Obs and Gynae Flashcards

1
Q

Abdo pain DDX in preggers and timing if known

A

Non Gyane

UTI
Pyelonephritis
Cholesystitis
Appendicitis
Pancreatitis
Ligament strain 
Rectus sheath haematoma
Gastroenteritis

Gynae

Miscarriage
Pre Eclampsia
Ovarian cyst rupture/ torsion 
Uterine torsion 
Uterine rupture T3
Fibroids T2
Abruption
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2
Q

Presentation of cholecystitis in preggers and management

A
Presentation
		Less likelly jaudice
		Pain, nausea and vomiting
	Diagnosis
		If appendicitis cannot be ruled out (presence of stone?) then lapaoroscopy
	Management
		Conserve
		Severe then lap chole - some risk of miscarriage/ pre term labour
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3
Q

Presentation, DDX adn Management of pyelonephritis in preggers

A
More common in congenital renal abnormalities, neuropathic bladder and stone
	Presentation
		Frequency
		Urgency
		May not have other symptoms
		May be severe with
			Tachy
			Vomiting
			Loin pain
	DDX 
		Hyperemesis gravidarum
	Management
		Blood and urine culture
		IV cefuroxime (2nd)
If septic - stat gentamicin
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4
Q

management of UTI in preggers

A

Management
Trimethaprim CI in T1
Nitrofluratoin CI in T3 (neonatal haemolytic anaemia)
Cefalexin (1st gen) first line
Argument for treasting asymptomatic bacteriuria due to risk of UTI
Follow up post cystiits with MSU to ensure resolution

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5
Q

Classical presentation of abruption adn complications

A
The triad 
		Abdo pain
		Uterine rigidity 
		Vaginal bleeding
	1 in 200 preggers
	Comps
		DIC - high rate up to 50%
		PPH
High fetal loss
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6
Q

Uterine perforation presentation

A
abdominal pain (may be vague)
		Tenderness (over scar)
		PV bleed (may be absent)
		Late T3/ Labour
		Signs
			Shock
			Maternal hypertension
			Cessation of contraction
			Dissapearence of presenting part of baby during labour
			Fetal distress (CTG)
		Post partum
Failure of PPH to cease with well contracted uterus
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7
Q

Uterine perforation RFs

A

C section - scar pain
Obstruction
High foceps delivery - (CI above ischael spine)Internal version - manual turning via vagina
Obstructed in multiparous - especially if oxytocin used
Previous cervical/ uterine surgery
Breech extractaction

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8
Q

Management of uterine perforation

A

If in labour then cat 1 CS
High flow O2
Crossmatch 6 units and fast transfusion
Repair may be possible unless involves cervix or vagina in which case hysterectomy
Post op abx - cef and metro?

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9
Q

Uterine torsion patho

A

When it rotates >90 deg
Adrenax mass
Fibroids
Congential asymmetrical uterine anomalies

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10
Q

Uterine torsion presention

A
Mid to late preggers
		Abdo pain
		Shock
		Tenderness
Urinary retention
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11
Q

Management of uterine torsion

A

Resus
Catheter ( may shows location of uterus)
Diagnostic lapaotomy
LSCS

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12
Q

Fibroids presentation in preggers

A
Abdo pain
		\+/- vomiting and low grade fever
		Localised peritoneal tenderness
			Last half of preggers or puerperium
Large for dates
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13
Q

Fibroids pathophysiology and investigation in preg

A
RF
		Afro Carribean
		Increase in size during preggers/ T2
	Investigation
		US
		Colour flow Doppler - Fibroids vs Myometrium
	Patho
		If pedunculated may become tort
		Red degendeation in 50% preggers= thrombosis of capsular vessels followed by venous enghorement and inflammation = pain
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14
Q

Fibroids management in preg

A

Bed rest and analgesia (resolution =4-7 days
Most in body so do not obstruct(tend to rise in preggers)
Obstructed = CS

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15
Q

OVarian torsio/ cyst rupture patho

A

x Uterine cysts are very common
>5cm troublesome unless symptomatic
Uterus growing raises and displaces ovaries
Venous return becoming oedematous eventually impeding arterial

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16
Q

Benign cyst presentation

A
Asymptomatic
			Chronic pain with full ache
			Irregular vaginal bleed
			Abdo swelling or mass (if malig then ascites)
Unilateral iliac fossa pain
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17
Q

Presentation torsion/ rupture

A

Torsion = severe pain and vomiting
Improve over 24hr as ovary starts to due
Rupture = torsion symptoms with shock/ ?bleeding

	Examination
		Adnexal mass
		Cervical excitation Bleeding/ discharge
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18
Q

Investigations of benign cysts

A
TVS
			Malignant (multilocaular cyst, wall projections, solid areas, mets, ascites, bilateral lesion
		Transabdo imagin
		ing if large
		>7cm then ?MRI
Staging CT/ MRI
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19
Q

management of acute torsion/rupture

A

Acute pain

Urgent laparoscopy after TVS

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20
Q

Management of benign cysts

A
Pre menopausal
			Preserve fertility and exclude malig
			Nothing if <5 cm and non malig.
			Follow up
			Vs laparoscopy (avoid spilling)
		Post meno
			Risk of Malignancy Index
			Repeat TVS and CA125 to folow up every 4 months
			Bilater oophorectomy
			High risk = staging
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21
Q

Fibroids patho and natural history and RFs

A

Benign SM tumours, 20% of white and 50% of black women
Normally regress after menopause

RF
AfroCarribean
Age - response to puberty/ oestrogen

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22
Q

Fibroids Symptoms

A

may be asymptomatic
menorrhagia
lower abdominal pain: cramping pains, often during menstruation
bloating
urinary symptoms, e.g. frequency, may occur with larger fibroids
subfertility

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23
Q

Diagnosis fibroids

A

TV US

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24
Q

Management fibroids

A

Management
symptomatic management with a levonorgestrel-releasing intrauterine system is recommended by CKS first-line
other options include tranexamic acid, combined oral contraceptive pill etc
GnRH agonists may reduce the size of the fibroid but are typically useful for short-term treatment
Hot flushes
Osteoporosis
surgery is sometimes neede if >3cm/ distoring uterine cavity: myomectomy, hysterscopic endometrial ablation, hysterectomy
uterine artery embolization
GnRhH before surgery to shrink

