OBG Flashcards
(421 cards)
1
Q
WHAT ARE THE TWO TYPES OF OVARIAN CYST
A
FOLLICULAR
LUTEAL
2
Q
WHAT ARE FOLLICULAR CYSTS
A
FUNCTIONAL CYSTS THAT OCCUR WITH HORMONAL CHANGES
THEY ARE ALWAYS SMALLER THAN 6CM
3
Q
WHY DO FOLLICULAR CYSTS OCCUR
A
WHEN OVULATION DOESNT OCCUR AND THE FOLLICLE KEEPS GROWING
4
Q
WHAT ARE THE TYPES OF LUTEAL CYSTS
A
GRANULOSA
THECA
5
Q
WHAT ARE GRANULOSA CYSTS
A
OF CORPUS LUTEUM
are luteal cysts that occur with hormonal changes
have 2 stages vascular and serous, in vascular they can haemorrage if there is rupture
6
Q
WHAT ARE THECA CYSTS
A
BAD ONLY OCCUR WITH HIGH LEVELS OF HCG AND ARE OFTEN ASSOCIATED WITH A HYDRATIFORM MOLE
7
Q
HOW WOULD YOU INVESTIGATE A CYST
A
US
LAPROSCOPY
8
Q
WHAT ARE SYMPTOMS OF AN OVARIAN CYSTS
A
USUALLY ASYMPTOMATIC UNLESS THEE IS TORSION OR RUPTURE
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
10
Q
WHAT ARE UTERINE FIBROIDS
A
BENIGN GROWTH OF UTERINE MUSCLE
11
Q
WHAT ARE THE TYPES OF UTERINE FIBROID
A
SUBMUCUS
INTRAMURAL
SUBSEROUS
PEDUNCULATED
INTERLIGAMENTAL
PARASITIC
12
Q
WHICH FIBROIDS CAN CAUSE ENLARGEMENT OF THE UTERUS
A
INTERMURAL
13
Q
WHICH FIBROIDS CAUSE PAIN AS THEY GROW
A
SUBMUCOUS
PEDUNCULATED CCAN CAUSE PAIN IF THEY GET TWISTED
14
Q
WHICH FIBROID TYPE ARE USUALLY ASYMPTOMATIC
A
SUBSEROUS
15
Q
WHAT IS THE PRESENTATION OF FIBROIDS
A
HEAVY MENSES
NON TREATABLE ANAEMIA
DISCOMFORT ON PRESSURE
PAIN
16
Q
HOW ARE FIBROIDS TREATED
A
ONLY IF SYMPTOMATIC
TREATED SURGICALLY VIA MYECTOMY OR HYSTERECTOMY
17
Q
HOW DO YOU DIAGNOSE FIBROIDS
A
BI MANUAL PELVIC EXAM
US
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
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
20
Q
HOW WOULD YOU DIAGNOSE CHRONIC PELVIC INFECTION
A
SWABS
- HIGH VAGINAL
- ENDOCERVICLE
TRANSVAGINAL US
21
Q
WHAT ARE TREATEMENT OPTIONS FOR CHRONIC PELVIC INFECTIONS
A
IVF + TUBAL REMOVAL
HISTORECTOMY AND PELVIC ORGAN CLEARENCE
22
Q
WHAT % OF PREGNANT WOMEN ARE AFFECTED BY PYLEONEPHRITIS
A
1%
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
24
Q
WHAT IS THE PRESENTATION OF UTI IN PREGNANCY
A
USUALLY ASYMPTOMIATIC
25
WHAT IS THE MOST COMMON PATHOGEN CAUSING UTI
E COLI (G -VE)
26
HOW WOULD YOU DIAGNOSE A UTI
MSU
DIPSTICK
CULTURES
BLOODS: CRP, ESR, ECC
27
WHEN IS TRIMETHOPRIM USED TO TREAT UTI
CYSTITIS IN 3RD TRIMESTER OR NON PREGNANT
28
WHAT ANTIBIOTICS ARE USED FOR CYSTITIS IN PREGNANCY
CEFALEXIN ALL THROUGHOUT PREGANCY
NUROFERONTOIN 1ST TRIMESTER
TRIMETHOPRIM 3RD TRIMESTER
29
WHAT ANTIBIOTICS ARE USED FOR PYLEONEPHRITIS IN PREGNANCY
CEFALEXIN
30
WHAT IS PELVIC CONGESTION
VASCULAR CONJESTION OF PELVIC ORGANS DUE TO VESSEL DILATATION CAUSING STASIS OF BLOOD
31
WHAT ARE THE SYMPTOMS OF PELVIC CONGESTION
PELVIC PAIN
PAIN OFTEN STARTING DURING OR AFTER PREGNANCY
DYSPYRUNEA
SYMPTOMS WORSE DUING MENSES
TENDERNESS AT ILLIAC FOSSA
32
HOW WOULD YOU INVESTIGATE FOR PELVIC CONGESTION
US
LAPROSCOPY
VENOGRAPHY (VERY INVASIVE AND UNPLESENT)
33
WHAT ARE TREATEMENTS FOR PELVIC CONGESTION
PROSTAGLANDINS
OOPHORECTOMY
34
WHAT IS PID
PELVIC INFLAMMATORY DISEASE IS A POLYMYCROBIAL DISEASE
USUALLY CAUSED BY INFECTION WITH CHAMYDIA OR GHONNOREA (OR BOTH)
USUALLY WITH ONE OTHER AEROBIC BACTERIA
35
HOW WOULD YOU DIAGNOSE PID
HIGH VAGINAL AND ENDOCERVICLE SWABS
BLOODS FOR ACUTE PHASE REACTANTS
TRANSVAGINAL SCAN
36
WHAT IS THE MANAGEMENT OF PID
1. FLUIDS
2. ANTIBIOTICS
3. NSAID
4. IUD/IUS REMOVAL
5. IMMOBILIZATION UNTIL PAIN IS BETTER
6. ABSTINENCE UNTIL INFECTION IS CLEARED
37
WHAT IS THE ANTIBIOTICS USED FOR CHAMYDIA
AZYTHROMYCIN
OR
DOXYCYLINE
38
WHAT IS THE ANTIBIOTIC USED FOR GONNOREA
CEFTRIAXONE (IM)
+
DOXYCYCLINE/AZYTHROMYCIN
39
WHAT IS THE ANTIBIOTIC USED FOR TRICHOMONIASIS
METRANIDOZOLE
40
WHAT ARE URETERIC CALICULI
AN ACCUMULATION OF EITHER
* CALCIUM OXOLATE
* STRIVATE
* URIC ACID
* CYSTINE
* MIXURE OF ABOVE
IN THE BLADDER/URETER
41
WHY DOES DEHYDRATION PREDISPOSE YOU TO URETERIC CALICULI
LEADS TO SUPERSATURATION OF URINE
42
WHAT ARE THE THREE COMMON AREAS IN WHICH THE URETERIC CALICULI GET STUCK
PELVIC - URETERIC JUNCTION
PELVIC BRIM
VESICO URETERIC JUNCTION
43
WHAT IS THE PRESENTATION OF A URETERIC CALICULI
SUDDEN SEVERE URILATERAL PAIN GOING LOIN TO GROIN
RIGORS
DYSURIA
HAEMATURIA
RETENTION
N+V
44
HOW WOULD YOU DIAGNOSE URETERIC CALICULI
UINE DIPSTICK - HAEMATURIA
BLOODS - CALCIUM, PHOSPHATE, URATE
X RAY (US)
CT
45
A PATIENT IS SHOWN TO HAVE A STONE \< 5MM WHAT IS THE MANAGEMENT?
WATCH AND WAIT
ENCOURAGE FLUIDS
SPONTANEOUS PASS
+ ANALGESIA (AND POTENTIALLY ABX)
46
A PATIENT IS SHOWN TO HAVE A STONE\> 5MM WHAT IS THE MANAGEMENT?
TAMSULOSIN
SHOCKWAVE LITHOTRIPSY OR PERCUTANEOUS NEPHROLITHOMY
ANALGESIA
(POTENTIALLY ABX)
47
WHAT IS ADENOMYOSIS
ENTROMETRIAL CELLS GROWING INTO THE UTERINE WALLS
48
HOW DOES ADENOMYOSIS DIFFER FROM ENDOMETRIOSIS
ENDOMETRAL CELLS ONLY GROW INTO WALL
IN ENDOMETRIOSIS THEY GROW OUTSIDE UTERUS
49
WHAT ARE SYMPTOMS OF ADENOMYOSIS
HEAVY MENSES
ENLARGED UTERUS
50
HOW DO YOU DIAGNOSE ADENOMYOSIS
CLINICALLY AND US/MRI CAN GIVE AN IDEA BUT A HYSTERECTOMY AND MICROSCOPY OF TISSUE SAMPLE IS ONLY TRUE DIAGNOSIS
51
WHAT ARE TREATEMENTS FOR ADENOMYOSIS
COMBINED ORAL CONTRACEPTIVE
GnRH ANALOGUES
UTERINE ARTERY AMBOLIZATION
ENDOMETRIAL ABLASION
52
WHAT IS ENDOMETRIOSIS
PROLIFERATION OF THE ENDOMETRIUM IN SITES OTHER THAN UTERINE MUCOSA
53
WHAT ARE SYMPTOMS OF ENDOMETRIOSIS
PAIN
DYSPYRUNEA
DISMENNOREA
PAIN ON DEFICATION
54
WHAT SRE THE SIGNS OF ENDOMETRIOSIS
INFERTILITY
RETROVETRED UTERUS
ADENAXAL MASS
VAGINAL - RECTAL SEPTUM MASS
55
HOW WOULD YOU DIAGNOSE ENDOMETRIOSIS
BIMANUAL PELVIC EXAM + SIMULTANEOUS VAGINAL AND RECTAL EXAM
LAPROSCPY
COMBINED ORAL CONTRACEPTIVE CHALLENGE
56
WHAT ARE TREATEMENTS OF ENDOMETRIOSIS
COMBINED ORAL CONTRACEPTIVE
ANDROGENS (INCREASE PERIFERAL OESTROGEN CONVERSION)
GnRH ANALOGUES
SURGERY
57
WHAT ARE SIDE EFFECTS OF COC
BREAST TENDERNESS
FLUID RETENTION
58
WHAT ARE SIDE EFFECTS OF ANDROGENS
WEIGHT GAIN
XS HAIR
59
WHAT ARE SIDE EFFECTS OF GnRH ANALOGUES
MENOPAUSAL SYMPTOMS
60
WHAT IS INCONTENENCE
INVOLUNTARY LEAKAGE OF URINE AFFECTING SOCIAL LIFE AND HYGENE
61
WHAT ARE THE TWO TYPES OF INCONTENENCE
OVERACTIVE BLADDER
STRESS INCONTENANCE
62
DEFINE OVERACTIVE BLADDER
INVOLUNTARY AND FREQUENT BLADDER CONTRACTIONS
63
DEFINE STRESS INCONTENENCE
SPHINCTER WEAKNESS WHERE URINE IS PASSED ON INCREASED BLADDER PRESSURE
64
WHAT IS THE PRESENTATION OF INCONTENENCE
PASSING URINE WHEN SNEEZING OR COUGHING
SENSE OF URGENCY
NOCTURIA
KEY IN DOOR SYNDROME
65
HOW DO YOU DIAGNOSE INCONTENENCE
FREQUENCY VOLUME CHART
RESIDUAL URINE MEASUREMENT USING IN OUT CATHETER
E PAQ
CONTRAST CYSTOGRAM FOR STRESS INCONTENENCE
66
WHAT IS E PAQ
A QUESTIONAIRRE LOOKING AT URINARY, VAINAL, BOWEL AND SEXUAL SYMPTOMS
67
WHAT IS URODYNAMIC TESTING
ARTIFICIALLY FILLING BLADDER AND ASKING PATIENT TO COUGH TO MEASURE BLADDER PRESSURE
68
WHAT IS THE TREATEMENT FOR STRESS INCONTENENCE
LIFESTYLE
BLADDER TRAINING
SURGERY
69
WHAT ARE TREATEMENTS FOR OVERACTIVE BLADDER
LIFESTYLE
OXYBUTAMINE (ANTICHOLINERGIC)
BOTOX
CATHETERS
VAGINAL OESTROGEN
70
WHAT IS A FISTULA
AN ABNORMAL COMMUNICATION OF THE URETER AND VAGINA
71
WHAT CAN CAUSE A FISTULA
TRAUMA
C SECTION
NECROSIS
72
73
74
75
WHAT IS A UTEROVAGINAL PROLAPSE
WHEN THE UTERUS PARTIALLY OR COMPLETELY PROTRUDES FROM THE CERVIX INTO THE VAGINAL CANAL
76
DESCRIBE A PRIMARY UTEROAGINAL PROLAPSE
DESCENT OF CERVIX INTO THE VAGINA THROUGH OS
77
DECRIBE A SECONDARY VAGINAL PROLAPSE
DESCENT OF CERVIC TO THE INTEROITUS
78
DECRIBE A TERTIARY VAGINAL PROLAPSE
DECSENT OF CERVIX THROUGH INTEROITUS
79
DECRIBE A QUATERNARY/TOTAL VAGINAL PROLAPSE
MOST OF UTERUS OUTSIDE INTEROITUS
80
HOW WOULD YOU DIAGNOSE A UTEROVAGINAL PROLAPSE
SIMS SPECULUM
ULTRASOUND
POTENTIALLY MRI
81
WHAT IS THE TREATEMENT OF A UTEROVAGINAL PROLAPSE
REASURRANCE
TREAT SYMPTOMATICALLY
physio
RING / SELF PESSARY
SURGERY
82
WHAT IS A RETROCELE
A POSTERIOR VAGINAL WALL PROLAPSE WHERE THE RECTAL PASSAGE BULGES INTO THE VAGINAL CANAL
83
WHAT IS THE PRESENTATION OF A RETROCELE
DIFFICULT BOWEL MOVEMENTS
PRESSURE FELT ON RECTUM
FEELING OF INCOMPLETE VOIDING
84
WHAT IS THE TREATEMENT OF A RETROCELE
SURGERY
85
WHAT IS A CYSTOCELE
AN ANTERIOS VAGINAL WALL PROLAPSE WHERE BLADDER PRESSES ON ANTERIOR VAGINAL WALL
86
WHAT IS THE PRESENTATION OF A CYSTOCELE
HESITATION
FREQUENCY
RECURRANT UTI
INCOMPLETE VOIDING AND RETENTION
87
WHAT IS THE TREATEMENT FOR CYSTOCELE
PHYSIO
PRESSARY
TOPICAL VAGINAL OESTROGEN
SURGERY
88
HOW WOULD YOU DEFINE A MISCARRIGE
THE SPONTANEOUS DISCHARGE OF A GESTATIONAL SACK BEFORE THE FETUS IS VIABLE
89
WHAT PROPORTION OF PREGNANCIES END IN MISCARRIGE
50%
90
WHAT ARE THE TYPES OF MISCARRIGE
THREATNED
INEVITABLE SEPSIS
MISSED
SPONTANEOUS SECOND TRIMESTER
RECURRENT
91
WHAT IS A THREATNED MISCARRIGE
BLEEDING FROM GENITAL TRACT AT EARLIEST STAGES OF PREGNANCY BUT NO PRODUCTS OF CONCEPTION ARE DISCHARGED
CERVIX REMAINS CLOSED
92
WHAT IS AN INEVITABLE MISCARRIGE
THE CERVIX OPENS AND THE PRODUCTS OF CONCEPTION ARE DISCHARGED
CAN BE COMPLETE OR INCOMPLETE
93
WHAT ARE THE SIGNS OF AN INCOMPLETE MISCARRIGE
PROLONGED ABDOMINAL PAIN AND PV BLEEDING
94
WHAT IS A SEPSIS MISCARRIGE
INFECTION CAUSING EXPULSION OF PRODUCTS OF CONCEPTION
95
WHAT ARE THE SIGNS OF A SEPTIC MISCARRIGE
UTERINE TENDERNESS
PURULENT VAGINAL DISCHARGE
PYREXIA
ALSO OCCURS POST MISSCARRIGE
96
WHAT IS A MISSED MISSCARRIGE
AN EMPTY GESTATIONAL SAC BEING DISCHARGED
THERE WAS FAILURE TO DEVELOP AFTER 7 DAYS
OFTEN WOMEN DO NOT REALISE THEY MISCARRY - SIMILAR TO PERIOD
97
WHAT IS A SPONTANEOUS SECOND TRIMESTER LOSS
SPONTANEOUS MEMBRANE RUPTURE WITH CERVICALE DILATATION WILL CAUSE A MISSCARRIGE
98
WHAT ARE RECURRENT MISSCARRIGES
3 OR MORE
