Inflammation: Fajar L. Gultom Departemen Patologi Anatomik FK UKI April 2019

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INFLAMMATION

Fajar L. Gultom
Departemen Patologi Anatomik FK UKI
April 2019
Definition
Response of vascularized tissue to
infections and damaged tissue that
bring cells and molecules of host
defense from the circulation to the
sites where needed to eliminate the
offending agents. (Robbins, 2015)
Sequence of events in
inflammatory Reaction

Robbin’s Basic Pathology 9th edition 2015


Inflammation
• Inflammation  protective response
• Without inflammation:
– Infection unchecked
– Wounds never heal
– Injured tissue  festering sores
Inflammation
• Components:
– Blood vessels  endothel lining
– Leucocytes  recruited  activated  ingest
n destroy micobes n dead cells
• Harmful consequences:
– Protective reaction in infection  local tissue
damage  self limited – no damage
– Contrast: autoimmune disease, allergies.
Inflammatory misdirected  againts
selftissues.
Robbin’s Basic Pathology 9th edition 2015
Inflammation
• Local and systemic inflammation
– Local response  systemic manifestation –
fever
– Disseminated bacterial infection  sepsis
 SIRS (systemic inflammatory syndrome)
• Mediators of inflammation
– Soluble factors produced by various cells/
plasma protein
– Initiate or amplify inflammatory response
Inflammation
• Acute n chronic inflammation
– Acute: initial, rapid response, exudation
fluid, plasma protein (edema), emigration
of leucocytes (PMN/neutrophils)
– Chronic: longer duration, tissue destruction
>>, lymphocytes n macrophages (MN)
• Termination of inflammation and tissue
repair
Robbin’s Basic Pathology 9th edition 2015
Inflammation reaction. A. Early: PMN. B. Late: Lymphocytes.

Robbin’s Basic Pathology 9th edition 2013


Causes
• Infections: bacterial, fungal, viral,
parasites
• Tissue necrosis: ischemia, trauma,
physical and chemical injury
• Foreign bodies: sutures, dirt, urate
crystal, cholesterol crystal
• Immune response: hypersensitivity -
autoimmune
Inflammation
• Vascular response
Vasodilatation, capilar permeability ↑
(histamin), activated endothel
• Cellular response
Leucocyte (PMN) emigration 
accumulated at area of infection/ injury
 elimination
• Activated by mediator
Acute Inflammation
• “Protective” Response
•Non-specific
Cardinal signs
• Rubor
• Tumor
• Calor
• Dolor
• Fungsio
laesa

http://inflam.jst.go.jp/en/illust/
Highly Recommended..
Pls read
Vascular Reactions
• Vasodilatation  erythema, stasis
blood flow
• Increased vascular permeability 
plasma protein, leucocyte, mediators
leave circulation  extravascular
• Fluid leak  edema
Vascular Reaction

Robbin’s Basic Pathology 9th edition 2015


Increased
vascular
permeability

Robbin’s Basic Pathology 9th edition 2015


Leucocytes Recruitment
• Lumen: margination, rolling, adhesion
• Migration across endothelium and vessel
wall
• Migration in the tissue toward
chemotactic stimulus
Multistep Leucocyte Migration

Robbin’s Basic Pathology 9th edition 2015


Leucocyte Activation and Removal
Offending Agents
• Phagocytosis
–Recognition and attachment,
engulfment, killing and degradation
• Destruction in phagolysosomes (ROS,
NO)
• Neutrophils  NET (Neutrophils
Extracellular Traps)
Leucocyte Activation

Robbin’s Basic Pathology 9th edition 2015


Phagocytosis

Robbin’s Basic Pathology 9th edition 2015


Neutrophil Extracellular Traps (NET)

Robbin’s Basic Pathology 9th edition 2015


Mediators of Inflammation
• Substances that initiate and regulate
inflammatory reactions
• Secreted by cells (macrophages, dendritic cells
and mast cells) or generated from plasma
protein
• Short lived
Mediators of Inflammation
Morphologic Patterns
Acute Inflammation
• Serous  watery
• Fibrinous  hemorrhagic
• Suppurative  pus
• Ulcerative
Serous Inflammation
Fibrinous
Purulent (abscess) Inflammation
Ulcerative
OUTCOMES OF
ACUTE INFLAMMATION
1) 100% complete RESOLUTION

2) SCAR

3)CHRONIC inflammation
Robbin’s Basic Pathology 9th edition 2015
TERIMA KASIH..

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