Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Toxicology Final > Toxic Responses of Kidney > Flashcards

Toxic Responses of Kidney Flashcards

1
Q

What functional tasks do the kidneys perform?

A
  • formation of ultra filtrate
  • bulk reabsorption
  • controls urine concentration- up to 25% of water and solute are reabsorbed
  • reabsorbs solute
  • fine-tuning in the balance between excretion and reabsorption of water, solute
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the functions of the kidneys?

A
  • excretion of metabolic wastes
  • regulation of: extracellular fluid volume, electrolyte composition, and acid base balance
  • synthesis and release of hormones (1,25 dihydroxy vitamin B, renin, erythropoietin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What percentage of cardiac output does the kidney receive?

A

20-25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What makes the kidney esp susceptible to toxicity?

A
  • concentrate toxicants in tubular fluid
  • metabolizes xenobiotics
  • glomeruli and interstitial are susceptible to attack by the immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

_____ of acute kidney injuries are secondary to medication use

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the value definitions of actor kidney injury?

A
  • sCr >1.5x baseline within 7 days

- urine volume <0.5 ml/kg/hr for 6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the mechanism of pre-renal injury?

A
  • impaired renal perfusion

- can be caused by bleeding, volume depletion, cardiac dysfunction or vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What medications can cause pre-renal damage?

A

bleeding: anticoagulants
v. depletion: diuretics, cathartics, emetics
cardiac dysfunction: BB, cardiotoxins
vasocontriction: NSAIDs, calcineurin inhibitors, cyclosporin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mechanism of renal damage?

A
  • intrinsic damage (in vasculature or glomerulus)

- vascular, glomerular, acute tubular necrosis, acute interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What medications can cause renal damage?

A
  • cyclosporine, tacrolimis, quinine, clopridogrel
  • ACE inhibitors, NSAIDs
  • acetaminophen, aminoglycosides, antifungals, chemotherapeutic agetns, contrast media
  • antimicrobials, NSAIDs, diuretics, antihistamines, PPIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the mechanism of post-renal failure?

A
  • obstruction of urine flow
  • kidneys fail rapidly
  • bladder dysfunction
  • crystal formation
  • retroperitoneal fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What drugs can contribute to post-renal failure?

A
  • anticholinerigics, antipsychotics
  • acyclovir, ciprofloxacine, methotrexate, sulfonamides
  • B blockers, methyldopa, hydralazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some of the risk factors of kidney injury?

A
  • pre-existing renal impairment
  • dehydration
  • cirrhosis, HF, DM
  • multiple nephrotoxic agents
  • seriously ill
  • advanced age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is chronic kidney disease usually caused by?

A
  • DM
  • HTN
  • secondary pathophysi processes triggered by AKI
  • long term exposure to nephrotoxic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What NSAIDs are the ones that cause kidney damage?

A

nonselective NSAIDs or COX-2 specific NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What kind of kidney damage do NSAIDs do?

A
  • pre-renal damage

- Acute interstitial nephritis

17
Q

What clinical manifestations does NSAID kidney injury take on?

A
  • increased plasma creatinine
  • decreased RBF and GFR
  • oliguria
18
Q

What is the mechanism in which aminoglycosides cause toxicity?

A
  • proximal tubular necrosis (freely filtered, accumulate in proximal tubule - bind to phospholipids within the plasma membrane as well)
  • interstitial nephritis
19
Q

What dosing changes can be made to avoid amino glycoside toxicity?

A

1 high dose of amino glycoside rather than TID will prevent toxicity

20
Q

What are the clinical manifestations of amino glycoside toxicity?

A
  • increased plasma creatinine
  • increased BUN
  • non-oliguric
  • electrolyte abnormalities
21
Q

What aminoglycosides are the most nephrotoxic vs the least?

A

gent > tobra > amikacin

22
Q

What can be done to prevent amino glycoside nephrotoxicity?

A
  • avoid in patients with risk factors
  • adjust dose for renal function
  • correct hypokalemia and hypomagnesemia
  • limit duration to 7-10 days
  • minimize other nephrotoxic agents
  • choose an amino glycoside with less nephrotoxicity
23
Q

What is the mechanism of radio-contrast media nephrotoxicity?

A
  • high osmolality, which can lead to acute tubular necrosis and vasoconstriction
24
Q

What is the clinical manifestation of radio contrast media nephrotoxicity?

A
  • within 24-48 hours post exposure
  • mild increase in sCr
  • usually non-oliguric
  • hyperkalemia, acidosis, hyperphosphatemia
25
Q

What are the patients that are at highest risk of nephrotoxicity if receiving radio-contrast dye?

A
  • GFR <60 and significant proteinuria
  • GFR < 60 and comorbidities
  • GFR < 45
  • GFR < 30
26
Q

What can be done to aid in prevention of nephrotoxicity with contrast dye?

A
  • avoid volume depletion
  • withhold NSAIDs for 24-48 hours prior to procedure
  • use smallest dose necessary
  • ensure hydration

Toxicology Final (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions