Workbook Questions Flashcards
Define phenotype
The observable physical characteristics of an individual as determined by their genes.
Should the external genitalia be ambiguous at birth, suggest what types of investigations could be carried out to determine sex
Information on karyotype, gonadal sex, hormonal tests, and anatomy
(e.g., palpation of gonads, length and diameter of any phallus, position of urethral meatus,
degree of labio-scrotal fold fusion, presence of vagina/pouch/urogenital sinus) (including ultrasound study).
Why are germ cells separated from somatic cells so early in development?
Germ cells need to remain undifferentiated and protected from influences arising during development of the rest of the body
Which tissue forms the matrix of the gonads into which
the primordial germ cells migrate.
Somatic mesenchymal tissue
An individual has a genotype of XXY. Will they have ovaries or testis? Explain your answer.
Testis
Y chromosome determines gonadal sex
Which gene on the short arm of the Y chromosome determines formation of the testes?
SRY gene (sex determining region of Y gene) also called TDF gene (testis determining factor)
In Turner’s syndrome (45,XO), the ovaries develop normally until the15th week of gestation, but then the ova begin to degenerate and disappear such that at birth the ovaries are mere streaks. Sometimes, the diagnosis will only occur at puberty. What
will be the presenting signs at puberty?
Primary amenorrhoea (failure to menstruate for the first time).
Failure of secondary sexual characteristics such as poor breast development as 2° sexual characteristics are dependent on ovarian hormones.
Also short stature.
Diagnosis is more usually made earlier if to peripheral lymphodema, redundant neck skin
and congenital heart disease are present.
Predict the gonads in an individual with a sex chromosome mosaic of XY, XX (or XO) cells?
Both ovarian and testicular tissue is present (sometimes in one gonad); this is true/primary hermaphroditism.
If, experimentally, the ovaries are removed from a fetus (castration) which internal genitalia develop?
Female
Which hormones prevent the spontaneous development of the female genitalia in the male and from which cells are they secreted?
Interstitial cells of Leydig in the testes secrete androgens, principally testosterone, from 9 weeks gestation.
Sertoli cells lie within the walls of the seminiferous tubules and secrete MIH (Müllerian inhibitory hormone; MIS Müllerian inhibitory substance).
What structures do the Müllerian ducts develop into?
uterine tubes
uterus
cervix
(upper vagina)
Which structures do the Wolffian ducts develop into?
epididymis
vas deferens
seminal vesicles
The prostate develops from the urogenital sinus in the male (under the influence of testosterone), but what does the urogenital sinus form in the female?
Lower part of the vagina
What do the following precursors develop into in the male & female respectively?
labioscrotal swelling
urethral folds
Male:
Labioscrotal swelling = scrotum
Urethral folds = ventral aspect of shaft of penis, incl spongy urethra
Female:
Labioscrotal swelling = labia majora
Urethral folds = labia minora
what is the homologous structure to the male glans penis in the female (both derived from the genital tubercle)?
Clitoris
Consider an individual with genotype XY, testicular development and normal secretion of testosterone and MIH. However, the fetal genitalia is insensitive to testosterone or DHT. Predict the consequences to
Wolffian ducts:
External genitalia:
Müllerian ducts:
Hence, summarize you findings with regards to internal and external genitalia.
Wolffian ducts: regress (these are androgen dependent)
External genitalia: female
Müllerian ducts: regress (since MIH secreted from testes)
The phenotype is female as labia, clitoris and vagina are present but no other internal
genitalia but remember the genotype is male. (testicular feminisation)
consider a female fetus (XX), who has excessive secretion of androgens from the adrenal glands.
What would be the affect on the following:
Wolffian ducts:
External genitalia:
Müllerian ducts:
Summarize your findings with regards to internal and external genitalia:
Wolffian ducts: promoted by the presence of the androgens
External genitalia: masculinised to a variable extent, since androgens cause the urethral fold to fuse
Müllerian ducts: present (as no MIH secreted)
External appearance male but genetically female with internal genitalia of both sexes.
What would occur in a male (XY) with low levels of MIH or resistance to MIH?
Where will you find the testes in such an individual & why
The presence of testicular testosterone will promotes male external genitalia and Wolffian ducts, but the Müllerian ducts are also retained. Hence, genetically and gonadally male but with internal genitalia of both sexes.
In the abdomen. They cannot descend. Failure to fully descend can be caused by mechanical obstruction by fibrous adhesions, shortened spermatic cord and narrowing of inguinal canal.
