{"id":6273,"date":"2026-05-27T21:22:18","date_gmt":"2026-05-28T01:22:18","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=6273"},"modified":"2026-06-04T22:10:14","modified_gmt":"2026-06-05T02:10:14","slug":"infarction-clinical-death-amputation-and-gangrene-case-application","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/infarction-clinical-death-amputation-and-gangrene-case-application\/","title":{"raw":"Section 11 Infarction, Clinical Death, Amputation and Gangrene Case Application","rendered":"Section 11 Infarction, Clinical Death, Amputation and Gangrene Case Application"},"content":{"raw":"<h3><span style=\"color: #1f5c99\"><strong>Infarction<\/strong><\/span><\/h3>\r\n<strong>Infarction<\/strong> refers to an area of dead cells resulting from oxygen deprivation caused by stoppage of blood flow - i.e., ischemia leading to coagulative necrosis.\u00a0 You are likely already familiar with the term <strong>myocardial infarction<\/strong> (heart attack).\u00a0 Other examples of infarction include ischemic stroke (brain infarction), and necrosis of extremities in severe frostbite or peripheral vascular disease.\r\n<h3><span style=\"color: #1f5c99\"><strong>Defining Death<\/strong><\/span><\/h3>\r\nWhat constitutes death has evolved over the last century, particularly with the advent of artificial ventilators and life-support systems.\u00a0 Today a person is typically declared <strong>clinically dead<\/strong> when the following criteria are met:\r\n<ul>\r\n \t<li>No electrical activity in the brain.<\/li>\r\n \t<li>No response to painful stimuli.<\/li>\r\n \t<li>Absence of cranial reflexes<\/li>\r\n<\/ul>\r\nThe brain and heart are the organs most critical to this determination, as both require continuous oxygen supply and cannot survive even brief periods of ischemia without permanent damage.\r\n<div class=\"textbox textbox--examples\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\"><strong>* Case Application:\u00a0 Diabetes, Ischemia, and Foot Amputation<\/strong><\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nThe most common cause of limb amputation in Canada is diabetes.\u00a0 This case study traces the full cellular pathway from disease to amputation:\r\n<table class=\"grid landscape\" style=\"border-collapse: collapse;width: 100%;height: 168px\" border=\"0\">\r\n<tbody>\r\n<tr style=\"height: 31px\">\r\n<td style=\"width: 10.6623%;height: 31px\"><strong><span style=\"color: #032c80\">Step 1<\/span><\/strong><\/td>\r\n<td style=\"width: 89.3377%;height: 31px\"><strong>Diabetes<\/strong> causes progressive blood vessel damage.\r\n\r\nAs vessel walls are damaged, they narrow, reducing blood flow to peripheral tissues - particularly the feet.<\/td>\r\n<\/tr>\r\n<tr style=\"height: 31px\">\r\n<td class=\"shaded\" style=\"width: 10.6623%;height: 31px\"><strong><span style=\"color: #032c80\">Step 2<\/span><\/strong><\/td>\r\n<td class=\"shaded\" style=\"width: 89.3377%;height: 31px\">Reduced blood flow causes <strong>ischemia<\/strong> of foot tissue:\u00a0 reduced oxygen (hypoxia), reduced nutrient and glucose, and accumulation of waste products.<\/td>\r\n<\/tr>\r\n<tr style=\"height: 31px\">\r\n<td style=\"width: 10.6623%;height: 31px\"><strong><span style=\"color: #032c80\">Step 3<\/span><\/strong><\/td>\r\n<td style=\"width: 89.3377%;height: 31px\">First sign of ischemia:\u00a0 <strong>cyanosis<\/strong> - a blue discolouration of the skin resulting from low hemoglobin oxygen saturation (below ~75%).<\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td class=\"shaded\" style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 4<\/span><\/strong><\/td>\r\n<td class=\"shaded\" style=\"width: 89.3377%;height: 15px\">Ischemia causes <strong>low ATP<\/strong> \u2192 Na<sup>+<\/sup>\/K<sup>+<\/sup> and Na<sup>+<\/sup>\/Ca<sup>2+<\/sup> <strong>pump failure<\/strong> \u2192 intracellular <strong>calcium<\/strong> accumulation \u2192 <strong>phospholipase and protease activation<\/strong> \u2192 cell membrane breakdown \u2192 cell swelling and <strong>lysis.<\/strong>\r\n\r\nSimultaneously, anaerobic metabolism generates lactic acid, lowering intracellular pH and further impairing of enzyme function.<\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 5<\/span><\/strong><\/td>\r\n<td style=\"width: 89.3377%;height: 15px\"><strong>Sensory neurons<\/strong> in the foot die (neuronal death).\r\n\r\nThe patient loses sensation in the foot - they may injure themselves (e.g., step on something sharp) without noticing.<\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td class=\"shaded\" style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 6<\/span><\/strong><\/td>\r\n<td class=\"shaded\" style=\"width: 89.3377%;height: 15px\">An undetected wound becomes <strong>infected.<\/strong>\r\n\r\nThe immune response is <strong>compromised<\/strong> by the same ischemia, so infection can spread unchecked.