I apologize, upon reviewing the document I do not feel comfortable providing a summary without proper context around the sensitive topic of pesticides.
Pharmacodynamics and Pharmacokinetics of Synthetic CannabinoidsNMS Labs
Presented on February 21, 2012 at the AAFS 64th Annual Scientific Meeting by Barry K. Logan, PhD, DABFT, NMS Labs National Director of Forensic Services and Wendy R. Adams, Ph.D., DABFT, Forensic Toxicologist
Introduction to Opioid analgesis, Terms, History, Classification, Morphine, Opioid receptors, Mechanism of action, Pharmacological actions of morphine, Pharmacokinetics, Adverse effects, Contraindications, Therapeutic uses
Presented by
B . Kranthi Kumar
Department of Pharmacology
Introduction to Physiological and pathological role of serotonin
Autocoids, Classification, synthesis ,Serotonergic receptors, Physiological actions, Pathophysiological role
Presented by
K.Firdous banu
Department of Pharmacology
Grant Moore
Section Head Toxicology
Canterbury Health Labs,
PO Box 151, Christchurch 8014
grant.moore@cdhb.govt.nz
(P27, Thursday 27, Ilott Theatre, 2.00)
Pharmacodynamics and Pharmacokinetics of Synthetic CannabinoidsNMS Labs
Presented on February 21, 2012 at the AAFS 64th Annual Scientific Meeting by Barry K. Logan, PhD, DABFT, NMS Labs National Director of Forensic Services and Wendy R. Adams, Ph.D., DABFT, Forensic Toxicologist
Introduction to Opioid analgesis, Terms, History, Classification, Morphine, Opioid receptors, Mechanism of action, Pharmacological actions of morphine, Pharmacokinetics, Adverse effects, Contraindications, Therapeutic uses
Presented by
B . Kranthi Kumar
Department of Pharmacology
Introduction to Physiological and pathological role of serotonin
Autocoids, Classification, synthesis ,Serotonergic receptors, Physiological actions, Pathophysiological role
Presented by
K.Firdous banu
Department of Pharmacology
Grant Moore
Section Head Toxicology
Canterbury Health Labs,
PO Box 151, Christchurch 8014
grant.moore@cdhb.govt.nz
(P27, Thursday 27, Ilott Theatre, 2.00)
Introduction to Histamine and Antihistamine
Role of histamine, Synthesis, Storage, release of histamine
Mechanism of action of histamine
Anti histamine, Therapeutic uses, Adverse effects
Presented by
Shaik Sabeena
Department of Pharmacology
Background, physiology, immunology and recommended managements for patients in chemotherapy-induced hypersensitivity reactions. Details both cytotoxic and monoclonal antibody therapies. Delivered at HSE South East Regional Ongology Meeting March 2016.
Organophosphate Poisoning Treatment - port headland doctor teaching (31-1-12)Bishan Rajapakse
This is an educational talk about the treatment of organophosphorus poisoning (OP) based upon a talk given at the Australasian college of Emergency Medicine, Annual scientific sessions Nov 2010, canberra. If you liked this presentation; please also check out this page created by one of my senior colleagues (and watch the video) :- http://curriculum.toxicology.wikispaces.net/2.2.7.4.5+Organophosphates
OP Poisoning - Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kole...Dr Ajith Venugopalan
Organophosphate Poisoning - Evaluation & Management
Toxicology
Emergency Medicine
- Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kolenchery, Ernakulam, Kerala, India
Introduction to Screening Models of Hepatoprotective Drugs
Liver toxicity, Drugs causing DILI, Markers of hepatotoxicity
List of hepatoprotectives, Functions of liver
Screening models of hepatoprotective drugs
Presented by
I. Sai Reddemma
Department of Pharmacology
Introduction to Histamine and Antihistamine
Role of histamine, Synthesis, Storage, release of histamine
Mechanism of action of histamine
Anti histamine, Therapeutic uses, Adverse effects
Presented by
Shaik Sabeena
Department of Pharmacology
Background, physiology, immunology and recommended managements for patients in chemotherapy-induced hypersensitivity reactions. Details both cytotoxic and monoclonal antibody therapies. Delivered at HSE South East Regional Ongology Meeting March 2016.
Organophosphate Poisoning Treatment - port headland doctor teaching (31-1-12)Bishan Rajapakse
This is an educational talk about the treatment of organophosphorus poisoning (OP) based upon a talk given at the Australasian college of Emergency Medicine, Annual scientific sessions Nov 2010, canberra. If you liked this presentation; please also check out this page created by one of my senior colleagues (and watch the video) :- http://curriculum.toxicology.wikispaces.net/2.2.7.4.5+Organophosphates
OP Poisoning - Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kole...Dr Ajith Venugopalan
Organophosphate Poisoning - Evaluation & Management
Toxicology
Emergency Medicine
- Dr. Ajith Venugopalan, EM, MOSC Medical College Hospital, Kolenchery, Ernakulam, Kerala, India
Introduction to Screening Models of Hepatoprotective Drugs
Liver toxicity, Drugs causing DILI, Markers of hepatotoxicity
List of hepatoprotectives, Functions of liver
Screening models of hepatoprotective drugs
Presented by
I. Sai Reddemma
Department of Pharmacology
Organophosphate poisoning - a brief toxicological study martinshaji
this is a brief study on organophosphate poisoning , as it being more common problem in the health sector and emergency medicine now a days , this will be much helpful among health professionals .........text me for more topics
martinsuaj369@gmail.com
thank you
Organophosphate poisoning national guidelinecharithwg
publication by Dr-C.Here the given information are based on recommendations by sri lankan medical specialists who have dealt with the issue for a long time. it is quite obvious using agro chemical to deliberate self harm is a tendency in developing countries. it is common in agricultural ares.all the information are correct according to my knowledge. all the materials used to publish the slideshow are international publications. you have the full right to download and read. my personal request is to submit your ideas to me. and suggest different topics. i like to see your responses. i hope you would manage patients like these some day though it is so sad to see such incidents. be confident. do good. do not harm. be kind. keep us in your memories.
