The document discusses various types of adverse drug reactions (ADRs) and events. It defines an ADR as any noxious change suspected to be caused by a drug taken at normal doses, and an adverse drug event as any untoward occurrence during treatment that may not be causally related. It describes types of ADRs including dose-related type A reactions, unpredictable type B reactions, chronic type C reactions, and withdrawal type E reactions. It also discusses factors influencing ADRs, grading of severity, classifications, mechanisms of hypersensitivity reactions, pharmacovigilance, and prevention of adverse effects.
ADE
INCIDENCE OF ADR
GREADING OF SEVERITY OF ADR
CLASSIFICATIONS
PHARMACOVIGILANCE
CATAGORIES
CAUSES OF ADR
DRUG INDUCED HEPATIC DYSFUNCTION
DRUG INDUCED ENDOCRINE DYSFUNCTION
DRUG INDUCED PHERIPHERAL NEUROPATHY
MANAGEMENT OF ADR
ADE
INCIDENCE OF ADR
GREADING OF SEVERITY OF ADR
CLASSIFICATIONS
PHARMACOVIGILANCE
CATAGORIES
CAUSES OF ADR
DRUG INDUCED HEPATIC DYSFUNCTION
DRUG INDUCED ENDOCRINE DYSFUNCTION
DRUG INDUCED PHERIPHERAL NEUROPATHY
MANAGEMENT OF ADR
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
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
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.
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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.
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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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
2. ADVERSE DRUG REACTION
Any noxious change which is
Suspected to be due to a drug
At doses normally used in man
May requires treatment or decrease in dose or
Caution in the future use of the same drug
3. ADVERSE DRUG EVENT (ADE)
Any untoward occurrence that may present during medical
treatment,
But
Does not necessarily have a causal relationship with the treatment
4. Incidence of ADR more
Polypharmacy
Elderly
Children
Patient with multiple diseases
Pregnancy
Malnourished
Immunosuppression
Drug Abusers and addicts
Develop
Immediately
or
• Prolonged medication
or
• After stopping.
5. GRADING OF SEVERITY OF ADVERSE
DRUG REACTIONS :
Minor : No therapy, antidote or prolongation of
hospitalization is required.
Moderate: Requires change in drug therapy, specific
treatment or prolongs hospital stay.
Severe: Potentially life-threatening, causes permanent
damage or requires intensive medical treatment.
Lethal : Directly or indirectly contributes to death of the
patient.
6. CLASSIFICATIONS OF ADR
Broadly
Type- A (Predictable)- Based on pharmacological
properties
Type- B (Non-predictable) – Based on
Immunological response and genetic makeup of
person
Augmented
Bizarre
Continuous
Delayed
Ending Use
Failure of Efficacy
7. TYPE A- AUGMENTED
These are based on the pharmacological properties of the drug so
can be predicted.
They are common and account for 75% of ADRs
Dose related and preventable mostly reversible.
Examples:-
Anticoagulants (e.g., warfarin, heparin) – bleeding
Anti-hypertensives (e.g.. α1-antagonists) – hypotension
Anti-diabetics (e.g. insulin) – hypoglycemia
8. TYPE B- BIZZARE OR
UNPREDICTABLE
Have no direct relationship to the dose of the drug or the
pharmacological mechanism of drug action.
Develop on the basis of:
Immunological reaction on a drug (Allergy)
Genetic predisposition (Idiosyncratic reactions)
More serious clinical outcomes with higher mortality and
morbidity.
Mostly require immediate withdrawal of the drug.
9. TYPE C – CHRONIC (CONTINOUS) USE
They are mostly associated with cumulative-long term
exposure
Example:-
Analgesic (NSAID)– interstitial nephritis, papillary sclerosis,
necrosis
10. TYPE D – DELAYED
They manifest themselves with significant delay
Teratogenesis -Thalidomide – Phocomelia (flipper-like fore limbs)
Mutagenesis/Cancerogenesis
Others:
Tardive dyskinesis – during L-DOPA Parkinson disease treatment
11. TYPE E – END OF USE
Drug withdrawal syndromes and rebound phenomenons
Example – sudden withdrawal of long term therapy with -
blockers can induce rebound tachycardia and hypertension
12. PHARMACOVIGILANCE (DAUP)
The 'science and activities relating to the detection, assessment,
understanding and prevention of adverse effects or any other
drug related problems’
The information generated is useful in educating doctors and in the
official regulation of drug use.
