Cardio - CHF, RAAS Flashcards Preview

Small Animal Medicine > Cardio - CHF, RAAS > Flashcards

Flashcards in Cardio - CHF, RAAS Deck (21)
Loading flashcards...
1

In the short-term, RAAS is _____. Why?

great; BP is maintained in the face of low CO

2

In the long-term, RAAS is _____. Why?

Terrible;

Cardiac fibrosis, renal damage, cytokine activation

3

What are the RAAS activation events?

  1. Juxtaglomerular apparatus releases renin
  2. Renin converts angiotensinogen to angiotensin I
  3. Angiotensin converting enzyme (ACE) converts ATI to ATII in the lungs

4

What do the jusxtaglomerular cells detect?

Low BP, renal blood flow, or sodium

High SNS tone

5

Where is angiotensinogen produced?

liver

6

Where is ACE produced?

endothelial cells in the lungs

7

What can you do if there is low BP?

Increase CO or VR (more volume or more vasoconstriction)

8

What are the actions of ATII?

  1. Increase volume
  2. Increase vascular resistance
  3. Negative effects on the heart

9

Where does ATII act?

PCT to cause Na and water retention

10

What does ATII stimulate?

Aldosterone release from the adrenals and ADH release from the posterior pituitary

11

Where does aldosterone act?

DCT to retain Na and water (K loss)

12

What does ADH do?

Inserts aquaporins into the DCT to allow for free water retention (without Na)

13

What effect does ADH have on thirst?

Increases it by stimulating the thirst center in the hypothalamus

14

What receptors does ATII bind and where?

AT receptors on the vessels leading to vasoconstriction

 

15

ATII binds to the _____ arterial in the glomerulus, causing ____ and increasing intraglomerular pressure to maintin the _____.

efferent, vasconstriction, GFR

16

What does ATII stimulate from the adrenal medulla?

Norepi release, which binds to alpha receptors on vessels causing vasoconstriction

17

What does ATII stimulate that acts as a potent vasoconstrictor?

ADH release

18

ATII --> excessive _____ retention --> _____ in a diseased heart

volume, CHF

19

What are the negative effects of ATII and aldosterone on the heart?

They are cardiotoxic and cause fibrosis, vascular smooth muscle proliferation --> SHT, cytokines and free radical formation that lead to myocyte death

20

ATII cause renal and arteriolar sclerosis leading to _____.

renal damage

21

What are the 4 purposes of pharmacological intervention on RAAS? 

  1. Improve pumping function
    1. Better BP so RAAS isn't stimulated
  2. Stop or counteract RAAS activation/actions
  3. Antihypertensive
    1. Counteracts vasoconstriction
  4. Cardio-protective agents
    1. Reduce fibrosis, CK formation, increased cell death, vascular disease

Decks in Small Animal Medicine Class (100):