All macroscopic slides. Part 3 of 3 of the clinical pathoanatomy course for medical students Plovdiv medical Uni. Part 1 and 2 cover microscopic slides.
This document discusses pericardial diseases and tumors of the heart. It describes different types of pericardial effusions and pericarditis such as serous, fibrinous, purulent, hemorrhagic, and caseous pericarditis. The causes, morphology, and characteristics of each type are provided. It also discusses primary and metastatic tumors of the heart, describing the most common types like myxomas, lipomas, and rhabdomyomas, and how they present and are diagnosed. Metastatic tumors commonly spread to the heart from the lungs, breast, or lymphomas.
PMU third/fourth year Clinical pathonanatomy Part 1BenjiH
Part one of the full clinical anatomy micro and macroscopic slides.
this part covers the first 32 microscopic slide topics. For medical students Plovdiv medical university.
The document discusses bronchiectasis, which is a disease characterized by permanent dilation of the bronchi and bronchioles caused by destruction of muscle and elastic tissue. It can be congenital or post-infectious. Morphologically, the bronchi and bronchioles are dilated up to 4 times normal size. Histologically, the walls show inflammation and fibrosis. Clinically, it presents with persistent cough and sputum. Complications include lung abscess, amyloidosis, and cor pulmonale.
- Hemangioma is a benign tumor of blood vessels characterized by increased and abnormal blood vessels. Cavernous hemangioma involves large, dilated vascular channels in the liver. It arises from endothelial cells and can cause abdominal pain from compression.
- Coronary artery atherosclerosis involves plaques with necrotic cores, cholesterol, and inflammatory cells that can rupture and cause thrombosis, potentially leading to myocardial infarction.
- Aortic aneurysm is an abnormal dilation of the aorta that can contain thrombi and cause emboli in the lungs through fragmentation. Medial calcification or Monckeberg's sclerosis involves calcification of medium arteries and can cause hypertension.
This document discusses several topics related to edema and fluid accumulation in the body:
1. It defines edema as increased fluid in the interstitial tissue spaces and describes different types of fluid accumulation depending on the anatomical location.
2. It categorizes the pathophysiologic causes of edema into increased hydrostatic pressure, reduced plasma osmotic pressure, sodium retention, and lymphatic obstruction.
3. It provides examples of conditions that fall under each category and can result in edema.
This document provides an outline and overview of lung cancer (bronchial carcinoma). It discusses the epidemiology, risk factors like smoking, pathogenesis, types, staging systems, clinical features, diagnosis, management including surgery and chemotherapy, complications, differential diagnosis, prognosis and conclusions. The respiratory system, normal physiology, and common radiological presentations are also outlined.
This document discusses pulmonary embolism (PE), which occurs when a blood clot breaks off and travels to the lungs. It defines PE and classifies the severity. Risk factors include prolonged bed rest, surgery, cancer, and inherited or acquired hypercoagulable states. Symptoms are often nonspecific but include chest pain and difficulty breathing. PE is caused by deep vein thrombosis (DVT) in the legs traveling to the lungs. The diagnosis is challenging due to vague symptoms but is important because untreated PE can be fatal.
This document discusses various types of heart disease including hypertensive heart disease, cardiomyopathies, valvular heart disease, and infective endocarditis. It provides details on the criteria, morphology, causes, and clinical features of each condition. Specifically, it describes how hypertensive heart disease can cause left or right ventricular hypertrophy and heart failure. It also explains the differences between dilated, hypertrophic, and restrictive cardiomyopathies and their causes and features.
This document discusses pericardial diseases and tumors of the heart. It describes different types of pericardial effusions and pericarditis such as serous, fibrinous, purulent, hemorrhagic, and caseous pericarditis. The causes, morphology, and characteristics of each type are provided. It also discusses primary and metastatic tumors of the heart, describing the most common types like myxomas, lipomas, and rhabdomyomas, and how they present and are diagnosed. Metastatic tumors commonly spread to the heart from the lungs, breast, or lymphomas.
PMU third/fourth year Clinical pathonanatomy Part 1BenjiH
Part one of the full clinical anatomy micro and macroscopic slides.
this part covers the first 32 microscopic slide topics. For medical students Plovdiv medical university.
The document discusses bronchiectasis, which is a disease characterized by permanent dilation of the bronchi and bronchioles caused by destruction of muscle and elastic tissue. It can be congenital or post-infectious. Morphologically, the bronchi and bronchioles are dilated up to 4 times normal size. Histologically, the walls show inflammation and fibrosis. Clinically, it presents with persistent cough and sputum. Complications include lung abscess, amyloidosis, and cor pulmonale.
- Hemangioma is a benign tumor of blood vessels characterized by increased and abnormal blood vessels. Cavernous hemangioma involves large, dilated vascular channels in the liver. It arises from endothelial cells and can cause abdominal pain from compression.
- Coronary artery atherosclerosis involves plaques with necrotic cores, cholesterol, and inflammatory cells that can rupture and cause thrombosis, potentially leading to myocardial infarction.
- Aortic aneurysm is an abnormal dilation of the aorta that can contain thrombi and cause emboli in the lungs through fragmentation. Medial calcification or Monckeberg's sclerosis involves calcification of medium arteries and can cause hypertension.
This document discusses several topics related to edema and fluid accumulation in the body:
1. It defines edema as increased fluid in the interstitial tissue spaces and describes different types of fluid accumulation depending on the anatomical location.
2. It categorizes the pathophysiologic causes of edema into increased hydrostatic pressure, reduced plasma osmotic pressure, sodium retention, and lymphatic obstruction.
3. It provides examples of conditions that fall under each category and can result in edema.
This document provides an outline and overview of lung cancer (bronchial carcinoma). It discusses the epidemiology, risk factors like smoking, pathogenesis, types, staging systems, clinical features, diagnosis, management including surgery and chemotherapy, complications, differential diagnosis, prognosis and conclusions. The respiratory system, normal physiology, and common radiological presentations are also outlined.
This document discusses pulmonary embolism (PE), which occurs when a blood clot breaks off and travels to the lungs. It defines PE and classifies the severity. Risk factors include prolonged bed rest, surgery, cancer, and inherited or acquired hypercoagulable states. Symptoms are often nonspecific but include chest pain and difficulty breathing. PE is caused by deep vein thrombosis (DVT) in the legs traveling to the lungs. The diagnosis is challenging due to vague symptoms but is important because untreated PE can be fatal.
This document discusses various types of heart disease including hypertensive heart disease, cardiomyopathies, valvular heart disease, and infective endocarditis. It provides details on the criteria, morphology, causes, and clinical features of each condition. Specifically, it describes how hypertensive heart disease can cause left or right ventricular hypertrophy and heart failure. It also explains the differences between dilated, hypertrophic, and restrictive cardiomyopathies and their causes and features.
This document contains summaries of various pathological conditions:
- Schwannoma is a usually benign nerve sheath tumor composed of Schwann cells that normally produce myelin.
- Glioblastoma is the most aggressive brain cancer, with non-specific initial symptoms like headaches and nausea.
- Melanoma is a skin cancer that develops in pigment cells and has a tendency to spread and cause serious illness.