99
WHAT ARE COMMON CAUSES OF MISCARRIGE
GENETIC DISORDERS INCOMPATIBLE WITH LIFE
ENDOCRINE : DECREASED PROGESTERIONE FROM PLACENTA OR CORPUS LUTEUM
MATERNAL ILLNESS OR DRUG USE
CERVICLE INCOMPLETENCY
AUTO IMMUNE DISEASES
100
WHAT WOULD A SECOND TRIMESTER MISSCARRIGE BE LIKE
A RAPID DELIVARY WHICH IS OFTEN PAINLESS AND BLOODLESS
101
WHAT OFTEN CAUSES CERVIACLE INCOMPLETENCY
PRIOR TRAUMA TO CERVIX
102
HOW WOULD YOU INVESTIGATE A MISCARRIGE
VAGINAL EXAM TO CHECK DILATATION
VAGINAL SWABS
US - TRANSVAGINAL AND ABDOMINAL
103
WHAT IS THE MANAGEMENT OF A MISCARRIGE
GIVE PROSTAGLANDINS - MISOPRASTOL
104
WHAT DO PROSTAGLANDINS (MISOPRASTOL) DO
PROMOTE UTERINE CONTRACTION AND EXPULSION
105
WHAT IS THE MANAGEMENT OF A RHESUS NEGATIVE MISCARRIGE
GIVE MISOPROSTOL
GIVE ANTI D IMMUNOGLOBULINS WHEN FETAL GESTATION IS OVER 12W
106
WHEN WOULD YOU INTERVENE SURGICALLY IN MISCARRIGE
IF INCOMPLETE MISCARRIGE
OR ESPECIALLY PAINFUL
107
WHAT SHOULD YOU INVESTIGATE FOR IN RECURRANT MISCARRIGES
LUPUS
PCOS
KARYOTYPE TESTING
CERVICLE CLEARENCE
108
WHAT IS AN ECTOPIC PREGNANCY
WHEN A FERTILIZED EGG ATTACHES OUTSIDE OF UTERINE CAVITY
109
WHERE DO ECTOPIC PREGNANCYS OCCUR MOST OFTEN
FALLOPIAN TUBES
110
WHAT ARE THE RISK FACTORS FOR AN ECTOPIC PREGNANCY
IUD/IUS
PREV ECTOPIC PREGNANCY
SURGERY TO UTERINE TUBES
111
WHAT IS THE PRESENTATION OF AN ECTOPIC PREGNANCY
SUDDEN SEVERE UNILATERAL PAIN
SHOULDER TIP PAIN (DUE TO DIAPHRAGM IRRITATION)
112
HOW DO YOU DIAGNOSE AN ECTOPIC PREGNANCY
PREGNANCY TEST
SMALL UTERUS FOR GESTATION
US
LAPROSCOPY
113
HOW WOULD YOU TREAT AN ECTOPIC PREGNANCY
METHOTREXATE IF UNDER 3CM
LAPSROSCOIC REMOVAL
TUBAL REMOVAL
114
WHAT IS THE PROBLEM WITH USING METHOTREXATE IN MANAGING ECTOPIC PREGNANCIES
MAY BE UNSUCCESSFUL
MAY CAUSE RUPTURE
115
WHAT IS THE PATHOPHYSIOLOGY OF PCOS
INCREASED ANDROGEN
DECREASED FSH AND LH
ANDROGENS CONVERTED TO TESTOSTERONE PERIFERALLY
116
WHAT ARE THE CYST TYPE IF PCOS
COLLICULAR
HAULTED FOLLICULAR DEVELOPEMENT
117
WHAT INVESTIGATIONS ARE REQUIRED FOR PCOS
US
BLOODS:
* LH NORMAL OR DECREASED
* FHS NORMAL OR DECREASED
* HIGH PROLACTIN!!!!
* HIGH TESTOSTERONE
118
WHAT IS PCOS
THE PRESENCE OF MULTPILE CYSTS WITHIN THE OVARY ABD XS ANDROGEN PRODUCTON FROM OVARIES AND ADRENAL GLANDS
119
WHAT IS THE PRESENTATION OF PCOS
OVERWEIGHT AND DIFFICULTY LOOSING WEIGHT
HIRTUISM
INFERTILITY
ACNE
AMENORRHOE OR OLIGOMENNORHEA
120
HOW WOULD YOU TREAT PCOS
MENSES:
* COC / CYCLICAL OESTROGEN
* METFORMIN
FERTILITY
* METFORMIN
* CLOMIFENE
* PREDNISOLONE
* IVF
SPRIONOLACTONE
HAIR REMOVAL AND ACNE TREATEMENTS
121
HOW DOES SPIRONOLACTONE HELP IN PCOS
HAS ANTIANDROGEN PROPERTIES
122
HOW DOES METFORMIN HELP IN PCOS
HELS ASSOCIATED INSULIN RESISTANCE AND REGULATES MENSES BOTH ALSO AIDING FERTILITY
123
HOW DOES CLOMIFENE HELP IN PCOS
INDUCES OVARIES
124
WHY SHOULD YOU BE CAUTIOUS OF PROLONGED CLOMIFENE
INCREASES RISK OF OVERIAN CANCER
NO MORE THAN 6 CYCLES
125
HOW DOES PREDNISOLONE HELP IN PCOS
REVERSES CARCADIAM RYTHMN AND SUPPRESSES PITUITARY ACTH
126
WHAT IS ANDROGEN INSENSITIVITY SYNDROME
WHEN AN INDIVIDUAL HAS CELLS WITH LITTLE TO NO RESPONSE TO ANDROGENS
127
WHAT CAUSES OF ANDROGEN INSENSITVITY SYNDROME
A GENETIC FAULT CAUSING THE BODY TO NOT RESPOND TO TESTOSTERONE
128
WHAT IS THE PATHOPHYSIOLOGY OF ANDROGEN INSENSITIVITY SYNDROME
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
129
WHAT ARE THE TYPES OF ANDROGEN IINSENSITIVITY SYNDROME
MILD
PARTIAL
COMPLETE
130
DESCRIBE MILD ANDROGEN INSENSITIVITY SYNDROME
ABNORMAL MALE GENETALIA
131
DESCRIBE PARTIAL ANDROGEN INSENSITIVITY SYNDROME
ABNORMAL INTERNAL MALE REPRODUCTIVE ORGANS BUT EXTERNALLY ARE NORMAL
132
DESCRIBE COMPLETE ANDROGEN INSENSITIVITY SYNDROME
NORMAL EXTERNAL FEMALE GENETALIA
133
WHAT IS THE PRESENTATION OF ANDROGEN INSENSITIVITY SYNDROME
INFERTILITY
FROM SPERM DEFECTS TO FULL FEMALE GENETALIA
134
HOW WOULD YOU DIAGNOSE ANDROGEN INSENSITIVITY SYNDROME
KARYOTYPE
GENETIC TESTING FOR ANDROGEN RECEPTOR INSENSITIVITY MUTATIONS
135
HOW WOULD YOU MANAGE ANDROGEN INSENSITIVITY SYNDROME
SEX ASSIGNMENT
GENITOPLASTY
GONADECTOMY
HRT
COUNCELLING
136
WHAT IS AMENNORHEA
ABSENCE OF PERIODS
137
WHAT IS PRIMARY AMENNORHEA
ABSENCE OF MENSES BY 14-16
WITH NORMAL SECONDARY SEXUAL CHARACTERISTICS AND GROWTH
138
WHAT IS SECONDARY AMENNORHEA
PREVIOSULY HAVING MENSES
THEN ABSENCE OF MENSES FOR 6M OR OVER
139
WHAT ARE THE MAIN CAUSES OF PRIMARY AMENORHEA
TURNERS SYNDROME
VAGINAL AGENESIS
ANDROGEN INSENSITIVITY SYNDROME
140
WHAT ARE CAUSES OF SECONDARY AMENORRHEA
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
141
WHAT INVESTIGATIONS ARE REQUIRED IN AMENNORHEA
BLOODS
* FSH, LH, OESTROGEN, PROLACTIN, T3/T4, TSH
PIUTITARY MRI
OVARIAN BIOPSY
GENETIC TESTING
142
YOU ARE TESTING A PATIENT WITH SECONDARY AMENORHEA WHOS BLOODS COME BACK AS
HIGH FSH AND LH
WHAT DOES THIS INDICATE
OVARIAN FAILURE
143
YOU ARE TESTING A PATIENT WITH SECONDARY AMENORHEA WHOS BLOOS COME BACK AS
HIGH PROLACTIN
WHAT DOES THIS INDICATE
LACTATION
144
HOW DO WE MANAGE AMENNORHEA
TREAT ANY MANAGABLE CAUSES
HRT UNLESS RESISTANT OVARIAN SYNDROME
145
