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Inflammation Mind Map Depicting Multiple Causes
Inflammation is a physiological condition involving the response of body tissues to harmful stimuli. It’s generally divided into two types: acute and chronic. Acute inflammation is a short-term response characterized by swelling, redness, increased temperature, and pain, while chronic inflammation is a more sustained reaction that can involve scarring and tissue damage. Diagnosis of inflammation typically involves observation of symptoms in various tissues along with imaging techniques such as X-ray or MRI scans. Common symptoms include pain, swelling, redness, heat sensation, fatigue, loss of mobility, and weight changes. With the help of EdrawMind, you can also create a detailed inflammation mind map for your academics-related project.
Edited at 2023-02-01 23:59:41
Inflammation Mind Map Depicting Multiple Causes
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INFLAMMATION
Over view of INFLAMMATION
Literally: inflammation means "burnout".
Scientifically: it is a physiological response to cell injury, associated with cellular vascular humoral events
Classification of inflammation
Acute Inflammation
Acute inflammation is the type of inflammation that presents within a short period of time (days) and is associated with neutrophils infiltration, or lymphocyte if caused by viral infection, all cardinal signs of inflammation are present
If acute inflammation does not heal it becomes chronic
Days or weeks
Mainly neutrophils
Cardinal signs All are present
Healing process Complete resolution
Chronic Inflammation
Inflammatory reaction over a prolonged period of time i.e., months to years, in which active inflammation plus a healing process occur at a time
It follows acute inflammation when the causative agent is not removed
Months or years
Mainly lymphocytes, and plasma cells, macrophages and monocyte.
Cardinal signs Some of them
Healing process By fibrosis
What are the Purposes of the Inflammatory Process
To localize the injury in a specific area,
To get rid of the cause of the injury
To repair the damaged area.
General Features of Inflammation
Inflammation is a complicated process
you will see one mediator with different functions on different tissues
Duration of inflammation can be long or short, hence there is acute, chronic, or sub-chronic
Effects of Inflammation
local effects
the killing of invading microorganisms
swelling
loss of function
Systemic effects
Leukocytosis
high white blood cells
increased neutrophils indicate acute inflammation with special bacterial infection
increased lymphocytes occur in viral infections or chronic inflammation.
Fever
commonest systemic effect of inflammation
produced by cytokines and interleukins , It improves the efficiency of leukocyte killing and impairs the replication of the invading organisms
Increased Acute Phase Reactant & ESR
due to an increased level of IL1, IL6, TNF…etc. and other proteins produced from the liver in association with inflammation
Beneficial Effect of Inflammation
Dilution effect
results in removal and washout of the bacterial toxins through the lymphatic system
promoting the immunity
by enhancing immune response after bringing microorganism to the adjacent lymph node
Provides WBCs. Antibodies. and proteins
provide cells and different proteins like fibrinogen, complement system, and nutrition to the sick cells
Harmful Effects of Inflammation
Swelling
resulting in obstruction of organs with lumen
Loss of Organ Function
inflamed organs lose their function,
Clinical Charecterestic and sign of inflammation
Cardinal Signs of inflammation
Redness (Rubor)
Swelling (Tumor)
Pain (Dolor)
Loss of Function (Functio laesa)
Clinical Presentations of Acute Inflammation
Serous formation
Type of inflammation with protein-poor fluid, for example, skin blister resulting from burning
Suppurative (Purulent formation)
This is a pyogenic inflammation and pus formation in the inflamed area
Ulcerative formation
Ulcer is a loss of continuity of epithelium in the skin or mucous membrane, it can be due to inflammatory damage
example, ulcerative colitis, peptic ulcer.
