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Therapeutics 5 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Estradiol brand name and therapeutic class

A

Vivelle-Dot, Alora, Climara, Femring, Estring, Vagifem, Divigel, Estrace

Hormone/Estrogen

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2
Q

Estrogens (conjugated) brand name and therapeutic class

A

Premarin

Hormone/estrogen

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3
Q

Medroxyprogesterone acetate brand name and therapeutic class

A

Provera

Hormone replacement

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4
Q

Progesterone brand name and therapeutic class

A

Prometrium

Hormone replacement

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5
Q

Venlafaxine HCL brand name and therapeutic class

A

Effexor XR

Antidepressant (SNRI)

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6
Q

Desvenlafaxine

A

Pristiq

Antidepressant (SNRI)

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7
Q

Paroxetine HCl brand name and therapeutic class

A

Paxil XR, Pexeva

Antidepressant (SSRI)

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8
Q

Fluoxetine HCl brand name and therapeutic class

A

Prozac, Sarafem

Antidepressant (SSRI)

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9
Q

Perimenopause

A

Start of menstrual cycle irregularity until 12 months after last menstrual cycle

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10
Q

Menopause

A

12 months after last menstrual cycle

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11
Q

Early menopause

A

Menopause at age 40-45

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12
Q

Estrogens

A

refers to estradiol, estrone, estriol, and synthetic estrogens

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13
Q

Progestogen

A

Refers to progesterone and synthetic progestins

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14
Q

ET

A

estrogen therapy

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15
Q

EPT

A

estrogen plus progesterone therapy

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16
Q

Menopause etiology

A

Occurs at average of age 51
Loss of ovarian function leads to hormonal deficiencies
Due to: natural aging, ovarian surgery, meds, pelvic irradiation
<25% of women experience menopause without symptoms
Symptoms may last months to years

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17
Q

Hormonal changes in menopause

A

Increase in FSH and LH

Decrease in estrone and estradiol

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18
Q

Symptoms of menopause

A

Vasomotor symptoms (hot flushes, night sweats)
Sleep disturbances
Mood changes
Decreased libido
Problems with concentration and memory
Arthralgia
Genitourinary symptoms- vaginal dryness and dyspareunia

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19
Q

Lab tests in menopause

A

Perimenopause: FSH on day 2 and 3 of the menstrual cycle greater than 10-12 IU/L
Menopause: FSH greater than 40IU/L

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20
Q

Nonpharm therapy for menopause

A

Hot flushes- layered clothing, lowering room temperature, decreasing spicy foods, caffeine, hot beverages, exercise
Vaginal symptoms: vaginal lubricants, moisturizers
Efficacy- little evidence, most women need additional therapy

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21
Q

Indications for treatment of menopause

A

Symptomatic women age <60 OR <10 years since menopause
Vasomotor symptoms +/- vaginal symptoms= systemic treatment
Vaginal symptoms only- topical treatment
Prevention of post-menopausal osteoporosis (in <60 year old postmenopausal women)

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22
Q

Treatment goals of menopause

A

Menopause is NOT a disease
Decrease symptoms
Improve QOL
Minimize AE

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23
Q

When should you avoid MHT?

A

Unexplained vaginal bleeding, stroke, TIA, MI, PE, VTE, breast or endometrial cancer, active liver disease

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24
Q

When should you use caution in MHT?

A

Diabetes, hypertriglyceridemia, active gallbladder disease, increased risk of breast cancer or CVD, migraine with aura

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25
Q

What do you need to evaluate before starting MHT?

A

CV and breast cancer risk

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26
Q

Benefits of MHT

A 
Decreased vasomotor symptoms
Decreased vaginal atrophy
Osteoporosis prevention and treatment 
Potential colon cancer risk reduction
Increased QOL, mood, cognition
Decreased dementia
Decreased DM
Less weight gain
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27
Q

Risks of MHT

A 
Breast cancer
CV disease
Endometrial cancer
Ovarian cancer
Lung cancer
VTE
Gallbladder disease
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28
Q

Treatment of menopause with intact uterus

A

Must have estrogen AND progesterone due to risk of endometrial hyperplasia

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29
Q

Duration of MHT

A

Based on patient symptom duration and risk factors
Should not be life-long, assess yearly
Generally accepted duration is 5 years or less
Taper slowly over several months to prevent rebound symptoms
Low dose intravaginal therapy can continue indefinitely

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30
Q

Estrogen therapy AE

A

Nausea, HA, breast tenderness, heavy bleeding

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31
Q

Route of administration of estrogen therapy

A

oral, transdermal, topical, IM, implanted pellets

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32
Q

Oral estrogens for menopause

A

Estradiol is most potent, but only 10% reaches circulation as free estradiol
Formulations: conjugated equine estrogens, micronized 17beta-estradiol, estradiol acetate, esterified estrogens, synthetic conjugated estrogens, estropipate

