Week 7 - Diuretics Flashcards

(24 cards)

1
Q

How does tubular reabsorption of sodium occur?

A

Sodium pumped across basolateral membrane by nakatpase
Sodium then moves across apical down conc gradient via transporter
Water follows
Potassium goes opposite way due to depleted positive charge left by removal of sodium

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2
Q

Which transporters are in the PCT

A

NaH antiporter, Na - glucose symporter and Na - amino acid symporter

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3
Q

Which transporters are in the loop of henle

A

NaK2Cl symporter

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4
Q

Which transporters are in early distal tubule?

A

NaCl symporter

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5
Q

Which transporters are used in the late DT and CD.

A

ENaC

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6
Q

Where are the principle cells?

A

collecting duct

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7
Q

What effect does aldosterone have on the transporters of the collecting tubule?

A

Increases expression of the nakatpase, ENaC and potassium channels

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8
Q

Where do loop diuretics work and what do they do?

A

They work in the TAL of LoH. They block the NaK2Cl cotransporter

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9
Q

Give two examples of a loop diuretic

A

Furosemide and bumetanide

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10
Q

Why are loop diuretics the most potent diuretic?

A

Because 25% of sodium is absorbed in the loop of henle via the nak2cl and the segments beyond have limited capacity to reabsorb the resulting flood of sodium and water

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11
Q

What are loop diuretics used in treatment?

A

Heart failure - use as a diuretic and vasodilatation which reduces after load and preload
Acute pulmonary oedema - furosemide given IV - rapid action
Fluid retention and oedema - nephrotic syndrome , renal failure, cirrhosis
Treat hypercalcaemia

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12
Q

Where are thiazides active and how do they work?

A

They work in the distal convoluted tubule and they work by inhibiting sodium chloride cotransporter

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13
Q

Give two examples of thiazides

A

Bendroflumethiazide and metalozone

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14
Q

What is different about the effect of blocking the sodium channel with loop diuretics and blocking it with thiazides?

A

LD decreases calcium absorption

Thiazides increases calcium absorption

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15
Q

What are the two types of potassium sparing diuretics?

A

1) inhibitors of the ENaC - amiloride

2) aldosterone antagonists - spironolactone

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16
Q

When should potassium sparing diuretics not be used?

A

When using ACE inhibitors, potassium supplements or patients with renal impairment - lead to hyperkalaemia

17
Q

When is spironolactone best suited for treatment?

A

Hypertension caused by primary hyperaldosteronism
As cites and oedema caused by cirrhosis
In addition to loop diuretics in heart failure

18
Q

What are the risks of using carbonic anhydrases

A

Can cause metabolic acidosis due to loss of HCO3- in urine

19
Q

What are carbonic anhydrases used for

A

Treatment of glaucoma as it reduces aqueous humour in eye by50%

20
Q

When would mannitol be used and what is it an example of?

A

Osmotic diuretic - treat cerebral oedema

21
Q

Glomerular disease leads to an increased in glomerular basement membrane permeability to protein, what will the effects of this be?

A

Increased protein lost in the urine, causing low plasma albumin resulting in low plasma oncotic pressure = peripheral oedema, reduced circulating volume, increased RAAS, sodium and water retention = expansion of ECF

22
Q

What is the pathogen exists of oedema and ascites in cirrhosis of the liver

A

Reduced albumin synth is liver causes low plasma albumin resulting in low plasma oncotic pressure = peripheral oedema. This results in increased venous pressure in splanchnic circulation - the high venous pressure and low oncotic pressure results in movement of fluid in peritoneal capillaries in to peritoneal cavity. Results in reduced circ volume = RAS activated = worse oedema

23
Q

What are the adverse effects of diuretics?

A

Potassium abnormalities
Hypovolaemia
Hyponatraemia
Uric acid levels in blood can precipitate attack of gout
Metabolic effects - glucose intolerance, increased ldl levels

24
Q

What do diuretics do?

A

Increase the fraction excretion of sodium by blocking reaborption of sodium by the tubule. Usually it is less than 1%