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Kofi: Pure clinical conditions 2 > Reproductive > Flashcards

Reproductive Flashcards

1
Q

Which factors affect transmission of genital infections?

A
  • Age
  • Ehtnicity
  • Socioeconomic status
  • Age at first sexual intercourse
  • Number of partners
  • Sexual orientation
  • Condom use
  • Menstrual cycle
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2
Q

What is the impact of stigma associated with STIs?

A

There is impact on health and well being of affected individuals and contacts

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3
Q

What are the general considerations made during diagnosis of STI?

A
  • Could be symptomatic or asymptomatic
  • Sexual history and physical examinations are essential
  • Diagnostic samples need to be collected from the correct sites
  • Every effort should be made to isolate/diagnose the offending organism
  • Prompt treatment and partner notification
  • Advice, counselling and education of the patient and contacts
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4
Q

What are the general principles of STI treatment?

A
  • Treatment (antibiotics, antiviral, topical creams)
  • Co-infections are common so screen for other STIs
  • Contact tracing
  • STI prevention
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5
Q

What causes chlamydia and what are the microbiolical features of it?

A
  • Chlamydia trachomatis

- Obligate intra-cellular bacterium

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6
Q

What are the symptoms of chlamydia in males?

A
  • Urethritis
  • Dysuria
  • Epididymitis
  • Proctitis
  • Prostatitis
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7
Q

What are the symptoms of chlamydia in females?

A
  • Mostly asymptomatic
  • Increased discharge
  • Post coital and intermenstrual bleeds
  • Dyspareunia
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8
Q

Apart from the genital tract, which regions can chlamydia trachomatis affect?

A
  • Ocular inoculation that manifest as conjunctivitis

- Pharyngeal infection which is usually asymptomatic

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9
Q

What test are used to diagnose chlamydia in men?

A
  • First catch urine NAAT
  • Urethreal swabs - less acceptable
  • Rectal and pharyngeal NAAT for extragenial sampling
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10
Q

What is used to treat chlamydia?

A
  • Doxycycline or Azithromycin 1st line

- Erythromycin or Ofloxacin 2nd line

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11
Q

What is the cause of gonorrhoea and what are the microbiological features of it?

A

Neisseria Gonorrhoeae

-Gram negative intracellular diploccus

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12
Q

What are the primary sites of infection for neisseria Gonorrhoeae?

A

-Urethra, Endocervix, Rectum, Pharynx, and Conjunctiva

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13
Q

What are the main symptoms of Gonorrhoea in men?

A
  • Urethral discharge
  • Dysuria
  • Anal discharge
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14
Q

What are the main symptoms of gonorhea in women?

A
  • Asymptomatic in women in most cases
  • Altered discharge
  • Lower abdominal pain
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15
Q

Which investigations are undertaken in the diagnosis of Gonorhea?

A
  • Microscopy of gram stained genital specimen in men more than women
  • NAATS
  • Cultures for confirmatory identification and antimicrobial testing
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16
Q

What is used in the treatment of gonorrhoea?

A
  • Intramuscular Ceftriaxone plus oral azithromycin
  • Spectinomycin as alternative in penicillin allergy
  • Test of cure
  • Partner Notification
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17
Q

Why is azithromycin used in combination with ceftriaxone?

A
  • Shown to boost action of ceftriaxone
  • Decreases chances of developing resistance to ceftriaxone
  • People how have an STI have an increased change of co-infections. Azithromycin covers clamydia as a co-infection
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18
Q

What is the cause of herpes?

A

Herpes Simplex Virus

HSV 1 - oral-labial herpes
HSV 2 - primary, non-primary or recurrent infection

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19
Q

What are the symptoms of Herpes?

A
  • Painful ulceration
  • Dysuria
  • Vaginal discharge
  • Can be asymptomatic
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20
Q

What are the systemic features of Herpes?

A
  • Fever

- Myalgia

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21
Q

What is used to diagnose HSV?

A
  • Virus detection of vesicle fluid or ulcer base

- Type specific Serology

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22
Q

What is the treatment for Herpes?

A
  • General advice
  • Aciclovir
  • Suppresive treatment for recurrent HSV
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23
Q

What is the recommendation give to patient with primary herpes in pregnancy?

A

-Caesarian section recommended

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24
Q

What is the organism that causes syphilis and what are its microbial features?

A
  • Treponema pallium

- Spirochete bacterium

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25
Q

What is the pathophysiology of syphilis?

A

1 - Painless ulcer
2 - Rash, mucosal lesion, multi system involvement

Latent- symptom-free for years

3 - Up to 40 years after initial infection (neurosyphillis, parenchymous, cardiovascular syphillis, Gummas)

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26
Q

What is trichomanas vaginalis?

A

Infection but flagellated Protozoa

Treated with metranidazole

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27
Q

Scabies can spread sexually. True/False

A

True. It can affect the genitalia and spread. Treatment is permethrin

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28
Q

What are anogenital warts?

A
  • Benign lesion caused by the HPV virus

- More than 100 HPV types

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29
Q

Which HPV types commonly cause genital warts?

A

Types 6 or 11

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30
Q

What are the features of anogenital warts?

A

-Benign, painless, epithelial or mucosal outgrowths

Found at

  • Penis
  • Vulva
  • Vagina
  • Urethra
  • Cervix
  • Perianal skin
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31
Q

Which strains of HPV are high risk oncogenic?

A

HPV 16

HPV 18

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32
Q

What is used in the diagnosis of Anogenital warts?

A

-Biopsy in atypical lesion or non-response treatment

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33
Q

What are the treatment measures for anogenital warts?

A
  • No treatment
  • Topical application
  • Physical ablation
  • HPV vaccination
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34
Q

What is bacterial vaginosis?

A

Common cause of abnormal discharge in women of childbearing age. Discharge often fishy

  • Gardnerella vaginalis
  • Treated with metronidazole
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35
Q

What is vulvovaginal candidiasis?

A
  • Caused by Candida albicans or non albicans candida species
  • Vaginal discharge typically curdy and non offensive, Vulval itch, Soreness, Dyspareunia

Treatment: Topical and oral azoles

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36
Q

What is pelvic inflammatory disease?

A

Result of infection ascending the endocervix causing endometriosis, salpingitis, parametrises, oophoritis, tubo-ovarian abscess and/or pelvic peritonitis.

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37
Q

What is the pathophysiology of pelvic inflammatory disease?

A
  • Ascending infection from endocervic and vagina
  • Infecgtion causes inflammation
  • Inflammationc causes damage which lead to damaged tubal epithelium and adhesion can then form
  • Some recovery of the tubal epithelium does occur
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38
Q

What is endometritis?

A

Inflammation of the endometrial lining

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39
Q

What is salpingitis?

A
  • Inflammation of the Fallopian tube
  • Neutrophils and macrophages invade and this form and inflammatory exudate
  • The tubes become filled with pus
  • Formation of adhesions and fibrin blocks the tubes
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40
Q

What are complications of salpingitis?

A

-Abscess can form which can spread around the ovaries or within the tube

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41
Q

What is the aetiology of pelvic inflammatory disease?

A

-Sexually transmitted disease

Example organisms

  • Chlamydia trachomatis
  • Neisseria Gonorrhoea
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42
Q

What are the clinical symptoms of Pelvic inflammatory diseases?

A
  • Pyrexia
  • Pain
  • Lower abdominal pain
  • Deep dyspareunia
  • Abnormal vaginal/ cervical discharge
  • Abnormal vaginal bleeding
  • Sexual history
  • STI
  • Contraceptive history
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43
Q

What is found on examination in patient with pelvic inflammatory diseases?

A 
Fever 
Lower abdominal tenderness (usually bilateral)
Bimanual examination 
-adnexal tenderness with or without a mass
-Cervical motion tenderness
-Speculum examination
-Lower genital infection
-Purulent cervical discharges
-Cervicitis
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44
Q

What are investigations undertaken in patients suspected with pelvic inflammatory diseases?

A
  • Urinary and/or serum pregnancy test
  • Endocervical and High vaginal swabs (absence of Clamydia trachomatis and Neisseria Gonorrhea doesnt exclude diagnosis)
  • Blood tests: WBC and CRP
  • Screening for other STIs including HIV
  • Diagnostic laparoscopy is gold standard - Can also perform adhesiolysis and drain abscesses
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45
Q

What are drugs used to treat PIDs?

A
  • Ceftriaxone
  • Docycline
  • Metranidazole
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46
Q

How are PIDs managed?

A
  • Low threshold for empirical treatment
  • Symptomatic management with analgesia and rest
  • Management of sepsis
  • Severe disease requires IV antibiotics and admission for observation and possible surgical intervention
  • Contcct tracing for partners and full screening for women
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47
Q

What are complications of PIDs?

A
  • Ectopic pregnancy
  • Infertility
  • Chronic pelvic pain
  • Fits-Hugh-Curtis syndrome
  • Reiter syndrome (disseminated chlamydial infection)
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48
Q

Where can gynaecological tumours arise?

A
  • Vulva
  • Cervix
  • Endometrium
  • Myometrium
  • Ovary
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49
Q

What are the clinical features of vulval tumours?

A
  • Uncommon
  • Women over 60 makes 2/3 of patient
  • Usually Squamous cell carcinoma
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50
Q

How are vulval squamous neoplastic lesions related to HPV infection?

A
  • 30% related to HPV infection and it usually HPV 16

- 70% are unrelated to HPV. Most occur due to longstanding inflammation and hyper plastic conditions of the vulva

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51
Q

What is VIN?

A
  • Vulvar intraepithelial neoplasia
  • Atypical squamous cells in the epidermis
  • In situ precursor of vulval squamous cell carcinoma
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52
Q

How does Vulval squamous cell carcinoma spread?

A
  • Spreads initially to inguinal, pelvic, iliac and para-aortic lymph nodes
  • Also spreads to lungs and liver
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53
Q

What are the treatment options for vulval squamous cell carcinoma?

