Hemodynamic Disorders Edema Elephantiasis

Total Page:16

File Type:pdf, Size:1020Kb

Hemodynamic Disorders Edema Elephantiasis 5/15/2020 Edema Hemodynamic Disorders • Excess accumulation of fluid in interstitial space or in serous cavity is called edema. • Types – Local edema Dr. Sadequel Islam Talukder – Generalized edema MBBS, M Phil (Pathology 1995, IPGMR) 5/15/2020 Sadequel Talukder, www.talukderbd.com 1 5/15/2020 Sadequel Talukder, www.talukderbd.com 2 • Generalized edema • Local edema – Hepatic edema – Acute inflammatory edema – Cardiac edema – Allergic edema – Renal edema – Edema due to impaired venous return of leg following – Nutritional deficiency edema • Long journey – Pregnancy edema • Long period of standing – Myxedema – Lymphedema following lymphatic obstruction – Unexplained edema • e.g. Filariasis 5/15/2020 Sadequel Talukder, www.talukderbd.com 3 5/15/2020 Sadequel Talukder, www.talukderbd.com 4 Elephantiasis • Clinical Types of Edema – Pitting edema • A non-pitting edema following lymphtaic – Non-pitting edema obstruction • Causes of edema/Pathophysiological Category • Accumulation of lymph in tissue – Increased hydrostatic pressure • Causes inflammation, fibrosis. – Decreased colloidal osmotic pressure • Fibrosis causes non-pitting edema. – Retention of salt and water – Lymphatic obstruction 5/15/2020 Sadequel Talukder, www.talukderbd.com 5 5/15/2020 Sadequel Talukder, www.talukderbd.com 6 1 5/15/2020 • Serous cavities – Peritoneal cavity - Excess accumulation of fluid is • All causes are found in hepatic edema called ascites. • Normally interstitial space and serous cavity – Pleural cavity - Excess accumulation of fluid is contains small amount of fluid. Excess amount called pleural effusion. of fluid cases edema. – Pericardial cavity - Excess accumulation of fluid is called pericardial effusion. – Synovial cavity - Excess accumulation of fluid is called synovial effusion. 5/15/2020 Sadequel Talukder, www.talukderbd.com 7 5/15/2020 Sadequel Talukder, www.talukderbd.com 8 • Anasarca – Severe generalized edema is called • Fluid comes out from vessels due to anasarca. It is usually seen in nephrotic – Hydrostatic pressure in blood vessels syndrome. – Colloidal osmotic pressure (COP) in interstitial • Primary lymphedema – Edema due to fluid malformation of lymphatics. • Fluid enters in blood vessels due to • Starling postulate- Fluid movement between – Tissue tension extracellular space and blood vessels depends on balance of hydrostatic and osmotic – Colloidal osmotic pressure of plasma (80% COP is pressure. maintained by albumin) 5/15/2020 Sadequel Talukder, www.talukderbd.com 9 5/15/2020 Sadequel Talukder, www.talukderbd.com 10 • Tissue where fluid easily accumulates Hepatic Edema – Eyelids – Scrotum – Ankle etc. • Edema in liver diseases is called hepatic • Tissue where fluid does not easily accumulates edema. – Palm – Cirrhosis – Sole – Hepatitis • Water moves – Carcinoma of liver etc. – From fluid of high hydrostatic pressure to low hydrostatic pressure – From low colloidal osmotic pressure to high colloidal osmotic pressure. 5/15/2020 Sadequel Talukder, www.talukderbd.com 11 5/15/2020 Sadequel Talukder, www.talukderbd.com 12 2 5/15/2020 • Pathogenesis of edema in cirrhosis • Hypoalbuminemia – Portal hypertension – Reduction of hepatic cell mass in cirrhosis • Contraction of liver due to extensive fibrosis in cirrhosis – Decreased albumin synthesis • Portal vein compression at porta hepatis. • Increased hydrostatic pressure in portal system. – Nutritional hypoalbuminemia • Transudation. – Transudation and generalized edema • Accumulation of fluid in peritoneal cavity and ascites. • Lymphatic obstruction at porta hepatis – Compression of porta hepatis – Impaired lymph drainage – Enhancement of ascites 5/15/2020 Sadequel Talukder, www.talukderbd.com 13 5/15/2020 Sadequel Talukder, www.talukderbd.com 14 • Secondary hypertension Cardiac Edema – Reduction of hepatic cell mass – Delayed aldosterone metabolism. Thus half life of • Edema due to heart disease is called cardiac aldosterone is increased. edema. – Aldosterone acts upon renal tubules and • Example – Right-heart failure/Congestive absorption of sodium and water. cardiac failure (CCF) – Increased volume of blood – Increased hydrostatic pressure – Transudation and generalized edema. 