The document discusses antidotes for poisoning treatment. It defines an antidote as a therapeutic substance used to counteract the toxic effects of a xenobiotic. Antidotes are classified based on their mode and site of action, and include physical, chemical, and pharmacological antidotes. Physical antidotes like activated charcoal work by adsorption. Chemical antidotes form non-toxic complexes with poisons or accelerate detoxification. Pharmacological antidotes counteract poisons by producing opposite effects, competing for receptors, blocking toxic receptors, or aiding normal function restoration. The proper use of antidotes with supportive care can significantly reduce morbidity and mortality from poisonings.
covered antidote definition, classification, mechanisms. also sodium nitrite drug with their molecular formula, molecular weight,physical properties,chemical properties,reactions ,uses etc.refered from various books and search from google also.for any queries comment below.
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
covered antidote definition, classification, mechanisms. also sodium nitrite drug with their molecular formula, molecular weight,physical properties,chemical properties,reactions ,uses etc.refered from various books and search from google also.for any queries comment below.
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
short and simple study on the topic of laxative and purgatives which is very usefull for the student , teachers, as well as health cares peoples. this study is done by the student with the help of teachers
short and simple study on the topic of laxative and purgatives which is very usefull for the student , teachers, as well as health cares peoples. this study is done by the student with the help of teachers
It will be of no value to remove the chemical from the patient’s stomach if he has stopped breathing or his heart is fibrillating. So always asses the patient first, then what must be done and in what order.
Mechanism of drug action (pharmacokinetic and pharmacodynamic )Ravish Yadav
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
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Drug interaction is defined as the pharmacological activity of one drug is altered by the concomitant use of another drug or by the presence of some other substance
The Drug whose Activity is effected by such an Interaction is called as a “Object drug.”
The agent which precipitates such an interaction is referred as the “Precipitant”.
Sanjo College of Pharmaceutical Studies, Physical Pharmaceutics I , 3rd semester B.Pharm, Complexation & protein binding, Classification in detail, determination methods, application of complexes in pharmacy.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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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.
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!
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
2. Treatment of Poisoning:
Supportive care
Activated charcoal for serious
oral poisonings
Occasional use of specific
antidotes or dialysis
Only rare use of gastric
emptying
3. • The proper use of antidotes in the
intensive care setting, when
combined with aggressive supportive
care, may significantly reduce the
morbidity and mortality associated
with many severe poisonings.
www.mcqsinpharmacology.com
4. ANTIDOTES
• According to WHO
“Antidote was defined as a therapeutic
substance used to counteract the toxic
action(s) of a specified xenobiotic.”
• antidotes reduce the overall burden of health
service in managing of poisoning cases
Supportive
therapy
correct
Antidote
↑↑
Pt.Survival
www.mcqsinpharmacology.com
6. According to Site of Action:
1. Interacts with the poison to form a non toxic
complex that can be excreted:e.g. Chelators
2. Accelrates the detoxification of the poison:e.g. N-
acetylcystine,thiosulfate
3. Decrease the rate of conversion of posion into
toxic metabolite:e.g.Ethanol,Fomepizole
4. Compete the poison for certain receptors.:e.g.
Nalaxone
5. Block the receptor through which the toxic effect
of the poison is mediated e.g.Atropine
6. Bypass the effect of Poison:O2 in the treatment
of CO and cyanide toxicity
7. Antibodies to the poison : digiband and antivenoms
7. Physical Antidote:
Agent use to interfere with poison
through physical properties, not
change their nature
a) Adsorbing: The main example is
activated charcol
b) Coating: A mixture of egg & milk
make a coat over the mucosa.
c) Dissolving: 10% alcohol or glycine
for carbolic acid
www.mcqsinpharmacology.com
8. CHARCOL:
(Universal Antidote)
• produced by heating pulverized carbonaceous
substances sawdust, peat, or coconut shells
• activation: Hot air to erode the internal
surfaces of the product and thereby increase its
adsorptive surface area.
