Electrolytes Flashcards
1
Q
What are the signs and symptoms of HYPERcalcaemia?
A
- weakness
- fatigue
- excessive thirst
- confusion
- bone and joint pain
- vomiting
- dehydration
- muscle spasms
- irregular heartbeat
- hypertension
- drowsiness
- polyuria
- memory problem
- abdominal pain
- depression
- coma
2
Q
What complications can arise from HYPERcalcaemia?
A
- Kidney Stones
- Renal Impairment
- Stomach Ulcers
- Osteoporosis
3
Q
What can cause HYPERcalcaemia?
A
- Hyperparathyroidism
- Familial hypocalciuric hypercalcaemia
- Granulomatous Disease
- laxatives
- Immobility = accelerated bone turnover such as Paget’s disease. Enhanced osteoclast activity and diminished osteoblast activity results in overall increased bone resorption. In some cases, hypercalcaemia of another cause is worsened by immobility.
- Renal = 1. In chronic renal failure, low calcium levels cause parathyroid gland hypertrophy (secondary hyperparathyroidism). Tertiary hyperparathyroidism occurs when the hypertrophied glands start to produce excess unregulated PTH autonomously, causing calcium levels to rise inappropriately
2. In end-stage renal disease and/or people receiving renal replacement therapy, treatment with calcium and calcitriol or vitamin D analogues may precipitate hypercalcaemia
3. Following renal transplantation, hypercalcaemia may occur due to pre-existing parathyroid hyperplasia and the restoration of 1,25-dihydroxyvitamin D3 production by the transplanted kidney
4. During the recovery phase of acute kidney injury (AKI), hypercalcaemia may result from rebound increases in levels of PTH and 1,25-dihydroxyvitamin D3. If the AKI was due to rhabdomyolysis, hypercalcaemia also results from subsequent mobilization of calcium deposited in muscle and soft tissue.
4
Q
What are the levels for mild, moderate and severe HYPERcalcaemia?
A
- Mild = 2.6- 3.00 mmol/L
- Moderate = 3.01- 3.40 mmol/L
- Severe = >3.40 mmol/L
5
Q
What drugs can lead to HYPERcalcaemia?
A
-Thiazide like diuretics
- Lithium may directly stimulate PTH secretion and increase renal calcium reabsorption. The effects are typically reversed on drug withdrawal. Lithium decreases the sensitivity of the calcium-sensing receptor to calcium, and it may also unmask pre-existing primary hyperparathyroidism
- Vitamin D
- Vitamin A = manifestations of vitamin A toxicity include dermatitis, alopecia, and hepatic dysfunction
- Calcium co-prescribed with antacids or calcium and vitamin D preparations (‘calcium-alkali syndrome’)
This syndrome is characterized by severe hypercalcaemia, renal impairment, and metabolic alkalosis.
6
Q
What are the treatment options for HYPERcalcaemia?
A
- Bisphosphonates (pamidronates disodium)
- Calcitonin
- Corticosteroids
7
Q
What are the levels for mild, moderate and severe HYPOnatraemia?
A
Hyponatraemia is defined as a serum sodium concentration of less than 135 mmol/L.
- Mild = 135–130 mmol/L.
- Moderate = 129–125 mmol/L
- Severe = < 125 mmol/L
8
Q
What are the rate of onset of HYPOnatraemia?
A
- Acute — duration of less than 48 hours.
- Chronic — duration of 48 hours or more.
9
Q
What are the causes of HYPOnatraemia?
A
- Medications (most commonly thiazide diuretics).
- Syndrome of inappropriate antidiuresis (SIADH)
- Underlying medical conditions e.g. heart failure, kidney disease, and liver disease.
10
Q
What are the symptoms of HYPOnatraemia?
A
Rapid change or severe hyponatraemia =
- vomiting
- headache
- drowsiness
- seizures
- coma
- cardio-respiratory arrest
Chronic hyponatraemia =
- increased risk of falls
- bone fractures
- osteoporosis
- gait instability
- concentration and cognitive deficits
The 3 C’s - Confusion, Convulsant, Coma- Mental Status Change
11
Q
What drugs can cause HYPOnatraemia?
A
- Thiazide and thiazide-like diuretics inhibit sodium chloride reabsorption in the distal tubules.
- Loop diuretics may also cause hyponatraemia, but this is more likely to occur when they are taken in combination with medications, such as angiotensin converting enzyme (ACE) inhibitors or spironolactone. Loop diuretics inhibit sodium chloride reabsorption in the ascending loop of Henle
- SSRIs (especially citalopram) are more frequently associated with hyponatraemia than other antidepressants. Older age and concurrent use of diuretics are the most important risk factors for development of SSRI-associated hyponatraemia
- Antipsychotics (such as haloperidol and phenothiazines)
- Carbamazepine. It is more frequent in the elderly or when concurrently used with diuretics or antipsychotics
12
Q
What are the different types of HYPOnatraemia?
A
- Hypotonic (or true) hyponatraemia (A hypotonic solution has a lower concentration of solutes than another solution)
- Hypovolemic (volume depletion) hyponatraemia occurs when the total body water and sodium content are both decreased but the relative decrease in total body sodium is greater than the decrease in total body water.
