The document provides information on the treatment of various types of poisonings and overdoses. It discusses the general principles of poisoning treatment which include stopping the source of poison, limiting absorption, supportive therapy, and specific antidotes. It then covers the treatment of specific types of poisonings and overdoses, including barbiturate poisoning, morphine overdose, organophosphate poisoning, and heavy metal poisoning. For each, it discusses symptoms, causes, diagnosis, and standard treatment approaches.
An antidote is a substance that can counteract a form of poisoning.Antidotes for anticoagulants are sometimes referred to as reversal agents.Antidote a medicine or other remedy for counteracting the effects of poison, disease, etc
This is the second part of my presentation. It is all about the review on Routes and rights of drug administration. The slide also covers IP & Drug Laws too.
Please find the power point on Organophosphate poisoning and its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
A catecholamine is a monoamine, an organic compound that has a catechol (benzene with two hydroxyl side groups at carbons 1 and 2) and a side-chain amine. Included among catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine. Release of the hormones epinephrine and norepinephrine from the adrenal medulla of the adrenal glands is part of the fight-or-flight response.
An antidote is a substance that can counteract a form of poisoning.Antidotes for anticoagulants are sometimes referred to as reversal agents.Antidote a medicine or other remedy for counteracting the effects of poison, disease, etc
This is the second part of my presentation. It is all about the review on Routes and rights of drug administration. The slide also covers IP & Drug Laws too.
Please find the power point on Organophosphate poisoning and its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
A catecholamine is a monoamine, an organic compound that has a catechol (benzene with two hydroxyl side groups at carbons 1 and 2) and a side-chain amine. Included among catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine. Release of the hormones epinephrine and norepinephrine from the adrenal medulla of the adrenal glands is part of the fight-or-flight response.
millions of poisoning cases are seen every year with several hundred dying but several more are unreported. A poison may be defined as any substances which if administered or comes in contact with living being produces ill-health.
Clinical symptoms and management of poisoningschiragmarwah1
This presentation contains relevant and genuine information regarding clinical symptoms and management of different types of poisonings such as Barbiturate poisoning, Morphine poisoning, Arsenic Poisoning, Organophosphate poisoning, and Lead Poisoning. Hopefully the contents in presentation will help the pharma students to understand the concept of poisoning in a better and appropriate way.
Regards:
Chirag Marwah
What is definition of poisoning?
Poisoning is injury or death due to swallowing, inhaling, touching or injecting various drugs, chemicals, venoms or gases. Many substances — such as drugs and carbon monoxide — are poisonous only in higher concentrations or dosages.
activated charcoal – sometimes used to treat someone who's been poisoned; the charcoal binds to the poison and stops it being further absorbed into the blood.
antidotes – these are substances that either prevent the poison from working or reverse its effects.
There are four major routes by which a chemical may enter the body:
Inhalation (breathing)
Skin (or eye) contact.
Swallowing (ingestion or eating)
Injection.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
- 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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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
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.
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
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. • Toxicology is the science that deals with the
study of poisons, their source, properties,
actions, detection and treatment of poisoning.
3. General principles of treatment
• Stop the source of poison
• Limit the absorption of poison
• Supportive therapy – ABC and coma cock tail
– Naloxone 2 mg
– Thiaine 100 mg
– Dextrose 50% 50 mL
• Specific therapy with antidotes
• Other measures
4. Other measures are
– Forced alkaline diuresis : Frusemide, Sodium
bicarbonate and IV fluids
– Forced acid diuresis : Frusemide, Ascorbic acid
and IV fluids
– Hemodialysis
5. General management
• Gut decontamination
• Management of respiratory failure
• Management of circulatory failure
• Management of fluid and electrolyte
imbalance
• Metabolic acidosis
• Convulsions
• Antidotes
6. Gut decontamination
• Emesis : Ipecac syrup 20-30 ml or Strong salt
solution or freshly prepared mustard powder
solution
• Do not induce emesis : Corrosive agent or
petroleum product or unconscious patient
• Stomach wash
• Activated charcoal / Medicoal
• Purgatives: MgSO4 20-30 g or Sod. Sulphate
20-30 g
12. Antidotes
• Physical antidote : Activated charcoal adsorbs
alkaloids
• Chemical antidote : acetic acid reacts with
alkalis, chelating agents bind heavy metals like
lead, arsenic, copper, mercury, etc.
• Pharmacological antidotes
13. Pharmacological antidotes
Toxic agent Antidote
Paracetamol N-Acetyl cysteine
Morphine and other opioids Naloxone
Heparin Protamine sulphate
Cyanide Sodium nitrate + Sodium thiosulphate
Organophosphates Atropine, Pralidoxime
Atropine Physostigmine
Copper D-Penicillamine
Iron Desferrioxamine
Arsenic Dimercaprol
Lead Calcium disodium edetate
Insulin Glucose
Methanol Ethanol
Carbon monoxide Oxygen
Warfarin Vit K1 oxide
14. Barbiturate Poisoning
Barbiturate poisoning is due to excessive doses of barbiturates. If death
occurs this is typically due to a lack of breathing.
Barbiturate overdose may occur by accident or purposefully in an attempt
cause death. The toxic effects are additive to those
of alcohol and benzodiazepines.
The lethal dose varies with a person's tolerance and how the drug is taken. The
effects of barbiturates occur via the GABA neurotransmitter. Exposure may be
verified by testing the urine or blood.
Treatment involves supporting a person's breathing and blood pressure. While
there is no antidote, activated charcoal may be useful. Multiple doses of
charcoal may be required.
Hemodialysis may occasionally be considered. Urine alkalinisation has not
been found to be useful.
While once a common cause of overdose, barbiturates are now a rare cause.
15. Symptoms
difficulty thinking, poor coordination, decreased level of
consciousness, and a decreased effort to breathe
(respiratory depression)
Mechanism
Barbiturates increase the time that the chloride pore of
the GABA receptor is opened, thereby increasing the
efficacy of GABA. In contrast, benzodiazepines increase
the frequency with which the chloride pore is opened,
thereby increasing GABA's potency
16. Treatment
Treatment involves supporting a person's breathing and blood pressure.
While there is no antidote, activated charcoal may be useful.
Multiple doses of charcoal may be required. Hemodialysis may occasionally be
considered. Urine alkalinisation has not been found to be useful.
If a person is drowsy but awake and can swallow and breathe without difficulty,
the treatment can be as simple as monitoring the person closely.
If the person is not breathing, it may involve mechanical ventilation until the
drug has worn off.
17. Morphine
Morphine is a pain medication of the opiate family.It can be
taken orally or injected; it is also often smoked. It acts
directly on the central nervous system (CNS) to increase
feelings of pleasure and warm relaxation and reduce pain,
and is often abused for this purpose. It can be taken for
both acute pain and chronic pain and is frequently used for
pain from myocardial infarction, kidney stones, and
during labor. Morphine can be administered by mouth,
by injection into a muscle, by injection under
theskin, intravenously, injection into the space around
the spinal cord, or rectally.
18. Symptoms
decreased respiratory effort, vomiting, nausea,
and low blood pressure. drowsiness, vomiting, and
constipation.
Adverse effects
Constipation
Hormone imbalance
19. Morphine Toxicity
A large overdose can cause asphyxia and death by respiratory
depression if the person does not receive medical attention
immediately.
Overdose treatment includes the administration of naloxone. The
latter completely reverses morphine's effects, but may result in
immediate onset of withdrawal in opiate-addicted subjects.
Multiple doses may be needed as the duration of action of
morphine is longer than that of naloxone.
The LD50 for humans of morphine sulphate and other
preparations is not known with certainty. One poor quality study
on morphine overdoses among soldiers reported that the fatal
dose was 0.78 mcg/ml in males (~71 mg for an average 90 kg
adult man) and 0.98mcg/ml in females (~74 mg for an average
75 kg female).
20. Organophosphate poisoning
Organophosphates are a common class of insecticides. But large doses
of organophosphates can also harm people and other animals.
