This document discusses cholinergic agonists and their mechanisms of action. It describes how acetylcholine is synthesized and metabolized by cholinesterase. It outlines the two main types of cholinergic receptors - muscarinic and nicotinic receptors. Muscarinic receptors have subtypes that mediate various effects in the heart, blood vessels, smooth muscles and exocrine glands. Nicotinic receptors are located at autonomic ganglia and the neuromuscular junction. Some cholinergic drugs like pilocarpine are used clinically for their effects on muscarinic receptors in the eye.
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.
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.
cholingeric and Anticholinesterase drug in detail .this ppt contains introduction ,mechanism of action ,pharmacological action ,uses and adverse effect of the drug
Acetylcholine (ACh):- is an organic chemical that functions in the brain
and body of many types of animals, including humans, as a
neurotransmitter—a chemical released by nerve cells to send signals
to other cells.Its name is derived from its chemical structure: it is an
ester of acetic acid and choline. Parts in the body that use or are
affected by acetylcholine are referred to as cholinergic.
Acetylcholine is the neurotransmitter used at the neuromuscular
junction—in other words, it is the chemical that motor neurons of
the nervous system release in order to activate muscles.
.Acetylcholine is also used as a neurotransmitter in the autonomic
nervous system, both as an internal transmitter for the sympathetic
nervous system and as the final product released by the
parasympathetic nervous system.
introduction ,classification of cholinergic receptor ,and its function ,anti cholinergic agents -atropine and its pharmacology ,semi synthetic and synthetic atropine substitutes
cholingeric and Anticholinesterase drug in detail .this ppt contains introduction ,mechanism of action ,pharmacological action ,uses and adverse effect of the drug
Acetylcholine (ACh):- is an organic chemical that functions in the brain
and body of many types of animals, including humans, as a
neurotransmitter—a chemical released by nerve cells to send signals
to other cells.Its name is derived from its chemical structure: it is an
ester of acetic acid and choline. Parts in the body that use or are
affected by acetylcholine are referred to as cholinergic.
Acetylcholine is the neurotransmitter used at the neuromuscular
junction—in other words, it is the chemical that motor neurons of
the nervous system release in order to activate muscles.
.Acetylcholine is also used as a neurotransmitter in the autonomic
nervous system, both as an internal transmitter for the sympathetic
nervous system and as the final product released by the
parasympathetic nervous system.
introduction ,classification of cholinergic receptor ,and its function ,anti cholinergic agents -atropine and its pharmacology ,semi synthetic and synthetic atropine substitutes
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
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.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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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.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
11. Cholinesterase enzyme -Types
• A specific (Acetylcholinesterase—AChE or true cholinesterase) and a
nonspecific (Butyrylcholinesterase—BuChE or pseudocholinesterase)
type of enzyme occurs in the body.
12.
13. Botulinum toxin
• Botulinum toxin A and B
are highly potent exotoxins
produced by Clostridium
botulinum.
• These neurotoxic proteins
cause long-lasting loss of
cholinergic transmission by
interacting with axonal
proteins involved in
exocytotic release of ACh.
14. Botulinum toxin
• Localized injection of minute quantity of botulinum toxin A (BOTOX)
can be used in the treatment of a number of spastic and other
neurological conditions due to overactivity of cholinergic
nerves, like blepharospasm, spastic cerebral palsy, strabismus,
spasmodic torticollis.
• It is increasing being employed as beauty treatment by removal of age-
related facial wrinkles.
15. Cholinoceptors
• Two classes of receptors for
ACh are recognized.
• Muscarinic- G protein coupled
receptor.
• Nicotinic- ligand gated cation
channel.
16. 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 and glands of gastrointestinal,
respiratory and urinary tracts, sweat glands, etc. and in the CNS.
17. Subtypes of Muscarinic Receptor
• Muscarinic receptors have been divided into 5 subtypes: M1, M2, M3,
M4 and M5.
• The first 3 are the major subtypes that are present on effector cells as
well as on prejunctional nerve endings, and are expressed both in
peripheral organs as well as in the CNS.
• The M4 and M5 receptors are present mainly on nerve endings in
certain areas of the brain and regulate the release of other
neurotransmitters.
18.
19.
20. Nicotinic Receptor
• Location- Autonomic Ganglia(NN) and
Neuromuscular Junction(NM).
• These receptors are selectively activated by
nicotine and blocked by tubocurarine or
hexamethonium.
• They are rosette-like pentameric structures which
enclose a ligand gated cation channel: their
activation causes opening of the channel and
rapid flow of cations resulting in depolarization
and an action potential.
23. CHOLINERGIC DRUGS
(Cholinomimetic, Parasympathomimetic)
• These are drugs which produce actions similar to that of ACh, either by
• Directly interacting with cholinergic receptors (cholinergic agonists) or
• By increasing availability of ACh at these sites (anticholinesterases).
