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mens health Flashcards

1
Q

What is benign prostatic hyperplasia?

A
  • Progressive condition
  • Affects the lower urinary tract (LUT)
  • Non-malignant (no cancer) growth of some components of the prostate —> prostate enlarges
    • Transitional zone
    • Anterior zone
    • Peripheral zone
    • Central zone
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2
Q

What is the components of the prostate?

A
  • Epithelial (glandular tissue) —> Growth stimulated by androgens
  • Stromal (smooth muscle) tissue —> Innervate (supply with nerves) by alpha 1 adrenergic receptors
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3
Q

what is the function of the prostate

A

Testosterone is converted to dihydrotestosterone (DHT) by enzyme type II 5-alpha reductase —> Used for growth of prostate

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4
Q

What is the pathophysiology of benign prostatic hyperplasia?

A
  • Possibly due to age and hormones
  • Static component (hormones)
    • Dihydrotestosterone —> Enlargement of prostate tissue —> Physical compression which constricts urethra —> Urethral obstruction
  • Dynamic component
    • Increased smooth muscle tissue and stimulation of alpha 1 receptors —> Constriction —> Narrowing of urethra outlet —> Urethral obstruction
  • Urethral obstruction
    • Early phase: Bladder muscle is able to force urine through narrowed urethra by contracting more forcefully
      • Long term: Bladder muscle (detrusor muscle) gradually becomes thicker (hypertrophy) to overcome obstruction —> Muscle decompensates upon achieving hypertrophy peak —> Detrusor muscle becomes irritable and/or overly sensitive (overactivity or instability) —> Contracts abnormally in response to small amounts of urine in bladder —> Urge to urinate frequently
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5
Q

What are the signs and symptoms of benign prostatic hyperplasia?

A
  • Often asymptomatic, if not occurs in 1/3 men older than 65 years old
  • Lower urinary tract symptoms: Weak stream, Increased frequency, Nocturia (urge to urinate at night), Intermittant stream, Incomplete emptying, Straining, Urgency
    • Note that these symptoms are not specific to BPH! Could also be for urinary tract infections, prostate or bladder cancer, diabetes mellitus
  • Obstructive/ voiding symptoms: Early phase
    • Hesitancy, weak stream, sensation of incomplete emptying, dribbling, straining, intermittent flow
  • Irritative/ storage symptoms: Long term (after several years if untreated)
    • Dysuria (painful urination), increased frequency, nocturia, increased urgency, urinary incontinence (lack of voluntary control)
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6
Q

Assessment of BPH

A
  • Digital Rectal Exam (DRE)
  • Ultrasonography
  • Maximum Urinary Flow Fate (Qmax)
  • Postvoid Residual (PVR)
    • <100ml normal
    • > 200ml inadequate emptying
  • Prostate specific antigen (PSA)
    • Might be elevated in BPH and positively correlated with prostate volume
    • Predict progression of BPH (>1.5 ng/mL)
    • Higher risk for prostate cancer
    • Not specific to BPH, but specific to prostate size
  • Evaluate Medication history
    • Anticholinergics: Decrease bladder muscle contractibility
      • Promotes smooth muscle relaxation, taken when trying to pass that last bit of urine out
      • Antihistamines, Tricyclic antidepressants (TCAs)
    • Alpha-1 adrenergic agonist: Contraction of prostate smooth muscles
      • Decongestants
    • Opioid Analgesics: Increase urinary retention
    • Diuretics: Increase urinary frequency
    • Testosterone: Stimulate prostate growth
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7
Q

what is the non pharma Management for BPH?

A
  • Limit fluid intake in evening
  • Minimise caffeine and alcohol intake
  • Educate patient to take time to empty bladder completely and often
  • Avoid medications that can exacerbate symptoms
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8
Q

when can we do non pharma for bph?

A

For mild symptoms or symptoms that are not bothersome —> Watchful waiting! do lifestyle changes; Reco at any stage if have LUTS secondary to BPH

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9
Q

when can we do pharma for bph?

A

Start if symptoms bothersome or complications occur

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10
Q

what if have bph and ed? what is the likelihood of cardiac comorb

A

high

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11
Q

what if have bph and ed? if likelihood of cardiac comorb is high, then dont initiate what? and cannot use what?

