RAAS Flashcards

1
Q

What are the two main processes of RAAS

A
  • Alteration of vascular tone

- Controlling Na+ levels

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2
Q

What kind of enzyme is renin

A

Proteolytic

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3
Q

What stimulates renin release

A
  • Sympathetic stimulation of beta-agonist receptors
  • Decreased glomerular filtration
  • Decrease in renal perfusion pressure
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4
Q

What does renin do

A

Converts angiotensinogen into angiotensin I

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5
Q

What does ACE do

A

Converts angiotensin I into angiotensin II

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6
Q

Where is ACE located

A

Primarily in endothelial cells in the lungs

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7
Q

What does angiotensin II do to blood vessels and via what receptors and mechanisms (2 pathways)

A

1) It is a potent vasoconstrictor via AT-1 receptors, a g-protein coupled receptor that increases Ca2+ levels and smooth muscle contraction
2) via increased noradrenaline from sympathetic nerves (NA another g-protein receptor ligand)

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8
Q

What does angiotensin II do in regards to natriuresis (2 pathways)

A

Stimulates aldosterone secretion which:

1) Increases apical Na+ channels
2) Aldosterone binds with mineralocorticoid receptor resulting in increased expression of ENac channels which are inserted in the basolateral membrane of cells of the collecting tubules resulting in Na+ reabsorption.
3) Increased tubular reabsorption of Na+

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9
Q

What are the two main drugs that target the RAAS

A

ACE inhibitors

Angiotensin receptor antagonists (ARBs)

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10
Q

More minor drugs that target RAAS (4)

A

Aldosterone antagonists
Calcium channel blockers
Diuretics
Beta-blockers

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11
Q

What does ACE-Is do and how

A

Mimics the section of angiotensin I that binds to ACE, binds to ACE itself and stops ACE from binding to angiotensin I (a competitive inhibitor)

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12
Q

What is an example of an ACE inhibitor

A

Cilazipril

anything that ends in ipril os probably an ACE inhibitor

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13
Q

What is the secondary effect of ACE inhibitors

A

ACE are also known as kininase II which degrades bradykinin (inflammatory mediators). Therefore ACE-Is increase bradykinin

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14
Q

What are two main adverse effects that stem from increased bradykinin that occur with ACE-is use

A

Dry cough and angioedema

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15
Q

Why does angioedema occur with ACE-Is use. Where does this most commonly occur?

A

Because of the increased levels of bradykinin which are inflammatory mediators that cause vasodilation and increased permeability.
Lips, larynx, pharynx. Can block airways!

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16
Q

How do angiotensin receptor blockers work

A

Through binding to the AT1 receptors that bind angiotensin II

17
Q

Example of an ARB

A

Losartan

18
Q

What is generally more effective ACE-Is or ARB

A

ACE-Is

19
Q

Why would you use an ARB over an ACE-Is

A

Less adverse effects (dry cough and angiodema)

20
Q

How do aldosterone antagonist works

A

Antagonist at the mineralocorticoid receptor stopping the EnaC channels. Act as diuretics as prevent Na+ reabsorption

21
Q

What is an example of an aldosterone antagonist

A

Spirolactone

22
Q

How do calcium channel blockers work

A

Block Ca2+ channels decreasing the contractility of muscles

23
Q

Two commonly prescribed Calcium channel blockers

A

Nifedipine, verapamil

24
Q

Three diuretics

A

Loop diuretics, thiazides, amiloride

25
Q

How do loop diuretics work

A

Block the reabsorption of Na+ through acting on the Na+ K+ Cl- symporter in the thick ascending limb

26
Q

How do thiazide diuretics works

A

By blocking Na+ reabsorption in the the distal convoluted tubule (Na+ Cl- exchangers)

27
Q

How do amilorides work

A

By blocking the EnaC channels in the late distal convoluted tubule preventing Na+ reabsorption

28
Q

How do beta blockers work

A

Competetive antagonist at Beta- adrenergic receptors,primarily B1
Decrease cardiac contractility and decrease renin secretion.

29
Q

Example of a beta blocker

A

Metoprolol