#separator:Tab
#html:false
#tags column:5
IMF-096-01-0001-en	Why is a pathological pattern not automatically a diagnosis, and how should interpretation proceed?	The same pattern can arise from several causes, and one cause can produce different patterns by dose, duration, tissue, reserve and treatment, so reasoning runs from mechanism to morphology and back to a ranked set of mechanisms.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0002-en	What determines whether a tissue adapts to increased demand by hypertrophy or by hyperplasia?	Hypertrophy enlarges cells by synthesising proteins and organelles and dominates where mature cells divide poorly, such as cardiac and skeletal muscle; hyperplasia increases cell number and requires tissue able to divide.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0003-en	Why is pressure-overload hypertrophy of the ventricle an adaptation with a cost?	Thickened myocardium meets the load but increases oxygen demand and stiffness and raises the eventual risk of failure.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0004-en	Through which cellular mechanisms does atrophy develop, and why does prolonged atrophy matter?	Lower protein synthesis, increased proteolysis and autophagy shrink cells; this conserves energy, but prolonged loss of specialised structures reduces reserve.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0005-en	What does squamous metaplasia in a smoker's airway gain and lose?	Squamous epithelium tolerates smoke better than ciliated columnar epithelium, but mucociliary clearance and local defence decline, and persistent stress creates a setting for dysplasia and malignancy.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0006-en	What distinguishes dysplasia from invasive cancer, and why can mild dysplasia regress?	Dysplasia is disordered growth with atypia, abnormal maturation and disturbed architecture but no invasion; mild dysplasia can regress once the initiating stimulus is removed, whereas severe dysplasia approaches carcinoma in situ.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0007-en	Why does crossing the basement membrane change a neoplasm's behaviour and treatment implications?	Invasion into supporting tissue gives neoplastic cells access to lymphatics, blood vessels, nerves and stroma.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0008-en	How does reduced oxidative phosphorylation lead to cell swelling in reversible injury?	Falling adenosine triphosphate weakens ion pumps, so sodium and water enter and potassium is lost, swelling cells and organelles (hydropic degeneration) and dilating the endoplasmic reticulum.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0009-en	Why does cytosolic calcium entry drive injury toward irreversibility?	Calcium activates phospholipases, proteases, endonucleases and energy-consuming enzymes, which attack membranes, proteins and nucleic acids while further draining energy.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0010-en	What nuclear changes mark irreversible injury, and in what usual order?	Chromatin first condenses (pyknosis), then fragments (karyorrhexis) and finally fades (karyolysis), although the exact sequence varies.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0011-en	Why might a blood biomarker of tissue injury be absent even though cells have died?	Biomarkers enter blood only when injury, release, distribution and clearance permit, so timing and kinetics can hide real cell death.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0012-en	What distinguishes coagulative from liquefactive necrosis in mechanism and typical setting?	In coagulative necrosis proteins and enzymes denature, so ghostlike architecture persists temporarily, as in ischaemic solid organs; in liquefactive necrosis tissue is digested to viscous material, as in cerebral infarction and abscesses.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0013-en	Why does apoptosis usually provoke less inflammation than necrosis, and when can it still harm tissue?	Caspases dismantle the cell into membrane-bound fragments that are rapidly cleared, keeping contents contained; extensive apoptosis or failed clearance can still affect tissue function.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0014-en	Why might even a regenerative organ heal by scar rather than regeneration?	Scar forms when injury is extensive, infection persists, perfusion remains poor or the supporting matrix is destroyed; fibrosis restores mechanical continuity but rarely specialised architecture.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0015-en	What distinguishes hyperaemia from congestion in mechanism and consequence?	Hyperaemia is active inflow from arteriolar dilation, as in exercise or inflammation; congestion is passive impaired outflow that distends veins and capillaries and can cause hypoxia, oedema and haemorrhage.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0016-en	How does chronic hepatic venous congestion injure the liver?	Impaired outflow causes centrilobular hypoxia with a mottled cut surface, and long-standing injury may progress to fibrosis.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0017-en	How do heart failure and severe protein loss each cause oedema through different forces?	Heart failure raises venous hydrostatic pressure, pushing fluid out; severe protein loss lowers the plasma oncotic pressure, largely generated by albumin, that draws fluid back into vessels.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0018-en	Why do exudates contain more protein than transudates, and why is the distinction imperfect?	Exudates arise from increased permeability or local inflammation, whereas transudates reflect altered hydrostatic or oncotic forces; diuretics, prolonged disease, bleeding, malignancy and mixed mechanisms alter composition.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0019-en	Why can a small intracranial bleed be catastrophic while repeated small occult losses cause a different problem?	The skull limits expansion, so a small intracranial volume matters greatly; repeated occult loss causes little haemodynamic change per episode but depletes iron.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0020-en	How does Virchow's triad explain why arterial and venous thrombi differ in composition?	Arterial thrombi form on disrupted plaque under high shear, driven by endothelial injury, and are platelet rich; venous thrombi form where stasis and coagulation dominate and contain abundant fibrin and red cells.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0021-en	How can a venous thrombus reach a systemic artery, and what determines an embolus's consequence?	A communication between venous and arterial circulations permits paradoxical embolism; outcome depends on embolus size, collateral supply, tissue sensitivity to hypoxia, and whether the obstruction is sterile or infected.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0022-en	What distinguishes the settings of white and red infarcts?	White infarcts occur in solid organs with end-arterial circulation; red infarcts occur with venous obstruction, loose tissue, dual blood supply or reperfusion.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0023-en	In shock, why does a normal or restored blood pressure not prove adequate perfusion?	Early compensation redistributes flow to maintain pressure, and after hypoperfusion endothelial dysfunction, capillary leak and microthrombosis can persist, so pressure recovery does not ensure microvascular flow.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending
IMF-096-01-0024-en	What is the practical sequence for reasoning from a pathological pattern to a final diagnosis?	Name the pattern, define its distribution and age, identify the threatened structure, then test plausible mechanisms against context; the diagnosis must explain morphology, physiology, timing and clinical evidence together.	Integrated Medical Foundations; chapter 96, TTS module 1; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: 64da707fc425905a13a8759dddfe66016de15d4ecb8030c939bcf8bf2120565a; editorial review pending	imf lang::en chapter::096 module::096-01 review::pending