A

Less than 2cm

-Vulvectomy and lymphadenectomy

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54
Q

What is the likely causes of CIN or cervical carcinoma?

A

-Almost all cases related to High risk HPVs

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55
Q

What are the most important high risk HPV in the pathogenesis of cervical carcinoma?

A
  • HPV 16

- HPV 18

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56
Q

What is the pathogenesis of HPV in CIN or cervical carcinoma?

A
  • Infection of immature metaplastic squamous cells in transformation zone
  • Production of viral proteins E6 and E7
  • These interfere with tumour suppressor proteins (p53 and RB) to cause inability of repair damaged DNA and increased proliferation of cells
  • Most genital HPV infectious transient and eliminated by immune response in months
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57
Q

What are the risk factors of Vulval squamous cell carcinoma, CIN, and Cervical Carcinoma?

A
  • Sexual intercourse
  • Early first marriage
  • Early first pregnancy
  • Multiple births
  • Many partners
  • Promiscuous partner
  • Long term use of OCP
  • Partner with carcinoma of the penis
  • Low socio-economic class
  • Smoking
  • Immunosuppression

slide 13

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58
Q

What does cervical screening involve?

A
  • Cells from the transformation zone are scraped off
  • Stained with Papanicolaou stain
  • Examined microscopically

-Can also test for HPV DNA in cervical cels through molecular method of screening

Start at age 25 and do it every 3 years till 50
Then every 5 years 50-65

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59
Q

What is done if an abnormal cervical screening is observed?

A
  • Coloscopy

- Biopsy

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60
Q

What is cervical intraepithelial neoplasia?

A

-Dysplasia of squamous cells within the cervical epithelium, induced by infection with high risk HPVs

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61
Q

What is the grading of cervical intraepithelial neoplasia?

A

CIN 1 - most regress spontaneously. Few progress
CIN 2 - proportion progresses to
CIN 3 - Carcinoma in situ. 10% Progresses to invasive carcinoma in 2-10 yrs and 30% regress

CIN 1 to CIN 3 takes 7 years

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62
Q

What is the treatment for CIN?

A
  • CIN 1: Follow up or cryotherapy

- CIN 2 and CIN 3: Superficial excision of transformation zone

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63
Q

What are the types of invasive cervical carcinoma?

A
  • Squamous cell carcinoma (80%)
  • Adenocarcinoma (15%)

Average Age - 45 years
May be exophytic or infiltrative

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64
Q

How does cervical carcinoma spread?

A
  • Locally to para-cervical soft tissues, bladder, ureters, rectum, vagina
  • Lymph nodes (para-cervical, pelvic, para-aortic)
  • Distally
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65
Q

How does cervical carcinoma present?

A
  • Screening abnormality

- Post-coital, intermenstrual or post-menopausal vaginal bleeding

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66
Q

How is invasive cervical carcinoma treated?

A

Microinvasive (5 yr survival = 100%)
-Treated with cervical cone excision

Invasive carcinoma (62% ten year survival)
-Treated with hysterectomy, lymph node dissection and if advanced, radiation and chemotherapy
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67
Q

What is endometrial hyperplasia?

A
  • Increased gland to stroma ratio
  • Frequent precursor to endometrial carcinoma
  • Endometrium line the internal cavity of uterus
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68
Q

What is associated with endometrial hyperplasia?

A
  • Annouvulation
  • Increased oestrogen from endogenous sources
  • Exogenous oestrogen
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69
Q

How is endometrial hyperplasia treated if complex and atypical?

A

Hysterectomy

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70
Q

What are the clinical features of endometrial adenocarcinoma?

A
  • Common invasive cancer of the genital tract

- Usually 55-75

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71
Q

What is the presentation of endometrial adenocarcinoma?

A

-Irregular or post menopausal vaginal bleeding

Early detection and cure often possible.

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72
Q

What are the macroscopic features of endometrial adenocarcinoma?

A

-Can be polyploid or infiltrative

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73
Q

What types of endometrial adenocarcinoma are there?

A

Endometrioid (more common)

  • Mimics proliferative glands
  • Arises from endometrial hyperplasia
  • Associated with unopposed oestrogen ad obesity
  • Spread by myometrial invasion and direct extension to adjacent structures, to local lymph nodes and distant sites

Serous carcinoma

  • Poorly differentiated, aggressive, worse prognosis
  • Exfoliates, travels through Fallopian tubes and implants on peritoneal surfaces
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74
Q

What is the commonest tumour of the myometrium?

A
  • Leiomyoid = fibroid
  • Benign tumour of myometrium
  • Often multiple
  • Tiny to massive, filling the pelvis
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75
Q

What is the presentation of leiomyoma?

A
  • Asymptomatic
  • Can cause heavy/painful periods
  • Urinary frequency
  • Infertility
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76
Q

What is a malignant tumour of myometrium?

A
  • Uterine leimysarcoma
  • Uncommmon (40-60 yrs)
  • Highly malignant
  • Doesn’t arise from leiomyomas
  • Metastasise to lungs
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77
Q

What are clinical features of ovarian tumours?

A
  • Approximately 80% are benign and generally occur at 20-45 yrs
  • Malignant tumours generally occur at 45-65 yrs
  • Malignant tumours generally occur at 45-65 yrs
  • Many are bilateral
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78
Q

How do ovarian tumours present?

A
  • Most are non-functional. Only produce symptoms when they become large and invade adjacent structures or metastasise
  • Hormonal problems
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79
Q

What are the symptoms of large non-functional tumours?

A
  • Abdominal pain
  • Abdominal distension
  • Urinary and Gastrointestinal symptoms
  • Ascites
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80
Q

What are the hormonal problems of ovarian tumours?

A
  • Menstrual disturbances

- Inappropriate sex hormones

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81
Q

What are the clinical features of malignant ovarian tumours?

A
  • 50% spread to other ovary
  • Spread to regional nodes and elsewhere
  • Some associated with BRCA mutations (carriers treated with prophylactic sapling-oophrectomy)
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82
Q

What is used in diagnosis of malignant ovarian tumours?

A

CA-125

-Monitor disease recurrence and progression

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83
Q

How are ovarian tumour classified?

A
  • Mullerian (ovarian) epithelium (endometriosis)
  • Germ cell
  • Sex cord-stromal cells
  • Metastases
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84
Q

What are the 3 main histological types of ovarian epithelial tumours?

A
  • Serous
  • Mucinous
  • Endometrioid

Many are cystic

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85
Q

What are risk fact for ovarian epithelial tumours?

A
  • Nulliparity or low parity
  • OCP protective
  • Heritable mutations eg BRCA1 and BRCA2
  • Smoking
  • Endometriosis
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86
Q

What are serous ovarian tumours?

A

-Often spread to peritoneal surfaces and omentum and commonly associated with ascites

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87
Q

What are mucinous ovarian tumours?

A
  • Often large, cystic masses which can be more than 25 kg
  • Filled with sticky, thick fluid
  • Usually benign or borderline
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88
Q

What is pseudomyxoma peritonei? (thought to be from micnous but not)

A
  • Extensive mutinous ascites
  • Epithelial implants on peritoneal surfaces
  • Frequent involvement f ovaries
  • Can cause intestinal obstruction
  • Most likely is extra-ovarian usually appendix
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89
Q

What is endometrioid ovarian tumour?

A
  • Tumour has tubular glad resembling endometrial glands
  • Can arise in endometriosis
  • 15-30% have associated endometrial endometrial endometriod adenocarcinoma probably arising separately
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90
Q

What are Germ cell ovarian tumours?

A
  • 15-20% of all ovarian neoplasms
  • Most are teratomas which are usually benign
  • Other types are malignant and include dysgerminoma, Yolk sac tumour, Choriocarcinoma, Embryonal carcinoma
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91
Q

What are the types of ovarian teratoma?

A
  • Mature (benign) is most common
  • Mono-dermal (highly specialised)
  • Immature (malignant) is rare and composed to tissues that resemble immature foetal tssue
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92
Q

What are the clinical features of ovarian mature teratomas?

A
  • Most are cystic
  • Most contain skin lie structures
  • Usually occur in young women
  • Bilateral in 10-15% of cases
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93
Q

What is usually contain in ovarian mature teratomas?

A
  • Contain hair and sebaceous material and can contain tooth structures
  • Often also tissue from other germ laters such as cartilage, bone, thyroid and neural tissue
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94
Q

What is the most common mono-dermal ovarian teratoma?

A

Struma ovarii

  • Benign
  • Composed entirely of mature thyroid tissue
  • May be functional and cause hyperthyroidism
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95
Q

What are ovarian sex cord-strumal tumours?

A
  • Derived from ovarian stroma
  • Produces Sertoli and Leydig cells leading cell in testes and Granulosa and Theca cells in the ovaries
  • Tumours reselling all of these four cell types can be found in the ovary
  • These tumours can be feminising or masculinising
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96
Q

What are the clinical features of granulosa cell tumours?

A
  • Most occur in post-menopausal women

- May produce large amounts of oestrogen

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97
Q

What may be produced in pre-pubertal girls and adult women due to granulosa cell tumours?

A
  • Precocious puberty in pre-pubertal girls

- Endometrial hyperplasia, endometrial carcinoma and breast disease in adult women

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98
Q

What are the clinical dealers of ovarian-seroli leading cll tumours?

A

Often functional. Peak incidence in teens or twenties

  • In children, may block normal female sexual development
  • In women can cause defeminisation and masculinisation
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99
Q

What tumours occur in the testes?

A
  • Germ cell tumours
  • Sex cord-stromal tumors (Sertoli cell tumours, Leydig cell tumours)
  • Lymphomas
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100
Q

What are types of germ cell tumours occurring in men?

