{"id":6269,"date":"2026-05-27T21:21:27","date_gmt":"2026-05-28T01:21:27","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=6269"},"modified":"2026-05-29T15:00:45","modified_gmt":"2026-05-29T19:00:45","slug":"four-types-of-necrosis","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/four-types-of-necrosis\/","title":{"raw":"Section 9 Four Types of Necrosis","rendered":"Section 9 Four Types of Necrosis"},"content":{"raw":"<span class=\"transcription-time-part\" style=\"text-align: initial;font-size: 1em\" data-time-start=\"1537.339\" data-time-end=\"1539.71\">When cells undergo necrosis, the resulting tissue damage ahs a characteristic appearance that depends on the cause and location of the injury.\u00a0 There are four main types of necrosis, each name for what the affected tissue looks like. <\/span>\r\n\r\n<strong><span style=\"color: #2e75b6\">1. Liquefaction Necrosis<\/span><\/strong>\r\n\r\nIn <strong>liquefaction necrosis,<\/strong> dead cells liquefy into a soupy, fluid-filled mass.\u00a0 This occurs because <strong>lytic enzymes<\/strong> release from the lysosomes of dying cells break down proteins and other cellular components.\u00a0 Liquefaction necrosis most commonly results from <strong>infection<\/strong> and follows this progression:\r\n<ul>\r\n \t<li>Cells die and release <strong>hydrolytic enzymes<\/strong> that digest surrounding tissue.<\/li>\r\n \t<li><strong>Macrophages<\/strong> arrive and release cytokines to recruit additional white blood cells, including <strong>neutrophils<\/strong> (also phagocytes), to the area.<\/li>\r\n \t<li><strong>Phagocytes<\/strong> engulf debris and if present, the infecting agent (e.g., bacteria, virus, fungi).<\/li>\r\n \t<li>If the bacteria resist phagocytosis, the infection persists and may require <strong>antibiotics.<\/strong>\u00a0 (Viral and fungal infections require <strong>antiviral<\/strong> and <strong>antifungal <\/strong>medications respectively).<\/li>\r\n \t<li>A fluid-filled space or <strong>abscess<\/strong> may form, particularly in closed tissue such as beneath the skin (e.g., from a splinter carrying bacteria).\u00a0 Treatment may include <strong>lancing<\/strong> the abscess to release fluid and deliver antibiotic therapy.\r\n<ul>\r\n \t<li>If the wound is open, the battle between bacteria and phagocytes may produce <strong>pus<\/strong> - a protein-rich fluid containing dead cells and cell debris.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n[caption id=\"attachment_2272\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189.jpg\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-2272 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189-300x199.jpg\" alt=\"Example of liquefactive necrosis\" width=\"300\" height=\"199\" \/><\/a> Liquefactive necrosis in the lung following angioinvasive aspergillosis, the most severe and aggressive form of invasive aspergillosis (caused by Aspergillus fungi infection). Liquefactive necrosis is a type of cell death characterized by a transformation of tissue into a liquid, viscous mass, which is often associated with microbial infections or internal chemical burns.[\/caption]\r\n\r\n<div class=\"textbox textbox--key-takeaways\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\"><strong>Special Case:\u00a0 Liquefaction Necrosis in the Brain<\/strong><\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nAlthough <strong>liquefaction necrosis<\/strong> is typically caused by infection, the <strong>brain<\/strong> is a notable exception:\u00a0 hypoxia in the brain also causes liquefaction necrosis rather than the coagulative necrosis induced by <strong>hypoxia<\/strong> in other organs.\u00a0 The reason is not fully understood, but it may be related to the brain's lower connective tissue content.\r\n\r\nA <strong>bacterial infection<\/strong> of the brain can similarly cause liquefaction necrosis, potentially forming a fluid-filled abscess visible on brain imaging.\r\n\r\n<\/div>\r\n<\/div>\r\n<strong><span style=\"color: #2e75b6\">2. Coagulative Necrosis<\/span><\/strong>\r\n\r\n<strong>Coagulative necrosis<\/strong> is the most common type and typically results from <strong>ischemia<\/strong> (in any organ other than the brain).\u00a0 \u00a0During ischemia, cells switch to anaerobic metabolism, generating large amounts of <strong>lactic acid<\/strong>.\u00a0 This acidic environment <strong>denatures proteins<\/strong> - including the lytic enzymes that otherwise liquefy the tissue.\u00a0 As a result, the dead tissue takes on a firm, pale yellow, cheese-like appearance.\r\n\r\nBecause the lytic enzymes are themselves denatured, the tissue is not dissolved into soup - it retains its structural outline (at least temporarily) while the cells within are dead.\u00a0 This is commonly seen in ischemic kidney tissue and in the heart following a <strong>myocardial infarction<\/strong> (heart attack).