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Repro Flashcards

0
Q

How is male female differentiation determined in the gonads?

A

Males have SRY gene expressed in primordial germ cells
Triggers degeneration of the cortex and development of the medulla
Releases androgens which maintain mesonephric duct and mullarian inhibiting substance degrading the paramesonephric

Females lack SRY in no primordial germ cells
Cortex develops and medulla degrades
Lack of androgens results in degradation of mesonephric duct, lack of mullarian inhibiting substance results in persistence of paramesonephric duct.

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1
Q

Where do the gonads develop from? What type of embryonic tissues are involved?

A

The urogenital ridge (intermediate mesoderm) and primordial germ cells (from the yoke sac)

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2
Q

What is the embryonic origin of the female internal genitalia?

A

Paramesonephric ducts fuse, and the (uterine) septum between them breaks down forming the uterus, cervix and upper vagina. The urogenital sinus (external) begins to cavitate forming the sinovaginal bulb then the lower vagina.

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3
Q

What are the parts of the indifferent genetalia? What do they form in males and females?

A

Genital tubercle - glans penis / clitoris
Genital folds - shaft, spongy urethra / labia minora, urethra, vagina
Genital swellings - scrotum / labia majora

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4
Q

How do the testis anchored to the abdomen? How do they descend?

A

Urogenital mesentery becomes caudal genital ligament attaching to posterior abdo
Gubernaculum descends from caudal testis to inguinal region.
Testis starts to descend down route of gubernaculum
Gubernaculum extends to scrotum
Outpouching of peritoneum follows anteriorly (processus vaginalis)

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5
Q

Why does the ovary stop descending?

A

Mechanical obstruction by mullarian duct

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6
Q

What forms the ligaments of the ovary?

A

Cranial genital ligament - suspensory lig. of ovary
Caudal genital ligament - ovarian lig. and round lig. of uterus
Parietal lateral plate mesoderm - broad ligament of uterus

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7
Q

Describe female gamete formation

A

Primordial germ cells
Replicate to 7million then die to 2 million
Oogonia
Enter meiosis then arrest at prophase 1
Primary oocyte
Surrounded by flat follicular cells
Primordial follicle
BIRTH
Most primordial follicles die leaving 40000
PUBERTY
1/12 20 primordial follicles start to mature
Follicular cells thicken and become cuboidal with multiple layers (granulosa). Secrete zona pellucidia. Connective tissue shell (theca)
Pre antral follicle
Fluid collects in granulosa
Antral follicle
Theca differentiates into theca interna and theca externa. Antrum expands
Mature (graffian) follicle.
Meiosis progresses to prophase 2
Primary oocyte to secondary oocyte and polar body
Ovulation

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8
Q

What are the stages of the menstrual cycle with rough times?

A

Follicular / proliferative - 0 to 12 days (some variability)
Ovulation - 12 to 14 days
Luteal / secretory - 14 to 28 days (fixed)

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9
Q

Describe spermatogenesis

A 
Primordial germ cells on sex cords
Spermatagonia 
BIRTH
PUBERTY
Sex cords hollow forming seminiferous tubules
Spermatagonia cluster around the edge
Some spermatagonia differentiate to a1 spermatagonia 
Undergo a fixed number of mitotic divisions all remaining joined by cytoplasm
Spermatocytes
Meiosis
Spermatids
Release into tubules
Maturation
Spermatozoa
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10
Q

What are hormones that influence levels of other hormones called?

A

Trophic

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11
Q

Describe the release of GnRH

A

Released into hypophesal portal circulation from hypothalamus median eminence. Pulsetile, slightly more frequent in the morning.

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12
Q

What characteristics are required of male sex hormone production to meet their reproductive needs?

A

Steady hormone concentration to ensure continuos sperm production. Slightly raised levels in early morning. Slightly raised levels when stimulated and reduced when stressed.

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13
Q

What do LH and FSH do in male gonads?

A

LH acts on laydig cells to release testosterone

FSH acts on sertoli cells to stimulate spermatogenesis and also releases inhibin

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14
Q

What do testosterone and inhibin do in males?

A

Testosterone has regulatory and determinative effects.
Regulatory includes maintenance of repro tract, behaviour, promoting spermatogenesis by acting on sertoli cells alongside FSH
Determinative effects include secondary sexual characteristics
Testosterone feedback negatively on GnRH and LH + FSH (reduces secretion of GnRH and sensitivity of Gonadotrophin to GnRH).

Inhibin feeds back negatively on FSH

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15
Q

Explain the hormone changes in the proliferative / follicular phase of mensturation and the effects on the oocyte.

A

Initially low oestrogen and inhibin therefore uninhibited GnRH secretion.
As GnRH secretion increases increased LH and FSH
FSH causes granulosa to develop and inhibin to be released
LH causes theca to release androgens which are converted to oestrogens by granulosa
As follicle grows oestrogen and inhibin increase. Oestrogen inhibits GnRH and reduces sensitivity of gonadotrophs.
LH falls a bit but FSH falls markedly preventing further oocytes from developing. Oestrogen continues to rise as the follicle grows.

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16
Q

What is the effect of rising oestrogen during the proliferative/follicular phase on the female?

A

Endometrial proliferation (stratum basalis producing a new stratum functionalis. Arterioles lengthen and penetrate the new stratum functionalis)
Myometrium grows and contracts more
Cervical mucus becomes thin and alkaline
Systemic changes in hair, skin, metabolism.

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17
Q

What happens during ovulation?

