Brainscape's Knowledge GenomeTM

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


See full index

Anki 3a exports > Obs and Gynae anki 1 > Flashcards

Obs and Gynae anki 1 Flashcards

1
Q

How can urinary incontinece be characterised?

A
  1. Overactive bladder/urge incontinence
  2. Stress incontinence
  3. Mixed incontinence
  4. Overflow incontince
  5. Functional incontinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is urinary incontinence investigated?

A
  1. Physical exam-in some cases to rule out pelvic organ prolapse and ability to contract pelvic floor muscles
  2. Bladder diary-minimum of 3 days
  3. Urinalysis-rule out infection
  4. Urodynamic studies-cystometry and cystogram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the management of stress incontinence

A

Conservative: avoid caffeine and fizzy drinks and excessive fluid intake-
Pelvic floor exercises
Medical: Duloxetine-ONLY if conservative doesn’t work and patients doesn’t want surgery
Surgical: GS: Mid urethral slings
Other surgeries: Incontinence pessaries, bulking agents, colposuscpension and fascial slings

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

How do mid-urethral slings work to treat stress incontinence?

A

Compress the urethra against a supportive layer and assist in the closure of the urethral sphincter during increased intra-abdominal pressures

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

How does colposuspension and facial slings work in treating stress incontinence

A

Involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the general conservative management of incontinence

A

Lifestyle advice: avoid caffeine and fizzy drinks, avoid excessive fluid intake
Pelvic floor exercises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the medical management of urge incontinence

A

Anticholinergics(antimuscarinics): inhibit the parasympathetic action of the detrusor muscle-
Oxybutinin, tolterodine, etc

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

Describe the symptoms of a genital prolapse

A

Pelvic discomfort or a sensation of ‘heaviness’
Visible protrusion of tissue from the vagina
Urinary symptoms such as incontinence, recurrent urinary tract infections or difficulties voiding
Defecatory symptoms, including constipation or incomplete bowel emptying
Sexual dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the management of a gential prolapse

A

If asymptomatic and mild: no treatment Conservative: Weight loss, smoking cessation, avoid heavy lifting, pelvic floor exercises
Ring pessary
Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the surgical management for a cystocele

A

Anterior colporrhaphy, colposuspension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the symptoms of a vaginal fistula

A

Incontinence-especailly if vesicovaginal(bladder and vagina)
Also: diarrhoea, nausea, vomiting, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is a vaginal fistula diagnosed?

A

Pelvic exam
Cystoscopy and urodynamic studies
Imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the management of vaginal fistulas

A

Conservative: catheterisation, antibiotics to prevent/treat infection
Surgical: fistula repair, tissue grafts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the aetiology of uterine fibroids

A

Unknown
Genetic, hormonal and environmental factors

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

How can uterine fibroids cause polycythaemia?

A

Secondary to autonomous production of erythropoeitin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are uterine fibroids diagnosed

A

Trans-vaginal ultrasound: Used to assess the size and location of the fibroids
MRI: Used if ultrasound does not provide enough detail to assess the fibroid for surgery
Biopsy: May be taken if there is any doubt over the diagnosis to differentiate the fibroid from other conditions such as endometrial cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the management of asymptomatic fibroids

A

No treatment, just review to monitor growth and size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the management of menorrhagia secondary to fibroids

A

Levonorgestrel intrauterine system (LNG-IUS)-Mirena coil first line
Mefenamic and TXA
COCP and oral/injectable progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does red degeneration of fibroids present?

A

-Severe abdominal pain
-Low grade fever
-Tachycardia
-Vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is red degeneration of fibroids managed?

A

Supportive: rest, fluids and analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the aetiology of ovarian cysts

A

Hormonal imbalances, endometriosis, pregnancy and pelvic infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe some symptoms of an ovarian cyst

A

-Asymptomatic
-Acute unilateral pain
Bloating/fullness in the abdomen
-Intra-peritoneal haemorrhage with haemodynamic compromise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the management of a simpole ovarian cyst in premenopausal women

A

<5cm: often resolve within 3 cycles
5-7cm: gynae referral and yearly US
>7cm: consider MRI or surgical evaluation-difficult to characterise with US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the management of ovarian cysts in postmenopausal women

A

Post-menopausal-concerning for malignancy
Check Ca125 and referall to gynaecology
High Ca125: 2 week cancer list
Normal Ca125: if simple cyst and >5cm: mUS every 4-6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How are persistent or enlarging ovarian cysts treated?

A

Surgical intervention-laparoscopy->ovarian cystectomy, sometimes with affected oophorectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How can benign ovarian cysts becharacterised?

A

Physiological/functional cysts
Benign germ cell tumours
Benign epithelial tumours
Benign sex cord stromal tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the features of follicular cysts

A

Represent the developing follicle
When these fail to rupture and release the egg the cyst can persist.
Typically on US they have thin walls and no internal structures

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

Describe the features of a corpus luteum cyst

A

Occur when the corpus luteum fails to break down and instead fills with fluid
They may cause symptoms such as pelvic discomfort, pain or delayed menstruation.
They are often seen in early pregnancy.

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

What is an endometrioma?

A

Lump of endometrial tissue within the ovary, occurring in patients with endometriosis.
They can cause pain and disrupt ovulation

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

Describe the features of dermoid cysts/germ cell tumours

A

Benign ovarian teratomas-
Come from germ cells
Can contain tissue types like skin, teeth hair and bone.
Torsion is more likely than with other ovarian tumours

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

Describe the pathophysiolgy of an ovarian torsion

A

Twisting of the adnexa and blood supply to the ovary leads to ischaemia. If the torsion persists, necrosis will occur, and the function of that ovary will be lost.

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

Describe the presentation of a patient with ovarian torsion

A

Sudden onset severe unilateral pelvic pain
Pain is constant and gets progressively worse
Associated with nausea and vomiting
Pain can also come and go if ovary twists and untwists intermittently

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

How is ovarian torsion diagnosed?

A

1st line: Pelvic US(transvaginal ideally, transabdominal as backup)->;’whirlpool sign’ free fluid in pelvis and oedema or ovary
Doppler-> reduced blood flow
Definitive->laparoscopic surgery

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

Describe the management of ovarian torsion

A

Urgent admission and gynae involvement
Laparoscopic surgery to:Untwist the ovary and fix it in place(de-torsion)
Remove the affected ovary (oophorectomy)
Laparotomy may be needed if large ovarian mass or malignancy is suspected

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

Describe the aetiology of lichen sclerosus

A

Thought to be autoimmune reaction-associated with T1DM
Also genetics and hormonal factors

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

Describe a typical presentation of a patient with lichen sclerosus

A

45-60yr old woman
Vulval itching
Soreness/pain
Skin tightness
Painful sex (superficial dyspareunia)
Erosions
Fissures
Koebner phenomenon

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

Describe the appearance of lichen sclerosus

A

“Porcelain-white” in colour
Shiny
Tight
Thin
Slightly raised
There may be papules or plaques

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

How is lichen sclerosus diagnosed?

A

Mostly clinical
Skin biopsy can be used to confirm the diagnosis-usually done if atypical features are present(e.g. doesn’t respond to treatment, clinical suspicion of cancer etc)
Blood tests to check for potential autoimmune conditions

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

Describe the management of lichen sclerosus

A

Topical corticosteroids(dermovate) to reduce inflammation and itching
Avoidance of soap in affected areas to prevent further irritation
Emollients to relieve dryness and soothe itching

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

Describe the role of tumour suppressor genes in cervical cancer

A

2 main tumour suppressor genes: P53 and pRb
HPV produces 2 main proteins: E6 and E7
E6 protein inhibits p53
E7 inhibits pRb
Therefore, HPV promotes the development of cancer by inhibiting tumour suppressor genes.

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

At what age are children vaccinated against HPV?

A

age 12-13 yrs

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

Describe the signs and symptoms of cervical cancer

A

Most commonly picked up on screening incidentally
Abnormal vaginal bleeding (intermenstrual, postcoital or post-menopausal bleeding)
Vaginal discharge
Pelvic pain
Dyspareunia (pain or discomfort with sex)
Urinary/bowel habit change
Abnormal white/red patches on cervix
Mass on PR exam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How is cervical cancer investigated and diagnosed?

A

-If symptoms-speculum exam and smear test
If abnormal appearance of cervix-urgent cancer referral for colposcopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is the cervical intraepithelial neoplasia determined?

A

Colposcopy NOT screening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the grades of cervical intraepithelial neoplasia

A

CIN I::mild dysplasia, affecting 1/3 the thickness of the epithelial layer likely to return to normal without treatment
CIN II: moderate dysplasia, affecting 2/3 the thickness of the epithelial layer, likely to progress to cancer if untreated
CIN III: severe dysplasia, very likely to progress to cancer if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What ages and how regularly is cervical cancer screening done in the UK

A

All women between ages 24-64
25-49 yrs: 3 yearly
50-64 yrs: 5 yearly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe the results obtained from cervical cancer screening cytology

A

Inadequate
Normal
Borderline changes
Low-grade dyskaryosis
High-grade dyskaryosis (moderate)
High-grade dyskaryosis (severe)
Possible invasive squamous cell carcinoma
Possible glandular neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is a cone biopsy used for?

A

Treatment for cervical intraepithelial neoplasia(CIN) and very early-stage cervical cancer.
It involves a general anesthetic.
The surgeon removes a cone-shaped piece of the cervix using a scalpel
This sample is sent for histology to assess for& malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How does Bevacizumab work for cancer treatment

A

Targets vascular endothelial growth factor A: which is responsible for the development of new blood vessels.
Reduces the development of new blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Where does endometrial cancer arise from

A

Endometrium of the uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the red flag symptoms for endometrial cancer

A

> 55yrs with post menopausal bleeding-suspected cancer pathway 2ww

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How is endometrial cancer investigated?

A

1)Trans-vaginal ultrasound: endometrial thickness >4mm
2)Hysteroscopy with endometrial biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How is endometrial cancer managed?

A

Surgery: hysterectomy with bilateral salpingo-oophorectomy-can be curative if limited
Radio/chemotherapy
Progesterone therapy sometimes used in frail elderly women not suitable for surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe the outcomes of endometrial hyperplasia

A
  1. Most return to normal
  2. 5% become cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How is endometrial hyperplasia treated?

A

Intrauterine system(mirena coil)
Continuous oral progesterones(levonorgestrel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How does adipose tissue result in increased oestrogen levels?

A

Contains aromatase->converts androgens.
More adipose tissue->more androgens converted to oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How common is ovarian cancer?

A

5th most common malignancy in femals

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

What might epithelial ovarian tumours contain?

A

Partially cystic so can contain fluid

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

How do germ cell ovarian tumours typically spread?

A

Via lymphatics

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

Describe the presentation of ovarian cancer

A

Typically present late-non-specific symptoms
Abdominal pain
Bloating
Early satiety
Urinary frequency or change in bowel habits
Later stages:Ascites(vascular growth factors increasing vessel permeability)
Pelvic, back and abdominal pain
Palpable pelvic or abdominal mass

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

How is CA125 used to guide further investigations when investigting a patient for possible ovarian cancer?

A

Raised CA125(>=35IU/mL)-> urgent US of abdomen and pelvis

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

How is ovarian cancer treated?

A

Surgery:If early disease-remove uterus, fallopian tubes, ovaries and infracolic omentectomy
Advanced-debulking surgery
Adjuvant/intraperitoneal chemotherapy
Biologics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the prognosis of ovarian cancer

A

80% have advanced disease at presentationAll stage 5 year survival is 46%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Why might an ovarian mass result in pain elsewhere?

A

Presses on the obturator nerve-> referred hip or groin pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How common is vulval cancer?

A

Rare-4% of gynae cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

At what age are the majority of vulval cancers diagnosed?

A

>60 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe the clinical features of a patient with vulval cancer

A

Lump on labia majora
Inguinal lymphadenopathy
Itching/discomfort in vulval area
Non healing ulcer
Changes in skin colour/thickening of vulva
Bleeding/discharge not related to the menstrual cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How is vulval cancer managed?

A

Surgery
Radical/wide local excision
Radical vulvectomy for multi-focal disease
Reconstructive surgery
Radiotherapy.chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is a molar pregnancy?

A

AKA hydatidiform mole
Spectrum of disorders known as gestational trophoblastic disease
Imbalance in no of chromosomes originating from the mother and father during conception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How can molar pregnancies be characterised?

A

Complete
Partial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe the presentation of a patient with a hydatidiform mole

A

Vaginal bleeding
Enlargement of uterus beyond the expected size for gestational age
Nausea and hyperemesis gravidarum
Thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How can a molar pregnancy cause enlargement of the uterus?

A

Excessive growth of trophoblasts and retained blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How can a molar pregnancy cause thryotoxicosis?

A

HCG closely related to TSH so able to activate receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How is a molar pregnancy diagnosed?

A

B-HCG-> higher than normal
Trans-vaginal US->‘snowstorm’ appearance, low resistance of blood vessel flow and absence of a foetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How are molar pregnancies managed?

A

Referral to a specialist centre-> reduce the risk of potential choriocarcinoma or invasion.
Suction curettage to remove them from the uterus.
Hysterectomy mif not fertility performed
Surveillance: bimonthly serum and urine hCG testing until levels are normal.

In the case of a partial mole, a repeat hCG test is done 4 weeks later - if normal, the patient is discharged from surveillance.In a complete mole, monthly repeat hCG samples are sent for at least 6 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How common is endometriosis?

A

Common-10% of women in reproductive years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Describe the symptoms of endometriosis

A

Chronic pelvic pain
Dysmenorrhoea
Dyspareunia
Subfertility
Non-gynaecological-> dysuria, urgency, haematuria
Cyclical rectal bleeding, if endometrium-like tissue grows outside the female reproductive system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the medical management of endometriosis

A

Analgesia-paracetemol/NSAIDs
Hormonal therapies-mirena coil, COCP, medroxyprogesterone acetate, Gonadotrophin releasing hormone agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Describe the surgical management of endometriosis

A

Diathermy of lesions
Ovarian cystectomy(for endometriomas)
Adhesiolysis
Bilateral oophorectomy(sometimes hysterectomy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How do patients with adenomyosis typically present?

A

Asymptomatic
Dysmenorrhoea
Menorrhagia
Dyspareunia
Infertility or pregnancy-related complications
(Older then endo, often post-menopausal women-enlarged boggy uterus’)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe the management of adenomyosis

A

Symptomatic: TXA/mefenamic acid
Mirena coil(first line)
COCP
Cyclical oral progesterones
GnRH agonists
Uterine artery embolisation
Hysterecomy-definitive treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

How is andorgen insensitivity syndrome diagnosed?

A

Buccal smear or chromosomal analysis to reveal 46XY genotype
After puberty: hormonal tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe the presentation of a patient with atrophic vaginitis

A

Vaginal dryness and discharge
Dyspareunia
Occasional spotting
Loss of pubic hair
Urinary symptoms like dysuria and recurrent UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Describe the management of atrophic vaginitis

A

Hormonal treatment:
Systemic hormone-replacement therapy (oral or transdermal)
Topical oestrogen preparations
Non-hormonal treatments:Lubricants, which provide short-term improvement to vaginal dryness, alleviating symptoms such as dyspareunia
Moisturisers, which should be used regularly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Describe the management of a miscarriage

A

Conservative: Allow POC to pass naturally-> repeat scan/pregnancy test
Medical: vaginal misoprostol
Surgical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How does vaginal misoprostol work as medical management for a msicarriage?

A

Stimulates cervical ripening and myometrial contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Describe the features of a threatened pregnancy

A

Painless vaignal bleeding <24 weeks(usually 6-9 weeks)
Bleeding but often less than menstruation
Cervical os closed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

How is a threatened pregnancy treated?

A

ReassuranceIf heavy: admit and observe
If >12 weeks, and rhesus negative: Anti D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Describe the features of an inevitable pregnancy

A

Heavy bleeding
Clots
Pain
Cervical os open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How is an inevitable miscarriage treated?

A

Reassurance, if heavy bleeding then admit and observe
If >12 weeks and rhesus negative : Anti D
Likely to proceed to a complete/incomplete miscarriage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Describe the features of a missed/delayed pregnancy

A

Gestational sac containing a dead fetus <2 weeks without symptoms of expulsion
Cervical os closed
Asymptomatic, light bleeding, discharge, pregnancy symptoms which disappear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

How is a missed/delayed miscarriage treated?

A

Reassurance, if heavy bleeding admit for observation
Low success rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Describe the features of an incomplete miscarriage

A

POC partly expelled
Symptom of bleeding/clots
Cervical os open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

How might a patient with a complete miscarriage present?

A

History of bleeding
Clots
POC
Pain
Symptoms settled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How are patients with complete miscarriages managed?

A

Discharged to GP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Describe the symptoms of a septic miscarriage

A

Infected POC
Rigors
Fever
Bleeding
Leukocytosis
Increased CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

How is a septic miscarriage treated?

A

IV antibiotics and fluids
Medical/surgical treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Describe the symptoms of a patient with an ectopic pregnancy

A

Pelvic pain: can be unilateral
Shoulder tip pain-irritation of diaphragm by intra-abdominal bleeding
Vaginal discharge/bleeding-decidua breaking down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Describe the conservative management of an ectopic pregnancy

A

Close follow up and repeat B-HCG’s
Not usually done

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Describe the medical management of an ecoptic pregnancy

A

IM methotrexate
Regular B-HCG checks : >15% decline by day 4/5 or repeat methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

How does methotrexate work as treatment in a patient with an ectopic pregnancy?

A

Disrupts folate dependent cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Describe the surgical management of an ectopic pregnancy

A

Tubal ectopics: laparoscopic salpingectomy (remove ectopic and tube)
If only one tube left: salpingotomy (cut in fallopian tube and remove ectopic)
B-HCG follow up until <5iU(negative)-> check for residual trophoblast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

How does amniotic fluid normally change throughout pregnancy?

A

Volune increases until 33 weeks
Platueaus at 33-38 weeks
Decreases at term to reach 500ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Describe the normal physiological cycle of amniotic fluid

A

Fetus breathes and swallows fluid, processed and voided through the bladder
Predominantly fetal urine output with some fetal secretions and placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

How does placental insufficiency cause oligohydramnios?

A

Blood flows to brain instead of kidneys so there is a lower fetal urine output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

How do patients with oligohydramnios present?

A

Potter’s syndrome:
Fetal compression: clubbed feet, facial deformity, congenital hip dysplasia
Lack of amniotic fluid:
pulmonary hypoplasia in fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Describe the management of oligohydramnios

A

Treat underlying cause and optimise gestation of delivery
Maternal rehydration to increase amniotic fluid volume if mild
Amnioinfusion: saline into amniotic fluid to increase volume
Deliver: may be induced-C-section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Describe the prognosis of patients with oligohydramnios

A

If 2nd trimester: poor prognosis
If premature delivery and pulmonary hypoplasia: respiratory distress at birth
PLacental insufficiency: higher rate of preterm deliveries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Describe the aetiology of polyhdramnios

A

50-60%: Idiopathic
1) Escess production due to increased fetal urination:
-Maternal diabetes
-Fetal anaemia
-Fetal renal disorders
-Twin to twin transfusion syndrome
2)Insufficient removal due to decreased fetal swallowing:
-Oesophageal duodenal atresia
-Diaphragmatic hernia
-Anencephaly
-Chromosomal disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How is polyhdramnios diagnosed?

A

USS: Measure amniotic fluid: AFI/MPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

How fast does cervical dilation typicaly progress?

A

Primiparous: 1cm every 2 hours
Multiparous: 1cm every hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Describe the physiology of the first stage of labour

A

Hormones(mostly prostaglandins and oxytocin) stimulate regular uterine contractions
That and pressure from presenting part of foetus->progressive dilation of the cervix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Describe the signs and symptoms of the first stage of labour

A

Regular, painful contractions
Progressive cervical dilation
Passage of blood stained mucus-‘show’
Rupture of membranes
Descent of foetal head into pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

How is the first stage of labour managed?

A

Pain relief-> epidural analgesia, nitrous oxide, opioids
Encourage mobility and changes in position to facilitate labour progression
Ensure hydration and nutritional support
Regular monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

How is the second stage of labour managed?

A

Instrumental delivery
C-section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

How long does the third stage of labour usually last?

A

Natural: 30-60 minutes
With oxytocin: 5-10 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

How is the 3rd stage of labour managed?

A

Controlled cord traction->gently to avoid uterine inversion/PPH
If retained placenta: manual removal or curettage may be necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

How is labour induction carried out?

A

Membrane sweep: insert finger into extenral os and separate membranes from cervix
Vaginal prostalgandins: Used to ripen cervix and induce contractions
Amniotony: artificial rupture of membranes
Ballon catheter: mechanically dilates cervix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Describe the aetiology of pre-term labour

A

Overstretching of uterus: multiple pregnancy, polyhydramnios
Foetal risk complications: pre-eclampsia, placental abruption
Uterus/cervical problems: fibroids, malformations
Infections: chorioamnionitis, sepsis, group B strep etc
Maternal co-morbidity: htn, diabetes etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

How might patients with pre term labour present?

A

Regular uterine contractsion/changes in cervical effacement or dilation/rupturing of membranes before onset of contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

How is pre term labour managed?

A

Corticosteroids: betamethasone/dex to assist foetal lung maturation
IV abx if increased risk of infection(penicillin)
Tocolytic agents may be used(nifedipine), risk of side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How is menopause diagnosed?

A

Clinically: absence of menarche for 12 months in someone >45
If <40: test FSH etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Describe the management of menopause

A

Conservative:
Lifestyle: regular exercise, weight loss, good sleep
Medical:HRT, SSRI’s
Vaginal lubricants/moisturisers
Clonidine for vasomotor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

In terms of time frames, when can HRT be given?

A

Cyclically: perimenopausal women still having periods
Continuously: Post menopausal not having periods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

How is HRT given cyclically?

A

Monthly: oestrogen every day of months and progesterone for last 14 days
Every 3 months: Oestrogen very day for 3 months and progesterone for the last 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

How can menopause result in dyspareunia?

A

Vaginal dryness from reduced oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

How can menopause result in urinary incontinence?

A

Caused by epithelial thinning as a result of decline in oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Describe the feedback systems that control the menstrual cycle

A

Moderate oestrogen levels-> negative feedback on HPG
High oestrogen with no progesterone-> positive feedback on HPG
Oestrogen +progesterone-negative feedback on HPG
Inhibin selectively inhibits FSH at anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

How much blood is usually lost during menses?

A

10-80ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Describe the epidemiology of PCOS

A

Common
Affects up to 1/4 of women during reproductive years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Describe the aetiology of PCOS

A

Hormonal imblanaces-unknown?HyperandrogenismInsulin resistance
Elevated levels of LH
Raised oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Describe the symptoms of PCOS

A

Oligomenorrhoea
Subfertility
Acne
Hirsutism
Obesity
Mood changes: depression, anxiety
Male pattern baldness
Acanthosis nigracans->secondary to insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Describe the rotterdam diagnositc criteria

A

> =2 of:
Polycystic ovaries(>12 cysts on imaging or ovarian volume >10cubic cm)
Oligo/an ovulation
Clinical or biochemical features of hyperandrogenism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

How is PCOS managed?

A

Conservative:Weight loss, exercise, educate on risks of diabetes.cvr.endometrial cancer
Medical for those not planning pregnancy:COCP
Metformin
Medical for those wanting to conceive:
Clomiphene-induces ovulation
Metformin
Gonadotrophins-induce ovulation
Surgical for those wanting to conceive:
Ovarian drilling: laparoscopic-damages hormone producing cells of ovary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

How can endometrial curettage result in Asherman’s syndrome

A

Damages basal layer of endometrium->heals abnormally creating adhesions connecting areas of the uterus that aren’t normally connected
Adhesions can bind uterine walls together or might seal the endocervix shut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

How do adhesions cause problems in Asherman’s syndrome?

A

Can cause physical obstruction and distort pelvic organs->menstrual abnormalities, infertility and recurrent miscarriages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

How might patient with Asherman’s syndrome present?

A

Secondary amenorrhoea(absent periods)
Significantly lighter periods
Dysmenorrhoea
Infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

How is Asherman’s syndrome diagnosed?

A

Hysteroscopy: GS-can also treat adhesions
Hysterosalpingography
Sonohysterography
MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

How is Asherman’s syndrome treated?

A

Dissect adhesions during hysteroscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

How are congenital uterine abnormalities diagnosed?

A

USS
Hysterosapingography
MRI-considered best

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

How are congenital uterine abnormailites managed?

A

Surgical intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Give some examples of congenital uterine malformations

A

Complete failure of duct fusion:
double vagina, double cervix, double uterus
Septate uterus
arcuate uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Give some examples of congenital vaginal abnormalities

A

Vaginal agenesis
Vaginal atresia
Mullerian aplasia-normal external genitalia but absense of vagina
transverse vaginal septa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

How might abnormalities of the hymen present?

A

Obstruciton of menstrual flow after puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Descriebe the pathogenesis of polyps

A

Involves oestrogen->stimulates endometrial growth
Can arise from hyperplasia of basal layer of endometrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

How are endometrial polyps diagnosed?

A

Speculum exam
USS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

How are endometrial polyps managed?

A

ASX in premenopausal: monitor
Symptomatic/postmenopausal/atypical: removed via hysteroscopic polypectomy
Histology of removed polyp to exclude malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Describe the presentation of a patient with PID

A

Bilateral abdominal pain
Vaginal discharge
Post-coital bleeding
Adnexal tenderness
Cervical motion tenderness
Fever
Dysuria and menstrual irregularities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

How is Fitz Hugh Curtis syndrome diagnosed and treated?

A

Normal LFTs
US rule out stones
Definitive dx: laparoscopy
Tx: abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

How is PID managed?

A

IM ceftriaxone+14 days oral doxycycline+metronidazole
2nd line: oral ofloxacin+oral metronidazole
Consider removal of IUD
Avoid unprotected sexual intercourse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Describe the epidemiology of urinary tract stones

A

CommonM>F
>65 yrs
Can be both renal and ureteric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Describe the aetiology of renal stones

A

Calcium oxalate-mc
Calcium phosphate
Cystine
Uric acid
Struvite
Indinavir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

How might patient with urinary tract calculi present?

A

Severe intermittent loin pain that can radiate ot the groin
Restlessness
Haematuria
N+V
Sedoncary infection of stone->fever/sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

How are renal stones managed?

A

Analgesia
Wait if <5mm
Medical expulsive therapy
Extracorporeal shockwave lithotripsy
Uteroscopy-pregnancy women
Prevention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

How can pituitary adenomas be classified?

A

Size -micro(<1cm) or macro(>1cm)
Hormonal status (secretory vs non secretory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Describe the symptoms of a prolactinoma in men

A

Macroadenomas:
Headache
Visual disturbance-bitemporal hemianopia
Hypopituitarism signs and sx
Excess prolactin:
Impotence
Loss of libido
Galactorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Describe the symptoms of prolacitnomas in women

A

Macroadenomas:
Headache
Visual disturbance-bitemporal hemianopia
Hypopituitarism signs and sx
Excess prolactin:
Amenorrhoea
Infertility
Galactorrhoea
Osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

How is a prolactinoma diagnosed?

A

MRI head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

How are prolactinomas treated?

A

Dopamine agonists: cabergoline, bromocriptine(inhibits release of prolactin)
Trans-sphenoidal surgery: those who can’t tolerate therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Describe the surface anatomy of the breast

A

Lateral border of sternum at mid axillary line
2nd and 6th costal cartilages
Superficial to pectoralis major and serratus anterior muscles
Circular body
Axillary tail

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Describe the mammary glands with regards to breast anatomy

A

Modified sweat glands-> ducts and secretory lobules
Each lobule consists of many alveoli drained by a lactiferous duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Describe the connective tissue stroma with regards to breast anatomy

A

Fibrous and fatty component
Fibrous stroma condenses to form suspensory ligaments
Attach and secure breast to dermis and underlying pectoral fascia
Separate secretory lobules of breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Describe the pectoral fascia with regards to breast anatomy

A

Flat sheet of connective tissue associated with pec major
Retromammaroy space-> layer of loose conective tissue between breast and pectoral fascia(used in reconstruction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Describe the medial vasculature of the breast

A

Internal thoracic(mammary) artery->branch of subclavian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Describe the lateral vasculature of the breast

A

Lateral thoracic and thoracocromial branches-> axillary
Lateral mammary branches->posterior intercostal arteries
Mammary branch-> anterior intercostal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

How does lymphatic drainage link into the presentation of patiens with breast cancer

A

Blockages of lymphatic drainage->lymph builds up in SC tissues->nipple deviation and retraction, peau d’orange
Metastasis can occur through lymph nodes->axillary mx, then can spread to liver, bones and ovary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Describe the nerve supply of the breast

A

Anterior and lateral cutaneous branches of 4th-6th IC nerves(autonomic and sensory nerve fibres)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Describe the epidemiology of fibroadenomas

A

Young women-early 20s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Describe the presentation of a patient with a fibroadenoma

A

Firm, non-tender breast mass
Rounded and smooth edges
Highly mobile on palpation-‘rubbery’ <3cm in diameter(mc 2.5cm)Usually slow growing and solitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Describe the management of fibroadenomas

A

Conservative: Leave, usually regress naturally post menopause
Surgical excision: considered if large, growing, causing significant symptoms or diagnostic uncertainty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Describe the epidemiology of fibrocystic breast disease

A

Most common benign breast condition
20-50 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Describe the aetiology of fibrocystic breast disease

A

Cumulative effect of cyclical hormone
Mostly oestrogen and progesterone-> multiple cysts and proliferative changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Describe the presentation of a patient with fibrocystic breast disease

A

Bilateral ‘lumpy’ breasts, most commonly in upper outer quadrant
Breast pain
Sx worsen with menstrual cycle and peak 1 week before menstruation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Describe the management of fibrocystic breast disease

A

Encourage use of soft, well-fitting bra
Analgesia for pain relief
Most resolve after menopause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Describe the eppidemiology of breast cancer

A

Commonest cancer in UK in women
2nd most common cause of cancer deaths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Describe the pathophysiology of breast cancer

A

Genetic mutations and damaged cellular signalling-> generation of malignant cells-> metastasise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Describe how breast cancer cells metastasize

A

Invasion through basement membrane
Intravasation(entry into circulation)
Circulation
Extravasation
Colonisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Describe the features of ductal carcinoma in situ

A

From epithelial cells
Confined to ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Describe the features of lobular carcinoma in situ

A

Arise from epithelial cells
Neoplastic cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Describe the features of invasive ductal carcinoma

A

Neoplastic proliferation of epithelial cells->ductal basement membrane->fatty tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Describe the features of medullary carcinoma

A

Younger people
Higher grade than invasive ductal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Describe some signs and symptoms of breast cancer

A

Unexplained breast/axillary mass in those >30 years
Nipple discharge
Nipple retraction
Skin changes-p’eau d’orange
Metastatic features: weight loss, bone pain, SOB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

How is breast cancer diagnosed?

A

1st line: imaging:>30yrs and clinical suspicion: mammogram
<30yrs: USS of axilla
2nd line: biopsy
Fine needle aspiration and cytology
Others:
Oestrogen/progesterone receptor testing,
HER2 receptor testing
CT if metastatic disease suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

Describe the stages of breast cancer

A

1A: <2cm, isolated to breast
1B: <2cm, minor axillary LN spread
2A: <2cm, spread to 1-3 ipsilateral lymph nodes
2B: 2-5cm, minor axillary node spread or >5cm with no nodal spread
3A: 4-9 ipsilateral LN spread/>5cm with 1-3 ipsilateral nodes
3B: Spread to skin, chest wall
3C: >10 axillary nodes/supraclavicular/parasternal/axillary spread
4: metastatic spread to other organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

How can bisphosphonates be used in the treatment of breast cancer?

A

Can help reduce recurrence in node-positive cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What are fibroadenomas?

A

Fibroadenomas-overgrowth of glandular and connective tissue resulting in blocked breast ducts and subsequent fluid accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Describe the general management of benign breast disease

A

Reassurance: often only need monitoring
Antibiotics: for infections like mastitis
Analgesics
Surgery: e.g. large fibroadenomas, persistent cysts, symptomatic intraductal papillomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

Describe the epidemiology of Paget’s disease of the nipple

A

Rare: <5% of all breast cancer patients
Most common in postmenopausal women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Describe the aetiology of Paget’s disease of the nipple

A

2 theories:
Epidermotrophic: underlying breasst cancer cells migrate to the nipple
Intraepidermal origin: originates in nipple itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Describe the signs and symptoms of a patient with Paget’s disease of the nipple

A

Eczema like rash on skin of nipple/areola(often crusty, red, inflamed, itchy)
Bloody nipple discharge
Non-healing skin ulcer
Changes to nipple-> retraction/inversion
Pain
Breast lump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

How is Paget’s disease of the nipple diagnosed?

A

Mammography/US
Punch biopsy of affected skin, nipple discharge cytology
MRI for staging in uncertain cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

How is Paget’s disease of the nipple different to eczema of the nipple?

A

Paget’s involves the nipple primarily and only latterly spreads to the areolar(opposite way around in eczema)

193
Q

How is Paget’s disease of the nipple treated?

A

Depends on underlying lesion
Simple mastectomy: remove entire breast and nipple and areeola
Modified radical mastectomy: remove some axillary lymph nodes
Lumpectomy
Chemo, radiation, hormonal

194
Q

Describe the latent phase of labour

A

Contractions(may be irregular)
Mucoid plug
Cervix beginning to efface and dilate(0-4cm)
Can last up to 2-3 days

195
Q

Describe the features of contractions

A

Starts in the fundus(pacemaker)
Retraction/shortenng of muscle fibres
Build in aplitude as labour progresses
Fetus forced down causing pressure on the cervix

196
Q

Describe the features of a gynaecoid pelvis

A

Inlet is slightly transverse oval
Sacrum wide with average concavitiy and inclination
Side walls straight with blunt ischial spines
Wide suprapubic arch

197
Q

How might midwives help with the delivery of the body stage of labour?

A

Gentle downward traction to assist with delivery of shoulder below suprapubic arch
Gentle upwads traction to assist delivery of posterior shoulder

198
Q

Describe the anatomy of the placenta and how it is connected to the fetus

A

Lobes which attach to the uterine wall
Connected to fetus via umbilical cord whcih has 2 arteries and a vein

199
Q

How is a ventouse used?

A

Cup is applied with centre over flexion point on fetal skull
During uterine contractons, traction applied perpendicular to cup

200
Q

At what age gestation is non invasive prenatal testing available?

A

From 10 weeks

201
Q

At what week gestation is CVS offered for?

A

11-14 weeks gestation

202
Q

How many weeks gestatin would amniocentesis be performed?

A

>15 weeks

203
Q

Describe the epidemiology of mastitis

A

Postpartum: 10-20% prevalence
Usually in first 6 weeks post birth
Increased risk in 1st time mothers and previous hx of mastitis

204
Q

Describe the aetiology if mastitis

A

Milk stasis->inflammatory response and potential secondary infection
Cracked/sore nipples-> S.aureus-> infective mastitis

205
Q

Describe the presentation of mastitis

A

Localised: painful, red, tender, hot breast
Systemic: fever, rigors, myalgia, fatigue nausea and headache
Usually unilateral-presents 1st week post partum

206
Q

How is mastitis diagnosed?

A

Mostly clinical
US to ID if suspicion of abscess-> done in secondary care

207
Q

How is mastitis managed?

A

Reassure lactating women they can continue to breastfeed
Advice on methods to faciliate milk expression
Analgesia
Oral/IV abx, surgery if abscess

208
Q

Describe the aetiology of a breast abscess

A

S.aureus mc through crack in nipple/through milk duct
Accumulation of milk, trauma to nipple skin from incorrect latch/pump

209
Q

Describe the presentation of a patient with a breast abscess

A

Fever/rigors
Malaise
Pain and erythema over an area of the breast
Possible presence of a fluctuant mass->might not be palpable
Hisotry of recent/ongoing mastitis

210
Q

How is a breast abscess diagnosed/investigated?

A

Breast USS-> visualise abscess and guide drainage
Diagnostic needle aspiration-> culture organism and evacuation

211
Q

How is a breast abscess managed?

A

Incision and drainage/needle aspiration(with/out US guidance)
Abx therapy targeted towards most likely causative organism

212
Q

Describe the epidemiology of bacterial vaginosis?

A

Mc cause of abnormal dishcarge in women of childbearing age
More common in sexually active women but not an STI

213
Q

Describe the pathophysiology of bacterial vaginosis

A

Disturbance of normal vaginal flora->decrease in number of lactobacilli bacteria

214
Q

How is bacterial vaginosis managed in pregnanct/lactating women?

A

Screening done antenatally and quick treatment if needed
Lower doses of metronidazole in lactating women

215
Q

Describe the epidemiology of vulvovaginal candidiasis

A

Highlyy prevalent: 20% of women/yr
Most women will experience it at some point in their lifetime

216
Q

Describe the aetiology of vulvovaginal candidiasis

A

Candida albicans- replicated by budding
Opportunistic infection vs hypersensitivity reaction

217
Q

Describe the symptoms of vulvovaginal candidiasis

A

Pruritus vulvae
Vaginal discharge-white, curd like
Dysuria

218
Q

How is vulvovaginal candidiasis diagnosed/inveestigated?

A

Usually history/clinical
Vaginal smear and mc+s-> blastospores, pseudohyphae and neutrophils

219
Q

Describe the management of vulvovaginal candidiasis

A

Intravaginal antifungal-> clotrimazole pessary
Oral antifungal->fluconazole
Vulva/topical steroid-> topical imidazole

220
Q

How is vulvovaginal candidiasis treated in pregnancy?

A

DO NOT use oral antifungals
Advise care with intravaginal treatment applicator
Saftynetting if not resolved in 7-14 days

221
Q

Describe the epidemiology of chlamydia

A

Most common STD in UK
Highest prevalence in 15-24 yr olds

222
Q

How is chlamydia transmitted?

A

Via unprotected vaginal, oral, anal sex
Skin to skin contact of genitalsVertical(mother to baby during delivery)

223
Q

Describe the signs and symptoms of chlamydia in men

A

Often asymptomatic: incubation period 7-21 days
Urethritis: dysuria, urethral discharge
Epididymo-orchitis: testicular pain
Epididymal tenderness
Mucopurulent discharge

224
Q

Describe the signs and symptoms of chlamydia in women

A

Asymptomatic often: incubation period 7-21 days
Dysuria
Discharge
Intermenstrual bleeding
Pain/tenderness

225
Q

Describe the signs and symptoms of chlamydia in neonates

A

Pneumonia
Conjunctivitis

226
Q

How is chlamydia diagnosed?

A

Women: vulvovaginal swab
Men: first catch urine sample
Analyze using nucleic acid amplification tests

227
Q

Describe the management of chalmydia in non-pregnant people

A

Doxycycline: 100mg twice daily for 7 days

228
Q

Describe the management of chlamydia in pregnant women

A

Azithromycin/erythromycin

229
Q

Describe the management of neonates with chlamydia

A

Oral erythromycin

230
Q

Describe the epidemiology of gonorrhoea

A

2nd most common STI after chlamydia-increased prevalence in 15-24yrs->Higher prevalence in MSM

231
Q

How is gonorrhoea transmitted?

A

Unprotected vaginal/oral/anal sex
Vertical transmission

232
Q

Describe the aetiology and pathology of gonorrhoea

A

Gram negative diplococcus neisseria gonorrhoea
Causes acute inflammation-> uterus, urethra, cervix, fallopian tube, ovaries, rectum, testicles, eyes, throat

233
Q

How do patients with gonorrhoea present?

A

Males: urethral discharge, dysuria
Women: discharge, dysuria, dyspareunia, pain
Dishcarge tends to be thin, watery green/yellow
Asymptomoatic especially when rectal/pharyngeal infection

234
Q

How is gonorrhoea diagnosed?

A

Females: endocervical/vaginal/urethral swab
Males: first pass urine(NAAT), urethral/meatal swab
Microsopcy, culture and NAAT

235
Q

How is gonorrhoea treated?

A

Singled dose 1g IM ceftriaxone
Screen/treat other infections-test of cure recommended

236
Q

Describe the symptoms of disseminated gonococcall infection

A

Tenosynovitis
Migratory polyarthritis
Dermatitis

237
Q

How is gonorrhoea treated in pregnancy?

A

Prophylactic abx+tx in pregnancy->ceftriaxone

238
Q

How are neonates with gonorrhoea managed?

A

Urgent referral and treatment
Long term damage and blindness

239
Q

Describe the epidemiology of genital herpes

A

Very common
15-24yrs

240
Q

Describe the pathophysiology of genital herpes

A

After infecting surface-> travels up to meet nearest ganglion and stays there until reactivated

241
Q

Describe the presentation of a patient with a primary genital herpes infection

A

Asymptomatic
Small, painful red blisters around genitals, can form open sores
Vaginal/penile discharge, dysuria, urinary retention
Flu like sx-> fever ,muscle aches, malaise, headaches
After 20 days: lesions crust and heal-> end of viral shedding

242
Q

Describe the presentation of a patient with an outbreak of a genital herpes infection

A

Usually shorter and less severe than initial infection
Burning, itching, painful red blisters

243
Q

How is genital herpes diagnosed?

A

Clinical hz and exam
Swab from abuse of ulcer-> NAAT

244
Q

Describe the management of genital herpes

A

Primary infection: aciclovir 400mgTD 5 days
Recurrent outbreaks: OTC analgesia, ice, topical lidocaine
Regular episodes: episodic aciclovir tx when sx begin

245
Q

Describe the management of herpes in pregnancy

A

Low risk of transmission with vaginal birth
Referral to GUM clinic and treat with aiclovir if 1st time HSV infection
If contracted in last trimester: antibodies not developed-> C-section

246
Q

Describe the features/management of neonatal herpes

A

Skin/eyes/mouth herpes(SEM)-antiviral tx
Disseminated herpes(DIS)-internal organs
CNS herpes-> encephalitis
DIS and CNS herpes associated with increased mortality

247
Q

Describe the aetiology of genital warts

A

90% HPV 6/11-low risk, not associated with cancer

248
Q

How do patients with genital warts typically present?

A

Asx
Painless warts of scrotum, penis, vagina, cervix, perianal skin, anus
Warts can be keratinised(hard) or non-keratinised(soft)
Extra-genital lesions: oral cavity, larynx, nasal cavity, conjunctivae

249
Q

How are genital warts diagnosed/

A

Usually from clinical exam/hx
Proctoscopy/vaginal speculum exam to check for internal warts
Biopsy for atypical lesions/suspected intraepithelial neoplastic lesions

250
Q

Describe the management of genital wwarts

A

Tx not always needed, can resolve spontaneously
Topical:Podophyllotoxin: antiviral to destroy clusters(BD 3 days then 4 days rest)
Imiquimod: immune response modifier for larger keratinised warts(3 times/week)
Physical:Cryotherapy
Surgical excisionElecrto/laser-surgery

251
Q

How does pregnancy impact genital warts?

A

No risk to babies but maternal warts can multiply/enlarge during pregnancy

252
Q

Describe the pathophysiology behind the HIV infection

A

Penetrates host CDD4 cell and empties its contents.
Single strands of viral RNA converted to double stranded DNA by reverse transcriptase and combined host DNA using integraseInfected cell divides, viral DNA read->creates viral protein chains and immature virus pushes out of cell, retaining some membranes
Virus matures when protease cuts viral protein chains and assemble to create a working virus, destroying a host cell

253
Q

How do CD4 levels change over the course of the HIV infection?

A

Seroconversion(producing anti-HIV antiibodies during primary infection)->flu-like sx->decrease in CD4 levels due to initial rapid replication-> extremely infectious
Latent phase: months-yrs: initial asx but increased susceptibility to infections

254
Q

How is HIV transmitted?

A

Unprotected sexual intercourse
Sharing needles
Medical procedures
Vertical transmission

255
Q

Describe the symptoms of the seroconversion stage of HIV

A

2-6 weeks post exposure
Fever
Muscle aches
Malaise
Lymphadenopathy
Maculoapular rash
Pharyngitis

256
Q

Describe the symptoms of the symptomatic stage of HIV

A

Weight loss
High temperature
Diarrhoea
Frequent opportunistic infections

257
Q

Describe the symptoms of the AIDS defining illness stage

A

Advanced stage: immune system significantly weakened
Deveopment of AIDS defining illnesses/infections/malignancies

258
Q

How is HIV diagnosed?

A

4th generation tests:ELISA-> test for serum/salivary HIV antibodies and p24 antigen
Reliable results 4-6 weeks post exposure
Contact tracing

259
Q

Describe the management of HIV

A

HAART: highly active antiretroviral therapy >=3 drugs: usually 2 nRTIs and 1 PI/NNRTI
Decreases viral replication and reduces risk of viral resistance emerging

260
Q

Describe the features of NNRTI’s

A

non-nucleoside reverse transcriptase inhibitors
E.g. nevirapineSE: P450 enzyme interaction, rashes

261
Q

Describe the features of protease inhibitors

A

E.g. indinavir, nelfanivir
SE: diabetes, hyperlipidaemia, central obesity, P450 enzyme inhibitirion

262
Q

Describe the features of integrase inhibitors

A

E.g. raltegravir, elvitegravir
Block the action of integrase(viral enzyme that inserts the viral genome into the DNA of the host cell)

263
Q

How is HIV managed in pregnancy and why?

A

Can be transmitted in utero, at delivery and through breast-feeding
Risk reduction strategies
C-section non longer recommended if undetectable viral load

264
Q

How is the risk of HIV transmission in pregnant women minimised?

A

Anttenatal antiretroviral therapy during pregnancy and delivery
Avoidance of breastfeeding
Neonatal post-exposure prophylaxis

265
Q

How do patients with a threatened miscarriage present?

A

Painless vaginal bleeding <24 weeks(usually 6-9 weeks)
Bleeding often less than menstruation

266
Q

How can the aetiology of polyhydramnios be classified?

A

Idiopathic
Excess production due to increased fetal urination
Insufficient removal due to decreased fetal swallowing

267
Q

How might a patient with polyhydramnios present?

A

Uterus feels tense/large for dates
Difficult to feel fetal parts on abdominal palpation

268
Q

How is polyhydramnios managed?

A

Usually no intervention needed
Treat underlying cause
Severe only: amnioreductionIndomethacin

269
Q

How is indomethacin useful for treating polyhydramnios?

A

Enhances water retention and decreases fetal urine output

270
Q

How is prolonged pregnancy managed?

A

Membrane sweeps-40 wks nulliparous, 41 wks in parousInduction of labour-41/42 weeks gestation
If 2 declined: twice weekly CTG monitoring and US with amniotic fluid measurement to predict fetal distress.
Might need C-section

271
Q

How do patients with placenta praevia present?

A

Painless bright red vaginal bleeding after 24 weeks
Sometimes pain if in labour
Can present with signs of shock if severe blood loss
Malpresentation of fetus due to abnormal placental position

272
Q

Describe the management of acute presentation of placenta praevia

A

ABCDE approach
If bleeding not controlled/in labour: C-section
Anti-D within 72 hours of bleeding onset if rhesus D negative

273
Q

How is placenta praevia managed if found in a 20 week scan

A

Placenta praevia minor: rpt scan at 36 weeks-likely to move
Major: rpt at 32 weeks and plan for delivery-> usually elective c-section
Advice about pelvic rest: no penetrative sexual intercourse and go hospital if major bleeding

274
Q

Describe the pathophysiology of placental abruption

A

Rupture of maternal vessels in basal layer of endometrium-> blood gathers and splits placental attachment from basal layer
Detached portion unable to function-> rapid fetal compromise

275
Q

How might patients with placental abruption present?

A

Painful vaginal bleeding
If in labour: may have pain between contractions
Abdominal pain: often sudden and severe
Hypovolaemic shock disproportionate to amount of vaginal bleeding visible

276
Q

How is placental abruption managed?

A

ABCDE resus including anti D if rh D negative
Tx dependent on health of fetus
Emergency delivery: usually C section, even if in-utero death
Induction of labour at term to avoid further bleeding if haemodynamically stable

277
Q

Describe the natural progressin of most breech babies

A

20% breech at 28weeks
Most revert to cephalic presentation spontaneously with only 3% still breech at term

278
Q

How is breeech presentation diagnosed?

A

Clinical:Head felt in upper uteris, buttocks and legs in pelvis
Fetal heart auscultates higher on maternal abdomen on US
20% not diagnosed until labour

279
Q

How might breech presentatin present at labour?

A

Fetal distress->meconium stained liquor
Vaginal exam: sacrum/foot felt through cervical opening

280
Q

Describe the management of breech presentation

A

External cephalic version: offered at 37 weeks to primiparous women
C-section
Vaginal breech birth

281
Q

How is abnormal fetal lie/malpresentation/malrotation diagnosed?

A

Abdominal exam
Confirm with US-> also ID predisposing abnormalities

282
Q

Describe the management of normal fetal lie

A

External cephalic version(ECV)-> 36-38 weeks gestation

283
Q

Describe the management of malpresentation

A

Breech: ECV before labour, vaginal birth, C section
Brow: c-section
Shoulder: c -section
Face: chin posterior: c section,
chin anterior: attempt normal labour

284
Q

Describe the management of malposition

A

90% spontaneously rotate during labour
If not: operative vaginal delivery/C-section

285
Q

Describe the pathophysiology of pre-eclampsia

A

High resistance, low flow uteroplacental circulation develops as constrictive muscular walls of spiral arterioles are maintained
Increase in BP, hypoxia-> systemic inflammatory response

286
Q

Describe the symptoms of pre-eclampsia

A

Headaches
visual changes
Epigastric pain
Sudden onset non-dependent oedema
Hyper-reflexia

287
Q

Describe the management of pre-eclampsia

A

Serial monitoring: BP, urinalysis, fetal growth scans, CTG
VTE-LMWH
Anti-hypertensives-labetalol, nifedipine, methyldopa
Delivery(give IM steroids if <35 weeks)
Post-natal: monitor for 24 hours post partum and BP for 5 days

288
Q

Descrbe the split of eclamptic seizures in the post natal, antepartumand intrapartum periods

A

Post-natal: mc-44%
Antepartum: 38%
Intrapartum: 18%

289
Q

Describe the symptoms of eclampsia

A

New onset tonic clonic seizure in presence of pre-eclampsia
Lasts 60-75 secs then post-ictal phase
May cause fetal distress and bradycardia

290
Q

Describe the management of eclampsia

A

Rescuscitation
ABCDE approach
Pt lie in left lateral position and secure airway and O2 therapy
Seizure control:Magensium sulphate
Monitor for signs of magensium poisoning
BP control:IV labetalol and hydralazine
Delivery of baby and placenta:Usually C-section
Monitoring:Fluid balance: prevent pulmonary oedema and AKI
Monitor platelets, transaminases and creatinine

291
Q

How long should a magnesium suflate drip be continued for after an eclamptic seizure?

A

48 hours after last seizure

292
Q

How is trichomoniasis transmitted?

A

Predominanly sexual

293
Q

Describe the epidemiology of trichomoniasis

A

Mc non-viral STI globally

294
Q

Describe the signs and symptoms of trichomoniasis in women

A

Profuse, frothy, yellow vaginal discharge
Vulvovaginitis
Dyspareunia
Strawberry cervix-may be seen
pH>4.5
Asx

295
Q

Describe the signs and symptoms of trichomoniasis in men

A

Usually asymptomatic
Non-gonococcal urethritis

296
Q

How is trichomoniasis diagnosed?

A

Direct microscopy and culture of the causative organism-> motile trophozoites
pH>4.5
Test for other STIs

297
Q

How is trichomoniasis treated?

A

Oral metronidazole for 5-7 days or single dose of 2g orally
Abstain from sex for a week
Screen for others
Contact tracing

298
Q

Describe the epidemiology of chancroid

A

Global incidence decreasing
Mc in tropical areas and greenland

299
Q

Describe the symptoms of chancroid

A

Painful genital ulcers which may bleed on contact-ulcers are sharply defined, ragged, undermined border
Painful inguinal lymphadenopathy
Sx 4-10 days after bacterium exposure

300
Q

How is chancroid diagnosed?

A

Usually clinical
Can culture and use PCR

301
Q

How is chancroid treated?

A

Antibiotics: ceftriaxone/azithromycin/ciprfloxacin
Analgesics
Incision/drainage of buboes

302
Q

Describe the presentatin of a patient with lymphogranuloma venereum

A

Stage 1: small painless pustule which later forms an ulcer
Stage 2: painful ingional lymohadenopathy-may from fistulaitng buboes
Stage 3: proctocolitis(can include rectal pain and discharge)

303
Q

How is lymphogranuloma venereum diagnosed?

A

PCR from swab of genital ulcer

304
Q

How is lymphogranuloma venereum managed?

A

oral doxycuclin 100mg twice daily for 21 days
Can also use: tetracycline, erythromycin

305
Q

How is lymphogranuloma venereum different to ‘normal’ chalmydia?

A

Normal chalmydia: urethritis and PID: Chlamydia trachomatis serovars D-> Klymphogranuloma venereum: serovards L1, L2, L3

306
Q

Describe the aetiology of balanitis

A

Mc: infective: bacterial and candidal
Autoimmune causes

307
Q

How is balanitis investigated/diagnosed?

