Session 5 Flashcards

(41 cards)

1
Q

Explain depolarisation

A

If extracellular K+ rises, resting membrane potential is decreased

Na+ ions in

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2
Q

Explain repolarisation

A

If extracellular k+ falls, resting membrane potential is increased (hyperpolarised)

K+ ions out

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3
Q

ECG trace in hypokalaemia

A

Peaked P wave
Prolonged PR
ST depression
Shallow T wave
Prominent U wave

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4
Q

ECG trace in hyperkalaemia

A

Wide, flat P wave
prolonged PR
Decreased R wave amplitude
Widened QRS
Depressed ST segment
Tall, peaked T wave

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5
Q

Intra and Extra cellular concentrations of K+

A

Intra- 130-140 mEq/L
Extra- 3.5-5.5 mEq/L (due to Na+Ka+ATPase)

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6
Q

Distribution of body water

A

60% fluids (40% solids)

In 60% = 1/3 ECF, 2/3 ICF

In 1/3 ECF = 75% interstitial fluid, 25% plasma

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7
Q

How do the intercalated cells control pH of blood

A

Acidosis: secrete H+ into tubule, reabsorb K+ and HCO3- into blood

Alkalosis: secrete K+ and HCO3- into tubule, reabsorb H+ into blood

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8
Q

Clinical features of hyperkalaemia

A

Can be asymptomatic
Muscle weakness, cardiac arrhythmis (impacts nerve conduction)

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9
Q

Hyperkalaemia can result from

A

Lack of excretion - (kidneys failing, AKI/CKD, potassium sparing diuretics, ACE inhibitor, aldosterone problem)

Release from cells- acidosis, lysis

Excess administration- too much fluids, medications

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10
Q

When is emergency treatment of hyperkalaemia needed

A

When there is more than 6.5mlmol/L or ECG changes

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11
Q

Emergency treatment of hyperkalaemia

A

Calcium gluconate- Ca2+ stabilises the myocardium, preventing arrhythmias

Insulin- drives K+ into cells to lower plasma concentrations, given with glucose to avoid hypoglycaemia

Calcium resonium- removes K+ by binding to it and increasing excretion. Only way to remove K+ without renal replacement therapy

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12
Q

Clinical effects of hypokalaemia

A

Muscle weakness, cramps and tetany (starts in lower extremities)

Vasoconstriction and cardiac arrhythmias

Impaired ADH action causing thirst, polyuria and no concentration of urine

Metabolic alkalosis due to increase in intracellular H+ concentration

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13
Q

Long term control of hyperkalaemia

A

Low potassium diet
Stop offending medications
Furosemide- enhances potassium loss in urine
Dialysis?

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14
Q

Causes of hypokalaemia

A

Reduced dietary intake (anorexia nervosa)
Increased entry into cells (alkalosis or noradrenaline release due to stress perhaps)
Increased GI losses
Increased urine loss

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15
Q

Treatment for hypokalaemia

A

Treat cause- diuretics, diarrhoea, poor oral intake

Give replacement:
Oral- banana, orange, Sando-K
IV- add KCL to IV bags
Potassium sparing diuretics= spironolactone, amiloride

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16
Q

K+ too high or low will cause

A

Nerve dysfunction and cardiac arrest

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17
Q

Excretion of K+

A

Kidneys excrete 80% of K+, bowel 20%

18
Q

Insulin will decrease k+ for appprox

19
Q

What is osmolality

A

Particles of solute per kg of solvent

20
Q

What is osmolarity

A

Particles of solute per litre of solution

21
Q

What is tonicity

A

Effective osmotic pressure gradient of two solutions separated by a semi permeable membrane

22
Q

Differences in movement between intracellular and extracellular

A

Intracellular: potassium is major cation, Cell membrane limits transport

Extracellular: Sodium is major cation, concentration gradients allow movement

23
Q

What is the TBW of a newborn baby

24
Q

What is TBW in elderly

25
Why do patients need fluids
Nil by mouth Malfunctioning gastro-intestinal tract Dehydration Fluid losses Abnormal electrolytes
26
What to think about when giving fluids
Maintenance fluids- day to day requirements Has patient lost any additional fluids
27
What happens when you give dextrose
Glucose taken up by cells rapidly (intracellular), H20 reduces osmolarity of all compartments equally
28
Movement of ions between spaces
Extracellular: Na+ can move between interstitial and intravascular (plasma and interstitium) Na+ K+ ATPase allows transport of Na+ out of intracellular space and K+ in
29
What happens when you give saline
Na+ remains in ECF, no change in osmolarity (no drive to move intracellular)
30
What happens when you give Hartman’s
Majority retained in extracellular space as osmolarity maintained with effective osmoles sodium, potassium and calcium
31
What happens when you give dextrose and saline
H20 reduces osmolarity of all compartments Saline remains in ECF Dextrose drawn into ICF
32
Why are maintained requirements different in hospital patients
Vasopressin (ADH) differences (drugs, pain, nausea, low ECV) Generally not sweating much RAAS, catecholamines, reduced caloric expenditure (stress response)
33
NICE guidelines for fluids
25-30ml/kg/day of water 1 mmol/kg/day of potassium, sodium and chloride 50-110g/day of glucose to limit starvation ketosis
34
What happens when you give a patient saline that isn’t needed
Expanded ECF
35
What happens when a patient drinks too much water
Water expands ECF Dilutes ECF (osmolarity decreased) Water moves from ECF to ICF due to difference in osmolarity until new eq. Reached
36
What happens to the fluid volumes of a bleeding person
Losing volume from ECF
37
What happens to fluid volumes in a patient vomiting
ECF decreases Osmolarity increases as more dehydrated Water moves from ICF to ECF
38
What happens to the fluid volumes of someone who drinks salt water in large volume
ECF volume increases Osmolarity increases Water moves from ICF to ECF
39
What would you give a 96kg man who is NBM
1 x Hartman’s 2 x 5% dextrose (+40 mmol KCL)
40
What would you give a 65kg person who is NBM
2L 0.18 NaCl, 4% dextrose with KCL added to the bags
41
What would you give a 65kg person who is vomiting
1L saline, 2L 5% dextrose with KCL added So saline can go ECF and dextrose can go ICF