Keef 1 Flashcards
85% of the nephrons in the kidney are _____ while 15% are ______.
85% cortical
15% medullary
What is the main distinguishing feature of juxtamedullary nephrons?
They have long loops of Henle that push into the medulla & even into the papillary region. These are responsible for creating the osmotic gradient in the interstitial space.
What type of tissue does the exchange happen across in nephrons in the kidney?
Simple squamous epithelium
T/F the cortical nephrons don’t have a loop of Henle & don’t significantly contribute to the osmotic gradient in the interstitial space.
False. They do have a loop of Henle. But it is true that they don’t significantly contribute to the osmotic gradient.
Where does the fluid go after it gets to the distal convoluted tubule of the cortical & juxtamedullary nephrons?
They both drain into the common collecting duct. Here stuff happens based off of the osmotic gradient created by the juxtamedullary nephrons.
Where is the nephron permeable to water & where is it not?
In areas where filtration dominates: like the glomerulus & PCT & descending limb of the loop of Henle it is very permeable. In areas where absorption dominates: like the ascending limb of the loop of Henle & the DCT…it is very impermeable.
When we talk about permeability…what tissue are we talking about?
We are talking about the simple squamous epithelium lining the nephron…it is made of tight jcns in areas that are impermeable.
What types of proteins make up the tight jcns b/w the epithelial cells in the nephron?
Claudin
Occludin
*in the paracellular space
What is something that could cause a rupture of the tight jcn b/w the epithelial cells?
Ischemia, Disease, Mutation
Bad situation.
What is the relationship b/w portions of the nephron, filtration/absorption, tight jcns, & resistance?
As you move from the glomerulus to the PCT to the loop to the DCT to the collecting duct…
Resistance increases.
This means that there are more tight jcns as you move along.
This means that the area is less permeable as you move along.
This means that less filtration happens & more absorption happens as you move along.
What is another name for antidiuretic hormone (ADH)?
arginine vasopressing (AVP)
What does ADH do to the nephron?
It greatly increases the permeability of the collecting duct (not by messing w/ the tight jcns) but by inserting aquaporins (proteins that create holes).
If ADH is not present…what happens to those aquaporins it inserted into the collecting duct?
They are taken out/degraded.
Where is the location of aquaporins that are always there–not dependent on ADH? Where is the location of aquaporins that are only present w/ the presence of ADH?
Aquaporins in the proximal convoluted tubule are always there.
Aquaporins in the collection duct are dependent on ADH.
What are the different capillaries that are found w/ the cortical nephron & juxtamedullary nephrons?
Both have glomerular capillaries (afferent arteriole leads into this capillary & efferent arteriole leads out)
After this they both have a peritubular capillary surrounding the nephron.
BIG DIFFERENCE:
Only the juxtamedullary nephrons have the vasa recta capillary (it surrounds the big long loop of Henle).
Which of the capillaries in the nephron are low pressure & which are high pressure?
High Pressure: the glomerular capillaries
Low Pressure: peritubular capillaries & the vasa recta
Where is the first point of resistance in the nephron?
The afferent arteriole. Another point of resistance is the efferent arteriole.
What percentage of the renal blood flow goes to the cortex & what percentage goes to the medulla?
90% to the cortex.
10% to the medulla
What makes up the juxtaglomerular apparatus?
Glomerulus & the nearby portion of the distal convoluted tubule…this includes the JGA cells & the macula densa. Also, the extraglomerular mesanangial cells.
What is the fcn of the JGA cells & the macula densa?
JGA cells secrete renin.
The macula dense sense the level of flow in the DCT & feedback to the JGA cells to secrete Renin.
What is tubuloglomerular feedback?
Mechanism that tries to keep a constant GFR.
If the macula densa cells in the DCT sense low NaCl caused by low flow…they release substances that will cause JGA cells to secrete Renin (eventual efferent arteriole constriction) & substances that directly dilate the afferent arteriole. This increases GFR.
What does low NaCl @ the macula densa translate to a GFR that is too low?
B/c if GFR is too low b/c arterial pressure is too low or something there will be less flow in general in the nephron…NaCl is absorbed into the interstitial space in the ascending limb of the loop of Henle…of course some of this salt stays in the filtrate…if the macula densa in the DCT senses less NaCl than normal–that indicates lower flow than normal & calls for increased pressure in the glomerulus.
What is the mediator in the mechanism of tubuloglomerular feedback that tries to correct a GFR that is too high?
Mediator: adenosine
What are the modulators in the mechanism of the tubuloglomerular feedback that tries to correct a GFR that is too high?
NOS 1, COX-2, Ang II