• Adsorption results from weak intermolecular
(Van der Waals) forces
• AC can prevent systemic absorption of drugs
when given within 1-2 h of ingestion
• The optimal dose is probably a 40:1 ratio (by
weight) of charcoal to drug
• contraindicated for iron, lithium, potassium, and
ethanol overdose
9. Chemical Antidote:
• Interact specifically with a toxicant,
or neutralize the toxicant.
e.g. metal chelators combine with metals to form
complexes that can then be eliminated by the
kidneys
Mainly act by two mechanisms:
Complex Formation:
Antidote make complex with the toxicant making it
unavailable to cross the membrane or to interact
with receptors
DMSA(dimercaprol and dimercaptosuccinic
acid are sulfohydral compounds that bind metal
such as arsenic acid ,lead.
www.mcqsinpharmacology.com
10. Sp. Binding agents like EDTA, defroxamine and
D-pencillamine act by chelation of metal
forming more water soluble complex
Antivenins and antibodies against digitoxin are
immunologicaly genrated agents that bind
specifically to the toxin or venom
Metabolic conversion:
Detoxification to less toxic product
Nitrite interact with hemoglobin and cyanide to
form cyanomethamoglobin , which is less toxic
than cyanide and interfare with the cyanide
access to cytochrome oxidase system.
11. Pharmacological antidote:
• counteract the effects of a poison by producing the opposite
pharmacological effects, e.g., ACHE inhibitors atropine
• Pharmacologic antidotes may
neutralize or antagonize the effects
of a toxicant.
• This type of antidote may act by
following 5 mechanism.
www.mcqsinpharmacology.com
12. 1. Preventing the formation of toxic
metabolites:
More effective when given immediately before
toxic metabolic activation
Example:
Ethanol and 4-methylpyrazole(4-MP) which
compete with the alcohol dehydrogenase which
prevent the formation of toxic intermediate from
ethylene glycol.
2. By Facilitation Of More Rapid Or Complete
Elimination Of A Toxicant :
Change the physiochemical nature of toxin,
allowing better glomerular filtration and prohibt
tubular reabsorption.
eg., molybdenum and sulfate for copper toxicity by
making water soluble complex,
13. 3. By competing with the Toxicant’s action at a
receptor site:
a) Antagonism:
Competitive antagonism:
Naloxone/Naltrexone: Opioid dependence,
longer action and affinity for mu receptor.
Flumenazil: Antagonist for Benzodiazepine
Atropine: organophosphate, carbamate and
other parasympathomimetic antidote.
It is also used to correct bradycardia caused by
morphine, digitalis, beta blockers etc
www.mcqsinpharmacology.com
14. Non Competitive Antagonism:
Calcium gluconate:
Used for Calcium channel blocker especialy
Verapamil
Black widow spider bite
Lead colic
Oxalic acid
Paralidoxime :ChE activator act by breaking Alkyl
phosphate ChE bond. It is used in
organophosphate toxicity.
Diacetyl Monoxyime(DAM): action same as PAM
but with more BBB penetration.
Physostigmine: Counteract the anticholinergic
effect
www.mcqsinpharmacology.com
15. 4. By blocking receptors responsible for the
toxic effect :
The physiologic effect induced by a toxin is
prevented by an antidote, although the toxicant is
unchanged and may still be active.
Example:
atropine blocks the physiologic effect of
acetylcholine at cholinergic synapse and
neuromuscular junction ,and in organophosphate
toxicity
www.mcqsinpharmacology.com
16. 5. By aiding in the restoration of normal
function:
The antidote promotes return to normal function
by repairing a defect or enhancing a function that
correct the effect of poison.
Example:
Methylene blue:
In nitrite poisoning, methylene blue interact with
reduced NADPH to reduce the ferric iron of
methemoglobin back to ferrous ion in hemoglobin,
which can again transport oxygen
Acetylcysteine :
Acetylcysteien supplies the precursor amino acids
for glutathione, which serves as biologic
antioxident against acetaminphen toxicosis
www.mcqsinpharmacology.com
J Med Toxicol. 2010 June; 6(2): 190–198. Activated Charcoal for Acute Poisoning: One Toxicologist’s Journey Kent R. Olson
Peat” partialy decomposed vegetable matter saturated with water, as fuel n fertilizer
use of charcoal for medicinal purposes dating as far back as 1550 BC
Charcoal is produced by heating pulverized carbonaceous substances such as sawdust, peat, or coconut shells to very high temperatures (600-900°C) followed by “activation” using steam or hot air to erode the internal surfaces of the product and thereby increase its adsorptive surface area.
Methemoglobinemia occurs when iron atoms in hemoglobin become oxidized. During oxidation, the iron atom loses an electron to an oxidant and is converted from the ferrous state (Fe2+) to the ferric state (Fe3+).
Oxidizing: Amynitrile is used in cyanide toxicity
Reducing:
Methylene Blue:
Methemoglobinemia occurs when iron atoms in hemoglobin become oxidized.
it is used with MetHb producers Nitrates,nitrites,Sulfonamide,Phenacitin etc