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Y2 LCRS Pharmacology and Therapeutics > renal system > Flashcards

renal system Flashcards

renal physiology: explain the physiology of the renal system and how drugs impact ionic composition

1
Q

what areas in kidney are targeted by diuretics

A

proximal tubule, loop of Henle, distal tubule

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2
Q

structure of proximal tubule cell

A

surround lumen with microvillis, with intersitium and capillaries outside of basal interdigitation

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3
Q

physiology of proximal tubule cells: transcellular movement of H2O and Na+

A

H2O and Na+ diffuse across apical membrane of proximal tubule cell (through channels), with Na+ being exchanged for K+ (Na+/K+-ATPase) at basal membrane to ensure Na+ concentration gradient, with interstitium having oncotic pressure to draw H2O across via channels

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4
Q

physiology of proximal tubule cells: paracellular movement

A

H2O, Na+, Cl-, HCO3- move into interstitium due to oncotic pressure gradient

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5
Q

physiology of proximal tubule cells: transcellular movement of glucose and amino acids

A

associate with Na+ and pumped across apical membrane of proximal tubule cell in exchange for H+

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6
Q

physiology of proximal tubule cells: transcellular movement of HCO3-

A

HCO3- and H+ react in lumen by carbonic anhydrase on apical membrane to form CO2 and H2O, which diffuse across apical membrane of proximal tubule cell; broken down IC to H+ and HCO3- by carbonic anhydrase, with H+ exchanged for Na+ (and amino acids/glucose) at apical membrane (H+ out, Na+ in), and with HCO3- pumped out of basal membrane along with Na+

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7
Q

physiology of proximal tubule cells: exportation of exogenous agents

A

exogenous agents e.g. glucoronides attached to drugs exported into lumen

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8
Q

% of filtered Na+ absorbed in proximal tubule

A

65-70%

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9
Q

physiology of descending limb of loop of Henle: transcellular pathway

A

H2O permeable, ion impermeable; H2O diffuses across cell from isotonic lumen to hypertonic interstitium via channels

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10
Q

physiology of ascending limb of loop of Henle: transcellular pathway

A

H2O impermeable, ion permeable; Na+, 2Cl- and K+ pumped in across apical membrane of ascending limb cell via triple transporter, with Na+ pumped out in exchange for K+, and K+ and Cl- pumped out together, across basal membrane (K+ can diffuse across apical membrane also, and Cl- can diffuse across basal membrane also)

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11
Q

physiology of ascending limb of loop of Henle: paracellular pathway

A

Na+ absorbed

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12
Q

describe countercurrent effect of kidney in loop of Henle

A

loop filled with isotonic fluid -> Na+ pumped from ascending limb (so fluid in ascending lumb decreases osmolarity) -> descending tubule increases osmolarity (permeable to water so water drawn into medullary interstitium) -> more fluid enters and forces fluid from descending to ascending limb, which has increased osmolarity -> second/third etc. round of Na+ pumping

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13
Q

how is countercurrent effect important in collecting duct

A

when aquaporins inserted, water flows into interstitium down concentration gradient

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14
Q

physiology of distal tubule cell: transcellular pathway H2O

A

late: early stage is H2O impermeable, but in late stage H2O diffuses in through AQP2 (apical) and into interstitium through AQP3/4 (basal), in presence of ADH (and V2)

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15
Q

physiology of distal tubule cell: transcellular pathway ions

A

early: Na+ and Cl- contransported across apical membrane, with Na+ exchanged for K+ at basal membrane, and K+ and Cl- cotransported across basal membrane; late: aldosterone binds to MR, increasing Na+ absorption

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16
Q

physiology of collecting duct cell: transcellular pathway

A

similar as distal tubule cell with regard to water and ions, with H2O reabsorbed in presence of ADH (and V2)

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17
Q

2 methods of action of diuretics in kidney

A

inhibit reabsorption of Na+ and Cl- (increase excretion), increase osmolarity of tubular fluid (decrease osmotic gradient across epithelia)

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18
Q

5 main classes of diuretics

A

osmotic diuretics, carbonic anhydrase inhibitors, loop diuretics, thiazides, K+-sparing diuretics

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19
Q

location of action of osmotic diuretics

A

proximal tubule, descending limb of loop of Henle, collecting duct

20
Q

location of action of carbonic anhydrase inhibitors

A

proximal tubule

21
Q

location of action of loop diuretics

A

ascending limb of loop of Henle

22
Q

location of action of thiazides

A

distal tubule (early)

