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AY Renal > Renal pharmacology > Flashcards

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
Q

When do loop diuretics tend to be used if hypertension?

A

If resistant to other diuretics or anti-hypertensive drugs (usually in the presence of renal insufficiency)

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26
Q

Adverse effects of loop diuretics

A 
Hypokalemia 
Metabolic alkalosis 
Hypovolaemia & hypotension 
Depletion of calcium & magnesium 
Gout
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27
Q

Examples of thiazide diuretics

A

Bendroflumethazide

Hydrochlorothiazide

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28
Q

How do thiazide diuretics work?

A

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

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29
Q

What percentage of sodium do thiazide & loop diuretics cause to be excreted?

A 
Loop = 10-15%
Thiazide = 5%
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30
Q

Why are thiazide diuretics especially useful in hypertension?

A

Possess an additional vasodilator action

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31
Q

How do thiazide diuretics enter the filtrate?

A

Absorbed in GI tract

Enter nephron by OAT mechanism

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32
Q

What are thiazide diuretics widely used in?

A

Mild heart failure

Hypertension

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33
Q

Why do ythiazide diuretic work in renal stone disease?

A

Reduced urinary excretion of calcium discourage calciu stone formation

34
Q

Why are thiazide diuretics used in nephrogenic diabetes inspids?

A

Diminshed vasopressin responsiveness of the collecting ducts = decreased urine volume

35
Q

Adverse effects of thiazide diuretics

A 
Hypokalaemia 
Metabolic alkalosis 
Hypovolaemia & hypotension 
Depletion of magesium (not calcium) 
Gout 
Male sexual dysfunction 
Impaired glucose tolerance
36
Q

How does aldosterone work?

A

Increases synthesis of Na+/K+ATPase

Increase synthesis of protein that activates the epithelial Na+ channel (ENaC)

37
Q

What does ADH do?

A

Increases the number of aquaporins in the cell mambrane

38
Q

Why do diuretics cause hypokalaemia & metabolic alkalosis?

A

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
Q

Examples of potassium sparing diuretics

A

Amiloride
Triamterene
Spironolactone
Eplerenone

40
Q

What is the mechanism of action of amiloride & triamterene?

A

Block the apical sodium channel decrease Na+ reabsorption

41
Q

Mechanism of action of spironolactone

A

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
Q

What effect does spironolactone have on Na & K excretion?

A

Increase Na excretion

Decrease K excretion

43
Q

What is spironolactone metabolised to in the GI tract?

A

canrenone

44
Q

How do amiloride & triamterene enter the nephron?

A

OCT system in proximal tubule

45
Q

Which is better absorbed in the GI tract amiloride & triamterene?

A

Triamterene

46
Q

When are potassium mainly used?

A

In cnjunction with other agents that cause potassium loss

47
Q

What can potassium sparing diuretics cause if given alone?

A

Hyperkalaemia

48
Q

What are aldosterne antagonist used in the treatment of?

A

Heart failure
Primary hyperaldosteronism (Conn’s syndrome)
Resistant essential hypertension
Secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)

49
Q

Example of osmotic diuretic

A

Mannitol IV

50
Q

Mechanism of action of osmotic diuretics

A

Increase osmolarity of the filtrate opposing the absorption of water in parts of the nephron that are freely permable to water

51
Q

Where is the major site of action in the kidney for osmotic diuretics?

A

Proximal tubule

52
Q

Why do osotic diuretics cause secondary decrease in sodium absorption?

A

As they make the filtrate more dilute thus changing the electrochemical gradient

53
Q

When are osmotic diuretics used for their effect on the kidney?

A

Prevention of acute hypovolaemic renal failure

54
Q

Why are osmotic diuretics used in acutely raised intracranial & intraocular pressure?

A

Solute does not entre eye or brain but increased plasma osmolarity extracts water from these compartments

55
Q

Example of carbonic anhydrase inhibitor

A

Acetazolamide

56
Q

Mechanism of carbonic anhydrase inhibitors

A

Increase excretion of bicarb with Na, K and water - alkaline diuresis & metaabolic acidosis

57
Q

When are carbonic anhydrase inhibitors as they are no longer used as diuretics?

A

Glaucoma followgin eye surgery
Prophylaxis of altitude sickness
Some forms of infantile epilepsy

58
Q

Where is aldosterone secreted from?

A

Adrenal cortex

59
Q

WHat do aldosterone do?

A

Enhances tubular Na reabsorption and salt retention
increases synthesis of Na?KATPase
Increases activity of Na channel (ENaC)

60
Q

Where is ADH secreted from?

A

Posterior pituitary

61
Q

What is the effect of ADH?

A

Enhanced water reabsorption

Increases number of aquaporins

62
Q

What are the 2 types of diabetes insipidus?

A

Neurogenic

Nephrogenic

63
Q

What is the cause of neurogenic diabetes insipidus?

A

Lack of ADH secretion from posterior pituitary

64
Q

Treatment of neurogenic DI

A

Desmopressin

65
Q

Why does desmopressin not cause increased BP?

A

Only activates V2 receptor not V1

66
Q

What is nephrogenic diabetes insipidus?

A

Inability of th enephron to respond to ADH

67
Q

What is usually the cause of nephrogenic DI?

A

recessive and X-linked mitation in V1 receptor gene (AVPR2)

68
Q

What inhibits the action of vasopressin on the kidney?

A

Lithium

Demeclocycline

69
Q

What is the mechanism of action of ‘aquaretic/vaptans’?

A

Act as competitve antagnists of vasopressin receptors

70
Q

When is tolvaptan used?

A

Syndrome of inappropriate ADH secretion (SIADH) to correct hyponatraemia

71
Q

Why do SGLT inhibitors target SGLT2 not SGLT1?

A

SGLT2 is almost exclusively confined to the proximal tubules

72
Q

Examples of SGLT2 inhibitors

A

Canagliflozin

Dapagliflozin

73
Q

How are prosaglandins formed?

A

From fatty acids arachnoid acid by COX 1&2

74
Q

What are the major prostaglandins produced in the kidney?

A

PGE2 - medulla

PGI2 - glomeruli

75
Q

When are prostaglandins synthesised?

A

In response to ischaemia, mechanical trauma, angiotensin II, ADH and bradykinin

76
Q

When do prostaglandins gain importance in terms of renal blood flow?

A

Under conditions of vasoconstriction or decreased effective arteria blood volume where they cause compensatory vasodilation

77
Q

ow do prostaglandins affect GFR?

A

Direct vasodilator effect upon afferent arteriole
Releasing renin leading to increased levels of angiotensin II that vasoconstricts the efferent arteriole - FILTRATION PRESSURE INCREASES

78
Q

What may precipitate acute renal filure in conditions where renal blood flow id dependent upon vascular prostaglandins?

A

NSAIDs

79
Q

What 3 drugs gives “triple whammy”?

A

ACEi (or ARB)
Diuretic
NSAID

80
Q

How is uric acid formed?

A

Catabloism of purine

AY Renal (15 decks)

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