Caused by Strychnine derived from Strychnos nuxvomica (Kuchila)
It is used to kill dogs, hence called Dog-buttons.
Seeds shape is concavo-convex.
It is odorless and bitter in taste.
Fatal dose: One crushed seed
Tests to identify Strychnine is.
Wenzel test
Sonenshein test
Strychnine is excitatory in action.
Important informationWetzel test is used in case of Carbon monoxide (CO) Poisoning
Active Principles
Strychnine: It is a more potent than one
Brucine: These two are alkaloids
Loganin: It is a glucoside.
Mechanism of Action
Acts on the anterior horn cell of the spinal cord (Renshaw cells)
Complete blockade of the Ventral horn of motor neurons and postganglionic receptor site.
Effects of glycine (inhibitory neurotransmitter) are inhibited in the spinal cord and brainstem.
Thus, the overall effect is excitatory.
Thus, this disease mimics the mechanisms of Tetanus.
Two phases are present
Convulsion
Convulsion phase is increased in this poisoning.
There may be 5-6 convulsions simultaneously.
Clonic convulsions are seen.
Relaxation
Normally duration of the relaxation phase is more compared to the convulsion phase.
But in this poisoning, the convulsion phase is elevated.
Cause of death is respiratory muscle spasm - Asphyxia.
Consciousness will be retained.
Differentiation between Tetanus and Strychnine poisoning
In Strychnine Poisoning
All muscles are affected at the same time.
External stimuli increase the convulsions.
In tetanus, there will be sequential muscle spasms.
Clinical Features
Tonus
Opisthotonus
Hyperextension of back.
Most characteristic feature.
Emprosthotonus
Hyperflexion of back.
Pleurothotonus
Lateral bending
Spasm
Risus Sadonicus
Spasm of facial muscles.
Tests
Wenzel test
Sonneschin test
Treatment
Avoid gastric lavage as there will be convulsions. (Gastric lavage is Contraindicated in Convulsions).
Controlling seizures
Keeping patients away from convulsion-triggering stimuli
Acidification of the urine
Antidote (to control seizures)
Phenobarbitone
Diazepam
Postmortem Findings
Rigor mortis
Mnemonic: ST Ea L
ST-Strychnine, Ea- Early, L- Long duration
Early in onset and long duration
Postmortem Caloricity
Body temperature increases after death due to increased muscle action.
Putrefaction
Rate of putrefaction is decreased.
Brain and spinal cord are to be preserved.
Important informationRate of putrefaction is decreased inMnemonic: SMCStrychnineMetallic poisoningCarbolic acid, Carbon monoxide, and Cyanide poisoning
2. Gelsemium Poisoning
It is inhibitory in action.
Cardiac Poisons
Mnemonic: Queen D O N A C
Caused by
Quinine
Digitalis
Oleander (yellow, white/pink)
Nicotina tabacum
Aconite
Cerebra odellum
1. Aconite Poisoning
It is also called blue rocket/ monks hood/ meetha zeher
Roots are conical in shape and tapered at the end with longitudinal ridges.
All parts are poisonous.
Roots and seeds are the most poisonous part.
Roots of Aconite are generally mistaken as Horseradish root
Active Principles
Aconitine
Pseudaconitine
Aconin
Mechanism of Action
Mainly acts on sodium channel (AcoNite, Na+ channel action).
Binds to voltage-dependent sodium channels and prolongs the action leading to
Excitation of sensory nerves
Sensory nerves are predominantly affected than motor nerves.
Paralyze the motor ganglia of the heart.
Respiratory center is slowed.
Tachycardia followed by Bradycardia is observed.
Cause of death is due to Cardiac arrhythmia (mostly Ventricular arrhythmia)
Hyperkalemia is also seen.
Signs and Symptoms
Tingling and numbness of mouth and throat (most characteristic symptom)
Sweet taste
Numbness and paranesthesia of face, perioral area, and progress to all over the body.
Weakness of four limbs
Twitching of muscles
Hippus sign: Alternate contraction and dilation of the pupil.
Xanthopsia: Visual illusion of yellow color around objects.
Hypotension, tachycardia, ventricular ectopic, cardiac arrhythmia with AV block
Fatal Dose: 1-2 gms of the root is fatal.
Treatment
Gastric lavage with warm saline.
Atropine for AV block.
Supportive treatment
Correction of hyperkalemia
Medicolegal Importance
Accidental poisoning by horseradish root
One of the ideal homicidal poisonings.
It mimics natural cardiac arrhythmia.
Destroyed by putrefaction.
2. Oleander Poisoning
A. Yellow Oleander
Also called Cerbera Thevetia or peela kaner.
All parts of the plant are poisonous.
Active Principles
Cerberin
Thevetin A and B
Neriifolin
B. Pink Oleander
It is termed as Nerium odorum or white oleander.
Active Principles
Oleandrin
Nerin
Folinerin
Rosagenin
Mechanism of Action of Oleander poisoning
Action is like digitalis.
Inhibition of Sodium-Potassium ATPase channel leading to
Brady/Tachycardia
AV block
Hyperkalemia
Treatment of Oleander Poisoning
Gastric lavage with warm saline
Antidote:Digibind (same as that of Digitalis)
Digibind binds to the Fab end of the antibody.
For AV block - Atropine
For hyperkalemia - Dextrose and Insulin
3. Digitalis Poisoning
Digitalis purpurea is also called purple Fox glove.
Mechanism of action
Inhibition of Sodium-potassium ATPase channel
Treatment
Treatment is same as Oleander poisoning.
4. Cerebra Odellum
Also called are Suicidal tree.
Active Principles
Cerberin
Cerebroside
Odolin
Odolotoxin
Treatment
BHIST regime
5. Nicotine
Most common substance abuse in India
Important informationMost common illicit substance in India is Cannabis
And that is everything you need to know about Spinal and Cardiac Poisons for your FMT paper. For more informative and interesting blog posts to upgrade your NEET PG preparation, download the PrepLadder App and keep following our blog.
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