RAS

Question 1

Effective Circulating Volume

Answer 1

Amount of blood in arterial tree, bc venous blood pretty static and useless. What your BP sensing mechs actually sense

Question 2

Fast vs Slow Responses to Maintain BP

Answer 2

BaroR -> symp response mediated vs. RAAS mediated

Question 3

Problem w/ Long Term Sympathetic Response

Answer 3

Increased SVR from arteriolar constriction can lead to organ ischemia long term

Question 4

Purpose of RAAS

Answer 4

To return effective circulating volume to normal by increasing plasma volume (not hematocrit bc that would increase viscosity)

Question 5

2 Mechs of Nephron to Detect Renal Perfusion

Answer 5

BaroRs in afferent arteriole (JG cells)

Amount of Cl- delivered to distal tubule Macula Densa cells (indirect marker for Na excretion)

Question 6

3 Factors that Induce Renin Secretion by JG Cells

Answer 6

Decreased perfusion pressure (BaroR)
Decreased delivery of Cl- to distal tubule (macula densa cells)
Beta1 Stimulation

Question 7

Renin Action

Answer 7

Converts angiotensinogen (constitutive from liver) to AT1

Question 8

Angiotensin Receptor Type 1 (AT1)

Answer 8

GPCR (uses guanidine) to activate PLC when activated by peptide hormone ATII

Question 9

5 Actions of ATII

Answer 9

Peripheral arterial vasoconstriction (SVR)
Constriction of efferent arteriole of glomerulus
Increased synth/release of aldosterone
Increased Na reabsorption in proximal tubule
Increased ADH hormone release

Question 10

Hypoperfusion in Kidneys

Answer 10

No actual damage to kidney, just decreased pressure pushing plasma through capillary pores so you develop kidney failure. ATII constricts efferent arteriole to increase pressure, so its production is essential to maintain GFR in volume depletion/hypotension/low CO states

Question 11

Aldosterone (synth, action, consequence)

Answer 11

Synth in zona glomerulosa of adrenal glands stimulated by ATII, and binds to R in Principle Cells of Distal Tubule. Increases reabsorption but enhances K+ secretion (to balance) so all patients with RAAS activation are prone to HYPOKALEMIA

Question 12

CNS Effect of ATII

Answer 12

Stimulates ADH release from hypothal, which acts on water reabsorption in colectiving ducts

Question 13

Direct ATII Effect on Kidney

Answer 13

Increase Na reabsorption in proximal tubule

Question 14

Macula Densa Cells

Answer 14

Sense Cl- delivery, when low release PGs to diffuse from distal tubule to JGs in afferent arteriole to produce renin

Question 15

3 Components of JGA

Answer 15

Macula Densa, JG cells, and Lacis cells (modified smooth muscle cells that help control constriction of aff arteriole)

Question 16

3/4 Long Term Consequences of RAAS Activation

Answer 16

Edema from Na retention
Increased afterload (SVR) from peripheral vasoconstriction
Remodelling of heart - arrhythmias/Cardiorenal syndrome - leads to fibrosis and scarring of heart and kidney (even when kidney is fine, so gets damage from cardiac problems)

Question 17

2 Helpful Drug Suffixes

Answer 17

"pril" = ACEi
"artan" = ARB (blocks AT1 receptor)

Question 18

Major Electrolyte Complication of RAAS Inhibition

Answer 18

Hyperkalemia, for opposite reason that you get hypokalemia w/ RAS activation

Question 19

Major Consideration w/ ACEi or ARBs

Answer 19

So teratogenic it’ll make your face fall off

Question 20

Side Effect w/ ACEi

Answer 20

ACE is also kininase, which breaks down bradykinin, so that’s inhibited so you get fluid leakage in throat and shit leading to cough

Question 21

BNP

Answer 21

Kinda does a lot of same things as RAS (efferent vasoconstriction and shit) but inhibits RAS, so heart’s mech to try to avoid that whole ordeal while still maintaining kidney function in cardiac disease