\r\n\r\nSome bacterial infections can cause coagulative necrosis rather than liquefactive necrosis, particularly when bacterial toxins induce ischemia.\u00a0 Similarly viral infections can also induce coagulative necrosis when they cause severe hypoxia in tissues.\r\n\r\n[caption id=\"attachment_6380\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis.png\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-6380 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-300x297.png\" alt=\"After a myocardial infarction, 2 lesions involving the myocardium and the papillary muscles are seen. A and B. Green arrows point to dark mottling, and the black arrows point to a yellow, softened lesion with red-tan borders; these correspond to a myocardial infarction in between 12 to 24 hours and10 to 14 days, respectively. Early coagulative necrosis appears as dark mottling due to regions of hyperemia, edema, and hemorrhage and inflammation. Ischemia leads to cells dying and cellular proteins denaturing in dying and dead cells. The nuclei of dying cells disintegrates and more proteins become denatured giving rise to later signs of coagulative necrosis - a yellow cheese-like mass. The area is infiltrated by neutrophils and macrophages that phagocytose necrotic cells.\" width=\"300\" height=\"297\" \/><\/a> After a myocardial infarction, 2 lesions involving the myocardium and the papillary muscles are seen. A and B. Green arrows point to dark mottling, and the black arrows point to a yellow, softened lesion with red-tan borders; these correspond to a myocardial infarction in between 12 to 24 hours and10 to 14 days, respectively. Early coagulative necrosis appears as dark mottling due to regions of hyperemia, edema, and hemorrhage and inflammation. Ischemia leads to cells dying and cellular proteins denaturing in dying and dead cells. The nuclei of dying cells disintegrates and more proteins become denatured giving rise to later signs of coagulative necrosis - a yellow cheese-like mass. The area is infiltrated by neutrophils and macrophages that phagocytose necrotic cells.[\/caption]\r\n\r\n[caption id=\"attachment_6383\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain.png\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-6383 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-300x201.png\" alt=\"Coagulative necrosis of the cardiomyocytes with absent nuclei and an interstitial neutrophilic infiltrate (black arrow) within 12-24 hours of infarction.\" width=\"300\" height=\"201\" \/><\/a> Coagulative necrosis of the cardiomyocytes with absent nuclei and an interstitial neutrophilic infiltrate (black arrow) within 12-24 hours of infarction. Note that the cardiomyocytes appear glassy and \"ghost-like\" as structural and striated proteins break down and \"melt\" together in homogenous mass.\u00a0 Compare this to the healthy cells in the slide below.[\/caption]\r\n\r\n[caption id=\"attachment_6390\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain.png\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-6390 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-300x229.png\" alt=\"Normal, healthy myocardiocytes with nuclei staining dark purple with H&amp;E dye.\" width=\"300\" height=\"229\" \/><\/a> Normal, healthy myocardiocytes with nuclei staining dark purple with H&amp;E dye.[\/caption]\r\n\r\n[caption id=\"attachment_6386\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain.png\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-6386 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-300x196.png\" alt=\"Well-formed granulation tissue with collagen deposition and neovascularization (black arrow). Granulation tissue consists of newly formed blood vessels (angiogenesis), specialized fibroblasts, macrophages and other white blood cells. As collagen deposition by specialized fibroblasts increases and cellular debris is phagocytosed a dense collagenous scar will develop. Fibrosis, or scarring, begins in around 2 weeks, and eventually, complete scar formation occurs in 2 months.\" width=\"300\" height=\"196\" \/><\/a> Assuming the patient survives the myocardial infarction, cellular debris will be cleared and scarring will take place. During this process, well-formed granulation tissue with collagen deposition and neovascularization (black arrow) will develop. Granulation tissue consists of newly formed blood vessels (angiogenesis), specialized fibroblasts, macrophages and other white blood cells. As collagen deposition by specialized fibroblasts increases and cellular debris is phagocytosed a dense collagenous scar will develop. Fibrosis, or scarring, begins in around 2 weeks, and eventually, complete scar formation occurs in 2 months.