A&piii-Test3-4-2

Front 1

renal function curve is also known as what

Back 1

renal urinary output curve

Front 2

renal funcation curve is based on what

Back 2

pressure

Front 3

with pressure diuresis and renal function curve as arterial pressure increaeses what happens to urinary volume and urine sodium output

Back 3

they increase

Front 4

at a mean arterial pressure of 50-60 how much urine output would occur

Back 4

little to none

Front 5

at a mean arterial pressure of 100 how much urine output would occur

Back 5

1 x normal

Front 6

at a mean arterial pressure of 160 how much urine output would occur

Back 6

5 x normal

Front 7

LONG term blood pressure regulation is primarily a function of what

Back 7

the KIDNEYS in regulating salt & water balance with nervous and hormonal input

Front 8

what is pressure diuresis

Back 8

increased arterial pressure produces increased renal WATER loss

Front 9

what is pressure natriuresis

Back 9

increased arterial pressure produces increased renal SALT loss

Front 10

the infinite feedback gain mechanism is based on what

Back 10

2 intersecting curves

1-renal fxn curve
2-salt & water intake curve

Front 11

where is equillibrium point of infinite feedback gain mechanism

Back 11

where 2 lines of the 2 curves intersect

Front 12

what are the determinants of LONG term arterial pressure

Back 12

1-shift the renal fxn curve along the pressure axis (d/t renal dysfunction)

2-alter the salt and water intake

Front 13

an abrupt increase TPR may produce a short term increase in arterial pressure--what occurs in the prescence of NORMAL renal function and renovascular fxn

Back 13

the arterial pressure will rapidly return to normal

Front 14

what is the MAIN determinant of ECF volume

Back 14

salt accumulation

Front 15

increased fluid osmolality does what

Back 15

stimulates the thirst center (causing you to want to drink)

Front 16

increased osmolality stimulates the HPA axis to do what

Back 16

secrete ADH

(causes you to absorb more water to compensate for increased osmolaltity)

Front 17

what are the mech by which salt accumulation increases ECF volume

Back 17

*increased fluid osmolality stimulates the thirst center

*increased osmolaltity stimulates the HPA axis to secrete ADH

Front 18

chronic HTN is almost always the result of what

Back 18

impaired renal fluid excretion

Front 19

what are the main complications of chronic HTN

Back 19

*excess workload on the heart

*injury to vasc endothelium

*neurovascular dz

*renal injury or failure

Front 20

what is volume loading HTN

Back 20

HTN resulting from excess accumulation of extracellular fluid

Front 21

what are examples of volume loading HTN

Back 21

*decrease in functioning renal mass and increased salt intake

*dialysis in renal failure

*primary aldosteronism

Front 22

most HTN pts have what kind of CO

Back 22

normal

Front 23

most HTN pts have what kind of peripheral resistance

Back 23

high

Front 24

most HTN pts have what kind of extracellular fluid volume

Back 24

normal

Front 25

increased TPR in HTN is it the cause of HTN or the result of HTN

Back 25

the result

Front 26

with volume loading HTN what is the CO initially

Back 26

HIGH d/t excess fluid load

Front 27

what is the end result w/ volume loading HTN

Back 27

HIGH peripheral resistance HTN

Front 28

aniotension II is a vasodilator or vasoconstrictor

Back 28

vasoCONSTRICTOR

Front 29

how does angiotension I get converted to angiotension II

Back 29

in the lungs

Front 30

angiotension II releases what

Back 30

aldosterone

Front 31

what is the function of aldosterone

Back 31

increase absorption of salt and water

Front 32

if a person has decreased renal perfusion what will happen regarding salt and water balance

Back 32

they will absorb MORE salt and water to get increased renal perfusion

Front 33

what are the actions of angiotension II

Back 33

*vasoconstriction

*decreased excretion of salt and water by kidneys

Front 34

how does angiotension II affect vasoconstriction

Back 34

*significant arteriolar constriction

*mild venous constriction

Front 35

how does angiotension II decrease salt and water exretion by the kidneys

Back 35

*direct effect on tubuar cells

*renal arteriolar constriction

*stimulates aldosterone release

Front 36

what is the onset of action of the renin-angiotensin system

Back 36

*slower in onset than nervous control

*begins to work in minutes

Front 37

when does renin-angiotensin system reach its full acute effect

Back 37

~ 20 min

Front 38

what in the body compensates for a wide variation in salt intake

Back 38

negative feedback in the renin-angiotensin system

Front 39

a 50 fold increase in salt intake will increase BP how much if renin system is intact

Back 39

4-6 mmHG

Front 40

a 50 fold increase in salt intake will increase BP how much is renin system is NOT intact

Back 40

50-60 mmHg (10 fold)

Front 41

with an increased salt intake and increased fluid volume and BP what happens to renin and angiotensin

