Revision Topics Flashcards

1
Q

Define hypernatraemia?

A

sodium > 145mmol/L

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2
Q

2 broad causes of hypernatraemia? What is it more commonly due to?

A

low water or too much sodium

Hypernatraemia is more commonly due to low water as opposed to sodium overload

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3
Q

In hypernatraemia the serum osmolality is always?

A

high

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4
Q

Causes of hypernatraemia?

A

dehydration
osmotic diuresis e.g. HHS in diabetes
diabetes insipidus
excess IV saline

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5
Q

Most common cause of hypernatraemia in the elderly?

A

dehydration

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6
Q

Presentation of hypernatraemia?

A

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

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7
Q

Management of hypernatraemia?

A

correct with caution so not to upset brain tissue, treat any underlying disorder and treat any dehydration

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8
Q

In cranial DI, nephrogenic DI and psychogenic polydipsia what is urine, serum osmolality and sodium concentration?

A

hypernatraemia
high serum osmolality
low urine osmolality

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9
Q

What are some reversible causes of nephrogenic diabetes insipidus?

A

hypercalcaemia and hypokalaemia
lithium is another cause and it is usually reversible on cessation of therapy but not always

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10
Q

Define hyponatraemia?

A

serum sodium < 135 mmol/L

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11
Q

Overview of the causes of hyponatraemia?

A

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

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12
Q

In true hyponatraemia the serum osmolality is?

A

low

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13
Q

Causes of hyponatraemia with a low urinary sodium (<20 mmol/L)?

A

Extra renal loss - diarrhoea, vomiting, sweating, burns
Hypervolaemic - fluid overload in heart failure, liver failure and nephrotic syndrome

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14
Q

Causes of hyponatraemia with a high urinary sodium? (> 20 mmol/L)

A

Renal loss - addisons, diuretics, diuretic stage of renal failure
Euvolaemic - SIADH or hypothyroid

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15
Q

Investigations for hyponatraemia?

A

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

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16
Q

Presentation of hyponatraemia?

A

confusion, lethargy, cognitive impairment, focal or generalised seizures
signs of hypo or hypervolaemia

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17
Q

Causes of SIADH?

A

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

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18
Q

Management of acute hyponatraemia?

A

acute symptomatic hyponatraemia is a medical emergency and should be corrected carefully using hypertonic saline

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19
Q

What do you need to assess in non acute hyponatraemia to decide treatment?

A

volume status
hypovolaemic
euvolaemic
hypervolaemic

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20
Q

Causes of hyponatraemia where the patient will be hypovolaemic?

A

addisons, diuretics, diarrhoea, vomiting, sweating, burns

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21
Q

Causes of hyponatraemia where the patient is hypervolaemic?

A

fluid overload in heart failure, liver failure or nephrotic syndrome

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22
Q

Causes of hyponatraemia where the patient is euvolaemic?

A

SIADH or hypothyroid

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23
Q

Treatment of hypovolaemic hyponatraemia?

A

IV saline replacement

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24
Q

Treatment of normovolaemic hyponatraemia (SIADH)?

A

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

25
Treatment of hypervolaemic hyponatraemia?
the underlying cause should be treated which is usually HF, AKI or liver cirrhosis, loop diuretics are often beneficial
26
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
27
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
28
4 causes of acute liver failure?
paracetamol OD alcohol viral hepatitis (usually A or B) acute fatty liver of pregnancy
29
Features of acute liver failure?
jaundice drowsiness/ possible confusion encephalopathy coagulopathy - raised PT hypoalbuminaemia renal failure is common (hepatorenal syndrome)
30
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
31
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
32
Activated charcoal can be used within _______
1hr of paracetamol overdose
33
What is the most prognostic factor in paracetamol overdose?
arterial ph
34
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
35
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
36
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
37
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.
38
Predominant symptoms of carcinoid syndrome?
diarrhoea, SOB, flushing and itching
39
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
40
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
41
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
42
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
43
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
44
ECG changes with hypocalcaemia?
prolongation of the QT interval
45
ECG changes with hypercalcaemia?
shortening of the QT interval
46
Causes of hypomagnaesemia?
diuretics PPIs TPN diarrhoea (acute or chronic) alcohol secondary to hypercalcaemia and hyperparathyroidism
47
Presentation of hypomagnaesemia?
similar to features of hypocalcaemia (could then go on to actually cause hypocalcaemia as the parathyroids need magnesium)
48
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.
49
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
50
Presentation of hypocalcaemia?
tetany, cramps, perioral paraesthesia, Trosseaus (BP cuff inflation causes tetany) and Chvosteks sign (tapping over facial nerve causes twitching)
51
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
52
Presentation of hypokalaemia?
muscle weakness, hypotonia, increased risk of digoxin toxicity
53
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
54
ECG changes on hypokalaemia?
u waves, small or absent T waves, prolonged PR interval, ST depression
55
What is a u wave on ECG?
deflection immediately following the T wave
56
Causes of hyperkalaemia?
AKI Potassium sparing diuretics (spironolactone, eplerenone) ARBs metabolic acidosis Addisons rhabdomyolysis massive blood transfusion foods (salt substitutes, bananas etc)
57
Px of hyperkalaemia?
weakness, paralysis, intestinal cramping
58
ECG changes for hyperkalaemia?
tall tented t waves