A

If have BPH and ED, likelihood to have cardiac comorbidities: Dont initiate PDE5i if have unstable angina as cannot use with nitrates

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12
Q

need to consider what before initiating meds for bph?

A

Considerations: LUTS severity (IPSS), prostate size, concurrent comorbidities, PSA value, Presence of irritative/ storage symptoms

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13
Q

what are the meds for bph?

A
  1. Alpha Adrenergic Antagonist
  2. 5 Alpha Reductase Inhibitors (5ARIs)
  3. Phosphodiesterase 5 Inhibitor (PDE5I)
  4. Combination Therapy
  5. Symptomatic relief: Anti-muscarinics
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14
Q

what is Alpha Adrenergic Antagonist for ?

A

Effective for mod-severe LUTS with small prostate <40g; Works on smooth muscles, not prostate size

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15
Q

what are the types of Alpha Adrenergic Antagonist ? and what are the diffs?

A
  • Non-selective: Antagnoise both peripheral vascular and urinary alpha-1 adrenergic receptors
    • Agents: Doxazosin, terazosin, prazosin (not reco for BPH)
    • Titrate slowly!!!! due to risk of hypotension and syncope (passing out)
    • Good for hypertensive patients that need additional lowering of bp
    • Avoid if have or had syncope
    • Not as a monotherapy if have hypertension AND BPH
  • Selective for urinary alpha-1 receptors (predominant receptors in prostate and LUT)
    • Agents: Alfuzosin, tamsulosin, silodosin
    • No need dose titrate: Lesser risk of hypotension
    • Good for non-hypertensive patients
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16
Q

whats the characteristics of Alpha Adrenergic Antagonist?

A
  • Wont reduce prostate size, wont prevent progression of BPH or need for surgery
  • Does not affect prostate specific antigen bc dont affect prostate size
  • Fast onset (days-weeks)
  • Signs and symptoms might recur if discontinue
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17
Q

whats the side effects for taking alpha adrenergic antagonist?

A
  • Muscle weakness, fatigue, ejaculatory disturbance, headache
    • Bedtime admin to decrease orthostatic effects
    • Non selective: Dizziness*, first dose syncope and orthostatic hypotension (bp drops upon sitting up)
    • Uroselective: Low to none peripheral vascular dilatation (so less hypotension or syncope), ejaculatory disturbance (Silodosin > Tamsulosin > Alfuzosin; Less sexual dysfunction than 5ARI)
    • Intraoperative floppy iris syndrome (IFIS)
      • Complicates cataract surgery: Surgery requires dilation of iris
      • MOA linked to blockage of alpha 1 receptors in iris dilator muscle
      • Mostly due to tamsulosin
      • Avoid if have planned cataract surgery until surgery done or hold at least 14 days before surgery)
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18
Q

what is 5 alpha reductase inhibitors for?

A

Effective for mod-severe LUTS with large prostate >40g or if want to avoid surgery or cannot tolerate SE of alpha 1 antagonist

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19
Q

how does 5 Alpha Reductase Inhibitors (5ARIs) work?

A
  • Inhibits 5-alpha reductase (Type II) —> decrease conversion of testosterone to DHT —> reduce prostate size
    • Slows disease progression, decrease need for surgery
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20
Q

what are the types of agents for 5 Alpha Reductase Inhibitors (5ARIs)?

A

Finasteride and Dutasteride

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21
Q

what are the characteristics for 5 Alpha Reductase Inhibitors (5ARIs)?

A
  • Can decrease PSA levels: Consider adding if initial PSA >1.5 ng/mL
    • Measure PSA before initiation
  • Slow onset (up to 6-12 months) to decrease prostate size
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22
Q

what are the side effects for 5 Alpha Reductase Inhibitors (5ARIs)?

A
  • Ejaculatory disorders (reduced semen during ejaculation or delayed ejaculation)
    • Higher risk than alpha antagonist
  • Decreased Libido (3 -8%)
  • Erectile Dysfunction (3-16%)
  • Gynecomastia and breast tenderness (1%)
  • Lesser risk of hypotension
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23
Q

who cannot use 5 Alpha Reductase Inhibitors (5ARIs)?

A

Contraindicated in preggos and child-bearing age females

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24
Q

who is Phosphodiesterase 5 Inhibitor (PDE5I) for?

A

Better effect on Younger age, low BMI and higher baseline symptoms

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25
Q

what is an agent for Phosphodiesterase 5 Inhibitor (PDE5I)?

A

Tadalafil

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26
Q

how can Phosphodiesterase 5 Inhibitor (PDE5I) be taken?

A
  • Add on therapy, esp with concomitant ED
    • Take without regards to timing of sexual activity
    • 5 mg OD if monotherapy for BPH-LUTS with or without ED
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27
Q

what are the side effects for Phosphodiesterase 5 Inhibitor (PDE5I)?

A

Same SE as 5ARIs

  • Ejaculatory disorders (reduced semen during ejaculation or delayed ejaculation)
    • Higher risk than alpha antagonist
  • Decreased Libido (3 -8%)
  • Erectile Dysfunction (3-16%)
  • Gynecomastia and breast tenderness (1%)
  • Lesser risk of hypotension
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28
Q

what are the characteristics for Phosphodiesterase 5 Inhibitor (PDE5I)?

A
  • Does not affect prostate size
  • Fast onset (days to weeks)
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29
Q

what are the side effects for Phosphodiesterase 5 Inhibitor (PDE5I)?

A

Significant hypotension!!!!!!!!

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30
Q

what are the combi therapy for bph?

A

Agents: 5 Alpha Reductase Inhibitors + Alpha Adrenergic Antagonist

  • Finasteride and Doxazosin
  • Dutasteride and Tamsulosin

5 Alpha Reductase Inhibitors + Phosphodiesterase 5 Inhibitor

Phosphodiesterase 5 Inhibitor + Alpha Adrenergic Antagonist —- RARE

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31
Q

when is combi therapy used for bph?

A

Effective for mod symptoms and enlarged prostate size >25g; Long-term use of combi is safe with only mild ADR

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32
Q

how does 5 Alpha Reductase Inhibitors + Alpha Adrenergic Antagonist work?

A

MOA: Alpha blockers onset within weeks, 5-ARIs onset in months

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33
Q

when can use 5 Alpha Reductase Inhibitors + Alpha Adrenergic Antagonist for bph?

A
  • Reserved for symptomatic patients with an enlarged prostate
  • After 6 months of combi therapy, consider to discontinue alpha-blocker if mod BPH
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34
Q

why is 5 Alpha Reductase Inhibitors + Phosphodiesterase 5 Inhibitor used for bph?

A

Can mitigate sexual ADR that arises from 5-ARIs/ concomitant ED

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35
Q

why is Phosphodiesterase 5 Inhibitor + Alpha Adrenergic Antagonist not really used for bph?

A

Rare —> Can cause severe life threatening hypotension

Wont reduce prostate size

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36
Q

what if rly need to use Phosphodiesterase 5 Inhibitor + Alpha Adrenergic Antagonist?

A
  • If really need to use, use uro-selective alpha-1
  • Stabilise/ optimise alpha 1 dose first before adding lowest effective dose possible of PDE5i
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37
Q

what is the symptomatic relief agent for bph?

A

Anti-muscarinics

Oxybutynin, tolterodine, solifenacin, trospium, darifenacin, fesoterodine

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38
Q

when is the symptomatic relief agent: Anti-muscarinics used for bph?

A
  • For irritative voiding symptoms, which mimic overactive bladder (OAB)

Criteria: Postvoid Residual <250ml (or 150ml for more conservative guidelines)

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39
Q

how does he symptomatic relief agent: Anti-muscarinics used for bph work?

A

MOA: Block muscarinic receptors in detrusor muscle —> decreases involuntary contraction of bladder

40
Q

What is erectile dysfunction?

A
  • Persistent (min 6 months) inability to achieve or maintain an erection of sufficient duration and firmness to complete satisfactory intercourse
  • Incidence
    • Low in men <40 yo, increases over age
41
Q

What is the physiology of erection?

A

note: cGMP causes vasodilation
note2: Flaccid state: Blood (arterial) flow into penis balances with blood flow exiting penis

  • ctivation of parasympathetic system: Acetylcholine (ACh)
    • ACh increases creation of nitric oxide —> increases activity of guanylate cyclase —> increases cyclic guanosine monophosphate (cGMP)
    • ACh and prostagladins E increases adenyl cyclase —> Increases cyclic adenosine monophosphate (cAMP)
    • Both causes smooth muscle surrounding Corpora Cavernosa relaxes and vasodilates, causing CC to fill up with blood (increases inflow)
  • Swelling causes compression of venules against tunica albuginea (decreases outflow)
42
Q

what is the Functional hormonal system in men?