[\/caption]\r\n\r\n<strong><span style=\"color: #2e75b6\">3. Caseous Necrosis<\/span><\/strong>\r\n\r\n<strong>Caseous necrosis<\/strong> is caused by particular types of <strong>infection<\/strong> rather than ischemia.\u00a0 Instead of dying as a result of hypoxia, cell death is induced by specific bacteria and fungal infections and the ensuing response by white blood cells.\r\n\r\nThe most common example is <strong>tuberculosis (TB)<\/strong> - a serious <strong>respiratory disease<\/strong> caused by the <strong>bacterium<\/strong> <em>Mycobacterium tuberculosis<\/em> and spread by respiratory droplets.\u00a0 Certain <strong>fungal respiratory infections<\/strong> (e.g., histoplasmosis, cryptococcosis, and coccidioidomycosis) can also result in caseous necrosis.\r\n\r\nIn these respiratory infections, the killing of lung cells attracts white blood cells, including <strong>macrophages<\/strong> to the area.\u00a0 The macrophages promptly wall off the infected area and release digestive chemicals causing the affected cells to disintegrate.\u00a0 The dead tissue has a cheese-like appearance, a necrotic zone that becomes enclosed within a <strong>granuloma<\/strong> (an aggregation of macrophages).\u00a0 When fully walled off (often with a rim of <strong>calcium),<\/strong> this is called a <strong>Ghon focus.<\/strong>\u00a0 The contained tissue has a soft, crumbly, cheese-like appearance, hence the name 'caseous' (from the Latin word for cheese).\r\n\r\nThe danger of TB lies in its ability to persist in latency.\u00a0 Live bacteria can remain viable inside the Ghon focus for years or even decades.\u00a0 If the person later becomes <strong>immunocompromised<\/strong> (due to aging, HIV, or another illness), the bacteria, can reactivate causing progressive lung destruction, form expanding cavities, and even spread through the bloodstream to other organ.\r\n\r\n[caption id=\"attachment_2275\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-2275 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-300x199.jpg\" alt=\"Example of caseous necrosis.\" width=\"300\" height=\"199\" \/><\/a> Caseous necrosis enclosed within a granuloma in the lung during the late stages of tuberculosis following infection by Mycobacterium. Caseous necrosis is a type of cell death where tissue structure is destroyed and is characterized by its \"cheesy\" appearance.[\/caption]\r\n\r\n<strong><span style=\"color: #2e75b6\">4. Fat Necrosis<\/span><\/strong>\r\n\r\n<strong>Fat necrosis<\/strong> is rare and occurs specifically in fatty tissues such as the <strong>pancreas<\/strong> or <strong>breast tissue.<\/strong>\u00a0 When cells in these tissues die, <strong>lipase<\/strong> (an enzyme that breaks down triglycerides) is released.\u00a0 Lipase cleaves <strong>triglycerides<\/strong> into <strong>glycerol<\/strong> and <strong>fatty acid chains<\/strong>.\u00a0 The freed fatty acids then bind to <strong>calcium,<\/strong> forming a chalky, soap-like residue.\u00a0 This white, chalky deposit is the hallmark of fat necrosis.\r\n\r\n[caption id=\"attachment_2274\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-2274 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-300x200.jpg\" alt=\"Example of fat necrosis\" width=\"300\" height=\"200\" \/><\/a> High magnification micrograph of fat necrosis, a type of cell death that only occurs in adipose cells and is caused by some form of physical trauma that results in injury\/loss of blood supply (ex. surgery). Hard lumps may form under the skin where fat necrosis occurs, though this can disappear over time.[\/caption]\r\n\r\n<div class=\"textbox textbox--examples\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\"><strong>\u2217 Real-World Story:\u00a0 Frostbite on Mount Everest - Beck Weathers<\/strong><\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nIn 1996, climber Beck Weathers was left for dead near the summit of Mount Everest.\u00a0 That day was filled with a tragic series of events.\u00a0 During the last day in the final push for the summit, as the climbers ascended from Camp IV, Beck lost his vision and was no longer able to navigate the steep and treacherous terrain.\u00a0 While waiting for the climbing party to return from summitting, Beck became severely hypothermic and the hypoxic conditions of being high altitude led to difficulties in maintaining consciousness.\u00a0 A storm had blown in as the climbing party was attempting the final ascent to the summit.\u00a0 While waiting, Beck slipped into a hypothermic coma for several hours and miraculously awoke and managed to walk back down to Camp IV by himself.\u00a0 On rejoining climbers in the camp, he appeared near death.\u00a0 Little did he know that storm and plunging temperatures would claim 8 lives that day.\r\n\r\nDuring extreme cold exposure at high altitude, the body vasoconstricts blood vessels in the skin - sacrificing the skin's circulation to protect vital internal organs.