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ChemPath Flashcards

1
Q

What % of the body is water?

A

60%

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2
Q

What is the ratio of fluid in the body in terms of intracellular:extracellular?

A

2:1

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3
Q

Which compartments make up the body’s extracellular fluid?

A

-Intravascular-Interstitial-Transcellular

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4
Q

What is the function of interstitial fluid?

A

Bathes cells + makes up the largest component of ECF

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5
Q

What is transcellular fluid/where is it?

A

Within epithelial lined spaces e.g. CSF, joint fluid, bladder urine, aqueous humour

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6
Q

What is osmolality?

A

The total number of particles in a solution

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7
Q

What are the units for osmolality?

A

mmol/kg

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8
Q

What is osmolarity?

A

2(Na + K) + urea + glucose

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9
Q

What are the units of osmolarity?

A

mmol/L

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10
Q

What are the determinants of osmolarity?

A

Physiological: sodium, potassium, chlorine, HCO3, urea, glucosePathological: endogenous (e.g. glucose), exogenous (e.g. ethanol, mannitol)

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11
Q

What is the osmolar gap?

A

The difference between osmolarity and osmolality

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12
Q

What is the normal range for osmolality?

A

275-295 mmol/kg

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13
Q

What is the normal range for sodium?

A

135-145 mmol/L

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14
Q

How much sodium is freely exchangeable and where is the rest of it?

A

70% - rest is complexed in bone

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15
Q

Is sodium predominantly intracellular or extracellular?

A

Extracellular

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16
Q

What maintains sodium levels?

A

Active pumping from ICF to ECF by Na+/K+ ATPase

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17
Q

Which fluid volume directly depends on sodium?

A

ECF

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18
Q

How should you manage mild hyponatraemia?

A

Treat the underlying cause not the sodium level provided it’s not severe

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19
Q

What are the features of symptomatic hyponatraemia?

A

-Nausea and vomiting (

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20
Q

What measure should you use to determine if someone has true hyponatraemia?

A

Osmolality

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21
Q

What might be the cause of hyponatraemia if serum osmolality is high?

A

Glucose/mannitol infusion

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22
Q

What might be the cause of hyponatraemia if serum osmolality is normal?

A

Spurious - drip arm samplePseudohyponatraemia: hyperlipidaemia, paraproteinaemia

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23
Q

What might be the cause of hyponatraemia if serum osmolality is low?

A

True hyponatraemia

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24
Q

What is TURP syndrome?

A

Hyponatraemia from water absorbed through a damaged prostate

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25
Q

If you have a hyponatraemic patient with a low osmolality, what measure should you look at next to determine the cause?

A

Hydration status and urinary Na

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26
Q

What are the causes of hyponatraemia where a patient is hypovolaemic with urinary sodium >20?

A

Renal - diuretics, Addison’s, salt losing nephropathies

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27
Q

What are the causes of hyponatraemia where a patient is hypovolaemic with urinary sodium

A

Non renal - vomiting, diarrhoea, excess sweating, third space losses (ascites, burns) - depending on fluid replacement

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28
Q

What are the causes of hyponatraemia where a patient is euvolaemic with urinary sodium >20?

A

SIADH, primary polydipsia, severe hypothyroidism

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29
Q

What are the causes of hyponatraemia where a patient is hypervolaemic with urinary sodium >20?

A

ARF, CRF

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30
Q

What are the causes of hyponatraemia where a patient is hypervolaemic with urinary sodium

A

Cardiac failure, cirrhosis, inappropriate IV fluid

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31
Q

What isWhat tests should you do in a patient who is hyponatraemic and euvolaemic?

A

TFT, short synacthen test, paired urine serum osmolality

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32
Q

What is the risk with rapidly correcting hyponatraemia?

A

Central pontine myelinolysis

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33
Q

What are the features of central pontine myelinolysis?

A

Pseudo bulbar palsy, paraparesis, locked-in syndrome

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34
Q

At what rate should you aim to correct hyponatraemia?

A

Increase Na+ by 1 mmol/l per hour

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35
Q

What are some causes of hyponatraemia pos surgery?

A

-Overhydration with hypotonic IV fluids-Transient increase in ADH due to stress of surgery

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36
Q

What are the laboratory criteria for a diagnosis of SIADH?

A

-True hyponatraemia-Clinically euvolaemic-Inappropriately high urine osmolality and increased renal sodium excretion (>20 mmol/l)-Normal renal, adrenal, thyroid and cardiac function

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37
Q

What are the causes of SIADH?

A

-Malignancy: small cell lung ca (most common), pancreas, prostate, lymphoma (ectopic secretion)-CNS disorders: meningoencephalitis, haemorrhage, abscess-Chest disease: TB, pneumonia, abscess-Drugs: opiates, SSRIs, carbamazepine

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38
Q

How is hypernatraemia defined?

A

Usually clinically significant - plasma Na+ >148 mmol/l

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39
Q

What are some common scenarios in which patients become hypernatraemic?

A

Iatrogenic, ITU patients

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40
Q

What are the symptoms of hypernatraemia?

A

ThirstConfusionSeizures and ataxiaComa

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41
Q

What is the risk of rapid correction of hypernatraemia?

A

Cerebral oedema

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42
Q

What are the causes of hypernatraemia in a hypovolaemic patient?

A

GI loss: vomiting, diarrhoeaSkin loss: excessive sweating, burnsRenal loss:-Loop diuretics-Osmotic diuretics (glucose, mannitol)-Renal disease (impaired concentrating ability)

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43
Q

What are the causes of hypernatraemia in a euvolaemic patient?

A

Respiratory loss: tachypnoeaSkin loss: excessive sweating, feverRenal loss: diabetes insipidusMisc: no water

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44
Q

What are the causes of hypernatraemia in a hypervolaemic patient?

A

Mineralocorticoid excess (Conn’s syndrome)Hypertonic saline

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45
Q

What are the clinical features of diabetes insipidus?

A

-Hypernatraemia (lethargy, thirst, irritability, confusion, coma, fits)-Clinically euvolaemic-Polyuria and polydipsia-Urine: plasma osmolality

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46
Q

What are the 2 main types of diabetes insipidus?

A

Cranial and nephrogenic

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47
Q

What is cranial diabetes insipidus?

A

Where there is a lack of/no ADH

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48
Q

What are the causes of cranial diabetes insipidus?

A

Head traumaTumourSurgery

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49
Q

What is nephrogenic diabetes insipidus?