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25
Comps of fibroids
red degeneration - haemorrhage into tumour - commonly occurs during pregnancy
26
Presentaiton of endometrial hyperlasia
IMB PMBMenorrhagia Dysmenorrhea
27
Management of endometrial hyperplasia
``` Management Simple High dose prog every 3-4 months Levonorgestrel IUD Rebiopsy after 6-12months Atypia Hysterectomy with bilat salpingo oophorectomy (risk of malignant progression ```
28
Chronic pelvic pain cause
Physical: IBS, interstitial cystitis, Chronic infection e.g. PID, endometriosis/adenomyosis, Neuopathic pain form previous laproscopies. Psychosexual: Depression, child abuse, Emotional problems, stress
29
Chronic pelivc pain management
Mnaagement MDT Consider GnRH analogie to supress ovaries if cylical, can predict outcome of hysterectomy DDX Pelvic congestion/ migraines (treat with migrain treatment) ``` BIo Exploration of depressive symptoms - SSRI? Trial of GnRH anologue as pain is cyclical Psycho CBT Pain clinic referral Social Exercise Diet Cognitive methods e.g. meditation ``` If GnRH does not improve symptoms oophorectomy less likely to work. If not then could trial a neuropathic pain modifier e.g. amitryptilline before offering surgery
30
Pathology/ RF endometrial hyperplasia
Abnormal proliferation of endometrium in excess if norm RF for endometrial cancer Continuous ostrogen = RF Obestity
31
Diagnosis of endometrial hyperplasia
``` Types - histology Simple Complex Simple atypical Foci of atypical that may lead to ca in older personsHR Complex atypical ``` Diagnosis Histological diagnosis
32
Miscarriage diagnoses
Threatened - bleeding and or pain and preggers Likely to mischarriage Closed cervix Up to 24 weeks Inevitable miscarriage Open cervical Os even if viable preggers with fetal heart beat POC may not be pased by inevitably will Incomplete miscariage Some POC have been passed Tissues and blood clot remain within uterus Cervix stays open Complete miscarriage Only say for fact if you have a scan prior showing a fetus Cervix now closed Resolution of symptoms No strict USS diagnosis CRL >7mm or gestational sac >25mm with no cardiac miscarriage is diagnostic of a miscarriage Septic miscarriage Infected More likely if didnt present with miscarriage and incomplete occured with infection of POC Rare if TOP is legal
33
Miscarriage US classoifed
Missed miscarriage/ early fetal demise# (not recognised) Failed preggers with no cardiac pulsitation on USS Blighted ovum/ Anembryonic pregnancy Failed preggers with empty gestation sac (previosly chorionic cavity identiyable at 3-5 weeks) Incomplete miscarriage/ Retained products of conception Echogenic mass of blood clot and tissue within the uterine cavity >20mm in AP diameter Complete miscarriage May be preggers of unknown location Empty uterine cavity roughly <20mm AP Must have seen IUP intrauterine preg or PUL preg unknow location
34
Causes of miscarriage
``` Chromosomal abnormality (most T1 = aneuploidy) Congenital abnormality Maternal disease (10% in T1) DM Acute illness Uterine anomalies Thrombophilia / APLS T2 =Cervical weakness, uterine abnormality or maternal disease, infection (CMV) ```
35
RFs miscarriage
``` Advancing maternal age 40 Previous miscarriage (3 = recurrent and threshold for investigation) Smoking Alchol (moderate to heavy) and drug use NSAIDs adn Aspirin Street drugs Folate def Consanguinity - cousins marrying DM ```
36
Conservative management missed Miscarriage
x Wait and watch Usually POC pass over 2 weeks but can be longer Step in after 2 weeks due to risk of infection Must have 24hr access to gynae service Adv Avoid rsks Can be at home Disadv Pain and bleeding can be unpredictable Takes longer May be unsuccessful Unpredictable - may be sudden heavy bleeding
37
Medical management missed miscarriage
Day 1 :Mifepristone (antiprogesterone - like with CL causes shedding?). Day 3: Misoprostol (prostaglandin) - Adv 85% effective Avoids surgery Outpatient Disadv Pain and bleeding may be unpleasant and or severe ADR drugs Need for emergency surgical management (SERPC)
38
Moa Mifepristone
Blocks prog causing decidual degen (part of endometrium that forms placenta, cervical softening and dilation, release of prostglandings and increase sensitivity to contractile effect of prostaglandins. Decidual breakdown leads to trophoblack detachment, Decreased HCG and therefore Decrease progesterone from Corpus luteumx
39
MoA Misoprostol
causes contraction along with dilation and softening of cervix
40
Surgical management of miscarriage
``` Suction curette to empty uterus 5 minutes under GA Day case Physically normall after 24 hrs Bleeding 24 hrs... Disadv Harder to do after 12 weeks due to suction method Perforation, bowel bladder Damage to cervix Asherman's syndrome = severe pevic infection, adhesions which block menstruation, pain during ovulation/ menstruation Cervical weakness Anaesthetic risk ```
41
What is recurrent miscarriage
Loss of >=3 consecutive preggers with same partner
42
Causes of recurrent miscarriage and management brief
x Balanced (Robertsonian translocations) Mother is phenotypically nomral btu 50-75% of games are unbalance Refer to clinical geneticist PIGD has LOWER rates of healthy pregnancy than natural conception Uterine anomalies E..g septum which can be removed Increased risk of uterine rupture with hystroscopy Antiphospholipid syndrome Bacterial vaginosis and T2 loss Thrombophilia e.g. Factor V Leiden mutation Alloimmune causes (both parents have same HLA alleells so cant protect fetus)
43
Diagnosis of APLS
3 miscarraiges in 10 weeks 1 fetal loss >10 weeks 1 normal birth with severe PE or FGR
44
Management of APLS
x Give aspirin from day of prositive preggers test Give LMWH from FHR seen Monitor Liver birth rate 80%
45
General management of recurrent miscarriage and investigation. outcome
Miscarriage clinic Test for APLA Thrombophilia screen Pelvic US and consider further if abnormal Karyotype fetal products in products of conception 75% achieve ongoing preggers with supportive care only
46
Diagnosis of PUL
No IU conception or ectopic on TVS but a positive preggers test
47
Cause of PUL
x Too small for TVS e.g. less skilled scanner Complete miscarriage Ectopic Failing PUL (never seen but self resolveing) Rare = HCG secreting tumour Persistent PUL Rare plateu of HCG without and trophoblastic seen on TVS or diagnostic laparoscopy or uterine currettage
48
Management PUL
HCG monitoring >66% rise in 48hrs reassuring (should double). Rescan at HCG=1500 (predicted) or 2 weeks <66% rise in 48hrs Monitor untill <15ui and contact senior Flucuating HCG continue expectant management or offer methotrexate Progesterone <20 suggests failing pregnancy, if asymptomatic repeat hCG in 7 days
49
Ectopic investigation
FBC, G&S (unless acute the cross match 6 units) Urine PT TVSbHCG Serum progesterone If not TVS then consider laparoscopy vs conservative
50
Location of most ectopics
``` Tubal (99) Ampullar (55) Fimbrial Less rare types e.g. Cornua Ovarian (0.5) Abdominal Cercival Uterine diverticulum, intramural, rudimentary horn - split off part due to Mallarian defect and bicornuate uterus (cornual)/ scar Heterotopic with IVF, ovuation induction. (ectopic and intrauterine together) ```
51
Risk factors for ectopic pregnancy
``` 1/3 have no risk factors Previous ectopic Tubal surgery e.g. Sterilization or reversal Tubal pathology Previous PID/ endometrosis Preggers with Cu IUCD POP Tobacco smoking Previous ectopic ```
52
Presentation of ectopic preggers
``` Unilateral pain RIF/LIF Irregular PV spotting/ bleeding Fainting, dizziness (rupture) Shoulder tip pain GI symptoms N&V although usually not prominent with low bHCG ```
53
Management ectopics
Expectant - where HCG falling Increasingly offered 24 hr access to gynae services Medical Criteria to meet Methotrexate single dose Follow up bHCG 25% need repeat MTX - 3 month contraception Longer resolution and follow up, avoid preggers for 3-6/12 months ADR: conjunctivitis, stomatitis, diarrhoea, abdo pain Surgical Laparoscopic/ laparotomy Salpingectomy (removal)/ otomy (incision) Ectomy If controlateral tube is patent Salpingotomy more persistent trophoblast rates and subsequent ectopcs (if woman wants more and other tube damaged) Follow up with HcG Invasive tissues If clinically unwell or patient unwell Need to get all trophoblastc tissue to prevent re surgery
54
Criteria for conservative management and medical management
expectant management of an ectopic pregnancy can only be performed for 1) An unruptured embryo 2) <30mm in size 3) Have no heartbeat 4) Be asymptomatic 5) Have a B-hCG level of <200IU/L and declining 6) Understand risks and willing for regular follow up Medical management of an ectopic pregnancy can only be performed for 1) An unruptured embryo 2) <30mm in size 3) Have no heartbeat 4) Be asymptomatic 5) Have a B-hCG level of <3000IU/L and declining Understand risks and willing for regular follow up
55
What is gestational disease
A spectrum of disorders of trophoblastic development arising from abnormal fertilsation.
56
Types of mole
``` Potentially pre-malignant Hydratidiform Mole/ Molar pregnacy Complete mole - empty egg, 1sperm Benign Paritial mole (egg and 2 sperm) more common Triploid e.g. 69XXX Less malignant and slower growing ``` Maligant Invasive mole Choriocarcinoma
57
Mole features
``` Bleedingin in T1 or early T2 Exaggerated symptoms e.g. hyperemesis Uterus large for dates Very high hCG (mimic TSH) Hypertension and hyperthyroidism may be seen No pain/ Aysymptomatic ```
58
Management of a mole
SERPC 3 national GTD centres Postal follow-up of serum and urine serial bHCG Anti D Contraception to avoid preggers in 12 months
59
Hyperemesis gravidum presentation (when)
``` Excessive nausea and vomiting in early pregnancy (although a very common in pregnancy and usually normal) Usually 6-12 weeks Dehydration Deranged bloods Ketosis Weight loss Nutritional deficiency Complications of all of above ```
60
Pathology of hyperemesis theories
Elevated HCG More common in twin/molar preggers Same alpha subunit TSH - linked to thyrotoxicosis Elevated oestrogen/ progesterone Helicobacter pylori - subclinical infection activitaed by altered immunity in preggers Psychological Difference in different pop and cultures
61
DIagnosis of hyperemesis
Hyperemesis gravidarum, diagnostic criteria triad: 5% pre-pregnancy weight loss dehydration electrolyte imbalance
62
DDX hyperemesis
``` Diagnosis of exlusion Normally no abso pain DDX infection UTI Gastroentertis Appendicitis Pancreatitis DDX metabolic Biochemical thyrotoxicosis Graves disease Addisons DKA Drugs Antibiotics, iron preps Tumours Hydratiform mole formation Choriocarcinoma Teratoma with elements of choriocarcinoma Germ cell tumours Islet cell tumour ```
63
Hyperemesis investigations
``` Urine PT Ketonria UTI Bloods FBC Haematocrit Ues K+ especially - Addisons and vomiting LFT and amylase TFT HCG USS exclude GTD/ multiple pregnacy ```
64
Hyperemesis complications
Wernicke's encephalopathy Mallory-Weiss tear central pontine myelinolysis (Na? low) Paralysis, dysphagia, dysarthria, neuro symptoms acute tubular necrosis fetal: small for gestational age, pre-term birth
65
Management hyperemesis
``` Rehydration - not with glucose as can precipitate Weernicke's, replace K Vitmains and nutrients Thiamine replacement and folic acid Vitamins B and C (Pabrinex) if Wernicke's enceph) Often cant tolerate oral Antiemetics Parenteral route initially Ranitidine Thromboprophylaxis Rarely Steroids - appetite stimulation TPN/ JEG Termination ```
66
Diagnosis of mole
Suspected on scan | Confirmed on histology only
67
6 week PV bleed history questions
``` Bleeding - how much and clots How many pads/ soaking etc Dizziness (from this) Spotting Gi symptoms Diarrhoea Rectal pressure (can get due to irritation from ectopic) Pain Shoulder tip pain ``` Preggers - may need to get parents or partner out LKMP Previous ectopic/miscarrage Planned unplanned unwanted PMHx - DM SH Consanguinous marriage Smoker Drugs
68
6 week PV bleed investigation
``` Bloods Coag clotting UE FBC Serum HCG Disrimminatory level >1500 Serial measurements- dobling time/rate of change Serum Prog >30 = likely viable or not Cautious on these predictions in early Blood group Rhesus status for surgey Imaging US scan Trans-abdominal (TA) Trans-vaginal (TV) Easier to see Free fluid = bleeding Urine Preggers test ```
69
Define abortion
Termination of pregnancy by the removal or expulsion from the uterus of a fetus or embryo prior to viability (24 weeks/20 weeks)
70
Complications of induced abortion public health worldwide
``` Comps worldwide Haemorrhage Infection DIC GA ```
71
Abortion law in UK
HSA 1 form must be signed by two doctors Premises approved by secretary of state Social abortion clause C & D - pregnancy <24 weeks unless fetal abnormality Consent 16-18 can consent as young people Less than 16 can consent to contraception/ including abortion Competency as per Gillick case, can consent tomedicak treatment Frasier allow medical practitioner to provide contraception advice <16. ensures confidentiality
72
Abortion proceedures <9 weeks
Early medical abortion (EMA) using mifepristone (antiprogesterone) + prostaglandin. Person signing is taking responsibility Conventional suction TOP should be avoided (higher failure) Earlier surgical abortion - manual vacuum aspiration (MVA), US guided/ checking falling HCG post abortion etc
73
Abortion proceedures 9-24 weeks
7-15 weeks Early medical TOP (EMTOP) up to 9 preferred Surgical preferred 9-15 via suction TOP Cervical prep with prostaglandin is an option pror to surgery and routine for nulliparous women or >10 week with multiparous Greater risk with high BMI Medical abortion for 9-15 - may be pain/ bleeding for a few weeks but safe >15/13 weeks Surgical by D&E - dilation and excision receded by cervical prep Beyond 18 is a 2 stage procedure >21 Medical top with Urea and KCL prior Induciton of labour with prostaglandins
74
Alternate medical methods
Cervagem (prostaglandin analogue) more expensive not used | Highly effective
75
Contra indications to medial abortion
``` Suspected ectopic prep Any risk of heavy bleeding Chronic renal failure Mifepristone -similar to aldosterone and electrolyte Hepatic falure (bleeding) Severe asthma or COAD CVD/ Prosthesis Long term steroids - electrolyte Allergy to Mifegyne (Mifepristone) Haemorrhagic disorders and treatment with anticoagulants ```
76
Complications of abortion
Low risk of haemorrhage, increases with weeks 4.5% get sepsis Can give prophylactic abc Uterine performation Cervical tears Dilated with prostagladin to prevent And widened with dilator Can tear wall causing bleeding or incontinence Failure (<1%) Post abortion Sepsis Trauma during cervical dilatation and curettage Fundal perforation with suction curette Uterine perforation and suction of a loop of bowel
77
PReventions of complicaiton of abortion
Early referral within 5 weeks Counselling for risk and options Day care procedure if possible under LA Patient info written and verban Investigation: STI screenig, Rh factor, FBC, blood group, BBVs US scan Cervial priming for STOP with dilator - prostaglandin Trained personal TOP
78
After care of surgical abortion
Anti D for Rh -ve Abx propho - STI - metronidazole 1g rectally at time of abortion and doxy 100mg BD orally for 7 days or azythromycin 1g orally on day of abortion Verbal and written info and comps and actions No sex/ tampons for 2 weeks Future contraceptive plans- prescribe where appropriate Follow up 2 weeks Contacts for physical and emotional help Communication with appropriate health professionals
79
Describe rhythm method theory
``` Calender/ rhythm/ safe period 14 days fixed 7 days ovulation time Rhythm method (sperm survival of 7 days – ovulation on day 14-15) based on temp) Fertilie if sex between 8-19 ```
80
Other "natural" contraceptions
``` Cervical mucus assessment BBT - temp Breast feeding 90% contraception in first 6 months Withdrawal Persona - LH surge Expensive and misleading ```
81
MoA COCP
1 ovulation suppression (primary) 2 penetration of Cx mucus 3 prevention of blastocyst implantation
82
Types of COCP
Phasic (fixed dose) Biphasic Triphasic ED - 7 days of placebo pulls
