General pathology covers the basic mechanisms of diseases whereas This book is intended to be a textbook of general pathology for health science students. Human Diseases: Systemic Approach - Text Only. by Vinay Kumar, Abul K. Abbas and Jon C. Aster. Robbins and Cotran Pathologic Basis of Disease - With Access. PDF | This book has been written primarily for medical students of pathology whose mother tongue is not English, and as an aid to the teachers.

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Book Review. TEXTBOOK OF GENERAL PATHOLOGY. Br Med J ; 2 doi: (Published 15 July ) Cite this as: Br. This book has been published in good faith that the material provided by author is . is devoted to General Pathology, whereas the remaining two-thirds cover. I do admire the way they simplified general pathology by using very simple language. This book in my opinion will be of great help to our undergraduates'.

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Then you can start reading site books on your smartphone, tablet, or computer - no site device required. Would you like to tell us about a lower price? If you are a seller for this product, would you like to suggest updates through seller support? This new edition of Walter and Israel General Pathology has been extended and comprehensively updated to take account of the many advances made in recent years. Adopting a multidiscipline approach, including histopathology, genetics, immunology, microbiology and haematology.

It describes the spectrum of pathological processes, with many helpful diagrams and illustrations. Postgraduate students of surgery and pathology will find it essential reading. Read more Read less. Customers who viewed this item also viewed.

Page 1 of 1 Start over Page 1 of 1. Fischer's Mastery of Surgery. Pharmacology and Pharmacotherapeutics. Proliferative Phase: Proliferation of granulation tissues start approximately four days after wounding and usually lasts until day 21 in acute wounds depending on the size of the wound. Remodeling or Maturation Phase: Remodeling can take up to two years after wounding and explains why apparently healed wounds can break down so dramatically and quickly if attention is not paid to the initial causative factors.

The best example of this situation is the surgical incision where contamination of the wound is minimized and the wound is closed by suturing, once the wound is sutured, the incision space fills with blood, which contains fibrin and blood cells and which subsequently clots, the surface of this clot becomes dehydrated and forms a scab.

Within 24 hours, neutrophils appear at the edges of the incision and the epithelium at the edges of the incision begins to proliferate, it migrates under the scab and forms a thin continuous epithelial layer.

By 72 hours, macrophages are usually the most numerous inflammatory cells and granulation tissue starts to develop, collagen fibers are present but do not bridge the incision site, the epithelial cells continue to proliferate under the scab and the epidermal covering over the incision becomes thicker.

By day 5, the incision space is filled with granulation tissue and collagen fibers begin to bridge the incision, the epidermis returns to its normal thickness and keratinised architecture. During the second week, there is continued accumulation of collagen fiber s and proliferation of fibroblasts, inflammatory cells and edema disappears and the process of blanching begins.

By the end of one month, there is a connective tissue scar that is devoid of inflammatory cells and is covered by an intact epidermis. Inflammatory phase of healing Day 3 Healing by Secondary Intention This type of healing occurs when injuries result in more extensive loss of tissues such as with infarction, inflammatory ulceration, and large surface wounds. In these situations, due to the large tissue defects, repair by regeneration is minimal and the defect is filled with granulation tissue.

Second intention healing differ from first intention healing in several ways, first the greater injury induce a more intense inflammatory response. Secondly, much more granulation tissue is formed, and thirdly wounds that are repaired by second intention healing undergo a phenomenon known as "wound contraction" whereby specialized granulation tissue fibroblasts called myofibroblasts contract and dramatically reduce the size of the wound.

Excessive granulation is characterized by the formation of a mass of granulation tissue protruding from the wound and prevents re-epithelialization. Such excesses are commonly refer red to as "proud flesh". Keloid formation also refer s to an aberration of wound healing resulting in the formation of large bulging scars, but it differ s from excessive scar in that it is caused by excessive collagenizat ion of the wound and not excessive formation of granulation tissue, this phenomenon is a common problem in darker people.

