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Shells33
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Familial,
Increased SNS activity,
Increased sodium retaining hormones,
low Potassium-Calcium dietary intake,
increased renin secretion,
deficiencies of nitric oxide and prostaglandins,
DM,
Obesity,
Neurogenic sleep apnea
are all causes of what type of hypertension? What % of total is this?
Primary or Essential Hypertension. 95% of all cases.
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What is the fundamental cause of primary hypertension?
salt and water retention is the final common pathway shared
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Renovascular (renal artery stenosis),
Renal parenchymal disease/chronic renal diseases (pyelonephritis or glomerulonephritis),
hyperaldosteronism (Conn syndrome)
Aortic Coarctation
pheochromocytoma
hyperadrenocorticism (Cushing Syndrome)
Pregnancy induced HTN
Exogenous substances
are all what types of causes of HTN?
Secondary or demonstrable causes
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What 3 things are responsible for short term control of BP?
- 1) SNS
- 2) total peripheral vascular resistance
- 3) cardiac pumping ability
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What is responsible for long term control of BP?
balancing fluid intake and output
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Describe the renal urinary output curve/renal function curve
as BP increases, UOP increases (diuresis and natriuresis
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Describe the Renal Output Curve and Na/H2O intake
- 2 curves:
- 1) Renal output of H2O and salt in response to rising BP
- 2) Net intake of Na and H2O
Over time, intake must equal output. Where the curves intersect is the "equilibrium point" (H2O and salt intake is at 1x normal, BP is at 100 mmHg)
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Describe the Infinite Feedback Gain Principle
As BP increases, UOP increases to more than intake, I/O is negative until BP normalizes and equilibrium point is reached again. The opposite is true for a decreased BP.
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What 2 ways can you change the equilibrium point of the renal function curve/intake curve?
- 1) shift arterial pressure level for the renal output curve to a different pressure
- 2) move the level of water/salt intake line
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How would you shift the equilibrium point to the left on the renal function curve?
restrict sodium and water intake
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What two things determine arterial pressure?
CO and TPR
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If renal function is normal, how long will it take to return BP back to normal? When would this not happen?
1 day - if renal vascular resistance is increased
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If kidneys are functioning, will a change in TPR increase the long-term arterial pressure?
No
The renal function curve must be altered. This is only done if you have an increase in renal vascular resistance.
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What 2 ways does increased fluid volume increase BP?
- 1) directly by increasing CO
- 2) indirectly by autoregulation of the arterioles in response to increased CO (increases TPR)
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What happens when sodium intake increases?
- ECF osmolality increases -->
- stimulation of thirst center and release of ADH-->
- increased ECFV
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What happens in the first stage of volume loading hypertension?
- CO, blood volume, ECFV, and BP all increase
- TPR decreases
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What causes the decrease in TPR during the first stage of volume loading htn?
baroreceptor reflex
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What is responsible for the increased BP in the first stage of volume loading hypertension?
increased CO
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What happens in the second stage of volume loading hypertension?
htn persists, CO returns to near normal, TPR increases
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What is responsible for the increased TPR during the second stage of volume loading hypertension?
The autoregulation of the arterioles have caused them to constrict to control flow --> increased TPR
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Where is reining synthesized, stored, and released?
juxtaglomerular cells in the afferent arterioles of the kidney
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Is renin a vasoactive substance?
no
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What triggers the release of renin?
low arterial pressure
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How does renin increase blood pressure?
- Renin -->
- angiotensin I -->
- angiotensin II (via ACE in pulm circ) -->
- vasoconstriction and renal retention of salt and water
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What deactivates angiotensin II?
angiotensinase
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What is responsible for the immediate increased in BP d/t RAAS system?
- angiotensin is a rapid vasoconstrictor -->
- 1) contraction of arterioles (more then veins) = increased TPR &
- 2) venous contraction --> increased venous return to heart (increases CO)
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What is responsible for the long term raise in BP d/t RAAS system?
increased fluid volume = increased BP d/t sodium and water retention
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What are the 2 major mechanisms by which the kidneys cause sodium and water retention in response to angiotensin?
- 1) direct renal effects
- - renal arteriole constriction (less flow, less UOP)
- - increased reabsorption of Na and H2O
- 2) aldosterone secretion
- - Na reabsorption, water follows
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What is the relationship between sodium intake and renin release?
As Na intake rises, renin release will near zero
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How does angiotensin II affect BP?
increases via vasocontriction
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How does aldosterone affect BP?
increases via Na retention and water follows
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How does SNS activity affect BP?
increases via contraction of renal vasculature --> increased reabsorption of Na/H2O and vasoconstriction
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How does endothelin affect BP?
increase via vasoconstriction
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How does atrial natriuretic peptide affect BP?
decreases via decreased reabsorption of Na/H2O
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How does Nitric Oxide affect BP?
decrease via vasodilation
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How does Dopamine affect the renal vessels?
at low doses it stimulates dopamine 1 receptors which stimulates natriuresis
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What are the 3 rapid response mechanisms (seconds to minutes) to control BP?
- 1) Baroreceptor feedback
- 2) CNS inschemic mechanism
- 3) Chemoreceptor mechanism
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What are the 3 intermediate response mechanisms (minutes to hours) to control BP?
- 1) Renin-angiotensin vasoconstriction
- 2) stress-relaxation mechanism (increased BP = increased wall stretch = relaxation)
- 3) capillary fluid shift mechanism
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What are the 2 long term mechanisms to control BP?
- 1) Renal-blood volume pressure mechanism
- 2) renin-angiotensin-aldosterone mechanisms
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