Cocaine is a powerful and addictive stimulant drug derived from the coca plant. It works by inhibiting the reuptake of dopamine in the brain's reward pathway, producing feelings of euphoria. Cocaine can be administered via multiple routes and has a fast onset of action and short duration. It is highly addictive due to how it activates the brain's reward system. Cocaine use can lead to numerous severe health issues and its withdrawal produces intense cravings. Treatment focuses on counseling, support groups, and some promising medications, but complete abstinence is very difficult for chronic users to achieve due to the biological and psychological aspects of cocaine addiction.
A POWER POINT PRESENTATION BY DR.SANGEETA CHOWDHRY & DR.SUNIL SHARMA, DEPARTMENT OF FORENSIC MEDICINE & TOXICOLOGY, GOVT. MEDICAL COLLEGE, JAMMU (JAMMU AND KASHMIR)
Toxicology
Volatile poisons
Ethyl alcohol (Ethanol)
It is colorless liquid with characteristic odor.
It is obtained from fermentation of food e.g. barley , bread or fruits.
The percentage of alcohol in beverages caries according to the type of alcoholic beverages.
Its most common ingested toxin throughout world,
Thousands of deaths occur due to overdose , suicide and accidental intake of alcohol.
Alcoholic beverage
The alcoholic content of different beverages are:
Beer:2-8%
Ligh wine:5-10%
Heavy wines:10-20%
Brany ,Rhum (rum),vodka and wisky:40-50% .
Absorption and elimination
Ethyl alcohol can be absorbed by the mucus membrane of the stomach and the upper part of the small intestine.
Absorption occurs more rapidly when its taken on an empty stomach. its delayed by the presence of food, especially fatty food.
After absorption : it reaches its maximal concentration in the blood after 0.5-1 hr.
About 90% of the amount absorbed is oxidized in the body into acetaldehyde and then into carbon dioxide + water +energy. the remaining 10% is excreted unchanged in the urine and breath.
The rate of oxidation of alcohol in the body after absorption is 0.1ml/hg/bodywt/hour.
The concentration of alcohol in the blood can be indirectly estimated by measuring its cocentration in alveolar air by aclometer.
Metabolism
Ethanol is oxidized to acetaldehyde by alcohol dehydrogenase and then metabolized into Co2 and water, this is considered the main path of metabolism , microsomal ethanol oxidizing system (MEOS) plays a minor rule.
Because of mucosal and hepatic metabolism , the oral dose yields a lower blood ethanol level than in equivalent
Administered I.V dose.
METHYL ALCOHOL (Methanol)
Methyl alcohol is widely used in industry and laboratories and hospitals as a solvent. Many cases of poisoning occurs due to adulteration of ethyl alcohol by adding methyl alcohol, or methyl alcohol is taken as a substitute for ethyl alcohol .
Metabolism
Methyl ALCOHOL is metabolized mainly in the liver by dehydrogenases to formaldehyde and formic acid, both are more toxic than methanol leading to blindness and acidosis .
Fatal Dose :
60-150 mls 15 mls is enough to cause visual effect.
Action:
retinal edema , optic atrophy , CNS depression, cyanosis, metabolic acidosis , neuritis optic and blindness
Fatal Period : variable
Fomepizole
Tobacco . Its definition, available forms , fatal dose , contents , pathophysiology , pharmacokinetics and toxicology. Diagnosis and treatment of toxicity.
A POWER POINT PRESENTATION BY DR.SANGEETA CHOWDHRY & DR.SUNIL SHARMA, DEPARTMENT OF FORENSIC MEDICINE & TOXICOLOGY, GOVT. MEDICAL COLLEGE, JAMMU (JAMMU AND KASHMIR)
Toxicology
Volatile poisons
Ethyl alcohol (Ethanol)
It is colorless liquid with characteristic odor.
It is obtained from fermentation of food e.g. barley , bread or fruits.
The percentage of alcohol in beverages caries according to the type of alcoholic beverages.
Its most common ingested toxin throughout world,
Thousands of deaths occur due to overdose , suicide and accidental intake of alcohol.