Failure of fusion of the two ends of the wound, or nonunion of bone fracture. Implantation of epidermal cells, giving rise to keratin filled cyst known as epidermoid cyst. Bacterial infection and pus discharge may take place if a wound is contaminated. Failure to close the wound. Neoplasia, Neo literally means new and plasia means formation, while scientifically defined as an abnormal growth of tissues exceeding and un-coordinating with the evoking stimuli loss of responsiveness to normal stimuli of growth.

Neoplastic cells tend to be monoclonal, or similar in their genetic makeup, indicating the same origin from one transformed cell.

Non- neoplastic proliferations such as reactions to inflammation have cells that are polyclonal in origin. Biological Behavior of Neoplasia: Neoplastic tissues behave as parasites, depending on the host nutrient, i. Autonomy of growth, i. Additionally, some neoplasms behave as benign while others behave as malignant. Special Characteristics of Malignant Neoplasm: Malignant growth is not inhibited by contact with surrounding cells, they are discohesive and transplantable favouring invasion and metastasis.

Tumour cells can bind to laminin and fibronectin in connective tissues, then secrete collagenases or proteases, and then invade the surrounding tissue. Neoplastic cells may attain "immortality" or the ability to keep dividing indefinitely.

Nomenclature of Neoplasia: There are general rules for nomenclature with few exceptions and the rules depend on the following factors: Parenchymal or mesenchymal origin. For better understanding, we have to know the following terminology.

The functioning cells, like gland, epithelial, and hepatic cells. The supporting stroma, fibrous, muscle, and bone tissue connective tissue. Nomenclature of Benign Tumours: Benign tumours are named by adding the suffix oma to the end of the name of the tissue or cells from which they arise. For example, benign tumours of fibrous tissues are called fibroma, while of cartilages named chondroma, moreover from glands are named adenoma, and from bone are named osteoma, papilloma a name given for tumors arising from surface epithelium like skin or gastrointestinal surfaces.

Basis of Nomenclature of Malignant Tumours: All malignant tumors are called cancer, cancer is a sea animal crab which has multiple fingers like structures for fixation and nutrition. Malignant tumors arising from epithelial tissues are named by adding suffix carcinoma to the name of tissue or cell of origin, so it will be adenocarcinoma for glandular epithelium, squamous cell carcinoma for tumor s arise from squamous epithelium…etc.

While those arising from mesenchymal connective tissue are named by adding the sufix sarcoma at the end of the name of cell or tissue of origin, so it will be fibrosarcoma for tumor arises from fibrous tissues,…etc. The following table gives you more examples. Some tumors are malignant in spite of that, ended with the suffix -oma e.

Malignant tumor of spermatocyte -Lymphoma: Malignant tumor of lymphoid tissue -Melanoma: Malignant tumor of melanocyte -Teratoma: Neoplasm that originates from germ cells, sperm or ova , and is composed of mixed tissue are named teratoma, If it has benign features it is called benign teratoma and if has malignant features it is named malignant teratoma. Benign epithelial neoplasms growing on any surface epithelium showing microscopic or macroscopic finger -like patterns.

A mass that projects above the epithelial surface to form a microscopically visible structure, e. This is not a neoplasm, it is a local malformed growth that resembles a tumour, and it grows at the same rate as the surrounding tissues do.

Amass composed of normal cells in a wrong location, e. Both hamartoma and choristoma are considered as malformations and not neoplasms, and they are distinguished from neoplasms by the fact that they do not exhibit continued growth. They are a group of tumor -like tissue masses which may be confused with neoplasms. Cytological features of malignancy: There are abnormal cytological findings at the level of cytoplasm and the nucleus associated with malignancy, and used by the pathologist to diagnose malignancy which includes: Different shape and size of cells or nucleus - Hyperchromatism: Normally the chromatin is finely stained - Abnormal Mitotic Figure: Increased number with abnormal shape Tri, quadri-polar.

Normally it is bipolar figure. Prominent and irregular nucleoli which normally should not be seen. Means a high degree of resemblance to the normal tissue of origin has good prognosis.

Moderate degree of resemblance to the tissue of origin moderate prognosis. Means no resemblance to the tissue of origin, sometimes are called anaplastic tumours. They have the worse prognosis. It means failure of the tumour to resemble the original tissue, i. The cells will be large bizarre, pleomorphic and multinucleated.

