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Pharmacology Flashcards

1
Q

name 6 classes of drugs which act on the kidney

A

diuretics
vasopressin receptor agonists/antagonists
SGLT2 (sodium-glucose co-transporter 2 inhibitors)
uricosuric drugs (promote excretion of uric acid)
drugs for renal failure
drugs altering pH of urine

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2
Q

what do diuretics do?

A

increase urine flow, normally by inhibiting reabsorption o electrolytes (sodium) in nephron
enhance excretion of salt and water in conditions where increased volume of ECF (e.g oedema/tissue swelling)

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3
Q

what causes oedema?

A

imbalance between rate of secretion and absorption of interstitial fluid
- hydrostatic pressure in capillary (Pc)
hydrostatic pressure in interstitial fluid (Pi)
- oncotic pressure of plasma (Mp)
- oncotic pressure of interstitial fluid (Mi)

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4
Q

calculation for formation of interstitial fluid?

A

(Pc-Pi) - (Mp - Mi)

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5
Q

name 3 disease states which can increase Pc or decrease Mp

A

nephrotic syndrome
congestive heart failure
hepatic cirrhosis with ascites

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6
Q

what causes nephrotic syndrome?

A

disorder of glomerular filtration allowing for large proteins (mainly albumin) to appear in urine

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7
Q

is protein in the urine always abnormal?

A

no

small proteins can occur in urine after heavy exercise

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8
Q

how does decreased plasma oncotic pressure cause oedema/

A

decreased Mp > increased formation of interstitial fluid > reduced blood volume and CO > activation of the RAAS > aldosterone and angiotensin II cause Na+ and H2O retention > only salt and water added back, not protein so protein concentration in the blood is diluted > reduces plasma oncotic pressure even further and increases Pc > oedema

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9
Q

how does heart failure cause oedema?

A

reduced CO > renal hypoperfusion > activation of RAAS > blood volume expands and protein conc decreases > increased Pc and decreased Mp > oedema

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10
Q

how does cirrhosis cause ascites?

A

increased pressure at portal vein + decreased albumin production > loss of fluid into peritoneal cavity > oedema/ascites > RAAS activated

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11
Q

how do diuretics work (diagram)?

A

..

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12
Q

how is Na+ reabsorbed in the proximal tubule and what blocks this?

A

Na+/H+ exchange
blocked by carbonic anhydrase inhibitors (diuretics)
- site of 70% of sodium reabsorption

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13
Q

how is Na+ reabsorbed in the thick ascending limb of loop of henle and what blocks this?

A

triple co-transporter - Na+/K+/2Cl-

blocked by loop diuretics

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14
Q

how is sodium reabsorbed in the early distal tubule?

A

Na+/H+ exchange
- blocked by CA inhibitors
Na+/Cl- (mainly)
- blocked by thiazide diuretics

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15
Q

how is Na+ reabsorbed in the collecting tubule and duct?

A

Na+/K+ exchange

- blocked by potassium sparing diuretics

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16
Q

what type of diuretic can cause hypokalaemia?

A

any which increases reabsorption of Na+ in distal tubule (apart from potassium sparing ones)

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17
Q

a small inhibition of reuptake of NaCl can cause a large increase in Na+ excretion, true or false?

A

true

- as so much sodium is filtered

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18
Q

where do most diuretics act?

A

apical membrane of tubular cells

- therefore must enter the filtrate to act on these cells

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19
Q

how can diuretics enter the filtrate?

A

glomerular filtration (cant enter glomerular filtration if bound to large plasma proteins)
organic anion transporter (transport acidic drugs - thiazides and loops)
organic cation transporter (transport basic drugs - triamterene and amiloride)

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20
Q

secretion of diuretic into the filtrate allows what?

A

concentrate the diuretic in the filtrate (urine)

gives pharmacological selectiveness of the drug (makes sure it only works in renal system)

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21
Q

describe the organic anion transporter

A

basolateral and apical transport processes
basolateral
- anions enter cell against conc gradient in exchange for α-KG via OAT channels
- α-KG enters cell against conc gradient via NaDC3 transporter
apical membrane
- once in the cell, anion crosses to the lumen via multidrug resistance proteins 2 and 4 and BCRP via primary active transport
- anion crosses from the lumen via OAT4 channel in exchange for α-KG

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22
Q

name drugs which use anion transporter

A 
diuretics
simvastatin
penicillin
NSAIDs
endogenous urate
23
Q

how do diuretics increase acute gout risk?

