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Endo/Eye/Derm - Women/Men > Men' Health Dr. Bossaer > Flashcards

Men' Health Dr. Bossaer Flashcards

Dr. Bossaer

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1
Q

What are the causes of erectile dysfunction?

A

-blood supply to the penis -> Vascular diseases
>Peripheral vascular disease
>Arteriosclerosis
>Hypertension, BP meds
>Coronary artery disease
>Smoking, Obesity

-nerve signals for stimulation -> Neurologic
>Diabetic -> peripheral neuropathy
>Alcohol use, CNS depressants, depression (psychological)
>Trauma (prostatectomy)

-Hormonal
>Aging
>Hypogonadism (low Testosterone)

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2
Q

Drugs that can cause ED

A

-Anticholinergics: Antihistamines, TCAs, SSRIs (fluoxetine, sertraline, fluvoxamine), Benztropine (anti-parkinsonian drugs)

-Dopamine antagonist: Phenothiazines (metoclopramide, promethazine > prochlorperazine)

-Estrogens, antiandrogens: Digoxin, spironolactone, ketocanozole

-CNS depressants: EtOH, barbituates, anticonvulsants, opioids

-decreasing penile blood flow: diuretics, ß-blockers, central sympatholytics (clonidine)

-Others: 5-alpha reductase, MAOIs, Lithium, Gemfibrozil

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3
Q

Which testosterone level is considered Hypogonadism?

A

< 300 ng/dl

normal: 300 -1100 ng/dl

symptoms: malaise, depression, decreased libido
treat with testosterone replacement ONLY when testosterone is low and symptomatic

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4
Q

Which formulation for testosterone replacement is preferred?

A

Parenteral - preferred IM injection of Testosterone

-oral is hepatoxic
-transdermal products are often messy/oily

products should mimic circadian rhythms (AM peak/PM troughs)
normal testosterone metabolites (estrogen and DHT)
should be inexpensive and easy to use

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5
Q

Considerations with Testosterone

A

-Na retention -> higher BP
-increased hemoglobin (polycythemia) - makes the blood thick and harder for things to move around
-increased risk for VTE and CV events
-increased risk for liver cancer and hepatic complications with ORAL formulations
-gynecomastia -> due to the metabolite estradiol
-high risk of fractures?

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6
Q

What is the peak time for most phosphodiesterase inhibitors (PDEs)?

A

30-90 min

should be taken 30 - 60 min prior

Sildenafil
Avanafil
Vardenafil

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7
Q

Which PDE has the greatest time to peak?

A

Tadalafil with 2hrs

should be taken 60-120 min prior

-it also has the longest half-life and duration (24-36h)

-it has a daily dose available: 2.5 - 5 mg

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8
Q

Which PDEs absorption rate is not affected by a fatty meal?

A

Tadalafil

for Avanafil: the delay in Cmax is not clinically significant, can be taken with meal

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9
Q

Which PDEs have a pre-intercourse dose of 5-20 mg?

A

Tadalafil
Vardenafil

For Sildenafil: 25-100 mg
For Avanafil: 100-200 mg

start with low dose in patients with hepatic impairment

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10
Q

Which enzyme affects the metabolism of PDEs?

A

CYP 3A4

for Sildenafil: CYP 3A4 and 2C9
for Vardenafil: CYP 3A4, 2C9, and 3A5

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11
Q

Cross-reactivity of Sildenafil (PDE)?

A

inhibits PDE-6 (eyes)
-visual disturbance, blurry vision, color changes

to some degree PDE-11 (muscles)

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12
Q

Cross-reactivity of tadalafil (PDE)?

A

inhibits PDE-11 (muscles)
-myalgia (lower back, arms, legs)
-flushing -> they cause vasodilation
-headache

to some degree with PDE-6

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13
Q

Counseling points

A

-it takes time to work (~ 1 hour)
-erection after 4hr -> ER due to ischemia (blood is trapped, no perfused blood entering)

-Hypotension: Sildenafil/vardenafil drop SBP 8 to 10 mm Hg
-caution with alpha antagonist - (vasodilate smooth muscle cells of blood vessels) (IR formulations)

-vision loss? -> ER
Nonarteritic anterior ischemic optic neuropathy (NAION), potentially irreversible

contraindicated with nitrates!!!

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14
Q

Benefits of Tadalafil daily use

A

-reserved for on-demand failure
-can be more spontaneous with sex life
-better efficacy over on demand-use
-less toxic
-also effective for BPH symptoms

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15
Q

A patient with ED who takes nitroglycerin, which is the best PDE?

A

Sildenafil on-demand, may be used even though it has a contraindication

it has a short half-life so it will interfere the least with nitrate

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16
Q

Flibanserin (Addyi): drug profile

A

mixed (serotonin) 5HT agonist/ 5HT antagonist originally studied for depression
indication: Hypoactive sexual desire disorder
100 mg nightly - to avoid syncope and accidental injury from falling

17
Q

ADE of Flibanserin

A

-hypotension, syncope, CNS depression

.-Contraindication:
Relative: EtOH use within 2 hours
Absolute CI: strong or moderate 3A4 inhibitors
-> Flucanozole (strong 2C19 inhibitor)
Absolute CI: hepatic impairment

18
Q

Female Sexual dysfunction - menopause

A

-in menopausal women suffer from vaginal dryness and atrophy, pain during intercourse

-> topical estrogen

19
Q

What are the 3 tissues of the prostate?

A

-Epithelial: prostatic secretion

-Stromal: stimulation -> muscle contraction -> urethra compression through abundant alpha receptors
2:1 stromal to epithelial, in BPH 5:1 -> so alpha 1 receptor is a drug target

-Capsule: on the outside, mostly connective tissue, alpha1-receptors

20
Q

What causes prostate growth?

A

-aging: more testosterone converted to DHT by 5-alpha-reductase, DHT has a greater affinity to intraprostatic androgen receptors

-2 types of 5-alpha-reductase
Type 1: hair follicles and sebaceous glands
Type 2: prostate, genital tissue, scalp

21
Q

Pathophysiology of BPH

A

Static (structural): obstruction due to enlarged prostate

Dynamic: increased muscle tone within the prostatic bladder neck

environmental (fight or flight)

drugs: alpha-adrenergic agonists:
-pseudoephedrine
-anticholinergics (TCA, antihistamines, phenothiazines - dopamine antagonists)
-EtOH, caffeine, diuretics

22
Q

Which drug classes are used for moderate cases of BPH?

A

small prostate: alpha-antagonist -> reduce muscle contraction

large prostate: alpha-antagonist PLUS 5-alpha reductase -> to also slow down the growth of the prostate (it took years to grow, so it may take months to shrink)

concomitant Erectile dysfunction: alpha-antagonist and/or tadalafil

23
Q

Alpha-antagonists MOA

A

-inhibit alpha-1-receptors in prostate/bladder neck
-relaxes smooth muscle of prostate/bladder neck
-relieves dynamic symptoms
-work after 2-4 weeks

-First-line (start with alpha-1-blocker to treat BPH)

24
Q

What are the Alpha-1-receptor subtypes

A

alpha-1A: prostate, bladder neck (target)

alpha-1B: vascular smooth muscle (we do not want to target those)

alpha-1D: prostate (target)

25
Q

ADE Alpha-1-antagonists

A

with older generations:
Hypotension and Orthostasis (dizziness when standing up)

-nasal congestion
-sexual (ejaculation) dysfunction: since alpha-1-receptors are blocked the penis cant push out the semen
-floppy iris syndrome: with tamsulosin and other alpha-blockers (caution in case of eye surgery)

26
Q

What are the early generation alpha-1-antagonists

A

-Prazosin
-Doxazosin
-Terazosin
not often used anymore

caution for Hypotension and Orthostasis

27
Q

3rd gens alpha antagonists

A

-Tamsulosin (Flomax): targets alpha-1A and 1D
0.4 - 0.8 mg QD

-Silodosin (Rapaflo): targets alpha-1A
8 mg QD

-Alfuzosin: technically 2nd gen, but clinically uroselective

28
Q

ADE 5-alpha reductase

A

anti-androgenic effects: lower the number of DHT (androgenic)
-sexual dysfunction: impotence, decreased libido, erectile dysfunction

-Gynecomastia
-Hair growth (finasteride -> target type 1 and type 2 5-alpha reductase)

Precaution:
hepatic disease
reduces PSA (prostate screening marker) by 50% due to reducing the size of the prostate

increased risk of AGGRESSIVE prostate cancer

29
Q

5-alpha reductase options

A

Finasteride for BPH (Proscar): 5 mg QD

Finasteride for Alopecia (Propecia): 1 mg QD

Dutasteride: 0.5 mg QD

anti-androgenic effects: decreased libido, impotence (Erectile dysfunction), gynecomastia, increased risk for AGGRESSIVE prostate cancer

-slow onset: 3-6 months
-no CV side effects

30
Q

What is the most effective way to treat symptoms of BPH?

A

combination of alpha-1-blockers and 5-alpha reductase

alpha-1-blocker: short-term improvement but the improvement doesn’t get greater with time

5-alpha-reductase: it takes longer to work, but the condition improves more with time, since the size of the prostate gets smaller

-consider for men with enlarged prostate and moderate to severe symptoms

31
Q

How does Tadafil (PDE inhibitor) work for BPH?

A

Because there are PDE-5 receptors in the bladder and around the prostate -> can cause muscle relaxation and easier urine outflow from the bladder

32
Q

MOA Vibegron & Mirabegron

A

ß3 agonist

-relaxation of the detrusor muscle during the storage phase of urination
-allowing the bladder to store more urine, so to not go to the bathroom so frequently, but doesn’t make it easier to urinate

-used when alpha-blockers don’t work

-dose: 25 mg daily, up to 50 mg

Endo/Eye/Derm - Women/Men (30 decks)

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