yazik.info Programming Netters Illustrated Human Pathology Pdf


Friday, August 30, 2019

Netter's Illustrated Human Pathology 2E (1) - Ebook download as PDF File .pdf), Text File .txt) or read book online. netters path. Netter's Illustrated Human Pathology Updated Edition: with Student Consult Netter's Gastroenterology 2nd Edition PDF Gastroenterology, Science Books. Netter's illustrated human pathology. Material. Type. Book. Language English. Title. Netter's illustrated human pathology. Author(S). L. Maximilian Buja (Author) .

Netters Illustrated Human Pathology Pdf

Language:English, Spanish, Japanese
Published (Last):30.09.2015
ePub File Size:20.54 MB
PDF File Size:17.68 MB
Distribution:Free* [*Register to download]
Uploaded by: JOLINE

In this article, we are sharing with our audience the genuine PDF download of Netter's Illustrated Human Pathology Updated Edition PDF using. International Society of. Neuropathology, pages. This is another addition Netter's Illustrated. Human Pathology. L. Maximilian Buja and Gerhard R. F. It is always fun to look at Netter drawings. Those of us who first encountered them in medical school were convinced they enhanced our.

This can be seen in type reaction Table The contact brought about by direct action of cytotoxic T lymphocytes on the allergy—type reaction with production of vasoproliferative factors cellular antigen. Basophil reactions are immune reaction. Basophil reaction of skin following recluse spider bites left.

T Cell T-cell immune reactions are divided into the lymphocytotoxic activation of phagocytes with typical tissue reactions in certain reaction classic type IV reaction or tuberculin-type cellular infectious diseases such as tuberculosis.

Granulomatous and other cytokines is caused by antigens such as heavy metals. Eczematous skin reaction. Granulomatous pneumonitis showing gross left and microscopic right features of pulmonary tuberculosis. The lymphocytotoxic reaction is certain arthropod reactions. Neural hyperplasia traumatic neuroma. There are at least 2 identified increased functional requirement. Follicular hyperplasia in lymph node with prominent germinal centers arrow. When hyperplasia becomes out of balance with vascular- compensate for the increased burden.

Intestinal glandular hyperplasia in columnar cells of polyp. Positive effects of hyperplasia deficiency or both by hypertrophy remains limited. Compensation for structural or functional after trauma traumatic neuroma.

Hyperplasia compen- in cell mass without cell division i. Hypertrophy is an increase functionally or structurally damaged area. It tissues. Examples are hyperplastic stimuli for hypertrophy: Regeneration may be complete with restitution of normal is initiated by growth factors produced by cells adjacent to the structure and function or incomplete. Benign neoplasias tumors. Typical dysplastic of physiologic apoptosis.

Left Corpus uteri showing multiple benign fibroleiomyomas. They are characterized by figure. Cellular atypia indicating malignant tumors are often designated by their tissue of origin with the affix potential is characterized by nuclear enlargement with hyper. Benign cellular polarity. Right Extensive metastases in liver of testicular tumor seminoma.

B epithelia from area of dysplasia. C epithelia with atypia indicative of carcinoma in situ D not yet invasive. It leads to tumorous growth patterns changes can be observed in proliferating mucosa of intestinal independent of or at the expense of surrounding cells and tissues.

Intestinal adenoma with focal atypia arrow in large intestine. Atypia refers to cellular changes. Middle Atypical glands arrow invading mucosa of gastric antrum. Dysplasia describes an ologic growth regulation with persistent activity of growth- abnormal structural regeneration that may become malignant. Tumors of mesenchymal origin by cellular atypia. Malignancy is morphologically defined epithelial origin are carcinomas.

Adenocarcinoma of colon. Malignant tumors of cachexia and infections. There are exceptions to this tion and staging. The degree prognosis. Rhabdomyosarcoma of foot. Classification hemolymphatic malignancies and astrocytoma. Most patients have primary or essential Progression of disease leads to luminal narrowing and the HTN due to a complex of genetic and environmental influ- development of complicated lesions as a result of surface ences.

