Page 160 - Textbook of Pathology, 6th Edition

144 and shape. These giant cells are not derived from ii) Immune status of host. Patients who are immuno-
macrophages but are formed from dividing nuclei of the suppressed from congenital or acquired immunodeficiency
neoplastic cells e.g. carcinoma of the liver, various soft tissue have lowered inflammatory response and spread of
sarcomas etc. infections occurs rapidly e.g. in AIDS, congenital immuno-
ii) Reed-Sternberg cells. These are also malignant tumour deficiency diseases, protein calorie malnutrition, starvation.
giant cells which are generally binucleate and are seen in iii) Congenital neutrophil defects. Congenital defects in
various histologic types of Hodgkin’s lymphomas. neutrophil structure and functions result in reduced
iii) Giant cell tumour of bone. This tumour of the bones has inflammatory response.
uniform distribution of osteoclastic giant cells spread in the iv) Leukopenia. Patients with low WBC count with
SECTION I
stroma. neutropenia or agranulocytosis develop spreading infection.
v) Site or type of tissue involved. For example, the lung
FACTORS DETERMINING VARIATION IN has loose texture as compared to bone and, thus, both tissues
INFLAMMATORY RESPONSE react differently to acute inflammation.
Although acute inflammation is typically characterised by vi) Local host factors. For instance, ischaemia, presence of
vascular and cellular events with emigration of neutrophilic foreign bodies and chemicals cause necrosis and are thus
leucocytes, not all examples of acute inflammation show cause more harm.
infiltration by neutrophils. On the other hand, some chronic
inflammatory conditions are characterised by neutrophilic 3. Type of Exudation
infiltration. For example, typhoid fever is an example of acute The appearance of escaped plasma determines the morpho-
inflammatory process but the cellular response in it is logic type of inflammation as under:
lymphocytic; osteomyelitis is an example of chronic
inflammation but the cellular response in this condition is i) Serous, when the fluid exudate resembles serum or is
mainly neutrophilic. watery e.g. pleural effusion in tuberculosis, blister formation
The variation in inflammatory response depends upon a in burns.
number of factors and processes. These are discussed below: ii) Fibrinous, when the fibrin content of the fluid exudate is
high e.g. in pneumococcal and rheumatic pericarditis.
1. Factors Involving the Organisms
iii) Purulent or suppurative exudate is formation of creamy
i) Type of injury and infection. For example, skin reacts pus as seen in infection with pyogenic bacteria e.g. abscess,
to herpes simplex infection by formation of vesicle and to acute appendicitis.
General Pathology and Basic Techniques
streptococcal infection by formation of boil; lung reacts to iv) Haemorrhagic, when there is vascular damage e.g. acute
pneumococci by occurrence of lobar pneumonia while to haemorrhagic pneumonia in influenza.
tubercle bacilli it reacts by granulomatous inflammation.
v) Catarrhal, when the surface inflammation of epithelium
ii) Virulence. Many species and strains of organisms may produces increased secretion of mucous e.g. common cold.
have varying virulence e.g. the three strains of C. diphtheriae
(gravis, intermedius and mitis) produce the same diphtherial MORPHOLOGY OF ACUTE INFLAMMATION
exotoxin but in different amount.
Inflammation of an organ is usually named by adding the
iii) Dose. The concentration of organism in small doses suffix-itis to its Latin name e.g. appendicitis, hepatitis,
produces usually local lesions while larger dose results in cholecystitis, meningitis etc. A few morphologic varieties of
more severe spreading infections.
acute inflammation are described below:
iv) Portal of entry. Some organisms are infective only if 1. PSEUDOMEMBRANOUS INFLAMMATION. It is
administered by particular route e.g. Vibrio cholerae is not inflammatory response of mucous surface (oral, respiratory,
pathogenic if injected subcutaneously but causes cholera if bowel) to toxins of diphtheria or irritant gases. As a result of
swallowed.
denudation of epithelium, plasma exudes on the surface
v) Product of organisms. Some organisms produce enzymes where it coagulates, and together with necrosed epithelium,
that help in spread of infections e.g. hyaluronidase by forms false membrane that gives this type of inflammation
Clostridium welchii, streptokinase by streptococci, its name.
staphylokinase and coagulase by staphylococci.
2. ULCER. Ulcers are local defects on the surface of an organ
produced by inflammation. Common sites for ulcerations are
2. Factors Involving the Host
the stomach, duodenum, intestinal ulcers in typhoid fever,
i) Systemic diseases. Certain acquired systemic diseases intestinal tuberculosis, bacillary and amoebic dysentery,
in the host are associated with impaired inflammatory ulcers of legs due to varicose veins etc. In the acute stage,
response e.g. diabetes mellitus, chronic renal failure, cirrhosis there is infiltration by polymorphs with vasodilatation while
of the liver, chronic alcoholism, bone marrow suppression long-standing ulcers develop infiltration by lymphocytes,
from various causes (drugs, radiation, idiopathic). These plasma cells and macrophages with associated fibroblastic
conditions render the host more susceptible to infections. proliferation and scarring.