This document provides an overview of local anesthesia, including its types, history, classification, mechanism of action, pharmacological actions, uses and techniques, adverse effects, and differences from general anesthesia. It discusses how local anesthetics work by reversibly blocking sodium channels in nerve fibers to inhibit nerve impulse conduction. Common local anesthetics and their properties, uses for surface, infiltration, nerve block, spinal and epidural anesthesia are summarized. Potential adverse effects including CNS, cardiovascular and local tissue toxicity are also outlined.
Local anesthetics explained in detail while keeping Anaesthesia point of view. it covers introduction,history mechanism of action,classification,individual drugs and systemic toxicity and more points presented by Dr Gaurav Joshi Resident doctor in dept of Anaesthesia (1st year).
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
EVERYTHING RELATED TO LOCAL ANESTHETICS LIKE DEFINITION, HISTORY INTRODUCTION PHYSIOLOGY MECHANISM OF ACTION ANATOMY OF NERVES CLASSIFICATIONS INDIVIDUAL DRUGS AND ITS USES LOCAL ANESTHETICS TOXICITY LOCAL ANESTHETIC SYSTEMIC TOXICITY (LAST) MANAGEMENT OF LAST ETC...
Local anesthetics explained in detail while keeping Anaesthesia point of view. it covers introduction,history mechanism of action,classification,individual drugs and systemic toxicity and more points presented by Dr Gaurav Joshi Resident doctor in dept of Anaesthesia (1st year).
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
EVERYTHING RELATED TO LOCAL ANESTHETICS LIKE DEFINITION, HISTORY INTRODUCTION PHYSIOLOGY MECHANISM OF ACTION ANATOMY OF NERVES CLASSIFICATIONS INDIVIDUAL DRUGS AND ITS USES LOCAL ANESTHETICS TOXICITY LOCAL ANESTHETIC SYSTEMIC TOXICITY (LAST) MANAGEMENT OF LAST ETC...
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
This set of 17 slides introduces students to the some of the basic physiological processes that are the targets of many analgesic drug classes. It is suitable for beginner/intermediate level learners.
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
This set of 17 slides introduces students to the some of the basic physiological processes that are the targets of many analgesic drug classes. It is suitable for beginner/intermediate level learners.
This is the presentation for B. Pharm. IV Semester Students. It includes details like introduction, mechanism of action, classification along with structures and nomenclature, synthesis, uses and adverse effects of General Anaesthetics.
“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
- 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
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CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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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
2. Contents
Anaesthesia and Its types
History of local anaesthetics
Classification
Mechanism of action
Pharmacological action
Uses and Techniques
Adverse effects
New approved drug
Difference between LAs and
GAs
3. Anaesthesia
• It is reversible condition induced by anaesthetic drug that cause reduction or complete
loss of response to pain or another sensation such as consciousness and muscle
movements during surgery or other invasive procedure that can be painful.
General Local
- Make whole body - That numbs specific
loss feeling movement targeted area of the
and consciousness body
- Remove pain in local area of body
without producing unconsciousness
ex: biopsy, dental care, surgery
4. Local Anesthetics
• Local anesthetics produce a transient and reversible loss of
sensation in a region of the body without loss of consciousness.
As a general rule, smaller nonmyelinated dorsal root type C
nerve fibers that carry pain and temperature sensations (and also
sympathetic type C unmyelinated postganglionic nerve fibers)
are blocked before larger, heavily myelinated type A fibers that
transmit sensory proprioception and motor functions.
• Most available local anesthetics are either esters or amides and
are usually linked to a lipophilic aromatic group and to a
hydrophilic, ionizable tertiary amine. Most are weak bases with
pKa values between 7 and 9 (except benzocaine, pKa 3.5) and at
physiologic pH they are primarily in the charged, cationic form.
• The potency of local anesthetics is positively correlated with
their lipid solubility, which may vary 16-fold, and negatively
correlated with their molecular size.
