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37 Cards in this Set

  • Front
  • Back
Tunica vaginalis, Tunica Albuginea
Viceral layer of the scrotum
Capsule of the testis
The two compartments of the testis and the cells they contain ?
The interstitium which contains leydig cells and the Seminiferous Tubules (Setu.) lined by sertoli cells
Function of Leydig and Sertoli cells
Leydig : secrete testosterone
Sertoli : Spermatogenesis
Order of tubules in testes
Setu – Tubuli recti – rete testis – mediastinum of testis – mediastinum of the testis – ductuli efferentes – epididymis and then vas deferns
Cells involved in mulerian duct regression
Sertoli cells, and they secrete mullerian duct inhibitory factor
Fxn of testosterone by Leydig cells
Leads to the development of the testicular ducts and is also converted to hihydrotestosterone which acts on the penis, scrotum
Describe the process of Spermatogenesis
Germ cells undergo maturation to become primary spermatocytes. Then they undergo meiosis to secondary spermatocytes. These then undergo a second meiotic division to become spermatids which mature while along the Sertoli cells and then are relased as mature spermatozoa
Ratio of sperm : Spermatids
Germ cells to Sertoli
2: 1
13:1
While infertility can have many causes like abnormal testes , gonadotropin deficiency, abnormal sperm etc, what are normal, immature , maturation, hypospermatogenesis and germ cell aplasia
b. Seen in hypopituitary state when testes are not exposed to LSH and FSH
c. Spermatogenesis does not progress beyond the primary spermatocyte
d. Maturations occurs but germ cells are few in number
e. End of hypospermatogenesis and is thought to be irreversible state of infertility
Two examples of testicular dysgenesis
Testicular Feminization – 46XY karyotype and is familial X-linked recessive. Failure of end organ response to testosterone. Geneticall ymale but phenotypically female ( pseudohermaphroditism)
Klinefelters syndrome – Male hypogonadism. Occurs when XXY happens. This is rarely diagnosed prior to puberty . The characteristic features are elongated body habitus and small atrophic testes. Lacks secondary male characteristics. FSH is increased, Serum testosterone is decreased and testis biopsy may show peritubular fibrosis and Leydig cell hyperplasia
Cryptorochism (3)
One or both testis fail to descend. Corrected by Orchiopexy. Complications of cryptorchism include infertility and increased risk of germ cell neoplasia
Torsion of testis
Inguinal defect (bell clapper anomality)
Occurs in 20s-30s
Can be corrected within 6 hrsortherwise hemorrhagic necrosis occurs when venous blood is obstructed and ischemic necrosis if arterial blood flow is.
Contralateral testis also is at a risk for this, so orchiplexy is performed
Cause of acute epididymitis or orchitis
A bacterial infection due to reflex from a urinary tract infection
Mimps Orchitis -5
Present in post pubertal boys who contract mumps
Affects 20% of overall boys
Painful, unilateral testicular swelling with edema
The inflammation is lymphoplasmacytic but can be suppurative
Can cause sterility in few cases
Idiopathic granulomatous Orchitis – what do you have to rule out first ?
Must r/o granulomas, sarcoidosis etc. Must also exclude seminoma because seminomas are associated with a marked granulomatous rxn
Malakoplakia
Granulamatous rxn seen in the bladder, prostate and epididymis/testis
Gross yellow nodule appearance with granulomatous rxn including intra and extra cellular Michaelis Gutman bodies
Neoplasia – intratubular Germ cell neoplasia (ITGCN) – px ? found in ? not found in ?
Proliferation of abnormal, neoplastic germ cells within semtub(in-situ tomor)
occurs in association with cryptorchidism, testicular dysgensis, infertility and germ cell tumors (ipsilateral 85%)
Not found in spermatocytic seminoma and teratomas in prepubertal boys
Seminoma – Px, %, age, variants, PagF cells
30% of all testicular germ cell tumors
most likely to exhibit a pure histologic, non-mixed patter
peak incidence in fourth decade
variants include classic and spermatocytic
seminomas may contain scattered placental like synchiotripblastic cells that stain for hCG
Classic Seminoma – gross, micro
Gross – homogenous, lobulated, gray white mass w/o hemorrhage or necrosis
Micro – largeu polyhedral tumor cells with ample clear cytoplasm, largue nuclei, prominent nucleoli, cytoplasm contains glycogen. Lymphocytic infiltrate is associated with this tumor in 80% of the cases. Granulomatous infiltrate in 20% of the cases
Spermatocytic Seminoma
Rare
Older men
No metastasis
Large mass
Tumor cells are pleomorphic
Smaller cells resemble secondary spermatogonia
Embryonal carcinoma
Peak incidence in 20-30 yr age group
Small poorly demarcated with foci of hemorrhage and necrosis (unlike seminomas)
may penetrate tunica into epididymis and cord
Teratoma -%, mets
4-9% of testis tumors
metastasize via lymphatics
metastasis may contain non-teratomous elements
When are teratomas benign and when malignant
These are benign prior to puberty and malignany after puberty
What are the variants of teratomas ?
Theyse show differentiation along endodermal, mesodermal and ectodermal lines and variants are mature teratoma, immature teratoma, teratoma with malignant transformation
Most common testis tumor in infants and children. Marker?
Yolk sac tumor – Pure in prepubertal setting but almost always mixed w. another cell type in adults. Tends to contain AFP
Choriocarcinoma ? form ? expresses
Tumor MUST contain both Synchiotrophoblasts and cytotrophoblasts elements
Rare in pure form in testis, and is usually mixed
Contains and expresses HCG
Mixed germ cell tumors ? % and mets
Make up approx 40% of testis tumors
Tend to occur around 30 years of age, metastasizes to lymphatics
One of the most common forms of cancer in men between the ages of 15-34 but only account for 1% of cancer in men /
GCT of the testis
Risk of germ cell neoplasia in patients with undescended testes ?
14%. Genetic influence is present
GCT markers ?
AFP, HCG – useful in diagnosis, staging and monitoring response to therapy
Treatment of GCT ?
Surgery, radiation or chemo depending on histology ( Seminoma vs non seminoma)
Staging ?
I – tumor confined to testis
II – metastases limited to retroperitoneal nodes below diaphragm
III – metastases outside the retroperitoneal nodes or above the diaphragm
Which is more aggressive ?NSGCT or seminomas ?
NSGCT – approx 70% of seminomas are clinical stage I, whereas approximately 60% of NSGCTs are clinical stage II or III. Even if primary mass in NSGCTs is small, the metastasis is large, especially choriocarcinomas
Sex-cord Gonal Stromal Tumors – Leydig - %, age, secr, prepubertal, PagF, type ?
2% of tumors
20s -60s commonly
Secretes androgens, or mixture of androgens, estrogens and other steroids
In prepubertal settings causes sexual precocity
Tumor cells contain crystals of Reinke
Benign
Sertoli cell tumors – fxn, gross,micro,type
May elaborate androgens or estrogens
Gross : homogenous gray white – yellow mass
Micro : tall columnar cells often forming cords which look like Semtubs
Mostly benign
Testicular lymphoma - %, age, type of lymphoma, grade
5%
Most common >60yrs old
Non Hodgkins lymphoma
High grade
So there is a lymphoma in the testis, what is your first thought regarding the origin of the disease ?
Well most lymphomas represent disseminated disease, but primary testis lymphomas can occur