Electrolytes + Acid Base Flashcards
What is Na+ used for?
Most abundant cation in extracellular fluid (135-145 mmol/L)
Used in transmission of nerve impulses
Influences contraction/relaxation of muscle
Maintains balance of fluids in body
Where is the one place that water does not follow sodium?
Ascending loop of Henle
- Countercurrent mechanism to concentrate urine
Give a four examples of Na+ and water imbalance:
Oedema - too much Na+ ( increase Na+ excretion)
Volume depletion - too little Na+ (reduce Na+ excretion)
Hyponatraemia - too much water (suppress ADH to increase water excretion)
Hypernatraemia - too little water (enhance ADH ro decrease water excretion)
Causes of hypernatraemia
Dehydration:
- Diuretics
- Diarrhoea
- Burns
- Surgery (drains)
- Intake restriction
Endocrine disturbance:
- Collecting duct abnormalities ()
- Hyperaldosteronism (Conn’s)
- Diabetes insipidus
- Cushing’s syndrome
High sodium intake
Symptoms of hypernatraemia:
Altered mental state
Irritability
Restlessness
Seizures
Muscle twitches
Hyperreflexia
GIT - nausea and vomiting
How does dehydration cause increased urea: creatinine?
In prerenal failure, urea increases disproportionately
Enhanced proximal tubular reabsorption of Na+ and water -> urea follows Na+
Approach to hyponatraemia?
Hypoosmolar (true)
Hypertonic
- Translocation of water from cells into ECF
- Pseudohyponatraemia ( increased lipids and protein) - normal/elevated serum osmolality
Dehydration?
Fluid overload?
Bulimia?
Approach to hypoosmolar hyponatraemia:
Hypovolaemic: Decreased total body water and Na
Euvolaemic: Increased TBW, no change in Na
Hypervolaemic: increased TBW and Na
What is hypovolaemic hypoosmloar hyponatraemia, and what are the causes?
Decreased TBW and Na
If U Na > 20, there will be dumping of Na
Causes:
Renal loss
- diuretics
- salt losing nephropathy (e.g., HIVAN)
- cerebral salt wasting
If U Na < 20, there will be retaining of Na (conc. urine)
Causes:
Volume depletion
- Vomiting
- diarrhoea
- 3rd space losses
- burns
- pancreatitis
- bowel lumen (e.g., ileus)
What is hypervolaemic hypoosmloar hyponatraemia, and what are the causes?
Increased TBW and Na
If U Na > 20
Causes:
- AKI
- CKD
If U Na <20
Causes:
-Nephrotic syndrome
-CCF
-Cirrhosis
-Primary polydipsia
What is euvolaemic hypoosmloar hyponatraemia, and what are the causes?
Increased in TBW, no change in Na
Causes:
SIADH
- Na dumping
- Low plasma Na (<130)
- Low plasma osmolality (<270)
- High urine:Na (>40)
- High urinary osmolality (>100)
Hypothyroidism
- Decreased ADH suppression
- Decreased GFR (Decreased clearance of ADH)
Addison’s
- Hyperpigmentation
- Low BP
- Low glucose
- Low Na
- Increased K + acidosis
What is SIADH?
Syndrome of inappropriate ADH secretion
- defect in osmoregulation due to ADH being inappropriately stimulated -> increased urine osmolality + urine Na
-Euvolaemic
-Normal thyroid function and cortisol levels
What are the causes of SIADH?
Respiratory:
- Paraneoplastic effect (e.g., small cell lung ca)
- Suppurative/cavitating lung disease
- Positive pressure ventilation
CNS:
- CVA/ cavernous sinus thrombosis
- meningitis/ encephalitis
- SOL
Drugs:
- Carbamazepine/ TCA/ SSRIs/ phenothiazines (incl maxalon)
What are the risks of managing low Na?
Risky!!
Acute hyponatraemia: ECF becomes hypotonic -> water drawn into cell -> oedema -> adapts -> osmoles pumped out -> oedema resolved
Acute hyponatraemia -> risk of cerebral oedema -> correcting too quickly -> ECF more hypertonic than ICF -> cells shrink -> central pontine myelinolysis
What is K+ used for?
Regulates intracellular enzyme function
Helps determine neuromuscular and cardiovascular excitability
Primarily found in muscle (most abundant cation)
How is K+ controlled?
Regulated by kidney (3.5 -5.5 mmol/L)
GIT absorbs K+
Causes of hyperkalaemia:
Pseudohyperkalaemia - severe leukocytosis/thrombocytosis or prolonged tourniquet time
High intake
Redistribution by drugs/acidosis
Movement out of cells - cellular destruction
- rhabdomyolysis
- tumour lysis syndrome
- necrotic tissue
Potassium sparing drugs (enalapril, losartan)
Impaired renal secretion (Cr >150)
Type 4 renal tubular acidosis
Which drugs cause increased K+?
Beta-blockers and NSAIDs (block renin)
Amiloride and Bactrim (block ENAC)
ACE-inhibitors and ARBs (block aldosterone)
Spironolactone and ketoconazole (blocks aldosterone)
Cyclosporin and Tacro (block distal K+)
Whay are the effects of hyperkalaemia?
Muscle twitches/cramps -> paraesthesia
Irritability and anxiety
Low BP
ECG changes
- Tented T waves
- Increased PR and QRS intervals
- Flattening and eventual absence of P waves
- QRS widens -> ventricular asystole/Afib
Dysrhythmia
Abdominal cramp
Diarrhoea
Treatment of hyperkalaemia:
Calcium gluconate (protect heart)
Insulin (shift K+ into cells (monitor glucose!))
Kexelate/Dialysis (remove K+)
Causes of hypokalaemia:
Pseudohypokalaemia - increased abnormal white cells (e.g., AML takes up extracellular K+)
Redistribution (K+ driven into cells)
- Insulin
- Beta 2 agonists (ventolin)
- Theophylline
- Metabolic alkalosis
- Aldosterone/Fludrocortisone
Extrarenal loss (GIT)
Intrarenal loss (acidosis/alkalosis)
What are the ECG changes with hypokalaemia?
U wave with T wave - apparent prolonged QT
Giant U waves
T wave inversion
ST segment depression
Prolonged PR interval
Approach to hypercalcaemia:
PTH-related
Non-PTH related
What are the causes of PTH related hypercalcaemia?
Primary hyperparathyroidism
Tertiary hyperparathyroidism
What are the causes of non-PTH related hypercalcaemia?
Malignancy - multiple myeloma, metastases
Granulomatous disease - sarcoid/TB/lymphoma
Drugs - Hydrochlorothiazide
Prolonged immobility
How does multiple myeloma present, and what are the complications?
Renal failure + hypercalcaemia + backache + anaemia
Complications:
- Anaemia
- Recurrent bacterial infection
- Osteolytic lesions
- Renal failure
- Hyperviscosity
What is acidosis?
Low pH (high H+)
Will look short of breath
Causes of increased anion gap metabolic acidosis:
Methylene glycol
Uraemia
DKA
Pancreatitis
Infection
Lactic acidosis
Exogenous drugs
Salicylates
