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42 terms

golomular filtration - exam 2

STUDY
PLAY
renal corpusule components
Composed of _______ and _______ capsule

Blood enters glomerulus by the___________ and leaves by the __________

Blood is filtered from glomerulus and the ultrafiltrate is collected in the ___________
glomerulus, Bowman's
afferent arteriole
efferent arteriole
Bowman's space
3 components of FILTRATION BARRIER
1 Fenestrated capillary- 1st layer of filteration have lots of pores that filter
2 Glomerular basement membrane- 2nd layer of filtration, secrete basil lamina that allow them to stick onto capilaries and help to filter
3 Slit diaphragm- last layer of filtration ( most outer) between pediciles, acts as a filter, filters on the bases of size and charge
Glomerular Filtration: Filtration Barrier
Capillaries:
SIZE - Fenestrations hold back ____ and larger __________ bigger than a certain size
CHARGE - The capillaries are are covered in laminin and fibronectin which repel ______charged molecules
Capillary epithelium is lined with ________
Capillary epithelium is perforated with large _______-
RBC,plasma proteins
negatively
polyanionic glycoproteins
pores
Glomerular Filtration: Filtration Barrier
Lamina rara:
CHARGE - Laminin, fibronectin and heparan sulphate repel ______ charged molecules
Contain proteins
negatively
polyanionic non-collagenous
Glomerular Filtration: Filtration Barrier

Lamina densa:
SIZE - Collagenous proteins filter ______only,
Contains collagenous ________
size
proteins
Glomerular Filtration: Filtration Barrier
Slit diaphragm: ________ (mostly nephrin) with holes in it.
SIZE - Holes filter based on ____ like Lamina densa
CHARGE - The supporting podocytes filter on basis of ______
Podocytes are covered with polyanionic glycoproteins
Slit diaphragm is perforated with ______ pores
Protein
size
charge
small
negatively charged molecules have a _______ time getting through the filtration barrier then positive charged molecules
plasma proteins ______ pass through protein barier because
harder
can not, they are large with a net negative charge
So conclusion, filtrate is therefore mostly protein free
which molecules will have the most difficult time crossing the filtration barrier
large and negatively charged molecules
WHAT DRIVES FLUID MOVEMENT OUT OF THE CAPILLARIES OF THE GLOMERULUS?
HYDROSTATIC AND ONCOTIC PRESSURE, THAT'S WHAT.
Hydrostatic pressure has the ______ influence on fluid movement. Blood pressure inside capillary pushes _____ but the fluid in Bowman's space also has a hydrostatic pressure and this pushes _____. However the Pc is ________ than Pbs so the net effect of hydrostatic pressure is to push plasma _____ of the glomerulus = drives filtration.
biggest
OUT
back IN
WAY bigger
out
Oncotic pressue is basically osmotic pressure caused by ___________. The filtration barrier prevents many proteins______the capillaries so therefore the protein concentration in the capillaries is _______ than the Bowman's space. This will generate an osmotic pull of fluid _______ the capillary (capillary oncotic pressure). Like hydrostatic pressure, this can go both ways
colloids (large proteins)
leaving
higher,INTO
HYDROSTATIC PRESSURE
is composed of
Capillary hydrostatic pressure (PC)
Bowman's space hydrostatic pressure (PBS)
ONCOTIC PRESSURE
is composed of what 2 preasures
Capillary oncotic pressure (πC)
Bowman's space oncotic pressure (πBS)- so small it barely matters
the net glomular filtration rate is determined by
forces pushing both IN and OUT and it is the balance of these forces which determines whether fluid moves into or out of the capillary.
why would cappillary onconic preasure increase
water is leaving cappillary but protein isn't leaving so force goes up
Use these numbers to work out the net filtration pressure at the feline glomerular capillary:

