1) Together, they inhibit ovulation better. Separately, you're correct; either oestrogen alone or progesterone alone can inhibit FSH or LH enough to prevent ovulation. But combining the two is synergistic and optimal from a contraceptive point of view. You'd never really give oestrogen alone because of its trophic and pro-thrombotic activity (among other things), but you can give progesterone alone (so called progesterone-only pills, POPs). So why doesn't everybody get POPs? Because they simply aren't as good, have to be taken more carefully, have more breakthrough bleeding, etc. If there are no contraindications (and there are a lot), OCP is the way to go.
Another way to think about it (though more in the context of dysfunctional uterine bleeding) is that the main problem with progesterone-only regimens is that over time the endometrium can become thin and atrophic and will slough unpredictably. That's what causes breakthrough bleeding on POPs. On the other hand, oestrogen is trophic and oestrogen-only regimens will lead to a thickened, hyperplastic endometrium that will break down and bleed heavily over extended periods of time, as seen in obese women with PCOS when they finally do have their periods. That what causes menometrorrhagia in PCOS. Because of both mechanisms, OCPs are the best drugs to regulate the menstrual cycle.
2) I have no idea what Goljan said, but testosterone increases hepatic lipase activity. As lipid content goes up, lipoprotein density goes down and size goes up. So if you think about what HDL and LDL comprise, you'll realize that hepatic lipase will 1) hydrolyze buoyant HDL2 into denser HDL3 which gets metabolized by the liver and 2) increase the number of LDL by literally splitting up the particles into smaller LDL. These smaller LDL particles can still circulate while the denser HDL3 particles can't. (By the way, when you administer testosterone you find an increase only the smallest kind of LDL, LDL-C, as you would expect since LDL gets hydrolyzed by hepatic lipase activity. LDL-C also happens to be the most dangerous kind of LDL.)
3) Also oestrogen increases SHBG which binds off excess androgens. When you do your clinicals, you'll learn that SHBG is probably one of the best tests to order to confirm PCOS (better than LH, FSH). But why are you doing biochemical testing for PCOS. Isn't PCOS a clinical or sonographic diagnosis? And you only need 2 of the 3 Rotterdam criteria even if you don't have an ultrasound. Wrong. There are other causes of late-onset virilization like atypical congenital adrenal hyperplasia that you need to rule out first. And don't forget to always get a prolactin! That's more for Step 2 and 3.
I've highlighted only the high-yield factoids.
