This document discusses cholinergic pharmacology. It defines cholinergic as relating to acetylcholine, the neurotransmitter of cholinergic neurons in the parasympathetic nervous system. It describes cholinergic drugs as those that combine with acetylcholine receptors to produce similar responses. Examples include choline esters, naturally occurring alkaloids, and synthetic alkaloids. Anticholinesterase agents work by inhibiting the enzyme acetylcholinesterase and prolonging the effects of acetylcholine. The document discusses the mechanisms, actions, interactions, and uses of various cholinergic drugs.
This presentation was given by me during my M.pharm.
It contains description, classification, mechanism of actions and therapeutic uses of Neuromuscular blockers.
This presentation was given by me during my M.pharm.
It contains description, classification, mechanism of actions and therapeutic uses of Neuromuscular blockers.
Sympatholytic drugs (Adrenergic blockers) bind to the adrenergic receptors and prevent the action of adrenergic drugs.
These are drugs which block the actions of sympathetic division or catecholamines (adrenaline and noradrenaline).
They are competitive antagonists at both α and β adrenergic receptors.
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
Sympatholytic drugs (Adrenergic blockers) bind to the adrenergic receptors and prevent the action of adrenergic drugs.
These are drugs which block the actions of sympathetic division or catecholamines (adrenaline and noradrenaline).
They are competitive antagonists at both α and β adrenergic receptors.
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
cholingeric and Anticholinesterase drug in detail .this ppt contains introduction ,mechanism of action ,pharmacological action ,uses and adverse effect of the drug
The parasympathetic division typically acts in opposition to the sympathetic autonomic nervous system through negative feedback control.
This action is a complementary response, causing a balance of sympathetic and parasympathetic responses.
Overall, the parasympathetic outflow results in the conservation and restoration of energy, reduction in heart rate and blood pressure, facilitation of digestion and absorption of nutrients, and excretion of waste products.
These are drugs that produce actions similar to that of Acetylcholine hence known as parasympathomimetics.
They act either by directly interacting with cholinergic receptors or by increasing the availability of Acetylcholine at these sites.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
2. What is cholinergic ?
Choline in cholinergic refers to acetylcholine , which is the neurotransmitter
of cholinergic neuron present in the parasympathetic nervous system.
Acetylcholine is also the neurotransmitter for postganglionic nerves in the
SNS (sweet glands, blood vessel & adrenal medulla)
3. What is Cholinergic drugs
• Acetylcholine is a neurotransmitter in the parasympathetic system. Drugs that combine
with acetylcholine receptors and produce similar responses in the end organ are called
Para sympathomimetic drugs. They are also called cholinergic or cholinomimetic
drugs.
• These are examples of para sympathomimetic agent :
1) Choline ester (acetylcholine , methacholine, carbachol, bethanechol)
2) Naturally occurring cholinomimetic alkaloids (pilocarpine, muscarine, arecoline)
3) Synthetic alkaloids (areclidine and oxotremorine)
4) Anticholinesterase agent:(i) reversible a) natural (physostigmine)
b) Synthetic (neo stigmine , edrophonium, demecarium, ambenonium,
benzoquinonium)
(ii)Irreversible (a number of organophosphorus compounds used mainly as insecticides
4. Acetylcholine
• Acetylcholine is an ester of choline and acetic acid. Acetylcholine is
synthesised in cholinergic nerve endings by following pathway:
5. • Choline is actively taken up by axonal membrane and acetylated with the
help of ATP and acetyl coenzyme-A (CoA) by the cytosolic enzyme choline
acetyltransferase present in axoplasma.
• It is then stored in ionic solution within small synaptic vesicles by an active
transport process, which can be blocked by vesamicol but some free ACh is
also present in the cholinergic terminals.
• Release of ACh from nerve terminals occurs in small amounts by the
process of exocytosis. A toxic substance botulinus toxin inhibits the release
of ACh.
• Its release, the ACh diffuses across the synaptic cleft to combine with
receptors on the postsynaptic cell.