Comparison between benign and malignant tumors. Benign tumors Malignant tumor Slowly growing mass Rapidly growing mass Regular surface, capsulated, not Irregular surfaces, Non-capsulated attached attached to deep structures to deep structures Noninvasive to another organ or Invasive to other organs tissues No spread or metastasis Spread and metastasis Well differentiated all the them Poorly differentiated, moderately or well differentiated No recurrence after surgery Recurrence after surgery No bleeding in cut surfaces Bleeding from cut surfaces is common Named by adding suffix —oma Named by adding suffix sarcoma or carcinoma Slight pressure effect on the Remarkable pressure effect on neighbouring neighbouring organ tissue Etiology of Neoplasm; Tumour formation is a multifactorial and multistep process, the following factors plays major role in its formation.

Genetic damage lies at the core of the etiology of tumour, there are four main types of genes responsible for the formation of tumours. A gene that normally produces growth factors when activated to oncogene they produce cancer - Cancer Suppressor Gene: A Gene that prevents cancer formation. Its absence leads to tumor formation. A gene that is responsible for apoptosis. Genes that is responsible for repairing errors in DNA synthesis. Their absence leads to tumor formation.

Examples of Oncogene: RAS Oncogene: Tumour Suppressor Genes: First recognized in retinoblastoma a rare paediatric tumour of the eye.

Text-Book of General Pathology

The RB tumour suppressor gene is a nuclear phosphoprotein that regulates the cell cycle, actitylate hypophosphorylated state in non-dividing cells and inactive hyperphosphorylated state in cell cycle.

Several cancers have mutations in the RB pathway. These are viruses containing viral oncogenes i. Viral oncogene may be inserted in the human genome near a human oncogenes it amplify them and make them over expressed, example of oncogenic viruses: Causing lymphoma and leukaemia in adults.

Causing benign squamous cell papillomas of the skin, and carcinoma of the cervix. Causing Burkett's lymphoma, Hodgkin disease and nasopharyngeal carcinoma. Infection is associated with liver cancer.

Cancer syndromes inherited as Mendelian patterns include familial retinoblastoma, familial adenomatous polyps of the colon, Neurofibromatosis types I and II while breast, ovarian, and colon cancer are none Mendelian inherited cancer. Carcinogenic agents are substance that has a role in tumour formation, and can be classified into 5-Chemical Carcinogens - Alkylating Agents: They are anticancer drugs like Cyclo- phosphamide, chlorambucil, busulfan, and melphalan in spite of that, they may produce cancers.

Related to gastric carcinoma. This are not chemical substances can be found naturally, like aflatoxin in ground-nuts that results hepatatic carcinoma. Asbestos which causes bronchogenic carcinomas, mesothelioma , Arsenic associated with skin cancer. UV light is a cause of skin cancer s; ionizing radiations, X-rays, atomic radiation, and atomic bomb have produced a variety of malignancies, especially leukaemia, lymphoma, in Hiroshima, Nagasaki, and in Chernobyl village in Russia.

These are potentially malignant lesions found in tissues and after a period of time they may transform into malignancy e. May transform into hepatic carcinoma. May transform into colonic carcinoma. Transforms into squamous cell carcinoma.

Dysplasia Disordered Growth This is an irreversible premalignant change affecting a focal area of epithelial tissues without invading the basement membrane, and represents a state between hyperplasia and carcinoma in situ preinvasive neoplasia. Most of the cases are on top of metaplastic changes from continuous stimuli, e. Dysplasia does not necessarily progress to cancer in all cases. Dysplasia Figure Invasive carcinoma Grades of Dysplasia: Affecting one layer of tissue.

More than one layer is affected. All layers are affected without breaching the basement membrane and also known as carcinoma in situ or preinvasive neoplasia. If the basement membrane is breached, this is known as invasive carcinoma.

Invasion and Metastasis of Cancer Metastasis: Means secondary spread of cancer in a remote area, for example, breast carcinoma metastasizes to the lung, liver , and bone marrow. Means local spread when it breaches the basement membrane and invade the neighboring tissue, local invasion occurs through a four-step process that includes: This occur s due to loss of the intercellular glue substance E.

