Physio_19.txt

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c_sopkovich
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64162
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Physio_19.txt
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2011-02-04 20:13:04
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Physiology
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Chapter 19
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  1. Rising pressure in the kidney
    has a direct effect to cause excretion of the excess fluid thus returning pressure back to normal
  2. Pressure diuresis
    an increase in pressure of only a few mmHg can double the renal output of water
  3. Pressure natiuresis
    increases pressure increases the amount of salt lost in the urine
  4. Even if the pressure is only 1 mmHg above normal the loss of fluid will be greater then the intake until pressure is brought back to the equilibrium point
  5. Infinite feedback gain of pressure
    the kidneys will adjust volume loss and gain to return pressure ot the equilibrium point
  6. Two ways in which the pressure equilibrium point can be changed from 100mmHg
    • shift the pressure level of renal output
    • change the level of the salt and water intake line
    • both caused by abnormalities
  7. An acute rise in TPR will cause a rise in arterial pressure
    • with normal functioning kidneys this pressure will not be maintained
    • Changing resistance anywhere in the body except the kidney does not change the equilibrium pioint for blood pressure
  8. Autoregulation and increased CO
    • As cardiac output increases the heart brain and muscles begin to autoregulate.
    • This leads to and increase in TPR and an increase in arterial pressure
    • a normal kidney will increase volume loss to compensate for the pressure change
  9. HTN and PVR
    The culprit for the increases pressure is not the increased PVR it is the increases intrarenal resistance that decreases fluid output and causes HTN
  10. Salt vs water on pressure
    • it has been shown the pure water is excreted as fast as in is taken in
    • Salt is not as easily excreted
  11. Indirect increase in salt on extracellular volume
    • excess salt increases the osmolarity and thus stimulates the thirst center in the brain
    • increased osmolariy stimulates the osmoreceptors in the hypothalamic-posterior pituitary gland to increase ADH production
    • Salt is the main determinant of extra cellular fluid volume, thereby increasing cardiac output and TPR leading to hypertension
  12. Chronic hypertension
    mean arterial pressure above 110
  13. Leathal effects of hypertension
    • excess workload of the heart leads to early heart failure and coronary heart disease
    • the high pressure usually damages vessels in the brain fallowed by a cerebral infarct
    • High pressure almost always causes damage to the kidney
  14. Loss of kidney mass
    • impair the bodys ability to regulate salt and water
    • the pressure will increase slightly
    • if given high salt water the pressure will increase greatly due to the inability to excrete salt
    • When given a high salt diet the cardiac output and volume will rise faster then the pressure, this is due to an initial fall in TPR.
    • The fall in TPR is due to the barorecptors trying to maintain a pressure. After 2-3 the baroreceptros adapt and do not prevent a pressure rise
    • After this autoregulaton to the higher cardiac output sets in and the TPR increases
  15. Long term HTN after an increase in fluid
    eventually the cardiac output and fluid volume will return to normal but the TPR will stay increased maintaining the HTN
  16. Two stages of volume loading HTN
    • first stage results form increase in fluid volume causing increased cardiac output. This increase in CO caused HTN
    • The second stage in colume loading HTN is chatachteized by high blood pressure and high TPR but in return of cardiac output
    • Thus the increased TPR occurs after HTN occurs and therefore is secondary HTN
  17. Autonomic renin release
    Beta 1
  18. JG cells
    • smooth muscle cells in the afferent arterials, they store prorenin
    • When pressure falls the JG cells split and release renin
  19. Two major effects of angiotensin 2
    • vasoconstriction of the arterioles, slightly n veins
    • The slight increase in venous tone shifts volume tot he heart to help pump against the constructer arterioles
    • Decresed excretion of salt and water.
