Disorders Of Fluid And Electrolyte Balacne Flashcards
Hyponatraemia, treatment
Water restriction Increase salt intake/diuretics Depends on severity and cause Aggressive-> central pontine myelinolysis RAA activated by increased salt delivery
Hyponatraemia, causes
1)Usually H2O retention secondary to excretion defects:
Advanced renal failure
Inability to suppress ADH secretion-> ECV depletion-> congestive heart failure, diuretics
SIADH
Hormonal changes eg cortisol deficiency, hypothyroidism
2)Primary polydipsia, often schizophrenia
3) reset osmostat H2O in to cells->cerebral edema, lightheaded ness, vomiting, lethargy, seizures,
Exercise associated Hyponatraemia
Salt loss through sweating and over consumption of fluids
May also involve ADH suppression through exercise stress
Hypotonic encephalopathy with fatal cerebral oedema
Pseudohyponatremia
In hyoerprotienaemia/hyolipidaemia
Artefactually low serum Na resulting from volume displacement from altered protien/lipid cons
Can be caused by hyperosmolar state
Water moves out of cells by osmosis-> increase ECV
Hypernatremia
Thirst is main defence mechanism Almost never happens in alert patient with access to water Occurs when thirst can't be expressed Causes: Mainly H2O loss and impaired thirst Na retention-> H2O out of cells-> decreased brain volume! lethargy, seizures Treatment: Decrease Na increase water
Hypovolemia, causes
Decreased ECV Causes Vasodilation Internal bleeding Aortic dissection Heart failure Hypoalbuminemia Hyponatraemia
Hypovolemia symptoms and treatment
Pale, cool, moist skin
Increased HR, weak pulse
Absolute-> intravascular fluid leaves body
Relative-> intravascular fluid only leaves vascular system
Replace fluid loss
Hypervolemia, causes
Liver disease
Congestive heart failure
Glomerulnephritis/kidney failure/nephritis
Hyperaldosteronism
Hypervolemia, symptoms
Ascites Edema Dysapnea High BP Cough Increased MVP Treatment: Na retention Fluid restriction Diuretics
Hypo and hyper osmolality
Hypo osmolality-> decrease osmolality of ECF
Increased fluid and decreased solutes
Hyponatraemia
Hyper osmolality-> increased osmolality of ECF
Hypokalaemia, causes
[K] mild no symptoms
[K] muscle weakness, ECG damage and arythmias, polyuria and polydipsia
Very common
Causes:
1) decreased net intake, may contribute but rarely sole reason
2) increased entry into cells:
Alkalosis (max decrease in K 0.4mmolm/l per 0.1pH
Insulin in hyperglycaemia
Beta2 adrenoceptor activation-> stress, hypoglycaemia, inhalers
3) increased GI losses
4) increased urinary losses:
Loop/thiazides diuretics-> increased aldosterone
Vomiting-> metabolic alkalosis
Mineralocorticoid excess-> aldosterone producing adenoma
Metabolic acidosis due to aldosterone
Importance of K distribution
Affects membrane potential =[Ki][Ko]
Transcellular shifts cause more symptoms than external balance
Increase [Ko]-> depolarise membrane-> more excitable;but persistent depolarisation inactivated Na channels-> decreased membrane excitability-> impaired cardiac conduction/muscle weakness
Decreased [Ko]-> hyper polarise membrane-> less excitable but in cardiac myocyctes increase membrane excitability due to removal of normal inactivation of Na channels
Factors influencing transcellular distribution of K, physiological factors
Basal-> primarily 3Na/2K ATPase
Inulin activates Na/K-> increases K uptake in to the cell
Catecholamines on beta2 receptors-> increase K uptake in to the cells and activates Na/K
Beta2 against-> increases K reabsorption via Na/K
Stimulated effects transient-> efflux due to decreased plasma K+
Lack of insulin or beta2 adrenoceptor antagonism implairs by doesn’t prevent K+ movement into cells
Can create a totally body deficit when K + moves in to cell
Or retention when K+ moves out
Exercise increases plasma K
Transcellular distribution of K+, pathological factors
Chronic disease especially renal
Extra cellular pH-> decreased pH-> increased K+ out, not for organic acids
Hyper osmolality, plasma K increased by solvent drag
Rate of cell breakdown-> severe trauma-> increase Ko
Renal tubular acidosis
Type 1:
Classic distal RTA, decrease in distal H secretion-> increased K secretion for electorneutrility as Na reabsorbed
Type 2:
Decreased proximal HCO3- reabsorption->increased K secretion
Rare hereditary disorders-> liddles, battlers, gitelmon
Consequences of hypokalaemia and treatment
Often no symptoms when mild More server: Muscle weakness or paralysis Cardia arrhythmia's Rhambdomyolysis Renal dysfunction: Polyuria, polydipsia Decreased ADH effect, decreased medullary gradient Increased ammoniagenesis Increased HCO3 reabsorption Treatment: KCl, KHCO3, oral or iv
Hyperkalaemia, causes
Extracellular [K+]>5.5mmol/l Causes: 1) increased intake 2) movement from inside to outside cells: Pseudohyperkalemia->Artefactually increase in serum K due to release from cells Metabolic acidosis Insulin deficiency+hyper osmolality Tissue catabolism-> rhabdomyolsis Beta adrenoceptor antagonism Servere exercise 3) decreased urinary excretion: Renal failure Hypovolemia Hyperaldosteronism
Consequences and treatment of Hyperkalaemia
Muscle weakness/ nerve paralysis Cardiac arythmias Treatment: 1) antagonism of membrane actions: Ca2+ restores membrane excitability Not long lasting 2) increased K entry into cells: Lasts several hours Insulin and glucose NaHCO3-> creates alkalosis Beta2 adrenoceptors agonists 3)removal of excess K Lasts several hours Asymptomatic patients Diuretics Cation-exchange resin Haemidialysis/peritoneal dialysis
