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INFLAMATORY REACTIONS

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is part of the complex biological response of vasculartissues to harmful stimuli, such as pathogens,damaged cells, or irritants. The classical signs of

acute inflammation are pain (dolor), heat (calor),redness (rubor), swelling (tumor), and loss offunction (functio laesa). Inflammation is a protectiveattempt by the organism to remove the injuriousstimuli and to initiate the healing process.

Inflammation is not a synonym for infection, even incases where inflammation is caused by infection.Although infection is caused by a microorganism,inflammation is one of the responses of the organism

to the pathogen. However, inflammation is astereotyped response, and therefore it is consideredas a mechanism of innate immunity, as compared toadaptive immunity, which is specific for eachpathogen.Without inflammation, wounds andinfections would never heal.

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Similarly, progressive destruction of the tissuewould compromise the survival of theorganism. However, chronic inflammation canalso lead to a host of diseases, such as hayfever, periodontitis, atherosclerosis,rheumatoid arthritis, and even cancer (e.g.,

gallbladder carcinoma). It is for that reasonthat inflammation is normally closely regulatedby the body.Inflammation can be classified aseither acute or chronic. Acute inflammation is

the initial response of the body to harmfulstimuli and is achieved by the increasedmovement of plasma and leukocytes(especially granulocytes )

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from the blood into the injured tissues.A cascade of biochemical events

propagates and matures theinflammatory response, involving thelocal vascular system, the immunesystem, and various cells within theinjured tissue. Prolonged inflammation,known as chronic inflammation, leads toa progressive shift in the type of cells

present at the site of inflammation andis characterized by simultaneousdestruction and healing of the tissue

from the inflammatory process

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Causes Burns Chemical irritants Frostbite Toxins Infection by pathogens

Physical injury, blunt or penetrating Immune reactions due to

hypersensitivity

Ionizing radiation Foreign bodies, including splinters, dirt

and debris Stress Trauma

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Types> Appendicitis

> Bursitis>Colitis>Cystitis

>Dermatitis>Meningitis>Phlebitis

> Rhinitis>Tendonitis>Tonsillitis

>Vasculitis

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CARDINAL SIGNAcute inflammation is a short-term process,usually appearing within a few minutes or

hours and ceasing upon the removal of theinjurious stimulus. It is characterized by fivecardinal signs:The acronym that may beused for this is "PRISH" for Pain, Redness,

Immobility (loss of function), Swelling andHeat.The traditional names for signs ofinflammation come from Latin:

> Dolor (pain)>Calor (heat)>Rubor (redness)

>Tumor (swelling)>Functio laesa loss of function

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The first four (classical signs) were described by Celsus(ca 30 BC–38 AD), while loss of function was addedlater by Galen even though the attribution is disputedand the origination of the fifth sign has also been

ascribed to Thomas Sydenham and Virchow.Rednessand heat are due to increased blood flow at body coretemperature to the inflamed site; swelling is caused byaccumulation of fluid; pain is due to release of

chemicals that stimulate nerve endings. Loss offunction has multiple causes.These five signs appear when acute inflammationoccurs on the body's surface, whereas acuteinflammation of internal organs may not result in thefull set. Pain only happens where the appropriatesensory nerve endings exist in the inflamed area—e.g.,acute inflammation of the lung (pneumonia) does notcause pain unless the inflammation involves the

parietal pleura, which does have pain-sensitive nerve

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DIFFERENT

Inflammatorydisorders

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Atherosclerosis- Atherosclerosis, formerlyconsidered a bland lipid storage disease, actuallyinvolves an ongoing inflammatory response.

Recent advances in basic science haveestablished a fundamental role for inflammationin mediating all stages of this disease frominitiation through progression and, ultimately, the

thrombotic complications of atherosclerosis.These new findings provide important linksbetween risk factors and the mechanisms ofatherogenesis. Clinical studies have shown that

this emerging biology of inflammation inatherosclerosis applies directly to humanpatients.

