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4th Year > Electrolyte Imbalance > Flashcards

Electrolyte Imbalance Flashcards

1
Q

causes of hyperkalaemia: intake

A

oral intake

blood transfusion

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2
Q

causes of hyperkalaemia: redistribution

A

acidosis
rhabdomyolysis
tumour lysis

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3
Q

causes of hyperkalaemia: urinary

A 
renal tubular acidosis type 4
renal failure 
adrenal insufficiency 
diabetes 
K+ sparing diuretics
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4
Q

immediate management of hyperkalaemia

A

ABCDE
fluid resuscitation (enhance renal perfusion and elimination)
bloods: FBC, U&E, CK, ABG
monitoring: ECG and blood pressure

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5
Q

why do you give calcium in hyperkalaemia

A

cardiac protection: antagonises the membrane excitability of the heart
DOES NOT LOWER SERUM K+

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6
Q

how can K+ be moved back INTO cells

A

insulin/dextrose: stimulates Na+/K+ ATPase

salbutamol: indirectly stimulates Na+/K+ ATPase

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7
Q

how does HCO3 move K+ into cells

A

decreases the concentration of H+ in the ECF
increases IC Na+ via the Na+/H+ exchanger and facilitates K+ shift into cells via the Na+/H+ ATPase
IN ADDITION TO insulin/dextrose or salbutamol

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8
Q

HCO3 should not be administered at the same time as…

A

Ca2+

can cause precipitation

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9
Q

what is the role of resonium (K+ binders) in hyperkalaemia

A

calcium resonium acts as a cation exchange
negatively charged polymer that exchanges the cation for K+ cars the intestinal wall
SLOW ACTING

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10
Q

definition of hyperkalaemia

A

serum K= >5.5 mmol/L
moderate = >6
severe = >7

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11
Q

what is the relationship between hyperkalaemia and acidosis

A

acidosis causes increased H+ in ECF which inhibits Na+/H+ exchanger
less sodium in transported into the cell which inhibits the Na+/K+ ATPase from moving sodium OUT and potassium IN leading to increase [K+]

hyperkalaemia stimulates the Na+-K+ ATPase to move sodium OUT of the cell
increased EC sodium stimulates the Na+/H+ exchanger leading to acidosis

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12
Q

effects of increased potassium on the heart and ECG changes

A

reduced myocardial excitability
depression of pacemaking and conducting tissues
bradycardia, conduction blocks, cardiac arrest

mild: peaked T waves
moderate: wide, flat P wave, prolonged PR
severe: prolonged QRS with abnormal morphology, high-grade AV block with slow junctional and ventricular escape rhythms, conduction blocks (BBB, fascicular)

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13
Q

causes of hypokalaemia: intake

A

inadequate intake

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14
Q

causes of hypokalaemia: redistribution

A 
alkalosis 
hypomagnesaemia 
glucose infusion 
periodic paralysis 
beta-agonists
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15
Q

causes of hypokalaemia: urinary

A 
steroids
DKA 
hyperaldosteronism 
Cushings
renal tubular acidosis 
diuretics
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16
Q

causes of hypokaelamia: non-urinary output

A

upper GI: vomiting
Mid GI: fistula
lower GI: diarrhoea
other: sweat, burns, bleeding, RRT

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17
Q

how does alkalosis cause hypokalaemia

A

reduced H+ stimulates Na/H+ exchanger to move sodium into cells and H+ out of cells
increased IC sodium stimulates NaK ATPase to move sodium out of cells and potassium in

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18
Q

how does DKA cause hypokalaemia

A

potassium moves out of the cell due to acidosis but is lost in urine

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19
Q

how does hypomagesaemia cause hypokalaemia

A

reduces the intracellular potassium concentration and promoting renal potassium wasting

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20
Q

how do steroids cause hypokalaemia

A

promote renal potassium loss

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21
Q

where is the main site of K+ homeostasis

A

kidney (responsible of 90% of daily K+ loss)

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22
Q

definition of hypokalaemia

A

mild: 3.0-3.5
moderate: 2.5-3.0
severe: <2.5

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23
Q

symptoms of hypokalaemia

A 
fatigue 
muscle cramps and weakness 
constipation 
rhabdomyolysis 
ascending paralyses 
resp failure 
arrhythmias 
medications
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24
Q

ECG signs of hypokalaemia

A 
increased amplitude and width of P wave 
prolonged PR 
T wave flattening and inversion 
ST depression 
U waves 
frequent SV and V ectopics 
SVTs 
potential for ventricular arrhythmias (VT, VF, TdP)
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25
Q

management of hypokalaemia

A

replace Mg2+ (allows faster correction of hypokalaemia)
give potassium
10-20 mmol/hr if non-acute
20 mol/10 min If life-threatening

