FINAL EXAM - Lecture 5 Flashcards
Clearance is always
volume of substance cleared from the plasma
If creatinine is being reduced, then
renal function is being reduced
When someone has acute hypertension, how does the kidney respond pre glomerular capsule? Say the map is 200mmHg
- Afferent arteriole would constrict to prevent as much overperfusion as possible, but it can only constrict so much.
Say the MAP is 200mmHg, what happens to the pressure in the GC? and what is the result of that?
90mmHg (normal 60mmHg), which would change our NFP, and increase our GFR. Reabsorption doesnt increase and we would produce insane amounts of urine. So, obviously, the afferent arterioles are good at maintaining blood flow.
What is a consequence of a low MAP, such as 50mmHg?
GFR decreases, so kidneys arent filtering as much, will elevate things the kidneys were supposed to filter
When we have chronic HTN or things like uncontrolled diabetes, what can happen to afferent arteriole?
may become stiff and calcified just like any other blood vessels, and wont be able to dilate as much to compensate for a drop in blood pressure.
What is another consequence of chronic HTN?
glomerular capsular gets beaten up from all the pressure, podocytes may break, scarring in capillary bed, altered filtration, structures may not stay together.
What is getting the MOST messed up by chronic HTN?
Glomerular capillary bed
Agent that effects efferent arteriole more
Angiotensin II
Still affects afferent, just efferent most.
Drugs will primarily relax which arteriole (pressors or dilators)
afferent arteriole MOST, but efferent arteriole will also be affected.
If we have high pressure/high GFR, macula densa would sense increased flow and do what?
Decrease angiotensin II to dilate the efferent arteriole
Where is majority of reabsorption occuring?
Proximal tubule, almost everything.
is there reabsorption happening at every segment of tubular structure?
Yes, some segments more than others.
what percentage of water is reabsorbed in the Proximal tubule?
2/3rds
Where is creatinine most concentrated in proximal tubule?
At the end. Water is being reabsorbed but creatinine isnt, so the concentration is going up the further you go down the tubule.
Where is the “sensory” area thats watching the numbers of sodiums and chloride?
macula densa. mostly watching for sodium.
How does the macula densa gauge the GFR?
by watching Na and Cl. If there is a higher amount of NaCl, it will detect that the GFR is higher than normal.
How does the macula densa know how much Na and Cl pass through?
Its counting how many molecules come through (maybe)
If GFR is low, what will macula densa do?
Increase Angiotensin II which will constrict efferent arteriole and increase GFR
What does angiotensin II do?
Increases salt reabsorption, and constricts efferent arteriole.
Where is the increased salt absorption from angiotensin II?
proximal tubule
What percent is normal of Na and Cl is reabsorbed in proximal tubule?
2/3rds
What are the consequences of the increased reabsorption of NaCl in proximal tubule even though GFR is normal?
Macula densa would detect low NaCl, increase angtiotensin II, which would constrict efferent arteriole and increase NaCl reabsorption, leading to elevated blood pressures in the glomerular capillary, causing damage if its a long term problem.
What kind of drug would you give if your NaCl reabsorption is elevated?
Angiotensin II blocker or ARB
For every glucose we reabsorb, we have to reabsorb
one sodium along with it, cause sodium is going down its concentration gradient (140:14)
What is the sodium concentration of initial part of proximal tubule?
140
If we have elevated glucose, this would be more glucose being filtered, and more being reabsorbed. How does this affect other reabsorption?
Increased sodium reabsorption, less sodium reaching macula densa, so macula densa would increase GFR. This is why diabetes destroys kidneys.
What ends up destroying kidneys in diabetes?
Hyperfiltration.
Increased glucose will increase sodium reabsorption, making macula densa think GFR is low, increasing angiotensin II, putting more pressure on glomerular capillaries
How are amino acids reabsorbed?
uses sodium concentration gradient, just like glucose (1:1 ratio)
What can create the same problem with diabetes hurting the kidneys?
