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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


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?



Why aren't TCA's commonly used for depression?

Side-effects and toxicity in overdose


What are common side effects of tricyclic anti-depressants?


dry mouth

blurred vision


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?




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


What are the risk factors for endometrial cancer?



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


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



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


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


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




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?


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




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?



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,



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






What are the causes of female infertility?

ovulatory disfunction (25%)


premature menopause


surgical removal


weight loss/stress

Sheehan’s syndrome

tubal dysfunction (25%)

previous PID



uterine abnormality


Why can hyperprolactinaemia cause infertility|?

Becasue prolactin inhibits GnRH


What are the different types of miscarriage?








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?


         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.



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


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?



Hypermesis gravidarum (associated with large amounts of beta HCG)



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



+ USS in following pregnancies


What is the management for ectopic pregnancy?

- medical: methotrexate

- surgical: laparoscopic salpingectomy/ salpinotomy for few indications



+ USS in following pregnancies


What are risk factors for ectopic pregnancy?

Pelvic inflammatory disease



Previous tubal surgery

Previous ectopic

Assisted conception


What are potential ectopic sites for ectopic pregnancy?

Fallopian tube is the most common (especially ampullary region)




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?


Higher risk in multiple pregnancy, polyhydramnios, pre-eclampsia, smokers


What is the presentation of placental abruption?


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


Multiple pregnancy


Pre-term rupture of membranes

Previous cervical surgery

Previous preterm deliver


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?



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



Blurred vision




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


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?


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


Urine protein/creatinine ratio


U and E



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?



Hypothalamic disorders


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, 




interventional radiology: uterine artery embolisation and MRI- guided ablation of fibroids may be possible in specialist centres


What are the complications of fibroids?


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


Pelvic malignancies


What is the definition of menorrhagia?

Heavy menstrual bleeding (more than 80ml per cycle)


What are potential investigations for menorrhagia?



Pelvic USS



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, 


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




chronic pelvic pain

dysmenorrhoea - pain often starts days before bleeding

deep dyspareunia


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?


NSAIDs, COCP, danazol/gestrinone, mirena IUS, GnRH agonist (leuprorelin), progesterone, levonorgestrel (LNG), GnRH analogues


remove endometriosis, goes from laparoscopic ablation of lesions to hysterectomy and bilateral salpingo-oophorectomy

pain management


What are causes of dysmenorrhoea?


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?


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)



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?


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


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




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







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?


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?


- 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 


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




Ovarian cyst accident / cyst rupture




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








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:



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


Family history (BRCA1 and BRCA2)

Early menarche late menopause

Nullparity, higher age at first pregnancy

Higher socioeconomic group



What is the screening programme for cervical cancer?

screening: 25-64   y/o, smear test every 3 years when <50 y/o, every 5 years when >50 y/o 


If low grade dyskariosis then repeat in 6 months


What is cervical intraepithelial neoplasia?

Abnormal cells in the cervix detected by biopsy and histological examination are classified as cervical intraepithelial neoplasia (CIN). Graded 1 to 3 according to the proportion of cervix affected.


What type of HPV virus is most assocaited with cervical cancer?

HPV 16 and 18 are highr risk subtypes


What does CIN grading measure?

Grading is determined by how abnormal the cells look under a microscope as well as how much of the cervical tissue is affected. 

Epithelial lining of the transdformation zone of the cervix is the part that is affected


When would you refer someone to colposcopy?

Three consecutive inadequate smear samples

Three borderline dmears (squamous)

Mild, moderate or severe dyskariosis

Suspected invasive disease


Dyskariosis (this is when the squamous epithelial cells have abnormal cytologic changes as well as charactersitic hyperchromatic nuclei and/or irregular nuclear chromatin). Another word for dyskariosis is dysplasia 


How is colposcopy carried out?

colposcopy involves inspection of ectocervix under magnification. Acetic acid and Lugol’s iodine is applied to identify abnormality. 


How is histological diagnosis of CIN achieved?

Histological diagnosis is achieved with biopsies of abnormal area


CIN staging

CIN 1: low grade dysplasia–will regress

CIN 2: moderate dysplasia – may regress

CIN 3: severe dysplasia – unlikely to regress


What is managemnt of CIN?

LLETZ (large loop excision of the transformation zone)

Thermal coagulation

Laser ablation


+ follow-up LBC at 6 months for cytology to check for recurrence of disease and to reassure, also regular smears are required after treatment to ensure adequate treatment


What is the pathogenesis of CIN?

HPV infects basal layers of cells, viral genes expressed as host cell matures, deregulation of host cycles as viral DNA is integrated in cells


What percentage of CIN 3 progresses to cervical carcinoma?



What are the features of dyskariosis?

dyskariosis (abnormal cells may be few, nucleus is increased in size and nuclear/cytoplasmic ratio, variation in size, shape, outline, coarse, irregular chromatin, nucleoli)


What is the presentation of cervical cancer?

asymptomatic or irregular PV bleeding, postcoital bleeding, intermenstrual bleeding, discharge, pain


late cases present with disease progression; renal failure following ureteric obstruction or bowel and bladder involvement


classical hard, craggy, bleeding cervix on pelvic examination or colposcopy


What are risk factors for cervical intraepithelial neoplasia?

HPV infection




Persistent infection


What are the investigations for cervical cancer?

Screening (prophylactic investigation)


Cervical biopsy


MRI of pelvis, CT of chest, abdomen, pelvis (to assess the spread)


What are the stages of cervical cancer?

stage 1 (carcinoma strictly confined to the cervix)

stage 2 (carcinoma that extends into the parametrium or upper 2/3 of vagina)

stage 3 (carcinoma has extended to pelvic side wall, lower 1/3 of vagina or causes hydronephrosis)

stage 4 (carcinoma that has extended beyond the pelvis)


What is the management of cervical cancer?

excision biopsy  for stage 1a, 

radical hysterectomy or chemo-radio for stage 1b or 2, chemo-radio for stage 2b-4, 


chemothrapy is cisplatin,

caesium insertion (brachy therapy) is another means of management 


What are the most common types of cervical cancer?

80-90% = squamous cell 

10-20% = adenocarcinoma


Ectocervix = squamous cell

Endocervix = columnar cell


What are the oncogenes made by papilloma viruses 16 and 18?

HPV 16 & 18 produces the oncogenes E6 and E7 genes respectively

E6 inhibits the p53 tumour suppressor gene

E7 inhibits RB suppressor gene


What are risk factors for cervical cancer?

Human papillomavirus (HPV), particularly serotypes 16,18 & 33 is by far the most important factor in the development of cervical cancer. Other risk factors include:


human immunodeficiency virus

early first intercourse, many sexual partners

high parity

lower socioeconomic status


What are the symptoms of stress incontinence?

urine leakage on coughing, laughing, sneezing, exercise, sexual intercourse. May be demonstrated on examination with a full bladder. Severity ranges from mild to severe.


(dysuria, haematuria, voiding symptoms (interrupted flow, recurrent UTI, straining to void, prolapse symptoms (vaginal lump, dragging sensation in vagina), bowel symptoms (anal incontinence, constipation, faecal evacuation, dysfunction, IBS))


What are investigations for stress incontinence?

MSSU, urodynamics

(3 day urinary diary, urine dipstick,

Post voiding residual volume assessment 

Urodynamics (indicated if surgery is contemplated)


What is the management for stress incontinence?

conservative: pelvic floor exercises, lifestyle changes (smoking cessation, lose weight, eat more healthily to avoid constipation, stop drinking alcohol or caffeine) tension free vaginal tape (for suburethral hammock theory) (TVT) or colposuspension but TVT is now 1st choice, physiotherapy (pelvic floor muscle training), 






tension-free vaginal tape, colposuspension, urethral bulking agents


What causes stress incontinence?

Defect in anterior vaginal wall and pubo-urethral ligament

Suburethral hammock


What are risk factrors for stress incontinence?





Medical problems

Increased intra abdominal pressure

Pelvic floor trauma


Connective tissue disease



What is management for urge incontinence and overactive bladder?

conversative: physiotherapy, bladder retaining, lifestyle modifications, normalise fluid intake, reduce caffeine, fizzy drinks, chocolate, stop smoking, weight loss, 



anticholinergics (oral or transdermal antimuscarinic), tri-cyclic antidepressants,



Botox injections, clam cystoplasty, urinary diversion


What is the difference between overactive bladder and urge incontinence?

involuntary loss of urine when there is involuntary detrusor activity 


symptoms of urgency and frequency with or without associated incontinence 


What is the name of the benign and malignant cels of the cartilage, bone and fibrous tissue?

