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Phase 3a > OBG > Flashcards

OBG Flashcards

1
Q

WHAT ARE THE TWO TYPES OF OVARIAN CYST

A

FOLLICULAR

LUTEAL

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2
Q

WHAT ARE FOLLICULAR CYSTS

A

FUNCTIONAL CYSTS THAT OCCUR WITH HORMONAL CHANGES

THEY ARE ALWAYS SMALLER THAN 6CM

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3
Q

WHY DO FOLLICULAR CYSTS OCCUR

A

WHEN OVULATION DOESNT OCCUR AND THE FOLLICLE KEEPS GROWING

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4
Q

WHAT ARE THE TYPES OF LUTEAL CYSTS

A

GRANULOSA

THECA

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5
Q

WHAT ARE GRANULOSA CYSTS

A

FUNCTIONAL AND OF CORPUS LUTEUM

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6
Q

WHAT ARE THECA CYSTS

A

BAD ONLY OCCUR WITH HIGH LEVELS OF HCG AND ARE OFTEN ASSOCIATED WITH A HYDRATIFORM MOLE

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7
Q

HOW WOULD YOU INVESTIGATE A CYST

A

US

LAPROSCOPY

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8
Q

WHAT ARE SYMPTOMS OF AN OVARIAN CYSTS

A

USUALLY ASYMPTOMATIC UNLESS THEE IS TORSION OR RUPTURE

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9
Q

WHY DO GRANULOSA CYSTS HAVE DIFFERENT PRESENTATIONS TO MOST OTHER OVARIAN CYSTS

A

BECAUSE THEY COME FROM CORPUS LUTEUM THEY SECRETE POGESTERONE MIMIKING AN ECTOPIC PREGNANCY

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10
Q

WHAT ARE UTERINE FIBROIDS

A

BENIGN GROWTH OF UTERINE MUSCLE

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11
Q

WHAT ARE THE TYPES OF UTERINE FIBROID

A

SUBMUCUS

INTRAMURAL

SUBSEROUS

PEDUNCULATED

INTERLIGAMENTAL

PARASITIC

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12
Q

WHICH FIBROIDS CAN CAUSE ENLARGEMENT OF THE UTERUS

A

INTERMURAL

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13
Q

WHICH FIBROIDS CAUSE PAIN AS THEY GROW

A

SUBMUCOUS

PEDUNCULATED CCAN CAUSE PAIN IF THEY GET TWISTED

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14
Q

WHICH FIBROID TYPE ARE USUALLY ASYMPTOMATIC

A

SUBSEROUS

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15
Q

WHAT IS THE PRESENTATION OF FIBROIDS

A

HEAVY MENSES

NON TREATABLE ANAEMIA

DISCOMFORT ON PRESSURE

PAIN

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16
Q

HOW ARE FIBROIDS TREATED

A

ONLY IF SYMPTOMATIC

TREATED SURGICALLY VIA MYECTOMY OR HYSTERECTOMY

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17
Q

HOW DO YOU DIAGNOSE FIBROIDS

A

BI MANUAL PELVIC EXAM

US

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18
Q

WHAT IS A CHRONIC PELVIC INFECTION

A

WHEN AN ACUTE INFECTION ISNT TREATED AND PROGRESSES TO DILATATION AND OBSTRUCTION OF TUBES FORMING ADHESIONS

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19
Q

WHAT ARE THE SIGNS AND SYMPTOMS OF CHRONIC PELVIC INFECTION

A

CHRONIC PELVIC PAIN

CHRONIC PURULENT VAGINAL DISCHARGE

EPIMENORRHOEA

DYSMENORRHOEA

INFERTILITY

RETROVERTED UTEROUS

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20
Q

HOW WOULD YOU DIAGNOSE CHRONIC PELVIC INFECTION

A

SWABS

  • HIGH VAGINAL
  • ENDOCERVICLE

TRANSVAGINAL US

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21
Q

WHAT ARE TREATEMENT OPTIONS FOR CHRONIC PELVIC INFECTIONS

A

IVF + TUBAL REMOVAL

HISTORECTOMY AND PELVIC ORGAN CLEARENCE

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22
Q

WHAT % OF PREGNANT WOMEN ARE AFFECTED BY PYLEONEPHRITIS

A

1%

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23
Q

WHAT IS THE PRESENTATION OF A UTI

A

LOIN/ABDO PAIN

SUPRAPUBIC PAIN (CYSTITIS)

OFFENSIVE SMELLING URINE

FREQUENCY

URGENCY

HAEMATURIA

DYSURIA

FEVER/RIGORS

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24
Q

WHAT IS THE PRESENTATION OF UTI IN PREGNANCY

A

USUALLY ASYMPTOMIATIC

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25
Q

WHAT IS THE MOST COMMON PATHOGEN CAUSING UTI

A

E COLI (G -VE)

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26
Q

HOW WOULD YOU DIAGNOSE A UTI

A

MSU

DIPSTICK

CULTURES

BLOODS: CRP, ESR, ECC

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27
Q

WHEN IS TRIMETHOPRIM USED TO TREAT UTI

A

CYSTITIS IN 3RD TRIMESTER OR NON PREGNANT

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28
Q

WHAT ANTIBIOTICS ARE USED FOR CYSTITIS IN PREGNANCY

A

CEFALEXIN ALL THROUGHOUT PREGANCY

NUROFERONTOIN 1ST TRIMESTER

TRIMETHOPRIM 3RD TRIMESTER

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29
Q

WHAT ANTIBIOTICS ARE USED FOR PYLEONEPHRITIS IN PREGNANCY

A

CEFALEXIN

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30
Q

WHAT IS PELVIC CONGESTION

A

VASCULAR CONJESTION OF PELVIC ORGANS DUE TO VESSEL DILATATION CAUSING STASIS OF BLOOD

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31
Q

WHAT ARE THE SYMPTOMS OF PELVIC CONGESTION

A

PELVIC PAIN

PAIN OFTEN STARTING DURING OR AFTER PREGNANCY

DYSPYRUNEA

SYMPTOMS WORSE DUING MENSES

TENDERNESS AT ILLIAC FOSSA

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32
Q

HOW WOULD YOU INVESTIGATE FOR PELVIC CONGESTION

A

US

LAPROSCOPY

VENOGRAPHY (VERY INVASIVE AND UNPLESENT)

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33
Q

WHAT ARE TREATEMENTS FOR PELVIC CONGESTION

A

PROSTAGLANDINS

OOPHORECTOMY

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34
Q

WHAT IS PID

A

PELVIC INFLAMMATORY DISEASE IS A POLYMYCROBIAL DISEASE

USUALLY CAUSED BY INFECTION WITH CHAMYDIA OR GHONNOREA (OR BOTH)

USUALLY WITH ONE OTHER AEROBIC BACTERIA

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35
Q

HOW WOULD YOU DIAGNOSE PID

A

HIGH VAGINAL AND ENDOCERVICLE SWABS

BLOODS FOR ACUTE PHASE REACTANTS

TRANSVAGINAL SCAN

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36
Q

WHAT IS THE MANAGEMENT OF PID

A
  1. FLUIDS
  2. ANTIBIOTICS
  3. NSAID
  4. IUD/IUS REMOVAL
  5. IMMOBILIZATION UNTIL PAIN IS BETTER
  6. ABSTINENCE UNTIL INFECTION IS CLEARED
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37
Q

WHAT IS THE ANTIBIOTICS USED FOR CHAMYDIA

A

AZYTHROMYCIN

OR

DOXYCYLINE

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38
Q

WHAT IS THE ANTIBIOTIC USED FOR GONNOREA

A

CEFTRIAXONE (IM)

+

DOXYCYCLINE/AZYTHROMYCIN

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39
Q

WHAT IS THE ANTIBIOTIC USED FOR TRICHOMONIASIS

A

METRANIDOZOLE

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40
Q

WHAT ARE URETERIC CALICULI

A

AN ACCUMULATION OF EITHER

  • CALCIUM OXOLATE
  • STRIVATE
  • URIC ACID
  • CYSTINE
  • MIXURE OF ABOVE

IN THE BLADDER/URETER

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41
Q

WHY DOES DEHYDRATION PREDISPOSE YOU TO URETERIC CALICULI

A

LEADS TO SUPERSATURATION OF URINE

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42
Q

WHAT ARE THE THREE COMMON AREAS IN WHICH THE URETERIC CALICULI GET STUCK

A

PELVIC - URETERIC JUNCTION

PELVIC BRIM

VESICO URETERIC JUNCTION

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43
Q

WHAT IS THE PRESENTATION OF A URETERIC CALICULI

A

SUDDEN SEVERE URILATERAL PAIN GOING LOIN TO GROIN

RIGORS

DYSURIA

HAEMATURIA

RETENTION

N+V

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44
Q

HOW WOULD YOU DIAGNOSE URETERIC CALICULI

A

UINE DIPSTICK - HAEMATURIA

BLOODS - CALCIUM, PHOSPHATE, URATE

X RAY (US)

CT

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45
Q

A PATIENT IS SHOWN TO HAVE A STONE < 5MM WHAT IS THE MANAGEMENT?

A

WATCH AND WAIT

ENCOURAGE FLUIDS

SPONTANEOUS PASS

+ ANALGESIA (AND POTENTIALLY ABX)

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46
Q

A PATIENT IS SHOWN TO HAVE A STONE> 5MM WHAT IS THE MANAGEMENT?

