Menstrual Disorders Flashcards
How is dysmenorrhoea classified?
Primary = menstrual pain occurring with no underlying pelvic pathology.
Secondary = menstrual pain that occurs with an associated pelvic pathology.
Outline the pathophysiology of dysmenorrhoea
No fertilisation = corpus luteum regresses = decline in progesterone = prostaglandin (PGF2α and PGE2) release by endometrial cells =
- spiral A vasospasm = ischemic necrosis, shedding of superficial endometrium
- increased myometrial contractions
How should primary dysmenorrhoea be managed?
Lifestyle = stop smoking
Pharmacological = - NSAIDs (inhib prostaglandin prod) and/or paracetamol - 3-6m trial of COCP, IUS
Non-pharmacological =
- heat
- Transcutaneous Electrical Nerve Stimulation (TENS)
How is amenorrhoea classified?
Primary = failure to start
Secondary = cessation for >6m (excluding preg)
Define oligomenorrhoea
irregular periods with intervals between menstrual cycles of more than 35 days and/or less than nine periods per year
Outline the HPG axis
What are the common causes of oligomenorrhoea?
PCOS
Contraceptive/Hormonal treatments
Perimenopause
Thyroid disease/Diabetes
Eating disorders/excessive exercise
Medications e.g. anti-psychotics, anti-epileptics
What are the causes of amenorrhoea?
HYPOTHALAMIC =
- Functional (eating disorders, exercise): suppress GnRH prod, subsequent low oestradiol levels, via ghrelin and leptin
- Chronic: psychiatric disorders, thyroid disease, sarcoidosis
- Kallmann syndrome
PITUITARY
- Prolatinoma
- Sheehan’s syndrome (necrosis sec to massive obstetric haemorrhage)
- Destruction of pit (radiation or autoimmune disease)
- Post-contraception amenorrhoea
OVARIAN
- PCOS
- Turners
- Premature ovarian failure
ADRENAL
- Adrenal hyperplasia
GENITAL
- Ashermann’s syndrome
- Imperforate hymen/Transverse vaginal septum
- Mayer-Rokitansky-Kuster-Hauser syndrome
How should menstrual irregularity be investigated?
Preg test
Blood test = TFTs, prolactin, FSH, LH, Oestradiol, Progesterone, Testosterone, 17 hydroxyprogesterone (congenital adrenal hyperplasia)
Karyotyping
US
Progesterone challenge test to elicit a withdrawal bleed:
- bleed = adequate levels of oestrogen however the patient is not ovulating (PCOS)
- no bleed = very low levels of oestrogen or an outflow obstruction
Hor should menstrual irregularity be managed?
Regulating periods = COCP, IUS
Hormone = cyclical hormone replacement therapy with oestrogen, Ca +vit D (post bone scan)
Symptoms = hair: COPC, acne = Abx, topical retinoids
Treat hyper/hypothryoidism
IVF - improve fertility
Surgery = tumour removal, correction of genital tract abnoramilties
What are the causes of heavy menstrual bleeding?
PALM: Structural Causes
- Polyp
- Adenomyosis
- Leiomyoma (Fibroid)
- Malignancy & hyperplasia
COEIN: Nonstructural Causes
- Coagulopathy
- Ovulatory dysfunction
- Endometrial
- Iatrogenic
- Not yet classified
How should heavy menstrual bleeidng be investigated?
Bloods = FBC, TFT, coag
US pelvis
Cervical smear
High vaginal and endocervical swabs
Pipelle endometrial biopsy
Hysteroscopy and endometrial biopsy
How can heavy menstrual bleeding be managed?
Levonorgestral-releasing intrauterine system (LNG-IUS) (thins endometrium and can shrink fibroids)
Tranexamic acid, mefanamic acid or COCP
Progesterone only: oral norethisterone (Taken day 5-26 of cycle), depo or implant
Endometrial ablation
Hysterectomy: partial, total
What is the role of FSH?
Bind granulosa cells = follicle maturation of primary follicles = secondary follicle
Theca interna appears = secondary follicles then prod low levels of oestrogen = inhib LH
Inhibin secretion begins = inhibits FSH = stops more follicles devel
In the follicular phase what keeps LH levels low?
Due to rising levels of GnRH LH should be rising
However FSH causes the devel of the follicle which prod low levels of oestrogen = which inhib LH secretion
After the first 10 days (mid-follicular phase) what affect does oestrogen have?
High levels now able to cause a +ve feedback = stim release of LH
FSH not released due to inhibin prod by the follicle
What causes the LH surge? What is the result of the LH surge?
+ve feedback from oestrogen levels that are now high
Continued release of GnRH
Result = ovulation of the most mature follicle releasing the oocyte
What is the role of inhibin?
-ve feedback = stops the secretion of FSH = as we don’t need anymore follicle maturing just yet
Describe the function of progesterone
-ve feedback on GnRH = stop release of FHS/LH
Stimulate endometrial growth = for egg to implant if fertilised
What causes the corpus luteum to degenerate?
As the corpus luteum degenerates what does that cause?
Progesterone inhibiting a further rise in LH
Result =
Progesterone levels fall = GnRH not inhibited = new cycle
Endometrial lining sheds as not maintained by progesterone
What are the causes of abnormal uterine bleeding (AUB)?
Abnormal clotting - vWD, thrombocytopenia, leukaemia
Pathology - fibroids, endometriosis, PID, polyps
Medical - hypothyroid, liver disease, Ca
How should abnormal uterine bleeding be investigated?
Hysteroscopy +/- biopsy
USS
Outline how abnormal uterine bleeding is medically treated
Tranexamic acid (for active bleeding) = inhibit plasminogen activation reducing fibrinolysis
NSAIDs = inhib PG and PGE2 binding to its receptor
Progesterone
- Norethisterone
- MIRENA-IUCD
OCP
GnRH
Ulipristal acetate
LARC/minipill/depot
How is abnormal uterine bleeding surgically treated?
Hysterectomy (removal of the uterus +/- ovaries + cervix)
Endometrial ablation = resection, roller ball, laser, cold coag, microwave, balloon, radiofrequency
