Lecture 6 (RAAS and Hemodynamics) Flashcards

1
Q

Function of Renin:

A

necessary for angiotensin II synthesis

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2
Q

Function of Angiotensin II:

A
  • vasoconstrictor
  • stimulates aldosterone secretion from adrenal cortex
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3
Q

Function of Aldosterone:

A
  • promotes Na+ conservation by kidneys; H2O follows Na+
  • increases intravascular volume
  • vasoconstrictor
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4
Q

All angiotensin II bioactivity in vascular smooth muscle and cardiac muscle is mediated by what receptor?

A

AT1

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5
Q

Actions of angiotensin II that lead to increased blood pressure (4):

A
  1. vasoconstriction
  2. block in high pressure baroreceptor activity
  3. increased aldosterone levels
  4. stimulation of norepi release from post-ganglionic SNS fibers
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6
Q

Angiotensin II can block high pressure baroreceptor input. How does this cause an increase in BP?

A
  • endogenous counter-response to elevated BP is neutralized.
  • SNS not shut off in response to elevated BP.
  • SNS has free-reign to maintain increased BP.
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7
Q

Where are receptors for RAAS (angiotensin II and aldosterone) located?

A
  1. myocardium
  2. vascular smooth muscle
  3. kidney
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8
Q

Effect of RAAS (aldosterone and angiotensin II) on the heart:

A
  • contributes to left ventricular hypertrophy
  • increased wall stress and oxygen demand
  • reduced ejection fraction
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9
Q

Effect of RAAS (aldosterone and angiotensin II) on vascular smooth muscle:

A
  • leads to tunica intima and tunica media thickening
  • can cause vascular stenosis
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10
Q

Effect of RAAS (aldosterone and angiotensin II) on the kidney:

A
  • impairs normal renal function
  • can lead to renal failure.
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11
Q

Treatments for hypertension:

A
  1. ACE inhibitors (angiotensin II)
  2. ARBs (AT1 receptors)
  3. Diuretics (aldosterone)
  4. Calcium channel blockers (amlodipine)
  5. beta-blockers (SNS)
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12
Q

Function of verapamil and cardizem:

A
  • blocks Type L calcium channels in the heart.
  • help reduce heart rate by increasing AV nodal delay.
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13
Q

Function of amlodipine:

A
  • blocks Type L calcium channels in vascular smooth muscle.
  • prevents vasoconstriction.
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14
Q

Primary hypertension:

A
  • hypertension due to an unknown cause.
  • treatable with general hypertension protocol.
  • ACE inhibitors, ARBs, calcium channel blockers, etc.
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15
Q

Secondary hypertension:

A
  • hypertension due to another medical condition.
  • not treatable with general hypertension protocol.
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16
Q

How, specifically, does using a beta-blocker decrease blood pressure?

A
  • beta-blockers block SNS effects on the heart.
  • decrease HR and inotropy, and therefore CO.
  • CO = SV x HR.
  • MAP = CO X TPR.
17
Q

General primary hypertension treatment protocol:

A
  • First:
    • thiazide diuretic
  • Second:
    • thiazide diuretic + ACE inhibitor/ARB
  • Third:
    • thiazide diuretic + ACE inhibitor/ARB + Ca2+ channel antagonist
18
Q

The four body systems involved in hypertension, and drugs that target their function:

A
  • cardiac
    • calcium channel blockers, beta-blockers
  • renal
    • diuretics, ACE inhibitors, ARBs
  • vascular smooth muscle
    • calcium channel blockers, ACE inhibitors, ARBs, alpha-1 receptor blockers
  • ANS
    • beta-blockers
19
Q

Blood vessels with the highest velocity and lowest velocity of flow:

A
  • highest velocity: aorta
  • lowest velocity: capillaries
20
Q

Blood vessels with the highest and lowest total cross-sectional area:

A
  • highest: capillaries
  • lowest: aorta
21
Q

Blood vessels with the highest and lowest transmural (wall) pressure:

A
  • highest: aorta
  • lowest: vena cava
22
Q

Total peripheral resistance equation:

A
  • TPR = (Pa - Pv)/Qt.
    • Qt = cardiac output (CO = SV x HR).
  • Pa - Pv = CO x R
23
Q

60% of total peripheral resistance is due to:

A
  • arteriolar resistance
    • Arterioles can undergo 4x changes in lumen diameter, which leads to up to a 256x change in conductance.
24
Q

Which blood vessel has the greatest influence over total peripheral resistance?

A

arterioles

25
Peak arterial pressure occurs at:
* the end of decreased/slow systolic ejection phase, which is the end of the T wave.
26
Lowest arterial pressure occurs at:
* the end of isovolumetric contraction. * immediately before the aortic valve opens
27
Draw ECG with arterial pressure graph underneath:
28
Where does systolic pressure normalize with diastolic pressure?
* right before entering the capillaries after traveling through the arterioles.
29
How do arterioles maintain a relatively constant capillary pressure?
* **by adjusting resistance to flow with precapillary sphincters.** * **ΔP = Q x R** * flow (Q) and capillary pressure remain relatively constant, so arterioles adjust arterial pressure going into capillaries via resistance.
30
The four Starling forces governing capillary filtration/exchange with the interstitial fluid:
1. Capillary hydrostatic pressure 2. Capillary oncotic pressure 3. Interstitial fluid hydrostatic pressure 4. Interstitial fluid oncotic pressure
31
What is oncotic pressure, and how does it affect capillary filtration?
* The tendency for fluids to be pulled toward proteins. * Albumin generates about 70% of the oncotic pressure in capillaries, which decreases capillary filtration into interstitial fluid.
32
On what end of capillaries is filtration the greatest?
* arteriole * Pcap \> Pif; filtration occurs * πif \> πcap; filtration occurs
33
Draw a capillary with starling force magnitudes:
34
What carries capillary filtrate in the interstitial fluid back to the venous system?
* lymphatic ducts
35
Lymphatic function is compromised if the amount of capillary filtrate in the interstitial fluid is greatly increased. This causes edema. How can this occur?
1. increased arterial pressure (increased Pcap) 2. increased venous pressure (increased Pcap) 3. a pathological increase in capillary permeability
36
When does edema occur?
* when there is increased capillary pressure that leads to increased filtration that overwhelms the lymphatic system.
37
The two types of diffusion that occurs from capillaries to interstitial fluid:
1. **via pores:** * water soluble molecules; rapid 2. **via plasma membrane:** * lipid-soluble molecules (gases); very rapid
38
The pressure drop across the arterial-venous tree is determined by what equation?
**Pa - Pv = CO x R** * R is determined by the arterial side, mostly by arterioles. (TPR = (Pa - Pv)/QT)