Workshop 6

Definition: The inflamation represents the common response of tissues to different pathogens. Depending on persistence of the etiological agents and of the type of tissue reaction inflammation could be: - ACUTE; - CHRONIC.

• • • It is a rapid response to an injurious agent, It has short duration (hours or days)2 weeks It implies three major changes: cellular, umoral and vascular

Vasculo-cellular changes in the inflammatory focus Vascular changes
 Changes of vascular caliber:
• • transitory vasoconstriction; vasodilation with the opening of the capillaries – Transudate formation

Cellular changes
Blood cells

 Changes of the blood circulation speed:
- Diminution of the blood flow;

 Leukocyte extravasation:
– margination and rolling; – adhesion and diapedesis; – migration in tissues. Inflammatory cells

 Changes in the vascular permeability:
– Exudate formation (rich in proteins).

Vascular changes

3. Incetinirea curentului sanguin in venule (staza)

Location of inflammation– in a vascularized connective tissue

Vascular changes

• •

Transitory vasoconstriction; Vasodilatation of the arterioles → opening of the entire capillary bed (calor and rubor)  with transudate formation; • The slowing of the circulation; • Increasing of the vascular permeability (microcirculation) =Endothelial cell contraction with intercellular space formation with exudate formation; • Producing of stasis with leucocyte margination;
Location of inflammatory focus – in a vascularized connective tissue

Cellular changes

Cellular changes / Leucocyte changes
• • • Leucocyte margination The leucocyte rolling on the endothelial surface; Diapedesis - the leucocyte movement outside of the vessel or migration of neutrophils


Neutrophil fagocitosis

The neutrophil
 It is the characteristic element of acute inflammation  Represents 70% from circulating leukocytes;  It has a polilobated nucleus (segmented leukocyte);  It contains 2 types of neutral granules (ME): - azurophile granules (lysosomes); - specific granules (alkaline phosphatase, lactofferin, lisosime and collagenase).  They have a very short life, of about 1-3 days  By destruction they release the lysosomal enzymes. ME

Coloraţia MGG


The macrophage
 It is the cell derived from monocyte;

 It appears in the inflammatory focus after the neutrophil;

Monocit (coloraţia MGG)

 It presents : - a renal shape nucleus; - abundant cytoplasm containing:
– – – – pinocytosis vacuoles; mitocondria; lisosomes secretory granules.


neutrophil diapedesis

Inflammatory exudate
• Inflammatory exudate = the result of all morphological changes in the inflammatory focus • Macroscopically
• the inflammatory exudate is a yellowish fluid riched in proteins (resembling with the blood serum/plasmatic fluid)

• Microscopically
• the inflammatory exudate is an intense eosinophilic fluid (increased amount of proteins)

Inflammatory exudate
• inflammatory exudate composition:
– plasma fluid, which is riched in proteins: albumin, globulin and fibrinogen; – cells: PMN, MF; – others: tissue debris & causative agent;

• depending on the severity and duration of the action of the causative agent
– there are variations in the exudate composition with the production of various types of inflammatory exudate

• the inflammatory exudate is the morphological substrate in different types of acute inflammations

• Serous exudate acute serous inflammation; • Fibrinous exudate acute fibrinous inflammation; • Purulent exudate: acute purulent inflammation; • Catharal exudate: catharal inflammation; • Haemorrhagic exudate: haemorrhagic inflammation;

Varieties of inflammatory exudate and acute inflammations

The serous exudate – increased fluid component (rich in proteins: albumins and globulins).

Serous alveolitis
In the alveolar walls :
 dilatation/congestion of parietoalveolar capillaries

 In alveolar lumen: serous exudate
 eosinophilic fluid;  a few neutrophils;  eritrocytes;  variable amount of bacteria. HE staining

Fibrinous exudate – rich in fibrin (fibrin=precipitation of fibrinogen as a network in the inflammatory focus).

Fibrinous alveolitis :
 In alveolar walls: – Dilatation/congestion of parietoalveolar capillaries  In alveolar lumen: fibrinous

exudate  It appears as a network merging through Kohn pores from an alveolus to another;  neutrophils;  eritrocytes;  Infectious agents.

Mallory staining

Fibrinous pericarditis
 On the surface of epicardium:

 Intense eosinophilic exudate - red network;  neutrophils;  eritrocytes.
 Epicardium:

 vascular dilation/congestion;  neutrophils.

HE staining

The purulent exudate is composed from:
      Neutrophiles; Macrophages; Eritrocytes; Necrotic debris; Fibrin; Bacteria.

The purulent inflammation can be: DIFFUSE LOCALISED

pus smear (MGG)

purulent exudate  rich in cellular elements
(espeacially, integre and altered neutrophils).

Purulent alveolitis :
 In alveolar walls: – Dilatation/congestion of parietoalveolar capillaries  In alveolar lumen: purulent exudate
      Neutrophiles; Macrophages; Eritrocytes; Necrotic debris; Less fibrin; Bacteria. HE staining

Purulent Leptomeningitis  The meninges is diffusely thickened
– –


purulent exudate; vascular dilatation/congestion.

 The dilated vessels: – leukocyte margination and diapedesis

HE Coloraţia HE

Purulent Leptomeningitis
– leukocyte margination and diapedesis

HE staining


• The abscess:
– localisated purulent inflammation;

– Recent – Chronic

Recent cerebral abscess
• Centrally:
– purulent exudate;

• At periphery:
– The fibrin wall.
Coloraţia HE

Cronic hepatic abscess • Centrally: cavity containing
purulent exudate;

 At the periphery: abscess wall = pyogenic membrane
 Interior part – fibrin network  Exterior part- connectivevascular tissue

HE Staining

Sign up to vote on this title
UsefulNot useful