Term
|
Definition
| most lethal neurotoxin that permanently opens neuronal Na channels so that neuron can no longer polarize |
|
|
Term
|
Definition
| blocks neuronal Na channels from passing Na, paralysis and respiratory arrest within minutes (blue ringed oxtopus and puffer fish)****mentioned in Dr. V AND Quock lecture |
|
|
Term
|
Definition
| excitotoxicity causing overactivation of NMDA and AMPA receptors with massive influx of Na and Ca ions resulting in neuronal death, cytochrome C release and production of ROS causing DNA damage |
|
|
Term
| organophosphate poisoning (transmissional) |
|
Definition
| Deporlarization blockade: blocks ACh re-uptake, ACh continues to activate receptors causing major muscle spasms and ultimate death |
|
|
Term
| cocaine toxicity (transmissional) |
|
Definition
| inhibition of DA and NE re-uptake, resulting in overactivation of DA (sympathetic overstimulation) causing cerebrovascular accidents and other actions like overactivation of seratonin/ muscarinic receptors |
|
|
Term
| organophosphates-induced delayed neuropathy OPIDN(axonopathy) |
|
Definition
| inhibition of neuropathy target esterase (NTE) causing swelling and degenration of axons in corticospinal motor tracts resulting in muscle weakness, ataxia and paralysis |
|
|
Term
| cisplatin-induced axonopathy |
|
Definition
| damage to organ corti, destruction of auditory and vestibular-balance occurring 3-4 days after drug administration (high pitch sounds most affected) |
|
|
Term
| vincristin-induced axonopathy |
|
Definition
| microtubuli interferance; symmetrical peripheral sensory-motor neuropathy resulting in paresthesia and severe motor weakness (ileus and orthostatic hypotension) |
|
|
Term
| lead-induced myelinopathy |
|
Definition
| mechanism not entirely understood, target of myelinopathy is CNS, induction of oxidative stress and apoptosis of neurons |
|
|
Term
| hecachlorophene-induced encephalopathy |
|
Definition
| inhibits respiratory D-lactase dehydrogenase and interferes with electron transport, it is a mitochondrial neurotoxin and causes spongiform (myelin: fluid filled) encephalopathy in cerebellum, hippocampus and brainstem |
|
|
Term
| nitrous oxide-induced myelinopathy |
|
Definition
| irreversibly oxidizes cobalt on methylcobalamine, inhibiting synthesis of methionine which is needed for the formation of myelin |
|
|
Term
| carbon monoxide-induced encephalopathy |
|
Definition
| induces platelet and endothelial release of NO formin free peroxynitrite radical causing mitochondrial dysfunction, capillary leakage, leukocyte sequestration and apoptosis, lipid peroxidation causes reversible demyelination of white matter |
|
|
Term
|
Definition
| taken up into dopamine neurons and attacks mitochondria and inhibits energy production, causing neuropathy and resembles advanced parkinsonism with major loss of dopamine activity |
|
|
Term
| methylmercury (MeHg) induced neuropathy, minamata disease |
|
Definition
| organic form of mercury (toxin found in large fish) that is most easily bioaccumulated casing major neuropathies in the brain and sever CNS and sensory damage |
|
|
Term
|
Definition
| organic form of mercury and the form of mercury that is most easily bioaccumulated |
|
|
Term
|
Definition
| cerebral palsy, blindness, deafness, growth retardation, mental retardation and microcephaly due to neuropathies in brain and spinal cord |
|
|
Term
| arsenic induced neurotoxicity |
|
Definition
| reacts with thiol on proteins and enzymes rendering them inactive leading to defects in protein composition and disorganization of cytoskeletal framework |
|
|
Term
| streptomycin-induced ototoxicity |
|
Definition
| aminoglycoside ototoxicity due to disruption of mitochondrial protein synthesis and formation of free radicals, apoptosis of cells and vestibular toxicities |
|
|
Term
| ANTAGonism of M2 receptors |
|
Definition
| increased conduction of AV and SA node, increased HR, increased O2 demand, exacerbation of angina, predisposition of other types of arrhythmias |
|
|
Term
|
Definition
