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ICM > Electrolytes > Flashcards

Electrolytes Flashcards

1
Q

Potassium

A

Potassium is a predominantly intracellular ion
Normal range is between 3.5 and 5.0mmol/l
It is absorbed from the small intestine
It’s entry into cells is controlled by the Na/K ATPase pump
It is 90% renally excreted
It regulates acid base balance and maintains the RMP

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2
Q

Hypokalaemia - Causes

A

Hyperkalaemia = K <3.5mmol/l and causes include:

  1. Redistribution: alkalosis, hypoMg, refeeding syndrome, drugs (beta agonists, catecholamines, insulin)
  2. Abnormal intake: inadequate intake or supplementation
  3. Abnormal losses: Urinary - steroids, DKA, hyperaldosteronism, diuretics, diuretic phase of AKI & GI - vomiting and diarrhoea
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3
Q

Hypokalaemia - Clinical Features

A

CNS: Weakness, cramps, paralysis, hyporeflexia
CVS: Hypertension (Na retention), dysrhythmias, tall wide P waves, T wave flatting and inversion, ST depression, U waves, prolonged QT, progression to ventricular arrhythmias
GI: Nausea, vomiting, constipation, ileus

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4
Q

Hypokalaemia - Management

A

Principles include:

  1. An A-E approach
  2. Replace potassium (and magnesium if necessary)
  3. Monitor ECG and electrolytes
  4. Prevent recurrence
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5
Q

Hyperkalaemia - Causes

A

Hyperkalaemia = K >5.5mmol/l and causes include:

  1. Redistribution: Acidosis, Rhabdomyolysis, tumour lysis, insulin deficiency (including DKA), haemolysis, drugs (sux, digoxin, beta-blockers)
  2. Abnormal intake: High potassium foods, blood transfusion
  3. Abnormal losses: Urinary - renal failure, adrenal insufficiency, drugs (potassium sparing diuretics, ACEi, ARBs)
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6
Q

Hyperkalaemia - Clinical Features

A

CVS: Hypotension, arrhythmias, wide flat P wave, prolonged PR, wide QRS, AV and conduction blocks, bradyarrhythmia, PEA or VFib
GI: Nausea, vomiting

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7
Q

Hyperkalaemia - Management

A

General principles include:

  1. An A-E approach
  2. Stop administration/ treat underlying cause
  3. Move potassium into cells: Salbutamol, Insulin-Glucose
  4. Protect the myocardium (calcium)
  5. Remove the potassium (diuretics/ RRT)
  6. Prevent recurrence
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8
Q

Magnesium

A

Magnesium is a predominantly intracellular ion
Normal range is 0.7-1.0mmol/l
Absorbed in the small intestine
50-60% stored in bone
Only a small amount renally excreted
Involved in enzyme systems such as ATPase, antagonises calcium

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9
Q

Hypomagnesaemia - Causes

A

Hypomagnesaemia is defined as a Mg <0.7mmol/l

Redistribution: Refeeding syndrome, insulin, post- parathyroidectomy
Abnormal intake: TPN, malabsorption, alcoholism (malnutrition)
Abnormal losses: Urinary: RTA, diuretics, polyuria, hyperaldosteronism, hypercalcaemia & GI: Vomiting, acute pancreatitis, diarrhoea

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10
Q

Hypomagnesaemia - Clinical features

A

Often co-exists with hypoCa, hypoK

CNS: Weakness, ataxia, tremor, coma
CVS: Hypertension, angina, arrhythmia, prolonged QT, signs of hypoK, VT (incl. Torsades)
GI: nausea, vomiting, abdominal pain

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11
Q

Hypomagnesaemia - Management

A

General principles include:

  1. Replace Mg
  2. Monitor ECG & electrolytes
  3. Prevent recurrence
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12
Q

Hypermagnesaemia - Causes

A

Hypermagnesaemia is defined as a Mg >1.0mmol/l

It is invariably iatrogenic

  1. Abnormal intake: excess supplementation, think obstetrics
  2. Abnormal losses: Urinary - renal failure
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13
Q

Hypermagnesaemia - Clinical Features

A

Magnesium antagonises Ca entry into cells

CNS: Weakness, coma
CVS: Conduction abnormalities
GI: Nausea/ vomiting

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14
Q

Hypermagnesaemia - Management

A

General principles include:

  1. An A-E approach
  2. Stop administration
  3. Give calcium (antagonises Mg)
  4. Monitor ECG and electrolytes
  5. Prevent recurrence
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15
Q

Phosphate

A

A predominantly intracellular ion
Normal phosphate is 0.85-1.4mmol/l
Absorbed in the small intestine
85% found in bone
PTH causes phosphate resorption from bone and reduces reabsorption in PCT
Calcitonin, Mg, Bicarbonate increase excretion
Needed for ATP

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16
Q

Hypophosphataemia - Causes

A

Defined as a PO4 <0.85mmol/l

Redistribution: Refeeding syndrome, respiratory alkalosis, insulin in DKA, glucagon, cortisol, adrenaline (causes intracellular shift)
Abnormal intake: Malnutrition, phosphate binders, malabsorption, TPN
Abnormal losses: Urinary: RTA, hyperaldosteronism; GI: diarrhoea; Other: Sweat, burns, bleeding

17
Q

Hypophosphataemia - Clinical Features

A

Often an incidental finding and co-exists with hypoK, hypoMg

Neuro: Proximal myopathy, weakness, smooth muscle dysfunction
CVS: Acute cardiomyopathy

18
Q

Hypophosphataemia - Management

A
  1. Replace phosphate
  2. Monitor (watch for hypoCa also)
  3. Prevent recurrence
19
Q

