Electrolyte disorders Flashcards

Question

Presentation of hypernatraemia

Answer 1

-Thirst -Weakness -Dizziness -Oliguria and concentrated urine. -More severe cases may result in confusion and weakness, and possibly tachycardia, and finally hypotension and coma

Answer 2

-Plasma urea is usually elevated due to a low urine flow rate, which is accompanied by increased tubular reabsorption of urea. -These findings, along with a urine osmolality of over 600 mosm/kg confirm water depletion. -EGFR, creatinine

Answer 3

-The treatment is to give enough water to replenish body water stores, accounting for any ongoing water losses. =This may be given enterally (drinking or NG tube) or parenterally as intravenous 5% glucose. -Treatment is by oral replacement of water in mild cases; 5% dextrose (i.v.) in moderate cases; and a combination of 5% dextrose and 0.9% (150mmol/l) saline (i.v.) if dehydration is severe, as volume expansion requires salt as well as water. Hypernatraemia should be corrected with great caution. Although brain tissue can lose sodium and potassium rapidly, lowering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death1. Although there are no clinical guidelines by NICE or Royal College of Physicians at present, it is generally accepted that a rate of no greater than 0.5 mmol/hour correction is appropriate1.

Answer 4

-Hyponatraemia is a problem of low plasma tonicity. Or you can consider it as a problem of excess body water. -Translocation of water into the circulation such as in severe hyperglycaemia (in which case plasma tonicity will be normal and there is no risk of cerebral oedema; POsm > 280 mOsm/L) -POLYDIPSIA: Excessive water intake (relative to kidney function) or low dietary solute (beer potomania, tea and toast) intake (in which the urine will be very dilute: UOsm < 100 mOsm/L) -Release of ADH in response to hypovolaemia (in which case the renin-angiotensin system will also be activated so that urinary sodium excretion is low: UNa < 30 mM) -Reduced body sodium: water depletion accompanied by excessive Na+ depletion – e.g. large electrolyte losses replaced largely by water drinking. Seen in Addison’s disease, for example, when kidneys fail to retain sodium. -Release of ADH in response to what the body perceives as hypovolaemia in low cardiac-output or vasodilated states such as heart failure or portal hypertension in liver cirrhosis (renin-angiotensin system will be activated so UNa < 30 mM) -Inappropriate release of ADH in euvolaemia in response to drugs, chest and CNS disease, pain, stress or as a paraneoplastic phenomenon = SIADH (UNa > 30 mM) -Hypovolaemia with manifest UNa >30, impair salt reabsorption within kidney (thiazide, renal salt-wasting, adrenal insufficiency) Urinary sodium > 20 mmol/l Sodium depletion, renal loss (patient often hypovolaemic) diuretics: thiazides, loop diuretics Addison's disease diuretic stage of renal failure Patient often euvolaemic SIADH (urine osmolality > 500 mmol/kg) hypothyroidism Urinary sodium < 20 mmol/l Sodium depletion, extra-renal loss diarrhoea, vomiting, sweating burns, adenoma of rectum Water excess (patient often hypervolaemic and oedematous) secondary hyperaldosteronism: heart failure, liver cirrhosis nephrotic syndrome IV dextrose psychogenic polydipsia

Answer 5

-Impaired urinary dilution =Thiazide -Renal salt wasting =NSAIDs/ antibiotics, PPIs (if AIN) -SIADH =Antidepressants (SSRIs, TCAs) =Antipsychotics =Anticonvulsants (carbamazepine) =Anti-cancer (cisplatin) =Opioids =MDMA -Reset osmostat =Venlafaxine, carbamazepine -Excessive thirst =MDMA

Answer 6

-Moderately severe= nausea, confusion, headache -Severe= vomiting, CNS, depression, seizures, coma -Rapid changes in sodium levels or severe hyponatraemia can cause symptoms such as vomiting, drowsiness, headache, seizures, coma, and cardio-respiratory arrest due to cerebral oedema and raised intracranial pressure. -Chronic mild hyponatraemia can lead to gait instability, falls, and concentration and cognitive deficits. -Acute hypernatremia (rapid onset)// rapid correction of chronic hyponatraemia= rapid increase in plasma sodium concentration= osmotic demyelination/ Central pontine myelinolysis, causing severe permanent brain damage -Rapid onset of acute hyponatraemia/ rapid correction of chronic hypernatremia= rapid decrease in plasma sodium concentration= cerebral oedema

