Learn the nor adrenergic transmission in ANS. Synthesis, storage ,release, uptake,metabolism of nor-adrenaline. Types of adrenoceptors. Agonist and antagonist of adrenoceptors.
Learn the nor adrenergic transmission in ANS. Synthesis, storage ,release, uptake,metabolism of nor-adrenaline. Types of adrenoceptors. Agonist and antagonist of adrenoceptors.
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
Sympatholytic drugs (Adrenergic blockers) bind to the adrenergic receptors and prevent the action of adrenergic drugs.
These are drugs which block the actions of sympathetic division or catecholamines (adrenaline and noradrenaline).
They are competitive antagonists at both α and β adrenergic receptors.
Neurotransmission (Latin: transmission "passage, crossing" from transmitter "send, let through"), is the process by which signalling molecules called neurotransmitters are released by the axon terminal of a neuron and bind to and react with the receptors on the dendrites of another neuron
complete and detail study on the topic of general anesthetics by the collaboration of teacher and students for the student , teachers and other health care professionals to learn more on the topics
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
Sympatholytic drugs (Adrenergic blockers) bind to the adrenergic receptors and prevent the action of adrenergic drugs.
These are drugs which block the actions of sympathetic division or catecholamines (adrenaline and noradrenaline).
They are competitive antagonists at both α and β adrenergic receptors.
Neurotransmission (Latin: transmission "passage, crossing" from transmitter "send, let through"), is the process by which signalling molecules called neurotransmitters are released by the axon terminal of a neuron and bind to and react with the receptors on the dendrites of another neuron
complete and detail study on the topic of general anesthetics by the collaboration of teacher and students for the student , teachers and other health care professionals to learn more on the topics
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.
General Anesthetics
Its help in the B pharma students and all science students.
Here give the full notes about General Anesthetics so read nd learn here also share with your friends,
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Agents that produces loss of consciousness are anesthetics.
They induce smooth and rapid effect for limited period. There are five stages of anesthesia. They are classified as INHALATION ANESTHETICS, ULTRA SHORT ACTING BARBITURATES and DISSOCIATIVE ANESTHETICS.
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.
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.
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
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
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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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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
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
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
3. What is Anaesthesia ???
Anaesthesia – is a reversible condition of comfort and quiescence
for a patient within the physiological limit before, during and after
performance of a procedure.
General anaesthesia – for surgical procedure to render the patient
unaware/unresponsive to the painful stimuli.
Drugs producing General Anaesthesia – are called General
Anaesthetics.
Local anaesthesia - reversible inhibition of impulse generation
and propagation in nerves.
4. In sensory nerves, such an effect is desired when painful
procedures must be performed, e.g., surgical or dental
operations.
Drugs producing Local Anaesthesia – are called Local
Anaesthetics e.g. Procaine, Lidocaine and Bupivacaine etc.
6. What Are
General
Anaesthetics ?
• Definition : Anesthesia (an =without,
aisthesis = sensation )
• The drugs which produce reversible
loss of all sensations and
consciousness.
• Generally administered by an
anaesthesiologist in order to induce or
maintain general anaesthesia to
facilitate surgery.
8. Stages Of
General
Anaesthesia
Stage-1 • Analgesia : Start from beginning of
anaesthesia administration and last upto loss of
consciousness, feels a dream like state,
reflexes and respiration remains normal
Stage-2 • Stage of delirium : From loss of
consciousness to beginning of irregular
respiration. Apparent excitement is seen.
Muscle tone increases. Jaws are tightly closed.
Heart rate and blood pressure may rise.
9. Stages Of
General
Anaesthesia
Stage-3 • Surgical anaesthesia : Extends from onset
of irregular respiration to cessation of spontaneous
breathing.
This has been divided into 4 planes:-
• Plane1:This plane ends when eyes become fixed
•Plane 2: Loss of corneal and laryngeal reflexes
•Plane 3:Pupil start dilating and light reflex
•Plane 4: Dilated pupil, decrease muscle tone ,BP •
falls
Stage-4 • Medullary paralysis : Respiratory and
vasomotor control ceases
10.
