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Urinary > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What is diuresis and what is a diuretic

A

• Diuresis – increased formation of urine by the kidney
• Diuretic - A substance /drug that promotes a diuresis
by increasing renal excretion of water AND sodium therefore reduction of ECF volume
• Clinical use: in conditions where Na+ and water retention cause expansion of ECF volume
eg Heart failure

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2
Q

Briefly how do diuretics act

A

• Diuretics act by blocking
reabsorption of sodium and water by the tubule
65% reabsoption in PCT, 25% in TAL, 5% in DCT, 2% CD
• Fraction excretion (FE) of Na
is usually <1%.
Diuretics increase the FE of Na

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3
Q

Descrbe tubular reabsorption in the late DCT and CD

A
  • Na-K ATPase in Basolateral membrane
  • Na+ enters via ENaC
  • Na+ reabsorption creates a negative potential in lumen
  • This favours secretion of K+ through K+ channels
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4
Q

How does aldosterone affect channels

A

•Aldosterone increases expression of
Na-K ATPase, ENAC & K+ channels
• Diuretics reducing ENaC activity also reduces K+ secretion .

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5
Q

What are mechanisms of action of diuretics

A

1) direct action on cellsto block Na+ transporters in the luminal membrane
2) By antagonising the action o aldosterone

No longer sued:

3) By modification of filtrate content - osmotic diuretic
4) by inhibiting activity of CA enzyme in PCT

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6
Q

Describe the action of diuretics on Na+ transporters

A
  1. By Direct Action on cells to block Na+ transporters in the luminal membrane
    — Drug is secreted into the lumen in the PCT Act from within the lumen on transporters
  • Loop diuretics –
    Act on Loop of Henle
    block NKCC2 cotransporter
  • Thiazide diuretics -
    Act on the early Distal Tubule
    block Na –Cl cotransporter
  • K+ sparing diuretics
    Act on Late DT & CD
    block Epithelial Na channels
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7
Q

Describe the action of diuretics in terms of andosterone inhibition

A
  1. By Antagonising the action of Aldosterone
    — Aldosterone acts on Principal cells of Late DT & CD to increase Na+ reabsorption via ENaC

Aldosterone antagonists – competitive inhibition of aldosterone receptor
Decrease Na reabsorption
Also have k+ sparing effect

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8
Q

Descrbe diuretics that are no longer used

A
  1. By Modification of Filtrate Content – Osmotic Diuretics
    - Small molecules freely filtered at
    glomerulus but not reabsorbed
    - Increases osmolarity of filtrate
    - reduces water & Na+ reabsorption
    throughout the tubule
  2. By Inhibiting activity of enzyme
    Carbonic anhydrase in the PCT
    to interferes with Na & HCO3- reabsorption in PCT
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9
Q

Give a summary of the classification of diuretics

A

See slide

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10
Q

How do loop diuretics act on LOH

A

Block NKCC2
• Na and Cl not absorbed so medullary tonicity is less
• This affects water reabsorption further down the tubule so less water is absorbed.
Net result: Na+ and water loss
• The K+ carried across apical membrane drifts back into lumen via K+ channels
• Creates a lumen positive potential
• Which helps to also to drive absorption of the positively charged ions Ca2+ and Mg2+ - diuretic impacts this

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11
Q

What are loop diuretics

A

Eg furosemide, butanide
— Very potent diuretics
— 25 - 30% of filtered sodium reabsorbed in Loop of Henle
— Segments beyond have limited capacity to reabsorb the resulting flood of Na & water

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12
Q

When are loop diuretics used

A

— Used in heart failure for treatment of symptoms (breathlessness, expansion of ECF volume -> oedema)

  • Diuretic effect
  • Vaso and venodilatation ( decreased after/preload)
  • Reduces symptoms but no effect on reducing mortality but do help sickness

— In Acute Pulmonary oedema Furosemide given iv for rapid action

— Used to treat fluid retention & oedema in :
nephrotic syndrome,
renal failure,
cirrhosis of liver (spironolactone preferred, Loop Diuretics added if needed)

— Useful in treatment of hypercalcaemia
• Impairs calcium absorption in the Loop of Henle
• increases urinary excretion of calcium
• Furosemide given together with IV fluids

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13
Q

How do Thiazide diuretics work

A

• Thiazide diuretics block Na – Cl transporter in DCT
• Secreted into lumen in PCT
• Travel downstream to act at DCT
• Increases Na+ (and H2O) loss in urine
• Unlike in Loop of Henle, blocking Na absorption increases Ca2+ absorption
• Reduces Ca2+ loss in urine
i.e. increases Ca2+ absorption

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14
Q

When are thiazides used

A

Eg bendroflumethiazide
• Less potent diuretics than loop diuretics
• Only 5% of sodium reabsorption inhibited
• Ineffective in renal failure
• Widely used in hypertension (vasodilatation)
• Higher incidence of hypokalaemia (more later)

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15
Q

Describe the mechanisms of K+ sparing diuretics

A
  1. Inhibitors of epithelial Na channels (ENaC).
    e. g. Amiloride
  2. Aldosterone antagonists :
    e. g. Spironolactone

Both groups of drugs
• Reduce ENaC activity (directly or indirectly)
• Reduce the loss of K+ - excreting less
• Both can produce life threatening
hyperkalaemia especially if used with ACE Inhibitors, K+ supplements or in patients with renal impairment
Both are mild diuretics affecting only 2% of Na+ reabsorption

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16
Q

When are aldosterone antagonists used

A

Most of the time used for non diuretic effects
Aldosterone antagonists – eg Spironolactone
• Shown to reduce mortality in heart failure - used in long term treatment of heart failure (non diuretic effect)
• Preferred drug for Ascites & oedema in cirrhosis
• Used as additional therapy in hypertension not controlled by ACEI+CCB+Thiazide
• Treatment of hypertension due to primary hyperaldosteronism (

17
Q

Wha are epithelial Na channel blockers used

A

Epithelial Na channel blockers eg Amiloride , Triamterene
• Mild diuretics with K+ sparing effect
• Usually used in combination with K+ losing diuretics such as Loop or Thiazide diuretics to minimise K+ loss

18
Q

How can loop and thiaziade diuretics lead to hypokalaemia

A

Increased Na+ & H2O delivery to late DT & CD

-> increased Na absorption by principal cells -> favourable electrical gradient for K+ excretion

-> Faster flow rate of
filtrate in tubule lumen -> K+ secreted into lumen is washed away faster.-> Lower K+ concentration in lumen Favourable chemical gradient for K+ secretion

19
Q

What are the effect of diuretics on circulatory Vol and how can this affect K+ secretion

A

Diuretics may lead to reduced circulatory volume
Activation of Renin Angiotensin System
Increased !ldosterone secretion
Increased Na absorption & K+ secretion
Hypokalaemia

20
Q

Hoe can K- sparing diuretics lead to hyperkalaemia

A

Epitheliall Na+ channel inhibitors -> Block ENaC ->*

Aldosterone antagonists -> Block of Action of Aldosterone ->Reduce activity of Na-K ATPase & Epithelial Na+ channels ->*

*-> Reduce Na+ reabsorption
Reduces potassium loss in urine
Hyperkalaemia

21
Q

How are K+ levels monitored when used diuretics

A

• Monitoring K+ levels during is vital
• The combination of Loop /thiazide diuretic with a K+ sparing diuretic (ENaC blocker or an Aldosterone antagonist) can be used to minimise changes in potassium
alternately
• Loop /thiazide diuretics can be used with potassium supplements if
necessary

22
Q

When should K+ sparing diuretics be avoided

A

K+ sparing diuretics (ENaC inhibitors or Aldosterone antagonists):
• Avoid use along with potassium supplements
• Avoid if renal function is impaired
These increase the risk of hyperkalaemia
• In concomitant use with ACEI / ARB – regular K+ monitoring required E.g. Use of ACEI & spironolactone in heart failure

23
Q

Whe are diuretics primarily used

A

Diuretics are used primarily to treat Conditions with ECF expansion & Oedema

24
Q

When does ECF expansion usually occur

A

Expansion of ECF is usually an adaptive response to reduced circulating volume
In Congestive Heart Failure this is due to
(1) drop in Cardiac output with reduced renal perfusion
(2) increased Systemic venous pressure → oedema (higher hydrostatic pressure)
fluid moves from intravascular to interstitial compartment
• Leading to activation of Renin Angiotensin System (RAAS)
→ Na+ & water retention -> expansion of ECF
DIURETICS ARE USEFUL IN SYMPTOMATIC MANAGEMENT BUT STILL NEED TO TREAT THE CAUSE

25
Q

What is nephrotic syndrome

A

Glomerular disease → increase in GBM permeability to protein
→ proteins filtered and lost in urine -> proteinuria
→ causes low plasma albumin
→ results in low plasma oncotic pressure
→ peripheral oedema
→ reduced circulatory volume → RAAS activated
→ Na & water retention → expansion of ECF & → more oedema
Diuretics manage symptoms but stil need to treat cause

26
Q

What is ascites

A

Distension of abdomen

27
Q

Describe oedema and ascites in cirrhosis of liver

A

Reduced albumin synthesis in liver
• causes low plasma albumin
• Leads to low plasma oncotic pressure -> Peripheral oedema

Portal hypertension
• Cause increased venous pressure in splanchnic (GI) circulation
• high venous pressure + low oncotic pressure
• Movement of fluid in peritoneal capillaries -> to peritoneal cavity (transudate)
• Ascites (free fluid in peritoneal cavity)

28
Q

What are adverse effects of diuretics

A

• Potassium abnormalities (discussed)
• Hypovolaemia – especially Loop diuretics
Low EC

29
Q

Describe the action of CA inhibitors

A 
Act on proximal tubule
E.g. Acetazolamide
• Inhibits action of Carbonic anhydrase in brush border &amp; PCT cell
• Can cause metabolic acidosis due to
loss of HCO3- in urine
• Useful in the treatment of Glaucoma
• Reduces formation of Aqueous
humor in eye by about 50%
30
Q

Descrbe osmotic diuretics eg mannitol

A
  • Small inert molecules
  • Increases plasma osmolarity thus drawing out fluid from tissues & cells (IV mannitol used to treat cerebral oedema)
  • In the kidney increases the osmolarity of filtrate
  • Acts by altering the driving force for renal water absorption, which is osmolarity.
  • Causes loss of water, Na+ and K+ in the urine
  • Not inhibitors of enzymes or transport proteins
31
Q

Wha are other substances with diuretic action

A

• Alcohol – inhibits ADH release
• Coffee - increased GFR and decreased tubular Na+ reabsorption
• Drugs which inhibit action of ADH on collecting ducts:
e.g. Lithium (used for bipolar affective disorder)

32
Q

Wha are diseased casing diuresis

A

Symptom - Polyuria
• Diabetes Mellitus – glucose in filtrate - osmotic diuresis
• Diabetes Insipidus (cranial)- increase ‘pure’ water loss
Decreased ADH release from post pituitary -> reduced absorption of water in collecting ducts -> diuresis
• Diabetes Insipidus (nephrogenic) – increased ‘pure’ water loss
Poor response of

Urinary (17 decks)

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