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renal > drugs acting on the kidney > Flashcards

drugs acting on the kidney Flashcards

1
Q

what are the role of diuretics?

A
  • increase urine flow, normally by inhibiting the reabsorption of electrolytes (mainly sodium salts) at various sites in the nephron
  • are used to enhance excretion of salt and water in conditions where an increase in the volume of extracellular fluid (i.e. oedema) causes tissue swelling
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2
Q

what causes oedema?

A

-oedema results from an imbalance between the rate of formation and the absorption of interstitial fluid

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3
Q

what is the formation of interstitial fluid proportional to?

A

formation of interstitial fluid= (Pc - Pi) - (Pip - Pii)

Pc= Capillary pressure (pushes out of capillary)
Pi= capillary pressure (moves both ways in capillary)
Pip= oncotic pressure (moves into the capillary)
Pii= oncotic pressure (moves out of capillary)
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4
Q

what diseases may causes an increase in Pc or decrease in Pip causing oedema?

A
  • nephrotic syndrome
  • congetive heart failure
  • hepatic cirrhosis with ascites
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5
Q

what is nephrotic syndrome?

A

-a disorder of glomerular filtration, allowing protein (largely albumin) to appear in the filtrate (proteinuria)

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6
Q

what effect does nephrotic syndrome have on oncotic pressure (Pip)?

A

it decreases it

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7
Q

what effect does decrease in oncotic pressure (Pip) from nephrotic syndrome have?

A

-this increases formation of interstitial fluid which can lead to oedema

  • increase in interstitial fluid also causes a decrease in blood volume + decrease in cardiac output
  • RAAS system becomes activated
  • Na+ and H2O retention
  • this increases capillary pressure (Pc) and due to water being added into the blood the oncotic pressure decreases further (Pip) leading to oedema getting worse
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8
Q

what causes congestive heart failure?

A

-reduced cardiac output

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9
Q

how does congestive heart failure cause oedema?

A
  • reduced cardiac output from congestive heart failure
  • subsequent renal hypo perfusion activates RAAS
  • expansion of blood volume contributes to increased venous and capillary pressures which, combined with reduced oncotic pressure (PiP) causes pulmonary and peripheral oedema
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10
Q

how does septic cirrhosis with ascites cause oedema?

A
  • increased pressure in the hepatic portal vein, combined with production of albumin causes loss of fluid in the peritoneal cavity and oedema (ascites)
  • activation of RAAS occurs in response to decreased circulating volume
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11
Q

role of diuretics in tubules

A
  • block sodium reabsorption

- block movement of accompanying water (in those parts of the tubule that are permeable to water)

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12
Q

where do loop diuretics affect in the tubule?

A

thick ascending limb of the loop of Henle

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13
Q

where do thiazide diuretics affect ?

A

-distal convoluted tubule

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14
Q

where do potassium sparing diuretics affect?

A

-collecting tubules

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15
Q

is H2O permeable in the ascending limb of the loop of Henle?

A

no

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16
Q

where is the site of action of thiazide, loop and potassium sparing diuretics?

A
  • apical membrane of tubular cells

- so if hydrophilic they must enter the filtrate to access that site

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17
Q

how my diuretics enter the filtrate?

A
  • glomerular filtration (for drug not bound to plasma protein)
  • secretion via transport process in the proximal tubule
  • two transport systems are important (the organic anion transporters and the organic cation transporters)
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18
Q

how do diuretics enter the cell using organic anion transporters at the basolateral membrane?

A
  • at the basolateral membrane organic anions (OA) enter cell by either diffusion or in exchange for alpha- ketoglutarate via OATs
  • alpha ketoglutarate is transported into cell (against a concentration gradient) via a Na+ decarboxylate transporter
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19
Q

how do diuretics enter the apical membrane using organic anion transporters?

A

-at the apical membrane, OA enters the lumen via either multi drug resistance protein 2 (MRP2) or OAT4 (in exchange for alpha ketoglutarate)

20
Q

mechanism of action of loop diuretics?

