Drug overdose

the ingestion or application of a drug or other substances in quantities greater than are recommended or generally practiced

-accidentally -deliberately

-benzodiazepines -analgesics -antidepressants this drugs are usually taken with alcohol

-narrow therapeutic window -steep dose-response curse (high dose+ high effect) -enzyme inhibitors (P450) -enzyme inducers -high toxic potential (kidney failure from antibiotics)

-polymorbidity polypharmacy -treatment lasting longer -chronic diseases -abuse -non-compliance -self-treatment -ordering different drugs from different dr.

dose causing toxicity/ dose providing efficacy

-aspirin -digoxin -lithium -aminoglycoside antibiotics

• quinidine -valproic acid

-immediate measures evaluation (ABC, history etc) -supportive measures (cardiac/respiratory arrest) -prevent absorption (activated charcoal, gastric lavage) -elimination (alkaline diuresis) -antidotes (using interaction in advantage) -psychiatric assessment

-recognise the poisoning -identify which agents are involved -assessment of how severe it was -prediction of toxicity

-A: airways B:breating C: circulation -protect the airway -vital signs, mental status, pupil size -pulse oxymetry, cardiac monitoring, ECG -IV access -cervical immobilization (if trauma suspected) -rule out hypoglycaemia (similar symptoms)

-gastric lavage -induce vomiting -activated charcoal

-it absorbs toxic substances or irritants + inhibits GI absorption -oral 25-100g -cannot absorb petroleum distillantes +inorganic acid and alkali + alcohol + metal ions + cyanide +lithium

-flushing of stomach contents via a tube from the nose into the stomach -saline is injected into the tube -patients are usually unconscious unless intubated

-renal elimination -forced alkaline diuresis -haemodialysis or hemoperfusion

-for severe poisoning -drug needs to be protein bound with low Vd -can be used long or short term if the kidney are damaged

infusion of NS+NAHCO3 eliminates acidic drug that mainly excreted by the kidney fluid and electrolytes disturbance may occur

-meds to stimulate urination or defecation to get rid of excess drug faster

mechanism: pharmacological antagonists ethanol and naloxone

enhance physiological function to compensate physostigmine

restore active site of drug target pralidoxime

bypass block glucagon

Sequester poison digibind

speed up excretion chlorine

no symptoms -->nausea & vomiting, malaise

-subclinical elevation of hepatic aminotransferases -increase of prothrombin time and total bilirubin -right upper quadrant pain, liver enlargement and tenderness -oliguria and renal function abnormalities

jaundice, confusion, elevation in hepatic enzyme, hyperammonaemia, bleeding diathesis hypoglycaemia, lactic acidosis, renal failure, death.

recovery phase

-GI bleeding and prolonged bleeding -activation of respiratory centre -interference with metabolism --> ATP isn't formed + a.a. isn't metabolised

40-50 mg/dL

3g (children) 30g (adults)

-metabolic acidosis --> acidic pH movement of salicylate into tissue -respiratory alkalosis --> more breathing = more CO2 -electrolyte imbalance --> vomiting + more renal excretion of bicarbonate

burning throat pain decrease urination double vision fever ringing in the ears or inability to here seizures stomach pain vomiting

-activated charcoal -fluid replacement --> to combat salicylate toxicity -urine alkalinization --> excretion of ionised acid form of salicylate

-renal failure -acute lung injury -persistent CNS disturbances -severe acid-base or electrolyte imbalance (after treatment) -hepatic compromise with coagulopathy

-respiratory depression -pinpoint pupil -decrease level of consciousness -hypotension and bradycardia

specific opioid receptor in CNS

antidote - naloxone

• I.V, I.M 04-2mg every 2-3 mins

BP changes arrhythmias seizures withdrawal

-organophosphate -irreversible anticholinesterases (AChE)

twitching fasciculations muscle weakness cyanosis elevated BP

-bronchoconstriction -increase secretion (blocked in airway) -sweating -GI -miosis (extensive dilation of pupil)

-anxiety -restlessness -confusion -headache

-clear airways -AChE regenerator Pralidoxime (antidote) i.v. 1-2g 15-30 min -treatment needs to start early -doesnt enter CNS because +ve charge -use atropine to control muscarinic excess

-reversible inhibitors -protect against excessive AChE inhibition --> when deatly poison is anticipated