A

Oestrogen levels climb. Switches to +ve feedback at hypothalamus and pituitary increasing LH levels +++. LH surge. LH breaks down theca externa collagen causing rupture and ovulation. This leaves the reminents of the follicle, the corpus haemorrhagicum.
As follicle ruptures oestrogen levels decrease, back to -ve feedback, LH and FSH drop.

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18
Q

What occurs in the secretory/luteal phase?

A

Corpus haemorrhagicum to corpus luteum.
Corpus luteum secretes oestrogen, progesterone and relaxin
Oestrogen decreases GnRH amount per pulse, progesterone decreases number of GnRH pulses and prevents any positive feedback from oestrogen.
O+P cause thickening of endometrium, thick acidic cervical mucus, increased body temp, metabolic changes, mammary changes.

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19
Q

How long does the corpus luteum last if no hCG is detected? What does it become? What happens?

A

14 days - becomes corpus albicans.

Decrease o+p, decrease blood supply to placenta, menses. Cycle starts again.

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20
Q

What are the strands of connective tissue that support the breast called? What causes laxity?

A

Suspensory ligaments

Age, strain

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21
Q

What is the structure of the glandular tissue of the breast?

A

Alveoli into lobules into 20 lobes

Lobes to secondary tubules to mammary duct to lactoferrous sinus to lactoferrous duct to nipple.

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22
Q

What determines breast size?

A

Amount of subcutaneous fat

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23
Q

What is the lymphatic drainage of the breast?

A

Sub areolar lymphatic plexus

Most to the axillary (pectoral), some to supra clavicular or deep cervical. Some medially to the parasternal

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24
Q

What is the histology of the ovaries?

A

Cortex with germ cells

Medulla connective tissue, blood vessels and nerves

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25
Q

What are the areas of the Fallopian tubes? What are their histology?

A

General - mucosa, lamina propria, muscular externa and serosa.

Fimbria
Infundibulum
Ampulla - heavily folded, bilayered muscle, cilliated columnar
Isthmus - lightly folded, trilayered muscle, peg cells
Intramural

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26
Q

What are the layers of the uterus?

A 
Compact and spongy stratum functionalis (endometrium)
Stratum basalis (endometrium)
Myometrium
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27
Q

What is the histology of the cervix?

A

Near the internal os - simple columnar
Near the external os - non keratanized stratified squamous

Junction is the squamatocolumnar junction.

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28
Q

What makes pre puberty and puberty distinct?

A

The repro system could work pre puberty but GnRH secretion is low (thus low LH and low sex steroids).

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29
Q

What triggers puberty?

A

Unknown - something from the brain
Maybe body weight - 47kg trigger for menarch (though actually proportion of genetically expected weight) possibly signalled by leptins.
Maybe light levels producing melatonin from pineal gland

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30
Q

Why might age of puberty decreased over generations?

A

Increased body weight

Increased exposure to light (artificial)

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31
Q

Define precocious puberty

A

Onset of puberty prior to 8 years old

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32
Q

What can cause precocious puberty?

A

Idiopathic
Pineal tumour
Meningitis
Ectopic GnRH tumours

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33
Q

Why would cause early onset secondary sexual characteristics but not fertility?

A

Ectopic sex steroid producing tumour

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34
Q

What is the order of development in females during puberty?

A

Thelarche - breast development
Andrenarche - pubic hair growth
Growth spurt
Menarche - menstruation

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35
Q

What is the age of onset of puberty in females?

What is the age of onset of menarche?

A

8-13

11-15

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36
Q

What hormones are responsible for female pubertal development?

A

Thelarche is oestrogen
Anderarche is testosterone
Growth is both
Menarche is LH and FSH

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37
Q

When does puberty begin in males?

A

9-14

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38
Q

What order do events occur in male puberty?

A

Testicular growth
Penis size
Adrearche
Growth spurt

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39
Q

Why do males grow taller than females?

A

Testosterone is a bigger driver of growth than oestrogen

Longer period of growth (though later onset)

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40
Q

Why does early puberty cause short stature?

A

Less normal growth before growth spurt and growth plates seal after a set time during puberty.

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41
Q

Why do females experience menarche?

A

Follicles running out therefore reduced oestrogen.

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42
Q

What are the stages and typical ages of menopause, what happens to hormone levels and fertility?

A

Pre-menopause (from 40 years) causing erratic ovulation and mensturation with reduced but not absent fertility. Corpus luteum doesn’t always form. Less oestrogen and inhibin lead to raised LH and FSH.
Menopause (around 50 years), no follicles left to develop, oestrogen and inhibin levels fall thus LH and FSH very high.

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43
Q

What are the symptoms of menopause?

A 
Hot flushes
Regression of uterine tissue
Loss of breast tissue
Loss of vaginal rugae
Vaginal dryness

Increased risk of osteoporosis
Increased risk of CVD

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44
Q

What are the sub classifications and definitions of amenorrhea?

A

Primary
Absence of menses aged 14 with no secondary sexual characteristics
Or
Absence of menses aged 16 with secondary sexual characteristics

Secondary
Menses in the past but none for 3 months if used to be regular or 9 months if used to be irregular.

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45
Q

What are the 2 most common cause of secondary amenorrhoea?

A

Preggers

Menopause

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46
Q

What are pituitary/hypothalamic causes of amenorrhoea?

A

Primary - congenital failure to produce gonadotrophins

Secondary - weight loss/anorexia nervosa, stress, exercise, pituitary necrosis, hyperprolactinaemia, haemochromatosis

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47
Q

What are gonadal causes of amenorrhoea?

A

Primary - chromosomal abnormalities (eg turners), receptor abnormalities (eg congenital adrenal hyperplasia)

Secondary - pregnancy, menopause, POS, drug induced

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48
Q

What are outflow tract causes of amenorrhoea?

A

Primary - mullarian agenesis, vaginal atresia (causes cryptomenorrhoea)

Secondary - endometrial adhesions (often follows dilation and cutterage abortions).

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49
Q

What sort of things should you ask in a history about amenorrhoea?

A 
? Preggers
Sexual Hx
Contraception
Weight change
Medications
Fhx (esp. Menopause)
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50
Q

What should you examine in an amenorrhoea consultation?

A 
BMI 
Hair distribution
Thyroid
Visual field
Breast discharge (hyperprolactinaemia)
Abdominal masses
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51
Q

What is the term for heavy periods?

A

Menorrhagia

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52
Q

What is the term for painful periods

A

Dysmenorrhoea

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53
Q

What is the term for infrequent periods?

A

Oligomenorrhoea

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54
Q

What are the layers surrounding the testis? What do they originate from?

A 
Tunica vaginalis (procerous vaginalis)
Spermatic fascia (transversalis fascia)
Cremastic fascia and muscle (internal oblique muscle)
External spermatic fascia (external oblique muscle)
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55
Q

How does the histology of the male reproductive tract change?

A

Rete testis - simple cuboidal
Ductus efferentes - cilliated simple columnar, simple columnar
Epididymis - psudostratified columnar with steriocilia
Vas deferans - psudostratified columnar with sparse steriocilia

There is increasing amounts of muscle as you move distally.

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56
Q

How is testicular temperature regulated?

A

Held outside of the body
Pampiniform plexus of veins helps cool arterial blood
Dartos muscle contracts the scrotum when cold

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57
Q

What is the lymphatic drainage of the testis? What is the clinical significance of this?

A

The para aortic nodes

They can’t be palpated

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58
Q

What is the arterial supply and venous drainage of the testis?

A

Arterial supply - testicular arteries from the abdominal aorta
Venous drainage - testicular veins - right to IVC left to left renal vein

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59
Q

What is contained in the spermatic cord?

A 
Testicular artery and vein
Lymphatics
Genital branch of genitofemoral nerve
Obliterated procerous vaginalis
Vas deferans
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60
Q

Where are the dartos and cremaster muscle located?

A

Dartos in the scrotum outside of the spermatic fascia

Cremaster in the middle layer of spermatic fascia

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61
Q

What is the innervation of the scrotum?

A

Anterior - genital branch of genitofemoral

Posterior - pudendal nerve from sacral plexus

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62
Q

Where in the prostate is bph more likely to effect? What about cancer?

A

Bph central zone

Ca peripheral zone

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63
Q

What are the cavities of the penis?

A

One corpus sponginosum

Two corpora cavenosa

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64
Q

What muscles are associated with the penis?

A

Bulbospongiosus

Ischiocavernosus

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65
Q

What lines make up the pelvic brim?

A

Lina terminalis made of arcuate line, pectineal line and pubic crest.
The sacral promonatory.

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66
Q

What are the three conjugates of the pelvis?

A

Anatomical - superior to sacral prominotory
Obstetric - middle to sacral prominotory (smallest)
Diagonal - inferior to sacral prominotory (easy to measure)

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67
Q

What is the entrance and exit to the true pelvis?

A

Entrance is the pelvic brim

Exit is pubic arch - ischial tuberosity - sacrotuberous ligament - coccyx

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68
Q

Differentiate a gynaecology from an android pelvis

A 
Gynacoid has 
a greater than 90 degree pubic arch
More oval brim
Less prominent ischial spines 
A wider greater sciatic notch (more posterior coccyx)
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69
Q

What is the arterial supply to the ovaries uterus and vagina?

A

The ovarian artery (ovary and anastomoses with uterine)
The uterine artery (uterus and anastamoses with both)
The internal pudendal artery (vagina)

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70
Q

What glands are found in the vaginal vestibule?

A

Bartholin / vestibular

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71
Q

Explain the uterine position

A

The uterus is usually antiverted (rotated forward with respect to the vagina axis) and antiflexed (rotated forward with respect to the axis of the cervix).
With a full bladder the uterus can become retroverted.

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72
Q

What are the pouches around the uterus?

A

Uterovesicular pouch - bladder to uterus

Retro uterine pouch - uterus to rectum

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73
Q

What are the pouches within the vagina at the point of connection to the cervix?
What is the medical application?

A

The anterior and posterior fornices

Posterior fornix used for withdrawing fluid from rectouterine pouch by culdocentesis

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74
Q

What is the lymphatic drainage of the uterus?

A

Fundus to aortic nodes
Body to external iliac
Cervix to external and internal iliac as well as sacral

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75
Q

What muscles make up the pelvic floor?

A

Levator ani - puborectalis, pubococcygeus, iliococcygeus, coccygeus
Piriformis

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76
Q

What is the nervous innervation to the pelvic floor?

A

Pudendal nerve (s2 3 and 4)

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77
Q

What is the perineum?
What are. It’s boundaries?

How can it be divided?

A

A fibromuscular sheet which closes the outlet to the true pelvis
Pubic symphysis to ischiopubic ramus to ischial tuberosity to sacrotuberous ligament to coccyx.
Divided into anterior and posterior triangles

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78
Q

What muscles anchor to the perineal body?

A

Bulbospongiosus
External anal sphincter
Transverse perineal

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79
Q

What passes through the pelvic floor?

A

The urogenital hiatus comprising of the:
Urethra
Vagina
Anus

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80
Q

What prevents vaginal prolapse?

