Medicine Notes Renal System Notes
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 ...
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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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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 ...
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