Testosterone can be administered parenterally , but it has more irregular prolonged absorption time and greater activity in muscle in enanthate , undecanoate , or cypionate ester form. These derivatives are hydrolyzed to release free testosterone at the site of injection; absorption rate (and thus injection schedule) varies among different esters, but medical injections are normally done anywhere between semi-weekly to once every 12 weeks. A more frequent schedule may be desirable in order to maintain a more constant level of hormone in the system.  Injectable steroids are typically administered into the muscle, not into the vein, to avoid sudden changes in the amount of the drug in the bloodstream. In addition, because estered testosterone is dissolved in oil, intravenous injection has the potential to cause a dangerous embolism (clot) in the bloodstream.
Your story is the most accurate I have read. 100% true for women and it was Accutane that did it to me almost 20 years ago. I can remember the exact moment my orgasm started to fade as I was having it and it never returned. It was like a light being dimmed as the orgasm sensation slowly got weaker and weaker during that last climax and never returned. Dull light tingling now with full muscle spasms after orgasm so my body has responded to stimulation but the pleasure sensation of orgasm has diminished to virtually nothing. So unless a person is suicidal from having bad acne and it is life and death, my advice is: No!!!!!
Finasteride results in a decrease of circulating DHT levels by about 65 to 70% with an oral dose of 5 mg and of DHT levels in the prostate gland by up to 80 to 90% with an oral dose of 1 or 5 mg.    Unlike inhibitors of all three isoenzymes of 5α-reductase like dutasteride , which can reduce DHT levels in the entire body by more than 99%,  finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II ( IC 50 = 313 nM and 11 nM, respectively).   In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1), although its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than 5α-reductase type I) and hence is unlikely to be of clinical significance.  As of 2012, the tissues in which the different isozymes of 5α-reductase are expressed are not fully clear, as different investigators have obtained varying results with different reagents , methods, and tissues examined.  However, the different isozymes appear to be widely expressed, most notably in the prostate gland and hair follicles.