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THE PATIENT > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What are the functions of the kidneys?

A
  • Maintain correct ionic balance of blood

- Remove waste products

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2
Q

How much blood passes through kidney in 24 hours?

A

120L

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3
Q

How much urine is produced in healthy individuals?

A

1.5L

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4
Q

What is one functional kidney unit called?

A

Nephron

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5
Q

What is the glomerulus?

A

dense capillary network

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6
Q

How does blood enter the glomerulus?

A

Through Afferent arteriole

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7
Q

How is fluid filtered out of the glomerulus and what is the process called?

A

Due to high hydrostatic pressure fluid and dissolved solutes are pushed out into capsular space
filtration

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8
Q

Where does blood go after it is filtered out of glomerulus?

A

Proximal convoluted tubule

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9
Q

From PCT where does filtrate go next?

A

Descending loop of henle then ascending loop of henle then the DCT

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10
Q

How does blood leave the glomerulus?

A

Through efferent arteriole

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11
Q

When filtrate is traveling along loop of henle and DCT what is it called?

A

tubular fluid

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12
Q

How does the tubular fluid get back into the cortex of the kidney?

A

Through DCT out of collecting duct

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13
Q

In what form does tubular fluid leave the collecting ducts?

A

Urine

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14
Q

What is the structure, function and role of the PCT?

A

 Has Leaky tight junctions between epithelial cells=Na+ diffuse down electrical conc gradient into epithelial cell this transport coupled with glucose, phosphate, AA’s, lactate, Cl-, K+ and proton extrusion
 60-70% Na+ reabsorption
 Actively secretes organic acids and bases via OAT transporter- creatinine, NSAID, penicillin , diuretics actively secreted into filtrate by OAT
 Ammonia- diffuses into filtrate down conc grad

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15
Q

What is the structure, function and role of the descending loop of henle?

A

 Surrounded by interstitial fluid= hypertonic to the filtrate
 Conc/tonicity increases as loop of henle descends
 Cells permeable to H20
 Water diffuses out of lumen down conc grad
 Countercurrent multiplier= concentrates interstitial fluid in renal medulla

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16
Q

What is the structure, function and role of the ascending loop of henle?

A

thick
 Low permeability cells to H2O
 20-30% active Na+ reabsorption
 Cortical end= top part= Na out via basolateral memb Na/K pump
 Creates gradient for Na to cross apical memb from lumen via Na/K/Cl transporter
 K= some absorbed from filtrate= most diffuses back out through apical memb K channels

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17
Q

What is the structure, function and role of the DCT?

A

 Impermeable to H2O
 7% Na+ reabsorbed down conc gradient
 Sodium actively reabsorbed via conc gradient set up by Na-K pump

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18
Q

What is the structure, function and role of the collecting tubule?

A

 Up to 15% Water reabsorbed from filtrate by aquaporin channels which are ADH mediated
 ADH binds to vasopressin releases aquaporin channels from vesicles they are stored in and they insert into apical memb
 Removal of filtered water= urine production

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19
Q

What are the functions of diuretics?

A
  • Increase Na+ and water secretion= produce natriuresis
  • Increased Na+ of filtrate= H2O follows
  • Directly acts on nephron cells or change filtrate composition
  • Small decrease in reabsorption= large increase in Na+ excretion
  • Diuretics apart from spironolactone actively secreted by PCT cells into lumen
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20
Q

What are the uses of diuretics?

A
  • Increase urine output
  • Reduces plasma volume and plasma concentrates so interstitial fluid drawn into blood = reduced oedema= no cardiac failure, no liver failure, no acute renal failure
  • Hyperaldosteronism= increases Na+ retention= increases plasma vol= stopped by diuretics
  • Reverses hypertension by reducing plasma volume
  • Acute renal failure= low blood flow to kidneys= small vol of dilute urine produced= diuretics increase excretion and aid urine production and kidneys concentrating powers
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21
Q

What are the examples of loop diuretics?

A
  • Furosemide, bumetanide, torasemide
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22
Q

List some advantages of bumetanide?

A

more lipid sol
higher bioavailability
diffuses passively into filtrate

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23
Q

What is the MOA of loop diuretics?

A
  • Inhibit Na+/K+/2Cl- carrier in the thick ascending limb
     Act on Cl- binding site of Na/K/Cl carrier
     Blocks K+/Cl- uptake= lost in urine
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24
Q

What are the outcomes of the MOA of loop diuretics?

A

no effect on Na+/H+ exchanger= Na+ in and H+ out
no effect on HCO3= continuously reabsorbed from filtrate= conc increased due to plasma vol reduction= alkalosis
increases Ca2+ and Mg2+ secretion= harmful die effect
reduced uric acid secretion= gout precipitation
Blocks Na+ reabsorption= more Na+ in distal part of nephron= reduced H2O absorption further

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25
Q

What other property or mechanism do loop diuretics exhibit?

A

Vasodilator mechanism

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26
Q

What are the different ways the vasodilator mechanism of loop diuretics could be caused?

A

reduced response to Ang II
Increased production of vasodilating PG’s
Reduced production of endogenous Na+/K+/ATP inhibitor= reduces vasoconstrictor properties
Exert K+ channel opening effect in resistance arteries

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27
Q

What are the examples of loop diuretics?

A
  • Furosemide, bumetanide, torasemide
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28
Q

What are the consequences if NSAIDs and loop diuretics are taken together?

A

Reduces diuretic action
NSAID block PGE2 production by competing for OAT
reduced Na+ and Cl- reabsorption in thick ascending loop
Reduce delivery of diuretics into renal tubule

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29
Q

What does the renal tubule consist of?

A

Loop of henle, DCT, collecting tubule

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30
Q

What are the outcomes of the MOA of loop diuretics?

A

no effect on Na+/H+ exchanger= Na+ in and H+ out
no effect on HCO3= continuously reabsorbed from filtrate= conc increased due to plasma vol reduction= alkalosis
increases Ca2+ and Mg2+ secretion= harmful die effect
reduced uric acid secretion= gout precipitation
Blocks Na+ reabsorption= more Na+ in distal part of nephron= reduced H2O absorption further

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31
Q

What other property or mechanism do loop diuretics exhibit?

A

Vasodilator mechanism

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32
Q

What are the different ways the vasodilator mechanism of loop diuretics could be caused?

A

reduced response to Ang II
Increased production of vasodilating PG’s
Reduced production of endogenous Na+/K+/ATP inhibitor= reduces vasoconstrictor properties
Exert K+ channel opening effect in resistance arteries

33
Q

What type of drug class to loop diuretics interact with?

34
Q

What are the consequences if NSAIDs and loop diuretics are taken together?

A

NSAID block PGE2 production by competing for OAT
reduced Na+ and Cl- reabsorption in thick ascending loop
Reduce delivery of diuretics into renal tubule

35
Q

What are the indications for loop diuretics?

A 
	Acute pul oedema
	Chronic HF
	Liver cirrhosis and ascites
	Nephrotic syndrome
	Renal failure
	Hypertension 
	Reduced renal function
	Hypercalcaemia
36
Q

What are the common side effects of loop diuretics?

A 
	Hypotension
	Hypokalemia 
	Metabolic alkalosis 
	Gout
	Hearing loss due to CN VII damage 
	Exacerbate diabetes 
	Increase effects and toxicity of digoxin and type 3 antidysrhythmic
37
Q

What effect do loop diuretics have on potassium?

A

Loss of potassium
higher conc of Na+ in filtrate as reabsorption inhibited by diuretic
more Na+ crossing apical memb
increases Na/K exchanger activity
more K into cell and diffuses out through apical K channels

38
Q

Describe the pharmacokinetics of loop diuretics?

A

 GIT absorption
 IV/oral
 Peak effect in less than 1 hr for IV= 30 min
 Strong binding to albumin= reaches site of action by PCT excretion
 Excreted in urine
 T1/2= 90 mins

39
Q

What are the indications of Thiazide + thiazide like diuretics?

A

 Hypertension
 Mild-mod CHF
 Oedema
 Nephrogenic diabetes insipidus

40
Q

What us the MOA of Thiazide + thiazide like diuretics?

A

Inhibit Na/Cl cotransporter
K+/cl- blocked
lost in urine

41
Q

What are the outcomes of the MOA of Thiazide + thiazide like diuretics?

A

no effect on Na+/H+ exchanger= Na+ in and H+ out
no effect on HCO3= continuously reabsorbed from filtrate= conc increased due to plasma vol reduction= alkalosis
increases Mg2+ secretion
decreases Ca2+ secretion
reduced uric acid secretion= gout precipitation

42
Q

What other effect do Thiazide + thiazide like diuretics exhibit?

A

vasodilator effects

43
Q

Describe the steps of the homeostatic mechanism used to limit hypotensive effects of diuretics during chronic dosing?

A

 Reduction in blood vol
 Increases renin release
 Ang I produced then to Ang II by ACE
 Ang II= vasoconstriction and aldosterone secretion
 Vasoconstriction= increased BP
 Aldosterone secretion= increased Na+ reabsorption = increased BP

44
Q

What is the MOA of Potassium sparing diuretics?

