Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
51 Cards in this Set
- Front
- Back
|
what are the steps in the RAS systems
|
angiotensin produced by liver
renin from kidney converts angiotensin to angiotensin 1 angiotensin 1 gets converted to angiotensin 2 by ACE from lungs |
|
|
what are the functions of angiotensin 2
|
increases sympathetic tone
increases BP via vasoconstriction increases Na/H2OI retention and K elimination increases ADH and aldosterone secretion which also cause fluid retention |
|
|
what does EPO do
|
drives RBC production
|
|
|
what does Vit D do
|
reabsorbs Ca, PO4, Mg
|
|
|
what does ADH do
|
promotes H2O reabsorption
|
|
|
what does Renin do
|
converts Ang > Ang 1
part of RAS and is released in response to decrease blood to glomeruli (volume depletion) |
|
|
what does Aldosterone do
|
reabsorption of Na/H2O
K excretion product of RAS |
|
|
what do prostaglandins do
|
they dilate the renal artery and afferent arteriole and this is how pt w/ renal failure maintain blood flow to their kidneys
|
|
|
what is GFR
|
rate at which plasma is filtered from glomerulus
|
|
|
what is normal GFR range
|
90-140 ml/min
|
|
|
what is the most accurate way to measure GFR
|
inulin clearance
|
|
|
what are the properties of inulin
|
not secreted, reabsorbed, or protein bound, ONLY FILTERED
|
|
|
what are the properties of creatine
|
filtered and secreted
|
|
|
what are the properties of BUN
|
filtered and reabsorbed
|
|
|
what are other factors that influence BUN levels
|
high protein diet
GI bleeding dehydration liver disease (decrease BUN) |
|
|
why can't you look at BUN or SCr solely as a marker of kidney function
|
in order to see changes in these values you need a decrease of 50% in GFR therefore a change of 120>70 is substantial but would only change the SCr from 1>1.2 which isn't a major change at all
|
|
|
what is the equation for Cockroft Gault
|
(140-age)weight / 72*SCr
multiply by 0.85 if female |
|
|
what is the equation for dosing weight
|
IBW + 0.4(ABW - IBW)
used when ABW > 120-130% of IBW |
|
|
what is the equation for IBW
|
M: 50 + 2.3* every inch over 5 ft
F: 45.5 + 2.3* every inch over 5 ft |
|
|
pre renal AKI results from what
|
decreased renal perfusion
|
|
|
with AKI what do you typically see in SCr and GFR
|
SCr increase of .5 or 50% increase
50% decrase in GFR |
|
|
what are symptoms of AKI in general
|
anuric <50 ml/min
oliguric <500 ml/min nonoliguric >500 ml/min |
|
|
why is it believed diuretics may increase pt outcome in AKI
|
pts that are nonoliguric have better outcomes then anuric pts meaning that urine production results in better outcomes but in reality diuretics don't better outcomes
|
|
|
pre renal AKI is typically reversed unless what
|
hypoperfusion is prolonged b/c it leads to ischemia (decrease blood flow to organ) and may result in ATN
|
|
|
what are some causes of pre renal AKI
|
volume depletion (vomit, hemorrhage)
altered intra renal hemodynamics(nsaid/ ace) decrease blood volume (decrease CO) renal artery oclusion (embolism, stenosis) |
|
|
what are the effects of ACE-I/ARB
|
they inhibit Ang 2 which is a vasoconstrictor therefore they dilate the Efferent arteriole and decrease pressure allowing for blood to get out easily
this decrease in pressure helps slow down glomerulosclerosis |
|
|
what are the down falls of ACE/ARB
|
if they decrease the pressure inside the glomerulus too much filtration no longer occurs efficiently therefore ACE/ARB MAY CAUSE ACUTE RENAL FAILURE
also causes a slight increase in SCr upon initial treatment |
|
|
what are the effects of NSAIDs/cyclosporin
|
NSAIDS inhibit prostaglandin synthesis therefore cause vasoconstrition of Afferent arteriole
cyclosporin is an immunosuppressant and causes vasoconstriction of afferent arteriole as well |
|
|
how do you manage pre-renal AKI
|
stop potentially nephrotoxic drugs (aminoglycosides, NSAIDS/ ARB/ACE)
correct volume deficit optimize cardiac function (dilators or vasoconstrictors) |
|
|
what is the cause of Intrinsic AKI
|
damage to the kidney itself (glomerulus, interstitium, tubules)
|
|
|
what is the cause of glomerulonephritis
|
immune complexes attack membrane resulting in poor filtration and loss of protein/albumin in the urine
|
|
|
presence of protein and albumin in the urine is a sign of what form of AKI
|
glomerulonephritis (intrinsic KI)
|
|
|
what are some autoimmune diseases that can cause glomerulonephritis
|
wegners - vasculitis (inflamation of BV)
good pastures - immune complexes attack basement membrane lupus |
|
|
how is glomerulonephritis managed
|
stop inflammation and prevent scarring
|
|
|
why would you use diuretics to treat glomerulonephritis
|
due to the decrease in blood albumin levels you have a decrease in oncotic pressure therefore fluid isn't kept in the veins and leaks into the interstitium leading to patients becoming volume overloaded
|
|
|
what is the cause of ATN
|
injury to the tubules due to ischemia or nephrotoxins (myoglobin, radiocontrast agents, aminoglycosides)
|
|
|
contrast induced nephropathy effects what part of the kidney
|
free radicals from the contrast dye damage the tubules
|
|
|
how can you prevent CIN
|
normal saline - dilutes dye and keeps enough fluid going to kidney to prevent ischemia
mukamist (acetylcysteine) - d/c after 4 doses Na bicarbonate may also be used dopamine/theophylin |
|
|
what is AIN
|
infiltration of inflammatory cells in the interstitium (you see eosinophils in high concentrations in improper areas)
|
|
|
what is the classic triad of acute interstitium nephortoxicty (AIN)
|
fever
rash eosinophils |
|
|
what are some causes of AIN
|
drug induced (PPI, PCN, furosemide, NSAID, rifampin, phenytoin)
lupus |
|
|
how do you treat AIN
|
corticosteroids
|
|
|
what is the cause of post renal AKI
|
obstruction
|
|
|
what is dopamines effect in the kidney
|
at low doses IV dopamine can bind to the dopamine Rc and cause increase blood flow and increase urine output
|
|
|
in CIN what happens to the SCr levels
|
25% (0.5mg/dL) increase in SCr from baseline
peaks after 3-5 days returns to baseline after 7-10 days |
|
|
what are some modifiable risk factors of CIN
|
amount of contrast given
multiple exposure to contrast w/in 24-48hrs hypotension (hypoperfusing kidney) anemia/blood loss ACEI/ARB Diuretics NSAIDS dehydration nephrotoxic antibiotics |
|
|
how is post renal AKI managed
|
remove the obstruction (nephrostomy, catheter placement)
diuresis after obstruction is removed is extreme and pt may become volume depleted |
|
|
what are some of the drugs that cause glomerulonephritis and what is an example of an infection
|
captopril, TZD, PCN, cocaine, rifampin
may also be due to acute post infection - staph/strep |
|
|
why would you give diuretics to treat glomerulonephritis
|
you have a decrease in albumin > decrease oncotic pressure > fluid leaks out of veins> pt becomes fluid over loaded
|
|
|
what is the normal BUN level
|
8-18
|
|
|
what are the modifiable CIN risk factors
|
ACE-I/ARB
diuretics hypotension volum of contrast given multiple contrast exposure over 24hrs anemia/blood loss NSAIDs dehydration |