| reduced conduction of AV and SA node, decrease HR, decreased O2 demand and reduced risk of angina |
|
|
Term
| OVER-excitation of B1 adrenergic receptors (result of excess of NE or epi) |
|
Definition
|
|
Term
| amphetamines (release of NE), Cocaine (blocks re-uptake NE) |
|
Definition
| overexcitation of B1 receptors, cardiac arrhythmias because heart is working harder than usual and can lead to cardiac event |
|
|
Term
|
Definition
| overexcitation of B1 receptors (Heart beats harder), transmission toxicity of neurons |
|
|
Term
| antimigraine and sympathomimetic |
|
Definition
| drug-induced coronary vasospasms leading to possible myocardial hypoxia and necrotic lesions to the heart |
|
|
Term
|
Definition
| inhibition of Na/K ATPase leading to increased Na/Ca exchanger to increase intracellular Ca resulting in increased contractility, too much cell cannot depolarize |
|
|
Term
| verapamil (isoptin) and diltiazem (cardiazem) |
|
Definition
| excessive bradycardia caused by blockade of Ca channels, decreased contractility (L-type) and decreased heart rate (T-type)...general weakening of heart |
|
|
Term
| antipsychotics, antihistamines (non-drowsy), azithromycin, viagra and cialis |
|
Definition
| can give rise to severe arrhythmias by blocking/ interfering with hERG K+ channel function which can lead to prolongation of Q-T interval and progress to torsades de pointes |
|
|
Term
| antiarrhythmic class IA: quinidine, procainamide, disopyramide |
|
Definition
| Drug-induced Q-T syndrome |
|
|
Term
| antiarrhythmic Class IC: encainide, flecainide |
|
Definition
| Drug-induced Q-T syndrome |
|
|
Term
| antiarrhythmic Class IIIL sotalol and amiordarone |
|
Definition
| Drug-induced Q-T syndrome |
|
|
Term
| Doxorubacin-induced cytotoxicity |
|
Definition
| breakdown product (semiquinone) forms complex with iron to make free radical which reacts with hydrogen peroxide forming peroxinitrite to cause cardiotoxicity |
|
|
Term
|
Definition
| Peroxinitrite cardio-toxicity AND mytochondrial dysfunction (oxidative stress) |
|
|
Term
|
Definition
| long term use causes mitochondrial dysfunction |
|
|
Term
|
Definition
| hypersensitivity myocarditis: NOT dose-dependent, occurs within a month |
|
|
Term
|
Definition
| vasoDILAtors, drug-induced vascular injury with long-term used |
|
|
Term
| vasopressin, angiotensin II, phenylephrine, epinephrine, methoxamine |
|
Definition
| vasoCONSTRICtors, drug-induced vascular injury with long-term used |
|
|
Term
| cholesterol (and oxygenated derivatives), organophosphates*, cadmium, arsenic mercury* |
|
Definition
| exacerbation of pre-existing vascular condition (atherosclerosis) |
|
|
Term
| propylthiouracil and ciprofloxacin* |
|
Definition
| drug-induced vasculitis, thickening, weakening, narrowing, scarring leading to necrosis of vessels |
|
|
Term
| Rifampin* (rifadin) hepatotoxicity |
|
Definition
| inhibition of transport IN and OUT of hepatocyte; increased UNconjugated AND conjugated bilirubin in blood (emia), may also increase glucuronyl transferase enzyme |
|
|
Term
| Sulfonamides* hepatotoxicity |
|
Definition
| compete for binding of albumin in blood; increased UNconnjugated ONLY, deposition in brain (kernicterus) and PERMANENT brain damage |
|
|
Term
|
Definition
| inhibits UDP glucuronic transferase and prevents glucuronidation of bilirubin, increasing UNconjugated ONLY...deposits in brain (kernicterus) and permanent damage--withdrawn |
|
|
Term
| Acetaminophen* hepatotoxicity |
|
Definition
| covalent binding to hepatocyte proteins in overdose due to toxic metabolite and depleted glutethione |
|
|
Term
|
Definition
| similar hepatocellular damage as APAP |
|
|
Term
|
Definition
| hypersensitivity; NOT dose-related cholestasis (simple accumulation of bile; jaundice/ puritis) |
|
|
Term
|
Definition
| hypersensitivity; DOSE-related cholestasis (simple accumulation of bile; jaundice/ puritis), mild and reversible |
|
|
Term
| ehtanol-induced steatosis |
|
Definition
| accumulation of NADH signals cells there is adequate energy source, inhibiting fat breakdown and increasing hepatocyte fat storage |