A

The uterosacral ligament acting as a sling
The arcus tendinous compressing the vagina
The perineal body anchoring the vagina in the perineum

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81
Q

What are the functions of the pelvic floor?

A

Support the pelvic organs preventing prolapse
Contributes to urinary continence (increased bladder pressure mimicked by increased sphincter pressure)
Contributes to bowel continence (puborectalis causes flexure in rectum)
Contributes to childbirth and truncal stability

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82
Q

What can cause pelvic floor weakness?

A 
Childbirth stretches the ligaments, muscles and nerves (pudendal) 
Age
Menopause
Obesity
Chronic cough
Connective tissue disease
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83
Q

Why is incidence of STIs rising?

A

Greater awareness so greater presentation with symptoms or for screening
Greater promiscuity and risky sexual behaviour
Decline in fear of HIV
Better diagnostics

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84
Q

Why may many STIs go unrecognised?

A 
Asymptomatic
Denial
Lack of awareness of symptoms
Embarrassment 
Presentation to GP not GUM (statistical only)
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85
Q

Who is most at risk of STIs?

A 
Young
Poor
Uneducated
Ethnic minorities
Early sex
Multiple partners at once
Unprotected sex
Many partners 
lack of confidence
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86
Q

As well as direct treatment what else should be carried out on discovering an sti?

A

Contact tracing
Anti clamydia treatment
Advice on abstinence until cured
Advice on future safe sex

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87
Q

What causes genital warts?
What treatment?
What other disease is associated with it?

A

Human papillomavirus
Nothing/cryotherapy/surgery
Associated with cervical cancer (HPV 16 and 18)

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88
Q

What causes herpes?
How does it present?
What treatment?

A

Herpes Simplex Virus (usually type 2 though can be 1)
Painful multiple blisters that ulcerate. First episode associated with fever.
Treat with acyclovir if severe, salt water baths to keep area clean

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89
Q

What causes chlamydia, how does it present, what is the treatment?

A

Chlamydia trachomatis
Gram -ve coccus or rod
Urethritis, Epididymitis, prostitis, cervicitis, salpingitis
Can cause conjunctivitis in neonates (trachoma)
Treat with doxycycline

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90
Q

What causes gonorrhoea, how does it present, what is a common complication, how do you treat?

A

Neisseria gonorrhoeae
A gram -ve intracellular diplococcus
Causes urethritis, proctitis, prostatitis, Epididymitis and is often asymptomatic in females
Can spread to skin and joints
Treatment is with IM ceftriaxone and oral ciprofloxacin

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91
Q

What is trichomoiasis, what are symptoms, what tests, what treatment?

A 
Trichomonas vaginalis 
Protazoa
Burning/itching to vagina with offensive smelling discharge
Perform culture 
Tx with metronidazole
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92
Q

What is syphilis, what are the stages of disease, what is Dx and Tx?

A

Treponema pallidum a spirochete
Painless ulcer to fever rash and lymphadonopathy to chronic granulomas to cvs and CNS pathology
Dx with dark field microscopy or serology
Tx with penicillin

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93
Q

What causes candidiasis, what are risk factors, what are symptoms, what is treatment?

A

Candidia albicans
Risk include dm, abx, ocp, pregnancy, steroids
Symptoms include white discharge and itch
Dx with smear
Txt with azoles, nystatin,

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94
Q

What is bacterial vaginosis, symptoms, Dx, Tx

A 
Non sexually. Transmitted
Gardnerella sp. mycoplasma, anaerobes
Offensive fishy discharge
Dx with wiff test
Tx with metranidazole.
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95
Q

What is PID?

A

An ascending infection causing endometriosis, salpingitis, parametritis, oophritis.

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96
Q

What are complications of PID?

A

Tuboovarian abscess
Adhesions
Pelvic peritonitis

97
Q

What are causative organisms of PID?

A

Neisseria gonorrhoea
Chlamydia trachomatis
Gardenella sp.

98
Q

What is the treatment for PID?

A

Causitive based:
Ceftriaxone
Doxycycline
Metronidazole

99
Q

When should PID be admitted to hospital?

A

Need for IV abx
Tuboovarian abscess
Pregnant
Unable to rule out surgical emergency

100
Q

What. Are future risks of PID?

A

Ectopic pregnancy
Infertility
Chronic pelvic pain
Peri hepatic adhesions

101
Q

How does PID present?

A 
Pyrexia
Pain (bilateral adenaxial tenderness)
Deep dysparaunia 
Abnormal discharge
Bleeding
102
Q

What are the phases of coitus?

A

Excitement
Plateau
Orgasm
Resolution

103
Q

What two mechanisms cause vasodilation in the excitement phase of coitus?

A

Decreased sympathetic stimulation

NO release

104
Q

How does decreased sympathetic stimulation cause vasodilation in coitus?

A

Decreased alpha 1 - decreased alpha q release - decreased phospholipase c - decreased pip2 to ip3 and dag - decreased ca2+ release and increased MLCP activity.

105
Q

How is nitric oxide released in the excitement phase of coitus?

A

Directly from nonadreneargic noncholinergic parasympathetic nerves.
Release of ACh from cholenergic nerves activating M3 on endothelial cells - increases alpha q - increases IP3 - increases Ca2+ - activates nitric oxide synthase converting arginine and oxygen to NO

106
Q

How does NO cause vasodilation?