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33
Q

Other (non oral) estrogen formulations

A 
Forgoes first pass metabolism and thus increased estradiol concentrations
Transdermal patch (Vivelle-dot, Alora, Climara)- continuous delivery of estradiol, causes skin reactions so much rotate site
Topical sprays, gels, emulsions- vary in drug absorption 
Estradiol pellets- insert subcutaneously, difficult to remove, can have increased estradiol levels for months after removal
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34
Q

Intravaginal estrogens

A 
Used in genitourinary symptoms
Can have systemic absorption 
Creams (premarin, estrace)
Tablet (vagifem)
Ring (Estring)
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35
Q

Progestogens AE

A

Irritability, weight gain, bloating, headache

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36
Q

Progestogens agents

A 
Should be used in combo with estrogens in anyone with an intact uterus 
Medroxyprogesterone acetate (Provera)
Micronized progesterone (Prometrium)
Norethindrone acetate (Aygestin)
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37
Q

Combo therapy of MHT`

A

Continuous EPT- estrogen daily and progestogen concomitantly for 12-14 days/month
Continuous combined EPT
Continuous long-cycle EPT- estrogen daily and progestogen concomitantly for 12-14 days every OTHER month
Intermittent combined EPT- 3 days estrogen alone, 3 days estrogen-progestogen

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38
Q

Why can’t you use COC in menopause?

A

The dosing is very different. You need more estradiol in menopause than in COC

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39
Q

Other hormonal therapies for menopause (bazedoxifene)

A

Conjugated estrogens/bazedoxifene
MOA- bazedoxifene is a selective estrogen receptor modulator (SERM)
Indicated in patients WITH a uterus and have vasomotor symptoms or for osteporosis prevention

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40
Q

BBW for MHT

A

Estrogen- endometrial cancer, probable dementia
Progestogen- Breast cancer
Both- Should not be used for prevention of CV disorders

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41
Q

Contraindications of MHT

A

Known, suspected, or history of breast cancer or other estrogen or progesterone positive neoplasia
Active deep vein thrombosis
Active or recent coronary thromboembolic disease (stroke, MI)
Active liver dysfunction or disease

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42
Q

Relative contraindications to MHT

A

HTN, hypertriglyceridemia, hypothyroidism, fluid retention, severe hypocalcemia, ovarian cancer

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43
Q

Alternatives to hormonal therapy for hot flushes

A

Antidepressants using similar doses to depression
-Venlafaxine, desvenlafaxine, paroxetine (Brisdelle is only one approved for this indication)
Megestrol acetate-antineoplastic progestin
Clonidine
Gabapentin

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44
Q

Selective estrogen receptor modulators (SERMs)

A

Estrogen agonists in bone tissue
Estrogen antagonists in breast and uterus tissues
Tamoxifen, raloxifene (reduces risk or osteoporosis and breast cancer), ospemifene (used for dyspareunia)
AE- hot flushes, leg cramps

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45
Q

Sexual differentiation

A

Genetic sex- XY or XX
Gonadal sex- Testes or ovaries
Phenotypic sex- male/female genital tract and external genitalia
Psychological sex

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46
Q

Male sex differentiation

A

XY chromosomes- presence of SRY gene (on Y chromosome). This is the sex-determining region of the Y and encodes TDF (testis determining factor)
Primordial gonads differentiate into fetal testes- sertoli and leydig cells

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47
Q

Sertoli cells

A

Make mullerian-inhibiting substance (MIS)/ Anti- mullerian hormone
This causes regression in the mullerian ducts

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48
Q

Leydig cells

A

Make testosterone which leads to the wolffian ducts transforming into epididymis, vas deferens, seminal vesicles, ejaculatory duct
Testosterone can turn into dihydrotestosterone which leads to the development of the penis, scrotum, and prostate

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49
Q

Sperm production temperature

A

Sperm production requires temperatures several degrees below normal body temperature, thus the function of the scrotum. Thus, a warmer or colder scrotum can impact fertility

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50
Q

Semen fluids

A

Epididymis H secretion decreases pH of luminal fluid
Seminal vesicle- secretion and storage of fructose- rich product, PG, ascorbic acid, fibrinogen and thrombin-like proteins
Prostate- secretion and storage of fluid rich in acid phosphate and protease (prostate specific antigen: PSA)
Cowper glands- mucus upon arousal

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51
Q

What happens during prostate removal?

A

Removal of the ductal connection thus all of the proximal fluid components of the ejaculate. The prostatic urethra is left intact.

