This document provides an overview of the autonomic nervous system (ANS) and cholinergic system. It defines key terms like neurons, the central and peripheral nervous systems. It describes the sympathetic and parasympathetic divisions of the ANS. The document outlines the cholinergic neurotransmitter acetylcholine, its synthesis and receptors. It discusses cholinergic drugs that act as agonists or antagonists at muscarinic and nicotinic receptors. Conditions like glaucoma and myasthenia gravis are summarized. Adverse effects of cholinergic drugs and treatment of organophosphate poisoning are also covered.
This is the lecture presentation for general concept of autonomic nervous system and cholinergic drugs.
The class is intended for BNS 1st year students.
This is the lecture presentation for general concept of autonomic nervous system and cholinergic drugs.
The class is intended for BNS 1st year students.
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.
introduction ,classification of cholinergic receptor ,and its function ,anti cholinergic agents -atropine and its pharmacology ,semi synthetic and synthetic atropine substitutes
Histamine, meaning ‘tissue amine’ (histos—tissue) is almost ubiquitously present in animal tissues and in certain plants, e.g. stinging nettle. Its pharmacology was studied in detail by Dale in the beginning of the 20th century when close parallelism was noted between its actions and the manifestations of certain allergic reactions. It was implicated as a mediator of hypersensitivity phenomena and tissue injury reactions. It is now known to play important physiological roles.
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.
introduction ,classification of cholinergic receptor ,and its function ,anti cholinergic agents -atropine and its pharmacology ,semi synthetic and synthetic atropine substitutes
Histamine, meaning ‘tissue amine’ (histos—tissue) is almost ubiquitously present in animal tissues and in certain plants, e.g. stinging nettle. Its pharmacology was studied in detail by Dale in the beginning of the 20th century when close parallelism was noted between its actions and the manifestations of certain allergic reactions. It was implicated as a mediator of hypersensitivity phenomena and tissue injury reactions. It is now known to play important physiological roles.
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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).
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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
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
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the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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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.
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2. Introduction to ANS
Neurons = A cell that received & send electrical signal
over long distance.
Nervous system = Brain + Spinal Cord + Ganglia +
Receptor organ.
CNS = Brain + Spinal Cord.
PNS = Other then Brain + Spinal Cord
ANS = Heart muscles, smooth muscles.
Sympathetic nerves system = adjust stress & prepare
the body for fight or flight.
Parasympathetic nerves system = adjust stress free,
rest and digest. 2
3. Introduction to ANS Con..
Somatic = ( voluntary ) neuron association with skittle
muscle influence voluntary movement.
Involuntary nerves = that control muscles of internal
organs- heart, blood vessels, exocrine glands, lungs,
stomach, viscera
Reflex = muscles contraction in response to stretching.
Hypothalamus = control – 1. Body temperature 2.
Hunger 3. Thirst 4. Body equilibrium.
Maintains homeostasis
Endocrinal, metabolic, immunological, emotional
activities, somatomotor, Integrates sensory. 3
4. Introduction to ANS Con..
Afferent nerves = nerve that care impulse toward
CNS.
Efferent nerves = nerve that care impulse away from
CNS.
Pre-ganglionic neuron = myelinated
Post-ganglionic neurons = non-myelinated
Ganglion = junction b/w pre & postganglionic fibers.
Nerve conduction = generate nerve impulse
Nerve transmission = transfer impulse one nerve to
another nerve or muscles.
4
9. Cholinergic system
Acetylcholine is the principal NT at nm junction.
