Water and Electrolytes Flashcards
W&E
Describe the normal distribution of body fluids
60% of the body is water
- 2/3rds in intracellular.
- Extracellular fluid is the intravascular fluid (including plasma and interstitial fluid)
- Osmolality = total amount of solute in water.
- Water moves down osmolar gradients.
- Extra and intracellular concentration of solutes must be the same otherwise water will move, but the compartments are made up of different salts.
- Osmolality is very tightly regulated between 285-295 mosmol/l. You lose the ability to concentrate your urine as you age (there is a much larger range of osmolality of urine - 50-1500 mosm/l than plasma).
W&E
Describe the normal composition of body fluids -> IC vs EC fluid
Osmolality is identical;
IC: main cation is K+ and anion is PO4-;
EC: main cation is Na+ and anion is HCO3- (and Cl-)
W&E
What are the causes of dehydration?
Vomiting and diarrhea • Alcohol • Diabetes mellitus • Diabetic ketoacidosis/hyperosmolar coma • Diabetes insipidus • Bleeding • Brain injury to posterior pituitary • Post-operative • Sepsis • Anorexia Burns – loss of skin resulting in loss of water and salts through exposed subcutaneous layers so it is difficult to know how much fluid someone is losing as you cant measure evaporated water – weigh them! • Earthquakes – hot, lack of water, bleeding, possible infections, muscle crush injuries and rhabomyolysis (this releases chemicals from muscles which cause renal failure) • Iatrogenic – chemotherapy may be emetic or nephrotoxic resulting in volume depletion, diuretics • Exercising
W&E
Why does blood urea rise when dehydrated?
As dehydrated and because kidneys aren’t perfused well so they can’t function
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What happens if you give someone IV hypertonic saline?
Increase circulating blood volume as water is also drawn out of cells, so increase in BP too (not indefinitely as water redistributes in the body)
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What happens if you give someone IV NaCl 0.9% saline?
Increase in circulating blood volume but increase in BP will be smaller as no osmotic difference between saline and blood plasma
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What happens if you give someone IV 5% dextrose?
Dextrose taken up into cells as metabolite so blood vol goes up for a short time only. Osmolality decreases as once the glucose is taken up it is like giving the patient water (diluting)
W&E
What are the functions of each part of the kidney - Glomerulus, PCT, LoH, DCT and CD?
G: filters 180L/day; PCT: Reabsorbs 70% of solutes and water, fluid reabsorption is mostly isosmotic, so solute conc in tubule is same as in plasma, so doesn’t help conc the urine. LoH: Desc = permeable to water and salt stays in, Thin = water permeable and salt diffuses out, thick = active reabsorption of Na via NaK2Cl pump. Asc pumps ions into the interstitial fluid, so the tubular fluid osmolality here decreases, and increases in the interstitial fluid. Desc: water moves out to counteract the now more concentrated interstitium; this makes the osmolality in desc tubular fluid higher than asc. The process is repeated since fluid is constantly flowing through the nephron. The result is a very concentrated interstitial fluid in the medulla, especially at the base of the loop. Conc of urine occurs since asc is impermeable to water, water cannot diffuse down the osmotic gradient into the medulla. DCT: Actively resorbs solutes (2-3%) via NaCl pump, with urine max dilute here. CD: ADH sensitive -> with ADH then water insensitive, so dilute urine
W&E
What is needed to make dilute urine?
Adequate fluid delivery, Na reabsorption into thick asc. and impermeable CD for water
W&E
What is needed to make concentrated urine?
Not too much fluid delivery/Na reabsorption in thick asc, ADH production should be normal, medullary hypertonicity must be normal
W&E
What are the 3 hormones involved in regulation of water reabsorption?
ADH, RAAS and ANP
W&E
What is the role of ADH in water reabsorption?
A nonapeptide synthesized by the hypothalamus and secreted from the posterior pituitary • Osmoreceptors sense the change in serum osmolality (NOT Na+ concentration) • 1% increase in ECF osmolality causes more ADH release (e.g. in fluid deprivation). • 1% decrease in ECF osmolality causes less ADH release (e.g. with water ingestion). • Non-osmotic stimuli also causing release include stress, hypoxia, pain and volume depletion. • MOA: 1) Direct vasoconstrictor, 2) NaCl reabsorption in the thick ascending limb of LOH, 3) Water retention in the collecting ducts • V2 receptor binding activates cAMP, which stimulates AQP2 incorporation into the apical membrane (i.e. tubular lumen of CD cell).