  20. Renin system after hemorrhage
    • strong enough to return pressure half way back to normal
    • Takes 20 minutess to become fully active
  21. Two ways angiotensin retains salt and water
    • direct action on the kidneys to retain salt and water
    • causes adrenal gland to secrete aldosterone in turn increasing salt and water retention
  22. Mechanism of water retention by angiotensin
    • constrict renal arterioles. DIminishes blood flow to the kidney, less fluid is filtered. Also the slow flow of blood reduces the pressure in the peritubular capillaries which causes rapid reabsorption form the tubules
    • Increase tubule cells to increase Na absorption
    • the direct effect of angitensin on the kidneys is 3-4 times more powerful then the secondary effect of aldosterone
    • Direct effect on the Na/H transporter
  23. Most important effect of angiotensin system
    • to allow a person to eat very small or very large amount of salt without causing a drastic change in extracellular fluid volume or arterial pressure
    • The initial effect of increased salt intake is to increase the extra cellular volume which in turn increases arterial pressure
    • the increase in presure increases renal blood flow which reduces the rate of renin secretion. THis leads to a decrease in Na reabsorption and a return of fluid volume to normal
    • The pressure will only rise 4-6 mmHg with a 50 fold increase in salt intake
  24. One kidney Goldblatt hypertension
    • if restriction is placed on the afferent renal arterial the pressure in the glomerulus will decrease
    • this leads to an increase in renin secretion and pressure rises quickly. Over the next few days pressure rises slowly from fluid retention
    • The systemic pressure will rise until it reaches an equilibrium, this pressure will be high enough to increase the pressure in the kidney to normal pressure
  25. Two kidney Goldblatt hypertension
    • When the afferent arterial to only one kidney is constricted the ischemic kidney will produce renin
    • non ischemic kidney will retain salt and water in response to the renin secretion
    • the ischemic kidney will increase salt and water retention in response to the decrease in pressure
    • This causes an increase in pressure until the kidney is non ischemic
  26. One of the common causes of renal hypertension in older people
    • patchy ischemic kidney disease
    • the ischemic patches will secrete renin that all the kidney tissue will respond to
  27. HTN by coarctation
    • when a constrictor is placed on the aorta above the renal arteries the pressure in the upper body rises but blood flow is deminished in the lower body
    • The kidneys secrete renin which increases the pressure in the upper body even more but returns the pressure and flow in the lower body to normal
    • The pressure in the lower body will be almost normal in coarctation
  28. Autoregulation in coarctation
    • pressure in the arms is 40-60mmHg above normal but blood flow is normal and blood flow in the legs where pressure is not elevated is normal
    • long term autoregulation develops and nearly completely controls blood flow to the need of the tissues and not in accordance of the pressure
  29. Preclampsia , toxemia of pregnancy
    • HTN that subsides after the baby is born
    • Believed to be from ischemia of the placenta and release of toxic factors causing HTN
    • The toxins inhibit the release og NO from endothelial cells causing vaso constriction and decreased renal filtration
    • autoimmune complex may cause a thickening of the glomerular membrane
  30. Neurologic HTN caused nby lose of baroreceptors
    • lose of the nerves leading from the baroreceptors or damage to the tracts solitaris in the medulla, this is where nerves connect to
    • Acute HTN since the response of the vaso motor center to the lose of input from the baroreceptors fades away and resets
  31. Primary HTN risk factors
    • obesity
    • sedentary lifestyle
    • Ohysical activity and weight loss are the first step in treating HTN
  32. Charateristics of primary HTN caused by weight gain
    • Cardiac output is increased due to the additional blood flow required by the extra tissue and increased metabolic demand of tissues
    • Increased sympathetic activity in obese patients. Leptin from fat cells may sitmulate the hypothalamus
    • Angiotensin 2 and aldosterone are increased in fat people. Partly from increased sympathetic tone
    • Impared function of pressure naturesis. Fat person with a pressure of 150 will become anuresis if pressure returns to a normal 100
  33. Two types of essential HTN
    • salt sensitive, may be due to loss of kidney tissue, abnormal function of the renin angiotenson system
    • non salt sensitive , intake of salt does not exacerbate the HTN
  34. Cappilary fluid shift
    • if pressure in the capillary falls fluid will be absorbed
    • if pressure increases fluid will be forced out

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