[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › General pathology # General pathology The why of disease: how a cell is injured and dies, how inflammation and repair work, how a thrombus, an infarct or shock happens, and how a tumour starts and spreads. Each mechanism links the DurgiPedia conditions where it shows and the physiology, biochemistry, histology and immunology behind it. 121 pages - Cell injury, adaptation and death - Inflammation - Tissue repair - Hemodynamic disorders - Neoplasia - Genetic disease - Paediatric pathology - Environmental pathology - Nutritional pathology - Aging - The pathology laboratory - A to Z ## Cell injury, adaptation and death Why a cell is injured, how it adapts and how it dies: necrosis, apoptosis and autophagy. - [**Causes of cell injury** Cells are hurt by lack of oxygen, physical forces, chemicals, germs, the immune system, faulty genes, poor nutrition and age. Topic](https://durgical.com/en/general-pathology/causes-of-cell-injury/) - [**Reversible vs irreversible cell injury: the point of no return** A hurt cell first swells and can recover; once its mitochondria and membranes are badly damaged, it is past the point of no return and dies. Mechanism](https://durgical.com/en/general-pathology/reversible-vs-irreversible-cell-injury-the-point-of-no-return/) - [**Mechanisms of cell injury: ATP, mitochondria, calcium, membranes and DNA** Most injuries act through a few shared paths: energy loss, broken mitochondria, excess calcium, free radicals, leaky membranes and DNA damage. Mechanism](https://durgical.com/en/general-pathology/mechanisms-of-cell-injury-atp-mitochondria-calcium-membranes-and-dna/) - [**Oxidative stress and free-radical injury** Free radicals are unstable molecules that steal electrons. When the body makes more than it can neutralize, they damage fats, proteins and DNA. Mechanism](https://durgical.com/en/general-pathology/oxidative-stress-and-free-radical-injury/) - [**Hypoxia, ischemia and reperfusion injury** Blocked blood flow starves cells of oxygen. Restoring flow is essential, but it can briefly add damage of its own: reperfusion injury. Mechanism](https://durgical.com/en/general-pathology/hypoxia-ischemia-and-reperfusion-injury/) - [**Chemical (toxic) cell injury: direct and after metabolism** Some toxins harm cells directly; others are harmless until the liver converts them into reactive molecules. Mechanism](https://durgical.com/en/general-pathology/chemical-cell-injury-direct-and-after-metabolism/) - [**Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous** Dead tissue looks different depending on the organ and the cause. The pattern on the slide is a clue to what happened. Lesion](https://durgical.com/en/general-pathology/patterns-of-necrosis-coagulative-liquefactive-caseous-fat-fibrinoid-gangrenous/) - [**Apoptosis: the intrinsic and extrinsic pathways** Apoptosis is a tidy, programmed suicide: the cell shrinks, cuts itself into packets and is eaten without causing inflammation. Mechanism](https://durgical.com/en/general-pathology/apoptosis-the-intrinsic-and-extrinsic-pathways/) - [**Apoptosis vs necrosis: the comparison table** Apoptosis is quiet, single-cell and planned. Necrosis is messy, affects many cells and causes inflammation. Topic](https://durgical.com/en/general-pathology/apoptosis-vs-necrosis-the-comparison-table/) - [**Other forms of cell death: necroptosis, pyroptosis, ferroptosis** Some cells burst open on purpose. These planned but messy deaths alarm the immune system and matter in infection and inflammation. Mechanism](https://durgical.com/en/general-pathology/other-forms-of-cell-death-necroptosis-pyroptosis-ferroptosis/) - [**Autophagy** Autophagy means self-eating: the cell wraps worn-out parts in a membrane and sends them to the lysosome to be recycled. Process](https://durgical.com/en/general-pathology/autophagy/) - [**Endoplasmic reticulum stress and the unfolded protein response** When too many proteins fold badly inside the ER, the cell slows production and makes more helpers; if that fails, it kills itself. Mechanism](https://durgical.com/en/general-pathology/endoplasmic-reticulum-stress-and-the-unfolded-protein-response/) - [**Hypertrophy: physiologic and pathologic** Hypertrophy is growth of an organ because its cells get bigger, not more numerous. The heart and muscles do this when they work harder. Process](https://durgical.com/en/general-pathology/hypertrophy-physiologic-and-pathologic/) - [**Hyperplasia: physiologic and pathologic** Hyperplasia is growth of a tissue because its cells multiply. It needs cells able to divide and usually stops when the stimulus ends. Process](https://durgical.com/en/general-pathology/hyperplasia-physiologic-and-pathologic/) - [**Atrophy** Atrophy is shrinkage of cells and organs when they get less work, blood, nerve supply, food or hormones. Process](https://durgical.com/en/general-pathology/atrophy/) - [**Metaplasia** Metaplasia is when one mature cell type is replaced by another that better withstands the stress. It protects, but can lead to cancer. Process](https://durgical.com/en/general-pathology/metaplasia/) - [**Fatty change (steatosis)** Steatosis is the build-up of fat droplets inside cells, mostly in the liver. It is reversible when the cause is removed. Lesion](https://durgical.com/en/general-pathology/fatty-change/) - [**Intracellular accumulations: cholesterol, proteins, hyaline, glycogen** Cells can fill up with fat, protein, glycogen or other material when they make too much, cannot process it or cannot get rid of it. Lesion](https://durgical.com/en/general-pathology/intracellular-accumulations-cholesterol-proteins-hyaline-glycogen/) - [**Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon** Pigments are coloured substances that build up in tissue. Some come from outside, like coal dust; others the body makes, like iron or bilirubin. Lesion](https://durgical.com/en/general-pathology/pigments-in-tissue-lipofuscin-hemosiderin-melanin-bilirubin-carbon/) - [**Pathologic calcification: dystrophic vs metastatic** Calcium can deposit in damaged tissue even when blood calcium is normal, or in healthy tissue when blood calcium or phosphate is high. Lesion](https://durgical.com/en/general-pathology/pathologic-calcification-dystrophic-vs-metastatic/) ## Inflammation Acute and chronic inflammation, its mediators and the granuloma. - [**Inflammation: the cardinal signs and its five steps** Inflammation is how living tissue answers injury or infection: it brings blood, fluid and white cells to the spot, cleans up, then repairs. Topic](https://durgical.com/en/general-pathology/inflammation-the-cardinal-signs-and-its-five-steps/) - [**Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate** In the first minutes of inflammation small vessels widen and leak, so protein-rich fluid and cells flood the tissue and cause swelling. Mechanism](https://durgical.com/en/general-pathology/vascular-changes-in-acute-inflammation-vasodilation-leakage-exudate-vs-transudat/) - [**Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxis** White cells leave the blood in steps: they roll on the vessel wall, stick firmly, squeeze between endothelial cells and crawl toward the injury. Process](https://durgical.com/en/general-pathology/leukocyte-recruitment-rolling-adhesion-transmigration-chemotaxis/) - [**Mediators of inflammation: the table to know** Inflammation is run by chemical messengers from cells and plasma; knowing who makes each one and what it does explains the signs