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4th Year > Electrolyte Imbalance > Flashcards

Electrolyte Imbalance Flashcards

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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
management of hypokalaemia
replace Mg2+ (allows faster correction of hypokalaemia) give potassium 10-20 mmol/hr if non-acute 20 mol/10 min If life-threatening
26
causes of hypermagnesaemia
iatrogenic (Mg infusion) | urinary: panel failure increases risk of accumulation
27
definition of hypermag
>2.2 mmol/l | toxic >4 mmol/
28
which other electrolyte disturbances is hypermag associated
hyperkal | hypocalc
29
symptoms of hypermag
>4 muscle weakness, hyporeflexia, N+V, hypotension due to vasodilation >10 coma, hypoventilation, neuromuscular paralysis, cardiac arrhythmia, bradycardia, death
30
ECG changes in hypermag
increased PR and QTc prolonged QRS peaked T waves and flattened P waves complete AV block and asystole
31
management of hypermag
dialysis is best calcium chloride 10% treats life threatening arrhythmia forced diuresis (IV saline and furosemide)
32
hypomag causes: intake
TPN malabsorption alcoholism
33
hypomag cause: redistribution
insulin | hungry bone syndrome
34
hypomag causes: urinary output
RTA diuretics polyuria from any cause
35
hypomag causes: non-urinary output
upper GI: NG suction lower GI: diarrhoea hypercalcaemia
36
definition hypomag
<0.75 mmol/l
37
pathophysiology of hypomag
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
symptoms of hypomag
``` Trousseau and Chvostek signs weakness/fatigue vertical nystagmus tetany seizures reversible blindness arrhythmia (TdP) hypokalaemic ECG vit D deficiency PTH resistance ```
39
management of hypomag
resus: treat dysrhythmias, seizures etc Iv magnesium replacement/oral correct other electrolyte abnormalities (hypokal and hypocalc) potassium-sparing diuretic is renal wasting
40
causes of hypercalc: intake
``` Ca2+ vitamin A or D hypomag hypovolaemia TPN ```
41
causes of hypercalc: redistribution
``` immobilisation malignancy hyperparathyroidism sarcoid litium adrenal insufficiency endocrine causes (thyrotoxicosis, acromegaly, phaeo) ```
42
urinary causes of hypercalc
thiazides
43
how is free ionised Ca2+ concentration related to pH
inversely related | increase in pH results in decreased Ca2+
44
how does vitamin D help calcium absorption
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
roles of vitamin D
increases intestinal absorption of Ca2+ increases renal Ca2+ reabsorption mobilises bone Ca2+ and PO4
46
which electrolyte states impact parathyroid secretion
increased PTH: hypocalc and hypomag | decreased PTH: hypercalc and hypermag
47
what are the functions of PTH
mobilises Ca2+ from bone increases renal Ca2+ reabsorption increases renal PO4 excretion increases formation o 1,25-dihydroxycholecalciferol
48
action of calcitonin
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
what are the most common causes of hypercalc
``` 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
hypercalc symptoms
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
investigations in hypercalc
confirm malignancy/bony involvement (R, CT etc) assess bone turnover (ALP) assess PTH
52
management of hypercalc
``` 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
causes og hypocalc: intake
Ca2+ vitamin D phenytoin (increased metabolism of vitamin D)
54
causes of hypocalc: redistribution
``` alkalosis citrate toxicity hyperphosphataemia pancreatitis tumour lysis syndrome rhabdomyolysis decreased bone turnover hypoPTH drus ```
55
causes of hypocalc: urinary
ethylene glycol cis-platin protamin loop diuretics
56
causes of hypocalc: non-urinary
bleeding plasmapheresis citrate RRT
57
history in hypocalc
``` personal numbness paraesthesias muscle cramps mild mental status changes (irritability) siezures tetany collapse ```
58
examination in hypocalc
``` 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
management of hypocalc
``` 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
causes of hyperphos
renal failure increased renal reabsorption cellular injury with release (tumour lysis, rhabdomyolysis, haemolytic, ischaemic gut) medication
61
clinical features of hyperphos are related to...
``` hypocalc precipitation of Ca2+ (nephrolithiasis) decreased vit D muscle cramps tetany hyperreflexia seizures prolonged QT ```
62
management of hyperphos
limit phosphate intake chance urinary excretion (saline, acetazolamide) dialysis oral calcium binders
63
causes of hypophos: intake
``` malnutrition phosphate binders vitamin D malabsorption TPN ```
64
causes of hypophos: redistribution
referring syndrome | insulin in DKA
65
causes of hypophos: urinary
diuretics osmotic diuresis hyperPTH proximal tubular dysfunction (Fanconi syndrome)
66
relationship between PTH and phosphate
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
symptoms of hypophos
``` SOB ventilator dependence weakness altered mental state heart failure symptoms shock ```
68
definition of hyponat
mild: 125-134 moderate: 120-124 severe: <120
69
types of Hyponatremia
hypoosmolar/hypotonic iso-osmolar hypertonic
70
causes of hypotonic/hypoosmolar Hyponatremia
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
how to differentiate between renal and non-renal hypovolaemic hyponat
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
causes of SIAADH
``` MAD CHOP malignancy ADH secretion (ectopic) drugs (SSRIs, ecstasy) CNS disease hormone deficiency (hypothyroidism, adrenal insufficient) others pulmonary ```
73
causes of isotonic hyponat
aka pseudohyponatramia marked hyperproteinaemia or hyperlipidaemia causes the lipid proportion of plasma to increase meaning there is a relative decrease in sodium
74
causes of hypertonic hyponat
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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