A

TAMSULOSIN

SHOCKWAVE LITHOTRIPSY OR PERCUTANEOUS NEPHROLITHOMY

ANALGESIA

(POTENTIALLY ABX)

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47
Q

WHAT IS ADENOMYOSIS

A

ENTROMETRIAL CELLS GROWING INTO THE UTERINE WALLS

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48
Q

HOW DOES ADENOMYOSIS DIFFER FROM ENDOMETRIOSIS

A

ENDOMETRAL CELLS ONLY GROW INTO WALL

IN ENDOMETRIOSIS THEY GROW OUTSIDE UTERUS

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49
Q

WHAT ARE SYMPTOMS OF ADENOMYOSIS

A

HEAVY MENSES

ENLARGED UTERUS

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50
Q

HOW DO YOU DIAGNOSE ADENOMYOSIS

A

CLINICALLY AND US/MRI CAN GIVE AN IDEA BUT A HYSTERECTOMY AND MICROSCOPY OF TISSUE SAMPLE IS ONLY TRUE DIAGNOSIS

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51
Q

WHAT ARE TREATEMENTS FOR ADENOMYOSIS

A

COMBINED ORAL CONTRACEPTIVE

GnRH ANALOGUES

UTERINE ARTERY AMBOLIZATION

ENDOMETRIAL ABLASION

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52
Q

WHAT IS ENDOMETRIOSIS

A

PROLIFERATION OF THE ENDOMETRIUM IN SITES OTHER THAN UTERINE MUCOSA

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53
Q

WHAT ARE SYMPTOMS OF ENDOMETRIOSIS

A

PAIN

DYSPYRUNEA

DISMENNOREA

PAIN ON DEFICATION

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54
Q

WHAT SRE THE SIGNS OF ENDOMETRIOSIS

A

INFERTILITY

RETROVETRED UTERUS

ADENAXAL MASS

VAGINAL - RECTAL SEPTUM MASS

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55
Q

HOW WOULD YOU DIAGNOSE ENDOMETRIOSIS

A

BIMANUAL PELVIC EXAM + SIMULTANEOUS VAGINAL AND RECTAL EXAM

LAPROSCPY

COMBINED ORAL CONTRACEPTIVE CHALLENGE

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56
Q

WHAT ARE TREATEMENTS OF ENDOMETRIOSIS

A

COMBINED ORAL CONTRACEPTIVE

ANDROGENS (INCREASE PERIFERAL OESTROGEN CONVERSION)

GnRH ANALOGUES

SURGERY

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57
Q

WHAT ARE SIDE EFFECTS OF COC

A

BREAST TENDERNESS

FLUID RETENTION

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58
Q

WHAT ARE SIDE EFFECTS OF ANDROGENS

A

WEIGHT GAIN

XS HAIR

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59
Q

WHAT ARE SIDE EFFECTS OF GnRH ANALOGUES

A

MENOPAUSAL SYMPTOMS

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60
Q

WHAT IS INCONTENENCE

A

INVOLUNTARY LEAKAGE OF URINE AFFECTING SOCIAL LIFE AND HYGENE

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61
Q

WHAT ARE THE TWO TYPES OF INCONTENENCE

A

OVERACTIVE BLADDER

STRESS INCONTENANCE

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62
Q

DEFINE OVERACTIVE BLADDER

A

INVOLUNTARY AND FREQUENT BLADDER CONTRACTIONS

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63
Q

DEFINE STRESS INCONTENENCE

A

SPHINCTER WEAKNESS WHERE URINE IS PASSED ON INCREASED BLADDER PRESSURE

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64
Q

WHAT IS THE PRESENTATION OF INCONTENENCE

A

PASSING URINE WHEN SNEEZING OR COUGHING

SENSE OF URGENCY

NOCTURIA

KEY IN DOOR SYNDROME

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65
Q

HOW DO YOU DIAGNOSE INCONTENENCE

A

FREQUENCY VOLUME CHART

RESIDUAL URINE MEASUREMENT USING IN OUT CATHETER

E PAQ

CONTRAST CYSTOGRAM FOR STRESS INCONTENENCE

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66
Q

WHAT IS E PAQ

A

A QUESTIONAIRRE LOOKING AT URINARY, VAINAL, BOWEL AND SEXUAL SYMPTOMS

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67
Q

WHAT IS URODYNAMIC TESTING

A

ARTIFICIALLY FILLING BLADDER AND ASKING PATIENT TO COUGH TO MEASURE BLADDER PRESSURE

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68
Q

WHAT IS THE TREATEMENT FOR STRESS INCONTENENCE

A

LIFESTYLE

BLADDER TRAINING

SURGERY

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69
Q

WHAT ARE TREATEMENTS FOR OVERACTIVE BLADDER

A

LIFESTYLE

OXYBUTAMINE (ANTICHOLINERGIC)

BOTOX

CATHETERS

VAGINAL OESTROGEN

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70
Q

WHAT IS A FISTULA

A

AN ABNORMAL COMMUNICATION OF THE URETER AND VAGINA

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71
Q

WHAT CAN CAUSE A FISTULA

A

TRAUMA

C SECTION

NECROSIS

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72
Q
A
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73
Q
A
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74
Q
A
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75
Q

