Revision Topics Flashcards
Define hypernatraemia?
sodium > 145mmol/L
2 broad causes of hypernatraemia? What is it more commonly due to?
low water or too much sodium
Hypernatraemia is more commonly due to low water as opposed to sodium overload
In hypernatraemia the serum osmolality is always?
high
Causes of hypernatraemia?
dehydration
osmotic diuresis e.g. HHS in diabetes
diabetes insipidus
excess IV saline
Most common cause of hypernatraemia in the elderly?
dehydration
Presentation of hypernatraemia?
in diabetes insipidus there is thirst, polydipsia and polyuria
other signs include CNS dysfunction - lethargy, weakness, confusion, myoclonic jerks and seizures
signs of dehydration and hypovolaemia may be present
Management of hypernatraemia?
correct with caution so not to upset brain tissue, treat any underlying disorder and treat any dehydration
In cranial DI, nephrogenic DI and psychogenic polydipsia what is urine, serum osmolality and sodium concentration?
hypernatraemia
high serum osmolality
low urine osmolality
What are some reversible causes of nephrogenic diabetes insipidus?
hypercalcaemia and hypokalaemia
lithium is another cause and it is usually reversible on cessation of therapy but not always
Define hyponatraemia?
serum sodium < 135 mmol/L
Overview of the causes of hyponatraemia?
Too little sodium:
Renal loss - addisons, diuretics, diuretic stage of renal failure
Extra renal loss - diarrhoea, vomiting, sweating, burns
Too much water:
Euvolaemic - SIADH or hypothyroid
Hypervolaemic - fluid overload in heart failure, liver failure and nephrotic syndrome
In true hyponatraemia the serum osmolality is?
low
Causes of hyponatraemia with a low urinary sodium (<20 mmol/L)?
Extra renal loss - diarrhoea, vomiting, sweating, burns
Hypervolaemic - fluid overload in heart failure, liver failure and nephrotic syndrome
Causes of hyponatraemia with a high urinary sodium? (> 20 mmol/L)
Renal loss - addisons, diuretics, diuretic stage of renal failure
Euvolaemic - SIADH or hypothyroid
Investigations for hyponatraemia?
in low sodium result first measure urine sodium, urine osmolality and plasma osmolality
if the plasma osmolality this is a pseudohyponatraemia
check then for addisions disease - are they hyperkalaemic, do a synacthen test
check their thyroid function
then look for signs of fluid overload
drug review - are they on diuretics
are there any obvious losses e.g. diarrhoea, burns
Presentation of hyponatraemia?
confusion, lethargy, cognitive impairment, focal or generalised seizures
signs of hypo or hypervolaemia
Causes of SIADH?
Neoplastic - ADH secretion by cancer - most commonly small cell lung cancer
Pulmonary - pneumonia, abscess, TB, aspergillosis, asthma, CF, positive pressure ventilation
CNS - abscess, meningitis, AIDs, subdural, SAH, CVA, head trauma, MS, GBS, Shy-Drager syndrome
Drugs
1. AVP analogues e.g. desmopressin, oxytocin, vasopression
2. stimulate AVP release/ action e.g. SSRIs, antipsychotics, anti-epileptics, NSAIDs, MDMA
Hereditary SIADH
Idiopathic SIADH
Management of acute hyponatraemia?
acute symptomatic hyponatraemia is a medical emergency and should be corrected carefully using hypertonic saline
What do you need to assess in non acute hyponatraemia to decide treatment?
volume status
hypovolaemic
euvolaemic
hypervolaemic
Causes of hyponatraemia where the patient will be hypovolaemic?
addisons, diuretics, diarrhoea, vomiting, sweating, burns
Causes of hyponatraemia where the patient is hypervolaemic?
fluid overload in heart failure, liver failure or nephrotic syndrome
Causes of hyponatraemia where the patient is euvolaemic?
SIADH or hypothyroid
Treatment of hypovolaemic hyponatraemia?
IV saline replacement
Treatment of normovolaemic hyponatraemia (SIADH)?
fluid restrict 1-1.5L
Demeclocycline - old fashioned antibiotic that uncouples AQP2 from vasopressin receptor
Tolvaptan - vasopressin receptor antagonist - may be useful but can induce thirst, are expensive, have limited availability and potentially may increase sodium levels too rapidly
Treatment of hypervolaemic hyponatraemia?
the underlying cause should be treated which is usually HF, AKI or liver cirrhosis, loop diuretics are often beneficial
Explain what central pontine myelitis is and what happens?
this occurs if you correct low sodium levels too quickly
sodium correction should be no more than 8 mmol/L per 24 hours
symptoms usually occur after 2 days and are often irreversible
presentation is seizures, disturbed consciousness, gait trouble, dysphagia, dysarthria, diplopia, acute tetraparesis
Explain what pseudohyponatraemia is?
sodium is low but osmolality is normal (or high)
physiological drop in sodium because another solute is high
e.g. high glucose and urea in diabetes
or high urea in renal disease
4 causes of acute liver failure?
paracetamol OD
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy
Features of acute liver failure?
jaundice
drowsiness/ possible confusion
encephalopathy
coagulopathy - raised PT
hypoalbuminaemia
renal failure is common (hepatorenal syndrome)
Some reasons someone with acute liver failure might be referred for transplant?
encephalopathy
oliguria or AKI
hypoglycaemia
metabolic acidosis
ph < 7.3 or bicarb < 18
In paracetamol OD when do you give acetylcysteine?