\u00a0 Beck had lost a glove in the storm and the hours that went by before being able to descend resulted in Beck's nose, cheeks, and hands being deprived of blood flow, oxygen and nutrients for too long.\u00a0 His hands reportedly looked like porcelain and his nose and cheeks had turned black.\u00a0 After the highest-altitude medical evacuation ever performed by a helicopter at the time (a risky challenge due to the thinness of the air), Beck required amputation of all four fingers and thumb of the left hand as well as his nose due to lost circulation in those tissues.\u00a0 Reconstructive surgery of his nose was performed using tissue from his ear and forehead.\r\n\r\n<em>The events of May 1996 are captured in the riveting movie 'Everest' as well as several books, including \"Into Thin Air by Jon Krakauer, \"Left for Dead: My Journey Home from Everest by Beck Weathers, \"The Climb: Tragic Ambitions on Everest\" by Anatoli Boukreev<\/em>.\r\n\r\n<\/div>\r\n<\/div>","rendered":"<p><span class=\"transcription-time-part\" style=\"text-align: initial;font-size: 1em\" data-time-start=\"1537.339\" data-time-end=\"1539.71\">When cells undergo necrosis, the resulting tissue damage ahs a characteristic appearance that depends on the cause and location of the injury.\u00a0 There are four main types of necrosis, each name for what the affected tissue looks like. <\/span><\/p>\n<p><strong><span style=\"color: #2e75b6\">1. Liquefaction Necrosis<\/span><\/strong><\/p>\n<p>In <strong>liquefaction necrosis,<\/strong> dead cells liquefy into a soupy, fluid-filled mass.\u00a0 This occurs because <strong>lytic enzymes<\/strong> release from the lysosomes of dying cells break down proteins and other cellular components.\u00a0 Liquefaction necrosis most commonly results from <strong>infection<\/strong> and follows this progression:<\/p>\n<ul>\n<li>Cells die and release <strong>hydrolytic enzymes<\/strong> that digest surrounding tissue.<\/li>\n<li><strong>Macrophages<\/strong> arrive and release cytokines to recruit additional white blood cells, including <strong>neutrophils<\/strong> (also phagocytes), to the area.<\/li>\n<li><strong>Phagocytes<\/strong> engulf debris and if present, the infecting agent (e.g., bacteria, virus, fungi).<\/li>\n<li>If the bacteria resist phagocytosis, the infection persists and may require <strong>antibiotics.<\/strong>\u00a0 (Viral and fungal infections require <strong>antiviral<\/strong> and <strong>antifungal <\/strong>medications respectively).<\/li>\n<li>A fluid-filled space or <strong>abscess<\/strong> may form, particularly in closed tissue such as beneath the skin (e.g., from a splinter carrying bacteria).\u00a0 Treatment may include <strong>lancing<\/strong> the abscess to release fluid and deliver antibiotic therapy.\n<ul>\n<li>If the wound is open, the battle between bacteria and phagocytes may produce <strong>pus<\/strong> &#8211; a protein-rich fluid containing dead cells and cell debris.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<figure id=\"attachment_2272\" aria-describedby=\"caption-attachment-2272\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189.jpg\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-2272 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189-300x199.jpg\" alt=\"Example of liquefactive necrosis\" width=\"300\" height=\"199\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189-300x199.jpg 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189-768x510.jpg 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189-65x43.jpg 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189-225x150.jpg 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189-350x233.jpg 350w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Aspergillosis_angioinvasive_3679097189.jpg 960w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-2272\" class=\"wp-caption-text\">Liquefactive necrosis in the lung following angioinvasive aspergillosis, the most severe and aggressive form of invasive aspergillosis (caused by Aspergillus fungi infection). Liquefactive necrosis is a type of cell death characterized by a transformation of tissue into a liquid, viscous mass, which is often associated with microbial infections or internal chemical burns.<\/figcaption><\/figure>\n<div class=\"textbox textbox--key-takeaways\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\"><strong>Special Case:\u00a0 Liquefaction Necrosis in the Brain<\/strong><\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>Although <strong>liquefaction necrosis<\/strong> is typically caused by infection, the <strong>brain<\/strong> is a notable exception:\u00a0 hypoxia in the brain also causes liquefaction necrosis rather than the coagulative necrosis induced by <strong>hypoxia<\/strong> in other organs.