Renal - Review Questions Flashcards

1
Q

analgesic nephropathy

A

chronic consumption of combinations of NSAIDs and/or APAP (more than 3 years)

papillary necrosis with chronic interstitial nephritis.

Klaassen, Curtis D.. Casarett & Doull’s Toxicology: The Basic Science of Poisons, 9th Edition (p. 786). McGraw-Hill Education. Kindle Edition.

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2
Q

aminoglycosides

A

S1 and S2 segments

phospholipidosis due to inhibition of lysosomal hydrolases

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3
Q

radioconstrast agents

A

third most common cause of AKI

altered renal perfusion due to high viscosity and direct effects on endothelial cells

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4
Q

NGAL

A

distal nephron damage

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5
Q

Halogenated hydrocarbons (e.g. chloroform)

A

cytochrome P450 metabolism -> reactive intermediate that covalently binds to nucelophilic groups on macromolecules

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6
Q

haloalkenes (tetrafluorethylene)

A

proximal tubular necrosis (S3 segment)

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7
Q

KIM-1

A

proximal tubular damage

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8
Q

charge and glomerular filtration

A

Filtration of anionic molecules tends to be restricted compared to that of neutral or cationic molecules of the same size; this is primarily due to the charge-selective properties of the GBM

Klaassen, Curtis D.; Watkins, John B.. Casarett & Doull’s Essentials of Toxicology, Third Edition (Lange) . McGraw-Hill Education. Kindle Edition.

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9
Q

cyclosporine

A

acute vasculopathy

chronic glomerular sclerosis and tubular atrophy (vasoconstriction)

The decrease in RBF and GFR is related to marked vasoconstriction induced by cyclosporine, and it is probably produced by a number of factors:

including an imbalance in vasoconstrictor and vasodilatory prostaglandin production,

increased production of the vasoconstrictor thromboxane and endothelin,

and activation of the renin-angiotensin system.

Klaassen, Curtis D.. Casarett & Doull’s Toxicology: The Basic Science of Poisons, 9th Edition (p. 788). McGraw-Hill Education. Kindle Edition.

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10
Q

Depleted uranium

A

renal tubular necrosis

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11
Q

Proximal tubule

A

S1 (pars convoluta): vascular lysosomal system

S2: the end of the convoluted segment and the initial portion of the straight segment.

S3 (pars recta): catabolism, glutathione transport, GGT activity

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12
Q

indomethacin

A

papillary necrosis

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13
Q

Acetaminophen

A

acute proximal tubular necrosis

biotransformation at recommended doses generally via conjugation to sulfate or glucuronic acid and excreted in urine (Phase I not needed)

High doses saturate conjugation capacity -> CYP2E1 biotransformation -> NAPQI

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14
Q

Von-Hippel Lindau (VHL) germline mutations

A

target hypoxia inducible factor (HIF) proteins for degradation

loss of VHL results in increased HIF1 expression -> neovascularization

loss of both alleles required for tumorigenesis -> retinal and brain hemangioblastomas, renal clear cell carcinomas, pheochromocytomas, pancreatic neuroendocrine tumors, endolymphatic sac tumors

mutations can be induced by trichloroethylene (TCE)

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