toxicology

Question 1

increased anion gap in paracetamol overdose

Answer 1

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).

Question 2

what are the risk factors for lithium toxicity in chronic users

Answer 2

Elderly Long-term therapy increases half-life of lithium Volume depletion Renal insufficiency

(Page 376).

Question 3

what are the serum levels for mild moderate and severe lithium toxicity?

Answer 3

mild-< 2.5 m eq/l
mod 2.5 to 3.5 meq/l
severe >3.5

Question 4

what are the features of mild toxicity

Answer 4

Tremor, ataxia, nystagmus, choreoathetosis, photophobia, lethargy

(Page 376).

Question 5

what are the features of modereate toxicityt

Answer 5

Agitation, fascicular twitching, confusion, nausea, vomiting, diarrhea, signs of cerebellar dysfunction

(Page 376).

Question 6

what are the features of severe toxicity

Answer 6

Seizures, coma, sinus bradycardia, hypotension

(Page 376).

Question 7

do levels correlate with toxicity

Answer 7

levels do not correlate with symptoms i9n acute toxcicity.they coprrelate more in chronic toxicity

Question 8

adverse effects of activated charcoal

Answer 8

lung toxicity

Question 9

which is also known as gi dialysis

Answer 9

multiple dosae activated charcoal

Question 10

what is the urinary ph to be attained in urinary alkanoization

Answer 10

ph > 7.5

Question 11

duration of action of naloxone

Answer 11

15 to 90 miniutes

Question 12

in which other toxicities are naloxone effective

Answer 12

valproate
lithium
ace inhiobitor

Question 13

dosage of naloxone

Answer 13

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).

Question 14

what is high dose insulin euglycaemia therapy ?

Answer 14

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).

Question 15

which sensory modality is most cvommonly affected in sLIYLATE poisoning

Answer 15

tinnitus and hearing

Question 16

what is the differene in saliylate poisoning between adults and children

Answer 16

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).

Question 17

what is the danger with mechanical ventilation in salicylate poisoning

Answer 17

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).

Question 18

what for of gut deontaination ay be used in saliylate

Answer 18

atiated haroal

Question 19

in case of paracetamol toxivity at which stage is hepato toxicity most marked ?

Answer 19

72 to 96 hours

Question 20

toxic dose of paracatamol

Answer 20

acute : 150 mg per kg or 10 g

cgronic :4 g

Question 21

toxic dose of salicylate

Answer 21

150 mg per kg

Question 22

feature of glycaemic control in salicylate poisoning

Answer 22

deranged glycaemic copntrol with low csf glucose

Question 23

feature of glycaemic control in salicylate poisoning

Answer 23

deranged glycaemic copntrol with low csf glucose

Question 24

in case of an unknown time of ingestion of paracetamol when should NAC be administered

Answer 24

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

Question 25

what are the zones of the rumack matthew normogram

Answer 25

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).

Question 26

compare the iv and oral formulations of nac

Answer 26

both are equally efficacious,however the iv formulation may be preferred for the convenience of a shorter regime ( 20 hrsa over 72 hrs )

Question 27

what are tyhe nac regimes ?

Answer 27

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).

Question 28

icu score to predict mortality in paracetamol toxicity

Answer 28

apache score greater than 15

Question 29

treatment for amphetamine hyperthermia

Answer 29

dantrolene

Question 30

organ affected in amphetamin e overdose

Answer 30

hepatic

Question 31

treatment for isopropranol toxicity

Answer 31

mainly supportive dialysis nin refractory coma opr shock fomepizole is not indicated

Question 32

indication of dialysis in alcohol toxicity

Answer 32

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).

Question 33

is amphertamine dialysable

Answer 33

no

Question 34

temperature aberration assosciated with barbiturate toxicity

Answer 34

hypothermia

Question 35

why is bdz poisoning a cxlinical diagnosis

Answer 35

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).

Question 36

is bdz dialysable

Answer 36

no

Question 37

for barbiturates is haemoperfusion more efficient than haemodialysis

Answer 37

no