Acute Kidney Injury (L4-L5) (exam 1)

are AKIs usually symptomatic or asymptomatic

asymptomatic

what are the non-preventable risk factors for AKI

CKD, HF, diabetes, peripheral vascular diseases, liver disease, >75 y/o

a pre-renal AKI happens when…

not enough blood is getting to the kidney

a pre-renal AKI happens when not enough blood is getting to the kidney which results in ________

ischemia (kidney cell death)

in a pre-renal AKI, not enough blood flows to the kidney, therefore it compensates by _________ Na+ output & activating RAAS

decreasing

in a pre-renal AKI, not enough blood flows to the kidney, therefore it compensates by decreasing ___ output & activating _____

Na+, RAAS

a ____-renal AKI results from compensation by decreasing Na+ and activation of RAAS

pre

in a pre-renal AKI, the RAAS is activated which leads to ______ urine output and _______ Na+ excretion

less, less

in a pre-renal AKI, the RAAS is activated which leads to less ________ & ______ output/excretion

urine, Na+

a pre-renal AKI results in _______ concentrated urine with _____ Na+

highly, low

a ____-renal AKI results in highly concentrated urine with low Na+

pre

a pre-renal AKI results in highly concentrated ______ with low ___

urine, Na+

what 3 things can cause a pre-renal AKI

intravascular volume depletion (dehydration, hemorrhage, urinary losses/diuretics)

reduced cardiac output (hypotension, HF, MI, calcium-channel blockers)

vascular obstruction (bilateral renal artery stenosis)

when diagnosing a pt with a pre-renal AKI, history should be taken to see if they have taken a ________ + _______ _________

thiazide + loop diuretic

upon physical examination for a pt with a pre-renal AKI, they will experience _______ _________

orthostatic hypotension (dizzy upon standing)

upon physical examination for a pt with a ____-renal AKI, they will experience orthostatic hypotension (dizzy upon standing)

pre

a fractional excretion of Na+ (FENa) <1% is indicative of a ____-renal AKI

pre

a fractional excretion of Na+ (FENa) ___% is indicative of a pre-renal AKI

<1%

the fractional excretion of Na+ (FENa) may not be accurate if the pt is ________ often or taking _________, and they should instead use the FEUrea

urinating, diuretics

the fractional excretion of Na+ (FENa) may not be accurate if the pt is urinating often or taking diuretics, and they should instead use the _______

fractional excretion of urea (FEUrea)

a fractional excretion of urea (FEUrea) of <35% is indicative of a ____-renal AKI

pre

a fractional excretion of urea (FEUrea) of ___% is indicative of a pre-renal AKI

<35%

what is the first step to management of a pre-renal AKI

rehydration (NOT with dextrose)

the first step of pre-renal AKI management is rehydration with _______ or _______, NOT dextrose

NS or lactated ringers (isotonic)

in rehydration for management of a pre-renal AKI, the pt should NOT be given _________

dextrose

an intrinsic AKI is caused by prolonged _____________ or ______________

pre-renal AKI or post-renal AKI

what are the 2 causes of intrinsic AKIs

tubular nephropathy (ATN or AIN)

glomerulonephropathy (GNs)

what is the most common (physiological, not DI) cause of any AKI

Acute Tubular Necrosis (ATN)

ATN in intrinsic AKI is prolonged ________, which leads to ischemia, which leads to necrosis of tubules, which leads to muddy brown ________ ______

hypotension (pre-renal AKI), granular casts

AIN in intrinsic AKI is __________-mediated, and the pt will present with _______ or _____ in addition to renal symptoms

autoimmune, fever or rash

GNs are usually due to __________ disease

autoimmune

in GNs the glomerular filtration of ________ is broken, therefore they get into the tubules and cause _________

protein, proteinuria

in GNs, a urine protein >_____g/day is considered nephrotic syndrome

3.5

in GNs, a urine protein >3.5 g/day is considered _________ syndrome

nephrotic

what is the most common sign of nephrotic syndrome

facial edema (& frothy urine)

