Disorders Of Fluid And Electrolyte Balacne Flashcards Preview

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Flashcards in Disorders Of Fluid And Electrolyte Balacne Deck (18)
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0
Q

Hyponatraemia, treatment

A
Water restriction 
Increase salt intake/diuretics
Depends on severity and cause 
Aggressive-> central pontine myelinolysis 
RAA activated by increased salt delivery
1
Q

Hyponatraemia, causes

A

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,

2
Q

Exercise associated Hyponatraemia

A

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

3
Q

Pseudohyponatremia

A

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

4
Q

Hypernatremia

A
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
5
Q

Hypovolemia, causes

A
Decreased ECV 
Causes
Vasodilation 
Internal bleeding 
Aortic dissection 
Heart failure
Hypoalbuminemia 
Hyponatraemia
6
Q

Hypovolemia symptoms and treatment

A

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

7
Q

Hypervolemia, causes

A

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

8
Q

Hypervolemia, symptoms

A
Ascites
Edema
Dysapnea
High BP
Cough
Increased MVP
Treatment:
Na retention
Fluid restriction
Diuretics
9
Q

Hypo and hyper osmolality

A

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

10
Q

Hypokalaemia, causes

A

[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

11
Q

Importance of K distribution

A

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

12
Q

Factors influencing transcellular distribution of K, physiological factors

A

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

13
Q

Transcellular distribution of K+, pathological factors

A

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

14
Q

Renal tubular acidosis

A

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

15
Q

Consequences of hypokalaemia and treatment

A
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
16
Q

Hyperkalaemia, causes

A
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
17
Q

Consequences and treatment of Hyperkalaemia

A
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