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toxi spring quiz 1 > nephrotoxicity > Flashcards

nephrotoxicity Flashcards

1
Q

list the soluble drug transporters

A
  • OATs/OCTs - organic anion and cation transporters
    • MOST IMPORTANT. TRANSPORT ALMOST ALL SUBSTANCES
  • OATPs - organic anion transporting polypeptides
  • PEPT - peptide transporters (amino acids and
  • peptides)
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2
Q

WHAT TYPE OF TRANSPORTER IS MATE

A
  • multi-drug and toxin extrusion - family of ABC transporters
    • ABC TRANSPORTERS TRANSPORT THINGS OUTSIDE THE CELL
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3
Q

EXPLAIN THE MECHANISM BY WHICH PROBENICID AS WELL AS SIMILIAR SUBSTRATE RESULT IN PENICILIN AND CEPHALOSPORIN EXCRETION

A
  • PENICILIN AND CEPHALOSPORINS ARE NORMALLY NT TOXIC
  • THEY HAVE TO COMPETE WITH PROBENICID FOR TRANSPORT INTO KIDNEY CELLS AND INTO URINE
  • PROBENICID IS A SUBSTRATE
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4
Q

EXPLAIN ADV. AND DISADVANTAGES OF PROBENICIN AS A SUBSTRATE FOR OTA

A
  • REDUCE ENTRY OF OTA INTO THE KIDNEY CELLS
  • BUT OTA IS GONNA ACCUMULATE IN BLOOD
  • AND ITS GONNA DAMAGE THE LIVER AND OTHER ORGANS INSTEAD
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5
Q

DISCUSS MECHANISM OF PARA-AMINO HIPPURIC ACID IN KIDNEYS

A
  • SAME AS PROBENICIN
    • IT IS A CO-SUBSTRATE
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6
Q

WHICH DRUGS ARE TRANSPORTED BY ABC TRASPORTERS

A
  • IVERMECTIN
  • FLOUROQUINOLONES
  • NOT GENTAMYCIN
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7
Q

KEY ENZYME FOR Glutathione conjugate
processing

A
  • N-acetyl-transferase (NAT1 and
    NAT2)
  • A renal-specific biotransformation pathway
  • A renal-specific biotransformation pathway
  • Slow and fast metabolizes of drugs (see sulfonamide sensitivity of dogs)
  • Bioactivation of certain halogenated benzenes and other toxins (benzene-ring structures)
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8
Q

NON TOXIC END PRODUCT OF GLUTATHIONE CONJUGATE PROCESSING

A
  • Mercapturic acid (renal end-product) in urine
  • N-acetyltransferase INACTIVATES THE toxic COMPOND
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9
Q

THE TOXIC COMPOUND OF GLUTATHIONE CONJUGATE PROCESSING

A
  • Venylthiole episulfonium ions
  • SITE SPECIFIC RENAL TOXICITY
  • animals with genetic polyphomophism will nt express more
    of N. ACETYL TRSANSFERASE leaing to the toxic pathway
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10
Q

AVANTAGE AND DISADVANTAGES OF METALLOTHIONEINS

A
  • BINDS METALS PREDOMINANTLY IN THE LIVER AND STOP LIVER DAMAGE
  • THE METAL COMPOUNDS GETS DEPOSITED IN KIDNEY N END P DAMAGED
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11
Q

DISCUSS THE MECHANISM FOR KIDNEY DAMAGE BY METALLOTHIONEINS (MT)

A
  • Heavy metals (particularly Cd:
    replaces Zn and binds to and
    induces MT - predominantly in the
    liver)
  • The MT complex is transported tothe kidney
  • In the kidney the MT complex is cleaved due to a pH shift
    • Free metal ions - accumulation- oxidative stress - cell injury/renal toxicity
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12
Q

DISCSS ROUND UP PESTICIDE TOXICIDE

A
  • Glycophosphate toxicity
  • Normally very safe
  • pesticide/herbicide
  • Combined with heavy
  • metals results in toxicity
  • Chronic kidney disease of
  • unknown origin
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13
Q

MECHANISM FOR ETHYLENE GLYCOSIDE

A
  • Acute acidosis
  • Decreased renal perfusion
  • Calcium oxalate crystals in the renal tubules
  • LD50 1.5 ml in cats; 5.5ml in
  • dogs
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14
Q

DISCUSS TX OF ETHELYNE GLYCOL

A
  • Ethylene glycol itself is not toxic,

the metabolites are

  • Therapy in dogs: 4-MP (fomepizol

or 4-methylpyrazone; Atizol®)
Inhibition of alcohol
dehydrogenase (only in higher
concentrations in cats!)