- Leiomyosarcoma arises from the muscular part of the uterus and is a malignant smooth muscle tumor.
Embolism is the obstruction of blood vessels by foreign material that travels through the bloodstream. There are several types of embolism classified by the material causing obstruction (solid, liquid, gas), source of obstruction (cardiac, arterial, venous), and whether infection is present. Common types include thromboembolism caused by blood clots, pulmonary embolism from clots blocking pulmonary arteries, fat/bone marrow embolism from tissue trauma, and amniotic fluid embolism during childbirth from amniotic material entering the mother's bloodstream. Embolisms can cause infarction of tissues and organs downstream from the obstruction depending on the location and size of the obstructing material.
This document provides information about myocardial infarction including:
- Myocardial infarction is caused by interruption of blood supply to the heart muscle, usually due to blockage of a coronary artery.
- Risk factors that can lead to coronary artery blockage include hypertension, hyperlipidemia, diabetes, and smoking.
- A thrombus or embolism in a coronary artery cuts off the blood supply, causing cell death in the affected heart muscle area.
- The location and size of the infarction depends on which coronary artery is blocked. Transmural infarcts that penetrate the full heart wall thickness are more likely to cause complications than smaller subendocardial infarcts.
2- ATHEROSCLEROSIS and its pathophysiologywajidullah9551
This document provides an overview of atherosclerosis and myocardial infarction for a pathology lecture. It begins with objectives to understand pathogenesis and complications of atherosclerosis and ischemic heart disease. Key topics to be discussed include risk factors for atherosclerosis, pathogenesis of atherosclerotic plaques, clinical complications such as coronary artery disease and stroke, and changes seen in myocardial infarction. Diagrams and descriptions of healthy blood vessels and the progression of atherosclerotic plaques from fatty streaks to raised lesions are also provided. The document concludes with sample test questions related to the material.
The document discusses the anatomy and disorders of the mediastinum. It begins by describing the anatomy of the different compartments of the mediastinum and structures contained within each. It then discusses various disorders that can arise in each compartment, including tumors, cysts, infections and others. Common tumors mentioned are thymoma, teratomas, and lymphomas. Clinical features, investigations, treatment and prognosis of different disorders are provided.
Thrombosis is caused by Virchow's triad of endothelial injury, stasis or turbulence of blood, and hypercoagulability. Endothelial injury is the most dominant influence and can lead to thrombosis in the heart or arteries. Alterations in normal blood flow such as stasis and turbulence bring platelets into contact with the endothelium and predispose to thrombosis. Hypercoagulability, either inherited or acquired, also increases the risk of thrombosis. Thrombi may embolize, causing partial or complete occlusion of vessels and ischemic necrosis of distal tissues. Pulmonary embolism is a common complication of deep vein thrombosis in the legs. Systemic embolism usually arises from intracard
Embolism is the obstruction of blood vessels by foreign particles carried in the bloodstream called emboli. The majority of emboli are thromboemboli originating from thrombi or blood clots that detach from vessel walls. Common types of emboli include solid materials like thrombi or tumors, liquid materials like fat or amniotic fluid, and gaseous materials like air. Pulmonary embolism is a potentially fatal condition caused by emboli blocking the pulmonary arteries, which can lead to sudden death or pulmonary infarction and complications like pulmonary hypertension. Other clinical manifestations of embolism include infarction of organs like the heart, brain, kidneys, liver, and spleen due to impaired blood flow.
Thrombosis is the formation of a blood clot within a blood vessel or cavity of the heart. Virchow identified three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can propagate or embolize, becoming lodged in another vessel and resulting in infarction of downstream tissue. Infarctions appear pale/white in solid organs and red/hemorrhagic in lungs/other tissues. Over time, infarcted tissue progresses from coagulative necrosis to phagocytosis and scar formation.
Based on the information provided about Mr. Gamal:
- CT angiography would likely reveal an abdominal aortic aneurysm, showing markedly increased aortic diameter below the renal arteries.
- The most probable cause in his case is atherosclerosis, given his risk factors of diabetes, hypertension, smoking history and hyperlipidemia.
- His risk factors are diabetes, hypertension, smoking history, obesity (BMI of 30), and hyperlipidemia.
- His condition would be classified as an atherosclerotic abdominal aortic aneurysm.
- Possible complications include rupture of the aneurysm, thrombosis/embolism, compression of adjacent structures, or occlusion of branches supplying organs like the kidneys or intestines
This document provides an overview of thromboembolism and its pathology. It discusses the Virchow triad of factors that predispose to thrombosis - endothelial injury, abnormal blood flow, and hypercoagulability. The key components and processes of thrombogenesis are described. Risk factors for deep vein thrombosis and the pathology of pulmonary embolism are also reviewed. The student is expected to understand the basic pathology of thrombogenesis and identify risk factors for thrombosis.
Valvular heart disease can cause stenosis or insufficiency of the valves. Degenerative valvular disease is caused by changes to the extracellular matrix of the valves like calcification or alterations in collagen and elastin. Calcific aortic stenosis causes calcified masses on the aortic valve cusps. Myxomatous mitral valve disease causes floppy, thickened mitral valve leaflets. Rheumatic valve disease principally causes mitral stenosis from thickened, scarred leaflets and cords. Infective endocarditis forms valve vegetations containing microorganisms. Cardiomyopathies are heart muscle diseases classified as dilated, hypertrophic, or restrictive based on morphological and functional patterns.
The document discusses diseases of the heart, specifically chronic ischemic heart disease and myocardial infarction. It describes the blood supply to the heart from the coronary arteries and the risks factors, causes, classifications, signs and symptoms, progression, complications and treatment of myocardial infarction. Key points include that myocardial infarction is mainly caused by blockages in the coronary arteries from atherosclerosis, and can lead to complications like arrhythmias, heart failure, cardiogenic shock or cardiac rupture if not properly treated.
Rheumatic heart disease is caused by rheumatic fever, which occurs after a streptococcal throat infection and causes inflammation of the heart valves. Genetic factors influence the risk of developing rheumatic heart disease. Acute rheumatic fever causes inflammatory lesions called Aschoff bodies in heart tissue that contain characteristic giant cells. Long-term rheumatic heart disease results in thickened and scarred heart valves that may become narrowed or insufficient.
Mitral stenosis is a narrowing of the mitral valve opening that blocks (obstructs) blood flow from the left atrium to the left ventricle. Mitral stenosis usually results from rheumatic fever, but infants can be born with the condition. Mitral stenosis does not cause symptoms unless it is severe
This document discusses various types of edema, thrombosis, and embolism. It defines edema as increased fluid in the interstitial tissue spaces. Thrombosis is the formation of a thrombus or blood clot within vessels. An embolism occurs when a piece of this thrombus breaks off and travels to lodge in another vessel. Common causes, presentations, and outcomes of these conditions are described.
15-pathology of hemodynamicsHEMODYNAMIC DISORDERS.pptLearta Asani
Edema is excess fluid accumulation in interstitial spaces that can occur systemically or locally. It is caused by increased hydrostatic pressure, reduced plasma oncotic pressure, sodium retention, or lymphatic obstruction. Generalized edema with profound swelling is called anasarca. Thrombosis is the formation of a clot (thrombus) within a blood vessel. It results from an interaction of platelets, damaged endothelial cells, and activation of the coagulation cascade. The major influences predisposing to thrombosis are endothelial injury, blood stasis, and hypercoagulability.