• Some of it succumbs on the way to rapid hydrolysis by two enzymes
namely acetylcholinesterase and plasma pseudo cholinesterase.
• Acetylcholinesterase is present in all the sites where acetylcholine acts and
has high specificity for acetylcholine as compared to other choline esters.
• Plasma cholinesterase is found in plasma and liver, it is non specific as it
can break down a number of drug with ester linkage.
8. Muscarinic receptors
• These receptors are selectively stimulated by muscarine and blocked by atropine.
• They are located primarily on autonomic effector cells in heart, blood vessels, eye
smooth muscles, sweet gland, gland in gastrointestinal, respiratory tract etc. and in the
CNS.
• G- protein coupled receptors.
• Divided into M1, M2, M3, M4 and M5.
• The first 3 are major subtypes that are present on effector cells as well as on
prejunctional nerve endings and both are expressed in peripheral organs as well as in
the CNS.
• M4 and M5 are present in certain area of brain and regulate the release of other
neurotransmitters.
9. • M1: The M1 is primarily a neuronal receptor located on ganglion cell and central
neurones, especially in cortex, hippocampus and corpus striatum.
• It play major role in mediating gastric secretion, relaxation of lower esophageal
sphincter(LES) on vagal stimulation and in learning, memory, motor functions,
etc.
• M2: cardiac muscarinic receptors are predominantly M2 and mediate vagal
bradycardia.
• Auto receptors on cholinergic nerve endings are also M2 subtype. Smooth
muscles express some M2 receptors as well as which, like M3 mediate
contraction.
• M3: Visceral smooth muscle contraction and glandular secretions are elicited
through M3 receptors, which mediate vasodilatation through EDRF release.
Together the M2 and M3 receptors mediate muscarinic action including
contraction of LES.
10. Nicotinic receptors
• Named after agonist nicotine.
• These receptor selectively activated by nicotine and blocked by tubocurarine or
hexamethonium. Their activation causes opening of the channel and rapid flow of
cations resulting in depolarization and action potential.
• Ligand gated ion channels.
• Divided into N1and N2
11. • N1: these are present at skeletal muscle endplate: are selectively
stimulated by phenyl trimethylammonium and blocked by
tubocurarine. They mediate skeletal muscle contraction.
• N2: these are present on ganglionic cells( sympathetic as well as
parasympathetic), adrenal medullary cell and in spinal cord and
certain area of brain.
• They are selectively stimulated by dimethyl phenyl pipierazinium
(DMPP), blocked by hexamethonium, and constitute the primary
pathway of transmission in ganglia
12. Cholinergic drugs
• These are drugs which produce action similar to the ACh, either by directly
interacting with cholinergic receptors or by increasing of availability of ACh.
• Some cholinergic agonist are acetylcholine, methacholine, carbachol, muscarine and
arecoline.
13. Actions
• Depending on the type of receptor through which it is mediated, the peripheral actions of ACh
are classified as muscarinic or nicotinic.
A. Muscarinic
• Heart : ACh hyperpolarize the SA nodal cells and decrease the rate of diastolic depolarisation. As
a result, rate of impulse generation is reduced – bradycardia or even cardiac arrest may occur.
• At the A-V node and His- Purkinje fibre refractory period(RP) is increased and conduction is
slowed: P-R interval increases and partial to complete A-V block may be produced. The force of
atrial contraction is markedly reduced and RP of atrial fibres is abbreviated.
• The cardiac muscarinic receptors are of the M2 subtype.
• Blood vessels: all blood vessels are dilated, though only few ( skin of face, neck, salivary glands)
receive cholinergic innervation.
• Muscarinic (M3) receptors are present on vascular endothelial cells: vasodilatation is mediated
through the release of an endothelium dependent relaxing factor(EDRF)which is nitric oxide.
• Stimulation of cholinergic nerves to the penis causes erection by releasing NO and dilating
cavernosal vessels through M3 receptors. This response is minimal with injected cholinergic
drugs.
