General Pathology Slides

General Pathology Slides
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Image No.	Slide Title	Description
K4		Liver - advanced cirrhosis (microscopic).	This is a trichrome stain, which stains collagen blue. The nodular appearance of regenerative liver parenchyma is typical of cirrhosis. The vacuolation in liver cells represents fat globules, commonly seen in alcoholic liver disease
K10		Colon- pseudomembranous colitis (microscopic).	This is a photomicrograph from a biopsy of colon of a patient treated with clindamycin for 5 days for an upper respiratory infection who developed diarrhoea. Multiple small yellow patches were seen on the colonic mucosa during sigmoidoscopy; the mucosa bled readily on removal of the membranous exudate. Note the typical volcanic eruption with a fibrinous coagulum in which there are numerous leucocytes (most being neutrophil polymorphs). This condition is not specific to the one antibiotic but results from alteration of the bowel flora and overgrowth of clostridium difficile (a commensal organism) which secretes an exotoxin. Questions Would this lesion heal without scar formation? What logical suggestions can you make with regard to, prevention? therapy?
K 12		Colon - Pseudomembranous colitis (Gross).	This is a postmortem specimen of entire colon; the mucosal surface shows extensive confluent yellow patches leaving virtually no identifiable normal colonic mucosa. This patient has tetracyclin treatment for an upper respiratory infection for a week, and developed severe watery diarrhoea. When admitted, she was in shock with serum albumin down to 1.5 gm%. In spite of extensive infusion with human serum albumin, she died after 3 days. The close-up appearance demonstrates marked hyperemia of the denuded mucosa. Comments: This is a severe, indeed fatal condition due to pseudomembanous colitis complicating antibiotic treatment. It serves to illustrate that unwarranted antibiotic therapy can be dangerous.
K 14		Vein - organising thrombus (microscopic).	The photomicrograph shows a vein with thrombus adherent to its wall on the right side, partially obstructing its lumen. Note the cells beginning to invade the thrombus, the first step in organisation. Questions What are the next steps in organisation? What is the end result of the process?
K15		Heart - acute myocardial infarction (microscopic).	This is a typical example of early ischemic coagulative necrosis of myocardium. The necrotic or dead myocytes are deeply acidophilic, stained red with eosin stain, attenuated, with loss of nuclei (top of photo). These necrotic myocytes are in sharp contrast to viable myocytes, which demonstrate preservation of cross striations, and presence of nuclei (bottom of photo). Questions Why is there no leucocytic infiltrate in the area of infarction? How would the necrotic area heal?
K21, 22 & 23		Heart - mural thrombus (microscopic).	A typical microscopic view of a thrombus showing coral-like growth of platelet aggregates, which are pink confluent masses on the H & E section. In the higher magnification (especially #23), you will clearly see granular masses of platelets surrounded by a thin layer of deeper pink fibrin strands that hold up the platelets, and then a zone of PMNL and other forms of leukocytes. Between the platelet columns are stagnant red cells. Comments: Formation of platelet columns is a living process, as it will require continuing blood flow to bring in platelets to contribute to a continuing growth. There is no evidence of organization, so the thrombus is fairly recent. Questions What are lines of Zahn? Is the example a red or a white thrombus?
K24		Liver amyloidosis (microscopic)	The liver cell cords are very much attenuated due to compression atrophy by eosinophilic extracellular deposits that are identified as amyloid by Congo red staining combined with polarization (most prominent in bottom of photo). The amyloid deposits also cause obliteration of sinusoids. Questions What would be the functional derangement in the liver? What other organs can be involved?
K25		Artery occluded by embolus	This is a low-power view of an artery. The lumen is almost completely occluded by thrombus. Notice there is attachment to the luminal wall at the 6 o'clock position. No atherosclerosis of the arterial wall is noted.
K26
K27		Artery with severe atherosclerosis	This is a low power view of an artery with severe stenosotic atherosclerosis of the wall. Only a tiny lumen remains.
K35		Stomach - Chronic ulcer (Microscopic).	A portion of the mucosal lining is disrupted exposing the submucosa, which is heavily infiltrated with dark blue cellular elements. Several cross sections of a gastric artery are seen in the deep portion of the ulcer. Overlying the ulcer is a thick inflammatory exudate; the cellular nature is not discernable at this low power. The adjacent mucosa shows hyperplasia of gastric glands (left). Comments: This slide is meant for low power orientation of a typical ulcer. You should examine the histologic slide of a gastric ulcer to understand the inflammatory process that has been going on in the ulcer. Questions What is a peptic ulcer? Besides the stomach, where else in the GI tract may peptic ulcers occur? How does an ulcer heal? How would a peptic ulcer bleed excessively? What factors influence the healing of a peptic ulcer? What are the typical clinical symptoms and signs of a peptic ulcer? What are the possible complications and sequelae of a peptic ulcer?
K36		Stomach - Ulcer base granulation tissue (Microscopic)	A close-up view on the ulcer base permits you to see the type of cellular components. You may have identified a few small fascicles of smooth muscle cells. Diffusely throughout are chronic inflammatory cells, fibroblasts and capillaries (mostly with empty lumen). Notice the vesicular nucleus of spindle-shaped fibroblasts that contain basophilic cytoplasm. Comments: In a persistent chronic ulcer, attempted repair has been unsuccessful. New granulation tissue will form at the base of necrotic old granulation tissue. The ulcer will unsuccessfully keep trying to heal. Examine the histologic section of a chronic gastric ulcer and try to define several zones of tissue showing various inflammatory reactions. Questions How is the name granulation tissue derived? What is the color of granulation tissue? Would it easily bleed? When is the collagen laid down?
