Lakhasly

Acute inflammation

• Immediate and early response to tissue injury (physical, chemical, microbiological, etc.)
• Vasodilation
• Vascular leakage and oedema
• Leukocyte emigration (mostly PMNs) Cardinal Signs These signs are:
• rubor (redness)
• tumour (swelling)
• calor (heat)
• dolor (pain)
• functio laesa, or loss of function (In the second century AD, the Greek physician Galen added this fifth cardinal sign).Examples: Urticaria, allergic rhinitis and bronchial asthma.Pathogenesis: a-increased capillary hydrostatic pressure b-increase capillary permeability c- increase osmotic pressure of tissue spaces
• Function: 1-dilute bacterial toxins MPT-104 PATHOLOGY PATHOLOGY 14 2-contains antibody and antitoxins 3-block lymphatics by compression so limiting spread of infection by lymphatics

5. Dilatation of lymphatic vessels: -dilated at inflammed area -Some lymphatics may be blocked by fibrin thrombi this increase oedema but limits spread of infection -Draining lymph nodes develop lymphadenitis Cellular response

• The cellular response of acute inflammation is marked by movement of phagocytic white blood cells (leukocytes) into the area of injury. Phagocytosis involves three distinct steps:
• Adherence plus opsonisation
• Engulfment
• Intracellular killing through enzymes, toxic oxygen and nitrogen products produced by oxygen-dependent metabolic pathways (nitric oxide, peroxyonitrites, hydrogen peroxide, and hypochlorous acid)
• If the antigen is coated with antibody or complement, its adherence is increased because of binding to complement.5- Pseudomembranous (Membranous) Inflammation: Characteristics & pathogenesis: Severe form of acute inflammation of mucous membranes caused by bacteria that produce exotoxins leading to mucosal necrosis and marked submucosal inflammation resulting in formation of false membrane composed of necrotic mucosal patches and excessive fibrin.The sequence of events in the cellular response to inflammation includes: S Pavementing S Emigration S Chemotaxis S Phagocytosis 1- Pavementing
• The release of chemical mediators (i.e., histamine, leukotrienes and kinins) and cytokines affects the endothelial cells of the capillaries and causes the leukocytes to increase their expression of adhesion molecules.- As this occurs, the leukocytes slow their migration and begin to marginate, or move to and along the periphery of the blood vessels 2- Emigration and chemotaxis
• Emigration is a mechanism by which the leukocytes extend pseudopodia, pass through the capillary walls by ameboid movement, and migrate into the tissue spaces.- It only occurs in special sites where the skin and subcutaneous tissues are thick and tough due to dense fibrous septa that extend between the deep fascia and the dermis; thus dividing the subcutaneous fat into compartments, therefore infection reaching these multiple compartments leads to multiple suppurative foci.MPT-104 PATHOLOGY PATHOLOGY 18 4- Catarrhal Inflammation: Characteristics: A mild form of acute inflammation of mucous membranes characterized by an exudate mixed with mucous secreted by the irritated mucous membrane.Characters and composition of pus: Pus is a non-coagulable (no fibrinogen) creamy alkaline yellowish or yellowish green fluid composed of: 1- Fluid exudate without fibrin (liquefied).It is worth noting that serous membranes may be affected by other types of inflammation other than serous and fibrinous, e.g. suppurative inflammation Gross Picture: The visceral and parietal layers of the serous membranes are thickened, reticulated, opaque and greyish in case of fibrinous type.Progressively fluid move into the tissues (increased vascular permeability and structural alteration of blood vessels) and cause swelling (tumour), pain, and impaired function.- Once they have exited the capillary, the leukocytes move through the tissue guided by secreted cytokines, bacterial and cellular debris, and complement fragments (C3a, C5a).II- Diffuse: Caused by Streptococcus haemolyticus bacteria, which produce hyaluronidase (the spreading factor) and streptokinase (fibrinolysin) which dissolves fibrin.iii- Pyaemia: Multiple small abscesses caused by septic emboli derived from septic thrombi due to septic inflammation of veins near the abscess (septic thrombophlebitis).Carbuncle Is a special type of localised suppurative inflammation characterised by multiple communicating deep subcutaneous abscesses, each of which opens onto the surface by a sinus i.e. multiple sinuses occur.- The process by which leukocytes migrate in response to a chemical signal is called chemotaxis 3- Phagocytosis
• During the next and final stage of the cellular response, the neutrophils and macrophages engulf and degrade the bacteria and cellular debris in a process called phagocytosis.Acute Suppurative Inflammation I- Suppurative Inflammation (Septic, Purulent or Pyogenic Inflammation) Caused by pyogenic organisms as Staphylococcus aureus, Streptococcus haemolyticus and others.Types of suppurative inflammation: Localised: Caused by Staphylococcus aureus bacteria, which produce coagulase enzyme that leads to fibrin deposition leading to localisation.MPT-104 PATHOLOGY PATHOLOGY 17 Site Occurs in loose connective tissues as subcutaneous tissues, areolar tissue of orbit, scrotum and pelvis. 4) inflammatory fluid exudate: It is the passage of protein rich fluid through the dilated capillary walls into the interstitial tissue at site of irritation.Microscopic Picture: The false membrane consists of necrotic patches, fibrin, bacteria and acute inflammatory cells.6- Other Types of Acute Non Suppurative Inflammation: Haemorrhagic Inflammation: Characterised by excessive erythrocytes within the exudate due to associated vascular damage.Abscess Abscess is a type of localised suppurative inflammation characterised by the formation of a cavity containing pus.c. Fistula: It occurs if evacuation of a deep abscess results in a tract communicating between two surfaces or hollow organs, this tract with two openings is called fistula.Differences between cellulitis and abscess Criteria Cellulitis Abscess Definition Acute diffuse suppurative inflammation.Microscopic Picture: Epithelial cells of the mucosa are swollen and vacuolated due to excess mucin (mucoid degeneration).The underlying submucosa shows dilated capillaries, fibrin and acute inflammatory cells (PMNs and macrophages).The exudation or movement of the fluid out of the capillaries and into the tissue spaces dilutes the offending agent.Dead neutrophils (called pus cells) release their proteolytic enzymes, which liquefy necrotic tissue and fibrin.4- Bacteria and bacterial pigments which may be yellowish (as in staphylococcal infections) or greenish (as in pyocyaneous infections).2- Large abscess: Because absorption of pus occurs at a very slow rate, a big abscess undergoes pointing and rupture (spontaneous evacuation), followed by healing.Complications of abscess: 1- Complications of evacuation and healing: a. Ulcer: It is a local defect or excavation of the surface (discontinuation of the epithelium).Microscopic Features: The subserosa shows dilated capillaries, fibrin and acute inflammatory cells.2.

