MSK, Reproduction and Psychiatry Summary Flashcards
How do anti-psychotics work?
Antipsychotics act as dopamine D2 receptor antagonists, blocking dopaminergic transmission in the mesolimbic pathways
What are the extrapyramidal side effects caused by traditional anti-psychotics?
Extrapyramidal side-effects
Parkinsonism
acute dystonia (e.g. torticollis, oculogyric crisis)
akathisia (severe restlessness)
tardive dyskinesia (late onset of choreoathetoid movements, abnormal, involuntary, may occur in 40% of patients, may be irreversible, most common is chewing and pouting of jaw)
What are the specific risks of antipsychotics in the elderly?
Increased risk of stroke
Increased risk of VTE
What are other side-effects of anti-psychotics?
antimuscarinic: dry mouth, blurred vision, urinary retention, constipation
sedation, weight gain
raised prolactin: galactorrhoea, impaired glucose tolerance
neuroleptic malignant syndrome: pyrexia, muscle stiffness
reduced seizure threshold (greater with atypicals)
sprolonged QT interval (particularly haloperidol)
What mood stabilsing agent can cause hypothyroidism?
Lithium
Why aren’t TCA’s commonly used for depression?
Side-effects and toxicity in overdose
What are common side effects of tricyclic anti-depressants?
drowsiness
dry mouth
blurred vision
constipation
urinary retention
What is low does amitryptiline used for?
low-dose amitriptyline is commonly used in the management of neuropathic pain and the prophylaxis of headache (both tension and migraine)
What joints are affected in rheumatoid arthritis?
MCP
PIP
What are the joints affected in osteoarthritis?
Large weight-bearing joints (hip, knee)
Carpometacarpal joint
DIP, PIP joints
What are X-ray findings in osteoarthritis?
Loss of joint space
Subchondral sclerosis
Subchondral cysts
Osteophytes forming at joint margins
What are x-ray findings on rheumatoid arthritis?
Loss of joint space
Juxta-articular osteoporosis
Periarticular erosions
Subluxation
What are the risk factors for endometrial cancer?
obesity
nulliparity
early menarche
late menopause
unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
diabetes mellitus
tamoxifen
polycystic ovarian syndrome
hereditary non-polyposis colorectal carcinoma
What are the features of endometrial cancer?
post-menopausal bleeding is most common feature, abnormal vaginal bleeding (change in pre-menstrual bleeding)
What is the investigation for endometrial cancer?
women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway
first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
hysteroscopy with endometrial biopsy
MRI pelvis
What is FIGO staging?
Endometrial cancer staging
(FIGO stage 1-4 according to depth of myometrial invasion, cervical involvement and lymph node involvement) and type (1 or 2)
stage 1 (carcinoma strictly confined to the uterus)
stage 2 (carcinoma extended to the endocervix (2A) or cervical stoma (2B))
stage 3 (spread to serosa of uterus, pelvic peritoneum or pelvic lymph nodes)
stage 4 (local metastasis to bladder/bowel (4A) or distant metastasis (4B))
What is the management for endometrial cancer?
localised disease is treated with total abdominal hysterectomy with bilateral salpingo-oophorectomy. Patients with high-risk disease may have post-operative radiotherapy
progestogen therapy is sometimes used in frail elderly women not consider suitable for surgery
What are protective factors for endometrial cancer?
Combined oral contraceptive pill
Smoking
What cancers is the oral contraceptive protective for?
Ovarian cancer and endometrial cancer
What are the risk factors for breast cancer?
BRCA1, BRCA2 genes - 40% lifetime risk of breast/ovarian cancer
1st degree relative premenopausal relative with breast cancer (e.g. mother)
nulliparity, 1st pregnancy > 30 yrs (twice risk of women having 1st child < 25 yrs)
early menarche, late menopause
combined hormone replacement therapy (relative risk increase * 1.023/year of use), combined oral contraceptive use
past breast cancer
not breastfeeding
ionising radiation
p53 gene mutations
obesity
previous surgery for benign disease (?more follow-up, scar hides lump)
What are the functions of oestrogen?
- Proliferation of endometrium
- Promotes development of genitalia
- Promotes growth of follicle
- Causes LH surge
- Responsible for female fat distribution
- Increases hepatic synthesis of transport proteins
- Upregulates oestrogen, progesterone and LH receptors
- Increases TBG levels
What are the functions of progesterone?
- Maintenance of endometrium and pregnancy
- Thickens cervical mucous
- Decreases myometrial excitability
- Increases body temperature
- Responsible for spiral artery development
What are the causative organisms for pelvic inflammatory disease?
Chlamydia trachomatis - the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis
What are the features of Pelvic Inflammatory Disease?
lower abdominal pain
fever
deep dyspareunia
dysuria and menstrual irregularities may occur
vaginal or cervical discharge
cervical excitation
perihepatitis (Fitz-Hugh Curtis Syndrome) occurs in around 10% of cases. It is characterised by right upper quadrant pain and may be confused with cholecystitis
What are the investigations for Pelvic Inflammatory Disease?
FBC, CRP, hCG (ensure negative), MSU, high vaginal swab, endocervical swabs, blood cultures if febrile, pelvic USS, screen for chlamydia and gonorrhoea (low vaginal swabs)
What is the treatment for Pelvic Inflammatory disease?
Low threshold for treatment
Oral oflaxacin and oral metronidaole
OR
Intramuscular ceftrioaxone and oral doxycycline and oral metronidazole
Surgical treatment may be indicated in the case of pelvic abscesses
What are complications of pelvic inflammatory disease?
Infertility
Chronic pelvic pain
Ectopic pregnancy
What are the features of dependant personality disorder?
Intense fear of separation and rejection
Clings to relationships, unfortunately this means that a lot of these people end up in abusive relationships. They hold on to someone who completely takes care of them. Lacks self confidence
Difficulty making simple decisions e.g what to eat.
How is the diagnosis of PCOS made?