Organophosphate poisoning can occur when you’re exposed to them
for too long or at high levels.
Organophosphates are typically colorless-to-brown liquids at room
temperature. Some may be unscented, while others have a fruit-like
smell.
ResearchersTrusted Source say as many as 25 million agricultural
workers across the developing world have at least one episode of
organophosphate poisoning per year. It’s being seen with more
frequency in areas where there is limited access to insecticide safety
gear, such as suits and breathing apparatuses.
Terrorist use of organophosphates is rare, but it has occurred. Sarin, an
organophosphate poison, has been intentionally used twice in terrorist
attacks in Japan.
21. Symptoms of organophosphate poisoning
Organophosphate poisoning can be short- or long-term. It can be caused by
large or small doses. The longer the exposure and the larger the dose, the
more toxic the effects. Symptoms can occur within several minutes or hours of
exposure.
MILD ORGANOPHOSPHATE EXPOSURE MAY CAUSE:
•narrowed, pinpointed pupils
•impaired, blurry vision
•stinging eyes
•runny nose
•watery eyes
•excess saliva
•glassy eyes
•headache
•nausea
•muscle weakness
•muscle twitching
•agitation
22. MODERATE SIGNS OF ORGANOPHOSPHATE EXPOSURE INCLUDE:
•very narrowed pupils
•dizziness
•disorientation
•coughing and wheezing
•sneezing
•difficulty breathing
•drooling or excessive phlegm
•muscle twitching and tremors
•muscle weakness
•fatigue
•severe vomiting and diarrhea
•involuntary urination and defecation
EMERGENCY SIGNS OF ORGANOPHOSPHATE POISONING INCLUDE:
•very narrowed pupils
•confusion
•agitation
•convulsions
•excessive body secretions, including sweat, saliva, mucus, and tears
•irregular heartbeat
•collapse
•respiratory depression or arrest
•coma
23. WHAT ARE THE COMPLICATIONS OF ORGANOPHOSPHATE
POISONING?
Organophosphate poisoning can cause several serious complications. These
include:
•metabolic disorders, such as hyperglycemia (high blood sugar) and glycosuria
(excess sugar in urine)
•diabetic ketoacidosis, in which your blood produces excess blood acids
•pancreatitis, or inflammation of the pancreas
•Cancer
•neurological problems, such as muscle weakness and twitching, poor
concentration, poor memory, and post-traumatic stress disorder
•fertility problems
•paralysis
24. What causes organophosphate poisoning
The people most at-risk for unintentional organophosphate
poisoning are those who live or work on or near farms. You
can also get organophosphate poisoning by consuming
contaminated food or water.
The most common unintentional exposure routes are
through breathing and contact with the skin.
People who intentionally expose themselves to
organophosphates tend to inhale and ingest it. These
concentrated, high doses are often fatal.
25. organophosphate poisoning Treatment
The first goal of treating emergency cases is stabilization.
Emergency care workers will:
•decontaminate your body to prevent further exposure
•stabilize your breathing
•use intravenous fluids to flush your system of toxins
In non-emergency cases, healthcare providers will still
administer some supportive therapy. They’ll pay close
attention to your breathing. Respiratory function is
weakened by organophosphate exposure.
Doctors may administer a drug called atropine to stabilize
your breathing. They may also administer pralidoxime,
which can help relieve neuromuscular problems.
26. In severe cases
doctors often prescribe benzodiazepines to prevent or stop seizures.
If you have been exposed to organophosphates in small doses and don’t need
to be hospitalized, you may administer a low dose of atropine to yourself using
a commercially prepared injection.
An injection of 10 mg diazepam is recommended for people exposed to
chemical attacks of organophosphates.
Age and weight Dose
adults and children who weigh more
than 90 pounds (41 kilograms)
2 milligrams (mg)
children weighing 42 to 90 pounds (19 to
41 kilograms)
1 mg
children weighing less than 42 pounds
(19 kilograms)
0.5 mg
27. •Heavy metal poisoning(Lead,Mercury and Arsenic)
Heavy metals are are elements that are naturally found in the earth.
They’re used in many modern-day applications, such as agriculture,
medicine, and industry.
Your body even naturally contains some. Zinc, iron, and copper, for
example, are necessary for regular body function, as long as they aren’t
present in toxic amounts.
Heavy metal poisoning occurs when your body’s soft tissues absorb too
much of a particular metal.
The most common metals that the human body can absorb in toxic
amounts are:
•mercury
•lead
•cadmium
•arsenic
28. You might be exposed to high concentrations of these
metals from food, air or water pollution, as well as
medicine, food containers with improper coating,
industrial exposure, or lead-based paint.
In the United States, heavy metal poisoning is very rare.
It only occurs when you’ve been exposed to a significant
amount of heavy metal, usually over a long period of
time.
But the popularity of over-the-counter (OTC) products
that claim to detoxify your body of heavy metals can
make it seem more common than it is.
.
29. Symptoms of heavy metal poisoning?
Common symptoms across several types of heavy metal poisoning include:
•diarrhea
•nausea
•abdominal pain
•vomiting
•shortness of breath
•tingling in your hands and feet
•chills
•Weakness
MERCURY POISONING SYMPTOMS:
•lack of coordination
•muscle weakness
•hearing and speech difficulties
•nerve damage in your hands and face
•vision changes
•trouble walking
30. Lead poisoning symptoms:
•constipation
•aggressive behavior
•sleep problems
•irritability
•high blood pressure
•loss of appetite
•anemia
•headaches
•fatigue
•memory loss
•loss of developmental skills in children
Arsenic poisoning symptoms:
•nausea, vomiting, and diarrhea
•red or swollen skin
•spots on your skin, such as warts or lesions
•unusual heart rhythm
•muscle cramps
Cadmium poisoning symptoms:
•fever
•breathing problems
•muscle pain
31. Causes of heavy metal poisoning
Heavy metals can enter your body in different ways. You might consume them
in the food you eat or absorb them through your skin, for example.
Here’s how you might be exposed to various heavy metals. Keep in mind that
heavy metal poisoning occurs with heavy or frequent exposure, usually over a
long period of time. Occasional exposure won’t lead to heavy metal poisoning.
Arsenic
•working near a hazardous waste site
•living in an area that has high levels in rocks, water, and soil
•ingesting insecticides, pesticides, or herbicides
•eating contaminated seafood or algae
•drinking contaminated water
Mercury
•mining, producing, or transporting mercury
•mining and refining gold and silver ores
•consuming contaminated fish or water
•manufacturing mirrors, X-ray machines, incandescent lights, or vacuum pumps
32. Lead
•living in a home with high levels of lead-based paint
•doing industrial construction work, radiator repair, or smelter operations
•being in firing ranges
•using kohl cosmetics
•applying progressive hair dyes, though the U.S. Food and Drug
AdministrationTrusted Source (FDA) is working to change this
•using foreign digestive remedies, calcium products, kohl, surma, kajal, or
progressive hair dyes
33. Diagonsis of heavy metal poisoning?
Doctors can usually check for heavy metal poisoning with a simple blood test
known as a heavy metals panel or heavy metal toxicity test.
To do the test, they’ll take a small blood sample and test it for signs of heavy
metals. If you have symptoms of heavy metal poisoning, but your blood test
only shows low levels, you doctor might do some additional testing.
These may include:
•kidney function tests
•liver function studies
•urine analysis
•hair analysis
•fingernail analysis
•electroardiograms
•X-rays
34. heavy metal poisoning treatment
For mild cases of heavy metal poisoning, just eliminating your exposure to
heavy metals can be enough to treat the condition. Depending on the
underlying cause, this might mean taking some time away from work or
changing your diet.
Your doctor can give you more specific recommendations on how to reduce
your exposure.
For more severe cases, the standard treatment is chelation therapy. This
involves giving medication, either through a pill or injection, that binds to the
heavy metals in your body.
These medications are known as chelators. As they bind to the metals,
chelators help to usher them out of your body as waste.