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LUSUMA Questions > Repro > Flashcards

Repro Flashcards

1
Q

State the normal ranges for the start of puberty, for males and females

A

Males: 9-14
Females: 8-13

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2
Q

Describe how the initiation of puberty is altered by external factors

A

Initiation of puberty is due to the increased pulsitile secretion of GnRH as the central mechanisms mature.

In females menarche relies upon the achievement of a critical weight of 47kg, therefore lifestyle factors such as diet and exercise can alter the timing of the initiation of puberty.

General influences of the onset of puberty includes involvement of the pineal gland. This secretes melatonin which is triggered by changes in day length.

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3
Q

Why can meningitis lead to precocious puberty?

A

Precocious puberty is where there are signs of puberty in children

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4
Q

Why may a patient who has precocious puberty due to a pituitary tumour have visual issues?

A

The pituitary gland lies within the pituitary fossa of the sphenoid bone just inferior to the optic chiasm.
If tumour growth is large there may be compression of the optic chiasm leading to compression of the optic nerves and restriction of visual fields.

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5
Q

Describe the sequence of events of puberty in girls and the age ranges associated with each

A

Breast bud (Thelarche) = first sign - 10-14
Growth spurt - 10-14
Pubic hair - 11-13
Menarche - 12-13

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6
Q

Describe the sequence of events of puberty in boys

A

Testicular volume - 11-16
Genitalia growth - 11-13
Growth spurt - 11-15
Pubic hair - 12-14

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7
Q

Explain why the testes grow in size during puberty

A

Increased GnRH increases spermatogenesis and androgen secretion initiates the growth of sexual accessory organs including glands.

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8
Q

Why do boys grow to be taller in stature than girls?

A

Growth velocity = 10.3cm/year compared to 9cm/year in females.

Growth period is longer and faster.

Females have more oestrogen secretion from the ovary than the male sertoli cells, which leads to earlier termination of epipheseal growth because the threshold of fusion is reached sooner.

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9
Q

Describe how the rate of growth differs in males and females

A

Males: 10.3cm/year
Females: 9cm/year

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10
Q

Describe the role of testosterone and oestrogen in increasing the height of males compared to females

A

Testosterone causes retention of minerals in the body to support bone and muscle growth.
Further to this, males secrete less oestrogen from their sertoli cells than the ovarian secretion in females. This means that it takes longer for epiphyseal fusion to occur

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11
Q

Describe the changes to the menstrual cycle that occur from the age of 40 prior to the menopause

A

The follicular phase shortens which leads to early or absent ovulation and an overall decrease in oestrogen production.
A result of this is increased LH and FSH - the latter more so due to loss of the negative feedback effect of inhibin

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12
Q

State the age range at which the menopause normally occurs

A

49-50 years old

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13
Q

Explain why FSH levels increase massively

A

No more follicles which means no oestrogen or inhibin production. This relieves the negative feedback affect on FSH and LH production. FSH levels increase more because usually inhibin keeps these levels lower.

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14
Q

List 4 symptoms of the menopause

A

Vascular - hot flush
Bone - increased occurance of fractures due to menopause-related osteoporosis
Oestrogen-sensitive tissues - changes in skin, breast involution

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15
Q

Explain why the menopause can lead to dysparenuia

A

Dysparenuia = painful or difficult sexual intercourse

Loss of vaginal rugae which leads to reduced ability to distend and decreased lubrication

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16
Q

Explain why the menopause can lead to osteoporosis

A

Loss of protective effect of oestrogen.

Bone reabsorption > bone deposition
This is due to reduced stimulation of osteoblasts.
Therefore bone density decreases (2.5cm/year) increasing the risk of osteoporosis

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17
Q

What are some side effects of HRT?

A

Linked to increased hormone levels:

Breast tenderness
Bloating
Fluid retention

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18
Q

Define primary amenorrhoea

A

Absence of menses by the age of 14 with no secondary sexual characteristics or by 16y.o with normal SSC

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19
Q

Define secondary amenorrhoea

A

Established menses has ceased.
3 months or longer in females with a regular cycle
9 months of longer in females with an irregular cycle

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20
Q

Define menorrhagia

A

Heavy vaginal bleeding - >80ml over a period of 7 days.

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21
Q

Define dysmenorrhoea

A

Painful menstruation

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22
Q

Metorrhagia

A

Abnormal bleeding from the womb

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23
Q

Describe the causes of primary amenorrhoea

A

Hypothalmic/pituitary causes: inadequate FSH leading to decreased oestrogen and therefore no stimulation of the endometrium

Gonadal/end organ: lack of response of the ovary to pituitary stimulation

Outflow tract abnormalities: HPO axis normal so period occurs but not visible.

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24
Q

Explain how Turner’s syndrome can cause primary amenorrhoea

A

45 X
Leads to gonadal dysgenesis
Inadequate ovary response to pituitary stimulation

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25
Q

Describe the pathophysiology of Kallman’s syndrome

A

Form of hypogonadotrophic hypogonadism - GnRH neurons fail to migrate into the hypothalamus during embryonic development.
This means that the release of GnRH is blocked or reduced and therefore the testes and ovaries do not develop.

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26
Q

Why may Kallman’s syndrome patients present with anosmia?

A
  • Problems with the olfactory bulb is the cause of prevention of GnRH neurone migration through it

or

  • Olfactory bulb missing or not fully developed as a result of Kallman syndrome
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27
Q

Describe what is meant by Asherman’s syndrome

A

Also known as intraauterine adhesions it is characterised by adhesions and/or fibrosis of the endometrium

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28
Q

How can exercise affect the menstrual cycle

A

Can lead to secondary amenorrhoea

Secondary hypothalmic disorder caused by increased stress due to excessive exercise. This leads to reduced GnRH production in order to conserve energy levels

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29
Q

State the two most common causes of secondary amenorrhoea

A

Pregnancy, menopause

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30
Q

Explain why severe bleeding during childbirth can lead to amenorrhoea

A

Sheehan’s syndrome is a hypopituitary disorder as a result of excessive blood loss and therefore reduced oxygen availability to the pituitary. It is also known as post-partum hypopituitarism.
This means that the pituitary doesn’t secrete FSH or LH to stimulate ovulation and the production of oestrogen.
Therefore endometrial growth doesn’t occur and so amenorrhoea occurs.

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31
Q

Describe the questions asked in an amenorrhoea history

A

Lifestyle - diet changes, weight loss, sexual history/health
Family history - age of menopause, history of amenorrhoea
Period history - age of onset, length of periods, regularity of cycles

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32
Q

Describe what is meant by dysfunctional uterine bleeding and how it is managed

A

Heavy periods with no recognisable pelvic pathology - this may be due to lack of ovulation or decreased oestrogen production leading to prolonged progesterione production.

Management with combined contraceptive pill or an intrauterine device is often affective.

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33
Q

Why can fibroids lead to menorrhagia?

A

Increased surface area

Increased blood supply to the uterus and neovascularisation

Increased tension leading to distortion of the uterine cavity. This means that the uterus is unable to contract down on the venous sinuses in the zona basalis and so excessive bleeding occurs

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34
Q

A patient presents to your with tiredness secondary to menorrhagia, why are they tired?