A

Where there is a receptor defect leading to insensitivity to ADH

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50
Q

What are the causes of nephrogenic diabetes insipidus?

A

InheritedLithiumChronic renal failure

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51
Q

How do you diagnose diabetes insipidus?

A

8 hour fluid deprivation test

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52
Q

What happens in a normal 8 hour fluid deprivation test?

A

Urine concentration rises to >600 mOsmol/kg

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53
Q

What happens in an 8 hour fluid deprivation test with primary polydipsia?

A

Urine concentrates >400-600 mOsmol/kg

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54
Q

What happens in an 8 hour fluid deprivation test with cranial diabetes insipidus?

A

Urine concentrates only after giving desmopressin

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55
Q

What happens in an 8 hour fluid deprivation test with nephrogenic diabetes insipidus?

A

Zero concentration of urine including after desmopressin

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56
Q

What is the normal range for potassium?

A

3.5-5.5 mmol/l

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57
Q

Is potassium mainly intracellular or extracellular?

A

Intracellular - only 2% is extracellular

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58
Q

What maintains potassium in the intracellular fluid?

A

Active pumping from ECF -> ICF by Na+/K+ ATPase

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59
Q

How much of potassium is freely exchangeable and where is the rest of it?

A

90% - rest is bound in RBCs, bone, brain tissue

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60
Q

What ion is potassium linked to (other than sodium)

A

H+ - as one moves into cells the other moves out

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61
Q

For every drop in pH of 0.1, what is the change in K+?

A

Increases by 0.7

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62
Q

How is hypokalaemia defined?

A

Potassium

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63
Q

What are the two main mechanisms of hypokalaemia?

A

Depletion or shift into cells - rarely ue to decreased intake

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64
Q

What are some common causes of hypokalaemia?

A

-GI loss-Renal loss: hyperaldosteronism, excess cortisol, increased sodium delivery to distal nephron, osmotic diuresis-Redistribution into cells: insulin, beta agonists, alkalosis

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65
Q

What are some rare causes of hypokalaemia?

A

Tubular acidosis type 1 + 2, hypomagnesaemia

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66
Q

How is hyperkalaemia defined?

A

Potassium >5.5 mmol/l

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67
Q

How common is hyperkalaemia compared to hypokalaemia?

A

Less common but more dangerous

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68
Q

What are the 3 main mechanisms behind hyperkalaemia?

A

Excessive intakeTranscellular movement (ICF>ECF)Decreased excretion

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69
Q

What are some causes of excessive potassium intake?

A

Oral (fasting)ParenteralStored blood transfusion

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70
Q

What are some causes of transcellular movement of potassium?

A

AcidosisInsulin shortageTissue damage/catabolic state

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71
Q

What are some causes of decreased excretion of potassium?

A

Acute renal failure (oliguric phase)CRF (late)K sparing diuretics (spironolactone)Mineralocorticoid deficiency (Addisons)NSAIDsACEI

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72
Q

What is a normal pH?

A

7.35-7.45

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73
Q

What is a normal CO2?

A

4.7-6.0 kPa

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74
Q

What is a normal bicarbonate?

A

22-30 mmol/L

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75
Q

What is a normal O2?

A

10-13 kPa

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76
Q

What is the equation for [H+] using CO2 and HCO3?

A

[H+] = 180 x ([CO2]/[HCO3])

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77
Q

What is the pH, bicarb and CO2 in metabolic acidosis?

A

Low pHLow bicarbNormal CO2 or low if compensated

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78
Q

What is the pH, bicarb and CO2 in metabolic alkalosis?

A

High pHHigh bicarbNormal CO2 or high if compensated

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79
Q

What is the pH, bicarb and CO2 in respiratory acidosis?

A

Low pHNormal bicarb or high if compensatedHigh CO2

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80
Q

What is the pH, bicarb and CO2 in respiratory alkalosis?

A

High pHNormal bicarb or low if compensatedLow CO2

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81
Q

What are the causes of metabolic acidosis?

A

Lactate build upDKARenal tubular acidosis

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82
Q

What are the causes of metabolic alkalosis?

A

Pyloric stenosisHypokalaemia

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83
Q

What are the causes of respiratory acidosis?

A

Lung injury - pneumonia, COPDDecreased ventilation

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84
Q

What are the causes of respiratory alkalosis?

A

Mechanical ventilationAnxiety/panic attack

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85
Q

What is ‘compensation’ (acid base)?

A

Return of pH towards normal at the expense of other values

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86
Q

What are the anion and osmolar gaps useful for?

A

Screening for organic poisoning, DKA, and to provide more information about a metabolic acidosis

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87
Q

How do you calculate the anion gap?

A

(Na+ + K+) - (Cl- + HCO3)

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88
Q

What is the anion gap?

A

Difference between the total concentration of principal cations and principal anions = concentration of unmeasured anions in plasma

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89
Q

What almost entirely makes up the anion gap?

A

Albumin

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90
Q

What is the normal range for the anion gap?

A

14-18 mmol/L

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91
Q

What are the causes of elevated anion gap metabolic acidosis?

A

KULTKetoacidosis (DKA, alcoholic, starvation)Uraemia (renal failure)Lactic acidosisToxins (ethylene glycol,methanol, paraldehyde, salicylate)

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92
Q

What defines mild hyponatraemia?

A

Sodium

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93
Q

What defines severe hyponatraemia?

A

Sodium

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94
Q

What is a normal osmolar gap?

A
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95
Q

how do you calculate the osmolar gap?

A

Osmolality (measured) - osmolarity (calculated)

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96
Q

What does an elevated osmolar gap mean?

A

That there is extra solute in the plasma e.g. ethylene glycol, ethanol, methanol, mannitol

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97
Q

Why is osmolar gap helpful?

A

To differentiate between causes of elected anion gap metabolic acidosis

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98
Q

What are the LFT markers of liver cell damage?

A

ALTASTAlk phosGGTBilirubin

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99
Q

What are the LFT markers of liver synthetic function?

A

Clotting (INR)AlbuminGlucose

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100
Q

What are the aminotransferases?

A

AST And ALT

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101
Q

What is a normal aminotransferase?

A
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102
Q

When are the aminotransferases raised?

A

When hepatocytes die

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103
Q

What is the pattern of aminotransferases in alcoholic liver disease?

A

AST:ALT = 2:1

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104
Q

What is the pattern of aminotransferases in viral liver disease?

A

AST:ALT =

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105
Q

What is a normal alkaline phosphatase?

