Acute Inflammation and inflammation types

Acute inflammation
Causes for inflammation
Cardinal signs of inflammation
Types of inflammation
Exudate
Transudate
Local complications
Systemic effects

1. Acute Inflammation
Dr Janane Nallaretnam
Department of Pathophysiology

2. Objectives

•Definition
•Cardinal features and vascular changes of acute inflammation
•Compare exudate and transudate
•Describe the cellular changes and their role in acute inflammation
•Describe the functions of chemical mediators
•Advantages and disadvantages of the acute inflammatory response
•Cells of inflammation
•Morphological patterns of acute inflammation
•Outcomes of acute inflammation

3. Inflammation
“Inflammation is a response of vascularized tissues to infections and
tissue damage that brings cells and molecules of host defense from
the circulation to the sites where they are needed, to eliminate the
offending agents”

•Reaction of vascularized living tissue to local injury

4. •Purpose
Eliminate injurious agent
Prevent the spread of injurious agent
Remove necrotic cells and tissue
Initiate tissue repairing process

•Usually inflammation promotes healing, but if it is uncontrolled it can
be harmful

5. Too much inflammation
•Autoimmune diseases
•Allergies
•Excessive prolonged infections by
microbes that resist eradication
(tuberculosis and viral hepatitis)
•Inflammatory reactions for chronic
diseases (rheumatoid arthritis,
atherosclerosis, lung fibrosis)
•Life-threatening hypersensitivity reactions
to insect bites, drugs and toxins
•Degenerative or genetic disorders - type 2
diabetes, Alzheimer disease and cancer

6. Too little inflammation
•Increased susceptibility to infections
•By bone marrow cancers, suppression of bone marrow by therapies
for cancer and graft rejection
•Inherited genetic abnormalities of leukocyte function

7. Causes of Inflammation
•Infections (bacterial, viral, fungal, parasitic) and microbial toxins
•Physical agents – burns, trauma, cuts, radiation
•Chemicals – toxins, caustic substances
•Tissue necrosis
•Foreign bodies - splinters, dirt, sutures
•Immune reactions

8. Cardinal signs of inflammation
•Heat (calor)
•Redness (rubor)
•Swelling (tumor)
•Pain (dolor)
•Loss of function (functio laesa)

9. •Redness - secondary to vasodilatation and increased blood flow
•Heat - localized increase in temperature and increased blood flow
•Swelling - increased vessel permeability, allowing fluid loss into the
interstitial space
•Pain - by stimulation of the local nerve endings, from mechanical and
chemical mediators
•Loss of function - due to pain and swelling

11. •Main components - vascular reaction and cellular response
•Both are activated by chemical mediators that are derived from
plasma proteins and various cells
•The defense mediators - phagocytic leukocytes, antibodies, and
complement proteins
•Inflammatory mediators
Promote the efflux of plasma
Recruitment of circulating leukocytes to the site
Activate the recruited leukocytes, enhancing their ability to
destroy and remove the offending agent

12. •The typical inflammatory reaction develops through a series of
sequential steps:
 Recognition of the injurious agent
 Recruitment of leukocytes
 Removal of the agent
 Regulation (control) of the response
 Resolution (repair)

14. 2 types
•Acute inflammation
•Chronic inflammation

15. Acute inflammation –
Polymorphonuclear neutrophils
(PMNs)
Chronic inflammation. Lymphocytes,
plasma cells, and few macrophages

16. Recognition of offending agents
•Cellular receptors for microbes
Toll-like receptors (TLRs) - in plasma membranes and endosomes of
phagocytes and dendritic cells
TLRs recognize motifs common to many microbes, often called pathogen-
associated molecular patterns (PAMPs)
Bacterial lipopolysaccharides, Bacterial proteoglycans, Double strand RNA
virus
Stimulate production of cytokines (induce inflammation), interferons and
membrane proteins that promote lymphocyte activation and potent immune
responses

17. •Sensors of cell damage
Cytosolic receptors - Damage-associated molecular patterns (DAMPs)
The receptors activate inflammasome, which induces the production of
cytokine interleukin-1
IL-1 recruits leukocytes and induces inflammation
The inflammasome also has been implicated in inflammatory reactions to
urate crystals (gout), cholesterol crystals (in atherosclerosis), lipids (in
metabolic syndrome and obesity- associated diabetes) and amyloid deposits
in the brain (in Alzheimer disease)
•Circulating proteins
Plasma proteins recognize and destroy blood-borne microbes and stimulate
inflammation
The complement system reacts against microbes and produces mediators of
inflammation
Mannose-binding lectin recognizes microbial sugars and promotes ingestion
of microbes and activation of the complement system
Collectins bind to microbes and promote phagocytosis