11. Difference Between General And Local Anaesthetics
Description General Local
Site of action CNS Peripheral nerves
Area Whole body Restricted areas
Consciousness Lost Unaltered
Preferential use Major surgery Minor surgery
Use in non-cooperative
patients
Possible Not possible
Poor health patient Risky Safer
Care for vital functions Essential Not needed
12. Mechanisms of
GA
Mayer and Overton (1901) pointed out a
direct parallelism between lipid/water
partition coefficient of the GAs and their
anaesthetic potency.
Minimal alveolar concentration (MAC) is
the lowest concentration of the anaesthetic in
pulmonary alveoli needed to produce
immobility in response to a painful stimulus
(surgical incision) in 50% individuals.
It is accepted as a valid measure of potency
of inhalational GAs, because it remains fairly
constant for most young adults.
The MAC of all inhalational anaesthetics
declines progressively as age advances
beyond 50 years.
13. The MAC of a number of GAs shows excellent correlation with their
oil/gas partition coefficient.
However, this only reflects capacity of the anaesthetic to enter into CNS
and attain sufficient concentration in the neuronal membrane, but not the
mechanism by which anaesthesia is produced.
The principal locus of causation of unconsciousness appears to be in the
thalamus or reticular activating system, amnesia may result from action in
cerebral cortex and hippocampus, while spinal cord is the likely seat of
immobility on surgical stimulation.
14. Recent findings show that ligand gated ion channels (but not voltage
sensitive ion channels) are the major targets of anaesthetic action.
The GABAA receptor gated Cl¯ channel is the most important of these.
Many inhalational anaesthetics, barbiturates, benzodiazepines and propofol
potentiate the action of inhibitory transmitter GABA to open Cl¯ channels.
Each of the above anaesthetics appears to interact with its own specific
binding site on the GABAA receptor, Cl¯ channel complex, but none binds
to the GABA binding site as such; though some inhaled anaesthetics and
barbiturates (but not benzodiazepines) can directly activate Cl¯ channels.
15. Action of glycine (another inhibitory transmitter which also activates Cl¯
channels) in the spinal cord and medulla is augmented by barbiturates,
propofol and many inhalational anaesthetics.
This action may block responsiveness to painful stimuli resulting in
immobility of the anaesthetic state.
Certain fluorinated anaesthetics and barbiturates, in addition, inhibit the
neuronal cation channel gated by nicotinic cholinergic receptor which may
mediate analgesia and amnesia.
On the other hand, N2O and ketamine do not affect GABA or glycine gated
Cl¯ channels. Rather they selectively inhibit the excitatory NMDA type of
glutamate receptor.
16. This receptor gates mainly Ca2+ selective cation channels in the neurones,
inhibition of which appears to be the primary mechanism of anaesthetic
action of ketamine as well as N2O.
The volatile anaesthetics have little action on this receptor.
Neuronal hyperpolarization caused by GAs has been ascribed to activation
of a specific type of K+ channels called ‘two-pore domain’ channels.
This may cause inhibition of presynaptic transmitter release as well as
postsynaptic activation.
17. Inhibition of transmitter release from presynaptic neurones has also been
related to interaction with certain critical synaptic proteins.
Thus, different facets of anaesthetic action may have distinct neuronal
basis, as opposed to the earlier belief of a global neuronal depression.
Unlike local anaesthetics which act primarily by blocking axonal
conduction, the GAs appear to act by depressing synaptic transmission.
20. Diethyl ether (C2H5 – O – C2H5)
• Colourless, highly volatile liquid with a pungent
odour.
• Boiling point = 35ºC
• Produces irritating vapours and are inflammable and
explosive.
• Pharmacokinetics: - 85 to 90 percent is eliminated
through lung and remainder through skin, urine, milk
and sweat
• Can cross the placental barrier.