the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
there is a staggered overdose* or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration; or
patients who present 8-24 hours after ingestion of an acute overdose of more than 150 mg/kg of paracetamol even if the plasma-paracetamol concentration is not yet available
patients who present > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal
acetylcysteine should be continued if the paracetamol concentration or ALT remains elevated whilst seeking specialist advice
Activated charcoal can be used within _______
1hr of paracetamol overdose
What is the most prognostic factor in paracetamol overdose?
arterial ph
Who has increased risk of developing hepatotoxicity following paracetamol OD?
enzyme inducing drugs
rifampicin, phenytoin, carbamazepine
malnourished patients
chronic alcohol intake
acute alcohol intake is not a risk factor and may actually be protective
Risk with acetylcysteine treatment? Management of this?
acetylcysteine can cause a non-IgE anaphylactoid reaction (ie a reaction that looks like anaphylaxis but is not IgE mediated)
this is treated by stopping the infusion and restarting at a lower rate
Explain what carcinoid syndrome is caused by?
this is a syndrome caused by secretion of serotonin and bradykinin from a carcinoid/ neuroendocrine tumour
(in some parts of body name carcinoid tumour is no longer used)
note that not all carcinoid tumours secrete hormones - most in the lungs dont secrete anything
they can secrete more hormones than just serotonin and bradykinin but carcinoid syndrome is specifically caused by secretion of these two hormones
Explain what vitamin deficiency can be caused by carcinoid syndrome and how this presents?
carcinoid syndrome can cause vitamin B3 (niacin) deficiency. This is because increased serotonin production uses up the things needed for niacin production. This presents as the 3ds - dementia, diarrhoea and dermatitis.
Predominant symptoms of carcinoid syndrome?
diarrhoea, SOB, flushing and itching
NICE reccomendations for routine fluid maintenance?
25-30ml/kg of water
1mmol/kg/day of sodium, potassium, chloride
50-100g/day glucose
Up to a maximum weight of 100kg
NICE reccomendations for routine fluid maintenance?
25-30ml/kg of water
1mmol/kg/day of sodium, potassium, chloride
50-100g/day glucose
Up to a maximum weight of 100kg
Crystalloid vs colloids?
Colloid vs crystalloid
Colloids are designed to stay in intravascular space as has bigger molecules
colloid examples: starches, dextrans, gelatins; or naturally occurring, such as human albumin or fresh frozen plasma (FFP
Crystalloids go across all compartments which you want in resuscitation
crystalloid examples: NaCl 0.9% and Hartmanns, 5% dextrose
What should be used for fluid resus?
- NICE recommends that fluid resus is best approached with a crystalloid solution rather than a colloid
- Most experts would recommend a balanced crystalloid e.g. Hartmanns because excessive amounts of 0.9% sodium chloride can result in hyperchloraemic metabolic acidosis
- Exception includes rhabdomyolysis (and AKI/ CKD) when 0.9% sodium chloride would be preferred initially because of the risk of hyperkalaemia
How should you give initial fluid for resus?
500ml over less than 15 minutes
if AKI would want to give NaCl 0.9% over Hartmanns otherwise Hartmanns is probably better
ECG changes with hypocalcaemia?
prolongation of the QT interval
ECG changes with hypercalcaemia?
shortening of the QT interval
Causes of hypomagnaesemia?
diuretics
PPIs
TPN
diarrhoea (acute or chronic)
alcohol
secondary to hypercalcaemia and hyperparathyroidism
Presentation of hypomagnaesemia?
similar to features of hypocalcaemia (could then go on to actually cause hypocalcaemia as the parathyroids need magnesium)
Is hypermagnaesmia common?
no much less common than hypo and severe presentations only really encountered in patients with end stage kidney disease. In healthy individuals excess intake is excreted by the kidneys.
Management of hypomagnaesemia?
if < 0.4 mmol/L or tetany or arrhythmias or seizure need IV replacement
if > 0.4 can give magnesium salts but should note that these cause diarrhoea
Presentation of hypocalcaemia?
tetany, cramps, perioral paraesthesia, Trosseaus (BP cuff inflation causes tetany) and Chvosteks sign (tapping over facial nerve causes twitching)
Causes of hypokalaemia?
hypokalaemia with alkalosis: vomiting, thiazides, and loops, cushings, conns
with acidosis: diarrhoea, renal tubular acidosis, acetazolamide, partially treated DKA (insulin pushes K into cells)
magnesium deficiency can also cause hypokalaemia in such cases normalising potassium level may be difficult until deficiency has been corrected
Presentation of hypokalaemia?
muscle weakness, hypotonia, increased risk of digoxin toxicity
What is important to consider about hypokalaemia?
it increases risk of digoxin toxicity so if someone is on a diuretic that causes hypokalaemia and on digoxin need to consider this
ECG changes on hypokalaemia?
u waves, small or absent T waves, prolonged PR interval, ST depression
What is a u wave on ECG?
deflection immediately following the T wave
Causes of hyperkalaemia?
AKI
Potassium sparing diuretics (spironolactone, eplerenone)
ARBs
metabolic acidosis
Addisons
rhabdomyolysis
massive blood transfusion
foods (salt substitutes, bananas etc)
Px of hyperkalaemia?
weakness, paralysis, intestinal cramping
ECG changes for hyperkalaemia?
tall tented t waves