Alcoholic beverage
The alcoholic content of different beverages are:
Beer:2-8%
Ligh wine:5-10%
Heavy wines:10-20%
Brany ,Rhum (rum),vodka and wisky:40-50% .
Absorption and elimination
Ethyl alcohol can be absorbed by the mucus membrane of the stomach and the upper part of the small intestine.
Absorption occurs more rapidly when its taken on an empty stomach. its delayed by the presence of food, especially fatty food.
After absorption : it reaches its maximal concentration in the blood after 0.5-1 hr.
About 90% of the amount absorbed is oxidized in the body into acetaldehyde and then into carbon dioxide + water +energy. the remaining 10% is excreted unchanged in the urine and breath.
The rate of oxidation of alcohol in the body after absorption is 0.1ml/hg/bodywt/hour.
The concentration of alcohol in the blood can be indirectly estimated by measuring its cocentration in alveolar air by aclometer.
Metabolism
Ethanol is oxidized to acetaldehyde by alcohol dehydrogenase and then metabolized into Co2 and water, this is considered the main path of metabolism , microsomal ethanol oxidizing system (MEOS) plays a minor rule.
Because of mucosal and hepatic metabolism , the oral dose yields a lower blood ethanol level than in equivalent
Administered I.V dose.
METHYL ALCOHOL (Methanol)
Methyl alcohol is widely used in industry and laboratories and hospitals as a solvent. Many cases of poisoning occurs due to adulteration of ethyl alcohol by adding methyl alcohol, or methyl alcohol is taken as a substitute for ethyl alcohol .
Metabolism
Methyl ALCOHOL is metabolized mainly in the liver by dehydrogenases to formaldehyde and formic acid, both are more toxic than methanol leading to blindness and acidosis .
Fatal Dose :
60-150 mls 15 mls is enough to cause visual effect.
Action:
retinal edema , optic atrophy , CNS depression, cyanosis, metabolic acidosis , neuritis optic and blindness
Fatal Period : variable
Fomepizole
Tobacco . Its definition, available forms , fatal dose , contents , pathophysiology , pharmacokinetics and toxicology. Diagnosis and treatment of toxicity.
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- 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
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 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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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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
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Cocaine
1.
2. WHAT IS COCAINE?
• Cocai ne (benzoyl -m hyl -ecgoni ne) (C 21N 4) i s
et 17H O
a cr yst al l i ne al kal oi d pr epar ed f r omt he l eaves
of t he Er yt hr oxyl on coca pl ant .
• Cocai ne i s a bi t t er , w t e, odor l ess, cr yst al l i ne
hi
dr ug.
• A ccor di ng t o t he N i onal I nst i t ut e of D ug A
at r buse
(N D ), cocai ne i s:“A pow f ul l y addi ct i ve dr ug
I A er
t hat can be sni f f ed, i nj ect ed, chew or sm
ed oked.”
3. CO NE HAS BEEN CLASSI FI ED AS A SCHEDU I I DRUG BY THE
CAI LE
UNI TED STATES.
4. FORMS OF COCAINE
1. C ocai ne hydr ochl or i de (pow ) : pr epar ed by
der
di ssol vi ng t he al kal oi d i n hydr ochl or i c aci d,
f or m ng a w er sol ubl e sal t .
i at
2. C ack cocai ne : pr oduced w
r hen cocai ne
hydr ochl or i de i s m xed w t h sodi umbi car bonat e
i i
and w er , and t hen heat ed.
at
5. ROUTE OF ADMINISTRATION
• C ocai ne can be adm ni st er ed as a dr ug of abuse i n t he
i
f ol l ow ng w
i ays :
• 1. Cocai ne hydr ochl or i de :
• Sni f f ed (i nt r anasal ),
• sm ng,
oki
• i nt r avenous i nj uct i on (i ncl udi ng bei ng m xed w t h her oi n
i i
or i ngest i on)
6. • 2. C ack cocai ne : i nhal at i on of vapour f r omheat ed
r
f oi l or pi pe.
