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Pharma > Drugs Used For The Treatment Of Hypertension III: Drugs Acting On The Renin-angiotensin-aldosterone System > Flashcards

Drugs Used For The Treatment Of Hypertension III: Drugs Acting On The Renin-angiotensin-aldosterone System Flashcards

1
Q

Where is renin produced?

A

Kidney

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2
Q

Where is angiotensinogen produced?

A

The liver

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3
Q

What is the action of renin?

A

Converts angiotensinogen to angiotensin I

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4
Q

Where is ACE found?

A

Plasma

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5
Q

What is the action of ACE?

A

Converts AT1 to AT2

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6
Q

What is the effect of ACE on bradykinin?

A

ACE inactivates bradykinin

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7
Q

What tissues does angiotensin II work on?

A

Adrenal cortex

Blood vessels

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8
Q

What receptors do angiotensin II work on?

A

AT-1

Angiotensin 2 type 1 receptors

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9
Q

What is the action of ACEIs?

A

Inhibit the conversion of AT1 to AT2

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10
Q

What is the action of ATII on the adrenal cortex?

A

Release of aldosterone

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11
Q

Which part of the adrenal cortex is aldosterone released from?

A

The zone glomerulosa

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12
Q

What is the effect of ATII on the blood vessels?

A

Vasoconstriction

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13
Q

What drug inhibits renin?

A

Aliskiren

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14
Q

What accumulates as a result of the action of aliskiren?

A

Angiotensinogen

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15
Q

What does the use of aliskiren prevent the accumulation of?

A

ATI

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16
Q

What does the use of ACEI result in the accumulation of ?

A

ATI and bradykinin

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17
Q

What does the use of ACEI result in the decreased formation of?

A

ATII

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18
Q

What is the receptor for ARBs?

A

Angiotensin II type 1 receptors

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19
Q

What are the effects of aliskiren, ARBs and ACEIs?

A

Vasodilation

Decreased aldosterone secretion

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20
Q

What is the action of aldosterone?

A

Na+ and water retention

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21
Q

Do ARBs interfere with bradykinin degradation?

A

No

As ACE is not affected when ARBs are used

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22
Q

Why are ARBs and ACEIs protective in diabetic nephropathy?

A

ATII constricts the efferent arterioles of the kidney. If ARBs and ACEs are used there is no ATII action so there is dilation of the efferent arteriole. Therefore filtration pressure and GFR decreases — this decreases the work of the kidney and reduces the risk of proteinuria.

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23
Q

What is the action of PG on the afferent arteriole of the kidney?

A

Vasodilation

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24
Q

When is there maximum filtration pressure and maximum GFR?

A

When PG dilates the afferent arteriole and ATII constricts the efferent arteriole

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25
Q

What is the clinical indication of aliskiren?

A

Mild to moderate hypertension

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26
Q

What are the clinical indications of ARBs and ACEIs?

A

Mild to moderate hypertension
Protective of diabetic nephropathy
CHF

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27
Q

What are the side effects of ACEIs, ARBs and aliskiren?

A 
Hyperkalemia
Acute renal failure in renal artery stenosis
Angioedemia 
Dry cough (only in ACEIs) 
Hypotension
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28
Q

When do we not use aliskiren, ACEIs, ARBs?

A

Pregnancy
Bilateral renal artery stenosis
Hypotension

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29
Q

Why does aliskiren, ARBs and ACEIs cause hyperkalemia?

A

Aldosterone promotes K+ wasting, if there is no aldosterone action then no K+ wasting resulting in hyperkalemia

30
Q

Why are ARBs, ACEIs and aliskiren not advised in renal artery stenosis?

A

In renal artery stenosis there is already a decreased GFR. If you prevent the vasoconstriction of the efferent arteriole via the use of one of these drugs, then the GFR decreases further as the filtration pressure is reduced.

31
Q

What are the enhancers of renin release?

A

Decreased blood flow or hypotension
NaCl excretion
SY stimulation via Beta 1 receptors

32
Q

What are the clinical indications for RAAS inhibitors?

A 
Hypertension
Diabetic nephropathy 
Metabolic syndrome: insulin sensitivity increases and insulin resistance decreases
CHF
IHD
LVH
33
Q

Which drugs do RAAS inhibitors interact with?