True or false:
Germ cells arise 3 weeks after conception
True
True or false:
Germ cells are haploid
False
True or false:
The para-mesonephric duct gives rise to the vas deferens
False
True or false:
The mesonephric duct is supported by MIH
False
What connects the seminiferous tubules to the epididymis.
Rete testis
True or false:
The vas deferens is c35 cm long in the adult human
False
Approx 24cm
True or false:
The gubernaculum connects the developing testis to the
posterior abdominal wall
False
Testes to scrotum
True or false:
The cervix arises from the Müllerian duct
True
True or false:
Testosterone causes the genital swellings (labioscrotal)
to develop into the shaft of the penis
False
Shaft of penis from urethral folds
True or false:
The primordial gonads arise ventral to the gut
False
True or false:
In the adult female human one ovum is normally produced
True
True or false:
Primary oocytes increase in number following puberty
False
True or false:
Oogonia are diploid cells
True
True or false:
Primordial follicles are surrounded by a theca
False
True or false:
In antral follicles thecal cells produce androgens
True
In the antral phase what do granulosa & thecal cells have receptors for respectively?
In the antral phase granulosa cells have receptors for_FSH_, thecal cells for_LH_.
True or false:
Ovulation is preceded by the completion of meiosis II
False
Only completed after fertilisation
True or false:
One type A spermatogonium produces up to 64 primary
spermatocytes
False
Each spermatogonium gives rise to 64 spermatozoa.
Also, it is the type B spermatogonium which gives rise to the daughter spermatocytes, with some type A remaining as resting cells to serve as an ancestor for later generations. (Be aware that classification of the spermatogonia varies in different texts but it is not necessary for you to
learn these).
True or false:
One primary spermatocyte normally produces 4 spermatids
True
True or false:
Sperm spend 12 days in the epididymis
True
between 6-12 days. They can be stored for much longer (weeks) in the vas deferens.
What hormone(s) does the corpus luteum secrete & under the influence of what
The corpus luteum secretes_progesterone__ and_oestrogen (oestradiol)_ under the control of__LH_
True or false:
Ovulation is stimulated by the LH surge
True
True or false:
One primary oocyte produces 4 ova
False
Whilst a primary oocyte goes through two meiotic division to produce an ovum
(including an ovulation and fertilization), non-functional first and second polar bodies are
formed at each stage.
True or false:
2% of sperm deposited in the vagina reach the site of
fertilisation in the ampulla of the fallopian tube
False
It is lower than 2%. Each ml of sperm (usually 1-4 mls ejaculated) contain tens of million sperm and only 200-300 of these will reach the site of fertilization in the ampulla of the uterine tube.
True or false:
The vas deferens passes anterior to the pubic bone
True
True or false:
The tunica vaginalis is a remnant of peritoneum
True
It is a peritoneal sac derived from the embryonic tunica vaginalis.
True or false:
The largest proportion of the volume of semen is from
the seminal vesicles
True
Up to 60% comes from the seminal vesicle and 1/3 from the prostate.
True or false:
The arterial supply of the testis is from the iliac arteries
False
It is from the testicular artery which has its origin in the aorta (remember the embryological origin of the testes).
discriminate between the roles of oestrogen in the early follicular phase and its role at ovulation.
In the early follicular phase, oestrogen at low levels exerts a negative (inhibitory) feedback on gonadotrophin release.
At ovulation, rising levels of oestrogen produces a positive (stimulatory) feedback, enhancing LH release thus promoting ovulation. (In fact the oestrogen enhances the LH releasing
mechanism to GnRH.)
At the menopause the ovary secretes dramatically less oestrogen. What will happen
initially to:
o plasma levels of FSH
o plasma levels of LH
o the secretion of GnRH from the hypothalamus?
FSH levels will rise considerably
LH levels will rise
GnRH levels will rise
Feedback from gonadal steroids much reduced
NB Several years after the menopause, these hormones return to lower levels.
Why are the changes in LH and FSH secretion at the menopause different?
No Inhibin secreted from ovary, so selective inhibition of FSH by Inhibin acting on pituitary gland no longer occurs and FSH levels rise more than LH
In pregnancy, once the placenta has developed it begins to secrete oestrogen and progesterone. The secretion is independent of LH and FSH. What will happen to: o plasma levels of FSH o plasma levels of LH o hypothalamic secretion of GnRH in a pregnant woman?
FSH levels will fall
LH levels will fall
GnRH levels will fall
Because placental oestrogen & progesterone exert negative feedback inhibition at both hypothalamus and pituitary
The drug clomiphene is an “anti-oestrogen” used in the treatment of infertility.
