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MD3002 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

What is the precursor of all steroids?

A

Cholesterol

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2
Q

What is the distribution of cholesterol?

A
  • Membrane lipid
  • In plasma associated with apoproteins, triacylglycerols & phospholipids in structures called lipoproteins
  • Cytosolic lipid droplets as cholesterol esters
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3
Q

What is the structure of Cholesterol?

A
  • Cyclopentanoperhydrophenanthrene nucleus

- 8-carbon aliphatic side chain

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4
Q

How is cholesterol synthesised?

A

From acetyl CoA in a multi-step process that occurs in the SER & cytosol

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5
Q

What is the rate limiting step in cholesterol synthesis?

A

Conversion of 3-hydroxy-3-methylglutaryl (HMG-CoA) to Mevalonate by HMG-CoA reductase

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6
Q

What are the 3 main physiological roles of cholesterol?

A
  1. Component of cell (plasma) membrane
  2. Precursor for the production of bile salts
  3. Precursor for all steroid hormones
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7
Q

What does cholesterol do as a component of the cell (plasma) membrane?

A
  • Decreases membrane fluidity
  • Decreases physical permeability to charged/polar compounds
  • Associated with formation of lipid rafts
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8
Q

What does cholesterol do as a precursor for the production of bile salts?

A

Uptake of fats & fat-soluble vitamins in GI tract

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9
Q

Give 3 examples of steroid hormones that cholesterol acts as a precursor to?

A
  1. Glucocorticoids
  2. Mineralocorticoids
  3. Sex steroids
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10
Q

Give 5 examples of what pregnenolone (from cholesterol esters) form into?

A
  1. Aldosterone
  2. Cortisol
  3. Testosterone
  4. Estradiol
  5. Progesterone
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11
Q

What are the 2 adrenal steroids?

A
  1. Mineralocorticoid aldosterone

2. Glucocorticoid cortisol

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12
Q

Where are the enzymes associated with biosynthesis of adrenal steroids located (2)?

A
  • Smooth endoplasmic reticulum (SER)

- Mitochondria

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13
Q

What is the side-chain cleavage enzyme that produces pregnenolone also known as?

A

20,22 desmolase

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14
Q

What happens if the synthesis of cortisol is prevented by any one of several dysfunctional enzymes?

A

Other steroid products might be produced in excess

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15
Q

In the biosynthesis of what 2 things are certain pathways shared?

A

Androgens as well as estrogens

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16
Q

What is the main cytochrome P-450 enzyme involved in steroidogenesis?

A

Cholesterol side chain cleavage (P-450SSC)

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17
Q

What is the gene associated with Cholesterol side chain cleavage enzyme (P-450SSC)?

A

CYP11A1

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18
Q

What does Aromatase enzyme (P-450arom) do?

A

Catalyzes a reaction essential for the production of estrogens

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19
Q

How many different P-450 enzymes have been identified in the human genome?

A

57

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20
Q

What are the 3 different structures making up the adrenal gland?

A
  • Capsule
  • Cortex
  • Medulla
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21
Q

What are the 3 different zones in the cortex of an adrenal gland?

A
  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona reticularis
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22
Q

What hormone does the Zona Glomerulosa produce in the adrenal gland cortex?

A

Mineralocorticoid (aldosterone)

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23
Q

What hormones does the Zona Fasciculata & Zona Reticularis produce in the adrenal gland cortex?

A
  • Glucocorticoids (cortisol)

- Androgens (DHEA) / sex hormones

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24
Q

Describe the course of the blood supply of the adrenal glands?

A

Enters cortex in subcapsular region & flows through anastomotic capillary beds while coursing through both cortex & medulla

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25
Q

What special cells does the adrenal medulla contain?

A

Chromaffin cells

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26
Q

What hormones does the chromaffin cells in the adrenal medulla secrete?

A
  • Epinephrine

- Small amount of norepinephrine

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27
Q

What does DHEA stand for?

A

Dehydroepiandrosterone

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28
Q

In a male human what is the preferred pathway for pregnenolone to from testosterone?

A

Pregnenolone –> DHEA –> Androstenediol –> oxidation of A ring –> Testosterone

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29
Q

What is the function of Leydig cells in testis?

A

They produce testosterone in the presence of luteinizing hormone (LH)

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30
Q

What is the function of Sertoli cells in testis?

A
  • FSH stimulates the Sertoli cells to secrete androgen-binding protein into lumen of seminiferous tubules
  • Binding of testosterone in lumen provides local testosterone supply for developing spermatogonia
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31
Q

What is the cross-link between Leydig cells and Sertoli cells?

A
  • Leydig cells make testosterone, which acts on Sertoli cells
  • Sertoli cells convert some of this to estradiol, which can act on Leydig cells
  • Sertoli cells generate growth factors that act on the Leydig cells
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32
Q

How does the biosynthesis of ovarian steroids differ to testicular steroids?

A

Ovaries have aromatase, which converts androgens to estrogens

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33
Q

What is the major product of the ovary follicle in the follicular phase?

A

Estradiol

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34
Q

What is the major product of the corpus luteum in the ovary?

A

Progestins

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35
Q

What happens in the follicular phase of the ovary?

A
  • LH primes the Theca cell to convert cholesterol to androstenedione
  • Androstenedione diffuses to the granulosa cell, whose aromatase activity has been stimulated by FSH
  • Aromatase converts androstenedione to estradiol
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36
Q

Why does Androstenedione have to diffuse from the Theca cell to the granolasa cell to be converted?

A

Theca cell lacks aromatase, it cannot generate estradiol from androstenedione

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37
Q

Where are the 2 places cholesterol is derived from?

A
  1. Diet

2. Synthesised in Liver

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38
Q

Describe the movement of cholesterol?

A

Transported to steroidogenic tissue primarily in form of LDL, taken up by receptor- mediated endocytosis & stored esterified to fatty acids in cytosolic lipid droplets

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39
Q

What are the 2 major sites for steroid hormone biosynthesis?

A
  1. Adrenal cortex

2. Gonads

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40
Q

What are the 5 major classes of plasma lipoproteins?

A
  1. Chylomicrons
  2. VLDL
  3. IDL (intermediate density lipoproteins)
  4. LDL
  5. HDL
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41
Q

What enzyme breaks cholesterol esters into free cholesterol?

A

Cholester Hydrolase

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42
Q

What does free cholesterol give rise to?

A

Pregnenolone

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43
Q

What is the fundamental reproductive unit of the female?

A

Single ovarian follicle, composed of one germ cell (oocyte), surrounded by endocrine cells

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44
Q

What is Menarche?

A
  • Beginning of menstrual cycles (average 11-13yr)

- Maturation of GnRH pulsatility so primarily hypothalamic

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45
Q

What are the different things which determine age at puberty for a female?

A
  • Genetics
  • Nutrition
  • Geographic location
  • Exposure to light
  • Body composition, fat deposition
  • Exercise
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46
Q

What is the female sexual cycle/menstrual cycle controlled by?

A
  • Gonadotropins

- Gonadal hormones

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47
Q

Describe the 3 phases in the ovarian cycle?

A
  1. Follicular phase (15days)
  2. Ovulatory phase (1-3days)
  3. Luteal phase (13day)
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48
Q

What are the 3 phases in the endometrial cycle?

A
  • Menstruation
  • Proliferative
  • Secretory
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49
Q

What is oogenesis?

A

Production of gametes (eggs) during the foetal period

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50
Q

What are the 4 functions of the ovaries?

A
  1. Oogenesis
  2. Maturation of oocyte
  3. Expulsion of mature oocyte (ovulation)
  4. Secretion of female sex steroid hormones (oestrogen & progesterone) & peptide hormone inhibin
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51
Q

What are the 5 stages in the development ovarian follicle?

A
  1. Primordial follicle
  2. Primary follicle
  3. Preantral follicle
  4. Early astral follicle
  5. Mature follicle
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52
Q

What is the mature version of an oocyte called?

A

Ovum

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53
Q

What does oogenesis involve?

A

Completion of meiosis which occurs at the time of fertilisation

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54
Q

How is oogonia produced?

A

In embryonic yolk sac by mitotic division (max 7 million) 3 weeks post conception

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55
Q

What happens to oogonia at 8-10weeks of gestation?

A

Prophase of 1st meiosis starts, becomes primary oocyte

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56
Q

What is the oogonia surrounded by?

A

Pre-granulosa cells

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57
Q

What is the oogonia also called?

A

Primordial follicle

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58
Q

Describe 1st phase of oogenesis occurring during foetal life?

A
  • Migrate to ovary
  • Colonise the cortex
  • Undergo mitosis
  • At 8-10weeks meiosis begins
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59
Q

What happens to the remaining oocytes which aren’t degenerated?

A

Arrested in meiotic prophase until last oocytes are ovulated (upto 50years)

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60
Q

What are the 2 most common cytogenetic abnormality which increases with maternal age?

A
  • Aneuploidy

- Down Syndrome

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61
Q

What happens in the 2nd phase of oogenesis at ovulation?

A
  • Meiosis resumes, 1st division is completed & haploid nuclei separated to form 2 cells
  • Cytoplasma unequally shared
  • Meiosis arrests again at metaphase II & secondary oocyte is ovulated
  • 2nd division of meiosis is only completed in those oocytes that are fertilised
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62
Q

What stimulates meiosis resuming in 2nd phase of oogenesis?

A

Lutenizing Hormone (LH)

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63
Q

What does the cytoplasm being unequally shared in the 2nd phase of oogenesis form?

A

Large secondary oocyte & polar body (which has no further role)

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64
Q

What are the 3 differences between spermatogenesis & Oogenesis?