<\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 7<\/span><\/strong><\/td>\r\n<td style=\"width: 89.3377%;height: 15px\">Dead tissue undergoes <strong>coagulative necrosis<\/strong>.\r\n\r\nIf <strong>gangrene<\/strong> develops (black discolouration from iron sulfide which forms as hemoglobin is degrade and iron binds to hydrogen sulfide release by colonizing bacteria)<\/td>\r\n<\/tr>\r\n<tr style=\"height: 15px\">\r\n<td class=\"shaded\" style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 8<\/span><\/strong><\/td>\r\n<td class=\"shaded\" style=\"width: 89.3377%;height: 15px\">If <strong>revascularization surgery<\/strong> is not possible, <strong>preventative amputation<\/strong> of the affected tissue is performed to stop infection from spreading into healthy tissue.<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<\/div>\r\n<\/div>\r\n<a style=\"font-weight: bold;font-size: 1em\" href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-2231 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-300x173.jpg\" alt=\"Vascular ischemia of the toes with the characteristic cyanosis (bluish-purple hue to skin).\" width=\"300\" height=\"173\" \/><\/a>\r\n\r\nVascular ischemia of the toes with the characteristic cyanosis (bluish-purple hue to skin).\r\n\r\n[caption id=\"attachment_2280\" align=\"alignnone\" width=\"300\"]<a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img class=\"wp-image-2280 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-300x275.jpg\" alt=\"Example of gangrene\" width=\"300\" height=\"275\" \/><\/a> Gangrene in the right foot in a person with diabetes. Gangrene is the death of tissue due to lack of blood flow or following serious bacterial infection, resulting in tissue break down and a greenish-black colour.[\/caption]\r\n\r\n<div class=\"textbox textbox--key-takeaways\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\"><strong>Regenerative Capacity of Different Organs<\/strong><\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nThe ability to recover from ischemic injury, infection, or other causes of damage depends heavily on the regenerative capacity of the affected tissue:\r\n<ul>\r\n \t<li><strong>Skin:<\/strong>\u00a0 High regenerative capacity.\u00a0 New cells replace damaged tissue through mitosis.<\/li>\r\n \t<li><strong>Bone:<\/strong>\u00a0 Good regenerative capacity.\u00a0 Fractures once set properly often heal within months.<\/li>\r\n \t<li><strong>Kidney:<\/strong> Limited regenerative capacity.\u00a0 Can increase in size modestly to compensate, but significant damage is largely permanent.<\/li>\r\n \t<li><strong>Heart:<\/strong>\u00a0 Very limited regenerative capacity.\u00a0 Cardiomyocytes (heart muscle cells) lost to infarction are largely replaced by scar tissue, reducing contractile function.<\/li>\r\n \t<li><strong>Brain and Spinal Cord:<\/strong>\u00a0 Minimal regenerative capacity.\u00a0 Neuronal loss is generally permanent, making strokes, traumatic brain and spinal cord injuries so consequential.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\nThis chapter has examined common terms used in pathophysiology as well as the full spectrum of cellular deterioration - from the quiet accumulation of materials inside aging cells, through two pathways of cell death (planned and unplanned), to the tissue-level consequences of four types of necrosis.\u00a0 These cellular events underlie virtually every disease process you will encounter throughout this course.","rendered":"<h3><span style=\"color: #1f5c99\"><strong>Infarction<\/strong><\/span><\/h3>\n<p><strong>Infarction<\/strong> refers to an area of dead cells resulting from oxygen deprivation caused by stoppage of blood flow &#8211; i.e., ischemia leading to coagulative necrosis.\u00a0 You are likely already familiar with the term <strong>myocardial infarction<\/strong> (heart attack).\u00a0 Other examples of infarction include ischemic stroke (brain infarction), and necrosis of extremities in severe frostbite or peripheral vascular disease.<\/p>\n<h3><span style=\"color: #1f5c99\"><strong>Defining Death<\/strong><\/span><\/h3>\n<p>What constitutes death has evolved over the last century, particularly with the advent of artificial ventilators and life-support systems.\u00a0 Today a person is typically declared <strong>clinically dead<\/strong> when the following criteria are met:<\/p>\n<ul>\n<li>No electrical activity in the brain.<\/li>\n<li>No response to painful stimuli.<\/li>\n<li>Absence of cranial reflexes<\/li>\n<\/ul>\n<p>The brain and heart are the organs most critical to this determination, as both require continuous oxygen supply and cannot survive even brief periods of ischemia without permanent damage.