Cartilage = chondroma - chondrosarcoma

Bone = osteochondroma - osteosarcoma

Fibrous tissue = fibroma - fibrosarcoma


What is the presentation of benign bone tumours?

Activity related pain


Pathological fracture


Neurovascular effects (limb weakness, numbness)


What are invesitagtions for bone tumours?


-XR  (lesion is inactive or aggressive), 

-CT (ossification and calcification)
-isotope bone scans (bone mets for staging)





There may be tumour biomarkers in the blood


What is the characteristic X-ray finding for osteochondroma?

bony projection of bone which is capped with cartilage - exotosis


What are characteristic X-ray findings for a giant cell tumour of the bone?


(note - giant cell tumours are benign tumours)

Giant cell tumour = forms multi-cystic bone lesions that look like soap bubbles


What are the characteristic features of osteosarcoma on x-ray?

Lytic bone lesions which form a sunburts effect

Osteosarcomas often cause the periosteum to lift and this is called codman's triangle


What are the characteristic features of Ewings sarcoma on x-ray?

Ewings sarcoma - forms lytic bone lesions that look like an onion ring appearance


What is the most common benign bone tumour?



What is the presentation for malignant bone tumour?


NOT- activity related

Deep-deated boring nature

Night pain

Difficulty weight bearing

Analgesics are usually ineffective



Pathological fractures


Joint effusion


Neurovascular effects


What is the management for malignant bone tumours?

chemotherapy, surgery, radiotherapy, referral to specialist Tumour Centre for soft tissue tumours, prophylactic internal fixation to prevent pathological fracture

fracture risk assessement is Mirel’s Scoring System (score 1-3 depending on site, pain, lesion type and size, if >8 then internal fixation before radiotherapy)


surgical excision, endoprosthetic replacement, chemotherapy, radiotherapy (in Ewing’s)


Where do secondary bone cancers often come from?

Be prepared for the laughing kid







What are malignant primary tumours of the bone?



Fibrosarcoma - fibrous tissue

Multiple myeloma - this is from plasma cells


What is the most common malignant bone tumour?



What is the pathogenesis of osteosarcoma?

assocaited mutations include abnormal pRB protein which is associated with retinoblastoma, also the p53 protein which is associated with li-fraumeni syndrome which is a multi - system cancer syndrome. Osteosarcoma is caused by osteoblast cells which are pleomorphic and produce too much osteoid tissue


Where does primary bone cancer often spread to?

primary bone cancer spreads to breast, bronchus, prostate, kidney, thyroid


Which is more common, primary or secondary bone tumour?

secondary bone tumour 25x commoner than primary


What is the gene assocaited with Ewings sarcoma?

associated with t(11;22) translocation which results in an EWS-FLI1 gene product


What is the most common soft tissue tumour?



What is the presentation of osteoarthritis?

patient over 45 and activity-related joint pain (pain after exertion) plus either morning stiffness < 30 minutes, reduced ROM, deformity


pain after exertion, 


IF linked to trauma, prolonged morning-related stiffness, rapid deterioration of symptoms, hot swollen joint then -> gout, other inflammatory arthrides, septic arthritis, malignancy


What is the name given to the osteophytes in the fingers?

patient over 45 and activity-related joint pain (pain after exertion) plus either morning stiffness < 30 minutes, reduced ROM, deformity


pain after exertion, 


If linked to trauma, prolonged morning-related stiffness, rapid deterioration of symptoms, hot swollen joint then -> gout, other inflammatory arthrides, septic arthritis, malignancy


What are the radiological features of OA?

Loss of joint space


Subchondral sclerosis

Subchondral cyst


What is the management of osteoarthritis?


analgesia (NSAIDs, codeins, topical capsaicin)

lifestyle changes (social, quality of sleep, especially weight loss)


occupational therapy

walking aids

intra-articular steroid injection

thermotherapy, electrotherapy, aids and devices)



arthroscopy (NICE advise only if symptoms of mechanical locking)

osteotomy (aims to correct malaligned joint)

arthroplasty (joint replacement, ex: total hip replacement)

arthrodesis (joint fusion)


What causes OA?

Inflamatory process

Progressive cartilage loss

Subchondral bone formation and bony osteophytes


May be secondary to trauma, infection or ceongenital conditions such as developmental dysplasia of the hip.


OA and RA comparison


What is the diagnosis of JIA?

age of onset <16y/o, duration of disease >6 weeks, presence of arthritis is assessed by joint swelling or 2 of the following: 

painful or limited joint motion




What are the three different types of idiopathic juvenile arthritis?

Polyarticular (5 joints or more)

Pauci articular (4 joints or less)

Stills disease which is systemic onset



What is the most common type of IJA?

Pauciarticular (this is 55%)



Polyarticular (25%)

Systemic onset (20%)


What type of autoantibody may be present in JIA?



What features may be present in JIA apart from joint pathology?

Type 1 pauciarticular = uveitis

Type 2 pauciarticular = iridocyclitis

Type 3 pauciarticular = iridocyclitis, dactylitis, potential family history of psoriasis

For pauciarticular constitutional symptoms are rare



Can be RF positive or RF negative

Constitutional sypmtoms such as low grade fever and malaise

RF negative = hepatosplenomegaly, growth abnormalities, mild anaemia

RF positive = erosions in X-rayoccur early, can be complicated by sjrogens, feltys, aortic regurgitation or pulmonary fibrosis




What are the symptoms of STILLs disease?

Spiking fever for at least 2 weeks (high in the evening normal in the morning).


Salmon red rash on trunk and thighs that accompanies the fever.


Can be brought on by scratching ( Koebner's phenomenon)


Generalised lymphadenopathy 50-75%. Non-tender.




Abdominal pain


With or without transaminases


Serositis (polyserositis, pericarditis in 36%). Tamponade and myocarditis is rare.


What is the presentation of osteomyelitis?

infant: failure to thrive, drowsy or irritable, metaphyseal tenderness + swelling, decreased range of motion positional change, commonest around knee

child: severe pain, reluctant to bear body weight, tender fever + tachycardia, malaise, fatigue, nausea, vomiting), reduced range of motion

adult: backache, history of UTI/urological procedure, history of diabetes, immunosuppression, commonest in thoracolumbar spine, limp, pain, general malaise, loss of appetite, fever, pseudoparalysis 


What is the likely causative organism in osteomyelitis?

Staph. aureus is the most common cause except in patients with sickle-cell anaemia where Salmonella species predominate.


What is the investigation for osteomyelitis?



Others include:

US, aspiration (swelling?), isotope bone scan, labelled white cell scan, MRI, FBC + WBC, ESR, CRP, CK, 3x blood cultures at peak of temperature, U&Es if ill dehydrated, bone biopsy, tissue swabs from up to 5 sites around implant at debridement in prosthetic infections but sinus tract and superficial swab results may be misleading (skin contaminants)


What is the management of osteomyelitis?

hydration and analgesia, 

rest & splintage, 

AB (choice depends on microbiology), IV AB for children, 

surgery is indicated for abscess drainage, debridement of dead/infected tissue, drainage of subperiosteal abscess, drainage of joint sepsis, 


Antibiotic therapy is usually:

flucloxacillin for 6 weeks

clindamycin if penicillin-allergic


What are risk factors for osteomyelitis?

diabetes mellitus

sickle cell anaemia

intravenous drug user

immunosuppression due to either medication or HIV

alcohol excess


What can predispose you to osteomyelitis?

Haematogenous spread in children and elderly

Local spread from site of infection (trauma in open fracture, bone surgery or joint replacement)

Secondary to vascular insufficiency


What are potential outcomes of osteomyelitis?



metastatic infection

pathological fracture

septic arthritis

altered bone growth


Where does osteomyelitis often start?

Starts at the metaphysis of long bones


What is the mean age of osteomyelitis?

