RENAL UROLOGY+ANATOMY, NEPHROTIC v. NEPHRITIC Flashcards
(45 cards)
2 types of nephrons
juxatmedullary- 15% of nephrons, INNER portion
cortical- 85% of nephrons, OUTER portion
role of nephrons
- juxtamedullary vs. cortical
- why would we direct blood flow between them?
juxtamedullary- primarily for urine concentration
- rebarbsorbs higher proportion fo filtrate
- uses more energy
cortical- less efficient at conserving fluid
- uses less energy
we can direct bloow flow to CONSERV E fluid or energy
renal corpuscle
- consists of
- function
consist of glomerulus and bowmans capsule
- moves fluid out of blood plasma and into bowmans capsule to be filtered
- majority of filtrate goes back into blood stream
filtration at glomerular level
filtrate must pass through
- fenestrated capillary membrane
- glomerular basement membrane
- podocyte foot processes
feedback loop for aldosterone secretion (RAAS system)
renin release from juxtaglomerular appartus to make angiotensinogen into angiotensin I, then into—angiotension II (by ACE)—-direct vasoconstriction effect on vessels, effect on Na and K
angiotensin II—stim adrenal cortex to release aldosterone—-aldosterone dec Na and water excretion—-inc extracellular fluid volume—-inc renal arterial mean pressure
action of aldosterone on principal cell of collecting duct
causes sodium reabsorption, potassium secretion
ADH effect
- dehydration vs. hypervolemia/hydration
acts on collecting duct to influence water and sodium secretion/reabsorption
- ADH present–> allows DCT and CD to be leaky and reabsorb water into salty medulla (good for dehydration/conserve and circulate fluid)
- ADH NOT present–> DCT and CD become impermeable to water, and water stays in filtrate, going to ureter to be peed out
countercurrent multiplier
- how does it work
process that uses energy to create an osmotic gradient in the renal medulla (henle loop, DCT, CD)
- maintaining NaCl gradient in interstitial fluid
- conserve water in response to ADH
- use vasa recta to exchange fluid and sodium between circulation and tubules
how does the NaCl gradient work
in desc. limb- water is being reabsorbed into the blood vessel due to the salty medulla
in asc limb- it is IMPERMEABLE to water, so it causes NaCl to move out of the tubule, and reabsorb into the medulla
- that constant movement of salt into the medulla drives the OSMOSIS and gradient for water to be reabsorbed into the blood vessel
glomerular filtration
- PGC v. PBS
PGC- glomerular capillary blood pressure
- moving from glomerulus into bowmans
- pressure is higher WITHIn the bowmans space to allow for drive of filtration
PBS- fluid pressure in bowmans space (where glomerular capillaries are)
- moving from bowmans into glomerulus
higher pressure in AFFERENT arteriole
what happens if there is an issue with PGC v. PBC
if there is higher pressure in areas other than the glomerular capillary space (ex: higher PBS than PGC), net filtration pressure and GFR will dec, leading to reduced filtration and fluid RETENTION
blood pressure/resistance effect on kidney
- sites of highest vascular resistance
high systolic pressure can cause irreversible damage
- largest vascular resistance at afferent and efferent arteriole
- intrinsic damage is due to vascular resistance
efferent arteriole constriction
- what can cause it
- what happens
cause ex) angiotensin II
- dec RBF (renal bf)
- inc PGC (resistance causes inc in pressure)
- inc GFR (inc PGC causes inc PGC)
- inc FF (filtration fraction)
afferent arteriole constriction
- what causes it
- what happens
cause ex) norepi, NSAIDS, prostaglandin inhibitors
- dec RBF, dec PGC, dec GFR, nl FF, dec end proximal fluid delivery
efferent arteriole DILATION
- what causes it
- what happens
causes ex) ACEi
- inc RBF
- dec PGC (dec resistance)
- dec GFR
- dec FF
afferent arteriole DILATION
- what causes it
- what happens
causes ex) prostaglandins
- inc RBF
- inc PGC
- inc GFR
- FF nl
- inc end proximal fluid delivery
trick for afferent v. efferent tone
efferent
- RBF opposite of PGC, GFR, FF
afferent
- RBF, PGC, GFR, FF all move same way
what percent of CO is received by kidneys
20-25%
systemic perfusion pressure in kidneys
90-100 mmHg is needed
OR risk damage in shock, dehydration, and ischemic events
kidney has HIGH O2 demand for renal metabolism
EPO secretion
- EPO stimulates BM to make more RBCs
- RBCs go to kidney and deliver O2
- feedback dependent on whether kidney is receiving enough bf and O2 to stimulate EPO to the BM to inc RBC production
CKD and EPO
in CKD- dysfunc of the kidney results in production of less EPO
- less EPO=less BM stim=less RBC produced= less O2 to kidneys (remember kidney needs LOTS OF O2!)
- this can cause ANEMIA
CKD and EPO
- tx
- supplements
giving these pts EPO stim drugs will mimick EPO and stim the BM to make more RBCs
- must supplement these pts with iron (anemia caused from CKD)
blood test for vit D levels vs. active vit D
appears as vit D 25,OH—> vitamin STORES in the body
Active vit D—> vit D1,25,OH
- becomes activated in the kidneys and can now be used by the body for bone production
PTH effect on kidney
PTH directly stimulate on kidney to make inactive into active form of vit D
- this is essential for calcium absorption in the small intestines