It has an important role in rational use of medicines, as it provides
the basis for assessing safety of medicines.
13. Various activities involved in pharmacovigilance are:
Postmarketing surveillance and other methods of ADR monitoring
such as voluntary reporting by doctors prescription event
monitoring.
Dissemination of ADR data through 'drug alerts', 'medical letters,'
advisories sent to doctors by pharmaceuticals and regulatory
agencies.
Changes in the labelling of medicines indicating
restrictions in use or statuary warnings, precautions,
or even withdrawal of the drug.
14. The Uppsala Monitoring Centre (Sweden) is the international
collaborating centre.
In India,
National centre is located at Ghaziabad
Peripheral Centres at Medical college levels and tertiary and above
hospitals
Reports generated by doctors, paramedical staff--to peripheral
centre...National centre...Uppsala Monitoring Centre...Compilation
of data..analysis of data..causal association is
confirmed..guidelines issued regarding the safe use of medicine or
(restricted use or withdrawal from the market)
15. PREVENTION OF ADVERSE EFFECTS TO DRUGS
Avoid inappropriate use of drugs .
Appropriate drug administration (Rational Therapeutics)
Dose
Dosage form
Duration
Route
Frequency
Technique
Ask for previous history of drug reactions and allergies
Always suspect ADR when new symptom arises after initiation of
treatment. ( No new drug for new symptom).
Ask for laboratory findings like serum creatinine etc.
16. Categorized into:
Side effects-
Secondary effects
Toxic effects
Intolerance
Idiosyncrasy
Drug allergy
Photosensitivity
Drug dependence
Drug withdrawal reactions
Teratogenicity
Mutagenicity and Carcinogenicity
Drug induced diseases (Iatrogenic disorders or Iatrogenicity)
17. SIDE EFFECTS
Unwanted often unavoidable Pharmaco-dynamic
effects.
Occur at therapeutic doses.
Predictable
Examples.
Benzodiazepines- Motor in coordination
H1 Anti-histaminics- Sedation
18. SECONDARY EFFECTS
Indirect consequences of a primary action of the drug.
E.g. corticosteroids weaken host defence
mechanisms so that latent tuberculosis gets activated.
19. TOXIC EFFECTS (Poisonous effect)
It is the dose and duration which makes a poison.... Paracelsus
Over dose or prolonged use.
The effects are predictable and dose related.
The CNS, CVS, kidney, liver, lung, skin and bone marrow are most
commonly involved in drug toxicity.
20. Toxicity may result from extension of the therapeutic
effect itself, e.g. complete A-V block by digoxin,
bleeding due to heparin.
Poisoning: Poison is a substance which endangers life
by severely affecting one or more vital functions.
21. Specific antidotes such as receptor antagonists, chelating
agents or specific antibodies are available for few poisons.
For others as well as for those poisons which have a
selective antagonist general supportive and symptomatic
treatment should be done.
These measures are:
1. Resuscitation and maintenance of vital functions:
maintenance of ABC , body temperature and blood
glucose.
2.Termination of exposure (decontamination)
3. Prevention of absorption of ingested poisons.
4. Hastening elimination of the poison by inducing
diuresis or altering urinary pH
22. INTOLERANCE
It is the appearance of characteristic toxic
effects of a drug in an individual at therapeutic
doses
It indicates a low threshold of the individual to
the action of a drug
Example:- Only few doses of carbamazepine
may cause ataxia in some people
23. IDIOSYNCRASY
It is genetically determined abnormal reactivity to a chemical.
The drug interacts with some unique feature of the individual,
not found in majority of subjects, and produces the
uncharacteristic reaction.
Example :-
Chloramphenicol produces nondose-related
serious aplastic anaemia in rare individuals.
Barbiturates cause excitement and mental confusion in some
individuals
24. DRUG ALLERGY
It is also called drug hypersensitivity.
