Electrolytes Flashcards

1
Q

How are sodium levels controlled?

A

Aldosterone acting on DCT and CD => increased reabsorption of Na via Na/K ATPase

Natriuretic peptides inhibit reabsorption of Na

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2
Q

How does a person with hyponatraemia present?

A

Anorexia, nausea, malaise

Headache, irritability, confusion, seizures

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3
Q

What investigations are done in hyponatraemia?

A
Serum sodium
Serum osmolality
Urine sodium 
Urine osmolality 
TFTs, 9am cortisol/synacthen test
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4
Q

What are some causes of hyponatraemia?

A

Water overload

GI loss, CCF, cirrhosis

SIADH, ACTH/glucocorticoid deficiency

Addison’s

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5
Q

How is hyponatraemia managed?

A

Asymptomatic - fluid restriction, treat underlying cause

Acute/symptomatic/dehydrated - Rehydrate with 0.9% NaCl

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6
Q

What can happen with rapid rehydration with hyponatraemia?

A

Central pontine myelinolysis

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7
Q

What is SIADH?

A

Excess release of ADH
Results in concentrated urine sodium, with hyponatraemia
No hypovolaemia, diuretic use or oedema

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8
Q

What are some causes of SIADH?

A

Malignancy - small cell lung cancer
CNS disorders - stroke, head injury
Drugs - SSRIs, opiates

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9
Q

How is SIADH managed?

A

Treat underlying cause
Fluid restriction
ADH receptor antagonists (vaptans)

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10
Q

How does a person with hypernatraemia present?

A

Lethargy, thirst, irritability

Signs of dehydration - reduced skin turgor, tachycardia, low BP, dry mucous membranes

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11
Q

What are some causes of hypernatraemia?

A

Dehydration - inadequate intake, diabetes insipidus, thirst impairment
Fluid loss - burns, vomiting, diarrhoea, diuretics
Sodium gain - IV fluids, Primary hyperaldosteronism

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12
Q

How is hypernatraemia managed?

A

Treat underlying condition, correct dehydration

IV 5% glucose
0.9% NaCl if hypovolaemic

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13
Q

What are complications of hypernatraemia?

A

Subarachnoid haemorrhage - shrinkage of brian

Quick correction can lead to cerebral oedema

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14
Q

What is diabetes insipidus?

A

Passing large volumes of dilute urine due to impaired water reabsorption
Renal - kidneys don’t respond to ADH
Cranial - reduced ADH secretion posterior pituitary

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15
Q

What are some cranial causes of diabetes insipidus?

A

Idiopathic
Genetic
Trauma

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16
Q

What are some nephrogenic causes of diabetes insipidus?

A

Inherited
CKD
Electrolyte imbalance

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17
Q

What investigations are done for diabetes insipidus?

A

Urine output >3L/day
U&E - hypernatraemia
Blood glucose - exclude DM

High serum osmolality
Low urine osmolality

Water deprivation test

18
Q

How is diabetes insipidus managed?

A

Treat underlying cause

Cranial - head MRI, check pituitary function
Desmopressin - ADH analogue

Nephrogenic - bendroflumethiazide, reduce salt intake, NSAIDs

19
Q

How are potassium levels controlled?

A

Mainly intracellular
Uptake into cells stimulated by insulin and catecholamines - via Na/K ATPase

Cation shift - fluctuation with H+

20
Q

How does a person with hypokalaemia present?

A

Mild - asymptomatic
Muscle weakness, tetany, hypotonia
Palpitations

21
Q

What ECG changes are seen in hypokalaemia?

A

Small/inverted T waves
U waves
Prolonged PR interval
Depressed ST interval

22
Q

What are some causes of hypokalaemia?

A

Loss of K - Thiazide/loop diuretics, vomiting, diarrhoea, hyperaldosteronism

Transcellular shift - alkalosis, insulin

Inadequate intake

23
Q

How is mild hypokalaemia (>2.5) managed?

A

Do ECG, repeat bloods

Oral K supplements

24
Q

How is severe hypokalaemia (>2.5) managed?

A

ECG, bloods

IV potassium

25
What are complications of hypokalaemia?
Arrhythmias Muscle weakness Contributes to digoxin toxicity
26
How does a person with hyperkalaemia present?
Weakness, fatigue Palpitations Chest pain Bradycardia
27
What are some causes of hyperkalaemia?
Renal - AKI, CKD, mineralocorticoid deficiency, drugs eg spironolactone, ACE inhibitors, ARB Tissue damage => release of K, eg rhabdomyolysis, trauma, burns Acidosis Drugs - digoxin, beta blockers
28
What ECG changes are seen in hyperkalaemia?
Wide QRS Tall T waves Small P waves Sinusoidal pattern
29
What is the management of hyperkalaemia?
ECG, check K levels again with ABG Stabilise heart - calcium gluconate Shift K into cells - insulin and dextrose, nebulised salbutamol Removal of K - calcium resonium, haemodialysis
30
What is the overall effect of parathyroid hormone?
Increase Calcium | Decrease phosphate
31
What are specific actions of PTH?
Increase osteoclast activity Increase reabsorption of calcium at kidney Decrease reabsorption of phosphate in kidney Increase hydroxylation of calcidiol => calcitriol (vitamin D) in kidney
32
What is the overall effect of vitamin D/calcitriol?
Increase Calcium | Increase phosphate
33
What are specific actions of vit D/calcitriol?
Increase absorption of Ca and PO4 from gut Increased reabsorption of Ca and PO4 from kidney Inhibition of PTH release Increase bone turnover
34
How does hypercalcaemia present?
Moans - depression, lethargy Bones - pain Stones - renal colic Groans - abdo pain, constipation, vomiting Inc threshold for AP => reduced neuronal activity
35
What are causes of hypercalcaemia?
Malignancy Primary hyperparathyroidism - adenoma Sarcoidosis Secondary/tertiary hyperparathyroidism - CKD
36
What investigations are required in hypercalcaemia?
FBC, 24hr Ca urine collection, CXR, isotope bone scan | PTH levels
37
How is malignancy identified as a cause of hypercalcaemia?
Low PTH levels - release of PTHrP | CT CAP
38
How is acute hypercalcaemia managed?
If Ca >3.5 and symptomatic: Correct dehydration with 0.9% saline IV bisphosphonates => inhibition of osteoclast Treat underlying cause eg chemo in malignancy, steroids in sarcoidosis
39
How does hypocalcaemia present?
``` Peri-oral paraesthesia Cramps Chvostek's sign Carpopedal spasm Laryngospasm ``` Dec threshold for AP => inc neuronal activity
40
What are causes of hypocalcaemia?
CKD, hypoparathyroidism (post-thyroidectomy) Vit D deficiency, osteomalacia Respiratory alkalosis - panic attack => hyperventilation => low co2
41
How is hypocalcaemia managed?
Mild - PO supplements | Severe - IV calcium gluconate