\u00a0 The reason is not fully understood, but it may be related to the brain&#8217;s lower connective tissue content.<\/p>\n<p>A <strong>bacterial infection<\/strong> of the brain can similarly cause liquefaction necrosis, potentially forming a fluid-filled abscess visible on brain imaging.<\/p>\n<\/div>\n<\/div>\n<p><strong><span style=\"color: #2e75b6\">2. Coagulative Necrosis<\/span><\/strong><\/p>\n<p><strong>Coagulative necrosis<\/strong> is the most common type and typically results from <strong>ischemia<\/strong> (in any organ other than the brain).\u00a0 \u00a0During ischemia, cells switch to anaerobic metabolism, generating large amounts of <strong>lactic acid<\/strong>.\u00a0 This acidic environment <strong>denatures proteins<\/strong> &#8211; including the lytic enzymes that otherwise liquefy the tissue.\u00a0 As a result, the dead tissue takes on a firm, pale yellow, cheese-like appearance.<\/p>\n<p>Because the lytic enzymes are themselves denatured, the tissue is not dissolved into soup &#8211; it retains its structural outline (at least temporarily) while the cells within are dead.\u00a0 This is commonly seen in ischemic kidney tissue and in the heart following a <strong>myocardial infarction<\/strong> (heart attack).<\/p>\n<p>Some bacterial infections can cause coagulative necrosis rather than liquefactive necrosis, particularly when bacterial toxins induce ischemia.\u00a0 Similarly viral infections can also induce coagulative necrosis when they cause severe hypoxia in tissues.<\/p>\n<figure id=\"attachment_6380\" aria-describedby=\"caption-attachment-6380\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis.png\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-6380 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-300x297.png\" alt=\"After a myocardial infarction, 2 lesions involving the myocardium and the papillary muscles are seen. A and B. Green arrows point to dark mottling, and the black arrows point to a yellow, softened lesion with red-tan borders; these correspond to a myocardial infarction in between 12 to 24 hours and10 to 14 days, respectively. Early coagulative necrosis appears as dark mottling due to regions of hyperemia, edema, and hemorrhage and inflammation. Ischemia leads to cells dying and cellular proteins denaturing in dying and dead cells. The nuclei of dying cells disintegrates and more proteins become denatured giving rise to later signs of coagulative necrosis - a yellow cheese-like mass. The area is infiltrated by neutrophils and macrophages that phagocytose necrotic cells.\" width=\"300\" height=\"297\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-300x297.png 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-150x150.png 150w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-768x760.png 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-65x64.png 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-225x223.png 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-350x346.png 350w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis.png 984w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-6380\" class=\"wp-caption-text\">After a myocardial infarction, 2 lesions involving the myocardium and the papillary muscles are seen. A and B. Green arrows point to dark mottling, and the black arrows point to a yellow, softened lesion with red-tan borders; these correspond to a myocardial infarction in between 12 to 24 hours and10 to 14 days, respectively. Early coagulative necrosis appears as dark mottling due to regions of hyperemia, edema, and hemorrhage and inflammation. Ischemia leads to cells dying and cellular proteins denaturing in dying and dead cells. The nuclei of dying cells disintegrates and more proteins become denatured giving rise to later signs of coagulative necrosis &#8211; a yellow cheese-like mass. The area is infiltrated by neutrophils and macrophages that phagocytose necrotic cells.<\/figcaption><\/figure>\n<figure id=\"attachment_6383\" aria-describedby=\"caption-attachment-6383\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain.png\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-6383 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-300x201.png\" alt=\"Coagulative necrosis of the cardiomyocytes with absent nuclei and an interstitial neutrophilic infiltrate (black arrow) within 12-24 hours of infarction.\" width=\"300\" height=\"201\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-300x201.png 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-1024x685.