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52
Q

Composition of semen

A
  1. ) Testis- sperm (5%)
  2. ) Seminal vesicle- mucoid material: fructose, ascorbic acid, inositol, and other compounds (60%)
  3. ) Bulobourethral/ Cowpers gland- mucus secretions (15%)
  4. ) Prostate- think, milky alkaline fluid: citric acid, calcium, phosphatases, and other (20%)
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53
Q

Gonadotropin secretion

A
  1. ) Fetal to 1st year- GnRH, gonadotropins, sex hormones secreted at relatively high levels
  2. ) Infancy to puberty- secretion rates very low, reproductive function quiescent
  3. ) At puberty- secretion rates increase markedly, large cyclical swings in female, starts period of active reproduction
  4. ) Later in life- gonads become less responsive to gonadotropins, reproductive function diminishes, ceases entirely in females
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54
Q

Testosterone is at the highest level in the

A

morning

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55
Q

Effects of estradiol in the male

A 
17beta estradiol (aromatase activity)
Epiphyseal closure, prevention of osteoporosis, feedback regulation of GnRH secretion
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56
Q

Pathologies of androgens in males in fetal development

A

Defect in 5alpha reductase- does not allow for DHT production. Male genitalia will not fully develop, high levels of testosterone during puberty lead to development of genitalia, but urethra does not extend through penile shaft
Androgen insensitivity- defect in androgen receptor- partial or complete. Complete insensitivity results in female appearance (Y chromosome, testes present)

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57
Q

Pathologies of androgens in males during postnatal life

A

Hyposecretion before puberty- eunuchs. Bones keep growing; patient grows tall but has feminine characteristics
Hyposecretion after puberty- may not change many secondary characteristics
Normally, testosterone is secreted throughout life, but is reduced with advancing age
Early excess secretion of testosterone leads to precocious puberty- early development of sex characteristics, lack of growth
Treat with GnRH analogs (histrelin, nafarelin, leuprorelin)

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58
Q

LH and FSH receptors

A

Closely related to TSH receptor
Coupled via G alpha s
McCune albright syndrome- precocious puberty
Activating mutations of LH receptor- male limited familial precocious puberty
Loss of function in FSH receptor- infertility in males and females. Females primarily amenorrhea

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59
Q

Exogenously administered androgens

A

Can achieve normal systemic levels of testosterone but not normal seminiferous tubule levels. Normalize secondary sexual characteristics but not spermatogenesis.
Exogenous testosterone will inhibit LH and FSH secretion (impaired spermatogenesis)
Anabolic steroids (modified androgens) may lead to decreased fertility and erectile dysfunction (via decrease androgernic activity)
Long term use leads to irreversible CV disease (cardiomyopathy, atherosclerosis)

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60
Q

During erection, what happens to the penis?

A

Corpora cavernosa becomes rigid

Corpus spongiosum remains pliable

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61
Q

Reflex pathways for erection

A

Descending CNS pathways triggered and either stimulatory or inhibitory
-Increase activity of neurons that release nitric oxide
-Decrease activity of sympathetic neurons
Input from penis mechanoreceptors
-spinal reflex system

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62
Q

Masters and Johnson sexual response cycle

A

Desire (libido)
Arousal (excitement)
Orgasm
Resolution

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63
Q

Physiology of penile erection

A

Sexual stimulation causes endothelial cell derived nitric oxide secretion.
This increases GTP, cGMP, and GMP

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64
Q

Erectile dysfunction

A

Failure to achieve a penile erection suitable for satisfactory sexual intercourse

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65
Q

ED causes

A

Organic-
hormonal: hypogonadism, hyperprolactinemia, hyperthyroidism
Neurovascular: spinal cord injury, neurologic conditions (PD), neuropathy (DM)
Anatomical: penile abnormalities

Psychogenic- relationship stress, performance anxiety, depression

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66
Q

Hormonal physiology of penile erection

A

Testosterone principally produced by testes- free 2%, majority bound to sex hormone-binding globulin
Highest levels in morning, lowest in evening (10pm)
Testosterone stimulates libido and increases muscle mass
Testosterone is activated to DHT which stimulates prostate gland growth, increases facial/body hair, induces baldness, and causes acne
Testosterone naturally decreases after age 40
Normal physiologic serum total testosterone 3,000-1,100 ng/dL

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67
Q

Common risk factors for ED

A

Same as CVD. There is a common pathway linking CVD and ED (endothelial dysfunction and atherosclerosis)
Age, smoking, diabetes, HTN, dyslipidemia, depression, obesity, sedentary lifestyle

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68
Q

Screening tools for ED

A

IIEF-5- can be used to monitor response

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69
Q

Medication causes of ED

A

Alcohol, nicotine, illicit drugs (amphetamines, barbiturates, cocaine, opiates, marijuana)
Analgesics (opiates)
Anticonvulsants (phenobarbital, phenytoin)
Antidepressants (SNRI, TCA, SSRI, MAOI, lithium)
Antihistamines
Antihypertensives (alpha blockers, beta blockers, CCBs, clonidine. methydopa, resserpine)
Antiparkinson agents (bromocriptine, levodopa, trihexyphenidyl)
Antipsychotics (chlorpromazine, haloperidol, pimozide, thioridazine, thiothixene)
CV agents (digoxin, disopyramide, gemfibrozil)
Cytotoxic agents (diuretics, spironolactone, thiazides)
Hormones and hormone active agents
Immunomodulators- interferon alfa
Tranquilizers- benzodiazepines