Pathology of hemodynamic disorders part 2 nov 2017 Dr. Sufia HusainSufia Husain
This document discusses various types of hemodynamic disorders including embolism, infarction, and shock. It provides detailed information on different types of embolism such as pulmonary thromboembolism, systemic thromboembolism, fat embolism, air embolism, and amniotic fluid embolism. It also describes the stages of shock, associated pathophysiology and morphological changes in tissues during the different stages of shock.
This document discusses infarcts, which are areas of ischemic necrosis caused by occlusion of the arterial supply or venous drainage. It defines infarcts and lists common causes like thrombotic occlusion. It describes different types of infarcts based on color, age, and presence of infection. Pathogenesis involves local hyperemia, edema, hemorrhage, and cellular changes leading to necrosis replaced by fibrous tissue. Gross morphology shows wedge-shaped lesions pointing toward the occluded vessel. Microscopy typically shows coagulative necrosis and inflammatory reaction at the periphery replaced by fibrous tissue. Commonly affected organs and outcomes are also outlined.
This document discusses infarcts, which are areas of ischemic necrosis caused by occlusion of the arterial supply or venous drainage. It defines infarcts and lists common causes like thrombotic occlusion. It describes different types of infarcts based on color, age, and presence of infection. Pathogenesis involves local hyperemia, edema, hemorrhage, and cellular changes leading to necrosis replaced by fibrous tissue. Gross morphology shows wedge-shaped areas pointing toward the occluded vessel. Microscopy shows coagulative necrosis and inflammatory reaction at the periphery replaced by fibrous tissue. Commonly affected organs and outcomes are also outlined.
The document discusses various types of aneurysms including their definition, causes, classifications, pathological features, complications, and treatments. It focuses on atherosclerotic, syphilitic, and dissecting aortic aneurysms. Atherosclerotic aneurysms most commonly involve the abdominal aorta in older males. Syphilitic aneurysms occur in tertiary syphilis and mainly affect the thoracic aorta. Dissecting aneurysms are caused by a tear in the aortic wall and often affect hypertensive males. Treatments discussed include surgical clipping or coiling for brain aneurysms, open surgical grafting or endovascular stenting for aortic and peripheral aneurysms.
This document contains summaries of various pathological conditions:
- Schwannoma is a usually benign nerve sheath tumor composed of Schwann cells that normally produce myelin.
- Glioblastoma is the most aggressive brain cancer, with non-specific initial symptoms like headaches and nausea.
- Melanoma is a skin cancer that develops in pigment cells and has a tendency to spread and cause serious illness.
- Leiomyosarcoma arises from the muscular part of the uterus and is a malignant smooth muscle tumor.
Embolism is the obstruction of blood vessels by foreign material that travels through the bloodstream. There are several types of embolism classified by the material causing obstruction (solid, liquid, gas), source of obstruction (cardiac, arterial, venous), and whether infection is present. Common types include thromboembolism caused by blood clots, pulmonary embolism from clots blocking pulmonary arteries, fat/bone marrow embolism from tissue trauma, and amniotic fluid embolism during childbirth from amniotic material entering the mother's bloodstream. Embolisms can cause infarction of tissues and organs downstream from the obstruction depending on the location and size of the obstructing material.
This document provides information about myocardial infarction including:
- Myocardial infarction is caused by interruption of blood supply to the heart muscle, usually due to blockage of a coronary artery.
- Risk factors that can lead to coronary artery blockage include hypertension, hyperlipidemia, diabetes, and smoking.
- A thrombus or embolism in a coronary artery cuts off the blood supply, causing cell death in the affected heart muscle area.
- The location and size of the infarction depends on which coronary artery is blocked. Transmural infarcts that penetrate the full heart wall thickness are more likely to cause complications than smaller subendocardial infarcts.
2- ATHEROSCLEROSIS and its pathophysiologywajidullah9551
This document provides an overview of atherosclerosis and myocardial infarction for a pathology lecture. It begins with objectives to understand pathogenesis and complications of atherosclerosis and ischemic heart disease. Key topics to be discussed include risk factors for atherosclerosis, pathogenesis of atherosclerotic plaques, clinical complications such as coronary artery disease and stroke, and changes seen in myocardial infarction. Diagrams and descriptions of healthy blood vessels and the progression of atherosclerotic plaques from fatty streaks to raised lesions are also provided. The document concludes with sample test questions related to the material.
The document discusses the anatomy and disorders of the mediastinum. It begins by describing the anatomy of the different compartments of the mediastinum and structures contained within each. It then discusses various disorders that can arise in each compartment, including tumors, cysts, infections and others. Common tumors mentioned are thymoma, teratomas, and lymphomas. Clinical features, investigations, treatment and prognosis of different disorders are provided.
Thrombosis is caused by Virchow's triad of endothelial injury, stasis or turbulence of blood, and hypercoagulability. Endothelial injury is the most dominant influence and can lead to thrombosis in the heart or arteries. Alterations in normal blood flow such as stasis and turbulence bring platelets into contact with the endothelium and predispose to thrombosis. Hypercoagulability, either inherited or acquired, also increases the risk of thrombosis. Thrombi may embolize, causing partial or complete occlusion of vessels and ischemic necrosis of distal tissues. Pulmonary embolism is a common complication of deep vein thrombosis in the legs. Systemic embolism usually arises from intracard
Embolism is the obstruction of blood vessels by foreign particles carried in the bloodstream called emboli. The majority of emboli are thromboemboli originating from thrombi or blood clots that detach from vessel walls. Common types of emboli include solid materials like thrombi or tumors, liquid materials like fat or amniotic fluid, and gaseous materials like air. Pulmonary embolism is a potentially fatal condition caused by emboli blocking the pulmonary arteries, which can lead to sudden death or pulmonary infarction and complications like pulmonary hypertension. Other clinical manifestations of embolism include infarction of organs like the heart, brain, kidneys, liver, and spleen due to impaired blood flow.
Thrombosis is the formation of a blood clot within a blood vessel or cavity of the heart. Virchow identified three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can propagate or embolize, becoming lodged in another vessel and resulting in infarction of downstream tissue. Infarctions appear pale/white in solid organs and red/hemorrhagic in lungs/other tissues. Over time, infarcted tissue progresses from coagulative necrosis to phagocytosis and scar formation.
Based on the information provided about Mr. Gamal:
- CT angiography would likely reveal an abdominal aortic aneurysm, showing markedly increased aortic diameter below the renal arteries.
- The most probable cause in his case is atherosclerosis, given his risk factors of diabetes, hypertension, smoking history and hyperlipidemia.
- His risk factors are diabetes, hypertension, smoking history, obesity (BMI of 30), and hyperlipidemia.
- His condition would be classified as an atherosclerotic abdominal aortic aneurysm.
