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FOCP > Women's health > Flashcards

Women's health Flashcards

1
Q

What is the classic presentation of placenta previa?

A

Painless vaginal bleeding in the third trimester. Bright red. Often stops spontanously

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2
Q

What is placenta praevia?

A

Abnormal placenta or covering of the cervical os

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3
Q

What are the types of placenta praevia?

A

Complete and marginal

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4
Q

What is the definition of complete placenta praevia?

A

Complete coverage of the cervical os by placenta

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5
Q

What is the defintion of marginal placenta praevia?

A

Leading edge of placenta is less than 2 cm from internal os, but not fully covering

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6
Q

What is the inherent risk of placenta praevia?

A

Haemorrhage

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7
Q

What causes the bleeding in the third trimester due to placenta pravia?

A

Develpent of lower uterine segment in third trimester, placental attachment is thinned in preparation of labour

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8
Q

What is the cause of placenta praevia?

A

Placental implantation is initiated by the embryo (embryonic plate) adhering in the lower (caudad) uterus. With placental attachment and growth, the developing placenta may cover the cervical os. However, it is thought that a defective decidual vascularization occurs over the cervix, possibly secondary to inflammatory or atrophic changes. As such, sections of the placenta having undergone atrophic changes could persist as a vasa previa.

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9
Q

What are the risk factors of placenta praevia?

A

Advancing maternal age, infertility treatment, previous c-section, multiparity, multiple gestation, short interpregnancy interval, previous uterine surgery or injury, previous or recurrent abortions, previous placentapraevia, nonwhite ethnicity, low socioeconomic status, smoking, cocaine use

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10
Q

What are the maternal complications of placenta praevia?

A

Haemorrhage, placental abruption, preterm delivery, post partum endometritis, mortality, septicemia, thrombophlebitis, need for hysterectomy

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11
Q

What are the fetal complications of placenta praevia?

A

Congenital malformations, low birth weight, SIDS, intrauterine growth restriction, jaundice, neonatal respiratory distress, abnormal foetal presentation, foetal anemia and Rh isoimmunization,

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12
Q

What should be aboided in patients with previous placenta praevia?

A

Decrease activity, avoid pelvic exam and intercourse maintain iron and folate,

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13
Q

What can be seen in the examination ofa patient with placenta praevia?

A

Haemorrhage, hypotension, tachycardia, soft, nontender uterus, normal foetal heart tones

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14
Q

What tests should be used to investigateplacenta pravia?

A

Rhcompatibility, fibrin split products, fibrinogen, PT aPTTT, FBC, blood type,

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15
Q

What imaging tests should be used to investigate placenta praevia>

A

US, transvaginal,, transabdominal, transperineal, translabial, MRI to plan pregnancy

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16
Q

How can haemorrhage be controlled during birth?

A

Oversewing the placental implantation site
Bilateral uterine artery ligation (O’Leary stitch)
Internal iliac artery ligation
Circular interrupted ligation around the lower uterine segment both above and below the transverse incision
Packing with gauze or tamponade with the Bakri balloon catheter
B-lynch stitch
Cesarean hysterectomy

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17
Q

What is placental abruption?

A

Premature separation of placenta from uterus

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18
Q

What does placental abruption usually present with?

A

Bleeding, uterine contractions, fetal distress, decreased foetal movement, abdominal or back pain, uterine tenderness, history of trauma, in second half of pregnancy

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19
Q

What are the complications of a placental abruption?

A

Haemorrhage into the decidua basalis, haematoma formation, separation of placenta from uterine wall, disruption of foetal blood flow, retroplacental blood in the peritoneal cavity, myometrium rupture

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20
Q

What is the classisification of placental abruption?

A

Class 0, 1, 2, 3

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21
Q

What are the characteristics of a class 0 placental abruption?

A

Asymp, diagnosis made after birth looking at organised blood clot in the placenta

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22
Q

What are the characteristics of a class 1 placental abruption?

A 
No vaginal bleeding to mild vaginal bleeding
Slightly tender uterus
Normal maternal BP and heart rate
No coagulopathy
No fetal distress
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23
Q

What are the characteristics of a class 1 placental abruption?

A

No vaginal bleeding to moderate vaginal bleeding
Moderate to severe uterine tenderness with possible tetanic contractions
Maternal tachycardia with orthostatic changes in BP and heart rate
Fetal distress
Hypofibrinogenemia (ie, 50-250 mg/dL)

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24
Q

What are the characteristics of a class 1 placental abruption?

A 
No vaginal bleeding to heavy vaginal bleeding
Very painful tetanic uterus
Maternal shock
Hypofibrinogenemia (ie, < 150 mg/dL)
Coagulopathy
Fetal death
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25
Q

Name 10 risk factors of placental abruption

A

High maternal age, low maternal age, smoking, cocaine use, alcohol, short placenta, maternal hypertension, retroplacental bleeding, idiopathic, retroplacental fibromyoma, male baby, maternal trauma, sudden decompression of uterus, previous placental abrubtion, prolonged rupture of membranes, low socioeconomic status

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26
Q

What are the signs of suspected foetal compromise?

A

Prolonged fetal bradycardia, repetitive, late decelrations, absence of foetal heart sounds, decreased short-term variability

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27
Q

What lab tests should be used to investigate placental abruption?

A

FBC, Fibrinogen, PT, aPTT, renal function tests, blood and Rh types, kleihuaer betke test

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28
Q

Why should renal function tests be done in patients with haemorrhage?

A

The hypovolemic condition brought on by a significant abruption also affects renal function.

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29
Q

Why should coagulation studies be done on patients with bleeding?

A

Can have disseminated intravascular coagulation

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30
Q

What is the kleihauer-betke test?

A

Finding foetal RBCs in maternal circulation, used for rH incompatible mothers

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31
Q

What imaging studies should be done on a patient with placental abruption?

A

US, non stress test,

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32
Q

What is the initial managemnt of placental abruption?

A

Continuous foetal monitoring, IV access, fluid resus, type and cross match blood, transfusion if needed, correct coagulopathy if present, give Rh immune globulin if necescary, corticosteroids for prem baby

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33
Q

When i vaginal delivery used for placental abruption

A

If foetal death has occurred due to placental abruption

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34
Q

What are the four classifications of hypertension in pregnancy?

A

Chronic hypertension preeclampsia -eclampsia, preeclampsia + chronic hypertension, transient hypertension of pregnancy

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35
Q

What is preclampsia?

A

Disorder of widespread vascular endothelial malfunction and vasospasm defined by hypertension and proteinuria

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36
Q

When can preeclampsia occur?

A

20 weeks gestation to 6 weeks post partum

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37
Q

What is the definition of preeclampsia?

A

BP >=140 mmhg or >=90mmhg, in two occasions, 4 hours apart or bp >= 160/110

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38
Q

What are the rf for preeclampsia?

A

Nulliparity, age over 40, black, chronic hypertension, renal disease, DM, BMI, twin gestation, antiphospholipid syndrome, family history antiotensinogen gene

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39
Q

What are the signs and symptoms of preeclampsia?

A

Headache, visual disturbances, altered mental status, dyspnea, oedema, weakness, malaise, clonus, blindness, epigastric or ruq abdo pain

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40
Q

What is eclampsia?

A

Seizures in a women with no other cause other than preeclampsia

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41
Q

What lab tests can be used to diagnose preeclampsia?

A

FBC, LFTs, uric acid, urine dipstic, US, cardiotocography

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42
Q

What is the management of severe preeclampsia?

A

Birth

Primary management is to stabilise Bp and prevent eclampsia (with the use of mg sulfate and aim for the delivery of the baby), fluid restriction (to prevent pulmonary oedema)

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43
Q

What is the criteria for delivery in preeclampsia?

A

Signs of foetal distress, ruptured membranes, uncontrollable BP, oligohydramnios, severe uterine growth restriction, severe oligouria, pulmonary oedema, severe serum creatinine, placental abruption, eclampsia, abdo tenderness, headache, low platelet count

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44
Q

What is the relationship between thromboembolism and pregnancy?

A

Pregnancy increases the risk of thromboembolism 4-5 times

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45
Q

What are the two manifestations of venous thromboembolisms?

A

DVT and PE

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46
Q

What are the complications of venous thromboembolisms

A

Pulmonary hypertension, post thrombotic syndrome, venous insufficiency

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47
Q

What tests are done in thromboembolisms and pregnancy?

A

Doppler US

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48
Q

How are thromboemnbolisms managed in pregnancy?

A

Low molecular weight Heparin

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49
Q

How does pregnancy cause thromboembolism

A

Hypercoagulability

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50
Q

What factors are increased in pregnancy (clotting cascade factors)

A

I, II, VII, VIII, IX, X

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51
Q

What is the definition of gestational diabetes?

A

Glucose intolerance with onset or first recognition in pregnancy

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52
Q

What tests are used for diagnosing DM in pregnancy?

A

Glucose challenge test, OGTT

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53
Q

What antenatal testing must be done in the first trimester for gestational DM?

A 
HbA1C
Blood urea nitrogen (BUN)
Serum creatinine
Thyroid-stimulating hormone
Free thyroxine levels
Spot urine protein-to-creatinine ratio
Capillary blood sugar levels
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54
Q

What antenatal testing must be done in the second trimester for gestational DM?

A

Spot urine protein-to-creatinine study in women with elevated value in first trimester
Repeat HbA1C
Capillary blood sugar levels

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55
Q

What antenatal imaging must be done for gestational DM?

