to respond

Poodle 1.5yrs, history of lethargy and poor appetite PE: recumbency and minimally responsive, positive skin tent, sunken eyes, tacky mm. TPR: hypothermic and bradycardia What’s you DDx, and what diagnostics would you run to confirm?

Hypoadrenocorticism QATS - mild hypoglycemia, azotemia, USG 1.018 CBC, chem, UA ECG

Poodle 1.5yrs, history of lethargy and poor appetite PE: recumbency and minimally responsive, positive skin tent, sunken eyes, tacky mm. TPR: hypothermic and bradycardia What type of supportive care would you give this patient?

Heat IV catch with fluids Emerg hyperkalemia treatment

What type of fluids should be given to addisons patient?

Saline Can have hyperkalemia, do NOT give fluids with K

What could you do to treat a hyperkalemia in an addisons patient?

Saline Calcium gluconate: cardioprotective Regular insulin with concurrent dextrose (draws potassium into cells and some diuretic effect) Bicarb - patient are acidotic

What CBC, Chem and UA results would you expect in an Addisons patient?

CBC - NO stress leukogram Chem- azotemia, hyponatremia, hyperkalemia UA- isosthenuric

What test is diagnostic or hypoadrenocorticism

ACTH stimulation test Endogenous ACTH levels -can be used to differentiate type

Endogenous ACTH is high in ________________ hypoadrenocorticism and low in _________forms

Primary; secondary and tertiary

What is the treatment for an acute Addisonian crisis ??

Restore blood volume rapidly: 0.9% NaCl Address life-threatening hyperkalemia: shock dose fluids then insulin/glucose, Ca gluconte, or Bicarb if nessessary GIVE GLUCOCORTICOIDS *** dexamethasone *** Give mineralocorticoids - DOCP/Fludricortisone

Which therapy for mineralocorticoids, also has some glucocorticoid effect?

Fludrocortisone

T/F: glucocorticoids maintence therapy is needed by all addisons patients

False More likely needed with DOCP

For maintenance therapy fo glucocorticoids, addisons patients should receive what type of dose?

Physiologic dose (0.25/kg/day) All owners should have some to give under conditions of stress (0.5-1.5 mg/kg/day)

How do you treat atypical hypoadrenocorticism ?

Glucocorticoids supplementation