Clinical Trials Flashcards
What are the statistics on self-poisoning in rural Asia?
Currently kills around 150,000 people are year
WHO: most important global means of suicide
Why did suicide rates in rural Asia rise in the 1970s-1990s?
During the green revolution when pesticides and fertilisers became commonplace
How was the rapid increase in suicide rates in rural Asia managed?
All class I pesticides were banned in 1995.
Engineering contols
What were solutions to due to high rates of suicide in rural Asia due to pesticides?
Improving medical care
Administrative controls- moving pesticides to safer storage
Engineering controls- banning harmful pesticides
What were the conclusions drawn from a RCT looking at containing pesticides within a locked container?
53,379 households recruited in a community based cluster RCT?
Each village was randomised to receive a container or not and followed for at least 3 years looking at all cases of self harm.
Similar rates of suicide within control and intervention arms with a large confidence interval interval
Concluded boxes were novel and not used long term
What is OP insecticide poisoning and how does it cause effects?
Organophosphate insecticide
Inhibits acetylcholinerestease which recycles ACh
Indigestion causes massive overstimulation of cholinergic receptors- causes fluid overload, foaming and drowning
The neuromuscular junction also stops working and get a range of symptoms including breathing failure, cardiovascular and digestion problems, convulsions and loss of consciousness
Why was there large variation in time between poisoning and death in OP insecticide poisoning patients?
This was partly because there was different types of long and short acting pesticides
What new treatment was tested on OP insectiside poison patients and why was this stopped?
- A new treatment tested out was charcoal- it absorbs the drug in the stomach before it is digested and enters the body
- However whether drinking activated charcoal benefited poisoned patients had inconclusive results
- Trial stopped after the death of a patient and local media outrage
What were two antidotes that could be given to patients suffering from OP insecticide poisoning?
Atropine, a muscarinic antagonist
Praildoxime, which reactivates acetylcholinesterase
Why can fluid eventually come out of the mouth after OP insecticide poisoning?
Excess ACh stimulates the bronchial and cholinergic receptors, causing airway secretions and bronchoconstriction
- Fluid passes down the airways, into the alveoli, reducing oxygen exchange
- Fluid eventually comes out of the mouth
What was the only problem with using atropine in OP insecticide poisoning and what was a potential solution?
Atropine turns off fluid production but does not increase its removal.
Addition of salbutamol stimulates sodium channels to remove water via salt removal
What were the results of the salbutamol and atropine RCT to treat OP insecticide poisoning?
Performed in Bangladesh
Comparing 2.5 and 5mg salbutamol nebulised against a saline placebo nebulised in addition to atropine and oxygen
Looked at oxygen saturations
Salbutamol had no effect- may be due to the fact it was nebulised but because of the fluid accumulation it may not even reach receptors
Was pralidoxime useful in treating OP insecticide poisoning?
Oximes reactive acetylcholinesterase
WHO expert guidance recommended high dose oximes
However it was later found the drug did not work and caused respiratory failure
What was causing the hyperlactaemia in dimethorate poisoning?
Lactate rises due to lack of aerobic respiration
Alot of trials unsuccessfully helped with ths issue
This was because they were looking at the wrong substance- it was cylohexane the solvent the pesticide was dissolved in that caused hyperlactaemia
What is rocuronium?
A nicotnic antagonist
