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Sex & Reproduction > SexReproFlashcards > Flashcards

SexReproFlashcards

1
Q

What is the function of breasts?

A

Production and secretion of milk

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2
Q

Where are breasts located/

A

Superior chest wall overlying the fascia coveirng the pectoralis muscles

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3
Q

What do breasts look like on histology?

A

15-25 lobes open into the nipple via lactiferous ducts

Interlobar connective tissue divides lobes into lobules

Each lobule ends in a terminal duct lobular unit (TDLU)

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4
Q

What is the functional unit of a breast?

A

TDLU - hormonally responsive and undergoes cyclic changes with menstrual cycle

PRoliferates and enlarges in pregnancy, with milk secretion during lactation

Atrophic changes after menopause

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5
Q

What is mastitis?

A

Breast inflammation

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6
Q

What are signs and symptoms of mastitis?

A

Tenderness, redness, induration

Ocacasionally forms an abscess

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7
Q

What are teh two types of mastitis?

A

Puerperal (lactational)

Non-puerperal (non-lactational)

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8
Q

What is lactational mastitis?

A

Duct obstuction and milk leakage (breast milk cytoines induce inflammatory response?)

Abscesses with staph and strep spp

Symptoms inclue pain, burning, redness ,fever and swelling

Diagnose iwth H&P, ultrasound to rule out abscess

Treat with antibiotics

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9
Q

What are symptoms of lactational mastitis?

A

pain, burning, redness, fever, swelling

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10
Q

How do you treat lactational mastitis?

A

Antibiotics

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11
Q

How does lactational mastitis present?

A

Pain, burning, redness, fever, swelling,

Duct obstruction and milk leakage

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12
Q

What do we see here?

A

Abscess formation in lactational mastitis

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13
Q

What can cause non-puerperal mastitis?

A

Duct ectasia, fat necrosis, granulomatous mastitis, inflammatory carcinoma

may present as a breast mass!

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14
Q

What are important factors of a history when evaluating a patient witha breast mass?

A
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15
Q

What are clinical exam features of breast masses that are useful for identifying malignancy vs benign?

A
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16
Q

What od we see here?

A

Duct ectasia - dilated duct

Non-puerperal mastitis

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17
Q

What is duct ectasia?

A

Non-puerperal mastitis that typically presents in older women

Duct dilation and secretory stasis, presenting with periductal inflammation and fibrosis

Signs and symptoms of mastitis

Antibiotics can be useful

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18
Q

What is fat necrosis non puerperal matitis?

A

sterile mastitis

Trauma, radiation or surgery that can damage fat cells

Inflammation, free fatty acids released complex with calcium to form soaps and can form white chalky deposits

May form lump

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19
Q

How are fat necrosis non puerperal mastitis treated?

A

Self-limited, goes away on own

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20
Q

What is granulomatous mastitis?

A

Inflammation caused by ruptured silicone breast implants or TB

Clinical history is helpful

Ultrasound or mammography can be used, but biopsy is diagnostic

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21
Q

What do we see here?

A

Wight foreign material and foreign body giant cells

Granulomatous mastitis

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22
Q

What is inflammatory carcinoma non puerperal mastitis?

A

Reddening of breast skin simulates dermatitis and ocurs in association with underlying breast cancer

Dermal lymphatic invasion by cancer cells leads to erythema nad edema ‘peau d’orange’ skin

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23
Q

What do we see here?

A

Dilated dermal lymphatic spaces distended by a tumor

inflammatory carcinoma non puerperal mastitis

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24
Q

What is fibrocystic change?

A

Benign condition of breast

affects 30-60% of reproductive aged women

Noncancerous breast lumpiness that can cause discomfort and related to menstrual cycle

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25
Q

When do women with fibrocystic change present typically?

A

30s

FIbrosis and cysts cause lumpiness over years

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26
Q

How is the lumpiness of fibrocystic change?

A

Freely mobile with smooth contours

Features of benignity

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27
Q

How is the discomfort of fibrocystic change?

A

Pain/tenderness peak before each menses and diminsih afterwards

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28
Q

How do you diagnose fibrocystic change?

A

Hystory and PHysical

If findings are intermediate - mammography then ultrasound, then biopsy

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29
Q

How does fibrocystic hcange look on histology?

A

Duct dilation and fibrosis

Apocrine metaplasia

+/- microcalcifications

may or may not epithelial hyperplasia

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30
Q

What do we see here?

A

Duct dilation (top)

Apocrine metaplasia (bottom)

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31
Q

What is the importance of duct epithelial hyperplasia in fibrocystic change?

A

Can indicate proliferative fibrocystic change (vs nonproliferative), which has an increased risk of progressing to cancer

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32
Q

What do we see here?

A

Series of fibrocystic change slides

Left: nonproliferative (no cancer risk)

mid: apocrine metaplasia with moderate proliferation (inreased risk)
right: atypical duct epithelial hyperplasia (4-5x risk of cancer)

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33
Q

How do you treat fibrocystic change?

A

Symptomatic releif

fitted bra for good support

painkilllers (NSIADS)

Heat or ice pack

Change hormonal supplements

decrease caffeine and chocolate

(disappears with age)

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34
Q

Abigail Ainsley, a 32-year-old woman previously unknown to you, presents to your office with a chief complaint of pain in her left breast of several months__ duration. She reports she has been otherwise healthy, has two young children (G2P2), and has no family history or personal history of breast cancer. On further questioning you elicit that the breast pain occurs just prior to her menses and resolves following menses. Physical examination reveals slightly lumpy (ropey) breasts, with the left showing a 2.5 cm cystic mass to the left of her areola. The mass is mobile and mildly tender. You perform an in-office ultrasound exam which confirms a cystic structure. You then aspirate the cyst and withdraw clear, straw-colored fluid. Post aspiration, she feels relief and the cyst is no longer palpable. What was it?

A

Fibrocystic change

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35
Q

What is phyllodes tumor?

A

Rare predominantly benign tumor

Phyllo = leaf (looks leaflike under microscope

Firm, mobile, circumscribed mass

Biopsy for diagnosis, surgical resection

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36
Q

What is this?

A

Breast enlargement

Well-circumscribed

MIcroscopic gland and stromal proliferation with stroma jutting inot glands

Phyllodes tumor

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37
Q

What is nipple discharge?

A

Any fluid that seeps form nipple

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38
Q

What are casues of nipple discharge?

A

Physiologic, result of trauma, stimluation, fibrocystic change, infection, abscess, benign tumor (fibroadenoma), cancer, or others

In men, must be investigated; in women, most are benign

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39
Q

What are signs that can help narrow your differential when considering nipple discharge?

A

Sore, red, pus = infection

Greenish discharge, thick, perimenopausal = mammary duct ectasia

Bloody or sticky = intraductal papilloma (most common cause)

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40
Q

What does pus and sore, red, warm breasts with discharge suggest?

A

Infection

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41
Q

What does thick, greenish nipple discharge in perimenopausal women suggest?

A

Mamary duct ectasia

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42
Q

What does bloody or sticky nipple discharge suggest?

A

Intraductal papilloma (most common cause

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43
Q

What are tests to run on nipple idscharge?

A

Sample of discharge and send to pathology

Mammogrand or ultrasound for cyst/masses

Biopsy for masses

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44
Q

What is the most common benign breast tumor?

A

Fibroadenoma

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45
Q

what is fibroadenoma?

A

Most common benign breast tumor

Most common tumor in young

Solitary, but may be miltuiple and iblatera

Painless, freely mobile, well circumscribe,d firm, rubbery

may grow during pregnancy

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46
Q

What are the characteristics of fibroadenoma?

A

Painless, freely mobile, well circumscribed mass, firm, rubbery

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47
Q

What is this?

A

Fibroadenoma

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48
Q

What is this?

A

Fibroadenoma

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49
Q

What are tests for fibroadenoma?

A

Mammorgraphy or ultrasound

Very young patients can be managed conservatively

Older patients - biopsy

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50
Q

How do you manage fibroadenomas?

