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Renal pharmacology Flashcards

1
Q

Examples of drugs that act on the kidneys

A

Diuretics
Vasopressin receptor agonist & antagonist
SGLT2 inhibitors
Uricosuric drugs

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2
Q

What is the general action of diuretics

A

Increase urine flow normally by inhibiting the reabsorption of electrolytes

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3
Q

What causes oedema?

A

Imbalance between the rate of formation and the rate of absorption of interstitial fluid

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4
Q

What forces affect the formation of interstitial fluid?

A

Capillary hydrostatic & oncotic pressure

Interstitial hydrostatic & oncotic pressure

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5
Q

Examples of conditions that increase the capilary hydrostatic pressure or decrease the interstitial oncotic pressure?

A

Nephrotic syndrome

Congestive heart failure

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6
Q

How does decreased interstitial oncotic pressure lead to oedema?

A 
Increased formation of interstitial fluid 
Decreased blood volume & CO
Activation of RAAS
Na+ and water retention 
Increased capillary hydrostatic pressure
Decreased interstitial oncotic pressure 
OEDEMA
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7
Q

Which drugs block Na+/H+ exchange in the proximal & distal convoluted tubules?

A

Carbonic anhydrase inhibitors

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8
Q

What class of drugs block Na+/K+/2Cl- co-transport in the ascending limb of the loop of Henle?

A

Loop diuretics

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9
Q

Which drugs block Na+/Cl- co-transport in the distal convoluted tubule?

A

Thiazide dirueticss

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10
Q

Which drugs block Na+/K+ exchange in the collecting tubule?

A

Potassium-sparing diuretics

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11
Q

Methods by which diuretics can enter the filtrate to act on the apical membrane?

A

Glomerular filtration

Secretion via transport process in the proximal tubule

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12
Q

Which 2 transport systems are important in transporting diuretics into filtrate?

A

OATs & OCTs

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13
Q

Which type of drug do OATs transport?

A

Acidic drugs (e.g. thiazide & loop diuretics)

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14
Q

Which type of drug do OCTs transport?

A

Basic drugs (e.g. triamterene & amiloride)

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15
Q

Which protein is OA- transported into the cell in exchange for in OATs at the basolateral membrane?

A

a-ketoglutarate

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16
Q

What transports a-KG into the cell?

A

Na-dicarboxylate transporter

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17
Q

How does OA- enter the lumen at the apical membrane?

A

Via MRP2 or OAT4

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18
Q

How does OC- enter the lumen at the apical membrane?

A

Via MRP1 or OC-/H+ antiporters

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19
Q

Example of loop diuretic

A

Furosemide

Bumetanide

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20
Q

Where on the triple co-transporter do loop diuretics bind?

A

Cl-

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21
Q

What efect does binding to the triple co-transporter have?

A

Decease tonicity of interstitium of medulla
Prevent dilution of filtrate in the thick ascending lib
Increase load of Na+ delivered to distal regions of the nephron (causing K+ loss)

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22
Q

Why are loop diuretics especially useful in heart failure?

A

Possess an additional venodilator effect that is beneficial in pulmonary oedema

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23
Q

How do loop diuretics enter the filtrate?

A

Absrobed in GI tract
Strongly bound to plasma protein
Enter nephron by OAT mechanism

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24
Q

In what conditions can loop diuretics be used to reduce salt & water overload?

A

Acute pulmonary oedema
Chronic kidney failure
Hepatic cirrhosis with ascites
Chronic heart failure Nephrotic syndrome

