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PR3152 (cleefy) > PR3152 IC19 (BPH/ED) > Flashcards

PR3152 IC19 (BPH/ED) Flashcards

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1
Q

what is the physiology of the prostate

A

1) epithelial cells (glandular): growth stimulated by androgens
2) stroma cells (smooth): innervated by alpha1 adrenergic receptors

testosterone is converted into DHT by 5alpha-reductase.

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2
Q

what is the pathophysiology of BPH?

A

1) static component
- hormone factors (testosterone -> DHT) = enlargement of prostate tissue

2) dynamic component
- increase smooth muscle tissue and agonism of alpha 1 receptors = narrowing of urethra

= urethral obstruction and other s/sx

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3
Q

what is the pathophysiology of BPH in the long term, relating to bladder

A

the detrusor muscle must contract hard to force the urine out of the narrow urethra = hypertrophy = at the highest level of hypertrophy, the detrusor muscle compensates = bladder becomes irritative and highly sensitive = contract abnormally w/ smallest amounts of urine = increase urinary frequency.

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4
Q

what is LUTS

A

lower urinary tract symptoms (LUTS)
- nocturia, frequency, urgency, intermittent stream, straining, weak stream, incomplete emptying

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5
Q

progression of BPH in males? relate to age

A

more patients are asymptomatic until 65yo, where 1/3 will start to develop symptoms.

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6
Q

what are the two types of s/sx for BPH?

A

1) obstructive/voiding (typically early on)
- sensation of incomplete emptying
- dribbling
- weak stream
- intermittent stream
- hesitancy
- straining

2) irritative/storage (after several years, when detrusor starts to decompensated)
- frequency
- urgency
- nocturia
- dysuria (pain during urination)
- urinary incontinence

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7
Q

assessment methods for BPH

A

1) maximum urinary flow rate (Qmax)

2) Prostate specific antigen (PSA)
- not specific to BPH, but can monitor BPH progression. PSA ideally <1.5, may indicate risk of prostate cancer.

3) Post void residual (PVR)
- <100 = normal
- >200 = urinary retention

4) digital rectal exam (DRE)

5) ultrasonography

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8
Q

IPSS

A

7 sections, total of 5 per section, up to 35 max points

also includes QOL, up to 6 points.

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9
Q

MOH LUTS

A

4 grades

I) QOL <3, PVR < 100, treatment not needed

II) QOL ≥3 PVR <100, phx

III) QOLNIL PVR >100, Qmax<10ml/s surgical option

IV) QOLNIL, (urine retention, recurrent UTI, bladder calculi, persistent macroscopic hematuria)
surgery TURP

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10
Q

medication risk factors for BPH

A

need to remove risk factor

opioid analgesics = increases urinary retention

anticholinergics (tricyclic antidepressants eg -triptylines, antihistamines) = block acetylcholine which send signals for bladder contraction = reduces bladder muscle contractility

testosterone = increase prostate size

diruetics = increase urinary frequency

alpha 1 agonists (decongestants) = contract prostate smooth muscles

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11
Q

when do you NOT need to initiate treatment for BPH

A

if patient has IPSS < 8 or

mod-severe (IPSSS≥8) with QOL <3

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12
Q

non phx measures for bPH

A

1) limit fluid intake at night
2) avoid caffeine or alcohol intake
3) counsel patient to have complete and frequent urination
4) avoid meds that worsen symptoms

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13
Q

what to consider when initiating treatment for BPH

A

comorbidities
IPSS (luts severity)
prostate size
PSA

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14
Q

describe the alpha adrenergic antagonists (types, onset, and any specific instructions) in BPH

A

alpha1 adrenergic antagonists

1) non-selective: affect the peripheral vascular and urinary a1 receptors
- DTP: doxazosin, terazosin, prazosin (P not used)
- risk of hypotension and syncope = require dose titration slowly.

2) selective: selectively affect the urinary a1 receptors
- SAT: silodocin, alfuzocin, tamsulosin
- do not require dose titration.

onset is days to weeks

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15
Q

indication of alpha adrenergic antagonists in BPH

A

for patients with moderate to severe LUTS with small prostate <40g

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16
Q

downsides to alpha adrenergic antagonists in BPH

A

no effect on PSA
s/sx recur if discontinue
does not reduce prostate size or reduce progression of disease (only helps with symptomatic management)

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17
Q

benefits to alpha adrenergic antagonists in BPH

including onset time

A

fast onset of days to weeks

potentially beneficial in patients with concomitant HTN

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18
Q

side effect profile for alpha adrenergic antagonists in BPH

A

general: muscle weakness, fatigue, headache, ejaculatory abnormalities

uroselective: ejaculatory abnormalities
S>T>A

non-selective: dizziness, first dose syncope, hypotension

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19
Q

what medical condition to check when initiating alpha adrenergic antagonists and what to do w med admin in BPH

A

check for IFIS
- intraoperative floppy iris syndorms

caused by alpha adrenal blocking at the iris dilator muscle, complicates cataract surgery - likely cause = tamsulosin

to stop alpha blockers at least 14 days before surgery

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20
Q

administration instructions for non-selective alpha adrenergic antagonists in BPH

A

to take at night to reduce risk of orthostatic hypotension

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21
Q

what (and when) is the indication for 5ARIs in BPH

A

patients with moderate to severe LUTS and prostate size >40g

patients who cannot tolerate SE of alpha blockers OR do not want surgery

consider initiating if PSA >1.5

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22
Q

what are the 5ARI drugs in BPH

A

finasteride and dutasteride

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23
Q

benefits of 5ARI in BPH?

A

reduces PSA levels (consider initiating if PSA >1.5)

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24
Q

downsides of 5ARI in BPH?

A

slow onset 6-12months

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25
side effect profile of 5ARI?
decreased libido increased risk ejaculation abnormalities vs alpha blockers erectile dysfunction gynaecomastia lesser HTN risk 5ARI increases the amount of circulating testosterone that (not converted to androgen) is now converted into estrogen, leading to development of female features = gynaecomastia
26
contraindications for 5ARI? | special population
women and children
27
additional labs to take before initiating 5ARI in BPH?
obtain PSA before starting as it is difficult to interpret after initiating
28
indications for PDE5i in BPH?
adjunctive therapy for BPH
29
administration and onset of PDE5i for BPH? include the drug approved | include the drug used
tadalafil adminster irregardless of sexual activity onset days to weeks
30
when should monotherapy for PDE5i for BPH be initiated?
low BMI, young age, higher baseline symptoms
31
who are more likely to benefit from combination therapy?
moderate luts (IPSS 8-19), QOL (5-6), prostate >25g
32
a1 antagonist + 5ari combination for BPH?
alpha blocker onset in weeks to help manage symptoms, while 5ari onset in months to control the size of prostate symptomatic patients with enlarged prostate after 6 months can consider discontinuing alpha blocker.
33
PDE5i + 5ari combination for BPH?
help to mitigate 5ari side effects causing sexual disturbance/concomitant ED however, risk of cardiac problems (commonly associated with ED patients) avoid nitrate use eg GTN
34
a1 antagonist + PDE5i combination for BPH?
not recommended due to significant risk of LIFE THREATENING hypotension. if initiated: start with optimising and stabilising alpha blocker dose before adding pde5i at the lowest dose
35
when should antimuscarinics be added for BPH? (and initiated when)
for irritative/storage symptoms initiate if patient PVR <250 (150 in some guidelines)
36
MOA of antimuscarinics for BPH
inhibits smooth muscle contraction of bladder (detrusor) by blocking muscarinic receptor = decrease involuntary contraction
37
name the antimuscarinic BPH agents?
SOFTT -(blaDAR) solifenacin oxybutinin fesoterodine tolerodine trospium darifenacin
38
what is the definition of erectile dysfunction (ED)?
>6 months unable to have or maintain erection to have satisfactory sexual intercourse
39
what is the physiology of erection
activation of parasympathetic nervous system: 1) ach increase = increases in cGMP 2) ach and prostaglandin E increase = increase in cAMP = combined to increase smooth muscle relaxation and vasodilation = corpus carvenosa fills with blood (inflow increased) = presses against the tunica albuginea (outflow decreased) = erection testosterone plays contributory role but should be assessed with patient symptoms. patient may have low testosterone but no ED
40
what are the normal testosterone levels
300- 1000 ng/dL 10.4 - 38.2 nmol/L
41
what is the physiology of detumescence?
parasympathetic deactivation - PDE5 degradation of cGMP to 5GMP = reduced smooth muscle relaxation and increased vasoconstriction sympathetic activation - a2 adrenergic receptors = induce smooth muscle contraction = reduced blood flow
42
what is the etiology of ED
1) organic 2) psychogenic 3) mixed 4) others: social habits (smoking, drinking, illicit drug use), obesity
43
what are the factors in organic ED
1) vascular 2) hormonal 3) neurological 4) medication-related causes
44
what are the vascular causes in organic ED
atherosclerosis DM HTN PVD
45
what are the hormonal causes in organic ED
related to lack of testosterone - hypogonadism - hyperprolactinemia (increased prolactin = decreased testosterone and sperm production)
46
what are the neurological causes in organic ED
primary: CNS disorders secondary: neuropathy, DM, urethral surgery
47
what are the medication-related causes to organic ED (include moa)
BADSBC 1) BP medications: methydopa, betablockers (except ), thiazide diuretics = decreased blood flow 2) Anticholinergic agents: 1st gen antihistamines, tricyclic antidepressants (e.g. -triptyline) = decreased Ach activity 3) Dopamine Antagonists: metoclopramide = dopamine related to sexual arousal/stimulation 4) SSRIs = increase serotonine in brain/decrease testosterone 5) BPH meds: 5ARIs = decreases testosterone 6) CNS depressants: benzodiazepines, anticonvulsants =suppress perception of psychic stimulus
48
what are the causes of psychogenic ED?
Malaise Loss of attraction Stress Performance anxiety Mental Disorders Sedation
49
EDdiagnosis/ evaluation criteria?