K44 & 45		Skin - Arthus reaction (Microscopic).	The lesion shown in these micrographs is produced in rabbit by giving homologous antiserum to bovine serum albumin intravenously, and then injected local intradermally bovine serum albumin. The hemorrhagic swelling developed in 10 hours, and the histologic sections were taken shortly after. This model is a passive immunization, but the phenomenon is identical to that seen in actively immunized rabbit with the same antigen. The lesion is characterized by leucoclastic angitis. The venules and a portion of arterioles are surrounded by abundant polymorpholeukocytes. There is marked vascular congestion, fibrinoid change in venular wall and diapedesis. Comments: If immunofluorescent stainings are done, one will be able to demonstrate deposition of IgG, complements and bovine serum albumin, thus immune complex mediated injury. Depletion of PMNL or complement will prevent the development of the process. Questions What is serum sickness? What is the mechanism of serum sickness? What are the tissues affected and what are the clinical symptoms? How does Arthus phenomenon differ from serum sickness? How should you treat a patient who has serum sickness?
K48 & 49		Lung - Pneumococcal pneumonia, stage of edema (Microscopic).	The alveolar septae demonstrate congestion. Alveoli contain pink finely granular or apparently homogenous proteinaceous fluid with relatively small numbers of polymorphonuclear leukocytes. Comments: Although the inflammatory nature of edema fluid is quite clear, the morphologic appearance is not specific for pneumococcal etiology. History, cultures and bacterial stains must be used to ascertain the diagnosis. Questions Where do you expect to find the Streptococci pneumoniae? How would the pulmonary edema fluid differ from that of acute congestive heart failure?
K50 & 51		Pneumococcal pneumonia, stage of red hepatization (Microscopic).	The cellular elements are increased markedly when compared to stage of edema especially rich in red cells. The alveolar septae remain hyperemic, and the alveolar cells are prominent. Comments: The features may be difficult to distinguish from pulmonary hemorrhage of other causes, except for presence of leucocytic infiltrates and alveolar epithelial hyperplasia.
K52 & 53		Pneumococcal pneumonia, stage of gray hepatization (Microscopic).	This is the peak stage in pneumococcal pneumonia with lobar distribution of consolidation distinctive on the gross examination. Microscopically, many polymorphs, mononuclear cells (macrophages), fibrin strands, and scarce red cells are present in the alveoli. The pores of Kohn are readily seen, as fibrin strands traverse through these natural anatomical passages between the two adjacent alveoli. Comments: You will notice the intactness of alveolar septae in spite of fibrinopurulent exudates in alveoli. Questions What is the last stage of pneumococcal pneumonia? Would the lung return to normal anatomical and functional state completely? By what mechanism do pneumococci (Streptococci) cause inflammation? What is the distinction between lobar and lobular consolidation? Why will pneumococcal pneumonia have the classical lobar distribution while staphylococcal pneumonia does not? Which one of the two, pneumococcus or staphylococcus, leaves pulmonary scarring more often?
K61, 62 & 63		Appendix - Acute appendicitis (Microscopic)	A low and two medium magnifications of acute appendicitis. Focal ulceration with hemorrhage in the mucosa, polymorphonuclear leucocytes infiltration in the mucosa and fibrinopurulent exudate in the lumen.
K68		Heart - Myocardial infarct (Gross)	The specimen shows transmural acute myocardial infarct of 7 day's duration. The necrotic tissue is yellow and surrounded by a ragged zone of hyperemia. The necrotic tissue has a yellow color almost similar to that of the epicardial fat. One of the papillary muscles is also affected by coagulative necrosis (center of photo). Comments: This patient lived for 7 days before he succumbed to rupture of the heart, which is not shown on this photograph. Transmural infarct is the consequence of thrombotic occlusion of the coronary artery that supplies this region. Questions What type of necrosis is this? If the patient survives, what would happen to this area? Why is the infarcted tissue pale in color? What is end artery supply? What other organs are supplied by end arteries?
K73		Aorta - Severe atherosclerosis with mural thrombus in aortic aneurysm (Gross).	The aortic intima shows extensive ulceration exposing the pultaceous material of atheroma. Some shiny flecks of material are cholesterol plates. Ulceration also leads to fresh thrombus formation, which is buffy-brown in color. Below the renal arteries (not too well shown) is an aneurysm about 7 cm in diameter. Lamellated thrombotic materials of variegated color fill up the dilated vascular lumen. Comments: This is the complicated phase of atherosclerosis in which ulceration, hemorrhage, calcification, thrombosis and aneurysm formations are common. Thrombosis will further aggravate the atherosclerotic process, and the disease process is a progressive one leading to other complications. Questions Which element of Virchow's triads is implicated in thrombosis on the plaques and in the aneurysm? Why did the mural thrombus grow so big and so thick without providing significant protection to the aneurysm, which may eventually blow out? Atherosclerosis is a complicated process, and much is yet to be studied and to be known. In the general pathology course, the student may be advised to read the section dealing with the theories on atherosclerosis, as the principles involve reaction to injury, repair, and control of cellular proliferation.