5/15/2020 Sadequel Talukder, www.talukderbd.com 15 5/15/2020 Sadequel Talukder, www.talukderbd.com 16 – Salt and water retention • Pathogenesis of cardiac edema • Impaired venous return • Decreased cardiac output – Increased hydrostatic pressure • Decreased renal blood flow -> Renin secretion from • Right heart failure causes impaired venous return juxtraglomerular system. • Increased blood volume in venous system. • Activation of renin angiotensin axis. • Increased hydrostatic pressure in blood. • Secretion of aldosterone -> absorption of sodium and • Transudation and generalized edema. water from renal tubules. • Increased blood volume. • Increased hydrostatic pressure in blood. • Transudation and generalized edema. 5/15/2020 Sadequel Talukder, www.talukderbd.com 17 5/15/2020 Sadequel Talukder, www.talukderbd.com 18 3 5/15/2020 Renal Edema • Pathogenesis of edema in nephritic syndrome • Edema following renal diseases is called renal – Proteinuria in nephrotic syndrome edema. • Mild to moderate proteinuria • Hypoalbuminemia • Renal diseases associated with edema • Decreased colloidal osmotic pressure – Nephritic syndrome (Syndrome in AGN) • Transudation and edema – Nephrotic syndrome 5/15/2020 Sadequel Talukder, www.talukderbd.com 19 5/15/2020 Sadequel Talukder, www.talukderbd.com 20 • Pathogenesis of edema in nephrotic syndrome – Massive proteinuria or heavy proteinuria • Oligouria in nephritic syndrome • Hypoalbuminemia – Retention of salt and water in blood. • Decreased colloidal osmotic pressure in blood. – Increased volume of blood • Transudation and edema • Massive or heavy proteinuria – Increased hydrostatic pressure in blood » Passage of protein (albumin) > 3.5 gm in 24 hours. – Transudation and edema 5/15/2020 Sadequel Talukder, www.talukderbd.com 21 5/15/2020 Sadequel Talukder, www.talukderbd.com 22 Clinical Importance of Edema Angioedema • Cardiac edema – 1st appear in dependent part, • Edema in Type-I and Type-III hypersensitivity like, ankle. reaction. • Renal edema - 1st appear in face • Edema involves in dermis and subcutaneous • Hepatic edema - 1st appear in abdomen tissue. [ascites] 5/15/2020 Sadequel Talukder, www.talukderbd.com 23 5/15/2020 Sadequel Talukder, www.talukderbd.com 24 4 5/15/2020 Pulmonary Edema Hypoxia in pulmonary edema • Accumulation of fluid in lung alveoli is called • Fluid in alveolar spaces cause scarcity of gas in pulmonary edema. alveoli. • Causes • Blood in interalveolar septal capillaries can not – Left ventricular failure obtain sufficient oxygen thus cellular hypoxia – Cerebral damage etc. throughout the body. 5/15/2020 Sadequel Talukder, www.talukderbd.com 25 5/15/2020 Sadequel Talukder, www.talukderbd.com 26 Cerebral Edema • Example of vesogenic edema – edema in – Primary and metastatic tumors of brain • Brain is susceptible to edema , because of – Brain abscess – Little room to expand – Infarction of brain etc. – Absence of lymphatics to carry away any excess fluid that accumulates. • Cytotoxic edema • Types – Accumulation of fluid in cells of gray matter. – Vesogenic edema – loss of blood brain barrier – Example – edema in ischemic brain function results from damage of capillaries or newly formed capillaries that have not yet established barrier causes edema. 