and the drugs. Topic](https://durgical.com/en/general-pathology/mediators-of-inflammation-the-table-to-know/) - [**Arachidonic acid metabolites in inflammation, and the drugs that block them** Cell membranes release arachidonic acid, which enzymes turn into prostaglandins and leukotrienes; most anti-inflammatory drugs block this pathway. Mechanism](https://durgical.com/en/general-pathology/arachidonic-acid-metabolites-in-inflammation-and-the-drugs-that-block-them/) - [**Histamine, serotonin, bradykinin and the plasma protein cascades** Histamine from mast cells and bradykinin from plasma make vessels leak within minutes; the clotting, kinin and complement systems are wired together. Mechanism](https://durgical.com/en/general-pathology/histamine-serotonin-bradykinin-and-the-plasma-protein-cascades/) - [**Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcer** Acute inflammation looks different depending on what leaks out: clear fluid, fibrin, pus or a gap in the surface. The pattern points to the cause. Lesion](https://durgical.com/en/general-pathology/patterns-of-acute-inflammation-serous-fibrinous-purulent-abscess-ulcer/) - [**Outcomes of acute inflammation: resolution, abscess, scar or chronic inflammation** Acute inflammation ends in one of four ways: full healing, a walled-off abscess, a scar, or a slow chronic process that keeps going. Topic](https://durgical.com/en/general-pathology/outcomes-of-acute-inflammation-resolution-abscess-scar-or-chronic-inflammation/) - [**When leukocytes injure tissue: proteases, oxidants and NETs** The weapons neutrophils use to kill microbes (enzymes, oxidants and DNA nets) can leak out and damage the body's own tissue. Mechanism](https://durgical.com/en/general-pathology/when-leukocytes-injure-tissue-proteases-oxidants-and-nets/) - [**Chronic inflammation: causes, cells and features** Chronic inflammation lasts weeks to years: injury, the immune reaction and attempts at repair go on at the same time, often ending in scarring. Process](https://durgical.com/en/general-pathology/chronic-inflammation-causes-cells-and-features/) - [**Granulomatous inflammation: caseating vs non-caseating, the causes to know** A granuloma is a tight ball of activated macrophages around something hard to kill; how it looks under the microscope points to the cause. Lesion](https://durgical.com/en/general-pathology/granulomatous-inflammation-caseating-vs-non-caseating-the-causes-to-know/) - [**Systemic effects of inflammation: fever, acute-phase proteins, leukocytosis, sepsis** Strong inflammation spills into the blood: cytokines cause fever, make the liver release acute-phase proteins and the marrow release white cells. Mechanism](https://durgical.com/en/general-pathology/systemic-effects-of-inflammation-fever-acute-phase-proteins-leukocytosis-sepsis/) ## Tissue repair Regeneration, wound healing and fibrosis. - [**Tissue repair: regeneration or scar; labile, stable and permanent cells** Damaged tissue heals either by growing back the same cells or by filling the gap with a scar; which one depends on the cells and the framework. Topic](https://durgical.com/en/general-pathology/tissue-repair-regeneration-or-scar-labile-stable-and-permanent-cells/) - [**Granulation tissue and scar formation** When a gap cannot regrow, new vessels and fibroblasts fill it with pink, grainy tissue that slowly turns into a pale collagen scar. Process](https://durgical.com/en/general-pathology/granulation-tissue-and-scar-formation/) - [**Healing of skin wounds: first and second intention** A clean cut with edges brought together heals fast with a thin scar; an open wound fills from the bottom up, shrinks and leaves a bigger scar. Process](https://durgical.com/en/general-pathology/healing-of-skin-wounds-first-and-second-intention/) - [**What delays healing: infection, diabetes, nutrition, glucocorticoids, poor blood flow** Wounds heal slowly when they are infected, poorly perfused or under pressure, or when the person has diabetes, is malnourished or takes steroids. Topic](https://durgical.com/en/general-pathology/what-delays-healing-infection-diabetes-nutrition-glucocorticoids-poor-blood-flow/) - [**Abnormal repair: chronic wounds, hypertrophic scar, keloid, contracture** Repair can fail in three ways: too little (a wound that will not close), too much (a raised scar or keloid), or a scar that shrinks and pulls. Lesion](https://durgical.com/en/general-pathology/abnormal-repair-chronic-wounds-hypertrophic-scar-keloid-contracture/) - [**Fibrosis in organs: TGF-β and the myofibroblast** When injury keeps coming back, organs fill with scar: TGF-β turns support cells into myofibroblasts that lay down collagen and stiffen the organ. Mechanism](https://durgical.com/en/general-pathology/fibrosis-in-organs-tgf-and-the-myofibroblast/) - [**Liver regeneration** The liver can regrow lost mass in weeks: the remaining liver cells divide until the organ reaches the size the body needs. Process](https://durgical.com/en/general-pathology/liver-regeneration/) ## Hemodynamic disorders Edema, congestion, hemorrhage, thrombosis, embolism, infarction and shock. - [**Edema and effusions: the four mechanisms** Edema is extra fluid outside the vessels. It appears when venous pressure rises, proteins fall, lymph is blocked or the kidney keeps salt. Mechanism](https://durgical.com/en/general-pathology/edema-and-effusions-the-four-mechanisms/) - [**Hyperemia and congestion (the nutmeg liver, heart-failure cells)** In both, an organ holds more blood. In hyperemia more flows in (active and red); in congestion it cannot get out (passive and bluish). Lesion](https://durgical.com/en/general-pathology/hyperemia-and-congestion/) - [**Hemorrhage: petechiae, purpura, ecchymosis, hematoma, and what blood loss does** Blood outside the vessels takes different forms by size and cause; its effect depends on how much, how fast and where it is lost. Lesion](https://durgical.com/en/general-pathology/hemorrhage-petechiae-purpura-ecchymosis-hematoma-and-what-blood-loss-does/) - [**Thrombosis and Virchow's triad** A thrombus is a clot that forms inside a living vessel. It comes from endothelial damage, abnormal flow or blood that clots too easily. Mechanism](https://durgical.com/en/general-pathology/thrombosis-and-virchow-s-triad/) - [**Hypercoagulable states: inherited and acquired** Some people clot too easily because of an inherited gene or an acquired situation, such as cancer, pregnancy or certain antibodies. Topic](https://durgical.com/en/general-pathology/hypercoagulable-states-inherited-and-acquired/) - [**Arterial vs venous thrombi; mural thrombi and lines of Zahn** Arterial thrombi are pale and platelet-rich; venous thrombi are red and rich in red cells. Lines of Zahn prove a thrombus formed in life. Lesion](https://durgical.com/en/general-pathology/arterial-vs-venous-thrombi-mural-thrombi-and-lines-of-zahn/) - [**What happens to a thrombus: propagation, embolism, dissolution, organization** A thrombus can grow, break off and travel, dissolve, or turn into scar tissue that sometimes lets blood through again. Process](https://durgical.com/en/general-pathology/what-happens-to-a-thrombus-propagation-embolism-dissolution-organization/) - [**Disseminated intravascular coagulation: how consumption causes both clots and bleeding** In DIC tiny clots form all over the body; by using up platelets and clotting factors, the patient also bleeds. Mechanism](https://durgical.com/en/general-pathology/disseminated-intravascular-coagulation-how-consumption-causes-both-clots-and-ble/) - [**Pulmonary