Fluod And Electrolyte Balance Flashcards

1
Q

What is the definition of osmolality?

A

Is the number of solute particles per unit of water.

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2
Q

How to calculate serum osmolality?

A

2[Na+] + [K+] + [glucose] + [urea] all in mmol

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3
Q

What is the osmolar gap?

A

Difference between measured and calculated osmolality and indicates the presence of a foreign substance

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4
Q

How much water is with the body

A

42 litres
ICF= 28 litres
ECF= 14 litres

Na main contributor to ECF osmolality.
K main contributor to ICF osmolality
K and Na cannot move freely requires active transport in the form of ATP

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5
Q

Functions of water

A

Structure of body
Transport vehicle
Hydrolysed food in the digestive system
Chemical reactions in the body cells
Water is obtained though diet and oxidative metabolism
Loss through kidneys, skin, lungs and gut.

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6
Q

Regulation of water if there is an increase in ECF osmolality (dehydration)

A

Stimulation of Antidiuretic hormone. Renal water reabsorption and small volume of urine.
Stimulation of hypothalamic thirst centre. Increase water intake.
Redistribution of water from ICF to ECF to increase ECF water

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7
Q

What can happen if there is a failure in restoring ECF volume.

A

Can lead to tissue death due to the lack of oxygen and vitamins and failure to remove waste.
Primary control mechanism for body fluid volume is renin angiotensin-aldosterone system.

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8
Q

Facts about sodium homeostasis?

A
  1. Regulates extracellular and vascular volume.
  2. Contributes to resting membrane potential and generation of action potential.
  3. Sodium lost through kidneys GIT and sweat.
    Dietary intake of sodium normally exceeds the body’s need.
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9
Q

Actions of renin-angiotensin-aldosterone system

A

Renin release in response to many factors including a decrease in sodium.
Angiotensinogen - angiotensin 1- angiotensin 11- angiotensin 111- aldosterone release.

Results in sodium reabsorption for exchange of urinary loss of H+ and K+.

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10
Q

Other hormones that help eliminate sodium?

A

Atrial natiuretic peptide= secreted from the right atrium. Increases urinary excretion of Na by inhibiting Na reabsorption

Dopamine= dopamine acts kn distal tubules to stimulate Na excretion.

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11
Q

What is hyponatraemia, signs and causes?

A

Clinical symptoms may depend on whether there is an excess of water.
Clinical signs include: headaches, confusion, fatigue, muscle cramps due to seizures.
If due to excess water other symptoms include:
Oedema
Hypertension
Haemodilution: due to dilutions effect.

Brain and nervous system disturbances.
Low osmolality

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12
Q

What are the different types of hyponatraemia?

A

Hypervolaemic hyponatraemia= lover failure is where total body water and Na are increased but the increase in water is much greater than increase in Na.
Euvolaemic hyponatraemia = SIADH, water overload. When total body water increases whilst Na is normal. Post surgery
Hypovalaemic hyponatraemia= lack of both Na and water however there is a greater loss of sodium.

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13
Q

What is SIADH?

A

It is syndrome of inappropriate Antidiuretic hormone secretion.
Common in elderly.
May take place after major trauma or sugary.
ADH acts on kidneys leading to water retention. Despite low osmolality, ADH production still continues.

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14
Q

Causes and signs and symptoms of hypernatraemia?

A

Less common but causes include dehydration leading to increased conc of solute particles.
Due to lack of fluid intake
Fluid also constantly lost in sweat and via lungs in addition to urine

Excess intake of sodium or retention in ECF
Both water and Na lost with prolonged vomiting, diarrhoea. When more water is lost relative to sodium.

Signs and symptoms: thirst, mental confusion, coma.

If due to water deficiency then other symptoms may include:
Hypertension
Haemoconcentration= raises protein concentration and blood cell count

Management: correct approx two thirds of loss in 24 hr and one third the next 24 hr.

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15
Q

What is diabetes insipidus:

A

Deficiency in ADH= disturbances in production or decrease in response in the kidney.

Cranial DI = a failure to secrete ADH from the posterior pituitary gland may be congenital or due to head injury.
Nephrogenic DI= kidneys fail to respond to ADH.
Dehydration as patients unable to conserve water
Results in reduced blood volume and hypernatremia

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16
Q

Importance of potassium?

