Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

C TO REVISE - PHASE 3A > WOMENS HEALTH - SEXUAL HEALTH, BREAST AND EXTRA CONDITIONS > Flashcards

WOMENS HEALTH - SEXUAL HEALTH, BREAST AND EXTRA CONDITIONS Flashcards

1
Q

CHLAMYDIA
What findings may there be on clinical examination in chlamydia?

A
  • Pelvic/abdo tenderness
  • Cervical excitation
  • Cervicitis
  • White/purulent discharge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CHLAMYDIA
What are some generic complications of chlamydia?

A
  • Reactive arthritis,
  • epididymitis,
  • PID,
  • endometriosis,
  • increased incidence of ectopic pregnancy,
  • most common preventable cause of infertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CHLAMYDIA
How would you manage chlamydia?

A
  • Test for other STIs, contraceptive advice, ?safeguarding if child.
  • Doxycycline 100mg BD for 7d (C/I pregnancy or breastfeeding).
  • 1g azithromycin stat dose in pregnancy (erythromycin or amoxicillin safe too)
  • Referral to GUM for partner notification + contact tracing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

GONORRHOEA
What are the local complications of gonorrhoea?

A
  • Urethral strictures
  • Epididymo-orchitis + salpingitis (can lead to infertility)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

GONORRHOEA
What are the systemic complications of gonorrhoea?

A
  • PID
  • Gonococcal arthritis (most common cause of septic arthritis in young adults)
  • Disseminated gonococcal infection as triad (tenosynovitis, migratory polyarthritis, dermatitis lesions can be maculopapular or vesicular)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

BACTERIAL VAGINOSIS
What are the risk factors of bacterial vaginosis?

A
  • Multiple sexual partners
  • Excessive vaginal cleaning
  • Recent Abx
  • Smoking
  • IUD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

BACTERIAL VAGINOSIS
What diagnostic criteria is used in BV?

A

Amsel’s (3/4)
- Thin, white discharge (can present asymptomatically)
- Vaginal pH using swab + pH paper >4.5
- Clue cells on cervical swab MC&S (endocervical or self-taken vaginal)
- Positive whiff test (add potassium hydroxide to get very strong fishy odour)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TRICHOMONAS VAGINALIS
What causes TV?
What is the structure of this organism?

A
  • Protozoan parasite, single-celled organism with flagella – trichomonas vaginalis
  • 4 flagella at front, 1 on back making it highly motile, attach to tissues + cause damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TRICHOMONAS VAGINALIS
What is the clinical presentation of TV?

A
  • PV discharge classically offensive, frothy + yellow/green.
  • Vulvovaginitis, itching, dysuria + dyspareunia.
  • May cause urethritis + balanitis in men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

TRICHOMONAS VAGINALIS
What might clinical examination of TV show?

A
  • Speculum = strawberry cervix (colpitis macularis) due to cervicitis + tiny haemorrhages on surface of cervix due to infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TRICHOMONAS VAGINALIS
What investigations would you do for TV?

A
  • Vaginal pH >4.5
  • Charcoal swab for MC&S (HVS, urethral swab or first-catch urine).
  • Microscopy shows motile trophozoites + wet microscopy shows polymorphonuclear leukocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

SYPHILIS
What is the clinical presentation of secondary syphilis?

A
  • Systemic (low grade fever, lymphadenopathy).
  • Maculopapular rash (trunk, soles + palms).
  • Condylomata lata (grey wart-like lesions around genitals + anus).
  • Alopecia
  • Buccal ‘snail track ulcers’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

SYPHILIS
What is the clinical presentation of tertiary syphilis?

A
  • Gummas (granulomatous lesions that can affect skin, organs + bones)
  • Aortic aneurysms
  • Neurosyphilis – tabes dorsalis (locomotor ataxia), paralysis, dementia,
  • Argyll-Robertson (prositutes) pupil - accomodates but does not react
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

SYPHILIS
What is an Argyll-Robertson pupil?

A

“Accommodates but does not react”
- Constricted pupil that accommodates when focusing on near object but does not react to light, often irregularly (small) shaped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SYPHILIS
What investigations would you do for syphilis?

A
  • Treponemal tests (enzyme immunoassay or haemagglutination assay)
  • Samples from site of infection tested with dark field microscopy or PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SYPHILIS
How would you manage syphilis?

A
  • Specialist GUM (full STI screening, contact tracing, contraceptive information).
  • Single dose IM benzathine benzylpenicillin or PO doxycycline if allergic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SYPHILIS
What is a potential adverse effect of treating syphilis?

A
  • Jarisch-Herxheimer reaction within a few hours of treatment
  • Fever, rash + tachycardia thought to be due to release of endotoxins following bacterial death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

GENITAL HERPES
What other specific symptoms may be seen in genital herpes?

A
  • Aphthous ulcers (small painful oral sores)
  • Herpes keratitis (inflammation of the cornea = blue)
  • Herpetic whitlow (painful skin lesion on finger/thumb)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GENITAL HERPES
What is the management or primary genital herpes contracted before 28w gestation?

A
  • Aciclovir during infection
  • Prophylactic aciclovir from 36w gestation onwards to reduce risk of genital lesions during labour + delivery
  • Asymptomatic at delivery can have vaginal if >6w from initial infection, if Sx then c-section
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

GENITAL WARTS
What are the investigations for genital warts?

A
  • Clinical diagnosis (may use magnifying glass or colposcope)
  • Application of acetic acid/vinegar produces acetowhite changes of surface
  • Biopsy if atypical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GENITAL WARTS
How is genital warts managed?

A
  • Prophylaxis with HPV vaccine for 12–13y (may be given to MSM, trans men/women + sex workers)
  • Topical podophyllotoxin cream/lotion or cryotherapy.
  • GUM contact tracing, contraceptive advice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

LICHEN SCLEROSUS
What phenomenon can occur in lichen sclerosus?

