Week 6: Womens' health (1) (menstrual cycle and micturition) Flashcards

1
Q

Menstrual bleeding history

A

Menstrual history

Menarche: How old were you when you started your period?

LMP: When was the first day of your last period?

Cycle: Are your cycles regular? How often do you get your period? How long does the bleeding last?

Other problems: Other than your periods being heavy, do you have any problems with them?

  • Painful periods (dysmenorrhoea can suggest endometriosis/fibroids)
  • Bleeding between cycles (intermenstrual bleeding can suggest STI/contraception problems/malignancy)
  • Bleeding after sex (post-coital bleeding can suggest ectropion/malignancy)
  • Long breaks between periods (amenorrhoea can be a feature of anorexia/hormonal problems such as hypothyroidism)

How heavy are your periods (e.g. how many times do you change you tampon/pad)

Complete a full gynaecological history

Sexual and contraception history:

  • Are you sexually active at the moment? Do you have a regular partner? How many partners have you had in the past 6 months?
  • Have you had a sexual health screen in the past? When? Have you ever been treated for an STI?
  • Have you noticed any changes to your vaginal discharge?
  • Have you noticed any rashes or itching around your vulva?
  • Do you have pain when you’re having sex (dyspareunia)?
  • Are you using contraception at the moment? Have you used anything in the past?
  • Is there any chance you could be pregnant (e.g missed pills)?

Cervical smears:

  • When was your last cervical smear? Are you up to date with your smears?
  • Have you been vaccinated against HPV?
  • Any abnormal smears?
  • Any treatment required?

Urinary questions:

  • Any problems with going to the toilet?
  • Are you passing urine more often (frequency)?
  • Do you have any burning or stinging on passing urine (dysuria)?
  • Do you have any problems with incontinence?
  • So you have the sensation of “dragging” in your vagina (prolapse)?

Brief obstetric history:

  • Have you ever been pregnant? Any miscarriages or terminations?
  • Do you have any children? How old are they? Were they vaginal deliveries or c-sections? Any complications?
  • Are you currently trying to to get pregnant or have plans for a baby soon? (this will have an impact on management)

PMH

Family history e.g. of heavy bleeding

Allergies

Drugs

e.g. contraception

Social history

  • effect on personal life, inc time off work or school
  • smoking
  • alcohol
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2
Q

gynecological examination

A

Clinical examination should be undertaken to assess for any anaemia and also to rule out potential organic causes of menorrhagia.

  • Note general appearance and BMI. Body fat is very important in relation to metabolism of steroid hormones.
  • Note any signs suggestive of endocrine abnormality (hirsutism, acne) or bruising.
  • Look at the tongue for pallor and the nails for koilonychia.
  • Examination of the abdomen always precedes pelvic examination; otherwise, large pelvic masses can be missed.
  • Pelvic examination may not always be appropriate (for example, in adolescents) but should be considered:
  • Where underlying pathology seems likely from the history.
  • When the levonorgestrel-releasing intrauterine system (LNG-IUS) is being considered as treatment.
  • Where initial treatment has not been effective.
  • Where relevant, ascertain that the cervical smear is up to date.
  • Inspect the cervix and take swabs if clinically indicated.
  • Where indicated, perform a bimanual examination. Abnormalities may include a bulky or grossly enlarged uterus, fixation of the uterus or tenderness.
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3
Q

urological history taking

A

History of presenting complaint

Key urological symptoms

Symptoms that are typically associated with urological disease include:

  • Dysuria: typically associated with urinary tract infection (UTI), including sexually transmitted infections (e.g. chlamydia, gonorrhoea).
  • Urinary frequency: commonly associated with UTIs.
  • Urinary urgency: may be associated with UTIs or detrusor instability.
  • Nocturia: associated with UTIs and prostate enlargement (e.g. benign prostatic hyperplasia).
  • Haematuria: associated with UTIs, trauma (e.g. catheter insertion) and renal tract cancers (e.g. bladder cancer, renal cancer).
  • Urinary hesitancy, terminal dribbling and poor urinary stream: associated with enlargement of the prostate (e.g. prostate cancer, benign prostatic hyperplasia).
  • Urinary incontinence: associated with a wide range of pathology including UTIs, detrusor instability and spinal cord compression (e.g. cauda equina syndrome).
  • Fevers and rigors: typically associated with pyelonephritis.
  • Nausea and vomiting: typically associated with pyelonephritis.
  • Weight loss: associated with malignancy and uraemia.
  • Uraemic symptoms: nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritis and confusion.