A

30-150 iu/L

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106
Q

When is ALP raised?

A

Cholestasis (intra or extra hepatic), bone disease, and ++ in pregnancy

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107
Q

What is a normal gamma GT?

A

30-150 iu/L

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108
Q

When is gamma GT elevated?

A

Chronic alcohol use, bile duct disease and metastases

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109
Q

What is gamma GT useful for?

A

To confirm hepatic source of ALP

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110
Q

What are the porphyrias?

A

A group of 7 disorders caused by deficiency in enzymes involved in haem biosynthesis, leading to a build up of toxic haem precursors

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111
Q

What is acute intermittent porphyria?

A

An autosomal dominant disorder in which there is an HMB (hydroxymethylbilane) synthase deficiency

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112
Q

What are the symptoms of acute intermittent porphyria?

A

NEUROVISCERAL ONLY:Abdo painSeizuresPsych disturbancesNausea and vomitingTachycardiaHypertensionSensory lossMuscle weaknessConstipationUrinary incontinence

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113
Q

Why are there no cutaneous manifestations in acute intermittent porphyria?

A

Absence of porphyrinogens

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114
Q

How do you diagnose acute intermittent porphyria?

A

ALA and PBG in urine - ‘port wine urine’

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115
Q

What are the precipitating factors in acute intermittent porphyria?

A

ALA syntheses inducers (steroids, ethanol, barbiturates)Stress (infections, surgery)Reduced caloric intake and endocrine factors (e.g. premenstrual)

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116
Q

How do you treat acute intermittent porphyria?

A

Avoid precipitating factorsAnalgesiaIV carbohydrate/haem arginate

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117
Q

What is acute porphyria with skin lesions?

A

Hereditary coproporphyria (HCP) + variegate porphyria (VP); autosomal dominant condition

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118
Q

What are the features of hereditary coproporphyria?

A

Neurovisceral and skin lesionsRaised porphyrins in faeces or urine

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119
Q

Which non-acute porphyrias have skin lesions only?

A

Congenital erythropoietic porphyriaErythropoietic protoporphyriaPorphyria cutanea tarda

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120
Q

What are the features of erythropoietic protoporphyria?

A

PhotosensitivityBurning, itching, oedema following sun exposure

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121
Q

What is porphyria cutanea tarda?

A

Inherited or acquired deficiency in uroporphyrinogen decarboxylase

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122
Q

What are the symptoms of porphyria cutanea tarda?

A

Vesicles (causing, pigmented, superficial scarring) on sun exposed sites

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123
Q

How do you diagnose porphyria cutanea tarda?

A

Increased urinary uroporphyrins and coproporphyrinsIncreased ferritin

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124
Q

What’s the treatment for porphyria cutanea tarda?

A

Avoid precipitants (alcohol,hepatic compromise), phlebotomy

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125
Q

Which pituitary hormones does GHRH stimulate?

A

GH

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126
Q

Which pituitary hormones GnRH stimulate?

A

FSH and LH

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127
Q

Which pituitary hormones TRH stimulate?

A

TSH, prolactin

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128
Q

Which pituitary hormones dopamine stimulate?

A

Inhibits prolactin

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129
Q

Which pituitary hormones CRH stimulate?

A

ACTH

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130
Q

What are the indications for a combined pituitary function test?

A

Assessment of all components of anterior pituitary function - particularly in pituitary tumours or following tumour treatment

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131
Q

What are the contraindications to doing a combined pituitary function test?

A

Ischaemic heart diseaseEpilepsyUntreated hypothyroidism (impairs the GH and cortisol responses)

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132
Q

What are the side effects of doing a combined pituitary function test?

A

Sweating, palpitations, loss of consciousnessRarely: convulsions with hypoglycaemiaWith the TRH injection may get transient symptoms of metallic taste in the mouth, flushing and nausea

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133
Q

What are the 3 components of the combined pituitary function test?

A

Insulin tolerance testThyrotrophin releasing hormone testGonadotrophin releasing hormone test

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134
Q

How do you interpret the insulin tolerance test?

A

Adequate cortisol response: increase from >170 nmol/L to >500 nmol/LAdequate GH response: increase to > 6mcg/L

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135
Q

What is a normal result in the thyrotrophin releasing hormone test?

A

TSH rise to >5 u/L (30 min value > 60 min value)

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136
Q

What is a result in the thyrotrophin releasing hormone test indicating primary hypothalamic disease?

A

IF the 60 min value > 30 min value

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137
Q

What is a result in the thyrotrophin releasing hormone test indicating hyperthyroidism?

A

TSH remains supressed

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138
Q

What is a result in the thyrotrophin releasing hormone test indicating hypothyroidism?

A

Exaggerated response

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139
Q

Why isn’t dynamic testing usually needed to diagnose hyperthyroidism?

A

Because current TSH assays are sensitive enough for basal levels to be adequate

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140
Q

What is a normal gonadotrophin releasing hormone test result?

A

Normal peaks can occur at 30 or 60 minutes/ LH should be >10U/L and FSH >2U/L

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141
Q

What is an inadequate gonadotrophin releasing hormone test result indicative of/

A

Can be a possible early indicator of hypopituitary

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142
Q

How is gonadotrophin deficiency diagnosed?

A

On basal levels:-Male - low testosterone in absence of increased basal gonadotrophinFemale - low estradiol without raised basal gonadotrophin and no response to clomiphene

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143
Q

How should pre pubertal children respond to the gonadotrophin releasing hormone test?

A

Should have no response of LH or FSH to LHRH

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144
Q

How will the pituitary respond in a gonadotrophin releasing hormone test in e.g. precocious puberty

A

Sex steroids present -> pituitary is ‘primed’ -> will respond to LHRH

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145
Q

What do you have to be careful of before the test with the gonadotrophin releasing hormone test?

A

Shouldn’t prime the pituitary with steroids

146
Q

What hormones will a pituitary tumour produce?

A

Any combination of pituitary hormones

147
Q

How is a pituitary micro adenoma defined?

A
148
Q

How is a pituitary macro adenoma defined?

A

> 10mm - usually aggressive

149
Q

What visual defect can a pituitary adenoma cause?

A

Bitemporal hemianopia due to compression of the optic chiasm

150
Q

What are the hormones of the anterior pituitary?

A

ADH and oxytocin

151
Q

What might cause excess ADH?

A

-LUNG: paraneoplasias: SCC, small cell, pneumonia-BRAIN: traumatic brain injury, meningitis-IATROGENIC: SSRIs, amitryptilline

152
Q

What is the effect of excess ADH?