A
  • Koebner phenomenon where signs + Sx worse with friction to skin
  • Can be worse with tight, rubbing underwear, scratching + incontinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HIV
What is HIV?
What is the pathophysiology of HIV?

A
  • RNA retrovirus that encodes reverse transcriptase
  • Binds to GP120 envelope glycoprotein to CD4 receptors which migrate to lymphoid tissue where virus replicates + produces billions of new virions
  • Reverse transcriptase makes single strand RNA > double stranded DNA + viral DNA is integrated to host cell’s DNA with enzyme integrase + core viral proteins synthesised + cleaved by viral protease
  • These then released + in turn infect new CD4 cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HIV
What tests can be used to investigation HIV?

A
  • Serum/salivary HIV enzyme-linked immunosorbent assay (ELISA)
  • Rapid point of care screening blood test for HIV antibodies
  • PCR testing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HIV
What are the considerations with HIV and pregnancy?

A
  • Normal vaginal delivery if viral load <50 copies/ml
  • Consider c-section if >50, but mandatory in >400
  • IV zidovudine 4h before c-section
  • Neonatal PO zidovudine if maternal viral load <50 if not triple ART both for 4–6w
  • No breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

HIV
What are the 4 main groups of HIV treatment?

A
  • Nucleoside reverse transcriptase inhibitors (NRTIs)
  • Protease inhibitors (PIs)
  • Integrase inhibitors (IIs)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea discharge?

A

Odourless purulent, can be green/yellow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

TRICHOMONAS VAGINALIS
What can it increase the risk of?

A

Contracting HIV by damaging vaginal mucosa
BV,
cervical cancer,
PID
pregnancy-related complications.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

SYPHILIS
What is the causative organism?

A

Treponema pallidum – spirochete (spiral-shaped) bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CANDIDIASIS
What are some risk factors?

A

Increased oestrogen (pregnancy, during menstrual years)
poorly controlled DM,
immunosuppression,
broad spectrum Abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

CANDIDIASIS
What treatment should be used in pregnancy?

A

Clotrimazole in pregnancy as fluconazole can cause congenital abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

BALANITIS
what are the causes?

A

candidiasis
dermatitis
bacterial
anaerobic
lichen planus
lichen sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

BALANITIS
what are the acute causes?

A

candidiasis
dermatitis
bacterial
anaerobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

BALANITIS
what is the treatment for bacterial infection?

A

flucloxacillin or clarithromycin if penicillin allergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

BALANITIS
what is the treatment for anaerobic balanitis?

A

saline washing
oral metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

LYMPHOGRANULOMA VENEREUM
what is it?

A

STI caused by serovars L1, L2 or L3 or chlamydia trachomatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

LYMPHOGRANULOMA VENEREUM
what are the clinical features?

A

Painless genital ulcer
Appears 3-12 days after infection
May not be noticeable e.g. if occurs inside the vagina
Inguinal lymphadenopathy
Proctitis, rectal pain, rectal discharge (in rectal infections)
Systemic symptoms such as fever and malaise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

LYMPHOGRANULOMA VENEREUM
what is the management?

A

Treatment is with antibiotics. Common regimes include:

Oral doxycycline 100 mg twice daily for 21 days
Oral tetracycline 2 g daily for 21 days
Oral erythromycin 500 mg four times daily for 21 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

CHANCROID
what are the causes?

A

Haemophilus ducreyi

Given its relatively high incidence in topical areas and Greenland, it is important to inquire in the history about recent travel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CHANCROID
what are the clinical features?

A

A painful genital lesion which may bleed on contact
Associated symptoms include painful lymphadenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

CHANCROID
what is the management?

A

The infection is treated using antibiotics (typically Ceftriaxone, Azithromycin or Ciprofloxacin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

COCP
What are the benefits of the COCP?

A
  • Effective contraception, rapid return of fertility after stopping.
  • Improvement in PMS, menorrhagia + dysmenorrhoea (acne in some).
  • Reduced risk of endometrial, ovarian, colon cancer + benign ovarian cysts.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

COCP
What are some side effects + risks with the COCP?

A
  • Unscheduled bleeding common in first 3m.
  • Breast pain + tenderness.
  • Mood changes + depression.
  • Headaches, HTN, VTE.
  • Small raise in risk of breast + cervical cancer (risk normalises after 10y taking pill).
  • Small raise in risk of MI + stroke.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

COCP
What are the UKMEC3 criteria for the COCP?

A
  • > 35 smoking <15/day.
  • BMI >35kg/m^2.
  • Controlled HTN.
  • VTE FHx in 1st degree relatives.
  • Immobility.
  • Known carrier of BRCA1/2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

POP
What is the main complaint/side effect of the POP?
What are some other side effects of the POP?

A
  • Unscheduled bleeding common in first 3m (if persists exclude other causes like STIs, pregnancy, cancer).
  • Changes to bleeding schedule one of primary adverse effects (40% regular bleeding, 40% irregular, prolonged or troublesome + 20% amenorrhoeic).
  • Breast tenderness, headaches + acne.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

POP
What are some risks of the POP?

A
  • Increased risk of ovarian cysts, small risk of ectopic pregnancy with traditional POP due to reduced ciliary action, minimal increased risk of breast cancer (returns to normal 10y after stopping).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

PROGESTERONE INJECTION
What is the mechanism of action of the progesterone injection?

A
  • Inhibits ovulation by inhibiting FSH secretion by the pituitary gland + prevents development of follicles in the ovary.
  • Thickens cervical mucus + alters endometrium to make it less favourable for implantation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

PROGESTERONE INJECTION
What are 3 unique side effects to the progesterone injection?

A
  • Weight gain
  • Reduced BMD (oestrogen maintains BMD + mostly produced by follicles in ovaries)
    – Makes depot unsuitable for those >45
  • Takes 12m for fertility to return after stopping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

PROGESTERONE INJECTION
What are some general side effects of the progesterone injection?

A
  • Acne.
  • Reduced libido.
  • Mood issues (depression).
  • Headaches.
  • Alopecia.
  • Skin reactions at injection sites.
  • Small rise in breast/cervical cancer risk.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

PROGESTERONE IMPLANT
What is the mechanism of action for the progesterone implant?

A
  • Inhibits ovulation.
  • Thickens cervical mucus.
  • Alters endometrium to make it less accepting to implantation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

PROGESTERONE IMPLANT
What are the side effects of the progesterone implant?

A
  • Problematic bleeding (20% amenorrhoeic, 25% frequent/prolonged bleeding, 33% infrequent, rest normal, can use COCP for 3m if problematic bleeding + no C/Is).
  • Can worsen acne, no STI protection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

PROGESTERONE IMPLANT
What are the risks with the progesterone implant?

A
  • Can be bent/fractured or impalpable/deeply implanted needing extra contraception until located (USS/XR), may need specialist removal.
  • Very rarely can enter vessels + migrate through body to lungs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

COILS
What are the contraindications to the coils?

A
  • PID or infection,
  • immunosuppression,
  • pregnancy,
  • unexplained bleeding,
  • pelvic cancer,
  • uterine cavity distortion (fibroids).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

COILS
What are the drawbacks of the IUD?

A
  • Procedure with risks for insertion/removal.
  • Can cause HMB/IMB which often settles.
  • Some women have pelvic pain.
  • No STI protection.
  • Increased risk of ectopic pregnancies.
  • Occasionally falls out.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

COILS
What is the mechanism of action for the IUS?

A
  • Progesterone component thickens cervical mucus.
  • Alters endometrium making less hospitable + inhibits ovulation in small # of women.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

COILS
What are the drawbacks of the IUS?

A
  • Procedure with risks for insertion/removal.
  • Can cause spotting or irregular bleeding.
  • Some women experience pelvic pain.
  • No STI protection.
  • Increased risk of ectopic pregnancies.
  • Occasionally falls out.
  • Increased incidence of ovarian cysts.
  • Systemic absorption can lead to progesterone Sx (acne, headaches, breast tenderness).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

EMERGENCY CONTRACEPTION
For the copper IUD, answer the following…
i) effectiveness?
ii) time frame?
iii) mechanism?
iv) extra notes?

A

i) 99% regardless of time in cycle
ii) <120h of UPSI or 120h after earliest estimated date of ovulation
iii) Toxic to sperm + ovum so inhibits fertilisation + implantation.
iv) Keep in until at least next period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

EMERGENCY CONTRACEPTION
For Ulipristal acetate, answer the following…
i) dose?
ii) effectiveness?
iii) time frame?
iv) mechanism?
v) extra notes?
vi) side effects?

A

i) Single 30mg dose
ii) Second most effective but decreases with time
iii) <120h
iv) Selective progesterone receptor modulator that inhibits ovulation
v) Vomiting within 3h then repeat dose
vi) Spotting + changes to next menstrual period, abdo/pelvic/back pain, mood changes, headaches, dizziness, breast tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

EMERGENCY CONTRACEPTION
For Ulipristal acetate, what are the pros and cons?

A

Pros
- More effective than levonorgestrel
- Can be used >1 in one cycle
Cons
- Avoid breastfeeding for 1w (express but discard)
- Avoid in severe asthma
- Wait 5d before starting COCP or POP with 7 or 2d extra contraception needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

EMERGENCY CONTRACEPTION
For levonorgestrel, answer the following…
i) dose?
ii) effectiveness?
iii) time frame?
iv) mechanism?
v) side effects?

A

i) Single 1.5mg dose (3mg if BMI >26kg/m^2)
ii) Least effective of group 84%
iii) <72h
iv) Stops ovulation + inhibits implantation
v) Spotting + changes to next menstrual period, diarrhoea, breast tenderness, dizziness, depressed mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

EMERGENCY CONTRACEPTION
For Levonorgestrel, what are the pros and cons?

A

Pros
- Safe during breastfeeding (Avoid for 8h to avoid infant exposure though).
- COCP/POP can start instantly but with extra contraception for 7/2d
- Use more than once in a menstrual cycle
Cons
- Less effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

FEMALE INFERTILITY
What are some risk factors of infertility?

A
  • Extremes of weight
  • Increasing age
  • Smoking
  • Alcohol/drug use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

ASSISTED CONCEPTION
What is the clinical presentation of ovarian hyperstimulation syndrome?

A
  • Mild = abdo pain + vomiting
  • Mod = N+V + ascites on USS
  • Severe = ascites, oliguria
  • Critical = anuria, VTE, ARDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

ASSISTED CONCEPTION
What are the risk factors for ovarian hyperstimulation syndrome?

A
  • Younger age.
  • Lower BMI.
  • PCOS.
  • Higher antral follicle count.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

ASSISTED CONCEPTION
What investigations would you do in ovarian hyperstimulation syndrome and what would they show?
How could you identify someone at risk?

A
  • Activation of RAAS > high renin
  • Haematocrit raised as less fluid in intravascular space
  • USS + serum oestrogen (high = risk) – monitor these to identify those at risk.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ASSISTED CONCEPTION
What is ovarian hyperstimulation syndrome?
What is it associated with?

A
  • Increased vascular endothelial growth factor (VEGF) from granulosa cells increases vascular permeability so fluid leaks from intravascular>extravascular space (oedema, ascites + hypovolaemia).
  • Gonadotrophins to mature follicles.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

BREAST CANCER
What are the 2 main genes involved in breast cancer and how do they act?

