Basics of Pathology

Learn how cells provide energy for growth and repair, form tissues, and build organs and systems, from primary tissues to pathogenesis at the cellular level.

Explore the three core cell components—the cell membrane, cytoplasm and organelles, and the nucleus—and learn their roles, membrane composition, and key structures like the nucleolus and nucleoplasm.

Explore the cell membrane's three main components—lipids (phospholipids and cholesterol), proteins (integral and peripheral), and carbohydrates—highlighting lipid bilayer structure, glycocalyx, and protein-mediated transport channels, carriers, enzymes, receptors, and pumps.

Learn how the semi-permeable cell membrane enables transport of ions, nutrients, and wastes through passive, active, and special mechanisms, including endocytosis, exocytosis, and transcytosis.

the cell membrane's semi permeability and fluidity permit fat soluble substances and small molecules to pass while blocking water soluble ones, enabling dynamic endocytosis and exocytosis with rapid hole repair.

Explore the six key functions of the cell membrane, including protective roles, selective permeability, absorptive and excretory activities, gas exchange, and maintenance of cell shape.

Explore cytoplasm and organelles, detailing secretory vesicles, lysosomes with protease, lipase, and amylase, rough and smooth endoplasmic reticulum, ribosomes, mitochondria, Golgi apparatus, and nucleus with nucleolus, nucleoplasm, chromatin, and metabolism.

Explore how normal cells adapt to stress through atrophy, hypertrophy, hyperplasia, and metaplasia, and differentiate reversible from irreversible cell injury, including necrosis and apoptosis, with inflammation.

Explore how cells alter their size, number, and phenotype in response to the external environment. Identify the four adaptations—atrophy, hypertrophy, hyperplasia, and metaplasia—and differentiate physiological from pathological responses.

Explore how physiological stress and pathological stimuli trigger cell injury when cells fail to adapt, and examine how adaptation, injury severity, duration, and type (mechanical, chemical, radiation, genetic) shape outcomes.

Explore genetic and acquired causes of cell injury. Oxygen deprivation is the primary driver, causing hypoxia and ischemia; include physical, chemical, microbial, immunological, and nutritional derangements.

Learn the reversible and irreversible cell injury concepts, where short-term ischemia causes reversible functional and structural changes, while persistent ischemia leads to irreversible cell death—the point of no return.

Investigate reversible cell injury, focusing on generalized cellular swelling and fatty change due to ischaemia. Learn how ATP depletion, Na+/K+ pump failure, and anaerobic glycolysis drive these changes.

Explore how persistent ischemia drives irreversible cell injury, triggering necrosis with mitochondrial dysfunction and membrane disruption, versus programmed apoptosis that minimizes inflammation to regulate tissue cell numbers.

necrosis is irreversible cell injury with membrane damage and intracellular leakage, triggering local inflammation; macrophages clear debris via phagocytosis and proteolysis, with six types including coagulative and liquefactive.

Apoptosis is regulated programmed cell death that removes extra cells via intrinsic and extrinsic pathways; apoptotic bodies provide a 'find me and eat me' signal to phagocytes, preventing inflammation.

Explore the intrinsic apoptosis pathway, detailing mitochondrial cytochrome c release regulated by the BCL2 family proteins, survival signals, and the caspase cascade that leads to cell death.

extrinsic apoptosis begins when a death inducer binds death receptors such as TNF receptors or Fas, activating FADD and caspases 8 and 9 to cause DNA degradation and cytoskeleton fragmentation.

Apoptosis is natural programmed cell death that removes unwanted cells without harming neighbors or causing inflammation. Necrosis is focal cell death from injury that damages nearby cells and triggers inflammation.

Inflammation is the protective vascularized-tissue response that delivers leukocytes and host-defense molecules to injury sites to remove microbes and necrotic debris, with neutrophils first and mast cells triggering vasodilation.

Acute inflammation rapidly delivers neutrophils to the injury site to kill microorganisms and remove the cause. Chronic inflammation lasts longer, driven by macrophages and lymphocytes with tissue destruction and healing.

Initiate acute inflammation by vessel dilation, leukocyte recruitment, and phagocytosis, with fluid and plasma protein exudation and neutrophil migration to the injured site, leading to resolution, fibrosis, or chronic inflammation.

Explain how vasodilation increases vessel diameter, reduces blood velocity, and raises blood flow to inflamed tissue via mediators such as histamine, serotonin, and prostaglandins, while promoting vascular permeability and edema.

Basics of pathology explains how dilated vessels recruit neutrophils to inflamed tissue through margination, rolling, adhesion, transmigration, and migration, guided by chemokines and selectin and integrin interactions.

Explain how neutrophils and macrophages perform phagocytosis to recognize, engulf, and kill microbes, forming phagolysosomes with lysosomal enzymes, reactive oxygen species, and nitric oxide.

Analyze how tissues resolve via healing by scarring when regeneration fails or fibrin exudation is abundant, with fibroblast recruitment and fibrin threads trapping calcium crystals leading to fibrosis.

Chronic inflammation features prolonged mononuclear cell infiltration, ongoing tissue destruction, and fibrosis-driven healing, caused by persistent infection, autoimmune reactions, or toxins, with mucous membrane, serous, fibrinous, hemorrhagic, and purulent forms.

Explore hypersensitivity reactions in pathology, detailing four types, immediate and delayed responses, and how antigens interact with immune response products to provoke exaggerated inflammation.

Describe type I hypersensitivity as an IgE-mediated, immediate reaction in a previously sensitized individual. Release histamine, leukotrienes, and prostaglandins from mast cells and basophils, causing urticaria, bronchospasm, and anaphylactic shock.

Activate antibody-mediated hypersensitivity by binding mismatched antibodies to cell surface antigens, triggering complement activation and cell injury, as seen in myasthenia gravis with IgG or IgM attacking acetylcholine receptors.

Explain how IgG-mediated immune complexes form and deposit in the vascular endothelium and glomerular basement membrane, activate neutrophils and complement, and drive acute glomerulonephritis.

Explore type IV delayed hypersensitivity, mediated by CD4 T lymphocytes, with antigen recognition triggering lymphokines and interferon gamma that recruit macrophages and form granulomas, as in tuberculosis.