Introduction to general Veterinary Pathology, Gross examination description, How to describe lesion while doing Gross/ macroscopic examination, Postmortem lesion description at basic leve
etiology, local names, definition, transmission, source of infection, epidemiology, pathogenesis, clinical signs, diagnosis, differential diagnosis, treatment prevention and control
ENHANCING THE EFFICIENCY OF POST MORTEM DIAGNOSIS BY IMPROVING THE POST MO...asha ann philip
A postmortem examination, is the examination of the body/carcass after death. Post mortem is performed to obtain an accurate cause of death and when done properly which involves looking at the animal as a whole, as well as looking at each individual organ within the body.The efficiency of postmortem diagnosis depends on facilities and techniques that are used during PM, thorough knowledge, health aspects/biosafety and other supporting diagnostic methods.
etiology, local names, definition, transmission, source of infection, epidemiology, pathogenesis, clinical signs, diagnosis, differential diagnosis, treatment prevention and control
ENHANCING THE EFFICIENCY OF POST MORTEM DIAGNOSIS BY IMPROVING THE POST MO...asha ann philip
A postmortem examination, is the examination of the body/carcass after death. Post mortem is performed to obtain an accurate cause of death and when done properly which involves looking at the animal as a whole, as well as looking at each individual organ within the body.The efficiency of postmortem diagnosis depends on facilities and techniques that are used during PM, thorough knowledge, health aspects/biosafety and other supporting diagnostic methods.
An overview of Inclusion body hepatitis-hydropericardium syndrome (IBH-HPS) a...Dr.Kedar Karki
IBH/HPS is an acute infectious disease characterized by typical hydropericardium, severe anaemia, necrotic hepatitis and high mortality. In natural outbreaks, the affected birds may not exhibit any clinical signs (Jaffery, 1988) except sudden heavy mortality (Ravikumar et al., 1997). Mortality rates in various outbreaks range from 15- 60% (Asrani et al., 1997).
An overview of Inclusion body hepatitis-hydropericardium syndrome (IBH-HPS) a...Dr.Kedar Karki
IBH/HPS is an acute infectious disease characterized by typical hydropericardium, severe anaemia, necrotic hepatitis and high mortality. In natural outbreaks, the affected birds may not exhibit any clinical signs (Jaffery, 1988) except sudden heavy mortality (Ravikumar et al., 1997). Mortality rates in various outbreaks range from 15- 60% (Asrani et al., 1997).
At the end of the class the students will be able to,
Explain the basic concept of pathology
Describe the Cellular & tissue changes.
Describe the Infiltration and regeneration
Elaborate the inflammation and infection
introduction to anesthesia introduction to anesthesiaone .pptxyeshiwasdagnew
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Difference between Apoptosis versus Necrosis and Types of Necrosis.pptxRukhshanda Ramzaan
Apoptosis Versus Nercosis
Apoptosis Necrosis
Predefined cell suicide or programmed cell death. Natural physiological Process. Involve one cell at a time. Cell shrinkage (Dense eosinophilic cytoplasm) Pyknosis (Condensation) and Karyorrhexis (fragmentation) of nuclear material Formation of membrane blebs and apoptotic bodies
Phagocytosis of apoptotic bodies by Macrophages
Caspase dependent pathway
No Inflammation (no immune response) Premature, unprogrammed cell death always pathological. Involve many cells Cell Swelling (Swelling of endoplasmic reticulum and mitochondria) and membrane blebs Pyknosis (condensation), Karyorrhexis (Fragmentation) and Karyolysis (lysis)of the nucleus. Breakdown of the plasma membrane, organelles (enzymatic digestion), leakage of cellular contents
Increased eosinophilia, Accumulation of Myelin figures (whorled precipitated Phospholipids)
Initiate Inflammation (Strong immune response)
Difference between reversible and irreversible cell injury,Mechanism of cell ...Rukhshanda Ramzaan
Cell Injury: Any change resulting in loss of the ability to maintain the normal or adapted homeostatic state.
Agents that cause cell injury
• Hypoxia / Ischemia (loss of blood supply)
• Microbial
• Parasitic
• Chemical
• Physical
• Trauma
• Genetic
• Nutritious
• Environmental
Types of Cell injury
Reversible Cell Injury
Pathologic changes that can be reversed in mild cellular injury when the stimulus is removed. Cell injury is reversible only up to a certain point otherwise it will be irreversible.