23
Q

location of action of K+-sparing diuretics

A

distal tubule (late) and collecting duct

24
Q

example of osmotic diutetic

A

mannitol

25
Q

example of carbonic anhydrase inhibitor

A

acetazolamide

26
Q

example of loop diuretic

A

frusemide

27
Q

action of frusemide on Na+ reabsorption from ascending limb of loop of Henle

A

inhibit Na+ and Cl- reabsorption in triple transporter, interfering with counter current effect

28
Q

action of frusemide on H2O reabsorption from ascending limb of loop of Henle

A

increase tubular fluid as interferes with counter current effect, increases tubular fluid osmolarity and decreases osmolarity of medullary interstitium, causing decrease of H2O reabsorption in collecting duct; powerful so can cause large amounts of water loss

29
Q

what action does frusemide have in common with thiazides

A

increased delivery of Na+ to distal tubule, increasing K+ loss (increase Na+/K+ exchange), causing hypokalaemia

30
Q

effect of frusemide on Ca2+ and Mg2+ reabsorption and why

A

loss of K+ recycling, so as K+ recycling drives positive lumen potential, Ca2+ and Mg2+ less well absorbed through paracellular route

31
Q

example of thiazide

A

bendrofluazide

32
Q

action of bendrofluazide on Na+ reabsorption from early distal tubule

A

inhibit Na+ and Cl- reabsorption (cotransport protein) in early distal tubule

33
Q

action of bendrofluazide on H2O reabsorption from distal tubule

A

increase tubular fluid osmolarity so decrease H2O reabsorption in collecting duct; less powerful as not affecting counter current effect

34
Q

what action does bendrofluazide have in common with loop diuretics

A

increased delivery of Na+ to distal tubule, increasing K+ loss (increase Na+/K+ exchange), causing hypokalaemia; less so than loop diuretics as affects later on and affect countercurrent

35
Q

effect of thiazides on Mg2+ and Ca2+

A

increase Mg2+ loss (hypokalaemia causing inhibition of distal tubular cell Mg2+ uptake), increase Ca2+ reabsorption (increased proximal Na+ and H2O reabsorption due to volume depletion, leading to increased passive proximal Ca2+ reabsorption)

36
Q

problem of thiazides and loop diuretics in macula densa cells (RAAS)

A

if take long-term, promote Na+ and water loss, so as reduced renal perfusion pressure and loss of Na+ concentration at distal convoluted tubule, more renin released from granular cells (bigger issue with loop diuretics as stops Na+ entering macula densa cell)

37
Q

2 examples of K+-sparing diuretics

A

amiloride, spironolactone

38
Q

S47

A

S47

39
Q

2 classes of K+-sparing diuretics

A

aldosterone receptor antagonists (spironolactone), inhibitors of aldosterone-sensitive Na+ channels (amiloride)

40
Q

mechanism of action of spironolactone

A

inhibits aldosterone action of pumping Na+ into distal tubule cell (blocks new Na+ channels being created), and Na+ pumping across basal membrane into interstitium (blocks new Na+/K+-ATPase being created)

41
Q

mechanism of action of amiloride

A

prevent Na+ being pumped into distal tubule cell through Na+ channels

42
Q

action of K+-sparing diuretics on Na+ reabsorption from distal tubule

A

inhibit Na+ reabsorption (and concomitant K+ secretion) in early distal tubule

43
Q

action of K+-sparing diuretics on H2O reabsorption from distal tubule

A

increase tubular fluid osmolarity so decrease H2O reabsorption in collecting duct (as furthest along, worst diuretic at preventing water reabsorption)

44
Q

action of K+-sparing diuretics due to decreased Na+ reabsorption from distal tubule

A

increased H+ retention (as reduced Na+/H+ exchange)

45
Q

5 common side effects of loop diuretics and thiazides

A

metabolic alkalosis (Cl- loss), hypovolemia, hyponatraemia, hypokalaemia, hyperuricemia

46
Q

common side effect of K+-sparing diuretics

A

hyperkalaemia (less Na+/K+ exchange)

47
Q

how is hyperuricemia a common side effect of diuretics

A

diuretic must get from bloodstream to other side of lumen, so excreted by kidney into lumen (accesses target); transport protein is same that excretes uric acid, so diuretic competes, so uric acid builds up in blood

Y2 LCRS Pharmacology and Therapeutics (68 decks)

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