Diuretics and IV fluids Flashcards

1
Q

Describe how 5% dextrose solution distributes across the body fluid compartments

A

It goes into all compartments- about 2/3 moves into the intracellular compartment and 1/3 stays in ECF.
This is because the dextrose is absorbed by the cells & increases their osmotic pressure so fluid moves into the cells. The dextrose is then metabolised, meaning not all the fluid will move in.

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2
Q

Describe how fluid distributes when given a 0.9% NaCl normal saline solution

A

It is isotonic to the ECF so will enter the ECF and stay there, because although volume has increased the osmotic pressure hasnt.

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3
Q

Describe what colloid is and how it will distribute into fluid compartments

A

Its a solution containing proteins (albumin). The theory is all the fluid should stay in the plasma because itll increase the oncotic pressure and the proteins wont move into the interstital space and so be good for treating burns. In reality it has little extra benefit over normal saline and is more expensive.

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4
Q

What is mannitol and how is it meant to work as a diuretic?

A

It is an osmotically active substance which is freely filtered at the glomerulus and not reabsorbed, thus increasing the osmolarity of the filtrate and so decreasing water (and Na+) reabsorbtion

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5
Q

Mannitol is not generally used as a diuretic anymore but what is it used for now?

A

It can be used to reduce intercranial pressure (eg after head trauma) and treat glaucoma. Both because it’ll increase osmotic pressure of the blood and cause fluid reabsobtion

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6
Q

Why can carbonic anhydrase inhibitors be used as diuretics? (They’re not really anymore)

A

They decrease Na and HCO3- reabsorbtion in the PCT so less water reabsobtion

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7
Q

Name a loop diuretic

A

Furosemide

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8
Q

How do loop diuretics work?

A

Block the NKCC in the ascending limb of the loop of henle.

Less NaCl reabsorbtion= less water reabsorbed

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9
Q

Why can loop diuretics (eg furosemide) cause hypocalcaemia and hypomagnesia/ treat hypercalcaemia?

A

Because normally the K+ bought in from NKCC will diffuse back out and make the lumen positive in relation to the cells so drive Mg2+ and Ca2+ reabsorbtion- since this is lost you also loose some reabsorbtion of Mg2+ an Ca2+

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10
Q

Which diuretic is the most potent?

A

Loop diuretics are very potent- as 25% reabsorbtion occurs in the loop.

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11
Q

When are loop diuretics used?

A

As theyre very potent theyre given in pulmonary odema as they quickly reduce ECF volume- esp if given IV.
They also vaso and venodilate so are used in heartfailure
They can also be used in cirrhosis, renal failure and neprotic syndrome

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12
Q

How do thiazide diuretics (eg cholothyazide) work?

A

They blood Na- Cl cotransporters (NCCT) in the DCT

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13
Q

When are thiazide diuretics used?

A

Theyre less potent and are mild venodilators so used in hypertension

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14
Q

What implications do thiazide diuretics have for Ca2+ reabsorbtion?

A

increase

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15
Q

How do thiazide and loop diuretics lead to K+ wasting (and so hypokalaemia)? (3)

A
  • Less Na+ is reabsorbed in the early nephron, so more is delivered to the principal cells of the collecting ducts, where Na+ absorption is linked to K+ secretion (so Na+ absorption will increase and K+ secretion will increase).
  • Also more fluid will be retained in the filtrate, leading to faster flow rate, secreted K+ is washed away faster- so favourable chemical gradient for K+ secretion.
  • ALSO diuretics may decrease circulating blood volume -> which activates RAAS-> aldosterone will increase Na+ reabsorption in the collecting ducts further, so further increasing K+ secretion
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16
Q

Which classes of diuretics are k+ sparing?

A

Amiloride (inhibits NHE and ENaC) and Aldosterone antagonists (spironolactone)

17
Q

How does amiloride work?

A
  • Inhibits NHE (so less Na+ reabsorption in PCT) (minor effect)
  • Also inhibits ENaC in collecting ducts, so less Na+ is reabsorbed so less reabsorption of water (also less excretion of K+)
18
Q

How do aldosterone antagonists work?

A

Aldosterone usually increase expression of ENaC and Na/K/ATPase in the collecting ducts, so less of this= less Na+ and so H20 reabsorption

19
Q

How potent are K+ sparing diuretics?

A

Mild as most Na+ has been reabsorbed by the time you get to the collecting ducts- often used with thiazide diuretics to minimise K+ loss

20
Q

Can you get hyperkalaemia with K+ sparing diuretics?

A

yes especially if used with an ACEi (will cause further drops in aldosterone), a K+ supplement or if they have renal impairment

21
Q

Why are diuretics used in nephrotic syndrome?

A

Nephrotic syndome= loss of protine in urine= loss of oncotic pressure= fluid accumulation in interstitial space= odema which needs reversing

22
Q

What diseases cause diuresis (polyuria)

A
  • Diabetes insipidus and mellitus
  • phychogenic polydipsia
  • hypercalcaemia
  • CKD (sometimes)
23
Q

State adverse effects of diuretics other than hypovalemia and K+ changes

A
  • hyponaturaemia
  • gout as increased uric acid in blood
  • metabolic effects- glucose intolerance
  • erectile dysfunction w/ thiazides
  • oestrogen like effects w/ spironolactone
  • metabolic acidosis w/ carbonic anhydrase inhibitors