This document defines and describes various pathological processes including degeneration, necrosis, apoptosis, gangrene, and calcification. It discusses four main types of degenerative cell changes: cellular swelling, fatty change, hyaline change, and mucoid change. It also describes five types of necrosis: coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Apoptosis is defined as a genetically programmed form of cell death. Gangrene is described as necrosis with superadded putrefaction. Pathologic calcification can be either dystrophic or metastatic.
This presentation mainly deals with granuloma formation and various factors involved in it. It describes the examples of granulomatous disorders and gives a details on how to seperate them on histopathology.It also describes type 4 hypersensitivty reaction concisely
Hi..! This presentation series is about 'Cell Injury'.. So, here is the 1st part- 'OVERVIEW OF CELLULAR NECROSIS' which I tried to explain in simplest way.. i hope that it will be helpful.. Plz like n do share... Thank You..!!
This presentation mainly deals with granuloma formation and various factors involved in it. It describes the examples of granulomatous disorders and gives a details on how to seperate them on histopathology.It also describes type 4 hypersensitivty reaction concisely
Hi..! This presentation series is about 'Cell Injury'.. So, here is the 1st part- 'OVERVIEW OF CELLULAR NECROSIS' which I tried to explain in simplest way.. i hope that it will be helpful.. Plz like n do share... Thank You..!!
Morphology of cell injury and Intracellular accumulationspptxvaishaliwasnik
MORPHOLOGY OF REVERSIBLE CELL INJURY
Common examples of morphologic forms of reversible cell injury are as under:
Hydropic change
2. Hyaline change
3. Mucoid change
4. Fatty change (discussed under intracellular accumulations)
1. HYDROPIC CHANGE
Hydropic change means accumulation of water within the cytoplasm of the cell.
Other synonyms used are cloudy swelling (for gross appearance of the affected organ) and vacuolar degeneration (due to cytoplasmic vacuolation).
Hydropic swelling is an entirely reversible change upon removal of the injurious agent.
ETIOLOGY
This is the commonest and earliest form of cell
injury from almost all causes.
The common causes include acute and subacute cell injury from various etiologic agents such as bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline etc.
PATHOGENESIS
Cloudy swelling results from impaired
regulation of sodium and potassium at the level of cell membrane.
This results in intracellular accumulation of sodium and escape of potassium.
This, in turn, is accompanied with rapid flow of water into the cell to maintain iso-osmotic
2. HYALINE CHANGE
The word ‘hyaline’ or ‘hyalin’ means glassy (hyalos = glass).
Hyalinisation is a common descriptive histologic term for glassy, homo geneous, eosinophilic appearance of proteinaceous material in haematoxylin and eosin-stained sections and does not refer to any specific substance.
Though fibrin and amyloid have hyaline appearance, they have distinctive features and
staining reactions and can be distinguished from non-specific hyaline material.
Hyaline change is seen in heterogeneous pathologic conditions and may be intracellular or extracellular.
INTRACELLULAR HYALINE
Intracellular hyaline is mainly seen in epithelial cells.
1. Hyaline droplets in the proximal tubular epithelial cells due to excessive reabsorption of plasma proteins in proteinuria.
2. Hyaline degeneration of rectus abdominalis muscle called Zenker’s degeneration, occurring in typhoid fever. The muscle loses its fi brillar staining and becomes glassy and hyaline.
3. Mallory’s hyaline represents aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury.
4. Nuclear or cytoplasmic hyaline inclusions seen in some viral infections.
5. Russell’s bodies representing excessive immuno glo bulins in the rough endoplasmic reticulum of the plasma cell
EXTRACELLULAR HYALINE
Extracellular hyaline commonly termed hyalinisation is seen in connective tissues.
1. Hyaline degeneration in leiomyomas of the uterus.
2. Hyalinised old scar of fi brocollagenous tissues.
3. Hyaline arteriolosclerosis in renal vessels in hyper tension and diabetes mellitus.
4. Hyalinised glomeruli in chronic glomerulonephritis.
5. Corpora amylacea seen as rounded masses of concentric hyaline laminae in the enlarged prostate in the elderly, in the brain and in the spinal cord in old age, and in old infarcts of the
lung.
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
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.
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.
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.
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
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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.
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?
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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.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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.
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.
2. DEGENERATION
Definition : It is defined as a retrogressive change in the
cell following a cell injury , more so in the cytoplasm than
the nucleus, caused by a factor which is not stong enough
to cause cell death.
It is a reversible cell injury.
4. CELLULAR SWELLING
It is the most common and earliest form of cell injury .
Results from impaired regulation of cellular volume
GROSS: The affected organ is enlarged , pale , the cut surface
bulges out .
MICROSCOPY :The cells are swollen with cytoplasmic granularity
and they compress the surrounding microvasculature.
HYDROPIC CHANGE : Small clear vacuoles are seen in the cells
Organs affected:
Kidney (Large white kidney ) , islets of Langerhans in DM
5.
