Class Flashcards
(35 cards)
Enumerate the contra-indications of emesis 7
-Corrosives: for fear of perforation of esophagus or stomach.
-Coma: for fear of suffocation or aspiration pneumonia.
-Convulsions: as vomiting and patient manipulation may stimulate convulsions.
-Kerosene (volatile hydrocarbons) for fear chemical pneumonitis. Chronic poisoning.
-Cardiac and elderly patients and vascular insufficiency.
-Infants below the age of 6 months (immature gag and airway protective reflexes).
Enumerate contraindications of gastric lavage
Are the same as for emesis with exception of:
-Coma & volatile hydrocarbons —> Lavage is allowable after inserting a cuffed endotracheal tube to prevent aspiration pneumonia.
-Convulsions—► Lavage can be performed under general anesthesia.
-Cardiac dysrhythmias must be controlled before gastric lavage is initiated, as insertion of the tube may create vagal response —► cardiac at rest.
Enumerate the poisons in which activated charcoal is ineffective (poorly absorbed)
C- Cyanide and Corrosives.
H-Heavy metals (Lead, Arsenic and Mercury).
A-Alcohols.
R-Rapid onset or absorption poisons (Cyanide and Strychnine).
C-Chlorine and iodine.
O-Others insoluble in water (substances in tablet form).
A–Aliphatic and poorly adsorbed hydrocarbons (petroleum distillates).
L—Lithium
Multiple dose activated charcoal (MDAC) is indicated in poisons that:
- Show enterohepatic circulation (TCA, Digitalis and Barbiturates)
- Stick to the stomach (Salicylate).
- Slow gut motility (Barbiturates & Morphine)
Enumerate the contraindications of whole bowel irrigation 6
a. Unprotected airway or compromised airway.
b. Bowel obstruction or perforation.
c. Clinically significant GIT bleeding.
d. Intractable vomiting.
e. Unstable vital signs.
f. Signs of leakage of illicit drug packets (e.g. tachycardia, hypertension, hyperthermia in a patient who has ingested cocaine packets); surgical consult should be obtained in this circumstance.
Discuss Ion trapping
Alteration of the urine pH (Ion Trapping):
Changing PH of urine —> the poison to be ionized ->poison can’t be reabsorbed through the cells of the renal tubule, as ionized drugs are poorly absorbable through cell membranes —> increase excretion.
Alkalization of urine as in salicylates and Acidification (not used due to SE).
Indicated in severely intoxicated patients, toxic serum drug level and progressive clinical deterioration
Enumerate the types of Antidotes 6
I. Physio-mechanical Antidotes e.g. Activated charcoal
II. Chemical Antidotes
III. Physiological or pharmacological antidotes; These produce effects opposite to that of poison e.g.: Glucagon in calcium channel blockers
IV. Competitive antagonist: at receptor site: naloxone in morphine poisoning
V. Dispositional antidotes: interfere with absorption, distribution ,metabolism or excretion of the poison .
VI. Chelating agents: These substances combine with metals forming nontoxic compounds that are easily excreted in urine e.g. Deferrioxamine: used for chelation of iron.
Enumerate the anti-cholinergic toxidromes
Atropine, hyoscine
Antihistamine (diphenhydramine)
TCAs (Imipramine, amitripyline)
Phenothiazines: Chlorpromazine
Give the MOA of Atropine (also hyoscine)
Peripheral: antagonize the muscarinic action of acetylcholine.
Central: stimulation followed by depression of central nervous system.
But, Hyoscine: Peripheral action is weaker & Central action is depression of central nervous system without initial stimulation.
Give the MOA of Antihistamines (diphenhydramine)
- Antagonize effects of histamine on H1 receptor.
- Anticholinergic action
- Large diphenhydramine overdose: Prolongation of QRS (sodium channel blockade).
Give the MOA of Imipramine (TCAs)
- Neurotransmitter reuptake inhibition: Norepinephrine, Dopamine and Serotonin.
- Receptor blockade: Cholinergic, Alpha adrenergic and Histaminic receptors.
