Download Chapter 27 Reproductive Endocrinology

Chapter 25 Urinary System
Urinary System
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Kidneys
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Ureters
2
Urinary Bladder
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Urethra
1
renal functions
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homeostasis of body fluids
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chemical waste removal
maintain blood volume
maintain blood osmolarity
maintain blood pH
maintain electrolyte levels
via:
making urine
gross anatomy
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renal cortex
outer
renal medulla
inner
renal pelvis
drains urine to ureter
nephron anatomy
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nephron
=
functional unit of urine formation
renal corpuscle
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glomerulus
capillary network
glomerular capsule
= Bowman’s capsule
renal tubules
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PCT
proximal convoluted tubule
loop of Henle
• descending and ascending limbs
DCT
distal convoluted tubule
collecting duct (? part of nephron )
blood vessels
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glomerulus
capillary bed
afferent arteriole
into glomerulus
efferent arteriole
out of glomerulus
peritubular capillaries
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line convoluted tubules
vasa recta
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capillaries deep into medulla
juxtaglomerular apparatus
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juxtaglomerular cells
produce renin
surround afferent arteriole
pressoreceptors
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macula densa cells
DCT/ ascending loop of Henle
filtrate volume, osmolarity
data
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> 800 L /day
blood into kidney
160 - 180 L/day
blood filtered into nephrons
1 -2 L /day
urine excreted
(all other capillaries of body only 4 L/day)
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filtrate
fluid in nephron
being processed
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urine
fluid out of nephron
final product
processes needed
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waste removal:
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a way to get wastes out of blood
a way to get good stuff back into blood
way to vary blood volume (BP)
water
way to vary blood osmolarity
Na
way to correct blood pH
HCO3what happens where ?
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waste removal
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early nephron
filtration
renal corpuscle
bulk reabsorption
PCT
secretion of wastes
PCT
blood volume/osm control
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distal nephron
varied reabsorption of Na
DCT
varied reabsorption of H2O collecting duct
glomerular filtration
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filters fluid out of plasma into Bowman’s capsule
glomerulus > 100x more permeable than other capillaries
How big should the holes be?
maintain BP must be high enough to force fluid into Bowman’s capsule
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55 mmHg in glomerulus
efferent arterioles thinner than afferent
net filtration pressure
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net filtration pressure NFP
=
force out - force in
force out:
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HPg
glomerular hydrostatic pressure (BP)
force in:
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OPg
colloid osmotic pressure
HPc
capsular hydrostatic pressure
NFP =
HPg
- (OPg + HPc)
NFP =
55
- (30
+ 15)
= 10
glomerular filtration rate
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GFR = filtrate formed per minute
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(both kidneys)
120 – 125 ml / min
180 L / day
factors:
surface area
membrane permeability
NFP
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NFP and GFR
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 systemic BP
 NFP  GFR
dehydration
 NFP  GFR
GFR homeostasis
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any change BP/Vol is a risk to GFR and waste elimination
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GOAL:
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constant GFR
GFR too high
lose nutrients , water
GFR too low
retain wastes
note: constant GFR
≠
not constant urine volume
Δ GFR ~ Δ NFP
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to change GFR
change glomerular BP
3 ways:
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afferent arteriole
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efferent arteriole
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systemic BP
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afferent arteriole:
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vasodilate
? glomerular BP
? GFR
vasoconstrict
? glomerular BP
? GFR
GFR regulation
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intrinsic controls
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afferent arteriole diameter
extrinsic controls
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sympathetic
hormones
GFR intrinsic controls
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GOAL: maintains constant GFR w/changing systemic BP
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myogenic mechanism
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= renal autoregulation
Intrinsic corrects for extrinsic BP/volume changes
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stretch smooth muscle - it contracts
 systemic BP

afferent arteriole vasoconstriction
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vasodilation
tubulo-glomerular feedback mechanism
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GFR
receptors = macula densa
 flow rate ; osmolality
afferent vasodilation
 flow rate ; osmolality
afferent vasoconstriction
GFR extrinsic controls
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homeostasis of systemic BP , not renal BP
 GFR
sympathetic n.s.
