The bundle of His extends through the interventricular septum and divides into right and left bundle branches Figure 16 gastritis vs heart attack purchase florinef canada. The pericardium consists of a closely apposed layer xiphoid gastritis discount florinef 0.1 mg free shipping, There are 3 anatomic patterns of distribution of the visceral pericardium or epicardium gastritis symptoms lightheadedness order 0.1 mg florinef overnight delivery, and an outer fibrous sac chronic gastritis rheumatoid arthritis discount florinef 0.1mg otc, coronary blood supply eosinophilic gastritis symptoms buy florinef with paypal, depending upon which of the the parietal pericardium gastritis diet x garcinia 0.1mg florinef visa. Crux is the region on the pericardial cavity which is lined by mesothelial cells and posterior surface of the heart where all the four cardiac normally contains 10-30 ml of clear diet to help gastritis order generic florinef, watery serous fluid gastritis burning pain in back generic 0.1mg florinef with visa. These patterns are as under: the endocardium is the smooth shiny inner lining of the Right coronary artery preponderance is the most myocardium that covers all the cardiac chambers, the cardiac common pattern. In this, right coronary artery supplies blood valves, the chordae tendineae and the papillary muscles. It to the whole of right ventricle, the posterior half of the is lined by endothelium with connective tissue and elastic interventricular septum and a part of the posterior wall of fibres in its deeper part. The valve cusps and semilunar leaflets are delicate and Balanced cardiac circulation is the next most frequent translucent structures. In this, the right and left ventricles receive blood collagen and elastic tissue and covered by a layer of supply entirely from right and left coronary arteries endothelium (valvular endocardium). The cardiac muscle, in is supplied by a branch of the right coronary while the order to function properly, must receive adequate supply of anterior part is supplied by a branch of the left coronary oxygen and nutrients. Most of blood flow to the In this, the left coronary artery supplies blood to the entire myocardium occurs during diastole. There are three major left ventricle, whole of interventricular septum and also coronary trunks, each supplying blood to specific segments supplies blood to a part of the posterior wall of the right of the heart (Fig. The anterior descending branch of the left coronary Coronary veins run parallel to the major coronary arteries artery supplies most of the apex of the heart, the anterior to collect blood after the cellular needs of the heart are met. For the purpose of pathologic discussion of heart diseases, they are categorised on the basis of anatomic region involved 3. The right coronary artery supplies the right atrium, the and the functional impairment. Accordingly, topics on heart remainder of the anterior surface of the right ventricle, the diseases are discussed in this chapter under the following headings: 1. It may be mentioned here that pattern of heart diseases in developing and developed countries is distinct due to difference in living standards. In children, valvular diseases are common all over the world, but in developing countries including India, infections, particularly rheumatic valvular disease, is the dominant cause compared to congenital etiology in affluent countries. On the other hand, ischaemic heart disease and hypertensive cardiomyopathy are the Figure 16. Heart failure is defined as the pathophysiologic state in which Acute heart failure. Sudden and rapid development of heart impaired cardiac function is unable to maintain an adequate failure occurs in the following conditions: circulation for the metabolic needs of the tissues of the body. In acute heart failure, there is sudden reduction in cardiac Etiology output resulting in systemic hypotension but oedema does not occur. Instead, a state of cardiogenic shock and cerebral Heart failure may be caused by one of the following factors, hypoxia develops. The most common and slowly as observed in the following states: most important cause of heart failure is weakening of the i) Myocardial ischaemia from atherosclerotic coronary ventricular muscle due to disease so that the heart fails to artery disease act as an efficient pump. The various diseases which may ii) Multivalvular heart disease culminate in pump failure by this mechanisms are as under: iii) Systemic arterial hypertension i) Ischaemic heart disease iv) Chronic lung diseases resulting in hypoxia and pulmo ii) Myocarditis nary arterial hypertension iii) Cardiomyopathies v) Progression of acute into chronic failure. This often results in well-maintained arterial pressure Increased mechanical load on the heart results in increased and there is accumulation of oedema. Though heart as an organ eventually fails as a whole, but i) Increased pressure load may occur in the following functionally, the left and right heart act as independent units. It is initiated by stress to the left ii) Increased volume load occurs when a ventricle is heart. The major causes are as follows: required to eject more than normal volume of the blood i) Systemic hypertension resulting in cardiac failure. This is seen in the following ii) Mitral or aortic valve disease (stenosis) conditions: iii) Ischaemic heart disease a) Valvular insufficiency iv) Myocardial diseases. Heart failure may be acute or chronic, right-sided or left Right-sided heart failure. However, some conditions affect the right ventricle primarily, failure can be explained on the basis of mutually inter producing right-sided heart failure. According to this concept, either of ii) Cor pulmonale in which right heart failure occurs due to the ventricles fails to eject blood normally, resulting in rise intrinsic lung diseases (Chapter 17). According to this hypothesis, clinical v) Myocardial disease affecting right heart. The Ultimately, however, dilatation decreases the force of mechanism of clinical manifestations resulting from heart contraction and leads to residual volume in the cardiac 421 Figure 16. These are as follows: Cardiac Hypertrophy i) Pulmonary stenosis and insufficiency ii) Tricuspid insufficiency Hypertrophy of the heart is defined as an increase in size iii) Mitral stenosis and/or insufficiency and weight of the myocardium. The basic factors that stimulate the hypertrophy of the Cardiac Dilatation myocardial fibres are not known. It appears that stretching of myocardial fibres in response to stress induces the cells to Quite often, hypertrophy of the heart is accompanied by increase in length. Other factors which may volume of blood in a chamber of the heart causes increase in stimulate increase in size of myocardial fibres are anoxia. Hypertrophy with or without dilatation may the cardiac chambers from the following causes may result involve predominantly the left or the right heart, or both in dilatation of the respective ventricles or both: sides. The common causes are as in left ventricular dilatation, tricuspid and/or pulmonary under: insufficiency in right ventricular dilatation) i) Systemic hypertension ii) Left-to-right shunts. The weight of the heart is increased above sites for the formation of new sarcomeres. However, excessive epicar nucleic acid content determinations have shown increase dial fat is not indicative of true hypertrophy. It is the most common and important trabeculae carneae are rounded and enlarged, while in form of heart disease in the early years of life and is present hypertrophy with dilatation these are flattened. The incidence is higher Microscopically, there is increase in size of individual in premature infants. It is attributed to multi degenerative changes and necrosis in the hypertrophied factorial inheritance involving genetic and environmental myocardium (Fig. Other factors like rubella infection to the mother a result of relative hypoxia of the hypertrophied muscle during pregnancy, drugs taken by the mother and heavy as the blood supply is inadequate to meet the demands of alcohol drinking by the mother, have all been implicated in the increased fibre size. Ventricular hypertrophy renders causing in utero foetal injury resulting in congenital the inner part of the myocardium more liable to ischaemia. Congenital anomalies of the heart may myofilaments comprising myofibrils, mitochondrial be either shunts (left-to-right or right-to-left), or defects changes and multiple intercalated discs which are active causing obstructions to flow. The chambers opened up at the apex show concentric thickening of left ventricular wall (white arrow) with obliterated lumen (hypertrophy without dilatation). The free left ventricular wall is thickened (black arrow) while the lumen is dilated (white arrow) (hypertrophy with dilatation). Left-to-Right Shunts (Acyanotic or Late Cyanotic Group) In conditions where there is shunting of blood from left-to right side of the heart, there is volume overload on the right heart producing pulmonary hypertension and right ventricular hypertrophy. At a later stage, the pressure on the right side is higher than on the left side creating late cyanotic heart disease. The smaller defects often close spontaneously, while larger defects remain patent and produce significant effects. In 90% of cases, the defect involves membranous septum involving combinations of shunts and obstructions are also and is very close to the bundle of His (Fig. It may be accompanied by situs increased pulmonary flow and increased volume in the inversus so that all other organs of the body are also left side of the heart. These effects are as under: transposed in similar way and thus heart is in normal position i) Volume hypertrophy of the right ventricle. However, isolated dextrocardia is ii) Enlargement and haemodynamic changes in the associated with major anomalies of the heart such as tricuspid and pulmonary valves. Left-to-right shunts remains unnoticed in infancy and childhood till pulmonary (Acyanotic or late cyanotic group) hypertension is induced causing late cyanotic heart disease 1. Right-to-left shunts (Cyanotic group) i) Fossa ovalis type or ostium secundum type is the most 1. Transposition of great arteries (4-10%) defect is situated in the region of the fossa ovalis (Fig. Aortic stenosis and atresia (4-6%) the defect is located high in the interatrial septum near the 3. B, the opened up chambers of the heart show a communication in the inter-ventricular septum superiorly (white arrow). The ductus produced due to left-to-right shunt at the atrial level with arteriosus is a normal vascular connection between the aorta increased pulmonary flow. Normally, the i) Volume hypertrophy of the