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Repro Flashcards

1
Q

What makes the primitive gonad?

A

-Intermediate mesoderm of urogenital ridge and primordial cells

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2
Q

What are primordial germ cells?

A

-Specialised population of cells derived from the yolk sac which migrate along the dorsal mesentery and populate the mesodermal stroma of the gonads and are the ‘seed of the next generation’

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3
Q

How does the presence of SRY genes influence development?

A

-Drives development of the male causing differentiation of the gonads into testis, the duct system and the external genitalia

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4
Q

Describe what happens to mesonephric (wolffian) duct system in a male

A
  • Mesonephric duct makes contact with urogenital sinus and ureteric buds begin to sprout causing development of metanephros
  • The urogenital sinus expands as smooth muscle appears in the walls creating independant openings for UBs and MDs as it absorbs the structures
  • Presence of androgens causes development of prostate, spongy urethra and vas deferens
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5
Q

Describe what happens to mesonephric (wolffian) duct system in a female

A
  • Mesonephric duct makes contact with urogenital sinus and ureteric buds begin to sprout causing development of metanephros
  • The urogenital sinus expands as smooth muscle appears in the walls creating independant openings for UBs
  • Lack of adrogens leads to regression of MDs and the development of the female internal and external genitalia
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6
Q

Describe what happens to the paramesonephric (mullarian) ducts in females
Why is this prevented in males?

A
  • PMDs appear as invaginations of urogenital ridge
  • As they develop and elongate pulling the peritoneum with it, cranially they open into abdo cavity and caudally they fuse at the midline
  • This develops to form the upper 1/3 vagina, cervix, uterus and uterine tubes by regression of the septum which was created by fusion
  • Mullarian inhibiting hormone released from the testis prevents development of PDS in males
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7
Q

How does the external genitalia of a fetus begin? Describe how these develop into both the male and femaly external genitalia

A
  • Genital swellings, genital tubercles and genital folds
  • Males = GT elongates and GF fuse on the ventral surface. This forms spongy urethra and is influenced by DHT
  • Females = lack of DHT causes GT to remain and open into a vestibule instead of elongating
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8
Q

Describe the testicular descent

A
  • Begin on the posterior abdominal wall at urogenital ridge (retroperitoneal)
  • Evagination of processes vaginalis derived from parietal peritoneum creates a pathway for the testis to pass through the inguinal canal and into the scrotum
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9
Q

Describe ovarian descent

A

-Start on posterior abdominal wall at urogenital ridge and are tethered to labioscrotal folds via gubernaculum. Drawn down but do not pass through inguinal canal as they are obstructed by the uterus and uterine tubes

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10
Q

What 3 factors during meiosis ensure genetic variation?

A
  • Crossing over
  • Random segregation
  • Independent assortment
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11
Q

Briefly describe spermatogenesis How long does it take?

A
  • Germ cells line the seminiferous tubules of the testis and become more differentiated towards the lumen. They are finally released as spermatids and carried to the epididymis by sertoli cell secretions and peristalsis where they become motile ad are now spermatozoa
    1) Spermatogonium(2n) undergoes mitosis -> Ad (2n replenishes stock) and ap spermatogonium/1 spermocyte(2n)
    2) 1spermocyte undergoes meiosis I and forms 2x 2spermatocyte (1n) 3) both 2 spermocytes undergo meiosis II and form 4xspermatid
    4) spermatids released and transported to epididymis becoming spermatozoa
  • 74 days
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12
Q

What is the spermatogenic wave and cycle?

A
  • Spermatogenic wave refers to how spermatogenesis generations spiral around each other within a seminiferous tubule as different germ cells differentiate at different times
  • The spermatogenic cycle refers to the time it takes for the same stage of differentiation to appear at the same point in the wave. approxmately 16 days
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13
Q

What are the main constituents of sperm and where do they come from?

A
  • Mostly seminal vesicle secretions (70%) containing a’a, citrate, PGs and fructose
  • Prostate secretions (25%) containg proteolytic enzymes
  • Sperm - 200-500mill
  • Bulbourethral secretions to neutralise and lubricate distal urethra
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14
Q

What is sperm capacitation?

A
  • The final maturation step which occurs in the female genital tract
  • Glycoproteins are removed from sperm head which activates signalling pathways and allows the sperm to bind to the zona pellucida of the oocyte to initate the acrosome reaction
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15
Q

Describe oogenesis before birth

A
  • Primordial germ cells in gonads differentiate into oogonia and proliferate by mitosis
  • Selected oogonia enter meiosis I whilst others continue in mitosis
  • Those which enter meiosis I are primary oocytes and arrest in prophase I and become individually surrounded by follicular cells forming a primordial follicle
  • By mid-gestation max number of oogonia are reached and selection occurs. Majority of oogonia undergo atresia
  • All surviving oogonia enter meiosis I and halt in prophase I and become primordial follicles
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16
Q

Describe oogenesis when puberty begins, includint the different stages of maturation

A
  • Degeneration of primordial follicles has been occurring since birth
  • At puberty approx 15-20 primordial follicles begin to mature passing through preantral, antral and preovulatory stages of maturation. Out of this 20 only 1 will make it to ovulation due to ongoing atresia
  • Preantral = primordial follicle grows and granulosa cells form and begin secreting zona pellucida
  • Antral = fluid filled spaces appear between granulosa cells and eventually coalesce to form an antrum. Theca interna/externa develop and this is now secondary follice
  • Preovulatory = Under influence of FSH and LH meiosis I is completed to produce 2 haploid cells of unequal size. Meiosis II begins but arrests before ovulation and is only completed upon fertilisation. The secondary follicle is now called the graafian follicle.
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17
Q

What induces ovulation and how?