Changes in reversible cell injury
Cellular Swelling: Due to accumulation of intracellular water and endoplasmic reticulum & mitochondria.
Clumping of chromatin.
Irreversible Cell injury
Pathologic changes that are permanent and cause cell death, they cannot be reversed to normal state.
Changes in irreversible cell injury
Irreversible injury is marked by severe mitochondrial vacuolization, extensive damage to plasma membranes, detachment of ribosomes from the granular endoplasmic reticulum (ER). Injury to lysosomal bodies leads to leakage of lysosomal enzymes into the cytoplasm and condensation, fragmentation and lysis of nuclei.
Cellular Response to cell Injury and Cellular Adaptations .pptxRukhshanda Ramzaan
Cellular Adaptations
ability of cells to respond to various types of stimuli and adverse environmental changes
Atrophy(decrease in cell size)
Hypertrophy(increase in cell size)
Hyperplasia(increase in cell number)
Metaplasia(change in cell type): Replacement of one differentiated cell type with another mature differentiated cell type that is not normally present in that tissue.
Dysplasia (increase in abnormal cell): Dysplasia is not cancer, but it may sometimes become cancer.
Terminologies used in Disturbances of Cell Growth which are not adaptations
Agenesis refers to the failure of an organ to develop during embryonic growth and development
Hypoplasia is the underdevelopment or incomplete development of a tissue or organ. It is technically not the opposite of hyperplasia (too many cells). Hypoplasia is a congenital condition, while hyperplasia generally refers to excessive cell growth later in life.
Aplasia is a birth defect where an organ or tissue is wholly or largely absent. It is caused by a defect in a developmental process.
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
- 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
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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
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
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
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.
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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. Learning Outcomes
• By the end of the lecture you should be able to:
• Define Pathology in two ways
• Define General Pathology
• Discuss about the Morphological Changes
• Explain lesion and types of the Lesion
• Define Gross examination and Histopathology
• How to describe the Lesion in Gross examination
3. Introduction to Pathology
•Pathology:
• Pathology is the study of Disease.
• Pathos – suffering, disease
• Logos – study
Disease?
*loss of ease
*a departure from a
normal state
The better we understand the disease, the better we
can diagnose & treat it
4. What‘s normal (When Body At Ease)
Anatomy
Physiology
Histology
Biochemistry
Genetics
Health is a state of an
individual living in
complete harmony with
his environment.
5. Pathology is the study of molecular, biochemical,
functional, & morphological changes in cells,
tissues, or organs in response to an INJURY
Let’s define again
Cell damage is cell injury
6. Agents that cause things to go wrong/ injury
Trauma
Microbial
Nutritious
Genetic
Chemicals
Parasitic
8. Pathology
General
Pathology
Concerned with the
basic reactions of
cells and tissues to
injurious stimuli
Systemic
Pathology
The application of
these basic reactions
to the various body
systems, or to various
specific diseases
9. Pathology
Clinical
Pathology
It includes certain laboratory
methods which help in making
the diagnosis e.g. urine
examination, blood
examination
Necropsy
& meat
inspection
Postmortem examination of
animals.
To determine the health of
animals both prior to death
(ante mortem) and after death
(post mortem)
10. Pathology covers Four aspects of a disease
process
Etiology ( cause of disease)
Pathogenesis
Morphological Changes (Lesions)
Clinical significant / Functional
Consequence
General/Systemic
Pathology
Practical
11. Morphological Changes (Lesion)
The structural
alterations in cells or
tissues
A lesion is any
damage or abnormal
change in the tissue
structure of an
organism, usually
caused by disease
Morphology study of forms and structures
12. Types of Lesion
Macroscopic or Microscopic morphological alteration occurring
in the tissue structure or function as the result of injury
Macroscopic or Gross Lesions
Can see through the naked eye
Gross Examination
Examination of tissue without
the help of a microscope
Microscopic or histopathology
Lesions
Can see through a microscope
Histopathology
Study of diseases tissue under a
microscope
Let’s define again the lesion
35. Revisiting Learning Outcomes
• By the end of the lecture you should be able to:
• Define Pathology in two ways yes/no
• Define General Pathology yes/no
• Discuss about the Morphological Changes yes/no
• Explain lesion and types of the Lesion yes/no
• Define Gross examination and Histopathology yes/no
• How to describe the Lesion in Gross examination yes/no
