Disease of the Adrenal Glands

Where are the adrenal glands located?

Cranial poles of the kidneys.

How many regions does the adrenal gland have?

Two — adrenal cortex and adrenal medulla.

What are the three layers of the adrenal cortex?

Zona glomerulosa, zona fasciculata, zona reticularis.

What does the zona glomerulosa secrete?

Aldosterone.

What does the zona fasciculata secrete?

Glucocorticoids, mainly cortisol.

What does the zona reticularis secrete?

Sex hormones — androgens and estrogens.

What hormones does the adrenal medulla produce?

Norepinephrine and epinephrine.

What hormone does the hypothalamus release to stimulate the pituitary?

CRH (corticotropic releasing hormone).

What hormone does the pituitary release to stimulate the adrenal cortex?

ACTH (adrenocorticotropic hormone).

What hormone does the adrenal cortex secrete?

Cortisol.

How does cortisol regulate ACTH and CRH?

Negative feedback on both pituitary and hypothalamus.

What are the catabolic effects of excess cortisol?

Breakdown of muscle, bone, and skin components to create glucose.

What does excess cortisol do to muscle?

Causes muscle atrophy of head, abdomen, and shoulders.

How does excess cortisol affect bone?

Decreases intestinal calcium absorption, increases renal calcium secretion, weakens bones.

How does excess cortisol affect skin?

Atrophy of sebaceous glands and hair follicles, symmetrical alopecia, calcinosis cutis.

How does excess cortisol affect blood vessels?

Thinning of vascular walls, hematomas.

How does excess cortisol affect the CNS?

Mood and behavior changes.

How does excess cortisol affect the liver?

Excess glycogen production → hepatomegaly.

How does excess cortisol affect the kidneys?

Increased GFR, increased water in filtrate, decreased urine specific gravity.

How does excess cortisol affect the immune system?

Decreases inflammatory response, increases susceptibility to infection.

What is the most common cause of hyperadrenocorticism (Cushing's)?

Pituitary‑dependent hyperadrenocorticism (PDH).

What causes PDH?

Excessive ACTH release from pituitary microadenoma → bilateral adrenal hyperplasia.

What percentage of Cushing's cases are PDH?

85%.

What is the second most common cause of Cushing's?

Functional adrenocortical tumor (ATH).

What percentage of Cushing's cases are ATH?

15%.

What is iatrogenic Cushing's?

Excessive or prolonged glucocorticoid administration.

Clinical signs of Cushing's?

Pendulous abdomen, bilateral alopecia, thin coat, hyperpigmentation, muscle atrophy, testicular atrophy, PU/PD, polyphagia, panting.

Serum chemistry findings in Cushing's?

Increased ALP, ALT, cholesterol, blood glucose; decreased BUN; lipemia.

Urine findings in Cushing's?

Hyposthenuria (1.000-1.008), increased urine cortisol:creatinine ratio.

Why are serum cortisol levels not specific for Cushing's?

Affected by stress.

What does the ACTH stimulation test identify?

Exogenous/iatrogenic Cushing's; evaluates adrenal cortex thickness.

What is the ACTH stim result for PDH and ATH?

Elevated cortisol.

What is the ACTH stim result for iatrogenic Cushing's?

Minimal response.

What does the Low Dose Dexamethasone Suppression Test identify?

Cushing's with 90% sensitivity.

Can the low‑dose dex test differentiate PDH from ATH?

No.

What is the normal response to low‑dose dex suppression?

Cortisol suppressed at all time points.

What is the Cushing's response to low‑dose dex suppression?

Cortisol remains elevated or suppresses then rebounds by 8 hours.

What does the High Dose Dexamethasone Suppression Test differentiate?

PDH vs ATH.

What is the high‑dose dex result for ATH?

Not suppressed.

What is the high‑dose dex result for PDH?

Suppressed.

What drug is used to selectively destroy adrenal cortex layers in Cushing's?

Mitotane (o,p'DDD, Lysodren).

What layers does mitotane destroy?