2 of the three
- Polycystic ovaries on USS
- Oligo ovulation or anovulation
- Clinical hirsuitism, acne or biochemical signs of hyperandrogenism
What are complications of PCOS?
Type 2 diabetes
Sleep apnoea
Cardiovascular risk
Endometrial hyperplasia and carcinoma
What are the investigations for PCOS?
Pelvic USS
Testosterone and sex-hormone binding globulin
Glucose tolerance test
BP
FSH:LH
What is the management for PCOS?
get BMI within 18-30 range, if BMI is normal
then use ovulation induction agent (clomiphene, gonadotrophins, GnRH, according to the group),
oral contraceptive pill
antiandrogen (combined hormonal contraception, spironolactone, eflornithine cream)
endometrial protection (CHC, progestogens, mirena US (progestin IUD) (remember that endometrial hyperplasia is a complication.
fertility (clomiphene/metformin)
Cosmetic theapies for hirsuitism
What is the largest cause of mortality in pregnancy women?
VTE/PE
What are the signs and symptoms of maternal DVT/PE?
asymptomatic, SOB/chest pain, unilateral leg welling/pain, unexplained tachycardia, calf muscle tenderness,
What are the signs of maternal DVT/PE?
haemoptysis, pleural rub
What are the investigations / diagnosis for maternal DVT/PE?
D-dimer is unreliable, use ECG, leg Doppler, CXR, CTPA, V/Q scans to assess mismatch
What is the management of maternal DVT/PE?
low molecular weight heparin, (WARFARIN IS TERATOGENIC)
thromboprophylaxis (stockings, increase mobility) should be considered in those with risk factors or following C section, for 6w post-partum
Why is there an increase risk of maternal PE/DVT?
pregnancy is hypercoagulable state: increase in fibrogen, factor VIII, VW factor, platelets, decrease in natural anticoagulants (antithrombin III), increse in fibrinolysis)
What are risk factors for DVT/PE?
older mothers, increasing parity, increased BMI, smokers, IV drug users, PET, dehydration (due to hyperemesis), decreased mobility, infections, operative delivery, prolonged labour, haemorrhage, blood loss >2L, previous VTE, FH of VTE, sickle cell disease
What is the definition of primary infertility?
primary infertility: unprotected sexual intercourse for over 1 year and no history of pregnancy
secondary infertility: unprotected sexual intercourse for over 1 year with a previous history of pregnancy
What might be in a males history for pirmary infertility?
change in shaving frequency (testosterone), mumps infection, STI (chlamydia/gonorrhoea), history of varicoceal repair, vasectomy, Klinfelter’s
What is the investigation for male infertility?
semen analysis, repeat semen analysis if required
CF screening if azoospermia,
fat and hair distribution,
STDs (chlamydia, gonorrhoea, NSTD),
caryotype (Klinefelter syndrome),
congenital absence of vas deferens,
What are the investigations for female infertility?
rubella immunity,
chlamydia,
TSH,
mid luteal progesterone if periods are regular, day 1-5 FSH, LH, PRL, testosterone if periods irregular, pelvic US, tubal patency test
What is managment for male infertility?
surgical sperm retrieval,
reversal of vasectomy,
donor insemination,
intra-uterine insemination,
IVF/ICSI (intracytoplasmic sperm injection,
injection of mature egg with single sperm,
overnight incubation), DI (?)
sperm donation
What is the managment for female infertility?
clomifene, gonadotrophins, laparoscopic ovarian drilling, GnRH, tubal surgery, oocyte donation
What are the casues of male infertility?
CF, testicular maldescent, testicular problem, pre-testicular (hypothalamus) or post-testicular. Previously mentioned that there can also be absence of vas deferens
failure of production (35%)
Klinfelter’s syndrome
previous mumps or TB
failure of transport
sterilisation
CF
impotence
What are the causes of female infertility?
ovulatory disfunction (25%)
PCOS
premature menopause
Turner’s
surgical removal
hyperprolactinaemia
weight loss/stress
Sheehan’s syndrome
tubal dysfunction (25%)
previous PID
endometriosis
sterilisation
uterine abnormality
Why can hyperprolactinaemia cause infertility|?
Becasue prolactin inhibits GnRH
What are the different types of miscarriage?
Threatened
Inevitable
Incomplete
Complete
Septic
Missed
What is a threatened miscarriage?
This is when there is bleeding from the gravid uterus before 24 weeks gestation, when there is a viable fetus and no evidence of cervical dilation. The uterus may remain viable and the pregnancy continues without any further problems. The cervix is closed in speculum examination.
What is an inevitable miscarriage?
when there is dilation of the cervix
What is an incomplete miscarriage?
When there is only partial expulsion of the products of conception
What is a complete miscarriage?
Complete expulsion of the products of conception
What is a septic miscarriage?
Following incomplete abortion there is always a risk of ascending infection into the uterus which can spread through the pelvis and is known as septic abortion
What is the definition of a missed miscarriage?
When the fetus has died but the uterus has made no attempt to expel the products of conception. No symptoms or could have bleeding vaginally. Gestational sac seen on scan. No clear fetus or fetal pole with no fetal heart seen in the gestational sac.
What is the aetiology of spontaneous miscarriage?
Abnormal conceptus
chromosomal, genetic, structural - It is estimated that 50% of spontaneous miscarriages may be due to abnormal chromosomes.
Uterine abnormality
congenital, fibroids - Congenital uterine abnormalities result from a failure of normal fusion of the mullerian ducts - incidence of spontaneous miscarriage in this group is estimated to be double that of the normal population. Submucosal fibroids are especially associated with spontaneous miscarriage due to distortion of the uterine cavity.
Cervical incompetence
Primary, secondary - The cervix opens prematurely with absent or minimal uterine activity and the pregnancy is expelled. Trauma to the cervix can be an important aetiological factor such as cone biopsy treatment?
Maternal
increasing age, diabetes - Hormonal imbalances are also said to be a cause of spontaneous miscarriage. The corpus luteum is essential for ensuring the survival of the pregnancy during the first 8 weeks of term. If the corpus luteum is to be removed surgically then abortion will usually occur within 7 days. In threatened miscarriage, those that continue to have inevitable miscarriages will have lower levels of progesterone than those that continue pregnancies to term.
Maternal causes of spontaneous miscarriage can include SLE, thyroid disease, acute maternal infection such as appendicitis, pyelitis. Maternal infection causes general toxic illness with high temperature that can stimulate uterine activity and loss of pregnancy.
Unknown
What is the presentation of a molar pregnancy?
Minor bleed, positive, pregnancy test, vomitting
Enlarged uterus
Feeling of pelvic pressure
What is the main finding in blood tests for molar pregnancy?
Increased beta HCG
What is a molar pregnancy?
Molar pregnancy is an abnormal form of pregnancy in which a non-viable fertilized egg implants in the uterus and will fail to come to term.
A molar pregnancy is a gestational trophoblastic disease which grows into a mass in the uterus that has swollen chorionic villi. These villi grow in clusters that resemble grapes. A molar pregnancy can develop when fertilized egg had not contained an original maternal nucleus. The products of conception may or may not contain fetal tissue. It is characterized by the presence of a hydatidiform mole. Molar pregnancies are categorized as partial moles or complete moles, with the word mole, being used to denote simply a clump of growing tissue, or a growth.
What is the difference between a complete and an incomplete hydatiform mole?
Complete = single sperm fertalises enucleate egg, this means that the moile only contains paternal DNA. There are no fetal cells and there is a risk of GTN (gestational trophoblastic neoplasia) - this includes invasive mole, choriocarcinoma and placental site trophoblastic tumour.
Partial = One normal egg cell fertilised by two normal sperm cells, usually triploid. Some fetal cells are evident such as amnion and RBC,s there isn’t really an association with choriocarcinoma.
What are risk factors for molar pregnancy?
Spontaneous abortion
Previous molar pregnancy
Infertility
Maternal age of extremes (less than or equal to 15 or older than 35)
Low dietary carotene (this is a precursor for vitamin A)
What are complications of molar pregnancy?
Malignancy
Hyperthyroidism
Hypermesis gravidarum (associated with large amounts of beta HCG)
Preeclampsia
What are the investigations for molar pregnancy?
Transvaginal ultrasound
Chest X-Ray to look for malignant spread
What is the management of molar pregnancy?
remove tissue by curretage, if beta hCG returns to normal then no further treatment, if beta hCG stays high (persistent disease) then cure by methotrexate
What is the presentation for a molar pregnancy?
period amenorrhoea +/- positive pregnancy test, +/- vaginal bleeding, +/- pain in the abdomen +/-GI or urinary symptoms,
syncope, lower abdominal pain, bleeding (normally light)
What is the investigation / diagnosis for ectopic pregnancy?
US scan (no intrauterine gestational sac, may see adnexal masses, fluid in pouch of Douglas), serum Beta HCG levels, serum progesterone levels, FBC, diagnostic laparoscopy
What is the management of ectopic pregnancies?
- medical: methotrexate
- surgical: laparoscopic salpingectomy/ salpinotomy for few indications
conservative
+ USS in following pregnancies
What is the management for ectopic pregnancy?
- medical: methotrexate
- surgical: laparoscopic salpingectomy/ salpinotomy for few indications
conservative
+ USS in following pregnancies
What are risk factors for ectopic pregnancy?
Pelvic inflammatory disease
Chlamydia
Gonorrhoea
Previous tubal surgery
Previous ectopic
Assisted conception
What are potential ectopic sites for ectopic pregnancy?
Fallopian tube is the most common (especially ampullary region)
Cervical
Abdominal
Ovarian
Uterine cesarean scar
What are the sypmtoms of ectopic pregnancy rupture?
Severe abdominal pain (may refer to shoulder with phrenic nerve irritation)
Rebound tenderness
Guarding indicates peritoneal irritation
Haemodynamic instability (feeling faint, syncope, tachycardia, hypotension, diaphoresis)
What are the causes of antepartum haemorrhage?
Placenta praevia
Placental abruption
APH of unknown origin
Local lesions of the genital tract
Vasa praevia (very rare)
What is the definition of primary and secondary postpartum haemorrhage?
primary PPH :>500 mL blood loss within first 24h delivery
secondary PPH: >500 mL blood loss after 24h of delivery
What is the presentation of post partumhaemorrhage?
may present with tachycardia, tachypnoea, hypotension if severe bleeding
What is the management of PPH?
obstetric emergency, resuscitation and treat cause (fluids, uterine massage, drugs to stimulate contractility (oxytocin, ergometrine)
if still bleeding then insertion of intrauterine balloon, uterine artery embolisation, uterine artery ligation, hysterectomy
What are the casues of PPH?
pathology: 4 Ts
tone (uterine atony) (commonest)
trauma (cervical, vagina and perineal tears)
tissue (retained placenta or membranes)
thrombin (coagulation disorder)
What is placenta praevia?
PLacenta partially or completely covers the lower uterine segment
What are the symptoms of placenta praevia?
Asymptomatic or can present with painless PV bleeding which can range from light to torrential.
What is the investigation for placenta praevia?
Low-lying placenta identified at 20 week anomaly ultrasound
Needs confirmation in third trimester as may migrate away from lower segment
What is the management of placenta praevia?
Delivery by caesarean section
What is the potential complication assocaited with placenta praevia?
Post-partum haemorrhage
What is placental abruption?
Premature separation of the placenta from the uterine wall
What might increase the chances of placental abruption?
Trauma
Higher risk in multiple pregnancy, polyhydramnios, pre-eclampsia, smokers
What is the presentation of placental abruption?
Pain
Vaginal bleeding
May be concealed and present with abdominal pain
Woody hard uterus is a classic sign
What is the management for placental abruption?
May have to do immediate C section in worst cases but vaginal delivery may be achieved
What are the complications of placental abruption?
complications include maternal shock, collapse, fetal death, maternal DIC (disseminated intravascular coagulation), renal failure, postpartum haemorrhage, ‘couvelaire uterus’
What is the definition of pre-term labour?
onset of labour before 37 completed gestational weeks. sign is contraction with evidence of cervical change on vaginal examination
What are risk factors for preterm labour?
Acute illness
Low BMI
Multiple pregnancy
Polyhydramnios
Pre-term rupture of membranes
Previous cervical surgery
Previous preterm deliver
Smoking
Uterine abnormalities
What is the managment of preterm labour?
The mother should deliver the baby in a unit where adequate facilities to care for the neonate are available
Medical = corticosteroids associated with significant reduction in neonatal death, respiratory distress syndrome and intraventricular haemorrhage in the newborn
Tocolytics = atosiban, nifedipine
Surgical = cervical cerclage for those at risk or identified as having a short cervix
What is the presentatino of syphillis?
primary: chancre lesion, raised painless papule with ulcerated centre, usually found at the site of inoculation; lymphadenopathy
secondary: widepsread mucocutaneous lesions, fever, malaise, headache, lymphadenopathy, sore throat
tertiary: characteised by gumma, usually found in liver, bone and testes
What is the organism responsible for syphillis?
Spirochaete - treponema pallidum
What is the presentation of syphillis?
primary: chancre lesion, raised painless papule with ulcerated centre, usually found at the site of inoculation; lymphadenopathy
secondary: widepsread mucocutaneous lesions, fever, malaise, headache, lymphadenopathy, sore throat
tertiary: characteised by gumma, usually found in liver, bone and testes
What are the investigations for syphillis?
microscopy of fluid from mucocutaneous lesions, veneral diseases research lab (VDLR), treponema pallidum haemagglutination assay (TPHA),
CXR, CT/MRI, lumbar puncture looking for complications
What is the treatment of syphillis?
Penicillin
What is the outcome of congenital syphillis?
Spontaneous abortion, birth defects
What are the features of cardiovascular syphillis?
Aortic aneurysmn
Aortic regurgitation
What are the features of neurosyphillis?
Tabes dorsalis
Brain atrophy
Argyll Robertson Pupil
What is the infective organism for Gonorrhoea?
Bacterial infection caused by Neisseria Gonorrhoeae
What is the presentation of gonorrhoea?
Purulent penile discharge
Often asymptomatic in women
What is the investigation for gonorrhoea?
Microscopy of discharge reveals characteristic gram-negative diplococci
What is the treatment for gonorrhoea?
Cephalosporin, widespread antibiotic resistance
What are the complications of gonorrhoea?
Septic arthritis - most common cause of monoarthritis in sexually active adults
What is the presentation of chlamydia?
female: usually none, sometime cervicitis/cystitis, lower abdominal pain, intermenstrual bleeding
male: often asymptomatic discharge, dysuria
What is the infective organism in chlamydia?
Chlamydia Trachomatis
What are the investigations for chlamydia?
enzyme immunoassays, nucleic acid amplification test, urine testing for Chlamydia
What is the treatment for chlamydia?
The two most commonly prescribed antibiotics for chlamydia are:
azithromycin – given as 2 or 4 tablets at once
doxycycline – given as 2 capsules a day for a week
Your doctor may give you different antibiotics, such as amoxicillin or erythromycin, if you have an allergy or are pregnant or breastfeeding. A longer course of antibiotics may be used if your doctor is concerned about complications of chlamydia.
What is a complication of chlamydia?
Peri-hepatitis (fitz hugh-curtis syndrome)
What is managment of HIV to prevent vertical transmission?
mother is given antiviral therapy anyway (highly active anti-retroviral therapy, HAART), C-section and no breastfeeding if high load of anti-viral (zidovudine) prior to delivery and given to infant, maybe vaginal delivery if low viral load
What is the presentation of vulkvovaginal candidosis?
usually asymptomatic, symptomatic trush (itching, discharge, classically thick, ‘cotton cheese’, but often just increased amount)
Itch and discharge
fissuring, erythema with satellite lesions, characteristic discharge
What is the investigation for vulvovaginal candidosis?
Gram stained preparation, culture
What is the treatment for vulvovaginal candidosis?
azole antifungals (clotrimazole (+ clotrimazole HC if vulvitis) and fluconazole)
What is the likely infective organism for vulvovaginal candidosis?
Candida albicans
What are the risk factors for vulvovaginal candidosis?
risk factors: diabetes, oral steroids, immune suppression including HIV, pregnancy, reproductive age group
What is the presentation of bacterial vaginosis?
usually asymptomatic, watery grey/yellow ‘fishy’ discharge, may be worse after period/sex, sometimes sore/itch from dampness,
What are the investigations for bacterial vaginosis>
Gram stained smear of vaginal discharge
What is the management of bacterial vaginosis?
Gram stained smear of vaginal discharge
What is the treatment for bacterial vaginosis?
oral metronidazole for 5-7 days
70-80% initial cure rate
relapse rate > 50% within 3 months
the BNF suggests topical metronidazole or topical clindamycin as alternatives
What is Amsel’s diagnostic criteria for diagnosing bacterial vaginosis?
Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present
thin, white homogenous discharge
clue cells on microscopy: stippled vaginal epithelial cells
vaginal pH > 4.5
positive whiff test (addition of potassium hydroxide results in fishy odour)
What is the bacterial change assocaited with bacterial vaginosis?
increased gardnerella, ureaplasma, mycoplasma, anaerobes, reduced lactobacilli
Bacterial vaginosis (BV) describes an overgrowth of predominately anaerobic organisms such as Gardnerella vaginalis. This leads to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH
What are typical antihypertensive agents used in chronic hypertension in pregnancy?
lifestyle changes
change in medication as ACE inhibitors like ramipril and enalopril cause birth defects and impaired growth), use angiotensin receptor blockers (losartan, candesartan), anti diuretics and lower dietary sodium. Aim to keep BP < 150/100 (labetolol (Beta blocker), nifedipine (ARB), methyldopa (alpha2 receptor adrenergic agonist), monitor for superimposed pre-eclampsia, if on beta-blockers for hypertension then monitor fetal growth,
What is the presentation of gestational hypertension?
Normal signs of hypertension
Headaches
Dizziness
Blurred vision
Epistaxis
Angina
Syncope
Signs of heart failure
What is the presentation of pre-eclampsia?
asymtomatic or headache, blurry vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands, face and legs, clonus, brisk reflexes, papilloedema, reduced urine output, convulsions, epigastric pain, right upper quadrant pain, visual disturbance, leg swelling
Eclampsia is characterised by tonic clonic seizures
Can also cause pulmonary oedema, cerebral haemorrhage, HELLP syndrome, placental abruption
HELLP syndrome is haemolysis, elevated liver enzymes and low platelets
What changes would you see in the blood in pre-eclampsia?
High Bp
Raised liver enzymes
Bilirubin
Raised urea and creatinine
Raised urate
Low platelets
Low haemoglobin
Signs of haemolysis
Features of DIC
What are the complications of pre-eclampsia on the fetus?
IUGR
Intrauterine death
Iatrogenic preterm delivery
What is the diagnostic criteria for pre-eclampsia?
creatinine ratio >30mg/mmol,
24h urine protein collection >300mg/day,
mild HT on two occasions or more, more than 4 hours apart or moderate to severe HT
What are the investigations for pre-eclampsia?
Serial blood pressure
Urinalysis
Urine protein/creatinine ratio
FBC
U and E
LFT
Coagualtion
Group and save if delivery thought to be likely
CTG to assess fetal well-being
What is the management of pre-eclampsia?
oral labetalol is now first-line following the 2010 NICE guidelines. Nifedipine and hydralazine may also be used
delivery of the baby is the most important and definitive management step - caesarean section
Magnesium sulphate is used to prevent seizures
Methyldopa can also be used for lowering blood pressure.
Steroids are given for fetal lung maturity
Induction of labour (avoid ergometrine - this precipitates
What are the complications of pre-eclampsia in the mother?
mother: eclampsia, severe HT, cerebral haemorrhage, stroke, hemolysis, elevated liver enzymes, low platelets, liver and renal failure, disseminated intravascular coagulation, renal failure, pulmonary oedema, cardiac failure,
impaired placenta perfusion,, growth, HELLP syndrome, pappiloedema, pulmonary oedema, placental abruption, disseminated intravascular coagulation
What is the effect of gestational diabetes on a baby?
on fetus: increased risk of congenital anomalies, perinatal mortality, macrosomial, shoulder dystocia, polyhydramnios
What are the effects of gestational diabetes on the mother?
on mother: diabetic nephropathy and retinopathy may deteriorate. Increased risk of miscarriage, pre-eclampsia and operative delivery
What is the management of gestational diabetes?
on mother: diabetic nephropathy and retinopathy may deteriorate. Increased risk of miscarriage, pre-eclampsia and operative delivery
Here is management of diabetes in pregnanct women
Important to note that there is increase in insulin requirement, early induction of labour and early feeding of baby to reduce neonatal hypoglycaemia
before pregnancy, to prevent malformations: make sure blood sugars are 4-7mmol/L pre-conception and HbA1c <6,5% (<48mmol/L), folic acid 5mg, dietary advice, retinal and renal assessement
during pregnancy, to prevent metabolic complications: increase insulin, can continue oral anti-diabetic agents, should be aware of hypos risk, watch for ketonuria/infections, repeat retinal assessement 28 and 34w, watch fetal growth, observe mother for PET, oral hypoglyacemics are usually avoided (according to book page 259)
giving birth: induction of labout at 38-39 weeks is the norm, consider C-section if significant fetal macrosomia, maintain blood glucose in labour with insulin-dextrose insulin infusion, continuous CTG fetal monitoring in labour, early feeding of baby to reduce neonatal hypoglycaemia, switch back to pre-pregnancy regimen for insulin post delivery
What are the complications of pre-exiswting diabetes in pregnancy?
increased risk of congenital fetal abnormalities (especially if blood sugars high peri-conception), miscarriage, pre-eclampsia, fetal macrosomia, polyhydramnios, operative delivery, shoulder dystocia, worsening of maternal nephropathy, retinopathy, hypoglycaemia, reduced awareness of hypoglycaemia, infections, stillbirth, increased perinatal mortality, neonatal death (impaired lung activity, neonatal hypoglycaemia, jaundice, obstruction of labour)
What is the definition of primary amenorrhoea?
never had period, either >14 and no secondary sexual characteristics or >16 and sexual characteristics
What are the investigations for primary amenorrhoea?
GnRH, hCG, TFT, LH, FSH, prolactin, chromosomal karyotype, pelvic USS, oestrogen, TSH, progesterone challenge test (oral progesterone for 5 days, if there is endogenous oestrogen and normal anatomy, withdrawal bleeding will occur), pregnancy test, testosterone?
What is management of primary amenorrhoea?
Gradual build up with estrogen
Effect on breast development
Add progesterone
Once maximum height potential is reached
At least 20 mg of estrogen dose
How can you interpret the progesterone withdrawal test?
So if there is anovulation then - progesterone given and then removed, bleeding 2-7 days later. This is dependant on sufficient estradiol concentration in the serum.
If no bleeding = Low serum estradiol, hypothalamic pituitary axis dysfunction, non-reactive endometrium, outflow tract abnormality such as cervical stenosis.
If it is not an outflow tract obstruction then it is likely to be due to low oestrogen. Withdrawal bleeding occurs after removal of oestrogen / progesterone therapy.
What are casues of amenorrhoea?