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Allergies-An allergic reaction, formally knownas type 1 hypersensitivity, is the result of aninappropriate immune response triggering

inflammation. A common example is hayfever, which is caused by a hypersensitiveresponse by skin mast cells to allergens. Pre-sensitised mast cells respond by

degranulating, releasing vasoactive chemicalssuch as histamine. These chemicals propagatean excessive inflammatory responsecharacterised by blood vessel dilation,

production of pro-inflammatory molecules,cytokine release, and recruitment ofleukocytes.

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Myopathies-Inflammatorymyopathies are caused by theimmune system inappropriatelyattacking components of muscle,

leading to signs of muscleinflammation. They may occur inconjunction with other immune

disorders, such as systemic sclerosis,and include dermatomyositis,polymyositis, and inclusion body

myositis

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Leukocyte defects-Due to the central roleof leukocytes in the development and

propagation of inflammation, defects inleukocyte function often result in adecreased capacity for inflammatory defensewith subsequent vulnerability to infection.

Dysfunctional leukocytes may be unable tocorrectly bind to blood vessels due tosurface receptor mutations, digest bacteria(Chediak-Higashi syndrome), or produce

microbicides (chronic granulomatousdisease). Additionally, diseases affecting thebone marrow may result in abnormal or fewleukocytes.

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Pharmacological-Certain drugs orexogenic chemical compounds are

known to affect inflammation. Vitamin Adeficiency causes an increase ininflammatory responses, and anti-

inflammatory drugs work specifically byinhibiting normal inflammatorycomponents. Certain illicit drugs such

as cocaine and ecstasy may exert someof their detrimental effects by activatingtranscription factors intimately involvedwith inflammation (e.g. NF-κB).

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Cancer-Inflammation orchestrates themicroenvironment around tumours,contributing to proliferation, survival andmigration. Cancer cells use selectins,chemokines and their receptors for invasion,migration and metastasis. On the other hand,

many cells of the immune system contributeto cancer immunology, suppressingcancer.Molecular intersection betweenreceptors of steroid hormones, which have

important effects on cellular development, andtranscription factors that play key roles ininflammation, such as NF-κB, may mediatesome of the most critical effects of

inflammatory stimuli on cancer cell

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Connection to depression-Thereis evidence for a link betweeninflammation and depression.Inflammatory processes can be

triggered by negative cognitions ortheir consequences, such as stress,violence, or deprivation. Thus,

negative cognitions can causeinflammation that can, in turn, leadto depression.

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Chronic inflammation and muscle loss-Both chronic and extreme inflammation are

associated with disruptions of anabolicsignals initiating muscle growth. Chronicinflammation has been implicated as part ofthe cause of the muscle loss that occurs with

aging. Increased protein levels of myostatinhave been described in patients withdiseases characterized by chronic low-gradeinflammation.Increased levels of TNF-α can

suppress the AKT/mTOR pathway, a crucialpathway for regulating skeletal musclehypertrophy, thereby increasing muscle

catabolism.

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Comparison between acute and chronicinflammation:

ACUTE CHRONIC

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  ACUTE CHRONIC

Causative agent Bacterial Pathogens, injured

tissues

Persistent acute inflammation

due to non-degradable

pathogens,viral infection,

persistent foreign bodies, orautoimmune reactions

Major cells involved neutrophils (primarily), basophils

(inflammatory response), and

eosinophils (response to

helminth worms and parasites),

mononuclear cells (monocytes,

macrophages)

Mononuclear cells (monocytes,

macrophages, lymphocytes,

plasma cells), fibroblasts

Primary mediators Vasoactive amines, eicosanoids IFN-γ and other cytokines,

growth factors, reactive oxygenspecies, hydrolytic enzymes

Onset Immediate Delayed

Duration  Few days Up to many months, or years

Outcomes Resolution, abscess formation,chronic inflammation Tissue destruction, fibrosis,necrosis

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