A

Watched, patient makes informed decision

Surgical removal for lesions that grow with time, or if there is concern for cancer

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51
Q

Who gets breast cancer/

A

Mean age = 60 years old, women mostly (men = 1%)

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52
Q

What are nongenetic risk factors for breast cancer?

A

Signs seem to point to excess estrogen exposure

Early menarche, late menopause
Nulliparity, low parity

No breast feeding

Long duration postmenopausal HRT

Obesity

Alcohol consumption

Ionizing radiation at young age

Atypical duct hyperplasia fibrocystic change

Family history

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53
Q

What are genetic risk factors for breast cancer?

A

BRCA genes (BRCA1 = 56-90%; BRCA2 37-84% risk; and also ovarian

TP53 mutation carriers have increased risk (Li-Fraumeni, SBLA syndrome = soft tissue and bone sarcomas, brain tumors, leukemias, and adrenocortical carcinomas)

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54
Q

What is the breast cancer pathogenesis?

A

Loss of tumor suppressor function (BRCA, TP53)

BRCA1 = 17q21

BRCA2 = 13q12-13

Well studied in Ashkenazi Jews

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55
Q

How does breast cancer present?

A

Breast lump, hard, nontender mass with irregular borders

Or in sreening mammograpy

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56
Q

Where is the most common location of breast cacner?

A

Upper outer quadrant

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57
Q

What are associated symptoms with breast cancer/

A

Redness + warmth, edema (peau d’orange), pain, skin or nipple retraction, discharge, eczematous nipple, axillary lymphadenopathy = sign of spread

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58
Q

What are signs/symptoms of advanced disaese?

A

Bone pain, jaundice, weight loss

Axillary lymphadenopathy indicates spread ot lymph nodes

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59
Q

What are the four main types of breast cancer/

A

Insitu duct = inraductal carcinoma = ductal carcinoma in situ (DCIS)

Invasive duct carcinoma (most common)

Lobular carcinoma in situ (LCIS)

Invasive lobular carcinoma

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60
Q

What are duct carcinoma in situ (DCIS)?

A

Precursor to invasive duct carcinoma

Typically discovered on screening mammography (no mass)

Suspicious calcifications on mammograms

May be multifocal multicentric, bilateral

Resection of suspicious area is treatment

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61
Q

How do DCIS present?

A

No mass = precursor to invasive duct carcinoma

Tpically present on mammography

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62
Q

How do you treat DCIS?

A

Resection

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63
Q

What do we see here?

A

Malignant epithelial cells growign within ducts but do not invade the duct basement membrane into the stroma

DCIS

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64
Q

What is the most common breast cancer?

A

Infiltrating duct carcinoma

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65
Q

How does infiltrating duct carcinoma present?

A

Mammography, mass or density with irregular borders +/- calcifications

Histologically can see irregular nests of ductal epithelial cells that invade stroma

Treat wiht resection

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66
Q

What do we see here?

A

Irregularly shaped nest of malignant cells infiltrating the pale fibrous stroma

Infiltrating duct carcinoma

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67
Q

What is LCIS?

A

lobular cacinoma in situ

Not a palpable mass

Not calcificated

Usually incidentally found

Histologically neoplastic epithelial cells repalce epithelium of the TDLU and enlarge it

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68
Q

What do we see here?

A

Lobule distended by carcinoma cells, basement membrane intact

LCIS

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69
Q

What is invasive lobular carcinoma?

A

More frequently bilateral than other type sof breat cancer

Similar to invasive duct carcinoma on mammography and gross apearance

Histologically, small, uniform malignant cells invade stroma in linear pattern (single file)

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70
Q

What is this?

A

Invasive lobular carcinoma

Single file pattern on infiltration by cancer cels into pale firous stroma

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71
Q

What are good prognosis breast cancers?

A

Medullary, mucinous, tubular, papillary carcinoma

paget’s disease = cancer cells in epidermis (almost always associated with DCIS or invasive duct carcinoma

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72
Q

What is this?

A

Mucinous carcinoma - tumor cells float in mucous pools = good prongosis

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73
Q

What is this?

A

Tubular carcinoma, small tubular formations = good prognosis

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74
Q

What is this?

A

Paget disease; pale tumor cells in epidermis = good prognosis

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75
Q

What are tests for breast cancer?

A

Mammography = screening or diagnostic (negative mammogram with palpable mass doesnt exclude cancer - perform biopsy)

Ultrasound = useful in young patients in determining cystic vs solid

MRI = high sensitivity, low specificity

Biopsy = definitive

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76
Q

What is the definitive test for breast cancer?

A

Biopsy . traetment shouldnt be undertaken without biopsy

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77
Q

How do you treat breast cancer/

A

Excision of biopsy-proven malignancy or mastectomy with option of reconstruction

Sentinel lymph node dissection

Post-surgical chemo, radiation, or hormone therapy

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78
Q

How are breast cancer patients followed up/

A

Every 3-6 months for 1st 3 years, and then less frequently

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79
Q

Where do breast cancers metastesize to?

A

Lymph nodes = axillary are most common, internal mammary, supraclavicular, infraclavicular

Distant sits = bone, lung, brain, liver

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80
Q

What are poor prognostic markers?

A

Lymph node involvement = most important

Tumor size

Tubular carcinoma and others are good prognosis

Histologic grade

Proliferation index

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81
Q

What are predictive markers that indicate response to therapy for breast cancer/

A

Estrogen receptor + tumors can be treated with tamoxifen and have lower risk of recurrence

HER2/neu gene amplification = patients respond to herceptin

Negative prognostic marker, as HER2 + tumors have increased risk of recurrenc eand death

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82
Q

A 59 yo lady, a new patient, presents to you with a chief complaint of a newly discovered breast lump.

You find out her mother had breast cancer at age 72, and there are no other known cancers in the family. She has otherwise been in good health, is married, postmenopausal, with two grown children. She has had regular mammograms and pap smears, which were normal. You palpate a small, firm, fixed lesion in her right breast, without being able to further define due to fatty tissue. Mammogram reveals

Biopsy shows

What do we suspect?

A

She has infiltrating duct carcinoma and needs surgery

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83
Q

What is this?

A

Inner vulva and vagina

not skin - no hair, glands, etc…

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84
Q

How does the vaginal epithelium synthesize glycogen?

A

Estrogen and progesterone stimulates the epithelium

Glycogen is main nutreitn for lactobacilli

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85
Q

What is the significance of glycogen produciton by vaginal glycogen?

A

Main nutrient for lactobacilli

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86
Q

What is the normal vaginal pH?

A

3.8-4.2

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87
Q

Why is the vaginal pH low?

A

Lactobacilli metabolize glycogen into lactic acid, responsible for lowering the pH to 3.8-4.2

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88
Q

What is inflammation of the vagina called? What typially causes it?

A

Vaginitis

Typically infection=

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89
Q

What is the most common vaginal disorder?

A

Vaginitis

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90
Q

What is vaginal discharge?

A

Change in amount, odor, color and/or consistency of secretions

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91
Q

What is the main symptom of vaginitis?

A

Discharge

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92
Q

What are the three main causes of vaginitis/vaginal discharge?

A

Gardnerella

Candida

Trichomonas

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93
Q

How do you workup vaginal discharge?

A

Obtain sample of discharge

Examine it under microscope

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94
Q

What is the most common cause of bacterial vaginitis (vaginosis)?

A

Gardnerella

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95
Q

What is the discharge typically associated with gardnerella?

A

scant grayish to milky white, malodorous and fishy smelling

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96
Q

What is the special test to identify gardnerella?

A

Amine test - fishy odor with 10% KOH

Saline wet mount

Will see clue cells - vaginal cells that are grainy looking since they are studded with bacteria

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97
Q

What is the second most common cause of vaginitis?

A

Candida (1st = gardnerella)

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98
Q

What vaginitis causes a thick, curdlike discharge?

A

Candida

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99
Q

What vaginitis can cause an appearance of erythematous skin?

A

Candida

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100
Q

How does candida cause vaginitis?

