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46 Cards in this Set
- Front
- Back
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microglobulins are...
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very small proteins
filtered thru glomerulus not in urine b/c nut for tubules endocytose into epis |
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solvent drag
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movement through non-tight jctns
resoprtion of Ca, K, Cl happens in late proximal tubule |
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transport mech for resorption of glucose
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-secondary active transport w/Na
-in proximal tubule |
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movement of glucose at glomerulus
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freely filtered
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characteristics of glucose reabsorption
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-secondary transport
-saturation (Vmax & Tm) -competative inhibition (sulfates, aa's, uric acid, organic molecules) DM has glucose in urine because saturation of transport |
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Tm for glucose
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Tm (transport maximum)
~400 mg/min (filtered load) GFR x Pg (plasma glucose conc) |
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plasma glucose concentration at which you exceed Tm
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glucose plasma concentration of ~200
after that will be excreted |
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splay
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difference between amount of glucose reabsorbed and excreted
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reabsorption of urea in proximal tubule
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passive reabsorbtion
depends on flow rate (low flow more absorbed) |
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renal secretion
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anions & cations:
creatinine (cation) (also epi, NE & DA) medications PAH (organic acids)-anion (cAMP, Bile acid salts, PGs, urate, oxalate) |
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meds excreted at kidney
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anions:
-diruetics -acetazolamide -PNC -probenecid -slicylates cations -atropine -isoproterenol -morphine -amiloride -quinine -cimetidine |
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calculation of RBF
(renal plasma flow) |
solve ERPF (GFR)
UV/RA pah RBF=RPF/1-Hct |
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amount of filtrate absorbed at proximal tubule
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ALWAYS 60%
b/v autoregulation (Starling & TG balance) |
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amount reabsorbed at PT
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ALWAYS 67% of filtrate & water
GT balance maintains (by increase filtration fraction) |
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GT balance
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maintains 67% reabsorption
starlings forces Unregulated |
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absorption at proximal tubule
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All
-HCO3 (70-85% at PT, 99.9% total) Early -tight jcts are tight -Na costransport, antiport w/H+ -Glucose & aa's cotrsp w/Na Late -tight jcts loose -K & Cl (& cations) in via solvent drag -water passive diffusion -H+ & organic acids secreted |
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absorption of HCO3
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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) |
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PT absorption of Na
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Lumen
-co w/ glucose or aa's -anti w/H+ -Na/K ATPase at BLM |
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PT absorption of Glucose & aa's
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co w/Na at lumen
out BLM b/c Na/K ATPase drives transporter |
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absorption of proteins at PT
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microglobulins
endocytosis (100%, dz state if urine is pos for microglobulins) |
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molecules absorbed by solvent drag
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K, Cl (& other anions)
in late PT Cl at principal cell (late DT & CD) |
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molecules secreted in PT
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H+ & organic acids (PAH, aspirin, EtOH)
& ammonia to buffer acids in tubule |
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primary function of:
PT LOH 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 |
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componants of LOH
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tDLH
- perm Na, H2O, urea TALH - active resorp Na, CL, K - active secretion H/K |
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transporter that drives CCM
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Na, 2CL, K cotransport
in TALH Furosimide inhibits |
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Early Distal Tubule Actions
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Macula Densa (if low solute or volume)
-signal JGA rls renin -relax afferents dilution of tubular fluid -Na/Cl channel -blocked by thiazides |
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cell types at late DT & CD
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principal
-resorption of Na, Cl, K & H2O intercalated -acid base balance |
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absorption of Na at principal cell
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(late DT & CD)
aldosterone dependent channel inhibited by K sparing diuretics |
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absorption of Cl at principal cell
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(Late DT & CD)
maintain ion balance in plasma takes K out via cotransport back in via solvent drag (based on Na level) |
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absorption of K at principal cell
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channel diffusion trade w/Na (K sparing diuretics)
co transport secretion w/Cl |
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affect of aldosterone on principal cell
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bind R
activate mRNA increase Na channels increase activity of Na/K ATPase (increases passive diffusion of K out to tubule) |
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aldosterone stimulated by
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i.e. renin rls
low NaCl (macula densa) low volume high K |
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ion flow at intercalated cell
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H+ pumped out
-H ATPase -H/K ATPase antiport K pumped in -H/K ATPase antiport increase production of HCO3 if acidosis no aquaporin |
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excretion of titratable acids
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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 |
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response to acidosis
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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 |
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movement of NH3/NH4
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passive & active from ascending limb to desc limb
passive into CD increases w/low pH urine |
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site of action & effect of aldosterone
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early DT/CD
increase expression (via mRNA) Na channels increase secretion of K |
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site of action & effect of AT II
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PT
increases PT reabsorption of NaCL & H2O via efferent arteriole constriction (JG's dilate afferents) |
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site of action & effect of ADH
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DT/CD
incraese expression (mRNA) of aquaporins increase H2O & urea reabsorption |
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site of action & effect of ANP
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DT/CD
increase Na excretion increases GFR |
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site of action & effect of PTH
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PT/TALH/DT
decrease PO4 reabsorption increase Ca reabsorption decrease activation 25 D (leading to increased Ca & PO4 reabsorption) |
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aldosterone secreted in response to
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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) |
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AT II released in response to
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same as aldosterone
low blood volume (baros) high plasma K (osmos) low DT Na (MDs sense) |
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ADH released in response to
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low blood volume
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ANP released in response to
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atrial stretch
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PTH released in response to
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decreased plasma Ca or 1,25 D
increased PO4 |