6 years old


What is management of chronic osteomyelitits?

long term AB (local: gentamicin cement, systemic: IV AB)

surgery (mutliple ops to eradicate)

deformity correction, massive reconstruction, amputation


What is the presentation of septic arthritis?

fever, warm, red, swollen, painful joint, may also be an erythematous rash 


in adults: acute pain in single large joint, limping, swollen red joint, refusal to move joint (knee, ankle, wrist) (reluctancy to make any movement, increase T° and pulse, increase tenderness)


What are investigations for septic arthritis?


FBC, WCC, ESR, CRP, blood cultures, XR, US, uric acid (exclude gout), Ab (exclude RA),


synovial fluid: 

aspiration, culture (cloudy?), increased leucocytes



MC&S (microscopy, culture, sensitivity)


urethral, cervical and anorectal swabs


XR: soft tissue swelling, joint distension, later juxta-articular osteoporosis, periosteal elevation, joint space narrowing, bony erosions and possible osteomyelitis 


What is the management of septic arthritis?

fluid and pain control, AB, surgical drainage  lavage, infected joint replacement, arthroscopy (knee, shoulder, ankle), arthrotomy, physiotherapy




synovial fluid should be obtained before starting treatment

intravenous antibiotics which cover Gram-positive cocci are indicated. The BNF currently recommends flucloxacillin or clindamycin if penicillin allergic

antibiotic treatment is normally be given for several weeks (BNF states 6-12 weeks)

needle aspiration should be used to decompress the joint

arthroscopic lavage may be required


What are potential routes of infection for septic arthritis?


Eruption of bone abscess

Direct invasion (penetrating wound, intra-articular injury, arthroscopy)

Dissemination from osteomyelitis


What are potential outcomes from septic arthritis?

Complete recovery


partial loss of the articular cartilage


Fibrous bony ankylosis


Joint destruction



What is the disease process of septic arthritis?

Articular cartilage is attacked by abcterial toxin and cellular enzyme


Complete destruction of the articular cartilage


source of infection can be from blood, adjacent sites (osteomyelitis, bone abscess) or it can be through direct introduction of the organism via trauma / instrumentation


What are the most common causative organisms for septic arthritis?

most common organism overall is Staphylococcus aureus

in young adults who are sexually active Neisseria gonorrhoeae should also be considered


What are differentials for septic arthritis?

acute osteomyelitis, trauma, irratable joint, haemophilia, rheumatic fever, gout, Gaucher’s disease


What is the presentation of fracture?


nerve, blood vessel, skin damage

visceral damage (pneumotheorax in rib fracture)

disruption to overlying soft tissue


What are the different types of fractures?

Fractures have a variety of names. Below is a listing of the common types that may occur:

Greenstick - Incomplete fracture. The broken bone is not completely separated.

Transverse - The break is in a straight line across the bone.

Spiral - The break spirals around the bone; common in a twisting injury.

Oblique - Diagonal break across the bone.

Compression - The bone is crushed, causing the broken bone to be wider or flatter in appearance.

Comminuted - The break is in three or more pieces and fragments are present at the fracture site.

Segmental - The same bone is fractured in two places, so there is a "floating" segment of bone.


Main types are open vs closed


What is the Gustilo - Anderson classification of fractures?

Grades are according to soft tissue injury:


Type 1: low-energy clean wound < 1 cm with minimal soft tissue injury and fracture communition

Type 2: Wound 1-10 cm with moderate soft tissue damage and fracture communition

Type 3: high-energy wound >10cm (3A no periosteal stripping, 3B periosteal stripping, 3C major vascular injury)



What is the managent for fractures?

ABC, analgesia, assess VTE risk and implement prophylaxis low-molecular weight heparin plus anti-embolism stockings if appopriate ie. hip fractures)


prophylaxis for crush syndrome, infection (open fractures), tetanus, as required  - compartment syndrome can follow on from crush syndrome so be prepared.


Crush syndrome causes acute tubular necrosis of the kidneys (rep


fracture-specific treatment: 


for displaced fractures


non operative: 

simple splinting: neighbouring strap (metacarpal fractures)

plaster of Paris: easily moulded, cheap. often applied acutely as a backslab to allow for swelling 

fibreglass cast: lighter, less bulky, more rigid (disadvantage if swelling occurs) and more durable than POP 


internal fixation Kirschner wire (screws and plates)

external fixation uniplanar or ring (ie. Ilizarov frame)




occupational therapy


What are complications of bone fracture?

minutes to hours complications (immediate): 

fat embolism


hours to days complications (early): 

compartement syndrome


wound infection

DVT and PE

neurovacular damage


weeks to months complications (late): 


Sudek’s atrophy


pseudoarthrosis - a joint formed by fibrous tissue bridging the gap between the two fragments of bone of an oldfracture that have not united

secondary osteoarthritis

chronic osteomyelitis

avascular necrosis

CRPS type 1

implant failure

psycholigcal & social aspects

complications from bed rest


What is the managment of dupytrens disease?

non-operative: radiotherapy

operative: partial fasciectomy (+ physio), dermo-fasciectomy (+ intense physio, no recurrence), arthodesis, amputation, percutaneous needle fasciotomy (potential recurrence, risk of nerve injury), collagenase (30% recurrence, radical, cost)


What is the aetiology of dupytrens disease?

Autosomal dominant but onset may be sex linked, white people disease


Which fingers are most commonly affected by dupuytrens diusease?

Ring finger follwed by little and middle fingers


What causes dupuytrens disease?

Formation of abnormal connective tissue within the palmar fascia


What are risk factors fordupuytrens disease?


Old age







How does dupuytrens disease progress?

Starts in the palms causing puckering of the skin. Metacarpophalangeal (MCP) joints affected before the proximal interphalangeal (PIP) joints.


What is the presentation of trigger finger?

clicking sensation with movement of digit, clicking may progress to locking, may have to use other hand to “unlock”


Lump in palm under pulley


What is the treatment for trigger finger?

Rest and medication – avoiding certain activities and taking non-steroidal anti-inflammatory drugs (NSAIDs) may help relieve pain.

Splinting – where the affected finger is strapped to a plastic splint to reduce movement.

Corticosteroid injections – steroids are medicines that can reduce swelling.

Surgery on the affected sheath – surgery involves releasing the affected sheath to allow the tendon to move freely again. It's usually used when other treatments have failed. It can be up to 100% effective, although you may need to take 2 to 4 weeks off work to fully recover.


What is the disease mechanism for trigger finger?

Trigger finger occurs if there's a problem with the tendon or sheath, such as inflammation and swelling. The tendon can no longer slide easily through the sheath and can bunch up to form a small lump (nodule). This makes bending the affected finger or thumb difficult. If the tendon gets caught in the sheath, the finger can click painfully as it's straightened.


Who is more likely to be affected by trigger finger?


Over 40

People who have had dupuytrens disease




What muscles are contained in the sheath which is inflamed in de quervain's tenosynovitis?

extensor pollicis brevis and abductor pollicis longus tendons


Who does de quervain's tenosynovitis usually affect?

Usually affects women who are aged 30-50 years old


What is the test for de quervains tenosynovitis?



What are the features of de quervains tenosynovitis?

  • pain on the radial side of the wrist
  • tenderness over the radial styloid process
  • abduction of the thumb against resistance is painful
  • Finkelstein's test: with the thumb is flexed across the palm of the hand, pain is reproduced by movement of the wrist into flexion and ulnar deviation


What is the managment for de quervains tenosynovitis?


steroid injection

immobilisation with a thumb splint (spica) may be effective

surgical treatment is sometimes required


What is the diagnosis of having a lump in dorsal foot - firm, non tender, change in size, smooth, occasionally lobulated, normally not fixed to skin or underlying tissue, never fixed to skin


Pain from pressure from shoewear

Pain from underlying problem



What is the management of ganglia?

Non - operative = aspiration

Operative = excision (including the root)


Where do ganglia arise from ?

Joint capsule, tendon sheath or ligament


What is the presentation of base of thumb OA?

pain (opening jars, pinching), stiffness, swelling, deformity, loss of function


What is the management of base of thumb OA?

non op: NSAIDs, splint, steroid injection

op: trapeziectomy (gold standard), fusion, replacement


What is the presenation median nerve injury

Ape-hand deformity - this is when you cannot abduct or oppose the thumb due to paralysis of the thenar muscles. Sensory deficit on volar aspect of thumb.


