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Life Cycles > Week 3 > Flashcards

Week 3 Flashcards

1
Q

General principles of contraception: 7 main strategies

A

1) Stop/block production of sperm
2) Block sperm entry into/past cervix
3) Thicken cervical mucosa: Progestin methods
4) Ligate/occlude/remove fallopian tube
5) Prevent ovulation (Progestin alone, Progestin + Estrogen Combo)
6) Avoid intercourse when ovulating
7) Thin endometrium to prevent implantation (Progestin)

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2
Q

Effects of exogenous Progestin (6)

A

1) Inhibits ovulation by suppressing function of HPO axis
2) Modifies midcycle surges of LH and FSH
3) Diminishes ovarian hormone production
4) Reduces activity of cilia
5) Produces endometrial changes unfavorable to embryo implantation
6) Thickens cervical mucus to impede sperm transit

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3
Q

Effects of exogenous estrogen (4)

A

1) Helps stabilize uterine lining → less breakthrough bleeding
2) Added suppression of FSH - less follicle development
3) Increases SHBG → less male effects (i.e. acne)
4) Reduces ovarian cancer, endometrial, colon cancer risks

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4
Q

Risks of estrogen

A

CLOTTING

Increases clotting factors 2, 7, 10, 12, 8, and fibrinogen → shift towards thrombus formation and prevention of clot dissolution → greater risk of venous and arterial clot formation

Higher estrogen = more clotting factors

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5
Q

Who should avoid contraception with estrogen?

A

Smoker > age 35

CAD, heart disease, history of clots (DVT, PE), uncontrolled HTN, diabetes with vascular changes

Migraines with aura

Active liver/gallbladder problems

Breast cancer (Estrogen dependent cancers)

Major surgery with prolonged immobilization

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6
Q

Copper IUD:

A

Creates inflammatory reaction in uterus

Copper acts as spermicide

Non-hormonal method

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7
Q

Emergency contraceptive options

A

prevent pregnancy AFTER sex

Mechanism: NOT the same as abortion pill, is basically contraceptives at a much higher dose

1) Plan B: Levonorgestrel, progestin only (75% efficacy)
2) Copper IUD: 99% effective
3) Ella: ulipristal acetate = progesterone receptor modulator, better efficacy than Plan B

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8
Q

Squamocolumnar junction of cervix

A

between stratified squamous epithelium of ectocervix and glandular columnar epithelium of endocervix

Area where 99% of HPV-associated cervical cancer arise

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9
Q

2013 recommendations for cervical cancer screening:

A

Cervical cytology screening should begin at age 21

Cervical cytology is recommended every 3 years for women between ages of 21-29 years

Cervical cytology screening with HPV co-testing is recommended every 5 years for women between age 30-65

Cervical cytology screening should stop for women at age of 65 years if she has been adequately screened and had not had CIN2 or CIN3 lesions for previous 20 years

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10
Q

Goal of screening for cervical carcinoma

A

Catch DYSPLASIA (CIN) before it develops into carcinoma

Progression from CIN –> carcinoma takes 10-20 years

PAP SMEAR = GOLD STANDARD

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11
Q

What do you do if you get an abnormal Pap smear test?

A

-Confirmatory colposcopy (visualization of cervix with magnifying glass) and biopsy

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12
Q

Limitations of the Pap smear?

A

Inadequate sampling of transformation zone (false negative screening)

Limited efficacy in screening for adenocarcinoma

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13
Q

Human Sexual Response Cycle

Four phases:

A

Excitement
Plateau
Orgasm
Resolution

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14
Q

Desire phase

A

no measurable physiologic changes, desire is different than attraction and can be augmented or inhibited by learned responses and experiences

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15
Q

Arousal/Excitement Phase

A

physiologic changes occur

1) Increased pulse and respiration
2) Shift blood flow to pelvis and genitalia
3) Shift in blood flow to skin
4) Nipple erection

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16
Q

Erection in men mechanism?