<\/p>\n<div class=\"textbox textbox--examples\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\"><strong>* Case Application:\u00a0 Diabetes, Ischemia, and Foot Amputation<\/strong><\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>The most common cause of limb amputation in Canada is diabetes.\u00a0 This case study traces the full cellular pathway from disease to amputation:<\/p>\n<table class=\"grid landscape\" style=\"border-collapse: collapse;width: 100%;height: 168px\">\n<tbody>\n<tr style=\"height: 31px\">\n<td style=\"width: 10.6623%;height: 31px\"><strong><span style=\"color: #032c80\">Step 1<\/span><\/strong><\/td>\n<td style=\"width: 89.3377%;height: 31px\"><strong>Diabetes<\/strong> causes progressive blood vessel damage.<\/p>\n<p>As vessel walls are damaged, they narrow, reducing blood flow to peripheral tissues &#8211; particularly the feet.<\/td>\n<\/tr>\n<tr style=\"height: 31px\">\n<td class=\"shaded\" style=\"width: 10.6623%;height: 31px\"><strong><span style=\"color: #032c80\">Step 2<\/span><\/strong><\/td>\n<td class=\"shaded\" style=\"width: 89.3377%;height: 31px\">Reduced blood flow causes <strong>ischemia<\/strong> of foot tissue:\u00a0 reduced oxygen (hypoxia), reduced nutrient and glucose, and accumulation of waste products.<\/td>\n<\/tr>\n<tr style=\"height: 31px\">\n<td style=\"width: 10.6623%;height: 31px\"><strong><span style=\"color: #032c80\">Step 3<\/span><\/strong><\/td>\n<td style=\"width: 89.3377%;height: 31px\">First sign of ischemia:\u00a0 <strong>cyanosis<\/strong> &#8211; a blue discolouration of the skin resulting from low hemoglobin oxygen saturation (below ~75%).<\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td class=\"shaded\" style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 4<\/span><\/strong><\/td>\n<td class=\"shaded\" style=\"width: 89.3377%;height: 15px\">Ischemia causes <strong>low ATP<\/strong> \u2192 Na<sup>+<\/sup>\/K<sup>+<\/sup> and Na<sup>+<\/sup>\/Ca<sup>2+<\/sup> <strong>pump failure<\/strong> \u2192 intracellular <strong>calcium<\/strong> accumulation \u2192 <strong>phospholipase and protease activation<\/strong> \u2192 cell membrane breakdown \u2192 cell swelling and <strong>lysis.<\/strong><\/p>\n<p>Simultaneously, anaerobic metabolism generates lactic acid, lowering intracellular pH and further impairing of enzyme function.<\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 5<\/span><\/strong><\/td>\n<td style=\"width: 89.3377%;height: 15px\"><strong>Sensory neurons<\/strong> in the foot die (neuronal death).<\/p>\n<p>The patient loses sensation in the foot &#8211; they may injure themselves (e.g., step on something sharp) without noticing.<\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td class=\"shaded\" style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 6<\/span><\/strong><\/td>\n<td class=\"shaded\" style=\"width: 89.3377%;height: 15px\">An undetected wound becomes <strong>infected.<\/strong><\/p>\n<p>The immune response is <strong>compromised<\/strong> by the same ischemia, so infection can spread unchecked.<\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 7<\/span><\/strong><\/td>\n<td style=\"width: 89.3377%;height: 15px\">Dead tissue undergoes <strong>coagulative necrosis<\/strong>.<\/p>\n<p>If <strong>gangrene<\/strong> develops (black discolouration from iron sulfide which forms as hemoglobin is degrade and iron binds to hydrogen sulfide release by colonizing bacteria)<\/td>\n<\/tr>\n<tr style=\"height: 15px\">\n<td class=\"shaded\" style=\"width: 10.6623%;height: 15px\"><strong><span style=\"color: #032c80\">Step 8<\/span><\/strong><\/td>\n<td class=\"shaded\" style=\"width: 89.3377%;height: 15px\">If <strong>revascularization surgery<\/strong> is not possible, <strong>preventative amputation<\/strong> of the affected tissue is performed to stop infection from spreading into healthy tissue.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/div>\n<\/div>\n<p><a style=\"font-weight: bold;font-size: 1em\" href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-2231 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-300x173.jpg\" alt=\"Vascular ischemia of the toes with the characteristic cyanosis (bluish-purple hue to skin).\" width=\"300\" height=\"173\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-300x173.jpg 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-1024x589.jpg 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-768x442.jpg 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-1536x884.jpg 1536w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-2048x1178.jpg 2048w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-65x37.jpg 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-225x129.jpg 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/Ischemia-scaled-1-350x201.jpg 350w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><\/p>\n<p>Vascular ischemia of the toes with the characteristic cyanosis (bluish-purple hue to skin).