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48 Cards in this Set
- Front
- Back
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glomerular filtration definition |
filtration of blood plasma by the renal glomerular caps; no proteins or blood cells cross |
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glomerular ultrafiltrate |
fluid with solute concentrations very similar to those in plasma; filtration of the blood plasma by the renal glomerular caps results in the formation of glomerular ultrafiltrate with solute concentrations that are similar to those in plasma; however protein and other high molecular weight compounds and protein bound solutes are present in much lower cencentrations so for the most part it doesn't contain them |
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the filtration barrier |
glomerulus with its afferent arteriole and efferent artierioles, distal tubule with masula densa, and glomerular caps with the visceral epi layer of bowman's capsule made up of podocytes; fenestrated endothelium and podocytes on them with their foot processes; between the interdigitation of the foot processes are filtration slits which are connected by a thin diaphragmatic structure called the slit diaphragm; glycoproteins with negative charge cover the podocytes, filtration slits, and filtration diaphragm |
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what forms the slit diaphragm |
nephrin, neph1, podocin, and other proteins organized on lipid rafts; these proteins may recruit other molecules involved in signaling events that control slit permeability; the extracellular domains of these proteins from adjacent podocytes may zip together to form the filtration slit |
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when there is a defect in these proteins |
result is the passage across the filtration barrier of protein which normally is not allowed through the slits |
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filtration barrier summary |
fenestrated endothelium; basement membrane; epithelial podocytes |
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filterability of things depends on what |
molecular weight, radius, and charge; weight= less than 5,500 Da; radius= less than 2nm; the glomerular filtration barrier carries a net negative charge that restricts the permeation of anions but enhances the permeation of cations |
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what happens if the glomerular barrier loses its negative charge |
increased permeability to negatively charges ions |
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forces that determine ultrafiltration |
PGC= glomerular cap hydrostatic pressure; pieBS= bowman's space oncotic pressure (which is pretty much 0); PBS= bowman's space hydrostatic pressure; pieGC= glomerular cap oncotic pressure; the GCs favor ultrafiltration and the BSs oppose the movement of fluid out of the cap; glomerular filtration rate (GFR)= Kf[(PGC-PBS)-(pieGC-pieBS)] where Kf is the ultrafiltration coefficient; in other words the glomerular filtration rate depends on the product of the ultrafiltration coefficient (the product of the hydraulic conductivity of the cap and the effective surface available for filtration) and the net Starling forces; the net driving force at any point int he glomerular cap is the difference between the hydrostatic pressure difference and the oncotic pressure difference |
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the starling forces along the glomerular caps |
because the afferent and efferent arterioles are in series, PGC is 50 mmHg which is approx 2x as high as in most other caps and it goes down very little between afferent and efferent arterioles; the hydrostatic pressure in the bowman's space is approx 10 mmHg and it changes little along the glomerular cap; as far as the oncotic driving forces, pie GC is 25 mmHg at the beginning of the cap; as a consequence of the production of a protein free ultrafiltrate the oncotic pressure of the fluid left behind in the glomerular cap rises progressively; the oncotic pressure in the bowman's space (pieGS) is very small because the ultrafiltrate for the most part has no protein |
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as you go along the glomerular cap network what increases? |
PBS+pieGC and when it increases to the point that it equals PGC+pieBS then there is no filtration (at the end of the cap)(filtration equilibrium)(pieGC is the one that rapidly increases); in between (where there is still a difference) then there is PUF (ultrafiltration pressure); remember pieBS is 0 |
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renal blood flow represents what percent of the cardiac output |
20% |
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decreased glomerular plasma flow leads to |
decreased GFR; filtration equilibrium is achieved earlier |
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increased glomerular plasma flow leads to |
increase in GFR; as renal plasma flow increases the oncotic pressure does not increase so rapidly and filtration equilibrium may not be achieved within the glomerular cap leading to - as RPF increases there is more GFR and - the surface area utilized for filtration increases |
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filtration fraction |
FF=GFR/RPF where FF=filtration fraction, GFR+ glomerular filtration rate (ml/min), and RPF=renal plasma flow (ml/min); this is the fraction of renal plasma flow that is filtered |
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renal microvascular features |
the renal vascular bed has 2 major resistances= the afferent and efferent arterioles; both can be regulated; it has 2 cap beds in series= afferent and efferent arteriolar resistances control both glomerular filtration rate and renal plasma flow, the peritubular caps provide nutrients for tubules and RETRIEVE THE FLUID THE TUBULES REABSORB |
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pressures along the renal vasculature |
there are significant pressure drops at both arterioles; the glomerular cap pressure is nearly constant along the cap and the peritubular cap pressure is quite low |
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control of pressure along the renal vasculature |
selective vasoconstriction or relaxation of the afferent and efferent arterioles allows for a highly sensitive control of the hydrostatic pressure in the glomerular cap and therefore of GFR |
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if there is an increase in afferent arteriole resistance and a decrease in efferent arteriole resistance |
the total resistance does not change and therefore the RPF would not change but PGC decreases with a possible decrease in GFR |
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if there is a decrease in afferent arteriole resistance and an increase in efferent arteriole resistance |
even though the total resistance has not changed and therefor total RPF has not changed there is a higher PGC which increases GFR |
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afferent arteriole vasoconstriction would cause |
a decrease in RPF, GFR, and PGC |
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efferent arteriole vasoconstriction would |
decrease RPF but initial increase in PGC and GFR; as resistance increases further GFR decreases because falling RPF dominates |
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peritubular caps originate from what and form what |