A

-LH surge causes an increase in collagenase activity inside the ovary-> matrix breakdown in graafian follicle and extrusion of oocyte by PG-induced muscular contraction

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18
Q

What is the corpus luteum? What is its function? What happens to it?

A
  • The granulosa and theca interna of the graafian follicle become vascularised under the influence of LH and begin to secrete progesterone and oestrogen
  • The hormones produced from CL stimulate the uterine mucosa to enter the secretory stage and prepare for implantation
  • If no fertilisation occurs within 14 days the CL undergoes apoptosis and regresses (corpus albicans) and decreased progesterone levels induce menses, if fertilisation occurs hCG maintains the CL until placenta developed (corpus luteum gravidatis)
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19
Q

What 6 hormones does the anterior pituitary secrete?

A
  • LH
  • FSH
  • TSH
  • ACTH
  • GH
  • Prolactin
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20
Q

How does the ant pituitary communicate with hypothalamas?

A

-Superior hypophyseal artery

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21
Q

Describe how the hypothalamic releasing hormones are released in to the superior hypophyseal artery? How do they exert their effect at the pituitary?

A
  • There is a basal secretion which is pulsatile in nature and is tied to the biological clock and external stimuli such as light and dark
  • Also under negative feedback control from circulating hormones
  • Bind to specific cell surface receptors and induce a second messenger which leads to the production of the corresponding hormone
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22
Q

Which hormone controls the secretion of FSH and LH? In what rhythm is it released?

A
  • Gonadotrophin releasing hormone

- Pulsatile every hour

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23
Q

How do LH and FSH exert their effects on a molecular level at the gonad?

A

-Bind to GPCRs at gonads which are coupled to Gas -> increased in AC activity -> increased cAMP -> Increased PKA -> leads to the production of the corresponding sex steroids

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24
Q

Under which hormonal control is the LH surge? Explain how this works?

A
  • High titres of oestrogen alone

- High titres of oestrogen decrease the threshold level of GnRH needed at the anterior pituitary in order to secrete LH.

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25
Q

How do moderate titres of oestrogen with progesterone modify the GnRH pulses?

A

-Oestrogen reduces the amplitude of pulses and progesterone reduces frequency

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26
Q

Which cells specifically do FSH and LH target in both the male and female? What do each of the cells produce?

A
  • Male = FSH targets sertoli cells causing ABG and inhibin secretion, LH targets leydig cells causing testosterone secretion
  • Females = FSH targets granulosa cells causing inhibin secretion and aromatase production. LH targets theca cells causing androgen production
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27
Q

What is the function of androgen binding globulin?

A

-binds to testosterone to keep it within the seminiferous tubule

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28
Q

What is the function of inhibin?

A

-Selectively inhibits FSH production

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29
Q

What will happen to spermatogenesis if testosterone levels increase? how is this prevented?

A

-Increase rate of spermatogenesis but also increase production of inhibin which will bring the rate back to normal

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30
Q

What is the dominant hormone in the luteal phase? When does production of this hormone begin and why? What phase does this mark the beginning of?

A
  • Progesterone
  • Begins just after ovulation, granulosa cells develop LH receptors and the remnants of the graafian follice undergoes leutinisation to produce corpus luteum.
  • Luteal phase
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31
Q

Describe the follicular phase of the ovarian cycle.

A
  • Small group of follicles are recruited independent of extragonadal signals
  • No sex steroid hormones means the hypothalamus is not inhibited and causes slow release of FSH and LH which drives follicular development
  • FSH binds to granulosa cells causing development by mitosis resulting in the production of inhibin and aromatase.
  • Inhibin inhibits the secretion of FSH to prevent development of additional follicles
  • Theca interna appears and is stimulated by LH to produce androgens
  • Androgens converted to oestrogen by aromatase
  • Oestrogen has +ve feedback on HPA and increased GnRH and Inhibin levels leads to LH surge
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32
Q

Describe the luteal phase of the ovarian cycle

A
  • Remnants of the graafian become vascularised and luteinised and form the corpus luteum
  • CL secretes oestrogen and progesterone which have a -ve feedback on HPA and prevent the production of FSH and LH -> system held in pause.
  • Oestrogen and progesterone stimulate secretory phase of uterine cycle to prepare the uterus for implantation
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33
Q

Describe the proliferative phase of the uterine cycle. When does this occur?

A
  • Oestrogen produced by the dominant follicle stimulates the endometrium of the uterus to proliferate
  • Occurs at the same time as the follicular phase of the ovarian cycle
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34
Q

Describe the secretory phase od the uterine cycle. When does this occur?

A
  • Progesterone produced by the corpus luteum causes the endometrium to become highly vascular, increases uterine secretions and decreases the motility of uterine smooth muscle
  • Occurs at the same time as the luteal phase
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35
Q

Summarise the actions of oestrogen during the follicular phase

A
  • Drives follicular development by increasing levels of GnRH, FSH and LH
  • Stimulates the uterine endothelium to proliferate
  • Stimulates think alkaline cervical mucus
  • Increases motility of uterine tube
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36
Q

Summarise the actions of progesterone during the follicular phase

A
  • Causes negative feedback of HPA putting cycle in pause
  • Stimulates vascularisation of endometrium
  • Decreases motility of uterus and uterine tubes
  • Stimulates acidic mucus
  • Causes changes in mammary tissue
  • Increases body temperature
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37
Q

What is the normal length of a menstrual cycle? Why can it vary?

