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Block 3 > MMT: renin angiotensin > Flashcards

MMT: renin angiotensin Flashcards

1
Q

What is the rate limiting step in the RAAS pathway?

A

Activating renin

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2
Q

What are the main steps of the RAAS pathway?

A
  1. Renin activates angiotensinogen to angiotensin I
  2. ACE converts angiotensin I to angiotensin II
  3. Angiotensin II increases aldosterone secretion and causes vasoconstriction
  4. Sodium and water retention/increased peripheral vascular resistance
  5. Increased blood pressure
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3
Q

Does increased blood pressure impact afterload or preload?

A

Increases afterload

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4
Q

Does increased sodium and water retention impact afterload or preload?

A

Increases preload

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5
Q

What other enzyme can ACE cleave? What is the significance of this?

A

Bradykinin: it affects its vasodilation ability

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6
Q

Describe the movement of blood through the glomerulus.

A
  1. Blood enters the afferent arteriole
  2. Blood moves through the proximal tubule
  3. Blood moves through the distal tubule
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7
Q

What mechanics facilitate filtration of blood in the glomerulus?

A

Hydrostatic pressure caused by the afferent arteriole having a larger diameter than the efferent arteriole

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8
Q

What does the macula densa do?

A

Senses salt; if it senses too little it will activate renin

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9
Q

What do the juxtaglomerular cells do?

A

They sense stretch; decreased stretch will cause them to release renin

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10
Q

What 3 factors stimulate renin release?

A
  1. Salt content (macula densa)
  2. Blood pressure (juxtaglomerular cells)
  3. SNS (beta 1)
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11
Q

How is further renin release inhibited?

A

Ang II acts on the JD cells via negative feedback

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12
Q

What are fast impacts of ang II?

A

Direct vasoconstriction, enhanced noradrenergic actions in the periphery, increased sympathetic discharge, and release of catecholamines from the adrenal medulla

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13
Q

How do angiotensin II receptors work?

A

They’re coupled to Gq and lead to calcium release

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14
Q

Describe the relationship between Ang II and SNS.

A

They kind of function like a positive feedback loop!

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15
Q

What are the effects of Ang II at the kidneys?

A

Increased sodium and water retention, aldosterone release, increased renal sympathetic tone, and renal vasoconstriction

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16
Q

How does Ang II impact GFR?

A

It constricts the efferent arteriole more than the afferent arteriole, supporting GFR and causing more filtration

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17
Q

Describe how Ang II impacts cardiomyocytes and the heart.

A

Increases myocyte hypertrophy and ECM deposition which leads to stiffness. It will also increase preload, afterload, and tension. All of these combined can be a major contributor to heart failure. The body uses the RAAS system to try to help, but ends up making it worse.

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18
Q

What is the MOA of ACE inhibitors?

A

Conversion of Ang I to Ang II is decreased, which leads to lower aldosterone, lower SNS, lower vascular tone, increased bradykinin

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19
Q

What is THE tell for an ACE inhibitor?

A

Increased bradykinin

20
Q

What happens to Ang I and renin as a result of ACE inhibitors?

A

They go up since Ang II isn’t being produced to lead to negative feedback

21
Q

What is the effect of renovascular disease on RAAS?

A

RAAS is ramped up to try to support GFR due to low blood flow coming in

22
Q

What happens if you give someone with renovascular disease ACE inhibitors?

A

Kidney injury or failure

23
Q

How do ACE inhibitors impact heart functions?

A

Preload decreases, afterload decreases, CO increases, and LVH decreases. This makes them first-line for chronic heart failure.

24
Q

Why give an ACE inhibitor to someone who has had an MI?

A

Decreased morbidity and mortality

25
Q

What 4 drugs do patients who have had an MI take?

A

Beta blocker, statin, aspirin, and ACE inhibitors

26
Q

What events can ACE inhibitors help decrease?

A

Nonfatal strokes, cardiovascular death, acute MI

27
Q

Describe diabetic nephropathy, and how we treat it.

A

The pressure in the glomerulus is too high, which can lead to injury and kidney function issues. They’re typically given ACE inhibitors to reduce BP and dilate the efferent arteriole, resulting in decreased pressure in the glomerulus.

28
Q

Protein in the urine is a sign of…

A

Diabetic nephropathy

29
Q

What are the adverse effects of ACE inhibitors?

A

Cough, angioedema, first dose hypertension, hyperkalemia

30
Q

What side effect is bradykinin responsible for in ACE inhibitors?

A

Cough and angioedema

31
Q

In what cases do you not give ACE inhibitors?

A

Those with history of angioedema, people taking renin inhibitors, people taking TMP-SMX, those with bilateral renal artery stenosis, and pregnancy

32
Q

What causes hyperkalemia in ACE inhibitors? Who is at higher risk?

A

Decreased aldosterone; those taking K sparing diuretics or TMP-SMX

33
Q

What is the MOA of ARBs?

A

AT1 antagonism

34
Q

What are ARBs commonly used for?

A

HTN and heart failure

35
Q

What are major side effects of ARBs?

A

Hyperkalemia, TMP-SMX contraindication, teratogenic

36
Q

With ARBs, which compounds increase?

A

Ang I, Ang II, and renin

37
Q

What is the MOA of aliskrein?

A

It is a renin antagonist

38
Q

What is aliskrein used for?

A

HTN, but it isn’t common

39
Q

What are the adverse effects of aliskrein?

A

Hyperkalemia, especially with ACEi or ARBs

40
Q

Blocking which adrenergic receptors will decrease renin release?

A

Beta 2 and alpha 2

41
Q

What drives aldosterone release?

A

Ang II and elevated K

42
Q

What are the prototypes for aldosterone antagonists?

A

Spironolactone and eplerenone

43
Q

Why are aldosterone antagonists used in heart failure?

A

They can prevent heart remodeling aka stiffness and thickening

44
Q

What are aldosterone antagonists used for?

A

Hypertension and chronic heart failure

45
Q

What are side effects of spironolactone?

A

Sexual dysfunction, hyperkalemia

Block 3 (21 decks)

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