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
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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
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.
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
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.
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
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
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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
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.
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
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.
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
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
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
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Role of Mukta Pishti in the Management of Hyperthyroidism
Adverse drug reaction pharmacology
1. ADVERSE DRUG REACTION FEB 2014
1
ADVERSE DRUG REACTION
Adverse Drug Reaction (ADR)
It is a response to a drug that is “noxious and unintended and which occurs in doses normally used for
the treatment, prophylaxis or diagnosis of disease or in the modification of physiological function”.
(WHO).
Adverse Events
It refers to any adverse effects that occur while the patient is taking a given drug. It is not necessary
that the event was a response related to the drug.
Side-effects
It is any effect caused by a drug other than the intended therapeutic effect whether it is beneficial,
neutral or harmful.
It can be based on the same therapeutic effect of the drug.
Examples
a. Atropine is used as a pre-anaesthetic medication as it decreases secretion, as side-effects it
causes dryness of mouth.
b. Codeine is used as an analgesic or cough suppressant, as side-effects leads to constipation.
This adverse effect is beneficial; it allows codeine to be used as an anti-diarrheal medication.
c. Minoxidil is an arterial vasodilator. It was first used to treat hypertension and was found to cause
hirsutism as side-effect. This side-effect explains the use of topical minoxidil in treating alopecia.
Toxic effect
It refers to the direct cell damaging (eg paracetamol on the liver) action of the drug often when used at
high dose.
All drugs are toxic in overdose.
Overdose can be:
1. Absolute: acute high dose of the drug is administered as in suicidal attempt or by accident.
2. Relative: the therapeutic dose of the drug is used but it may turn out toxic because of
underlying abnormalities in the patient.
Examples:
a. Paracetamol at a dose of 4g /day therapeutic dose can lead to fulminant liver failure in a
patient suffering from alcohol liver disease.
b. When gentamicin is given to a patient with pre-existing renal impairment, ototoxicity is
more likely to occur.
Types of ADR
1. Type A reaction (augmented reaction).
It also known as quantitative intolerance and is dose related.
It depends on:
a. The duration of the treatment,
b. Total intake of the drug,
2. ADVERSE DRUG REACTION FEB 2014
2
c. Capacity of the drug to accumulate or gets deposited in certain tissues
2. Type B (Bizarre reaction)
It is also known as qualitative intolerance.
It is non-dose dependent and can occur from single dose of the drug.
Two main types of type B reactions are:
a. Hypersensitivity reaction.
b. Idiosyncrasy.
Possible mechanism of pathogenesis of type B reactions are:
I. Receptor abnormality
II. Abnormal biological system that is apparent only in the presence of the drug.
III. Any pharmaceutical variation.
IV. Drug-drug interaction.
V. Immunological.
Hypersensitivity reactions (drug allergy)
Drug allergy is an immunologically mediated reaction producing symptoms which are unrelated to the
pharmacological effects and doses of the drug.
It occurs in 5-10% of the population.
Only a few drugs (mol wt>10,000) are large enough to act as effective antigen or immunogens and are
capable of initiating an immune response on their own.
Most drugs/metabolites (hapten) must be converted to antigen by linkage to body protein.
Hypersensitivity reaction can be humoral or cell mediated.
Type I: Anaphylactic reaction
Drug specific antibody of IgE type combines with the Fc segment of mast cell. Upon re-exposure to the
antigen, degranulation of the mast cell occurs with release of histamine and other mediators which
leads to manifestation like hypotension, broncho-spasm, headache, flushing, laryngeal oedema,
urticaria, rash...
Treatment: Epinephrine 0.5 ml of 1:1000 IM
Hydrocortisone 100-200 mg, Iv 6-8 hourly (max of 400mg/day).
Chlorpheniramine 10 mg IV 6-8 hourly till pruritus and rashes decrease.
Salbutamol nebuliser or IVI of aminophylline for bronchospasm.
Supportive treatment.
Type II: Cytotoxic reaction
Drug antibody Ig G/ Ig M complex adhere to the surface of the blood cells and cause activation of
complements.
It manifests as hemolytic anaemia, agranulocytosis, thrombocytopenia, collagen vascular disease.
Type III Immune complex vasculitis (serum sickness/ Arthus reaction)
Drug antibody complex precipitates on the vascular wall and activates complement and ultimately
triggers an inflammatory response. It is characterised by fever, lymphadenopathy, arthralgia, myalgia,
interstitial nephritis and neuropathy.
3. ADVERSE DRUG REACTION FEB 2014
3
Type IV(delayed cell mediated).
The drug is bound to the surface of T-lymphocytes with production of lymphokine and cause an
inflammatory response.
Steven’s Johnson reaction is an example of such a reaction.
Examples of drugs that are likely to cause allergic reaction
Antibiotics (Penicillin anaphylactic reaction and cephalosporin in particular), vaccines, monoclonal
antibodies, insulin…
Idiosyncratic reaction
It is a functional term which does not apply to any mechanism of toxicity.
Immunological phenomenon cannot be proved. It is likely to have a genetic predisposition.
Examples of idiosyncratic reactions:
1. Individual with G6PD deficiency are likely to suffer from hemolytic anaemia with oxidizing agents like
primaquine, sulfa drugs (sulphonamides), quinolones, metronidazole, chloroquine,
high dose of vitamin C.
2. Prolonged apnoea by succinylcholine in patient with atypical cholinesterase.
3. Anaphylactoid reaction with aspirin.
4. Chloramphenicol : bone marrow suppression and agranulocytosis.
Comparison between type A and type B reaction:
ADR Type A Type B
Dose relationship Present Absent
Frequency More common Less common
Mortality rate Lower Higher
Treatment Stop/reduce dose Stop the drug at once.