K74, 75 & 76		Lung - Miliary tuberculosis (Microscopic)	Miliary tuberculosis follows hematogenous dissemination of the infectious organism, Myco. tuberculosis. All tubercles are of about the same size and same age of development, clearly nodular, have a thin rim of lymphocytes, masses of epithelioid cells some of which transform into Langhans' giant cells, and central caseous necrosis. Fibrosis is slight at this stage. The remaining pulmonary parenchyma appears normal. Comments: Miliary hematogenous dissemination may occur following primary tuberculosis in childhood or reactivation of tuberculosis in an adult. Organisms are filtered out in many organs, including lungs, liver, spleen, bone marrow and kidneys. A wide variety of clinical and laboratory findings may be confusing at times to render diagnosis difficult. Histopathologically, the features are distinctive. Questions Examine the slides thoroughly to become familiar with the caseous type of granulomatous inflammation. What would be the evolution of these granulomas if the patient survived? From what is the term miliary tubercles derived? Is a granuloma composed of granulation tissue? What is an epithelioid cell? From what precursor is the cell derived? Are there functional differences between epithelioid cells and macrophages? Why do caseous tubercles tend to undergo calcification? Is the patient highly infectious in this form of tuberculosis? to his relatives, nurses, and doctors? to pathologists and their assistants conducting the autopsy?
K80		Normal jejunal mucosa (Microscopic)	The ratio of villi to the crypt is about 4:1, which is normal. Contrast this slide with slide #81, subtotal villous atrophy of sprue. Note the interspersed goblet cells and serration of the lateral surface of the villi, which is typical for normal jejunal mucosa.
K81		Villous atrophy in Sprue (gluten enteropathy, Celiac disease) (Microscopic)	This biopsy is taken per-orally from the jejunum. There is total loss of villi, but there is hypertrophy of the crypts, which show cellular hyperplasia. There is a moderate round cell infiltrate in the lamina propria. Comments: This condition is called subtotal villous atrophy, seen characteristically in gluten sensitive enteropathy, in which patients have malabsorption. Compare with K80, normal jejunal mucosa.
K84		Infarct of bowel (Gross)	This is an overview of the abdomen a the time of autopsy. The dusky red and distended loops of small bowel intertwine within the peritoneal cavity, but are apparently free from each other, as there has been very little inflammatory exudate. Some proximal segments of bowel are distended to 4-5 cm in diameter.
K85		Fibrinopurulent peritonitis (Gross)	The abdominal cavity contains matted loops of bowel covered by (foul-smelling) fibrinopurulent exudate. Bright yellow strands of exudates cling on the hyperemic bowel serosa between the loops and on the liver surface (top of the slide). Cloudy brown liquid exudate is seen in the lower of the slide. Comments: Acute fibrinopurulent peritonitis is an outcome of many disorders affecting the abdominal viscera. The consequences are the same.
K89		Fat emboli in glomerulus (Microscopic)	This is an oil-red 0 stain for fat showing red globules of fat in glomerular capillaries. The section has been prepared by freezing the block of tissue to allow the section to be cut. If it had been processed by embedding in paraffin the conventional way, the fat would have been dissolved out and optically empty holes would be seen where the fat had been. Questions How do the fat emboli get to the renal glomeruli? Do you expect to see other organ involvement when there is renal glomerular involvement?
K 90		Kidney - infarct involving the entire right kidney	Compare with left. The infarct must include renal artery as it is globally affected.
K91		Kidney - infarcts of renal cortex due to vasculititis (Gross)	A portion of kidney has been bisected showing renal cortex and medulla and in particular the cortico-medullary junction where arcuate and interlobar arteries and veins are located. The infarcted renal cortex exhibits a sharply defined bright yellow appearance, partially bordered by a hyperemic zone. At the corticomedullary junction is a cross section of a thrombosed artery, which has just entered the renal parenchyma. Comments: The yellow appearance is typical of ischemic necrosis of the kidney, which has an end arterial blood supply. The underlying causes of renal arterial occlusion can be many. Here it is related to polyarteritis nodosa. Questions Would infarcted renal cortex regenerate? Can you suggest causes other than vasculitis for renal infarcts?
K94		Acute pancreatitis with fat necrosis (Gross)	A cross section of the pancreas showing brownish pancreatic parenchyma, around and within which are specks and patches of chalk-white or creamy deposits. Comments: This a typical example of enzymatic necrosis, in which fatty tissue within and around the pancreas, and also the abdominal fat and mesentry are subjected to lipase digestion. The fatty acid so formed binds calcium to form the creamy soapy substance. Questions How do pancreatic enzymes become activated to cause enzymatic necrosis? If the fat necrosis is extensive, what would be the serum calcium level? Is this type of calcification dystrophic or metastatic?