- Possible complications include rupture of the aneurysm, thrombosis/embolism, compression of adjacent structures, or occlusion of branches supplying organs like the kidneys or intestines
This document provides an overview of thromboembolism and its pathology. It discusses the Virchow triad of factors that predispose to thrombosis - endothelial injury, abnormal blood flow, and hypercoagulability. The key components and processes of thrombogenesis are described. Risk factors for deep vein thrombosis and the pathology of pulmonary embolism are also reviewed. The student is expected to understand the basic pathology of thrombogenesis and identify risk factors for thrombosis.
Valvular heart disease can cause stenosis or insufficiency of the valves. Degenerative valvular disease is caused by changes to the extracellular matrix of the valves like calcification or alterations in collagen and elastin. Calcific aortic stenosis causes calcified masses on the aortic valve cusps. Myxomatous mitral valve disease causes floppy, thickened mitral valve leaflets. Rheumatic valve disease principally causes mitral stenosis from thickened, scarred leaflets and cords. Infective endocarditis forms valve vegetations containing microorganisms. Cardiomyopathies are heart muscle diseases classified as dilated, hypertrophic, or restrictive based on morphological and functional patterns.
The document discusses diseases of the heart, specifically chronic ischemic heart disease and myocardial infarction. It describes the blood supply to the heart from the coronary arteries and the risks factors, causes, classifications, signs and symptoms, progression, complications and treatment of myocardial infarction. Key points include that myocardial infarction is mainly caused by blockages in the coronary arteries from atherosclerosis, and can lead to complications like arrhythmias, heart failure, cardiogenic shock or cardiac rupture if not properly treated.
Rheumatic heart disease is caused by rheumatic fever, which occurs after a streptococcal throat infection and causes inflammation of the heart valves. Genetic factors influence the risk of developing rheumatic heart disease. Acute rheumatic fever causes inflammatory lesions called Aschoff bodies in heart tissue that contain characteristic giant cells. Long-term rheumatic heart disease results in thickened and scarred heart valves that may become narrowed or insufficient.
Mitral stenosis is a narrowing of the mitral valve opening that blocks (obstructs) blood flow from the left atrium to the left ventricle. Mitral stenosis usually results from rheumatic fever, but infants can be born with the condition. Mitral stenosis does not cause symptoms unless it is severe
This document discusses various types of edema, thrombosis, and embolism. It defines edema as increased fluid in the interstitial tissue spaces. Thrombosis is the formation of a thrombus or blood clot within vessels. An embolism occurs when a piece of this thrombus breaks off and travels to lodge in another vessel. Common causes, presentations, and outcomes of these conditions are described.
15-pathology of hemodynamicsHEMODYNAMIC DISORDERS.pptLearta Asani
Edema is excess fluid accumulation in interstitial spaces that can occur systemically or locally. It is caused by increased hydrostatic pressure, reduced plasma oncotic pressure, sodium retention, or lymphatic obstruction. Generalized edema with profound swelling is called anasarca. Thrombosis is the formation of a clot (thrombus) within a blood vessel. It results from an interaction of platelets, damaged endothelial cells, and activation of the coagulation cascade. The major influences predisposing to thrombosis are endothelial injury, blood stasis, and hypercoagulability.
Pathology of hemodynamic disorders part 2 nov 2017 Dr. Sufia HusainSufia Husain
This document discusses various types of hemodynamic disorders including embolism, infarction, and shock. It provides detailed information on different types of embolism such as pulmonary thromboembolism, systemic thromboembolism, fat embolism, air embolism, and amniotic fluid embolism. It also describes the stages of shock, associated pathophysiology and morphological changes in tissues during the different stages of shock.
This document discusses infarcts, which are areas of ischemic necrosis caused by occlusion of the arterial supply or venous drainage. It defines infarcts and lists common causes like thrombotic occlusion. It describes different types of infarcts based on color, age, and presence of infection. Pathogenesis involves local hyperemia, edema, hemorrhage, and cellular changes leading to necrosis replaced by fibrous tissue. Gross morphology shows wedge-shaped lesions pointing toward the occluded vessel. Microscopy typically shows coagulative necrosis and inflammatory reaction at the periphery replaced by fibrous tissue. Commonly affected organs and outcomes are also outlined.
This document discusses infarcts, which are areas of ischemic necrosis caused by occlusion of the arterial supply or venous drainage. It defines infarcts and lists common causes like thrombotic occlusion. It describes different types of infarcts based on color, age, and presence of infection. Pathogenesis involves local hyperemia, edema, hemorrhage, and cellular changes leading to necrosis replaced by fibrous tissue. Gross morphology shows wedge-shaped areas pointing toward the occluded vessel. Microscopy shows coagulative necrosis and inflammatory reaction at the periphery replaced by fibrous tissue. Commonly affected organs and outcomes are also outlined.
The document discusses various types of aneurysms including their definition, causes, classifications, pathological features, complications, and treatments. It focuses on atherosclerotic, syphilitic, and dissecting aortic aneurysms. Atherosclerotic aneurysms most commonly involve the abdominal aorta in older males. Syphilitic aneurysms occur in tertiary syphilis and mainly affect the thoracic aorta. Dissecting aneurysms are caused by a tear in the aortic wall and often affect hypertensive males. Treatments discussed include surgical clipping or coiling for brain aneurysms, open surgical grafting or endovascular stenting for aortic and peripheral aneurysms.
Similar to PMU third/fourth year Clinical pathoanatomy Part 3 (20)
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
2. 1. Benign Nephrosclerosis
Arteriolosclerotica (Macroscopic):
Patchy ischemic atrophy with focal
loss of parenchyma
Granular appearance
Diffuse Pin-point haemorrhages on
cortical surface.
Kidneys are slightly smaller than
normal
Essential hypertension/ diabetes
mellitus, benign because there is
little altered function of the
kidneys but increased risk for renal
failure.
Accelerated (malignant) stage of
essential HT
Left: Malignant hypertension
(300/150mmhg) – a
complication/sequelae of benign form,
leads to focal haemorrhaging which
obscures the corticomedullary junction
3. 2. Hypertensive heart – macro:
• Increased peripheral vascular resistance
and cardiac workload induces
remodelling of the myocardium. This is
seen as concentric left ventricular
hypertrophy a.k.a “Cor hypertonicum”.
• Normal thickness = 5-9mm, borderline =
13/14mm, hypertrophic = > 15mm
• The rest of the heart is relatively
unchanged. Secondary right ventricular
hypertrophy may occur after
hypertension induced left sided heart
failure and pulmonary hypertension.
• Complications of hypertensive heart
disease: increased risk of myocardial
infarction (larger mass of muscle to be
supplied with O2), arrhythmias, heart
failure, aortic dissection, aneurysms,
accelerated atherosclerosis due to
endothelial injury, nephrosclerosis,
hypertensive retinopathy, cerebral
vascular accident (stroke).
4. 3. Atherosclerosis Aortae (Macro):
FIRST STAGE - Fatty streak (white arrows)
Thin, flat, yellow
Non-protruding linear streaks
Present from very young age, even
birth
Increase in number until young
adulthood then stabilise or may
regress
Reversible with lifestyle modification
occur at areas of turbulent flow such
as around the orifices of branching
vessels of the aorta.
