Electrolyte Imbalances Flashcards
What is the normal range for calcium?
Normal adjusted calcium level is 2.2 to 2.6mmol/L for albumin.
What is the role of calcium?
Calcium is important for action potentials, muscle contraction, hormone secretion and blood coagulation.
What is pseudohypocalcaemia?
Pseudohypocalcaemia is where low albumin causes a reduction in bound calcium.
What is hypocalcaemia?
Hypocalcaemia is a value below 2.1 mmol/L which occurs due to:
->Hypoparathyoridism
->Low Vitamin D from renal failure, liver cirrhosis or low dietary intake or lack f sunlight
->Tissue injury due to release of both calcium and phosphate causing precipitation of crystals
->Acute pancreatitis due to high lipid content binding to calcium
->Frequent blood transfusions due to content of EDTA and citrate binding to calcium
-> Acute respiratory alkalosis
-> Hyperphosphataemia
-> Excessive bisphosphonates
What is the cause of hypoparathyroidism?
->Magnesium deficiency
->Autoimmune disease
->Congenital conditions like DiGeorge syndrome
thyroidectomy
-> Radiotherapy for Graves’ disease or thyroid cancer
-> thyroidectomy
What are the signs of hypocalcaemia on ECG?
Prolonged ST, prolonged QT and arrythmias like torsades de pointes
What is the clinical presentation of hypocalcaemia?
Tetany, perioral paraesthesia, muscle stiffness and cramps, SOB and diaphoresis (sweating)
Clinical signs include Chvostek’s sign and Trousseau’s sign.
What is tetany?
Involuntary repetitive spasming of the peripheral nerves after a stimulus due to low calcium causing a loss of regulation of the cardiac membranes.
What is Chvostek’s sign?
A sign of hypocalcaemia: involuntary twitching of the facial muscles after pressing on the ipsilateral facial nerve
What is Trousseau’s sign?
A sign of hypocalcaemia: placing blood pressure cuff over 3 minutes on causes involuntary cargo pedal spasm
What are the causes of low vitamin D?
-> Low Vitamin D arises from renal failure, liver cirrhosis or low dietary intake or lack f sunlight
-> High levels of phosphate due to suppression of Vitamin D 1a-hydroxylase
-> Induction of cytochrome P450 which causes breakdown of calcitriol by medications like phenytoin and carbamezapine
Why does acute respiratory alkalosis cause hypocalcaemia?
Promotes the binding of albumin to calcium
Why does hyperphosphataemia causes hypocalcaemia?
Hyperphosphataemia promotes calcium deposition in bone and skeletal muscle and inactivation of vitamin D 1-alpha hydroxylase
What is the management of hypocalcaemia?
IV or parenteral calcium like calcium gluconate and calcium chloride with a continuous infusion best for maintained effect
Vitamin D supplementation if necessary
IV magnesium
Patients with arrythmias, prolonged QT on ECG and severe symptoms like tetany and seizures should immediately be started on treatment.
What is hypercalcaemia?
Hypercalcaemia is greater than 2.6 mmol/L
What is the clinical presentation of hypercalcaemia?
“stones, bones, groans and psychiatric overtones’’
-> Kidney stone formation
-> Depression, anxiety and confusion
->Constipation, lethargy and weakness due to: ->High Ca2+ hyper stabilises the membrane, reducing depolarisation and causes hyporeflexia and slow muscle contraction
->Hypercalcemia can cause dehydration, nephrogenic diabetes insipidus by reducing the sensitivity of the kidneys to ADH
->Type 1 renal tubular acidosis, occurring in the DCT
What is the cause of hypercalcaemia?
Malignancy:
->Excessive PTH due to adenoma, diffuse hyperplasia or carcinoma
->Malignancy due to PTHrP release in paraneoplastic syndrome
->Osteopathic metastases in breast, lung and multiple myeloma
Medications
-> Medications like thiazide diuretics which increase calcium reabsorption
-> lithium
Hormonal regulation
-> Paget’s disease due to excessive bone remodelling that causes misshapen, large and weak bones
-> Hyperthyroidism due to thyroid hormones promoting bone resoprtion
-> excess vitamin D
-> Sarcoidosis and granulomatous disorders and lymphomas cause excess calcitriol production
-> Adrenal crisis due to reduced aldosterone action for Ca2+ excretion
Miscellaneous:
-> rhabdomyolysis due to release of Ca2+ stores
What are the ECG findings for hypercalcaemia?
bradycardia, shortened QT, ST elevation, arrythmias, J/Osborn wave which is associated also with hyperthermia
-> Membranes are overstimulated, so less likely to fire
What is the treatment of hypercalcaemia?
First line treatment: IV Hydration due to polyuria causing dehydration and achieving dilution
Once patient is euvoluemic, loop diuretics like furosemide inhibit the Na-CL- K+ transporter
Glucocorticoids to reduce Ca2+ intestinal absorption
IV or IM calcitonin
Bisphosphonates: inhibit osteoclasts resorption
Steroids with lymphoma or granulomatous disease
What is the level for hyponatremia?
Sodium level below 135 meq/L is considered hyponatremia.
How does hyponatremia present?
Hyponatremia presents with fatigue, nausea, vomiting at acute levels. In chronic levels, it can cause confusion and seizures to occur.
What is the hypovolemic causes of hyponatremia?
Hypovolemia due to nausea, vomiting, renal tubular acidosis, cerebral salt wasting and diuretics which cause loss of sodium through fluids. This should be treated with isotonic saline.
What is the euvolemic causes of hyponatremia?
Related to ADH due to SIADH, reset osmostat, glucocorticoids and hypothyroidism which promotes water rebbsorption and causes lower sodium. This should be treated with water restriction and tolvaptan, a V2 receptor antagonist.
What are the hypervolemic cases of hyponatremia?
Hypervolemia due to fluid retention with heart failure, liver cirrhosis and advanced renal failure, where there is dilutional hyponatremia.
This should be treated with sodium and water restriction.
What are the causes of pseudohyponatremia?
Pseudohyponatremia can occur due to hyperglycaemia, osmotic diuretic, azotemia and elevation of serum lipid.
What is cerebral salt wasting?
Cerebral salt wasting is where there is insufficiency Na+ reabsorption that results in volume depletion and ADH secretion to compensate which reduces na+ levels by promoting water reabsorption.
How is hyponatremia investigated?
1) Obtain electrolyte for sodium and adjust for glucose
2) measure urine osmolality and specific gravity
-> high urine osmolality indicates high water content, may related to high ADH or primary polydipsia or renal failure
3) assess volume status
4) urine Na+ excretion
What is the cause of metabolic acidosis and hyperkalemia?
Primary adrenal sufficiency
What is the cause of metabolic acidosis and hypokalemia?
Volume depletion from diarrhoea
What is the cause of Metabolic alkalosis + hypokalemia?
Vomiting and diuretics due to loss of H+ ions from acid or reduced Na+ reabsorption.
What is the cause of hyponatremia with high uric acid and blood uric acid?
SIADH and cerebral salt wasting due to increased action of ADH on urea reabsorption along with water.
What is the cause of hypovolemic hyponatremia with low urine na+?
Nausea or vomiting.
What is the cause of hypovolemic hyponatremia with high urine Na+?
Diuretic use and primary adrenal insufficiency
-> Hyponatremia can be treated with volume depletion with IV hypotonic saline
What is the cause of euvolemic hyponatremia with low urine Na+?
Primary polydipsia and low dietary intake of salt.
What is the cause of euvolemic hyponatremia with high urine Na+?
SIADH, reset osmostat, cerebral salt wasting, secondary adrenal insufficiency, hypothyroidism and adrenal insufficiency due to changes in ADH
What is the cause of hypervolemic hyponatremia with low urine Na+?
Congestive heart failure
Liver cirrhosis
What is the cause of hypervolemic hyponatremia with high urine Na+?
Renal failure
-> Treatment with fluid restriction
What is the risk of correction of hyponatremia?
Osmotic demyelination: characterised by coma, personality changes, confusion, coma and paraparesis
What is the risk of use of tolvaptan?
