Toxicology Flashcards
CO is the leading cause of death by poisoning (closed areas AC, car). How does CO primarily act (two)?
- Displacing oxygen from hemoglobin (Hb)
CO has more than 200 times higher affinity to Hb than O2
CO displaces oxygen –produces carboxy-hemoglobin - Impairing oxygen release from Hb
CO reduces the ability of oxyhemoglobin to deliver oxygen to the peripheral tissues
How do you treat CO poisoning?
100% O2 UNDER PRESSURE bc will displace much faster (20 min. max).
What is Hyperoxia & Oxygen Toxicity and what are the risk factors?
Breathing oxygen at higher than normal partial pressures (>21% atm. Pressure). Risk factors: hypercapnia due to COPD, working at depth, narcotic withdrawal. Deep sea diving. Also, CO poisoning, decompression sickness
What is the treatment of Hyperoxia & Oxygen Toxicity?
prevention, minimum O2 dose possible, anti-epileptics
How does Hyperoxia & Oxygen Toxicity happen?
Production of reactive oxygen intermediates (ROIs), superoxide anion, hydroxyl radical, H2O2
What are the clinical features of Hyperoxia & Oxygen Toxicity?
Lungs: increase susceptibility to mucous plugging, atelectasis, 2ry infection by impairing mucociliary clearance & decrease immune cell function
Oxygen toxicity: tracheobronchial & alveolar damage, pulmonary interstitial fibrosis
Eye: retinal detachment and retrolental fibroplasia (esp. newborns during resuscitation)
Seizures
NO2is a relatively insoluble deep lung irritant capable of producing _____.
pulmonary edema
Severe exposure of ozone (O3) can cause deep lung irritation, with _____ when inhaled at sufficient concentrations.
pulmonary edema
Where can you find benzene (toluene)?
octane boost in fuel –Formula 1, airplanes; airplane glue, paint-thinners, rocket fuel, component of gasoline
What are the acute toxic effects of benzene?
depression of CNS and
Aplastic anemia
What is the chronic toxic effects of benzene?
leukemia
Does toluene cause aplastic/leukemic effects and why is it abused?
No; abused due to intoxication symptoms (euphoria, dizziness, sleep)
What are the sources of cyanide?
inhalation of smoke produced by the burning of plastics, fruit seeds (e.g., apricots and cherries, apple, plum, peach), lima bean, and raw almond
*****Which drug causes cyanide toxicity?
nitroprusside
What is the mechanism of cyanide poisoning?
Cyanide produces toxicity by binding avidly to ferric iron (Fe3+), which prevents its reduction to the ferrous form (Fe2+). Fe2+ is involved in the cytochrome oxidase a3 electron-transport system.
Inhalation of cyanide may produce a _____ demise, whereas symptoms may be _____ if the cyanide is ingested orally
rapid, delayed
What are the Cyanide toxic symptoms?
hypoxia including headache, anxiety, agitation, confusion, lethargy, seizures and coma, shortness of breath, abdominal pain, nausea and vomiting, cherry red skin color (increased venous hemoglobin oxygen saturation). Cyanide does not directly cause cyanosis
What are the treatments for cyanide toxicity?
Cyanide Antidote Kit contains amyl nitrite pearls, sodium nitrite, and sodium thiosulfate. Another antidote Hydroxocobalamin can be administered in the absence of the cyanide antidote.
How do you return Methemoglobin + Sodium thiocyanate to Hb when treating cyanide poisoning?
Methylene blue
_____ turns Hb to methemoglobin which has high affinity for cyanide radical and forms cyanomethemoglobin. This may release cyanide from cytochrome oxidase a3.
Nitrite
Sodium thiosulfate is given to form _____ which is poorly dissociable and is excreted in the urine
Sodium thiocyanate
*****What are the clinical features of lead poisoning?
blue line on gum margin, low IQ, dense metaphyseal band on x-ray, microcytic anemia, basophilic stippling RBC, blood lead increased
*****What do you use to treat (chelator) iron poisoning (hemochromatosis)?
deferoxamine (excreted by urine)
*****What is the treatment of lead poisoning > 44μg/dl?
Blood lead > 44μg/dl, edetate calcium disodium (EDTA), succimer, dimercaprol, penicillamine
*****What is the treatment of lead poisoning > 70μg/dl?
IV EDTA+dimercaprol
*****What is the chelator (treatment) of lead?
EDTA
What is the chelator (treatment) of copper (Wilson’s disease)?
Penicillamine
What is the chelator (treatment) of arscenic?
British anti-lewisite
What is the treatment of mercury?
dimercaprol or succimer
What are the clinical features of Wilson’s (copper builds up in liver and blood)?
parkinsonism, cirrhosis, neuropsychiatric symptoms, Kayser-Fleischer ring, Serum ceruloplasmin (copper carrying protein) decreases (<20mg/dl)
*****What are acute iron toxicity?
necrotizing gastritis, vomiting, abdominal pain and bloody diarrhea
*****How do you diagnose primary or secondary hemochromatosis?
Serum ferritin, liver biopsy—iron staining (Prussian blue)
Quick recall of toxic drugs and their antidotes.
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