A

First trimester - Ultrasonographic assessment for pregnancy dating and viability
Second trimester - Detailed anatomic ultrasonogram at 18-20 weeks and a fetal echocardiogram if the maternal glycohemoglobin value was elevated in the first trimester
Third trimester - Growth ultrasonogram to assess fetal size every 4-6 weeks from 26-36 weeks in women with overt preexisting diabetes; perform a growth ultrasonogram for fetal size at least once at 36-37 weeks for women with gestational diabetes mellitus

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56
Q

What is the management of gestational diabetes?

A

Diet, insulin, glyburide, metformin, prenatal obstertic management, management of neonate

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57
Q

What are the maternal complications of gestational diabetes?

A

Diabteic retinopathy, renal disease, hypertension

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58
Q

What are the foetal complications of gestational diabtes?

A

Miscarriage, birth defects, neural tube defects, cardiovascular defects, growthrestriction in t1D, obesity,high BW (marcrosomia), metabolic syndrome, SV rf, perinatal mortality, birth injury, resp problems,post natal hyperbilirubinaemia, resp problems, hypocalcemia

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59
Q

What are the rf for gestational diabetes?

A

Severe obesity, FH, PMH, glycosuria, polycystic ovarian syndrome

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60
Q

What is the rhesus factor?

A

RBC surface antigen

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61
Q

What is Rh incompatibility?

A

Women with Rh- blood is exposed to Rh+ blood and develops Rh antibodies

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62
Q

How can Rh incompatibility occur?

A

Exposure secondary to fetomaternal haemorrhage during pregnancy (Spontaneous or induced abortion, trauma, obstetric procedures, delivery), exposure duue to rh+blood transfusion

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63
Q

How long do Rh antibodies last once produced?

A

Forever

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64
Q

What can maternal Rh antibodies do to a fetus?

A

Haemolytic anaemia

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65
Q

Why are first borns usually not affected by Rh incompatibility?

A

Maternal Rh antibodies take a month to circulate after sensitization

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66
Q

What does sensitization refer to in rh incompatibility?

A

Exposure of Rh+ blood to Rh- mother that starts the production of Rh antibodies

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67
Q

What are the factors that affect the risk and severity of sensitization in Rh incompatibility?

A

Multiparity, volume of trnasplacental haemorrhage, extent of maternal immune response, concurrent presence of ABO incompatibility

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68
Q

What occurs in infants mildly affected by Rh incompatibility?

A

little to no anaemia, hyperbilirubinaemia

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69
Q

What occurs in infants moderately affected by Rh incompatibility?

A

Anaemia + hyperbilirubinaemia/jaundice

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70
Q

What occurs in infants severely affected by Rh incompatibility?

A

Kernicterus

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71
Q

What is kernicterus?

A

Neurological syndrome caused by deposition of bilirubin into CNS

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72
Q

What are the signs and symptoms of kernicterus?

A

Loss of moro reflex, posturing, poor feeding, inactivity, bulging fontanelles, high-pitched, shrill, cry, seizures

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73
Q

How long does kernicterus take to develop?

A

Several days after delivery

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74
Q

What are the complications of kernicterus?

A

Hypotonia, hearing loss, mental retardation

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75
Q

What is erythroblastosis fetalis?

A

Life threatening complication of Rh incompatibility in infants, characterised by hemolytic anemia and jaundice

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76
Q

What are the causes of Rh incompatibility (name 5)

A

Ectopic pregnancy placenta praevia, placental abruption, abdominal, pelvic trauma, lact of prenatal care, invasice obstetric procedures, spontaneous abortion, in utero feotal death

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77
Q

What tests are used to diagnose Rh incompatibility?

A

Rosette screening test, Kleihauer-Betke, determination of rh blood type

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78
Q

What are the postnatal tests done in Rh inncompatibility?

A

Examine cord blood for fetal blood type, Coomb test for antibiotic caused haemolytic anaemia, elevated serum bilirubin,

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79
Q

What is intrahepatic chlestasis of pregnancy?

A

Reversiblehormone influenced cholestasis developed in late pregnancy to genetically predisposed individuals

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80
Q

What is the pathophysiology of intrahepatic cholestasis o pregnancy>

A

Defect in excretion of bile salts > increased serum bile acids > deposited in skin > pruritus

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81
Q

What are the complications of intrahepatic cholestasis of pregnancy?

A

Pruritus, Sudden foetal death

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82
Q

What is usually done in intrahepatic cholestasis of pregnancy?

A

Induced birth

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83
Q

When is the preferred delivery time in intrahepatic cholestasis of pregnancy?

A

37 weeks

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84
Q

What is the typical presentation of intrahepatic cholestasis of pregnancy?

A

Pruritis, no rash, starts on sole of feet and palms progressint to trunk and face, worse at night. Steatorrhea, vit K deficiency, jaundice

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85
Q

What are the lab tests for intrahepatic cholestasis of pregnancy?

A

Serum bile acid, bilirubin, LFTs, cholic acid, chenodeoxycholic acid, transaminase, PT,PTT, INR

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86
Q

What medications are used to treat intrahepatic cholestasis of pregnancy?

A

Phenobarbitol, hydroxyzine, glutathione precursors, dexamethasone, cholestyramie, ursodeoxycholic acid, antihistamines

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87
Q

What is the defintion of breech presentation?

A

Foetus is in a longtitudinal lie withbuttocks or feet closest to cervix

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88
Q

Does increasing gestational age increase or decrease the incidence of breech presentation?

A

Decrease

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89
Q

What are the predisposing factors of breech presentation?

A

Prematurity, uterine malformation, fibroids, polyhydramnos, placenta previa, foetal abnormalties (CNS malformation, neck masses, aneuploidy), multiple gestations

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90
Q

What are the types of breech presentation?

A

Frank breech, comlete breech, footling

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91
Q

What is the definition of a frank breech?

A

Hips flexed, knees extended (pike position)

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92
Q

What is the defintion of a complete breech?

A

Hips and knees flexed (cannonball position)

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93
Q

What is the defintion of footling or incomplete breech presentation

A

One or both hips extended, foot presenting

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94
Q

What is the mort common type of breech?

A

Frank

ly my dear, I don’t give a damn

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95
Q

What are the types of vaginal breech delivery?

A

Spontaneous, assissted, total breech extraction

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96
Q

What is the most commpn type of vaginal breech delivery?

A

Assisted

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97
Q

What occurs in assisted breech delivery?

A

Infant spontanously delivers up till umbilicus, maneuvers are initiated to assit to deliver the rest of the baby

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98
Q

Whe is spontanous breech delivery used?

A

Preterm or nonviable deliveries

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99
Q

What occurs in total breech extraction?

A

Fetal feet are grasped, fetus is extracted

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100
Q

When is total breech extraction used?

A

For second twin

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101
Q

What are the complications of vaginal breech delivery?

A

Fetal head entrapment, nuchal arms, cervical spine injury, cord prolapse

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102
Q

What is the process for a vaginal breech delivery?

12 steps

A

Fetal membranes are left intact as long as possible, pinard maneuver to facilitate delivery of legs, no trction exerted on foetus til umbilicus is past the perinum, dry towl arounf infant;s hips to help traction, assistant applies transfundal pressure, once scapula is visible, rotate infant 90o and sweep ant. arm out of vagina by pressing on inner elbow, rotate babie 180o in reverse direction, get other arm out, rotate baby till back is anterior, fetal head should be maintained flexed, take baby out

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103
Q

WHat are the types of twins?

A

Monozygotic, dizygotic, [dichorionic, diamniotic], [monochorionic, diamniotic], [Monochorionic, monoamniotic]

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104
Q

What type of twins are dizygotic twins?

A

Dichorionic diamniotic

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105
Q

When must the egg split to create dichorionic, diamniotic monozygotic twins?

A

0-3 days aft fertilization

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106
Q

When must the egg split to create monochorionic, diamniotic monozygotic twins?

A

4-8 days aft fertilization

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107
Q

When must the egg split to create monochorionic, monoamniotic monozygotic twins?

A

8-12 days post fetilization

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108
Q

When must the egg split to create conjioned twins?

A

13 days aft. fertilization

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109
Q

What is the foetal complications of multifetal birth?

A

Prem, twin-twin transfusion sundrome, cerebral palsy, still birth, neonatal death

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110
Q

What is the maternal complications of multifetal birth?

A

Preterm labour, preterm premature rupture of membranes, PE, placental abruption, preeclampsia, postpartum haemorrhage

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111
Q

What is the most reliable test to detect multifoetal pregnancy?

A

Ultrasound

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112
Q

What is the definition of labour?

A

Physiological process during which fetus, membranes, umbilical cord and placenta are expelled from the uterus

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113
Q

How many stages of labour are there?

A

3

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114
Q

What does the first stage of labour begin and end with?

A

Regular uterine contractions and ends with complete cervical dilation at 10 cm

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115
Q

WHat is the first stage of labour devided into?

A

Latent and active phase

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116
Q

What occurs in the latent phase of the first stage of labour?

A

Mild, irregular uterine contractions that soften and chorten the cervix, contractions become more rhythmic and stronger

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117
Q

What occurs in the active phase of the first stage of labour?

A

starts with 3-4 cm of cervical dilation, characterized by rapid cervical dilation and decent of pr`esenting fetal part

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118
Q

What does the second stage of labour begin and end with?

A

Complete cervical dilation

ends with delivery of fetus

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119
Q

What is considered prolonged labour in a nulliparous woman?

A

> 3 hours w/ regional anaesthesia >2 hrs without anaesthesia

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120
Q

What is considered prolonged labour in a multiparous woman?

A

> 2 hours w/ regional anaesthesia >1 hrs without anaesthesia

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121
Q

What does the third stage of labour begin and end with?

A

Delivery of fetus

delivery of placenta and fetal membranes

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122
Q

What is considered prolonged for the third stage of labour?

A

> 30 min

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123
Q

How can the third stage of labour be actively managed?

A

Oxytoxin, prostaglandins, ergot alkaloids, cord clamping, cutting, controlled traction of umbilical cord

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124
Q

What are the seven steps in the mechanism of labour?

A 
Engagement
descent
flexion
internal rotation
extension
restitution and external rotation
expulsion
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125
Q

What management can be done in the first stage of labour?

A

Helping woman find a comfy position, periodic assessment of frequency and strength of contractions, changes in cervix and fetus station and position
Monitoring of HR

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126
Q

What management can be done in the second stage of labour?

A

Continuing observation, forceps, vacuum or c-section
Help mum find a comfy position
Episiotomy
Delivery maneuvers

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127
Q

What are the delivery maneouvers?

A

Head held in mid position till delivery, check fetus neck for wrapped umbilical cord, deliver ant. shoulder, help deliver post. shoulder, gentle traaction, cord cut, baby is stimulated then dried

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128
Q

What are the three signs that indicate that the placenta has seprated from the uterus?

A

Uterus contracts and rises, umbilical cord suddenly lengthens, gush of blood

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129
Q

What pain relief can be given to delivering mothers?

A

Meperidine, fentanyl, nalbuphine, butorphanol, morphine

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130
Q

What anaesthesia can be given to expectant mothers?

A

Epidural, spinal, combined

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131
Q

What is preterm labour?

A

Presence of uterine contractions of sufficient frequency and strength to effect progressive3 effacement and dilation of cervix prior to term gestation

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132
Q

What is the window of defintion of preterm labour?

A

20-27 weeks gestaation

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133
Q

What are the risks/causes of preterm labour?

A

Decidual haemorrhage, (abruption), uterine overdistention (multiple gestation, polyhydramnios), cervical incompetence (trauma, cone biopsy), uterine distortion, cervical inflammation, maternal inflammmation/fever, hormonal changes, uteroplacental insufficiency

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134
Q

what can cause uteroplacental inufficiency

A

Hypertension, insulin dependent diabetes, drug abuse, smoking, alcohol consumption

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135
Q

What can be done in a physical assessment for preterm labour?

A

Integrity of cervix with digital and speculum, cervical length (short cervical length is a warning sign)

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136
Q

What lab tests can be used for risk assessment of preterm labour/

A 
Rapid plasma reagin test
Gonorrheal and chlamydial screening
Vaginal pH/wet smear/whiff test
Anticardiolipin antibody (eg, anticardiolipin immunoglobulin [Ig] G and IgM, anti-beta2 microglobulin)
Lupus anticoagulant antibody
Activated partial thromboplastin time
One-hour glucose challenge test
TORCH
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137
Q

What medications can be used to manage preterm labour (or reduce the risk)

A

Progesterone reduces the risk, tocolytic agents can reduce contractions (mg sulphate, indomethacin, nifedipine)

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138
Q

What is shoulder dystocia?

A

One or both shoulders become impacted against the bones of the maternal pelvis, as shown in the image below

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139
Q

Why does shoulder dystocia occur?

A

Either the shoulder dimensions are too large or maternal pelvis is to narrow to permit shoulder rotation to oblique pelvis

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140
Q

What are the direct antenatal RF of shoulder dystocia?

A

PH, fetal macrosomia, diabtes, impaired glucose tolerance,

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141
Q

What are the rf of moacrosomia?

A

Excessive weight gain during pregnancy, maternal obesity, asymmetric accelerated fetal growth postterm pregnancy, parity,

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142
Q

What are the intrapartum rf for shoulder dystopia?

A

Precipiuous second stage (<20min) operative vaginaldelivery, prolonged second stage

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143
Q

What are the contraindications for management in shoulder dystocia ( and why)

A 
Fundal pressure (increases risk of permanant brachial plexus injury),
Strong lateral traction, head rotation beyond 90o
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144
Q

What fetal maneuvers can be used to treat shoulder dystocia>

A

Rubin, post-arm delivery, woods screw, cephalic replacement, shute forceps, cleidotomy

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145
Q

What maternal maneuvers can be used to treat shoulder dystocia?

A

McRoberts, ramp, lateral decubitis, all fours, suprapubic pressure, symphysiotomy

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146
Q

What are the complications of shoulder dystocia?

A

Postpartum haemorrhage, perineal laceration, neonatal claviacl fracture, fractured humurus, brachial plexus injury, neonatal hypoxic ischaemic encephalopathy, sudden fetal circulatory collapse

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147
Q

What is the definition of intrauterine growth restriction?

A

Conditions that cause the fetus to not achieve it’s genetically determined potential size

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148
Q

What are the maternal causes of intrauterine growth restriction?

A

Chronic hypertension, pregnancy associated hypertension, cyanotic HD, diabetes, hemoglobinopathies, autoimmune disease, protein calorie malnutrition, smoking, substaance abuse, uterine malformations, thrombophilias, prolonged high altitude exposure

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149
Q

What are the placental or umbilical causes of intrauterine growth restriction?

A

Placental abnormalities, twin to twin ttransfusion syndromes, chronic abruption, placenta praevia, cord abnormalities, abnormal cord insertion, multiple gestations

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150
Q

What is the pathophysiology of intrauterine growth restrictions?

A

Gas exchange and nutrient delivery to fetus isn’t suffiecient for it to thrive

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151
Q

What tests can be done to investigate intrauterine growth restriction?

A

Fetal karyotype, maternal serology for infectious processes, environmetal exposure history, US

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152
Q

What are the complications of IUGR?

A

C section, death, prematurity, compromise in labour, need for induced labour

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153
Q

What can cause increased mortality of fetuses in IUGR?

A

NEC, thrombocytopenia, temp instability, renal failure

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154
Q

How is IUGR screened for?

A

Fundal height from US

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155
Q

What is the definition of postterm pregnancy?

A

Extends after 42 weeks

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156
Q

WHat are the three management plans of postterm pregnancy?

A

Elective labour induction, expectant pregnancy management, antenatal testing

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157
Q

What are the fetal and neonatal risrks of postterm pregnancy?

A

SIDS, perinatal mortality, asphyzia, inttrauterne infection, meconium aspiration, neonatal acidaemia, low apgar scores, macrosomia, birth injury, prolonged labour, shoulder dystocia, cepahalopelvic disproportion, postmaturity

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158
Q

What are the maternal complications of postterm pregnancies?

A

Labor dystocia, perineal injury, c section, emotional impact, hamorrhage, enomyometritis

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159
Q

What is episiotomy?

A

Surgical incision of perineum performed to widen vaginal opening

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160
Q

What are the short-term benefits of episiotomy?

A

Ease of repair compared to spontaneous laceration, reduction of laceration, decreased postpartum pan

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161
Q

What are the long term benefits of episiotomy?

A

Prevents prolapse, sexual dysfunction, incontinence, asphyxiam cranial trauma, cerebral haemorrhage, shoulder dystoia

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162
Q

What are the complications of episiotomy?

A

Extension of severe perineal lacerations, dyspareunia, pelvic floor dysfunction

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163
Q

What are the indications for episiotomies?

A

difficult deliveries, delivery in nonreassuring fetal status, to avoid serious maternal laceration

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164
Q

What are the contraindications to episiotomy?

A

In vaginal delivery, need consent,, not in IBD and severe perineal malformations

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165
Q

What i the leading cause of maternal mortality?

A

Post-partum haemorrhage

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166
Q

What is the definition of postpartum haemorrhage?

A

Blood loss>500mL following vaginal delivery or >1000mL following c-section

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167
Q

What are the risk factors of postpartum haemorrhage?

A

Retained placenta, failure to progress during the second stage of labour, placenta accreta, lacerations, instrumental delivery, large for dates baby, hypertensive disorders, induction of labour, augmentation of labour with oxytocin, obesity, SNRIs

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168
Q

What are the causes of postpartum haemorrhage?

A

Tone, tissue, trauma, thrombosis

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169
Q

How can post partum haemorrhages be prevented?

A

Active management of the third stage of labour

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170
Q

What does the active management of labour entail?

A

Oxytocin upon delivery of baby
Early cord clamping anf cutting
gentle cord traction when uterus is well contracted

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171
Q

What are the presentation symptoms of postpartum haemorrhage?

A

Apart from MASSIVE BLOOD LOSS?

Hypovolaemic shock: Palpitations, tachycardia, dizziness, weakness, sweating, pallor, oligouria, collapse, ar hunger

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172
Q

What tests postpartum haemorrhage?

A

FBC, baseline coag, crossmatch thould be reflected

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173
Q

How is postpartum haemorrhage managed?

A

Fluid resus, blood transfusion, correct coagulation problem, management of underlying cause

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174
Q

What is the most common cause of postpartum infection after a vaginal delivery?

A

Local spread of colonized bacteria

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175
Q

What is the most common infection in the postpartum period?

A

endometritis

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176
Q

WHat are the postpartum infections? 8

A

Post-surgical wound infections, perineal cellulitis, mastitis, resp. complications from anaesthesia, retained products of conception, endometritis, UTIs, pelvic phlebitis

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177
Q

When are wound infections more common?

A

After c-sections

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178
Q

What are the risk factors of endometritis?

A

C-section, prolonged rupture of membranes, prolonger use of foetal monitering, anemia, lower ses

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179
Q

Where are the sources of bacteria in endometritis?

A

Bowel, cervix, vagina, perineum

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180
Q

What bactueria are the most common cause of postpartum wound infection?

A

Staph and strep

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181
Q

What are the risk factors of UTIs and GTIs after birth?

A

Duration of labour, use of internal monitoring devices, number of vaginal exams

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182
Q

What are the most common pathogens of GTIs?

A

Polymicrobial:

clostridium, E. coli, bacteroides

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183
Q

What is the most common cause of mastitis?

A

Bacteria spread from infant’s mouth or throat during breastfeeding

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184
Q

What is the most common causative agent in mastitis?

A

Stap. A

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185
Q

What can mastitis cause?

A

thrombosis

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186
Q

What are the causitive organisms of UTIs?

A

Klebsiella, proteus, enterobacter

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187
Q

WHat are the general risk factors of postpartum infections?

A

History of c-section, premature rupture of membranes, frequent cervical exam, internal foetal monitoring, preexisting infection, diabetes, nutritional status, obesity

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188
Q

What are the complications of postpartum infections?

A

Scarring, infertility sepsis, septic shock death

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189
Q

What are the signs of endometritis?

A

Lower abdo tenderness, adnexal and parametrial tenderness, temp elevation, scanty, odourless lochia, foul-smelling lochia

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190
Q

What are the signs of a wound infection?

A

Erythema, oedema, tenderness out of proportion with postpartum pain, discharge from site

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191
Q

What are the signs of mastitis?

A

tender, engorged, erythematous breasts, usually unilateral

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192
Q

What are the signs of septic pelvic thrombophlepitis?

A

palpable pelvic veins, tachycardia out of proportion to fever

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193
Q

What investigations can be done in postpartum infections?

A

FBC, electrolytes, blood culture, urinalysis, cervical or uterine cultures, lactate, wound cultures, coag studies

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194
Q

What imaging studies can be done for pelvic problems?

A

Pelvic US, contrast enhanced CT or MRI

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195
Q

WHat percent of women experience mood disturbance after pregnancy?

A

85

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196
Q

What hormonal factors are risk factors for postpartum depression?

A

Abnormally sensitive to hormanal changes, may develop symptoms when treated with exogenous estrogen or progesterone

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197
Q

What are the psychological rf for post partum depression?

A

Inadequate social support, maritial discord/dissatisfaction, recent negative life events, partner violence, employment

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198
Q

What are the biological rf for postpartum depression?

A

FH, PMH, gestational diabetes

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199
Q

When d the symptoms of postpartum blues peak?

A

4th-5th day after birth

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200
Q

How are postpartum blues treted?

A

With support and reassurance

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201
Q

What are the presentations of postpartum depression?

A

Depressed mood, tearfullness, anhedonia, loss of appetite, fatigue, insomnia, suicidal thoughts, intense sadness, anxiety, despair

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202
Q

When does postpartum depression develop?

A

first 3 postpartum months

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203
Q

How is postpartum depression treated?

A

SSRIs, SNRIs, TCAs

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204
Q

What is the most severe form of postpartum psychiatric illness?

A

Postpartum psychosis

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205
Q

How is most at risk of postpartum psychosis?

A

PMH, history of bipolar disorder

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206
Q

When does postpartum psychosis usually onset?

A

within 2 weeks

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207
Q

What are the symptoms of postpartum psychosis?

A

Manic episode, restlessness, insomnia, irritability, rapidly shifting mood, disorganized behaviour, delusions, hallucinations

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208
Q

What happens with a diagnosis of post-partum psychosis?

A

Psychiatric emergency, inpatient treatment

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209
Q

What is the management of psotpartum psychosis?

A

Mood stabilizer (carbamazepine, lithium, valpoic acid) with antipsychotic and benzo

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210
Q

What is an important consideration in the medical managemtn of postpartum psychosis?

A

Most medications will be secreted into breast milk

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211
Q

What is the definition of c section?

A

Delivery of foetus through surcical incisions in abdominal wall and uterine wall

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212
Q

What are the maternal indications of c-section?

A

Repeat c-section, obstructive lesions in ential tract, pelvic abnormailities, cardiac conditions

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213
Q

What are the foetal indications of c-section delivery?

A

Infection, dystocia, breech presentation, foetal distress, congential malformation, infection, prolonged acidaemia,

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214
Q

When is c-section done to benefit both mom and foetus

A

Labour is contraindicated, placenta praevia, placenta accreta, cephalopelvic disproportion

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215
Q

What ar the contraindications of c-section?

A

Maternal stuatus may be compromised, if foetus has an abnormality that is non compatible with life

216
Q

What is the preop management of c-section?

A

preop fasting of at least 2 hours from clear liquids, 8 hpurs from a meal, placement of IV line, infusion of IV fluids, foley catherer, external foetal monitor, preop antibiotc prohylaxis, evaluation by surgeon and anaesthesiologist

217
Q

What lab testin is done befor c-section?

A

FBC, blood type and screen cross match, screening for HIv, hep B, syphylis, coag studies, US

218
Q

What is the procedure of csection delivery? 6+1

A
  1. Laprotomy
  2. Hysterotomy
  3. foetal delivery
  4. Utrine repair
  5. Closure
  6. Contraception if requested
219
Q

What is the post-op management of c-section?

A

Routine assessment, monitoring of vital signs, palpation of fundus, IV fluids, analgesia, ambulation, breastfeeding commences, discharge on day 2-4, refrain from sexual intercoarse

220
Q

What are the complications of csection?

A

Increase in maternal mortality and morbidity, infection, thromboembolic problems, anaesthetic complications, surgical injury, uterine atony, delayed return of bowel function

221
Q

What are the indications for forceps delivery?

A

Prolonged second stage of labour, suspicion of immediate or potential foetal compromise, shortening second stage of labour benefit of the mother
foetal malposition breech vaginal delivery

222
Q

What are the prerequisites for forceps delivery?

A

Head must be engaged, cervix must be fully dilated, retracted, no disproportion between pelvic head and foetal head, membranes must be ruptured, patient must have adequate analgesia, adequate facilities,

223
Q

What are the contraindications of forceps delivery?

A

Contradication to vaginal delivery inability to consent, cervis is not fully dilated, inability to determine the presentation anf foetal head position, inadequate pelvic size,, cephalopelvic disproportion, absence of analgesia, inadequate facilities and staff, insufficient experienced operator

224
Q

How should the patient be prepared preop for forceps delivery?

A

Anaesthesia, lithotomy position

225
Q

What is the definition of an etopic pregnancy

A

Embryo implants outside the uterine cavity

226
Q

What are the risk factors of ectopic pregnancy

A

Low ses, age, pmh, fh, smoking, IUD

227
Q

What is the clinical presentation of ectopic pregnancies?

A

scanty, dark Abnormal vaginal bleeding, lower abdo pain, collapse, syncope, shoulder tip pain, amenorrhea

228
Q

What are the signs of an eectopic pregnacy?

A

Tachycardia, hypotension, collapse, abdominal and rebound tenderness, tender adnexum, cervical os is closed, uterus is smaller than expected

229
Q

How are ectopic pregnancies investigated?

A

Pregnancy test, Transvaginal US, quantitative serum HCG, laproscopy

230
Q

How is ectopic pregnancy managed?

A

Blood is cross matched, Anti D if needed, laproscopy, systemic single dose of methotrexate

231
Q

What is polycystic ovarian disease?

A

Diagnosis of exclusion made by irregular periods, Hirsutism, raised serum testosterone or signs on ultrasound

232
Q

What test is diagnostic for polycystic ovary?

A

Transvaginal US

233
Q

Whaat can be seen in polycystic ovaries in a transvaginal US?

A

Mutliple, small (2mm-8mm) follicles in an enlarged ovary

234
Q

WHat is tha pathophysiology of polycystic ovaries?

A

Disprdered (raised LH), peripheral insulin resistance w/ compensatory raised insulin leads to increased ovarian nd adrenal androgen production. This disrupts folliculogenesis, leading to excess small ovarian follicles and irregular or absent ovulation. Raised peripheral androgens cause hirsutism anf acne

235
Q

Whatare the clinical features of a patient with polycystic ovarian syndrome?

A

Obese, acne, hirsutism, oligomenorrhea/ amennorrhea, miscarriage

236
Q

What investigations can be done on a patient with polycystic ovaries

A

FSH (raised in ovarian failure) prolactic (prolactinoma), TSH, serum testosterone, transvaginal scan

237
Q

What are the complications of polycystic ovarian syndrome?

A

T2D, gestational D, endometrial cancer

238
Q

How is polycystic ovarian syndrome treated?

A

Diet advice, antiandrogens cyproterone acetate, spironolactone, metformin

239
Q

What are fibroids?

A

Benign tumours of the myometrium

240
Q

What are the types of fibroids?

A

Subserou polyp, subserous, intracavity polyp, intamural, mubmucosal, cervical

241
Q

What are the possible causes of fibroid growth?

A

Oestrogen and progesterone

242
Q

WHat are the clinial features of fibroids?

A

Menstrual problems: menorrhagia, intermenstrual loss, dysmenorrhea, increased urinary frequency, retention, hydronephrosis, reduced fertility, solic mass in pelvis or abdomen palpaple in exam

243
Q

When do fibroids often stop growing?

A

Menopause

244
Q

What can occur with fibroids an pregnancY?

A

Orem labour, malpresentation, transverse lie, obstructer labour, postpartum haemorrhage, red degenration

245
Q

What are the complications of fibroids?

A

torsion of pedunculated fibroid, red degenration, hyaline/cystic degenration, calcification, leiomyosarcoma

246
Q

What is the relationship between HRT and fibroids?

A

Continues fibroid growth aft menopause

247
Q

How are fibroids investigated?

A

US, MRI, la[rpscp[y, hysteroscopy, HB concentration

248
Q

How are fibroids treated?

A

Hysteroscopic surgery embolization

249
Q

What is hyperemesis gravidarum?

A

When nausea and vomiting in early pregnancy are so severe the cause dehrdation, weight loss or electrolyte imbalance

250
Q

How is hyperemesis gravidarum managed?

A

IV rehydration, antiemetics, thiamine, psychological support

251
Q

What is the definition of endometriosis?

A

Presence and growth or endometrium-like tissue outside the uterus

252
Q

Is endometriosis more or less common in nulliparous women?

A

More

253
Q

Where can endometriosis occur?

A

Pelvis, uterosacral ligaments, on or behind ovaries, umbilicus, abdo. ound scars, vagina, bladder, rectum, lungs

254
Q

What is an endometrioma and what does it look like?

A

Accumulted altered blood due to endometriosis that is dark brown and looks like a chocolate cyst Found in ovaries

255
Q

What can endometriosis cause?

A

Inflammation, progressive fibrosis, adhesions, frozen pelvis

256
Q

What is the possible cause of endometriosis?

A

Retrograde menstruation, metaplasia of coelomic cells

257
Q

What are the symptoms of endometriosis?

A

Chronic cyclical pelvic pain, dysmeorrhe before menstruation, subfertility, deep dyspareunia, pain on passing stool during menses, ,emstrual pronlems

258
Q

What are the symptoms of a ruptured chocolate cyst?

A

Acute pain

259
Q

What do cyclical haematuria, rectal bleeding or umbilical bleeding suggest?

A

Severe endometriosis

260
Q

What are the signs of endometriosis?

A

Tenderness, thickening behind uterus or in adnexa, retroverted and immobile uterus, retrovaginal node

261
Q

How can endometriosis be investigated?

A

Laproscopy, transvaginal US, MRI, serum cncer antigen

262
Q

What can be seen laproscopically that is indicative of endometriosis?

A

Active lesions- red vesicles or punctuate marks on peritoneum
Less active- White scars or brown spots
severe disease - extensive adhesions, endometriomata

263
Q

How is endometriosis treated?

A

drugs to surpress ovarian activity, analgesia, progestogens, GnRH analogs, combined oral contraceptive, laser or bipolar diathermy

264
Q

How do treatments for endometriosis work?

A

Either mimic pregnancy or mimic menopause

265
Q

What is the link between endometriosis and fertility?

A

More severe the endometriosis, the greater the chance of subfertility
Escision of ovariam endometrioma cysts improves fertility

266
Q

How are women with epilepsy counselled before becoming pregnant?

A

Seizure control with as few medications as possible at lowest dose, with folic acid supplementation

267
Q

What does of folic acid is given to espectant mothers with epilepsy?

A

5mg/day

268
Q

What epileptic medication must be avoided in pregnancy?

A

Sodium valproate

269
Q

What is sodium valproate associated with in terms of pregnancy?

A

Higher rate of congenital abnormalities, lower intelligence in children

270
Q

What seizure medication is best for expectant mothers?

A

Carbmezipine, iamotrigine

271
Q

What is a molar pregnancy?

A

Trophoblastic tissue, which normally invades into endometrium, proliferates more aggressively than usual. HCG is usually secreted in excess

272
Q

What is a hydatidiform mole?

A

Trophoblastic proliferation is localized and non-invasive

273
Q

What are the types of hydatidiform moles?

A

Complete and partial

274
Q

What is a complete mole?

A

Onr sperm fertilizes empty oocyte and undergoes mitosis. No foetal tissue, just a proliferation of swollen chorionic villi

275
Q

WHat is a partial mole

A

Two sperms in one oocyte, with variable evidence of a foetus

276
Q

What is a choriocarcinoma?

A

Matastasis from an invasive molar pregnancy

277
Q

What are the risk factors for molar pregnancies?

A

Extrees of age, asians

278
Q

What are the clinical fetues of molar pregnancies?

A

Heavy vaginal bleeding severe vomiting, large uterus, early pre-eclampsia, hyperthyroidism

279
Q

How are molar pregnancies investigated?

A

US, Highe serum hCG, histology

280
Q

What does an US of a molar pregnancy show?

A

Snowstorm

281
Q

What are the complications of molar pregnancies?

A

Recurrence, malignant trophoblastic disease

282
Q

hat is cervical ectropion?

A

When columnar epithelium of endocervix is visible as a red area around the os on the surfaceof the cervix

283
Q

What causes cervical ectropion?

A

Eversion of the cervix

284
Q

In whom are cervical ectropions common?

A

Pregnant, young, on the pill

285
Q

What is the clinical presentation of cevical ectropion?

A

Asymp, postcoital bleeding, vaginal discharge

286
Q

How are cervical ectropions treated?

A

Cryotherapy without anaesthetic

287
Q

WHat must be done before a cervical ectropion is treated?

A

A smear and colposcopy

288
Q

Why must a smear and colposcopy be done before a cervical ectropion is treated?

A

to exclude cervicalcancer

289
Q

What are cervical polyps?

A

Benign tumours in the endocervical epithelium

290
Q

WHo re cervical polyps most common in

A

age>40

291
Q

What are the sizes of cervial polyps?

A

<1 cm

292
Q

What ais the clinical presentation of cervical polyps?

A

intramenstrual bleeding or post coital bleeding

293
Q

How are cervical polyps treated?

A

Avulsed without anaesthetic

294
Q

What is pelvic inflammatory disease?

A

Salpingitis caused by an STI

295
Q

What are the risk factors for pelvic inflammatory disease?

A

Multiple partners, not using barrier contraception

296
Q

What is protective for pelvic inflammatory disease?

A

Combined oral contraceptive

297
Q

What can cause an asymp STI to spread into the pelvis?

A

Spontaneous, uterine instrumentation, laproscopy, dye test, intrauterine devices, miscarriage, complications of child bearth, descending infection

298
Q

What organisms can cause pelvic inflammatory disease?

A

Polymicrobial, chlamydia, gonococcus,

299
Q

What are the symptoms of pelvic inflammatory disease?

A

Asyp, subfertility, mestrual problems, bilateral lower abdo pain, abnormal vaginal bleeding or discharge, fever, cervical excitation,

300
Q

What are the signs of pelvic inflammatory isease>

A

tachycardia, high fever, lower abdo peritonism, bilateral adnexal tenderness, cervical excitation, pelvic mass (abscess)

301
Q

WHat investigations can be done for pelvic inflammatory disease?

A

Endocervical swabs, blood culture, FBC, CRP, perlvic US, laproscopy, fimbral biopsy

302
Q

What are the complications of pelvic inflammatory disease?

A

Abscess, pyoselpinx, tubal obstruction, subfertility, chronic pelvic infection, pelvic pain, ectopic pregnancy

303
Q

What are the signs and symptoms of chronic pelvic inflammatory disease?

A

Chronic pelvic pain, dysmenorrhea, deep dyspareunia, heavy and irregular menses, chronic vaginal discharge, subfertility, abdominal and adnexal tenderness, fixed retroverted uterus

304
Q

What can be seen in a transvaginal US in chroic pelvic inflammatory disease?

A

Fluid collections in fallopian tubes, surrounding adhesions

305
Q

What is the best diagnostic tool for chronic pelvic inflammatory disease?

A

Laproscopy

306
Q

How is chronic pelic inflammatory disease treated?

A

Anaelgesics and antibiotics
Adhesiolysis - cuts adhesions
Salpingectomy

307
Q

What can cause chronic pelvic inflammatory disease?

A

Improper treatment o acute pelvic inflammatory disease

308
Q

What are the causes of vaginal discharge?

A

Physiological, infection, trichomonas vaginitis, atrophic vaginitis, foreign body, malignancy

309
Q

What cause physiological vaginal discharge?

A

Increases around pregnancy and ovulation and due to combined oral pill. exposure of columnar epithelium in cercival eversion can cause this

310
Q

What are the most common vaginal infections?

A

Bacterial: candidiasis, chlamydia, gonorrhea, trichomonas vaginitis

311
Q

What causes atrophic vaginitis,?

A

Oestrogen deficiency before menarche, lactatio, aft menopause

312
Q

How is atrophic vaginitis treated?

A

Oestrogen cream, HRT,

313
Q

What are the common foreign bodies that can cause vaginal discharge?

A

Swabs after childbirth, retained tampons

314
Q

WHat does a non itchy, non offensive, clear vaginal discharge suggest?

A

Ectropion

315
Q

How is cervical ectropion treated?

A

Cryotherapy

316
Q

What does a non itchy, acidotic, fishy-smeling grey-whote vaginal dicharge suggest?

A

Bacterial vaginosis

317
Q

What does an itchy, red, non-offensive white vaginal discharge suggest?

