Electrolytes And Water Flashcards

1
Q

What is osmolality?

A

Number of solute particles in 1 kg of solvent

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2
Q

What is osmolarity?

A

The number of solute particles per 1L of solvent

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3
Q

What is osmotic pressure?

A

The osmotic activity due to unequal concentrations of molecules across a membrane

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4
Q

What is tonicity?

A

The osmotic pressure exerted by a solute particles that aren’t freely permeable across a membrane. This can cause cells to swell or shrinks

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5
Q

What is colloid osmotic pressure?

A

The osmotic pressure across capillary walls due to plasma proteins

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6
Q

What allows organs and cells to be more complex?

A

Compartmentalisation

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7
Q

What keeps compartments intact?

A

Homeostatic mechanisms

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8
Q

Does fluid input have to equal fluid outtake?

A

Yes

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9
Q

Does electrolyte input equal electrolyte losses?

A

Yes

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10
Q

What happens to hypertonic cells?

A

Cells shrink

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11
Q

What happens to hypotonic cells?

A

They swell

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12
Q

Body fluid compartments - What is ICF and ECF?

A

Intracellular fluid
Extracellular fluid

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13
Q

What can you split ECF into?

A

Plasma and interstitial fluid

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14
Q

How does water and electrolytes enter and leave the body?

A

Via plasma

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15
Q

Can plasma levels change the levels of interstitial and intracellular fluid?

A

Yes

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16
Q

What is not freely exchanged between the plasma and interstitial fluid?

A

Plasma

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17
Q

What controls movement of fluid/electrolytes between plasma and interstitial fluid?

A

Hydrostatic pressure and oncotic pressure.

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18
Q

What separates the ICF and ECF>

A

Cell Membranes

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19
Q

What governs te movement of water?

A

Osmotic pressures

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20
Q

What is isotonic?

A

Concentration of osmotically active solutes is equal between ICF and ECF

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21
Q

Water moving out of cells are?

A

Hypertonic

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22
Q

Water moving into cells are?

A

Hypotonic

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23
Q

What are commonly measured electrolytes in the body?

A

Sodium
Calcium
Potassium
Chloride
Bicarbonate
Magnesium

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24
Q

Where is sodium a major cation of and what are the anions?

A

Extracellular and chlorides and bicarbonate are the anions

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25
Q

Where is potassium the major Cation of and what are the anions?

A

Intracelllar and the anions are phosphate

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26
Q

How are the gradiants of sodium and potassium kept?

A

Sodium potassium pumps

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27
Q

What are involved in the U/Es profile?

A

Urea,
Creatinine,
sodium
Potassium

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28
Q

Homeostatic of potassium - fundamental principles?

A

Potassium intake = potassium outtake

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29
Q

Homeostatic of potassium - how do you get potassium in the body?

A

Ingested via gut and excreted in urine

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30
Q

how is potassium homeostasis done?

A

Cells of the kidney tubules secrete K+ into the urine or into the blood depending on if excess is to be excreted into urine or if there is a deficit and K+ needs to be retained

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31
Q

How is potassium homeostasis regulated?

A

plasma K+ concentration and by aldosterone (responding) to plasma K+ concentrations

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32
Q

how do potassium disorders usually develop?

A

Movement of potassium between ICF and ECF
Problems with renal handling of potassium
Inappropriate intake of potassium

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33
Q

if someone comes in with high potassium how do you treat them and wh?

A

Insulin as this encourages cells to take up potassium

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34
Q

what is hyperkalaemia?

A

increased plasma concentrations of potassium

35
Q

what does hyperkalaemia do to the body?

A

= DECREASES the excitability of muscle
= Usually asymptomatic
= Effects muscular function (eg muscle weakness)
= Cardiac arrythmias resulting in chest pain

36
Q

what causes hyperkalaemia?

A

= Kidney unable to adequately excrete: Acute renal failure/Chronic renal failure
= ICF – ECF shifts: Cell Lysis/Exercise/Metabolic acidosis/Increased plasma osmolality
= Deficiency of hormones that act to push K+ into cells/out in the urine eg aldosterone insufficient
= Increased intake from the gut (unlikely unless there is a further cause, usually renal)

37
Q

what is hypokalaemia?

A

decreased plasma concentrations of potassium

38
Q

What does hypokalaemia do to the body?

A

= Increases excitability of muscle
= Usually asymptomatic but if severe you get muscle weakness, muscle cramps, constipation, paralysis and cardiac arrythmias.

39
Q

what causes Hypokalaemia?

A
  • insufficient intake - anoerxia, alcholism
  • shifts of potassium into cells: alkalosis, increase in hormones that push potassium into cells/increase urinary excretion (conns tumour)
  • Abnormal loss from the gut: diarrhoea
  • Abnormal Loss into urine: hyperaldosteronism, diuretics.
40
Q

Water Homeostasis - what is sodium and water homesotasis regulated by?

A

Adjusting ECF volume and ECf osmolarity

41
Q

What does ECF volume adjustments maintain?

A

High blood pressure which is controlled by the RAAS systems

42
Q

How is hypertension caused by salt?