WHAT IS ATROPHIC VAGINITIS
THINNING OF VAGINAL WALLS
VAGINA BECOMING DRY AND INFLAMMED
146
WHAT CAUSES ATROPHIC VAGINITIS
FALLING OESTROGEN LEVELS
147
WHATS IS THE PRESENTATION OF ATROPHIC VAGINITIS
VAGINAL DRYNESS
VAGINAL BLEEDING AND DISHCHARGE
DYSPURUNEA
RECURRANT UTI
148
HOW WOULD YOU DIAGNOSE ATROPHIC VAGINITIS
SWABS TO RULE OUT INFECTION
SPECULUM
149
HOW WOULD YOU TREAT ATROPHIC VAGNITIS
LUBRICANT
EMMOLIANT
TOPICAL OESTROGEN
HRT
150
WHAT IS SUPERFICIAL DYSPYRUNEA
PAIN SURING SEX AT VAGINAL ENTRANCE / CANAL
151
WHAT ARE CAUSES OF SUPERFICIAL DYSPYRUNEA
INFECTIONS
INTROITUS NARROWING
ATROPHIC VAGINITIS
LICHEN SCLEROSIS
152
WHAT IS DEEP DYSPYRUNEA
PAIN DURING INTERCOURSE UPON DEEP PENETRATION FELT IN ABDOMEN
153
WHAT ARE CAUSES OF DEEP DYSPYRUNEA
PID
RETROVERTED UTERUS
OVARIAN PROLAPSE INTO POUCH OF DOUGLAS
ENDOMETRIOSIS
NEOPLASTIC DISEASE
POST OP SCARRING DUE TO DECREATED UTERINE MOTILITY
154
HOW WOULD YOU DEFINE THE MENAUPAUSE
CESATION OF MENSES FOR 12 MONTHS
155
WHAT IS THE AVERAGE AGE FOR STARTING MENAUPAUSE
51Y
156
HOW WOULD YOU DESCRIBE PERIMENAUPAUSE
THE PERIOD LEADING UPTO MENAUPAUSE CHARACTERISED BY IRREGULAR PERIODS AND MENAUPAUSAL SYMPTOMS
157
WHAT ARE SYPTOMS OF MENAUPASE / PERIMENAUPAUSE
HOT FLUSHES
MOOD SWINGS
UROGENITAL ATROPHY
DECREASED LIBIDO
VAGINAL DRYNESS
DRY ITCHY SKIN
DECREASED CONFIDENCE
JOINT AND MUSCLE PAIN
158
DESCRIBE THE PHYSIOLOGY OF MENAUPAUSE
DEACREASED EGGS SO DECREASED OESTROGEN
DECREASED OESTROGEN MEANS LESS NEGATIVE FEEDBACK OF PITUITARY MEANING LESS GnRH
HIGHER FSH LH CAUSING IRREGULAR MENSES
159
WHAT IS THE MANAGEMENT OF MENAUPAUSE
HRT
CLONIDINE
160
WHAT ARE THE TYPES OF HRT AND WHEN ARE THEY GIVEN
COMBINED
* UTERUS
OESTROGEN ONLY
* HYSTERECTOMY
CYCLICAL
* ANY WOMAN STILL IN PERI MENAUPAUSE
161
WHY IS OESTROGEN ONLY HRT NOT GIVEN TO WOMEN WITH UTERUS
LACK OF PREOGESTERONE AND HIGH OESTROGEN WILL INCREASE ENDOMETRIAL PROLIFERATION INCREASING RISK OF CANCER
162
WHAT ARE CONS OF HRT
INCREASED RISK OF BREAST CANCER
INCREASED RISK OF CVD AND STROKE
INCREASED RISK OF VTE
163
WHAT ARE BREAST CANCER RISKS IN HRT
PROGESTERONE IS DRIVING FORCE
OESTROGEN ONLY IN BRACA
RISK REDUCES AFTER STOPPING
164
WHY IS TRANSDERMAL BETTER IN SOME GROUPS (AND WHICH)
HIGH VTE RISK GROUPS AS
PASSES FIRST PASS METABOLISM SO DOESNT AFFECT CLOTTING FACTORS
165
WHAT IS PREMATURE OVARIAN INSUFFICIENCY
PERI MENAUPAUSE UNDER 40 YEARS
166
HOW CAN YOU DIAGNOSE PREMATURE OVARIAN INSUFFICIENCY
TWO FSH TESTS 4 WEEKS APART
NO PERIOD IN 4 MONTHS
PREGNANCY TEST
PELVIC US
167
WHAT IS THE PRESENTATION OF PREMATURE OVARIAN INSUFFICIENCY
IRREGULAR AND MISSED PERIODS
MENAUPAUSAL SYMPTOMS
INFERTILITY
168
HOW DO YOU MANAGE PREMATURE OVARIAN INSUFFICIENCY
HRT
CALCIUM AND VIT D SUPPLIEMNTS
IVF
169
WHAT CAUSES PREMATURE OVARIAN INSUFFICIENCY
IDOPATHIC
ALSO
FRAGILE X OR TURNERS
ADDISONS
CHEMO
LOW FOLLICLE NUMBER
170
CHAT ARE CERVICLE POLYPS
A BENIGN OR CANCEROUS GROWTH ON THE CERVIX
171
WHAT IS THE PRESENTATION OF A CERVIACLE POLYP
INTERMENSTRUAL BLEEDING
BLEEDING DURING PREGNANCCY (ANTEPARTUM BLEEDING)
POST COITAL BLEEDING
WHITE/YELLOW DISCHARGE
172
HOW DO YOU DIAGNOSE CERVICLE POLYPS
SPECULUM
COLPOSCOPY + BIOPSY
173
HOW DO YOU TREAT CERVIACLE POLYPS
REMOVAL WITH RING FORCEPS AND CAUTERISATION
174
WHAT IS A PRIMARY POST PARTUM HAEMORRAGE
BLEEDING FROM GENITAL TRACT
OVER 500ML
DURING DELIVARY OR WITHIN 24 HRS AFTERWARDS
175
WHAT ARE CAUSES OF PRIMARY POST PARTUM HAEMORRAGE
THE 4 TS
TONE
* Uterine atony from - prolonged labour - twins - multiparus
TISSUE
* Retained placental tissue
THROMBIN
* decreased thrombin from LMWH
TRAUMA
176
WHAT BLOOD VOLUME CLASSES AS A MAJOR PRIMARY POST PARTUM HAEMORRAGE
1500ML +
177
WHAT IS THE MOST COMMON CAUSE OF PRIMARY POST PARTUM HAEMORRAGE
(TISSUE) PLACENTAL SITE BLEEDING
178
WHAT IS THE DEFINITION OF SECONDARY POST PARTUM HAEMORRAGE
ABNORMAL VAGINAL BLEEDING UPTO 6 WEEKS AFTER DELIVARY
179
WHAT CAUSES SECONDARY POST PARTUM HAEMORRAGE
RETAINED PLACENTAL TISSUE
UTERINE INFECTION
TROPHOBLASTIC DISEASE
180
WHAT ARE THE SIGNS OF A MILD SECONDARY POST PARTUM HAEMORRAGE
MILD BLEEDING
ASYMPTOMATIC
NON TENDER UTERUS
(NORMAL WOMAN BLEEDING MORE THAN SUPPOSED TO)
181
WHAT ARE THE SIGNS OF A SEVERE SECONDARY POST PARTUM HAEMORRAGE
HEAVY BLEEDING
PAIN
FEVER + SIGNS OF INFECTION
182
HOW WOULD YOU MANAGE A SEVERE SECONDARY POST PARTUM HAEMORRAGE
ABX (IV) EMPIRICAL THEN
BLOOD CULTURES, URYNALISIS AND SWABS TO CONFIRM ABX CHOICE
UTERINE CLEARENCE (SUREGRY)
183
HOW WOULD YOU MANAGE A PRIMARY POST PARTUM HAEMORRAGE
FLUIDS
BLOODS
if placenta is retained : CONTROLLED CORD EXPULSION
if placenta is expulsed : OXYTOCIN \> HARTMANS \> ERGOMETRIN \> PROSTAGLANDINS (MYSOPROSTOL) \> BIMANUAL COMPRESSION \> SURGERY
184
HOW WOULD YOU MANAGE A MILD SECONDARY POST PARTUM HAEMORRAGE
OBSERVE AND MONITOR
185
WHAT ARE THE CAUSES OF ANTEPARTUM HAEMORRAGE
CERVICAL LESIONS AND POLYPS (OR CANCERS)
VASA PREVIA
PLACENTA PREVIA
INFECTIONS
PLACENTAL HAEMORRAGE
186
WHAT IS PLACENTA PREVIA
WHEN THE PLACENTA IS OVER THE OS IN THE THIRD TRIMESTER
187
WHY CANT PLACENTA PREVIA BE DIAGNOSED BEFORE THE THIRD TRIMESTER