A
  • BRCA1 = mutation of C17, 60-80% lifetime risk, stronger incidence
  • BRCA2 = mutation of C13, 45% lifetime risk
  • Tumour suppression genes that act as inhibitors of cellular growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

BREAST CANCER
What are some other genetic mutations associated with breast cancer?

A
  • TP53 (Li Fraumeni)
  • Peutz-Jeghers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

BREAST CANCER
What tumour marker can be used to monitor response to breast cancer treatment and disease recurrence?

A
  • CA 15-3
70
Q

BREAST CANCER
Reconstruction surgery can either be primary (immediately) or delayed.
What are the pros and cons of primary reconstruction?

A
  • Increased skin preservation options, reduced psychological trauma
  • May delay chemo/radiotherapy if complications, radiotherapy may ruin results (fibrosis)
71
Q

BREAST CANCER
Reconstruction surgery can either be primary (immediately) or delayed.
What are the pros and cons of delayed reconstruction?

A
  • Minimal risks of delay in adjuvant therapies, healthy tissue used to recreate breast
  • Limited skin preservation options, psychological impact (no breast)
72
Q

BREAST INFECTION
What is the management of non-lactational mastitis?

A
  • Same as lactational mastitis (flucloxacillin or erythromycin) but + metronidazole
73
Q

BREAST INFECTION
What is the most common cause of mastitis?
What is there a caution with?

A
  • S. Aureus then anaerobes (esp. non-lactational)
  • Repeated incision in non-lactational abscess as can develop mammary fistula which is difficult to treat
74
Q

GYNAECOMASTIA
What are some pathological causes of gynaecomastia?

A
  • Drugs (spironolactone, oestrogen, anabolic steroids)
  • Marijuana
  • Liver failure
  • Testicular failure or tumour (Can produce beta-hCG)
75
Q

DUCT ECTASIA
What is the management?

A

Expectant management
If symptoms persist then operation to remove affected ducts may be offered

76
Q

BREAST CANCER
what is tamoxifen?

A

tamoxifen inhibits the oestrogen receptor on breast cancer cells
It increases survival by 15-25% in woman with ER+ cancer
give for 10 years in higher risk women

77
Q

BREAST CANCER
what are the complications of tamoxifen?

A

hot flushes
nausea
vaginal bleeding
rarely thrombosis and endometrial cancer

78
Q

BREAST CANCER
what are aromatase inhibitors?

A

letrozole
Inhibit aromatase enzyme responsible for the conversion of androgens to oestogen in post-menopausal woman
slightly better anticancer efficacy than tamoxifen

79
Q

BREAST CANCER
what are the side effects of aromatase inhibitors?

A

hot flushes
reduced bone density
joint pains

80
Q

PAGET’S DISEASE OF THE NIPPLE
what are the risk factors?

A
  • old age
  • FHx of breast cancer
  • Previous breast cancer
  • overweight
  • excess alcohol
  • smoking
  • risk factors for breast cancer
81
Q

1* AMENORRHOEA
What is primary amenorrhoea?

A

Absence of menstruation by –
- 14y if no secondary sexual characteristics (more indicative of a chromosomal abnormality)
- 16y with secondary sexual characteristics (breast buds)

82
Q

1* AMENORRHOEA
What is the difference between hypogonadotrophic hypogonadism and hypergonadotrophic hypogonadism?

A
  • Deficiency in gonadotrophins (LH + FSH) stimulating ovaries due to abnormal hypothalamus or pituitary means they do not respond by producing sex hormones (oestrogen)
  • Gonads fails to respond to stimulation of gonadotrophins meaning no negative feedback + increasing amounts of FSH/LH
83
Q

1* AMENORRHOEA
What are some causes of hypogonadotrophic hypogonadism?

A
  • Constitutional delay (temporary delay, no pathology, ?FHx)
  • Hypopituitarism
  • Kallmann’s (failure to start puberty + anosmia)
  • Excessive exercise, dieting or stress causes hypothalamic failure
  • Endo = Cushing’s, prolactinoma, thyroid
  • Damage (cancer, surgery)
84
Q

1* AMENORRHOEA
What are some causes of hypergonadotrophic hypogonadism?

A
  • Turner’s syndrome XO
  • Congenital absence of ovaries
  • Previous damage to gonads (torsion, cancer, infections like mumps)
85
Q

1* AMENORRHOEA
What are some other causes of primary amenorrhoea and how may they present?

A
  • Congenital adrenal hyperplasia (tall, deep voice, facial hair)
  • Androgen insensitivity syndrome (46XY but female phenotype)
  • Congenital malformations of genital tract (if ovaries unaffected = secondary sexual characteristics but no menses)
  • Gonadal dysgenesis (no ovaries or uterus form)
86
Q

1* AMENORRHOEA
What are some first line investigations for primary amenorrhoea?

A
  • Examination = signs of puberty, PV exam, BMI, visual fields
  • FBC + ferritin (anaemia), U+E for CKD, anti-TTG for coeliac, urinary beta-hCG crucial
87
Q

1* AMENORRHOEA
What hormonal blood tests would you do for primary amenorrhoea?

A
  • FSH + LH (low or high)
  • TFTs, prolactin (if indicated)
  • Free androgens raised in PCOS, AIS + CAH
  • Insulin-like growth factor I used for screening for GH deficiency
88
Q

2* AMENORRHOEA
What is secondary amenorrhoea?
What is oligomenorrhoea?

A
  • Previously normal menstruation ceases for >3m in a non-pregnancy woman
  • Where menses are >35d apart (up to 6m), can be ovarian normality but exclude PCOS
89
Q

2* AMENORRHOEA
What are the causes of secondary amenorrhoea?

A
  • Pregnancy (most common), breastfeeding, menopause (physiological)
  • Iatrogenic (contraception)
  • Hypothalamic/pituitary
  • Ovarian causes (PCOS, POI)
  • Thyroid, uterine pathology (Asherman’s)
  • Excessive exercise, stress or eating disorders
90
Q

2* AMENORRHOEA
What are the hypothalamic or pituitary causes of secondary amenorrhoea?

