andrology m.hassan & m.a.wadood

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Andrology Urology Department Under-graduate courses By Moh.Hassan, MBBcH Revised by M.A.Wadood , MD, MRCS

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Basic andrology presentation

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Page 1: Andrology  M.hassan & M.A.Wadood

Andrology

Urology Department

Under-graduate courses

By Moh.Hassan, MBBcH Revised by M.A.Wadood , MD, MRCS

Page 2: Andrology  M.hassan & M.A.Wadood

Erectile Dysfunction

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Page 3: Andrology  M.hassan & M.A.Wadood

Blood supply of penis

Arterial supply by the internal pudendal artery,

Venous drainage

1. Intracavernosal drainage

into subtunical venules.

2. Extracavernosal drainage.

(a) deep dorsal veins.

(b) cavernosal and crural veins.

(c) superficial dorsal vein.

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Page 4: Andrology  M.hassan & M.A.Wadood

Vascular Physiology of Erection

1. Nitric oxide

• Following sexual stimulation, Nitric oxide

diffuses into the corporal smooth muscle and

induces smooth-muscle relaxation.

2. Venous outflow resistance

• Filling of the lacunar spaces stretches the

subtunical venules to create venous outflow

resistance and a further increase in

intracavernosal pressure.

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Page 5: Andrology  M.hassan & M.A.Wadood

Vascular Physiology of Erection

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Page 6: Andrology  M.hassan & M.A.Wadood

Erectile Dysfunction

• Erectile dysfunction is the persistent

inability to obtain and maintain an

erection sufficient for sexual

intercourse

• Infertility is the inability to produce

offspring, which is usually not caused

by impotence.

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Page 7: Andrology  M.hassan & M.A.Wadood

Causes of ED

Vasculogenic impotence

1. Arterial disease: Atherosclerosis is a common

cause of organic impotence.

2. Venogenic impotence : an increase in corporal

smooth-muscle tone during stress or anxiety induce

a functional venous leak.

Diabetes mellitus in up to 75% of diabetic patients .

Renal failure 50% of dialysis-dependent uremic

patients.

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Page 8: Andrology  M.hassan & M.A.Wadood

Neurologic lesions affect erectile function at

many levels:

1. Intracerebral

2. Spinal cord

3. Peripheral nerves

Endocrine disorders less than 5%.

1. Hypogonadotropic hypogonadism

2. Hypergonadotropic hypogonadism

3. Hyperprolactinemia

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Causes of ED

Page 9: Andrology  M.hassan & M.A.Wadood

Trauma

1. Pelvic.

2. Perineal trauma.

Postoperative or iatrogenic impotence.

1. Aortic or peripheral vascular surgery.

2. Renal transplantation

3. Pelvic suergery or irradiation.

4. Cavernosal-spongiosal shunts

5. Neurosurgical procedures.

Drugs.

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Causes of ED

Page 10: Andrology  M.hassan & M.A.Wadood

Sexual history The onset, duration, and

circumstances of the erection problem.

• Psychogenic cause: sudden onset of impotence

or impotence under some circumstances.

• Organic cause: gradual deterioration of erectile

quality with preservation of libido

Medical history DM, hypertension, smoking, and

hyperlipidemia, liver, renal, vascular, neurologic,

psychiatric, or endocrine disease.

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Evaluation of ED

Page 11: Andrology  M.hassan & M.A.Wadood

• Physical examination of body habitus and

secondary sexual characteristics (Gynecomastia, the

penile length, fibrotic region, or deformity of the corporal

bodies).

• Laboratory tests Hormonal status is adequately

assessed by serum serum testosterone, LH & prolactin.

• Specialized tests

Vascular testing

Duplex ultrasonography to assess cavernosal artery

diameter and flow velocity.

Cavernosography and cavernosometry.

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Evaluation of ED

Page 12: Andrology  M.hassan & M.A.Wadood

Sex therapy For Patients with psychogenic impotence .

Oral therapy

1. Oral phosphodiesterase inhibitors (sildenafil, Tadelafil,

Vardenafil)

increase intracellular concentration of cGMP causing

corporal smooth-muscle relaxation and erection.

Side effects headaches, dyspepsia & visual color changes

Contraindications: nitrate therapy, severe uncontrolled

hypertension, severe cardiac malfunction

2. Androgen replacement: for patients with androgen

deficiency

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Treatment of ED

Page 13: Andrology  M.hassan & M.A.Wadood

PDE5 inhibition with sildenafil

PDE5

cGMP

GMP

GTP

Sexual stimulation

Smooth

muscle

relaxation

of the

cavernosal

arteries &

the corpora

Erection

Corpus cavernosum

NO

NANC

NO=nitric oxide; NANC=nonadrenergic-noncholinergic neurons;

PDE5=phosphodiesterase type 5

Page 14: Andrology  M.hassan & M.A.Wadood

Nonsurgical therapy

Intracavernous pharmacotherapy Alprostadil alone or in

combination with papaverine and/or phentolamine mesylate

may be injected intracavernosally.

Transurethral alprostadil

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Treatment of ED

Page 15: Andrology  M.hassan & M.A.Wadood

Surgical therapy

Inflatable prostheses: consist of a pair of inflatable

cylinders, a reservoir, a pump, and tubing to connect these

components.

Noninflatable prostheses: a pair of silicone rods

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Treatment of ED

Page 16: Andrology  M.hassan & M.A.Wadood

Male Infertility

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Page 17: Andrology  M.hassan & M.A.Wadood

Normal Hypothalamic Pituitary

Gonadal Axis

• Hypothalamus site of production of GnRH, which reaches

the anterior pituitary via the portal system.