right atrium and right ductus closes functionally within the first or second day of ventricle. Its persistence after 3 months of age is considered ii) Enlargement and haemodynamic changes of tricuspid abnormal. These effects are as follows: i) Volume hypertrophy of the left atrium and left ventricle. Right-to-Left Shunts (Cyanotic Group) In conditions where there is shunting of blood from right side to the left side of the heart, there is entry of poorly Figure 16. The effects on the heart are as follows: i) Pressure hypertrophy of the right atrium and right ventricle. Tetralogy of Fallot is the most position of the aorta, pulmonary trunk, atrioventricular common cyanotic congenital heart disease, found in about orifices and the position of atria in relation to ventricles. There is complete transposition of the great arteries with aorta arising from the right ventricle and the pulmonary trunk from the left ventricle, as well as transposition of the great veins so that the pulmonary veins enter the right atrium and the systemic veins drain into the left atrium. This results in a single large common vessel receiving blood from the right as well as left ventricle. In tricuspid atresia, there is absence of tricuspid orifice and instead there is a dimple insufficiency such as claudication and coldness. In tricuspid stenosis, the there is development of collateral circulation between pre tricuspid ring is small and the valve cusps are malformed. Children are cyanotic since birth and live for a few weeks ii) Preductal or infantile type: the manifestations are or months. There is often associated Congenital obstruction to blood flow may result from interatrial septal defect. Preductal coarctation results in obstruction in the aorta due to narrowing (coarctation of aorta), right ventricular hypertrophy while the left ventricle is obstruction to outflow from the left ventricle (aortic stenosis small. Cyanosis develops in the lower half of the body and atresia), and obstruction to outflow from the right while the upper half remains unaffected since it is supp ventricle (pulmonary stenosis and atresia). The most common localised narrowing in any part of aorta, but the constriction congenital anomaly of the aorta is bicuspid aortic valve which is more often just distal to ductus arteriosus (postductal or does not have much functional significance but predisposes adult), or occasionally proximal to the ductus arteriosus it to calcification (page 450). Congenital aortic atresia is rare (preductal or infantile type) in the region of transverse aorta: and incompatible with survival. Congenital aortic stenosis to the point of entry of ductus arteriosus which is often may be of three types: valvular, subvalvular and closed (Fig. The aorta i) Valvular stenosis: the aortic valve cusps are is dilated on either side of the constriction. The aortic valve is recognised in adulthood, characterised by hypertension may have one, two or three such maldeveloped cusps. In all these cases, there is pressure hypertrophy of the left ventricle and left atrium, and dilatation of the aortic root. Isolated pulmonary stenosis and atresia do not cause cyanosis and hence are included under acyanotic heart diseases. The changes in these conditions are as under: Pulmonary stenosis: It is the commonest form of obstructive congenital heart disease comprising about 7% of all congenital heart diseases. Pulmonary stenosis is caused by fusion of cusps of the pulmonary valve forming a diaphragm-like obstruction to the outflow of blood from the right ventricle and dilatation of the pulmonary trunk. Atherosclerosis produces gradual luminal narrowing that may eventually lead to ‘fixed’ coronary I. The general coronary thrombosis, ulceration, haemorrhage, rupture and aspects of atherosclerosis as regards its etiology, pathogenesis aneurysm formation. Here, a brief account of the specific features in pathology of lesions in atherosclerotic coronary artery disease in particular the attacks of acute coronary syndromes, which include acute are presented. Atherosclerotic lesions in coronary arteries death, are precipitated by certain changes superimposed on are distributed in one or more of the three major coronary a pre-existing fixed coronary atheromatous plaque. These arterial trunks, the highest incidence being in the anterior changes are as under: descending branch of the left coronary, followed in 1. About one acute coronary episodes are often precipitated by sudden third of cases have single-vessel disease, most often left anterior changes in chronic plaques such as plaque haemorrhage, descending arterial involvement; another one-third have two fissuring, or ulceration that results in thrombosis and vessel disease, and the remainder have three major vessel disease. Almost all adults show atherosclerotic plaques are brought about by factors such as sudden coronary artery scattered throughout the coronary arterial system. However, spasm, tachycardia, intraplaque haemorrhage and hyper significant stenotic lesions that may produce chronic cholesterolaemia. Transmural acute myocar reduction in the cross-sectional area of a coronary artery or dial infarction is often precipitated by partial or complete its branch. The initiation of thrombus occurs due cm from the coronary ostia, more often at or near the bifurca to surface ulceration of fixed chronic