The E. Attachments of malignant cell to collagen and loss cellular junction - Degradation of the Extra Cellular Matrix: Tumour cells then secrete proteases which cause degradation of the E.

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M and type IV collagenase. B Protease inhibitors thus can be used as therapeutic agents to treat tumours. Movements of malignant cell from its site, this step occur sunder the effect of certain chemotactic factors, e. Distant Spread Metastasis: It is the presence of a tumour cell away from its primary original site, without continuity with it.

Distant spread can occur by: The most important step in metastasis is angiogenesis new vessel formation in primary tumour site, then local invasion of the blood vessel with intravasation and transport through the circulation and arrested in micro-vessel in liver, lung or bones, followed by extravasations of cells from the vessels and forming of micro-metastasis, then proliferate to form macrometastasis tumors.

Steps of cancer metastasis Routes of Spread of Cancer: This includes the following ways intracavitary spread through cavities, such as the peritoneum, pleura, etc, for example, gastric carcinoma metastasize through the peritoneal cavity to ovaries called Krukenberg's tumour, lymphatic spread via the lymphatic vessels , haematogenous spread: Krukenberg's tumour Stages of Cancer: Generally speaking tumors can be sub divided clinically into stage I-IV depending on the degree of metastasis and size of the tumor.

Stage I: Tumor confined to the site of origin Stage II: Cancer has spread to regional structures neighboring tissues invasion of adjacent structures. Stage IV: Cancer has spread to distant sites. Also, there is another system for staging called the TNM system: Includes, T0, T1, T2,and T3. Node Involvement: No involvement N0, involvement N1 Extent of Spread: No metastasis M0.

Metastasis M The Stage may influence choice of management, i. Grading of Cancer: This is microscopic sub-categorization of tumours depends only on cytological and histological findings which affects prognosis and method of management of some tumours.

There are three methods of grading as shown in the table below, depending on the degree of resemblance to the original tissue differentiation. As discussed above some factors cause a cell to be transformed into a neoplastic cell that is not controlled by normal body processes Probably most severely transformed cells die because they are too abnormal to function or they are abnormal enough for the body's immune system to destroy them.

However, if the factors promoting neoplasia persist, a transformed cell may sometimes give rise to a clone that does continue to grow. There are "pre-cancerous" conditions in which malignant neoplasia is more likely to occur but not in every case: In these cases, there is ongoing cellular proliferation for repair of damaged tissue, often from ongoing inflammation, abnormal cell proliferation leads to a greater likelihood for mutations to occur.

Transformation Concept of Progression and Heterogeneity of Tumors: Progression of cancer means gradual acquisition of fully neoplastic characteristics, i. Finally full malignant neoplasia.

Progression is not necessarily accompanied by increase tumor size. The concept of "tumor progression" holds that subclones may arise over time from the original malignant clone, these subclones may differ from the original clone in specific characteristics such as invasiveness, metastatic potentiality, and response to therapy.

The sub-clones may arise from acquisition of additional mutations and genes. Showed different abilities of different cell in one tumor As progression of tumor take place, different cell in the tumor developed different hallmarks e.

Especially in tumors infiltrating nearby organs, for example pancreatic carcinoma infiltrating bile duct resulting in obstructive jaundice. Commonly occur s in colonic, gastric, and renal cell carcinomas - Infection: Often due to luminal obstruction like pneumonia, urinary tract infection In carcinoma of the ovary, bladder, and colon all of them may ruptured.

Systemic Effects: Due to malnutrition, chronic bleeding, cytotoxic drugs and bone marrow involvement. Diagnosis of Neoplasia - Clinical Diagnosis: Depends on symptoms and signs of neoplasia, loss of weight, anemia…etc.

Measuring tumor marker may help in diagnosis, follow up and to predict the prognosis. They are proteins produced by the neoplastic cells, for example prostate specific antigen in prostatic neoplasm, alkaline phosphates in bone tumors. Fine needle aspiration for cytology especially in breast neoplasm or fluid cytology from ascetic aspiration or pleural fluid, looking for the cytological features of cancers in smears.