6. FATTY CHANGE
Occurs due to intracellular accumulation of neutral
fats.
CAUSES:
Excess alcohol consumption,obesity malnutrition
,starvation ,diabetes mellitus, chronic ilnesses , late
pregnancy, hypoxia , hepatotoxins [ carbontetra
chloride , chloroform , ether,aflatoxins ] certain
drugslike estrogen steroids tetracycline etc.
Liver is the most common organ affected . Other
organs affected are heart, kidney and skeletal muscle.
7. FATTY LIVER
Gross :The organ is enlarged yellow tense glistening capsule and rounded
margins. C/S – bulges and pale yellow and greasy to touch.
8. MICROSCOPY
Fat in the cytoplasm of the hepatocytes is seen as
clear area which may vary from minute droplets in the
cytoplasm of a few hepatocytes [microvesicular] to
distension of the entire cytoplasm of most cells by
coaslesced droplets [macrovesicular] pushing the
nucleus to the periphery of the cell.
Occ. the adjacent cell containing fat, rupture
producing fatty cysts
Special stains such Sudan III & IV,Sudan black Oil
red O can be employed to demonstrate fat in the
tissue
9.
10. HYALINE CHANGE
Hyaline is a glassy homogenous material that stains pink in
H&E sections.
Two types :
1. Intra cellular (epithelial )
2. Extra cellular (connective tissue)
11. Intra cellular (epithelial ) hyaline :
1. Zenkers degeneration in typhoid.
2. Mallory’s hyaline in ALD
3. Russel bodies in plasma cells
Extra cellular (connective tissue) hyaline
1. Hyaline degeneration of splenic capsule , leiomyomas of uterus.
2. Hyaline arterisclerosis in HT and DM.
3. Copora amylacea in prostate.
13. DEF OF NECROSIS
Focal death along with degradation of
tissue by hydrolytic enzymes liberated
by cells. accompanied by
inflammatory reaction.
14. NECROSIS
DEF.-It refers to spectrum of morphological
changes that follows cell death in living tissue
largely resulting from progressive degradative
action of enzymes on lethally injured cell.
Irreversible cell injury.
Nucleus – pyknosis, karyolysis, karyorrhexis.
Cytoplasm – homogenous ,intensely eosinphilic.
16. COAGULATIVE
NECROSIS
Mc , caused by sudden cessatiion of blood flow.
Organs commonly affected are kidney , heart , spleen.
17. Gross :they are pale or anemic & wedge shaped with the
base resting under the capsule & apex pointing towards the
medulla.
18. Microscopy: the hallmark
of coagulative necrosis is
that architectural outlines
of cells may be preserved
although the cellular
details are lost.
19. LIQUEFACTIVE
NECROSIS
Occurs commonly due to ischemic injury and bacterial
and fungal infections.
Due to degradation of tissue by the action of powerful
hydrolytic enzymes.
Eg : infarct brain , abcess cavity
20. well defined,soft with
liquified centre
containing necrotic
debris later a cyst wall
is formed
-
The cystic space contains necrotic
cell debris & macrophages
containing phagocytosed material.
The cyst wall is formed by
proliferating capillaries
,inflammatory cells and
proliferating glials cells.
21. CASEOUS NECROSIS
It is found in the centre of tuberculous foci
It combines features of both coagulative ana liquefactive
necrosis.
23. Microscopy :The necrosed foci are
structureless ,granular eosinophilic
The surrounding tissue shows chacteristic
granulomatous
reaction
24. CAUSES hypoxia,chemical and physical agents.
Microbial agents and immunologic injury.
Changes---cell digestion by lytic enzymes.& denaturation of proteins.
manifested morphologically by changes in nucleus &cytoplasm.
CYTOPLASM ---EOSINOPHILIC/WITH
VACUOLATION OR DYSTROPHIC
CALCIFICATION.
NUCLEUS—
PYKNOSIS/KARYOLYSIS/KARYORRHEXIS.
25. Types of necrosis
5 types.
1)Coagulative necrosis---common type. caused by ischaemia. less
commonly by bacterial or chemical agents.
Organs—HEART,KIDNEY & SPLEEN.
GROSS: Focii of coagulative necrosis ;pale firm &slightly swollen. With
progression, becomes yellowish softer & shrunken .
26. Microscopy — cells can be recognized as
merely having ghost architecture. the
nuclear and cytoplasmic characters are
lost. Cells swollen &more eosinophilic
along with nuclear changes described. It is
infiltrated by inflammatory cells.
Dead cells are phagocytosed./granular
debris/fragments of cells.
32. 2)Liquifactive necrosis--- combination of ischemic injury and
bacterial or fungal infection. action of strong powerful hydrolytic
enzymes. eg; infarct brain, abscess.
Gross— soft with liquefied centre containing necrotic debris. Later
cyst wall is formed.
Microscopy— necrotic cell debris/macrophages with phagocytosed
material. Cyst wall—proliferating capillaries, inflammatory cells, and
gliosis in case of brain. fibroblasts.