5/15/2020 Sadequel Talukder, www.talukderbd.com 27 5/15/2020 Sadequel Talukder, www.talukderbd.com 28 • Interstitial edema Infarct and Infarction – Example – Edema in noncommunicating type hydrocephalus. Fluid comes out across the • Localized area of ischemic necrosis either due ependymal lining of ventricles and accumulates in to sudden arterial occlusion or impaired the periventricular white matter. venous return is called infarct and the phenomenon is called infarction. *Cerebral edema is more dangerous, because, the • Types cerebrum may herniate through foramen magnum and patient may die. • Based on presence or absence of infarction – Septic infarct – presence of infection in infarct. – Bland infarct - absence of infection in infarct. 5/15/2020 Sadequel Talukder, www.talukderbd.com 29 5/15/2020 Sadequel Talukder, www.talukderbd.com 30 5 5/15/2020 • Based on color – Pale or anemic infarct • Effects of abnormal blood flow – Red or hemorrhagic infarct – Arterial dilatation causes increased blood flow. It is called hyperemia. Most common cause of infarct – Sudden arterial occlusion causes infarction. – Arterial occlusion, caused by thrombus or – Diminised arterial blood flow cases atrophy embolus 5/15/2020 Sadequel Talukder, www.talukderbd.com 31 5/15/2020 Sadequel Talukder, www.talukderbd.com 32 • Characteristics of pale infarct • Characteristics of red infarcts – Caused by arterial occlusion – Caused by impaired venous return – Occurs in solid organs – heart, kidney, liver, spleen – Occurs in loose and previously congested tissue, etc. like – Edema usually absent. • Intestine (in strangulated inguinal hermia, intestinal • Atheroma and myocardial infarction obstruction) • Lung – Superimposed thrombus formation on coronary • Testis (in testicular torsion) artery atheroma -> occlusion of artery and • Overy (in twisting of ovary) ischemic necrosis. • Valva etc. – Usually, edema present. 5/15/2020 Sadequel Talukder, www.talukderbd.com 33 5/15/2020 Sadequel Talukder, www.talukderbd.com 34 • Impaired venous return and infarct • Oxygen content of blood – Impaired venous return causes stasis of
Recommended publications
  • General Pathologic Anatomy
    МІНІСТЕРСТВО ОХОРОНИ ЗДОРОВ'Я УКРАЇНИ Харківський національний медичний університет GENERAL PATHOLOGIC ANATOMY Manual for practical classes in pathomorphology for English-speaking teachers ЗАГАЛЬНА ПАТОЛОГІЧНА АНАТОМІЯ Методичні розробки до занять з патоморфології для англомовних викладачів медичних закладів Затверджено вченою радою ХНМУ. Протокол № 15 від 15.06.2017. Харків ХНМУ 2017 1 General pathologic anatomy : мanual for practical classes in patho- morphology for English-speaking teachers / comp. I. V. Sorokina, V. D. Markovskiy, I. V. Korneyko et al. – Kharkov : KNMU, 2017. – 64 p. Compilers I. V. Sorokina V. D. Markovskiy I. V. Korneyko G. I. Gubina-Vakulik V. V. Gargin O. N. Pliten M. S. Myroshnychenko S. N. Potapov T. V. Bocharova D. I. Galata O.V. Kaluzhina Загальна патологічна анатомія : метод. розроб. до занять з пато- морфології для англомовних викладачів мед. закладів / упоряд. І. В. Сорокіна, В. Д. Марковський, І. В. Корнейко та ін. – Харків : ХНМУ, 2017. – 64 с. Упорядники I. В. Сорокіна В. Д. Марковський І. В. Корнейко Г. І. Губіна-Вакулик В. В. Гаргін О. М. Плітень М. С. Мирошниченко С. М. Потапов Т. В. Бочарова Д. І. Галата О. В. Калужина 2 Foreword Pathomorphology, one of the most important medical subjects is aimed at teaching students understanding material basis and mechanisms of the development of main pathological processes and diseases. This manual published as separate booklets is devoted to general pathological processes as well as separate nosological forms. It is intended to the English-medium students of the medical and dentistry faculties. It can be used as additional material used for individual work in class. It can also be used to master the relevant terminology and its unified teaching.
