Cushings & Addison's Disease Flashcards
What are the important functions fo adrenal glands?
They secrete steroids hormones such as:
- Glucocorticoids
- Mineralocorticoids
- Androgens
How are steroids hormones made?
Stressors triggers the hypothalamus to cause the pituitary gland to produce corticotrophin-releasing hormone (CRH) to stimulate the anterior pituitary gland to produce adrenocorticotrophic hormone (ACTH) which stimulates secretion from the adrenal cortices.
What does cortisol do and where is it secreted from?
- Secreted form the adrenal cortex
- Increased secretion occurs within 1-2mins after stimulation from ACTH
- Peaks at 15mins
- Transported by plasma proteins (albumin and globulin)
- Anti-inflammatory effects
- Suppresses the immune system
- Processed and deactivated by the liver and kidneys
What is aldosterone and where is it secreted?
- Secreted by the adrenal cortex
- Regulated by the renin-angiotensin system
- Primary mineralocorticoid
- Promotes reabsorption of sodium ions in the kidneys
- Water follows sodium reabsorption and therefore plays a role in maintaining blood pressure
What is hypoadrenocorticism (Addison’s) disease?
- Atrophy of bilateral adrenal cortex - idiopathic
- Could be caused by hyperA medication
- Minimum of 85-90% of Adrenocortical cells loss before clinical signs appears
- Affects young to middle age female dogs
What is Addisonian’s crisis?
- Acute collapse and hypovolemic shock
- pale MM
- slow or increased CRT
- profound weakness
- bradycardia in 1/3 dogs instead of usual tachycardia
- hyperkalemia
- severe GI hemorrhage
- metabolic acidosis
- cutaneous hyperpigmentation
What are the laboratory findings of Addison’s dz?
- Hyponatremia
- Hyperkalaemia (synergies AV node blockers to cause Brady)
- Azotemia
- Mild to moderate anion gap
- Metabolic acidosis
- Na/K ratio is low <27:1
- Low urine specific gravity (<1.030)
- 30% cases has Hypercalcemia (due to low Ca excretion)
- Hypoglycemia (due to low hepatic gluconeogenesis)
- Hypochlonemia
- Abnormal phosphorus
- Normal WBC count which is abnormal
- Mild hypoalbuminemia (>2.0gm/dL)
What are the rads and ECG abnormalities seen in hyperA patients?
- Microcardia due to hypovolemia
- Megaoesophagus
- Bradycardia due to hyperkalemia (tall peaked T waves)
What is the only way to determine the absence or presence of hypoadrenocorticism (Addison’s)?
- ACTH stimulation test - assess adrenal reserve capacity
* Cortisol levels are stable in plasma or serum for as long as 5 days at room temperature
What is endogenous ACTH concentrations?
- This is a test to differentiate between primary and secondary hypoadrenocorticism.
- Plasma must be drawn and centrifuged immediately, then frozen in plastic tubes
What is the treatment for hypoadrenocorticism (Addison’s)?
- Treat hypotension, hypovolemia, electrolyte and acid/base abnormalities and provide glucocorticoid replacement
- Death is generally the result of hypovolemia not hyperkalemia
- IVF is first-line treatment
- 0.9%NaCl due to hyperkalemia and hyponatremia
- If hypoglycemia - 5% dextrose
- Steroid - dexamethasone SP(0.25-1.0mg/lb) is drug of choice as it will not interfere with ACTH stim test result
- Hydrocortisone hemisuccinate or hydrocortisone phosphate (1.2mg/lb slow IV) - post ACTH stim test
- Prednisolone sodium succinate (2-10mg/lb) - rapid acting glucocorticoid
- Hyperkalemia
- IVF dilution
- life-threatening = calcium gluconate (0.4-1.0mg/kg over 10-20 minutes) - helps protect myocardium form adverse effects by resetting the action potential threshold
- IV glucose (2-5ml/lb) of 10% solution over 30-60 mins as when glucose enters cells, potassium follows
- insulin (0.03-0.06U/lb) IV or IM to aid movement of potassium into cells
- 20ml 10% dextrose given for each unit of insulin given to prevent hypoglycaemia
- bicarbonate only if <12mEq/L with profound metabolic acidosis
What is the maintenance therapy for hypoadrenocorticism?
- Initial tx with both glucocorticoids and mineralocorticoid
- Prednisolone PO or prednisone (0.2-0.5mg/lb/day q12) should be continued for 3-4 weeks
- dosages to be tapered by 50% per week until discontinued
- Long term management with mineralocorticoid replacement :
- fludrocortisone acetate (both mineralocorticoid and glucocorticoid) (Florine’s 0.02 mg/kg/d Po) or
- desoxycortiocosterone pivalate (DOCP 2.2 mg/kg IM or SQ for 25-30 days)
- Electrolyte levels to be checked every 4-7 days for the first 1-2weeks, then 3-4 months through the first year
Where does hyperadrenocorticism (Cushing’s) result from?
- Most commonly from the pituitary (80-85%), causing excessive secretion of ACTH, which leads to excessive cortisol secretion.
- both adrenal cortices become hyperplastic as a result.
- mostly due to a pituitary tumour. - Adrenal tumour (15-20%)
- usually unilateral
- ultrasound needed for diagnosis - Iatrogenic causes
- due to prolonged or excessive exposure to glucocorticoids
What age and what sex of dogs does HyperA (Cushing’s) affect?
> 6 years and females
What are the clinical signs of HyperA (Cushing’s)?
- polydipsia
- polyphagia (excessive hunger)
- polyuria
- weight gain / obesity
- enlarged abdo (weakening of abdo muscles)
- thinning of hair and sometimes alone is
- panting / increased RR
- lethargy
- muscle weakness
Other:
- Bruise easily
- Heat intolerance
- calcinosis cutis (calcium deposits on the skin)
- Skin hyperpigmentation
- Neuropathies (nerve pain)
- Myopathies (muscle)
- Likely to develop secondary diabetes mellitus due to increased insulin resistance from cortisol
- Hepatomegaly
- elevated Alk phos, amino transferase, cholesterol with normal bilirubin
- Hypertension
