On the right side of WebSlide 174 is a muscular artery and its companion vein. Focusing on the artery first, note the prominent internal and external elastic laminae, which are stained pink in this slide. The tunica media contains several layers of circumferential smooth muscle mixed with collagen. The tunica adventitia which is slightly thinner than the tunica media grades into surrounding fatty connective tissue. The companion vein is just below and the the left of the artery. Note the thickness of the wall compared to the overall diameter of the lumen.
Slide UMich 042, is from abdominal mesentery and offers another opportunity to compare a muscular artery with its companion vein[example]. Observe the same features of arteries and veins noted above. Recall that a unique characteristic of larger veins is the presence of longitudinal bundles of smooth muscle in the adventitia, which can be observed in this specimen [example]. Also present are numerous arterioles and venules [example] (and also associated nerve fibers --recall that these structures occur together as neurovascular bundles)
This is a portion of the inferior vena cava cut in cross section. The original circumference of 10-15 mm is only partly sampled in your slide.
Note the following:
Variable intima with some longitudinal fibers, including smooth muscle [example].
Disorganized media consisting of 3-5 layers of circular smooth muscle) [example].
Thick adventitia with plentiful longitudinal smooth muscle bundles like islands in a sea of collagen [example], with vasa vasorum [example] and surrounding connective tissue --note that the connective tissue of the adventitia here has frayed apart somewhat, so a lot of the empty spaces seen here are due to this artificial separation.
Look at both stains. Note that a precise junction between the intima and media (i.e. a distinct internal elastic lamina) is not easy to recognize in either the trichome[example] or H&E-stained[example] sections. Unfortunately, the endothelial layer is mostly absent in both slides. The transition from the media to adventitia, however, can be easily recognized in both trichome[example] and H&E-stained[example] sections. NOTE: The radial folds [see orientation] in these sections are artifacts due to the elastic nature of the vessel and are not vasa vasorum, although examples of these small vessels may be found usually at the transition from the media to adventitia (look for spaces containing RBCs) [example].
Slide 98HE is stained with H&E and Slide 98-N is a similar section stained with Aldehyde Fuchsin-Masson. You should look at both stains. Locate the atrioventricular sulcus that contains a branch of the coronary arterial system (a muscular artery that exhibits moderate intimal thickening) embedded in the epicardial fat. Look at the connective tissue present between the ventricle and atrium. This is part of the cardiac skeleton into which cardiac muscle inserts. A leaflet of an A-V valve takes origin from the cardiac skeleton. Look at the atrial and ventricular endocardium, consisting of an endothelial lining and the underlying connective tissue (the endothelium is often stripped away during processing, but there are some areas where it has been preserved). With low power, locate the Purkinje fibers present immediately beneath the ventricular endocardium in the H&E[example] and trichrome-stained[example] sections (note the appearance of these fibers in cross and longitudinal orientations). These conducting fibers are larger and paler staining than the cardiac muscle fibers. Note the meshwork arrangement of the cardiac muscle fibers in the myocardium. These slides also offer excellent views of capillaries within the myocardium [example].
The interventricular septal connective tissue is present, and, in most sections, a distinct unit of specialized cardiac muscle, the A-V bundle (of His), traverses the septal connective tissue (a thin group of muscle fibers surrounded by dense c.t.). The A-V bundle is easiest to see in slide 99HM, [example], although you should also be able to recognize it the H&E-stained section[example] as well. In these slides, the bundle fibers are cut in cross section and they are similar in size and staining to that of normal cardiac muscle fibers, although in some of your sections the fibers may more closely resemble Purkinje fibers (which is what they are). On one side of the section, a leaflet of the aortic valve[example] is present. On the other side, portions of an A-V valve[example] are present, as are bits and pieces of collagenous chordae tendinae. In slide 99HE, there is a piece of chorda tendinae actually attached to the valve [example] , whereas in slide 99M, the pieces are unattached and out in the ventricular lumen (the attachment site is out of the plane of section [example] .
Cardiovascular System Pathology
Text (Robbins Basic Pathology, 8th ed.):
Ch. 10, The Blood Vessels, pp. 339-363, 369-371, 377-378
Ch. 11, The Heart, pp. 379-382, 388-417
A 55-year-old man complaining of chest pain was admitted to the hospital. His clinical evaluation quickly led to the diagnosis of myocardial infarction, primarily involving the left ventricle. The patient appeared restless, anxious, and markedly dyspneic. He appeared pale and his extremities were cool to the touch. Bradycardia was present and the patient was hypotensive. Shortly after admission, the patient developed pulmonary edema and liver failure and unfortunately died a week later. Slide 32 is from the patient's liver.
Once you've thought of the answer to the question above, click here to see what the lungs look like. The field of view that opens is an alveolus which should normally be filled with just air, but there is clearly more than just air here. The large cells are macrophages stuffed with glossy brown pigment.
What is this pigment and where did it come from?
In terms of hemodynamics, what is happening in the lungs?
These sections of arteries came from a 62-year-old hypertensive diabetic who had generalized lesions of this sort.
Focus on the section on the right side of the slide [example] since it's easier to make out what's left of the original lumen of the vessel, which is lined by a simple squamous endothelium [example].
About 2/3 of the original lumen has been taken up an athersclerotic plaque, within which you can see "foam cells" [example] that have ingested cholesterol.
The cholesterol accumulation is so great that it also collects extracellularly as large, elliptical "crystals" (also called cholesterol clefts) --of course, since they are lipid, they are extracted with tissue processing, so they appear as empty spaces.
Within the plaque, you may also see amorphous, basophilic debris [example], which are examples of dystrophic calcification.
What are the possible fates of this sort of lesion?
This 63-year-old patient had a “heart attack” and died shortly thereafter. The immediate cause of his death was an irreversible cardiac arrhythmia.
First, we'll focus on an area of healthy myocardium [example]. Be sure you can identify it as cardiac muscle.
Next, we'll move into the area of the infarct [example], which is a bit darker staining. The increased eosinophilia is due to protein coagulation within the dead cardiomyocytes. The areas of basophilia are streams of neutrophils coming in as part of the acute inflammatory process. Zoom in on an area [example] and note that the general structure of the cardiomyocytes is preserved, but the nuclei in the necrotic cells are faded or completely absent (karyolysis) and the cytoplasm is markedly more eosinophilic compared to normal cardiomyocytes [example] and the extracellular space around the necrotic cells is filled with inflammatory cells.
What type of inflammatory cells are these?
About how much time had elapsed between the time of the infarction and the time that this sample was obtained?
Can you predict in general histologic terms what would have happened to this tissue over time had this patient survived? (Slide 49 [WebScope][ImageScope] illustrates some of this.) What are some of the complications that the patient might have had to deal with?
A 19-year-old student presented to the campus health service complaining of transient knee and hip joint pains of one week’s duration. He had become febrile 2 days prior to seeking medical attention. Physical examination revealed swollen knee joints and small painless subcutaneous swellings located in the scalp and over the elbows. One week later, a heart murmur thought to be due to mitral regurgitation was detected. Congestive heart failure soon developed and the patient succumbed despite aggressive medical treatment. Slide 50 is prepared from the autopsy material.
What epicardial abnormality is present [hint] and how might this have been clinically manifested on physical examination of the living patient?
Valvular endocardial fibrin deposits (excrescences) are present in the slide [example]. What would these deposits have looked like grossly? If the patient had survived, what would be the clinical significance of these endocardial fibrin deposits?
What myocardial abnormalities are present? [hint] Based on these findings and the symptoms, what is the diagnosis?
What are some of the possible complications that might have arisen if the patient had survived this particular episode?