A

Iron-deficiency anaemia caused by excessive blood loss during menstruation.

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35
Q

Why are progesterone analogues used to manage menorrhagia?

A

Progesterone is anti-mitogenic therefore inhibiting the affects of oestogen on the endometrium. This means that the uterine lining is thinner.

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36
Q

The scrotum develops from the genital folds. Name the homologue in the female

A

Labia majora

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37
Q

Name the muscle which forms the scrotal rugae

A

Dartos muscle

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38
Q

Explain why the scrotal rugae are important for the function of the testis

A

Spermatogenesis requires tight regulation of temperature. These rugae give a greater surface area for heat exchange

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39
Q

How is the innervation of the anterior and posterior aspect of the scrotum different?

A

Anterior - lumbar plexus

Posterior (and inferior) - sacral plexus

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40
Q

Describe the course of descent of the testes

A

Develop on the mesonephric ridge in the retroperitoneum. These descend through the deep inguinal ring lateral to the inferior epigastric vessels -> through inguinal canal and superficial inguinal ring -> into the scrotum

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41
Q

State the condition where blood forms between the layers of tunica vaginalis

A

Haematocoele

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42
Q

How can a haematocoele be differentiated from a hydrocoele

A

Transilluminecence - haematocoele appears pink whereas hydrocoele is clear/white

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43
Q

State two functions of the pampiniform plexus

A

Venous drainage of the spermatic cord/scrotum

Thermoregulation - allows for heat to cross from arterial to venous drainage

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44
Q

Explain why metastatic testicular cancer can be difficult to palpate until late

A

Testicular cancer metastasis’ via the lymphatics but the lymphatic drainage is the paraortic nodes which are deep and difficult to palpate in the back

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45
Q

From superficial to deep, name the layers of the spermatic cord

A

External spermatic fascia - formed from the external oblique aponeurosis

Cremasteric muscle & fascia
- formed from the internal oblique aponeurosis

Internal spermatic fascia - from the transversalis fascia

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46
Q

Name the artery found in the spermatic cord which is a branch of the inferior vesical artery

A

Artery to vas deferens

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47
Q

Describe the clinical importance of the cremasteric reflex

A

Stimulation of the cremasteric reflex causes elevation of the testis. This helps to thermoregulate the testis to provide the optimal environment for spermatogenesis.

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48
Q

What is the histology of the vas deferens and how does this relate to it’s function?

A

Pseudostratified epithelium which 3 smooth muscle layers.

Contraction of the smooth muscle helps to propel sperm through the duct and into the urethra

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49
Q

Describe the course of the vas deferens

A

Begins after the epididymis.
Travels through the spermatic cord and transverses the inguinal canal
Tracks around the pelvic side wall
Passes between the bladder and ureter
Forms the dilated ampulla, posterior to the bladder
Opens into the ejaculatory duct

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50
Q

State the anatomical location of the seminal vesicle

A

Between the bladder and the rectum

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51
Q

Describe the relations of the prostate…

a) Anterior
b) Posterior
c) Superior
d) Inferior

A

a) Urethral sphincter
b) Ampulla of rectum
c) Neck of the bladder
d) Urethral sphincer & deep perineal muscles

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52
Q

Why does benign prostatic hyperplasia occlude the urethra earlier than malignancy of the prostate?

A

BPH is most commonly in the central or transitional zone of the prostate. This surrounds the prostatic urethra therefore hyperplasia is likely to occlude the vessel.

Malignancy affects the peripheral zones which means that it needs to be significantly enlarged to occlude the urethra

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53
Q

Describe the routes of metastasis of prostate cancer

A

Lymphatic - into the internal iliac and sacral nodes

Venous drainage - into the internal vertebral plexus which metastasises to the vertebrae and potentially the brain.

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54
Q

Explain why the corpus spongiosum is not surrounded by tunica albuginea

A

Derived from the genital tubercle not the genital folds therefore not covered by the tunica albuginea in development?

Furthermore, the tunica albuginea is involved in maintenance of the erection and it is important it doesn’t surround the corpus spongiosum as this may restrict the spongy urethra which travels through.

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55
Q

Why is the membranous urethra difficult to catheterise?

A

This is where the urethra transverses the perineum which means that it is not very distensable and therefore resistance is likely to be met during catheterisation

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56
Q

Where does urine collect if the urethra is pierced proximal to the perineum

A

Recto-vesicle pouch (pouch of douglas)

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57
Q

What is the blood supply to the penis?

A

Internal pudendal artery - a branch of the internal iliac artery

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58
Q

What is the innervation of the penis?

A

S2-S4
Sensory/sympathetic = pudendal nerve
Parasympathetic = prostatic nerve plexus

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59
Q

A patient presents with severe unilateral testicular pain. What is the likely diagnosis and why is there a risk of necrosis to the testicle?

A

Testicular torsion.

This usually occurs above the upper pole of the testicle which poses a risk of occlusion of the testicular artery. If this occurs then blood supply to the testicle is prevented and cellular death and necrosis occurs.

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60
Q

Name the 3 muscles which form levator ani and state the nerve roots of innervation

A

Pubococcygeus
Iliococcygeus
Puborectalis

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61
Q

What are the functions of the levator ani?

A

Support of the pelvic viscera

(Puborectalis) Sphincter for the vagina & rectum - Forms a sling around the distal GI tract at the ano-rectal junction to maintain 90 degree angle of the ano-rectal anal

Resists increased abdominal pressure during straining

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62
Q

Name the muscles of the pelvic floor which help to maintain an erection

A

Bulbospongiosum

Ischiocavernosum

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63
Q

Why is it important that an episiotomy spares the perineal body?

A

This is the attachment of many important muscles. If this is damaged then the pelvic floor will be weakened which increases the risk of pelvic viscera/vaginal/rectal prolapse

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64
Q

Outline the borders of the anterior perineal triangle

A

Also known as the urogenital triangle

Pubic symphysis (anterior)
Ischiopubic rami (lateral)
Imaginary line between the 2 ischial tuberosities (posterior)
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65
Q

Describe the contents of the perineal triangle in the male

A

External genitalia and urethra

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66
Q

Where is the ischiorectal fossa and why may infection be dangerous?

A

The ischiorectal fossa is a fat filled space inferior to the obturator internus and levator ani.

Infection may lead to an ischiorectal abcess, which although treatahle there is a risk of “Fournier’s Gangrene”.

This is a type of necrotizing fascitis affecting the perineum and is a urological emergency

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67
Q

State some risk factors for STD’s

A
  • Age (25-30 highest peak)
  • Many sexual partners
  • Unprotected sex
  • Certain ethnicities at higher risk of different infections (e.g. black carribean - gonorrhoea)
  • Risky sexual behaviours

etc

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68
Q

Describe 3 important factors to enquire about in a sexual history

A

Are they sexually active?
Are they in a relationship and are they or their partner having sex outside of that relationship?
What contraceptive and protective methods do they use?

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69
Q

Describe how STDs are managed in general

A

Thorough history from the patient followed by an examination.
Differential diagnosis made followed by tests based on raised suspicion.

