Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology / Renal Medicine > Electrolyte Disturbances for Finals > Flashcards

Electrolyte Disturbances for Finals Flashcards

1
Q

Which electrolyte is most common in:

1) Intracellular fluid
2) Interstitial fluid
3) Plasma (not an electrolyte)

A

1) K+
2) Na+
3) Protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is oedema?

A

Increase in interstitial fluid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some of the causes of increased interstitial fluid (i.e. that seen in oedema)?

A

Increased hydrostatic pressure e.g. from Na+ and K+ retention in heart failure
Reduced oncotic pressure e.g. hypoalbuminaemia in nephrotic syndrome
Obstruction to lymphatic flow
Increased vascular permeability e.g. in infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When might you administer a colloid fluid replacement?

A

To increase circulating volume of fluid e.g. in haemorrhage, sepsis, burns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the composition of colloid fluid replacement?

A

Examples: gelofusin

Contain larger molecules which stay in the intravascular space longer than crystalloids - used to replace or increase the volume of circulating fluid e.g. in haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the composition of crystalloid fluid replacement?

A

Example: 0.9% sodium chloride (saline)

Contain small molecules which pass easily between the intravascular (plasma) and interstitial spaces. On IV administration, about 1/3 will stay in the intravascular space, while the rest will go to the extravascular (interstitial) compartment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens when the effective arterial blood volume (EABV) is decreased?

A

Activation of extra-renal and intra-renal volume receptors in the large vessels of the heart and the afferent arterioles of the kidney respectively. Leads to sodium and water reabsorption in the kidneys and an increase in circulating volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of hypovolaemic hyponatraemia?

A

Measure urinary sodium to assess whether renal or extra-renal cause of hyponatraemia…

  • Renal cause: Diuretics, renal failure, adrenocortical insufficiency (Addison’s)
  • Extra-renal cause: Vomiting and diarrhoea, haemorrhage, burns, pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the normal value for serum sodium?

A

135 - 145 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the normal value for serum potassium?

A

3.5 - 5.0 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the normal value for bicarbonate on ABG?

A

22 - 28 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is the anion gap calculated?

A

(Na + K) - (HCO3 + Cl)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a normal anion gap?

A

10 - 18 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes a normal anion gap metabolic acidosis?

A

Loss of bicarbonate from kidneys or GI tract e.g. vomiting, diarrhoea, renal tubular acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is it appropriate to calculate the anion gap from an ABG sample?

A

To work out the cause of a metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List some ECG changes seen in hyperkalaemia

A

Tall, tented T waves
Small P waves
Broad QRS complexes
…may progress to VT or VF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How can you treat hyperkalaemia with no ECG changes?

A

Treat the underlying cause
Review medications
Consider calcium resonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the emergency management for hyperkalaemia (K+ > 6.5 mmol/L)?

A 
DR ABCDE
Continous cardiac monitoring
10mL 10% calcium gluconate over 10 minutes
10units Actrapid in 50mL 20% glucose
Consider nebulised salbutamol
Dialysis in retractable hyperkalaemia
Stop the cause e.g. if drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

True / False: Rhabdomyolysis is a cause of hyperkalaemia?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What effect does K+ have on digoxin toxicity?

A

Hypokalaemia exacerbates digoxin toxicity so it’s important to keep higher levels of K+ on commencement of digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What signs would you see on an ECG in hypokalaemia?

A

Small or inverted T waves
Prominent U waves
Long PR interval
Depressed ST segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If someone is found to be hyponatraemic, what is the first step in the investigations?

A

Assess fluid status

23
Q

What are the causes of hypervolaemic hyponatraemia?

A 
The 'failures':
Renal failure
Nephrotic syndrome
Heart failure
Liver failure
24
Q

List some drug causes of hyponatraemia

A 
Thiazide diuretics
SSRIs
Anti-epileptics: Phenytoin and valproate
ACE inhibitors
Omeprazole (can cause SIADH)
25
Q

Why is it important not to replace fluids too quickly in hyponaetraemia?

A

Can cause central pontine myelinolysis

26
Q

What does calcium resonium down?

