Electrolyte Imbalance Flashcards
Describe the steps of Calcium Homeostasis
- Ca too high
- Ca too low
- thyroid produces calcitonin to decrease renal Ca absorption and inhibit osteoclast activity. Parathyroid is suppressed
- parathyroid produces PTH which acts to increase osteoclast activity and increase renal vitamin D activation
active vitamin D increases renal and intestinal Ca absorption
- What is the pathophysiology of primary hyperparathyroidism?
- What is the most common cause of primary hyperparathyroidism?
- PTH secretion increased. Ca is raised as a consequence
2. parathyroid gland adenoma
Describe clinical features of primary hyperparathyroidism
- nephrolithiasis
- polyuria and polydipsia
- bone, muscle and joint pain
- loss of appetite and weight loss
- nausea and constipation
- fatigue
- depression
What is the pathophysiology of secondary hyperparathyroidism?
excessive secretion of PTH in response to hypocalcaemia/hyperphosphataemia
- raised PTH
- low Ca
What are the 2 most common causes of secondary hyperparathyroidism?
- CKD
- poor dietary Ca intake/vitamin D deficiency
What is the pathophysiology of tertiary hyperparathyroidism?
persistent secondary hyperparathyroidism
- parathyroid hyperplasia results in autonomous PTH secretion
- Name causes of hypoparathyroidism
2. What are the metabolic consequences of hypoparathyroidism?
1. post operative - thyroidectomy; radical neck dissection autoimmune congenital infiltration radiation
- hypocalcaemia
hyperphosphataemia
- What are the major biochemical derangement associated with a low GFR?
- What are the major biochemical derangements associated with tubular dysfunction?
- raised urea, creatinine, potassium and phosphate; reduced Ca; Acidotic
- normal urea and creatinine; decreased potassium and phosphate; Alkalotic
- What derangements are associated with thiazide/loop diuretic use?
- decreased sodium and potassium; increased bicarb and urea
What are the biochemical/electrolyte derangements associated with:
- Addion’s
- Cushings?
- Conn syndrome
- Diabetes Insipidus
- SIADH
- hyperkalaemia, hyponatraemia, raised urea
- hypokalaemia, hypernatraemia; raised bicarb
- hypokalaemia; raised bicarb; sodium normal or raised
- raised sodium and plasma osmolality
- hyponatraemia; decreased plasma osmolality
Describe signs and symptoms of hyponatraemia
- anorexia
- nausea
- malaise
- headache
- irritability
- confusion
- decreased GCS
- seizures
What are the causes of:
1. hypovolaemic hyponatraemia?
- euvolaemic hyponatraemia?
- hypervolaemic hyponatraemia?
- D&V, burns, pancreatitis, diuretics, mineralocorticoid deficiency (Addison’s), osmotic diuresis
- drugs - thiazides, carbamazepine, vincristine, ecstasy
adrenal insufficiency
hypothyroidism
SIADH
3. cirrhosis
heart failure
AKI
CKD
nephrotic syndrome
- how is hyponatraemia managed?
2. Why does care need to be taken with the management of hyponatraemia
- correct underlying cause
fluid restriction if chronic and asymptomatic - don’t correct fluid status/sodium levels rapidly as can lead to central pontine myelinolysis
What is the most concerning complication associated with hyperkalaemia?
myocardial hyperexcitiability leading to VF and cardiac arrest
Name concerning signs and symptoms of hyperkalaemia
- fast, irregular pulse
- chest pain
- palpitations
- weakness
- light headedness
- tall inverted T waves
- small P waves
- wide QRS