Synthesize, store, release ACh
Sites of ACh release
Ganglia: pre-ganglionic fibres of ANS (both sympathetic
& para-sympathetic)
Post-ganglionic parasympathetic nerve endings
Sweat glands
Skeletal muscles
Adrenal medulla
CNS: brain, spinal cord
9
18. Cholinomimetic Agents
i. Reversible AntiChEs
a) Tertiary
Physostigmine
Tacrine
b) Quarternary
Neostigmine
Pyridostigmine
Edrophonium
ii. Irreversible anticholinesterases
a) Organophosphates
Miotics
Dyflos (DFP)
Ecothiophate
Insecticides
Malathion (Licel), Parathion
Diazinon (Tik-20)
War gases: Sarin, Soman, Tabun
b) Carbamates: Propoxur (Bagyon)
18
B. Indirectly acting agents (ACh enhancers/amplifiers)
19. Cholinergic drugs
Chemicals that act at the same site as ACh
Mimic actions of ACh
Acetylcholine
Muscarinic actions
Heart (M2): Depress SA, reduces heart rate, force
of contraction, decrease conduction velocity
Blood vessels: relax vascular smooth muscles,
dilates blood vessels of skin & mucous membrane,
BP
19
20. Acetylcholine
Smooth muscle: tone of all other non-vascular smooth
muscles
GIT: peristalsis (M3)
Urinary bladder (M3): contract detrussor, relax trigone of
bladder, promotes voiding of urine
Bronchus (M3): contraction: Bronchospasm
Secretory glands:
Enhance secretions (GI secretions-M1)
Eye (M3): miosis (circular muscles of iris), accommodation,
drainage of aqueous humor, ciliary muscle contraction
20
22. Acetylcholine
Uses
PO: Destroyed in GIT
Not used therapeutically
Esters of ACh
Carbachol: longer DOA
Used in glaucoma
Bethanechol: hypotonia of bladder & GI smooth
muscles, post op paralytic ileus, urinary retention
Adverse effects
Diarrhea, flushing, salivation, sweating, bradycardia,
hypotension, Bronchospasm, syncope
22
24. Glaucoma
Increased IOP
Causes
Blockage of drainage of aqueous humor
Increased formation of aqueous humor
Management
Decrease formation of aqueous humor
Timolol, betaxolol, levobunolol
Adrenaline, acetazolamide, Apraclonidine, brimonidine.
Increase drainage of aq humor
Carbachol, pilocarpine, physostigmine, latanoprost
24
25. Alkaloids
Arecoline
– Chief alkaloid of areca or betel nuts
– Muscarinic & nicotinic receptors
– Enhances salivary secretion
– No therapeutic indication
Muscarine
– Quaternary amine
– Muscarinic receptors
– Found in mushrooms (Amanita muscaria)
– Small amounts edible
– Large amounts poisonous
– Effects: fall in BP, temporary pause of heart beat,
Antidote: ATROPINE
25
26. Anticholinesterases
The agents inhibiting the action of
acetylcholinesterase are called anti
acetylcholinesterase (AntiCHEs) or
Cholinesterase inhibitors
26
27. Anticholinesterases
i. Reversible AntiChEs
a) Tertiary
Physostigmine
Tacrine
b) Quarternary
Neostigmine
Pyridostigmine
Edrophonium
ii. Irreversible anticholinesterases
a) Organophosphates
Miotics
Dyflos (DFP)
Ecothiophate
Insecticides
Malathion (Licel), Parathion
Diazinon (Tik-20)
War gases: Sarin, Soman, Tabun
b) Carbamates: Propoxur (Bagyon)
27
29. • Physostigmine - only anticholinesterase capable
of crossing the blood brain barrier. Is more lipid
soluble.
• Used as an antidote for overdosage of
anticholinergics such as:
atropine, antihistamines, TCA, phenothiazines.
• Glaucoma.
• Pyridostigmine - drug of choice for patients
with Myasthenia gravis.
30. • Neostigmine - prototype anticholinesterase agent.
Used for long-term treatment of myasthenia gravis
and as an antidote for tubocurarine and other non-
depolarizing agents in surgery.
• Donepezil -
• Used in the treatment of mild to moderate
Alzheimer’s disease.
• Helps to increase or maintain memory and
learning capabilities.
31. • Cobra bite – edrophonium (prevent respiratory
paralysis.
• atropine poisoning – Physostigmine
(antogonizes both central and peripheral effects).
• Alzheimer’s Disease – Donepezil,
galantamine, tacrine, rivastigmine.
