Salicylate poisoning can occur from ingesting derivatives of salicylic acid like aspirin. It causes metabolic disturbances as salicylates uncouple oxidative phosphorylation, increasing oxygen consumption and heat production. This can lead to hyperventilation, tachycardia, fever, hypoglycemia and metabolic acidosis. Treatment involves gastric decontamination, fluid resuscitation, urinary alkalinization and hemodialysis in severe cases to enhance renal excretion of the toxin. Prognosis is generally good with acute ingestion but worse with chronic use due to increased risks of mortality and morbidity.
General principles involved in management of poisoning- by rxvichu!!RxVichuZ
Hellow friends!!! I am back....with my 13th ppt!!
This ppt is regarding TOXICOLOGY,which happens to be my 1st....and i am happy to release the same on INDEPENDENCE DAY!!
Wishing a very happy and blissful Independence Day to all....i release my toxicology ppt regarding GENERAL PRINCIPLES IN POISONING MANAGEMENT.....
Since its my 1st attempt in Toxicology, i would love to hear ur reviews, and comments....so that i can improve in upcoming editions......
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General principles involved in management of poisoning- by rxvichu!!RxVichuZ
Hellow friends!!! I am back....with my 13th ppt!!
This ppt is regarding TOXICOLOGY,which happens to be my 1st....and i am happy to release the same on INDEPENDENCE DAY!!
Wishing a very happy and blissful Independence Day to all....i release my toxicology ppt regarding GENERAL PRINCIPLES IN POISONING MANAGEMENT.....
Since its my 1st attempt in Toxicology, i would love to hear ur reviews, and comments....so that i can improve in upcoming editions......
Keep reading...thanks for ur support!!!
With love and regards,
Vishnu.R.Nair (rxvichu-alwz4uh!!)
:) :)
Drug induced liver injury (DILI) and HepatotoxicityDr. Ankit Gaur
In this presentation I have tried to explain the defination, Mechanism of drug induced liver injury (DILI) and hepatotoxicity with the help of few examples.
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
Please find the power point on Management of antipsychotic overdose. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Drug induced liver injury (DILI) and HepatotoxicityDr. Ankit Gaur
In this presentation I have tried to explain the defination, Mechanism of drug induced liver injury (DILI) and hepatotoxicity with the help of few examples.
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
Please find the power point on Management of antipsychotic overdose. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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
7. Salicylates
• Derivatives of Salicylic acid
• Acetyl Saliclic acid.
• Sodium Salicylate.
• Methyl Salicylate.
WILLOW TREE
8. SALICYLIC ACID AKA Orthohydroxy Benzoic
Acid
• Hoffman, a chemist at Bayer Company first synthesised acetyl salicylic
acid in the laboratory in 1897.
• ASPIRIN was coined in 1899.
9. Uses :
1. Sodium salicylate and acetyl salicylic acid:
a)Antipyretic
b)Analgesic
c) Antiplatelet
2. Para Amino Salicylic acid : A second line drug in treating Tuberculosis.
3. Bismuth Salicylate : Traveller’s Diarrhoea.
10. Uses :
4. New Derivatives :
a) Mesalamine (5 ASA) – Used in IBD.
b) Diflunisal - difluorophenyl derivative of salicylic acid more potent
than aspirin in the treatment of musculoskeletal sprains and
osteoarthritis.
c) Benorylate - ester of aspirin and paracetamol with less incidence of
gastric irritation and bleeding.
11. Uses :
5. Locally acting salicylates :
a) Salicylic acid is a keratolytic agent.
b) Methyl salicylate is also used as a flavouring agent for candy.
c) Homomenthyl salicylate (homosalate) is a sunscreen agent.
d) Trolamine salicylate cream is used in the management of
osteoarthritis
12. Toxicokinetics
• Salicylates are rapidly absorbed from the stomach and intact Skin.
• Salicylates distribute well into plasma, saliva, milk, and spinal,
peritoneal and synovial fluid and into body tissues including kidney,
liver, lung and heart.
• Metabolism occurs chiefly in the liver-
broken down into salicyluric acid, ether glucoronide, ester
glucoronide, and gentisic acid and Excreated In urine.
14. PATHOPHYSIOLOGY
A. CENTRAL NERVOUS SYSTEM
1) Increased central respiratory drive:Mechanism unclear.