What can cause median nerve palsy?

Wrist lacerations

Carpal tunnel syndrome



Which nerve is likely to be affected in fracture of humeral condyles?

Ulnar nerve


What is the presenation of ulnar nerve palsy?

•motor deficit - claw hand, hypothenar & 1st dorsal interosseous wasting


Sendory deficit is in little finger


What is the presentation of radial nerve palsy?

Motor wasting (wrist drop - extensors)

Sensory deficit - 1st web space dorsally



What is the presentation of klumpkes palsy?

claw hand (affects small muscles of hand, wasting of intrinsic muscles of hand, decreased sensaton over T1 dermatome)


What is the presentation of erb's palsy?

waiter’s tip position, arm is adducted and IR, elbow is extended and pronated, wrist is flexed, decreased sensation over C5, C6 dermatomes


What causes klumpkes palsy?

breech delivery, T1 damage (upward traction): occurs with shoulder disclocation or cervical rib


What causes erbs palsy?

birth injury or fall on side of neck (downward traction): forced contralateral neck adbuction


Shoulder dystocia


What is the diagnosis if there is tenderness in the anotomical snuff box?

Scaphoid fracture



What are the complications of scaphoid fracture?

avascular necrosis in proximal part of scaphoid (AVN) (because blood supply is distal to proximal), non-union


Who is more predipsposed to DDH?

More common in girls

More common in the left hip

Common in the eastern euroean demographic


What increases your chances of getting DDH?

First born


Breech presentation

Family history

Lower limb deformities



What are clinical features of DDH?

Ortolani's sign and Barlow's sign


One leg appears longer than the other

Uneven skin folds in the buttocks

One leg dragging behind the other


What is the treatment of DDH?

Pavlik harness

Surgery may be needed if your baby is diagnosed with DDH after they're 6 months old, or if the Pavlik harness has not worked

Surgical options include:

closed reduction – the ball is placed in the socket without making any large cuts (incisions)

open reduction – an incision is made in the groin to allow the surgeon to place the ball in the socket


What is the disease process of Perthes disease?

Part or all of the femoral head (top of the thigh bone: the ball part of the ball-and-socket hip joint) loses its blood supply and may become misshapen. This may lead to arthritis of the hip in later years.


What are the symptoms of perthes disease?

hip pain: develops progressively over a few weeks


stiffness and reduced range of hip movement


What are X-Ray findings of perthes disease?

x-ray: early changes include widening of joint space, later changes include decreased femoral head size/flattening


How is diagnosis of perthes disease achieved?

plain x-ray

technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms persist


What are complications of perthes disease?

Premature fusion of growth plates



Phases =

Avascular necrosis

Fragmentation - revascularisation (pain)

Reossification - bony healing

Residual deformity


What is the treatment for Perthes disease?

To keep the femoral head within the acetabulum: cast, braces

If less than 6 years: observation

Older: surgical management with moderate results

Operate on severe deformities


Who is SCFE more likely to be seen in?

More likely to be seen in overweight children (more likely to be male)


Typical age is 9-14 years


What are the classifications of SCFE?

Acute v chronic (3 weeks)

Syable vs unstable


What is the presentation for SCFE?


Pain in hip or knee

Externally rotated posture and gait

Reduced internal rotation, especially in flexion

Plain X-Rays


What are the differences between acute slip and chronic slip?

Acute Slip:

In an acute slip, pain in the hip is so severe that your child is unable to walk or stand. You may notice that one leg seems shorter than the other. They won't want to move their hip because it is painful. You may notice that their leg is turned outwards.


Chronic Slip:


Walking may be painful

Pain worse on excersize


Leg on affected side may be shorter

Muscle wasting on affected side


What are investigations for SCFE?

Physical examination


CT scan


If avascular necrosis is suspected then an MRI or a bone scan may be necessary


What are complications of SCFE?

Avascular necrosis:

Stable slips (able to bear weight) have a low risk of AVN

Unstable slips (unable to bear weight) have a high risk of AVN



Early osteoarthritis


What is the radiographical sign of SCFE?



What is the commonest cause of hip pain in children?

Transient synovitis


What is the common history for transient synovitis?

Typical age group = 2-10 years
Acute hip pain associated with viral infection


What would separate transient synovitis from septic arthritis?

apyrexial, allowing joint to be examined, low CRP, normal WCC, not that unwell (as opposed to septic artheritis and osteomyelitis)


What is the presentation of rheumatoid arthritis?

joint pain exacerbated by movement, morning stiffness, immobility, poor function, , joint swelling, affects various joints,


systemic symptoms, non-specific: fatigue/lethargy (secondary fibromyalgia due to dysregulation of the HPA axis), weight loss, anaemia, anorexia, mild fever


specific: eyes, lungs (interstitial lung disease, fibrosis), nerves, skin, kidneys, muscles (sarcopenia), bones (osteoporosis), secondary Sjogren’s syndrome, liver (elevated acute-phase response, anaemia of chronic disease (IL6 increases hepatocyte production of hepcidin, an iron-regulatory hormone)


long term: CVS (altered lipid metabolism, elevated acute-phase reactants, increased endothelial activation), malignancy


2010 EULAR/ACR RA classification depends on joint involvement, serology, acute-phase reactants, duration of symptoms


disease activity score: 

DAS 2,4 represents clinical remission

DAS >5,1 represents eligibility for biologic therapy


joints: swollen, warm, tender joints, limitation of movement


joint deformities: swan neck, boutonniere, subluxation


lymphadenopathy, splenomegaly, rheumatoid nodules, muscle weakness, evidence of amyloidosis and vasculitis


diagnosis criteria: need 4 out of 7 (RF RISES)

Rheumatoid factor

Finger/hand joint involvement

Rheumatoid nodules

Involvement of 3 or more joints

Stiffness - early morning

Erosions/decalcification on XR

Symmetrical arthritis


What would bloods show you on rheumatoid arthritis

bloods: ESR + CRP (degree of synovial inflammation), anaemia of chronic disease, low albumin (correlates directly with disease severity), neutropenia (in Felty’s syndrome)


What are immunology results for RA?

rheumatoid factor IgG, IgM

anti-cyclic citrullinated antibodies (anti CCP, ACPA)



What are findings on X-ray of RA?

Loss of joint space

Peri-articular erosions

Juxta articular osteoporosis



What are the features of synovial fluid on RA?

Incerased WBC

Increased protein


What is the presentation for shoulder dyslocation?


Decreased movement

Loss of deltoid coutour

Arm held internally rotated and adducted


What is the management for shoulder dyslocation?

Firstly consider anaesthesia / sedation

Closed reduction (e.g Kocher's)

Open reduction if closed reduction techniques fail

Immobalise the arm for 3 weeks





When are posterior disocations more likely to happen?

Secondary to epileptic seizures


What is the most common type od seizure?



Who is affected by frozen shoulder?

It is most common in middle-aged females. The aetiology of frozen shoulder is not fully understood.


diabetes mellitus: up to 20% of diabetics may have an episode of frozen shoulder


What are the features of adhezive capsulitis?

Features typically develop over days

external rotation is affected more than internal rotation or abduction

both active and passive movement are affected

patients typically have a painful freezing phase, an adhesive phase (decreased ROM especially on internal rotation and a recovery phase

bilateral in up to 20% of patients

the episode typically lasts between 6 months and 2 years


What is the management of rozen shoulder?


no single intervention has been shown to improve outcome in the long-term

treatment options include NSAIDs, physiotherapy, oral corticosteroids and intra-articular corticosteroids


What is the difference between golfers elbow and tennis elbow?


Which disc when prolapsed would cause :

sensory loss on the little toe and sole of foot

Motor weakness in plantar felxion of the foot

Reflex change in ankle jerk

Disc = L5/S1

Actual root value = S1


Which disc when prolapsed would cause:

Sensory loss on the great tow and first dorsal webspace

Motor weakness of the EHL and cause no change in reflex?

Disc = L4/5 

Actual root value = L5


Which disc when prolapsed would cause:

Sensory loss in medial aspect of lower leg

Motor weakness in the quads

Reflex change in the knee jerk 

Disc = L3/L4

Actual root value = L4


Where is a cervical prolapse most likely to happen?