A

SIADH -> euvolaemic hyponatraemia

153
Q

What are the causes of ADH failure?

A

-Diabetes insipidus-Neurogenic (failure of production, 50% idiopathic)-Nephrogenic (commonly iatrogenic from lithium, also hypercalcaemia, renal failure)-Dipsogenic (failure/damage to the hypothalamus and thirst drive, hypernatraemia without increased thirst response)

154
Q

What is diabetes insipidus?

A

Increased diuresis due to either failure of production or insensitivity to ADH, leads to decreased urine osmolality and increased serum osmolality

155
Q

What does oxytocin do?

A

Increases uterine contraction and expulsion of milk

156
Q

What can you given in failure of oxytocin production e.g. to help breastfeeding?

A

Syntocinon

157
Q

What can you use as an oxytocin antagonist in tocolysis?

A

Atosiban

158
Q

What are the causes of normal TSH with an abnormal T4?

A

-Assay interference-Changes in TBG-Amiodarone

159
Q

What are the causes of low TSH?

A

-High T4 or high T3: hyperthyroidism-Normal T3 and T4: subclinical hyperthyroidism-Low T4: central hypothyroidism (hypothalamic/pituitary disorder)

160
Q

What are the causes of a high TSH?

A

-Low T4: hypothyroidism-Normal T4: treated or subclinical hypothyroidism (look for associated increased cholesterol)-High T4: TSH secreting tumour or thyroid hormone resistance-Later low TSH and low T3 and T4: sick euthyroidism (with any severe illness)

161
Q

What are causes of hyperthyroidism with high uptake?

A

Graves disease (40-60%, F>M 9:1, autoantibodies ++, high uptake on isotope scan)Toxic multi nodular goitre (30-50%, high uptake)Toxic adenoma (5%, ‘hot nodule’ on isotope scan)

162
Q

What are causes of hyperthyroidism with low uptake?

A

Subacute deQuervain’s thyroiditis - self limiting post viral painful goitrePostpartum thyroiditis

163
Q

What is the treatment for hyperthyroidism with high uptake?

A

Beta blocker and antithyroid therapy (carbimazole/propylthiouracil)Can also use radio iodine or surgery

164
Q

Why is propylthiouracil not really used now?

A

Risk of aplastic anaemia

165
Q

What can you use propylthiouracil for in high uptake hyperthyroidism?

A

To block and replace or titrate to TSH

166
Q

What is the treatment for hyperthyroidism with low uptake?

A

Symptomatic - beta blockers and NSAIDs for de Quervain’s

167
Q

What are the autoimmune causes of hypothyroidism?

A

Primary atrophic hypothyroidismHashimoto’s thyroiditis

168
Q

What are the features of primary atrophic hypothyroidism?

A

Diffuse lymphocytic infiltration and atrophy, no goitre

169
Q

What are the features of Hashimoto’s thyroiditis?

A

Plasma cell infiltration and goitre. Elderly females. May be initial Hashitoxicosis. ++ autoantibody titres

170
Q

What are the non autoimmune causes of hypothyroidism?

A

-Iodine deficiency (common worldwide)-Post thyroidectomy/radioiodine-Drug induced: antithyroid drugs, lithium, amiodarone

171
Q

What is the treatment for hypothyroidism?

A

Thyroid replacement therapy

172
Q

What are the 5 kinds of thyroid neoplasia?

A

PapillaryFollicularMedullaryLymphomaAnaplastic

173
Q

What are the features of papillary thyroid cancer?

A

> 60% cases30-40 years oldSurgery +/- radioiodineThyroxine to lower TSH

174
Q

What are the features of follicular thyroid cancer?

A

25%Middle agedWell differentiated but spreads earlySurgery + radioiodine + thyroxine

175
Q

What are the features of medullary thyroid cancer?

A

5% originates in parafollicular cellsLinked to MEN2Produce calcitonin

176
Q

What are the features of lymphoma thyroid cancer?

A

5% MALT originRisk factor: chronic HashimotosGood prognosis

177
Q

What are the features of anaplastic thyroid cancer?

A

RareElderlyPoor response to any treatment

178
Q

What are the causes of Cushing’s?

A

Pituitary tumour (85%, Cushing’s disease)Adrenal tumour 10%Ectopic ACTH producing tumour 5%Iatrogenic: steroid use

179
Q

What are the causes of Addisons?

A

AutoimmuneTBTumour depositsAdrenal haemorrhageAmyloid deposits

180
Q

What are the causes of Conn’s?

A

Adrenal tumour

181
Q

What are the causes of Phaeo?

A

Adrenal medulla tumour = increased adrenaline

182
Q

What are the symptoms and signs of Cushing’s?

A

Moon faceBuffalo humpStriae, acneHypertensionDiabetesMuscle weakness (proximal myopathy)Hirsutism

183
Q

What are the symptoms and signs of Addison’s?

A

High potassiumLow sodium and glucosePostural hypotensionSkin pigmentationLethargyDepression

184
Q

What are the symptoms and signs of Conn’s?

A

Uncontrollable hypertensionHigh sodiumLow potassium

185
Q

What are the symptoms and signs of phaeo?

A

HypertensionArrhythmiasDeath if untreated

186
Q

What investigations should you do in Cushing’s?

A

Low dose dexamethasoneHigh dose dexamethasoneCortisol levels

187
Q

What investigations should you do in Addison’s?

A

SynACTHen test

188
Q

What investigations should you do in Conn’s?

A

Aldosterone:renin ratio

189
Q

What investigations should you do in phaeo?

A

Plasma + 24h urine met adrenaline measurement/catecholamines + VMA

190
Q

How should you treat Cushing’s?

A

Treat the underlying cause e.g. surgical removal of lesion

191
Q

How should you treat Addison’s?

A

Hormone replacement: hydrocortisone/fludrocortisone if primary adrenal lesion

192
Q

How should you treat Conn’s?

A

Aldosterone antagonists/K sparing diuretics: spironolactone, eplerenone, amiloride

193
Q

How should you treat phaeo?

A

Alpha blockadeBeta blockadeThen surgery when blood pressure well controlled

194
Q

What are the signs of phenytoin toxicity?

A

Ataxia and nystagmus

195
Q

What are the signs of digoxin toxicity?

A

ArrhythmiasHeart blockConfusionXanthopsia (seeing yellow)

196
Q

What are the signs of lithium toxicity?