WHAT IS A UTEROVAGINAL PROLAPSE

A

WHEN THE UTERUS PARTIALLY OR COMPLETELY PROTRUDES FROM THE CERVIX INTO THE VAGINAL CANAL

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76
Q

DESCRIBE A PRIMARY UTEROAGINAL PROLAPSE

A

DESCENT OF CERVIX INTO THE VAGINA THROUGH OS

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77
Q

DECRIBE A SECONDARY VAGINAL PROLAPSE

A

DESCENT OF CERVIC TO THE INTEROITUS

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78
Q

DECRIBE A TERTIARY VAGINAL PROLAPSE

A

DECSENT OF CERVIX THROUGH INTEROITUS

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79
Q

DECRIBE A QUATERNARY/TOTAL VAGINAL PROLAPSE

A

MOST OF UTERUS OUTSIDE INTEROITUS

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80
Q

HOW WOULD YOU DIAGNOSE A UTEROVAGINAL PROLAPSE

A

SIMS SPECULUM

ULTRASOUND

POTENTIALLY MRI

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81
Q

WHAT IS THE TREATEMENT OF A UTEROVAGINAL PROLAPSE

A

REASURRANCE

TREAT SYMPTOMATICALLY

physio

RING / SELF PESSARY

SURGERY

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82
Q

WHAT IS A RETROCELE

A

A POSTERIOR VAGINAL WALL PROLAPSE WHERE THE RECTAL PASSAGE BULGES INTO THE VAGINAL CANAL

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83
Q

WHAT IS THE PRESENTATION OF A RETROCELE

A

DIFFICULT BOWEL MOVEMENTS

PRESSURE FELT ON RECTUM

FEELING OF INCOMPLETE VOIDING

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84
Q

WHAT IS THE TREATEMENT OF A RETROCELE

A

SURGERY

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85
Q

WHAT IS A CYSTOCELE

A

AN ANTERIOS VAGINAL WALL PROLAPSE WHERE BLADDER PRESSES ON ANTERIOR VAGINAL WALL

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86
Q

WHAT IS THE PRESENTATION OF A CYSTOCELE

A

HESITATION

FREQUENCY

RECURRANT UTI

INCOMPLETE VOIDING AND RETENTION

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87
Q

WHAT IS THE TREATEMENT FOR CYSTOCELE

A

PHYSIO

PRESSARY

TOPICAL VAGINAL OESTROGEN

SURGERY

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88
Q

HOW WOULD YOU DEFINE A MISCARRIGE

A

THE SPONTANEOUS DISCHARGE OF A GESTATIONAL SACK BEFORE THE FETUS IS VIABLE

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89
Q

WHAT PROPORTION OF PREGNANCIES END IN MISCARRIGE

A

50%

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90
Q

WHAT ARE THE TYPES OF MISCARRIGE

A

THREATNED

INEVITABLE SEPSIS

MISSED

SPONTANEOUS SECOND TRIMESTER

RECURRENT

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91
Q

WHAT IS A THREATNED MISCARRIGE

A

BLEEDING FROM GENITAL TRACT AT EARLIEST STAGES OF PREGNANCY BUT NO PRODUCTS OF CONCEPTION ARE DISCHARGED

CERVIX REMAINS CLOSED

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92
Q

WHAR IS AN INEVITABLE MISCARRIGE

A

THE CERVIX OPENS AND THE PRODUCTS OF CONCEPTION ARE DISCHARGED

CAN BE COMPLETE OR INCOMPLETE

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93
Q

WHAT ARE THE SIGNS OF AN INCOMPLETE MISCARRIGE

A

PROLONGED ABDOMINAL PAIN AND PV BLEEDING

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94
Q

WHAT IS A SEPSIS MISCARRIGE

A

INFECTION CAUSING EXPULSION OF PRODUCTS OF CONCEPTION

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95
Q

WHAT ARE THE SIGNS OF A SEPTIC MISCARRIGE

A

UTERINE TENDERNESS

PURULENT VAGINAL DISCHARGE

PYREXIA

ALSO OCCURS POST MISSCARRIGE

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96
Q

WHAT IS A MISSED MISSCARRIGE

A

AN EMPTY GESTATIONAL SAC BEING DISCHARGED

THERE WAS FAILURE TO DEVELOP AFTER 7 DAYS

OFTEN WOMEN DO NOT REALISE THEY MISCARRY - SIMILAR TO PERIOD

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97
Q

WHAT IS A SPONTANEOUS SECOND TRIMESTER LOSS

A

SPONTANEOUS MEMBRANE RUPTURE WITH CERVICALE DILATATION WILL CAUSE A MISSCARRIGE

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98
Q

WHAT ARE RECURRENT MISSCARRIGES

A

3 OR MORE

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99
Q

WHAT ARE COMMON CAUSES OF MISCARRIGE

A

GENETIC DISORDERS INCOMPATIBLE WITH LIFE

ENDOCRINE : DECREASED PROGESTERIONE FROM PLACENTA OR CORPUS LUTEUM

MATERNAL ILLNESS OR DRUG USE

CERVICLE INCOMPLETENCY

AUTO IMMUNE DISEASES

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100
Q

WHAT WOULD A SECOND TRIMESTER MISSCARRIGE BE LIKE

A

A RAPID DELIVARY WHICH IS OFTEN PAINLESS AND BLOODLESS

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101
Q

WHAT OFTEN CAUSES CERVIACLE INCOMPLETENCY

A

PRIOR TRAUMA TO CERVIX

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102
Q

HOW WOULD YOU INVESTIGATE A MISCARRIGE

A

VAGINAL EXAM TO CHECK DILATATION

VAGINAL SWABS

US - TRANSVAGINAL AND ABDOMINAL

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103
Q

WHAT IS THE MANAGEMENT OF A MISCARRIGE

A

GIVE PROSTAGLANDINS - MISOPRASTOL

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104
Q

WHAT DO PROSTAGLANDINS (MISOPRASTOL) DO

A

PROMOTE UTERINE CONTRACTION AND EXPULSION

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105
Q

WHAT IS THE MANAGEMENT OF A RHESUS NEGATIVE MISCARRIGE

A

GIVE MISOPROSTOL

GIVE ANTI D IMMUNOGLOBULINS WHEN FETAL GESTATION IS OVER 12W

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106
Q

WHEN WOULD YOU INTERVENE SURGICALLY IN MISCARRIGE

A

IF INCOMPLETE MISCARRIGE

OR ESPECIALLY PAINFUL

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107
Q

WHAT SHOULD YOU INVESTIGATE FOR IN RECURRANT MISCARRIGES

A

LUPUS

PCOS

KARYOTYPE TESTING

CERVICLE CLEARENCE

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108
Q

WHAT IS AN ECTOPIC PREGNANCY

A

WHEN A FERTILIZED EGG ATTACHES OUTSIDE OF UTERINE CAVITY

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109
Q

WHERE DO ECTOPIC PREGNANCYS OCCUR MOST OFTEN

A

FALLOPIAN TUBES

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110
Q

WHAT ARE THE RISK FACTORS FOR AN ECTOPIC PREGNANCY

A

IUD/IUS

PREV ECTOPIC PREGNANCY

SURGERY TO UTERINE TUBES

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111
Q

WHAT IS THE PRESENTATION OF AN ECTOPIC PREGNANCY

A

SUDDEN SEVERE UNILATERAL PAIN

SHOULDER TIP PAIN (DUE TO DIAPHRAGM IRRITATION)

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112
Q

HOW DO YOU DIAGNOSE AN ECTOPIC PREGNANCY

A

PREGNANCY TEST

SMALL UTERUS FOR GESTATION

US

LAPROSCOPY

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113
Q

HOW WOULD YOU TREAT AN ECTOPIC PREGNANCY

A

METHOTREXATE IF UNDER 3CM

LAPSROSCOIC REMOVAL

TUBAL REMOVAL

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114
Q

WHAT IS THE PROBLEM WITH USING METHOTREXATE IN MANAGING ECTOPIC PREGNANCIES

A

MAY BE UNSUCCESSFUL

MAY CAUSE RUPTURE

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115
Q

WHAT IS THE PATHOPHYSIOLOGY OF PCOS

A

INCREASED ANDROGEN

DECREASED FSH AND LH

ANDROGENS CONVERTED TO TESTOSTERONE PERIFERALLY

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116
Q

WHAT ARE THE CYST TYPE IF PCOS

A

COLLICULAR

HAULTED FOLLICULAR DEVELOPEMENT

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117
Q

WHAT INVESTIGATIONS ARE REQUIRED FOR PCOS

A

US

BLOODS:

  • LH NORMAL OR DECREASED
  • FHS NORMAL OR DECREASED
  • HIGH PROLACTIN!!!!
  • HIGH TESTOSTERONE
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118
Q

WHAT IS PCOS

A

THE PRESENCE OF MULTPILE CYSTS WITHIN THE OVARY ABD XS ANDROGEN PRODUCTON FROM OVARIES AND ADRENAL GLANDS

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119
Q

WHAT IS THE PRESENTATION OF PCOS

A

OVERWEIGHT AND DIFFICULTY LOOSING WEIGHT

HIRTUISM

INFERTILITY

ACNE

AMENORRHOE OR OLIGOMENNORHEA

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120
Q

HOW WOULD YOU TREAT PCOS

A

MENSES:

  • COC / CYCLICAL OESTROGEN
  • METFORMIN

FERTILITY

  • METFORMIN
  • CLOMIFENE
  • PREDNISOLONE
  • IVF

SPRIONOLACTONE

HAIR REMOVAL AND ACNE TREATEMENTS

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121
Q

HOW DOES SPIRONOLACTONE HELP IN PCOS

A

HAS ANTIANDROGEN PROPERTIES

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122
Q

HOW DOES METFORMIN HELP IN PCOS

A

HELS ASSOCIATED INSULIN RESISTANCE AND REGULATES MENSES BOTH ALSO AIDING FERTILITY

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123
Q

HOW DOES CLOMIFENE HELP IN PCOS

A

INDUCES OVARIES

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124
Q

WHY SHOULD YOU BE CAUTIOUS OF PROLONGED CLOMIFENE

A

INCREASES RISK OF OVERIAN CANCER

NO MORE THAN 6 CYCLES

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125
Q

HOW DOES PREDNISOLONE HELP IN PCOS

A

REVERSES CARCADIAM RYTHMN AND SUPPRESSES PITUITARY ACTH

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126
Q

WHAT IS ANDROGEN INSENSITIVITY SYNDROME

A

WHEN AN INDIVIDUAL HAS CELLS WITH LITTLE TO NO RESPONSE TO ANDROGENS

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127
Q

WHAT CAUSES OF ANDROGEN INSENSITVITY SYNDROME

A

A GENETIC FAULT CAUSING THE BODY TO NOT RESPOND TO TESTOSTERONE

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128
Q

WHAT IS THE PATHOPHYSIOLOGY OF ANDROGEN INSENSITIVITY SYNDROME

A

FETUS IS UNRESUPONSIVE TO TESTOSTERONE CAUSING A GENETICALLY MALE FETUS TO NOT BE ABLE TO DEVELOP THEIR MALE REPRODUCTIVE ORGANS PROPERLY AND SO WILL HAVE DISORDERS OF SECUAL DIFFERENTIATION

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129
Q

WHAT ARE THE TYPES OF ANDROGEN IINSENSITIVITY SYNDROME

A

MILD

PARTIAL

COMPLETE

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130
Q

DESCRIBE MILD ANDROGEN INSENSITIVITY SYNDROME

A

ABNORMAL MALE GENETALIA

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131
Q

DESCRIBE PARTIAL ANDROGEN INSENSITIVITY SYNDROME

A

ABNORMAL INTERNAL MALE REPRODUCTIVE ORGANS BUT EXTERNALLY ARE NORMAL

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132
Q

DESCRIBE COMPLETE ANDROGEN INSENSITIVITY SYNDROME

A

NORMAL EXTERNAL FEMALE GENETALIA

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133
Q

WHAT IS THE PRESENTATION OF ANDROGEN INSENSITIVITY SYNDROME

A

INFERTILITY

FROM SPERM DEFECTS TO FULL FEMALE GENETALIA

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134
Q

HOW WOULD YOU DIAGNOSE ANDROGEN INSENSITIVITY SYNDROME

A

KARYOTYPE

GENETIC TESTING FOR ANDROGEN RECEPTOR INSENSITIVITY MUTATIONS

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135
Q

HOW WOULD YOU MANAGE ANDROGEN INSENSITIVITY SYNDROME

A

SEX ASSIGNMENT

GENITOPLASTY

GONADECTOMY

HRT

COUNCELLING

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136
Q

WHAT IS AMENNORHEA

A

ABSENCE OF PERIODS

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137
Q

WHAT IS PRIMARY AMENNORHEA

A

ABSENCE OF MENSES BY 14-16

WITH NORMAL SECONDARY SEXUAL CHARACTERISTICS AND GROWTH

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138
Q

WHAT IS SECONDARY AMENNORHEA

A

PREVIOSULY HAVING MENSES

THEN ABSENCE OF MENSES FOR 6M OR OVER

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139
Q

WHAT ARE THE MAIN CAUSES OF PRIMARY AMENORHEA

A

TURNERS SYNDROME

VAGINAL AGENESIS

ANDROGEN INSENSITIVITY SYNDROME

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140
Q

WHAT ARE CAUSES OF SECONDARY AMENORRHEA

A

GONADOTROPHIN FAILURE CAUSED BY

  • ANOREXIA
  • KALLMANS
  • HYPOTHALAMIC PITUITARY DISEASE

OVARIAN FAILURE

  • PREM FAILURE OR RESISTENT OVARIAN FAILURE

ENDOCRINE

  • HYPOTHYROIDISM
  • CUSHINGS

ANDROGEN XS

  • CAH
  • GONADAL OR ADRENAL TUMOUR
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141
Q

