Anticholinergic drugs work by blocking the effects of the neurotransmitter acetylcholine at muscarinic receptors in the central and peripheral nervous systems. The main anticholinergic drugs discussed are atropine, glycopyrrolate, and scopolamine. Atropine is a naturally occurring tertiary amine that can cross the blood-brain barrier and exert central effects. Glycopyrrolate is a synthetic quaternary ammonium compound that does not cross the blood-brain barrier and lacks central effects. Scopolamine is similar to atropine but is more potent and lipid soluble, allowing it to more easily cross the blood-brain barrier and exert greater central antimuscarinic effects than atrop
Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
cholingeric and Anticholinesterase drug in detail .this ppt contains introduction ,mechanism of action ,pharmacological action ,uses and adverse effect of the drug
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
2. ANTICHOLINERGIC DRUGS
Anti cholinergic drugs
Are those which antagonise the effect of neurotransmitter
Acetylcholine (ACh) on autonomic effectors & in the CNS
exerted through “Muscarinic receptors”. Though nicotinic
antagonists also block certain actions of Ach, they are
referred to as “Ganglion blockers” & “Neuromuscular
blockers”
• Muscarinic receptor site-
• Heart
• Salivary glands
• Smooth muscles of GIT
• Genitourinary tract
• Urinary bladder
3. • Nicotinic acetyl choline receptor site-
– Nerve endings of neuromuscular junction.
• Acetylcholine is also the neurotransmitter at
postganglionic nicotinic receptors located at
the NMJ (Neuromuscular junction) &
autonomic ganglia.
• Effects of anticholinergic drugs at nicotinic
cholinergic receptors is little / nil as compared
at muscarinic receptors.
• Anticholinergic drugs are considered –
selectively antimuscarinic.
4. Naturally Occurring (Tertiary Amine)
Atropine Scopolamine
(Alkaloids of belladonna plants
Synthetic compound
(Glycopyrrolate)
(Quaternery Ammoniums
Derivatives)
• More potent than parent
compounds
• Lack CNS activity because of
poor penetration in brain
7. Mechanism of action
• Anticholinergic are the class of drugs that
block the neurotransmitter acetylcholine in
CNS and PNS.
• Anticholinergic drugs combine reversibly with
muscarinic cholinergic receptors thus
preventing access of neurotransmitter
acetylcholine in these sites.
8. Muscarinic Receptor Subtypes
M1 M2 M3 M4 M5
Location • CNS
• Stomach
• Heart
• CNS
• Airway
Smooth
Muscle
• CNS
• Salivary
glands
• Airway
smooth
muscle
• Vascular
endothelial
cells
• CNS
• Heart
• CNS
Clinical Effects • Hydrogen
Ion Secretion
• Bradycardia • Salivation
• Bronchodilati
on
• Vasodilation
? ?
Clinically
selective drugs
available
Yes No No No No
9. Atropine
• Atropine sulphate is a tertiary amine & the
naturally occuring levorotatory form is active.
• Administered IV/IM in a range of 0.01-0.02
mg/kg upto adult dose of 0.4-0.6 mg.
• Larger IV doses upto 2 mg may be required to
completely block the cardiac vagal nerves in
treating severe bradycardia.
10. Pharmacological Actions
• CNS :
-Atropine has CNS stimulant action. However
these effects are not appriciable at low doses.
-Atropine stimulates many medullary centres –
vagal, respiratory, vasomotor.
- It depresses vestibular exitation and has anti-
motion sickness property.
- It supresses tremor & rigidity of parkinsonism.
- High doses cause cortical exitation, restlessness,
disorientation, hallucination & delirium followed
by respiratory depression & coma.
11. • CVS :
- Most prominent effect is to cause tachycardia
due to blockade of M2 receptors at SA node.
• Eye :
- Topical instillation of atropine causes
mydriasis, abolition of light reflex and
cycloplegia resulting in photophobia &
blurring of near vision.
12. • Smooth muscles :
- All visceral smooth muscles that receive
parasympathetic motor innervation are relaxed
by atropine due to M3 blockade.
- Tone & amplitude of contractions of stomach &
intestine are reduced, the passage of chyme is
slowed – constipation may occur & spasm may be
relieved.
- Atropine causes bronchodilatation & reduces
airway resistance especially in COPD & Asthma
patients.
- Atropine has relaxant action on ureter & urinary
bladder.
13. • Glands :
- Atropine markedly decreases sweat, salivary,
tracheobronchial & lacrimal secretions by M3
blockade.
- Skin & eyes become dry, talking & swallowing
may be difficult.