A
  • estosterone: Encourage libido
    • 300-1000ng/dl (10.4-38.2 nmol/L)
    • To assess symptoms, as there isnt always a direct relation between level and ED
43
Q

What is the physiology of detumescence?

A

note: serotonin may inhibit sexual arousal

  • Deactivation of parasympathetic system
    • cGMP is deactivated by phosphodiestarase type 5 (PDE-5; predominant enzyme in penis) —> Stops vasodilation
    • Necessary as cannot stay hard forever —> Subsides erection
  • Activation of sympathetic system: Exercise, nervous, anxious —> Cannot get hard
    • Induces smooth muscle contraction via alpha-2 adrenergic receptors of arterioles —> Reduction of blood flow
44
Q

What is the etiology of erectile dysfunction?

A
  • Organic ED*
    • Compromised vascular systems
      • Arteriosclerosis
      • Peripheral vascular disease
      • Hypertension
      • Diabetes
    • Compromised nervous systems
      • Hypogonadism
      • Hyper-prolactinemia: Suppress testosterone production
        • Prolactin is produced in anterior pituitary gland
    • Compromised hormonal systems
      • Central: Spinal cord trauma/ disorder, Stroke, CNS tumor
      • Peripheral: Diabetes, Neuropathy, Urethral surgery
    • Medication induced
      • Anticholinergics: Tricyclic antidepressant (TCA), Phenothiazines (first gen antipsychotic)
      • Decrease ACh activity
  • Psychogenic ED: Due to thoughts or feelings
    • Malaise
    • Loss of attraction
    • Stress
    • Performance anxiety
    • Mental disorders
    • Sedation
  • Mixed ED: Combi of organic and psychogenic ED
  • Others: Smoking, Excessive ethanol intake, illicit drug use, obesity
45
Q

What are the signs and symptoms of erectile dysfunction?

A
  • Loss of interest in sexual activities
  • Depression
  • Performance anxiety
  • Embarrassment
  • Anger
  • Low self-esteem
  • Disharmony in relationship
46
Q

what is the Assessment of ED

A
  • Signs and symptoms
  • Sexual health inventory for men (SHIM)
    • Mild to no ED: 17-21 points
    • Mod to severe ED: <11 points
  • Workup to identify underlying causes of ED
    • Medical history/ Medications
    • Social history
    • Surgical history
    • Lab results: Blood glucose, lipid profile, testosterone
47
Q

why need access CVD if have ED?

A
  • ED might be an early symptom of unidentified comorbid CVD
  • Sexual activity —> sympathetic activation may increase BP and HR —> increase MI risk
  • Stages of CVD
    • Low risk: okay for sexual activity and treatment
    • Unknown/ not low risk: Stress test to evaluate exercise capacity
    • Unstable or severe symptomatic: Defer sexual activity and treatment until condition stabilized
48
Q

what is the Non-pharmacology for ed?

A
  • Modify risk factors
    • Stop smoking, Control weight, Control glucose/ BP/ lipids, Exercise, Decrease alcohol
  • Psychotherapy
  • Devices: Vacuum erection devices (VEDs)
  • Surgery: Penile implant
49
Q

what is the Pharmacology for ed?

A
  1. Phosphodiesterase 5 Inhibitor (PDE5I)
  2. Testosterone Replacement
  3. Alprostadil
  4. Yohimbine
50
Q

what is the first line for ed?

A

Phosphodiesterase 5 Inhibitor (PDE5I)

51
Q

how does Phosphodiesterase 5 Inhibitor (PDE5I) work for ed?

A

Inhibit PDE 5 enzyme which induces catabolism of cGMP —> enhance cGMP activity —> induce smooth muscle relaxation —> erection

Require sexual stimulation to work

52
Q

what are the agents for Phosphodiesterase 5 Inhibitor (PDE5I) ?

A

sildenafil
vardenafil
tadalafil
avanafil

53
Q

which Phosphodiesterase 5 Inhibitor (PDE5I) agent has the longest doa?

A

taladafil of 36h, so can take once daily orally

54
Q

how to admin Phosphodiesterase 5 Inhibitor (PDE5I) agents?

A

empty stomach: sildenafil, vardenafil
regardless of food: tadalafil, avanafil

55
Q

what is the avevrage onset of Phosphodiesterase 5 Inhibitor (PDE5I) agents?

A

within an hour

56
Q

when to give lower dose of Phosphodiesterase 5 Inhibitor (PDE5I) ?

A
  • Lower initial dose if:
    • > 65yo
    • Also taking alpha blockers
    • Renal failure
    • Also taking CYP3A4 inhibitors which will increase PDE5i conc: Erythromycin, cimetidine, ketoconazole, itraconazole, clarithromycin, grapefruit or grapefruit juice, ritonavir, saquinavir
57
Q

what are the side effects of Phosphodiesterase 5 Inhibitor (PDE5I) ?

A
  • Headache, rhinitis, flushing, muscle and back pain, dizziness, hypotension
  • Prolonged erections and priapism: MUST seek ED treatment if >4hours
    • Blood is trapped in penis yikes
  • Sudden hearing loss (but very rare!!!)
    • May also have tinnitus and dizziness
  • QTc Prolongation: Vardenafil
  • Muscle pain: Tadalafil with PDE 11 affinity
  • Ocular issues: Sildenafil, Vardenafil (affinity to PDE6 in retina)
    • Reversible with colour discrimination (difficulty discriminating blue from green)
    • Sensitive to light
    • Nonarteritic Anterior Ischemic Optic Neuropathy (NAION)
      • Ischemia of optic nerve due to hypoperfusion (reduced blood flow) caused by PDE5i
      • Risk factors: DM, smoking, HTN, CVD, dyslipidemia, age >50y/o
      • IMMEDIATELY DISCONTINUE
58
Q

what are the Drug interactions for phosphodiesterase 5 inhibitors?

A
  • AVOID combining Nitrates + PDE5i, if not fatal hypotension
    • Avoid nitrates for 12h after avanafil, 24 hrs after sildenafil or vardenafil, 48hrs after tadalafil
  • Hypotension risk increases with use of multiple antihypertensives
  • AVOID combining PDE5i + Alcohol , if not hypotension
  • AVOID combining CYP3A4i + PDE5i (3A4 substrates), if not cannot be metabolised which causes an increase in PDE5i conc —> toxicity
59
Q

how to monitor Phosphodiesterase 5 Inhibitor?

A
  • Efficacy: Check for factors that may contribute to failure
    • Administration with food if any
    • Timing and frequency of dosing
    • Lack of adequate sexual stimulation
    • Titration to maximum dose
    • Treat with diff PDE5i or use other more invasive therapy if modifiable factors all addressed

make sure to check for changes in cardiac health status!

60
Q

when to use Testosterone Replacement for ed?

A

First line for symptomatic hypogonadism (insuff production of testosterone or sperm) as confirmed by (i) decreased libido and (ii) low serum testosterone conc

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

61
Q

what are the side effects for testosterone replacement?

A
  • Irritability, aggressive behaviour, undesirable hair growth, increased BP, hepatotoxicity, dyslipidemia, polycythemia (increase in RBC)
  • Prostatic hyperplasia (hence contraindicated for prostate cancer)
62
Q

when to monitor when using testoterone replacement for ed?

A

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

63
Q

what is Alprostadil for ed?

A

Prostaglandin E1 analog

64
Q

how does Alprostadil work for ed?

A

Stimulates adenyl cyclase to increase cAM —> induce smooth muscle relaxation —> erection

No need sexual stimulation to work (unlike PDE5i)

65
Q

what is the onset for Alprostadil for ed?

A

Fast onset: 5-10 mins

66
Q

what to NOT take when taking Alprostadil for ed?

A

DDIs: Do not use with PDE5i

67
Q

what are the agents for Alprostadil for ed?

A

Intraurethral alprostadil pellet
- DOA: 30-60 min

Intracavernosal alprostadil
- Preferred over intraurethral due to better efficacy BUT also higher risk of priapism, bleeding, hematoma, fibrosis
- cons: Injection, invasiveness, lack of spontaneity
- Titrate in healthcare setting to duration of ≤1 hr, then self administered no more than x3/ week

68
Q

what are the side effects Intraurethral alprostadil pellet for ed?

A

Pain, warmth or burning sensation in the urethra, voiding (urinate) difficulties, bleeding or spotting, priapism (penis stuck at rigid erection even without stimulation), vaginal burning or itching in partner

69
Q

is Yohimbine reco for ed?

A

no..

70
Q

drug for ED that has highest risk of priapism

A

intracavernosal alprostadil

71
Q

what are the characteristics of bph?

A

note: Benign so not cancerous

  • Enlarged prostate
    • Healthy prostate creates fluids in semen and force semen through urethra upon ejaculation
  • Often >50 years old: Frequency of disease increases with age
  • BPH is dependent on androgen 5-alpha dihydrotestosterone (5alpha-DHT)
  • Testosterone secreted by testicles and adrenal glands and travels to prostate gland via bloodstream to be quickly metabolised into DHT by 5alpha-reductase
72
Q

how to treat bph?

A
  • Surgery (last resort)
  • Pharmacology
73
Q

what is the Goal of treatment for bph?

A
  • Relieve lower urinary tract symptoms
    • Obstructive symptoms: Urge but cant urinate, weak flow, slow flow
    • Irritative symptoms: Urinary frequency increased (night urination), Hard to empty bladder
  • Slow progression of BPH
  • Improve QOL
74
Q

whats the characteristics for ed?

A
  • Inability to develop or keep an erection
  • Often occurs when blood flow to penis is limited or nerves are damaged often by consistent hyperglycemia in diabetes
  • Mostly treatable
75
Q

what are the Risk factors for ed?

A
  • Alcohol
  • Tobacco use
  • Enlarged prostate
  • Psychological factors: Stress
  • Sleep disorders
76
Q

whats the Physiological process for ed?

A

Sexual arousal —> Nerves release chemicals to increase blood flow to penis —> Corpus cavernosum traps blood during erection —> Spongy muscle tissue relaxes and traps blood, making penis firm —> Erection

77
Q

what are the male pharmacology for bph?

A
  1. Tamsulosin PO (alpha-blocker/ alpha-adrenergic antagonists)
  2. Finasteride PO (5 alpha-reductase inhibitor)
78
Q

what are the male pharmacology for ed?

A
  1. Sildenafil (Phosphodiesterase 5 (PDE5) inhibitor)
79
Q

what is tamsulosin (alpha antagonist) for bph?

A

Small molecule

for Patients with moderate to severe symptomatic BPH regardless of prostate size

80
Q

how does tamsulosin po (alpha for bph) work?

A

Reversibly blocks alpha-1 receptors in prostate and smooth muscle of bladder —> inhibits vasoconstriction induced by endogeonus catecholamines and relaxes smooth muscle of bladder and urethra —> improves urodynamics (increase flow rate and relieves obstruction and tension)

81
Q

what are the types of alpha-1?

A
  • Alpha-1 subtypes: Selectivity for alpha-1 A receptors (blood vessels and prostate) over alpha-1 B (blood vessels and heart)
    • Very minimal effect on blood pressure but useful in BPH
82
Q

does tamsulosin po (alpha for bph) have fast onset and long duration of action?

A
  • Outcome after a few hours or days after admin
    • Effect on urinary storage (holding urine) and passing urine is maintained for a longer period of time
    • Delay or remove need for surgery or catheterization
83
Q

how is the pkpd for tamsulosin po (alpha for bph)?

A
  • A
    • Well absorbed orally
    • 0.4mg OD
  • D
    • Highly bound to plasma proteins so stay in blood circulation —> Small Vd (0.2L/kg)
  • M
    • Metabolised by CYP450 (CYP3A4, 2D6) —> Take note of DDI and FDI with pomelo
    • half life ~10-15h so can dose OD
  • E
    • ~10% excreted unchanged in urine because metabolised in liver
      • Made need dose adjustments for renal insufficiency
84
Q

what is the adr for tamsulosin po (alpha for bph)?

A
  • Abnormal ejaculation
  • Back pain
85
Q

who should avoid taking tamsulosin po (alpha for bph) ?

A
  • Heart patient that concurrent uses another alpha-1 adrenoceptor antagonist to regulate heart function —> dw to have multiple drugs acting on alpha 1 receptors
    • Eg. Prazosin: Non-selective alpha 1 blocker
86
Q

what does 5 alpha-reductase do?

A

5 alpha-reductase converts testosterone to DHT that causes prostate to grow or hair loss in males

87
Q

how does Finasteride PO (5 alpha-reductase inhibitor for bph) work?

A

Competitively inhibits action of 5 alpha-reductase (does not touch androgen receptor) —> Inhibits production of DHT —> Decrease prostate size (X BPH) and increases hair growth (X androgenetic alopecia) —> Improve urine flow, reduces acute retention of urine and surgery for prostate transurethral resection and prostatectomy

88
Q

how long does Finasteride PO (5 alpha-reductase inhibitor for bph) take to work?

A

May take up to 6months to see BPH clinical effect after treatment initiation

89
Q

what to monitor upon taking Finasteride PO (5 alpha-reductase inhibitor for bph)?

A
  • Monitoring parameters: Serum prostate-specific antigen (PSA) levels which decreases with finasteride
    • 2-3 months after initiation, if >1 .5ng/mL means BPH
90
Q

what is the pkpd for Finasteride PO (5 alpha-reductase inhibitor for bph)?

A
  • A
    • Well absorbed orally
    • Higher dose (5mg) OD for BPH
    • Lower dose (1mg) for hair growth
    • Good bioavailability
    • No dosage readjustment needed for renal insufficiency, liver failure, elderly patient
  • D
    • Highly plasma protein bound —> Low Vd
  • M
    • Metabolised by liver by CYP3A4
    • Half life 6h
  • E
    • 50% excreted unchanged in faeces while metabolites excreted in urine and faeces
      • Not mainly excreted in urine so dont really need dose adj for renal insufficiency patients
91
Q

what is the adr for Finasteride PO (5 alpha-reductase inhibitor for bph)?

A
  • Loss of libidio and sexual potency
  • Gynaecomastia (rare): Increase in breast gland tissues
92
Q

who should avoid Finasteride PO (5 alpha-reductase inhibitor for bph)?

A
  • Women and children
  • PREGGOS
93
Q

how does erection occur?

A

Sex stimulation releases nitric oxide in corpora cavernosa —> Activates guanylate cyclase (cGMP) which increases production of cyclic guanosine monophosphate (cGMP) in corpora cavernosa —> Relaxes smooth muscle in blood vessels to allow dilation and increased blood flow

94
Q

how does sildenafil (Phosphodiesterase 5 (PDE5) inhibitor for ed) work?

A
  • Specifically inhibits phosphodiesterase type-5 (PDE5) in penis —> Inhibits breakdown of cGMP so increases cGMP levels —> Prolonged smooth muscle relaxation in blood vessels within penis —> Fills penis with blood to cause erection
  • Tissue specificity to male reproductive system: PDE5 is highly expressed in corpora cavernosa and vasculature but poorly in myocardium
95
Q

what is the pkpd for sildenafil (Phosphodiesterase 5 (PDE5) inhibitor for ed)?

A
  • A
    • Well absorbed orally
    • 5mg OD: Start with lowest dose (note that guys might be greedy!!!!!)
    • Onset 30-60min quite fast
    • Good bioavailability F=0.4
    • No dosage readjustment needed for patients with renal insufficiency, liver failure, for elderly depends on heart function
    • DOA: 12h
  • D
    • Widely distributed, so large Vd of more than 5-8L
  • M
    • Metabolised by liver (CYP3A4 major, CYP2C9 minor)
    • t1/2 4h
  • E
    • Metabolites excreted mainly in faeces and lesser in urine, the v little remaining excreted unchanged in urine (thus no renal adjustment for renal insuff needed)
96
Q

whats the adr for sildenafil (Phosphodiesterase 5 (PDE5) inhibitor for ed)?

A
  • Headache
  • Flushing
  • Dyspepsia (stomach discomfort)
  • Dizziness
  • Back pain
  • Blur vision; Blue-green tint of vision
  • Priapism (Penis maintains a prolonged, rigid erection w/o stimulation)
97
Q

who should avoid taking sildenafil (Phosphodiesterase 5 (PDE5) inhibitor for ed)?

A
  • Cardiac patients on nitroglycerin (GTN)
    • Because GTN releases nitric oxide to increase cGMP for vasodilation and smooth muscle relaxation —> if take both drugs together —> synergistic effect on cGMP levels —> Excessive vasodilation —> Significant drop in BP —> Severe hypotension

finals (8 decks)

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