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Medical Instructor, Indiana Wesleyan University

Reaction-to-injury hypothesis cholesterol test diy buy generic gemfibrozil 300 mg line, first described in 1973 cholesterol levels pdf order cheap gemfibrozil line, and modified in 1986 and 1993 by Ross cholesterol test gp cheap 300mg gemfibrozil with visa. Monoclonal theory cholesterol genetic test buy cheap gemfibrozil on-line, based on neoplastic proliferation of smooth muscle cells, postulated by Benditt and Benditt in 1973. This theory is most widely accepted and incorporates aspects of two older historical theories of atherosclerosis-the lipid theory of Virchow and thrombogenic (encrustation) theory of Rokitansky. The original response to injury theory was first described in 1973 according to which the initial event in atherogenesis was considered to be endothelial injury followed by smooth muscle cell proliferation so that the early lesions, according to this theory, consist of smooth muscle cells mainly. The modified response-to-injury hypothesis described subsequently in 1993 implicates lipoprotein entry into the intima as the initial event followed by lipid accumulation in the macrophages (foam cells now) which according to modified theory, are believed to be the dominant cells in early lesions. The role of haemodynamic forces in causing endothelial injury is further supported by the distribution of atheromatous plaques at points of bifurcation or branching of blood vessels which are under greatest shear stress. Endothelial injury causes adherence, aggregation and platelet release reaction at the site of exposed subendothelial connective tissue and infiltration by inflammatory cells. Smooth muscle cell proliferation is also facilitated by biomolecules such as nitric oxide and endothelin released from endothelial cells. Intimal proliferation of smooth muscle cells is accompanied by synthesis of matrix proteins-collagen, elastic fibre proteins and proteoglycans. C, Smooth muscle cell proliferation into the intima and ingrowth of new blood vessels. However, following is the generally accepted role of key components involved in atherogenesis, diagrammatically illustrated in. It has been known for many years that endothelial injury is the initial triggering event in the development of lesions of atherosclerosis. Actual endothelial denudation is not an essential requirement, but endothelial dysfunction may initiate the sequence of events. Numerous causes ascribed to endothelial injury in experimental animals are: mechanical trauma, haemodynamic forces, immunological and chemical mechanisms, metabolic agent as chronic dyslipidaemia, homocystine, circulating toxins from systemic infections, viruses, hypoxia, radiation, carbon monoxide and tobacco products. As stated already, chronic dyslipidaemia in itself may initiate endothelial injury and dysfunction by causing increased permeability. As apparent from the foregoing, endothelial injury exposes subendothelial connective tissue resulting in formation of small platelet aggregates at the site and causing proliferation of smooth muscle cells. This causes mild inflammatory reaction which together with foam cells is incorporated into the atheromatous plaque. The lesions enlarge by attaching fibrin and cells from the blood so that thrombus becomes a part of atheromatous plaque. This hypothesis is based on the postulate that proliferation of smooth muscle cells is the primary event and that this proliferation is monoclonal in origin similar to cellular proliferation in neoplasms. The monoclonal proliferation of smooth muscle cells in atherosclerosis may be initiated by mutation caused by exogenous chemicals. However, the clinical disease states due to luminal narrowing in atherosclerosis are caused by fully developed atheromatous plaques and complicated plaques. Fatty streaks and dots on the intima by themselves are harmless but may be the precursor lesions of atheromatous plaques. They are especially prominent in the aorta and other major arteries, more often on the posterior wall than the anterior wall. The opened up inner surface of the abdominal aorta shows a variety of atheromatous lesions. While some are raised yellowish-white lesions raised above the surface, a few have ulcerated surface. Orifices of some of the branches coming out of the wall are narrowed by the atherosclerotic process. They may be either in the form of small, multiple dots, about 1 mm in size, or in the form of elongated, beaded streaks. Microscopically, fatty streaks lying under the endothelium are composed of closely-packed foam cells, lipidcontaining elongated smooth muscle cells and a few lymphoid cells. Gelatinous lesions develop in the intima of the aorta and other major arteries in the first few months of life. Microscopically, gelatinous lesions are foci of increased ground substance in the intima with thinned overlying endothelium. A fully developed atherosclerotic lesion is called atheromatous plaque, also called fibrous plaque, fibrofatty plaque or atheroma. Unlike fatty streaks, atheromatous plaques are selective in different geographic locations and races and are seen in advanced age. These lesions may develop from progression of early lesions of the atherosclerosis described above. Most often and most severely affected is the abdominal aorta, though smaller lesions may be seen in descending thoracic aorta and aortic arch. The major branches of the aorta around the ostia are often severely involved, especially the iliac, femoral, carotid, coronary, and cerebral arteries. Grossly, atheromatous plaques are white to yellowishwhite lesions, varying in diameter from 1-2 cm and raised on the surface by a few millimetres to a centimetre in thickness. Cut section of the plaque reveals the luminal surface as a firm, white fibrous cap and a central core composed of yellow to yellow-white, soft, porridgelike material and hence the name atheroma. Microscopically, the appearance of plaque varies depending upon the age of the lesion.