A

Activates guanylyl cyclase converting GTP to cGMP. cGMP activates PKG increasing action of MLCP
increasing PMCA and SERCA reducing Ca2+ (and thus decreasing MLCK)
Increases k+ permiability hyperpolarising the cell

107
Q

Other than vasodilation how does the body ensure blood pools in the penis during erection?

A

Constriction of the venous outflow by bulbospongiosus and ischiocavernosus

108
Q

What are possible causes of erectile disfunction?

How prevalent is it?

A

40% at 40, 50% at 50 etc
Rupture of there fibrous sheath around the corpora cavenosa and corpus sponginosum
Psychological
Meds eg. anti hypertensives, anti depressants
Vascular disease

109
Q

How can erectile dysfunction be treated?

A

Councilling

Viagra - inhibits phosphodiesterase 5 preventing breakdown of cGMP

110
Q

What is the arterial supply to the penis?

A

Superficial and deep arteries of the penis - branches of the internal pudendal off the internal iliac. Deep gives off helicine arteries.

111
Q

What is the arterial supply to the scrotum?

A

Posterior scrotal off the internal pudendal

Anterior scrotal off the external pudendal

112
Q

What occurs during the plateau phase of coitus in males?

A

Bulbourethral glands secrete an alkali fluid
Sperm propelled through epididymis, vas into prostate, mixed with secretions from seminal vesicles and prostate.
Some sperm may leak out

113
Q

What occurs at orgasm in the male?

A

Sns (L1 and L2) cause contraction of the glands and ducts, closure of the bladder sphincter and rhythmic contraction of the pelvic floor, perineal muscles and hip muscles propelling sperm out.

114
Q

How many sperm per ml ejeculate?

How many ml per ejeculation?

A

20-200 million per ml

2-4 ml per ejeculate

115
Q

What percentages of sperm should be healthy in an ejeculate?

A

More than 60% swimming

Less than 30% abnormal

116
Q

What do the seminal vesicles contribute to ejeculate?

A

Clotting factors
Fructose
Alkaline
60% volume

117
Q

What does the prostate contribute to ejeculate?

A

Acid
Proteolytic enzymes
Citric acid and acid phophotase
25% volume

118
Q

What occurs in the resolution phase?

A

Relaxation of muscles

Constriction of blood vessels

119
Q

What happens to ejeculate after it is deposited in the women?

A

The Proteolytic enzymes break down the clotting factors releasing the sperm
Capacitiation occurs where the mucosal surface breaks down the glycoprotein coat from the acrosmal region

120
Q

What is a sperms lifespan in the female?

What is an ovums lifespan?

A

Sperm 48-72 hrs (maybe up to 120 hrs)
Ovum 6-24 hrs
Thus fertile period for sex 3 days (maybe 5) before and 1 day after ovulation

121
Q

What days should be avoided in the rhythm method of contraception?

A

Days 7-16 post onset of menses. Assumes ovulation on day 12 - 14.

122
Q

What methods of barrier contraception are available?

A

Condom
Diaphragm - not complete barrier, holds sperm in vagina reducing survival time.
Cap

123
Q

Define infertility. What is the prevalence?

A

Inability to conceive in spite of regular unprotected intercourse for 1 year.
Effects 15% of couples
Only 5% still infertile after 2 years

124
Q

He can infertility be subdivided?

A

Primary - female has not been pregnant before

Secondary - female has been pregnant before (successful or not)

125
Q

What percentages of infertility are
Male problems
Female problems
Unexplained problems

A

Male - 20-25
Female - 45-60
Unexplained - 20-30

126
Q

What are the main groups of problems causing infertility?

A 
Coital problems (e.g. Erectile disfunction)
Anovulation (similar to amenorrhoea - inc. chemo/radio therapy)
Tubal occlusion (eg. Post PID)
Abnormal/absent sperm (can be due to testicle disease, brain disfunction, loss of control of bladder sphincter)
127
Q

When does the developing embryo embed fully into the uterine wall?

A

Day 9

128
Q

What does implantation of the embryo in the uterus require?

A

Breach of the epithelium
Establish villi for exchange
Anchor itself in with cytotrophoblasts

129
Q

What are primary placental villi?

A

Proliferated cytotrophoblast within syncytiotrophoblast

130
Q

What are secondary villi?

A

Cytotrophoblast covering proliferated chorionic plate mesoderm within syncytiotrophoblast

131
Q

What are tertiary villi? When do they begin to develop?

A

Mesenchyme core develops blood vessels. Cytotrophoblast reaches the outer of the syncytiotrophoblast creating a shell.

132
Q

What happens to tertiary villi in the second trimester?

A

Differentiation into spanning stem villi and side branched free villi

Regression of cytotrophoblast in villi reducing layers of diffusion

133
Q

What does the external layer of cytotrophoblast do in the second trimester? What is the resultant condition if this fails?

A

Invades the maternal blood vessels undergoing epithelial to endothelial transition. This widens the vessels lowering resistance.

Failure of this process results in eclampsia / preeclampsia

134
Q

What is the layer of the endometrium called:
Underneath the fetus
Atop the fetus
Opposite the fetus

A

Under - decidua basalis
Atop - decidua capsularis
Opposite - decidua parietalis

135
Q

How do the different decidua change as the fetus grows?

A

Decidua capsularis fuses with decidua parietalis

136
Q

What will twins share if they form from
separate zygotes
a single blastocyst with two inner cell masses
a single inner cell mass with two primitive streaks

A

Separate zygotes = separate amnions and placentas
Split inner cell mass = separate amnions and shared placenta
Two primitive streaks = shared amnion and placenta

137
Q

What are the functions of a placenta?

