this is a series of notes on general pathology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.
This presentation is for those who want to understand the basics of reversible cell injury.
You can also get more idea from my youtube channel:
Harshit Jadav I Medical Wala
this is a series of notes on general pathology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.
This presentation is for those who want to understand the basics of reversible cell injury.
You can also get more idea from my youtube channel:
Harshit Jadav I Medical Wala
this is a series of notes on general pathology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.
The term necrosis is derived from a greek word nekros which means dead body.
Definition: Necrosis is defined as local or focal death of cells along with degradation of tissues by hydrolytic enzymes released from lysosome of the cell.
It is often associated with surrounding inflammatory reaction.
Necrosis is a series of morphological changes that follows cell death due to the irreversible cell injury/lethal cell injury/pathological cell injury.
CONTENTS,
Introduction
Necrosis
Fates of necrotic cells
Patterns of tissue necrosis
Causes of cell injury
The biomechanism of cell injury
Clinicopathological correlations; examples of cell injury and necrosis
Apoptosis
Causes of apoptosis
Apoptosis in physiologic conditions
Apoptosis in pathologic conditions
Mechanism of Apoptosis
The Mitochondrial pathway of Apoptosis
The Death receptor pathway of Apoptosis
Clearance of Apoptotic cells
Examples of Apoptosis
Summary
References
This report, prepared by the student at the College of Dentistry, Hassan Atheed , in the third phase discusses scientific topics, but it maybe did not be 100% complete.
Cell injury (cell death): it is the variable changes in morphological and functional properties of cell occurs due to internal or external causes (ex. Chemical, physical, infectious and genetic agents), that obligate cell to respond for preserving normal hemostasis (adaptation) or death (necrosis) when the injury factors sever cell unable to adept, cell may also killed by another pathway even when it have the ability to adept for saving other cells and tissue by programed cell death (apoptosis).
حسن عضيد
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
This is a powerpoint presentation on the Topic of Male and female genital tract, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics
This is a presentation on the topic of Adaptations, Cell injury and cell death, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
This is a presentation on the topic of hemodynamic disorders, thromboembolic diseases and shock, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
This is a presentation on the topic of Inflammation and repair, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
This is a presentation on the topic of cytology of the breast, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
This is a presentation covering all techniques in histopathology. Comprehensive coverage of all related aspects.. Useful for postgraduate Pathology students and practitioners.
This is a presentation on most common applications of immunohistochemistry in breast lesions. Prepared by Dr Ashish Jawarkar, Assistant professor in pathology, Parul Institute of Medical sciences and research Vadodara
This is a powerpoint presentation of Immunohistochemistry of lesions of prostate. This presentation will be helpful for postgraduate pathology students and practitioners alike. We are also on youtube. Please visit our channel at https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw
Dear all, Pathologybasics is out with a new series of power point presentations on general Pathology.. Following is link presentation on seventh and the most difficult to understand chapter of robbins.. chapter 7,neoplasia. Any suggestions/feedback/constructive criticism are welcome on facebook.com/pathologybasics or pathologybasics@gmail.com
Dear all, Pathologybasics is out with a new series of power point presentations on General Pathology.. Following is link presentation on amyloidosis covered in chapter 6 of Robbins. Remaining topics will be uploaded as a separate presentation soon.
Dear all, Pathologybasics is out with a new series of power point presentations on Systemic Pathology.. Following is link presentation on 12th chapter of robbins - the heart.This presentation includes valvular heart diseases, endocarditis, cardiomyopathies, pericardial diseases and tumors of the heart. Remaining topics will be uploaded as a separate presentation soon.
Cellular adaptations, injury and death.. Lecture 1Ashish Jawarkar
This is a series of lectures on general pathology useful for undergraduate and postgraduate pathology students. The ppts here have are enriched with explanatory pictures as well as useful video links.. hope you find them useful
This is a series of notes on clinical pathology, useful for postgraduate students and practising pathologists. It covers all internal and external quality control techniques. The topics are presented point wise for easy reproduction.
CSF - Cerebrospinal fluid examination - from tapping to pathological diagnosisAshish Jawarkar
This is a series of notes on clinical pathology, useful for undergraduate and postgraduate students, as well as practising pathologists. Prepared from standard text books with data in tabular and easily readable format
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
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
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.
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The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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NVBDCP.pptx Nation vector borne disease control program
Necrosis
1. 1
General Pathology Notes (Robbins)
By Dr. Ashish Jawarkar
Chapter 1 : CELLULAR RESPONES TO STRESS AND TOXIC INSULTS:
ADAPTATION, INJURY AND CELL DEATH
TOPIC 2. CELL INJURY AND NECROSIS
Overview
1. definition
2. types – reversible, irreversible (necrosis,apoptosis)
3. causes
4. timeline
5. Mechanisms of cell injury (necrosis)
6. morphology
7. necrosis vs apoptosis
8. patterns of necrosis
9. molecular basis
*definition and types
Cells exposed to stress
Adaptation (hypertrophy/hyperplasia/atrophy/metaplasia)
Continued stress, no more adaptation possible
Cell injury
Reversible cell injury
Irreversible cell injury
(necrosis & apoptosis)
Notes on General Pathology – Apoptosis….By Dr. Ashish V. Jawarkar
Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes
2. 2
*Causes of cell injury
1. O2 deprivation, nutritional imbalances
2. Physical agents – trauma, heat, cold, UV light, shock
3. Chemical agents – cyanide, arsenic, pollutants
4. Infectious agents
5. Deranged immunity
*Timeline
Reversible
Injury
Biochemical
alterations
effect
cell
function
irreversible cell injury
Minutes
Ultrastructural
changes
Days
Light
Microscopic
Changes
Gross
Morphologic
Changes
*Mechanisms of Cell injury (Necrosis)
1. Damage to membranes (plasma, lysosomal,mitochondrial)
2. Failure of calcium pump
3. Accumulation of free radicals
4. Mitochondrial membrane damage and depletion of ATP
5. Protein misfolding and DNA damage
1. Damage to membranes
Plasma membrane damage
Lysosomal membrane damage
Osmotic imbalance
Leakage of metabolites
leakage of
(DNAases, RNAases, Proteases etc.)
