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Kidneys and Renal functions > Drugs and the Kidney > Flashcards

Drugs and the Kidney Flashcards

1
Q

How are kidneys related to drug excretion?

A

The kidney is the most important organ for eliminating drugs from body

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2
Q

How are drugs metabolised and excreted?

A

Most are metabolised by the liver to an inactive compound that can be excreted by kidney

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3
Q

How does drug polarity effect its excretion by the kidneys?

A

Kidney excretes polar (charged) drugs more readily than non-polar (uncharged) drugs
Non-polar (uncharged drugs) can be reabsorbed by kidney

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4
Q

How does the kidney excrete durgs?

A
  • Glomerular filtration
  • Tubular reabsorption
  • Tubular secretion
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5
Q

How much of the renal plasma flow is filtered by glomerulus?

A

Approximately 20% renal plasma flow is filtered through the glomerulus

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6
Q

How does size of molecules effect glomerular filtration?

A

Glomerular capillaries allow drugs of MW < 20kDa to be filtered freely, but not when bound on albumin (albumin MW ~ 68kDa)

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7
Q

How does the drug Warfarin’s size aid its function?

A

Anti-coagulant drug warfarin
98% bound to albumin : 2% into filtrate
This results in a long half-life – stays in the body a long time

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8
Q

What is the disadvantage of warfarin having a long half life due to their molecular size?

A

Issues of toxicity with continued dosing – e.g. excess bleeding

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9
Q

Where does tubular secretion of drugs occur?

A

Occurs mainly in proximal tubule

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10
Q

How are charged drugs secreted?

A

Non-specific cation and anion transporters for charged drugs or metabolites, e.g.
Morphine (weak base) – cation transporter
Penicillin (weak acid) – anion transporter

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11
Q

What is the polarity of most drugs metabolised and excreted?

A

Most drugs are weak acids or bases – degree of ionization depends on drug pKa and pH of environment

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12
Q

How does the non-specificity of the drug transporters effect their excretion?

A

Competition can occur between drugs at these transporters (as they are non-specific, no selective binding sites)

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13
Q

Explain how competition between penicillin and probenecid affects their half life

A

e.g. Penicillin (antibiotic) and Probenecid (removes uric acid, treat gout).
If Probenecid is administered with Penicillin, half-life of penicillin is increased – both act at anion transporter

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14
Q

What is the effect of diuretics on the kidneys?

A

Diuretics cause an increase in urine output (diuresis)

Many diuretics also produce increased Na (natriuresis) / and K excretion (hypokalaemia)

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15
Q

What are the consequences of over using diuretics?

A

Can cause hypertension, acute pulmonary oedema, heart failure

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16
Q

What are the 2 major groups of diuretics?

A
  1. Osmotic diuretics

2. Electrolyte affecting diuretics

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17
Q

What is the effect of osmotic diuretics?

A
  • Mainly affect H₂O excretion
  • Water
  • Ethanol (↓ADH release)
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18
Q

What is the role of Electrolyte affecting/K-sparing diuretics?

A
  • Increase in electrolyte excretion
  • Carbonhic anhydrase inhibitors
  • Loop diuretics
  • Thiazides
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19
Q

How do diuretics cause their effects?

A

Diuretic agents act at specific sites (6 sites along PCT (1+2) and DCT (3-6)) of the nephron and collecting ducts

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20
Q

What occurs at site 1 (PCT) due to diuretics?

A

Site 1:
Re-absorption of Na
with passive movement of organic molecules (glucose, amino acids) and H2O

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21
Q

What happens at Site 2 on PCT due to diuretics?

A

Re-absorption of Na in exchange for H - Role of carbonic anhydrase

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22
Q

Explain the events of site 3 on the DCT after taking diuretics

A

Loop of Henle - Site 3:
Transport of NaCl by Na/K/2Cl co- transporter
Thick ascending LoH impermeable to H2O
ICFV in this region becomes hypertonic
Re-absorption of H2O from CD (controlled by ADH)

23
Q

What happens at site 4 along the DCT in response to diuretics?

A

Site 4:

Re-absorption of Na/Cl (co-transporter), followed by H2O

24
Q

What events occur at site 5 on DCT after taking diuretics?

A

Site 5:

Na is reabsorbed (through ENaC channels) in exchange for K efflux (through K channels) - stimulated by aldosterone

25
Q

Outline what occurs at site 6 of the DCT in response to diuretics

A

Site 6:
Another Na-H exchanger - also stimulated by aldosterone

Sites 5 and 6 can produce K loss (in response to Na reabsorption) and alkalosis (due to increased proton excretion)

26
Q

Outline the features of the osmotic agent Mannitol

A

e.g. Mannitol - usually administered i.v.
Inert substances, freely filtered but not reabsorbed
High concentrations → ↑ Osmolarity in tubules → ↓ Reabsorption of H2O
Acts at PCT, DCT, and collecting duct
Little effect on electrolyte excretion

27
Q

What are the uses of mannitol?