- Hypervolemic (volume overload) hyponatraemia occurs when the total body water and sodium content both increase but the relative increase in total body water is greater than the increase in total body sodium, resulting in oedema
- Euvolemic (normal volume status) hyponatraemia occurs when the total body water increases but the total body sodium remains unchanged, thereby producing a dilutional effect.
- Hypertonic (or hyperosmolar) hyponatraemia can be caused by severe hyperglycaemia (the high levels of glucose draw intracellular water into the extracellular space) or administration of an active osmolyte (such as mannitol)
13
Q
What drugs can cause of HYPOnatraemia?
A
- Thiazide and thiazide-like diuretics inhibit sodium chloride reabsorption in the distal tubules
- Loop diuretics may also cause hyponatraemia, but this is more likely to occur when they are taken in combination with medications, such as angiotensin converting enzyme (ACE) inhibitors or spironolactone.
Loop diuretics inhibit sodium chloride reabsorption in the ascending loop of Henle. - Selective serotonin reuptake inhibitors (SSRIs) — SSRIs (especially citalopram)
- Antipsychotics (such as haloperidol and phenothiazines
- Carbamazepine, more frequent in the elderly or when concurrently used with diuretics or antipsychotics
- Drugs that increase the production, or potentiate the action, of ADH (SIADH):
Opioids.
ACE inhibitors and angiotensin-II receptor antagonists (AIIRAs).
Proton pump inhibitors (such as omeprazole and lansoprazole).
Anticonvulsants (such as sodium valproate, lamotrigine, and leviteracetam).
Amiodarone.
Theophylline.
Dopamine antagonists (metoclopramide and domperidone).
Antidiabetics (insulin, chlorpropamide, and tolbutamine).
Nonsteroidal anti-inflammatory drugs.
MDMA (ecstasy).
-Drugs that cause loss of ADH inhibition (SIADH):
Nonsteroidal anti-inflammatory drugs (particularly in combination with thiazide diuretics or heart failure).
-Drugs that produce exogenous ADH:
Desmopressin.
Oxytocin.
14
Q
What are the other causes of HYPOnatraemia?
A
- Heart Failure = Hyponatraemia in heart failure is primarily caused by a low cardiac output. Although there is an increase in plasma volume in heart failure, the effective circulating arterial volume is depleted and this stimulates sodium and water retention by the release of ADH, renin (subsequently leading to increases in angiotensin II), and noradrenaline.
- Liver disease = Hyponatraemia in liver failure may be triggered by reduced effective arterial blood volume from systemic vasodilation and arteriovenous shunting of blood. The reduced effective blood volume can activate baroreceptor-mediated ADH release leading to water retention
- Kidney diseases = The reduction in renal function may cause hyponatraemia through non-osmotic stimulation of ADH release
- Third spacing = occurs when too much fluid moves from the blood vessels into the interstitial or ‘third” space’ (the nonfunctional area between cells)
Bowel obstruction, pancreatitis, sepsis, or muscle trauma may markedly reduce effective circulating blood volume through fluid leakage from blood vessels. The reduced effective blood volume can activate baroreceptor-mediated ADH release leading to water retention. - SIADH = Characterized by excessive insuppressible release of ADH either from the posterior pituitary gland, or an abnormal non-pituitary source. The excessive action of ADH produces a state of water excess without major sodium retention.
SIADH is a common cause of hyponatraemia and can result from malignancy (for example small cell lung cancer, gastrointestinal tract cancers), central nervous system disorders (e.g. subarachnoid haemorrhage, meningitis, encephalitis), pulmonary disease (e.g pneumonia), or other non-specific causes (e.g medications, pain, nausea, stress, general anaesthesia). It can also be idiopathic. - Endocrine disorders = are an uncommon cause of hyponatraemia.
In primary adrenal insufficiency, hyponatraemia is partly explained by mineralocorticoid deficiency, which results in increased excretion of sodium in the urine. A combination of hyponatraemia and hyperkalaemia is suggestive of Addison’s disease.
15
Q
What are the treatment option for HYPOnatraemia?
A
- Sodium Chloride
- Sodium Bicarbonate
- For syndrome of inappropriate antidiuretic hormone secretion (SIADH): Fluid restriction is recommended. If there is no clear cause for SIADH following initial investigations, CT chest/abdomen/pelvis and MRI head may be arranged to exclude underlying malignancy.
Tolvaptan (a vasopressin V2-receptor antagonist) is indicated in adults for the treatment of hyponatremia secondary to SIADH.
-Acute hyponatraemia with moderate or severe symptoms: Hypertonic saline restores serum sodium concentration to a safe level to correct any cerebral oedema and reduce the risk of complications.
- Acute hyponatraemia with mild or no symptoms:
Non-essential parenteral fluids and medications that can provoke hyponatraemia are stopped and treatment is directed at the underlying cause. - Chronic hyponatraemia without moderate or severe symptoms: Non-essential supplementary fluids and medications that can provoke hyponatraemia are stopped and treatment is directed at the underlying cause.
- People with hypervolaemia: Fluid restriction is recommended to prevent further fluid overload.
- People with hypovolaemia: Extracellular volume is restored with infusion of 0.9% saline.