From top to bottom: Severe. Moderate and mild
atherosclerosis
THIRD STAGE – Atheromatous
plaque
Reddish brown mural
thrombi
Ulceration of intimal surface
Irregular shaped white-
yellow atheromatous
plaques
Calcifications
Plaques become more
confluent/ join up the
further the disease
progresses.
5. FOURTH STAGE – complicated plaque (unstable)
Fates:
1. Plaque may grow around the branch points
of vasa vasorum (own vessels) of the aorta
leading to atrophy of tunica media. This
weakens the wall and can lead to
atherosclerotic dissection or aneurysm.
2. Hemorrhage of weak neovascularisation in
the plaque may lead to a hematoma which
expands the plaque to occlude the lumen,
subsequent infarction.
3. Ulceration and rupture of the plaque can
release cholesterol (fat) emboli leading to
stroke, MI or PE.
4. Dystrophic calcification which hardens the
artery leading to changes in pulse, blood
pressure and further endothelial damage.
Calcific fragments can break off into
circulation (calcific emboli) and cause
infarction.
5. Re-canalisation: rare but the plaque can be
invades by endothelial cells which re-open a
larger lumen. A compensatory response.
Common location of atherosclerosis:
1. Coronary As => IHD and MI
2. Carotids => vascular dementia, berry aneurysms, cerebral stroke
3. Renal Artery => Stenosis and Secondary hypertension, renal infarction.
4. Iliac As/ Femoral => dry gangrene of feet, intermittent claudication.
5. Aorta => Mesenteric ischemia, dissection, aneurysm
6. Retinal arteries => amaurosis fugax/ acute temporary vision loss
Retinal
embolus,
gangrene,
renal stenosis,
berry
aneurysm.
6. 4. Myocardial Infarction (Macro):
Collagen deposition healed MI
Discrete pale
infarct with
hyperaemic border
Large transmural MI
Often multi-focal lesions
Initially; Red-purple blotchy
areas (hemorrhage and
reperfusion injury)
Progression: Yellow border
which extends inwards
(collagen/ granulation tissue)
and hyperaemic border.
Finally; Bright pale yellow/
white/ grey scar
Can lead to HF, arrhythmia.
Aneurysm, cardiac tamponade
7. 5. Fibrous endocarditis (Macroscopic):
Rheumatic (post-infectious) type endocarditis. The other two types
are 1). Infective (ulcero-polypotic) and 2). Non infective which is
further subdivided into a). NBTE (marantic) and b). Libman-sacks
(verrucous - SLE, anti-phospholipid syndrome)
Chronic valvulitis of mitral valve
In rheumatic
valvopathy we see
fusion of
commissures, sterile
fibrin vegetations and
shortened thickened,
fused chordae.
8. 6. Ulcero-polypotic Endocarditis (infectious) – macroscopic:
Bacterial/ septic endocarditis characterised by the
formation of pedunculated masses/ vegetations of fibrin
or thrombin mixed with bacterial colonies and
calcifications adhered to an ulcerative heart valve.
Acute forms = S. aureus or GABHS infection
Subacute forms = Strep. Viridans, Strep pyogenes and
Staph. Epidermidis
2 predisposing factors are required:
1). BACTEREMIA (anything from poor oral hygiene/ teeth
brushing micro-traumas – full blown sepsis)
2). Damage to or structural abnormality of valve endocardium
– allows for adherence of passing bacterial colonies.
Vegetations are multiple, large and friable
Tendency to break off as septic- thrombo emboli
More common on left side of heart – mitral and aortic
valves.
Ulceration of valve cusps, rupture of chordae tendineae.
Local destruction may be rapid and severe
Complications include: heart murmur, arrhythmia, AV
block, pericardial effusion, cardiogenic shock, acute heart
failure, stroke or pulmonary thromboembolism, brain,
heart or lung abscesses, meningitis, glomerulonephritis,
sepsis.
9. 7. Fibrinous pericarditis (gross appearance);
Dry course granular pericardial surface
Fibrinous exudate with stringy adhesions between
external epicardial surface and the inner surface of the
pericardium.
Fibrin has pale yellowish colour
Shaggy rough “Bread and Butter” appearance.
Clinically; pericardial friction rub can be heard.
Haemorrhagic
pericarditis
10. 8. Emphysema bullosa (macro):
5 classifications – 1. centri-acinar/ centrilobular, 2. pan-acinar/ panlobular, 3.
paraseptal (distal lobular), 4. irregular (paracictricial) and 5. mixed.
Multiple, large dilations most commonly under the pleura
Lungs are large, hyperinflated, pale and with little blood
Evidence of chronic smoking often evident; tar deposits
Complications: Spontaneous pneumothorax if they
burst, collapse of terminal bronchioles – pneumonia,
abscesses, pulmonary fibrosis, atelectasis, respiratory
failure, cor pulmonale, chronic bronchitis (often
concurrent), increased risk of lung cancer.
11. 9. Bronchopneumonia (lobular pneumonia)
abscedens – macro:
• Patchy areas of consolidation
• Usually bilateral.
• Hemorrhage and brighter areas of alveolar
purulent exudate.
• Consolidation matches the distribution/ shape of
the pulmonary lobules hence the name.
• This type of pneumonia is most often acquired in
hospital settings.
• Staph Aureus, Klebsiella, E-coli and Pseudomonas
are common culprits.
• Poorly defined areas are usually grey-red to tan
yellow in colour.
• Cavitary lesions/ abscesses may develop amongst
the consolidation.
• Areas of consolidation are firmer than healthy
areas. They also appear raised on cut section.
12. 10. Silicosis – Gross:
Upper lobe is usually affected earlier in the disease
Early lesions = multiple small pale to black ( if coal dust also present)
nodules progressing to hard collagenous scars.
Fibrosis tends to occur more at the hilar lymphnodes and pleura.
Nodules may have undulating/ irregular or stellate shaped edges due to
traction from the thick fibrosis. They may cavitate centrally due to
tuberculosis or ischemia.
Nodules range from 1-5mm.
Well circumscribed
Pleura is thickened, may
have adhesions to chest wall
If severe, or in concurrence
with COPD, may lead to cor
pulmonale.
Silicosis does not seem to
increase risk of bronchogenic
carcinomas, unlike
asbestosis.
13. 11. Lung Carcinoma - Gross:
Most common and fatal cancer
90% of lung cancers are associated with smoking
Cancers most commonly arise in the hilum
(centrally) and less often in the periphery
Classification of lung cancers:
1). Bronchogenic (most common type)
TWO subtypes of bronchogenic Ca:
a). NSCLC (non small cell lung ca -85%)
b). SCLC (small cell lung cancer – 15%)
Of NSCLC, adenocarcinoma is most common = 40%
Followed by Squamous = 30% and Large cell = 15%
1. Adenocarcinoma:
Strong assoc. with scarred areas and chronic
damage
Lobulated or spiculated shaped mass
May have central area of fibrosis or necrosis
More common in upper lobes, prefers periphery.
