Renal System Flashcards
ureter
tube that brings urine to bladder
kidney stones
form by precipitation and crystallization of increase concentration of minerals and ions
too large, get stuck in renal pelvis, ureter or urethra
nephron
functional unit of kidneys
main parts> renal corpuscle and tubule
renal corpuscles
filters blood and turns into filtrate
3 part
bowman’s capsule, glomerulus, juxtaglomerular apparatus
glomerulus
specialized leaky capillaries
tubule
tube structure made of single layer of epithelial cells
bowman’s capsule/renal capsule
outside of renal corpuscle
-where fluid filters into
-surrounds glomerulus
-cellular part made of podocytes
Juxtaglomerular apparatus
composed of late ascending limb of loop of henle then enters and exits afferent and efferent arterioles
macula densa cells
specialized cells in late ascending limb of loop of henle
detects concentration of Na and Cl in filtrate
detect how fast filtrate is flowing
types of nephrons
cortical 80% and juxtamedullary 20%y
difference between cortical and juxtamedullary nephrons
jux- nephron next to medulla, cort- upper cortex
jux-long loop of henle, cort-short
juz-vasa recti-help with [] urine
cort- peritubular capillaries
blood flow to kidneys in cortical nephrons
afferent arterioles > glomerulus >efferent arterioles > peritubular capillaries > venule > renal vein
processes of nephron
filtration + reabsorption + secretion and excretion
formula for excretion
filtration - reabsorption +secretion = excretion
barriers to filtration
size of fenestration and size of spaces between endothelial cells
-space between fibers of basal lamina
-spaces between podocytes
fenestrations
additional holes in endothelial cells
-size limits what can be filtered out of blood into bowman’s space
basal lamina
sticky tissue that connects endothelial cells to podocytes
-composed of collagen and negative charged glycoproteins
-filter plasma
0the negative charge prevents them from moving through basal lamina
podocyte
inside bowman’s capsule, specialized cells
-prevent some fluid filtration by wrapping around glomerulus
-long projections
slit space
between podocytes
-blood can move through here
-larger items can’t pass
-limits how much volume of fluid is filtered
endothelial cells
make up capillaries
-have fenestrations
net filtration pressure
-sum of Hydrostatic pressure of glomerular capillaries
colloid osmotic pressure of glomerular capillaries
hydrostatic pressure of bowman’s capsule
colloid osmotic pressure of bowman’s capsule
-=10 mm HG
glomerular filtration rate
-quantity of fluid and solutes dissolved in water filtered into bowman’s space from glomerular caps
-influenced by BF (more, than more)
-^GFR more solutes and h2o are excreted
usually L/day
Hydrostatic pressure of glomerular capillaries
blood pushed through vessels by heart’s pumps
-as blood flows through glomerulus capillary, fluid is forced into capsule space
-this P favours filtration
-largest force that promotes filtration
colloid osmotic pressure of glomerular capillaries
-proteins in blood don’t filter into capsular space b/c size and change
-proteins generate force, drawing water to where proteins flow
-force inhibits filtration
hydrostatic pressure of bowman’s capsule
-fluid filters, it fills capsule space
-fluid movement out of tubule is slow
-the back pressure of fluid in capsule limits more fluid from filtering capsule space
-inhibits fluid filtration
colloid osmotic pressure of bowman’s capsule
-if proteins could filter in capsular space, proteins pull fluid in
-positive force that favours filtration
-usually doesn’t exist =0
-must be accounted for b/c if presence affects fluid filtration
NFP equation
[HSP glo + COP B] - [HSP B + COP glo]
myogenic response
-increase blood flow in glomerulus, increase pressure, increase GFR
-myogenic response will reduce GFR
-reflexive contraction of afferent arterioles > this reduces blood flow, decrease GFR
tubuloglomerular feedback -high
-if blood pressure increases, increase the amount of fluid filtered
- when Na and Cl level in filtrate are too high or fluid flow is too high, macula dense cells release a paracrine factor that stimulate afferent arterioles (constrict) therefore decrease rate of fluid filtration
tubuloglomerular feedback- low flow
if low fluid flow rate or low [ ] in filtrate, macula densa cells release nitric oxide
-this causes smooth muscle to relax in afferent arteriole therefore increase GFR
afferent arteriole constricts
-when they vasoconstrict, decrease blood enter glomerulus
-hydrostatic pressure would decrease
-decrease GFR
efferent arteriole constricted
-when they vasoconstricted, decrease blood leaves glomerulus
-hydrostatic pressure would increase
-increase GFR
vasoconstriction of afferent and efferent arterioles
caused by angiotensin II
-result is decrease GFR
estimating the GFR
excretion= filtration - reabsorption + secretion
how to measure GFR
-use creatinine (waste product in blood)
-why bad is increase skeletal muscle, increase creatinine produced
creatinine in urine x urine/day divide by creatinine plasma
creatinine
-not perfect measurement because some creatinine is secreted in tubule
-overestimates GFR
other methods to measure GFR
inulin, blood urea nitrogen, serum creatinine
inulin
-plant polysaccharide
-given via intravenous, isn’t produced by kidneys
=then [ ] of inulin in blood and filtered bt kidneys
-epithelial cells of tubule don’t recognize, so inulin is not reabsorbed or secreted so 100% is excreted
-quite invasive
blood urea nitrogen (BUN)
-partially reabsorbed by tubules so doesn’t show all filtration
-[ ] of urea in blood can determine if less urea is being filtered
-measures nitrogen in urea
-however high protein diet and strenuous exercise can increase urea levels in blood
serum creatinine
-quick way to estimate GFR
-of serum creation levels increase in blood, can indicate kidneys are no longer filtering as much fluid
-normal values is different for different people
