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Week 2 Flashcards

1
Q

Oocyte

A

germ cell 4N, undergoes meiosis I and II to form mature oogonia

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2
Q

Oogenesis:

what happens in Meiosis I? When does this occur?

A

4N primary oocyte → undergoes Meiosis I (recombination, DNA exchange between non-sister chromatids) → Primary Oocyte (4N)

Occurs during fetal life, arrests at prophase of meiosis I

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3
Q

Oogenesis:

when does Meiosis I resume?

what do you have at the end of meiosis I?

A

Meiosis I does not resume until LH surge just before ovulation

→ 2N, haploid SECONDARY OOCYTE (ovulated) + polar body 1 (2N)

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4
Q

Secondary oocyte

A

2N, haploid

Secondary oocyte arrested in meiosis II until fertilization

If unfertilized, ovulated secondary oocyte degenerates

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5
Q

Primary Oocyte

A

4N, diploid

arrested at prophase of meiosis I until ovulation

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6
Q

Oogenesis:

Meiosis II

when does it occur?
what do you have at the end?

A

doesn’t occur until fertilization

2N oocyte → fertilized oocyte (1N, haploid) + 2nd polar body (1N)

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7
Q

The menstrual cycle:

Lasts _____ days

2 main phases and their duration?

A

28 days

Follicular Phase: proliferative, day 1-14

Luteal Phase: secretory (day 15-28)

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8
Q

What phase of the menstrual cycle is more variable - Follicular or Luteal?

A

Follicular - length can vary

Luteal - Most consistent duration, always precedes onset of menses by 14 days

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9
Q

4 main steps of follicular phase of menstrual cycle

A

1) Development of follicle
2) Upregulation of LH/FSH receptors on Theca/Granulosa cells → increased sensitivity to LH/FSH
3) Estradiol levels increase –> proliferation of endometrium
4) Ovulation: day 14

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10
Q

Follicular growth is fastest during the _____ week of the follicular phase

A

2nd

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11
Q

What is estradiol doing during the earlier parts of the follicular phase?

what are the levels of FSH, LH, and progesterone?

A

FSH/LH suppressed by negative feedback of estradiol

**Progesterone, FSH, and LH levels LOW during follicular phase

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12
Q

Cervical mucus consistency during follicular vs. luteal phase

A

Follicular: High estrogen → thin, watery, cervical mucus

Luteal: High levels of progesterone → Thick, viscous cervical mucus, impenetrable by sperm

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13
Q

Ovulation

A

day 14

Estrogen levels rise throughout follicular phase → peaks → REVERSAL of negative feedback → POSITIVE FEEDBACK → LH surge

Estrogen levels decrease just after ovulation, then rise again during luteal phase

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14
Q

Luteal phase main steps (2)

A

1) After egg is ovulated → follicle becomes corpus luteum → progesterone
2) High levels of progesterone- -> Proliferation of tortuous spiral arteries and glandular secretions from endometrial lining (prepare endometrium for fertilized egg) AND Increase basal body temperature

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15
Q

What happens at the end of the luteal phase if fertilization does NOT occur

A

Corpus luteum regresses → estrogen/progesterone levels decrease abruptly → shed endometrial lining

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16
Q

What happens at the end of the luteal phase if fertilization DOES occur

A

hCG and progesterone from corpus luteum maintains endometrial lining

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17
Q

Primordial Follicle

A

Oogonia + somatic (PRE granulosa) cells

Oocyte arrested at prophase of Meiosis I in primordial follicle

Present by 6 months of life

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18
Q

Primary Follicle = _______ + ________ + _________ under the basement membrane

A

primary oocyte + zona pellucida + single layer of cuboidal granulosa cells under BM

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19
Q

Zona pellucida

A

glycoprotein coat surrounding primary oocyte, facilitates sperm attachment and fertilization

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20
Q

Secondary Follicle = _______ + ________ + _________ under the basement membrane

A

Primary oocyte + Zona Pellucida + several layers of cuboidal granulosa cells + BM

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21
Q

Preantral follicles (3)

A

1) Primordial follicle
2) Primary follicle
3) Secondary follicle

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22
Q

Antral follicles (2)

A

1) Tertiary Follicle

2) Graafian follicle

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23
Q

Tertiary follicle = _______ + ________ + _________ under the basement membrane + _______ and _________ outside the BM

A

primary oocyte + zona pellucida + granulosa cell layers + BM + Theca interna/Theca externa

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24
Q

Meiotic division which gives rise to secondary oocyte occurs in _______ follicle just before _______

A

Meiotic division which gives rise to secondary oocyte occurs in graafian follicle just before ovulation