- Cardiovascular effects:
* Myocardial effects: Direct Quinidine like effect —>conduction defects and arrhythmias.
* Hypotension due to: direct myocardial depression, peripheral vasodilatation (alpha blocking) and increased capillary permeability.
Give the MOA of Amitriptyline (TCAs)
- Neurotransmitter reuptake inhibition: Norepinephrine, Dopamine and Serotonin.
- Receptor blockade: Cholinergic, Alpha adrenergic and Histaminic receptors.
- Cardiovascular effects:
* Myocardial effects: Direct Quinidine like effect —>conduction defects and arrhythmias.
* Hypotension due to: direct myocardial depression, peripheral vasodilatation (alpha blocking) and increased capillary permeability.
Give the MOA of Chlorpromazine (Phenothiazine)
- Receptor blockade: Cholinergic, Alpha adrenergic, Histamine and Dopamine receptors.
-Blockade of Dopamine receptors causes Extrapyramidal Manifestations & increased Prolactin (amenorrhea galactorrhea syndrome).
- CVS effects: the same as TCA
- CNS effects: Depression of:
- Cerebral cortex —> Coma and Seizures may occur.
- Respiratory center -> Respiratory failure.
- Chemoreceptor trigger zone (CTZ) -»Antiemetic action.
- Heat regulatory center (HRC) -> Hyperthermia or Hypothermia
Discuss the antidotes of anti-cholinergic toxidromes
Physostigmine in case of atropine & antihistamines:
- It reverses the peripheral & central anticholinergic effects.
- It is indicated in severe cases.
- It should be given under cardiac monitoring & should not be given as a constant infusion for a long time.
- It is contraindicated with wide QRS complex, bradycardia, and bowel or bladder obstruction.
Sodium bicarbonate in case of TCAs is indicated for: Conduction defects, Arrhythmias, asthma and Metabolic acidosis.
- Mechanism: Alkalinization: promotes dissociation of the tricyclic antidepressant from sodium channels. Increased plasma sodium to helps to drive sodium through sodium channels.
- Dose: IV bolus dose, followed by continuous IV infusion with dextrose) to maintain alkalinization.
Discuss the Opioid toxidromes (CNS depressants)
1- Opium contains more than 20 alkaloids such as morphine & codeine.
-Morphine is only injected & has no smell.
-Codeine is an antitussive
1- Heroin is a semisynthetic derivative of morphine, with analgesic properties superior to morphine and cough-suppressant properties superior to codeine. Heroin is 2-4 times more addictive than morphine; it is neither used medically nor manufactured legally.
2- Fentanyl, meperidine, methadone and tramadol are synthetic opioids.
Fentanyl is 25-50 times more potent than heroin and 50-100 times more potent than morphine.
Discuss the MOA of Opioid toxidromes
They exert their effects by interacting with specific opioid receptors.
Opioids interact with [mu, kappa and delta receptors] causing a mixture of stimulations and depressions but mainly depressions.
Tramadol binds to μ-opioid receptors only. It also inhibits the reuptake of noradrenaline and serotonin
CNS manifestations of opioid poisoning
-The patient feels euphoria (sense of well being and relief of pains) due to depression of Sensory cortex followed by dysphoria (distress, anxiety and fear).
- Gradual deterioration of consciousness (drowsy, stupor then comatose) due to depression of Consciousness.
-Cyanosis due to depression of respiratory center.
- Circulatory collapse due to depression of vasomotor center.
-Vomiting due to stimulation of vomiting center.
-The pupils are constricted pin pointed pupil (ppp) and non- reactive due to stimulation of Pupillo-constrictor center.
Discuss the CVS, respiratory and gastrointestinal manifestations of opioid poisoning
CVS: slow full pulse due to vagal center stimulation
Respiratory: Non-cardiogenic pulmonary edema and slow deep respirations due to stimulation of vagal center
GIT: constipation and diminished bowel sounds
Discuss the treatment of Opioid poisoning
- Supportive measures: ABCs
- GIT decontamination: Gastric lavage Using cuffed endotracheal tube even if alert (rapid CNS depression), and Even in case of injected morphine (morphine is re-excreted in the stomach). Local charcoal also for adsorption
- Antidote:
-Atropine blocks vagal stimulation and increase HR.
-Naloxone (Narcan): reverses respiratory depression
-Nalmefene: new opioid antagonist
-Naltrexone: used in opioid addiction treatment - Symptomatic treatment
- Elimination of poison from blood: Hemodialysis is ineffective due to high volume of distribution
Give the MOA of Sedative hypnotic toxidromes (CNS depressants); Barbituates like phenobarbital and Benzodiazepines like diazepam
Both act by enhancing the binding of y-aminobutyric acid (GABA) to GABA receptors. GABA receptors inhibit post-synaptic nerve impulse transmission.
Barbiturates causing GABA dependent chloride-channels to stay open for a longer period of time,
benzodiazepines causing chloride- channels to open more frequently.
Give the clinical CNS manifestations of Sedative hypnotic toxidromes (CNS depressants); Barbituates like phenobarbital and Benzodiazepines like diazepam
- CNS manifestations: Confusion, memory deficit, poor judgment, vertigo, slurred speech, and ataxia.
-Mild drowsiness up to coma.
-Barbiturates coma characterized by being deep & prolonged, with slow weak pulse, slow shallow respiration, hypotension and hypothermia, Muscle flaccidity with diminished reflexes and may end in respiratory failure (central asphyxia).
-Benzodiazepines coma is Low-grade coma (in most comatose patients arousal occurs within 12-36 hrs. following an acute overdose).
Give the CVS, Respiratory system, skin and renal manifestations of sedative hypnotic toxidromes (CNS depressants); Barbituates like phenobarbital and Benzodiazepines like diazepam
- CVS manifestations: Hypotension due to direct myocardial depression & vasodilatation.
- Respiratory manifestations:
* R.C. depression (in barbiturates only) which results in hypoventilation & apnea.
* Pneumonia (in barbiturates only) which may occur due to:
–Prolonged coma.
–Inhibition of the protective reflexes (cough reflex).
–Aspiration pneumonia following vomiting of gastric contents.
- Non-cardiogenic pulmonary edema in (barbiturates only): In rare cases respiratory arrest may occur following rapid IV administration in benzodiazepines.
- Skin manifestations: Blisters “bullae” over pressure points.
- Renal manifestations in barbiturates only:
Renal failure due to:
* Hypotension —► decreased perfusion.
* Rhabdomyolysis (due to prolonged coma).
Investigations in barbiturate and diazepam poising
- Routine investigations:
- Renal function test in cases of barbiturates: Acute renal failure. - Toxicological screen.
- CPK in cases of barbiturates: high (due to rhabdomyolysis).
- Chest X-ray in cases of barbiturates: pneumonia and non- cardiogenic pulmonary edema.
Discuss the treatment of sedative hypnotic toxidromes (CNS depressants) poisoning
- Supportive treatment: ABC.
- GIT decontamination: Emesis: not recommended since rapid neurologic deterioration is known to occur.
*Gastric Lavage: with cuffed endotracheal tube up to several hours after the overdose due to decreased GIT motility.
*Activated charcoal.
* MDAC: in phenobarbital toxicity only (enterohepatic circulation). - Elimination of the poison from blood:
* Forced alkaline diuresis: for long acting barbiturates only
* Hemodialysis and hemoperfusion have been successfully utilized in all types of barbiturate overdoses (most effective for long-acting barbiturates)
* Hemodialysis and hemoperfusion are ineffective in benzodiazepines
*Charcoal hemoperfusion is more effective than hemodialysis only in barbiturates. - Symptomatic treatment:
- Antidote: Flumazenil (Anexate) in benzodiazepines only:
*Action: Flumazenil is a competitive BZ receptor antagonist.
* Dose: IV, over 30 sec, may be repeated at 1-min. interval up to a maximum total dose of 3 mg.
