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 injuryCells are hurt by lack of oxygen, physical forces, chemicals, germs, the immune system, faulty genes, poor nutrition and age.Topic
• Reversible vs irreversible cell injury: the point of no returnA 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
• Mechanisms of cell injury: ATP, mitochondria, calcium, membranes and DNAMost injuries act through a few shared paths: energy loss, broken mitochondria, excess calcium, free radicals, leaky membranes and DNA damage.Mechanism
• Oxidative stress and free-radical injuryFree radicals are unstable molecules that steal electrons. When the body makes more than it can neutralize, they damage fats, proteins and DNA.Mechanism
• Hypoxia, ischemia and reperfusion injuryBlocked blood flow starves cells of oxygen. Restoring flow is essential, but it can briefly add damage of its own: reperfusion injury.Mechanism
• Chemical (toxic) cell injury: direct and after metabolismSome toxins harm cells directly; others are harmless until the liver converts them into reactive molecules.Mechanism
• Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenousDead tissue looks different depending on the organ and the cause. The pattern on the slide is a clue to what happened.Lesion
• Apoptosis: the intrinsic and extrinsic pathwaysApoptosis is a tidy, programmed suicide: the cell shrinks, cuts itself into packets and is eaten without causing inflammation.Mechanism
• Apoptosis vs necrosis: the comparison tableApoptosis is quiet, single-cell and planned. Necrosis is messy, affects many cells and causes inflammation.Topic
• Other forms of cell death: necroptosis, pyroptosis, ferroptosisSome cells burst open on purpose. These planned but messy deaths alarm the immune system and matter in infection and inflammation.Mechanism
• AutophagyAutophagy means self-eating: the cell wraps worn-out parts in a membrane and sends them to the lysosome to be recycled.Process
• Endoplasmic reticulum stress and the unfolded protein responseWhen too many proteins fold badly inside the ER, the cell slows production and makes more helpers; if that fails, it kills itself.Mechanism
• Hypertrophy: physiologic and pathologicHypertrophy is growth of an organ because its cells get bigger, not more numerous. The heart and muscles do this when they work harder.Process
• Hyperplasia: physiologic and pathologicHyperplasia is growth of a tissue because its cells multiply. It needs cells able to divide and usually stops when the stimulus ends.Process
• AtrophyAtrophy is shrinkage of cells and organs when they get less work, blood, nerve supply, food or hormones.Process
• MetaplasiaMetaplasia is when one mature cell type is replaced by another that better withstands the stress. It protects, but can lead to cancer.Process
• 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
• Intracellular accumulations: cholesterol, proteins, hyaline, glycogenCells 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
• Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbonPigments are coloured substances that build up in tissue. Some come from outside, like coal dust; others the body makes, like iron or bilirubin.Lesion
• Pathologic calcification: dystrophic vs metastaticCalcium can deposit in damaged tissue even when blood calcium is normal, or in healthy tissue when blood calcium or phosphate is high.Lesion

Inflammation

Acute and chronic inflammation, its mediators and the granuloma.

• Inflammation: the cardinal signs and its five stepsInflammation is how living tissue answers injury or infection: it brings blood, fluid and white cells to the spot, cleans up, then repairs.Topic
• Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudateIn the first minutes of inflammation small vessels widen and leak, so protein-rich fluid and cells flood the tissue and cause swelling.Mechanism
• Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxisWhite cells leave the blood in steps: they roll on the vessel wall, stick firmly, squeeze between endothelial cells and crawl toward the injury.Process
• Mediators of inflammation: the table to knowInflammation 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
• Arachidonic acid metabolites in inflammation, and the drugs that block themCell membranes release arachidonic acid, which enzymes turn into prostaglandins and leukotrienes; most anti-inflammatory drugs block this pathway.Mechanism
• Histamine, serotonin, bradykinin and the plasma protein cascadesHistamine from mast cells and bradykinin from plasma make vessels leak within minutes; the clotting, kinin and complement systems are wired together.Mechanism
• Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcerAcute 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
• Outcomes of acute inflammation: resolution, abscess, scar or chronic inflammationAcute inflammation ends in one of four ways: full healing, a walled-off abscess, a scar, or a slow chronic process that keeps going.Topic
• When leukocytes injure tissue: proteases, oxidants and NETsThe weapons neutrophils use to kill microbes (enzymes, oxidants and DNA nets) can leak out and damage the body's own tissue.Mechanism
• Chronic inflammation: causes, cells and featuresChronic inflammation lasts weeks to years: injury, the immune reaction and attempts at repair go on at the same time, often ending in scarring.Process
• Granulomatous inflammation: caseating vs non-caseating, the causes to knowA granuloma is a tight ball of activated macrophages around something hard to kill; how it looks under the microscope points to the cause.Lesion
• Systemic effects of inflammation: fever, acute-phase proteins, leukocytosis, sepsisStrong inflammation spills into the blood: cytokines cause fever, make the liver release acute-phase proteins and the marrow release white cells.Mechanism

Tissue repair

Regeneration, wound healing and fibrosis.

• Tissue repair: regeneration or scar; labile, stable and permanent cellsDamaged 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
• Granulation tissue and scar formationWhen a gap cannot regrow, new vessels and fibroblasts fill it with pink, grainy tissue that slowly turns into a pale collagen scar.Process
• Healing of skin wounds: first and second intentionA 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
• What delays healing: infection, diabetes, nutrition, glucocorticoids, poor blood flowWounds heal slowly when they are infected, poorly perfused or under pressure, or when the person has diabetes, is malnourished or takes steroids.Topic
• Abnormal repair: chronic wounds, hypertrophic scar, keloid, contractureRepair 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
• Fibrosis in organs: TGF-β and the myofibroblastWhen injury keeps coming back, organs fill with scar: TGF-β turns support cells into myofibroblasts that lay down collagen and stiffen the organ.Mechanism
• Liver regenerationThe liver can regrow lost mass in weeks: the remaining liver cells divide until the organ reaches the size the body needs.Process

Hemodynamic disorders

Edema, congestion, hemorrhage, thrombosis, embolism, infarction and shock.

• Edema and effusions: the four mechanismsEdema is extra fluid outside the vessels. It appears when venous pressure rises, proteins fall, lymph is blocked or the kidney keeps salt.Mechanism
• 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
• Hemorrhage: petechiae, purpura, ecchymosis, hematoma, and what blood loss doesBlood outside the vessels takes different forms by size and cause; its effect depends on how much, how fast and where it is lost.Lesion
• Thrombosis and Virchow's triadA thrombus is a clot that forms inside a living vessel. It comes from endothelial damage, abnormal flow or blood that clots too easily.Mechanism
• Hypercoagulable states: inherited and acquiredSome people clot too easily because of an inherited gene or an acquired situation, such as cancer, pregnancy or certain antibodies.Topic
• Arterial vs venous thrombi; mural thrombi and lines of ZahnArterial 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
• What happens to a thrombus: propagation, embolism, dissolution, organizationA thrombus can grow, break off and travel, dissolve, or turn into scar tissue that sometimes lets blood through again.Process
• Disseminated intravascular coagulation: how consumption causes both clots and bleedingIn DIC tiny clots form all over the body; by using up platelets and clotting factors, the patient also bleeds.Mechanism
• Pulmonary thromboembolism: where it comes from and what it doesA 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
• Systemic (arterial) thromboembolismEmboli that travel in the arteries nearly always start in the left heart and end up in the legs, brain, gut, kidney or spleen.Mechanism
• Fat, air and amniotic fluid embolismNot every embolus is a clot: fat, gas bubbles, amniotic fluid, cholesterol crystals, bacteria and tumour can travel too.Topic
• Infarction: red vs white, and what decides the damageAn 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
• The myocardial infarct over time: what the pathologist sees from hours to monthsDead 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
• Shock: types, stages and the organs it damagesIn shock the blood does not bring enough oxygen to the tissues. If not corrected, cells switch to anaerobic metabolism and organs fail.Mechanism
• How septic shock developsIn septic shock the defence against infection runs out of control: mediators widen the vessels, make them leaky and switch on clotting.Mechanism
• Watershed areas and the organs most sensitive to ischemiaWhen pressure falls, neurons suffer first, along with the zones at the far end of two arterial territories, called watershed areas.Topic

Neoplasia

Nomenclature, cancer biology, carcinogens, spread, grading, staging and markers.