A

Usually clinical-hx and exam
Swab for mc+s/PCR->bacteria or candida albicans
If doubt/extensive skin changes: biopsy

308
Q

Describe the general treatment of balanitis

A

Gentle saline washes
Wash properly under foreskin
1%hydrocortisone for a short period
Treat underlying cause

309
Q

How is balanitis due to dermatitis treated?

A

Mild potency steroid- hydocortisone

310
Q

How is balanitis due to lichen sclerosus treated?

A

High potency topical steroids
Clobetasol
Circumcision can help

311
Q

How is balanitis due to candidiasis treated?

A

Topical clotrimazole for 2 weeks

312
Q

How is syphilis transmitted?

A

Direct contact with syphilis sores or rash during vaginal, anal or oral sex
Vertical: mother to child

313
Q

Describe the features of primary syphilis?

A

Chancre-painless ulcer at the site of sexual contact
Local non-tender lymphadenopathy
Often not seen in women(lesion can be on the cervix)

314
Q

Describe the lesion associated with the primary syphilis infection

A

Painless
Round, indurated base
Heals spontaneously within 3-8 eeks

315
Q

Describe the features of secondary syphilis

A

Systemic: fevers, malaise etc
Rash on trunks, palms and sores buccal ‘snail track’ ulcers
Condylomata lata (painless warty lesions on genitalia)

316
Q

Describe the features of tertiary syphilis

A

Gummas(granulomatous lesions of skin and bones)
Ascending aortic aneurysms
neurological: demenita, paresis, tabes dorsalis, argyll-robertson pupil)

317
Q

Describe the features of congenital syphilis

A

Presents shortly after birth or later in infancy
Rash: palms/soles, mucous patches/leisons in motuh/nose/genitals
Feever
Blunted upper incisor teeth(Hutchinson’s teeth), ‘mulberry’ molars
Rhagaades( linear scars at angle of mouth)
Keratitis
Saber shins
Saddle nose
Neruological; seizures, developmental delay

318
Q

How can serological tests for syphilis be divided?

A

Non-treponemal tests
Treponemal specific tests

319
Q

Describe the features of non-treponemal tests for syphilis

A

Not-specific for syphilis: false positives
Based on reactivity of serum from infected patients to a cardiolipin cholesterol-lecithin antigen
Negative after treatment

320
Q

Describe the features of treponemal specific tests?

A

More complex and expensive but sspecific for syphilis
Qualitative

321
Q

Describe the treatment pf syphilis

A

IM benzathine penzylpenicillin
Tertiary/late latent: longer course of IM penicillin
Neurosyphilis: IV penicillin G for 10-14 days

Backup for penicillin allergy: doxycycline

322
Q

How might patients with intraductal papilloma present?

A

Bloody discharge from the nipple
With/without a palpable mass
May have breast tenderness

323
Q

How are intraductal papillomas treated?

A

Severe cases might need surgery

324
Q

How can breast cysts be classified?

A

Microcysts: seen on imaging but too small to be felt
Macrocysts: 1-2cm: large enough to be felt

325
Q

How might patients with mammary duct ectasia present?

A

Tender lump arounf areola +/- thick green nipple discharge
If ruptures: local inflammation-> ‘plasma cell mastitis’

326
Q

Describe the treatment for mammary duct ectasia

A

Surgical intervention may be needed if symptomatic

327
Q

Describe the epidemiology of HELLP syndrome

A

Rare
Significant cause of maternal and perinatal morbidity/mortality

328
Q

Describe the aetiology of HELLP syndrome

A

Unknown
Related to abnormal placentation, endothelial cell injury and generalized inflammatory response

329
Q

Describe the presentation of patients with HELLP syndrome

A

N+V
RUQ pain-> liver distention
Lethargy
Headaches
Blurred vision
Peripheral oedema

330
Q

Describe the maangement of HELLP syndrome

A

Definitive: deliver baby
Steroids: accelerate fetal lung maturation
Blood transfusions to manage anaemia and thrombocytopenia

331
Q

Describe the epidemiology of cord prolapse

A

Relatively rare
Higher risk in breech presentations and multiple pregnancies

332
Q

Describe the pathology of cord prolapse

A

Usually membrane rupture-> amniotic fluid egress-> descent of umbilical cord
Cord compression-> against maternal soft tissues or bony pelvis->fetal hypooxia

333
Q

How might patients with cord prolapse present?

A

Abnormal fetal heart rate: mc varibable/prolonged decelerations
Palpable umbilical cord
Sudden onset of sympotms post rupture of membranes
Patient reported sensation

334
Q

How is a cord prolapse investigates/diagnosed?

A

Clinical
USS
Cardiotocoography(CTG)
Speculum exam

335
Q

How is cord prolapse managed?

A

Immediate delivery of fetus-> instrumental or C section
‘knees chest’ position to reduce pressure on cord
Avoid exposure and handling of cord, reducing into vagina
Use of tocolytics like terbutaline to stop uterine contractions

336
Q

Describe the pathophysiology of vasa praevia

A

Abnormal placental development
Fetal membrane development: persistence of membranous vessels
Fetal vessel vulnerability: prone to rupture

337
Q

How can vasa praevia be classified?

A

Type 1 and Type 2
Ramified or funic

338
Q

Describe the signs and symptoms of vasa praevia

A

Painless vaginal bleeding
Rupture of membranes
Fetal bradycardia/resulting fetal death
Also:Foetal anaemia

339
Q

How is vasa praevia diagnosed?

A

Transabdominal/TV USS-most cases now diagnosed antenatally
Can use MRI and prenatal testing

340
Q

How is vasa praevia managed?

A

Elective C-section prior to rupture of membranes: 35-36 weeks gestation
Emergency C-section if premature labour or membranes rupture
Prompt neonatal resus

341
Q

Describe the epidemiology of peruperal psychosis

A

Rare: 1-2/1000 childbirths

342
Q

Describe the aetiology of peurperal psychosis

A

Unknown
Hormonal changes post childbirth
Genetics
Psychosocial stressors
Sleep deprivation

343
Q

Describe the signs and symptoms of peurperal psychosis

A

Paranoia
Delusions: Capgras
Hallucinations-command
Manic episodes
Depressive episodes
Confusion

344
Q

How is peurperal psychosis diagnosed?

A

Clinical
Thorough psych evaluation
Rule out: thyroid disorders, sepsis etc

345
Q

Describe the management of peurperal psychosis

A

Admit to mother/baby mental health unit: especially if Capgras/command hallucinations
Antipsychotics: olanzapine and quetiapine
Mood stabilisers in some cases
CBT

346
Q

Describe the epidemiology of postpartum depression

A

Prevalent: 10-20% of mothers

347
Q

Describe the aetiology of postpartum depression

A

Multifactorial
Biological: hormones, melatonin, cortisol, inflammatory processes, genetics
Psychological
Social

348
Q

Describe the signs and symptoms of postpartum depression

A

Persistents low mood and anhedonia
Low energy
Sleep issues-important to distinguish between baby’s fault and depression
Poor appetite
Concerns relating to bonding with baby, caring for baby etc

349
Q

How is baby blues different to postpartum depression?

A

MIlder: mood swings, irritability, anxiety and tearfullness
Sx present within first 2 weeks after birth and resolve spontaneously

350
Q

How is postpartum depression diagnosed?

A

Clinical
Edinburgh postnatal depression scale >13
ule out risk of psychosis-risk assessment really important
Physical exam: anaemia, hypothyroidism to rule out organic causes

351
Q

Describe the management of postpartum depression

A

Self-help, CBT, ITP(interpersonal therapy)
Antidepressants(SSRIs)
Severe: admission to mother baby mental health unit

352
Q

How is baby blues managed?

A

Reassurance and support
Regular health visitor checks to check in with mother

353
Q

Define pre-term labour

A

Onset of regular uterine contractions accompanied by cervical changes occuring before 37 weeks gestation

354
Q

Define pre-term birth

A

Delivery of a baby 20-37 weeks gestation

355
Q

Define premature rupture of membranes

A

Rupture of membranes at least one hour before onset of contracitons

356
Q

Define prolonged premature rupture of membranes

A

Rupture of membranes over 24 hours before onset of labour

357
Q

Define pre-term premature rupture of membranes

A

Early rupture of the membranes before 37 weeks gestation

358
Q

Describe the epidemiology of preterm prelabour rupture of the membranees

A

Occurs in around 2% of all pregnancies
Associated with 40% of preterm delvieries

359
Q

How is PPROM diagnosed?

A

Sterile speculum exam: look for pooling of amniotic fluid in posterior vaginal vault
Avoid digital exam: risk of infection
If no pooling: test fluid for placental alpha microglobulin protein(PAMG-1) or insulin like growth factor binding protein 1
USS-oligohydramnios

360
Q

How is PPROM managed?

A

Admission
Regular observations to check for chorioamnionitis
Oral erythromycin for 10 days
Antenatal corticosteroids: reduce risk of respiratory distress syndrome
Delivery should be considered at 34 weeks gestation

361
Q

Describe the aetiology of postpartum haemorrhage

A

4T’s:Tone: mc: uterine atony(failure of uterus to contract after delivery)
Trauma(tears)
Tissue(retained placenta etc)
Thrombin(clotting/bleeding disorder)

362
Q

Describe the initial management of PPH

A

Life threatening emergency: ABCDE approach
2 14 gauge large bore peripheral cannulas
Lie flat
Bloods including group and save
Commence warm crystalloid infusion

363
Q

Describe the mechancial strategies that can be used to manage postpartum haemorrhage

A

Palpate uterine fundus and rub it to stimulate contractions
Catheterisation to prevent bladder distention and monitor urine output

364
Q

Describe the medical management of postpartum haemorrhage

A

IV oxytocin: slow IV injection then infusion; ergometrine slow IV(unless hx of htn)
carboprost IM(unless hx of asthma)
sublingual misprostol

365
Q

Describe the surgical management of postpartum haemorrhage

A

If medical options fail to control bleeding:
Intrauterine balloon tamponde-if uterine atony as cause
B-lynch suture,
ligation of uterine/internal iliac arteries
If severe: hysterectomy as life-saving procedure

366
Q

How is secondary postpartum haemorrhage managed?

A

Depends on underlying cause
Abx for infection
Surgical evacuation for retained products of conception

367
Q

Describe the pathophysiology of rhesus negative pregnancy

A

15% of mothers rhesus negative
If rh negative mother delivers a rh positive child, a leak of fetal red blood cells can occur
Causes anti D-IgG antibodies to form in mother
Maternal anti-D antibodies can cross placenta in subsequent pregnancies and cause rhesus haemolytic disease if baby is rhesus positive
Can also occur in first pregnancy due to leaks

368
Q

Give some examples of sensitisation events in rhesus negative pregnancies

A

Antepartum haemorrhage
Placental abruption
Abdo trauma
ECV
Miscarriage if gestation >12 weeks
Termination of pregnancy
Delivery of rh positive infant
Ectopic pregnancy
Amniocentesis, CVS, fetal blood sampling

369
Q

How is rhesus heamolytic disease prevented and screened for?

A

Test for D antibodies in all rhesus negative mothers at booking
Anti-D given to non-sensitised rh negative mothers at 28 and 34 weeks-prophylaxis(once sensitisation occurs can’t be undone)

370
Q

How is rhesus negative pregnancy managed?

A

Screening/prevention strategies
Give Anti-D immunoglobulin as soon as possible but always within 72 hours when a sensitisation even occurs

371
Q

Describe the medical management of termination of pregnancy

A

Mifepristone(first orally) then misoprostol 24-48 hours after
Misoprostol can be repeated 3 hourly(max 5) until expulsion
Takes time: hours to days
Pregnancy test required in 2 weeks: multi-level pregnancy test-measures level of HCG not just positive or negative

372
Q

How is trichomoniasis vaginalis managed in pregnancy?

A

Same: oral metronidazole 400-500mg twicce a day for 5-7 days
High dose not recommended in pregnancy/breastfeeding(no 2g single dose)

373
Q

Describe the symptoms of uterine rupture

A

Sudden severe abdominal pain which persists between contractions
Shoulder tip pain-diaphragmatic irritation)
Vaginal bleeding

374
Q

Describe the signs of a uterine rupture

A

O/E: regression of presenting part
Abdominal palpation: scar tenderness and palpable fetal parts
Fetal monitoring: fetal distress/absent heart sounds
Significant haemorrhage: signs of shock: tachycardia, hypotension

375
Q

Describe the management of a uterine rupture

A

ABCDE appproach
C-section
Uterus either repaired or removed
Decision-incision interval should be under 30 minutes

376
Q

Define gestational diabetes

A

Glucose intolerance on OGTT with:
Fasting blood glucose >=5.6mmol/L
2 hour plasma glucose levels >=7.8mmol/L

377
Q

Describe the epidemiology of gestational diabetes

A

5% of pregnancies
2nd most common medical disorder complicating pregnancies

378
Q

How might patients with gestational diabetes present?

A

Often asx
Polyuria
Thirst
Fatigue

379
Q

How is gestational diabetes diagnosed?

A

OGTT: fasting >=5.6, 2 hour: >=7.8-REMEMBER 5,6,7,8
HbA1c: distinguish between gestational and pre-existing diabetes early on
Urinalysis: check for glycosuria

380
Q

Describe the management of gestational diabetes

A

Fasting glucose <7mmol/L: lifestyle : diet and exercise. Give it 1-2 weeks then metformin if targets not met, then insulin added
>=7mmol/L: start insulin (short acting not long acting)
6-6.9mmmol/L + complications like macrosomia or hydramnios: offer insulin
Glibenclamide only for women who can’t use metormin/doesn’t work and decline insulin

381
Q

Describe the management of pre-existing diabetes in pregnancy

A

Weight loss if BMI >27
Stop oral hypoglycaemimcs except metformin and start insulin
Folic acid 5mg/day until 12 weeks
Detailed anomaly scan at 20 weeks including 4 chamber view of heart and outflow tracts
Tight glycaemic control reduces complication rates
Treat retinopathy: can worsen in pegnancy

382
Q

Describe the normal changes in blood pressure in pregnancy

A

Usually falls in the 1st trimester and continues to fall until 20-24 weeks
After this: BP usually increases to pre-pregnancy levels by term

383
Q

How should pregnant patients with hypertension be classified?

A

Pre-existing hypertension
Pregnancy induced hypertension/gestational hypertension
Pre-eclampsia

384
Q

Describe the management of pre-existing hypertension in pregnancy

A

STOP ACE inhibitor or angiotensin 2 receptor
SWAP for alternative: labetalol whilst waiting specialist review
Nifedipine if asthmatic

385
Q

Describe the features of pregnancy induced hypertension

A

Hypertension occuring in the 2nd half of pregnancy(after 20 weeks)
No proteinuria, no oedema5-7% of pregnancies

386
Q

Describe the management of pregnancy induced hypertension

A

Oral labetalol/nifedipine/hydralazine
Typically resolves within 1 month after birth

387
Q

Describe the features of pre-eclampsia

A

Pregnancy induced hypertension associated with proteinuria(>0.3g/24hrs)
Oedema may occur but less commonly used now as a criteria
5% of pregnancies

388
Q

Describe the epidemiology of Group B strep infection

A

Mc asx commensal bacterium in GI and GU tracts
25% of pregnant women estimated to be carriers
Can cause severe illness to mother and infant during transmission during delivery

389
Q

How might Group B strep infection be investigated?

A

No current routine screening test for pregnant women as colonisation status can change through pregnancy
GBS culture may be done in certain cirumstances

390
Q

How is Group B strep infection managed?

A

Intrapartum antibiotic prophylaxis-benzylpenicillin
Abx IV during labour and delivery

391
Q

Describe the management of obesity in pregnancy

A

5mg folic acid not 400mcg
Screening for gestational diabetes with OGTT at 24-28 weeks
BMI >35: Birth in consultant led obstetric clinicBMI>=40: Antenatal coonsultation with ostetric anaesthetist and plan made in advance

392
Q

How is cephalopelvic disproportion managed?

A

Trial of labour
Instrumental vaginal delivery-may need episiotomy
C-section

393
Q

How is prolonged labour managed?

A

ID causes and evaluate progress of labour
Medical:Artificial rupture of membranes
IV oxytpcin to augemnt contractions
Pian management: epidural, nitrous oxide etc
Surgical:Operative delivery
C-section
Postpartum:Monitor closely for infection
Active management of 3rd stage of labour: uterotonic agents
Ensure adequate analgesia

394
Q

Describe the clinical features of obstetric cholestasis

A

Pruritus: intense-typically worst in palms, soles, abdomen
Jaundice: dark urine and pale stools in about 20% of patients
General fatigue and malaise
GI sx: nausea and appetite lossRUQ abdominal pain
Raised bilirubin in >90% of cases

395
Q

How is obstetric cholestasis managed?

A

Chlorphenamine and emollients to reduce itching
Induction of labour at 37-38 weeks
Ursodeoxycholic acid
Vitamin K supplementation->minimise risk of bleeding

396
Q

Describe the prognosis of obstetric cholestasis

A

High recurrence: 45-90% in subsequent pregnancies

397
Q

Describe the aetiology of chorioamnionitis

A

Bacteria ascending from vagina into uterus
Mc: Group B strep, E.coli and anaerobic bacteria

398
Q

How is chorioamnionitis diagnosed?

A

Usually clinical
Blood tests and cultures to confirm and ID causative organism

399
Q

How is chorioamnionitis managed?

A

IV broad sectrum abx: sepsis 6 protocol
Monitoring of fetus and mother for complications
Early delivery might be needed-C section

400
Q

Describe the management of FGM in the UK

A

Illegal in UK-immediate child protection referrral if child at risk
Anterior episiotomy during second stage of labour under local anaesthetic or regional block
Deinfibulation surgery: important to protect urethra

401
Q

Describe the clinical features of shoulder dystocia

A

Difficult delivery of fetal face/chin
Retraction of fetal head-turtle neck sign
Failure of restitution
Failure of descent of fetal shoulders following delivery of head

402
Q

Describe the management of shoulder dystocia

A

Immediately call for senior help
Do not apply fundal pressure-can lead to uterne rupture
McRoberts maneouevre
All fours position
Internal rotational manoeuvers
Episiotomy-won’t remove bony obstruction but will allow space for internal manoeuvers
Cleidotomy/symphysiotomy: not 1st line-associated with significant maternal morbidity]
Zavanelli manoeuvre-also dangerous

403
Q

Define anaemia in pregnancy

A

Hb:1st trimester: <110g/L
2/3 triester: <105g/L
Postpartum: <100g/L

404
Q

lDescribe some clinical features of anaemia

A

Asx
Dizziness, fatigue, dyspnoea: normal pregnancy
Pallor
Koilonychia
Angular cheilitis

405
Q

How is anaemia diagnosed/investigated in pregnancy?

A

FBC
Folate to check for folate deficiency
Check for beta thalassaemia and sickle cell

406
Q

Describe the risk of congenital rubella syndrome?

A

Risk high as 90% in first 8-10 weeks
Damage rare after 16 weeks

407
Q

Describe the epidemiology of congenital rubella syndrome

A

Rare now due to MMR vaccine

408
Q

How is rubella transmitted ot the fetus in congenital rubella syndrome?

A

Virus can cross the placenta and affect the developing fetus

409
Q

How is congenital rubella syndrome diagnosed?

A

Serology to confirm rubella infection-IgM raised in women recently exposed to virus
Audiology tests for hearing impairment
Opthalmology for eye abnormalities
Echos for congenital heart defects

410
Q

How is congenital rubella syndrome managed?

A

During pregnancy: discuss with local health protection unit
Advised to keep away from people who might have rubella
Offer MMR vaccine in post natal period
Neonates: primarily supprotive and symptomatic-monitor progress and manage long-term complications

411
Q

How can perineal tears be classified?

A

1st, 2nd, 3rd, 4th degree

412
Q

Describe the features of a first degree perineal tear

A

Superficial damage with no muscle involvement
Do not require any repair

413
Q

Describe the features of a second degree perineal tear

A

Injury to perineal muscle but not involving the anal sphincter
Require suturing on ward by suitably experienced midwife or clinician

414
Q

Describe the features of a third degree perineal tear

A

Injury to perineum involving the anal sphincter complex(external anal sphincter(EAS) and internal anal sphincter(IAS)
3a: <50% EAS thickness torn
3b: >50% EAS thickness torn
3c: IAS torn
Require repair in theatre by suitably trained clinician

415
Q

Describe the features of a fourth degree perineal tear

A

INjury to perineum involving the anal sphincter complex(EAS and IAS) and rectal mucosa
Require repair in theatre by suitably trained clinician

416
Q

Describe the management of perineal tearss

A

1st degree: no repair
2nd: suturing
3rd/4th: surgical repair under regional or general anaesthetic
Broad spectrum abx and laxatives given post surgery

417
Q

Describe the epidemiology of amniotic fluid embolism

A

Rare but significant cause of maternal morbidity and mortality

418
Q

Describe the aetiology of an amniotic fluid embolism

A

Not known fully
Amniotic fluid can enter maternal circulation and form embolism-> block circulation like a blood clot especially in lung
Fluid also triggers inflammatory response within mother’s immune system-> DIC

419
Q

Describe the signs and symptoms of an amniotic fluid embolism

A

Tachypnoea
Tachycardia
Hypotension
Hypoxia
DIC
Cyanosis and MI
Chills, shivering, sweating, anxiety and coughing

420
Q

How is an amniotic fluid embolism diagnosed?

