Exam 4-Reproductive Flashcards
Female Reproductive Growth/Masses
- polycystic ovary syndrome (PCOS)
2. Ovarian cysts
Polycystic ovary syndrome
Key features: decrease ovulation, increase androgens; assoicated with obesity, metabolic syndrome, ovarian and uterine cancer
** a condition in which the ovaries produce an abnormal amount of androgens, male sex hormones
Obese women: PCOS»_space; insulin resistance, increase insulin levels»_space; androgen secretion
FSH low, LH high»_space; increase androgens that convert to estrogen in the periphery»_space; continued FSH decrease, LH increase
Follicles fail, anovulation and cysts develop
Ovarian cysts
Follicular-benign unilateral cysts occur when follicle stimulated but doesn’t develop to maturity; rupture and regress
Corpus luteum-form in vascular corpus luteum; may rupture and cause abnormal uterine bleeding
Female Reproductive Track Cancers
- Cervical
- Uterine
- Ovarian
Cervical cancer
Etiology: HPV types 16 & 18 lead to dysplasia
Dysplastic cells initially precancerous, may progress to in situ (transformation zone) and invasive
S/S: usually asymptomatic, but can have vaginal bleeding, abrnormal discharge
Risk factors: Young women higher risk b/c columnar epithelial cells cover more of cervix (more sensitive to metaplasia)
Txt: HPV screening 30-65 years old. Screen if there is an abnormal pap.
Uterine Cancer
Pathology:
Involves glandular epithelium; unopposed estrogen
Most common symptom = abnormal uterine bleeding d/t altered epithelium; especially post menopause
Type I (hyperplasia) Type II (invades muscle)
S/S: unusual vaginal discharge, which can be foul-smelling, pus-like or blood-tinged.
pain during intercourse.
pelvic pain or pressure.
pain or feeling of pressure in the pelvis, lower abdomen, back or legs.
pain during urination, difficult urination or blood in the urine.
Risk Factors: older than 50, obese, take estrogen by itself without progesterone
Txt: sx to remove uterine, chemo, radiation
Ovarian cancer
Pathology- some associated with BRCA1 &2 genes; mesoderm derived cells migrate to ovary; other cells attach to ovary, transplanted” cell growth enhanced, metastasize. People who have the BRCA gene can be dx 10 yr before women without gene
Types-epithelial (develop from surface of epithelium from single cell); germ cell (due to meiosis error)
S/S: usually asymptomatic until tumors grow very large; vague abd distention, loss of appetite, and pelvic pain
Risk factors: hx endometriosis, early menarche, late menopause, nulliparity
Txt: sx to remove tumor, radiation, chemo
Breast Diseases
- Benign breast disease
- Breast cancer
- Male gynecomastia
Benign breast disease
Fibrocystic (nonproliferative)-cysts may regress, calcify, become chronically inflamed and fribrose
Ductal, lobular (proliferative)
- without atypia-numerous etiologies; types of lesions, generally present as defined mass; risk of cancer low
- with atypia-cells with altered structure without features of cancer cells; however risk of cancer increased
Breast cancer
Patho: r/t pregnancy, hormone influence, breast density, geneticsl lifestyle
Common subtypes: estrogen receptor, progesterone receptor; HER2; estrogen, progesterone, HER2 negative
Carcinoma in situ
Inflammation related
Invasive
Male gynecomastia
r/t to estrogen: testosterone imbalance, idiopathic, aging, obesity, adverse drug reaction, neoplasm
How does genetics influence breast cancer
BRCA1, BRCA2-normal function is tumor suppresion (role = DNA repair), therefore when mutated, it becomes dominant susceptibility genes (females and males; not limited to breast cancer)
Generally ductile epithelial cancers; heterogeneous and highly complex
Gene addiction-oncogenes and nononcogenes
Phenotype plasticity-unintentional development during cancer progression
Stem cells-origin, how continues to grow
How does lifestyle influence breast cancer
Ionizing radiation (as causitive factor and facilitating susceptibility). Diets high in fat and red meat, low fiber. Inconsistent positive association with alcohol intake, smoking, postmenopausal weight gain and obesity (but conflicting data)
Male reproductive track cancers
- Testicular cancer
2. Prostate cancer (adenocarcinoma)
Testicular cancer
young and middle aged males; germ cell etiology (seminoma, nonseminoma)
Primary manifestation is pain; may or may no have a mass