|
|
Term
| tetracycline-induced steatosis |
|
Definition
| DOSE-dependent after large IV doses, inhibiting protein synthesis (notably VLDL transport proteins) out of hepatocytes |
|
|
Term
| tetracycline-induced steatosis |
|
Definition
| DOSE-dependent after large IV doses, inhibiting protein synthesis (notably VLDL transport proteins) out of hepatocytes |
|
|
Term
| methotrexate (rheumatrex), amiodarone* (Cordarone) and methyldopa (Aldomet) |
|
Definition
| causes IRREVERSIBLE chronic liver failure with fibrous, scar tissue |
|
|
Term
| erythromycin, amiodarone*, fluoxatine, imipramine, and haloperidol |
|
Definition
| cause phospholipidosis PLUS Q-T prolongation |
|
|
Term
| chloroquine, hydroxychloroquine and quinine (don't mix up with quinidine--antiarrhythmic) |
|
Definition
| causes phospholipidosis PLUS myopathy and NEUROlogic damage |
|
|
Term
| aminoglycosides* (gentamycin, tobramycin, amikacin) |
|
Definition
| causes phospholipidosis PLUS NEPHROtoxicity (acute tubular necrosis--all aminoglycosides) |
|
|
Term
|
Definition
| hepatotoxicity AND acute intersticial nephRITIS |
|
|
Term
|
Definition
| hemodynamic renal failure, actune intersticial nephritis, acute tubular necrosis, glomerularnephritis (MCD and thin basement membrane nephrotoxicity |
|
|
Term
|
Definition
| increased vasoDILAtion, decreased profusion, and decreased glomerular filtration rate leading to hemodynamic renal failure (ischemia) |
|
|
Term
| cyclooxygenase inhibitors (ibuprofen, aspirin) |
|
Definition
| decreased facilitation of renin leading to decreased profusion and glomerular filtration leading to hemodynamic renal failure |
|
|
Term
| aminoglycosides* (gentamycin, kenamycin) |
|
Definition
| acute tubular necrosis from phospholipidosis of mitochondria and ROS formation in proxymal tubules leading to necrosis |
|
|
Term
|
Definition
| AVOID co-administration with Amphoteracin B due to additive nephrotoxicity |
|
|
Term
|
Definition
| acute tubular necrosis due to increased vasoCONSTriction with increased oxy demand and increased permeability (leakage) leading to necrosis of PROXIMAL and DISTAL tubules |
|
|
Term
|
Definition
| hyperbilirubinemia (unconj and conj) AND minimal change disease (glomerularnephritis) |
|
|
Term
|
Definition
| minimal change disease (glomerularnephritis); function impaired but no visible change |
|
|
Term
|
Definition
| regionalized scarring of the glomerulus; Focal Segmental Glomerularsclerosis |
|
|
Term
| NSAIDs*, mercury*, penicillamide, gold therapy |
|
Definition
| cause thin basement membrane nephropathy; presents with blood in urine but not functional issue |
|
|
Term
|
Definition
| thin basement membrane nephropathy,MeHg induced neuropathy, and exacerbation of pre-existing vascular conditions (atherosclerosis) |
|
|
Term
|
Definition
| causes membrane proliferative glomerularnephritis due to intraglomerular magnesium and immune cell/debris deposition |
|
|
Term
| cytotoxic drugs (cancer patients) |
|
Definition
| urate nephropathy, urate crystallization in ureters (post-renally) due to cell destruction and liberation of purines/ pyrimidines that are broken down to uric acid due to xanthineoxidase |
|
|
Term
|
Definition
| hyperbilirubinemia (UNconju ONLY) AND drug-induced crystallurea |
|
|
Term
| ciprofloxacin*, sulfonamides* |
|
Definition
| drug-induced crystallurea; drugs that are not very soluble in urine and precipitate out to form crystals that deposit in kidneys |
|
|
Term
|
Definition
| causes drug-induced vasculitis AND drug-induced crystallurea |
|
|
Term
|
Definition
| causes cirrhosis AND retroperitoneal fibrosis |
|
|
Term
| Methotrexate* and ergot derivatives (methysergide/ergotamine) |
|
Definition
| causes Retroperitoneal Fibrosis where fibrous tissue deposits to the back end of peritoneal cavity that also covers kidneys and ureters leading to obstruction of urine |
|
|
Term
|
Definition
| superoxidide ion, hydrogen peroxide, hydroxyl radical |
|
|
Term
| normal cellular anti-oxidants |
|