A

Opportunisitc pathogen - infection upon vaginal pH alteration

See erythematous skin, normal cervix, dysuria

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101
Q

Patient presents with erythematous vulva, normal cervix, dysuria and thick curdlike discharge. What do you think?

A

Candida

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102
Q

What do you see under the microscope in candida vaginitis?

A

fungal hyphae

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103
Q

What is the most prevalent nonviral STI in the US?

A

Trichomonas

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104
Q

What is trichomonas?

A

Uniflagellate protozoan that resides in lower female genital tract and male urethra that overgrows when the pH changes

Can cause vaginitis with discharge and cervico-vaginal petechial lesions (strawberry spots)

Produces profuse, frothy greenish foul-smelling discharge

Tx with metronidazole to patient and partner

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105
Q

What is the discharge seen with trichomonas?

A

Frothy greenish, profuse, foul-smelling discharge

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106
Q

How do you treat trichomonas vaginitis?

A

Metronidazole

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107
Q

What do you see in trichomonas vaginitis under microscopy?

A

Motile organisms on wet mount

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108
Q

What are STIs that are not primarily characterized by vaginal discharge?

A

Mucopurulent endocervicitis (gonorrhea, chlamydia trachomatis D-K)

Vulvar papular lesion which ulcerates (treponema, hemophilous, klebsiella, chlamydia trachomatis L1-L3)

Anogenital vesicles (HSV)

Anogenital warts (HPV)

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109
Q

What organism causes gonorrhea?

A

Neisseria gonorrhea

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110
Q

What is the typical presentaiton fo gonorrhea?

A

Typically asymptomatic

Can present with urethritis (more common in males) with copious pus-like discharge from glands of lower genital tract

May cause pelvic inflammatory disease if untreated - may lead to fallopian tube scarring and infertility

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111
Q

What is a consequence of not treating gonorrhea?

A

Pelvic inflammatory disease whcih can cause fallopian tube scarring and infertility

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112
Q

What is chlamydia trachomatis?

A

Most common bacterial STI in US

Serovars D-K causes mucupurulent cervicitis and pelvic inflammatory disease (may be asymptomatic)

Serovars L1-L3 cause lymphogranuloma venereum in Asia, Africa and S. America as a painless papule followed by inguinal lymphadenopathy

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113
Q

What serovars of chlamydia trachomatis causes mucopurulent cervicitis and PID?

A

D-K

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114
Q

What serovars of chlamydia trachomatis cause lymphogranuloma venereum?

A

L1-L3

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115
Q

What is the life cycle of chlamydia trachomatis?

A

Obligate intracellular bacterium

Unique in that it exhibits both intracellular and extracellular forms

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116
Q

What are risk factors for pelvic inflammatory disease?

A

Young age, sexual activity

Low socioeconomic status

African americans

Multiple partners

Failure to use barrier methods

Douching

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117
Q

What are complications of untreated chlamydia trachomatis?

A

Pelvic inflammatory disease with resultant fallopian tube scarring and increaed risk for ectopic pregnancy

Can form adhesions and be associated with chronic pelvic pain

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118
Q

What is lymphogranuloma venereum?

A

Caused by chlamydia L strains - more invasive and infect skin and underlying soft tissue -> lymphadenopathy

Primary lesion is painless genital papule which may ulcerate

May have systemic manifestations (fever, myalgia, arthralgia)

Can cause ulceration and hypertrophy of genitalia, arthirtis, fistula formation of rectum bladder vagina or vulva

Tx with antimicrobials

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119
Q

What are consequences of untreated chlamydia L?

A

Ulceration and hypertrophy of genitalia, arthritis, fistula formation of rectum, bladder, vagina, or vulva

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120
Q

What is the guiding principle of treatment for STIs?

A

Treat patient AND partner

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121
Q

What is most important in differentiating infectious etiologies of genital lesions?

A

Pathology lab - identify the organism

Many can look similar

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122
Q

What organism causes syphilis?

A

Treponema pallidum

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123
Q

What is the primary lesion in syphilis?

A

Painless chancre

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124
Q

What does secondary syphilis look like?

A

maculopapular rash on trunk and extremities (including palms and soles)

Whitish lesions on mucous membranes (condylomata lata)

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125
Q

When you see condylomata lata and a maculopapular rash on palms and soles, what are you thinking?

A

Secondary syphilis

Seen 4-10 weeks after primary infection

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126
Q

How does chancroid present?

A

Painful papule - soft chancre - ulcerates

Inguinal lymphadenopathy may break through skin (buboes)

Lymph nodes need drainage and if untreated can cause ulceration and fistula formation

Gram stain needed for diagnosis

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127
Q

What organism causes chancroid?

A

Hemophilus ducreyi

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128
Q

What do you see on microscopy of chancroid?

A

School of fish appearance of hemophilus ducreyi on gram stain

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129
Q

What is granuloma inguinale?

A

Painless papule that may ulcerate

No inguinal lymphadenopathy, but may cause tissue destruction (penile autoamputation has been reported) if untreated

Caused by Klebsiella granulomatis (donovanosis)

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130
Q

What disease does klebsiella granulomatis (donovanosis) cause?

A

Granuloma inguinale

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131
Q

How does granuloma inguinale look on microscopy?

A

Donavan bodies (donavanosis - Klebsiella granulomatis)

Biopsy with Wright-Giemsa stain is gold standard for diagnosis

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132
Q

What is the most common cause of genital ulcers in US?

A

HSV (2)

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133
Q

How does herpes cause infection/ulcers?

A

Enters through skin and travels to nerve roots

In outbreak, travels down nerve to original site of infection causing redness and blisters

Can be systemic - fever, malaise, headache, myalgia

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134
Q

What can you see on microscopy of herpes?

A

Tzanck stain shows Herpes vi ral cytopathic effect: multinucleated giant cells

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135
Q

What do you suspect from this Tzanck stain?

A

Herpes viral cytopathic effect

Multinucleated giant cells with ground glass appearance of nuclei

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136
Q

What virus classically causes genital warts?

A

HPV

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137
Q

What do you think this could be?

A

Whitish warty lesions, on the patients right side

Likely caused by HPV - take biopsy to confirm

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138
Q

What are the low risk HPV serotypes?

A

6,11 - intracellular virus in episomal form

Causes warts, low grade lesions

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139
Q

What HPV serotypes are high risk?

A

16, 18

Integrate into host DNA and are associated with high grade lesions and cancer

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140
Q

How is HPV thought to contribute to tumor formation?

A

Integration of viral DNA into host DNA causes aberrant overexpression of viral E6 and E7 genes

E6 caues degradation of p53 and E7 interferes with Cyclin A and p105 RB (whcih are important in cell cycle regulation)

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141
Q

What viral proteins are implicated in tumorigenisis in HPV infection?

A

E6 and E7

E6 = p53 degradation

E7 = inteference with cyclin A, p107 and p105 RB

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142
Q

What do we see here?

A

Koilocytes

HPV cytopathic effect

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143
Q

What is a koilocyte?

A

Raisin-like nuclei with surrounding space

Seen in HPV infection (HPV cytopathic effect)

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144
Q

What does this look like?

A

Condyloma acuminatum

HPV infection

Biopsy is gold standard

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145
Q

Emily Ernstweiler, an 18 year old female previously unknown to you, presents to your office with a chief complaint of vulvar pain and dysuria for the past week. She has been previously healthy, started her menses at age 13 and has had fairly regular 28 day menstrual cycles with duration of bleeding of 3

days. She became sexually active during this past month with a boy from her English class. On physical exam, you notice a number of symmetrical, ulcerated lesions on her labia majora bilaterally

What do you think?

A

Herpes infection

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146
Q

What is lichen sclerosus?

A

Most common vulvar dermatologic disorder

A type of vulvar dystrophy

Patchy white, thin skin (parchment paper skin)

Unknown etiology

Causes pruritis, painful intercourse, in troital stenosis, flattening and fusion of labial folds

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147
Q

What is this?

A

Lichen sclerosus

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148
Q

How do you treat lichen sclerosus?

A

Corticosteroids

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149
Q

What do you see here?

