This document discusses various drugs and their dependence liability. It describes how dependence develops from repeated drug administration and involves tolerance, physical withdrawal, and psychological craving. Different classes of drugs are listed with their typical dependence liability, from very strong for narcotics to weak or absent for LSD and cannabis. The mechanisms, effects, metabolism, and treatment approaches are summarized for several specific drugs, including nicotine, ethanol, cannabis, LSD, and cocaine.
Drug dependence
It is a physical or psychological condition resulting from repeated administration of mood-altering drugs.
It is a state characterized by a compulsion to take the drug on a continuous or periodic basis in order to experience its euphoriogenic effects.
If a mood-altering drug is unavailable, then the individual develops certain withdrawal symptoms.
Physical dependence + Psychological dependence
Drug addiction
Drug habituation
Drug abuse
Habit-forming drug
Drug dependence
It is a physical or psychological condition resulting from repeated administration of mood-altering drugs.
It is a state characterized by a compulsion to take the drug on a continuous or periodic basis in order to experience its euphoriogenic effects.
If a mood-altering drug is unavailable, then the individual develops certain withdrawal symptoms.
Physical dependence + Psychological dependence
Drug addiction
Drug habituation
Drug abuse
Habit-forming drug
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
Parasympatholytics are the drugs that block or inhibit the actions of acetylcholine at postganglionic nerve endings and cholinergic receptors. They are also referred to as anticholinergics or cholinergic blocking agents or antispasmodics.
Anticholinergic drugs include atropine and related drugs- atropine is the prototype. Atropine is obtained from the plant Atropa belladonna. Atropine and scopolamine (hyoscine) are the belladonna alkaloids. They compete with acetylcholine for muscarinic receptors and block this receptors-they are muscarinic antagonists.
Diagnosis and treatment of amphetamine abuseAsra Hameed
Amphetamine is a stimulant and an appetite suppressant. It stimulates the central nervous system (nerves and brain) by increasing the amount of certain chemicals in the body. This increases heart rate and blood pressure and decreases appetite, among other effects.
Amphetamine is used to treat narcolepsy and attention deficit disorder with hyperactivity (ADHD).
Amphetamine may also be used for purposes other than those listed in this medication guide.
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
Parasympatholytics are the drugs that block or inhibit the actions of acetylcholine at postganglionic nerve endings and cholinergic receptors. They are also referred to as anticholinergics or cholinergic blocking agents or antispasmodics.
Anticholinergic drugs include atropine and related drugs- atropine is the prototype. Atropine is obtained from the plant Atropa belladonna. Atropine and scopolamine (hyoscine) are the belladonna alkaloids. They compete with acetylcholine for muscarinic receptors and block this receptors-they are muscarinic antagonists.
Diagnosis and treatment of amphetamine abuseAsra Hameed
Amphetamine is a stimulant and an appetite suppressant. It stimulates the central nervous system (nerves and brain) by increasing the amount of certain chemicals in the body. This increases heart rate and blood pressure and decreases appetite, among other effects.
Amphetamine is used to treat narcolepsy and attention deficit disorder with hyperactivity (ADHD).
Amphetamine may also be used for purposes other than those listed in this medication guide.
This presentation covers the nature and features of drug dependence. It also gives coverage to different psychological or biological models of drug addiction.
Drug Dependence & Abuse - Presentation by Akshay AnandAkshay Anand
A presentation on Drug Dependence and Drug Abuse that explains in brief about the various practices of substance abuse and dependence and the medicinal agents and drugs that can be used to overcome or treat such abuses. This was presented as a part of curriculum by Akshay Anand in Sree Siddaganga College of Pharmacy during May 2013.
Effective treatment for drug addiction in Mindheal Homeopathy clinic ,Chembur...Shewta shetty
"Drug Addiction- drug addiction is characterized by the use of narcotic drugs or alcohol excessively so that when its usage is stopped withdrawal symptoms are manifested in the body. Drug addiction is a complex but treatable condition. It can be treated by proper rehabilitation of the patient along with mindheal therapy."/>
Homeopathic Doctor - Dr. Anita Salunke homeopathic clinic for Drug Addiction ...Shewta shetty
Homeopathic Doctor Anita Salunke practices in Chembur, Mumbai, India in her homeopathic clinic Mindheal. Find more information about homeopathic treatment at Mindheal. Welcome to safe, sure and effective homeopathic treatment Drug Addiction
This presentation describes various movement disorders and its management strategies with particular focus of management of parkinson's disease. It gives basic overview of the drugs also.
