Anatomy and physiology Flashcards

1
Q

Describe the sexual differentiation of the internal and external genitalia during embryogenesis

A

In both sexes, the Mullerian and Wolffian ducts originate from the mesoderm. Gonadal development is dependent on the SRY gene on Chromosome Y.
In male embryos, Sertoli cells produce AMH (Anti-Mullerian hormone), which causes suppression of the Mullerian duct. The Wolffian duct develops into the external genitalia.
In female embryos, there is no AMH produced, so the Mullerian duct develops into the internal genitalia.

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2
Q

Describe the external female genitalia.

A
  • Mons pubis
  • Clitoris
  • Labia majora and labia minora
  • Urethral opening
  • Vaginal opening
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3
Q

What are the natural barriers to pathogens in the vagina?

A
  • Stratified squamous epithelium with tight junctions
  • Glycogen rich epithelium (stimulated by E2), which provides substrate for Bacillus to produce lactic acid, maintaining the pH of the vagina at ~4.5
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4
Q

Describe the organs/tissues bordering the vagina (Ant-post + lateral).

A

Anteriorly: base of the bladder + 2/3s of urethra (fused)

Posteriorly:

  • Upper 1/3: Pouch of Douglas
  • Middle 1/3: Middle rectum
  • Lower 1/3: Perineal body

Laterally: Levator ani muscles, ureters, pelvic fascia.

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5
Q

Describe the support of the vagina. Why is this important?

A

Main support comes from the levator ani muscles (pelvic floor/pelvic diaphragm). These are: iliococcygeus, pubococcygeus, and puborectalis.
Also 3 levels of ligaments and fascia:
-Level 1: Apical support. Uterosacral ligaments attach cervix to sacrum, cardinal ligaments attach lateral fornices to pelvic wall.
-Level 2: Midvaginal support. Pelvic fascia.
-Level 3: Perineal body.

**Defects in any of these structures will predispose to prolapse. eg. Level 1- uterine/vaginal vault prolapse, Level 2- rectocele/cystocele, Level 3- ant/post wall prolapse

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6
Q

Describe the gross anatomy of the uterus

A
  • Body
  • Fundus (top)
  • Cornu (where tubes enter)
  • Isthmus (lower part into cervix)
  • Cervix
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7
Q

Through which ligament do the Fallopian tubes run through?

A

Broad ligament

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8
Q

Describe the attachments of the ovaries

A
  • Attached to pelvic wall by suspensory ligament of the ovaries (receive blood supply + nerves through this)
  • Attached to uterus by ovarian ligament and mesovarium of the broad ligament
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9
Q

Describe the blood supply of the pelvic organs. What is significant about the uterine artery?

A
  • Ovary receives blood supply from the ovarian artery (branch of the aorta)
  • Anterior branch of the internal iliac forms the uterine A, vaginal A, vesical A, middle rectal A, pudendal -> vulval A

The uterine A supplies uterus, ureters, cervix, upper vag. It runs in the broad ligament with the ureter, and thus both are at risk of damage during hysterectomy.

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10
Q

Describe the lymphatic drainage of the pelvic organs. Why is this relevant and important to know?

A

Overall: inguinal -> ex iliac -> common iliac -> para-aortic

External genitalia-> femoral + superficial inguinal nodes
Cervix-> stepwise or straight to para-aortic
Ovaries -> straight to para-aortic

  • Infections of the external genitalia eg. HSV can cause enlarged inguinal nodes
  • Ovarian cancer can disseminate quickly
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11
Q

Which is the main nerve supplying the external genitalia?

A

Pudendal nerve (S2-S4). Supplies sensation to vulva, anus, and levator ani

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12
Q

What are some possible Mullerian tract abnormalities? How common are they?

A
  • Affect up to 6% of the population
  • Obstruction: eg. Imperforate hymen
  • Duplication: eg. partial, total, uterine septum
  • Agenesis: Rokitansky syndrome (no uterus, cervix)
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13
Q

Describe the physiology of the normal menstrual cycle

A

Hypothalamus releases pulsatile GnRH –> stimulates pituitary FSH and LH production
-LH stimulates theca cells to produce androgens
-FSH stimulates follicles to grow, and stimulates aromatase to convert androgens to oestrogen
As follicles grow, they produce more oestrogen, which downregulates FSH. This leads to a relative lack of FSH, causing only one dominant follicle (that has become independent of FSH) to keep growing. The other follicles undergo atresia. The dominant (Graffian) follicle develops fully and produces large amounts of oestrogen. High oestrogen triggers the pituitary to go from negative feedback to positive –> big LH surge triggering ovulation.
After ovulation, the follicle becomes the corpus luteum, and produces progesterone and oestrogen. This stimulates the endometrium to undergo hyperplasia (oestrogen) and secrete glycoproteins (progesterone) to prepare for implantation. When implantation does not occur, the corpus luteum degrades and the lack of hormonal support causes the endometrium to shed in the process of menstruation.

