Electrolyte Abnormalities Flashcards

1
Q

what is hyponatraemia?

A

sodium < 135 mmol/L

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2
Q

what is the presentation of hyponatraemia?

A
  • anorexia
  • nausea
  • malaise
  • headache and irritability
  • decreased GCS and confusion
  • weakness
  • seizures
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3
Q

what are the main causes of hyponatraemia?

A

SIADH
diuretics - esp thiazide
heart failure

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4
Q

how is hyponatraemia sub-categorised?

A
  • hypotonic (inc hypovolaemic, euvolaemic and hypervolaemic)
  • isotonic
  • hypertonic
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5
Q

what is hypotonic hyponatraemia caused by, generally?

A

an increase in intravascular volume (but the subcategories are based on total body water differences)

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6
Q

describe hypovolaemic hyponatraemia

A

there is a deficiency in both total body water and sodium

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7
Q

describe the pathophysiology of hypovolaemic hyponatraemia

A

low fluid volume due to decreased total body water causes ADH release. ADH causes water retention which increases intravascular volume (even though total body water is decreased), diluting the Na.

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8
Q

what are the causes og hypovolaemic hyponatraemia?

A
  • diuretics (thiazide)
  • intrinsic renal disease
  • mineralocorticoid deficiency (Addison’s disease)
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9
Q

describe euvolaemic hyponatraemia

A

total body water remains the same but water moves into the intravascular space, diluting the sodium

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10
Q

what are the causes of euvolaemic hyponatraemia?

A

SIADH - causes increased resorption of water by the kidney (can be euvolaemic or hypervolaemic)
iatrogenic (surgery causes impaired water excretion, certain types of surgical procedures)

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11
Q

describe hyervolaemic hyponatraemia

A

excess total body water means that there is also excess intravascular fluid, causing dilution of sodium

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12
Q

what are the causes of hypervolaemic hyponatraemia?

A
  • chronic renal failure
  • congestive heart failure
  • liver cirrhosis
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13
Q

what is redistributive hyponatraemia?

A

hypertonic hyponatraemia
- hypertonic blood with excess osmolytes causes water to shift from the intracellular to the extracellular compartment (into blood), diluting the extracellular sodium.

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14
Q

what can cause redistributive hyponatraemia?

A

hyperglycaemia

or administration of hypertonic fluids

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15
Q

what is pseudohyponatraemia?

A

isotonic hyponatraemia

= artefact produced by high serum lipid or protein levels

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16
Q

what investigations are carried out in a patient with hyponatraemia?

A
  • serum sodium concentration
  • U&E
  • creatinine
  • glucose
  • serum osmolality
  • urine sodium concentration - SIADH
  • CT brain, chest, abdomen/pelvis (malignancy)
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17
Q

what is the management of hyponatraemia?

A
acute (<48 hours):
- hypertonic (3%) saline (give in 100 ml increments - up to 300 ml initially over 10 mins)
- treat underlying cause 
chronic:
hypovolaemic:
- give isotonic fluid (250 - 1000 ml boluses to maintain BP)
- treat underlying cause 
hypervolaemic:
- fluid restriction - 1 L/day 
- treat underlying cause
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18
Q

what rate of correction of sodium is aimed for in hyponatraemia and why?

A

up to 8 mmol/L/day correction over 24 hours

- to avoid central pontine myelinolysis

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19
Q

what is SIADH?

A

body produces too much ADH, which causes excess retention of water by the kidneys

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20
Q

what is the normal action of ADH?

A
  • produced by the hypothalamus and released from the posterior pituitary
  • acts on aquaporin 2 receptors in the distal convoluted tubule, increasing the number of aquaporin receptors on the apical surface of cells and increasing water reabsorption
21
Q

what are the causes of SIADH?

A
  • brain injury (meningitis, subarachnoid haemorrhage)
  • malignancy - small cell lung adenocarcinoma can produce ADH
  • drugs - carbamazepine/SSRIs/amitriptylline
  • infectious - lung/cerebral abscess/ atypical pneumonia
  • hypothyroidism
22
Q

what are the symptoms/signs of SIASH?