Zona fasciculata and zona reticularis.

Why is prednisone given during mitotane induction?

To counteract side effects.

How often is mitotane maintenance therapy given?

Every 2-7 days.

What test monitors mitotane therapy?

ACTH stimulation test.

What drug works best for PDH but has poor overall response?

Anipryl (L‑deprenyl).

What antifungal drug inhibits cortisol synthesis?

Ketoconazole.

What is hypoadrenocorticism?

Addison's disease.

Causes of Addison's disease?

Idiopathic, immune‑mediated, fungal, trauma, hereditary, iatrogenic.

Typical signalment for Addison's?

Clinical signs of Addison's?

Depression, lethargy, weakness, anorexia, weight loss, vomiting, diarrhea, PU/PD, dehydration, bradycardia.

What is an Addisonian crisis?

Acute collapse, arrhythmia, bradycardia, hypovolemic shock; medical emergency.

What may precipitate an Addisonian crisis?

Stress.

Serum changes in Addison's?

Eosinophilia, lymphocytosis, increased PCV/TP, azotemia, hypercalcemia.

Electrolyte changes in Addison's?

Hyponatremia and hyperkalemia.

What Na:K ratio suggests Addison's?

Na < 23, K > 27.

Urine specific gravity in Addison's?

ECG changes in Addison's?

Wide/flattened P waves, increased PR interval, increased T wave amplitude, bradycardia.

Diagnostic test for Addison's?

ACTH stimulation test (low cortisol values).

Treatment for acute Addisonian crisis?

IV NaCl (40-80 mL/kg/hr), dexamethasone, sodium bicarbonate, glucose if hypoglycemic.

Chronic treatment for Addison's?

Fludrocortisone (Florinef), Percorten, prednisone.

What is a pheochromocytoma?

Catecholamine‑producing tumor of adrenal medulla.

What hormones increase in pheochromocytoma?

Norepinephrine and epinephrine.

Clinical signs of pheochromocytoma?

Hypertension and tachycardia.

Treatment for pheochromocytoma?

Adrenalectomy.

When are many pheochromocytomas diagnosed?

Post‑mortem.

What two electrolyte abnormalities are associated with hypoadrenocorticism (Addison's Disease)?

hyponatremia, hyperkalemia

What liver induction enzyme is typically elevated in animals with hyperadrenocorticism (Cushing's)?

alkaline phosphatase

When running a low dose dexamethasone suppression test, samples are taken at what three times?

0 hour (baseline), 4 hour post, 8 hour post

What is actually measured when running a low dose dexamethasone suppression test?

serum cortisol

Prednisone, prednisolone, dexamethasone are all under what class of drugs?

glucocorticoids

________________ is a mineralocorticoid and is responsible for __________ retention and __________ excretion?

aldosterone, sodium, potassium

_____________________ is the most commonly prescribed drug to treat hyperadrenocorticism?

trilostane (vetoryl)

The majority of cases of hyperadrenocorticism (Cushing's) are __________________ dependent?

pituitary

List three clinical signs of hyperadrenocorticism (Cushing's disease).

PU/PD, pot bellied, ravenous appetite, symmetrical alopecia, calcinosis cutis

What does waxing and waning mean?

symptoms come and go

A dog presents in an Addisonian crisis — what is the most likely arrhythmia you would see on ECG?

sinus bradycardia

A dog in an Addisonian crisis would have very spiked __________ wave on ECG?

T

Name a hormone produced in the adrenal medulla.

epinephrine

What stimulation test is commonly used to diagnose hypoadrenocorticism (Addison's disease)?

ACTH

Why do we call hypoadrenocorticism the great imitator?

because its vague, intermittent symptoms can mimic many other illnesses, making it difficult to diagnose

Rapid administration of what fluid type is used during an Addisonian crisis?

0.9% NaCl

Monthly injections of ____________________ are commonly used to treat hypoadrenocorticism (Addison's disease)?

Percorten (V)

What is the name of a catecholamine‑producing tumor in the adrenal medulla?

Pheochromocytoma