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PM3A: Autumn > Male Reproductive System > Flashcards

Male Reproductive System Flashcards

1
Q

What is role of the testis

A

Sperm and hormone production

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2
Q

What are the three principle cell types involved in the testis and their roles

A
  1. Leydig cells- occupies space between tubules (outside tubules)
  2. Sertoli Cells- within tubules- starts off spermatogenesis
  3. Germ Cells- within tubules and lumen- when it gets to lunial surface it becomes sperm (washed away when ejaculated)
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3
Q

Describe the hypothalamic pituitary regulation of LH and FSH in male

A

GnRH (Gonadotrophin Releasing hormone) neurones in hypothalamus are stimulated

Production of LH and FSH to produce gonadotroph cells in anterior pituitary (systemic circulation)

LH is made by Leydig cells which becomes testosterone (androgens)

FSH is made by sertoli cells which becomes inhibin

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4
Q

Which two hormones in the testicular system have a negative feedback in LH and FSH secretion

A

Inhibin and Testosterone

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5
Q

What are the effects of androgen (testosterone) mainly before birth

A

Synthesised in fatal leydig cells in response to maternal hCG to cause descent of testes into scrotum

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6
Q

How is T converted to DHT

A

5-alpha reductase enzyme

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7
Q

What are the effects of androgen (testosterone) after birth (puberty)

A

Promotes growth and maturation of reproductive system
Penis enlargement and scrotum enlargement

Scrotum darkening

Enlargement of epididymis, prostate, seminal vesicles

Essential for spermatogenesis

Development of sex drive and controls gonadotrophin secretion

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8
Q

What are the secondary sex characteristics that androgens develop

A

Promotes muscle growth responsible for male body confirmation:

Increased protein synthesis
Decrease protein degradation
Increase lean:fat ratio
Promotes bone growth at puberty

Induces male pattern of hair growth

Deepening of voice

Skin thickens and sebaceous glands do (acne)

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9
Q

What is the andropause

A

Decreased testosterone production, reduced testicular androgen response to LH

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10
Q

What are physical changes in the andropause

A

Loss of muscle mass

Shrinking reproductive organs- penis, testicles, accessory glands

Loss of libido, increased stimulus for erection

Longer refractory period

Osteoporosis

Depression and reduced energy

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11
Q

How does erectile dysfunction occur

A

Nervousness- performance

Guilty- adultery

Relationship problems

Depression and exhaustion

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12
Q

What are the common physical causes of erectile dysfunction

A

Deterioration of arteries- common in older men with high blood pressure (atherosclerotic plaque blocks blood flow to penis)

Smoking

Diabetes

Excessive alcohol- whisky dick

Obese and out of condition

Side effects of drugs: anti-hypertensives and anti-depressants

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13
Q

What are the three different regions of the penis called and their anatomy

A

Corpus caverosum- parallel spongy columns

Central corpus spongiosum (enclosing urethra)

Cavernous sinuses- erectile tissue rich in tiny pool shaped blood vessels- fills with blood during erection

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14
Q

Describe the stages of an erection occurring (4)

A
  1. Psychogenic or tactile stimulation triggers the release of Ach (acetylcholine) from parasympathetic nerve endings
  2. Neuronal nNos is released from cavernous nerve which decreases noradrenaline
  3. Increased eNOS (endothelial nitric oxide synthase) in the vascular endothelial cells
  4. Increase of nitric oxide (NO) causes dilation of smooth muscles and increased blood supply into corpus cavernous and corps spongiosum
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15
Q

Describe the biochemical process of an erection

A
  1. Ach produced, neuronal nNos stimulates eNos
  2. NO synthesised diffuses into vascular smooth muscle
  3. Once inside nitric oxide binds to and activates guanylyl cyclase, converts GTP to cGMP
  4. cGMP activates protein kinase G
  5. PKG activation: promotes vascular smooth muscle relaxation via
    hyperpolarisation (K+ channels opening)
    Endoplasmic reticulum sequestration of Ca2+
    Inhibition of Ca2+ channels stops influx
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16
Q