A

Exchange of gasses, nutrients, waste and IgG
Metabolism producing glycogen, cholesterol and TAGs
Hormone synthesis

138
Q

What hormones does the placenta produce?

A

human chorionic Gonadotrophin
Human chorionic somatomammotrophin (lactotrophin)
Human chorionic thyrotrophin
Human chorionic corticotrophin

139
Q

When does the placenta take over progesterone and oestrogen synthesis form the corpus luteum?

A

Around week 11

140
Q

What drugs easily cross the placenta?

When is the most vulnerable period?

A

Warfarin
Thalidomide
Alcohol
Anticonvulsants

Weeks 3-8

141
Q

What common infections can cross the placenta?

A 
Varicella zoster
Rubella
Treponema pallidum
Toxoplasma gondii
Cytomegalovirus
142
Q

What cvs changes occur in pregnant women?

A 
Increase blood volume (30-50%)
Increase sv, co and hr (35, 40 and 15%)
Decreased bp 
Decreased TPR 
Increased rbcs
143
Q

What is the likely cause of hypotension in a third trimester pt.

A

Ivc compression

144
Q

What changes happen to the urinary system in a pregnant pt?

A

Increased GFR, renal plasma flow and clearance of creatine, protein, uric acid, bicarbonate etc.
Dilation of ureters / urethra

145
Q

What effect does dilatation of the ureters and urethra have?

A

Decreased urine flow with increased risk of uti. This can lead to pyelonephritis and preterm labour.

146
Q

What maternal changes occur in the respiratory system?

A 
Diaphragm elevated
Chest diameter increases
O2 requirement raises
Minute vol increased
Tidal vol increased
RR stays the same
147
Q

What is the risk of pH changes in pregnant women?

A

Co2 from fetus and progesterone causes increased minute volume. This causes respiratory alkalosis.
Renal excretion of hco3 increases in compensation.
This removes a lot of the buffering capacity leaving pt at risk of metabolic acidosis (nb also has increased ketone production).

148
Q

Why do thyroid levels remain the. Same during pregnancy?

A

There is increases t3/t4 from hCT
However there is also increased TBG
So cancel each other out!

149
Q

What GI changes occur during pregnancy?

A 
Contents move (appendix to ruq) 
Relaxation of smooth muscle opens sphincters and slows contractions - gord and constipation
150
Q

What haematology changes occur during pregnancy?

A

Increased fibrin
Decreased fibrinogen
Therefore pro thrombotic state

Increased volume ++
Increased RBC +
Therefore physiological anaemia

151
Q

Immune system in pregnancy is…

A

Suppressed to reduce risk of rejection

152
Q

What is the O2 diffusion gradient set up across the placenta?

A

Marginally raised maternal pO2 - 14kPa

Very low umbilical vein pO2 - 4kPa

153
Q

How does the fetus cope with such a low umbillical vein pO2?

A

HbF is very high affinity so is 70% saturated at 4kPa
Fetal blood has a higher haemoglobin concentration (18-20g/dl)
Double Bohr effect - co2 diffuses to maternal circulation decreasing maternal affinity for O2 whilst fetal affinity increases.

154
Q

Why is HbF so high affinity?

A

It can’t bind 2.3bpg due to no beta chain

155
Q

Why does progesterone cause a higher respiratory minute volume?

A

Lower maternal co2 so a gradient is established at the placenta allowing removal of fetal co2

156
Q

How does fetal umbilical vein blood bypass the liver?

A

Ductus venosus

157
Q

What directs the flow of blood through the fetal right atria (IVC to foramen ovale and SVC RV)

A

Crista dividens

158
Q

How is the brains oxygenation ensured in the fetus

A

Blood from the LV diverts to the brain prior to the more deoxygenated blood from the ductus arteriosus joining and lowering oxygen saturation.

159
Q

How does fetal circulation rapidly switch to adult circulation?

A

Breath lowers pulmonary pressure allowing blood to flow through lungs
Raised pressure in left atrium as it returns closing foramen ovale
Increased O2 content of blood closes ductus arteriosus and ductus venosus due to wall contraction.

160
Q

Why does the fetus ‘breath’ amniotic fluid in utero? When does this start?

A

To condition resp muscles

From around 20 weeks

161
Q

What is the function of amniotic fluid?

A

Mechanical protection

Moist environment preventing dehydration

162
Q

How does amniotic fluid volume change during a pregnancy?

A

Slow increase initially (10ml at 8 weeks)
Rapid increase to term (1000ml at 38 weeks)
Drop after term (300ml at 42 weeks)

163
Q

How is amniotic fluid produced?

A

Early pregnancy - diffuses over skin (non-keratinised)
Late pregnancy - fetal urine

Kept low by swallowing into GI tract. Debris left forms meconium.

164
Q

Why may neonates be jaundiced?

A

Fetus unable to conjugate bilirubin thus excreted over placenta
Neonates may not be able to do this straight away thus can be jaundiced for a short time.

165
Q

When should fetal movements be felt? What is this called?

A

17 weeks

The quickening.

166
Q

How can fetal growth be measured?

A

Crown rump length
Biparietal diameter
Abdominal circumference

167
Q

What are usual symphysis fundal heights?

A

1cm from the symphysis per week - only palpable at week 20 +

168
Q

What would a normal biparietal diameter and a reduced abdominal circumference indicate?

A

Reduced fetal nutrient and O2 supply

169
Q

What is a normal birth weight?

A

2500 - 4500g usually 3500g.

170
Q

When does the resp system complete development? Why?