8. O SET & D R TI O O A TI O
N UA N F C N
FO C C I N D
R O A E EPEN S O TH R U O
D N E O TE F
A M N STR TI O .
DI I A N
Route onset Duration
inhalation 7S 20 min
IV 15 S 22-30 min
Nasal 3 min 45-90 min
oral 10 min 60 min
9. COCAINE MECHANISM OF ACTION
• Cocaine binds to dopamine re-uptake transporters on the pre-
synaptic membranes of dopaminergic neurones.
• This binding inhibits the removal of dopamine from the synaptic
cleft and its subsequent degradation by monoamine oxidase in
the nerve terminal.
10. COCAINE MECHANISM OF ACTION
• Dopamine remains in the synaptic cleft and is free to bind to its
receptors on the post synaptic membrane, producing further
nerve impulses.
• This increased activation of the dopaminergic reward pathway
leads to the feelings of euphoria and the ‘high’ associated with
cocaine use.
11. WHEN GIVEN LOCALLY
• Cocaine produces anesthesia by inhibiting excitation of nerve
endings or by blocking conduction in peripheral nerves.
• This is achieved by reversibly binding to and inactivating sodium
channels.
• Sodium influx through these channels is necessary for the
depolarization of nerve cell membranes and subsequent
propagation of impulses along the course of the nerve.
• When a nerve loses its ability to propagate an impulse, the
individual loses sensation in the area supplied by the nerve.
12. THERAPEUTIC USES OF COCAINE
• Cocaine is used by health care professionals to temporarily numb the lining
of the mouth, nose, and throat (mucous membranes) before certain medical
procedures (e.g., biopsy, stitches, wound cleaning).
• It is an anesthetic that works quickly to numb the area about 1-2 minutes
after application.
• Cocaine also causes blood vessels to narrow, an effect that can decrease
bleeding and swelling from the procedure.
• It is also sometimes used in palliative care of terminally ill patient.
13. METABOLISM OF COCAINE
Serum half life of 45-90 minutes
Only 1% of the drug is recovered in urine after ingestion
Cocaine can be detected in blood or urine only for several
hours after its use
Cocaine metabolites are detectable for 2-5 days
Hair analysis provides a very sensitive marker for cocaine use
within the preceding weeks to months
14. EFFECTS OF COCAINE
1. Initial Low Doses :
A. Physical Effects :
1. Tachycardia, tachypnoea,
2. hypertension,
3. Dilated pupils (& flattened lenses),
4. sweating
5. reduced appetite, reduced need for sleep, reduced lung function,
6. dry mouth,
7. impaired motor control & performance of delicate skills and driving.
15. B- Psychological Effects :
1. Euphoria, sense of well being,
2. impaired reaction time and attention span,
3. impaired learning of new skills.
20. SYSTEMATIC FINDINGS
CARDIOVASCULAR SYSTEM :
Acute Cardiovascular Pathology
Cocaine is directly toxic to cardiac myocytes, and this cardiotoxic
effect does not depend on the
route of administration, and may not necessarily have to occur
at large doses. Neither does it
appear that pre-existing cardiovascular pathology is a pre-
requisite for cocaine toxicity
21. Acute Myocardial Infarction
• The mechanism of cocaine related myocardial infarction is
likely to be multifactorial in nature, and could be related to focal
vasoconstriction of coronary arteries, or spasm of these
arteries.
• Cocaine acts both directly and indirectly on vascular smooth
muscle, via-adrenergic
stimulation (noradrenaline) and an independent, dose-related
effect.
• Cocaine also increases coronary vascular resistance at a time
when it is increasing heart rate and myocardial oxygen demand
22. • Cardiac Arrhythmias
• Cocaine is a Class II antiarrhythmic agent, and exerts its actions
by blocking sodium channels.
• In large doses it is arrhythmogenic, possibly due to it’s effects
on catecholamines rather than any direct effect, or due to
secondary arrhythmias following cardiac
ischaemia due to prolonged coronary artery vasoconstriction.
