INFLAMMATORY

PROCESS
Bryan M. Espiritu, RN, MAN
INFLAMMATION=SETTING ON FIRE
• A response of vascularized tissues to infections and
damaged tissues.
• Brings cells and molecules of host defense from the
circulation to the sites where they are needed in order to
eliminate the offending agents.
• It is a protective response that is essential to rid the host
of both the initial cause of cell injury (toxin and microbes)
and the consequences of such injury (necrotic tissues).
• Without inflammation, infections would go unchecked,
wounds would never heal, and injured tissues might
remain permanent festering sores.
• NON-SPECIFIC DEFENSE
COMPONENTS
• Major participants are the leukocytes and the blood
vessels.
• Vessels dilate and increase their permeability.
• Leukocytes get recruited and activated to ingest and
destroy microbes.
HARMFUL CONSEQUENCES OF
INFLAMMATION
• Protective inflammation is also accompanied by local
tissue damage.
• Typically, these harmful consequences are self-limited
and resolved as the inflammation abates, leaving little to
no damage.
• Autoimmune diseases, allergies, inadequately controlled
inflammation process sometimes become the cause of
the disease, causing a dominant and injurious damage.
LOCAL AND SYSTEMIC RESPONSE
• Local Response: Inflammation focused on the
tissue reaction.
• Systemic Response: Inflammation reaction
causes widespread pathologic abnormalities
Local and Systemic Effects of
Inflammation

• Local effects
• Capillary dilatation
• Increased capillary permeability
• Attraction of leukocytes
• Migrate to site of injury
• Adhere to endothelium of small blood vessels

• Systemic effects: fever, leukocytes

TYPES
• Acute Inflammation
• Initial, rapid response to infection and tissue damage.
• Typically develops within minutes to hours.
• Short-lived, lasts for several hours or a few days.
• More prominent in the reactions of the innate immunity.
• Its main characteristics are: 
Exudation of fluid and plasma proteins (Edema)
Leukocyte migration, predominantly neutrophils (PMN)
• Chronic Inflammation
• Longer in duration.
• Associated with more tissue destruction.
• Presence of lymphocytes and macrophages.
• Proliferation of blood vessels.
• Deposition of connective tissues.
• More prominent in the reactions of the adaptive immunity.
CAUSES
• INFECTIONS
• Bacterial, viral, fungal, parasitic infections and toxins.
• Most common and medically important cause of inflammation.
• Elicit varied inflammatory response from acute to chronic and from
localized to systemic
CAUSES
• TISSUE NECROSIS
• Elicits inflammation regardless the cause of cell death.
• Ischemia
• Trauma
• Physical and Chemical Injury

• Molecules released from the necrotic cells trigger inflammation.

CAUSES
• FOREIGN BODIES
• They can cause tissue injury or they carry microbes.
• Can be exogenous or endogenous.
• Urate Crystal can cause inflammation gout.
• Cholesterol Crystals can cause inflammation in atherosclerosis.
• Lipids can cause inflammation in obesity-associated metabolic
syndrome.
CAUSES
• IMMUNE REACTIONS
• Also called hypersensitivity.
• Normally protective immune system damages individual’s own
tissues.
• Immune response can be directed against self-antigens such that
of autoimmune diseases.
• It can also be a reaction to normal substances in the environment
such that of allergies.
• These are harder to cure because the inflammation is persistent.
• The inflammation of this kind is usually elicited by cytokines
produced by T-lymphocytes
STEPS OF INFLAMMATORY
RESPONSE
• 1. Recognition
• 2. Recruitment
• 3. Removal
• 4. Regulation
• 5. Resolution and Repair
Local and Systemic Effects of Inflammation
HISTORICAL HIGHLIGHTS (CARDINAL
SIGNS OF INFLAMMATION)
• Clinical features of inflammation were described and
written in Egyptian papyrus dated 3000 B.C.
• Celsus described the four cardinal signs of inflammation:
•  Calor (Heat)  Rubor (Redness)  Tumor (Swelling)  Dolor (Pain)
• Rudolph Virchow added the fifth cardinal sign (Loss of function).
• John Hunter: “Inflammation is not a disease but a stereotypic
response that has a salutary effect on the host”
THE BASIS OF THE FIVE CARDINAL
SIGNS
• Increased blood flow due to vascular dilatation gives
REDNESS AND HEAT.