SOCRATES

Associated symptoms

  • red flags
    • fever
    • weight loss
    • night sweats
  • systemic enquiry
    • palpitations or chest pain
    • SoB
    • abdominal pain
    • confusion
    • muscle wasting
    • uraemic frost

PMH

Allergies

Drug history (some relevant examples)

  • Diuretics (e.g. furosemide): a common cause of nocturia and can cause acute kidney injury.
  • Alpha-blockers: commonly used to treat prostatic enlargement
  • Nephrotoxic medications (e.g. ACE inhibitors, NSAIDs): may cause acute or chronic kidney injury.
  • Antibiotics: commonly required for recurrent UTIs and may be prescribed as prophylaxis.

Family hisotry

Social history

  • type of accom
  • who they live with
  • ADL
  • carer input
  • smoking
  • alcohol
  • recreational drug use
  • diets and fluids
  • occupation

Closing

  • summarise key points
  • make sure to have included ICDE
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4
Q

urinary examination

A
  • General - look for fever and signs of infection and systemic illness.
  • Abdominal - a tender enlarged bladder with dullness to percussion well above the symphysis pubis, often almost to the level of the umbilicus.
  • Genitourinary:
  • In men, look for phimosis or meatal stenosis, as well as urethral discharge and genital vesicles.
  • In women, look for evidence of:
  • Vulval or vaginal inflammation or infection.
  • Cystocele, rectocele or uterine prolapse.
  • Pelvic mass (eg, retroverted gravid uterus, uterine fibroid, gynaecological malignancy).
  • Per rectum (PR) - check anal tone, prostatic size, nodules, tenderness, etc and exclude faecal impaction[6].
  • Neurological - look for evidence of prolapsed disc or cord compression by checking lower limb power and reflexes as well as perineal sensation.
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5
Q

hormonal production summary (menstrual cycle)

A
  • Hypothalamus: GnRH
  • Anterior pituitary: FSH and LH (work on the theca and granulosa cells)
  • Ovaries- progesterone and oestrogen (theca cells (converted from androgen by the granulosa cells)
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6
Q

Cycle length- what is normal

A
  • Normal duration 21-35 days (28 day av)
  • Day 14 usually ovulation → time for the follicle to mature
    • Variation is due to length of follicular phase
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7
Q

Disruption to cycle

A
  • Physiological factors
    • Pregnancy
    • Lactation
  • Emotional stress
  • Body weight
  • Infertility
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8
Q

2 cycles occurring in paralllel

A
  • Ovarian cycle- 2 phases
    • Pre- ovulation- follicular phase
    • Post ovulation- luteal phase
    • Uterine cycle- 2 phases
      • Pre-ovulation
        • Period
        • Proliferative
      • Post-ovulation
        • Secretory
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9
Q

The Hypothalamic-Pituitary-Gonadal (HPG) Axis

A

The hypothalamus, anterior pituitary gland and gonads (ovaries) work together to regulate the menstrual cycle.

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10
Q

summarise how the HPG axis causes ovulation

A
  • GnRH from the hypothalamus stimulates luteinising hormone (LH) and follicular stimulating hormone (FSH) release from the anterior pituitary gland.​
  • LH and FSH are gonadotropins that act primarily on the ovaries in the female reproductive tract
    • FSH binds to granulosa cells to stimulate follicle growth and also permits the conversion of androgens produced by the theca cells to oestrogen.
      • Also stimulates inhibin à which exerts negative feedback on FSH
    • LH binds to theca cells which produces androgens (need converting to oestrogen and progesterone (aromatase produced by granulosa cells)
  • Oestrogen and the HPG axis (levels of LH and FSH)
    • Moderate levels of oestrogen exerts a negative feedback effect on the HPG axis
    • At a high levels of oestrogen, negative feedback is converted to positive feedback to the HPG axis à leads to surge in LH (not FSH due to inhibin) à leading to ovulation
  • Oestrogen in the presence of progesterone (i.e. once the follicle is secreting a high level of progesterone in the luteal/ secretory phase) exerts negative feedback on the HPGà preventing the development of another follicle
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11
Q

the ovarian cycle isFSH binds to

A

granulosa cells and stimulates follicle growth and also permits the conversation of androgens produced by the theca cells to oestrogen