BECAUSE OFTEN ATTACHES LOW BUT AS UTERUS EXPANDS GOES UPWARDS NO LONGER BEING PREVIA
188
HOW WOULD YOU DIAGNOSE PLACENTA PREVIA
US
189
IN A SITUATION OF ANTEPARTUM HEAMORRAGE IN A PATIENT KNOWN TO HAVE PLACENTA PREVIA WHAT WOULD BE YOUR MANAGEMENT
SPECULUM
CTG
MONITOR BLEEDS
CHECK MATERNAL FBC
IF IN DISTRESS C SECTION
190
IN A WOMAN WITH PLACENTA PREVIA HOW IS DELIVARY PREPARED FOR
MATCH MUMS BLOOD TYPE AND HAVE BLOODS READY
POSTPONE DELIVARY AT 37 WEEKS THEN C SECTION
191
WHEN CAN VAGINAL DELIVARY BE ATTEMPTED IN A CASE OF PLACENTA PREVIA
IN GRADES I AND II OF PLACENTA PREVIA WHERE THE PLACENTA IS NOT DIRECTLY OVER THE OS
192
WHAT IS A VAGINAL WALL HEAMATOMA
A POOLING OF BLOOD AT THE VAGINAL ENTRANCE, VAGINA, OR VULVA
193
WHAT TYPES OF VAGINAL WALL HEAMATOMA ARE THERE
SUPERFICIAL
DEEP
194
WHERE DO SUPERFICIAL VAGINAL HAEMATOMA OCCUR
BELOW THE INSERTION OF LEVATORI ANI DISTENDS HE PERINEUM
195
WHAT IS THE PRESENTATION OF A SUPERFICIAL VAGINAL HAEMATOMA
PAIN
A VISIBLE BRUISE
196
HOW DO YOU TREAT SUPERFICIAL HAEMATOMAS
DRAINING
VESSELS LIGATED AND COMPRESSED: ARTRIAL/VEINS
DRAIN INSERTED
197
WHERE DO DEEP VAGINAL HAEMATOMAS OCCUR
DEEP TO INSERTION OF LEVATOR ANI AND WASNT VISIBLE EXTERNALLY
198
WHAT IS THE PRESENTATION OF A DEEP VAGINAL WALL HAEMATOMA
CHRONIC PELVIC PAIN
URINARY RETENTION
UNEXPLAINED ANAEMIA
BULGING UPPER VAGINAL WALL
199
WHAT COMMONLY CAUSES DEEP VAGINAL WALL HAEMATOMA
INSTRUMENTAL DELIVARIES
200
HOW WOULD YOU DIAGNOSE A DEEP VAGINAL WALL HAEMATOMA
SPECULUM
US
201
HOW WOULD YOU TREAT A DEEP VAGINAL WALL HAEMATOMA
DRAIN VIA INCISION
INSERT DRAIN
VAGINAL PACKING
CATHETER
ABX AND TRANSFUSION
202
WHAT ARE THE TYPES OF PLACENTAL ATTACHEMENT
ACRETA (THROUGH ENDOTHELIUM)
INCRETA (TO MYOMETRIUM)
PERCRETA (TO SEROSA)
203
HOW WOULD YOU DIAGNOSE PLACENTA ACCRETA
US
AT SECOND AND THIRD TRIMESTER
204
WHAT IS THE DEFINITION OF A PLACENTAL HAEMORRAGE
SEPARATION OF PLACENTA FROM UTERINE WALL
205
WHAT ARE THE TYPES OF PLACENTAL HAEMORRAGE
REVEALED
CONCEALED
CONCEALED AND REVEALED
206
WHAT ARE THE SIGNS OF PLACENTAL ABRUPTION
PAIN
PV BLEEDS
HARD UTERUS
LONGITUDINAL LIE
207
HOW WOULD YOU MANAGE A PLACENTA HAEMORRAGE
IV INSERT AND GIVE HEAMOCRIT
CLOTTING PROFILE
TRANSFUSIONS
CCG
?C SECTION
208
WHAT ARE THE KEY DIFFERENCES ON PRESENTATION BETWEEN PLACENTA PREVIA AND A PLACENTAL ABRUPTION
PREVIA
PAINLESS BLEEDS
SOFT UTERUS
ABRUPTION
PAIN
HARD UTERUS
209
HOW WOULD YOU TREAT A PLACENTAL ATTACHEMENT DISORDER
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
WHAT ARE COMPLICATIONS OF A PLACENTAL ABRUPTION
CLOT FORMS CAUSING SYSTEMIC INTRAVASCULAR COAGULATION
COUVELERE UTERUS
PPH
HYPOVULAEMIA CAUSING RENAL UBULAR NECROSIS
211
WHAT IS UTERINE INVERSION
A RARE COMPLICATION WHERE THE UTERINE FUNDUS PROTRUDES THROUGH THE CERVIX
212
WHEN IS UTERINE INVERSION LIKELY TO OCCUR
DURING PLACENTAL DELIVARY ESP IF PLACENTA IS ADHERENT OR FUNDAL
213
WHAT ARE THE TYPES OF UTERINE NVERSION
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
WHAT IS THE PRESENTATION OF UTERINE INVERSION
SEVERE PAIN
VSIBLE UTERUS
PPH
SHOCK + BRADYCARDIA
215
HOW DO YOU MANAGE UTERINE INVERSION
FLUIDS AND BLOODS
REPOSITION UTERUS MANUALLY
ASSESS IF SURGERY NEEDED / TAKE TO SURGERY
ABX
216
WHAT ARE CERVIACLE EROSIONS
WHEN GLANUDLAR CELLS (USUALLY FOUND INSIDE CERVICAL CANAL) GROW ON THE NECK OF THE CERVIX
217
WHAT CAUSES CERVICLE EROSIONS
HORMONAL CHANGES
THE PILL
PREGNANCY
218
WHAT IS THE PRESENTATION OF CERVICLE EROSIONS
INTERMENSTURAL BLEEDS
PREGANCY BLEEDS
DYSPYRUNEA
POST COITAL BLEEDS
219
HOW DO YOU DIAGNOSE CERVIACLE EROSIONS
COLPOSCOPY
220
WHAT ARE TREATEMENTS FOR CERVIACLE EROSIONS
NO TREATEMENT UNLESS SYMPTOMATIC
CAUTERISATION
221
WHAT IS VASA PREVIA
ONE OF THE BRANCHES OF THE UMBILLICAL VESSELS LIES OVER THE CERVIACLE
222
WHY IS VASA PREVIA DANGEROUS
IF THERES ROM THE PRESSURE WILL CAUSE VESSELS TO BUST AND BABY TO BLEED AND DIE
223
HOW DO YOU DIAGNOSE VASA PREVIA
US + DOPPLER
224
HOW DO YOU MANAGE VASA PREVIA
A PLANNED C SECTION AT 35-36 WEEKS TO AVOID ROM
225
WHAT IS THE HISTOLOGICAL TYPE OF ENDOMETRIAL CANCER
AN ADENOCARCINOMA
226
WHAT ARE THE RISK FACTORS OF ENDOMETRIAL CANCERS
OBESITY
OESTROGEN ONLY HRT
DIABETES
LATE MENOPAUSE
227
WHAT IS THE CARDINAL SIGN OF ENDOMETRIAL CANCER
POST MENOPAUSAL BLEEDING
228
WHAT ARE THE OTHER SIGNS OF ENDOMETRIAL CANCER
BLOATING
BACK/LEG/PELVIC PAIN
TIERDNESS
NAUSEA
+ RED FLAGS
229
HOW WOULD YOU INVESTIGATE FOR ENDOMETRIAL CANCER
VAGINAL EXAMINATION
TRANSVAGINAL US
ENDOMETRIAL BIOPSY
230
WHAT IS THE TREATMENT FOR ENDOMETRIAL CANCER
HYSTERECTOMY
+/- PELVIC LYMPH NODES
RADIOTHERAPY
PROGESTERONE THERAPY (ONLY FOR INDIVIDUALS WHO CANT TOLERATE MORE)
231
WHAT IS OLIGOHYDRAMNIOUS
LOW AMNIOTIC FLUID WITH AMNIOTIC FLUID INDEX
232
WHAT ARE CAUSES OF OLIGOHYDRAMNIOUS
IMPAIRED PLACENTAL FUNCTION
RENAL ANGIOGENESIS
PREMATURE ROM
URINARY TRACT MALFORMATIONS
233
WHAT ARE THE CONSEQUENCES OF OLIGOHYDRAMNIOUS
IUGR
PULMONARY HYPERTENSION
RDS
CLUBBED FOOT
WRY NECK
INCREASED RISK OF CORD COMPRESSION DURING CONTRACTIONS CAUSING HYPOXIA
234