1) signs and symptoms 2) SHIM (sexual health inventory for men) <11 = moderate to severe ED (mild is 17-21; goes up to 25 max) 3) patient medical history for underlying causes - social history, med/medication history, surgical history, lab results (lipid, glucose, testosterone)
50
why should CVS evaluation be initatied in ED patients?
1) possible early symptom of unidentified CVS problems 2) sexual intercourse = increase in sympathetic activation = BP and HR = risk of myocardial infarction
51
CV risk factors for ED and what to do?
if unknown or not low risk: test exercise capacity using exercise stress test. if unstable/severe symptomatic CVD: defer sexual activity until the condition stabilises cardiac rehab and regular exercise needed to reduce the risk of CV complications with sexual activity
52
non phx measures for ED?
1) address modifiable RF: control weight, BP, lipids, glucose exercise stop smoking decrease alcohol 2)psychotherapy 3) vacuum erection device (ved) 4) surgery eg. penile implant
53
what are the PDE5i agents for ED? include special instructions
SVTA Sildenafil - take with food. hepatic and renal dose adjustment Vardenafil - take with food. hepatic adjustment Tadalafil - long duration of action 36h - can be taken daily (OD) - take irregardless food. hepatic and renal dose adjustment Avanafil - take irregardless food.
54
when to lower dose of PDE5i for ED?
if - age >65 - taking alpha blocker - renal failure - cyp3a4 inhibitors e.g. macrolide, cimetidine, conazole antifungal, protease inhibitors
55
what are the SE for PDE5i
muscle and back pain (*pde11 in MSK*) headache, rhinitis, flushing, dizziness, hypotension (*relax arteries throughout body = increase flow*) priapism (for more than 4h = goA&E) sudden hearing loss (rare) (*due to increased blood flow to the ear*) ocular problems (*PDE6*): - sensitivity to light - colour discrimination problem (blue-green tinting of vision)
56
what are the food + drug interactions for PDE5i
X nitrates X antihypertensives X cyp3a4 inhibitors X alcohol = hypotension
57
what are the monitoring parameters for PDE5i (efficacy and safety) | E.G. if failure reported also
efficacy -If failure reported; * Administration with food? * Timingandfrequencyofdosing * Lack of adequate sexual stimulation * Titration to maximum dose * If all modifiable factors are addressed, may be treated with a different PDE5 inhibitor or proceed with other more invasive therapy safety * BP * Side effects * Drug interactions * Changes in cardiac health status
58
when to initiate testosterone for ED?
symptomatic gonadism with 1) reduced serum testosterone (should fall below the normal range of 300-1100ng/dl OR 10.4-38.2nmol/L) 2) decreased libido
59
SE of testosterone for ED?
circulatory system related - polycythemia - increase BP - dyslipidemia mood - irritability - aggression other organs - hepatotoxicity - prostatic hyperplasia others - undesirable hair growth
60
dosage forms of testosterone for ED?
Dosage forms: IM injection, buccal, patches, topical gel, body spray, nasal spray & PO
61
monitoring freq of testosterone for ED?
within 1-3 months monitoring then every 3-6 months. if no effect after 3 months = discontinue
62
MOA of alprostadil
prostaglindin E analog = stimulate production of cAMP = increased vasodilation and smooth muscle relaxation = erection no need for sexual stimulation for effect
63
onset, DOA, DDI, SE of alprostadil
5-10min onset for intraurethral = 30-60min duration of action DDI: PDE5i SE: pain, warmth or burning sensation in the urethra, voiding difficulties, bleeding or spotting, priapism, partners may experience vaginal burning or itching | no need sexual stimulation
64
intraurethral alprostadil pellets vs intracavernosal alprostadil
intracarvenosal has better efficacy BUT higher risk of priapism, bleeding, hematoma, fibroids + disadvantages: fear of needles, invasiveness, lack of spontaneity, complicated administration technique
65
titration for alprostadil intracavernosal
titrate in healthcare setting to erection that is maintain for ≤1 hr self administer no more than 3 times per week
66
what is yohimbine
alpha 2 antagonist controversial
67
side effect specific to tadalafil (more likely)
muscle pain due to afinity to pde11
68
side effect specific to vardenafil
QTC prolongation
69
PDE5i more likely to cause ocular problems( what + explain reasoning)
NAOINS: nonartertic anterior ischemic optic neuropathy - sildenafil and vardenafil - due to PDE5i causing hypoperfusion to the optic nerve resulting in ischemia
70
risk factors for NAION + counselling (PDE5i induced) | non artheritic ischemic optic neuropathy
DM, smoking, htn, cvd, dyslipidemia, >50yo if sudden vision loss/decreased vision = stop and go doctor
71
counselling points of PDE5i with nitrates?
12h: avanafil 24h: sildenafil and vardenafil 48h: tadalafil

PR3152 (cleefy) (13 decks)

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