This document discusses nervous system agents called adrenergic agonists and antagonists, as well as cholinergic agonists and anticholinergics. It describes their mechanisms of action, effects, indications, pharmacokinetics, contraindications and cautions. Adrenergic agonists bind to adrenergic receptors to mimic epinephrine. They increase heart rate, contractility and blood pressure. Alpha-specific agonists primarily bind to alpha receptors. Beta-specific agonists primarily bind to beta receptors and are used for bronchodilation. Adrenergic antagonists competitively block adrenergic receptors. Cholinergic agonists mimic acetylcholine to stimulate muscarinic receptors and
This presentation was delivered over two days to second year pharmacy students enrolled in a course in pharmacology & toxicology. This lecture is designed to accompany Goodman & Gilman's (12e) chapter 11.
This presentation contains drugs which blocks the adrenergic system e.g receptor blockers like alpha and beta receptor antagonists, adrenergic neuron blocking agents in details.various animated pictures are also included to make the presentation interesting as well as i have used various diagrams and tables to have better understanding of the topic. Thank you.
A power point presentation on "Drugs affecting coagulation and anticoagulants" suitable for undergraduate medical students. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
This presentation was delivered over two days to second year pharmacy students enrolled in a course in pharmacology & toxicology. This lecture is designed to accompany Goodman & Gilman's (12e) chapter 11.
This presentation contains drugs which blocks the adrenergic system e.g receptor blockers like alpha and beta receptor antagonists, adrenergic neuron blocking agents in details.various animated pictures are also included to make the presentation interesting as well as i have used various diagrams and tables to have better understanding of the topic. Thank you.
A power point presentation on "Drugs affecting coagulation and anticoagulants" suitable for undergraduate medical students. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
Serotonin is major neurotransmitter and affects the physiology of our body. Serotonin antagonists are used in various pathological conditions of body. This is a small presentation showing feature of serotonin.
Adrenoceptors are membrane bound receptors located throughout the body on neuronal and non-neuronal tissues where they mediate a diverse range of responses to the endogenous catecholamines- noradrenaline and adrenaline.
They are G protein coupled receptors.
Binding of catecholamine to the receptor is responsible for fight or flight response.
Serotonin is major neurotransmitter and affects the physiology of our body. Serotonin antagonists are used in various pathological conditions of body. This is a small presentation showing feature of serotonin.
Adrenoceptors are membrane bound receptors located throughout the body on neuronal and non-neuronal tissues where they mediate a diverse range of responses to the endogenous catecholamines- noradrenaline and adrenaline.
They are G protein coupled receptors.
Binding of catecholamine to the receptor is responsible for fight or flight response.
Brief description of all vasoactive peptides with their synthesis, receptors on which they act and mode of action along with their agonist or antagonists. Also including their effects on human body.
About pharmacological classification of sympathetic nervus system both sympathomimetics and sympatholytics drug and all about his pharmacokinetics and pharmacodynamics action on body
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
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.
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
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.
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- 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
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. ADRENERGIC AGONISTS
• Drugs that has effects similar to epinephrine
(adrenaline)
• Sympathomimetic agent
MECHANISM OF ACTION
1. Bind to receptors directly
– Bind to receptors and copy actions of natural transmitters
(catecholamine)
2
4. ADRENERGIC AGONISTS
2. Promote release of norepinephrine
– By acting on sympathetic nervous system to release
norepinephrine
– Ex that promote receptor activation = amphetamine &
ephedrine
4
5. 3. Inhibit norepinephrine uptake
– Results in accumulation of
norepinephrine in the synaptic
cleft and ↑activation of
receptors
5
6. ADRENERGIC AGONISTS
4. Inhibit activation of epinephrine
– Drugs inhibit monoamine oxidase to make more
epinephrine available for release
6
7. ADRENERGIC AGONISTS
• EFFECTS OF ADRENERGICS AT RECEPTORS
1. Alpha 1
– Located in vascular tissues & smooth muscles
2. Alpha 2
– Located in sympathetic nerve endings
3. Beta 1 receptor
– Primarily in the heart
4. Beta 2
– Smooth muscles of lungs
– Arterioles of skeletal muscles
– Uterine muscle
7
8. ADRENERGIC AGONISTS
1. Alpha 1
– Located in vascular tissues & smooth muscles
1. ↑ Force of heart contraction
2. Vasoconstriction = ↑ BP
3. Dilate pupils
4. ↓GI Secretions
5. ↑bladder and prostate contraction
8
9. ADRENERGIC AGONISTS
2. Alpha 2 (opposite to alpha1)
– Located in sympathetic nerve endings
1. Inhibit norepinephrine release
2. Dilates blood vessels
3. ↓ GI motility
4. ↓ BP
3. Beta 1 receptor
– Primarily in the heart
1. ↑ Heart rate and force of contraction
2. ↑ secretion of renin
3. ↑ BP
9
10. ADRENERGIC AGONISTS
4. Beta 2
– Smooth muscles of lungs
– Arterioles of skeletal muscles
– Uterine muscle
1. Dilates bronchioles
2. Promote GI and uterine relaxation
3. ↑ Blood sugar thru glycogenolysis
10
11. ADRENERGIC AGONISTS
• Alpha & Beta-Adrenergic Agonist
– Epinephrine, norepinephrine, dopamine, dobutamine, ephedrine,
mephentemine and metaraminol
– ACTION:
1. ↑ HR with ↑ myocardial contractility
2. Dilation of bronchi resulting to increased depth and rate
3. ↑ BP due to vasoconstriction
4. Breakdown glucose stores to produce energy
5. Dilation of pupils and ↑ sweating
11
12. Alpha & Beta-Adrenergic Agonist
INDICATION:
• Tx of hypotensive states or shock
PHARMACOKINETICS
• Absorbed after injection or passage through
mucus membrane
• Metabolized in liver
• Excreted in urine
12
13. Alpha & Beta-Adrenergic Agonist
CONTRAINDICATIONS:
• With pheochromocytoma
– Systemic overload could be fatal
• Ventricular fibrillation
– ↑ HR and oxygen consumption caused by these drugs
exacerbate symptoms
CAUTION
– Any kind of peripheral vascular disease – exacerbate
by systemic vasoconstriction
13
15. ALPHA-SPECIFIC ADRENERGIC AGONIST
INDICATIONS:
• Clonidine = tx for HPN
• Phenylepinephrine
– Can be found in cold and allergy medications
– Cause vasoconstriction to decrease swelling & congestion
associated with rhinitis
• Midodrine = tx orthostatic hypotension who do not
respond to other therapies.
15
16. ALPHA-SPECIFIC ADRENERGIC AGONIST
PHARMACOKINETICS
• Peak level in 20-45min
• Distributed in body
• Metabolized in liver
• Excreted in urine
CONTRAINDICATIONS:
• Severe hypotension and tachycardia
• Narrow angle glaucoma
• pregnancy
16
18. CONTRAINDICATIONS
• Isoproterenol is contraindicated in:
– + allergy
– Pulmonary hypertension
– During anesthesia with halogenated hydrocarbon
– Eclampsia
– Uterine hemorrhage
– Intrauterine death
18
19. CAUTION
• With diabetes
• Thyroid disease
• Vasomotor problems
• Degenerative heart disease
• Hx of stroke
19
20. ADRENERGIC ANTAGONIST
ALPHA & BETA-SPECIFIC BLOCKERS
ACTION:
– Competitively block the effects of norepinephrine at
both alpha & beta receptors
– Result to ↓blood pressure, ↓ PR and ↑renal
perfusion
20
21. ALPHA & BETA-SPECIFIC BLOCKERS
INDICATION = HPN
CONTRAINDICATION:
• Not recommended <18yo
• Bradycardia/heart blocks
• Asthma, shock or heart failure
• Pregnancy and lactation
CAUTION:
• DM pt as it can:
– mask symptoms of hyperglycemia and hypoglycemia
– Constrict peripheral vessels =reduced blood flow
21
22. ALPHA-SPECIFIC BLOCKERS
ACTION:
– Block postsynaptic alpha1 receptor resulting to ↓
in vascular tone and vasodilation.
INDICATION:
– BENIGN PROSTATIC HYPERTROPHY
– HPN
22
23. BETA-SPECIFIC BLOCKERS
ACTION:
– Blocks beta receptors in heart and in
juxtaglomerular apparatus
– ↓HR, contractility and excitability
INDICATION:
– Cardiovascular problem
• HPN, angina, migraine and HA
• Prevent reinfarction
23
26. CHOLINERGIC AGONISTS
• Stimulate PNS
• Copy the action of acetylcholine
Acetylcholine
– Neurotransmitter located at the ganglions and
parasympathetic terminal nerve endings that acts on the
receptors found in organs, tissues and glands
– Stimulate skeletal muscle contraction
26
28. CHOLINERGIC AGONISTS
DIRECT ACTING CHOLINERGICS
ACTION:
– React directly with receptor sites to cause the same
reaction as acetylcholine
– Stimulate muscarinic receptors within the PNS
28
29. CHOLINERGIC AGONISTS
DIRECT ACTING CHOLINERGICS
ACTION:
PNS effects
– ↓HR and myocardial contractility
– Vasodilation
– Bronconstriction
– ↑bronchial secretions
– ↑ GI activity
– ↑ bladder tone
– Relaxed GI sphincter
– Papillary constriction
29
31. CHOLINERGIC AGONISTS
INDIRECT-ACTING CHOLINERGICS
ACTIONS
• React chemically with acetylcholinesterase in synaptic cleft to
prevent breakdown of acetylcholine(Ach)
• Result: Ach is released from presynaptic nerve remains in the
area and accumulates, stimulating the Ach receptors
• Permits skeletal muscle stimulation, which ↑ force of muscular
contraction
31
34. ANTICHOLINERGICS
• Block the Ach receptors at muscarinic
cholinergic receptor sites, responsible for
mediating the effect of PNS
• Depress salivation and bronchial
secretions, dilate bronchi, relax GI & GU
tracts, relax pupils
34
35. ANTICHOLINERGICS
INDICATION
• ↓ Secretions before anesthesia
• Tx Parkinsonism
• Restore cardiac rate & BP after vagal stimulation during surgery
• Relieve bradycardia
• Relieve pylorospasm & hyperactive bowel
• Relax bladder detrusor muscles
• Peptic ulcer
• Control of rhinorrhea
• Antidote for cholinergic drugs
• Ophthalmic agent to cause mydriasis
35