• These anesthetics are selected for use on the basis of the
5. History of Local Anesthesia
• First local anesthetic to be discovered was cocaine, an alkaloid from the leaves of the plant Erythroxylon
coca, found in the highlands of Peru
• pure alkaloid first isolated by Neimann
• von Anrep, 1880, was the first to describe the sensory anesthetic action of subcutaneous injection and
recommended its use as such, however this was not acted upon
• in 1884, S. Freud used the CNS actions to wean a colleague from opioid addiction
• Koller, at about the same time as Freud, introduced its topical use into ophthalmology
• Hall, in 1884 introduced its use into dentistry and in the following year Halsted demonstrated its efficacy
in blocking conduction in nerve trunks
• Corning, also in 1885, produced spinal anesthesia in dogs however it was several years before this was
used in surgery
• the search for chemical substitutes for cocaine began in 1892, with the work of Einhorn & colleagues ®
procaine in 1905
• Lofgren synthesized lignocaine in 1943 and since then, with exception of chloroprocaine, all new local
anesthetics introduced into clinical practice have been amino-amides
6. Pharmacological Classification
• Injectable
1. Low potency, short duration: Procaine, Chlorprocaine
2. Intermediate potency and duration: Lidocaine,
Priocaine
3. High potency, long duration: Tetracaine, Bupivacaine,
Ropivacaine
• Surface
1. Soluble: cocaine, lidocaine, tetracaine, benoxinatel
2. Insoluble: Benzocaine, Butylaminobenzoate,
Oxehazaine
7. Mechanism of action
• Location: Local anaesthetic
receptor are located in the Na+
channel of axonal membrane
• Structure: The receptor consists of
two gates:
1. Activated gate or “m” gate
2. Inactivated gate or “h” gate
• The activation of ‘h’ gate is mainly
responsible for blocking of Na+
channels
8. • Resting state
• In resting phase ‘m’ gate closed so Na+ ion could not passed
• In local anaesthetic phase Equilibrium is established between
ionized cation form and base form
• There are in axonal membrane permeability of ionized cationic
form is very less so it gets converted into the base form which
have high permeability to the axonal membrane
• Thus local anaesthetic enter into the axonal membrane, and in
that base get converted into ionized cationic form and it has
higher binding capacity to local anaesthetic receptor
9. • Activated state: in this state when ‘m’ gate is
open along with the ‘h’ gate the ionized
cationic form bind to the local anaesthetic
receptor which causes the closing of ‘h’ gate
and thus the inactivated state is obtained
• Inactivated state: in this state the ‘h’ gate is
closed, Na+ ion could not passed to the
channel and then causes block of the
conduction of impulses
• The effect of concentration on LA on nerve
fibre:
I. a=untreated nerve fibre (normal conduction
of impulse)
II. b, c, d =treated nerve fibre, increasing
concentration of LA, as conc. Of LA increase
rise in action potential and max.
depolarization decreases that causing
10. Pharmacological action
1. Central nervous system: All LAs are capable of producing a
sequence of stimulation followed by depression.
• Cocaine is a powerful CNS stimulant causing in sequence
euphoria—excitement—mental confusion—rest-lessness—tremor
and twitching of muscles— convulsions—unconsciousness—
respiratory depression—death, in a dose-dependent manner.
• Procaine and other synthetic LAs are much less potent in this
regard. At safe clinical doses, they produce little apparent CNS
effects. Higher dose or accidental i.v. injection produces CNS
stimulation followed by depression.
• Lidocaine, on the contrary, can initially cause drowsiness and
lethargy, but higher doses produce excitation followed by
depression like others. The basic action of all LAs is neuronal
inhibition; the apparent stimulation seen initially is due to inhibition
of inhibitory neurons. At high doses, all neurons are inhibited and
flattening of waves in EEG is seen.
11. 2. Cardiovascular system: In Heart LAs are cardiac
depressants, but no significant effects are observed at
conventional doses.
• At high doses or on i.v. injection, they decrease
automaticity, excitability, contractility, conductivity and
increase effective refractory period (ERP). They have a
quinidine like antiarrhythmic action.
• Procaine is not used as antiarrhythmic because of short
duration of action and propensity to cause CNS effects,
but its amide derivative procainamide is a classical
antiarrhythmic. At high plasma concentrations
electrophysiological properties of heart may be markedly
altered, QTc interval is prolonged and LAs can themselves
induce cardiac arrhythmias.
• Bupivacaine is relatively more cardiotoxic and has
produced ventricular tachycardia or fibrillation. Lidocaine
12. • In Blood vessels LAs tend to produce fall in BP. This is
primarily due to sympathetic blockade, but high
concentrations, as obtained locally at the site of
injection, do cause direct relaxation of arteriolar
smooth muscle.
• Bupivacaine is more vasodilatory than lidocaine, while
prilocaine is the least vasodilatory. Toxic doses of LAs
produce cardiovascular collapse.
• Cocaine has sympathomimetic property; causes local
vasoconstriction, marked rise in BP and tachycardia.
13. Uses and Techniques
1. Surface anaesthesia: Amethocaine is used as
surface anaesthetic for eye, throat, urethra,
rectum and skin. Benzocaine and lignocaine HCL
are used as all purpose surface anaesthetic except
for eye. Dibucaine is use for ear, rectum and skin.
2. Infiltration anaesthesia: in this procedure the
nerve ending are anaesthetized by direct
exposure of drug, subcutaneously. Procaine and
lidocaine 2% are commonly used. They are mixed
with adrenaline to prolong action.
• Nerve block or conduction block where the drug is
injected very close to the nerve ex: brachial plexus
14. 3. Spinal anaesthesia: in this procedure the LA without adjuvants is injected into the
subarachnoid space. Its level in space is adjusted by using solution with higher or
lower specific gravity than that of CSF, as vehicle. Lidocaine and Bupivacaine is most
used drug.
4. Epidural anaesthesia: LA is injected outside the dura. Combined spinal-epidural
analgesia is induced by injecting LA intrathecally with additional dose given by
epidural route. Spinal, epidural analgesia and their combination are termed as
neuraxial analgesia.
5. Blood vessels: LAs tend to produce fall in BP. This is primarily due to sympathetic
blockade, but high concentrations, as obtained locally at the site of injection, do
cause direct relaxation of arteriolar smooth muscle. Bupivacaine is more vasodilatory
than lidocaine, while prilocaine is the least vasodilatory. Cocaine has
sympathomimetic property, increases sympathetic tone, causes local vasoconstriction,
marked rise in BP and tachycardia.
15. 6. Headache and migraine can be addressed by injections to the major
occipital nerve or by the intranasal or intravenous application of
lidocaine . Trigeminal neuralgia has been successfully treated with 10%
lidocaine injections and with trigger point injections
7. Postherpetic neuralgia (PHN) could be successfully treated with local LA
injections. In most recent studies, however, neural therapy was only used
in combination with steroids therefore, a clear conclusion on the value of
local anesthetics alone cannot be drawn
• A promising approach to ophthalmic PHN is the topical use of lidocaine in
eye drops. Similarly, the topical use of 5% lidocaine plaster has been
established as a first-line option for treating patients with PHN.
16. Adverse effects
(1) CNS effects are light-
headedness, dizziness, auditory and
visual disturbances, mental
confusion, disorientation, shivering,
twitching, involuntary movements,
finally convulsions and respiratory
arrest.
(2) Cardiovascular toxicity of LAs
is manifested as bradycardia,
hypotension, cardiac arrhythmias
and vascular collapse.
17. local tissue toxicity of LAs is low. However,
wound healing may be sometimes delayed.
Addition of vasoconstrictors enhances the
local tissue damage; rarely necrosis results.
