This document summarizes local anesthetics, including their mechanisms of action, types, uses, and side effects. It discusses how local anesthetics reversibly block sodium channels to cause temporary loss of sensation. The two main types are amides and esters, with amides being more potent and longer-lasting. Common local anesthetics and their properties are outlined. The document also reviews techniques for local anesthesia including infiltration, nerve blocks, epidurals, and Bier's block. Potential complications and contraindications are mentioned.
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
local anaesthesia is defined as a loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings
Or an inhibition of the conduction process in peripheral nerves; no loss of consciousness occurs
Local anesthetics interfere with the excitation process in the nerve membrane in one or more of the following ways:
1) Altering the basic resting potential of the nerve membrane
2) Altering the threshold potential (firing level)
3) Decreasing the rate of depolarization*
4) Prolonging the rate of repolarization
A teaching slide set describing the mechanisms of action and clinical use of local anaesthetics. This session is a basic introduction to the pharmacodynamics and pharmacokinetics of local anaesthetics. It is aimed at preclinical medical or dental students, or students in the early years of a pharmacology degree.
The presentation gives a detailed overview of local anesthetics. This presentation made very effectively, covering mostly all the important sub topics. It will be definitely useful for all the students Comment your response regarding the presentation.
THIS ppt explains in brief about general anesthesia for under graduates. It includes brief classification, mechanism of action, side effects of some important drugs. concepts like diffusion hypoxia, second gas effect, balanced anesthesia and pre- anaesthetic medication are discussed.
Local anaesthetics – a brief outlook by Rxvichu!!RxVichuZ
This is my 24th ppt!
Its on LOCAL ANESTHETICS.............It comprises varying drugs, their potencies, and other details....
Useful for 2nd year students.....and for reference!
Do check...n send ur reviews!
Thank you!
@rxvichualwz4uh!
:) :)
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
local anaesthesia is defined as a loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings
Or an inhibition of the conduction process in peripheral nerves; no loss of consciousness occurs
Local anesthetics interfere with the excitation process in the nerve membrane in one or more of the following ways:
1) Altering the basic resting potential of the nerve membrane
2) Altering the threshold potential (firing level)
3) Decreasing the rate of depolarization*
4) Prolonging the rate of repolarization
A teaching slide set describing the mechanisms of action and clinical use of local anaesthetics. This session is a basic introduction to the pharmacodynamics and pharmacokinetics of local anaesthetics. It is aimed at preclinical medical or dental students, or students in the early years of a pharmacology degree.
The presentation gives a detailed overview of local anesthetics. This presentation made very effectively, covering mostly all the important sub topics. It will be definitely useful for all the students Comment your response regarding the presentation.
THIS ppt explains in brief about general anesthesia for under graduates. It includes brief classification, mechanism of action, side effects of some important drugs. concepts like diffusion hypoxia, second gas effect, balanced anesthesia and pre- anaesthetic medication are discussed.
Local anaesthetics – a brief outlook by Rxvichu!!RxVichuZ
This is my 24th ppt!
Its on LOCAL ANESTHETICS.............It comprises varying drugs, their potencies, and other details....
Useful for 2nd year students.....and for reference!
Do check...n send ur reviews!
Thank you!
@rxvichualwz4uh!
:) :)
Dr rowan molnar anaesthetics study guide part ivDr. Rowan Molnar
Dr rowan molnar anaesthetics study guide part iv
Identifies (hopefully confirms!) anaesthetic agent being used
Measures inspiratory & expiratory concentrations
Expiratory (alveolar) concentration enables calculation of MAC fraction or multiple – i.e. estimation of anaesthetic depth.
Now mandatory when inhalational anaesthetic agents are used.
Dr Rowan Molnar,
Dr Rowan Molnar Anaesthetics,
Dr Rowan
“Local Anaesthetics”
These are agents which upon topical application or local injection cause reversible loss of pain sensation in a restricted area of the body. They act by blocking both sensory and motor nerve conduction to produce temporary loss of sensation without loss of consciousness.
Mechanism of action
These drugs reversibly prevent the generation and propagation of impulses in all excitable membranes including nerve fiber by stabilizing the membrane.
Local anesthetics block the nerve conduction by decreasing the entry of Na+ during action potential. They interact with a receptor situated within the voltage sensitive Na+ channel and raise the threshold of Na+ channel opening.
Therefore, Na+ can’t enter into the cell in response to an impulse which prevents depolarisation. Thus, action potential is not generated.
This action affecting the depolarization which leads to failure of conduction of impulse without affecting the resting membrane potential (RMP) is known as membrane stabilizing effect.
History- Cocaine is a naturally occurring compound indigenous to the Andes Mountains, West Indies, and Java.
It was the first anesthetic to be discovered and is the only naturally occurring local anesthetic; all others are synthetically derived.
Cocaine was introduced into Europe in the 1800s following its isolation from coca beans. Sigmund Freud, the noted Austrian psychoanalyst, used cocaine on his patients and became addicted through self-experimentation.
In the latter half of the 1800s, interest in the drug became widespread, and many of cocaine's pharmacologic actions and adverse effects were elucidated during this time. In the 1880s, Koller introduced cocaine to the field of ophthalmology, and Hall introduced it to dentistry
Pharmacology of local aesthetics and its mechanism of action, adverse effects and uses of local aesthetics with a note on the techniques of local aesthetics
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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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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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
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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.
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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
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
2. Drugs that cause reversible loss of sensory
perception specially of pain in a restricted
area of the body, when applied topically or
local injection.
LA if applied to a mixed nerve—sensory and
motor impulses are interrupted—resulting in
muscular paralysis and loss of autonomic
control.
3. Reversibly block the impulse conduction
Transient loss of sensation
Local anaesthesia blockade
C,B > Aδ > Aα,ß,γ
6. E S T E R S
Short duration of action
Less intense anesthesia
Higher risk of
hypersensitivity -PABA.
Hydrolyzed by Plasma
Cholinesterase in blood.
Rarely used for Infiltration
anesthesia But useful for
topical anesthesia on
mucous membranes.
A M I D E S
Produce more intense and
longer lasting anesthesia
Bind to alpha1 acid glyco-
protein in plasma
Rarely cause hypersensitivity
reactions- no cross
reactivity with ESTER L A s
Not hydrolyzed by Plasma
Cholinesterase, but in liver
7. Vasoconstrictor is a substance used to keep the
anesthetic solution in place at a longer period and
prolongs the action of the drug
Vasoconstrictor delays the absorption which slows
down the absorption into the bloodstream
Vasoconstrictor used ---the natural hormone called
epinephrine (adrenaline).
8. Blockage of membrane depolarisation in all excitable
tissues, usually intended on peripheral nerve
Membrane stabilizer
They prevent the
Initiation and propa-
Gation of the nerve
Impulse by reducing
the passage of Na
9. Effects of LA: injection as acid (hydrochloric salt)=
ionized form at physiological pH dissociation to
free base (lipid soluble) passage through cell
membrane to interior of axon re-ionisation
enter and blockage of Na+-channel and thereby
preventing influx of Na+ no generation of AP
conduction blockade
They block nerve conduction by reducing the
permeability of Na ions during depolarisation
10. Should not be coadministered for nerve block in areas such
as fingers and toes that are supplied with end-arteries
because it may cause ischemia or necrosis
It should be used cautiously in patients in labour and in
patients with thyrotoxicosis or cardiovascular disease.
11. Usually at range 7.6 – 8.9
Decrease in pH shifts equilibrium toward the ionized
form, delaying the onset action.
Lower pH, solution more acidic, gives slower onset
of action
Presence of Pus and inflammation will retard the
action of LA. ( probably low acidic pH)
12. Most widely used Amide linked LA and most
versatile ana.
Has variety of applications like Local, nerve block,
spinal, epidural, IVRA.
When used locally action starts within 3 mts and
causes vasodilatation.
Overdose causes muscle twitchings, convulsions,
cardiac arrhythmias, fall in BP, coma, respiratory
arrest.
Most popular ant arrhythmic drug
13. • Standard agent for infiltrations, regional blocks or
topical
• Short onset time, intermediate duration of action
• Class Ib antiarrhythmic properties
• Medium toxicity
• Maximal recommended dose: 3 mg/kg, 6 mg/kg with
vasconstrictor
14. A potent long acting ---Amide linked LA available in
India, most widely used allover.
Not used for IVRA but all others like local, spinal
epidural blocks.
Action lasts for 2 to 3 hours. Strength for epidural is
0.25 to 0.5 % solution.
Has high lipid solubility, distributes more in tissues
than in blood
15. It is similar to Bupivacaine
One of the metabolites are toxic and can cause
Methamoglobinemia
Used for Nerve Blocks and IVRA.
16. Causes more sensory block, than motor block the
advantage taken in during Caesarean Section.
(Walking Epidural)
Bupivacaine is more prone to prolong QTc interval
and induce ventricular tachycardia or Cardiac
depression----( Membrane Stabilization action ) (
toxic doses and accidental entry into vessel)-should
not be used for IVRA.
Longest acting LA available in India now.
17. 1. Surface anesthesia
2. Infiltration anesthesia
3. Conduction block a. Field block b. Nerve Block
4. Spinal anesthesia
5. Epidural anesthesia
6. I V R A (Bier’s Block)
18. Amethocaine ---eye, throat, urethra, rectum and
skin.
Benzocaine and Lidocaine hydrochloride—same ---
except for eye.
Procaine is unsuitable as a surface ana. Because of
its poor penetrating power
Lignocaine --4 % topical solution, 2 % Jelly
2 % vials for injections
19. Eutectic : Lowering of melting point of two solids
when they are mixed.
combination of Lidocaine and Prilocaine.
For Pediatric purpose. It can penetrate intact skin.
I v .cannula inserting.
Split skin graft harvesting
Other superficial procedures.
20. Mech. of action : Nerve endings as exposed to the
drug there by action.
Procaine, Lignocaine 2 % are used either with or
without Adrenaline 1 : 2,00,000
C/I : blocking where end arteries are involved either
for Penis, or for Digits, C A D patients.
21. Drug is injected close to the nerve or big nerve
trunks eg. Brachial Block, Sciatic, Femoral Nerve,
Radial, Ulnar Nerves.
22. LA is injected into the subarachnoid space.
Injection is made heavy by adding dextrose or light
by adding saline.
When the anesthetic in injected outside the dura,
the technique is known as Epidural anesthesia.
Lignocaine, Bupivacaine the two agents most
commonly used regularly in anesthesia practice.
24. Intravenous regional anesthesia
Agent of choice------ Lignocaine (Xylocaine )
20 to 40 ml of 0.5 % Lidocaine is used
Used for only for Upper Limb orthopedic surgeries
and others on Up. Limb.
25.
26. We have seen all Local actions of LA s
Systemic action when given IV : Bupivacaine is
relatively more cardiotoxic , produces ventricular
tachycardia or fibrillation.
Lidocaine has little effect on contractility and
conductivity, used as antiarrhythmic.
The prominent cardiac action of Xylocaine is
suppression of automaticity in ectopic foci.
27. Depression of function of CNS and CVS when high
plasma concentrations are reached
CNS toxicity : usually before cardiovacular effects
First signs of excitation due to initial blockade of
inhibitory pathways
mild: circumoral tingling, metallic taste, tinnitus,
visual disturbance, slurred speech
moderate: altered consicous state, convulsions
Later sings of generalized CNS depression with
potentially fatal toxicity: coma,respiratory arrest
28. 1.Bradycardia, 2.Hypotension 3.Headache
4.Cauda Equina syndrome 5.Septic meningitis
EPIDURAL ANESTHESIA :
Here the drug is injected outside the dura. Drug
spread is restricted to a specific region causes fewer
complications.
29. Allergic reactions: common with ESTERS like
Procaine, caused by para-aminobenzoic acid (also
found to cause arachnoiditis), less common with
AMIDES, then mostly through preservatives
Drug interactions: i.e. Anticholinesterases, other
competing drugs hydrolyzed by Plasma CE
Attention with heavy sedation with anticonvulsants:
may mask early signs of toxicity
Methaemoglobinaemia: after large doses Prilocaine