General Reaction Patterns

Published on 19/03/2015 by admin

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Last modified 19/03/2015

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General Reaction Patterns

Pathologic anatomy, gross and microscopic, is the science of identifying and interpreting morphologic patterns and relating them to the physiologic and pathologic functions of a living organism. Pathology thus helps to elucidate the pathogenesis of diseases and to determine their classification. To correctly register morphologic changes, students of pathology must possess a solid knowledge of the normal composition and appearance of cells and tissues (i.e., normal anatomy and histology). Deviations from such normal appearances require pathologic interpretation. The student also should bear in mind 2 basic principles of pathologic anatomy:

1. All morphologic changes represent a dose-dependent effect in a “time-space window.” That is, first, below a lower-dose threshold of functional alterations, no morphologic lesions occur despite the patient’s apparent illness, and, second, there is a time delay between the occurrence of a functional disturbance and the development of morphologic changes (called morphogenesis). Space refers to the fact that morphologic lesions are most extensive at the site of “toxic impact” and become less severe (and possibly less typical) with increasing distance. This should be kept in mind when taking biopsies for pathologic evaluation.

2. Whatever the quality of injury, the living organism reacts with a limited number of patterns. There are variations to these patterns, which may provide us with clues to the etiology of the injury, but no entirely new reactions can be expected, even when a new pathologic agent (such as human immunodeficiency virus) arises.

Therefore, however clear pathologic anatomical lesions seem to be, the final evaluation with regard to the disease must result from a clinicopathologic correlation, i.e., from the careful evaluation of all the physical, biochemical, and anatomical findings.

General Reaction Patterns

This chapter covers 5 complex reaction patterns that apply equally to all cells, tissues, and organ systems:

1. Degeneration and atrophy

2. Apoptosis and necrosis

3. Inflammation and immunity

4. Regeneration, hypertrophy, and hyperplasia

5. Dysplasia, atypia, and neoplasia

Degeneration is the morphologic cell response to acute injury (i.e., reversible injury), which does not cause immediate cell death. Atrophy of individual cells or of their organized groups (tissues and organs) indicates a persistently catabolic metabolism that is not immediately lethal. Apoptosis and necrosis are distinct forms of cell death after irreversible cell injury. Inflammation is a microvascular response characterized by alterations in blood circulation (hyperemia, prestasis, and stasis), increased vascular permeability, exudation of blood fluids (edema, fibrinous exudates), margination and emigration of blood cell components, and passive expulsion of red blood corpuscles (hemorrhage). Activation of the immune system may result in different morphologic forms of inflammation depending on the nature of the initiating antigen (exogenous or autoimmune, soluble or particulate) and the reacting component of the immune system (T-cell or B-cell system). Regeneration, hypertrophy, and hyperplasia are forms of functional or structural repair or both of damaged cells and tissues. Neoplasia (“new growth”) is a disturbance of physiologic growth regulation with persistent activity of growth-promoting factors or loss of proliferation inhibition functions (or of physiologic apoptosis). It leads to benign or malignant tumorous growth patterns independent of or at the expense of surrounding cells and tissues.

All reaction patterns vary according to differences in composition of the reacting tissue or organ (e.g., extent of vascularization, amount of connective tissue, amount and distribution of parenchymatous cells and their respective regenerative potential) and to the quality and quantity of the (exogenous or endogenous) stimulus. Because the normal tissue composition is known and additional reactive changes can be observed with the unaided eye or with the help of a microscope, the character of the pathologic change reveals the nature of the stimulus and thus of the etiologic agent. Meticulous morphologic interpretation therefore contributes to the elucidation of the etiology and pathogenesis of diseases. This is the essential task and responsibility of the practitioner of general pathology.

The following figures provide examples of the 5 reaction patterns in different tissues and organs.

TABLE 1-1

BASIC TYPES OF B-CELL AND T-CELL IMMUNOREACTIONS *

Gell and Coombs Type	Alias	Mechanism
B-cell reactions
Type I IR	Allergic IR Atopic IR Anaphylactic IR	Cytophilic antibodies (e.g., IgE) bind to mast cells; antigen binding to these cell-bound antibodies causes mast cell degranulation with release of vasoactive mediators (e.g., histamine), which initiate the microvascular inflammatory response (thrombocytes and eosinophils cooperate).
Type II IR	Toxic or cytotoxic IR	Complement-binding antibodies (on antigen binding) activate complement cascade, members of which initiate inflammatory response by activating cell chemotaxis and phagocytosis, ultimately causing toxic cell and tissue damage.
Type III IR	Immunocomplex IR	Persistence of antigen-antibody complexes are recognized by the immune system as foreign and induce the production of secondary anticomplex antibodies (i.e., anti-antibodies, such as rheumatoid factor); these bind and activate complement and cause tissue lesion through complement components (see above).
T-cell reactions
Type IV IR	Cell-mediated IR T-cell cytotoxic IR CTL response	a. Direct destruction of target antigenic cells by binding of CTL, Fas-related induction of apoptosis, and/or release of perforin and granzymes b. T-cell cytokine response activation of macrophages: granulomatous (e.g., IFN-γ, TNF) reaction c. T-cell cytokine response activation of mast cells: basophil reaction (e.g., IL-3, IL-5) d. T-cell cytokine response: activation of vasoproliferative factors (e.g., IL-3, IL-8)

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