Disorders of electrolytes and water

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Disorders of electrolytes and water

• 3rd Year Notes
• Dr Niroj Obeyesekere

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The extracellular fluid compartment

• In adults, body water 60
• ICF 2/3
• ECF 1/3
• Capillary endothelial membrane divides ECF into,
• Intravascular - plasma
• Extravascular
• Extravascular compartment can be divided into,
• Interstitial water (25 of TBW)
• Transcellular water (4 of TBW)
• Transcellular CSF, gastro-interstitial fluid
  and fluid in eyes and serous surfaces.

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• ICF and ECF are in osmotic equilibrium.
• Na salts being the most abundant salt in the ECF,
  are the most important determinant of ECF.
• The most fundamental characteristic of fluid and
  electrolyte homeostasis is the maintenance of ECF
  volume and circulatory stability.

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Tonicity and osmolality
Osmolality of a solution is the number of osmoles of solute per kilogram of solvent . Osmolality is a property of a particular solution and is independent of any membrane. Tonicity is a property of a solution in reference to a particular membrane. Urea hyperosmolar but isotonic High glucose in untreated DM hyperosmolar and hypertonic
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Water balance and renal water excretion

• Individuals maintain a physiologic serum
  osmolality between 285 290 mOsm/kg.
• We can excrete hypertonic or hypotonic urine in
  relation to plasma.
• This is done by counter- current system present
  in the kidney.

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Nephron and collecting duct
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The counter-current system
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The counter current system

• Renal cortex osmolality 290mOsm/kg renal
  medulla 1200 mOsm/kg.
• Thin descending loop permeable to water, but
  relatively impermeable to Na.
• Thin ascending limp and TAL are essentially
  impermeable to H20.

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Counter current system

• Fluid entering thin descending limb is 290
  mOsm/kg.
• However, the na re-absorption that occurs in the
  thick ascending limb increases osmolality in the
  medulla.
• Active Na-H pump (in the TALH) and Na-Cl-K co
  transporter.(the site of action of loop
  diuretics)
• This hyperosmolar fluid drags water out of thin
  descending limb and fluid entering ascending limb
  is hyperosmolar compared to plasma.
• But this osmotic gradient can be used to deliver
  hypotonic urine to the distal tubule. (at any
  level in the ascending limb the osmalality is
  less than the surrounding tissue)

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Vasopressin

• Also known as arginine vasopressin or ADH
• Secreted by the hypothalamus.
• Secreted in response to osmotic and non-osmotic
  stimuli.
• These osmo-receptors are located in the
  hypothalamus.
• Substances that are restricted to the ECF such as
  hypertonic saline or mannitol act as effective
  osmoles and enhances osmotic water release. This
  stimulates ADH.
• But, urea and glucose cross cell membranes freely
  so no change cell volume and therefore does not
  effect ADH release.
• Non-osmolar - decreased effective circulating
  volume (HF, cirrhosis), nausea, postoperative
  pain and pregnancy.

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Action of vasopressin collecting tubules
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Thirst and osmolality
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Control of serum sodium

• Counter-current mechanism
• Hypothalamic receptor and vasopressin
• Thirst
• Serum osmolality 2(na) BUN/2.8 glucose/18
• Hyperglycemia is a cause of hyponatraemia. A
  decrease of 1.6mmol of na per 5.6mmol/l increase
  in BSL.

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Approach to hyponatraemia
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Assessing volume state

• General appearance sunken orbits (rare),
  moribund appearance of severe dehydration,
  thirst.
• Face dry mucus membranes
• Neck JVP patterns. (very important)
• Hands, chest skin turgor
• BP postural drop and/or tachycardia
• Oedema

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JVP

• Internal jugular medial to sternomastoid
  muscle.
• Measure with patient at 45 degrees.
• The height is measured from the sternal angle.
• Differences between carotid and jugular
  pulsation. Jugular 1 visible but not palpable,
  2- complex wave form two flickers, 3- moves with
  respiration normally decreases with inspiration,
  4- when pressed fills from above.