Clomiphene exerts a weak oestrogenic effect, sufficient to achieve uptake and binding
by to oestrogen receptors. It then reduces the concentration of oestrogen receptors
inhibition of the process of receptor replenishment. Thus, the hypothalamic-pituitary axis
blinded to the endogenous oestrogen level in the circulation. It is given for 5 days at the
start of the menstrual cycle. What will be the effects on:
o GnRH secretion
o plasma levels of FSH and LH
of treatment with clomiphene?
GnRH secretion will rise as the true oestrogen signal is falsely lowered and negative feedback inhibition is diminished.
LH & FSH secretion will also rise, with a larger increase in LH levels
What would be the effects on gonadotrophin secretion of a constant moderate dose of a progesterone like drug?
How might these effects be different if the dose is much lower? In this case which parts
of the reproductive system might still be affected?
Progesterone enhances negative feedback of natural oestrogen
At moderate doses this will reduce LH and FSH secretion
And inhibit positive feedback of oestrogen, so no LH surges
And ovulation is suppressed
At lower doses, there is no inhibition of LH surges
Ovulation will probably still occur
But progestogens will affect cervical mucus, inhibiting sperm transport
If the anterior pituitary gland is transplanted to another site in the body the secretion of
LH, FSH, TSH, GH and ACTH falls to negligible levels. Why?
The transplanted anterior pituitary, however, hypersecretes prolactin. Why?
A major part of control of prolactin secretion is inhibition by dopamine.
Releasing hormones are diluted to ineffective concentrations in the general circulation.
The portal nature of the hypophyseal vessels normally ensures that releasing hormones reach
the pituitary at relatively high concentration
Prolactin secretion control is removed if the anterior pituitary is transplanted and the dopamine is diluted in the
general circulation
The major hypothalamic hormone inhibiting prolactin secretion is dopamine (prolactin
inhibitory hormone). The actions of dopamine are mimicked by the drug bromocriptine
and antagonised by drugs like haloperidol, metoclopramide and domperidone. What will
happen to prolactin levels if a woman is given bromocriptine?
They should fall, as it mimics the inhibitory effect of dopamine on lactotrophs
Prolactin and, particularly, hyperprolactinaemia, suppresses fertility by disturbing the pulsatile release of GnRH. What do you think might happen to the fertility of a woman given metoclopramide?
Fertility may be reduced, as prolactin levels rise because the inhibitory effects of dopamine are themselves inhibited since metoclopramide inhibits dopamine
Increasing levels of prolactin will produce a spectrum ranging from inadequate luteal phase function to anovulation and amenorrhoea with complete GnRH suppression. Fertility will be
affected at all points..
In some women, impaired fertility is associated with a loss of the normal daytime fall in prolactin levels. Which drug would you choose to lower prolactin levels and restore fertility?
Bromocriptine; mimics dopamine
What are the normal age ranges for the following in girls: Thelarche Adrenarche Growth Spurt Menarche
Thelarche – breast enlargement 8-11 years
Adrenarche – pubic hair 11-12 years
Growth Spurt 10-14 years
Menarche 11-15 years
Precocious puberty is defined as physical signs of sexual maturation before 8 years or menarche before 10 years old. Why might precocious puberty be stimulated by meningitis?
Irritation and inflammation stimulating early rises in GnRH secretion
True precocious puberty is caused by premature secretion of gonadotrophins - mostly idiopathic, but can be caused by CNS lesions (hypothalamic tumours, post-encephalitis neurofibromas etc.).
Hence, irritation and inflammation such as meningitis can stimulate early rises in GnRH secretion.
What are the effects of precocious puberty on a bone growth? Would you expect a girl to be shorter or taller as an adult because of precocious puberty?
The growth spurt begins earlier and is terminated earlier, so that epiphyses may close at an earlier stage of growth, making the individual shorter.
Delayed puberty commonly present as primary amenorrhoea, which is failure to
menstruate by the age of 16 years. What possible explanations might you consider if:
(i) plasma LH and FSH levels are in the normal range?
(ii) plasma LH and FSH levels are very low?
(i) If gonadotrophin levels are normal, then either the ovary is not responding to them so no steroids are produced, or if the tissues are not responding to the steroids that are produced. If no steroids are produced, however FSH & LH levels should be raised. Another possibility is that menstruation is occurring, but the products are not shed because of a vaginal or cervical problem
(Also, consider some forms of androgen insensitivity syndrome - these XY individuals will have external female genitalia as their tissues do not respond to androgen - but their male gonad will produce MIH so they will not have internal female ducts and will present with primary
amenorrhoea. Breast development is often normal or enhanced as the small amount of gonadal oestrogen and adrenal oestrogen is not opposed by androgen. Body hair is normal to scanty.)
