renal Flashcards
(38 cards)
list the anatomy of renal corpuscle
BC: epithelical cells (where fluid filters into) // podocytes
fused on top of basal lamina
glomerulus: endothelial cells
many femestration
3 barriers to filtratio.
split byw podocyte
basal lamina
glomerula pore size
order of blood glow in kidney
aorta/ cia renal artery / afferent, glomerulus, efferrent arteriole/ peritubular capill // renal gein towards inf vena cava
NFP
(P gc + coloid osmotic of BC) - (PEe BC + coloid osmotic of Gc)
2 factors affectinng GFR
- NFP- renal blood flow and BP
2, filtratio. coefficient
(SA for Gv available for filtration
permeable of barrier btw capil & Bc$
compare myogrnic response vs tubuloglomerular feedback
1/ High bp/ aff.ar constricts / ion channels open / smoth muscle cell depol : VG Ca channel open / aff.a constrict
Less blood flow, GFR
2/ high GFR / flow in tubule and mac.densa ce increase : paracrine from
mac.d signal to aff.-
constrict
if efferent arteriolr constrixt?
P GC and GFR woidl increase bcs thereymore blood in corpiscle
gice versa
how to calculate filtered load
=Xasma x GFR
cause of diabetes mellitus?
more filtered load glucose -> more glucose in filtrate -> bcs saturated Na/glucose symporter not all gets reabsorbed -> creates glucosknaria (glucose inurine) aand osmotic diulesis (more urine vol)
ascending limb vs distal convoluted tube
- DCT reavsorbs Ca
- no paracae transport
3 parathyroid hmn affects DCT
tell me tb concentra of filtrate along the tubule
proximal: same Osm 300
decendign: reabosrb water <Osm 1400
ascending: decrease Osm 100
collecting fuct: reabsord ion and water / increase Osm / 300 1000 1400
how osmoreceptor affect Warer avsorvtion
Increase plasma osmolarity -> shrivel -> trigger ADH -> bund to recpe (collec duct) -> more AQII -> water water reabsorption
barorexep - Water reabsorption.?
Decrease total body water / ECf -> less blood vol & BP -> send less AP to hypotha-> trogger ADH -> water resorption
compare with and without ADH, the effect on urine?
w/ ADH: low volume of concentrated urine
w/o aDH: large vol of diluted urine
Osmoreceptor’s role in ADH?
< plasma Osm, (high->low) shrink, trigger ADH which binds to recep in collecting duct -> creates more aQII -> more water reabsorption
Baroreceptor’s role in H20 handling?
> total body water/ ECF, > blood volume/ BP, barorecep send less AP to the hypothalamus, trigger ADH, more water reabsorption
RAAS vs ANP
renin angiotensen aldersterone vs atrial natriuretic peptide
increse Na+ reabsorption when vol are high vs decrease when vol are high
how renin leads to aldersterone production
liver releases angiotensinogen regardless of Na+ lvl -> justaglomerular cell releases renin when Na+ lvl are low -> cleave into angiotensin I -> angiotensin II with ACE -> aldersterone
between ADH, angiotensin II, aldersterone, ANP- type of hmn
only aldersterone is steroid. the rest is peptide
how angiotensin II increase Na + reabsorption
in proximal tubule, increase the activity of Na+/K+ ATPase and Na+/H
decrese GFR by constricting afferent/efferent -> less filtrate -> more Na+
how aldersterone increase Na+ reabsorption
in collecting duct,
increase Na+ K+ CHANNELS, increase the activity of Na+/K+ ATPase, increase gene expression (more protein expression)
how ANP decrease Na+ reabsorption
High Na+/ ECF/ BP -> cardical atrial cell releases ANP
(1) aldersterone production decreased (2) afferent arteriole dilates -> less GFR
-> less Na+ reabsorption
regulation of renin via chemoreceptor
(in macula densa cell)
If low Na+ lvl pass the macula densa cell, justaglomerular cell trigger renin
regulation of renin via baroreceptor in carotid sinus
low BP -> baroreceptor send less AP to the juxtaglomerular cells -> trigger renin