The usual sources of water intake are ingested liquids, foods fruits and vegetables and endogenous metabolic water production. The sources of water output comprise: Osmolality and Tonicity: The total solute concentration tonicity of body fluids is maintained constant, osmolality is defined by the ratio of total body solute in total body water, and it is regulated at — m.

Body Water Distribution: The proportion of intracellular water to extra cellular water is 2: The proportion of interstitial to intracellular water is 3: Table These are separated from plasma by an additional epithelial layer. Assessment of Extra-cellular Fluid: Extracellular fluid volume status can be assessed clinically by measuring the level of consciousness, the presence of thirst, moistness of mucosal surfaces, skin turgor, heart rate, blood pressure, and urine output.

Mechanisms of Water Homeostasis: Water is regulated by an interaction between osmoreceptors and volume receptors in carotid body and hypothalamus , ADH or vasopressin , and the kidney.

The mechanisms contributing to water balance can be outlined as mechanisms involving: Urine concentrating mechanism - Osmoreceptors: Activated by pain, stress, volume, and thirst sensors. Further reabsorption occur s in the descending limb of the loop of Henle, and in the collecting ducts, due to the action of Arginine Vasopressin which is also named anti-diuretic hormones ADH. Antidiuretic hormone is stimulated by the following mechanism: Increased plasma tonicity or osmolarity detected by hypothalamic osmoreceptors stimulate ADH secretion.

Reduced plasma volume can be detected by cardiovascular volume receptors stimulate ADH secretion. Fall in arterial blood Pressure detected by cardiovascular baroreceptor s stimulate ADH secretion. Adrenaline, angiotensin II, hypothyroidism, hypoadrenalism. Nicotine barbiturates, vincristine -Miscellaneous: Nausea and vomiting, hypoglycemia, stress, and heat, stimulate ADH secretion.

ADH inhibition involves mechanisms which are the vice versa of the above mention i. Association between osmolality and ADH releases. Water Loss Dehydration In dehydration, fluids from the blood and the space between the cells together called extracellular space are lost first, followed by loss of fluid from the cells intracellular space , dehydration can be categorized into isotonic, hyper tonic and hypotonic type, depending on how it affects the tonicity of the extracellular fluids, when dehydration does not affect the concentration of sodium in the extracellular fluid, it is called isonatremic dehydration also named isotonic or iso-osmolar dehydration, however when dehydration results in an increased sodium concentration of the extracellular fluid, called hypernatremic dehydration also named hyper tonic or hyperosmolar dehydration.

If you ask why is it important to know the dehydration types iso-, hyper -, or hypotonic , the answer because this can suggest the etiology of dehydration and the way of management. Excess of Water Over Hydration: In this condition the amount of water in the body is increased, there are two types of over -hydration, increased water intake or retaining water in the body, drinking more water than the kidneys can get rid of causes too much water to collect in the body.

Retaining water happens with several medical conditions associated with inappropriate ADH secretion. When too much water is collected in the body, it can lead to water intoxication or low levels of sodium in the blood hyponatremia and this can be dangerous and fatal.

Physiological Role of Sodium: Role of sodium is to maintain the followings - Osmolality: Sodium maintains plasma and extracellular fluid osmolality by being the principal osmotically active solute. Increases or decreases in total body sodium, lead to increase or decrease in the extracellular fluid and plasma volume. Sodium has an essential role in transmembrane potential differences that are responsible for excitability in nerve, and muscle fibres.

Rates of sodium transport potentially affect a variety of metabolic pathways because Na-KATPase is a major gate in the cells. Sodium balance is maintained by a variety of mechanisms outlined below, generally speaking sodium is regulated by water and water is regulated by sodium, both processes, maintain a constant osmolality m.

Abnormalities in serum sodium levels need to be interpreted in relation to the extracellular fluid volume status. This is done by sensor s for osmolalaity, pressure, and volume, distributed in the following organs: This an important mechanism for regulating sodium, that starts in the proximal tubule where e.

Role of aldestrone in sodium and potassium metabolism Disorders of Sodium - Hyponatremia a dilutional state due to too much water , results in low plasma sodium.