A
  1. Females, mitotic proliferation of oogonia occurs prior to birth. Males, spermatogonia proliferate after puberty
  2. Females, meiotic divisions of oocyte produces only 1 mature ovum. Males, produce 4 mature spermatozoa
  3. Females, 2nd meiotic division is completed only upon fertilisation. Males, products of meiosis (spermatids) undergo substantial differentiation in maturing process
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65
Q

Describe the male spermatogenesis?

A
  • Continuous
  • Lower temperature required
  • Meiosis begins at puberty
  • Results in production of infinite numbers of sperm (testis have stem cell population)
  • Results in production of motile gametes
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66
Q

Describe the female oogenesis?

A
  • Discontinous (periods of arrest)
  • Normal body temperature
  • Meiosis begins before birth
  • Results in production of finite numbers of oocytes (no stem cells)
  • Results in production of immotile gametes
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67
Q

What do the eggs in ovaries exist in?

A

Follicles

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68
Q

What is step 1 to follicular development?

A

Primordial follicle= single layer of granolas cells around oocyte

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69
Q

What is step 2 to follicular development?

A

Oocyte size increases, multiple layers of granulosa cells & separation of oocyte from granulosa cells by thick layer of material

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70
Q

What is step 3 to follicular development?

A

Cytoplamic processes cross the zona pelucida & form gap junctions with oocyte & nutrients & chemical messengers are passed to oocyte

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71
Q

What is step 4 to follicular development?

A

Follicle grows by mitosis of granulosa cells & some differentiate to become theca

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72
Q

What is step 5 to follicular development?

A

Antrum begins to form amongst granulosa cells from fluid they secrete

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73
Q

Describe Small Follicles (Primordial)?

A
  • Most numerous
  • Non-growing
  • Oocyte nucleus is in meiotic prophase
  • Single layer of follicular cells (granulosa cells)
  • Secrete anti-Müllerian hormone (AMH)
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74
Q

What do anti-Müllerian hormone (AMH) levels tell us?

A

Reflect the ovarian follicular reserve & therefore can be measured to assess ovarian ageing

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75
Q

Describe Medium Follicles (Primary)?

A
  • Follicular (granulosa) cells divide, forming 3 layers around the oocyte
  • Growth is independent of hormones
  • Takes 85days (3 cycles) to reach 3 layers of follicular cells
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76
Q

How many oocytes may a female lose?

A

~650 per cycle

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77
Q

Describe Large follicles (Secondary, antral, Graafian, preovulatory)?

A
  • Zona pellucida (egg shell) develops & enclosing the oocyte & masking its antigens
  • Rapid mitotic division in follicular cells forms many layers
  • Antrum develops & fills with fluid
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78
Q

What does the FSH do to medium follicles?

A

Stimulates rapid development of medium follicles over 14days leading to either ovulation/atresia

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79
Q

Initial follicular growth is ________ of hormones and takes _______?

A
  • Independent

- 85 days

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80
Q

Final follicular growth is dependent on _____ and takes ________?

A
  • FSH

- 10-14 days

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81
Q

What effect does LH surge have on the chemical mechanics of ovulation?

A

Induces prostaglandin endoperoxide synthase in granulosa cells (sets up pseudoinflammatory response)

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82
Q

What effect does FSH (some LH) have on the chemical mechanics of ovulation?

A

Stimulates release of plasminogen activator from granulosa cells (converts plasminogen to plasmin)

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83
Q

What effect does Prostaglandins E & F have on the chemical mechanics of ovulation?

A

Release lysosomal enzymes that digest follicular wall

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84
Q

What effects does “stigma” have on the chemical mechanics of ovulation?

A
  • Forms on surface of follicle, balloons out, forms vesicle and ruptures
  • Oocyte expelled
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85
Q

What 2 things is the process of ovulation facilitated by?

A
  • Intrafollicular pressure

- Contraction of smooth muscle in theca

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86
Q

How is the corpus luteum formed?

A
  • Mature follicle discharges its astral fluid & egg, collapses around antrum & undergoes rapid transformation
  • Granulosa cells enlarge, & form gland-like corpus luteum
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87
Q

What 3 things does the Corpus luteum secrete?

A
  • Oestrogen
  • Progesterone
  • Inhibin
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88
Q

What happens to the corpus luteum if no egg is fertilised?

A

Development reaches max within ~10 days & rapidly degenerates by apoptosis

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89
Q

What happens half way through the follicular phase?

A

One follicle becomes dominant and matures

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90
Q

What are the 2 anterior pituitary gonadotopins in a female?

A
  • LH

- FSH

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91
Q

What are the 2 gonadal sex hormones in a female ?

A
  • Oestrogen

- Progesterone

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92
Q

What is the hormonal pattern of FSH in a female?

A

Increases in early part of follicular phase, then steadily decreases throughout remainder of cycle EXCEPT small midcycle peak

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93
Q

What is the hormonal pattern of LH in a female?

A
  • Constant during most of follicular phase, then large midcycle increase (LH surge) peaking ~18h before ovulation
  • Then rapid decrease with further slow decline during the luteal phase
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94
Q

What is the hormonal pattern of Oestrogen in a female?

A
  • Low & stable for 1st week, increases rapidly in 2nd weeks, starts to decline before LH peak
  • Then 2nd increase due to corpus luteum in last few days of cycle.
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95
Q

What is the hormonal pattern of Progesterone in a female?

A
  • Low level due to ovary release during follicular phase with small increase just before ovulation
  • Soon after ovulation, large increase due to CL release, then similar pattern to oestrogen
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96
Q

What is the hormonal pattern of Inhibin in a female?

A

Similar pattern to oestrogen ie. increases in late follicular phase, remains high during luteal phase, decreases as corpus luteum degenerates

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97
Q

How does oestrogen have NEGATIVE feedback effects on ovarian hormones?

A

In low plasma conc, causes anterior pituitary to secrete less FSH & LH during early & middle follicular phase in response to GnRH & also may INHIBIT hypothalamic neurons that secrete GnRH

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98
Q

How does inhibin have NEGATIVE feedback effects on ovarian hormones?

A

Acts on pituitary to INHIBIT the secretion of FSH throughout cycle

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99
Q

How does oestrogen have a POSITIVE feedback effect on ovarian hormones?

A
  • Increasing dramatically, causes anterior pituitary cells to secrete more LH & FSH in response to GnRH which triggers ovulation
  • Can also STIMULATE hypothalamic neurons that secrete GnRH
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100
Q

How does progesterone have a NEGATIVE feedback effect on ovarian hormones?

A

High plasma conc, in presence of oestrogen, INHIBIT hypothalamic neurons that secrete GnRH, preventing LH surges during luteal phase & pregnancy

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101
Q

When is the concentration of FSH in the blood at its maximum?

A

During follicular phase of the menstrual cycle

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102
Q

In the 1st week of the follicular phase what does FSH stimulate?

A

Growth of medium sized follicles

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103
Q

During the follicular phase what do granulosa cells express?

A

FSH receptors

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104
Q

What are granulosa cells homologous with?

A

Sertoli cells of the testis

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105
Q

What does Luteinising hormone (LH) stimulate during the secretory phase?

A

Steroid hormone synthesis by the corpus luteum

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106
Q

What are Theca cells similar to?

A

Leydig cells in males

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107
Q

What diffuses from the Theca cells to the Granulosa cells during the early & middle follicular phases?

A

Androgen (androstenedione) through basement membrane

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108
Q

How is an LH surge formed?

A

Dominant follicle secretes large amounts of oestrogen which acts on anterior pituitary (& hypothalamus) to cause LH surge

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109
Q

What does LH surge trigger?

A

Ovulation & formation of corpus luteum

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110
Q

What is the action of LH mediated by?

A

Granulosa cells

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111
Q

What does oestrogen cause?

A
  • Mid-cycle shift from negative to positive feedback
  • Caused by up regulation of receptors (GnRH) when oestrogen levels increase
  • Resulting in LH & FSH surge prior to ovulation
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112
Q

What are the 5 effects of LH surge on ovarian function?

A
  1. Oocyte completes 1dt meiotic division & undergoes cytoplasmic changes that prepare the ovum for implantation
  2. Antrum size & blood flow to follicle increase
  3. Granulosa cells release progesterone & decrease release of oestrogen
  4. Enzymes & prostaglandins breakdown follicular-ovarian membranes which rupture
  5. Remaining granulosa cells of ruptured follicle are transformed into corpus luteum
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113
Q

What are the 7 functions of granulosa cells?

A
  1. Nourish oocyte
  2. Secrete chemical messengers
  3. Secrete antral fluid
  4. Site of action for oestrogen & FSH (early & middle follicular phase)
  5. Express aromatase
  6. Secrete inhibin
  7. Site of action for LH induction of changes in oocyte & follicle culminating in ovulation & formation of corpus luteum
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114
Q

What does aromatase do?

A

Converts androgen (from theca cells) to oestrogen

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115
Q

What things happen if no implantation in the luteal phase?

A
  • hCG does not appear in blood
  • Corpus luteum dies
  • Progesterone & oestrogen decreases
  • Menstruation occurs & next menstrual cycle begins
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116
Q

What is the timeline of events which occur when there is enough oestrogen from ovary?

A

LH surge induced –> ovulation –> corpus luteum degenerates –> decrease (oestrogen/progesterone) secretion –> FSH & LH increase enough for new follicle growth

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117
Q

What happens if progesterone remains high?

A

Levels of LH & FSH will be suppressed & ovulation will NOT occur ie. in pregnancy

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118
Q

How does progesterone remain high in pregnancy?

A

Human chorionic gonadotrophin produced by placenta maintains corpus luteum which continues to secrete progesterone

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119
Q

What is used for oral contraceptive pills/why?

A

Oestrogen as it suppresses LH & FSH & prevents ovulation

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120
Q

What are the 11 other things oestrogen stimulates?

