Scrotal mass pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Niloofarsadaat Eshaghhosseiny, MD[2]
Overview
The pathophysiology of testicular cancer depends on the histological cell subtypes and findings. Most testicular cancers derived from the lack of differentiation of primordial germ cell into spermatogonia. Germ cells testicular tumor have some genetic component while most sex cord stromal testicular cancer are hormonal dependent. Most testicular cancers derived from the lack of differentiation of primordial germ cell into spermatogonia. Germ cells testicular tumor have some genetic component while most sex cord stromal testicular cancer are hormonal dependent. Most gross pathology of testicular tumors look similar on the physical appearance.On microscopic histopathological analysis of testicular cancer, fried-egg appearance is the characteristic finding of seminoma; marked nuclear atypia is the characteristic finding of embryonal carcinoma; hyaline-type globules, and Schiller-Duval bodies are characteristic findings of yolk sac tumor ; syncytiotrophoblasts and cytotrophoblast cells are the characteristic findings of choriocarcinoma, Polymorphism with"spirene" chromatin for spermatocytic. Inadequate fixation of the lower pole of the testis to the tunica vaginalis causes testicular tortion . If fixation is absent , the testis may torse (twist) on the spermatic cord, lead to produceischemia from reduced arterial inflow and venous outflow obstruction . Testicular torsion etiology include (eg, trauma, vigorous physical activity) or spontaneously. Acquired hernias due loss of mechanical integrity of the abdominal wall muscles and tendons . primary hernia due Genetic or systemic extracellular matrix disorders and defective wound healing after laparotomy and hernia repairs may predispose to incisional hernias.
Pathophisiology
Physiology
Scrotal is extention of abdominal wall contains testis , tunica vaginalis ,spermatic cord,epididimysis and appendix testis.Testis has seminiferous tubules that has germ cells,sertoli cells, and leydig cells .Germ cells develop into spermatogenesis and produce gametes.Sertoli secrete inhibin and leydig cell produce testostrone.[1]The normal physiology of germ cells is production of gametes which are reproductive cells.After migration of these cells to gonads, they udergo meiosis to produce gametes.[2]
Phatogenesis
- It is understood that varicocele is the result of dilation of pampiniform venous plexus along spermatic cord.[3]
- The pathophysiology of testicular cancer depends on the histological subtype.[4]
- Testicular tortion is produced by Inadequate fixation of the lower pole of the testis to the tunica vaginalis causes testicular tortion . If fixation is absent , the testis may torse (twist) on the spermatic cord, lead to produceischemia from reduced arterial inflow and venous outflow obstruction[5]
- Epididimytis pathophysiology is due to spread of microorganism from urethra ,prostate , vesicle seminal or hematogenous pathogen.[6]
Genetics
Genes involved in the pathogenesis of testicular germcell tumors include:
Genes involved in the pathogenesis of testicular tortion include:
Associated Conditions
Conditions associated with testicular cancer include:
Gross Pathology
On gross pathology, purple color to testicular capsule , hemorragic parynchima are characteristic findings of testicular tortion. [10]
Microscopic Pathology
On microscopic histopathological analysis, edema of interstice, slight blood extravasation, and desquamation of the germ cells are characteristic findings of first grade of testicular tortion.In grade 2 characterized by necrosis of germ cells, and in grade 3 we have fully hemorragic infarction of testis.[11]
References
- ↑ Djureinovic D, Fagerberg L, Hallström B, Danielsson A, Lindskog C, Uhlén M; et al. (2014). "The human testis-specific proteome defined by transcriptomics and antibody-based profiling". Mol Hum Reprod. 20 (6): 476–88. doi:10.1093/molehr/gau018. PMID 24598113.
- ↑ Cinalli RM, Rangan P, Lehmann R (2008). "Germ cells are forever". Cell. 132 (4): 559–62. doi:10.1016/j.cell.2008.02.003. PMID 18295574.
- ↑ OʼReilly P, Le J, Sinyavskaya A, Mandel ED (2016). "Evaluating scrotal masses". JAAPA. 29 (2): 26–32. doi:10.1097/01.JAA.0000476208.04443.ca. PMID 26757064.
- ↑ Shaw J (2008). "Diagnosis and treatment of testicular cancer". Am Fam Physician. 77 (4): 469–74. PMID 18326165.
- ↑ Gordhan CG, Sadeghi-Nejad H (2015). "Scrotal pain: evaluation and management". Korean J Urol. 56 (1): 3–11. doi:10.4111/kju.2015.56.1.3. PMC 4294852. PMID 25598931.
- ↑ Marnay-Gulat C (1967). "[Parathyroid activity and vitamin D. Observations on rats, chickens and guinea pigs]". Arch Sci Physiol (Paris). 21 (4): 475–84. PMID 4294852.
- ↑ Korkola JE, Houldsworth J, Chadalavada RS, Olshen AB, Dobrzynski D, Reuter VE; et al. (2006). "Down-regulation of stem cell genes, including those in a 200-kb gene cluster at 12p13.31, is associated with in vivo differentiation of human male germ cell tumors". Cancer Res. 66 (2): 820–7. doi:10.1158/0008-5472.CAN-05-2445. PMID 16424014.
- ↑ Al-Ajmi N, Al-Maghrebi M, Renno WM (2013). "(-)-Epigallocatechin-3-gallate Modulates the Differential Expression of Survivin Splice Variants and Protects Spermatogenesis During Testicular Torsion". Korean J Physiol Pharmacol. 17 (4): 259–65. doi:10.4196/kjpp.2013.17.4.259. PMC 3741481. PMID 23946684.
- ↑ Bogefors C, Isaksson S, Bobjer J, Kitlinski M, Leijonhufvud I, Link K; et al. (2017). "Hypogonadism in testicular cancer patients is associated with risk factors of cardiovascular disease and the metabolic syndrome". Andrology. 5 (4): 711–717. doi:10.1111/andr.12354. PMID 28544654.
- ↑ "StatPearls". 2019. PMID 31550101.
- ↑ Mikuz G (1985). "Testicular torsion: simple grading for histological evaluation of tissue damage". Appl Pathol. 3 (3): 134–9. PMID 3842075.