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Physiology: Kidney > Drugs and the kidney > Flashcards

Drugs and the kidney Flashcards

1
Q

Excretion of drugs by the kidney

A

Takes place in

  • Glomerular filtration
  • Tubular reabsorption
  • Tubular secretion
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2
Q

Glomerular filtration of drugs

A

Some drugs may/may not bind to albumin. Only 20% of renal plasma flow is filtered in the glomerular. Glomerulus capillaries allow the drug of MW <20kDa to be filtered freely, but not when bound albumin.

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3
Q

What is the clinical importance of glomerular filtration for drugs?

A

Anti-coagulant drug warfarin
98% bound to albumin: 2% into the filtrate
Results in a long half -stay in the body along
Issues of toxicity with continued dosing - e.g. excess bleeding

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4
Q

Tubular secretion of drugs

A

Occurs mainly in the proximal tubule
Non-specific cation and anion transporters for charged drugs or metabolites
- Morphine (a weak base) - cation transporter
- Penicillin (weak acid) - anion transporter
Most drugs are weak acids or bases - degree of ionization depends on drug pKa and pH of the environment

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5
Q

Diuretics

A

An increase in urine output also produces Na (natriuresis)/ and K excretion (hypokalaemia).
Very important drugs - hypertension, acute pulmonary oedema, heart failure.

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6
Q

Increase in electrolyte excretion

A

Carbonic anhydrase inhibitors
Loop diuretics
Thiazides
K- sparing diuretics

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7
Q

Site 1 PCT

A

Reabsorption of Na with passive movement of organic molecules (glucose, amino acids) and water

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8
Q

Site 2 of PCT

A

Reabsorption of Na in exchange for H - the role of carbonic anhydrase

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9
Q

SIte 3 Loop of Henle

A
  • Transport of NaCl by a co-transport for Na, K, 2Cl
  • Thick ascending Loop of Henle is not permeable to water
  • Interstitial fluid in this region becomes hypertonic
  • Re-absorption of water from the collecting duct (controlled by ADH)
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10
Q

Site 4 DCT

A

Re-absorption of NA/Cl (co-transport), followed by water

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11
Q

Site 5 DCT

A

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

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12
Q

Site 6 DCT

A

Another Na- H exchanger - also stimulated by aldosterone

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13
Q

Agents that mainly affect H2O excretion

A

Osmotic agents
Mannitol - usually administered i.v.
Inert substances, freely filtered but not reabsorbed
High concentrations - increases osmolarity in tubules - decreases reabsorption of water
Act at PCT, DCT, and collecting duct
Little effect on electrolyte excretion

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14
Q

Use of osmotic agents

A

Reduces intracranial and intraocular pressure
Prevent acute renal failure
Agents that affect electrolyte excretion
Carbonic anhydrase inhibitors

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15
Q

How does intracranial and intraocular pressure decrease?

A

Mannitol doesn’t enter the CNS- creates an osmotic gradient - water leaves the CNS (into plasma)

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16
Q

How do drugs reduce renal failure

A

Mannitol can prevent Anuria

Distal nephron can dry up when filtration is very low

17
Q

How do osmotic agent affect electrolyte excretion

A
  • Drugs increase urine flow by increasing excretion of Na (natriuresis)
  • NaCl is the major determinant of extracellular fluid (ECF) volume
  • Increase NaCl excretion - decrease ECF vol- decrease blood vol, decrease Cardiac output- decrease in oedema
18
Q

Carbonic anhydrase inhibitors

A

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

19
Q

Loop diuretics

A

Frusemide
Powerful diuretics with rapid effect
Inhibit Na/K/Cl co-transport at the thick ascending loop of Henle (site 3)
Decrease 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) - increase water loss

20
Q

Uses of loop diuretics

A

Chronic heart failure - decrease ECFV, decrease CVP, decrease CO
Vasodilatation - by increase PGs in blood vessels
Acute renal failure- increase renal blood flow
Acute pulmonary oedema- decrease capillary pressure

21
Q

Side effects of loop diuretics

A 
Significant loss of K - hypokalemia 
Metabolic alkalosis (compensatory)
22
Q

Thiazide drugs

A

Moderately powerful diuretics
Inhibit Na/Cl uptake via co-transporter at distal convoluted tubule
Compensation mechanisms
Site 5: Na uptake via ENaC- K excretion - K loss
Site 6: Na uptake via Na/H exchanger - H loss
Decrease BV - increase RAAS, increase aldosterone - increase Na reabsorption (site5/6) - increase K/H loss

23
Q

Uses of thiazide

A 
Treatment of hypertension 
diuresis causes decrease BV- decrease CO
The major effect is causing vasodilation - decrease TPR
Mild heart failure - decrease ECFV
Oedema
24
Q

Side effects of thiazide drugs

A

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

25
Q

K- sparing diuretics

A

Weak diuretic action

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

26
Q

Spironolactone

A

The competitive antagonist of aldosterone at sites 5 and 6. CVS diseases linked to overproduction of aldosterone - volume overload, e.g. heart failure

27
Q

Amiloride

A

Blocks ENaC at site 5, Reduces Na reabsorption and K loss

28
Q

Captopril

A

Inhibition of angiotensin-converting enzyme - decrease Ang 2 formation - Decrease aldosterone

29
Q

NSAIDs

A

Prevent formation of prostaglandins (PGs) by inhibiting COX
PG are important for vasodilation in the afferent renal arterioles
Hence, COX and PGs formation is important for renal blood flow and GFR
Importantly: NSAIDs are contraindicated in renal failure
Exacerbate issues of poo GFR

30
Q

Drugs that induce kidney damage

A 
NSAIDs
Radiocontrast agents
Aminoglycosides (gentamicin)
Lithium (bipolar disorders)
Cyclosporine (anti - rejection)
Chemotherapy drugs

Physiology: Kidney (14 decks)

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