Pale, solid, whitish mass
Well circumscribed but not encapsulated
Anthracotic pigments (from smoking)
Has four subtypes
Bronchogenic Lung Cancers (hilar/ centrally located – most
likely squamous cell carcinomas)
14. Peripherally located carcinomas – later identified to
be adenocarcinomas.
2. Squamous cell ca:
Arises centrally from main
bronchi
Massive necrosis
Cavitation
Hemorrhages
Strong assoc. with smoking
Grey-white fleshy tumour
May cause bronchiectasis,
atelectasis, recurrent
pneumonia.
Tendency to invade hilum and
surrounding parenchyma
15. 12. Esophageal diverticulum – macroscopic:
Visible outpouching of wall of Esophagus
Contains ALL layers of wall (true diverticulum)
Rare = pseudo diverticulum – only mucosa or
submucosa
2 types by etiology: A). Congenital (more
common in upper Esophagus or at level of
carina) B). Acquired: 1. Pulsion (from
increased intraluminal pressure) or 2.
Traction (pulled by the formation of
adhesions, fibrosis)
Three types by location: 1. proximal
(zenkers), 2. mid-esophageal (usually traction
type) and 3. epiphrenic (distal)
Zenkers diverticulum is a pulsion type
acquired esophageal diverticulum in
hypopharyngeal location – due to esophageal
obstructions.
Complications: diverticulitis (hyperaemia/
wall thickening, leucocyte infiltration, peri-
diverticular edema, muco-purulent exudates,
hemorrhage, perforation and subsequent
pneumomediastinum or subcutaneous
emphysema in neck, esophageal cancer.
Opened post-mortem specimen of the oesophagus. An oesophageal
diverticulum with creamy exudates and a hard foreign body (bone)
adherent to the oesophageal wall (arrow).
16. 13. Acute stomach ulcer – gross :
Less than 1cm
Round shape
Well defined margins
Sometimes confluent
Dark brown – black colour due to formation of hematin.
Fibrinoid necrosis centrally in pit of ulcer
Surrounding tissue is hyperaemic
Most common location: lesser curvature of stomach, if
lesion occurs on greater curvature suspect ulcerating gastric
carcinoma.
Subtypes of ulcer = A). Curling's ulcer (severe burns) and B).
Cushing's ulcer – due to hemodynamic changed due to brain
injury/ elevated ICP.
17. 14. Chronic gastric ulcer with
perforation - gross :
Round/ oval shape
4-6 cm in diameter (larger than
acute ulcers)
Depth variable – may extend
through all layers; submucosa,
muscle layer and adventitia
Sides are hyperaemic, bulging
and overhanging
Base is firm due to fibrosis –
callus of the ulcer.
Floor may be relatively clean,
active hemorrhage or fully
perforating the gastric wall.
Mucosal folds radiate outward
from ulcer margins.
18. 15. Gastric carcinoma:
Variable presentation; as large solitary mass,
non-healing ulcer or diffuse infiltrative
burrowing process (linitis plastica).
Four types: 1). Polypoid/ papillary exophytic
growth 2). Fungating (raised margins with
central ulceration 3) ulcerative with infiltrating
margins 4). Linitis plastica (wall becomes thick
and rigid)
Wall thickening, rugal fold flattening
Hemorrhage and necrosis (signs of aggression)
19. 16. Micronodular liver cirrhosis – gross:
Nodules are less than 3mm (macro = 3mm
– 3cm).
Diffuse involvement of all hepatic lobules.
Fat deposition may be seen – although less
than in fatty liver disease, this gives the
organ a tawny brown-yellow appearance.
Normal liver is rich maroon red/brown.
Surface is granular and studded with
nodules.
Thick fibrose septae may be seen on cut-
section.
In severe disease the organ shrinks.
20. 17: Cholelithiasis - gross:
Gallbladder wall may be hypertrophic (thick,
contracted, calcified and firm organ) or
atrophic (large, flaccid, distended, pale and
grey organ).
Diffuse mural hyperaemia – mucosa is bright
red, mucinous or muco-purulent exudate
(empyema)
Abscesses may form in the wall.
Stones can be of FOUR kinds:
1). Cholesterol stones – oral or polygonal with
flattened facets, smooth, yellow-white.
2). Pigment stones – due to increased
unconjugated bilirubin often as a result of
haemolysis. These stones are small, numerous,
mulberry shape and jet black.
3). Calcium stones – grey/white, hard and small.
4). Mixed stones – most common type, a
laminated stone comprised of alternating deposits
of the contents of the other stones
21. 18. Malignant Non H Lymphoma - (macro):
Solid tumours of the lymphnodes – usually
cervical. One third of time they affect extranodal
sites – the tonsils, GIT and spleen.
Grossly the appearance of HL and NHL are very
similar., the differences are in behaviour, labs and
microscopic examination.
Normal lymphnode capsule invaded and destroyed
Surrounding fat tissue is invaded forming thick
tracts investing multiple lymphnodes – matted,
firm texture upon palpation.
NHL in lymphnodes near pancreas
22. 19. Hodgkin's lymphoma spleen (macro):
! DO NOT CONFUSE “Porphyry spleen” with “Sago” or “lardaceous”
spleen.
Porphyry spleen is caused by Hodgkin's lymphoma and is
characterised by multiple nodular leucocyte tumour infiltrates.
BOTH Sago spleen and lardaceous spleen are caused by amyloidosis
of the organ – characterised by diffuse granular amyloid deposits.
This can be due to hereditary amyloidosis (abnormal protein
synthesis) or secondary to chronic inflammatory conditions e.g.
rheumatoid arthritis, Inflammatory bowel disease etc, due to
plasma cell disorders that produce too much immunoglobulins or
senile amyloidosis– due to old age and other idiopathic causes.
These are shown on the next slide for comparison
Porphyry spleen:
Scattered grey-
white nodules
Can be singular
and large or
multiple and
smaller.
Nodules coalesce
over course of
disease
# of nodules =
prognostic (>5 =
bad).
24. 20. Nephrosclerosis
(glomerulonephritic type - macro):
A.k.a diffuse sclerosing GN.
Symmetrically and severely
atrophic kidneys - shrunken and
only weigh 1/3rd of a healthy
kidney.
Surface is finely granular and
cortex is thinned
Pelvis and calices are relatively
spared, medulla unremarkable.
Capsule may be adherent to
cortex.
25. 21. Chronic pyelonephritis with
calculus – gross:
• Coarsely granular and nodular
surface of kidney.
• Kidney is asymmetrical and
irregular in shape.
• Kidney is heavily scarred and
shrunken, capsular scarring and
retractions correspond to
involvement and dilation/ blunting
of the underlying calyx.
• Blunting of papillae, papillary
necrosis is common.
• Abscesses and cysts may be seen
• Calculi are common in the renal
pelvis and proximal ureter, as a
result ureter may be dilated.
26. 22. Polycystic kidney gross:
• A congenital/ genetic disease that
runs in families causing progressive
cystic change in the kidneys with age,
pain, high blood pressure and renal
failure.
• Kidneys are massively enlarged and
multi-cystic with replacement of the
entire cortex.
27. 23. Renal Cell Carcinoma – gross:
• Large, round, well-defined
masses that usually occur and
one of the poles of the kidney.