thromboembolism: where it comes from and what it does** A clot from the leg veins travels through the right heart to the pulmonary artery. By its size it is silent, causes an infarct, or kills. Mechanism](https://durgical.com/en/general-pathology/pulmonary-thromboembolism-where-it-comes-from-and-what-it-does/) - [**Systemic (arterial) thromboembolism** Emboli that travel in the arteries nearly always start in the left heart and end up in the legs, brain, gut, kidney or spleen. Mechanism](https://durgical.com/en/general-pathology/systemic-thromboembolism/) - [**Fat, air and amniotic fluid embolism** Not every embolus is a clot: fat, gas bubbles, amniotic fluid, cholesterol crystals, bacteria and tumour can travel too. Topic](https://durgical.com/en/general-pathology/fat-air-and-amniotic-fluid-embolism/) - [**Infarction: red vs white, and what decides the damage** An infarct is an area of tissue killed by lack of blood. It is white in solid organs with one artery and red in loose tissue or with a dual supply. Lesion](https://durgical.com/en/general-pathology/infarction-red-vs-white-and-what-decides-the-damage/) - [**The myocardial infarct over time: what the pathologist sees from hours to months** Dead heart muscle changes in a set order: hours of little change, days of neutrophils, a week of macrophages, and weeks to make a scar. Lesion](https://durgical.com/en/general-pathology/the-myocardial-infarct-over-time-what-the-pathologist-sees-from-hours-to-months/) - [**Shock: types, stages and the organs it damages** In shock the blood does not bring enough oxygen to the tissues. If not corrected, cells switch to anaerobic metabolism and organs fail. Mechanism](https://durgical.com/en/general-pathology/shock-types-stages-and-the-organs-it-damages/) - [**How septic shock develops** In septic shock the defence against infection runs out of control: mediators widen the vessels, make them leaky and switch on clotting. Mechanism](https://durgical.com/en/general-pathology/how-septic-shock-develops/) - [**Watershed areas and the organs most sensitive to ischemia** When pressure falls, neurons suffer first, along with the zones at the far end of two arterial territories, called watershed areas. Topic](https://durgical.com/en/general-pathology/watershed-areas-and-the-organs-most-sensitive-to-ischemia/) ## Neoplasia Nomenclature, cancer biology, carcinogens, spread, grading, staging and markers. - [**Naming tumours: -oma, carcinoma, sarcoma, and the misleading names** A tumour's name tells you its tissue of origin and whether it is benign or malignant, but a few famous names break the rules. Topic](https://durgical.com/en/general-pathology/naming-tumours-oma-carcinoma-sarcoma-and-the-misleading-names/) - [**Benign vs malignant tumours: the comparison table** Benign tumours stay put and look like their tissue; malignant ones invade, spread and look abnormal. Metastasis settles the question. Topic](https://durgical.com/en/general-pathology/benign-vs-malignant-tumours-the-comparison-table/) - [**Differentiation and anaplasia: how a tumour cell looks under the microscope** The more a tumour looks like its normal tissue, the better differentiated it is. Anaplasia means the cells have lost that likeness. Lesion](https://durgical.com/en/general-pathology/differentiation-and-anaplasia-how-a-tumour-cell-looks-under-the-microscope/) - [**Dysplasia and carcinoma in situ** Dysplasia is disordered growth in a lining; when it fills the whole thickness without crossing the basement membrane, it is carcinoma in situ. Lesion](https://durgical.com/en/general-pathology/dysplasia-and-carcinoma-in-situ/) - [**Invasion and metastasis: the metastatic cascade, step by step** To spread, a cancer cell must let go of its neighbours, break through tissue, travel in vessels and grow in a new organ. Few cells manage all of it. Process](https://durgical.com/en/general-pathology/invasion-and-metastasis-the-metastatic-cascade-step-by-step/) - [**Pathways of spread and the usual metastatic sites** Cancers spread through three routes: across body cavities, through lymphatics and through blood. Each cancer has favourite destinations. Topic](https://durgical.com/en/general-pathology/pathways-of-spread-and-the-usual-metastatic-sites/) - [**The hallmarks of cancer** Every cancer, whatever its organ, acquires the same set of abilities: to grow without orders, ignore brakes, avoid death, live forever and spread. Topic](https://durgical.com/en/general-pathology/the-hallmarks-of-cancer/) - [**Oncogenes: RAS, MYC, HER2, BCR-ABL and the table to know** Oncogenes are growth genes stuck in the ‘on’ position. One altered copy is enough to push a cell to divide. Topic](https://durgical.com/en/general-pathology/oncogenes-ras-myc-her2-bcr-abl-and-the-table-to-know/) - [**Tumour suppressor genes: RB, TP53, APC, BRCA and the two-hit hypothesis** Tumour suppressors are the cell's brakes. Cancer needs both copies broken, and people born with one broken copy get cancer earlier. Topic](https://durgical.com/en/general-pathology/tumour-suppressor-genes-rb-tp53-apc-brca-and-the-two-hit-hypothesis/) - [**The cell cycle in cancer: cyclins, CDKs and checkpoints** Cells divide only when cyclin-CDK engines are switched on and checkpoints agree. Cancer jams the engines on and cuts the checkpoint wires. Mechanism](https://durgical.com/en/general-pathology/the-cell-cycle-in-cancer-cyclins-cdks-and-checkpoints/) - [**Evading cell death and replicating without limit: BCL2 and telomerase** Cancer cells switch off their own self-destruct programme and rebuild the ends of their chromosomes so they can divide forever. Mechanism](https://durgical.com/en/general-pathology/evading-cell-death-and-replicating-without-limit-bcl2-and-telomerase/) - [**Tumour angiogenesis** A tumour cannot grow beyond a tiny size without its own blood vessels, so it learns to order new ones, mainly through VEGF. Mechanism](https://durgical.com/en/general-pathology/tumour-angiogenesis/) - [**How tumours evade the immune system** The immune system can recognise and kill cancer cells. Tumours that survive learn to hide from T cells and to switch them off. Mechanism](https://durgical.com/en/general-pathology/how-tumours-evade-the-immune-system/) - [**Genomic instability: mismatch repair, BRCA and xeroderma pigmentosum** When DNA repair fails, mutations pile up much faster. That is why defects in repair genes cause hereditary cancers. Mechanism](https://durgical.com/en/general-pathology/genomic-instability-mismatch-repair-brca-and-xeroderma-pigmentosum/) - [**Multistep carcinogenesis: the adenoma–carcinoma sequence** Cancer is not one mutation but several, gained over years. Colon cancer shows it best: normal mucosa, then a polyp, then cancer. Process](https://durgical.com/en/general-pathology/multistep-carcinogenesis-the-adenoma-carcinoma-sequence/) - [**Translocations, amplifications and epigenetic changes in cancer** Besides point mutations, cancers swap chromosome pieces, copy genes many times and silence genes without changing their sequence. Topic](https://durgical.com/en/general-pathology/translocations-amplifications-and-epigenetic-changes-in-cancer/) - [**Chemical carcinogens: initiation, promotion and the table to know** Some chemicals damage DNA and start a cancer; others only push already damaged cells to multiply. Both steps are needed. Mechanism](https://durgical.com/en/general-pathology/chemical-carcinogens-initiation-promotion-and-the-table-to-know/) - [**Radiation