atheromatous plaque, tion of the arteries, suggesting the role of haemodynamic ultimately causing complete luminal occlusion. The atherosclerotic fragments of thrombotic material are then dislodged which plaques in the coronaries are more often eccentrically located are embolised to terminal coronary branches and cause bulging into the lumen from one side (Fig. Another infrequent cause of coro Some cases of acute coronary episodes are caused by local nary occlusion is from hypercoagulability of the blood such aggregates of platelets on the atheromatous plaque, short of as in shock, polycythaemia vera, sickle cell anaemia and forming a thrombus. Contusion of a coronary artery from penetrating probably be responsible for coronary vasospasm in the injuries may produce thrombotic occlusion. Extension of dissecting aneurysm of the correlation, American Heart Association (1995) has classified aorta into the coronary artery may produce thrombotic human coronary atherosclerosis into 6 sequential types in coronary occlusion. Rarely, congenital, mycotic and syphi ascending order of grades of lesions as shown in Table 16. Development of lesions in the coronaries is not always accompanied by cardiac disease. Coronary ostial narrowing suddenness of onset, duration, degree, location and extent may result from extension of syphilitic aortitis or from aortic of the area affected by myocardial ischaemia, the range of atherosclerotic plaques encroaching on the opening. Various types of inflammatory involvements matic state at one extreme to immediate mortality at another of coronary arteries or small branches like in rheumatic (Fig. Asymptomatic state (Buerger’s disease), Takayasu’s disease, Kawasaki’s disease, tuberculosis and other bacterial infections may contribute to B. Sudden cardiac death bland thrombi, or from vegetations of bacterial endocarditis; the term acute coronary syndromes include a triad of acute rarely fat embolism and air embolism of coronary circulation myocardial infarction, unstable angina and sudden cardiac may occur. More often, the lesions lie in a branch of paroxysmal pain in the substernal or precordial region of the major coronary trunk so that collaterals prevent the chest which is aggravated by an increase in the demand infarction. Many patients pectoris with some differences in their pathogenesis: may die within the first few hours of the onset, while i) Stable or typical angina remainder suffer from effects of impaired cardiac function. This is the most common circulation through anastomotic channels over a period of pattern. A regular and well-planned exercise programme of pain following physical exertion or emotional excitement encourages good collateral circulation and improved cardiac and is relieved by rest. This pattern of occur in young people under the age of 40 years, particularly angina is characterised by pain at rest and has no relation in those with major risk factors to develop atherosclerosis ship with physical activity. The exact pathogenesis of like hypertension, diabetes mellitus, cigarette smoking and Prinzmetal’s angina is not known. After menopause, this sex as ‘pre-infarction angina’ or ‘acute coronary insufficiency’, difference gradually declines but the incidence of disease this is the most serious pattern of angina. It is characterised among women never reaches that among men of the same by more frequent onset of pain of prolonged duration and age. Myocardial ischaemia is brought about by one or more of the following mechanisms: i) Diminised coronary blood flow. Rupture of an atherosclerotic plaque exposes the subendothelial collagen to platelets which Figure 16. In general, slowly-developing mised lumen), aortic stenosis or haemorrhagic shock. Superimposed coronary in coronary atherosclerotic plaques in the form of thrombosis is frequently encountered in these cases too, and superimposed coronary thrombosis due to plaque rupture hence the beneficial role of fibrinolytic treatment in such and plaque haemorrhage is frequently encountered in cases patients. According to the degree of thickness of the ventricular wall Plaque haemorrhage and thrombosis may occur together involved, infarcts are of two types (Fig. Infarcts are most frequently involving the full thickness of ventricular wall and the subendocardial (laminar) infarcts affecting the inner located in the left ventricle. These are as under to infarction due to its thin wall, having less metabolic (Table 16. Critical coronary narrowing (more often in the right atrium, usually accompanying the infarct than 75% compromised lumen) is of great significance in the of the left ventricle. Atherosclerotic plaques with infarction because it is supplied by the oxygenated blood in superimposed thrombosis and intramural haemorrhage are the left atrial chamber. Accordingly, there are three regions of reduced coronary perfusion due to coronary atherosclerosis myocardial infarction (Fig. Stenosis of the left circumflex coronary artery is seen least most common (40-50%). Its area of involvement is the lateral wall anterior part of the left ventricle including the apex and the of the left ventricle. Stenosis of the right coronary artery is the next most changes in the myocardial infarction vary according to frequent (30-40%). It involves the posterior part of the left the age of the infarct and are therefore described ventricle and the posterior one-third of the interventricular sequentially (Table 16. The transmural infarcts, which by definition involve the entire thickness of the ventricular wall, usually have a thin rim of preserved subendocardial myocardium which is perfused directly by the blood in the ventricular chamber.