    [Show full text]
  • Heart Failure • Cor Pulmonale • Hypertensive Heart Disease
    DISEASES OF THE HEART - content • Cardiac hypertrophy and congestive heart failure • Cor pulmonale • Hypertensive heart disease • Ischemic heart disease • Valvular diseases • Myocardial diseases • Congenital heart diseases • Diseases of the pericardium • Cardiac neoplasms Normal values assessed by echocardiography • Free wall thickness: RV: 3-4 mm, LV: 10-11 mm • End-diastolic volume (EDV) 120 ml • End-systolic volume (ESV) 50 ml • Stroke volume (SV) 70 ml Weight: women: 300 gs, men: 350 gs HYPERTROPHY OF THE HEART • The cardiac myocytes are permanent cells (not able to enter the cell cycle) and, therefore, are not able to proliferate • Increase in work load increase in size and pumping capacity of ventricular myocytes • Weight > 400 g • Types: concentric dilative Concentric hypertrophy Pathogenesis An obstruction of outflow in systole (i.e., hypertension, aortic valve stenosis) the LV increases the end-systolic pressure pressure overload concentric remodeling and hypertrophy Morphologic features of concentric hypertrophy of LV: small lumen; markedly increased wall thickness (> 20 mm); increased mass (> 500 g) Clinical features of pressure-overloaded LV - symptomless for a long period - pump failure occurs lately - risk of sudden cardiac death Dilative hypertrophy Pathogenesis Aortic/mitral valve incompetence leads to diastolic backflow the regurgitated extra volume of blood is accepted with the dilation of the LV an increased EDV is ejected into the circulation during the next systole (volume overload) excentric remodeling and
    [Show full text]
  • Pathology.Pre-Test.Pdf
    Pathology PreTestTMSelf-Assessment and Review Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example, and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. Pathology PreTestTMSelf-Assessment and Review Twelfth Edition Earl J. Brown, MD Associate Professor Department of Pathology Quillen College of Medicine Johnson City, Tennessee New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto Copyright © 2007 by The McGraw-Hill Companies, Inc.
    [Show full text]
  • Coronary Thrombosis
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1935 Coronary thrombosis Joseph F. Linsman University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Linsman, Joseph F., "Coronary thrombosis" (1935). MD Theses. 568. https://digitalcommons.unmc.edu/mdtheses/568 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. -------- Ii CORONARY THROMBOSIS A ~ri:NIOR THESIS BY JOSEPH FRANCIS LINS~Mill College of Medicine, University ot N&hraska 'f "" Table of Contents Pages Introduction------------------------------------------- i-iii Historical Review ----------'...-----------------------------1-7 Ineidene• ----------------------------------------------- 8-11 Etiological Factors------------------------------------ 12-22 Relationship to Arteriosclerosis Relationship to Angina Pectoris Relationship to F.ypertension Relationship to Diabetes Relationship to Syphilis Relationship to Heredity, Physical Type, Work, Weight, and Habits Relationship to Other Diseases Pathogenesis and Pathology----------------------------23-34 SymptollS and Signs------------------------------------35-58
    [Show full text]
  • Human Pathology Slide Sets
    HUMAN PATHOLOGY SLIDE SETS Cat #: CH-PATH1 - CARDIAC DISEASES SLIDE SET - 16 slides 1 - Human myocardial hypertrophy sec. 2 - Cardiac muscle fatty degeneration sec. 3 - Human brown atrophy of myocardium sec. 4 - Human myocardial hypertrophy sec. 5 - Myocardial infarction sec. 6 - Human aortitis sec. 7 - Rheumatic endocarditis sec. 8 - Bacterial myocarditis sec. 9 - Semi-organized fibrous pericarditis sec. 10 - Rheumatic myocarditis sec. 11 - Angioma sec. 12 - Coronary atherosclerosis sec. 13 - Cardiac muscle of Keshan disease sec. 14 - Cardiac muscle lipofuscin sec. 15 - Cardiac muscle cell coagulation necrosis sec. 16 - Viral myocarditis sec. Cat #: CH-PATH2 - VASCULAR DISEASES SLIDE SET - 17 slides 1 - Mixed thrombus sec. 2 - Hyaline thrombus sec. 3 - Hemorrhagic infarct of lung sec. 4 - Renal anemic infarct sec. 5 - Chronic venous congestion of liver sec. 6 - Sanguineous apoplexy sec. 7 - Anemic infarct of spleen sec. 8 - Pulmonary congestion (heart-failure cells) sec. 9 - Pulmonary amniotic embolism sec. 10 - Human infarct of brain 11 - Organized thrombus sec. 12 - Intravenous thrombus sec. 13 - Fibrinoid necrosis of vascular wall sec. 14 - Atherosclerosis sec. 15 - Transparent thrombus sec. 16 - Takayasu's sec. Cat #: CH-PATH3 - HEMATOLOGIC DISEASES SLIDE SET - 12 slides 1 - Non-Hodgkin lymphoma sec. 2 - Hodgkin lymphoma sec. 3 - Human tissue system histiocytosis 4 - Acute lymphoblastic leukemia (L1) 5 - Acute lymphoblastic leukemia (L2) 6 - Acute lymphoblastic leukemia (L3) 7 - Acute leukemia bone marrow cells differentiated (M0) 8 - Immaturate acute myeloid leukemia (M1) 9 - Maturate acute myeloid leukemia (M2) 10 - Acute promyelocytic leukemia (M3) 11 - Acute monocytic leukemia (M4) 12 - Acute monocytic leukemia (M5) 13 - Acute hemolytic anemia 14 - Megaloblastic anaemia B12 deficiency anemia MEDICAL & SCIENCE MEDIA 17 Cat #: CH-PATH4 - URINARY DISEASES SLIDE SET - 27 slides 1 - Vitreous degeneration of renal arteriole sec.
    [Show full text]
  • Status of the Myocardium and Infarct-Related Coronary Artery in 19 Necropsy Patients with Acute Recanalization Using Pharmacolog
    JACC Vol. 9. No. 4 785 April I<J 87:785- 80 I MORPHOLOGIC STUDIES Status of the Myocardium and Infarct-Related Coronary Artery in 19 Necropsy Patients With Acute Recanalization Using Pharmacologic (Streptokinase, r-Tissue Plasminogen Activator), Mechanical (Percutaneous Transluminal Coronary Angioplasty) or Combined Types of Reperfusion Therapy BRUCE F. WALLER, MD, FACC,* DONALD A. ROTHBAUM, MD, FACC,t CASS A. PINKERTON, MD, FACC,t MICHAEL J. COWLEY, MD, FACC,§ THOMAS J. LlNNEMElER, MD, FACC,t CHARLES ORR, MD, FACC,t MICHAEL IRONS, MD,t ROBIN A. HELMUTH , MD,II EDWARD R. WILLS, MD,II CHARLES AUST, MOil Indianapolis. Indiana and Richmond. Virginia In acute myocardial infarction, myocardial salvage is 14 (74%) had hemorrhagic myocardial infarction and dependent on rapid restoration of blood flow. Phar­ they all received pharmacologic or combined forms of macologic (streptokinase, recombinant tissue-type plas­ reperfusion therapy. The remaining five patients (26%) minogen activator), mechanical (percutaneous translu­ had nonhemorrhagic (anemic) infarction and were treated minal coronary angioplasty, guide wire perforation) or with balloon angioplasty therapy alone. Increased lu­ combined forms of reperfusion therap y can accomplish minal cross-sectional area was present in 8 of 9 patients this goal, but their effects on infarcted myocardium and with acute balloon angioplasty but severe coronary ath­ vessel occlusion site have not been compared at necropsy. erosclerotic plaque remained in 9 of 10 patients without The heart of 19 necropsy patients who had received var­ acute balloon angioplasty. Severe hemorrhage sur­ ious forms of acute reperfusion therap y was studied: rounded angioplasty sites in all four patients who also 14 had pharmacologic or combined forms of reperfusion received streptokinase or tissue-type plasminogen acti­ therapy (13 streptokinase and I tissue-type plasminogen vator.
    [Show full text]
  • Annals of Surgery
    ANNALS OF SURGERY Vol. 171 April 1970 No. 4 Neurological Complications of Carotid Artery Surgery JAi s E. BLAiN, M.D., RiciLuA D. CHAPMAN, M.D., EDWIN J. WYLIE, M.D., F.A.C.S. From the Department of Surgery, University of California School of Medicine, San Francisco, California POSTOPERATIVE stroke is the most fre- rological deficit or acute progression of an quent and most disastrous complication of old deficit occurred after 55 (9%) of these cerebrovascular reconstructive surgery. Pa- operations. In most instances postoperative tients who undergo operation on the ca- neurological deficits, when viewed retro- rotid arteries are particularly vulnerable. spectively, resulted from an unwise deci- Since prevention of stroke is the primary sion to operate or an error in surgical man- objective of most carotid artery operations, agement. In three additional patients the technics to prevent it at the time of opera- postoperative deficit was merely a gradual tion are of paramount importance. Post- progression of a preoperative deficit and operative neurological deficits in our pa- was not related to the operation. A tabula- tients who had carotid operations were re- tion of the severity of the deficits and the viewed to determine causes and to assess ultimate neurological status of the patients the value of methods designed to prevent is shown in Table 1. Visual disturbances, these deficits. dysphagia, and monoparesis are examples Six hundred thirteen endarterectomies of deficits classified as mild. Under moder- for occlusive or ulcerating lesions at the ate deficits we included hemiparesis. Se- carotid bifurcation were performed in 488 vere deficit was applied to complete uni- patients between October, 1958 and June, lateral paralysis (hemiplegia) with or 1969.
    [Show full text]
  • 17. Vascular Pathology III. Heart Failure 1
    17. Vascular pathology III. Heart failure DISEASES OF THE HEART Content Cardiac hypertrophy and congestive heart failure Cor pulmonale Hypertensive heart disease Ischemic heart disease Valvular diseases Myocardial diseases Congenital heart diseases Diseases of the pericardium Cardiac neoplasms HYPERTROPHY OF THE HEART AND HEART FAILURE Normal values assessed by echocardiography Free wall thickness: RV: 3-4 mm, LV:10-11 mm End-diastolic volume (EDV) 120 ml, end-systolic volume (ESV) 50 ml, stroke volume (SV) 70 ml Weight: women: 300 gs, men: 350 gs Hypertrophy of the heart The cardiac myocytes are permanent cells (not able to enter the cell cycle) and, therefore, are not able to proliferate Increase in work load increase in size and pumping capacity of ventricular myocytes Weight > 400 g Types: concentric or dilative Concentric hypertrophy Pathogenesis An obstruction of outflow in systole (i.e., hypertension, aortic valve stenosis) the LV increases the end-systolic pressure pressure overload concentric remodeling and hypertrophy Morphology Concentric hypertrophy of the LV: small lumen; markedly increased wall thickness (> 20 mm); increased mass (> 500 g) Clinical features of pressure-overloaded LV Symptomless for a long period Pump failure occurs lately Risk of sudden cardiac death Dilative hypertrophy Pathogenesis Aortic/mitral valve incompetence leads to diastolic backflow the regurgitated extra volume of blood is accepted with the dilation of the LV an increased EDV is ejected into the circulation during the
    [Show full text]
  • Inhalt 11..23
    Contents 1 Fundamentals of Pathology Pathology .............................. 2 Signs of Death .......................... 5 Methods Equivocal Signs of Death Brain Death Disease ................................ 5 Unequivocal Signs of Death Etiology Causal Pathogenesis Statistics ............................... 5 Formal Pathogenesis Clinical Course Autopsy ................................ 5 2 Cellular Pathology Nuclear Lesions ........................ 6 Inclusions ............................. 12 Forms of Nuclei Amorphous inclusions Chromosomes Crystalline inclusions Particulate inclusions DNA Repair Defects ..................... 6 Xeroderma pigmentosum Oncofetal Lesion ....................... 12 Ribosome-lamellae complexes Chromosome Abnormalities .............. 6 Annulated lamellae layers Change in the Size of the Nucleus ........ 8 Mitochondria-lamellar-layer complexes Relation of Nucleus to Cytoplasm Nuclear Euploidy Lesions of the Smooth Endoplasmic Nuclear Polyploidy Nuclear Aneuploidy Reticulum (SER) ...................... 14 Chromatin Change ...................... 8 Quantitative Change ................... 14 Heterochromatin Condensation Proliferation of SER Dyskaryosis Atrophy of the SER Perinuclear Hyperchromatosis Morphologic Change ................... 14 Karyolysis Formation of Vesicles in the SER Inclusions .............................. 8 „Cytoplasmic Nuclei“ Cytoplasmic inclusions Inclusions ............................. 14 Paraplasmic inclusions Change in the Number of Nuclei ......... 10 Golgi Lesions ........................