and cancer: ultraviolet and ionizing** Sunlight damages the DNA of skin cells; X-rays and other high-energy radiation break DNA anywhere in the body. Both can lead to cancer. Mechanism](https://durgical.com/en/general-pathology/radiation-and-cancer-ultraviolet-and-ionizing/) - [**Oncogenic viruses and H. pylori: the table to know** Some viruses, one bacterium and a few parasites can cause cancer, either by switching off the cell's brakes or by keeping tissue inflamed for years. Topic](https://durgical.com/en/general-pathology/oncogenic-viruses-and-h-pylori-the-table-to-know/) - [**Cancer epidemiology: age, environment, predisposing conditions (and Colombia)** Who gets cancer depends on age, habits, infections, where one lives and a few inherited genes. Many cancers can be prevented. Topic](https://durgical.com/en/general-pathology/cancer-epidemiology-age-environment-predisposing-conditions/) - [**Hereditary cancer syndromes: the table to know** A few families inherit a faulty cancer gene. Their cancers appear younger, in several organs and in several relatives. Topic](https://durgical.com/en/general-pathology/hereditary-cancer-syndromes-the-table-to-know/) - [**Paraneoplastic syndromes: the table to know** Some cancers cause symptoms far from the tumour, through hormones they make or antibodies the body makes against them. Topic](https://durgical.com/en/general-pathology/paraneoplastic-syndromes-the-table-to-know/) - [**Local effects of tumours and cancer cachexia** A tumour harms by pressing, blocking, bleeding and breaking things nearby, and by making the whole body waste away. Mechanism](https://durgical.com/en/general-pathology/local-effects-of-tumours-and-cancer-cachexia/) - [**Grading and staging: what TNM means** The grade says how abnormal the cancer cells look; the stage says how far the cancer has spread. The stage usually matters more. Topic](https://durgical.com/en/general-pathology/grading-and-staging-what-tnm-means/) - [**Tumour markers: serum and tissue, and what each one is for** Markers are molecules that point to a cancer: some are measured in blood to follow treatment, others are stained in the biopsy to name the tumour. Topic](https://durgical.com/en/general-pathology/tumour-markers-serum-and-tissue-and-what-each-one-is-for/) - [**Precancerous conditions: when chronic inflammation, metaplasia or hyperplasia raise the risk** Some long-lasting conditions make a cancer more likely in that tissue. Most never turn into cancer, but they are watched. Topic](https://durgical.com/en/general-pathology/precancerous-conditions-when-chronic-inflammation-metaplasia-or-hyperplasia-rais/) ## Genetic disease Mendelian and nonclassic inheritance, and chromosome disorders. - [**Mendelian inheritance: autosomal dominant, recessive and X-linked** When a disease depends on a single gene, it passes through families in predictable patterns that let us estimate each child's risk. Topic](https://durgical.com/en/general-pathology/mendelian-inheritance-autosomal-dominant-recessive-and-x-linked/) - [**How a single gene causes disease: enzymes, receptors and structural proteins** An altered gene makes a protein that is missing, works badly or gets in the way; the kind of protein explains the disease and how it is inherited. Mechanism](https://durgical.com/en/general-pathology/how-a-single-gene-causes-disease-enzymes-receptors-and-structural-proteins/) - [**Chromosome abnormalities: number and structure** An extra chromosome, a missing one, or a piece lost or moved alters many genes at once and causes syndromes with several malformations. Topic](https://durgical.com/en/general-pathology/chromosome-abnormalities-number-and-structure/) - [**Trisomies 21, 18 and 13, and the 22q11.2 deletion** The three trisomies that reach birth and the commonest microdeletion have features typical enough to be recognised when the newborn is examined. Topic](https://durgical.com/en/general-pathology/trisomies-21-18-and-13-and-the-22q11-2-deletion/) - [**Sex chromosome disorders: Klinefelter and Turner** An extra X chromosome in a male (Klinefelter) or a missing one in a female (Turner) mainly affects the gonads, height and puberty. Topic](https://durgical.com/en/general-pathology/sex-chromosome-disorders-klinefelter-and-turner/) - [**Nonclassic inheritance: repeat expansions, mitochondrial genes, imprinting, mosaicism** Some genetic diseases break Mendel's rules: they worsen from one generation to the next, pass only through the mother, or depend on which parent gave the gene. Topic](https://durgical.com/en/general-pathology/nonclassic-inheritance-repeat-expansions-mitochondrial-genes-imprinting-mosaicis/) - [**Genomic imprinting: Prader–Willi and Angelman** Some genes work only when they come from the father and others only from the mother; losing the active copy causes disease even if the other is intact. Mechanism](https://durgical.com/en/general-pathology/genomic-imprinting-prader-willi-and-angelman/) - [**Multifactorial (complex) disorders** The commonest diseases, such as type 2 diabetes and hypertension, arise from many genes of small effect added to the environment. Topic](https://durgical.com/en/general-pathology/multifactorial-disorders/) ## Paediatric pathology Prematurity, diseases of the newborn and childhood tumours. - [**Prematurity and fetal growth restriction** Being born too early or growing too little in the womb leaves organs immature or without reserves, and explains much of newborn disease. Topic](https://durgical.com/en/general-pathology/prematurity-and-fetal-growth-restriction/) - [**Neonatal respiratory distress syndrome: surfactant and hyaline membranes** The preterm lung lacks enough surfactant; the alveoli collapse on breathing out and the baby tires from the effort of breathing. Mechanism](https://durgical.com/en/general-pathology/neonatal-respiratory-distress-syndrome-surfactant-and-hyaline-membranes/) - [**Necrotizing enterocolitis: why the premature gut is vulnerable** In the preterm baby, an immature gut, newly arrived bacteria and feeding combine into an inflammation that can kill the bowel wall. Mechanism](https://durgical.com/en/general-pathology/necrotizing-enterocolitis-why-the-premature-gut-is-vulnerable/) - [**Fetal hydrops: immune and nonimmune** The fetus builds up fluid in the skin and several body cavities, nearly always because its heart fails, it is very anaemic or its lymph drainage does not work. Mechanism](https://durgical.com/en/general-pathology/fetal-hydrops-immune-and-nonimmune/) - [**Sudden infant death syndrome: what is known** It is the unexpected death of a healthy baby during sleep that stays unexplained after a full investigation; sleeping on the back greatly lowers the risk. Topic](https://durgical.com/en/general-pathology/sudden-infant-death-syndrome-what-is-known/) - [**Tumours of infancy and childhood** Children's cancers differ from adult ones: they arise from embryonic tissues, are often small round blue cell tumours, and many are cured. Topic](https://durgical.com/en/general-pathology/tumours-of-infancy-and-childhood/) - [**Cystic fibrosis: from the CFTR channel to organ damage** A faulty chloride channel leaves secretions thick; mucus plugs the bronchi, pancreatic ducts and gut, and sweat comes out very salty. Mechanism](https://durgical.com/en/general-pathology/cystic-fibrosis-from-the-cftr-channel-to-organ-damage/) ## Environmental pathology Tobacco, alcohol, drugs, metals, heat, cold, radiation and trauma. - [**Tobacco: how smoking injures tissue** Tobacco