Physio Exam 3 Renal 2

Front 1

Together the endothelial wall, basement membrane, and podocyte processes form the

Back 1

filtration barrier

Front 2

The basement membrane
is composed of negatively
charged proteins such as

Back 2

Collagen Type IV, Laminin,
Proteoglycans, and
Fibronectin

Front 3

To be filtered a substance must pass

Back 3

1) The endothelial cell pores of the glomerular capillary
2) The acellular basement membrane
3) The filtration slits between the foot processes of podocytes

Front 4

Filtration slits between
podocyte foot processes
are traversed by

Back 4

by a thin
diaphragm known as the
filtration slit diaphragm with
pores of 40 – 140 Angstroms

Front 5

Membrane spanning
proteins are also linked with

Back 5

intracellular “adaptor” proteins
that link with proteins in the
glomerular basement
membrane.

Front 6

Filtration decreases with

Back 6

increasing size (42 A not filtered)
negatively charged molecules

Front 7

Multi-focal glomerular disease resulting in proteinuria and possible hematuria
in more severe cases

Back 7

Nephrotic Syndrome

Front 8

what accompanies significant protein loss?

Back 8

edema

Front 9

Minimal Change Disease

Back 9

Unknown etiology,
possibly related to T-cell dysfunction and production
of glomerular permeability factor. Most common
example of nephrotic syndrome in young children

Front 10

Autoimmune

Back 10

Systemic Lupus erythematosus,
an autoimmune disease causing inflammation and
damage to glomerulus

Front 11

Hereditary

Back 11

: Alport’s Syndrome, caused by a mutation in one of the Type
IV Collagen genes (usually COL4A5 genes) of the glomerular basement
Membrane.

Front 12

Infection:

Back 12

: HIV-related nephropathy, Post-streptococcal glomerulonephritis

Front 13

Diabetic nephropathy

Back 13

: Diabetes mellitus is the leading cause of end stage renal failure. Both metabolic cellular damage and glomerular hyperfiltration may result from elevated blood glucose

Front 14

Diabetic nephropathy

Back 14

Diabetes mellitus is the leading cause of end stage renal failure. Both metabolic cellular damage and glomerular hyperfiltration may result from elevated blood glucose

Front 15

Starling equation

Back 15

slide 8

Front 16

Elevation of oncotic pressure in capillaries from afferent to efferent is important because

Back 16

high level of filtration leaves behind plasma protein and becomes more concentrated creating an inward force

Front 17

Starling forces determined by

Back 17

Renal Blood Flow and therefore indirectly determines GFR

Front 18

Autoregulation of RBF and GFR once they plateau around 90 mmHg

Back 18

Myogenic or tubuloglomerular

Front 19

Myogenic autoregulation

Back 19

Dependent on cardiovascular system

Front 20

Tubuloglomerular feedback

Back 20

dependent on macula densa, allows GFR to mediate RBF.

Front 21

Myogenic and tubuloglomerular feedback depend on

Back 21

vascular resistance

Front 22

As renal artery pressure is increased, afferent arteriole resistance would

Back 22

increase and renal blood flow would decrease as well as GFR

Front 23

Decrease in Efferent resistance as renal artery pressure

Back 23

increases

Front 24

Changes in renal artery pressure have a larger effect on

Back 24

the regulation of afferent arteriolar resistance

Front 25

Myogenic autoregulation mechanism depends on

Back 25

stretch activated calcium channels in smooth muscle

Front 26

See myogenic autoregulation

Back 26

slide 11

Front 27

As myogenic mechanism increases pressure

Back 27

resistance increases and this reduces RBF and GFR

Front 28

Tubuloglomerular mechanism

Back 28

Signal is generated as abnormal increase in renal blood flow->GFR increases and [Na+] increase is sensed by macula densa and exerts a contraction of smooth muscle

Front 29

Cellular Control of Tubuloglomerular Feedback

Back 29

1) [NaCl] increases in thick ascending tubule. NKCC2 pump, pumps NaCl into macula densa
2)Stimulation of Na/K Atpase and it pumps Na out of macula densa
3)ADP increases in macula cell
4)Ca2+ increases in cell leading to ATP increase
5)ADP and ATP high in cell. ADP broken down into adenosine and pumped out of cell
6)Adenosine + ATP bind adenosine type A1 receptor or purinergic A2 receptor in smooth muscle of afferent arterioles
7) Afferent arterioles vasoconstrict and this cuts blood flow to glomerulus and GFR plateaus
Renin secretiion decreases, leading to decrease in Ang II which causes vasorelaxation so this is counterproductive, but renin affects mostly efferent arterioles

Front 30

Constricting afferent arteriole leads to
Pressure in glomerulus(Pgc)
GFR
RBF

Back 30

all decrease

Front 31

Constricting efferent arteriole
Pgc
GFR
RBF

Back 31

Increase
Increase
Decrease

Front 32

Dilation of efferent arteriole
Pgc
GFR
RBF

Back 32

decreases
decreases
increases

Front 33

Dilation of afferent arteriole
Pgc
GFR
RBF

Back 33

all increase

Front 34

Normally sympathetic tone
is minimal, but following
hemorrhage the baroreceptor
reflex induces

Back 34

constrinction.Effects predominate at the
afferent arteriolesn (constriction). Helps to increase MAP at
the expense of renal function

Front 35

Produced following
a hemmorhage to attenuate effects
of systemic vascoconstrictors and
prevent renal ischemia. Therefore,
NSAIDS are contra-indicated with
hemmorhagic shock

Back 35

prostaglandins

Front 36

A vasodilator that will
locally increase RBF and GFR in
response to increased sheer stress.
Also counteracts systemic vasocon-
strictors.

Back 36

Nitric Oxide

Front 37

Elevated levels cause
decrease in RBF and GFR. Elevated
in diabetes mellitus

Back 37

Endothelin