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70
Q

First line therapies for ED

A

lifestyle modifications
Medication changes if needed
Oral phosphodiesterase-5 inhibitor if not contraindicated

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71
Q

2nd line therapy for ED

A

Intraurethral or intracavernosal alprostadil (Caverject)

Vacuum device

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72
Q

PDE-5 inhibitors and CV risk

A

Low risk- patient can be started
Intermediate risk- pt should undergo complete CV workup and treadmill stress test to determine tolerance to increased myocardial energy. Reclassify as low or high risk
High risk- contraindicated, recommend against sexual intercourse

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73
Q

PDE isoenzymes

A

Isoenzyme type 1- vasculature
Isoenzyme type 5- corpus cavernosum of penis and vasculature of the lung
Isoenzyme type 6- rods and cones of eyes
Isoenzyme type 11- striated muscle

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74
Q

PDE-5 inhibitor MOA

A

Competitive, reversible inhibition of PDE-5 found in genital tissues
Requires sexual stimulation for effect
Efficacy around 60-80%

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75
Q

PDE-5 inhibitor agents

A

Avanafil (Stendra), Sildenafil (Viagra), Tadalafil (cialis), Vardenafil (Levitra, Staxyn)

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76
Q

Sildenafil

A

PDE-5 inhibitor
25 to 1000 mg orally 30 to 60 minutes before sexual activity
Lower dose in pts taking 3A4 inhibitors, hepatic/renal impairment, age >65 years
Onset of action: 30 minutes
Duration of action: 4-12 h

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77
Q

Vardenafil

A 
PDE-5 inhibitor
5 to 20mg 1 hour before sexual actibity
Lower dose in patients take 3A4 inhibitors, hepatic impairment, age >65
Onset of action- 30-60 minutes
Duration of action- 4-6 h
78
Q

Avanafil

A

PDE-5 inhibitor
50-200 orally 15 to 30 minutes before sexual activity
Lower dose in patients taking 3A4 inhibitors and hepatic impairment
Onset of action- 25-40 minutes
Duration of action- 6+ hours

79
Q

Tadalafil

A

PDE-5 inhibitor
5 to 20 mg 30 min to 36 hours before activity. Consider 2.5-5mg QD for men who take >2times/week
Lower dose in patients taking 3A4 inhibitors, hepatic/renal impairment
Onset of action- 45 min
Duration of action- 24-36 h

80
Q

Which PDE-5 inhibitors do fatty meals decrease absorption?

A

Sildenafil, vardenafil

81
Q

Which PDE-5 inhibitors are affected by alcohol?

A

Avanafil- >3 drinks increases risk of hypotension

Tadalafil- >5 drinks increases risk of hypotension, dizziness, HA, tachycardia

82
Q

Which PDE-5 inhibitors work on isoenzyme type 1?

A

Sildenafil, vardenafil

83
Q

Which PDE-5 inhibitors work on isoenzyme type 6?

A

Sildenafil
Vardenafil
Moderate avanafil

84
Q

Which PDE-5 inhibitor works on isoenzyme type 11?

A

Tadalafil

85
Q

50mg sildenafil=

A

10mg vardenafil, 10mg tadalafil, 100mg avanafil

86
Q

Contraindications of PDE-5 inhibitors

A

Concomitant use of any type of nitrate (withhold for 24-48 hours after PDE-5 inhibitor)

87
Q

Precautions with PDE-5 inhibitors

A

Concomitant alpha 1 antagonists therapy (use uroselective)
QT prolongation with vardenafil
Use caution with CVD, hypotension, HTN, MI, stroke within 6 months, life-threatening arrhythmias, penile deformities, renal or stroke hepatic dysfunction, and degenerative retinal disorders

88
Q

AE of PDE-5 inhibitors

A

HA, nasal stuffiness, nausea, dizziness
Flushing (lowest with tadalafil)
Dyspepsia (lowest with avanafil)
Myalgias (lowest with vardenafil and avanafil)
Visual impairment (blurred vision, impaired color perception, color tinge to vision) (highest with sildenafil)

89
Q

Patient education for PDE-5 inhibitors

A

Patients must engage in sexual stimulation for response
Sildenafil and vardenafil should be taken on an empty stomach
Continue for 5-8 doses before dose failure is declared
Dose titration may be required
Avoid excessive EtOH use
Smoking cessation, weight loss
Involve sexual partner
Staxyn- take w/o liquids

90
Q

Alprostadil

A

Used for ED
MOA: Prostaglandin E1 increases cAMP
Intracavernosal injection more effective than intraurethral pellets
Some experts recommend a combo of alprostadil with papaverine and phentolamine- improves efficacy and decreases ADR

91
Q

Hypogonadism

A

Primary- Leydig cells of the testes slowly and progressively decrease testosterone production
Symptoms: decreased libido, erectile dysfunction, gynecomastia, small testes, reduced growth of body hair and beard, decreased muscle mass, increased body fat
If left untreated may lead to anemia and osteoporosis

92
Q

Evaluation of testosterone deficiency algorithm

A

Measure TT, If less than 300, repeat TT, measure LH, and measure Hct
If Hct >50% and second TT <300 withhold testosterone therapy and refer
If LH low or normal and second TT <300, test prolactin. If prolactin is normal than testosterone deficiency is confirmed
If Hct <50%, high/normal LH, and second TT <300, testosterone deficiency confirmed
PSA testing in pts >40

93
Q

Treatment algorithm of hypogonadism

A

Patient meets criteria for testosterone deficiency and is a candidate for therapy
Need to do CV risk assessment before initiating therapy
Exogenous testosterone- gels/creams, patch, buccal, IM, SQ pellet, nasal spray
Alternative- SERM, hCG, AI

94
Q

Monitoring testosterone therapy/ dosing changes

A

If the patient is achieving therapeutic levels without symptom improvement, consider testosterone cessation 3-6 months after starting treatment.
Lab testing every 6-12 months
Dose adjust or change modalities if not effective. Consider changing to exogenous testosterone.

95
Q

Testosterone replacement therapy controlled

A

CIII

96
Q

Advantages of testosterone injections (testosterone cypionate, testosterone enanthate)

A

No daily administration (IM every 2-4 weeks)
Inexpensive
Flexible dosing
Sometimes injected at home in the US

97
Q

Disadvantages of testosterone injections (testosterone cypionate and testosterone enanthate)

A

Injection site pain, fluctuations in testosterone levels may lead to variations in symptoms (mood, libido) that may increase with longer intervals, may causemore increases in hematocrit and hemoglobin than topical
Rare cough after injection

98
Q

Advantages of gel testosterone (Androgel)

A

Less skin irritation than patches

99
Q

Disadvantages of gel testosterone (Androgel)

A

skin irritation and odor
Risk of skin to skin transfer to another person (need to wash hands after application and wear clothes over application site)
Pumps must be primed prior to first use

100
Q

Application of gel testosterone (Androgel)

A

Do not apply to genitals
Do not apply to abdomen (exception is Androgel 1%)
Do not swim or wash for 2 hours after applying (5 hours for Androgel 1%)

101
Q

Testosterone therapy AE

A

Erythrocytosis
Acne/oily skin
Detection of subclinical prostate cancer
Growth of prostate cancer
Reduced sperm production and fertility
Formulation specific
IM- fluctuation in mood/libido, injection site pain, coughing
Gel- potential risk of transfer, skin irritation
Buccal- alterations to taste, irritation of gums
Pellet implants- infection, expulsion of pellets

102
Q

Contraindications of testosterone therapy

A

Contraindicated in men with breast or prostate cancer

103
Q

Monitoring of testosterone therapy

A

Topical, oral/buccal- within 4 weeks
IM- after cycle 4
Pellets- 2 and 12 weeks after each insertion
Goal- mid-normal range (450-600 ng/dL)
Monitor every 6-122 months once stabilized

104
Q

Labs for testosterone therapy

A

Hg/HCT- measure every 6-12 months or sooner to maintain HCT levels below 54%
PSA- in men without a h/o prostate cancer may need monitoring. Need to monitor in men with prostate cancer

105
Q

Other treatments for SD

A

Vacuum erection device

Penile prostheses

106
Q

Hypoactive sexual desire disorder (HSDD)

A

In females, most common sexual dysfunction
Recommend a 3-6 month trial of testosterone
Alternative therapy is flibanserin or bremelanotide

107
Q

Flibanserin BBW

A

Use with moderate/strong 3A4 inhibitors
Hepatic impairment
Alcohol use

108
Q

Two major functions of the prostate

A

Secrete fluids that make up a portion of the ejaculate volume
Provide secretions with antibacterial effect

109
Q

Three types of tissues in the prostate

A

1.) Epithelial
2.) Stromal (smooth muscle tissue)- embedded with predominantly alpha 1a adrenergic receptors
#.) Capsule

110
Q

Diagnosis of BPH

A

Histological diagnosis based on proliferation of glandular epithelial tissue, smooth muscle, and connective tissue

111
Q

Epidemiology of BPH

A

Most common prostate problem for men >50

Increases exponentially after age 40

112
Q

Pathophysiology of BPH

A

Exact etiology is unknown, however, it is thought to be multifactorial and related to testosterone
5a reductase type 1 and 2
Imbalance between growth and apoptosis leads to increases in cellular mass

113
Q

BPH leads to

A

BPE, BPO, and LUTS

114
Q

Static vs dynamic factors of BPH

A

Static- anatomic enlargement, produces physical block at bladder neck and obstructs urinary outflow
Dynamic- excessive alpha adrenergic tone results in contraction of the prostate around urethra

115
Q

Clinical presentatio of BPH

A

LUTS
Obstructive- unable to empty all of bladder
Irritative- storage issues, post void residual, frequent urination

116
Q

Medication related symptoms of BPH

A

Testosterone- gets converted to DVT and increases prostate mass
a-adrenergic agonists- phenylephrine vasoconstricts around urethra
b-adrenergic agonists
Anticholinergics
Diuretics
Avoid CCBs and Benzos

117
Q

Disease progression of BPH

A

Symptoms vary over time
Majority of patients will have stable symptoms when evaluated 4 years after initial BPH diagnosis
Most men with mild disease improve without treatment in 2-5 years
Markers of worsening symptoms and complications- prostate gland size 30-40 g, PSA >1.4 ng/mL

118
Q

Complications of BPH

A

Acute, painful urinary retention can lead to renal failure
Persistent or intermittent gross hematuria when tissue growth exceeds blood supply
Overflow urinary incontinence or unstable bladder
Recurrent urinary tract infection that results from urinary stasis
Bladder diverticula
Bladder stones
Chronic renal failure from long-standing bladder outlet obstruction

119
Q

Goals of treatment for BPH

A

Control symptoms
Reduce risk of complications
Delay need for surgical intervention

120
Q

IPSS

A

Ranks BPS symptoms

Lower points= less symptoms

121
Q

BPH mild disease treatment

A

Watchful waiting
Reassess every 6-12 months by looking at IPSS, urinary flow rate, PVR urine volume, prostate size
Educate patient about disease and behavior modification

122
Q

Behavior modification for BPH

A

Restrict fluids before bedtime or going somewhere with limited bathroom access
Limit caffeine, alcohol, and spicy food
Do bladder training or pelvic floor exercises
Treat and prevent constipation
Increase activity; avoid sitting for long periods of time
Avoid drugs that could exacerbate voiding symptoms

123
Q

Treatment algorithm for BPH

A

Alpha blockers are DOC, if pt also has ED he can start with PED5 as initial therapy
Lack or incomplete response to alpha blocker- consider trial of PDE5 or add on 5ARI if prostate is >30cc

124
Q

2nd generation alpha 1 receptor antagonist

A 
Used for BPH
Prazosin (not recommended dur to short T1/2)
Terazosin
Doxazosin
Alfuzosin (clinically uroselective)
125
Q

3rd generation alpha 1 receptor antagonist

A

Used for BPH
Selective for alpha 1 A subtype
Choose because they decrease risks of AE
Tamsulosin, silodosin

126
Q

alpha 1 receptor antagonist MOA

A

Relaxes smooth muscle in the prostate and bladder neck
Improve AUA symptom score within 2-6 weeks
Increase urinary flow rate
Reduce PVR urine volume
Durable clinical benefit
Effectiveness is dose dependent (start low and titrate)
No effect on prostate volume, does not reduce PSA levels. Just decreases the effects associated with increases in alpha receptors

127
Q

Alpha 1 receptor antagonists AE

A

All- HA, malaise, fatigue, URI/nasal congestion
Doxazosin, terazosin- first dose syncope, orthostasis, dizziness
Tamsulosin- Floppy iris syndrome, decreased libido
Terazosin- impotence
Ejaculatory dysfunction- tamsulosin and silodosin

128
Q

When should you avoid tamsulosin?

A

In severe sulfa allergy

129
Q

Floppy iris syndrome

A

Alpha blockers block alpha-1 receptors in the iris
This prevents the iris from fully dilating during eye cataract surgery
Pupillary constriction occurs despite use of mydriatic agents and iris billows out
Cannot be on alpha blockers before cataract surgery

130
Q

Uroselective alpha 1 receptor antagonists

A

Tamsulosin, Rapaflo, Uroxatral

131
Q

Onset of alpha 1 receptor blockers

A

Days-weeks

132
Q

5 alpha reductase inhibitors MOA

A

block 5-alpha reductase II which inhibits the conversion of testosterone to DHT

133
Q

5-alpha reductase inhibitors indication

A

Indicated for management of LUTS/BPH with prostatic enlargement as judged by prostate volume of >30cc on imaging, a prostate specific antigen >1.5 ng/dL, or palpable prostate enlargement on DRE
Reduce prostate size by 15-25%
Increases peak urinary flow rate
Improves voiding symptoms
Durable clinical benefit, it does not become less effective over time

134
Q

5 alpha reductase inhibitor agents

A

Finasteride (type II only)
Dutasteride (type I and II)
Onset is 3-6 months

135
Q

5-alpha reductase inhibitors AE

A 
Decreased libido, ejaculatory disorder, ED
Breast changes can also occur
Decrease PSA (need to get baseline)
Prostate cancer
"post finasteride syndrome"
Pregnancy category X
136
Q

PDE-5 inhibitors in BPH

A

Tadalafil is only one FDA approved
Relaxes smooth muscle in the prostate and bladder neck (increases cGMP)
Good to use if patient has ED and BPH
Leads to significant improvement in voiding symptoms, but little improvement in urinary flow rate or reduction in PVR urine volume.
Takes 4 weeks to work

137
Q

Anticholinergic agents in BPH

A

Add on therapy for irritative voiding symptoms
Caution in acute urinary retention
Agents- tolteridone, oxybutynin, trospium, solifenacin, darifenacin, fesoterodine

138
Q

Mirabegron

A

B3-adrenergic agonist used in BPH
Increases urinary bladder capacity and interval between voiding
AE- HTN, URI

139
Q

Finasteride/Tadalafil combo

A

For patients with a significantly enlarged prostate
D/C alpha-blockers at least 1 day prior to initiation
Provides a small benefit over finasteride alone for symptom relief in men with prostate volume >30 cc
Only studied for 26 weeks

140
Q

Which BPH treatments relax prostatic smooth muscle?