A

Clinical
Exclude other causes-no definitive diagnostic test

421
Q

Describe the management of an amniotic fluid embolism

A

Immediate transfer to ICU, MDT care
Oxygen, fluid resus
Correction of any coagulopathy
FFP if prolonged PT
Cryoprecipitate for low fibrinogen
Platelet transfusion for low platelets

422
Q

Describe the management of hyperemesis gravidarum

A

Simple:Rest and avoid trigggers
Bland, plain food, ginger
P6(wrist) acupressure1st line meds:antihistamines: oral cyclyzine/promethazinephenothiazines: oral prochlorperazine or chlorppromazine
2nd line:Oral odansetron
Oral metoclopramide/domperidone-5 DAYS MAX
Thiamine and folic acid supplementation
Atacids
Thromboembolic stockings and LMWH -dehydration

423
Q

How is hyperemesis gravidarum managed in hospital?

A

Normal saline with added potassium for rehydation
Antiemetics

424
Q

Describe the management of hypothyroidism in pregnancy

A

Levothyroxine: usual dose increased by 25-50mcg due to increased metabolic demand

425
Q

Describe the aetiology of acute fatty liver of pregnancy

A

LCHAS mutation->accumulation of fatty acid metabolites in placenta->shunted into maternal circulation and accumulate in maternal liver

426
Q

How is acute fatty liver of pregnancy investigated/diagnosed?

A

Raised:AST/ALT
Bilirubin
Creatinine
Ammonia
Lactate
Serum uric acid
Leukocytosis,
low-normal platelets,
normocytic normochromic anaemia
Coagulopathy: prolonged PT, hypofibrinogenaemia and elevated D dimer

427
Q

Describe the management of acute fatty liver of pregnancy

A

Curative: delivery of the fetus
Maternal stabilisation: correct hypoglycaemia, coagulopathy and hypertension
After delivery: close monitoring-if ongoing deteriorattion in liver function post birth-transfer to liver transplant facility

428
Q

Describe the management of the thyrotoxic phase of postpartum thyroidits

A

Propanolol for sx control
Not usually treated with anti-thyroid drugs as thyroid not overactive

429
Q

Describe the treatment of the hypothyroid phase of postpartum thyroidits

A

Usually treated with thyroxine

430
Q

Describe the presentation of a patient with obstructed labour

A

Widest diameter of fetal sckull remains stationary above the pelvic brim
Prolonged labour: >12 hours
Premature rupture of membranes
Mother has abnormal vital signs
Bandls’ ring
Foul smelling meconium from mother’s vagina
Oedema of vulva/cervix
Caput
Malpresentation/malposition of fetus
Poor cervical effacement
Assess using vaginal exam

431
Q

Describe the management of obstructed labour

A

Saline for dehydration
catheter to drain bladder
May need C section or instrumental delivery

432
Q

Describe the epidemiology of intrauterine growth restriction

A

3-7% of newborns
Increased prevalence in low/middle income countries->maternal malnutrition and infection

433
Q

Describe the signs and symptoms of intrauterine growth restriction

A

Decreased fetal movement
Abnormal fundal height for gestational age
Complications like pre-eclampsia and stillbirh

434
Q

How is intrauterine growth restriction managed?

A

Close monitoring of fetal growth and wellbeing
Management of maternal conditions contributing
Consideration for early delivery if fetus is in distress/conditions worsens

435
Q

Describe the aetiology of ovarian hyperstimulation syndrome

A

Excessive response to hormones->multiple follicles mature and enlarge->all transform into corpus luteum->overproduction of oestrogen, progesterone and local cytokines, especially vascular endothelial growth factor->increased membrane permeability and loss of fluid from intravascular compartment

436
Q

Describe the signs and symptoms of ovarian hyperstimulation syndrome

A

Bloating
Abdo pain
Oedema
Pleural effusions
Ascites
Weight gain

437
Q

How is ovarian hyperstimulation syndrome diagnosed?

A

Routine bloods: evaluate haemoconcentration and detect potential organ dysfunction
CXR: ID pleural effusion

438
Q

Describe the management of ovarian hyperstimulation syndrome

A

Supportive-tailored to severity of condition
Simple analgesia for discomfort
Might need ICU and close monitoring if severe

439
Q

Describe the features of fetal varicella syndrome

A

Skin scarring
Eye defects: microphthalmia
Limb hypoplasia
Microcephaly
Learning difficulties

440
Q

Describe the management of chickenpox exposure in pregnancy

A

If doubt about previous infection: check blood urgently for varicella antibodies
Oral aciclovir now first choice for post exposure prophylaxis(used to be VZIG)-should be given day 7-14 after exposure not immediately

441
Q

Describe the management of chickenpox in pregnancy

A

Seek specialist advice
Oral aciclovir >=20 weeks and presents within 24hrs of rash onset <20 weeks: aciclovir ‘considered with caution

442
Q

Describe the pathophysiology of placental insufficiency?

A

Placental vascular remodeling is affected-> placental functioning progressively deteriorates.
This process affects the placental blood flow, leading to fetal hypoxemia, or low levels of oxygen in the blood, and restriction of fetal growth.

443
Q

How might placental insufficiency present?

A

Usually no observable sx
Decreased fetal movement
Intrauterine growth restriction
Prematurity
Stillbirth

444
Q

How is placental insufficiency diagnosed/investigated?

A

Doppler USS: evaluate fetal and placental circulations-> regular screening
MRI if inconclusive

445
Q

Describe the management of placental insufficiency

A

<34 weeks: delay delivery: low dose aspirin, vitamin C and E, heparin
>34 weeks: prompt delivery

446
Q

How is a pregnant women at high risk of VTE treated?

A

LMWH throughout antenatal period and input from experts

447
Q

If a pregnant woman has 3 risk factors for VTE how should this be managed?

A

LMWH from 28 weeks and continued nutil 6 weeks postnatal

448
Q

If a diagnosis of DVT is made shortly beefore delivery in a pregnant woman, how long should treatment be continued for?

A

At least 3 months

449
Q

How can twin pregnancies be classified?

A

Zygosity
Chorionicity
Amnionicity

450
Q

How can monozygotic twwins be further classified?

A

Dichorionic + daimniotic: 2 different sacs
Monochorionic + diamniotic: same outer sac, two inner sacs
Monochorionic + monoamniotic: same sacs

451
Q

Describe the epidemiology of twins

A

2/3: dizygotic
1/3: monozygotic
^When conceived naturally

452
Q

Describe the management of twins

A

Rest
USS for diagnosis and monthly checks
Additional iron and folate
More antenatal care(weekly when >30 weeks)
Precautions at labour(2 obstetricians present)
75% of twins deliver by 38 twins, if longer, most twins are induced at 38-40 weeks

453
Q

Describe the aetiology of twin-to-twin transfusion syndrome

A

Precipitated by anastamoses of umbilical vessels betwween 2 fetuses in the placenta of monochorionic twins

454
Q

How is twin-to-twin transfusion syndrome diagnosed?

A

Monochorionic twins: regular USS to monitor
Observe fluid levels in each amniotic sac, measure size of twins and assess blood flow in umbilical cord and placenta

455
Q

Describe the management of twin-to-twin transfusion syndrome

A

Laser transection of problematic vessels in utero-can increase survival rate, high mortlaity for both twins without tx

456
Q

Describe the symptoms of UTI in pregnancy

A

Frequent urination
Dysuria
Lower abdo pain
Fever
Haematuria

457
Q

Describe the management of asymptomatic bacteriuria in pregnancy

A

Nitrofurantoin and cefalexin mc used
If Group B strep ID d: intrapartum prophylactic abx to reduce risk of transmission

458
Q

Describe the treatment for a UTI in pregnant women

A

nitrofurantoin for 7 days(avoid at term)
Amoxicillin/cefalexin

459
Q

Describe the symptoms of puerperal infection

A

Fever
Abdo pain
Tachycardia
Abnormal discharge
Foul smelling lochia(postpartum bleeding)
Tenderness/pain in pelvic area
Sepsis signs: hypotension, tachypnoea etc

460
Q

Describe the maangement of puerperal infection

A

Abx-broad spectrum initially: ceftriaxone and metronidazole
Fluids
Analgesia
Prevention: good hygiene practices during childbirth and postpartum care
Close monitoring
Drainage of abscesses if needed

461
Q

Describe LH and FSH in Turners

A

Raised LH
Raised FSH

462
Q

Describe LH and FSH in Kallman’s

A

Low LH
Low FSH

463
Q

Describe the general function of blood hormones

A

Oestrogen: sex development-females
Progesterone: uterine development
Testosterone: sex development males
FSH and LH: ovarian functionality

464
Q

Describe the management of primary amenorrhoea

A

Primary hypo: COCP
Primary hyper: GnRH analogue

465
Q

Descrieb the management of secondnary amenorrhoea

A

Lifestyle: stress/weight management
Treat underlying cause
Surgical: tumour/cyst removal

466
Q

For how long/how frequently do a couple need to be having unrpotected sexual intercourse to be cnsidered infertile?

A

2 years despite sex 3-4 times/wweek

467
Q

How can causes of infertility be classified?

A

Genetics
Ovulation/endocrine
Tubal abnormalities
Uterine abnormalities
Endometriosis
Cervical abnormalities
Testicular disorders
Ejaculatory disorders

468
Q

Give some ovulation/endocrine disorders that can cause infertility

A

PCOS
Pituitary tumours
Sheehan’s syndrome
Hyperprolactinaemia
Cushing’s
Premature ovarian failure

469
Q

Give some tubal abnormalities that can cause infertility

A

Congenital anatomical abnormalities
Adhesions
Can be secondary to PID(- gonorrhoea, chlamydia)

470
Q

Give some uterine abnormalities that can cause infertility

A

Bicronate uterus
Fibroids
Asherman’s syndrome

471
Q

How is infertility investigated in women?

A

Bedside:Thorough hx including PMH, sexual history and past pregnancies
Speculum and bimanual exam-e.g. fibroids
STI screen
Bloods:Serum progesterone testing
Prolactin
LH/FSH
Anti-mullerian hormone
TFTsImaging:
TV USS
Hysterosalpingography
Laparoscopy and dye

472
Q

How is infertility investigated in men?

A

Bedside:Thorough hx including PMH, sexual history past children
Testicular exam: e.g. varicocele
Semen analysis: evaluate sperm count, motility and morphology
Bloods:Serum testosterone
LH/FSHTFTs

473
Q

Describe the conservative management of infertility

A

Folic acid
Weight loss: BMI 20-25
Smoking cessation and alcohol advice
Stres reduction strategies
Advice sexual intercourse every 2-3 days

474
Q

Describe the aetioloy of mastitis

A

Bacterial infection

475
Q

What is an intraductal papilloma

A

Benign tumour of breast ducts

476
Q

What is a radial scar

A

benign sclerosing breast lesion

477
Q

Describe the aetiology of fat necrosis

A

response to adipose tissue damage

478
Q

Describe the etiology of fibrocystic breast disease

A

Increased hormonal response response resulting in inflammation and fibrosis

479
Q

Describe the aetiology of mammary duct ectasia

A

Inflammation and dilation of large breast ducts

Anki 3a exports (11 decks)

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