A

Candiasis

318
Q

What does an itchy, grey-green, red, acidotic and offensive vaginal discharge suggest?

A

Trichomonas vaginitis

319
Q

What does a variable-pH, offensive, red-brown vaginal discharge suggest?

A

Malignancy

320
Q

How is bacterial vaginosis treated?

A

Antibiotics

321
Q

How is trichomonas treated?

A

Antibiotics

322
Q

How is vaginal candiasis treated?

A

Imidazoles

323
Q

What dies a acidotic, red clear vaginal discharge suggest?

A

Atrophic vaginitis

324
Q

What is the clinical presentation of the rupture of ovarian cysts?

A

Pain

325
Q

What causes the pain in ovarian cyst rupture?

A

Torsion, haemorrhage

326
Q

What are the side effects of ovulation induction?

A

Multiple pregnancy, breast and ovarian carcinoma, ovarian hyperstimulation syndrome

327
Q

What increases the risk of multiple pregnancy in ovulation stimulation?

A

Clomifene or gonadotrophins

328
Q

What is ovarian hyperstimulation syndrome?

A

Cloifene or gonadotrophins overstimulate the ovaries causing follicular enlargement

329
Q

What can be seen in severe cases of ovarian hyperstimulation syndrome?

A

Hypovolaemia, ascites, thromboembolsim, PE, electrolyte imbalance

330
Q

How is severe ovarian hyperstimulation treated?

A

Fluid resus, electrolyte monitoring, thrombolysis

331
Q

How is ovarian hyperstimulation syndrome prevented?

A

Using lowest does of gonadotrophin, cancellation of HCG

332
Q

How is ovulation induced?

A

Treatment of anovulation, lifestyle changes, gonadotrophin, climofene

333
Q

What is the definition of asoospermia

A

No sperm

Can be obstructive or non obstructive(testicular failure, fsh is high)

334
Q

WHat is oligospermia?

A

<20 million/mL

335
Q

What is severe oligospermia?

A

<5 illion/mL

336
Q

Whattis asthenospermia?

A

No or little motility

337
Q

What are the causes of abnormal/absent sperm relase?

A

Varioceole, idiopathuc, antisperm antiboies, drug exposure, infection, testicular abnormalities, obstruction, CF, congenital abnormailities, Kallmanns syndrome

338
Q

How is male subfertility investigated?

A

Sperm analysis

339
Q

How is oligospermia treated?

A

Intrauterine insemination

340
Q

How is severe oligospermia treated?

A

IVF

341
Q

How is azoopermia treated?

A

Investigation, karyotype, SPerm retriva and IVF

342
Q

What general advice is given for male subfertility?

A

Reduce drug exposure, lifestyle changes

343
Q

What drugs can cause male subfertility?

A

Alchohol, smoking, recreational, industrial solvents

344
Q

What are the causes of anovulation?

A

Ovarian failure, PCOS, hypothalamic hypogonadism, thyroid dysfunction, hyperprolactinaemia

345
Q

How is anaovulation investigated?

A

Mid-luteal progesterone, prolactin, fsh, Lh, testosterone, TSH levels, US,

346
Q

What is urinary stress incontinence?

A

Involuntary loss of urine when bladder exceeds max urethral pressure in absenceof detruser muscle contraction

347
Q

What are the causes of urinary stress incontinence?

A

Pregnancy, vaginal delivery, forceps, prolonged labour, obesity, age

348
Q

What is the pathophysiology of stress urinary incontinence?

A

Bladder neck slips below pelvic floor cause support is weak

349
Q

What are the symptoms of utodynamic stress incontinence?

A

Frequeny, urgency, psychological, affects QOL

350
Q

What are the signs of urodynamic stress incontinence

A

Cystoeole or urethrocoele with coughing

351
Q

What investigations can be done for urodynamic stress incontinence?

A

Urine dipstick, cystometry

352
Q

What is the onservative management of urodynamic incontinence?

A

Pelvic floor exercises

353
Q

What is the medical treatment of urinary stress incontinence?

A

Duloxetine, HRT, oestrogen supplimentation

354
Q

WHat are the surgical treatments for urinary stress inontinence?

A

mid-urethral sling rpocedures

355
Q

What is detrusor overactivity?

A

Involuntary detrusor contractions during filling phases that are either sponatneous or provoked

356
Q

What is the pathophysiology of detrusor overactivity?

A

Detrusor contraction is usually interpreted by the body as urgency, and if it happens enough, bladder will release

357
Q

What are the symptoms of detrusor overativity?

A

Urge incontinence, urgency, frequency, nocturia

358
Q

How is detrusor overactivity managed?

A

Reduce caffeine and fluid intake, bladder training, antimuscuranics, intravignal oestrogen (if vaginal atrophy is present), botox or sacral nerve stiulation.

359
Q

What are thr sims of antenatal care? 7

A

Detect and manage pre-existing maternal disorders that might afect pregnancy outcome
Prevent, or dectect and manage maternal and foetal compliacations of pregnancy
Detect congenital foetal problems if requested by the mother
Plan with the mother, the safest and most satisfacoty form of delivery
Educate about minor conditions of pregnancy and gove lifestyle advice

360
Q

When is the first appointment of pregnancy made?

A

9-11 weeks of gestation

361
Q

What is the purpose of the first appointment?

A

Screen for possible complcations, gestation of pregnancy is checked

362
Q

What occurs in the 12 week scan?

A

Gestation is confirmed, viability is assessed, multiple pregnacy is diagnosed, screening for chromosomal abnormalities

363
Q

Hos are chromosomal abnormailities screened for in the 12 week scan?

A

Nuchal translucency, beta-HCG, PAPPA

364
Q

What blood tests are done during antenatal checks?

A

FBC, serum antibodies, blood glucose level, syphilis, HIV and heps B screening, rubella immunity, rhesus status, blood type and cross match

365
Q

What other tests are done in antenatal appointments?

A

Urine dipstick, urine culture

366
Q

When is the anomoly scan?

A

20 weeks

367
Q

What are the antenatal visits?

A

16, 20, 25, 28, 34, 36, 38, 40, 41

368
Q

What happens at the 16 week check?

A

Results for screening tests for chromosonal abnormalities and booking blood tests ahould be specifically reviewd. alternatively triple test

369
Q

What happens at the 25 week check?

A

Nulliparous women, fundal height

370
Q

What happens on the 28 and 34 week check?

A

Fundal height is measured, FBC and antibodies are checked. Glucose levels test, anti-D given to rhesus- women

371
Q

What happens on the 31 week check?

A

Fundal height, blood tests from 28 weeks are reviewed

372
Q

What happens on the 36, 38 and 40 week check?

A

Fundal height, foetal lie, presentation

373
Q

What happens at the 41 week check?

A

Fundal height, foetal lie, presentation, membrane sweep i offered, indicuction of labour is offered

374
Q

What are the minor conditions of pregnacy?

A

Itching, symphyis pubis dysfunction, abdo pain, heartburn, backache, constipation, ankle oedema, leg cramps, carpal tunnel, vaginits tiredness

375
Q

What are the physiological changes in pregnancy?

A

Weight gain, genital tract, blod, cv system, lung changes, renal blood flow, glomerular filtration rates increase, reduced gut motility, delayed gastric emptying, constipation, thyroid enlargement

376
Q

What are the changes seen in the genital tract in pregnacy?

A

Uterues weight increases, muscle atrophy, increased blood flow an contractilitym cervix siftens, effaces in third trimester

377
Q

What are the changes in blood due to pregnancy?

A

Blood volume, red cell mass, WBC increase, HB decreases

378
Q

What are the changes seen in the CV system due to pregnancy?

A

Increased CO, reduced PR, BP falls mid pregnancy

379
Q

What are the changes seen in the lungs due to pregnancy?

A

Tidal volumee increases

380
Q

What is the definition of miscarriage?

A

Fetus dies or delivers dead before 24 weeks

381
Q

What is the definition of threatened miscarriage?

A

There is bleeding but the foetus is still alive, uterus is the expected size for dates and os is closed

382
Q

What is the definition of inevitable miscarriage?

A

Bleeding is heavy, fetus may be alive, cervical os is open. Miscarriage is about to occur

383
Q

What is the definition of incomplete miscarriage?

A

Some foetal parts have been passed, but Os is still open

384
Q

What is the definition of complete miscarriage?

A

All foetal tissue has been passed, Bleeding has been diminished. Uterus is no longer enlarged. Os is closed

385
Q

What is a septic miscarriage?

A

Contents of uterus are infected, causing endometritis. Vaginal loss is offensive, fever can be absent. Peritonism and abdo pain can occur

386
Q

What is a missed miscarriage?

A

Fetuss has not developped, or has died in utero

387
Q

What are the clinical features of a miscarriage?

A

Bleeding, Pain from uterine contractions, uterine size and state od os depending on type of miscarriage

388
Q

How are possible miscarriages investigated?

A

Early PAU, history, exam, urine pregnancy, US, FBC, rhesus group

389
Q

How are miscarriages managed?

A

Admission for ectopic pregnancies, resus or heavy bleeding Products of conception are removed by specum=lum and polyp forceps. Swabs, antiD

390
Q

What are the complications of miscarriage?

A

Sepsis, blood loss

391
Q

What is the definition of recurrent miscarriage?

A

Three or more miscarriages in suscession

392
Q

What are the causes of recurrent miscarriages?

A

Antiphospholipid antibodies, Chromosomal defects, anatomical factors, infection, obesity, PCOS, higher maternal age

393
Q

What is the most common vulval prblem?

A

Pruritis, soreness, burning, superficial dyspareunia

394
Q

What are the benign disorders of the vulva?

A

Lichen simplex, lichen planus, lichen scerosus

395
Q

What are the causes for pruritis vulvae?

A

Infections: candiasis, vulval warts, pubic lice, scabies

dermatological issues, neoplasia

396
Q

What us the classic presentation of lichen simplex?

A

Long history of pruritis and soreness, labia majora is thickened with hyper or hypo pigmentation

397
Q

What is the classic presentation of lichen planus>

A

Irritation with flat, papular, purplish lesions in the anogenital area, can affect hair, nails and mucus membranes

398
Q

What is the classic presentation of lichen scerosus?

A

Vulval epithelium is thin with loss og collagen. Associated with autoimmune stuff. pink white papules

399
Q

What are vulval pain syndromes?

A

Spontaneous genralized vulval pain

400
Q

When is vulval candiasis common?

A

Diabetics, pregnancy, antibiotic use, immunity is compromised

401
Q

What can cause infections in the vulva?

A

Herpes simplex, vulval warts, syphylis, donovanosis, candidiasis

402
Q

What can cause bartholin’s gland cyst?

A

Blockage of bartholin’s duct

403
Q

What does the bartholin’s gland do?

A

Secrete lubricant in anticipation of coitus

404
Q

What can commonly cause infection of the bartholin’s gland?

A

Staph or ecoli

405
Q

What is the presentation of a bartholin’s gland abscess?

A

Acutely painful, large, tender, red swelling/

406
Q

What is introtial damage?

A

Overtightening, incorrect apposition at perineal repair or extensive scar tissue presenting with su[perficial dysparaunia. Commonly after child birth.

407
Q

What are vaginal cysts?

A

Congenital cysts that arise in the vagina

408
Q

What are the appearance of vaginal cysts?

A

Smooth white appearamce, sometimes can be as large as a golf ball

409
Q

What is vaginal adenois?

A

When columnar epithelium is seen in the squamus cell epithelium of the vagina

410
Q

What is associated with vaginal adenosis?

A

Pregnant moms with diethylstilboestrol, genital tract abnormalities

411
Q

What is the risk with vaginal adenosis?

A

Can turn into malignancy?

412
Q

What are the two types of vulval intraepitheliulial neoplasia?

A

Caused by HP

Due to lichen simplex, causing lucjen sclerosis

413
Q

What is the most common type of vulval carcinomas?

A

Squamous cell epithelium

414
Q

What are thclinica features of vulval carcinoma?

A

Pruritis, bleeding, discharge, mass, can have late presentatio, ulcer or mass, enlarged inguinal lympnodes

415
Q

Where is a vulval carcinoma most likely to present?

A

Labia majora or clitoris

416
Q

What is a stage 1 vulval carcinoma?

A

Tumour <2 cm, no nodes involved

417
Q

What is a stage 2 vulval carcinoma?

A

Tumour > 2cm, no nodes involved

418
Q

What is a stage 3 vulval carcinoma?

A

Tumour has spread through to perineum, urethra, vagina or anus/ nodes on one side are affected

419
Q

What is a stage 4 vulval carcinoma?

A

Tumour is in rectum, bladder, bone or distant metastasis, and/or nodes are invlved bilaterally

420
Q

How is vulval carcinoma usually treated?

A

Wide ocal incision and groin lymphadectomy, preop, post op or palliative radiotherapy

421
Q

What is the most common genital tract carcinoma?

A

Endometrial cancer

422
Q

What is the mst common type of endometrial cancer?

A

Adenocarcinoma

423
Q

What is the biggest risk for endometrialcancer?

A

High ratio of oestrogen to progesterone

424
Q

What are the risk factors of endometrial cancers?

A

Exogenous eostrogen without progesterone, obesity, POCS, nulliparity, late menopause, ovarian granulosa cell tumours, tamoxifen, HTN and diabetes

425
Q

What is the premalignant disease of endometrial carcinoma?

A

Endometrial hyperplassia with atypia

426
Q

What are the clinical features of endometrial cancer?

A

Postmenopausal bleeding, irrguglar or intramenstual bleeding, cervical smear, atrophic vaginitis may co-exist

427
Q

What are stage 1(a,b,c) endometrial carcinomas?

A

Lesions confined to the uterus

a) in endometrium only
b) deepest invasion <0.5 of endometrial thickness
c) deepest invasion >0.5 of myometrial thickness

428
Q

What are stage 2 (a,b) endometrial cancers?

A

Lesions in cervix and uterus

a) in endocervical glands only
b) in cervical stroma

429
Q

What are stage 3 (a,b,c) endometrical cancers

A

Tumour invades through the uterus

a) invades the serosa and or adnexa and positive cytopogy
b) vaginalmets
c) pelvic or para aortic mets

430
Q

What are stage 4 (a,b) endometrical cancers

A

Further spread

a) in bowel and bladder
b) distant mets

431
Q

How are endometrial carcinomas investigated?

A

transvaginal US, endometrual biopsy, staging after hysterectomy

432
Q

How are endometrial carcinomas treated?

A

Hysterectomy and bilateral salpingectomy, peritoneal washing
Adjuvant treatment dependent on staging
Radio, chemo, progesterone

433
Q

Where is recurrence of endometrial cancers most likely?

A

Within three years in vagina

434
Q

What is the most common type of cervical carcinomas?

A

Squamous cell

435
Q

What is the premalignant condition of cervical cencers?

A

Cervical intraepithelial neoplasia

436
Q

What is the most common cause of cervical cancer?

A

HPV, immunosupression can increase spread

437
Q

What are the clinical features of a cervical cancer?

A

Can be asymp, postcoital bleedinf, IMB, PMB, offensive vaginal discharge, uraemia, haematuria, rectal bleeding, pain, visible ulcer or mass

438
Q

What are the characteristics of a stage 1 (ai, aii, bi, bii) cervical carcinomas?

A

Lsions confined to cervix,
ai) microinvasion <3mm from basement membrane, <7mm across, no lymp or vascular space involvement
aii) Invasion >3mm, <7mm across, <5mm deep
bi tumour sze <4cm
bii) invasion >4 cm

439
Q

What are the characteristics of cervical carcinomas of stage 2 (a,b)?

A

Invasion into vaginna, but not on the pelvic side wall

a) invasion of upper 2/3 of vagina but not parametrium
b) invasion of parametrium

440
Q

What are the characteristics of stage 3 cervical carcinomas?

A

Invasion of lower vaginal wall or pelvic wall, or causing ureteric obstruction

441
Q

What are the characteristics of stage 4 cervical carcinomas?

A

Invasion of bladder or rectal mucosa, or beyond the true pelvis

442
Q

How is cervical carcinoma investigated?

A

Biopsy of tumour, vaginal and rectal exam, colposcopu and MRI, FBC and Us and Es to check fitness for surgery

443
Q

What are the indicatiors for poor prognosisin cervical carcinomas?

A

LN involvement advanced clinical stage, large primary tumour, early recurrence

444
Q

What is the issue with ovarian cancer?

A

Silent nature of the carcinoma means that presentation tends to be late

445
Q

What is the most likely type of ovarian carcinoma?

A

epithelial

446
Q

What are the risk facotrs of epithelial cancers?

A

Number of ovulations: therefore, early menarchy, nulliparity, late menopause, lynch syndrome, braca genes

447
Q

What are protective factors of ovarian cancers?

A

Pregnancy, the pill, breastfeeding

448
Q

What are the clinical features of ovarian cancers?

A

tend to present in stage 3 or 4, with abdo distension, pain, abnormal bleeding, metastasisis symptoms, cachexia, abdo or pelvic mass, asites

449
Q

What are the characteristics of a stage 1 (a,b,c) ovarian cancer?

A

Disease macroscopically confined to ovaries
a) one ovary is affected, capsule is intact
b? both ovaries are affeted capsule is intact
c) one/both ovaries affected, capsule is not intact, or malignant cells in abdo cavity

450
Q

What are the characteristics of a stage 2 ovarrian carcinoma?

A

Disease is beyond the ovaries but confined to the pelvis

451
Q

What are the characteristics of a stage 3 ovarian carcinoma?

A

Disease is beyond the pelvis but is confined to the abdomen

omentum, small bowel and peritoneum are frequently involved

452
Q

What are the characteristics of a stage 4 ovarian carcinoma?

A

Disease is beyonf the abdomen, like lungs or liver

453
Q

How is ovarian carcinoma investigated?

A

US, tumour markers(ca 125- inflammation of pelvic peritoneum), Fbc, u and e, LFTs, car,

454
Q

How is ovarian carcinoma treated?

A

laprotomy (abdo hysterectome + bilat. salpingectomy, and removal of omentum), chemo, radio

455
Q

What is the pear index?

A

Measurement of the efficacy of contraception, risk of pregnancy per 100 woomen per year of using the given method

456
Q

What contraception is used for adolescents typically?

A

Combined oral pill with condom to prevent STIs

457
Q

What contraception is used for older women typically?

A

Oral contraceptive, IUDs, sterilization

458
Q

What are the types of hormonal contraceptives?

A

Progesterone pill, combined pill, IUS, patch or ring

459
Q

How does the combined pill?

A

Negative feedback on GnRH, inhibiting ovulation

460
Q

How is the combined pill taken?

