Kidney Toxicity (Table) Flashcards

(39 cards)

1
Q

Mechanisms of chemically induced AKI:

Diuretics, ACE, ARBS, Antihypertensives

A

Pre-renal

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2
Q

Mechanisms of chemically induced AKI:

NSAIDS, Radiocontrast Agents, Cyclosporine, Tacrolimus, Amphotericin B

A

Vasoconstriction

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3
Q

Mechanisms of chemically induced AKI:

Sulfonamides, Methotrexate, Acyclovir, Triamterene, Ethylene glycol, Protease inhibitors

A

Crystalluria

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4
Q

Mechanisms of chemically induced AKI:

Aminoglycosides, Cisplastin, vancomycin, Pentamidine, Radiocontrast agents, Heavy metals, haloalkane and haloalkene

A

Tubular Toxicity

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5
Q

Mechanisms of chemically induced AKI:

Cyclosporine, Mitomycin C, Tacrolimus, Cocaine, Conjugated estrogens, Quinin

A

Endothelial Injury

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6
Q

Mechanisms of chemically induced AKI:

Gold, Pencillamine, NSAIDS

A

Glomerulopathy

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7
Q

Mechanisms of chemically induced AKI:

Antibiotics, NSAIDs, Diuretics

A

Interstitial Nephritis

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8
Q

Glomerular Injury:

Impair glomerular ultrafiltration
without significant loss of structural
integrity and decrease GFR

A

Cyclosporine,
Amphotericin B, and
Gentamicin

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9
Q

● ↓ GFR by renal vasoconstriction
● ↓ Glomerular capillary ultrafiltration
coefficient (Kf)

A

Amphotericin B

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10
Q

Interacts with anionic sites on the
endothelial cells → ↓ GFR and Kf

A

Gentamicin

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11
Q

T/F: Gentamicin drug has
a narrow therapeutic index

A

True

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12
Q

Renal vasoconstriction and vascular
damage, injurious to the glomerular
endothelial cell

A

Cyclosporine

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13
Q

Drugs that causes glomerular injury

A

Cyclosporine,
Amphotericin B, and
Gentamicin

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14
Q

drugs that causes LOOP OF HENLE/DISTAL TUBULE/
COLLECTING DUCT INJURY

A

Amphotericin B, Methoxyflurane, Cisplastin

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15
Q

The initial target of abusive consumption of analgesics is the

A

Medullary interstitial cells > Degenerative changes in the
medullary capillaries > Loops of Henle > Collecting ducts

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16
Q

The acute nephrotoxicity induced
by HgCl2 is characterized by
proximal tubular necrosis and AKI
within 24 to 48 hours after
administration

17
Q

Can cause brain defects and affect
kidneys

18
Q

seafood
exposed in industrial waste

19
Q

produces proximal
tubule dysfunction (S1 and S2
segments) and injury that may
progress to chronic interstitial
nephritis

20
Q

primary cellular target of
chloroform is the ______ with no primary damage to the
glomerulus or the distal tubule

A

proximal tubule

21
Q

Proteinuria, glucosuria, ↑ BUN levels

22
Q

is the
penultimate nephrotoxicant of Tetrafluoroethylene

A

Cysteine S-conjugate

23
Q

The products of the reaction are
ammonia, pyruvate, and a reactive
thiol that is capable of binding
covalently to cellular
macromolecules, causing cellular
damage

A

Tetrafluoroethylene

24
Q

________________ of bromobenzene
and other halogenated benzenes is
critical for their nephrotoxicity

A

Biotransformation

25
Metabolizes bromobenzene and conjugates it to glutathione, and releases it as a form that can cause nephrotoxicity
Hepatic cytochrome P450
25
26
1000-fold more potent than bromobenzene
Diglutathione conjugate of the hydroquinone
27
are products of molds and fungi, and a number of mycotoxins produce nephrotoxicity
Mycotoxins
28
↓ urine osmolality, GFR and RBF, glycosuria, ↑urinary enzyme excretion
Citrinin nephrotoxicity
29
Found on corn and corn products
Fumonisins B1 and B2
30
nephrotoxicity in rats and rabbits
Fumonisins B1 and B2
31
↑ urine volume, ↓ osmolality, ↑ low and high MW proteins
Fumonisins B1 and B2
32
Aristolachia and I genera
Aristolochic acids and aristolactams
33
can lead totubular dysfunction, proteinuria, interstitial fibrosis
Aristolochic acids and aristolactams
34
Proximal tubular necrosis with increases in BUN and plasma creatinine, ↓ GFR, and clearance of para-aminohippurate
Acetaminophen
35
reversible on withdrawal of the drug
NSAIDs
36
NSAIDs: _________ RBF and GFR by _______
↓ RBF and GFR by oliguria
37
Chronic consumption of NSAIDS
> 3 years
38
Characterized by non oliguric renal failure with ↓ GFR, ↑ serum creatinine, and proteinuria
Aminoglycosides