32. Myasthenia Gravis (Myo + asthenia)
Autoimmune disorder
Reduction in number of free NM
receptors
Causes: Development of
antibodies directed to Nicotinic
receptors at muscle end plate
Reduction in number by 1/3rd of NM
receptors
Structural damage to NM junction
Weakness & easy fatigability on
repeated activity, with recovery after
rest
32
33.
34. Myasthenia gravis – Treatment
Neostigmine: improve muscle contraction by allowing ACh
released fromprejunctional endings to accumulate.
Neostigmine – 15to 30mg. orally every 6 hrly
Dose frequency is Adjusted according to the response
Pyridostigmine – less frequency of dosing
35. Other drugs: Corticosteroids (prednisolone 30-60 mg
/day induces remission and 10mg daily or on
alternate days can be used for maintenance therapy. )
– immunosuppression
Inhibits production of NRantibodies .
Both azathioprine and cyclosporine also inhibitNR-
antibody synthesis by affecting T-cells.
Removal of antibodies by plasmapheresis (plasma
exchange) is another therapeutic approach.
36. Anticholinesterases
Uses
Glaucoma
Reverse effects of mydriatic
To prevent/break adhesions between iris & lens
Myasthenia gravis
Reverse effects of muscle relaxants
Post op paralytic ileus/ urinary retention
Belladona (atropine) poisoning: Physostigmine DOC
Alzheimer’s disease
36
37. Cholinergic Agents: Adverse Effects
Adverse effects are a result of overstimulation of the PNS.
Cardiovascular: – Bradycardia, hypotension, conduction
abnormalities (AV block and cardiac arrest)
CNS: – Headache, dizziness, convulsions
Gastrointestinal: – Abdominal cramps, increased
secretions, nausea, vomiting
Respiratory: Increased bronchial secretions, bronchospasm
Other: Lacrimation, sweating, salivation, miosis
37
38. Drug Adverse Effects of Cholinergic Agents
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Miosis
Salivation
Lacrimation
Urination
Bronchoconstriction
Defaecation
Decreased heart rate
39. Acute toxic effects of irreversible
cholinesterase inhibitors (OP poisoning )
• These agents are lipid soluble
• Can enter the body by the eye,skin, respiratory system and GI
tract.
• organophosphate insecticides (malathion, parathion) or nerve
gases (sarin, tabun, soman)
• These agents cause excessive cholinergic
stimulation (muscarinic) and neuromuscular blockade
40. • Cholinergic crisis occurs because the
irreversible anticholinesterase poison binds to
the enzyme acetylcholinesterase and
inactivates it.
• Thus, acetylcholine remains in cholinergic
synapses causing excessive stimulation of
muscarinic and nicotinic receptors.
41. Treatment of OP poisoning
Emergency treatment includes:
• Decontamination of clothing
• Flushing poison from skin and eyes
• Activated charcoal and lavage for GI
ingestion
• Atropine to counteract the muscarinic
effects (2mg IV every 10 min till pupil
dilates, max 50-100 mg)
42. • To relieve the neuromuscular blockade by
nicotinic effects, give pralidoxime, a
cholinesterase reactivator.
• Pralidoxime causes the anticholinesterase
poison to release the enzyme
acetylcholinesterase.
• Give Pralidoxime as soon as possible as if too
much time passes, the poison bond becomes
too strong (aging) for the pralidoxime to work.
• Other oximes- obidoxime, diacetylmonoxime
Editor's Notes
Nicotinic selectively activated by nicotine, Muscarinic muscarine (from a toxic mushroom)
Pehle Khao Phir Dil Lagao:
M1: GIT (gastric glands); M2: Heart; M3: in eye, Heart, Lungs (bronchus), bladder; M4, 5: CNS
Blood vessels DONOT have muscarinic innervation; whenever there is stimulation of M3 receptors, release of NO, that causes VD
Directly acting: on muscarinic receptors
Indirectly acting: increase the level of ACh at synapse
SC inj of Bethanechol in urine retention. Other ROA: oral
Methacholine: highly sensitive to myocardium