Treatment may involve antibiotics; contact screening and advice about safe sex

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70
Q

State the strains of HPV associated with cervical cancer

A

HPV 16 & 18

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71
Q

Explain why cervical cancer screening is not offered to those under 25

A

The test has low sensitivity and validity in those under 25. For example the number of false positives is high and therefore it’s positive predictive value is low.

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72
Q

Describe how genital warts can be treated

A

Generally resolves on it’s own.

May be given topical podophyllin

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73
Q

State the organism responsible for chlaymydia

A

Chlamydia trachomatis

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74
Q

Explain how chlamydia can cause perihepatitis

A

Infection may spread through the abdominal cavity (pelvic inflammatory disease) and cause fibrotic lesions on the surface of the liver to the peritoneum.

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75
Q

Describe how chlamydia is diagnosed

A

First void urine in both males and females or endocervical/urethral swabs in females.

Diagnosed using NAAT (nucleic acid amplification techniques) such as immunofluoscence and PCR because it does not grow on standard media.

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76
Q

Describe the triad of Reiter’s syndrome

A

This is a male specific complication of chlamydia infection.

  • Urethritis
  • Conjunctivitis
  • Arthritis
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77
Q

Describe the process of gram staining

A
  1. Application of crystal violet
  2. Application of iodine
  3. Alcohol wash
  4. Application of counterstain
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78
Q

A patient is swabbed and gram negative diplococci are found. State the likely diagnosis

A

Neisseria species - if from the genital tract it may be Neisseria gonorrhoea

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79
Q

Describe the presentation of gonorrhoea

A

Females - mostly assymptomatic but may have endocervitis or urethritis.

Males - urethritis, epididymitis

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80
Q

Explain why azithromycin is given alongside ceftriaxone for gonorrhoea

A

Because there is commonly a co-infection with chlamydia trachomatis

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81
Q

Describe the presentation of a herpes simplex infection

A

Genital herpes

Presents as extensive painful ulceration. May have secondary effects of dysuria.

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82
Q

Classify the virus according to its genome

A

Double stranded DNA

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83
Q

Explain why herpes infections can be recurrent

A

They often remain as a latent, assymptomatic infection in the dorsal root ganglia

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84
Q

State the infectious cause of syphilis

A

Treponema Pallidum

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85
Q

Describe the stages of a syphilis infection

A
  1. Indurated, painless ulcer
  2. 6-8 weeks later: fever, rash, lymphadenopathy, mucosal lesions
  3. Latent stage - may last several years
  4. Neurosyphilis
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86
Q

A patient presents to you with urethritis and cervicitis: give 2 differential diagnoses

A

Chlamydia

Gonorrhoea

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87
Q

A patient presents to you with a painless ulcer on their penis. What is the likely diagnosis and why?

A

Syphilis

Because the more common cause of ulceration, genital herpes, presents with extensive painful ulcerations.

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88
Q

Give 3 causes of genital ulceration

A

Syphilis
Genital herpes
Genital warts

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89
Q

A patient presents with painful, swollen lymph nodes in their groin. Give 3 differentials

A

Genital herpes
Syphilis
Gonorrhoea

(+ malignancy; chancroid; infections in the lower limb)

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90
Q

Upon swabbing, gram negative cocci bacilli are found (following presentation of painful lymphadenopathy), what is the likely cause?

A

Neisseria Gonorrhoeae

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91
Q

A patient presents with vaginal discharge

a) Give 3 differentials
b) Describe 2 tests used to distinguish

A

a) Bacterial vaginosis
Vulvovaginalis candidiasis
Trichomonas vaginalis

b) vaginal smear (+culture) - usually using a wet mount which means a sample of discharge is mixed with salt solution on a microscope slide

KOH Whiff Test - potassium hydroxide added to a sample of discharge to see whether a strong fishy odor is produced

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92
Q

What is the cause of a positive KOH whiff test?

A

Bacterial vaginosis - a change in the balance of vaginal flora such as Gardnerella

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93
Q

Describe the causes of genital thrush

A

Known as a “yeast” infection this is usually due to protozoa such as Candida albicans or other species that are part of the GI or vaginal flora.

Thrush usually occurs when the normal flora is disturbed such as when on antibiotics.

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94
Q

How is candida albican infection managed?

A

Sometimes left to resolve but may require topical azoles or treatment with nystatin.

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95
Q

Why can thrush arise after antibiotics?

A

Normal flora of the vagina affected by the antibiotics which means that there is less environmental competition for the candida species to thrive

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96
Q

Define pelvic inflammatory disease

A

The result of infection ascending from the endocervix, causing endometritis, salpingitis, parametritis, oophoritis, tubo-ovarian abscess and/or pelvic peritonitis

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97
Q

Describe the route that an infection must take to cause pelvic peritonitis

A

Vagina -> cervix -> uterus -> fallopian tubes

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98
Q

What is the most common causative organism

A

Chlamydia trachomatis or Neisseria gonorrhoea

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99
Q

Describe the difference between parametritis and salpingitis

A

Salpingitis is inflammation of the fallopian tubes.

Parametritis is inflammmation of the ligaments around the uterus (broad or round ligament)

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100
Q

Your patient has RUQ pain. Explain how this may be due to PID?

A

A severe complication of PID is Fitz-Hugh-Curtis syndrome which is where chlamydial infection has undergone transabdominal spread to affect the liver. It causes capsular infection (note that the hepatic parenchyma is not effected) which leads to fibrosis on the surface of the liver and fibrotic lesions between the liver and the peritoneum.

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101
Q

Your patient has a fever, raised WBC, abdominal pain and discharge

A

Chlamydia or gonorrhoea infection that has caused systemic infection or pelvic inflammatory disease.

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102
Q

Explain why PID increases your risk of ectopic pregnancy in the future?

A

Causes fibrosis and narrowing of the fallopian tubes due to inflammation and adhesion formation. This means that following ovulation the egg may not be able to travel through the tubes and therefore implant in the peritoneum or within the fallopian tube itself.

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103
Q

How does the coil affect your risk of PID?

A

During insertion and removal there is a risk of transmitting infection from the skin.

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104
Q

Why is the pill protective against PID?

A

The pill causes hormonal changes and changes in the intrauterine environment (such as pH changes) which disfavours bacterial growth and therefore protective against PID.

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105
Q

State a differential diagnosis for PID with regards to:

a) gynaecological
b) GI
c) Urinary

A

a) Ectopic pregnancy
b) Appendicitis
c) Urinary tract infection

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106
Q

Describe how appendicitis can be ruled out on examination for PID?

A

Appendicitis will be tender in the lower right quadrant whereas PID tends to have bilateral and adnexal tenderness.

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107
Q

Describe the pattern of pain associated with PID?

A

Lower abdominal, bilateral pain.

On examination there is adnexal tenderness and cervical motion tenderness

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108
Q

What is meant by cervical excitation?