converting L/day to ml/min
1000ml
1440 min
GFR lower than expected
-with age, natural decline in renal function
-too much lower, kidneys are no longer functioning as they should
kidney failure GFR
15ml/min
normal GFR
180L/day or 125 ml/min
chronic kidney disease (CKD)
-progressive disease can result in complete kidney failure
-damage can’t be reversed but slowed + stay
-nephrons damaged can’t heal
5 stages
stage 1-2 of CKD
mild decrease in GFR, may not experience symptoms
stage 3 of CKD
GFR decrease further, symptoms swelling in hands and feet b/c less blood being filtered
stage 4 of CKD
last stage before kidney failure, move severe symptoms
stage 5 of CKD
kidney failure > no longer functioning to support body
-dialysis or transplant
filtered load
how much of each substance is filtered
-calculated using GFR
= [substance] plasma x GFR
percentage excreted
= [total excreted/ filtered load ] x100
normal excretion rate of Na
0.5-2.5%
normal excretion rate of K
6-9%
normal excretion rate of Mg
3-5%
tubule function
-99% of filtrate is reabsorb
-based on types of transporters in tubule epithelial cells
proximal tubule reabsorption
glucose, AA, h2o, Na, K, cl
transporter type; reabsorption
descending limb reabsorption
h2o, + minimal Na
ascending limb reabsorption
Na, K, Cl
distal convoluted tubule reabsorption
Na, K, CL, Ca
collecting duct reabsorption
na and h2o
paracellular transport
between epithelial cells or though cells across luminal and basolateral membrane
transcellular transport
reabsorption or secretion
-uses channels or protein carriers across tubule membrane
channels
small protein-lined pores that permit specific molecules them
uniporters
allow movement of single molecule through membrane
-protein carriers that bind to molecules
-facilitated transport
glucose uniporter
symporters
facilitated transport + secondary active transport
-permits 2 or more molecules same direction
-1 molecule must move down [] gradient
-Na/glucose symporter
antiporters
-permits 2 or more molecules in different direction
-called exchangers
-1 molecules must move down [] gradient
-facilitated transport
Na/H antiporter
primary active transporters
uses ATP against [] gradient
-every tubule cell has Na/k atpase
regulation at level cellular location
channels and transports only function when in right location (cell membrane)
-h2o channels
regulation at level of activity
protein carriers bind to specific molecules and change shape
-protein carriers can work faster by hormones
-Na/H exchanger
regulation at level of gene expression
more molecules can move across membrane if more channel/ protein carriers
-make more by making copies in DNA > exporting as messager RNA in proteins
proximal tubule transport
reabsorbs almost everything
Na/AA symporter location, regulated
in proximal tubule
-luminal
-not to hormones
-binds to protein symporter >conformation change
-Na goes down [] gradient, bring AA with it
Na/glucose symporter location, regulated
in proximal tubule
luminal
-not by hormones
-Na goes down [] gradient
-Na makes protein carrier change (conformation)
-glucose doesn’t favour going in proximal tubule, Na bring it with protein carrier
in proximal tubule
Na/H exchanger location, regulated
in proximal tubule
-luminal
-responsive to angiotensin 2
-Na goes down [] gradient
-antiporter of H(H in opposite direction)
-Na reabsorbed, H secreted
Na/K ATPase location, regulated
in proximal tubule
basolateral
-responsive to angiotensin 2
-uses ATP to change conformation
-against [] gradient
-3 Na out, 2K in
-primary active transport
maintains low []
aquaporin channel 1 location, responsive
in proximal tubule
luminal
-not by hormones
-h20 move to higher solute
-diffusion osmosis> not facilitated
paracellular responsive
in proximal tubule
-h2o, K, Cl
-not by hormones
-movement between tubule cells
high to low []
aquaporin channel 2/3 location, responsive
in proximal tubule
basolateral
-not by hormones
inside tubule cell to interstition space then reabsorbed in blood
-diffusion osmosis> not facilitated
AA uniporter location, responsive
in proximal tubule
-basolateral
-not by hormones
-AA that were just reabsorbed into cytosol move across basolateral membrane into interstitial space by themselves
high to low []
glucose uniporter location, responsive
in proximal tubule
basolateral
-not by hormones
-high to low []
-cytosol to interstitial space
-move by itself (protein carrier)
glucosuria
-Na/glucose symporters in proximal tubule have limited capacity, so not all glucose is reabsorbed, therefore in urine
-causes less h2o in proximal tubule b/c it follows glucose
decrease h20 reabsorption, increased urine V
osmotic diuresis
increase urine V due to increase levels of solute excretion
descending loop of henle
-reabsorbs few substance from filtrate (mainly h2o)
-both luminal and basolateral membrane have aquaporin 1
-favourable gradient for h20 movement b/c high[] of solutes of extracellular fluid in medulla
ascending loop of henle
impermeable to h2o
-paracellular transport of h20 is prevented by tight junction proteins adhering epithelial cells together
-paracellular transport of ions (Na)
NA/Cl/K symporter, Na and Cl are moving down [] gradient
principal cells
-in collecting duct
-make up majority of epithelial cells
-responsive to variety of hormones that regulate h2o and Na balance
collecting duct cells
principal cells, intercalated cell A and B
intercalated cell
responsive to changes in plasma pH
aquaporin channel 2 location, regulated
in collecting duct
luminal
responsive to ADH
aquaporin channel 3/4 location
in collecting duct
basolateral
out tubule cell
Na channel location, regulation
in collecting duct
luminal
-responsive to aldosterone
-Na move high to low []
K channel location, regulation
in collecting duct
luminal
-responsive to aldosterone
moving in collecting duct’s lumen
Na/K ATPase location, regulated
in collecting duct
-basolateral
responsive to aldosterone
Na 3 out, 2 K in
-uses ATP