Acute inflammation

• Immediate and early response to tissue injury (physical, chemical, microbiological, etc.)


• Vasodilation


• Vascular leakage and oedema


• Leukocyte emigration (mostly PMNs)
  Cardinal Signs
  These signs are:


• rubor (redness)


• tumour (swelling)


• calor (heat)


• dolor (pain)


• functio laesa, or loss of function (In the second century AD, the Greek physician Galen
  added this fifth cardinal sign).
  Response to inflammation:


• Vascular response.


• Cellular response.
  Vascular reactions

1. Brief arteriolar vasoconstriction lasts few second or minutes only and it is due to direct
   stimulating action. followed by vasodilation


2. passive vasodilation
   Blood vessels in the affected area lose their reactivity to nervous and humoral stimuli and
   passive vasodilation occurs.
   The chemical substances as histamine from mast cells, serotonin from platelets and
   bradykinin and kallikrein from damaged cells.
   Progressively fluid move into the tissues (increased vascular permeability and structural
   alteration of blood vessels) and cause swelling (tumour), pain, and impaired function.
   The exudation or movement of the fluid out of the capillaries and into the tissue spaces dilutes
   the offending agent. As fluid moves out of the capillaries, stagnation of flow and clotting of
   blood in the small capillaries occurs at the site of injury.
   This aids in localizing the spread of infectious microorganisms.
   Accounts for warmth and redness
   Opens microvascular beds.


3. Slowing of the blood stream: It is due to:
   a- Swelling of the vascular endothelium.
   b- increase in the capillary bed due to opening of all cappilaries in the area of inflammation
   c- Haemoconcentration due to escape of large amount of fluid portion of blood.