A
  • 21 to 35 days

- Varying length in follicular cycle becuase luteal phase is constant +/- 2 days due t lifespan of CL

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38
Q

Give 3 causes of menorrhagia

A
  • Hypothyroid
  • Abnormal clotting (idiopathic thrombocytopenia)
  • Fibroids (benign tumours of the endometrium increases bs to uterus)
  • Iatrogenic (copper coil)
  • PCOS
  • Obesity (increases oestrogen)
  • Progesterone contraception
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39
Q

Give 3 causes of amenorrhoea

A
  • Pregnancy
  • Anorexia (low oestrogen)
  • Primary (absent ovaries, primary ovarian failure, excessive prolactin)
  • Cryptomenorrhoea (cervical stenosis, imperforate hyman)
  • Tumours
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40
Q

Define thelarche, pubarche, menarche and adrenache. State the order in which they occur in girls and boys

A
  • Thelarche -> development of breast
  • Pubarche -> development of axillary and pubic hair
  • Menarche -> first menstrual period
  • Adrenarche -> onset of increased androgen secretion
  • Girls = thelarche, adrenarche, pubarche then menarche
  • Boys = genital development, adrenarche, pubarche, spermatogenesis
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41
Q

Describe the difference between the growth spurt in males and females

A

-Earlier and shorter in girls due to oestrogen causing closure of the epiphyseal growth plates

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42
Q

What is the typical age of onset of puberty for males and female? What factors influence this in females?

A
  • Males = ~12.5 years
  • Females = ~11.5 years
  • For females there is a critical weight of 47kg due to the relationship between adipose tissue and oestrogen production. (obese children start early)
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43
Q

Describe the hormonal changes and consequences at the start of puberty in a male

A
  • From about 10 years old FSH and LH slowly begin to rise and spermatogenesis and androgen secretion begin at a very low level (adrenals secrete androgens but too low to initiate puberty)
  • At a sufficient level androgens stimulate growth of prostate, testis and drive development of secondary sexual characteristics
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44
Q

Describe the hormonal changes and consequences at the start of puberty in a female

A
  • From about 8 years old FSH and LH slowly begin to rise and oestrogen begins to be produced.
  • At sufficient levels oestrogen feeds back on HPA axis and menses is initiated via the LH surge
  • Oestrogen also drives progression of secondary sexual characteristics of growth of internal and external genitalia and subcut fat distribution
  • Adrenals increase androgen production and this drives pubarche
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45
Q

What effect do androgens have on bone and muscle?

A

-Cause retention of minerals to stimulate growth

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46
Q

What is precocious puberty? Give some causes

A
  • Onset of puberty before 8 in girls and 9 in boys
  • Idiopathic
  • Gonadotropin dependant causes eg hormone secreting tumour (rare)
  • Gonadotropin independent causes eg meningitis
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47
Q

What is precious pseudopuberty? Give some causes

A
  • Development of secondary sexual characteristics independent of HPG axis
  • Alternative source of sex steroids eg anabolics
  • Congenital adrenal hyperplasia
  • Choriocarcinoma of gonads
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48
Q

Define delayed puberty. Give some causes

A
  • Initial physical changes of puberty not present by 13 in girls (or amenorrhoea at 16) or 14 in boys or that the length of puberty is greater then 5 years
  • Hypergonadotrophic hypogonadism causes (gonadal failure eg turners, atresia or chemotherapy)
  • Hypogonadotrophic hypogonadism causes (hypothalamic/pituitary lesions)
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49
Q

Briefly describe the menopause and its effects

A
  • Follicular phase begins to shorten and ovulation can be early or absent as primary follicles begin to run out
  • Eventual cessation of the menstrual cycle for at least 12 months due to lack of follicles, produces a huge decline in oestrogen levels and a concomitant rise in FSH and LH
  • Uterus endometrium regresses and myometrium shrinks, Reduced vaginal tone, involution of breasts, skin changes, reduction in pelvic tone, risk of osteoporosis as bone density decreases
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50
Q

Describe the blood supply and venous drainage of the testis

A
  • Teasticular arteries straight from the abdominal aorta

- R testicular vein -> IVC, L testicular vein -> L renal vein -> IVC

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51
Q

What does the spermatic cord contain?

A
  • Vas deferens
  • Testicular artery, cremasteric artery, artery to vas deferens
  • Genitofemoral nerve
  • Lymphatics
  • Surrounded by Pampiniform plexus
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52
Q

What is the pampiniform plexus?

A

-A sophisticated drainage system which acts as a heat exchanger as spermatogenesis is optimal at a few c below body temp

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53
Q

Describe the layers of the testis from superficial to deep

A
  • Skin
  • Subcut tissue
  • Dartos fascia
  • External spermatic fascia (external oblique apon)
  • Cremasteric muscle and fascia
  • Internal spermatic fascia
  • Tunica vaginalis (peritoneum)
  • Tunica albuginea (fibrous capsule)
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54
Q

Define the terms hydrocoele, haematocoele, varicocoele and spermatocoele

A
  • Hydrocoele = serous fluid in tunica vaginalis
  • Haematocoele is blood in tunica vaginalis
  • Varicocoele is swollen varicosities of the pampiniform plexus (aching pain)
  • Spermatocoele is an epididymal cyst
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55
Q

How are the testis innervated?