Most commonly C5/6


Where is a thoracic prolapse most likely to happen?



What is the presentation of cauda equina syndrome?

injury or precipitating event

symptoms located in buttock bilaterally, leg pain, back pain, varying dysaethesiae + weakness; leg weaknees together with absent reflexes

bowel and/or bladder sphincter dysfunction (urinary retention +/- incontinence overflow)

saddle anaesthesia, loss of anal tone & anal reflex


What are investigations for cauda equina syndrome?


PR exam

Lumbar CT myelogram if MRI is contraindicated


What are the causes of cauda equina syndrome?

compression of cauda equina due to:

central lumbar disc prolapse (commonest), 

cord tumours, vertebral mets

trauma (burst, fracture disc, spinal stenosis)

infection (epidural abscess)

iatrogenic (spinal surgery or manipulation, spinal epidural injection)


What is the main complication assocaited ith cauda equina syndrome?

if admission + MRI scan + operation >48h then may result in permanent dysfunction of bladder and anal sphincter


Which condition is better walking up hill vs worse walking downhill?

Spinal claudication


What are the two classifications of spinal cord injury?

Complete and incomplete


complete: no motor or sensory function distal to lesion, no anal squeeze, no sacral sensation, ASIA grade A, no chance of recovery

incomplete: some function is present below site of injury, more favourable prognosis


Patterns of injury:

patterns of injury: 


central cord syndrome

anterior cord syndrome

Brown-Sequard syndrome


What is the management for spinal cord injury?

prevent a secondary insult, particularly in patients with incomplete injuries 


Airway- C spine control


Breathing- ventilation and oxygenation


Circulation- fluids, consider neurogenic shock (low BP and HR, loss of sympathetic tone, injuries about T6, TREAT WITH vasopressors)


Disability- assess neuro function including PR and perianal sensation, logrolling




surgical fixation for unstable fractures (vast majority fixed from posteriorly, pedicle screws preferred method)



long-term management: spinal cord injury unit- intermediate term, physiotherapy, occupational therapy, psychological support, urological/sexual counselling


What is the presentation of central cord syndrome?

Weakness of arms moreso than legs, perianal sensation and lower extremity power is preserved


What is the presentation for anterior cord syndrome?

Fine touch and proprioception is preserved, profound weakness


(Fine touch is in the ventral spinothalamic pathway which is in the anterior portion of the spinal cord)


Complete motor paralysis below the level of the lesion due to interruption of the corticospinal tract

Loss of pain and temperature sensation at and below the level of the lesion due to interruption of the spinothalamic tract

Retained proprioception and vibratory sensation due to intact dorsal columns

Autonomic dysfunction may be present and can manifest as hypotension (either orthostatic or frank hypotension), sexual dysfunction, and/or bowel and bladder dysfunction

Areflexia, flaccid internal and external anal sphincter, urinary retention and intestinal obstruction may also be present


What is the presentation of traumatic subarachnoid haemorrhage?

Immediately unconscious and in cardiac arrest

Sudden onset - headache 'the worst headache in my life'

Neck stiffness



What are investigations for Traumatic subarachnoid haemorrhae?


Cerebral angiogram


What is the cause of paget's disease of the bone?

Excessive bone resorption follwoed by disorganised compensatory bone formation


What are is the cause of pagets disease of the bone?

Unclear, possible causes include 

Slow virus infection of osteoclasts

Mutations of SQSTM1, RANK genes involved in Osteoclasts' function regulation


What are signs and symptoms of Pagets diseas of the bone?

Affects femur, lumbar vertebrae and the skull

Bone pain

Pathological fractures

Bony malformations (enlarged skull, bowing of long bones)

Increased temperature (hypervascularity)

Arthritis in assocaited joints

Hearing impairment (sclerosis of the skull bones, cranial nerve compression)

Decreased ROM


What are X ray findings of Paget's disease of the bone?

Osteoporisis circumscripta (well defined osteolytic lesions of the skull in early course)

Cotton wool appearance 

Squaring of vertebrae seen on lateral X-ray

Tam O'shanter sign (enlarged overriding frontal bone)


Bone scan scintigraphy is a potential investigation (focal increased radionuclide uptake)


What are bloods in paget's disease?

Normal Ca2+ but raised alkaline phosphatase


What is the treatment of Paget's disease?

don’t treat if asymptomatic uness in skull or area needing surgery

do not treat based on raised alkaline phosphatase alone

use IV bisphosphonate therapy and one-off zoledronic acid infusion

calcitonin for severe pain/extensive lytic disease


What are complications of Paget's disease?


Heart failure - excessive demand on the heart dues to increased hypervascularity

Neural tissue compression

Rarely - malignant transformation (osteosarcoma)


What is a bone biopsy finding of pagets disease of the bone?

Mosaic pattern of lamellar bone

Large numerous osteclasts with up to 100 nuclei normal is 5-10)

Affected bone marrow field is filled with highly vascular stroma


What is osteomalacia?

normal bony tissue but decreased mineral content

rickets if when growing

osteomalacia if after epiphysis fusion


What is the presentation of osteomalacia?

rickets: knock-knee, bow leg, features of hypocalcaemia

osteomalacia: bone pain, fractures, muscle tenderness, proximal myopathy


What are the types of osteomalacia?

vitamin D deficiency e.g. malabsorption, lack of sunlight, diet

renal failure

drug induced e.g. anticonvulsants

vitamin D resistant; inherited

liver disease, e.g. cirrhosis


What are the investigations for osteomalacia?

low 25(OH) vitamin D (in 100% of patients, by definition)

raised alkaline phosphatase (in 95-100% of patients)

low calcium, phosphate (in around 30%)

PTH is raised

x-ray: children - cupped, ragged metaphyseal surfaces; adults - translucent bands (Looser's zones or pseudofractures)


What is the management of osteomalacia?

calcium with vitamin D tablets


What is the cause of pathophysiology of osteogenesis imperfecta?

abnormality in type 1 collagen due to decreased synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides


What are the features of osteogenesis imperfecta?

fragile bones from mild trauma or even daily acts of life

other non-bone clinical features

growth deficiency

defective tooth formation (dentigenesis imperfecta)

hearing loss

blue sclera

scoliosis/barrel chest

ligamentous laxity (Beighton score)

easy bruising


What is management of osteogenesis imperfecta?

surgical: treat fractures

medical: IV bisphosphonates (to prevent fractures)

social: education and social adaptations

genetic: genetic counselling for parents and next generation


What are the two ways of assessing osteoporosis fracture risk?




What are the advantages and limitations of qFracture?

qfracture only uses data from the UK

Can be used for patients aged 30-99 which is better than FRAX (40-90)


When is it necessary to order a bone mineral density scan for osteoporosis?

Alongside a fracture assessment to make results more accurate  (intermediate risk as assessed by the FRAX test requires a BMD scan)

before starting treatments that may have a rapid adverse effect on bone density (for example, sex hormone deprivation for treatment for breast or prostate cancer).

in people aged under 40 years who have a major risk factor, such as history of multiple fragility fracture, major osteoporotic fracture, or current or recent use of high-dose oral or high-dose systemic glucocorticoids (more than 7.5 mg prednisolone or equivalent per day for 3 months or longer).


What are risk factors for osteoporosis?

Family history

Female sex

Increasing age

Deficient diet

Sedentary lifestyle


Premature menopause

Low body weight

Caucasians and Asians


What is the management of osteoporosis?

Family history

Female sex

Increasing age

Deficient diet

Sedentary lifestyle


Premature menopause

Low body weight

Caucasians and Asians


What is the management of osteoporosis?

Minimise risk factors

Ensure good calcium and Vitamin D status

Falls prevention strategies

Medications - hormone replacement therapy


Side effects of HRT - increased risk of blood clots increased risk of breast cancer with extended use into late 50's/early 60's

Increased risk of heart disease and stroke if used after large gap from menopause.


Selective oestrogen receptor modulator raloxifene - only effective in preventing vertebral body fractures - doesn't affect hip fractures.