14. • Smooth muscle : Smooth muscle in most organs is contracted (mainly
through M3). Tone and peristalsis in the gastrointestinal tract is
increased and sphincters relax → abdominal cramps and evacuation
of bowel.
• Peristalsis in ureter is increased. The detrusor muscle contracts while
the bladder trigone and sphincter relaxes→ voiding of bladder.
• Bronchial muscles constrict, asthmatics are highly sensitive →
dyspnoea, precipitation of an attack of bronchial asthma.
• Glands : Secretion from all parasympathetically innervated glands is
increased via M3 and M2 receptors: sweating, salivation, lacrimation,
tracheobronchial and gastric secretion.
• Secretion of milk and bile is not affected.
15. • Eye : contraction of circular muscle of iris → meiosis.
• Contraction of ciliary muscle → spasm of accommodation, increased
outflow facility, reduction in intraocular tension (especially in
glaucomatous patients).
B. Nicotinic
• Autonomic ganglia: Both sympathetic ganglia and parasympathetic are
stimulated. This effect is manifested at higher doses. High dose of ACh
given after atropine causes tachycardia and rise in BP due to stimulation of
sympathetic ganglia and release of catecholamine.
• Skeletal muscles : Iontophoretic application of ACh to muscle endplate
causes contraction of the fibre. Intra-arterial injection of high dose can
cause twitching and fasciculations, but i.v. injection is generally without any
effect(due to rapid hydrolysis of ACh).
C. CNS
• ACh injected i.v. does not penetrate blood-brain barrier and no central
effects are seen.
• Direct injection into brain, or other cholinergic drugs which enter brain,
produce a complex pattern of stimulation followed by depression.
16. Interactions
• Anticholinesterases potentiate ACh, methacholine to less extent and
have only additive action with carbachol or bethanechol, depending
upon the role of ChE in the termination of action of the particular
choline ester.
• Adrenaline is a physiological antagonist.
17. Uses
• Choline esters are rarely, if ever, clinically used.
• ACh is not used because of evanescent and non selective action.
• Methacholine was occasionally used to terminate paroxysmal
supraventricular tachycardia but is obsolete now.
• Bethanechol has been used in postoperative/postpartum non
obstructive urinary retention, neurogenic bladder, congenitalss
megacolon and gastroesophageal reflux.
18. Cholinomimetic alkaloids
• Pilocarpine : it is obtained from the leaves of pilocarpus microphyllus and
other species. It has muscarinic actions and also stimulates ganglia- mainly
through ganglionic muscarinic receptors.
• It causes sweating, salivation and increases other secretions as well.
• Small doses generally cause fall in BP, but higher doses elicit rise in BP and
tachycardia which is probably due to ganglionic stimulation (through
ganglionic muscarinic receptors).
• In the eyes, it penetrates cornea and causes miosis, ciliary muscle
contraction and fall in intraocular tension lasting 4-8 hours.
• Pilocarpine is used only in the eye as 0.5-1% drops.
• Muscarine : it occurs in poisonous mushrooms Amanita muscaria and
Inocybe species and has only muscarinic actions it is not used
therapeutically but is of toxicological importance.
• Muscarine ix non selective agonist of the muscarinic acetylcholine receptor.
19. • Mushroom poisoning : refers to harmful effects from ingestion of toxic
substances present in mushroom. Amanita phalloides account for major
cause of mushroom poisoning. Three type of poisoning is known.
1. Muscarinic type(early mushroom poisoning) :this is due to Inocybe and
related species.
2. Hallucinogenic type: hallucinogenic mushroom toxicity is caused by
ingestion of fungi containing ibotenic acid, muscimol, psilocybin. These
compound activate amino acid receptors and block muscarinic receptors
in the brain and show hallucinogenic property.
3. Phalloidin type( late mushroom poisoning):it is due to peptide toxins
found in A. phalloids, Galerina species. These inhibit RNA and protein
synthesis.