(ii) If gonadotrophin levels are low, then the problem is likely of pituitary or hypothalamic origin. Some examples are pituitary tumours. Anorexia nervosa, malnutrition and psychogenic causes also lead to hypo gonadotropic hypogonadism. Check serum prolactin and consider imaging for a cranial lesion.
If plasma LH & FSH are in the normal range & other secondary sexual characteristics were present what possible explanation would you consider for primary amenorrhoea?
The ovary may not be responding, so ovulation does not occur and a cycle of steroid secretion is not properly established.
A boy is brought to you by his parents, concerned that he is behind his classmates in pubertal development.
What would you examine to assess his stage of puberty?
To assess stage of puberty check height, weight, body hair, genitalia, bone age.
Also ask about medical history and medications.
Delayed puberty is lack of sexual maturation by age 15 - majority have constitutional delay - which is quite benign - and which represents normal variation - often familial. Such boys will eventually undergo a normal puberty and attain normal height.
Constitutional delay is most probable in a healthy boy with delayed growth and bone age.
Consider a 14 year old boy with query delayed puberty. What proportion of normal 14 year olds would be expected not yet to be exhibiting signs of puberty? What factors in his history might
make you feel that he is in this group?
The proportion would be very low (3-5%) since puberty in boys visibly begins between 9 and 14 years with scrotum and testicular development, however, full maturity may not be complete until
early 20’s (e.g., facial hair).
If he has good general health and nutrition, also if a brother was a “late developer”, you would suspect constitutional delay of puberty and would give reassurance.
Serious systemic illness (e.g. diabetes, malabsorption) can delay puberty
Explain what is meant by ‘bone age’. How will this help in establishing puberty delay?
Accelerated growth is one of the earliest signs of precocious puberty and bone age can be determined with hand-wrist films and compared with standards for the patient’s chronologic age.
If his bone age is inconsistent with (behind) his chronologic age then constitutional delay is likely.
What is the normal growth spurt for boys in puberty?
How is this measured?
Growth spurt in boys is approx 10cm/year
height comparisons over time are useful.
When does the growth spurt occur in relation to other events in pubertal development in boys?
The growth spurt starts about 12 months after the first signs of puberty (increase in testicle size due to FSH induced increase in seminiferous tubules).
Why may parents not notice the early signs of puberty in boys?
Early signs of puberty in boys are the increase size of testes followed by reddening of scrotal skin and elongation of penis-his parents may not be aware that these changes are occurring.
Is a boy with delayed puberty likely to be producing sperm?
High intra-testicular levels of testosterone are needed for spermatogenesis-so it is doubtful.
If there is a problem of delayed puberty, what test would you use to distinguish between defects in the gonads and defects primarily in the hypothalamus/pituitary?
If FSH is low, suspect hypothalamic/pituitary.
If testosterone is low, suspect hypogonadism.
What is the lower age limit of normal puberty in boys?
10 yrs
How would you clinically assess the stage of puberty?
Height, weight, genitals, body hair, bone age.
What are the possible consequences of early puberty
Short stature-premature growth spurt - epiphyseal closure
What are the common causes of early puberty in boys?
True precocious puberty - premature secretion of gonadotrophins - leads to testicular androgen production and sperm production and virilisation - mostly idiopathic.
Can be caused by CNS
lesions, thus evaluation and follow-up is needed. Precocious pseudopuberty results from secretion of androgens from adrenal glands or testis, virilisation occurs but not sperm
production (most commonly caused by adrenal hyperfunction-congenital adrenal hyperplasia).
A patient has isosexual precocity, which is manifest in males as virilisation, but no more. What disorders of the adrenal gland may cause these signs?
How might you differentiate between them?
He may have adrenal hyperfunction - congenital adrenal hyperplasia (from 21-hydroxylase
or Il-hydroxylase deficiency)
or an adrenocortical tumour.
Congenital adrenal hyperplasia: Biochemical tests of enzyme levels (patients have elevated
serum 17-hydroxyprogesterone levels).
Adrenal tumours can be seen by imaging studies - sonography, CT, NMR.
There is a gradual depletion of ovarian follicles as a woman proceeds toward the menopause such that the secretion of oestrogen declines dramatically. What will happen to plasma levels of the following hormones?
FSH
LH
GnRH
Why do these changes occur?
FSH: rises considerably
LH: rises
GnRH: rises
As gonadal steroid production falls there is loss of negative feedback to the pituitary and hypothalamus.
Why are the changes in LH and FSH secretion different in menopause?
No inhibin from ovary so selective inhibition of FSH no longer occurs and it thus rises more than LH.