facial edema (& frothy urine) are the most common signs of _________ syndrome

nephrotic

GNs can be treated with __________ therapy, or we can just treat the symptoms like proteinuria, hyperlipidemia, HTN, edema

immunosuppressive

______ & ______ can both be used in the treatment of GNs since they cause efferent arteriole vasodilation

ACE-Is & ARBs

ACE-Is & ARBs can both be used in the treatment of GNs since they cause ______ arteriole vaso________

efferent arteriole vasodilation

using ACE-Is or ARBs in the treatment of GNs causes vasodilation off the efferent arteriole which _________ glomerular pressure and therefore __________ the amount of proteins filtered into the tubules

decreases, decreases

although using ACE-Is and ARBs can lead to a decrease in the amount of proteins filtered into the tubules, they can also cause an ___________ SCr (due to _____ creatine filtered into the urine)

increased, less

a _____-renal AKI happens when there is an obstruction of the outflow of urine to the bladder/ureters

post

a post-renal AKI can lead to __________, which is when urine backflows into the kidneys

hydronephrosis

in a post-renal AKI, backflow of urine into the kidneys (hydronephrosis) can cause an _________ pressure in the nephrons which leads to interstitial kidney damage

increase

a _____-renal AKI can be caused by kidney stones

post

kidney stones are cause by a buildup of calcium ________ or calcium _________

oxalate, phosphate

the treatment for kidney stones that are >10mm and will not pass on their own is medical expulsive therapy with________

Tamsulosin

treatment for kidney stones that are <5mm and will likely pass on their own is ____________ and pain management

hydration (PO or IV fulids)

FOR ANY PATIENT WITH AN AKI, DOSE ADJUST ___________ ______________ MEDS!

RENALLY ELIMINATED

in hospitalized pts the easiest way to detect a DI AKI is an __________ SCr

increased

in hospitalized pts the easiest way to detect a DI AKI is an increased ____

SCr

in an outpatient setting DI AKIs can be detected by what 3 symptoms

decreased urination

hypervolemia/edema

nausea/loss of appetite

what is the best way to prevent DI AKIs

avoid nephrotoxic drugs in patients with AKI risk factors

what is pseudo renal disease

increased SCr d/t competitive inhibition of creatine secretion in proximal tubule

pseudo renal disease is an __________ SCr d/t competitive inhibition of creatine secretion in proximal tubule

increased

pseudo renal disease is an increased SCr d/t competitive inhibition of __________ secretion in proximal tubule

creatine

pseudo renal disease is an increased SCr d/t competitive inhibition of creatine secretion in _________ tubule

proximal

what 2 drugs can cause pseudo renal disease

Trimethoprim (Bactrim) & Dronaderone

DI pre-renal AKI can be caused by any medications that _______ blood volume

reduce

DI pre-renal AKI can be caused by any medications that reduce _______ ________

blood volume

________ diuretics can cause DI pre-renal AKIs

loop

loop diuretics can cause pre-renal AKIs if the dose is too high since they will ________ vascular volume and therefore ________ renal blood flow/filtration, which will in turn _________ SCr & AKI

decreased vascular volume, decrease renal blood flow/filtration

increase SCr & AKI

ACE-Is and ARBs block ________ to illicit ______ renal artery vaso________

RAAS, efferent dilation

ACE-Is or ARBs usually have little to no effect on SCr, unless the pt has _________ _________ _______ _________

bilateral renal artery stenosis

_______ or _______ are contraindicated in pts who have bilateral renal artery stenosis since they block the RAAS compensatory mechanism

ACE-Is or ARBs

normally in bilateral renal artery stenosis, the _____ is compensatory and causes efferent arterial vaso__________, but taking an ACE-I or ARB will cause efferent arterial vaso__________