• Naming tumours: -oma, carcinoma, sarcoma, and the misleading namesA 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
• Benign vs malignant tumours: the comparison tableBenign tumours stay put and look like their tissue; malignant ones invade, spread and look abnormal. Metastasis settles the question.Topic
• Differentiation and anaplasia: how a tumour cell looks under the microscopeThe more a tumour looks like its normal tissue, the better differentiated it is. Anaplasia means the cells have lost that likeness.Lesion
• Dysplasia and carcinoma in situDysplasia is disordered growth in a lining; when it fills the whole thickness without crossing the basement membrane, it is carcinoma in situ.Lesion
• Invasion and metastasis: the metastatic cascade, step by stepTo 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
• Pathways of spread and the usual metastatic sitesCancers spread through three routes: across body cavities, through lymphatics and through blood. Each cancer has favourite destinations.Topic
• The hallmarks of cancerEvery cancer, whatever its organ, acquires the same set of abilities: to grow without orders, ignore brakes, avoid death, live forever and spread.Topic
• Oncogenes: RAS, MYC, HER2, BCR-ABL and the table to knowOncogenes are growth genes stuck in the ‘on’ position. One altered copy is enough to push a cell to divide.Topic
• Tumour suppressor genes: RB, TP53, APC, BRCA and the two-hit hypothesisTumour suppressors are the cell's brakes. Cancer needs both copies broken, and people born with one broken copy get cancer earlier.Topic
• The cell cycle in cancer: cyclins, CDKs and checkpointsCells divide only when cyclin-CDK engines are switched on and checkpoints agree. Cancer jams the engines on and cuts the checkpoint wires.Mechanism
• Evading cell death and replicating without limit: BCL2 and telomeraseCancer cells switch off their own self-destruct programme and rebuild the ends of their chromosomes so they can divide forever.Mechanism
• Tumour angiogenesisA tumour cannot grow beyond a tiny size without its own blood vessels, so it learns to order new ones, mainly through VEGF.Mechanism
• How tumours evade the immune systemThe immune system can recognise and kill cancer cells. Tumours that survive learn to hide from T cells and to switch them off.Mechanism
• Genomic instability: mismatch repair, BRCA and xeroderma pigmentosumWhen DNA repair fails, mutations pile up much faster. That is why defects in repair genes cause hereditary cancers.Mechanism
• Multistep carcinogenesis: the adenoma–carcinoma sequenceCancer is not one mutation but several, gained over years. Colon cancer shows it best: normal mucosa, then a polyp, then cancer.Process
• Translocations, amplifications and epigenetic changes in cancerBesides point mutations, cancers swap chromosome pieces, copy genes many times and silence genes without changing their sequence.Topic
• Chemical carcinogens: initiation, promotion and the table to knowSome chemicals damage DNA and start a cancer; others only push already damaged cells to multiply. Both steps are needed.Mechanism
• Radiation and cancer: ultraviolet and ionizingSunlight 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
• Oncogenic viruses and H. pylori: the table to knowSome 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
• 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
• Hereditary cancer syndromes: the table to knowA few families inherit a faulty cancer gene. Their cancers appear younger, in several organs and in several relatives.Topic
• Paraneoplastic syndromes: the table to knowSome cancers cause symptoms far from the tumour, through hormones they make or antibodies the body makes against them.Topic
• Local effects of tumours and cancer cachexiaA tumour harms by pressing, blocking, bleeding and breaking things nearby, and by making the whole body waste away.Mechanism
• Grading and staging: what TNM meansThe grade says how abnormal the cancer cells look; the stage says how far the cancer has spread. The stage usually matters more.Topic
• Tumour markers: serum and tissue, and what each one is forMarkers 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
• Precancerous conditions: when chronic inflammation, metaplasia or hyperplasia raise the riskSome long-lasting conditions make a cancer more likely in that tissue. Most never turn into cancer, but they are watched.Topic

Genetic disease

Mendelian and nonclassic inheritance, and chromosome disorders.