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26
Q

causes of hypermagnesaemia

A

iatrogenic (Mg infusion)

urinary: panel failure increases risk of accumulation

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27
Q

definition of hypermag

A

> 2.2 mmol/l

toxic >4 mmol/

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28
Q

which other electrolyte disturbances is hypermag associated

A

hyperkal

hypocalc

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29
Q

symptoms of hypermag

A

> 4
muscle weakness, hyporeflexia, N+V, hypotension due to vasodilation
10
coma, hypoventilation, neuromuscular paralysis, cardiac arrhythmia, bradycardia, death

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30
Q

ECG changes in hypermag

A

increased PR and QTc
prolonged QRS
peaked T waves and flattened P waves
complete AV block and asystole

31
Q

management of hypermag

A

dialysis is best
calcium chloride 10% treats life threatening arrhythmia
forced diuresis (IV saline and furosemide)

32
Q

hypomag causes: intake

A

TPN
malabsorption
alcoholism

33
Q

hypomag cause: redistribution

A

insulin

hungry bone syndrome

34
Q

hypomag causes: urinary output

A

RTA
diuretics
polyuria from any cause

35
Q

hypomag causes: non-urinary output

A

upper GI: NG suction
lower GI: diarrhoea
hypercalcaemia

36
Q

definition hypomag

A

<0.75 mmol/l

37
Q

pathophysiology of hypomag

A

Mg deficiency leads to drop in ICF K+ and rise in ICF Na+
elevation in resting potential and a rise in inward Ca2+ current
this causes enhanced neurological and cardiac irritability
magnesium is required for potassium reabsorption by the kidneys
ASSOCIATED WITH HYPOKAL AND HYPOCALC

38
Q

symptoms of hypomag

A 
Trousseau and Chvostek signs 
weakness/fatigue 
vertical nystagmus 
tetany 
seizures 
reversible blindness 
arrhythmia (TdP)
hypokalaemic ECG 
vit D deficiency 
PTH resistance
39
Q

management of hypomag

A

resus: treat dysrhythmias, seizures etc
Iv magnesium replacement/oral
correct other electrolyte abnormalities (hypokal and hypocalc)
potassium-sparing diuretic is renal wasting

40
Q

causes of hypercalc: intake

A 
Ca2+
vitamin A or D 
hypomag
hypovolaemia 
TPN
41
Q

causes of hypercalc: redistribution

A 
immobilisation 
malignancy 
hyperparathyroidism 
sarcoid 
litium
adrenal insufficiency 
endocrine causes (thyrotoxicosis, acromegaly, phaeo)
42
Q

urinary causes of hypercalc

A

thiazides

43
Q

how is free ionised Ca2+ concentration related to pH

A

inversely related

increase in pH results in decreased Ca2+

44
Q

how does vitamin D help calcium absorption

A

cholecalciferol is formed in the skin
liver converts it to 25-hydroxycholecalciferol
kidney proximal tubules convert that to 1,25-dihidroxycholecalciferol
helps calcium absorption in the intestine
controlled by parathyroid hormone

45
Q

roles of vitamin D

A

increases intestinal absorption of Ca2+
increases renal Ca2+ reabsorption
mobilises bone Ca2+ and PO4

46
Q

which electrolyte states impact parathyroid secretion

A

increased PTH: hypocalc and hypomag

decreased PTH: hypercalc and hypermag

47
Q

what are the functions of PTH

A

mobilises Ca2+ from bone
increases renal Ca2+ reabsorption
increases renal PO4 excretion
increases formation o 1,25-dihydroxycholecalciferol

48
Q

action of calcitonin

A

antagonist of PTH
secreted from thyroid gland in response to hypercalc, catecholamines, gastrin
inhibits the mobilisation of bone Ca2+, increases renal Ca2+ and PO4 excretion

49
Q

what are the most common causes of hypercalc

A 
malignancy (inappropriate release of PTH-related peptide from tumour cells - lung, breast, prostate, colon, T-cell malignancies)
post-hypocalc hypercalc
adrenal insufficiency 
prolong immobilisation 
Mg2+ metabolism disorder 
TPN
hypovolaemia 
iatrogenic
50
Q

hypercalc symptoms

A

stones, bones, groans and moans
GI: smooth muscle relaxation = constipation, anorexia, nausea, vomiting
neuro: lethargy, hypotonia, confused, coma
renal: polyuria, dehydration, stone, dehydration
CVS: arrhythmia

51
Q

investigations in hypercalc

A

confirm malignancy/bony involvement (R, CT etc)
assess bone turnover (ALP)
assess PTH