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vasoconstricts all blood vessels, afferent arteriole
shunts blood to other organs for emergency
GFR  or unchanged
renin-angiotensin mechanism
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raises systemic BP
juxtaglomerular cells
produce renin
angiotensin II
systemic vasoconstriction  GFR
efferent vasoconstriction  GFR
autoregulation maintains minimal GFR changes
tubular secretion
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from peritubular capillaries into filtrate
mostly in PCT
adds stuff to filtrate :
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wastes
• creatinine , ammonia (NH4+)
• urea , uric acid
• medications and toxins
to  blood pH (DCT)
H+
K
+
aldosterone
(collecting ducts)
tubular reabsorption
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reabsorbs the good stuff
through tubular cells and capillary wall
PCT
most reabsorption here
• all nutrients
• electrolytes
• water
- glucose, AA, small proteins
loop of Henle
water
DCT
Na+
collecting ducts
PCT - reabsorption of sodium
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diffusion into tubular cell (from filtrate)
active transport from tubular cell to interstitial fluid
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Na / K pump
provides energy for reabsorption of other solutes
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diffusion into peritubular capillary
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this creates:
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osmotic pressure toward capillary
electrical gradient
anions follow +
concentration gradient of all solutes
• water follows Na
• dilutes solute concentration in capillary
PCT - passive reabsorption of solutes
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anions
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Cl-
water
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follow Na
HCO3osmosis
obligatory water reabsorption
lowers concentration of solutes in tubule cell and capillary
solutes follow water
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toward low solute concentration
= diffusion
lipids
urea
cations
K+ Ca++
Mg++
PCT - secondary active transport of solutes
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cotransport with Na+
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Na+ active transport out of tubular cell
Na+ diffuses into tubular cell
solutes cotransport into tubular cell
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fascilitated diffusion to capillary
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transport maximum Tm
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max amt able to reabsorb each solute
# carriers in cell membrane
amino acids, cations, glucose
glucose
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glucose Tm 375 mg/min
hyperglycemia
> Tm
glucosuria
PCT - other solutes
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small proteins
endocytosis
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wastes
not reabsorbed
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urea
from AA
uric acid
from nucleic acids
creatinine
from creatine
loop of Henle - reabsorption
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reabsorbs some H2O and Na
see countercurrent mechanism below
early nephron review
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25% of water , 10% of NaCl remain in filtrate at D
CT
wastes remain
filtrate ~ 100 mOsm
filtration and reabsorption is relatively constant in the
not controlled by hormones
early nephron
distal nephron preview
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we need to be able to:
control blood volume (BP)
control blood osmolarity
this is done by varying:
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amount H2O reabsorbed
amount Na reabsorbed
this is controlled by:
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aldosterone
ADH
reabsorption in DCT and cortical Collecting Duct
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Na / K ATPase
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reabsorbs Na into blood
secretes K into filtrate
Aldosterone
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increases Na/K channels and ATPase
stim by:
low BP or BV (via angiotensin)
low Na (via tubulo-glomerular mechanism)
hyperkalemia
effect of Aldosterone
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result:
increased blood osmolarity
slight increase blood volume
K loss
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water
reabsorbed only if ADH
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same Na/K pump
DCT vs PCT
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PCT
obligatory
DCT
only if Aldosterone
water
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PCT
obligatory
DCT/CD only if ADH
reabsorption in collecting duct
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water reabsorption
=
urine concentration
DCT and Collecting ducts are impermeable to water
require aquaporins
ADH
facultative water reabsorption
osmosis
no Na A.T.
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water follows Na
Na already in medulla
why can’t we use Na pumps?
effects of ADH
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w/o ADH
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no water reabsorbed
urine osmolarity ~ 100 mOsm
maximum amt urine produced
w/ ADH :
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water reabsorbed
urine osmolarity varies
facultative water reabsorption
300 – 1200 mOsm
ADH
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hypothalamus -
posterior pituitary
stim by:
high blood osmolarity
low BP
via angiotensin
affects tubule cells of CD
G protein / cAMP system
stim aquaporin production
graded effect
inhib by:
alcohol
diuretic drugs
low osmolarity
loop of Henle – a casual view
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reabsorbs Na and H2O from filtrate
reabsorbs more Na than H2O
leaves the excess Na in the medulla
this high Na concentration has osmotic force at CD
countercurrent mechanism
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countercurrent mechanism
flow in opposite directions
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countercurrent multiplier
loop of Henle
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creates Na gradient in medulla
countercurrent exchanger
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vasa recta
maintains Na gradient in medulla
goal:
Na gradient to reabsorb H2O from collecting ducts
countercurrent multiplier
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creates NaCl gradient in medulla
ascending limb
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active transport of NaCl to medulla
impermeable to water
maintains osmotic gradient of medulla
descending limb
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NaCl out
water out
osmosis of water to medulla
impermeable to NaCl
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NaCl loss from ascending limb creates water loss from descending limb
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Water loss from descending limb creates NaCl loss from ascending limb
result of loop
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decreased urine volume
dilute urine ~ 100 mOsm
creates Na gradient in medulla
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for use by collecting duct
countercurrent exchanger
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vasa recta
maintains osmotic gradient of medulla
reabsorbs NaCl and H2O from medulla
leaves the extra NaCl in medulla
NaCl
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descending vasa recta
absorbs NaCl
ascending vasa recta
loses NaCl
water
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ascending vasa recta absorbs water
via colloid oncotic pressure
distal nephron review
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increase blood osmolarity
aldosterone
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increase BV ; same OsM
aldosterone + ADH
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increase BV ; decrease OsM
ADH
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decrease BV and Osm
ANP
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dilute urine
no hormones
diuretics
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increase urinary output
decrease blood volume
decrease tissue edema
glucosuria
via osmotic diuresis
alcohol
inhibits ADH
caffeine
inhibits Na reabsorption (PCT)
diuretic drugs inhibit Na pumps (DCT, ascending loop)
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Lasix
diuril
K sparing diuretics
block K loss (DCT)
allow Na reabsorption (PCT, Henle)
renal clearance
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rate at which substance is removed from blood
measures GFR and renal disease
RC = UV / P
U
=
concentration of substance in urine
V
=
rate of urine formation
P
=
concentration of substance in plasma
renal clearance (part 2)
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inulin
amt excreted = amt filtered
its RC = GFR
~ 125 ml/min
used as standard
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RC < 125
substance reabsorbed
RC > 125
substance secreted
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glucose
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drugs are secreted
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contains:
water
wastes - urea, uric acid , creatinine
urobilinogen
electrolytes
minerals
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pH
~6
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abnormal
glucose
protein
bacteria
WBC
RBC
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pH balance
RC = 0
completely reabsorbed
RC used to determine dosage
urine
(4.5 – 8.0)
other renal functions
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 H+ secretion / HCO3- reabsorption
erythropoietin
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 RBC production
Vit D
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skin:
cholesterol
 ergocalciferol
kidney:
ergocalciferol  calciferol
 Ca
absorption
++
(digestive)
= active Vit D