Menstruation + Disorders Flashcards
(47 cards)
1
Q
Describe the anatomy of the female reproductive tract
A
*Refer to Netters/web for further pictures
2
Q
Explain the physiology of the menstrual cycle
A
Refer to menstrual cycle lecture notes in SEM4 Repro for further info/understanding
3
Q
What happens in menstruation itself?
A
- endometrium develops secondary to ovarian cycle
- oestrogen proliferates endometrium
- progesterone maintains endometrium
- failure of conception
- regression of corpus luteum
- fall in oestrogen and progesterone
- distal ischaemia + vasodilatation leads to tissue breakdown + bleeding
- 36 hours after bleeding, endometrial regeneration begins
4
Q
What is important to ask about in a menstrual history?
A
- LMP
- cycle length
- menarche
- regularity
- quantity of blood loss
- associated clots
- duration of menses
- IMB/PCB/PMB
- associated pain (dysmenorrhoea)
5
Q
What is menopause and when does it happen?
A
- permanent cessation of menstruation due to loss of ovarian follicular function
- there is a transitional period (perimenopause) from approx 5 years prior to final menstrual period (FMP) up to one year after the FMP
- avg age of menopause = 51
6
Q
What is premature menopause?
A
Defined as menopause before age of 40
7
Q
What are the symptoms of menopause?
A
- reduced fertility
- menstrual irregularities (shortening -> irregular -> absent)
- vaso-motor -> hot flushes, sweats, palpitations
- oestrogen dependent tissue atrophy -> vaginal dryness
- osteoporosis
Menopause results from diminished ovarian reserve -> reduced primordial follicles lead to lower ovarian function, which results in lower oestrogen levels giving rise to symptoms.
8
Q
What is primary amenorrhoea?
A
- failure to start menstruating (by age 16)
- in the presence of normal growth and secondary sexual characteristics
- avg age of menarche in UK = ~12
- needs investigation in:
- 16yr old
- 14yr old with no breast development
9
Q
What is secondary amenorrhoea?
A
- when periods stop for >6 months*
- in a woman who has previously menstruated
- other than due to pregnancy
*some sources say 3 months
10
Q
What is oligomenorrhoea?
A
- infrequent periods
- with a cycle of >35 days
11
Q
Primary amenorrhoea can cause great anxiety. In most patients puberty is just late (often familial), and reassurance is all that is needed. In some the cause is structural or genetic.
So what needs to be asked/checked?
A
- has she got normal external secondary sexual characteristics? if so, are the internal genitalia normal?
- causes can be the same as for secondary amenorrhoea (coming up)
- if she’s not developing normally, examination and karyotyping may reveal Turner’s syndrome or AIS - the aim of treatment is to help the patient to look normal, to function sexually and if possible, to enable her to reproduce if she wishes
12
Q
What are the 5 categories of causes of oligo-menorrhoea?
A
- physiological
- hypothalamic
- pituitary
- ovaries
- other
13
Q
What are physiological causes of oligo-amenorrhoea?
A
- pre-pubertal
- post-menopausal
- pregnant or lactating
14
Q
What are the hypothalamic causes of oligo-amenorrhoea?
A
- primary -> rare, due to congenitally reduced GnRH
-
secondary:
- usually psychological factors/stress
- low body fat/anorexia
- excess exercise (up to 44% of competitive athletes have amenorrhoea)
15
Q
What are pituitary causes of olig-amenorrhoea?
A
- hyperprolactinaemia (most common) -> hyperplasia or adenoma suppresses the pituitary and gonads (Rx w/ dopamine agonist eg. bromocryptine)
- hypo- or hyperthyroidism
- severe systemic disease eg renal failure
- rare -> pituitary tumours + necrosis (Sheehan’s syndrome)
16
Q
What are the ovarian causes of oligo-amenorrhoea?
A
-
acquired:
- PCOS -> extremely common, usually causes oligomenorrhoea
- premature menopause -> 1 in 100
- tumours
-
congenital:
- turner’s syndrome (45XO) -> short stature, poor secondary sexual characteristics
- disorders of sexual differentiation
17
Q
What are some other causes of olig-amenorrhoea not mentioned?