A

Skin showing epidermal thinning with loss of rete ridges and superficial dermal sclerosis

Lichen sclerosis

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150
Q

Kelly Kalleidoscope is a 34-year-old lady, a mother of two (G2P2) who presents to your office for a follow up of her recent Pap smear which was abnormal, with a high-grade squamous intraepithelial lesion (HSIL). On colposcopic examination of her cervix, you identify an area showing abnormal blood vascular pattern and perform a biopsy. You inform Kelly that the abnormal area is larger than the biopsy sample and, if the Pathology report confirms your suspicion of a high-grade lesion, she will have to return to have the entire lesion excised. The Pathology Lab reports cervical intraepithelial neoplasia II (CIN II, moderate dysplasia). You telephone Kelly with this news and advise her to return at her next convenience for a loop electroexcision procedure (LEEP).

Which portion of the cervix tends to be involved (hence, must be excised in order to ensure optimal treatment)?

A

Transformation zone

151
Q

What is cervicitis?

A

Inflammation of cervix

Most common disorder of cervix

Most commonly caused by agents of STI

Treated with antimicrobials and is almost always curable

152
Q

What do we see here?

A

Cervical histology

See ectocervix - external os and endocervical glands (internal)

153
Q

What is the cervical transformation zone?

A

High incidence area for devleopment of intraepithelial (precancerous) lesions

Squamo-columnar junction

T-zone moves upward in cervical canal during a woman’s lifetime

154
Q

What are cervical intraepithelial neoplasias (CINs)?

A

Formerly called dysplasias (refers to abnormal maturation of epithelium)

155
Q

What are risk factors for CIN?

A

Early age of first sexual encounter

Multiple sexual partners

High-risk male partner

Multiple pregnancies

Early age first marriage

Unstable marriage

Low socioeconomic status

Cigarette smoking

Immunosuppresion

History of STI, especially HPV

156
Q

What is an associated infection with CINs?

A

HPV in >80% of CINs and 99.7% of cervical cancers

157
Q

How is CIN (cervical dysplasia) graded?

A

mild, moderate, severe

Mild = CIN I -> abnormal maturation involving lower 1/3 of epithelium

Moderate = CIN II -> Abnormal maturation involving lower 1/2 to 2/3 of epithelium

Severe = CIN III -> Abnormal maturation involving full thickness of epithelium

158
Q

What is pap smear?

A

Screening test for cerivcal cancer

Has decreased incidence of invasive cervical cancer

There are established guidlines for followup of abnormal pap smears

159
Q

What is ASCUS on pap smear?

A

Atypical squamous cells of uncertain significance - not treated

160
Q

What is ASC-H on pap smear?

A

Atypical squamous cells of which a high-grade lesion cannot be excluded - not treated

161
Q

What is LSIL on pap smear?

A

Low-grade squamous intraepithelial lesion - not treated

162
Q

What is HSIL on pap smear?

A

High-grade squamous intraepithelial lesion - treated, removed

163
Q

What does a cell whose nucleus takes up more than 50% of the cell volume on pap smear indicate?

A

HSIL - needs to be treated -> excision or removal by freezing or burning

164
Q

What is colscopy?

A

Lesions that look significant can be sampled by colposcopy - biopsy and send to path lab

165
Q

What do we see on left, right?

A

Left - LSIL = low grade squamous intraepithelial lesion (lower 1/3)

Right = HSIL = high grade squamous intraepithelial lesion (full thickness)

166
Q

What can happen to untreated intraepithelial lesions?

A

Regress, persist, or progress

167
Q

What does cervical cancer look like on pathology?

A
168
Q

Millie Millhauser is a new patient of yours. She presents with a chief complaint of postcoital bleeding. She is a 50 year old waitress, mother of two, notable for her flaming red hair and bright red finger nails. She had gone through a stormy divorce three years ago and has had four boyfriends since then. Her current __beau__ is an ex-convict. Millie is a long-time, heavy cigarette smoker with a long history of abnormal Pap smears, but doesn__t recall what the diagnoses were.

What do you tell her?

A

Your differential includes either cervical or endometrial cancers, so you will want to repeat pap smear or biopsy

169
Q

Nikki Nickelbaum is a 25 year old nulliparous, obese woman, who presents to your office with a complaint of decreased menses (once every 4 or so months, called oligomenorrhea). Her periods when they come, tend to be heavy, lasting around 7 days, and she goes through two boxes of Kotex pads (sanitary napkins) per period. Nikki says she has had bad acne since puberty (age 13). On pelvic exam you find no abnormalities, and no masses are palpated

What lab tests do you order?

A

Need to rule out pregnancy, thyroid problem, or CNS problem (prolactinoma)

170
Q

What influences the ovaries to secrete estrogen and progesterone?

A

Hypothalamus and pituitary peptide hormones

171
Q

What changes does the endometrium undergo on a monthly basis?

A

Proliferative (growth) phase

Secretory (stop growth and secretion) phase

Pregnancy causes endometrium to convert to gestational phase; if not, menstrual breakdown

172
Q

What do we see here?

A

Proliferative phase of endometrium (estrogen phase)

Mitosis in gland and stromal cells

173
Q

What do we see here?

A

Early secretory phase of endometrium

Cytoplasmic vacuoles in gland cells

174
Q

What do we see here?

A

Mid secretory phase of endometrium

Glands begin to distend with intraluminal secretions

175
Q

What do we see here?

A

Late secretory phase of endometrium

Post secretory glands begin to involute

176
Q

What do we see here?

A

Menstrual phase of endometrium

Gland and stromal cell death and endometrial tissue dissolution

177
Q

What does this show?

A

Menstrual cycle

178
Q

What is metrorrhagia?

A

Bleeding between periods

Causes include endometrial polyp, uterine cancer, hormone replacement therapy

179
Q

What is menorrhagia?

A

Heavy bleeding during menses

Causes leiomyomas (fibroids), pregnancy complications, adenomyosis, IUDs, endometrial hyperplasia, malignancy, dysfunctinoal uterine bleeding

180
Q

What is menometrorrhagia?

A

Combination of menorrhagia and metrorrhagia

181
Q

What is endometrial hyperplasia?

A

Abnormal growth causing thickness of endometrial mucosa and increaed gland-to-stroma ratio

Considered precancerous

Estrogen is implicated in pathogenesis

Associated with microsatellite instability, defects in DNA mismatch repari genes, and PTEN tumor suppressor mutations

182
Q

How does endometrial hyperplasia present clinically?

A

Abnormal uterine bleedgin (any type)

Abnormal vaginal discharge

Abnormal glandular cells on pap smear (AGUS)

Ultrasound can assess endometrial thickness, but endometrial BIOPSY is GOLD STANDARD

183
Q

What is the gold standard of diagnosis for endometrial hyperplasia?

A

Biopsy

184
Q

What is this a progression of?

A

Endometrial hyperplasia

185
Q

What is the gland-to-stroma ratio in typical endometrium?

A

Glands make up ~<50% of endometrium

Good amoutn of stroma between, and are separate from neighbors

186
Q

What is characteristic of simple endometrial hyperplasia?

A

Swiss Cheese hyperplasia

Mildly crowded, some dilatation

187
Q

What is characteristic of complex endometrial hyperplasia?

A

Animal cracker hyperplasia

Moderately crowded glands, complex shapes

188
Q

What is characteristic of atypical endometrial hyperplasia?

A

Severely crowded glands with nuclear atypia

189
Q

Which endometrial hyperplasia has the greatest risk of progression to cancer?

A

Atypical hyperplasia

190
Q

How can the relative risk of the different types of endometrial hyperplasia be remembered?

A

Penny, nickel, quarter (simple, complex, atypical = 1%, 5%, 25% respectively)

Risk of developing cancer

191
Q

What is the most common pelvic genital cancer in women?

A

Endometrial carcinoma (adenocarcinoma)

192
Q

What is endometrial carcinoma (adenocarcinoma)?