WHAT INVESTIGATIONS ARE REQUIRED IN AMENNORHEA

A

BLOODS

  • FSH, LH, OESTROGEN, PROLACTIN, T3/T4, TSH

PIUTITARY MRI

OVARIAN BIOPSY

GENETIC TESTING

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142
Q

YOU ARE TESTING A PATIENT WITH SECONDARY AMENORHEA WHOS BLOODS COME BACK AS

HIGH FSH AND LH

WHAT DOES THIS INDICATE

A

OVARIAN FAILURE

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143
Q

YOU ARE TESTING A PATIENT WITH SECONDARY AMENORHEA WHOS BLOOS COME BACK AS

HIGH PROLACTIN

WHAT DOES THIS INDICATE

A

LACTATION

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144
Q

HOW DO WE MANAGE AMENNORHEA

A

TREAT ANY MANAGABLE CAUSES

HRT UNLESS RESISTANT OVARIAN SYNDROME

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145
Q

WHAT IS ATROPHIC VAGINITIS

A

THINNING OF VAGINAL WALLS

VAGINA BECOMING DRY AND INFLAMMED

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146
Q

WHAT CAUSES ATROPHIC VAGINITIS

A

FALLING OESTROGEN LEVELS

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147
Q

WHATS IS THE PRESENTATION OF ATROPHIC VAGINITIS

A

VAGINAL DRYNESS

VAGINAL BLEEDING AND DISHCHARGE

DYSPURUNEA

RECURRANT UTI

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148
Q

HOW WOULD YOU DIAGNOSE ATROPHIC VAGINITIS

A

SWABS TO RULE OUT INFECTION

SPECULUM

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149
Q

HOW WOULD YOU TREAT ATROPHIC VAGNITIS

A

LUBRICANT

EMMOLIANT

TOPICAL OESTROGEN

HRT

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150
Q

WHAT IS SUPERFICIAL DYSPYRUNEA

A

PAIN SURING SEX AT VAGINAL ENTRANCE / CANAL

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151
Q

WHAT ARE CAUSES OF SUPERFICIAL DYSPYRUNEA

A

INFECTIONS

INTROITUS NARROWING

ATROPHIC VAGINITIS

LICHEN SCLEROSIS

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152
Q

WHAT IS DEEP DYSPYRUNEA

A

PAIN DURING INTERCOURSE UPON DEEP PENETRATION FELT IN ABDOMEN

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153
Q

WHAT ARE CAUSES OF DEEP DYSPYRUNEA

A

PID

RETROVERTED UTERUS

OVARIAN PROLAPSE INTO POUCH OF DOUGLAS

ENDOMETRIOSIS

NEOPLASTIC DISEASE

POST OP SCARRING DUE TO DECREATED UTERINE MOTILITY

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154
Q

HOW WOULD YOU DEFINE THE MENAUPAUSE

A

CESATION OF MENSES FOR 12 MONTHS

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155
Q

WHAT IS THE AVERAGE AGE FOR STARTING MENAUPAUSE

A

51Y

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156
Q

HOW WOULD YOU DESCRIBE PERIMENAUPAUSE

A

THE PERIOD LEADING UPTO MENAUPAUSE CHARACTERISED BY IRREGULAR PERIODS AND MENAUPAUSAL SYMPTOMS

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157
Q

WHAT ARE SYPTOMS OF MENAUPASE / PERIMENAUPAUSE

A

HOT FLUSHES

MOOD SWINGS

UROGENITAL ATROPHY

DECREASED LIBIDO

VAGINAL DRYNESS

DRY ITCHY SKIN

DECREASED CONFIDENCE

JOINT AND MUSCLE PAIN

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158
Q

DESCRIBE THE PHYSIOLOGY OF MENAUPAUSE

A

DEACREASED EGGS SO DECREASED OESTROGEN

DECREASED OESTROGEN MEANS LESS NEGATIVE FEEDBACK OF PITUITARY MEANING LESS GnRH

HIGHER FSH LH CAUSING IRREGULAR MENSES

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159
Q

WHAT IS THE MANAGEMENT OF MENAUPAUSE

A

HRT

CLONIDINE

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160
Q

WHAT ARE THE TYPES OF HRT AND WHEN ARE THEY GIVEN

A

COMBINED

  • UTERUS

OESTROGEN ONLY

  • HYSTERECTOMY

CYCLICAL

  • ANY WOMAN STILL IN PERI MENAUPAUSE
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161
Q

WHY IS OESTROGEN ONLY HRT NOT GIVEN TO WOMEN WITH UTERUS

A

LACK OF PREOGESTERONE AND HIGH OESTROGEN WILL INCREASE ENDOMETRIAL PROLIFERATION INCREASING RISK OF CANCER

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162
Q

WHAT ARE CONS OF HRT

A

INCREASED RISK OF BREAST CANCER

INCREASED RISK OF CVD AND STROKE

INCREASED RISK OF VTE

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163
Q

WHAT ARE BREAST CANCER RISKS IN HRT

A

PROGESTERONE IS DRIVING FORCE

OESTROGEN ONLY IN BRACA

RISK REDUCES AFTER STOPPING

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164
Q

WHY IS TRANSDERMAL BETTER IN SOME GROUPS (AND WHICH)

A

HIGH VTE RISK GROUPS AS

PASSES FIRST PASS METABOLISM SO DOESNT AFFECT CLOTTING FACTORS

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165
Q

WHAT IS PREMATURE OVARIAN INSUFFICIENCY

A

PERI MENAUPAUSE UNDER 40 YEARS

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166
Q

HOW CAN YOU DIAGNOSE PREMATURE OVARIAN INSUFFICIENCY

A

TWO FSH TESTS 4 WEEKS APART

NO PERIOD IN 4 MONTHS

PREGNANCY TEST

PELVIC US

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167
Q

WHAT IS THE PRESENTATION OF PREMATURE OVARIAN INSUFFICIENCY

A

IRREGULAR AND MISSED PERIODS

MENAUPAUSAL SYMPTOMS

INFERTILITY

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168
Q

HOW DO YOU MANAGE PREMATURE OVARIAN INSUFFICIENCY

A

HRT

CALCIUM AND VIT D SUPPLIEMNTS

IVF

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169
Q

WHAT CAUSES PREMATURE OVARIAN INSUFFICIENCY

A

IDOPATHIC

ALSO

FRAGILE X OR TURNERS

ADDISONS

CHEMO

LOW FOLLICLE NUMBER

170
Q

CHAT ARE CERVICLE POLYPS

A

A BENIGN OR CANCEROUS GROWTH ON THE CERVIX

171
Q

WHAT IS THE PRESENTATION OF A CERVIACLE POLYP

A

INTERMENSTRUAL BLEEDING

BLEEDING DURING PREGNANCCY (ANTEPARTUM BLEEDING)

POST COITAL BLEEDING

WHITE/YELLOW DISCHARGE

172
Q

HOW DO YOU DIAGNOSE CERVICLE POLYPS

A

SPECULUM

COLPOSCOPY + BIOPSY

173
Q

HOW DO YOU TREAT CERVIACLE POLYPS

A

REMOVAL WITH RING FORCEPS AND CAUTERISATION

174
Q

WHAT IS A PRIMARY POST PARTUM HAEMORRAGE

A

BLEEDING FROM GENITAL TRACT

OVER 500ML

DURING DELIVARY OR WITHIN 24 HRS AFTERWARDS

175
Q

WHAT ARE CAUSES OF PRIMARY POST PARTUM HAEMORRAGE

A

THE 4 TS

TONE

  • Uterine atony from - prolonged labour - twins - multiparus

TISSUE

  • Retained placental tissue

THROMBIN

  • decreased thrombin from LMWH

TRAUMA

176
Q

WHAT BLOOD VOLUME CLASSES AS A MAJOR PRIMARY POST PARTUM HAEMORRAGE

A

1500ML +

177
Q

WHAT IS THE MOST COMMON CAUSE OF PRIMARY POST PARTUM HAEMORRAGE

A

(TISSUE) PLACENTAL SITE BLEEDING

178
Q

WHAT IS THE DEFINITION OF SECONDARY POST PARTUM HAEMORRAGE

A

ABNORMAL VAGINAL BLEEDING UPTO 6 WEEKS AFTER DELIVARY

179
Q

WHAT CAUSES SECONDARY POST PARTUM HAEMORRAGE

A

RETAINED PLACENTAL TISSUE

UTERINE INFECTION

TROPHOBLASTIC DISEASE

180
Q

WHAT ARE THE SIGNS OF A MILD SECONDARY POST PARTUM HAEMORRAGE

A

MILD BLEEDING

ASYMPTOMATIC

NON TENDER UTERUS

(NORMAL WOMAN BLEEDING MORE THAN SUPPOSED TO)

181
Q

WHAT ARE THE SIGNS OF A SEVERE SECONDARY POST PARTUM HAEMORRAGE

A

HEAVY BLEEDING

PAIN

FEVER + SIGNS OF INFECTION

182
Q

HOW WOULD YOU MANAGE A SEVERE SECONDARY POST PARTUM HAEMORRAGE

A

ABX (IV) EMPIRICAL THEN

BLOOD CULTURES, URYNALISIS AND SWABS TO CONFIRM ABX CHOICE

UTERINE CLEARENCE (SUREGRY)

183
Q

HOW WOULD YOU MANAGE A PRIMARY POST PARTUM HAEMORRAGE

A

FLUIDS

BLOODS

if placenta is retained : CONTROLLED CORD EXPULSION

if placenta is expulsed : OXYTOCIN > HARTMANS > ERGOMETRIN > PROSTAGLANDINS (MYSOPROSTOL) > BIMANUAL COMPRESSION > SURGERY

184
Q

HOW WOULD YOU MANAGE A MILD SECONDARY POST PARTUM HAEMORRAGE

A

OBSERVE AND MONITOR

185
Q

WHAT ARE THE CAUSES OF ANTEPARTUM HAEMORRAGE

A

CERVICAL LESIONS AND POLYPS (OR CANCERS)

VASA PREVIA

PLACENTA PREVIA

INFECTIONS

PLACENTAL HAEMORRAGE

186
Q

WHAT IS PLACENTA PREVIA

A

WHEN THE PLACENTA IS OVER THE OS IN THE THIRD TRIMESTER

187
Q

WHY CANT PLACENTA PREVIA BE DIAGNOSED BEFORE THE THIRD TRIMESTER

A

BECAUSE OFTEN ATTACHES LOW BUT AS UTERUS EXPANDS GOES UPWARDS NO LONGER BEING PREVIA

188
Q

HOW WOULD YOU DIAGNOSE PLACENTA PREVIA

A

US

189
Q

IN A SITUATION OF ANTEPARTUM HEAMORRAGE IN A PATIENT KNOWN TO HAVE PLACENTA PREVIA WHAT WOULD BE YOUR MANAGEMENT

A

SPECULUM

CTG

MONITOR BLEEDS

CHECK MATERNAL FBC

IF IN DISTRESS C SECTION

190
Q

IN A WOMAN WITH PLACENTA PREVIA HOW IS DELIVARY PREPARED FOR

A

MATCH MUMS BLOOD TYPE AND HAVE BLOODS READY

POSTPONE DELIVARY AT 37 WEEKS THEN C SECTION

191
Q

WHEN CAN VAGINAL DELIVARY BE ATTEMPTED IN A CASE OF PLACENTA PREVIA

A

IN GRADES I AND II OF PLACENTA PREVIA WHERE THE PLACENTA IS NOT DIRECTLY OVER THE OS

192
Q

WHAT IS A VAGINAL WALL HEAMATOMA

A

A POOLING OF BLOOD AT THE VAGINAL ENTRANCE, VAGINA, OR VULVA

193
Q

WHAT TYPES OF VAGINAL WALL HEAMATOMA ARE THERE

A

SUPERFICIAL

DEEP

194
Q

WHERE DO SUPERFICIAL VAGINAL HAEMATOMA OCCUR

A

BELOW THE INSERTION OF LEVATORI ANI DISTENDS HE PERINEUM

195
Q

WHAT IS THE PRESENTATION OF A SUPERFICIAL VAGINAL HAEMATOMA

A

PAIN

A VISIBLE BRUISE

196
Q

HOW DO YOU TREAT SUPERFICIAL HAEMATOMAS

A

DRAINING

VESSELS LIGATED AND COMPRESSED: ARTRIAL/VEINS

DRAIN INSERTED

197
Q

WHERE DO DEEP VAGINAL HAEMATOMAS OCCUR

A

DEEP TO INSERTION OF LEVATOR ANI AND WASNT VISIBLE EXTERNALLY

198
Q

WHAT IS THE PRESENTATION OF A DEEP VAGINAL WALL HAEMATOMA

A

CHRONIC PELVIC PAIN

URINARY RETENTION

UNEXPLAINED ANAEMIA

BULGING UPPER VAGINAL WALL

199
Q

WHAT COMMONLY CAUSES DEEP VAGINAL WALL HAEMATOMA

A

INSTRUMENTAL DELIVARIES

200
Q

HOW WOULD YOU DIAGNOSE A DEEP VAGINAL WALL HAEMATOMA

A

SPECULUM

US

201
Q

HOW WOULD YOU TREAT A DEEP VAGINAL WALL HAEMATOMA

A

DRAIN VIA INCISION

INSERT DRAIN

VAGINAL PACKING

CATHETER

ABX AND TRANSFUSION

202
Q

WHAT ARE THE TYPES OF PLACENTAL ATTACHEMENT

A

ACRETA (THROUGH ENDOTHELIUM)

INCRETA (TO MYOMETRIUM)

PERCRETA (TO SEROSA)

203
Q

HOW WOULD YOU DIAGNOSE PLACENTA ACCRETA

A

US

AT SECOND AND THIRD TRIMESTER

204
Q

WHAT IS THE DEFINITION OF A PLACENTAL HAEMORRAGE

A

SEPARATION OF PLACENTA FROM UTERINE WALL

205
Q

WHAT ARE THE TYPES OF PLACENTAL HAEMORRAGE

A

REVEALED

CONCEALED

CONCEALED AND REVEALED

206
Q

WHAT ARE THE SIGNS OF PLACENTAL ABRUPTION

A

PAIN

PV BLEEDS

HARD UTERUS

LONGITUDINAL LIE

207
Q

HOW WOULD YOU MANAGE A PLACENTA HAEMORRAGE

A

IV INSERT AND GIVE HEAMOCRIT

CLOTTING PROFILE

TRANSFUSIONS

CCG

?C SECTION

208
Q

WHAT ARE THE KEY DIFFERENCES ON PRESENTATION BETWEEN PLACENTA PREVIA AND A PLACENTAL ABRUPTION

A

PREVIA

PAINLESS BLEEDS

SOFT UTERUS

ABRUPTION

PAIN

HARD UTERUS

209
Q

HOW WOULD YOU TREAT A PLACENTAL ATTACHEMENT DISORDER

A

C SECTION OR IF NO DISTRESS INDUCE W SYNTOCIN

POST OP OXYTOCIN AND ANTIBIOTICS

REMOVAL OF PLACENTA EITHER SURGICALLY OR WITH METHOTREXATE

ARTERY LIGATION

210
Q

WHAT ARE COMPLICATIONS OF A PLACENTAL ABRUPTION

A

CLOT FORMS CAUSING SYSTEMIC INTRAVASCULAR COAGULATION

COUVELERE UTERUS

PPH

HYPOVULAEMIA CAUSING RENAL UBULAR NECROSIS

211
Q

WHAT IS UTERINE INVERSION

A

A RARE COMPLICATION WHERE THE UTERINE FUNDUS PROTRUDES THROUGH THE CERVIX

212
Q

WHEN IS UTERINE INVERSION LIKELY TO OCCUR

A

DURING PLACENTAL DELIVARY ESP IF PLACENTA IS ADHERENT OR FUNDAL

213
Q

WHAT ARE THE TYPES OF UTERINE NVERSION

A

INCOMPLETE: TO CERVICLE OS

INCOMPLETE: THROUGH THE CERVICAL OS

COMPLETE: VISIBLE OUTSIDE THE CERVIX AT THE INTEROITUS

COMPLETE: TOTALLY PROTRUDING AND CAN HAVE VAGINAL INVERSION

214
Q

WHAT IS THE PRESENTATION OF UTERINE INVERSION

A

SEVERE PAIN

VSIBLE UTERUS

PPH

SHOCK + BRADYCARDIA

215
Q

HOW DO YOU MANAGE UTERINE INVERSION

A

FLUIDS AND BLOODS

REPOSITION UTERUS MANUALLY

ASSESS IF SURGERY NEEDED / TAKE TO SURGERY

ABX

216
Q

WHAT ARE CERVIACLE EROSIONS

A

WHEN GLANUDLAR CELLS (USUALLY FOUND INSIDE CERVICAL CANAL) GROW ON THE NECK OF THE CERVIX

217
Q

WHAT CAUSES CERVICLE EROSIONS

A

HORMONAL CHANGES

THE PILL

PREGNANCY

218
Q

WHAT IS THE PRESENTATION OF CERVICLE EROSIONS

A

INTERMENSTURAL BLEEDS

PREGANCY BLEEDS

DYSPYRUNEA

POST COITAL BLEEDS

219
Q

HOW DO YOU DIAGNOSE CERVIACLE EROSIONS

A

COLPOSCOPY

220
Q

WHAT ARE TREATEMENTS FOR CERVIACLE EROSIONS

A

NO TREATEMENT UNLESS SYMPTOMATIC

CAUTERISATION

221
Q

WHAT IS VASA PREVIA

A

ONE OF THE BRANCHES OF THE UMBILLICAL VESSELS LIES OVER THE CERVIACLE

222
Q

WHY IS VASA PREVIA DANGEROUS

A

IF THERES ROM THE PRESSURE WILL CAUSE VESSELS TO BUST AND BABY TO BLEED AND DIE

223
Q

HOW DO YOU DIAGNOSE VASA PREVIA

A

US + DOPPLER

224
Q

HOW DO YOU MANAGE VASA PREVIA

A

A PLANNED C SECTION AT 35-36 WEEKS TO AVOID ROM

225
Q

WHAT IS THE HISTOLOGICAL TYPE OF ENDOMETRIAL CANCER

A

AN ADENOCARCINOMA

226
Q

WHAT ARE THE RISK FACTORS OF ENDOMETRIAL CANCERS

A

OBESITY

OESTROGEN ONLY HRT

DIABETES

LATE MENOPAUSE

227
Q

WHAT IS THE CARDINAL SIGN OF ENDOMETRIAL CANCER

A

POST MENOPAUSAL BLEEDING

228
Q

WHAT ARE THE OTHER SIGNS OF ENDOMETRIAL CANCER

A

BLOATING

BACK/LEG/PELVIC PAIN

TIERDNESS

NAUSEA

+ RED FLAGS

229
Q

HOW WOULD YOU INVESTIGATE FOR ENDOMETRIAL CANCER

A

VAGINAL EXAMINATION

TRANSVAGINAL US

ENDOMETRIAL BIOPSY

230
Q

WHAT IS THE TREATMENT FOR ENDOMETRIAL CANCER

A

HYSTERECTOMY

+/- PELVIC LYMPH NODES

RADIOTHERAPY

PROGESTERONE THERAPY (ONLY FOR INDIVIDUALS WHO CANT TOLERATE MORE)

231
Q

WHAT IS OLIGOHYDRAMNIOUS

A

LOW AMNIOTIC FLUID WITH AMNIOTIC FLUID INDEX

232
Q

WHAT ARE CAUSES OF OLIGOHYDRAMNIOUS

A

IMPAIRED PLACENTAL FUNCTION

RENAL ANGIOGENESIS

PREMATURE ROM

URINARY TRACT MALFORMATIONS

233
Q

WHAT ARE THE CONSEQUENCES OF OLIGOHYDRAMNIOUS

A

IUGR

PULMONARY HYPERTENSION

RDS

CLUBBED FOOT

WRY NECK

INCREASED RISK OF CORD COMPRESSION DURING CONTRACTIONS CAUSING HYPOXIA

234
Q

WHAT ARE TREATMENTS FOR OLIGOHYDRAMNIOUS

A

C SECTION AS SOON AS SAFE

235
Q

WHAT ARE THE TYPES OF MALPRESENTATION

A

FACE

BROW

OCCIPITO-POSTERIOR

OCCIPITO-ANTERIOR

TRANSVERSE

236
Q

DESCRIBE A FACE PRESENTATION

A

FETAL HEAD IS HYPEREXTENDED SO FACE IS PRESETING

237
Q

HOW WOULD YOU DESCRIBE A BROW PRESENTATION

A

THE FETAL HEAD IS MIDWAY BETWEEN FLEXED VERTEX AND FACE

THE MOST UNFAVOURABLE POSITION

238
Q

DESCRIBE AN OCCIPITO-POSTERIOR PRESENTATION

A

A MALPRESENTATION OF FETAL HEAD OF -20% OF ALL CEPHALIC PRESENTATIONS

ASSOCIATED WITH BACK PAIN AND A LONG PAINFUL LABOUR

239
Q

WHAT IS DEEP TRANSVERSE ARREST

A

A HALT DURING THE NORMAL ROTATION MEANING HEAD IS OCCIPITO-TRANSVERSE

240
Q

WHAT ARE THE STAGES OF NORMAL FETAL HEAD ROTATION

A

DESCENT

ENGAGEMENT

NECK FLEXION

INTERNAL ROATION: OP>OT>OA

CROWNING

EXTENSION OF PRESENTING PART

RESITITUTION

INTERNAL ROTATION

LATERAL FLEXION

241
Q

HOW DO YOU ASSESS PRESENTATIONS

A

PALPATE LIE

PALPATE LOWER UTERUS AND BALLOT

ASSESS ENGAGEMENT

242
Q

HOW DO YOU MANAGE MALPRESENTATIONS

A

C SECTION

243
Q

WHAT IS A CORD PROLAPSE

A

OCCURS WHEN ANY PART OF THE CORD LIES ALONGSIDEOR INFRONT OF THE PRESENTING PART OF THE BODY

244
Q

WHAT ARE RISK FACTORS OF CORD PROLAPSE

A

DISPLACEMENT OF THE PRESENTING PART

IRREGULAR SURFACE OF PRESENTING PART (IE NOT HEAD) CAUSING POOR MOULDING

ARM

245
Q

HOW DO YOU MANAGE A CORD PROLAPSE

A

KNEES TO CHEST

FILL BRADDER

DIGITAL DISPLACEMENT OF CORD AND PUT WARM PAD AT VAGINAL OPENING

C SECION ASAP UNLESS THERES NO TIME THEN INSTRUMENTAL

246
Q

WHAT IS OBSTRUCTED LABOUR

A

WHEN THERE IS NORMAL UTERINE CONTRACTION BUT DELAYS IN LABOUR DUE TO CHILD BEING PHYSIOLOGICALLY BLOCKED

247
Q

WHAT IS THE MOST COMMON CAUSE OF OBTRUCTED LABOUR

A

CEPHALOPELVIC DISPROPORTION

248
Q

WHY MIGHT THERE BE CEPHALOPELVIC DISPROPORTION

A

MACROSOMIA

SMALL PELVIT INLET

249
Q

WHEN IS IT OKAY TO TRY PV DELIVARY IN CEPHALOPELVIC DISPROPORTION

A

WHEN THERES GOOD MOULDING

(CHECK AT ISCHEAL SPINES)

250
Q

WHAT IS THE MANAGEMENT OF OBSTRUCTED LABOUR

A
251
Q

HOW LONG SHOULD LABOUR LAST IN A NULLIPARUS WOMAN

A

LATENT = HRS - DAYS

ACTIVE S1 = 8-18HRS

ACTIVE S2=5-12HRS

252
Q

HOW LONG SHOULD LABOUR LAST IN A MULTIPARUS WOMAN

A

LATENT= HRS - DAYS

ACTIVE S1= 0-3HRS

ACTIVE S2= 0-2HRS

253
Q

DEFINE WHAT A LATENT STAGE IS

A

CEVIX < 4CM

IRREGULAR WEAK CONTRACTIONS (1/10)

EACH CONTRACTION LASTING APROX 30S

254
Q

WHAT IS THE DEFINITION OF ACTIVE LABOUR

A

CERVIX AT 4-10CM

REGULAR STRONG CONTRACTIONS (3/10)

EACH CONTRACTION LASTING 90S

255
Q

WHAT ARE THE STAGES OF LABOUR

A

STAGE 1- LATENT AND ACTIVE PHASE

STAGE2-PUSHING BABY

STAGE3-DELIVERING PLACENTA

STAGE 4-UTERINE INVOLUTION

256
Q

WHAT TYPE OF CANCER IS CERVICLE CANCER

A

SQUAMOUS CELL CARCINOMA

257
Q

WHAT IS THE MOST COMMON CANCER IN WOMEN UNDER 30

A

CERVICEL CANCER

258
Q

WHAT CAUSES CERVICLE CANCER AND WHY?

A

HPV

HAS E6+7 RECEPTORS BLOCKING TUMOUR MARKERS P53 AND RB RESPECTIVELY

259
Q

WHAT TEST IS USED TO SCREEN FOR CERVICLE CANCER AND DESCRIBE IT

A

SMEAR TEST

COLLECTS CELLS AT OPENING OF CERVIX (TRANSFORMATION ZONE) DETECTING PRECANCEROUS CELLS

DONE EVER 3 YEARS AGES 25-49Y

AND AFTER 50 EVERY 5 Y

260
Q

HOW DO YOU TREAT CERVICLE CANCER

A

LLETZ LOOPS

HYSTERECTOMY

TUMOURS >4CM NEED CHEMO AND RADIO

261
Q

WHAT TYPE OF CANCER IS OVARIAN CANCER

A

EPITHELIAL CELL CARCINOMA

262
Q

WHAT ARE SX OF OVERIAN CARCINOMA

A

ASYMPTOMATIC (SX VERY GENERIC AND MIMIC OTHER THINGS)

  • IBS LIKE
  • URINARY FREQUENCY
  • ABDO PAIN RADIATING TO BACK

UNTIL LATE STAGE

263
Q

WHAT ARE RF FOR OVARIAN CANCER

A

BRCA 1 + 2

LINKED TO HOW MANY TIMES YOUVE OVULATED BEFORE

264
Q

AT WHAT STAGE OF DISEASE DO WOMEN USUSALLY PRESENT

A

STAGE 3 +

265
Q

HOW WOULD YOU INVESTIGATE OVARIAN CANCER

A

BLOODS: CA125

US

CT

266
Q

WHY IS CA 125 NOT SPECIFIC

A

ELEVATED IN FIBROIDS/CYSTS

267
Q

WHAT IS THE TREATEMENT FOR OVARIAN CANCER

A

SURGERY

CHEMO

268
Q

WHAT KIND OF CANCER IS VULVAL CANCER

A

SQUAMOUS CELL CARCINOMA

269
Q

WHAT ARE RISK FACTORS FOR VULVAL CACER

A

HPV

LICHEN SCLEROSIS

270
Q

WHAT ARE SX OF VULVAL CANCER

A

ITCHING

SORENESS

PAINFULLPASSING URINE

271
Q

WHAT IS THE TREATEMENT FOR VULVAL CANCER

A

CHEMO

RADIO

272
Q

WHAT TYPE OF CANCER IS VAGINAL CANCER

A

SQUAMOUS CELL/ADENOCARCINOMA

273
Q

DESCRIBE THE AETIOLOGY OF VAGINAL CANCER

A

PRIMARY VAGINAL CANCER IS RARE

ONCE VAGINAL CANCER HAS SPREAD IT BECOMES TERMINAL IN MOST CASES

274
Q

WHAT ARE RISK FACTORS FOR VAGINAL CANCER

A

VIN

HPV

275
Q

WHAT IS VIN

A

VAGINAL INTRAEPITHELIAL NEOPLASIA

276
Q

WHAT ARE SYMPTOMS OF VAGINAL CANCER

A

POST COITAL BLEED

POST MENOPAUSAL BLEEDING

LUMPS AND MASSES

FREQUENCY

DYSURIA

CONSTIPATION

PELVIC PAIN

277
Q

HOW DO YOU Ix VAGINAL CANCER

A

SPECULUM

BI MANUAL EXAMINATION

COLPOSCOPY +/- BIOPSY

278
Q

WHAT ARE Tx FOR OPTIONS FOR VAGINAL CANCER

A

LUMPECTOMY

VAGINECTOMY

HYSTERECTOMY

RADIOATION/CHEMO

279
Q

WHAT IS GESTATIONAL TROPHOBLASTIC DISEASE

A

PREGNANY RELATED TUMOURS WHICH ARE VERY RARE

THESE ARISE FROM THROPHOBLASTS

280
Q

WHAT ARE THE TYPES OF GTD

A
  1. HYDRATIFORM MOLE
  2. INVASIVE MOLES
  3. CHORIOCARCINOMAS
  4. PLACENTAL SIGHT TROPHOBALSTIC TUMOUR
  5. EPITHELIAL TROPHOBLASTIC TUMOUR
281
Q

DESCRIBE A HYDRATIFORM

A

EGG NOT CONTAINING MATERNAL NUCLEUS IS FERTILIZED AND THEN IMPLANTS - THESE GROW INTO GRAPE LIKE STRUCTURES WHICH ARE BENIGN

RISKS OF IT BECOMING MALIGNANT

282
Q

WHAT IS AN INVASIVE MOLE

A

AN EGG WHICH DOES NOT CONTAIN A MATERNAL NUCLEUS IS FERTILIZED AND IMPLANTS THEN GROWS INTO THE MUSCLE WALL OF THE NUCLEUS

283
Q

WHAT IS A CHORIOCARCINOMA

A

PLACENTAL ATTACHEMENT CELLS BECOMING MALIGNANT

HIGHLY RESPONSIVE TO CHEMO

GREAT SURVIVAL RATE

284
Q

WHAT ARE RISK FACTORS FOR GTD

A

AGED 20-35Y

PREV GTD

ASIAN

285
Q

HOW DOES GTD PRESENT

A

MIMICS PREGNANCY

ENLARGED UTERUS

PELVIC PAIN

HYPEREMISIS

286
Q

HOW DO YOU DIAGNOSE A GTD

A

+VE PREG TEST

PICKED UP AT 15W SCAN

287
Q

WHY IS BIOPSY CONTRAINDICATED IN GTD

A

HIGHLY VASCULAR

288
Q

HOW DO YOU TREAT GTD

A

EVACUATION/HYSTERECTOMY (SURGERY)