A
- pregnancy-related
- asherman’s syndrome (uterine adhesions after a D+C)
- post-pill amenorrhoea
18
Q
What are relevant investigations for oligo-amenorrhoea?
A
- b-hCG urine dip -> exclude pregnancy
- assess ovarian + pituitary function -> FSH + oestradiol
- low E2 w/ high FSH = ovarian
- low E2 w/ low FSH = pituitary or hypothalamic
- prolactin, thyroid function
- serum androgens -> PCOS
- imaging -> USS of vagina and uterus for structural abnormalities
19
Q
What is the treatment for oligo-amenorrhoea?
A
- Rx related to cause
- premature ovarian failure cannot be reversed but HRT is necessary to control symptoms of oestrogen deficiency + protect against osteoporosis
- pregnancy can be achieved with oocyte donation + in vitro fertilization techniques
20
Q
What is the treatment for HPA malfunction in regards to stress, weight loss and exercise?
A
- if mild, there is sufficient activity to stimulate enough ovarian oestrogen to produce an endometrium
- if severe, axis shuts down (eg anorexia)
- reassurance + advice on diet or stress management or psych help if appropriate
- she should be advised to use contraception as ovulation may occur at any time
- if she wants fertility restored now, or reassurance of seeing a period, mild dysfunction will respond to clomifene but a shut-down axis will need stimulation by GnRH
21
Q
What is menorrhagia?
A
- defined clinically as excessive menstrual blood loss that interferes w/ a woman’s quality of life
- objectively classified as >80ml blood loss per cycle
- up to 33% of women complain of heavy menstrual bleeding
- most common gynaecological symptom
- look for signs + symptoms of anaemia
22
Q
What are the most common causes of menorrhagia?
A
- fibroids (30%)
- polyps (10%)
23
Q
How do you classify causes of menorrhagia depending on the underlying pathology?
A
- endocrine (anovulation): pcos, hyperprolactinaemia, thyroid dysfunction (hypo particularly), HPA dysfunction (perimenopause, adolescent), dysfunctional corpus luteum
- structural: fibroids, polyps, endometriosis, adenomyosis, uterine + cervical cancers
- pregnancy complication: miscarriage, choriocarcinoma, ectopic
- infection: endometritis, salpingitis
- iatrogenic: IUCD, anticoags, tamoxifen, HRT, herbs (ginseng, ginkgo, soya)
- systemic: haem/coag disorders, chronic liver and renal disease
- physiological: altered synthesis of uterine vasodilatory prostanoids, reduced endothelin expression, inc fibrinolysis, perturbed endometrial regeneration, overproduction of NO
24
Q
Enquiring into the history can help to narrow down on the underlying cause of the menorrhagia. For example, asking about thyroid symptoms, haem symptoms etc. Similarly examination will also help with this.
What investigations can be useful to manage menorrhagia?
A
-
bloods:
- serum/urine pregnancy test
- FBC
- TFTs
- serum free testosterone
- clotting screen: PT/APTT, vWd
-
imaging:
- ultrasound
- hysteroscopy + directed endometrial biopsy (D+C)
- (pipell biopsy)?
- hysterosalpingography (HSG)
25
Menorrhagia: Which women require a **hysteroscopy** _over_ an ultrasound as the first-line imaging modality?
* **women w/ suspected submucosal fibroids, polyps or endometrial pathology**
* whether have symptoms such as persistent intermenstrual bleeding OR they have risk factors for endometrial pathology
* if declined -\> offer pelvic USS
* for larger fibroids, offer pelvic USS
26
Menorrhagia: In which examples is an **ultrasound** the first-line imaging modality?
* women w/ suspected adenomyosis
* offer **transvaginal USS**
* when they have significant dysmenorrhoea **or**
* a bulky, tender uterus on examination that suggests adenomyosis
27
When agreeing treatment options for menorrhagia with women, what needs to be taken into account?
* the woman's **preferences**
* any **comorbidities**
* presence or absence of fibroids (incl size, number + locations), polyps, endometrial pathology or adenomyosis
* other symptoms such as pressure and pain
28
What is the step-wise **medical** management of menorrhagia?
