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5. Morphology acute inflammation
Morphological patterns of acute inflammation
Dominating pattern
1. Exudation
2. Necrosis and fibrinous exudation
3. Necrosis
1. DOMINATING PATTERN: EXUDATION
Types according to the extent of vascular permeability
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Serous inflammation
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Fibrinous inflammation
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Purulent inflammation
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Hemorrhagic inflammation
SEROUS INFLAMMATION
Exudate: watery, relatively protein-poor fluid, with scanty fibrin
Occurs
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On serous membranes (pleura, pericardium, peritoneum, synovium, meninges, conjunctiva)
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On respiratory/GI mucosa
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In the skin
On serous membranes
Causes
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Immune complexes in systemic lupus erythematosus (SLE): peritonitis, pleurisy, pericarditis  termed ”serositis”
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Viruses: meningitis, pericarditis, conjuctivitis
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Long-term exercise (e.g., long distance running)  synovitis
Morphology

Normally, the serous membrane is smooth and has a glistening surface.

In serous inflammation, it becomes reddish and opaque.
Outcome
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May heal completely
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May transform to fibrinous inflammation
On respiratory/GI mucosa
The mucous secretions dominate in the exudate because the mucous glands become stimulated  catarrhal inflammation
Causes
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Allergic reaction (hay fever) - rhinitis with profuse nasal discharge
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Viruses - airways: rhinitis, pharyngitis, bronchitis (sore throat, coughing)
- small bowels: enteritis (watery diarrhoea)
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Cold in children: rhinitis, pharyngitis, bronchitis
Gross features: the affected mucosa is hyperemic, swollen, and is covered by abundant mucous exudate
Outcome
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May heal completely
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Airways: superinfection with bacteria  mucopurulent rhinitis or tracheobronchitis
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May be lethal: rotavirus-induced enteritis
Serous inflammation of the larynx
Causes

Infection (Haemophilus influenzae, viruses)
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Drugs through allergic mechanisms
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Inhalation of toxic gases
Clinical consequence: sudden onset of hyperemia and swelling of mucosa of the vocal cords and epiglottis  edema of larynx
 airway obstruction  on occasion, death
Serous inflammation in the skin
Blister: serous exudate accumulates in the epidermis or along the epidermal-dermal junction
Vesicle; if larger than 5 mm: bulla
Causes
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Mechanical irritation (friction), burns
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Herpes virus varicellae-induced chickenpox or shingles
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Autoimmune: pemphigus
Outcome

May heal completely

Superinfection with St. aureus: the blisters are filled with pus (pustula)  sepsis may develop

Lethal: burns involving large areas
FIBRINOUS INFLAMMATION
Exudate: high content of fibrinogen  coagulates into a thick fibrin coating
Occurs on serous membranes or in the lungs
Causes on serous membranes
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Viruses: pleurisy, pericarditis, meningitis
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Chronic uremia: pericarditis
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Immune complexes in SLE: serositis, arthritis
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Irritation: adjacent to pulmonary infarction (pleurisy), myocardial infarction (pericarditis); joints - arthritis
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5. Morphology acute inflammation
Morphology

Macro: the serous membrane is opaque and reddish, and is covered by coagulated fibrin

Micro: the fibrin appears as homogeneous masses of eosinophilic material
Outcome
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May be removed by fibrinolysis  heals completely
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Abundant fibrin is converted to granulation tissue  fibrous strands bridge serous surfaces (adhesions)
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Bacterial superinfection  purulent inflammation
Clinical feature: fibrinous pleurisy or pericarditis  friction rub, thoracic pain
Fibrinous inflammation of the lungs: lobar pneumonia
Causative agent: Streptococcus pneumoniae. The entire lobe is affected; the exudate is localized in the alveoli
Morphology

