Menstrual Disorders Flashcards

1
Q

How is dysmenorrhoea classified?

A

Primary = menstrual pain occurring with no underlying pelvic pathology.

Secondary = menstrual pain that occurs with an associated pelvic pathology.

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2
Q

Outline the pathophysiology of dysmenorrhoea

A

No fertilisation = corpus luteum regresses = decline in progesterone = prostaglandin (PGF2α and PGE2) release by endometrial cells =

  1. spiral A vasospasm = ischemic necrosis, shedding of superficial endometrium
  2. increased myometrial contractions
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3
Q

How should primary dysmenorrhoea be managed?

A

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)
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4
Q

How is amenorrhoea classified?

A

Primary = failure to start

Secondary = cessation for >6m (excluding preg)

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5
Q

Define oligomenorrhoea

A

irregular periods with intervals between menstrual cycles of more than 35 days and/or less than nine periods per year

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6
Q

Outline the HPG axis

A
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7
Q

What are the common causes of oligomenorrhoea?

A

PCOS

Contraceptive/Hormonal treatments

Perimenopause

Thyroid disease/Diabetes

Eating disorders/excessive exercise

Medications e.g. anti-psychotics, anti-epileptics

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8
Q

What are the causes of amenorrhoea?

A

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
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9
Q

How should menstrual irregularity be investigated?

A

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
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10
Q

Hor should menstrual irregularity be managed?

A

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

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11
Q

What are the causes of heavy menstrual bleeding?

A

PALM: Structural Causes

  • Polyp
  • Adenomyosis
  • Leiomyoma (Fibroid)
  • Malignancy & hyperplasia

COEIN: Nonstructural Causes

  • Coagulopathy
  • Ovulatory dysfunction
  • Endometrial
  • Iatrogenic
  • Not yet classified
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12
Q

How should heavy menstrual bleeidng be investigated?

A

Bloods = FBC, TFT, coag

US pelvis

Cervical smear

High vaginal and endocervical swabs

Pipelle endometrial biopsy

Hysteroscopy and endometrial biopsy

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13
Q

How can heavy menstrual bleeding be managed?

A

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

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14
Q

What is the role of FSH?

A

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

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15
Q

In the follicular phase what keeps LH levels low?

A

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

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16
Q

After the first 10 days (mid-follicular phase) what affect does oestrogen have?

A

High levels now able to cause a +ve feedback = stim release of LH

FSH not released due to inhibin prod by the follicle

17
Q

What causes the LH surge? What is the result of the LH surge?

A

+ve feedback from oestrogen levels that are now high

Continued release of GnRH

Result = ovulation of the most mature follicle releasing the oocyte

18
Q

What is the role of inhibin?

A

-ve feedback = stops the secretion of FSH = as we don’t need anymore follicle maturing just yet

19
Q

Describe the function of progesterone

A

-ve feedback on GnRH = stop release of FHS/LH

Stimulate endometrial growth = for egg to implant if fertilised

20
Q

What causes the corpus luteum to degenerate?
As the corpus luteum degenerates what does that cause?

A

Progesterone inhibiting a further rise in LH

Result =

Progesterone levels fall = GnRH not inhibited = new cycle

Endometrial lining sheds as not maintained by progesterone

21
Q

What are the causes of abnormal uterine bleeding (AUB)?

A

Abnormal clotting - vWD, thrombocytopenia, leukaemia

Pathology - fibroids, endometriosis, PID, polyps

Medical - hypothyroid, liver disease, Ca

22
Q

How should abnormal uterine bleeding be investigated?

A

Hysteroscopy +/- biopsy

USS

23
Q

Outline how abnormal uterine bleeding is medically treated

A

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

24
Q

How is abnormal uterine bleeding surgically treated?

A

Hysterectomy (removal of the uterus +/- ovaries + cervix)

Endometrial ablation = resection, roller ball, laser, cold coag, microwave, balloon, radiofrequency