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-768x513.png 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-65x43.png 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-225x150.png 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain-350x234.png 350w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Coagulative-Necrosis-HE-stain.png 1484w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-6383\" class=\"wp-caption-text\">Coagulative necrosis of the cardiomyocytes with absent nuclei and an interstitial neutrophilic infiltrate (black arrow) within 12-24 hours of infarction. Note that the cardiomyocytes appear glassy and &#8220;ghost-like&#8221; as structural and striated proteins break down and &#8220;melt&#8221; together in homogenous mass.\u00a0 Compare this to the healthy cells in the slide below.<\/figcaption><\/figure>\n<figure id=\"attachment_6390\" aria-describedby=\"caption-attachment-6390\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain.png\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-6390 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-300x229.png\" alt=\"Normal, healthy myocardiocytes with nuclei staining dark purple with H&amp;E dye.\" width=\"300\" height=\"229\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-300x229.png 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-1024x780.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-768x585.png 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-65x50.png 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-225x171.png 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain-350x267.png 350w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Normal-Myocardiomyocytes-HE-stain.png 1264w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-6390\" class=\"wp-caption-text\">Normal, healthy myocardiocytes with nuclei staining dark purple with H&amp;E dye.<\/figcaption><\/figure>\n<figure id=\"attachment_6386\" aria-describedby=\"caption-attachment-6386\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain.png\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-6386 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-300x196.png\" alt=\"Well-formed granulation tissue with collagen deposition and neovascularization (black arrow). Granulation tissue consists of newly formed blood vessels (angiogenesis), specialized fibroblasts, macrophages and other white blood cells. As collagen deposition by specialized fibroblasts increases and cellular debris is phagocytosed a dense collagenous scar will develop. Fibrosis, or scarring, begins in around 2 weeks, and eventually, complete scar formation occurs in 2 months.\" width=\"300\" height=\"196\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-300x196.png 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-1024x670.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-768x503.png 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-65x43.png 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-225x147.png 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain-350x229.png 350w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2026\/05\/Myocardial-Infaction-Granuloma-HE-stain.png 1467w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-6386\" class=\"wp-caption-text\">Assuming the patient survives the myocardial infarction, cellular debris will be cleared and scarring will take place. During this process, well-formed granulation tissue with collagen deposition and neovascularization (black arrow) will develop. Granulation tissue consists of newly formed blood vessels (angiogenesis), specialized fibroblasts, macrophages and other white blood cells. As collagen deposition by specialized fibroblasts increases and cellular debris is phagocytosed a dense collagenous scar will develop. Fibrosis, or scarring, begins in around 2 weeks, and eventually, complete scar formation occurs in 2 months.<\/figcaption><\/figure>\n<p><strong><span style=\"color: #2e75b6\">3. Caseous Necrosis<\/span><\/strong><\/p>\n<p><strong>Caseous necrosis<\/strong> is caused by particular types of <strong>infection<\/strong> rather than ischemia.\u00a0 Instead of dying as a result of hypoxia, cell death is induced by specific bacteria and fungal infections and the ensuing response by white blood cells.<\/p>\n<p>The most common example is <strong>tuberculosis (TB)<\/strong> &#8211; a serious <strong>respiratory disease<\/strong> caused by the <strong>bacterium<\/strong> <em>Mycobacterium tuberculosis<\/em> and spread by respiratory droplets.\u00a0 Certain <strong>fungal respiratory infections<\/strong> (e.g., histoplasmosis, cryptococcosis, and coccidioidomycosis) can also result in caseous necrosis.<\/p>\n<p>In these respiratory infections, the killing of lung cells attracts white blood cells, including <strong>macrophages<\/strong> to the area.\u00a0 The macrophages promptly wall off the infected area and release digestive chemicals causing the affected cells to disintegrate.\u00a0 The dead tissue has a cheese-like appearance, a necrotic zone that becomes enclosed within a <strong>granuloma<\/strong> (an aggregation of macrophages).