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Flashcards in Week 7 - Diuretics Deck (46):
1

Explain tubular reabsorption of Na and H2O in PCT

-NaKATPase on basolateral membrane sets up an Na gradient
-Na symporter on apical membrane allows Na to enter the cell down its concentration gradient
-Water follows by osmosis

2

Name the Na transporters of the PCT

-Na:glucose
-Na:a'a
-NHE

3

Name the Na transporters of the loop of henle

-NaKCC2

4

Name the Na transporters of the DCT

-NCCT

5

Name the Na transporters of the late DCT and CD

-ENaC

6

Describe Na resorption and K secretion in Late DCT and CD

-Occurs in principle cells
-NaKATPase on basolateral membrane sets up a Na Gradient
-Na enters the cell via a channel called ENaC
-Influx of Na+ produces a lumen negative potential which favours K+ secretion through K channels

7

What are the effects of aldosterone at a molecular level?

-Increases expression of NaKATPase, ENaC and K channel

8

What is meant by a potassium sparing diuretic?

-A diuretic which also decreases potassium secretion in its mechanism of action eg spironolactone

9

Which diuretics work by direct action? What is meant by this?

-Loop Diuretics
-Thiazide Diuretics
-K sparing diuretics
-> The diuretics work by directly acting on Na transporters to block them and prevent resorption and this water resorption

10

Which channels do loop diuretics work on?

-NKCC2 in LoH

11

Which channels do thiazide diuretics work on?

-NCCT in early DCT

12

Which channels do K sparing diuretics work on?

-ENaC in late DCT and CD

13

How do direct action diuretics reach their target site?

-They are secreted into the lumen in the PCT

14

Explain how a diuretic would work by antagonising the action of aldosterone? Name an example

-Aldosterone increases the expression of NaKATPase, ENaC and K channels in late DCT and CD, thus it works to increase Na and water resorption
-Competitive inhibition of aldosterone would decrease expression of these channels and thus increase renal excretion of Na and water
eg spironolactone

15

Explain how some diuretics work by modification of filtrate. Give an example

-These diuretics are small molecules which are free filtered at the glomerulus but are not reabsorbed
-They increase the osmolarity of the filtrate and thus decrease water resorption
eg mannitol

16

Explain how inhibiting the activity of carbonic anhydrase would ace as a diuretic

-Inhibition of CA -> decreased CO2 and H20 entering the cell
-Decreased activity of NHE
-Decreased Na and H2O resorption

17

Give an example of a loop diuretic

-Furosemide

18

Give an example of a diuretic which inhbits ENaC

-Amiloride

19

Which diuretics work in PCT?

-CA inhibitors

20

What is essential to ensure the continual action of NKCC2 in the loop?

-Diffusion of K back into the lumen so it can be used again

21

Which diuretic also helps to drive reabsorption of Ca and Mg?

-Loop diuretics

22

Why does decreasing resorption in the loop increase renal excretion?

-Segments downstream have limited capacity for reabsorption and thus cannot reabsorp the flodding of Na and water

23

Why are loop diuretics used in HF?

-Diuretic effect
-Vaso and venodilation reduce after/pre load

24

When are loop diuretics used?

To treat fluid retention and oedema in
-HF
-Nephrotic syndrome
-renal failure
To treat hypercalcaemia as impairs Ca resorption in the loop

25

When are thiazide diuretics used?

-Hypertension

26

Which diuretics are the least potent at Na resorption?

-K sparing

27

In what situations are K sparing diuretics contraindicated and why?

-When pt on ACE inhibitor, K supplements or patients with renal impairment
-Can lead to life threatening hyperkalaemia

28

Explain why ACE inhibitor and K sparing diuretics can cause hyperkalaemia when used together

-ACE inhibitor blocs angiotensin I to angiotensin II
-Decrease angiotensin II results in decreased aldosterone
-Decreased aldosterone increases k retention as K secretion is decreased
-K aring diuretics also cause K retention
-Together can lead to hyperkalaemia

29

When is spironolactone used?

-Hypertension due to primary hyperaldosteronism (conn's syndrome)
-Ascites and oedema in cirrhosis
-In addition to loop diuretics in HF

30

What groups of diuretics are not currently used?

-Inhibitors of carbonic anhydrase
-osmotic diuretics

31

What is an adverse effects of carbonic anhydrase inhibitor diuretics?

-Metabolic acidosis as it decreases the resorption of HCO3

32

When are carbonic anhydrase inhibitors used?

-Glaucoma as reduces aqueous humor formation

33

What is IV mannitol used to treat?

-Cerebral oedema

34

Why is there expansion of ECF in congestive heart failure?

-Increased systemic venous pressure -> oedema as fluid moves into ECF due to increased hydrostatic pressure
-Decreased CO stimulates RAAS which increased Na and H2O retention

35

Why does nephrotic syndrome lead to increased ECF?

-Increase in glomerular basement membrane to protein
-proteins such as albumin lost in urine
-Results in a lower oncotic pressure leading to peripheral oedema
-causes low circulating volume and activation of RAAS
-Na and water retention leads to more oedema

36

Why does peripheral oedema ensue in liver cirrhosis?

-Reduced albumin synthesis in liver ->Low plasma oncotic pressure ->Peripheral oedema -> Decreased CO due to low blood volume activates RAAS -> worsening oedema

37

Why does ascites occur in liver cirrhosis?

-Portal hypertension leads to an increased systemic pressure in GI circulation
-Increased hydrostatic pressure, coupled with low oncotic pressure, causes fluid to move from peritoneal capillaries to peritoneal cavity
-Decreased CO due to low blood volume activates RAAS -> worsening ascites

38

What does the rate of K secretion in DCT depend on?

-Concentration gradient of K across apical membrane
-Rate of Na absorption

39

How do loop and thiazide diuretics lead to K loss?

1)Increased Na and H2o delivery to late DCT and CD
-Increased Na resorption by ENaC
-Favours K secretion via creating lumen negative potential
2) increased flow rate -> increased removal of K in lumen -> increased conc gradient favours K secretion

40

What can you do when giving diuretics to ensure that hyper/hypokalaemia doesnt develop?

-Monitor electrolyte levels
-Give a K sparing diuretic (amiloride/spironolactone) with a K loosing diuretic (loop/thiazide) to minimise K change

41

Why can loop diuretics cause hypovolaemia?

-Decreases ECF volume by causing excretion of Na and H2O
-Loop diuretics are the most potent as the segments distal do not have capacity to resorb much water

42

List some adverse effects of diuretucs

-Potassium disturbance
-Hypovolaemia
-Hyponatraemia
-Gout

43

Why can loop and thiazide diuretics lead to gout?

-Increase uric acid levels in the blood

44

Name some substances with diuretic effects

-Alcohol
-Coffee
-Lithium

45

Name some disease which cause diuresis

-Diabetes mellitus
-Diabetes insipidus

46

What is a diuretic? When are they used?

-A substance/drug that increases urine formation via promoting renal excretion of water and sodium in order to reduce ECF volume