21. • Advantages –
-Can be used without
complicated apparatus
-Potent anaesthetic and good
analgesic
-Muscle relaxation
-Wide safety of margin
-Respiratory stimulation and
bronchodilatation
-Does not sensitize the heart to
adrenaline
-No cardiac arrythmias
-Can be used in delivery
-Less likely hepato or
nephrotoxicity
• Disadvantages
-Inflammable and explosive
-Slow induction and unpleasant
-Struggling, breath holding,
salivation and secretions
(drowning)
-Atropine
-Slow recovery
-Nausea & vomiting
- Cardiac arrest
- Convulsion in children
- Cross tolerance – ethyl alcohol
22. Nitrous oxide/laughing gas (N2O)
• NH4NO3 (s) → 2 H2O (g) + N2O (g)
• Colourless, odourless inorganic gas with sweet taste
• Non-inflammable and non-irritating, but of low potency
• Very potent analgesic, but not potent anaesthetic
• Carrier and adjuvant to other anaesthetics – 70% + 25-
30% + 0.2-2%
• As a single agent used wit O2 in dental extraction and in
obstetrics
23. • Advantages:
-Non-inflammable and non-
irritant
-Rapid induction and
recovery
-Very potent analgesic (low
concentration)
-No effect on heart rate and
respiration
– mixture advantage
-No nausea and vomiting
-Post anaesthetic not marked
-Nontoxic to liver, kidney and
brain
• Disadvantages:
-Not potent alone
(supplementation)
-Not good muscle relaxant, not
-Hypoxia, unconsciousness cannot
be produced without hypoxia
-Inhibits methionine synthetase
(precursor to DNA synthesis)
-Inhibits vitamin B-12 metabolism
-Dentists, OR personnel, abusers at
risk
-Gas filled spaces expansion
(pneumothorax) - dangerous
24. Halothane
• Fluorinated volatile liquid with sweet odour, non-
irritant non-inflammable and supplied in amber
coloured bottle
• Potent anaesthetic (if precise control), 2-4% for
induction and 0.5-1% for maintenance
• Boiling point - 50ºC
• Pharmacokinetics: 60 to 80% eliminated
unchanged. 20% retained in body for 24 hours and
metabolized
• Delivered by the use of a special vapourizer
• Not good analgesic or relaxants
• Potentiates NM blockers
25. • Advantages:
-Non-inflammable and nonirritant -
Abolition of Pharyngeal and laryngeal
reflexes
-Bronchodilatation – preferred in
asthmatics
- Potent and speedy induction &
recovery
- Controlled hypotension
- Inhibits intestinal and uterine
contractions – external or internal
version
- Popular anaesthetic in developing
countries
- can be used in children for induction and
maintenance and adult maintenance
• Disadvantages:
- Special apparatus
- Vapourizer
- Poor analgesic and muscle relaxation
- Myocardial depression – direct depression of Ca++ and also
failure of sympathetic activity – reduced cardiac output (more
and more)
- Hypotension – as depth increases and dilatation of vascular beds
- Heart rate – reduced due to vagal stimulation, direct depression
of SA node and lack of Baroreceptor stimulation
- Arrythmia
- Sensitize heart to Adrenaline
- Respiratory depression – shallow breathing (PP of CO2 rises)
assisted ventilation
- Decreased urine formation – due to decreased GFR - Hepatitis: 1
in 10,000
- Malignant hyperthermia: Abnormal Ryanodine receptor
- Prolong labour
26. Enflurane
• Non-inflammable, with mild sweet odour and
boils at 57ºC
• Similar to halothane in action, except better
muscular relaxation
• Depresses myocardial force of contraction and
sensitize heart to adrenaline
• Induces seizure in deep anaesthesia and
therefore not used now - Epileptiform EEG
• Metabolism one-tenth that of halothane-- does
not release quantity of hepatotoxic metabolites
• Metabolism releases fluoride ion-- renal toxicity
27. Isoflurane
• Isomer of enflurane and have
similar properties but slightly
more potent
• Induction dose is 1.5 – 3% and
maintenance dose is 1 – 2%
• Rapid induction (7-10 min) and
recovery
• By special vapourizer
28. • Advantages:
- Rapid induction and recovery -
Good muscle relaxation
- Good coronary vasodilatation
- CO maintained, HR increased –
beta receptor stimulation
- Less Myocardial depression than no
myocardial sensitization to
adrenaline
- No renal or hepatotoxicity
- Low nausea and vomiting
- No dilatation of pupil and no loss
of light reflex in deep anaesthesia
- No seizure and preferred in
neurosurgery
- Uterine muscle relaxation
• Disadvantages:
- Pungent and respiratory irritant
- Special apparatus required
- Respiratory depression--
prominent
- Maintenance only, no induction
- Hypotension
- ß adrenergic receptor stimulation
- Costly (Desflurane and
Sevoflurane ----- read yourself)
29. Intravenous Anaesthetics
• For induction only
• Rapid induction (one arm brain circulation time)
• For maintenance not used
• Alone – supplemented with analgesic and muscle relaxants.
