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Medicine Notes Renal System Notes

Control Of Body Fluid Osmolarity (Water Balance) Notes

Updated Control Of Body Fluid Osmolarity (Water Balance) Notes

Renal System Notes

Renal System

Approximately 31 pages

These notes helped me achieve a mark of 78% in my renal system exam, which is the equivalent of a 1st. The notes are based on a series of lectures on the subject. This is a very good, thorough and in depth review of the nervous system. They are very clearly laid out and easy to follow. They cut out unnecessary information on the topic, making the notes very concise, and fast to get through. Anyone studying medicine, or any other subject requiring knowledge of the renal system (e.g. physiology or ...

The following is a more accessible plain text extract of the PDF sample above, taken from our Renal System Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Lecture 11 & 12

Control of Body Fluid Osmolarity (water balance)

  • Why do we need to regulate fluid osmolarity and stay in water balance?

    • Osmolarity= Conc. of solution expressed as (m)osmoles of solutes per litre of solution

    • Osmolarity of solution represents ‘pulling power’ it exerts in drawing water across

    • Depends on number of particles, not size

    • Osmolarity of plasma and ECF maintained at 285mOsm/L (+/- 4%) (N.B. not 300 mOsm/l)

    • Increased ECF osmolarity leads to withdrawal of water from cells=cell shrinkage

    • Reduced ECF leads to water entering cells=swelling

    • ECF osmolarity maintained constant despite wide variations in

      • Water and salt intake

      • Obligatory extra-renal losses of water and salt (e.g. sweat, expiration)

  • How do we maintain constant ECF osmolarity?

    • Stabilised by regulating body water (not salt)

    • Physiological control over both water intake (via thirst) and water output (urination)

    • Must compensate for

      • Water generated via metabolism (not under physiological control)

      • ‘Obligatory’ water loss via other routes (gut, skin, respiratory system. Either not under physiological control or is regulated for purposes other than water balance)

  • Typical human water ‘balance sheet’ in 24hr period

    • Intake

      • Dinking 1500ml

      • Water in food 500ml

      • Water from metabolism 400ml

      • TOTAL 2400ml

    • Output

      • Urine 1500ml (cannot be reduced <500ml)

      • Respiration 400ml

      • Skin 400ml

      • Faeces 100ml

      • TOTAL 2400ml

  • Control of water excretion by ADH (VASOPRESSIN): an overview

    • Rate of water excretion set by ADH (vasopressin)

    • ADH=peptide hormone from posterior pituitary gland (PPG), below hypothalamus

    • Increases water permeability of cortical & medullary collecting ducts (possibly DCT)

    • Absence of ADH, walls of distal nephron impermeable to water

    • ADH binds V2 receptors in basolateral membranes of principle cells in distal parts of nephron

    • Up-regulates expression of AQUAPORINS which are then inserted into apical cell membrane

    • Water then moves osmotically from tubular fluid in distal nephron into surrounding interstitial and then blood

  • Renal effects of ADH (vasopressin)

    • No ADH in blood

      • Over hydration diuresis

      • Cells that line cortical and medullary collecting duct are impermeable to water

      • Na+ and Cl- do pass out but no H2O without ADH

      • So urine more and more dilute as it passes down

      • 80mOsm/L and 15-20ml/min (urine)

    • Maximal ADH in blood

      • Dehydration Anti-Diuresis

      • ADH binds to V2 receptors

      • Inserts aquaporins into cortical & medullary collecting ducts

      • Water will move until osmotic equilibrium is reached

      • Urine very concentrated as max. osmolarity set up by renal medulla

      • In diabetes

        • Glucose adds to osmolarity of tubules so water stays in tubules and not reabsorbed=Diuresis

  • Regulation of release of ADH from PPG

    • Mechanism

      • Increased ECF osmolarity detected by osmoreceptors in hypothalamus, which shrink leading to increased frequency of nerve impulses along hypothalam0-hypophyseal tract

      • Supraoptic & paraventricular nuclei (hypothalamus)=site of synthesis of ADH

      • Increased frequency of nerve impulses causes secretion of the ADH from hypothalamo-hypophyseal nerve terminals

      • ADH moves to PPG and is secreted from there

    • Level of ADH in blood controlled by negative feedback

      • Increased blood osmolarity detected by hypothalamus osmoreceptors

        • Raised blood osmolarity and low blood volumes also lead to sensation of thirst

      • Increased release of ADH from PPG

      • Insertion of aquaporins in distal nephron cell membranes

      • Increased water permeability of distal nephron

      • Increased reabsorption of water from distal nephron (under influence of medullary osmotic gradient)

  • Effect of circulating blood volume in regulating ADH release

    • Decreased blood volume (hypovolaemia)

      • Decreased venous return (volume receptors, B receptors in walls of great veins, right atrium. LOW PRESSURE side of circulation)

      • Decreased BP (baroreceptors in carotids and aortic arch. HIGH PRESSURE)

    • Hypothalamus gets these signals leading to THIRST and INCREASED ADH

  • Regulation of thirst

    • Sensation of thirst induced by

      • Stimulation of hypothalamic osmoreceptors (via raised plasma osmolarity)

        • Effect can be mimicked by injecting hypotonic saline

      • Hypovolaemia detected by CV stretch receptors

    • Thirst sensation ‘switched off’ before drink has been absorbed (receptors thought to be stretch receptors in pharynx &/or stomach)

    • Thirst system can maintain water balance when ADH release/action impaired (DI)

  • Relative physiological ‘status’ of osmoreceptors vs. volume receptors

    • In physiological states, info from osmoreceptors dominates regulation of thirst and ADH

      • Very small changes in plasma osmolarity trigger changes in ADH release and sensation of thirst (detect changes <1%)

    • In pathological states (e.g. haemorrhage), regulation dominated by input from volume receptors

      • Situations where osmoreceptors & volume receptors not working in tandem

      • Fairly wide variation in ECF osmolarity are tolerated

      • Release ADH and hold urine

  • Summary of factors regulating release of ADH

    • Increased by

      • Fall in body volume

      • Rise in osmolarity of ECF

      • Sleep, fright, exercise

    • Decreased by

      • Alcohol

  • Reduced output/effectiveness of ADH: DIABETES INSIPIDUS

    • Symptoms

      • Excretion of large volumes of dilute urine

      • Thirst

    • Two forms

      • PITUITARY (CENTRAL) DI

        • No/reduced synthesis or release of ADH (time of dehydration)

        • Can be successfully treated by

          • Self administered nasal spray that provides ADH replacement

      • NEPHROGENIC (PERIPHERAL) DI

        • Produce ADH, but kidney does not respond

        • Lack of response by kidney to circulating ADH

        • Can result from

          • No/reduced V2 receptors on BL membranes, distal nephron

          • Mutation of gene that regulates synthesis of aquaporins

        • Water balance can only be maintained by increased water intake to compensate for increased water excretion

    • Both forms, if left untreated= rise if ECF osmolarity and fall in circulating blood volume (hypovolaemia) and BP

  • Overproduction of ADH

    • Water retention=HYPERVOLAEMIA

    • ...

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