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25
Corpus Luteum
remnant of ovulated ovarian follicle, no oocyte present Highly vascular → LH/FSH stimulate progesterone/estrogen secretion Produces high levels of progesterone which supports pregnancy
26
Corpus Luteum if fertilization does NOT occur
No fertilization → CL degenerates (becomes fibrosed) 11 days after ovulation (Corpus Albicans)
27
Corpus Luteum if fertilization DOES occur
Conception and ongoing pregnancy occur → -Remaining cells of ovulated follicle become corpus luteum Placental production of hCG (a-subunit similar to LH) stabilizes corpus luteum and thus progesterone production for first 9 weeks until placenta able to make progesterone independently Regresses after first few weeks → Corpus Albicans
28
Large growing follicles containing eggs are needed to produce _______
estradiol
29
Local autocrine/paracrine factors influencing follicular matruation
Interleukins, growth factors (VEGF → increase blood flow to developing follicles) -Activin --Inhibin
30
Activin autocrine/paracrine effects
augments FSH, suppresses androgen production in theca cells (increases estrogen)
31
Inhibin autocrine/paracrine effects
later in follicular phase, enhances LH stimulation of androgen synthesis in theca cells → more substrate for estrogen synthesis in granulosa cell → LH surge
32
Dominant follicle
single follicle that ovulates each cycle Determined by local hormonal milieu (more estrogen, better blood supply, more FSH receptors, more granulosa cell proliferation, more aromatase activity, more inhibin)
33
2-Cell Theory of Sex Steroid Production
TWO cell types needed to produce estradiol Theca → produce androgens that are taken up by Granulosa cells Granulosa cells → convert androgen → estradiol
34
Layers of Endometrium
1) Stratum basalis | 2) Stratum Functionalis (Stratum spongiosum + Stratum Compactum) --> shed during menstruation
35
Stratum basalis
deepest layer, adjacent to myometrium, does not change appreciably during menstrual cycle Permanent stromal tissue Contains endometrial glands Basal layer that regenerates stratum functionalis each cycle
36
Stratum spongiosum
thick intermediate layer between basalis and compactum part of stratum funcitonalis
37
Stratum Compactum
superficial layer of endometrium part of stratum funcitonalis
38
Spiral arteries
pass through basal layer into stratum functionalis Hormonally sensitive Constrict in response to hormonal shifts → stratum functionalis becomes ischemic → sheds
39
Straight arteries
feed stromal layer of endometrium Do NOT infiltrate endometrium very deeply
40
Endometrial Phases: (3)
1) Menstrual phase 2) Secretory phase 3) Proliferative phase
41
Menstrual Phase
lasts 5 days = Menses Endometrial ischemia (spiral artery constriction) → shedding of stratum functionalis → menstrual effluvium (blood, necrotic epithelium, necrotic stroma, inflammatory cells, fibrin deposits) Corpus luteum degenerates → fall in progesterone/estrogen
42
Secretory Phase
in response to high progesterone (secreted by corpus luteum) Endometrial glands become more tortuous and secrete glycogen rich substance capable of sustaining conceptus before placenta forms Endometrial stroma becomes increasingly edematous
43
Proliferative Phase:
in response to ovarian estrogen Endometrial stroma proliferates, becomes thicker/highly vascular Tubular glands of stratum compactum invaginate, elongate, and become more coiled
44
Cryptorchidism
Undescended testis (Unilateral or bilateral) Impaired spermatogenesis due to increased intra-abdominal temperature -increased risk of germ cell tumors in undescended testis AND contralateral side - Atrophy evident as early as age 2 - Contralateral testis may also regress
45
Varicocele
Dilated veins in pampiniform plexus due to increased venous pressure Due to venous valve insufficiency Typically LEFT side (or bilateral in 10%) due to increased resistance to flow from L gonadal vein --> L renal vein -Can cause infertility (increased temperature) "bag of worms" on palpation does NOT transilluminate
46
cryptochidism -what lab values?
- LOW INHIBIN, INCREASED FSH and LH - TESTOSTERONE: low in bilateral, normal in unilateral Normal testosterone because Leydig Cells unaffected by temperature
47
Nonspecific Epididymitis/Orchitis
destruction, necrosis, and abscess formation | Due to urinary tract infection
48
Causes of Epididymitis/Orchitis in children vs. sexually active adults vs. elderly
Children - associated with urinary tract malformation (gram neg rods) Sexually active adults - C. trachomatis, N. gonorrhoeae Elderly - Enterobacteria
49
Mumps orchitis
