MU NURS 611- ADV PATHO - EXAM 4 REVIEW -
REPRODUCTIVE SYSTEM QUESTIONS &
DETAILED COMPLETE ANSWERS
1. primary excessive endometrial prostaglandin production; painful periods;
dysmen- produces 10x as much prostaglandin F (potent myometrial stimulant
orrhea and vasoconstrictor)
2. elevated levels uterine hypercontractility, decreased blood flow to uterus, increased nerve
of hyper- sensitivity = pain
prostaglandin
s results from endometriosis, endometritis (infection), pelvic inflammatory
disease, obstructive uterine/vaginal anomalies, uterine fibroids, pulps,
3. secondary tumors, ovarian cysts, pelvic congestion syndrome, nonhormonal IUDs
dys-
menorrhea
4. polycystic cause unknown, may be genetic; no single factor fully accounts for
ovar- ian abnormalities
syndrome
(PCOS)
1/
8
, MU NURS 611- ADV PATHO - EXAM 4 REVIEW -
REPRODUCTIVE SYSTEM QUESTIONS &
DETAILED COMPLETE ANSWERS
5. hyperandr cardinal feature in pathogenesis of PCOS; glucose intolerance/insulin
o- genic resistance, hyperinsulinemia often run parallel and markedly aggravate it;
state affects follicular growth, insulin attects follicular decline by suppressing
apoptosis and enabling follicles to survive
2/
8
REPRODUCTIVE SYSTEM QUESTIONS &
DETAILED COMPLETE ANSWERS
1. primary excessive endometrial prostaglandin production; painful periods;
dysmen- produces 10x as much prostaglandin F (potent myometrial stimulant
orrhea and vasoconstrictor)
2. elevated levels uterine hypercontractility, decreased blood flow to uterus, increased nerve
of hyper- sensitivity = pain
prostaglandin
s results from endometriosis, endometritis (infection), pelvic inflammatory
disease, obstructive uterine/vaginal anomalies, uterine fibroids, pulps,
3. secondary tumors, ovarian cysts, pelvic congestion syndrome, nonhormonal IUDs
dys-
menorrhea
4. polycystic cause unknown, may be genetic; no single factor fully accounts for
ovar- ian abnormalities
syndrome
(PCOS)
1/
8
, MU NURS 611- ADV PATHO - EXAM 4 REVIEW -
REPRODUCTIVE SYSTEM QUESTIONS &
DETAILED COMPLETE ANSWERS
5. hyperandr cardinal feature in pathogenesis of PCOS; glucose intolerance/insulin
o- genic resistance, hyperinsulinemia often run parallel and markedly aggravate it;
state affects follicular growth, insulin attects follicular decline by suppressing
apoptosis and enabling follicles to survive
2/
8