Answer 7

-History and examination =Drugs, clinical conditions, intercurrent illness (gastroenteritis), chronic illness (anorexia), fluid intake and nocturnal polyuria -Serum sodium -Plasma osmolality (POsm): high= hypertonic, low= hypotonic -Urine osmolality (UOsm); estimate ADH, low (100)= ADH not acting, high= acting -Urine sodium concentration (UNa)

Answer 8

-Mild (130-135): Debated risks of osteoporosis, neurocognitive defects -Moderate (125-130) -Profound (<125) real risks of cerebral oedema and ODS -Acute= duration known to be <48hrs -Chronic= duration unknown or >48hrs -By volume status (deplete, normal, expanded) -High risk of ODS (osmotic demyelination syndrome)= hypokalaemia, EtOH, malnutrition, liver disease

Answer 9

1. Exclude hyperglycaemia and other causes of non-hypotonic hyponatremia (translocational): plasma osmolality (<275) 2. Is hypotonic hyponatremia acute or severe symptoms? =Yes: medical emergency: consider immediate treatment with hypertonic saline (seek senior help) 3. If not, urine osmolality =<100 consider primary polydipsia, low solute intake, beer potomania =>100 4. Urine sodium concentration =<30 mmol/l: low effective arterial blood volume ==If ECF expanded: HF, liver cirrhosis, nephrotic syndrome ==If ECF reduced: D&V, third spacing, remote diuretics =>30 mmol/l ==Diuretics, kidney disease, all other causes ==If ECF reduced: vomiting, primary adrenal insufficiency, renal salt wasting, cerebral salt wasting, occult diuretics ==If ECF normal: SIAD, secondary adrenal insufficiency, hypothyroidism, occult diuretics -Duration of hyponatremia: is it acute or chronic? =acute: develops over a period of < 48 hours =chronic: develops over a period > 48 hours -The severity of hyponatremia: what is the sodium level? =mild: 130-134 mmol/L =moderate: 120-129 mmol/L =severe: < 120 mmol/L -Symptoms: is the patient symptomatic? =Early symptoms may include: headache, lethargy, nausea, vomiting, dizziness, confusion, and muscle cramps =Late symptoms may include: seizures, coma, and respiratory arrest -Suspected aetiology of the hyponatraemia: =hypovolemic hyponatraemia/clinically =dehydrated: diuretic stage of renal failure, diuretics, Addisonian crisis =euvolemic hyponatraemia: SIADH =hypervolaemic hyponatraemia: heart failure, liver failure, nephrotic syndrome

Answer 10

-Acute symptomatic hyponatraemia= hypertonic saline (seek expert help) -Primary polydipsia= reduced water intake -Low solute intake= dietary review, supplemental Na and K -Hypovolaemia hyponatraemia= ICV 0.9% NaCl. For dehydrated patients, administer 0.9% (isotonic) saline (150 mmol/l NaCl) to replenish volume. -Volume expanded= loop diuretics (or water restriction) -SIADH= water restriction (furosemide or V2R antagonists) -Aim to correct chronic hyponatraemia slowly (5 mM/day, no more than 10) -Chronic hyponatreamia without severe symptoms =If a hypovolemic cause is suspected normal, i.e. isotonic, saline (0.9% NaCl) this may sometimes be given as a trial if the serum sodium rises this supports a diagnosis of hypovolemic hyponatraemia if the serum sodium falls an alternative diagnosis such as SIADH is likely =If a euvolemic cause is suspected fluid restrict to 500–1000 mL/day consider medications: demeclocycline vaptans (see below) =If a hypervolemic cause is suspected fluid restrict to 500–1000 mL/day consider loop diuretics consider vaptans -Acute hyponatreamia with severe symptoms =Patients with acute, severe (<120 mmol/L) or symptomatic hyponatraemia require close monitoring, preferably in an HDU or above setting. =Hypertonic saline (typically 3% NaCl) is used to correct the sodium level more quickly than would be done in patients with chronic hyponatraemia.

Answer 11

Vasopressin/ADH receptor antagonists (vaptans): these act primarily on V2 receptors - antagonism of V2 receptors results in selective water diuresis, sparing the electrolytes They should be avoided in patients who have hypovolemic hyponatremia Vasopression/ADH receptor antagonists can stimulate the thirst receptors leading to the desire to drink free water. They can be hepatotoxic in patients with underlying liver disease.