A
  • act on the loop of henle
  • block the cotransporter molecule preventing active transport of sodium, potassium and water into the interstitial fluid (resulting in more water, potassium and sodium in urine)
21
Q

give examples of loop diuretics

A
  • furesomide

- bumetanide

22
Q

side effects of loop diuretics?

A
  • hypokalameia
  • hypotension
  • AKI
  • urinary retention (where outflow restricted and increase in production of urine)
  • worsen diabetic control (hyperglycaemia)
  • exacerbate gout
  • ototoxicity (damage to inner ear)
23
Q

role of thiazide diuretics?

A

-decrease sodium and water in the body

24
Q

what are thiazide diuretics used to treat?

A
  • hypertension

- oedema

25
Q

examples of thiazide diuretics?

A
  • bendroflumethiazide

- indapamide

26
Q

what part of the kidneys do thiazide diuretics affect?

A

distal tubule

27
Q

mechanism of action of thiazide diuretics?

A
  • act on the distal tubule
  • blocks thiazide sensitive sodium chloride co transporter, blocking reabsorption of sodium and chloride from the filtrate into the blood
28
Q

what are examples of potassium sparing diuretics?

A
  • amiloride
  • triamterene
  • spironolactone
  • eplerenone
29
Q

mechanism of action of amiloride and triamterene?

A

-block the apical sodium channel and decrease Na+ reabsorption

30
Q

mechanism of action of spironolactone and eplerenone?

A

-compete with aldosterone for binding to intracellular receptors preventing the actions of the steroid described previously

31
Q

what’s an example of an osmotic diuretic?

A

mannitol IV

32
Q

why must osmotic diuretics be administered by IV?

A

-as they are membrane impermanent

33
Q

where are the major sites of action of osmotic diuretics?

A
  • proximal tubule where most iso osmotic reabsorption of water occurs
  • secondarily also decrease sodium reabsorption in the proximal tubule (larger fluid volume decreases sodium concentration and electrochemical gradient for reabsorption)
34
Q

when are osmotic diuretics used?

A
  • in prevention of acute hypovolaemic renal failure to maintain urine flow
  • in urgent treatment of acutely raised intracranial and intraocular pressure. The solute does not enter the eye, or brain, but increased plasma osmolality extracts water from these compartments
35
Q

what are side affects of osmotic diuretics?

A

-transient expansion of blood volume and hyponatramia

36
Q

what is an example of a carbonic anhydrase inhibitor?

A

-acetazolamide

37
Q

role of carbonic anhydrase inhibitors?

A
  • increase excretion of HCO3 with Na+ and H2O

- results in alkaline diuresis and metabolic acidosis

38
Q

what are carbonic anhydrase inhibitors useful in?

A
  • glaucome and following eye surgery (to reduce intraocular pressure by suppressing formation of aqueous humour)
  • prophylaxis of altitude sickness
  • some forms of infantile epilepsy
39
Q

what is diabetes insipidus?

A
  • symptoms similar to diabetes mellitus (thirst, polydipsia, polyuria)
  • disturbance of signalling by vasopressin (ADH)
  • neurogenic diabetes insipidus (lack of vasopressin secretion from the posterior pituitary)
40
Q

what is neurogenic diabetes insipidus treated with?

A

-desmopressin

41
Q

what is neurogenic diabetes insipidus?

A

-lack of vasopressin secretion from the posterior pituitary

42
Q

what is nephrogenic diabetes insipidus?

A

-inability of the nephron to respond to vasopressin

43
Q

what are aquaretics or vaptans?

A

-act as competitive antagonists of vasopressin receptors (which occur as V1A, V1B and V2 GPCR subtypes)

44
Q

what do V1A receptors mediate?

A

-vasoconstriction

45
Q

what do V2 receptors mediate?

A

H2O reabsorption in collecting tubules by directing aqua poring 2 (AQP2) containing vesicles to the apical membrane

46
Q

what does blockade of V2 receptors cause?

A

-excretion of water without accompanying Na+ and thus raises plasma Na+ concentration

47
Q

what is used to correct hyponatramia in SIADH?

A

tolvaptan

renal (37 decks)

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