Negative effects of SERMS- hot flushes if taken close to menopause, increased clotting risks, lack of protection at hip site



Bisphosphonates are the main Rx option


Oral Bisphosphonates generally the first line of treatment

Adequate Renal function required

Adequate Calcium and Vitamin D status

Good Dental Health and Hygiene advised

Notify dentist on Bisphosphonates

Encourage regular check ups / well fitting dentures


Alendronate - this is one of the popular bisphosphonates used to treat osteoporosis



Side effects of bisphosphonates -



Not safe when eGFR<30 mls/min


Atypical femoral shaft fractures

Drug Holiday for 1-2 years

Usually after 10 years Oral Bisphosphonates


Bisphosphonates can also cause osteonecrosis of the jaw. - very rare


Even though you increase the chance of atypical femoral shaft fracture - you are still 200 times more likely to break your hip by osteoporosis than bisphosphonates


Denosumab - this is a monoclonal antibody against RANKL


The RANK L ligand is responsible for regulating osteoclast activity


Denosumab requires a subcutaneous injection every 6 months - safer in patients with significant renal impairment than bisphosphonates.


Osteoclasts do not get the signal to resporb bone

There is no negative feedback signal to osteoblasts continue to lay down bone


Side effects of Denosumab:

Allergy / rash

Symptomatic hypocalcaemia if given when vitamin D deplete


Atypical femoral shaft fracture?


Teriparatide - intermittent human parathyroid hormone - this is the first portion of parathyroid hormone - makes osteoblasts lay down bone - only anabolic bone treatment (only treatment that actually aids in the laying down of bone


Side effects of Teriparatide - injection site irritation


What are diseases that increase the chances of osteoporosis?

Endocrine: glucocorticoid excess (e.g. Cushing's, steroid therapy), hyperthyroidism, hypogonadism (e.g. Turner's, testosterone deficiency), growth hormone deficiency, hyperparathyroidism, diabetes mellitus

Multiple myeloma, lymphoma

Gastrointestinal problems: inflammatory bowel disease, malabsorption (e.g. Coeliacs), gastrectomy, liver disease

Rheumatoid arthritis

Long term heparin therapy

Chronic renal failure

Osteogenesis imperfecta, homocystinuria




Another list from Laszlo's table:


risk factor endocrine:

thyrotoxicosis, hyper and hypoparathyroidism, Cushings, hyperprolactinaemia, hypopituitarism, low sex hormone levels (


rheumatoid arthritis, ankylosing spondylitis, polymyalgia rheumatica, osteomalacia


inflammatory- UC and Crohns 

liver- PBC, CAH, alcoholic cirrhosis, viral cirrhosis (hepC)

malabsorption- CF, chronic pancreatitis, coeliac disease, Whipple’s disease, short gut syndromes, ischaemic bowel

medication, chronic renal failure

medications, steroids, PPI, enzyme inducting antiepileptic medications, aromatase inhibitors, GnRH inhibitors, warfarin


What is the mechanism of osteoporosis?

metabolic bone disease characterised by low bone mass and micro architectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk 


What medications might predispose you to osteoporosis?



Enzyme inducting antiepileptic mediations

Aromatase inhibitors

GnRH inhibitors



What is the pathophysiology associated with lupus?

There is environmental damage of DNA - release of nuclear antibodies. Antinuclear antibodies and antigens form immune complexes (this is a type 3 hypersensitivity reaction, these immune complexes deposit themselves in tissues)

Organs affected = kidneys, skin, joints and heart

Individuals may develop antibodies which target certain molecules such as phosphilipids on red or white blood cells marking them for phagocytosis (this is a type 2 hypersensitivity reaction)


What is the presentation of SLE?

classification criteria (any 4 “ORDER HIS ANA): 

Oral ulcers

malar Rash

Discoid rash (raised, scarring, permanent marks, alopecia)

Exaggerated photosensitivity

Renal disorders (significant proteinuria or cellular casts in urine)

Haematological (low WCC, platelets, lymphocytes, haemolytic anaemia)

Immunological (anti ds-DNA, SM ( I think this is anti-smith, cardiolipin, lupus anticoagulant, low complement)

Serositis (pleurisy or pericarditis)

Arthritis/arthralgia (2 joints at least)

Neuro (unexplained seizures or psychosis)

ANA (anti-nuclear Ab)



Also has fever


What are complications of SLE?

Cardiovascular disease:

Libman–Sacks endocarditis, myocardial infarction (MI)


Serious infections; renal failure; hypertension


Antiphospholipid syndrome:

Hypercoagulable state; individuals

prone to develop clots (e.g. deep vein

thrombosis, hepatic vein thrombosis,



What are the blood results for SLE?


Coomb’s +ve haemolytic anaemia, neutropenia, lymphocytopenia, thrombocytopenia, increased ESR, normal CRP, renal profile


What is the management of lupus?

management depends on organ threat: 

mild/moderate- hydroxychloroquine,
- azathioprine, methotrexate, mycophenolate, NSAIDs, anti-malarials, low-dose steroids

severe- cyclophosphamide, rituximab, steroids, immunosuppressants


What is noticeable about lupus arthritis?

This is SLE arthritis - notice how there is no bone damage - In lupus the deformity arises because the ligaments become weak.


What is the pathophysiology of scleroderma?

T helper cell mediated immune response, causes a chronic inflammatory response resulting in excessive collagen deposition and damage to microvasculature



What are the two different types of scleroderma?

Limited (80%)


Skin involvement limited to

fingers, forearms,face

Late visceral involvement

Some individuals develop

CREST syndrome:

Calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia


Associated with anticentromere antibodies

Relatively benign

Diffuse (20%)

Widespread skin involvement

Early visceral involvement

Rapid progression

Associated with

anti-DNA topoisomerase I



Poor prognosis


What are the signs and symptoms of scleroderma?

Raynaud phenomenon


Cutaneous changes of face, extremities:

Skin thickening, tightening, sclerosis (most common); edema, erythema (precede sclerosis)


GI involvement

Esophageal fibrosis

dysphagia, GI reflux


Small intestine involvement

abdominal pain, obstructions,

constipation, diarrhea, malabsorption syndrome (weight loss, anemia)

Pulmonary involvement with interstitial



Right-sided cardiac dysfunction/

pulmonary hypertension

Cardiac involvement

Pericardial effusions, myocardial fibrosis

congestive heart failure, arrhythmias


Renal involvement (diffuse disease)

fatal hypertensive crisis (rare)


How is the diagnosis of scleroderma made?


Upper endoscopy

Esophageal fibrosis/reflux esophagitis



Serologic tests

▫↑ANAs in almost all individuals with

systemic sclerosis; low specificity

↑ACAs highly specific (limited) - anticentromere antibodies


Anti-topoisomerase I antibodies (anti-Scl-70) highly specific (diffuse)


Complete blood count (CBC)

Anemia due to malabsorption, increased serum creatinine due to renal dysfunction


Clinical presentation

Skin thickening, swollen fingers,

Raynaud's phenomenon, GI reflux


Pulmonary function tests


Restrictive ventilatory defect due to pulmonary interstitial fibrosis


Are antinulear antibodies and RF present in scleroderma?

ANA positive in 90%

RF positive in 30%


What is the treatment for scleroderma?


What is the cause of sjogren's syndrome?

Chronic autoimmuned infalmmatory disease

Lymphocytic infiltration

Destruction of exocrine glandsof eyes and mouth


What are the causes of sjogrens?

Primary = sicca syndrome

Secondary (to other autoimmune diseases, RA is the most common)


What are signs and symptoms of sjogrens?

Dry eyes (irritation, itching foreign body sensation, keratoconjuncitivits)

Oral dryness reflecting salivary hypofunction

Salivary gland enlargement (parotid, subamndibular etc)

Extraglandular manifestations (MSK symptoms such as arthralgias and arthritis, rashes, interstitial nephritis, vasculitis)


What are blood results for sjogren's?




Increased ESR


What are the findings in the urine for sjogren's?

Proteinuria/haematuria reflecting glomerulonephritis


What would you find in a salivary gland biopsy in sjogren's?

Focal lymphocyte foci (collections of tightly aggregated lymphocytes)


What are serological tests for Sjogren's?

rheumatoid factor (RF) positive in nearly 100% of patients

ANA positive in 70%

anti-Ro (SSA) antibodies in 70% of patients with PSS

anti-La (SSB) antibodies in 30% of patients with PSS

also: hypergammaglobulinaemia, low C4


What test can measure tear production in Sjogren's?