A
  1. Growth of ovary & follicle
  2. Growth of smooth muscle & proliferation of epithelial linings of reproductive tract
  3. External genitalia growth, particularly during puberty
  4. Breast growth, particularly ducts & fat deposition during puberty
  5. Female body configuration development
  6. Fluid secretion from lipid-producing skin glands
  7. Bone growth & cessation of bone growth
  8. Vascular effects
  9. Feedback effects on hypothalamus & anterior pituitary
  10. Prolactin secretion
  11. Protects against atherosclerosis
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121
Q

What effect does oestrogen have on the Fallopian tubes?

A

Increases contractions & ciliary activity

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122
Q

What effect does oestrogen have on the uterus?

A
  • Increase myometrial contraction & responsiveness to oxytocin
  • Stimulates secretion of abundant, watery cervical mucus
  • Prepares endometrium for progesterone’s actions by inducing progesterone receptors
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123
Q

What effect does oestrogen have on the vagina?

A

Increases layering of epithelial cells

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124
Q

What are the 8 other effects of progesterone?

A
  1. Converts oestrogen-primed endometrium to actively secreting tissue suitable for implantation of an embryo
  2. Induces thick, sticky cervical mucus
  3. Decreases contractions of fallopian tubes & endometrium
  4. Decreases proliferation of vaginal epithelial cells.
  5. Stimulates breast growth (glandular tissue)
  6. Inhibits milk-inducing effects of prolactin.
  7. Feedback effects on hypothalamus & anterior pituitary
  8. Increases body temperature.
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125
Q

What inhibits the secretion of GnRH & gonadotropins during the luteal phase?

A

Combination of progesterone, oestrogen and inhibin

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126
Q

What is the mean length of the menstrual cycle?

A

Mean 28days (3/- 3.95) for about 40 years

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127
Q

What is Menopause?

A
  • Occurs at ~45-55yrs (51yrs avg) & marks end of natural fertility
  • Exhaustion of primordial follicles so primarily ovarian
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128
Q

When are human females sexually receptive to males?

A

Throughout their cycle

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129
Q

How long is the menstrual phase?

A

~3-5 days in a typical 28 day cycle

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130
Q

What happens during the 1. menstrual phase?

A

Epithelial lining of uterus (endometrium) degenerates which is part of ovarian follicular phase

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131
Q

What happens during the 2. proliferative phase

A
  • Menstrual flow ceases
  • Under influence of oestrogen, endometrium thickens
  • Growth of underlying smooth muscle (myometrium)
  • Synthesis of receptors for progesterone in endometrial cells
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132
Q

How long does the 2. proliferative phase last?

A

~10 days until ovulation

part of follicular phase

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133
Q

What is the proliferative phase dominated by?

A

Estradiol 17β

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134
Q

Describe the proliferative phase histology?

A
  • Repair of lining epithelium after menstruation
  • Proliferation & thickening of stroma
  • Simple test tube shaped glands
  • Induction of synthesis of intracellular receptors for progesterone
  • Contractility & excitability of myometrium increases
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135
Q

When does the 3. secretory phase occur/ how long does it last?

A
  • Soon after ovulation

- ~12 days long

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136
Q

What happens during the 3. secretory phase?

A
  • Endometrium increases secretory activity under influence of progesterone acting on oestrogen-primed tissue
  • Effect on endometrial glands
  • Coincides with ovarian luteal phase
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137
Q

What effects does the 3. secretory phase have on the endometrial glands & why?

A
  • Become coiled, filled with glycogen, blood vessels become more numerous, enzymes accumulate in glands & connective tissue
    – Making endometrium hospital environment for implantation & nourishment of developing embryo
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138
Q

What is the secretory phase dominated by?

A

Progesterone

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139
Q

Describe the secretory phase histology?

A
  • Proliferation/thickening of stroma
  • Spiral arteries develop alongside complex,
    hacksaw shaped glands
  • Secretion in the glands is rich in glycoprotein sugars & amino acids
  • Enlargement of myometrial cells but depressed overall excitability
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140
Q

What is lost during the ischaemic phase?

A

Steroid support

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141
Q

Describe the ischaemic phase histology?

A
  • Constriction of spiral arteries
  • Ischemia & collapse of endometrium
  • Separation of basal & functional layers
  • Functional layer is shed as menstrual bleeding
  • Increase in neutrophils
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142
Q

How much blood is lost in each menstrual phase?

A

30-80mls normal

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143
Q

Describe the bleeding in the menstrual phase?

A

Bleeding without clotting, endogenous fibrinolytic activity

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144
Q

What happens to oestrogen & progesterone levels during the menstrual cycle days 1-5?

A

Low because the previous corpus luteum is regressing

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145
Q

What is the effect of LOW oestrogen & progesterone in the menstrual cycle?

A
  • Endometrial lining sloughs
  • Secretion of FSH & LH is released from inhibition & plasma conc increase
  • Severe growing follicles are stimulated to mature
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146
Q

What is the major event which occurs at day 7 of the menstrual cycle?

A

Single follicle (usually) becomes dominant

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147
Q

What is the major events which occur during days 7-12 of the menstrual cycle?

A
  • Plasma oestrogen increases due to secretion by dominant follicle so endometrium stimulated to proliferate
  • LH & FSH decrease due to oestrogen & inhibin negative feedback so degeneration of non-dominant follicles
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148
Q

What are the major evens which occur at days 12-13 during the menstrual cycle?

A
  • LH surge induced by increased plasma oestrogen
  • Oocyte induced to complete 1st meiotic divisions & undergo cytoplasmic maturation
  • Follicle stimulated to secrete digestive enzymes & prostoglandins
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149
Q

What are the major events at day 14 during menstrual cycle?

A

Ovulation is mediated by follicular enzymes & prostaglandins

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150
Q

What are the major events at days 15-25 of the menstrual cycle?

A
  • Corpus luteym forms & under influence of low LH, secretes oestrogen & progesterone increasing plasma conc
  • Secretory endometrium develops
  • Secretion of LH & FSH inhibited
  • No new follicles develop
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151
Q

What are the major events at days 25-28 of the menstrual cycle?

A
  • Corpus luteum degenerates
  • Plasma oestrogen & progesterone conc decrease
  • Endometrium begins to slough at conclusion of day 28, new cycle begins
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152
Q

What is the ovarian follicular phase equivalent to?

A

Uterine menstrual & proliferative phases

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153
Q

What is the ovarian luteal phase equivalent to?

A

Uterine secretory phase

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154
Q

What is oligomenorrhoea?

A

Infrequent light periods

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155
Q

What is metrorrhagia?

A

Irregular bleeding

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156
Q

What is polymenorrhoea?

A

Frequent periods

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157
Q

What is amenorrhoea?

A

No periods

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158
Q

Describe the causes of dysmenorrhoea?

A
  • Overproduction of prostaglandins produced by endometrium in response to decrease in plasma oestrogen & progesterone
  • May account for systemic symptoms ie. nausea, vomiting, headache
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159
Q

How common is Premenstrual syndrome (PMS)?

A

3/4

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160
Q

How common is premenstrual dysphoric disorder (PMDD)?

A

3-8%

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161
Q

Describe symptoms of premenstrual dysphoric disorder (PMDD)?

A
  • Anxiety
  • Mood swings
  • Headaches
  • Bloated
  • Change in appetite
  • Joint pain
  • Tender enlarged breasts
  • Abdo pain
  • Clumsiness
  • Depression
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162
Q

What may be the cause of the symptoms associated with premenstrual dysphoric disorder (PMDD)?

A

Fall of progesterone (anxiolytic effects) at end of the cycle

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163
Q

What are the primary causes of amenorrhoea?

A
  • Anatomical/congenital abnormality ie. underdevelopment or absence of uterus/vagina
  • Genetic ie. Turner’s syndrome
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164
Q

What are the secondary causes of amenorrhoea?

A
  • Pregnancy
  • Lactation
  • Exercise/nutrition
  • Menopause
  • Polycystic ovarian syndrome
  • Latrogenic (surgery, medication)
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165
Q

What are the effects of amenorrhoea?

A
  • Estrogen deficiency can cause hot flushes, vaginal dryness

- Loss of bone mineralisation causing reduction in peak bone mass & osteopenia/osteoporosis

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166
Q

What is “natural” breast feeding?

A
  • Feeding ad lib & with baby sleeping with mother & feeding though the night
  • Female may experience lactational amenorrhoea decreasing likelihood of pregnancy until weaning occurs
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167
Q

How common is polycystic ovary syndrome (PCOS)?

A
  • 10% of reproductive age woman

- Most common reproductive problem

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168
Q

What are the characteristics of polycystic ovary syndrome (PCOS)?

A
  • Hyperandrogenemia
  • Oligomenorrhea
  • Obesity (ethnicity of women)
  • Hirsutism (hairiness & acne)
  • Infertility
  • Enlarged cystic ovaries
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169
Q

What is the biochemical spectrum of polycystic ovary syndrome (PCOS)?

A
  • Elevated oestrogen from peripheral armatase, or low from anovulation
  • Elevated free testosterone
  • Insulin resistance
  • Elevated anti Müllerian hormone
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170
Q

What are the different types of Polycystic ovary syndrome (PCOS) therapies?

A
  • Weight control (difficult)
  • Cycle regulation (oral contraceptive pill)
  • Anti androgen therapy (cyproterone acetate)
  • Cosmetic hair removal
  • Ovulation induction
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171
Q

Where is prolactin synthesised & released?

A

Anterior pituitary gland

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172
Q

What is prolactin production normally controlled by?

A
  • Hypothalamic prolactin inhibitory factor (PIF), shown to be dopamine
  • Stress inhibits dopamine release which allows prolactin levels to rise
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173
Q

How does dopamine have an effect on prolactin production?