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Isotonic and hypetonic hyponatremia

• Non hypotonic hyponatremia is diagnosed by the
  presence of an osmolar gap.
• Osmolar gap difference between measured plasma
  osmolality and calculated osmolality. Serum
  osmolality 2(na) BUN/2.8 glucose/18
• If there is a osmolar gap then its due to
  pseudohyponatremia or the presence of a non
  sodium effective osmole in the circulation. But
  it has to be effective osmole

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pseudohyponatremia

• Sodium biological activity is determined by the
  concentration in plasma water. So true hypotonic
  hypontremia is a decreased concentration of na in
  the aqeous phase of plasma.
• Plasma is 93 water and 7 proteins and lipids.
• So in states of hyperlipidemia or
  hyperproteinemia the na is reduced even thouhg
  the concentration remains the same
• Eg . HIV, Hep C, IVIG
• Direct vs indirect ISE

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Hypertonic/isotonic hyponatremia

• Effective osmole attracting water from cells to
  plasma. So cells are shrunken.
• Hyperglycemia, mannitol and IVIG.
• Isotonic TURPs isomotic fluid

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Hypotonic hyponatremia adaptive responses

• Cells are swollen.
• Ie brain in a confined space. How do we
  compensate?
• Ancient trait by activating a mechanism called
  RVD volume regulatory decrease in which
  osmotically active solutes are extruded from the
  cell. Eg K, CL,(10 -20 dcerase) organic
  osmolytes (upto 90 decrease) and limit brain
  swelling.

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Brain adaptations

• Blood brain barrier. impedes substances that
  are not lipid soluble. Capillary endothelium and
  astrocyte end feet. Not neurons so astrocytes are
  swollen and not neurons. Through aquaporin 4.
• Acute vs chronic hyponatremia . Less than 24 vs
  more than 48 hrs.
• Physiology in hypertonicity organic osmolytes
  are transported in cells opposite of
  hyponatremia. Eg taurine.

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Brain adaptive responses

• In chronic hypertonicity these transporters are
  upregulated. Helps explain the stubborn
  persistence of osmolytes in pts with
  hypernatremia and resultant cerebral oedema that
  occurs when corrected too quickly/
• In chronic hypoNa these transporters are
  downregulated. And are slow to return to cells
  esp when corrected too quickly. osmotic
  demyelination syndrome
• Usually 1 day after so aim for 10 -12 mq/l a day.

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Acute hyponatremia

• Some interesting bits.
• 1. exercise induced. ultra long marathon runner
  56 km or more. Can get Hypona. Their AVP is up
  even with a normal Na. this most likely due to
  volume drop than osmotic issue. Also BNP,
  cortisone.
• Sweat glands 90k run 8.6 l of sweat.
• Sweat glands have a secretory coil. Which
  produces isomotic sweat and a reabsorptive duct
  which actively reabsorbs Na.

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Exercise induced hypona

• Na is via the amiloride sensitive channel and Cl
  is through the cystic fibrosis transmembrane
  channel. So when not much sweat hypotonic
  sweat. High sweat na reabsortpion is rate
  limited.
• Increase loss of na and AVP increase may decrease
  na.
• Other causes psychosis and post operative, ectasy

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Chronic hyponatremia

• Is an abnormality of free water excretion. Most
  have a increased vasopressin release.
• Decrease effective volume ie. Heart failure,
  liver failure. Easy dx.
• Difficult between true vs euvolemic hyponatremia.
  (siad)

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siad

• 1. hypoosmolality
• 2. urine that is less than maximally dilute gt100
• 3. absence of diuretics
• 4. urine na concentration more than 30
• 5. reversal of na wasting with water restriction
• Gold standard bt true vs euvolamic- isotonic
  saline reduced vasopressin release and urine
  becomes dilute. Hard to differentiate.

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Symptoms

• Fatigue vomiting, consuion, dysarthria, gait
  disturbances and lethargy,
• Seizures, coma.
• Gait like having a BAL 0.06 gait and tandem
  gait tests.

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causes

• 1. drugs
• 2.tumours small cell lung cancers ectopic
  prduction of vasopressin
• 3. pneumonia
• 4.endocrine addisons and hypothyroidism.
• 5. meningitis
• 6. ABI

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Rx

• Fluid
• Water restrict
• Vasopressin antagonists in heart failure