Lecture 5 Final Flashcards
,How does the autoregulation work in the system?
Increase in pressure > increase glomerular pressure > increase GFR > increase UOP > lowers systemic pressure
What makes it a good thing to have a slowed down velocity in the ascending vasa recta?
after reabsorption, as it goes up to a lower concentration, there’s an opportunity for the proteins to move back into the renal interstitium. If the flow is too fast, that chance is decreased and leads to a “washout”
What happens to the kidneys during chronic HTN?
Unregulated high BP: (Unlikely)
If the Pressure is “200mmHg”, the AA will constrict but not enough to reduce pressure to the GCs “90mmHG” instead of 60mmHg showing an increase of +30 NFP when originally it’s 10mmHG so now it’s 40mmHG.
Kf = 12.5 x 40 = 500ml/min. 124ml is reabsorbed leaving a urine output of 376ml/min
What happens to normal kidney autoregulation if the BP is low?
the AA will relax, causing an increase in flow to the GCs pressure
What happens to the autoregulation after exposure to prolonged HTN
the arterioles tend to stiffen and elasticity is decreased so it is unable to handle low BP. Podocytes will also start to show wear and tear and structures to the GCs are weakened. Fenestrations and slit pores may be bigger than usual as well.
What is damaged the most when exposed to prolonged HTN?
Glomerular Capillary beds
Is it uncommon to have the efferent arteriole constrict while the afferent arteriole dilate?
No, this is usually how it goes.
What “agent” affects the efferent arteriole more?
Angiotensin II
Which drugs affect the afferent arteriole more?
B-blockers, Ca Ch Blockers
Which drugs affect the afferent and efferent arterioles?
Pressors
T/F: Angiotensin II only constricts the efferent arteriole.
False, it constricts both but mainly constricts the efferent arteriole more.
What effects does a reduced Angiotensin II have?
Dilated efferent arteriole.
T/F: Reabsorption occurs throughout the renal tubule segment.
True, just different segments reabsorb more than others.
What is 2/3 reabsorbed in the PCT?
Water
What happens to Cr concentration if it is not reabsorbed in the PCT?
Increases in the tubule the further it gets.
If there’s a high concentration of Na+ and Cl- at the Macula Densa, the GFR is?
Increased
If the Na+ and Cl- concentration at the Macula Densa is low, this means the GFR is?
decreased
What’s another term for when the Macula Densa is sensing the the Na+, Cl- concentrations?
“Geiger counter”
Correlation of GFR to Na concentration?
High GFR > High Na concentration
Low GFR > Low Na concentration
If GFR is low, what happens?
Angiotensin II increases > efferent arteriole constricts > increase GFR, increase Na reabsorption in the PCT
What happens if the GFR is normal but Na reabsorption is increased? What causes this?
Treatment?
(ok if acute but damaging the GCs if chronic)
- Macula Densa thinks that GFR is low and will activate angiotensin II to increase GFR more than normal.
- DM2 > hyperfiltration > kidney fx
TX: ACEi, ARBs
Where is glucose mainly reabsorbed? What if we have a high level of glucose?
- in the PCT, and it usually reabsorbs 1 glucose with 1 Na+ through the SGLT (2nd transport).
- we’d have more glucose reabsorption + Na+ as well.
Normally the PCT can handle the reabsorption of increased glucose but only to a certain point until it is saturated. then what happens?
The Macula Densa will detect the low Na level and will release angiotensin II to offset the imbalance.
Amino acids are small and easy to filter. Normally 1 amino acid is reabsorbed for every Na.
T/F; Increase amino acids in the blood > increase Na reabsorption (1:1 AA/Na) > MD sense low Na > increase angiotensin II > increase GFR pressure
True!
But places a huge wear and tear on the GCs > renal failure
T/F: The PCT is the only where glucose can be reabsorbed.
True
What is the “apical” side of the cell?
It’s where the tubular lumen and tubular cell are connected
The wall of the tubular cell that is on the interstitial side.
Basolateral side
Secondary transporter for glucose
SGLT1; SGLT2
T/F: As you go further down the tubule, the glucose concentration gets higher.
False, it should be zero.
How does glucose get reabsorbed?
Through the SGLT on the apical wall and through the Glut transporter of basolateral wall to the interstitium.
In the S1 segment, what does glucose use to be reabsorbed?
90% use SGLT2 (apical side), GLUT2 (basolateral side)
1Na+:1 glucose
low affinity
In the S2 segment, what does glucose use to be reabsorbed?
Very few in S3.
10% use SGLT1 (apical side), GLUT1 (basolateral side)
2Na+:1 glucose
High affinity bc its more diluted here
If there’s 100mg/dl of glucose,
1.25 dl/min of plasma flow. What is the filtration rate?
125mg/min of glucose filtered
What does “threshold” mean for glucose?
This is when you start to see glucose in the urine
Once you are at a glucose 1:1 rate passed the threshold, this is called?
Transport maximum
Where is the Macula Densa located?
TAL
AKA speedometer
GFR
Which electrolyte is the GFR more sensitive to?
Na+
What is released if the Macula Densa thinks the GFR is too low?
Renin > binds agiotensinogen (liver) > angiotensin I > binds to ACE (lungs) > angiotensin II
Source of renin
Juxtaglomerular cells
What are risks for taking ACEi?
Since ACE is from the lungs, you can be at risk for having lung issues (congestion/cough)
What else happens when the angiotensin II causes the efferent arteriole to constrict?
NO causes the afferent arteriole to dilate as well.
What other risks are there if there’s glucose in the urine?
Glucose are sticky and leave residue causing breeding ground for bacteria.
Miracle weight loss drugs (SGLTi) causes risks…
Glucose excretion l/T cells looking “funny” that may trigger immune cell response. Better off having less glucose intake.