A

Tremor (early)LethargyFitsArrhythmiaRenal failure

197
Q

What are the signs of gentamicin toxicity?

A

TinnitusDeafnessNystagmusRenal failure

198
Q

What are the signs of theophylline toxicity?

A

ArrhythmiasAnxietyTremorConvulsions

199
Q

What is phenytoin mainly used for?

A

Seizures

200
Q

What is digoxin mainly used for?

A

Arrhythmias

201
Q

What is lithium mainly used for?

A

Relapse of mania in bipolar disorder

202
Q

What is gentamicin mainly used for?

A

Uncontrolled infection

203
Q

What is theophylline mainly used for?

A

COPD, asthma - relaxes bronchial smooth muscle

204
Q

What are the interactions and cautions of phenytoin?

A

At high levels the liver becomes saturated leading to a surge in blood levels

205
Q

What are the interactions and cautions of digoxin?

A

Levels increased with hypokalaemiaReduce dose in renal failure and elderly

206
Q

What are the interactions and cautions of lithium?

A

Excretion impaired by hyponatraemia, decreased renal function and diuretics

207
Q

What are the interactions and cautions of gentamicin?

A

Mostly use single daily dosing. Monitor peak and trough level before next dose

208
Q

What are the interactions and cautions of theophylline?

A

Variation in half life e.g. 4 hours in smokers and 8 hours in non-smokers, 30 hours in liver disease. Level increased by erythromycin, cimetidine and phenytoin

209
Q

How do you treat phenytoin toxicity?

A

Omit/reduce dose

210
Q

How do you treat digoxin toxicity?

A

Digibind (digoxin immune Fab)

211
Q

How do you treat lithium toxicity?

A

RF may need haemodialysis

212
Q

How do you treat gentamicin toxicity?

A

Omit/reduce dose

213
Q

How do you treat theophylline toxicity?

A

Omit/reduce dose

214
Q

What is the normal range for calcium?

A

2.2-2.6 mmol/L

215
Q

Where is calcium in the body?

A

45% ionised = free = biologically active50% bound to albumin, therefore affected by albumin level (use corrected calcium)

216
Q

What are the two main hormones in calcium metabolism?

A

PTH1,25 (OH)2 D - calcitriol

217
Q

What are the actions of PTH?

A

Increases tubular 1alpha hydroxylation of bit DMobilises calcium from boneIncreases renal calcium reabsorptionIncreases renal phosphate excretion

218
Q

What are the actions of calcitriol?

A

Increases calcium and phosphate absorption from the gutBone remodelling

219
Q

What is this condition?-High calcium-Low PO4-Increased or normal PTH-Increased or normal ALP-Normal vitamin D

A

Primary hyperparathyroidism

220
Q

What is this condition?-Low or normal calcium-High PO4-High PTH-High ALP-Normal vitamin D

A

Secondary hyperparathyroidism

221
Q

What is this condition?-High calcium-Low PO4-Increased PTH-Increased or normal ALP-Normal vitamin D

A

Tertiary hyperparathyroidism

222
Q

What is this condition?-Low calcium-High PO4-Low PTH-Low or normal ALP-Normal vitamin D

A

Hypoparathyroidism

223
Q

What is this condition?-Low calcium-Low PO4-Increased PTH-Increased ALP-Low D

A

Rickets/osteomalacia

224
Q

What is this condition?-Normal calcium-Normal PO4-Normal PTH-High ALP-Normal vitamin D

A

Paget’s disease

225
Q

What is this condition if there is bone loss?-Normal calcium-Normal PO4-Normal PTH-Normal ALP-Normal vitamin D

A

Osteoporosis

226
Q

What is the primary defect in primary hyperparathyroidism?

A

Increased PTH (80% parathyroid adenoma)

227
Q

What is the primary defect in secondary hyperparathyroidism?

A

Renal osteodystrophy

228
Q

What is the primary defect in tertiary hyperparathyroidism?

A

Autonomous PTH secretion post renal transplant

229
Q

What is the primary defect in hypoparathyroidism?

A

Low levels of PTHPrimary: DiGeorge syndromeSecondary: post thyroid surgery

230
Q

What is the primary defect in rickets/osteomalacia?

A

Vitamin D deficiency

231
Q

What is the primary defect in PAget’s disease?

A

Remodelling of bone

232
Q

What is the primary defect in osteoporosis?

A

Bone loss

233
Q

What should be the first step in determining the cause of hypercalcaemia?

A

Albumin

234
Q

If a patient is hypercalcaemic with high albumin, what might the cause be?

A

If urea is high - dehydrationIf urea is normal - cuffed

235
Q

If a patient is hypercalcaemic with low or normal albumin, what should be the next investigation?

A

Phosphate

236
Q

If a patient is hypercalcaemic with low/normal albumin and low phosphate what might the cause be?

A

Primary or tertiary hyperparathyroidism (confirm with raised PTH)

237
Q

If a patient is hypercalcaemic with low/normal albumin and high phosphate what might the next investigation be?

A

ALP

238
Q

If a patient is hypercalcaemic with low/normal albumin, high phosphate and high ALP what might the cause be?

A

Increased bone turnoverBone metastasisThyrotoxicosisSarcoidosis (increased 1alphaOH)

239
Q

If a patient is hypercalcaemic with low/normal albumin, high phosphate and normal ALP what might the cause be?

A

MyelomaExcess vitamin DSarcoidMilk alkali syndrome (and increased bicarbonate)

240
Q

What are the symptoms of hypercalcaemia?

A

Stones (renal)Bones (pain)Groans (psych)Moans (abdo pain)PolyuriaMuscle weakness

241
Q

How should you treat hypercalcaemia?

A

Correct dehydrationBisphosphonatesCorrect cause e.g. chemo for cancer

242
Q

What should be the first investigation in a patient who is hypocalcaemic?

A

Phosphate

243
Q

What are the causes of hypocalcaemia with raised phosphate?

A

Chronic kidney diseaseHypoparathyroidism (including post thyroid surgery)PseudohypoparathyroidismHypomagnesaemia

244
Q

What are the causes of hypocalcaemia with normal/low phosphate?

A

OsteomalaciaAcute pancreatitisOver hydrationRespiratory alkalosis (low ionised/active Ca2+)

245
Q

What is a cause of finding hypocalcaemia as an artefact?

A

Hypoalbuminaemia

246
Q

What are the symptoms of hypocalcaemia?

