FINAL EXAM - Lecture 9 Flashcards
Classifications of renal failure include
Renal insufficiency, renal failure, and end stage renal disease
Whats your % of normal GFR with renal insufficiency?
20-50%
Whats your % of normal GFR with Renal failure?
5-20%
Whats your % of normal GFR with with ESRD?
<5%
Whats your % of normal GFR with CHRONIC renal failure?
<25%
Worst type of chronic renal failure is
ESRD
What are we looking for after surgical procedures?
Acute renal failure from anesthetics during operation
What causes ARF?
A massive stressor to the system, such as hypotension, nephrotoxic drugs, or anesthetic drugs that cause hypotension.
How does sux cause ARF?
Sux causes excess potassium release from cells, causing extra stress on kidneys to filter potassium.
Why are volatile anesthetics nephrotoxic?
Flourine (e.g. isoflourane)
Acute renal failure has a mortality of
90%
Far less serious version of ARF and what is the rate of occurence?
AKI, 7% of patients. Will have to stay in hospital. Also, this is why you cant leave after surgery until you pee.
What can you look at post-op lab wise if the patient isnt urinating?
Look at their creatinine before and after procedure.
What are the 2 organ systems in danger for flouride?
CNS and kidneys
Why can GFR disguise the lack of renal blood flow?
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.
Discuss autoregulation in entire kidney, but also the medulla vs the cortex
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.
What are the pros and cons of the medullary nephrons having terrible autoregulation?
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.
If we have excess potassium, how can we get rid of it?
-Non-potassium sparing diuretic
-Insulin
-Beta agonist (such as albuterol)
-Kaexelate (long term)
How does insulin lower serum potassium levels?
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.
If we eat a bunch of sugar, the body will store it in
fat cells, liver, and muscle cells.
if we eat a meal, what happens with insulin receptors and glut-4 transporters?
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.
If we eat a high potassium meal (such as ______ and _________), it will stimulate what?
potatoes; bananas; insulin binding, Na/K pump, and glut-4 transporters
How do beta agonists decrease serum potassium?
Increased SNS -> increased adrenaline (norepi and epi) -> binds to beta receptors -> speed up Na/K pump cycling rate, tucking potassium inside the cell.
Why is beta-receptor stimulation lowering potassium useful for the body?
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!
