Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|