  • Also stimulates inhibin à which exerts negative feedback on FSH
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12
Q

LH binds to

A

theca cells

which produces androgens (need converting to oestrogen and progesterone (aromatase produced by granulosa cells)

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13
Q

the ovarian cycle is split into

A

follicular phase

(ovulation)

luteal phase

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14
Q

Follicular phase

A
  • Growth of follicles stimulated by FSH (which is secreted by the AP → stimulated by GnRH release from hypothalamus (stimulated by activin secreted by granulosa cells))
    • Primordial follicles → primary follicles à secondary follicles → tertiary follicles
    • One of these follicles then becomes the ‘graafian follicle’ or dominant→ oocyte will be released during ovulation
  • As time goes by FSH levels reduce due to the release of inhibin
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15
Q

dominant follicle

A

graafian follicle

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16
Q

why does the level of FSH decrease overtime

A

due tot he release of inhibin

17
Q

why does LH surge

A

due to certain level of oestrogen being produced by the graafian cell

18
Q

ovulation

A
  • 1 day event
  • Due to spike in LH (day 14)à surge in oestrogen
  • Oocyte bursts out of follicle
  • Level of oestrogen suddenly drops due to disruption in granulosa cell membrane
19
Q

lutueal phase

A
  • Empty follicle becomes the corpus luteum
  • Produces oestrogen and progesterone (used in the menstrual cycle)
    • Exerts negative feedback on LH and FSH to the hypothalalmus à therefore levels remain low
    • Will last for the rest of the cycle (14 days) if not fertilsed à will degenerate/involute to become the corpus albicans
    • If egg is fertilised it will stay for longer, stimulated by HCG, which is secreted by fertilised egg, until the placenta can take over endocrine role
    • Cycle is restarted if egg is not fertiles and FSH levels will begin to increase again
20
Q

the coprus luteum (empty follicle) produces

A

Produces oestrogen and progesterone

  • Exerts negative feedback on LH and FSH to the hypothalalmus à therefore levels remain low
21
Q

how long is the luteul phase

A

14 days

22
Q

the uterine cycle is split into

A
  • menstrual phase
  • proliferative phase
  • secretory phase
23
Q

Menstrual phase

A
  • When period occurs → shedding of lining of the endometrium
  • When follicles (in ovarian cycle) start to grow)
24
Q

Proliferative phase (of the endometrium)

A

mainly oestrogen

  • Early proliferative= sparse glands, straight
  • Late proliferative – thicker functional layer, glands coiled
25
Q

Secretory phase →mainly progesterone

A
  • Secretory-endometrial thickness at maximum, very coiled glands, coiled arterioles
  • Day 21→ best time for implantation
  • Therefore most fertile time is few days before and after ovulation
  • If egg not fertilised, CL degenerates, reduction in O and P → loss of endometrial lining→ menstrual phase
26
Q

If you have a fertilised egg…

A

HCG will be released (syncytiotrophoblast… prevents CL from degenerating… CL releases oestrogen and progesterone which maintains the endometrium → perfect environment for implantation)

27
Q

uterine layer histology

A
  • Endometrium= epithelium and stroma
    • Functional layer- responsive to hormone- shed in menstruation
    • Basal layer- develops into new functional layer (constant blood supply)
  • Myometrium
  • Perimetrium
28
Q

steroid hormone action on the endometrium: oestrogen

A
  • Thickening of endometrium
  • Increases fallopian tube function- cilia which waft oocyte along fallopian tube
  • Growth and motility of myometrium
  • Produces thin alkaline cervical mucus- for sperm
  • Vaginal changes
  • Changes skin, hair, metabolism
29
Q

steroid hormone action on the endometrium: progesterone

A
  • Further thickening of endometrium (secretory)
  • Thickening of myometrium and reduction of motility- to stop implanted embryo from being expelled
  • Thick acidic cervical mucus
  • Development of breast tissue
  • Increased body temp
  • Metabolic changes
  • Electrolyte changes
30
Q

storage phase of micturition

A

When urine is stored in the bladder. Under control by the sympathetic and somatic nervous system.