A
  • Seminomas

- Non-seminomatous germ cell tumours (Yolk sac tumours, Embryonal carcinomas, Choriocarcinomas, Teratomas)

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101
Q

Which tumours commonly metastasise to the ovaries?

A

Mullerian tumours from

  • Uterus
  • Fallopian tubes
  • Contralateral ovary
  • Pelvic peritoneum
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102
Q

What other tumours metastasise to the ovaries?

A
  • Gastrointestinal tumour and breast
  • Krukenberg tumour : mestastatic gastrointestinal tumour within the ovaries which is often bilateral and from the stomach
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103
Q

What covers the corpus cavernosa in the penis?

A

Fibrous capsule (Tunica albuginea)

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104
Q

Which structure derived from the peritoneum covers the testes and what is it’s structure?

A

Tunica Vaginalis

  • Parietal layer
  • Cavity
  • Visceral layer
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105
Q

Where does spermatogenesis occur?

A

Semineferous tubules

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106
Q

Where does the sperm mature and learn to swim (motile)?

A

In the Epididymis

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107
Q

What is the rete testis?

A

Hilum of the testes where things go in and come out

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108
Q

What is a hydrocoele?

A

A collection of serous fluid within the tunica vaginalis. It is most commonly due to a failure of the processus vaginalis to close.

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109
Q

What are sertoli cells?

A

Sertoli cells are the somatic cells of the testis that are used for spermatogenesis. They are vital for maturation of sperm by providing nutrition and hormonal support to germ cells

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110
Q

What is the purpose of Leydig cells?

A
  • Sit outside of tubules and are involved in testosterone synthesis.
  • Involved in lipid metabolism
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111
Q

Why does the left testicle hang lower than the right?

A

Greater resistance for drainage for the left so it hangs lower

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112
Q

What is testicular torsion?

A

Testicular torsion occurs when the spermatic cord twists upon itself. This causes an increase in the pressure in the region and this leads to occlusion of the testicular artery, resulting in necrosis of the testes.

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113
Q

Why are the testicles sutured after receiving a testicular torsion?

A

The individual normally has a predisposition for the spermatic cord to twists upon itself

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114
Q

How is the spermatic fascia formed?

A

-Testes evaginate the abdominal wall as they are pulled through the gubernaculum.

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115
Q

What are the fascial coverings of the spermtic cord?

A
  • External spermatic fascia
  • Cremaster muscle and fascia
  • Internal spermatic fascia
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116
Q

What is the anatomical course of the vas deferens?

A
  • It is continuous with the tail of the epididymis.
  • Travels through the inguinal canal.
  • Moves down the lateral pelvic wall in close proximity to the ischial spine.
  • Turns medially to pass between the bladder and the ureter.
  • Joins the duct from the seminal vesicle to form the ejaculatory duct.
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117
Q

Which part does BPH and prostate cancers affect?

A
  • BPH affects the transitional zone

- Prostate cancers tend to affect the peripheral zone

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118
Q

Why does BPH present earlier than prostate carcinomas?

A

The BPH affect the transitional zone whereas prostate carcinoma is usually in the peripheral zone. This means that symptoms (trouble urinating) presents earlier

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119
Q

What occurs at the pelvic floor during catheterisation?

A

It is the narrowest part of the urethra so increased resistance so you have to keep pushing

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120
Q

What are the functions of the penis?

A
  • Expulsion of urine via urethra
  • Deposition of sperm in female genital tract
  • Removal of competitors’ sperm
  • Attraction of mates
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121
Q

How does an erection form?

A
  • Vasodilation in penile arterioles and compression of veins.
  • Sinusoidal relaxation
  • Tunica albuginea is thick and doest expand so more blood.
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122
Q

How is vasodilation initiated in an erection?

A

By parasympathetic stimulation

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123
Q

How is an erection terminated?

A

Vasoconstriction of arterioles

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124
Q

Which nervous system control emission and ejaculation?

A

Sympathetic Nervous system

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125
Q

What is the structure of the penis?

A

2 corpus Cavinosum

1 Corpus spongiosum

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126
Q

Why do women sometimes get a sharp pain at ovulation?

A

The oocyte pops out of the ovary and breaches the peritoneum. Parietal peritoneum surround the ovary and is filled with somatic nerves which innervate it

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127
Q

How are the collagen fibres of the tunica albuginea of the penis arranged?

A

Arranged at right angles to each other.

There are circumferential collagen fibres and parallel collagen fibres

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128
Q

What symptoms do ovarian cysts present with?

A
  • Can rupture or undergo torsion which gives you pain
  • Bloating
  • Stretching
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129
Q

What are the parts of the uterus?

A
  • Fundus (top)
  • Body (middle)
  • Cervix (bottom)
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130
Q

What is the appearance of the cervix in pregnant woman?

A

-Slit like appearance

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131
Q

What is the appearance of the cervix when the woman hasn’t been pregnant?

A

-Circular appearance

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132
Q

What are the symptoms experienced as the foetus grows?

A
  • Acid reflux due to mechanical compression
  • Hormones makes lower oesophageal sphincter leaky
  • Constipation
  • Urinary frequency increases due to bladder being squashed
  • Extreme stretch of ligamentous structures
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133
Q

What is the most common site for ectopic pregnancies?

A

Ampulla

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134
Q

What is important to confirm when a young woman presents with abdominal pain?

A

You need to confirm with a pregnant test as if its a ruptured ectopic pregnancy, the woman can bleed to death due to pregnant.

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135
Q

What is the function of the Peg cels?

A

They nourish and maintain the egg

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136
Q

What moves the egg into the uterine tube?

A

The fimbriae

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137
Q

How can infection spread into the peritoneum through the vaginal canal?

A

The uterine tube open into the peritoneal cavity so infection can spread into the peritoneum from the vaginal canal

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138
Q

What is the broad ligament?

A

Peritoneal fold.

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139
Q

What is the round ligament?

A

Remnants of the gubernaculum.

-Pulls the gonads down from the top of the abdomen to the pelvis

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140
Q

What is the suspensory ligament?

A

Neurovascular pathway bulging into the peritoneum.

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141
Q

Where is the mesometrium?

A

-Largest part of the broad ligament and covers the uterus up to the lateral pelvic wall

Runs laterally to cover the external iliac vessels, forming a distinct fold over them. The mesometrium also encloses the proximal part of the round ligament of the uterus.

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142
Q

What is the mesosalpinx?

A

Originates superiorly to the mesovarium, enclosing the fallopian tubes. Hangs from the tubes

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143
Q

What is the mesovarium?

A
  • Part of the broad ligament associated with the ovaries
  • Projects from the posterior surface of the broad ligament and attaches to the hilum of the ovary, enclosing its neurovascular supply. It does not cover the surface of the ovary itself.

(Imagine it suspending the ovary)

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144
Q

What is the blood supply and drainage to the uterus?

A
  • Uterine artery for supply

- Uterine veins for drainage

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145
Q

What is the lymphatic drainage of the uterus?

A

Iliac, Sacral, Aortic and Inguinal lymph nodes

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146
Q

What is the epithelium lining the vagina?

A

Stratified squamous epithelium

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147
Q

Why is there lots of glycogen in the vagina?

A

Favourite food for lacto-bacilli. Maintains acidic pH due to conversion of glycol to lactic acid. This acts as defence against infection

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148
Q

How does the structure of the Fallopian tube facilitate transport of the ovum towards the uterus?

A

-Tissue structure has cilia which help to waft the egg to the uterus

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149
Q

Why could there be pain in shoulder top following ruptured ectopic pregnancy?

A
  • Internal bleeding could irritate the diaphragm
  • This can irritate the phrenic nerve which has sensory nerve roots at C3, C4 and C5
  • This can lead to pain at the shoulder
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150
Q

What can be palpated at the:
A. Posterior fornix
B. Lateral fornix
C. Anterior fornix

A

A. Assessment of the rectouterine pouch
B. Assessment of the adnexal masses
C. Uterus

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151
Q

What is the purpose of the menstrual cycle?

A

Preparation of

  • Gamete via the ovarian cycle
  • Endometrium by the uterine cycle
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152
Q

What are the control mechanism of the menstrual cycle?

A

Gonadotrophins acting on the ovary

Ovarian steroids:

  • Acting on tissues of the reproductive tract
  • Acting to control the cycle
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153
Q

Outline the HPO axis control of the menstrual cycle

A
  • GnRH produced by the hypothalamus
  • Acts on the anterior pituitary to release the gonadotrophins: FSH and LH
  • Gonadotrophins act on the ovary to promote follicular development and produce ovarian hormone like steroid hormones and inhibit
  • The gonadal hormones act to control the system
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154
Q

What happens if GnRH release is continuous rather than intermittent?

A
  • Continuous exposure of the GnRH receptors to GnRH lead to them becoming desensitised
  • FSH and LH production stops
  • Gonadal steroid production stops
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155
Q

What are the feature of the start of the menstrual cycle?

A
  • No ovarian hormone
  • Early development of follicles begin
  • Low steroid and inhibit levels
  • Little inhibition at hypothalamus or anterior pituitary
  • Free from inhibition
  • FSH levels are rising
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156
Q

What is the effect of FSH in the menstrual cycle?

A
  • Bind to granulosa cells
  • Follicular development continues
  • Theca interna appears
  • Follicle now capable of oestrogen secretion
  • Inhibin secretion begins
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157
Q

What occurs in the mid-follicular phase?

A
  • Need a nominate a dominant follicle
  • Prevention of recruitment of any further follicles
  • The follicular oestrogen is now at a concentration that it can exert positive feedback at hypothalamus and anterior pituitary
  • Gonadotrophin levels rise
  • Follicular inhibit rising which seleively inhibits FSH production for m the anterior pituitary
  • Effect on LH only
158
Q

What are the hormonal changes resulting in ovulation?

A
  • Circulating estradiol and inhibit rise rapidly
  • Oestradiol production no longer dependant on FSH
  • Surge in LH production
  • Progesterone production begins as the granulose cels become responsive to LH
  • Modulation of GnRH pulse generator
159
Q

What is completed and started in ovulation?