Boils and Furuncles formation
Focal skin collection of abscess commonly in hair follicles. Boils are smaller
Pseudo-membranous formation
Following clostridia, or diphtheria infection, characterized by the formation of pseudo-membrane composed of (necrotic tissue + coagulated fibrin + neutrophils and macrophage + bacteria)
Acute Inflammation
Control of Acute Inflammation
vascular, cellular, and humeral events
Vascular Events
changes in vessel caliber, blood flow
increased vascular permeability
: leakage of fluids and protein from the vessels due to histamine and other chemical mediators
prolonged leakage is due to damage to the wall of blood vessels
The protein-rich fluid that leaves the circulation is called an exudate
All plasma protein can be found in the exudates, especially fibrinogen
fibrinogen is converted to fibrin during the healing process
Changes in the vascular flow
start with rapid vasoconstriction for a few seconds
then vasodilatation results in hyperemia and redness
15 minutes later, there is stasis of blood flow
Decreased movement of the blood flow; hence allows fluid, proteins, and cells to get out of the intravascular compartment to the inflamed area
Factors responsible for stasis Include
adhesion of WBCs to endothelium consequently slowing of the flow
vasodilatation of the blood vessels in the inflamed area
Recruitment
Cells move out of the vessels into the area of inflammation recruited by chemotactic agents. Inflammatory cells become activated to phagocytize offending materials, this process occurs in steps as follows
Margination and Rolling of WBCs
Moving from axial flow to the margin of the vessels is called margination
Activation and adhesion
Marginated leukocytes begin to roll on the endothelial surface by forming transient adhesion molecules via the selectin family of proteins
E-selectin on endothelial cells
P-selectin on endothelial cells and platelets
L-selectin on leukocytes
Migration of Leucocytes
Passage of the cells across the wall of blood vessels and moved to reach the site of inflammation due to the effect of chemical mediators gradient (chemotaxis)
Chemotaxis
A process resulted from certain products of WBCs, platelets, and microorganisms, which attracts WBCs towards the inflammation area according to the high concentration of that substance
Phagocytosis
Define as engulfment and internalization of foreign bodies in the phagosome and digestion
steps in phagocytosis
the adhesion of the particle to be phagocytosed to the cell surface
Then the phagocyte ingests the attached particle by sending out pseudopodia around it
Then met and fused so that the particle lies in a phagocytic vacuole (called a phagosome)
then bounded to small bodies containing enzymatic compounds called lysosomes, to form phagolysosomes. In which intracellular killing of microorganisms occurs
Phagocytic cells
neutrophils
polymorph nuclear cells
eosinophils
monocytes
Humeral Events (Chemical Mediators)
Chemical mediators are the cornerstone in controlling the inflammatory Process
Mediators are substances produced by, from damaged tissues or bacteria, also from endothelial cells, WBCs, and platelet (locally)
They can be produced systemically from the liver
They control
vascular and cellular events
produce the cardinal signs in acute and chronic inflammation
they act locally
on the neighboring cells (paracrine) or on themselves (autocrine).
Example of action
permeability
margination
chemotaxis
vasodilation and vasoconstriction
fever and pain
phagocytosis
Out come of Acute Inflammation
Resolution
Complete restoration of the structures and functions of inflamed tissue
Steps of the resolution
Removal of inflammatory exudates, fibrin, and cells completely
Increase of lymphatic drainage to get rid of all debris (remaining parts of cells)
Cessation of vascular events of inflammation
Regeneration of lost specialized cells (return of normal structure)
Fibrosis
it is a feature of chronic inflammation that occurs in three situations
if heavy deposition of fibrin or failure to be removed completely
if there is a large amount of tissue necrosis or the tissue cannot regenerate like cardiac and CNS tissues
Formation of Abscess
Occurs with pyogenic bacteria or fungal infection.
Developing of Chronic Inflammation
acute Process continues as chronic inflammation.