The plaques involve the aorta and its ma. Myocardial infarcts undergo septal defect [ASD]. The more acute myocardial infarcts. Slowly thrombosis. Larger healed infarcts can develop into ventricular aneurysms. A massive acute myocar- macrophages and T lymphocytes. In spite of significant advances in predisposing to gangrene of the lower extremities.

They usually platelet aggregation and vasospasm can precipitate myocar- arise from randomly occurring defects in embryogenesis. The 3 the occluded coronary artery. Sudden luminal occlusion due to thrombosis of an tions.

As myocardium is lost from one or protein. Acute changes in plaques associated with the cardiovascular system in the early fetus. Myocardial necrosis begins in major pathophysiologic categories of congenital heart dis. The pathogenesis tion. Medial degenerative disease. RHD involving a tricuspid valve. The condition may der involving the skin. Aortic valvular pleural and pericardial effusions.

Granulomatous inflammation dissecting aneurysms of the ascending thoracic aorta. Viral infections are associated with verse or descending thoracic aorta type B. Pericardial involvement is often manifest as or as a result of hemodynamic stress accelerated by HTN. Hy- pharyngitis. Key clinical features of IE are fever and stroke.

Infections of a logically. Pulmonary and tricuspid valvular disease is pro- parenchymal disease. Failure of the right ventricle RV leads to sis and calcification of a tricuspid valve.

Cor pulmonale refers to isolated right IE. Myocar- Medial degeneration develops as a result of a genetic de. Most of the inflammation resolves without con. Most cases begin as fail. Both dissecting and nondissecting aneurysms are prone to Cardiomyopathies are diseases of the heart muscle.

Mitral valve incompetence regurgitation results tricular hypertrophy. Cardiovascular syphilis is a form of tertiary syphilis as a component of a defined disease process usually origi- with ascending aortic aneurysm.

Restrictive cardiomyopathy typically has a relatively matic heart disease RHD. Bacterial infections produce neutrophil-rich suppu- origin in the ascending thoracic aorta type A or the trans. In both acute and subacute IE. Mitral valve stenosis is virtually always due pensation to an increased stress is accomplished by ven. Etio- external rupture leading to exsanguination. Acute IE is produced by highly viru- microvascular damage in the form of hyperplastic arteriolo.

Aortic valvular stenosis results from chronic ure of the LV as manifest by fatigue and progressive pulmo. The most common primary tumor of the heart in most common primary tumor of the heart in infants and chil- adults is the myxoma. The in the myocardium as well as ventricular cavity obstruction. Obstruction of the Circulation Without Shunt Coarctation of the aorta. Most VSDs result from leading to late onset of cyanosis Eisenmenger syndrome. Membranous Type Congenital heart disease results from malformations of the heart although some are located in the muscular interventricular and major vessels that develop during embryogenesis and are septum.

The surgically corrected. A general classification of congenital malforma. If not tions of the heart and major vessels is presented in Table As a result of the left-to-right shunt. Some of these anomalies produce PDA is another type of high-pressure left-to-right shunt producing vascular rings that can compress the trachea and esophagus. Other anomalies of Failure of this connection to close results in PDA. Because left-to-right shunting occurs at low tissue.

This ASD occurs as a result of formation of the septum primum and septum secundum results in defective formation of septum primum and septum secundum a common atrium.

Failure of the region of the foramen ovale. Cleft anterior mitral cusp Cleft medial septal tricuspid cusp L. The VSD component is in the atrioventricular canal. The ASD closed membranous interventricular septum. The complete component is low in the interatrial septum because of failure of endocardial-cushion defect. The partial membranous VSD. Com- defects. Depending on the severity of the overrides the VSD. Transposition of truncal swellings becomes involved in partitioning the truncus.

The lower diagram shows the tally complete transposition of the great vessels. In transposition. Next to transposition of The postductal type of coarctation leads to the anomaly. There are 2 major types: Postductal type Preductal type demonstrating erosion of costal Adult Infant. The patient presents with HTN in the resulting in clinical problems in early childhood. Less severe congenital aortic tion.

The congenital of the LV and ascending aorta. There is a dense. LVOT obstruction leads to underdevelopment hypoplasia stenoses are compatible with longer survival. In severe congential aortic malforma. This constellation of anomalies constitutes the because of hemodynamic turbulence that leads to fibrosis and hypoplastic left heart syndrome.

The ductus population and can give rise to aortic stenosis in adulthood arteriosus is open. The photomi- arteriosclerosis. The fatty streak is the most The lesion of established fibrous capsule and lipid-rich core containing foam cells and atherosclerosis is the atherosclerotic fibrous or atheromatous cholesterol crystals. Atherosclerosis progresses asymptomatically for years visceral arteries. Genetic ment of atherosclerosis are a diet high in saturated fats and susceptibility.

According to the response to until a clinical threshold is reached. The onset of symptoms may injury hypothesis. The major treatable risk factors for develop- vessel wall to multifactorial and repetitive injury.

Most symptomatic disease is associated with the Coronary atherosclerosis leads to progressive lumen. Nonatheromatous causes of myocardial ischemia include luminal narrowing of one or more of the coronary arteries by congenital coronary anomaly.

Subendocardial intramural myocardial With right bundle branch block Acute anteroseptal. Transmural duration approximately 15 minutes. Lesions myocardial injury. Myocardial necrosis generally begins after 45 minutes of coronary artery give rise to inferior posteroapical and posterior severe ischemia and extends from the subendocardium into the myocardial infarcts.

With resorption of muscle thin wall and mural thrombi. Myocardial infarction. Complicated by right bundle branch block. Seen in longitudinal section of heart Thrombi Infarct Acute posterior subendocardial infarct. Lesions of the left circumflex coronary artery subepicardium in a wave-front fashion over a period of approxi.

This illustration shows various failure or ventricular fibrillation. If the patient survives. Mural thrombi can form over the infarct and give rise to granulation tissue. Seen in coronal section of heart Ventricular septum Healed anterolateral Area of infarct. In hypertrophied infarct and dilated heart secondary to hypertension: Right ventricular hypertrophy indicative of heart failure Area of infarct recent Healed posterior infarct.

During healing. During the first 2 to 3 thinned infarcted wall may expand to form a ventricular aneu- weeks. These cardiac tamponade. Over that. These ruptures output. Other severe time. This is generally fatal. In some cases. With rupture of left ventricle. Patients at highest risk are those reaction to occur and seal off a region of pericardium.

This gives rise to a wide-mouthed pseudoaneurysm in regions without fibrosis. Endocrine output. The pathophysiologic basis of HTN is excessive arteriolar is secondary to a recognizable lesion or disease. HTN disease. Parenchymal constriction leading to increased peripheral vascular resistance. The fundamental etiology of HTN is unknown in most disorders and coarctation of the aorta are less common.

This condition is known as essential.

In severe malignant HTN. An associated nant HTN. Malignant HTN is characterized by arteriolosclerosis. Benign amorphous eosinophilic material composed of degenerated HTN is characterized by mild to moderate increase of blood smooth cells and deposited plasma proteins.

Cut surface Hyalinization of an afferent arteriole. The characteristic vascular lesion of benign essential ischemic injury develops rapidly. G Necrosis of a glomerulus G and of an afferent arteriole A A Kidney in malignant phase of essential hypertension. Typically found in essential hypertension Malignant phase of essential hypertension.

Hyaline arteriolo- pressure and an asymptomatic period of several years before the sclerosis with associated small cortical scars hyaline arteriolone- inevitable onset of symptoms and end-organ damage hence.

A A In arteriolosclerosis of essential hypertension Granular arteriolosclerotic kidney. Hyperplastic condition is not truly benign.

Cardiac hypertrophy is an by a thick wall and a relatively small chamber volume. When the limits of compensation are hypertrophy. May or may not be present tall R waves in V4. In hypertension without cardiac failure Left Ventricle Thickened muscle wall Cardiac hypertrophy. The cardiac death. With greatly hypertrophied L. Concentric Hypertrophy Hypertension. The reached. In chronic hypertension x-ray evidence may be minimal Cross section of heart.

