FINAL EXAM - Lecture 9

Question 1

Classifications of renal failure include

Answer 1

Renal insufficiency, renal failure, and end stage renal disease

Question 2

Whats your % of normal GFR with renal insufficiency?

Answer 2

20-50%

Question 3

Whats your % of normal GFR with Renal failure?

Answer 3

5-20%

Question 4

Whats your % of normal GFR with with ESRD?

Answer 4

<5%

Question 5

Whats your % of normal GFR with CHRONIC renal failure?

Answer 5

<25%

Question 6

Worst type of chronic renal failure is

Answer 6

ESRD

Question 7

What are we looking for after surgical procedures?

Answer 7

Acute renal failure from anesthetics during operation

Question 8

What causes ARF?

Answer 8

A massive stressor to the system, such as hypotension, nephrotoxic drugs, or anesthetic drugs that cause hypotension.

Question 9

How does sux cause ARF?

Answer 9

Sux causes excess potassium release from cells, causing extra stress on kidneys to filter potassium.

Question 10

Why are volatile anesthetics nephrotoxic?

Answer 10

Flourine (e.g. isoflourane)

Question 11

Acute renal failure has a mortality of

Answer 11

90%

Question 12

Far less serious version of ARF and what is the rate of occurence?

Answer 12

AKI, 7% of patients. Will have to stay in hospital. Also, this is why you cant leave after surgery until you pee.

Question 13

What can you look at post-op lab wise if the patient isnt urinating?

Answer 13

Look at their creatinine before and after procedure.

Question 14

What are the 2 organ systems in danger for flouride?

Answer 14

CNS and kidneys

Question 15

Why can GFR disguise the lack of renal blood flow?

Answer 15

GFR can be increased by constricting efferent arteriole with drugs which would raise the GFR, and since urine output is normal you can think that the kidney is well perfused. But doesnt necessarily mean the kidney is getting adequate blood flow.

Question 16

Discuss autoregulation in entire kidney, but also the medulla vs the cortex

Answer 16

Autoregulation in the kidney has great autoregulation with a sloped regulator line.

Autoregulation in the renal cortex has almost perfect autoregulation with a completely flat regulator line.

Autoregulation in the medullary nephrons/vesa recta capillaries has terrible autoregulation and it almost is just a straight slanted line even with the regulator.

Question 17

What are the pros and cons of the medullary nephrons having terrible autoregulation?

Answer 17

Pros are it allows us to control blood pressure and volume by getting rid of excess fluid when pressure is high and filtering less when blood pressure is low.

The cons are that hypotension can cause ischemia very easily, and it greatly impacts the kidney even though they are a small percentage of total nephrons.

Question 18

If we have excess potassium, how can we get rid of it?

Answer 18

-Non-potassium sparing diuretic
-Insulin
-Beta agonist (such as albuterol)
-Kaexelate (long term)

Question 19

How does insulin lower serum potassium levels?

Answer 19

Obviously cells have Na/K ATPase pumps.

Insulin receptors on the cell wall are tied to Na/K pumps and also Glut-4 transporters, and when they are stimulated, it speeds up both of these pumps.

Giving them excess insulin will speed up these pumps and pump potassium into the cell.

Question 20

If we eat a bunch of sugar, the body will store it in

Answer 20

fat cells, liver, and muscle cells.

Question 21

if we eat a meal, what happens with insulin receptors and glut-4 transporters?

Answer 21

Insulin is secreted and binds to receptor, and glut-4 transporters move to cell wall to allow the sugar eaten during that meal to come in.

Question 22

If we eat a high potassium meal (such as ______ and _________), it will stimulate what?

Answer 22

potatoes; bananas; insulin binding, Na/K pump, and glut-4 transporters

Question 23

How do beta agonists decrease serum potassium?

Answer 23

Increased SNS -> increased adrenaline (norepi and epi) -> binds to beta receptors -> speed up Na/K pump cycling rate, tucking potassium inside the cell.

