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LR Renal > Peter's Pharmacology > Flashcards

Peter's Pharmacology Flashcards

1
Q

List 5 types of drug that act on the kidney

A
  • Diuretics
  • ADH receptor agonists
  • ADH receptor antagonists
  • SGLT2 inhibitors
  • Uricosuric drugs
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2
Q

What are the 2 main uses for diuretics?

A
  • To increase urine flow

- To offload oedema

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3
Q

How do diuretics…
- Increase urine flow
- Offload oedema
…?

A
  • Increase urine flow:
    By inhibiting the reabsorption of Na+ in the nephron, resulting in reduced H2O reabsorption as H2O follows Na+. H2O follows Na+ out in the urine
  • Offload oedema:
    As increased excretion of Na+ and H2O in the urine reduces extracellular fluid volume
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4
Q

Why does oedema occur?

A

When there is an imbalance between the rate of formation and the rate of absorption of interstitial fluid

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5
Q

What is the principal force driving H2O…
- out of the capillaries and into the interstitial fluid
- from the interstitial fluid back into the capillaries
…?

A
  • Out of the capillaries and into the interstitial fluid:
    Hydrostatic pressure in the capillary i.e., H2O attracted to lower H2O conc. in the interstitial fluid
  • From the interstitial fluid back into the capillaries:
    Oncotic pressure of the plasma (mainly driven by plasma proteins, esp. albumin) i.e., H2O attracted to the PP’s in the capillaries
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6
Q

Starling forces state that formation of interstitial fluid is proportional to…?

A

(Hydrostatic pressure in capillary - Hydrostatic pressure in interstitial fluid) - (Oncotic pressure in capillary - Oncotic pressure in interstitial fluid)

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7
Q

Diseases that…
-Increase/decrease hydrostatic pressure in the capillary
and/or
-Increase/decrease oncotic pressure in the capillary
… produce oedema?

A

Diseases that increase hydrostatic pressure in the capillary or diseases that decrease oncotic pressure in the capillary produce oedema

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8
Q

List 3 diseases that can cause oedema

A

Nephrotic syndrome
Congestive heart failure
Hepatic cirrhosis w/ ascites (as resistance to blood flow through the liver increases capillary pressure)

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9
Q

The normal glomerulus is permeable to H2O, electrolytes, and most low weight compounds. It is impermeable to large plasma proteins.

How is this changed in nephrotic syndrome?

A

Nephrotic syndrome is a disorder of glomerular filtration, allowing large plasma proteins (mainly albumin) to enter the filtrate and appear in the urine (proteinuria)

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10
Q

? urine is a sign of proteinuria

A

Frothy

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11
Q

Why does nephrotic syndrome cause oedema?

A
  • Filtration of plasma proteins results in decreased plasma oncotic pressure (as there is less protein in the capillaries)
  • This increases the formation of interstitial fluid (as H2O is driven out of the capillaries), leading to oedema
  • As H2O is driven out of the capillaries, blood volume and CO decrease
  • The kidneys receive less blood flow and so RAAS is activated to increase BP
  • Aldosterone causes reabsorption of Na+ and H2O
  • This further decreases plasma oncotic pressure as the blood is being diluted by retained H2O
  • Further decrease in plasma oncotic pressure causes more oedema
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12
Q

How do diuretics help treat nephrotic syndrome?

A

By inhibiting the reabsorption of Na+ in the nephron. This causes increased excretion of Na+ in the urine, which in turn causes increased H2O excretion in the urine, as H2O follows Na+ movement

Increased excretion of H2O and Na+ in the urine reduces ECF volume

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13
Q

What are the 3 major sites of diuretic action in the nephron?

A
  • Thick ascending limb of the Loop of Henle
  • Early distal convoluted tubule
  • Late distal tubule, collecting tubule and collecting duct
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14
Q

X diuretics act on Y transporters in the thick ascending loop of Henle to block Na2+ reabsorption

A

X - loop

Y - Na+/K+/2Cl- co-transporters

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15
Q

X diuretics act on Y transporters in the early distal convoluted tubule to block Na2+ reabsorption

A

X - Thiazide

Y - Na+/Cl- co-transporters

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16
Q

X diuretics act on Y transporters in the late distal tubule, collecting tubule and collecting duct to block Na2+ reabsorption

A

X - Potassium-sparing

Y - Na+/K+ exchangers

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17
Q

The site of action of most diuretics (except Spironolactone) is the apical membrane of tubular cells. By what 3 mechanisms can diuretics enter the filtrate to act on the apical membrane of tubular cells?

A
  • Glomerular filtration (as the drug is not bound to plasma protein and so can be be filtered into the tubular fluid)
  • Secretion via organic anion transporters (OATs) in the proximal tubule (transport acidic drugs)
  • Secretion via organic cation transporters (OCTs) in the proximal tubule (transport basic drugs)
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18
Q

Describe how secretion of organic anions into the tubular fluid occurs via organic anion transporters (OATs) in the proximal tubule

A
  • OA- enters the basolateral membrane of the tubular cell from the blood stream via active transport by OAT1, 2, & 3 in exchange for alpha-KG
  • OA- also enters the apical membrane of the tubular cell from the filtrate via active transport by OAT4
  • OA- exits over the apical membrane into the tubular fluid via active transport proteins MRP2/4 and BCRP
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19
Q

Describe how secretion of organic cations into the tubular fluid occurs via organic cation transporters (OCTs) in the proximal tubule

A
  • OC+ enters the basolateral membrane of the tubular cell from the blood stream on OCT2 transporter down its concentration gradient
  • OC+ exits over the apical membrane into the tubular fluid via active transporters MATE and MDR1
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20
Q

Which diuretics use…
- Organic anion transporters (OATs)
- Organic cation transporters (OCTs)
…?

A

OATs - thiazide and loop diuretics

OCTs - potassium-sparing diuretics

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21
Q

Why do loop and thiazide diuretics enter the nephron by the OAT mechanism?

A

They are strongly bound to plasma protein, and so cannot be filtered at the glomerulus

They must instead enter the filtrate by secretion in the proximal tubule, via the OAT mechanism (as they are acidic)

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22
Q

Describe the mechanism of action of loop diuretics

A

They block sodium reabsorption in the thick ascending loop of Henle by inhibiting the Na+/K+/Cl- triple transporter via binding at its Cl- site

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23
Q

What effect does inhibition of the Na+/K+/Cl- transporter have on the tubular cell?

A

Na+, K+ and Cl- are not reabsorbed

Therefore…

  • The interstitium of the medulla is less concentrated
  • Dilution of the filtrate in the thick ascending loop of Henle is prevented (dilution of filtrate is its function)
  • Na+ load to the distal regions of the nephron is increased, therefore increasing K+ loss
  • Excretion of Ca2+ and Mg2+ is increased
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24
Q

Why are loop diuretics called ‘high ceiling’ diuretics?

A

Because they are the diuretic that causes the most profound diuresis

This is due to their action in the thick ascending limb of the loop of Henle, which is responsible for reabsorption of ~25% of filtered Na+

They cause this large amount of filtrate to instead be excreted

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25
Q

What are the clinical uses of loop diuretics?

A
  • To reduce salt and water overload e.g., CKD, nephrotic syndrome, acute pulmonary oedema, chronic heart failure
  • To increase urine output in AKI
  • As an add-on treatment in hypertension (often in the presence of renal insufficiency)
  • To reduce acute hypercalcaemia
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26
Q

Why might loop diuretics be less effective in nephrotic syndrome?

A

As they travel bound to proteins, the loop diuretics may prefer to bind to the protein found in the filtrate in nephrotic syndrome, instead of the Na+/K+/Cl- triple transporter

This means they will be excreted alongside the proteinuria

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27
Q

Why are loop diuretics especially useful for pulmonary oedema caused by heart failure?

A

They possess an additional, indirect, venodilator effect which acts even before diuresis

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28
Q

What are the main side effects of using loop diuretics?

A 
Hypokalaemia
Metabolic alkalosis
Hypocalcaemia
Hypomagnesaemia
Hyperuricaemia -> gout
Hypovolaemia and hypotension (due to decreased circulating fluid volume)
Dose-related hearing loss
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29
Q

What are the contraindications and cautions of loop diuretic use?

A

Contraindications:

  • Severe hypovolaemia
  • Dehydration

Cautions:

  • Severe hypokalaemia
  • Severe hyponatraemia
  • Hepatic encephalopathy
  • Gout
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30
Q

Name the 2 principal loop diuretics

A

Furosemide

Bumetanide

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31
Q

What is the mechanism of action of thiazide diuretics?

A

They block sodium reabsorption in the early distal convoluted tubule by inhibiting the Na+/Cl- co-transporter via binding at its Cl- site

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32
Q

What effect does Na+/Cl- co-transporter inhibition have on the tubular cell?

A

Na+ and Cl- are not reabsorbed

Therefore…

  • Dilution of the filtrate in the early distal convoluted tubule is prevented (as it is impermeable to water here)
  • Na+ load to the distal regions of the late distal convoluted tubule and collecting tubule is increased, therefore increasing K+ loss
  • Reabsorption of Ca2+ is increased (this is opposite to loop diuretics, unsure why)
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33
Q

Why do thiazide diuretics produce a modest diuresis when compared to loop diuretics?

A

Due to their site of action in the early distal convoluted tubule, which is responsible for reabsorption of ~5% of filtered Na+ (as opposed to ~25% in loop diuretics)

This means they cause only ~5% of filtered Na+ to be excreted

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34
Q

What are the clinical uses of thiazide diuretics?

A
  • Mild heart failure
  • Hypertension (as an add-on treatment)
    (main 2)
  • Severe resistant oedema or pulmonary oedema (in combo with a loop agent)
  • Renal stone disease
  • Nephrogenic diabetes insipidus
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35
Q

Why are thiazide diuretics useful as an add-on anti-hypertensive agent?

A

They possess an additional, indirect, venodilator effect

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36
Q

Why can thiazide diuretics be used in renal stone disease?

A

Increased Ca2+ reabsorption reduces urinary excretion of Ca2+ which discourages Ca2+ stone formation in the urinary tract

The most common renal stones are formed by aggregates of calcium oxalate

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37
Q

What are the main side effects of thiazide diuretic use?

A

Hypokalaemia
Metabolic alkalosis
Hyperuricaemia
Hypomagnesaemia (not hypocalcaemia, which is an advantage in elderly patients with osteoporosis)
Hypovolaemia and hypotension (due to decreased circulating fluid volume)
Erectile dysfunction
Impaired glucose tolerance in diabetics

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38
Q

What are the contraindications and cautions for thiazide diuretic use?

A

Contraindications:
-Hypokaelamia

Cautions:

  • Hyponatraemia
  • Gout
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39
Q

Name the 2 principal thiazide diuretics

A 
Bendroflumethiazide
Chlortalidone (a thiazide-like diuretic)
40
Q

Why can loop and thiazide diuretics cause hypomagnesaemia (+ hypocalcaemia in loop diuretics)?

A

Because they inhibit K+ reabsorption and increase K+ loss

K+ reabsorption normally drives Ca2+ and Mg+ paracellular reabsorption
unsure why Ca2+ is not reduced in thiazides

41
Q

Why can loop and thiazide diuretics cause hyperuricaemia and gout?

A

Uric acid and loop/thiazide agents compete for the OAT mechanism in the proximal tubule

This means more uric acid remains in the blood stream

42
Q

Why can loop and thiazide diuretics cause hypokalaemia and metabolic alkalosis?

A

As they reduce Na+ reabsorption, they increase the load of Na+ delivered to the distal nephron

Increased Na+ in the distal nephron stimulates increased reabsorption of Na+ in exchange for a K+ and a H+, which are excreted in the urine

43
Q

Describe the cellular mechanisms involved in hypokalaemia caused by loop and thiazide diuretics

A
  • Increased Na+ load enhances Na+ reabsorption through ENaC in the late distal tubule and collecting tubule
  • Enhanced reabsorption of Na+ makes the tubular lumen more negative, which attracts K+
  • Increased driving force on K+ leads to increased secretion of K+ through ROMK and BK channels
  • K+ secreted into the tubular fluid is washed away by the increased urinary flow rate
44
Q

Why do potassium-sparing diuretics enter the tubular cell by the OCT mechanism?

A

They are strongly bound to plasma protein, and so cannot be filtered at the glomerulus

They must instead enter the filtrate by secretion in the proximal tubule, via the OCT mechanism (as they are basic)

45
Q

What is the mechanism of action of the potassium-sparing diuretics…
- Amiloride and Triamterene
- Spironolactone and Eplerenone
…?

A
  • Amiloride and Triamterene:
    They block sodium reabsorption in the late distal convoluted tubule and collecting tubules and ducts by blocking the tubular cells apical ENaC sodium channels
  • Spironolactone and Eplerenone
    They block sodium reabsorption in the late distal convoluted tubule and collecting tubules and ducts by competing with aldosterone for binding to intracellular receptors
46
Q

What effect does aldosterone binding to intracellular receptors usually have?

A

Aldosterone acts via cytoplasmic receptors to…

  • Increase activation of ENaC channels (reabsorb Na+)
  • Increase expression of ENaC
  • Increase expression of Na+/K+ ATPase (reabsorbs Na+ and secretes K+)
47
Q

What effect does potassium-sparing diuretic action have on the tubular cell?

A

Na+ is not reabsorbed and K+ is not secreted

  • Blocks entry for Na+ reabsorption (ENaC channels)
  • Decreases synthesis of ENaC channels (which reabsorb Na+)
  • Decrease synthesis of Na+/K+ ATPase (reabsorbs Na+ and secretes K+)

This means Na+ excretion is increased, and K+ excretion is decreased

48
Q

Why do potassium sparing diuretics have little diuretic action?

A

Due to their site of action in the late distal convoluted tubule and collecting tubule + ducts, which are responsible for reabsorption of ~2% of filtered Na+ (as opposed to ~25% in loop diuretics and ~5% in thiazide diuretics)

This means they cause only ~2% of filtered Na+ to be excreted

49
Q

Action of Spironolactone and Eplerone depends on circulating levels of…?

A

Aldosterone

as they compete with it for access to cytoplasmic aldosterone receptors

50
Q

Spironolactone and Eplerone gain access to the tubular cell from the apical/basolateral membrane?

A

Basolateral

all other diuretics use the apical membrane

51
Q

What is the major use for potassium-sparing diuretics?

A

In conjunction with other agents that cause potassium loss (e.g., thiazide or loop diuretics)

52
Q

What conditions are potassium-sparing diuretics used to treat? (4)

A
  • Heart failure
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Resistant essential hypertension
  • Secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)
53
Q

What is the major side effect of potassium sparing diuretics? What implications does this have?

A

When given alone, they cause hyperkalaemia

Therefore, they are always used alongside an agent that causes potassium loss e.g., thiazide or loop diuretics

54
Q

What side effect can be seen with Spironolactone?

A

Breast tissue growth

55
Q

What are the contraindications for the use of potassium-sparing diuretics? (3)

A
  • Severe renal impairment
  • Hyperkalaemia
  • Addison’s disease (as they block aldosterone receptors)
56
Q

What is the major site of Na+ reabsorption in the nephron?

A

The proximal convoluted tubule (67% of filtered Na+ is reabsorbed here)

57
Q

Which drugs block Na+ reabsorption in the proximal convoluted tubule? How?

A

Carbonic anhydrase inhibitors

By blocking the Na+/H+ exchanger

58
Q

What effect does blocking the Na+/H+ exchanger on the tubular cells in the proximal convoluted tubule have?

A

Na+ is not reabsorbed and H+ is not excreted

This results in increased Na+ and HCO3- excretion in the urine which leads to alkaline diuresis (alkaline urine) and metabolic acidosis

59
Q

Why are carbonic anhydrase inhibitors no longer used as diuretic agents?

A

They lose their effectiveness after a couple of days

60
Q

What are carbonic anhydrase inhibitors now used for?

A
  • Glaucoma and following eye surgery (to reduce IOP)
  • Prophylaxis of altitude sickness
  • Some forms of infantile epilepsy
61
Q

What are osmotic diuretics?

A

Drugs that inhibit the reabsorption of Na+ and H2O in the nephron by altering osmotic driving forces along the nephron

62
Q

Give an example of an osmotic diuretic

A

IV mannitol

63
Q

Why are osmotic diuretics given IV?

A

They are membrane impermeable because they are extremely polar

64
Q

Describe the mechanism of action of osmotic diuretics

A
  • Once given IV, the diuretic enters the nephron by glomerular filtration
  • It is not reabsorbed because it is highly polar and so stays in the filtrate
  • This increases the osmolarity of the filtrate
  • This attracts H2O, opposing its reabsorption and meaning it is retained in the tubular fluid
  • This secondarily reduces Na+ reabsorption because the tubular fluid is now more dilute
65
Q

What is the major site of action of osmotic diuretics? Why?

A

The proximal tubule because this is where most of the iso-osmotic reabsorption of water occurs

66
Q

What are the clinical uses of osmotic diuretics?

A
  • In severe hypovolaemia to maintain urine flow to prevent AKI
  • In the urgent treatment of acutely raised ICP or IOP
67
Q

What are the possible side effects of osmotic diuretics? (2)

A
  • Transient expansion of blood volume

- Hyponatraemia

68
Q

What conditions can cause osmotic diuresis?

A
  • Hyperglycaemia

- Iodine-based radiocontrast dyes in imaging

69
Q

How can hyperglycaemia cause osmotic diuresis?

A

When reabsorptive capacity of the proximal tubule for glucose (by SGLT1 and 2) is exceeded, glucose remains in the filtrate and retains fluid

70
Q

How can hyperglycaemia cause osmotic diuresis?

A

When reabsorptive capacity of the proximal tubule for glucose (by SGLT1 and 2) is exceeded, glucose remains in the filtrate and retains fluid

71
Q

ADH is a hormone which is secreted from the posterior pituitary in response to increased blood osmolality. How does ADH act on the kidneys?

A
  • ADH binds to V2 GPCR’s on the basolateral membrane of collecting tubule cells
  • This increases production of cAMP
  • This increases the number of aquaporins in the apical membrane of the tubular cell
  • More H2O is reabsorbed
72
Q

What condition can be treated with an ADH receptor agonist?

A

Neurogenic diabetes insipidus

73
Q

Describe the use of ADH receptor agonists in the treatment of neurogenic diabetes insipidus

A

Desmopressin is a synthetic analogue of ADH. It selectively binds to V2 ADH receptors in the collecting tubule of the kidneys to cause H2O retention

74
Q

Why can ADH agonists not be used to treat nephrogenic DI?

A

It is caused by inability of the nephron to respond to ADH, as opposed to decreased ADH secretion

There is no current pharmacological treatment

75
Q

When would ADH receptor antagonists be used?

A

To cause excretion of H2O without accompanying Na+ loss, resulting in increased plasma Na+ (opposite to diuretics)

76
Q

What are the ADH receptor antagonists called?

A

‘Vaptans’ e.g., Tolvaptan

77
Q

What is Tolvaptan licensed to treat in the UK?

A

To correct hyponatraemia in SIADH

78
Q

Normally, 100% of filtered glucose is reabsorbed in the proximal tubule by sodium glucose co-transporters (SGLT) 1 and 2. In what circumstance would glucose appear in the urine?

A

If filtrate concentration of glucose exceeds the renal threshold (~11 mmol/l)

79
Q

What transporters move glucose…

  • Into the apical membrane of the tubular cell from the tubular fluid
  • Out of the basolateral membrane of the tubular cell, into the interstitium
A

SGLT1/2 take glucose into the tubular cell across the apical membrane by active transport

GLUT2/1 transporters allow glucose to leave across the basolateral membrane of the cell by facilitated diffusion

80
Q

SGLT2 and 1 transport glucose into the cell against its concentration gradient by coupling its movement to…?

A

Na+ influx

81
Q

What are the differences between SGLT2 and SGLT1?

A

SGLT2:

  • Found in the proximal part of the proximal tubule
  • Mediates ~90% of glucose reabsorption
  • Transporter stoichiometry is 1 Na+:1 glucose
  • Has a lower affinity for glucose but a greater capacity for binding

SGLT1:

  • Found in the distal part of the proximal tubule (and also in the intestines)
  • Mediates ~10% of glucose reabsorption in the kidneys
  • Transporter stoichiometry is 2Na+:1 glucose
  • Has a higher affinity for glucose but a lower capacity for binding
82
Q

How do SGLT2 inhibitors have their effect?

A

They block SGLT2 receptors in the proximal tubule of the nephron, causing reduced reabsorption of glucose into the bloodstream

83
Q

Reduced reabsorption of glucose results in…?

A

Excretion of ~25-30% of the filtered glucose into the urine (glycosuria)

84
Q

Name 3 SGLT2 inhibitors

A

Canagliflozin
Dapagliflozin
Empagliflozin

85
Q

Why are SGLT2 inhibitors good for treating T2DM?

A

They cause…

  • Excretion of glucose
  • Reduction of HbA1c (glycated Hb)
  • Weight loss (due to calorie loss through glucose in urine and mild osmotic diuresis)
86
Q

What are the side effects of SGLT2i?

A

Increased incidence of genital bacterial and fungal infections (due to glycosuria)

Apart from that, they have limited adverse effects

87
Q

What are the 2 major prostaglandins synthesised by the kidney?

A

PGE2

PGI2

88
Q

Where is…
-PGE2
-PGI2
… synthesised in the kidney?

A

PGE2: the medulla

PGI2: macula densa cells in the glomeruli

89
Q

When are prostaglandins produced by the kidney?

A

COX 1 and 2 enzymes increase prostaglandin synthesis in response to renal insult e.g., ischaemia, mechanical trauma, ADH etc.

90
Q

Under normal conditions, how do prostaglandins affect renal blood flow and GFR in the kidneys?

A

They have little effect on either of these

91
Q

When do prostaglandins start to have an important role in kidney function?

A

When renal blood flow is compromised

92
Q

What is the function of prostaglandins when renal blood flow is low?

A

To increase blood flow to the glomerulus and to maintain adequate glomerular filtration pressure

93
Q

How do the prostaglandins
- Increase blood flow to the glomerulus
- Maintain adequate glomerular filtration pressure
…?

A

They cause vasodilation of the afferent arteriole which increases blood flow to the glomerulus

They cause vasoconstriction of the efferent arteriole which increases glomerular filtration pressure

94
Q

Why are NSAIDs nephrotoxic?

A

They inhibit COX enzymes

which synthesise the prostaglandins that maintain RBF and GFR in times of low renal blood supply

95
Q

Why do ACEIs/ARBs, diuretics and NSAIDs cause a ‘triple whammy’ effect?

A

ACEIs/ARBs block RAAS which inhibits efferent arteriolar vasoconstriction

Diuretics decrease plasma volume and therefore decrease renal blood flow

NSAIDs inhibit prostaglandins which inhibits afferent arteriolar vasodilation and efferent arteriolar vasoconstriction

96
Q

What are uricosuric agents?

A

Drugs used in the treatment of gout that block reabsorption of urate in the proximal tubule

97
Q

Why are uricosuric agents rarely used in the treatment of gout anymore?

A

They have been replaced by Allopurinol, which inhibits urate synthesis

LR Renal (16 decks)

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