Signs of hyponatremia The cause of a low level of sodium can be broken down into the following types: Sample errors accompanied by normal osmolality of the extracellular fluid caused by severe hyperproteinaemia, hypertriglyceridaemia and sample taken from a vein just after IV fluid. True Hyponatraemia: Plasma sodium is low, and can be classified according to the extracellular fluid volume into the following causes. Which is due to a dispropor tionately greater reduction in total body sodium than in total body water , and is accompanied by features of extracellular fluid depletion, this can be due to renal losses from diuretics, gastrointestinal losses, skin losses, and intraperitoneal losses.

Which is associated with increased body water and normal total body sodium this can be due to arginine vasopressin excess or a reset osmostat. Which is associated with a disproportionately greater reduction in total body water than in total body sodium, and is accompanied by features of expanded extracellular fluid volume.

Oedematous states responsible may be due to congestive heart failure, cirrhosis of the liver , nephrotic syndrome or renal failure. Which is secondary to water shifts from the intracellular to the extracellular compartment, and associated with normal total body water and total body sodium. The extracellular fluid osmolality and tonicity are high, This can be associated with severe hyperglycemia.

It is associated with the following pathophysiological mechanisms: Which is due to a total body water deficit that is dispropor tionately greater than total body sodium deficit, this is associated with renal losses e.

Which is due to an increase in total body sodium that is disproportionately greater than the increase in total body water , this is either iatrogenic caused by hyper tonic saline, or associated with primary hyperaldosteronism. This is caused by either renalwater losses diabetes insipidus or increased insensible water losses, and is associated with a normal total body sodium content.

Potassium Metabolism Potassium is the major cation in the intracellular fluid, the serum level ranges between 3. Functions of Potassium: Generation of transmembrane potentials, thereby affecting the electrical excitability of tissues, a cofactor in enzymatic reactions, responsible for normal cell volume by being the predominant intracellular solute, maintenance of cell polarity, maintenance of acid—base balance, Potassium Balance: Potassium homeostasis is maintained by a balance between intake, excretion, and distribution between the compartments, ninety per cent of the total body potassium is available for exchange, allowing for major shifts between body compartments.

Factors Stimulating Intracellular Movements of Potassium: Alkalosis, mainly metabolic type, insulin, beta-adrenergic agonists catecholamines , high extracellular potassium concentration, hyperosmolarity of the extracellular fluid. Factors Stimulating Potassium Exit from Cells: Acidosis, mainly respiratory type, low osmolarity of the extracellular fluid, glucagon, beta- adrenergic blockade, alpha-adrenergic agonists catecholamines , cell injury.

Renal Control of Potassium: Serum potassium is normally maintained between 3. This process, in the kidney depends on the net effect of the following factors: Renal secretion of potassium depends on Na-K-pump, and H-K pump in the tubule under the effect of reninin-angiotensin system.

Reduction of serum potassium less than 3. True Hypokalaemia: Types and causes of hyperkalemia include the followings o Pseudo-Hyperkalemia: Improper blood collect ion with haemolysis; marked leukocytosis; marked thrombocytosis due to exit from the cells.

Reduced excretion in acute renal failure; potassium-sparing diuretics, increased supplements intake or release of pota sium in ; rhabdomyolysis, hemolytic states, extracellular shifts of pota sium in acidosis; beta blocker s, cell destruction tumor lysis.

Mechanisms of Heamostasis - Intact Blood Vessel: Intact blood vessels prevents both bleeding and thrombosis at the same time through a negative charge of the endothelium, which repels negatively charged platelets, and vasoconstriction of blood vessels when injured to prevent bleedings.

Thus any reduction in the number or abnormality in function results in bleeding. These are circulating proteins in an inactive form, but when trauma occurs will be activated in a cascade manner each one activate the other factor I to factor XIII, there are three pathways for activation, starting in an intrinsic or extrinsic way ending with common pathway.

General Pathology for Veterinary Nurses

Fibrinolytic factor s are proteins that prevent propagation of thrombus formation localizations of thrombus in one site. Plasminogen is the main fibrinolytic factor. The absence of these factor s results in excessive thrombosis. Like Protein S, C, antithrombin III, which inactivate active coagulation factor, so prevent further thrombosis, lack of these inhibitor s result in thrombosis.