A

increased penile blood flow due to relaxation of penile arteries and corpus cavernosal smooth muscle

Mediated by release of NO from nerve terminals and endothelial cells → cGMP synthesis in smooth muscle cells → muscle relaxation, increased blood flow to corpus cavernosum

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17
Q

Plateau Phase

A

heightened state of arousal, physiologic changes are stable

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18
Q

Orgasm Phase

A

series of rhythmic contractions of the perineal muscles

Male → 3-7 ejaculatory spurts of seminal fluid

Female → elevation of “orgasmic platform” (posterior vaginal wall - levator ani, pubococcygeus)

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19
Q

Resolution phase

Males

A

orgasm followed by obligatory resolution phase - return to baseline, further stimulation cannot produce excitement

Varies in length from 5 minutes to 24 hours or longer

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20
Q

Resolution phase

Females

A

resolution not always obligatory, can have repeated orgasm without resolution to a basal state

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21
Q

Medical Model of Sexual Dysfunction: 4 parts

A

Sex is a physiologic process

Sexual dysfunctions result from alterations in physiology

Alterations come from “blocks” or interruptions in the sexual response cycle

Emotional responses may alter or stop response cycle

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22
Q

PDE5 inhibitors

A

Sildenafil, Vardenafil, Tadalafil

Inhibits breakdown of cGMP

No effect on absence of sexual stimulation

Side effects: headaches, dizziness, flushing, sudden hearing loss, anterior optic neuropathy

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23
Q

Desire Phase Disorders: (2)

A

almost always due to performance anxiety or aversion

1) Low Libido - Hypoactive Sexual Desire Disorder:
2) Inhibited sexual desire - Sexual Aversion Disorder:

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24
Q

Hypoactive Sexual Desire Disorder

A

Causes: Chronic disease, depression, hypoestrogenic states

Persistently or recurrently deficient sexual/erotic thoughts or fantasies and desire for sexual activity

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25
Q

Sexual Aversion Disorder

A

Results of pain or other dysfunction

Sexual aversion and HSDD are a continuum

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26
Q

Dyspareunia

A

pain with intercourse

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27
Q

Vaginismus

A

involuntary spasm of muscles around outer third of vagina

Makes penetration impossible

Causes: pain, religious orthodoxy, negative parental attitudes

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28
Q

Primary ovarian tumors: list them

A

1) Epithelial neoplasms (60-70% of ovarian tumors)
- Serous
- Mucinous
- Endometroid
- Clear cell

2) Germ cell (15-20%)
-Teratomas
-Dysgerminoma
-Yolk Sac tumor
Choriocarcinoma

3) Sex Cord Stromal Neoplasms: 5-10%
- Granulosa cell tumors
- Fibromas and thecomas
- Sertoli-Leydig cell tumors

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29
Q

Major risk factors for ovarian tumors?

A

Infertility, unopposed estrogen > 10 years, family history, nulliparity
BRCA1 and 2

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30
Q

BRCA1 and BRCA2

  • what chromosomes?
  • results in what kind of cancer?
A

BRCA1: Ch17
BRCA2: Chr13

DNA repair genes

Breast and ovarian cancer risk

Typically high grade SEROUS carcinoma*

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31
Q

Epithelial ovarian neoplasms can be ______, _______ or _________.

4 subtypes?

A

benign, borderline, or malignant

  • Serous
  • Mucinous
  • Endometroid
  • Clear cell
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32
Q

Epithelial ovarian neoplasms are derived from __________ that lines the ovary and fallopian tubes

–> fimbriated end of fallopian tube may be origin

A

coelomic epithelium

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33
Q

Benign epithelial ovarian neoplasms = ________

main features?
in pre or post menopausal women?

A

Cystadenomas

Single cyst, simple, flat lining

Usually in PREmenopausal women (30-40 years)

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34
Q

Malignant epithelial ovarian neoplasms = ________

main features?
in pre or post menopausal women?

A

Cystadenocarcinomas

  • Complex cysts with thick, shaggy, lining
  • Hemorrhage, necrosis, rapidly increasing abdominal girth

Usually in POSTmenopausal women (60-70 yrs)

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35
Q

Serous epithelial ovarian neoplasm

Main features?
main buzz words (2)

what serum marker is elevated?

A

Full of water fluid, usually also cystic
Most frequent subtype

1) HIERARCHICAL BRANCHING* cuboidal cells (resemble tubal epithelium, but without cilia)
2) PSAMMOMA BODIES*

Increased CA-125 marker

BRCA1 –> increased risk for SEROUS carcinoma

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36
Q

Mucinous epithelial ovarian neoplasm

Main features?
main buzz words (1)

A

full of mucus-like fluid, usually also cystic

Huge tumors

1) Can have GOBLET CELLS** present

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37
Q

Clear cell epithelial ovarian neoplasm

2 main buzzword features

A

Very rare, but may be aggressive

1) Associated with ENDOMETRIOSIS**
2) “HOBNAIL CELLS” - nuclei bulging into cystic space without apparent cytoplasm**

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38
Q

Endometrioid epithelial ovarian neoplasm

Main buzzword/fetature?