Pc = 58 mmHg
Pbs = 18 mmHg
πc = 22 mmHg
πbs = 0 mmHg
18 mmHg= net filtration preasure
____ is the biggest of Starling's Forces, and therefore the biggest determinant of ____. It makes sense, then, that the easiest way for the kidney to modulate GFR is to keep a tight handle on ____. It does this by carefully regulating blood flow through the _________.
Pc, GFR
Pc
glomerulus
If it's easier for blood to enter the glomerulus than leave it, this will __________and therfor ____________
If it's easier for blood to leave the glomerulus than enter it, this will ______________and therfor ____________
increase Pc and therefore increase GFR
reduce Pc and therefore reduce GFR
The thing that makes it "easier" or "harder" for blood to enter/leave the glomerulus is the resistance to blood flow provided by the ______________
so when afferent arterial dialates GFR _______
and dialation of the effererent arterial will __________GFR
afferent/efferent arterioles.
will increase
decrease
Disease states alter GFR because they change ___________
Starling's Forces
Disease states decrease GFR, consider the example of schistosomiasis. Changing the ____________ or ___________ of filtration apparatus will change GFR
permeablilty and/or surface area
if the filtration barrier gets chewed up it stops filtering and just lets anything through (ie proteins and RBC). This failure to filter = _________GFR = renal failure.
reduced
The key to realizing why a decreased Kf decreases GFR lies in the definition of GFR - it's the filtration rate across all FUNCTIONING glomeruli. If disease destroys the filtration apparatus, then __________ can't functionally filter, so overall GFR goes _______.
glomerulus
down
Kf CHANGES
Kf = (permeability of capillary) x (filtration surface area)
Most disease states decrease Kf
Glomerular disease is an excellent example
PC CHANGES
In acute renal failure, PC can decrease due to impaired renal perfusion. This causes decrease in GFR
πC CHANGES
Plasma protein levels can increase and decrease
↑ πC = ↓ GFR
↓ πC = ↑ GFR
PBS CHANGES
Obstructions (uroliths, plugs) can increase PBS
↑ PBS = ↓ GFR
↓ PBS = ↑ GFR
dialated aferent arteriole and normal efferent arteriole _____blood flow and _____GFR
increase, increase
Glomerular filtration is governed by forces pushing fluid out of the glomerulus and forces push fluid back into glomerulus. These forces are _________ and _____________.
hydrostatic pressure and oncotic pressure
_________________ pressure is the most important factor. Pc (and therefore GFR) can be changed by adjusting the resistance of afferent and efferent arterioles
Capillary hydrostatic
Autoregulation is the intrinsic ability of an organ to maintain___________at a nearly constant rate despite changes in __________ pressure
blood flow, arterial perfusion
Changes in BP can have 2 major consequences to the kidney and autoregulation helps to offset these consequences:
Autoregulation helps to prevent damage to kidneys by controlling the __________ to the glomeruli despite fluctuations in BP. ______remains relatively constant over a wide range of BP.
autoregulation controls RBF to PREVENT CHANGES IN _____.
blood flowing,RBF
GFR
Autoregulation works to maintain a steady state_________and _____ despite changes in systemic blood pressure.
blood flow,GFR
Goal of renal autoregulation
1. Prevent damage to _______caused by spiking BP (maintain constant blood flow despite changes in BP
2. Prevent fluctuations in BP from changing delivery of filtrate to ________ (maintain constant GFR despite changes in BP)
glomeruli
tubules
2 mechanisms
1. MYOGENIC MECHANISM
TRIGGER: Fluctuations in ___ change transmural pressure in _____ arteriole
Increased BP elicits ________ and decreased blood flow
Decreased BP elicits ___________ and increased blood flow
2. TUBULOGLOMERULAR FEEDBACK
TRIGGER: Fluctuations in___ change ____meaning distal tubule fluid composition is altered
1. Low/High GFR produces low/high___
2. Low/High ion concentration sensed by __________
3. JGA changes arteriole resistance to autoregulate ______
much slower
BP, AFFERENT
constriction
dilation
BP,GFR
ultrafiltrate
macula densa
GFR
Renin is an important molecule as it is critical to generating angiotensin II - this is one of the key molecules that change _________
arteriolar resistance!
function of ANGIOTENSIN II:
Systemic arteriolar ____________ to increase blood pressure
Increases __________ secretion (adrenal cortex)
Promotes _____secretion (pituitary) and thirst
Increases tubular_____uptake
vasoconstriction
aldosterone
ADH
NaCl
REDUCING GFR

If GFR is high, ____in the distal tubule fluid will be high and therefore more than usual will move to the cells of the _______.
_________ is the important mediator of this process
We know __________ in the extraglomerular mesangial cells are activated and that this increases ____. We think this Ca2+ then moves through gap junctions into afferent ________ cells (which causes them to contract) and into JG cells (inhibits renin release).
Finally, we know that ________ and _________can modulate this whole process
Cl- ,macula densa.
Adenosine
adenosine receptors
Ca2+
smooth muscle
nitric oxide and angiotensin II
INCREASING GFR
1. Low Na+ K+ and Cl- sensed by NKCC2 on apical surface of MD
2. MD releases _________
3. PGE2 causes afferent arteriole ________ (INCREASES GFR) and stimulates JG to release ______, increasing________
4. Angiotensin II in the bloodstream
Causes systemic ____________(INCREASES GFR)
Preferentially contracts _____________arteriole (INCREASES GFR)
Increases ______ production from MD (INCREASES GFR)
Negatively feedbacks onto contralateral kidney to stop ________release
prostaglandin E2 (PGE2
vasodilation, renin, angiotensin II
vasoconstriction
efferent over afferent
PGE2
renin
toxicity and acute renal failure
1. ________ depletion or systemic hypotension
2. systemic ____________
afferent ________
3. ______________ GFR
4. release __________
5. afferent ____________
6. normalized _________
toxisity prevent the release of _________which causes acute renal failure by preventing the negative feedback
volume
vasoconstriction
vasoconstriction
reduce
prostiglandin
vasodialation
GFR
prostiglandin
role of myogenic mechanism =
reponse time =
importance
protection aginst injury
fast
No myogenic mechanism, no autoregulation
role of Tubuloglomerular Feedback
reponse time=
importance
regulation of GFR
slower
Less important, works with other mechanisms to control GFR and fluid homeostasis