A

Expands fluid compartments leading to hypertension

43
Q

What regulates the ECF volume?

44
Q

what system and how is ECF osmolarity regulated?

A

Regulated to prevent swelling/shrinking of cells by the ADH system

45
Q

What regulates osmolarity?

46
Q

Water Homeostasis - How does water enter the body and leave the body?

A

Drinking water and gut and then leaves via lungs, faeces, skin, and sweat as insensible loses and urine as the only sensible loss

47
Q

Water homeostasis - how does the body control intake and excretion of water? - when water is low

A

If you dont drink the concentration of sodium rises increasing osmolality. The hypothalamus detects this increasing osmolarity and stimulates thirst response and release of ADH from the glands. The ADH tells the kidney to increase the water uptake from urine and therefore more concentrated urine.

48
Q

Water homeostasis - how does the body control intake and excretion of water? - high water in the body?

A

osmolarity decreases hypothalamus senses this and stops thirst signalling and ADH release, leads to kideny retaining less water and you produce a dilute urine.

49
Q

what would the biochemistry of diabetes insipidous?

A

high sodium, high urea, high chloride,

50
Q

What would happen to ADH if you had cranial Diabetes insipidous?

A

not being released

51
Q

What would happen to ADH if you had nephrongenic diabetes insipidous?

A

Nothing but kidneys cant respond to it

52
Q

Can tumours produce ADH?

53
Q

what can hyponatraemia cause and why?

A

cerebral oedema due to hypotonicity and movement of fluid into cells (swelling)

54
Q

what does the brain have to keep brain cells isotonic during slowly developing hyponatraemia?

A

a compensatory mechanism

55
Q

what would happen if hyponatraemia is corrected too quickly and why?

A

Osmotic demyelnination syndrome - because the ECF is hypertonic compared to the new osmolarity of the brian cells i.e the cells shrink

56
Q

Sodium Homeostasis - what does changes in sodium concentration cause?

A

fluid shifts

57
Q

Is it the amount of sodium or concentration of sodium which that determines the volume of body water?

58
Q

what does too much sodium do?

A

Expands ECF

59
Q

What does too little sodium do?

A

contracts ECF

60
Q

what is hyponatraemia?

A

low sodium in the blood

61
Q

what is hypernatraemia?

A

high levels of sodium in the blood

62
Q

what does expanded ECF give you?

A

hypertension

63
Q

What does contracted ECF give you?

A

hypotension

64
Q

What does the RAAS system do?

A

reclaim salt from urine back into plasma

65
Q

where do you get sodium from?

A

dietary sodium caused by a salt craving

66
Q

How do excrete sodium?

A

sweat, faeces, urine

67
Q

What is the RAAS system?

A

renin-angiotensin-aldosterone system

68
Q

the RAAS system - low blood pressure

A

Low blood pressure acts on kidneys which releases renin to work on angiotensinogen to generate angiotensin 1 which is turned into angiotensin 2 by ACe. Angiotensin 2 can work on the adrenals to release aldosterone which instructs kidney to retain salt bringing bp up

69
Q

What is the pathway from decreased ECf volume (hypovolaemia) to ECF expanding?

A

Decreased ECF - Low BP - RAAS activates - reclaimed sodium - ECF expands

70
Q

What is the pathway from increased ECf volume (hypervolaemia) to ECF contracting?

A

Increased ECF - high BP - RAAS supresses - sodium wasted - ecf contracts

71
Q

what is an oedema?

A

Accumulation of excess fluid within the intersitial space

72
Q

Does hydrostatic pressure push fluid out of capillaries and does oncotic pressure pull fluid into capillaries?

73
Q

what would distruption ot the capillary hydrostatic pressure or the oncotic pressure lead to?

A

excess movement of fluid into tissue

74
Q

What is chronic cardiac failure and what does this do to the hydrostatic pressure?

A

decline in hearts ability to prump blood which increases capillary hydrostatic pressure (fluid out capillary)

75
Q

what is nephrotic tissue and how does this affect oncotic pressure?

A

kidneys lose large amounts of protien which results in a decrease in the oncotic pressure (fluids leaks out of the capillary).

76
Q

Do nephrotic syndrome and chronic cardiac failure lead to tissue oedema?

77
Q

in oedemas are patients hypervalemic but the body acts as though they are hypovalemic?

A

yes because they percieve the abnormal circulation as a low effective circulating volume.

78
Q

what is the pathway between decreased effective circulating volume and ECF expanding?

A

decreased effective circulating volume - low bp - RAAS activation - sodium is reclaimed - ECF expands.

people may become hyponatraemic

79
Q

Do people with mass bleeds retain water?

A

yes because they are loosing lots of body fluid.

80
Q

causes of hyponatraemia?

A

SIADH
acute or chronic renal failure
Oedematous states

81
Q

Causes of hypernatraemia?

A

Usually dehydration
Diabetes Insipidua
Very rarely it reflect a gain of salt

82
Q

What is hyponatraemia associated with?

A

Normal volume status, hypervolaemia or hypovolaemia

83
Q

What is hypernatraemia usually associated with?

A

th low volume but can be associated with Normalvolume status or hypervolaema