A

impair ability to secrete urate out of the blood and into the urine (organic anion transporter)

24
Q

describe organic cation transporter

A

basolateral membrane
- organic cations enter cell via OCT2 channel driven by -ve potential, against conc gradient
apical membrane
- cation enters the lumen in rate limiting manner via electroneutral multidrug and toxin extrusion transporters (MATES) an active transport via MDR1

25
what drugs use organic cation transporter?
``` diuretics atropine metformin morphine procainamide catecholamines ```
26
...
blocks triple transporter > low intracellular Na+ > drives reabsorption of Na+
27
...
...
28
what are the 2 principle loop diuretics and how do they work in general terms?
furosemide bumetanide inhibit the triple transporter by binding to the Cl- site and thus
29
what is the impact of inhibiting the triple transporter?
decrease tonicity of medulla interstitium prevent dilution of filtrate in thick ascending limb increase load of Na+ delivered to distal nephron causing K+ loss increased excretion of calcium and magnesium causes 15-25% of filtered Na+ to be excreted
30
what additional action of loop diuretics can be helpful in acute pulmonary oedema before the diuretic action kicks in?
venodilator action
31
which loop is better in heart failure?
bumetonide
32
pharmacokinetics of loop diuretics?
absorbed by GI tract (subject to variation in CHF) bind to plasma protein enter nephron via OAT
33
indications for loop diuretics?
reduce salt and water overload associated with cardiac/renal failure, cirrhosis or nephrotic syndrome to increase urine volume in AKI treat hypertension to reduce acute hypercalcaemia
34
how may nephrotic syndrome affect loop diuretic action?
reduce effectiveness | drug binds to high amount of protein in urine
35
contraindications for loop diuretics?
severe hypovolaemia or dehydration | use with caution in hypokalaemia/hyponatraemia, hepatic encephalopathy and gout
36
side effects of loop diuretics?
low electrolyte states (including metabolic alkalosis due to H+ secretion) hypovolaemia/hypotension hyperuricaemia (gout) dose-related hearing loss
37
where is the triple transporter found in the nephron?
thick ascending limb of loop of henle
38
what do thiazide diuretics block?
sodium chloride co-transporter
39
principle thiazide and thiazide-like diuretics?
``` bendroflumethiazide thiazide like - chlortalidone - indapamide - metolazone ```
40
what do thiazide like diuretics do?
inhibit Na+/Cl- co-transporter by binding to Cl- site and therefore - prevent dilution of filtrate/urine in early distal tubule - increase load of Na+ delivered to collecting tubule causing K+ loss - increased reabsorption of calcium causes up to 5% of filtered Na+ to be secreted (modest diuresis)
41
additional action of thiazides?
vasodilator action | - benefit in hypertension
42
pharmacokinetics of thiazides?
well absorbed from GI tract | enter nephron via OAT mechanism
43
indications for thiazides?
mild heart failure hypertension (indapamide or chlotalidone) severe resistant oedema renal stone disease (reduced Ca2+ excretion discourages Ca2+ stone formation- less calcium in urine so less likely to precipitate out) nephrogenic diabetes (reduced ADH response in collecting ducts)
44
contraindications for thiazides?
hypokalaemia | use with caution - hyponatraemia, gout
45
side effects of thiazides?
``` hypokalaemia metabolic alkalosis hypovolaemia/hypotension hypomagnesia (not hypocalcaemia) hyperuricaemia (gout) erectile dysfunction impaired glucose tolerance ```
46
which diuretic is best to use in elderly person with osteoporosis and why?
thiazide | - don't cause loss of calcium
47
function of aldosterone?
acts via cytoplasmic receptors to increase reabsorption of Na+ in the late distal and collecting tubule via increasing ENac (sodium) channel and Na+/K+ ATPase
48
how does aldosterone affect potassium?
increased Na+ reabsorption = increased K+ excretion
49
how does Na+ reabsorption cause K+ excretion?
charge separation makes lumen more -ve and depolarizes the luminal/basolateral membrane this causes an increased driving force of K+ across the luminal membrane leading to enhanced secretion of K+ (Sgk1 increases ROMK K+ channel numbers in apical membrane) secreted K+ is washed away by increased urinary flow rate that also indirectly activates the ROMK channel leading to development of hypokalaemia
50
name 4 potassium diuretics?
amiloride triamterene spironolactone eplerenone
51
how do amiloride and triamterene work?
enter nephron via organic cation transport system in proximal tubule and block apical sodium channels in collecting tubules and decrease Na+ reabsorption
52
how does spironolactone and eplerenone work?
enter cell via basolateral membrane and compete with aldosterone for binding to intracellular cytoplasmic receptors preventing the actions of steroid described previously - increase Na+ excretion - decrease K+ excretion
53
indications for potassium sparing diuretics?
``` given in conjunction with other agents that cause potassium loss (as they cause hyperkalaemia) ... . . . ```
54
contraindications of potassium sparing diuretics?
//

Renal (34 decks)

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