lecture 19 Flashcards

1
Q

how is covid19 related to the angiotensin 2 disease state

A

SARSCoV2 spike proteins bind to target cells via angiotensin converting enz 2 > inhibition of ACE2 + decreased ACE2 expression in infected cells > higher circulating levels of Ang2

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2
Q

what are the harmful effects of ang2 and how does body stop it

A

ang2 can cause damage to tissues
- in alveoli = decrease lung uptake oxygen
- in cardiac myoc = CHF
can also cause inflammation and apoptosis

stop by ACE2 break down to ang1-7 and can bind to MAS1 R to counteract harmful effects

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3
Q

how does BV correlate with BP

A

= increase BV = increase pressure on walls of blood vessels
= increase BV > increase venous return to heart > increased stroke volume > increased cardiac output > increased BP

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4
Q

how does increased SNS input to kidney act contribute to hypertension

A

increase SNS input to kidneys > increase renin > increase ang2 = decreased renal Na secretion = BV increases BP increases (these effects can contribute to chronic hypertension)

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5
Q

what is renal SNS involvement in hypertension

A

efferent renal sns act. usually increases hypertension
- (chronic lowlevel renal nerve stim induces hypertension)
- sympatholytic drugs decrease BP

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6
Q

how can the renin-angio system be manipulated to clinically decrease BP

A

inhibition via
AT1 anta
ACE inhibi
b blockers

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7
Q

whats AT1 R anta clinically useful for + ex

A

useful for lowering BP
- Cozaar = angiotensin 2 R blocker (ARB)
- decrease vasocon
- decreases release of aldosterone

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8
Q

whats ACE inhibitors clinically useful for + ex

A

useful for lowering BP
- inhibits ACE > deccrease amount of angiotensin 2 produced = lower BP

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9
Q

whats b blocker clinically useful for + ex

A

lowering BP
- decrease ang2 production
- inhibit renin release from JG cells caused by SNS act
- b blocker decrease BP by inhibiting the blood pressure increasing effects of ang2 (vasocon + incr salt intake + increase water in)

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10
Q

What is CHF

A

heart failture due to reduction of contractility of heart > decrease stroke volume > decrease BP > this decrease cardiac output causes activation of compensatory system (Vasopressin RAS SNS) and to increase fluid retention to increase volume of blood delivered to heart
- increase volume stretches muscles (result in decreasing SV and fluid accumulation in tissues)

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11
Q

describe starling’s law

A

drop in BP causes increase fluid retention > increased volume of blood increases stroke volume
The greater that the heart muscle is stretched during diastole the greater the force of contraction during systole

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12
Q

CHF in the right side of the heart

A
  • failure of right ventricle = accumulation of blood in right heart + venous system >blood vessels accum in capillaries = weaker + fluid build up in tissue > edema (more pronounced in lower extremities due to grav)
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13
Q

CHF in the left side of the heart

A
  • failure of left side = accumulation of blood in pulmonary circulation > blood in lungs = cant breath
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14
Q

treatments for CHF?

A

AT1 anta - decrease effects of ang2 > decrease retention of Na and water and decrease vasocon
ACE inhib - decrease production of ang2
b blockers - decrease SNS mediated production of ang2
diuretics - increase excretion of na and water by kidneys (loop stronger than thiazide)

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15
Q

describe function of loops of henle, thick ascending limb, distal con tubule

A

loop of henle = sire for water reabsorption driven by hyperosmotic interstitium of renal medulla
thick ascending limb = site of Na K Cl reuptake transport
distal convoluting tub = site of na reuptake trans

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16
Q

describe diuretic action in renal tub

A
  • in thick ascending limb: loop diuretics inhibit the Na K Cl symporter > decreases Na absorp (normally reabsorbs 25% of Na+ load)
  • in distal con tub: thiazide diuretics inhibit Na Cl transporter (normally 5%)
17
Q

the renin-angiotensin-system is antagonized by _____ peptides and released with _____

A

natriuretic peptides - increase sodium excretion and released with hypervol

18
Q

what are the 2 natriuretic peptides

A

Atrial natriuretc peptide (ANP) is produced by
smooth muscle cells in the heart atria
Brain-type natriuretic peptide (BNP) is produced
by the CNS as well as the heart ventricles

19
Q

what tissues does natriuretic peptides act on

A

vasculature (induce dilation) and kidneys (increase glomerular filtration rate, Increase excretion of sodium, Decrease release of renin)

20
Q

what are natriuretic peptides effect on vasculature

A

induce dilation
reduce calcium released from SR + reduce calcium sensitivity of contractile proteins = lower BP

21
Q

what are natriuretic peptides effect on kidney to increase filtration rate

A
  • causes relaxation of glomerular cells > increases SA for filtration of blood = diuresis
22
Q

what are natriuretic peptides effect on kidney to increase sodium excretion

A

inhibit Na reabsorption in kidney tubules so inhibit Na chs = diuresis

23
Q

what are natriuretic peptides effect on kidney to decreases release of renin

A

decreases ang2 lvls > decreases aldosterone levels > decrease vasoconstriction

24
Q

whats ACE inhibitors clinically useful for + ex

A

useful for lowering BP
- inhibits ACE > decrease amount of angiotensin 2 produced = lower BP