fluid and electrolyte balance Flashcards
what electrolytes and anions in ECF
Na+, Cl- and HC03
what electrolytes and anions in ICF
K+, proteins and phosphate
how is water excreted and what controls it? what secretes what controls it
Water excretion by the kidney is very tightly controlled by arginine vasopressin (AVP) also called ADH secreted from the posterior pituitary gland according to the osmolality.
A rising osmolality promotes the secretion of AVP, causing water to be retained by the kidney.
A declining osmolality switches the secretion off.
concentration of sodium in circulation
135-145mmol/L maintains serum osmolality
100-300mmol per day intake in the west
how is na+ lost
kidneys, sweat, poo, vommit( OTC diaralyte has electrolytes.
Na needs to be regulated otherwise hypotension
what controls na urinary output homeostasis
Aldosterone: na and water retention and k+ excretion
Atrial natriuteric peptide: secreted from cardiocytes of the right atrium of the heart. It increases urinary sodium excretion
explain RAAS system
at the end : increase reabsorption of na and h20 and decrease cardiac output
what is the science name for low sodium and what are the causes, clinical symptoms and clinical signs?
hyponatraemia
Loss of Sodium; e.g. vomiting diarrhoea, loss from burns, fistulae, Addison’s disease.
Water retention; inappropriate secretion of ADH (SIAD), e.g. post trauma or inappropriate treatment with iv dextrose
Clinical symptoms: nausea, malaise, headache, lethargy and a reduced level of consciousness. Seizures and coma are not seen usually until Na+ Conc. < 110-115 mmol/l.
Clinical signs: signs of volume depletion e.g. hypotension, decreased urine output, decreased consciousness, decreased skin turgor, soft/ sunken eyeballs, dry mucous membrane, increased pulse
-demeclocycline- for hyponatraemia
toxicity of which drug is made worse by hyponatraemia
Lithium- causes lithium retention and causes toxicity bc narrow therapeutic index.
what is hypernatraemia and what causes it
Water depletion:
water intake e.g. post-op ( due to unconciousness or nil by mouth) or dysphagia.
Excessive water loss, diabetes insipidus (failure of ADH), sweating, hyperventilation
Sodium retention
Excessive intake e.g. over infusion of saline, salts etc.
Excessive adrenocortical hormones e.g. Conn’s syndrome and Cushing’s syndrome
potassium serum levels
K+ is the major ICF cation, 2% of body content being in the ECF (serum level is 3.5-5mmol/l)
Potassium intake is variable, 30-100mmol/day in the UK.
The kidney excretes the bulk of ingested potassium (20-100mmol/day), with some lost in the faeces (~5mmol/day).
Serum potassium conc. does not vary appreciably in response to water loss or retention. However, factors that cause even a small or sudden shift of intracellular potassium will cause a big change in the ECF K+ conc.
how does k+ move, cellular paths and in acids and alkaline situations?
Cellular uptake of potassium is stimulated by insulin.
A reciprocal relationship exists between K+ and H+ ions. In acidosis, H+ ions conc. , K+ ions are displaced from the cells into ECF to maintain electroneutrality. The opposite occurs in alkalosis. Hence, H+ ions changes cause marked alteration in serum K+ conc.
One of the main functions of potassium is to maintain excitability of neuromuscular tissue.
what’s name for high k+ and what’s the causes
Is caused by: Renal failure Mineralocorticoid deficiency (hypoaldosteronism (Addison’s disease)) Acidosis Hormonal effects-low plasma insulin Severe tissue damage Excessive doses of K+ sparing diuretics, what others? Excessive doses of K+ supplements
how k+ clinical symptoms
Clinical symptoms;
Hyperkalaemia results in an enhanced state of excitability of cells. The main effects are on cardiac and skeletal muscle. In many cases, cardiac signs appear and lead to death before skeletal muscle symptoms appear.
Cardiac toxicity manifests as the sudden development of cardiac irregularity, tachycardia, ventricular fibrillation and asystole. Sudden death from cardiac arrest is common.
name for low k+? and what are causes?
hypokalaemia may be caused by:
- gastrointestinal losses eg. vomiting, diarrhoea or surgical fistula
- renal losses in renal tubular failure
- drug induced: diuretics, corticosteroids
patients with hypokalaemia may have sever muscle weakness, neurological and cardiac arrhythmia
what is the calcium serum level
2.2-2.6mmol/l
factors that control calcium homeostasis
vitamin d and parathyroid hormone PTH
PTH is secreted from the parathyroid glands in response to low unbound plasma calcium. It causes an;
Increase in osteoclastic resorption of bone
Increase in renal tubular reabsorption of calcium
Increase synthesis of 1,25-(OH)2D3
Increase intestinal absorption of calcium
Calcium calculation
About half of serum calcium is bound to proteins, mostly to albumin.
Unbound calcium is the biologically active fraction of the total calcium in plasma and maintenance of its concentration within tight limits is required. It is this fraction that is recognised by the parathyroid gland.
Laboratories routinely measure total calcium concentration (both bound and unbound).
This may give to problems in interpreting results, as changes in serum albumin concentration cause changes in total calcium concentration.
E.g. if albumin concentration falls, total serum calcium is low because the bound fraction is decreased.
Corrected calcium (mmol/L)= Total measured calcium + 0.02 (40-albumin)
hypocalcaemia causes
- vit d deficiency: malabsorption, inadequate diet, lack of sun
- renal disease: unable to synthesise 1,25-DHCC
Hypocalcaemia symptoms and management
- numbness and tingling and burning in extremities
- tetany occurs when levels are 1.5-1.6mmol/l
- prolonged hpocalcaemia can interfere with metabolism of the lens and cause cataracts
management:
- calcium supplemets
- calcitriol or alfacacidol can be given
hypercalcaemia causes and clinical signs
causes of high calcium:
- vitamin d oversode
- hyperparathyroidism
- neoplasms
- Bone disease: pagets
clinical signs of hypercalcaemia:
- heart: cardiac arrhythmias
- neurological and physc: legsrthy, confusion, dementia, depression
renal: thirst, polyuria - gi: anorexia, constipation, n and v
what are the functions of the kidney
- regulation of water, electrolytes and acid base balance
- excretion of urea, creatinine and uric acid
- produced hormones eg renin and erythop
Cockcroft and Gault equation for egfr
GFR= A X (140 – age(years)) X weight (kg) Serum Creatinine (µmol/L)
Where A=1.23 for males, A = 1.04 for females
considerations for obese patients for egfr calculations?
To normalise the calculation, use ideal body weight where fat is likely
to be the major contributor to body mass
IBW male = 50 + (2.3 x height in inches over 5 feet) IBW female= 45.5 + (2.3 x height in inches over 5 feet)
Many other formulas used:
Ideal body weight (kilograms) = Constant + 0.91 (Height - 152.4)
Where:
Constant = 50 for men; 45.5 for women
Height in centimetres
limitations in GFR calculations
- not valid in pregnancy
- not valid in elderly
- amputees
- vegans
- bodybuilders