    [Show full text]
  • Vascular Pathology in the Aged Human Brain
    Acta Neuropathol (2010) 119:277–290 DOI 10.1007/s00401-010-0652-7 REVIEW Vascular pathology in the aged human brain Lea Tenenholz Grinberg • Dietmar Rudolf Thal Received: 24 June 2009 / Revised: 3 February 2010 / Accepted: 4 February 2010 / Published online: 14 February 2010 Ó The Author(s) 2010. This article is published with open access at Springerlink.com Abstract Cerebral atherosclerosis (AS), small vessel lesions (WMLs) and lacunar infarcts. In this review, we disease (SVD), and cerebral amyloid angiopathy (CAA) demonstrate the relationship between AS, SVD, and CAA are the most prevalent arterial disorders in the aged brain. as well as their contribution to the development of vascular Pathogenetically, AS and SVD share similar mechanisms: tissue lesions and we emphasize an important role for apoE plasma protein leakage into the vessel wall, accumulation in the pathogenesis of vessel disorders and vascular tissue of lipid-containing macrophages, and fibrosis of the vessel lesions as well as for BBB dysfunction on WML and wall. CAA, on the other hand, is characterized by the lacunar infarct development. deposition of the amyloid b-protein in the vessel wall. Despite these differences between CAA, AS and SVD, Keywords Atherosclerosis Á Small vessel disease Á apolipoprotein E (apoE) is involved in all three disorders. Cerebral amyloid angiopathy Á Brain infarction Á Such a pathogenetic link may explain the correlations Hemorrhages Á White matter lesions between AS, SVD, CAA, and Alzheimer’s disease in the brains of elderly individuals reported in the literature. In addition, AS, SVD, and CAA can lead to tissue lesions Introduction such as hemorrhage and infarction.
    [Show full text]
  • 1. Pathology of Cellular Injury and Death 1
    1. Pathology of cellular injury and death What is disease? A condition in which the presence of an abnormality causes a loss of normal health Manifests in signs and symptoms: subjective: e.g., pain; objective: confirmed by diagnostic tests Duration of disease: short lasting – acute long lasting – chronic Outcome: varies; can be lethal What is pathology? The study (logos) of suffering (pathos) Devoted to the study of the cause of the disease (etiology) the mechanism(s) of disease development (pathogenesis) the structural alterations induced in cells and tissues by the disease (morphologic change) the functional consequences of the morphologic changes (clinical significance) The morphologic change of an organ can be focal (localized abnormality) or diffuse Teaching program of pathology for medical students General pathology Basic reactions of cells and tissues to abnormal stimuli, i.e. common features of various disease processes in various cells and tissues Systematic pathology The descriptions of specific diseases as they affect given organs or organ systems The descriptions and terms are the basis of medical language PATHOLOGY OF CELLULAR INJURY AND DEATH Cells react to adverse influences by 1) reversible cell injury: changes that can be reversed when the stimulus is removed 2) irreversible cell injury: changes that cause cell death 3) cellular adaptation: stimuli result in new but altered state that maintains the viability of the cell Intracellular mechanisms particularly vulnerable to cellular injury Maintenance of membrane integrity (critical for ionic and osmotic homeostasis of the cell) Aerobic respiration (oxidative phosphorilation and ATP production in mitochondria) Synthesis of enzymes and structural proteins Common cellular injuries 1.
    [Show full text]
  • Pathology of Cellular Injury and Death. Cellular Adaptations
    What is disease? • A condition in which the presence of an abnormality causes a loss of normal health • Manifests in signs and symptoms subjective: e.g., pain objective: confirmed by diagnostic tests • Duration of disease: short lasting - acute long lasting - chronic • Outcome: varies; can be lethal What is pathology? • The study (logos) of suffering (pathos) • Devoted to the study of - the cause of the disease (etiology) - the mechanism(s) of disease development (pathogenesis) - the structural alterations induced in cells and tissues by the disease (morphologic change) - the functional consequences of the morphologic changes (clinical significance) • The morphologic change can be focal (localized abnormality) or diffuse Teaching program of pathology for medical students General pathology • Basic reactions of cells and tissues to abnormal stimuli, i.e. common features of various disease processes in various cells and tissues Systematic pathology • The descriptions of specific diseases as they affect given organs or organ systems The descriptions and terms used are the basis of medical language Students are expected to attend the lectures, the autopsy and histopathology practicals, and the organ demonstrations. Attendance at the practicals the attendence is always verified. There is no possibility for missed practicals to be repeated later. Students who are absent from more than 25% of the practicals, automatically fail the semester. The grade achieved in the fall-semester examinations will be calculated from the sum of the following: - the first mid-term assessment (maximum 5 points) - the second mid-term assessment (max. 5 points) - the histology examination (max. 5 points) - the autopsy examination (max. 5 points) - the final test (max.
    [Show full text]