Most com. Cardiac condition is termed congestive heart failure CHF. Because the dominant symptoms left. The failure may be left-sided. Vacuolation of cardiac thiamine administration Tachycardia. This illustration shows the major usually result from pulmonary or systemic venous congestion. In response to impaired left ventricular output. The subsequent increased glomerular vascular peritubular capillaries. The sodium and water retention contribute resistance produces increases in filtration fraction and colloid to the development of edema associated with CHF.

Right and left ventricle in left ventricular failure due to hypertension. When the heart reaches a critical weight of atrial fibrillation and formation of mural thrombi. Stress of the atria can result in tory hypertrophy. Following atrial fibrillation in hypertension Infarct Left ventricle X-ray: Cardiac enlargement and Right right pleural effusion ventricle Hypertrophy. In response to load on the heart can produce failure and cardiac dilatation chronic stress.

Heart failure results in progressive ventricular dilatation of the hypertrophied LV. A severe acute or primarily. Hypertrophy and dilatation of L. Because of the dual disease.

Without infarction. Acute Cor Pulmonale Cor pulmonale. Acute strain on the right heart is produced by a massive circulation from the pulmonary arteries and bronchial arteries. A thromboembolus of sufficient magnitude may infarcts.

A thromboembolus usually circulation. Pulmonary infarcts do occur in the presence of thrombo- cause sudden death because the obstruction of the pulmonary emboli and impaired systemic circulation associated with vasculature produces pulmonary HTN and acute right-sided heart preexistent CHF.

In leads V1 and V2 as well as S. With great distention of pulmonary trunk and Aorta main pulmonary arteries. Chronic obstructive emphysema with cor pulmonale Hypertrophy and dilatation of R. Prominent P waves in leads II. The heart exhibits significant hypertrophy and recurring pulmonary thromboembolic disease or chronic dilatation of the RV with a normal-sized LV unless the patient pulmonary parenchymal diseases.

Chronic Cor Pulmonale Chronic cor pulmonale typically develops in response to and emphysema. Lower abdominal aorta Lower abdominal aorta. The cavity of the atheroscle- that accompanies the severe atherosclerosis. The frequent occurrence of abdominal aortitis.

Netter’s Illustrated Human Pathology

Less frequently. Lower abdominal aorta the renal arteries and the bifurcation Severe atherosclerosis. Atherosclerotic aneurysms of atherosclerotic aortic aneurysms is due to the medial weakening the iliofemoral arteries also occur.

Aortic root external rupture and life-threatening exsanguinations. In the aorta between Aneurysm. Severe disease gives rise exsanguination. Frequently associated with cystic medial necrosis Dilation of ascending aorta and aortic ring.

The lesions. Myxomatous degeneration of the mitral valve typically develops. With a dilated annulus and incompetent orfice Dilated ascending aorta Prolapsed leaflets of mitral value Marfan syndrome. The weakened and dilated aorta is prone to medial connective tissue.

Severe cystic medial on the LV. In develop distal tears and become chronic with the potential for most cases. Some dissections aneurysm. In type A dissections. Blood pressure control is key in the treatment of any lumen under systemic pressure. The hematoma dissects longitudinally to split the are prone to external rupture into the mediastinum or pericardial media.

Type A dissections. RF generally affects involvement manifests as spontaneous uncoordinated movements children between the ages of 5 and 15 years. Stained with Human heart muscle.

Rheumatic fever 10 to 14 days later much longer gap for chorea Skin Nervous system Streptococcal chorea throat infection DAYS 1 5 10 15 20 25 30 35 40 45 50 Malaise Temp. Ten to 14 days after of the extremities Sydenham chorea. Rheumatic vegetations on mitral valve Characteristic distribution of myocardial Well-developed Aschoff body. The connective tissue accompanied by inflammatory cellular cardiac valvular lesions consist of small. The cardiac inflamma- pancarditis composed of fibrinous pericarditis.

RHD is produced by inflammation of all components of the heart particularly the mitral and aortic valves. In interstitial tissue between the variety of cells. Swelling along line of fascicles of muscle Aschoff cells closure of the valve cusp represents healing of vegetative material.

Acute thrombi verrucae along the line of closure of the valves. Composed of Photomicrograph of mitral valve in acute Aschoff bodies. These dium. A vicious process of organization and healing.

The organization and healing of the inflammation. Fusion of right cusp and posterior cusp. Some fusion of chordae tendineae Mitral and thickening of cusps at contact areas.

The inflammation of the cycle of increased hemodynamic turbulence and wear and tear cardiac valves elicits a granulation tissue response with ingrowth ensues. Anterior cusp has typical convexity. This murmur at the cardiac apex. With some thickening of wall resulting from mitral stenosis.

In rheumatic mitral stenosis.

Viewed from below and left: Increased pulmonary venous produced by obstruction of the orifice and regurgitation of blood pressure. On both surfaces of mitral Heart valve. This valvular pathology is Healing of the inflammation leads to progressive valvular histiocytic myocarditis. In an area of segmental necrosis of blood vessel demonstrated by immunofluorescence Interstitial edema. The process interstitial myocarditis and progressive myocardial fibrosis.

After acute illness. The valvular lesions also The valvular lesions can be clinically silent or can result of mild inflammation and associated surface endothelial give rise to serious symptoms due to embolization of the vegeta- damage.

The lesions are frequently associated with disseminated tions. Predisposing illnesses are those that along the line of closure of the valvular leaflets Lambl initiate a systemic reaction. Sometimes there is no obvious site of infection. The bacteria or other aureus. Some absence of systemic conditions in the host chronic alcoholism. Whether IE follows an acute On bicuspid aortic valve Aortic valve Vegetations Vegetations Mitral valve Early vegetations of Left bacterial endocarditis. Early Lesions Infective endocarditis generally involves the cardiac valves.

These thrombi. The toxic products of the bacteria etc. Development of vegetations. The surface thrombi generalized inflammatory reaction to a bacteremia or fungemia grow to become vegetations.

Containing clumps of Deposit of platelets and organisms stained dark. As part of a incites an accelerated inflammatory reaction. Advanced Lesions Progression of the inflammation can lead to the perforation of a which leads to progressive valvular incompetence and cardiac valve leaflet or it can spread onto the chordae tendineae.

A major goal of clinical management is to make the to chordal rupture. The inflammation may also invade the diagnosis and institute high-dose intravenous antibiotic therapy to valvular annulus.

Vegetations extending onto On underaspect as well as on atrial chordae tendineae with rupture surface of mitral valve of two chordae. Vegetations of bacterial endocarditis. The patient may present with severe left-to-right shunting. Multiple pulmonary infarcts. Infection of the right-sided cardiac valves is pneumonia due to seeding of the lungs with infected vegetations.

Small thromboemboli lead to petechial hemorrhages in the highly virulent organisms. Remote Embolic Effects Embolization of infected vegetations is a serious complication of produces infarcts of the tissue supplied by an end artery.

Infected emboli to one or more coronary result from inflammatory damage to the vessel wall.

Intraluminal obstruction myocardial abscesses. Larger infected thomboemboli. In vessel of ocular Infarct of brain with secondary hemorrhage from fundus arrow with embolism to right anterior cerebral artery. With IE. Cardiac involvement. Revealing multiple intramural and subepicardial abscesses with pericarditis Muscular wall of ventricle Mastoiditis Tonsillitis. Systemic give rise to bacteremia or fungemia. Hand infection Central mass of bacteria surrounded by leukocytes.

The heart may also be involved with various protozoal valvular involvement. Pericardial involvement consists of a fibrinous cytes and by variable amounts of myocardial necrosis.

The exudate often accompanied by a serous effusion. The type of extent of inflammatory cellular infiltrate exceeds the amount of inflammatory cellular infiltrate provides information about the necrosis. Diffuse cellular infiltration of bundle of His Diffuse and patchy interstitial edema. Atrial or ventricular mural thrombi or both may disease not originating in the myocardium or systemic disease form as a result of poor contractile function.

The likely causes for development of cardiomegaly. Little or no fibrosis of endocardium. The myocardium with cardiac involvement.

Dilated congestive cardiomyopathy. IHSS is characterized motion of the anterior mitral leaflet toward the bulging interven- pathologically by asymmetrical ventricular septal hypertrophy tricular septum. The IHSS the left ventricular free wall. The abnormal condition that produces obstruction of the LVOT at the subvalvu. Myocytes in the affected myocardium myosin. Endomyocardial biopsy is used to distinguish amyloidosis and senile cardiac amyloidosis. Cardiac amyloidosis and severe fibrosis normal-sized heart.

Myocardial degen. Restrictive Cardiomyopathy Cardiac involvement occurs most frequently in primary systemic cardiomyopathy. The the tricuspid valve in a small percentage of cases. Some fusion at each commissure. Significant rheumatic lesions affect mitral. RHD is only one of a tion dominated by incompetence insufficiency.

Aortic valve stenotic and incompetent from fusion of all three Tricuspid commissures. Chronic RHD results in clinically significant pathology which results in incompetence. Patients with valvular are responsible for most valvular heart disease necessitating aortic stenosis experience left ventricular hypertrophy.

Netter’s Illustrated Human Pathology

With tension on chordae tendineae. RHD can produce aortic stenosis. They surgical intervention. In the United States. Some degree tion.

The redundant valve composed of white. A atrium with each systole. The mitral degeneration can give rise to progressive mitral regurgita- prolapse is readily detected by echocardiography.

Progression of the clicks and a short systolic murmur heard at the cardiac apex.

Rupture of a chordae tendineae. The redundant valve prolapses into the left tion and secondary degenerative change of the mitral valve. The lesions are composed of primitive of nondifferentiated small mesenchymal cells in an abundant myocytes spider cells. The rhabdomyomas may occur as part of myxoid stroma. The most be single or multiple and have a subendocardial. It occurs most commonly in the left atrium and the tuberous sclerosis complex. In infants and much less frequently than metastatic tumors of the heart but more children.

These tumors may often than the rare primary sarcomas of the heart. Characteristically originating from interatrial septum and almost filling L. Anterior view left and frontal view right Carcinoma Carcinoma Metastasis of bronchial carcinoma to heart wall Lymphangial spread of metastatic bronchial carcinoma. Tuberculosis produces granulomatous Treatment may involve percutaneous panied by pericardial effusion. T wave inversion in all leads except aVR and V1. Fluid accumulation in the pericardium can result in infections.

Pericardial disease also can result from metastatic of clear fluid with low protein content a transudate. Bacterial infections produce pericardiocentesis or a surgically produced pericardial window.

Viral tumors. In the age of hemodialysis. Severe adhesive pericarditis can produce the clinical relatively common cause of adhesive pericarditis. The lesions can heal with aneurysm delayed cardiac tamponade due to hemopericardium. Gunshot or stab wounds of the chest can hemorrhagic necrosis of the myocardium.

Multiple contusions of heart. All of these lesions can produce acute cardiac the heart muscle known as a cardiac contusion. The lesions show decompensation. Disruption and separation of myocardial fibers. The lesion can be produce lacerations or perforations of various parts of the heart. A decelerative impact With obvious subepicardial force extravasations of blood Contusion Pathogenesis and variable course of cardiac contusion Subendocardial Transmural Subepicardial Cardiac contusion hemorrhage.

Other traumatic lesions include rupture of the life-threatening condition necessitates rapid evacuation of the interventricular septum.

This formation. Chronic forms include such pathogeneti. COPD may terns and are classified as bacterial pneumonias. Most bacterial and viral monary blood flow. They heal with focal or diffuse scarring and potential to expand. It can be caused by a number of different respiratory diseases. In situ COPD follows either increased resistance to airflow e. Pneumocystis carinii tually. Recurrent which must be distinguished from primary lung tumors. Their local ex- cally different entities as idiopathic pulmonary fibroses tension and metastatic spread determine their prognosis.

Only patients in early stages of acute RLD may recover ties of diagnostic pathology and form the basis for determining completely. RLD occurs in acute and alveolar lining cells or as sarcomas.

Although extrapulmonary disorders such as chest abnormali- ties. In addition. Mycobac- terium tuberculosis. Infections of the lung present with different pathologic pat- bronchiectasis. In these As in other organs.

They are classified ac- chronic forms. TLC increased in obstruction but expiratory flow rate decreased. COPD follows increased resistance to airflow by reduced intrapulmonary blood flow. ERV residual vol. L n Normal volume loop. COPD is caused by a number of L Normal Obstruction Maximal expiratory flow-volume curves. Ex breathing shaded areas increased.

RV Lung vol. In severe ction obstruction tidal breathing may coincide with MEFV curve. It is accompanied by repeated muscular hypertrophy. Impaired genetic Pseudomonas invasion ciliary clearance and colonization Genetic defect Mucus Lungs structurally normal at Increased goblet cells Obstruction of small birth but prone to infection in airway epithelium arrow airways by mucus mainly in airways at first with increased submucosal and pus due to unknown genetic defect gland size Infection Group of small airways distended with pus and mucus.

Chronic abscess formation. Mucus inspissation blocks the airways. Although abnormally viscid mucus in all secretory glands. Emphysema is sema expands in interstitial septae after acute overinflation of the classified by anatomical nature and location in the lobule: It may spread to the mediastinum and subcutaneous lungs after inhalation of toxic materials.

Diaphragm not to ribs evident. Patient had chronic CO2 retention. Interstitial emphy- activity e.. The pathogenesis is thought to be an imbalance between emphysema results from enhanced focal destruction of air space increased inflammatory elastolysis and decreased antiprotease walls with confluence of multiple air spaces.

Bilateral giant apical bullae No hyperinflation. Severe coughing with expectoration of a glandular hypertrophy. Status asthmaticus is a severe persistent broncho- their breakdown products Charcot-Leyden crystals. The etiology and pathogenesis is multifactorial metaplasia of bronchial epithelium. It leads to severe mucus clumps Curschmann spirals.

Bronchial lumina are often occluded by characteristic mucoid sputum with masses of eosinophils and mucous plugs. Palmitic Dipalmitoyl paraquat. The morphology is represented by factor leads to a loss of type I alveolar cells and a reactive diffuse alveolar damage DAD.

Glucose Gycerophosphate bodies e. Glucose Other lipids cytotoxic drugs. Progressive fibroblast develops subsequent to diffuse alveolar epithelial and vascular proliferation leads to fibrosis. Other Shock of any cause. The formation of hyaline membranes composed of With Electron eosinophilic hyaline photomicrograph.

The decrease in functioning surfactant genic pulmonary infiltrates. Pathology of hyaline membrane disease Atelectasis. Alveolar and interstitial edema proliferation of type II alveolar cells. Alveolar cell diverse and often cannot be identified from the morphologic necrosis may occur with focal hemorrhage and capillary micro. High-power section inset above shows macrophages with vacuolated cytoplasm filling alveolar space. Extensive subpleural and interalveolar fibrosis. Intense fibrosis and bullous arrow throughout both lungs.

Small nodular and miliary densities Chronic bagassosis. Alveolar walls thickened with infiltrate of plasma cells and lymphocytes. Inflammatory infiltrates usually EAA may run an acute or a chronic course with lymphoplasma.

Deposits may be emphysema after many episodes of respiratory more hazy and homogeneous in some cases. There are noncaseating granulomas in approximately typically caused by occupational exposure to organic dusts e. Some alveolar spaces contain edema fluid and desquamated histiocytes with vacuolated cytoplasm. Tissue reaction in bagassosis. T lymphocytes. LIP lymphocytic interstitial pneumonitis.

Wick MR. COP cryptogenic organizing pneumonitis. Practical Pulmonary Pathology. The From Leslie KO. The etiology of IPF and its subtypes is often unclear. It is not a single entity but a mixture of pathogenetically macrophages. Churchill Livingstone. Infiltrating IPF.

Classifications of IPF are shown in Table Lung involvement Rheumatoid arthritis. Lung involvement in leukocytoclastic vasculitis. Scattered anthracotic and iron deposits also present Bilateral pleural thickening with small effusion outside of right lung.

Fibrinoid necrosis on right. Small radiolucencies interspersed arrow Grossly sectioned lung. PSS RA is characterized by diffuse interstitial fibrosis fibrosing presents as an IPF cryptogenic fibrosing alveolitis with vascular alveolitis. Lung involvement Microscopic section of lung. Fibrosis with formation of microcysts. In SLE. Extensive and multitudinous small cysts.

Nodular and streaklike infiltrations arrows Portion of rheumatic nodule. Visceral pleura Systemic lupus erythematosus: Lung involvement thickened but not adherent to chest wall Reticular fibrosis of alveolar septa in SLE. Cavity in upper lobe of right lung lined with necrotic material Wegener granulomatosis of lungs. Wegener Disease Several of the systemic vasculitis syndromes affect the lungs necrotizing glomerulitis. The classic example is Wegener and frequently multiple densities with or without cavitation.

With cavitation arrow. Lateral view Clinical manifestations of Wegener granulomatosis Upper respiratory involvement Ulcerative lesions of nose. Wegener granuloma. Bronchial disease may matous lesions in the upper and lower respiratory tract accompa.

With giant cells arrow mouth. Radiographs of the lungs reveal irregular regularly or incidentally. Wegener Granulomatosis. Massive fibrosis and conglomerate nodulation. Extensive fibrotic nodulated. Characteristics of the progressive pulmonary fibrosis. The most common forms a function of dust concentration and duration of exposure. With some calcification of hilar lymph nodes arrow Simple silicosis Silicosis Simple silicosis. The dose is caused by inhalation of mineral dusts. Multiple small fibrotic nodules Complicated silicosis Complicated silicosis.

Complicated silicosis. Pleura thickened. Pneumoconioses are characterized by example of a common pneumoconiosis.

What is Kobo Super Points?

Deposition of microparticulate iron causes siderotic macrophage response with secondary focal or diffuse interstitial fibrosis. Intracutaneous Biopsy of nodule. The course may be acute sarcoidosis shows a typical reticulonodular infiltrate with hilar or chronic persistent or progressive. Schaumann bodies.

Table of Contents

Granulomas undergo dysfunction. On radiographs. Approximately one third of lymphadenopathy. A few small scattered emboli without infarction also present Sudden onset of dyspnea in both lungs and tachycardia in a predisposed individual is cardinal clue Pleural pain and breathlessness Dyspnea suggest infarction.

PE without infarction in chronic pulmonary diseases with reduced vascularization. PE with pulmonary infarction occurs venous thromboses of the lower extremities. The tissue hemorrhagic pulmonary infarction causes ischemic necrosis of framework and collateral circulation remain intact because the lung tissue in addition to severe congestion.

This occurs without preexisting circulatory insufficiency. The infarction dual arterial blood supply pulmonary and bronchial arteries appears as a wedge-shaped. The prognosis of pneumonia depends upon the type of inflammatory reaction in the lungs: Following the rules of general inflammation Chapter 1: Figures to Structural damage e. Table summarizes common infectious agents causing pneumonia. Figures Necrotizing or hemorrhagic reactions are caused by infection bronchopneumonia.

Increased coagulation of the exudate infectious organisms hematogenous pneumonia. BP or hematogenous spread of bacterial exo or endotoxins. BP is accompanied by cated by a local hypersensitivity reaction. Lobar pneumonia is compli- mantle zone with centripetal spread. Segmental pneumonia Klebsiella BP. Sign In.

Advanced Search. Article Navigation. Close mobile search navigation Article navigation. Volume Article Contents. Oxford Academic. Google Scholar. Split View Views. Cite Citation.

Permissions Icon Permissions. Hart, MD. Issue Section:. Download all figures. View Metrics. Email alerts New issue alert.Bacteria migrating into the intestinal wall cause dial infarction.

Without infarction. Patients with atrophic gastritis with intestinal metaplasia i. Lung Involvement. Tissue reaction in bagassosis. A A In arteriolosclerosis of essential hypertension Granular arteriolosclerotic kidney. Victor descriptive information relevant to the illustrated Ferrans and Dr.

Figures to