Hyperphosphataemia - Causes

A

Defined as a PO4 >1.4mmol/l

Redistribtion: Rhabdomyolysis, tumour lysis, malignant hyperpyrexia, haemolysis, acidosis
Abnormal intake: Increased intake, enemas, VitD intoxication
Abnormal losses: Urinary: Renal failure, hypo parathyroid sim, hypoMg

20
Q

Hyperphosphataemia - Clinical Features

A

Binds with calcium to cause HypoCa
Neuro: Tetany
Renal: Calculus formation

21
Q

Hyperphosphataemia - Management

A
  1. Stop administration
  2. Bind phosphate (aluminium hydroxide)
  3. Remove phosphate (RRT and volume repletion)
  4. Monitor
  5. Prevent recurrence
22
Q

Calcium

A

A predominantly extracellular ion
Normal concentration in plasma is 2.2-2.6mmol/l
Exists in plasma as free ions, bound to proteins (40-50%) and diffusible complexes
PTH ensures control of ionised calcium by INCREASING release from bone, reabsorption from DCT, converting VitD to increase GI absorption
Calcitonin released from thyroid opposes PTH

23
Q

Hyopcalcaemia - Causes

A

Hypocalcaemia is defined as a serum Ca <2.2mmol/l

Redistribution: Alkalosis, citrate toxicity, blood administration, hyperphosphataemia, pancreatitis, tumour lysis, rhabdomyolysis, hypoparathyroidism, drugs (PPIs, SSRIs)
Abnormal intake: Low dietary Ca, low VitD, phenytoin (increases VitD metabolism)
Abnormal losses: Urinary: ethylene glycol, cisplatin, loop diuretics; Other: bleeding, plasmapheresis, citrate RRT

24
Q

Hyopcalcaemia - Clinical Features

A

Neuro: Mental state changes, tetany, facial muscle contracture, carpopedal spasm
CVS: Prolonged QTc, AV block, Torsades

25
Q

Hypocalcaemia - Management

A
  1. Replace Ca (Nb Ca Chloride contains 3x calcium ions as Ca Gluconate)
  2. Monitor
  3. Prevent recurrence
26
Q

Hypercalcaemia - Causes

A

Defined as a serum Ca >2.6mmol/l

Redistribution: Immobilisation, malignancy, hyperparathyroidism, sarcoid, lithium toxicity, adrenal insufficiency, thyrotoxicosis
Abnormal intake: Calcium, VitA or VitD, hypoMg, hypovolaemia, TPN
Abnormal losses: Urinary: thiazide diuretics

27
Q

Hypercalcaemia - Clinical Feature

A

Groans (constipation)
Bones (bony pain)
Moans (psychosis)
Stones (renal calculi)

Also malaise, weakness, hyporeflexia

28
Q

Hypercalcaemia - Management

A
  1. IV hydration
  2. Bisphosphonates
  3. Loop Diuretics
  4. Monitor
  5. Prevent recurrence
29
Q

Sodium

A

Sodium is a major extracellular ion with roles in regulating ECF, preserving osmolality and maintaining tubuloglomerular feedback
Normal range is 135-145mmol/l
Absorbed in the small intestine
Reabsorption in nephron influenced by RAAS, ADH, thirst, beta stimulation at PCT
99% reabsorbed

30
Q

Hyponatraemia - Causes

A

Hyponatraemia is defined as a Na <135mmol/l
Unlike other electrolytes - classified according to volume status

Hypovolaemic: Total body water low but with disproportionate Na loss = vomiting, diarrhoea, excess sweating
Euvolaemic: Most common = SIADH, glucocorticoid deficiency, hypothyroid, beer potomania, polydipsia
Hypervolaemic: Essentially dilutional (kidney unable to excrete water) = nephrotic syndrome, CCF, cirrhosis

31
Q

Hyponatraemia - Clinical features

A

Neuro: signs result from a change in osmotic gradient which can result in seizures, comas and death (milder symptoms include headache, nausea, poor balance, confusion, muscle fatigue).

32
Q

Hyponatraemia - Management

A

Overaggressive treatment risks dymelination!

If severe <115 with severe symptoms then give sodium chloride 3% to increase sodium by 5mmol/l
Otherwise/ thereafter correct slowly (<12mmol/l/24h)

33
Q

Hypernatraemia - Causes

A

Defined as a serum sodium >145mmol/l

Abnormal intake (low free water intake): unable to drink water, impaired thirst mechanism (malignancy)
Abnormal intake (sodium overload): large volumes of hypertonic NaHCO3  or hypertonic saline; hyperaldosteronism (though usually negated by water intake)
Abnormal losses (free water losses): Renal: osmotic diuresis (recovery from AKI, poorly controlled DM, loop diuretics/ mannitol); GI: diarrhoea, vomiting; Other: Burns.
34
Q

Hypernatraemia - Clinical Features

A

Neuro: Lethargy, weakness, irritability, seizures, coma, death

PLUS signs of hypovolaemia

Urine osmolality: High (>500) = pure volume depletion; Low (<150) = DI
Serum osmolality: Alway High (>295mosm/kg)

35
Q

Hypernatraemia - Management

A
  1. A-E approach
  2. Oral water (or IV 5% glucose) fluid replacement: Calculate free water deficit and replace 50% in first 24h
  3. Monitor Na: 2mmol/l/h drop in first 2-3h followed by 0.5mmol/l/h thereafter
  4. Treat underlying cause/ co-existing electrolyte abnormalities

Also:

  • Desmopressin if DI
  • Consider loop diuretic if therapeutic excess
36
Q

What is the definition of BE?

A

The amount of acid or alkali to restore 1L of blood to pH 7.4 at PCO2 5.3 and body temperature

37
Q

What is the StdBE

A

StdBE is corrected to a Hb concentration of 50g/dL and is defined in terms of a litre of extracellular fluid

ICM (16 decks)

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