Parkinson's disease (PD) is a neurodegenerative disorder that affects predominately dopamine-producing (“dopaminergic”) neurons in a specific area of the brain called substantia nigra. ... People with PD may experience: Tremor, mainly at rest and described as pill rolling tremor in hands .
In this presentation we will discuss Parkinsonism and other movement disorders, Pathophysiology of parkinsonism and its types, drugs used in Parkinsonism and their pharmacology and briefly discuss the drugs used to treat other movement disorders like tourettes syndrome, Huntington chorea etc.
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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
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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
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.
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.
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
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.
2. TypeType ExamplesExamples Dependence liabilityDependence liability
Narcotic analgesicsNarcotic analgesics MorphineMorphine Very strongVery strong
DiamorphineDiamorphine Very strongVery strong
General CNS depressantsGeneral CNS depressants EthanolEthanol StrongStrong
BarbituratesBarbiturates StrongStrong
MethaqualoneMethaqualone ModerateModerate
GlutethimideGlutethimide ModerateModerate
AnaestheticsAnaesthetics ModerateModerate
SolventsSolvents StrongStrong
Anxiolytic drugsAnxiolytic drugs BenzodiazepinesBenzodiazepines ModerateModerate
Psychomotor stimulantsPsychomotor stimulants AmphetaminesAmphetamines StrongStrong
CocaineCocaine Very strongVery strong
CaffeineCaffeine WeakWeak
NicotineNicotine Very strongVery strong
Psychotomimetic agentsPsychotomimetic agents LSDLSD Weak or absentWeak or absent
MescalineMescaline Weak or absentWeak or absent
PhencyclidinePhencyclidine ModerateModerate
CannabisCannabis Weak or absentWeak or absent
3. Drug dependenceDrug dependence
Dependence is defined as a compulsive cravingDependence is defined as a compulsive craving
that develops as a result of repeatedthat develops as a result of repeated
administration of the drug.administration of the drug.
Dependence occurs with a wide range ofDependence occurs with a wide range of
psychotropic drugs, acting by many differentpsychotropic drugs, acting by many different
mechanisms.mechanisms.
The common feature of dependence-producingThe common feature of dependence-producing
drugs is that they have a positive reinforcingdrugs is that they have a positive reinforcing
action ('reward') associated with activation ofaction ('reward') associated with activation of
the mesolimbic dopaminergic pathway.the mesolimbic dopaminergic pathway.
4. dependence is often associated with (i)dependence is often associated with (i)
tolerance to the drug, which can arise by varioustolerance to the drug, which can arise by various
biochemical mechanisms; (ii) a physicalbiochemical mechanisms; (ii) a physical
abstinence syndrome, which varies in type andabstinence syndrome, which varies in type and
intensity for different classes of drug; (iii)intensity for different classes of drug; (iii)
psychological dependence (craving), which maypsychological dependence (craving), which may
be associated with the tolerance-producingbe associated with the tolerance-producing
biochemical changes.biochemical changes.
Psychological dependence, which usuallyPsychological dependence, which usually
outlasts the physical withdrawal syndrome, is theoutlasts the physical withdrawal syndrome, is the
major factor leading to relapse among treatedmajor factor leading to relapse among treated
addicts.addicts.
Though genetic factors contribute to drug-Though genetic factors contribute to drug-
seeking behaviour, no specific genes have yetseeking behaviour, no specific genes have yet
been identified.been identified.