• A cocaine-induced rise in
intracellular calcium may also be responsible.
23. RESPIRATORY SYSTEM
Non-specific findings at autopsy include pulmonary edema and
congestion, possible due to excess catecholamine release.
Specifically, cocaine use has been associated with :
granulomas in the lungs, and this may represent either
impurities in the drug, or more likely poly drug abuse
Spontaneous pneumothorax or pneumopericardium
Haemoptysis
Pulmonary hypertension
24. GASTROINTESTINAL TRACT
The pathological findings in the gastrointestinal tract of a
cocaine abuser are similar to those found in experimental
animals treated with high levels of catecholamines, i.e.:
Ulceration and perforation
Ischaemic colitis
Severe bowel ischaemia and gangrene (vasoconstriction of
mesenteric vasculature)
Peptic ulcer perforation (due to a disruption of the internal
elastic lamina of the small
vessels supplying the ulcerated area
25. URINARY SYSTEM
Cocaine use is known to have caused:
• Renal infarction
• Renal thrombosis
• Haemolytic uraemic syndrome
• Rhabdomyolysis with myoglobinuric renal failure
26. CENTRAL NERVOUS SYSTEM
• Due to cocaine’s ability to produce hyperpyrexia, combined with
it’s effects on neurotransmitters, the drug may contribute to
seizure formation as well as hyperthermia. Seizures may be
‘primary’, due to cocaine lowering the seizure threshold, or
‘secondary’ to cardiac effects such as ventriculartachycardia
and fibrillation.
27. 11 WAYS TO DIE FROM COCAINE DRUG
ADDICTION
1. Acute hypertensive crises - quickly elevating blood pressure - blows out a
weak blood vessel in brain causing cerebral hemorrhage.
2. Hypertension chronic users may weaken blood vessels in their brain. Die
from strokes or complications after.
3. Acute hypotension - no blood with oxygen to the brain causing an
anaphylaxis - allergic reaction.
4. Status epilepticus - repeated convulsions - increased EEG activity.
5. C.N.S. Rebound - physical and emotional depression - depressed
medullary/respiratory centers of the brain knock you OUT - this is the most
common cause of cocaine death.
28. 6. Hyperpyrexia - Cocaine can raise the body to an extremely high
temperature. May feel cold on the outside. Shows bruising easily - temp 106
degrees (anal)
7. Pulmonary insult - heat fumes and chemicals in lungs cause lungs to
collapse.
8. Paranoid miscalculation - accidental death due to delusions and
hallucinations.
9. Suicide - during post-cocaine depression
10. Needle borne - infections from needle use.
11. Allergic Reaction - anticholinesterase (enzyme) deficiency 10-20 mg. of
cocaine will kill them - the drug never gets destroyed and recycles continuously
throughout the body.
29. COCAINE RISK FOR ABUSE OR DEPENDENCE
Community-based interview surveys suggest that up to one in six persons
who use cocaine will become dependent.. Users
Heavier users and users who take the drug Intravenously or by smoking
are more likely to become dependent than lighter users or intranasal and
oral users..addicts
The greater abuse potential of intravenous or smoked cocaine is attributed
to the faster rate of drug delivery to the brain (within 10 seconds), & faster
onset of psychological effects . Route
This faster onset is associated with a more intense pleasurable response
(the so-called "rate hypothesis" of psychoactive drug action
30. COCAINE ADDICTION
• Why is cocaine so highly addictive?
• Next to methamphetamine,* cocaine creates the greatest
psychological dependence of any drug. It stimulates key
pleasure centres within the brain and causes extremely
heightened euphoria.
• The addictive properties of cocaine are thought to be due to
brain dopamine D2-receptor stimulation.
31. Cycle of Cocaine Addiction
This addiction has biological, behavioral & psychological aspects
Cocaine
Use
EUPHORIA
Positive Reinforcement
Brain Reward Neuroadaptations
Cocaine
Seeking
Behavior CRAVING
Negative Reinforcement
Treatment interventions are designed to reduce euphoria & craving