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14
Q

Describe the role of prostaglandins during the menstrual cycle and clinical relevance.

A

PGs are involved in the process of ovulation and in menstruation. Supposedly, blocking PGs may inhibit ovulation. Blocking PGs (with NSAIDs) during menstruation also decreases blood loss and pain.

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15
Q

Describe the process of puberty in females

A

GnRH pulsatility begins around 8-9 years, causing LH and FSH release –> oestrogen increase.
The rising oestrogen stimulates the development of secondary sex characteristics, starting with breast development, then pubic and axillary hair, and finally menstruation.

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16
Q

Define precocious puberty and name some causes.

A

Onset of puberty before the age of 8 years in F.
Causes can be divided into central (increase in LH and FSH) or peripheral (independent oestrogen production).
Central PP is usually idiopathic in girls, though other causes include any CNS pathology such as pituitary tumours, infection, injury.
Peripheral precocious puberty is usually caused by congenital adrenal hyperplasia, or by sex steroid producing tumours in the adrenals or gonads.

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17
Q

Define delayed puberty and name some causes.

A

Delayed puberty is lack of development of secondary sex characteristics by the age of 14 years. This is not the same thing as primary amenorrhoea.
Causes can be divided into hypergonadotrophic (high LH + FSH) and hypogonadotrophic (low LH + FSH).
Hypergonadotrophic causes include Turner syndrome, Fragile X, iatrogenic causes eg. pelvic radiotherapy, or immunological.
Hypogonadotrophic causes include Kallmann syndrome, CNS tumours, FHA, or chronic illness.

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18
Q

Describe the features of Turners syndrome. Why is there often delayed puberty?

A

Turners syndrome is a genetic condition caused by the absence of one X chromosome (in all cells or some cells eg. mosaicism), with the genotype 45XO.
Affected individuals may have short stature, webbed neck, wide carrying angle, barrel chest with widely-spaced nipples, etc. There is also an association with several medical complications, including aortic coarctation, deafness and renal anomalies.
In Turner’s, the ovaries do not fully develop and are termed ‘streak gonads’. As a result, LH and FSH production during the onset of puberty fails to stimulate oestrogen production, and secondary sex characteristics do not develop and menarche does not occur.

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19
Q

What are the types of DSD? Describe.

A
  • Turners syndrome. 45XO.
  • 46 XY gonadal dysgenesis: genotypically male, but testis do not develop (one cause is SRY gene mutation/loss) so the affected individual has female external genitalia. This means the individual is phenotypically female but without functioning ovaries.
  • 46 XY DSD: male testes develop but are insensitive to androgens, meaning external genitalia do not virilise (become male). Individuals are phenotypically female, but with male internal genitalia.
  • 46 XX DSD: also known as congenital adrenal hyperplasia. Adrenal androgens result in partial virilisation, causing ambiguous genitalia at birth.
  • 5a reductase deficiency: 46XY but androgens cannot be converted to the most active form, leading to partial virilisation and ambiguous genitalia.
20
Q

Define the different types of amenorrhoea and name several causes.

A

Primary amenorrhoea: no onset of periods by 15 years in girls with secondary sex characteristics, or by 13 in those without.
Secondary amenorrhoea is the cessation of menses for a period of 6 or more months in the absence of pregnancy.
Causes can be divided into:
Hypothalamic: CNS pathology (tumours, infection, radiation), Kallmann’s, FHA
Pituitary: CNS pathology (tumours), Sheehan’s, pituitary apoplexy, iatrogenic (surgery, radiation)
Ovarian: PCOS, Turners, Fragile X, immunological, iatrogenic
Endometrial: Mullerian tract abnormalities eg. absent uterus, imperforate hymen

21
Q

A 15 year old girl attends adolescent gynae clinic after referral from her GP as she has not yet started her periods. Describe your approach to reaching a diagnosis.

A
  • Full history, focusing on growth and development, nutrition + exercise, PMH, FHx of puberty onset.
  • Examination: looking for signs of genetic conditions eg Turners, Fragile X, secondary sex characteristics, and pelvic exam to check for outflow tract obstruction
  • Ix: bloods (LH +FSH, oestrogen, TFTs) karyotype, USS, consider cranial imaging/pelvic imaging if indicated.
22
Q

A 40 year old woman attends the GP. She reports that she has not had a period in 6 months. What else would you want to know from the history, and what investigations might you consider?

