Escolar Documentos
Profissional Documentos
Cultura Documentos
Presented
By
Ahmed El-Rashedy
Professor & Previous Head
of Pathology Department
Al-Azhar University
Inflammation
Def.: It is a series of vital reaction of a living tissue in
response to an irritant.
Types of irritants: Irritant is a stimulus causing either
reversible or irreversible cell injury. Irritants include:
1. Physical agents: Heat, Coldness, Trauma, Severe
pressure.
2. Chemical agents: Acids, Alkali, Corrosives.
3. Irradiations: whether ionizing or non-ionizing.
4. Allergens: whether injectable (aspirin, penicillin) ,
Ingestible drugs ( sulphonamide) or foods as egg,
chocolate, fish, meat or inhaled as dust or perfumes.
5. Biological agents: Fungi, Bacteria, Viruses,
Parasites, etc.
Acute
Chronic
1. Onset
2. Irritant
Sudden
Severe.
Gradual
Mild.
3. Duration
Longer (months-years)
4. Course
Rapidly progressive
Slowly progressive
5. Exudate:
A) Fluid part.
B) Cellular part
Excess
Moderate
Little
Excess
Polymorphs (Neutrophils).
Pus cells ( Dead polymorphs).
RBCs.
Macrophages.
Eosinophils.
Plasma cells.
Lymphocytes.
Macrophages(Histiocytes).
Giant cells.
Fibroblasts.
Eosinophils.
From tissue histiocytes.
6. Types of cells
7.
Origin
of From blood monocytes.
macrophages
8. Arrangement
Diffuse.
9. Vascular changes Mild.
Perivascular or diffuse.
Marked.
Acute
Chronic
11. Repair
Follow.
Associate.
12.Granulation tissue
Absent
Present
13.Fibrosis
Absent
Marked.
14.Toxemia
Severe.
Mild.
15.CardinalSigns
Redness hotness
Absent except swelling.
pain swelling loss of
function.
present.
usually absent.
Total
leucocytic count is normal
or decrease
16.General changes as
fever and leucocytosis
17.Types
Chemical Mediators
Def.: They are chemical substances released in response to an
inflammatory process mediating it.
Origin:
1. Plasma.
2. Inflammatory cells.
3. Damaged tissue.
Classification: They are classified into:
1. Group I: Vasoactive amines as histamine & serotonin.
2. Group II: plasma proteases which are subdivided into:
A) Kinin system: as Bradykinin & Kallikerin.
B) Complement system: particularly C3a, C5a, C5b, C9.
C) Coagulation-fibrinolytic system: as fibrinopeptides & fibrin
degradation products.
3.Group III: Arachidonic acid derivatives as prostaglandins &
leukotrienes.
4.Group IV: Lysosomal constituents as acid proteases (acting on
intracellular proteins) & neutral proteases (acting on extracellular
proteins).
Action
1. Vasoconstriction
Leukotrienes.
2. Vasodilatation
Prostaglandins.
3. Increased Capillary
permeability
Leukotrienes.
Vasoactive amines (Histamine & Serotonin).
Bradykinin.
Complements ( C3a & C5a ).
Platelet activating factor (PAF).
4. Pain
Prostaglandins.
Bradykinin.
5. Fever
Prostaglandins.
Interleukin -1(IL-1) & Tumor necrosis factor (TNF).
6. Chemotaxis
Leukotrienes.
C5a.
Bacterial Products.
7. Tissue damage
Fluid exudate
2. Cellular exudate.
1. Composition:
Cellular exudate
Acute inflammatory cells:
Polymorphs or neutrophils or
polymorphonuclear
leukocytes
(PNLs) .
Pus cells (dead PNLs).
Macrophages.
Eosinophils & Mast cells.
RBCs.
Chronic inflammatory cells:
Lymphocytes.
Plasma cells.
Macrophages or Histiocytes.
Giant cells.
Eosinophils.
RBCs.
Fibroblasts.
2. Function:
Fluid exudate
Cellular exudate
Dilution of toxins.
Provides
antibodies
(antitoxins & precipitins).
Fibrin acts by:
1.Blocking the meshes of
the tissue &thus localizing
the infection.
2. Acts as a scaffold or
railway upon which PNLs
traverse.
3. Helps the repair which
starts early at the site of
fibrin.
1.PNLs:
Active phagocytosis that is the engulfing of
irritant & digesting it through release of their
mediators (lysosomal or lytic enzymes).
2. Macrophages( Scavenger cells):
They are derived from blood monocytes thus
they engulf microorganisms and necrotic
debris converting them into soluble
substances through their own lysosomal
enzymes as well as wash them out to
prepare the inflamed area for healing.
