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Pharmacology and Therapeutics 2 Y2 > Diuretics > Flashcards

Diuretics Flashcards

1
Q

permeability of proximal tubule cells to sodium and water

A

Very permeable

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2
Q

Explain effect of the oncotic force in the kidney

A
  • Throughout the kidney there is a protein-based osmotic force (oncotic pressure) that draws water out of the lumen back into the blood
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3
Q

The paracellular route At the PCT allows …

A

Electrolytes and water

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4
Q

Where is carbonic anhydrase found in the PCT

A

On the apical cell surface and within the cell

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5
Q

What does carbonic anhydrase do

A

allows the cell to convert CO2 and H2O to H+ and HCO3- and vice versa

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6
Q

What does the apical carbonic anhydrase do and why

A

HCO3- and H+ will be converted to CO2 and H2O on the apical side of the cell, this CO2 and H2O can then enter the cell easily by diffusion

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7
Q

What does the intracellular carbonic anhydrase do

A

converts CO2 and H2O to H+ and HCO3-

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8
Q

Once intracellular carbonic anhydrase has formed H+ and HCO3-, what happens to the ions?

A

The HCO3- is then transported into the blood with Na

The H+ ions are used in an antiport protein to swap Na+ and H+ at the apical cell membrane

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9
Q

What transports water into the blood?

A

It does it itself through the osmotic gradient

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10
Q

How does Na enter the PCT cells? (2)

A

There is free movement of Na+ into the cell, accompanied by movement using Na/H antiporters

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11
Q

How are glucose and amino acids moved into PCT cells?

A

coupled to sodium movement

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12
Q

what does the PCT absorb?

A

Glucose, amino acids, H2O, Na, CO2

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13
Q

what does the PCT excrete?

A

H and exogenous drugs

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14
Q

how does the PCT recognise exogenous drugs to excrete

A

Big polar conjugate side chains that have been added on to the drugs

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15
Q

Permeability of the descending limb of the LOH to water?

A

Very permeable

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16
Q

General permeability of the ascending limb of the LOH to water? (exception?)

A

Impermeable (a little bit can move paracellularly)

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17
Q

Basal side of the membrane of the cells of the kidney lumen faces…

A

Blood

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18
Q

Apical side of the membrane of the cells of the kidney lumen face …

A

Lumen

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19
Q

Transport proteins in the DL of the LOH?

A

Not many

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20
Q

Transport proteins in the AL of the LOH?

A

Na+/Cl-/K+ triple transporter (apical)

Na/K ATPase (basal)

K/Cl cotransporter (basal)

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21
Q

what does the Na+/Cl-/K+ triple transporter do (numbers)

A

2x Cl- moved and 1x Na+ and K+ from the lumen to inside the cell

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22
Q

Which surface of the ALoftheLOH has the Na+/Cl-/K+ triple transporter

A

Apical

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23
Q

What travels paracellularly in the AL of LOH

A

Water and Na (heavily restricted)

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24
Q

Reason for the countercurrent gradient?

A
  • Promote water movement from the collecting duct Creates an osmotic gradient for water to move out of the collecting duct, into the interstitium and eventually into the blood (when vasopressin recruits aquaporins)
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25
Q

High osmolarity means concentration of water is …

A

Low

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26
Q

High osmolarity means concentration of dissolved stuff is …

A

High

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27
Q

Water moves from regions of X osmolarity to X osmolarity

A

Low to high

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28
Q

Transporters on apical surface of DCT?

A

Na/Cl cotransporter

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29
Q

Transporters on basal surface of DCT?

A

Na/K ATPase

K/Cl cotransporter

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30
Q

Effect of aldosterone on DCT, binds to what and this does what (2)

A

mineralocorticoid, binds to mineralocorticoid receptor and causes increased capacity of cells to reabsorb sodium. via More sodium channels apically and more Na+/K+ ATPase basally

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31
Q

Effect of vasopressin on DCT, binds to what and this does what (2)

A

binds to the V2 receptor, causes movement of AQP2 apically

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32
Q

Which AQP is found apically

A

AQP2

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33
Q

Which AQP is found basally

A

AQP3/4

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34
Q

Job of diuretics? (2)

A

increase excretion of salt/water in the urine

  1. Inhibit the reabsorption of Na+ and Cl- i.e. increase excretion
  2. Increase the osmolarity of tubular fluid i.e. decrease the osmotic gradient across the epithelia
35
Q

5 classes of diuretics?

A
  1. OSMOTIC DIURETICS e.g. mannitol
  2. CARBONIC ANHYDRASE INHIBITORS e.g. acetazolamide
  3. LOOP DIURETICS e.g. frusemide (furosemide)
  4. THIAZIDES e.g. bendrofluazide (bendroflumethiazide)
  5. POTASSIUM SPARING DIURETICS e.g. amiloride, spironolactone
36
Q

Where do osmotic diuretics work?

A

PCT, LOH, CD

37
Q

Where do carbonic anhydrase inhibitors work?

A

PCT

38
Q

Where do loop diuretics work?

A

AL of the LOH

39
Q

Where do thiazides work?

A

Distal tubule start

40
Q

Where do potassium sparing diuretics work?

A

Distal tubule end

41
Q

What diuretics act on the PCT?

A

Osmotic diuretics and carbonic anhydrase inhibitors

42
Q

What diuretics act on the LOH?

A

Osmotic diuretics

43
Q

What diuretics act on the AL of the LOH?

A

Loop diuretics

44
Q

What diuretics act on the start of the DCT?

A

Thiazides

45
Q

What diuretics act on the end of the DCT?

A

Potassium sparing diuretics

46
Q

What diuretics act on the CD?