* **_mirena IUS_** - releases levonorgestrel into endometrial cavity -\> atrophy (reduces bleeding -\>86% @ 3months)
* **antifibrinolytics** eg. tranexamic acid (49%)
* **NSAIDs** eg. mefenamic acid (29%)
* **COCP** (20-30%)
* **progestogens** IM eg. Norethisterone
* **GnRH** agonists rarely
29
What is the surgical treatment for menorrhagia?
* **endometrial ablation**
* **uterine artery embolisation** or **myomectomy**: for women wishing to retain fertility w/ fibroids \>3cm
* **hysterectomy**: for women not wishing to retain fertility and fibroids \>3cm
30
**Intermenstrual bleeding** (IMB) is defined as bleeding from the vagina at any time in the menstrual cycle other than normal menstruation.
What are the **causes** of IMB?
* **mid-cycle bleeding** - physiological oestrogen surge
* **contraception**: COCP, injection, IUCD
* **cervix**: polyps, infection (chlamydia, gonorrhoea), cancer, polyps, ectropion
* **vagina**: adenosis, vaginitis, tumours
* **uterus**: polyps, cancer, adenomyosis, fibroids
* **pregnancy** related eg. ectopic pregnancy
31
**Post-coital bleeding** (PCB) is more likely to originate from the vagina or cervix than the endometrium. This symptom is the classical symptom of cervical carcinoma, which should always be suspected in PCB.
What are the causes of PCB?
* **vaginal:** vaginitis, carcinoma
* **cervix**:
* cervicitis
* _polyps_
* _carcinoma_ - the most likely malignant cause of PCB
* trauma - even quite minor lesions may cause severe PCB if co-existent coag disorder
* _ectropion_
32
After taking a thorough focused history and examination, what **investigations** would you like to do for IMB and PCB, if indicated?
* cervical smear
* endocervical or vaginal swab
* blood tests - FBC, clotting, TFTs
* pregnancy test
* pelvic ultrasound
* hysteroscopy + endometrial biopsy
* ? MRI
* colposcopy
Do these in context of history + exam
33
What is **primary** dysmenorrhoea?
* **pain w/ no organ pathology**
* associated w/ anovulatory cycle
* worse during first day or two
* cramping lower abdomen pain, back + groin pain
34
What is the management of primary dysmenorrhoea?
* excess prostaglandins cause painful uterine contractions producing ischaemic pain
* therefore **NSAIDs** inhibit PGs eg. mefenamic acid during menstruation so reduce contractions + hence pain
* **paracetamol** is a good alternative to NSAIDs
* in pain w/ ovulatory cycles, ovulation suppression w/ **COCP** can help
* **cervical dilatation** during _childbirth_ may relieve it but surgical dilatation may render cervix _incompetent_
35
What is secondary dysmenorrhoea?
* pain w/ associated pathology
* associated with **deep** dyspareunia
36
What are the causes of **secondary** dysmenorrhoea?
* endometriosis
* adenomyosis
* adhesions
* fibroids
* ovarian cysts / tumours
* pelvic inflammatory disease
37
What investigations can be done where secondary dysmenorrhoea is suspected?
* cervical swabs
* FBC, WBC, CRP, b-hCG, tumour markers (Ca125)
* USS
* MRI
* hysteroscopy +/- biopsy
38
What is the treatment for secondary dysmenorrhoea?
* **treatment of cause is best plan**
* may be w/ hormonal contraception
* IUCDs increase dysmenorrhoea, except Mirena which usually reduces it
39
What are the **differences** in presentation between primary and secondary dysmenorrhoea?
* primary begins **6-12 months after menarche**, whereas secondary begins **at** menarche or **several years** after
* primary has 'spasmodic' lower abdo pain radiating to **back + thighs**, secondary feels 'congested'
* primary occurs just before mensturation + ends before bleeding stops, secondary is prior to menses, increasing through luteal phase
* primary responds well to **NSAIDs**, secondary is refractory to NSAIDs
40
Dysfunctional uterine bleeding (DUB) is exessive uterine bleeding, usually affecting pre-menopausal women that is _not_ due to pregnancy or recognisable uterine or systemic disease.