A
  • History: characterise her menstrual cycle history, including any irregular cycles, heavy bleeding, etc. Pregnancy/breastfeeding. Symptoms of POI eg. hot flushes, poor sleep and concentration, vaginal dryness. Recent weight loss/diet changes/stress. Thyroid symptoms. Visual changes, galactorrhoea. Symptoms of androgen excess (unlikely cause). PMH.
  • Examination: general, abdo + pelvis. Looking for signs of chronic illness, thyroid disease, vaginal dryness.
  • Ix: bloods (FSH+ LH, oestrogen, prolactin, TFTs). Consider cranial imaging if indicated.
23
Q

What are the diagnostic criteria of PCOS? Name some other common features.

A

-Menstrual irregularity (amenorrhoea, oligomenorrhoea (>35 day cycles, <9 cycles per year))
-Clinical/biochemical hyperandrogenism
-Polycystic ovarian morphology (>12 follicles one 1+ ovary, or 1+ ovary >/= to 10cm3)
Other common features include being overweight/obese and insulin resistance (may have acanthosis nigricans)

24
Q

What are the treatments for PCOS?

A

Management of PCOS needs to take into account the fertility goals.
-For all women: encourage diet + exercise, with aim to loose weight + improve insulin resistance.
-If not wanting to conceive:
COCP (regulates cycles, reduces HA symptoms), LNG-IUS (good for preventing endometrial hyperplasia, no effect on HA symptoms), or cyclical progesterone (regulate cycles). Cyproterone acetate (usually combined with E2, reduces HA symptoms), spironolactone (reduces HA symptoms).
-If wanting to conceive:
Clomifene citrate 1st line to induce ovulation. Alternatives include OI with other agents eg. hMG, or IVF.
-Can also consider metformin if there is insulin resistance. This also can regulate cycles and improve HA symptoms in addition to helping with weight loss.

25
Q

What is premenstrual syndrome?

A

Collection of physiological and psychological symptoms experienced in a cyclical pattern prior to the onset of menstruation due to the fluctuating hormone levels.
Includes: bloating and weight gain, mood changes eg. lability, depression, abdominal cramps, fatigue, headache.

26
Q

What is the management of PMS?

A
  • Conservative: diet and exercise can improve mood and fatigue, relieve cramping
  • Mild: stress management eg. yoga, vitamins (B6, Mg)
  • Mod/severe: SSRIs/CBT either continuous or in luteal phase, or cycle suppression with COCP/prog/LNG-IUS
  • Resistant: referral to gynae. GnRH analogue with HRT, surgery with HRT.
27
Q

What are the normal changes to metabolism in pregnancy? How should diet change?

A

During pregnancy, energy requirements increase by about 14%. Therefore, women should eat about 200-300 extra calories per day. This should include higher amounts of protein, and vits/minerals like iron, folic acid, Vit C.

28
Q

How does weight change during pregnancy?

A

There is also normal weight gain during pregnancy of about 25% or 10-15kg. This is due to hormonal effects increasing energy deposits (eg. insulin sensitivity early in pregnancy leading to increased stores of glycogen and fat) as well as the weight of the baby, placenta, breast tissue, amniotic fluid, and increased blood volume.

29
Q

How does maternal anatomy change (genital tract, joints, breasts, skin) during pregnancy and how does this lead to symptoms experienced in pregnancy?

A

Genital tract: uterus undergoes hyperplasia and rotates to the right, hypertrophy of uterine ligaments, cervix becomes oedematous + softens + mucus plug
Ortho: Relaxation of pelvic joints and ligaments -> back pain, neck pains + numbness, carpal tunnel, etc.
Breasts: grow and increase vascularity -> tenderness, warmth
Skin: striae gravidarum (abdo), striae distensae (thighs), chloasma gravidarum (butterfly pigment on face), linea nigra (abdo)

30
Q

How does the maternal GI system change during pregnancy? What symptoms can arise as a result?

A

GI: decreased oesophageal sphincter strength, decreased peristalsis and gastric emptying –> (constipation, N+V, heartburn)
GB: increased cholesterol and bile salts, decreased gallbladder emptying –> cholestasis of pregnancy (itching)
Liver: increased albumin and proteins (globulin, fibrinogen)

31
Q

How does the maternal urinary system change during pregnancy? What symptoms can arise as a result?

A

Increased pressure and relaxation of the ureters –> reflux and stasis –> increased risk of UTIs
Increased GFR –> increased frequency and output, some glycosuria

32
Q

How does the maternal CVS change during pregnancy? What symptoms can arise as a result?

A

Increased CO (increased HR and SV), decreased PVR
–> signs of hypovolaemia can be masked because there is good compensation
-Some ECG changes normal, soft systolic ejection murmur normal
Can lead to symptoms of tiredness, dyspnoea, palpitations, syncope

33
Q

How does maternal haematology change during pregnancy? What symptoms can arise as a result?

A
  • Increased RBC production with dilutional anaemia
  • Increased WBC (neutrophils) but poor T/B cell responses –> increased susceptibility to viral infections
  • Increased thrombosis risk: increased stasis + coagulability
34
Q

How does maternal endocrinology change during pregnancy? What symptoms can arise as a result?

