Long term control of BP Flashcards

1
Q

What is long term control of blood pressure mediated by?

A
  • revolves around the control of plasma volume by the kidney and involves 3 horemone systems
  • Renin-angiotensin-aldersterone system
  • Antidiuretic factor ( ADH, vasopressin)
  • atrial natriuretic peptide
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2
Q

State the functions fo the kidney

A
  • extrection of waste products
  • maintainence of ion balance
  • regulation of pH
  • regulation of osmolarity
  • regulation of PV ( used to regulate MAP)
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3
Q

Describe the regulation of PV by the kidneys

A

-Starling’s forces= balance between hydrostatic pressure and osmotic pressure.

  • countercurrent system creates high OSMOLARITY outside the collecting duct
  • control over the Na+ transport determines how big the osmotic gradient is
  • control over the permeability of the collecting duct to water determines if water follows that osmotic gradient or not
  • hence, you can control how much water is lost in the urine + how much is retained
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4
Q

The effect of making the collecting duct permeable to water + vise versa

A
  • lots of water reabsorption, little urine and increases PV. Small volume of hyperosmotic(concentrated) urine.
  • making collecting duct impermeable to water will result in little reabsorption + lots of urine ( diuresis) and reduction in PV. Large volume of hypo-osmotic(less concentrated) urine
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5
Q

Where is renin produced?

A

-from juxtaglomerular ( granule cells) of the kidney

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6
Q

What triggers renin production?

A

Low MAP

  • juxtaglomerular apparatus is activated by sympathetic nerves.
  • decreased distension of afferent arterioles ( the renal baroreflex),
  • decreased delivery of Na+/Cl- through the tubule

All of this are signs of low MAP

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7
Q

Function of renin

A

converts inactive angiotensin>angiotensin l

- this is is converted into Angiotensin ll by angiotensin converting enzyme

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8
Q

Function of angiotensin ll

A

Stimulates the release of aldesterone from the adrenal cortex;
-this increases Na+ reasborption in the loop of Henle, hence reduces diuresis and icnreases PV

Increases release of ADH from posterior pituitary gland

  • increases water permeability of the collectig duct, hence reducing diuresis and icnreases PV
  • increases thirst

All of the above increases MAP

Vasoconstriction
-increases TPR

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9
Q

Is the renin-angiotensin-aldersterone system a negative or positive feedback system?

A

-negative feedback system as multiple mechanisms detect any decrease in MAP, stimulates release of renin which evokes mechanisms to increase MAP

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10
Q

Where is ADH produced?

A
  • synthesised in the hypothalamus

- released from posterior pituary gland

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11
Q

What triggwea ADH release?

A
  • decrease in blood volume ( sensed by cardiopulmonary baroreceptors and relayed via the medullary cardiovascular centres)
  • an increase in osmolarity of ISF ( sensed by smoreceptors of hypothalamus)
  • circulating angiotensin ll ( triggered by renin-angiotensin -alderesterone system)

All of the above are signs of low PV and/or MAP

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12
Q

Function of ADH

A
  • increases permeability of collecting duct to H20 + reduces diuresis and increases PV
  • causes vasoconstriction (hence aka vasopressin)

Both increases MAP
-another negative feedback system as many systems decrease any decrease in MAP>ADH> multiple mechanisms activated to increase MAP

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13
Q

Where is atrial natriutetic peptide produced?

A

ANP produced in and releleased from myocardial cells in atria

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14
Q

What triggers ANP release?

A

increased distension of atrium

A sign of increased MAP

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15
Q

Function of ANP

A
  • increases excretion/secretion of Na( natriuresis)
  • inhibits release of renin
  • acts on medullary CV centres to reduce MAP

All of these decreases MAP

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16
Q

Negative feedback of ANP

A

detects increase in MAP > ANP > evokes multiple mechanisms to reduce MAP

17
Q

Identify receptors involved in sensing plasma volume (BP indirectly)

A
  • cardiopulmonary receptors
  • juxtaglomerular cells of the kidney
  • macula densa cells of the kidney ( cells of distal convulated tubule, part of juxtaglomerular apparatus where DCT meets with afferent arteriole)
18
Q

Describe how chronic hypotension results in right sided heart failure

A

Pulmonary hypotension incolves there being high blood pressure in the pulmonary arterioles, so this high so not all the blood pumped in the right ventricle will go into pulmonary circulation as it requries more strength/energy to overcome this increased pressure. Hence, increased afterload occurs and overtime the right ventricle will adapt through hypetrophy but this may not be enough which will decrease SV + Pooling of the blood will occur into the systemic pulmonary circulation.
-Symptoms include a leg oedema, hepatomegaly,, raised JV[

19
Q

How can this lead to left side heart failure?

A

Due to pooling of blood in pulmonary circualtion, less blood will be getting pumped into the systemic circulation, increasing volume and pressure in pulmonary circulation.
-caused by acute MI, mitral valve regugitation, etc

20
Q

Why can right sided HF lead to a pulmonary oedema

A

due to high pulmonary pressure, leakage of ISF of pulmonary capillaries into the lungs will occur . Fluid accumulates in intersitial space=pulmonary oedema
-there is an imbalance of starling’s forces

21
Q

What is starling’s forces

A

-balance betweeen hydrostatic pressure and osmotic pressure

22
Q

How does an oedema affect gas exchange?

A

-fluid build up will decrease the diffusion distance thus decreasing gas exchange. Affects mainly O2 as it is less soluble in water vs CO2