A

symptoms and signs of hyponatraemia

  • anorexia
  • nausea
  • malaise/weakness
  • irritability / headache
  • low GCS
  • confusion
  • seizures
23
Q

what investigations are carried out when suspecting SIADH?

A
  • fluid status
  • serum sodium (hyponatraemia <135)
  • serum potassium and cortisol (considering Addison’s disease as alternative cause of hyponatraemia)
  • plasma osmolality (reduced)
  • urine osmolality (high due to water reabsorption)
  • urine sodium concentration (high due to water reabsorption (>40 mmol/L - normal is 20))
  • TFTs - hypothyroidism is a cause of SIADH
  • imaging (e.g. CXR for cancer - can be a cause of SIADH)
24
Q

how would you manage SIADH?

A
  • treat underlying cause
  • fluid restriction
  • replace Na - IV or orally (careful not to correct Na too rapidly)
25
Q

what is hypernatraemia?

A

serum sodium >145 mmol/L

26
Q

what are the causes of hypernatraemia?

A
  • iatrogenic (most common) -giving hypertonic fluids (patient will be hypervolaemic)
  • dehydration ( burns, diarrhoea vomiting, burns) (patient will be hypovolaemic)
  • diabetes insipidus
27
Q

what are the symptoms of hypernatraemia?

A
  • thirst
  • irritable
  • seizures
  • muscle spasms
  • nausea and vomiting
28
Q

what investigations are carried out when suspecting hypernatraemia?

A
  • full history
  • U&Es
  • FBC - haemoatocrit, to look for dehydration
  • blood osmolarity
  • urine osmolarity
  • urine output
  • imaging (CT head - hypopituitarism which can be causing cranial DI)
29
Q

what is the management of hypernatraemia?

A
  • give 0.45% NaCl if euvolaemic or 0.9% NaCl if hypovolaemic
  • aiming for a 12 mol/L/day decrease in sodium
30
Q

what is hypocalcaemia?

A

serum calcium <2.2 mmol/L

31
Q

what is the presentation of hypocalcaemia?

A
  • mild - asymptomatic
  • paraesthesia
  • carpopedal spasm
  • muscle cramps
  • tetany
  • ckvostek’s sign (tapping the facial nerve in front of the ear below the zygomatic arch causes a muscular spasm)
  • trousseau’s sign (inflating a pressure cuff above systolic BP and keeping it there induces a carpopedal spasm)
  • prolonged QT interval (can lead to heart block or VF)
  • laryngospasm
  • bronchospasm
  • dementia, confusion and papilloedema when prolonged
32
Q

what are the causes of hypocalcaemia?

A
  • hypoparathyroidism (causing decreased Ca absorption)
  • 2ry hyperparathyroidism (caused by low vitamin D levels which causes low Ca levels which leads to hyperparathyroidism)
  • chronic kidney disease (reduced active vitamin D and increase in serum phosphorous levels which binds Ca)
  • acute pancreatitis
33
Q

what investigations need to be carried out when suspecting hypocalcaemia?

A
  • U&E
  • creatinine (renal function)
  • amylase (for pancreatitis)
  • serum phosphate
  • serum PTH levels
  • vitamin D levels
  • ECG to rule out long QT (can occur in hypocalcaemia)
34
Q

how would you manage hypocalcaemia?

A
  • IV calcium gluconate
  • Oral Ca preparations alongside IV
  • Oral vitamin D
35
Q

what are the symptoms of hypercalcaemia?

A
  • Moans (tired, depressed, confused)
  • Groans (constipation, pancreatitis, peptic ulcers)
  • Stones (kidney stones, polyuria)
  • Bones (Muscle and bone aches)
  • polyuria and polydipsia
  • ectopic calcification (deposition of calcium in tissues)
36
Q

what are the causes of hypercalcaemia?

