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Life Cycles > Week 2 > Flashcards

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
Q

Corpus Luteum

A

remnant of ovulated ovarian follicle, no oocyte present

Highly vascular → LH/FSH stimulate progesterone/estrogen secretion

Produces high levels of progesterone which supports pregnancy

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26
Q

Corpus Luteum if fertilization does NOT occur

A

No fertilization → CL degenerates (becomes fibrosed) 11 days after ovulation (Corpus Albicans)

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27
Q

Corpus Luteum if fertilization DOES occur

A

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

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28
Q

Large growing follicles containing eggs are needed to produce _______

A

estradiol

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29
Q

Local autocrine/paracrine factors influencing follicular matruation

A

Interleukins, growth factors (VEGF → increase blood flow to developing follicles)

-Activin

–Inhibin

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30
Q

Activin autocrine/paracrine effects

A

augments FSH, suppresses androgen production in theca cells (increases estrogen)

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31
Q

Inhibin autocrine/paracrine effects

A

later in follicular phase, enhances LH stimulation of androgen synthesis in theca cells → more substrate for estrogen synthesis in granulosa cell → LH surge

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32
Q

Dominant follicle

A

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)

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33
Q

2-Cell Theory of Sex Steroid Production

A

TWO cell types needed to produce estradiol

Theca → produce androgens that are taken up by Granulosa cells

Granulosa cells → convert androgen → estradiol

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34
Q

Layers of Endometrium

A

1) Stratum basalis

2) Stratum Functionalis (Stratum spongiosum + Stratum Compactum) –> shed during menstruation

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35
Q

Stratum basalis

A

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

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36
Q

Stratum spongiosum

A

thick intermediate layer between basalis and compactum

part of stratum funcitonalis

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37
Q

Stratum Compactum

A

superficial layer of endometrium

part of stratum funcitonalis

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38
Q

Spiral arteries

A

pass through basal layer into stratum functionalis

Hormonally sensitive

Constrict in response to hormonal shifts → stratum functionalis becomes ischemic → sheds

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39
Q

Straight arteries

A

feed stromal layer of endometrium

Do NOT infiltrate endometrium very deeply

40
Q

Endometrial Phases: (3)

A

1) Menstrual phase
2) Secretory phase
3) Proliferative phase

41
Q

Menstrual Phase

A

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
Q

Secretory Phase

A

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
Q

Proliferative Phase:

A

in response to ovarian estrogen

Endometrial stroma proliferates, becomes thicker/highly vascular

Tubular glands of stratum compactum invaginate, elongate, and become more coiled

44
Q

Cryptorchidism

A

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
Q

Varicocele

A

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
Q

cryptochidism

-what lab values?

A
  • LOW INHIBIN, INCREASED FSH and LH
  • TESTOSTERONE: low in bilateral, normal in unilateral

Normal testosterone because Leydig Cells unaffected by temperature

47
Q

Nonspecific Epididymitis/Orchitis

A

destruction, necrosis, and abscess formation

Due to urinary tract infection

48
Q

Causes of Epididymitis/Orchitis in children vs. sexually active adults vs. elderly

A

Children - associated with urinary tract malformation (gram neg rods)

Sexually active adults - C. trachomatis, N. gonorrhoeae

Elderly - Enterobacteria

49
Q

Mumps orchitis

A

atrophy due to blood supply restriction

Pubertal or adult males

1 week after parotid swelling

Unilateral in most cases (70%)

Infertility uncommon

50
Q

Tuberculous orchitis

-what does it effect first - epididymus or testis?

A

Effects epididymis → then testis

Usually part of systemic disease

Formation of caseating granulomas

51
Q

Syphilis inflammatory disease of the testes

-what does it effect first - epididymus or testis? why?

A

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
Q

Inflammatory disease of the testes: (4)

A

1) Nonspecific Epididymitis/Orchitis
2) Mumps orchitis
3) Tuberculous orchitis
4) Syphilis

53
Q

Hydrocele

A

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
Q

Testicular Germ Cell Tumors (6)

A

1) Seminoma
2) Spermatocytic seminoma

Non-seminoma:

3) Yolk sac (endodermal sinus) tumor
4) Choriocarcinoma
5) Teratoma
6) Embryonal Carcinoma

6) Mixed

55
Q

Testicular Germ Cell Tumors

A

> 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
Q

Testicular Germ Cell Tumors:

Predisposing factors?

A

Cryptorchidism

genetic factors

dysgenesis

chromosomal changes (Kleinfelter)

57
Q

Seminoma

response to chemo?
serum markers?
frequency?
can produce what?

A

Most common testicular tumor (50%)

Radiosensitive and chemosensitive - good prognosis

Serum markers negative

In rare cases, may produce hCG

58
Q

Seminoma

appearance?