19. •Exudate : Extravascular fluid with high protein concentration and cellular
debris
To deliver fibrin, inflammatory mediators and immunoglobulins to the site of damage
Dilutes toxins to reduce tissue damage
Increases lymphatic drainage to deliver antigens and pathogens to lymph nodes to
initiate an immune reaction
•Transudate : Fluid with low protein content, little or no cellular material
and low specific gravity
•Edema : Excess fluid in interstitial tissue or serous cavities; it can be either
an exudate or transudate
•Pus :Purulent exudate, is an inflammatory exudate rich in leukocytes
(mostly neutrophils), debris of dead cells and microbes

20. Exudate Transudate
Due to increase vascular
permeability
Due to imbalance between
hydrostatic and osmotic force
High protein content Low protein content (usually
albumin)

High neutrophil content and
rich in cellular debris
Little or no cellular material
High specific gravity > 1.020

Low specific gravity < 1.012

Clinically expressed as non
pitting edema
Clinically expressed as pitting
edema

22. Exudation of fluid
•Fluid flow across the vessel walls is
controlled by a combination of hydrostatic
pressure (the pressure exerted by a fluid
which forces fluid out) and oncotic pressure
(osmotic pressure exerted by proteins
which draws fluid in) “Starling’s Forces”
•Vasodilation of arterioles leads to increased
hydrostatic pressure and as a result, higher
fluid movement out of vessels
•Increased vessel permeability allows
proteins to move into the interstitium,
leading to increased colloid pressure and
further increasing fluid movement out of
vessels

23. Acute inflammation

3 major components:

•Increase blood flow

•Increased vascular
permeability

•Emigration of the
leukocytes from the
microcirculation

24. Changes in vascular flow and caliber
(hemodynamics)

•Vasoconstriction – transient,
inconstant
•Vasodilation – first arterioles,
then capillaries, then venules
Histamine like mediators on
vascular smooth muscle
Result in increased blood flow (heat
and erythema)
Increased permeability of the
microvasculature
Albumin-rich fluid (an exudate)
leaking into extravascular tissue

25. •Slowed circulation – Loss of fluid and increased vessel diameter lead
to slower blood flow, concentration of red cells in small vessels, and
increased viscosity of the blood
Stasis of blood flow
Engorgement of small vessels and blocked with slowly moving red cells
Vascular congestion and erythema of the tissue
•Leukocyte margination – PMNs become oriented at vessel periphery
and start to stick
Leukocytes mainly neutrophils accumulate along the vascular endothelium
Endothelial cells are activated by mediators and express increased levels of
adhesion molecules
Leukocytes adhere to the endothelium and they migrate through the vascular
wall into the interstitial tissue

27. Vascular permeability (leakage)

•Retraction of endothelial cells
Opening of endothelial spaces by chemical mediators
(histamine, bradykinin, leukotrienes)
Rapidly after exposure to mediator (within 15 to 30 minutes)
Main sites for rapid increase in vascular permeability -
postcapillary venules
• Endothelial injury
Direct injury – e.g. toxic burns, chemicals
Results endothelial cell necrosis and detachment
Leucocyte dependent injury – damages endothelial cells
causing gaps to form between them
By ROS and enzymes from leucocytes
Cytoskeletal re-organization forming gaps between cells
It is mediated by cytokines (IL-1 and TNF)

30. •Increased transcytosis – production of
channels within the endothelial cell to
allow movement of proteins and fluid
between cells. It is mediated by vascular
endothelial growth factor (VEGF)

31. Lymphatic Vessels and Lymph Nodes
•Lymphatic vessels proliferate during inflammatory reactions
•Lymph flow is increased to drain edema fluid that accumulates because of
increased vascular permeability
•Lymphangitis and Lymphadenitis
•This constellation of pathologic changes is termed reactive or
inflammatory lymphadenitis
•Presence of red streaks near a skin wound is a telltale sign of an infection in
the wound
•This streaking follows the course of lymphatic channels and indicates the
presence of lymphangitis; it may be accompanied by painful enlargement
of the draining lymph nodes (lymphadenitis)

32. Recognition of microbes or dead cells induces several responses in leukocytes that
are collectively known as leukocyte activation

33. Leukocyte recruitment to sites of inflammation
•Leukocyte adhesion to endothelium
Margination
White cells assume a peripheral position along the
endothelial surface
Rolling
Selectins - weak interactions between leukocytes and
endothelium
E-selectin on endothelial cells
P-selectin on platelets and endothelium
L-selectin on the surface of most leukocytes
E-selectin and the ligand for L-selectin are
expressed on endothelium only after
stimulation by IL-1 and tumor necrosis factor
(TNF)

35. Firm adhesion
Integrins
When the rolling leukocytes encounter the chemokines, the cells are
activated and their integrins undergo conformational changes and cluster
together, thus converting to a high-affinity form
TNF and IL-1, activate endothelial cells to increase their expression of
ligands for integrins

•Transmigration of leukocyte through endothelium
Diapedesis – neutrophils relax the junctions between the endothelial cells so
they can move across the endothelium
Mainly in postcapillary venules
Platelet endothelial cell adhesion molecule-1 (PECAM-1) expressed on
leukocytes and endothelial cells, mediates the binding events needed for
leukocytes to traverse the endothelium
Leukocytes pierce the basement membrane by secreting collagenases

37. •Chemotaxis of Leukocytes
Chemotaxis – neutrophils are attracted towards the site of injury by
chemical attractants
C5a from complement system
Bacterial and mitochondrial products (low-molecular-weight N-formylated
peptides - N-formyl-methionyl-leucyl-phenylalanine)
Products of arachidonic acid metabolism leukotriene B4 (LTB4)
Cytokines (chemokine family e.g., IL‐8)

38. •Opsonization - process were the organisms
are rendered more palatable to the
phagocytic cells
•Opsonin are substances which make it
easier for phagocytes to recognize the
targets
E.g.-the bacteria are opsonized by antibodies
before they get phagocytosis by neutrophils and
macrophages
•Common opsonins-Immunoglobulins,
Complement products, Fibronectin and etc
•Once phagocytosed the intracellular
organisms are killed by forming free
radicals

39. Leukocyte infiltration varies with the age of the inflammatory response
and the type of stimulus
•Bacterial infection - neutrophils
•Viral infections - lymphocytes
•Hypersensitivity reactions - activated lymphocytes,
macrophages and plasma cells
•Allergic reactions – eosinophils

40. Clearance of the offending agent
•Phagocytosis
Attachment of leukocyte with offending agent
Mannose receptors, scavenger receptors and receptors for opsonins
Engulfment
Killing and degradation

Activation of phagocytes are done by microbes, necrotic debris, and
various mediators

42. Intracellular destruction of microbes
•Reactive Oxygen Species
Superoxide Anion (O2–)
In neutrophils, this oxidative reaction is tightly
linked to phagocytosis, and is called the
respiratory burst
H2O2
Hypochlorous Acid (HOCl)
(•OH)
•Nitric Oxide (NO)
•Granule Enzymes and Other Proteins
lysozyme, collagenase, gelatinase, lactoferrin,
plasminogen activator, histaminase, and
alkaline phosphatase

43. Neutrophil Extracellular Traps
•Extracellular fibrillar networks
•They concentrate anti-microbial substances at
sites of infection and prevent the spread of the
microbes by trapping them
•Infectious pathogens (bacteria and fungi) and
inflammatory mediators (e.g., chemokines,
cytokines, and complement proteins)
•It consists of viscous meshwork of nuclear
chromatin that binds and concentrates granule
proteins (anti-microbial peptides and enzymes)
•During NET formation, neutrophils will loose
their nuclei, leading to the death of the cells
(NETosis)
•NETs also have been detected in the blood
during sepsis
•The nuclear chromatin in the NETs (histones and
DNA) may be a source of nuclear antigens in
systemic autoimmune diseases, particularly
lupus

44. Inflammatory mediators

45. •Produced by cells or from plasma
•Active mediators are produced only in response to various molecules
that stimulate inflammation (microbial products and substances
released from necrotic cells)
•Short-lived
•One mediator can stimulate the release of other mediators
Complement activation stimulate the release of histamine
Cytokine TNF acts on endothelial cells stimulate the production IL-1 and many
chemokines