4. inflammatory fluid exudate: It is the passage of protein rich fluid through the dilated
   capillary walls into the interstitial tissue at site of irritation.
   Pathogenesis:
   a-increased capillary hydrostatic pressure
   b-increase capillary permeability
   c- increase osmotic pressure of tissue spaces

• Function:
  1-dilute bacterial toxins
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  2-contains antibody and antitoxins
  3-block lymphatics by compression so limiting spread of infection by lymphatics

5. Dilatation of lymphatic vessels:
   -dilated at inflammed area -Some lymphatics may be blocked by fibrin thrombi this increase
   oedema but limits spread of infection -Draining lymph nodes develop lymphadenitis
   Cellular response

• The cellular response of acute inflammation is marked by movement of phagocytic white
  blood cells (leukocytes) into the area of injury.


• Two types of leukocytes participate in the acute inflammatory response - the
  granulocytes and monocytes.
  The sequence of events in the cellular response to inflammation includes:
  S Pavementing
  S Emigration
  S Chemotaxis
  S Phagocytosis
  1- Pavementing


• The release of chemical mediators (i.e., histamine, leukotrienes and kinins) and
  cytokines affects the endothelial cells of the capillaries and causes the leukocytes to increase
  their expression of adhesion molecules.


• As this occurs, the leukocytes slow their migration and begin to marginate, or move to and
  along the periphery of the blood vessels
  2- Emigration and chemotaxis


• Emigration is a mechanism by which the leukocytes extend pseudopodia, pass through the
  capillary walls by ameboid movement, and migrate into the tissue spaces.


• The emigration of leukocytes also may be accompanied by an escape of red blood cells.


• Once they have exited the capillary, the leukocytes move through the tissue guided by
  secreted cytokines, bacterial and cellular debris, and complement fragments (C3a, C5a).


• The process by which leukocytes migrate in response to a chemical signal is called
  chemotaxis
  3- Phagocytosis


• During the next and final stage of the cellular response, the neutrophils and
  macrophages engulf and degrade the bacteria and cellular debris in a process called
  phagocytosis.
  Phagocytosis involves three distinct steps:


• Adherence plus opsonisation


• Engulfment


• Intracellular killing through enzymes, toxic oxygen and nitrogen products produced by
  oxygen-dependent metabolic pathways (nitric oxide, peroxyonitrites, hydrogen peroxide, and
  hypochlorous acid)


• If the antigen is coated with antibody or complement, its adherence is increased
  because of binding to complement. This process of enhanced binding of an antigen caused by
  antibody or complement is called opsonisation.
  Acute Suppurative Inflammation
  I- Suppurative Inflammation (Septic, Purulent or Pyogenic Inflammation) Caused by
  pyogenic organisms as Staphylococcus aureus, Streptococcus haemolyticus and others.
  Mechanism of pus formation:
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1. Pyogenic organisms cause:
   a- Remarkable necrosis.
   b- Attraction of huge number of neutrophils.
   c- Death of many neutrophils due to high virulence of the bacteria.