A

Meiosis 1 is completed

Meiosis 2 is started

160
Q

How is the mature oocyte extruded?

A

It is extruded through the capsule of the ovary

161
Q

What are the effects of LH after ovulation?

A
  • Folicle is lutenised
  • Oestrogen and progesterone are secreted in large quantities
  • Inhibin continues to be produced
162
Q

What is the effect of progesterone on LH production?

A

-LH is suppressed by progesterone via negative feedback

163
Q

Describe the luteal phase.

A
  • Corpus luteum formed and produced progesterone, oestrogens from androgens. It also produced inhibin
  • Production of progesterone is promoted
  • Corpus luteum regresses spontaneously however in the absence of further rise in LH
164
Q

What is the effect of oestrogen on the endometrium?

A

-Proliferates and secretes

165
Q

What is the effect of progesterone on the endometrium?

A

-Secretion

166
Q

What is the endometrium?

A

Specialised epithelium

167
Q

What is the uterus made of?

A
  • Muscular wall called the ‘Myometrium’
  • Endometrium which is the epithelial layer. Has a functional layer which is hormone responsive and sheds if no pregnancy occurs. Functional layer is developed on the basal layer
168
Q

What occurs at the end of the menstrual cycle?

A
  • Absence of further rise in LH means the corpus luteum regreses
  • Dramatic fall in gonadal hrmone
  • Relieving of the negative feedback
  • Resets to start again
169
Q

What are the series of changes the uterus undergoes in the menstrual cycle?

A
  • Early proliferative: Glands sparse and straight
  • Late proliferative: Functional layer has doubles and the glands are now coiled
  • Early secretory: Endometrium max thickness and very pronounced coiled glands
  • Late secretory: Glands adopt characteristic saw tooth appearance
170
Q

If the ovum is fertilised, which hormone is produced to support the corpus luteum and what by?

A
  • Human chorionic gonadotrophin (HCG)

- Syncytiotrophoblast

171
Q

How does the corpus luteum support the pregnancy?

A

It produces steroid hormone which support the pregnancy

172
Q

What controls the HPO axis throughout most of pregnancy?

A
  • The placenta
  • Oestrogen and Progesterone
  • Responsible for maintaining the pregnancy state
  • Take over from corpus luteum by 11th week
173
Q

What are the actions of progesterone in the luteal phase?

A
  • Further thickening of the endometrium into secretory form
  • Thick, acid cervical mucus
  • Thickening of the myometrium but reduction of motility
  • Changes in mammary tissue
  • Increased body temperature
  • Metabolic changes
  • Electrolyte changes
174
Q

What is the normal duration of the menstrual cycle?

A

21-35 days

175
Q

What are the action of oestrogen in the follicular phase?

A
  • Fallopian tube function
  • Thickening of the endometrium
  • Growth and motility of the myometrium
  • Thcnk alkaline cervical mucus
  • Vaginal changes
  • Changes in skin, hair, metabolism
176
Q

Which phase affect variation in the cycle duration?

A

Follicular phase

177
Q

What is the luteal phase strictly controlled to?

A

14 days +/-2 days

178
Q

Which physiological factors affect the menstrual cycle?

A
  • Pregnancy

- Lactation

179
Q

What are some non-physiological factors that affect the menstrual cycle?

A
  • Emotional stress

- Low body weight

180
Q

What is the effect of moderate levels of oestrogen on the HPO axis and high levels?

A

Moderate levels - Negative Feedback. Reduce GnRH

High levels - Positive feedback. Increase GnRH so increase in LH

181
Q

What is the effect of the high oestrogen and progesterone on the HPO axis?

A

Negative feedback

182
Q

What is primary amenorrhea?

A

Failure to establish menstruation by 16 years

183
Q

What is secondary amenorrhea?

A

Cessation of previously normal menstruation for greater than 6 months

184
Q

What is oligomenorhea?

A

Infrequent menstruation

185
Q

What is menorhaggia?

A

A complain of excessive menstrual blood loss over consecutive cycles

186
Q

What is dysmenorrhoea?

A

Pain during menses associated with ovulatory cycles

187
Q

What is dysfunctional uterine bleeding?

A

Heavy and irregular menstrual bleeding that occurs secondary to anovulation

188
Q

What is PMS?

A

Cyclical disorder occurring in the latter half of the menstrual cycle .Symptoms can be physical psychological and resolve with onset of menstruation

189
Q

What is premenstrual dysphoric disorder?

A

Severe end of the PMS spectrum with extreme mood symptoms

190
Q

What are some causes of amenorrhoea?

A
  • Physiologic causes such as prepubertal, pregnancy and menopause
  • Pathology at the various levels of endocrine control such as hypothalamic, pituitary, ovarian, uterine

Gonadotrophin levels indicate the level of the pathology

191
Q

What are the structural causes of menstrual disorders??

A
  • Agenesis/hypoplasia at any level of the genital tract
  • Leiomyoma - uterine fibroids
  • Imperforate hymen, vaginal septal
  • Asherman’s syndrome
  • Cervical stenosis
192
Q

What are the causes of menorrhagia?

A
  • Uterine fibroids
  • Uterine polyps
  • Endometrial cancer
  • Bleeding diathesis
  • Drugs like warffarin
  • Copper IUCD
193
Q

What causes irregular bleeding?

A
  • Hormonal Contraception
  • STI’s/PID
  • Cervical ectopy or pathology which normally results in postcoital bleeding
  • Endometrial pathology such as polyp or cancer
  • Ovarian cyst secreting hormones
194
Q

What causes dysmenorrhoea?

A
  • Primary dysmenorrhoea is idiopathic and due to response of the uterus to local prostaglandins hence painful contractions.
  • Secondary dysmenorrhea can be due to endometriosis or obstructed menses
195
Q

What are the features of PMS?

A
  • Subjective
  • Cyclical
  • Can be distressing and even debilitating
196
Q

What are environmental inferences on puberty?

A
  • Triggered by changes in day length
  • Involvement of pineal gland
  • Secretion of melatonin
197
Q

What is the critical weight for girls to begin puberty?

A

47kg

198
Q

What is the effect of significant weight loss in women?

A

The reproductive cycle ceases

199
Q

What are the sequence of changes girls follow in puberty?

A

9-13

  1. Breast bud appears
  2. Pubic hair growth
  3. Growth spurt
  4. Onset of menstrual
  5. Pubic hair becomes adult like
  6. Breast become adult like
200
Q

Why does pubic hair grow?

A

It is a response to oestrogen and testosterone levels

201
Q

What are the sequence of changes boys follow in puberty?

A

10-14 years of age

  1. Genital develpment (Testosterone)
  2. Pubic hair growth
  3. Spermatogenesis
  4. Growth spurt
  5. Genitalia becomes adult like
  6. Pubic hair becomes adult like
202
Q

How does accelerated osmotic growth stop?

A

Epiphyseal fusion in response to oestrogen

-Ended earlier in girls

203
Q

What is accelerated somatic growth?

A

Period of growth that pepends on growth hormone and sex steroids in both sexes

  • It is earlier and shorter in girls
  • It is longer and faster in men so larger growth spurt
204
Q

What triggers the onset of puberty?

A

Switching on the HPG axis. Done by:

  • Increased stimulation of hypothalamus-pituitary-gonadal axis
  • Gradual activation of GnRH
  • Increases frequency and amplitude of LH pulses
  • Gonadotropins stimulate secretion of sexual steroids
  • Extragonadal hormonal changes
205
Q

What happens if GnRH secretion is blocked?

A

-Lack of gonadotrophin synthesis and secretion and reproductive development. GnRH plays a critical role in reproductive maturation

206
Q

What are the characteristics of hypothermic releasing hormones?

A
  • Secretion in pulse tied to the internal biological clock
  • Act on specific membrane receptors
  • Transduce signals via secondary messengers
  • Stimulate release of stored pituitary hormones
  • Stimulate synthesis of pituitary hormones
  • Stimulates hyperplasia and hypertrophy of target cells
  • Regulates it own receptor
207
Q

What does the GnRH stimulate in the anterior pituitary gonadotrophs?

A

Stimulates production of

  • Luteinizing hormone
  • Follicle Stimulating hormone

GnRH Released Every 1.3 hours

208
Q

What is leptin?

A

Adipocyte derived protein hormone that signal information about energy stores to the CNS and plays an important role in regulating neuroendocrine function.

209
Q

How can leptin affect the reproductive cycle?

A
  • If deficient, associated with reproductive dysfunction

- Leptin can accelerate the onset of reproductive function

210
Q

How is leptin released?

A

Pulsatile release pattern significantly associated with the variations in LH

211
Q

What are the effects of growth hormone secretion from the pituitary?

A
  • Increases TSH
  • Increased metabolic rate
  • Promote tissue growth
  • Increases androgens so retention of minerals in body to support bone and muscle growth

Growth spurt

212
Q

How is the anterior pituitary connected to the hypothalamus?

A

Superior hypophyseal artery

213
Q

Describe the sleep dependant nocturnal rise in LH

A
  • Increase in sleep related LH
  • Stimulates a nocturnal rise in Testosterone
  • Could account of early pubertal changes seen in males
214
Q

Describe the hormonal control of puberty in an overview.

A

Brain > Hypothalamus > Pituitary > Increase in LH and FSH levels > Gonadal development > Androgens and oestrogen

215
Q

Describe the HPG axis in a male

A
  • LH stimulates Leydig cells in testis
  • Production of steroid hormone testosterone (mostly testes)
  • Testosterone levels remain constant in the medium long term
  • Circadian rhythm and environmental stimuli have an effect
216
Q

What do the seminefrous tubules require?

A

Testosterone (functioning leydig cells)

217
Q

What is the control of Sertoli cells?