A
  • malignancy most commonly (ectopic production of parathyroid-related peptide or ectopic calcitriol or osteolysis from bone tumours)
  • granulomatous conditions such as sarcoidosis and TB
  • Drugs - thiazide diuretics and vitamin D supplements
  • primary hyperparathyroidism (parathyroid gland adenoma)
  • dehydration (urea raised)
37
Q

what investigations are carried out when suspecting hypercalcaemia?

A
  • serum calcium
  • U&Es
  • PTH levels
  • Vitamin D levels
  • Alkaline phosphatase (bony mets or liver involvement in sarcoidosis)
  • albumin levels - low in malignancy
  • phosphate levels - affected in hyperparathyroidism
  • phosphate levels
  • X-rays - bone abnormalities
38
Q

what is the management of hypercalcaemia?

A
  • treat underlying cause
  • 0.9% saline to flush out the Ca
  • Bisphosphonates IV (to reduce bone turnover)
  • denosumab - used when resistant to bisphosphonates
39
Q

what is the presentation of hypokalaemia?

A
  • asymptomatic when mild
  • weakness (beginning in lower extremities and extending upwards)
  • muscle pain
  • constipation
  • respiratory failure
  • ileus (due to involvement of GI muscles)
  • paraesthesia
  • tetany
40
Q

what are the causes of hypokalaemia?

A
  • renal tubular acidosis
  • hypomagnasaemia
  • K-losing diuretics (bendroflumethiazide, furosemide)
  • high aldosterone levels - hyperaldosteronism (inc Conn’s syndrome), Cushing’s disease, Renal artery stenosis
  • diarrhoea, vomiting (causes alkalosis and therefore hypokalaemia)
  • inadequate K replacement in IV fluids whilst nil by mouth
41
Q

what investigations are carried out when suspecting hypokalaemia?

A
  • U&E
  • Serum bicarbonate
  • Serum glucose
  • Serum magnesium (low Mg)
  • ECG
42
Q

what is seen on an ECG when a patient has hypokalaemia?

A
  • Flat T waves
  • ST depression
  • Prominent U waves
43
Q

how would you manage hypokalaemia?

A
  • mild - potassium replacement (potassium chloride supplements). review after 3 days. if needed, consider repeating replacement. if taking thiazide diuretic consider adding a k sparing diuretic
  • if severe, give Iv K cautiously and slowly (NEVER give IV K as a stat bolus)
44
Q

what is the presentation of hyperkalaemia?

A
  • weakness and fatigue
  • muscle paralysis
  • shortness of breath
  • palpitations/chest pain
  • bradycardia
45
Q

what are the causes of hyperkalaemia?

A
  • ischaemia/necrosis
  • infection
  • trauma - crush injuries
  • autoimmune - SLE
  • acidosis (e.g. in DKA)
  • Addison’s disease (aldosterone low- less K excreted)
  • CKD/AKI
  • K-sparing diuretics (spironolactone, amiloride)
  • ACEi/ARBs
  • neoplasia (tumour lysis syndrome, malignancies)
  • haemolytic anaemia, causing K release from RBCs
46
Q

what investigations are carried out when suspecting hyperkalaemia?

A
  • FBC (normochromic, normocytic anaemia suggests acute haemolysis)
  • U&E
  • capillary blood glucose and plasma glucose
  • ABG (acidosis)
  • Creatinine (renal cause)
  • 24 hr urine output - for renal causes
  • ECG
47
Q

what is seen on an ECG in hyperkalaemia?

A
  • tall tented T waves
  • no P waves
  • wide QRS
  • bradycardia
48
Q

how would you manage hyperkalaemia that is causing ECG changes or K>7 mmol/L?

A
  • Stop medications that can be causing the hyperkalaemia (spironolactone, amiloride, ACEi/ARBs)
  • IV calcium gluconate to protect the heart
  • Insulin and dextrose (causes K to move into cells)
  • sodium bicarbonate if acidotic
  • salbutamol (IV or nebulised) (drives K into cells)
  • calcium resonium + lactulose (binds K in intestines and removes it via faeces)
  • Dialysis - gold standard for removing K from body