The document discusses the autonomic nervous system (ANS) and acetylcholine (Ach) neurotransmission. The ANS controls involuntary functions and is divided into the parasympathetic (PSN) and sympathetic (SNS) systems. Ach is the main neurotransmitter of the PSN and SNS. It binds to muscarinic and nicotinic receptors. Cholinergic drugs like anticholinesterases inhibit Ach breakdown, increasing its effects. They are used to treat conditions like myasthenia gravis but have side effects like excessive secretions. The document covers the synthesis, storage, release and effects of Ach in detail.
complete explanation with amicable pictures regarding CNS stimulants and cognitive enhancers.useful for both UG and PG students.references from different books and authors
clinical pharmacology,clinical,injections,pharmacological,what is pharmacology,lethal injection drugs,pharmacology definition,Plus review of anatomy of the ANS
cholinergic receptors definetion and classifcation to 1-nicotinic and 2-muscarinic ...and their subtybes ..... then the sites and the mechanism ... and last the drugs effect
This presentation covers an introduction to Autonomic Nervous System.. only enough to understand the actions of cholinergic and anticholinergic drugs. This presentation does not include anticholinergic drugs.
complete explanation with amicable pictures regarding CNS stimulants and cognitive enhancers.useful for both UG and PG students.references from different books and authors
clinical pharmacology,clinical,injections,pharmacological,what is pharmacology,lethal injection drugs,pharmacology definition,Plus review of anatomy of the ANS
cholinergic receptors definetion and classifcation to 1-nicotinic and 2-muscarinic ...and their subtybes ..... then the sites and the mechanism ... and last the drugs effect
This presentation covers an introduction to Autonomic Nervous System.. only enough to understand the actions of cholinergic and anticholinergic drugs. This presentation does not include anticholinergic drugs.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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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.
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
1. AUTONOMIC NERVOUS SYSTEM
•System autonomous from voluntary or conscious
control e.g. digestion, secretion of juices, pH,
temperature control, endocrine secretions,
metabolism.
•Inervation of visceral and vascular smooth
muscles of heart, exocrine and endocrine glands.
•Two types of efferents from CNS i.e. autonomic
efferents and somato motor efferents.
•Afferent neurons convey impulses from peripheral
organs to CNS for integration e.g. via vagus nerve
which convey impulses from viscera.
•Efferent neurons are divided into parasympathetic
(cholinergic), sympathetic (adrenergic) and enteric
system.
2. Basic Anatomy of ANS
• Two divisions: PSN and SNS
• Two neuron patterns: preganglionic neurons (cell bodies
in CNS), post ganglionic (cell bodies in autonomic
ganglia)
• PSN is connected to the CNS via Cranial nerves III, VII,
IX, X and the Sacral outflow
• PSN ganglia usually lie close to or within the target
organ.
• Sympathetic outflow leaves CNS in thoracic and lumbar
spinal roots.
• Sympathetic ganglia form two paravertebral chains plus
some prevertebral or midline ganglia.
• Enteric system – controls gastric motility and secretion
but receives inputs from ANS.
3. PHYSIOLOGY OF ANS
• Most of the time PSN and SNS exert opposite
effects. Net effect depends on predominant
system. SNS is associated with flight and fright
while PSN is associated with repose.
• Some organs are innerverted by only one
system e.g. spleen, sweat glands, most blood
vessels and hair follicles – adrenergic. Ciliary
muscles of the iris, adrenal medulla, exocrine
glands of stomach and pancrease – cholinergic.
• Cerebral circulation is not regulated by either
PSN, SNS – but by chemical environment and
perfusion pressure in the capillaries.
4. NEURO TRANSMISSION IN ANS
• MAIN neurotransmitters – Ach, NA
• NANC – ATP, VIP, neuropeptide, nitric oxide,
substance p, 5HT, gabba, Dopamine (principle
of co- transmission)
• Above may also be neuromodulators
• Other neuro modulators – enkephalins,
adenosine, prostaglandins, somatostatin, TRH,
GRH, CCK, ATP.
• Neuro modulators can act presynaptically as
neurotransmitters in some circumstances.
• Neuromediators e.g. cyclic Amp, cyclic GMP, the
so called second messengers.
5. Neuro chemical transmission in ANS
• Precussors – depolarization
Ca2+ - Synthesis – storage into
vesicles – post synaptic activity –
termination of action.
• Drug /Chemical intervention can occur at
any of the above steps.
6. Cholinergic Transmission
• Transmitter – Ach – (CNS, ANS)
• Cholinergic neurons release Ach and are located
as follows:-
• Post ganglionic parasympathetic nerve ending
• Post ganglionic SNS to sweat glands and hair
follicles.
• Preganglionic neurons to autonomic ganglia and
supra renal medulla.
• Somato motor nerves to skeletal muscles
• In the CNS.
• Cilia in respiratory tract and fallopian tubes
• SAN
7. Synthesis, Storage release of Acetycholine
• Precussor – choline (vit B group)
• Taken into neurons by active transport system –
Na+ choline co transporter.
• Acetyl group donated to choline by Acetyl CoA.
(via choline acetyl transferase.
• Storage of Ach into vesicles
• Release of Ach due to depolarization and influx
of Ca2+. (exocytosis)
• Post synaptic action
• Termination of action by acetyl cholinesterase in
the synaptic cleft.
• Cholinesterase enzymes are of two types, true
cholinesterase (Ach) and pseudo cholinesterase
(Butyrl cholinesterase ( Buche).
8. Effects of drugs on cholinergic
transmission
• Inhibition of choline uptake by inhibiting Na+ choline co
transporter – Hemicholinium
• Blocks storage of Ach in synaptic vesicles by preventing
active transport of Ach – Vesamicol.
• Blocks release of Ach by exocytosis – Botulinium (from
botulinium) and tetanus toxin (clostridium).
• Stimulate release of Ach from the vesicles and its
depletion – black widow spider toxin.
• Blocks effects of Ach at receptors:
• 1) Non depolarizing neuromuscular blockers –
tubocurarine
• 2) Depolarizing neuromuscular blockers -
suxamethonium
• Prevents degradation of Ach by cholinesterase i.e
anticholinesterases – neostigmine, pyridostigmine.
9. Receptors of Acetylcholine
• Muscarinic – effects produced by Ach
correspond to those of poisonous
mushroom, Amanita muscara.
• Nicotinic – effects produced by Ach on
these receptors found at autonomic
ganglia and neuromuscular junction (NMJ)
correspond to those of nicotine.
10. Muscarinic Receptors
• Stimulated by muscarine and blocked by
atropine.
• Found in autonomic effector cells of the heart,
blood vessels, eye, smooth muscles and glands
of git, respiratory, urinary tract, sweat glands,
CNS, and autonomic ganglia.
• Muscarinic receptor sub types M1 – M5 (M1,
M2, M3 major sub types)
• M1 (neural) M2 (cardiac), M3 (glandular) M4 and
M5 (CNS) – may be involved in regulating
release of other neuro transmitters.
11. Nicotinic receptors
• Nm (N1) (Neuro muscular junction) and Nn (N2)
found in autonomic ganglia, suprarenal medulla
and CNS.
• Main mechanism of action on activation is by
opening of cationic channels (Na+, K+, Ca2+
(N2) and depolarization.
• Antagonists: N1 (d-tubocurarine, α
bungarotoxin)
• - N2 (Hexamethonium
&trimethaphan)
• Main effect of activation of N1 receptors is
contraction of skeletal muscle.
• Main effect of activation of N2 receptors is
transmission of impulse in autonomic ganglia
and release of catecholamine.
• Agonists: N1, N2 – Ach, nicotine.
12. Pharmacological effects produced on
activation of muscarinic receptors
• M1 – mediates gastric secretion, relaxes
lower esophageal sphincter on vagal
stimulation. May play a role in learning,
memory and motor functions.
• M2 – Mediate vagal bradycardia
• M3 – Visceral smooth muscle contraction,
glandular secretions and vasodilation via
release of EDRF (NO)
13. Cholinergic drugs
• Also called cholinomimetics (effects equivalent to those
of Ach) or parasympathomimetics (effects same as PSN
stimulation)
Classification
• Direct acting cholinergic receptor agonist e.g choline
esters Ach, bethanecol, carbachol, methacholine
• Plant alkaloids: muscarine, nicotine, pilocarpine,
arecoline.
• Indirect acting cholinergic receptor agonists:
• Reversible cholinesterase inhibitors. Neostigmine,
physostigmine, pyridostigmine, edrophonium, donepezil,
carbamate insecticides e.g carbaryl (Sevin) propoxur
(Baygon).
• Irreversible cholinesterase inhibitors - organophosphates
(malathion, diazinon isoflurophate, echothiophate )
• Drugs that increase Ach release: cisapride,
metochlorpropamide
• Other cholinergic receptor agonists: sildenafil.
14. Summary of pharmacological effects of
Acetylcholine
Muscarinic effects:
a) Heart –
– Bradycardia via M2 receptors
– AVN and His purkinje – conduction decreases
(i.e increase PR interval)
– Force of atrial and ventricular contractions
decreases.
15. Summary of pharmacological effects of
Acetylcholine (Continued)
b) Blood vessels
Most blood vessels are not affected by cholinergic system.
• Vasodilation of some blood vessels(penile and salivary) by
inhibiting release of noradrenaline.
• Vasodilation is also caused via M3 receptors which when
activated release EDRF (NO)
• Ach stimulates M3 receptors on cavernosal vessels, releasing
NO and causing vasodilation and penile erection.
c) Smooth muscles
• Ach acts via M3 receptors, causing contraction of smooth
muscles of most organs:
• Increases in git tone and peristalysis. Relaxation of
sphincters and evacuation of bowel.
• Ureter: Contraction of detrusor muscles and relaxation of
sphincter muscles – voiding of urine.
• Bronchi – Broncho constriction. Contra indicated in
asthmatics.
16. Summary of pharmacological effects of
Acetylcholine (Continued)
d) Glands
• Increased secretion via M3 and M2 receptors leading to
sweating, salivation, lacrimation, tracheo bronchial and
gastric secretions.