atrophy due to blood supply restriction Pubertal or adult males 1 week after parotid swelling Unilateral in most cases (70%) Infertility uncommon
50
Tuberculous orchitis -what does it effect first - epididymus or testis?
Effects epididymis → then testis Usually part of systemic disease Formation of caseating granulomas
51
Syphilis inflammatory disease of the testes -what does it effect first - epididymus or testis? why?
Effects testis → then epididymis (effect inner part of testi first due to obliterative endarteritis) Congenital or acquired Plasma cells, lymphocytes present Obliterative endarteritis Gummas
52
Inflammatory disease of the testes: (4)
1) Nonspecific Epididymitis/Orchitis 2) Mumps orchitis 3) Tuberculous orchitis 4) Syphilis
53
Hydrocele
Fluid collection within the tunica vaginalis (serous membrane covering testicle and internal surface of scrotum) Associated with incomplete closure of processus vaginalis leading to communication with the peritoneal cavity (infants) or blockage of lymphatic drainage (adults) TRANSILLUMINATED scrotal swelling
54
Testicular Germ Cell Tumors (6)
1) Seminoma 2) Spermatocytic seminoma Non-seminoma: 3) Yolk sac (endodermal sinus) tumor 4) Choriocarcinoma 5) Teratoma 6) Embryonal Carcinoma 6) Mixed
55
Testicular Germ Cell Tumors
>95% of testicular tumors Pure or mixed (germ cell is pluripotent - tumor is pluripotent) Metastases can vary from primary Tends to occur in young men (15-30 yrs) PAINLESS testicular enlargement
56
Testicular Germ Cell Tumors: Predisposing factors?
Cryptorchidism genetic factors dysgenesis chromosomal changes (Kleinfelter)
57
Seminoma response to chemo? serum markers? frequency? can produce what?
Most common testicular tumor (50%) Radiosensitive and chemosensitive - good prognosis Serum markers negative In rare cases, may produce hCG
58
Seminoma appearance?
LARGE cells + CLEAR cytoplasm + CENTRAL nuclei --> resemble SPERMATOGONIA hematogenous mass with NO hemorrhage or necrosis
59
Embryonal carcinoma appearance
IMMATURE, PRIMITIVE cells that may produce GLANDS forms HEMORRHAGIC MASS with NECROSIS
60
Embryonal carcinoma response to chemo? aggressive or not? age effected?
Chemosensitive - BUT chemo may result in differentiation into another type of germ cell tumor** Aggressive, with early hematogenous spread Presents in 30's
61
Embryonal carcinoma serum markers? May also have increased _____ or ______
PLAP, placental lactogen, hCG May also have increased AFP or B-hCG
62
Yolk sac (endodermal sinus) tumor appearance?
Malignant tumor that resembles yolk sac elements Schiller-Duval Bodies (glomerulus-like structures) are seen on histology
63
Yolk sac (endodermal sinus) tumor - most common tumor in who? - what is usually elevated? - Prognosis
Most common testicular tumor in CHILDREN alpha-fetoprotein (AFP) elevated Prognosis relatively good
64
Choriocarcinoma appearance?
Malignant tumor of syncytiotrophoblasts and cytotrophoblasts (placenta-like tissue, but villi are absent)
65
Choriocarcinoma
Spreads early in BLOOD B-hCG characteristically elevated --> can lead to hypothyroidism or gynecomastia (a-subunit of hCG similar to FSH, LH, and TSH) Very rare, and aggressive with high rate of mets
66
Teratoma appearance?
tumor composed of mature fetal tissue derived from 2-3 embryonic layers Teratoma is benign in females, but MALIGNANT in males
67
Teratoma
Malignant transformation is common (any component can transform) Chemoresistant - slow to progress, but may undergo malignant change
68
Mixed germ cell tumors
Germ cell tumors are usually mixed Prognosis is based on the worst component
69
Sex cord / Stromal Tumors in Males
Usually benign 1) Leydig cell tumor 2) Sertoli cell tumor
70
Leydig cell tumor
usually produces androgen --> causes precocious puberty in children, gynecomastia in adults
71
Sertoli cell tumor
Comprised of tubules and is usually clinically silent
72
Condyloma Acuminatum
Benign warty growth on genital skin Due to HPV 6 or 11 Characterized by koilocytic change
73
Lymphogranuloma venereum
Necrotizing granulomatous inflammation of the inguinal lymphatics and lymph nodes Sezually transmitted disease caused by Chalmydia trachomatis (serotypes L1-L3) Eventually heals with fibrosis Perianal involvement may result in rectal stricture
74
Carcinoma in situ of the penis
plaque-like lesions, full thickness dysplasia replacing full thickness of squamous cells precursor to squamous cell carcinoma
75
Bowen's disease
Carcinoma in situ of the penile shaft or scrotum that presents as LEUKOPLAKIA
76
Erythroplasia of Queyrat
Carcinoma in situ of the GLANS that presents as ERYTHROPLAKIA
77
Bowenoid papulosis