Arecoline : it is found in betel nut Areca catechu and has muscarinic as well
as nicotinic actions. It has prominent CNS effect: has been tried in dementia
as an enhancer of cognitive functions, but not found useful- has no
therapeutic use.
20. Specific examples of cholinergic
drugs
o Direct – acting
• Bethanechol (urecholine) – raise the tone &motility of the bladder &Gl tract (should cause
urination with in 60 minutes in a pt. with urinary retention)
• Pilocarpine (pilocar) – used to constrict pupil, which lower intraocular pressure (glaucoma)
o Indirect – acting
• Neostigmine (prostigmin) – given for the diagnosis & treatment of myasthenia gravis – it
causes skeletal muscle contractions
• Donepezil (Aricept ) – used to treat mild – moderate Alzheimer’s disease- it raise ACh in the
brain &helps raise or maintain memory or learning capabilities (manages the symptoms , it
is not a cure)
21. Anticholinesterases
• Anticholinesterase are agent which inhibit ChE, protect ACh from
hydrolysis – produce cholinergic effects in vivo and potentiate ACh both
in in vivo and in vitro.
Classification :
A) Cholinesterase inhibitors or reversible anticholinesterase :
• carbamates
1. Natural :Physostigmine
2. Synthetic : Neostigmine, Pyridostigmine, Edrophonium, Rivastigmine,
Donepezil, Galantamine
3. Acridine: tacrine
23. AChEs – Chemistry
• Anti-ChEs are either esters of Carbamic acid or derivative of
phosphoric acid.
• Carbamates : R1- non popular tertiary amino N, e.g.
physostigmine(lipid soluble); other – R1 quaternary amino N+ (lipid
insoluble)
• Organophosphates: All are highly lipid soluble except ecothiophate.
24. Mechanism of action
• Normally acetylcholinesterase (AchE) hydrolyses acetylcholine
• The active sites of AchE is made up of two subsites – anionic and
esteratic
• The anionic site serve to bid a molecule pf ACh to the enzyme.
• Once the ACh is bound, the hydrolytic reaction occurs at a second
region of the active site called the esteratic subsite.
• The AChE itself gets acetylated at serine site
• Acetylated enzyme react +water = acetic acid and choline
• Choline immediately taken up by the high affinity choline uptake
system presynaptic membrane
25. • Anticholinesterases also react with the enzyme ChEs in similar fashion like Acetylcholine
• Carbamates – carbamylate the active site of the enzyme
• Phosphates – phosphorylate the enzyme
• Both react similar fashion covalently with serine
• Carbamylated (reversible inhibitor ) react with water slowly and the esteractic site is
freed and ready for action – 30 minutes(less than synthesis of fresh enzyme)
• But, phosphorylated (irreversible ) react extremely slowly or not at all – takes more time
than synthesis of fresh enzyme
- sometime phosphorylated enzyme losses one alkyl group and become resistant to
hydrolysis
• Edrophonium and tacrine react only at anionic site – short acting while
organophosphates react only at esteratic site.
26. Pharmacological actions
• Ganglia : anti- ChEs stimulate ganglia primarily through muscarinic receptors
present there
• High doses cause persistent depolarisation of the ganglionic nicotinic receptors
and blockage of transmission.
• CVS: cardiovascular effect are complex. Where as muscarinic action would
produce bradycardia and hypertension, ganglionic stimulation would tend to
increase heart rate and BP.
• action on medullary centres (stimulation followed by depression)
• The overall effect are often unpredictable and on the agent and its doses.
• Skeletal muscle: after treatment with anti- ChEs, the Ach released by a single
nerve impulse is not immediately destroyed- rebinds to the same receptors
• Activates prejunctional fibres→ repetitive firing → twitching and fasciculations.
• Increases force of contraction in muscle
• Higher doses cause persistent depolarization of endplate resulting in blockade of
neuromuscular transmission→ weakness and paralysis.
27. Pharmacokinetics
• Physostigmine: It is rapidly absorbed from g.i.t. and parenteral sites.
Applied to the eye , it penetrates cornea freely. It crosses blood brain
barrier and is disposed after hydrolysis by Che.