• Pituitary: anterior pituitary secretes 2 hormones (gonadotropins)

Luteinizing hormone (LH) released into systemic

circulation in a pulsatile fashion. LH is the major stimulus

to testosterone production by Leydig's cells. testosterone

exerts a -ve feedback on pituitary LH release.

Follicle-stimulating hormone (FSH) is responsible for

initiation and maintenance of spermatogenesis (Sertoli's

cells

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Page 18: Andrology  M.hassan & M.A.Wadood

Normal Hypothalamic Pituitary

Gonadal Axis

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Page 19: Andrology  M.hassan & M.A.Wadood

Male Infertility

• Definition : the inability to achieve a

pregnancy resulting in live birth after 1 year of

unprotected intercourse (primary infertility).

• Incidence : male factor can be identified in

nearly 50% of these couples

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Page 20: Andrology  M.hassan & M.A.Wadood

Evaluation of the Infertile male

History

• The duration of the marriage and attempts to conceive

• if either partner has been previously married.

• History of undescended testicles, hypospadias, gynecomastia, mumps,

herniorrhaphy or scrotal surgery.

• Retrograde or absent ejaculation is most often caused by diabetic

autonomic neuropathy, sympatholytic drugs, or retroperitoneal surgery.

Physical examination

1. Testes. The size and consistency.

2. Spermatic cord. Any asymmetry, the presence of varicoceles,

gynecomastia or galactorrhea.

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Page 21: Andrology  M.hassan & M.A.Wadood

Semen analysis is the single most important.

• collected after 3 days of abstinence from ejaculation.

• On at least two occasions.

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Evaluation of the Infertile male - Laboratory evaluation

Parameter Normal range

Ejaculate volume 1.5-5.0 mL

Sperm denisty > 20 million/mL

Motility > 60%

Forward progression > 2 (scale 0-4)

Morphology > 60% normal

Agglutination No

Pyospermia No

Page 22: Andrology  M.hassan & M.A.Wadood

Hormonal assays (In severely oligospermic or azoospermic)

• FSH, LH, testosterone and prolactin

Genetic assessment (karyotyping) for Azoospermia

chromosome number (e.g, Klinefelter's syndrome, 47XXY).

chromosome structure (e.g., abnormal Y translocations).

Radiologic evaluation

Transrectal ultrasonography (TRUS) is now the initial

diagnostic modality for documenting ejaculatory duct

obstruction and seminal vesicle/vasal absence or aplasia

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Evaluation of the Infertile male

Page 23: Andrology  M.hassan & M.A.Wadood

Male Reproductive Abnormalities

• Low-volume azoospermia

1. Ejaculatory duct obstruction (acquired or

congenital).

2. Congenital bilateral absence of the vas

deferens (CBAVD)

• Normal-volume azoospermia

1. Vasal or epididymal occlusion may be

congenital or acquired.

2. Spermatogenic failure Clinical clues to this

diagnosis include small testes ©

Page 24: Andrology  M.hassan & M.A.Wadood

Male Reproductive Abnormalities

• Hypergonadotropic hypogonadism

1. Klinefelter's syndrome: karyotype (47,XXY). Testes are

small and firm. Gynecomastia. Hormonal evaluation shows

elevated LH and FSH, testosterone may be low.

2. XX male syndrome is seen in 1 in 10,000

3. Bilateral mumps or viral orchitis, radiation,

chemotherapy, and other toxic/inflammatory insults

suppress spermatogenesis.

• Oligoasthenospermia Low sperm density and poor

sperm motility often coexist. Due to varicocele, toxins or idiopathic.

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Page 25: Andrology  M.hassan & M.A.Wadood

Varicocele

• the most common cause of oligospermia.

• unilateral (on the left) in 80% of patients.

• bilateral in 18% of patients.

• Varicocele have been reported in about 15% of the fertile

male population.

• varicocele is seen in 40% of infertile

males.

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Page 26: Andrology  M.hassan & M.A.Wadood

Treatment of ED

Low-semen-volume azoospermia (<1.0 mL)

1. Ejaculatory duct obstruction is diagnosed with TRUS.

• Transurethral resection if TRUS has defined a midline cystic

structure.

2. Vasal aplasia sperm retrival and ICSI.

Normal-semen-volume azoospermia cause is

Primary spermatogenic failure (FSH levels are elevated).

• Testicular sperm extraction (TESE) may retrieve sperms

and ICSI is done.

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Page 27: Andrology  M.hassan & M.A.Wadood

Treatment of ED

Ejaculatory dysfunction

• Treated by either:

Penile vibratory stimulation or

Rectal probe electroejaculation

Retrograde ejaculation

• use post-ejaculate urine specimen and sperm

retrieval and ICSI.

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Page 28: Andrology  M.hassan & M.A.Wadood

• Oligoasthenoteratospermia

1. Elimination of spermatotoxin.

2. Medical therapy. Clomiphene citrate, hCG, tamoxifen

citrate, oral kallikrein, pentoxifylline, and folinic acid.

3. Surgical therapy. (varicocelectomy)

improves SA in 40 - 70% of patients.

• Pregnancy occurs in 40% of couples within

1 year of treatment.

4. Assisted reproductive techniques (ARTs)

a. Intrauterine insemination (IUI).

b. Intracytoplasmic sperm injection (ICSI)

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Treatment of ED

Page 29: Andrology  M.hassan & M.A.Wadood

Thank You