1. Inflammation 2

2. Local signs in acute inflammation:
1-Redness
2-Hotness
3-Swelling
4-Pain
5-Loss of function
Pain; is due to:
Stretching of tissue by inflammatory exudate with irritation of nerve endings.
Release of mediators as prostaglandins and bradykinin

3. Morphology of acute inflammation
severity of the inflammatory response
its specific cause
tissue involved
Morphology of acute inflammation
modify the basic, producing distinctive appearances.
The vascular and cellular reactions that characterize acute inflammation are reflected in the morphologic appearance of the reaction.
The severity of the inflammatory response, its specific cause, and the particular tissue involved can all modify the basic morphology of acute inflammation, producing distinctive appearances

4. Morphological patterns of acute inflammation
I-Non suppurative inflammation
II-Suppurative inflammation

5. Morphological patterns of acute inflammation
I-Non suppurative inflammation
Serous
Fibrinous
Catarrhal
Allergic
Pseudomembranous
Necrotizing
Hgic

6. vesicles in herpes pericardial effussion
1-Serous inflammation
Exudate:
Watery
Abundunt
protein poor
Examples:
Skin blister
vesicles in herpes pericardial effussion
Depending upon the site of injury, this fluid is derived either from the serum or from the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities e.g.

7. 2-Fibrinous inflammation
More severe injury
greater vascular permeability
large molecules (such as fibrinogen) to pass through endothelial barrier
Serous sacs.
Lung alveoli in lobar pneumonia.

8. Grossly: 2-Fibrinous inflammation Bread &butter appearance
The fibrin is precipitated on the inner surface of the parietal layer and on the outer surface of the visceral layer. So the serous membranes appear opaque and rough giving bread and butter appearance

9. 2-Fibrinous inflammation
Microscopically:
fibrin appears as an eosinophilic meshwork of threads
Fate
-Resolution (fibrinolysis)
-Organization
Fate: - degraded by fibrinolysis, and the accumulated debris may be removed by macrophages, resulting in restoration of the normal tissue structure (resolution).
- ingrowth of fibroblasts and blood vessels (organization), leading ultimately to scarring that may have significant clinical consequences.
suppurative inflammation and acute non-suppurative inflammation

10. 2-Fibrinous inflammation
Lung alveoli in lobar pneumonia.
Microscopically:
fibrin threads +
Inflammatory cells

11. 3- Catarrhal inflammation:
Mild
In mucous membranes
Eg. common cold
Gross:
Mucoid discharge
becomes yellow
Mic:
Swollen mucus cells edema
neutrophils

12. 4-Allergic inflammation
Cause :
Antigen antibody reaction
excess exudates
> edema
EOSINOPHILS
in tissue & blood
Eg:
1.Eczema 2.Urticaria
3.Allergic rhinitis
4.Bronchial Asthma

13. Patchy mucosal necrosis Inflammation rich in fibrin
5-Pseudo membranous inflammation:
Severe - mucous membrane
Bacterial
Exotoxin
Patchy mucosal necrosis
Inflammation rich in fibrin
Pseudomembrane
Diffuse to blood>
severe toxemia
powerful exotoxin → patchy necrosis
Pathogenesis:
The bacteria remain on the mucosal surface and produce powerful exotoxin resulting in patchy necrosis.
The exotoxin diffuses to the submucosa leading to acute inflammation with formation of exudate rich in fibrin that mixes up with the necrotic mucosa to form the pseudomembrane.
The exotoxin is absorbed in the blood causing severe acute toxaemia.

14. 5-Pseudo membranous inflammation:
Upper Resp tract :Diphtheria
Large intestine:Bacillary dysentery
Grossly: PSEUDOMEMBRANE
Mic:
Causative organism
Necrotic mucosa
Fibrin threads
PNL
RBCs
grayish white
loosely attached to the underlying tissue
easily detached
leaving bleeding ulcers
Diphtheria
Bacillary dysentery
pseudomembrane is grayish white, dirty, loosely attached to the underlying tissue and can be easily detached leaving bleeding ulcers

15. 6-Haemorrhagic inflammation
Severe
destruction of wall of
bl. vs with haemorrhage
acute haemorrhagic pneumonia
7-Necrotizing inflammation
with extensive necrosis
Vincent angina

