Figure 6.1.1 Papillary endothelial hyperplasia. This lesion arose in a hemorrhoidal area in a patient who had undergone radiation treatment for cervical squamous carcinoma. There is hemorrhage and amorphous debris.

Figure 6.1.2 Papillary endothelial hyperplasia. There is abundant fibrin deposition.

Figure 6.1.3 Papillary endothelial hyperplasia. There are cores of fibrin coated by a monolayer of endothelial cells.

Figure 6.1.4 Papillary endothelial hyperplasia. At high magnification, the endothelial cells are not large. Compare them to the lymphocyte at the upper right.

Figure 6.1.5 Papillary endothelial hyperplasia. The amorphous fibrin debris in this field probably reflects prior radiation treatment.

Figure 6.1.6 Angiosarcoma. This is a solid proliferation of atypical cells.

Figure 6.1.7 Angiosarcoma. There is some vasoformation, but the nuclei are enlarged compared to the adipocyte nuclei in the field.

Figure 6.1.8 Angiosarcoma. This example extends along a preexisting vessel. The malignant cells are hyperchromatic.

Figure 6.1.9 Angiosarcoma. Note the hyperchromatic nuclei.

Figure 6.1.10 Angiosarcoma. The nuclei form a monolayer on the right but are “piled up” on the left.

Figure 6.2.1 Condyloma lata. The eye-catching feature in this image is the dense chronic inflammation. Even at this magnification, it appears lymphoplasmacytic. There is pseudoepitheliomatous hyperplasia at the right.

Figure 6.2.2 The squamous epithelium appears reparative, and intercellular bridges can be seen in the basal layer.

Figure 6.2.3 Condyloma lata. This is an immunostain for treponemal organisms. It is fairly specific (it also reacts with the organisms responsible for intestinal spirochetosis) but not terribly sensitive. As such, patients should be tested serologically, and the immunostain is not necessary.

Figure 6.2.4 Squamous cell carcinoma. There is ulceration but little chronic inflammation. There is desmoplasia in this field.

Figure 6.2.5 Squamous cell carcinoma. There is no in situ component in this example, but it shows necrosis. There is minimal chronic inflammation.

Figure 6.2.6 Squamous cell carcinoma. This basaloid example has invaded through the muscularis mucosae. There is some colorectal-type mucosa at the left. Many squamous cell carcinomas of the anal region arise at the junction of the squamous and columnar mucosa.

Figure 6.3.1 Condyloma. Note that most of the lesion is composed of epithelium rather than stroma. The epithelium is quite thick.

Figure 6.3.2 Condyloma. This image shows enlarged nuclei and koilocytic atypia in which there is a large perinuclear halo around many nuclei. Condyloma acuminatum is equivalent to anal intraepithelial neoplasia (AIN1/low-grade AIN/mild dysplasia).

Figure 6.3.3 Condyloma. As noted above, the stromal component is a minor one.

Figure 6.3.4 Fibroepithelial polyp (anal tag). This lesion is “all stroma,” with a coating of reactive squamous epithelium.

Figure 6.3.5 Fibroepithelial polyp (anal tag). These are reactive surface changes. The vacuoles around some of the squamous cells are small compared to the perinuclear halos that characterize condylomas.

Figure 6.3.6 Fibroepithelial polyp (anal tag). This example had a focus of AIN3, high-grade AIN on its surface. It is important to check the surface of even the most mundane-appearing squamous areas in the anus, including the surface of hemorrhoids.

Figure 6.4.1 Stromal changes in fibroepithelial polyps. Since such lesions are constantly traumatized, they are prone to both reparative epithelial changes as well as reactive stromal changes. This lesion has squamous epithelial edema and a cellular stroma.

Figure 6.4.2 Stromal changes in fibroepithelial polyps. Higher magnification of the lesion shown in Figure 6.4.1.

Figure 6.4.3 Stromal changes in fibroepithelial polyps. This polyp has rather striking changes, but there is no mitotic activity, and the peculiar large fibroblasts have low nuclear-to-cytoplasmic ratios.

Figure 6.4.4 Kaposi sarcoma involving the anal canal. The hemosiderin and cellularity are both clues.

Figure 6.4.5 Epithelioid sarcoma–like hemangioendothelioma/pseudomyogenic hemangioendothelioma involving the anal area. Even if one is not familiar with this rare tumor, it clearly is far more cellular than the pseudosarcomatous change seen in Figure 6.4.3.

Figure 6.4.6 Epithelioid sarcoma–like hemangioendothelioma/pseudomyogenic hemangioendothelioma involving the anal area. Higher magnification of the tumor shown in Figure 6.4.5.

Figure 6.5.1 Reactive squamous changes. The nuclei lack hyperchromasia and mature toward the surface.

Figure 6.5.2 Reactive squamous changes. Well-glycogenized mucosa showing maturation.

Figure 6.5.3 Reactive squamous changes. The basal layer is expanded and mitotically active as part of reactive changes, but note that there is edema such that the intercellular bridges are readily apparent. They are difficult to see in nonreparative basal cells.

Figure 6.5.4 Anal intraepithelial neoplasia. This example is at the transition with colorectal-type mucosa. In this example of low-grade dysplasia, enlarged nuclei are easily identified even at low magnification.

Figure 6.5.5 Anal intraepithelial neoplasia. This high-grade example is quite hyperchromatic.

Figure 6.5.6 Anal intraepithelial neoplasia. At high magnification, it is impossible to see squamous bridges.