A

Binds K+ in the gut, reducing it’s absorption and thus gradually lowering levels of potassium

27
Q

List some drug causes of hyperkalaemia

A 
Potassium sparing diuretics e.g. spironolactone, eplenerone
Loop diuretics e.g. furosemide
Beta blockers
ACE-Inhibitors
Digoxin
Ciclosporin
28
Q

In a patient who is hyponatraemic and hypovolaemic, what is the next step in the investigation / management of the hyponatraemia?

A

Measure urine sodium

29
Q

In a patient who is hyponatraemic and euvolaemic, what is the next step in the investigation / management of the hyponaetraemia?

A

Measure urine osmolality

30
Q

What is the cause of hyponatraemia when the urine osmolality is raised?

A

SIADH

31
Q

How can you tell if hyponatraemia is caused by SIADH?

A

Urine osmolality raised

32
Q

What is vasopressin?

A

Anti-diuretic hormone

33
Q

What are the clinical features of diabetes insipidus?

A

Polyuria
Polydipsia
Nocturia
Dilute urine

34
Q

How is diabetes insipidus classified?

A

Nephrogenic

Cranial

35
Q

What is the mechanism of cranial diabetes insipidus?

A

Impaired production of ADH by the pituitary

36
Q

What is the mechanism of nephrogenic diabetes insipidus?

A

Resistance to the action of ADH

37
Q

What is the key investigation in diabetes insipidus?

A

Water deprivation test

38
Q

How is the water deprivation test performed?

A

Serum and urine osmolality, urine volume and body weight measured hourly for up to 8 hours, while the patient is fasting and deprived of water or other fluids

39
Q

What is a normal result from the water deprivation test?

A

Serum osmolality within normal range

Urine osmolality rises i.e. concentrated urine

40
Q

What result from a water deprivation test would lead you to suspect diabetes insipidus?

A

High serum osmolality

Minimal rise in urine osmolality i.e. no concentration of urine

41
Q

How do you differentiate between nephrogenic and cranial diabetes insipidus?

A

Give desmopressin and measure urine osmolality for a further 2-4 hours after water deprivation test:

  • Urine osmolality stays the same = Nephrogenic DI (no response to the ADH analogue)
  • Urine osmolality rises by more than 50% = Cranial DI (the kidneys have responded to the ADH analogue)
42
Q

What is desmopressin?

A

Vasopressin (ADH) analogue

43
Q

What are the causes of cranial diabetes insipidus?

A

Trauma e.g. post-head injury
Pituitary surgery
Tumours e.g. craniopharyngioma

44
Q

What are the drug causes of nephrogenic diabetes insipidus?

A

Lithium

Dimeclocycline

45
Q

What are the causes of nephrogenic diabetes insipidus?

A 
Drugs: Lithium, dimeclocycline
Electrolyte abnormalities: Hypokalaemia, hypercalcaemia
Renal tubular acidosis
Sickle cell disease
Congenital: Mutation in ADH receptor
46
Q

What is the treatment for cranial diabetes insipidus?

A

Desmopressin

47
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Treat the cause
Bendroflumethiazide 5mg daily
NSAIDs

48
Q

What is the mechanism by which NSAIDs treat diabetes insipidus?

A

Lower urine volume and plasma sodium by inhibiting prostaglandin synthase (prostaglandins locally inhibit the action of ADH)

49
Q

What actions does anti-diuretic hormone have?

A

Causes concentration of urine by water reabsorption in the collecting tubules
Causes vasoconstriction in response to low BP

50
Q

List some triggers for ADH production

A

High serum osmolality
Low BP
Low circulating blood volume

51
Q

List some causes of SIADH

A

Malignancy: Small cell lung cancer, proste cancer, pancreatic cancer
Brain: Meningitis, tumour
Lung: Pneumonia, lung abscess, TB
Drugs: Carbamazepine, opiates, SSRIs, sulphonylureas

52
Q

What would you find on investigation of a patient with SIADH?

A

Low plasma osmolality, ‘inappropriate’ urine osmolality
High urine sodium
Low serum sodium
Normal renal, adrenal, thyroid function
Normal volume status (Euvolaemic hyponatraemia)

53
Q

What is the treatment for SIADH?

A

Fluid restriction
Treat underlying cause
Dimeclocycline - Reduces response of kidneys to ADH
Correct slowly to avoid central pontine myelinolysis

Endocrinology / Renal Medicine (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions