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Yr 2 - Renal > Pharmacology and the Kidney > Flashcards

Pharmacology and the Kidney Flashcards

1
Q

Describe the RAAS system

A
  1. Blood pressure drops
  2. Renin released by the kidneys
  3. Angiotensinogen produced by the liver is converted to angiotensin I by renin
  4. ACE convert angiotensin I to angiotensin II in the lungs
  5. (Effects of angiotensin II - vasoconstriction)
  6. Aldosterone released by adrenal cortex (effects of aldosterone)
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2
Q

What are effects of aldosterone?

A

Sodium and water retention, potassium excretion –> increases blood pressure

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3
Q

What do beta blockers inhibit?

A

Renin release

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4
Q

Side effect of ACE inhibitors?

A

Cough - can cause bradykinin accumulation (as ACE normally breaks down bradykinin)

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5
Q

What is bradykinin?

A

A vasodilator

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6
Q

What drugs may be used instead of ACEi?

A

Angiotensin II receptor antagonists (but less data available for these drugs)

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7
Q

What type of cells contain renin?

A

Granular cells

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8
Q

What is renin release stimulated by?

A

Decreased pressure in afferent arteriole

Sympathetic nervous system

Changes in conc of chloride, osmotic conc

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9
Q

What is effect of ACEi?

A

Inhibit conversion of angiotensin I to angiotensin II so inhibit the vasoconstrictive effects of angiotensin II

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10
Q

How does ACEi act on the kidneys?

A

Act on efferent arteriole (prevents vasoconstriction due to lack of angiotensin II)

This modulates intra-glomerular pressure and increases sodium and water excretion

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11
Q

Why does ACEi act on efferent arteriole?

A

The efferent arteriole has a smaller diameter in the basal state; as a result, further constriction at this site will produce a greater increase in resistance than at the afferent arteriole.

This decreases pressure

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12
Q

What is the intra-glomerular pressure?

A

Pressure responsible for filtration

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13
Q

What are the indications that ACEi is needed?

A

Hypertension, cardiac failure, CKD

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14
Q

What are possible side effects of ACEi?

A

Hypotension (consider holding if AKI or risk of AKI)

Hyperkalaemia

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15
Q

How may ACEi lead to hyperkalaemia?

A

Decreased aldosterone levels (aldosterone normally increases levels of potassium released in urine)

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16
Q

What are examples of ACEi?

A
  • Ramipril
  • Lisinopril

(tend to end in -pril)

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17
Q

What are dangers of ACEi surrounding pregnancy?

A

Warn woman taking that she must not get pregnant as these can cause foetal abnormalities

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18
Q

What is effect of angiotensin receptor blockers (ARBs)?

A

Inhibit vasoconstrictive effect of angiotensin II on receptor

  • Acts on efferent arteriole
  • Modulates intra-glomerular pressure
  • Increases sodium and water excretion
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19
Q

Why do ARBs act on efferent arteriole?

A

The efferent arteriole has a smaller diameter in the basal state; as a result, further constriction at this site will produce a greater increase in resistance than at the afferent arteriole.

This decreases pressure.

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20
Q

What are indications that ARBs are needed?

A
  • Hypertension
  • Cardiac failure
  • CKD (reduces intra-renal pressure)
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21
Q

What are possible side effects of ARBs?

A
  • Hypotension (consider holding if AKI or risk of AKI)

- Hyperkalaemia

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22
Q

How may ARBs lead to hyperkalaemia?

A

Decreased aldosterone levels (aldosterone normally increases levels of potassium released in urine)

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23
Q

What are examples of ARBs?

A
  • Valsartan

- Irbesartan

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24
Q

Are there similar dangers of ARBs with pregnancy?

A

Yes

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25
Q

What are diuretics?

A

Drugs that increase salt and water excreted in urine

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26
Q

What are osmotic diuretics?

A

Inhibits reabsorption of water and sodium in regions of the kidney that are highly permeable to water

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27
Q

What are carbonic anhydrase inhibitors?

A

Weak diuretics, with the main site of action in the proximal tubular lumen and cell.

Reduce formation of bicarbonate and H+ ions by inhibiting carbonic anhydrase

This reduces bicarb and N+ reabsorption via the Na+/HCO3- cotransporter so promotes renal excretion of Na+, K+, bicarb and water.

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28
Q

How do loop diuretics work?

A

Inhibit the Na+/K+/2Cl co-transporter in the loop of Henle (in the kidney). This reduces Na, Cl and K reabsorption leads to increased loss in the urine, water follows this so excess water is lost

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29
Q

How can loop diuretics ease symptoms of oedema?

A

Less fluid remains in bloodstream which eases symptoms of oedema (accumulation of fluid) due to heart failure

30
Q

What are thiazides?

A

A weak diuretic

31
Q

How do thiazides work?

A

Promote diuresis by inhibiting the sodium/chloride cotransporter located in the distal convoluted tubule of a nephron

Inhibits sodium uptake so increases excretion of sodium and water

32
Q

What are indications that loop diuretics are required?