Question 24

Why is beta-receptor stimulation lowering potassium useful for the body?

Answer 24

If we are active and firing more action potentials, and during every action potential, potassium is pushed outside the cell, then that means high activity will raise your potassium extracellularly. So if we are going to be active and raise extracellular potassium, we need that beta-receptor stimulation to tuck the potassium BACK into the cell. fixes the problem before it even becomes a problem!

Question 25

If we were to take a high dose beta blocker, and you have high activity, what can happen?

Answer 25

Hyperkalemia! you no longer have that system that tucks potassium back into the cells.

Question 26

What is Kaexelate?

Answer 26

Helps prevent potassium absorption in GI system, takes awhile to get rid of it but can be used to treat a chronic issue.

Question 27

What increases H+ secretion and HCO3- reabsorption?

Answer 27

Increased PCO2
Increased H+/decreased HCO3-
Decreased extracellular fluid volume
Increased ANGII
Increased Aldosterone
Hypokalemia

Question 28

What decreases H+ secretion and HCO3- reabsorption?

Answer 28

Decreased PCO2
Decreased H+, increased HCO3-
Increased extracellular fluid volume
Decreased Aldo and ANGII
Hyperkalemia

Question 29

Where is acid base balance occuring in kidney?

Answer 29

Mostly PCT, also collecting duct with intercalated cells

Question 30

What are our intercalated cells MOSTLY secreting?

Answer 30

protons. can do bicarb, but mostly protons.

Question 31

Why does elevated PCO2 drive H+ secretion and HCO3- reabsorption?

Answer 31

If we have more CO2 everywhere in kidney, we will have more H+ everywhere.

More CO2, means more CO2 + h20 being reabsorbed in tubular cells. That means more carbonic acid forming, and more breaking apart to secrete H+ back into tubule and HCO3- into interstitium.

Question 32

why does increased ANGII cause H+ secretion?

Answer 32

Binds to AT1 in PCT, causing speeding up of Na/K pump, then NHE.. so more H+ secretion. Which also leads to HCO3- reabsorption.

Question 33

Why does increased extracellular fluid volume drive H+ secretion? (2 ways)

Answer 33

in one way — Higher pressure, higher GFR, leads to more ANGII.

Also, more extracellular volume means more H+ that end up in the blood by osmolarity, so they will be filtered and secreted.

Question 34

Why does aldosterone increase H+ secretion?

Answer 34

Acts in distal tubule on intercalated cells, speeding up H+ ATPase pumps. thats it.

Doesnt become a problem until aldosterone levels are extraordinarily high, such as an aldo secreting tumor or overactive adrenal gland, causing alkalosis.

Question 35

why does hypokalemia cause H+ secretion?

Answer 35

Low K+ outside cell means the cells will secrete more K+ to compensate for it. Less potassium inside the cell decreases the charge of it, so to fix the charge it will have more H+ inside the cell. if there is more H+ in the PCT or DT cells, that will increase likelihood that protons will be exchanged for Na+ (PCT) or pumped out by H+ ATPase pump (DT).

Question 36

If there is increased H+ in the body, what does this do to potassium?

Answer 36

More H+ going into cells will kick K+ out of the cell and cause hyperkalemia.

Question 37

What are the way acidosis causes hyperkalemia? Which one is the PRIMARY way?

Answer 37

PRIMARILY: H+ kicks K+ out of the cell
Decreased pH will affect enzyme activity, reducing speed of Na/K pump, keeps extracellular K+ outside the cell.

Question 38

if someone takes an Ace-inhibitor, how is there BP affected with low salt intake, normal, and high salt intake? How does this affect the bodies response to hemmorhage?

Answer 38

Low BP, normal BP, and still normal BP! Low ace means less sodium reabsorption.

Less compensation to raise BP since you dont have RAAS to increase salt and water reabsorption, more likely to be hypotensive.

Question 39

How can you have a natural, non-pharmacological ACE-inhibitor?

Answer 39

High salt diet