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46 Cards in this Set

  • Front
  • Back
microglobulins are...
very small proteins
filtered thru glomerulus
not in urine b/c nut for tubules
endocytose into epis
solvent drag
movement through non-tight jctns
resoprtion of Ca, K, Cl
happens in late proximal tubule
transport mech for resorption of glucose
-secondary active transport w/Na
-in proximal tubule
movement of glucose at glomerulus
freely filtered
characteristics of glucose reabsorption
-secondary transport
-saturation (Vmax & Tm)
-competative inhibition
(sulfates, aa's, uric acid, organic molecules)

DM has glucose in urine because saturation of transport
Tm for glucose
Tm (transport maximum)

~400 mg/min
(filtered load)

GFR x Pg (plasma glucose conc)
plasma glucose concentration at which you exceed Tm
glucose plasma concentration of ~200

after that will be excreted
difference between amount of glucose reabsorbed and excreted
reabsorption of urea in proximal tubule
passive reabsorbtion
depends on flow rate
(low flow more absorbed)
renal secretion
anions & cations:

creatinine (cation)
(also epi, NE & DA)
PAH (organic acids)-anion
(cAMP, Bile acid salts, PGs, urate, oxalate)
meds excreted at kidney

calculation of RBF
(renal plasma flow)
solve ERPF (GFR)
UV/RA pah

amount of filtrate absorbed at proximal tubule
b/v autoregulation
(Starling & TG balance)
amount reabsorbed at PT
ALWAYS 67% of filtrate & water
GT balance maintains (by increase filtration fraction)
GT balance
maintains 67% reabsorption
starlings forces
absorption at proximal tubule
-HCO3 (70-85% at PT, 99.9% total)

-tight jcts are tight
-Na costransport, antiport w/H+
-Glucose & aa's cotrsp w/Na

-tight jcts loose
-K & Cl (& cations) in via solvent drag
-water passive diffusion

-H+ & organic acids secreted
absorption of HCO3
mostly at proximal tubule
Na/K ATPase
Na/HCO3 costransport at BLM
Na/H+ antiport at lumen
CA on luminal membrane (only place CA extracellular)
PT absorption of Na
-co w/ glucose or aa's
-anti w/H+
-Na/K ATPase at BLM
PT absorption of Glucose & aa's
co w/Na at lumen
out BLM b/c Na/K ATPase drives transporter
absorption of proteins at PT
endocytosis (100%, dz state if urine is pos for microglobulins)
molecules absorbed by solvent drag
K, Cl (& other anions)
in late PT

Cl at principal cell (late DT & CD)
molecules secreted in PT
H+ & organic acids (PAH, aspirin, EtOH)

& ammonia to buffer acids in tubule
primary function of:
DT (early)
DT (late) & CT
PT- passive resorb 67% filtrate
LOH- 20% filtrate & water
DT (early)
-MD cells signal JGA
-dilution of tubular fluid
Late DT & CCD
-hormone reg reabsorption of solute & water
componants of LOH
- perm Na, H2O, urea

- active resorp Na, CL, K
- active secretion H/K
transporter that drives CCM
Na, 2CL, K cotransport
Furosimide inhibits
Early Distal Tubule Actions
Macula Densa (if low solute or volume)
-signal JGA rls renin
-relax afferents

dilution of tubular fluid
-Na/Cl channel
-blocked by thiazides
cell types at late DT & CD
-resorption of Na, Cl, K & H2O

-acid base balance
absorption of Na at principal cell
(late DT & CD)
aldosterone dependent channel
inhibited by K sparing diuretics
absorption of Cl at principal cell
(Late DT & CD)
maintain ion balance in plasma

takes K out via cotransport
back in via solvent drag
(based on Na level)
absorption of K at principal cell
channel diffusion trade w/Na (K sparing diuretics)
co transport secretion w/Cl
affect of aldosterone on principal cell
bind R
activate mRNA
increase Na channels
increase activity of Na/K ATPase
(increases passive diffusion of K out to tubule)
aldosterone stimulated by
i.e. renin rls

low NaCl (macula densa)
low volume
high K
ion flow at intercalated cell
H+ pumped out
-H ATPase
-H/K ATPase antiport

K pumped in
-H/K ATPase antiport

increase production of HCO3 if acidosis

no aquaporin
excretion of titratable acids
In intercalated cells
secrete PO3 (best buffer)
secrete H+ (ATP ase or exchange for K in)
acid picks up (in tubule)
HCO3 (gen'd when rls H+) out to interstitium
response to acidosis
more glutamine at proximal tubule (& more NH4 secreted)
more movement NH4/NH3 from asc to desc
more NH3 available in med to diffuse & trap H+ excreted in CD
movement of NH3/NH4
passive & active from ascending limb to desc limb

passive into CD

increases w/low pH urine
site of action & effect of aldosterone
early DT/CD

increase expression (via mRNA) Na channels

increase secretion of K
site of action & effect of AT II

increases PT reabsorption of NaCL & H2O

via efferent arteriole constriction

(JG's dilate afferents)
site of action & effect of ADH

incraese expression (mRNA) of aquaporins

increase H2O & urea reabsorption
site of action & effect of ANP

increase Na excretion
increases GFR
site of action & effect of PTH

decrease PO4 reabsorption
increase Ca reabsorption
decrease activation 25 D
(leading to increased Ca & PO4 reabsorption)
aldosterone secreted in response to
low blood volume
high plasma K
low DT Na (MDs sense)
(renin released from JG via cAMP when MD, osmos or baros sense above situation)
AT II released in response to
same as aldosterone

low blood volume (baros)
high plasma K (osmos)
low DT Na (MDs sense)
ADH released in response to
low blood volume
ANP released in response to
atrial stretch
PTH released in response to
decreased plasma Ca or 1,25 D
increased PO4