General management of poisoning involves stabilization, evaluation, gastrointestinal decontamination if recent, urinary alkalinization for some toxins, haemodialysis/haemoperfusion, lipid emulsion therapy, supportive care, and antidotes if available. Stabilization focuses on airway, breathing, circulation. Evaluation includes examination. Gastrointestinal decontamination includes activated charcoal orally or via tube for some toxins within 1 hour, or whole bowel irrigation for sustained release drugs. Urinary alkalinization enhances excretion of weak acids/bases. Haemodialysis/haemoperfusion effectively removes some toxins. Lipid emulsion therapy counters cardiac effects of some lipophilic drugs. Supportive care monitors until effects
Poisoning
Poison
Medicinal Poisoning
Environmental Poisoning
Factors Affecting Environmental poisoning
Drug Poisoning
Role of Pharmacist to Prevent Poisoning
Diagnosis
Treatment
Poisoning is a lethal disruption of body’s physilogical machanism by the induction of an exogenic biological or chemical agent.
A poison is any substance that is harmful to your body.
Poisons may include-
Prescription or over-the-counter medicines taken in doses that are too high
Overdoses of illegal drugs
Carbon monoxide from gas appliances
Household products, such as laundry powder or furniture polish
Pesticides
Indoor or outdoor plants
Metals such as lead and mercury
poisoning, its types and emergent management.bhartisharma175
it explain about definition, causes, types of poison, severity , diagnostic evaluation, complication of poisoning, emergent management, supportive management and nursing management.
Poisoning
Poison
Medicinal Poisoning
Environmental Poisoning
Factors Affecting Environmental poisoning
Drug Poisoning
Role of Pharmacist to Prevent Poisoning
Diagnosis
Treatment
Poisoning is a lethal disruption of body’s physilogical machanism by the induction of an exogenic biological or chemical agent.
A poison is any substance that is harmful to your body.
Poisons may include-
Prescription or over-the-counter medicines taken in doses that are too high
Overdoses of illegal drugs
Carbon monoxide from gas appliances
Household products, such as laundry powder or furniture polish
Pesticides
Indoor or outdoor plants
Metals such as lead and mercury
poisoning, its types and emergent management.bhartisharma175
it explain about definition, causes, types of poison, severity , diagnostic evaluation, complication of poisoning, emergent management, supportive management and nursing management.
Poisoning is one of the very alarming topic now a days. This presentation will give you a basic idea on poisoning, drug poisoning, animal poisoning, plant poisoning, household poisoning, industrial poisoning, treatment of poisoning e.t.c
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
Heart failure (HF) is a common cardiovascular condition with increasing incidence and prevalence. Unlike western countries where heart failure is predominantly a disease of elderly, in India it affects younger age group. Heart failure is a chronic condition in which the heart cannot pump enough blood and oxygen to support other organs in your body.
Poisoning is one of the very alarming topic now a days. This presentation will give you a basic idea on poisoning, drug poisoning, animal poisoning, plant poisoning, household poisoning, industrial poisoning, treatment of poisoning e.t.c
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
Heart failure (HF) is a common cardiovascular condition with increasing incidence and prevalence. Unlike western countries where heart failure is predominantly a disease of elderly, in India it affects younger age group. Heart failure is a chronic condition in which the heart cannot pump enough blood and oxygen to support other organs in your body.
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
Alcoholic liver disease is a result of over-consuming alcohol that damages the liver, leading to a buildup of fats, inflammation, and scarring. It can be fatal.
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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!
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.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. General management of poisoning can be done by:-
• Stabilization
• Evaluation
• Gastrointestinal decontamination
• Urinary alkalinisation
• Haemodialysis and haemoperfusion
• Lipid emulsion therapy
• Supportive care
• antidotes
3. Stabilisation & evaluation:-
• Assessment & correction of life threatening problems, if present.
• Attention must be paid to the air way, breathing, circulation,
depression of CNS.
• If patient is not in crisis i.e he is alert with normal speech &pulse,
proceed to a complete, thorough, & systemic examination.
4. Gastrointestinal decontamination:-
• Patients who have ingested potentially life –threatening quantities of
toxins may be considered for gastrointestinal decontamination if
poisoning has been recent.
• Induction of emesis is no longer used.
5. 1.Activated charcoal-
• Given orally as slurry, absorbs toxins in the bowel as a result of its large
surface area.
• If given sufficiently early, it can prevent absorption of an important
proportion of the ingested dose of toxin.
• Efficacy decreases with time & current guidelines do not advocate use
more than 1hour after overdose in most circumstances.
• However, use after a long interval may be reasonable when a delayed
release preparation has been taken or when gastric emptying is delayed.
• Some toxins do not bind to activated charcoal so it will not affect their
absorption.
6. • In patients with impaired swallowing or a reduced level of
consciousness, activated charcoal, even via nasogastric tube, carries a
risk of aspiration pneumonitis, which can be reduced by protecting
the airway with a cuffed endotracheal tube.
• Multiple doses of activated charcoal (50g 6 times daily in an adult)
may enhance the elimination of some drugs at any time after
poisoning.
• Recommended for serious poisoning with some substance.
• This interrupts enterohepatic circulation or reduces the concentration
of free drug in the gut lumen, to the extent the drug diffuses from the
blood bowel back to be absorbed on to the charcoal : so called gastro
intestinal dialysis.
• Laxative is generally given- to reduce the risk of constipation or
intestinal obstruction by charcoal briquette formation in the gut
lumen.
7. • Evidence suggests that single or multiple doses of activated charcoal
do not improve clinical outcomes after poisoning with pesticides or
oleander.