2. Dead neutrophils (called pus cells) release their proteolytic enzymes, which liquefy
   necrotic tissue and fibrin. The liquefied material mixed with pus cells and fluid exudate form
   pus.
   Characters and composition of pus:
   Pus is a non-coagulable (no fibrinogen) creamy alkaline yellowish or yellowish green fluid
   composed of:
   1- Fluid exudate without fibrin (liquefied).
   2- Cells: A large number of pus cells, PMNs, some macrophages and some erythrocytes.
   3- Necrotic fragments (sloughs) and liquefied necrotic tissue.
   4- Bacteria and bacterial pigments which may be yellowish (as in staphylococcal infections)
   or greenish (as in pyocyaneous infections).
   Types of suppurative inflammation:
   Localised:
   Caused by Staphylococcus aureus bacteria, which produce coagulase enzyme that leads to
   fibrin deposition leading to localisation. The most common forms of localised suppurative
   inflammation are:
   a. Abscess. b. Boil (furuncle). c. Carbuncle.
   II- Diffuse:
   Caused by Streptococcus haemolyticus bacteria, which produce hyaluronidase (the spreading
   factor) and streptokinase (fibrinolysin) which dissolves fibrin. The most common forms of
   diffuse suppurative inflammation are:
   a. Cellulitis. b. Suppurative appendicitis. c. Diffuse septic peritonitis.
   Abscess
   Abscess is a type of localised suppurative inflammation characterised by the formation of a
   cavity containing pus. It is commonly caused by staphylococcal infection. It can occur in any
   organ, but is most common in the subcutaneous tissues.
   Fate of abscess:
   1- Small abscess: Pus may be absorbed, followed by healing.
   2- Large abscess: Because absorption of pus occurs at a very slow rate, a big abscess
   undergoes pointing and rupture (spontaneous evacuation), followed by healing.
   Complications of abscess:
   1- Complications of evacuation and healing:
   a. Ulcer: It is a local defect or excavation of the surface (discontinuation of the epithelium).
   It is due to separation of inflammatory necrotic tissue and defective healing.
   b. Sinus: It is a blind ended tract between a deep abscess and the surface, e.g. a peritoneal
   abscess may cause sinuses on the abdominal wall.
   c. Fistula: It occurs if evacuation of a deep abscess results in a tract communicating between
   two surfaces or hollow organs, this tract with two openings is called fistula. Ano-rectal fistula
   complicating a perianal abscess is an example.
   d. Keloid.
   e. Hemorrhage e.g. hemoptysis when a large abscess opens into a bronchus.
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   2- Putrefaction: e.g. putrefaction of a lung abscess by saprophytes (a type of bacteria) leading
   to gangrene.
   3- Spread of infection:
   a. Direct spread leads to abscess enlargement.
   b. Lymphatic spread leads to lymphangitis and lymphadenitis.
   c. Blood spread may lead to:
   i- Toxaemia: Bacterial toxins circulating in the blood.
   ii- Septicaemia: Large number of virulent bacteria & their toxins circulating in blood.
   Commonly fatal.
   iii- Pyaemia: Multiple small abscesses caused by septic emboli derived from septic thrombi
   due to septic inflammation of veins near the abscess (septic thrombophlebitis).
   4- Compression effects: e.g. in case of brain abscess and liver abscess.
   5- Chronicity: If the abscess is neither evacuated spontaneously nor surgically, it gets
   surrounded by fibrosis and becomes a chronic abscess. Pus dries and dystrophic calcification
   may occur. Examples:
   a. Chronic breast abscess: May be clinically mistaken for a tumour.
   b. Chronic lung abscess.
   Furuncle (Boil)

• Staphylococcal infection of the hair follicles (folliculitis) is common in the face of males
  and axilla of females.


• Folliculitis may regress, or progress to suppuration leading to formation of small abscess
  related to the hair follicle called furuncle or boil.


• Furuncles are commonly multiple (furunculosis).
  Carbuncle
  Is a special type of localised suppurative inflammation characterised by multiple
  communicating deep subcutaneous abscesses, each of which opens onto the surface by a sinus
  i.e. multiple sinuses occur.


• It only occurs in special sites where the skin and subcutaneous tissues are thick and tough
  due to dense fibrous septa that extend between the deep fascia and the dermis; thus dividing
  the subcutaneous fat into compartments, therefore infection reaching these multiple
  compartments leads to multiple suppurative foci.


• Sites of carbuncle include back of neck, scalp & buttocks.