A
  • Sensitive to FSH

- Inhibin negatively feeds back on the anterior pituitary to decrease FSH

218
Q

Which cells produce a tight junction in the seminiferous tubules and why?

A

Sertoli cells

-Prevent blood and sperm mixing to prevent an immune reaction

219
Q

What is the primary target cells of FSH and LH in the female and the effect?

A
  • Ovarian granulose cells
  • Theca interna

Stimulate sex hormone synthesis and control gamete production

220
Q

Where is inhibin realised from?

A

Granulosa cells of corpus luteum

221
Q

What is the function of inhibin?

A
  • Inhibits the secretion of FSH

- Has a small inhibitory effect on LH

222
Q

What do germ cells do after colonising the gonad?

A
  • Proliferate by mitosis
  • Reshuffle genetically and reduce haploid by meiosis
  • Cytodifferentiate into mature gametes
223
Q

What are the features of oogenesis?

A
  • Usually 1 ovum per 28 day menstrual cycle
  • One ovum with unequal division of cytoplasm and 3 polar bodies formed
  • Starts in the foetus
  • Ends at menopause
  • Non motile gametes
  • Last stage of meiosis 2 occurs in the oviduct
224
Q

What are the features of spermatogenesis?

A
  • Huge number of sperm reduced (200 million)
  • 4 spermatids formed with no polar body formation and equal division of cytoplasm
  • Starts at puberty
  • Continuous production from puberty throughout adult life
  • Motile gametes
  • All stages are completed in the testes
225
Q

What are the main functions of meiosis?

A
  • Reduction of chromosome number to 23
  • Ensures gametes is genetically unique
  • Used only in production of sperm and eggs
  • 2 successive cell divisions
  • Production of 4 daughter cells
226
Q

How many mature oocytes are formed in the female?

A

1

The rest are polar bodies

227
Q

What does genetic variation arise from?

A
  • Crossing over (exchange of DNA between 2 homologous chromosomes)
  • Independent assortment (random orientation of each bivalent along the metaphase plate with respect to other bivalents)
  • Random segregation (random distribution o alleles among four gametes)
228
Q

Where do the seminiferous tubules concentrate the sperm?

A

Ductus deferentes

229
Q

Describe spermatogenesis

A
  • Spermatogonia divide by mitosis to give Ad spermatogonium(resting) and Ap spermatogonium(active)
  • Ap spermatogonium maintain stock and from puberty onwards produce type B spermatogonia which give rise to primary spermatocyte
  • Primary spermatocyte divide by meiosis giving rise to secondary spermatocytes then spermatids
  • Each primary spermatocyte divides to form 4 haploid spermatids which differentiate into spermatozoa
230
Q

What is the definition of the spermatogenic cycle?

A

The time it take for the appearance of the same stage within a segment of the tubule

231
Q

What is the definition of the spermatogenic wave?

A

Distance between the same stage is called the spermatogenic wave

232
Q

Describe the process that results in the differentiation of the spermatids to spermatozoa.

A
  • Spermatids are related into the lumen of seminiferous tubules
  • They remodel as the pass down seminiferous tubules. through the rete testis and ductile efferentes and into epididymis to finally form spermatozoa
233
Q

Where are secretions for semen released from?

A
  • Seminal vesicle secretions (about 70%)
  • Secretion of prostate (about 25%)
  • Sperm (about 2-5%)
  • Bulbourethral gland (less than 1%)
234
Q

What is released from the prostate?

A
  • Proteolytic enzymes
  • Milky slightly acidic fluid
  • Citric acid, acid phosphatase
235
Q

What is secreted form seminal vesicle?

A
  • Amino acids
  • Citrate (better than glucose as less completion from bacteria)
  • Fructose
  • Prostagladins
236
Q

What is released for the bulbourethral gland?

A

Mucoproteins which help lubricates and neutralised acidic urine in distal urethra

237
Q

What is sperm capacitation?

A

Conditions in the female genital tract stimulate:

  • Removal of glycoproteins and cholesterol from sperm membrane
  • Tail movement changes from beat to whip like action
  • Activation of sperm signalling pathways
  • Allow sperm to bind to the bona pellucida of oocyte and initiate acrosome reaction
238
Q

When does maturation of oocytes begin?

A

Before birth

239
Q

Describe the maturation of germ cells before birth

A
  • Germ cells colonise the gonadal codex and differentiate oogonia
  • Oogonia then proliferate rapidly by mitosis
  • By end of the 3rd month oogonia are arranged in clusters surrounded by flat epithelial cells
  • Majority then continue to divide by mitosis but some enter meiosis and these arrest in prophase of meiosis 1 and are called primary oocytes
  • Max number of germ cells reached mid gestation
  • Cell death then begins and oogonia and primary oocytes begin to degenerate. by 7th moth most oogonia degenerated
  • All surviving primary ones have now entered meiosis 1 and are individually surrounded by layer of flat epithelial cells called follicular cells.
  • Follicular cells are now called primordial follicle cells
240
Q

Describe maturation of oocytes at puberty

A

15-20 oocytes start to mature each month passing through 3 stages

  1. Preantral
  2. Antral
  3. Preovulatory
241
Q

What is the preantral stage?

A

As Primordial follicles begin to grow

  • Surrounding follicular cells change from flat to cuboidal and proliferate to produce a stratified epithelium of granulosa cells
  • Granulosa cells secrete layer of glycoprotein on oocyte forming the bona pellucida
242
Q

What is the antral stage?

A

As development continues

  • Fluid filled spaces appear between the granulosa cells and these come together to form the antrum
  • Several follicles begin to develop with each ovarian cycle and usually one will reach maturity
243
Q

Describe the features of the preovulatory phase

A
  • Surge in LH induces this stage
  • Meiosis 1 is complete resulting in 2 haploid daughter cells of unequal size due to one cells revving most of the cytoplasm and the other (1st polar body) receiving none.
  • Each daughter cells now has 23 chromosomes and 46 chromatids
  • Cell enters meiosis 2 but arrest in metaphase 2
  • Meiosis 2 is only completed if the oocyte is fertilised otherwise the cell degenerates
244
Q

What stimulates growth of the follicle during ovulation?

A

FSH and LH

245
Q

What is the mature follicle called when it is 2.5cm in diameter?

A

Graafin follicle

246
Q

What stimulate collagenase activity?

A

LH surge

247
Q

What is the function of prostaglandins in relation to LH?

A

Increase response to LH and cause local muscular contractions in ovarian wall

248
Q

Give an overview of ovulation

A
  • Rapid growth of follicle several hours before ovulation occurs
  • Graffin follicle formation
  • Local muscular contractions in ovarian wall and increase in collagenase activity
  • Oocyte is extruded and breaks free from ovary
249
Q

How is the corpus leteum formed?

A

-Remaining granulosa and theca internal cells become vascularised and develop yellowish pigment and change into lutein cells which form the corpus luteum

250
Q

What is the function of the corpus luteum?

A

-Stimulates the uterine mucos to enter secondary stage in preparation for the embryo implantation

251
Q

How is the oocyte transported?

A
  • Fimbriae sweep over surface of ovary shortly before ovulation
  • Uterine tube begins to contract rhythmically
  • Oocyte carried into tube by sweeping movement s of fimbriae and by motion of cilia on epithelial lining
  • Oocyte is then propelled by peristaltic muscular contractions of the tube and by cilia in the mucosa
  • If fertilised, oocyte reaches uterine lumen in 3 to 4 days
252
Q

What forms the corpus albicans?

A

-If fertilisation does not occur corpus luteum degenerates and forms mass of fibrotic scar tissue which is the corpus albicans.

253
Q

Why does menstrual bleeding occur?

A

Progesterone production decreases

254
Q

Where is the fertilisation site?

A

Ampulla of uterine tube

255
Q

Outline the human sexual response?

A
  • Excitement phase (phychogenic and/or somatogenic stimuli)
  • Plateau phase
  • Orgasm phase
  • Resolution phase (return to haemodynamic norm followed by a refractory period)
256
Q

What is the parasympathetic innervation of the penis?

A
  • Pelvic nerves and pelvic plexus
  • Cavernous nerve to corpora and vasculature
  • Fibres from the lumbar and sacral spinal levels
257
Q

What is the neurophysiology of an erection?

A
  • Inihibiton of sympathetic arterial vasoconstrictor nerve
  • Activation of PNS
  • Activaton of non-adrenergic, non-cholinergic, autonomic nerves to arteries to release Nitric Oxide
258
Q

How is NO made and what is the role?

A
  • Post ganglionic fibres release ACh
  • ACh bonds to M3 receptors on endothelial cells
  • Rise in Ca2+ and activation of NOS and formation of NO
  • Nitric Oxide diffuses into vascular smooth muscle and causes relaxation
  • NO also released directly from nerves
259
Q

What are causes of erectile dysfunction?

A
  • Psychological
  • Tears in fibrous tissue of corpora cavernosa
  • Vascular
  • Drugs
260
Q

What is emission?

A

Emission

  • Movement of semen into prostatic urethra
  • Contraction of Smooth muscle in prostate, vas deferent and spinal vesicles
261
Q

What is ejaculation?

A

Expluson of semen

  • Contraction of glands and ducts
  • Bladder internal sphincter contracts preventing retrograde ejaculation
  • Rhythmic striatal muscle contractions
262
Q

How does the cervical mucus vary through the menstrual cycle?

A
  • Oestrogen leads to thin and stretchy mucus lining

- Oestrogen and progesterone form a thick and sticky plug

263
Q

What is the fertile windrow of oocytes and spermatozoa?

A

Spermatozoa - 48-72 hours

Oocytes - 6-24 hours

264
Q

What is the fertile period?

A

Sperm deposition up to 3 days prior to ovulation or day of ovulation

265
Q

What is acrosome?

A
  • Derived from Golgi region of developing spermatid
  • Contains enzymes
  • Necessary for fertilisation
266
Q

What is the acrosome reaction?

A
  • Sperm pushes through corona radiata
  • Binding of sperm surface receptor to ZP3 glycoprotein of zona pellucida
  • Triggers acrosome reaction
  • Digestion of zona pellucida
267
Q

What is the cortical reaction?

A

If fertilisation occurs, there is a fusion of plasma membrane to block polyspermy

268
Q

How does the completion of meiosis 2 occurs when there is fertilisation?

A
  • Series of calcium waves are activated following fusion of oocyte and sperm membranes
  • Resumption of meiosis 2 occurs
  • Pronuclei move together
  • Mitotic spindle forms leading to cleavage
269
Q

What is significant about a morula?

A

Each cells at this stage of development is totipotent

270
Q

How does the blastocyst form and hatch?

A
  • Differetion to form inner and outer cell mass
  • Formation of blastocyst
  • Blastocyst hatches from zona pellucida
  • No longer constrained so now free to enlarge
  • Can interact with uterine surface to implant
271
Q

How is implantation controlled?

A
  • Endometrium controls degree of implantation
  • Transformation of endometrium into decidua In presence of the conceptus
  • Decidual reaction provides the balancing force for the invasive force of the trophoblast
272
Q

What are methods of contraception?

A
  • Natural
  • Barrier
  • Hormonal
  • Prevention of implantation
  • Sterilisation
  • Emergency contraception
273
Q

What are advantages and disadvantages of abstinence?

A

Advantages
-100% reliable method of contraception

Disadvantages
-No sex

274
Q

What are advantages and disadvantages of barrier contraceptions?

Male and female condoms
Diaphragm caps

A

Advantages

  • Reliable
  • Protection from STIs
  • Male condom is widely available

Diadvantages

  • Disrupt romantic nature of sexual intercouree
  • Reduces sexual pleasure
  • Danger of expiring
  • Allergy/Sensitivity to latex/Spermicide
275
Q

What is the effect of moderate/high doses of progesterone as a contraceptive pill?

A
  • Enhance negative feedback fo natural oestrogen so reduction in LH and FSH
  • Inhibits positive feedback of oestrogen so no LH surge and no ovulation
276
Q

What is the effect of lower disease of progesterone as a contraceptive pill?

A

-Thickens cervical mucus

Ovulation still likely

277
Q

What is the combined contraceptive pill and its action?

A

Synthetic oestrogen and progesteron taken for 21 days (+- 7 day placebo)

  • Prevents ovulation
  • Reduces endometrial receptivity to inhibit implantation
  • Thickens cervical mucus to inhibit penetration of sperm
278
Q

What are advantages and disadvantages of combined oral contraceptive pill?

A
  • Can relive menstrual disorders
  • Reduces risk of ovarian cancer and endometrial cancer

Disadvantages

  • Interaction with other medications
  • Contraidications and side effects
  • Increased risk of breast cancer, cervican cancer, VTE, MI, Stroke
  • No protection from STIs
279
Q

What are methods of giving high dose progestogen as a contraceptive and its actions?

A
  1. Intramuscular injections given at intervals
  2. Progestogen pill

99% effective

Action

  • Inhibits ovulation
  • Thickens cervical mucus
  • Prevent endometrial proliferation
280
Q

What are the advantages and disadvantages of the progestogen implant?

A

Advantages

  • Reliable
  • LARC
  • It can be useful for women who can’t use contraception that contains oestrogen
  • Natural fertility return quickly when removed

Diadvantages

  • Minor procedure to insert
  • Side effects
  • No STI protection
281
Q

What are the advantages and disadvantages of low dose progestogen only pill?

A

Advantages

  • Quickly reversible
  • It does not interrupt sexual intercourse
  • Can be used where the COCP is contraindicated

Disadvantages

  • User dependant
  • Menstrual problems are common
  • Interacts with other medication
  • Risk of ectopic pregnancy
  • Does not protect from STI’s
282
Q

What are method of inhibiting implantation?

A

-Intrauterine system
Progestogen-rleasing plastic device that works for 3-5 years. It prevents impantating and reduces endometrial proliferation.

-Intrauterine device
Plastic device with added copper. Works for 5-10 years
Copper is toxic to ovum and sperm
Also causes endometrial inflammatory reaction to prevent implantation and changes the consistency of cervical mucus

283
Q

What are the advantages and disavantages of IUD and IUS?

A

Advantages

  • Convenient
  • Long duration of action

Disadvantages

  • Insertion may be unpleasant
  • Risk of uterine perforation
  • Menstrual irregularity
  • Doesn’t prevent STI
  • Displacement/expulsion may occur
284
Q

What are methods of sterilisation?

A
  • Vasectomy (the vas deferens is interrupted to prevent sperm entering ejaculate
  • Tubual Ligation/Clipping (Fallopian tubes cut or blocked to stop ovum travelling from the ovary to the uterus)
285
Q

What are methods of ermgency contraception?

A
  • Emergency IUD
  • Emergency pill with ulipristal acetate
  • Emergency pill with levonorgestrel
286
Q

What are advantages and disadvantages of progestogen injections?

A

Advantages

  • Reliable
  • Does not interrupt sexual intercourse
  • Can be useful for women who can’t use COCP

Disadvantages

  • Appointment needed every 12 weeks
  • Contraindications and side effects
  • Delay in fertility returning
  • No STI protection
287
Q

What are the principles of lactational amenorrhea method of contraception?

A
  • Breastfeedng delays the return of ovulation after childbirth
  • Sucking stimulus disrupts release of GnRH
  • Affect feedback cycle of HPG axis
  • Relise on exclusive breast feeding and is only effect for up to 6 months after giving birth
288
Q

What are advantages and disadvantages of lactational amenorrhea method of contraception?

A

Advantages
-No hormone/contraindications

Disadvantages

  • Unreliable
  • No STI prevention
289
Q

What are advantages and disadvantages of withdrawal method and fertility awareness methods?

A

Advantages
-No devices/hormones

Disadvantages

  • Not reliable (some sperm release in pre ejaculate, will power reliant)
  • No protection for STI’s
290
Q

What is the week of 2’s?

A

Two distinct cell layers

Outer cell mass

  • Syncytiotrophoblast
  • Cytotrophoblast

Inner cell mass becomes the bilaminar disk

  • Epiblast
  • Hypoblast
291
Q

What are 2 cavities in the embryo?

A
  • Amniotic cavity

- Yolk sac

292
Q

How is the embryo suspended in the chorionic cavity?

A

-Connecting Stalk

293
Q

What is the fate of embryonic spaces?

A
  • The yolk sac disappears
  • The amniotic sac enlarges
  • The chorionic sac is occupied by the expanding amniotic sac
294
Q

What does implantation achieve?

A

Establishes the basic unit of exchange
-Primary villi: early finger-like projections of trophoblast
-Secondary villi: invasion of mesenchyme into core
-Tertiary villi: invasion of mesenchyme core by fetal vessels
Anchor the placenta
Establish maternal blood flow within the placenta

295
Q

What does implantation achieve?

A
  • Implantation is interstitial (the uterine epithelium is breached and the conceptus implants within the stroma)
  • The placental membrane becomes progressively thinner as the needs of the fetus increase
  • In the human one layer of trophoblast ultimately separates maternal blood from fetal capillary wall (but the two circulations never mix)
296
Q

What is a chorionic villus?

A

The placenta is a specialisation of the chronic villus. The chorion fondusum is the outer layer and has fingerlike projections. This allows finger-like projections from trophoblast that have vessels to allow for good exchange.

297
Q

What are the possible implantation defects?

A
  • Impantation in the wrong place (Ectopic pregnancy, Placenta praevia)
  • Incomplete Invasion (Placental Insufficiency, Pre-Eclampsia)
298
Q

Why is ectopic pregnancy bad?

A
  • No decidua therefore no control

- The conceptus can invade into tissues

299
Q

How does the chorionic villus change from first semester to third semester?

A

First trimester - Thicker barrier

Third Trimester - Thinner barrier

300
Q

What is the blood vessels to the umbilicus?

A
  • Two umbilical arteries to transport deoxygenated blood from fetes to placenta
  • Umbilical vein to transport Oxygenated blood from placenta to fetus
301
Q

Which hormones are produced by the placenta?

A

Protein

  • Human chorionic gonadotrophin
  • Human chorionic somatomammotrophin
  • Human chorionic thyrotrophin
  • Human chorionic corticotrophin

Steroid

  • Progesterone
  • Oestrogen
302
Q

What is hCG?

A
  • Hormone produced in the first 2 months of pregnancy
  • Supports secretory function of corpus luteum
  • Produced by syncytiotrophoblast therefore pregnancy specific
  • Excreted in eternal urine and therefore used as a basis for pregnancy testing
303
Q

How do placental hormones influence maternal metabolism?

A
  • Progesterone increases appetite in order to lay down fat stores which will be called upon later in pregnancy
  • hCS/hPL increases glucose availability to fetus. Causes insulin resistance in maternal tissue so other stores are used by mother so the foetus gets glucose
304
Q

What are transport functions of the placenta?

A
  • Simple diffusion (water, electrolytes, urea/uric acid, gases)
  • Facilitated diffusion (applies to glucose transport)
305
Q

How does gas exchange occur in the placenta?

A
  • Simple diffusion
  • Diffusion barrier is small and decreases as pregnancy proceeds
  • Flow limited, not diffusion limited. Low stores of fetal oxygen so needs adequate low
  • Gradient of partial pressure is required so fetal pO2 must be lower than maternal pO2 which increases marginally.
306
Q

Describe active transport in the placenta

A

Specific transporters expressed by syncytiotrophoblast for:

  • Amino acids
  • Iron
  • Vitamins
307
Q

How does transfer of passive immunity occur?