A

Dopamine carried from neurosecretory cells in arcuate nucleus via hypophyseal portal system to anterior lobe of pituitary where it modulates secretion of prolactin

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174
Q

What does Hyperprolactinaemia cause?

A
  • Inhibit FSH & LH leading to amenorrhea

- Inappropriate lactation, libido loss

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175
Q

What can pituitary tumours (macro adenoma) cause?

A

Constrict blood supply to pituitary, preventing PIF from reaching anterior pituitary causing prolactin levels to rise = hyperprolactinaemia

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176
Q

What is the surgical approach to pituitary tumour?

A

Via nasal cavity & sphenoid air sinus

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177
Q

How are prolactinomas treated?

A

Dopamine agonist- Bromocriptine or Cabergoline

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178
Q

What is premature ovarian failure (POF)?

A

Menopause in women <40yrs (idiopathic, autoimmune disorders, genetic disorders such as fragile X, chemotherapy, radiation)

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179
Q

How can symptoms of menopause be treated?

A

Oestrogen replacement (hormone replacement therapy - HRT)

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180
Q

What is the definition of infertility according to OED in 2012?

A

Not fertile; unfruitful, unproductive, barren, sterile

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181
Q

What is the definition of infertility in a medical sense?

A

People who have difficulties (of may find it impossible) to have children naturally

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182
Q

What 3 ways is infertility described as being?

A
  • Dysfunction (not a disease)
  • Socially constructed disease
  • “Terrible disease affecting our sexuality & well being”
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183
Q

What are the 3 steps to parenthood?

A
  1. Begetting- bring child into existence through reproduction
  2. Gestating- child grows inside the woman
  3. Caring- post-birth role
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184
Q

What are the different types of parents?

A
  • Intentional parents
  • Genetic parents
  • Gestational mother
  • Nurturing parents
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185
Q

How many couples may have difficulty conceiving?

A

~1/6 couples

~3.5 million people

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186
Q

What is the % for number of couples who are infertile?

A

~5%

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187
Q

After 3 years of trying to conceive without success, what is the % chance of pregnancy occurring within the next year?

A

25% or less

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188
Q

What are the 3 factors affecting a woman fertility?

A
  • Abnormal ovulation (polycystic ovary syndrome, early menopause)
  • Blockage of Fallopian tubes
  • Age
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189
Q

What are the 3 factors affecting a mans fertility?

A
  • Low sperm count/quality

- Damage to testicle and/or failure to ejaculate

190
Q

What are the different methods to treat infertility/ assisted reproductive technologies?

A
  • Intrauterine insemination (IUI)
  • In vitro fertilisation (IVF)
  • IVF with intracytoplasmic sperm injection (ICSI)
  • Use of donor sperm/eggs
  • Surrogacy
191
Q

What are the 5 steps to in vitro fertilisation?

A
  1. SUPPRESS (GnRH agonist)
  2. STIMULATE (FSH)
  3. MATURATION (hCG)
  4. EGG COLLECTION (ultrasound transvaginal aspiration/laparoscopy)
  5. TRANSFER after 2-6days , use ultrasound, use progesterone for luteal phase support
192
Q

What are the risks associated with IVF?

A
  • Ovarian hyperstimulation syndrome (can occur due to super ovulation in response to drugs)
  • Transferral of several embryos (multiple births)
  • Welfare of the child (1990: need for father. 2008: need for supportive parenting)
193
Q

What is the definition of “supportive parenting”?

A

Woman shall not be provided with treatment services unless account has been taken of WELFARE of any child born of the treatment & any other child who may be affected by the birth

194
Q

What are the guidelines for IVF in Scotland for <40 years old?

A
  • 3 cycles if:
  • Infertility with an appropriate cause of any duration
  • Unexplained infertility of 2yrs (heterosexual)
  • Unexplained infertility following 6-8 cycles of donor insemination (same sex)
195
Q

What are the guidelines for IVF in Scotland for 40-42yrs old?

A
  • 1 cycle if:
  • No IVF before
  • No evidence of low ovarian reserve
  • Discussion of implications of IVF & pregnancy at this age
196
Q

What is the HFEA statistic (%) for successful IVF in UK (2014)?

A

26.5% of IVF treatments, using own fresh eggs

197
Q

How much does 1 IVF cycle cost?

A

~£3500

198
Q

Who/when was the 1st test tube baby?

A

1978 - Louise Brown

199
Q

What 2 things do the Human fertilisation & embryology authority (HFEA) regulate?

A
  • Treatment (inspect & license clinics)

- Research (licenses for human embryo research)

200
Q

What was the case regarding homosexual couples using IVF?

A

NHS Greater Glasgow & Clyde (2009)- NHS said no, but then overturned that decision

201
Q

What was the case regarding single women using IVF?

A

Elizabeth Pearce (Ealing PCT)- using sperm bought from the uS, and IVF funded by NHS

202
Q

What are the ethical issues surrounding Gametes in IVF?

A
  • Frozen: must state for how long & what happens in event of death
  • Donated: is it ok to pay donors? Limit to number of children created? Should children be able to find out biological parents?
203
Q

What is the UK limit of how many children a person can create via IVF?

A

10 families

204
Q

What are the ethical issues surrounding embryos in IVF?

A
  • Use immediately, freeze, discard, research
  • How many should be made?
  • How many should be implanted?
  • What do we do with spares?
205
Q

What are the ethical issues surrounding reproductive tourism?

A
  • Cost
  • Waiting lists
  • Avoid legal restrictions
206
Q

What is “3 parent IVF”?

A

IVF with mitochondrial replacement

207
Q

What is IVF with mitochondrial replacement?

A
  • Allows those at risk of passing on certain mitochondrial conditions to avoid risk
  • Pro-nuclear transfer or maternal spindle transfer
208
Q

What are the 4 considerations regarding IVF with mitochondrial replacement?

A
  1. Modification of embryos & changing germline
  2. Implications for identity & status of mitochondrial donor
  3. General views on permissibility of techniques
  4. Licensing models & further regulatory issues
209
Q

What is the main difference between pronuclear & maternal spindle transfer?

A
  • Pronuclear transfer repair is done AFTER fertilisation

- Maternal spindle transfer repair is done BEFORE fertilisation

210
Q

What did the “House of Commons” say regarding IVF with mitochondria replacement?

A

Tuesday 3 February 2015 MPs voted by 382-128 to amend the Human Fertilisation & Embryology Act 2008 & ALLOW mitochondrial donation

211
Q

What did the “House of Lords” say regarding IVF with mitochondria replacement?

A

Tuesday 24 February 2015 peers voted by 280-48 to ALLOW mitochondrial donation to be licensed for use

212
Q

What did the HFEA say regarding IVF with mitochondria replacement?

A

15th December 2016, APPROVED use of mitochondrial donation in certain, specific cases

213
Q

When/where was the 1st approved clinic application of mitochondrial replacement?

A

16th March 2017 in Newcastle HFEA approved

214
Q

What is Partial surrogacy?

A

Surrogate mother inseminates herself with commissioning father’s sperm

215
Q

What is full surrogacy?

A

IVF (commissioning couple’s egg & sperm mixed in vitro then transferred

216
Q

What does the Surrogacy Act 1985 say?

A

Surrogacy agreements are not unlawful but they are unenforceable

217
Q

Who is the legal mother from birth in the UK?

A

The surrogate mother

218
Q

What are 2 key reports regarding surrogacy?

A
  1. Brazier Report

2. Warnock Report

219
Q

What is sexual differentiation?

A

Male & females become structurally & functionally dissimilar

220
Q

What is sex determination?

A

Initiation of the male differentiation pathway by SRY gene

221
Q

Describe the human somatic cells?

A
  • 22 pairs of autosomes

- 1 pair of sex chromosomes (XX or XY)

222
Q

Describe the female somatic cells?

A
  • 46, XX

- HOMOgametic

223
Q

Describe the male somatic cells?

A
  • 46, XY

- HETEROgametic

224
Q

Describe the oocyte somatic cells?

A
  • 23

- X

225
Q

Describe the spermatozoa somatic cells?

A
  • 23, X or…

- 23, Y

226
Q

What do not normally influence gonad differentiation?

A

Autosomes or “X” chromosomes

227
Q

What is in control of the genetic determinant of sex?

A

Presence or absence of Y chromosome

228
Q

What happens once gonadal differentiation is initiated?

A

Developing gonad releases gonadal hormones that trigger cascades producing sexual dimorphism of reproductive tract

229
Q

Describe the Y chromosome?

A
  • Small
  • DNA condesned
  • Encodes ~48genes involved in skeletal growth, tooth development
  • Few genes involved with testis development
  • Has regulatory gene which indirectly controls formation of testes
230
Q

Where are many of the genes required for testis development?

A

Autosomes or X chromosome

231
Q

What happens to the chromosomes in XY females?

A

Part of short arm of Y chromosome is missing or mutated

232
Q

What happens to the chromosomes in XX males?

A

Section of Y chromosome translocated to autosome or X chromosome

233
Q

What is the SRY gene?

A

Sex-determining region of the Y chromosome which encodes a DNA binding protein (transcription factor) that regulates expression of genes on other chromosomes responsible for testes differentiation

234
Q

What are the 2 distinct cell types that the testes & ovaries are formed by?

A
  1. Somatic mesenchyme

2. Primordial germ cells

235
Q

How is the genital ridge formed?

A

Proliferation of surface epithelium & condensation of mesenchyme forming sex cords

236
Q

Gonads are identical in both sexes until the _____ of development?

A

7th week

237
Q

Where do the primordial germ cells (PGCs) originate?

A

Epiblast & 1st identifiable in wall of yolk sac (~2 weeks)

238
Q

What is the movement of primordial germ cells?

A

Migrate into genital ridge (by week 6) driven by chemotaxis & become surrounded by primitive medullary sex cords

239
Q

What happens if the migration of Primordial germ cells (PGCs) fails to enter the genital ridge?

A

Gonads do NOT develop as PGCs have inductive influence but no role during sexual dimorphism

240
Q

Describe the gonadal differentiation of a MALE?

A
  • SRY gene = primitive sex cords proliferate & penetrate medulla = TESTIS CORDS
  • Testis cords become looped, contract with ingrowing mesonephric tubule called Rete testis
  • Primordial germ cells come to reside within developing testis cords
241
Q

What do mesodermal cells differentiate into in the cords of a male gonad?

A

Sertoli cells

242
Q

What does mesenchyme tissue in interstitial spaces develop into in a male?

A

Leydig cells & start to secrete testosterone by 8th week

243
Q

What do the male gonads appear like by the 20th week?

A

Testis cords are horseshoe-shaped, composed of germ cells & Sertoli cells

244
Q

Describe the gonadal differentiation of a female?

A
  • Absence of Y = degeneration of primitive sex cords
  • 2nd set of cords form from mesenchyme (cortical cords) & by 12weeks these form distinct cell clusters around the germ cells
245
Q

How are primordial follicles formed in the female gonads?

A

Cells proliferative & surround each oogonium (germ cell) with epithelial layer of follicular cells

246
Q

What happens to the genital ducts in embryo at 7-8 weeks?

A

Dual ductal systems that are precursors to male & female internal genitalia

247
Q

What do Wolffian (mesonephric) ducts give rise to?

A

Male genital ductal system

248
Q

What do the Müllerian (paramesonephric) ducts give rise to?

A

Female genital ductal system

249
Q

Does the developmental path depend on hormones secreted by developing ovary?

A

NO

250
Q

In males, what does the SRY act in conjunction with?

A

Other transcription factors such as SOX9 & SF-1 (steroidogenic factor-1) to stimulate differentiation of Sertoli & Leydig cells

251
Q

What do the Sertoli cells express & why?

A

Anti-Müllerian hormone (AMH) which leads to regression of Müllerian ducts & prevents female structures

252
Q

What does Leydig cells start secreting/ what does this do?

A

Testosterone which supports development of Wolffian ducts & leads to virilisation

253
Q

What happens in absence of any hormones?

A

Wolffian ducts degenerate & Müllerian ducts develop forming fallopian tubes

254
Q

What does WNT4 (ovary-determining gene) do?

A
  • Up-regulates DAX1= inhibits function of SOX9, preventing male program
  • Regulates expression of other genes responsible for ovarian differentiation
255
Q

What forms the lower vagina?

A

Paramesonephric tubercle (region called sinovaginal bulbs)

256
Q

When is the vaginal outgrowth complete?

A

20 weeks

257
Q

Like gonads, external genitalia are initially ______?

A

Bipotential

258
Q

What does the developmental path for external genitalia depend on?

A

Presence or absence of androgens

present in male, absent in female

259
Q

Describe Turner’s Syndrome?

A
  • 45, XO
  • Deficiency in ovarian steroids
  • Lack of secondary sex characteristics (pubic hair, breasts) & infertility
  • Short stature, webbed neck, skeletal deformities
260
Q

Describe Triple X syndrome?

A
  • 47, XXX
  • “Super female”
  • Undiagnosed due to few symptoms apart from being very tall
261
Q

Describe Klinefelter syndrome?

A
  • 47, XXY
  • Small testis with decreased spermatogonia
  • Male phenotype
  • Incomplete virilization & breast enlargement after puberty
262
Q

Describe XYY syndrome?

A
  • 47, XYY
  • “Super males”
  • Undiagnosed due to few symptoms apart from being taller
263
Q

Describe Sex reversed syndrome ?

A
  • 46, XXSXR
  • Testis
  • Have female genes
264
Q

Describe (DSD) Pseudohermaphroditism?

A

Individual with gonads appropriate to genotype but external genitalia of opposite sex

265
Q

Give an example of a DSD syndrome due to endocrine signalling between gonads & developing tissues?

A
  • Androgen-insensitivity syndrome

- 46, XY karyotype

266
Q

Describe (DSD) Androgen-Insensitivity syndrome?

A
  • Testis initially normal but tissues lack androgen receptor so unresponsive to testosterone
  • Wolffian ducts degenerate without support of androgens
  • Testes secrete normal AMH, female ducts degenerate
  • Female external genitalia develops but have undescended testes
267
Q

Describe (DSD) Congential Adrenal Hyperplasia?

A
  • XX with ovaries
  • Fetal adrenals are over-active & secrete large amounts of steroid hormones, some have androgenic action
  • Development of Wolffian ducts & formation of male external genitalia
  • No AMH secreted so female ducts persist
  • 2 DUCTAL SYSTEMS!
268
Q

What are the 2 different compartments in the cross section of seminiferous tubules?

A
  • Intratubular compartment

- Peritubular compartment

269
Q

What are the 2 major compartments in the testes?

A
  1. Semiinferous tubules

2. Interstitial spaces

270
Q

Describe the seminiferous tubules of the testes?

A
  • ~250m total length
  • Developing germ cells
  • Sertoli (sustentacular) cells
271
Q

Describe the interstitial spaces of the testes?

A
  • Leydig cells (synthesize androgens)

- Blood & lymph vessels

272
Q

What is the function of having 2 separate compartments in the testes?

A
  • Separate “blood-testis barrier”
  • Prevents immune reaction to spermatozoa
  • Separates fluids of different composition
273
Q

What is spermatogenesis?

A

Production of mature spermatozoa from undifferentiated germ cells (primordial germ cell)

274
Q

What are the 3 stages of spermatogenesis?

A
  1. Mitotic proliferation
  2. Meiotic (reduction) division
  3. Cell modelling (spermiogenesis)
275
Q

What is the different types of cells which lead up to the production of spermatozoa?

A

Primordial germ cell –> Spermatogonia –> Primary spermatocyte –> Secondary spermatocyte –> Spermatids –> SPERMATOZOA

276
Q

How long is the gap between 1st mitotic division & release of spermatozoa?

A

74 days

277
Q

Spermatogenesis occurs in _____, initiated every ______>

A
  • Waves (4-5 cells at different stages of development)

- 16 Days

278
Q

How often does spermiogenesis occur?

A

~200 million/day

2300/second

279
Q

What are the 4 different parts to a sperm?

A
  1. End piece
  2. Principle piece
  3. Middle piece
  4. Head
280
Q

What happens at the end of differentiation?

A
  • Cytoplasmic links broken
  • Spermatozoa released into tubule lumen
  • Sperm virtually immobile
281
Q

What does the large amounts of fluid secreted by Sertoli cells help the movement of?

A

Flushes developing spermatozoa from seminiferous tubules, through the rete testis into epididymis

282
Q

How is motility of spermatids suppressed?

A

Epididymal fluid

283
Q

If ejaculated spermatozoa are placed with oocytes in vitro fertilization _____ occur immediately. They need to undergo _______?

A
  • Doesn’t

- Capacitation (normally occurs in female reproductive tract 2-6hrs)

284
Q

What 2 changes happen to the sperm due to female reproductive tract (2-5hr)?

A
  • Hyperactivation by progesterone (increased flagellar beats)
  • Head acquires capacity to initiate acrosome reaction
285
Q

What % of sperm in humans show morphological abnormalities?

A

Upto 30% (sperm quality poor)

286
Q

What is a normal sperm count?

A

50-150 x 10*6/ml

287
Q

What is sub fertility?

A

< 20 x 10*6/ml

oligozoospermia

288
Q

What is Azoospermia?

A

Absence of sperm in the ejaculate

289
Q

What is Asthenozoospermia?

A

Low sperm motility (<50% moving)

290
Q

What is Teratozoospermia?

A

High proportion of abnormally-shaped sperm

291
Q

What is Antiserum antibodies?

A

Abnormal immune response to sperm

292
Q

What are the 4 different types of hormones the testes synthesis?

A
  1. Testosterone (steroid) by Leydig cells
  2. Estrogens (steroid) but Sertoli & Leydig cells
  3. Inhibins (polypeptides) by Sertoli cells
  4. Oxytocin (polypeptide) by Leydig cells
293
Q

What is the steroid hormone biosynthesis in the testis?

A

Acetate –> Cholesterol –> Progesterone –> Testosterone –> Estrogens

294
Q

When/What happens if testosterone production is prevented?

A
  • Spermatogenesis ceases

- Blocked when primary spermatocyte enters meiotic prophase

295
Q

What happens if blood testosterone is low?

A

Few stem cells with begin cell division but the whole process will still take 74 days

296
Q

How does the pituitary gland & hypothalamus have a role in testicular function?

A

Hypothalamus secretes gonadotrophin-releasing hormone (GnRH) which causes anterior pituitary to secrete gonadotrophins from the gonadotroph cells

297
Q

What hormones does the anterior pituitary/Adenohypophysis produce?

A
  1. GONADOTROPHS- basophilic cells, secrete LH & FSH (glycoproteins). Most secrete 1, some both
  2. LACTOTROPHS- acidophilic cells, secrete prolactin (polypeptide)
298
Q

What hormones does the posterior pituitary/Neurohypophysis produce?

A

NEUROSECRETORY NEURONES- secrete arginine vasopressin (AVP) & oxytocin (peptides)

299
Q

What must GnRH be for it to be effective?

A

Released into portal blood in PULSES every hr

300
Q

What does high and low GnRH amplitiude & frequency each synthesis and secrete?

A
  • HIGH: LH

- LOW: FSH

301
Q

What happens if LH secretion is too low?

A

Testosterone is low, spermatogenesis halts

302
Q

What is the function of FSH?

A

Required for maximum sperm production, acts of Sertoli cells

303
Q

What does FSH, binding to Sertoli cells FSH receptors, cause in increase in?