• It is more common in diabetics due to low immunity and infection usually starts as a boil
  then spreads causing a carbuncle.
  Cellulitis
  Cellulitis is an acute diffuse suppurative inflammation, more common in diabetics.
  Differences between cellulitis and abscess
  Criteria Cellulitis Abscess
  Definition Acute diffuse suppurative
  inflammation.
  Acute localised suppurative
  inflammation.
  Aetiology Caused by Streptococcus
  haemolyticus.
  Caused by Staphylococcus
  aureus.
  Character of
  causative
  agent.
  Bacteria secrete fibrinolysin &
  hyaluronidase
  Bacteria secrete coagulase.
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  Site Occurs in loose connective
  tissues as subcutaneous tissues,
  areolar tissue of orbit, scrotum
  and pelvis.
  Occurs in any organ or tissue but
  is most common in subcutaneous
  tissue.
  Characters
  of pus.
  a. Thin, because fibrinolysin
  antagonizes fibrin deposition;
  thus the amount of liquefied
  fibrin within pus is small.
  b. Sanguineous i.e. contains
  numerous erythrocytes.
  c. Contains many sloughs due to
  more extensive necrosis.
  a. Thick due to the presence of
  large amount of liquefied fibrin.
  b. Contains few erythrocytes.
  c. Contains few sloughs.
  Spread Spread of infection is more
  common (direct, lymphatic &
  blood spread).
  Spread of infection is less
  common.
  Acute Non-Suppurative Inflammation
  1- Serous Inflammation:
  Characterised by excessive serous fluid poor in fibrin. This fluid is either derived from
  blood (exudate) or from secretions of the mesothelial cells (in case of inflammation of
  serous membranes).
  *Examples:
  a. Skin blisters due to skin burns.
  b. Epidermal vesicles due to herpes
  simplex viral infection.
  c. Inflammation of serous memb (pleura, pericardium and peritoneum).
  2- Fibrinous Inflammation:
  Characterised by an exudate rich in fibrin, with a little fluid component.
  *Examples:
  a. Lobar pneumonia: The excessive fibrin participates in consolidation of the affected areas.
  b. Adult hyaline membrane disease (adult respiratory distress syndrome):
  c. Inflammation of serous membranes.
  3- Serofibrinous Inflammation
  As shown above, inflammation of serous membranes may be of the serous type (sometimes
  referred to as the wet type of serofibrinous inflammation) or fibrinous type (sometimes
  referred to as the dry type of serofibrinous inflammation). It is worth noting that serous
  membranes may be affected by other types of inflammation other than serous and fibrinous,
  e.g. suppurative inflammation
  Gross Picture:
  The visceral and parietal layers of the serous membranes are thickened, reticulated, opaque
  and greyish in case of fibrinous type.
  The serous sac contains abundant serous fluid (effusion) in case of the serous type.
  Microscopic Features:
  The subserosa shows dilated capillaries, fibrin and acute inflammatory cells.
  In case of fibrinous inflammation, the serosal layer is covered by a thick network of fibrin
  entangling acute inflammatory cells.
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  4- Catarrhal Inflammation:
  Characteristics: A mild form of acute inflammation of mucous membranes characterized by
  an exudate mixed with mucous secreted by the irritated mucous membrane. *Examples: a.
  Catarrhal rhinitis (common cold) b. Catarrhal appendicitis.
  Gross Picture:
  Swollen hyperemic mucosa pouring a discharge of serous fluid mixed with mucous.
  Microscopic Picture:
  Epithelial cells of the mucosa are swollen and vacuolated due to excess mucin (mucoid
  degeneration). The submucosa shows dilated capillaries, PMNs, macrophages and fibrin.
  5- Pseudomembranous (Membranous) Inflammation:
  Characteristics & pathogenesis: Severe form of acute inflammation of mucous membranes
  caused by bacteria that produce exotoxins leading to mucosal necrosis and marked
  submucosal inflammation resulting in formation of false membrane composed of necrotic
  mucosal patches and excessive fibrin.
  Examples: a. Diphtheria. b. Bacillary dysentery.
  Gross Picture:
  The original mucous membrane is replaced by another (false) membrane, which appears
  yellowish gray, thick and adherent. If forcibly removed, it leaves a bleeding surface and is
  reformed rapidly.
  Microscopic Picture:
  The false membrane consists of necrotic patches, fibrin, bacteria and acute inflammatory
  cells. The underlying submucosa shows dilated capillaries, fibrin and acute inflammatory
  cells (PMNs and macrophages).
  6- Other Types of Acute Non Suppurative Inflammation:
  Haemorrhagic Inflammation:
  Characterised by excessive erythrocytes within the exudate due to associated vascular
  damage. Example: Small pox.
  Necrotizing Inflammation:
  Characterised by extensive necrosis in association with inflammation.
  Example: Cancrum oris.
  Allergic Inflammation:
  The underlying cause of inflammation is hypersensitivity. There are usually many
  eosinophils.
  Examples: Urticaria, allergic rhinitis and bronchial asthma.