HISPOLOGICAL SAMPLE

METHOTREXATE

RADIOTHERAPY FOR METS

289
Q

WHAT IS A DURAL PUNCTURE LEAK

A

WHEN PERFORMING AN EPIDURSL THE DURA IS PUNCTURED CAUSING A CSF LEAK

290
Q

WHAT ARE THE SYMPTOMS OF A DURAL PUNCTURE

A

HEADACHE WHICH IMPROVES ON LYING DOWN

NECK STIFFNESS

PHOTOPHOBIA

291
Q

HOW DO YO TREAT A DURAL PUNCTURE

A

BLOOD PATCH

292
Q

WHAT IS URINARY RETENTION

A

ONSET OF INABILITY TO COMPLETELY MICTURATE REQUIRING CATHETERISATION

293
Q

WHAT CAN CAUSE URINARY RETENTION

A

ANAESTHESIA

DAMAGE TO PUDENAL NERVE

UROGENITAL SWELLING AND OEDEMA

294
Q

WHAT CAN DAMAGE THE PUDENAL NERVE

A

VAGINAL DELIVARY

INSTRUMENTAL DELIVARY

PROLONGED LABOUR

295
Q

WHAT ARE COMPLICATIONS OF URINARY RETENTION

A

BLADDER DYSFUNCTION

UTI

CATHETER RELATED INJURY

296
Q

WHEN IN PREGNANCY ARE YOU AT HIGHEST RISK OF VT

A

FISRT THREE WEEKS AFTER DELIVERY

297
Q

WHAT ARE THE RISK FACTORS FOR VT

A

PREV VT

ANTENATAL LMWH

C SECTION

BMI>40

35Y+

MULTIPLE PREGNANCYIES

IMMOBILITY

298
Q

WHAT IS THE TREATEMENT FOR A VT

A

LMWH

299
Q

WHAT PROFYLAXIS WOULD YOU GIVE TO A HIGH RISK VT WOMAN

A

10D PROFYLACTIC PMWH POST DELIVARY

PRE DELIVARY FROM 28 W

300
Q

WHAT PROFYLAXIS WOULD YOU GIVE TO A HIGH RISK VT PREGNANCY

A

PROFYLACTIC LMWH FROM 28W

6 WEEKS PROFYLACTIC LMWH POST DELIVERY

301
Q

WHAT ARE THE HORMONES WHICH DRIVE BREAST MILK PRODUCTION

A

OXYTOCIN

PROLACTIN

302
Q

WHAT IS THE MECHANISM OF OXYTOCIN

A

DRIVES EJECTION OF BREAST MILK

BABY SUCKLING DRIVES OXYTOCIN PRODUCTION BY POSTERIOR PITUITARY GLAND

303
Q

WHAT IS THE MECHANISM OF PROLACTIN

A

DRIVES PRODUCTION OF MLK

BABY SICKLING DRIVES PROLACTIN PRODUCTION BY ANTERIOR PITUITARY GLAND

304
Q

WHAT CELLS DOES OXYTOCIN ACT ON

A

MYOEPITHELIAL CELLS

305
Q

WHAT CELLS DOES PROLACTIN ACT ON

A

LACTOLYTES

306
Q

WHAT IS LACTOGEN

A

A PROLACTIN LIKE HORMONE PRODUCES BY THE PLACENT WHICH DECREASES MATERNAL INSULIN AND FACILITATES ENERGY SUPPLY TO FOETUS

307
Q

WHAT IS LACTOFERRIN

A

A MOLECULE WHICH BINDS IRON IN BREAST MILK HELPING BABY ABSORB IRON WHILST INHIBITING BACTERIAL PROLIFERATION

308
Q

WHAT ARE THE BENEFITS OF BREAST FEEDING

A

SUPPRESSES OVULATION

BOOSTS BABYS IMMUNE SYSTEM

BONDING

REDUCES RISKS OF BREAST AND OVARIAN CANCER AND OSTOPOROSIS (18MONTHS BREAST FEEDING)

309
Q

WHAT IS THE PUERPERIUM

A

PERIOD OF TIME FROM DELIVERY OF THE PLACENTA TO 6 WEEKS AFTER BIRTH

310
Q

WHAT ARE THE THREE STAGES OF THE PUEPERIUM

A
  1. RETURN TO PREPREGNANT STATE
  2. INDUCTION AND SUPPORESSION OF LACTATION
  3. TRANSITION TO PARENTHOOD
311
Q

WHAT ARE THE PHYSIOLOGICAL CHANGES THAT OCCUR WHEN RETURNING TO PRE PREGNANT STATE

A

RETURN OF UTERUS TO THE ORIGINAL POSITION WITH MUSCLE ISCHEMIA, AUTOLYSIS AND PHAGOGENESIS

UTERUS TAKES 6-8 WEEKS TO SHRINK AND SOFTEN

SHEDDING OF DECIDUA AND HORMONAL CHANGES

312
Q

WHAT IS DECIDUA

A

BLOOD AND OTHER CONTENTS IN UTERO AFTER PREGNANCY

313
Q

WHAT IS LOCHIA

A

THE SHEDDED DECIDUA

314
Q

WHAT ARE THE TYPES OF LOCHIA

A
  • RUBURA:
    • 0-4 DAYS
    • RED IN COLOUR
    • BLOOD AND FOETAL MEMBRANES
  • SEROSA
    • 4-10D
    • BROWN
    • WOUND DISCHARGE (WBC) AND MUCUS
  • ALBA
    • 10-28D
    • WHITE
    • CELL SHEDDING
315
Q

WHAT ARE SEVERE COMPLICATIONS OF THE PUEPERL PERIOD

A

SEPSIS

PPH

ECLAMPSIA

THROMBOSIS

UTERINE PROLAPSE

POST DURAL PUNCTURE HEADACHE

BREAST ABCESS

PSYCHOSIS

316
Q

DEFINE SEPSIS

A

INFECTION WITH SYSTEMATIC MANIFESTATIONS

317
Q

DEFINE SEVERE SEPSIS

A

SEPSIS WITH ORGAN DYSFUNCTION OR HYPOPERFUSION

318
Q

DEFINE SEPTIC SHOCK

A

PERSISTANCE OF HYPOPERFUSION DESPITE FLUID RESUS

319
Q

WHAT ARE THE SIGNS OF SEPSIS

A

B - bp <90 systolic

U - urine output < 30ml/hr

H - HR>130 bpm

F - further tests ie cultures, temp (high), wcc (high), blood glucose (high)

L - lactate high

O - o2<90%

320
Q

WHAT IS THE MANAGEMENT OF SEPSIS

A

FLUIDS

BLOOD CULTURES

URINALYSIS AND CULTUES

O2

IV ABX EMPIRICALLY UNTIL CULTURES RETURN

321
Q

WHAT IS THE DEFINITION OF PRE ECLAMPSIA

A

BP>140/90

+PROTEINURIA

AFTER 20 WEEKS GESTATION

322
Q

WHEN DOES PRE-ECLAMPSIA TURN TO ECLAMPSIA

A

WITH START OF CONVULSIONS

323
Q

WHAT ARE RF FOR PREECLAMPSIA

A

OBESITY

OLD AGE

KIDNEY DISEASE

HTN

DIABETES

FAMILY HX OF PRE ECLAMPSIA

324
Q

WHAT ARE SYMPTOMS OF PRE ECLAMPISA

A

SWELLING OF HANDS AND FACE

PITTING OEDEMA

HEADACHES

FLASHING LIGHTS

ABDO PAIN

HYPERREFLEXIA

325
Q

WHAT IS THE PROFYLXIS FOR PRE ECLAMPSIA

A

APSRIN LOW DOSE DAILY UP UNTIL DELIVARY

326
Q

HOW DO YOU MANAGE PRE ECLAMPSIA

A

LABETALOL

PREDNISOLONE + MAGNESIUM SULPHATE 24 HRS PRE DELIAVRY

DELIVER PLANNED AT 37-38 WEEKS

327
Q

Define a show

A

a plug of mucus and blood which is ‘delivered’ at the start of labour

328
Q

define ‘waters breaking’

A

a ruputre of membranes and amniotic sac

329
Q

what are the indicaions of waters breaking

A

show

rupture of membranes

contractions

330
Q

what is the purpurse of contractions

A

efface and dilate the cervix and then help move baby

331
Q

what is the definition of active labour

A

4-10 cm

coordinate strong

frequent contractions

332
Q

how long does active labour last in primigravida

A

12-13 hrs

333
Q

how long does active labor last in multigravida

A

6-9hrs

334
Q

describe phase 1 of labour

A

consists of of labour and active phase

335
Q

describe the second phase of labour

A

power - forceful contractions

passage

passenger

336
Q

what are the cardinal movements of a baby

A

descent until engaged at ischeal spines

rartation once babys head is flexed

babys head mves under ischeal spines

once baby is OA it is expulsed

baby roatates CP and shoulders are passed

337
Q

phase 3 of labour is ?

A

uterine contractions causing placental separation

338
Q

phase 4 of labour

A

uterine involution and the return to pre pregnanct stage

339
Q

hormones used in labour

A

progesterone

oestrogen

prostaglandins

relaxin

endorphins

adrenaline

340
Q

what is the role of relaxin in labour

A

loosens tendons and ligaments makng pelvis more flexible

341
Q

what causes prostaglandin synthesis

A

presence of oxitocin

pressure on cervix

342
Q

what is the role of prostaglandins in labour

A

cervicle ripening

343
Q

what is the role of oxitocin in labour

A

promotes uterine contractions

ripens cervix

344
Q

what is the role of preogesterone in early pregnancy

A

proliferation and vascularisation of endometrial strome

promotes maternal quiescence

increases maternal ventilation

promotes glucose deposition

345
Q

what is the role of prostaglandin in late pregnancy

A

prevents labour onset

prevents lacttaion

prengthens pelvic muscles

346
Q

where is progesterone produced

A

corpus luteum

placenta (trophoblastst)

347
Q

where is oestrogen produced in pregnancy

A

at start corpus luteum

then fetal liver and adrenal glands as well as maternal ovaries

348
Q

what is the role of oestrogen during pregnancy

A

growth and correct placental function

promoting maternal breast development

increases endometrial progesterone recepors

349
Q

describe the HPG axis

A
350
Q

describe the physiology of ovulation

A

fsh causes follicular development

dominant follicle developms

causes and increase in LH and oestrogen

FSH has -ve feedback on LH by anterior pituitary gland until theres LH surge

causing ovulation

351
Q

describe the effecst of FSH+LH on follicular cells

A

LH acts on thecal cells

FSH acts on granulosa cells

theca cells produce testosterone which granulosa cells change to oestrogen

352
Q

describe the menstrual cycle

A

ant. pituitary releases FSH and LH

FSH rises quickly and follicles start developing

there is a slow rise in oestrogen (which LH drives) due to the negative feedback of FSH on LH until theres LH surge

ovulation occurs

Once follic;e bursts ut becomes corpus leuteum which produces progesterine which has -ve affect on pituitary