46. Actions of mediators in
inflammation

47. Tumor Necrosis Factor and Interleukin-1
•Important roles in leukocyte
recruitment by promoting adhesion of
leukocytes to endothelium and
migration through vessels
•Activated macrophages and dendritic
cells
•TNF also produced by T lymphocytes
and mast cells
•Some epithelial cells also produce IL-1
•Stimuli for secretion - microbial
products, foreign bodies, necrotic cells

48. Main functions
•Endothelial activation
•Activation of leukocytes and
other cells
•Systemic acute-phase
response
•TNF regulates energy balance
by promoting lipid and protein
catabolism and by suppressing
appetite

49. Cytokines

50. Complement

51. Local complications of Acute Inflammation

•Damage to normal tissue –substances produced by neutrophils and
released in phagocytosis
•Obstruction of tubes, e.g. bile duct, intestine due to compression by
surrounding swelling
•Exudate: Compression e.g. cardiac tamponade
•Loss of fluid as exudate, e.g. burns
•Pain and loss of function

52. Systemic Effects of Acute Inflammation

•Fever
Pyrogenic substances (IL-1 and TNF) are released and stimulate the
hypothalamus to increase the body temperature
PG can also cause fever
Prostaglandin synthesis is inhibited by aspirin
•Leukocytosis
IL-1 and TNF produce accelerated release of leucocytes from the bone
marrow
Macrophages and T lymphocytes also stimulate the further release of other
leucocytes

53. •Acute phase response - change in the level of some plasma proteins
as the liver changes its pattern of protein synthesis
Decreased appetite, increased pulse rate, altered sleep patterns and changes in
plasma concentration of acute phase proteins such as:
C-reactive protein (CRP) (clinically useful in assessing the level of inflammation)
Alpha-1 antitrypsin
Haptoglobin
Fibrinogen
Serum amyloid A protein
•Shock
Clinical syndrome of circulatory failure, often fatal
If bacterial products or inflammatory mediators spread around the body in
the blood stream, leading to body-wide inflammation
Dramatic drop in blood pressure by widespread vasodilation and increased
vascular permeability

54. Disorders related to acute inflammation
Rare diseases

•Hereditary angio-oedema (‘angioneurotic oedema’)
•Alpha-1 antitrypsin deficiency
•Inherited complement deficiencies
•Defects in neutrophil function
•Defects in neutrophil number
•Deficiency of NADPH oxidase that generates superoxide, therefore
no oxygen‐dependent killing mechanism (chronic granulomatous
disease)

55. Acute inflammatory termination
•Inflammation mediators - short half-lives and degrade after release
•Neutrophils - short half-lives in tissues (apoptosis within hours to a
day or two after leaving the blood)
•Stop signals
Proinflammatory leukotrienes to anti-inflammatory lipoxins
 Liberation of anti-inflammatory cytokines (transforming growth factor-β
(TGF-β) and IL-10 from macrophages and other cells)
•Neural impulses (cholinergic discharge)- inhibit TNF production in
macrophages

57. Cells of Inflammation
•Neutrophils
•T and B lymphocytes
•Monocytes and Macrophages
•Eosinophils
•Basophils

58. Neutrophil
•First inflammatory cell for tissue injury
•Phagocytosis

59. T and B lymphocytes

•T lymphocytes – mediate cellular immune response
•Plasma cells
Differentiated B cells
Produce antibodies

60. Eosinophils

•Allergic reactions
•Parasite-associated inflammatory reactions
•Chronic inflammation
•Modulates mast cell-mediated reactions

61. Monocytes and Macrophages

•Microglia, Kupffer cells, sinus histiocytes, alveolar macrophages
•Circulate as monocytes and reach site of injury within 24 –48 hrs
•Activated by T cell‐derived cytokines, endotoxins, and other products
of inflammation

62. Basophils

•Allergic hypersensitivity reactions
•Mast cells and basophils contain cell surface
receptors for IgE
•Mast cells - connective tissues (lung and
gastrointestinal mucosal surfaces, the dermis)
•Cytoplasmic granules contain acid
mucopolysaccharides (including heparin), serine
proteases, chemotactic mediators for neutrophils
and eosinophils and histamine
•Stimulation of mast cells and basophils also leads
to the release of products of arachidonic acid
metabolism and cytokines ( TNF and IL-4)

63. Morphologic patterns of acute inflammation
Based on Exudate:
•Serous Inflammation
•Catarrhal inflammation
•Fibrinous Inflammation
•Purulent (Suppurative) Inflammation, Abscess
•Ulcers

