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TOXICOLOGY > Kidney > Flashcards

Kidney Flashcards

1
Q

kidney is not responsible for release of

A

angiotensin

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2
Q

kidney is responsible for

A

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

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3
Q

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

A

20-25%

one of the reasons they are so susceptible

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4
Q

risk factors for acute kidney injury include

A

dehydration
advance age
cirrhosis

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5
Q

are all nsaids nephrotoxic

A

yes

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6
Q

glomerulus function

A

formation of ultrafiltrate

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7
Q

proximal function

A

bulk reabsorption of solute and water

80%

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8
Q

distal function

A

controls urine concentration

up to 25% of water and solute reabsorbed

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9
Q

loop on henle function

A

reabsorbs solute

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10
Q

collecting duct function

A

fine tuning in the balance between excretion and reabsorption of water

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11
Q

kidney responsible for synthesis and release of which hormones

A

1,25-dihydroxy vit D
renin
erythropoietin

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12
Q

what makes the kidney susceptible to toxicity

A

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

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13
Q

what defines acute kidney injury

A

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

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14
Q

mechanism of prerenal AKI

A

impaired renal perfusion

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

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15
Q

drugs that cause prerenal AKI

A

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

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16
Q

mechnism of renal aki

A

intrinsic damage in the kidney

vascular, glomerular, and tubular

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17
Q

drugs causing vascular renal aki

A

vascular - cyclosporin, tacrolimue, quinine, clopidogrel

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18
Q

drugs causing glomerular renal AKI

A

acei

nsaid

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19
Q

drugs causingacute tubular necrosis (ischemic injury in tubules)

A 
acetaminophen
aminoglycoside
antifunal
chemo agents
iodinated contrast dye
20
Q

drugs causing acute interstitial nephritis (hypersensitivity)

A 
antimicrobials
nsaid
diuretic 
antihistamine
PPI
21
Q

mechanism of post renal aki

A

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

22
Q

drugs causing bladder dysfunction the post renal aki

A

anticholinergic

antipsychotic

23
Q

drugs that form crystal and cause post renal aki

A

acyclovir
ciprofloxacin
methotrexate
sulfonamides

24
Q

drugs that cause retroperitoneal fibrosis and cause post renal aki

A

beta blockers
hydralazine
methyldopa
bromocriptine

25
Q

risk factors for AKI

A 
preexisting renal impairment
dehydration (diuresis, vomiting, diarrhea, hemorrhage)
cirrhosis, heart faillure, diabetes
multiple nephrotoxic agents
seriously ill
advanced age
26
Q

cause of chronic kidney disease

A

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

27
Q

how do nsaids damage the kidney

A

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

28
Q

clinical manifestation of nsaid kidney damage

A

increased plasma creatinine
decreased renal blood flow and GFR
oliguria

29
Q

how do you prevent nsaid kidney damage

A

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

30
Q

mechanism of aminoglycoside kidney damage

A

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

31
Q

type of kidney damange with aminoglycosides

A

interstitial nephritis

proximal tubular necrosis

32
Q

clinical manifestations of AG renal damamge

A

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

33
Q

prevention of aminoglycoside renal damage

A 
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
34
Q

additional risk factors for AG toxicity

A

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

35
Q

why is once daily dosing less toxic

A

uptake of the drug is saturable

36
Q

aki indidence in iodinated contrast media

A

almost never when no risk factors

50% in high risk

37
Q

iodinated contrast medica mechanism of renal damage

A

high osmolality

acute tubular necrosis and vasocontraction

38
Q

first gen media

A

ionic monomers

highly hyperosmolal

39
Q

second gen media

A

nonionic monomers

lower osmolality

40
Q

newest generation media

A

nonionic, dimers
iso-osmolal
least risk but costly

41
Q

range osmolality of iodinated contrast media

A

ionic monomers >nonionic monomers > nonionic dimers

42
Q

clinical manifestations of iodinated contrast media damage

A 
rapid decline within 24-48hr
mild increase in serum creatinin
non-oliguric
hyperkalemia
acidosis
hyperphosphatemia
43
Q

additional risk factors for contrast media

A 
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
44
Q

patients at risk of kidney damage with contrast media

A

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

45
Q

prevention of kidney damage with contrast media

A

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

46
Q

tubule most commonly affected by drug induced renal toxicity

A

proximal

47
Q

analgesic nephropathy

A

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

TOXICOLOGY (24 decks)

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