A

-Anterior by lumbar plexus and posterior by sacral plexus

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56
Q

Describe the course of vas deferens

A

-Leaves epididymis-> spermatic cord -> inguinal canal -> deep inguinal ring -> pelvis side wall -> passes between bladder and ureter -> joins with seminal vesicle to form ejaculatory duct

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57
Q

Describe the anatomical location and the organisation of the prostate. Explain where BPH and Prostate Ca occur and what the consequences of this are

A

-Fibromuscular gland which lies between the bladder and the rectum
-Divided into zones:
Central zone formed by the wolffian ducts and peripheral zones formed by the UGS
-BPH occurs in the central zone so enlargement causes compression of the internal urethral orifice which is in contact with the anterior surface
-Prostate cancer occurs in the peripheral zones so considerable enlargement needs to occur before it creates any symptoms so it presents later increasing the chance of spinal/brain mets

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58
Q

Describe the internal structure of the penis

A
  • Pair of copora cavernosa dorsally (Erectile tissue)

- Corpus spongiosum ventrally (spongy tissue surrounding urethra)

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59
Q

What arteries supply the penis?

A

-Internal pudendal and internal iliac

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60
Q

What are the functions of bulbospongiosus and ischiocavernosus?

A
  • Bulbospongiosus wraps around root of penis and helps expel residual urine
  • Ischiocavernosus compresses veins to help maintain erection
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61
Q

Describe the anatomical landmarks of a pelvis and state which factors make a gynaecoid pelvis

A
  • Iliac crest
  • Linea terminalis (entry to true pelvis)
  • Ischial spine
  • Ischial tuberosity
  • Sacrum
  • Coccyx
  • Round intel, straight side walls, not prominent ischial spines, curved sacrum, subpubic arch >90
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62
Q

What are pelvic conjugates?

A

-Distances between the anterior and posterior pelvis:
Obstetric from sacral prominance to pubic symphysis
Diagonal from sacral prominence to inferior pubic symphysis
Anatomical from sacral prominance to superior pubic symphysis

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63
Q

Name the anatomical parts of the uterine tubes and uterus

A
  • Abdominal ostium, fimbrae, infundibulum, ampulla, and uterine ostium
  • Fundus, isthmus, body, cervix
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64
Q

What is the broad ligament? Describe its sections

A
  • Transverse fold of peritoneum which contains the uterine tubes and ovarian vessels
  • Split into mesometrium which is the entire ligament
  • Mesosalpinx is the section of the broad ligament covering the uterine tube
  • Mesovarium is the section covering the ovary
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65
Q

What is the round ligament?

A
  • Former gubernaculum which attaches ovaries to labia majora folds through inguinal canal.
  • Made by round ligament of the ovary which reflects off the side wall of the uterus and becomes round ligament of uterus
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66
Q

What does the suspensory ligament contain?

A

-Ovarain vessels

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67
Q

What is meant by the uterus being anteverted and anteflexed?

A
  • Anteverted refers to the angle of the between the axis of the cervix and axis of the vagina
  • Anteflexed refers to the angle between the axis of the uterus and axis of the cervix
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68
Q

What are the main 2 ligaments which provide visceral support to the uterus?

A
  • Transverse cervical -> Thickening at the base of the broad ligament to provide lateral stability of cervix
  • Uterosacral -> Opposes pull of round liganent
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69
Q

Describe the innervation to the vagina

A
  • Inferior 1/5 somatic innervation from pudendal

- Superior 4/5 and uterus from uterovaginal plexus

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70
Q

What are bartholin glands?

A

-Greater and lesser vestibular glands

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71
Q

Give 3 possible reasons for the increasing incidence of STIs

A
  • Better diagnostic equipment
  • Better awareness of screening
  • True increase in transmission due to changing sexual and social behaviours
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72
Q

How is a diagnosed STI managed?

A
  • Short course/single dose of antibiotics
  • Screen for co-infection
  • Contact tracing
  • Sexual health education
  • Advice on contraception
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73
Q

What STI is caused by HPV? What strains of HPV are most likely to cause this STI? With what are strains 16 and 18 associated? How is the STI treated?

A
  • Anogenital warts
  • Strains 6 and 11
  • Cervical cancer
  • Spontaneous resolution within 2 years, cryotherapy
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74
Q

What STI does chlamydia trachomatis cause? What type of bacteria is it?What symptoms can it cause? How is it diagnosed? What is the treatment?

A
  • Chlamydia
  • Obligate intracellular anaerobe (needs special culture medium)
  • Urethritis, epididymitis/cervicitis, prostatits/salpingitis but often asymptomatic
  • Swabs subjected to NAAT and 1st void urine to NAAT
  • Azithromycin or doxycycline. Erythromicin in children
75
Q

What STI does herpes simplex virus cause? What symptoms does it cause? Whch strain is associated with the STI? Is the virus curable? How is it diagnosed? How is it treated?

A
  • Herpes
  • Painful mucosal ulcerations, inguinal lymphadenopathy and dysuria
  • HSV 2
  • Remains dormant in dorsal root ganglia causing recurrent outbreaks
  • PCR of vesicle fluid
  • Aciclovir for first and serious outbreaks
76
Q

What STI does Neisseria Gonorrhoeae cause? What type of bacteria is it?What symptoms can it cause? How is it diagnosed? What is the treatment?

A
  • Gonorrhoeae
  • Gram neg intracellular diplococcus
  • Urethritis, pharyngitis, discharge or asymptomatic
  • Swab or urine NAAT
  • Ceftriaxone and azithromycin
77
Q

What STI does Treponema Pallidum cause? What type of bacteria is it? With who is it associated? What symptoms can it cause? How is it diagnosed? What is the treatment?