Vasoconstrictors should not be added for
ring block of hands, feet, fingers, toes and
penis . Bupivacaine has the highest local
tissue irritancy.
• (4) Hypersensitivity reactions like rashes,
angioedema, dermatitis, contact
sensitization, asthma and rarely
anaphylaxis occur. These are more
common with ester-linked LAs, but rare
with lidocaine or its congeners. Cross
reactivity is frequent among ester
compounds, but not with amide-linked
18. Method Uses Drugs Side Effects
Surface
anaesthesia
Nose, mouth, bronchial area
(usually in spray form), cornea,
urinary tract Not effective for skin
Lidocaine,
tetracaine,
(amethocaine),
dibucaine,
benzocaine
Risk of systemic toxicity when high concentrations
and large areas are involved
Infiltration
anaesthesia
Direct injection into tissues to
reach nerve branches and
terminals Used in minor surgery
Most
Adrenaline (epinephrine) or felypressin often added
as vasoconstrictors (not with fingers or toes, for fear
of causing ischaemic tissue damage) Suitable for
only small areas, otherwise serious risk of systemic
toxicity
Intravenous
regional
anesthesia
LA injected intravenously distal to
a pressure cuff to arrest blood
flow; remains effective until the
circulation is restored Used for
limb surgery
Mainly lidocaine,
prilocaine
Risk of systemic toxicity when cuff is released
prematurely; risk is small if cuff remains inflated for
at least 20 min
19. Method uses Drug Side effects
Nerve block
anesthesia
LA is injected close to nerve trunks (e.g.
brachial plexus, intercostal or dental nerves)
to produce a loss of sensation peripherally
Used for surgery, dentistry, analgesia
Most
Less LA needed than for infiltration
anesthesia Accurate placement of the
needle is important Onset of
anesthesia may be slow Duration of
anesthesia may be increased by
addition of vasoconstrictor
Spinal
anesthesia
LA injected into the subarachnoid space
(containing cerebrospinal fluid) to act on
spinal roots and spinal cord Glucose
sometimes added so that spread of LA can be
limited by tilting patient Used for surgery to
abdomen, pelvis or leg, mainly when general
anesthesia cannot be used
Mainly lidocaine
Main risks are bradycardia and
hypotension (owing to sympathetic
block), respiratory depression (owing
to effects on phrenic nerve or
respiratory center); avoided by
minimizing cranial spread
Postoperative urinary retention
(block of pelvic autonomic outflow) is
common
Epidural
anesthesia
LA injected into epidural space, blocking
spinal roots Uses as for spinal anesthesia; also
for painless childbirth
Mainly lidocaine,
bupivacaine
Unwanted effects similar to those of
spinal anesthesia but less probable,
because longitudinal spread of LA is
reduced Postoperative urinary
retention common
20.
21. Character Local Anesthetics General Anesthetics
Site of action Local nerve fibers CNS
Mechanism of action
Generally blocks conduction and
generation of nerve impulse
CNS depression directly
Patient conscious Present Absent
Pain sensation and other reflex activity Locally lost Generalized loss of consciousness
Muscular relaxation Locally Generally whole body
Use of preanesthetic medication Not required Required
Use During minor surgical operation Major surgical operations
Toxicity Less toxic
More toxic if dose not properly handle
may cause neurological disorder.
Difference between Local Anesthetics and General Anesthetics
22. •Reference:
pharmacology and pharmacotherapeutics by R.S
satoskar, Nirmala N. Rege, Raakhi K. Tripathi, S.D.
Bhandarkar
KDT essential of medicinal pharmacology
http://cmro.in/index.php/jcmro/article/view/317
https://www.slideshare.net/mobile/ParasuramanParasur
aman/local-anaesthetics-63457069
https://www.nysora.com/foundations-of-regional-
anesthesia/pharmacology/clinical-pharmacology-local-
anesthetics/