• Mendelian inheritance: autosomal dominant, recessive and X-linkedWhen a disease depends on a single gene, it passes through families in predictable patterns that let us estimate each child's risk.Topic
• How a single gene causes disease: enzymes, receptors and structural proteinsAn 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
• Chromosome abnormalities: number and structureAn extra chromosome, a missing one, or a piece lost or moved alters many genes at once and causes syndromes with several malformations.Topic
• Trisomies 21, 18 and 13, and the 22q11.2 deletionThe three trisomies that reach birth and the commonest microdeletion have features typical enough to be recognised when the newborn is examined.Topic
• Sex chromosome disorders: Klinefelter and TurnerAn extra X chromosome in a male (Klinefelter) or a missing one in a female (Turner) mainly affects the gonads, height and puberty.Topic
• Nonclassic inheritance: repeat expansions, mitochondrial genes, imprinting, mosaicismSome 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
• Genomic imprinting: Prader–Willi and AngelmanSome 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
• Multifactorial (complex) disordersThe commonest diseases, such as type 2 diabetes and hypertension, arise from many genes of small effect added to the environment.Topic

Paediatric pathology

Prematurity, diseases of the newborn and childhood tumours.

• Prematurity and fetal growth restrictionBeing born too early or growing too little in the womb leaves organs immature or without reserves, and explains much of newborn disease.Topic
• Neonatal respiratory distress syndrome: surfactant and hyaline membranesThe preterm lung lacks enough surfactant; the alveoli collapse on breathing out and the baby tires from the effort of breathing.Mechanism
• Necrotizing enterocolitis: why the premature gut is vulnerableIn the preterm baby, an immature gut, newly arrived bacteria and feeding combine into an inflammation that can kill the bowel wall.Mechanism
• Fetal hydrops: immune and nonimmuneThe 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
• Sudden infant death syndrome: what is knownIt 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
• Tumours of infancy and childhoodChildren's cancers differ from adult ones: they arise from embryonic tissues, are often small round blue cell tumours, and many are cured.Topic
• Cystic fibrosis: from the CFTR channel to organ damageA faulty chloride channel leaves secretions thick; mucus plugs the bronchi, pancreatic ducts and gut, and sweat comes out very salty.Mechanism

Environmental pathology

Tobacco, alcohol, drugs, metals, heat, cold, radiation and trauma.

• Tobacco: how smoking injures tissueTobacco smoke carries thousands of chemicals that inflame the airways, damage blood vessels and mutate DNA in many organs.Mechanism
• Alcohol: how it injures the liver, brain, heart and fetusBreaking down alcohol creates acetaldehyde and an excess of NADH; these injure the liver, pancreas, brain, heart and developing fetus.Mechanism
• Injury by therapeutic drugs: the classic examplesMedicines can injure tissue through their predictable toxicity or through rare immune or genetic reactions; some cases are exam classics.Topic
• Drugs of abuse: cocaine, opioids, amphetamines, cannabisDrugs of abuse injure the heart, brain, lungs and other organs through their action on neurotransmitters and through the way they are used.Topic
• Heavy metals: lead, mercury, arsenic and cadmiumLead, mercury, arsenic and cadmium bind proteins and enzymes; each one damages its own favourite organs: blood, brain, nerves, kidney or skin.Topic
• Air pollution and occupational exposuresPolluted air outdoors, smoke from cooking fires indoors and dusts at work damage the lungs and the heart, and some cause cancer.Topic
• Thermal injury: burns, hyperthermia and hypothermiaToo much heat or cold destroys skin and tissue and, when the whole body is affected, can cause shock, organ failure or arrhythmias.Mechanism
• Mechanical and electrical injury: abrasion, contusion, laceration, woundsBlunt and sharp forces leave typical wounds on the body; electric current burns deep along its path and can stop the heart.Lesion
• Ionizing radiation injuryIonizing radiation breaks DNA directly and through free radicals; dividing tissues fail first, and cancer may appear years later.Mechanism
• Health effects of climate changeA warming climate brings more heat waves, floods and droughts, spreads mosquito-borne infections and worsens air quality and food supply.Topic

Nutritional pathology

Malnutrition, vitamin deficiencies and obesity.

• Severe acute malnutrition: marasmus and kwashiorkorChildren who lack enough food waste away (marasmus) or swell with oedema (kwashiorkor); both weaken immunity and can be fatal.Topic
• Cachexia, anorexia nervosa and bulimiaCachexia is inflammatory wasting that eating alone does not reverse; anorexia and bulimia are eating disorders with serious body effects.Topic
• Vitamin deficiencies: what each one does to tissueEach missing vitamin leaves its own mark: night blindness, soft bones, bleeding gums, nerve damage, rash or large red cells.Topic
• Obesity: leptin, adipokines and its consequencesFat 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
• Diet, cancer and systemic diseaseWhat people eat shapes the risk of colorectal and gastric cancer, liver cancer, high blood pressure, atherosclerosis and diabetes.Topic

Aging

How cells and organs age.

• Cellular aging: telomeres, DNA damage, senescence and proteostasisCells age because damage builds up, telomeres shorten, repair weakens and some cells stop dividing and release inflammatory signals.Mechanism
• How organs age: normal changes vs diseaseOrgans lose reserve with age. Knowing what is normal aging and what is disease avoids both overtreatment and missed diagnoses.Topic

The pathology laboratory

Biopsy, frozen section, cytology, immunohistochemistry, molecular pathology and autopsy.

• Biopsy: excisional, incisional, core needle, punch and fine-needle aspirationA biopsy takes a piece of tissue to look at under the microscope; the technique chosen decides what the pathologist can answer.Technique
• Frozen section: the intraoperative consultationWhile the patient is still in theatre, the pathologist freezes a piece of tissue, cuts it and answers one specific question within minutes.Technique
• Immunohistochemistry: the principle and the markers to knowAn antibody that recognises a protein binds to it in the section, and a colour reaction shows which cells carry it.Technique
• Cytology: the Pap test, fine-needle aspiration and body fluidsCytology looks at loose cells that were scraped, aspirated or floating in a fluid; it is cheap and fast, ideal for screening.Technique
• From specimen to report: fixation, margins and the pathology reportThe specimen travels from theatre to microscope in several steps; the final report gathers what is needed to stage and treat.Technique
• Special stains in diagnosis: Congo red, Prussian blue, PAS, Ziehl–Neelsen, GramWhen H&E is not enough, a chemical stain gives amyloid, iron, glycogen or microbes a colour of their own.Technique
• Molecular pathology: PCR, FISH, sequencing and liquid biopsyMolecular tests read the genes of a tumour or a microbe to confirm the diagnosis and choose the treatment.Technique
• The autopsy: clinical and medicolegalAn autopsy examines the body after death to find out what the person died of and which diseases they had.Technique

A to Z

• Abnormal repair: chronic wounds, hypertrophic scar, keloid, contractureTissue repair · Lesion
• Air pollution and occupational exposuresEnvironmental pathology · Topic
• Alcohol: how it injures the liver, brain, heart and fetusEnvironmental pathology · Mechanism
• Apoptosis vs necrosis: the comparison tableCell injury, adaptation and death · Topic
• Apoptosis: the intrinsic and extrinsic pathwaysCell injury, adaptation and death · Mechanism
• Arachidonic acid metabolites in inflammation, and the drugs that block themInflammation · Mechanism
• Arterial vs venous thrombi; mural thrombi and lines of ZahnHemodynamic disorders · Lesion
• AtrophyCell injury, adaptation and death · Process
• AutophagyCell injury, adaptation and death · Process
• Benign vs malignant tumours: the comparison tableNeoplasia · Topic
• Biopsy: excisional, incisional, core needle, punch and fine-needle aspirationThe pathology laboratory · Technique
• Cachexia, anorexia nervosa and bulimiaNutritional pathology · Topic
• Cancer epidemiology: age, environment, predisposing conditions (and Colombia)Neoplasia · Topic
• Causes of cell injuryCell injury, adaptation and death · Topic
• Cellular aging: telomeres, DNA damage, senescence and proteostasisAging · Mechanism
• Chemical (toxic) cell injury: direct and after metabolismCell injury, adaptation and death · Mechanism
• Chemical carcinogens: initiation, promotion and the table to knowNeoplasia · Mechanism
• Chromosome abnormalities: number and structureGenetic disease · Topic
• Chronic inflammation: causes, cells and featuresInflammation · Process
• Cystic fibrosis: from the CFTR channel to organ damagePaediatric pathology · Mechanism
• Cytology: the Pap test, fine-needle aspiration and body fluidsThe pathology laboratory · Technique
• Diet, cancer and systemic diseaseNutritional pathology · Topic
• Differentiation and anaplasia: how a tumour cell looks under the microscopeNeoplasia · Lesion
• Disseminated intravascular coagulation: how consumption causes both clots and bleedingHemodynamic disorders · Mechanism
• Drugs of abuse: cocaine, opioids, amphetamines, cannabisEnvironmental pathology · Topic
• Dysplasia and carcinoma in situNeoplasia · Lesion
• Edema and effusions: the four mechanismsHemodynamic disorders · Mechanism
• Endoplasmic reticulum stress and the unfolded protein responseCell injury, adaptation and death · Mechanism
• Evading cell death and replicating without limit: BCL2 and telomeraseNeoplasia · Mechanism
• Fat, air and amniotic fluid embolismHemodynamic disorders · Topic
• Fatty change (steatosis)Cell injury, adaptation and death · Lesion
• Fetal hydrops: immune and nonimmunePaediatric pathology · Mechanism
• Fibrosis in organs: TGF-β and the myofibroblastTissue repair · Mechanism
• From specimen to report: fixation, margins and the pathology reportThe pathology laboratory · Technique
• Frozen section: the intraoperative consultationThe pathology laboratory · Technique
• Genomic imprinting: Prader–Willi and AngelmanGenetic disease · Mechanism
• Genomic instability: mismatch repair, BRCA and xeroderma pigmentosumNeoplasia · Mechanism
• Grading and staging: what TNM meansNeoplasia · Topic
• Granulation tissue and scar formationTissue repair · Process
• Granulomatous inflammation: caseating vs non-caseating, the causes to knowInflammation · Lesion
• Healing of skin wounds: first and second intentionTissue repair · Process
• Health effects of climate changeEnvironmental pathology · Topic
• Heavy metals: lead, mercury, arsenic and cadmiumEnvironmental pathology · Topic
• Hemorrhage: petechiae, purpura, ecchymosis, hematoma, and what blood loss doesHemodynamic disorders · Lesion
• Hereditary cancer syndromes: the table to knowNeoplasia · Topic
• Histamine, serotonin, bradykinin and the plasma protein cascadesInflammation · Mechanism
• How a single gene causes disease: enzymes, receptors and structural proteinsGenetic disease · Mechanism
• How organs age: normal changes vs diseaseAging · Topic
• How septic shock developsHemodynamic disorders · Mechanism
• How tumours evade the immune systemNeoplasia · Mechanism
• Hypercoagulable states: inherited and acquiredHemodynamic disorders · Topic
• Hyperemia and congestion (the nutmeg liver, heart-failure cells)Hemodynamic disorders · Lesion
• Hyperplasia: physiologic and pathologicCell injury, adaptation and death · Process
• Hypertrophy: physiologic and pathologicCell injury, adaptation and death · Process
• Hypoxia, ischemia and reperfusion injuryCell injury, adaptation and death · Mechanism
• Immunohistochemistry: the principle and the markers to knowThe pathology laboratory · Technique
• Infarction: red vs white, and what decides the damageHemodynamic disorders · Lesion
• Inflammation: the cardinal signs and its five stepsInflammation · Topic
• Injury by therapeutic drugs: the classic examplesEnvironmental pathology · Topic
• Intracellular accumulations: cholesterol, proteins, hyaline, glycogenCell injury, adaptation and death · Lesion
• Invasion and metastasis: the metastatic cascade, step by stepNeoplasia · Process
• Ionizing radiation injuryEnvironmental pathology · Mechanism
• Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxisInflammation · Process
• Liver regenerationTissue repair · Process
• Local effects of tumours and cancer cachexiaNeoplasia · Mechanism
• Mechanical and electrical injury: abrasion, contusion, laceration, woundsEnvironmental pathology · Lesion
• Mechanisms of cell injury: ATP, mitochondria, calcium, membranes and DNACell injury, adaptation and death · Mechanism
• Mediators of inflammation: the table to knowInflammation · Topic
• Mendelian inheritance: autosomal dominant, recessive and X-linkedGenetic disease · Topic
• MetaplasiaCell injury, adaptation and death · Process
• Molecular pathology: PCR, FISH, sequencing and liquid biopsyThe pathology laboratory · Technique
• Multifactorial (complex) disordersGenetic disease · Topic
• Multistep carcinogenesis: the adenoma–carcinoma sequenceNeoplasia · Process
• Naming tumours: -oma, carcinoma, sarcoma, and the misleading namesNeoplasia · Topic
• Necrotizing enterocolitis: why the premature gut is vulnerablePaediatric pathology · Mechanism
• Neonatal respiratory distress syndrome: surfactant and hyaline membranesPaediatric pathology · Mechanism
• Nonclassic inheritance: repeat expansions, mitochondrial genes, imprinting, mosaicismGenetic disease · Topic
• Obesity: leptin, adipokines and its consequencesNutritional pathology · Mechanism
• Oncogenes: RAS, MYC, HER2, BCR-ABL and the table to knowNeoplasia · Topic
• Oncogenic viruses and H. pylori: the table to knowNeoplasia · Topic
• Other forms of cell death: necroptosis, pyroptosis, ferroptosisCell injury, adaptation and death · Mechanism
• Outcomes of acute inflammation: resolution, abscess, scar or chronic inflammationInflammation · Topic
• Oxidative stress and free-radical injuryCell injury, adaptation and death · Mechanism
• Paraneoplastic syndromes: the table to knowNeoplasia · Topic
• Pathologic calcification: dystrophic vs metastaticCell injury, adaptation and death · Lesion
• Pathways of spread and the usual metastatic sitesNeoplasia · Topic
• Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcerInflammation · Lesion
• Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenousCell injury, adaptation and death · Lesion
• Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbonCell injury, adaptation and death · Lesion
• Precancerous conditions: when chronic inflammation, metaplasia or hyperplasia raise the riskNeoplasia · Topic
• Prematurity and fetal growth restrictionPaediatric pathology · Topic
• Pulmonary thromboembolism: where it comes from and what it doesHemodynamic disorders · Mechanism
• Radiation and cancer: ultraviolet and ionizingNeoplasia · Mechanism
• Reversible vs irreversible cell injury: the point of no returnCell injury, adaptation and death · Mechanism
• Severe acute malnutrition: marasmus and kwashiorkorNutritional pathology · Topic
• Sex chromosome disorders: Klinefelter and TurnerGenetic disease · Topic
• Shock: types, stages and the organs it damagesHemodynamic disorders · Mechanism
• Special stains in diagnosis: Congo red, Prussian blue, PAS, Ziehl–Neelsen, GramThe pathology laboratory · Technique
• Sudden infant death syndrome: what is knownPaediatric pathology · Topic
• Systemic (arterial) thromboembolismHemodynamic disorders · Mechanism
• Systemic effects of inflammation: fever, acute-phase proteins, leukocytosis, sepsisInflammation · Mechanism
• The autopsy: clinical and medicolegalThe pathology laboratory · Technique
• The cell cycle in cancer: cyclins, CDKs and checkpointsNeoplasia · Mechanism
• The hallmarks of cancerNeoplasia · Topic
• The myocardial infarct over time: what the pathologist sees from hours to monthsHemodynamic disorders · Lesion
• Thermal injury: burns, hyperthermia and hypothermiaEnvironmental pathology · Mechanism
• Thrombosis and Virchow's triadHemodynamic disorders · Mechanism
• Tissue repair: regeneration or scar; labile, stable and permanent cellsTissue repair · Topic
• Tobacco: how smoking injures tissueEnvironmental pathology · Mechanism
• Translocations, amplifications and epigenetic changes in cancerNeoplasia · Topic
• Trisomies 21, 18 and 13, and the 22q11.2 deletionGenetic disease · Topic
• Tumour angiogenesisNeoplasia · Mechanism
• Tumour markers: serum and tissue, and what each one is forNeoplasia · Topic
• Tumour suppressor genes: RB, TP53, APC, BRCA and the two-hit hypothesisNeoplasia · Topic
• Tumours of infancy and childhoodPaediatric pathology · Topic
• Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudateInflammation · Mechanism
• Vitamin deficiencies: what each one does to tissueNutritional pathology · Topic
• Watershed areas and the organs most sensitive to ischemiaHemodynamic disorders · Topic
• What delays healing: infection, diabetes, nutrition, glucocorticoids, poor blood flowTissue repair · Topic
• What happens to a thrombus: propagation, embolism, dissolution, organizationHemodynamic disorders · Process
• When leukocytes injure tissue: proteases, oxidants and NETsInflammation · Mechanism

Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Representative model, for educational purposes only.