A
  • Fetal immune system is immature
  • Receptor mediated process maturing as pregnancy progresses
  • Immunoglobulin class-specific
  • IgG only. Concentration in fetal plasma exceed this in maternal circulation
308
Q

Why is the placenta not a true barrier?

A
  • Teratogens can access the fetus via the placenta
  • Unintentional outcomes from physiological process. Haemolytic disease of the newborn secondary to Rhesus incompatibility of mother and fetus. Can lead to destruction of metal erythrocytes. It can be prophylactically treated
309
Q

What are examples of harmful substances and the placenta?

A
  • Thalidomide (Limb defects)
  • Alcohol (FAS and ARND)
  • Therapeutic drugs (anti-epileptic drugs, warfarin, ACE inhibitors)
  • Drugs of abuse (dependancy in the fetus and newborn)
  • Maternal smoking
310
Q

What are the periods of susceptibility to teratogenesis?

A

Pre embryonic
-Lethal effects

Embryonic

  • More sensitive
  • Narrow windows for some systems

Fetal
+/- sensitive

After embryonic period, risk of structural defects very low
-Except CNS as development occurs throughout

311
Q

What are the components of the matron-fetal exchange that happens at the placenta?

A
  • Fetal circulation
  • Umbilical arteries (deoxygenated blood)
  • Umbilical vein (oxygenated blood)
  • Fetal capillaries within chorionic villi (increase surface area)
  • Uterine arteries
  • Uterine veins (maternal blood lakes in the intervillous spaces)
312
Q

What factors increase fetal O2 content?

A
  • Fetal haemaglobin variant
  • Fetal haematocrit is increased over that in the adult
  • Increased maternal production of 2,3 DPG secondary to physiological respiratory alkalosis of pregnancy
  • Double Bohr effect
313
Q

What is the fetal haemoglobin variant?

A
  • 2 alpha subunits plus 2 gamma subunits

- Greater affinity fo oxygen because it doesn’t bind 2,3-DPG as effectively as HbA

314
Q

Describe the double Bohr effect in materno-fetal exchange.

A
  • As CO2 passes into intervillous blood, pH decreases
  • Bohr effect
  • Decreasing affinity of maternal Hb for O2
  • At the same time, as CO2 is lost, pH rises in the fetus
  • Bohr effect
  • Increasing affinity fo Hb for O2
315
Q

How does the concentration gradient for CO2 transfer form?

A
  • Maternal physiological adaptation to pregnancy
  • Progesterone-driven hyperventilation
  • Hence lower pCO2 in maternal blood
316
Q

What is the double Haldane effect?

A
  • As Hb gives up O2, it can accept increasing amounts of CO2
  • Fetus gives up CO2 as O2 is accepted
  • No alteration in local pCO2
317
Q

Describe the fetal circulation.

A
  • Receives oxygenated blood from mother via placenta in umbilical vein
  • Lungs are non functional so they are bypassed
  • Returns to the placenta via umbilical arteries
318
Q

What are the 3 shunts found in the fetal circulation?

A
  • Ductus Venosus
  • Foramen ovale (Right atrium to left atrium to by pass lungs)
  • Ductus arteriosus (pulmonary trunk to aorta)
319
Q

What is the purpose of the ductus venosus?

A
  • Connects umbilical vein carrying oxygenated blood to the IVC
  • Blood enters the right atrium so blood is shunted around the liver to maintain most of the saturation
320
Q

What is the purpose of the foramen ovale?

A
  • Right atrial pressure is getaner than in the left atrium in the foetus
  • Forces leaves the foramen ovale part and blood flow into left atrium
  • Free border of septum secundum forms a crest
  • Creates two streams of blood flow
  • Majority of blood flow to Left atrium and the minor flows to Right ventricle
321
Q

Why is the ductus arteriosus needed?

A
  • Shunts blood from Right ventricle and Pulmonary trunk to Aorta
  • Minimuses drop in O2 saturation
322
Q

What is the fetal response to hypoxia?

A
  • HbF and Hb is increased
  • Redistribution of flow to protect supply to heart and brain
  • Fetal heart rate slows in response to hypoxia reduce O2 demand
323
Q

What is the effect of chronic hypoxaemia?

A
  • Growth restriction

- Behavioural changes

324
Q

How is hypoxia detected in the foetus?

A
  • Fetal chemoreceptors detect decreased pO2 or increased pCO2
  • Vagal stimulation then leads to bradycardia
325
Q

Which hormones are necessary for foetal growth?

A
  • Insulin
  • IGF1 and IGF2
  • Leptin
326
Q

What are the effects of nutrition on fetal growth during pregnancy?

A
  • Can cause symmetrical or asymmetrical growth restriction

- Can influence health in later life

327
Q

What is the dominant cellular growth mechanism in the first, second, and third trimester?

A

First trimester - Hyperplasia
Second trimester - Hyperplasia and Hypertrophy
Third trimester - Hypertrophy

328
Q

What is the purpose for amniotic fluid?

A
  • Amniotic sac encloses embryo/fetus in amniotic fluid
  • Protection
  • Contributes to development of lungs
329
Q

How is the amniotic fluid produced and recycled?

A
  • Fetal urinary tract produced urine by 9 weeks
  • Fetal lungs
  • Fetal GI tract (Swallowed and absorbs water and electrolytes. Debris and intestinal secretions accumulates in Gut to form meconium)
  • Placenta and fetal membranes
330
Q

What is the composition of amniotic fluid?

A
  • 98% water

- Plus electrolytes, cretinne, urea, bile pigment, renin, glucose, hormones and fetal cells, lung and Venice caseosa

331
Q

What is amniocentesis?

A
  • Sampling of amniotic fluid
  • Allows for collection of fetal cels
  • Useful diagnostic test
332
Q

How is the bilirubin metabolised in the foetus and why?

A
  • During gestation, clearance of fetal bilirubin id handle efficiency by the placenta
  • Foetus cannot conjugate bilirubin
  • Immaturity of liver and intestinal processes for metabolism, conjugation and excretion
  • Physiological jaundice common
333
Q

What is the pattern of growth during development?

A
  • Embryonic period is characterised by intense activity but absolute growth is very small
  • Growth and weight gain accelerate in fetal period

Embryo - Intense morphogenesis and differentiation; little weight gain; placental growth most significant
Early fetus - Protein deposition
Late fetus - Adipose deposition

334
Q

How do body proportions change during detail period?

A
  • At 9 weeks the head is approx half crown-rump length

- Thereafter, body length and lower limb growth accelerates

335
Q

What is an obstetric ultrasound scan?

A
  • Safe method that can be used early in pregnancy to calculate age. This can rule out ectopic and number of foetuses.
  • Routinely carried out at 20 weeks to assess fetal growth and fetal anomalies
336
Q

How is crown-rump length used to date the pregnancy?

A
  • Measured between 7 and 13 weeks to date the pregnancy and estimate delivery date
  • Scan at T1 also used to check location, number, viability
337
Q

How can the fetal age be estimated?

A
  • Last menstrual period (prone to inaccuracy)

- Development criteria

338
Q

How is biparietal diameter used to date the pregnancy?

A
  • Distance between the parietal bones of the fetal skull

- Used in combination with other measurements to date pregnancies in T2 and T3

339
Q

How is abdominal circumference and femur length to date the pregnancy?

A
  • AC and FL used in combination with biparietal diameter for dating an growth monitoring
  • Also useful for anomaly detection
340
Q

How are birth weight classified?

A

3500g - Average
<2500g - suspects growth restriction
>4500g - macrosomia (maternal diabetes)

341
Q

Why can babies have a low birth weight?

A
  • Premature
  • Constitutionally small
  • Suffered growth restriction
342
Q

Describe an overview of the development of the Respiratory system?

A
  • Lungs develop relatively late
  • Embryonic development creates only the broncho pulmonary tree
  • Functional specialisation occurs in the fetal period
  • Stage of development has major implication for pre-term survival. Terminal sac stage is crucial by 24 weeks
343
Q

Outline the stages of lung development.

A

Pseudoglandular Stage - Duct system (bronchioles) forms with the bronchopulmonary segment created during the embryonic period. (Wks 8-16)

Canalicular stage - Formation of respiratory bronchioles budding from bronchiole formed previously (Wks 16-26)

Terminal sac stage - Terminal sacs begin to bud from respiratory bronchioles. Differentiation of Type 1 and Type 2 pneumocytes. Surfactant. (Wks 26)

344
Q

How are lungs prepared to assume full burden at birth at T2 and T3?

A
  • Breathing movement to condition the respiratory musculature
  • Fluid filled (amniotic) which is crucial for normal lung development
345
Q

What is respiratory distress syndrome?

A
  • Insufficient surfactant production
  • Often affects infant born prematurely so if delivery pre-term in unavoidable then glucocorticoid treatment to increase surfactant production
346
Q

Describe an overview of the urinary system.

A
  • Fetal kidney function begins in week 10
  • Fetal urine is a major contributor to amniotic fluid volume
  • Fetal kidney fucntion is not necessary for survival but without it there is oligohydramnios
347
Q

What is the importance of amniotic fluid volume?

A

Oligohydramnios

  • Too little
  • Can cause placental insufficiency and fetal renal impairment

Polyhydramnios

  • Too much
  • Fetal abnormality due to inability to swallow so recycling process is implicated
348
Q

Describe the overview of nervous system.

A
  • First to being development and last to finish
  • Corticospinal tract required for coordinated voluntary movement being to form in the 4th month
  • Myelination of brain only begins in 9th month
349
Q

When does movement develop in the foetus?

A
  • No movement until after 8th week

- After large repertoire of movement develop to practise for post-natal life (suckling, breathing)

350
Q

What is quickening?

A
  • Maternal awareness of fetal movement from 17 weeks onwards
  • Low cost, simple method of antepartum fetal surveillance
  • Reveal those fetuses requiring follow-up
351
Q

What is parturition?

A

-Transition from pregnancy to non-pregnant state

352
Q

What is labour?