A

Alpha 1 antagonists

PDE5-inhibitors

141
Q

Which BPH treatments decrease prostate size

A

5ARI

142
Q

Which BPH treatment halts disease progression?

A

5ARI

143
Q

Which BPH treatment has CV AE

A

A1-antagonist, PDE5-i, Anticholinergics, beta 3 agonist

144
Q

Which BPH therapy causes efficacy in relieving BOO

A

A-1antagonists
5ARI
PDE5-i

145
Q

Which BPH therapy decreases PSA?

A

5ARI

146
Q

F/U of BPH

A

Evaluate 4-12 weeks after initiating treatment

Wait 3-6 months for longer onset drugs (5ARIs)

147
Q

M3 receptor of the bladder

A

parasympathetic stimulation of the M3 receptor by ACh causes contraction and the ability to urinate

148
Q

B3 receptors in the bladder

A

Inhibitory

Causes relaxation and sodium release

149
Q

Physiology of urinary incontinence

A

Any disruption in the integration of musculoskeletal and neurologic function can lead to loss of normal bladder control

  1. ) bladder fills- detrusor muscle relaxes, beta receptor mediated (bladder fills), pelvic floor and urethral sphincter contracts (alpha receptor mediated)
  2. ) first sensation to void- bladder half full, urination voluntarily inhibited until appropriate time
  3. ) Normal desire to void- bladder full)
  4. ) Micturition- cholinergic mediated, detrusor muscle contracts and pelvic floor relaxes
150
Q

Epidemiology of urinary incontinence `

A

Highly prevalent, more common in women
Substantial impact
Associated with decreased QoL, decreased personal/social activities, increased psychological stress

151
Q

Stress incontinence

A

F>M

Risk factors: weak pelvic floor muscles (childbirth, pregnancy, menopause); post-urologic surgery in men

152
Q

Urge incontience

A

Risk factors: increased age, neurologic disease (stroke, PD, MS, spinal cord injury, chronic bladder outlet obstruction

153
Q

Functional incontinence

A

Common causes: musculoskeletal limitations (OA, RA, PD, stroke) or cognitive impairment

154
Q

Overflow incontinence

A

Common causes: bladder outlet obstruction, diabetic neuropathy, spinal cord injuries, MS

155
Q

Overactive bladder

A

Detrusor muscle contracts before bladder is full

156
Q

Clinical presentation of urinary incontinence

A

lower abdominal fullness, hesitancy, straining, decreased force of stream, incomplete bladder emptying, frequency, urgency, abdominal pain, increase PVR
Urgency, frequency (>8 times/day), nocturia (>1 void/night), enuresis

157
Q

Clinical evaluation of incontinence

A

Symptoms, history, physical exam, urinalysis
Bladder diary- liquid intake, number of trips to bathroom, activities during leakage, strength of urge to void, accidental leaks

158
Q

Reversible causes of urinary incontinence

A 
Delirium
Infection
Atrophic vaginitis/urethritis
Psychiatric disorders
Pharmacologic agents
Excessive urine output
Restricted mobility
Stool impaction
159
Q

Meds than decrease bladder contractility (cause retention and overflow UI)

A 
ACE
Antidepressants
Antihistamines
Antimuscarinics
Antiparkinsonian agents
Antipsychotics
beta agonists
CCBs
Opioids
Sedatives, hypnotics
Skeletal muscle relaxants
160
Q

Meds that increase detrusor irritability or CrCl (cause urge UI)

A

Alcohol, caffeine, diuretics, acetylcholinesterase inhibitors

161
Q

Meds that increase urethral sphincter tone (cause retention and overflow UI)

A

Alpha agonists
Amphetamines
TCAs

162
Q

Meds that decrease urethral sphincter tone (cause stress UI)

A

Alpha 2 antagonists

163
Q

Diagnostic tests for UI

A

Stress incontinence- cough stress test
OAB- urodynamic; urinalysis should be negative
Overflow- assessment of PVR; renal function tests to rule out renal failure due to chronic urinary retention

164
Q

Goals of treatment for UI

A

Reduce or eliminate symptoms
Increase QOL
Prevent negative consequences associated with incontinence
Clinical- rashes, pressure sores, skin and UTIs, falls
Psychological/social- embarrassment, isolation, depression, anxiety, dependency