Back 41

they are decreased

Front 42

what occurs in one kidney goldblatt

Back 42

acute renal artery constriction produces a rapid rise in renin and blood pressure

Front 43

early phase in one kidney goldblatt is d/t

Back 43

angiotensin-induced vasoconstriction

Front 44

later phase in one kidney goldblatt is d/t

Back 44

salt and water reabsorption

Front 45

in one kidney goldblatt when the arterial pressure reaches a level where there is adequate perfusion of the constricted renal artery what occurs

Back 45

*renal artery pressure returns to normal

*renin secretion returns to normal

Front 46

what to 2 kidney goldblatt

Back 46

partial occlusion of one renal artery produces decreased profusion pressure and release of renin

Front 47

what is the result of two kidney goldblatt

Back 47

increased angiotension and aldosterone which also cause the normally perfused kidney to retain salt and water (b/c of the global effect when renin is released)

Front 48

what s "patchy" kidney dz

Back 48

small localized areas of inadequate perfusion secrete renin leading to a "global" response from the remaining healthy renal tissue

Front 49

what is coarctation of the aorta

Back 49

constriction of the aorta distal to the branches feeding the head and neck but proximal to the renal arteries

Front 50

what results from coarctation of the aorta

Back 50

HTN proximal to constriction and normotension distal

Front 51

in the upper body (proximal to the constriction) with coarctation of the aorta what type of blood flow and PVR will there be

Back 51

*NORMAL blood flow despite HTN

*increased PVR

Front 52

with coarctation of the aorta what will the BP be in the upper body

Back 52

HIGH (HTN)

Front 53

with coarctation of the aorta what will the BP be in the lower body (distal to the constriction)

Back 53

NORMAL

Front 54

what are the other names for preeclampsia

Back 54

*toxemia of pregnancy

*hypertensive disorder of pregnancy

*PIH

Front 55

what is preeclampsia believed to be the result of

Back 55

belived to result when ischemic areas of the placenta release substances toxic to vascular endothelium into the bloodstream

Front 56

what leads to vasoconstriction in preeclampsia

Back 56

decreased release of nitric oxide and other vasodilators

Front 57

what renal problem might occur with preeclampsia

Back 57

it might directly produce glomerular membrane thickening which requires higher pressures for kidneys to adequately fxn

Front 58

when does neurogenic HTN occur

Back 58

*following sympathetic discharge d/t excitation or anxiety

*may occur following disruption of the baroreceptor nerves

Front 59

what occurs if there is disruption of the baroreceptor nerves

Back 59

*loss of inhibitory impulses leads to over active vasomotor center & increased SNS outflow

Front 60

if there is disruption of baroreceptor nerves will BP reflexes return to normal

Back 60

YES

-effect dimishes over ~ 2 days d/t central resetting and BP returns to normal

Front 61

when does autonomic hyperreflxia occur

Back 61

after a spinal injury following return of spinal refexes

Front 62

what is the incidence of autonomic hyperreflexia

Back 62

~ 85% above T6

-rare below T10

Front 63

what are the hallmarks of autonomic hyperreflexia

Back 63

HTN and reflex bradycardia

Front 64

what initiates autonomic hyperreflexia

Back 64

stimulus such as surgery or distension of a hollow viscus (i.e. bladder overfillng)

Front 65

how is autonomic hyperreflexia managed

Back 65

*with a short acting vasodilator (like nipride)

*prevent with adequate anesthesia

Front 66

when may autonomic hyperreflexia be seen

Back 66

as early as 24 hrs after spinal injury

(as soon as spinal reflexes return)

Front 67

with autonomic hyperreflexia what will occur above the level of transection

Back 67

vasodilation

Front 68

with autonomic hyperreflexia what will occur below the level of transection

Back 68

vasoconstriction

Front 69

is autonomic hyperreflexia more common with higher or lower spinal injuries

Back 69

higher

(the higher the injury the more common)

Front 70

excess wt gain accounts for what % risk for primary HTN

Back 70

60-70

Front 71

what are the characteristics of primary HTN

Back 71

*increased CO

*increased SNS activity

*increased angiotension II & aldosterone levels

*impaired pressure naturesis
(retention of salt & water)

Front 72

when does salt sensitivity increase

Back 72

with age

Front 73

what is the treatment for primary HTN

Back 73

*weight loss

*increased physical activity

*drugs that produce renal vasodilation

*drugs which decrease reabsorption of salt and water

Front 74

what are drug that produce renal vasodilation

Back 74

*b-blockers

*ca channel blockers

*ACE or ARB

Front 75

how would drugs produce renal vasodilation

Back 75

*inhibition of SNS output or blockade of effect (b-blockers)

*direct relaxation of vascular smooth muscle (ca channel)

*block of renin-angiotensin system (ACE/ARB)

Front 76

what are drugs that decrease absorption of salt and water

Back 76

*diuretics

*natriuretics