\u00a0 When fully walled off (often with a rim of <strong>calcium),<\/strong> this is called a <strong>Ghon focus.<\/strong>\u00a0 The contained tissue has a soft, crumbly, cheese-like appearance, hence the name &#8216;caseous&#8217; (from the Latin word for cheese).<\/p>\n<p>The danger of TB lies in its ability to persist in latency.\u00a0 Live bacteria can remain viable inside the Ghon focus for years or even decades.\u00a0 If the person later becomes <strong>immunocompromised<\/strong> (due to aging, HIV, or another illness), the bacteria, can reactivate causing progressive lung destruction, form expanding cavities, and even spread through the bloodstream to other organ.<\/p>\n<figure id=\"attachment_2275\" aria-describedby=\"caption-attachment-2275\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-2275 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-300x199.jpg\" alt=\"Example of caseous necrosis.\" width=\"300\" height=\"199\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-300x199.jpg 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-1024x678.jpg 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-768x509.jpg 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-1536x1018.jpg 1536w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-2048x1357.jpg 2048w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-65x43.jpg 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-225x149.jpg 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Tuberculosis_-_Sub-pleural_primary_Ghon_focus_6596011395-scaled-1-350x232.jpg 350w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-2275\" class=\"wp-caption-text\">Caseous necrosis enclosed within a granuloma in the lung during the late stages of tuberculosis following infection by Mycobacterium. Caseous necrosis is a type of cell death where tissue structure is destroyed and is characterized by its &#8220;cheesy&#8221; appearance.<\/figcaption><\/figure>\n<p><strong><span style=\"color: #2e75b6\">4. Fat Necrosis<\/span><\/strong><\/p>\n<p><strong>Fat necrosis<\/strong> is rare and occurs specifically in fatty tissues such as the <strong>pancreas<\/strong> or <strong>breast tissue.<\/strong>\u00a0 When cells in these tissues die, <strong>lipase<\/strong> (an enzyme that breaks down triglycerides) is released.\u00a0 Lipase cleaves <strong>triglycerides<\/strong> into <strong>glycerol<\/strong> and <strong>fatty acid chains<\/strong>.\u00a0 The freed fatty acids then bind to <strong>calcium,<\/strong> forming a chalky, soap-like residue.\u00a0 This white, chalky deposit is the hallmark of fat necrosis.<\/p>\n<figure id=\"attachment_2274\" aria-describedby=\"caption-attachment-2274\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-2274 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-300x200.jpg\" alt=\"Example of fat necrosis\" width=\"300\" height=\"200\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-300x200.jpg 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-1024x683.jpg 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-768x512.jpg 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-1536x1024.jpg 1536w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-2048x1366.jpg 2048w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-65x43.jpg 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-225x150.jpg 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Fat_necrosis_-_very_high_mag-scaled-1-350x233.jpg 350w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-2274\" class=\"wp-caption-text\">High magnification micrograph of fat necrosis, a type of cell death that only occurs in adipose cells and is caused by some form of physical trauma that results in injury\/loss of blood supply (ex. surgery). Hard lumps may form under the skin where fat necrosis occurs, though this can disappear over time.<\/figcaption><\/figure>\n<div class=\"textbox textbox--examples\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\"><strong>\u2217 Real-World Story:\u00a0 Frostbite on Mount Everest &#8211; Beck Weathers<\/strong><\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>In 1996, climber Beck Weathers was left for dead near the summit of Mount Everest.\u00a0 That day was filled with a tragic series of events.\u00a0 During the last day in the final push for the summit, as the climbers ascended from Camp IV, Beck lost his vision and was no longer able to navigate the steep and treacherous terrain.\u00a0 While waiting for the climbing party to return from summitting, Beck became severely hypothermic and the hypoxic conditions of being high altitude led to difficulties in maintaining consciousness.\u00a0 A storm had blown in as the climbing party was attempting the final ascent to the summit.\u00a0 While waiting, Beck slipped into a hypothermic coma for several hours and miraculously awoke and managed to walk back down to Camp IV by himself.