3. Double Jeopardy What is happening? Remember me False or True Think wisely Look closely 20 20 20 20 20 40 40 40 40 40 60 60 60 60 60 80 80 80 80 80 100 100 100 100 100
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5. Regarding Chlorinated hydrocarbon which is true ,& which is false? 1)They affect primarily axonal membranes ,resulting in neuronal irritability & excitation 2)Elimination of some of them can be increased by cholestyramine 40 gram orally every 8 hours 3)The first sign of toxicity may be the acute onset of seizure without peripheral signs & symptoms 4)Seizure activity is usually non self limiting lasting 1-2 weeks 5)Ventricular dysrhythmia are most likely to occur during seizure activity due to high circulating catecholamines & other metabolic abnormalities
6. A38 y old farm worker presents to the ED with hypersalivation, urinary incontinence, diarrhea, & muscle weakness after being in a recently sprayed field. He has prominent wheezing & is producing copious amounts of clear sputum. Which of the following statements is TRUE of the treatment for this condition? 1)Atropine should be administered as 1 mg IV every 5 mints until muscle weakness has resolved 2)Supportive care is the only appropriate treatment for this condition 3)Pralidoxime will regenerate cholinesterase molecules if given any time after exposure 4)Atropine & Pralidoxime work synergistically to treat this condition
7. *The pt is having symptoms of cholinergic crisis evidenced by the symptoms given, as well as his recent exposure to the sprayed field, it is unknown exactly whether the agent is organophosphate or carbamate.While both agents inhibit cholinesterase, thus causing accumulation of Ach in neurons of CNs, & autonomic as well as NMJ, organophosphate do so irreversibly. *Atropine & pralidoxime are the two main antidote used for these types of pts . Atropine should be given to adult every 5 mint until muscrininc effects are reversed. Atropine has no effect on muscle weakness. *Pralidoxime acts by regenerating phosphorylated ach –cholinesterase & may also directly detoxify free organophosphate molecules if given as early as within the first 48 hours of ingestion. Its use with atropine appears to be synergistic .
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16. Regarding Roundup ? 1)Most of its exposure happens through ingestion due to its poor skin absorption 2)The critical elements in diagnosis is history of ingestion 3)Both hydrofluoric acid ingestion & Roundup have the clinical findings of hyperkalemiea & AG metabolic acidosis 4)Ionized Ca level will be low
17. *In case of sever toxicity with this substance what ECG changes would u see? *Cause of its toxicity? *Mention 3 Negative prognostics indicators?
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19. Regarding Pyrethrins & pyrthroids? 1)MOST of them are absorbed int the fat ,so cumulative toxicity form problem 2) Addtion of piperonyl butoxide reduce their toxicity 3)Both of them cause allergic reactions 4)They affect sodium channel mediated & GABA Calcium channels
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21. Which is true which is false: 1) Cholinesterase inhibitor include bradycardiea or tachycardia , hypotension or hypertension, miosis or mydriasis 2)In chlorinated hydrocarbon exposure catecholamine is avoided 3)Rapid cooling & substrate provision (glucose) are the most important therapies in substituted phenol toxicity
22. *What is this, for what used? *What is the recommended concentration to be used in children? * Mention 3 factors that can increase its toxicity?
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25. Which is true regarding Bipyrindal compounds? 1)Diquat is poorly absorbed through the skin 2) Paraquat induced pulmonary injury usually occurs over 1- 3 weeks 3)Successful therapeutic intervention for paraquat toxcictry is extremely time dependant & pt outcome depends on the history 4)ALL pts with ingested paraquat requires hospitalization 5)All of the above 6) Non of the above
26. *Mention 3 clinical features of DNP toxicity? * what is characteristic about the site of skin or mucus absorption?
27. *What is this? which group? *what is its target organ of toxicity & why?
28. *To which group I belong?? *Target organ affected? * When the serious toxic effect develop?
29. *what is this? *With which group of pts they can get it ? in which group of people ?reversible or not
30. *What are theses ? What insecticides are extracted from them? How? *what is there predominant form of toxicity? * counseling? Cute ,but toxic !!!
31. *What is this? For what purpose it is used? *Mechanism of toxicity?
32. Insert Text for Question Category 5 – 100 points *Which sort of insecticides is this ?For what it is used? *Mechanism of toxicity ? *Best drugs for Dysrhythmia causes by it?