WHAT ARE TREATMENTS FOR OLIGOHYDRAMNIOUS
C SECTION AS SOON AS SAFE
235
WHAT ARE THE TYPES OF MALPRESENTATION
FACE
BROW
OCCIPITO-POSTERIOR
OCCIPITO-ANTERIOR
TRANSVERSE
236
DESCRIBE A FACE PRESENTATION
FETAL HEAD IS HYPEREXTENDED SO FACE IS PRESETING
237
HOW WOULD YOU DESCRIBE A BROW PRESENTATION
THE FETAL HEAD IS MIDWAY BETWEEN FLEXED VERTEX AND FACE
THE MOST UNFAVOURABLE POSITION
238
DESCRIBE AN OCCIPITO-POSTERIOR PRESENTATION
A MALPRESENTATION OF FETAL HEAD OF -20% OF ALL CEPHALIC PRESENTATIONS
ASSOCIATED WITH BACK PAIN AND A LONG PAINFUL LABOUR
239
WHAT IS DEEP TRANSVERSE ARREST
A HALT DURING THE NORMAL ROTATION MEANING HEAD IS OCCIPITO-TRANSVERSE
240
WHAT ARE THE STAGES OF NORMAL FETAL HEAD ROTATION
DESCENT
ENGAGEMENT
NECK FLEXION
INTERNAL ROATION: OP\>OT\>OA
CROWNING
EXTENSION OF PRESENTING PART
RESITITUTION
INTERNAL ROTATION
LATERAL FLEXION
241
HOW DO YOU ASSESS PRESENTATIONS
PALPATE LIE
PALPATE LOWER UTERUS AND BALLOT
ASSESS ENGAGEMENT
242
HOW DO YOU MANAGE MALPRESENTATIONS
C SECTION
243
WHAT IS A CORD PROLAPSE
OCCURS WHEN ANY PART OF THE CORD LIES ALONGSIDEOR INFRONT OF THE PRESENTING PART OF THE BODY
244
WHAT ARE RISK FACTORS OF CORD PROLAPSE
DISPLACEMENT OF THE PRESENTING PART
IRREGULAR SURFACE OF PRESENTING PART (IE NOT HEAD) CAUSING POOR MOULDING
ARM
245
HOW DO YOU MANAGE A CORD PROLAPSE
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
WHAT IS OBSTRUCTED LABOUR
WHEN THERE IS NORMAL UTERINE CONTRACTION BUT DELAYS IN LABOUR DUE TO CHILD BEING PHYSIOLOGICALLY BLOCKED
247
WHAT IS THE MOST COMMON CAUSE OF OBTRUCTED LABOUR
CEPHALOPELVIC DISPROPORTION
248
WHY MIGHT THERE BE CEPHALOPELVIC DISPROPORTION
MACROSOMIA
SMALL PELVIT INLET
249
WHEN IS IT OKAY TO TRY PV DELIVARY IN CEPHALOPELVIC DISPROPORTION
WHEN THERES GOOD MOULDING
| (CHECK AT ISCHEAL SPINES)
250
WHAT IS THE MANAGEMENT OF OBSTRUCTED LABOUR
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251
HOW LONG SHOULD LABOUR LAST IN A NULLIPARUS WOMAN
LATENT = HRS - DAYS
ACTIVE S1 = 8-18HRS
ACTIVE S2=5-12HRS
252
HOW LONG SHOULD LABOUR LAST IN A MULTIPARUS WOMAN
LATENT= HRS - DAYS
ACTIVE S1= 0-3HRS
ACTIVE S2= 0-2HRS
253
DEFINE WHAT A LATENT STAGE IS
CEVIX \< 4CM
IRREGULAR WEAK CONTRACTIONS (1/10)
EACH CONTRACTION LASTING APROX 30S
254
WHAT IS THE DEFINITION OF ACTIVE LABOUR
CERVIX AT 4-10CM
REGULAR STRONG CONTRACTIONS (3/10)
EACH CONTRACTION LASTING 90S
255
WHAT ARE THE STAGES OF LABOUR
STAGE 1- LATENT AND ACTIVE PHASE
STAGE2-PUSHING BABY
STAGE3-DELIVERING PLACENTA
STAGE 4-UTERINE INVOLUTION
256
WHAT TYPE OF CANCER IS CERVICLE CANCER
SQUAMOUS CELL CARCINOMA
257
WHAT IS THE MOST COMMON CANCER IN WOMEN UNDER 30
CERVICEL CANCER
258
WHAT CAUSES CERVICLE CANCER AND WHY?
HPV
HAS E6+7 RECEPTORS BLOCKING TUMOUR MARKERS P53 AND RB RESPECTIVELY
259
WHAT TEST IS USED TO SCREEN FOR CERVICLE CANCER AND DESCRIBE IT
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
HOW DO YOU TREAT CERVICLE CANCER
LLETZ LOOPS
HYSTERECTOMY
TUMOURS \>4CM NEED CHEMO AND RADIO
261
WHAT TYPE OF CANCER IS OVARIAN CANCER
EPITHELIAL CELL CARCINOMA
262
WHAT ARE SX OF OVERIAN CARCINOMA
ASYMPTOMATIC (SX VERY GENERIC AND MIMIC OTHER THINGS)
* IBS LIKE
* URINARY FREQUENCY
* ABDO PAIN RADIATING TO BACK
UNTIL LATE STAGE
263
WHAT ARE RF FOR OVARIAN CANCER
BRCA 1 + 2
LINKED TO HOW MANY TIMES YOUVE OVULATED BEFORE
264
AT WHAT STAGE OF DISEASE DO WOMEN USUSALLY PRESENT
STAGE 3 +
265
HOW WOULD YOU INVESTIGATE OVARIAN CANCER
BLOODS: CA125
US
CT
266
WHY IS CA 125 NOT SPECIFIC
ELEVATED IN FIBROIDS/CYSTS
267
WHAT IS THE TREATEMENT FOR OVARIAN CANCER
SURGERY
CHEMO
268
WHAT KIND OF CANCER IS VULVAL CANCER
SQUAMOUS CELL CARCINOMA
269
WHAT ARE RISK FACTORS FOR VULVAL CACER
HPV
LICHEN SCLEROSIS
270
WHAT ARE SX OF VULVAL CANCER
ITCHING
SORENESS
PAINFULLPASSING URINE
271
WHAT IS THE TREATEMENT FOR VULVAL CANCER
CHEMO
RADIO
272
WHAT TYPE OF CANCER IS VAGINAL CANCER
SQUAMOUS CELL/ADENOCARCINOMA
273
DESCRIBE THE AETIOLOGY OF VAGINAL CANCER
PRIMARY VAGINAL CANCER IS RARE
ONCE VAGINAL CANCER HAS SPREAD IT BECOMES TERMINAL IN MOST CASES
274
WHAT ARE RISK FACTORS FOR VAGINAL CANCER
VIN
HPV
275
WHAT IS VIN
VAGINAL INTRAEPITHELIAL NEOPLASIA
276
WHAT ARE SYMPTOMS OF VAGINAL CANCER
POST COITAL BLEED
POST MENOPAUSAL BLEEDING
LUMPS AND MASSES
FREQUENCY
DYSURIA
CONSTIPATION
PELVIC PAIN
277
HOW DO YOU Ix VAGINAL CANCER
SPECULUM
BI MANUAL EXAMINATION
COLPOSCOPY +/- BIOPSY
278
WHAT ARE Tx FOR OPTIONS FOR VAGINAL CANCER
LUMPECTOMY
VAGINECTOMY
HYSTERECTOMY
RADIOATION/CHEMO
279
WHAT IS GESTATIONAL TROPHOBLASTIC DISEASE
PREGNANY RELATED TUMOURS WHICH ARE VERY RARE
THESE ARISE FROM THROPHOBLASTS
280
WHAT ARE THE TYPES OF GTD
1. HYDRATIFORM MOLE
2. INVASIVE MOLES
3. CHORIOCARCINOMAS
4. PLACENTAL SIGHT TROPHOBALSTIC TUMOUR
5. EPITHELIAL TROPHOBLASTIC TUMOUR
281
DESCRIBE A HYDRATIFORM
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
WHAT IS AN INVASIVE MOLE
AN EGG WHICH DOES NOT CONTAIN A MATERNAL NUCLEUS IS FERTILIZED AND IMPLANTS THEN GROWS INTO THE MUSCLE WALL OF THE NUCLEUS
283
WHAT IS A CHORIOCARCINOMA
PLACENTAL ATTACHEMENT CELLS BECOMING MALIGNANT
HIGHLY RESPONSIVE TO CHEMO
GREAT SURVIVAL RATE
284
WHAT ARE RISK FACTORS FOR GTD
AGED 20-35Y
PREV GTD
ASIAN
285
HOW DOES GTD PRESENT
MIMICS PREGNANCY
ENLARGED UTERUS
PELVIC PAIN
HYPEREMISIS
286
HOW DO YOU DIAGNOSE A GTD
+VE PREG TEST
PICKED UP AT 15W SCAN
287
WHY IS BIOPSY CONTRAINDICATED IN GTD
HIGHLY VASCULAR
288
HOW DO YOU TREAT GTD
EVACUATION/HYSTERECTOMY (SURGERY)
HISPOLOGICAL SAMPLE
METHOTREXATE
RADIOTHERAPY FOR METS
289
WHAT IS A DURAL PUNCTURE LEAK
WHEN PERFORMING AN EPIDURSL THE DURA IS PUNCTURED CAUSING A CSF LEAK
290
WHAT ARE THE SYMPTOMS OF A DURAL PUNCTURE
HEADACHE WHICH IMPROVES ON LYING DOWN
NECK STIFFNESS
PHOTOPHOBIA
291
HOW DO YO TREAT A DURAL PUNCTURE
BLOOD PATCH
292
WHAT IS URINARY RETENTION
ONSET OF INABILITY TO COMPLETELY MICTURATE REQUIRING CATHETERISATION
293
WHAT CAN CAUSE URINARY RETENTION
ANAESTHESIA
DAMAGE TO PUDENAL NERVE
UROGENITAL SWELLING AND OEDEMA
294
WHAT CAN DAMAGE THE PUDENAL NERVE
VAGINAL DELIVARY
INSTRUMENTAL DELIVARY
PROLONGED LABOUR
295
WHAT ARE COMPLICATIONS OF URINARY RETENTION
BLADDER DYSFUNCTION
UTI
CATHETER RELATED INJURY
296
WHEN IN PREGNANCY ARE YOU AT HIGHEST RISK OF VT
FISRT THREE WEEKS AFTER DELIVERY
297
WHAT ARE THE RISK FACTORS FOR VT
PREV VT
ANTENATAL LMWH
C SECTION
BMI\>40
35Y+
MULTIPLE PREGNANCYIES
IMMOBILITY
298
WHAT IS THE TREATEMENT FOR A VT
LMWH
299
WHAT PROFYLAXIS WOULD YOU GIVE TO A HIGH RISK VT WOMAN
10D PROFYLACTIC PMWH POST DELIVARY
PRE DELIVARY FROM 28 W
300
WHAT PROFYLAXIS WOULD YOU GIVE TO A HIGH RISK VT PREGNANCY
PROFYLACTIC LMWH FROM 28W
6 WEEKS PROFYLACTIC LMWH POST DELIVERY
301
WHAT ARE THE HORMONES WHICH DRIVE BREAST MILK PRODUCTION
OXYTOCIN
PROLACTIN
302
WHAT IS THE MECHANISM OF OXYTOCIN
DRIVES EJECTION OF BREAST MILK
BABY SUCKLING DRIVES OXYTOCIN PRODUCTION BY POSTERIOR PITUITARY GLAND
303
WHAT IS THE MECHANISM OF PROLACTIN
DRIVES PRODUCTION OF MLK
BABY SICKLING DRIVES PROLACTIN PRODUCTION BY ANTERIOR PITUITARY GLAND
304
WHAT CELLS DOES OXYTOCIN ACT ON
MYOEPITHELIAL CELLS
305
WHAT CELLS DOES PROLACTIN ACT ON
LACTOLYTES
306
WHAT IS LACTOGEN
A PROLACTIN LIKE HORMONE PRODUCES BY THE PLACENT WHICH DECREASES MATERNAL INSULIN AND FACILITATES ENERGY SUPPLY TO FOETUS
307
WHAT IS LACTOFERRIN
A MOLECULE WHICH BINDS IRON IN BREAST MILK HELPING BABY ABSORB IRON WHILST INHIBITING BACTERIAL PROLIFERATION
308
WHAT ARE THE BENEFITS OF BREAST FEEDING
SUPPRESSES OVULATION
BOOSTS BABYS IMMUNE SYSTEM
BONDING
REDUCES RISKS OF BREAST AND OVARIAN CANCER AND OSTOPOROSIS (18MONTHS BREAST FEEDING)
309
WHAT IS THE PUERPERIUM
PERIOD OF TIME FROM DELIVERY OF THE PLACENTA TO 6 WEEKS AFTER BIRTH
310
WHAT ARE THE THREE STAGES OF THE PUEPERIUM
1. RETURN TO PREPREGNANT STATE
2. INDUCTION AND SUPPORESSION OF LACTATION
3. TRANSITION TO PARENTHOOD
311
WHAT ARE THE PHYSIOLOGICAL CHANGES THAT OCCUR WHEN RETURNING TO PRE PREGNANT STATE
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
WHAT IS DECIDUA
BLOOD AND OTHER CONTENTS IN UTERO AFTER PREGNANCY
313
WHAT IS LOCHIA
THE SHEDDED DECIDUA
314
WHAT ARE THE TYPES OF LOCHIA
* 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
WHAT ARE SEVERE COMPLICATIONS OF THE PUEPERL PERIOD
SEPSIS
PPH
ECLAMPSIA
THROMBOSIS
UTERINE PROLAPSE
POST DURAL PUNCTURE HEADACHE
BREAST ABCESS
PSYCHOSIS
316
DEFINE SEPSIS
INFECTION WITH SYSTEMATIC MANIFESTATIONS
317
DEFINE SEVERE SEPSIS
SEPSIS WITH ORGAN DYSFUNCTION OR HYPOPERFUSION
318
DEFINE SEPTIC SHOCK
PERSISTANCE OF HYPOPERFUSION DESPITE FLUID RESUS
319
WHAT ARE THE SIGNS OF SEPSIS
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
WHAT IS THE MANAGEMENT OF SEPSIS
FLUIDS
BLOOD CULTURES
URINALYSIS AND CULTUES
O2
IV ABX EMPIRICALLY UNTIL CULTURES RETURN
321
WHAT IS THE DEFINITION OF PRE ECLAMPSIA
BP\>140/90
+PROTEINURIA
AFTER 20 WEEKS GESTATION
322
WHEN DOES PRE-ECLAMPSIA TURN TO ECLAMPSIA
WITH START OF CONVULSIONS
323
WHAT ARE RF FOR PREECLAMPSIA
OBESITY
OLD AGE
KIDNEY DISEASE
HTN
DIABETES
FAMILY HX OF PRE ECLAMPSIA
324
WHAT ARE SYMPTOMS OF PRE ECLAMPISA
SWELLING OF HANDS AND FACE
PITTING OEDEMA
HEADACHES
FLASHING LIGHTS
ABDO PAIN
HYPERREFLEXIA
325
WHAT IS THE PROFYLXIS FOR PRE ECLAMPSIA
APSRIN LOW DOSE DAILY UP UNTIL DELIVARY
326
HOW DO YOU MANAGE PRE ECLAMPSIA
LABETALOL
PREDNISOLONE + MAGNESIUM SULPHATE 24 HRS PRE DELIAVRY
DELIVER PLANNED AT 37-38 WEEKS
327
Define a show
a plug of mucus and blood which is 'delivered' at the start of labour
328
define 'waters breaking'
a ruputre of membranes and amniotic sac
329
what are the indicaions of waters breaking
show
rupture of membranes
contractions
330
what is the purpurse of contractions
efface and dilate the cervix and then help move baby
331
what is the definition of active labour
4-10 cm
coordinate strong
frequent contractions
332
how long does active labour last in primigravida
12-13 hrs
333
how long does active labor last in multigravida
6-9hrs
334
describe phase 1 of labour
consists of of labour and active phase
335
describe the second phase of labour
power - forceful contractions
passage
passenger
336
what are the cardinal movements of a baby
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
phase 3 of labour is ?