• Pale beige-yellow appearance
against the healthy red kidney.
• Centred in the cortex, may have
pseudocapsule exteriorly and
disrupt the smooth contour of the
kidney while invading the
medulla or renal sinus interiorly.
• May be cystic in appearance
(bottom right image) or have
multiple hemorrhages, focal
necrosis or calcifications within
the mass – a sign of its aggressive
behaviour.
• Often invades the renal vein and
vena cava.
28. Kidney abscess – Macro:
• Round to ovoid pale yellow
lesions.
• Associated with purulent
infections of the kidney – either
due to hematogenous spread or
an ascending UTI, can also be
caused by renal tuberculosis
(bottom right image).
• Well circumscribed
• Frequently multitudinous –
especially in acute pyelonephritis
where many small abscesses are
dotted around the capsular
surface and cortex of enlarged
firm red kidneys (top left image).
29. 24. Hypertrophy of prostate - gross:
Benign prostatic hyperplasia mostly
affects the peri-urethral and transitional
area of the gland.
Gland enlarges to over 5/6cm and can
weigh 100g+. Normal size = 3-4cm.
Yellow – white nodules of variable size.
Enlarged gland can be seen pushing
prominently out into bladder lumen.
May compress urethra “slit-like
appearance” on cut section.
30. 25. Carcinoma of urothelium of bladder
– Macro:
Two classifications: 1). Epithelial
origin – more common 2). Non-
epithelial origin.
Urothelial (transitional) cell
carcinoma constitutes 90% of
epithelial tumours. Others include
squamous cc, adenocarcinoma, small
cell and mixed.
More common in males, 5th decade
of life.
Non-papillary type usually bulky,
large and ulcerative.
Papillary type urothelial ca:
fused and branched fern-like pattern.
Exophytic, free-floating.
Lateral wall most commonly
affected, then posterior wall and
trigone.
Usually small – less than 2cm
May be single or multiple
May infiltrate lamina propria and
deep in detrusor muscle
31. 26. Seminoma testis – macro:
• Most common malignant
tumour of testis (45%). It is of
the GERM CELL class of
tumours.
• Uniform solid tan to pale
cream, grey- white mass.
• Necrosis and hemorrhage are
uncommon and minimal.
• If spontaneous regression
occurs, scarring may be the
only indicator of its occurrence.
• Homogenous and lobulated,
well circumscribed.
• Testis is usually enlarged,
seminoma may replace entire
testicular tissue.
• Usually confined to just the
testis in 90% of cases.
32. 27. Tubal abortion - macroscopic:
Less than 1% of all pregnancies.
Increased risk in patients with history of
pelvic inflammatory disease.
Embryo, placenta and amniotic sac are
formed as normal.
This is followed by rupture of the tube
around the 2nd – 6th week of gestation.
May cause massive bleeding
intraperitoneally.
Foetus either dies immediately or soon
after rupture, it may be absorbed,
calcified (lithopaedion), extruded into
peritoneum or the products of
conception may become septic.
Grossly the affected ovarian tube is
usually dilated/ distended, hyperaemic.
It may contain what appears to be a
hematoma.
Products of conception are often visible
– embryo, chorionic villi
Tube may be intact or ruptured.
33. 28. Molar pregnancy – macro:
There are four main categories of
trophoblastic gestational disease:
1) Partial mole
2) Complete mole
3) Invasive mole
4) Choriocarcinoma
Partial mole:
Placental tissue exists but is immature and
abnormal – admixed with hydropic villi that
tend to be smaller and more numerous
than in complete mole.
Fetal parts and gestational sac may be seen
Complete mole:
Hydropic villi which appear as fluid-filled
semi-transparent vesicles or variable size
“Bunch of grapes” appearance.
Normal fetal parts are absent
Normal placental structures are absent
Invasive mole: Fluid filled vesicles extend into
myometrium. Uterus may be perforated.
Appears as erosive haemorrhagic lesion.
Partial molar pregnancies
Complete molar
pregnancy
Partial mole
34. 29. Carcinoma of cervix – macro:
Classification of cervical disease:
1). Inflammatory cervical lesions.
2). Non-neoplastic cervical proliferations (eg. squamous
metaplasia, polyps)
3). SIL (squamous intraepithelial lesion or CIN (cervical
intraepithelial lesion).
- CIN 1 = (Less than 1/3rd of epithelium affected or
Mild dysplasia) = low grade SIL
- CIN 2 (1-2/3rds involved or moderate dysplasia)
- CIN 3 (full thickness/ severe dysplasia or in situ
carcinoma – doesn’t invade basement membrane!)
[CIN 2+ 3 = High grade SIL]
Grossly: squamous cell carcinoma is most common
(75% of cases) followed by adenocarcinoma (20%).
Squamous Cell Carcinoma:
Red, friable indurated lesion.
Can be ulcerated or elevated granular lesion
Variable morphology: Exophytic, papillary, polypoid,
nodular and ulcerative forms have been observed.
Can be invasive and infiltrate surrounding
structures. May be necrotic and haemorrhagic.
Associated with HPV 16 + 18 infection.
35. 30. Carcinoma of endometrium – macro:
Most common in post-menopausal women (55-65).
Previous pregnancies have a protective effect.
Most present grossly as polypoid/ fungating masses.
Uterus is often asymmetrically enlarged
Invasion into the muscular layer is usually present from
an early stage.
Earliest symptom = abnormal uterine bleeding (AUB).
Soft and homogenous growth. May sometimes be
heterogenous – with foci of necrosis and hemorrhage
on cut surface.
Some cases present as simple endometrial thickening –
the lining in this case is red, abundant and friable to
touch.
Usually has a favourable prognosis.
Types include: 1), endometrioid 2). Serous 3). Clear cell
adenocarcinoma and 4). Mixed type
Has five stages of progression:
STAGE 1 - body of uterus only
STAGE 2 – body and cervix
STAGE 3 – extra-uterine but remains in true pelvis
STAGE4 – Distant metastasis
36. 31. Krukenberg metastasis in Ovaries - gross:
Metastatic type tumour of the ovaries (5-10% of all
ovarian tumours are metastasis), krukenberg is almost
always bilateral (80%).
It is a mucin rich signet- ring adenocarcinoma with
gastric origin.
Other origins include breast and colon. Rarely the
primary tumour may be located in the
gallbladder, biliary tract, urinary bladder or
cervix.
Prognosis of this tumour is extremely poor.
Small, multinodular surface with extensive
extra-ovarian spread.
Metastatic tumours are most difficult to
distinguish from mucinous type primary
tumours of the ovary.
Scattered growth with intervening normal
ovarian parenchyma
Multiple vascular emboli nearby
Similar characteristics to primary tumour
– whichever that may be.
May have multiple cysts.
Lymph and blood vessel invasion
37. 32. Breast Cancer - gross:
1. Invasive ductal carcinomas usually
form a solid mass with a variable
consistency.
2. Tumours with abundant
desmoplastic stroma are firm to
hard and grey-white in
appearance.
3. The presence of microcalcifications
may impart a gritty consistency.
4. There may be yellow-white streaks
of necrosis and foci of
hemorrhage.
5. Extensively necrotic tumours may
develop cystic change.
