Tylenol Case Study en people near Chicago, Illinois, died soon after taking Tyle
ID: 213158 • Letter: T
Question
Tylenol Case Study en people near Chicago, Illinois, died soon after taking Tylenol. The symptoms that they experienced before dying were dizziness, confusion, headache, and shortness of breath. Autopsy results indicated that they died from suffocation, even though the oxygen level in their blood was above normal. The concentrations of other metabolites associated with cellular respiration were also measured and the results are shown in the table below: MetaboliteAverage Level I for Normal Level Glucose Pyruvate NAD NADH Vietims 99 HM 27 uM 10 400 HM 25 uM 7511M 50 . What, ultimately, killed the people that ingested the cyanide? Why did their autopsy indicate that they died of suffocation, even though they had above-normal levels of oxygen in their blood? .Explanation / Answer
QUESTION 1 ANSWER =Tylenol or paracetamol or acetaminophen is a para-amino phenol derivatives . paracetamol does not stimulate RESPIRATION OR AFFECT ACID-BASE BALANCE AND DOES NOT INCRTEASE CELLULAR METABOLISM .IT HAS NO EFFECT ON CVS.
ACUTE PARACETAMOL POISONING- IT OCCURS ESPASILLY IN SMALL CHILDREN WHO HAVE LOW HEPETIC GLUCURONIDE CONJUGATING ABILITY. IF A LARGE DOSE GRATER THAN 150mg or 10 g in an adult is taken serious toxicity can occurs. fatility is common with grater then 250mg per kg.
early manifestation are just nausea vomating abdominal pain and liver tenderness with no impairment of consciousness. after 12 hour centrilobular hepetic necrosis occurs which may be accompanied by renal tubular necrosis.
mechenism of toxicity N- acetyl-p-benzoquinoneimine is highly reactive arylating minor metabolite of paracetamol which is detoxifiedc by conjugation with glutathione. when a very large dose of paracetamol is taken glucuronidation capacity is saturated more of the minor metabolite is formed- hepatic glutathione is depleted and this metabolite bind covlently to proteins in liver cells causing necrosis.
QUESTION 2 ANSWER= it produce cellular hypoxia by binding of ferric ion speciallyt that present in cytochrome oxidase system. when it is bind to this enzyme complex electron transport chain is inhibited then ATP IS NOT PRODUCED . due to this result cellular utilization of oxygen decreases. but present in blood.
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