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Renal > 3.4: Drugs Acting on the Kidney 1 > Flashcards

3.4: Drugs Acting on the Kidney 1 Flashcards

1
Q

Name some drugs acting on the kidney? (5)

A

Diuretics

Vasopressin Receptor Antagonists or Agonist (VASOPRESSIN = ADH)

Inhibitors of Sodium-Glucose Co-Transporter 2 (SGLT2)

Uricosuric Agents

Those used in renal failure

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2
Q

Function of diuretics?

A

Increasing urine flow by inhibiting reabsorption of sodium at sites in nephron

(Sodium follows water)

Also used to enhance excretion of salt and water in conditions where there is accumulation of fluid (Eg: Lymphoedema)

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3
Q

Most commonly used drugs in renal conditions?

A

Diuretics

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4
Q

How does oedema occur?

A

Due to imbalance in the Starling forces

There is an imbalance between interstitial fluid formation and reabsorption

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5
Q

Describe the forces involved in oedema?

A

Capillary pressure pushes water in interstitium

Capillary oncotic pressure pulles water back into capillaries (due to plasma proteins)

Interstital fluid pressure pushes water into the capillary

Intersitital fluid oncotic pressure pulls water into the interstitium

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6
Q

Give the equation for formation of interstitial fluid?

A

(Capillary pressure - Capillary oncotic pressure) - (Interstitial fluid pressure - Intersitial fluid oncotic pressure)

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7
Q

Oedema is caused by either an:

INCREASE/DECREASE in capillary pressure?

INCREASE/DECREASE in interstitial fluid pressure?

A

INCREASE in capillary pressure drives oedema formation

DECREASE in interstitial fluid pressure drives oedema formation

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8
Q

Name some conditions that cause oedema?

A

Nephrotic Syndrome

Congestive Cardiac Failure

Hepatic Cirrhosis with Ascites

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9
Q

Describe the nephrotic syndrome?

What is seen in the urine?

A

This is a disorder of the glomerulus

This allows protein (mainly albumin) to appear in the filtrate

Normally, large plasma proteins cannot pass through the glomerulus

There is proteinuria

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10
Q

Describe how the nephrotic syndrome causes oedema?

A

Plasma proteins leave the blood and enter the filtrate

This causes decreased capillary oncotic pressure and increases interstitial oncotic pressure

This causes increased intersitial fluid volume (causing oedema)

There is also decreased BP and CO due to loss of fluid

This causes RAAS activation

This retains sodium and water

This is good as it increases BP however the capillary pressure increases and the capillary oncotic pressure decreases

Leads to increased capillary pressure

Again, leads to oedema

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11
Q

Frothy urine suggests?

A

Loss of protein
Eg: Nephrotic Syndrome

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12
Q

In nephrotic syndrome, RAAS is activated due to the detection of?

What detects this?

A

Decreased in blood volume

Detected by juxtaglomerular apparatus

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13
Q

Treatment of nephrotic syndrome causing oedema?

A

DIURETIC

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14
Q

Describe how congestive heart failure causes oedema?

A

Reduced CO

There is renal hypoperfusion

Detected by juxtaglomerular apparatus

Causes activation of RAAS

Reabsorption of sodium and water

This increases capillary pressure and decreases oncotic pressure

This leads to more water moving into intersitial fluid causing oedema

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15
Q

In congestive cardiac failure, where specifically is oedema a big problem?

A

Pulmonary Oedema

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16
Q

Describe how hepatic cirrhosis with ascites causes oedema?

A

Increased pressure in the hepatic system

Active liver disease causes decreased albumin

Decreased albumin means decrease oncotic pressure

Fluid is lost to the interstitial fluid

Causes swelling and ascites

Ascites = Abdominal Oedema

Again, RAAS is activated

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17
Q

Describe (briefly) how diuretics work?

A

Space around cells is swollen with excessive fluid

Addition of diuretic causes increased output of water and salt (excreted in urine)

This means the blood leaving the kidney is haemoconcentrated and volume is reduced

This causes increased oncotic pressure

This can remove fluid from the intersitial space

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18
Q

Describe a side effect due to massive diuretic loss?

A

Thrombosis and collapse

Due to hypovolaemia

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19
Q

Diuretics work by preventing reabsoprtion of.. and make us pee out water.

A

Diuretics work by preventing reabsoprtion of sodium and makes us pee out water

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20
Q

Describe sodium reabsorption in the proximal convoluted tubule?

Describe the diuretic action here?

A

Na+ reabsorption (passive Cl- absorption)

Na+/H+ exchanger (Reabsorbs sodium)

Carbonic Annhydrase inhibitors block the Na+/H+ exchanger

NO LONGER USED

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21
Q

Describe sodium reabsorption in the thick ascending loop of Henle?

Describe diuretic action here?

A

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

Blocked by loop diuretics

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22
Q

Describe sodium reabsorption in the distal convoluted tubule?

A

Na+/H+ exchanger

Na+/Cl- Co-transporter

Sodium/hydrogen exchanger is blocked by carbonic annhydrase inhibitors

Sodium/Chloride co-transporter is blocked by thiazide diuretics

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23
Q

Describe sodium reabsoprtion at the distal collecting tubule?

Describe diuretic action here?

A

Na+/K+ exchanger

Blocked by potassium sparing diuretics

24
Q

What blocks sodium reabsorption at each point?

A

1 = No diuretic action

2 = Carbonic Annhydrase Inhibitors

3 = Loop Diuretics

4 = Carbonic Annhydrase Inhibitors

5 = Thiazide Diuretics

6 = Potassium Sparing Diuretics

25
Q

Describe? sodium reabsorption at each point

A
  1. Na+ reabsorption, passive Cl- absorption
  2. Na+/H+ exchanger
  3. Na+/k+/2cl- co-transporter (triple transporter)
  4. Na+/H+ exchanger
  5. Na+/Cl- co-transporter
  6. Na+/K+ exchanger
26
Q

Describe the effect of diuretics on potassium levels?

A

Most diuretics (Eg: Loop and Thiazide) cause potassium loss and hypokalaemia

Potassium sparing diuretics retain potassium

27
Q

A very LARGE/SMALL proportion of NaCl and H20 that is filtered via the ……. is reabsorbed.

This means a small inhibition of reuptake can cause a marked INCREASE/DECREASE in Na+ excretion

Fill in the blanks?

A

A very LARGE proportion of NaCl and H20 that is filtered via the glomerulus is reabsorbed

This means a small inhibition of reuptake can cause a marked INCREASE in Na+ Excretion

28
Q

What is the site of action of many diuretics (Eg: Loop, Thiazides, Potassium Sparing)?

What is the siginificance of this?

What is the exception?

A

The Apical Membrane

The diuretics must be in the filtrate to reach the site of action

Spironolactone is the exception

29
Q

How do diuretics enter the filtrate? (2 Methods)

A
  1. Glomerular Filtration (for drugs not bound to plasma protein)
  2. Secretion via transport processes in the proximal tubule (for drugs bound to plasma protein)
30
Q

What are the two transport systems invovled in diuretic secretion into the proximal tubule?

A

Organic Anion Transporters (OATs) transport acidic drugs - eg: Thiazides and Loop Agents

These work in proximal tubule, loop of henle and distal tubule

Organic Cation Transporters (OCT) transport basic drugs - eg: Triametere, Amiloride

This work in the collecting ducts

31
Q

Secretion (of diuretics into the proxiaml tubule) results in the concentration of the diuretic in the filtrate being HIGHER/LOWER than the concentration of diuretic in the blood?

A

Secretion of diuretics into the proximal tubule results in a higher concentration of diuretic in the filtrate than in the blood

32
Q

What do loop diuretics block?

Where do they work?

A

The triple co-transporter (Na+/K+/2Cl-)

Thick ascending limb of the loop of Henle

33
Q

Describe how loop diuretics work (in detail)?

*Also mention calcium

A

Block the Na+/K+/2Cl- (Triple co-transporter)
Specifically blocks the chloride binding site

This prevents reabsorption and causes increased urine production and increased sodium, chloride and potassium excretion

Calcium and magnesium can also not be reabsorbed as they rely on an electrochemical gradient set up by the triple co-transporter and potassium recycling

  1. Block triple co transporter to prevent reabsorption
  2. Prevents water reabsorption
  3. Prevents calcium and magnesium reabsorption
  4. More urine produced that contains electrolytes
34
Q

Name two commonly used loop diuretics?

A

Furosemide

Bumetanide

35
Q

Describe the speed of action of Furosemide and Bumetanide?

A

Work very rapidly

‘High ceiling agents’

Causes 15-25% of filtered Na+ to be excreted

36
Q

Describe an additional action of loop diuretics (Furosemide and Bumetanide)?

What is this important in?

A

Venodilator action

Beneficial in pulmonary oedema due to heart failure

37
Q

Describe loop diuretics absorption from GI tract?

Do they bond well or poorly to plasma proteins?

How do they enter the nephron?

A

Absorbed well from GI tract

Bind strongly to plasma protein

Enters nephrons via OAT mechanism (organic anion transport)

38
Q

Clinical indications for loop diuretics?

A
  • To reduce salt and water in acute pulmonary oedema, chronic kidney failure, hepatic cirrhosis with ascites, chronic heart failure, nephrotic syndrome
  • Hypertension (2nd line)
  • Hypercalcaemia
39
Q

Adverse effects of loop diuretics?

A
  • Hypokalaemia
  • Metabolic Alkalosis
  • Hypovolaemia and hypotension (especially in elderly)
  • Depletion of calcium and magnesium
  • Increased plasma uric acid
40
Q

Describe how Thiazide Diuretics work?

Where do they work?

Affect on calcium?

A

Block sodium reabsoprtion by blocking the Na+/Cl- co-transporter

Work in the distal convoluted tububle

Causes increased reabsorption of calcium

41
Q

Give some examples of thiazide diuretics?

A

Benzoflumethiazide

Hydrochlorothiazide

42
Q

Do thiazide diuretics cause a modest or large diuresis?

Do loop diuretics cause a modest or large diuresis?

A

Thiazide = 5% excretion, modest diuresis

Loop = 25%, large diuresis

43
Q

Describe an additional action of thiazide diuretics?

What condition is this useful in?

A

Vasodilator Action

Useful in hypertension

44
Q

Thiazide Diuretics:

  • GI tract absorption?
  • How does it enter nephrons?
A

Well absorbed from GI Tract

Enters nephrons via the OAT (Organic Aninon Transport Mechanism)

45
Q

Clinical indications for thiazide diuretics?

A

Mild Heart Failure

Hypertension

Also in:

  • Renal stones
  • Severe resistant oedema (+ loop agent)
  • Nephrogenic Diabetes Insipidus
46
Q

Side effects of thiazide diuretics?

A

Hypokalaemia

Metabolic Alkalosis

Hypovolaemia and Hypotension

Depletion of magnesium (not calcium)

Hyperuricaemia (uric acid)

Male Sexual Dysfunction

Impaired Glucose tolerance

47
Q

Match the drug to the side effect:

  • Loop Diuretic
  • Thiazide Diuretic
    1. Depletion of calcium and magnesium
    2. Depletion of magensium
A

Loop Diuretic = Decreased calcium and magnesium

Thiazide Diuretic = Decreased magneisum ONLY

48
Q

Why do loop diuretics and thiazide diuretics cause potassium loss?

A
  1. Causes hypovolaemia which turns on RAAS. Adolsterone stimulates Na+/K+ exchanger causing potassium loss
  2. Decreased sodium reabsorption means more sodium uptake in distal tubules by epithelial Na Channels (ENaCs). This causes stimulation of Na/K co-transporter and potassium loss
  3. Potassium channels (KOMK) secrete K+ into the urine
49
Q

What is often used alongside thiazides to try to combat hypokalaemia?

A

ACE Inhibitors

These block angiotensin 2 and therefore adolesterone production

50
Q

Name some potassium sparing diuretics?

A

Amiloride

Triamterene

Spironolactone

51
Q

Describe how amiloride and triameterene work?

A

Block sodium channels

Decrease Na reabsorption

52
Q

Describe how Spironolactone and Eplereone work?

A

Compete with aldosterone for binding site

This causes decreased expression of a gene and reduced synthesis of a protein mediator that activates Na+ channels

Also causes decrease numbers of Na+/K+/ATPase pumps in basolateral membrane

Reduces transepithelial movement of sodium which reduces potassium secretion

53
Q

Spironolactone:

  • High or low diuretic action?
  • How do they work?
  • Affect on Na+ and K+?
  • Absorption from GI tract?
A

Low Diuretic Action

Competitve antagonists with adolsterone

Increase Na+ excretion, decrease K+ excretion

Well absorbed from GI tract

54
Q

Amiloride and Trimaterene:

  • Action?

How does it enter nephron?

GI tract absorption?

A

Blocks sodium channels in collecting duct

Enters nephron via OCT (Organic Cation transport system) in proximal tubule

Triameterene well absorbed

Amiloride poorly absorbed

55
Q

Clinical indications for potassium sparing diuretics?

A
  • Use in conjunction with hypokalaemia causing diuretics
  • Heart failure
  • Primary adolsteronism (Conn’s)
  • Resistant essential hypertension
  • Secondary adolsteronsim (due to hepatic cirrhosis with ascites)

Renal (34 decks)

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