64. Serous Inflammation
•Exudation of cell poor fluid into spaces
•Thin, watery exudate
•Injury to surface epithelia or into body cavities
(peritoneum, pleura, or pericardium)
•Fluid is not infected by destructive organisms
and does not contain large numbers of
leukocytes
Eg; The skin blister from a burn or viral infection

65. •Fluid may be derived from the plasma (increased vascular
permeability) or from the secretions of mesothelial cells (by local
irritation)
•Accumulation of fluid in cavities - Effusion
•Effusions consisting of transudates also occur in noninflammatory
conditions, such as reduced blood outflow in heart failure or reduced
plasma protein levels in some kidney and liver diseases
•Effusions into body cavities:
Serous: transudate with mainly edema fluid and few cells
Serosanguinous: an effusion with red blood cells
Fibrinous (serofibrinous): fibrin strands are derived from a protein-rich
exudate
Purulent: numerous PMN's are present, called "empyema" in the pleural
space

66. Skin blister
Epidermis separated from the dermis by a
focal collection of serous effusion

67. •Right pleural effusion - clear, pale yellow fluid (serous effusion)
•Lung collapse - due to pressure induced by the fluid

68. Catarrhal inflammation
•Inflammation of mucous membranes
•Secretion of mucus
•Infections
eg Rhinitis in common cold (Rhinovirus)

69. Fibrinous Inflammation

•Fibrinous exudate will form when vascular
leaks are large or because of local
procoagulant stimulus
•Fibrinogen will come out of from the blood,
fibrin is formed and deposited in the
extracellular space
•In the lining of body cavities - meninges,
pericardium and pleura
•Histology
Fibrin - an eosinophilic meshwork of threads or
amorphous coagulated mass

70. •Fibrinous exudates may be removed by fibrinolysis
and clearing of other debris by macrophages
•But if the fibrin is not removed, it may stimulate
the ingrowth of fibroblasts and blood vessels and
thus lead to scarring
•Conversion of the fibrinous exudate to scar tissue
is called organization
•When this occurs within the pericardial sac it
leads either to opaque fibrous thickening of the
pericardium or development of fibrous strands
that reduce and may obliterate the pericardial
space

71. •Fibrinous pericarditis
Visceral and parietal surfaces
stuck together by fibrin

Separation of the two layers –
Bread and butter appearance

72. Pseudomembranous inflammation: surface necrosis

•Bacterial toxins damage the mucosal lining,
produce a membrane composed of necrotic
tissue
•Eg; Corynebacterium diphtheriae produces
a toxin causing pseudo membrane
formation in the pharynx and trachea
•A greenish-yellow exudate covers most of
the mucosal surface
•Severe injury may be associated with
extensive epithelial necrosis with sloughing
•This creates large shallow ulcers

73. •Fibrin, dead epithelium, neutrophils, red cells and bacteria mix
together to produce a false membrane covering the affected mucosa
Eg; Pseudomembranous enterocolitis

74. Purulent (Suppurative) Inflammation

•Pus
•Neutrophils, necrotic cells and
edema fluid
•Certain bacteria (e.g., staph.
aureus, St. pyogenes, Pneumococci,
gonococci, meningococci and E.
coli) produce this localized
suppuration
•Pyogenic (pus-producing) bacteria
Eg: Acute appendicitis

75. •Acute appendicitis
•Lt; serosal surface with tan-yellow fibrino purulent
exudate
•Rt; lumen filled with pus
•Pus is a thick creamy yellow or blood-stained fluid

76. Abscess
•Localized collections of pus buried in a tissue / organ or a confined
space
•Once pus begins to accumulate in a tissue, it become surrounded by a
pyogenic membrane (emerging capillaries, neutrophils and occasional
fibroblasts)
•Bacteria within the abscess cavity are relatively inaccessible to
antibodies and antibiotic drugs (acute osteomyelitis, an abscess in the
bone marrow cavity is difficult to treat)
•Site: skin, subcutaneous tissue, internal organs (brain, lung, liver,
kidney)

77. •Central region - mass of necrotic leukocytes and tissue cells
•Around the necrotic foci -zone of preserved neutrophils and outside
this may be vascular dilation, fibroblastic proliferation, indicating the
beginning of repair
•Abscess may become walled off and ultimately replaced by
connective tissue

79. •Pus is usually liberated through an
epithelial surface and rest of the tissue is
healed with a scar
•If it is discharged into blood vessels
multiple abscess and septicemia occurs
•Multiple bacterial abscesses in
bronchopneumonia
•Pus may solidify, calcify and later form a
calcific nodule
•With a partial discharge of pus chronic
sinus occurs
•With the discharge in to two epithelial
surfaces fistula occurs