Carcinoma in situ of the penis that presents as multiple reddish papules seen in younger patients (40s) relative to Bowen disease and erythroplasia of Queyrat Does NOT progress to invasive carcinoma
78
Squamous cell carcinoma of the penis
Malignant proliferation of squamous cells of penile skin Typically in patients 60-80 years of age Ulcerating rolled up lesion, highly destructive Precursor lesion: carcinoma in situ
79
Risk factors for Squamous cell carcinoma of the penis
High risk HPV (2/3 of cases) Lack of circumcision - foreskin acts as nidus for inflammation and irritation ir not properly maintained
80
Prostate anatomy: __________ zone surrounds the urethra __________ zone surrounds the ejaculatory duct that empties into prostatic urethra ________ zone is in the outer regions of the prostate
Transition zone Central zone Peripheral zone
81
________ zone is where prostate cancer typically arises ___________ zone is where Benign Prostatic Hyperplasia usually occurs
Peripheral zone = cancer Transition zone = BPH
82
Acute Prostatitis
Acute inflammation of the prostate, usually due to bacteria Presents with dysuria, fever, chills Prostate is tender and boggy on digital rectal exam Prostatic secretions show WBCs, culture reveals bacteria pus filled, focal or diffuse polymorphonuclear inflammation
83
Acute Prostatitis causes in young adults vs. older adults
- Chalmydia, N. gonorrhoeae in young adults - E. Coli, Pseudomonas in older adults Can be iatrogenic due to catheter insertion
84
Chronic Prostatitis
Chronic inflammation of the prostate presents as pelvic or low back pain Prostatic secretions show WBCs, but cultures are NEGATIVE Mononuclear cell inflammation Often associated with atrophy Typically asymptomatic Unclear etiology
85
Benign Prostatic Hyperplasia (BPH)
hyperplasia of prostatic stroma and glands (typically in transition zone - central periuretheral zone of prostate) Age-related change NO INCREASED RISK for cancer Blacks > whites > Asians
86
Pathophysiology of BPH
Related to DHT: - T --> DHT via 5a-reductase - DHT acts on androgen receptor of stromal and epithelial cells resulting in hyperplastic nodule
87
Clinical features of BPH
1) Problems starting and stopping urine stream 2) Impaired bladder emptying with increased risk of infection and hydronephrosis 3) Dribbling 4) Hypertrophy ofbladder wall smooth muscle (increased risk for bladder diverticula) 5) Microscopic hematuria 6) PSA may be slightly elevated (<10) due to increased number of glands
88
Treatment of BPH (4)
1) a1-antagonists (terazosin) --> relax smooth muscle (can also lower BP) 2) Selective a 1A-antagonists (temulosin) --> can be used in normotensive individuals to avoid a1B effects on blood vessels 3) 5a-reductase inhibitor --> block formation of DHT, takes months for results, can also treat male pattern baldness 4) TURP
89
Adenocarcinoma of the prostate epidemiology
Most common non-skin cancer of adult males Second leading cause of male cancer death, > 200,000 new cases per year, > 27,000 deaths per year More men die WITH PCa than of it Main risk factors = age, race (black > white > asian), and diet (high saturated fat)
90
Adenocarcinoma of the prostate
Malignant proliferation of prostatic glands Usually clinically silent -arises in PERIPHERAL and POSTERIOR region of prostate --> no urinary sx
91
Prostate cancer screening
Begin at age 50 with DRE and PSA PSA --> increases with age due to BPH -PSA > 10 --> highly worrisome Decreased % free PSA is suggestive of cancer because cancer makes bound PSA Prostatic biopsy used to confirm presence of carcinoma = GOLD STANDARD
92
Adenocarcinoma of the prostate Appearance
Small, invasive, glands with prominent (large) nucleoli Infiltrative pattern Single cell layer (loss of basal cells) Perineural invasian
93
How and where does prostate cancer spread?
Lymphatically AND hematogenously to axial skeleton (spine or pelvis) Presents as low back pain and increased ALK PHOS, PSA, and prostatic acid phosphatase (PAP)
94
Gleason grading system
based on ARCHITECTURE ALONE (NOT NUCLEAR ATYPIA) Multiple regions of tumor assessed because architecture varies from area to area Score (1-5) assigned for two distinct areas then added to produce final score (2-10) --> higher is worse prognosis
95
Treatment of Prostate cancer
Prostatectomy (localized disease) Hormone suppression (reduce T and DHT) --> Leuprolide (GnRH analog), or Flutamide (androgen receptor inhibitor)
96
Prostatic intraepithelial neoplasia
Can be noninvasive precursor to some prostate cancers (30-50% of prostates with PIN harbor prostate cancer) Genetic and molecular changes similar to PCa Frequency increases with age

Life Cycles (8 decks)

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