Thrombus is a coagulated solid mass composed of blood constituents platelets, fibrin, WBS and RBCs which develops in an artery, vein or capillary or heart champers.

Pathogenesis of thrombosis: A- Damage to the endothelial lining of a blood vessel. B- Abnormal blood flow Stasis or turbulence. C- Increased coagulablity of blood, i. Virchow triads of thrombosis Endothelial Injuries and Thrombosis: There are two main reasons for thrombosis in cases of endothelial injury. Binding of platelets to th ese surfaces, mediated by a Von Willebrand factor , leads to formation of platelet aggregates and initiates the formation of thrombi.

Causes of Endothelial injury Cell Associated with Thrombosis - Hemodynamic injury in high blood pressure. Varicose Veins: Associated with deep vein thrombosis. Prolonged Immobility: Lying in bed or sitting long times e. Tissue Damage: Conditions that cause massive tissue destruction, such as crush trauma, burns or surgery are commonly complicated by thrombosis.

Pregnancy and Obstetrical Complications: Generally speaking, pregnancy, forceps delivery and pelvic manipulation predisposes to thrombosis, also oral contraceptives and steroid hormones increase the risk of thrombosis. Circulatory Disturbances: Major circulatory disturbances such as myocardial infarction and stroke, are important risk factor s.

Thrombosis in tumours is related to the release of thromboplastin, which promotes coagulation. Macroscopic Features of Thrombi: Large thrombi formed in the veins, arteries, and heart of a living person has typical macroscopical features that distinguish them from postmortem clots which includes the followings: Thrombi formed by the deposition of platelets and fibrin, which forms a white layer , then RBCs deposit on it forming a red layer on which a new layer of fibrin and platelets is deposited, these alternating white and red lines are called lines of Zhan.

Thrombi are held together with fibrin that does not permeate all layers uniformly but leaves cleavage lines between the white and red layers. Most thrombi will crumble along cleavage lines when bent or compressed with the finger.

The friability of thrombi accounts for the fact that they may detach and embolize. Thrombi are attached to the surface of the vessel or heart chamber in which they are formed. At autopsy, such veins appear completely filled and widened Postmortem Clots Appearance: Postmortem clots are formed from blood that does not circulate, owing to the forces of gravity RBCs sediment and are separated from plasma.

Such clots do not fill or expand the blood vessels in which they are found. Postmortem thrombi can be easily removed from the blood vessels at autopsy. Comparison, thrombus and clot features Thrombus Clot Occurrence During life After death Morphology White and red layer, Lines Red currant jelly, and yellow of Zhan are formed chicken appearance Texture Friable fragments Pliable no fragment Ability of moldings Moldings' taking the shape No molding of the vessel Attachment Attached to the wall Not attached to the wall Arterial Thrombosis: Common sites are coronary, cerebral, mesenteric, and renal artery Clinical Features: The main clinical feature is due to obstruction of blood supply resulting in infarction according to the location, e.

Venous Thrombosis: It is the most common form of clinically diagnosed thrombosis.The effects of inflammation can be both local and systemic. Cells in the chronic inflammatory process tend to produce substances that add new tissue, such as collagen and new blood vessels, many of these changes also represent the repair process, and there is a blurry continuum between chronic inflammation and the whole repair process.

Bilirubin formed from biliverdin will give it a yellowish colour. Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury. Sub-cellular Alteration in Irreversible Cell Injury Effects of injurious agents on organelles and cellular components varies, some forms of cell injury affect particular organelles and have unique manifestations, e. Razan Ali rated it liked it Nov 16, Swelling is a sign of inflammation which may result in obstruction of lumen as in acute laryngitis, or increase intracranial pressure in encephalitis and ischemic injury if obstruction of blood supply take place.

For example, benign tumours of fibrous tissues are called fibroma, while of cartilages named chondroma, moreover from glands are named adenoma, and from bone are named osteoma, papilloma a name given for tumors arising from surface epithelium like skin or gastrointestinal surfaces.

Payment Methods accepted by seller. Comparison Between Acute and Chronic Inflammation: