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Gynecology & Obstetrics

State exam 2015/2016

Gynecology & Obstetrics State exam 2015/2016

Contents

Triplet 1

1

1.A

Pelvic inflammatory disease

1

1.B

Diagnosis and differentia diagnosis of Ectopic pregnancy

2

1.C

Postpartum haemorrhage

3

Triplet 2

5

2.A

Puberty physiology, pathology

5

2.B

Standard examination methods in prenatal care

9

2.C

Malpresentation of the vertex

12

Triplet 3

15

3.A

Menstruation cycle

15

3.B

Anatomy of the female genitalia

18

 

19

3.C Positio alta occipitalis anterior

20

Triplet 4

20

4.A

Gynecological examination of women (medical history, physical examination, digital

examination)

20

4.B

Hyperprolactinemia and galactorrhea

24

4.C

Development of the placenta and abnormality of placental development

26

Triplet 5

30

5.A

Colpitis and vaginosis

30

5.B

Life Cycle of a Woman

31

5.C

Birth shock

32

Triplet 6

38

6.A

Cancer screening in gynecology

38

6.B

Amenorrhea

38

6.C

Preeclampsia

43

Triplet 7

44

7.A

Treatment of endometriosis associated infertility

44

7.B

Fertilization and fetal development

45

7.C

Puerperal infections

46

Triplet 8

47

8.B

Ethical issues in gynecology, obstetrics and assisted reproduction

49

8.C

Intrauterine hypoxia, causes and diagnosis

50

Triplet 9

53

9.A

Pelvic pain syndrome

53

9.B

Legislation on assisted reproduction practice in Europe

54

9.C

Placenta Praevia

55

Triplet 10

57

10.A

Regulation of the menstrual cycle

57

10.B

Evaluation of fetoplacental function

58

10.C

Kidney and urinary tract diseases in pregnancy

59

Triplet 11

61

11.A

Dysmenorrhoea and dyspareunia

61

11.B

First stage delivery

62

11.C

Eclampsia

63

Triplet 12

64

12.A

Chlamydial, Mycoplasmal and Ureaplasmal infections

64

12.B

Second stage delivery

66

12.C

Endocrine disorders in pregnancy

67

Triplet 13

71

13.A

PCOS syndrome

71

13.B

Third stage delivery

71

13.C

Preterm birth

73

Triplet 14

75

14.A

Vulvar dystrophies and vulvitis

75

14.B

Ectopic pregnancy

76

14.C

Diabetes mellitus and pregnancy

77

Triplet 15

79

15.A

Endometriosis

79

15.B

Endocrine disorders and female reproduction

80

15.C

HELLP syndrome

81

Triplet 16

83

16.A

Evalutation and Management of the Infertile Couple

83

16.B

USG in pregnancy

88

16.C

Forceps and vacuum delivery

89

Triplet 17

91

17.A

Influence of male factors on treatment of fertility/sterility

91

17.B

Spontaneous abortion

92

17.C

Anaemia in pregnancy

93

Triplet 18

94

18.A

Anovulation Treatment and Management

94

18.B

Thrombophilias in Pregnancy

95

18.C

Breech presentation and delivery

97

Triplet 19

99

19.A

Assisted reproductive techniques

99

19.B

Changes in the reproductive system /uterus and ovaries/ during pregnancy

100

19.C

Asynclitic birth

101

Triplet 20

102

20.A

Cervicitis and endometritis

102

20.B

Gestational trophoblastic disease

103

20.C

Rhesus incompability

105

Triplet 21

106

21.A

Adnexitis and parametritis

106

21.B

Fetoplacentar unit function

108

21.C

Failure of uterine contractions during labour

109

Triplet 22

111

22.A

Preservation of fertility in cancer patients, cryopreservation of gametes and embryos

111

22.B

Central nervous and respiratory system development

113

22.C

Pregnancy and delivery in cardiac disease

116

Triplet 23

117

23.A

Pelviperitonitis and peritonitis diffusa

117

23.B

The development of the cardiovascular system and fetal blond circulation

118

23.C

Abruptio placentae praecox

119

Triplet 24

120

24.A

Benign lesions of the vulva, vagina and cervix uteri

120

24.B

Termination of pregnancy

122

24.C

Hypertensive disorders of pregnancy

123

Triplet 25

125

25.B

Prenatal care

126

25.C

The transverse and oblique fetal presentation

127

Triplet 26

128

26.A

Benign tumors of the uterus

128

26.B

Physiological changes during Pregnancy

129

26.C

HIV/AIDS during pregnancy

131

Triplet 27

133

27.A

Malignant tumors of uterus

133

27.B

Sexual transmission diseases

134

27.C

Intrauterine Fetal Death causes, diagnosis, treatment

137

Triplet 28

139

28.A

Medical Definition of Climacterium

139

28.B

Management of normal labor

140

28.C

Coagulation disorders in pregnancy

142

Triplet 29

144

29.A

Uterine descensus and prolapse

144

29.B

Implantation of the embryo and implant failure

146

29.C

Post-term pregnancy and induced labour

147

Triplet 30

150

30.A

Prevention and early diagnosis of malignant tumors in gynecology

150

30.B

Secondary amenorrhea

151

30.C

Premature rupture of membranes

152

Triplet 31

154

31.A

Urinary incontinence in women

154

31.B

Differential diagnosis of ectopic pregnancy

155

31.C

Genetic birth defects

157

Triplet 32

159

32.A

Cervical cancer

159

32.B

Cardiotocograph plus ST analysis of fetal electrocardiogram and pulse oximetry

162

32.C

Multiple pregnancy

165

Triplet 33

167

33.A

Precancerous lesions of the vulva, vagina and cervix uteri

167

33.B

Screening for congenital birth defects in pregnancy

169

33.C

Bleeding in pregnancy causes, diagnosis, therapy

171

Triplet 34

175

34.A

Vaginal and vulvar cancer

175

34.B

The Newborn Infant postpartum treatment and examination

175

34.C

Complications of 3 rd stage of labour

177

Triplet 35

179

35.A

Breast cancer

179

35.B

Latest news on hormone replacement therapy

180

35.C

Uterine rupture

181

Triplet 36

182

36.A

Non-epithelial ovarian cancer

182

36.B

Planned parenthood and contraception

183

36.C

Umbilical Cord Pathology /Abnormalities

185

Triplet 37

188

37.A

Benign tumors of the ovary

188

37.B

Obstetrical analgesia and anaesthesia

189

37.C

Premature infant

190

Triplet 38

192

38.A

Benign breast diseases

192

38.B

Abnormal puerperium

198

38.C

Sectio Cesarea

204

Triplet 39

207

39.A

Hormonal treatment in gynecology

207

39.B

Imaging modalities/methods in obstetrics and gynecology

209

39.C

Injuries of fetus and newborn

210

Triplet 40

212

40.A

Hormonal contraception

212

40.B

Development of the urogenital system and malformations of female genitalia

214

40.C

Maternal death

216

HIV/AIDS:

216

Triplet 41

216

41.A

Hormonally active ovarian tumors

217

41.B

Infectious diseases in pregnancy

221

41.C

IUGR

225

42.A

Diagnosis of amenorrhoea

227

42.B

Anthropozoonosis and pregnancy

231

42.C

Abnormal puerperium

233

Triplet 43

234

43.A

Gynecology Preventive Care

234

43.B

Normal puerperium

235

43.C

Abnormalities of pelvis and birth canal

236

Triplet 44

239

44.A

Pediatric and Adolescent Gynecology

239

44.B

Hormones of the Placenta

240

44.C

Critical conditions in obstetrics

240

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Triplet 1

1.A

Pelvic inflammatory disease

Definition When infections ascend from cervix or vagina into upper genital tract.

