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endo y3s1 > IC19 Erectile dysfunction > Flashcards

IC19 Erectile dysfunction Flashcards

1
Q

definition

incidence

A
  • Persistent (at least 6 months) inability to achieve/ maintain erection for sufficient duration & firmness to complete sexual intercourse
  • Affects QOL
  • Increased incidence with age (>40years)
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2
Q

How erection works

changes in BF

A

Smooth muscle relaxes → more space for blood to enter
Changes in blood flow:
* Corpora cavernosa fills up with blood ⇒ increases inflow
* Swelling → compression of venules against tunica albuginea ⇒ reduced outflow

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3
Q

flaccid vs erection (difference in BF)

A

Flaccid
Blood flow into penis = blood flow out of penis

Erection
Erection arterial flow into penis > venous outflow

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4
Q

How erection works
activation by PNS

ACh, Prostaglandins + overall effect

A

Ach
* increases creation of nitric oxide (NO)
* Increases activity of guanylate cyclase
* Increases cyclic guanosine monophosphate (cGMP)

Ach & prostaglandins E
* Increases adenylyl cyclase
* Increases cyclic adenosine monophosphate (cAMP)

Overall effect
Smooth muscle relaxation & vasodilation ⇒ increase blood inflow

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5
Q

Functional hormonal system

purpose of testosterone, testing & treatment

A
  • Testosterone → encourage libido (sexual drive)
    Low testosterone ≠ ED, may have normal sexual fx
  • No need to test for patients with no symptoms
  • If have symptoms + low testosterone levels ⇒ can replace
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6
Q

physiology of detumescence

A

1. Deactivating PNS
* cGMP deactivated by phosphodiesterase type 5 [PDE5]
* Vasodilation stops & vasoconstriction occurs
* Prevents inflow of blood to penis

2. Activated SNS
* Induces smooth muscle contraction via α2 adrenergic receptors of arterioles
* Reduction in blood flow

3. Serotonin
Postulated inhibitory effects on sexual arousal

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7
Q

etiology of ED

A
  1. organic
  2. psychogenic
  3. mixed
  4. others
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8
Q

etiology: (1) organic
systems affected

A

Vascular: lack of BF entering penis due to narrowing of vessels
* Atherosclerosis, peripheral vascular disease (PVD), HTN, DM

Hormonal
* Hypogonadism → reduced testosterone
* Hyper-prolactinemia → suppression of testosterone production

Nervous: loss of sensation

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9
Q

etiology: (1) organic
medication induced + MOA

A

BP control
* Clonidine, Methyldopa, Beta Blockers (with the exception of Nebivolol), Thiazides Diuretics
* Decreases penile BF

Anticholinergics
* Tricyclic antidepressants, 1st generation AH, phenothiazines
* Decreases ACh activity

Dopamine antagonists
* Metoclopramide
* Dopamine can cause sexual arousal/ stimulation

Serotonin Selective Reuptake Inhibitors (SSRIs)
* Increases Serotonin in brain/ Decreased testosterone

5ARIs
* Finasteride, Dutasteride
* Decreases testosterone

CNS depressants
* Benzodiazepines, anticonvulsants
* Suppress perception of psychic stimulus (increased drowsiness)

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10
Q

etiology: (2) psychogenic

A

Due to thoughts/ feelings (psychological) rather than physical pathology

Malaise, loss of attraction, stress, performance anxiety, mental disorders, sedation

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11
Q

etiology: (4) others

A

Social habits: smoking, excessive alcohol intake, illicit drug use
Obesity

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12
Q

signs & symptoms of ED

A
  • Loss of interest in sexual activities, performance anxiety
  • Depression, anger, low self-esteem, embarrassment
  • Disharmony in a relationship
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13
Q

evaluation of ED

Sexual health inventory for men (SHIM)

A

Signs & symptoms
Sexual health inventory for men (SHIM)
* Mild to no ED: 17 - 21 points
* Moderate to severe ED: <11 points

Workup to identify underlying causes of ED
* Medical hx/ medications → organic causes
* Social hx
* Surgical hx
* Lab results → blood glucose, lipid profile, testosterone (only if symptomatic)

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14
Q

evaluation for CVD

indication, reasoning, when to test, management of CVD

A
  • Required for all patients with ED
  • Possible early symptom of comorbid CVD
    Sexual activity → SNS activation may increase BP & HR ⇒ increased risk of MI

When to test
* Low risk of CVD: ok
* unknown/ not low risk: exercise stress testing to evaluate exercise capacity
* unstable/ severe symptomatic CVD: defer until condition stabilise

Cardiac rehabilitation & regular exercise → good for reducing risk of CV complications with sexual activity

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15
Q

non-pharmacological management

A

Address modifiable RF
* Stop smoking, weight control, control glucose/ BP/ lipids, exercise, decrease alcohol intake

Psychotherapy
Devices: vacuum erection devices
Surgery: penile implant

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16
Q

pharmacological management

A
  1. PDE5 inhibitor
  2. testosterone replacement
  3. alprostadil
17
Q

(1) PDE5i: MOA

A
  • inhibit PDE5 enzyme which induces catabolism of cGMP
  • enhance cGMP activity → induce smooth muscle relaxation ⇒ erection
18
Q