K99		Haemorrhagic infarct and massive pulmonary embolism (gross).	First orient yourself with respect to right and left lungs. The right main pulmonary artery is blocked by an impacted mass of thrombus. The right lower lobe shows a haemorrhagic infarct. The pulmonary artery to the left lower lobe also contains an embolus. Heavily pigmented lymph nodes are not relevant to the embolic process illustrated. Both lungs are rather brown, suggesting passive venous congestion. Comments: Haemorrhagic infarction of the lung is the typical consequence of pulmonary embolism in patients who have pre-existing circulatory impairment or a hypoxic condition and who live for a sufficient length of time after the impacting of the embolus to allow the infarct to develop. Obstruction of the pulmonary circulation by the impaction of massive emboli in the main pulmonary arteries as seen at A and C in this example results in sudden death (i.e., within 2 or 3 minutes). Therefore, the right lower lobe infarct (B) seen here was not due to the visible emboli but to a previous embolic event. Questions Comment on the circulation of blood to the lungs. Where do the bronchial arteries come from? What determines the clinical outcome in pulmonary embolism? Analyse this from first principles. Confirm your conclusions by reading Robbins and Kumar, pages 407-409. What condition might cause passive congestion of the lungs?
K 102		Thrombus in valve pocket of a leg vein (Gross)	The vein has been opened longitudinally to reveal the delicate semilunar valve tissue. Arising from the valve pocket is a red-yellow variegated mural thrombus apparently adherent to the vein wall. Comments: This is the initial site of thrombus formation in a leg vein. Questions Which one of Virchow's triad is mainly responsible for the thrombus forming in the valve pocket? What kind of thrombus is it? Is it white or red? Could this one dislodge to cause pulmonary embolism? How do you prevent thrombus formation in the valve pockets?
K103		Heart - Acute myocardial infarct (Gross)	This is a septal cut (a cut made through the septum, between left and right ventricles) to show typical acute myocardial infarction. Confluent bright yellow necrotic areas and interspersed with hemorrhagic streaks mainly at the boundary zone. Comments: The lesion has developed in three days, giving the typical appearance of an acute myocardial infarct. Questions: What is the histopathologic basis for the dark red streaks bordering the infarct? If the patient survives, what does this infarcted myocardium eventually become?
K104		Acute myocardial infarct (Microscopic	This is the early histologic appearance of an acute myocardial infarct (of 1 day's duration). The necrotic myofibers are deeply acidophilic and show loss of nuclei. Leucocytic infiltration has not yet occurred.
K105		Acute myocardial infarct (Microscopic)	The lesion is estimated to be of 10 day's duration. The necrotic muscles have become fragmented and partly resorbed. The resorption area is heavily infiltrated with mixture of lymphocytes, plasma cells, and many fibroblasts. A few neutrophils may be identified. Comments: The healing of an infarct is an ongoing process, regionally variable because of variable blood supply that brings in the cellular elements and humoral factors necessary for repair. Questions Can you do something to accelerate healing of an infarct? Where do these fibroblasts come from? Do you expect to see regenerating myocardial cells? Explain.
K106		Squamous metaplasia of bronchus (Microscopic)	The normal ciliated columnar epithelial cells are totally replaced by non-keratinizing stratified squamous epithelium. Comment: Squamous metaplasia is a reversible process, provided the irritative cause is removed. Questions 1. Define the term metaplasia. 2. Give 5 examples of metaplasia, not restricted to the squamous cell type. 3. What are the causes of squamous cell metaplasia of bronchus? 4. What may be the functional derangement in a bronchus that has extensive squamous cell metaplasia?
K108		Cardiac hypertrophy (concentric type) (Gross)	This heart demonstrates classical concentric hypertrophy of myocardium, resulting in small ventricular cone-shaped chamber. The thickness of the left ventricular wall measures 25 mm (Normal 15 mm). Notice the papillary muscle which is also very plump. The aortic valve is normal. Comments: There is no aortic valvular deformity to account for left ventricular hypertrophy. There is no myocardial fibrosis. Questions 1. What is the common cause of cardiac hypertrophy in such a case? 2. What is the normal heart weight and the normal left ventricular wall thickness?
K109		Cardiac hypertrophy (eccentric type) (Gross)	Compare with K108. This picture, K109, also shows a big heart, weighing 600 gms. The left ventricular wall thickness is about 12 mm. The ventricular chamber, however, demonstrates a marked degree of dilatation and appears globular in shape. There are small white patches on the endocardial surface of the anterior septum; these are foci of endocardial fibrosis. Questions 1. Comment on the major difference(s) between the abnormalities in this heart and that depicted in K108. Can one state evolve towards the other? And vice-versa? 2. What is the likely cause of this condition? 3. Note the large orifices of the coronary arteries in the coronary sinuses of Valsalva. Suppose they had been much narrowed by atherosclerosis; what then might have occurred during the evolution of this condition?
K114		Pulmonary tuberculosis (gross)	The picture shows the cut surface of one lung. The disease process is more severe and more extensive in the upper lobe. The scattered pale lesions of caseating tuberculosis are of two types: (a) moderately large (mostly 1 to 3 cm in greatest overall dimension), rather uniform opaque, solid-looking areas. These are foci of tuberculous broncho-pneumonia (b) much less frequent, small (less than 1 cm) cavitated lesions with a perceptible small, ragged cavity. These are examples of endobronchial spread of tuberculosis (from a chronic focus not present on this plane of section of the lung) Comment: Mycobacterium tuberculosis elicits, in man, a chronic inflammatory response. The appearance and spread of the lesions depends on the anatomical structure of the tissue affected (in this case, lung) and the balance between virulence of the infecting organism and host resistance, especially the latter. In this autopsy case, host resistance has become low and the infection (from a chronic fibro-caseous lesion not in the picture) is now spreading via the airways (endobronchial spread) setting up new lesions in the mucosa of small bronchi. The infecting organism has also been aspirated into the pulmonary lobules (acini) giving rise to tuberculous broncho-pneumonia. Tuberculous bronchopneumonia was common in the 19th century and was called galloping consumption by Victorians (see various novels and operas). Questions 1. What factors may lower host resistance to tuberculous infection? 2. When tubercle bacilli are disseminated via the blood stream (rather than the airways as here), what term is given to the form of the disease which results? 3. What is the cause of the small black spots and the black strip under the pleura?