Answer 12

-Osmotic demyelination syndrome (central pontine myelinolysis) =Can occur due to over-correction of severe hyponatremia =Usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma =Patients are awake but are unable to move or verbally communicate, also called 'Locked-in syndrome’

Answer 13

Acute severe hypercalcaemia is a medical emergency because it can cause cardiac dysrhythmia and coma

Answer 14

-Detected in parathyroid glands -PTH acts in bone gut and kidney to mobilise calcium from bone stores and modify excretion -Vit D activated in liver an kidney: gut promotes absorption -Calcium receptor in renal tubule: produces dilute urine in hypercalcaemia =Hypercalcaemia causes the kidney to make a dilute urine. (This effect is mediated in the loop of Henle, mimicking a loop diuretic such as furosemide.)

Answer 15

Hypercalcaemia may be due to excessive PTH secretion (in primary: adenoma or tertiary hyperparathyroidism: chronic kidney disease as glands hyperplastic) or due to other causes such as malignancy, in which PTH levels are suppressed (PTHrP)/ release calcium from bones (osteolytic lesions, myeloma) -FHH: mutations in calcium sensing receptor= negative feedback at higher set point -Vit D ingestion, sarcoidosis, lymphoma, TB: granulomatous produces Vit D -Immobilisation, thyrotoxicosis, milk-alkali Two conditions account for 90% of cases of hypercalcaemia: 1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients 2. Malignancy: the commonest cause in hospitalised patients. This may be due to a number of processes, including; PTHrP from the tumour e.g. squamous cell lung cancer bone metastases myeloma,: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells for this reason, measuring parathyroid hormone levels is the key investigation for patients with hypercalcaemia

Answer 16

-Impaired urinary Ca excretion =Thiazide =Calcium-containing antacid preps (milk-alkali) =Lithium -Increased absorption =Vitamin preparations =Calcium-containing antacid preps (milk-alkali) -Stimulation of PTH secretion =Lithium -Reduced bone buffering =Vitamin A =Anti-oestrogen

Answer 17

-Thrones (toilet): polyuria, thirst, volume depletion -Groans: peptic ulcer, pancreatitis, constipation -Moans: fatigue, depression, delirium -Stones: kidney stones, nephrocalcinosis -Bones: osteoporosis -Features of malignancy corneal calcification shortened QT interval on ECG hypertension

Answer 18

-Classification: <3 mM mild 3-3.5 mM moderate >3.5 mM severe (cardiac dysrhythmia, seizures) -History =Symptoms of hypercalcaemia and duration =Symptoms of underlying causes, e.g. weight loss, night sweats, cough =Family history =Drugs including supplements and over-the-counter preparations -Examination: volume deplete, malignancy, Assess for cognitive impairment, Fluid balance status. For underlying causes, including neck, respiratory, abdomen, breasts, lymph nodes -ECG: short QTc -Bloods: calcium adjusted for albumin, phosphate, PTH, U&E 1. PTH: =High/not low in primary hyperparathyroidism =-If low or normal then... 2. PTHrP and vitamin D metabolites =High PTHrP: malignancy =High vit D: granulomatous diseases/ vit D intoxication =If normal... 3. Multiple myeloma testing =Abnormal: MM =Normal: consider milk-alkali syndrome

Answer 19

-Volume resuscitation with copious IV 0.9% NaCl (4-6L in 24 hours) -IV bisphosphonates (takes days to work) =Zoledronic acid 4mg over 15 mins -Additional treatments addressing underlying cause -Second line: glucocorticoids, calcimimetics, parathyroidectomy The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days Other options include: calcitonin - quicker effect than bisphosphonates steroids in sarcoidosis Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.

Answer 20

The clinical history combined with parathyroid hormone levels will reveal the cause of hypocalcaemia in the majority of cases Causes vitamin D deficiency (osteomalacia) chronic kidney disease hypoparathyroidism (e.g. post thyroid/parathyroid surgery) pseudohypoparathyroidism (target cells insensitive to PTH) rhabdomyolysis (initial stages) magnesium deficiency (due to end organ PTH resistance) massive blood transfusion acute pancreatitis

Answer 21

As extracellular calcium concentrations are important for muscle and nerve function many of the features seen in hypocalcaemia seen a result of neuromuscular excitability Features tetany: muscle twitching, cramping and spasm perioral paraesthesia if chronic: depression, cataracts ECG: prolonged QT interval Trousseau's sign carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic wrist flexion and fingers are drawn together seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people Chvostek's sign tapping over parotid causes facial muscles to twitch seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people

Answer 22

Contamination of blood samples with EDTA may also give falsely low calcium levels.

Answer 23

severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes intravenous calcium chloride is more likely to cause local irritation ECG monitoring is recommended further management depends on the underlying cause