Chronic Inflammation
characterized by the following changes
Diminished polymorphs cells and presences of macrophages, (epithelioid, and giant cells), plasma cells, and lymphocytes
Vascular budding and formation of new capillaries
(angiogenesis)
Proliferation of fibroblast and fibrosis
in an attempt of healing
Causes of chronic inflammtion
Persistant infection
By microorganism that is difficult to eradicate
hypersensitivity diseases
Excessive and inappropriate activation of the immune system
autoimmune diseases
unregulated immune responses to against microbs
inflammatory bowel disease
Prolonged exposure to toxic agents
Endogenous
Exogenous
Organization in chronic inflammation
inflammatory cells in chronic inflammation tend to add new tissue such as collagen and new blood vessels, these changes also represent the repair process this is called organization
We can say that chronic inflammation is characterized by tissue destruction, and attempts of repair, happening at a time
Patterns of chronic inflammation
Granuloma with caseation: like TB, fungal infection,
is a chronic inflammation, in which epithelioid cells accumulate inclusters with central necrosis, and giant cells are surrounded by lymphocytes, plasma cell, and fibrous tissue in a peripheral zone.Inflammatory cell-forming granuloma includes macrophages,plasma cells, and lymphocytes
Macrophages
Macrophages in granuloma are derived from circulating monocyte, when reaching the inflammatory site, they become epithelioid cells with powerful secretary activity, or become giant cells
Several macrophages fused together and became powerful phagocytic cells called giant cells
Types of Giant cells
Langhan’s Giant Cell
Resulted from the fusion of several macrophages, and has multiple nuclei, arranged in a horseshoe pattern, in tuberculosis.
Foreign Body Giant Cells
results from the fusion of several macrophages, with multiple nuclei, arranged in a scattered pattern found in the granuloma of the foreign body together with lymphocytes, plasma cells, and fibroblast
Lymphocytes
TH1 cells that recognize the antigen on the antigenpresenting cells and are responsible for the secretion of interferon-gamma, fibroblast growth factor, transforming growth factor-beta… etc
Plasma cells
responsible for antibody formation
Caseating Granulomatous Inflammation
causes include Tuberculosis, it is a granuloma containing Langhan's giant cell + central caseous necrosis. Other causes of Granulomatous diseases include leprosy, syphilis, sarcoidosis, and foreign bodies
Noncaseating granuloma: Sarcoidosis, Crohn's disease, foreign body
Ill-defined granuloma: syphilis
Organized chronic inflammation: chronic bacterial infection
Ulcerative chronic inflammation: chronic gastric ulcer
Examples of chronic inflammation
TUBERCULOSIS
What is it
Chronic granulomatous disease that affects the lung, intestine,kidney, bones, and other organs, caused by the following species of mycobacteria
Mycobacterium Tuberculosis
Aerobic, alcohol acid-fast bacilli (AAFB), stains by Zeil Nelson method (ZN), cultured in Lewenstein Jenson media (L.J media).
Mycobacteria Bovis
Encountered from cow's milk causes abdominal tuberculosis
Atypical Mycobacteria
Causes opportunistic disease in immunecompromised individuals and includes, M. avium, M. Intracellular, M. scrafulatum, M. kansassi.
Types
Primary Tuberculosis
Primary tuberculosis occurs in persons who are exposed to the bacillus for the first time, i.e. non-immunized. In the lung primary complex is formed, which is composed of primary lesion and enlarged hilar lymph nodes
Primary Lesion (Gohn’s Focus): It is a subplueritic lesion of 1-2cm diameter in the midzone of the lung. Microscopically it shows central caseation and granuloma
Hilar Lymphadenopathy: The bacillus reaches the draining lymph node where extensive reaction takes place causing enlargement of lymph node and caseation, the lesion here is larger than that in the primary lesion.
Secondary (Post-Primary) TB
it occurs because of a re-infection, a reactivation of dormant disease, or direct progression of primary TB to disseminated disease.
Granulomas of secondary TB are found in the lung apices, kidneys, meninges, marrow and other organs.
Granulomas are the major cause of tissue damage in secondary TB. Cavities are a common feature of secondary TB, and necrotic lesions may rupture into vessels or airways spreading mycobacteria throughout the body or releasing them in airspaces
Comarison between primary and secondary TB
Primary T.B
Occurs in
(childhood)
1st time infection
Non immunized persons
Methods of infection
exogenous by
Inhalation
Ingestion
Direct contact
Site of 1ry complex
Lung, Intestine, Tonsils, Skin, Nose
Reaction of the body against bacilli
Primary complex
Secondary T.B
Occurs in
Non immunized persons
2nd time infection
In a patient had 1ry infection or B.C.G vaccine
Methods of infection
Endogenous due to reactivation.