K117		Pneumococcal pneumonia, stage of edema (Microscopic)	There is little difference in appearance between this lesion and simple pulmonary edema, except for more fibrin in the exudate. Comments: Without clinical history or culture data, the diagnosis of pneumococcal pneumonia of first stage is impossible. There are many other causes of acute pulmonary edema such as inhalation of fumes, toxic gases, products of combustion as seen, for example, in fire victims. Questions 1. By what mechanisms do pneumococci spread from alveolus to alveolus and from lobule to lobule? 2. Does the pneumococcus produce a toxin that is responsible for the pneumonic process? 3. Why does consolidation in pneumococal pneumonia tend to be lobar in distribution, and fairly uniform in the stage of progression, as if the disease progresses in unison throughout the entire lobe?
K127		Infarct of spleen (Gross)	A portion of spleen has lost its dark red color and become buff-brown (white infarct). It is sharply defined. Comments: This is an example of an infarct of the spleen of some duration. A thin whitish rim may represent a zone of granulation tissue, which has already laid down collagen. Questions 1. What is the proximate cause of a splenic infarct? 2. List three conditions which give rise to 1 above. 3. Explain the difference between a ‘white’ and a ‘red’ infarct.
K129		Foreign body granuloma in pilonidal cyst (microscopic)	The fibrovascular tissue contains three yellow ovoid cross sections of hair shafts (right of photo) that have provoked giant cell reaction (left of photo). In addition, fibrocytes, pigmented macrophages, lymphocytes and plasma cells are present. Comments: The lesion represents foreign body induced chronic inflammation and foreign body granuloma formation. Questions 1. Name a few other examples of foreign body granulomatous inflammation. 2. What is the outcome of foreign body granulomatous inflammation?
K130		Acute and chronic inflammation, nonspecific type (microscopic)	There is a mixed cellular infiltrate. The magnification is adequate for recognition of PMNL (polymorphonuclear leucocytes), plasma cells, and fibroblasts. A few scattered lymphocytes are also present. Comments: The micrograph is provided for recognition of various cellular elements in acute and chro nic inflammation in the tissue. No specific etiology can be defined here.
K131		Acute pyogenic inflammation (microscopic)	This is a typical example of an acute suppurative inflammatory reaction. The predominant inflammatory cells are overwhelmingly neutrophils. Admixed in between are mononuclear cells. The suppurative inflammation is very early, as there is no cellular debris accumulation yet. Arterial and venous engorgement is evident. Comments: The picture was taken from a slide of acute appendicitis. Appendectomy was performed some 10 hours after the onset of clinical symptoms.
K140		Bacterial endocarditis (microscopic)	The vegetation on the valve is examined microscopically. It is shown to be composed of mixture of fibrin mesh-works, colonies of bacteria which appear as bluish granular material, and leukocyte-rich exudate. Comments: Owing to the lack of firm anchorage of these bacteria infested thrombi, septic embolization is an important complication.
K141		Myocardial abscess (microscopic)	A focal suppurative lesion composed of collections of polymorphs cells debris, necrotic myofibers and colonies of bacteria in the myocardium. Comments: This is a typical example of an abscess in its early stage of development. Its causative agent is also shown. Questions 1. Define abscess and empyema. 2. How does the infective agent reach the myocardium?
K144		Hyaline droplet change of renal epithelium (microscopic)	The proximal renal tubular cells are swollen and contain many discrete acidophilic cytoplasmic globules of variable sizes. The adjacent tubules show dilatation of the lumen, flattening of epithelial cells and desquamation of cells into the lumen. Comments: This patient had renal failure due to hemoglobinuric nephrosis following development of gas gangrene. Excretion of excessive hemoglobin into the kidney led to the development of this characteristic hyaline droplet change. Questions 1. Many different and unrelated things may account for the appearance of hyaline material in cells and in interstitial tissue. Name three other situations (See Robbins and Kumar, page 26, if you need help). 2. In this case, are the renal tubular cells working less effectively or more effectively than normal? 3. In the light of your answer to 2 above, can this change reasonably be called a cellular degeneration?
K145		Necrotizing arteritis in testes (microscopic)	The small muscular artery shows club-like swelling and luminal expansion, representing a focal aneurysmal formation. This is associated with focal destruction of muscular wall, fibrin deposition both within the lumen side and outside the vascular wall, and leucocytic infiltration. The vascular lumen is, in fact, poorly delineated. This is another example of fibrinoid necrosis. Comments: This is a classical example of necrotizing vasculitis, consistent with polyarteritis nodosa or hypersensitivity angiitis, many of which are immune-complex mediated disorders. In this case, it is a small muscular artery; in other cases, it may be large vessels or veins. Questions 1. What may be the consequences when the artery becomes necrotic and inflamed, if the kidney is the organ/system involved? 2. How would you prove that this is immune-complex mediated injury?
