A&P final Flashcards
What would expect the osmolarity to be in the PCT in a state of conservation?
What would you expect the renal interstitium around the PCT to be?
300mOsm
water is permeable here to ISF should be the same
300mOsm
What would you expect the osmolarity to be in the descending loop of Henle in a state of conservation?
What would you expect the renal interstitium around the descending loop of Henle to be?
1200mOsm
water is permeable here so ISF should be the same
1200mOsm
Which pump is found in the thin ascending loop of Henle?
Is water permeable here?
Na/Cl pump
Not very permeable
what percent of what gets filtered is reabsorbed in the thick ascending limb?
25%
what is an example of what the osmolarity of the thick ascending limb could be in a period of conservation?
100mOsm
Why is the 100mOsm in a period of conservation concentration at the thick ascending loop of Henle interesting?
Because the interstitium is really concentrated in comparison, and even during a period of conservation, the osmolarity in the tubule is getting really low.
Nothing really changes that this segment is the diluting segment, (i.e how much ADH, how much angiotensin II is there). During states of conservation and states of excess it will always be the diluting segment.
The osmolarity of the last part of the distal tubule should be
the same as it is in the interstitium surrounding it.
It is permeable to water and should therefore be in balance.
The osmolarity of the last part of the collecting duct should be
the same as it is in the interstitium surrounding it.
It is permeable to water (under normal circumstances) and should therefore be in balance.
The kidney can’t concentrate the urine any more than it can concentrate the _____
why is this?
renal interstitium
Water permeability is based on osmosis so it will go towards the more concentrated area until it is balancded
What would expect the osmolarity to be in the PCT in a state of excess?
What would you expect the renal interstitium around the PCT to be?
300mOsm
water is permeable here to ISF should be the same
300mOsm
What would expect the osmolarity to be in the descending loop of Henle in a state of conservation?
What would you expect the renal interstitium around the descending loop of Henle to be?
600mOsm
water is permeable here to ISF should be the same
600mOsm
What makes the difference in the concentration of the renal interstitium at the descending loop of Henle in a state of conservation vs. excess?
ADH.
ADH helps us reabsorb water and urea during states of conservation but it is not playing a role during states of excess so that we do not retain as much water
What changes would you see in a nephron in a state of conservation vs a state of excess?
- The renal ISF at the loop of Henle would be a lot more concentrated during conservation
- the distal convoluted tubule will be permeable to water during conservation
- the collecting duct will be permeable to water and urea during conservation
- the urine will be much more dilute during excess
What similarities would you see in a nephron in a state of conservation vs a state of excess?
- the PCT will have similar/same osmolarities in the tube and in the ISF in both states
- The Diluting segment will have similar/same osmolarities in the tube and in the ISF
Why are people put on diuretics?
To lower blood pressure or prevent further heart failure
Diuretics cause an increase in fluid _______ from the body
excretion
Where does the fluid come from that is excreted when using diuretics?
extracellular fluid volume
What happens when you are exposed to a diuretic for the first time?
You dump a lot of urine
what is lost when someone is taking diuretics?
electrolytes and water
If you diurese 1L of fluid, how much of that will come from the plasma?
200cc.
This is enough to lower blood pressure
ECF fluid is made up of what compartments?
1/5 = plasma
4/5 = interstitium
Why do you see an increase in urine when you give a second, third, fourth, etc. dose of a diuretic?
The first time you give the drug you will see an increase in urine d/t the drug “skimming” off the top and taking the extra fluid from the ECF. subsequent doses are only maintaining this new level.
However, you will see an increase in urine output with those doses d/t water building up over the hours between the dose.
If you start off with 1000cc and the initial dose takes off 200cc then the new balance is 800cc. Over the next few hours you gain 200cc and when you take your next dose you lose 200ccs bringing you back down to your new balance.
Why is long term therapy more focused on diuretics than drugs like an alpha receptor blocker?