165
Q

Nonpharm for UI

A

1st line to all patients
Toilet proximity, safe path to bathroom, raised toilet seats, grab bars, toilet substitutes, weight loss if overweight, smoking cessation

166
Q

Bladder training

A

Retrain pelvic mechanisms and the CNS to inhibit urge sensation between voids
Used in patients with urge incontinence in patients without cognitive impairment

167
Q

Habit training

A

Individualized toileting scheduled to preempt involuntary voiding
Used in patients with urge incontinence WITH cognitive impairment

168
Q

Pelvic floor muscle exercises

A

Muscle contraction and relaxation to reduce incontinence by producing urethral closure and decreasing central nervous system stimulation of detrusor muscle
Used for urge and/or stress incontinence in patients without cognitive impairment

169
Q

Prompted and scheduled voiding

A

Indicated for urge incontinence for patients WITH cognitive impairment

170
Q

Red flags for UI

A

If present, refer to specialist
Associated pain, persistent hematuria or proteinuria, significant pelvic organ prolapse, previous pelvic surgery or radiation, suspected fistula, elevated postvoid residual

171
Q

Guideline for treatments of UI

A

Behavioral modifications 1st line
Oral antimuscarinics or beta 3 adrenergic agonists as second line
Prefer ER forms due to lower rates of dry mouth
Transdermal oxybutynin may be offered

172
Q

UI clinical principles

A

Inadequate symptom control and/or AE- dose modification or switch drugs
Should not use antimuscarinics in pts with narrow angle glaucoma
Use caution in patients with impaired gastric emptying or history of urinary retention
Manage constipation and dry mouth before abandoning an effective antimuscarinic therapy
Use caution in frail patients

173
Q

Stress UI treatment options

A

Duloxetine, antimuscarinics, topical. estrogen

174
Q

Overflow UI treatment options

A

alpha antagonists (tamsulosin in women), 5ARI (men)

175
Q

Urge incontinence treatment options

A

Antimuscarinics
Beta 3 agonists
Intravaginal estrogen for women

176
Q

Antimuscarinic agents for UI

A

Inhibits muscarinic receptors resulting in decreased urinary bladder contraction, increased residual urine volume, and decreased detrusor muscle pressure
Reduces UI frequency by 50%
Agents have similar efficacy
Oxybytynin, tolteridone, fesoterodine, trospium, solifenacin, darifenacin

177
Q

Which antimuscarinic causes QT prolongation?

A

Solifenacin

Tolterodine

178
Q

Which antimuscarinics are nonselective?

A

Oxybutynin, tolterodinee, fesoterodine

179
Q

Which antimuscarinics are selective?

A

Trospium, Solifenacin, Darifenacin

180
Q

Which antimuscarinic is a prodrug?

A

Fesoterodine

181
Q

Which antimuscarinic is impacted by food?

A

Trospium

Take 1 h before or 2 h after meals

182
Q

Antimuscarinic AE

A

Dry mouth, dry eyes, constipation, urinary retention, cognitive impairment, dizziness, visual changes, HA, thirst

183
Q

Oxybutynin AE

A

IR- orthostatic hypotension, sedation, weight gain

transdermal- pruritis, erythema, application site

184
Q

Which anticholinergics cause the most dry mouth, visual disturbances, dizziness, and constipation?

A

Oxybutynin

185
Q

Contraindications and precautions of antimuscarinics

A 
Urinary retention
Gastric retention
Severely decreased GI motility
Angioedema
Myasthenia gravis
Uncontrolled narrow angle glaucoma
Worsening hepatic/renal condition or concomitant drug therapy
Mental status change or risk for falls
186
Q

Beta 3 agonists

A

Modestly effective in reducing urinary frequency and incontinence
Relaxation of detrusor smooth muscle during storing phase increases bladder capacity
Mirabegron and Vibegron
Both increase digoxin levels

187
Q

B3 agonists AE

A

Mirabegron- HTN, nasopharyngitis, UTI, HA

Vibegron- GI (constipation, D, N, xerostomia), nasopharyngitis, HA, PVR, urinary retention

188
Q

Precautions with beta 3 agonists

A

Mirabegron- urinary retention, severe uncontrolled HTN (>180/110), increased effect of narrow therapeutic index drugs that are 2D6 substrates, QT prolongation, angioedema
Vibegron- urinary retention

189
Q

Duloxetine

A

Used for stress incontinence, but not FDA approved

190
Q

Topical/vaginal estrogens for UI

A

Topical for stress incontinence
Intravaginal for urge incontinence
Increases urethral tone
Mild benefit

191
Q

Bethanechol

A

Cholinergic stimulation of detrusor
Used for overflow incontinence but only FDA approved for urinary retention
Take on an empty stomach
AE- flushing, abdominal cramps, diarrhea, acute exacerbation of asthma

192
Q

Onabotulinumtoxin A

A

Botox
FDA approved for UI
Can only be used if pt will self-catheterize
Repeat doses no sooner than 12 weeks

Therapeutics 5 (6 decks)

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