• Effect on secretions from intestine, and pancrease is not
marked except for HCL
• Secretion of milk and bile not affected.
e) Eye
• Miosis due to contraction of circular muscle of iris.
• Contraction of ciliary muscle causes spasm of
accommodation, increased outflow of aqueous humour
and reduction in intraocular tension – useful in
glaucoma.
17. Pharmacological effects
continued
CNS
• I.V Ach, no crossing BBB, no effect.
• Direct injection of Ach into brain or
administration of cholinergic agonists that enter
the brain may cause tremors, hypothermia,
increased locomotor activity - all via M1
receptors.
• Selective M1 agonists are being developed to
treat dementia because they improve cognition.
18. Nicotinic effects of acetylcholine
Nicotinic effects of acetylcholine
• Stimulates sympathetic and parasympathetic
ganglia.
• At high doses, stimulate sympathetic ganglia
leading to NA release (tachycardia and BP
increase)
• Contraction of skeletal muscles by interacting
with nicotinic receptors at motor end plate.
• High doses intra arterially – twitching and
fasciculation. I.V no effect because of rapid
hydrolysis of Ach.
19. Reversible cholinesterase inhibitors
(anticholinesterases)
Reversible cholinesterase inhibitors (anticholinesterases)
• Form weak bonds with cholinesterase.
• Inhibit degradation of Ach at all cholinergic synapses; leading to its
accumulation.
• Lipid soluble agents e.g physostigmine can cross BBB causing marked
CNS effects but with less effect on NMJ. They also cause muscarinic
and ganglion stimulant effects.
• Lipid insoluble agents e.g neostigmine, edrophonium and pyridostigmine
have marked effect on skeletal muscle and ganglia but less effect on
muscarinic sites and CNS.
• Duration of action vary
– Edrophinium short acting
– Physostigmine, pyridostigmine, prostigmine, ambenonium –medium
acting.
– Demecarium – long acting.
Summary of pharmacological actions of anticholinesterases
• Stimulate ganglia via muscarinic receptors.
• High doses block nicotinic receptors and prevent neuro muscular
transmission.
20. CVS
• Bradycardia and Hypotension (muscarinic)
• Ganglia - HR increase, BP increase, higher doses
cause a decrease in heart rate and blood pressure.
• Medullary centre – stimulation followed by depression.
• Overall effect is complex and depends on agent and
dose.
Skeletal muscle
• Twitching and fasciculation due to increase in
concentration of Ach.
• Higher doses – persistent depolarization and NMJ
blockade leading to weakness and paralysis.
Glands
• Increase secretions – git, respiratory, urinary, eye.
• (Homework, pharmacokinetics of reversible ACHE)
21. Irreversible cholinesterase inhibitors
• Mainly organo phosphates, DFP, (dyflos),
Echothiophate ( therapeutically useful agents),
insecticides which include parathion, malathion,
diazinon, dimethoate and war gases e.g. tabun,
soman, sarin.
• Highly lipid soluble and are absorbed from all sites
in the body(skin, mucous membrane,CNS.)
• They form strong covalent bonds with esteratic site
of cholinesterase – long duration of action.
• Effects of organophosphate poisoning are due to
excessive Ach at muscarinic and nicotinic
receptors (see handout).mgt-
supportive,atropine.pralidoxime.
22. Therapeutic uses of cholinergic agonists.
• Ach not useful because of non selective action.
• Methacholine – paroxysmal supraventricular
tachycardia (not used any more).
• Bethanecol – post operative or post partum
urinary retention and management of
gastroesophageal reflux.
• Pilocarpine – eye drops for glaucoma.
• Physostigmine eye drops for glaucoma
• Metocholorpropamide (plasil) - blocks DA
receptors in CTZ, cholinomimetic, therefore used
in nausea and vomiting.
• Cisapride – 5HT4 agonist with cholinomimetic
action which was used in nausea and vomiting.
Has been discontinued.
23. Therapeutic uses of agonists (continued)
• Sildenafil is a phosphodiesterase inhibitor,
preventing degradation of cyclic GMP. Increase
cyclic GMP in corpus cavernosum of the penis
causes vasodilation.
• Sildenafil potentiates vasodilator action of Ach,
increasing penile blood flow and can therefore
be used in male erectile dysfunction.
• Mysthenia gravis (MG) - neostigmine and
pyridostigmine are used.
• Drugs contraindicated in myasthenia gravis
include: aminoglycosides, quinine, quinidine
• Edrophonium I.V is used for diagnosis of MG.
24. Therapeutic uses continued
• Overdose with neuromuscular blocking drugs
e.g. tubocurarine (edrophonium 10mg I.V).
• Poisoning with atropine, tricyclic antidepressants
(TCA) and antipsychotic agents –
(physostigmine is used).
• Alzheimer's disease – due to degeneration of
cholinergic neurons in CNS and loss of memory.
Treated by:
• physostigmine
• Donepezil, tacrine ,rivastigmine, galantamine
(centrally acting anticholinesterases)
• Choline – to enhance synthesis and release of
Ach
• Nootropic agents e.g Piracetam