A

Perioral paraesthesiaCarpopedal spasmNeuromuscular excitability (Trousseau’s and Ckvostek’s sign)

247
Q

What’s the treatment for hypocalcaemia?

A

Mild: give calciumChronic kidney disease: alfacalcidolSevere: 10% calcium gluconate IV

248
Q

What are the risk factors for renal stones?

A

DehydrationAbnormal urine pH (meat intake, renal tubular acidosis)Increased excretion of stone constituentsUrine infectionAnatomical abnormalities

249
Q

What are the causes of calcium stones?

A

Most patients are normocalcaemicResults from:-Hyperoxaluria: increased intake/absorption etc-Hypercalciuria: increased intake/renal leak

250
Q

How are calcium stones managed preventatively?

A

Avoid dehydrationReduce oxalate intakeMaintain Ca intakeThiazides -> hypocalciuricCitrate (alkalinise urine)

251
Q

How common are mixed calcium stones and how do they appear on X-ray?

A

~45% - radioopaque

252
Q

How common are calcium oxalate stones and how do they appear on X-ray?

A

~35% - radioopaque

253
Q

How common are calcium phosphate stones and how do they appear on X-ray?

A

~1% - radioopaque

254
Q

How common are triple phosphate ‘struvite’ stones and how do they appear on X-ray?

A

~10% - radiopaque ‘staghorn’

255
Q

How common are uric acid stones and how do they appear on X-ray?

A

~5% - radiolucent

256
Q

How common are cysteine stones and how do they appear on X-ray?

A

~1-2% - radiolucent

257
Q

How common are xanthine stones?

A

Rare

258
Q

What investigations should be done in recurrent stones?

A

Serum : Cr, bicarb, Ca, phosphate, urate, PTH (if hypercalcaemic)Stone analysisSpot urine: pH, MCS, amino acids, albumin24h urine: volume (>2.5L), Ca, oxalate, urate, citrate

259
Q

When are amylase levels high?

A

Acute pancreatitis - >10x upper normal limit

260
Q

What is the most common usage of creatine kinase?

A

Marker of muscle damage

261
Q

What are the forms of creatine kinase?

A

CK-MM - skeletal muscleCK-MB 1 + 2 - cardiac muscle

262
Q

When are creatine kinase levels raised?

A

Physiological - Afro-Caribbeans (10x normal), MI (>10x normal), statin related myopathy, rhabdomyolysis

263
Q

Where does alkaline phosphatase come from?

A

High concentrations in liver, bone, intestine and placenta

264
Q

When is alkaline phosphatase raised?

A

Physiological: pregnancy (3rd trimester), childhood growth spurtPathological: ->5x ULN: bone (Paget’s, osteomalacia), liver (cholestasis, cirrhosis)-

265
Q

Which troponin are clinically useful?

A

I and T - myocardial injury biomarkers

266
Q

When should you measure troponin?

A

At 6 hours and then 12 hours post onset of chest pain (100% sensitivity and 98% specificity at 12-24 hours)Remains elevated for 3-10 days

267
Q

What are the diagnostic criteria for an MI?

A

Either of:1) Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) and at least one of: ischaemic symptoms, pathologic Q waves on ECG, ECG changes indicative of ischaemia, coronary artery intervention2) Pathologic findings of an acute MI

268
Q

What are the lipoproteins in order of density?

A

Chylomicron

269
Q

What is PCSK9 and what mutation of it is significant?

A

Binds LDLR and promotes its degradationLoss of function mutation of PCSK9 -> low LDL

270
Q

How is PCSK9 clinically useful?

A

Novel form of LDL-lowering therapy is anti-PCSK9 Mab

271
Q

Why is lipoprotein (a) clinically significant?

A

Risk factor for cardiovascular disease - treat with nicotinic acid

272
Q

What are the forms of primary hypercholesterolaemia and what mutations are involved?

A

Familial hypercholesterolaemia (type II) - autosomal dominant (LDLR, apoB, PCSK9) or autosomal recessive (LDLRAP1)Polygenic hypercholesterolaemia - several polymorphismsFamilial hyperalpha0lipoporteinaemia - CETP deficiencyPhyosterolaemia - ABC G5 and G8

273
Q

What are the forms of primary hypertriglyceridaemia and what deficiencies/problems are involved?

A

Familial type I - lipoprotein lipase or apoC II deficiencyFamilial type V - apia V deficiency (sometimes)Familial type IV - increased synthesis of triglyceride

274
Q

What are the forms of primary mixed hyperlipidaemia?

A

Familial combined hyperlipidaemiaFamilial dysbetalipoproteinaemiaFamilial hepatic lipase deficiency

275
Q

What are the forms of hypolipidaemia and what deficiencies/problems are involved?

A

Beta-lipoporteinaemia - MTP deficiencyHypo-beta-lipoproteinaemia - truncated apoB proteinTangier disease - HDL deficiencyHypoalpha-lipoproteinaemia - apoA-1 mutations (sometimes)

276
Q

Vitamin AWhat’s another name for it?What happens in deficiency?What happens in excess?How do you test for it?

A

RetinolDeficiency - colour blindnessExcess - exfoliation, hepatitisTest - serum

277
Q

Vitamin DWhat’s another name for it?What happens in deficiency?What happens in excess?How do you test for it?

A

CholecalciferolDeficiency - osteomalacia/ricketsExcess - hypercalcaemiaTest - Serum

278
Q

Vitamin EWhat’s another name for it?What happens in deficiency?How do you test for it?

A

TocopherolDeficiency - anaemia, neuropathy,?malignancy, IHDTest - serum

279
Q

Vitamin KWhat’s another name for it?What happens in deficiency?How do you test for it?

A

PhytomenadioneDeficiency - defective clottingTest - PTT

280
Q

What are the fat soluble vitamins?

A

A, D, E, K

281
Q

What are the water soluble vitamins?

A

B1, B2, B6, B12, C, folate, B3

282
Q

Vitamin B1What’s another name for it?What happens in deficiency?How do you test for it?

A

ThiaminDeficiency - beri-beri, neuropathy, Wernicke syndromeTest - RBC transketolase

283
Q

Vitamin B2What’s another name for it?What happens in deficiency?What happens in excess?How do you test for it?

A

RiboflavinDeficiency - glossitisTest - RBC glutathione reductase

284
Q

Vitamin B6What’s another name for it?What happens in deficiency?What happens in excess?How do you test for it?