• Neostigmine and congeners : these are poorly absorbed orally. They
don’t effectively penetrate cornea or cross blood brain barrier. They
are partially hydrolysed and partially excreted unchanged.
• Organophosphates : these are absorbed from all sites including intact
skin and lungs. They are hydrolysed as well as oxidized in the body.
28. Uses
• Physostigmine
1. Used as miotic drops to decrease IOP in Glaucoma.
2. To antagonize mydriatic effect of atropine
3. To break adhesions between iris and cornea alternating with mydriatic drop
4. In Belladonna poisoning &Phenothiazine poisoning
5. Alzheimer’s disease
6. Atropine is antidote in physostigimine poisoning.
• Neostigmine
1. Used in treatment of Myasthenia Gravis to increase muscle strength
2. Post – operative reversal of neuromuscular blockade
3. In gastric atony paralytic ileus, urinary bladder atony
4. Cobra snake bite
5. Produces twitchings & fasciculations of muscle leading to weakness
29. • Myasthenia gravis : Myasthenia gravis is an autoimmune disorder affecting 1 in
10000 population – reduction in number of N1 receptor
• Structural damage to the neuromuscular junction – weakness and easy
fatigability on repeated activity, with recovery after rest.
• Neostigmine and its congeners improve muscle contraction by allowing ACh
released from prejunctional endings to accumulate and act on receptors over a
larger area and by directly depolarizing the endplate.
• Treatment is usually started with neostigmine -15 to 30 mg orally every 6 hourly.
Adjusted according to the response.
• Myasthenic crisis : acute weakness of respiratory muscles
• It is manged by the tracheobronchial intubation and mechanical ventilation.
• Generally, i.v. methylprednisolone pulse therapy is given while anti- ChEs are
withheld for 2-3 days followed by their gradual reintroduction.
• Thymectomy produces gradual improvement in majority cases.
• Overtreatment with anti-ChEs also produces weakness by causing persistent
depolarization of muscle endplate.
30. Diagnostic test for myasthenia gravis
A. Ameliorative test: edrophonium 2-10 mg injected slowly i.v.
improves muscle strength.
B. Provocative test myasthenics are highly sensitive to d- tubocurarine;
0.5 mg i.v. causes weakness in them but is ineffective in non
myasthenics. This is test hazardous: for positive pressure respiration
must be at hand before performing
31. Anticholinesterase poisoning
• AChEs are easily available and extensively used as agricultural and
household insecticide and homicidal poisoning
• Complex effect – Muscarinic , nicotinic and CNS actions.
• Sign and symptoms:
1. Irritation in eye, lacrimation, salivation, tracheo-bronchial secretion,
blurring of vision, defecation and urination.
2. Fall in BP, tachy or bradycardia and CVS collapse
3. Muscular fasciculations, weakness and respiratory paralysis
4. Irritability, disorientation, ataxia, convulsions and coma.
32. Treatment
• Termination of exposure to the poison – fresh air wash the skin and gastric lavage according to
need.
• Maintain patent airway, positive pressure respiration if it is failing.
• Supportive measures – maintain BP, control of convulsions with judicious use of diazepam.
• Specific antidote- Atropine – 2mg i.v. every 10 minutes till dryness of mouth or atropinisation( up
to 200mg/kg)
• Cholinesterase reactivators – oximes:
• Pralidoxime (2-PAM) and Obidoxime Diacetyl monoxime (DAM)
• Oximes have generic formula R-CH=N-OH
• Provides reactive group OH to the enzyme to reactivate the phosphorylated enzymes – million
times faster.
• PAM has quaternary nitrogen of PAM gets attaches to anionic site of the enzyme and react with
phosphorus atom at esteratic site
• Forms Oxime- phosphonate complex making esteratic site free
• No effective in Carbamate poisoning
• Dose : 1-2 gm i.v. slowly maximum 12 gms/24 hrs and 20-30 hrs mg/kg/hrs continuous i.v.
infusion.