Hypoadrenocorticism & Hyperadrenocorticism

Question 1

What maintains vasomotor tone?

Answer 1

Cortisol increase vascular sensitivity to catecholameines

Question 2

What is the difference between primary & Secondary hypoaddrinocorticism?

Answer 2

Primary: Lack of functional adrenals

Secondary: Lack of stimulation of adrenals (lack of ACTH, pituitary affected etc)

Question 3

Describe how Cortisol is releases starting with the brain

Answer 3

Paraventricular nucleus

CRH & Vasopressen Hypothalamus

ACTH from from anterior pituitary

Cortisol from the Adrenal Cortex

Cortisol down regulates CRH and ACTH.

Question 4

3 main causes of Typical Addisons (adrenal destruction of all 3 layers usually)

Answer 4

1. Immune mediated
2. Infiltrative

• Fungal infections
• Neoplasia
• Amyloidosis
• Coagulopathy

3. Iatrogenic (tied to mitotane, trilostane therapy)

Question 5

What is atypical primary addison’s?

Answer 5

Zona fasciculata and zona reticularis are affected. (zona granulosa is not). Loss of glucocorticoids and sex hormones (?). Gradual descruction, electroytes tend to not be affected

Question 6

Secondary Addison’s

Answer 6

Can be due to head trauma, usually only glucocorticoids are affected (mineralocorticoids are ok)

Question 7

Iatrogenic addison’s

Answer 7

Usually due to drugs (mitotane, trilostane) given for treatment of cushing’s that inhibit the production of glucocorticoids or adrenocorticol lysis causing a loss in glucocorticoids & mineralocorticoids (corticosteroids)

Question 8

Signalment of Addison’s

Answer 8

Young-to-middle aged female dogs

(poodle, great dane, white terrier)

(families: bearded collie, portugues water dog, leonburger, novascotia retriever)

Question 9

Clinical signs of Addison’s

Answer 9

Basic bunch similar to diabetes:
PU/PD
Diahrea/vomiting
weakness
dehydration/slow CRT

Others:

Hair loss
Hypothermia
weak pulse
bradycardia

GI Hemorrhage

Painful abdomen

Previous response to therapy

Waxing & waning

(a lot of the signs look like shock)

Question 10

How do you recognize an Addisonian crisis

Answer 10

Collapse

Bradycardia (hyperkalemia)

Hypotension/Shock/Hypovolemia/Pale or injected mucous membranes (lack of aldosterone = decreased Na/Cl/H2O)

Hypothermia

GI hemorrhage

Question 11

Na+/K+ ratio in Addison’s crisis

Answer 11

Na+/K+ ratio < 27

Question 12

Clinicopathologic abnormalities in Addison’s

Answer 12

Na+/K+ ratio < 27
Hyperkalemia **
Hyponatremia
Hypochloremia

Acidosis
Hyperphosphatemia (due to high urea & creatanine)
Pre-renal Azotemia (medullary washout)
+/- Hypercalcemia (may be opposite to phosphorus is PTH is working?? but here we tend to find phosphorus as high, perhaps because sodium is low)
USG < 1.030
Hypoglycemia
Hypoalbumenia
Elevated AST/ALT
Hyperbilirubinemia
Anemia (normocytic, normochromic)
Eosinophilia
Lymphocytosis

Question 13

Stress Leukogram

Answer 13

Neutrophilia

Lymphopenia

Monocytosis

Question 14

What do you see in radiographs with addison’s

Answer 14

microcardia

hypo-perfused lung fields

narrowed vena cava

Sometimes (rarely) megaesophogus

Question 15

Concentration (baseline) of cortisol to rule out addison’s?

What if you can’t rule it out?

Answer 15

> 55 nmol/L

If less than 55nmol/L inject with ACTH

a) if less than 30, inject with ACTH, wait 1 hour, test… still 30? Addison’s.

Question 16

Dexamethasone w.r.t. Addison’s

Answer 16

• can still be used with ACTH stimulation test. Other glucocorticoids do: wait 24 hours after administering.
• Tends to be good for treatment
• 0.25 mg/kg IV at first

Question 17

Lifelong treatment of Addisons can include

Answer 17

Deoxycorticosterone or DOCP (replaces minarlocorticoids) or Fludrocortisone acetate

Glucocorticoids - prednisone

Question 18

Etiology of hyperadrenocorticism

Answer 18

Dogs & cats - 85% Pituitary dependant

15% adrenal tumour

Rare in cats

Question 19

What are 3 ways to diagnose hyperadrenocortisism

Answer 19

Urine cortisol: creatanine ratio (expect cortisol to be high - sensitive, not specific)

ACTH stimulation test (expect either a somewhat independantly high or responsive cortisol or if pituitary-dependant, then a huge response)

Low Dex suppresion test or LDDST (dex doesn’t properly (temp or none) suppress the levels - can differentiate between types, high sensitivity, low specificity)

HDDST - differentiation of PDH and AT

Ultrasound - for adrenal tumours

Endogenous ACTH levels (high in PDH)

Question 20

Potential complications of Hyperadrenocorticism

Answer 20

• Hypertension
• Proteinuria
• Thromboembolic disease
• Pulmonary thromboembolism dyspnea
• Urinary tract infection (similar to DM)
• Calcinosis cutis (due to all the cortisol secretion, should resolve on its own)
• Macroadenoma in PDH dogs can cause neuro signs

Question 21

Treatments for hyperadrenocorticism (to get cortisol between 50-150 nmol/L)

Answer 21

Best 2: Mitotane, Trilostane (blocks enzyme intermediatein production of cortisol)

Ketoconazole (50% effective, hepatotoxicity possible), selegeline (< 20% effective)

Question 22

Adrenal tumour types

Answer 22

Cortisol-secreting tumours (adenomas or carcinomas)

Pheochromocytoma (excess catecholamines: tachycardia, hypertension)

Non-secreting tumours (adenomas)