  • Ethanol: competition for alcohol

dehydrogenase

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15
Q

cs of ethelyn glycol intoxication

A
  • 0.5-12hrs: vomiting, ataxia, polyuria
  • Cardiopulmonary symptoms: tachypnea, tachycardia
  • 4EX. Oxalate nephrosis: anorexia, azotemia, oliguria
  • leading to kidney failure
  • Rapid intervention is required:
  • Interrupt exposure: induce vomiting (binds poorly to
    • activated charcoal, bentonite is better)
    • Correct metabolic acidosis: Na-bicarbonate
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16
Q

discuss toxicity of melamine

A
  • Feed contamination: technical melamine contains residual amounts of cyanuric acid
  • Melamine and cyanuric acid - amorphous brownish crystals in collective duct and urinary bladder: may result in acute renal failure
    • Migration agent from plastic?
    • Disease not reproducible with melamine
  • Melamine toxicity is completely documented - no renal toxicity
17
Q

WHICH toxin affects the DT

A
  • Distal tubular damage
  • in contrast to other toxins
    causing proximal tubular damage
  • Melamine plus cyanuric acid complexes
18
Q

MELAMINE TOXICITY

A

China September 2008: large scale fraude with
infant formula to which melamine was added to
pretend a higher protein content (interferes with
protein measurement)
Thousands of infants with renal failure
Therapy: symptomatic, prognosis is poor

19
Q

TOXICITY FOR GENTAMICINE

A
  • Nephrotoxicity - neurotoxicity -ototoxicity
  • Substrates for OAT1 and OAT3;
    • down regulation of OAT expression following continuing exposure
  • Time-dependent passive reabsorption; active secretion
  • Concentration dependent bacterial killing
20
Q
  • TOXICITY OF GENTAMYCIN DEPENDS ON
A
  • Duration of treatment
  • Cumulative dose
  • Average daily dose
  • Peak and trough serum
  • concentrations
  • Concurrent diuretic use
  • Underlying disease status
  • Previous exposure to
  • aminoglycosides
21
Q

THIS DRUG CAUSE HYPERTENTION LEADING TO CARDIOPATHY AND CHRONIC RENAL INSUFICIENCY

A
  • Melengestrol acetate
  • Long-term glucocorticoid treatment
  • THIS CONDITION IS CALLED AMES: Apparent Mineralocorticoid Excess
    Syndrome (liquorice) IN PPLE
22
Q

mechanism by which hypertension causing drugs like Melengestrol acetate cause renal damage

A

Inhibition of 11-β-hydroxy-steroid
dehydrogenase

23
Q

drugs causing PT damage

A

Aminoglycosides
Amphotericin B
Cisplatin

24
Q

rugs causing distal tubular damage

A

NSAIDs
ACE-inhibitors
Cyclosporin
Lithium salts

25
Q

drugs causing tubular obstruction

A

Sulfonamides
Propoylene glycol

26
Q

drugs causing intestitial nephritis

A

β-lactams (cephalosporins)
Vancomycin
Sulfonamides
Ciprofloxacin
NSAIDs
Cimetidine, ranitidine
Furosemide
Thiazides
Phenytoine

27
Q

theraupetic measures for renal toxicity

A
  • Improving renal secretion and excretion
  • Enforced diuresis: only in patients with maintained renal function
    • Furosemide (nephrotoxic in high dosages) -
    • infusions (saline, electrolytes)
  • Modulate urinary pH
    • more acidic: ammonium chloride
    • more basic: sodium-bicarbonate, sodium citrate
28
Q

plant toxin used to lose wt but cause renal damage

A

Aristolochic acid

29
Q

this enzyme is a specific marker for pt damage

A

ggt

it is a brush border enzyme

30
Q

non specific pt damage enzymes

A
  • non-specific cell necrosis
  • AP and LDH

toxi spring quiz 1 (6 decks)

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