Long term, the body figures out a way around those drugs by changing ADH, angiotensin, or one of the many other factors that feeds into blood pressure. Assuming the patient is responsive to diuretics, it is a much better long term management strategy.
what effect does salt intake have on angiotensin II?
it decreases it and therefore decreases the amount of salt that we reabsorb
If we have high levels of angiotensin II and we increase salt intake, what will happen?
our bp will increase
What advice can we give to patients with chronically high angiotensin II levels?
decrease salt and water intake and BP should be okay
if you have low levels of angiotensin II, what do you worry about?
low blood pressure.
low angiotensin II means low aldosterone which means low salt intake which means lower water intake which means low blood pressure
Do we ask patients to stop taking ACE inhibitors before surgery?
No. Research shows that these have minimal effects, however it can lead to us having a harder time managing hypotension in the OR. We would rather have a hemodynamically stable patient going into the OR though so we deal with it.
If you have a patient that only eats Little Ceasers, what do you anticipate in the OR?
The patient to have really low angiotensin II levels d/t the long term elevated Na+ levels. This essentially has the same effect as an ACE inhibitor. We would anticipate having a harder time managing hypotension in the OR
What would cause elevated angiotensin II levels?
stenosis in the renal artery of ONE kidney
-low Pcap
-Low GFR
-low NaCl at the macula densa
-MD releases angiotensin II
-constricts efferent arteriole
-drives up GFR
The Angiotensin II works on BOTH kidneys, but the healthy kidney doesn’t have any issues. It does decrease renin a little but it isn’t enough to overcome the angiotensin II effects.
This leads to kidney damage over time.
What drugs help with increased blood pressure d/t stenosis in one of the kidneys leading to increases angiotensin II levels?
ACE inhibitors
ARBS
renin inhibitors
what kind of pressure does Dr. Smidt have at the dentist office?
high pressure
What is one reason we take blood pressure frequently (at dr./dentist office)
to give us a heads up that something is wrong in the body. Could be due to stenosis in the kidney. You don’t want that to run unopposed for a long period of time, permanent damage is imminent
Why do we use salt so much on our food?
MOA?
It enhances our ability to taste food!
Taste buds are electrically excitable cells with receptors in them for food stuffs. When food binds to the sensor then it changes cell wall permeability to ions which can elicit an action potential. They have Na+ and K+ channels on them. Increases Na+ intake raises membrane potential which makes the food receptors on them easier to excite and therefore have more taste!
Why don’t Cl- inhibit taste buds?
There aren’t any Cl- channels on the taste bud for them to get into the cell
Why is Mrs. Dash not a good replacement for salt?
It is a potassium supplement that does help to excite the taste bud cell but it doesn’t take very much at all and the supplements are usually “overkill” so it ends up making the food taste funny instead.
If you eat a lot of extra salt and drink a lot of water with it, what does the negative feedback system look like in the kidney?
increased salt=increases blood pressure
increased salt concentration in the blood
increased salt concentration at the glomerular capillaries
increased filtration of salt
MD sees a lot of salt and decreases renin release
which decreases angiotensin II and aldosterone
which makes us reabsorb less salt and water
which decreases blood pressure
blood volume will also increase
increases systemic bp
increases Pcap
increases filtration
increases Na+ at the MD
MD decreases angiotensin II and aldosterone
which makes us reabsorb less salt and water
which decreases blood pressure
If a healthy person increases their salt/water intake, what happens to their bp?
it goes up momentarily until the body has time to deal with it. but the kidneys typically take care of the problem very quickly
(slight slant in the “normal” line for BP)
Describe non salt-sensitive HTN
Our body still regulates blood pressure when we intake salt/water but the starting point for blood pressure is high.
(should be a straight up with a small slant line. More of a slant than a normal bp person indicating that they do have a little bit of a harder time regulating.)
Describe salt-sensitive HTN
Renal vascular HTN
-stenotic renal artery
-over expression of the RAA system
the kidneys struggle to get rid of the Na+ that it takes in
What kind of HTN do African Americans, also prevalent in some parts of Asia, have? How does this relate to African Africans?