<\/p>\n<figure id=\"attachment_2280\" aria-describedby=\"caption-attachment-2280\" style=\"width: 300px\" class=\"wp-caption alignnone\"><a href=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1.jpg\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-2280 size-medium\" src=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-300x275.jpg\" alt=\"Example of gangrene\" width=\"300\" height=\"275\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-300x275.jpg 300w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-1024x938.jpg 1024w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-768x703.jpg 768w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-1536x1406.jpg 1536w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-2048x1875.jpg 2048w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-65x60.jpg 65w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-225x206.jpg 225w, https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-content\/uploads\/sites\/1961\/2024\/09\/GangreneFoot-scaled-1-350x320.jpg 350w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><figcaption id=\"caption-attachment-2280\" class=\"wp-caption-text\">Gangrene in the right foot in a person with diabetes. Gangrene is the death of tissue due to lack of blood flow or following serious bacterial infection, resulting in tissue break down and a greenish-black colour.<\/figcaption><\/figure>\n<div class=\"textbox textbox--key-takeaways\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\"><strong>Regenerative Capacity of Different Organs<\/strong><\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>The ability to recover from ischemic injury, infection, or other causes of damage depends heavily on the regenerative capacity of the affected tissue:<\/p>\n<ul>\n<li><strong>Skin:<\/strong>\u00a0 High regenerative capacity.\u00a0 New cells replace damaged tissue through mitosis.<\/li>\n<li><strong>Bone:<\/strong>\u00a0 Good regenerative capacity.\u00a0 Fractures once set properly often heal within months.<\/li>\n<li><strong>Kidney:<\/strong> Limited regenerative capacity.\u00a0 Can increase in size modestly to compensate, but significant damage is largely permanent.<\/li>\n<li><strong>Heart:<\/strong>\u00a0 Very limited regenerative capacity.\u00a0 Cardiomyocytes (heart muscle cells) lost to infarction are largely replaced by scar tissue, reducing contractile function.<\/li>\n<li><strong>Brain and Spinal Cord:<\/strong>\u00a0 Minimal regenerative capacity.\u00a0 Neuronal loss is generally permanent, making strokes, traumatic brain and spinal cord injuries so consequential.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<p>This chapter has examined common terms used in pathophysiology as well as the full spectrum of cellular deterioration &#8211; from the quiet accumulation of materials inside aging cells, through two pathways of cell death (planned and unplanned), to the tissue-level consequences of four types of necrosis.\u00a0 These cellular events underlie virtually every disease process you will encounter throughout this course.<\/p>\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:\/\/commons.wikimedia.org\/wiki\/File:Ischemia.JPG\"><a rel=\"cc:attributionURL\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Ischemia.JPG\" property=\"dc:title\">Private: Ischemia<\/a>  &copy;  <a rel=\"dc:creator\" href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Doc_James\" property=\"cc:attributionName\">James Heilman<\/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:\/\/commons.wikimedia.org\/wiki\/File:GangreneFoot.JPG\"><a rel=\"cc:attributionURL\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:GangreneFoot.JPG\" property=\"dc:title\">Private: GangreneFoot<\/a>  &copy;  <a rel=\"dc:creator\" href=\"https:\/\/commons.wikimedia.org\/wiki\/User:Doc_James\" property=\"cc:attributionName\">James Heilman<\/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><\/ul><\/div>","protected":false},"author":1370,"menu_order":13,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-6273","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":3,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6273","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":9,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6273\/revisions"}],"predecessor-version":[{"id":6643,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6273\/revisions\/6643"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/3"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/6273\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=6273"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=6273"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=6273"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=6273"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}