Notes on General Pathology – Apoptosis….By Dr. Ashish V. Jawarkar
Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes
3. 3
2. Failure of Ca2+ pump
Calcium influx
Activation of leaked enzymes (DNAases, RNAases)
Alteration of mitochrondrial
Membrane permeability
3. Accumulation of free radicals
Generation of free radicals
ROS
1. Redox rns in
Normal metabol
2. Radiation
3. Inflammn
4. CCl4
5. Transition metals
(Fenton rn#)
6. NO
FENTON RN
H202 + Fe2+
O2Super
Oxide
Fe3+ + OH + OH-
SOD
H2O2
fenton rn
+Fe2+
Hydrogen
Peroxide
OH
Hydroxyl
Radical
MITOCHONDRIA
Removal of free radicals done by
1. SOD (superoxide dismutase) – mitochondria
2. Glutathione peroxidase – mitochondria
3. Catalase – peroxisome
Pathologic effects of ROS
1. Fatty acid oxidation and disruption of membranes, organelles
2. Protein oxidation and loss of enzyme activity, protein misfolding
3. DNA oxidation and mutations and breaks
Notes on General Pathology – Apoptosis….By Dr. Ashish V. Jawarkar
Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes
4. 4
4. Mitochondrial membrane damage and depletion of ATP
Mitochondrial membrane damaged by
1. increased cytosolic calcium
2. ROS
3. hypoxia
4. mutations in mito genes
Activation of caspases
(apoptosis)
Due to leakage of cyto c
Alteration of mitochondrial membrane permeability
Due to leakage of H+
H+ leakage and Loss of membrane potential
Decreased Oxidative Phosphorylation
Decreased ATP generation
Detachment of Ribosomes
Failure of Na+ pump
Increased anaerobic
Glycolysis
Decreased protein synthesis
Influx of Na +, Ca2+
H2O
Lactic acidosis
Increased lipid deposition
Cellular swelling
ER swelling
Clumping of nuclear
chromatin
Notes on General Pathology – Apoptosis….By Dr. Ashish V. Jawarkar
Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes
5. 5
*Morphology
GROSS
Light
Microscopy
REVERSIBLE INJURY
1. Pallor
2. Turgor
3. Increased weight
1. Cellular swelling
2. vacuolar
degeneration/hydropic
change – clear vacuoles in
cytoplasm that represent
pinched off segments of ER
NECROSIS
1. Cytoplasm –
a. eosinophilia – due to loss of
cytoplasmic RNA
b. Glassy appearance – due to loss
of glycogen particles
c. Moth eaten app – due to
vacuolation
2. Cell membrane –
a. Myelin figures – membrane
fragments collect in cytoplasm
b. Calicification – of myelin figures
3.
a.
b.
c.
Ultra
structure
Plasma membrane – blebs, loss of
microvilli
Nucleus –
Karyoloysis – lysis of chromatin
Pyknosis – nuclear shrinkage
Karyorrhexis – chromatin
condenses into solid shrunken
basophilic mass
Plasma membrane – discontinuities
Cytoplasm – Myelin figures
Nucleus – disaggregation of
granular and fibrillar elements
Mitochondria - Large amorphous
densities
ER – dilatation and detachment of
ribosomes
Mitochondria – amorphous
densities
*Patterns of tissue necrosis
1. COAGULATIVE NECROSIS
Gross: The tissue is firm. Eg of localized coagulative necrosis is infarct.
Microscopy: preserved cell outlines, loss of nuclei, inflammatory infiltrate
2. CASEOUS NECROSIS (cheese like, in TB)
Gross: friable white app of necrotic area
Notes on General Pathology – Apoptosis….By Dr. Ashish V. Jawarkar
Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes
6. 6
Microscopy: Granuloma – central necrosis with lysed cells forming amorphous
debris, surrounded by inflammatory cells and epithelioid cells
3. LIQUEFACTIVE NECROSIS (necrosis in CNS)
Characterized by digestion of dead tissue – transformation into liquid viscous
mass
Gross: Abscess cavity formation with ragged margins
Microscopy: Necrotic material is creamy yellow containing dead leucocytes
4. GANGRENOUS NECROSIS
1. coagulative necrosis occurring in a limb that has lost its blood supply
2. occurs in multiple tissue planes
3. superimposed bacterial infection causes liquifactive necrosis – wet
gangrene
5. FAT NECROSIS
Refers to focal areas of fat destruction occurring due to release of pancreatic
enzymes into substance of pancreas and peritoneal cavity
Seen in acute pancreatitis
Gross: Pancreatic enzymes liquefy membranes of fat cells in peritoneum, split
triglycerides, produce saponification and deposition of calcium, chalky white
areas
Microscopy: shadowy outlines of fat cells, basophilic calcium deposits,
inflammatory reaction
6. FIBRINOID NECROSIS
Seen in immune reactions like SLE and other vasculitic syndromes
Seen in the wall of blood vessels
Microscopy: The wall of the vessels show circumferential bright pink areas of
necrosis and inflammation. Its basically immune complex deposition with
extravasated fibrin.
Notes on General Pathology – Apoptosis….By Dr. Ashish V. Jawarkar
Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes