Cells Of  The Exudate

Granulocytes (Neutrophils, eosinophils, and basophils)

Monocytes (and tissue macrophages)

Lymphocytes

Neutrophils (polymorphs).

Characteristics

(1) Cell of acute inflammation.

(2) Actively motile.

(3) Phagocytic.

(4) Respond to chemotactic agents like.

Complement products.

Bacterial products.

Tissue breakdown

Lysosomal enzymes of other polymorphs

Functions

(1) Phagocytosis and intracellular digestion of bacteria.

(2) Exocytosis of lysosomal enzymes to digest dead tissue as the first step in the process of repair.

Eosinophils

Characteristics

(I) Cell of allergjc and immunologic inflammation.

(2) Motile and phagocytic but less so than a neutrophil.

(3) Response to chemotaxis similar to neutrophil. In addition, it is also responsive to antigens and antigen-antibody complexes.

(4) Steroids cause depletion of eosinophils.

Functions

(1) Contain most of the lysosomal enzymes that polymorphs have

(2) control of Histamine release and degradation in inflammation

Basophils (and mast cells)

Characteristics

(1) Contain coarse metachromatic granules.

(2) Contain, histamine and proteolytic enzymes

Functions

Histamine: release which causes some of the changes of inflammation and allergic

reactions. .

Monocytes .

Blood monocytes form a component of. the mononuclear phagocytic system (MPS), the other being tissue macrophages The tissue macrophages may be :

(a) Fixed phagocytic. cells:

• Kuffer cell of liver.
• Sinusoidal lining cells of spleen and lymph nodes.
• Pleural and peritoneal macrophages
• Alveolar macrophages.
• Microglial cells.

(b) Wandering macrophages or tissue histiocytes.

The tissue histiocytes are derived from blood monocytes.

Characteristics

.(1)Seen in inflammation of some duration, as they -outlive polymorphs.

(2) Actively phagocytic and motile.

(3) Fuse readily to from giant cells in certain situations.

Function

(1) Phagocytosis.

(2) Lysosomal enzyme secretion.

(3) Site of synthesis of some components of complement.

(4) Antigen handling and processing before presenting it to the Immune  competent cell.

(5) Secretion of lysosyme and interferon.

Giant cells can be

(A) Physiological

Syncytiotrophoblast, megakatyocytes, striated muscle, osteoclast.

(B) Pathological:

Foreign body: in the presence of particulate foreign matter like talc, suture material etc. and in certain infections_e g fungal.

Langhan's type: a variant of foreign body giant cell seen in tuberculosis.

Touton type in lipid rich situations like Xanthomas, lipid granulomas etc.

(iv) Aschoff cell in rheumatic carditis.

(v) Tumour gjant cells e.g. Reid-Sternberg cell in Hodgkin's Lymphoma, giant cells in any malignancy.

Lymphocytes and Plasma cells

These are the small mononuclear cell comprising the immune system

They are less motile than_macrophages and  neutrophils and are seen in chronic inflammation and immune based diseases.

Agranulocytosis. Severe neutropenia with symptoms of infective lesions.

Drugs. are an important cause and the effect may be due to .
-Direct toxic effect.
-Hypersensitivity.

Some of the 'high risk drugs are.
-Amidopyrine.
-Antithyroid drugs.
-Chlorpromazine, mapazine.
-Antimetabolites and other drugs causing pancytopenia.

Bloodpicture:  Neutropenia with toxic granules in neutrophils. Marrow shows decrease in granulocyte precursors with toxic granules in them.

Systemic Candidiasis (Candidosis; Moniliasis)

Invasive infections caused by Candida sp, most often C. albicans, manifested by fungemia, endocarditis, meningitis, and/or focal lesions in liver, spleen, kidneys, bone, skin, and subcutaneous or other tissues.

Infections due to Candida sp account for about 80% of all major systemic fungal infections.

Symptoms and Signs

Esophagitis is most often manifested by dysphagia. Symptoms of respiratory tract infections are nonspecific, such as cough. Vaginal infections cause itching, burning, and discharge. Candidemia usually causes fever, but other symptoms are typically nonspecific. Sometimes, a syndrome develops resembling bacterial sepsis, with a fulminating course that may include shock, oliguria, renal shutdown, and disseminated intravascular coagulation.

Hematogenous endophthalmitis starts as white retinal plaques that can cause blindness as destructive inflammation progresses, extending to opacify the vitreous and causing potentially irreversible scarring. Most often, there are no symptoms in early stages of Candida endophthalmitis. If treatment is not begun before symptoms appear, significant or even total loss of vision is likely to occur in the affected eye. In neutropenic patients, eye involvement is more often manifested by retinal hemorrhages; papulonodular, erythematous, and vasculitic skin lesions may also develop.

Nephrosclerosis
 Disease of the renal arteries.

 Clinical manifestations:
 (1) Benign (arterial) nephrosclerosis →  Caused by the formation of atherosclerotic plaques in the renal artery. Results in narrowing of the arterioles.

(2) Malignant nephrosclerosis → Caused by malignant hypertension. Common signs of malignant hypertension include severe hypertension, retinal hemorrhages, and hypertrophy of the left ventricle. Results in inflammatory changes in the vascular walls, which may lead to rupture of the glomerular capillaries.

Eczematous Dermatitis
Eczematous dermatitis includes a large category of skin lesions characterized by severe pruritus and distinctive gross and microscopic features.
 - type I hypersensitivity is involved with atopic dermatitis in patients who have an allergic history.
 - type IV hypersensitivity is involved in contact dermatitis (poison ivy).
 - acute eczematous dermatitis is characterized by a weeping, pruritic rash, while a chronic eczematous dermatitis presents with dry, scaly, plaque-like thickening of the skin, a process called lichenification.  

The Specific Immune Response

Definition

The immune response comprises all the phenomenon resulting from specific interaction of cells of the immune-system with antigen. As a consequence of this interaction cells  appear that mediate cellular immune response as well cells that synthesis and secrete immunoglobulins

Hence the immune response has 2 components.

1. Cell mediated immunity (CMI).

2:. Humoral immunity (antibodies)

(I) Macrophages. Constituent of the M. P. S. These engulf the antigenic material.

(i) Most of the engulfed antigen is destroyed to' prevent a high dose paralysis of the Immune competent cells.

(ii) Some of it persists in the macrophage, retaining immunogenecity for continued stimulus to the immune system.

(iii)The antigenic information is passed on to  effectors cells. There are two proposed mechanisms for this:

(a) As messenger RNA with code for the specific antibody.

(b) As antigen-RNA complexes.

(2) Lymphocytes. There are 2 main classes recognized by surface characteristics.

(A) T-Lymyhocytes (thymus dependant) :- These are responsible for cellular immunity . On exposure to antigen 

• They transform to immunoblasts  which divide to form the effectors cells.
• They secrete lymphokines These are
  • Monocyte migration inhibition factor
  • Macrophage activation factor
  • Chemotactic factor
  • Mitogenic factor
  • Transfer factor
  • Lymphotoxin which kills target cell
  • Interferon.
  • Inflammatory factor which increases permeability. .
• Some remain as 1onglived memory cell for a  quicker recognition on re-exposure
• They also modify immune response by other lymphocytes in the form of “T – helper cells “ and “T-suppressor” cells
• They are responsible for graft rejection

(B) B-Lymphocytes (Bursa dependent). In birds the Bursa of Fabricious controls

these cells. In man, its role is taken up by," gut associated lymphoid tissue)

(i) They are responsible for antibody synthesis. On stimulation they undergo blastic transformation and then differentiation to plasma cells, the site of immunoglobulin synthesis.

(ii) They also form memory cells. But these are probably short lived.

(C) In addition to T & B lymphocytes, there are some lymphocytes without the surface markers of either of them. These are 'null' cells-the-natural Killer (N,K.) cells and cells responsible for antibody dependent cellular-cytotoxicity.

(3) Plasma cells. These are the effectors cells of humoral immunity. They produce the immunoglobins, which are the effector molecules.