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  1. What is AUA scoring?
    • 0-7: mild to asx
    • 8-19: sympomatic-moderate
    • 20-35: severe with complications
  2. What do urine flow labs show?
    PVR > 30 ml, uroflowmetry <10mL/sec
  3. What causes the prostate to enlarge?
    5 alpha reductase converts testosterone to DHT in the prostate, and DHT causes prostatic enlargement
  4. What exacerbates BPH obstruction?
    • Anticholinergics (antihistamines, TCA, phenothiazines=>decrease/weaken detrusor tone)
    • Alpha-adrengeric (ephedrine, phenylephrine, pseudoephedrine)=> increase bladder sphinctor tone
  5. In what types of pts is surgery recommended for BPH?
    Pts with urinary retention needing permanent catheterization; those with malignancy, severe complications, or medical tx resistance
  6. List the 2G alpha 1 blockers
    • Alfuzosin
    • Doxazosin
    • Terazosin
    • Alfuzosin is the only one that is really safe to use
  7. How are 2g alpha 1 blockers titrated?
    • day 1-3: 1 mg HS
    • Day 4-14: 2 mg HS
    • Week 2-3: 5 mg HS
    • Week four on ward: 10 mg HS
  8. What are the advantages of alpha 1 blockers?
    • onset 2-4 weeks
    • 6-10 year durable
  9. What are the disadvantages of alpha 1 blockers?
    • Orthostatic HTN
    • CHF (particularly doxazocin)
  10. Name the 3G alpha 1A blocker
  11. What are the advantages and disadvantages of Flomax?
    • Advantages: less orthostatic HOTN
    • Disadvantages: retrograde ejaculate, cataract surgery, sulfa allergy, interaction with phosphodiesterase type-5 (except tadalafil)
  12. What is the indication for 5 alpha reductase inhibitors?
    Pts with prostate enlargement > 40 grams
  13. What are the two 5 alpha reductase inhibitors?
    Finasteride, dutasteride
  14. What are the advantages of 5 alpha reductase inhibitors?
    • no orthostatic HOTN
    • 4-6 year durable
  15. What are the disadvantages of the 5 alpha reductase inhibitors?
    • Onset within 6mo
    • Decreased libido
    • gynecomastia
    • ED
    • PSA reduction of 50% which means you might not be able to detect prostate carcinomas
    • Increased rate of high grade carcinomas
  16. What is the indication for combo therapy for BPH?
    Resistant therapy or high risk of progression
  17. What are the causes of urinary incontinence?
    • Dementia
    • Infection
    • Atrophic urethritis/vaginitis
    • Pharmaceuticals (anticholinergics, alpha blockers, sedatives, narcotics)
    • Psychological
    • Excessive urine output
    • Restricted mobility
    • Stool impaction
  18. How do you tx urge incontinence?
    • Anticholinergics
    • Oxybutin (a non-selective anticholinergic) is the DOC
    • Selectives are tolterodine, trospium, solifenacin, darifenacin
  19. How is ditroban dosed?
    • Ditroban: non-selective anticholinergic for stress incontinence
    • Titration from 2.5 mg BID to 5mg TID over months
  20. Why is long acting ditropan better than nl length?
    • Ditropan: non-selective anticholinergic
    • Less ADRs
    • Titration is less (5mg QD to 30 mg daily over weeks)
  21. What are ADRs of non-selective anticholinergics?
    • Tachycardia
    • Confusion
    • Cognitive impairment
    • Constipation
    • Dry mouth
    • Vision changes
  22. Which selective anticholinergic is associated with the cypP450 system?
  23. Which selective anticholinergic is destroyed by antacids?
    Detrol LA
  24. Which selective anticholinergic is associated with less CNS ADRs?
  25. What makes trospium not a great drug?
    • Trospium: selective anticholinergic
    • Oral absorption <10%, expensive
  26. Which selective anticholinergics actually have questionable selectivity?
    Solifenacin and Darifenacin
  27. What is darifenacin's advnatage over IR oxybutynin?
    Dry mouth may be < than IR oxybutynin
  28. How do you tx stress incontinence?
    • Vaginal estrogens
    • Alpha adrenergic agonists
    • Duloxetine (Cymbalta)
  29. How do you tx overflow incontinence due to bladder outlet obstruction?
    alpha blockers
  30. How do you tx overflow incontinence due to bladder underactivity?
    Cholinergic agonist (Urocholine)
  31. What is the formal definition of ED?
    Persistent ED (at least 6mo), inability to achieve or maintain an erection of sufficient duration and firmness to complete satisfactory intercourse through caginal penetration
  32. What are vascular sources of ED?
    HL, ESRD, smoking, HTN
  33. What are neurologic causes of ED?
    Stroke, DM, prostate surgery
  34. What are hormonal sources of ED?
    Excess PRL and/or decreased testosterone
  35. What are drug induced causes of ED?
    5 alpha reductase inhibitors, anti-HTN, psychiatric medicines, alcohol, illicit drugs, cigarette smoking, some diuretics
  36. Which HTN meds contribute to ED?
    • HCTZ, BB, alpha blockers (methyldopa, clonidine)
    • Therefore pt should use ACE-I, ARBs, CCB
  37. What psych meds contribute to ED?
    TCA, antipsychotics, benzos
  38. Why is intracavernosal testosterone replacement DCd?
    Unnatural, non-spontaneous erection
  39. Why are Phosphodiesterase inhibitors (type 5) used in ED?
    They inhibit the enzyme, enhancing effects of nitric oxide-activated increases in cGMP
  40. What do you educate patients about when taking phosphodiesterase inhibitors?
    • Don't take with food, and need foreplay
    • Failure after 8 unsuccesful uses
  41. What is the timing of the different phosphodiesterase inhibitors?
    Levitra and Viagra 60 mins before, cialis 30 min
  42. Which ED drugs are associated most with hypotension?
    Viagra and Levitra, 5-6mmHg decrease
  43. Which ED drugs are associated with vision loss?
  44. Which ED drugs are associated with myalgia?
  45. What are the phosphodiesterase inhibitor DI?
    • Nitrates
    • Alpha blockers (either reduce PDE-5 dose or separate by 4+ hours)
    • Vasodilators
    • Cyp3A4 inhibitors (macrolide abx, antifungal agents, protease inhibitors)
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for my upcoming pharm exam
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