DUB usually presents as heavy, prolonged or frequent uterine bleeding.
What is the **pathophysiology** behind DUB?
* **DUB is believed to occur as a result of the derangement of the cyclical sex hormonal stimulation orchestrated by follicular development**
* in DUB, endometrial tissue breakdown located in superficial layer of endometrium occurs either focally in scattered areas of the endometrium (resulting in **breakthrough spotting**) or diffusely throughout the endometrial cavity (resulting in **heavier withdrawal bleeding**)
* such derangements of endometrial tissue necrosis are believed to occur due to vascular alterations associatd w/ continuous **oestrogen** stimulation unopposed by progesterone (_anvoulatory_ DUB) or irregular progesterone stimulation due to dysfunctional CL (_ovulatory_ DUB)
* while proliferative endometrium is encountered in anovulatory DUB, ovulatory DUB is not appreciated histologically
41
The goal is to restore normal menstrual bleeding pattern and to treat associated complications, most commonly anaemia. Exclusion of pregnancy or underlying pelvic or systemic diseases is the most important initial step in the management of DUB.
What is the treatment for DUB?
1. **progestogens** (oral or IUD)
2. COCP
3. surgery
* D+C +/- hysteroscopy (retain fertility)
* endometrial ablation/resection
* hysterectomy
42
What is premenstrual syndrome (PMS)?
Premenstrual syndrome (PMS) is characterised by cyclical, physical, and behavioural symptoms occurring in the luteal phase of the normal menstrual cycle. Symptoms may extend into the first few days of menses.
The symptoms cannot be an exacerbation of another disorder and they must interfere with some aspects of the woman’s life.
43
Healthcare professionals should elicit the woman's belief about the cause of the symptoms, previous treatments used, and whether symptoms improved with treatment.
A full medical history, including medication, contraceptive history, and use of recreational drugs and alcohol should be part of the evaluation. A history of sexual abuse should be explored with every woman as some evidence suggests a relationship between prior abuse and increased sensitivity to hormonal changes and mood disorders.
What are the **symptoms** of PMS?
* risk factors - post-pubescent, premenopausal, FHx, mood disorders
* abdominal bloating (days before menses, resolves at menses)
* fatigue
* breast tenderness
* headaches (like a tension headache)
* depressed mood, irritability + internal tension
* labile mood
* adverse effect on life
* increased appetite
* forgetfulness and difficulty concentrating
* other subjective symptoms
44
How is the diagnosis made for PMS?
* symptom diary should be kept to show symptom predominance in the luteal phase + symptom-free interval between menses
* if cyclical symptoms not found, physician should consider other diagnoses such as mood/affective disorders or substance abuse
45
Describe the normal physiology of the HPO axis
The gonadotropin hormones FSH and LH are secreted by the pituitary gland. FSH is necessary for the development of the immature ovum, (i.e. the primordial follicle in the ovary), and LH triggers ovulation. The secretion of FSH and LH from the pituitary gland is under the control of gonadotropin releasing hormone (GnRH) from the hypothalamus, and the hypothalamus in turn is controlled by the levels of the ovarian steroid hormones oestrogen and progesterone in the blood by means a feedback mechanism.
46
What drugs target the HPO axis?
* **GnRH** -\> buserelin etc. if applied continuously, inhibits FSH/LH release. Gonderelin is used in a pulsatile fashion to induce FSH/LH release
* **LH + FSH analogues** -\> induce ovulation
* **anti-progestogens** -\> used in ToP
* **anti-oestrogens** -\> treatment of breast cancer (tamoxifen) + to induce ovulation by preventing negative feedback by endogenous oestrogens (clomifene)
47
What are some _common_ causes of abnormal uterine bleeding?
* amenorrhoea
* menorrhagia
* IMB
* PCB
* dysmenorrhoea
* amenorrhoea - PCOS, starvation, stress, hyperprolactinaemia
* menorrhagia - fibroids, polyps
* IMB - malignancy, infections, polyps/fibroids
* PCB - cervical pathology; cancer, polyp, ectropion
* dysmenorrhoea - fibroids, adenomyosis, endometriosis, PID