If the enzyme is present gastritis diet çíàêè purchase cheap florinef, Conditions associated with excessive accumulation of dark pigment is identified in pigment cells gastritis symptoms of 0.1 mg florinef mastercard. In diabetes mellitus gastritis symptoms yahoo answers purchase florinef 0.1mg amex, there is intracellular accumulation of amelanotic melanoma from other anaplastic tumours gastritis bacteria safe florinef 0.1mg. Glycogen deposits in diabetes mellitus generalised and localised hyperpigmentation and are seen in epithelium of distal portion of proximal convolu hypopigmentation: ted tubule and descending loop of Henle gastritis symptoms light headed florinef 0.1mg discount, in the hepatocytes gastritis diet shopping list order 0.1mg florinef mastercard, in beta cells of pancreatic islets chronic gastritis forum generic florinef 0.1mg mastercard, and in cardiac muscle cells gastritis menu discount 0.1mg florinef visa. In glycogen storage diseases or glycogenosis, there is defec pigmentation on the skin of face, nipples, and genitalia and tive metabolism of glycogen due to genetic disorders. A similar appear conditions along with other similar genetic disorders are ance may be observed in women taking oral contraceptives. There are 2 broad categories of b) Peutz-Jeghers syndrome is characterised by focal peri-oral pigments: endogenous and exogenous (Table 3. Melanin f) Dermatopathic lymphadenitis is an example of deposition of melanin pigment in macrophages of the lymph nodes Melanin is the brown-black, non-haemoglobin-derived draining skin lesions. It is synthesised in the iii) Generalised hypopigmentation:Albinism is an extreme melanocytes and dendritic cells, both of which are present degree of generalised hypopigmentation in which tyrosinase in the basal cells of the epidermis and is stored in the form of activity of the melanocytes is genetically defective and no cytoplasmic granules in the phagocytic cells called the melanin is formed. Albinos have blond hair, poor vision and melanophores, present in the underlying dermis. However, sometimes tyrosinase is squamous and basal cell cancers of the skin in such present but is not active and hence no melanin pigment is individuals. In such cases, the presence of tyrosinase can be iv) Localised hypopigmentation: a) Leucoderma is a form of partial albinism and is an inherited disorder. Haemoprotein-derived pigments i) Haemosiderin Melanin-like Pigments ii) Acid haematin (Haemozoin) c. Lipofuscin (Wear and tear pigment) required for break-down of homogentisic acid which then B. Injected pigments (Tattooing) alkaptonuria, if allowed to stand for some hours in air, turns black due to oxidation of homogentisic acid. Hepatocytes in patients haemoglobin is liberated which is taken up by macrophages of Dubin-Johnson syndrome, an autosomal recessive form where it is degraded and stored as haemosiderin. A few of hereditary conjugated hyperbilirubinaemia, contain examples are as under : melain-like pigment in the cytoplasm (Chapter 21). The changing colours of a bruise or a black eye are caused by the pigments like biliverdin and bilirubin which are Haemoprotein-derived Pigments formed during transformation of haemoglobin into haemosiderin. Haemoproteins are the most important endogenous Brown induration in the lungs as a result of small haemor pigments derived from haemoglobin, cytochromes and their rhages as occur in mitral stenosis and left ventricular failure. For an understanding of disorders of Microscopy reveals the presence of ‘heart failure cells’ which haemoproteins, it is essential to have knowledge of normal are haemosiderin-laden alveolar macrophages. In disordered iron metabolism and transport, Systemic overload with iron may result in generalised haemoprotein-derived pigments accumulate in the body. There can be two types of patterns: these pigments are haemosiderin, acid haematin (haemozoin), bilirubin, and porphyrins. Iron is stored in the tissues in 2 forms: Ferritin, which is iron complexed to apoferritin and can be identified by electron microscopy. Haemosiderin, which is formed by aggregates of ferritin and is identifiable by light microscopy as golden-yellow to brown, granular pigment, especially within the mononuclear phagocytes of the bone marrow, spleen and liver where break-down of senescent red cells takes place. Haemosiderin is ferric iron that can be demonstrated by Perl’s stain that produces Prussian blue reaction. In this reaction, colourless potassium ferrocyanide reacts with ferric ions of haemosiderin to form deep blue ferric-ferrocyanide (Fig. Excessive storage of haemosiderin occurs in situations when there is increased break-down of red cells, or systemic overload of iron due to primary (idiopathic, hereditary) haemochromatosis, and secondary (acquired) causes such as in thalassaemia, sideroblastic anaemia, alcoholic cirrhosis, Figure 3. Another variety of haematin pigment is formalin pigment formed in blood-rich tissues which have been preserved in acidic formalin solution. Excess of bilirubin or hyper bilirubinaemia causes an important clinical condition called jaundice. Normal bilirubin metabolism and pathogenesis of jaundice are described in Chapter 21. Hyperbilirubinaemia may be unconjugated or conjugated, and jaundice may appear in one of the following 3 ways: a) Prehepatic or haemolytic, when there is excessive destruc tion of red cells. Excessive accumulation of bilirubin pigment can be seen Parenchymatous deposition of haemosiderin occurs in the in different tissues and fluids of the body, especially in the parenchymal cells of the liver, pancreas, kidney, and heart. Skin and sclerae Reticuloendothelial deposition occurs in the liver, spleen, become distinctly yellow. Porphyrins are normal pigment present i) Increased erythropoietic activity: In various forms of in haemoglobin, myoglobin and cytochrome. Porphyria chronic haemolytic anaemia, there is excessive break-down refers to an uncommon disorder of inborn abnormality of ofï€ haemoglobin and hence iron overload. It results from genetic deficiency of further compounded by treating the condition with blood one of the enzymes required for the synthesis of haem, transfusions (transfusional haemosiderosis) or by parenteral resulting in excessive production of porphyrins. The deposits of iron in these cases, termed as genetic deficiency is precipitated by intake of some drugs. Porphyrias are broadly of 2 types—erythropoietic and absorption of iron even when the intake is normal, is known hepatic. These have defective dominant disease associated with much more deposits of iron synthesis of haem in the red cell precursors in the bone than cases of acquired haemosiderosis. These may be further of 2 subtypes: by triad of pigmentary liver cirrhosis, pancreatic damage Congenital erythropoietic porphyria, in which the urine is resulting in diabetes mellitus, and skin pigmentation. On the basis of the last two features, the disease has come to be red due to the presence of uroporphyrin and coproporphyrin. Bones and iii) Excessive dietary intake of iron: A common example of skin show red brown discolouration. The excess of iron gets deposited in various organs a normal erythroid precursors but have a defect in synthesis including the liver causing pigment cirrhosis. Acid haematin or following: haemozoin is a haemoprotein-derived brown-black pigment Acute intermittent porphyria is characterised by acute containing haem iron in ferric form in acidic medium. But it episodes of 3 patterns: abdominal, neurological, and psycho differs from haemosiderin because it cannot be stained by tic. There is Prussian blue (Perl’s) reaction, probably because of formation excessive delta aminolaevulinic acid and porphobilinogen of complex with a protein so that it is unable to react in the in the urine. Haematin pigment is seen most commonly in chronic Porphyria cutanea tarda is the most common of all malaria and in mismatched blood transfusions. Porphyrins collect in the liver and small quantity malarial pigment can also be deposited in macrophages and is excreted in the urine. Most of the patients have associated Inhaled Pigments 43 haemosiderosis with cirrhosis which may eventually develop the lungs of most individuals, especially of those living in into hepatocellular carcinoma. The skin photosensitivity with acute abdominal and neurological most commonly inhaled substances are carbon or coal dust; manifestations. These substances may produce occupational lung diseases called pneumoconiosis Lipofuscin or lipochrome is yellowish-brown intracellular (Chapter 17). The pigment particles after inhalation are taken lipid pigment (lipo = fat, fuscus = brown). Some of the pigment-laden often found in atrophied cells of old age and hence the name macrophages are coughed out via bronchi, while some settle ‘wear and tear pigment’. It is seen in the myocardial fibres, in the interstitial tissue of the lung and in the respiratory hepatocytes, Leydig cells of the testes and in neurons in senile bronchioles and pass into lymphatics to be deposited in the dementia. However, By light microscopy, the pigment is coarse, golden-brown extensive deposition of particulate material over many years granular and often accumulates in the central part of the in coal-miners’ pneumoconiosis, silicosis, asbestosis etc. In the heart muscle, the change is provoke low grade inflammation, fibrosis and impaired associated with wasting of the muscle and is commonly respiratory function. The pigment Ingested Pigments can be stained by fat stains but differs from other lipids in being fluorescent and having acid-fastness. The examples are as under: By electron microscopy, lipofuscin appears as intralysoso i) Argyria is chronic ingestion of silver compounds and mal electron-dense granules in perinuclear location. These results in brownish pigmentation in the skin, bowel, and granules are composed of lipid-protein complexes. Lipofuscin represents the collection of indigestible material ii) Chronic lead poisoning may produce the characteristic blue in the lysosomes after intracellular lipid peroxidation and is lines on teeth at the gumline. Unlike in normal iii) Melanosis coli results from prolonged ingestion of certain cells, in aging or debilitating diseases the phospholipid end cathartics. The lipofuscin pigment granules are seen in the cytoplasm of the myocardial fibres, especially around the nuclei. There is presence of abundant coarse black carbon pigment in the septal walls and around the bronchiole. The examples of injected pigments are prolonged use of ointments containing mercury, dirt left accidentally in a wound, and tattooing by pricking the skin with dyes. Autolysis can occur in the living body when it is surrounded by inflammatory reaction (vital reaction), but the term is generally used for postmortem change in which there is complete absence of surrounding inflammatory response. Autolysis is rapid in some tissues rich in hydrolytic enzymes such as in the pancreas, and gastric mucosa; intermediate in tissues like the heart, liver and kidney; and slow in fibrous tissue. Morphologically, autolysis is identified by homogeneous and eosinophilic cytoplasm with loss of cellular details and remains of cell as debris. Necrosis can be caused by various agents such as hypoxia, chemical and physical agents, microbial agents, immunological injury, etc. A, Cell necrosis is identified irreversible cell injury in necrosis of all types (Fig. Morphologically this condensation of nuclear chromatin and fragmentation of the cell into change is identified as homogeneous and intensely membrane-bound apoptotic bodies which are engulfed by macrophages. The common examples are infarct brain 45 cytoplasmic vacuolation or dystrophic calcification. This process is morphologically Grossly, the affected area is soft with liquefied centre seen as characteristic nuclear changes in necrotic cell. Morphologically, there are five types of necrosis: coagulative, liquefaction (colliquative), caseous, fat, and fibrinoid necrosis. This appearance is partly attributed to the histotoxic effects of lipopolysaccharides present in the capsule of the Grossly, foci of coagulative necrosis in the early stage are tubercle bacilli, Mycobacterium tuberculosis. With progression, they Microscopically, the necrosed foci are structureless, become more yellowish, softer, and shrunken. The Microscopically, the hallmark of coagulative necrosis is surrounding tissue shows characteristic granulomatous the conversion of normal cells into their ‘tombstones’ i. Eventually, occurring at two anatomically different locations but the necrosed focus is infiltrated by inflammatory cells and morphologically similar lesions. These are: following acute the dead cells are phagocytosed leaving granular debris pancreatic necrosis, and traumatic fat necrosis commonly in and fragments of cells (Fig. Lique lipases from injured or inflamed tissue that results in necrosis faction or colliquative necrosis occurs commonly due to of the pancreas as well as of the fat depots throughout the ischaemic injury and bacterial or fungal infections. It occurs peritoneal cavity, and sometimes, even affecting the extra due to degradation of tissue by the action of powerful abdominal adipose tissue. The affected area on right shows cells with intensely eosinophilic cytoplasm of tubular cells but the outlines of tubules are still maintained. The interface between viable and non-viable area shows non specific chronic inflammation and proliferating vessels. The necrosed area on right side of the field shows a cystic space containing cell debris, while the surrounding zone shows granulation tissue and gliosis. Fat necrosis hydrolyses neutral fat present in adipose cells has the staining properties of fibrin. The leaked out free fatty acids immune complex vasculitis, autoimmune diseases, complex with calcium to form calcium soaps (saponification) Arthus reaction etc), arterioles in hypertension, peptic discussed later under dystrophic calcification. Grossly, fat necrosis appears as yellowish-white and firm Microscopically, fibrinoid necrosis is identified by deposits. Formation of calcium soaps imparts the necrosed brightly eosinophilic, hyaline-like deposition in the vessel foci firmer and chalky white appearance. Necrotic focus is surrounded by nuclear debris of Microscopically, the necrosed fat cells have cloudy neutrophils (leucocytoclasis) (Fig. Local haemor appearance and are surrounded by an inflammatory rhage may occur due to rupture of the blood vessel. Fibrinoid necrosis is programmed cell death’ having significance in a variety of characterised by deposition of fibrin-like material which physiologic and pathologic conditions (apoptosis is a Greek Figure 3. There is eosinophilic, amorphous, granular material, while the periphery shows granulomatous inflammation. The vessel appearance of adipocytes, coarse basophilic granular debris while the wall shows brightly pink amorphous material and nuclear fragments of periphery shows a few mixed inflammatory cells. The characteristic cell death is activated (‘cell suicide’) and is unaccompanied morphologic changes in apoptosis seen in histologic and by any inflammation and collateral tissue damage. Involvement of single cells or small clusters of cells in responsible for mediating cell death in a wide variety of the background of viable cells. The apoptotic cells are round to oval shrunken masses Physiologic Processes: of intensely eosinophilic cytoplasm (mummified cell) 1. Organised cell destruction in sculpting of tissues during containing shrunken or almost-normal organelles development of embryo. Normal cell destruction followed by replacement proliferation such as in intestinal epithelium. Cell death by cytotoxic T cells in immune mechanisms such