A
  • Syphilis
  • Spirochete
  • Males and MSM
  • Multistage disease ->1= indurated painless ulcer, 2 = fever, rash ulcerations, lymphadenopathy, 3= latent and symptom free for years, 4=neurosyphilis -> tabes dorsalis, cardiovascular syphilis and gummas
  • ELISA
  • IM penecillin
78
Q

What STI does Trichomonas Vaginalis cause? What type of organism is it?What symptoms can it cause? How is it diagnosed? What is the treatment?

A
  • Trichomonas Vaginitis
  • Flagellated protozoa
  • Thin, frothy, offensive discharge, irritation and dysuria,
  • Wet preperation and culture
  • Metronidazole
79
Q

What are the causes of bacterial vaginosis? What symptoms can it cause? How is it diagnosed? What is the treatment?

A
  • Gardnerella spp. anaerobes
  • Scant fishy discharge
  • Clinically by pH of urine and smell and a gramstain of discharge
  • Metronidazole
80
Q

What is vulvovaginal candisiasis? What causes it? What are the symptoms? Give some risk factors, how is it treated?

A
  • Vaginal thrush
  • The fungus candida albicans
  • Profuse, white, itchy, lumpy discharge
  • Antibiotics, oral contraceptives, pregnancy, steroids, diabetes
  • Topical azoles eg clotrimazole
81
Q

What makes up the pelvic floor and what are its functions?

A

1) Pelvic diaphragm = levator ani, coccygeus and fascia
2) Perineum
- Contribute to continence and resist rises in intrabdominal pressure

82
Q

Describe the muscles of the pelvic diaphragm

A

-Levator ani made up of puborectalis, pubococcygeus and ileococcygeus and coccygeus

83
Q

What is the perineum? How is it split into anterior and posterior? How is it innervated?

A
  • A diamond shaped area mared by the coccyx, ischial tuberosities and the pubic symphysis
  • An imaginary line spilts the perineum into urogenital triangle and anal triangle
  • S2,3,4 pudendal
84
Q

Describe the contents within the anterior peritoneum (urogenital triangle)

A
  • Contains deep transverse perineal muscle and the external urethral sphincter between two layers of fascia. There is the urogenital hiatus to allow passage of the vagina and/or urethra
  • The inferior layer of fascia is known as the perineal membrane and provides structural support
  • Below the perineal membrane there is the bulbospongiosus, the ischocavernosis and the superficial transverse perineal muscle
85
Q

What is the perineal body?

A

-Fibromuscular junction between anterior and posterior perineum to which many muscles attach

86
Q

Describe the contents of the posterior perineum

A
  • External anal sphincter
  • Puborectalis part of levator ani
  • Anus
  • Ischiorectal fossae
87
Q

What is the clinical significance of the ischiorectal fossae?

A

-Infection can track to the glutes

88
Q

How does the pelvic floor aid continence?

A
  • Exerts pressure on sphincters in order to resist changes in intrabdominal pressure
  • Weakness of these muscles pushes bladder/anus through hiatus leading to incontinence
89
Q

What is PID?

A

-The result on an infection extending from the endocervix causing and vagina causing inflammation of pelvic structures including the endometrium, salpinx and ovaries. May lead to tubo-ovarian abscesses or adhesion. Often polymicrobial

90
Q

What is a tubo-ovarian abscess?

A

-Inflammatory exudate fills salpinx causing inflammation to extend to serosa and pus to oose from the tube attaching the tube to the side wall causing a blockage

91
Q

Give some possible complications of PID

A
  • Infertility

- Ectopic pregnancy, Fitz-hugh-curtis, reiter syndrome

92
Q

What is Fits-hugh-curtis syndrome?

A

-PID which spreads to the liver causing liver adhesions

93
Q

What is reiters syndrome?

A
  • Disseminated chlamydial disease

- Conjunctivitis, Urethritis and arthritis

94
Q

What are the symptoms of PID?

A

-Fever, lower abdo pain, dyspareunia, discharge, bleeding, sepsis

95
Q

Give some differential diagnoses of PID

A
  • Pyelonephritis
  • Appendicitis
  • UTI
  • Ectopic pregancy
96
Q

What happens to sperm during ageing?

A

-Decreases in quantity and quality

97
Q

What is the purpose of PGs in semen?

A

-Increase motility of female genital tract

98
Q

What happens in males during the sexual response?

A
  • Activation of parasymp NS causes penile erection due vasodilation of BVs
  • contraction of ischiocavernosus maintains erection
  • Activation of sympathetic nervous system causes ejaculation but have cortical control
99
Q

What happens in females during the sexual response?

A
  • Seceretions for lubrication, clitoris engorges, inner 2/3 vagina lengthens and increases in tone, uterus elevates, breasts increase n size and nipples become erect
  • Orgasmic platform in lower 1/3 vagina contracts rhythmically
100
Q

What happens to the vagina with age?

A

-Decreased lubrication, decreased venocongestion, decreased desire, loss of elasticity and decreased rhythmic contractions

101
Q

Describe what happens from deposition of sperm to fertilisation

A

-Sperm has a hard life and has to break its way through the thick cervical mucus covering the external os. Once in the female genital tract it can survive 5 days. It makes its way up the uterine tube and if it happens to bump into an oocyte it has to make its way through the corona radiata and then the zona pellucida. It takes 300 other soilders to dispers the ZP. When reaching the zona pellucida the acrosomal reaction begins ane enzymes digest ZP to make a path for fusion of sperm with oocyte pm

102
Q

Give 4 reasons for sexual dysfunction

A
  • Psychological
  • Drugs eg statins, OCP
  • Vascular -> atherosclerosis (le riche)
  • Physical damage
103
Q

How is polyspermy blocked after fertilisation?