A

This is performed on bimanual or speculum examination and results in an unpleasant or painful sensation upon contact of the cervix. If there is tenderness then it is suggestive of pelvic pathology

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109
Q

Describe the antibiotic management of PID for inpatients and outpatients

A

Inpatient - IV ceftriaxone; doxyclycline; metronidazole

Outpatient - IV cefriaxone; PO doxycycline; PO metronidazole

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110
Q

Explain why some patients with PID may need inpatient treatment

A

There is a risk of further complications including obstruction and sepsis therefore close monitoring of response to treatment is needed in order to ensure an improvement in the patient’s health

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111
Q

Describe how the rates of sperm production differ between a 20 year old and 50 year old man

A

Slight decline in rate of production and the quality of the sperm produced

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112
Q

State the 5 phases of coitus

A
  1. Excitement Phase
  2. Plateau Phase
  3. Orgasmic Phase
  4. Expulsion/Ejaculation
  5. Resolution Phase
113
Q

What system is involved in the stimulation of the excitement phase?

A

Limbic system (activation of parasympathetic nerones and inhiition of thoracolumbar sympathetic neurones)

114
Q

What changes occur in the plateau phase?

A

Contraction of the ischiocavernosus (impedes venous return) leading to a rise in intracavernosus pressure and therefore decreased arterial inflow.

Stimulation of accessory glands - 5% of ejaculate

115
Q

What is the functions of the secretions from the Cowper and Littre glands?

A

Lubricate the distal urethra

Neutralise acidic urine in the urethra

116
Q

What reflex is involved in emission?

A

Thoracolumbar sympathetic reflex

117
Q

What occurs during the emission phase?

A

Contraction of smooth muscle in ductus deferens, ampulla, seminar and vesicle and prostate
Internal and external urethral sphincters contract

The result is that the semen is pooled in the urethral bulb

118
Q

What reflex is involved in the ejaculation/expulsion phase?

A

Spinal reflex with cortical control - Sympathetic nervous system

119
Q

Outline the processes involved in ejaculation

A

Sympathetic nervous system stimulation.
Filling of the internal urethra stimulates the pudendal nerve
-> contractions of the genital organs, ischiocavernosus and bulbocavernosus
-> expulsion of semen

120
Q

What nervous pathway is involved in the resolution phase of the male sexual response?

A

Thoracolumbar sympathetic pathway

121
Q

State the nerve roots of the pudendal nerve

A

S2-4

122
Q

How does the pudendal nerve help to maintain an erection?

A

Causes contraction of the ischiocavernosus muscle which leads to an impeded venous return

123
Q

Describe the pathway by which NO is produced and how it acts to cause smooth muscle relaxation

A

Stimulation of the parasympathetic neurones on M3 receptors leads to an increase in calcium influx which stimulates eNOS. This increases NO production

NO is a powerful smooth muscle relaxant as it acts via cGMP and PKG to reduce intracellular calcium and therefore reduces the occurrence of calcium-induced calcium release

124
Q

Why is NO production important for erectile function?

A

Causes arteriolar smooth muscle dilation in the corpora cavernosa which leads to penile latency (filling) and tumescence (erection).

125
Q

Viagra inhibits cGMP breakdown: how can this help manage erectile dysfunction?

A

This leads to maintained erection.

cGMP is responsible for activation of PKG which acts via various methods to reduce the intracellular calcium concentration in smooth muscle.
Therefore if this is available for longer then vasodilation occurs for longer and the venous drainage of the penis is impeded for longer.

126
Q

Give 3 classes of drug which cause erectile dysfunction

A

Alcohol
Beta-blockers
Diuretics

127
Q

Give 3 non-drug causes of erectile dysfunction

A

Loss of desire
Psychological reasons - decending inhibition of spinal reflexes
Trauma - tears in the fibrous tissue of corpora cavernosa which means that it cannot get erect

128
Q

State the nerve which controls emission and ejaculation and give its nerve routes

A

Hypogastric Nerve

T10-L2

129
Q

Describe the events which occur during ejaculation

A

Urethral bulb swelling leads to stimulation of the pudendal nerve which leads to contractions of the genital organs, the ischiocavernosus and the bulbocavernosus muscles.

Internal urethral sphincter contracts
Contraction of glands and ducts

130
Q

State the normal number of spermatozoa in 1ml of sperm

A

20-200x10^6

131
Q

State the acceptable proportions with abnormal morphology and the normal proportions swimming forward vigorously

A

Acceptable abnormal: 60%

132
Q

Explain why there is fructose and prostaglandins in the seminal vesicle secretions

A

Fructose - energy source

Prostaglandins - increase sperm motility and female genital smooth muscle contraction

133
Q

Describe the function of acid phosphatase that is released in the prostate gland

A

This re-liquifys semen after approximately 10-20 minutes to give them motility in the female tract

134
Q

Describe how the spermatozoa mature within the vagina

A

Capacitation

Removal of the protein cost of sperm
Acrosomal enzymes exposed
Tail movement changes from beat to whip-like action

This is due to exposure to the female tract.

135
Q

Describe the processes of the acrosome reaction

A

Proteins on the sperm head bind to ZP3 proteins of the zona pellucida
Signalling mechanism involving Ca2+
Acrosomal enzymes digest path through the ZP
One sperm penetrates: fusion of plasma membranes

136
Q

Describe the Fast Block corticol reaction

A

Electrical change - wave of depolarisation across the cytoplasm

137
Q

Describe Slow Block cortical reaction

A

Ca2+ released from ER - induces exocytosis of cortical granules

These release enzymes to stimulate adjacent cortical granules

Wave of exocytosis occurs around the oocyte in 3 dimensions

138
Q

Describe the changes which occur in the female gamete immediately after fertilisation?

A

Oocyte undergoes meiosis II and the second polar body is expelled

Fusion of the nucleuses of each gamete to form the zygote.

139
Q

How long after fertilisation does implantation occur?

A

6 days after ovulation (thus ~5 days after fertilisation)

140
Q

Describe how the size of the chorionic cavity and the amniotic sac changes after week 2

A

Amniotic sac enlarges as the chorionic sac begins to pinch away. Eventually an embryochorionic membrane is formed which is where the amnion and chorion become composite membranes

141
Q

Explain what is meant by the term haemochondrial

A

There is only one cell layer of trophoblast between the maternal spiral arteries and the fetal capillary circulation

142
Q

Compare and contrast the structures of primary, secondary and tertiary villi

A

Primary - projection of syncitiotrophoblast cells
Secondary - mesenchyme has begun to invade. Thinner layer of syncitiotrophoblast cells around the outside of each villi. The cells within the mesenchyme are pluripotent and bring macrophages and small capillaries into the villi
Tertiary - mesenchyme is invaded by fetal vessels as the fetal circulation becomes established.

143
Q

Describe how the endometrium is prepared for implantation

A

Oestrogen - in the preovulatory stages oestrogen is produced by the growing follicle. This stimulates cellular proliferation in the endometrium - the preparatory stage.

Post ovulation and in the presence of the corpus luteum progesterone is secreted. This stimulates the endometrium to become secretory so that glands form and spiral arteries invade.

144
Q

Explain why massive peripartum bleeding occurs in placenta accreta

A

Placenta accreta is where the embryo has implanted into the myometrium. This is a highly vascular area which is not adapted to form a fetomaternal circulation therefore the vessels formed are not adapted for the function and are prone to rupture (????)

145
Q

Describe how the location of the foetal villi changes during development

A

Location of the villi is centred over a small area known as the villus chorion. The villi grow in length into the endometrium and the chorionic plate grows larger - to the size of a small dinner plate

146
Q

Describe as the interhaemal distance and surface area of the placenta changes in development

A

Surface area increases - large amount of branching

Interhaemal distance decreases - cytotrophoblast layer is lost

147
Q

What is the metabolic function of the placenta?