as in graft-versus-host disease and rejection reactions. The nuclear chromatin is condensed or fragmented on the outer surface of apoptotic cell facilitates early (pyknosis or karyorrehexis). The cell membrane may show convolutions or projections appearance of inflammatory cells. Triggers for signalling program or loosely floating apoptotic cells after losing contact, with med cell death act at the cell membrane, either intra each other and basement membrane as single cells, or may cellularly or extracellularly. These include the following: result in major cell loss in the tissue without significant i) Withdrawal of signals required for normal cell survival change in the overall tissue structure. Staining of chromatin condensation (haematoxylin, initiated into self-destruct mode, the programme inbuilt in Feulgen, acridine orange). Annexin V as marker for apoptotic cell membrane having ‘caspase’ is derived from: c for cystein protease; asp for phosphatidylserine on the cell exterior. Biochemical processes get activated either by coming in contact with some etiologic underlying the morphologic changes are as under: agent of cell injury agent or by unknown mechanism. Appearance of phosphatidylserine on the outer surface appropriately called a death receptor because on coming in of cell membrane. Definition Programmed and coordinated cell death Cell death along with degradation of tissue by hydrolytic enzymes 2. Morphology i) No Inflammatory reaction i) Inflammatory reaction always present ii) Death of single cells ii) Death of many adjacent cells iii) Cell shrinkage iii) Cell swelling initially iv) Cytoplasmic blebs on membrane iv) Membrane disruption v) Apoptotic bodies v) Damaged organelles vi) Chromatin condensation vi) Nuclear disruption vii) Phagocytosis of apoptotic bodies by macrophages vii) Phagocytosis of cell debris by macrophages 4. Thus, it may regulate the apoptotic examples of necrotising inflammation are: gangrenous process by binding to some related proteins. The net effect on the mitochondrial membrane is variant form of wet gangrene called gas gangrene. The above mechanisms lead to proteolytic this form of gangrene begins in the distal part of a limb due actions on nucleus, chromatin clumping, cytoskeletal to ischaemia. The typical example is the dry gangrene in the damage, disruption of endoplasmic reticulum, mitochondrial toes and feet of an old patient due to arteriosclerosis. It is usually initiated in one of the toes which membrane changes which promote their phagocytosis. The gangrene spreads slowly upwards until appear on the outer surface of the cells in apoptosis, which it reaches a point where the blood supply is adequate to keep facilitate their identification by adjacent phagocytes and the tissue viable. The phagocytosis is unaccompanied between the gangrenous part and the viable part. The type of necrosis is usually coagulative due usually brings about complete separation with eventual to ischaemia. The gangrenous area is dry, shrunken and dark and is separated from the viable tissue by clear line of separation. Histologically, there is necrosis with smudging of the venous, and less commonly, arterial blood flow from tissue. The toxic products formed by bacteria are absorbed Wet Gangrene causing profound systemic manifestations of septicaemia, and finally death. The spreading wet gangrene generally Wet gangrene occurs in naturally moist tissues and organs lacks clear-cut line of demarcation and may spread to such as the mouth, bowel, lung, cervix, vulva etc. Bed sores occurring in a bed-ridden patient due to is soft, swollen, putrid, rotten and dark. The classic pressure on sites like the sacrum, buttocks and heels are the example is gangrene of bowel, commonly due to other important clinical conditions included in wet gangrene. The part Wet gangrene usually develops rapidly due to blockage of is stained dark due to the same mechanism as in dry gangrene (Fig. Histologically, there is coagulative necrosis with stuffing of affected part with blood. The line of demarcation between gangrenous segment and viable bowel is generally not clear-cut (Fig. It is a special form of wet gangrene caused by gas-forming clostridia (gram-positive anaerobic bacteria) which gain entry into the tissues through open contaminated wounds, especially in the muscles, or as a complication of operation on colon which normally contains clostridia. Clostridia produce various toxins which produce necrosis and oedema locally and are also absorbed producing profound systemic manifestations. Grossly, the affected area is swollen, oedematous, painful and crepitant due to Figure 3. Line of demarcation between gangrenous segment and the viable bowel is not clear-cut. Subsequently, the affected tissue becomes dark black and Metastatic calcification, on the other hand, occurs in foul smelling. Microscopically, the muscle fibres undergo coagulative Etiology and pathogenesis of the two are different but necrosis with liquefaction. Large number of gram-positive morphologically the deposits in both resemble normal bacilli can be identified. Histologically, in routine H and E stained sections, calcium salts appear as deeply basophilic, irregular and granular clumps.
Discount florinef online master card. What Are The First Signs Of Gastritis?.
Syndromes
Excessive vaginal bleeding (2 - 7 days following the overdose)