A

*Resemble normal endometrial glands - same appearance as uterine endometrioid tumors

**→ MUST exclude metastasis from uterine tumor

Usually are malignant

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39
Q

Sex Cord Stromal Neoplasms

Include what 3 subtypes?

A

Granulosa cell tumors

Fibromas and thecomas

Sertoli-Leydig cell tumors

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40
Q

Granulosa cell tumors

2 buzzword histology features?

Presentation?

A

Neoplastic proliferation of granulosa cells

Often produce estrogen → presents with signs of estrogen excess

1) Call-Exner Bodies** (resembles primitive follicle)
2) and nuclear grooves

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41
Q

Fibromas

A

benign tumor of fibroblasts

can get Meig’s Syndrome

Appears fibrous and pink

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42
Q

Meig’s Syndrome

A

Associated with pleural effusions and ascites = Meig’s Syndrome

Resolves with removal of tumor

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43
Q

Sertoli-Leydig cell tumors

A

Recapitulates developing testis
-Composed of Sertoli cells that form tubules and Leydig cells with characteristic Reinke crystals

May produce androgen → hirsutism and virilization

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44
Q

Germ Cell Tumors

subtypes?

A

1) Mature and Immature Teratomas
2) Dysgerminoma
3) Yolk sac tumors (aka endodermal sinus tumor)
4) Choriocarcinoma

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45
Q

Mature cystic teratoma

Females

A

BENIGN in females

Composed of fetal tissue derived from two or three embryologic layers (skin, hair, bone, cartilage, gut, etc.)

Usually occurs in reproductive years

Can be bilateral

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46
Q

Struma ovarii

A

teratoma composed primarily of thyroid tissue

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47
Q

Immature teratoma

Females

A

malignancy
Microscopic identification of immature neuroepithelium

Tightly packed small dark cells with lots of mitoses

Grading based on amount of immature neural tissue (more is worse)

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48
Q

Dysgerminoma

histological appearance?
prognosis?
what is elevated in serum?

A

Composed of large cells with clear cytoplasm and central nuclei (resemble oocytes) - Female counterpart to seminoma

Can be bilateral

Good prognosis

Serum LDH elevated

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49
Q

Yolk Sac Tumors (aka endodermal sinus tumor)

Histology?
Buzz word for histology?

Elevated serum levels of what?

A

Malignant tumor that mimics yolk sac

Most common germ cell tumor in children

High AFP

Contains SCHILLER-DUVAL BODIES (glomerulus-like structures)

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50
Q

Choriocarcinoma

malignant tumor composed of what two cell types?

Mimics what tissue?

How does it spread?

What is elevated in the patients serum?

Response to chemo?

A

Malignant tumor composed of cytotrophoblasts and syncytiotrophoblasts

Mimics placental tissue but villi are ABSENT

Small, hemorrhagic with early hematogenous spread

High B-hCG

Poor response to chemo

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51
Q

Krukenberg Tumor

A

metastatic mucinous tumor, involves both ovaries

Most commonly metastatic GASTRIC CARCINOMA

SIGNET RING CELL morphology

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52
Q

Pseudomyxoma peritonei

A

“Jelly Belly”

Mucin throughout abdomen

Can be due to mucinous tumor of the appendix with metastasis to the ovary

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53
Q

Fallopian Tube Pathology:

Intraepithelial Carcinoma (TIC):

A

Precursor lesion to most ovarian high grade serous carcinomas

Derived from fimbriated end of fallopian tube

Typically p53 mutations

54
Q

Ectopic pregnancy

A

Implantation of fertilized ovum at site other than uterine wall

Most common (90%) in fallopian tube

Key risk factor is scarring (PID)

Rupture = medical emergency,

Can cause hematosalpinx (bleeding into fallopian tube)

Presentation: lower abdominal pain after missed period

55
Q

Inhibin A vs. B

A

Inhibin A - important in luteal phase

Inhibin B - important in follicular phase of menstrual cycle

56
Q

Approach to evaluating Disturbances in Menstrual Cycle:

