19. Adrenergic & Angiotensin Block in CHF Flashcards Preview

CVPR Exam I > 19. Adrenergic & Angiotensin Block in CHF > Flashcards

Flashcards in 19. Adrenergic & Angiotensin Block in CHF Deck (21)
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1
Q

What is the difference in SE btw an ACE-inhibitor and an ARB?

A

all the same except with ARBs, no cough and less angioedema

2
Q

What are the ACE inhibitors’ side effects?

A
  1. cough (dry, nonproductive) 2. hyperkalemia 3. angioedema 4. renal problems 5. neutropenia 6. hypotension
3
Q

ACE is an enzyme produced in the ____.

A

lungs

4
Q

How is the RAAS stimulated?

A
  1. hypovolemia 2. low NaCL
5
Q

Hydralazine is a _____.

A

vasodilator

5
Q

ACE inhibitors end in -_____.

A

opril

6
Q

Name the 2 vasodilators that are most commonly used.

A
  1. hydralazine 2. isosorbide
7
Q

What is stage B HFrEF?

A

heart structure problem w/o symptoms

8
Q

ACE inhibitors block both ____ and ____.

A

angiotensin conversion to angiotensin-II AND bradykinin conversion to its inactive fragments

8
Q

What does angiotensin II do?

A
  1. vasoconstriction 2. increased sympathetic output 3. increased aldosterone production and Na+ reab 4. increased ADH release 5. increased thirst
10
Q

The ARBs end in -_____.

A

sartan

11
Q

What is stage C HFrEF?

A

structural disease w/ symptoms

12
Q

ARBs mainly have an effect on the ____ receptor.

A

AT1

14
Q

What is your target creatinine clearance level?

A

< 30

15
Q

What does digoxin do?

A

increases CO and SV

16
Q

Angiotensinogen is a zymogen produced in the ____.

A

liver

17
Q

High bradykinin causes?

A

a cough, remodeling of the LV, and vasodilates

18
Q

If your pt is stage C HFrEF and is black, add ____ in addition to the beta blocker and ACEI/ARB.

A

hydralazine and isosorbide

19
Q

Bradykininogen is a zymogen produced in the ____.

A

liver

20
Q

What is stage D HFrEF?

A

refractory - hospitalized pts

21
Q

Why do African Americans need a vasodilator, too?

A
  1. they get HFrEF at an earlier age 2. their HFrEF is more advanced 3. they have a higher rate of mortality and hospitalizations 4. they have more TGF-beta (increased fibrosis) 5. they have increased vasothelin 6. sometimes they’re NO synthetase deficient 7. the RAAS is decreased