A
  • CKD
  • Nephrotic syndrome
  • Hypertension
  • Cardiac failure
33
Q

What are possible side effects of loop diuretics?

A
  • Hypovolaemia

- Hypokalaemia (can be used with potassium sparing diuretic)

34
Q

What are indications that thiazides are required?

A
  • CKD
  • Nephrotic syndrome
  • Hypertension
  • Cardiac failure
35
Q

What are possible side effects of thiazides?

A

Hypovolaemia

36
Q

What is effect of Spironolactone?

A

Inhibits aldosterone

This prevents sodium reabsorption in exchange for potassium

37
Q

What is spironolactone also referred to as?

A

Potassium sparing diuretic

38
Q

What are the indications that spironolactone is required?

A
  • Cardiac failure

- Liver cirrhosis (ascites)

39
Q

What is ascites?

A

Abnormal buildup of fluid in the abdomen

40
Q

What is common cause of ascites?

A

High blood pressure in the veins that bring blood to the liver (portal hypertension), which is usually due to cirrhosis.

41
Q

What are possible side effects of spironolcatone?

A

Hyperkalaemia

42
Q

What is amiloride?

A

Potassium sparing diuretic

43
Q

How does amiloride work?

A

Inhibits sodium reabsorption in exchange for potassium

Removes sodium and water

44
Q

What are the most potent diuretics?

A

Loop diuretics

45
Q

When is amiloride is required?

A

To prevent hypokalaemia

46
Q

What are possible side effects of amiloride?

A

Hyperkalaemia

47
Q

How is vitamin D activated?

A

Hydroxylated in liver and then kidneys into calcitriol

48
Q

What is effect of calcitriol?

A

Increase absorption of dietary calcium and phosphorus

49
Q

How do healthy kidneys deal with calcium and phosphorus?

A

Decrease excretion of calcium

Increase excretion of phosphorus

50
Q

If vitamin D is not activated, what happens?

A

Poor absorption of dietary calcium

Parathyroid glands sense low blood calcium and increase PTH secretion

This causes bones to release calcium and phosphorus –> can lead to bone disease and osteoporosis

51
Q

What are vitamin D analogues?

A

A form of synthetic vitamin D

Hydroxylated by liver to active form

52
Q

What are effects of vitamin D analogues?

A

Increases uptake of calcium and phosphate from gut

53
Q

What are possible side effects of vitamin D analogues?

A
  • Hypercalcaemia

- Hyperphosphataemia

54
Q

What is erythropioetin?

A

Stimulates erythropoiesis. Produced by cells in the interstitium of the kidneys.

55
Q

What is erythropioetin secretion stimulated by?

A

Hypoxia

56
Q

Erythropioetin is given as a subcutaneous injection when eGFR drops below what?

A

eGFR < 15

57
Q

What are potential side effects of erythropiotein?

A
  • Hypertension (can lead to strokes)

- Pure red cell aplasia (rare)

58
Q

What does reduced renal perfusion lead to?

A

Decreased transglomerular pressure, therefore decreased GFR

59
Q

How do prostaglandins act on kidney?

A

Vasodilate afferent arteriole (to increase flow)

60
Q

How do NSAIDs affect kidney?

A

Inhibit prostaglandins (reduce perfusion which can be dangerous)

61
Q

What is effect of RAAS system on efferent arteriole? What does this lead to?

A

Vasoconstriction (Ag II), this increases transglomerular pressure and restores GFR

62
Q

What is effect of ACEi and ARBs on efferent vasoconstriction?

A

Inhibit this which decreases transglomerular pressure and decreases GFR

63
Q

What are dangers of ACEi and ARBs in AKI?

A

Can induce renal failure

64
Q

Are penicillins excreted by the kidneys?

A

All penicillins except Flucloxacillin are excreted by the kidneys

65
Q

What can accumulation of penicillin lead to?

A

CNS side effects (including seizures)

66
Q

What can accumulation of opioid analgesics due to poor renal excretion lead to?

A

Accumulation of active metabolites (especially morphine, pethidine and codeine) can lead to increased incidence of CNS side effects and respiratory depression

67
Q

What are the opiates with minimal renal excretion?

A
  • Fentanyl
  • Oxycodone
  • Hydromorphone
68
Q

What can accumulation of digoxin lead to?

A

Bradycardia, visual disturbances, mental confusion

Aggravates hyperkalaemia

69
Q

What can accumulation of hypoglycaemic agents lead to? How can this be reduced?

A

Hypoglycaemia

  • Aggravates hyperkalaemia
  • Reduce dose
  • Monitor drug level
70
Q

What can accumulation of metformin lead to?

A

Poor excretion by kidneys leads to lactic acidosis and hypoglycaemia

71
Q

What herbal medicines are implicated in interstitial nephritis?

A

Chinese herbal medicines with aristocholic acid implicated in interstitial nephritis

Cat’s Claw has anti-inflammatory properties
implicated in causing AKI and hypotension with antihypertensives

Remember to ask patient !

Yr 2 - Renal (16 decks)

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