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MBCHB3 RBF > Lecture 8: ACE inhibitors > Flashcards

Lecture 8: ACE inhibitors Flashcards

1
Q

What are the pathophysiological effects of RAAS?

A
  • Increased activity in Congestive cardiac failure and hypertension
  • Adverse CV effects
    i.e Cardiac hypertrophy
    i.e Atherosclerosis development and plaque rupture
    i.e Proinflam/pro-oxidant
  • Close relationship with SNS
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2
Q

What does ACE do in addition to ANG conversion?

A

ACE -> Breakdown substance P.

Substance P and Bradykinin augment NO release.

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3
Q

What does ANG2 do on the AT-1?

A
  • Aldosterone
  • Vasoconstriction
  • Inc. salt retention
  • Inc. SNS tone
  • Inc. endothelin
  • Inc. VSM hypertrophy
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4
Q

What is the MoA of ACEi?

A

ACE inhibitors
- Inhibit ACE
= Dec ANG2 activity and conc. of other vasoactive peptides
- Increase bradykinin levels (can be beneficial for the heart)

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5
Q

How do ANG2 antagonists work?

A

Block AT1

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6
Q

Where are AT1 receptors found?

A
  • Kidney
  • Heart
  • Vascular SM
  • Adrenal glands
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7
Q

What are the pathophysiological effects of ANG 2?

A

Cardiomyocyte
- Hypertrophy
- Increased O2 consumption
- Impaired relaxation.

Fibroblast
- Fibrosis

Peripheral artery
- Vasocon
- VSM hypertrophy

Coronary art
- Vasocon
- Atherosclerosis

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8
Q

What type of drug blocks AT1?

A

“sartan’

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9
Q

What are the pathophysiological effects of aldosterone?

A

CM
- Hypertrophy

Fibroblast
- Fibrosis

Peripheral art.
- Vasocon
- Endothelial dysf.

Kidney
- K loss
- Na retention

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10
Q

What happens with long term ACE use?

A

First few weeks plasma benefits:
- Dec ANG 2
- Dec aldo

but later
- ANG2 and aldo increase BECAUSE of chymase activity (A1-A2)
- BUT bradykinin levels increase = vasorelaxation and endothelial function inc.

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11
Q

Compare and contrast ACE vs AT1 blockers:

A

ACE
- Acutely lowers ANG2 and ALDO but chronically this is normalised
- However increased bradykinin is good.

AT1
- Non-competitive block
- Prevents ANG2 function

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12
Q

What are the effects of ACEi and AIIA?

A

Vasodilation
- Dec. art and venous pressure
- Dec. ventricular preload and afterload

Dec. blood volume
- natriuresis (lose Na)
- Diuresis

Dec. SNS activity

Dec. cardiac and vascular hypertrophy

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13
Q

What are some ACE inhibitors?

A

Main one: Cilazapril

others:
Captopril
Enalapril
etc etc

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14
Q

What are some AIIA?

A

Main one: Candesartan

  • Losartan
  • Valsartan
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15
Q

What are the considerations of ACE and AIIA?

A

Be careful with patients that have chronic kidney disease

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16
Q

What are the ACE indications?

A
  • Hypertension (AB) + (CD)
  • Congestive heart failure
17
Q

Write some notes on ACE use in hypertension:

A
  • Monotherapy then combination
  • Diuretic + ACEi (Synergistic combination)
18
Q

Write some notes on ACE use in HFrEF:

A

AS part of multiple treatments
- ACEi
- Diuretic
- Beta blocker
- Aldosterone antagonist

19
Q

What are the AIIA indications?

A

In ACEi intolerant patients

  • Hypertension
  • HF
    -> Candesartan licensed
    -> Dont use ACEi and AIIA, C/I
20
Q

What are common treatment regimes for hypertension?

A

Diuretic + ACEi + Vasodilator

21
Q

What are some common treatment regimes for heart failure?

A

Diuretic + ACEi (OR AIIA) + B-blocker + Spironolactone

22
Q

What are the SE of ACE?

A
  • Dry cough (Bradykinin/Sub P stimulate C-fibres in lungs)
  • Hyperkalemia
  • Renal Fx deterioration
  • Hypotension
  • Angiooedema
23
Q

What are the SE of AIIA?

A
  • Dry cough
  • Hyperkalemia
  • Renal Fx deterioration
  • Hypotension
  • Angiooedema
24
Q

What are the real cautions when using ACE and AIIA?

A
  • Hyperkalemia
  • Renal impairment
  • Volume depletion / diuresed patients

Absolute contradindications
- Bilateral renal stenosis
- Pregnancy

25
Q

What is bilateral renal art stenosis a C/I?

A

ANG2 required in these patients to constrict the efferent arteriole to maintain pressure across glomerulus. Otherwise AKI.

26
Q

Why is ACE / AIIA C/I in pregenacy?

A

Cross placental and cause renal defects and hypotension

27
Q

What are the non-BP lowering effects of ACE?

A

Cardio-protective
- Beneficial effects independent of lowering BP

  • Reduced incidence of developing new db
28
Q

Whats the role of ANG2 and db?

A

ANG2:
- Inc. SNS
- Pro inflam and oxidant
- Impairs insulin signalling
- Impairs pancreas function
- Reduced insulin sensitivity

29
Q

Is there any added benefits of blocking renin directy?

A

No

MBCHB3 RBF (39 decks)

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