- Exogenous due to reinfection
Site
Any site, but mainly lung & intestine
Reaction of the body against bacilli
Tubercles in solid organs
SARCOIDOSIS
Sarcoidosis is not infectious. However, clinically and pathologically, simulates tuberculosis
It is a chronic non-caseating granulomatous inflammatory disease that affects multiple organs in the body, commonly, the lungs and lymph glands
• Clinically: there are abnormal masses or nodules composed of granulomas in certain organs of the body. The following picture showing the affected organs
SYPHILIS
A chronic infective granuloma caused by spirochete microorganisms (treponema pallidum)
Transmitted mainly by
Direct sexual intercourse
Non-venereal type by touching the syphilitic lesion.
Blood transfusion
Transplacental transmission from infected mother to her fetus
Stage of syphilis
Primary
Duration
Two weeks from infection
Name of the lesion
Chancre formation
Affected organs
Skin and mucous membranes
Secondary
Duration
Two months from 1ry
Name of the lesion
Condyloma lata
Affected organs
All organs
Tertiary
Duration
2-10 years from 2ry
Name of the lesion
Gumma formation
Affected organs
cvs, cns…gummas in all organs
Chemical Mediators
Chemical mediators of inflammationFEATURES
Account for all the events of inflammation.
Perform their biological activities by binding to specific receptors on target cells or on the cells that produce them.
Short-lived.
Have the potential to cause cellular damage
Effects of Mediators
Mediators have several effects associated with vascular or cellular events
Vasoconstriction: Caused by histamine, thromboxane A2, leukotrienes, PAF.
Vasodilatation: prostaglandins, and nitric oxide.
Increased Vascular Permeability: Histamine, serotonin, leukotrienes, and bradykinin.
Chemotaxis: C5a,TNF, IL8.
Fever: IL1, IL6, TNF, prostaglandin.
Pain: Prostaglandin, bradykinin
Sources of mediators
Plasma-derived mediators
Complement activation
increases vascular permeability (C3a,C5a)
activates chemo-taxis (C5a)
opsonization (C3b,C3bi)
Factor XII (Hageman factor) activation
Its activation results in the recruitment of four systems: the kinin, the clotting, the fibrinolysis, and the compliment systems
Cell-derived chemical mediators
Produce from inflammatory cells like PAF, IL1……ETC
CLASSIC MEDIATORS
CYTOKINES /CHEMOKINES
CYTOKINES are PROTEINS produced by MANY cells, LYMPHOCYTES, and MACROPHAGES, and has numerous roles in acute and chronic inflammation
CHEMOKINES are small proteins that are attractants for PMNs and other inflammatory cells
PLATELET ACTIVATING FACTOR (PAF)
LYSOSOME CONSTITUENTS
FREE RADICALS
NEUROPEPTIDES
HISTAMINE
SEROTONIN
COMPLEMENT
KININS
CLOTTING FACTORS
EICOSANOIDS
NITRIC OXIDE
VIP Chemical Mediators
IL-1, TNFα: produced by macrophages are Both are considered the most important mediators of acute and chronic inflammation
produced by macrophages are Both are considered the most important mediators of acute and chronic inflammation
IL-1, TNFα
Local effects
Vascular effect
Increases WBCs adhesion molecules in the blood vessels
Procoagulant effect
Cellular effect
Activation and release of cytokines
Fibroblast effects
Increases proliferation and cpllagen synthesis
In healing and repair
Systematic effect
increase fever
Increase acute phase protien
Increase WBCs
IL-10, Interferon α, Transforming growth factor β.