83
CI COCP
``` Hypertension Migraine Smoker >35 History of Cerbro or CVD Breast cancer DM with retinopathy/ comp Severe cirrhosis Gallbladder disease History of OCP related cholestasis ? CYP modifiers ```
84
ADRs Oestrogen
Bloatedness, breast fullness leg cramps, headache, PV bleed, VTE, Migraines worse,
85
ADRs Progesteron
xIrritability, weight gain, hirtsuitism, irregular periods, premenstrual depression, low mood, low libido, breast tenderness
86
Beneftits of COCP
Less bleeding, regular, less anaemic, less dysmenorrhoea Endometriosis - less pain, less dysperiunea Premenstrual tension- less PID - less risk Fewer Ectopic pregers due to anovulation Less benign breast disease Less functional ovarian cyst Ovarian, endometrial and colorectal Ca less
87
Long term health risks COCP
Increased risk of breast and cervical ca, VTE, stroke, IH
88
Other methods of oestrogen delivery as contraception
``` Patch Delay of 48hrs then barrier for 7 and consider emergency contraception NuvaRing (oestrogen ring) Lunelle injection monthly combined Lovelle vaginal combined pills ```
89
IUD time span, use and SE
``` Up to 10 yrs Above 40 can be longer and can leave Copper Licensed for emergency contraception and better Instant Primarily prevent fertilisation May also prevent implantation ``` Bleeding pattern change - heavier with copper Progesterone - risk of ovarian cysts increased Explosion PID Rare: uterine perforation
90
Nexplanon MoA, use, when is it effective
Releasing Etonogestron over 3 years Ovulation suppression main Takes 7 days Effective imediately if <5 days inserted after period
91
Mirena use and when is it effective
Up to 5 yrs 20mg LNG / day Not for emergency Takes 7 days
92
MoA of oral levonorgestal emergency
Emergency Oral levonorgestrel 1.5mg stat | Anti ovulation
93
History regarding prenatal diangosis and why
Maternal age Maternal disease DM First few weeks of control really important (6 weeks heart is formed) Epilepsy Medication esp in 1st trimester Folic acid 5mg per day start from planning prior to birth Previous obs history Child with aneuploidy (abnormal number of chromo) Genetic disorder Structural abnormality Consanguinity Are you and your partner related? Parent with known balanced translocation Exposure in pregnancy-drug related malformations Antiepileptics Warfarin Vit A - acne Intrauterine infection Rubella CMV Ask have you been unwell recently or travelled? If seroconvert first time during pregnancy Pass to embryo May get long term sequelae (1-2%) e.g. Sensorineural defness or learning disability Parvovirus Zika Recent travel
94
Maternal blood screen for prenatal dianosis
Haemoglobinopathy Thalassaemia Sickle cell disease VDRL/ RPR screening - Venereal disease research laboratory Syphilis HIV, Hep B AFP screening Produced in fetal liver and small bowel Raised level associated with open neural tube defect, gastroschisis (unlike exomphalos no peritoneum and not a herniation through umbilicus), cystic hygroma, congenital nephrosis, teratoma, fetal infection, oesophageal atresia, late preggers probs too Maternal Rhesus antibody Anti D at 28 and 32 offered for second pregges to prevent risk Combined first trimester serum screening for Trisomy 21, 18 and 13 Look for free foetal DNA from blood system from October 2018
95
Describe Down's screening - combined test
Combined test detects 75%, 3% FP Uses NT, hCG and preg associated plasma protein a PAPA, woman's age 11-13+6. Higher rates for trisomy 18 and 13
96
Other causes for raised nuchal lucency?
ystic hygroma (lymph sac in neck), cardiac malformations, thoracic compressive syndromes- congenital diaohragmatic hernia, congenital infections
97
Cut off for blood test for Down's Screening
1 in 150 before further is offered
98
Dating scan purpose
ibilitity - HB Accurate dating Detection of fetal abnormalities Anencephaly Large anterior abdo wall defects Cystic hygroma Nuchal translucency Twin determination and chorionicity Cytocitiy Zygocity - 2 completly split - monozygous same egg and sperm 2 sepearate egg and sperm then dizigous Chorionicity = number of placentas One egg and one sperm split, own membrane and own placenta Dichorionic, diamniotic monochorionic (one placenta) Diamniotic (2 sacs) Most monozygotic twin preggers Monochorionic, monoamniotic have high mortality due to cords getting twisted Worst is when babies don't separate = conjoined twins, higher mort Can only tell chorionicity and amniocity on scan unless opposite sex or sharing placenta
99
Anomaly scan purpose
``` bility Measurements (growth) Liquor volume Fetal anatomy Placental location Previa - can cover internal os - life threatening bleed Assessment of normal variants/ soft markers for aneuploidy, renal-pelvic dilatation, choroid plexus cysts •nuchalfold •short femur •choroidplexus cysts •echogenic focus in heart •dilated renal pelvis •talipes equinovarus (club foot) Not perfect detection. CVD particularly low Normal shaped cerebellum 98% of spinal sbifida ruled out DM can have sacral probs Frontal bossing Absent nasal bone - downs Cleft lip Normal variants Nuchal fold >6mm Ventriculomegaly ```
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When is amniocentesis performed? facts too
After 15 weeks gestation] Under direct US 15-20ml using a 22G needle Culture of amniocytes, harvesting and banding Karyotyping p to 3 weeks 1% risk of miscarriage also preterm delivery and chronic liquor leak
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Indications for amniocentesis
Assessment of fetal karyotupe if risk of Downs, USS findings, parental translocation, maternal request Measurement of AFP and ACHE (being negative) - ?congenital nephrosis Virology screen PPROM (Preterm (<37week) prematuure rupture of membranes) to rule out chorioamnionitis Loss of barrier so can get infected OD 450 (amniotic bilirubin scan)-haemolytic disease
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Use of Chorionic Villus Sampling, risks, when is it performed, how,
``` Results = 1 week, (can be 2 days) After 10 weeks ideally US guided TA or Tcervical 2 cell lines True mosaic or contamination ```
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Risks of CVS
``` 1% get mosaic result from placental mosacism Mum contamination (false positive) 1% risk of failure Transmission of BBV 1-2% Miscarriage ```
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How to terminate >21
Painful As part of procedure do KCl inject into heart Distressing for parents if baby has signs of life Induction of labour with prostaglandins preceded by fetocide after 22 weeks of gestation in many countries PEG2 - Oxytocin after ROM
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Explain PIGD
``` FISH analysis At 8 cell satage Indication Known parental translocation Increased age FH X linked recessive ```
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Explain quadruple test
Quadruple test 16 weeks Dating scan, AFP, unconjugated estriol, BHCG, inhibin A, womens age 15-20 weeks
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Integrated test
Expensive | NT and PAPP-A in 1st then quaruple in 2nd
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How long is a normal cycle
* Length 24-32 (not normal to be 28 every time over years) | * Regularity best between 20-40, longer after menarche, shorter pre-menopause
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Normal cause for PCB and follow up
post coital bleed, normally cervix as lesions of vagina rare and epithelium thick. Check smears and lesion on cervix
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Cause of menorrhagia
``` ○ Abnormal clotting § Von Willebrands, thrombocytopenia, platelet disorders, coat disorder, leukaemia ○ Pathology § Fibroids (benign tumour of muscle § Adenomyosis/ endometriosis § IUCD - copper makes heavier § PID § Polyps -heavy ○ Metabolic/ Medical § Hypothyroid § Liver disease § SLE § Cancer Polyps/ pro contraception • DUB ○ 60% primary menorrhagia ○ Dysfunctional uterine bleeding ○ Diag by exclusion No recognisable pathology, preggers or general condition disorder ```
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Risk factors for Menorrhagia
• Age 40_ • Correlation in twins - hereditary • +Ve parity Uterine pathology fibroid or endometrial abnormality, endometrial cancer in post menopausal
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Brief history menorrhagia
History How much Clots Flooding Subjective vs objective assessment ○ Only 50% with subjective menorrhagia have > normal loss Only 60% of women with MBL >80ml consider their periods heavy
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Investigations into menorrhagia
``` Hb TFTs and coag if needed Pregnancy test TVUS Investigations futher • Hysteroscopy +/- Biopsy • Cancer rare in menstruating but increases towards menopaus ○ Smear if due • Consider STI screen Subserous vs submucosal fibroid - more bleeding ```
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Treatment of menorrhagia (with 1st 2nd and 3rd line)
* Tranexamic acid - antifibrinolytic (2nd or for baby) * NSAID/ Fenamates (not in handbook) • Progestrogens ○ Norethisterone (not in handbook) ``` ○ Mirena-IUCD ○ Depot/ IM prog 3rd § Irreg bleeding ○ OCP 3rd • GnRH analogues ``` ``` • Ulipristal acetate Surgical ○ Hysterectomy - dont need ovaries § Risks □ ○ Endometrial ablation § Resection § Roller ball § Laser - old § Cold coat § Microwave § Balloon- thermal current - common § Radio frequency (controlled thermal damage)- also common. 1-2mins ```
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MoA and SE transexamic acid
x ○ Inhibit plasminogenhibition of tPA and uPA thus reduce fibronoylsis ○ Reduce 50% of MBL ○ Side effect nausea, dizziness, tinnitus, dont give to us of PE DVT etc
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MoA and efficacy of NSAID/ Fenamate for menorrhagia
○ Inhibit PG and binding to PGE2 § Reduce platelet aggregation ○ Reduce MBL by 20-44.5% ○ Pain killer too
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Efficacy and ADR of Norethisterone for menorrhagia
§ No literal administration § 21/28 with a break reduce MBL § Nause, headache, bloated ness, weight weigh, skin rash, adverse on lipids, breast tenderness (think early prey symptoms/ last half)
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Efficacy of Mirena IUCD for menorrhagia
``` 1st line 80% reduction 3 months, 97% at 1 year) § 5 years § Major reduction in MBL § Some BTB (break through bleed( § Not increase ectopic or PID ```
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GnRh analogue mOA and ADR
○ Large dose actually inhibits pit (after brief stimulation) ○ = menopause ○ Hot flushes, osteoporosis ○ Temporary?
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Ulipristal acetate MoA and ADR
○ Prog antagonist ○ Help shrink fibroids and may help fibroids ○ Can grow back after ○ abdominal pain; acne; breast pain; dizziness; endometrial thickening; headache; hot flushes; hyperhidrosis; malaise; menstrual disturbances; myalgia; nausea; oedema; ovarian cyst (including rupture); pelvic pain; uterine haemorrhage
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Risks of hysterectomy
Bleeding, Bowel, bladder, ureter damage, infection e.g. peritonitis, wound infection, Scarring, VTE, early menopause (with ovaries).
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Effectiveness of endometrial ablation for menorrhagia
Expect 30% amen, 30% failure, 40% llight
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Causes of amenorrhea
``` Pathological Brain - Pit/ hypothalmic □ Stress □ Psychoactive drugs ○ Cryptomenorrhea (hidden) e.g. imperforate hymen ○ Uterine/ endometrial/ Ovaries • Physiological ○ Prepubertal ○ Preg ○ Menopause ```
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Cause/ pathology of PCOS
○ Heterogenous endocrine disorder with unknown aetiology ○ FAmilial clustering/ RF ○ 90% Amennorhea ○ US - string of pearls = diag • Patho ○ Recruit follicles which get stuck and dont get to follicular ovulation stage ○ Each produce oestrogen and androgen ○ No prog so no ovulation and infertile ○ Ovarian theaca cell hyperplasia leading to enlargement with icing sugar coating ○ Tendency to DM due to insulin resistance ○ Characterised by § Hypersecretion of androgens § Increased pilsatile secretion of LH § Theca cell (follicle) hyperplasia leading to ovarian enlargement § Anovulation Insulin resistance
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Clinical features of PCOS
``` ○ Oligo/ amen ○ Dysfunctional uterine bleeding ○ Obesity ○ Hurtsuitis ○ Acne ○ INfert String of pearls ```
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Biochemical features PCOS
§ Increased LH/FSH § Decreased Sex Hormone Binding Blobulin (SHBG) § Raised free androgen index (FAI) Increased serum insulin
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DDX PCOS
``` ○ Anovulatiory cycles ○ CAH - congenital adrenal hyperplasia ○ Androgen secreting tumours ○ Cushings’s syndromes (also oligo) ○ Hypothalamic dysfunction ○ Female athlete triad ○ Eating disorder ○ Hyperprolactineamia Thyroid disorders ```
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Long term comps PCOS
``` ○ MIscarriage ○ Gestational diabetes ○ NIDDM ○ Hypertension ○ CVD Endometrial hyperplasia/ carcinoma (oestrogen) Ovarian ca ```
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Management PCOS
``` ○ Weight adjustment ○ COCP ○ Cyproterone acetate d ○ Cyclical progestogen ○ Metform ○ Ovulation induction in fertility § Something citrate Ovarian drilling ```
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What is cypropterone acetate and important ADR
§ Antiandrogen § Normal ones can cause meningioma § Some prog functions § With oestrogen
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Causes of dysmennorhea
``` Primary dysmennorhea Often with anovulation after menarchy Excessive prostagladins = contractions and ischaemic pain Secondary Adenomyosis Endometriosis PID Fibroids Ovarian cancer (less likely endometrial) ```
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Treatment dysmennorhea
``` Primary NSAIDs e.g. mefanamic acid Paracetamol If ovulatory cycle then COCP can help Hyoscine butylbromide (SM anti-spasmodics) unreliable Secondary Treat cause IUCDs can increase- levonogesterol may help ```
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Absolute CI OCP
``` Migraine with aura Breastfeeding <6 weeks post-partum Age 35 or over smoking 15 or more cigarettes/day Systolic 160mmHg or diastolic 95mmHg Vascular disease History of VTE Current VTE (on anticoagulants) Major surgery with prolonged immobilisation Known thrombogenic mutations Current and history of ischaemic heart disease Stroke (including TIA) Complicated valvular and congenital heart disease Current breast cancer Nephropathy/retinopathy/neuropathy Other vascular disease Severe (decompensated) cirrhosis Hepatocellular adenoma Hepatoma Raynaud's disease with lupus anticoagulant Positive antiphospholipid antibodies ```
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Define menopause and peri-menopause
Permanent cessation of menstruation due to the loss of ovarian follicular activity (12 months amen) • Peri menopause- the period from the beginning of symptoms of approaching menopause and ending 12 months after the final menstrual period
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Symptoms of menopause
``` ○ Hot flush and sweats ○ Irritability ○ Lack of conc ○ depression ○ Loss of libido ○ INcrease bone loss ○ Increase CVD risk ○ Vaginal dryness ○ Dowager’s hump due to osteoporosis and spontaneous collapse § Resp function too ```
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Diagnosis menopause
``` ○ Age ○ Cessation of menstruation ○ Atophy ○ ? Role of hormone profile - NICE do not recommend ○ ? Role of ovarian biopsy DDX thyroid and psych ```
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Management options menopause
○ Diet and exercise ○ ERT and prog if they have a uterus = HRT § Prog reduce the increased risk of endometrial hyperplasia and carcinoma with unopposed oestrogen in non-hysterectimized women ○ E.g. Stradiol or premarin and meedroxyprogesterone acetate, Duphaston (Provera), ○ Sequential or continuous § Retro gem cont with 12-14 of prog causing bleeding, less prog so possible less CVD risk § Continue less likely for period ○ COCP Monophasis or triphasic