• Body temperature :
- Rise in body temperature occur at high doses due
to both inhibition of sweating as well as
stimulation of temperature regulating centre in
the hypothalamus.
- Children are highly succeptible to Atropine fever.
• Local anaesthetic : Atropine has mild anesthetic
action on the cornea.
14. • Sensitivity of different organs & tissues to
atropine varies & can be graded as –
• Saliva, sweat, bronchial secretion > eye,
bronchial muscle, heart > smooth muscle of
intestine, bladder > gastric glands & smooth
muscles.
15. Uses
• As anti-secretory :
- Pre-anesthetic medication : reduces excessive
salivation & respiratory secretions.
- Peptic ulcer : decreses gastric secretions &
provide symptomatic relief in peptic ulcer now
been superseded by H2 blockers.
• As anti-spasmodic :
- If there is no mechanical obstruction intestinal &
renal colic, abdominal cramps symptomatic relief
is affordable.
- Gastritis, gastric hypermortility.
- To relive urinary frequency & urgency.
16. • Can be given in patients of Bronchial Asthma
• As mydiatric & cycloplegic.
• As cardiac vagolytic
• For central actions in Parkinsonism as an
adjuvant to levodopa.
• To antagonise muscarinic effects of anti-
Cholinesterase i.e OP Poisoning with dose 2mg
IV with repeated doses and early mushroom
poisoning.
17. Side effects
• Belladona poisoning due to drug overdose.
• Dry mouth, difficutly in swallowing and talking.
• Dry ,flushed and hot skin.
• Fever difficulty in micturition , decreased bowel
sounds.
• Dilated pupil, photophobia, blurring of near
vision.
• Excitement, ataxia, delirium, hallucination.
• Convulsion and coma may occur in severe
poisoning.
18. • Treatment :
Physostigmine 15- 60 micro gram / kg IV every
1- 2 hourly.
• Contraindications :
- Narrow angle glaucoma
- BPH
- Hyperthyroidism
- CAD
19. Glycopyrolate
• Glycopyrolate is a synthetic product that differs from
atropine in being a quaternary amine.
• The pre-medication dose is 0.005 – 0.01 mg/kg upto 0.2-0.3
mg in adults.
• Clinical consideration :
• Because of its quaternary structure, glycopyrolate can’t
cross BBB & is almost devoid of CNS & Opthalmic activity.
• Potent inhibition of salivary gland & respiratory tract
secretions is the primary rationale for using glycopyrolate
as pre-medication.
• Heart rate increases after IV administration.
• It has longer duration of action than atropine sulphate i.e 2-
4 hrs.
20. Scopolamine
• Scopolamine is a naturally occuring tertiary amine.
• It’s dose is 0.3-0.5 micro gram I/M.
• Clinical Consideration :
• Lipid soluble.
• Easy penetrate BBB.
• More potent antisialagogue than Atropine & causes
greater CNS effects
• Clinical doses results in restlessness, drowsiness,
amnesia, dizziness & delirium.
• It has the added virtue of preventing motion sickness.
• The lipid solubility allows trans-dermal absorption &
has been used to prevent post-operative nausea &
vomiting
• Best avoided in patients with closed angle glaucoma.
21. Differences
Atropine Glycopyrrolate
1. Lipid solubility - Lipid soluble - Poorly soluble (Quaternary
ammonium compound)
2. Blood brain
barrier crossing
- Good - Minimum ability of crossing
BBB
3. Metabolization - 50% from liver -
4. Excretion - 18% unchanged - 80% unchanged
5. Treatment - bradycardia at low dose
- 0.2 – 0.4 mg IV
-Dose for intra operative
bradycardia
1.2 mg
-Max dose for bradycardia
3 mg
Hiccups (Occurring after
laryngeal mask placement)
Intra operative bradycardia
22. Differences
Atropine Glycopyrrolate
7. Effect on smooth
muscles
Decreases tone of smooth
muscles of biliary tract & ureter
8. Antisialagauge
effect
- Less then scopolamine More
9. T½ - 2.3 hrs Prolonged in uremic patients
1.25 hrs
24. Central Anticholinergic Syndrome
• Anticholinergic drugs like scopolamine, atropine can
enter central nervous system (CNS) and produce some
unusual symptoms which are characterized in a
syndrome which is known as central anticholinergic
syndrome.
Symptoms are -
– Restlessness
– Hallucination to somnolence
– Unconsciousness
Glycopyrrolate does not easily cross BBB & not likely
cause CACS.
25. • References :-
Stoelting’s Pharmacology & Physiology.
Morgan & Mikhail’s Clinical Anesthesiology.
KD Tripathi Essentials of Medical Pharmacology.