A
  • Increased oestrogen + progesterone + HPL (placenta)
  • Increased bhCG during early pregnancy (CL then placenta)
  • T3 +T4 increase
  • Cortisol increases
  • Prolactin increases
35
Q

Name some causes of abnormal menstrual bleeding

A

Abnormal menstrual bleeding can be classified using the FIGO PALM-COEIN system which divides causes of bleeding into structural and non-structural.

Structural causes:
Polyp: endometrial, cervical 
Adenomyosis
Leiomyoma 
Malignancy (endometrial, cervical, vaginal)
Non-structural causes:
Coagulopathy
Ovulatory disorder
Endometrial: DUB 
Iatrogenic
Not classified
36
Q

What is the definition of HMB?

A

> 80 ml period or periods lasting >7 days or both

37
Q

What are some causes of HMB?

A

Fibroids (30%), adenomyosis, polyps, coagulopathy, thyroid dysfunction, IUDs, drugs, cancer

38
Q

A 30 year old woman comes to gynae clinic because she has very heavy periods. What would you like to know?

A
  • HMB: quantify blood loss (pads + tampons, flooding), clots, length of bleeding, effect on life, onset. Bleeding at any other time. Tried anything for it?
  • Cycles: LMP, length, regularity, pain
  • Gynae as appropriate: discharge, urine + bowel symptoms
  • Anaemia: SOB, fatigue, dizziness
  • Gynae Hx (smears, contraception, sexual), Obs Hx
  • PMH and DHx, allergies
  • FHx: bleeding disorders, cancers
  • SHx: impact, job, smoking
39
Q

A 30 year old woman comes to gynae clinic because she has very heavy periods. They have been heavy for the past 2 years. Her cycles are regular and 30 days long, the periods last for about 5 days and she uses 5-6 tampons a day and occasionally leaks. She does not have significant pain during her periods, and does not have any symptoms of anaemia. Her smears are up to date, she is not sexually active and is not taking contraception. She has no other PMH and is not on any medications.
What would you like to do next, and why?
What are the management options for this woman?

A

Examination: abdo and pelvis to palpate for bulky uterus indicating fibroids/adenomyosis, inspect the vagina and cervix to look for abnormalities

Investigations: like to do a FBC and TVUSS if any suspicion of fibroids or uterine pathology

Management: partially depends on cause. If no large fibroids or endometrial pathology:

  • LNG-IUS/Mirena is best. May need 6 months to settle irregular bleeding. 1/3 will have no periods.
  • If not: tranexamic acid during periods, NSAIDs, COCP, progestogen-only mini pill.
40
Q

Describe the management of fibroids.

A

<3cm: use pharmacological management, either non-hormonal (tranexamic acid/NSAIDs) or hormonal (LNG-IUS, CHC, progestogen-pill)
-Endometrial ablation, hysteroscopic removal of submucosal fibroids

> 3cm:

  • Pharmacological as appropriate, usually less effective
  • Uterine artery embolisation
  • Surgery: myomectomy (fertility-sparing), hysterectomy +/- pretreatment with GnRH analogues to shrink
41
Q

Name some causes of dysmenorrhoea

A

Dysmenorrhoea can be primary or secondary. Primary dysmenorrhoea is usually normal. Secondary may be due to fibroids, endometriosis, PID, cervical stenosis

42
Q

A 26 year old woman comes to the GP complaining of painful periods. What do you want to know?

A
  • Pain: when did this start? How bad is the pain? When is it in relation to the bleeding? Do you take anything for it? How has it been impacting your life?
  • Cycles: LMP, regularity, length, periods, HMB, IMB/PCB
  • Gynae symptoms: other pain (dyspareunia), dyschaezia, discharge
  • Other gynae history, smears, contraception, sexual Hx
  • Obs Hx
  • PMH, DHx
  • SHx: smoking, alcohol
43
Q

A 26 year old woman comes to the GP complaining of painful periods. What will you look for on examination?

A
  • Abnormal cervix: cervical stenosis
  • Cervical excitation: PID
  • Fixed uterus: adhesions/PID
  • Enlarged/bulky uterus: fibroids
  • Rectovaginal nodules/uterosacral ligament nodules: endo
44
Q

What are the management options for dysmenorrhoea?

A

Conservative: heat, exercise
Pharmacological: NSAIDs/paracetamol, hormonal treatment eg. COCP, LNG-IUS (best), POP
Surgery where appropriate: adhesiolysis, excision of endometriosis, hysterectomy

45
Q

Describe the management of endometriosis.

A

Pharmacological:

  • NSAIDs/paracetamol
  • Hormonal: patient decision making tool on NICE. LNG-IUS, COCP, POP, etc.

Surgical:

  • Laparoscopic excision of endometriosis, endometrioma removal
  • Hysterectomy