3 things you want to check, and 2 things you do NOT want to check

A

1) Exclude pregnancy (B-hCG)
2) Rule out high prolactin
3) DO NOT need androgen levels or GnRH stimulation test
4) Draw LH and FSH levels in first 5 days after menses starts (normally LH=FSH)

57
Q

Hypogonadotropic Hypogonadism (women)

A

low LH, FSH, and estradiol with amenorrhea

58
Q

Hypogonadotropic Hypogonadism (women)

causes

A

1) Congenital GnRH deficiency (Kallmann Syndrome)

2) Acquired GnRH deficiency
- Hypothalamic amenorrhea

59
Q

Hypothalamic amenorrhea

A

Acquired GnRH deficiency

defects in amount of frequency of GnRH pulses - usually do to stress, exercise, or poor nutrition

60
Q

Hypergonadotropic hypogonadism (women)

A

high FSH and/or LH, low estradiol and amenorrhea

61
Q

Hypergonadotropic hypogonadism (women)

two congenital causes

1 acquired cause

A

1) Congenital:
- Turner Syndrome
- Gonadal dysgenesis (XO, XX/XO)

2) Acquired:
- Premature ovarian insufficiency (POI)

62
Q

Premature ovarian insufficiency (POI)

  • definition
  • pathophys
A

ovarian failure before age 40

Typically due to autoimmune process (associated with autoimmune thyroid disease, T1DM, celiac, pernicious anemia)

63
Q

Premature ovarian insufficiency (POI)

presentation (symptoms)
labs?

A

Presentation: irregular menses, without moliminal symptoms (breast tenderness, bloating, and cramping)

LABS:

  • FSH levels rise before LH levels due to loss of inhibin
  • FSH>LH in early follicular phase, low E2
64
Q

Hyperandrogenic anovulation:

3 causes

A

1) Polycystic ovarian syndrome (PCOS)
2) Tumors causing hirsutism
3) Obesity induced anovulation

65
Q

Polycystic ovarian syndrome (PCOS)

mechanism?

A

-high amplitude GnRH pulses causes oversecretion of LH

high LH –> theca cell stimulation and over production of androgens

decreased FSH causes follicular degeneration with fluid filled cyst formation

66
Q

PCOS

presentation

Labs?

A

Presentation: irregular menses, anovulation, hirsutism, acne, obesity, insulin resistance

Labs:

  • High LH/FSH > 2.5/1
  • Increased androgens (testosterone and DHEAS)
67
Q

Patients with PCOS are at increased risk for what?

A

increased risk of endometrial cancer (estrogen unopposed by progesterone), insulin resistance, diabetes, HTN, cardiac disease

68
Q

Tumors causing hirsutism

pathophysiology?

A

virilizing tumors of ovary (testosterone producing) or adrenals (DHEA-S producing)

69
Q

Tumors causing hirsutism

presentation?
labs?

A

Presentation: rapid onset, male pattern balding, hair on upper chest and back, clitoromegaly

Labs: Testosterone > 200 or DHEAS > 800 suggest TUMOR

70
Q

Obesity induced anovulation

labs and presentation?

A

normal puberty and cycles until high weight

Labs: LH=FSH (normal) and mild elevations in androgens

71
Q

Mechanism of estrogen agonist action?

how does this differ from estrogen antagonist action?

A

AGONIST:

  • diffuse through membrane → enter nucleus and bind to an ER → conformational change → receptor dimerization
  • ER dimers bind ERE in promoter regions of target genes → recruit co-activators → initiate transcription

ANTAGONIST
-antagonists of ERs also promote dimerization and DNA binding, but causes different conformational change and recruits co-REPRESSORS and REDUCES transcription

72
Q

Effects of estrogen on development? (3)

A

Promote development of vagina, uterus, and breast

Secondary sex characteristics-axillary/pubic hair, fat distribution

Accelerated growth phase and closing of epiphyses of long bones at puberty

73
Q

Physiologic effects of estrogen (4)

A

1) Breast growth
2) Endometrial growth → activates endometrium in proliferative phase
3) Decrease bone osteoclast function
4) Liver - Decreases LDL, increase HDL, increase clotting factors

74
Q

Adverse effects of estrogen administration (8)

A

1) Clotting

2) Endometrial and breast cancer
- -> Endometrial cancer risk reduced if given with progestin

