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2402 Supp > 2402 REPRO(M) > Flashcards

2402 REPRO(M) Flashcards

1
Q

Flaccid state

A

Sympathetic nervous system keeps smooth
muscle in the corpus cavernosa and blood
vessels (arterioles) contracted

Maintains unhindered bidirectional blood
flow –> prevents blood retention

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2
Q

Erect state

A

Sexual stimulation –> release of
neurotransmitters from the cavernous nerve
terminals

Smooth muscle relaxes

Allows more blood in and clamps down on
veins (so blood can’t escape)

Erection results

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3
Q 
External stimuli (erection)
- Begins with the brain via
A
  • Visual
  • Smell
  • Imaginary
  • Touch
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4
Q

NANC nerves:

A

nor-adrenergic and nor-cholinergic

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5
Q

Stimulation pathway:

A
  1. NANC nerve
    - -> Ca+2 influx
    - -> production of nitric oxide (NO)
  2. Cholinergic nerve
    - -> Release of Ach
    - -> Activation of muscarinic receptor on endothelial cell
    - -> NO release
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6
Q

Nitric Oxide (NO) pathway

A
  1. NO activates guanylate cyclase which converts
    GTP –> cGMP
  2. cGMP activates protein kinaseG
  3. Phosphorylates certain proteins:
    - -> Opens K channels
    - -> Closes Ca+2 channels
    - -> Ca+2 back into SR
    - -> Reduced intracellular Ca+2

** Smooth muscle relaxation

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7
Q

Prostaglandin Pathway

A
  1. PGE1 binds to its receptor (G protein coupled
    receptor) on CC smooth muscle cells
  2. Activates adenylate cyclase
  3. Converts ATP –> cAMP
  4. cAMP activates protein kinaseA
  5. Phosphorylates certain proteins to cause **Nitric Oxide Pathway
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8
Q

Inhibiting the erect state:

A

Adrenergic nerve

  • -> release of NA
  • -> muscle contraction (detumescence)
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9
Q

Alprostadil

A

Incr. PGE1

Injection into CC tissue
Efficient

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10
Q

Alprostadil side effects

A 
• Pain (PGE1)
• Painful erection (priapism) lasting
>8h
• Redness/lump
• Rash/Itching
• Trouble urinating
• Feeling faint
• Permanent damage to penis/fibrosi
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11
Q

Papaverine

A

Less commonly used

• Mechanism of action not completely known, but
proposed to inhibit phosphodiesterase 5

  • Causes vasodilation
  • Only used if alprostadil use is contraindicated
  • Does not induce localised pain
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12
Q

Phentolamine (Inhibition)

A

• Mechanism of action is via vasodilation as a
result of potent competitive antagonism of α1
adrenoceptors

• Generally used along with papaverine and/or
alprostadil (Trimix, also available as a gel)

• Trimix has to be formulated by a pharmacist and
used within 1-6 months (>90% effective).

  • Dose is 50 to 200 ul depending on severity of problem (increase dose in 25 ul increments)
  • Prescribed when single dose therapy has failed
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13
Q

Phosphodiesterase 5

(PDE5) inhibitors

A

• Need to take the pills 1
-2h before intercourse
(time to reach
tmax)

• ~70% effective in healthy patients

• Inhibits hydrolysis of cGMP
–> longer residence of cGMP
–> prolonged smooth
muscle relaxation

• Still need stimulation coming from the NANC
nerves

• The ‘fils’ are eventually metabolised/inactivated
by liver P450 3A4

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14
Q

(PDE5) Inhibitors

Side Effects:

A
  • Visual isturbances
  • Indigestion
  • Headaches and dizziness
  • Unstable angina
  • Bladder pain
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15
Q

ED drugs may be ineffective from:

A

Diabetes

Veno-occlusive disorders

Hypogonadal patients

Prostate removal

Smoking

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16
Q

Explain how diabetes can inhibit effective ED drugs

A
  1. Endothelial dysfunction
  2. Increased contractile sensitivity
  3. Reduced NO signalling
  4. Diabetic neuropathy
17
Q

Explain how veno-occlusive disorders can inhibit effective ED drugs

A

Simply can’t get enough blood vessel dilation

–> Drug intervention is useless

18
Q

Explain how hypogonodal disorders can inhibit effective ED drugs

A

Reduced testosterone

–> Testosterone regulates NOS & PDE5

19
Q

Explain how prostate removal can inhibit effective ED drugs

A

Surgery can damage the penile nerve bundle

  • -> No signalling from the brain
  • -> Can damage the whole organ
20
Q

The flaccid smoker :(

A
  1. Damages endothelial cells
  2. Respond by releasing
    vasoconstrictors
  3. Hardens blood vessels
  4. Cumulative reduced penile blood flow
21
Q

The prostate

A
  • Doughnut shaped structure sitting just inferior
    to the bladder and anterior to the rectum
  • Surrounds proximal end of the urethra (usually
    20-30 cm3
    in size)
  • Consists of glandular, connective and smooth
    muscle tissue. Blood is supplied by the
    hypogastric artery
  • Its job is to secrete a milky, slightly alkaline
    fluid that contributes ~ 25% of semen volume
  • The secreted fluid also contains citrate (to feed
    sperm ATP production) and enzymes that
    liquefy coagulated semen (eg. prostate specific
    antigen or ‘PSA’)
22
Q

Benign Prostatic Hyperplasia

A
  1. Enlargement of the prostate due to nodular prostatic
    remodelling of the stroma and endothelium and inflammation
  2. Remodelling and inflammation begin in the transition zone
    usually and is characterised by an increase in cell numbers and
    increase in cell size (advanced)
  3. Hyperplasia and hypertrophy are stimulated by androgens
  4. Enlargement
23
Q

Benign Prostatic Hyperplasia: Symptoms

A

**Pushes on bladder and rectum and constructs urethra, leading
to:

  • Abdominal pain
  • Difficulty urinating and slow urine flow
  • Incontinence (by pushing on bladder)
  • Feeling of urinary ‘urgency’
  • Pain can be worse in the cold or when stressed
24
Q

DHT is…..

A
  • Produced by the enzyme 5α reductase (5AR)
  • Important in promoting prostate development, growth and differentiation
  • A very potent androgen, 5x more potent than testosterone
  • Binds the testosterone receptor with higher affinity than testosterone and binds longer
  • The cause of male patterned balding due to high local 5AR levels in the scalp

• BPH pathogenesis results from chronic inflammatory reactions induced by the growing prostate
stromal cells

25
Q

Benign Prostatic Hyperplasia: Treatment

A

RETURN NORMAL URINARY FUNCTION!
1. Drug treatments to inhibit 5AR (Decr. DHT and reduce prostate size)

2. Drug treatments to inhibit prostate smooth muscle contraction and reduce
urinary obstruction (α1 adrenergic antagonists)

Final straw:
• surgical removal of prostate

26
Q

Benign Prostatic Hyperplasia: Treatment

A 
Finastride:
Also used for androgenic alopecia
• 6 month treatment for men with >30 cm3
prostate
• Pharmacokinetics - ~60% bioavailability, t½
~8h

Dutasteride:
Pharmacokinetics - ~60% bioavailability, t½
~ 5 days
• better and more consistent therapy than
finasteride
• Ideally the drug of choice

27
Q

Benign Prostatic Hyperplasia: Treatment Side Effects (Dutasteride, and Finastride)

A

• ED, ejaculation problems and reduced libido
• Male breast enlargement
• May increase the chances of male breast cancer, so need
to monitor changes in breast tissue

28
Q

A1 Adrenergc Antagonists:

A

Reduce the degree of smooth muscle contraction in the prostate

Reduce pressure on the urethra and increase urinary flow (5AR inhibitors are better if they can be tolerated or are not contraindicated)

29
Q

Alfuzosin and Tamsulosin

A

Only indication is for BPH

• α1A selective (specific for the capsule of the
prostate grand and bladder neck)

• Little effect on α2 & 1 receptors and
therefore less likely to cause cardiac side
effects

• Less effective against BPH than prazosin and
terazosin, but also less hypotension.

30
Q

Prazosin and Terazosin

A

Can be used as 3rd line drugs in hypertension

More effective in BPH treatment than alfuzosin
and tamsulosin, but dose titration needed to
minimise hypotensive effects

31
Q

A1 Adrenergc Antagonists: Treatment Side Effects (Alfuzosin and Tamsulosin, Prazosin and Terazosin)

A 
Common
Hypotension, 
dizziness, 
fatigue, 
‘floppy iris syndrome’,
nasal congestion, 
first dose hypotension

Rare
Vision disturbances,
tachycardia,
palpitations

2402 Supp (5 decks)

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