Pregnancy
PCOS
Hypothalamic disorders
Hyperprolactinaemia
Ovarian failure / menopause
Thyroid disease
Anatomical disorders of outflow
What is the definition of secondary amenorrhoea?
absence of menstruation > 6 months in a woman who has previously menstruated
What are signs of secondary amenorrhoea?
hirsutism and other androgen-linked features (enlarged clitoris, acne, deep voice)
What is management for secondary amenorrhoea?
control BMI, HRT if premature ovarian insufficiency, emotional support
anatomical causes: surgery for imperforate hymen/transverse septum
What are causes of secondary amenorrhoea?
causes: pregnancy, breast feeding, contraception, polycystic ovaries, early menopause, thyroid disease, cushing’s, raised prolactin (medication related or prolactinoma), hypothalamic, androgen secreting tumour (high testosterone), Sheehans syndrome (pituitary failure), Asherman’s syndrome (intrauterine adhesions)
What are is the presentation for female pelvic organ prolapse?
“mass down below”, “dragging sensation”
vaginal: feeling/seeing a bulge, sensation of bulge, difficulty in inserting tampons, dyspareunia
urinary: hesitancy, incomplete emptying, poor stream, prolonged stream, urinary incontinence, frequency/urgency, manual reduction of prolapse to start or complete void
bowel: incontinence of void/flatus, feeling of incomplete emptying, straining, urgency, digital evacuation to complete defecation, splinting or pushing on or around the vagina or perineum to start or complete defecation
What are investigations for POP?
POP quantification (POPQ score) stage 0-6, measure of cm, USS/MRI (thickness of levator ani), urodynamics (exclude concurrent UTI), IVU (view ureters, bladder and kidneys with contrast), renal USS (if suspicion of obstruction)
What is the managment of female pelvico organ prolapse?
prevention: avoid constipation, manage chronic chest pathology (COPD, asthma), smaller family size, muscle training (PFMT)? (cannot treat fascial cases)
conservative: pelvic floor exercises, ring and shelf pessaries (except if inability to hold it for 2 weeks)
surgical: vaginal hysterectomy, anterior and posterior vaginal wall repair
+ perineometer, biofeedback, vaginal cones, electrical stimulation,
What causes female pelvico organ prolapse?
Caused by weakening of pelvic floor normally secondary to child birth
What is the presentation of fibroids?
usually asymptomatic or dysmenorrhoea (painful periods), menorrhagia (excessive bleeding), pelvic pain, pressure symptoms on bladder, intermenstrual bleeding (for submucous or intramural types), bloating
What are investigations for fibroids?
large fibroids are palpable abdominally, uterus may be enlarged on pelvic examination
Transvaginal USS, Pelvic USS, hysteroscopy?
What is the management of fibroids?
same as menorrhagia
medical treatment is less efficient if fibroids are large and distort the cavity
only if symptomatic myomectomy, hysteroctomy, transcervical resection (submucous), GnRH analogues or ulipristal acetate to temperarily shrink the fibroids (pre-op)
progestin IUD, tranexamic acid, OCP,
surgery
interventional radiology: uterine artery embolisation and MRI- guided ablation of fibroids may be possible in specialist centres
What are the complications of fibroids?
Pain
Malpresentation/obstruction of labour
What are the different types of fibroids?
smooth muscle growth, can be:
submucosa (protrude into uterine cavity)
intramural (within uterine wall)
subserosal (project out of uterus into peritoneal cavity)
What causes fibroids?
Benign tumour arising from the myometrium
What are the causes of menorrhoagia?
Uterine fibroids
Dysfunctional uterine bleeding
Coagulopathies
Pelvic malignancies
What is the definition of menorrhagia?
Heavy menstrual bleeding (more than 80ml per cycle)
What are potential investigations for menorrhagia?
FBCs
TFTs
Pelvic USS
hCG
Hysteroscopy and endometrial biopsy if simple treatment fails or suspicous features
What is the treatment of menorrhagia?
medical: progesterone only pill, tranexamic acid, mefenamic acid, combined oral contraceptive, mirena, GnRH analogues,
surgery:
trans-cervical resection of submucous fibroids, endometrial ablation, myomectomy, hysterectomy
What is the presentation of endometriosis?
dysmenorrhoea, deep dyspareunia, chronic pelvic pain, ovulation pain, infertility, dyschezia (pain of defecation), tenderness or palpable nodules on bimanual examination, frozen pelvis
Passmedicine:
chronic pelvic pain
dysmenorrhoea - pain often starts days before bleeding
deep dyspareunia
subfertility
non-gynaecological: urinary symptoms e.g. dysuria, urgency, haematuria. Dyschezia (painful bowel movements)
on pelvic examination reduced organ mobility, tender nodularity in the posterior vaginal fornix and visible vaginal endometriotic lesions may be seen
What would you find on examination of endometriosis?
adnexal masses or tenderness
nodules or tenderness in posterior vaginal fornix or uterosacral ligaments,
fixed (because of fibrous scar tissue) retroverted uterus,
rectovaginal nodules
What are the investigations for endometriosis?
laparoscopy (gold standard) look for clear, red, bluish lack or with lesions,
pelvic MRI for deep endometriosis, if severe disease is suspected and surgical planning necessary
pelvic USS can diagnose endometrioma (chocolat cyst) or large nodules
What is managment of endometriosis?
medical:
NSAIDs, COCP, danazol/gestrinone, mirena IUS, GnRH agonist (leuprorelin), progesterone, levonorgestrel (LNG), GnRH analogues
surgical:
remove endometriosis, goes from laparoscopic ablation of lesions to hysterectomy and bilateral salpingo-oophorectomy
pain management
What are causes of dysmenorrhoea?
Endometriosis
Pelvic adhesions
Chronic PID
Ovarian cysts
Pelvic venous conegestion
Uterine fibroids
What is the presentation of adenomyosis?
dysmenorrhoea, dysparenunia, menorrhagia, bulky tender uterus
Endometriosis doesn’t have menorrhagia by the looks of it so this would be the key difference between the two
What are the investigations for adenomyosis?
MRI, hysterectomy and histological diagnosis as diagnostic is often flawed
What is the managment for adenomyosis?
Hormonal contraception for heavy/painful periods (mirena US, progestogens, combined OCP)
What is the definition of adenomyosis?
Presence of endometrial tissue in the myometrium
What is the presentation of ovarian cancer?
non-speciifc bowel symptoms (indigestion, early satiety, loss of appetite, altered bowel habit/pain, bloating, discomfort, weight loss)
overlap with IBS symptoms
pelvic mass (asymptomatic or pressure symptoms), adnexal mass on pelvic examination,
late-stage disease may present as a large pelvic mass, ascites, palpable lymph nodes and pleural effusion
How is the diagnosis of ovarian cancer made?
diagnosis: Ca125 (carcinoma antigen), pelvic USS,
staging: pelvic MRI/CT chest/abdomen/pelvis, colonoscopy/OGD may be indicated is there is a possibility of primary GI malignancy, US guided biopsy of omentum, staging (1-4)
stage 1 (tumour limited to ovaries)
stage 2 (tumour involves one or both ovaries with pelvic extension
stage 3 (tumour with peritoneal implants outside the pelvis or retroperitoneal and or inguinal nodes)
stage 4 (tumour with distant metastasis)
Diagnosis is difficult and often relies on diagnostic laparotomy
What is the managment of ovarian cancer?
protective: OCP, prophylactic oophorectomy, having many children
Platinum based chemotherapy
stage 1:
total abdominal hysterectomy and bilateral salpingoophorectomy and omentectomy +/- chemotherapy
stage 2:
stage 1 + /- lymphadenectomy with surgical effort to remove all disease
stage 3:
stage 2 +/- neoadjuvant chemotherapy to reduce tumour mass before surgery
stage 4:
stage 3 + pallative chemotherapy
What are genes associated with ovarian cancer?
genes associated: BRAC1, BRAC2, HNPCC/Lynch type 2 familial cancer syndrome
What is the most common type of ovarian cancer?
around 90% of ovarian cancers are epithelial in origin, with 70-80% of cases being due to serous carcinomas
What are risk factors for ovarian cancer?
FH, >30 y/o, FH (2 or more relatives), cancer gene mutation carriers)
for risk (combines menopausal status, ultrasound score and CA 125) use RMI I score (if 250 or greater then referral to specialist team)
What are potential causes for raised CA125?
CA 125 (glyco-protein antigen) can indicate malignancies (ovary, colon/pancreas and breast) and benign conditions such as menstruation, PID, endometriosis, liver disease, recent surgery, effusions
What is the presentation of endometrial cancer?
post-menopausal bleeding is most common feature, abnormal vaginal bleeding
What is the investigation for endometrial cancer?
women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway
first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
hysteroscopy with endometrial biopsy
MRI pelvis/CT chest, abdomen, pelvis for staging
What is the staging of endometrial cancer?
(FIGO stage 1-4 according to depth of myometrial invasion, cervical involvement and lymph node involvement) and type (1 or 2)
stage 1 (carcinoma strictly confined to the uterus)
stage 2 (carcinoma extended to the endocervix (2A) or cervical stoma (2B))
stage 3 (spread to serosa of uterus, pelvic peritoneum or pelvic lymph nodes)
stage 4 (local metastasis to bladder/bowel (4A) or distant metastasis (4B))
What is the management of endometrial cancer?
surgery:
stage 1: total abdominal hysterectomy and bilateral salpingoophorectomy
stage 2: radical total abdominal hysterectomy (TAH) + bilateral salpingoophorectomy (BSO) + radiotherapy +/- lymphadenactomy
stage 3: surgery + radiotherapy or radiotherapy alone
stage 4: palliative radiotherapy (with progesterone if advanced stage)
other:
peritoneal washings (all laparoscopically), chemo if high risk histology, radiotherapy (external beam or caesium insertion)
What are the two common types of endometrial cancer?
type 1 (commonest): endometrioid adenocarcinoma, linked to excess oestrogen, hyperplasia with atypia precursor
type 2: uterine serous & clear cell carcinoma, high grade, more aggressive, worse prognosis, generally older ladies, serous intraepithelial carcinoma precursor
95% is adenocarcinoma
What are risk factors for endometrial cancer?
Obesity
Tamoxifen therapy (although antagonistic with respects to breast tissue tamoxifen may serve as an agonist at other sites. Therefore risk of endometrial cancer is increased cancer)
Early menarche / late menopause
Oestrogen secreting tumours
HRT
Endometrial hyperplasia with atypia
Genetic predisposition (lynch syndrome)
What is the presentation of menopause?
lack of menstruation for >1 year
hot flushes and night sweats (vasomotor symptoms)
vaginal dryness/soreness (vasomotor symptoms)
dyspareunia (vasomotor symptoms)
atrophy and thinning of vaginal epithelium
overactive bladder symptoms (urgency, frequency)
mood changes,
loss of libido
osteoporosis
increase in cardiovascular risk
What are hormonal findings for menopause?
FSH and LH ar high
Oestrogen is low
What are the relevant investigations for menopause?
DEXA scan for bone density
LH
FSH
Oestrogen
Progesterone
What are the different forms of hormone replacement therapy?
Combined (oestrogen and progestogen) for a women with a uterus
Oestrogen alone for those with hysterectomy
Can be given sequentially (monthly withdrawal bleeding) or can be given continuously (period free)
What does HRT increase the risk of?
VTE
Breast cancer
Endometrial cancer
Gall bladder disease
Vascular disease
What are investigations for downs syndrome in utero?
first trimerster screening: combined test
nuchal translucency, hCG and PAPP-A (pregnancy associated plasma protein A), AFP (alpha fetoprotein)
first and second trimester: intergrated test
combined test and ALP (alpha fetoprotein), oestriol, inhibin A
second trimester: quadruple test
hCG, estriol, AFP, inhibin A
second trimester: anomaly USS
if risk is <1 in 250 then are offered chorionic villus sampling or amniocentesis
What is the risk of having a baby with Down’s syndrome if the woman is aged 40?
around 1%
What are the symptoms of PID?
constant lower abdominal pain, purulent vaginal discharge, deep dyspareunia, pyrexia, irregular PV bleeding, adnexal tenderness
dysuria, irregular periods
What is the cassical sign of PID?
