Inflammation is the body's response to infection, injury, or irritation. It is characterized by redness, swelling, heat, and pain at the site of injury or infection. When tissue is damaged, chemicals are released that cause blood vessels to become leaky and allow immune cells like neutrophils and macrophages to migrate to the injured site. These cells destroy and remove pathogens, limit their spread, and initiate tissue repair. Acute inflammation resolves quickly, while chronic inflammation persists long-term and can damage tissue over years.
inflammation is the body's immune system's response to an irritant. The irritant might be a germ, but it could also be a foreign object, such as a splinter in your finger.
Inflammation is a fundamental process for human survival, this lecture covers the basics of the process, its components and affects. Developing an understanding of this process will enable the student to comprehend this omnipresent process and how it is directly linked to our survival.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
inflammation is the body's immune system's response to an irritant. The irritant might be a germ, but it could also be a foreign object, such as a splinter in your finger.
Inflammation is a fundamental process for human survival, this lecture covers the basics of the process, its components and affects. Developing an understanding of this process will enable the student to comprehend this omnipresent process and how it is directly linked to our survival.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Introduction, History , Types of inflammation, Cellular events, Vascular events, Morphology of inflammation, Systemic effects of inflammation, Fate of inflammation
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Introduction, History , Types of inflammation, Cellular events, Vascular events, Morphology of inflammation, Systemic effects of inflammation, Fate of inflammation
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Inflammation by Dr. Amit T. Suryawanshi, Oral Surgeon, Pune All Good Things
Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.
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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.
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.
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
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
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
- 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
1. Definition
“An inflammation
is a more or less
coordinated series
of responses by the
body to injuries and
infections”. Or
While various exogenous stimuli can cause
direct cell injury & the same stimuli also
incite a complex reaction in vascularized
connective tissues call inflammation
The characteristics of the
inflammatory response are
swelling, redness, heat,
& pain-acne
When tissue is
injured or invaded
by microbes, a
series of more or
less predictable
events ensues.
INFLAMMATION
Acute: Short duration
immediate & early
responses to injury
Chronic: Long duration
impacts even in
years
Inflammation
2. time -- hyperacute (peracute), acute,
subacute, and chronic inflammation;
the main inflammatory
manifestation - alteration,
exudation, proliferation;
the degree of tissue damage -
superficial, profound (bordered, not
bordered);
characteristic picture -
nonspecific, specific;
immunopathological
mechanisms
•allergic (reaginic) inflammation,
•inflammation mediated by cytotoxic antibodies,
•inflammation mediaded by immune complexes,
•delayed-type hypersensitivity reactions.
According to different criteria, inflammatory responses can
be divided into several categories. The criteria include:
3. An increased blood supply to the tissue ''in danger''.
It is performed by vasodilation.
The inflamed tissue looks like containing greater number of vessels.
Increased capillary permeability
caused by retraction of the
endothelial cells.
This permit comparatively larger
molecules to escape from the
capillaries, and thus allows the
soluble mediators of immunity to
reach the site of inflammation.
Leukocytes migrate out of the
capillaries into the surrounding
tissues.
In the earliest stages of
inflammation, neutrophils are
particularly prevalent, but later
monocytes and lymphocytes also
migrate towards the site of
infection.
Three major events occur during this response :
4. Main humoral and cellular components involved in the amplification
and propagation of both acute and chronic inflammation
5. There are two categories of factors capable to induce the
damage of cells and tissues - endogenous and exogenous.
Endogenous damaging factors include
immunopathological reactions, and some neurological and
genetical disorders. Exogenous factors can be divided into:
mechanical
(traumatic
injury),
physical
(extremely low or
high
temperature,
ionising
irradiation,
microwaves),
chemical (caustic
agents, poisons,
venoms,
genotoxic and
proteotoxic
compounds),
nutritive
(deficiency of
oxygen, vitamins
and basic
nutrients),
biological
(viruses,
microorganisms,
protozoan and
metazoan
parasites).
Factors involved in cell damage
6. The acute inflammatory response is an effective way to isolate an infection
and to attract the macrophages, neutrophils, and lymphocytes that can attack
and overcome it,
This can occur because of an
autoimmune
disease (such as
rheumatoid
arthritis),
because of
persistence of
an infection
(such as
tuberculosis),
because of
repeated tissue
injuries
("tennis
elbow"),
or because of
cancer.
Impact of acute Inflammation on Body of Host
7. Under some conditions it can persist for long
periods of time, becoming a chronic
inflammatory response.
Often the chronic inflammation causes a mass
of activated macrophages, lymphoctes, and
antigen that form a tumor-like lump called a
granuloma.
Apparently one of the central activators of a
chronic immune response is gamma-
interferon, which is also essential for normal
immune responses.
chronic inflammations are treated variously
with drugs like aspirin and ibuprofen (non-
steroidal anti-inflammatory drugs), steroids,
or drugs that block extravasation.
Impact of chronic Inflammation on Body of Host
8.
