Transcript cholinergic
Antidotal therapy involves antagonism
chemical inactivation of an absorbed poison
or
The pharmacodyamics of a poison can be altered by
competition at a receptor (naloxone therapy in the
setting of heroin overdose)
Physiological antidote (glucagon in the setting of
propranolol overdose)
Anti-venoms and chelating agents bind and directly
inactivate poisons
The biotransformation of a drug can also be altered
by an antidote (fomepizole will inhibit alcohol
dehydrogenase and stop the formation of toxic acid
metabolites from ethylene glycol and methanol)
Many drugs used in the supportive care of a
poisoned patient (anticonvulsants, vasoconstricting
agents, etc.) may be considered nonspecific
functional antidotes
Antidotes can significantly reduce morbidity and
mortality rates but are potentially toxic if used for
inappropriate reasons….their use requires correct
identification of a specific poisoning or syndrome
THE
IDENTIFICATION
OF
VARIOUS
TOXIC
SYNDROMES REQUIRES INTEGRATING OF DATA
PROVIDED
BY BOTH
PHYSICAL
THE VITAL SIGNS AND
EXAMINATION
TO
ELICIT
MANIFESTATIONS SPECIFIC TO AN INTOXICANT
THIS
COLLECTION
OF
MANIFESTATION
(TOXICOLOGIC SYNDROMES) MAY ASSIST IN THE
DIAGNOSIS WHEN THE AGENT IS UNKNOWN AND
MAY HELP IN ANTICIPATING MANIFESTATIONS THAT
WILL DEVELOP
CHOLINERGIC
ANTICHOLINERGIC
SYMPATHOMIMETIC
NARCOTIC
WITHDRAWAL
•
CENTRAL NERVOUS SYSTEM:
•
BRAIN
SPINAL CORD
PERIPHERAL NERVOUS SYSTEM
SOMATIC NERVOUS SYSTEM
AUTONOMIC NERVOUS SYSTEM
•
AUTONOMIC NERVOUS SYSTEM
PARASYMPATHETIC
SYMPATHETIC
CHOLINERGIC
ACETYLCHOLINE
ADRENERGIC NOREPINEPHRINE
•
AUTONOMIC NERVOUS SYSTEM
CHOLINERGIC
ACETYLCHOLINE RELEASE & BREAKDOWN
FOUND AT :
ALL AUTONOMIC GANGLIA
POSTGANGLIONIC PARASYMPATHETIC FIBERS
FEW SYMPATHETIC FIBERS - SWEAT GLANDS
NEUROMUSCULAR JUNCTION
ADRENAL MEDULLA
•
AUTONOMIC NERVOUS SYSTEM
CHOLINERGIC
RECEPTORS:
MUSCARINIC: CARDIOVASCULAR, GI,
URINARY, LUNGS
NICOTINIC: AT ALL GANGLIA,
NEUROMUSCULAR JUNCTION
•
AUTONOMIC NERVOUS SYSTEM
SYMPATHETIC ( ADRENERGIC )
NOREPINEPHRINE RELEASE & REUPTAKE AT MOST
POSTGANGLIONIC SYMPATHETIC NEURONS
RECEPTORS = 1
2 1 2 3
CHOLINERGIC
THREE WAYS TO ENHANCE CHOLINERGIC ACTIVITY:
1. CHOLINERGIC MEDICATIONS
PILOCARPINE = MIOSIS (glucoma)
BETHANECHOL = URINARY STIMULANT
2. ACETYL CHOLINESTERASE INHIBITORS:
ORGANOPHOSPHATES & CARBAMATES
3. PLANTS: AMANITA MUSCARIA (WEAK)
CLITOCYBE
DUMBELS (direct or indirect-AchEI)
DEFECATION
URINATION
MIOSIS
•ANTIDOTE: atropine /
pralidoxime
•Administer activated
charcoal orally
BRONCHOSPASM / BRADYCARDIA
EXCESSIVE SALIVATION
LACRIMATION
SEIZURES, SECRETIONS, SWEATING
THINK: ANTI AND ATROPINE
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ANTIHISTAMINES
ANTIPSYCHOTICS
ANTISPASMODICS
ANTIEMETICS
ANTIPARKINSON
TCAs
PLANTS: Atropa belladonna, JIMSON
WEED (Datura stramonium), HENBANE
(Hyoscyamus niger)