16. Morphological patterns of acute inflammation
I-Non suppurative inflammation
II-Suppurative inflammation

17. II- Suppurative (purulent) inflammation:
.Pyogenic org.
.Marked tissue necrosis
Strong PNL chemotaxis
Dead PNL
Proteolytic enzymes liquefy necrotic tissue
mixes with inflammatory exudate
Staph
Strept
Meningiococci
E.coli
Def :Acute inflammation ccc by pus formation
Causative organism : Pyogenic bacteria
Pathogenesis of pus formation:
Pyogenic organisms
marked tissue necrosis
strong chemotaxis to PNL
Many neutrphils are killed by bacteria resulting in release of proteolytic enzymes (from dead neutrophils) that liquefy the necrotic tissue which mixes with the inflammatory exudates forming pus.
PUS

18. Composition of pus ?

20. II- Suppurative (purulent) inflammation:
strept
Localized
a.Abscess
b.variants
Diffuse
a.cellulitis
b.Phlegmnous
Staph

21. Empyema: Localized suppurative inflammation Staph aureus
a.Abscess
Localized suppurative inflammation
> cavity filled with pus
Staph aureus
Coagulase enzyme
Fibrinogen to
fibrin
localize infection
Empyema:
Pus in hollow organ

22. Pathogenesis of abscess1
Organism
Marked tissue necrosis
Strong chemotaxis
Central necrotic 2
Vascular phenomena
>pyogenic membrane = dilated congested capillaries, many neutrophils & organisms 3
Neutrophils die
>Proteolytic enzymes
>Liquefy periphery of necrotic area
>Pus
pyogenic membrane which is composed of many dilated congested capillaries, many neutrophils and the organisms.

23. How many zones in the abscess?
Central necrotic zone
Mid zone containing pus
Peripheral zone (pyogenic membrane) 3 1 2

24. Pathogenesis of abscess(cont.)5
abscess enlarges by further necrosis & liquefaction 6
coagulase enzyme→
transforming fibrinogen into fibrin
localize the suppuration 7
Pain
Open & discharge pus
The tension inside the abscess cavity gradually ↑→pain

25. Where abscess opens? Deep > Sinus Subcutaneous tissue kidney :
covering epidermis undergo necrosis and pus escapes
Deep > Sinus
kidney :
into the calyces & contents discharged with urine
narrow tract which connects abscess cavity with surface outside (sinus) ↓
blind end deeply & open end on the surface

26. II- Suppurative (purulent) inflammation:
Localized
Abscess
variants
Diffuse
cellulitis
Phlegmnous
Localized
Abscess
variants
Diffuse
cellulitis
Phlegmnous

27. Furuncle b.Variants of abscess (boil) Related to
hair follicle or sebaceous glands
Staph. aureus.
Face, back of neck & axilla

28. More in Back of neck & scalp
carbuncle
Pus is found in multiple loculi separated by f.t strands
Loculi open on the surface by multiple openings
More in Back of neck & scalp
PDF:DM
Each suppurative loculus develops in the same way as an abscess.

29. Complications of abscess
Chronic abscess
Blood spread >Toxemia –pyemia –bacteremia
Lymphatic spread>lymphangitis - lymphadenitis
Complications of healing:
-ulcer- keloid- sinus- fistula

30. Ulcer
Ulcer: 
Sinus
Local defect of skin or mucosal surface d.t necrosis and sloughing of cells of the skin, mucosa of the mouth, stomach, intestines, or genitourinary tract.
abnormal tract lined by septic granulation tissue connecting a cavity to the outside-has a blind end.
Abnormal tract lined by septic granulation tissue connecting 2 cavities or between hollow viscera & the surface
Sinus
Differs from sinus as it is opened from both ends
Fistula

31. Sinus
fistula

32. Fistula : Abnormal tract lined by septic granulation tissue connecting 2 cavities or between hollow viscera & the surface
Types of fistula
Congenital: thyroglossal
Inflammatory
Neoplastic
vesicovaginal fistula
in case of carcinoma of
the urinary bladder.
 Congenital; thyroglossal fistula.
 Inflammatory; appendicular fistula complicating acute suppurative appendicitis

33. Fistula
Vagina & rectum

34. a.Abscess b.variants a.cellulitis b.Phlegmnous
II- Suppurative (purulent) inflammation:
Localized
a.Abscess
b.variants
Diffuse
a.cellulitis
b.Phlegmnous
Localized
Abscess
variants
Diffuse
cellulitis
Phlegmnous

35. Diffuse Suppurative inflammation
Cellulitis
CT of orbit –pelvis-scrotum
Subcutaneous tissue
Phlegmonous
Mucous membrane

36. Cellulitis Streptococci Streptokinase Hyaluronidase Fibrinolysin
dissolve the mucopolysaccharide matrix
spread of infection
Stap aureus