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25
When do loop diuretics tend to be used if hypertension?
If resistant to other diuretics or anti-hypertensive drugs (usually in the presence of renal insufficiency)
26
Adverse effects of loop diuretics
``` Hypokalemia Metabolic alkalosis Hypovolaemia & hypotension Depletion of calcium & magnesium Gout ```
27
Examples of thiazide diuretics
Bendroflumethazide | Hydrochlorothiazide
28
How do thiazide diuretics work?
Inhibit Na+/Cl- carrier to prevent th edilution of urine in the early distal tubule Increase the load of Na+ delivered to collecting tubule (causing K+ loss) Increase reabsorption of calcium
29
What percentage of sodium do thiazide & loop diuretics cause to be excreted?
``` Loop = 10-15% Thiazide = 5% ```
30
Why are thiazide diuretics especially useful in hypertension?
Possess an additional vasodilator action
31
How do thiazide diuretics enter the filtrate?
Absorbed in GI tract | Enter nephron by OAT mechanism
32
What are thiazide diuretics widely used in?
Mild heart failure | Hypertension
33
Why do ythiazide diuretic work in renal stone disease?
Reduced urinary excretion of calcium discourage calciu stone formation
34
Why are thiazide diuretics used in nephrogenic diabetes inspids?
Diminshed vasopressin responsiveness of the collecting ducts = decreased urine volume
35
Adverse effects of thiazide diuretics
``` Hypokalaemia Metabolic alkalosis Hypovolaemia & hypotension Depletion of magesium (not calcium) Gout Male sexual dysfunction Impaired glucose tolerance ```
36
How does aldosterone work?
Increases synthesis of Na+/K+ATPase | Increase synthesis of protein that activates the epithelial Na+ channel (ENaC)
37
What does ADH do?
Increases the number of aquaporins in the cell mambrane
38
Why do diuretics cause hypokalaemia & metabolic alkalosis?
Increased Na load causes enhanced Na reabsorption Makes lumen more negative Increased driving force on K+ (& H+) across the membrane causing K+ (& H+) to be washed away = hypokalaemia & metabolic alkalosis
39
Examples of potassium sparing diuretics
Amiloride Triamterene Spironolactone Eplerenone
40
What is the mechanism of action of amiloride & triamterene?
Block the apical sodium channel decrease Na+ reabsorption
41
Mechanism of action of spironolactone
Compete with aldosterone for binding to intracellular receptors causing decreased gene expression and reduced synthesis of a protein mediator that activates Na+ channels in the apical membrane Decreased numbers of Na+/K+ATPase pumps in the basolateral membrane
42
What effect does spironolactone have on Na & K excretion?
Increase Na excretion | Decrease K excretion
43
What is spironolactone metabolised to in the GI tract?
canrenone
44
How do amiloride & triamterene enter the nephron?
OCT system in proximal tubule
45
Which is better absorbed in the GI tract amiloride & triamterene?
Triamterene
46
When are potassium mainly used?
In cnjunction with other agents that cause potassium loss
47
What can potassium sparing diuretics cause if given alone?
Hyperkalaemia
48
What are aldosterne antagonist used in the treatment of?
Heart failure Primary hyperaldosteronism (Conn's syndrome) Resistant essential hypertension Secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)
49
Example of osmotic diuretic
Mannitol IV
50
Mechanism of action of osmotic diuretics
Increase osmolarity of the filtrate opposing the absorption of water in parts of the nephron that are freely permable to water
51
Where is the major site of action in the kidney for osmotic diuretics?
Proximal tubule
52
Why do osotic diuretics cause secondary decrease in sodium absorption?
As they make the filtrate more dilute thus changing the electrochemical gradient
53
When are osmotic diuretics used for their effect on the kidney?
Prevention of acute hypovolaemic renal failure
54
Why are osmotic diuretics used in acutely raised intracranial & intraocular pressure?
Solute does not entre eye or brain but increased plasma osmolarity extracts water from these compartments
55
Example of carbonic anhydrase inhibitor
Acetazolamide
56
Mechanism of carbonic anhydrase inhibitors
Increase excretion of bicarb with Na, K and water - alkaline diuresis & metaabolic acidosis
57
When are carbonic anhydrase inhibitors as they are no longer used as diuretics?
Glaucoma followgin eye surgery Prophylaxis of altitude sickness Some forms of infantile epilepsy
58
Where is aldosterone secreted from?
Adrenal cortex
59
WHat do aldosterone do?
Enhances tubular Na reabsorption and salt retention increases synthesis of Na?KATPase Increases activity of Na channel (ENaC)
60
Where is ADH secreted from?
Posterior pituitary
61
What is the effect of ADH?
Enhanced water reabsorption | Increases number of aquaporins
62
What are the 2 types of diabetes insipidus?
Neurogenic | Nephrogenic
63
What is the cause of neurogenic diabetes insipidus?
Lack of ADH secretion from posterior pituitary
64
Treatment of neurogenic DI
Desmopressin
65
Why does desmopressin not cause increased BP?
Only activates V2 receptor not V1
66
What is nephrogenic diabetes insipidus?
Inability of th enephron to respond to ADH
67
What is usually the cause of nephrogenic DI?
recessive and X-linked mitation in V1 receptor gene (AVPR2)
68
What inhibits the action of vasopressin on the kidney?
Lithium | Demeclocycline
69
What is the mechanism of action of 'aquaretic/vaptans'?
Act as competitve antagnists of vasopressin receptors
70
When is tolvaptan used?
Syndrome of inappropriate ADH secretion (SIADH) to correct hyponatraemia
71
Why do SGLT inhibitors target SGLT2 not SGLT1?
SGLT2 is almost exclusively confined to the proximal tubules
72
Examples of SGLT2 inhibitors
Canagliflozin | Dapagliflozin
73
How are prosaglandins formed?
From fatty acids arachnoid acid by COX 1&2
74
What are the major prostaglandins produced in the kidney?
PGE2 - medulla | PGI2 - glomeruli
75
When are prostaglandins synthesised?
In response to ischaemia, mechanical trauma, angiotensin II, ADH and bradykinin
76
When do prostaglandins gain importance in terms of renal blood flow?
Under conditions of vasoconstriction or decreased effective arteria blood volume where they cause compensatory vasodilation
77
ow do prostaglandins affect GFR?
Direct vasodilator effect upon afferent arteriole Releasing renin leading to increased levels of angiotensin II that vasoconstricts the efferent arteriole - FILTRATION PRESSURE INCREASES
78
What may precipitate acute renal filure in conditions where renal blood flow id dependent upon vascular prostaglandins?
NSAIDs
79
What 3 drugs gives "triple whammy"?
ACEi (or ARB) Diuretic NSAID
80
How is uric acid formed?
Catabloism of purine

AY Renal (15 decks)

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