A

Taken every day for 3 weeks, then one week without, having a withdrawal bleed

461
Q

How effective is the contraceptive pill?

A

0.2 PI

462
Q

What are the contraindications of the combined pill?

A

Venous thrombosis, stroke, IHD, HTN, igraine with aura, active breast/endometrial cancer, Pregnancy, thrombophilia, smokers>35, more than 15/day, BMI>40, diabetes w/ vascular complications, active/chronic liver disease

Smokers, chronic inflammatory disease, renal impairment, diabetes, age>40, breastfeeding, high BMI

463
Q

What are the side effects of progesterone?

A

Depression, PMS, bleeding, amenorrhea, acne, weight gain, reduced libido

464
Q

WHat are the common side effects of oestrogen?

A

Nausea headaches increased mucus, fluid retention and weight gain, occasionally HTN, breast tenderness and fullness, bleeding

465
Q

What are the complications of progesterone and oestrogen pills?

A

Venous thrombosis, MI, stroke, focal migraine, HTN, jaundice, liver, cervical amd brest cancer

466
Q

How does the progesterone only pill work?

A

Makes cervical mucus hostile to sperm

467
Q

What are the ide effects of progesterone pill?

A

Spotting, PMS, Mastalgia, weight gain, functional ovarian cysts

468
Q

What does the implant contain?

A

Progestrone

469
Q

Wheren are implants implanted?

A

Upper arm, subdermall, local anaesthetic

470
Q

What is the efficacy of implants?

A

<1 PI

471
Q

What are the side effect of the implant?

A

Irregular bleeding in the first year

472
Q

Does the implant significanantly affect fertility?

A

No

473
Q

What are the types of emergency contraception?

A

Morning after pill, IUD

474
Q

What is the morning after pill

A

Single doese (1.5mg) of progesterone levonorgestre, within 24 hours ideally (72 hours) after unprotected intercoarse

475
Q

What are the side effects of the morning after pill?

A

Vomitting, menstrual disturbances in the next cycle

476
Q

When is the IUD used?

A

72 hours aft unprotected sex (up to 5 days aft expected day of ovulation

477
Q

What are the types of barrier contraceptives?

A

Male condoms, female condoms, diaphragm, caps, spermicides

478
Q

What are the types of IUD?

A

Copper containing hormone containing

479
Q

How do copper IUDs work?

A

Copper ions are toxic to sperm, block implantation

480
Q

How do hormone containing devices work

A

Release progesterone

481
Q

What is the efficacy of IUDs?

A

0.5 PI

482
Q

What are the complications of IUDs?

A

Expulsion of IUD, pain, carvical shock, perforation of uterine wall, heavier or more painful micturition, ectopic pregnancy

483
Q

What are the contraindications of IUDs?

A

Endometrial or cervical cancer, undiagnosed vaginal bleeding, recent/active pelvic infecction, breast cancer, HIV, previous ectopic pregnancy, excessive menstrual loss, mutliple sex partners, young, nulliparous

484
Q

How are women sterilized?

A

Tubes compressed with clips, prevents egg and sperm meeting

485
Q

What is the efficacy of getting your tubes tied?

A

0.5 PI

486
Q

What are the grounds for abortion after 24 weeks in England?

A

Continuation of pregnancy would lead to greater risk for woman.
Termination will prevent grave physical or mental harm to woman, Child would suffer from severe handicaps

487
Q

What are the surgical methods of abortion>

A

Suction crettage, dilation and evacuation

488
Q

When is surgical cutterage used?

A

7-13 weeks

489
Q

When is dilation and evacuation used?

A

13 weeks

490
Q

What are the medical methods of abortion?

A

Mifepristone plus prostaglandin

491
Q

When is mifepristone used for abortion?

A

Less than 7 weeks, 7-9 weeks, 13-24 weeks aft 22 weeks for feticide

492
Q

What are the complications of abortions

A

Haemorrhage, infection, uterine porforation, cervical trauma, failure

493
Q

Wat is the definition of prolapse?

A

Descent if uterus and or vaginal walls within the vagina

494
Q

The laxity f which ligaments contributes to prolapse?

A

transverse cervical and uteroscacral ligaments

495
Q

The weakness of which muscles is contributing to prolapse?

A

Levator ani muscles

496
Q

What are the types of prolapse?

A

Uterus, post vaginal wall, ant vaginal wall

497
Q

What are the types of uterine prolapse?

A

1-3

498
Q

What happpens in 1st degree prolapse?

A

Cervix is still in vagina

499
Q

What happens in second degree uterine prolapse?

A

at introitus

500
Q

What happens in 3rd degree uterine prolapse?

A

Entire uterus comes out of vagina

501
Q

What are the types f ant. vaginal wall prolapses?

A

Cystocoele, urethrocoele

502
Q

What is a cystocoele?

A

Prolapse of bladder forming a bulge in ant vaginal wall

503
Q

What is a urethrocoele?

A

4 cm long urethra bulges in lower ant. wall

504
Q

What are th types of post vaginal wall prolapses?

A

Rectocoele, enterocoele

505
Q

What is an enterocoele?

A

Prolapse of pouch of douglas (peritoneal cavity) into post. vaginal wall, usually contains small bowe

506
Q

What is a rectocoele?

A

Prolapse of rectum forming a bulge in the middle of post. wall

507
Q

What are the causes of prolapse?

A

Weakened support of pelvic organs, increased strain on supports

508
Q

What causes weakened support of pelvic organs?

A

Vaginal delivery, pudendal nerve damage, mechanica damage, prolonged delivery, instrumental delivery, poor suturing or perineal tears, bearing down before full dilation, oestrogen deficiency, iatrogenic (aft hysterectomy), genetics

509
Q

What causes incresed strain on the supports?

A

Obesity, pelvic masses, chronic cough

510
Q

What are the symptoms of rolapse?

A

Dragging sensation, lump,worse at the end of daay or when standing up, ulceration, bleeding, urinary frequency, incomplete bladder emptying, stress incontinence,difficulty defaecation

511
Q

What does an examination of prolapse reveal?

A

Sims speculum to reveal prolapse

512
Q

What investigations should be doen on a patient with prolapse?

A

Pelvic ultrasound, cystometry

513
Q

How is prolapse managed?

A

Weight reduction, pessearies, surgical treatment

514
Q

WHat are the types of pessaries?

A

Shelf, ring

515
Q

What are the surgical treatments of prolapse?

A

Vaginal hysterectomy, sacrospinous colpopexy, tension free vaginal type, meshes

516
Q

What are the types of ovarian tumour like conditions?

A

Endometriotic cyst - endometriosis in ovaries, chocolate cyst
Functional cysts

517
Q

What are the types of ovarian cancer?

A

Epithelial tumour - cyst adenoma - clear = serous, murky = mucinous
Endometriod, clear cell carcinoma (from bladder) brenner tumour.
Germ cell - teratoma (younger ace group), dysgermimoma
Sex cord tumours - granulous a cell tumous, thecomas, fibromas

Secondary malignancy from breast and GI tract, krukenburg

518
Q

What is adenomyosis?

A

Presence of endometrial gland tissue on myometrium, at least 2-3 mm below the endometrial surface

519
Q

What are the causes of maternal collapse?

A

Sepsis

520
Q

What are the rf of maternal sepsis?

A

Obesity, diabetes, anaemia, vaginal discharge, PMH, immunocompromised, prolonged spontaneous rupture of membranes

521
Q

How is sepsis assessed in obstetrics?

A

Modified Early Obstetric Warning Score

522
Q

How is maternal sepsis managed?

A

Broad spectrum antibiotics, fluids, IV immunoglobulins ( staph and strep), delivery of baby

523
Q

What antibiotics can be used in pregnancy?

A

Co-amox, metronidazole, clindamycin, piperacillin-tazobactam, gentamicin.

524
Q

What is an amniotic fluid embolism?

A

Adverse reaction when amniotic fluid enters circulatory system

525
Q

When does an amniotic fluid embolism occur?

A

Birth, labour, vaginal or section, abortion, amniocentesis

526
Q

What are the symptoms of amniotic fluid embolism?

A

Cardiac arret, rapid resp failure: fetal compromise, vomiting, nausea, seizures, anxiety, swearing, shivering, discolouration
Haemorrhage
Renal failure

527
Q

How is amniotic fluid embolism investigated?

A

Obs, u and e, abg, ECG (lhf), ctg, PT, clotting

528
Q

How is amniotic fluid embolisms managed?

A

O2 therapy, ventilation. Pulmonary artery catheter, drugs to control Bp. Blood transfusions,

529
Q

What Is the treatment of cervicalIN!

A

Cutting diathermy under local anaesthetic

530
Q

What is the most common type of cervical cancer?

A

Squamous cell

531
Q

What is the most common cause of Cervical cancer?

A

HPV

532
Q

Why does obesity increase the risk of endometrial cancer?

A

Oestrogens are fat based

533
Q

What’s the commonest cause of post menopausal bleeding?

A

Atrophic vaginitis

534
Q

What are the types if ovulation disorders?

A

Hypothalamic pituitary failure, hypothalamic pituitary ovarian dysfunction, ovarian failure

535
Q

How is hypothalamic pituitary failure?

A

Anorexics

Advised to moderates exercise levels, increase BMI

536
Q

How is ovarian failure treated?

A

Donated egg

537
Q

How is ovarian reserve checked?

A

AMH (high indicates more)

FSH (low indicates more)

FOCP (12 decks)

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