• Directly acting
• Indirectly acting- Anticholinesterases (eg. Physostigmine, Neostigmine etc).
24. ACTIONS (of ACh as prototype)
• A. Muscarinic actions
• 1. Heart
• ACh hyperpolarizes the SA nodal cells and decreases their rate of
diastolic depolarization. As a result, rate of impulse generation
is reduced—bradycardia or even cardiac arrest may occur.
• At the A-V node and His-Purkinje fibres refractory period (RP) is
increased and conduction is slowed: P-R interval increases and partial
to complete A-V block may be produced.
• The cardiac muscarinic receptors are of the M2 subtype.
25. ACTIONS (of ACh as prototype)
• 2. Blood vessels
• Muscarinic (M3) receptors are
present on vascular endothelial
cells: vasodilatation is primarily
mediated through the release of
an endothelium dependent
relaxing factor (EDRF) which is
nitric oxide (NO).
26. ACTIONS (of ACh as prototype)
• 3. Smooth muscle
• Smooth muscle in most organs is contracted (mainly through M3 receptors).
• GIT-Tone and peristalsis in the gastrointestinal tract is increased and sphincters
relax---abdominal cramps and evacuation of bowel.
• Genitourinary tract-Peristalsis in ureter is increased. The detrusor muscle
contracts while the bladder trigone and sphincter relaxes --- voiding of bladder.
• Respiratory system-Bronchial muscles constrict, asthmatics are highly sensitive -
-- bronchospasm, dyspnoea, precipitation of an attack of bronchial asthma.
27. ACTIONS (of ACh as prototype)
• 4. Exocrine Glands
• Secretion from all parasympathetically innervated glands is increased
via M3 receptors:
• sweating,
• salivation,
• lacrimation,
• increased tracheobronchial and gastric secretion.
28. ACTIONS (of ACh as prototype)
• 5. Eye
• Contraction of ciliary muscle--- spasm
of accommodation, increased outflow
of aqueous humour ,
• Reduction in intraocular tension
(especially in glaucomatous patients).
30. ACTIONS (of ACh as prototype)
• 5. Eye
• Contraction of circular muscle of iris---Miosis.
31. ACTIONS (of ACh as prototype)
• B. Nicotinic actions
1. Autonomic ganglia
• Both sympathetic and parasympathetic ganglia 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
catecholamines.
32. ACTIONS (of ACh as prototype)
• B. Nicotinic actions
• 2. Skeletal muscles
• Acetylcholine released from nerve endings stimulates NM receptors
resulting in skeletal muscle contraction
• But i.v. injection is generally without any effect (due to rapid
hydrolysis of ACh).
33.
34. • Interactions
• Anticholinesterases potentiate Acetylcholine markedly.
• Atropine and its congeners competitively antagonize muscarinic
actions.
35. Choline esters-Uses
• Choline esters are rarely, if ever, clinically used.
• ACh is not used because of transient and nonselective action.
36. Choline esters-Uses
• Bethanechol
• Used in postoperative/postpartum nonobstructive urinary retention,
neurogenic bladder to promote urination.
• Side effects are prominent: belching, colic, involuntary
urination/defecation, flushing, sweating, fall in BP, bronchospasm.
37. Choline esters-Uses
• Methacoline
• Can be administered by inhalation for the diagnosis of bronchial
airway hyperreactivity.
• Fall in FEV1 by 20% is suggestive of Bronchial Asthma.
39. Pilocarpine
• Applied to the eye, it penetrates cornea and promptly causes miosis,
ciliary muscle contraction and fall in intraocular tension lasting 4–8
hours.
• Pilocarpine is used only in the eye as 0.5–4% drops.
• It is a third-line drug in open angle glaucoma.
• An initial stinging sensation in the eye and painful spasm of
accommodation(due to contraction of ciliary muscle) are frequent side
effects.
43. Pilocarpine
• Other uses as a miotic are—
• to counteract mydriatics after
they have been used for testing
refraction.
44. Pilocarpine
• Other uses as a miotic are—
• To prevent/break adhesions of iris
with lens or cornea by alternating it
with mydriatics.
45. 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.
46. Mushroom poisoning
• Depending on the toxic principle present in the particular species, at
least 3 types of mushroom poisoning is known.
• Muscarine type (Early mushroom poisoning)
• Hallucinogenic type
• Phalloidin type (Late mushroom poisoning)
47. Early mushroom poisoning
• Muscarine type due to Inocybe and related
species.
• Symptoms characteristic of muscarinic actions
appear within an hour of eating the mushroom,
• Symptoms- salivation, lacrimation, abdominal
colic, diarrhea, visual disturbances and
bronchospasm.
• Treatment- Atropine(1-2 mg intramuscularly
every 30 minutes).
Inocybe