9. Acute Inflammation: Has 3 major components:
• Heat (colour)
• Redness (Nubor)
• Swelling (Tumor)
• Pain (Dolor)
• Loss of function
(Functio-laesa)
Alteration in
vascular caliber
that lead to local
increase in
blood supply
=Vasodilatatio
n
Structural
changes in
micro
vasculature that
permit plasma
protein to leave
the circulation
Emigration of
leukocytes from
microcirculation
& accumulation
in focus of
injury
These three
process
accounts for fine
classical local
sign of acute
inflammation :
10. After Adhering endothelial cells leukocytes squeezed between them & migrate through vascular wall into
interstitial tissues, a process called emigration.
As the stasis developed, leukocytes (principally neutrophils) begin to settle out of the flowing blood &
accumulate along the vascular endothelial surface, a process called migration.
This cause RBC to become more concentrated, thereby increase blood viscosity & slowing the circulation.
These changes are manifested microscopically numerous dilated small vassals, pocket with erythrocytes called stasis.
Subsequently, microvasculature become more permeable resulting in extraduction of protein rich fluid into
extra-vascular tissues.
After an inconstant & transient vasoconstriction of arterioles, vasodilatation occur.
Arterioles are involve first resulting in opening of new micro-
vascular beads in the area of infection
Local increase in blood flow cause the redness (erythrema) and
warmth characteristically seen in acute inflammation
Vascular Changes: A-Change in vascular flow & Caliber
11. Vasodialation
+Increased Blood Flow
Vascular Hydrostatic
Pressure
Filtration of Fluid From
Capillary=Fluid:
Transdute =Ultrafiltrate
of Blood Plasma
Increased Vascular
Permeability
Permit the flow of
protein rich fluid &
even cells into
interstitum
This movement of fluid
cause the reduced in
intravascular OP while
interstitial OP increases
OUTFLOW of water &
Ions into extra-vascular
tissue which
accumulation is called
EDMA
Vascular Changes: B-Increased Vascular Permeability
INCREASED
ECLIPASED
Permit
12. Endothelial Cell Contraction
In-vitro System
Direct Endothelial Injury
Leukocytes Dependent Endothelial Injury
Increase Transcytosis
How Permeability Increases?
13. leads to widening of
intracellular gap elicited
by histamine,
bradekinine,
leukotrinase, etc., & it is a
reversible process.
Cellular contraction
occur rapidly after
binding of mediators
to a specific
receptors (short-
lived)
Only these
endothelial lining of
venules 20-60m
undergo contraction;
while endothelium
in capillary &
arteries are remain
unaffected.
1-Endothelial Cell Contraction
14. Functional mechanism is another mechanism
resulting vascular permeability
2-In-vitro System
Cytokines like TNF,
IL-1 etc
Structural
reorganization of
cytoskeleton
Endothelial Cell
Junction are
disrupted
Start after 2-4 hrs & persists upto 24 hrs
15. 3-Direct Endothelial Injury Seen after serious injury
Causing Vascular leakage by endothelial cells necrosis & detachment
Detachment is often associated with palate adhesion & Thrombosis
This reaction is known as Immediate Sustain response which affect
vacuoles, capillary and arterioles
This may cause Delayed Prolong Leakage that begain after 2-12 hrs &
last for several hrs or even a day
e.g. Mild to modrate thermal injury, X-ray/UV radiation & Certain bacterial
toxins
It is Attributable to apoptosis & action of Cytokines
16. 4-Leukocytes Dependent Endothelial Injury
May occur as a consequences of Leukocytes
accumulation during inflammatory responses
Such Leukocytes may activate the release of
TOXIC OXYGEN SPECIES & PROTEIOLYTIC
ENZYMES
which thus cause endothelial injury or
detachment, largely restricted to those tissues
where leukocytes can adhere to endothelium
17.
18. 1-the activation of a number of
proteolytic enzymes including
plamin, fibrin, kallikrein, and
complement
2-These cause localized increases
• in vascular permeability,
• smooth muscle contraction (blood vessels
are made of two kinds of cells-- smooth
muscles and endothelial cells), and
• production of chemotactic molecules like
some fragments of the complement proteins
(C3a, C5a).
3-These chemotactic molecules lure
(attract=ensnare) various cell types
out of the blood stream, by binding to
specific receptors on their cell surface
and inducing a migratory behavior
out of the blood stream into the
tissues.
4-The first cells to extravasate are
neutrophils followed subsequently
monocytes (macrophages that
haven't yet made a commitment)
and lymphocytes. Several
coordinated activities mediate this
process.
Reactions in Inflammation:When tissue is injured or invaded by
microbes, a series of more or less predictable events ensues.
19. 5-First, bradykinin, fibrin, and complement
act on endothelial cells to increase their
permeability.
Second, release of "mediator" molecules by
activated macrophages induces increased
permeability of the blood vessel, and serves
as chemotactic factors for cells.
Several of the macrophage released
cytokines, including IL-1, IL-6 and TNF-
alpha, have widespread activities
throughout the body, not just at the site of
the injury.