uterine contractions causing placental separation
338
phase 4 of labour
uterine involution and the return to pre pregnanct stage
339
hormones used in labour
progesterone
oestrogen
prostaglandins
relaxin
endorphins
adrenaline
340
what is the role of relaxin in labour
loosens tendons and ligaments makng pelvis more flexible
341
what causes prostaglandin synthesis
presence of oxitocin
pressure on cervix
342
what is the role of prostaglandins in labour
cervicle ripening
343
what is the role of oxitocin in labour
promotes uterine contractions
ripens cervix
344
what is the role of preogesterone in early pregnancy
proliferation and vascularisation of endometrial strome
promotes maternal quiescence
increases maternal ventilation
promotes glucose deposition
345
what is the role of prostaglandin in late pregnancy
prevents labour onset
prevents lacttaion
prengthens pelvic muscles
346
where is progesterone produced
corpus luteum
placenta (trophoblastst)
347
where is oestrogen produced in pregnancy
at start corpus luteum
then fetal liver and adrenal glands as well as maternal ovaries
348
what is the role of oestrogen during pregnancy
growth and correct placental function
promoting maternal breast development
increases endometrial progesterone recepors
349
describe the HPG axis
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350
describe the physiology of ovulation
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
describe the effecst of FSH+LH on follicular cells
LH acts on thecal cells
FSH acts on granulosa cells
theca cells produce testosterone which granulosa cells change to oestrogen
352
describe the menstrual cycle
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
what are gonadotrophins
glycoproteins :
fsh
lh
hcg
354
what is a female steriod
oestrogen
355
what do thecal cells do
synthesis progesterone and testosterone from cholesterol
356
what is the role of granulosa cells
to turn the testosterone made bythecal cells to oestrogen
357
how does implantation occur
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
what is the purpose of the decidua
permits invasion of blastocyst and implantation causing uterine stromal enlargement and proliferation of uterine natural killer cells
359
what is the limiting factor of stromal invasion
decdua basalis
360
what can cause placental mediated diseases
poor remodelling of spiral arteries
361
what is a morola
a solid ball of cells resulting from the division of a fertilized ovum
362
what is a lacunae
a small depression which fills with maternal blood this is where the placents begins
363
what is the vascular supply of the umbilical cord
x2 arteries - deoxygenated
x1 vein- oxygenated
364
what structures does teh ectoderm form
nervous system]epidermis
hair
eye lense
365
what structures does a mesoderm form
skeleton
dermis
muscles
vascular
urogenital
366
what structures does the endoderm form
GI tract
pancreas
liver
thyroid
367
what are implications of pregestational diabetes in pregnancy on the mother
increased risk of:
pre eclampsia
instrumental/c section delivery
368
what are implications of pregestational diabetes in pregnancy on the fetus
misscarrige/still birth
fetal abnormalities
macrosomia
prem baby
shoulder distocia/erbs palsey
NICU admission (RDS,jaundice, hypoglycaemia)
369
a T2 diabetic woman comes to you and asks about conception and pregnancy advice. what would that be?
maintain HBA1C\<48
take folic acid
stop ACEi and satins
regular retinal screening
GFR monitoring + albumin
370
what is the management of a T1 diabetic woman in pregnancy
insulin on bolus regime
metformin
if Hypo = glibenclamide
371
what is the leading cause of maternal death in UK
thrombotic events associated with pregnancy
372
why does pregnancy put you in a thromboembolic state?
increase in coagulation factors and decrease in anticoagulation factors
decreased fibrinolysis
increase in venous stasis
373
what are the risk factors for a clot in pregnancy
icreased age
increased BMI
operative delivary
smoking
sickle cell
pre eclampsia
374
how would you investigate a clot in pregnancy
US + doppler
VQ scan
or in PE
CTPA
venous perfusion scan
if sustepcting venous sinus embolism = CT head
375
how do you manage embolic events in pregnancy
LMWH
WARFRIN = TETROGENIC!!!
376
what are maternal complications of renal disease
accelerated irreversible renal failure
hypertension
pre eclampsia
increased c section risk
377
what are fetal complications of renal disease
IUGR
prematurity
still birth
congenital abnormalities due to drug therapies
378
how does renal physiology change in pregnancy
GFR increases by 50%
serum creatinine, urate and albumin falls
379
what is the management of renal disease in pregnancy
STOP ACEi+ARB
start labetalol, folic acid and low dose asprin
regular fetal survailence
380
why is it important to screen pregnant women with renal disease for UTI's
the risk to pregancies with renal disease is very high
381
what are the implications of epilepsy on pregnancy for mother
increase frequency of siezures
increased risk of sudden epileptic death
382
what are the implications of epilepsy on pregnancy for fetus
increased riskof congenital abnormalities (medications)
still birth due to hypoxia caused in prolonged seizures/ status epilipticus
383
what congenital abnormalities does serum valopate cause in fetus'
neural tube defects
congenital heart defects
lowered IQ
cleft pallette
384
what is the managment of epilepsy in pregnancy
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
what changes in pregnancy which may cause or exaccerbate anaemia
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
what are maternal risks of mild anaemia
dizziness meaninf + risk in falls
387
what are fetal risks of mild anaemia
+ risk of neonatal anaemia
388
what are maternal risks of severe anaemia
fainting meaning + risk in falls
increased risk of mortality duing childbirth due to blood loss
389
what are fetal risks of severe anaemia
prem baby
low birth weight
increased risk of severe neonatal anaemia
390
how do you diagnose anaemia in pregnancy
FBC
iron studies
391
management of anaemia in pregnancy
iron
folate
b12
if very severe : blood transfusions
392
how common is asthma in pregnancy
5-10%
393
what are maternal implications of asthma
1/3rd of asthmatics become worse and in 3rd trimester there is + risk of exacerbations
394
what are fetal implications of asthma
decreased perfusion so there + risk of IUGR
prem delivary due to maternal deterioration
pre-eclampsia
395
how do you manage uncomtrolled asthma in pregnancy
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396
what is the Px of obstetric cholestasis
intense itching
* wthout a rash
* mainly on palms and feet
commonly in 2nd+3rd trimester
397
investigations for obstetric cholestasis
AST
ALT
urine bile acides + serum
398
what are maternal complications of obstetric cholestasis
pruritis
prolonged clotting time (+ PPH risk)
399
what are fetal complications of obstetric cholestasis
prem
still birth (due to +++ bile acids)
400
what is the Mx of obstetric cholestasis
uredeoxycholic acids
oral water soluble vit K
induce labour at 37 w
401
why shoudld post natal contraception that contains oestrogen be avoided in abstetric cholestasis
because oestrogen is potential cause of obstetric cholestasis and may prolong Sx
402
why is the incidence of cardiac disease increasing in pregnant women
age of pregnancy is + so + risk of ischemic heart disease
survavival of congenital heart disease is much better now
403
what are the maternal implications of heart disease in pregnancy
increased risk of heart failure
pre eclampsia
404
what are the baby implications of heart disease in pregnancy
IUGR
prem
miscarrige
405
what cardiac pathologies have highest risk in prenancy
fixed cardiac output pathologies
eg
* aortic stenosis
* coarctation of aorta
* prosthetic valves
406
what cardiac pathologies have lowest risk in prenancy
regurgent lesions
eg
* AD
* VSD
* mitral or aortic incompetence
407
how do yo Ix the effects of cardiac disease in pregnancy
maternal echo
maternal ECG
fetal serial growth scans
fetal doppler
BP monitoring
408
Mx of cardiac disease in pregnancy
LMWH (anticoagulants)
inotropes (cardiomyopathies)
labetalol (aortic stenosis + miral stenosis + mitral prolapse)
Abx to prevent endocarditis
409
What is the management of Endocarditis in pregnancy
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
why are women with cardiac disease at high risk of heart failure in the post partum changes
large haemodynamic changesin labour a
411
what are maternal implications of hypothyroidism in pregnancy
increased risk of PPH
412
what are fetal implications of hypothyroidism in pregnancy
miscarrige
neurodevelopmental inpairement and developmental delay
413
how would you manage hypothyroidism in pregnancy
thyroxine
iodine suppliments
414
when is thyroid control most important in pregnacy
1st trimester
415
why is hypothyroidism uncommon in pregnancy
autoimmune state (main cause = graves) it usually resolves in pregnancy
416
what are maternal implications of hyperthyroidsim in pregnancy
Thyrotoxicosis
cardiac failure (due to thyrotoxicosis)
pre eclampsia
417
what are fetal implications of hyperthyroidsim in pregnancy
still born
IUGR
prem baby
418
why would thyrotoxicosis occur
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
how would you manage hyperthyroidism in pregnancy
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
what is contraindicated in the managment of hyperthyroidism in pregnancy
carbimazole = fetal abnormalities
radioactive iodine
421