A 
Late:
Embryonic period - bronchopulmonary tree only
8-16 bronchioles develop 
16-26 respiratory bronchioles develop
Only after 26 weeks do alveoli develop

Because the lungs are not needed in utero

171
Q

Why are steroids beneficial in pre term deliveries?

A

Encourage surfactant production reducing chance of respiratory distress.

172
Q

When is the cvs definitive?

What should the heart rate be like?

A

Around 15 weeks

Variable! Constant indicates pathology

173
Q

What would happen in fetal kidney failure?

A

Oligohydramnios

174
Q

When does fetal movement begin (note NOT detectable)

A

Week 8

175
Q

What can the spacial location of the fetus be described as at term?

A

Lie - relationship of long axis of fetus and long axis of uterus
Presentation - which part of fetus is next to pelvic inlet
Position - what is the orientation of the presenting part

176
Q

What is the normal spacial location of the fetus at term?

A 
Longitudinal lie
Head presenting (cephalic) 
Head flexed (presenting smallest diameter)
177
Q

What initiates labour. What causes this?

A

High oestrogen to progesterone ratio caused by a fall in progesterone.
Unsure on cause of fall in progesterone

178
Q

What happens when labour is initiated by falling progesterone?

A

Placenta secretes progesterone which effaces cervix

Contractions amplify

179
Q

How does progesterone efface the cervix?

A

Decreases collagen density and aggregation of fibres

Increases gag

180
Q

How does progesterone influence contractions?

A

Increases calcium release from SR in myometrium causing contraction.

181
Q

What is the ferguson reflex?

A

Stretch of the uterus due to prostaglandin mediated calcium release triggers oxytocin release from the posterior pituitary
Oxytocin causes decreased threshold for action potential increasing contractility so feeding back positively causing more oxytocin release.

182
Q

How is labour ensured to be progressive?

A

Ferguson reflex is. Positive feedback so oxytocin levels rise
Brachystasis of muscles ensures advancing of fetus down birth canal.

183
Q

How does the fetus move as it progresses down the birth canal form the normal lie presentation and position?

A 
Internally rotates
Exits vagina (risk of tear)
Rotates
Extends to deliver shoulders
Pops out.
184
Q

What occurs in the third stage of labour?

A

Strong uterine contractions to cut placental blood flow and sheer off placenta and expel.

185
Q

What can be used to enhance uterine contraction in the third stage of labour?

A

Oxytocin drugs

186
Q

What are the three general catagories of causes of. Labour problems?

A

Power
Passage
Passenger

187
Q

Why do breasts enlarge at puberty?

A

Breast adipose tissue is oestrogen sensitive

188
Q

What changes occur to the breast during pregnancy?

A

Hypertrophy

Alveolar cells differentiate to be able to secrete milk

189
Q

What is initial breast milk called

What is in it

A

Colostrum

Protein
IgG

190
Q

What is in normal breast milk?

Where is each component from in the breast?

A 
Water 
Sugar (cytoplasm)
Fat (smooth ER)
Proteins (rER via golgi)
Minerals
191
Q

How is milk secretion controlled?

A

During pregnancy high progesterone to oestrogen inhibits secretion

On delivery fall allows secretion

Suckling inhibits dopamine increasing prolactin stimulating milk production for next time (thus low stimulation for one feed lowers amount in next)

Suckling and anticipation of suckling trigger oxytocin release. This contracts the myoepithelial cells squeezing the milk out of the breast.

192
Q

What are the benefits of breast feeding?

A

Fewer neonatal infections
Bonding
Decreased Ca breast risk

193
Q

What are the symptoms of breast disease?

A

Masses
Pain
Discharge
External changes (nipple deviation, crusting, puckered skin etc)

194
Q

What makes nipple discharge more / less worrying?

A

Unilateral / Bilateral
Spontaneous / Cyclical with menstrual cycle
Bloody or serous / Milky

195
Q

What makes breast pain more or less worrying?

A

Constant / cyclical

Localised / diffuse or bilateral

196
Q

What are some non neoplastic lesions of the breast?

A

Mastitis
Duct ectasia
Fat necrosis
Fibrocystic changes

197
Q

What are some neoplastic non malignant changes of the breast?

A

Fibroadenoma
Epithelial hyperplasia
Papilloma

198
Q

What is the borderline tumour of the breast?

What is it?

A

Philloides
A dark mass, lobed and clefted containing blood vessels.
Covered in epithelium
5% malignant

199
Q

What are the malignant tumours of the breast?

A

Ductal carcinoma in situ DCIS
Invasive ductal carcinoma no special type IDC NST
Invasive lobular carcinoma

200
Q

What is the commonest breast lesion?

What is the commonest invasive malignant breast lesion?

A

Fibrocystic changes

IDC NST

201
Q

What are the risk factors for Ca breast?

A 
Female gender
Uninterrupted menses (no kids)
Early menarche
Late menopause
COCP
No breast feeding
Obesity previous Ca breast
Family Hx of hereditary Ca breast (10%)
202
Q

What is mastitis?

A

Usually a staphylococcus aureus infection in nipple cracks during lactation/feeding. Causes erythema and pain in breast with systemic pyrexia. Can lead to abscess.

203
Q

Differentiate duct ectasia from DCIS

A

Duct ectasia is dilation and inflammation of the ducts near the nipple. Causes peri areolar masses and nipple discharge. Ducts contain macrophages and debris partially full.
DCIS has proliferated epithelial cells filling the lumen with central necrosis and calcification visible on a mammogram. Myoepithelial cells around duct are intact. If it reaches the nipple can cause Paget’s disease of the breast (red crusty skin)

204
Q

What are multiple small, mobile, smooth, pale breast masses likely to be?

A

Fibroadenomas

A mixed mass of stromal and epithelial cells

205
Q

What are risk factors for vulval carcinoma?

A 
HPV 16+18
Chronic irritation (lichen sclerosus, squamous hyperplasia)
206
Q

What is the precursor lesion for vulval cancer?

What is it?

A

VIN
Vulval intraepithelial neoplasm

Mitotic activity above the basal layer
Presents as scaly itchy red patches

207
Q

What types of vulval cancer are there?

A

Vulval squamous cell carcinoma - warty keatotic plaques
Basal cell carcinoma - pearly white pigmented nodule
Malignant melanoma
Adenocarcinoma

208
Q

What are risk factors for cervical cancer?

A 
HPV 16+18
Long term OCP use
Immunosuppression
Familial 
Early first and lots of pregnancies
209
Q

Why does ocp increase cervical cancer risk?

A

Causes cervical eversion exposing columnar epithelium to acid vagina.

210
Q

What are cervical precursor lesions?

A

CIN and CGIN
Cervical intraepithelial neoplasm and cervical glandular intraepithelial neoplasm.

CIN - graded 1-3 based on loss of differentiation. Can be detected at the surface as all cells abnormal.

211
Q

How are CIN cells highlighted at a colposcopy?

A

Acetic acid

212
Q

What types of cancer effect the cervix?

A 
SCC
adenocarcinoma 
Sarcoma
Neuroendocrine
Adenosquamous carcinoma
Lymphoma
213
Q

What are symptoms of cervical cancer?

A

Post coital or inter menstural bleeding

214
Q

Where does cervical cancer spread?

A

Uterus
Fistula to bladder/bowel
Lymph (para cervical, para aortic, pelvic)

215
Q

What is the prognosis of cervical cancer?

A

CIN grade 1 >99% cure

Overall 60%

216
Q

What types of endometrial tumours are there?

A

Type 1 - adenocarcinomas (oestrogen sensitive, locally invading)
Type 2 - adenocarcinomas (clear cell/serous)
Carcinosarcoma
Stromal sarcoma

217
Q

What are the risk factors for endometrial tumours?

A 
Nulliparous
Early menarch
Late menopause
Obesity
HRT
Diabetes
218
Q

What are benign myometrial tumors called? What are their features?

A

Leiomyoma (fibroid)
Smooth muscle benign tumour
Usually multiple
Oestrogen dependant so reduce post menopause
Schemes heavy/painful periods and infertility

219
Q

What are malignant myometrial tumours?

What do they not origionate from?

A

Leiomyosarcomas

Not derived from leiomyoma

220
Q

What types of ovarian tumours are there?

A

Epithelial
Sex cord stromal
Germ cell neoplasms

221
Q

What are epithelial ovarian tumours?

How do they present?

A

Serous, mucinous, endometrial or clear cell classifications
No precursors
Present late
Symptoms include mass, hormone disturbance, ascities and obstruction/perforation post metastasise

222
Q

What do sex cord stromal tumours often cause?

A

Precocious puberty as produce sex steroids

223
Q

What are the two germ cell neoplasms?

A

Mature teratoma (produces mix of mature tissues, hair, teeth etc) benign

Immature teratoma (primitive tissues) malignant

224
Q

What are the gestational tumours?

A

Hydatidiform mole - can penetrate myometrium and invade! Either 1 set of maternal and 2 of paternal dna or just 2 paternal dna

Choriocarcinoma - malignant trophoblast tumour

225
Q

Are primary liver tumours more commonly benign or malignant?

A

Malignant

226
Q

Where do secondary liver tumours usually origionate?

A 
GI tract (via portal) 
Breast
227
Q

What are some. Benign liver tumours?

A

Adenomas of. Hepatocytes or bile ducts

Hemangiomas

228
Q

What malignant tumours of the liver are there?

A

Hepatocellular carcinoma
Cholangiocarcinoma
Hepatoblastoma

229
Q

When might you perform an abdominal xray?

A

Acute abdo pain
Obstruction
Exacerbation IBD
Renal colic

230
Q

Why would a small bowel not usually be visible on an abdo X-ray?

A

Shows bowel gas patterns and due to fast transit there is little gas in the small bowel

231
Q

How can you differentiate the small and large bowel?

A

Small is central and contains valvulae conniventes

Large is peripheral and has houstral patterning

232
Q

What sizes of bowel on an X-ray would be worrying?

A

Small bowel greater than 3cm
Large bowel greater than 6cm
Cecum greater than 9cm

233
Q

What is the. X-ray sign for volvulus?

A

Coffee bean sign

234
Q

What could suggest inflammation on a abdo X-ray?

A

Mucosal thickening
Featureless colon
Bowel oedema
Thumb printing

235
Q

What calcifications may be of note on an abdo X-ray?

A

Appendicoliths
Renal calculi
Blood vessels
Pancreatitis

236
Q

When may a chest X-ray be useful in abdo diagnosis?

A

Erect chest X-ray showing gas under diaphragm - ? Perforation

237
Q

What can barium be used to show? When should an alternative be used?

A

Motility
Size
Backflow
Outpouchings

Should not be used in perforations - use a water soluble contrast!

238
Q

What is abdo ct used for?

A

Ca staging
Acute abdo investigation
Inflammatory bowel disease

239
Q

When is MRI particularly useful?

A

Hepatobillary and pancreatic disease

240
Q

What is the big disadvantage of ultrasound

A

User dependant results

PPE (12 decks)

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