• Increased vascular permeability gives edema causing

TISSUE SWELLING.

• Certain chemical mediators stimulate sensory nerve

endings giving PAIN. Nerves also stimulated by
stretching from edema.

• Pain and swelling result in loss of FUNCTION.

RECOGNITION OF MICROBES AND
CELL DAMAGES
• CELLULAR RECEPTORS
• SENSORS OF CELL DAMAGE
• OTHER CELLULAR RECEPTORS
• CIRCULATING PROTEINS
Complement System
• Classical Pathway – recognizes pathogen’s surface
• Lectin Pathway – mannose-binding lectin binds to mannose on
pathogen surface
• Alternative Pathway – recognizes antigen-antibody complexes
4 Phases of Inflammation
• Vascular
• Think blood vessels
• Cellular
• Think WBC’s
• Formation of
Exudate
• Fluid & neutrophils
• Healing
• regeneration or repair
of tissue
 Vascular Phase: Blood Vessels

• Injury occurs
• Mediators intervene
• Vasodilation occurs
• Capillaries become
more permeable
• Swelling and
movement of fluid
occurs
Cellular Phase – Think WBC’s
• Injury occurs
• Chemotaxis begins
• White blood cells rush in to
help
• Neutrophils
• Monocytes
• Macrophages
Chemical Mediators
Coordinators of the
inflammatory response
• Histamine
• Prostagladins
• Cytokines
 Chemical mediators of
inflammation
• Vasoactive amines
• Histamine
• Serotonin (5-HT)
• Neuropeptides
• Substance P
• Plasma proteases and the complement system
• Action of Hageman factor
• Arachidonic acid metabolites
• Prostaglandins
• Leukotrienes
• Lipoxins
• Cytokines
• IL-1, TNF etc.
• Chemokines (CXC and CC)
• Nitric oxide and oxygen-derived free radicals
 Chemical mediators of
inflammation
• PREFORMED
Histamine, Serotonin

• NEWLY SYNTHESISED
Prostaglandins
Leucotrienes
Platelet activating factor
Cytokines
Nitric oxide

• LOCAL AND SYSTEMIC

 Vasodilation:
Prostaglandins, NO

Increased vascular permeability:

Histamine, serotonin, C3a, C5a, bradykinin,
Leukotrienes C4, D4, E4, platelet activating factor

Chemotaxis, leukocyte activation:

C5a, leukotriene B4, bacterial products, chemokines (IL-8)