Schirmer's test: filter paper near conjunctival sac to measure tear formation


What is the treatment for Sjogren's?

artificial saliva and tears

pilocarpine may stimulate saliva production


Moderate to severe SS = immunosuppressive treatment


What are complications of Sjogren's?

Peridontal complications, oral infections, mucosal assocaited lymphoid tissue lymphoma


There is a marked increased risk of lymphoid malignancy (40-60 fold).


Who is more likely to be affected by Sjogren's?

Sjogren's syndrome is much more common in females (ratio 9:1).


What is the disease mechanism of granulomatosis with polyangitis (wegners)?

B cell mediated release of free radicals from neutrophils

Free radicals damage neighbouring endothelial cells - vasculitits


granulomatosis with polyangitis only affects small vessels (nasopharynx, kidneys and lungs)


What is the triad of granulomatosis with polyangitis?

Focal necrotising vasculitis

Necrotizing granulomas in the upper airway, lungs

Necrotizing glomerulonephritis (renal vasculitis)


What aere the signs and symptoms of granulomatosis with polyangitis?

Chronic pain (oral ulcers, bloody nasal mucus, chronic sinusitis, saddle nose)

Haemoptysis, dyspnoea, cough, pleuritic chest pain (inflammation of the lung vessels)

Decreased urine production, hypertension, haematuria, red cell casts, proteinuria (glomerular filtration)






What is the blood marker for granulomatosis with polyangitis?



What are the features of polymyositis and dermatomyositis?

Polymyositis = proximal muscle weakness

Dermatomyositis = proximal muscle weakness + gottron's papules and heliotrope rash


What is the specific antibody for polymyositis?

Jo-1 (this is a specific ANA profile)


What disease affects large vessles?

Giant cell arteritis

Takayasu arteritis


What type of vasculitis affects medium sized vessels?

Kawasaki's disease

Polyarteritis nodosa


What is the diagnostic criteria for giant cell arteritis?

3 of the following:

Age at onset (over 50 years)

New headache

Temporal artery tenderness / reduced pulsation

ESR greater than or equal to 50

Abnormal temporal biopsy


Other signs and symptoms include:

Jaw claudication

Transient unilateral vision loss

Carotid bruits, decreased pulse in arms, aortic regurgitation

Tender palpable nodules, absent temporal pulse

Increased risk of aortic dissection, aortic aneurysm


How do we diagnose giant cell arteritis?

Extremely elevated ESR (over 100mm/hr)

Temporal artery biopsy


What is the general treatment for multi-system autoimmune diseases?


What is the treatment for GCA?



What is the treatment for Wegners?


Cyclophosphamide / rituximab


What is SICCA syndrome?

Sicca syndrome is a variant of Sjögren syndrome characterized by xerostomia and keratoconjunctivitis without rheumatoid arthritis.


(dry mouth, dry eyes and RA)


What type of hypersensitivity is present in Sjogren's syndrome? (in reference to the destruction of lacrimal and salivary glands)

Type 4


What are the symptoms of ankylosing spondylitis?

inflammatory back pain, 

limitation of movements in antero-posterior as well as lateral planes at lumbar spines, 

limitation of chest expansion, 

bilateral sacroiliitis on XR

Achilles tendonitis, dactylitis


cardiac-aortic incompentence, heart block

pulmonary-restrictive disease, apical fibrosis


osteoporosis and spinal fractures

neurological- AAD and cauda equina syndrome

renal-secondary amyloidosis

Tenderness over sacroiliac joints (grading of radiographic sacroilitis (grade 0-4 on ASAS classification)


What are the investigations for ankylosing spondylitis?

X-ray of lungs (remember they have apical fibrosis and restrictive lung disease)




What are the findings of bloods on ankylosing spondylitis?

Chronic anaemia

RhF negative

Increased ESR


What are the findigns of ankylosing spondylitis on imaging?

XR (sacroiliitis, juxta-articular sclerosis, syndesmorphyte formation, marginal erosion, fusion of adjacent vertabrae (bamboo spine)), disk calcification, pseudoarthritis; MRI



sacroilitis: subchondral erosions, sclerosis

squaring of lumbar vertebrae

'bamboo spine' (late & uncommon)

syndesmophytes: due to ossification of outer fibers of annulus fibrosus

chest x-ray: apical fibrosis


What is a classical presentation of ankylosing spondylitis?

typically a young man who presents with lower back pain and stiffness of insidious onset

stiffness is usually worse in the morning and improves with exercise

the patient may experience pain at night which improves on getting up


What clinical test could be used to show reduced forward flexion in ankylosing spondylitis?

Schober's test


What is the management of ankylosing spondylitis?


Occupational therapy


DMARDs (sulfasalazine)

Anti-TNF therapy (such as etanercept and adalimumab)

Treatment of osteoporosis

Joint replacement surgery and spinal surgery


What are the nail changes associated with psoriatic arthritis?


Transverse nail ridging

Nail pitting


What are clinical features of psoriatic arthritis?

Asymmetric large joint arthritis, axial arthritis, asymmetric sacroiliitis, peripheral small joint arthritis, DIP joint arthritis, and arthritis mutilans





What are the joint pattern for the following conditions?

Psoriatic arthritis

Reactive arthritis

Enteropathic arthritis

Ankylosing spondylitis

AS = Axial

Enteropathic = Axial and peripheral

Psoriatic = Axial and asymmetrical peripheral

Reactive = Axial and asymmetrical peripheral


What are blood findings in psoriatic arthritis?

Raised ESR

RhF negative

ANA negative


What are imaging findings in psoriatic arthritis?

imaging: XR (para-marginal erosions, fluffy periosteal bone formation, bony ankylosis, asymmetrical sacroiliitis


What is the management for psoriatic arthritis?

sulfasalazine, methotrexate, leflunomide, cyclosporine, anti-TNF therapy, anti-IL-17 and IL-23, steroids, physiotherapy and occupational therapy, axial disease treated similar to ankylosing spondylitis




What infections might cause reactive arthritis?

Infections include- Salmonella, Shigella, Yersinia, Campylobacter, Chlamydia trachomatis or pneumoniae, Borrelia, Neisseria and streptococci

Infections- throat, urogenital & GI


What is the presentation of reactive arthritis?

mono or oligoarthritis, dactylitis and enthesitis also seen, disease may be systemic with skin and mucous membrane involvement (keratoderma blenorrhagica, circinate balanitis, urethritis, conjunctivitis, iritis)

Reiter’s syndrome (arthritis, urethritis and conjunctivitis)


What is the management of reactive arthritis?

acute: NSAID, joint injection (if infection excuded), AB in chlamydia infection (contacts as well)

chronic: NSAID, DMARD (ex: sulphasalazine, methotrexate)


What diseases might predispose you to enteropathic arthritis?

Commonly associated with inflammatory bowel disease (Crohn’s or UC)

Rarely seen with infectious enteritis, Whipple’s disease and Coeliac disease


What is the presentation of enteropathic arthritis?

can be both peripheral and axial disease, enthesopathy commonly seen


If there is arthritis with IBD / Crohn's it's important to suspect enteropathic origin


What is the crystal in both gout and pseudogout?

Gout = monosodium urate

Pseudogout = Calcium pyrophosphate


What are the causes of gout?

Increased production of uric acid (Purines)

Diet high in red meat, shellfish, anchovies

Increase in cell turnover

Cancer treatment - tumour lysis syndrome

Polycythemia vera (5-10% develop gout)

Lesch-Nyhan syndrome (HGPRT deficiency)

Dehydration, alcoholic beverage consumption - decreased clearance of uric acid

Chronic kidney disease


What are risk factors for gout?

Age (20-30+ years of hyperuricaemia increases the risk




Drugs that decrease urate excretion and increase production (thiazides, aspirin)

Chronic lead toxicity


What is the difference in crystal histology for gout and pseudogout?

Gout = needle shaped, negatively birefringent

Pseudogout = Rhomboid, positively birefringent


What are the complications of gout?

Stone passage causing renal colic

Renal failure - death in 20% of individuals with chronic gout



What is the clinical presentation for gout?


monoarthritis, severe pain lasting 7-10 days, most commonly first metatarsophalangeal joint (podogra)



gouty tophi on pinnae, hands +/- polyarthritis


What are findings on imaging of gout? (US, radiographical, CT)

Joint destruction, bony erosions (rarely present on the first acute episode)

Imaging findings tend to become more likely with disease duration


X-Ray - radiolucent uric acid nephrolithiasis


What is acute flare therapy for gout?