A

Major action in intracellular fluid.
Critical for many cell functions.
Controlled by kidneys and GI tract
Aldosterone secretion is stimulated by hyperkalaemia and renin

H+ and K+ ions neutralise the membrane potential generated by active Na+ reabsorption.
As most of K+ is within the cells plasma K+ does not reflect body K+.

17
Q

Causes and features of hypokalaemia?

A

Causes GI tract loss, renal loss and drug induced hypokalaemia.

Main signs are: neuromuscular eg muscle weakness and depression. And cardiac arrhythmias.
Kidneys: polyuria, polydipsia

Treatment: potassium salts given orally or IV. ECG monitoring and slow infusion.

18
Q

Clinical features of hyperkalaemia and management.

A

SERIOUS ELECTROLYTE EMERGENCY!
First manifests as cardiac arrest without signs and symptoms
Lowers resting membrane potential and shortens cardiac action
Causes: renal failure, release of K from damaged cells, tissue trauma or burns.

Management: immediate! Infusion of insulin and glucose. K will move into cells.
Severe cases: oral ion exchange resins are given resonium A will stop or reverse a slow rise in K.
Severe cases in which hyperkalaemia cannot be controlled requires dialysis

19
Q

How is H+ produced?

A

During cellular metabolism
From diet oxidation of sulphur containing amino acids.
Metabolism also forms CO2 excreted by lungs
In solution CO2 forms carbonic acid thus upsetting acid base status.

20
Q

What is a buffer?

A

Is a solution that resists changed in pH when small quantities of acids or alkali are added to it. It bind to H+ allowing a balance between acid and base.
Buffers do not remove H+ from body

Lungs, erythrocytes and kidneys are main tissues involved in maintaining acid base balance.

Body contains number of buffers: Hb (plasma)
Proteins (ICF) and bicarbonate important in ECF.

21
Q

Give formulation involving bicarbonate, H+ and carbonic acid and explain equation.

A

H+ + HCO3- = H2CO3 = CO2 + H2O

Addition of H+ will drive reaction to the right increasing carbonic acid and consuming bicarbonate ions.
Fall in H+, dissociation of carbonic acid into H+.

22
Q

3 ways body removes H+ ions and saves bicarbonate?

A

Renal control= recovery of HCO3-
Renal control= renal H+ excretions
Respiratory control= transport of CO2

23
Q

Regeneration of bicarbonate has not met excretion why?

A

Most of the filtered HCO3- is reclaimed in the proximal tubule.

24
Q

How is H+ secreted by the renal vessels?

A

Ammonia is produced in renal tubular cells by the hydrolysis of glutamine to glutamate.

25
Q

Transport of CO2 via blood cells and lungs

A

Very little CO2 is produced in red cells so CO2 produced by the tissues lasses into the cell down a conc gradient. Final product released is bicarbonate.

The reverse process occurs in the lungs: CO2 diffuses in the alveoli and is excreted I’m expired air,

26
Q

Step by step guide in how blood is taken to measure PO2 and PCO2.

A

Arterial or arterialised capillary blood is taken.
No air bubbles in sample to exclude any effect on analytes.
Small amount of heparin (anticoagulant)
Sample taken to lab immediately in ice water to stop glycolysis occurring as lactic acid is produced.
Temperature of patient is assumed 37
Patient must be relaxed and breathing settled.

27
Q

Features of metabolic acidosis?

A

Primary disorder is a decrease in bicarbonate.
Hyperventilation
Causes: renal disease decrease H+ secretion
Diabetic ketoacidosis
Lactic acidosis

Results in anion gap: [cations]-[anions]
Anion gap will increase in metabolic condition that increase production of acids.

28
Q

What is metabolic alkalosis?

A

Primary disorder is an increase in bicarbonate.
Clinical picture: hypoventilation, confusion and cramps.
Causes: loss of H+ in gastric fluid
Ingestion of absorbable alkali.
Potassium deficiency
Excessive reabsorption of HCO3.

29
Q

What is respiratory acidosis?

A

Primary disorder due to increase in PCO2.
Causes are due to insufficient gas exchange:
Airways obstruction
Depression of respiratory centre
Neuromuscular disease eg motor neuron
Pulmonary disease eg pneumonia

Acute cases: acute respiratory problem
Chronic causes: usually impaired alveolar ventilation.

30
Q

What is pulmonary alkalosis?

A
Primary disorder is a decrease in PCO2.
Clinical picture: Hyperventilation
Causes due to excessive gas exchange
Hysterical hyperventilation= anxiety 
Raised intracranial pressure