Definition
| glutethione peroxidase, superoxidase dismutase, and catalase |
|
|
Term
| Ferrous iron (Fe++), asbestos |
|
Definition
| cause fenton reaction converting to ferric ion by hydroxyl rdical |
|
|
Term
| doxyrubacin*, mitomycin C, and carbon tetrachloride (degreaser) |
|
Definition
| radical induced damage that spreads to lipid peroxidation: large areas of cell membranes causing a chain reaction with each new phospholipid |
|
|
Term
|
Definition
| leads to emphasema due to free radicals that destroy enzymes that normally maintain elastic qualities of lung |
|
|
Term
| xenoestrogen*, phytoestrogens, diethylsilbestrol(DES)*, and bisphenol A (BPA) |
|
Definition
| estrogen receptors: endocrine disruptors that cause toxicity by binding and activating nuclear receptors |
|
|
Term
|
Definition
| synthetic estrogen used to prevent miscarriage, causing vaginal cancer of the daughters of women who took the drug |
|
|
Term
| Aryl-hydrocarbon receptor ligands(AhR)...PCB's |
|
Definition
| change in protein production and cell proliferation by indirectly altering gene expression causing ultimate cell death |
|
|
Term
|
Definition
| produced by cyanobacteria (blue-green algae), selectively taken up by hepatocyte, covalent binding to cell and destroy enzymes that regulate cytoskeleton ultimately causing hemorrhage |
|
|
Term
| Aflatoxin (fungal), cyclophosphamides (anti-cancer), Benzo-A-Pyrene (cigarette smoke)* |
|
Definition
| covalent binding directly to DNA |
|
|
Term
|
Definition
| forces Na channels to stay open so axon cannot polarize, like batrachotoxin***but for insects |
|
|
Term
|
Definition
| inhibits enzymes containing iron in the electron transport chain, interferes with mitochondria and proton grandient...caused by smoke inhalation |
|
|
Term
|
Definition
|
|
Term
|
Definition
| entanercept (Enbrel), Adalimumab (Humira), Infliximab (Remicade)...death receptor antagonists (stops cell death) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| B cell lymphoma-2 receptors |
|
Definition
| inhibit the ONLY intrinsic (mitochondrial) apoptotic pathway |
|
|
Term
| Fas/ CD95, TRAIL receptors, caspase |
|
Definition
| Pro-apoptotic ligands(tumor necrosis factors and caspase) that EXTRINSICally promote cell |
|
|
Term
|
Definition
| inhibit cell death, decreases inflammation and is used for MI or stroke to save cells |
|
|
Term
|
Definition
| Bax, Bak, Bad, Bid and Bim...target cells for cell DEATH |
|
|
Term
|
Definition
| inhibit apoptosis BOTH extrinsically (caspase/TNF) and intrinsically (mitochondria) |
|
|
Term
|
Definition
| pro-apoptotic, used for cancer |
|
|
Term
|
Definition
| B cell lymphoma-2 receptor that inhibits ONLY INTRINSIC (mitochondria) |
|
|
Term
|
Definition
| inhibit apoptosis ONLY extrinsically by caspase inhibition |
|
|
Term
|
Definition
| naturally occurring produced by fungi growing on corn, grains, peanuts; control storage conditions to prevent poisoning |
|
|
Term
| ethidium bromide, acridine orange |
|
Definition
| intercalation (covelent binding) directly to DNA; displaces replication enzymes causing reading frame shift and/or mutation |
|
|
Term
|
Definition
|
|
Term
| tumor suppressor (de-acitvation) |
|
Definition
|
|
Term
| estrogen xenoestrogens*, AhR ligands |
|
Definition
| chemicals that cause cell receptor or change gene expression to alter cell growth/ death; does NOT interact with DNA directly |
|
|
Term
|
Definition
| stimulate cell proliferation in E2 sensitive tissues |
|
|
Term
|
Definition
| issue for fetus non-immunized or not previously exposed pregnant women, causing fetal defects: blindness, cataracts, mental retardation etc. |
|
|
Term
|
Definition
| used for morning sickness (contrast to DES for miscarriages), casing major birth defects highly time-dependent and only one dose needed |
|
|
Term
|
Definition
| (isotretinoid)...derivatives of Vit A cause malformations of fetus |
|
|
Term
|
Definition
| Pro-apoptotic by antagonizing the inhibition of intrinsic pathway of Bcl-2, essentially promoting INTRINSIC apoptotic pathway |
|
|
