1. Cell injury refers to changes in a cell's internal and external environment due to stresses like lack of oxygen, toxins, or infections.
2. Causes of cell injury include hypoxia, physical and chemical agents, microbes, immunological reactions, nutritional imbalances, and genetic factors.
3. Cellular responses to injury include reversible changes like fatty change and swelling, or irreversible cell death through necrosis or apoptosis. Adaptive changes like hypertrophy and hyperplasia can also occur.
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 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
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
This ppt on basic Introduction of General Pathology including the etiology and pathogenesis and their factors .
General Pathology into simple terms for you to understand and use in your exam.
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
This ppt on basic Introduction of General Pathology including the etiology and pathogenesis and their factors .
General Pathology into simple terms for you to understand and use in your exam.
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
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
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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.
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
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.
2. Introduction
General considerations……
• Adapt or die!
• Reaction patterns in a given cell/tissue is often limited
• Degree of injury is a function of type, duration and
severity of insult
3. Definition
Cell injury: The effect of a variety of stresses due to
etiological agents a cell encounters resulting in changes in
its internal & external environment.
Cellular response to stress vary & depends upon
1. Host factors: type of cell & tissue involved
2. Factors pertaining to injurious agent : extent & type of
cell injury.
4. Introduction
• Pathology: the study (logos) of suffering (pathos)
• Four aspects of a disease process that form the core of
pathology
1. its cause (etiology)
2. Mechanisms of its development
( pathogenesis)
3. Structural alterations induced in cells &
organs ( morphological changes)
4. Functional consequences of the
morphologic changes ( Clinical significance)
5. Causes of cell injury
Genetic causes
Acquired causes -Hypoxia and ischemia
-Physical agents
-Chemical agents and drugs
-Microbial agents
-Immunological agents
-Nutritional derangements
-Psychological factors
6. Causes of cell injury
Acquired causes
1. Oxygen Deprivation
Ischemia ( loss of blood supply from impeded arterial flow
or reduce venous drainage)
Local e.g. embolus
Systemic e.g. cardiac failure
Hypoxia ( deficiency of oxygen causing cell injury by
reducing aerobic oxidative respiration)
Oxygen problems e.g. altitude
Haemoglobin problems e.g. anaemia
Oxidative phosphorylation
E.g. cyanide poisoning
7. Causes of cell injury
2. Physical agents
Direct Physical Effects
- Exposure of tissue to extreme heat or cold results in
direct injury that is often irreversible, resulting in a
pattern of coagulative necrosis.
- Sudden changes in pressure can cause cellular
disruption (e.g. a hammer blow to the thumb).
- Electrical currents can cause direct breakdown of
cellular membranes that may be irreversible.
8. Causes of cell injury
3. Chemical agents & drugs:
Common poisons (arsenic, cyanide, mercury)
interfere with cellular metabolism. If ATP levels
drop below critical levels, affected cells will die.
The list of pharmaceuticals that may have toxic
effects on cells is enormous. Some act directly, but
most have their effect through breakdown
metabolites. Metabolism of alcohol (a type of drug)
to acetaldehyde is one example.
9. Causes of cell injury
4. Microbial agent
Injuries by microbes include infections caused by Fungi,
Rickettsiae, Bacteria, parasites and Viruses
5. Immunologic agents: Double –edged sword’- protects the
host against various injurious agents but it may also cause
cell injury.
Hypersensitivity reactions
Anaphylactic reactions to a foreign body
Autoimmune diseases
10. Causes of cell injury
6. Nutritional Imbalances:
Dietary insufficiency of protein, vitamins and/or
minerals can lead to injury at the cellular level due
to interference in normal metabolic pathways.
Dietary excess
can likewise lead to cellular and tissue alterations
that are detrimental e.g. fat is the biggest
offender, or excess ingestion of "health
supplements"
11. Causes of cell injury
7. Psychogenic diseases: No specific biochemical or
morphologic changes in acquired mental diseases.
problems of drug addiction, alcoholism & smoking results
in various organic diseases such as liver damage, chronic
bronchitis, lung cancer, peptic ulcer, HT, IHD etc,
8. Genetic derangements: result in a defect as severe as the
congenital malformations associated with down
syndrome, caused by chromosomal abnormalities.
Inborn error of metabolism arising from enzymatic
abnormalities.
12. Causes of cell injury
9. Iatrogenic causes
10. Idiopathic diseases: ‘Unknown cause’. Exact cause
is undetermined.
Most common form of HT ( 90%) is idiopathic ( or
essential ) HT.
11. Ageing: it is result of a progressive decline in the
proliferative capacity & life span of cells and the
effects of continous exposure to exogenous influences
that result in progressive accumulation of cellular and
molecular damage.
16. Adaptation
In case of severe stress, the narrow range
of alteration in structure & function is not
sufficient, the cell undergoes an altered
but steady state e.g. atrophy, hypertrophy.
17. Cellular responses
1. Cellular adaptations:
Increased functional demand
↓
cell adapt to the changes
↓
expressed morphologically
↓
revert back to normal after the stressed is removed.
18.
