PA5.1-6 | Hemodynamic Disorders — Glossary

Reversible ischaemic or toxic necrosis of renal tubular epithelium (especially proximal tubule and loop of Henle), the commonest cause of acute kidney injury in shock and ICU settings; regenerates with adequate supportive care.

Entry of amniotic fluid containing fetal squames, lanugo, and surfactant into maternal venous circulation at delivery, triggering an anaphylactoid reaction, acute respiratory failure, and DIC; rare but highly fatal.

Severe, generalised subcutaneous oedema involving the entire body, typically caused by profound hypoalbuminaemia or massive sodium/water retention.

A blood clot that formed during life at a site of endothelial injury or turbulence; characterised by firm adherence to the vessel wall and microscopic lines of Zahn.

Diffuse alveolar damage with hyaline membrane formation, alveolar oedema, and refractory hypoxia complicating sepsis, trauma, or aspiration; the pulmonary manifestation of multi-organ dysfunction in shock.

Centrilobular fibrosis of the liver resulting from long-standing chronic venous congestion; represents the fibrotic endpoint of nutmeg liver, rarely progressing to true cirrhosis.

Life-threatening compression of the heart by pericardial fluid (haemopericardium or effusion), producing Beck's triad: hypotension, muffled heart sounds, and raised jugular venous pressure.

The yellow-white upper layer of a postmortem clot, formed by plasma and leukocytes that separate by gravity before the blood sets; distinguishes postmortem clotting from antemortem thrombus.

Sustained venous back-pressure causing persistent tissue engorgement, hypoxia, parenchymal cell loss, and eventually fibrous replacement of the affected organ.

A form of ischaemic cell death in which cell outlines (ghost cells) are preserved despite complete nuclear loss, because structural proteins denature rather than dissolve; the dominant pattern in most organ infarcts except brain.

Passive engorgement of tissue with deoxygenated blood due to impaired venous outflow; the affected tissue appears dusky red to cyanotic and is cool.

The dark red lower layer of a postmortem clot, formed by settled red blood cells embedded in fibrin; paired with the chicken-fat layer as a diagnostic pair for postmortem formation.

Massive uncontrolled release of pro-inflammatory cytokines (TNF-α, IL-1, IL-6) in response to infection, causing systemic vasodilation, endothelial injury, and multi-organ dysfunction in septic shock.

A clinical technique of pressing a glass slide or finger firmly against a skin lesion to determine whether it blanches; haemorrhagic lesions (petechiae, purpura) do not blanch because blood is outside vessels.

Widespread microvascular thrombosis driven by excess thrombin generation (in sepsis, obstetric catastrophes, trauma), which consumes clotting factors and platelets simultaneously, producing paradoxical bleeding.

A pattern in which two separate arterial sources supply the same tissue (e.g., lung: pulmonary + bronchial arteries); occlusion of one vessel allows the second to reflux blood into the necrotic zone, producing haemorrhagic infarction.

A large (> 1 cm) area of cutaneous haemorrhage ('bruise') that undergoes sequential colour change (blue-black → green → yellow-brown) as haemoglobin is metabolised to biliverdin and haemosiderin by macrophages.

Massive, non-pitting lymphoedema of the lower limbs, genitalia, or breasts due to chronic lymphatic obstruction by Wuchereria bancrofti (filariasis).

Lodgement of an abnormal mass (embolus) within the vascular system at a site distant from its origin, carried there by the bloodstream; the embolus may be solid, liquid, or gaseous.

A vascular pattern in which a single terminal artery supplies a tissue segment with no collateral anastomosis; occlusion invariably causes pale infarction because no alternative blood source exists.

Protein-rich inflammatory fluid (> 3 g/dL, specific gravity > 1.020) produced when endothelial injury increases vascular permeability, allowing plasma proteins to leak into the interstitium.

A clinical triad of hypoxia, neurological dysfunction, and petechiae appearing 24-72 hours after long-bone fracture, caused by bone marrow fat globules entering the circulation and obstructing pulmonary and cerebral capillaries.

The end stage of infarct healing, in which granulation tissue matures into dense, acellular collagen that permanently replaces the necrotic zone; appears grey-white and firm.

A dead cell in coagulative necrosis whose architectural outline persists on H&E but whose nucleus is absent; a reliable marker of ischaemic infarction in solid organs.

Provisional repair tissue containing new capillaries, fibroblasts, and macrophages that grows into the necrotic zone of an infarct after the first week, preceding scar formation.

A localised collection of blood within tissue (e.g., subdural, intramuscular, retroperitoneal); may cause mass effect, compression, and ischaemia of adjacent structures.

An insoluble intracellular storage form of iron derived from the degradation of haemoglobin; deposits appear golden-brown on H&E and stain blue with Prussian blue (Perls) stain.

Haemosiderin-laden alveolar macrophages found in the lungs of patients with chronic left heart failure; they appear golden-brown on H&E and stain blue with Prussian blue (Perls) stain.

Active engorgement of a tissue with oxygenated blood due to arteriolar dilatation; the affected tissue appears bright red and is warm to touch.

The red, congested border around an early infarct (hours to 1–2 days), formed by reactive vasodilation and inflammatory hyperaemia in the viable tissue adjacent to the necrotic zone.

An increased tendency to thrombosis due to inherited defects (Factor V Leiden, Protein C/S deficiency, antithrombin deficiency) or acquired conditions (malignancy, pregnancy, antiphospholipid syndrome); the third element of Virchow's triad.

An area of ischaemic coagulative necrosis caused by obstruction of the arterial supply or venous drainage of a tissue, most commonly by thrombosis or embolism.

Dissolution of the cell nucleus in necrosis, leaving a cell with no visible nuclear material; one of the three microscopic forms of nuclear death (alongside karyorrhexis and pyknosis).

Protein-energy malnutrition in children characterised by adequate caloric intake but severe protein deficiency, resulting in hypoalbuminaemia, pitting oedema, ascites, and hepatic steatosis.

Accumulation of lactate in the blood (>2 mmol/L) due to anaerobic glycolysis when tissue oxygen delivery is insufficient; the hallmark of Stage 2 progressive shock and a key resuscitation target.

Alternating pale (platelet-fibrin) and dark (red cell) laminae visible in arterial thrombi on gross section, produced by undulating pulsatile flow; their presence confirms ante-mortem formation in a flowing vessel.

Cell death characterised by complete dissolution of tissue architecture into a liquid mass; the dominant pattern in brain infarction due to the high lipid content of neural tissue.

An outer membrane component of gram-negative bacteria that binds TLR4/CD14 on macrophages, triggering the cytokine storm that initiates septic shock pathogenesis.

The system of lymphatic vessels that returns excess interstitial fluid to the circulation; its impairment results in protein-rich, non-pitting lymphoedema.

Macroscopic appearance of the chronically congested liver — alternating dark red centrilobular congested zones and pale periportal fatty zones resembling the cut surface of a nutmeg; caused by right heart failure.

Abnormal accumulation of fluid in the interstitial tissue spaces or body cavities, resulting from an imbalance in Starling forces or impaired lymphatic drainage.

The process by which fibrovascular granulation tissue grows into a thrombus from the vessel wall, converting it to connective tissue over days to weeks, as part of the healing/fate pathway.

An antemortem thrombus that has been partially or fully replaced by fibrovascular granulation tissue and later collagen, sometimes with recanalised channels restoring partial flow.

A grey-white, firm infarct occurring in solid organs with end-arterial supply (heart, kidney, spleen), where arterial occlusion leaves no residual blood to colour the necrotic zone.

Pinpoint (1–2 mm) haemorrhages in skin or mucous membranes caused by thrombocytopaenia, platelet dysfunction, or small-vessel vasculitis; do not blanch on pressure.

A calcified organised old thrombus within a vein, detectable as a rounded calcification on plain X-ray, reflecting the end-stage of the organisation fate.

The osmotic pressure exerted by plasma proteins (predominantly albumin) that draws fluid from the interstitium back into the capillary; normal value approximately 25 mmHg.

A clot that forms passively after cardiac arrest by stagnation of blood; not attached to the vessel wall, gelatinous, and shows a characteristic bi-layer of yellow-white 'chicken-fat' over dark red 'currant-jelly'.

A haemorrhagic, wedge-shaped area of necrosis in the lung, usually caused by a pulmonary embolus lodging in a pulmonary artery, with blood re-entering via bronchial collaterals to produce the red colour.

Haemorrhagic patches larger than petechiae (3–5 mm or more) in the skin or mucosae; do not blanch on pressure; caused by thrombocytopaenia, coagulopathy, or vasculitis.

Formation of new capillary channels through an organised thrombus, partially restoring blood flow; the final step of the organisation-and-recanalization fate of thrombi.

An infarct in which blood re-enters the necrotic zone due to venous occlusion, dual blood supply, or reperfusion, producing a red-blue haemorrhagic appearance; occurs in lung, bowel, and gonads.

A large thromboembolus that straddles the bifurcation of the main pulmonary artery, causing sudden fatal obstruction of the entire pulmonary outflow and acute cor pulmonale.

Haemorrhagic necrosis of a loop of bowel following mesenteric venous or arterial occlusion, producing a dark red-purple to black gangrenous segment corresponding to a mesenteric vascular territory.

A state of systemic hypoperfusion of tissues leading to cellular hypoxia and dysfunction; classified as hypovolaemic, cardiogenic, distributive (septic/anaphylactic/neurogenic), or obstructive based on mechanism.

The four hydrostatic and oncotic pressure gradients across the capillary wall that determine the net direction and magnitude of fluid movement between plasma and interstitium.

Pathological formation of a solid mass (thrombus) from blood constituents within the intact vascular system in a living subject, distinguished from normal haemostatic clot by its pathological context and extent.

Protein-poor oedema fluid (< 3 g/dL, specific gravity < 1.012) produced by haemodynamic imbalance without vascular injury — characteristic of heart failure, cirrhosis, and nephrotic syndrome.

Three factors predisposing to thrombosis: endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability; proposed by Rudolf Virchow in 1856 and still the dominant teaching framework.

Bilateral haemorrhagic necrosis of the adrenal glands complicating meningococcal septicaemia, caused by DIC-mediated vascular thrombosis and haemorrhage in the adrenal cortex; classically associated with Neisseria meningitidis.

Boundary region between the terminal distributions of two major arterial territories (e.g., anterior and middle cerebral arteries); most vulnerable to ischaemia in hypotensive shock due to 'last-field' positioning in the arterial tree.

The characteristic conical shape of an end-arterial infarct, with its base at the organ capsule and its apex pointing toward the occluded vessel (hilum or root).

An infarct in a solid organ with end-arterial supply where the dense tissue prevents blood re-entry into the necrotic zone; appears pale yellow-white with a hyperaemic rim; occurs in kidney, spleen, and myocardium.