Hypoadrenocorticism & Hyperadrenocorticism Flashcards
What maintains vasomotor tone?
Cortisol increase vascular sensitivity to catecholameines
What is the difference between primary & Secondary hypoaddrinocorticism?
Primary: Lack of functional adrenals
Secondary: Lack of stimulation of adrenals (lack of ACTH, pituitary affected etc)
Describe how Cortisol is releases starting with the brain
Paraventricular nucleus
CRH & Vasopressen Hypothalamus
ACTH from from anterior pituitary
Cortisol from the Adrenal Cortex
Cortisol down regulates CRH and ACTH.
3 main causes of Typical Addisons (adrenal destruction of all 3 layers usually)
- Immune mediated
- Infiltrative
- Fungal infections
- Neoplasia
- Amyloidosis
- Coagulopathy
- Iatrogenic (tied to mitotane, trilostane therapy)
What is atypical primary addison’s?
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
Secondary Addison’s
Can be due to head trauma, usually only glucocorticoids are affected (mineralocorticoids are ok)
Iatrogenic addison’s
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)
Signalment of Addison’s
Young-to-middle aged female dogs
(poodle, great dane, white terrier)
(families: bearded collie, portugues water dog, leonburger, novascotia retriever)
Clinical signs of Addison’s
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)
How do you recognize an Addisonian crisis
Collapse
Bradycardia (hyperkalemia)
Hypotension/Shock/Hypovolemia/Pale or injected mucous membranes (lack of aldosterone = decreased Na/Cl/H2O)
Hypothermia
GI hemorrhage
Na+/K+ ratio in Addison’s crisis
Na+/K+ ratio < 27
Clinicopathologic abnormalities in Addison’s
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
Stress Leukogram
Neutrophilia
Lymphopenia
Monocytosis
What do you see in radiographs with addison’s
microcardia
hypo-perfused lung fields
narrowed vena cava
Sometimes (rarely) megaesophogus
Concentration (baseline) of cortisol to rule out addison’s?
What if you can’t rule it out?
> 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.
Dexamethasone w.r.t. Addison’s
- 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
Lifelong treatment of Addisons can include
Deoxycorticosterone or DOCP (replaces minarlocorticoids) or Fludrocortisone acetate
Glucocorticoids - prednisone
Etiology of hyperadrenocorticism
Dogs & cats - 85% Pituitary dependant
15% adrenal tumour
Rare in cats
What are 3 ways to diagnose hyperadrenocortisism
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)
Potential complications of Hyperadrenocorticism
- 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
Treatments for hyperadrenocorticism (to get cortisol between 50-150 nmol/L)
Best 2: Mitotane, Trilostane (blocks enzyme intermediatein production of cortisol)
Ketoconazole (50% effective, hepatotoxicity possible), selegeline (< 20% effective)
Adrenal tumour types
Cortisol-secreting tumours (adenomas or carcinomas)
Pheochromocytoma (excess catecholamines: tachycardia, hypertension)
Non-secreting tumours (adenomas)