Endometritis, salpingitis, tubo-ovarian abscess & pelvic peritonitis.

Main causes: Chlamydia. Trachomatis, Neisseria. Gonorrhoeae (Mycoplasma & anaerobes).

Sometimes in laparoscopically proven PID, no bacterial cause is found.

Incidence unknown (~ 2/3 asymptomatic).

Clinical presentation:

None to very severe.

Onset of symptoms usually in first part of menstrual cycle.

Chlamydial PID is usually milder than gonococcal PID.

Lower abdominal pain is the most common symptom.

Increased vaginal discharge, irregular bleeding, postcoital bleeding, dyspareunia (pain

during sex), cervicitis. Adnexal & cervical tenderness on examination.

May be Pyrexia (fever) ?

Palpable adnexal mass. ?

Diagnosis:

No specific symptoms, signs or lab tests.

Made by clinical findings.

Differential diagnoses: appendicitis & ectopic pregnancy.

Pregnancy test.

Laparoscopy + microbiology of upper & lower genital tract ("gold standard").

Not always available/appropriate in mild cases.

Treatment:

Do not delay (no waiting for test result).

Outpatient, Oral antibiotics for mild to moderate cases.

I.V therapy in severe cases.

Hospitalization if diagnostic uncertainty, severe case or failure to respond to oral therapy.

Antibiotic combination: Cefoxitin + Doxycycline + Metronidazole + Ofloxacin + Ceftriaxone????

Analgesia.

No sex until both partners, completed treatment (in case of STD).

In moderate (severe) cases - review 23 days to ensure improvement.

Lack of response, requires further investigation, I.V therapy, surgery.

All patients should be seen after treatment to check clinical response & medication completed.

1

Complications:

- Main complications from PID are due to tubal damage.

- Tubal infertility.

- Ectopic pregnancy (x6-10).

- Chronic abdominal or pelvic pain.

- Hysterectomy.

- Repeats in 1/3.

- Infection of liver capsule (perihepatitis).

1.B

Diagnosis and differentia diagnosis of Ectopic pregnancy

Definition:

Non-intrauterine pregnancy (ovarian, cervical or intra-abdominal).

Usually tubal.

Major cause of mortality!

Clinical presentation:

Pelvic tenderness and/or cervical excitation and/or shoulder tip pain due to diaphragmatic irritation from haemoperitoneum.

Pain, amenorrhea (abnormal absence of menstruation) & vaginal bleeding.

Diagnosis:

The date of the last menstrual period, date of pregnancy test & symptoms suggesting pelvic

infections. Pelvic examination should be gentle to avoid tubal rupture.

hCG which does not increase > 66% in 48 hours increases the likelihood of ectopic pregnancy.

Treatment:

Resuscitation & blood transfusion may be required.

Management depends on the overall clinical picture, the scan result and the serum level of

hCG. Tubal pregnancy can be managed by:

o

Laparotomy

o

Laparoscopy

o

medically or by observation alone.

If shocked (hypotensive

)

- immediate pregnancy test (ectopic pregnancy) & consider urgent

laparotomy if positive. If hemodynamically stable, a laparoscopic approach to the surgical management of tubal pregnancy is preferable to an open approach.

hCG should be rechecked in 48 hours. If levels are not doubled, steady or only slightly reduced, consider a laparoscopy.

In a well woman with a positive UPT and an empty uterus on transvaginal ultrasound, a serum hCG level is performed. If the level is over 1500 IU/l, consider a laparoscopy.

2

Methotrexate is an option for ectopic pregnancy with minimal symptoms, clinically stable &

hCG level < 3000 IU/l. Laparoscopic salpingectomy or salpingotomy is appropriate.

Postoperative tracking of serum hCG is necessary following salpingotomy, to identify cases

complicated by persistent trophoblast. Expectant management is an option for clinically stable asymptomatic women with an ultrasound diagnosis of ectopic pregnancy and a decreasing serum hCG, initially less than 1000 IU/l.

When serum hCG levels are below the discriminatory zone (<1000 IU/l) and there is no pregnancy (intra-or extra-uterine) visible on transvaginal ultrasound scan, the pregnancy can be described as being of unknown location (pregnancy of unknown location or PUL).

If women are managed expectantly, serial serum hCG measurements should be performed until hCG levels are less than 15 IU/l.

Non-sensitized Rh- woman with a confirmed or suspected ectopic pregnancy should receive anti-D immunoglobulin.

Differential diagnosis:

Miscarriage, continuing intrauterine pregnancy, PID, Appendicitis, Salpingitis

Ruptured corpus luteum cyst or ovarian follicle.

Spontaneous abortion or threatened abortion, Ovarian torsion.

Cervical cancer, dysmenorrhea, placenta previa.

UTI.

Complications:

Infertility.

Infections.

Bleeding, shock, death.

1.C

Postpartum haemorrhage

Definition Bleeding after delivery.

Primary postpartum haemorrhage:

Risk factors: multiparity, multiple pregnancy, fibroids, polyhydramnios, placenta previa & long labour.

Blood loss > 500 ml < 24h of delivery.

Secondary postpartum hemorrhage:

Any significant loss 24h - 6 weeks from delivery.

Usually due to infection and/or retained products of conception.

More likely in women with a past history of postpartum hemorrhage.

Important to treat anaemia in the antenatal period.

Oxytocin (after delivery).

3

Main causes of PPH:

Atony: retained placenta (90%). Normally, contraction of the uterus in the third stage of labour causes compression of blood vessels & bleeding stops.

Trauma: Episiotomy, a vaginal or cervical laceration or a rupture in the uterine wall.

Lacerations of genital tract after an instrumental delivery.

Coagulation problems: usually disseminated intravascular coagulation (DIC).

Clinical presentation:

Bleeding is usually obvious, but, an atonic uterus can fill up without obvious external loss & the first real sign can be cardiovascular collapse (shock).

Easy to underestimate the real loss.

The most critical factors are the signs of shock, pallor, tachycardia & falling BP.

Palpate the abdomen to assess the size and tone of the uterus.

If uterus is atonic, a contraction can be stimulated by abdominal massage.

I.V access should be established with 2 wide-bore cannulas & blood taken for hemoglobin, hematocrit, platelets, clotting & crossmatch.

Oxytocin i.v. should be given to further contract the uterus, followed by a oxytocin infusion.

Crystalloid and/or colloid should be rapidly infused to maintain the circulating volume.

A urinary catheter should be inserted to aid compression of the uterus & to measure urine

output. If placenta has not been delivered, gently attempt at controlled cord traction.

In Hemorrhage + placenta accreta consider a hysterectomy.

Treat DIC with fresh frozen plasma or cryoprecipitate.

Techniques to stop hemorrhage are aimed at either maintaining compression of the uterus or applying pressure on the placental bed.

o

By suture, intrauterine Balloons & surgical packs.

o

Hysterectomy indicated, especially in uterine rupture or placenta accreta.

o

Internal iliac artery ligation (only for atony).

o

Radiologically guided internal iliac artery embolization.

The decision is usually between conservative management with antibiotics, or arranging for an evacuation of retained products with antibiotic cover under anesthesia.

In the first week the evacuation can often be carried out digitally.

However, in the presence of persistent bleeding, USG to observe the spontaneous resolution of intrauterine hematoma & identify retained products.

4

Triplet 2

2.A

Puberty physiology, pathology

Definition:

Puberty should transform a girl into a fertile woman.

Puberty encompasses: an adolescent growth spurt the acquisition of secondary sexual characteristics the onset of menstruation (menarche) & the establishment of ovulatory function.