3.Eosinophils:
They are increased (eosinophilia) in :
a)Allergic conditions: as Urticaria &
Bronchial asthma.
b) Parasitic diseases: as Bilharziasis,
Amoebiasis , Leishmaniasis..etc.
They produce IgE.
4. Mast cells: They release vasoactive
amines that act in the inflammatory process.
Fluid exudate
2. Function:
Cellular exudate
5. Lymphocytes:
They function in both humoral (B-cells) & in
cell-mediated response( T- cells that produce
lymphokines group of chemical mediators).
6. Plasma cells:
They arise from B-lymphocytes & function in
humoral immunity through producing
immunoglobulins (antibodies).
7. Giant cells:
They function in phagocytosis of F.B. ,
bacteria or tumor cells.
8. Fibroblasts:
Active cells synthesize the collagen fibers,
growth factors and proteoglycans of ground
substance & basement membranes.
Transudate
High ( > 3 gm % )
Low ( < 3 gm % )
High
Low
3. Cellular content
Hypercellular
(rich in cells)
Hypocellular
(Poor in cells)
4. Specific gravity
> 1018
< 1018
5.Coagulation on standing
Present
Absent
6. Origin
Plasma
Interstitial fluid
or serous fluid
Inflammation
1. Protein content
2. Fibrinogen content
7. Example
Acute Inflammation
Suppurative ( Pyogenic or Septic)
Localized
1. Abscess.
2. Boil (Furuncle = small abscess).
3. Carbuncle ( Multilocular abscess).
I)Abscess
Def.:
Localized suppurative inflammation caused mainly
by staphylococci.
Pathogenesis:
Staphylococci produce coagulase enzyme that
converts fibrinogen into fibrin , thus, localizes the
infection.
I) Abscess
Pathology:
A) Early:
The abscess is formed of two layers:
1. Central core of necrotic tissue.
2. Outer pyogenic layer.
B) Late:
1. Central core of necrotic tissue.
2. Intermediate pus ( by liquefaction of the necrotic
tissue).
3. Outer pyogenic layer.
N.B. Pus is formed of :
1.Liquefied necrotic tissue.
2.Living & dead bacteria.
3.Living & dead polymorphs.
4.Fluid exudate.
5.Fibrin threads.
6.Few RBCs.
I) Abscess
Fate :
Due to the increased osmotic pressure inside the abscess, fluid is dragged
from the surroundings with increased tension within the abscess causing
severe throbbing pain followed by spontaneous rupture & drainage.
Complications:
A) Local:
1. Sinus:
A tract with one opening joining the abscess cavity with skin surface.
2. Fistula:
A tract with two openings joining two hollow organs or a hollow organ with
skin surface.
3. Ulcer :
Persistent loss of the epithelial continuity.
4. Chronicity:
A conversion of acute into chronic abscess (Table discussed later).
5. Local spread:
Dissemination into the surrounding tissues e.g. pyogenic liver abscess
spreads into the lung.
I) Abscess
B) Systemic:
1. Toxemia: Presence of bacterial toxins (whether endotoxins or exotoxins)
circulating in the blood stream.
2. Bacteremia: Temporary presence of only low virulent bacteria circulating in
the blood stream usually without any symptoms (asymptomatic).
3. Septicemia: Presence of highly virulent bacteria & their toxins circulating in
the blood stream.
4. Pyemia: Presence of bacterial clumps or septic emboli circulating in the blood
stream to reach organ(s) causing multiple abscesses.
It is two types:
a)Portal pyemia: Septic emboli carried to the liver by portal circulation.
b)Systemic pyemia: Septic emboli carried to different organs including the liver
by general circulation.
5. Systemic spread:
a)Through lymphatics (Lymphangitis) into the draining lymph nodes
(lymphadenitis).
b)Through systemic or pulmonary circulation giving pyogenic single abscess in
different organ or lung respectively.
Chronic abscess
2. Content
3. Cell type
By incision
By excision
Absent
May occur
1. Wall
4. Treatment
5. Calcification
II)Boil (Furuncle)
Def.: It is a small abscess related to hair follicle or to a sebaceous gland.
Multiple small abscesses related to several hair follicles cause a condition
known as Furunculosis.
III) Carbuncle
Def.: It is multilocular abscess with multiple sinuses discharging pus.
Site: It occurs commonly in the nape (back of the neck) of a diabetic
patient.
Acute Inflammation
Suppurative ( Pyogenic or Septic)
Diffuse ( = Cellulitis)
Def.: Cellulitis is a diffuse acute suppurative inflammation caused by
streptococci.
Pathogenesis: Streptococci release lytic enzymes (hyaluronidase &
fibrinolysin) that produce lysis of the tissue with diffuse pattern of
inflammation.
Sites:
1. Orbit.
2. S.C. of hands & feet.
3. Pelvic soft tissue.
Pathology:
1. Widespread slowly formed & thinner pus (than in abscess).
2. Marked RBCs formation (Sanguineous).
Complications:
Systemic complications (through blood & lymphatic spread like those of
acute abscess) commonly occur.
Treatment: Medical in form of:
1. Antibiotics.
2. Anti-inflammatory drugs.
Acute Inflammation
Non - suppurative ( Aseptic)
N.B.:
Tetany means carpo - pedal spasm due to hypocalcaemia as a result
of hypoparathyroidism.
Tetanus is an infective disease
characterized by necrosis &
putrefaction by Clostridium tetani.
Chronic Inflammation
Def.: A pathological condition characterized by persistence of the irritant
producing a progressive tissue damage together with a similar degree of
repair ( Fibrosis & regeneration ).
Characteristics:
1.Aggregation of chronic inflammatory cells forming a mass called granuloma.
2.The arterioles in the chronic inflammatory area showed thick wall & narrow
lumen ( End-arteritis obliterans= EAO).
3.The fluid exudate is scanty while the cellular exudate is abundant in chronic
inflammation.
Terminology
The term of inflammation ends by the suffix itis that is added to
the name of the affected organ.
The followings are examples of inflammation:
1. Encephalitis: inflammation of the brain tissue.
2. Meningitis: inflammation of the leptomeninges.
3. Dacryocystitis: inflammation of the lacrimal gland.
4. Blepharitis: inflammation of the eyelid.
5. Keratitis: inflammation of the cornea.
6. Iridocyclitis: inflammation of the iris & ciliary body.
7. Dermatitis: inflammation of the skin.
8. Rhinitis: inflammation of the nose.
9. Otitis media: inflammation of the middle ear.
10. Labyrinthitis: inflammation of the internal ear.
11. Glossitis: inflammation of the tongue.
12. Cheilitis: inflammation of the lips.
13. Stomatitis: inflammation of the mouth.
Terminology
14. Pneumonia: inflammation of the pulmonary alveoli.
15. Pneumonitis: inflammation of the lung interstitium.
16. Pleurisy: inflammation of the pleura.
17. Vasculitis: inflammation of an artery.
18. Phlebitis: inflammation of a vein.
19. Lymphangitis: inflammation of a lymph vessel.
20. Lymphadenitis: inflammation of a lymph node.
21. Gastritis: inflammation of the stomach.
22. Enteritis: inflammation of the small intestine.
23. Colitis: inflammation of the colon.
24.Proctitis: inflammation of the rectum.
25.Omphalitis: inflammation of the umbilicus.
26.Hepatitis: inflammation of the liver.
Terminology
27.Nephritis: inflammation of the renal tissue.
28.Pyelitis: inflammation of the renal pelvis.
29.Cystitis: inflammation of the urinary bladder.
30.Cholecystitis: inflammation of the gall bladder.
31.Cholangitis: inflammation of the bile duct.
32.Myometritis: inflammation of smooth muscle of uterus.
33.Endometritis: inflammation of lining epithelium of uterus.
34.Parametritis: inflammation of pelvic connective tissue.
35.Funnicultis: inflammation of the spermatic cord.
36.Orchitis: inflammation of the testis.
37.Palanitis: inflammation of the glans penis.
38.Salpingitis: inflammation of the Fallopian tube.
39.Synovitis: inflammation of the synovial membrane.
Terminology
40.Osteomyelitis: inflammation of bone cortex & marrow.
41.Dactylitis: inflammation of the terminal phalanx.
42.Onycolitis: inflammation of the nail bed.
43.Panniculitis: inflammation of the subcutaneous tissue.
44.Arthritis: inflammation of the joint.
45. Neuritis: inflammation of the nerve.
46.Osteitis: inflammation of the bone.
47.Chondritis: inflammation of the cartilage.
48.Tendenitis: inflammation of the tendon.
49.Fasciitis: inflammation of the fascia.
50.Myositis: inflammation of the muscles.
51.Parotitis: inflammation of the parotid gland.
52.Sialadenitis: inflammation of the salivary gland.
53.Cellulitis: acute diffuse suppurative inflammation.
Prof. Dr. Ahmed Elrashedy
Thank You