3) Postmenopausal bleeding
4) Nausea, breast tenderness
5) Anorexia, vomiting, diarrhea
6) HTN
7) Increased migraine headache frequency
8) Gallstones

75
Q

Contraindications of estrogen use (4)

A

1) History of breast or endometrial cancer
2) Vaginal bleeding
3) Acute liver disease
4) Active thrombosis

76
Q

Menopausal Hormonal Therapy: ESTROGEN (3)

A

want lowest effective dose and for shortest duration

1) Vasomotor symptoms → systemic treatment
2) Vulvovaginal and urogenital complaints (vaginal dryness, pruritus) → local application vaginal products preferred
3) Prevention of osteoporosis → ONLY consider if pt at SIGNIFICANT risk of osteoporosis

77
Q

Physiologic vs. pharmacologic administration of estrogen

A

“Physiologic replacement” → hypoestrogenic menopausal symptoms
5-10 mcg ethinyl estradiol

“Pharmacologic suppression” of ovulation
20-35 mcg ethinyl estradiol in oral contraceptive

78
Q

Medroxyprogesterone (megestrol)

A

Progesterone type

less effect on pituitary, mainly peripheral actions (endometrial tissue)

79
Q

Norethindrone

A

Progesterone type

1st gen progesterone

80
Q

Levonorgestrel

A

Progesterone type

2nd gen progesterone

→ increased androgenic actions**

81
Q

Desogestrel-norethynodrel-norgestimate

A

Progesterone type

3rd gen progesterone

*LOWER ANDROGENIC ACTIONS
higher VTE risk

82
Q

Drospirenone

A

4th gen progesterone

antimineralocorticoid and antiandrogenic activity → increased VTE risk

83
Q

Effect of progesterone on endometrium?

A

*ANTI-ESTROGENIC action on ENDOMETRIAL proliferation

84
Q

Progesterone

adverse reactions

A

Depression, somnolence headache

Breast enlargement/tenderness

Nausea

Elevated BP, edema, weight gain

Osteoporosis (suppress FSH and LH → estradiol levels lower)

85
Q

Raloxifene

mechanism?

A

SERM

Agonist activity on BONE receptors (increase bone mineral density) and LIVER receptors (decrease LDL and total cholesterol)

ANTAGONIST activity (growth promoter) in UTERINE and BREAST tissue

86
Q

Raloxifene

use?

what are the benefits of Raloxifene over Tamoxifen?

A

Prevention of osteoporosis, postmenopausal therapy

Raloxifene has NO effect on breast or endometrial tissue → no increased risk of breast cancer

87
Q

Adverse effects of Raloxifene?

A

Still have increased clotting (via hepatic synthesis of clotting factors)

Hot flashes

88
Q

Tamoxifen

how does it differ from Raloxifene in mechanism and use?

A

has receptor action in endometrial → increase risk of endometrial cancer (NOT present in Raloxifene), but still protects against breast cancer

Use: treatment and prevention of breast cancer

89
Q

Adverse reactions of tamoxifen? (3)

A

Increased incidence of endometrial cancer (5 FOLD!)

Hot flashes

Thromboembolic disorders

90
Q

Drug interactions with oral contraceptives?

A

drugs that induce or enhance estrogen metabolism (CYP450) → reduction in contraceptive effect

Rifampin, anticonvulsants (phenytoin, carbamazepine, phenobarbital), griseofulvin

91
Q

Lichen sclerosis

A

smooth white plaques/papules
- Thinning of epidermis and fibrous (sclerosis) of dermis**

  • Presents as LEUKOPLAKIA with parchment-like vulvar skin
  • Typically in postmenopausal women - possible autoimmune etiology
  • Benign - can have slightly increased risk for SCC
92
Q

Lichen Simplex Chronicus

A

hyperplasia of vulvar squamous epithelium

  • LEUKOPLAKIA + leathery vulvar skin
  • Associated with chronic irritation and scratching
  • NO increased risk of SCC (benign)
93
Q

Condyloma acuminatum:

A
  • verrucous (cauliflower), multifocal
  • Caused by HPV 6 and 11
  • Hyperkeratosis (thickened stratum corneum with “ghost” nuclei) and parakeratosis (especially papillae tips)
  • Hypergranulosis and elongated rete ridges

**Koilocytes (crinkly raisin)
Rarely progresses to carcinoma

94
Q

Molluscum contagiosum

A

flesh colored, pearly skin lesions

Endophytic growth with eosinophilic inclusions
Self-limited (no tx)
Benign

95
Q

Trichomonas:

A

flagellated protozoan infection
Frothy yellow discharge
Dysuria, dyspareunia
“Strawberry cervix” on colposcopy

96
Q

Candida:

A

normal, but can overgrow (DM, abx, pregnancy)

Curd-like discharge and pruritis

97
Q

Vulva drains to ____ lymph nodes

A

inguinal

98
Q

Vulvar Intraepithelial Neoplasia (VIN):

A

Nuclear atypia (Koilocytic) and lack of maturation = DYSPLASIA

  • Increased mitoses, full thickness dysmaturity (cells at surface look the same as those near the base)
  • Precursor lesion for SCC
99
Q

Vulvar Carcinoma:

A

carcinoma from squamous epithelium lining vulva
Rare

Presents as LEUKOPLAKIA

Caused by HPV (high risk 16 and 18) or non-HPV causes (e.g. long standing lichen sclerosis)

100
Q

HPV-Associated SCC:

A

Females, less than 60 years

VIN is precursor lesion

10-20 yrs from initial infection until tumor forms

Appearance: infiltrating irregular nests of malignant squamous cells eliciting a desmoplastic stromal response

101
Q

Inflammatory associated SCC:

A

Females > 70 years

HPV negative

Lichen sclerosus/d-VIN precursor lesions
Prominent keratin pearls in well-differentiated carcinoma + increased mitoses, and pink cytoplasm

102
Q

Extramammary Paget Disease:

A
  • Malignant epithelial cells in epidermis of vulva
  • Presents as erythematous, pruritic, ulcerated vulvar skin
    Represents carcinoma in situ with NO underlying carcinoma (ISOLATED TO EPIDERMIS)
  • Paget disease OF NIPPLE almost always associated with underlying carcinoma
103
Q

Extramammary paget disease must be distinguished from ____

A

Melanoma

Pagets = PAS+, keratin +, S100-

Malignant Melanoma: PAS-, keratin-, S100+

104
Q

Embryonal rhabdomyosarcoma:

A

aka sarcoma botryoides
- Malignant mesenchymal proliferation of immature skeletal muscle

  • Presents as bleeding + grape-like mass protruding from vagina or penis of a child (<5yrs)
  • Rhabdomyoblast
105
Q

Rhabdomyoblast

A

characteristic cell of rhabdomyosarcoma

Cytoplasmic cross-striations
Desmin +, Myogenin +

106
Q

Adenosis:

A

focal persistence of columnar epithelium in the upper vagina (derived from MULLERIAN DUCT)

Columnar epithelium of upper vagina typically replaced by squamous epithelium of lower ⅓ of vagina during development

Increased incidence in females we were exposed to DES in utero

107
Q

Clear cell adenocarcinoma:

A

Malignant proliferation of glands with clear cytoplasm

Rare - Associated with DES vaginal adenosis

108
Q

Vaginal carcinoma:

A

Carcinoma arising from squamous epithelium lining the vaginal mucosa

  • Usually related to high risk HPV
  • Precursor lesion = VAIN (vaginal intraepithelial neoplasia)
  • Spreads to regional lymph nodes:
109
Q

Lower 1/3 of vagina drains to ____ lymph nodes

A

inguinal

110
Q

Upper 1/3 of vagina drains to ____ nodes

A

Iliac

111
Q

Endocervical polyps:

A
  • Can cause “spotting”
  • Curettage curative
  • Dilated mucus-secreting glands and inflammation
112
Q

Cervical Intraepithelial Neoplasia (CIN)

A

Koilocytic change, disordered cellular maturation, nuclear atypia, increased mitotic activity within cervical epithelium
Precursor lesion to SCC

113
Q

CIN grades:

A

higher grade = more likely to progress to SCC

CIN I = < ⅓ thickness of epithelium
CIN II = < ⅔ thickness of epithelium
CIN III = slightly less than entire thickness of epithelium
CIS = entire thickness of epithelium

114
Q

Cervical Squamous Cell Carcinoma (6)

A
  1. Invasive carcinoma that arises from cervical epithelium
  2. Typically in middle-aged women (age 40-50 yrs)
  3. Presentation: vaginal bleeding, post-coital bleeding, cervical discharge
  4. HPV related malignancy (16/18)
  5. Related to immunodeficiency (cervical carcinoma = AIDS defining illness)
  6. *Unlike endometrial cancers, the STAGING of cervical cancers is based on clinical features
115
Q

Cervical cancer: Adenocarcinoma in situ: (AIS)

A

15% of cervical cancer cases
HPV related

Histology: hyperchromasia, mucin depletion, luminal mitoses, high N:C

116
Q

Endometrial Polyps:

A

hyperplastic protrusion of endometrium

Presents as abnormal uterine bleeding

Dense pink stroma, haphazardly arranged glands

117
Q

Acute endometrits

A

bacterial infection of endometrium usually due to retained products of conception

Presents as fever, abnormal uterine bleeding, pelvic pain

Increase PMNs in stroma and glands

Curettage curative

118
Q

Chronic endometritis

A

Chronic inflammation of endometrium

Plasma cell and lymphocyte infiltrate

Causes: retained products of conception, chronic PID (Chlamydia, Gonorrhea, etc.), IUDs, TB

Presents as abnormal uterine bleeding, pain, and INFERTILITY

119
Q

Endometriosis/Adenomyosis

A

Endometrial glands AND stroma OUTSIDE uterine endometrial lining

*Adenomyosis: (endometrial glands and stroma WITHIN UTERINE WALL), uterine myometrium involvement

Extrauterine = endometriosis
Most common site of involvement is ovary → “Chocolate cyst”
Can increase risk for carcinoma at site of endometriosis (especially in ovary)

120
Q

Presentation of endometriosis/adenomyosis

A

dysmenorrhea, may cause Infertility

121
Q

Endometrial hyperplasia

A

hyperplasia of endometrial glands relative to stroma

Due to unopposed estrogen (obesity, PCOS, estrogen replacement)

Presents as postmenopausal bleeding

Can progress to carcinoma

Most important predictor for progression is presence of CELLULAR ATYPIA

122
Q

Simple hyperplasia:

A

increased gland to stroma ratio

Rarely progresses to cancer
Treated with progestins

123
Q

Complex hyperplasia:

A

+/- cytologic atypia

Glandular crowding and architectural complexity
5-30% progress to cancer

124
Q

Leiomyoma:

A

BENIGN neoplastic proliferation of smooth muscle arising from myometrium

Related to estrogen exposure

Multiple, spherical, firm, “white whorled”, WELL CIRCUMSCRIBED*
Most common uterine tumor

125
Q

Treatment of leiomyoma

A

Surgery, embolization, GnRH agonist, nothing

126
Q

Leiomyosarcoma

A

Malignant proliferation of smooth muscle arising from myometrium

Arise de novo (NOT from leiomyoma)

Usually in postmenopausal women

SINGLE lesion with areas of NECROSIS and HEMORRHAGE

INFILTRATING polypoid mass

Most common uterine sarcoma

Rapid increase in size, metastasizes to lungs, low survival

127
Q

Endometrial carcinoma

A

malignant proliferation of endometrial glands
Most common invasive carcinoma of female genital tract

Usually presents as postmenopausal bleeding, but many asymptomatic

128
Q

Type I endometrial carcinoma:

A

endometrioid adenocarcinoma

Molecular pathway: PTEN → KRAS → b-catenin

HYPERPLASIA pathway - arises from endometrial hyperplasia

Minimal invasion/spread

Endometrioid histology (looks like normal endometrium)

Perimenopausal - age 60

129
Q

Risk factors for endometrial carcinoma

A
  1. Genetics: HNPCC (MMR genes and microsatellite instability)
    - MLH1 and MSH2 gene mutations - typically
    - SOMATIC mutations (non-germline)
    - Colon + endometrial cancer
  2. Unopposed estrogen (PCOS, obesity, etc.)
130
Q

Type II endometrial carcinoma:

A

serous adenocarcinoma
Postmenopausal* - 70 years

  • Aggressive - Disseminated at presentation
  • 10-20% of endometrial cancers
  • Papillary structures, psammoma bodies
131
Q

Molecular pathway of Type II endometrial carcinoma

A

53 driven**
SPORADIC pathway
Carcinoma arises in atrophic endometrium with no evident precursor lesion

132
Q

Staging vs. Grading of uterine cancers:

A

Uterine cancers: Prognosis depends on STAGE (extent of spread)

Life Cycles (8 decks)

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