Endocrine changes: reactivation of the hypothalamic-pituitaryovarian axis.

Gonadotrophins (GnRH - FSH & LH) release, lead to production of ovarian estrogen, which initiates the physical changes of puberty.

External signs of puberty usually occur in a specific order.

Adolescent growth spurt is an early feature.

This acceleration in growth is dependent on growth hormone as well as gonadal steroids.

Menarche (first menstruation) is a late feature.

Breast development, which is primarily under the control of ovarian estrogens, is described in 5 stages (Tanner stages of breast development).

The appearance of the breast bud is followed by pubic & axillary hair, mainly under the influence of ovarian & adrenal androgens (Tanner stages of pubic hairdevelopment).

The age of menarche is ~ 13.

This has been attributed to improvement in socioeconomic conditions, nutrition & general health.

Influence of body weight: attainment of a critical body weight (48 kg).

Body fat increases to ~ 22% of body weight.

Delay of a critical body weight may delay menarche (Malnutrition, Slow growth before & after birth, Twins, Athletic training& Eating disorders).

Anorexia nervosa can cause both primary & secondary amenorrhoea & a halt in pubertal progress.

95% of normal girls attain stage 2 breast development by age 13.

5

50% will complete all stages of puberty by age 16.

The bone age, which is an index of physiological maturation, correlates closely with the menarche.

It can be measured by an X-ray of the hand.

80% of girls begin to menstruate at a bone age of ~13.

Menstrual cycles tend to be irregular as ovulation is initially infrequent.

Most girls take several months / a year to establish a regular cycle.

Pathologic puberty:

Delayed puberty: absence of physical manifestations of puberty by age 13.

Primary amenorrhoea: no menstruation by the age of 14 accompanied by failure to develop secondary sexual characteristics OR no menstruation by age 16 in the presence of normal sexual development.

Arrested puberty: puberty starts without normal progression.

Constitutional delay: normal but inherently late in entering puberty.

o

Although these individuals are usually of short stature & have usually been shorter than their peers for years, their height is generally appropriate for their bone age.

o

All stages of development are delayed.

o

They may be considered to be physiologically immature, with a functional deficiency of gonadotrophin-releasing hormone (GnRH) for their chronological age, but not for their stage of physiological development.

o

On attaining a bone age of 1113 years they can be expected to enter puberty.

o

Associated with:

Conditions affecting weight.

Systemic disease.

Malnutrition.

Anorexia nervosa.

o

Restoration of weight usually results in spontaneous onset of puberty.

6

CNS tumors: interference with GnRH synthesis / secretion / stimulation of the pituitary gland (craniopharyngioma).

Primary (peripheral) gonadal failure (hyper-gonadotrophic hypogonadism):

o

Hypogonadism due to an impaired response of the gonads to the gonadotropins (FSH&LH) resulting in a lack of sex steroid production (estrogen & progesteron)& elevated gonadotropin levels (as an attempt of compensation by the body).

o

May present as either congenital (usually)/ acquired.

o

There are many different etiologies of HH.

1) Congenital causes:

Chromosomal abnormalities (resulting in gonadal dysgenesis) - Turner's syndrome, Klinefelter's syndrome, Swyer's syndrome, XX gonadal dysgenesis, & mosaicism.???????

Defects in the enzymes involved in the gonadal biosynthesis of the sex hormones.

Gonadotropin resistance: FSH insensitivity &LH + FSH resistance due to mutations in the GNAS gene.

2) Acquired causes (due to damage / dysfunction of the ovaries):

Ovarian torsion.

Premature ovarian failure.

Ovarian resistance syndrome.

Trauma, surgery, autoimmunity, chemotherapy, radiation, infections (STD), toxins & drugs (anti androgens, opioids, alcohol).

Diagnosis:

Hormone panel: FSH, LH, estradiol, prolactin & thyroid.

History & physical examination.

Pelvic USG.

Karyotype.

X-ray for bone age.

7

Pelvic CT / MRI.

Treatment (cause dependent):

They will require hormone replacement therapy, until age 50.

The first stage in treatment is to achieve apparently normal puberty by estradiol.

Commonly, ongoing estrogen replacement is with the combined oral contraceptive pill (COCP).

Precocious puberty:

Signs of sexual maturation < 8 years.

The growth spurt is a striking feature.

Menstruation usually brings the girl to medical checkup.

Intracranial lesions:

This is the next most likely cause, particularly in younger girls.

An intracranial lesion resulting from encephalitis, meningitis, hydrocephaly / a small space- occupying lesion, may trigger premature reactivation of the hypothalamic-pituitaryovarian axis.

Feminizing tumors of the ovary / adrenal may give rise to vaginal bleeding without signs of pubertal development.

Diagnosis of precocious puberty:

Hormone panel: FSH, LH, estradiol & thyroid.

X-ray of the hand to determine bone age.

USG of abdomen & pelvis.

Radiological skeletal survey of the long bones.

Cranial CT / MRI.

8

The goal is To arrest or regress of the physical signs of puberty&in particular menstruation.

To avert the rapid advance in bone age, as premature fusion of the epiphyses would compromise the final height of the child.

The introduction of GnRH agonists, which suppress gonadotrophin secretion for constitutional & cerebral precocious puberty.

Sexual abuse:

This is the involvement of dependent sexually immature children & adolescents in sexual activity they do not truly comprehend, to which they are unable to give informed consent & which violates social taboos / family roles.

Particular attention should be paid to bleeding, bruising / any other area of injury.

2.B

Standard examination methods in prenatal care

Antenatal care is a screening program aimed at identifying problems at an early stage to minimize the risks to mothers & their babies.

For health promotion, preparation for labour, parenthood & surveillance of risk.

The initial visit ideally 8 - 10w, every 4 weeks until 30w, every 2w until 32w & then every week.

&

spontaneous labour. The duration of labour, mode of delivery, birth weight, sex, neonatal outcome & postnatal complications.

or

Past

obstetric

history:

previous

pregnancies

labours,

gestation

at

delivery

&

induced

Medical & surgical history: Previous operations, particularly gynaecological procedures (cone biopsy may predispose to cervical incompetence) & blood transfusions received? Hypertension, diabetes, heart disease, renal disease, epilepsy, asthma, thyroid dysfunction.

Family history: potential inherited conditions, thalassemia, cystic fibrosis, sickle cell anaemia, chromosomal disorders & structural abnormalities.

History of present pregnancy: The date of the first day of the last menstrual period & details of the menstrual cycle before conception. Correlation with early pregnancy, USG dating is important.

Social & drug history: drugs taken, during the pregnancy. Alcohol, smoking & drug abuse. Evidence of socioeconomic deprivation. Identification of matters relating to child protection necessitates (social work department).

9

Examination: pulse rate, BP, weight & height.

A BMI > 30 is potential for complications.

Abdominal examination: approximate indication of the uterine size, identify abnormal

masses & other abnormalities. There is no indication for a routine vaginal examination, perform cervical cytology if overdue.

USG: fetal viability?, gestational age, identifies multiple pregnancy.

Measure nuchal translucency & diagnose fetal anomalies (anencephaly).

Urine analysis: protein & glucose.

Blood test: CBC (anaemia & thrombocytopenia). Blood group ABO + Rh + presence of red cell

antibodies. Rubella status: check mothers immunity.

Hemoglobin electrophoresis (sickle cell anaemia or thalassemia).

Hepatitis B status.

Serology for syphilis.

HIV.

Discuss screening options for chromosomal & structural abnormalities.

Mothers at the extremes of reproductive age are at increased risk of obstetric complications, particularly hypertensive disorders & perinatal mortality.

The incidence of proteinuria pre-eclampsia in a second pregnancy is x1015 greater if there was pre- eclampsia in the first pregnancy.

Those who have had a previous instrumental delivery usually have a normal delivery next time.

In general, those with a previous C section for a non-recurrent indication, e.g. breech, fetal distress or relative cephalopelvic disproportion (CPD) secondary to fetal malposition should be offered vaginal birth, although repeat elective C section may be recommended in certain circumstances.

Smoking is associated with low-birth-weight babies.

follow-up has demonstrated intellectual & emotional impairment. Increased risk of placental abruption, preterm labour, intrauterine fetal demise & sudden infant death syndrome (SIDS).

Although there is no evidence to support an association with fetal abnormality, long-term

Alcohol & drug abuse carry significant fetal risks. Avoid in pregnancy! May continue working providing she is not 2 tired.

Moderate exercise is likely to be of benefit and should be encouraged.

Antenatal surveillance: used to identify obstetric complications. Gestational hypertension & pre- eclampsia. BP & urinalysis, checked every visit.

‘Small for gestational age’ (SGA): birth weight < 10th percentile.

‘fetal growth restriction’ (FGR): ‘a fetus which fails to reach its genetic growth potential’. Carries a significant risk of antenatal & intrapartum asphyxia, intrauterine death, neonatal hypoglycemia, long-term neurological impairment & perinatal death.

10

USG will identify, most small babies.

Impaired glucose tolerance test & diabetes: If family history of diabetes, previous large-for- gestational-age baby or persistent glycosuria.

Hemolytic disease: Maternal IgG antibodies to fetal red cell antigens cross the placenta & may lead to fetal hemolysis, anaemia & "hydrops fetalis".

Initial sensitization usually occurs in previous delivery, but may occur with vaginal bleeding at

any stage, amniocentesis, external cephalic version or an unrecognized event (silent fetomaternal transfusion). The most significant antibody is Rh antigen (Rh- mothers may develop against Rh+ fetal cells).

All women should be screened for anti-red cell antibodies at booking & again in the 3rd

trimester. Those with antibodies require further investigation.

o Rh- women without sensitization are recommended to receive 2 doses of anti D.

Breech presentation: associated with multiple pregnancy, bicornuate uterus, fibroids, placenta praevia, polyhydramnios & oligohydramnios.

Confirmed by USG.

Planned C section at term is associated with less perinatal mortality & less serious neonatal morbidity.

Anaemia As there is a physiological fall in hemoglobin (Hb) as pregnancy advances.

Oral FeSO4 if Hb <10 g/dl or if the mean corpuscular volume (MCV) is low (<80 fl).

Check folate, B12 & ferritin before deciding on therapy.

Parenteral iron should never be given in thalassemia!

Polyhydramnios (Excess of liquid) In the 2nd & 3rd trimesters, liquor is produced by fetal kidneys and is swallowed by the fetus. Diagnosed by USG (a single pool >8 cm in depth, and/or an amniotic fluid index > 90th percentile).

Caused by Increased production from high urine output Macrosomia, diabetes, recipient of

twintwin transfusion, "hydrops fetalis", Gastrointestinal obstruction, Esophageal atresia, duodenal atresia, bowel obstruction or Hirschsprung’s disease Poor swallowing because of neuromuscular problems or mechanical obstruction Anencephaly, myotonic dystrophy, maternal myasthenia, facial tumor, macroglossia or micrognathia. Associated with: placental abruption, malpresentation, cord prolapse, carrying a large-for-

gestational-age infant requiring a caesarean section, perinatal death. Antibody titers should be checked to exclude alloimmune haemolytic disease.

Increased

complications.

antenatal

fetal

surveillance

+

increased

awareness

of

the

risks

of

intrapartum

Prolonged pregnancy (> 42 weeks) Is associated with an increased perinatal mortality due to ‘unexplained’ intrauterine death, intrapartum hypoxia and meconium aspiration syndrome.

Sweeping the membranes By vaginal examination and inserting a finger through the internal os to separate the membranes from the uterine wall, thus releasing endogenous prostaglandins.

11

Induction of labour after 41 weeks reduces the incidence of fetal distress & meconium staining & reduced C section rate.

Fetal monitoring by fetal movement charts, cardiotocography (CTG), biophysical profile scoring & Doppler flow velocity studies.

Fetal cardiotocography (CTG): indication of fetal well-being at a particular moment but has little longer-term predictive value.

Fetal biophysical profile (BPP): five parameters are assessed.?????

Doppler flow velocity: of umbilical arteries indicates placental vascular resistance.

Useful in pregnancies considered at risk of hypoxia due to impaired placental function.

In severe compromise, diastolic flow may stop altogether or may even reverse.

Abnormal waveforms (absent or reduced - end diastolic flow) are associated with an increased risk of structural & chromosomal abnormalities.

risk of structural & chromosomal abnormalities. 2.C Malpresentation of the vertex Definition: ➢

2.C

Malpresentation of the vertex

chromosomal abnormalities. 2.C Malpresentation of the vertex Definition: ➢ "presentation": the part of the

Definition:

"presentation": the part of the fetus presenting to the pelvic inlet.

Normal presentation is vertex.

Malpresentation’ describes any non-vertex presentation (face, brow, breech, other part of the body).

Clinical presentation:

'Malposition’ is when the head, coming vertex first, does not rotate to occipitoanterior (persistent occipitotransverse / occipitoposterior).

The presenting diameter is dependent on the degree of flexion / extension of the head (deflexed & brow presentations have a wide diameter).

12

Fetal neurocranium: occipital, sphenoid, parietal, temporal & ethmoid bones joined by frontal, sagittal, lambdoid & coronal sutures.

Moulding’: change in shape of the skull during labour due to the birth canal shape.

Face presentation: associated with anencephaly (rare), edema & bruising. Usually only recognized after the onset of labour.

o If the face is swollen it is easy to confuse with a breech presentation.

Brow presentation: least favorable.

o The head may flex to become a vertex presentation / extend to a face presentation.

Treatment:

C section may be required.

Complications:

Increased risk for injuries to the uterus / birth canal (bleeding) & abnormal labor ("failure to progress").

Fetal distress: tachycardia / bradycardia.

Caput: Edema of fetal head.

Fetal neurocranium: occipital, sphenoid, parietal, temporal & ethmoid bones joined by frontal, sagittal, lambdoid & coronal sutures.

Moulding’: change in shape of the skull during labour due to the birth canal shape.

Face presentation: associated with anencephaly (rare), edema & bruising. Usually only

Definition:

"presentation": the part of the fetus presenting to the pelvic inlet.

Normal presentation is vertex.

Malpresentation’ describes any non-vertex presentation (face, brow, breech, other part of the body).

Clinical presentation:

'Malposition’ is when the head, coming vertex first, does not rotate to occipitoanterior (persistent occipitotransverse / occipitoposterior).

13

The presenting diameter is dependent on the degree of flexion / extension of the head (deflexed & brow presentations have a wide diameter).

recognized after the onset of labour.

o If the face is swollen it is easy to confuse with a breech presentation.

Brow presentation: least favorable.

o The head may flex to become a vertex presentation / extend to a face presentation.

Treatment:

C section may be required.

Complications:

Increased risk for injuries to the uterus / birth canal (bleeding) & abnormal labor ("failure to

progress"). Fetal distress: tachycardia / bradycardia.

Caput: Edema of fetal head.
Caput: Edema of fetal head.

14

Triplet 3

3.A

Menstruation cycle

Definition:

Monthly series of changes a woman's body goes through in preparation for the possibility of pregnancy.

Each month, one of the ovaries releases an egg (ovulation) & hormonal changes prepare the uterus for pregnancy.

The menstrual cycle can be described by changes in uterus or ovary.

The endometrial cycle results from the growth & shedding of the uterine lining.

At the end of the menstrual phase, the endometrium thickens again (proliferative phase).

After ovulation, endometrial growth stops, the glands become more active & full of secretions (secretory phase).

Endometrial changes are controlled by the ovarian cycle.

The average duration of the ovarian cycle is 28 days (follicular, ovulation & post ovulatory or luteal phase).

If the cycle is prolonged, the follicular phase lengthens (longer time to ovulation) but the luteal phase remains constant at 14 days.

Fundamental to normal cycle: hypothalamic-pituitaryovarian axis + responsive follicles in ovaries + a functional uterus.

to normal cycle : hypothalamic-pituitary – ovarian axis + responsive follicles in ovaries + a functional

15

The hypothalamus controls the cycle & influenced by higher centers (anxiety or stress can change the cycle).

Hypothalamus --> pituitary by gonadotrophin-releasing hormone (GnRH).

GnRH stimulates --> follicle-stimulating hormone (FSH) & luteinizing hormone (LH).

FSH stimulates growth of follicles (follicular phase) & sex hormone secretion (estradiol).

LH stimulates sex hormone production (testosterone, converted by FSH to estradiol).

production (testosterone, converted by FSH to estradiol). The mid-cycle surge of LH which triggers rupture of

The mid-cycle surge of LH which triggers rupture of the mature follicle (ovulation).

Post-ovulatory production of progesterone by the corpus luteum is also under the influence of LH.

The ovarian cycle:

I. Follicular phase Days 18: FSH + LH rise in response to the fall of estrogen & progesterone at menstruation.

This stimulates development of 1020 follicles. With growth of the dominant follicle, estrogen levels increase.

II. Days 914: The primary follicle transforms into a Graafian follicle (oocyte inside).

Follicular maturation is associated with increase in the production of estradiol by the developing follicle.

As the estrogen level rises, the release of both gonadotrophins is suppressed (negative feedback).

III. Ovulation (Day 14): rapid enlargement of the follicle, followed by protrusion from the surface of the ovarian cortex & rupture of the follicle with extrusion of the oocyte (ovulation).

Some women can identify the time of ovulation because they experience a short-lived pain in iliac fossa.

The final rise in estradiol concentration is thought to be responsible for the subsequent mid- cycle surge of LH & FSH (positive feedback).

16

 

Immediately before ovulation there is a precipitous fall in estradiol & increase in progesterone.

IV.

Luteal phase (Days 1528): The Graafian follicle forms the corpus luteum.

 

This is the major source of sex hormones (estrogen & progesterone) secreted by the ovary in the postovulatory phase.

Progesterone levels peak 1 week after ovulation (day 21 of 28-day cycle).

During the luteal phase gonadotrophin levels remain low until the regression of the corpus luteum (days 2628).

If conception & implantation occur, the corpus luteum does not regress, because it is maintained by hCG secreted by the trophoblast.

The detection of the presence of hCG in a sample of urine forms the basis of pregnancy testing.

If conception & implantation do not occurr, the corpus luteum regresses, progesterone levels fall & menstruation starts.

The fall of sex hormones (estrogen & progesterone) allows the FSH + LH levels to rise & start the next cycle.

The uterine cycle:

The cyclical production of sex hormones (estrogen & progesterone) by the ovary induces changes in the uterus (endometrium & cervical mucus).

The endometrium: has a superficial layer which is shed during menstruation & a basal layer which regenerates the superficial layer during the subsequent cycle.

I. Proliferative phase: During the follicular phase in the ovary, the endometrium is exposed to estradiol.

After menstruation, the secretion of estradiol from the ovary brings about repair & regeneration of the endometrium + growth & proliferation of glands, blood vessels.

II. Secretory phase: After ovulation, progesterone production prepares the endometrium for implantation.

III. Menstrual phase: Normally, the luteal phase of the ovary lasts for 14 days, at the end of which regression of the corpus luteum is associated with a decline in ovarian sex hormones (estradiol & progesterone).

This fall (estrogen & progesterone) is followed by intense spasmodic contraction of the endometrial arterioles & ischemic necrosis (shedding the superficial layer & bleeding).

The vasospasm & uterine contractions at the time of the menstrual flow is by prostaglandins.

17

Basal body temperature: rises ~ 0.5°C following ovulation & sustained until menstruation (progesterone's effect on hypothalamus). Should conception occur, this higher temperature is maintained throughout pregnancy.

Breast changes: very sensitive to sex hormones (estrogen & progesterone). During the normal cycle, breast swelling occurs in the luteal phase in response to increasing progesterone levels.

Psychological changes: changes in mood with increased emotional lability in late luteal phase (falling levels of progesterone).

For menstrual cycle regulation see question 10/A

3.B

Anatomy of the female genitalia

External & internal genitalia:

Blood supply:

o

Perineum from internal pudendal artery.

o

Uterine, Vesical & vaginal arteries from internal iliac artery.

o

Ovarian vessels from abdominal aorta (inside suspensory ligament).

Innervation:

o

Perineum from pudendal nerve (Sacral plexus (S2, S3, S4)).

o

Uterus & Vagina from hypogastric nerves & Sacral plexus.

o

Ovary from ovarian plexus.

S4)). o Uterus & Vagina from hypogastric nerves & Sacral plexus. o Ovary from ovarian plexus.

18

19

3.C

Positio alta occipitalis anterior

Definition:

Malpresentation, the head is high above the pelvic inlet during the first stage of labor.

Head position is with the sagittal suture in the "anterior/posterior" axis.

There is a delayed labor (non progressing) & C section is usually the way to deliver safely.

Triplet 4

4.A

examination, digital examination)

Gynecological examination of women (medical history, physical

Gynecological history:

Usual history-taking with questions about the presenting complaint, its history & associated

problems. Past medical history, drugs & allergies.

Social status, family history & general systemic enquiry.

Menstrual cycle, fertility, pelvic pain, urogynaecological & obstetric - histories.

Menstrual history: The pattern of bleeding?

o

The simple phrase ‘tell me about your periods’

o

The bleeding pattern of the menstrual cycle is expressed as a fraction. A cycle of 4/28 means the woman bleeds 4 days every 28 days.

Bleeding too little (Amenorrhoea): is the absence of periods.

Primary amenorrhoea: no menstruation by age 16.

Secondary amenorrhoea: no menstruation > 6 months.

Oligomenorrhoea: infrequent periods (> 42 days cycle).

Climacteric: peri-menopausal time when periods become less regular & increasing menopausal symptoms.

Menopause: time after last ever period (assessed retrospectively).

Bleeding too much (menorrhagia): Loss > 80 ml during regular menstruation. It is very difficult to accurately assess, how heavy the periods are.

Blood clots are not normal! Symptoms of anaemia may also be present.

A history of the menstrual cycle since menarche (the first period) can reveal changes in the bleeding pattern.

20

Bleeding at the wrong time It is important to ask specifically about bleeding, brown, or bloody discharge between periods (inter-menstrual bleeding), or after intercourse (postcoital bleeding). Can point to abnormalities of cervix or uterine cavity.

Postmenopausal bleeding (PMB): bleeding > 1 year after the last period.

Undiagnosed abnormal bleeding requires further investigation!

Fertility history:

Last menstrual period (LMP) This question is vital & should be followed with whether that

period came at the expected time (normal character?). Contraception: sexually active? contraception?

o

Problems with chosen contraceptives & why they were stopped.

Postmenopausal: hormone replacement therapy? any symptoms of menopause?

Cervical smears: Women age's 20 - 64 are invited for cervical screening every 3 - 5 years.

Any previous abnormalities should be noted & colposcopic investigation or treatment?.

If > 50, it may be relevant to discuss breast screening.

Pelvic pain history: Painful periods (Dysmenorrhoea) is a common problem & its effects on lifestyle is important.

The cramping pain of primary dysmenorrhoea is most intense just before & during the early

stages of a period. Young women are particularly affected & the pain has usually been present from the time of the first period.

Usually not associated with structural abnormalities and may improve with age or after a pregnancy.

Secondary dysmenorrhoea: menstruation was not painful in the past & more likely indicates pelvic pathology.

Progressive dysmenorrhoea: the intensity of the pain increases throughout menstruation, may suggest endometriosis.

Pain before or during periods is likely to be of gynecological origin.

It is vital to take a urinary & lower gastrointestinal history as urinary tract infection or irritable bowel syndrome may present with pelvic pain.

Any pain is likely to be worse if the person is anxious, stressed or depressed.

Chronic pelvic pain is particularly affected by psychosomatic factors.

Pain on intercourse (dyspareunia) has two main types (superficial & deep).

Deep dyspareunia: associated with pelvic pathology that restrict uterine mobility (scarring, adhesions, endometriosis, masses).

Superficial dyspareunia: from local abnormalities at the vaginal orifice or 2 low lubrication.

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It can also be due to a voluntary or involuntary contraction of the muscles of the pelvic floor referred to as ‘vaginismus’.

Vaginal discharge: normal or associated with cervical ectopy & if offensive or irritant, can indicate infection.

It can also suggest neoplasia of the cervix or endometrium.

Enquire about the duration, amount, color, smell & relationship to cycle.

Urogynaecological history: Urinary incontinence? Incontinence after exercise, coughing, laughing or straining can suggest stress incontinence.

Other urinary symptoms: frequency & nocturia? dysuria or haematuria may suggest bladder infection or pathology.

Prolapse: vaginal discomfort, dragging sensation, feeling of something ‘coming down’.

The Uterus & vaginal walls (anterior & posterior) can prolapse.

I. Gynaecological examination:

Signs of gynecological disease are not limited to the pelvis (anaemia, pleural effusions,

visual field defects, lymphadenopathy). Done by speculum, taking a cervical smear & bimanual pelvic examination.

A female chaperone should always be present!

The examination requires full explanation & verbal consent.

II. Inspection: hair distribution & vulvar skin.

The vulva can be a site of chronic skin conditions (eczema, psoriasis, warts, cysts of the

Bartholin’s glands & cancers). Ulceration may imply herpes, syphilis, trauma or malignancy.

Look at the perineum & gently part the labia to inspect the vaginal orifice.

Perineal scars are usually secondary to tears or episiotomy during childbirth.

Asking the woman to cough may reveal stress incontinence or the bulge of a prolapse.

III. Physical examination:

1. Speculum examination:

Inspect the vagina for atrophic vaginitis & discharge. A creamy or mucous discharge is normal.

A yellow-greenish frothy discharge is seen with Trichomonas vaginalis.

A grey-green fishy discharge suggests bacterial vaginosis.

Purulent cervical discharge with gonorrhoea.

Increased mucous discharge with chlamydial cervicitis.

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2. Vaginal Swabs: should be taken from the vaginal fornices or the cervical canal (endocervical).
2.
Vaginal Swabs: should be taken from the vaginal fornices or the cervical canal (endocervical).
The cervical os is small & round in the nulliparous, bigger & more slit-like in parous
women.
Inspect cervical mucosa for any changes
Threads from an IUCD may be present.
3.
Taking a cervical smear: in mid - late follicular phase (not during menstruation).
The most commonly used technique involves using liquid-based cytology and a
broom-type sampling device (endocervical + ectocervix).
4.
Check for prolapse:

Coughing will show a bulge of the posterior wall if a rectocele is present.

When the posterior wall is held back, coughing will demonstrate the bulge of a cystocele and/or uterine descent.

23

Digital examination:

1. Pelvic examination:

Apply lubricating gel to the gloved fingers of the right hand. Part the labia with the index and middle fingers of the left hand. Gently slip the right index finger into the vagina. If comfortable, slip the middle finger in below the index finger, making room posteriorly to avoid the sensitive urethra.

The cervix feels like the tip of a nose and protrudes into the top of the vagina.

2. Digital pelvic examination: palpate the cervix & record irregularities or discomfort.

3. Cervical excitationis when touching the cervix causes intense pain & implies active pelvic inflammation.

Assess the position of the uterus. It is usually anteverted (cervix is posterior & uterine body anterior).

Retroverted uterus (cervix is anterior & uterine body posterior).

The fingers should be manipulated behind the cervix to lift the uterus. With the left hand above the umbilicus, feel through the abdomen for the moving uterus.

Bimanual examination: Examination of the uterus & adnexa.

Assess mobility, regularity & size of uterus.

The adhesions of endometriosis, infection, surgery or malignancy fix the uterus & make the

bimanual examination more uncomfortable. Asymmetry of the uterus may imply fibroids.

Feel for adnexal masses in the vaginal fornices lateral to the cervix on each side.

4.B

Hyperprolactinemia and galactorrhea

Hyperprolactinemia Definition:

Presence of abnormally high levels of prolactin in the blood.

Normal < 500 mIU/L [20 ng/mL].

Prolactin is a hormone produced by the pituitary gland that is primarily associated with lactation & plays a vital role in breast development during pregnancy.

Clinical presentation:

> Typical history of oligomenorrhea, amenorrhea or infertility, which generally results from prolactin suppression of gonadotropin-releasing hormone (GnRH) & galactorrhea (spontaneous flow of breast milk).

May be a part of normal body changes during pregnancy & breastfeeding.

May be caused by diseases affecting the hypothalamus & pituitary gland, drugs, medicinal herbs, heavy metals, diseases of liver, kidneys, ovaries & thyroid.

24

Nonpuerperal hyperprolactinemia: pituitary adenomas produce prolactin (prolactinomas).

Diagnosis:

Secretion is pulsatile: it increases with sleep, stress, pregnancy & chest wall stimulation or trauma.

Must be drawn after fasting.

The presence of a pituitary tumor may cause visual-field defects or headache.

Treatment:

Asymptomatic Patients (idiopathic or microprolactinoma) can be monitored without treatment.

Depending on etiology

 

o

Hypothyroidism should be given thyroid hormone replacement therapy.

o

Surgery/radiotherapy for tumors.

o

Estrogen replacement.

o

Change drug causing the problem.

Bromocriptine (dopamine agonist).

Complications:

Persistent associated hypogonadism can lead to osteoporosis, blindness, hemorrhage & infertility.

Galactorrhea definition:

A milky nipple discharge unrelated to the normal milk production, also in those who have

never had children or after menopause.

Not a disease, but it could be a sign of an underlying problem.

Excessive breast stimulation, medication side effects or disorders of the pituitary gland all may contribute to galactorrhea.

Often from hyperprolactinemia.

May be idiopathic.

Clinical presentation:

Persistent or intermittent milky nipple discharge (no blood).

Nipple discharge involving multiple milk ducts.

Spontaneously leaked or manually expressed nipple discharge.

One or both breasts affected.

25

Absent or irregular menstrual periods.

Headaches or vision problems (pituitary tumor).

Diagnosis:

A physical exam for breast lumps & suspicious areas.

Analysis of fluid discharge (fat droplets present help confirm the diagnosis of galactorrhea).

A blood test (prolactin & TSH levels).

A pregnancy test.

Mammography & USG.

Head CT/MRI (pituitary gland).

Treatment:

Cause dependent.

Complications:

Cause dependent.

4.C

development

Development of the placenta and abnormality of placental

The interface between mother & fetus to fulfill critical roles such as preventing allograft rejection of fetus, fetal nutrient supply, respiratory gas exchange & transfer of toxic metabolic waste into the maternal blood circulation for elimination.

The placenta also functions as an endocrine organ producing steroid and protein hormones for the protection of pregnancy.

placenta also functions as an endocrine organ producing steroid and protein hormones for the protection of

26

1. Placental abruption: Premature separation of placenta from uterus (> 20w - before birth). A

1.

Placental abruption:

Premature separation of placenta from uterus (> 20w - before birth).

A significant cause of third-trimester bleeding associated with fetal + maternal morbidity & mortality.

Patients with this condition typically present with bleeding, uterine contractions & fetal distress.

Classification (class 0-III):

Based on extent of separation (partial vs. complete) & location of separation (marginal vs. central).

Etiology unknown!

Risk factors:

- Maternal hypertension (most common).

- Maternal trauma.

- Smoking.

- Drug abuse.

- Sudden decompression of uterus (premature rupture of membranes, birth of the first twin

- Chorioamnionitis.

- Previous placental abruption.

- Subchorionic hematoma.

27

Presentation:

One or more of the following (may be asymptomatic):

- Vaginal bleeding.

- Contractions.

- Abdominal tenderness (even uterine tetany).

- Decreased fetal movement.

- Idiopathic premature labor.

- Fetal death.

Diagnosis:

No digital examination on a bleeding pregnant patient!!!

Pelvic examination in placenta previa can produce profuse vaginal bleeding.

History of hypertension or any other risk factor.

Shocked (hypotensive), pregnant & obvious vaginal bleeding

may be placental abruption.

USG will show fetal movements, vital signs, location of placenta, bleeding.

External fetal monitor.

Blood test (CBC, clotting profile, BUN).

Management: not in emergency settings.

Continuous external fetal monitoring.

Fluid resuscitation (crystalloids or blood).

Vaginal delivery (preferred if fetus died).

C section: often necessary for fetal or maternal stabilization.

Hysterectomy: uncontrolled bleeding

last step after correction of coagulopathy, ligation of

the uterine artery, administration of uterotonics

Complications:

Hemorrhage into the decidua basalis, usually followed by vaginal bleeding.

Compromised fetal blood supply (due to compression).

Penetration of blood through the thickness of the uterine wall.

Uterine rupture.

Miscarriage.

Maternal hypovolemic shock.

Prognosis:

Class 0 - I good prognosis.

Class III fetal & maternal death may follow.

2.

Placenta Praevia

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A rare, obstetric complication in which the placenta is inserted partially / wholly in the lower uterine segment. Because of placental migration during pregnancy the diagnosis is made by USG, only > 34w.

A leading cause of antepartum hemorrhage (vaginal bleeding).

Classification:

Minor: in lower uterine segment, but does not cover the internal os.

Major: In lower uterine segment& covers the internal os.

Risk factors: uterine scars (previous C section, surgery, trauma, uterine cancer, infection), drug abuse, previous placenta previa, idiopathic.

Clinical presentation: often present with painless, bright red vaginal bleeding (usually ~32w). This bleeding often starts mildly & may increase as the area of placental separation increases.

Should be suspected if there is bleeding > 24w.

Diagnosis: USG (> 34w).

Treatment: depends on presentation and progression.

Any danger to fetus / mother

Emergency C section.

If no acute danger & bleeding stops

vaginal delivery possible & in major - elective C section.

Continue as a risk pregnancy until term & then: In minor -

Complications:

Maternal: Antepartum hemorrhage, Malpresentation, Abnormal placentation&Postpartum hemorrhage.

Increased risk of puerperal sepsis &postpartum hemorrhage because the lower segment, contracts less well postpartum.

Fetal: IUGR, Premature delivery&Death.

3. Placenta accrete/incretta/percretta See Question 13/B

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Triplet 5

5.A

Colpitis and vaginosis

Colpitis (Vaginitis): Inflammation of the vagina.

May result in abnormal discharge, itching, pain, often associated with an irritation / infection of the vulva, dyspareunia (pain during sex).

Usually due to infection.

1)

Bacterial vaginosis (BV): infection & Inflammation of the vagina.

Disturbance between normal flora & pathogens.

Risk factor for getting an STD & HIV.

Douching (washing the vagina), Sex & multiple sex partners increases the risk of BV.

Etiology unknown!

Clinical presentation: may by asymptomatic. Abnormal vaginal discharge, fish like odor, itching, burning during urination.

Diagnosis: clinical presentation + smear test.

Treatment: depending on test results / antibiotics (metronidazole / Clindamycin).

Complications: other superinfection / STD, premature labor, PID & infertility.

2)

Yeast infections:

usually by Candida albicans. Same as above.

Clinical manifestation: mainly itching & white, thick discharge that looks like cottage cheese.

Treatment: anti fungal ("azole" family), miconazole / fluconazole.

3)

Trichomoniasis (parasite, STD): same as above.

Treatment: metronidazole.

4)

Vaginal atrophy (atrophic (non infectious) vaginitis): same as above.

Vaginal sprays, douches, perfumed soaps, scented detergents & spermicidal products may cause an allergic reaction or irritate vulvar & vaginal tissues. Thinning of the vaginal lining a result of decreased hormone levels (estrogen) following menopause / surgical removal of your ovaries can also cause vaginal itching & burning.

Treatment: topical estrogen & avoid irritating factors.

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5.B

Life Cycle of a Woman

The 7 ages of women:

Intrauterine.

Neonatal (< 28 day).

Childhood (< puberty).

Adolescent (<18).

Fertile (< 45).

Climacterium, menopause (45 - 55).

Senium (> 55).

Intrauterine age:

Normal vs. abnormal (congenital abnormalities).

Genetic disorders Down, Edward, Patau, Triploidy, XO, XXY, XXX

).

Structural disorders congenital heart disease, NTD, abdominal wall defects, genitourinary abnormalities, lung disorders

Congenital infections Toxoplasmosis, Rubella, CMV, HSV, HIV, HCV, HBV, syphlilis

Prenatal diagnosis: Serological screening (triple test-AFP, HCG, estriol), USG (nuchal translucency), amniocentesis, chorionic villus sampling.

Neonatal age:

After birth hypoxia, Apgar score (max 10) skin color, muscle tone, response to stimulation.

Physical birth injury brachial plexus, facial nerve, skeletal, soft tissue, caput succedaneum, cephalic hematoma.

RDS (respiratory distress syndrome) by a deficiency of surfactant in lungs (premature).

Infections.

Surgical correction of fetal abnormalities.

Hyperbilirubinemia.

Diagnosis of metabolic disorders - Phenylketonuria, Congenital Hypothyroidism, Cystic Fibrosis (CF).

Childhood:

Development of skeleton, body, endocrinology.

31

Early diagnosis of genetic disorders & abnormal genital tract development.

Genitalia trauma.

Alien body in vagina.

Infections of vulva & vagina.

Violence (abuse) somatic & psychical.

Normal puberty (telarche, pubarche, menarche).

Adolescent growth spurt.

Acquisition of secondary sexual characteristics.

Onset of menstruation (menarche).

Establishment of ovulatory function.

Pathological puberty:

Precocious puberty signs of sexual maturation < 8 years.

Delayed puberty absence of physical manifestations of puberty by 13 years.

5.C

Birth shock

In the mother:

Postpartum Shock state due to complications.