List at least 5 effects of oestrogen depletion that menopausal women may experience.
hot flushes
poor sleep
vaginal/urethral atrophy dysparunia/dysuria
breast atrophy
mood change/depression
osteoporosis/posture & height change/increased fracture risk
changing cholesterol/lipid profile & possible increased risk of CHD
What treatments or preventive measures might you consider for menopause problems?
Oestrogen HRT Calcium
(HRT is comprised usually of a mixture of oestrogens and progesterone, which are either
synthetic or extracted from pregnant mares’ urine.)
What are the disadvantages of using HRT
Increased risk of thromboembolism, breast cancer.
Why are oestrogen-only preparations not given to women who have not had a hysterectomy
Unopposed oestrogens cause proliferation of uterine lining with a risk of endometrial cancer. Progesterone inhibits this.
How are fibroids diagnosed?
Most fibroids are asymptomatic.
The most common symptom is abnormal bleeding, typically menorrhagia and the women is usually in her 40s.
Large fibroids may be palpable on bimanual examination (irregularly shaped uterus) examination by anaesthesia and curettage or by laparoscopy.
ultrasound may show the presence of a mass but may not distinguish other ovarian tumours.
How would you assess whether menstrual blood loss is sufficiently great to have
adverse effects?
Menorrhagia is usually defined as menstrual loss greater than 80ml which will produce
anaemia. Assess by pad and tampon counts and measuring haemoglobin/haematocrit levels.
What options are there for treating fibroids (i) in a woman under 35, (ii) in a woman
nearing the menopause?
Treatment options
It is common for women in their forties to have a hysterectomy, which usually involves removal of both uterus and ovaries. What might be the advantages and disadvantages of removing the ovaries as well as the uterus? What evidence bases would you quote in
helping a woman to decide whether to have her ovaries removed?
Strictly speaking a hysterectomy is the removal of the uterus.
Women in their forties may be counselled on the risks and benefits of bilateral oophorectomy in
conjunction with hysterectomy.
Potential benefits include, avoidance of ovarian pathology in the future(although some ovarian
type tumours can arise from the peritoneum de novo)
Potential disadvantage, sudden onset of menopause as the albeit aging ovary is removed and
loss of ovarian androgen.
Define genotype
The genetic makeup of an individual as defined by the particular sets of genes they possess.
What are the main public health messages required to limit STIs?
Practice safer sexual behaviour Age at first intercourse Total number of partners Number of concurrent partners Frequency of partner switching Sexual orientation Specific at-risk sexual practices Use correct barrier contraception techniques consistently Seek better sexual health education Seek early treatment for suspected STI Attend for regular screening if at risk Avoid teenage pregnancy Avoid alcohol abuse and illicit drug use
What factors influence the effectiveness of public health campaigns for STIs?
Changing societal norms
Targeted advertising and education
Peer group pressure and social activities
Socio-economic factors
Poverty
Educational and social disadvantage
Unemployment
Teenage conception and pregnancy
Ready and confidential access to GUM clinics and other health practitioners
Awareness of serious risks associated with some STIs
Colin aged 19, presents to you somewhat embarrassed. For the past two days he has
experienced pain on passing urine, and a urethral discharge. He has no previous history
of genital urinary problems and is normally fit and healthy. On examination he has no
fever, the discharge from his urethra is creamy, and there is a slight reddening of the
surrounding glans penis.
What key things will you need to know about his history?
Details of recent sexual contacts
Timing
Partner(s)
Nature of sexual activity and sexual orientation
Have partners sought advice or treatment?
Are partners symptomatic?
Previous STIs and complications
Overseas travel and place of residence
Underlying diseases, including HIV, HBV and HCV status
Participation in commercial sex
Recent antibiotic use and history of allergies
Colin aged 19, presents to you somewhat embarrassed. For the past two days he has
experienced pain on passing urine, and a urethral discharge. He has no previous history
of genital urinary problems and is normally fit and healthy. On examination he has no
fever, the discharge from his urethra is creamy, and there is a slight reddening of the
surrounding glans penis.
What possible infections will you consider?
Chlamydial urethritis
Gonococcal urethritis
Non-specific urethritis (NSU)
A Gram stain of the urethral discharge shows intracellular Gram negative diplococci (ie. cocci in pairs).
What is your diagnosis?
Gonococcal urethritis
For Gonococcal urethritis, What antibiotics will you consider, and why?
Ceftriaxone 500 mg IM single dose (many gonococci resistant to other agents)
PLUS
Azithromycin (single large oral dose 1g) (co-treatment for chlamydia and enhances treatment for gonorrhoea)
Subsequent investigation of the urethral discharge from a patient with Gonococcal urethritis reports the specimen as positive for Chlamydia trachomatis as well.