Cervical excitation
What are investigations for pelvic inflammatory disease?
FBC, CRP, hCG (ensure negative), MSSU, high vaginal swab, endocervical swabs, blood cultures if febrile, pelvic USS, screen for chlamydia and gonorrhoea (low vaginal swabs)
What is the management of PID?
medical:
- mild: oral ofloxacin + metronidazole for 14 days
- moderate: intramuscular ceftriaxone + oral doxycycline + metronidazole for 14 days
severe: inpatient IV therapy if clinically unwell and severe
surgical:
may be indicated in severe cases with evidence of pelvic abscess
prevention: contact tracing for sexual partners
What are the differentials for lower abdominal pain in a young woman?
Ectopic pregnancy
Appendicitis
Endometriosis
IBS
Ovarian cyst accident / cyst rupture
UTI
What are potential causative organisms for PID?
Causative organisms
Chlamydia trachomatis - the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis
What are potential complications of PID?
infertility (10-20% after first episode), ectopic pregnancies, chronic pelvic pain, Fitz-Hugh-Curtis syndrome (in 10% cases)
What is the presentation of breast cancer?
hard lump, fixed mass, tethering to skin, dimpling of skin, often painless lump or thickening in breast, discharge or bleeding, change in size or contours of breast, change in colour of areola, redness or pitting of skin over the breast like the skin of an orange
What are the investigations for breast cancer?
triple assessement of any breast lump (clinical examination, radiological investigation (mammography/US) and biopsy)
FNA cytology, core biopsy, mammography, US, sentinel lymph node biopsy (assess lymphatic spread), nipple scrape (Paget’s disease) or use discharge for analysis if present,
What are staging investigations for breast cancer?
staging investigations: Hb FBC, U&Es, LFTs, CXR, CT thorax and abdomen, isotope bone scan if lymph node spread,
What is the screening programme for breast cancer in Scotland?
he Scottish Breast Screening Programme invites women aged between 50 and 70 years old for screening every three years. Women over 70 years old are able to attend through self-referral.
What are the subtypes of breats cancer?
Non-invasive = Ductal carcinoma in situ, lobular carcinoma in situ
Invasive = Invasive ductal carcinoma (most common)
Invasive lobular carcinoma and its variants
Where does breast cancer spread to?
Local skin
Pectoral muscles
Lymphatic axillary and internal mammary nodes
Blood
Bone
Lungs
Liver
Brain
What is the purpose of histological assessment of breast cancer?
Histological assessment should be carried out to assess tumour type and to deter- mine oestrogen and progesterone receptor (ER/PR) status and HER2 status
What is management of breast cancer?
wide local excision or mastectomy, removal of sentinel lymph node;
hormonal markers predict response to hormonal treatment (trastuzumab herceptin)
antihormonal therapy is tamoxifen or chemotherapy
tumours <4cm usually are eligible for breast conservation therapy
if sentinal node biopsy contains tumour then radiotherapy on all of the axillary lymph nodes or remove all (clearance)
micrometastases are treated with hormonal therapy or chemo
trastazumab to patients with over expression of Her2 (monoclonal Ab)
+follow up (yearly mammograms for 10 years)
What is the hormone therapy for breast cancer?
What Type of Hormone Therapy do we Usually Give?
If premenopausal – tamoxifen for 5 years
If postmenopausal – tamoxifen for 5 years if excellent prognosis.
BUT others get an aromatase inhibitor, eg ANASTROZOLE for 5-10 years
What type of breast cancers responds well to hormonal therapy?
About 70% of breast cancers are ER positive. They respond well to treatment with hormonal therapies.
Most commonly used hormone therapy drugs used to treat breast cancer are:
tamoxifen
aromatase inhibitors (anastrozole, exemestane and letrozole)
goserelin (Zoladex)
fulvestrant (Faslodex)
Who usually receives chemotherapy for breast cancer?
Node posistive
Stage 3
Mastectomy vs wide local excision?
What genes can result in breast cancer?
Both genetic and hormonal factors play a role; about 5–10% of breast cancers are hereditary and occur in patients with mutations of BRCA1, BRCA2, AT or TP53 genes
What drug can be used to treat HER 2 positive breast cancer?
Some breast cancers have high numbers of receptors for the protein HER2 (human epidermal growth factor 2). They are called HER2 positive breast cancers. About 1 in 7 women (15%) with early breast cancer have HER2 positive cancer. A drug called trastuzumab (Herceptin®) is an effective treatment for this type of breast cancer.
What are triple negative breast cancers?
If the cancer does not have receptors for either HER2 or the hormones oestrogen and progesterone, it is called triple negative breast cancer. It affects up to 1 in 5 women (15–20%) with breast cancer and is more common in younger women
What is the TNM staging of breast cancer?
Tumour (T)
T1 – 0-2cm
T2 - 2-5cm
T3 - >5cm
T4 – fixed to skin or muscle
Nodes (N)
N0- none
N1 – nodes in axilla
N2 – large or fixed nodes in the axilla
Metastases (M)
M0 – none
M1 - metastases
What is the tool which calculates prognosis for breast cancer?
Nottingham prognosis index
This accounts for tumour size, lymph node score and grade score
How many women are affected by breast cancer?
1 in 8
What are risk factors for breast cancer?
Female sex
Age
Family history (BRCA1 and BRCA2)
Early menarche late menopause
Nullparity, higher age at first pregnancy
Higher socioeconomic group
HRT
CIN staging
CIN 1: low grade dysplasia–will regress
CIN 2: moderate dysplasia – may regress
CIN 3: severe dysplasia – unlikely to regress
OA and RA comparison
What is the treatment for scleroderma?
What is the general treatment for multi-system autoimmune diseases?
Gout vs Pseudogout comparison