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Risks and beenfits of HRT
``` ○ Risks of HRT § Unapposed oestrogen: □ Endometrial cancer □ Ovarian cancer? § Breast cancer § IHD ? § Gall blasser § Stroke § VTE § Uterine bleed § Lipid profile neg affected § Thrombophilia profile neg affected ○ Benefits Less vasomotor symptoms Improvement in urogenital and sexual function symptoms Osteoporotic fracture reduction (only if lifelong and sustained) Reduced Colorectal cacner by 1/3 ?alz ?CVD, Ovarian Alz ```
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Cyclical vs combined HRT?
x Women should be prescribed cyclical combined HRT if their LMP was less than 1 year ago and continuous combined HRT if they have: taken cyclical combined for at least 1 year or it has been at least 1 year since their LMP or it has been at least 2 years since their LMP, if they had premature menopause (menopause below the age of 40)
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Route for HRT
``` ○ Oral ○ Transdermal ○ Implant ○ Transvaginal ○ Nasal ○ Local ○ Patch Prog: Transderm, oral, IUS ```
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Symptom specific treatment alternatives to HRT
``` • Prevention of osteoporosis ○ Bisphosphonates ○ Calcium and Vit D ○ Raloxifene § SERM § Increase hot flush and VTE § Less action on breast and uterine bleeding ○ Exercise • Vaginal dryness - lubricants or vaginal oestrogen transderm • Vasomotor symptoms ○ SSRI ○ Clonidine (less efficacy) - alpha 2 in brain stem cuasing less TPR ( Gabapentin ```
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Contraception around menopause
x • Stop <50 years is amenorrhic 2 years • Stop >50 if 1 year Stop COCP in >50 after 2 years post amen or POP
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Diagnosis of hypertension in preggers
>=140/90 on 2 occasions more than 4 hrs apart or a single reading of the diastolic BP >110 Korotkoff phase V should be used (when it stops as per normal)
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What is significant proteinuria? | Next investigations?
• 2+ more of protein on urinanalysis is significant • Protein:creatinine ratio is acceptable measure ○ <30mg/mol implies non-significant proteinuria ○ >30 prompt 24hr urine collection • >300mg in 24hrs is abnormal MSU and C&S but infection unlikely if absence of symptoms (more likely to be preeclampsia)
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Classifcation of hypertensive disorders of preggers?
• Preeclampsia (only cause in T3) • Gestation hypertension/ proteinuria (only one possible) • Chronic hypertension • Pre-eclampsia superimposed on chronic hypertension (15-25% of chronic hypertensive cases) Differentiating this from gestational hyp can be difficult as pre eclamp can be without proteinuria
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Normal variation of BP in preggers?
Drops MAP by -5mmHg from 0 to 21 weeks then returns to normal by 40
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Risks, and urate in chronic hypertension in preggers?
• Risks are mainly related to superimposed PET (pre eclapmptic toxaemia • Normal urate • WIth proteinuria IUGR common Abortion 1/50
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BP target in chronic/ secondary hypertension in preggers?
xKeep BP in all women below 150/100 with urgent treatment If BP >140/90 on 2 occasions then transfer to consultant led labour ward Agitation and restlessness is sign of underlying problem in women with HYT
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Define pre eclampsia
○ Miltisystem disorder ○ Usually recognised by new onset hypertension (140/90) and protein urea (>300mg) in the second half of preggers that resolves after delivery Can occur with or without HYT or without or with/out proteinuria but will have other symptoms
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Pathophysiology of pre eclampsia
○ Two stage placental disease concept § Abnormal trophoblastic invasion and adaptation of spiral arteries □ Converts muscular layer to trophoblast cells (dilated) - Trophoblast fails to invade maternal spiral arterioles □ If not then poor dilation and resistance to blood flow □ Reduction of vasodilators PGI2 and NO in endothelium □ Maternal plasma vol fails to expand □ Placenta fails to be a low pressure supply system § Placental ischaemia affecting maternal and fetal circ e.g. HYT to compensate
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Complications of pre eclampsia
``` • CNS ○ MAP >125 then intracranial haemorrhage/ cortical blindness risk ○ Cerebral oedema/ eclampsia • Renal ○ Renal tubular necrosis, renal cortical necrosis • Resp ○ Pulmonary oedema ○ ARDS • Liver ○ Haemorrhage beneath capsule ○ Hepatic rupture ○ Acute fatty liver of preggers ○ HELLP § Hemolysis § Elevated liver enzymes (EL) § Low platelet count (LP) • Thrombosis ○ High risk ○ Microangiopathic haemolysis/ DIC • PLacenta infarction/ placental abruption • Fetus ○ FGR - fetal growth restriciton ○ Preterm death Preterm labour ```
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Risk factors for pre eclampsia
``` ○ Socio-demograph § Age >40 § SESEthnicity § Smoking reduces risk? ○ Preggers § Nulliparous § Multiple preggs § Previous pre eclapsia § Hydrops (oedema/ fluid in fetal compartment e.g. rhesus disease), trophoblastic diseas ○ Medical Hx § PAst HYT (on pill too) § FHx Lupus or CKD or other systemic/ autoimmune ```
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Clinical features of pre eclampsia and biochem
``` • Symptoms ○ Headache ○ Visual disturbance ○ Epigastric pain (not sure why) ○ Oedema, can be usual too, non dependent ie..e face and hands in pre eclampsia only ○ Vomiting • Signs ○ Hyper reflexia/clonus ○ Oedema Epigastric tenderness and RUQ ``` ``` ○ Abnormal blood results § Raised urea and creatinine § Raised urate § Low platelets Elavated ALT/AST ```
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INvestigation (asessment of risk)
``` • Bedside ○ Blood pressure level § Diastolic for preeclampsia § Systolic for maternal morbidity ○ Proteinuria § Fetal risk § Protein:creatinine ratio • Bloods ○ FBC - anaemia, Platelet count ○ Ues Uric acid ○ LFTs ○ +/- coag screen - PT, APTT (DIC) • Fetal movements ○ Slowing of movements not good as non essential activity reduced • CTG ○ Cardiac topograph ○ Only if reduced movement • Umbilical Doppler ○ Notching • US ○ Fetal size - FGR ○ Liquor Volume • If baby well on admission Can prolong pregnancy if mother stable ```
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Managment pre eclampsia
``` • Early intervention ○ IF BP >140/90 refer ○ Antenatal Day Assessment Units ○ Closer monitoring ○ Assess the need for therapy • Admit if ○ BP >170/110 ○ OR ○ BP >140/90 and Sig symptoms § Proteinuria 2+/300 § Sig symptoms • Meds ○ Acute then Oral Labetalol first line if >160/110 § Also hydralazine or nifidipine • Chronic meds ○ Labetalol ○ If not the methyldopa or nifidipine rolongation of preggers • If no convulsions • A few days allows use of steroids Ø A week may increase fetal survaval Ø However ○ Fetal signs of compromise, delivery is necessary ○ Better small and healthy than big and compromised Ø Deliver on labour ward ```
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Prevention pre eclampisa
• Antenatal care appropriate ○ Appropriate RFs indentified in T1 (before onset) ○ After 20 weeks monthly visits or fortnightly after 34 in primigravida ○ Clear history • Primary ○ Rest and exercise (not strong) ○ Ca shops but no effect on baby outcome ○ No benefit of Vt C and E Low dose aspirin if high risk women
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Fetal risks of severe hypertension in preggers
``` • Direct effect of disease ○ Intra-uterine growth restriction • From intervention ○ Premature delivery ○ Intervention ○ Cerebral haemorrhage ○ Pneumothorax • Related to both Cerebral palsy ```
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MoA, use, ADR and CI methyldopa
§ Methyldopa □ NOt if history of dep □ Stop PN due to risk of PN dep □ ADR tiredness/dry mouth/ GI/ dep Mechanism - metabolised to methynoradrenaline and stimulates alpha adrenergic receptors 250mg BD increased over 2 days up to 3g CI - history of depression, pheochromocytoma, acute porphyrias
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MoA labetalol, ADR, CI
Alpha and beta blocker □ Combined beta alpha blocker □ Not in T1DM as prevents hypos or asthma ADR - scalp tingling/ headaches/ wakness/ liver damage/ GI disturbances
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Postnatal BP monitoring after PE.
○ Daily BP monitoring for 2 days post birth ○ Once 3-5 days after birth Medical review 2 weeks after transfer
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Define eclampsia
Generalised convulsions during preggers, labour or <=7 days postpartum and not caused by epilepsy or other neurological disorder
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Pathophysiology of eclampsia (3 theory_
More sensitive to vasoconstrictors Prothrombotic - microthrombi reduce perfusion Leaky caps - increased in ISF, cerebral oedema
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Management of exlampsia
``` A-E appraoch Catheterise for urine output - Restrict fluids to <80ml/hr Labetalol 20mg IVI (or hydralazine) ○ Magnesium sulphate § Prevention (IVI) - high risk § Treatment ○ Senior review ○ Deliver once stable Neuroimaging should be performed urgently in any women with focal neurology or not recovered from seizure ```
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Complications of eclampsia
○ Cardiac failure and pulmonary oedema Plasma protein less and cap leakage MM 2-4% mort and baby 10-30%
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Define infertility and infecundity
Infertility Inability of a couple to conceive after 12 months+ of unprotected intercourse (6 months for women over 35) Infecundity (the inability of a couple to produce live birth) Potential e.g. how much people can, natural ability to reproduce
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Caues infertility broadly
``` Ovulation defect Male factor Tubal disease Unexplained (25% each) Endometriosis (prev in infertile increased) Uterine factors Other ```
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When are women most fertile and when does this start to decline?
Most fertile 20-31More pronounced post 37 and steep after 40
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Male and female factors that warrant early investigation
``` Male Cryptorchidism Chemi-Radiotherapy Previous urogenital surgery History of STDs Varicocele Abnormal semen analysis Female Age >35 Previous ectopic Known tubal disease History of PID/ STDs Tubal or pelvic surgery Chemo-Radiotherapy Amenorrhoea Olygomenorrhoea ```
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Causes of anovulation (ovaries)
``` PCOS 2 of 3 criteria Causes 80% String of pearls Weight related Either obese or under weight Ovarian failure Removed Chemo Autoimmune ovarian dysfunction Hyperprolactinaemia ```
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Tubal pathology causing infertility
PID most common chlamyd or gonn Adhesion e.g. endo Congenital abnormality
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History infertility
``` Age Duration of fertility Type of infertility Menstrual cycle - ovulating? Tubal surgery/ PID Menorrhagia/ Dysmenorrhoea/ pelvic pain Pelvic surgery ``` How often having sex
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Examination findings infertility
``` BMI (19-30 for NHS funding) Body hair distribution Galactorrhoea Secondary sexual characteristics Pelvic Structural abnormalities fixed or tender uterus Abdominal Swabs clamyd and gonn ```
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History male
General health Alcohol/ smoking Previous surgery Previous infection e.g. mumps in adulthood Surgery e.g. Hernia History of undescended or trauma in childhood Sexual dysfunction - erectile/ ejaculatory Undescended testes
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Examination in male
Scrotum - varicocele Testicular size Position - undescended testes Prostate - chronic infection
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Investigation in female
Female - Follicular LH, FSH (Day 2) Luteal phase prog (D21 - week before period) Rubella status 5%not vaccinated/ with cover Give 2 vaccines Avoid preggers for 2 months due to live vaccine If in preggers then discuss with local health protection unnit and post natal MMR Tests of tubal patency Hysterosalpingogram (uses dye) XR Diagnostic laproscopy and dye (if ?tubal patency) HyCoSy hystero-salpingo contrast sonography (sane as hysterosalpingogram but with US) Additional Clamyd Female - pelvic US - also for PCOS Hysteroscopy (not needed routinely) Prolactin/ TFTs (not needed routine) Testosterone/ SHBG/ Free androgen binding index (NNR)
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Investigation in male
Semen analysis x1 if normal If abnormal then repeat after 70 days due to sperm cycle Normally >20mil/ml, normal motility >50%, normal morph >30%, Volume >2ml Antisperm antibodies Mixed agglutination reaction/ immunobead tests Occurs from sperm in ummune system e.g. anal sex, blood-testis barirer e.g. surgery or orchitiis Only affect if in repro tract FSH/LH/ Testosterone FSH >20/30 then primary testicular failure FSH 1-10 = likely obstruction Vasogram FSH low then hypogondaism US seminal vesicles and prostate
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Management of fertility in PCOS
Weight loss Clomiphene citrate for PCOS (SER) Antioestrogen drug to reduce level -causing stimulation of FSH and LF stimulating follicular growtg via neg feedback inhibition Days 2-6 of cycle 50mg OD Need to monitor follicular growth via US Gonadotrophins/ pulsatile GNRH 2nd line or if low oestrogen with normal FSH Injected and expensive, needs US monitoring for hyperstimulation Metformin Help with weightloss and possibly ovulation but off licence Laproscopic ovarian drilling Needlepoint diathermy into ovary to try to reduce LH. 50% success and lasts for 12-18months
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Risks of fertility treatment in POCS
x Risks Hyperstimulation of ovary: Bloating, nausea, SOB, Pleural effusion, excessive weight gain Twins
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Management of infertility in prolactin, weight, male factors, or if no cause found
``` Dopamine probs (hyperprolactinaemia) Agonists e.g. Bromocriptine/ cabergoline Weight 18-30 BMI Tubal Surgery IVF Male factor IVF/ IUI intrauterine insemination Lifestyle - smoking, weight ICSI - intracytoplasmic sperm injection (one by one) Donor insemination ``` ``` No cause 2 years of trying Folic acid BMI Regular sex every 2-3 days Smoking/ drinking advice ```
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Aeitiology endometriosis
Outside of endometrium Predominantly in pelvis Responds to cyclical hormonal changes Can achieve preggers too Rare post menopausal - oestrogen dependent Aetiology - multiple theories Retrograde menstruation - most blood comes out butmay go retrograde and deposit in abdomen Coelomic metaplasia Metaplasic change in peritoneum (Coelomic) which will or won't accept retrograde menstruation May spread haematological or lymphatic and can be found anywhere
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Presentation endometriosis
Asymptom Most common is dysmenorrhoea Cyclical May be constnd lower abdo pain due to adhesions Dyschezia (pain on defication) Heavy period Dyspareunia Epistaxis, rectal bleeding, PCB- post coital bleeding with period Little correlation between symptom and severity of disease Infert - exact mechanism unknown
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Examination of endometriosis
