toxicology Flashcards
increased anion gap in paracetamol overdose
This is seen with chronic ingestion of a normal dose in thin malnourished patients and is thought to be due to glutathione deficiency. The accumulating acid is pyroglutamic acid.
(Page 199).
what are the risk factors for lithium toxicity in chronic users
Elderly Long-term therapy increases half-life of lithium Volume depletion Renal insufficiency
(Page 376).
what are the serum levels for mild moderate and severe lithium toxicity?
mild-< 2.5 m eq/l
mod 2.5 to 3.5 meq/l
severe >3.5
what are the features of mild toxicity
Tremor, ataxia, nystagmus, choreoathetosis, photophobia, lethargy
(Page 376).
what are the features of modereate toxicityt
Agitation, fascicular twitching, confusion, nausea, vomiting, diarrhea, signs of cerebellar dysfunction
(Page 376).
what are the features of severe toxicity
Seizures, coma, sinus bradycardia, hypotension
(Page 376).
do levels correlate with toxicity
levels do not correlate with symptoms i9n acute toxcicity.they coprrelate more in chronic toxicity
adverse effects of activated charcoal
lung toxicity
which is also known as gi dialysis
multiple dosae activated charcoal
what is the urinary ph to be attained in urinary alkanoization
ph > 7.5
duration of action of naloxone
15 to 90 miniutes
in which other toxicities are naloxone effective
valproate
lithium
ace inhiobitor
dosage of naloxone
If a patient is not opioid dependent, a reasonable starting dose is 2 mg, increasing to 10 mg (in increments) if there is no response.
(Page 1320).
what is high dose insulin euglycaemia therapy ?
During druginduced shock, insulin shifts myocardial fatty acid oxidation to carbohydrate oxidation, which increases contractility, left ventricular pressure, and rate of change of developed pressure. Enhanced fatty acid oxidation, such as occurs after epinephrine administration, transiently increases contractility at the expense of increased myocardial oxygen consumption.32
(Page 1321).
(Page 1320).
which sensory modality is most cvommonly affected in sLIYLATE poisoning
tinnitus and hearing
what is the differene in saliylate poisoning between adults and children
in children respiratory alkalosis is uncoon.Since acidosis enhances transfer of the salicylate ion across the blood–brain barrier, it is necessary to employ more active therapy at lower salicylate concentrations in children.
(Page 1516).
what is the danger with mechanical ventilation in salicylate poisoning
The concern with airway management in these patients is due to the mechanical ventilator’s inability to match the patient’s respiratory function (both primary respiratory alkalosis and compensation from the metabolic acidosis).
(Page 1516).
what for of gut deontaination ay be used in saliylate
atiated haroal
in case of paracetamol toxivity at which stage is hepato toxicity most marked ?
72 to 96 hours
toxic dose of paracatamol
acute : 150 mg per kg or 10 g
cgronic :4 g
toxic dose of salicylate
150 mg per kg
feature of glycaemic control in salicylate poisoning
deranged glycaemic copntrol with low csf glucose
feature of glycaemic control in salicylate poisoning
deranged glycaemic copntrol with low csf glucose
in case of an unknown time of ingestion of paracetamol when should NAC be administered
nac therapy should be started if both liver emzymes and apap levels are elevated ( > 5 micg/ml as per hall and schmidt but time yto be less than 24 hours)
OR
even if only apap levels are elevated
what are the zones of the rumack matthew normogram
The Rumack-Matthew nomogram for predicting acetaminophen hepatoxicity. This nomogram allows for stratification of patients into categories of probable hepatic toxicity, possible hepatic toxicity, and no hepatic toxicity, based on the relationship between acetaminophen level and time after ingestion. When this relationship is known, N-acetylcysteine (NAC) therapy is indicated for acetaminophen levels above the lower nomogram line.
(Page 1207).
compare the iv and oral formulations of nac
both are equally efficacious,however the iv formulation may be preferred for the convenience of a shorter regime ( 20 hrsa over 72 hrs )
what are tyhe nac regimes ?
The oral loading dose of NAC is 140mg/kg. This is followed by a dose of 70mg/kg every 4 hours for 17 doses. There
(Page 1208).
The most commonly used 21-hour scheduling of IV NAC includes a loading dose of 150mg/kg over 1 hour, followed by 50mg/kg over 4 hours, then 100mg/kg over 16 hours.112
(Page 1208).
icu score to predict mortality in paracetamol toxicity
apache score greater than 15
treatment for amphetamine hyperthermia
dantrolene
organ affected in amphetamin e overdose
hepatic
treatment for isopropranol toxicity
mainly supportive
dialysis nin refractory coma opr shock
fomepizole is not indicated
indication of dialysis in alcohol toxicity
Hemodialysis can be performed concurrently with fomepizole if clinically indicated. Hemodialysis is indicated for serum levels above 50mg/dL (for both ethylene glycol and methanol), significant acidosis (pH <7.25), renal failure, or deteriorating vital signs. Specifically in the case of methanol, hemodialysis is indicated if there are vision abnormalities at time of diagnosis.132
(Page 1209).
is amphertamine dialysable
no
temperature aberration assosciated with barbiturate toxicity
hypothermia
why is bdz poisoning a cxlinical diagnosis
Some benzodiazepines, such as clonazepam, are not metabolized to frequently tested metabolites and will therefore not be detected by urine drug screens. Others, such as alprazolam, will undergo insufficient metabolism to reach the testing threshold for a positive urine drug test, so therapy should be based more on clinical information.155-157
(Page 1210).
is bdz dialysable
no
for barbiturates is haemoperfusion more efficient than haemodialysis
no