Macro: the affected lobe is consolidated, resembles to the liver by palpation (hepatisation)
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Micro: fibrin fills the alveolar spaces, days later the exudate turns into purulent
Outcome
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Heals completely
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Complications develop, such as lung abscess
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Results in death
PURULENT INFLAMMATION
General features

Neutrophil granulocytes predominate in the exudate

Causative agents: pus-forming (pyogenic) bacteria, e.g., Staphylococcus, Streptococcus, Neisseria

Pus: viscous, creamy fluid composed of bacteria, viable and dead NGs, debris of liquefied tissues, exuded plasma
proteins

Sites: skin, deep tissues, preformed cavities, serosal surfaces, airways, urethra
Abscess
Liquefactive necrosis-induced cavity filled with pus

Sites: in the skin, perianal region, internal organs, brain, etc.

Deep-seated abscesses have a tendency to break through intramuscular septa. Eventually, the pus reaches a
surface, where it is discharged. Sinus tract (fistula): the channel draining the abscess

Healing: by fibrosis
Surgical drainage is often necessary to eliminate abscesses from deep sites
Purulent inflammation of the skin: abscesses and cellulitis; fequent in diabetics!
Abscesses of skin adnexa
Causative agent: Staphylococcus aureus
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Folliculitis - suppuration of a hair follicle

Furuncle (boil) - suppuration of a hair follicle + subcutaneous tissue
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Carbuncle - suppuration of several hair follicles + subcutaneous tissue
Cellulitis (erysipelas; phlegmon)
Caused by Streptococcus pyogenes

The bacteria produce hyaluronidase, which digests dermal connective tissue leading to diffuse spread of bacteria and
formation of purulent exudate along the dermis.

Clinical features: rapidly spreading, erythematous cutaneous swelling on the face, or on the body or an extremity in
middle-aged persons. The rash has a sharp, well-demarcated, serpiginous border + systemic symptoms: fever and
fatigue.

Responds to antibiotics
Pus accumulation in preformed cavities: empyema
Clinically important:
Empyema of
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gallbladder
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paranasal sinuses (maxillary, sphenoidal, ethmoidal, frontal)  complication: purulent meningitis
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middle ear (purulent otitis media): mainly in children; complication  perforation of the tympanic membrane
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thorax; healing: granulation tissue  secondary calcification: callus of pleura
Purulent inflammation of serous membranes

Acute purulent peritonitis: after perforation of an abdominal organ; the peritoneal surface is hyperemic and red, and is
covered by creamy exudate

Acute purulent meningitis: bacteria reach the subarachnoid space and induce purulent exudation
Outcome
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Both are frequently lethal
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In survivors, healing with fibrosis  adhesions
Purulent inflammation of respiratory mucous membranes

Mucous membranes form a tube, therefore, the exudate may appear distal to the primary site. The affected mucosa
is swollen, red and is covered by mucopurulent or purulent exudate
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Acute purulent bronchitis: with coughing, the exudate infects other parts of the bronchial tree and alveoli
(bronchopneumonia) and also appears as purulent sputum
Outcome
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5. Morphology acute inflammation
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•
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May heal completely
May turn into chronic
May result in death
Acute purulent urethritis
Caused by Neisseria gonorrhoeae, sexually-transmitted disease, termed gonorrhoea

Manifests as purulent discharge

Complications: purulent inflammation of the prostate, seminal vesicle, epididymis, and testis
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If untreated: healing by fibrosis  infertility
HEMORRHAGIC INFLAMMATION
Sufficient vascular damage  hemorrhages
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In the bladder: hemorrhagic cystitis, caused by Gram-negative bacteria; the bladder mucosa is swollen, hyperemic
and displays focal hemorrhages  hematuria
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In the lungs: if influenzavirus infects the alveoli  severe alveolar damage  hemorrhagic pneumonia; frequently
fatal
2) NECROSIS AND FIBRINOUS EXUDATION DOMINATES: PSEUDOMEMBRANOUS INFLAMMATION
Pathomechanism: a response of mucous surface to certain bacteria/fungi. The surface epithelium becomes necrotic  plasma
exudates from the submucosal vessels onto the necrotic surface, its fibrinogen content coagulates, and encloses the necrotic
epithelium  pseudomembrane
Pseudomembranous colitis

Clostridium difficile infection after antibiotic therapy eradicating normal bacterium flora of the gut
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Grossly, plaques of yellow fibrin and inflammatory debris adhere to a reddened mucosa; severe cases: enterocolitis

Clinical features: odorous diarrhea + septicotoxicosis
Outcome:
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May heal completely

May heal with granulation tissue
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May be lethal
3) NECROSIS DOMINATES
Comprises
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Necrotizing soft tissue infections
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Necrotizing pancreatitis
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Necrotizing inflammation caused by viruses
Necrotizing soft tissue infections
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Soft tissues: dermis, subcutis, superficial and deep fasciae, and muscles
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Etiology: via trauma or surgical wounds bacteria enter into the soft tissues
Prototype: necrotizing fasciitis; involves the extremities, the perineum and genital area (Fournier’s gangrene) and the
abdominal wall

Highly virulent, exotoxin-producing (e.g., Streptococcus) and/or gas producing bacteria (e.g., anaerobs, Clostridium
perfringens) proliferate, and the toxins cause thrombosis of the perforating vessels  inflammatory necrosis of fascia
and surrounding tissues

If gas production is abundant, extensive necrosis of tissues occurs (gas gangrene)
Clinical features
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Intense pain and swelling of the involved site, the overlying skin is erythematous and warm; myalgia
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Rapid spread reaching 2-3 cm/h septic shock within 24 hours; high mortality rate
Necrotizing inflammation of the pancreas
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Pancreatic proenzymes become activated within the pancreas
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Autodigestion and enzymatic necrosis of parenchyma and vessels
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Acute inflammatory reaction  acute necrotizing-hemorrhagic pancreatitis + systemic inflammatory response sy
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Frequently lethal
Necrotizing inflammation caused by viruses
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Viruses are small intracellular parasites, use host cell metabolism for their replication.
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Electron microscopy is necessary to visualize them;
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Certain viruses induce inclusion bodies which can be observed by light microscopy.
Pathomechanism of necrosis of virus-infected cells
1) Cytopathic viruses directly lyse cells, eg., respiratory epithelial cells. Cell lysis is a special form of necrosis. E.g.,
influenzavirus infection
2) Host CD8+ cytotoxic lymphocytes cause necrosis of virus-infected parenchymal cells: acute viral hepatitis, acute viral
myocarditis
Influenzavirus infection
Epidemic rhinitis and pharyngitis + tracheobronchitis
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Grossly: acute catarrhal or serohemorrhagic inflammation with intense intense mucosal hyperemia
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LM: necrosis of epithelial cells, lymphocytic and histiocytic infiltration of mucosa, mucus hypersecretion
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Clinical features: sudden onset, high fever, myalgias, cough, catarrhal discharge from nose
Outcome

Heals completely
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5. Morphology acute inflammation
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Complications: bacterial superinfection  purulent tracheobronchitis; the virus may infect the alveoli hemorrhagic
pneumonia
Lethal in patients with chronic heart disease, elderly people, in immunosuppressed individual
COMPARISON OF FEATURES OF MICROBIAL AND VIRAL INFECTION
Acute inflammation induced by bacteria

E.g.: bronchopneumonia
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Responding cells: neutrophils kill the bacteria + systemic signs: fever (IL-1, TNF from neutrophils and macrophages),
leukocytosis (WBC >12000/ul; qualitatively granulocytosis); increase in acute phase proteins
Acute inflammation induced by viruses
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E.g.: infectious mononucleosis
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Responding cells: T-lymphocytes eliminate the viruses + systemic signs: fever, leukocytosis (WBC >12000/ul;
qualitatively lymphocytosis); increase in acute phase proteins
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