19. Adaptive response:
Hypertrophy: An increase in the size of cells and
,with such change ,an increase in the size of the organ
( without any change in the number of cells)
Hypertrophied organ has no new cells ,just large cells.
Atrophy : shrinkage in the size of the cell substance
is known as atrophy.
Hypoplasia : Term used for developmentally small
size.
Aplasia: Extreme failure of development so that only
rudimentary tissue is present.
20. Adaptive response
Hyperplasia: An increase in number of cells in an
organ or tissue resulting in enlargement of the organ
or tissue.
Metaplasia: Reversible change in which one adult
cell type ( epithelial or mesenchymal) is replaced by
another adult cell type.
A regressive change in the adult cells manifested by
variation in their size, shape & orientation.
Commonly associated with chronic inflammation and
irritation or is seen adjacent to cancerous change.
There is tendency to develop into cancer in some
cases.
21. Adaptive response
Intracellular accumulations : one of the
manifestations of metabolic derangements in cells is
the intracellular accumulations of abnormal amounts
of various substance.
1. A normal cellular constituent- water, lipid, proteins
& carbhohydrates.
2. An abnormal substance
Exogenous : minerals or products of infectious
agents
Endogenous : products of abnormal synthesis or
metabolism
3. Pigments
22. HEART( lipid accumulation)
lipid accumulation in two forms:
1.Tigroid effect: bands of yellowed myocardium
alternating with bands of darker, red brown
myocardium uninvolved in patients with profound
anemia
2.Diffuse ,uniform appearance of myocardium e.g:
Diphtheritic myocarditis & severe anemia.
23. Cellular responses : Subcellular
changes
Residual effects of reversible cell injury persist in cell
as evidence of cell injury at Subcellular level
(Subcellular changes) or metabolites may accumulate
within the cell (Intracellular accumulations).
24. Cellular responses:
Reversible & Irreversible cell injury
Cell injury :
If the cell’s adaptive capability is exceeded or if adaptive response
is not possible, cell injury develops.
Two types
1. Reversible cell injury ( Degeneration ):stress is mild to
moderate ; injured cell may recover.
2. Irreversible cell injury ( Necrosis ) : Persistent & severe form of
cell injury leads to cell death.
25. Reversible change
Fatty change ( Steatosis)
Abnormal accumulation of triglycerides within
parenchymal cells.
Organs:
1. Liver ( common , organ involved in fat metabolism)
2.Heart
3. Muscle
4.Kidney
26. Fatty change ( Steatosis)
Causes :
1. Toxins ( Alcohol abuse)
2.DM
3. Protein malnutrition
4.Obesity
5.Anoxia
6.kwashiorkor in children
29. Foam cells
Accumulation of triglycerides, cholesterol & cholesterol
esters in phagocytic cells.
Scavenger macrophages, whenever in contact with the
lipid debris of necrotic cells or abnormal forms of
plasma lipids become stuffed with lipid becoz of
phagocytic activities.
Cytoplasm becomes vacuolated & are called as ‘ FOAM
CELLS’. E.g: Atheroslcerosis of aorta
31. Fatty Liver: Microscopy
Appears as clear vacuoles within parenchymal cells
D/D: Intracellular accumulations of water &
polysaccharides ( glycogen) produce clear vacuoles.
1. Lipids:
Avoidance of fat solvents used in paraffin embbeding.
Frozen section : to identify fat.
Special stains: Sudan IV, Oil Red- O (orange red ),
Osmic acid, Sudan black( color: black )
32. Fatty Liver: Microscopy
2. Glycogen: PAS ( Periodic Acid Schiff )
Reaction
3. Water/ Fluid with a low protein
content :
Neither fat nor glycogen can be
demonstrated.
33. Cellular swelling/ cloudy swelling
Organs: kidney ,liver
Causes: ischemia, hypoxia, effect of poison.
Mech : cells are incapable to maintain ionic and fluid
homeostasis.
Gross: organ is swollen, c/s bulges outwards, pale, hazy
& has a grey parboiled appearance. Soft in consistency.
Microscopy: cells are swollen, indistinct cell margins
and cytoplasm filled with eosinophilic(proteinaceous )
granules and cell borders might be grayed releasing
granules.
34. Reversible cell injury
Hydropic degeneration :
vacuoles appear in the cytoplasm.
In extreme forms ,cells get distended with fluid &
rupture, resulting in death of cells. e.g. blisters,
Microvasculature of organ is compressed by swollen
cells ( hepatic sinusoids, capillaries of renal cortex)
resulting in pallor of the organ
35. Irreversible cell injury
Necrosis: Death of a cell or group of cells in the
midst of living tissue.
1. Coagulative necrosis
2.Liquefactive necrosis
3. Caseous necrosis
4.Fat necrosis
5.Fibrinoid necrosis
6.Gangrenous necrosis
Apoptosis: Programmed cell death.
36. Classification of morphologic forms
of cell injury
1. Reversible cell injury
2. Irreversible cell injury
3. Programmed cell
death
4. Deranged cell
metabolism
5. After-effects of
necrosis
Retrogressive changes
Cell death –necrosis
Apoptosis
Intracellular
accumulation of lipid,
protein, carbhohydrate
Gangrene, pathologic
calcification.