LC Exam 1 Week 2 Flashcards
Phases of spermatogenesis
- Proliferative (self renewal as well)
- Meiotic
- Spermiogenic (maturation)
Progression of spermatogenesis
Spermatogonia (2N, 2C) -> 1˚ (2N, 4C) -> 2˚ (1N, 2C) -> Spermatid (1N, 1C) -> Mature spermatozoon
Types of spermatogonia
Adark (self renewing) -> Apale -> B
All 2N
Give rise to 1˚
Spermiogenesis phases
- Golgi phase (to head, acrosomal vesicles)
- Cap phase (vesicles will become cap)
- Acrosomal phase
- maturation phase (centrioles to tail, attract mito)
extra cytoplasm cast off (may stimulate new round)
Spermiation
End of spermiogenesis
Released into lumen by sertoli cell
Epididymis function
Mature sperm
Head: concentrait
Body: maturation (mobility, fertilization capability)
Tail: storage
Disorders that decrease SHBG
Insulin resistance
Metabolic syndrome
Diabetes
Normal aging
Pituitary related hypogonadism: levels and examples
Low T and low FSH/LH Prolactinoma Tumor/mass effect Hemachromatosis (classically: bronze skin) Autoimmune hypophysitis
OSA effects on testosterone
Mildly decreased T levels
Erectile dysfxn (decreased NO, cGMP)
CPAP
Acquired hypertrophic hypogonadism
Traums/torsion Mumps orchitis Alcohol (direct toxin) Diabetes Radiation/chemo Autoimmune testicular failure Gonadotrope pituitary tumor (high FSH, +/- LH, low T)
Recommended for normal/low
Diet/lifestyle modification
Cardiac risk and testosterone therapy
Appears to be within the first 90 days
Low FSH/LH, testosterone
Genetic: Kallman
Acquired: narcotics, GC’s, hemochromatosis, tumor, XRT, stress, illness
Not real: OSA, get T assay (SHBG)
High FSH/LH, low testosterone
Primary testicular failure (XXY, trauma)
Gonadotrope pituitary tumor
Tunica vaginalis
Peritonem taken with descent
Injury can fill with fluid (hydrocele)
Tunica albugenia
Fibrosis, tough, capsule
Cryptorchidism
Most: superficial inguinal canal
Wrong temperature for sperm production
Usually unilateral, but bilateral atrophy w/out tx (infertility)
5x risk of seminoma
Orchiopexy by 2 years decreases risk to 2x
47XXY pathogenesis
Dysgenesis of seminiferous tubules: low inhibin, high FSH
Abnormal Leydig: low T, high LH, high E2 conversion
Varicocele
90% of the time left side (due to left renal artery)
Bag of worms appearance
Assoc. with left sided renal cell carcinoma
Testicular torsion
Venous before arterial
Blood pumps in, can’t pump out
Failure of testes to attach to inner lining of scrotum (via process vaginalis)
Inflammatory dz leading to orchitis
- Chlamydia (D-K), gonorrhea (young)
- E. coli and pseudo (old)
- Mumps (1 wk post parotid, unilateral)
- Syphilis
- Gran/autoimmune (TB)
Three general types of testicular tumors
- Germ cell tumors (malignant)
- Sex cord stromal tumors (benign or malignant)
- Lymphoma: diffuse large B-cell (>60 y/o)
Germ cell tumors
Seminoma (good prognosis, large cells, clear cytoplasm, central nuclei)
Non-seminoma:
Embryonal carcinoma (primitive, glandular, necrosis, differentiation with chemo, AFP and/or ß-hCG)
Yolk sac (Schiller-Duval bodies, AFP)
Choriocarcinoma (ß-hCG, FLßT)
Teratoma (malignant in males, AFP and/or ß-hCG)
Mixed (most common)
Sex cord stromal tumors
Usually benign
Leydig cell tumor: androgen secretion (precocious puberty, gynecomastia, Reinke crystals)
Sertoli cell: tubules, clinically silent
Condyloma acuminatum
HPV 6, 11
Koilocytic change (raisin nucleus)
Benign warty growth
Verrucous carcinoma
HPV associated
More destructive
Non-met
In situ SCC of the penis
- Glans: erythroplasia of Queyrat (erythroplakia)
2. Shaft: Bowen disease (leukoplakia)
Testis cancer serum markers
AFP
ß-hCG
Placental like alk phos
LDH
Penile malignancies
Epithelial (95%): SCC, Basal cell, melanoma
Mesenchymal (5%): tissue sarcomas
BPH
usually around transition zone (periurethral)
Age related change
Related to DHT stimulation on stromal and epithelial cells resulting in hyperplastic nodules
BPH treatment
alpha-1 antagonist: terazosin
5alpha reductase inhibitors
Prostate inflammation
Acute: lymphs, STI/UTI bugs
Chronic: mononuclear, granulo form, atrophy assoc.
Prostatic atrophy
Increased cancer risk concrete formation (associated with chronic inflammation)
Prostatic carcinoma
Western/environment risk Biopsies (blind, random) gold standard Multifocality Gleason grading: based soley on architecture Mets to spine 20-30 years for natural history
Menstrual cycles phases
- Follicular phase
- Ovulation
- Luteal phase
Primordial follicles
Oogonia + somatic cells (pre-granulosa cells)
Ovarian/pituitary hormones
LH stimulates theca cells to produce androgens
FSH stimulates granulosa cells to convert androgens to E2
Oogenesis
1˚ oocyte begin meiosis I during fetal life and finish just prior to ovulation (prophase = pause)
Meiosis 1 results in 2˚ plus polar body
Corpus luteum
Progesterone secretion
Small/large cells + capillaries
Some estrogen
Stablized by hCG from placenta
Follice =
oocyte + granulosa cell
FSH an LH functions in menstrual cycle
FSH: stimulates granulosa proliferation
LH: fosters granulosa lutenization
Is atresia related to selection of the dominant follicle?
NO
Lymph drainage of lady bits
Vulva + lower 1/3 vagina (UGS) = inguinal, para-aortic
Cervix + upper 2/3 vagina (parameso) = iliac
Epithelial progression through female tract
Vulva: keratinizing squamous
Vagina: non-keratinizing squamous
Cervical, endocervical: glandular (singular)
Uterus: glandular (multi)
Vulva condyloma
6, 11
Koilocytes, hyper parakartosis
Vulva infection
Trichomonas -> strawberry cervix
Candida -> pH change, curdlike d/c, itch
Actinomyces -> sulfer granules, copper IUD
VIN
Leukoplakia, 16, 18
- HPV associated SCC - BM invasion
- Non-HPV (Lichen sclerosis, thin parchment paper)
Paget extramammilary dz
PAsKET'S dz PAS+ KEraTin + S100- (otherside of ') Ery, puritic, ulcerated
Melanoma of the vulva
PAS-
Keratin-
S100+