It is an immunologically mediated reaction producing
stereotype symptoms which are unrelated to the
pharmacodynamic profile of the drug.
It generally occur even with much smaller doses and have
a different time course of onset and duration.
25. Allergic reactions occur only in a small
proportion of the population exposed to the
drug .
History of prior sensitization may or may not be
evident.
The drug or its metabolite acts as antigen (AG)
or more commonly hapten (incomplete antigen)
and induce production of antibody
(AB)/sensitized lymphocytes.
26. TYPES OF ALLERGIC REACTIONS
A) HUMORAL
1. Type I/ anaphylactic reactions.
2. Type-II / cytolytic reactions.
3. Type-Ill / retarded or Arthus reactions.
B) CELL MEDIATED
Type-IV (delayed hypersensitivity) reactions.
27. PHOTOSENSITIVITY
It is a cutaneous reaction resulting from drug induced sensitization of the
skin to UV radiation.
The reactions are of two types:
a) Photo-toxic :- (T-S)
a) Drug or its metabolite Accumulates in the skin,
b) absorbs light and undergoes a Photochemical reaction followed by
c) Photobiological reaction resulting in
d) Tissue damage (sunburn-like),
a) i.e. erythema, edema, blistering , hyper pigmentation,
desquamation.
The shorter wave lengths (290-320 nm, UVB) are responsible
28. (b) Photo-allergic: (A-L)
Drug or its metabolites induce a cell mediated immune response which on
exposure to
Light of longer wave lengths (320-400 nm, UV -A)
Produces a papular or eczematous contact dermatitis like picture.
Drugs involved are sulfonamides, sulfonylureas, griseofulvin, chloroquine,
chlorpromazine
29. DRUG DEPENDENCE
Use of drugs for personal satisfaction
Higher priority than other basic needs, often in the face of known
risks to health.
Physical dependence It is an altered physiological state produced by
repeated administration of a drug which necessitates the continued
presence of the drug to maintain physiological equilibrium.
Discontinuation of the drug results in a characteristic withdrawal
(abstinence) syndrome.
Drugs producing physical dependence are opioids, barbiturates and
other depressants including alcohol and benzodiazepines
30. Drug abuse :
Refers to use of a drug by self medication in a manner and
amount that deviates from the approved medical and social
patterns in a given culture at a given time.
Drug addiction
It is a pattern of compulsive drug use characterized by
overwhelming involvement with the use of a drug. Procuring
the drug and using it takes precedence over other activities
31. Drug habituation (Psychological dependence)
It denotes less intensive involvement with the drug, so that its
withdrawal produces only mild discomfort.
Consumption of tea, coffee, tobacco, social drinking are
regarded habituating, physical dependence is absent
32. DRUG WITHDRAWAL REACTIONS
Sudden interruption of therapy with certain other drugs results in
adverse consequences, mostly in the form of worsening of the
clinical condition for which the drug was being used
Example: Acute adrenal insufficiency may be precipitated by
abrupt cessation of corticosteroid therapy.
33. TERATOGENICITY (Teratos- Monster)
Drug to cause foetal abnormalities when administered to the
pregnant mother.
Drugs can affect the foetus at 3 stages-
(i) Fertilization and implantation-conception to
17 days-failure of pregnancy which often goes unnoticed.
(ii) Organogenesis-18 to 55 days of gestation most vulnerable
period, deformities are produced.
(iii) Growth and development-56 days onwards
developmental and functional abnormalities
can occur,
e.g. ACE inhibitors , Thalidomide, Warfarin, Barbiturates,etc.
34. MUTAGENICITY AND CARCINOGENICITY
Cause genetic defects and cancer respectively.
Reactive intermediates which affect genes and may cause
structural changes in the chromosomes
Even without interacting directly with DNA, certain
chemicals can promote malignant change in genetically
damaged cells, resulting in carcinogenesis.
Examples- anticancer drugs, radioisotopes, estrogens,
tobacco,etc.
35. DRUG INDUCED DISEASES
These are also called iatrogenic (physician induced)
diseases, and are functional disturbances (disease) caused
by drugs .
Hepatitis by isoniazid and Rifampicin
Peptic ulcer by salicylates and corticosteroids
Retinal damage by chloroquine