A
  • Sheehan’s syndrome = pituitary necrosis following PPH
  • Pituitary tumour like prolactinoma leading to hyperprolactinaemia which prevents GnRH
  • Trauma, radiotherapy or surgery
91
Q

2* AMENORRHOEA
How does excessive stress or eating disorders cause secondary amenorrhoea?

A
  • Hypothalamus reduces GnRH in times of stress > hypogonadotrophic hypogonadism to prevent pregnancy in adverse situations
92
Q

2* AMENORRHOEA
What hormonal tests would you do in secondary amenorrhoea?

A
  • Urine/blood beta-hCG
  • High FSH (POI)
  • Low FSH/LH (hypgonadotrophic hypogonadism)
  • High LH or LH:FSH ratio suggests PCOS
  • Free androgen raised in PCOS
  • Mid-luteal (day 21) progesterone to check ovulation happened
  • Prolactin + TFTs if indicated
93
Q

2* AMENORRHOEA
What is the management of…

i) hyperprolactinaemia?
ii) hypothalamic failure?

A

i) Bromocriptine or cabergoline (dopamine agonists)
ii) GnRH replacement

94
Q

POI
What are some causes of POI?

A
  • Majority idiopathic
  • Iatrogenic (chemo/radio, oophorectomy)
  • Autoimmune (coeliac, T1DM)
  • Genetic (FHx, Turner’s)
  • Infections (mumps, TB, CMV)
95
Q

POI
What are the complications of POI?

A
  • Higher risk of conditions due to lack of oestrogen > CVD, stroke, osteoporosis, dementia + cognitive impairment + Parkinsonism
96
Q

FGM
What is the WHO classification for the types of FGM?

A
  • 1 = partial or total clitoridectomy
  • 2 = excision
  • 3 = infibulation
  • 4 = all other non-medical harmful procedures incl. pricking, piercing, incising
97
Q

MACROSOMIA
What are the causes of macrosomia?

A
  • Constitutionally large or familial (parental height + weight)
  • Maternal diabetes, previous macrosomia, obesity or rapid weight gain
  • Overdue
  • Male baby
98
Q

INFECTIONS + PREGNANCY
What is Parvovirus?
What are the adverse effects?
What is the management?

A
  • Parvovirus B19 can give viral Sx then ‘slapped cheeks’ (erythema infectiosum)
  • Worse <20w = suppresses foetal erythropoiesis causing anaemia + foetal hydrops, death, pre-eclampsia-like (mirror) syndrome in women
  • Maternal IgM + IgG, supportive, refer to foetal medicine to monitor
99
Q

INFECTIONS + PREGNANCY
What is the management of HIV in pregnancy?

A
  • Normal vaginal delivery if viral load <50 copies/ml if. not c-section (IV zidovudine 4h before)
  • Neonatal zidovudine PO if maternal viral load <50 if not triple ART, both for 4–6w
  • Breastfeeding C/I
100
Q

THYROID + PREGNANCY
What is the management of hyperthyroidism in pregnancy?

A
  • Propylthiouracil is choice in 1st trimester (associated with maternal hepatic injury)
  • Carbimazole C/I until 2nd trimester as causes foetal abnormalities
  • If mother has stimulating antibodies, monitor foetal growth with USS
101
Q

THYROID + PREGNANCY
Is hypothyroidism in pregnancy common?
What is the prognosis of untreated hypothyroidism in pregnancy?
What is the management?

A
  • Yes
  • Early foetal loss + congenital hypothyroidism leading to impaired neurodevelopment
  • Aim for adequate replacement with levothyroxine (safe), especially in 1st trimester
102
Q

THYROID + PREGNANCY
What is post-partum thyroiditis?

A

3 stages –
- Thyrotoxicosis (3m)
- Hypothyroidism (3–6m)
- Normal thyroid function
Sx control of thyrotoxicosis, treat hypothyroidism with levothyroxine
Just need TFTs to Dx if within 12m of giving birth + Sx

103
Q

PREMATURITY
What is the prophylaxis for prematurity and how do they work?

A
  • Progesterone gel or pessary decreases activity of myometrium + prevents cervix remodelling in preparation for delivery
  • Cervical cerclage = ≥1 sutures to strengthen + keep cervix closed
  • ‘Rescue’ cerclage to halt delivery
104
Q

PREMATURITY
What are the indications for…

i) progesterone prophylaxis?
ii) cervical cerclage?
iii) ‘rescue’ cerclage?

A

i) Cervical length <25mm on TVS at 16–24w
ii) Cervical length <25mm on TVS at 16–24w, previous premature birth or cervical trauma (colposcopy, cone biopsy)
iii) Cervical dilatation without ROM at 16–27+6 with no infection, bleeding or contractions

105
Q

PREMATURITY
What is the acute management of prematurity?

A
  • Senior obs + neonate input
  • Foetal monitoring (CTG)
  • Tocolytics
  • Corticosteroids
  • IV magnesium sulfate
  • Consider delayed cord clamping or cord milking (increases circulating blood volume + Hb in baby)
106
Q

AMNIOTIC EMBOLISM
What are some risk factors for amniotic fluid embolism?
Presentation?

A
  • Increasing maternal age + ARM
  • Often around time of labour + delivery but can be postpartum
  • Sx = SOB, sweating, anxiety, seizures, haemorrhage
  • Signs = hypoxia, tachycardia + hypotension, may lead to cardiac arrest
107
Q

MATERNAL SEPSIS
What are the investigations for maternal sepsis?

A
  • Monitor Maternal Early Obstetric Warning Score (MEOWS)
  • Warning signs of sepsis (3Ts white with sugar)
108
Q

MATERNAL SEPSIS
What are the warning signs of sepsis?

