Water and electrolyte Metabolism Flashcards by Jessica A

Total Body Water

42L

How well did you know this?

Not at all

Perfectly

Water distribution percentages

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

How well did you know this?

Not at all

Perfectly

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

F. except in the kidney

How well did you know this?

Not at all

Perfectly

ECF osmolality

282-295 osmol/kg of water

How well did you know this?

Not at all

Perfectly

A rising ECF osmolality promotes/switches off secretion of AVP

Promotes

How well did you know this?

Not at all

Perfectly

AVP causes

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

How well did you know this?

Not at all

Perfectly

ECF osmolality comprises

Na, Cl, HCO3, glucose and urea

How well did you know this?

Not at all

Perfectly

ICF osmolality comprises

K
Phosphates

How well did you know this?

Not at all

Perfectly

Interstitial fluid comprises two pressures

Colloid osmotic pressure
Oncotic pressure

How well did you know this?

Not at all

Perfectly

Evidences of cerebral dysfunction

Drowsiness
Coma

How well did you know this?

Not at all

Perfectly

Total body sodium in a 70kg man

3700 mmol

How well did you know this?

Not at all

Perfectly

What percentage of total body sodium is exchangeable

75%

How well did you know this?

Not at all

Perfectly

Sodium concentration interval

135-145 mmol/L

How well did you know this?

Not at all

Perfectly

Urinary Sodium output is regulated by

Aldosterone
Atrial Natriuretic Peptide

How well did you know this?

Not at all

Perfectly

Aldosterone stimulation is stimulated by

Decreased ECF volume

How well did you know this?

Not at all

Perfectly

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

Renin
Angiotensin
Aldosterone

How well did you know this?

Not at all

Perfectly

Atrial Natriuretic peptide is a polypeptide hormone secreted by

Cardiocytes of the right atrium of the heart

How well did you know this?

Not at all

Perfectly

ANP increases/decreases sodium excretion

Increases

How well did you know this?

Not at all

Perfectly

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

Aldosterone
AVP

How well did you know this?

Not at all

Perfectly

ECF contraction can lead to

Development of pre-renal uraemia
Stimulation of AVP secretion
Stimulation of aldosterone secretion

How well did you know this?

Not at all

Perfectly

Causes of Oedematous Hyponatremia

CCF
Nephrotic Syndrome
Inappropriate IV saline

How well did you know this?

Not at all

Perfectly

Treatment of hyponatremia (oedematous)

Diuretics
Fluid restriction

How well did you know this?

Not at all

Perfectly

Causes of Non-oedematous hyponatremia

SIAD
Renal failure
Increased intake eg compulsive water drinking

How well did you know this?

Not at all

Perfectly

Causes of Hyponatremia due to sodium loss from GIT or Urine

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

How well did you know this?

Not at all

Perfectly

What disease is due to aldosterone deficiency

Addisons disease

Examples of aldosterone antagonists

Spironolactone or Triamterine

Diagnosis of hyponatremia due to Na loss

Hypotension Tachycardia

Regarding SIAD, What type of hyponatremia?

Non oedematous hyponatremia

Regarding SIAD, level of sodium in ICF

Normal total body sodium

Regarding SIAD, level of sodium in ECF

Hyponatraemic

Regarding SIAD, what level of blood pressure

Normal, normotensive

Concerning SIAD, glomerular filtration rate is

is normal

Concerning SIAD, Serum urea and creatinine are

Normal

Hyponatremia caused by SIAD can be induced by

Thiazide Diuretics

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

F. There is non osmotic AVP stimulation

Non-osmotic stimuli in SIAD include

Reduction in circulating blood volume Nausea and vomiting Pain

There is a continued natriuresis in SIADH T/F

Hyponatremia with natriuresis only occurs in SIADH T/F

F. Also occurs in adrenal failure and renal disorders

Features of Hyponatremia patients that have water overload

No oedema Normal serum Normal creatinine Normal blood pressure

Water overload is treated by

Fluid restriction

Causes of hypernatremia

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

Clinical Presentation of Hypernatremia

Dehydration in water loss and indication of fluid overload (hypervolemia) in Na retention - INCREASED JVP PULMONARY OEDEMA

Management of Hypernatremia

Give oral fluids slowly or 5% dextrose slowly

Total body potassium

3600 mmol

% of potassium intracellular and extra cellular

98% intracellular, 5% extra cellular

Intake interval of potassium per day

30-100 mmol

Excretion dependent on glomerular filtration T/F

What % of K is lost in faeces

Interval of Potassium concentration in the body

3.3-5 mmol/L

Cellular uptake of potassium is stimulated by

Insulin

Clinical effects of hypokalemia

Severe weakness Hyporeflexia Cardiac Arrhythmias Cardiac arrest

ECG changes concerned with Hypokalemia

Flattened T waves Prominent U wave Increased sensitivity to digoxin

Causes of hypokalemia

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

What drug(s) induce hypokalemia

Thiazide diuretics Corticosteroids Cabenoxolone

Treatment of hypokalemia

Oral potassium supplements Intravenous potassium

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

20mmol/hour ECG

Commonest and most serious electrolyte emergency encountered in clinical practice

Hyperkalemia

Clinical feature of hyperkalemia includes muscle weakness T/F

ECG changes of hyperkalemia

Widened QRS complex Peaked T waves

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

7mmol/L

Causes of hyperkalemia

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

Treatment of hyperkalemia

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

What does high anion gap indicate?

Lactic acidosis

Fluids

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

Water -

5% dextrose

Isotonic NaCl

0.9% NaCl

Sodium bicarbonate-

1.26%

Reference range of Hydrogen ions in the body

35-45 nmol/L

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

F. Sulphur containing amino acids

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

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

What happens to H and bicarbonate in metabolic acidosis

H is high or normal Bicarbonate is always low

Diseases associated with metabolic acidosis

Renal disease Diabetic ketoacidosis Lactic acidosis

In respiratory acidosis, what happens to H and PCO2

Both raised

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

Commonest cause of metabolic alkalosis

Prolonged vomiting

Diseases associated with metabolic alkalosis

Nasogastric suction Conns syndrome

Respiratory compensation of metabolic alkalosis leads to

Elevated PCO2

Water and electrolyte Metabolism Flashcards

(77 cards)