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• Histology is the study of microscopic anatomy, focusing on the various cells and components of human tissue
• Histopathology studies disease manifestation through microscopic anatomy, relying on both macroscopic and microscopic observation of organs and tissues
• Histotechnology involves preparing tissues for microscopic examination, including fixation, tissue sectioning, and staining, with actual microscopic examination performed by trained pathologists
• Cells are the basic unit of tissue, traditionally divided into epithelial and mesenchymal types
• Cellular adaptation includes reversible functional and structural responses to physiologic stresses and pathologic stimuli, leading to new altered steady states allowing the cell to survive and function
• Cellular adaptation can result in hypertrophy (increase in cell size), hyperplasia (increase in cell number), atrophy (decrease in cell size or metabolic activity), and metaplasia (change in cell phenotype)
• Inflammation is a protective response designed to remove the initial cause of cell injury (e.g. microbes, toxins) and the consequences of such injury (e.g. necrotic cells and tissues)
• Hypertrophy refers to an increase in tissue or organ size due to enlarged individual cells, which can be physiological (normal) or pathological (disease-related)
• Pathological hypertrophy can be seen in conditions like hypertension causing the heart muscle to become hypertrophic, particularly the left ventricle
• Without inflammation, infections would go unchecked, wounds would never heal, and injured tissues might remain permanent sores
• Hyperplasia is an increase in the number of cells in a tissue or organ, often occurring as a compensatory mechanism to repair tissue damage, and can be physiologic or pathologic
• Inflammation is generally beneficial to the body, but it can also be detrimental
• Physiologic hyperplasia can occur in situations like hormonal changes during pregnancy or compensatory growth of liver tissue after injury
• Examples of inflammation-related conditions include fever, asthma, and rheumatoid arthritis
• Pathological hyperplasia, like endometrial hyperplasia, can increase the risk of developing cancer
• Inflammation occurs only in living tissues; necrotic or dead tissue cannot mount an inflammatory response
• Metaplasia involves the conversion of one differentiated cell type to another, such as in smokers where bronchial epithelium changes to squamous epithelium
• Agents causing inflammation include infective agents like bacteria, viruses, immunological agents, physical agents like heat, cold, and chemical agents like organic and inorganic poisons
• Dysplasia, characterized by disordered cellular development, can progress from metaplasia and hyperplasia, often seen in epithelial cells with cellular proliferation and cytologic changes
• Signs of inflammation include redness, swelling, heat, and pain; a fifth sign, Functio laesa, was added by Robert Virchow
• Atrophy is a decrease in the size and function of a cell, tissue, or organ, caused by conditions like reduced functional demand, hormonal stimulation, nutrient supply, or aging
• The chronology of inflammation involves initiation, amplification, destruction, and termination stages
• In the initiation stage of inflammation, soluble mediators are activated, and inflammatory cells are recruited to the area
• Atrophy is a decrease in the size and function of a cell, tissue, or organ, caused by conditions like reduced functional demand, hormonal stimulation, nutrient supply, or the normal process of aging
• Factors determining variation in inflammatory response include type of injury and infection, virulence, dose, immune status of the host, and type of tissue involved
• Physiological atrophy examples include limb size difference after being in a cast and cellular atrophy in aging heart muscle and brain
• Inflammation can be classified as acute (short duration, early body reaction, resolves quickly) or chronic (longer duration, persistent) depending on the defense capacity of the host and duration of response
• Pathological atrophy types: starvation, ischemia, autophagy in kidneys, neuropathy-induced, endocrine, pressure (e.g., Chinese foot binding), and idiopathic atrophy
• Acute inflammation involves alterations in vascular caliber, structural changes in the microvasculature, and emigration of leukocytes from the microcirculation
• Cell injury results when cells are stressed severely, exposed to damaging agents, or have intrinsic abnormalities, progressing through reversible and irreversible stages
• Causes of cell injury include hypoxia, ischemia, physical agents, chemical agents, infectious agents, immunologic reactions, genetic derangements, nutritional imbalances, aging, and psychogenic diseases
• Pathogenesis of cell injury involves the type, duration, and severity of the injurious agent, the target cell's type, status, and adaptability, and underlying intracellular phenomena like mitochondrial damage and cell membrane damage
• Reversible cell injury may manifest as hydropic change, hyaline change, mucoid change, or fatty change, with hydropic change being the most common form of cell injury
• Altered vascular permeability in acute inflammation causes the accumulation of edema fluid in the interstitial compartment, leading to swelling at the local site of inflammation
• Altered vascular permeability in inflammation:

  • Initial stage: fluid escape due to vasodilation and elevated hydrostatic pressure, transudate in nature
  • Subsequent stage: inflammatory edema (exudate) appears by increased vascular permeability of microcirculation
• Irreversible cell injury leads to nuclear changes like pyknosis, karyolysis, and karyorrhexis, culminating in cell death through necrosis
• Necrosis involves degradative and inflammatory reactions after tissue death caused by injury, with enzymatic digestion occurring through autolysis and heterolysis
• Transudate vs Exudate:

  • Transudate: initial stage, transudate in nature
  • Exudate: subsequent stage, inflammatory edema, appears by increased vascular permeability of microcirculation
• Patterns of tissue necrosis include coagulative necrosis (common type caused by irreversible focal injury) and liquefactive necrosis (characterized by digestion, softening, and liquefaction of tissue)
• Mechanisms of increased vascular leakiness:

  1. Contraction of endothelial cells:

  • Affects venules exclusively while capillaries and arterioles remain unaffected
  • Endothelial cells develop temporary gaps between them due to their contraction, mediated by histamine, bradykinin, and other chemical mediators