52
Q

management of hypercalc

A 
increase excretion
- IV fluids 
- loop diuretics (decrease absorption in Loop of Henle)
- steroids (inhibits effects of Vit D)
reduce release 
- calcitonin
bisphosphonates (inhibit osteoclasts)
53
Q

causes og hypocalc: intake

A

Ca2+
vitamin D
phenytoin (increased metabolism of vitamin D)

54
Q

causes of hypocalc: redistribution

A 
alkalosis
citrate toxicity 
hyperphosphataemia 
pancreatitis 
tumour lysis syndrome 
rhabdomyolysis 
decreased bone turnover 
hypoPTH
drus
55
Q

causes of hypocalc: urinary

A

ethylene glycol
cis-platin
protamin
loop diuretics

56
Q

causes of hypocalc: non-urinary

A

bleeding
plasmapheresis
citrate RRT

57
Q

history in hypocalc

A 
personal numbness 
paraesthesias
muscle cramps 
mild mental status changes (irritability)
siezures 
tetany 
collapse
58
Q

examination in hypocalc

A 
Chvostek sign (tapping facial nerve anterior to ear causes facial muscle spasm)
trousseau sign (inflate BP cuff, traps median nerve, carpal spasm)
arrhythmias (long QT)
heart failure
59
Q

management of hypocalc

A 
treat cause 
oral Ca2+
replace Mg2+
vitamin D 
IV calcium 
- symptomatic 
ionised <0.8 mmol
CCB overdose 
hypermag 
hypocalc with high inotrope requirement 
massive transfusion 
post cardiopulmonary bypass
60
Q

causes of hyperphos

A

renal failure
increased renal reabsorption
cellular injury with release (tumour lysis, rhabdomyolysis, haemolytic, ischaemic gut)
medication

61
Q

clinical features of hyperphos are related to…

A 
hypocalc 
precipitation of Ca2+ (nephrolithiasis)
decreased vit D 
muscle cramps 
tetany 
hyperreflexia 
seizures 
prolonged QT
62
Q

management of hyperphos

A

limit phosphate intake
chance urinary excretion (saline, acetazolamide)
dialysis
oral calcium binders

63
Q

causes of hypophos: intake

A 
malnutrition 
phosphate binders 
vitamin D 
malabsorption 
TPN
64
Q

causes of hypophos: redistribution

A

referring syndrome

insulin in DKA

65
Q

causes of hypophos: urinary

A

diuretics
osmotic diuresis
hyperPTH
proximal tubular dysfunction (Fanconi syndrome)

66
Q

relationship between PTH and phosphate

A

PTH increases phosphate and Ca2+ release from bone, but increases excretion in kidney by inhibiting reabsorption in the proximal tubule
vitamin D from the kidneys acts on jejunum to increase absorption of Ca2+ and phosphate

67
Q

symptoms of hypophos

A 
SOB
ventilator dependence 
weakness 
altered mental state 
heart failure symptoms 
shock
68
Q

definition of hyponat

A

mild: 125-134
moderate: 120-124
severe: <120

69
Q

types of Hyponatremia

A

hypoosmolar/hypotonic
iso-osmolar
hypertonic

70
Q

causes of hypotonic/hypoosmolar Hyponatremia

A

solute depletion/dilution

hypovolaemic: loss of H2O and Na from the ECF - increased ADH secretion - decreased free H2O excretion and H2O retention - hyponat
euvolaemic: SIADH, psychogenic polydipsia, hypotonic IVF therapy, adrenal insufficiency, hypothyroidism
hypervolaemic: increase in total body Na+ and H2O but H2O is out of proportion to Na+

71
Q

how to differentiate between renal and non-renal hypovolaemic hyponat

A

urinary Na+ <10 mmol = extra-renal (kidney is reabsorbing Na+ so there is less in the urine)
urinary Na+ >20 mmol = renal (kidney should be holding on to Na+ if hypovolaemic)

72
Q

causes of SIAADH

A 
MAD CHOP
malignancy
ADH secretion (ectopic)
drugs (SSRIs, ecstasy)
CNS disease 
hormone deficiency (hypothyroidism, adrenal insufficient)
others 
pulmonary
73
Q

causes of isotonic hyponat

A

aka pseudohyponatramia
marked hyperproteinaemia or hyperlipidaemia causes the lipid proportion of plasma to increase meaning there is a relative decrease in sodium

74
Q

causes of hypertonic hyponat

A

osmotically active particles in the plasma induces movement of H2O from the ICF to ECF, meaning the serum Na+ decreases
can be caused by glucose, mannitol, sorbitol, radio contrast

inability to excrete H2O will initially lower osmolality ut increased urea will cause it to normalise

4th Year (3 decks)

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