Why do you think such mixed infections are common?
Common at risk behaviours and associated factors
Long-term asymptomatic infection
High prevalence rates of Chlamydia trachomatis infection
Identical mode of transmission
What is the likelihood of the partner of a patient with Chlamydia/Gonococcal urethritis being infected?
Depending on the following factors the risk of her being infected with Chlamydia trachomatis and/or Neisseria gonorrhoeae, though not necessarily symptomatic, may be anywhere upwards
of 50 %!
Adherence to strict barrier contraception
Frequency of intercourse
Duration of sexual relationship
Time of acquisition of the STI by her partner
Concurrent genital inflammation or ulcers?
How would you manage the asymptomatic partner of a patient with Chlamydia/Gonococcal urethritis
Detailed history
Physical Examination
Diagnostic investigations
Endocervical smear and swab for microscopy and culture of N. gonorrhoeae
First-void urine and/or endocervical smear for C. trachomatis (+/- N. gonorrhoeae) detection by
nucleic acid amplification (NAA) test
Pharyngeal and/or rectal swabs for culture of N. gonorrhoeae
Screening investigations
Syphilis serology
pap smear cytology
cervical swabs for HPV detection by hybrid capture?
serology for blood and body-fluid borne viruses – HIV, HBV, HCV
If positive treat for Chlamydia +/- gonorrhoea
Advice regarding need to abstain until treated or cleared of infection – potentially infectious
despite being completely asymptomatic!
Advice regarding need for return visit
Counselling, advice, and basic sexual health education
Julie, aged 27 comes to see you. She has noticed a slight increase in vaginal discharge but is otherwise well. On questioning you establish that she had unprotected sex with a casual partner 5 days ago. She has no steady sexual partner.
What possible infecting organisms will you consider?
Normal physiological variation! Candida spp. – fungus Bacterial vaginosis – Perturbed normal flora including Gardnerella vaginalis and Mycoplasma hominis Trichomonas vaginalis – protozoa Chlamydia trachomatis Neisseria gonorrhoeae
Julie, aged 27 comes to see you. She has noticed a slight increase in vaginal discharge but is otherwise well. On questioning you establish that she had unprotected sex with a casual partner 5 days ago. She has no steady sexual partner.
You examine Julie and find that she is tender in the right upper quadrant of her
abdomen.
What structures will you be considering as the reasons for this tenderness?
How might tenderness in these structures be linked to her other symptoms?
Liver Gall bladder Right kidney Stomach, pancreas, small or large intestine Lung or pleura
Fitz-Hugh Curtis syndrome due to perihepatitis – C. trachomatis or less commonly N. gonorrhoeae
Julie, aged 27 comes to see you. She has noticed a slight increase in vaginal discharge but is otherwise well. On questioning you establish that she had unprotected sex with a casual partner 5 days ago. She has no steady sexual partner.
You decide to perform a pelvic examination and decide to undertake some investigations for infections.
From where will you take swabs?
Endocervical smear and swab for microscopy and culture of N. gonorrhoeae
Endocervical swab for detection of C. trachomatis by NAAT
Urethral swab for culture of N. gonorrhoeae
Throat and/or rectal swabs for culture of N. gonorrhoeae
First-void urine for detection of C. trachomatis(+/- N. gonorrhoeae) by NAAT
Mid stream urine (MSU) for microscopy and culture of UTI pathogens
Cervical smear for cytology
Cervical swab for HPV detection
High vaginal smear and swab – Candida, Trichomonas, bacterial vaginosis (BV)
Julie, aged 27 comes to see you. She has noticed a slight increase in vaginal discharge but is otherwise well. On questioning you establish that she had unprotected sex with a casual partner 5 days ago. She has no steady sexual partner.
You decide that Julie does indeed have a sexually transmitted infection.
Apart from offering her treatment with appropriate antibiotics, what other advice
should you give her?
Abstain until both partner and herself, and any other sexual contacts, have been treated
effectively
Measures to minimise risk of future STI
Advice on correct use of barrier methods of contraception
Need to attend for a return visit – ‘test of cure’ investigations?
Basic sexual health education and advice regarding regular screening option
What is the ‘illness iceberg’? How does this concept apply in the case of sexually transmitted infections?
Only a small percentage of those infected with a pathogen may manifest symptoms and/or
signs of illness
Many STIs exhibit this phenomenon – Chlamydia, HPV, HSV, even syphilis may only manifest
with transient and minor evidence of primary disease
Potential large infectious reservoir – needs to be identified and treated promptly – CONTACT TRACING
Helena attended the family planning clinic a few weeks ago and elected to start taking
oral contraceptives. She has come to you now because she has developed genital
itching and a white discharge.
What organism will you consider in this case?
Why might the organism have grown at this particular time?
Candida spp. – fungus which can be part of the normal vaginal flora
Trichomonas vaginalis – sexually transmitted protozoan pathogen
Bacterial vaginosis – perturbed vaginal flora
Oral contraceptive use is associated with increased incidence of vulvo-vaginal thrush
Overgrowth of the yeasts is favoured by high oestrogen levels
Helena attended the family planning clinic a few weeks ago and elected to start taking
oral contraceptives. She has come to you now because she has developed genital
itching and a white discharge.
What conditions in the vagina will promote organism growth
Perturbed normal flora – broad spectrum antibiotic use
Warmth and humidity – climate, clothing, obesity
Oral contraceptives and pregnancy – oestrogen levels
Glucose levels – diabete mellitus
Steroid therapy
Menstrual cycle-associated changes – pre-period symptoms
Colonisation with a recalcitrant Candida species or strain
Helena attended the family planning clinic a few weeks ago and elected to start taking
oral contraceptives. She has come to you now because she has developed genital
itching and a white discharge.
What are the principles of treatment of this condition?
Does it constitute a sexually transmitted infection
Withdraw or control risk-factors
Obtain high vaginal smear and swab for microscopy and culture – many diagnoses may be
made clinically without laboratory investigation
Treat only if significantly symptomatic
Use first-line topical azoles (e.g. clotrimazole)
Consider oral fluconazole for more problematic cases
If recurrent or unusually severe investigate for resistant yeast and/or other unidentified risk
factors
Consider treating partner to reduce frequency of ‘re-infection’
No, as the aetiological agent is typically part of the normal vaginal flora
Jane aged 18, presents with a two day history of painful genital ulcers, mild fevers and a
painful swelling in her left groin. During the past few hours she has experienced marked
dysuria.
What other aspects of the history are you going to seek?
Sexual history – partner(s), timing, symptoms in partner(s)
History of previous STIs
History of previous genital ulcers, vesicle, or rashes
History of cold sores or primary gingivostomatitis
History of recent drug or antibiotic use and known allergies
Etc
Jane aged 18, presents with a two day history of painful genital ulcers, mild fevers and a
painful swelling in her left groin. During the past few hours she has experienced marked
dysuria.
What are the possible aetiological agents?
How would you confirm your diagnosis?
Herpes simplex virus typically type 2 (but may be HSV1)
Haemophilus ducreyi – tropical STI (chancroid)
Klebsiella granulomatis– tropical STI (granuloma inguinale)
Treponema pallidum – syphilis but lesions rarely multiple
Behcet’s syndrome or erythema multiforme – non-infectious aetiology
Smear and swab of vesicle fluid or ulcer base – herpes PCR
Syphilis serology and other investigations as per normal GUM assessment
Jane aged 18, presents with a two day history of painful genital ulcers, mild fevers and a
painful swelling in her left groin. During the past few hours she has experienced marked
dysuria.
How would you manager her illness?
A diagnosis of primary genital herpes warrants immediate aciclovir treatment
Oral aciclovir if outpatient management appropriate
Otherwise consider hospitalisation and IV aciclovir
Features of primary genital herpes
Mild fever and systemic symptoms
Inguinal lymphadenopathy
Extensive genital ulceration including spread to adjacent skin
Prolonged illness – up to two or more weeks!
Marked dysuria and possible acute urinary retention
Consider use of indwelling urinary catheter
Analgesia and other supportive measures
Advise regarding risk of recurrence
HSV2 (90 % patients experience recurrence within 1 year)
HSV1 (25 % patients experience recurrence within 1 year)
If recurrences persist for > 1 year, frequency unlikely to decline
Advise regarding possible transmission to others even whilst asymptomatic
Advise regarding issues related to current or future pregnancies
Frequent recurrences
Patients may recognise trigger factors and/or herald symptoms
Long-term continuous or periodic suppressive aciclovir therapy
What is inflammation of the Fallopian (uterine ) tubes called?