A

PyridoxineDeficiency - dermatitis/anaemiaExcess - neuropathyTest: RBC AST activation

285
Q

Vitamin B12What’s another name for it?What happens in deficiency?How do you test for it?

A

CobalaminDeficiency - pernicious anaemiaTest - serum B12

286
Q

Vitamin CWhat’s another name for it?What happens in deficiency?What happens in excess?How do you test for it?

A

AscorbateDeficiency - scurvyExcess - renal stonesTest - plasma

287
Q

FolateWhat happens in deficiency?How do you test for it?

A

Deficiency: megaloblastic anaemia, neural tube defectTest: RBC folate

288
Q

Vitamin B3What’s another name for it?What happens in deficiency?

A

NiacinDeficiency: pellagra - 3 D’s: DementiaDermatitisDiarrhoea

289
Q

IronWhat happens in deficiency?What happens in excess?How do you test for it?

A

Deficiency - hyochromic anaemiaExcess - haemochromatosisTest: FBC, Fe, ferritin

290
Q

IodineWhat happens in deficiency?How do you test for it?

A

Deficiency: goitre, hypothyroidTest: TFT

291
Q

ZincWhat happens in deficiency?

A

Dermatitis

292
Q

CopperWhat happens in deficiency?What happens in excess?How do you test for it?

A

Deficiency - anaemiaExcess - Wilson’s diseaseTest: Cu, caeroplasmin

293
Q

FluorideWhat happens in deficiency?What happens in excess?

A

Deficiency - dental cariesExcess - fluorosis

294
Q

Which metabolic disorders are screened for in the UK?

A

PhenylketonuriaCongenital hypothyroidismCystic fibrosisSickle cell diseaseMCADD

295
Q

What is the problem in phenylketonuria?

A

Phenylalanine hydroxyls deficiency

296
Q

What causes congenital hypothyroidism and how do you screen for it?

A

Dysgenesis/agenesis of the thyroid glandTSH levels to screen

297
Q

What is the main problem in cystic fibrosis and how is it screened for?

A

Mutation in CFTR -> viscous secretions -> ductal blockatesImmune reactive trypsin to screenIf positive, DNA mutation detection

298
Q

What is MCADD and how do you screen for it?

A

Medium chain acyl CoA dehydrogenase deficiency - a fatty acid oxidation disorderAcylcarnitine levels by tandem mass spectrometry to screen

299
Q

How are the urea cycle disorders inherited?

A

Autosomal recessive except for ornithine transcarbamylase deficiency - X linked

300
Q

What are the red flags for urea cycle disorders?

A

Vomiting without diarrhoeaHyperammonia and respiratory alkalosisEncephalopathyChange in diet

301
Q

What is the treatment for urea cycle disorders?

A

Remove ammoniaReduce ammonia production

302
Q

What are the organic acidurias?

A

Group of metabolic disorders that disrupt amino acid metabolism, particularly branched chain amino acids (leucine, isoleucine and valine)

303
Q

How do organic acidurias present in neonates?

A

Unusual odoursLethargyFeeding problemsTruncal hypotoniaLimb hypertoniaMyoclonic jerks

304
Q

What is seen on blood tests in organic acidurias?

A

Hyper ammonia with metabolic acidosis and high anion gap (not lactate)Hypocalcaemia, neutropenia, thrombocytopenia, pancytopenia

305
Q

Other than as a neonate, how might an organic aciduria present?

A

As a chronic intermittent form with recurrent episodes of:Ketoacidotic comaCerebral abnormalitiesReye syndrome

306
Q

What are the features of Reye syndrome?

A

Vomiting, lethargy, confusion, seizures, decerebration, respiratory arrest

307
Q

What are the triggers for Reye syndrome?

A

Salicylates, antiemetics, valproates

308
Q

What is the most common kind of galactosaemia and what does it do?

A

Galactose-1-phosphate uridylyltransferase deficiency (Gal-1-PUT) is the most severe of the 3 known disorders, in which raised Gal-1-PUT causes liver and kidney disease

309
Q

How does Gal-1-PUT deficiency present?

A

VomitingDiarrhoeaConjugated hyperbilirubinaemiaHepatomegalyHypoglycaemiaSepsis

310
Q

What lab investigations should you do in Gal-1-PUT deficiency?

A

Urine reducing substancesRed cell Gal-1-PUT

311
Q

What are the common features of the glycogen storage disorders?

A

Result from defects in glycogen synthesis or breakdown. Commonly have muscular, liver, and other consequences. All are due to enzyme deficiencies.

312
Q

How many glycogen storage disorders are there?

A

11

313
Q

What causes glycogen storage disorder type 1 and what’s another name for it?

A

Von Gierke’s disease - glucose-6-phosphatase deficiency

314
Q

What is the pathology in GSD Type I?

A

Excessive glycogen storage but also prevents glucose export from gluconeogenetic organs

315
Q

How does GSD type I present?

A

Lactic acidosisConvulsionsHypoglycaemia: irritability, pallor, cyanosis, hypotonia, tremors, loss of consciousness, apnoeaHepatomegalyHyperlipidaemiaHyperuricaemiaNeutropenia

316
Q

What is the pathophysiology in lysosomal storage diseases?

A

Intraorganelle substrate accumulation leading to organomegaly and consequent dysmorphia and regression

317
Q

What lab investigations should you do in lysosomal storage diseases?

A

Urine mucopolysaccharides and oligosaccharidesLeucocyte enzyme activity

318
Q

What is the treatment for lysosomal storage diseases?

A

Bone marrow transplantExogenous enzymes

319
Q

What are perioxisomal disorders?

A

A disorder in the metabolism of very long chain fatty acids and biosynthesis of complex phospholipids

320
Q

What is the neonate profile of perioxisomal disorders?

A

Severe muscular hypotonia, seizuresHepatic dysfunction - mixed hyperbilirubinaemiaDysmorphic signs

321
Q

What is the infant profile of perioxisomal disorders?

A

Retinopathy (often leading to early blindness)Sensorineural deafnessMental deficiencyHepatic dysfunctionLarge fontanelle, osteopenia of long bones, calcified stippling

322
Q

What lab investigation should you do for perioxisomal disorders?

A

Very long chain fatty acids

323
Q

What is the general pathology in mitochondrial disorders?

A

Defective ATP production leads to multi system disease especially affecting organs with a high energy requirement e.g. brain, muscle, kidney, retina, and endocrine organs

324
Q

What are the features of Barth syndrome?

A

Presents at birthCardiomyopathyNeutropeniaMyopathy

325
Q

What are the features of MELAS?