A

Reduce intracranial and intraocular pressure
Prevent acute renal failure
Excretion of some types of poisoning

28
Q

How does Mannitol reduce intercranial pressure?

A

Mannitol does not enter the CNS → creates an osmotic gradient
→ H2O leaves the CNS (into plasma)

29
Q

How does Mannitol administration prevent acute renal failure?

A

Mannitol can prevent ANURIA

Distal nephron can dry up when filtration is very low

30
Q

How do electrolyte excretion agents work?

A

Drugs increase urine flow by increasing excretion of Na (natriuresis)
– where Na goes → H2O follows (osmosis)

31
Q

Which electrolyte is the major determinant of ECFV ?

A

NaCl is the major determinant of extracellular fluid (ECF) volume

32
Q

Explain the effects of increased NaCl excretion

A

↑ NaCl excretion → ↓ ECF vol → ↓ Blood vol → ↓ Cardiac output → ↓ Oedema

33
Q

Name a carbonic anhydrase (CA) inhibitor

A

Acetazolamide

34
Q

Outline the features and functions of acetazolamide

A

Mild diuretics
Inhibit the activity of CA - decrease formation of protons in the luminal cells of PCT (Site 2)
Loss of NaHCO3 into lumen - loss of H2O
Also used in non-renal effects - in glaucoma, aqueous humor formation is dependent on CA activity

35
Q

What kind of drug is frusemide?

A

Powerful loop diuretic that produces rapid effects (i.v)

36
Q

What are the roles of frusemide?

A

Inhibit Na/K/Cl co-transporter at thick ascending loop of Henle (Site 3)
↓ Reabsorption of Na, K, and 2Cl – marked loss of these electrolytes

Prevents concentration of cortico-medullary interstitial fluid and therefore reduces effect of ADH on the collecting duct (less osmotic drive) - ↑ H2O loss

37
Q

What are the clinical uses of frusemide?

A

Chronic heart failure
↓ ECFV, ↓ CVP, ↓ CO

Vasodilatation
by increase PGs in blood vessels

Acute renal failure
↑ renal blood flow

Acute pulmonary oedema
↓ Capillary pressure

38
Q

What are the major side effects of using diuretics?

A 
Significant loss of K → hypokalaemia
Metabolic alkalosis (compensatory, see thiazides)
39
Q

Name a thiazide drug

A

E.g. Bendrofluazide

40
Q

Outline features of Bendrofluazide

A

Moderately powerful diuretics

Inhibit Na/Cl uptake via co-transporter at distal convoluted tubule (Site 4)

41
Q

What are the compensatory mechanisms initiated by bendrofluazide?

A

Site 5: Na uptake via ENaC - K excretion – K loss

Site 6: Na uptake via Na/H exchanger – H loss

42
Q

What is the effects of decreased BV?

A

↓BV → ↑RAAS, ↑aldosterone → ↑Na re-absorption (sites 5/6) - ↑↑ K/H loss

43
Q

What are the uses of Bendrofluazide?

A

Treatment of hypertension
Diuresis causes ↓ BV → ↓ CO
Major effect is causing vasodilatation → ↓ TPR

Mild heart failure - ↓ ECFV
Oedema

44
Q

What are the major side effects of Bendrofluazide?

A

Hypokalaemia (loss of K)
Metabolic alkalosis (loss of H)
Hypercalcemia (Increased Ca/Na exchanger)
Hypotension (too much vasodilatation)

45
Q

Describe the diuretic action of K-sparing diuretics

A

Weak diuretic action

46
Q

Where do K-sparing diuretics act?

A

Act at end of DCT and collecting duct (Sites 5 + 6)

47
Q

What is the role of K-sparing diuretics?

A

Important as they cause K retention- counter the powerful electrolyte secretions of diuretics such as frusemide

48
Q

Name a few K-sparing diuretics

A

Spironolactone
Amiloride
Captopril

49
Q

Describe the functional features of Spironolactone

A

Competitive antagonist of aldosterone
at sites 5 and 6
CVS diseases linked to overproduction of aldosterone → volume overload, e.g. Heart failure

50
Q

What are the effects of Amiloride?

A

Blocks ENaC at site 5

Reduces Na reabsorption and K loss

51
Q

What does the K-sparing diuretic Captopril cause?

A

Inhibition of angiotensin- converting enzyme - ↓ Ang II formation - ↓ aldosterone

52
Q

What are nephrotoxic drugs?

A

These are drugs that induce kidney damage

53
Q

List examples of nephrotoxic drugs

A 
NSAIDs (commonly prescribed drugs)
Radiocontrast  agents
 Aminoglycosides (gentamicin)
Lithium (bipolar disorder)
Cyclosporine (anti-rejection)
Chemotherapy drugs
54
Q

How do NSAIDs cause kidney damage?

A

NSAIDs prevent formation of prostaglandins (PGs) by inhibiting COX
PGs are important for vasodilatation in the afferent renal arterioles
Hence, COX and PGs formation is important for renal blood flow and GFR

Kidneys and Renal functions (14 decks)

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