If the surrounding structures are involved, what is this called?
salpingitis
PID- if abscess develops may be called tubo-ovarian abscess
List the symptoms of PID
Lower abdominal pain, dyspareunia (+/- vaginal discharge) fever,(+/- menstrual abnormalities)
What is the differential diagnosis from PID (listed by anatomical structures affected) of:
bladder conditions
bowel conditions
gynaecological conditions
bladder conditions
cystitis, bladder stones
bowel conditions
irritable bowel syndrome, inflammatory bowel disease, appendicitis
gynaecological conditions:
ovarian cysts, endometriosis, ectopic pregnancy, torsion
What investigations would you perform to confirm a diagnosis of PID?
ultrasound, laparoscopy, swabs from endocervix, swabs from peritoneum if laparoscopy is done
What organisms are involved in PID?
Most episodes of PID will be polymicrobial, including organisms such as Chlamydia trachomatis, Neisseria gonorrhoeae, mycoplasmas, bacteriodes + other anaerobes
How would you manage a patient with PID?
medication:
analgesia, antibiotic / antimicrobial against specific organism, and broad spectrum antibiotics with good anaerobic coverage.
advice:
bed rest, if hospitalised, Semi-Fowler position to drain pus into pelvis
Aggressive antibiotic Treatment, particularly in young nulliparous patients.
What are the potential sequelae of PID?
chronic recurring infection, increased risk of ectopic pregnancy, impaired fertility, chronic pelvic pain
How can patients prevent PID & associated complications?
barrier contraceptives, STD screening, screening of partner, early treatment of STIs, avoidance of promiscuity
The uterine tubes lie in the free edge of which ligament?
Broad
List the mechanisms, which facilitate movement of an ovum along the duct?
Cilia & smooth muscle contraction (peristalsis)
Explain how infection may spread to the peritoneum from the female reproductive tract
The opening of the uterine tube at the infundibulum into the peritoneal cavity allows infection such as gonorrhea to spread from the vagina and cervix, via the uterus and uterine tubes into the peritoneal cavity.
What may be the consequence of infection in the uterine tubes?
Adhesions, which do not allow an ovum to pass through to the uterus. Hence, this may cause infertility or an ectopic pregnancy.
List some common & very rare sites of implantation in ectopic pregnancy
Common: fimbrial, ampullary, isthmic or interstitial (of the uterine tubes); ovary
Rare: Pouch of Douglas, abdominal viscera.
Where would pain be felt with an ectopic pregnancy implanted in the ampulla of the uterine tubes?
Explain why pain may be felt at the shoulder tip following rupture of an
ectopic pregnancy?
Pain from an ectopic pregnancy is felt in the lower abdominal quadrants
If lying down blood in the peritoneal cavity may collect beneath the diaphragm irritating the phrenic nerve.
Since this nerve originates with cutaneous nerves from C3, 4 and 5, pain may be referred to the dermatomes for these segments; i.e. shoulders.
Pain felt in the lower quadrants is due to stretching and tearing of the peritoneum.
Blood passing from the vagina is usually withdrawal bleeding (not a result of bleeding at the site of the rupture), caused by reduction in the hormone hCG which maintains the corpus luteum and hence prepares the endometrium for implantation.
A ruptured ectopic pregnancy at this site may cause a dangerous haemorrhage.
Describe the arterial blood supply to the uterine tubes?
It is an anastomotic system of the ovarian and uterine arteries.
The lateral reflection of the peritoneum off the body of the uterus forms which ligament?
Broad ligaments (which also contain uterine vessels)
The broad ligament may be subdivided. The mesentery of uterus is also called the mesometrium.
The mesosalpinx is mesentery of the uterine tube, whilst the mesovarium is that part of the broad ligament that suspends the ovary.
Histologically, what are the three layers of the uterus and which of these layers is shed during menstruation?
Perimetrium (outer)
Myometrium (consisting of three muscle layers)
Endometrium (inner)
consisting of the stratum functionalis - shed during menstruation
and the stratum basalis (which produces new stratum functionalis after each menstruation)
The endometrial lining of the uterus is of which type of epithelial cells?
How does this compare to the cervical canal epithelium?
Simple columnar epithelium (either are ciliated or have microvilli) with glycogen producing glands changing from simple to highly coiled over the course of the uterine cycle.
Tall columnar cells, with branched glandular cells, which form an alkaline mucus.
How does the epithelium of the body of the uterus change during the uterine cycle
menses days 1 – 4 :
desquamation of 2/3, bleeding
days 5 – 7 :
rapid re-growth from remaining epithelial cells
days 7 – 14 :
endometrial re-growth is completed
This concludes the proliferative phase
days 14 – 28 :
Secretary phase includes endometrial thickening, enlargement of
glandular cells, oedematous, proliferation of white cells.
3 layers : compact superficial zone spongy middle zone (glandules) inactive basal layer
As menses approach the arteries go in to spasm, retracting back to the deeper layers evoking ischaemia.