Copyright © 2004-2013 Duke University School of Medicine
|
Cell Injury, Death, and Inflammation |
||
Robbins Basic Pathology: |
|
|
Learning Resources |
Slide 1 [WebScope][ImageScope] Liver: Steatosis (“fatty infiltration,” etc.) This slide is from the liver of a 54-year-old alcoholic who died of heart failure. At autopsy, the liver was enlarged (2800 gm, as compared to the expected normal of 1700 gm), and had a paler than usual color, almost uniformly throughout the organ. Look at the lighter staining area on the right side of the slide and note all of the apparent empty spaces in the cells [example], which are lipid inclusions caused by dysfunction and injury to the liver cells. In many places, the liver cells are so engorged with lipid [example] that they almost look like adipocytes, and, indeed, there probably are some true adipocytes mixed in but DO NOT worry about trying to tell them apart --the point about this slide is just to show lipid inclusions.
Slide 42 [WebScope][ImageScope] Lung: Early Chronic Passive Congestion - Hemosiderin pigment This specimen of lung was obtained from a 66-year-old patient who had been in congestive cardiac failure prior to death. In this condition, the heart does not pump blood out very efficiently, so it starts to back up in the lungs and peripheral tissues. In the lungs in particular, blood starts to spill out of the capillaries and into surrounding tissues. Resident macrophages then ingest the red blood cells and break down the hemoglobin into hemosiderin, which is evident as rather large, glassy-brown granules. In fact, the macrophages are so engorged with hemosiderin that it may be difficult to even see their nuclei except in few instances where they are sectioned just right and/or they haven't quite stuffed themselves so much [example].
Slide 12 [WebScope][ImageScope] Artery: Atherosclerosis - lipid inclusions and dystrophic calcification These sections of arteries came from a 62-year-old hypertensive diabetic who had generalized lesions of this sort.
Slide 8 [WebScope][ImageScope] Kidney: Infarction - Coagulative necrosis and Acute Inflammation This specimen of kidney was obtained from a patient that had a small clot in the aorta that broke loose and lodged into a small branch of a renal artery causing the infarction of a triangle-shaped wedge of tissue. The healthy tissue is on the right side of the slide and should be examined first. We haven't studied the histology of the kidney, so don't worry about the particulars, but note the tangles of capillary loops called "glomeruli" [example] where blood is initally filtered and all of the tubules lined by simple cuboidal epithelium modify the filtrate (mostly by resorbtion) to produce urine. Then, move over to the infarcted area [example], and note that the general structure of the cells is preserved, hence the term "coagulative", but there are no nuclei, so the tissue is most definitely dead.
Slide 2 [WebScope][ImageScope] Heart: Lipofuscin pigment, Coagulative Necrosis, and Acute Inflammation (myocardial infarct) This 63-year-old patient was admitted to the hospital for a “heart attack.” He was stabilized and transferred to the intensive care unit but then died shortly thereafter. The immediate cause of his death was an irreversible cardiac arrhythmia.
Slide 15 [WebScope][ImageScope] Appendicitis: Suppurative Inflammation with Liquefactive Necrosis This slide shows the appendix that was removed from 16-year-old with appendicitis. The slide contains one more-or-less longitudinal section and two cross-sections of the appendix. The lower left cross section [example] is from a relatively uninflamed area (this is near the area where the surgeons cut to remove the appendix) that shows the normal architecture of the appendix. Being a GI organ, the layers are similar that which you've seen in Webslide 0032 of the ileum [ImageScope] [WebScope]. Starting from the lumen of the appendix, the layers consist of:
The lower right cross section shows inflamed tissue [example] consisting mostly of neutrophils, thus allowing you to classify this generally as acute inflammation. As to further classifying the morphological type of acute inflammation seen in this particular area, we would say that it is suppurative or purulent because of the purulent exudate consisting of cell debris and neutrophils (pus). The inflammatatory response is so great that it has caused necrosis of the epithelial tissue and the underlying loose connective tissue, which has been completely obliterated and all that is left is a mass of eosinophilic cell debris [example] (the slight basophilic tinge seen here are actually masses of bacteria that pick up the hemotoxylin stain because of the DNA in them). As to the specific type of necrosis, we would say this is liquefactive. In the outer layer of connective tissue, a slightly different kind of acute inflammation is seen [example]. Masses of neutrophils are present, so the inflammation is "purulent", but we can also amorphous tangles of fibrin [example] that have leaked out of the nearby blood vessels, so it also somewhat "fibrinous," or, putting the terms together, "fibrinopurulent." The point here is not to get hung up so much on nomencalture but to realize that the processes can occur together and have different clinical consequences: the suppurative element weakens the wall of the appendix leading to the risk of rupture, which would be disastrous. The fibrinous element may lead to "organization" or fibrosis in the outer wall and possible attachment to other parts of the bowel or body cavity lining and could cause an obstruction, which would be equally problematic.
Slide 3 [WebScope][ImageScope] Spleen: Granulomatous Inflammation with Caseous Necrosis This spleen is from a 28-year-old patient who died of a systemic tuberculosis infection.
Slide 0143 [WebScope] [ImageScope] Breast: foreign body reaction / chronic inflammation This slide was obtained from breast tissue in which a silicon implant ruptured thus initiating a persistent foreign body reaction and therefore further demonstrates some of the features of chronic inflammation. Rather than polymorphonuclear neutrophils, the primary inflammatory cells are mononuclear (monocytes and lymphocytes). The monocytes differentiate into macrophages which then fuse into multi-nucleated giant cells [example] in an attempt to deal with the implant material. The lymphocytes may be seen scattered amongst the surrounding connective tissue [example]. Recall that lymphocytes are characterized by small, dark, round nuclei.
Slide 68 [WebScope] [ImageScope] Lung: Chronic Inflammation associated with asthma This slide is of lung tissue from a 24 year old who died due to complications associated with asthma. We haven't yet studied lung tissue in detail, so don't worry about trying to identify any of the particular structures. Instead, just focus on the epithelial lining of the two large airways shown in the slide (the airways are surrounded by plates of hyaline cartilage which you should be able to identify). One of the airways is relatively clear of debris [example] whereas the other is filled with a fibrinous exudate [example]. Zoom in on the epithelium lining the airway, and you should be able to recognize the pseudostratified, ciliated columnar epithelium, although it is not quite in as good a shape as the normal trachea (UMich Slide 40 - [ImageScope] [WebScope]) that you studied in the Epithelium lab. Look deep to the epithelium in the underlying loose connective tissue, and note the massive infiltration of eosinophils [example] which is often observed in many chronic inflammatory conditions affecting the GI and respiratory tract.
|
|