A

Osmotic diuretics

47
Q

Example of a loop diuretic?

A

Frusemide

48
Q

How do loop diuretics work? (2)

A

Inhibit Na+ K+ and Cl reabsorption in ascending limb – 30% less water reabsorbed in the CD due to increased ions in tubular fluid

Increase tubular fluid osmolarity/decrease osmolarity of medullary interstitium

49
Q

What transporter do loop diuretics target?

A

Na/K/Cl triple transporter

50
Q

How do loop diuretics cause an increased K loss

A

Na/K/Cl not absorbed in the AL of LOH, DT tries to desperately absorb Na via Na/K exchanger (and Na/Cl co transporter), meaning potassium is going to be lost from blood to try Na in

51
Q

How do loop diuretics cause an increase in Ca/Mg ion loss (K recycling)

A

K+ recycling – potassium is constantly reabsorbed but also lost This constant movement of potassium constantly replenishes positive charge in the lumen which contributes to the net positive charge in the lumen – this causes calcium and magnesium and sodium (all positive) to be ‘repelled’ via the paracellular route back to the blood – Reducing this K+ recycling causes more loss of Na, Ca and Mg

52
Q

What transporter do thiazides target

A

Na/Cl cotransporter in early distal tubule

53
Q

What % of water loss do loop diuretics cause

A

about 30%

54
Q

Action of loop diuretics on Na reabsorption?

A

Inhibit Na+ K+ and Cl reabsorption in ascending limb – 30% less water reabsorbed

55
Q

Action of thiazides on Na reabsorption?

A

Inhibit Na+ and Cl- reabsorption in early distal tubule – 5-10%

56
Q

Action of loop diuretics on H2O reabsorption?

A

Increase tubular fluid osmolarity/decrease osmolarity of medullary interstitium, so less water is absorbed in the CD

57
Q

Action of thiazides on H2O reabsorption?

A

Increase tubular fluid osmolarity so causes decreased H2O reabsorption in the collecting duct

58
Q

Action of thiazides on K?

A
  • Increase delivery of Na+ to distal tubule and increase K+ loss (via increasing Na+/K+ exchanger as the Na+ is trying to be absorbed by the DT)
59
Q

Action of thiazides on Mg and Ca?

A

Increased­ Mg2+ loss and ­ increased Ca2+ reabsorption (unknown reasons, happens after chronic diuretic use)

60
Q

Problem with chronic thiazide and loop diuretic use?

A

They cause hyponatraemia over time, stimulating renin secretion (low sodium passing through lumen of distal tubule after chronic use sensed by the macula densa) – this increases sodium and water reabsorption by stimulating aldosterone (a rebound effect)

61
Q

What do we do to fight the rebound effect of thiazides and loop diuretics

A

give diuretics in conjunction with ACE inhibitors

62
Q

2 classes of K sparing diuretics?

A
  1. ALDOSTERONE RECEPTOR ANTAGONISTS (MR inhibitors)

2. INHIBITORS OF ALDOSTERONE-SENSITIVE Na+ CHANNELS

63
Q

Effectiveness of K sparing diuretics? (%)

A

5% water loss, not v powerful

64
Q

Action on Na+ reabsorption of K sparing diuretics?

A

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

65
Q

Action on H20 reabsorption of K sparing diuretics?

A

Increase tubular fluid osmolarity -> Decrease H2O reabsorption in the collecting duct

66
Q

Permeability of distal tubule to water?

A

Only permeable with AQP

67
Q

Where do AQPs act?

A

DCT

68
Q

What do ALDOSTERONE RECEPTOR ANTAGONISTs do

A

Bind to MR in distal tubule cell stopping aldosterone from increasing Na channels apically and Na/K exchangers basally

69
Q

What do INHIBITORS OF ALDOSTERONE-SENSITIVE Na+ CHANNELS

A

Block Na channels in the DCT which were in place by aldosterone effects

70
Q

What is amiloride an example of

A

INHIBITORS OF ALDOSTERONE-SENSITIVE Na+ CHANNELS

71
Q

What is spironolactone and example of

A

ALDOSTERONE RECEPTOR ANTAGONISTS

72
Q

Example of INHIBITORS OF ALDOSTERONE-SENSITIVE Na+ CHANNELS

A

Amiloride

73
Q

Example of ALDOSTERONE RECEPTOR ANTAGONISTS

A

Spironolactone

74
Q

How do K sparing diuretics lead to H+ retention

A

Decrease reabsorption of Na+ to distal tubule increase H+ retention (decrease Na+/H+ exchange)

75
Q

Side effects of K sparing diuretics? Why?

A

Hyperkalemia as there is less Na/K exchange

76
Q

Side effects of thiazides and loop diuretics? (5)

A

Hypovolemia, hyponatremia, hypokalaemia, metabolic acidosis, hyperuricemia

77
Q

Side effects of carbonic anhydrase inhibitors?

A

Metabolic acidosis

78
Q

How do loop diuretics and thiazides cause hyperuricemia

A

because they directly affect the transporter than moves uric acid into the lumen

79
Q

What does a build up of uric acid in blood lead to

A

Gout

80
Q

What can diuretics be used to treat (2)

A

Hypertension

Heart failure

81
Q

First line treatment for hypertension?

A

Thiazides

82
Q

Why use thiazides as antihypertensives instead of other diuretics

A

Chronic use of thiazides is associated with vasodilation

Could be associated with eNOS, Ca channel antagonism and K channel opening

83
Q

Why do you lose the diuretic effect after using a diuretic for about 6 weeks? How do you amend this

A

Renin increase, to fix give an ACEi

Pharmacology and Therapeutics 2 Y2 (24 decks)

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