RAAS, constriction (to increase glomerular pressure back up), dilation

blocking the compensatory RAAS mechanism by ACE-Is or ARBs will continually ___________ SCr

increase

NSAIDs block _________-mediated vasodilation and can cause afferent artery vasoconstriction

prostaglandin

NSAIDs block prostaglandin-mediated vaso_________ and can cause afferent artery vasoconstriction (which will then decrease glomerular pressure/filtration and increase SCr)

dilation

NSAIDs block prostaglandin-mediated vasodilation and can cause __________ artery vasoconstriction (which will then decrease glomerular pressure/filtration and increase SCr)

afferent

NSAIDs block prostaglandin-mediated vasodilation and can cause afferent artery vasoconstriction which will then _________ glomerular pressure/filtration and __________ SCr

decrease, increase

__________ block prostaglandin-mediated vasodilation and can cause artery vaso constriction which will in turn decrease glomerular pressure/filtration and increase SCr

NSAIDs

cyclosporine & tacrolimus are _____________ used for transplant patients

immunosuppressant

_________ & __________ are immunosuppressants used for transplant patients

cyclopsporine & tacrolimus

cyclosporine & tacrolimus cause vaso__________ of afferent renal artery which can cause chronic ischemia

constriction

cyclosporine & tacrolimus cause vasoconstriction of _________ renal artery which can cause chronic ischemia

afferent

cyclosporine & tacrolimus cause vasoconstriction of afferent renal artery which can cause chronic _______

ischemia

DI pre-renal AKIs caused by cyclosporine or tacrolimus are considered _______-related

dose (can lower dose instead of discontinuing)

DI intrinsic glomerular disease is an ________ disease due to a drug _________

autoimmune, allergy

DI autoimmune glomerular disease causes __________ which can damage the glomerulus

proteinuria

DI autoimmune ____________ disease causes proteinuria which can damage the ________

glomerular, glomerulus

what 4 drugs can cause DI glomerular disease

NSAIDs, lithium, quinolones, bisphosphates

NSAIDs, lithium, quinolones, and bisphosphates can cause DI _____________ disease

glomerular

to manage DI glomerular disease we must _________ the offending drug, and then is renal function does not improve we could give _________

discontinue, steroids

____________ are the classic cause for DI acute tubular necrosis

aminoglycosides (AGs)

aminoglycosides (AGs) are the classic cause for DI ____________________

acute tubular necrosis (ATN)

when giving AGs (which can cause ATN), we want to have _______ troughs in order to give kidneys a ‘rest’

low

AGs are almost 100% filtered in the ________

glomerulus

~10% of AGs accumulate in the __________ of the proximal tubule, which will cause _____________ of the proximal tubule

lysosomes, autodigestion

damage to the proximal tubule caused by AGs will cause __________ reabsorption and _________ urine output

decreased, increased

damage to the proximal tubule caused by __________ will cause decreased reabsorption and increased urine output

aminoglycosides

____________ can be misleading d/t the uncommon mechanism of increasing urine output

aminoglycosides

AGs can be misleading d/t the uncommon mechanism of __________ urine output

increasing

for management of DI intrinsic acute tubular necrosis we should discontinue ___________ and start an alternative antibiotic

aminoglycosides

for management of DI intrinsic acute tubular necrosis we should d/c the aminoglycosides and also start _______ to make sure the high urine output does not cause dehydration/pre-renal AKI

normal saline

vancomycin can also cause DI ___________________, but its mechanism is unknown

acute tubular necrosis (ATN)

vancomycin DI acute tubular necrosis damage is _____________-dependent

concentration

IV radiographic contrast media causes DI __________________ due to renal vasoconstriction

acute tubular necrosis (ATN)

IV radiographic contrast media causes DI acute tubular necrosis due to renal vaso_________

constriction

IV radiographic contrast media causes a slow increase in SCr and is non-__________, which means there is not a decrease in _______ ________

oliguric, urine output