\u00a0 On rejoining climbers in the camp, he appeared near death.\u00a0 Little did he know that storm and plunging temperatures would claim 8 lives that day.<\/p>\n<p>During extreme cold exposure at high altitude, the body vasoconstricts blood vessels in the skin &#8211; sacrificing the skin&#8217;s circulation to protect vital internal organs.\u00a0 Beck had lost a glove in the storm and the hours that went by before being able to descend resulted in Beck&#8217;s nose, cheeks, and hands being deprived of blood flow, oxygen and nutrients for too long.\u00a0 His hands reportedly looked like porcelain and his nose and cheeks had turned black.\u00a0 After the highest-altitude medical evacuation ever performed by a helicopter at the time (a risky challenge due to the thinness of the air), Beck required amputation of all four fingers and thumb of the left hand as well as his nose due to lost circulation in those tissues.\u00a0 Reconstructive surgery of his nose was performed using tissue from his ear and forehead.<\/p>\n<p><em>The events of May 1996 are captured in the riveting movie &#8216;Everest&#8217; as well as several books, including &#8220;Into Thin Air by Jon Krakauer, &#8220;Left for Dead: My Journey Home from Everest by Beck Weathers, &#8220;The Climb: Tragic Ambitions on Everest&#8221; by Anatoli Boukreev<\/em>.<\/p>\n<\/div>\n<\/div>\n<div class=\"media-attributions clear\" prefix:cc=\"http:\/\/creativecommons.org\/ns#\" prefix:dc=\"http:\/\/purl.org\/dc\/terms\/\"><h2>Media Attributions<\/h2><ul><li about=\"https:\/\/www.flickr.com\/photos\/pulmonary_pathology\/3679097189\/\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.flickr.com\/photos\/pulmonary_pathology\/3679097189\/\" property=\"dc:title\">Private: Aspergillosis,_angioinvasive_(3679097189)<\/a>  &copy;  <a rel=\"dc:creator\" href=\"https:\/\/www.flickr.com\/people\/30950973@N03\" property=\"cc:attributionName\">Yale Rosen<\/a>    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/\">CC BY-SA (Attribution ShareAlike)<\/a> license<\/li><li about=\"https:\/\/www.researchgate.net\/publication\/347692788_Educational_Case_Myocardial_Infarction_Histopathology_and_Timing_of_Changes\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.researchgate.net\/publication\/347692788_Educational_Case_Myocardial_Infarction_Histopathology_and_Timing_of_Changes\" property=\"dc:title\">Myocardial Infaction Coagulative Necrosis<\/a>  &copy;  Ghafoor, Mariam; Kamal, Maria; Nadeem, Urooba; Husain, Aliya    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/\">CC BY-NC-ND (Attribution NonCommercial NoDerivatives)<\/a> license<\/li><li about=\"https:\/\/www.researchgate.net\/publication\/347692788_Educational_Case_Myocardial_Infarction_Histopathology_and_Timing_of_Changes\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.researchgate.net\/publication\/347692788_Educational_Case_Myocardial_Infarction_Histopathology_and_Timing_of_Changes\" property=\"dc:title\">Myocardial Infaction Coagulative Necrosis H&amp;E stain<\/a>  &copy;  Ghafoor, Mariam; Kamal, Maria; Nadeem, Urooba; Husain, Aliya    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/\">CC BY-NC-ND (Attribution NonCommercial NoDerivatives)<\/a> license<\/li><li about=\"https:\/\/www.researchgate.net\/publication\/270653788_Endoplasmic_reticulum_stress_response_in_spontaneously_hypertensive_rats_is_affected_by_myocardial_ischemia_reperfusion_injury\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.researchgate.net\/publication\/270653788_Endoplasmic_reticulum_stress_response_in_spontaneously_hypertensive_rats_is_affected_by_myocardial_ischemia_reperfusion_injury\" property=\"dc:title\">Normal Myocardiomyocytes H&amp;E stain<\/a>  &copy;  Guo, Xiao-Fu & Yang, Xiang-Jun    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY (Attribution)<\/a> license<\/li><li about=\"https:\/\/www.researchgate.net\/publication\/347692788_Educational_Case_Myocardial_Infarction_Histopathology_and_Timing_of_Changes\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.researchgate.net\/publication\/347692788_Educational_Case_Myocardial_Infarction_Histopathology_and_Timing_of_Changes\" property=\"dc:title\">Myocardial Infaction Granuloma H&amp;E stain<\/a>  &copy;  Ghafoor, Mariam; Kamal, Maria; Nadeem, Urooba; Husain, Aliya    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/\">CC BY-NC-ND (Attribution NonCommercial NoDerivatives)<\/a> license<\/li><li about=\"https:\/\/www.flickr.com\/photos\/pulmonary_pathology\/6596011395\/\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.flickr.com\/photos\/pulmonary_pathology\/6596011395\/\" property=\"dc:title\">Private: Tuberculosis_-_Sub-pleural_primary_(Ghon)_focus_(6596011395)<\/a>  &copy; 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