Liver failure, therefore LFT monitoring is required
What is the treatment of cerebral salt wasting?
Hypertonic saline
What is the treatment of SIADH?
Fluid restriction or salt tablets and loop diuretics
What are the acute symptoms of hyponatremia?
Acute symptoms are seizures and cerebral oedema and risks of this outweighs demyelinations syndrome.
What are the chronic symptoms of hyponatremia?
Chronic symptoms include cognitive deficits and gait disturbances.
What is the value for hypernatremia?
Sodium level is over 145mEq/L is considered hypernatremia.
What is the clinical manifestation of hypernatremia?
Clinical mainfestations of hypernatremia are identical to hyponatremia with:
Fatigue, headache, fever, intense thirst, nausea, confusion, seizures and coma
What regulates levels of sodium?
Na+ levels are regulated by ADH which promotes loss of Na+ in urine.
Aldosterone promotes rebasorption of Na_
What are the hypovolemic causes of hypernatremia?
Hypovolemia due to deficit of Na+ from water loss associated with:
-> The use of osmotic + loop diuretics
-> Post-obstructive renal disease
-> Extra-renal losses with sweating, burns and diarrhoea that should be treated with hypotonic saline. There is typically a high urine osmolality
Treatment is with isotonic saline.
What are the signs of Hypovolemia?
Features are poor skin turgor, hypotension, tachycardia and dry mucous membranes.
What are the euvolemic causes of hypernatremia?
Euvolemic hypernatremia occurs due to loss of total body water, associated with:
Central diabetes insipidus due to trauma, malignancy, infiltrative disorders like sarcoma
Nephrogenic diabetes insipidus like
-> lithium, demeclocyline, cisplatin and amphotecrin, Chronic hypercalcaemia
->Chronic hypokalemia
->Renal diseases like amyloidosis -> Pregnancy
This should be treated with water replacement.
What are the hypervolemic causes of hypernatremia?
Hypervolemic hypernatremia occurs due to increased in total body water due to:
Conn’s syndrome, Cushing’s syndrome, hypertonic dialysis excess administration if saline and intake of sodium carbonate tablets.
This should be treated with diuretics and water replacement.
What is diabetes insipidus?
Diabetes insipidus is a resistance to effect of ADH for water reabsorption. This can cause high serum osmolality in solutes and urine is high in water, causing low osmolality.
What is complete diabetic insipidus?
Complete DI is where plasma osmolality exceeds urine due to water loss in urine.
Central will have greater urine osmolality than nephrogenic because there is no circulating ADH compared to nephrogenic where kidneys are unresponsive to ADH
What is partial diabetic insipidus?
Partial DI is where urine osmolality exceeds plasma due to some water rebasorption from regions where ADH is effective
What is the difference in urine osmolality between central and nephrogenic diabetes insipidus?
Central DI will have greater urine osmolality than nephrogenic because there is no circulating ADH compared to nephrogenic where kidneys are unresponsive to ADH
What is acute hypernatremia?
Acute hypernatremia is onset less than 48 hours and should be corrected within 24 hours
What is chronic hypernatremia?
Chronic hypernatremia is onset exceeding 48 hours and should be corrected by 10mg/L every 24 hours e.g 165 -> 155 in 24 hours
How should diabetes insipidus be treated?
Dextrose solution with water
What is a normal value for potassium?
3.5mmol/L to 5.2 mmol/L
What is clinical presentation of hypokalemia?
Muscle weakness in the legs especially, cramps, ileum and rhabdomyolysis
Arrythmias like atrial fibrillation
What are the signs of hypokalemia on ECG?
ECG will show ST depression, T wave inversion and prominent U waves.
What regulates the levels of potassium?
Aldosterone and cortisol which promotes the loss of K+ in the urine.
What is the cause of hypokalemia?
->Low intake:
Malnutrition from starvation or anorexia
-> Loss of potassium through vomiting and diarrhoea
Substance induced:
->Loop and thiazide diuretics promoting renal loss of K+
-> Laxative abuse
-> Chronic ingestion of liquorice
->Amphotecirin B (membrane permeability)
->High levels of mineralcorticoids or glucocorticoids with Conn’s syndrome and Cushing’s disease
Physiological
-> Type 1 and 2 Renal tubular acidosis
-> Hypomagnesiaemia
-> Insulin
-> Catecholeamines
-> Alkalosis
-> High cell proliferation which causes sequestering of potassium intracellularly
Why do catecholeamines cause low K+?
Activation of B2 receptors causes an intracellular shift of potassium into cells.
What is Liddell syndrome?
Genetic condition that causes pseudo Hyperaldosteronism where there is a mutation that increases the number of EnaC Na+ channel on the collecting duct for sodium reabsorption that causes persistent hypertension and Hypokalemia metabolic alkalosis
How does alkalosis affect potassium levels?
It promotes the loss of K+ and decreased reabsorption/ Acidosis promotes absorption of potassium.
What is secondary aldosteronism?
Secondary aldosteronism is characterised by high levels of renin due to renal vascular disease that causes hypoperfusion or a renin secreting tumour that promotes high levels of aldosterone and renin.
What is pseudohyperaldosteronism?
Pseudohyperaldosteronism due to Cushing’s syndrome or glucocorticoids as cortisol can act on mineralcorticoid receptors and promote hypertension. This can also occur due to LIddel’s syndrome.
What is pseudohypoklaemia?
release of potassium from cells due to
Fist clenching or prolonged use of tourniquet during phlebotomy
Increased cell count like erythrocytes is and thrombocytosis
How is hypokalemia investigated?
History
Checking magnesium levels
Acid base balance
Metabolic alkalosis with hypokalemia due to vomiting or laxative use, hyperaldosteronism and salt wasting nephropathy
Metabolic acidosis with hypokalemia due to diarrhoea or laxative use, diabetic ketoacidosis and type 1 and 2 renal tubular acidosis
How is hypokalemia treated?
Sodium gluconate to stabilise cardiac membranes
IV fluid with potassium chloride
Oral potassium chloride
What is hyperkalemia?
serum potassium levels are above 5.5 mmol/L
What are the clinical manifestations of hyperkalemia?
muscle weakness
Paraesthesia and fasiculation due to excitability of tissues
Cardiac condition abnormalities
How does hyperkalemia affect the ECG?
ST segment depression
Widening of PR interval and QRS interval
Tall Peaked waves
Sine wave where blending of QRS complex and T wave occurs
What are the causes of hyperkalemia?
Cell lysis from tumour lysis, Haemolysis and rhabdomyolysis
Acidosis
Renal failure
Insulin deficiency
Low aldosterone levels assoicated with:
-> Addison’s disease
-> Diabetic nephropathy and NSAID use
-> Use of ACE inhibitors and heparin
-> Excessive use of aldosterone receptor antagonists
->Use of trimethoprim
Which medications can cause hyperkalemia?
Potassium sparing diuretics
Mineralcorticoid and glucocortocids
Beta blockers
Digoxin toxicity
Calcineurin inhibitors
How is hyperkalemia treated?
IV calcium is an acute therapy which antagonises activity of potassium at cell membrane
Insulin with dextrose solution
Beta 2 agonists to stimulate potassium entry into cells
Sodium bicarbonate should only be used if metabolic acidosis is present
What is normal levels of phosphate?
Normal levels of phosphate are between 0.81-> 1.45 mmol/L and phosphate tends to be contained within cells typically.
What is considered a low level of phosphate?
Normal levels of phosphate are between 0.81-> 1.45 mmol/L and phosphate tends to be contained within cells typically.
What are the consequences of low phosphate?
Dysfunctional bone metabolism
Reduction in ATP generation for energy metabolism involved in contraction
Reduction in 2,3 DPG which increases haemoglobin affinity of oxygen and reduces disassociation of oxygen to tissue, causing hypoxia
What is the cause of hypophoosphataemi?
-> Malabsorption
-> Malnutrition in alcoholics
->Loss of PO42-
->Vitamin D deficiency
Hyperparathyroidism due to excessive osteolysis
-> Fanconi syndrome
->Re feeding syndrome that can cause low K+, magnesium and phosphate due to insulin
->Hungry bone syndrome following parathyroidectomy where there is high mineralisation of bone
-> Resp/metabolic Alkalosis
What is Fanconi syndrome?