W&E
What is the role of the RAAS in water reabsorption?
Ang2 -> Vasoconstriction; Increased Na and water retention; Stimulates aldosterone release. • Many drugs target this system: direct renin inhibitors, ACE inhibitors, ARBs • Patients must stop taking these drugs if they get volume depleted e.g. with vomiting
W&E
What is the role of ANP in water reabsorption?
Polypeptide released from cardiac myocytes due to stretch. ANP has opposite effects compared to the other systems: • Increases urinary excretion of Na and water • Inhibits Na resorption by the collecting duct • Inhibits renin production and aldosterone secretion • Vaptans interfere with this system
W&E
What is the mechanism of water balance when fluid is ingested/deprived?
When fluid ingestion increases (e.g. 5 pints of beer), serum osmolality decreases • There is thirst suppression • Decrease in ADH release • More water excretion (to make maximally dilute urine) • With fluid deprivation serum osmolality increases • Thirst increases • Increase in ADH release • More water reabsorption and urine becomes concentrated
W&E
How is too much water lost through the kidneys?
No ADH (born without it, or drugs suppressing release) • Kidney insensitive to ADH • Thick ascending limb NaKCl2 channel blocked • Other solutes carrying water through the kidney, especially glucose • Alcohol and caffeine (block cAMP in tubular cells) • Drugs inhibiting ADH • Excess ANP
W&E
What are the different symptoms of dehydration at 1, 2, 3-4, 6, 8 and 20% of weight loss?
• 1% weight loss thirst • 2% weight loss more thirst, vague discomfort and loss of appetite • 3-4% weight loss increased RBC concentration, lethargy, apathy, nausea and emotional instability • 6% weight loss tingling limbs, heat exhaustion and increased body temperature • 8% weight loss dizziness, confusion and delirium • 20% weight loss death
W&E
What are the clinical features of dehydration and why are they important?
You can distinguish between intracellular and intravascular fluid depletion -> Intravascular depletion: postural hypotension (intravascular depletion); Intracellular/interstitial depletion: tachycardia, low skin turgor, sunken eyes, dry mouth and thirst • You can use an electric current to measure the resistance of water through the body to measure dehydration.
W&E
What are the biochemical features of dehydration?
High serum osmolality • High serum Na • High/low or normal serum K/Mg/Ca • High serum urea • High Hb
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How do you treat dehydration?
If fluid is lost -> replace fluid, give water. If salt and water then give saline; get other solutes balanced too
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How is sodium balance maintained in the kidney?
x
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What are the buffer systems present in the body?
Normal pH range is 7.35-7.45, with H20 H+ + OH-. Bicarbonate and pCO2 are the 2 main buffer systems
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What is the role of bicarbonate in pH?
Reg by kidneys; if low in met acidocis = 1) Renal failure, mineral-corticoid deficiency, lower GI losses (diarrhoea) – usually present with a high chloride. 2) Due to excess acids (lactate and ketones) – do not usually present with a high chloride and therefore have an anion gap present. if high in met alkalosis = Usually due to fluid losses in upper GI tract or on diuretics NB: Base excess is clinically used alongside bicarbonate to assess acid-base status to improve accuracy (normal = 0, normal range -2 to +2, if positive implies excess base).
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What is the anion gap?
The anion gap is the difference between positive and negatively charged electrolytes. Normal 8-16. Calculation: Anion Gap = Na+ – Cl- - HCO3
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What is the main issue with hyperkalaemia and what are the features?
Abnormal ECG -> Tented T waves (ventricular repolarisation affected), loss of P waves (atrial depolarisation), broad QRS (ventricular depolarisation) and bradycardia
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How is pH regulated in the body?
Increase breathing -> pCO2 decreasing, resp alkalosis, caused by type 1 resp failure (pneumonia or PE) and hyperventilation; decrease breathing -> pCO2 increases, resp acidosis
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How do changes in K integrate with changes in pH and bicarbonate?
Causes of high K = met acidosis, low K = met alkalosis; Met acidosis + hypoK = renal tubular disease, urinary diversion -> NB: check anion gap, as ketones and lactates are the cause and aren’t measured.
W&E
How do we compensate for changes in pH?
NB: high pH = cramps/tetany as pH affects Ca ionisation which affects muscle excitability; low pH = breathlessness, causing strong resp drive. Resp compensation is fast and metabolic compensation is slow
