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Clinical Pathology > Water and electrolyte Metabolism > Flashcards

Water and electrolyte Metabolism Flashcards

1
Q

Total Body Water

A

42L

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2
Q

Water distribution percentages

A

ICF - 66% (28L)
ECF - 33% (14L)
Plasma - 8% (3.5L)
Interstitial (11L)

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3
Q

Osmotic concentrations of the ICF and ECF are always equal T/F

A

F. except in the kidney

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4
Q

ECF osmolality

A

282-295 osmol/kg of water

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5
Q

A rising ECF osmolality promotes/switches off secretion of AVP

A

Promotes

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6
Q

AVP causes

A

Water to be retained by the kidneys with reduction of urine production

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7
Q

ECF osmolality comprises

A

Na, Cl, HCO3, glucose and urea

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8
Q

ICF osmolality comprises

A

K
Phosphates

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9
Q

Interstitial fluid comprises two pressures

A

Colloid osmotic pressure
Oncotic pressure

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10
Q

Evidences of cerebral dysfunction

A

Drowsiness
Coma

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11
Q

Total body sodium in a 70kg man

A

3700 mmol

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12
Q

What percentage of total body sodium is exchangeable

A

75%

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13
Q

Sodium concentration interval

A

135-145 mmol/L

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14
Q

Urinary Sodium output is regulated by

A

Aldosterone
Atrial Natriuretic Peptide

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15
Q

Aldosterone stimulation is stimulated by

A

Decreased ECF volume

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16
Q

Cells of the JG apparatus sense decrease in BP and secrete ……….., ………… then …………….

A

Renin
Angiotensin
Aldosterone

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17
Q

Atrial Natriuretic peptide is a polypeptide hormone secreted by

A

Cardiocytes of the right atrium of the heart

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18
Q

ANP increases/decreases sodium excretion

A

Increases

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19
Q

……………. and ………….. interact to maintain normal volume and concentration of ECF

A

Aldosterone
AVP

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20
Q

ECF contraction can lead to

A
  1. Development of pre-renal uraemia
  2. Stimulation of AVP secretion
  3. Stimulation of aldosterone secretion
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21
Q

Causes of Oedematous Hyponatremia

A

CCF
Nephrotic Syndrome
Inappropriate IV saline

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22
Q

Treatment of hyponatremia (oedematous)

A

Diuretics
Fluid restriction

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23
Q

Causes of Non-oedematous hyponatremia

A

SIAD
Renal failure
Increased intake eg compulsive water drinking

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24
Q

Causes of Hyponatremia due to sodium loss from GIT or Urine

A

Vomiting - Pulmonary Stenosis
Diarrhoea
Fistula
Urinary loss
Aldosterone Deficiency
Aldosterone Antagonists

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25
Q

What disease is due to aldosterone deficiency

A

Addisons disease

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26
Q

Examples of aldosterone antagonists

A

Spironolactone or Triamterine

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27
Q

Diagnosis of hyponatremia due to Na loss

A

Hypotension
Tachycardia

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28
Q

Regarding SIAD, What type of hyponatremia?

A

Non oedematous hyponatremia

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29
Q

Regarding SIAD, level of sodium in ICF

A

Normal total body sodium

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30
Q

Regarding SIAD, level of sodium in ECF

A

Hyponatraemic

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31
Q

Regarding SIAD, what level of blood pressure

A

Normal, normotensive

32
Q

Concerning SIAD, glomerular filtration rate is

A

is normal

33
Q

Concerning SIAD, Serum urea and creatinine are

A

Normal

34
Q

Hyponatremia caused by SIAD can be induced by

A

Thiazide Diuretics

35
Q

In SIAD there is osmotic AVP stimulation and if they are exposed to excess water load they become hyponatraemic T/F

A

F. There is non osmotic AVP stimulation

36
Q

Non-osmotic stimuli in SIAD include

A

Reduction in circulating blood volume
Nausea and vomiting
Pain

37
Q

There is a continued natriuresis in SIADH T/F

A

T

38
Q

Hyponatremia with natriuresis only occurs in SIADH T/F

A

F. Also occurs in adrenal failure and renal disorders

39
Q

Features of Hyponatremia patients that have water overload

A

No oedema
Normal serum
Normal creatinine
Normal blood pressure

40
Q

Water overload is treated by

A

Fluid restriction

41
Q

Causes of hypernatremia

A
  1. Excess sweating
  2. Diarrhoea in children
  3. Excess sodium intake or retention
  4. Na bicarbonate in the correction of acidosis
  5. Conn’s syndrome
  6. Cushing’s syndrome
42
Q

Clinical Presentation of Hypernatremia

A

Dehydration in water loss and indication of fluid overload (hypervolemia) in Na retention -

INCREASED JVP
PULMONARY OEDEMA

43
Q

Management of Hypernatremia

A

Give oral fluids slowly or
5% dextrose slowly

44
Q

Total body potassium

A

3600 mmol

45
Q

% of potassium intracellular and extra cellular

A

98% intracellular, 5% extra cellular

46
Q

Intake interval of potassium per day

A

30-100 mmol

47
Q

Excretion dependent on glomerular filtration T/F

A

T

48
Q

What % of K is lost in faeces

A

5%

49
Q

Interval of Potassium concentration in the body

A

3.3-5 mmol/L

50
Q

Cellular uptake of potassium is stimulated by

A

Insulin

51
Q

Clinical effects of hypokalemia

A

Severe weakness
Hyporeflexia
Cardiac Arrhythmias
Cardiac arrest

52
Q

ECG changes concerned with Hypokalemia

A

Flattened T waves
Prominent U wave
Increased sensitivity to digoxin

53
Q

Causes of hypokalemia

A
  1. GIT losses – vomiting, diarrhoea, fistula
  2. Renal losses – from renal disease, diuretic therapy or increased aldosterone production (Conns Syndrome)
  3. Drug induced – thiazide diuretics and corticosteroids. Cabenoxolone has mineralocorticoid activity
  4. Alkalosis causes a shift of potassium from the ECF to the ICF
54
Q

What drug(s) induce hypokalemia

A

Thiazide diuretics
Corticosteroids
Cabenoxolone

55
Q

Treatment of hypokalemia

A

Oral potassium supplements
Intravenous potassium

56
Q

Intravenous potassium should not be given faster than ………… mmol/h and should be monitored by

A

20mmol/hour
ECG

57
Q

Commonest and most serious electrolyte emergency encountered in clinical practice

A

Hyperkalemia

58
Q

Clinical feature of hyperkalemia includes muscle weakness T/F

A

T

59
Q

ECG changes of hyperkalemia

A

Widened QRS complex
Peaked T waves

60
Q

At what level of serum potassium is there a risk of cardiac arrest

A

7mmol/L

61
Q

Causes of hyperkalemia

A
  1. Renal disease
  2. Mineralocorticoid deficiency (Addison’s disease, patients on aldosterone antagonists eg SPIRONOLACTONE or TRIAMTERENE
  3. Acidosis
  4. K released from damaged cells
  5. Artefactual increase in haemolysis serum
62
Q

Treatment of hyperkalemia

A
  1. Infusion of insulin and glucose
  2. Infusion of calcium gluconate
  3. Dialysis
  4. Cation exchange resin e.g Resonium A
63
Q

What does high anion gap indicate?

A

Lactic acidosis

64
Q

Fluids

A
  1. Water
  2. Isotonic NaCl
  3. Plasma
  4. 1.26% Na2CO3
  5. K supplements
65
Q

Water -

A

5% dextrose

66
Q

Isotonic NaCl

A

0.9% NaCl

67
Q

Sodium bicarbonate-

A

1.26%

68
Q

Reference range of Hydrogen ions in the body

A

35-45 nmol/L

69
Q

Oxidation of the nitrogen containing amino acids of proteins is a source of hydrogen ions in the body T/F

A

F. Sulphur containing amino acids

70
Q

Arterial blood gas values, H+, Bicarbonate, PCO2, PO2

A

H+ - 35-46 nmol/L
Bicarbonate - 18-31mmol/L
PCO2 - 4-6kP (36-46mmHg)
PO2 - 11-15kP (85-105mmHg)

71
Q

What happens to H and bicarbonate in metabolic acidosis

A

H is high or normal
Bicarbonate is always low

72
Q

Diseases associated with metabolic acidosis

A

Renal disease
Diabetic ketoacidosis
Lactic acidosis

73
Q

In respiratory acidosis, what happens to H and PCO2

A

Both raised

74
Q

There’s hypoxia and overbreathing in respiratory alkalosis T/F

A

T

75
Q

Commonest cause of metabolic alkalosis

A

Prolonged vomiting

76
Q

Diseases associated with metabolic alkalosis

A

Nasogastric suction
Conns syndrome

77
Q

Respiratory compensation of metabolic alkalosis leads to

A

Elevated PCO2

Clinical Pathology (5 decks)

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