6-Some of these activities recruit
•leukocytes-increased vascular permeability
•and adhesion molecules on endothelial cells;
•some induce "systemic" non-specific actions
•like fever and production of
•"acute phase proteins" that inhibit microbial growth:
•some help activate a specific immune responses;
•and some even help promote the healing response,
such as proliferation of fibroblasts
Reactions in Inflammation:When tissue is injured or invaded by
microbes, a series of more or less predictable events ensues-2
20. Third, the recruited leukocytes
enter the damaged tissue and
can begin to attack the
microorganisms causing the
infection, digest damaged cells
and tissues, and initiate an
immune response.
However, antigen-presenting
cells such as macrophages are
necessary to this activation;
macrophages can pick up
bacteria or other foreign
materials at the site of injury
and reenter the blood stream
where they can eventually
encounter and present to
lymphocytes.)
Reactions in Inflammation:When tissue is injured or invaded
by microbes, a series of more or less predictable events ensues.
21. Extravasation of leukocytes and lymphocytes, for example, seems to depend on a
complex series of interactions between the membranes of the blood cells and the endothelial cells of
the blood vessels. A variety of cell surface receptors, cell adhesion molecules, and secreted
chemokines induce tight, specific interactions among the cell types, followed by migration between
endothelial cells and out of the blood vessel.
In addition to direct cell-cell interactions, there are also long range interactions that direct
cells out of the blood stream and into the tissues at specific locations. These are mediated by
chemokines (a special subclass of cytokines) that are released by a variety of lymphoid and myeloid
cell types and that act through chemokine receptors to act as "chemo-attractants", luring cells along
a concentration of chemokines to a particular location.
All chemokine receptors known are G-protein coupled receptors that activate a variety of
second messenger systems to mediate, among other things, directional cell movement.
While the acute inflammatory response is an effective way to isolate an infection and to attract the
macrophages, neutrophils, and lymphocytes that can attack and overcome it, under some
conditions an inflammatory response can persist for long periods of time, becoming a chronic
inflammatory response. This can occur because of an autoimmune disease (such as rheumatoid
arthritis), because of persistence of an infection (such as tuberculosis), because of repeated tissue
injuries ("tennis elbow"), or because of cancer. Often the chronic inflammation causes a mass of
activated macrophages, lymphoctes, and antigen that form a tumor-like lump called a granuloma.
Apparently one of the central activators of a chronic immune response is gamma-interferon, which
is also essential for normal immune responses. Chronic inflammations are treated variously with
drugs like aspirin and ibuprofen (non-steroidal anti-inflammatory drugs), steroids, or drugs that
block extravasation. Presumably inhibitors of IFN- would also be effective, but I don't know of
any that are available. The hottest news in anti-inflammatory drugs are the so called Cox
(cyclooxygenase) inhibitors that are much more specific than other NSAIDs in blocking
inflammation.
23. Inflammation
Triggered by tissue damage due to infection, heat,
wound, etc.
Four Major Symptoms of Inflammation:
1. Redness
2. Pain
3. Heat
4. Swelling
May also observe:
5. Loss of function
24. Functions of Inflammation
1. Destroy and remove pathogens
2. If destruction is not possible, to limit
effects by confining the pathogen and its
products.
3. Repair and replace tissue damaged by
pathogen and its products.
25. Stages of Inflammation
1. Vasodilation: Increase in diameter of blood vessels.
Triggered by chemicals released by damaged cells:
histamine, kinins, prostaglandins, and leukotrienes.
2. Phagocyte Migration and Margination: Margination
is the process in which phagocytes stick to lining of
blood vessels.
Diapedesis (Emigration): Phagocytes squeeze
between endothelial cells of blood vessels and enter
surrounding tissue.
26.
27. Stages of Inflammation
(Continued)
Phagocytes are attracted to site of infection through
chemotaxis.
Phagocytes destroy microbes, as well as dead and
damaged host cells.
3. Tissue Repair: Dead and damaged cells are
replaced.
28. Antimicrobial Substances:
I. Complement System: Large group of serum
proteins that participate in the lysis of foreign cells,
inflammation, and phagocytosis.
Two mechanisms of complement activation:
1. Classical Pathway: Initiated by an immune reaction
of antibodies.
2. Alternative Pathway: Initiated by direct interaction
of complement proteins with microbial
polysaccharides.
Both pathways cleave a complement protein called C3,
which triggers a series of events.
29.
30.
31. Consequences of Complement
Activation:
1. Cytolysis: Due to the formation of a membrane attack
complex (MAC) which produces lesions in microbial
membranes.
2. Inflammation: Complement components (C3a)
trigger the release of histamine, which increases
vascular permeability.
3. Opsonization: Complement components (C3b) bind
to microbial surface and promote phagocytosis.
4. Inactivation of Complement: Regulatory proteins
limit damage to host cells that may be caused by
complement.
32.
33.
34. II. Interferons: Antiviral proteins that interfere with
viral multiplication.
Small proteins (15,000 to 30,000 kDa)
Heat stable and resistant to low pH
Important in acute and short term infections.
Have no effect on infected cells.
Host specific, but not virus specific.
Interferon alpha and beta: Produced by virus
infected cells and diffuse to neighboring cells.
Cause uninfected cells to produce antiviral
proteins (AVPs).
Interferon gamma: Produced by lymphocytes.
Causes neutrophils to kill bacteria.