smoke carries thousands of chemicals that inflame the airways, damage blood vessels and mutate DNA in many organs. Mechanism](https://durgical.com/en/general-pathology/tobacco-how-smoking-injures-tissue/) - [**Alcohol: how it injures the liver, brain, heart and fetus** Breaking down alcohol creates acetaldehyde and an excess of NADH; these injure the liver, pancreas, brain, heart and developing fetus. Mechanism](https://durgical.com/en/general-pathology/alcohol-how-it-injures-the-liver-brain-heart-and-fetus/) - [**Injury by therapeutic drugs: the classic examples** Medicines can injure tissue through their predictable toxicity or through rare immune or genetic reactions; some cases are exam classics. Topic](https://durgical.com/en/general-pathology/injury-by-therapeutic-drugs-the-classic-examples/) - [**Drugs of abuse: cocaine, opioids, amphetamines, cannabis** Drugs of abuse injure the heart, brain, lungs and other organs through their action on neurotransmitters and through the way they are used. Topic](https://durgical.com/en/general-pathology/drugs-of-abuse-cocaine-opioids-amphetamines-cannabis/) - [**Heavy metals: lead, mercury, arsenic and cadmium** Lead, mercury, arsenic and cadmium bind proteins and enzymes; each one damages its own favourite organs: blood, brain, nerves, kidney or skin. Topic](https://durgical.com/en/general-pathology/heavy-metals-lead-mercury-arsenic-and-cadmium/) - [**Air pollution and occupational exposures** Polluted air outdoors, smoke from cooking fires indoors and dusts at work damage the lungs and the heart, and some cause cancer. Topic](https://durgical.com/en/general-pathology/air-pollution-and-occupational-exposures/) - [**Thermal injury: burns, hyperthermia and hypothermia** Too much heat or cold destroys skin and tissue and, when the whole body is affected, can cause shock, organ failure or arrhythmias. Mechanism](https://durgical.com/en/general-pathology/thermal-injury-burns-hyperthermia-and-hypothermia/) - [**Mechanical and electrical injury: abrasion, contusion, laceration, wounds** Blunt and sharp forces leave typical wounds on the body; electric current burns deep along its path and can stop the heart. Lesion](https://durgical.com/en/general-pathology/mechanical-and-electrical-injury-abrasion-contusion-laceration-wounds/) - [**Ionizing radiation injury** Ionizing radiation breaks DNA directly and through free radicals; dividing tissues fail first, and cancer may appear years later. Mechanism](https://durgical.com/en/general-pathology/ionizing-radiation-injury/) - [**Health effects of climate change** A warming climate brings more heat waves, floods and droughts, spreads mosquito-borne infections and worsens air quality and food supply. Topic](https://durgical.com/en/general-pathology/health-effects-of-climate-change/) ## Nutritional pathology Malnutrition, vitamin deficiencies and obesity. - [**Severe acute malnutrition: marasmus and kwashiorkor** Children who lack enough food waste away (marasmus) or swell with oedema (kwashiorkor); both weaken immunity and can be fatal. Topic](https://durgical.com/en/general-pathology/severe-acute-malnutrition-marasmus-and-kwashiorkor/) - [**Cachexia, anorexia nervosa and bulimia** Cachexia is inflammatory wasting that eating alone does not reverse; anorexia and bulimia are eating disorders with serious body effects. Topic](https://durgical.com/en/general-pathology/cachexia-anorexia-nervosa-and-bulimia/) - [**Vitamin deficiencies: what each one does to tissue** Each missing vitamin leaves its own mark: night blindness, soft bones, bleeding gums, nerve damage, rash or large red cells. Topic](https://durgical.com/en/general-pathology/vitamin-deficiencies-what-each-one-does-to-tissue/) - [**Obesity: leptin, adipokines and its consequences** Fat tissue is an endocrine organ; in obesity it sends wrong signals to the brain and inflames the body, causing diabetes, liver and heart disease. Mechanism](https://durgical.com/en/general-pathology/obesity-leptin-adipokines-and-its-consequences/) - [**Diet, cancer and systemic disease** What people eat shapes the risk of colorectal and gastric cancer, liver cancer, high blood pressure, atherosclerosis and diabetes. Topic](https://durgical.com/en/general-pathology/diet-cancer-and-systemic-disease/) ## Aging How cells and organs age. - [**Cellular aging: telomeres, DNA damage, senescence and proteostasis** Cells age because damage builds up, telomeres shorten, repair weakens and some cells stop dividing and release inflammatory signals. Mechanism](https://durgical.com/en/general-pathology/cellular-aging-telomeres-dna-damage-senescence-and-proteostasis/) - [**How organs age: normal changes vs disease** Organs lose reserve with age. Knowing what is normal aging and what is disease avoids both overtreatment and missed diagnoses. Topic](https://durgical.com/en/general-pathology/how-organs-age-normal-changes-vs-disease/) ## The pathology laboratory Biopsy, frozen section, cytology, immunohistochemistry, molecular pathology and autopsy. - [**Biopsy: excisional, incisional, core needle, punch and fine-needle aspiration** A biopsy takes a piece of tissue to look at under the microscope; the technique chosen decides what the pathologist can answer. Technique](https://durgical.com/en/general-pathology/biopsy-excisional-incisional-core-needle-punch-and-fine-needle-aspiration/) - [**Frozen section: the intraoperative consultation** While the patient is still in theatre, the pathologist freezes a piece of tissue, cuts it and answers one specific question within minutes. Technique](https://durgical.com/en/general-pathology/frozen-section-the-intraoperative-consultation/) - [**Immunohistochemistry: the principle and the markers to know** An antibody that recognises a protein binds to it in the section, and a colour reaction shows which cells carry it. Technique](https://durgical.com/en/general-pathology/immunohistochemistry-the-principle-and-the-markers-to-know/) - [**Cytology: the Pap test, fine-needle aspiration and body fluids** Cytology looks at loose cells that were scraped, aspirated or floating in a fluid; it is cheap and fast, ideal for screening. Technique](https://durgical.com/en/general-pathology/cytology-the-pap-test-fine-needle-aspiration-and-body-fluids/) - [**From specimen to report: fixation, margins and the pathology report** The specimen travels from theatre to microscope in several steps; the final report gathers what is needed to stage and treat. Technique](https://durgical.com/en/general-pathology/from-specimen-to-report-fixation-margins-and-the-pathology-report/) - [**Special stains in diagnosis: Congo red, Prussian blue, PAS, Ziehl–Neelsen, Gram** When H&E is not enough, a chemical stain gives amyloid, iron, glycogen or microbes a colour of their own. Technique](https://durgical.com/en/general-pathology/special-stains-in-diagnosis-congo-red-prussian-blue-pas-ziehl-neelsen-gram/) - [**Molecular pathology: PCR, FISH, sequencing and liquid biopsy** Molecular tests read the genes of a tumour or a microbe to confirm the diagnosis and choose the treatment. Technique](https://durgical.com/en/general-pathology/molecular-pathology-pcr-fish-sequencing-and-liquid-biopsy/) - [**The autopsy: clinical and medicolegal** An autopsy examines the body after death to find out what the person died of and which diseases they had. Technique](https://durgical.com/en/general-pathology/the-autopsy-clinical-and-medicolegal/) ## A to Z - [**Abnormal repair: chronic wounds, hypertrophic scar, keloid, contracture**](https://durgical.com/en/general-pathology/abnormal-repair-chronic-wounds-hypertrophic-scar-keloid-contracture/) Tissue repair · Lesion - [**Air pollution and occupational exposures**](https://durgical.com/en/general-pathology/air-pollution-and-occupational-exposures/) Environmental pathology · Topic - [**Alcohol: how it injures the liver, brain, heart and fetus**](https://durgical.com/en/general-pathology/alcohol-how-it-injures-the-liver-brain-heart-and-fetus/) Environmental pathology · Mechanism - [**Apoptosis vs necrosis: the comparison table**](https://durgical.com/en/general-pathology/apoptosis-vs-necrosis-the-comparison-table/) Cell injury, adaptation and death · Topic - [**Apoptosis: the intrinsic and extrinsic pathways**](https://durgical.com/en/general-pathology/apoptosis-the-intrinsic-and-extrinsic-pathways/) Cell injury, adaptation and death · Mechanism - [**Arachidonic acid metabolites in inflammation, and the drugs that block them**](https://durgical.com/en/general-pathology/arachidonic-acid-metabolites-in-inflammation-and-the-drugs-that-block-them/) Inflammation · Mechanism - [**Arterial vs venous thrombi; mural thrombi and lines of Zahn**](https://durgical.com/en/general-pathology/arterial-vs-venous-thrombi-mural-thrombi-and-lines-of-zahn/) Hemodynamic disorders · Lesion - [**Atrophy**](https://durgical.com/en/general-pathology/atrophy/) Cell injury, adaptation and death · Process - [**Autophagy**](https://durgical.com/en/general-pathology/autophagy/) Cell injury, adaptation and death · Process - [**Benign vs malignant tumours: the comparison table**](https://durgical.com/en/general-pathology/benign-vs-malignant-tumours-the-comparison-table/) Neoplasia · Topic - [**Biopsy: excisional, incisional, core needle, punch and fine-needle aspiration**](https://durgical.com/en/general-pathology/biopsy-excisional-incisional-core-needle-punch-and-fine-needle-aspiration/) The pathology laboratory · Technique - [**Cachexia, anorexia nervosa and bulimia**](https://durgical.com/en/general-pathology/cachexia-anorexia-nervosa-and-bulimia/) Nutritional pathology · Topic - [**Cancer epidemiology: age, environment, predisposing conditions (and Colombia)**](https://durgical.com/en/general-pathology/cancer-epidemiology-age-environment-predisposing-conditions/) Neoplasia · Topic - [**Causes of cell injury**](https://durgical.com/en/general-pathology/causes-of-cell-injury/) Cell injury, adaptation and death · Topic - [**Cellular aging: telomeres, DNA damage, senescence and proteostasis**](https://durgical.com/en/general-pathology/cellular-aging-telomeres-dna-damage-senescence-and-proteostasis/) Aging · Mechanism - [**Chemical (toxic) cell injury: direct and after metabolism**](https://durgical.com/en/general-pathology/chemical-cell-injury-direct-and-after-metabolism/) Cell injury, adaptation and death · Mechanism - [**Chemical carcinogens: initiation, promotion and the table to know**](https://durgical.com/en/general-pathology/chemical-carcinogens-initiation-promotion-and-the-table-to-know/) Neoplasia · Mechanism - [**Chromosome abnormalities: number and structure**](https://durgical.com/en/general-pathology/chromosome-abnormalities-number-and-structure/) Genetic disease · Topic - [**Chronic inflammation: causes, cells and features**](https://durgical.com/en/general-pathology/chronic-inflammation-causes-cells-and-features/) Inflammation · Process - [**Cystic fibrosis: from the CFTR channel to organ damage**](https://durgical.com/en/general-pathology/cystic-fibrosis-from-the-cftr-channel-to-organ-damage/) Paediatric pathology · Mechanism - [**Cytology: the Pap test, fine-needle aspiration and body fluids**](https://durgical.com/en/general-pathology/cytology-the-pap-test-fine-needle-aspiration-and-body-fluids/) The pathology laboratory · Technique - [**Diet, cancer and systemic disease**](https://durgical.com/en/general-pathology/diet-cancer-and-systemic-disease/) Nutritional pathology · Topic - [**Differentiation and anaplasia: how a tumour cell looks under the microscope**](https://durgical.com/en/general-pathology/differentiation-and-anaplasia-how-a-tumour-cell-looks-under-the-microscope/) Neoplasia · Lesion - [**Disseminated intravascular coagulation: how consumption causes both clots and bleeding**](https://durgical.com/en/general-pathology/disseminated-intravascular-coagulation-how-consumption-causes-both-clots-and-ble/) Hemodynamic disorders · Mechanism - [**Drugs of abuse: cocaine, opioids, amphetamines, cannabis**](https://durgical.com/en/general-pathology/drugs-of-abuse-cocaine-opioids-amphetamines-cannabis/) Environmental pathology · Topic - [**Dysplasia and carcinoma in situ**](https://durgical.com/en/general-pathology/dysplasia-and-carcinoma-in-situ/) Neoplasia · Lesion - [**Edema and effusions: the four mechanisms**](https://durgical.com/en/general-pathology/edema-and-effusions-the-four-mechanisms/) Hemodynamic disorders · Mechanism - [**Endoplasmic reticulum stress and the unfolded protein response**](https://durgical.com/en/general-pathology/endoplasmic-reticulum-stress-and-the-unfolded-protein-response/) Cell injury, adaptation and death · Mechanism - [**Evading cell death and replicating without limit: BCL2 and telomerase**](https://durgical.com/en/general-pathology/evading-cell-death-and-replicating-without-limit-bcl2-and-telomerase/) Neoplasia · Mechanism - [**Fat, air and amniotic fluid embolism**](https://durgical.com/en/general-pathology/fat-air-and-amniotic-fluid-embolism/) Hemodynamic disorders · Topic - [**Fatty change (steatosis)**](https://durgical.com/en/general-pathology/fatty-change/) Cell injury, adaptation and death · Lesion - [**Fetal hydrops: immune and nonimmune**](https://durgical.com/en/general-pathology/fetal-hydrops-immune-and-nonimmune/) Paediatric pathology · Mechanism - [**Fibrosis in organs: TGF-β and the myofibroblast**](https://durgical.com/en/general-pathology/fibrosis-in-organs-tgf-and-the-myofibroblast/) Tissue repair · Mechanism - [**From specimen to report: fixation, margins and the pathology report**](https://durgical.com/en/general-pathology/from-specimen-to-report-fixation-margins-and-the-pathology-report/) The pathology laboratory · Technique - [**Frozen section: the intraoperative consultation**](https://durgical.com/en/general-pathology/frozen-section-the-intraoperative-consultation/) The pathology laboratory · Technique - [**Genomic imprinting: Prader–Willi and Angelman**](https://durgical.com/en/general-pathology/genomic-imprinting-prader-willi-and-angelman/) Genetic disease · Mechanism - [**Genomic instability: mismatch repair, BRCA and xeroderma pigmentosum**](https://durgical.com/en/general-pathology/genomic-instability-mismatch-repair-brca-and-xeroderma-pigmentosum/) Neoplasia · Mechanism - [**Grading and staging: what TNM means**](https://durgical.com/en/general-pathology/grading-and-staging-what-tnm-means/) Neoplasia · Topic - [**Granulation tissue and scar formation**](https://durgical.com/en/general-pathology/granulation-tissue-and-scar-formation/) Tissue repair · Process - [**Granulomatous inflammation: caseating vs non-caseating, the causes to know**](https://durgical.com/en/general-pathology/granulomatous-inflammation-caseating-vs-non-caseating-the-causes-to-know/) Inflammation · Lesion - [**Healing of skin wounds: first and second intention**](https://durgical.com/en/general-pathology/healing-of-skin-wounds-first-and-second-intention/) Tissue repair · Process - [**Health effects of climate change**](https://durgical.com/en/general-pathology/health-effects-of-climate-change/) Environmental pathology · Topic - [**Heavy metals: lead, mercury, arsenic and cadmium**](https://durgical.com/en/general-pathology/heavy-metals-lead-mercury-arsenic-and-cadmium/) Environmental pathology · Topic - [**Hemorrhage: petechiae, purpura, ecchymosis, hematoma, and what blood loss does**](https://durgical.com/en/general-pathology/hemorrhage-petechiae-purpura-ecchymosis-hematoma-and-what-blood-loss-does/) Hemodynamic disorders · Lesion - [**Hereditary cancer syndromes: the table to know**](https://durgical.com/en/general-pathology/hereditary-cancer-syndromes-the-table-to-know/) Neoplasia · Topic - [**Histamine, serotonin, bradykinin and the plasma protein cascades**](https://durgical.com/en/general-pathology/histamine-serotonin-bradykinin-and-the-plasma-protein-cascades/) Inflammation · Mechanism - [**How a single gene causes disease: enzymes, receptors and structural proteins**](https://durgical.com/en/general-pathology/how-a-single-gene-causes-disease-enzymes-receptors-and-structural-proteins/) Genetic disease · Mechanism - [**How organs age: normal changes vs disease**](https://durgical.com/en/general-pathology/how-organs-age-normal-changes-vs-disease/) Aging · Topic - [**How septic shock develops**](https://durgical.com/en/general-pathology/how-septic-shock-develops/) Hemodynamic disorders · Mechanism - [**How tumours evade the immune system**](https://durgical.com/en/general-pathology/how-tumours-evade-the-immune-system/) Neoplasia · Mechanism - [**Hypercoagulable states: inherited and acquired**](https://durgical.com/en/general-pathology/hypercoagulable-states-inherited-and-acquired/) Hemodynamic disorders · Topic - [**Hyperemia and congestion (the nutmeg liver, heart-failure cells)**](https://durgical.com/en/general-pathology/hyperemia-and-congestion/) Hemodynamic disorders · Lesion - [**Hyperplasia: physiologic and pathologic**](https://durgical.com/en/general-pathology/hyperplasia-physiologic-and-pathologic/) Cell injury, adaptation and death · Process - [**Hypertrophy: physiologic and pathologic**](https://durgical.com/en/general-pathology/hypertrophy-physiologic-and-pathologic/) Cell injury, adaptation and death · Process - [**Hypoxia, ischemia and reperfusion injury**](https://durgical.com/en/general-pathology/hypoxia-ischemia-and-reperfusion-injury/) Cell injury, adaptation and death · Mechanism - [**Immunohistochemistry: the principle and the markers to know**](https://durgical.com/en/general-pathology/immunohistochemistry-the-principle-and-the-markers-to-know/) The pathology laboratory · Technique - [**Infarction: red vs white, and what decides the damage**](https://durgical.com/en/general-pathology/infarction-red-vs-white-and-what-decides-the-damage/) Hemodynamic disorders · Lesion - [**Inflammation: the cardinal signs and its five steps**](https://durgical.com/en/general-pathology/inflammation-the-cardinal-signs-and-its-five-steps/) Inflammation · Topic - [**Injury by therapeutic drugs: the classic examples**](https://durgical.com/en/general-pathology/injury-by-therapeutic-drugs-the-classic-examples/) Environmental pathology · Topic - [**Intracellular accumulations: cholesterol, proteins, hyaline, glycogen**](https://durgical.com/en/general-pathology/intracellular-accumulations-cholesterol-proteins-hyaline-glycogen/) Cell injury, adaptation and death · Lesion - [**Invasion and metastasis: the metastatic cascade, step by step**](https://durgical.com/en/general-pathology/invasion-and-metastasis-the-metastatic-cascade-step-by-step/) Neoplasia · Process - [**Ionizing radiation injury**](https://durgical.com/en/general-pathology/ionizing-radiation-injury/) Environmental pathology · Mechanism - [**Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxis**](https://durgical.com/en/general-pathology/leukocyte-recruitment-rolling-adhesion-transmigration-chemotaxis/) Inflammation · Process - [**Liver regeneration**](https://durgical.com/en/general-pathology/liver-regeneration/) Tissue repair · Process - [**Local effects of tumours and cancer cachexia**](https://durgical.com/en/general-pathology/local-effects-of-tumours-and-cancer-cachexia/) Neoplasia · Mechanism - [**Mechanical and electrical injury: abrasion, contusion, laceration, wounds**](https://durgical.com/en/general-pathology/mechanical-and-electrical-injury-abrasion-contusion-laceration-wounds/) Environmental pathology · Lesion - [**Mechanisms of cell injury: ATP, mitochondria, calcium, membranes and DNA**](https://durgical.com/en/general-pathology/mechanisms-of-cell-injury-atp-mitochondria-calcium-membranes-and-dna/) Cell injury, adaptation and death · Mechanism - [**Mediators of inflammation: the table to know**](https://durgical.com/en/general-pathology/mediators-of-inflammation-the-table-to-know/) Inflammation · Topic - [**Mendelian inheritance: autosomal dominant, recessive and X-linked**](https://durgical.com/en/general-pathology/mendelian-inheritance-autosomal-dominant-recessive-and-x-linked/) Genetic disease · Topic - [**Metaplasia**](https://durgical.com/en/general-pathology/metaplasia/) Cell injury, adaptation and death · Process - [**Molecular pathology: PCR, FISH, sequencing and liquid biopsy**](https://durgical.com/en/general-pathology/molecular-pathology-pcr-fish-sequencing-and-liquid-biopsy/) The pathology laboratory · Technique - [**Multifactorial (complex) disorders**](https://durgical.com/en/general-pathology/multifactorial-disorders/) Genetic disease · Topic - [**Multistep carcinogenesis: the adenoma–carcinoma sequence**](https://durgical.com/en/general-pathology/multistep-carcinogenesis-the-adenoma-carcinoma-sequence/) Neoplasia · Process - [**Naming tumours: -oma, carcinoma, sarcoma, and the misleading names**](https://durgical.com/en/general-pathology/naming-tumours-oma-carcinoma-sarcoma-and-the-misleading-names/) Neoplasia · Topic - [**Necrotizing enterocolitis: why the premature gut is vulnerable**](https://durgical.com/en/general-pathology/necrotizing-enterocolitis-why-the-premature-gut-is-vulnerable/) Paediatric pathology · Mechanism - [**Neonatal respiratory distress syndrome: surfactant and hyaline membranes**](https://durgical.com/en/general-pathology/neonatal-respiratory-distress-syndrome-surfactant-and-hyaline-membranes/) Paediatric pathology · Mechanism - [**Nonclassic inheritance: repeat expansions, mitochondrial genes, imprinting, mosaicism**](https://durgical.com/en/general-pathology/nonclassic-inheritance-repeat-expansions-mitochondrial-genes-imprinting-mosaicis/) Genetic disease · Topic - [**Obesity: leptin, adipokines and its consequences**](https://durgical.com/en/general-pathology/obesity-leptin-adipokines-and-its-consequences/) Nutritional pathology · Mechanism - [**Oncogenes: RAS, MYC, HER2, BCR-ABL and the table to know**](https://durgical.com/en/general-pathology/oncogenes-ras-myc-her2-bcr-abl-and-the-table-to-know/) Neoplasia · Topic - [**Oncogenic viruses and H. pylori: the table to know**](https://durgical.com/en/general-pathology/oncogenic-viruses-and-h-pylori-the-table-to-know/) Neoplasia · Topic - [**Other forms of cell death: necroptosis, pyroptosis, ferroptosis**](https://durgical.com/en/general-pathology/other-forms-of-cell-death-necroptosis-pyroptosis-ferroptosis/) Cell injury, adaptation and death · Mechanism - [**Outcomes of acute inflammation: resolution, abscess, scar or chronic inflammation**](https://durgical.com/en/general-pathology/outcomes-of-acute-inflammation-resolution-abscess-scar-or-chronic-inflammation/) Inflammation · Topic - [**Oxidative stress and free-radical injury**](https://durgical.com/en/general-pathology/oxidative-stress-and-free-radical-injury/) Cell injury, adaptation and death · Mechanism - [**Paraneoplastic syndromes: the table to know**](https://durgical.com/en/general-pathology/paraneoplastic-syndromes-the-table-to-know/) Neoplasia · Topic - [**Pathologic calcification: dystrophic vs metastatic**](https://durgical.com/en/general-pathology/pathologic-calcification-dystrophic-vs-metastatic/) Cell injury, adaptation and death · Lesion - [**Pathways of spread and the usual metastatic sites**](https://durgical.com/en/general-pathology/pathways-of-spread-and-the-usual-metastatic-sites/) Neoplasia · Topic - [**Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcer**](https://durgical.com/en/general-pathology/patterns-of-acute-inflammation-serous-fibrinous-purulent-abscess-ulcer/) Inflammation · Lesion - [**Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous**](https://durgical.com/en/general-pathology/patterns-of-necrosis-coagulative-liquefactive-caseous-fat-fibrinoid-gangrenous/) Cell injury, adaptation and death · Lesion - [**Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon**](https://durgical.com/en/general-pathology/pigments-in-tissue-lipofuscin-hemosiderin-melanin-bilirubin-carbon/) Cell injury, adaptation and death · Lesion - [**Precancerous conditions: when chronic inflammation, metaplasia or hyperplasia raise the risk**](https://durgical.com/en/general-pathology/precancerous-conditions-when-chronic-inflammation-metaplasia-or-hyperplasia-rais/) Neoplasia · Topic - [**Prematurity and fetal growth restriction**](https://durgical.com/en/general-pathology/prematurity-and-fetal-growth-restriction/) Paediatric pathology · Topic - [**Pulmonary thromboembolism: where it comes from and what it does**](https://durgical.com/en/general-pathology/pulmonary-thromboembolism-where-it-comes-from-and-what-it-does/) Hemodynamic disorders · Mechanism - [**Radiation and cancer: ultraviolet and ionizing**](https://durgical.com/en/general-pathology/radiation-and-cancer-ultraviolet-and-ionizing/) Neoplasia · Mechanism - [**Reversible vs irreversible cell injury: the point of no return**](https://durgical.com/en/general-pathology/reversible-vs-irreversible-cell-injury-the-point-of-no-return/) Cell injury, adaptation and death · Mechanism - [**Severe acute malnutrition: marasmus and kwashiorkor**](https://durgical.com/en/general-pathology/severe-acute-malnutrition-marasmus-and-kwashiorkor/) Nutritional pathology · Topic - [**Sex chromosome disorders: Klinefelter and Turner**](https://durgical.com/en/general-pathology/sex-chromosome-disorders-klinefelter-and-turner/) Genetic disease · Topic - [**Shock: types, stages and the organs it damages**](https://durgical.com/en/general-pathology/shock-types-stages-and-the-organs-it-damages/) Hemodynamic disorders · Mechanism - [**Special stains in diagnosis: Congo red, Prussian blue, PAS, Ziehl–Neelsen, Gram**](https://durgical.com/en/general-pathology/special-stains-in-diagnosis-congo-red-prussian-blue-pas-ziehl-neelsen-gram/) The pathology laboratory · Technique - [**Sudden infant death syndrome: what is known**](https://durgical.com/en/general-pathology/sudden-infant-death-syndrome-what-is-known/) Paediatric pathology · Topic - [**Systemic (arterial) thromboembolism**](https://durgical.com/en/general-pathology/systemic-thromboembolism/) Hemodynamic disorders · Mechanism - [**Systemic effects of inflammation: fever, acute-phase proteins, leukocytosis, sepsis**](https://durgical.com/en/general-pathology/systemic-effects-of-inflammation-fever-acute-phase-proteins-leukocytosis-sepsis/) Inflammation · Mechanism - [**The autopsy: clinical and medicolegal**](https://durgical.com/en/general-pathology/the-autopsy-clinical-and-medicolegal/) The pathology laboratory · Technique - [**The cell cycle in cancer: cyclins, CDKs and checkpoints**](https://durgical.com/en/general-pathology/the-cell-cycle-in-cancer-cyclins-cdks-and-checkpoints/) Neoplasia · Mechanism - [**The hallmarks of cancer**](https://durgical.com/en/general-pathology/the-hallmarks-of-cancer/) Neoplasia · Topic - [**The myocardial infarct over time: what the pathologist sees from hours to months**](https://durgical.com/en/general-pathology/the-myocardial-infarct-over-time-what-the-pathologist-sees-from-hours-to-months/) Hemodynamic disorders · Lesion - [**Thermal injury: burns, hyperthermia and hypothermia**](https://durgical.com/en/general-pathology/thermal-injury-burns-hyperthermia-and-hypothermia/) Environmental pathology · Mechanism - [**Thrombosis and Virchow's triad**](https://durgical.com/en/general-pathology/thrombosis-and-virchow-s-triad/) Hemodynamic disorders · Mechanism - [**Tissue repair: regeneration or scar; labile, stable and permanent cells**](https://durgical.com/en/general-pathology/tissue-repair-regeneration-or-scar-labile-stable-and-permanent-cells/) Tissue repair · Topic - [**Tobacco: how smoking injures tissue**](https://durgical.com/en/general-pathology/tobacco-how-smoking-injures-tissue/) Environmental pathology · Mechanism - [**Translocations, amplifications and epigenetic changes in cancer**](https://durgical.com/en/general-pathology/translocations-amplifications-and-epigenetic-changes-in-cancer/) Neoplasia · Topic - [**Trisomies 21, 18 and 13, and the 22q11.2 deletion**](https://durgical.com/en/general-pathology/trisomies-21-18-and-13-and-the-22q11-2-deletion/) Genetic disease · Topic - [**Tumour angiogenesis**](https://durgical.com/en/general-pathology/tumour-angiogenesis/) Neoplasia · Mechanism - [**Tumour markers: serum and tissue, and what each one is for**](https://durgical.com/en/general-pathology/tumour-markers-serum-and-tissue-and-what-each-one-is-for/) Neoplasia · Topic - [**Tumour suppressor genes: RB, TP53, APC, BRCA and the two-hit hypothesis**](https://durgical.com/en/general-pathology/tumour-suppressor-genes-rb-tp53-apc-brca-and-the-two-hit-hypothesis/) Neoplasia · Topic - [**Tumours of infancy and childhood**](https://durgical.com/en/general-pathology/tumours-of-infancy-and-childhood/) Paediatric pathology · Topic - [**Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate**](https://durgical.com/en/general-pathology/vascular-changes-in-acute-inflammation-vasodilation-leakage-exudate-vs-transudat/) Inflammation · Mechanism - [**Vitamin deficiencies: what each one does to tissue**](https://durgical.com/en/general-pathology/vitamin-deficiencies-what-each-one-does-to-tissue/) Nutritional pathology · Topic - [**Watershed areas and the organs most sensitive to ischemia**](https://durgical.com/en/general-pathology/watershed-areas-and-the-organs-most-sensitive-to-ischemia/) Hemodynamic disorders · Topic - [**What delays healing: infection, diabetes, nutrition, glucocorticoids, poor blood flow**](https://durgical.com/en/general-pathology/what-delays-healing-infection-diabetes-nutrition-glucocorticoids-poor-blood-flow/) Tissue repair · Topic - [**What happens to a thrombus: propagation, embolism, dissolution, organization**](https://durgical.com/en/general-pathology/what-happens-to-a-thrombus-propagation-embolism-dissolution-organization/) Hemodynamic disorders · Process - [**When leukocytes injure tissue: proteases, oxidants and NETs**](https://durgical.com/en/general-pathology/when-leukocytes-injure-tissue-proteases-oxidants-and-nets/) Inflammation · Mechanism Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. 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