Pharm Flashcards
Name two drug classes that were emphasized to cause ED
B-blockers (switch to ACE/ARB if possible)
SSRIs
Recreational drugs/EtOH
What is the MOA of PDE5-inhibitors?
Blocks the degradation of cGMP in the corpus cavernosum, allowing it to accumulate and increase vascular flow
Name 3 important PDE5-inhibitors
Sildenafil
Vardenafil
Tadalafil
Compare sildenafil, vardenafil, and tadalafil
All three are PDE5-inhibitors
All should be taken ~1 hr before sexual activity
Tadalafil has the longest half-life and can be effective up to 36 hours post dose
Vardenafil and tadalafil are relatively contraindicated with a-blockers such as prazadosin and doxasin
All PDE5-inhibitors are STRONGLY CONTRAINDICATED for use with nitro products!
What are the AE Wooten emphasized with PDE5-inhibitors?
- Headache
- Hypotension
- Flushing
(Not emphasized by Wooten but discussed in clin med:
- Visual abnormalities are common with most PDE5-inhibitors
- Tadalafil associated with back pain/myalgia
- Priapism, more common with injectables)
What is the name and MOA of the injectable ED drug we discussed?
Alprostadil
It is an E1 prostaglandin, and increases the production of cAMP, thereby increasing smooth muscle relaxation –> increased blood flow
What is a first line treatment for priapism?
Psuedoephedrine
What are four drug classes Wooten discussed for treatment of BPH?
- a1 blockers
- 5-a-reductase inhibitors
- PDE5-inhibitors
- Antimuscarinics (not for use as monotherapy; can add to an a1-blocker)
What is the first line treatment for BPH, and what is the MOA of those drugs?
a1 blockers:
- Afluzasin
- Tamsulosin
These block a-adrenergic receptors, specifically preventing constriction of stromal tissue that might otherwise interfere with urethral function. AKA they reduce dynamic factor (stromal smooth muscle tone).
What are Finasteride and Dutasteride used to treat, and what are their MOA?
Finasteride and dutasteride are 5-a-reductase inhibitors, used to treat BPH (second line).
They inhibit the conversion of testosterone –> DHT, and since DHT increases prostate size, 5-a-reductase inhibitors work to reduce the size of the prostate. They reduce static factor (compression of urethra).
These take a little while to work and have more AE than a1 blockers.
What use, other than treatment of ED, does tidalifil have?
Tidalifil (a PDE5-inhibitor) is also sometimes used to treat BPH (3rd line) as it may slightly reduce prostate size.
Your patient presents with acute prostatitis and he is at low risk of STIs. What is the first line therapy?
A FQ such as levofloxacin 500-750 mg 10-14 days
Alternatives:
TMP/SMX for 10-14 days
Cipro 10-14 days (try to reserve if possible)
Your patient presents with chronic bacterial prostatitis. What is an appropriate therapy?
Per Banderas:
(Chronic >/= 4 weeks)
Levofloxacin 750 x 4 weeks (everything else I see says treat for 6-12 weeks?)
Alternatives:
Cipro x 4 weeks
TMP/SMX x 1-3 months!
Your patient is a 21 YO otherwise healthy female presenting with lower UTI. What is an appropriate therapy?
Acute, uncomplicated cystitis:
TMP/SMX PO BID x 3 days if <20% resistance in area per antibiogram
Alternatives:
Nitro x 5 days
Fosfomycin x 1 day (less efficacious)
Augmentin x 3-7 days
You performed a pre-treatment C&S on a patient that you diagnosed with cystitis. After 3 days the results show resistance to the empiric treatment that you prescribed, however, her symptoms have improved. Why might this be and what action should you take?
Per Banderas: These antibiotics concentrate in the urine. C&S studies are based on serum concentrations of antibiotics. If the patient is symptomatically better, it is likely that the urine concentration of antibiotic was sufficiently high to overcome the resistance, and her treatment does not need to be changed.
But in clin med we said to change antibiotics so ?