39. 4)fat necrosis —acute pancreatic
necrosis,traumatic fat necrosis.
Gross-yellowish white &firm deposits.micro
—cloudy appearance with inflammatory
cells.
5)Fibrinoid necrosis —fibrin like
material.seen in examples of immunologic
injury.
Micro—brighitly eosinophilic hyaline
material in vessel walls etc.
42. PATHOLOGIC CALCIFICATION
When calcium getrs deposited at sites other than bone
and enamel it is called as pathologic or heterotopic
calcification.
Two types :
1. Dystrophic
2. Metastatic
43. DYSTROPHIC
Deposits of Ca salts in dead and
degenerated tissue.
Ca metab . is normal
Sr Ca levels normal
Causes : necrosis,infarcts,
thrombi,atheromas , Monckebergs
sclerosis etc
METASTATIC
Deposits of Ca salts in normal
tissue
Deranged
Hypercalcemia
Hyperparthyroidism,bony
destructive lesions ,prolonged
immobilisation etc
46. “ A FORM OF CELL DEATH DESIGNED TO ELIMINATEA FORM OF CELL DEATH DESIGNED TO ELIMINATE
UNWANTED HOST CELLS THROUGH ACTIVATION OFUNWANTED HOST CELLS THROUGH ACTIVATION OF
COORDINATED , INTERNALLY PROGRAMMED SERIESCOORDINATED , INTERNALLY PROGRAMMED SERIES
OF EVENTS REGULATED BY A SET OF GENE PRODUCTSOF EVENTS REGULATED BY A SET OF GENE PRODUCTS ”
DEFINITION
51. CELL DELETION IN INTESTINAL CRYPT EPITHELIA
CELL DEATH IN TUMORS
DEATH OF NEUTROPHILS IN ACUTE INFLAMMATION
DEATH OF IMMUNE CELLS
IN DUCT OBSTRUCTION
VIRAL HEPATITIS ( Councilman bodies )
CELL DEATH PRODUCED BY INJURIOUS STIMULI
( In low doses )
63. APOPTOSIS NECROSIS
Cell shrinkage Cell swelling
No inflammatory response Inflammatory response
Death of single cells Death of many contiguous cells
Cytoplasmic blebbing Plasma membrane disruption
Chromatin condensation Nuclear swelling & lysis
Intact lysosomes & other Lysosomal breakdown
organelles
Fragmentation of nucleus & Cell lysis & disentegration
cytoplasm
Phagocytosis by adj ‘ cells Phagocytosis by infl ‘ cells
Physiological & path ‘ stimuli Hypoxia , toxins mainly
Apoptotic bodies Damaged organelles
Programmed cell death Cell death by ATP depletion
64.
65.
66.
67. Necrosis Apoptosis
Morphological changes
Loss of membrane integrity
Begins with swelling of cytoplasm and
mitochondria
Ends with total cell lysis
No vesicle formation, complete lysis
Disintegration (swelling) of organelles
Membrane blebbing, but no loss of integrity
Aggregation of chromatin at the nuclear
membrane
Begins with shrinking of cytoplasm and
condensation of nucleus
Ends with fragmentation of cell into smaller
bodies
Formation of membrane bound vesicles
(apoptotic bodies)
Mitochondria become leaky due to pore
formation involving
proteins of the bcl-2 family.
68. Necrosis Apoptosis
Physiological significance
Affects groups of contiguous cells
Evoked by non-physiological
disturbances (complement
attack, lytic viruses, hypothermia,
hypoxia, ischemica,
metabolic poisons)
Phagocytosis by macrophages
Significant inflammatory response
Affects individual cells
Induced by physiological stimuli (lack of
growth
factors, changes in hormonal
environment)
Phagocytosis by adjacent cells or
macrophages
No inflammatory response
69. GANGRENE necrosis of tissue with superadded putrifaction.usually coagulative.
3types.
DRY GANGREN—seen in distal part of limb due to
ischemia. eg toes & FEET IN ATHEROSCLEROSIS
THROMBOANGITISOBLITERANCE.RAYNAUDS.
GROSS-DRY,SHRUNKEN,DARK BLACK.MICRO—
SMUDGING OF TISSUE/INFL.GRANULATION
TISSUE.
71. Wet gangrene —moist tissues. Diabetic foot.high
growth of bacteria.bed sores.venous blockage
commonly than arterial.due to
thrombosis,embolism.
Gross —soft swollen ,putrid rotten dark. eg-
bowel gangrene.
Micro —coagulative necrosis with blood,.
uleration, inflammatory infiltrate. No clear line of
demarcation.
72. P – 779/83. Extensive Gangrene of small intestine.
73.
74.
75.
76. Gas gangrene
special form of wet gangrene—gas forming clostridia
infectswounds. ms., colonic operation.
GROSS—Swollen, oedematous, crepitant/ dark black,
foul smelling.
Microscopy—ms. fibres show coagulative necrosis with
liquefaction. gm +bacilli can be identified.