A

3Ts white with sugar –
- Temp <36 or >38
- Tachycardia >90bpm
- Tachypnoea >20bpm
- WCC >12 or <4
- Hyperglycaemia >7.7mmol/L in absence of diabetes

109
Q

MATERNAL SEPSIS
What are the SEPSIS 6 components?

A

BUFALO (3 in, 3 out) –
- Blood cultures (out)
- Urine output by catheter (hourly, out)
- Fluids resus (IV, in)
- Abx (IV broad-spec, in)
- Lactate (ABG, out)
- Oxygen (high flow SpO2 >94%, in)

110
Q

PUERPERIUM
What are some drug contraindications in breastfeeding?

A
  • Abx (ciprofloxacin, tetracyclines, chloramphenicol)
  • Psych drugs (lithium, BDZs)
  • Amiodarone, aspirin
  • Carbimazole, methotrexate
  • Sulfonylureas
  • Cytotoxic drugs
111
Q

PUERPERIUM
What are the pros + cons of breast feeding?

A
  • Readily available good nutrition, cheaper, contraceptive effect, decrease childhood infections (gastroenteritis), decrease in necrotising enterocolitis
  • Feed more often, uncomfortable + pain (mastitis)
112
Q

SHEEHAN’S SYNDROME
What is Sheehan’s syndrome?

A
  • Drop in circulating blood volume leads to avascular necrosis of the pituitary gland
  • Ischaemia + infarction of anterior pituitary cells as supplied by hypothalamo-hypophysial portal system which is susceptible to rapid drops in BP after PPH
113
Q

SHEEHAN’S SYNDROME
How does Sheehan’s syndrome present?
What is the management?

A
  • Reduced lactation (lack of prolactin)
  • Amenorrhoea (lack of LH + FSH > HRT)
  • Hypothyroidism (lack of TSH > levothyroxine)
  • Adrenal insufficiency (lack of ACTH > hydrocortisone)
114
Q

NEWBORN SCREENING
What is the process of the newborn blood spot conditions screen (Guthrie/heel-prick)?

A
  • Screening on day 5–9
  • Residual blood spots stored for 5 years (part of consent process) for research
115
Q

NEWBORN SCREENING
What conditions does the newborn blood spot screen for?

A

3 genetic –
- Sickle cell disease
- Cystic fibrosis
- Congenital hypothyroidism
6 inherited metabolic –
- Phenylketonuria
- Medium-chain acyl-CoA dehydrogenase deficiency
- Maple syrup urine disease
- Isovaleric acidaemia
- Glutaric aciduria type 1
- Homocystinuria

116
Q

NEWBORN SCREENING
What specifically is tested for in…

i) cystic fibrosis?
ii) congenital hypothyroidism?
iii) phenylketonuria?

A

i) Immunoreactive trypsinogen
ii) TSH
iii) Phenylalanine

117
Q

PREGNANCY PHYSIOLOGY
What hormones increase in regards to the anterior pituitary gland?

A
  • ACTH = rise in steroid hormones (cortisol, aldosterone) = improves autoimmune conditions (RA) but susceptible to DM + infections
  • Prolactin = suppresses FSH + LH
  • Melanocyte stimulating hormone = increased skin pigmentation (linea nigra + melasma = brown pigmentation)
118
Q

PREGNANCY PHYSIOLOGY
What other hormones rise in pregnancy?

A
  • T3/T4
  • HCG = doubles every 48h until plateau at 8–12w then gradual fall
  • Progesterone
  • Oestrogen
119
Q

PREGNANCY PHYSIOLOGY
What changes occur to the uterus in pregnancy?

A
  • Increase from 100g–1.1kg
  • Hyperplasia + hypertrophy of myometrium
  • Decidual spiral arteries remodelled for wide bore low resistance
120
Q

PREGNANCY PHYSIOLOGY
What changes occur to the cervix in pregnancy?

A
  • Increased oestrogen = ?cervical ectropion + increased discharge
  • Before delivery, prostaglandins break down collagen in cervix = dilate + efface
  • Chadwick’s sign = early pooled deoxygenated blood > blue tinge
121
Q

PREGNANCY PHYSIOLOGY
What changes occur to the vagina in pregnancy?

A
  • Oestrogen > hypertrophy of vaginal muscles + increased PV discharge
  • Makes bacterial + candida infection more common
122
Q

PREGNANCY PHYSIOLOGY
In terms of the cardiovascular system in pregnancy, what…

i) increases?
ii) decreases?

A

i) Blood volume, plasma volume, CO (as increased SV + HR)
ii) Peripheral vascular resistance (can cause flushing + hot sweats) + BP in early-mid pregnancy but returns to normal by term

123
Q

PREGNANCY PHYSIOLOGY
What CVS anatomical changes are there?

A
  • Diaphragmatic elevation > heart displaced upwards/left so apex moved laterally
  • Increased ventricular muscle mass + increased LV/LA size
  • Altered QRS (LAD), ECG changes (inverted T waves) + flow (ES) murmurs
124
Q

PREGNANCY PHYSIOLOGY
In terms of the respiratory system, what are the mechanical changes?

A
  • Increased subcostal angle, pulmonary blood flow + tidal volume
  • Decreased vital capacity + functional residual capacity
  • Progesterone causes trachea-bronchial smooth muscle relaxation
125
Q

PREGNANCY PHYSIOLOGY
In terms of the respiratory system, what are the biochemical changes?

A
  • Increased oxygen consumption (20%) + RR
  • Compensated resp alkalosis may occur as increased pO2 + reduced pCO2 (facilitates foetal CO2 excretion), renal HCO3- excretion to prevent this
  • Increased 2,3 DPG to promote maternal Hb to release oxygen
126
Q

PREGNANCY PHYSIOLOGY
In terms of the renal system, what…

i) increases?
ii) decreases?