Fanconi syndrome where there is a defect in the PCT reducing glucose, phosphate, protein and uric acid absorption. It is characterised by metabolic acidosis and, causing glucosuria and hypophosphataemia.
How does alkalosis cause hypophospataemia?
Increased pH stimulating phosphofructokinase For generation of ATP -> ADP that ends to depletion of potasssium
What does high urinary excretion of phosphate necessitate for investigation?
Investigate vitamin D, PTH levels and Fanconi syndrome
What does low urinary excretion of phosphate necessitate for investigation?
Investigate nutrition, GI malabosprtion, medications containing antacids with patients with GERD or GI losses from diarrhoea
Which medications cause low phosphate?
Intake of phosphate binders like antacids or calcium acetate
What is hyperphosphataemia?
Hyperphosphataemia is over 1.45 mmol/L and typically induces hypocalcaemia, with clinical presentation related to this:
tetany, Perioral paraesthesia, Muscle stiffness and cramps, SOB due to diaphragmatic spasms and Diaphoresis
What are the causes of hyperphosphataemia?
->Decreased Urinary excretion
-> Renal failure
-> Excess Vitamin D
-> Hypoparathyroidism
-> Acromegaly
-> Tumour lysis syndrome and Rhabdomyolysis due to release of intracellular contents
-> Lactic acidosis
Why does acromegaly cause hyperphosphataemia?
Acromegaly causes excessive growth hormone which stimulates phosphate reabsorption in the PCT.
Why does hypoparathyroidism cause hyperphosphataemia?
Due to reduced action of PTH for reducing renal phosphate absorption.
What is pseudohyperphosphataemia?
High levels of paraproteinemia which occurs in Multiple myeloma.
Hyperlipidaemia, hyper bilirubin anemia and chronic infection can also cause pseudo hyperphosphataemia
What is the treatment for hyperphosphataemia?
Haemodialysis, low phosphate diet or phosphate binders for impaired renal function
Treating Underlying condition
Phosphate binders include calcium salts like acetate
What is the normal level of magnesium?
Normal magnesium levels are between 0.85 to 1.10 mmol/L
Where is the majority of magnesium stored?
Majority of magnesium is stored in bones or within cells, with a minority free inn the plasma.
Where is magnesium absorbed?
Majority of magnesium absorption is in the ascending limb of the loop of Henle and relies on movement based on Na+ and Cl-
What is the clinical presentation of hypomagnesaemia?
Clinical presentation of hypomagnesiaemia is typically caused by secondary electrolyte abnormalities associated with hypokalemia and hypercalcaemia.
There is a risk of afibrillation ventricular arrythmias such as MI, prolonged QT, congestive heart failure and digoxin toxicity
What is the cause of hypomagnesaemia?
-> Alcohol overuse which reduces tubular absorption of magnesium
-> Use of PPIs which reduces gut absorption
->Chronic diarrhoea and inflammation of the bowel causes loss of magnesium
-> Osmotic diuresis from diabetes
-> Loop and thiazide diuretics, amphotecrin B, aminoglycosides and cisplatin
What is the treatment of hypomagnesaemia?
Treatment of hypomagnesiaemia should consider how abrupt increases from IV infusion inhibit magnesium reabsorption in loop of Henle so targ
Arrythmias and hypokalemia should receive IV magnesium
Asymptomatic- oral repletion of magnesium
What is hypermagnesamia
Hypermagnesmia is over 1.1 mmol/L
What is the clinical presentation of hypermagnesaemia?
Bradycardia, hypotension
Reduced reflexes, muscle weakness, drowsiness and parasympathetic blockade with dry mouth, dilated pupils and urinary retention
What is the cause of hypermagnesaemia?
Renal failure
IV infusion when treating conditions like ecclampsia
Tumour lysis syndrome
What is the treatment of hypermagnesaemia?
Treatment is dependent on renal function
Low GFR: furosemide and IV saline
Stage 5 GFR or Anuria AKI: dialysis
