Physiology: Sodium and Water Balance Flashcards

1
Q

What is syndrome of inappropriate ADH (SIADH)?

A

Non-osmotic stimuli common in disease e.g. hypovolaemia/hypotension, pain, nausea/vomiting, stimulate ADH release which is inappropriate for the osmolar state

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2
Q

How might syndrome of inappropriate ADH present?

A

Patient in hospital with other illness retains more water due to excess ADH, occurs slowly so no hyponataemia symptoms but incidental finding on bloods

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3
Q

Name the body compartments which 5% dextrose is able to enter

A

Plasma, interstitial fluid, intracellular fluid compartment

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4
Q

Why does water follow sodium?

A

Water follows solute by osmosis; as sodium concentration is greater than any other solute, in practice water follows sodium

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5
Q

If plasma osmolarity decreases, ADH will ________

A

Decrease

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6
Q

When is low/high sodium very serious?

A

If Na+ is very low or very high, which can cause symptoms

Symptomatic hypo/hypernatraemia indicates very high or low Na+ - life-threatening (e.g. altered consciousness, confusion, N+V, fitting)

If Na+ has fallen or risen rapidly to current level, it may be serious even if concentration falls within normal reference range

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7
Q

Why are loop diuretics effective in the management of oedema?

A

An oedematous patient has too much water and sodium - treat with loop diuretics which cause loss of sodium (and water)

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8
Q

Describe the clinical presentation of hypernatraemia

A

Coughing, shortness of breath

Tiredness

Pulmonary oedema

Pleural effusion

Ascites

Swelling in ankles and legs

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9
Q

_______ is present and can move between all body compartments, whereas ______ is confined to the ECF

A

Water, sodium

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10
Q

Describe the effect of decreased levels of ADH

A

Decreased plasma osmolarity → decreased ADH → less aquaporins in DCT and CD cells of the kidney → less water reabsorbed in kidney → large volume of dilute urine (low osmolarity)

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11
Q

ADH is released by the ______ pituitary

A

Posterior

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12
Q

Name the main mineralocorticoid

A

Aldosterone

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13
Q

If there is too much mineralocorticoid activity, there will be ____ of sodium

A

Gain

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14
Q

_____natraemia can be caused by too little sodium or too much water

A

Hyponatraemia

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15
Q

If plasma osmolarity increases, ADH will ________

A

Increase

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16
Q

Why will the effects of too much/too little sodium will produce more clinical evidence of changes than water gain or loss?

A

Sodium is confined to the ECF, whereas water loss or gain is distributed through all body compartments

17
Q

_______natraemia can be caused by too much sodium or too little water

A

Hypernatraemia

18
Q

Name the body compartments 0.9% saline is able to enter

A

Plasma, interstitial fluid

19
Q

Name some causes of hypernatraemia

A

↑ Na+ intake

↓ Na+ loss

↑ H2O loss e.g. diabetes insipidus

↓ H2O intake e.g. very young or very old - quite common

20
Q

Describe the clinical presentation of hyponatraemia

A

Increased pulse

Dry mucous membranes

Soft/sunken eyeballs

Decreased skin turger

Decreased consciousness

Decreased urine output

Postural decrease in blood pressure

21
Q

Describe the effect of increased levels of ADH

A

Increased plasma osmolarity → increased ADH → more aquaporins in DCT and CD cells of the kidney → more water reabsorbed in kidney → small volume of concentrated urine (high osmolarity)

22
Q

Name the body compartments plasma/blood is able to enter

A

Plasma

23
Q

What is mineralocorticoid activity?

A

Steroids with mineralocorticoid activity result in Na+ reabsorption in renal tubules in exchange for K+/H+, increasing Na+ levels

24
Q

Oedema stimulates the release of ___ and ________, which ends up making the oedema worse

A

ADH, aldosterone

25
Q

Name some causes of hyponatraemia

A

↑ Na+ loss

↓ Na+ intake

↓ H2O excretion e.g. SIADH - most common

↑ H2O intake (compulsive water drinking)

26
Q

Why is sodium confined to the ECF?

A

Due to Na+/K+ transporter in the plasma membrane

27
Q

What causes oedema?

A

Oedema signifies effective circulating (vascular) volume depletion due to an altered balance of Starling forces at capillary level resulting in increased flow of fluid from the vascular system into the interstitium