31. Thiopentone sodium:
• Barbiturate: Ultra short acting
---Water soluble
• Alkaline
• Dose-dependent suppression of CNS
activity
• Dose: 3-5mg/kg iv (2.5%) solution –
15 to 20 seconds Pharmacokinetics:
-Redistribution
-Hepatic metabolism (elimination half-
life 7-12 hrs)
-CNS depression persists for long (>12
hr)
32. • Disadvantages:
- Depth of anaesthesia
difficult to judge
- Pharyngeal and laryngeal
reflexes persists
- Apnoea – controlled
ventilation
- Respiratory depression
- Hypotension (rapid) – shock
and hypovolemia – CVS
collapse
- Poor analgesic and muscle
relaxant
- Gangrene and necrosis
- Shivering and delirium
• Advantages:
- Rapid induction
- Does not sensitize
myocardium to adrenaline
- No nausea and vomiting
- Non-explosive and non-
irritant
- Short operations (alone)
Other uses: convulsion,
psychiatric patients and
narcoanalysis of criminals –
by knocking off guarding
33. Propofol
• Rapid onset and have a short
duration of action
• Highly protein bound in vivo and is
metabolized by conjugation in the
liver
• Very good anesthetic for induction
and maintaince of anesthesia with
no accumulation effect
• Side-effects are pain on injection,
hypotension and transient apnea
following induction
• Used for the induction, maintenance
of GA and sedation
• Useful for day-case surgery
34. Ketamine
• Dissociative anaesthetic
• NMDA Receptor Antagonist
• Cardiovascular stimulant
• Catatonia, analgesia, and amnesia without
loss of consciousness
• Useful for anesthetizing patients at risk for
hypotension and bronchospasm and for
certain paediatric procedures
35. Etomidate
• Rapid induction
• Minimal change in cardiac function and
respiratory rate
• Not analgesic
• Cause pain on injection and nausea
postoperatively
• Prolonged administration may cause adrenal
suppression
37. Introduction
• Local anaesthetics (LAs) are drugs which upon topical application or
local injection cause reversible loss of sensory perception, especially
of pain, in a restricted area of the body.
• They block generation and conduction of nerve impulse at any part of
the neuron with which they come in contact, without causing any
structural damage.
• Thus, not only sensory but also motor impulses are interrupted when
a LA is applied to a mixed nerve, resulting in muscular paralysis and
loss of autonomic control as well.
38. Features Of
Local
Anaesthetics
Should have quick onset of action
Should not be irritating to skin & mucous
membranes
Duration of action must be long enough to
allow desired surgery to be completed
Should be effective on both injection & local
application
Should have low Systemic toxicity
39. Should not cause any permanent damage on any
tissue.
Should be relatively free from producing allergic
reaction.
Should be stable in solution and readily undergo
biotransformation.