A

Physiologic process by which fetus is expelled form the uterus to outside world

353
Q

What is delivery?

A

-Method of expulsion of the fetus, transforming fetus to neonate

354
Q

What are the physiological stages of labour?

A
  1. Creating of the birth canal and descent of fetal head into it
  2. Changes in uterine contractions to expulsive, descent of the fetus through the birth canal and delivery
  3. Expulsion of the placenta and contraction of the uterus. usually lasts between 5 and 15 minutes but can go up to 30-60 minutes depending on circumstances
355
Q

What are the clinical stages of labour?

A

Stage 1 - Interval between onset of labour and full dilatation of the cervix
Stage 2 - Time between full dilation of the civic and delivery
Stage 3 - Starts with completed birth of the baby and end with complete expulsion of placenta and membranes

356
Q

What are the latent and active phases occuring during labour?

A

During Stage 1
-Onset of labour with slow cervical dilatation but softening. Last a variable time (latent)

  • Faster rate of change and regular contractions (active)
  • Descent and rotation of the head internally. Crowning where the head stretches perineal muscle and skin. Extension of head and external rotation. Shoulder rotate and deliver followed rapidly by the body (passive).
  • Maternal effort to expel the fetus and achieve birth (active)
357
Q

How is labour initiated?

A

Unclear mechanism

  • Prostagladins (lipid) promote labour but don’t initiate.
  • Produced mainly in myometrium and decidua
  • Production controlled by oestrogen:progesterone ratio
  • Powerful contractor of smooth muscle
358
Q

How is contractility regulated in labour?

A
  • Progesterone inhibits contractions so it’s levels fall
  • Oestrogen increases gap junctional communication between smooth muscle cells to increase contractility
  • Mechanical stretching of uterine smooth muscle increases contractility.
  • Prostaglandins caused increase in Ca2+ per action potential
  • Oxytocin increase action potential and lowers threshold
359
Q

What is the role of oxytocin in labour?

A
  • Initiate uterine contractions
  • Action inhibited in pregnancy by progesterone, relaxin and low number of oxytocin receptors
  • Increased number of gap junctions to aid communication between muscle cells
  • By 36 weeks increased number of oxytocin receptors in myometrium therefore uterus can respond to pulsatile release of oxytocin from posterior pituitary gland. Oxytocin release controlled by hypothalamus
360
Q

What is cervical ripening?

A

Cervix collagen in proteoglycan matrix

Prostaglandins trigger ripening which involves

  • Reduction in collagen
  • Increase in glucosaminoglycans
  • Increase in hyaluronic acid
  • Reduced aggregation of collagen fibres
361
Q

What is effacement and dilatation?

A

Change to the cervix result in the Labour cervix offering less resistance to presenting part.

362
Q

What is the size of the birth canal?

A
  • Diameter of presentation of the foetus is 9.5cm

- Birth canal is determined by pelvis and the pelvic inlet is typically 11 cm and softening of ligaments may increase it

363
Q

What are the changes that occur to the pelvic floor vagina and perineum to allow for labour?

A
  • Levator ani fibres stretch

- Thinning of central portion of the perineum to almost transparent structure

364
Q

What happens to muscle in myometrium during labour?

A
  • Contractions from two poles of uterus ho to the funds and upper part of the uterus
  • After each contraction, length of each myometrium muscles of uterus can not return to former length
  • Becomes shorter and shorter
  • Contraction and retraction
365
Q

What are principles of inducing labour?

A
  • Stimulate release of prostagldins (membrane rupture)
  • Artificial prostaglandins
  • Synthetic oxytocin
  • Anti-progesterone agents
366
Q

How can delivery be facilitated by intervention?

A
  • Caesaerian seton

- Operative delivery (forceps, vacuum extraction)

367
Q

How does separation and descent of the placenta occur?

A
  • Marked reduction in size of uterus due to powerful contraction and retraction
  • Size of placental site therefore reduced
  • Inelastic placenta squeezed by contraction
368
Q

How is bleeding controlled in labour?

A
  • Powerful contraction/retraction of uterus especially action of interlacing muscle fibres which cobstricts blood vessels running though the myometrium
  • Pressure exerted onplacental site by walls of contracted uterus
  • Blood clotting mechanism
369
Q

How does the neonate establish independent life?

A
  • Neonate takes first breath (stimuli are trauma, cold, light, noise)
  • Lungs expand
  • Alveoli inflate and inflation maintained by surfactant
  • Regular breathing enables by neonatal brain pathways triggered at birth
  • Reduced pulmonary vascular resistance
  • Increase arterial pO2
370
Q

What is the hormonal control of growth and development of mammary tissue?

A
  • Hypertrophy in pre-existing alveolar-lobular structures in the breast.
  • Formation of new alveolae by budding from milk ducts with proliferation of milk collecting ducts
  • Hormones used are progesterone, oestrogen, prolactin, growth hormone, adrenal steroids
  • High levels of lactogenic hormone in pregnancy but only minimal amounts of milk hit of progesterone and oestrogen inhibit lactogenic hormones.
371
Q

How is milk produced?

A
  • Prolactin controlled
  • Released by action of suckling at a nipple that has become exquisitely sensitive post delivery.
  • Neuro-endocrine reflex causes less dopamine and increase VIP.
  • Prolactin levels and milk production are dependent on the frequency and duration of suckling.
  • Levels are at their highest in the early puerperium and reduce slowly, only returning to normal after weaning.
372
Q

Which hormone is reposbile for milk let down?

A

Oxytocin

  • Causes contraction of the myoepithelial cells situated around the alveolae to cause them to contract and expel the milk into the milk collecting ducts.
  • Milk collecting ducts have longitudinal muscle cells, which are also stimulated, causing them to dilate and improve the free flow of milk towards the nipple along these dilated ducts.
373
Q

What controls the release of hormone in milk let down?

A

Oxytocin

  • Release is stimulated by suckling, seeing or hearing the baby but is also readily inhibited by emotional stress or anxiety.
  • 90-minute cycle of ‘let down’ irrespective of suckling, because oxytocin is released in a pulsatile manner from the pituitary.
374
Q

How does cessation of lactation occur?

A
  • Key to maintaining milk production is sufficient suckling stimulation at each feed to maintain prolactin secretion and to remove accumulated milk.
  • If suckling stops, milk production ceases gradually. Due to turgor induced damage to secretory cells and low prolactin level. Suppression can also be achieved via steroids
375
Q

What is the result of damage to the neuroendocrine axis of breastfeeding?

A
  • Inadequate emptying of secreting glands of the breast to feed the infant
  • Distension and atrophy of glandular epithelium.
376
Q

What are the functions of the pelvic floor muscles

A
  • Support the pelvic organs
  • Maintain urinary and faecal continence (bladder and rectum)
  • Maintain intra-abdominal pressure during coughing, vomiting, sneezing and laughing
  • Facilitate defaecation and micturition
  • Facilitate childbirth
377
Q

What are the components of the levator ani muscles from medial to lateral?

A
  • Puborectalis
  • Pubococcygeus
  • Illiococcygeus
378
Q

What is the function of the perineal body?

A
  • Fibrous point of insertion of the elevator ani muscles

- Support of the perineal structures rely on it

379
Q

Which muscles make up the pelvic side walls?

A
  • Obturator internus

- Piriformis

380
Q

What makes up the pelvic floor (diaphragm) ?

A
  • Levator ani
  • Coccygeus
  • Urogenital diaphragm
  • Perineal body
  • Perineal muscles
  • Posterior compartment
381
Q

What makes up the deep layer of the perineal muscles?

A
  • Compressor urethra and external urethral sphincter

- Deep transverse perineal

382
Q

What makes up the superficial layer of perineal muscles?

Pubic symphysis to Ischial tuberosity

A
  • Ischicavernoousus
  • Bulbospongiosus
  • External anal sphincter
  • Superficial transverse perineal
383
Q

What is the innervation of the pelvic floor musculature?

A

-Pudendal nerve

S2,S3,S4 keeps shit of the floor

384
Q

How can damage to pelvic body occur?

A

Childbirth in women

  • Muscles strecthced
  • Nerve damage
  • Perineal body disrupted
  • Episiotomy
385
Q

What is the blood supply to the pelvic floor?

A

Blood supply - Internal and external pudendal nerves and drains via corresponding veins

Lymphatic - Inguinal nodes

386
Q

What are examples of pelvic floor dysfunction?

A
  • Pelvic organ prolapse

- Incontinence

387
Q

What is pelvic organ prolapse?

A
  • Loss of support for the uterus, bladder, colon or rectum leading to prolapse of one or more organs into the vagina
  • Can affect body image and cause depressive symptoms and is more than an anatomical defect
  • Common problem
388
Q

What are causes and risk factors of pelvic organ prolapse?

A

Aetiology is complex

Risk factors:

  • Age
  • Parity
  • Vaginal delivery-4x increased risk after 1stchild; 11x increase after >/= 4 deliveries
  • Postmenopausal oestrogen deficiency.
  • Obesity and causes of chronic raised intra-abdominal pressure
  • Gennective connective tissue disorder
  • Neurological
389
Q

What are structures involved in an episiotomy?

A
  • Vaginal epithelium
  • Transverse perineal muscle
  • Bulbocavernosus muscle
  • Bulbospongiosus
  • Perineal skin
390
Q

What is an episiotomy?

A

Cutting the vagina medial laterally

391
Q

What are complications of an episiotomy?

A
  • Haemorrhage
  • Extension to the anal sphincters
  • Infection
  • Perineal pain
  • Dyspareunia
  • Cosmetic disfigurement due to poor alignment during suturing
392
Q

What are the types of FGM?

A

Type 1 - Removal of clitoris
Type 2 - Removal of vulva and clitoris
Type 3 - Removal of vulva, clitoris and infibulation
Type 4 - All the above + sewing up

Kofi: Pure clinical conditions 2 (5 decks)

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