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Total body water and its distribution
~60% of body weight
2/3 intracellular, 1/3 extracellular
Daily water intake sources
Drinks ~60%, food ~30%, metabolic water ~10%
Daily water loss routes
Urine ~60%, lungs + skin (insensible) ~28%, sweat ~8%, faeces ~4%
⚠ Your notes said: '8% precipitation' — it is perspiration (sweat).
Main intracellular ions
K⁺, phosphate, Mg²⁺ (+ proteins)
Main extracellular ions
Na⁺, Cl⁻, HCO₃⁻
Which ion determines ECF volume?
Na⁺ — Na⁺ retention expands ECF, Na⁺ loss shrinks it
RAAS: hypovolaemia → kidney releases _____ → angiotensinogen → _____ (vasoconstriction) → adrenal _____ → Na⁺ + water retention
renin | angiotensin II | aldosterone
ADH (vasopressin) — trigger and action
Trigger: ↑ plasma osmolality (osmoreceptors) or ↓ volume
Action: inserts aquaporin-2 in collecting duct → water reabsorption
⚠ Your notes said: 'ADH stimulates Na⁺ and water retention' — Na⁺ retention is aldosterone's job.
ANP — source and action
Atrial myocytes (stretch) → ↑ GFR, ↓ Na⁺/water reabsorption → natriuresis + diuresis, ↓ BP
Two stimuli for true thirst
1. Cellular dehydration (↑ ECF osmolality)
2. ↓ blood volume
Where are the osmoreceptors for thirst?
In/near the thirst centre of the hypothalamus
Define hypodipsia
Decreased ability to sense thirst (common in elderly)
Polydipsia types: _____ (water loss: DM, DI, diarrhoea), _____ (renal failure, CHF), _____ (schizophrenia)
symptomatic/true | inappropriate/false | psychogenic
Define diabetes insipidus
Deficiency of or resistance to ADH → inability to concentrate urine → 3–20 L/day dilute urine + polydipsia
Central vs nephrogenic DI
Central: ↓ ADH synthesis/release
Nephrogenic: kidneys don't respond to ADH
When does DI become dangerous?
When the patient can't drink (unconscious, infant, no water) → hypertonic dehydration
Isotonic / hypertonic / hypotonic saline examples
Isotonic: 0.9% NaCl (240 – 349 mOsm, department lecture)
Hypertonic: 3% NaCl
Hypotonic: 0.45% NaCl
Normal plasma osmolality: 275 – 295 mOsm/kg
⚠ Your notes listed hyperosmolar diabetic coma and DKA as HYPOtonic states — both are HYPERtonic.
Darrow–Yannet principle
Any non-isotonic change in ECF causes a net water shift between ECF and ICF until osmolality equalises
Define dehydration
↓ ECF volume from inadequate intake, excessive loss, or both
Dehydration severity by % body weight loss
Mild ~2%, moderate ~5%, severe ≥ 8%
Clinical signs of dehydration
Thirst, weight loss, ↓ urine output, tachycardia, ↑ haematocrit, dry mucosa, ↓ skin turgor
Isotonic dehydration: definition + example
Na⁺ and water lost in proportion
No shift between compartments
E.g. haemorrhage, burns
Hypotonic dehydration: definition, shift, example
Loss of Na⁺ > water → ECF hypotonic → water moves into cells (cell swelling, brain oedema)
E.g. vomiting/diarrhoea or sweating replaced with plain water, diuretics, Addison's
⚠ Your notes said: 'profuse sweating' as the example — sweating alone gives hypertonic dehydration.
Hypertonic dehydration: definition, shift, example
Loss of water > Na⁺ → ECF hypertonic → water leaves cells (cellular dehydration, intense thirst)
E.g. sweating, DI, osmotic diuresis in DM, no access to water
Isotonic hyperhydration — example
Gain of water + Na⁺ in proportion: excess isotonic saline infusion, heart failure, nephrotic syndrome → ECF oedema
Hypotonic hyperhydration (water intoxication): shift + examples
Water gain > Na⁺ → water moves into cells → cerebral oedema
E.g. psychogenic polydipsia, SIADH, acute renal failure + fluids
Hypertonic hyperhydration: shift + examples
Na⁺ gain > water → water leaves cells
E.g. Conn's syndrome, hypertonic saline, drinking sea water
Causes of fluid overload (hypervolaemia)
Excess fluid/Na⁺ intake, CHF, cirrhosis, renal failure, SIADH, normal post-operative response
Clinical signs of fluid overload
Weight gain, oedema, ↑ BP, jugular venous distension, dyspnoea, crackles, pleural effusion → pulmonary oedema
SIADH
Excess ADH → water retention → hyponatraemia with concentrated urine (hypotonic hyperhydration)
Hyponatraemia: range, causes, danger
Na⁺ < 135 mmol/L
SIADH, diuretics, HF, cirrhosis, polydipsia, Addison's
Water into brain cells → cerebral oedema, seizures
Correct slowly
Hypernatraemia: range, causes, effects
Na⁺ > 145 mmol/L
Water loss (DI, sweating, osmotic diuresis), poor intake
Cells shrink → thirst, confusion
Hypokalaemia: range, causes, ECG
K⁺ < 3.5 mmol/L
Vomiting, diarrhoea, diuretics, hyperaldosteronism, insulin, alkalosis
Weakness, ileus, flat T, U waves, arrhythmias
Hyperkalaemia: range, causes, ECG
K⁺ > 5.0 mmol/L
Renal failure, K⁺-sparing drugs/ACEi, Addison's, acidosis, cell lysis
Peaked T, wide QRS → VF/asystole
Acid–base and K⁺ shifts
Acidosis → K⁺ leaves cells (hyperkalaemia)
Alkalosis → K⁺ enters cells (hypokalaemia)
Body water by age
Infant ~70–75%, adult ~60%, elderly ~50–55% of body weight
ECF as % of body weight and its split
ECF ≈ 20% of body weight: interstitial ~15%, plasma ~5%
Normal plasma osmolality and its formula
275–295 mOsm/kg
≈ 2×Na⁺ + glucose + urea (mmol/L)
Why are infants and the elderly most at risk of dehydration?
Infants: high water turnover, large surface area, immature kidneys, can't ask for water
Elderly: ↓ total water, hypodipsia, ↓ renal concentrating ability, diuretics
Psychogenic polydipsia
Compulsive drinking (often > 5 L/day), e.g. in schizophrenia → hypotonic hyperhydration (water intoxication, hyponatraemia)
How do you assess a patient's fluid status?
History, daily weight (best single measure), intake/output chart, vital signs (pulse, BP, orthostasis), skin turgor, mucous membranes, JVP/oedema
Labs: Na⁺, osmolality, urea:creatinine, haematocrit, urine specific gravity
EXAMINER ASKS: A patient has lost fluid through diarrhoea and drunk only plain water. What type of dehydration and what happens to his cells?
Hypotonic dehydration: salt-rich loss, water replaced → ECF hypotonic → water moves into cells → cell swelling (cerebral oedema risk), no thirst
EXAMINER ASKS: Why is a patient with hypertonic dehydration intensely thirsty but one with hypotonic dehydration is not?
Thirst follows ECF osmolality: hypertonic ECF pulls water out of osmoreceptor cells → thirst. Hypotonic ECF swells them → thirst is suppressed despite volume loss.
EXAMINER ASKS: Why must hypernatraemia be corrected slowly?
Brain cells adapt by making idiogenic osmoles
Rapid dilution makes water rush in → cerebral oedema (and the reverse — rapid correction of chronic hyponatraemia → osmotic demyelination)
15-MINUTE NOTES / Write your note sheet for essay 14 Water-electrolyte balance – dehydration, hyperhydration
1. Body water by age + compartments (ICF 40%, ECF 20%), intake/loss
2. Electrolytes ICF vs ECF; Na⁺ sets ECF volume; osmolality 275–295
3. Regulation: RAAS, ADH, ANP, thirst; DI vs SIADH
4. Tonicity + Darrow–Yannet principle
5. 3×2 table: iso/hypo/hypertonic de- and hyperhydration with water shift + example
6. Clinical signs + assessment
7. Na⁺ and K⁺ disorders
Draw: the 3×2 table with ICF and ECF boxes and arrows showing which way water moves in each of the 6 states