A
  • Fast block -> Electrical charge in oocyte causes depolarisation of PM
  • Slow block -> Exocytosis of cortical granules cause formation of zona pellucida again
104
Q

What is syngamy?

A
  • Oocyte completes meiosis II and expels polar body

- Sperm and oocyte pronuclei fuse with each other this is sungamy

105
Q

Define infertility. Give some causes

A
  • Failure to conceive within 1 year
  • Coital problems
  • Anovulation, PCOS, endometriosis, low sperm count
106
Q

Describe the hormone levels in the following conditions:

i) Menopause
ii) Ovarian failure
iii) HP failure
iv) PCOS

A

i) high LH/FSH low oestrogen
ii) High LH/FSH low oestrogen
iii) All low
iv) increased ratio of LH:FSH and normal oestrogen

107
Q

How can ovulation be induced clinically?

A
  • Anti-oestrogen eg clomiphene -> prevents oestren neg feedback on HPA causing increased GnRH and LH/FSH = ovulation
  • Gonadotrophin analogues
108
Q

When is the pre-embryonic, embryonic and fetal period?

A
  • Pre-embyonic = 1-2 weeks
  • Embyonic = 3-8 weeks
  • Fetal = 8+ weeks
109
Q

What happens to the conceptus immediately after fertilisation to implantation?

A
  • Conceptus undergoes cleavage and begins to divide to produce a morula
  • Morula undergoes compaction and an inner cell mass and outer cell mass is produced
  • The outercell mass develops into the syncytiotrophoblast and cytotrophoblast
  • The inner cell mass develops into the epiblast and the hypoblast forming the amniotic cavity and primitive yolk sac respectively
  • Attaches to uterine epithelium high on the posterior uterine wall over embryonic pole and implants into endometrium
  • Implantation defect fixed by fibrin plug
110
Q

Describe how the syncytioblast develops to initially set up haematological exchange with the mother

A

-Syncytioblast develops and invades maternal sinusoids forming lacunae within the syncytioblasts and uroplacental circulation begins

111
Q

What is gastrulation? V briefly describe it

A
  • The establishment of the three germ layers from the bilaminar disk in the embryo
  • Primitive streak appears on epiblast and cells migrate into the streak and differentiation of the 3 germ layers occurs
112
Q

What happens to the amniotic sac and yolk sac after implantation?

A

-The yolk sac disappears and the amniotic sac enlarges and binds to the chorion

113
Q

What happens to the placental membrane throughout gestation?

A

-It becomes progressively thinner

114
Q

Describe the formation and progession of placetal villi as a unit of exchange with the mother

A
  • Primary villi form due to proliferations of the cytoblast forming projections into syncytioblast.
  • Chorionic villi regress except from in area of placenta. Here they develop into secondary villi during gastrulation as they become infiltrated by mesenchymal cells
  • Develop into tertiary villi when the mesenchymal core differentiates into foetal vessels.
115
Q

What is the purpose of decidual cells?

A

-They are incorporated into the placenta and ensures invasion o f the conceptus during implantation is appropriate -> decidua basalis

116
Q

Why can uncontrolled invasion occur in ectopic pregnancy?

A

-Only the uterine endometrium has pre-decidual cells which monitor invasion

117
Q

What is pre-eclampsia?

A

-Inadequate remodelling of the spiral arteries in that the lining is not replaced by syncytioblast and remains maternal lining producing a highly resistant vascular bed. Requires a high blood pressure to over come the resistance which is dangerous for mother and baby

118
Q

What are the 3 ways in which Monozygotic twins are produced?

A
  • Cells split at morula stage and have 2 blostocyst cavities, 2 placentas
  • Two bilaminar discs appear producing 2 amnoitic cavities 1 placenta
  • 2 primitive streaks appear producing one amnion and 1 placenta
119
Q

How is the placenta anchored to decidua basalis? What are intervillous spaces?

A
  • The tertiary cytotrophoblastic villi develop to form a single layer shell around the syncytiotrophoblast and anchor it to the decidua basalis
  • The spaces between the chorionic villi are intervillous spaces and are filled with maternal blood
120
Q

How does deoxygenated blood exchange with the placenta?

A

-Paried umbilical arteries branch into chorionic villi and waste products diffuse into the intervillous space across the placental membrane

121
Q

What makes up the placental membrane? How does it change between the 1st trimester and term?

A
  • Foetal capillary
  • cytotrophpblast
  • Syncytiotrophoblast
  • Placental barrier thins during gestation to optimise diffusion
122
Q

What is the metabolic function of the placenta?

A

-To synthesis glycogen, cholesterol and FAs

123
Q

What endocrine functions does the placenta have?

A
  • Secrete progesterone in order to maintain the HPA in pause

- Secretes Hcg to support corpus luteum during establishment of placenta

124
Q

What is a molar pregnancy?

A

-Pregnancy which only contains outer cell mass eg placenta

125
Q

What is the function of human Placental Lactogen?

A

-Increase glucose availability to featus

126
Q

What is a choriocarcinoma?