Fever:
IL-1, IL-6, TNF, prostaglandins

Pain:
Prostaglandins, bradykinin

Tissue damage:
Neutrophil and macrophage lysosomal enzymes, oxygen
metabolites
NO
Formation of Exudates
• Exudation – the process by which fluid, proteins, and
blood cells from the vascular system escapes into the
interstitial tissue or to the body cavities.
• EXUDATE – high protein concentration and contains cellular
debris, this is an implication that there is increased permeability
triggered by some sort of tissue injury.
• TRANSUDATE – low protein and little to no cellular debris, it is
essentially an ultrafiltrate of the blood, this is an implication of
osmotic or hydrostatic imbalances in the vessels, without an
increase in the permeability of the vascular walls.
• EDEMA – denotes an excess of fluid in the interstitial tissue or
serous cavities, can be both an exudate and transudate.
• PUS – purulent exudate rich in leukocytes and cell debris.
Healing Phase
CHRONIC INFLAMMATION
• CAUSES OF INFLAMMATION
• Persistent Infection
• Hypersensitivity Diseases
• Prolonged exposure to toxic agents
Cells of the chronic inflammatory
response
• Lymphocytes
• Monocytes/ macrophages
• Plasma cells
GRANULOMATOUS INFLAMMATION
• Characterized by collections of activated macrophages,
often Tlymphocytes and sometimes associated with
central necrosis.
• A cellular attempt to contain an offending agent that is
difficult to eradicate.
• Strong lymphocytes lead to macrophage activation and
cause injury to normal tissues.
• Epitheloid Cells are activated macrophages that develop
abundant cytoplasm and begin to resemble epithelial
cells.  Giant Cells are fused, multinucleated activated
macrophages.
Types of Inflammation
• Acute inflammation • Chronic inflammation
• Short duration
• Longer duration
• Edema
• Lymphocytes & macrophages
• Mainly neutrophils
predominate
• Fibrosis
• Granulomatous
• New blood vessels
inflammation (angiogenesis)
• Distinctive pattern of chronic
inflammation
• Activated macrophages
(epithelioid cells)
predominate
• +/- Multinucleated giant cells
Types of Inflammation: acute vs. chronic
Types of repair: resolution vs. organization (fibrosis)
 Infection
• Inflammatory process caused by disease-
producing organisms
• “itis”: suffix indicates an infection or inflammatory
process such as appendicitis, hepatitis, colitis
• Cellulitis: acute spreading infection at any site
• Abscess: infection associated with breakdown of
tissues, formation of pus
 Definition
Infection is the invasion and multiplication of
microorganisms in body tissues, which may
be unapparent or the result of local cellular
injury caused by competitive metabolism,
toxins, intracellular replication, or antigen-
antibody response.

An infection is the invasion of a

susceptible host by pathogens or
microorganisms, resulting in
disease.
Infection

• Septicemia: overwhelming infection

where pathogenic bacteria gain access to
bloodstream
• Pathogenic: capable of producing disease
• Virulence: a measure of severity of
disease
• Host: affected individual or animal
 Infection
• Involves the relationship between invading
organism and defenses of the body
 Infection
• Factors influencing the outcome
• Virulence of organism
• Numbers of invading organisms
• Host resistance
 Chronic Infection

• State in which the pathogenic organism

and the host are evenly matched
• Relatively quiet, smoldering inflammation,
associated with repeated attempts of the
body at healing
• Predominant cells: lymphocytes, plasma
cells, and monocytes
Chain of
Infection
Natural
Defenses
• Skin (Barrier, Shedding of Cells)
• Mouth (Mucosa, Saliva)
• Eye (Tearing, Blinking, Eyelashes)
• Respiratory Tract (Cilia, Macrophages)
• Urinary Tract (Flow of Urine)
• GI Tract (Acidity, Peristalsis)
• Vagina (Normal Flora, pH)
 Inflammatory
Response
Vascular and Cellular Responses
• Acute inflammation
• Rapid vasodilation occurs, allowing more blood near the location of the injury.
• Chemical mediators released to increase the permeability of small blood vessels-
edema occurs
• Pain r/t swelling.
• (WBCs) arriving at the site.
• Phagocytosis occurs in which neutrophils and monocytes consume bacteria.
• Leukocytosis: WBC count is normally 5,000 to 10,000/mm3 but typically rise to
15,000 to 20,000/mm3 and higher during inflammation.
Inflammatory Exudate
• Accumulation of fluid and dead tissue cells and WBCs forms an exudate at the site of
inflammation.
• Serous, Purulent, etc.
Tissue Repair
• Damaged cells replaced with healthy new cells, which go through a maturation stage
• If inflammation is chronic, tissue defects sometimes fill with fragile granulation tissue
 Localized Infection Systemic Infection
• swelling, redness, • fever, leukocytosis,
heat, pain or malaise, anorexia,
tenderness, and loss nausea, vomiting,
of function in the lymph node
affected body part. enlargement, or organ
failure.
 Risk Factors

• Age
• Chronic Conditions
• Lifestyle
• Travel History
• Heredity
• Occupation
• Procedures
• Nutrition
Thank You