What kind of drugs work for these patients?
non-renin form of Salt-sensitive HTN
African Africans don’t have this type of HTN. It has something to do with the genetics
ACE inhibitors
How do osmotic diuretics work? Example of this type of drug
Mannitol
Vitamin C 5,000 IU’s
The drug is heavily filtered but not reabsorbed. Stays in the tubule and collects water as it is excreted.
How do ARBS and ACE inhibitors work?
They effect constriction at the efferent arteriole.
Effects how much Salt and electrolytes are reabsorbed in the PCT.
These are AT1 dependent process. So less interaction with Angiotensin II at the AT1 receptor, less reabsorption you’ll have at the PCT.
What do K+ sparing diuretics effect?
aldosterone portion of principal cells
What is the normal blood concentration of creatinine
1mg/dL
what is normal filtration in dL?
1.25dL/min
How much creatinine does a healthy person filter each minute?
Creatinine blood concentration: 1mg/dL
filtration: 1.25dL/min
=1.25mg/min creatinine filtered OR filtered load
How to solve for excretion.
What is filtered plus what is secreted minus what is reabsorbed
If creatinine system is balanced then excretion rate should =
rate of production
If we have a spontaneous single nephrectomy, what would our creatinine clearance be?
Normal:
Creatinine blood concentration: 1mg/dL
filtration: 1.25dL/min
=1.25mg/min creatinine filtered OR filtered load
Nephrectomy:
Creatinine blood concentration 1mg/dL
Filtration: 0.625dL/min
= 0.625mg/min creatinine filtered OR filtered load
If we have a spontaneous single nephrectomy, describe what happens with the plasma concentration and creatinine excretion?
Plasma concentration of creatinine increases until creatinine excretion and production are equal again.
It has to go up in the plasma by double because we stopped excreting it and the only way to go from half the excretion rate back to total excretion is to double the amount of creatinine in the small amount of fluid now being filtered.
The one kidney left can, over time, increase it’s filtration to make up for this extra creatine so that eventually the single kidney now excretes the same amount that is produced again
How does the healthy kidney in a patient with a unilateral nephrectomy increase its work without having too much damage?
physiological hypertrophy
How much does the healthy kidney in a patient with a unilateral nephrectomy increase its GFR by?
50%
What is the single nephron GFR?
62.5nanoliters/min
what is the volume excreted per nephron?
0.75nanoliters/min
How many nephrons would you have left if you lose 75% of your nephrons
500,000
what is the total GFR if you lose 75% of your nephrons?
a little lower than 40ml/min
d/t the nephrons having bad hypertrophy
What would be the single nephron GFR if you lose 75% of your nephrons?
80 nanoliters/min
what is the volume excretion for all nephrons in a normal kidney and in one that you have lost 75% of the nephron?
1.0ml/min!
they are the same because the 25% of nephrons that are left over pick up the extra work load. This will kill off that 25% faster but is a good compensation mechanism short term.
What is the volume excreted per nephron in a kidney who has lost 75% of it’s nephrons?
3.0nanoliters/min
This is 4 times the normal!!! this will have a huge impact on the nephrons that remain, killing them faster than normal.
Renal failure treatments
Na+ restrictions
water restrictions
K+ restrictions
protein restrictions
Renal failure problems
hypernatremia
hypervolemia
hyperkalemia
hypertension
acidosis
What is the normal osmolality of the body?
300mOsm
How much of our total body water is made of ICF?
2/3
How much of our total body water is made of ECF?
1/3
If we add isotonic saline, what happens to the body fluid compartments?
Increases ECF compartment. Some will go into the plasma and but majority will go into the interstitium.
If we add hypotonic saline, what happens to the body fluid compartments?
Lower overall osmolarity in all the compartments.
Some will stay in the ECF but some will now move into the ICF compartment because the ICF will be more concentrated than the ECF.
If we add hypertonic saline, what happens to the body fluid compartments?
Increase overall osmolarity in the compartments.
It will pull fluid from the ICF into the ECF because now the ECF is more concentrated than the ICF.
Is water permeable in the thick ascending limb?
No. This is why it is called the diluting segment. 25% of solutes get reabsorbed but no water leaves the tubule
