Addisons disease/ crisis

"Pathophysiology"
1. Brought about by the destruction of the Adrenal gland - usually via an auto-immune pathway
  1. Destruction leads to marked decreases in Aldosterone and Cortisol (adrenocortical hormones released natually from the adrenal gland)
    1. ALDOSTERONE
      1. Acts on the Kidneys to improve blood pressure
        Increases blood volume by increasing water retention - caused by heightened sodium and chloride re-absorption & increased potassium excretion
    2. CORTISOL
      1. Acts in response to stress
        Reduces sodium loss, aids in metabolism, increases blood sugar level (via insulin) & suppresses the immune system
    3. Reductions in these hormones cause dramatically lowered blood pressure and volume due to water loss and less sodium/chloride retention
"Clinical signs"
1. Non -specific = mimics other diseases therefore making it difficult to diagnose
2. Loss of body condition
  1. Anorexia
  2. Emesis
  3. Diarrhoea
  4. Increased water loss
    1. Dehydration
  5. Gastroenteritis
3. Hypotension
  1. Circulatory collapse
  2. Shock
4. Increased potassium levels
  1. Bradycardia
  2. Irregular heart beat
5. Hypoxia due to lessened perfusion
  1. RENAL FAILURE
6. Increased ACTH release from pituitary
  1. Hyperpigmentation of the skin
"Diagnosis"
1. ACTH stimulation test
  1. Adrenocorticotrophic hormone is usually released from the anterior pituitary in order to stimulate the adrenal gland to produce Cortisol
    1. A healthy animal will have heightened cortisol levels following injection whereas an Addison's sufferer will have no change
  2. Blood test prior to injection. 1ml synthetic ACTH injected (Synactin). Blood test 1 hour post injection.
"Aims of treatment"
1. Acute medical emergency
  1. Stabilise patient ASAP
2. FLUIDS
  1. Support vascular systems & reduces shock
    1. NO HARTMANS- contains K +
  2. Sodium chloride (Saline) administered to reduce hyperkalaemia and improve sodium and chloride levels
3. STEROIDS
  1. Synthetic glucocorticoid (Prednisolone sodium succinate)
  2. Short-course Preds once stable - not long term as animal cna usually cope with glucocorticoid insufficiency (Cortisol)
  3. Once stable maintained on a synthetic minercorticoid (Florinef) in order to compensate for Aldosterone reduction
4. HYPERKALAEMIA
  1. Dangerous in an emergency situation - capable of causing serious cardiac dysfunction
    1. Small dose of insulin causes cellular uptake of Potassium - therefotre lowering blood concentration
      1. Ahee and Crowe, 2000
      2. NO steroids in this situation until insulin has stopped being effective as they can promote insulin resistance
NURSING TREATMENT
1. MONITORING
  1. Regular electrolyte measurements
  2. Temp
  3. Fluids
2. Regular trips outside to toilet if capable
  1. Potentially incontinent - INKA pad
  2. Check hygiene constantly
  3. Not weeing = need diruetics
3. Offer renal diet when stable
4. Home ASAP to prevent stress
5. Recumbent patient - comfy bed & regular turning
6. Recommend home visits & zylkene to reduce stress

Next up

Addisons disease/ crisis

Description

Resource summary

Similar

	Created by becky.rawlinson about 11 years ago