Reproductive/Breast Pathology Flashcards

1
Q

common symptoms of brest disesases

A

pain, palpable masses, nipple discharge

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2
Q

Are the common symptoms of breast diseases specific for cancer?

A

No, they can also represent fibrotic growths or cysts; however, the older the patient, the greater the chance it is malignant.

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3
Q

At what age should women start screening and why?

A

Age 40; younger than 40 the breast tissue is too dense.

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4
Q

Characteristics and uses of mammography

A
  • detects density
  • shows architectural distortions
  • identifies calcifications
  • can show changes over time (which can be indicative of certain pathologies)
  • does not detect all breast cancers (~10% of breast cancers not detected by mammography, can be detected by palpation)
  • can be used to guide a biopsy needle
  • 85-90% predicative
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5
Q

Causes of acute mastitis

A
  • infectious or non-infectious (bacterial = staph or strep)
  • plugged breast ducts
  • typically associated with women who are breast feeding (1st month, postpartum)
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6
Q

consequences of acute mastitis

A
  • breast abscesses

- necrosis

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7
Q

What is the usual cause of fat necrosis?

A

trauma (esp. from a seat belt during a car accident)

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8
Q

examples of fibrocystic changes

A
  • fibrosis
  • cysts
  • palpable changes (can make detection of breast cancer difficult)
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9
Q

which type of fibrocystic changes has the higher risk of cancer?

A

aggressively proliferative type with atypia

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10
Q

characteristics of breast cysts/fibrocystic changes

A
  • 20-40 yrs old
  • doesn’t typically occur after menopause
  • can calcify
  • can look like cancer on a mammogram
  • 60% of women have microscopic cysts associated with epithelial tissue
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11
Q

characteristics of benign neoplasms of the breast

A
  • most common = fibroadenomas
  • mostly connective tissue, well circumscribed
  • don’t remove unless uncomfortable
  • usually occurs in patients < 30 yrs.
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12
Q

incidence of breast carcinoma

A
  • rarely occurs in patients < 25 yrs
  • affluent societies with highest incidence regardless of race –> environmental causes
  • about 30% incidence by 70 yrs old, 30% of cases are fatal
  • about 250,000 new cases of breast cancer/yr in the US
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13
Q

breast carcinoma and genetics

A
  • 5-10% of cases = inherited (single strong gene factor; BRCA 1 and 2 are the most common inherited genes)
  • 20-30% of cases = family tendency (not a single strong gene, but a pattern of occurrence in families)
  • 70-80% of cases = no familial pattern, just chance
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14
Q

causative factors of breast carcinoma

A
  • diet high in animal fats
  • obesity
  • delayed first pregnancy
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15
Q

symptoms of breast carcinoma

A
  • pain
  • masses (assessed by palpation, mammography, ultrasound, MRI, or tissue biopsy)
  • swollen, pitted surface (“peau d’orange” - orange peel)
  • enlarged axillary lymph nodes
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16
Q

Prognosis of breast carcinoma

A
  • based on size, axillary node status, and distant metastasis
  • 5 year survival: stage 0 = 92%, stage IV = 13%
  • if the tumor expresses estrogen/progesterone receptors if often responds to hormone therapy; higher estrogen receptors in postmenopausal
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17
Q

Invasive carcinomas make up _____% of cases of breast cancer.

A

75-85

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18
Q

characteristics of breast carcinomas

A
  • generally all are adenocarcinomas, originating from epithelial cells in the terminal ducts
  • most are ductal and the incidence increases with age (there are invasive and non-invasive types)
  • lumpectomies to remove smaller masses
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19
Q

characteristics/risk factors for cervical cancer

A
  • HPV-associated squamous cell neoplasms most common
  • risk factors: multiple sex partners, immunosuppression, early age of first sexual contact, oral contraception for more than 5 yrs, nicotine use
20
Q

what are the most common causes of excessive uterine bleeding?

A
  • polyps
  • endometritis
  • endometrial hyperplasia
  • cancers
  • anovulatory cycles (associated with malformation of hypothalamus/pituitary)
21
Q

Causes of endometrial polyps

A
  • hypertension
  • obesity
  • late menopause
  • < 2% progress to cancer
22
Q

characteristics of leiomyoma

A
  • benign smooth muscle neoplasm
  • estrogen dependent
  • bleeding and pain
  • may cause infertility
  • very frequent (about 10-15%)
23
Q

risk factors and treatment of endometrial cancer

A
  • risk factors: obesity, diabetes, hypertension

- treatment: hysterectomy (treatment of choice) with radiation and chemotherapy as adjuncts

24
Q

cause of endometritis

A
  • infections (chlamydia and neisseria)

- often associated with IUDs

25
Q

cause and treatment of endometrial hyperplasia

A
  • exaggerated responses due to excessive estrogen/excessive ovarian activity (lacks opposition from progesterone)
  • treatment: progesterone; hysterectomy
26
Q

what is preeclampsia?

A
  • secondary hypertension in pregnant women of at least 20 weeks gestation
  • often associated with diabetes
  • exact cause is unknown, but appears to be associated with abnormal circulation in the placenta
27
Q

what are the two types of ovarian masses

A
  • non-neoplastic cysts (follicular cysts)

- neoplastic (ex. endometrioid)

28
Q

characteristics of neoplastic ovarian masses

A
  • most are sporadic (90%)
  • contraceptives can decrease risk
  • treatment: total hysterectomy with removal of surrounding tissue and chemotherapy
  • 10% hereditary (BRCA 1 and 2)
  • most present at an advanced stage
29
Q

symptoms of ovarian masses

A
  • pelvic pain
  • pelvic mass (go figure)
  • abdominal bleeding
  • ** no effective screening method for ovarian cancer (unlike cervical cancer)
30
Q

what are the stages of the menstrual cycle?