Inhibitory cytokines of acute inflammation
when released they stop the inflammatory process
Then followed by resolution and healing
HISTAMINE
From Mast Cells, basophils
Action
POWERFUL Vasodilator
Vasoactive “amine”
When IgE fixed on mast cell it produce alergy
SEROTONIN
(5HT, 5-Hydroxy-Tryptamine)
Production from, Platelets and EnteroChromaffin Cells
Action: vasodilatation,
COMPLEMENT SYSTEM
Multiple sites of action, but cell LYSIS is the main
KININ SYSTEM
BRADYKININ is KEY component
production from plasma protiens
ACTIONS
Increased permeability
Smooth muscle contraction like uterus, (NON vascular)
PAIN
CLOTTING FACTORS
Location
circulating plasma
Function
Coagulation
production of fibrin
Prostaglandins
(thromboxanes included)
FUNCTION
Pain
Fever
Clotting
Lipoxins
Function
INHIBIT chemotaxis
Vasodilatation
Counteract actions of leukotrienes
Leukotrienes
FUNCTIONS
Chemotaxis
Vasoconstriction
Increased Permeability
Platelet-Activating Factor(PAF)
Phospholipid
From MANY cells, like eicosanoids
ACTIVATE PLATELETS, powerfully
NEUROPEPTIDES
Produced in CNS (neurons)
SUBSTANCE P
NEUROKININ A
NITRIC OXIDE
Potent vasodilator
Produced by the enzyme nitric oxide synthetase on arginine.
FREE RADICALS
O2 (SUPEROXIDE)
H2O2 (PEROXIDE)
OH- (HYDROXYL RADICAL)
TISSUE DESTRUCTION
EICOSANOIDS
(ARACHIDONIC ACID DERIVATIVES)
Produced From the phospholipid Part of cell membranes by Arachidonate cascade
Prostaglandin (incl. Thromboxanes)
Leukotrienes
Lipoxins (newly discovered)
Arachidonate cascade
Oxygenated derivatives are formed via three major pathways including
cyclooxygenase (COX)
lipoxygenase (LOX)
The three pathways, are collectively known as the 'arachidonate cascade.' Each pathway is named after the enzyme that catalyzes the committed step.
The prostanoids – prostaglandins and thromboxanes – are formed via the COX pathway COX1 AND 2. Nonsteroidal anti-inflammatory drugs like aspirin inhibit prostanoid formation
Leukotrienes are formed through a LOX pathway.
Certain anti-asthmatic drugs inhibit 5-lipoxygenase or leukotriene receptor signaling
Lipid mediators
Membrain Phospholipid
Lyso-PAF
PAF Platelet aggregation
Eosinophil chemotaxis
Neutrophil activation
Arachidonic acid
Lipoxygenase pathway
Leukotriene A4
Leukotrienes B4
Neutrophil chemotaxis
Leukotraienes C4 ,D4, E4
SRS-1 Bronchial smoth muscle contraction
SRS-1 = Slow reacting substances of anaphylaxis
Prostaglandin G2
Prostaglandins
Increase vascular permeability
Vascular dilation
Neutrophil chemotaxis
Other effects
Thromboxan
vasoconstriction
Platelet aggregation
Other effects
Comarison between Chronic and Acute Inflammtion
Acute Inflammation
Caustive agent
Pathogens
Injured tissue
major cells involved
Neutrophils
Mononuclear cells ( monocytes , macrophages )
Primary mediators
Vasoactrive amines
Eicosanoids
Onset
Immediate
duration
few days
Outcomes
Resolution
Abscess formation
Chronic inflammtion
Cronic
Caustive agent
Persistent acute inflammation due to non-degradable pathogens
persistent foreign bodys
Autoimmune reactions
major cells involved
Mononuclear cells ( monocytes , macrophages lymphocytes , plasma cells) ,
fibroblasts
Primary mediators
Interferon gamma (IFN-γ) and other cytokines
Growth factors
reactive oxygen species
Hydrolatic enzymes
Onset
Delayed
duration
up to many months or years
Outcomes
Tissue distruction
Fibrosis