(1) PDE5i: indication & requirements

A

First line agents → that is if no symptomatic hypogonadism (lack of testosterone)
REQUIRES sexual stimulation → then can cause & enhance erection
Failure rates ~30-40%

19
Q

(1) PDE5i: drugs available

A
  1. sildenafil
  2. tadalafil
  3. vardenafil
  4. avanafil
20
Q

(1) PDE5i: sildenafil

starting dose, dose range, onset & duration of action, dose adj, food

A
  • 50 mg PO 1 hour before intercourse
  • 25-100 mg
  • 15-60 mins
  • 4h
  • Empty stomach
  • May require hepatic & renal dose adjustments
21
Q

(1) PDE5i: tadalafil

starting dose, dose range, onset & duration of action, dose adj, food

A
  • 5 mg PO up to 36 hours before intercourse
  • 5-20 mg
  • 2.5-5 mg PO daily (Daily dose)
  • 15 mins - 2 hours
  • 36h
  • Regardless of food
  • May require hepatic & renal dose adjustments
22
Q

(1) PDE5i: vardenafil

starting dose, dose range, onset & duration of action, dose adj, food

A
  • 10 mg PO 1 hour before intercourse
  • 5-20 mg
  • 25-60 mins
  • 4h
  • Empty stomach
  • May require hepatic dose adjustments
23
Q

(1) PDE5i: avanafil

starting dose, dose range, onset & duration of action, dose adj, food

A
  • 100 mg PO 30 mins before intercourse
  • 50-200 mg
  • 15-30 mins
  • 6h
  • Regardless of food
24
Q

(1) PDE5i: indications for lower dose

A
  • Patients ≥ 65y/o
  • those taking alpha blockers
  • Patients with renal failure
  • Taking CYP3A4 Inhibitors: may increase the serum concentrations of PDE5 Inhibitors
25
Q

(1) PDE5i: SE

general + specific for each drug

A
  • Headache, rhinitis, flushing, muscle & back pain, dizziness, hypotension
  • Prolonged erections & priapism
    Must seek ED treatment if >4 hours
  • Sudden hearing loss (very rare)
    May be present with tinnitus & dizziness
  • QTc prolongation (Vardenafil)
  • Muscle pain (esp Tadalafil with PDE11 affinity)
  • Ocular problems (sildenafil & vardenafil with affinity to PDE6 in retina)
    Reversible problems with colour discriminating (blue from green)
    Sensitivity to light
    ischemia of optic nerve due to hypoperfusion caused by PDE5i
    Risk factors: DM, smoking, HTN, CVD, dyslipidemia, and age >50 y/o
    Patients with sudden decreased vision or vision loss to stop use and look for immediate medical attention
26
Q

(1) PDE5i: DDI

A
  • nitrates + PDE5I ⇒ potentially fatal hypotension
    Should avoid nitrates 12 hours after avanafil, 24 hours after sildenafil/ vardenafil & 48 hours after tadalafil
  • Increased risk of hypotension: Using multiple antihypertensives & Alcohol intake
  • CYP3A4 inhibitors ⇒ increases concentration of PDE5I
27
Q

(2) testosterone replacement: purpose

A

Restore serum testosterone levels to normal range (300–1100 ng/dL; 10.4– 38.2 nmol/L)

28
Q

(2) testosterone replacement: indication

A

hypogonadism with symptoms ⇒ first line
(1) decreased libido
(2) low serum testosterone concentrations

29
Q

(2) testosterone replacement: SE

c/i

A

irritability, aggressive behaviour, undesirable hair growth, BP, hepatotoxicity, dyslipidemia, polycythemia, prostatic hyperplasia (C/I for prostate Cancer)

30
Q

(2) testosterone replacement: dosage form

A

IM injection, buccal, patches, topical gel, body spray, nasal spray & PO

31
Q

(2) testosterone replacement: monitoring

A

serum testosterone within 1–3 months and at 6- to 12- month intervals
* discontinue if no improvement after 3 months

32
Q

(3) alprostadil: MOA

A
  • prostaglandin E1 analog stimulates adenyl cyclase → increased cAMP
  • Induce smooth muscle relaxation ⇒ erection
33
Q

(3) alprostadil: background

sexual stimulation, onset, DDI

A
  • NOT REQUIRE sexual stimulation
  • Fast onset: 5-10 mins
  • DDI: cannot use with PDE5I
34
Q

(3) alprostadil: dosage forms

A
  1. intraurethral pellet
  2. intracavernosal
35
Q

(3) alprostadil: intraurethral pellet

duration of action

A

30-60 mins

36
Q

(3) alprostadil: intraurethral pellet

SE

A
  • pain, warmth or burning sensation in the urethra
  • Voiding difficulties, bleeding or spotting
  • Priapism
  • partners may experience vaginal burning or itching
37
Q

(3) alprostadil: intracavernosal

benefits

A

Better efficacy; preferred route

38
Q

(3) alprostadil: intracavernosal

risks & disadvantages

A
  • higher risks of priapism, bleeding, hematoma, fibrosis

Disadvantages:
* Fear of needles, invasiveness
* lack of spontaneity
* Complicated administration technique

39
Q

(3) alprostadil: intracavernosal

titration

A

Titration in healthcare setting to duration of ≤1 hr, then self-administered no more than 3x per week

endo y3s1 (16 decks)

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