A

5-15 yearsMitochondrial encephalopathy, lactic acidosis, and stroke like episodes

326
Q

What are the features of Kearns-Sayre?

A

12-30 yearsCPEORetinopathyDeafnessAtaxia

327
Q

What are the causes of hyperglycaemia?

A

CorticotrophinSomatotrophin: those with gigantism and acromegaly are at vastly increased risk of contracting T2DMCatecholaminergicSecondary to increased insulin resistance or absolute deficiency

328
Q

How common is diabetes in the UK?

A

About 2 million - 90% T2DM

329
Q

What makes a diagnosis of diabetes mellitus?

A

Typical symptoms plusFasting glucose >7, oral glucose tolerance test >11.1, or random glucose >11.1 ORWithout symptoms but with 2 of the above testsNICE recommends HbA1c >48 as one of these tests

330
Q

What glucose test results are classed as impaired glucose tolerance?

A

Random or oral glucose tolerance test >7.8 but

331
Q

What glucose test result counts as impaired fasting glucose?

A

Fasting glucose >6.1 but

332
Q

What is the difference in risk between impaired glucose tolerance, impaired fasting glucose, and diabetes?

A

IGT and IFG have the same microvascular risks as WHO classified diabetes but microvascular complications are seen more frequently in diabetics

333
Q

What are the causes of hyperinsulinaemic hypoglycaemia?

A

Iatrogenic insulin, sulfonylurea excess, insulinoma

334
Q

What are the causes of hypoinsulinaemic hypoglycaemia with positive ketones?

A

Alcohol binge with no food, pituitary insufficiency, Addison’s, liver failure

335
Q

What are the causes of hypoinsulinaemic hypoglycaemia with negative ketones?

A

Non-pancreatic neoplasms: fibrosarcomata, fibromata

336
Q

What are some causes of hypoglycaemia in adults with low insulin and low C peptide?

A

FastingStrenuous exerciseCritical illnessEndocrine deficiency (hypopituitarism, adrenal failure)Liver failureAnorexia nervosa

337
Q

What are some causes of hypoglycaemia in neonates?

A

Ketones present, FFA present: premature, IUGR, comorbidityKetones absent, FFA present: inherited metabolic disorder

338
Q

What are the features of non-islet tumour hypoglycaemia?

A

Low glucose, low insulin, low C-peptide, low FFA, low ketonesTumours that cause a paraneoplastic syndrome, secreting, ‘big IGF-2’ which binds to IGF-1 and insulin receptors

339
Q

What are some of the common problems in low birth weight neonates?

A

Respiratory distress syndromeRetinopathy of prematurityIntraventricular haemorrhagePatent ductus arteriolesNecrotising enterocolitis

340
Q

What are some of the differences in renal function in children as opposed to adults?

A

Functional maturity of GFR by 2 years but low GFR for surface area. Less reabsorption than adult due to short proximal tubule (but usually adequate for small filtered load). Reduced concentrating ability due to shop troops of Henle and distal collecting ducts. Persistent sodium loss due to distal tubule being relatively aldosterone-insensitive

341
Q

Why do children have a high insensible water loss?

A

High surface areaHigh skin blood flowHigh metabolic/respiratory rateHigh transepidermal fluid loss

342
Q

What are some causes of hypernatraemia specific to neonates?

A

Intraventricular haemorrhageSodium bicarbonate when treating acidosis

343
Q

When does hypernatraemia become uncommon in paediatrics?

A

After 2 weeks - usually associated with dehydration

344
Q

What defines ‘prolonged’ neonatal jaundice?

A

> 14 days if term or >21 days in preterm

345
Q

What kind of hyperbilirubinaemia is always pathological in neonates?

A

Conjugated

346
Q

What is a normal GFR?

A

120ml/hr

347
Q

How does GFR change with age?

A

Age related decline of ~1ml/hr/year

348
Q

Define ‘clearance’ in relation to renal function

A

The volume of plasma that can be completely clear of a marker substance in a unit of time

349
Q

When does clearance = GFR?

A

Marker is not bound to serum proteins AND is freely filtered by the glomerulus AND is not secreted/absorbed by tubular cells

350
Q

What ist he gold standard measure of GFR and why isn’t it used?

A

Inulin - but requires a steady state infusion and difficult to assay, so reserved for research purposes only

351
Q

What marker is used in clinical practice to measure renal function and how do we measure it?

A

CreatinineVery variable between individuals so we use it to monitor trends over timeDifferent equations use serum creating with variable combinations of age, weight, sex, ethnicity to estimate GFR

352
Q

What do you use a single sample of urine for?

A

Dipstick testingMicroscopic examinationProteinuria quantification (protein:creatinine ratio)

353
Q

What can you use a 24h urine collection for?

A

Proteinuria quantification (now usually do protein:creatinine ratio instead)Creatinine clearance estimationElectrolyte estimationStone forming elements

354
Q

What ca you see on urine microscopy?

A

CrystalsRBCsWBCsCastsBacteria

355
Q

What are the 3 kinds of acute kidney injury?

A

Pre renal - reduced renal perfusion with no structural abnormalityRenal: vascular, glomerular, tubular, interstitialPost-renal: obstruction to urinary flow

356
Q

Describe stage 1 chronic kidney disease, its GFR, and its prevalence

A

Kidney damage with normal GFR>90 GFR3.3% prevalence

357
Q

Describe stage 2 chronic kidney disease, its GFR, and its prevalence

A

Mildly decreased GFR60-89 = GFR3% prevalence

358
Q

Describe stage 3 chronic kidney disease, its GFR, and its prevalence

A

Moderately decreased GFR30-59 = GFR4.3% prevalence

359
Q

Describe stage 4 chronic kidney disease, its GFR, and its prevalence

A

Severely decreased GFR15-29 = GFR0.2% prevalence

360
Q

Describe stage 5 chronic kidney disease, its GFR, and its prevalence

A

End stage kidney failureGFR

361
Q

What are the commonest causes of chronic kidney disease?

A

DiabetesAtherosclerotic renal diseaseHypertensionChronic glomerulonephritisInfective or obstructive uropathyPolycystic kidney disease

362
Q

What are the consequences of chronic kidney disease?

A

Progressive failure of homeostatic function (acidosis, hyperkalaemia)Progressive failure of hormonal function (anaemia, renal bone disease)Cardiovascular disease (vascular calcification, uraemic cardiomyopathy)Uraemia and death

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