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Renal > Drug Induced Nephrotoxicity > Flashcards

Drug Induced Nephrotoxicity Flashcards

1
Q

Kidney and drug filtration

A

Kidney can filter small drug molecules and those NOT bound to plasma proteins

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2
Q

Kidney and drug excretion

A

Active tubular secretion in proximal tubule that involves 2 carrier systems (acids, bases)

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3
Q

Reabsorption of weak acids, bases by

A

Passive diffusion

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4
Q

Rate of reabsorption depends on

A

Urinary pH and lipid solubility of UNionized drug whether acidic or basic

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5
Q

Drug metabolism in the kidney

A

Just like in the liver ie involves oxidation, acetylation, conjugation NOTE: less specific than in the liver CP450 with oxidation

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6
Q

Reasons for kidneys susceptibility to adverse effects of drugs

A
  1. High blood flow 2. Ability to concentrate drugs in tubules—> expose tubules to high concentrations of drug 3. Metabolize drugs—> active metabolites 4. Large surface area of tubular epithelium provides site for interaction
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7
Q

Mechanism of Acute Renal Failure

A
  1. Altered intraglomerular hemodynamics 2. Vasoconstriction 3. Acute tubular necrosis 4. Aminoglycosides 5. Acetaminophen 6. Acute interstitial nephritis 7. Tubular obstruction ( crystal nephropathy) 8. Thrombotic microangiopathy 9. Rhabdomylosis 10. Osmotic nephrosis
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8
Q

Altered intraglomerular hemodynamics and ARF

A

NSAIDS and ACE-I→ deccline in blood prssure/ renal blood flow → prerenal failure

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9
Q

Altered intraglomerular hemodynamics and NSAIDS

A

NSAIDS

inhibit vasodilator effects of prostaglandins

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10
Q

Altered intraglomerular hemodynamics and ACE-I

A

ACE-I

inhibit Ang 2 acivity→ affect kidnyes ability to regulate glomerular pressure → decreased GFR

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11
Q

Captopril and ARF

A

Captopril: ACE-I

induces ARF in patients with decreased renal blood flow ie pt with bilateral Renal Artery Stenosis, shock, hypovolemia.

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12
Q

Reversibility of ARF induced by ACE-I and NSAIDs

A

Reversible after discontinuation

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13
Q

Vasoconstriction and ARF mainly associated with which drugs

A

Main mechanism of ARF in Cylosporine and vasopressors

ALSO: Amphoterecin B, radiocontrast media

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14
Q

Cyclosporin and vasocostriction→ ARF

A

Causes dose and concentration dependent predominating preglomerular vasoconstrition → reduced renal plasma flow and GFR→ ARF

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15
Q

How is the nephrotoxicity associated with cyclosporin managed

A

Reduced dose

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16
Q

Acute tubular necrosis and ARF

A
  • Mostly caused by drugs that are excreted by the kidney
  • Direct tubuar toxicity→ tubuoepithelial injury in PCT
17
Q

Drugs associated with acute tubular necrosis → ARF

A
  1. Gentamycin
  2. Amphoterecin B
  3. Antiviral
  4. Cisplatin
  5. Acetaminophen (in cases of overdose + usualy acompained by hepatic failure)
  6. Radiocontrast media
18
Q

Aminoglcosides and ARF pathophysiology

A

Aminoglycosides:

  • highly cationic
  • actively reabsorbed in PCT→ high concntrations in cotex
  • accumulate within lysosomes→ interfere with protein synthesis and miochondrial function→ NECROSIS
19
Q

Reversibility of Aminoglycosides→ARF

A

Reversible after discontinuation of drug

20
Q

Acute interstitial nephritis→ ARF mediated by

A

Inflammation of interstitium and tubules

21
Q

Acute interstitial nephritis→ ARF pathophysiology

A

Idiosyncratic non dose dependent hypersensitivity reaction

22
Q

Acute interstitial nephritis→ ARF associated with which drugs

A
  1. Antibiotics (penicillins, cephalosporins, sulfonamides, quinolones)
  2. NSAIDS
  3. ANtivirals (acyclovir)
23
Q

Crystal nephropathy an ARF pathophysiology

A

Drugs that produce crystals (pH DEPENDENT) insoluble in urine → precipitate in lumen of DT→ obstruct renal flow + interstitial reaction

24
Q

Crystal nephropathy → ARF associated with which drugs

A
  1. Antivirals (acyclovir)
  2. ANtibiotics (sulfonamides, ciprofloxacin)
  3. METHOTREXATE
25
Q

Thrombotic miroagiopathy→ ARF pathophysiology

A
  1. formation of platelet thrombi in microcirculation
  2. secondary mechanism of immune mediated
  3. direct endothelial toxicity

Result in severe renal failure

26
Q

Drugs implicated in Thrombotic microangiopathy→ARF

A
  • CYCLOSPORIN
  • Chemotherepeutics eg mitomycin-c
  • antiplatelet drugs eg ticlopidine
27
Q

Rhabdomylosis associated with

A

STATINS

esp if adminostered with other drugs

may occur with other drugs

28
Q

Osmotic Nephosis assoicated with

A

Hyperosmolar agents

radiocontrast media, plasma expanders, Ig

29
Q

Oveview of drug induced CRF

A
  • presents as tubulointerstitial disease
  • assocaited with analgesics (NSAIDs) cyclosporin, lithium, cisplatin
  • renal injury may be irreversible (lithium, cyclosorin)
30
Q

Analgesic nephropathy→CRF

A
  • associated with long term use of analgesics
  • characterized by interstitial nephritis and renal papllary necrosis
  • cobinations eg. acetaminophen and aspirin→more toxic than single drug because aspirin deplete the glutathione that detoxofies the active metabolote of aceta
31
Q

Nephrotic syndrome associated with which drug

A

NSAIDs

immunological

MINIMAL CHANGE NEPHROTIC SYNDROME

32
Q

Patient related RF for drug-induced nephrotoxicity

A
  • age >60
  • volume depletion
  • diabetes
  • heart failure
  • spesis
  • shock
  • GFR,60ml/min/1.73m2
  • exposure to multiple nephrotoxins
  • Race
  • sex
  • allergies
  • genetic variations
33
Q

Drugs with inherent nephrotoxic effect

A
  • Aminoglycosides
  • Amphoterecin B
  • Cisplatin
  • Cyclsporine
  • Contrast dye

NOTE: Risk factor for drug induced nephrotoxicity

34
Q

drugs whos nephrotoxicity is dose dependent

A
  • Acyclovir
  • NSAIDs

NOTE: Risk factor for drug induced nephrotoxicity

35
Q

other dug related RF

A
  • repeated exposure
  • immune effexts
  • drug interations
36
Q

Prevention

A
  • awareness of nephrooxicity of drugs and combinations
  • correct rf
  • elderly more succeptible
  • avoid dehydration esp in high risk pt
  • adjust daily dosage to onhoig alteration in GFR cockcroft gault formula
  • Limit daily dosage and duration of treatment with NSAIDs
  • alternatives

Renal (9 decks)

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