No LA in use today satisfy all of these criteria
, however all anesthetics do meet a
majority of them.
40. Chemistry
All local anesthetics are weak bases,they have
amphiphilic property
Consist of hydrophilic secondary or tertiary amine on
one side
Lipophilic aromatic residue on other side
ØTwo are joined by an alkyl chain through an ester
or amide linkage
42. Advantage of Amide LAs over Ester LAs
• Produce more intense and longer lasting anaesthesia .
• Bind to α1acid glycoprotein in plasma.
• Not hydrolyzed by plasma esterase's.
• Rarely causes hypersensitivity reaction.
43. Classification
1.InjectableAnaesthetic
(a)Low Potency, Short Duration
ex. Procaine, Chloroprocaine
(b)Intermediate potency and
duration
ex. Lidocaine, Prilocaine
(c)High potency and long duration
ex. Tetracaine, Bupivacaine,
Ropivacaine, Dibucaine
2.SurfaceAnaesthetic:
(a)Soluble
ex. Cocaine, Lidocaine, Tetracaine
(b)Insoluble
ex. Benzocaine, Butyl-amino-
benzoate, Oxethazaine benoxinate
45. Mechanism of action of LAs
LA blocks the nerve conduction by reducing entry of Na+
through the voltage gated channels
Due to this, they block the initiation & propagation of nerve
impulse.
At higher doses it also blocks
-Voltage gated Ca2+ channels
-K+channels
46. Pharmacokinetics
Absorption:-
Local anesthetics are absorbed when ingested.
Some local anesthetics may be absorbed in toxic amounts after
topical use.
Absorption after an injection depends on drug solubility in lipid
and in water, tissue vascularity and local anesthetic and
vasoconstrictor effects on local circulation.
Distribution:-
Amides-wide distribution –I.V.-lipophilic taken up by highly
perfused organs-then moderately perfused.
Ester type- short plasma half life
47. Metabolism and excretion:-
Esters are hydrolyzed by plasma and liver esterases.
Longer-acting esters are often metabolized more slowly.
Patients with altered pseudo-cholinesterase activity may be highly
sensitive to these drugs.
Amides are metabolized in the liver by cyp450.-N-dealkylation
then hydrolysis except prilocaine- hydrolysis first-o toludine-can
cause methemoglobinemia.
Patients with severe hepatic damage or advanced congestive heart
failure may be unusually sensitive to these drugs.
Some amides are partially excreted unchanged in the urine.
Acidification can enhance excretion.
49. Precautions and interactions:-
Aspirate lightly to avoid intravascular injection.
Inject the LA slowly &take care not to exceed the maximum
safe dose, especially in children.
Propranolol may reduce metabolism of lidocaine and other
amide LAs by reducing hepatic blood flow.
Vasoconstrictor (Adr) containing LA should be avoided for
patients with ischemic heart disease, cardiac arrhythmia,
uncontrolled hypertension those receiving β-blockers or
tricyclic antidepressants.
51. Surface Anaesthesia
• Application of a local
anesthetic to nose, mouth,
throat, tracheobronchial tree,
esophagus.
• Onset & duration depends on
the site, the drug, its
concentration and form.
• Absorption of soluble LAs
from mucous membrane is
rapid.
52. Infiltration Anaesthesia
• Injection of LA directly into
tissue under the skin.
• Used primarily for surgical
procedures.
• LAs most frequently used are
lidocaine (1%), bupivacaine
(0.25%), etidocaine(0.5-1%),
ropivacaine(0.5-1%),
mepivacaine(1-3%) and
prilocaine(1-4%).
• Mix with adrenaline
(1:20000) to prolong the
action
53. Conduction block
• Injected around nerve trunks
so that area distal to injection
is anaesthetised and paralyzed
• Choice of LA and
concentration is mainly
determined by the required
duration of action.
• Lidocaine for intermediate
duration of action.
• Longer lasting anesthesia
bupivacaine may be selected.
