28 January 2021: Textbook Updates

We have posted updates of the following topics:

Cervix > Benign / nonneoplastic epithelial lesions > Nabothian cysts
by Gulisa Turashvili, M.D., Ph.D.
Topic summary: Variably shaped, cystically dilated benign endocervical glands. Single or multiple yellow-white mucin filled cysts usually measuring up to 1.5 cm, rarely reaching 4 cm. Most common type of cervical cyst, typically incidental, not requiring treatment. Reactive process due to chronic inflammation and healing. Usually asymptomatic; large cysts may be symptomatic or present with vaginal discharge. Deep or large cysts may mimic malignancy on imaging. Excellent prognosis. Sometimes excision may be performed in large complex cystic lesions raising the differential diagnosis of gastric type endocervical adenocarcinoma.

Cervix > General > Staging
by Carlos Parra-Herran, M.D.
Topic summary: Staging of cervical cancer follows the International Federation of Obstetrics and Gynaecology (FIGO) system updated in 2019 and the American Joint Committee on Cancer (AJCC) system that was last updated in 2017 and still mirrors the previous FIGO staging. Stage is the most important prognostic variable in cervical cancer. According to the FIGO 2019 update, imaging and pathology can be used, when available, to supplement clinical findings of tumor size and extent. Pathological findings supercede imaging and clinical findings; in other words, pathology findings can now modify the clinical stage (former versions of FIGO staging dictated otherwise).

Eye > General > Staging-conjunctiva melanoma
by Martin Hyrcza, M.D., Ph.D., M.Sc.
Topic summary: Based on AJCC 8th edition staging system; used for melanomas arising from bulbar and palpebral conjunctiva, the caruncle and the fornices. Not applicable to primary eyelid skin melanomas or to uveal melanomas with secondary involvement of conjunctiva. Regional lymph nodes are the preauricular, parotid, postauricular, submandibular and cervical. There are currently no proposed prognostic groups. Registry data collection variables include tumor thickness, i.e. depth of invasion measured in millimeters into substantia propria from the surface of the conjunctiva, presence or absence of epithelioid cytology, mitotic count and margin status.

Lymph nodes & spleen, nonlymphoma > Lymph node & spleen-nonlymphoid neoplasms > Acute lymphoblastic leukemia / lymphoma
by Morgan Hrones, M.D., Patricia Tsang, M.D., M.B.A.
Topic summary: Acute lymphoblastic leukemia / lymphoma is a highly aggressive neoplasm of precursor lymphoid (blast) cells with 2 main subtypes: B-ALL / LBL and T-ALL / LBL. Characterized by neoplastic proliferation of clonal precursor B cells or T cells that typically have blastic cytomorphology. Bone marrow or nodal involvement. Idiopathic and likely multifactorial. Diagnosis involves multimodal pathologic evaluation with some combination of morphology, flow cytometry, immunohistochemistry, cytogenetics, FISH, PCR, NGS and clinical laboratory tests. Treatment: multiagent chemotherapeutic regimen stratified based on epidemiology, presentation and other patient specific associated characteristics of the disease, as well as presence of specific cytogenetic abnormalities and therapeutic response to initial induction.

Muscle & peripheral nerve nontumor > Muscular dystrophies > Becker and Duchenne muscular dystrophy
by Yanel De Los Santos, M.D., Jesse L. Kresak, M.D.
Topic summary: Becker muscular dystrophy (BMD) is caused by dystrophin (DMD) gene mutations on chromosome Xp21, which decreases / alters dystrophin production and causes variable progressive proximal weakness in childhood, progressing to paralysis by adulthood. Duchenne muscular dystrophy (DMD) is also caused by DMD gene mutations, which causes severe progressive muscle weakness, progressive cardiorespiratory compromise in adulthood and death. Both BMD and DMD are X linked and therefore are seen almost exclusively in males. Typically affects proximal muscle groups, especially the lower extremities, with variable cardiomyopathy. Diagnosis relies on clinical features in combination with genetic testing and creatinine kinase levels. No curative treatment for the X linked dystrophinopathies.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s