A
  • RNA & Protein synthesis
  • Energy metabolism
  • cAMP
  • Inhibin secretion
  • ABP secretion
  • Fluid secretion
  • Androgen & FSH receptors
304
Q

What are the contents of the spermatic cord?

A
  • Testicular artery (from Ao L2) & pampiniform plexus
  • Artery to vas
  • Cremasteric artery (from inferior epigastric)
  • Vas
  • Lymph from testis (to para-aortic nodes)
  • Closed remnant of processus vaginalis
  • Genital branch of genitofemoral nerve
  • Sympathetic (efferent & afferent to testis)
  • Ilio-inguinal nerve (L1)
305
Q

What could happen if the processus vaginalis did not close off?

A

Lead to cysts and/or hydrocele

306
Q

How does the spermatic cord begin & end?

A

Begins at deep ring, completed as it picks up external spermatic fascia from external oblique at superficial ring

307
Q

What is the L1 cremaster reflex?

A

Ipsilateral testicular retraction on stroking upper, medial thigh due to cremaster muscle supply by genital branch of genitofemoral nerve

308
Q

Where does the referred pain go from the testis and why?

A
  • Peri-umbilical region

- Sympathetic nerves derived from lesser splanchnic nerve T10 & 11

309
Q

What makes up the cremasteric (middle layer) fascia & muscle?

A

Transversus abdominis & internal oblique

310
Q

What does the external oblique form?

A

External spermatic fascia

311
Q

What does the transversalis fascia form?

A

Internal spermatic fascia

312
Q

What does the parietal peritoneum form?

A

Loops down developing spermatic cord as processes & tunica vaginalis

313
Q

Where is the scrotum & testis suspended?

A

Inferior to urogenital triangle, outside the body

314
Q

What testis is lower than the other?

A

Left lower than right

315
Q

Describe the skin of the scrotum?

A
  • Rugose
  • No fat
  • Dartos muscle (smooth, sympathetic genital branch of genitofemoral)
  • Midline raphe divided by septum
316
Q

Name the different scrotal fascia layers?

A
  • Tunica vaginalis (visceral & parietal)
  • Internal cremasteric fascia
  • External spermatic fascia
  • Dartos fascia
317
Q

What makes up Dartos fascia?

A

Colles’ perineal fascia (continuous with Scarpa’s) & Dartos muscle (camper’s)

318
Q

What 2 things does the Scarpa’s fascia fuse with in the thigh below the inguinal ligament?

A
  • Fascia lata

- Perineal body

319
Q

What are “blue swimming trunks, but front only” a sign of?

A

Bruising trapped under Scarpa’s & Colles’

320
Q

What are the 2 different nerve supplies of the scrotum?

A
  • ANTERIOR 1/3: L1, ilio-inguinal, genitofemoral

- POSTERIOR 2/3: S2 & S3 via scrotal branches of perineal branches of Pudendal nerve

321
Q

What are the 2 different blood supplies of the scrotum?

A
  • ANTERIOR 1/3: deep & superficial external pudendeal branches of femoral
  • POSTERIOR 2/3: internal pudendal branch of internal iliac
322
Q

What are the 2 different venous supplies of the scrotum?

A
  • ANTERIOR 1/3: deep & superficial external pudendal veins to great saphenous
  • POSTERIOR 2/3: internal pudendal
323
Q

What is the lymph drainage of the scrotum?

A

Superficial inguinal nodes

324
Q

Describe the movement of sperm in the testis?

A

Seminiferous Tubules –> Rete testis in mediastinum –> via efferent ductules –> Epididymis

325
Q

What are the 3 different parts of the epididymis (post-lat)?

A
  1. Head
  2. Body
  3. Tail becoming vas
326
Q

What is the function of the tough capsule of tunica albuginea?

A

Maintains internal pressure to help transport of sperm

327
Q

What can be the clinical problem of the epididymis & testis?

A

Testicular torsion, rotate on pedicle = necrosis

328
Q

What is the appendix epididymis?

A

Remnant of the proximal end of mesonephric duct

329
Q

What is the Appendix testis & Prostatic utricle?

A

Remnants of the paramesonephric duct

330
Q

Describe the 3 different tunics/coats of the testis?

A
  1. VAGINALIS (visceral & parietal), potential space for movement, sinus of epididymis
  2. ALBUGINEA, fibrous, forms mediastinum & septae
  3. VASCULOSA with branches of testicular vessels
331
Q

What does the left & right testicular veins (from pampiniform plexus) drain into?

A
  • LEFT: left renal vein

- RIGHT: IVC

332
Q

What is Varicocele?

A

Visible/Palpable in the scrotal skin, mass of varicose veins in the spermatic cord

333
Q

Where does the vas deferens emerge into the abdomen?

A

Lateral to inferior epigastric artery, then lies on lateral wall of pelvis

334
Q

Vas deferens leaves scrotum, ______ to epididymis?

A

Medial

335
Q

What part of the vas deferens unites with the duct from seminal vesicle to form ejaculatory duct?

A

Dilated ampullary end of vas

336
Q

What 3 things in the male urethra prevent compression?

A
  1. Bulbo-urethral
  2. Mucous glands
  3. Corpus spongiosum
337
Q

What happens to the internal sphincter during ejaculation?

A

Contracts (sympathetic) to prevent back flow of semen

338
Q

Where does the ejaculatory duct enter the urethra?

A

Veru montanum

339
Q

What is the “false pelvis”?

A

Posterior abdominal wall, iliacus covering the iliac bones

340
Q

Obturatory internus lines _______, Levator ani forms _______?

A
  • Pelvic lateral wall

- Muscular pelvic floor

341
Q

What does the diamond-shaped perineum contain anteriorly & posteriorly?

A
  • ANTERIOR: genitalia & urethra

- POSTERIOR: anal canal & ischia-anal fossae

342
Q

What divides the perineum (pudendal region) into deep & superficial compartments?

A

Perineal membrane

343
Q

What 2 things enclose the greater & lesser sciatic foramina?

A
  • Sacrospinous ligament

- Sacrotuberous ligament

344
Q

Describe the piriformis muscle?

A
  • From sacrum to greater trochanter
  • Forms posterior pelvic wall
  • Divides greater sciatic foramen
345
Q

Describe the obturator internus muscle?

A
  • From obturator membrane & adjacent bone to greater trochanter
  • Forms lateral pelvic wall
  • Overlying obturator fascia, giving origin to pelvic levator ani
346
Q

What is the tendinous arch?

A

Thickening of obturator fascia for attachment of levator ani

347
Q

What passes out of the greater sciatic foramen into the buttock and what happens to it next?

A
  • Pudendal nerve
  • Then curves posterior to ischial spine, sacrospinous ligament & coccygeus to run forward into perineum below levator ani
348
Q

What 2 muscles makes up the pelvic floor/pelvic diaphragm?

A
  1. Coccygeus

2. Levator ani

349
Q

Describe the 2 divisions of levator ani muscle?

A
  1. Iliococcygeus (S3, 4)

2. Pubo-coccygeus: divided into pubo -rectalis, -vaginalis/prostaticus, -urethralis (S3, 4)

350
Q

What is the function of the pelvic floor/ “bowl” structure?

A
  • Support of viscera
  • Maintenance of urinary & faecal continence
  • Augments external anal & urethral sphincters
  • Forms vaginal sphincter
351
Q

What does each side of the levator ani muscle meet in the midline to form?

A

Anococcygeal raphe & perineal body/central tendon of perineaum just anterior to anal canal & posterior to vagina in female

352
Q

What is the nerve supply of puboprostaticus muscle?

A

Direct branches from S3, 4

353
Q

Where may the obturator lymph nodes be located?

A

Lateral pelvic walls, alongside Obturator Neurovascular bundle

354
Q

What are the somatic, conscious, voluntary pelvic nerves?

A
  • Ventral rami of L4,5 & S1,2,3,4 from anterior sacral foramina –> lumbosacral plexus
  • Pudendal nerve S2,3,4 to pelvic floor & voluntary sphincters
  • Direct branches from S3,4 to pelvic floor muscles
355
Q

Describe the sympathetic trunks (autonomic) which supply the pelvis?

A
  • Bilateral

- Give sacral splanchnics, superior hypogastric plexus sending left & right branches to pelvic plexuses

356
Q

What are the nerve roots of parasympathetic pelvic splanchnics (autonomic)?

A

S2,3,4

357
Q

What does the thoracic sympathetic trunk give off?

A
  1. Greater splanchnic nerve T5-9 (foregut)
  2. Lesser splanchnic nerve T10-11 (midgut)
  3. Least splanchnic nerve T12 (hindgut)
358
Q

What do the splanchnic nerves from?

A

Pre-aortic plexus & synapse in ganglia at coeliac trunk, SMA & IMA

359
Q

Describe the sympathetic trunks?

A
  • Anterior to sacrum & duse as ganglion impar opposite coccyx
  • Carry pre-ganglionic nerves T10-L2 and emerge as white rami communicates to sympathetic trunks
  • Then give sacral splanchnic nerves to pelvic plexus
360
Q

Describe the Pelvic (inferior hypogastric) plexus?

A
  • From superior hypogastric plexus
  • Carrying fibres from lesser & least splanchnic nerves T10,11,12
  • “Boosted” bu sacral splanchnics
  • Afferent & efferent
361
Q

Describe Pelvic Splanchnics?

A
  • Afferent & efferent parasympathetic fibres S2,3,4
  • Join pelvic plexus
  • Splanchnic & somatic nerves (pudendal) carry both motor & sensory fibres
362
Q

Where is the pelvic plexus located?

A

In fascia lateral to rectum, seminal vesicles & prostate (cervix & vaginal fornices) & posterior aspect bladder. In angle between internal iliac & inferior vesical arteries

363
Q

What sends branches to control recto-anal, urinary & reproductive/sexual function?