A
  • menstrual stage: menses
  • follicular stage: proliferative, estrogen the predominant hormone
  • luteal stage: secretory
  • fertile window: last 5 days of follicular stage + ovulation
  • as populations age they spend more time in menopause of andropause
31
Q

characteristics of natural estrogens

A
  • steroid hormones derived from cholesterol (synthetic estrogens may not be steroids)
  • cross cell membranes and activate receptors inside the cell to modulate the expression of genes
  • different forms:
    > EstrONE (predominant during menopause, “E1”)
    > EstraDIol (predominant during repro years, most
    active form of estrogen, “E2”)
    > EstraTRIol (predominant during pregnancy and
    produced by the placenta, “E3”)
32
Q

Synthetic estrogens

A
  • steroidal = ethinyl estradiol

- non-steroidal = diethylstilbesterol

33
Q

physiological functions of estrogen

A
  • sexual maturity
  • increased CNS excitability (seizure inducing?)
  • increased endometrial and uterine growth
  • maintains skin elasticity
  • reduces bone absorption
  • alters plasma lipids - increases HDLs and triglycerides, reduces LDLs
  • increases blood coagulabiltiy
34
Q

clinical uses of estrogens

A
  • primary hypogonadism
  • postmenopasual problems
  • treatment of acne
  • reduce some repro organ neoplasms
35
Q

guidelines for use of estrogen

A
  • use smallest does for the shortest period of time possible

- local creams preferred to minimize systemic exposure

36
Q

adverse effects of estrogen use

A
  • postmenopausal bleeding
  • nausea
  • breast tenderness
  • migraines
  • hypertension
  • hyperpigmentation (especially around the eyes)
  • increased risk for some cancers (breast and endometrial)
  • smoking dramatically increases the risk of cardiovascular disease
37
Q

contraindications for use of estrogen

A
  • liver diseases (slowed metabolism)
  • breast/endometrial cancers
  • thrombolytic disorders
38
Q

characteristics of progestins

A
  • made from cholesterol
  • present in males, but less than females
  • progesterone is the most important progestin in humans
  • precursor to many steroid hormones: estrogen, androgen, adrenocortical steroids (cortisol), testosterone, estradiol
39
Q

effects of synthetic progestins

A
  • half life = 5 min (short acting)
  • increase fat deposition
  • decrease CNS excitability (antiseizure?)
  • increase aldosterone (increased Na+ retention, increased BP, increased water retention and blood volume)
  • increased body temperature
  • increases insulin and insulin response to glucose
40
Q

clinical uses of progestins

A
  • replacement therapy
  • oral contraception
  • long-term ovarian suppression (for cases of dysmenorrhea or endometriosis; no issue of bleeding or clotting like with estrogens)
41
Q

risks/contraindications for progestins

A
  • breast cancer risk

- severe hypertension or heart disease is a risk

42
Q

2 main categories of hormonal contraception

A
  • combination (estrogen and progesterone) - decreases ovulation (approaching 100%) and decreases conception/implantation
  • progestin only (less effective, about 80-90%) - decreases ovulation (50-80%), thicken mucus and reduces sperm penetration, impairs implantation, less side effects
43
Q

methods of delivery for hormonal contraceptives

A
  • combinations: monophasics (constant doses of both estrogen and progesterone), biphasics (dosage of one or both change once during the cycle), and triphasics (dosages change 2 times during the cycle)
  • progestin only: “minipill”, fewer side effects but less effective
  • implantable: efficacy 2-4 yrs (ex. Norplant)
  • injections: IM, sustained effects
  • intravaginal rings
  • IUDs with and without estrogen/progestin
  • Transdermal combinations
44
Q

side effects of combinations

A
  • typically reverse when contraceptive is discontinued
  • reduced ovarian function and size
  • increased breast size and tenderness
  • increased thrombolytic events
  • increased heart rate and BP
  • hyperpigmentation, especially around the eye
  • mild nausea, breakthrough bleeding, headaches
  • interactions with antibiotics that disrupt GI normal flora (ex. amoxicillin) because absorption of the contraceptives is dependent on these bacteria
  • reduced sebum production in the skin (can cause dry skin and help treat acne)
45
Q

side effects of estrogen only replacement

A
  • increased risk of ovarian, endometrial, and breast cancer after 10 yrs of use
  • nausea, breast tenderness, migraines, hypertension (these effects are dose dependent)
46
Q

uses of contraceptives/hormone replacements

A
  • oral contraception
  • menstrual disorders, irregularity, heavy discharge
  • acne
47
Q

clinical uses/effects of testosterone

A
  • can be converted to estradiol via aromatase enzyme –> adverse effects in men that have too much testosterone
  • hormone replacement therapy in males
  • treatment of gynecological disorders in females (engorged breasts after child birth, uterine bleeding in postmenopausal women, etc.)
  • protein anabolic effects (replace muscle loss)
  • growth stimulation (can prematurely close growth plates in adolescents)
  • counter age-related muscle loss
  • masculinization in women
  • when abused for muscle strength/building, can cause acne, aggressiveness, and “roid rage”