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Medicine 3 > Reproduction > Flashcards

Reproduction Flashcards

1
Q

What does FSH stimulate in the ovaries?

A

Development of ovarian follicles

Secretion of oestrogen and inhibin

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2
Q

What does LH stimulate in the ovaries?

A

Oestrogen production

Conversion of Graafian follicle into corpus luteum

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3
Q

What is the action of progesterone?

A

Causes endometrium to become receptive to implantation of a fertilised ovum

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4
Q

What is the action of the corpus luteum?

A

Secrete progesterone

Secretes oestrogen to negatively feedback on GnRH production

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5
Q

How is a Graafian follicle formed?

A

At the beginning of menstrual cycle.
10-20 early follicles proliferate to secondary follicles (due to FSH)
Only one matures fully and becomes the Graafian follicle

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6
Q

What happens to the Graafian follicle after ovulation?

A

Proliferation to form the corpus luteum which secretes progesterone

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7
Q

What causes the midcycle surge in LH?

A

Alteration in oestrogen feedback at pituitary.
Oestrogen usually inhibits GnRH secretion however when a threshold is released, feedback switches from negative to positive, leading to a gonadotrophin surge.

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8
Q

What hormone changes lead to menstruation?

A

Fall in LH secretion leads to a reduction in corpus luteum progesterone secretion. Lack of progesterone leads to menstruation

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9
Q

What hormone changes prevent menstruation in fertilisation?

A

Fertilised ovum secrets a hormone with similar actions to LH. This continues stimulating corpus luteum to produce progesterone which prevents menstruation. This secretion of progesterone continues until placenta takes over

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10
Q

How does the menstrual cycle reset?

A

Death of corpus luteum and drop in oestrogen and progesterone secretion remove negative feedback on pituitary, leading to an increased secretion of GnRH again.

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11
Q

What are the two compartments of the seminiferous tubules?

A

Tubular (germinal) and extra-tubular (endocrine)

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12
Q

How are the spermatocytes protected from interstitial fluid in the testis? Why is this important?

A

Unidirectional tight junctions. Important to prevent immune response against sperm antigens

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13
Q

What is the role of Sertoli cells?

A

Secrete nutrients for developing sperm

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14
Q

What is the role of LH in spermatogenesis?

A

LH stimulates Leydig cells to produce testosterone

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15
Q

What is the role of testosterone in spermatogenesis?

A

Binds to Sertoli cell receptors

Induces FSH receptors on Sertoli cells

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16
Q

What is the role of FSH in spermatogenesis?

A

Stimulates Sertoli cells to produce androgen binding protein (ABP)

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17
Q

What is the role of androgen binding protein (ABP) in spermatogenesis?

A

Binds and carries testosterone to ductal system

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18
Q

Describe the vasculature in the spermatic cord

A

Testicular artery runs along with the vas deferens and pampiniform veins form a plexus around artery (ideal for heat exchange)

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19
Q

Describe the structure and purpose of the vas deferens

A

3 muscular layers, fibroelastic lamina and inner ciliated epithelium. Purpose is to transport and store sperm

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20
Q

What is the purpose of seminal vesicles (mucosal folds)?

A

Secrete seminal fluid

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21
Q

Describe the composition of seminal fluid

A

Fructose (energy)
Prostaglandins (contraction of smooth muscle in male + female tract)
Proteins
Amino acids
Alkaline secretions (neutralise acidic vagina)
Fibrinogen

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22
Q

What is the function of the prostate gland?

A

Collection of concentric secreting glands which open into urethra to secrete seminal fluid

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23
Q

What complications can the prostate gland cause in older men?

A

Enlargement (compresses urethra)

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24
Q

What is the purpose of bulbourethral glands?

A

Secrete lubricant into urethra and neutralises acidic urine. Precedes semen in emission

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25
Q

Describe the physiology of a penile erection

A

Closure of arterio-venous anastomosis
More blood into Helicine arteries
Smooth muscle relaxes and cavernous spaces fill with enlarged blood vessels under high pressure
Compression of emissary veins, reducing outflow

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26
Q

What is endothelium-derived relaxant factor (EDRF)?

A

Nitric oxide

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27
Q

How is sidenafil useful to treat erectile dysfunction?

A

Inhibits action of phosphodiesterase 5 (PDEV) which usually deactivates cGMP. Use of sidenafil maintains levels of cGMP leading to prolonged action of NO

28
Q

How is the acidic environment inside the vagina created?

A

Glycogen secreted by epithelial mucosa

Glycogen broken down by commensalism lactobacilli- leads to production of lactic acid and acid pH

29
Q

Why is the vagina environment acidic?

A

To deter pathogens such as Candida albicans (vaginal thrush)

30
Q

What are the two parts of the cervix?

A

Ectocervix - portion projecting into vagina through the external OS
Endocervix - passageway between external OS and uterine cavity, terminates at internal OS

31
Q

What is the purpose of the endocervical epithelium?

A

Columnar epithelium with deep invaginations that secrete mucin. Sperm can rest here

32
Q

What is the purpose of endocervical mucin?

A

Lubrication for sex
Bacterial protection
Allows ascent of sperm into uterus

33
Q

What is the metaplastic epithelium in the cervix?

A

The zone where squamous ectocervix epithelium meets columnar endocervix epithelium (irritation of exposed columnar cells to acidic vagina)

34
Q

What is a Nabothian cyst?

A

Cyst formed by cervical mucin production blocked by squamous metaplasia

35
Q

What is a major causative agent for cervical cancer?

A

Human papillomavirus

36
Q

What different types of human papillomavirus cause different pathologies?

A

Types 6 and 11 - genital warts

Types 16 and 18 - cervical cancer

37
Q

Where in the Fallopian tube does fertilisation occur?

A

The ampulla

38
Q

Where in the Fallopian tube does super capacitation occur?

A

The isthmus

39
Q

How are sperm cells attracted to the oocyte waiting in the ampulla?

A

Granulosa cells of oocyte secrete chemo-attractants which are detected by odorant receptors in plasma membrane of sperm head

40
Q

Describe the acrosome reaction in the sperm cell

A

ZP3 binds to receptor on sperm head
Calcium influx causes acrosome swelling due to depolymerisation of F-actin between acrosome and sperm-head membrane
Acrosome fuses with plasma membrane of head
Exposure of ZP2 receptor which can bind to ZP2 on zona pellucida
Acrosin release aids digestion of pathway through zona pellucida

41
Q

How is polyspermy prevented?

A

Cortical reaction - release of cortical granules that cleaves ZP2 and hydrolysis binding region of ZP3 to prevent further sperm binding

42
Q

Describe the events post fusion of sperm and ZP

A

Secondary oocyte completes meiosis and one set of chromosomes dispatched as second polar body. Remaining chromosomes pair with paternal chromosomes to make diploid egg

43
Q

Why are all mitochondria maternally derived?

A

Fertilised egg receives its mitochondria from maternal cytoplasm

44
Q

What are the two divisions of the blastocyst?

A

Trophoectoderm - forms placenta

Inner cell mass - forms embryo

45
Q

How does the fertilised egg communicate with the mother to prevent menstruation?

A

Secretes human chorionic gonadotrophin (hCG), an analogue of LH. Binds to ovarian LH receptors on granulose cells of corpus luteum which then continues to secrete progesterone

46
Q

What are syncytiotrophoblasts? What are their purpose?

A

Multinucleated tissue layers without cell boundaries. Formed when cytotrophoblast cells (proliferation of trophoblast cells) fuse together. Form finger like projections into endometrium to burrow in

47
Q

How does the developing blastocyst obtain nutrition from the endometrium?

A

Syncytial fingers tap uterine glands and use it’s milk (histiotrophic nutrition)

48
Q

What are the functions of the placenta?

A

Nutrition
Respiration
Immunological barrier
Endocrine funtion

49
Q

Describe the primary villi of the placenta

A

Columns of syncytiotrophoblast that grow into endometrium in the first trimester:
Free villi - project into maternal blood
Anchoring villi - project deep into endometrial tissue to anchor placenta

50
Q

How do secondary villi develop in the placenta?

A

Extra-embryonic mesoderm invade into primary villi

51
Q

How do tertiary villi develop in the placenta?

A

Formation of primitive capillary plexus within villi due to haematopoetic stem cells in extra-embryonic mesoderm

52
Q

How does placental fetal circulation establish?

A

Connection between fetal vessels in chorionic villi with umbilical stalk vessels

53
Q

How is maternal blood flow to placenta optimised?

A

Extra-villous trophoblasts invade maternal spiral arteries and replace artery endothelium and smooth muscle cells. Artery remains open and dilated - no longer maternal control

54
Q

How is fetal blood oxygenated?

A

Umbilical arteries carry de-oxygenated fetal blood to placenta. Umbilical vein takes oxygenated blood back to fetus

55
Q

What is pre-eclampsia?

A

Reduced invasion of spiral arteries leading to reduced maternal blood flow to placenta

56
Q

Describe the maternal physical changes during pregnancy

A

Uterine enlargement
Mammary gland development
Ventricular wall muscle mass increase in heart to cope with increased maternal cardiac output
Changes in calcium concentrations in maternal bone
Weight gain

57
Q

Describe cardiovascular changes during pregnancy

A

Increased cardiac output and decreased peripheral resistance

58
Q

Describe the changes in maternal blood during pregnancy

A

Decreased Hb concentration

Reduced haematocrit and RBC count

59
Q

Describe maternal oxygen consumption during pregnancy

A

Oxygen consumption in tissues increased
Pulmonary ventilation increased
PCO2 decreased + increased blood flow = high PO2 on maternal side of placenta

60
Q

Describe the anatomical changes to the kidney during pregnancy

A

Enlargement due to increase vascular volume.

Dilation of calyces, renal pelvis and ureter (higher chance of UTI)

61
Q

Describe the physiological changes to the kidney during pregnancy

A

Increased RPF and GFR. Changes in tubular re-absorption

62
Q

Why do pregnant women have glycosuria?

A

Increased RPF = more filtered glucose (exceeds maximal rate of reabsorption)

63
Q

Describe glucose homeostasis in the mother during pregnancy

A

All fetal glucose comes from mother
Early pregnancy - progesterone increases appetite and increased insulin secretion (lipogenesis and fat storage)
Mid pregnancy onwards - increased gluconeogenesis, mobilisation of FFA (lipolysis) and ketones for fuel.

64
Q

How does the fetus avoid maternal rejection?

A

Placenta is a structural barrier stopping direct contact of maternal blood with fetal blood. Maternal immune cells cannot cross syncytiotrophoblasts into fetus.
Syncytial knots shed into maternal circulation, phagocytosed by maternal immune cells, fetal HLA presented and conversion of maternal T cells to suppressor cells.
Spiral artery invading extravillous trophoblast cells (EVTs) present HLA-G which is recognised by killer cells and leads to inhibition of cytokine production

65
Q

How does the fetus gain passive immunity from the mother?

A

Maternal IgG can cross the placenta and provide immunity to fetus

66
Q

What are the complications of the Rhesus antigen in pregnancy?

A

If mother is Rhesus negative and fetus is Rhesus positive then can mount immune response against fetus in second pregnancy (due to mingling of blood during parturition and creation of antigens)

67
Q

How does the mother prepare for postnatal nutrition?

A

Prolactin inhibited during pregnancy by oestrogen and progesterone. After parturition, drop in these hormones allows prolactin dominance and begins lactogenesis

Medicine 3 (8 decks)

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