What does calmodulin do and how is it activated

A

Aids phosphorylation of myosin light chains (MLC)

Activated by free intracellular calcium

17
Q

Where are MLCs (myosin light chain) found and their roles

A
  1. Subunits on myosin heads

2. When phosphorylated, they cross bridge on myosin heads and actin filaments cause cellular contraction

18
Q

What is the mechanism of action of viagra

A
  1. Competitively inhibits enzyme responsible for degradation of cGMP to GMP (phosphodiesterase type 5)
  2. Stabilisation of cGMP- prolonged action of second messenger
  3. Greater more sustained dilation of sinusoidal smooth muscle via PKG (needed to reduce free cytosolic calcium ion concentration)
  4. Engorgement of erectile tissue with blood
19
Q

What are the common side effects of viagra

A

Flushing
Headache
Nasal Congestion (vasodilation elsewhere)

20
Q

What are the less common side effects of viagra

A

Blurred vision
Loss of hearing
Bladder pain
Dizziness, pain on urination

21
Q

What is priaprism

A

Persistent painful erection lasting longer than four hours in absence of sexual desire

22
Q

What are the two types of priaprism

A

Ischaemic- no flow

Non-ischaemic- high flow (excess arterial supply)

23
Q

How do you treat priaprism

A

Intracavernosal injection of alpha adrenoceptor agonist

24
Q

What is the function of the prostate gland

A

Secretion of slightly alkaline prostatic fluid that is mixed with sperm and secretions from other accessory glands

25
Q

What is Benign prostatic hyperplasia (BPH) and its symptoms

A

Enlargement of prostate with age

Symptoms:
Hesitancy- interrupted, weak urine system
Urgency, leaking or dribbling
Frequent urination at night

26
Q

How do you treat benign prostatic hyperplasia (BPH) and drug examples

A
  1. Alpha adrenoceptor blockers:
  2. 5 alpha reductase inhibitors- finasteride
  3. Minimal invasive surgery
27
Q

Describe the use of alpha adrenoceptor blockers in BPH and give examples

A

Relaxes muscle fibres within prostate- therefore reducing obstruction to urine flow

Does not reduce prostate size

Examples: Tamsulosin (flomax) and terazosin

28
Q

What are the risk factors for prostate cancer?

A

Age: increases with age (mostly over 50s)

Family History: 2 and a half more likely if father or brother hasn’t been diagnosed

Ethnicity: afro carribeans are 3 times more likely than whites

Diet: typical western diet his in saturated fats and red meat

29
Q

What are the symptoms of prostate cancer (similar to early BPH)

A

Hesitant
Interrupted weak urine system
Urgency and leaking or dribbling
Most frequent night urination

30
Q

How do you diagnose prostate cancer (7)

A

Urine test- rules out infection

Above negative- blood test to measure PSA (prostate specific antigen)

DRE- digital rectal examination

TRUS (trans-rectal-ultra-sound)

CT scan

MRI scan

Bone scan with or without x rays

31
Q

What are the three different types of prostate cancer

A

Localised- affecting only prostate

Locally advanced

Advanced (metastasis- typical to bone)

32
Q

How do you treat localised prostate cancer

A

Active surveillance

Radiotherapy

Surgical prostatectomy

33
Q

How do you treat locally advanced prostate cancer

A

Hormone therapy

Tumour growth often androgen dependent- block androgen production or action

Surgical castration

34
Q

how does hormone therapy related to prostate cancer work

A

Down regulation of GnRH receptors- blocking of LH secretion and androgen secretion

Blocks androgen synthesis directly

Block androgen receptor

35
Q

What are the different types of hormone therapy in prostate cancer and give examples

A

Injection and implants- stop testosterone production (GnRH agonists that down regulate the GnRH receptor on pituritary gonadotroph cells)

Examples:
Goserelin- ZOLDADEX

36
Q

Give some examples of anti-androgens

A

Bicalutamide

FLutamide

Cyproterone acetate

PM3A: Autumn (20 decks)

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