NB: Anaphylactoid reaction mimicks anaphylactic reaction but it does have any immunological basis.
Drugs causing anaphylactoid reaction: aspirin, paracetamol, N-acetyl-cysteine, succinylcholine, d-
tubocurarine, mivacurium, iron, iodine containing contrast…
3. Type C (continuous reaction).
It occurs on the long term use of a particular drug.
Examples:
Analgesic nephropathy, tardive dyskinesia with prolonged use of anti-psychotics, chloroquine induced
retinopathy…
4. Type D (delayed effects).
Teratogenicity and carcinogenesis.
Teratogenicity
It is the ability of a drug to induce physical malformation in the foetus when such a drug is administered
to the pregnant woman. The stage of organogenesis (18-55days) is the most vulnerable period).
4. ADVERSE DRUG REACTION FEB 2014
4
Examples of teratogenic drugs:
Thalidomide: Was used as sedative/hypnotics and for the relief of morning sickness. It caused
phocomelia, Amelia and multiple defects.
Phenytoin, valproate, carbamazepine: fetal hydantoin syndrome and neural tube defects characterized
by microcephaly, facial dysmorphism, limb defects (hypoplastic phalanges).
Warfarin: growth retardation with nose, ears and hand defects.
Tetracycline: deformed and discoloured teeth and retarded bone growth.
Carcinogenesis
The female offspring of women who were exposed to stilboesterol during their child-bearing age have
been shown to develop vaginal cancers.
Type E (ending of use)
Example :
Acute adrenal crisis will occur upon abrupt discontinuation of a corticosteroid in a patient who was
treatment for more than 3 weeks with a corticosteroid (suppression of HPA axis).
Sudden withdrawal of high doses of β-blockers in hypertensive patients causes rebound increase in
blood pressure (up-regulation of receptors).
Abrupt stoppage of nasal decongestants following chronic use leads to rebound congestion (down
regulation of receptors).
Photosensitivity
These are cutaneous reactions resulting from drug induced sensitization of the skin to UV radiation. It is
of two types:
a. Photo-toxicity: the drug or its metabolite accumulates in the skin and absorbs the light (UVB) and
cause tissue damage by a chemical reaction. It ressembles sun-burn (erythema, oedema, blistering,
hyperpigmentation).
Examples: Amiodarone, thiazides, fluoroquinolones, sulfones…
b. Photo-allergic reaction: it is a cell-mediated immune response and on exposure to sunlight, it gives
eczematous like picture.
Examples: Sulphonamides, sulfonylureas, griseofulvin, terbinafine.
Iatrogenic disease
Physician induced disease.
Examples:
1. Steroid induced hypertension, diabetes mellitus, osteoporosis.
2. Broadspectrum antibiotic induced candidiasis.
3. Hydralazine/procainamide induced SLE.
4. Isoniazid induced hepatitis.
5. ADVERSE DRUG REACTION FEB 2014
5
Addiction (psychological dependence).
It consists of compulsive, relapsing drug use despite negative consequences and at times is triggered by
cravings. It includes strong feeling of euphoria and the reward pathway is stimulated.
Examples: caffeine, cocaine, tobacco…
Dependence (physical dependence)
Altered physiological state produced by repeated administration of a drug such that when the drug is
abruptly discontinued, characteristic withdrawal syndrome occurs.
Examples: opioids, alcohol, benzodiazepines, sympathomimetics vasoconstrictors, bronchodilators.
Steven’s Johnson syndrome
Stevens-Johnson syndrome is an immune-complex–mediated hypersensitivity complex that
typically involves the skin and the mucous membranes. It is a minor form of toxic epidermal
necrolysis, with less than 10% body surface area (BSA) involved.
Etiology
1. Infectious
2. Drug-induced
3. Malignancy-related
4. Idiopathic
Drugs that are implicated:
1. Antibiotics: Penicillins and sulfa drugs are prominent; ciprofloxacin has also been
reported.
2. NSAIDS
3. Anticonvulsant drugs: carbamazepine, oxcarbamazepine, phenytoin, valproate,
lamotrigine.
4. Modafinil (Provigil)
5. Allopurinol
6. TNF-alpha antagonists (eg, infliximab, etanercept, adalimumab
7. Sertraline
8. Pantoprazole
9. Tramadol
Treatment
1. No specific treatment.
2. Symptomatic treatment in the form of fluid resuscitation, calamine lotion.
3. Corticosteroid therapy.
4. Immunosuppressant.
5. Human intravenous immunoglobulin (IVIG) has been described as both treatment and
prophylaxis.
6. ADVERSE DRUG REACTION FEB 2014
6
Toxic Epidermal Necrolysis (TEN), Lyell’s Syndrome
It is a life-threatening dermatologic disorder characterized by widespread erythema, necrosis,
and bullous detachment of the epidermis and mucous membranes, resulting in exfoliation and
possible sepsis and/or death.
Mucous membrane involvement can result in gastrointestinal hemorrhage, respiratory failure,
ocular abnormalities, and genitourinary complications.
The most commonly implicated agents include the following:
1. Sulfonamide antibiotics
2. Antiepileptic drugs
3. Oxicam nonsteroidal anti-inflammatory drugs
4. Allopurinol
5. Nevirapine
6. Abacavir
7. Lamotrigine
Treatment
Same as for Steven’s Johnson syndrome.