Likely explanation may be the direct stimulation of medullary regulatory activity.
Hyperventilation predominates early in the course of salicylate toxicity resulting in
respiratory alkalosis,decreased ionized calcium, and compensatory renal excretion of
potassium, sodium, and bicarbonate.
2) Seizures and coma Etiology:
As glucose utilization increases, a decrease in brain glucose concentrations may occur
producing a relative CNS hypoglycemia despite normal blood glucose concentrations.
15.
16. B. METABOLIC:
• Uncoupling of oxidative phosphorylation leads to a disruption in
cellular metabolism due to the interference of the Kreb’s cycle
and impaired carbohydrate and lipid metabolism.
• Substrates are metabolized but the energy produced is dissipated
as heat instead of being used to produce adenosine triphosphate
(ATP).
• The basal metabolic rate increases, placing increased demands on
the cardiorespiratory system.
• Excess lactic acid results from nonmitochondrial ATP production.
17.
18.
19. Disrupted cellular metabolism produces:
1. Increased oxygen consumption; compensatory increase in heart rate.
(tachycardia)
2. Increased CO2 production due to abnormal cellular respiration.
(hypercapnea)
3. Increased heat production (hyperthermia)
4. Patient’s commonly present with hyperglycemia but increased
glucose utilization, impaired glucose production, and eventually
reduced tissue glucose concentrations may lead to (hypoglycemia)
5. Increased production of organic acids (metabolic acidosis)
25. Diagnosis
History :
• Amount
• Approximate time of ingestion
• Possibility of long-term ingestion
• Potential co-ingestants
• Presence of other medical conditions (eg, cardiac, renal diseases)
Physical examination:
• Vital signs.
• CVS
• Chest
• Abdomen
• CNS
26. Laboratory markers:
• Serum salicylate:
Low serum levels early after acute ingestion do not preclude toxicity .
Levels should be obtained every 2 hours until a decrease is noted on two
consecutive measurements.
• Acute ingestions of non–enteric-coated aspirin should result in peak serum
levels by 6 hours after ingestion. A delayed increase may be seen in patients
with a salicylate pharmacobezoar , patients who have ingested enteric-coated or
sustained-released products (due to delayed absorption), and patients with
worsening acidosis.
• Acute toxicity, levels ranging from 31 to 100 mg/dL
• Chronic toxicity, toxic levels may be as low as 30 to 40 mg/dL
28. • ABG
• CXR
• ECG
• Abdominal imaging:
- Suspicion of aspirin concretion & pharmacobezoar- US, CT,
Endoscopy.
• Hepatic, hematologic, and coagulation profiles - Obtain for patients
with clinical evidence of moderate to severe toxicity
.
29. Treatment
1. Fluid resuscitation :
Correction of dehydration with 0.9% sodium chloride or lactated Ringer
solution,
• 10 to 20 mL/kg/h over 1 to 2 hours until a good urine flow is
established of at least
2 to 3 mL/kg/h
2. GI decontamination:
Gastric lavage in the first hr (warmed NS 38C,protect airway) Activated
charcoal in the first 4 hr, 1-2g/kg (maximum 100g) Whole-bowel
irrigation (WBI) with polyethylene glycol{enteric coated or slow release
formulas, 2 L/h (20 mL/kg/h) until the rectal effluent is clear}
30. 3. Urinary alkalinization with sodium bicarbonate: Moderate to severe
toxicity.
• 1 to 2 mEq/kg of sodium bicarbonate IV bolus, then infusion of DW5% with
100 to 150 mEq of sodium bicarbonate and 20 to 40 mEq of potassium
chloride in each liter at a rate of 1.5 to 2.5 mL/kg/h.Goal urine output is 2
to 3 mL/kg/h.
4. Hemodialysis:
• Management of patients with salicylate poisoning and a serum salicylate
level >100 mg/dL after acute ingestion or >40 mg/dL after chronic
ingestion, altered mental status, renal failure, pulmonary edema,
progressive clinical deterioration, refractory acidosis, or failure to respond
to more conservative therapy.
31. Prognosis
• The prognosis in patients with acute salicylate poisoning is very good:
the mortality rate is 1%, and the morbidity rate is 16% The prognosis
is worse in patients with chronic salicylate poisoning: the mortality
rate is 25%, and the morbidity rate is 30%