A

-Malgnancy of the chorion

127
Q

Describe haemolytic disease of the newborn

A
  • Regards Rh blood group incompatibility between fetus and mother
  • Occurs on second child
  • If mother exposed to 1st childs blood during delivery who is Rh+ she will make anti-Rh+ve antibodies
  • If a future child is Rh+ve the IgG antibodies can cross the placenta and begin attacking the foetus
128
Q

Describe the CVS changes which occur in a mother during pregnancy

A
  • 50% increase in blood vol (therefre increase SV, HR=CO)
  • Decreased TPR due to progesterone causing SM relaxation
  • Decreased BP in 1 and 2, normal in 3
129
Q

Describe the renal changes which occur in a mother during pregnancy

A
  • Increased GFR causing increased creatinine clearance and decreased urea in blood
  • Incresed urinary frequency
130
Q

Describe the Respiratory changes which occur in a mother during pregnancy

A
  • Increased tidal volume

- Increased resp rate due to high CO2 and progesterone

131
Q

Describe the metabolism changes which occur in a mother during pregnancy

A
  • Increase insulin resistance and a switch to gluconeogenesis-> glucose spared for facilitated diffusion across placenta. Caused by progesterone and hPL
  • Increased lipolysis
  • Increased T3/T4/TBG
132
Q

What is gestational diabetes? Give some risk factors

A
  • Hyperglycaemia due to improper insulun response which doesnt persist post-partrum
  • PCOS, FHx T2DM, obesity, advancing age
133
Q

Describe the GI changes which occur in a mother during pregnancy

A
  • Constipation due to SM relaxation by progesterone
  • Displacement of viscera
  • Biliary tract stasis
134
Q

Describe the haematological changes which occur in a mother during pregnancy

A
  • hypercoaguable due to increase in fibrinogen and clotting factors and vascular stasis due to progesterone
  • Anaemia
135
Q

How are the gas gradients achieved between mother and baby?

A

1) Increased maternal 2,3-BPG due to progesterine promotes T state and O2 dissociation
2) Foetal Hb has 2a and 2g chains. g chains have a lower affinity for 2,3-BPG meaning HbF has higher affinity for O2 then HbA
3) Double bohr effect -> CO2 passes into intervillous blood from fetus -> Decreased local pH promoting T state -> more O2 given up. The loss of CO2 from foetal blood promotes the R state -> O2 rapidly taken up into foetal blood
4) Progesterone driven hyperventilation causes more CO2 to be blown off causing a gradient between foetal and maternal blood
5) Double haldane effect -> As maternal blood gives up O2 can take up more CO2 and vice versa

136
Q

Describe the foetal response to hypoxia

A

1) Increased HbF
2) Redistribution of flow to heart and brain
3) Slowing of foetal HR to reduce O2 demand

137
Q

What hormones are required for foetal growth?

A
  • Insulin
  • IGF 1/2
  • Leptin
138
Q

What is the main hormone present in T1 involving growth of the foetus? what type of growth is involved?
What is the main hormone present in T2/3 involving growth of the foetus? what type of growth is involved?

A
  • IGF II
  • Nutrient independent
  • IGF I
  • Nutrient dependant
139
Q

What type of growth occurs between week 0-20? 20-28? 28?-

A
  • Hyperplasia
  • Hyperplasia and hypertrophy
  • Hypertrophy
140
Q

What is the function of the amniotic fluid? How much amniotic fluid at 8 weeks compared to 38?

A
  • Protection and lung development

- 10ml vs 1L

141
Q

Why does the amniotic fluid decrease post EDD?

A

-Placental senescence

142
Q

Describe the circulation of amniotic fluid

A

-Produced by the foetal kidneys and recycles by the lungs, GIT and placenta

143
Q

What is lanugo and vernix caseosa?

A
  • Both mechanisms of protecting neonates skin
  • lanugo is fine hairs
  • Vernix caseosa is white, cheese like substance
144
Q

How does the foetus handle bilirubin?

A

-Placenta handles bilirubin as liver immature

145
Q

What is the majority of the babys length at the beginning of the foetal period?

A

-Head is half CRL

146
Q

How is the foetus assessed during pregnancy?

A
  • Foetal movements -> reported by mother
  • Regular measurements of symphysis fundal height
  • USS
147
Q

How is the foetal age estimated in T1?

A
  • Last menstrual period (prone to inaccuracy)
  • Crown Rump Length by USS (becomes inaccurate further into pregnancy due to variation in size)
  • Biparietal diameter, abdominal circumference and femur length
148
Q

What is the average birthweight? What weight is suggestive of growth restriction/macrosomia?

A
  • 3500g
  • <2500g = growth restriction
  • > 4500g = macrosomia
149
Q

Desribe the development of the resp tract in the foetus. Why can survival of premature birth depend on the development of the resp tract.

A
  • One resp diverticulum in embryonic period then no further development until foetal period
  • Over the remaining weeks there is slow development of the bronchioles, resp bronchioles and alveoli
  • Surfactant is produced late in gestation when the t2 pneumocytes develop. Without surfactant Neonates get respiratory distress syndrome.
150
Q

How is respiratory distress syndrome avoided if there is a known premature birth?

A

-Glucocorticoid injection in the mother to stimulate surfactant production

151
Q

Why is amniotic fluid crucial for lung development?

A

-Allows baby to do breathing movements and develop the musculature needed for life

152
Q

Give 2 causes of oligohydramnios

A
  • Placenta insufficiency

- Foetal kidney atresia

153
Q

When is pre-term birth?

A

-Before 36 weeks

154
Q

What is classed as post-term?