A

Pelvic plexuses & Pudendal nerves

364
Q

Where does the internal iliac artery originate from?

A

Common iliac opposite SI joint at level of L5 disc

365
Q

What does the internal iliac artery supply?

A
  • Buttock & medial thigh, posterior pelvic & abdominal walls, pelvic viscera & perineum
  • Gluteal branches contribute to anastomoses around hip = collateral circulation for lower limb
366
Q

Describe the internal iliac vein?

A
  • Joins external iliac to form common iliac, forming IVC
367
Q

What is the anal canal a site of?

A

Porto-systemic anastomosis

368
Q

What is the head of the spermatozoon made of?

A
  • Nucleus

- Acrosome

369
Q

What happens is vasa efferentia is blocked?

A

Seminiferous tubules & testis swell

370
Q

How long does it take sperm & fluid to travel through vasa efferentia & epididymis?

A

6-12 days

371
Q

What are the concentration changes to spermatozoa in epididymis?

A

100-fold

5x107/ml entering & 5x109/ml leaving

372
Q

What are the sperm modelling changes to spermatozoa in epididymis?

A
  • Nuclear condensation & acrosome shaping completed

- Cytoplasmic droplet shed

373
Q

What are the metabolism changes to spermatozoa in the epididymis?

A
  • Increase dependence on external fructose for glycolytic energy
  • Little oxidative metabolism
  • Increase intracellular pH (due to NA+/H+ exchange)
374
Q

What are the motility changes to spermatozoa in the epididymis?

A
  • Increase disulphide bridges between proteins in outer dense fibres of tail
  • [cAMP] rises in the tail
  • Acquires capacity for forward movement
375
Q

What are the membrane changes to spermatozoa in the epididymis?

A

Composition of various components change

376
Q

Where is the seminal fluid mainly formed?

A

Accessory glands

377
Q

What is exploited by infectious agents (ie. Hep B, HIV)?

A

Seminal fluid

378
Q

What are the different glands in the male and describe the type of seminal fluid they produce?

A
  1. TESTES: 0.1-0.2ml, contains spermatozoa
  2. SEMINAL VESICLE: 1-3ml, alkaline, gelantinous
  3. PROSTATE: 0.5-1ml, acidic, watery
  4. BULBOURETHRAL GLANDS: 0.1-0.2ml, viscous, clear
379
Q

What are the 6 major constituents of male ejaculate & where are they produced?

A
  1. Spermatozoa (testes)
  2. Fructose (seminal vesicle & ampulla)
  3. Inositol (testes & epididymis)
  4. Citric acid (prostate)
  5. Glycerlyphosphorylcholine (epididymis)
  6. Acid phosphatase (prostate)
380
Q

What is the function of fructose in the male ejaculate?

A

Anaerobic energy metabolism

381
Q

What is the function of inositol in the male ejaculate?

A

Osmotic ballast

382
Q

What is the function of citric acid in the male ejaculate?

A

Ca2+ chelater- depresses semen coagulation

383
Q

What is the function of glycerlyphosphorylcholine in the male ejaculate?

A

Source of choline in phospholipid metabolism

384
Q

What is the function of acid phosphatase in the male ejaculate?

A

Cleaves choline from glycerophosphorylcholine

385
Q

What causes the penis to become turgid so to allow semen to be introduced into female genital tract?

A
  • Haemodynamic changes involving the corpora cavernosa (singular=corpus cavernosum)
  • Sinuses along most of the length of the penis
386
Q

What 3 things can produce arousal in the male reproductive system?

A
  1. Erotic psychological stimulio (visual, olfactory)
  2. Tactile stimuli at level of brain
  3. Tactile stimuli can also mediate local spinal reflexes
387
Q

What is the sympathetic role in the male reproductive system?

A
  • Lower thoracic & lumbar spinal segments

- Maintains flaccidity

388
Q

What is the parasympathetic role in the male reproductive system?

A
  • Control centre in sacral spinal segments

- Increased activity produces turgidity

389
Q

Describe how the Erection Centre in the sacral spinal cord mediated the erection reflex in the male reproductive system?

A
  • Dilatation of arterioles to c. cavernosa & c. spongiosum
  • Closing of arteriovenous shunts that normally bypass the c. cavernosa
  • Probably also occupation of veins draining penis
390
Q

Describe the parasympathetic relaxation of vascular smooth muscle in the male penis?

A
  • Involves ACh acting on vascular endothelial cells
  • Indirectly triggers release nitric oxide (NO)
  • NO causes relaxation of vascular smooth muscle
391
Q

What can result in the failure to obtain an erection in the male penis?

A
  • Mechanical damage to the c. cavernosa
  • Obstruction of arteries to penis
  • Drugs that block parasympathetic actions
  • Psychological factors
392
Q

How is stress associated with high sympathetic activity preventing a male erection?

A

NA causes vasoconstriction of penile arterioles & so inhibits erection

393
Q

How does the sympathetic nervous system mediate male ejaculation?

A
  • Ejaculation centre in lower thoracic & lumbar spinal cord
  • Signals to ducts of genital tract & bulbocavernosus muscle at base of penis
394
Q

What is the emission phase in male ejaculation?

A
  • Smooth muscle contraction in walls of genital tract

- Expels semen into urethral bulb

395
Q

What is the expulsion phase in male ejaculation?

A
  • Rhythmic contractions of penis & bulbocavernosus muscle
  • Ejects semen in spurts
396
Q

What is male ejaculation normally followed by?

A

Refractory phase of 10mins - 1hr

397
Q

Describe the 3 different compositions of the male ejaculate (not uniform)?

A

1st- PROSTATE: rich in acid phosphatase & citric acid
2nd- VAS DEFERENS: rich in spermatozoa
3rd- SEMINAL VESICLE: rich in fructose

398
Q

What happens to the male ejaculate if it lingers somewhere?

A

Coagulation followed by liquefaction

399
Q

What does tumescence mean?

A

Swollen/becoming swollen, due to sexual arousal

400
Q

What does a PDE V inhibitor?

phosphodiesterase 5

A

It stops cGMP from being degraded by PDE V which allows the penile erection to last longer

401
Q

What are the different surfaces of the bladder?

A
  • Superior
  • Infero-lateral x2
  • Base (trigone between ureteric orifices & neck)
402
Q

Describe the apex of the bladder?

A
  • Upper aspect of pubic symphysis
403
Q

What is the distance of the 2 ureters in an empty and full bladder?

A

EMPTY: 2.5cm
FULL: 5cm

404
Q

What is the median umbilical ligament?

A

Remnant of embryonic urachus, extends from apex

405
Q

Describe the mucous membrane of the different parts of the bladder?

A
  • Over the DETRUSOR: loose & “ruckled”

- Over TRIGONE: smooth, fixed

406
Q

Where is the bladder neck in the female?

A

Above pelvic floor so pressure of pelvic organs & levator ani contribute to urinary continence

407
Q

What are the different ligaments in the male & female that support the bladder?

A
  • Puboprostatic (male)

- Pubovesical (female)

408
Q

What forms the puboprostatic & pubovesical ligaments in the pelvis?

A

Fibromuscular & fascial condensations from pelvic floor

409
Q

What part of the bladder has NO peritoneum?

A

Apex

410
Q

What are the different pouches which support the bladder?

A
  • Rectovesical

- Vesico-uterine & Recto-uterine in female

411
Q

What are the bladder relations in the male?

A
  • Superior: peritoneum, ilium, sigmoid

- Base: rectovesical pouch, septum, rectum, vas deferens, seminal vesicle

412
Q

What is the arterial supply of the bladder?

A
  • Internal iliac, anterior trunk
  • Superior vesical
  • Inferior vesical (replaced by vaginal in female)
413
Q

What is the main principle with the arterial supply of the bladder?

A

Pelvic organs are supplied by arteries to adjacent organs

414
Q

What are the veins draining the bladder?

A
  • Plexus on inferolateral surface of bladder
  • Drain directly into internal iliac veins
  • Male drain to prostatic plexus –> internal iliac
415
Q

What may the male prostatic plexus/veins communicate with?

A

Valveless veins of the vertebral plexuses (Batson) facilitating potential prostatic tumour spread

416
Q

What are the 3 lymph plexuses of the bladder?

A
  1. Mucosa
  2. Muscle
  3. Serosa
417
Q

What is the main lymph drainage of the bladder?

A

Nodes on external iliac artery

418
Q

What are the different nerve supplies of the bladder?

A
  • Anterior part of pelvic plexus that passes the rectum
  • Detrusor parasympathetic (afferent & efferent) from pelvic splanchnic S2,3,4 via pelvic plexus
  • Sympathetic to preprostatic sphincter & some detrusor from T12, L1,2 via pelvic plexus
  • Parasympathetic in female bladder neck
419
Q

Whats at surgical risk around the rectum?

A

Pelvic plexus

420
Q

Describe the urethra in a male?

A
  • Bladder neck, preprostatic urethra with internal sphincter
  • Prostatic urethra receiving ejaculatory duct
  • External sphincter surrounding membranous urethra
  • Spongy urethra in bulb of penus & then corpus spongiosum
421
Q

Describe the preprostatic part of the male urethra?

A
  • From bladder neck to upper aspect of verumontanum (colliculus seminalis)
  • Surrounded by genital, preprostatic/internal sphincter & smooth muscle from bladder wall passing into urethra & prostate
422
Q

Describe the prostatic part of the male urethra?

A
  • Closer to anterior aspect prostate
  • Emerges anterior to apex
  • Urethral crest causes crescentic section with sinuses each side
  • Verumontanum with utricle & ejaculatory ducts each side
423
Q

How many ducts open into the prostatic sinuses?

