DNA damage is correlated positively with poor semen parameters, especially low sperm concentration and low sperm motility, leukocytospermia, and oxidative stress.
DFI has been shown to be the etiology of idiopathic infertility.
Elevated DNA fragmentation index (DFI) is associated with poorer results in conventional IVF.
DFI is usually lower in ejaculated sperm compared with sperm obtained from testicular tissue.
Elevated DNA fragmentation is not associated with lower in-vivo pregnancy rates.
oligospermia with counts less than 10 mil/mL.
LH, prolactin, and free testosterone.
FSH, LH, and prolactin.
testosterone and FSH.
FSH and inhibin
FSH and LH.
Y-chromosome microdeletion exists in 50% of patients with azoospermia.
25% of all infertile males will have structural and numerical chromosomal abnormalities.
CFTR mutations are identified in only 10% of patients with congenital bilateral absence of vas deferens (CBAVD).
None are true.
Genetic testing with karyotype and Y-chromosome microdeletion is indicated for all patients with azoospermia or severe oligospermia.
EJDO will often present with low-volume azoospermia.
Seminal vesicle width greater than 12 to 15 mm is suggestive of obstruction.
Normal volume azoospermia is a common presentation for EJDO.
In a patient with suspected EJDO, seminal pH will usually be around 8.
If any sperm is found in seminal vesicle aspiration at the time of transrectal ultrasonography (TRUS), the diagnosis of EJDO is confirmed.
Scrotal ultrasound is recommended for the diagnosis and potential treatment of subclinical varicoceles.
Venography is the gold standard for the diagnosis of varicocele and is usually performed at the time of venous embolization.
Abdominal ultrasonography is indicated in men with unilateral absence of the vas deferens or CBAVD that is not associated with CFTR mutation due to an increased incidence of upper tract anomalies.
Testicular microlithiasis are noted in 3% of subfertile men but are not thought to be a precursor for testicular cancer.
Testicular germ cell tumors are more common in men with infertility, and a screening ultrasound is recommended when there is any concern on physical examination.
presence of elongated spermatids in the seminiferous tubules.
patients with normal sperm counts.
small testis size.
elevated FSH and LH levels.
the presence of only Sertoli cells and Leydig cells in the biopsy tissue.
Pretesticular etiologies of azoospermia are usually endocrine in nature.
Low-volume azoospermia with normal testis size and palpable vas is a common presentation for testicular failure.
Testicular cause of azoospermia is also known as primary testis failure.
Secondary testis failure is characterized by high serum gonadotropin levels and small testis size.
Post-testicular causes constitute 40% of cases of azoospermia.
Teratospermia is a common finding and of minimal clinical significance in the absence of bizarre morphology.
Only 25% of males presenting for an infertility evaluation will have normal bulk semen parameters.
Endocrinopathies are rarely observed in oligospermic males with sperm counts greater than 10 mil/mL.
Asthenospermia is often iatrogenic from delayed processing in the andrology laboratory.
a lower degree of oxidative stress due to excessive venous pooling.
higher testosterone levels in the peritesticular vasculature, which inhibit spermatogenesis.
excess turbulent flow through dilated veins that causes a pressure injury to the testicle.
heat injury from excess pooling of blood in dilated spermatic veins.
reflux of splenic metabolites, which is directly gonadotoxic.
dull ipsilateral scrotal pain.
adolescent males with ipsilateral testis size reduction of 20% compared with the contralateral testis.
a clinical varicocele in an infertility patient with an elevated DNA fragmentation index.
a clinical varicocele in a male with known infertility.
a subclinical varicocele in a patient with abnormal semen parameters.
Spontaneous fertilization rates of 75%
Improvement in semen parameters in men with genetic infertility (e.g., Y-chromosome microdeletion)
An average increase in motility by 20%
Improved semen parameters in about two thirds of patients
No improvement in semen parameters in azoospermic patients
These patients often have low FSH levels and small testes.
The level of the cryptorchid testis is not predictive of spermatogenic impairment.
Mechanisms for cryptorchid-induced testis failure include testicular dysgenesis, impaired endocrine axis, immunologic damage, and obstruction.
Both unilateral and bilateral cryptorchidism have equivalent effects on male fertility.
The literature does not support improved fertility with early orchiopexy.
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