54. Field block:
• Produced by injecting the LA
subcutaneously in the
surrounding area of nerve so
that all nerves coming to
particular field are blocked.
• Herniorrhaphy, Appendicectom
y,dental procedures, scalp
stitching, operations on forearms
and legs etc.
• Larger area can be
anaesthetized with lesser drug
compared to infiltration.
Nerve Block:
• local anesthetic is injected around a nerve that
leads to the operative site.
• Usually more concentrated forms of local
anesthetic solutions are used.
eg. radial nerve block, ulnar nerve block so on.
• Nerve block lasts than field block or infiltration
anaesthesia.
• Lidocaine (1.5%), mepivacaine(1.5%),
bupivacaine (0.25- 0.35%) can be used.
55. Epidural Anaesthesia
• Spinal dural space is filled with semi
liquid fat through which nerve root
travel Injected in this space- acts
primarily on nerve roots and small
amounts permeates through
intravertebral foramina to produce
multiple paravertebral blocks.
• Used to produce analgesia or
anaesthesia in surgical and obstetric.
• Divided into 3 categories depending
on site of action:
1.Thoracic:
2.Lumbar:
3.Caudal:
56. Spinal Anaesthesia
• Injected into the
subarachnoid space
between L2-3 or L3-4 of
the spinal cord .
• Suitable LA like
lidocaine(3-5%),
bupivacaine (0.5-
0.8%), tetracaine(0.3-
0.5%).
• Primary site of action is
cauda equina rather than
spinal cord.
• Used to anaesthetize lower
abdomen and hind limbs.
57. • Use of hyperbaric(in7.5-10% glucose) or hypobaric (in distilled water)
solution of LA .
• Proper positioning of the patient is also limiting the block to the desired
level.
• Advantages over general anaesthesia are:
Safer Produces good analgesia and muscle relaxation without loss of
consciousness Cardiac, pulmonary, renal disease and diabetic pose less
problem.
58. • Complication of spinal anaesthesia:
Respiratory paralysis Hypotension Headache
Cauda equina syndrome Septic meningitis
• Contraindications:
Hypotension & hypovolemia
Infant & children's - control of level is difficult Vertebral abnormalities -
kyphosis
59. Intravenous regional anaesthesia:
• Also referred as Bier’s
block & used for upper
limb and orthopedic
procedures.
• Regional analgesia
produced within 2-5min
and last till 5- 10min.
• Only ¼ of the
injected drug enters
systemic circulation
when tourniquet is
removed.
• Bradycardia can occur
and bupivacaine should
not be used because of
higher cardio toxicity.
60. • Commonly used drug with LA
• Adrenaline –to prolong the effect of
LA and to reduce the toxicity by
reducing absorption from local area.
• Hyaluronidase-enzyme which cause
depolymerization of hyaluronic acid
and increase the permeability of
injected fluid.
63. Cocaine
• First local anaesthetic obtained from
leaves of plant Erythroxylon Coca.
• It is no more in use nowadays because
of its corneal toxicity, addicting nature
etc.
64. Procaine
• First synthetic local anaesthetic
• Used as a small area infiltration
and spinal anaesthetic.
• It is poorly absorbed from
mucous membrane so no topical
use.
• 2% injection is the usual
preparation.
65. Lignocaine • Most commonly used LA
• In ophthalmology 4% [topical]
and 2% [infiltration] solutions
are commonly used.
• It has quick onset of action and
high degree of penetration.
• The drug is recommended for
topical, nerve block, infiltration
and epidural injection and for
dental analgesia.
• It may cause drowsiness.
66. Bupivacaine
• Onset of action is slow
• A 0.75% solution produce
anaesthesia and akinesia for 8-12
hours.
• In ophthalmic practice, usually
a combination of 2%
lignocaine,0.75% bupivacaine
and 7.5 TRU of hyaluronidase is
used for periocular injection, and
surgery of any kind may be
performed on such type of
anaesthetized eye.