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Renal > Drugs that Act on the Kidneys III > Flashcards

Drugs that Act on the Kidneys III Flashcards

1
Q

What is an example of an osmotic diuretic?

A

Mannitol IV

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2
Q

What are osmotic diuretics?

A

Membrane impermeant polyhydric alcohols = pharmacologically inert

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3
Q

How do osmotic diuretics enter the nephron?

A

By glomerular filtration = are not reabsorbed

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4
Q

What effect do osmotic diuretics have on the filtrate?

A

Increase the osmolarity = opposes the absorption of water in parts of the nephron that are freely permeable to water

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5
Q

Where is the major site of action in the kidneys of osmotic diuretics?

A

The proximal tubule = area where most iso-osmotic reabsorption of water takes place

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6
Q

What is the secondary action of osmotic diuretics in the proximal tubule?

A

Decrease sodium reabsorption = larger fluid volume decreases sodium concentration and electrochemical gradient for reabsorption

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7
Q

What are the uses of osmotic diuretics?

A

Prevention of acute hypovolaemic renal failure to maintain urine flow
Urgent treatment of acutely raised intracranial and intra-ocular pressure

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8
Q

What are the adverse effects of osmotic diuretics?

A

Transient expansion of blood volume, hyponatraemia

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9
Q

How can hyperglycaemia cause osmotic diuresis?

A

Reabsorptive capacity of proximal tubule for glucose is exceeded = glucose remaining in filtrate retains fluid

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10
Q

How can iodine-based radiocontrast dyes cause osmotic diuresis?

A

Dye filtered at glomerulus but not reabsorbed = constitutes osmotic load

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11
Q

What is an example of a carbonic anhydrase inhibitor?

A

Acetazolamide = increases excretion of HCO3-with Na+, K+ and H2O

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12
Q

What do carbonic anhydrase inhibitors cause?

A

Alkaline diuresis and metabolic acidosis

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13
Q

What conditions are carbonic anhydrase inhibitors used to treat?

A

Glaucoma and following eye surgery
Prophylaxis of altitude sickness
Some forms of infantile epilepsy

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14
Q

What are the benefits of alkanising urine?

A

Relief of dysuria, prevention of weak acid crystallisation, enhanced weak acid excretion

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15
Q

What does aldosterone cause in the kidneys?

A

Enhanced tubular Na+ reabsorption and salt retention

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16
Q

What does ADH cause?

A

Enhanced H2O reabsorption

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17
Q

What are the symptoms of diabetes insipidus?

A

Similar to diabetes = polyuria, thirst, polydipsia

Urine is copious and dilute

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18
Q

What is neurogenic diabetes insipidus?

A

Lack of ADH secretion from posterior pituitary = treated with desmopressin

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19
Q

What is desmopressin?

A

Synthetic analogue of ADH with V2 selectivity

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20
Q

What is nephrogenic diabetes insipidus?

A

Inability of nephron to respond to ADH = rare, caused by recessive and X-linked mutations in AVPR2

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21
Q

What are some substances that inhibit the action of ADH?

A

Lithium, demeclocycline, vaptans

22
Q

What are vaptans?

A

Act as competitive antagonists of ADH receptors = V1A, V1B, V2

23
Q

What do V1A receptors mediate?

A

Vasoconstriction

24
Q

What do V2 receptors mediate?

A

H2O reabsorption in collecting tubule = direct AQP2-containing vesicles to apical membrane

25
Q

What does block of V2 receptors cause?

A

Excretion of water without accompanying Na+ = raises plasma Na+ concentration

26
Q

What are some indications of vaptan use?

A

Hypervolaemic hyponatraemia = to reduce preload

Tolvaptan can be used in syndrome of inappropriate ADH to correct hyponatraemia

27
Q

What are some examples of vaptans?

A 
Conivaptan = V1A and V2 antagonist
Tovaptan = V2 antagonist
28
Q

Where does reabsorption of glucose occur?

A

In the proximal tubule of the kidney mediated by SGLT1 and SGLT2

29
Q

When does glucose appear in the urine?

A

Reabsorption normally 100% = glucose only appears in urine if filtrate concentration of glucose exceeds renal threshold (about 11 mmol/l)

30
Q

Where are SGLT1 and SGLT2 expressed?

A 
SGLT1 = by enterocytes and the kidneys 
SGLT2 = almost exclusively confined to the proximal tubule
31
Q

What effect do drugs that selectively block SGLT2 have?

A

Only have an effect on renal reabsorption of glucose

32
Q

How much glucose is reabsorbed by SGLT1 and SGLT2?

A 
SGLT2 = S1 segment, reabsorbs up to 90% 
SGLT1 = S2 and 3 segments, reabsorbs up to 10%
33
Q

How is glucose reabsorbed in the proximal tubule?

A

By secondary active transport and the apical membrane and facilitated diffusion at the basolateral membrane

34
Q

How do SGLT1 and SGLT2 transport glucose against a concentration gradient?

A

By coupling it to Na+ influx

35
Q

What is the transport stoichiometry of SGLT1 and SGLT2?

A 
SGLT1 = 2Na+:1 glucose, high affinity, low capacity
SGLT2 = 1Na+:1 glucose, low affinity, high capacity
36
Q

What does SGLT2 inhibition result in?

A

Glucosuria

37
Q

What are some examples of SGLT2 inhibitors?

A

Canagliflozin, dapagliflozin, empagliflozin

38
Q

What are the effects of SGLT2 inhibitors?

A

Excretion of glucose, decrease in HBA1c, weight loss

Adverse effects = genital bacterial and fungal infections

39
Q

What are prostaglandins?

A

Part of prostanoid family = formed from fatty acid arachidonic acid by COX 1 and 2

40
Q

What are some features of prostaglandins?

A

Act as vasodilators and are natriuretic

Synthesised in response to ischaemia, mechanical trauma, angiotensin II, ADH and bradykinin

41
Q

What are the two major prostaglandins synthesised by the kidney?

A 
PGE2 = medulla
PGI2 = glomeruli
42
Q

What effect do prostaglandins have in normal conditions?

A

Have very little effect on renal blood flow or GFR

43
Q

Under what conditions do prostaglandins cause compensatory vasodilation?

A

During decrease effective arterial blood volume or vasoconstriction

44
Q

How do prostaglandins affect GFR?

A

Direct vasodilator effect upon afferent arteriole
Releases renin leading to increased levels of angiotensin II
Vasoconstricts efferent arteriole (increases filtration pressure)

45
Q

Why can NSAIDs cause acute renal failure in conditions where renal blood flow is dependent on prostaglandin compensatory action ?

A

Inhibit COX so may reduce prostaglandins = occurs in liver cirrhosis, heart failure and nephrotic syndrome

46
Q

What is three drugs make up the “triple whammy” effect that may cause acute renal failure in conditions dependent on compensation by prostaglandins?

A

ACE inhibitors/ARBs, diuretics and NSAIDs

47
Q

What is uric acid formed as a result of?

A

Purine synthesis

48
Q

What does elevated plasma urate predispose to?

A

Gout

49
Q

What are some examples of uricosuric agents?

A

Probenecid and sulfinpyrazole = may help treat gout by blocking absorption of urate in proximal tubule

50
Q

What are the points of action of uricosuric agents?

A

Urate secretion = blocked by low sub-therapeutic doses

Urate secretion and reabsorption = blocked by therapeutic doses, net effect is enhanced excretion

Renal (36 decks)

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