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Urinary > Session 5 > Flashcards

Session 5 Flashcards

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

A

6 hours

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

A

75%

24
Q

What is TBW in elderly

A

45%

25
Q

Why do patients need fluids

A

Nil by mouth
Malfunctioning gastro-intestinal tract
Dehydration
Fluid losses
Abnormal electrolytes

26
Q

What to think about when giving fluids

A

Maintenance fluids- day to day requirements

Has patient lost any additional fluids

27
Q

What happens when you give dextrose

A

Glucose taken up by cells rapidly (intracellular), H20 reduces osmolarity of all compartments equally

28
Q

Movement of ions between spaces

A

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
Q

What happens when you give saline

A

Na+ remains in ECF, no change in osmolarity (no drive to move intracellular)

30
Q

What happens when you give Hartman’s

A

Majority retained in extracellular space as osmolarity maintained with effective osmoles sodium, potassium and calcium

31
Q

What happens when you give dextrose and saline

A

H20 reduces osmolarity of all compartments

Saline remains in ECF

Dextrose drawn into ICF

32
Q

Why are maintained requirements different in hospital patients

A

Vasopressin (ADH) differences (drugs, pain, nausea, low ECV)

Generally not sweating much

RAAS, catecholamines, reduced caloric expenditure (stress response)

33
Q

NICE guidelines for fluids

A

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
Q

What happens when you give a patient saline that isn’t needed

A

Expanded ECF

35
Q

What happens when a patient drinks too much water

A

Water expands ECF
Dilutes ECF (osmolarity decreased)

Water moves from ECF to ICF due to difference in osmolarity until new eq. Reached

36
Q

What happens to the fluid volumes of a bleeding person

A

Losing volume from ECF

37
Q

What happens to fluid volumes in a patient vomiting

A

ECF decreases
Osmolarity increases as more dehydrated

Water moves from ICF to ECF

38
Q

What happens to the fluid volumes of someone who drinks salt water in large volume

A

ECF volume increases
Osmolarity increases

Water moves from ICF to ECF

39
Q

What would you give a 96kg man who is NBM

A

1 x Hartman’s
2 x 5% dextrose (+40 mmol KCL)

40
Q

What would you give a 65kg person who is NBM

A

2L 0.18 NaCl, 4% dextrose with KCL added to the bags

41
Q

What would you give a 65kg person who is vomiting

A

1L saline, 2L 5% dextrose with KCL added

So saline can go ECF and dextrose can go ICF

Urinary (20 decks)

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