In the newborn:

Transient depression of muscle tone & deep tendon reflexes in newborns after birth.

Usually lasts < 24 - 48 hours.

May happen in vaginal or cesarean deliveries.

Worldwide, 1 woman dies every minute, every day from a complication of pregnancy!

In developed countries, maternal death is uncommon.

Major causes of mortality:

1. Unexpected collapse

2. Amniotic fluid embolism.

3. Retained placenta.

4. Uterine inversion.

5. Uterine rupture.

6. Hemorrhage.

32

7.

Eclampsia.

8. Pulmonary embolism (PE).

Remember that there are often two lives at stake & in most emergencies minutes or even seconds count.

‘Resuscitate the mother & you will resuscitate the fetus’.

An obstetric emergency can cause profound lifelong psychological problems for both the mother & partner. This can manifest itself as postnatal depression, post-traumatic stress syndrome & fear of becoming pregnant.

The aim is to resuscitate the mother & then (and only then) to consider the welfare of the fetus.

4

H:

1.

Hypoxia,

2.

Hypovolemia,

3.

Hypo/hyperkalaemia,

4.

Hypothermia.

4

T:

1.

Thromboembolism,

2.

Toxic (including anesthesia),

3.

Tamponade,

4.

Tension pneumothorax.

Eclampsia (including magnesium toxicity).

Amniotic fluid embolus.

The decision for peri-mortem C section should be made by 4 minutes if there is no response to active resuscitation & the delivery by 5 minutes (the ‘4-minute rule’).

Amniotic fluid embolism:

One of the most catastrophic conditions that can occur in pregnancy (rare).

Etiology unknown:

Breakdown occurs in the barrier separating mother & fetus, allowing a bolus of amniotic fluid to enter the maternal circulation, moves to the pulmonary circulation & produces massive perfusion failure, bronchospasm & shock.

May be an anaphylactoid reaction to fetal antigens entering the maternal circulation.

Can occur at any time in pregnancy but it mostly occurs in labour, after vaginal delivery & following C section.

Risk factors:

- Multi-parity,

- placental abruption,

33

- intrauterine death,

- precipitate labour,

- termination of pregnancy,

- abdominal trauma,

- amniocentesis.

Clinical presentation:

 

o

Usually develops almost instantaneously & the diagnosis must be considered in all collapsed obstetric patients.

o

Some or all signs & symptoms.

o

Classically a woman in late stages of labour or immediately postpartum starts to gasp for air, starts fitting & may have a cardiac arrest.

o

There is often a profound disseminated intravascular coagulopathy (DIC) with massive hemorrhage, coma & death.

o

There are inevitably signs of fetal compromise.

o

Chills, Shivering, Sweating, Anxiety, Coughing, Cyanosis, Hypotension, Bronchospasm Tachypnoea, Tachycardia, Arrhythmias, Myocardial infarction, Seizures, DIC.

Diagnosis:

Autopsy.

In a surviving patient by finding fetal squames in washings from the bronchus or in a

sample of blood from the right ventricle. In the acute situation, as there is no single clinical or laboratory finding which can diagnose or exclude. The diagnosis is made clinically by exclusion.

Management:

This is primarily supportive & should be aggressive.

There is, however, no evidence that any specific type of intervention significantly improves

maternal prognosis. Initial therapy to support cardiac output & management of DIC.

If the woman is undelivered, an immediate C section, providing the mother can be stabilized.

A chest X-ray often show pulmonary edema & increase in right atrial + ventricular size

The ECG demonstrates right ventricular strain & there is metabolic acidosis.

Aggressive fluid replacement, maintenance of cardiac output with a dopamine infusion, treatment of anaphylaxis with adrenaline (epinephrine), salbutamol, aminophylline and hydrocortisone.

Treatment of DIC with fresh frozen plasma & cryoprecipitate treatment of hemorrhage after delivery with Syntocinon, ergometrine, carboprost (Haemabate) or misoprostol & uterine massage.

34

Prognosis:

Neonate: very poor, mortality rate ~ 60% & survivors usually suffer neurological impairment.

Maternal: outcome in mothers who have suffered a cardiac arrest is complicated by the fact that many are left with serious neurological impairment.

Venous thromboembolic disease:

In pregnancy the balance of the clotting system is altered towards clot formation.

Increased levels clotting factors & reduced levels of anticoagulants.

The gravid uterus causes a degree of mechanical obstruction to the venous system & leads to peripheral venous stasis in the lower limbs.

Venous thromboembolic disease is the commonest direct cause of maternal mortality in the UK (> 50% of deaths occur antenatally, mostly 1st trimester).

Thromboembolism may be asymptomatic but usually presents with symptoms of calf tenderness, cough & chest pain.

Essential to make a definitive diagnosis, not just for the current pregnancy but also for next pregnancies.

Hematological testing (blood test) for D-dimers is not helpful in pregnancy!

Doppler USG is particularly useful for identifying femoral veins.

It is safe and should be the first-line investigation.

X-ray venography is more specific (radiation exposure!).

Pregnancy is not a contraindication to chest X-ray and/or a ventilationperfusion scan any radiation risks are outweighed by the benefits of accurate diagnosis.

A normal scan virtually excludes the diagnosis of pulmonary embolism.

A CT pulmonary arteriogram (CTPA) may also be appropriate, especially if a large pulmonary embolism is suspected.

Treatment:

DVT or pulmonary embolism (PE) in pregnancy is with intravenous (i.v.) or subcutaneous (s.c.) heparin, continued into labour.

Continuing anticoagulation for 612 days.

Once anticoagulants are stopped, women should be screened for thrombophilias.

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Thromboembolic risk factors in pregnancy & postpartum:

Age > 35 years, Obesity (> 80 kg), 4th pregnancy or more, Gross varicose veins, Current infection, Pre-eclampsia, Immobility prior to surgery (> 4 days), Major current illness (heart or lung disease), cancer, inflammatory bowel disease, nephrotic syndrome, Caesarean section, particularly emergency caesarean section, Extended major pelvic or abdominal surgery (hysterectomy), Women with a personal or family history of deep vein thrombosis (DVT), pulmonary embolism (PE) or thrombophilia, paralysis of lower limbs, antiphospholipid antibody.

Breathlessness and syncopal episodes are present in 90% of normal pregnancies, atrial ectopic beats are common, and up to 96% of normal women may have an audible ejection systolic murmur.

Potential hemodynamic problems? A very close follow-up by a multidisciplinary team is mandatory and a careful plan should be made for delivery. Serious consideration of pregnancy termination is advisable in women with Eisenmenger’s syndrome, primary pulmonary hypertension, or pulmonary veno-occlusive disease.

With atrial fibrillation, anticoagulation is required to prevent atrial clot forming and subsequent embolic problems.

Severe cardiac disease can cause problems at delivery, particularly in those with prosthetic valves, aortic stenosis, severe mitral stenosis, left ventricular dysfunction, or pulmonary hypertension.

Cardiac disease and delivery Labour should be conducted in a high-dependency or intensive care unit, possibly with central venous catheter monitoring, aiming for a vaginal delivery.

Particular care is required in the immediate postpartum period as the increased circulating volume following uterine retraction may lead to fluid overload and congestive failure.

Myocardial infarction (MI) is rare in pregnancy but is the commonest cardiac cause of maternal mortality.

Peripartum cardiomyopathy (rare), associated with hypertension in pregnancy, multiple pregnancy, high multi-parity & increased age.

Presents with sudden onset of heart failure and on chest radiology or echocardiography - grossly dilated heart.

Retained placenta:

Failure to deliver the placenta within 30 minutes of delivery.