353
Q

what are gonadotrophins

A

glycoproteins :

fsh

lh

hcg

354
Q

what is a female steriod

A

oestrogen

355
Q

what do thecal cells do

A

synthesis progesterone and testosterone from cholesterol

356
Q

what is the role of granulosa cells

A

to turn the testosterone made bythecal cells to oestrogen

357
Q

how does implantation occur

A

progesterone produced from corpus leuteum allows for implantation

fetal blastocysys produce hCG

prevents luteal death so progesterone continues

At day 20-24 endothelium is sticky and there is implantation into the stroma which then proliferates over the blastocyst

358
Q

what is the purpose of the decidua

A

permits invasion of blastocyst and implantation causing uterine stromal enlargement and proliferation of uterine natural killer cells

359
Q

what is the limiting factor of stromal invasion

A

decdua basalis

360
Q

what can cause placental mediated diseases

A

poor remodelling of spiral arteries

361
Q

what is a morola

A

a solid ball of cells resulting from the division of a fertilized ovum

362
Q

what is a lacunae

A

a small depression which fills with maternal blood this is where the placents begins

363
Q

what is the vascular supply of the umbilical cord

A

x2 arteries - deoxygenated

x1 vein- oxygenated

364
Q

what structures does teh ectoderm form

A

nervous system]epidermis

hair

eye lense

365
Q

what structures does a mesoderm form

A

skeleton

dermis

muscles

vascular

urogenital

366
Q

what structures does the endoderm form

A

GI tract

pancreas

liver

thyroid

367
Q

what are implications of pregestational diabetes in pregnancy on the mother

A

increased risk of:

pre eclampsia

instrumental/c section delivery

368
Q

what are implications of pregestational diabetes in pregnancy on the fetus

A

misscarrige/still birth

fetal abnormalities

macrosomia

prem baby

shoulder distocia/erbs palsey

NICU admission (RDS,jaundice, hypoglycaemia)

369
Q

a T2 diabetic woman comes to you and asks about conception and pregnancy advice. what would that be?

A

maintain HBA1C<48

take folic acid

stop ACEi and satins

regular retinal screening

GFR monitoring + albumin

370
Q

what is the management of a T1 diabetic woman in pregnancy

A

insulin on bolus regime

metformin

if Hypo = glibenclamide

371
Q

what is the leading cause of maternal death in UK

A

thrombotic events associated with pregnancy

372
Q

why does pregnancy put you in a thromboembolic state?

A

increase in coagulation factors and decrease in anticoagulation factors

decreased fibrinolysis

increase in venous stasis

373
Q

what are the risk factors for a clot in pregnancy

A

icreased age

increased BMI

operative delivary

smoking

sickle cell

pre eclampsia

374
Q

how would you investigate a clot in pregnancy

A

US + doppler

VQ scan

or in PE

CTPA

venous perfusion scan

if sustepcting venous sinus embolism = CT head

375
Q

how do you manage embolic events in pregnancy

A

LMWH

WARFRIN = TETROGENIC!!!

376
Q

what are maternal complications of renal disease

A

accelerated irreversible renal failure

hypertension

pre eclampsia

increased c section risk

377
Q

what are fetal complications of renal disease

A

IUGR

prematurity

still birth

congenital abnormalities due to drug therapies

378
Q

how does renal physiology change in pregnancy

A

GFR increases by 50%

serum creatinine, urate and albumin falls

379
Q

what is the management of renal disease in pregnancy

A

STOP ACEi+ARB

start labetalol, folic acid and low dose asprin

regular fetal survailence

380
Q

why is it important to screen pregnant women with renal disease for UTI’s

A

the risk to pregancies with renal disease is very high

381
Q

what are the implications of epilepsy on pregnancy for mother

A

increase frequency of siezures

increased risk of sudden epileptic death

382
Q

what are the implications of epilepsy on pregnancy for fetus

A

increased riskof congenital abnormalities (medications)

still birth due to hypoxia caused in prolonged seizures/ status epilipticus

383
Q

what congenital abnormalities does serum valopate cause in fetus’

A

neural tube defects

congenital heart defects

lowered IQ

cleft pallette

384
Q

what is the managment of epilepsy in pregnancy

A

high dose folic acid

carbamezipine

careful delivery and post partum plan

  • with inceased Vit K dose if necessary. as anticonvulsants can cause decreased vit K
385
Q

what changes in pregnancy which may cause or exaccerbate anaemia

A

theres a x2-3 increase in iron requirement

a x10-20 increase in folate requirements

an increased plasma volume and RBC side causing physiological anaemia

386
Q

what are maternal risks of mild anaemia

A

dizziness meaninf + risk in falls

387
Q

what are fetal risks of mild anaemia

A

+ risk of neonatal anaemia

388
Q

what are maternal risks of severe anaemia

A

fainting meaning + risk in falls

increased risk of mortality duing childbirth due to blood loss

389
Q

what are fetal risks of severe anaemia

A

prem baby

low birth weight

increased risk of severe neonatal anaemia

390
Q

how do you diagnose anaemia in pregnancy

A

FBC

iron studies

391
Q

management of anaemia in pregnancy

A

iron

folate

b12

if very severe : blood transfusions

392
Q

how common is asthma in pregnancy

A

5-10%

393
Q

what are maternal implications of asthma

A

1/3rd of asthmatics become worse and in 3rd trimester there is + risk of exacerbations

394
Q

what are fetal implications of asthma

A

decreased perfusion so there + risk of IUGR

prem delivary due to maternal deterioration

pre-eclampsia

395
Q

how do you manage uncomtrolled asthma in pregnancy

A
396
Q

what is the Px of obstetric cholestasis

A

intense itching

  • wthout a rash
  • mainly on palms and feet

commonly in 2nd+3rd trimester

397
Q

investigations for obstetric cholestasis

A

AST

ALT

urine bile acides + serum

398
Q

what are maternal complications of obstetric cholestasis

A

pruritis

prolonged clotting time (+ PPH risk)

399
Q

what are fetal complications of obstetric cholestasis

A

prem

still birth (due to +++ bile acids)

400
Q

what is the Mx of obstetric cholestasis

A

uredeoxycholic acids

oral water soluble vit K

induce labour at 37 w

401
Q

why shoudld post natal contraception that contains oestrogen be avoided in abstetric cholestasis

A

because oestrogen is potential cause of obstetric cholestasis and may prolong Sx

402
Q

why is the incidence of cardiac disease increasing in pregnant women

A

age of pregnancy is + so + risk of ischemic heart disease

survavival of congenital heart disease is much better now

403
Q

what are the maternal implications of heart disease in pregnancy

A

increased risk of heart failure

pre eclampsia

404
Q

what are the baby implications of heart disease in pregnancy

A

IUGR

prem

miscarrige

405
Q

what cardiac pathologies have highest risk in prenancy

A

fixed cardiac output pathologies

eg

  • aortic stenosis
  • coarctation of aorta
  • prosthetic valves
406
Q

what cardiac pathologies have lowest risk in prenancy

A

regurgent lesions

eg

  • AD
  • VSD
  • mitral or aortic incompetence
407
Q

how do yo Ix the effects of cardiac disease in pregnancy

A

maternal echo

maternal ECG

fetal serial growth scans

fetal doppler

BP monitoring

408
Q

Mx of cardiac disease in pregnancy

A

LMWH (anticoagulants)

inotropes (cardiomyopathies)

labetalol (aortic stenosis + miral stenosis + mitral prolapse)

Abx to prevent endocarditis

409
Q

What is the management of Endocarditis in pregnancy

A

in low risk pregnancies:

  • amoxicillin PO 1hr before labour and then 6hrly during labour

in standard risk pregnancies

  • ampicillin IV + gentamycin IV at onset of labour and repeated 8hrly

is theres a penicillin allergy give vancomycin IV 12hrly and at start of labour

410
Q

why are women with cardiac disease at high risk of heart failure in the post partum changes

A

large haemodynamic changesin labour a

411
Q

what are maternal implications of hypothyroidism in pregnancy

A

increased risk of PPH

412
Q

what are fetal implications of hypothyroidism in pregnancy

A

miscarrige

neurodevelopmental inpairement and developmental delay

413
Q

how would you manage hypothyroidism in pregnancy

A

thyroxine

iodine suppliments

414
Q

when is thyroid control most important in pregnacy

A

1st trimester

415
Q

why is hypothyroidism uncommon in pregnancy

A

autoimmune state (main cause = graves) it usually resolves in pregnancy

416
Q

what are maternal implications of hyperthyroidsim in pregnancy

A

Thyrotoxicosis

cardiac failure (due to thyrotoxicosis)

pre eclampsia

417
Q

what are fetal implications of hyperthyroidsim in pregnancy

A

still born

IUGR

prem baby

418
Q

why would thyrotoxicosis occur

A

in first trimester baby doesnt have a thyroid

means that Thyroid stimulating antibodies cross the placenta and to mums thyroid to help support baby

this increases thyroid dimand and can cause thyrotoxicosis (thyroid storm)

419
Q

how would you manage hyperthyroidism in pregnancy

A

propylthiouracil

  • blocks release of thyroxine and convestion of T4>T3 in periferies

check TSG every 4-6 weeks

fetal tachycarda monitoring after 32 weeks (>/= 160bpm shows fetal thyroid dysfunction)

420
Q

what is contraindicated in the managment of hyperthyroidism in pregnancy

A

carbimazole = fetal abnormalities

radioactive iodine

421
Q
A

Phase 3a (22 decks)

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