L3 Pathology Circulatory Disturbance III (CVS) PDF

Level 2 Semester 3  Module CIBL309  Lecture Title Circulatory disturbance III (Ischemia, infarction and gangrene)  Instructor information Dr/ Sarah Nabil Nasif MD Assistant professor of Pathology email: [email protected] I...

Level 2 Semester 3  Module CIBL309  Lecture Title Circulatory disturbance III (Ischemia, infarction and gangrene)  Instructor information Dr/ Sarah Nabil Nasif MD Assistant professor of Pathology email: [email protected] Ischemia Definition: Reduction of arterial blood supply to a tissue. Types: 1-ACUTE ISCHEMIA (Sudden Complete Arterial Occlusion) 2-CHRONIC ISCHEMIA (Gradual Incomplete Arterial Occlusion) 1-ACUTE ISCHEMIA a )Thrombosis (particularly on top of atherosclerosis) b) Embolism Thrombosis and embolism are the most two common causes. c) Surgical ligature of an artery b) Strangulation of vessels d) Twisting of vessels as those of ovary and testis. e) Severe arterial spasm as in i) Raynaud's disease f) Buerger's disease (inflammatory occlusion of vessels in heavy smoking middle-aged males), g) Frost bite: h) Severe arterial compression, Effects: Depend on the efficiency of collaterals: a) Occlusion of an end artery or artery with poor collaterals results in ischemic necrosis (Infarction or gangrene). b) Occlusion of an artery with good collaterals may cause no significant effects. 2-CHRONIC ISCHEMIA Causes: A) Atherosclerosis B) Endarteritis; as in syphilis C) Arterial compression e.g by tumors. Effects: a) With efficient collaterals: no effects. b) With poor collaterals, the following effects occur: i) Pain on exercise e.g angina pectoris (cardiac pain) and intermittent claudication (lower limb muscle pains). ii) Patchy cell injury that gradually leads to patchy fibrosis of the affected tissue e.g myocardial fibrosis in case of coronary atherosclerosis Infarction Definition: An infarct is an area of ischemic necrosis due to sudden ischemia.. Aetiology: 1 -Arterial occlusion by thrombus or embolus represents about 99% of cases; 2-Extensive venous obstruction may rarely lead to ischemia. Types of infarction: Infarction may be pale (anemic) or red (hemorrhagic). 1 -Infraction Due to Arterial Occlusion 2-Infarctions Due to Venous Occlusion 1 -Infraction Due to Arterial Occlusion The occluded artery has poor collateral (end artery), therefore immediately after occlusion no blood reaches the area which appears pale. After 24 hours blood collects in the area following dilatation of the poor arterial collaterals. Thus the infarction appears red. After 36 hours, the necrotic cells within the infarction become swollen. This results in: a) Solid organs as heart, kidney, spleen and brain, the blood cells within the ischemic area are squeezed outside the area; thus the infarct appears pale and is called Pale or anaemic infarction. b) Loose richly vascularized tissues as lung, much blood is trapped inside the ischemic area and will not be squeezed out, so the infarct appears red and is called Red hemorrhagic infarction. 2-Infarctions Due to Venous Occlusion (with or without arterial occlusion) are Red haemorrhagic infarction, these include infarction of intestine, ovary and testis due to twisting of their vessels and brain infarction in case of jugular vein thrombosis. General pathological features of infarction: Gross The infarction is usually pyramidal or wedge- shaped with its apex at the site of vascular occlusion and its base at surface of the organ. This is due to the fan distribution of end arteries. (2) When the infarction base is a serosal surface (pleura, pericardium, or peritoneum) it shows fibrinous exudates (due to fibrinous inflammation). (3) Margins of the infarction are hyperemic due to inflammation. (4) Early the infarction is swollen, but later it becomes contracted due to healing. (5) Infarction may be pale or haemorrhagic. 2)Microsopic picture: (1)The infarction is an area of coagulative necrosis. The necrotic cells exhibit pyknosis, karyorrhexis or karyolysis and appear swollen. They retain their structural outlines for sometimes but later become structureless. In case of CNS infarction in which necrosis is of liquefactive type, the area is structureless from the start. (2) The margins of the infarction show dilated capillaries and some inflammatory cells. (3) The rest of the organ appears normal except in case of lung infarction where the lung shows picture of chronic venous congestion. Fate: (a) Small infarction: Necrotic tissues are removed by macrophages; then granulation tissue fills the defect followed by fibrosis (b) Large infarction: Gets surrounded by a fibrous capsule and its substance may show dystrophic calcification. General reactions: As fever, leukocytosis, increased sedimentation rate and elevation of certain serum enzymes as transaminase in myocardial infarction. Clinical effects: They vary according to site of infarction eg: Hemiplegia occurs if the internal capsule of the brain is affected Chest pain and hemoptysis in lung infarction Gangrene GANGRENE Definition: It is massive tissue necrosis followed by putrefaction. Gangrene can involve any part of the body; the most common sites include the toes, fingers, feet, and hands. Risk factors: Any factor result in cut off blood supply to the affected part, as: - Injury or trauma, such as a crush injury, a severe burn, or frostbite - Diseases that affect the circulation of blood, such as arteriosclerosis, diabetes mellitus, smoking, or Raynaud's disease - Infection of wounds Causes: 1) Necrosis: Is caused by acute ischemia or bacterial toxins. 2) Putrefaction: caused by saprophytic bacteria which break down the protein of the necrotic tissue →hydrogen sulphide that gives the tissue a foul odor. Hydrogen sulphide unites + the iron of hemoglobin →iron sulphide →stains the gangrenous tissue black. Types of Gangrene: 1) Dry gangrene. 2) Moist gangrene. 3) Infective gangrene. 4) Gas gangrene. I. DRY GANGRENE Etiology: caused by arterial occlusion which may be caused by: 1) Thrombus. 2) Embolus. 3) Thromboangitits obliterans (Buerger's disease). 4) Raynaud's disease → spastic occlusion. 5) Surgical ligature. Pathogenesis : 1) Gangrene occurs when there is arterial occlusion with poor collateral circulation. 2) As the arterial supply is only occluded venous and lymphatic drainage and surface evaporation occur, so the gangrene will be of the dry type. 3) The commonest example of dry gangrene is senile gangrene of the lower limb which usually affects old males Senile Gangrene Predisposing factors: 1) Atherosclerosis: common in old age, predisposes to arterial thrombosis and poor collateral circulation. 2) Weak heart action and low blood pressure causes vascular stasis. 3) Low body resistance due to nutritional disturbances, nephritits, anaemia. Arterial occlusion is either spontaneously or follows slight injury as that caused by tight shoes. Pathological features of senile gangrene 1) Distal to the occlusion: Massive necrosis occurs. The affected part is: Pale and cold due to ischemia, Lost sensations. Later on it stains red by escaped blood from necrotic vessels. Drainage and evaporation of blood and tissue fluid → dryness →shrunken and mummified Pathological features of senile gangrene 2) Saprophytic bacteria as bacillus subtilis and diphtheroids invade the necrotic tissue and cause putrefaction and blackish discoloration. Pathological features of senile gangrene 3) The gangrenous part irritates the living one and initiates its inflammation with thrombosis of its vessels and further tissue necrosis → progression of the gangrene. Pathological features of senile gangrene 4) When gangrene reaches level with good blood supply it stops. The toxic products of putrefaction act as an irritant →zone of acute inflammation in the neighboring healthy part which appears as a red line between the healthy and gangrenous part (Line of demarcation). Pathological features of senile gangrene 5) From the healthy side granulation tissue grows towards the gangrenous part with the formation of a groove on the surface called line of separation. This groove may slowly deepen until it separates the gangrenous part leaving a stump II. MOIST GANGRENE Etiology: It is caused by sudden arterial and venous occlusion. It occurs mainly in internal organs as the intestine from which no fluid evaporation can occur. Characterized by: 1- Rapid putrefaction and progression due to presence of tissue fluids. 2- Poor line of demarcation. 3- Absent line of separation. 4- Severe toxemia. Examples: 1) Moist Gangrene of the Intestine 2) Moist Gangrene of the Limb 3) Diabetic Gangrene III. INFECTIVE GANGRENE Definition: A subtype of moist gangrene in which bacteria cause tissue necrosis and putrefaction. Pathogenic bacteria cause tissue necrosis by its toxins then saprophytic bacteria act on dead protein causing putrefaction. IV. GAS GANGRENE Definition: It is infective gangrene mainly of muscles occurring in deep wounds characterized by gases production (hydrogen, carbon dioxide, hydrogen sulphide). - It is characterized by sever toxemia. - The wound is contaminated by soil containing anaerobic spores. - Tissue destruction causes local ischemia which favors germination of the spores  Recommended references https://www.clinicalkey.com/student/content/book/3-s2.0- B9780323353175000041#hl0001115 https://www.clinicalkey.com/student/content/book/3-s2.0- B9780323353175000041