6. The tumours that are composed
largely of neoplastic and
inflammatory cells without much
stroma tend to be soft and
fleshy and bulge when they are
sectioned.
38. A B
A: Clearly visible nipple retraction in advanced stage breast cancer
B: Peau d’orange - skin appears
studded with dimples like an orange
peel.
40. 33. Macroglossia (acromegaly) - gross:
A form of “true” macroglossia (the tongue is indeed larger)
whereas “pseudo-macroglossia” is a relative macroglossia –
where the tongue appears larger due to the oral cavity or
mandible (micrognathia) being smaller the normal.
Caused by muscular hypertrophy of tongue tissue in response to
excessive growth hormone. The oral cavity is often enlarged also.
Most cases of acromegaly are caused by a benign
functional (secretory) adenoma of the pituitary gland.
Acromegaly is usually undiagnosed until the age of
30 to 50. If it occurs before the fusing of the
epiphyseal growth plates at the end of puberty, it is
known as gigantism – due to prolonged bone growth.
Differential diagnosis of macroglossia:
Congenital true macroglossia:
- Mucopolysaccharidosis
- Idiopathic tongue muscular hypertrophy
- Haemangioma
- Lymphangioma
Acquired true macroglossia:
- Amyloidosis (most common cause in adults)
- Hypothyroidism (myxoedema)
- Sarcoidosis, lymphoma, trauma, TB, syphilis, actinomycosis
41. 34. Nodular goiter –
macroscopic:
Unlike simple goiters,
multinodular goiters are
asymmetrical and very large,
weighing on average between
200-700g but can grow to be
as large as 2kg!
Nodularity and poor
encapsulation
Haemorrhages are common
Scarring is abundant as is
cystic degeneration and focal
calcifications.
Individual nodules are variable
in size with dominant ones
often larger than 10cm.
Surface is bumpy and irregular
Brown gelatinous colloid
collections may be seen on
cut surface.
42. 35. Diabetic glomerulosclerosis - macroscopic:
Renal lesions appear around 10-20 years
after onset of diabetes.
Major symptoms include; proteinuria,
glucosuria, progressive decrease in renal
function, increased recurrence of
pyelonephritis, edema and hypertension
may manifest as late-stage symptoms.
Gross features include:
- Slight to moderate symmetrical enlargement
of the size of the kidneys.
- Subcapsular cortical surface is finely granular
and dark red in colour.
- Cortex is thinned
- Atherosclerotic changes to renal vessels,
renal stenosis and subsequent renal atrophy.
- Pyelonephritic features may be observed
(due to the predisposition of glycosuria to
precipitate infections); deep irregular surface
scars and retractions, dilated and deformed
calyces, renal calculi, cysts and if active
infection was occurring; multiple micro-
abcesses.
43.
44. 36. Glioma – gross:
Gliomas are tumours of the glial cells; astrocytoma,
glioblastoma, oligodendrogliomas, ependymomas and
choroid plexus papilloma. They are the most common
brain tumour group and comprise 40%.
Astrocytoma is the most common glioma:
- Found in mid- late life (40-60yo).
- Most often located in cerebral hemispheres, sometimes
in spinal cord but can occur anywhere (optic nerves,
brainstem, cerebellum etc).
- Have a tendency to progress from low grade to high
grade and transform into glioblastoma multiforme.
- They are grey-white, cystic or solid masses, gradually
grow and therefore clinical symptoms are insidious.
- Signs of transformation to aggressive glioblastoma
includes acceleration in symptom progression, yellow,
hemorrhages, focal necrosis, poor margins and
heterogenous
soft consistency.
Astrocytoma
Glioblastoma
Glioblastoma
Glioblastoma
45. 37. Meningioma – gross:
Most common location is along falx cerebri
and parasagittal (25%), calvarium convexity
(20%), sphenoid wing (20%), suprasellar (10%),
posterior fossa (10%).
It may occur in the orbit – congenital cause of
exophthalmos. May occasionally occur at
cerebellopontine angle and mimic acoustic
neuromas.
Tan, quite spherical or hemi-spherical, well-
defined margins, may be lobulated, firm,
fibrose. Usually meningiomas are solitary.
May contain focal calcific precipitates.
1-10cm in size, overlying skull may have
reactive thickening (hyperostosis) and
sclerosis.
Attached to dura (Note: it does not originate
from the dura, it arises from the arachnoid
layer!)
Broad base, may be solid, cystic or gelatinous
in texture. When removed they leave a pit/
depression in the underlying cerebral
hemisphere. Clinical symptoms depend on
location; paresis, seizures, headaches, vision
changes, language impairment, memory loss.
46. 38. Neurinoma – macroscopic:
Does not occur in CNS only peripheral
nerves; spinal nerve roots, cranial nerves.
Pontocerebellar angle near internal
acoustic meatus is a very common site –
affecting CN VIII (vestibulocochlear nerve).
Arise from Schwann cells that make
myelin sheath on sensory, motor and
autonomic nerves.
Encapsulated, solid, sometimes cystic,
eccentric enlargement.
When they are rich in collagenous tissue
they are subclassified as neurofibromas
(neurofibromatosis).
“Pepples in
shoe” pain
sensation is a
distinctive
symptom of
lower limb
neuroma.
47. 39. Fibrocavernous TB of lungs –
gross:
Apices of lungs are most heavily
affected. Usually bilateral
involvement. Unilateral hilar
lymphnodes involvement (kids).
Thick fibrose non-compliant
upper lobes, pleura may be
thickened, bronchial stricture
and bronchiectasis due to
deformity, displacement and
traction.
Multiple granulomas with
central caseous (cheese-like)
necrosis. There may be focal
hemorrhages and cavitation.
Miliary type TB features
multiple diffuse micro-
abscesses throughout the lungs.
It indicates hematogenous
spread and may be associated
with TB meningitis, renal TB,
bone TB and has a poor
prognosis.
48. 40. Renal Tuberculosis – gross:
Young to middle aged adults.
Renal involvement may be
indolent, insidious taking
anywhere from 10-30 years to
manifest after primary TB
infection.
Onset of symptoms as unilateral
renal impairment and less often,
renal failure.
Multiple large cavities filled with
thick, yellowish caseous necrosis.
Liquefaction and cavity formation.
Secondary or concomitant
infection - bacterial abscesses.
Contraction and fibrosis may lead
to irregularity and deformity of the
cortical surface.
Correlating clinical symptoms
include; flank pain, increased
frequency, blood and pus in urine,
fever, dysuria as well as signs of
renal insufficiency.
49. 41. Luetic aneurysm – gross:
Aortic intima has fine or
course, irregular foldings.
Scattered foci of fibrosis
(pearly-white nodules) along
the intima creating
characteristic “tree-bark”
appearance.
Typical feature of advanced or
tertiary stage of syphilis
infection.
Ascending aorta and aortic
arch are most frequently
impacted.
Superimposing
atherosclerotic changes are
frequent. The cerebral vessels
may also be affected by
syphilitic vasculitis
Aorta lumen is dilated, walls
are hardened, fibrotic and
thickened, there is
replacement of the atrophied
tunica media muscle.