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The main distinction of promyelocyte from myeloblast is in the cytoplasm which contains azurophilic (primary or non-specific) granules cholesterol test variation buy 300mg gemfibrozil amex. The myelocyte is the stage in which specific or secondary granules appear in the cytoplasm cholesterol pills recall buy gemfibrozil 300mg otc, and accordingly cholesterol levels vldl order gemfibrozil canada, the cell can be identified at this stage as belonging to the neutrophilic cholesterol test false positive cheap gemfibrozil 300mg line, eosinophilic or basophilic myelocyte. Primary granules also persist at this stage but formation of new primary granules stops. The nucleus of myelocyte is eccentric, round to oval, having somewhat coarse nuclear chromatin and no visible nucleoli. The myeloid cells up to the myelocyte stage continue to divide and, therefore, comprise mitotic or proliferative pool. The metamyelocyte stage is 10-18 m in diameter and is characterised by a clearly indented or horseshoe-shaped nucleus without nucleoli. The metamyelocytes are best distinguished from the monocytes by the clumped nuclear chromatin while the latter have fine chromatin. Band form is juvenile granulocyte, 1016 m in diameter, characterised by further condensation of nuclear chromatin and transformation of nuclear shape into band configuration of uniform thickness. The mature polymorphonuclear leucocytes, namely: the neutrophils, eosinophils and basophils, are described separately below. Monocyte-Macrophage Series the monocyte-macrophage series of cells, though comprise a part of myeloid series alongwith other granulocytic series, but are described separately here in view of different morphologic stages in their maturation. The monoblast is the least mature of the recognisable cell of monocyte-macrophage series. It is very similar in appearance to myeloblasts except that it has ground-glass cytoplasm with irregular border and may show phagocytosis as indicated by the presence of engulfed red cells in the cytoplasm. However, differentiation from myeloblast at times may be difficult even by electron microscopy and, therefore, it is preferable to call the earliest precursor of granulocytic series as myelomonoblast. The promonocyte is a young monocyte, about 20 m in diameter and possesses a large indented nucleus containing a nucleolus. The cytoplasm is basophilic and contains no azurophilic granules but may have fine granules which are larger than those in the mature monocyte. The mature form of monocytic series is described below, while the transformed stages of these cells in various tissues. In man, the bone marrow and the thymus are the primary lymphopoietic organs where lymphoid stem cells undergo spontaneous division independent of antigenic stimulation. These sites actively produce lymphocytes from the germinal centres of lymphoid follicles as a response to antigenic stimulation. Myeloblast 10-18 m Round or oval Fine meshwork Very fine 2-5 Scanty, blue, agranular, Auer rods may be seen Lymphoblast 10-18 m Round or oval Slightly clumped Fairly dense 1-2 Scanty, clear blue, agranular 347 Feature 1. It includes migration of immature lymphocytes to other organs such as the thymus where locally-produced factors act on them. In man, the B cells are derived from the bone marrow stem cells, while in birds they mature in the bursa of Fabricius. After antigenic activation, B cells proliferate and mature into plasma cells which secrete specific immunoglobulin antibodies. Lymphoid Series the maturation stages in production of lymphocytes are illustrated in. The lymphoblast is the earliest identifiable precursor of lymphoid cells and is a rapidly dividing cell. It is a large cell, 10-18 m in diameter, containing a large round to oval nucleus having slightly clumped or stippled nuclear chromatin. The nuclear membrane is denser and the number of nucleoli is fewer (1-2) as compared with those in myeloblast (2-5). The distinguishing morphologic features between the myeloblast and lymphoblast are summarised in Table 14. This stage is an intermediate stage between the lymphoblast and mature lymphocyte. These young lymphocytes are 9-18 m in diameter, contain round to indented nucleus with slightly stippled or coarse chromatin and may have 0-1 nucleoli. It also normally undergoes minor degree of diurnal variation with a slight rise in the afternoon. The total white cell count is normally high in pregnancy and following delivery, usually returning to normal within a week. The pathological variations in white cell values together with brief review of their morphology and functions are considered below. It consists of a characteristic dense nucleus, having 2-5 lobes and pale cytoplasm containing numerous fine violet-pink granules. These lysosomal granules contain several enzymes and are of 2 types: Primary or azurophilic granules are large and coarse and appear early at the promyelocyte stage. When the absolute neutrophil count falls below 2,500/l, the patient is said to have neutropenia and is prone to develop recurrent infections. Drugs, chemicals and physical agents which induce aplasia of the bone marrow cause neutropenia. Occasionally, certain drugs produce neutropenia due to individual sensitivity such as: anti-inflammatory (amidopyrine, phenylbutazone), antibacterial (chloramphenicol, cotrimoxazole), anticonvulsants, antithyroids, hypoglycaemics and antihistaminics. Heavy, dark staining, coarse toxic granules are characteristic of bacterial infections. In bacterial infections such as in septicaemia, cytoplasmic vacuolation may develop. These include the following: i) Sex chromatin is a normal finding in 2-3% of neutrophils in female sex. It consists of a drumstick appendage of chromatin, about 1 m across, and attached to one of the nuclear lobes by a thin chromatin strand.

Rarely cholesterol lowering foods eggs order gemfibrozil 300 mg online, congenital cholesterol level in quail eggs discount gemfibrozil 300 mg online, mycotic and syphilitic aneurysms may occur in coronary arteries and produce similar occlusive effects cholesterol medication efficacy buy 300mg gemfibrozil overnight delivery. Compression of a coronary from outside by a primary or secondary tumour of the heart may result in coronary occlusion cholesterol ratio wiki order gemfibrozil 300 mg without prescription. Depending upon the suddenness of onset, duration, degree, location and extent of the area affected by myocardial ischaemia, the range of changes and clinical features may vary from an asymptomatic state at one extreme to immediate mortality at another. Sudden cardiac death the term acute coronary syndromes include a triad of acute myocardial infarction, unstable angina and sudden cardiac death. It is characterised by paroxysmal pain in the substernal or precordial region of the chest which is aggravated by an increase in the demand of the heart and relieved by a decrease in the work of the heart. Stable or typical angina is characterised by attacks of pain following physical exertion or emotional excitement and is relieved by rest. The pathogenesis of condition lies in chronic stenosing coronary atherosclerosis that cannot perfuse the myocardium adequately when the workload on the heart increases. This pattern of angina is characterised by pain at rest and has no relationship with physical activity. It may occur due to sudden vasospasm of a coronary trunk induced by coronary atherosclerosis, or may be due to release of humoral vasoconstrictors by mast cells in the coronary adventitia. It is characterised by more frequent onset of pain of prolonged duration and occurring often at rest. Multiple factors are involved in the pathogenesis of unstable angina which include: stenosing coronary atherosclerosis, complicated coronary plaques. More often, the lesions lie in a branch of the major coronary trunk so that collaterals prevent infarction. Many patients may die within the first few hours of the onset, while remainder suffer from effects of impaired cardiac function. A significant factor that may prevent or diminish the myocardial damage is the development of collateral circulation through anastomotic channels over a period of time. A regular and well-planned exercise programme encourages good collateral circulation and improved cardiac performance. About 5% of heart attacks occur in young people under the age of 40 years, particularly in those with major risk factors to develop atherosclerosis like hypertension, diabetes mellitus, cigarette smoking and dyslipidaemia with familial hypercholesterolaemia. After menopause, this sex difference gradually declines but the incidence of disease among women never reaches that among men of the same 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 undergo aggregation, activation and release reaction. These events contribute to the build-up of the platelet mass that may give rise to emboli or initiate thrombosis. There are some differences in the pathogenesis of the transmural infarcts involving the full thickness of ventricular wall and the subendocardial (laminar) infarcts affecting the inner subendocardial one-third to half. Critical coronary narrowing (more than 75% compromised lumen) is of great significance in the causation of such infarcts. Atherosclerotic plaques with superimposed thrombosis and intramural haemorrhage are significant in about 90% cases, and non-atherosclerotic causes in the remaining 10% cases. This is because subendocardial myocardium is normally least well perfused by coronaries and thus is more vulnerable to any reduction in the coronary flow. Superimposed coronary thrombosis is frequently encountered in these cases too, and hence the beneficial role of fibrinolytic treatment in such patients. Infarcts have been classified in a number of ways by the physicians and the pathologists: 1. According to the anatomic region of the left ventricle involved, they are called anterior, posterior (inferior), lateral, septal and circumferential, and their combinations like anterolateral, posterolateral (or inferolateral) and anteroseptal. According to the degree of thickness of the ventricular wall involved, infarcts are of two types. According to the age of infarcts, they are of two types: i) Newly-formed infarcts called as acute, recent or fresh. Right ventricle is less susceptible to infarction due to its thin wall, having less metabolic requirements and is thus adequately nourished by the thebesian vessels. Atrial infarcts, whenever present, are more often in the right atrium, usually accompanying the infarct of the left ventricle. Left atrium is relatively protected from infarction because it is supplied by the oxygenated blood in the left atrial chamber. The region of infarction depends upon the area of obstructed blood supply by one or more of the three coronary arterial trunks. Feature Definition Frequency Distribution Pathogenesis Coronary thrombosis Epicarditis Transmural Infarct Full-thickness, solid Most frequent (95%) Specific area of coronary supply > 75% coronary stenosis Common Common Subendocardial Infarct Inner third to half, patchy Less frequent Circumferential Hypoperfusion of myocardium Rare None 431 Figure 16. Stenosis of the left anterior descending coronary artery is the most common (40-50%). The region of infarction is the anterior part of the left ventricle including the apex and the anterior two-thirds of the interventricular septum. It involves the posterior part of the left ventricle and the posterior one-third of the interventricular septum. Stenosis of the left circumflex coronary artery is seen least frequently (15-20%). The gross and microscopic changes in the myocardial infarction vary according to the age of the infarct and are therefore described sequentially (Table 16.