originate from efferent arterioles of the superficial glomeruli; the caps form juxtamedullary nephrons known as vasa recta that follow the tubules and enter the medulla |
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peritubular caps functions |
deliver oxygen and nutrients and take up the interstitial fluid that the renal tubules reabsorb by following the Starling forces that normally favor absorption (ultrafiltration elevates plasma oncotic pressure and the efferent arteriole resistance drops the postglomerular hydrostatic pressure so the effect is a large net absorptive pressure that remains along the length of the peritubular cap) |
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when there is an increase in the FF, the oncotic pressure in the peritubular caps |
increases (so after it being equal to the oncotic pressure at the end of the glomerular caps) leading to higher PT absorption; the inverse is also true (decreases in FF decrease PT absorption) |
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autoregulation of the RBF and GFR |
stabilizes the filtered load of solutes and protects the renal caps against increases in perfusion pressure that could lead to structural damage but is not important for physiological regulation of Na balance and during physiopathological states where the systemic changes in hormonal and sympathetic regulation effects dominate; the kidney responds to a rise in renal arterial pressure with proportional increase in the resistance of the afferent renal arterioles; efferent arteriole resistance does not change; includes myogenic and tubuloglomerular feedback |
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tubuloglomerular feedback- increase in mean arterial pressure |
increase in mean arterial pressure leads to increase in glomerular cap pressure RPF and GFR leads to increase Na and Cl delivery to macula densa and JG apparatus leads to increase contraction of nearby vascular smooth muscle cells leads to increase in afferent arteriolar resistance leads to normalization in GFR |
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myogenic response |
the afferent arterioles have the inherent ability to respond to changes in vessel circumference by contracting or relaxing; the mechanism is the opening of stretched activated, non selective cation channels in vascular smooth muscle which leads to increased cytosolic Ca, depolarization, and contraction |
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other forms of regulation of RBF and GFR |
renin-angiotensin-aldosterone axis; sympathetic nerves; arginine vasopressin; atrial natriuretic peptide; modulate renal hemodynamics and renal Na reabsorption |
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renin-angiotensin-aldosterone |
the dominant effect is that of afferent and more pronounced efferent vasoconstriction; in terms of renal hemodynamic effects the most important member is AII whose dominant effect is that on afferent and more pronounced efferent vasoconstriction- it decreases RBF and to a lesser degree GFR, the FF goes up |
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sympathetic nerves |
nerve fibers from the sympathetic celiac plexus supply the kidney; the nerve endings are primarily alpha adrenergic; these nerve endings are found in association with afferent arteriole, efferent arteriole, mesangial cells, and juxtaglomerular apparatus; a small increase in sympathetic activity augments renin and aldosterone release and results in preferential efferent vasoconstrction; strong stimulation markedly increases both resistances and results in drastic decreases in RBF and GFR |
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arginine vasopressin |
secreted in the posterior pit mainly secondary to changes in osmolality although hemodynamic changes will also cause release of this hormone; main effect increase water reabsorption (antidiuretic hormone); hemodynamic effects= it increases vascular resistance, it does not affect RBF and GFR, it decreases blood flow to the renal medulla maintaining its hypertonicity essential for concentrating urine, only in cases of severe decreases in effective circulating volume produces systemic vasoconstriction |
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atrial natriuretic peptide |
increase in effective circulating volume leads to increase in atrial pressure leads to atrial myocytes release ANP; effects= vasodilation of afferent and vasoconstriction of the efferent arteriole, increase in RBF and GFR, and inhibition of secretion of renin and AVP |
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other vasoactive agents |
epinephrine, dopamine, endothelins, prostaglandins, leukotrienes, and nitric oxide |
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epinephrine is released by |
cromaffin cells of adrenal medulla similar to norepinephrine |
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dopamine does what |
low doses vasodilates, and at higher doses vasoconstricts |
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endothelins so what and what is the stimuli for their release |
they are potent vasoconstrictor peptides that act locally; stimuli for their release include AII, epi, high dose AVP, thombins, and shear stress |
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prostaglandins do what |
prevent/modulate excessive vasocosntriction |
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leukotrienes do what and their release is stimulated by what |
have local effects and their release is stimulated in inflamation; they have a vasoconstrictor effect |
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nitric oxide is produced where and has what effect |
is produced in endothelial cells and has a vasodilatory effect |
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key concepts: glomerular ultrafiltrate is what |
fluid with solute concentrations very similar to those in plasma; it contains no protein and no blood cells |
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key concepts: fultration barrier is what |
endothelial cells, basement membrane, and podocytes |
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key concepts: what determine the filterability of solutes across the glomerular filtration barrier |
molecular size, electrical charge, and shape |
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key concepts: determinants of glomerular ultrafiltration |
hydrostatic pressure in glomerular cap, oncotic pressure in bowman's space, oncotic pressure in glomerular cap, hydrostatic pressure in bowman's space, and ultrafultration coefficient |
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key concepts: relation of renal blood flow and GFR |
renal blood flow indirectly affects GFR |
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key concepts: the renal vascular bed has 2 major resistances= |
the afferent and efferent arterioles which can both be regulated |
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key concepts: the 2 cap beds of the renal vascular bed |
afferent and efferent arteriolar resistances control both GFR and renal plasma flow; the peritubular caps provide nutrients for tubules and RETRIEVE THE FLUID THE TUBULES REABSORB |
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key concepts: regulation of RBF and GFR |
hormonal changes (RAAS, sympathetic nerves, AVP, and ANP) induce changes in vascular resistance that regulate RBF and GFR |