A

Most common pelvic genital cancer in women

Usually in older women

Can be seen in younger womeon with unopposed estrogenic stimulation (polycystic ovarian syndrome)

Bleeding facilitates detection of early stage disease -> better prognosis than others

193
Q

Why do endometrial carcinomas have better prognoses than other gyn cancers?

A

bleedign facilitates early detection

194
Q

How does an endometrial adenocarcinoma look like grossly?

A

Uterus containing cancer will show thickend, ragged mucosal lining or polypoid mass(es)

Malignancy of glandular epithelium = adeno carcinoma

195
Q

How does an endometrial adenocarcinoma appear histologically?

A

Back-to-back arrangement of glands (cribriforming)

Due to invasion of storma by malignant gland-forming cells until they become confluent

196
Q

What do we see here?

A

Endometrial adenocarcinoma

197
Q

What are the two types of endometrial adenocarcinoma?

A

Type I = features unopposed estrogen and can occur premenopausal, low grade, lesser invasion, indolent

Type II - no unopposed estrogen and occurs postmenopausally only, high grade, deep invasion, aggressive (p53)

198
Q

What is the most common tumor of the uterus?

A

Leiomyoma - benign smooth muscle cell neoplasm

More common in African Americans than caucasians

1/3 are symptomatic (menorrhagia)

199
Q

Who gets leiomyomas more commonly?

A

African americans

200
Q

How do leimyomas present?

A

only 1/3 are symptomatic with menorrhagia

201
Q

What do we see here?

A

Leiomyoma

202
Q

What do we see here?

A

Uterine leiomyoma

203
Q

What is adenomyosis?

A

Similar clinical picture to leiomyoma (abnormal uterine bleeding or menorrhagia)

Physical exam can distinguish since adenomyosis causes SYMMETRIC enlargement of uterus (leiomyoma is irregular enlargement)

Downgrowth of endometrial tissue into myometrium

204
Q

What is the difference between adenomyosis and leiomyoma?

A

Adenomyosis presents w/ symmetrical enlargement of the uterus

Leiomyoma is irregular enlargement of the uterus

Adenomyosis is the result of downgrowth of endometrial tissue into myometrium

Leiomyoma is a neoplasm of myometrium

205
Q

What is leiomyosarcoma?

A

Malignant counterpart of leiomyoma (arise de novo and not from leiomyomas)

Very RARE

Present with abnormal uterine bleeding

Diagnostic histologic features include high mitotic count, nuclear atypia and necrosis

206
Q

What is PID?

A

Pelvic inflammatory disease (pus in dere)

Infection of upper reproductive tract (uterus, ovaries, fallopian tubes and adjacent soft tissues)

Result of ascending ifnection of vagina and cervix (Typically neisseria and chlamydia)

Risk factors include multiple partners, history of STI, history of sexual abuse)

Symptoms include - lower abdominal pain, abnormal vaginal discharge (may or may not be present)

207
Q

What are some symptoms of PID?

A

Lower abdominal pain

+/- abnormal vaginal discharge

Fever and pelvic tenderness

208
Q

What are risk factors for PID?

A

Multiple partners

Hx of STI

Sexual abuse hx

209
Q

What are things on the differential diagnosis with PID?

A

Appendicitis, cervicitis, UTI, endometriosis, ovarian tumor

210
Q

What are sequellae of untreated or delayed diagnosis of PID?

A

Chronic pelvic pain from scarring

Tubal infertility

Tubo-ovarian abscess

211
Q

Where do the ovaries lie?

A

Posterior aspect of uterus, connected via posterior ovarian ligament and behind/in the broad ligament

212
Q

What is female pseudohermaphroditism?

A

Most common cause of sexual ambiguity of the newborn - congenital adrenal hyperplasia

Normal 46XX karyotype, normal internal genitalia (uterus, ovaries, fallopian tubes), but external genitalia appears ambiguous or male

Due to exposure of fetus to excess male hormones

213
Q

What is the most common cause of sexual ambiguity of the newborn

A

Congenital adrenal hyperplasia (Female pseudohermaphroditism)

46XX female with internal genitalia intact, but external ambiguous d ue to excess male hormones before birth

214
Q

What is male pseudohermaphroditism?

A

46 XY - gonadal defects or end organ defects

215
Q

What determines the development of external male genitalia?

A

Testosterone

216
Q

How does fetal development of the genitourinary tract unfold?

A
217
Q

What is the “default” sex?

A

Female

218
Q

What is the function of mullerian inhibiting factor?

A

Stimulates male duct (mesonephric) development and regression of female (paramesonephric)

219
Q

What is the female internal genitalia duct system?

A

Paramesonephric ducts give rise to uterus, fallopian tubes, upper vagina

220
Q

What is the male internal duct system?

A

Mesonephric ducts

Give rise to vas deferens, epididymis, seminal vesicles

221
Q

Where do Mullerian inhibiting factor and testosterone act?

A

Locally - MIF stimulates Wolffian ducts and inhibits mullerian ducts; Testosterone stimulates external genitalia

222
Q

What are the karyotypes of individuals with mixed gonadal dysgenesis or true hermaphroditism?

A

Can be normal or not or mosaic

223
Q

What is a true hermaphrodite?

A

Internal duct development corresponds to adjacent gonad with ambiguous external genitalia

3/4 raised as males

(Mixed gonadal dysgenesis has persistent mullerian duct regardless of adjacent gonad)

224
Q

What is mixed gonadal dysgenesis?

A

Persistent mullerian duct regardless of adjacent gonad

Streak gonad

1/3 raised as males

(True hermaphroditism has internal duct development that corresponds to adjacent gonad

225
Q

46 yo woman

__ Completed child bearing and desired to have her internal genital organs removed due to her history

__ Gonad is pictured:

What__s your diagnosis

A

True hermaphrodite

226
Q

What is turner syndrome?

A

45X0 or mosaic (45XO/46XX)

Short stature, webbed neck, low-set hairline, shield chest, underdeveloped secondary sex characteristics

Gonadal Dysgenesis

227
Q

This is the internal genitalia of what type of patient?

A

Turner Syndrome

Hypoplastic uterus and fallopian tubes

228
Q

What is this? We’re looking at internal genitalia

A

Streak gonad

Fibrous streak instead of ovary

229
Q

What are the three non neoplastic ovarian cysts?

A

Functional (follicular) cysts

Endometriotic cysts

Polycystic ovarian syndrome (PCOS)

230
Q

What is a functional cyst?

A

Benign cysts that tend to occur in women of reproductive age

Size > 2cm

Follicle fails to release egg and fluid is not resorbed

Typically asymptomatic but can present with pelvic pain, abnormla uterine bleeding, dyspareunia

Most regress in 60 days

231
Q

What is this?

A

Follicular (Functional) cyst

232
Q

What is endometriosis/endometriotic cysts?

A

Cells from lining of uterus appear to grow outside uterine cavity (ovaries)

10-15% of reproductive-age women

Symptoms worsen around menses (pelic pain, dysmenorrhea, dyspareunia, dysuria)

Common finding in women with infertility

233
Q

What is this?

A

Endometriotic cyst

Endometrial tissue in ovary

234
Q

What causes endometriosis?

A

Unknown - may be genetic, may be estrogen-related

235
Q

What is the gross apperance of endometriosis?

A

Cysts that contain turbid brownish content (“chocolate cysts”)

236
Q

How does endometriosis appear histologically?

A

Endometrial-like glands and stroma, recent and remote hemorrhage - may cycle with menstrual cycle

237
Q

What is polycystic ovarian syndrome?

A

One of most common female endocrine disorders

5-10% of reproductive age women

Leading cause of female subfertility

“String of pearls” finding on ultrasoudn - thick, sclerotic cortical ring

– Release of excess LH by anterior pituitary, or high levels of blood insulin, or reduced sex hormone binding globulin (resulting in excess androgens, elevated LH:FSH ratio)

Oligomenorrhea, secondary amenorrhea, infertility, hyperandrogenemia (hirsutism and acne), metabolic syndrome

238
Q

What is this?

A

“string of pearls” arrangemnt of ovary

Polycystic ovarian syndrome (PCOS)

239
Q

What is this?