``` NAD Thickened/ nodular uterosacral ligs Fixed retroverted uterus Uterine/ovarian enlargement Forniceal tenderness Uterine tenderness ```
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Investigation endometriosis
``` Vulval/ cervical swabs - CT and NG NAAT Bloods if ?PID e.g. dysmennorrhea WCC, CRP - PID CA125 - Endometriosis and malignancy TVUS - Fibroids (unlikely), ovarian endometriotic cysts Laproscopy and biopsy Active endometriosis - Powder-burn spots Chocolate cysts Inactive endometriosis Scars Pertioneal defects ```
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Management endometriosis
Cure not guaranteed Varying treatmetn Depends on fertility issues Type and severity of symptoms Therapies tried and failed Patients wishes No baby wanted COCP - supress ovulation Continuous prog therapy (MPA) Medroxyprogesterone acetate IUS GnRH analogues (nasal spray/ implants += HRT add back therapy Osteoporosis after 6 months Danazol androgenergic+ antiestogen Severe androgenic side effects Given in PCOS for andrenergic stuff too Wanting the babez Mefenamic acid (not great in preggers) (painful period )/ transexamic acid (heavy) Symptomatic benefit Surgical Laparoscopic - diathermy, laser TAH + BSO (ovaries too due to oestrogen) Rsk of bladder, ureteric, bowel injury Risk of subtotal hysterectomy/ role of HRT Fertility Cant give hormones as will negatively addect fert Only do laprascopic diathermy ablation or cystectomy Assisted hormones Clomiphene citrate Gonadotrophs/ pulsitile GnRh Can give mefenamic acid or transexamic acid Mefanamic mid cycle will block ovulation
185
Adenomyosis RF
Multiparous towards end of reproductive life
186
Adenomyosis presentation
Endometrial tissue within myometrium dysmenorrhoea menorrhagia enlarged, boggy uterus
187
Adenomyosis diagnosis
Diagnosed by histology post hysterectomy or MRI or 3D/4D scan
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Managemet HELLP
MG SO4 IV dexamethason Control of BP Replacement of blood products
189
Presentation vulva ca
``` Pruritus Bleeding Discharge Signs Ulcer - rolled edges Mass Inguinal nodes (met cancer) ```
190
RFs vulval ca
``` 50% due to HPV Elderly HPV, HIV, SLE, Iatrogenic immunosupression Smoking 95% squamous ```
191
Investigation vulval cancer
x` Biopsy Ketes Punch Biopsy Forceps Push into skin and twist Get a bit of normal and a bit of abnormal
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Staging of vulval cancer
Stage 1- 1mm including epidermis and portion of epidermis Stage 2 = 3cm penetration Stage 3 = invasion
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Management of vulval cancer
``` Bloods FBC G&S Clotting Ues Imaging ECG CXR CT to see extent of involvement Management 1 - wide local incision. If 1mm go 1.5mm. Advances Radical vulvectomy Removal of whole perineum and lymph nodes Butterfly exision ```
194
Cervical cancer screening method
PAP smear and liquid based cytology | Calassification/ reporting - dyskaryosis and invasion
195
Frequency of cervical screenign
Age 25-50 every 3 50-65 every 5 +65 selected patients only
196
When to refer for culposcopy?
Inadequate or boarderline on 3 occassions | Dyskaryosis on 1 occasion or abnormal glandular cell
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Abnormal findings on culposcopy Location and diagnosis of Cervical intraepithelial neoplasia
x Low power binocular microscopy of cervix Look for feature suggestive of CIN or invasion Abnorm vasc pattern e.g. mosicism Abnormal staing of tissue (aceto-white, brown iodine) Especially at junction
198
Treatmetn of CIN 1-3
``` CIN 1 - most regresses Mananagement of CIN II 2 week wait Treatment e.g. punch biopsy and cold coagulation 6 month follow up screen CIN III See-and-treat Desrtuctive Cryocautery Diathermy Laser vaporisation Excisitional (LLETZ = best), cold knife cone Follow up colposcopy 6 months Annually for 10 yearsafter ```
199
Prevention of HPV
Gardasil: 6,11,16,18 • Cervarix:16 & 18 3 IM injections giving 5 years protection
200
Pathophysiology of HPV in cervical and histological diagnosis
``` x Most common cause is HPV causing koilocytosis Most the time regressed to norml a Unlikely with immunosuppression CIN1 - basal layers metaplasia CIN2 More meta CIN3 from base outwards (see below) Invasive Whole progression takes years 2/3 squamous 15% adeno Squamous 90%/ Adeno 10% ```
201
RF cervical ca
``` Age 45-55 Young age at first intervourse Multiple sexual partners Long term COCP Immunosuppression/ HIVHPV: STI Smoking ```
202
Presentation of cervical ca
``` PCB Intramenstual bleeding - between periods Discharge/ odour PMB None Advanced Fistulae Renal failure Nerve root pain Lower limb oedema Signs Visible or palpable lesion ```
203
Spread of cervical cancer and consequent symptoms/comps
``` Lateral pelvic wall locally to uterer Posterior or anterior to Retum/Bladder Local to Uterus or Vagina Ureter Hydronephrosis Uraemia AKI Colicky pains Retention Haematuria Bowel Blood Tenesmus Constipation ```
204
Management of establish cervical ca by stage
1a - microinvasion but confired to cervic Large loop excision of transformation zone (LLETZ) Heated wire - superficial area scraped off I-Iia - beyond cervix but not pelvic side wall or lower 1/3 vagina Radical surgery/ radiotherpay Total abdonimal hysterectopy Bilater salinpingectomy (Tubectomy = tying tubes, salpingectomy = entire tubes) >Iia - (III = pelvic spread, IV = distant spread) Chemoradiotherapy Surgery just increases mortality and morbidity Radical trachelectomy = cervicectomy
205
Complications of cervical ca treatment
``` Surgery Infection VTEHaemorrhage Vesicovaginal fistula Bladder dysfunctionLymphocyst formationShort Vagina Radiotherapy Vaginal dryness Vaginal stenosis Radiation cystitis Radiation proctitis Loss of ovarian function ```
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Uterine/ endometrial cancer pathophysiology and types
Most from endometrium | Adenocarcinoma
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Risk factors for endometrial cancer
``` Tamoxifen - more sensitive to effects of oestrogen in uterus Unopposed oestroogen - hyperplastic Exogenous Obesity (36%) PCOS Nullip Late menopause Tamoxifen DM PCOS/HNPCC/ Lynch ```
208
Protective against endometrial ca
COCP/ POP | HRT combined
209
Presentation endometrial ca
PMB (most common) - 10% with have malig Irregular periods - if in perimenopausal period IMB Normal exam
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Diagnosis of endometrial ca
``` US - thickening of endometrium TV best >3mm is abnormal >5mm cut off Biopsy - diagnosis Hysteroscopy Or D&C - dilation of cervic and curretage Pipelle biospy - push catheter in and shave bit off - outpatient try first CT and MRI - staging ```
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Where can mets occur
``` Rare with type 1 Intraperitoneal Lung Bone Brain Type 2 Mets more likely CT Chest Abdo Pelvis MR Pelvis ```
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Staging of endometrial FIGO
``` x FIGO 1- Limited to myometrium (80%) 2- Cervical spread 3- Uterine serosa Ovaries Tubes Vagina Pelvic/ para-aortic LN 4- Bldder/ bowel Distant mets ```
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Management endometrial cancer
``` Surgical hysterectomy BSO Total with cervix Sub total is just uterus Total hysterectomy with bilat salphingo oophorectomy Radiotherapy Adjuvent Neoadjuvent Primary Hormonal Progestatgens (oral or intauterine) Only some are response - prog opposes oestrogen and prevents growth Chemo if admanced Combination if more advanced Prognosis Ia >90% 5 year All 65% ```
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Ovarian ca presentation
``` Bloating Clothes tight Vague symptoms Loss of apetit/ early saity Silent Dyspepsia Unfreq Mass/ascites/ cachexia/ breasts Pain Anorexia N&V Weight loss Vaginal bleeding Change in bowel habit (rare) ```
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Spread of ovarian ca/ staging
Later get omental caking | Initially local invasion
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RFs ovarian cancer
``` Repro Early menarche 11yrs Lat menopause >49 Nullip Frequent trauma to epithelial surface 60-70s HRT Oval induction Familiar BRACA1/2 HNPCC Family history Decreased risk COCP Preggers Breastfeeding Hysterectomy Oophorectomy Sterilisation ```
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Types of ovarian cancer
``` Surface epithelium (85-90%) Epithelial tumours Most common Serous/ mucinous/ endometriod/ Clear/ transition. S&M most common Can be benign or malignant Germ cell Follicle cells Dysgermnioma Yolk Sac Choriocarcinoma Dermoid (benign teratoma) most common More commonly benign Stroma Sex cord-stromal Thecoma Granulosa cell Sertoli-Leydig cell Fibroma Secondary malig Gastric cancers Lymphomas No pre malignant stage ```
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Investigations ovarian cax
Bloods FBC, UE, LFT Ca125 (Epithelial), ``` CEA Imaging TVA (TV US) CXR (pre op) CT to assess peritoneal, omental and retroperitoneal disease ```
219
Down side to CA125
``` xUp to 80% EOC Poor specificity premenopausal Also in Ca pancreas, breast colon, lung Menstruation, PID, Endometriosis Liver disease, ascities, pleural and pericardial effusion Recent laparotomy ```
220
Staging of ovarian cacner
1 - Ovaries 2 - pelvic organs 3 - Peritoneal cavity, omentum, lymph 4- Distant mets, liver parenchyma, lung
221
Treatment ovarian cancer
``` Epithelial Surgery and chemo Staging laparotomy TAH & BSO and debulking Platinum (Cisplatin, carboplatin) and Taxane (paclitaxel) (MOA = microtubual formation in cell division) If one ovary then just oophorectomy is possible Non-epithelial Young women Extremly chemo-sensitive Conservative/ chemo Recurrent disease = palliative chemo ```
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Define small for dates and large for dates
Describes anthropometric variables (AC or EFW) <10th pop centile for gestational weight >95th centile = Large for dates 2
223
How is growth assessed in preggers
Abdo palpation. Umbilicus 20weeks - 1cm each way 20-30% sensitivity 20 weeks and at the xiphoid sternum from 36 weeks. Head free until 37 in nulliparous but less in multiparous SFH 30-40% sensitivity US measurement Sensitivity 90-95% Commonly used head circ abdo circ and femur length
224
How customised are growth charts?
To mother based on ethnicity, BMI | X used along dotted line (average)
225
Risks of SFD
FD disproportionately to perinatal morbid and mort Main contributor to association is FGR rather than SFD Means can FGR can decrease at one point and risk increases but SFD may be more due to a normal FGR earlier Increased morbidity and mortality is a result of intrauterine hypoxia, acidaemia, prematurity (often iatrogenic) and neonatal complications
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Causes of small for dates
``` Normal small Constitutionally small, healthy baby Abnormal small Chromosmomal abnormlaities (T2), syndromes (from beginnning), congenital malormations (from beginning) Infected Small Infection during preggers (CMV often) Check Igs - depends when. Some IgA can linger though so not sure when occurred Can measure retrospectively with kept booking bloods Starved Small Placental FGR Poor placentation (T3) Smoking Materal disease (T3) Multiple preggers Wrong Small Incorrect Dates or measurements ```
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Placental factors on size- adequate transfer dependent on?
Uteroplacental blood flow from uterine artery to placena (which artery which) Fetoplacental blood flow (umbilical to placent) Villous structure (interface of maternal and fetal blood) Tunic media in spiral arteries normally destroyed - no control ie free flow. In preeclampsia it is still there ie vasoconstriction still occurs
228
Investigation into placental FGR and when
Doppler of uterine artery ie blood flow impedence Can see flow in systole and diastole Severe reverse flow in diastale IN 24-26 weeks Good NPV, Poor PPV Mainly tertiary if mother has history of SGA babies Stage 1 - flow in both Stage 2 - flow in systole - diastolic effected - diastolic notching Stage 3 - reverse flow in diastole
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Signs of cause of SGA on US
Placenta - low liver glycogen so asymetrical growth restriciton Liquor volume - go down in placenta Centile position UmA doppler - small placena MCA doppler - in brainz, shunting to brain if low supply. High shows fetal redistribution
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Signs if aneuploidy/ infection
Markedly small, velocity may be reduced, symmetrical growth Variable amniotic fluid - normal or increased Normal UMA Doppler
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Signs of placental IUGR
Reduced amnio ASymmetrical FGR MCA increased High resistance UMA flow and decreasing BPP (abnormal)
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How to monitor if SFD e.g. different way
Assess material RFs Assess for presence of maternal disease Continue monitoring for pre-eclampsia with BP and urine checks in reguar intervals ``` Fetal surveillance Serial growth measrements every 2-4 weeks Fetal wellbeing surveillance Maternal perception of movements Not always reliable Maternal doppler Amniotic volume measurements Biophysical profile Umbilical artery only good in high risk Better predictor of abnormal CTG and NICU (Neonatal intensive care) on admission Uterine doppler Good for screening not surveillance Notching = high risk MCA Increased flow is danger to baby Surveillance useful Should increase in T3 Venous doppler Information about the 'pump' Ductus venosus RHF - evidence in ductus venosus Waveform deterioration predicts chages in BPS (biopsysical profile score/ manning score) ```
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When to delivery FGR??
Normal UAD - delay delivery until >37 weeks AREDF - (absent or resversed end-diastolic flow in the umbicial artery) if gestation >34/40 even if normal additional assessment <34 if CTG abnormal, BPP (biophysical profle on CTG and 4 Us parameters e.g. actvity) abnormal or other Doppler parameters abnormal Mode depends on gestation, presentation, foetal condition and maternal factors
234
Risks of preterm delivery/ FGR baby?
Increased need for resus Hypothermia and hypoglycaemia RDS & NEC (necrotizing enerocolitis
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Cause of large for dates?
Uterine fibroids Pelvic mass Polyhydramnios Maternal obesity ``` Why is the fetus large? Maternal Daibetes Obesity Increased materal age Multiparity Large status Fetal Consitiutional Male gender Postmaturity Genetic disorder (Beckwith Wiedeman) ```
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Implications of LFD
``` Maternal Prolonged labour Operative delivery Postpartum haemorrhage Genital tract trauma ``` ``` Fetal Birth injury Perinatal asphyxia from difficult delivery Shoulder dystocia/Erb’s palsy Hypoglycaemia Childhood obesity Metabolic syndrome ```
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Management LFD
Exclude maternal diabetes Absence of polyhydramnios treat as normal (due to polyuria in baby) Maternal diabetes and macrosomia offer C section Early recourse to intervention where there is delay in labour - mainly due to shoulder dystocia Monito hypoglycaemia in neonatal period
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Long term risks of SGA and LGA
LGA - More risk of metabolic | SGA - More risk of HYT and DM and CVD
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How does diabteres cause SGA?
Diabetes can affect placenta - microvasc disease (IDDM) and cause SGA
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When to give steroids?
<35 weeks and inducing then give steroids | If CTG - heart rate tracing abnormal then inducing
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Risk factors for GRF
``` Mother Age BMI Smoking (highest lifestyle factor) Alcohol Substance abuse Domestic Violence Due to abruptions Trauma/ haemorrhage into placenta Prescription and OTC drugs High altitude Pregnancy Previous FGR Highest Recurrent fetal loss Second highest Previous unexplained SB Raised AFP Infetion Placental pathology (praevia cirumvallata) Medical History Hypertension Haemoglobinopathies APLS Collagen vasc disorders Renal disease ```
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Innervation of bladder
``` Autonomic parasympathetic S2,3,4 Contract detrusor muscle during voiding Forms reflex Some higher control Sympathetic fibres T12-L2 Sphincter muscles mediated by sympathetic T12-L2 Relax detrusor and constrict sphincter Brain affects this UMN palsy - causes detrusor hyperreflexia Voluntary control Somatic S2,3,4 to external sphincter/ pelvic floor during storage, relaxation during voiding Pelvic nerve Contains sensory efferent And Parasympathetic Hypogasric nerve Sympathetic ```
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Forces involved in continence
Bladder pressures Detrusor Abdo pressure (weight coughing sneezing) Urethral Abdo pressure (above pelvic floor) - unless prolapse Urethral pressure from sphincter Pelvic floor if functioning properly - blood supply also affects Abdo cancels out in the above formula Pelvic floor - neck can slip under pelvic floor and Abdo pressure only acting on bladder not urethral making incontinence more likely. Detrusor overactivity e.g. MNS - if everything in tact may just get urge
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Incontinence history questions including specific questions
``` Symptoms Urgency - overwhelming desire to void Urge incontinence (leak) - associatd with leak Stress incontinence (leak when coughing) Frequency >8 per day Nocturia >2 per night Hesitancy - delay in commencing stream Dysuria - brief discomfort while/ after voiding History Stress or urge symptoms predominant - many have mixed Urge suggests detrusor overactivity Stress suggests Overfilled bladder e.g. stricture How frequent are symptoms Severity measures Amount Pad use, size and number Lifestyele modifications - e.g. Toilet mapping Fluid intake Associated symptoms Prolapse Faecal symptoms (up to 75%) Obstetric history Birthweight Forceps delivery Perineal trauma duration of second stage Previous surgery Hysterectomy Pelvic floor repair Incontinence ops Medical and fam Lung disease - bronchiectasis - coughing CTD Diabetes Hypertension - diuretics Move diuretic Doxazacin - alpha blocker\ ```
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Examination incontinence
``` Obesity Scars Abdo/pelvic massess Visible incontinence Prolapse - cough or bend down Pelvic floor tone from inside the vagina Mobile bladder neck - positional May be prolapse - cystocoele, urethrocoele Urodynamic stress CNS Middle years - MS Urge Often littlle leakage May be leakage on coughing Signs of CNS involvement e.g. MS ```
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Normal birth weight
2.5-4.5kg (3.5 normal) 5.5-10lb
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Investigation incontinence urge
Urinalysis Screen for infection - UTI could contribute to urge and leak Sign of stone/tumor Active infection can cause false dig at cytometry of detrusor over-activity so must check first Mid stream specimen far better than catheter but still false pos If using reagent strip Pos with symptoms = treat Pos without symptoms = formal MSSU - midstream specimen of urine Diaries 3-7 days Intake, functional bladder vol and freq Intake excessive >2l Confirm symptoms Used as adjunct to bladder drill Inclides drinks Amount of urine passed And leak or change pad Pad tests Object measure of leakage Duration 1 hr to 24 hrs Shorter test of dubious value Poor reproducibility 24 hr at home is best >50g unlikely to get better without surgery <50g then physio etc amy help US (bladder scan) Indicated in urge incontinence to find post void residule urine. ``` Qualiative tools May capture QoL issues Disease specifc QoL questionnaries King's Health care BFLUTs IIQ and UDI Generic SF 36 Few data on outcomes ```
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Investigation if incontinence and recurrent UTI, haematuria or pain. advantages?
``` IVP (Intravenous pyelogram) Investigation Recurrent UTI Haematuria PAin Recurrent UTI, haematuria, pain Painfulbladder syndrome? IVP producedure IV Contrast Xray before (check stone) During (filtering and should show blockages) After voiding (shows any incomplete emptying) Some risks but picks up more stones than US ``` ``` Cystoscopy Indications Haematuraia Recurrent UTI Painful bladder "sensory urgency" LA or GA Allows biopsies ```
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Investigation stress incontinence
``` Urinalysis Screen for infection - UTI could contribute to urge and leak Sign of stone/tumor Active infection can cause false dig at cytometry of detrusor over-activity so must check first Mid stream specimen far better than catheter but still false pos If using reagent strip Pos with symptoms = treat Pos without symptoms = formal MSSU - midstream specimen of urine Diaries 3-7 days Intake, functional bladder vol and freq Intake excessive >2l Confirm symptoms Used as adjunct to bladder drill Inclides drinks Amount of urine passed And leak or change pad Pad tests Object measure of leakage Duration 1 hr to 24 hrs Shorter test of dubious value Poor reproducibility 24 hr at home is best >50g unlikely to get better without surgery <50g then physio etc amy help ``` ``` Qualiative tools May capture QoL issues Disease specifc QoL questionnaries King's Health care BFLUTs IIQ and UDI Generic SF 36 Few data on outcomes ```
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Causes of Urodynamic stress incontinence
Commonest in women Sphincter not sufficient for abdo pressure ``` Causes Incompetent urethral sphincter Childbirth Menopause Prolapse Chronic cough Positional displacement - (most) - neck below floor during cough Intrinsic weakness (few) ```
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Detrusor overactivity causes/ RFs/ triggers
POORLY UNDERSTOOD Pressure from detrusor > spjincter tone HISTORY of childhood aneuresis (involuntary at night)/ UTIs May be post incontinence surgey May be neurological disease Commonest in men - prostate/ obstruction Neurogenic detrusor overactivity is common Triggers Running water Key in door Washing hands
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Cystometry overactivity
``` Functional test of bladder funciton Capacity Flow rate and voiding function Demonstrate leakage with intravesical pressure - during voiding Objective diagnosis - if unclear Not fool proof Exaimine pressure during cycle Measure pressure through small pressure in bladder Abdo pressure in rectuum Bladder- abdo = detrusor pressure Detrusor over time Cough checks Normally 0 as muscle is quiescent throughout - actively relax Record urine passed/ leaked Fill with saline at room temp 50ml/min Ask to report all bladded sensation Normally aware at 150ml = first desire May be suppressed, CNS? Strong desire More difficult to suppress and may reappear and become stronger May be able to distract Urgency Subjective - distractions affect too Inflammation then symptoms at lower vol e.g. Cystitis ```
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General incontinence treatmetn
``` General Pelvic floor first Continence care/ bladder care - 1.5-2.5l fluid a day Tea, coffee, alcohol avoid Mobility aids or downstairs toilets Pads, bedpans, commodes ```
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UDSI treatment non surgical
(Systems of stress dont need urodynamics before surgery unless other symptoms) Physio Examined to ensure pelvic floor correctly (just telling is ineffective in 40% due to wrong muscles) Effective in 50-70% Use biofeedback Cones - retain heavier cone using pelvic floor muscles (same efficacy of exercises) Electrical stimulation Meds Duloxetine 40mg 80% women say sig help
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MoA duloxetine
xreuptake inhibited or 5HT adn NA in Onuf's nucleus in sacral spinal cord (pudendal nerve), increases external (striated) sphincter tone and improved bladder capacity
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ADR duloxitine
Abdo pain, abnormal dreams, anxiety, GI upset, Diarrhoea/ Constipation, Sympathetic: Sweating, palpitation, insomnia, anxiety, tremor,
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Surgical UDSI treatmetn inclujding comps
``` Tension free vaginal tape most common Day case Less comps Bladder injury Outside peritoneum Tape exposed - chronic pain, surgery to correct LA Burch colposuspesion Old Suture in vaginal fascia Also treat cystocoele (prolapse Comps Voiding difficulty Detrusor overactivity Enterocoele formation Other tapes Transobturator tapes Diff route Periurethral injections Collagen Silicone PVC 50-75% success Can be repeated NOT anterior repair ```
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Detrusor overactivity management non surgical
``` Difficult to treat Behavioural therapies Bladder retraining first line Bladder drills Alarms and timers Contraction of pelvic floor reduces sensation Electrical stimulation High frequency applied to pudendal nerves Success 75% Often must be repeated Drug treatment Ach - muscarinic recptors 25-50% efficacy Poor compliance ```
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Types of muscurinic antagonists
``` Oxybutynin Severe SE Drymouth Tolterodine Specific to muscarinic receptor Less side effects Slow release available Solifenacin As effective as tolterodine Less side effects Trospium Second line drug Propiverine Second line ```
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Detrusor overactivity management surgical
``` Botulinum Good for nerogenic DOA Not as good for idiopathic Surgery End stage Clam enterocystoplasty Augments bladder size by adding in some ileum Self catherisation 5% malignant change at 10 yrs Urinary diversion Ileostomy Continent reservoir diversion ```
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Mixed incontinence treatmetn
Individualised discussion Conserve measures for stress Can consider surgery - urgency persists in up to 70%
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Prolapse predisposing factors
``` Age Menopause Parity CTD Obesity Smoking ```
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Symptoms prolapse
``` "something coming down" Backache or lower abdo pain Urinary incontience Faecal incontinence Difficulty with micturition or defacation Bleeding/ discharge Apareunia Inability to perform sex# ```
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Type of prolapse
Cystocele: Bladder bulges into vagina due to weakness in wall Rectocele: Posterior vaginal wall prolapse, Rectum buldges into vagina Enterocele: Herniation of peritoneal sac between vagina and rectum (often with bowel)
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Degrees of uterine prolapse
1st - cervix visible when perineum depressed (contained within vagina) 2nd- Cervix prolapsed through introitus (entrance) with fundus remaining in pelvis 3rd degree - procidentia (complete prolapse), entire uterus is outside
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Treatmetn of prolapse
``` Nothing Pessaries Easy and effective Minimal SE Ridgid block into vagina Also support bladder -may help stress incontinence Surgery Remove lump Restore organs to correct places Correct incontinence Preserve sexual finciton Wide range of procedures Comps Recurrent prolapse 10-15% Haemorrhage and Vault haematoma Vault infection DVT New incontinence Ureteric or bladder injury ```
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Other causes of incontinence e.g. continuous dribbling in african, post STI in male, Function incontinence.
``` Continuous dribbling Vesicovaginal fistula if prolonged labour from foreign country Post STI in male Stricture Functional incontinence Brain pathology Overflow Prostate ```
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RFs perinatal mental health
``` <16 Unrealistic ideas of motherhood Pre existing MHI FH MH Volatile or absent family relationships Social isolaton - foreign language Lack of positive support partner Poor or inadequate antenatal care Preg Comps Social problem ``` ``` Access care not good e.g. Substance misuse Migrant, asylum seeker, refugee <20 Domestic abuse Poverty Homeless ```
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Ways to risk assess and detect early perinatal metnal health
``` Brief screen in antenatal booklet (Whooley and Arrol) Can develop later Also GAD 2 - 2 item If high then GAD 7 Also Edinburgh postnatal depression scale EPDS (14-15) and Becks depression inventory ```
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Prevention of mental health post partum
Preconceptual counselling in psych patients Contraception use and pregnancy plans Implications of preggers and childbirth on mental illness and risk of relapse ``` Prevention Use the lowest possible dose Pre conceptual counselling Risk assess ante and post Education of HCPs Specialist mental healthcare team Protocols/ Guidelines for mgx of women at risk Documented mgx plan of at risk patients Antenatal and parenting classes Provision of home help and lengthening of hospital stays ```
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What is postpartum blues, treatment
Some alteration in their emotional state between the 3rd and 10th day postpartum Mild to significant Drop in progesterone Self-limiting 48hrs to 2 weeks Reassurance and support - health visitor Anxious, tearfull irritable
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Postnatal depression syptoms and onset and treatment
Mild in 7% Labile mood, irrtability, probs with coping and anxiety, symptoms similar to depression Can start first week postpartum - peak at 3 months Psychological as effective as antidepressants Preventative strategies are modified antenatal classes and postnatal peer support groups. Severe major postnatal depresson Affects 3-5% of all women Develops in early weeks post-delivery 1st 3 weeks rest between 10-12 week Symptoms are overt guilt, worthlessness, anxiety, panic attacks, anorexia, loss of concentration, anhedonia 1/3 obsessional thoughts of harm coming to baby Mangaement CBT SSRI 6 month therapy Recurrence risk 30-50%
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Puerperal psychosis symptoms and onset
Psychiatric emergency 1-2 per 1000 deliveries A third are manic and 2/3 depressive psychosis Abrupt onset by day 5 Peak onset at 2 weeks May present later - 3 months Irritablity, insomina, labile mood and behaviours, disorganised behaviour, delusions, hallucinations, high risk of suicide, disorientation
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Treatment puerperal psychosis
Manage MDT in mother baby unit Good recovery Emergency referral to specialist team Target affective symptoms: mood stabilizaer/ antidepressant/ ECT Target psychotic symptoms: 2nd gen atypical antipsychotic and long acting benzo Therapy, reassurance, emoptional support (family) MDT - health visitors, community psychiatric nurse High risk then admit to mother baby psych unit Risk of recurrence is 50% higher if preggers within 2 years of recurrence
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Lithium in pregnancy
Lithium, - ebsteins anomaly and neonatal hypothyroidism (offered cardiac scan), hypotonia, poor reflexes and arrhythmia Weened over 4 weeks if discovered use in preggers
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SSRI use in pregnancy, paroxetine adn fluocetine
SSRI - miscarriage, LBW and pulmonary hypertension Paroxetine - fatal cardiac death/ defect Fluoxetine is safer Antidep and antipsych can cause withdrawal e.g. Relucant to feed etc SSRI withdraw normally self limiting Poor adaptation Jitteriness Irritability Poor gaze control Can adjust feeding to avoid dose of drug Paroxetine worst Longer withdrawral for fluoxetine but thought to be best Treatmetn rarely needed Breast feed ok
277
Olanzapine in preggers
GDM, Fetal macrosomia | Antidep and antipsych can cause withdrawal e.g. Relucant to feed etc
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Anti-epileptics/ mood stabilisers in pregnancy
Carbamazepine = cleft lip Lamotrigene risk of Steven Johnson Antimanic - sedation, poor feeding, behavioural effects, develomental milestone, long term