• Substances poorly absorbed by activated charcoal:-
MEDICINES
iron lithium
CHEMICALS
acid mercury
alkalis methanol
ethanol
ethylene glycol
8. 2.Gastric aspiration and lavage-
• It is infrequently indicated in acute poisoning.
• Not effective than activated charcoal.
• Complication are common especially aspiration.
• Use is justified for poisons which are not absorbed by
activated charcoal
9. 3.Whole bowel irrigation-
• Enhance the elimination of ingested packets of illicit drugs or slow
release tablets such as iron & lithium.
• Involves the administration of large quantities of osmotically balanced
Polyethylene glycol & electrolyte solution.
• Usually by a nasogastric tube, until the rectal effluent is clear.
• Contraindication- inadequate air way protection, haemodynamic
instability, gastrointestinal haemorrhage, obstruction or ileus.
• May precipitate nausea and vomiting, abdominal pain & electrolyte
disturbances.
10. Use of gastric decontamination methods:-
o single dose activated charcoal may be considered if a patient has
ingested a potentially toxic amount of a poison up to 1hour
previously.
multi dose activated charcoal – life threatening amount of
carbamazepine, dapsone, phenobarbital, quinine or theophylline.
o gastric lavage should not be employed routinely, if ever, in the
management of poisoned patients.
11. oWhole bowel irrigation should be considered for:
poisoning with sustained – release or emetic coated drugs
patients who have ingested substantial amounts of iron
removal of ingested packets of illicit drugs.
12. Urinary alkalinisation:-
• Urinary excretion of weak acids and bases is affected by urinary PH,
which changes the extent to which they are ionized.
• Highly ionized molecules pass poorly through the lipid membranes &
therefore little tubular reabsorption occurs &urinary excretion is
increased.
• If the urine is alkalinized (PH>7.5) by the administration of sodium
bicarbonate, weak acids (eg: salicylates, methotrexate) are highly
ionized, resulting in enhanced urinary excretion.
13. • Urinary alkalinisation is currently recommended for patients with
clinically significant salicylate poisoning when the criteria for
haemodialysis are not met.
• Complications- alkalaemia, hypokalaemia, occasionally alkalotic
tetany.
• Hypocalcaemia may occur but is rare.
14. Haemodialysis and haemoperfusion:-
• Enhance the elimination of poisons - have small volume of
distribution &a long half life after overdose.
• Appropriate when poisoning is sufficiently severe to justify invasive
elimination methods.
• The toxin must be small enough to cross the dialysis membrane –
haemodialysis or must bind to activated charcoal – haemoperfusion.
• Haemodialysis may also correct acid – base balance & metabolic
disturbances associated with poisoning.
16. Lipid emulsion therapy:-
• Lipid rescue is used for management of poisoning with lipid soluble
agents, such as local anaesthetics, tricyclic antidepressants, calcium
channel blockers & lipid- soluble beta blockers propranolol.
• It involves intravenous infusion of 20% lipid emulsion at an initial dose
of 1.5mL/Kg/min , followed by a continuous infusion of
0.25mL/Kg/min until there is clinical improvement.
• The elevated myocardial concentration of free fatty acids induced by
intralipid administration may also have beneficial effects on
myocardial metabolism &performance by counteracting the inhibition
of myocardial fatty acid oxidation produced by local anaesthetics.
17. • This reverses cardiac depression by enabling increased ATP synthesis
&energy production.
• Animal studies have suggested efficacy and case reports of use in
human poisoning have also been encouraging, with recovery of
circulatory collapse reported in cases where other treatment
modalities have been unsuccessful.
• No controlled trails of this technique have been performed, however,
&as a result, its efficacy remains uncertain.
18. Supportive care:-
• For most poisons, antidotes and methods to accelerate elimination
are inappropriate, unavailable or incompletely effective.
• Outcome is dependent on appropriate nursing and care, & on
treatment of complications.
• Patient should be monitored carefully until the effects of any toxins
have dissipated.
19. EXAMPLES OF CAUSATIVE AGENTS MANAGEMENT
coma Sedative agents Appropriate airway protection &
ventilatory support
Pressure area& bladder care
Identification & treatment of
aspiration pneumonia
seizures NSAIDs
Anticonvulsants
TCAs
theophylline
Appropriate airway& ventilatory
support
IV benzodiazepine (eg: diazepam
10-20mg, lorazepam 2-4mg)
Correction of hypoxia, acid base &
metabolic abnormalities
Acute dystonias Typical antipsychotics
metoclopramide
Procyclidine, benzatropine or
diazepam
20. EXAMPLES OF CAUSATIVE AGENTS MANAGEMENT
HYPOTENSION
Due to vasodilations
Due to myocardial suppression
Vasodilator antihypertensives
Anticholinergic agents
TCAs
Beta blockers
Calcium channel blockers
TCAs
IV fluids
Vasopressors
Optimisation of volume status
Inotropic agents
VENTRICULAR TACHYCARDIA
Monomorphic, associated with QRS
prolongation
Torsades de pointes, associated
with QTc prolongation
Sodium channel blockers
Anti arrhythmic drugs(quinidine,
amiodarone, sotalol)
Antimalarials
Organophosphate insecticides
Antipsychotic agents
Antidepressants
Antibiotics(erythromycin)
Correction of electrolyte& acid
base abnormalities &hypoxia
Sodium bicarbonate
Magnesium sulphate,2g Iv over 1-
2mins, repeated if necessary
21. Antidote:-
• Antidotes are available for some poisons.
• Examples- By specific antagonism –isoprenaline for beta blockers
chelation- desferrioxamine for iron
reduction –methylene for dapsone