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Thus cholesterol levels heart disease myth order gemfibrozil 300 mg free shipping, the scar formed in a sutured wound is neat due to close apposition of the margins of wound; the use of adhesive tapes avoids removal of stitches and its complications cholesterol clarity order 300mg gemfibrozil with amex. Healing by Second Intention (Secondary Union) this is defined as healing of a wound having the following characteristics: i) open with a large tissue defect cholesterol in yard eggs cheap gemfibrozil, at times infected; ii) having extensive loss of cells and tissues; and iii) the wound is not approximated by surgical sutures but is left open cholesterol medication causing cough purchase 300mg gemfibrozil overnight delivery. The basic events in secondary union are similar to primary union but differ in having a larger tissue defect which has to be bridged. Hence healing takes place from the base upwards as well as from the margins inwards. The healing by second intention is slow and results in a large, at times ugly, scar as compared to rapid healing and neat scar of primary union. As a result of injury, the wound space is filled with blood and fibrin clot which dries. There is an initial acute inflammatory response followed by appearance of macrophages which clear off the debris as in primary union. A, the open wound is filled with blood clot and there is inflammatory response at the junction of viable tissue. B, Epithelial spurs from the margins of wound meet in the middle to cover the gap and separate the underlying viable tissue from necrotic tissue at the surface forming scab. C, After contraction of the wound, a scar smaller than the original wound is left. However, the proliferating epithelial cells do not cover the surface fully until granulation tissue from base has started filling the wound space. In this way, pre-existing viable connective tissue is separated from necrotic material and clot on the surface, forming scab which is cast off. Granulation tissue is formed by proliferation of fibroblasts and neovascularisation from the adjoining viable elements. With time, the scar on maturation becomes pale and white due to increase in collagen and decrease in vascularity. Specialised structures of the skin like hair follicles and sweat glands are not replaced unless their viable residues remain which may regenerate. Contraction of wound is an important feature of secondary healing, not seen in primary healing. Due to the action of myofibroblasts present in granulation tissue, the wound contracts to one-third to onefourth of its original size. Wound contraction occurs at a time when active granulation tissue is being formed. Bacterial contamination of an open wound delays the process of healing due to release of bacterial toxins that provoke necrosis, suppuration and thrombosis. Surgical removal of dead and necrosed tissue, debridement, helps in preventing the bacterial infection of open wounds. Complications of Wound Healing During the course of healing, following complications may occur: 1. Implantation (epidermal) cyst formation may occur due to persistence of epithelial cells in the wound after healing. Healed wounds may at times have rust-like colour due to staining with haemosiderin. Some coloured particulate material left in the wound may persist and impart colour to the healed wound. Cleanliness of wound Infection Margins Sutures Healing Outcome Complications Primary Union Clean Generally uninfected Surgical clean Used Scanty granulation tissue at the incised gap and along suture tracks Neat linear scar Infrequent, epidermal inclusion cyst formation Secondary Union Unclean May be infected Irregular Not used Exuberant granulation tissue to fill the gap Contracted irregular wound Suppuration, may require debridement 170 5. A weak scar, especially after a laparotomy, may be the site of bursting open of a wound (wound dehiscence) or an incisional hernia. Excessive formation of collagen in healing may result in keloid (claw-like) formation, seen more commonly in Blacks. Hypertrophied scars differ from keloid in that they are confined to the borders of the initial wound while keloids have tumour-like projection of connective tissue. An exaggeration of wound contraction may result in formation of contractures or cicatrisation. The collagens are a family of proteins which provide structural support to the multicellular organism. It is the main component of tissues such as fibrous tissue, bone, cartilage, valves of heart, cornea, basement membrane etc. Collagen is synthesised and secreted by a complex biochemical mechanism on ribosomes. The collagen synthesis is stimulated by various growth factors and is degraded by collagenase. Regulation of collagen synthesis and degradation take place by various local and systemic factors so that the collagen content of normal organs remains constant. On the other hand, defective regulation of collagen synthesis leads to hypertrophied scar, fibrosis, and organ dysfunction. Other types of collagen are non-fibrillar and amorphous material seen as component of the basement membranes. Morphologically, the smallest units of collagen are collagen fibrils, which align together in parallel bundles to form collagen fibres, and then collagen bundles. Plasma fibronectin is synthesised by the liver cells and is trapped in basement membrane such as in filtration through the renal glomerulus. Tissue fibronectin is formed by fibroblasts, endothelial cells and other mesenchymal cells. It is responsible for the primitive matrix such as in the foetus, and in wound healing.