Kidney

Question 1

kidney is not responsible for release of

Answer 1

angiotensin

Question 2

kidney is responsible for

Answer 2

synthesis of renin
acidbase balance
reabsorption of electrolytes
regulation of extracellular fluid

Question 3

although kidneys constitute 0.5% of total body mass how much of the resting cardiac output do they recieve

Answer 3

20-25%

one of the reasons they are so susceptible

Question 4

risk factors for acute kidney injury include

Answer 4

dehydration
advance age
cirrhosis

Question 5

are all nsaids nephrotoxic

Answer 5

yes

Question 6

glomerulus function

Answer 6

formation of ultrafiltrate

Question 7

proximal function

Answer 7

bulk reabsorption of solute and water

80%

Question 8

distal function

Answer 8

controls urine concentration

up to 25% of water and solute reabsorbed

Question 9

loop on henle function

Answer 9

reabsorbs solute

Question 10

collecting duct function

Answer 10

fine tuning in the balance between excretion and reabsorption of water

Question 11

kidney responsible for synthesis and release of which hormones

Answer 11

1,25-dihydroxy vit D
renin
erythropoietin

Question 12

what makes the kidney susceptible to toxicity

Answer 12

lots of blood flow so toxins in circulation delivered to kidney in large amounts
concentrate toxicants in tubular fluid
metabolism of xenobiotics occurs in kidney
glomeruli and interstitium are susceptible to attack by the immune system

Question 13

what defines acute kidney injury

Answer 13

abrupt decline in GFR
srcr increase? >0.3mg/dl in 48hr
srcr >1.5 x baseline within 7 days
urine volume <0.5ml/kg/hr for 6 hr

Question 14

mechanism of prerenal AKI

Answer 14

impaired renal perfusion

reduced renal blood flow through vasoconstriction, volume depletion and decreased cardiac output

Question 15

drugs that cause prerenal AKI

Answer 15

bleeding - anticoagulant
volume depletion - diuretic, cathartic
CV dysfunction - beta blocker
vasoconstriction - nsaid, cyclosporin

Question 16

mechnism of renal aki

Answer 16

intrinsic damage in the kidney

vascular, glomerular, and tubular

Question 17

drugs causing vascular renal aki

Answer 17

vascular - cyclosporin, tacrolimue, quinine, clopidogrel

Question 18

drugs causing glomerular renal AKI

Answer 18

acei

nsaid

Question 19

drugs causingacute tubular necrosis (ischemic injury in tubules)

Answer 19

acetaminophen
aminoglycoside
antifunal
chemo agents
iodinated contrast dye

Question 20

drugs causing acute interstitial nephritis (hypersensitivity)

Answer 20

antimicrobials
nsaid
diuretic 
antihistamine
PPI

Question 21

mechanism of post renal aki

Answer 21

obstruction of urine flow
not common
kidneys fail rapidly
due to bladder dysfunction, crystals forming, retroperitoneal fibrosis

Question 22

drugs causing bladder dysfunction the post renal aki

Answer 22

anticholinergic

antipsychotic

Question 23

drugs that form crystal and cause post renal aki

Answer 23

acyclovir
ciprofloxacin
methotrexate
sulfonamides

Question 24

drugs that cause retroperitoneal fibrosis and cause post renal aki

Answer 24

beta blockers
hydralazine
methyldopa
bromocriptine

Question 25

risk factors for AKI

Answer 25

``` preexisting renal impairment dehydration (diuresis, vomiting, diarrhea, hemorrhage) cirrhosis, heart faillure, diabetes multiple nephrotoxic agents seriously ill advanced age ```

Question 26

cause of chronic kidney disease

Answer 26

deterioration of renal function due to DM, HTN, AKI, nephrotoxic chemicals chronic interstitial nephritis

Question 27

how do nsaids damage the kidney

Answer 27

prerenal - decrease prostaglandins causes vasoconstriction and decreased renal blood flow also acute interstitial nephritis

Question 28

clinical manifestation of nsaid kidney damage

Answer 28

increased plasma creatinine decreased renal blood flow and GFR oliguria

Question 29

how do you prevent nsaid kidney damage

Answer 29

avoid nsaids amoung high risk patients creatinine should be monitored closely avoid nsaids prior to procedures involving radiocontrast

Question 30

mechanism of aminoglycoside kidney damage

Answer 30

proximal tubular necrosis - freely filtered and accumulate in proximal tubule, bind to phospholipids within the plasma membrane interstitial nephritis

Question 31

type of kidney damange with aminoglycosides

Answer 31

interstitial nephritis | proximal tubular necrosis

Question 32

clinical manifestations of AG renal damamge

Answer 32

increased plasma creatinine increased BUN non oliguric - polyuria bc lose concentrating ability electrolyte abnormalities

Question 33

prevention of aminoglycoside renal damage

Answer 33

``` adjust dose for renal function correct hypokalemia and hypomagnesemia limit duration to 7-10days minimize concomitant nephrotoxic meds monitor therapy choose one with less nephrotoxicity once daily regimen ```

Question 34

additional risk factors for AG toxicity

Answer 34

elevated plasma drug concentrations - get peak and trough levels daily prolonged duration of therapy type: gent>tobra>amikacin frequency of dosing

Question 35

why is once daily dosing less toxic

Answer 35

uptake of the drug is saturable

Question 36

aki indidence in iodinated contrast media

Answer 36

almost never when no risk factors | 50% in high risk

Question 37

iodinated contrast medica mechanism of renal damage

Answer 37

high osmolality | acute tubular necrosis and vasocontraction

Question 38

first gen media

Answer 38

ionic monomers | highly hyperosmolal

Question 39

second gen media

Answer 39

nonionic monomers | lower osmolality

Question 40

newest generation media

Answer 40

nonionic, dimers iso-osmolal least risk but costly

Question 41

range osmolality of iodinated contrast media

Answer 41

ionic monomers >nonionic monomers > nonionic dimers

Question 42

clinical manifestations of iodinated contrast media damage

Answer 42

``` rapid decline within 24-48hr mild increase in serum creatinin non-oliguric hyperkalemia acidosis hyperphosphatemia ```

Question 43

additional risk factors for contrast media

Answer 43

``` dose - higher is more toxicity type - higher osmolarity more toxicity intraarterial more toxic than IV interventional angiography higher than diagnostic PCI reduced renal perfusion heart failure, multiple myeloma ```

Question 44

patients at risk of kidney damage with contrast media

Answer 44

<60 GFR and proteinuria >500mg/d <60 GFR and comorbidities (diabetes, liver fialure, heart failure) GFR <45

Question 45

prevention of kidney damage with contrast media

Answer 45

avoid volume depletion withhold nsaids 24-48hr before use smallest dose use iso-osmolal agent or nonionic low osmolal agent hydration wiht IV isotonic saline premedicate with acetylcysteine (NAC) for antioxidant properties

Question 46

tubule most commonly affected by drug induced renal toxicity

Answer 46

proximal

Question 47

analgesic nephropathy

Answer 47

renal papillary necrosis and chronic interstitial nephritis caused by acetaminophen, nsaid, asa