A

Polycystic ovarina syndrome (PCOS)

240
Q

What are the three broad categories of ovarian tumors?

A

Epithelial (surface or germinal epithelium)

Germ cell tumors (oocyte)

Sex cord/stromal tumors (follicle cells)

241
Q

What age women are at greatest risk for malignant ovarian masses?

A

Prepubescent children and postmenopausal women

242
Q

What is an ovarian mass in a reproductive age woman most likely to be?

A

Functional cyst or endometrioma

243
Q

How do you work up an ovarian mass?

A

Patient’s age

Characteristic of mass on pelvic exam

Radiographic appearance

244
Q

What are physical findings of a benign ovarian mass?

A

Mobile, cystic, smooht, unilateral

245
Q

What are physical findings of a malignant ovarian mass?`

A

Fixed, solid, nodular, bilateral

246
Q

You find mobile, cystic, smooth unilateral ovarian mass, what do you think?

A

Benign

247
Q

You find fixed, solid, nodular, bilateral ovarian masses. What do you thinK?

A

Malignant

248
Q

How do benign ovarian masses appear on ultrasound?

A

Simple cyst <10cm

Septations < 3mm unilateral

Calcification (teeth)

249
Q

How do malignant ovarian masses appear on ultrasound?

A

Solid +/- cystic

Septations >3mm

Bilateral

Ascites

250
Q

What lab tests do you order on a patient with an ovarian mass?

A

hCG - pregnancy marker, and seen in some malignant germ cell tumors

AFP, LDH (young girls) - malignant germ cell tumor marker

CA125 - postmenopausal women suspected of having ovarian cancer

251
Q

What are epithelial tumors of the ovary?

A

70% of all primary ovarian neoplasms

Most are benign and serous cystadenoma is most common; they are also ost common malignant primary ovarian neoplasms

Typically post-menopause

252
Q

Tanya Tannenbaum is a 65- year-old nulliparous Caucasian female, who presents to your office with a 6 month history of increasing waist size even though she seems to be eating less. She complains of occasional shortness of

breath even at rest. She denies any nausea, vomiting, or vaginal bleeding. Prior to this, she had always been healthy. What is the diagnosis you suspect?

A

Mucinous cystadenoma

Ovarian carcinoma

Uterine malignancy

All possible

253
Q

What is the most common malignant epithelial neoplasm in the ovaries?

A

Papillary serous carcinoma

254
Q

This is an ovarian malignancy. What is it?

A

Papillary serous carcinoma - papillary structures lined by malignant epithelial cells

255
Q

What are risk factors for ovarian cancer?

A

Ovulation

High fat diet

Talc exposure

Genetics (BRCA1 or 2; Lynch Syndrome aka HNPCC)

256
Q

What are germ cell tumors?

A

2nd most common ovarian neoplasms after epithelial tumors - most are benign (90%) and called dermoids

257
Q

What are dermoids?

A

Benign ovarian neoplasms (germ cell tumors)

Removal recommended

258
Q

Who gets malignant germ cell tumors?

A

girls and teenagers

259
Q

What are biologic markers for germ cell tumors?

A

AFP and hCG

260
Q

What is dysgerminoma?

A

Most common malignant germ cell tumor

COmposed of primordial germ cells

Show good resopnse to radiation and chemo

261
Q

What is a mature cystic teratoma?

A

Most common benign germ cell tumor

Composed of mature tissues from any of the germ line layers (ecto,meso, endoderm)

MAjority are benign

262
Q

Lora Lane is a 25 year old with normal medical history who recently experienced amenorrhea, beginning breast atrophy, deepening of her voice, and beginnings of a beard.

A

May have elevated testosterone

May have an adrenal problem

May have ovarian tumor

May have sex-cord stromal tumor

263
Q

What are sex-cord stromal tumors?

A

10% of primary ovarian neoplasms

Arise from follicle cells (granulosa, theca)

May produce sex hormones (estrogen, testosterone) with clinical consequences (feminization or masculinization)

264
Q

What is a granulosa cell tumor?

A

Most common malignant sex cord/stromal tumor

Low-grade malignatn tumor

265
Q

What are fibrothecomas?

A

Most common benign sex cord/stromal tumors

1/3 are inert, 1/3 secrete estrogen and 1/3 secrete androgen

266
Q

AK is a 64 yo lady who complains of increasing abdominal girth and diffuse lower abdominal discomfort for the past six weeks. She has a feeling of fullness in the upper abdomen. Her appetite has been poor in the past few months, but she gained 8 pounds. She has no gynecologic or urinary symptoms. She has been postmenopausal for 14 years, and her past history and family history are unremarkable.

What could it be?

A

Could be benign, malignant, GI or GYN issue

267
Q

AK is a 64 yo lady who complains of increasing abdominal girth and diffuse lower abdominal discomfort for the past six weeks. She has a feeling of fullness in the upper abdomen. Her appetite has been poor in the past few months, but she gained 8 pounds. She has no gynecologic or urinary symptoms. She has been postmenopausal for 14 years, and her past history and family history are unremarkable.

Physical exam:

Reveals a pale, normal-appearing lady. Notable findings include a distended abdomen with a prominent fluid wave and shifting dullness.

Bimanual and rectovaginal exam reveal a 15x10 cm, irregular, nodular mass fixed to the right pelvic sidewall and extending across the midline

What could it be?

A

Ovarian cancer

268
Q

AK is a 64 yo lady who complains of increasing abdominal girth and diffuse lower abdominal discomfort for the past six weeks. She has a feeling of fullness in the upper abdomen. Her appetite has been poor in the past few months, but she gained 8 pounds. She has no gynecologic or urinary symptoms. She has been postmenopausal for 14 years, and her past history and family history are unremarkable.

Physical exam:

Reveals a pale, normal-appearing lady. Notable findings include a distended abdomen with a prominent fluid wave and shifting dullness.

Bimanual and rectovaginal exam reveal a 15x10 cm, irregular, nodular mass fixed to the right pelvic sidewall and extending across the midline

Labs:

Hemoglobin and Hct are decreased slightly, otherwise normal

Radiology:

Abdominal CT scan shows a 6x12 cm irregular mass in the mid-abdomen anterior to the stomach; a 15x10 cm pelvic structure consisting of the uterus and right ovary, which is replaced by a partly solid, partly cystic irregular mass that extends to the right pelvic sidewall, compressing the sigmoid colon. The left ovary is irregular and enlarged to 4x6 cm.

Abdominal paracentesis removes 6000 ml of straw-colored fluid, sent to CytoPathology.

What could it be?

A

Serous adenocarcinoma (most common ovarian carcinoma

Refer to Gyn Oncologiest

269
Q

When does embryonic circuliation begin?

A

When placenta forms (21 days)

270
Q

When does the placenta form?

A

21 days

271
Q

What are funcitons of the placenta?

A

Provide maternal nutrients and oxygen to fetus

Clear fetal waste

Confer passive immunity by transfer of maternal antibodies

Produce hCG, hPL, estrogens, and progesterone

272
Q

What is the funciton of progesterone on the pregantn mother?

A

Smooth muscle relaxation

273
Q

What is the effect of human placental lactogen on the pregnant mother ?

A

HPL causes breast growth and lactation; diabetogenic

274
Q

What is the effect of hCG on the pregnant mother?

A

Nausea

Maintains corpus luteum

275
Q

What aer circulatory system physiologic changes in pregnance?

A

Increasd venous return, cardiac output and blood volume; Decreased blood pressure

276
Q

What are respiratory physiologic changes in a pregnant woman?

A

Increased oxygen consumption

277
Q

What are urinary physiologic changes in a pregnant woman?

A

Renal blood flow increases causing increased urine formation

278
Q

What are digestive physiologic changes in a pregnant woman?

A

Increased transit time (better absorption, but constipation occurs)

Progesterone relaxes smooht muscle tissue

279
Q

How is pituitary funciton changed in pregnancy?

A

Increased oxytocin (mostly during labor and lactation) from posterior pituitary

Increasd prolactin, corticotropin, thyrotropin, and GH from anterior pituitary

Decreased FSH, LH from anterior pituitary

280
Q

What is the function of oxytocin in pregnancy?

