Manipulating Kidney Function

Question 1

Tubulo-glomerular feedback is influenced heavily by the __________ system.
__________ Drugs inhibit this process.

Answer 1

influenced by the RAAS
NSAID drugs inhibit it/

Question 2

When tubular fluid is high, the GFR is…..

Answer 2

reduced (less time)

Question 3

What is the role of the RAAS in the Kidney?

Answer 3

Angiotensin II constricts the efferent arteriole and enhances Sodium and water absorption by the Proximal Convoluted Tubule

Question 4

What is the role of Prostoglandin and NO in the kidney?
What drugs inhibit this?

Answer 4

They act as vasodilators
They also signal renin release to protect the afferent arteriole from excessive vasoconstriction when blood pressure drops
NSAIDs inhibit this (target COX-1 and COX-2 which are involved in renin secretion)

Question 5

The diuretic mechanism of action (ADH) aims to… (3)

Answer 5

Inhibit sodium chloride reabsorption to increase salt and water excretion
Counter act salt and water retention in heart failure
Activate Renin secretion

Question 6

What is the most common type of diuretic used in practice?

Answer 6

Loop Diuretics- specifically Furosemide

Question 7

Where and how do Loop Diuretics work?

Answer 7

Act on the Ascending loop of Henle to ensure more water stays in the tubules to allow Diuresis

Question 8

How do Loop Diuretics reach their site of action?

Answer 8

Heavily plasma protein bound- secreted by Proximal Convoluted Tubule to reach the loop of henle

Question 9

When given I/V what is the onset, peak and duration of Furosemide?

Answer 9

Onset- 5 mins
Peak effect- 30 mins
Duration- 2 hours

Question 10

Can Furosemide be used to treat Hypercalcaemia?

Answer 10

Yes- increases the excretion of calcium by inhibiting calcium co transporters in the Loop of Henle

Question 11

Where do Thiazidine Diuretics exert their action?

Answer 11

Act on the early distal tubule

Question 12

How do Thiazidine Diuretics work?

Answer 12

Bind to the Chlorine site of the NaCl co transporter- The NaCl transporter normally facilitates the absorption of sodium from the distal tubules back to the interstitium- blocking it promotes calcium retention in the blood

Question 13

What is the onset, peak and duration of action of Thiazidine Diuretics?

Answer 13

Onset- 1 hour
Peak- 4 hours
Duration- 6-12 hours

Question 14

Why is there a risk of Hypokalaemia when using Thiazidine Diuretics?

Answer 14

Thiazidines cause RAAS activation- Aldosterone from the RAAS pathway enhances the excretion of K+

Question 15

What can we use to reduce the risk of Hyperkalaemia with Diuretic use?

Answer 15

Use potassium sparing diuretics- act on the cortical connecting tubule to inhibit aldosterone and prevent sodium reabsorption which prevents excessive excretion of K+ in urine

Question 16

Which Potassium Sparing Diuretic is a competitive antagonist on the Aldosterone receptors?

Answer 16

Spironolactone

[Triamterene and Amiloride are non competitive]

Question 17

What is the main adverse action of diuretics?

(not hyperkalaemia)

Answer 17

They’re all vasodilatory so can reduce preload and cause Hypovolaemia (reduced blood circulating)

Question 18

How do NSAIDs and Renal Prostoglandins interact?

Answer 18

In heart failure- Renal Prostoglandins are Natriuretic (salt losing), NSAIDs increase salt and water retention to reduce the efficacy of the diuretics