As the bladder fills the rugae distend and a constant pressure in the bladder (intra-vesicular) is maintained- stress-relaxation phenomenon. Can have up to 150ml of urine in bladder before pressure changes.

  • Involved relaxation of the detrusor muscles of the bladder
  • Contraction of both the internal (IUS) and external (EUS) urethral sphincters
  • Detrusor muscle- sympathetic nervous control
  • IUS- sympathetic nervous control
  • EUS- somatic nervous control
31
Q

outline storage phase

A
  1. To stimulate storage, impulses from the cerebral cortex travel to the pons (slow impulses) via afferent sensory neurones
    • Pons is responsible for coordinating the actions of the urinary sphincters and the bladder
    • Area involved in storage phase= pontine continence centre (L (lateral)- region of the pons)
  2. Stretch receptors of sensory neurones (afferent) detect stretch in the detrusor muscle of the bladder – send feedback to 2 locations:
    • Sensory neurone enters the spinal cord between S2-S4 (S2, S3, S4 keeps the poo and wee off the floor) but ascends to higher levels of the spinal cord where they synapse at T10-L2 with sympathetic pre-ganglionic neurones
    • Stretch receptors in detrusor muscle also send feedback to the cerebral cortexà allows us to know when we need to wee
  3. Impulses travel from the spinal cord to the bladder via the sympathetic hypogastric nerve (nerve roots T10-13) and have an effect on the:
    1. Detrusor muscles- relaxation of the bladder wall via stimulation of B3- adrenoreceptors in the fundus and the body of the bladder
    2. Internal urethral sphincter (IUS)- contraction of IUS via stimulation of alpha1- adrenoreceptors at the bladder neck
    3. EUS is under voluntary somatic control
      • Impulses travel to the EUS via the pudendal nerve (S2-4) to nicotinic (cholinergic) receptors on the striated muscle resulting in contraction of the sphincter
    4. L (lateral) centre important for deferring micturition
      • Sends actions down through the cord which stimulate the pudendal motor neurones
      • Maintains continence
32
Q

EUS (external urinary sphincter)

A
  1. under voluntary somatic control

Impulses travel to the EUS via the pudendal nerve (S2-4) to nicotinic (cholinergic) receptors on the striated muscle

33
Q

IUS under

A

sympathetic nervous control

34
Q

voiding phase is under

A

paraysmpathetic control

35
Q

outline the voiding phase

A
  1. Afferent nerves (sensory S2-4) of the bladder signal the need to void around 400ml of filling, this signal projects to the cerebrum and pontine micturition centre (M (medial)- centre)
  2. Upon the voluntary decision to urinate, neurones of the pontine micturition centre fire to excite the sacral preganglionic neurones.
  3. There is subsequent parasympathetic stimulation to the Pelvic Nerve (S2-4) causing a release of ACh, which works on M3 muscarinic ACh receptors on the detrusor muscle, causing it to contract and increase intra-vesicular pressure.
  4. When we decide to wee, M centre (in pontine micturition centre) sends inhibitory impulses to L centre (Onuf’s nucleus, with a resultant reduction in :
    • Sympathetic stimulation to the internal urethral sphincter causing relaxation.
    • Relaxation of external sphincter by inhibiting the pudendal nerve à micturition can proceed
36
Q

summary of micturition nerves

A
37
Q

duloxetine

A
  • Treatment for Stress UI (also depression and anxiety)
    • NA and Serotonin uptake inhibitor
    • Increases activity of the pudendal nerveà keeping EUS closed
    • Facilitates sphincter acidity during urine storage and not during voiding, maintains the bladder-sphincter synergy
38
Q

B3 agonist. e.g. Mirabegron

A
  • stimulation of B3 causes detrusor muscle to relax and therefore increase the bladders capacity