A

Involved in uterine contrations of labor and postpartum uterine involution

Causes contraction of myoepithelial cells leading to ejection of milk from TDLUs into large ducts

281
Q

What is the effect of pregnancy on adrenal funciton?

A

INcreased cortical secretions - mobilizes amino acids for fetus; sodium resorption causes fludi retention

282
Q

What is the effect of preganncy on the thyroid?

A

Enlarges thyroid, increased thyroxine production

283
Q

What is the effect of pregnancy on parathyroid?

A

Enlarges - causes calcium resorption from maternal bones if needed by fetus

284
Q

How does uterine fundus hight above pubic symphisis relate to stage of pregnancy?

A

Each cm ~ week pregnant

285
Q

What changes do you see in hematocrit in pregnancy?

A

Decreases - dilutional (anemai in pregnancy is marked by Hgb < 11 or Hct < 33%)

286
Q

What is weight gain in pregnancy the result of?

A

Mother (uterus, breasts, blood, fat, other) cause ~ 13 lbs

Fetus causes ~6-9 lbs

Placenta, membranes, fluids cause ~ 4 lbs

287
Q

What are Leopold’s maneuvers?

A

Use abdominal palpation to ascertain position of fetus

288
Q

What is cephalic or vertex presentation?

A

Fetus has head down in abdomen of mother

289
Q

What is the first stage of labor?

A

Onset of labor contractions thru full dilation of cervix

290
Q

What is the second stage of labor?

A

From full cerix dilation to delivery of fetus

291
Q

What is the third stage of labor?

A

From delivery of fetus to delivery of placenta

292
Q

What are the three stages of labor?

A

1 - from onset of contracitons to full dilation

2 - from full dilation to delivery of baby

3- from delivery of baby to delivery of placenta

293
Q

What are mechanical factors of parturition?

A

Stretch of uterine smooth musculature (increases contractility; stretched by fetal growth)

Stretch of uterine cervix ( feedfback mechanism from cervix increases contractions)

294
Q

What are hormonal factors of parturition?

A

Estrogen increases uterine contractility

Progeserone decreases uterine contractility

E/P ration increases near term

Oxytocin increases contractions during labor

Prostaglandins soften cervix and cause contractions

295
Q

What is the E/P ratio and why is it important in partuition?

A

Estrogen/Progesterone

INcreases near term

Estrogen increases uterine contractility; progesterone decreases it

296
Q

What assesses the newborn’s need for resuscitation?

A

APGAR score

297
Q

What is normal blood loss durign labor?

A

< 500 mL

298
Q

What are identical twins?

A

From single ovum

299
Q

What are fraternal twins?

A

From two ova

300
Q

What proportion of twins are identical? What proportion are fraternal?

A

1/3 identical; 2/3 are fraternal

301
Q

What is the etiology of double ovum (fraternal) twins?

A

Inherited propensity

302
Q

What is the etiology of single ovum (identical) twins?

A

Chance splitting of the ovum

303
Q

Twins are boy and girl; what type of twins are they?

A

Fraternal - by definition; Must have come from two ova and two sperm

Identical are one ova, one sperm; then splits after fertilization

304
Q

What are dizygous twins?

A

Fraternal - associated with multiple ovulation

Increased frqency with increased maternal age, parity

Frequency dependent on races and ethnicity

305
Q

What are monozygous twins?

A

Result of division of a fertilized ovum

Fairly constant frequency worldwide - chance

Unclear cause

306
Q

How can the placentas of twins develop?

A

Devision of fertilized ovum < 3 days => dichorionic-diamniotic placenta

Division at 3-8 days => monochorionic-diamniotic placenta

Divisoin at 8-13 days => monochorionic-monoamniotic placenta

Divison > 13 days => conjoined twins

307
Q

What is dichorionic, diamniotic placenta?

A

Fraternal twins, typically; or if divisoin of identical occurs at < 3 days

308
Q

What is a complication of monochorionic- monoamniotic placenta?

A

Luckily it is a rare occurance

Can cause cord tangling

309
Q

What are pregnancy complications of twins?

A

Preterm labor

Discordant fetal growth

Pregnancy-induced HTN

Anemia

Others

310
Q

KL__s face, hands and lower legs appear edematous. Her pulse is 92, respiratory rate 18, BP 160/110, temperature normal. HEENT, neck, heart and lung exams are otherwise normal except for a 2/6 systolic ejection murmur loudest at the left sternal border. Breast exam is significant for bilateral fullness and slight tenderness diffusely. Abdominal exam reveals a nontender uterus with fundal height 38 cm, fetus is in a longitudinal lie, vertex presentation. Dipstick urinalysis reveals 3+ proteinuria.

What do you suspect?

A

Preeclampsia - HTN and proteinuria

311
Q

What are the signs and symptoms of preeclampsia?

A

HTN = sys > 140 or diastolic > 90

Proteinuria > 300mg in 24 hr

Symptoms of heaache, RUQ pain

Hematologic or liver enzyme abnormalities

312
Q

What defines preeclampsia?

A

Hypertension after 20 weeks gestation in previously nonhypertensive woman

Proteinuria over 300mg/24hr or at least 3+ on two random urine samples at least 4 hours apart

313
Q

What are lab abnormalities in preeclampsia?

A

HELLP (hemolysis; elevated liver enzymes; low platelets) - microangiopathic thrombangitis

314
Q

What is eclampsia?

A

Occurance of new-onset grand mal seizures in a woman with preeclampsia

315
Q

What is teh effect of preeclampsia on the fetus/placenta?

A

Mild cases can show no changes

But severe clases can cause small placenta with multiple infarcts

Placental trophoblast cells have not adequately invaded into maternal vasculature and maternal blood vessels fail to show normal changes of pregnancy

316
Q

An ultrasound exam reveals a “snowstorm” pattern of ehoes filling the uterine cavity without a fetus

A

Hydatidiform mole

317
Q

When do you see extremely high hCGs?

A

Hydatidiform mole

318
Q

What is a hydatidiform mole?

A

Benign placental neoplasm that has excess paternal chromosomes

Complete or partial

Complete: all placental villi are abnormal; no fetus

Partial: some villi are normal; may be fetus

319
Q

What type of hydatidiform mole is this?

A

Complete

320
Q

What type of hydatidiform mole is this?

A

Partial

321
Q

What factors influence expression of human sexuality?

A

Age, culture, religion, previous experiences, physcial conditions, partner(s), availability

322
Q

What is dyspareunia?

A

Pain on intercourse

Can be caused by inflammation, inadequate vaginal lubrication, trauma, other gynecologic problems, or a structural problem

323
Q

What is the human sexual resopnse?

A

Multisystem autonomic nervous relex that can be reinforced or inhibted by physiological, psychological and social factors

324
Q

What is a broad distinction between the men and women human sexual response?

A

Women resopnd more to consciousness of being desired as a whole person; Men’s satisfaction is more visceral senstion

325
Q

What are the 4 Masters and Johnson stages of sexual response?

A

1) excitement
2) plateau
3) orgasm
4) resolution

326
Q

What occurs in females during the excitement phase of sexual response?

A

Vasodilation and congestion of all erectile tissue

Breasts enlarge and vaginal ostium opens

Vestibular gland secretions and vaginal mucosal exudations cause moistening

327
Q

What occurs in men during the excitement phase of sexual response?

A

Vasodilation and congestion of vessels in corpora cavernosa cause erection

Scrotal skin and dartos muscle contract and draw testes up

328
Q

What occurs during the plateau phase of sexual response in women?

A

Vasocongestion increases

Uterine ligaments contract and lift uterus into alignment with pelvic axis

Cervix dilates

Lower 1/3 of vag engorges and upper 2/3 balloons

Pulse doubled and RR rises; involuntary pelvic thrusts

329
Q

What occursduring the plateau phase of men sexual response?