A

K+ sparing diuretics
Lithium (can increase Li toxicity)
Antidiabetic drugs (hypoglycemic effects may be enhanced)
Cytostatics and immunosuppressants (there is a risk of hypersensitivity)

34
Q

Name the ACEIs

A 
Captopril
Fosinopril 
Zofenopril
Perindopril
Enalapril
Lisinopril
Ramipril
35
Q

How are ACEIs administered?

A

Orally

36
Q

Where are the ACEIs eliminated?

A

The kidney (apart from fosinopril)

37
Q

Which ACEI is not eliminated in the kidney?

A

Fosinopril

38
Q

Where is Fosinopril eliminated?

A

Partly in the liver

39
Q

Which of the ACEIs are pro drugs?

A

Fosinopril
Zofenopril
Perindopril
Enalapril

Ramipril

40
Q

Where and how are the pro-drugs ACEIs activated and how?

A

Hydrolysis in the liver

41
Q

Where does glucuronidation of ACEIs take place?

A

The liver

42
Q

What is the bioavailability of ACEIs?

A

Mild to moderate

43
Q

What is the plasma half life of Captopril?

A

2h

44
Q

What is the plasma half life of Fosinopril?

A

4h

45
Q

What is the plasma half life of Zofenopril?

A

5-6h

46
Q

What is the plasma half life of Perindopril?

A

9h

47
Q

What is the plasma half life of Enalapril?

A

11h

48
Q

What is the plasma half life of Lisinopril?

A

12.5h

49
Q

What is the plasma half life of ramipril?

A

15h

50
Q

Which ACEI has the longest plasma half life?

A

Ramipril

51
Q

Which ACEI has the shortest half life?

A

Captopril

52
Q

What is the mechanism of action of ACEIs?

A

There is a decrease in ATII which leads to decreased aldosterone secretion. There is decreased Na+ and water retension which reduces pre and after load — decreasing the work of the heart.

In addition decreased ATII results in a decrease in peripheral vascular resistance which results in a decrease in BP.

53
Q

Name the ARBs

A 
Losartan
Eprosartan
Valsartan
Candesartan
Irbesartan
Telmisartan
54
Q

Which ARB has the largest bioavailability?

A

Irbesartan

55
Q

Which ARB has the smallest bioavailability?

A

Eprosartan

56
Q

Which ARB has the longest plasma half life?

How long is it?

A

Telmisartan

> 20h

57
Q

Which ARBs has the shortest plasma half life?

What is it?

A

Losartan

2-3h

58
Q

Why would you use ARBs over ACEIs?

A

If the patient has tried ACEIs and developed dry cough or angioedema

59
Q

What are the effects of ARBs?

A

Arteriolar and venous dilation and block of aldosterone secretion.

Decreased BP and Na+ and H20 retention

60
Q

What is the dose of Valsartan?

A

1 x 80-320mg

61
Q

How is aliskiren administered?

A

Orally

62
Q

How is aliskiren eliminated?

A

Without inactivation (mainly)

63
Q

In reference to aliskiren, when is P-glycoprotein involved?

A

Absorption and biliary excretion

64
Q

What are the drug interactions of aliskiren?

A

P-glycoproteins inducers (e.g., Rifampicin) decrease the bioavailability

P-glycoproteins inhibitors (e.g., ketoconazole, verapamil) enhance the plasma level.

65
Q

What should be avoided when ACEI are prescribed?

A

Potassium supplements and potassium sparing diuretics

66
Q

Why should potassium sparing diuretics be avoided when using ACEI?

A

Because it can cause hyperkalemia

aldosterone promotes the retention of Na and H20 and the excretion of K. If there is no aldosterone action, then K is not increased therefore there is the risk of hyperkalemia when used with potassium sparing diuretics.

67
Q

What may occur when ACEI are introduced to patients with HF who are already taking high dose diuretics?

A

Profound first dose hypotension

68
Q

What should be checked before starting ACEI? (or before increasing the dose)

A

Renal function and electrolytes

69
Q

When should ACEI be completely avoided?

A

in patients with severe bilateral renal artery stenosis (or severe stenosis of the artery supplying a single functioning kidney).

70
Q

When should ACEI be used with caution?

A

if the patient may have undiagnosed or clinically silent renovascular disease: this includes patients with peripheral vascular disease or those with severe generalised atherosclerosis.

Pharma (23 decks)

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