A

i) Blood flow to kidneys (so GFR), aldosterone (Na + water reabsorption + Retention), protein excretion
ii) Serum creatinine, urate + albumin

127
Q

PREGNANCY PHYSIOLOGY
What can happen in terms of the urinary system?
What is a consequence of this?
What else contributes?

A
  • Dilatation of ureters + collecting system > physiological hydronephrosis (more R)
  • Increased risk of UTIs
  • Decreased ureter tone/peristalsis = urinary stasis
128
Q

PREGNANCY PHYSIOLOGY
What 4 forces/pressures govern fluid retention in pregnancy?

A
  • Capillary (hydrostatic) pressure of blood in vessel = draws fluid OUT
  • Interstitial fluid colloid oncotic pressure of proteins in interstitial fluid = draws fluid OUT
  • Interstitial fluid pressure of tissues surrounding vessel = draws fluid IN
  • Plasma colloid oncotic pressure (albumin) = draws fluid IN
129
Q

PREGNANCY PHYSIOLOGY
Why does pregnancy cause dilutional anaemia?
What is the purpose of this?

A
  • Increased RBC production = higher iron, folate + B12 requirements
  • Increased ECF + plasma volume MORE than RBC volume leading to lower red cell conc (haematocrit) + lower Hb conc
  • Facilitates placental perfusion
130
Q

PREGNANCY PHYSIOLOGY
In terms of haematology in pregnancy, what…

i) increases?
ii) decreases?

A

i) WBCs, ESR, d-dimers, ALP
ii) Platelets, albumin

131
Q

PREGNANCY PHYSIOLOGY
What are the metabolic changes are there in pregnancy?

A
  • Early = post-prandial glucose plasma peak lower due to fat deposition + glycogen storage
  • Late = higher for longer + maternal insulin resistance (via hPL) for foetal glucose sparing
  • Maternal insulin rises during most of pregnancy
132
Q

PREGNANCY PHYSIOLOGY
What are the changes to the skin and hair in pregnancy?

A
  • Linea nigra + melasma
  • Striae gravidarum
  • General pruritus (?OC)
  • Spider naevi + palmar erythema
  • PP hair loss normal, improves within 6m
133
Q

PREGNANCY PHYSIOLOGY
What facilitates blastocyst implantation in pregnancy?

A
  • Increased GFs, proteolytic enzymes + inflammatory mediators
  • Not rejected as change in self/non-self pattern recognition molecules (HLA + MHC proteins)
134
Q

PREGNANCY PHYSIOLOGY
In pregnancy, what changes to the humoral and cell-mediated immunity?

A
  • Humoral = unchanged, plenty of circulating Th2 cells to fight infections (antibodies)
  • Cell-mediated = reduced as progesterone down regulates production of Th1 cells (phagocytes, cytotoxic T lymphocytes)
135
Q

PREGNANCY PHYSIOLOGY
What is the impact of dampening Th1 production?
What are the implications?

A
  • Shift to increased Th2 production (bias) to protect foetus
  • Pre-eclampsia, IUGR + miscarriage do not have a Th2 bias
136
Q

REPRODUCTION
What are the different stages in follicular genesis and what stage in the cell cycle are they?

A
  • Primordial follicles = diploid, arrested at prophase I
  • Primary follicle = diploid, undergoing meiosis I
  • Secondary follicle = haploid, once meiosis I complete
  • Antral (Graafian) follicle = haploid, frozen in metaphase II
137
Q

REPRODUCTION
What happens when follicles reach the secondary follicle stage?

A
  • Granulosa cells express FSH receptors = oestrogen production to grow
  • Theca cells express LH receptors = steroidogenesis
138
Q

REPRODUCTION
What happens at ovulation?

A
  • LH surge = smooth muscle of theca externa contracts
  • Follicle bursts + secretes enzymes puncturing hole in ovary
  • Fimbriae of fallopian tubes sweeps oocyte up, surrounded by zona pellucida
  • Leftover follicle > corpus luteum
139
Q

REPRODUCTION
How does fertilisation occur?

A
  • Sperm enters fallopian tube + attempts to penetrate through corona radiata + zona pellucida via acrosome reaction
  • Fusion of sperm + egg = zygote
140
Q

REPRODUCTION
What happens immediately after fertilisation?

A
  • Cell rapidly divides > mass of cells (morula) travels to uterus
  • Fluid filled cavity (blastocele) expands to form blastocyst (>80 cells) with outer layer (trophoblast) + inner layer (embryoblast)
141
Q

REPRODUCTION
When does the blastocyst reach the uterus?
What happens?

A
  • 8–10d after ovulation
  • Trophoblast cells undergo adhesion to stroma of endometrium
  • Outer layer of trophoblast (syncytiotrophoblast) forms projections into the stroma
142
Q

REPRODUCTION
Once the blastocyst has implanted, what happens to the stroma?
What signifies blastocyst implantation?

A
  • Cells of stroma convert into decidua to provide nutrients (decidual reaction)
  • Syncytiotrophoblast produces hCG to maintain corpus luteum
143
Q

REPRODUCTION
When does the embryonic disc develop further?
What does it develop into?

A
  • 5w
  • Foetal pole with 3 layers = ectoderm (outer), mesoderm (mid), endoderm (inner)
144
Q

REPRODUCTION
What tissues does the…

i) ectoderm
ii) mesoderm
iii) endoderm

produce?

A

i) Skin, hair, nails, teeth, CNS
ii) Heart, muscle, bone, connective tissue, kidneys, blood
iii) GI tract, lungs, liver, pancreas, thyroid, reproductive

145
Q

REPRODUCTION
When do actual organs begin to develop?

A
  • 6w foetal heart forms + starts to beat
  • 8w all major organs start development
146
Q

REPRODUCTION
How does the placenta develop?