K150		Steatosis – accumulation of fat in liver cells.	The white ‘holes’ represent accumulation of fat which is cleared in histologic processing and appears as empty spaces (see K89 for special stains to demonstrate fat in histologic preparations).
K152		Mallory’s hyaline in liver cells (Microscopic)	The swollen liver cells contain flocculent acidophilic cytoplasmic inclusions known originally as alcoholic hyaline. Comment: Mallory’s hyaline is composed of intermediate filaments derived from the hepatocyte cytoskeleton.
K156		Vacuolar change in renal and tubular epithelium (Microscopic)	marked vacuolar change of renal proximal tubular cells typical of hypokalemic nephropathy. Question: Is vacuolar change a reversible or irreversible cellular degeneration
K158		Renal glomerulus with lupus glomerulitis (microscopic)	The glomerulus, though normal in cellularity, exhibits irregular but widespread wire-loop thickening along the capillary loops. The thickening is pink and is composed of immune complexes (see K159).
K159		Renal glomerulus with lupus glomerulitis (Immunofluorescent staining for IgG) (microscopic)	An immunofluorescent stain for IgG reveals confluent granular deposits involving extensively the periphery of the capillary loops.
K160		Renal glomerulus with lupus glomerulitis (Immunoperoxidase staining for Complement, C₃ (microscopic)	Similar confluent granular deposits are demonstrated for C₃along the periphery of glomerular capillary loops.
K161		Fibrinoid necrosis of small muscular renal artery in systemic sclerosis (microscopic)	The arterial intima is thickened, resulting in marked lumen stenosis. The intimal plaque shows eosinophilic fibrin deposits semicircumferentially in the intima. Additionally, a few foam cells are seen. Comments: Such eosinophilic alteration of vascular wall is known as fibrinoid change, often denoting, though not always, collagen vascular disease.
K162		Fibrinoid necrosis of renal vessel in systemic sclerosis (Immunofluorescent staining for IgM) (microscopic)	Heavy immunoglobulin IgM deposits are demonstrated in the concentric intimal lesion and in the muscle coat.
K184 & 185		Acute Inflammation - leukocyte margination & emigration (microscopic)	The venules are very congested with their lumens jam packed with red cells. Pavementing of neutrophils is seen along the vascular wall with small numbers of leukocytes out of the vessel wall in No. 184. No. 185 shows more interstitial edema with an increased number of extravascular leucocyte; margination of leukocytes is also evident in the venular lumen.
K189		Macrophages in an inflammatory lesion (microscopic)	The slide shows a loose aggregate of cells, most of which are macrophages. These cells are round, oval or egg-shaped in contour and have abundant granular or foamy and granular cytoplasm. Nuclei are usually eccentric, sometimes markedly so, and sometimes bean-shaped. Comments: The character of the cytoplasm of macrophages depends to a large extent on what the cells have ingested. They are the adaptable helpers of the clean up crew. Questions 1. To what system do these cells belong? 2. What is the ultimate origin of the cells in this system? 3. What other morphologically distinct form of differentiation can such cells develop? (Think granuloma) 4. Suppose that in the lesion illustrated there had been previous haemorrhage and the blood was now breaking down in the tissues, what might you expect to find in the cytoplasm of some macrophages? (Think haemoglobin catabolism)
K199		Pneumococcal lobar pneumonia (gross)	The picture shows the costal surface of the left lung. Identify the apex, upper lobe, oblique fissure (rather distorted and splayed open in its middle third) and lower lobe. The lower lobe and a small part of the upper lobe just across the middle third of the oblique fissure are dark red and solid-looking. The pleural surface of this part of the lung is dull due to the presence of fibrinous exudate.
K200		Pneumococcal pneumonia (bacterial stain) (microscopic)	Gram (+) diplococci (blue) are demonstrated mostly intracellularly within the leucocytes by Gram stain. Comments: Bacterial stain of sputum will identify the diplococci (streptococci pneumoniae) readily. Cultures will be helpful and strains can be identified.
K210		Acid fast bacilli (Acid fast stain) (microscopic)	Within the caseous lesion, numerous red bacilli are present. It is said that when one bacillus is demonstrable in the section, 1 million tubercle bacilli per gram of tissue are present.
K211		Mixed pyogenic and granulomatous inflammation in coccidioidomycosis (microscopic)	Mixed foci of neutrophils and giant cell granulomas are clearly seen. Variable numbers of histiocytes, epithelioid cells and plasma cells are also present. The distinctive large round bodies of 50-70 micron in diameter, showing a thick clear cell wall and large central nuclear mass, are typical for Coccidioides immitis, a highly infective fungal organism. Comment: The disease is prevalent in Western USA , especially in the San Joaquin Valley of California.
K214		Lipoid pneumonia in lung (microscopic)	In the alveoli, histiocytic and lymphocytic infiltration and giant cells are noted. Small and large vacuoles are intracellular and extracellular lipid globules that have been aspirated into the lung. Some plasma cells and elongated fibrocytes are present. Fibrosis is minimal here. Questions: 1. Under what conditions and in what kind of patients might there be aspiration of food and milk, mineral oils, and cod-liver oil? 2. Is the fat shown here endogenous or exogenous fat? 3. What do you expect to find in the sputum to make the diagnosis of this condition?
K215		Chronic granulomatous inflammation with asteroid body in giant cell (microscopic)	One of the giant cells contain a distinctive star-like cytoplasmic inclusion. Otherwise, other changes and cellular infiltrations are typical of granulomatous inflammation. Comments: Though not invariable, the asteroid body in the giant cell is seen in sarcoidosis. Electron microscopy has shown that the asteroid body is composed of bundles of mature collagen fibres, which have been engulfed by the giant cell.
K216		Sarcoma	showing cytological features of malignant cells; nuclear pleomorphism, hyperchromatism, nucleolar prominence and increased nuclear cytoplasmic ratio.
K217		Sarcoma	showing many mitotic figures. Questions 1. What does the presence of many mitotic figures indicate? 2. Does this feature necessarily indicate malignancy?
K218		Abnormal mitosis (tripolar)	Question 1. What is the significance of abnormal mitoses?
K219		Fibroma
K220		Fibrosarcoma	Question 1. What cytological features distinguish fibrosarcoma from fibroma?
K223		Angioma
K224		Angiosarcoma
K225		Lipoma
K226		Liposarcoma
K228		Squamous papilloma of skin	Note thickening of squamous epithelial layer but with a distinct, sharply demarcated lower border.
K229		Squamous carcinoma of skin.	Note the epithelial character of the lesion but with an indistinct lower border showing infiltration of the dermis.
K230		Squamous carcinoma of skin	Higher power of squamous carcinoma of skin to show cellular features of keratinization, indicating differentiation.
K231		Adenoma of colon, a premalignant neoplasm of glandular epithelium.	Note the papillary growth pattern, each papilla being lined by regular epithelium
K233		Mixed tumor of salivary gland.	Note a portion of normal salivary gland (left of photo) at the periphery of the well circumscribed lesion, mainly composed of basophilic cartilage-like tissue.
K234		Mixed tumor of salivary gland.	This higher power shows both mesenchymal and epithelial elements which constitute the mixed tumor.
K235		Teratoma of testis.	Note elements from all three germ layers; glandular elements (endoderm), muscle and connective tissue (mesoderm), and neural elements (ectoderm).
K236		Hemangioma of liver
K237		Hemangioma of liver.	The lesion consists of vascular channels in a dense connective tissue stroma, and the lesion may be considered as a benign overgrowth of tissue native to the organ, i.e., a hamartoma.
K238		Follicular carcinoma of thyroid, well differentiated.	The neoplastic follicles closely resemble the mature cells of origin.
K239		Follicular carcinoma of thyroid, poorly differentiated.	The neoplastic follicles and cells have only slight resemblance to their native counterparts.
K240		Undifferentiated carcinoma of thyroid.	The neoplastic cells have no resemblance to the mature cells of origin and are bizarre with tumor giant cells an no follicle formation. What differences would you expect in the prognoses for patients with the neoplasms shown in K238, 239 and 240? On what else might it depend besides the grade of the neoplasm?
K241		Leiomyoma of stomach.	Note the discrete, well-demarcated growth of a benign neoplasm.
K242		Carcinoma of stomach.	Note the diffusely infiltrate growth without well-defined margins of a malignant neoplasm.
K243		Basal cell carcinomas of skin (clinical picture).	One of these lesions is well circumscribed with pigmented, heaped up margins and central ulceration. The other, beside the nose, has a more diffuse, infiltrative growth. Note: Basal cell carcinomas, though locally infiltrative, rarely metastasize. They are described as being locally malignant.
K244		Basal cell carcinoma. (microscopic)	Note nests of basal cells infiltrating the dermis.
K245		Glioma of brain (gross)	These are malignant tumors derived from the glial cells. They infiltrate locally but usually do not metastasize.
K246		Carcinoma (breast) in lymphatic channels. (microscopic)
K247		Metastatic carcinoma (breast) in axillary lymph node. (microscopic)
K248		Tumor in a vein. (microscopic)
K249		Liver metastases (gross)	Question 1. Where are the likely primary sites?
K250		Metastatic adenocarcinoma of liver. (microscopic)
K251		Lung metastases (gross)	Question 1. Where are the likely primary sites?
K252		Ulcerated carcinoma of stomach. (gross)
K253		Mesenteric and serosal metastases (gross) from carcinoma of stomach.
K254		Pericardial metastases (gross) from bronchogenic carcinoma.
K255		Cervical dysplasia.	Note some disorderly arrangement and loss of polarity of the cells in the lower part of the cervical epithelium. Question 1. What is the possible evolution of such a lesion?
K256		Cervical carcinoma in-situ.	Note the disarray of the cells throughout the entire thickness of the epithelium, loss of polarity and presence of malignant cytological features. Question 1. What is the likely evolution of such a lesion?
K257		Invasive squamous carcinoma of cervix.	Nests of malignant cells are invading deep to the epithelium.
K258		cervical carcinoma	Extensive cervical carcinoma causing obstruction of lower end of ureter with hydroureter (gross) and hydronephrosis.
K259		Fibroadenoma of breast (gross).	Note uniform, well-circumscribed tumor.
K260		Fibroadenoma of breast (microscopic).	Note small ducts in a loose stroma and a thin capsule.
K261		Infiltrating duct carcinoma (microscopic).	Note loss of orderly growth pattern and malignant cytologic features.
K262		Carcinoma of breast (gross)	Note subareolar tumor with ill-defined margins and inversion of the nipple.
K263		Carcinoma of breast (microscopic).	Note the infiltrating character of the neoplastic cells with a marked desmoplastic stromal response. This latter feature imparts a very hard consistency to the tumor.
K264		Intraduct carcinoma of breast (microscopic) (in situ carcinoma).
K267		Metastatic carcinoma (breast) extensively plugging lung lymphatics (gross).
K268		Metastatic tumor (breast primary) in liver (gross).
K271		Squamous cell carcinoma of lung (microscopic).	This low power photomicrograph shows well defined masses of closely packed cells interdigitating with each other like shingles on a roof - a habit common to squamous epithelial cells. Note the large nuclei with prominent nucleoli, occasional densely staining, shrunken (pyknotic) nuclei and mitotic figures. Also the tendency of small clusters of cells near the centers of the clusters to be larger, polygonal rather than elongated and to have pink, ground glass like cytoplasm: this is due to the development of keratin within them. These clusters of cancer cells are set in, and sharply demarcated from, a stroma composed of connective tissue cells (fibroblasts) and their products, namely ground substance and collagen which are not resolved in this micrograph.
K272		Squamous cell carcinoma of lung (microscopic, high power).	This micrograph is a high power view of the lesion shown in K271. A single cluster of cancer cells is shown. Note the ballooning of six or seven cells near the centre, due to keratinisation, the prominent nucleoli and the mitosis (in anaphase) which appears near the top of the picture two-thirds of the way along the upper margin to the right (when the slide is inserted in the projector with the orientation spot at top right. A small amount of stroma is present, best seen along the bottom of the micrograph.
K273		Bronchogenic carcinoma (gross).	Note white tumor mass filling right lower lobe bronchus (black arrow) and infiltrating lung parenchyma of lower lobe. Also, dilated distal airways with retained and infected secretions (bronchiectasis). Surviving lung parenchyma is airless because of atelectasis and pneumonic consolidation.
K274		Bronchogenic carcinoma (gross).	Note extensive infiltration of lung by nodules of tumor and an abscess cavity. Slides K273 and 274 require and reward careful study. They show graphical the secondary effects of bronchial obstruction as well as the carcinoma causing it. Seek help from your instructor if you have difficulty with these slides.
K276		Well differentiated adenocarcinoma (micro) of rectum.
K277		Annular constricting carcinoma of rectum (gross).
K279		Liver metastases from carcinoma of rectum (gross).
K280		Tumor in upper lobe of the left lung (gross).	Note extensions through the pleural surface
K281		Undifferentiated small cell carcinoma of lung (micro), oat cell type.
K282		Metastatic tumor in the brain (micro) (from oat cell carcinoma of lung).	Note multiple tumor nodules at junction of gray and white matter.
K283		Metastatic tumor in liver (gross) from oat cell carcinoma of lung.
K284		Metastatic tumor in the brain with hemorrhage into the ventricle.
K285		Hyperplasia of adrenal gland (gross).	The gland weighed 30 gm (normal 8 gm). The gland showed diffuse cortical hyperplasia due to ectopic ACTH secretion from oat cell carcinoma of lung.
K286		Clindamycin induced pseudomembranous colitis (microscopic).	Higher magnification of slide No. 10.
K304		Mural thrombus - heart (gross)	Apex of left ventricle. Greatly hypertrophied and dilated. Thrombus is attached to endocardium (lower left of photo). (Atlas of Pathologic Anatomy, Wilhelm Doerr, 1978).
K314		Acute myocardial infarct: rupture of papillary muscle (gross)	The picture shows the interior of the left side of the heart. Orient yourself by identifying the left atrium above, the mitral valve, its chordae and papillary muscles, and the cut wall of the left ventricle. Now study the papillary muscles and observe that one of them (the anterior one) has ruptured and presents two ragged torn ends. The muscle has been infarcted and the necrotic tissue lacking cohesive strength, has ruptured. Comments: This complication of myocardial infarction is fortunately unusual, as it nearly always leads to a rapidly fatal outcome. Questions: 1. What is the haemodynamic effect of rupture of a papillary muscle? (Consider the normal function of the mitral valve). 2. Why is such rupture usually fatal?
K315		Marantic endocarditis of aortic vale with normal control (2 panel slide) (gross)	Project the slide so that the panel with the normal aortic valve appears in the upper part of the screen; note the three shiny, well defined, clean-looking cusps and the sinuses of Valsalva. Now, compare the aortic outflow tract from the patient, which is shown in the lower panel. Note the abundant, light brown, granular vegetations on the ventricular aspects of the cusps. There are also two (one small, one rather larger) vegetations adherent to the aortic intima just above the non-coronary cusp. Comments: From a patient with advanced carcinoma of stomach who also had other thrombotic manifestations including thrombosis of major veins. See also K316.
K316		Embolic occlusion of small cerebral artery (microscopic)	The photomicrograph shows a small artery deep in the brain. The lumen is occluded by a grey-pink mass of thrombus. The crescentic space at its upper and right margin is artefact due to shrinkage during processing. Comments: It is often difficult to be sure whether an occlusive thrombus has developed in situ or has arrived from elsewhere by embolism. In this patient, there were multiple examples and a source of emboli in the form of marantic endocarditis of left sided heart valves (see K315). Furthermore, the artery wall is healthy. This example was found in one hippocampus, a temporal lobe structure involved in memory mechanisms, and was associated with a small recent infarct.


Pathology: Image Database	2007 — Faculty of Medicine Memorial University of Newfoundland