A

-42+ weeks

155
Q

Describe the stages of labour

A
  • Onset = increased prostaglandins and cervix ripens, uterine contractions increase in amplitude via ferguson reflex, brachystasis and dilation of cervix
  • 2= urge to push initiated as presenting part appears in birth canal (crowning), head flexes and rotates internally, head delivered, externally rotates and extends, shoulders rotate and deliver
  • 3=Hard contraction of the uterus causing sheering of the placenta and delivery within 10 mins
156
Q

What is the lie, presentation and vertex?

A
  • Lie is the relationship of the long axis of the baby to the uterus (normally flexed)
  • Presentation refers to which part of the baby is adjacent to pelvic inlet (usually head)
  • Vertex refers to the long axis of the baby in relation to the presenting part
157
Q

How is the birth canal canal created in labour?

A
  • Softening of ligaments of pelvis by MMPs
  • Expansion of soft tissues via cervical ripening -> reduction in collagen and increase in ECM tiggered by prostaglandins
158
Q

Describe contractions throughout gestation

A

-Pacemaker cells cause contractions occur throughout pregnancy but early they are low amplitude every 30 mins. Mid-gestation they are lower in frequency but higher in amplitude (braxton hicks). Labour they are variable amplitude then increase in frequency and amplitude

159
Q

What happens in parturition to generate the force for delivery?

A
  • Myometrium thickens during pregnancy
  • At the end of gestation oestrogen becomes dominant over progesterone and this causes PGs to increase. This leads to a rise Ca conc during APs making contractions more forceful. Also oxytocin lowers the threshold for APs increasing the frequency of APs and stimulates the placenta to produce PGs
160
Q

What is the ferguson reflex?

A

-the uterus contracts and pushes the babys head into uterus -> detected by posterior pituitary -> released oxytocin -> causes uterus to contract more -> enter positive feedback loop

161
Q

Where is oxytocin secreted from?

A

-Posterior pituitary (mother and fetus)

162
Q

What actions can be taken in post-partum haemorrhage?

A
  • Oxytocin inection

- Fundal massage

163
Q

What is bracchystasis?

A

-Uterus contracts more than it relaxes causing the presenting part to be driven into cervix

164
Q

What effect do contractions of the uterus and brachystasis have on the cervix?

A

-Causes cervical effacement and dilation

165
Q

Describe the stages of lactation

A
  • Mammogenesis -> during pregnancy high progesterone = hypertrophy of breast tissue and differentiation of cells to become capable of producing milk
  • Lactogenesis -> synthesis of milk containing fats, proteins and sugars. Neutrophils enter alveoli to prevent infection
  • Galactokinesis -> ejection of milk by contraction of myoepithelia cells surrounding alveoli. Stimulated by oxytocin. Oxytocin stimulated by mechanical stimulation of the nipple and breast
  • Galactopoesis -> maintenance by the neuro-endocrine reflex of oxytocin being stimulated by suckling. Prolactin production stimulated by suckling causes production of the milk for the next feed
166
Q

What is the difference between colostrum and milk?

A

-Colostrum contains less fat and sugars and more proteins eg IgG

167
Q

What breast signs would present a flag?

A
  • Unilateral discharge
  • Hard craggy palpable mass
  • Non-cyclical and focal pain
168
Q

Give 3 differentials for a palpable mass?

A
  • Invasive carcinoma
  • Fibroadenoma
  • Cysts
169
Q

Why are mammograms more useful in the older patient?

A

-More fatty tissue is easier to visualise

170
Q

When is mammographic screening?

A

-47->73 every 3 years

171
Q

What is of concern on a mammogram and what does it indicate?

A
  • Density -> Invasive carcinoma, fibroadenoma or cyst

- Calcification -> DCIS, benign tumour

172
Q

What is polythelia?

A

-Additional nipple

173
Q

What is acute mastitis? How does it present?

A
  • Inflammatory infection during lactation usually from staph accessing cracks in nipples
  • Presents with pyrexia, erythematous painful breast
174
Q

Name 3 benign epithelial lesions of the breast

A
  • Gynaecomastia
  • Fibrocystic change
  • Fibroadenoma
  • Phyllodes
175
Q

What is fibrocystic change?

A

-Mass in the breast caused by cyst formation and fibrosis

176
Q

What is a fibroadenoma?

A

-A stromal tumour which presents as a mobile mass which can be multiple, bilateral and often large

177
Q

What is a phyllodes? How is it treated?

A
  • Rare benign mass which is borderline malignant
  • Very large and cause atypical cellular stroma
  • May reccur
  • Wide margin excision
178
Q

What is gynaecomastia? Give some causes

A
  • Enlargement of male breast which can be unilateral or bilateral
  • Anabolic steroids, spironolactone, liver cirrhosis, klinefelters
179
Q

What type of breast cancer is most common?

A

-Adenocarcinoma

180
Q

Give some risk factors for Br Ca

A
  • Genetics -> BRCA1 gene
  • Obesity
  • Null parity
  • Early periods/late menopause
  • OCT/HRT
181
Q

What is a ductal carcinoma in situ?

A
  • Malignant lesion of the breast which is limited to ductule cells and is non invasive
  • Has a central camedo calcification
182
Q

What is Paget’s disease of the breast?

A

-DCIS which has extended to the nipple skin -> unilateral, red and crusting

183
Q

What is an invasive breast carcinoma? How can it present?

A
  • Carcinoma which invades into the stroma, Lymphatics and BVs
  • Can present as palpable mass, lymphadenopathy, peau d’orange (blockage of lymphatics causing an oedematous breast and hair follicles pull down as attached to dermis)

PPE (15 decks)

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