A

15-20

424
Q

Describe the prostate & its function?

A
  • Acid seminal secretion
  • Fibromuscular & glandular
  • In tough capsule & supported by puboprostatic ligaments
  • Has base, apex, posterior, inferiolateral x2 sufaces
425
Q

What is in the slightly acid seminal secretion of the prostate?

A
  • Acid phosphatase
  • Amylase
  • Prostate specific antigen (PSA)
  • Fibrinolysin
426
Q

What lies posterior to the prostate?

A
  • Denonvillier’s fascia

- Rectum

427
Q

When would you describe the prostate as having lobes?

A

Only in foetus

2 lateral & a median

428
Q

What are the 3 different zones of the prostate?

A
  1. Transition 5%, around urethra anterior to ejaculatory ducts
  2. Central 25%, behind transition, contains ejaculatory ducts
  3. Peripheral 70%, around transition & central
429
Q

What abnormality can commonly occur in the Transition zone of the prostate?

A

Benign prostatic hypertrophy (BPH)

430
Q

What abnormality can commonly occur in the Peripheral zone of the prostate?

A

Carcinoma

431
Q

How much does the normal & BPH prostate weight?

A
  • Normal: 8-40g

- BPH: 150g+

432
Q

What resides in the superior surface of the bladder?

A

Loops of ileum & sigmoid colon

433
Q

What is the arterial supply of the prostate & urethra?

A
  • Prostate & Proximal male urethra: inferior vesical

- Female Urethra: vaginal & internal pudendal

434
Q

What is the venous drainage of the prostate & urethra?

A
  • Prostate & Male Urethra: vesical & prostatic plexuses –> internal iliac vein
  • Female Urethra: vaginal & internal pudendal veins
435
Q

What is the main lymph drainage of the prostate and proximal urethra in the male?

A

Internal iliac nodes

436
Q

What 3 types of nerve supply does the urethra & prostate require?

A
  1. Somatic motor for control of striated muscle (external sphincter)
  2. Autonomic (sympathetic & parasympathetic)
  3. Sensation
437
Q

Whats the nerve supply of the urethra & prostate?

A
  • S2,3,4 Pudendal nerve (somatic motor & sensory)
  • Parasympathetic pelvic splanchnics to pelvic plexus
  • Sympathetic L1,2 via superior hypogastric plexus to pelvic plexus
438
Q

Describe the 1. Storage part of Micturition (urination)?

A
  • Detrusor parasympathetic control, counteracted via sympathetics = bladder relax & fill without increase in tension
  • Stretch receptors send signals via parasympathetic pelvic splanchnics to cord S2,3,4 & trigger reflexes in parasympathetic efferents to cause detrusor contraction = AUTONOMIC STRETCH REFLEX
439
Q

When does the Autonomic stretch reflex prevail?

A

Untrained infant so the bladder empties automatically when full

440
Q

Describe the 2. “Full” causing desire to micturate (urinate)?

A
  • With training, afferents ascend up spinal cord trigger cortical inhibition in frontal lobe
  • Superimposes cortical control on “M” centre in pons that in turn (reticulospinal & corticospinal pathways) controls/stimulates preganglionic parasympathetic neurones S2,3,4 cord = VOID
441
Q

What does the “M” centre stand for?

A

Micturition centre in the pons

442
Q

Describe the 3. Void part of Micturition (urination)?

A
  • 1y neurones stimulate 2y neurones in bladder wall ganglia, causing detrusor contraction
  • Simultaneous relaxation of external urethral sphincter (striated) by pudendal nerve & contraction of abdominal wall
  • Sensation of urine in urethra maintains reflex
443
Q

What happens if you transect the spinal cord above S2 (after stroke)?

A

Loss of cortical control cause return to automatic infant reflex of the bladder emptying when full

444
Q

What happens if the sacral segments S2,3,4 are destroyed?

A

Detrusor is paralysed & bladder distends until there is overflow incontinence

445
Q

What are the 3 frequent disorders of the prostate?

A
  1. Benign prostatic hyperplasia
  2. Carcinoma
  3. Prostatitis
446
Q

Describe Benign Nodular Hyperplasia?

A
  • Common
  • Non-neoplastic (hormonal imbalance)
  • Nodular hyperplasia of glands & storm
  • Not premalignant
  • Obstructs urine flow
  • Infection
  • Treatable
447
Q

Describe Benign Prostatic Hyperplasia?

A
  • Transition zone & peri-urethral glands
  • Nodules of glands & stroma
  • Compress & elongate urethra
  • Interferes with urethral sphincter
  • Urinary retention
448
Q

Describe acute & chronic urinary retention?

A
  • ACUTE: painful

- CHRONIC: painless, more gradual

449
Q

Describe Prostate Carcinoma?

A
  • Prostatic intraepithelial neoplasia precursor
  • Adenocarcinoma usually >50yrs
  • Latent or indolent (incidental) carcinoma
450
Q

Describe Adenocarcinoma of the prostate?

A
  • Posterior subcapsular area
  • Asymmetric firm enlargement
  • Metastasises (esp to bone)
451
Q

Describe Latent or indolent (incidental) carcinoma of the prostate?

A
  • Microscopic incidental focus
  • Common, incidence high in old age
  • Lesions dormant, metastases in 30% after 10yrs
452
Q

What does the Gleason score of a prostate cancer show?

A
  • Differentiation

- Distribution

453
Q

What is the different stage TN of prostate cancer?

A
  • Direct
  • Via lymphatics
  • Via blood
454
Q

How does prostate cancer present?

A
  • Urinary symptoms
  • Incidental finding on rectal examination
  • Bone metastases
  • Lymph node metastases
455
Q

How do you diagnose prostate cancer?

A
  • Imaging: ultrasound, MRI, isotope bone scan
  • Cystoscopy
  • Biochemistry PSA
  • Haematology: bone marrow involvement
  • Biopsy
456
Q

How do you treat prostate cancer?

A
  • Oestrogen
  • GnRH analogues
  • Orcidectomy
  • Radiotherapy
  • Radical prostatectomy
457
Q

What are the different penis & scrotum abnormalities?

A
  • Venereal infection
  • Hypospadias: urethral opening on inferior aspect
  • Epispadias: often accompanied by abnormal development of bladder
  • Phimosis: narrowing of foreskin
  • Paraphimosis: retracted foreskin of male cannot be returned to normal
  • Bowen’s disease (non-invasive)
  • Invasive squamous cell carcinoma
  • Peyronie’s disease: scar tissue causing penis to bend during erection
458
Q

Describe Intraepithelial carcinoma of the penis?

A
  • Bowen’s disease
  • Occur anywhere on penis erythematous patch Kerototic surface
  • Raised red plaque
459
Q

Describe Invasive squamous carcinoma of the penis?

A
  • Rare in UK
  • HPV
  • Glans penis or inner aspect of prepuce
  • Nodule or plaque
  • Metastasises to inguinal lymph nodes
460
Q

Describe carcinoma of the scrotum?

A
  • Chimney sweeps & arsenic workers
  • Nodular ulcerated mass
  • Squamous carcinoma
  • Inguinal nodes
  • Possible ulceration
461
Q

What are the different urethral abnormalities?

A
  • Congenital valves
  • Rupture
  • Stricture
  • Gonococcal
  • Non-gonococcal (non-specific)
  • Warts
  • Transitional cell carcinoma
462
Q

What are the different developmental & cystic lesions of the testicles?

A
  • Undescended testis (cryptorchidism)
  • Hydrocoele
  • Haematocoele
463
Q

What are the different orchitis/inflammations of the testis?

A
  • Mumps orchitis
  • Idiopathic granulomatous orchitis
  • Syphilitic orchitis
464
Q

Describe testicular tumours?

A
  • Uncommon but treatable
  • Young & old men
  • Aetiology unknown but undescended tests is predisposing factor (x10 risk)
  • In situ neoplasia does occur & is precursor
465
Q

What are the 2 most common testicular tumours?

A
  • Seminoma 40%

- Teratoma 32%

466
Q

What is the presentation of testicular tumours?

A
  • Painless unilateral enlargement of testis
  • Secondary hydrocele
  • Symptoms from metastases
  • Retroperitoneal mass
  • Gynaecomastia
467
Q

Describe Seminoma?

A
  • Commonest
  • Germ cell origin
  • 30-50yrs
  • Classical type
  • Spermatocytic type
  • Anaplastic type: with syncytiotrophoblast giant cells (gynaecomastia)
  • Combined type
  • Produce hCG
468
Q

Describe Teratoma?

A
  • Germ cell origin
  • 20-30yrs
  • More aggressive
  • Differentiated type
  • Intermediate type
  • Undifferentiated type
  • Trophoblastic type
  • beta-hCG & alpha-fetoprotein useful markers
469
Q

What are different non-germ cell tumours?

A
  • Malignant lymphoma: elderly men
  • Leydig cell tumour: may produce androgens
  • Sertoli cell tumour
  • Metastatic tumours
470
Q

What the 4 different stages of testicular tumours?

A
  • Stage I: confined to testis & its coverings
  • Stage II: involves testis & para-aortic lymph nodes
  • Stage III: involves lymph nodes in mediastinum &/or supraclavicular region
  • Stage IV: visceral metastases
471
Q

What are the different causes of male infertility?

A
  • Endocrine disorders: GnRH deficiency, oestrogen excess
  • Testicular lesions: cryptorchidism, abnormal spermatogenesis
  • Post-testicular lesions: obstruction of efferent ducts
472
Q

What are the different abnormalities of the epididymis & spermatic cord?

A
  • Congenital
  • Epididymal cysts & spermatocoeles
  • Varicocoele
  • Torsion of spermatic cord & testis
  • Inflammatory lesions: epididymo-orchitis
  • Tumours: rare

MD3002 (15 decks)

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