A

LARGE cells + CLEAR cytoplasm + CENTRAL nuclei –> resemble SPERMATOGONIA

hematogenous mass with NO hemorrhage or necrosis

59
Q

Embryonal carcinoma

appearance

A

IMMATURE, PRIMITIVE cells that may produce GLANDS

forms HEMORRHAGIC MASS with NECROSIS

60
Q

Embryonal carcinoma

response to chemo?
aggressive or not?

age effected?

A

Chemosensitive - BUT chemo may result in differentiation into another type of germ cell tumor**

Aggressive, with early hematogenous spread

Presents in 30’s

61
Q

Embryonal carcinoma
serum markers?

May also have increased _____ or ______

A

PLAP, placental lactogen, hCG

May also have increased AFP or B-hCG

62
Q

Yolk sac (endodermal sinus) tumor

appearance?

A

Malignant tumor that resembles yolk sac elements

Schiller-Duval Bodies (glomerulus-like structures) are seen on histology

63
Q

Yolk sac (endodermal sinus) tumor

  • most common tumor in who?
  • what is usually elevated?
  • Prognosis
A

Most common testicular tumor in CHILDREN

alpha-fetoprotein (AFP) elevated

Prognosis relatively good

64
Q

Choriocarcinoma

appearance?

A

Malignant tumor of syncytiotrophoblasts and cytotrophoblasts (placenta-like tissue, but villi are absent)

65
Q

Choriocarcinoma

A

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
Q

Teratoma

appearance?

A

tumor composed of mature fetal tissue derived from 2-3 embryonic layers

Teratoma is benign in females, but MALIGNANT in males

67
Q

Teratoma

A

Malignant transformation is common (any component can transform)

Chemoresistant - slow to progress, but may undergo malignant change

68
Q

Mixed germ cell tumors

A

Germ cell tumors are usually mixed

Prognosis is based on the worst component

69
Q

Sex cord / Stromal Tumors in Males

A

Usually benign

1) Leydig cell tumor
2) Sertoli cell tumor

70
Q

Leydig cell tumor

A

usually produces androgen –> causes precocious puberty in children, gynecomastia in adults

71
Q

Sertoli cell tumor

A

Comprised of tubules and is usually clinically silent

72
Q

Condyloma Acuminatum

A

Benign warty growth on genital skin

Due to HPV 6 or 11

Characterized by koilocytic change

73
Q

Lymphogranuloma venereum

A

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
Q

Carcinoma in situ of the penis

A

plaque-like lesions, full thickness dysplasia replacing full thickness of squamous cells

precursor to squamous cell carcinoma

75
Q

Bowen’s disease

A

Carcinoma in situ of the penile shaft or scrotum that presents as LEUKOPLAKIA

76
Q

Erythroplasia of Queyrat

A

Carcinoma in situ of the GLANS that presents as ERYTHROPLAKIA

77
Q

Bowenoid papulosis

A

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
Q

Squamous cell carcinoma of the penis

A

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
Q

Risk factors for Squamous cell carcinoma of the penis

A

High risk HPV (2/3 of cases)

Lack of circumcision - foreskin acts as nidus for inflammation and irritation ir not properly maintained

80
Q

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

A

Transition zone

Central zone

Peripheral zone

81
Q

________ zone is where prostate cancer typically arises

___________ zone is where Benign Prostatic Hyperplasia usually occurs

A

Peripheral zone = cancer

Transition zone = BPH

82
Q

Acute Prostatitis

A

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
Q

Acute Prostatitis causes in young adults vs. older adults

A
  • Chalmydia, N. gonorrhoeae in young adults
  • E. Coli, Pseudomonas in older adults

Can be iatrogenic due to catheter insertion

84
Q

Chronic Prostatitis

A

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
Q

Benign Prostatic Hyperplasia (BPH)

A

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
Q

Pathophysiology of BPH

A

Related to DHT:

  • T –> DHT via 5a-reductase
  • DHT acts on androgen receptor of stromal and epithelial cells resulting in hyperplastic nodule
87
Q

Clinical features of BPH

A

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
Q

Treatment of BPH (4)

A

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
Q

Adenocarcinoma of the prostate

epidemiology

A

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
Q

Adenocarcinoma of the prostate

A

Malignant proliferation of prostatic glands

Usually clinically silent

-arises in PERIPHERAL and POSTERIOR region of prostate –> no urinary sx

91
Q

Prostate cancer screening

A

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
Q

Adenocarcinoma of the prostate

Appearance

A

Small, invasive, glands with prominent (large) nucleoli

Infiltrative pattern

Single cell layer (loss of basal cells)

Perineural invasian

93
Q

How and where does prostate cancer spread?

A

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
Q

Gleason grading system

A

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
Q

Treatment of Prostate cancer

A

Prostatectomy (localized disease)

Hormone suppression (reduce T and DHT) –> Leuprolide (GnRH analog), or Flutamide (androgen receptor inhibitor)

96
Q

Prostatic intraepithelial neoplasia

A

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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