A
  • Block Na+ reabsorption
  • Block Na+/K+ exchange in collecting tubule= limited diuretic action
     Act on nuclear R
     Blocks synthesis of Na/K pump and ENaCs
45
Q

What are the side effects of Thiazide + thiazide like diuretics?

A

 Increased urine frequency so take in morning
 Erectile dysfunction
 Hypokalaemia
 Impaired glucose tolerance

46
Q

Describe the pharmacokinetics of Thiazide + thiazide like diuretics?

A

 Oral only
 Excreted in urine
 Bendro= 2.5mg daily in hypertension= peak effect 4-6 hr lasts 8-12 hrs
 Chlortalidone= 25mg OD= peak effect 2-6hrs lasts 72 hrs

47
Q

How can K+ depletion be reduced?

A 
	More fruit juice
	More instant coffee
	More bananas 
	K+ supplements alone or combo with diuretic
	Use K+ sparing diuretics
48
Q

What class of drugs are Potassium sparing diuretics?

A

Aldosterone antagonists

49
Q

What are examples of Potassium sparing diuretics?

A

Spironolactone, eplerenone

50
Q

What is the MOA of spironolactone?

A 
inhibits aldosterone
no mineralocorticoid receptors activated
no upregulation of the expression of the gene for Na/K pump and epithelial sodium channel called ENaC
Directly blocks Na+ reabsorption
Blocks K+ influx across basolateral memb
reduced K+ in filtrate= less K+ lost
51
Q

What are the indications of spironolactone?

A

o Primary hyperaldosteronism
o Ascites caused by liver cirrhosis
o Oedema
o Mod-severe HF

52
Q

What are the indications of eplerenone?

A

o Left ventricular failure after MI

53
Q

What are the side effects of Potassium sparing diuretics?

A

 Hyperkalemia
 GI upset
 Gynaecomastia
 Menstrual disorders/testicular atrophy

54
Q

What class of drugs interact with Potassium sparing diuretics?

55
Q

What happens if ACEI and Potassium sparing diuretics interact?

A 
	Increases hypotensive effect
	Excessive K retention 
	ACEI block Ang I to Ang II
	Reduced aldosterone secretion and reduced vasodilation 
	Reduced vasodilation= reduced BP
56
Q

Describe the pharmacokinetics of spironolactone?

A

o Good gut absorption
o Metabolised to canrenone t1/2= 16 hrs
o Slow onset of action

57
Q

Describe the pharmacokinetics of eplerenone?

A

o Short elimination half life

58
Q

Name 2 other diuretics?

A

Triamterene + amiloride

59
Q

What is the MOA of Triamterene + amiloride?

A
  • Inhibit Na+ reabsorption

- Block luminal Na channels in collecting tubules

60
Q

What is a disadvantage of Triamterene + amiloride?

A
  • Limited diuretic actions
61
Q

What are the side effects of Triamterene + amiloride?

A

 Hyperkalaemia

62
Q

What are the contraindications of Triamterene + amiloride?

A

renal impairment

drugs that increase K +

63
Q

Describe the pharmacokinetics of Triamterene?

A

o Good oral absorption

o Partial liver metabolization

64
Q

Describe the pharmacokinetics of amiloride?

A

o Less absorption
o Slower onset
o Excreted unchanged in urine

65
Q

What are combined diuretic therapies?

A 
Co-amiloride= amiloride + furosemide
Co-amilozide= amiloride + hydrochlorothiazide
66
Q

What are the indications for Co-amiloride?

67
Q

What are the indications for Co-amilozide?

A

hypertension, CHF, oedema

68
Q

Name an osmotic diuretic?

69
Q

What is the MOA of osmotic diuretics?

A
  • Filtered in glomerulus not reabsorbed
  • Increases filtrate osmolarity by drawing water from PCT, ascending LOH and CD epithelial cells into filtrate
  • Increase excretion of H2O and Na+
70
Q

What are the indications for osmotic diuretics?

A

 Cerebral oedema
 Raised intraocular pressure
 Acute renal failure

71
Q

What combination of diuretics maintains K balance?

A

osmotic + loop/thiazide

72
Q

What are the side effects of osmotic diuretics?

A

 Hyponatremia
 Headache
 Nausea
 Vomiting

73
Q

Which class of diuretics are weak?

A

potassium sparing

74
Q

What is the site of action of Loop diuretics?

A

Loop of henle

75
Q

What is the site of action of thiazide diuretics?

76
Q

What is the site of action of potassium sparing diuretics?

A

DCT and collecting tubule

77
Q

What is the site of action of amiloride?

A

Collecting tubule

78
Q

What is the site of action of mannitol?

THE PATIENT (8 decks)

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