Drugs and the kidney Flashcards

1
Q

What is excreted more readily by the kidney?

A

→polar compounds more than non polar compounds

→non polar compounds can be reabsorbed by the kidney

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2
Q

What are the three methods of drug excretion by the kidney?

A

→ Glomerular filtration
→ Tubular reabsorption
→ Tubular secretion

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3
Q

What size do drugs have to be to be freely filtered?

A

→Smaller than 20 kDA it is freely filtered

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4
Q

What are drugs bound to that doesn’t allow them to be filtered?

A

→ when bound to albumin

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5
Q

What is the clinical importance of whether a drug is bound to albumin or not and give an example?

A

→ Warfarin
→ 98% bound to albumin
→ long half life - stays in the body for long

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6
Q

How are drugs that are not bound removed?

A

→ removed by secretion

→ non specific cation and anion transporters for charged drugs

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7
Q

How is morphine removed?

A

→ Cation transporter

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8
Q

How is penicillin removed?

A

→ Anion transporter

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9
Q

What does the degree of drug ionization depend on?

A

→ pKa and pH of environment

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10
Q

What do diuretics cause?

A

→ Increase in urine output (diuresis)

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11
Q

What do diuretics increase?

A

→ Na+ (natriuresis)

→ K+ excretion (hypokalaemia)

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12
Q

What are diuretics used for?

A

→hypertension
→acute pulmonary oedema
→ heart failure

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13
Q

What are the two major groups of diuretics?

A

→ affecting H2O excretion

→ increasing electrolyte excretion

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14
Q

What are the diuretics that affect water excretion?

A

→ water
→ ethanol (decreases ADH release)
→ osmotic diuretics

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15
Q

What are the diuretics that increase electrolyte excretion?

A

→ Carbonic anhydrase inhibitors
→ loop diuretics
→ Thiazides
→ K+ sparing diuretics

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16
Q

What is reabsorbed at the PCT and how (site 1 +2) ?

A

→ 65% of Na+ is reabsorbed
→ by the Na+ and glucose symporter
→ Na+/H+ antiport

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17
Q

What is reabsorbed at the descending looP?

A

→ Pure water

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18
Q

What is reabsorbed at the ascending loop ( site 3) ?

A

→ NaCl
→ K+
→ Cl-

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19
Q

What is reabsorbed at the DCT and how (site 4-6) ?

A

→ NaCl and H2O 4
→ Na+ through the eNAC channels in exchange for K+ - stimulated by aldosterone - 5
→ Na+/H+ exchanger - stimulated by aldosterone -6

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20
Q

How is mannitol usually administered?

A

→ I.V

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21
Q

What is mannitol and how does it pass through the kidney?

A

→ Inert substance

→ Freely filtered but not reabsorbed

22
Q

What do high concentrations of mannitol do?

A

→ Increase osmolarity in the tubules

→decrease reabsorption of H2O

23
Q

Where does mannitol act?

A

→ PCT
→ DCT
→ Collecting duct

24
Q

What are the uses of mannitol?

A

→ reduce intracranial and intraocular pressure

25
Q

How does mannitol reduce intracranial pressure?

A

→ Does not enter CNS
→ creates an osmotic gradient
→ H2O leaves the CNS into the plasma

26
Q

How does mannitol prevent acute renal failure?

A

→ if GFR drops very low
→ distal nephron can dry up
→ osmotic pressure in the tubule increases
→ water reabsorption decreases

27
Q

How do diuretics that affect electrolyte excretion work?

A

→ Increase urine flow by increasing excretion of Na+

→ Where Na+ goes H2O follow

28
Q

What is the major determinant of ECFV?

A

→ Na+

29
Q

What happens with increased NaCl excretion?

A
decreased ECF (RAAS activated)
↓
decreased blood volume 
↓
decreased cardiac output 
↓
oedema
30
Q

What is an example of a carbonic anhydrase inhibitor?

A

→ acetazolamidee

31
Q

How do carbonic anhydrase inhibitors increase urine output?

A

→ Inhibit CA activity
→ decrease formation of protons in luminal PCT cells ( site 2)
→ Loss of Na+ HCO3- into lumen
→ loss of H2O

32
Q

What non-renal things are dependent on carbonic anhydrase activity?

A

→ glaucoma

→ aqueous humor formation

33
Q

What are the most powerful diuretics called?

A

→ Loop diuretics (furosemide)

34
Q

What do loop diuretics do?

A

→ Inhibit Na/K/Cl co-transporter at thick ascending LoH
→ decreases reabsorption of Na, K and 2 Cl-
→ prevents concentration of interstitial fluid and reduces the effect of ADH on collecting duct

35
Q

What do loop diuretics do in chronic heart failure?

A

→ decrease ECFV
→ decrease pressure
→ decrease cardiac output

36
Q

What do loop diuretics do in acute renal failure?

A

→ Increased renal blood flow

37
Q

What do loop diuretics do in acute pulmonary oedema?

A

→ Decrease capillary pressure

38
Q

How do loop diuretics cause vasodilation?

A

→ Increasing PGs in blood vessels

39
Q

What are side effects of loop diuretics?

A

→ loss of K+

→ metabolic alkalosis (compensatory)

40
Q

What do thiazide diuretics do?

A

→ Inhibits Na/Cl uptake via co-transporter at DCT

41
Q

What are the uses of thiazide diuretics?

A

→ Hypertension
→ Decreased blood volume
→ decreased cardiac output

42
Q

What is the effect of thiazide diuretics?

A
→ compensation mechanisms
→ Less Na+ reabsorbed so more Na+ inside tubule 
→ More Na+ in the eNAC
→ balanced by further outflow of K+ 
→ more Na+ so further loss of H+ 
→ hypokalemia occurs
43
Q

Flowchart for what happens if blood volume drops

A
BV decreases
↓
increased RAAS
↓
increased aldosterone
↓
Increased Na+ reabsorption 
↓ 
Increased K+/H+ loss
44
Q

What are the side effects of loop diuretics?

A

→ Hypokalaemia ( loss of K+)
→ Metabolic alkalosis (loss of H+)
→ Hypercalcaemia ( increased Ca/Na exchanger)
→ Hypotension (too much vasodilation)

45
Q

Why are K+ sparing diuretics important?

A

→ cause K+ retention

→ counter powerful electrolyte secretions of diuretics such as furosemide

46
Q

Where do K+ sparing diuretics act?

A

→ End of DCT and collecting duct

47
Q

What is spironolactone?

A

→ competitive antagonist of aldosterone at sites 5&6

48
Q

What does amiloride do?

A

→ Blocks eNAC at site 5

→ reduces Na+ reabsorption and K+ loss

49
Q

What does captopril do?

A

→ Inhibits angiotensin converting enzyme
→ decreased angiotensin II formation
→ Decreased aldosterone

50
Q

What are nephrotoxic slides?

A

→ NSAIDs
→ prevent formation of prostaglandins by inhibiting COX
→ COX and PG formation is important for renal blood flow and GFR