279
Benzos in prenancy
Lorazepam/ Zolpidem ok as shorter half life
280
SSRIs and TCAs that are ok in preg
FINA - Fluoxitine, imipramine, noritramine, amitriptalline OK
281
What is first stage of labour? how long?
Cervix up to 10cm dilation Length starts at 4cm Before is latent - regular contraction but not effacing Mucus plug comes out - is it snotting like nose or fresh bleeding
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Passage in labour?
``` Pelvis unliekely cause unless RTA but rare Cervix - may have scarred, may tear Vaginal septums - just tear FGM - nasty tear to bladder and bowel Deinfibulation to open up and prevent tears Soft tissues Lower uterine segment Cervix Vagina Vulva (external female sex organs) Pelvic floor Perineum ```
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The powers in labour?
Fundal dominance of contractions The uterus polarises into an upper segment and lower segment Contractions are rhythmic and occur every 3-4 minute (2-3 in 10) and every 2-3 minutes in advanced labour (3-5). Note 5 is probably too much - slow up syncioxtocin
284
The passenger in labour? / terms
Lie Long Oblique Transverse Presntation Ceohalic Vertex (occoiput leading - most common cephalic) Brow Face Breech Shoulder Denominator - part of fetus used as reference point to describe position in materal pelvis (occiput, mentum, sacrum, acromino) usually occiput OP really slows labour down Position Relation of denominator to maternal pelvis Occipitoanterior, occipitotransverse, occipitoposterior ``` Moulding of fetal cranium + depending on how much you can get finger through Shows last trick has been used. +3 due to malposition Capput Egg head going down within 24 Engagement How much can feel out of pelvis Usually 2/3 fifths Usually occurs in 3 term Nulitips usually not until larbor ```
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Mechanism of labour
``` Engagement Flexion So occipital presentation Descent Internal rotation Extension External rotation (shoulders through spine) ```
286
Monitoring during labour including drugs
``` Obs Hydration Analgesia Pethidine Gas and air Water Antacids Risk of theatre Bladder care Position Not flat - hypensensitive due to major vessels Sitting up - left lateral tilt 3rd stage Active management Oxytocics and controlled cord traction Waiting can take 45mins Perineum ``` ``` Fetal wellbeing Fetal heart monitoring 15mins in first stage Continuous in high risk Colour of liquid Clear or straw If blood If meconeum then monitor ```
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Describe station in labour
``` widest part of head (biparietal diameter) to ischeal spine - can be plus too If through should be vaginal If not through then C seciton an option Low risk 0.5 cm per hr dilation Different in high risk = 1cm/hr ```
288
Define failure to progress?
``` x 1hr after full dilation call doctor 2hr if epidural Indications Lots of caput moulding Haematuria Maternal Exhaustion 20 hours or more if you are a first-time mother, and 14 hours or more if you have previously given birth ```
289
Causes of failure to progress
``` Powers Ineffective uterine activityy Hypotonic contractions Incoordinate contractions ?Dehydration, exhaustion, ketosis ``` ``` Passage Abnormal bony pelvis Cervical dystocia - rigid/ edematous Mechanical obstruction Rigid Perineum ``` ``` Passenger Macrosomia Hydrocephalus Abnormal diameter presenting Abnormal attitude, malpresentation or malposition ```
290
Management of powers in failure to progress
``` xManagement Hydration Analgesia Amniotomy Oxytocin infusion Delivery if appropriate ```
291
Management of passage in failure to progress
x Managemnt C section Episiotomy
292
Management of passenger in failure to progress
``` Management C section Correct malposition Instrumental delivery x ```
293
Dangers of breech
``` C section 5-10x less liely to have mort and morbidity Often with twin - i.e. second Undiagnosed breech with emergency Probs Cord prolapse With or before fetus Compromises blood flow to fetus Trapped aftercomng head Intracranial haemorrhage Internal injuries Usually iatrogenic ```
294
Indications of suspected fetal compromise
Passage of meconium Non reasuring CTGs Good NPV Poor PPV High sensitivity, low specificity Confirmed by fetal acid-base (fetal scalp blood sampling) If unable to perform FBS, delivery by speediest route Baseline tachy or brady Reduced beat-to-beat variability (flat) Absence of acceleration (non-reactive) Presence of deceleration
295
Causes of fetal compromise
``` Uterine hypersimulation (iatrogenic from oxytocin) Hypotension Poor fetal tolerance of labour (IUGR) Cord compression Infection Maternal disease ```
296
Management of suspected fetal compromise
Rectify reversible causes e.g. Maternal hypotension Left lateral position Stop oxytocics Confirm compromise by blood sampling where possible deliver by speediest route if unable to correct or if significant acidosis
297
Risks of VBAC
2/1000 chance of death instead of 1/1000 Risks Emergency C section Uterine scar dehiscence/ rupture 0.5-1% Risk higher with more than one previous CS
298
Common precautions with VBAC
IV access and G&S Continuous electrical fetal monitoring Avoid prolonged labour Augmentation/ induction should be senior decision only More likely with placenta previa
299
Placental invasion disease
Accreta into muscle - placenta attaches to myometriua as opposed to just decidua basalis Increta Villi invade myometrium Perccreta - adjacent organ (bladder) Invade through perimetrium/ serosa Risk of bleeding so interventional radiologist and vasc surgeons
300
Operative delivery of baby instrumental indications
If retinal detachment, Pneumothorax and dont want to push too hard Failure to progress in 2nd stage Fetal distress in 2nd stage
301
Complications of operative instrumental
``` x Failure Fetal trauma Maternal trauma Postpartum haemorrhage Urinary retention ```
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Pre requisits for instrumental
``` Trained operator Full dilatation Absent membranes Cephalic presentation Clearly defined position Presenting part engaged No evidence of CPD = Cephalopelvic disproportion (obstruction) - cant have everything on head Adequate analgiesia Peudendal nerve block may help Empty bladder ```
303
C section indications
``` Failure to progress Fetal distress Maternal reasons Malpresentation/ Malposition Failed instrumental delivery ```
304
Complications c section
``` Transient tachypnea of newborn (TTN) Retained fetal lung fluid, supportive tx abx O2 Haemorrhage Infection Bladder/ bowel injury Thromboembolic disease Requirement for blood transfusion Fetal trauma ```
305
Shoulder dytocia definition
Inability to deliver shoulders after delivery of head | Anterior shoulder does not enter the pelvic inlet
306
Shoulder dystocia Risks
``` Fetal death Asphyxia with resulting hypoxic damage Birth trauma (erbs - waiters tip internal rotated, fracture) Maternal trauma PPH ```
307
RF shoulder dystocia
Macrosomic fetus DM High maternal BMI Prolonged labourRotational instrumental delivery
308
Managemnet shoulder dystocia
Episiotomy McRoberts position Flex and abduct hips Other obstetric manoeuvres
309
Breech RFs
``` Uterine fibroids/ malformation Placenta previa Polyhydramnios/ oligohydramnios Fetal abnormality e.g. CNS malformation or chromosomal disorder Prematurity ```
310
Management of Breech
``` x External cephalic version Elective C section Vaginal breech delivery <36 weeks most will turn spontaneously 36 weeks then external cephalic version 60% success 37 in multipaous women Still breech then planned c section or Vaginal ```
311
Physiological causes of lumps
``` Coronal papillae Vulval papillae Keratotic wart Fordyce spots Haemangiokeratoma Hair follicles Pearly penile papules Scrotal follicles Skin tags Tyson's glands Vestibular papillosis ```
312
PAthological ddx lumps on perineum
``` Penile (meatal) warts Molluscum Contagiosum Lichen planus Secondary syphilis (above) (Condylomata lata) Carcinoma in situ VIN ```
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Presentation of genital warts
``` Keratinised (dry/ hairy skin) Non keratinised (warm/moist/ nonhairy) Aymptomatic Painless Itching "sore" Bleeding from urethra or anus (internal lesion) Distorion of urine flow (internal lesion) Anus ```
314
Pathophysiology of genital warts - how common is HPV infection? method of infection
``` HPV 1% have genital warts 25% no contact 60% prior infection 14% The rest subclinical infection 60% infectivity rate during sex Incubation long from 2 weeks to 8 months 4 months mean Replicate in basal layer, assemble in ```
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Management of warts. Order of success and recurrence
Explaination - implication on health etc Condoms useless Asymptomatic viral shedding Phsyological impact/ counselling Cryotherapy, podophyllotoxin and imiquimod all as effective (Podo may be more), imiqui lowest recurrence then cryto then podo
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Podophyllotoxin MoA, Use.
``` Non keratinised Podophyllotixin MoA Antimitotic Followed by local tissue necrosis HPV-infected cells reduce and warts shrink Solution (penile) or cream (vulval) Use 4-5/52 3/7 a week followed by 4/7 rest Avoid sex after (damage condoms) ```
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Imiquimod moa, use
MoA Stimulates innate and aquired immune response NKC activity and macrophage NO secretion Augments T cell activity and B cell proliferation and differentiation Induces cytokine production Interferones, TNFa and IL2 Not directly antiviral (maybe why it is better at remission? Use 3/7 for 16weeks
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LN2 best for which type of warts?
Keratinised
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Management of cervical warts
Gynae for colposcopy
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Managemetn of warts in preggers?
``` Often first presentation More difficult to treat Low risk of vertical transmission Home therapies are teratogenic Spontaneous resolution in puerperium Cryo only treatement (needs weekly) Risks RLP - round ligament pain Obstruction Treatment Cryoablation Surgical removal/ LSCS if extreme Avoid topicals ```
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When to refer for warts treatment?
``` Unsure of diag Cercial or vaginal warts Intrameatal or anal warts Not responding to treatment <16 Other genital symptoms Increased chance of other infection MSM Non-UK partner ```
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Sexual history PC female and tactics
Explain confidentiality Maintain privacy Simple language ``` Vagnal discharge - not neccessarily STI e.g. Thrush BV Genital lumps Warts Intermenstrual and post-coital bleeding Deep and superficial dyspareunia Location of pain Enters = superficial e.g. Thrush Deep inside = PID Dysuria and urinary frequency Abdominal pain PID Ectopic Rectal symptoms ```
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Sexual history PC male
``` Urethral discharge Dysuria and freq Genital lumb Testicular pain/swelling Swelling Epidydimal orchitis Rectal symptoms MSM ```
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Other reasons male and female present GUM
``` Females STI contact/ sexual assaults/ contraception/ TOP/sexual dysfunction Males MSM Sexual dysfunction and assaults ```
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Gyane history female GUM
``` Gynae Preggers Normal Still birth Miscarriage Menstual Reg How long LMP Heavy/ painful Smear Contraception What ```
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Social history for GUM
``` Alc Smoke Recreational drugs IVDU Chem sex - sex on drugs Domestic violence ```
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Sexual hisotry GUM
``` Past history of STI Last episode of sex How long getting STI to picking up on test = window. Clamyd and Gonn = 2 weeks to show up. Reg/ casual/ one off Male/ Female partner Sexual Contact - regular or contact Casual high suspicion of STI Difficulty with partner notification Duration of relationship Shorter then higher risk Sex with condoms Type of sex Particularly MSM Insertive/ receptive, active/ passive, top/ bottom Partner symptoms Partner details for contact BBI risk assessment How many partners in last 6 months - Hep C IVDU Partner IVDU MSM Women ask if parter MSM Where are partners/ patient from Africa risk Partners have virus Viral load Treatment Immunosupresed Blood products before 1985 Paid for sex or been paid for sex Tattoos/ piercing abroad PEP - limits risk fo getting HIV from sex ```
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Male sexual examination
``` Feelin in inguinal or groin region Insepect pubic area and scrotum Scratch Rashes Inspect penic Fully retract foreskin Palpate scrotal contents Tenderness over epidydimis = epidydimal orchitis MSM Perianal Anal/ rectal examination with proctoscope and for swbas ```
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Investigation male and time to show on test
``` Urine - Chlam + Gonn Discharge - on slide - evidence on Gonn Culture plate for Gonn - abx Blood HIV - window 1 month (no longer 6 months) Syph Hep B + C Hep B - 2 month Hep C - 6months MSM swabs from rectum and pharyngeal ```
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Female exanination
``` Lithotomy position Visulisation Inspect and palpate inguinal region Inspect public area, labia majora, minora and perianal areas Speculum exam Lube on Insert sideways When in rotate 90 deg and open See cervix Any bleeding Collect discharge from posterior fornix Bimanual exam Abdo pain Vaginal Same- 2 fingers 90degrees Push against cervic - pain -cervical something Analrectal in left lateral Oral cavity Skin Lymphoreticular system Eyes Joints Reactive arthritis ```
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Investigation female STI
High vaginal loop swab and pH - TV, BV, Candida Vivovaginal swab dual NAAT - Chlamyd and gonn Bloods Optional High vaginal charcole - MC+S, candida Gon ciltures - urethral and endocervical DGM - Dark gram microscopy Dark lesion?Shancre HSV PCR - ulcer Urinalysis Preggers test Self take a lt of swabs
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Causative organisms of PID
Chlamyd - risk increases with subsequent infection ?Hypersensitivity response Gonn more severe - attach to host cell via pili Neutrophilic infiltrate and abscess formation Gonn symptoms more likely than Chlamydia More systemic symptoms Tubo-ovarian cyst 10-40% untreated in chlamyd = PID Anaerobes etc in older women and of lesser importance Mycoplasmal PID Mild/ moderate similar to chlamyd
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Symptoms PID
``` Cervical Inflam Tenderness Discharge Deep dyspareunia Endometritis Menstrual irreg Menorragic IMB Secondary dysmennorhea PCB Midline abdon pain Not related to menses Constant Worse during or after sex Salpingitis Erythema Edema Exudate - discharge Lowblat abdo pain Peritonitis/ Appendicitis/ Perisigmoiditis/ perihepatitis Systemic Fever Asymptomatic ```
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Complications PID
``` Fitz-Hugh-Curtis Capsule of liver infalmmed Chlamydia mostly Cause adhesion - Violin-string adhesions Tubo- ovarian abscess Chronic pelvic pain Infert - Adhesions Increased episodes increases riks of tubal occlusion with each infection Increased risk of ectopic preggers In adnexae Recurrence Women with HIV have more severe symptoms ```
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Differentials PID
``` UTI/ Cystitis GI IBSIBDApprendicitis Gynae Ovarian cyst (torsion or rupture) Endometriosis Ectopic ```
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RFs PID
``` Young age Low SES Multople partners <25 yrs Low educational attainment TOP/ misscariate Instrumentation of uterus (loss of barrier of cervix) Barrier methods of contracep (decrease risk) Hormonal (increase)Timing of menses Appendicitis Coil insertion Low SES New sexual partner ```
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Signs PID
``` Cervical excitation Bimanual - pain, tenderness Lower abdo tenderness - bilateral Adnexal mass Tubes - either side of uterus) (abscess) ```
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Diagnosis PID
``` Clinical diagnosis difficult Uterine/adnexal tenderness or cervical motion tenderness can be diagnostic Cervical discharge Do not wait if high suspicion despite no investigation results Bedside Obs - oral temp >38.3 Bloods ESR CRP WCC Only if mod/ severe PID Imaging not usefel TVS Hydrosalpinx/free fluid/ abscess MRI/CT may confirm other DDX Neither is routine Procedural Preggers test most important Swabs Test for CT, NG, MG (myocplasma but not very available) vulvovaginal/ endocervical NAAT for CT and NG Culture for NG WBCs/ saline microscopy (Vaginal wet mount) of discharge - Absences of vaginal/ endocervical pus cells has high NPP for BV, TV and Candida Absence does not exclude as not swabbing higher infection site Definitive with laparoscopy Endometrial biopsy possible Doppler flow studies possible ```
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Management PID
``` Rest Analgesia Broad spectrum abx IV if temp >38 Admit fo obs if severe disease, preggers or suspected tubo ovarian abscess Abstinence until both partners treated ``` Empirial treatment Low threshold for treatment as delay may lead to worse outcome Esp if RFs, new onset lower bilat abdo pain, tenderness Unless Preggers ... Several regimens to cover common organisms over 2 weeks e.g: 500 mg IM ceftriaxone - gonn (also with erythro due to resistence) 100mg bd Doxy - chlamyd and inflam 400mh bd Metron - anaerobes Moxifloxacin if mycoplasma suspected IV until 24 hrs post improvement clinically Contact tracing with full screen and minimum treatment of Azithro 1g stat
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When to hospitalised PID
``` Surgical emergency Acutely unwell Not tolerate oral Not respond oral Abscess Pressers ```
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Follow up PID
``` 72hrs If no improvement - remove IUC if in sity (risk of preggers in last 7/7 adn consider emergency contra) - normally just leave in Consider IV 2-4weeks Ensure symptoms resolved Check compliance Metronidazole not nice Folllow up contacts and screening ```
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Surgical manage,ent PID
Surgical management Laparoscopic drainage +/- division of adhesion US guided drainage of cervical collections
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PID in pregnancy
Uncommon Cervical plug prevents infection Associated with increase in maternal and fetal morbid`ity IV therapy recommended
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Pathophysiology of hSV, types and stages
Herpes is seasonal September/October to March/April Herpes = to creep in latin (histological = dendritic) ``` Herpes - morbidity for life assocaited with infidelity Skin to skin transmission First episode followed by recurrences Asymptomatic carriage Pathogen Icubation 3-14days 4 stages Initially Tiny vesicar lesion Become blisters Ulcerate Resolve 2-3 weeks in primary Recurrence 2-3 days long, max 5 days Erosive vs ulcerated lesion Loss of epidermis only (erosive) - blisters Ulcer - both layers lost HSV 1 more common fron sex (i think) but both possible HSV 2 mouth??? Herpetic whitlow = finger or thumb - extrasexual ```
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Presentation HSV
``` Excruciatingly painful Dysuria When urine touches thighs or labia outside body - peeing on glass No frequency-rather desire not to pass urine Local A rash Leisons May just be within cervix DDX cervical cancer - stops girl going throgh cervical cancer May have discharge Can be analgenital Even without anal sex Systemc Myalgia Headache Tiredness (Fluy) Used any chemical agents recently Exlude chemical dermatitis Cervicitis May or may not get dicharge ```
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Examination HSV
Vulval swelling Multiple lesions with dendritric appearence Different lesions at different stages May just see oedema or swelling or no ulceration
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Investigation HSV
``` Swab - can do self swab Nucleic acid amplification technology Full STD screen Sypis serology Suspect unless proven otherwise On the rise HIV antibody test PCR Highly sensitivty ```
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Recurrence and prev of types of HSV
``` Types Type 2 higher recurrence Normally 4 in first year Type 1 Morecommon ```
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Managment HSV
Sick note/rest Analgesia Saline washing - urinate in bath or topical lignocaine gel If retention may need suprapubic catheterise Systemic antiviral 5 days Aciclovir or valaciclovir (way more expensive) Vaseline Avoid sexual contact Maximal benefit after 5 days. Natural history is self limiting
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Complications HSV
``` Urinary retention Adhesions - vaginas needed release Men frenulum repair Meningism Emotional distress Recurrence Herpes encephaltis Erosive vulvitis ```
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Is HSV serology useful?
xMany asymptomatic shedders 50% women 60% men seroconvert without being recognised Explains why serology is a waste of time Condoms only reduce if sore on glands or shaft
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HSV in pregnancy
HSV in preggers If recurrent episode low risk Primary infection in last trimester- C section Not enough time for antibody transfer NO place for swabbing in last trimester Occasional use prophylactic therapy in last trimester Discordant couples (one with one without) no UPSI (unprotected sex) in preggers Only time HSV serology considered Want to ensure its not first presentation Otherwise child gets herpes encephalitis - 80% mortality IF man herpes positive then ask to not have unproteced sex
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DDX HSV (genital soreness)
``` UTIThrush Rampant rabbit Sex toy can cause too Fixed drug eruptions Pheophylinnes Barbiturates Bechets Apthosis T cell triggered e.g. nutrition def Trauma Stress Hormones Allergies Genetics Lichen planus Pemphigus Malignance Trauma -physical/ chemical dermatitis Herpes zoster VIN/ CIN ```
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Syphilis pathology inc incubation
Treponema Pallidum Primary Icubation 9-90 days Secondary Incubation 6weeks to 6 months
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Presentation syphilis (stages)
Primary Chancre (painless ulcer) Oral Genital Perianal Lymphadenopathy Secondary Systemic symptoms Papular lesions on trunc Mucous patches on tongue Macular papular but on hands and feet Alopecia - eye brows too Chancre mucous membrane and scrotum Tertiary CVD - aortitis Neurology- asymptomatic, tabes dorsalis, dementia
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Diangosis syphilis
Dark ground microscopy Shooting stars Treponemal PCR STI Scren
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DDX syphilis
``` Haemophilus ducreyi/ chancroid Lymphogranuloma Venerum Granuloma inguinale Scabies Phthirus pubis Apthous ulcer ``` Behcets Recurrent orogenital ulceration Fixed drug eruption Erosive balanitis (nonspecific) Inflammation Environment Physical trauma Infection Extramammary Pagets disease
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What is haemophilus ducreyi?
Irregular painful ulcers Necrotising base Management Macrolide e.g. azithro
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What is lymphogranuloma venerum
Chlamydia tachomatis L1,2,3 serovars Small non-secript ulcer followed by florid (unilateral) lymphadenopathy and ano-genital syndrome
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Granuloma inguinale?
AKA donovanosis Klebsiella glandulomatis "beefy ulceration"
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Scabies on genitals
Crusted, inducated lesions on genitals Itchy
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Phthirus pubis?
Pubic hair - crab lice
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Causes of erosive balanitis?
Inflammation Environment Physical trauma Infection
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NAtural history typhilis
Primary and scondary may last 2 yrs - infections Latent Tertiary Tabes CVS
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Managemtn syphilis
Benzathine Penicillin IM stat If tertiary ten IV penicillin
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How long after birth need no contraception?
21 days
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Risk of transmission of BBV from needlestick
Hep B 1 in 3 Hep C 1 in 30 HIV 1 in 300
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Management of needlestick injury general
First aid measurement Wash and encourage to bleed (don't rub) Inform senior - relieved from duties Incident reporting later Risk assess by occupational health or GU doctor May need HIV post-exposure prophylaxis - start within 1 hr May need HBV booster Source patient RFs Known positives Viral load Big factor Nature of exposure Hollow vs solid needle Size of bore Gloves Skin puncture/ broken skin/ intact skin/ mucous membrane Time to first aid measures Recipient HBV vaccine status
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Management of specifiv BBV from needlestick
HIV PEP (post exposure prophylaxis) for 28 days Triple anti-retroviral drugs Start within 72 hrs (earlier better) Hep B May need booster immunisation May need HBIG If incompletely vaccinated/ poor responder and if patient HBSAg positive Hep C None available
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Testing post needle stick
HIV HBsAg HCV - Anti- HCV initially Recipeint Original blood sample sored Further tests at 6,12,24 weeks depending on curcumstances Waiting Safe sex Good infection control Avoid blood donation
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How does HIV cause harm?
nto host DNA Reverse transcripase to make DNA from genomic RNA
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Acute ilness in HIV? when?
Seroconversion illness (50-70% After 2-6 weeks)
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Long term consequences of HIV infection
Opportunistic infections TB Candida, pneumocystis Viral (HSV, CMV) Protoxoal Toxoplasma CNS - encephalopathy Malignancy -lymphoma, Kaposi sarcoma Wasting syndrome Weight loss >10% with diarrhea or chronic weakness and doccumented fever >30 days not attributable to concurrent condition
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How to test for HIV
4th gen combo assay (EIA Detects Anti-HIV antibodies Detects p24 antigen Shorter window period -2 weeks (4 weeks to be safe) Confirmatory test in lab if positive - immunoblot Look for other antigen RNA detection by PCR for viral load Second sample to confirm patient ID
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Pregnancy treatment HIV
Pregnancy Give antivirals HAART to mother throughout pregnancy Risk of premature labour and GDM Delivery If viral load <50 then vaginal ok If above 50 or not on HAART then C section Postpartum Avoid breast feeding (Carbergoline to supress lactation) HAART/ Zidovudine to baby within 4 hrs If high risk give Co-trimoxazole (PCP)
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Managemnt and monitoring in HIV
Highly active anti-retroviral therapy (HAART) Monitoring HIV viral load CD4 counts +/-HIV genotypic +/- drug resistance testing Routing bloods Hep B/c, EBV, CMV, TB Treat/ prevent opportunistic infections HAART Monitor CD4 and viral loads ?monthly at first then?6 monthly Refer to counseling for psychological suppport Advice regarding potential partner notification Counsel risk of opportunistic infection adn advise seeing help Management of CVD risk factors - higher risk of CVD Manage of bone diesease RFs e.g. smoking, alcohol, vit D
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Hepatitis presentation acute
Fever RUQ Jaundioce Malaise Anorexia, nasuea Dark urine, pale stool Fulminant hep - transplant? Cant distinguish from features Suportive management
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Hep B pathogen and problems
Partially ds DNA Symptomatic (incubation 2-6 months) <10% children, 30-50% adults Acute hep Fulminant hep Asymptomatic 1% mort Chronic hep 90% infants, <3% adults Asymptomatic or symptomatic carrier Cirrhosis HCC (100x risk)
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definition of acute vs chronic hep B
Acute vs chronic Hep B is <>6 moths
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Markers of current infection HBV
HBsAg = current infection (Ag = component of virus) Anti HBc - current or previous infection
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Marker of current or previous infection HBV
HBsAg = current infection (Ag = component of virus) Anti HBc - current or previous infection
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Marker of immunisation
Anti HBs - Immunisation
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Markers of infection
E antigen - high infectivity Anti-Hbe - high infectivity resolved
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Markers of body response to HBV
IgM = first reponse IgG = subsequent response
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Prevention of HBV
Lifestyle Vaccine 0,1,6 month doses Check anti HBs Pre and post exposure HBIG Post exposure prophylaxis Neonates of infected mother Needlestick
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When might one use HBIG?
Lifestyle Vaccine 0,1,6 month doses Check anti HBs Pre and post exposure HBIG Post exposure prophylaxis Neonates of infected mother Needlestick
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Management of HBV
Admit if unwell Refer to ID/ Hep/ GuM Notify PHE Full serological testing Baseline FBC LFT Clotting AFP Liver US Immunisations Hep A Houshold against Hep B Lifestyle Avoid transmission to others Avoid alcohol Breastfeed ok if baby immnunised Antvirals Speciialist
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bREAST feeding in HBV
fine
389
Management of Hep B in preggers
If mopther is surgace antigen pos then give Hep vaccine and 0.5ml HBIG within 12 hours of birth and further vaccine at 1-2 months and 6 months Not trasmitted by breast feeding unlike HIV
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Hep D who gets? presentation
Defective virus only funciton if HBsAg present BBV Co-infection with HBV More sympotmatic More likely to appear clear With chronic HBV Symptomatic flare High risk of chronic liver disease
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HCV pathogen presentation
Enveloped single-stranded RNA Acute Asymptomatic or mild -6 week incubation (2-26) 20% Clear infection 80% progress to chronic infection Cirrhosis HCC
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Serology HCV
Anti-HCV used Marks current or past infection Postiivite after 4-10weeks Antiody provides incomplete protection and reinfection is possible HCV RNA Distinguish current from past infection If present then infectious
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Management HCV
Lifestyle Weight loss Avoid alcohol Smoking Vaccine Hep A and B Acute Monitor to check clearance Drugs Sofosbuvir etc, older e.g. pegylated interferon and ribavirin Chronic Monitor for liver fibrosis and HCC
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Hep A and E transmission, presentation, RFs, prevention
Faeco-oral transmission (Or blood rare) Acute Asymtpomatic Or symptoms 2-8weeks Severity more with age Pregnant have high mortality No Chronic RF Travel MSM IVDU Prevention Hep A vaccine
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Foetal FFN?
Fetal fibronectin (fFN) is a protein that is released from the gestational sac. Having a high level has been shown to be related with early labour, and depending on the level different probabilities can be calculated for labour within one week, two weeks etc. Having a high level however does not mean that early labour is definite, some women will go to term even with a raised fFN