Disorders Of Fluid And Electrolyte Balacne

Question 0

Hyponatraemia, treatment

Answer 0

Water restriction 
Increase salt intake/diuretics
Depends on severity and cause 
Aggressive-> central pontine myelinolysis 
RAA activated by increased salt delivery

Question 1

Hyponatraemia, causes

Answer 1

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,

Question 2

Exercise associated Hyponatraemia

Answer 2

Salt loss through sweating and over consumption of fluids
May also involve ADH suppression through exercise stress
Hypotonic encephalopathy with fatal cerebral oedema

Question 3

Pseudohyponatremia

Answer 3

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

Question 4

Hypernatremia

Answer 4

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

Question 5

Hypovolemia, causes

Answer 5

Decreased ECV 
Causes
Vasodilation 
Internal bleeding 
Aortic dissection 
Heart failure
Hypoalbuminemia 
Hyponatraemia

Question 6

Hypovolemia symptoms and treatment

Answer 6

Pale, cool, moist skin
Increased HR, weak pulse
Absolute-> intravascular fluid leaves body
Relative-> intravascular fluid only leaves vascular system
Replace fluid loss

Question 7

Hypervolemia, causes

Answer 7

Liver disease
Congestive heart failure
Glomerulnephritis/kidney failure/nephritis
Hyperaldosteronism

Question 8

Hypervolemia, symptoms

Answer 8

Ascites
Edema
Dysapnea
High BP
Cough
Increased MVP
Treatment:
Na retention
Fluid restriction
Diuretics

Question 9

Hypo and hyper osmolality

Answer 9

Hypo osmolality-> decrease osmolality of ECF
Increased fluid and decreased solutes
Hyponatraemia
Hyper osmolality-> increased osmolality of ECF

Question 10

Hypokalaemia, causes

Answer 10

[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

Question 11

Importance of K distribution

Answer 11

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

Question 12

Factors influencing transcellular distribution of K, physiological factors

Answer 12

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

Question 13

Transcellular distribution of K+, pathological factors

Answer 13

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

Question 14

Renal tubular acidosis

Answer 14

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

Question 15

Consequences of hypokalaemia and treatment

Answer 15

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

Question 16

Hyperkalaemia, causes

Answer 16

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

Question 17

Consequences and treatment of Hyperkalaemia

Answer 17

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