80. Eg; Osteomyelitis is complicated by chronic sinuses connecting the
infected bone to the surface of the skin
•Allow the pus from the site of inflammation to drain
Route along the pus was discharged may persist as a sinus tract (connection
between the tissue and a surface (epidermal or epithelial))
Tract may be lined by granulation tissue and/or by epithelium derived from
the surface

81. •Sometimes, it will produce a fistula (abnormal connection between
two epithelial surfaces or an epithelial surface and the skin)
Eg; segment of ileum that is inflamed in Crohn’s disease may become adherent
to the bladder
Inflammation will spread to the bladder wall, a tract connecting the ileum and
the bladder may form
A similar process can produce fistulae between the ileum and another
segment of bowel, the vagina or the skin

82. •Abscess that involves the skin is
called “Boil” or “furuncle”
•Usually caused by staphylococcal
infection, which involve a hair
follicle and surrounding tissue

•Carbuncles are clusters of furuncles
•Multiple loci open at the surface by
sinuses

83. Cellulitis
•An acute diffuse suppurative inflammation
•Usually by streptococci, which secrete
hyaluronidase & streptokinase enzymes
that dissolve the ground substances and
facilitate the spread of infection
•Can occur anywhere on body, the most
common location is the lower leg
•If untreated, the infection can spread to
lymph nodes and bloodstream and
become life-threatening

84. Complications of suppurative inflammation
•Bacteriemia - (endocarditis, meningitis)
•Sepsis (massive bacteriemia) - septic fever, septic shock
•Thrombophlebitis - secondary inflammation of the vein
•Embolization - pyemia - hematogenous abscesses (infected
infarctions)
•Lymphangitis, lymphadenitis
•Gangrenous - secondary modification by bacteria wet gangrene –
appendicitis
•Necrosis - inflammatory necrosis of the surface - ulcer (skin, gastric)

85. Ulcers

•Local defect, or excavation, of the surface of an organ or tissue
•Produced by the sloughing of inflamed necrotic tissue
•Ulceration can occur only when tissue necrosis and resultant
inflammation exist on or near a surface
• Commonly in
mucosa of the mouth, stomach, intestines, or genitourinary tract
skin and subcutaneous tissue of the lower extremities in older persons with
circulatory disturbances that predispose to extensive ischemic necrosis
•Acute and chronic inflammation often coexist in ulcers, such as peptic
ulcers of the stomach or duodenum and diabetic ulcers of the legs

86. •In acute stage - intense polymorphonuclear infiltration and vascular
dilation in the margins of the defect
•With chronicity, the margins and base of the ulcer develop fibroblast
proliferation, scarring, the accumulation of lymphocytes,
macrophages and plasma cells
Eg; Chronic peptic ulcer stomach

87. Chronic duodenal ulcer
Low-power cross-section view of a duodenal ulcer crater with an acute
inflammatory exudate in the base

89. Outcomes of acute inflammation
•Complete resolution
 Injury is limited or short
 Little tissue destruction
 Damaged parenchymal cells can regenerate
•Healing by connective tissue replacement (scarring, or fibrosis)
After substantial tissue destruction
Tissues that are incapable of regeneration or when there is abundant fibrin
exudation in tissue or in serous cavities (pleura, peritoneum) that cannot be
adequately cleared
In all these situations, connective tissue grows into the area of damage or
exudate, converting it into a mass of fibrous tissue

90. •Progression to chronic inflammation
Failure to eliminate a pathological insult or inability to trigger
resolution
May be evident as a prolonged acute response with continued
influx of neutrophils and tissue destruction
Eg; failure of acute bacterial pneumonia may lead to extensive
tissue destruction and formation of a cavity leads to chronic lung
abscess

91. Beneficial effects of Acute inflammation

•Dilution of Toxins by the edema fluid
•Production of protective antibodies and promote immunity
•Fibrin meshwork formation that forms a scaffold for inflammatory cell
migration and limits the spread of infections

92. Harmful effects of Acute inflammation

•Swelling and edema that can be life threatening
e.g. acute epiglottitis
•Tissue pressure increases that contributes to tissue necrosis
•Digestion of adjacent viable tissue
•Sever damaging allergic reaction
•Generalized increase in vascular permeability can cause shock

93. Thank you