Increased amino acids in blood.
but its usually not the same scale as glucose, because you arent eating while you sleep unlike uncontrolled diabetes where your blood sugar is high in your sleep.
Where are the glucose reabsorption transporters in the kidney?
Only the proximal tubule.
What is the side of the cell called that makes up the wall of the tubular lumen? rear wall of that cell that makes up interstitial side?
apical; basolateral
if we want to make glucose non-existent in tubule, how do you get rid of the rest of it?
SGLT with Na+ cant do it, would need to use energy.
If glucose in the tubular cells is higher than the side of the interstitium, how does glucose get across to interstitium?
Just uses it concentration gradient to get across and passively cross the basolateral side through glut-2 transporters. but if the concentration gradient is higher in the interstitium, it would require energy.
Early parts of proximal tubule is called ____ and later is called________________
S1; S2 and S3
Where is majority of glucose reabsorbed? what %? How much sodium is required?
S1 segment, SGLT transporters (90%) 1Na+:1 glucose
What transporter gets glucose out the basolateral side of cell in S1 segment?
Glut-2
What is the effiency and affinity of SGLT2 transporters?
highly efficient, low affinity though.
What types of transporters are on S2 and S3 segment? what percent of glucose? How much sodium is required?
basal side SGLT1, 10%.
Basolateral side GLUT-1
2Na+:1 glucose
What is the affinity of SGLT1 transporters?
High affinity, because its lower capacity/lower density and needs to get rid of the rest of glucose.
why does SGLT1 require more sodium?
because the fluid is more diluted
Where is there the least amount of SGLT?
S3
The amount of glucose being filtered is entirely dependent on the
plasma glucose concentration
If our GFR is 1.25dL/min, and normal glucose is 100mg/dL, we should have how much glucose being filtered per minute?
1.25 x 100 = 125mg/min
If we have a GFR of 140mL/min, and a glucose of 80mg/dL, what is our amount of glucose being filtered per minute?
GFR = 1.4dL/min (convert to dL to match glucose)
1.4dL/min x 80mg/dL = 112mg/min (cross out dL)
When you see filtered load, it means
stuff that has dissolved in plasma thats being filtered.
if its freely filtered it means you can take what equation to figure out how much is being filtered out?
Concentration x flow = quantity of stuff filtered
The point at which glucose is no longer being completely reabsorbed, and it should show up in urine
threshold.
The book says this occurs at 200mg/dL, but schmidt thinks its lower than that
When the SGLT transport is maxxed out, the excretion of glucose ratio to excess glucose is
1:1. it’s maxxed out, so any excess glucose beyond that will not be reabsorbed and all of it will be excreted in urine because those pumps are saturated.
At what glucose level will transport maximum be reached?
300mg/dL. Any excess glucose will be excreted in urine.
At what point is glucose a 1:1 ratio of being filtered to being excreted in urine?
300mg/dL. Every molecule of glucose above 300mg/dL will not be reabsorbed. When its below 300, extra glucose is being reabsorbed but some is also excreting in urine.
Where is the macula densa?
Thick ascending loop of henle, right before DCT.
Where is the GFR speedometer located?
Macula densa
What releases the renin when the macula densa thinks GFR is too low?
Juxtaglomerular cells above the afferent and efferent arterioles
Renin will convert what into what?
Angiotensinogen to angiontensin I
Where is angiotensinogen produced?
liver
Angiotensin I is turned into what by what?
Angiotensin II via ACE (angiotensin converting enzyme)
Where is ACE found?
large amounts in the lungs
ANG II does what to efferent and afferent arteriole?
constricts efferent arteriole and dilates afferent arteriole
How does the afferent arteriole dilate?
Nitric oxide.
What is a consequence of a SGLT inhibitor?
everything downstream of glucose that isnt getting reabsorbed, causes excess glucose downstream in urethra and makes it a breeding ground for bacteria, causes its sticky and may cause immune to destroy them too cause they now look funny.