A

Glycogenolysis
Fatty acid metabolism
Cholesterol metabolism

148
Q

Why does insulin resistance occur during pregnancy?

A

The placenta produces human placental lactogen which has anti-insulin properties. This increases the glucose availability for the fetus

149
Q

Describe the consequences of poorly managed gestational diabetes

A

Macrosomic fetus - too much glucose available to the fetus
Stillbirth
Increased risk of congenital defects

The latter 2 are a result of the maternal ketoacidosis that occurs in poorly managed diabetes

150
Q 
Name a molecule which travels by the following across the placenta:
a) simple diffusion
b) facilitated diffusion
c) active transport
D) receptor mediated endocytosis
A

a) gases; water
b) glucose
c) amino acids; urea
d) immunoglobulins (IgG)

151
Q

Why is the rhesus group of the mother especially important during pregnancy?

A

The fetal circulation may occasionally mix with the maternal. If there is a mismatch of blood types then the maternal immune system will produce IgG against that blood type which will cause haemolytic disease in the fetus

152
Q

Name 3 teratogenic infections

A

Zika virus
Varicella zoster
Syphillis

153
Q

Give some features of babies with the following congenital infections:

a) syphilis
b) toxoplasma
c) rubella

A

a) intellectual disability, hearing loss
b) hydrocephalus, cerebral calcifications, microphthalmia
c) cataracts, glaucoma, heart defects, hearing loss, tooth abnormalities

154
Q

Name 3 risk factors for gestational diabetes

A

BMI >30
Previous pregnancy where baby >10pounds at birth
Family history

155
Q

Explain why gestational diabetes increases the risk of peripartal erbs palsy

A

Gestational diabetes increases the risk of a macrosomal baby.
This increases the risk of obstruction during childbirth - if this affects the shoulders then there is a risk of erbs palsy during delivery due to a stretch of the brachial plexus

156
Q

Describe the CVS changes of pregnancy

A

Progesterone causes smooth muscle relaxation which has many effects on the CVS.

  • decreases systemic vascular resistance
  • decreases after load
  • increases stroke volume and cardiac output (thus increases preload)
  • increase in heart rate
  • decrease in blood pressure (T1/2 only)
157
Q

Why is there an increased risk of varicose veins in pregnant women?

A

Progesterone causes smooth muscle relaxation, causing venodilation and potential pooling of blood within the veins.

Varicose veins are painful, distended veins in the leg.

158
Q

Describe the potential consequences of varicose veins

A

Bleeding from the skin
Ulcers
Infection
DVT - stasis of blood increases the risk of thrombus formation

159
Q

Explain why BP is low initially but increases back to normal levels later in pregnancy

A

Increased production of blood plasma and RBCs which increases the stroke volume and cardiac output of the heart, therefore increasing blood pressure.

Furthermore there is increased angiotensin II which encourages water and sodium retention

160
Q

Explain why serum creatinine levels fall during pregnancy

A

Progesterone increases the pre and post glomerular resistance vessels which increases the GFR and renal blood flow.
This means that creatinine clearance increases (40-50%) and therefore plasma creatinine levels drop

161
Q

Why are pregnant women at increased risk of UTIs?

A

Relaxation of smooth muscle by progesterone affects the ureters and the kidneys which means that there is an increased risk of stasis of urine.

162
Q

Describe the changes to ventilation found in pregnancy

A

Physiological hyperventilation - due to progesterone acting on the respiratory centres to increase respiratory drive. Doesn’t always occur

Increased alveolar and minute ventilation (15%)

163
Q

Why is there an increased risk of metabolic acidosis in pregnancy?

A

Increased respiratory ventilation means that there is reduced paCO2
Increased urinary excretion of bicarbonate cannot counteract this and therefore metabolic acidosis occurs

164
Q

Why does insulin resistance occur in pregnancy and why is there an increased risk of ketoacidosis?

A

hPL - anti insulin, ensures there is adequate circulating glucose for the fetus

However this means that the mother has to undergo gluconeogenesis by breakdown of protein, a biproduct of this system is ketones which exert an acidic effect.

165
Q

Why is there an increased risk of constipation and gallstones in pregnancy?

A

Effect of progesterone on the gastrointestinal smooth muscle (causes it to relax).

Constipation - Reduced peristalsis and contraction of the colonic smooth muscle.
Gall stones - effect on the biliary tree

166
Q

Explain why there is an increased risk of DVT in pregnancy

A

Pro thrombotic state - in preparation for childbirth

Plus increased venodilation and therefore venous pooling (stasis of blood) increases the risk.

167
Q

Describe the consequences of maternal smoking on the fetus

A

Teratogenic effects

Cleft lip/palate, intrauterine growth retardation, premature delivery

168
Q

Describe the impact of premature delivery on the baby’s lungs

A

Respiratory distress syndrome

Lungs have not matured to be able to secrete surfactant (from type II cells) therefore risk of alveolar spaces collapsing: high resistance airways.

169
Q

Why are babies who are born prematurely from gestational diabetic mothers at an increased risk of hypoglycaemia?

A

High amount of circulating insulin because they will have been exposed to high glucose concentrations in-utero

170
Q

State the diagnostic criteria for pre-eclampsia

A

New onset hypertension (>140mmHg systolic and/or >90mmHg diastolic) based on two measurements taken at least 4 hours apart, occurring in a pregnant woman after 20 weeks gestation.

With proteinuria - urinary excretion of >0.3g protein/24hours

171
Q

Describe some of the signs of pre-eclampsia. What is the suggested Pathogenesis?

A

Signs/symptoms:
Severe headaches, vision problems, heartburn, nausea or vomiting

Pathogenesis:
Cytotrophoblasts failed to migrate into the spiral arteries to form the maternal endometrium. This means that the maternal circulation is high resistance and therefore the systemic blood pressure has to increase to compensate.

172
Q

Why is hyper-reflexia an important sign of pre-eclampsia?

A

Suggests neurological involvement which is a severe risk factor for progression to eclampsia

173
Q

Describe the factors which create a high concentration gradient between the mother and the fetus

A

Higher fetal haematocrit & haemoglobin
Fetal haemoglobin higher affinity for O2

Double Bohr effect - pH decreases as O2 passes from mother to fetus. pH rises in fetal circulation as CO2 is lost

Double haldane effect - increase in CO2 concentration displaces oxygen from haemoglobin and in turn binding of oxygen with haemoglobin displaces CO2 from blood (both fetal and maternal)

174
Q

Explain why HbF does not release oxygen freely into the tissues

A

Very high affinity for oxygen - displays a hyperbolic curve rather than sigmoid curve

175
Q

Explain why the foetus is deprived of oxygen during labour

A

Contraction of the uterine muscles compresses the uterine vessels that supply the placenta.

176
Q

How does the foetal heart rate change if in distress?

A

Slows (bradycardia)

177
Q

Explain why it is important for the mother to have lower pCO2 than normal

A

Provides a concentration gradient for CO2 removal in the placenta.

178
Q

Why are foetal shunts required to supply sufficient oxygen to the fetus?

A

As there is very little O2 storage in the foetal circulation it is important that the O2 supply is diverted to the developing systems and organs rather than the organs which have little function in the foetus (e.g. Lungs) or a high metabolic demand (e.g. Liver)

179
Q

Describe 4 foetal shunts

A

Foramen ovale - from the RA->LA - prevents blood from going to the lungs
Ductus arteriosus - pulmonary artery->aorta
Ductus venosus - bypasses the liver
Crista dividens - allows a minor portion of blood to flow into the RV

180
Q

Describe how the foetal shunts close after birth

A

Umbilical artery & ductus arteriosus- vasoconstriction due to increased O2 saturation and decreased prostaglandins

Umbilical veins & ductus venosus - stasis of blood & clot formation leads to closure due to fibrosis

Foramen ovale - hypoxic pulmonary vasoconstriction is relieved which means that pressure LA>RA and therefore foramen ovale closes

181
Q

Describe the development of the foetal lungs

A

Embryonic period - only the pulmonary trunk formed, no gas exchange

Weeks 6-18 - pseudoglandular stage - duct system formed
Weeks 18-26 - canalicular stage - respiratory bronchioles formed, some terminal sacs
26-term - Terminal sac formation and the differentiation of the pneumocytes

182
Q

Explain why oligohydramnios can negatively affect respiratory development

A

Amniotic fluid is required for the development of the lungs as it prepares the lungs for the full burden and helps to develop the ciliary motion of the epithelia
Furthermore the lungs undertake breathing movements to practise and condition the musculature, which requires the lumens to remain open by the amniotic fluid.

183
Q

Give 2 causes of oligohydramnios

A

Excess loss of fluid - e.g. Rupture of amniotic membranes

Decrease in fetal urine production/excretion - e.g. Decreased renal perfusion (may be a result of chronic hypoxia)

184
Q

Give 3 causes of polyhydramnios

A

Problems with swallowing - e.g. Neuromuscular disorders, brain abnormalities, atresia of upper GI, foetal hypoxia

Problems with fetal urination (increased) - e.g. Foetal anaemia causing increased cardiac output

185
Q

Why may the mother be jaundiced during pregnancy?

A

Fetal bilirubin is handled efficiently by the placenta therefore maternal jaundice is pathological.

Potential causes include:
Acute fatty liver of pregnancy
Hepatitis infection
Cholelithiasis - linked back to the progesterone associated GI problems

186
Q

How may maternal jaundice be treated?

A

Depends on the cause:

Cholelithiasis - requires surgical intervention to remove gallstone
Acute fatty liver disease - early delivery - usually resolves with complete recovery

187
Q

Explain the significance of foetal abdominal circumference in monitoring gestational diabetes

A

Foetal abdominal circumference is associated with the birth weight therefore it is a good marker for control of gestational diabetes as it correlates with possible macrosomia

188
Q

Describe how you’d measure crown-rump length. When is this a useful measure?

A

Typically measured using ultrasound imagery, it is the measurement from the top of the head to the bottom of the buttocks.

This is useful for determining the gestational age, for example if the conception date is ambiguous.

189
Q

How does the head size change as a proportion of CRL in development?

A

By week 9 the head is >50% of the total CRL
Week 12 - change in proportions seen with head approximately 1/3
Towards the end of gestation and at full term the head is approximately 1/4 of CRL

190
Q

How do the methods of foetal weight gain differ between the early and late foetal periods?

A

Early - protein deposition

Late - adipose deposition

191
Q

Describe how the position of the uterine fundus changes during pregnancy

A

12 weeks gestation - pubic symphysis
20 weeks - umbilicus
36 weeks - xiphoid process of the sternum
Term - regression

192
Q

Explain the significance of the fundal:symphysis height

A

Proportional to the gestational age.
If too short or two long could be a sign of Incorrect dating or abnormal growth of the fetus (e.g. Growth restriction vs macrosomia) or presence of twins

193
Q

State 3 ways in which the foetal age can be estimated

A

Last menstrual period
Crown rump length
Biparietal diameter of the head

194
Q

Compare the causes of low and high birth weights

A

Low birth weights - growth restriction e.g. Chronic hypoxia, malnutrition. Or if the mother is small

High birth weights - gestational diabetes, maternal obesity/diabetes

195
Q

State the stage of respiratory development that the following form:

a) respiratory bronchioles
b) surfactant produced
c) ducts develop in bronchopulmonary segments

A

a) canalicular stage
b) terminal sac stage
c) pseudoglandular stage

196
Q

Why is survival impossible if the neonate is born prior to the terminal sac stage

A

Because there has been no alveolar sac development and therefore there is no site for gas exchange which means that the foetus is non-viable

197
Q

What is the importance of foetal movements in assessing CNS development?

A

The CNS is the earliest system to begin development and the last to complete it.
Movements begin from week 8 as development continues, including the tracts required for voluntary movements. Therefore if there is a change in the foetal movements it may suggest impairment in the development of the CNS

198
Q

Give 2 causes of symmetrical and 2 causes of assymetrical growth restriction

A

Asymmetrical - head sparing, restriction in weight followed by length.
E.g. Severe malnutrition, pre-eclampsia

Symmetrical - global, developed slowly throughout gestation
E.g. Anaemia, maternal substance abuse, early intrauterine infection

199
Q

Define labour

A

Medical term used to describe going from a pregnant state to a non-pregnant state

200
Q

Describe the difference between spontaneous abortion and pre-term labour

A

Spontaneous abortion =

201
Q

Describe how the uterine fundus changes throughout pregnancy

A

Fundus moves away from the pubic symphysis during early/mid pregnancy (fundal-symphysis height grows)
However in late pregnancy, approximately 2 weeks before full term, the fundus height drops as the position of the baby enters the pelvic inlet.

202
Q

What are the 3 factors described when assessing the foetus’ arrangement in the uterus?

A

a) lie - position of the fetus with relation to the mothers spine
b) presentation - what part has entered the pelvic inlet first
c) vertex - position of the baby’s body in relation to the presenting part

203
Q

State the landmark used to indicate the foetus’ position

A

Anterior fontanel

204
Q

Describe the limiting factors of the size of the birth canal

A

Laxity/angle of the public symphysis

Length of the sacral prominence

205
Q

Why is the oestrogen:progesterone ratio important in the first stage of labour?

A

First stage of labour is the preparation of the birth canal which includes cervical ripening.
Cervical ripening is induced by prostaglandin which is not released until the oestrogen:progesterone ratio increases (more oestrogen to progesterone)

206
Q

Explain the importance of the hormone relaxin in expanding the birth canal

A

Relaxin causes disruption in collagen synthesis and the extracellular matrix of ligaments and fibrous tissue. This allows for the cervix to relax and for the ligaments in the pelvis to become more lax.

207
Q

Describe a complication of the relaxation of the pelvic ligaments

A

Weakened support of the pelvic viscera which increases the risk of pelvic organ prolapse

208
Q

Describe the roles of prostaglandins in the first stage of labour

A

Cervical ripening - disrupts synthesis of collagen; decreases glycosaminoglycan synthesis which disrupts the extracellular matrix; reduced collagen aggregation therefore relaxes the cervix

Increases the amplitude and frequency of uterine contractions - increases intracellular calcium concentrations; contributes to the Ferguson reflex

209
Q

State the prostaglandins responsible for cervical ripening

A

F2x & E2

210
Q

Explain the term cervical effacement

A

Cervical effacement is also known as cervical ripening and is the thinning and relaxation of the cervix.

Note that this doesn’t occur until late in pregnancy (due to decrease in hCG which changes the oestrogen:progesterone ratio) which is beneficial as it prevents premature labour.

211
Q

How do oxytocin and prostaglandins differ in their action on uterine contractions?

A

Oxytocin - strengthens contractions of the uterus
Prostaglandins - increases the frequency of contractions (by increasing [Ca2+]i and positively feedback to the posterior pituitary to stimulate more oxytocin release

212
Q

Describe the Ferguson reflex

A

Mechanical stimulation of the uterus due to prostaglandin secretions leads to an increase in oxytocin production via positive feedback to the posterior pituitary.
Oxytocin increases mechanical stimulation of the uterus and stimulates the placenta to increase prostaglandins further which leads to a continued positive feedback loop.

This leads to an increase in frequency and force of contractions.

213
Q

Explain how the smooth muscle of the uterus is well adapted for its function in labour

A

Tight junctions between cells mean that it acts as a syncitium so that contraction occurs across the whole muscle.
Thick myometrium = stronger contractions.
Capable of brachystasis - unique to uterine smooth muscle this means that it contracts more than it relaxes

214
Q

State the dilatation at which the first stage of labour is complete

A

10cm

215
Q

Describe the change in maternal behaviour in the second stage of labour

A

Mother has the urge to bear down and will want to push

216
Q

Describe how the foetus position alters as it moves through the birth canal

A

Head flexes as it reaches the pelvic floor (reduces presentation diameter)
Internally rotates which stretches the vagina and perineum
Head rotates and extends as the head is delivered

217
Q

Why can giving oxytocic drugs help to prevent post-part up haemorrhage?

A

Encourages further uterine contractions to compress on the spiral arteries and the arteries within the myometrium thus reducing blood loss

218
Q

Explain why retention of the placenta is associated with heavy PPH?

A

Placenta recieves 500-800ml of blood per minute which continues if it is not sheared off.

This is 10-15% of the cardiac output which means that a huge amount of blood can be lost, very quickly.

219
Q

Define post-partum haemorrhage and give 3 causes

A

PPH = loss of 500-1000ml of blood within 24 hours of delivery

Retention of the placenta; failure of uterus to contract; blood clotting problems; tear of the uterus

220
Q

Describe the Pathophysiology of sheehans syndrome.

A

A form of primary hypopituitarism due to ischaemic necrosis as a result of blood loss and hypovolaemia during childbirth

221
Q

Why is the posterior pituitary unaffected in Sheehans syndrome?

A

The posterior pituitary is a down-growth of the diencephalon (forebrain) which means it’s blood supply is protected by the cerebral autoregulation mechanisms (myogenic autoregulation) when hypovolaemic shock occurs. Therefore ischaemia doesn’t occur as it does in the anterior pituitary in Sheehans syndrome.

222
Q

Describe the relationships of the female tract to other systems of the body

A

Relation to GI tract posteriorly via the rectouterine pouch (pouch of Douglas)
Relation to the urinary tract anteriorly via the uterovesicle pouch

223
Q

Why are the ovaries intraperitoneal?

A

Although they originated on the posterior abdominal wall they descended into the peritoneum and became enclosed by the broad ligament which is also known as the mesovarium and is therefore considered intraperitoneal.

224
Q

How are the ovaries supported in their position?

A

Suspensory ligament - connects the ovaries to the posterior abdominal wall - not a true ligament but consists of the ovarian artery and veins and lymphatic drainage. Connects to the ovaries at the inferior pole.

Ovarian ligament - connects the ovaries to the uterus holding in position.

225
Q

How does the venous drainage differ between the left and right ovaries?

A

Right ovary drain via the gonadal veins directly into the inferior vena cava
Left ovary drains via the left ovarian vein into the left renal vein

226
Q

What are the attachments of the uterine tube?

A

Attaches medially to the fundus of the uterus

Continuous attachment along its length to the broad ligament which gives it some movement.

227
Q

State the part of the uterine tube where fertilisation occurs

A

Ampulla

228
Q

Why are ectopic pregnancies dangerous?

A

Tissues needed for implantation are not present - including the lack of decidual cells which limit the level of implantation into the tissue.
This means that there is a severe risk of haemorrhage as the foetus grows

229
Q

How is the broad ligament formed?

A

Growth and fusion of the paramesonephric ducts into the midline pulls the peritoneum over it to form the broad ligament.

230
Q

Why is the lymphatic drainage of the fundus to the superficial inguinal lymph nodes?

A

Drainage of the fundus is via the round ligament of the uterus which continues to the labia Majora and therefore drains into the inguinal nodes.

231
Q

Describe the route that a needle must take to reach the pouch of Douglas from the vagina

A

Must pass through the posterior fornix of the vagina (fornices are out pockets of vagina around the cervix)

232
Q

Name the blood vessels which supply the uterus

A

Uterine artery - anterior division of the internal iliac artery
Ovarian artery - same as above

233
Q

Why is the rich anastomoses of the uterus important for its function?

A

Blood supply needs to be rich so that:

  • maternofetal blood supply can be established if fertilisation and implantation is successful
  • large amount of smooth muscle needs a good blood supply for delivery of fetus if gestation is successful
234
Q

Name the 3 ligaments that support the uterus

A

Broad ligament
Round ligament
Uterosacral ligament - opposes the anterior pull of the round ligament to maintain anteversion

235
Q

State the remnants of the gubernaculum in the female

A

Suspensory ligament
Ovarian ligament
Round ligament

236
Q

Describe the innervation of the perineum

A 
Pudendal nerve (S2-4)
Some contribution from the ilioinguinal nerve
237
Q

Name the plexus from which the ovaries are drained?

A

Pampiniform plexus

238
Q

Why can you not palpate ovarian cancer that has spread via the lymphatics?

A

Ovaries drain into the para-aortic lymph nodes due to their developmental origin.
This area is not palpable due to its position.

239
Q

Describe the lymphatic drainage of the fundus, body and cervix of the uterus

A

Fundus - inguinal lymph nodes (some para-aortic)
Body - external iliac
Cervix - external & internal iliac nodes and sacral nodes

240
Q

Describe the innervation of the vagina

A

Inferior 1/5 = pudendal nerve

Superior 4/5 = uterovaginal plexus

241
Q

Explain how innervation of structures differ above and below the pelvic pain line

A 
Above = inferior thoracolumbar spinal ganglia
Below = S2-4 ganglia
242
Q

Name the structures which form the pelvic inlet

A

Pubic crest
Iliopectineal line
Ala of sacrum and sacral prominatory

243
Q

What is the difference between the diagonal and obstetric conjugates

A 
Diagonal = sacral prominatory to inferior border of the pubic symphysis
Obstetric = sacral prominatory to midpoint of public symphysis
244
Q

Give 3 differences between gynaecoid and android pelvises

A

Gynaecoid - round inlet, straight side walls, sub-pubic arch >90
Android - heart shaped inlet, prominent medially projecting ischial spines, sub-pubic arch ~50

245
Q

Describe the Pathophysiology of endometriosis

A

Endometrium found outside the womb.

Possibly due to retrograde menstruation where the endometrium flows through the Fallopian tubes; possibly genetic, immune dysfunction or spread through bloodstream

246
Q

State the location where endometrial carcinoma is most likely to occur

A

Superior/posterior part of the body

247
Q

Describe how the origin and control of the anterior and posterior pituitary differs

A

Anterior pituitary = endocrine; developed from ectoderm tissue of the stomatodeum. Controlled via hormones from the hypothalamus.

Posterior pituitary = neuroendocrine; developed from the forebrain. Controlled via neuronal stimulation.

248
Q

Name 5 hormones released by the anterior pituitary

A 
FSH
LH
Prolactin
TSH
ACTH
249
Q

Why are only small amounts of hypothalamic hormone needed to activate the pituitary?

A

Large population of each cell type and stimulation activates a cascade reaction which amplifies the stimulation.

250
Q

How does GnRG release occur?

A

From the hypothalamus, secreted in a pulsatile fashion approximately once per hour.
Under the influence of the brain, body weight and circulating hormones.

251
Q

How does the HPG-axis control reproduction in the male?

A

GnRH stimulates FSH and LH release from the anterior pituitary which act on Sertoli Cells and Leydig cells respectively.
Leydig cells then secrete testosterone which negatively feedback to hypothalamus (reduces GnRH) but increases the effect of FSH in the Sertoli cells and stimulates maturation of the internal genitalia.
FSH stimulates spermatogenesis.
Sertoli cells also produce Inhibin inch negatively feed back on FSH.

252
Q

Why does FSH act on Sertoli cells to allow spermatogenesis to occur?

A

Because Sertoli cells are within the stroma where the spermogonia are and control the rate of spermatogenesis.

253
Q

What is the effect of Inhibin and prolactin on LH?

A

Both positively feedback to enhance the effect of LH on Leydig cells.

254
Q

How does the location of Sertoli and Leydig cells differ in the testis?

A

Sertoli cells form the blood-testis barrier whereas Leydig cells are within the interstitial spaces.

255
Q

Why does the level of oestrogen rise throughout the follicular stage?

A

Increased LH receptors due to increased number of granulosa cells which secrete oestrogen.

256
Q

How does the increasing level of oestrogen alter the HPG axis?

A

Oestrogen in high concentrations positively feedback to the hypothalamus to increase GnRH and therefore increase LH production which causes an LH surge.

257
Q

Describe the role of progesterone in the HPG axis

A

Produced by the corpus luteum in the post-ovulatory stage.
Prevents high oestrogen from producing a GnRH surge which means that the frequency of GnRH pulses reduces.
Furthermore it acts on Gonadotrophs to prevent new follicle development.

258
Q

Where is Inhibin secreted from in the male?

A

Sertoli cells

259
Q

How does Inhibin help to regulate the rate of spermatogenesis?

A

Inhibits LH which means that Leydig cells receive less stimulation and therefore produce less testosterone which decreases the rate of spermatogenesis.

260
Q

What are the functions of testosterone in the male?

A

Determinative effects - deepened voice, penis growth, body/facial hair

Regulatory effects - maintenance of internal genitalia, anabolic action, behavioural effects

261
Q

Describe the role of the following in follicular development:

a) LH
b) FSH

A

a) (antral phase) stimulates the theca interna to produce androgens and (pre-ovulatory) stimulates granulosa cells and increases collagenase activity
b) binds to granulosa cells to increase oestrogen production (from androgens) and stimulate growth.

262
Q

Why does the function of progesterone require oestrogen?

A

Oestrogen “primes” the cells for progesterone stimulation.

263
Q

List 4 functions of progesterone in the luteal phase

A
  1. Fallopian tube - decrease motility, secretion and cilia action
  2. Endometrium - further thickening, increase secretion, development of the spiral arteries
  3. Cervical mucus thickening, acidification & inhibition of sperm transport
  4. Elevates basal body temperature
264
Q

Why does the endometrium shed once the corpus luteum degenerates?

A

Because there is no secretion of progesterone and therefore no hormones to maintain the spiral arteries. This means that they collapse and necrosis and apoptosis of the stratum functionalis layer occurs.

265
Q

Why is FSH present in greater levels than LH at the start of the cycle?

A

Because there is no inhibition of it’s production from inhibin which is secreted from granulosa cells later in the cycle.

266
Q

Why can a progesterone pill be used as a contraceptive?

A

Prevents oestrogen from causing an LH surge therefore it prevents ovulation.

267
Q

How does the regulation of the corpus luteum differ if the ovum is fertilised or not?

A

If the ovum is not fertilised then it regresses spontaneously

If it is fertilised then the syncitiotrophoblasts produce hCG which maintains the corpus luteum

268
Q

Why can giving a dopamine agonist aid fertility?

A

Dopamine inhibits prolactin. Prolactin promotes oestrogen and progesterone production which means that overall it has an inhibitory effect on the development of a follicle.
Therefore increasing dopamine will increase the chances of follicular development.

269
Q

Why will an anti-oestrogen drug (such as clomiphene) aid fertility?

A

Oestrogen negatively feedbacks to the hypothalamus to prevent GnRH.
Anti-oestrogen drugs prevent this inhibition therefore up-regulating the HPG axis which means that more follicles can develop and there is a greater chance of successful ovulation.

270
Q

What is the fate of the corpus luteum?

A

No fertilisation - spontaneously regresses

Fertilisation - maintained by hCG but spontaneously regresses after ~12 weeks.

Forms a pale structure called the corpus albicans which slowly shrinks.

271
Q

What is the function of peg cells of the fallopian tube?

A

Produce mucous to help transport the sperm to the egg.

272
Q

Cilia are upregulated by oestrogen, how does this help fertilisation?

A

The cilia beat the oocyte along the ampulla and the sperm towards the oocyte which increases the chances of them meeting and fertilisation occuring.

273
Q

What is the structural difference between the stratum basalis and stratum functionalis?

A

Stratum basalis contains glands and remains the same thickness throughout the cycle whereas the stratum functionalis is predominantly cellular with coiled arteries and changes in depth depending on the time in the menstrual cycle.

274
Q

State the epithelium found in the upper cervix

A

stratified columnar - the same as the uterus

275
Q

What is the clinical significance of the squamocolumnar junction?

A

This is the point where there is an abrupt change in epithelial type, also described as the transition zone, and is the site where metaplasia can occur.

276
Q

Oestrogen favours glycogen deposition in the vagina. How can this help to prevent infection?

A

Reduces the pH of the vagina which is not favourable for many bacterial species.
it also promotes lactobacilli colonisation which promotes a natural microbiota environment which out competes colonisation of other bacteria.

277
Q

What are the impacts of oestrogen on the breast?

A

Induces ductal component
Causes fat deposition and stromal growth

Indirectly enhances lobuloalveolar development

278
Q

State the proportion of ovarian cancer that occurs in the germinal epithelium

A

90-95%

LUSUMA Questions (2 decks)

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