A

Intensity of erection increases; testes enlarge via congestion

Seminal fluid arrives at urethra via sympathetic nerve stimulation ov vas deferens, seminal vesicels and prostate

pre-ejaculate discharge may contain sperm

Pulse doubled and RR rises; involuntary pelvic thrusts

330
Q

What occurs during the orgasm phase of sexual response in women?

A

Pulse and RR double resting rate; Pelvic floor contraction

Climactic sensation

331
Q

What occurs during the orgasm phase of sexual response in men?

A

Pulse and RR double resting rate; Pelvic floor contraction

Climactic sensation - strong contractions pass along penis causing ejaculation - intensity related to volume

332
Q

What occurs during the resolution of sexual resopnse in men? women?

A

Pulse, RR, BP return to normal

Sweating

Vasocongestion receds over 5 minutes

Complete relaxation

Detumescense of erectile tissue in women and in men

333
Q

What is infertility?

A

Symptom of one or more disease states involving one or both male and female partners

334
Q

What are different features tha tmust be evaluated in infertility?

A

Anatomical

Hormonal/metabolic

Infectious

Autoimmune

Genetic

Environmental

Psychologic

335
Q

What is definition of infertility?

A

Involuntary inability to conceiv after one year of unprotected intercourse

336
Q

What factors play a significant role in infertility?

A

Maternal age > 35; paternal age > 40

337
Q

What are factors that limit the ability of couples to seek medical advice for infertility?

A

Economic

Social/religious/family

Psychological

338
Q

Do fertility drugs make you fertile?

A

No only make you produce more eggs

339
Q

What are important aspects of the sexual history in evaluating infertility?

A

Frequency of sex

Technique/position

Lubricants

Coital timing

Timing - clear mucous (ovulation predictor kits)

340
Q

What proportion of infertility cases are caused by female factors? male factors? unexplained/dual factors?

A

Female = 40-50%

Male = 30-40%

Dual/unexplained = 15-20%

341
Q

What are components from a male patient’s history that can affect fertility?

A

General health

Age

Lifestyle (tub baths, jacuzzi, ritual baths, bicycle seats)

Prior pregnancies

Infectious causes (STDs, prostatis, epididymitis, urethritis)

Varicocele

Toxic Exposure - (Lead, pesticides, solvents, petrochemicals, heavy metals)

342
Q

What is the first step of evaluation of infertility when you resort to lab testing?

A

Day 2 or Day 3 blood hormone tests (FSH, Estradiol, LH, Prolactin, TSH)

343
Q

What is the second test to perform for infertility when you resort to lab testing?

A

Post-coital exam - determines if sperm delivery and survival is adequate

344
Q

What can cause bad post-coital tests?

A

POstition, lubricants, hostile mucus, sperm abnormalities

345
Q

How can you bypass hostile mucus?

A

Intrauterine insemination (IUI)

Put sperm in sterile medium and basically inject it up into the uterus

346
Q

What is a step to evaluate infertility when you have resorted to lab testing and have evaluated that hormonal levels are good at day 2-3 and that postcoital exam is normal?

A

Day 21 to day 25 progesterone blood tests (one or a series of them)

Can identify a short luteal phase

347
Q

What is a test to perform once you have ruled out hormonal levels on day 2-3; progesterone on days 21-25; and post coital test is normal?

A

Hysterosalpingogram - x-ray of uterus and tubes

Performed on day 7, 8 or 9 of cycle (after flow finishes but before ovulation occurs)

Can identify various abnormalities

348
Q

What is a way to evaluate parts of the female GU tract that cannot be assessed by x-ray?

A

Laproscopy - to identify endometriosis, fibroid tumors, pelvic adhesions

349
Q

What lifestyle modifications can help improve fertility?

A

Avoid too much: alcohol, exercise, smoking, drugs and self-prescried heerbs

350
Q

What hormone imbalances can cause infertility?

A

Tyroid (TSH should be < 2)

Prolactin elevation

Low progesterone

Anovulation (PCOS or hypogonadotropic due to stress)

351
Q

How do oyu best treat infectious etiologies of infertility?

A

Tx both partners simultaneously with same antibiotics

352
Q

What are 5 mechanismms to acheive contraception?

A

Prevention of embryo formation (barrier)

Ovulation/egg prevention (hormonal)

Spermicide

Tubal occlusion/destruction
Combined effects

353
Q

What is the perfect use rate (of contraception)?

A

What percentage of women fail in 1 year with this method, in perfect usage

354
Q

What is the typical use rate (of contraception)?

A

What percentage of women will fail in 1 year in typical use

355
Q

What is the continuation rate (of contraception)?

A

What percentage of women continue this method after 1 year of use

356
Q

What is the perfect/typical use rate of using no contraception?

A

85%

357
Q

What are four common barrier methods?

A

Condoms (male and female)

Diaphragm

Cervical cap

Contraceptive sponge

358
Q

What are the two main types of hormonal contraception/

A

Combined hormonal contraception

Progestin/progesterone only contraception

359
Q

How do hormonal contraception methods work?

A

Suppress HPO axis by high levels of exogenous estrogen and progestin and thus prevent follicle formation and ovulation by negative feedback

Also thin cervical mucus and endometrial lining

360
Q

What is a difference between combined estrogen/progestin pills and progestin only pills?

A

Progestin only are continuous - amenorrhea (no drop off of progesterone levels0

Combined you have placebo (every month or three months) - which produces menstruation

361
Q

What are the two IUD types availabile in the US?

A

Copper (Paragard IUD) - secretes copper as a spermicide

Levonorgestrel (Mirena IUD) - secretes levonorgestrel - thickens cervical mucus, thins endometrial lining, spermicidal, and blocks ovulation

362
Q

What is the mirena IUD?

A

Levonorgestrel secreting IUD

Multiple contraceptive actions, including thickening of cervical mucus, thinning of endometrial lining, spermicidal effects, and ovulation

363
Q

What is the Paragard IUD?

A

Copper IUD - spermicidal - increase in uterine and tubal fluids containing copper ions, enzymes, prostaglandins, and WBCs that impair sperm function

364
Q

What is a permanent method of contraception?

A

Tubal occlusion

365
Q

What are four methods of tubal occlusion?

A

Post-partum tubal ligation

Laprascopic bipolar fulguration

Laprascopic unipolar fulguration

Laprascopic clips

366
Q

What is an essure coil?

A

Placed hysteroscipially in tubal ostia; provides tubal occlusion within 3 months

Permanent contraception

367
Q

What is Emergency Contraception?

A

Plan B - not to be used as contraception, not as effective as any form of contraception

Decreases chances of getting pregnant by 85% if used within 5 days after event

368
Q

35 y/o para 3 who presents to your office requesting permanent sterilization. What do you recommend?

A

Tubal occlusion - permanent, but cant go back

Laprascopic

Should consider vascetomy

369
Q

19 y/o para 0 who is sexually active with a history of chlamydia treated 2 months ago presents to the Adolescent Health Center to discuss contraceptive options. What do you discuss?

A

STI risk (cant do IUD with recent history of STI)

Use multiple methods - i.e. condom! STI is far more dangerous than pregnancy

370
Q

26 y/o para 2 with history of DVT in pregnancy s/p 1st trimester abortion presents to your office for a contraceptive evaluation. What do you discuss?

A

DVT, and abortion - not ready for other child

Bad option are estrogen products

Recommend IUDs

371
Q

23 y/o para 1 who presents to office for contraceptive evaluation. She was recently on OCP, but stopped due to side effects, and forgetting to the pill everyday. Issues to discuss?

A

COmpliance is an issue

IUD could be considered

Patch or nuvaring coudl be considered (less frequent)

372
Q

17 y/o para 0 who presents to the clinic because the condom broke last night during intercourse. She consistently uses condoms as her form of contraception. What do you tell her?

A

Plan B

Counseling on proper condom use

373
Q

What is sexual dysfunction?

A

Exists only if the person or couple is distressed by a particular aspect of their sexual response, rather than on the basis of an “objective” criterion

374
Q

What are categories of sexual dysfunction?

A

Disorders of: desire, arousal or orgasm; or painful intercourse

Sex & Reproduction (1 decks)

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