A
  • Syncytiotrophoblast forms chorionic villi with foetal blood vessels
  • Those nearest connecting stalk most vascular, cells proliferate + become placenta at about 10w
147
Q

REPRODUCTION
What role does the placenta play in immunity?

A
  • IgG crosses placenta to give foetus immunity
  • Primary immune deficiency hypogammaglobulinaemia can occur in babies whose mothers did not have high enough IgG during pregnancy
148
Q

REPRODUCTION
What are the main hormones produced by the placenta?

A
  • hCG (maintain corpus luteum)
  • Oestrogen
  • Progesterone
  • Human placenta lactogen
149
Q

REPRODUCTION
What is the role of oestrogen in pregnancy?

A
  • Softening tissue > more flexible, allows muscles + ligaments of uterus and pelvis to expand + cervix become soft
  • Enlarges + prepares breasts + nipples for breast feeding
  • E3 declines with foetal distress, E2 increases endometrial progesterone receptors
150
Q

REPRODUCTION
What is the role of progesterone in pregnancy?

A
  • Produced by corpus luteum until 10w
  • Initially prepares endometrium for implantation by proliferation, vascularisation + decidual reaction
  • Later, maintains pregnancy by preventing contraction
  • Relaxation elsewhere > heartburn, constipation, hypotension
151
Q

REPRODUCTION
What is the role of human placental lactogen in pregnancy?

A
  • Diabetogenic as raises blood glucose levels to help increase nutrient supply + helps convert mammary glands into milk secreting tissue
152
Q

MENSTRUAL CYCLE
what are the roles of FSH and LH?

A

FSH - enables production of oestrogen
LH - enables production of progesterone

153
Q

MENSTRUAL CYCLE
what are the stages of the ovarian cycle?

A

follicular phase
luteal phase

154
Q

MENSTRUAL CYCLE
what happens during the follicular phase?

A
  • rising levels of FSH stimulates developing follicles to produce oestrogen
  • oestrogen inhibits FSH leading to one dominant follicle
  • follicle starts developing LH receptors
  • egg completes first meiotic division
  • oestrogen levels cause positive feedback leading to LH surge
155
Q

MENSTRUAL CYCLE
what causes the LH surge at the end of the follicular phase?

A

oestrogen levels cause positive feedback leading to LH surge

156
Q

MENSTRUAL CYCLE
what happens during the luteal phase?

A
  • follicle becomes corpus luteum (lifespan of 14 days)
  • corpus luteum secretes progesterone which peaks 7 days after ovulation unless maintained by pregnancy
  • falling progesterone causes menstrual bleeding
157
Q

MENSTRUAL CYCLE
What occurs during ovulation?

A
  • Follicle (dominant) with most FSH receptors continues developing
  • Secretes further oestrogen which at a threshold causes spike in LH (+ slight rise in FSH) causing release of ovum on day 14
158
Q

MENSTRUAL CYCLE
What happens if the egg is fertilised?

A
  • Syncytiotrophoblast of embryo secretes human chorionic gonadotropin (hCG) which maintains corpus luteum
159
Q

MENSTRUAL CYCLE
What happens if the egg is not fertilised?

A
  • hCG absence > corpus luteum degenerates into corpus albicans
  • Fall in progesterone + oestrogen causes endometrium to breakdown + menstruation occurs
  • FSH + LH levels rise
  • Stromal cells of endometrium release prostaglandins to encourage endometrium breakdown + uterine contraction
160
Q

MENSTRUAL CYCLE
What are the stages of the menstrual cycle?

A
  • Menstruation (Days 1-5)
  • Proliferation (Days 6-14)
  • Ovulation (Day 14)
  • Secretion (Days 16-28)
161
Q

MENSTRUAL CYCLE
What happens during the menstrual phase?

A
  • falling levels of progesterone cause shedding of endometrium
  • spasm of spiral arteries
  • ischaemic necrosis
  • generalised inflammation
162
Q

MENSTRUAL CYCLE
What happens in the proliferative phase?

A
  • endometrium grows under influence of oestrogen
  • oestrogen causes hyperplasia of the endometrium
  • early development of glands and spiral arterioles
163
Q

MENSTRUAL CYCLE
What happens in the early secretory phase of the menstrual cycle?

A
  • after ovulation progesterone predominates
  • changes from focusing on growth to preparing for implantation
  • development of complex glands, increased spiral arterioles
  • endometrial cells produce and store glycogen
164
Q

MENSTRUAL CYCLE
What happens in the late secretory phase of the menstrual cycle?

A
  • Cervical mucus thickens + less hospitable for sperm
  • Decrease in oestrogen + progesterone > spiral arteries collapse + constrict + functional layer prepares to shred
165
Q

CONTRACPETION
What is the method of action for COCP?

A

Inhibits ovulation

166
Q

CONTRACEPTION
what is the method of action for POP (excluding desogestrel)?

A

Thickens cerivcal mucus

167
Q

CONTRACEPTION
What is the method of action for desogestrel POP?

A

Primary = inhibits ovulation
Also thickens cervical mucus

168
Q

CONTRACEPTION
What is the method of action for injectable contraceptives (e.g. depo)?

A

Primary = inhibits ovulation
Also thickens cervical mucus

169
Q

CONTRACEPTION
What is the method of action for IUD?

A

Decreases sperm motility and survival

170
Q

CONTRACEPTION
What is the method of action for IUS?

A

Primary = prevents endometrial proliferation
Also thickens cervical mucus

171
Q

EMERGENCY CONTRACEPTION
What is the method of action for levonogestrel?

A

Inhibits ovulation

172
Q

EMERGENCY CONTRACEPTION
What is the method of action for ulipristal acetate?

A

Inhibits ovulation

C TO REVISE - PHASE 3A (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions