Electrolyte abnormalities Flashcards
PTH has many actions - all serving to increase plasma Ca2+ levels.
State what they are [5]
- Increasing osteoclastic resorption of bone - occurs rapidly
- Increasing intestinal absorption of Ca2+ - slow response
- Activation of 1,25-dihydroxyvitamin D (calcitriol) in the kidney
- Increasing renal tubular reabsorption of Ca2+
- Increasing excretion of phosphate
State 4 roles of calcitriol [4]
(active form of vitamin D)
- Increased Ca2+ and phosphate absorption in the gut
- Increased Ca2+ and phosphate reabsorption in the kidney’s
- Inhibits PTH release - negative feedback
- Enhanced bone turnover by increasing numbers of osteoclasts
What is the role of calcitonin? [2]
Where is it produced? [1]
Lowers Ca2+ & P levels by:
- Inhibits Ca2+ absorption by intestines
- Inhibits Ca2+ reabsorption in kidney
- Promotes osteoblasts, inhibits osteoclasts
Secreted by C cells of thyroid
Hypercalcaemia has what effect on urine and thirst? [1]
Causes polyuria and polydipsia
How should you manage acute hypercalcaemia? [1]
What drug should you prescribe if Ca2+ remains elevated? [1]
- Give IV saline alone
- If Ca still high - give bisphosphinates; pamidronate: prevent bone resorption by inhibiting osteoclast activity. Single dose of 4mg will normalise serum Ca2+ levels within a week
Describe the causes of [3]
Primary hyperparathyroidism
Secondary hyperparathyroidism
Tertiary hyperparathyroidism
Primary hyperparathyroidism:
- is caused by uncontrolled parathyroid hormone production by a tumour of the parathyroid glands
- this leads to a raised blood calcium (hypercalcaemia)
Secondary hyperparathyroidism:
- is where insufficient vitamin D or chronic kidney disease reduces calcium absorption from the intestines, kidneys and bones.
- this result in low blood calcium (hypocalcaemia).
- The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone.
- The serum calcium level will be low or normal, but the parathyroid hormone will be high.
Tertiary hyperparathyroidism:
- when secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated
- hyperplasia (growth) of the parathyroid glands occurs as they adapt to producing a higher baseline level of parathyroid hormone
- Then, when the underlying cause of the secondary hyperparathyroidism is treated, the baseline parathyroid hormone production remains inappropriately high.
- In the absence of the previous pathology, this high parathyroid hormone level leads to the inappropriately high absorption of calcium in the intestines, kidneys and bones, causing hypercalcaemia. Treatment is surgically removing part of the parathyroid tissue to return the parathyroid hormone to an appropriate level.
State the most likely cause of:
Primary hyperparathyroidism [2]
Secondary hyperparathyroidism [2]
Tertiary hyperparathyroidism [1]
Primary hyperparathyroidism
* Solitary adenoma (80%)
* Hyperplasia (20%)
Secondary hyperparathyroidism
* Vit D deficiency (reduced intake)
* CKD - difficulty making Vit D
Tertiary hyperparathyroidism
- Secondary hyperparathyroidism
How would you investigate for hypercalcaemia if PTH is high? [1]
How would you investigate for hypercalcaemia if PTH is low? [1]
PTH high: indicates hyperparathyroidism
- USS
- SestaMibi Scan
- Parathyroid venous sampling
PTH low: indicates cancer:
- test for PTH related Peptide (PTHrP) - but can’t measure this - so do local body signs of cancer and further tests
Give differential diagnosis of primary hyperparathyroidism [3]
Thiazide like diuretics [1]
Lithium [1]
Tertiary hyperparathyroidism [1]
Acute severe hypercalcaemia is a MEDICAL EMERGENCY.
State how you would treat a ptx suffering from acute severe hypercalcaemia [4]
- Rehydrate with IV 0.9% saline fluids - to prevent stones
- Furosemide: loop diuretic that increases Ca2+ excretion
- Give bisphosphonates (to prevent bone resorption by inhibiting osteoclasts) after rehydration e.g. IV PAMIDRONATE
- Measure serum U&E’s daily and serum Ca2+ 48hrs after initial treatment
- Can give glucocorticoid steroids e.g. ORAL PREDNISOLONE in myeloma, sarcoidosis and vitamin D excess
How do you treat ptx with hypocalcaemia:
With < 1.9 Ca2+, no symptoms? [2]
With < 1.9 Ca2+, symptoms? [2]
< 1.9 with no symptoms
- Oral calcium supplements
- If due to severe vitamin D def, treat with high dose vit D (Calcitriol)
< 1.9 with symptoms
- IV calcium gluconate
Describe the causes of primary and secondary hypoparathyroidism [2]
Primary hypoparathyroidism:
- caused by autoimmune DiGeorge syndrome (Congenital familial condition in which the parathyroid glands fail to develop;
- idiopathic hypoparathyroidism
Secondary hypoparathyroidism
- After parathyroidectomy or thyroidectomy surgery. most common cause)
State the overarching causes of hypocalcaemia [8]
- Secondary to increased serum phosphate levels: CKD
- Severe vitamin D deficiency
- Reduced PTH production:
Primary hypoparathyroidism
& Secondary hypoparathyroidism - Radiation
- Hypomagnesaemia - Mg is required for PTH secretion
- Pseudohypoparathyroidism: failure of target cell response to PTH due to owing to a mutation in the Gs alpha-protein (GNAS1), which is coupled to the PTH receptor
- Pseudopseudohypoparathyroidism: Same phenotypic defects as pseudohypoparathyroidism e.g. short stature; but without any abnormalities of Ca2+ metabolism
- Drugs: Calcitonin - decreases plasma Ca2+ and phosphate; Bisphosphonates - reduce osteoclast activity resulting in reduced Ca2+
- ACUTE PANCREATITIS
Hyperkalaemia is associated with which change acid/base change? [1]
Why? [1]
Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule.
- H+ / K+ channel tries to excrete H in exchange for K
Name some pathological causes of hyperkalaemia [6]
AKI
CKD
Hypoaldosteronism
Addison’s disease
Stoma leak
Metabolic acidosis
Massive haemoysis
Name 5 drugs / classes which may cause hyperkalaemia due to impaired excretion of K
ACE inhibitors
Spirolactone
NSAIDs
Heparin
Ciclosporin
ketoconazole
tacrolimus
High dose trimethoprim
Name3 drugs / classes which may cause hyperkalaemia due to increased cellular release [3]
Insulin deficiency
Digoxin toxicity
Beta blockers
The diagnosis of hyperkalaemia is based on a laboratory sample of plasma potassium being ≥ [] mmol/L.
> 5.5
Describe the treatment algorithim for treating hyperkalaemia
All patients with severe hyperkalaemia (≥ 6.5 mmol/L) or ECG changes
- IV calcium gluconate: to stabilise the myocardium
- insulin/dextrose infusion: short-term shift in potassium from ECF to ICF; (10U soluble insulin) in 25g glucose (50mL of 50% or 125ml of 20% glucose)
- Nebulised salbutamol
All patients with moderate-to-severe hypokalaemia should have an ECG.
What are typical ECG changes you’d expect to see?
Flat T waves
ST depression
Prominent U waves
Prolonged PR
Describe the management plan of hypokalaemia
All patients with moderate or severe hypokalaemia should have a 12 lead ECG.
Mild-Moderate:
- oral replacement - e.g. SANDO-K
Severe hypokalaemia:
- intravenous replacement typically with 40 mmol of KCL in 1 litre of normal saline.
- Correct Magnesium: as low magnesium causes renal potassium wasting and may prevent potassium correction