5. Pharmacological approaches to treating drug dependencePharmacological approaches to treating drug dependence
MechanismMechanism ExamplesExamples
Substitution, to alleviateSubstitution, to alleviate
withdrawal symptomswithdrawal symptoms
Methadone, used short-term to blunt opiateMethadone, used short-term to blunt opiate
withdrawalwithdrawal
Benzodiazepines, to blunt alcohol withdrawalBenzodiazepines, to blunt alcohol withdrawal
Long-term substitutionLong-term substitution Methadone substitution for opiate addictionMethadone substitution for opiate addiction
Nicotine patches or chewing gumNicotine patches or chewing gum
Blocking responseBlocking response Naltrexone to block opiate effectsNaltrexone to block opiate effects
Mecamylamine to block nicotine effectsMecamylamine to block nicotine effects
Immunisation against cocaine to produce circulatingImmunisation against cocaine to produce circulating
antibody (not yet proven)antibody (not yet proven)
Aversive therapiesAversive therapies Disulfiram to induce unpleasant response to ethanolDisulfiram to induce unpleasant response to ethanol
Modification of cravingModification of craving Bupropion (antidepressant)Bupropion (antidepressant)
Naltrexone (blocks opiate receptors-also of value inNaltrexone (blocks opiate receptors-also of value in
treating other addictions)treating other addictions)
Clonidine (α-adrenoceptor agonist)Clonidine (α-adrenoceptor agonist)
Acamprosate (NMDA-receptor antagonist)Acamprosate (NMDA-receptor antagonist)
6. Pharmacology of nicotinePharmacology of nicotine
At a cellular level, nicotine acts on nicotinicAt a cellular level, nicotine acts on nicotinic
acetylcholine receptors, mainly of the α4β2 subtype,acetylcholine receptors, mainly of the α4β2 subtype,
to cause neuronal excitation. Its central effects areto cause neuronal excitation. Its central effects are
blocked by receptor antagonists such asblocked by receptor antagonists such as
mecamylamine.mecamylamine.
At the behavioural level, nicotine produces a mixtureAt the behavioural level, nicotine produces a mixture
of inhibitory and excitatory effects.of inhibitory and excitatory effects.
Nicotine shows reinforcing properties, associated withNicotine shows reinforcing properties, associated with
increased activity in the mesolimbic dopaminergicincreased activity in the mesolimbic dopaminergic
pathway, and self-administration can be elicited inpathway, and self-administration can be elicited in
animal studies.animal studies.
7. Pharmacology of nicotinePharmacology of nicotine
Electroencephalography changes show anElectroencephalography changes show an
arousal response, and subjects reportarousal response, and subjects report
increased alertness, accompanied by aincreased alertness, accompanied by a
reduction of anxiety and tension.reduction of anxiety and tension.
Peripheral effects of nicotine result mainly fromPeripheral effects of nicotine result mainly from
ganglionic stimulation: tachycardia, increasedganglionic stimulation: tachycardia, increased
blood pressure and increase gastrointestinalblood pressure and increase gastrointestinal
motility. Tolerance develops rapidly to thesemotility. Tolerance develops rapidly to these
effects.effects.
8. Nicotine is metabolised, mainly in the liver,Nicotine is metabolised, mainly in the liver,
within 1-2 hours. Its inactive metabolite,within 1-2 hours. Its inactive metabolite,
cotinine, has a long plasma half-life andcotinine, has a long plasma half-life and
can be used as a measure of smokingcan be used as a measure of smoking
habits.habits.
Nicotine replacement therapy (chewingNicotine replacement therapy (chewing
gum or skin patch preparations) improvesgum or skin patch preparations) improves
the chances of giving up smoking, but onlythe chances of giving up smoking, but only
when combined with active counselling.when combined with active counselling.
11. Effects of ethanolEffects of ethanol
Ethanol acts as a general CNSEthanol acts as a general CNS
depressant, similar to volatile anaestheticdepressant, similar to volatile anaesthetic
agents, producing the familiar effects ofagents, producing the familiar effects of
acute intoxication.acute intoxication.
Several cellular mechanisms areSeveral cellular mechanisms are
postulated: inhibition of calcium channelpostulated: inhibition of calcium channel
opening, enhancement of GABA actionopening, enhancement of GABA action
and inhibitory action at NMDA-typeand inhibitory action at NMDA-type
glutamate receptors.glutamate receptors.
12. Effective plasma concentrations:Effective plasma concentrations:
threshold effects: about 40 mg/100 mlthreshold effects: about 40 mg/100 ml
(5 mmol/l)(5 mmol/l)
severe intoxication: about 150 mg/100severe intoxication: about 150 mg/100
mlml
death from respiratory failure: about 500death from respiratory failure: about 500
mg/100 ml.mg/100 ml.
Main peripheral effects are self-limitingMain peripheral effects are self-limiting
diuresis (reduced antidiuretic hormonediuresis (reduced antidiuretic hormone
secretion), cutaneous vasodilatation andsecretion), cutaneous vasodilatation and
delayed labor (reduced oxytocindelayed labor (reduced oxytocin
secretion).secretion).
Neurological degeneration occurs inNeurological degeneration occurs in
heavy drinkers, causing dementia andheavy drinkers, causing dementia and
peripheral neuropathies.peripheral neuropathies.
13. Effects of ethanolEffects of ethanol
Long-term ethanol consumption causes liver disease,Long-term ethanol consumption causes liver disease,
progressing to cirrhosis and liver failure.progressing to cirrhosis and liver failure.
Moderate ethanol consumption has a protective effectModerate ethanol consumption has a protective effect
against ischemic heart disease.against ischemic heart disease.
Excessive consumption in pregnancy causes impairedExcessive consumption in pregnancy causes impaired
fetal development, associated with small size, abnormalfetal development, associated with small size, abnormal
facial development and other physical abnormalities, andfacial development and other physical abnormalities, and
mental retardation.mental retardation.
Tolerance, physical dependence and psychologicalTolerance, physical dependence and psychological
dependence all occur with ethanol.dependence all occur with ethanol.
Drugs used to treat alcohol dependence includeDrugs used to treat alcohol dependence include
disulfiram (aldehyde dehydrogenase inhibitor),disulfiram (aldehyde dehydrogenase inhibitor),
naltrexone (opiate antagonist) and acamprosate (NMDA-naltrexone (opiate antagonist) and acamprosate (NMDA-
receptor antagonist).receptor antagonist).
17. CannabisCannabis
Main active constituent is Δ9-tetrahydro cannabinol (THC),Main active constituent is Δ9-tetrahydro cannabinol (THC),
though pharmacologically active metabolites may bethough pharmacologically active metabolites may be
important.important.
Actions on CNS include both depressant andActions on CNS include both depressant and
psychotomimetic effects.psychotomimetic effects.
Subjectively, subjects experience euphoria and a feeling ofSubjectively, subjects experience euphoria and a feeling of
relaxation, with sharpened sensory awareness.relaxation, with sharpened sensory awareness.
THC also shows analgesic and antiemetic activity,THC also shows analgesic and antiemetic activity,
Peripheral actions include vasodilatation, reduction ofPeripheral actions include vasodilatation, reduction of
intraocular pressure and bronchodilatation.intraocular pressure and bronchodilatation.
Cannabinoid receptors belong to the G-protein-coupledCannabinoid receptors belong to the G-protein-coupled
receptor family, linked to inhibition of adenylate cyclase andreceptor family, linked to inhibition of adenylate cyclase and
effects on calcium and potassium channel function, causingeffects on calcium and potassium channel function, causing
inhibition of synaptic transmission.inhibition of synaptic transmission.
18. CannabisCannabis
Anandamide, an arachidonic acid derivative, is anAnandamide, an arachidonic acid derivative, is an
endogenous ligand for the CNS cannabinoid receptor; itsendogenous ligand for the CNS cannabinoid receptor; its
function has not yet been ascertained.function has not yet been ascertained.
Cannabinoids are less liable than opiates, nicotine orCannabinoids are less liable than opiates, nicotine or
alcohol to cause dependence but may have long-termalcohol to cause dependence but may have long-term
psychological effects.psychological effects.
Nabilone, a THC analogue, has been developed for itsNabilone, a THC analogue, has been developed for its
antiemetic property.antiemetic property.
Though cannabinoids are not available for clinical use,Though cannabinoids are not available for clinical use,
trials are in progress for symptomatic treatment oftrials are in progress for symptomatic treatment of
multiple sclerosis and AIDS.multiple sclerosis and AIDS.