ANTICHOLINERGIC (ATROPINE,
ANTIHISTAMINES, TCA's)
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HOT AS A HARE
RED AS A BEET
DRY AS A BONE
BLIND AS A BAT
MAD AS A HATTER
The bowel and bladder lose their tone
….and the heart runs alone
ANTICHOLINERGIC
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Mydriasis
Blurred vision
Fever
Dry skin
Flushing
Ileus
Urinary retention
Tachycardia
Hypertension
Psychosis
Myoclonus
Seizures
ANTIDOTE:
physostigmine /
treat symptoms
Maintain an open airway and assist ventilation
if needed
Treat (if they occur):
Hyperthermia….external rapid cooling
Coma
Rhabdomyolysis (Hematest-positive urine or
high
serum
creatine
phosphokinase
level)…..I.V fluids, alkalinize of urine
Seizures…..benzodiazepine
A small dose of physostigmine (0.5–1 mg IV in an
adult), given to patients with severe toxicity
Precaution: can cause AV block, asystole, and
seizures, especially in patients with tricyclic
antidepressant overdose
Neostigmine,
a
peripherally
acting
cholinesterase inhibitor, may be useful in
treating anticholinergic-induced ileus
Decontamination: administer activated charcoal
orally (gastric lavage no needed)
SYMPATHOMIMETIC (COCAINE,
AMPHETAMINES)
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MYDRIASIS
TACHYCARDIA
HYPERTENSION
FEVER
SWEATING
SEIZURES
ANTIDOTE:
benzodiazepines
Alpha-adrenergic
syndrome
(phenylpropanolamine and phenylephrine)
Hypertension with reflex bradycardia
The pupils are usually dilated
Beta-adrenergic
syndrome (albuterol,
metaproterenol, theophylline, and caffeine)
Beta-2–mediated vasodilation may cause
hypotension. Tachycardia is common
NARCOTIC
Papaver somniferum
“ poppy plant”
NARCOTIC (HEROIN, METHADONE)
MIOSIS
CNS DEPRESSION
BRADYCARDIA
HYPOTENSION
HYPOVENTILATION
HYPOTHERMIA
COMA
ANTIDOTE:
naloxone
DEATH
WITHDRAWAL
WITHDRAWAL: (ALCOHOL, NARCOTICS, SEDATIVE
- HYPNOTICS, antiHTN DRUGS
• DIARRHEA
•
CRAMPS
• MYDRIASIS
•
LACRIMATION
• TACHYCARDIA
•
SEIZURES
• HYPERTENSION
•
HALLUCINATIONS
ANTIDOTE:
benzodiazepines
HYPERMETABOLIC SYNDROME
Phenol
compound,
dinitrophenol,
pentachlorophenol herbicides
CONVULSION
RESTLESSNESS
FEVER
HYPERPNEA
TACHYCARDIA
METABOLIC ACIDOSIS
TORSION–HEAD AND NECK SYNDROME:
idiosyncratic reaction with extrapyramidal manifestation
Amantadine, H1 receptor antagonist
(brompheniramine), levodopa,
phenothiazines, sertraline
DYSPHONIA
OCULOGYRIC CRISIS
RIGIDITY
TREMOR
TORTICOLLIS
CASE 5: A 22 Y.O. MALE IS BROUGHT IN BY POLICE.
DURING THE ARREST THEY SUSPECT HE
SWOLLOWED SOMETHING. THE PATIENT REFUSES TO
ANSWER YOUR QUESTIONS.
T 100.8 (38C) R 24
PULSE 130
B/P 148/98
DIALATED PUPILS, AGITATED, NO TRACK MARKS
WHAT SUBSTANCE BEST FITS?
WHY?
WHAT TREATMENT?
WHY?
SPECIFIC ANTIDOTES
Muscle relaxant
K+ channel
activator/vasodilator
Somatostatin analogue
/ inhibit insulin
Peripheral neuropathy
due to pyridoxine
depletion