Anti-inflammatory treatment ASAP 

GLucocorticoids (oral and or intraarticular injections)

NSAIDs (naproxen, indomethacin)

Colchicine (inhibits leukocyte migration)

Biological agents (IL-1 inhibitors)


What is management and prevention of gout?

Limit medications that alter urate balance (e.g thiazides, aspirin)

Initiate medications that decrease uric acid levels

Xanthine oxidase inhibitors (allopurinol, febuxostat)

Uricosuric medications (increase urate excretion at the kidney)

Uricase medications - mimic enzyme that catalyzes urate conversion

Other interventions =

  • management of obesity/diabetes
  • Diet modification (avoidance of soda, red meat and seafood)
  • Alcohol moderation
  • Increase in physical activity


Note for uricosuric medications:

Gouty patients with normal or low excretion of uric acid (underexcretors) may be candidates for treatment with uricosuric drugs with little risk of urinary calculi. Measurement of the amount of excreted urate has also been recommended to identify these patients.




Gout vs Pseudogout comparison


What are the causes of pseudogout?


Hereditary component

Secondary to previous joint damage, hyperparathyroidism, haemachromatosis, hypothyroidism, ochronosis, diabetes


What are risk factors for pseudogout?

Usually affects individuals over 50 years

Decreased magnesium levels


What is treatment of pseudogout?

Acute flares:




Management and prevention:



What is the presentation of polymyalgia rheumatica?

typically patient > 60 years old

usually rapid onset (e.g. < 1 month)

aching, morning stiffness in proximal limb muscles (not weakness) - typically lasts more than 1 hour

also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats


Muscle power is normal


What are investigations for polymyalgia rheumatica?

ESR > 40 mm/hr

Increased CRP

note CK and EMG normal

reduced CD8+ T


You tend to find that there is a dramatic response to steroids


What are causes of polymyalgia rheumatica?

Genetic defects (assocaited with HLA DR4)

Exposure to adenovirus / human parovirus B19


What is the treatment for polymyalgia rheumatica?

Low dise corticosteroids

The condition can regress after 1 or 2 years (or it can remain chronic)


What condition is polymyalgia rheumatic closely related to?

Giant cell arteritis


How long is a cast recquired for the following tpes of fractures?


Green stick


Buckle = 3/4 weeks

Greenstick = 4-6 weeks

Complete = 6 weeks


What are potential complications of fractures?

Compartment syndrome



Superficial radial nerve injury

Posterior interosseous nerve injury


What is a galeazzi fracture?

fracture of radial shaft with dislocation of the distal radio-ulna joint


What is a monteggia fracture?

Fracture of proximal ulna with dislocation of radial head


What is the most common type of fracture in a child?

Forearm fracture - 80% of which occur in the distal third


What is the presentation for hallux valgus (forefoot problems)

bunions, pressure symptoms from shoe wear, pain from crossing over of toes, metatarsalgia


What are the investigations for hallux valgus?

clinical, XR (determine severity of underlying bony deformity, exclude associated degenerate change)


What are non-operative methods of management for hallux valgus?


shoe wear modification (wide +/- high toe box)

orthotics to offload pressure/correct deformity

activity modification



What is the operative management of hallux valgus?

 (if non-operative fails or unacceptable to patient):

release lateral soft tissues

osteotomy 1st metatarsal +/- proximal phalanx


What is the aetiology of hallux valgus?

Genetic foot wear


What os the pathophysiology of hallux valgus?

lateral angulation of great toe

tendon pull realigned to lateral of centre of rotation of toe worsening deformity

vicious cycle of increased pull creating increased deformity

sesamoid bones sublux - less weight goes through great toe

as deformity progresses abnormalities of lesser toes occur


What is the presentation of hallux rigidus?

Stiff big toe


Pain (often at extreme of dorsiflexion)

Limited ROM


What is the managment of hallux rigidus?


- Activity modification, shoe wear with rigid sole, analgesia



cheilectomy (remove dorsal bone impingement) 

arthrodesis = 1st MTPJ fusion (gold standard, permanent)



What causes hallux rigidus?

unknown, possibly genetic (typical shape of metatarsal head is slightly pointed rather than rounded), possible multiple microtrauma


O/A of the first MTP?


What is hammer toe?

hammer toe is flexion between proximal and intermediate phalanx of any lesser toe 


What is claw toe?

Flexion between proximal and intermediate phalynx AND between intermediate and distal phalynx of any lesser toe


What is mallet toe?

mallet toe is flexion between intermediate and distal phalanx of any lesser toe


What is non-operative treatment for lesser toe deformities?

activity modification, shoe wear (flat shoes with high toe box to accomodate deformity)

orthotic insoles (metatarsal bar/dome support)


What is operative treatment of lesser toe deformities?

flexor to extensor transfer

fusion of interphalageal joint

release of metatarsophalangeal joint

shortening osteotomy of metatarsal


What is the cause of lesser toe deformities?

Imbalance between flexors/extensors

Shoe wear


Rheumatoid arthritis



What are the rheumatoid forefoot management options?




- 1st MTPJ arthrodesis (this is also a treatment in hallux rigidus)

2-5th toe excision arthroplasty


What is midfoot arthritis management?



XR guided injections



What is the pathophysiology of midfoot arthritis?

Post-traumaic arthritis


Rheumatoid arthritis


What are the signs and symptoms for plantar fibromatosis?

asymptomatic unless very large or on weightbearing area


What is the cause of plantar fibromatosis?

Progressive connsctive tissue build up


What is the management of plantar fibromatosis?

non operative: 

avoid pressure, shoewear/orthotics



excision (80% recurrence)


radiotherapy (80% recurrence)


combination surgery/radiotherapy (higher complications risk, less recurrence)


What are the tests for achilles tendon rupture?

Simmonds - squeeze test

Matles test - angle of dangle


What are investigations for achilles tendonopathy?




What is the management for achilles tendonopathy?


activity modification, weight loss, shoe wear modification (slight heel), physiotherapy (eccentric stretching), extra-corporeal shockwave treatment, immobolisation (in below knee cast)



Gastrocnemius recession

Release and debridement of tendon


What are the symptoms of plantar fasciitis/fasciosis?

pain first thing in the morning, pain on weight bearing after rest (post-static dyskinesia), pain located at origin of plantar fascia, frequently long-lasting (2 years or more)


What are the investigations for plantar fasciitis/fasciosis?

diagnosis is clinical mainly, XR, USS and MRI 


What is the management of plantar fasciitis/fasciosis?

rest, change training, streching of Achilles, ice, NSAIDs, orthoses (heel pads), physiotherapy, weight loss, injections (corticosteroid (good in short term but may make conditon worse long term), night splinting


newer/3rd line treatment: 

extracorporeal shockwave therapy

topaz plasma coblation

nitric oxide

platelet rich plasma

endoscopic/open surgery


What is the pathophysiology of plantar fasciitis/fasciosis?

chronic degenerative change, fibroblast hypertrophy, absence inflammatory cells, disorganised and dysfunctional blood vessels and collagen, avascularity, can’t make extra cellular matrix required for repair and re-modelling -> (microtears?)


What are the risk factors for plantar fasciitis/fasciosis?

athletes associated with high intensity or rapid increase in training, running with poorly padded shoes or hard surfaces, obesity, occupations involving prolonged standing, foot/lower limb rotational deformities, tight gastro-soleus complex 


What tendon dysfunction might cause medial or lateral pain and cause medial heel to move inwards and downwards?

Tibialis posterior tendon dysfunction


What is the sign for tibialis posterior tendon dysfunction?

clinical diagnosis (double & single heel raise; heel should swing for valgus to varus as heel rises)


What are the investigations for tibialis posterior tendon dysfunction?


MRI to assess tendon


What is the management of tibialis posterior tendon dysfunction?

orthoses or surgery (reconstruction of tendon (tendon transfer), triple fusion (subtalar, talonavicular and calcaneocuboid)


What is the managment of diabetc foot ulcer?



modify the main detriments to healing (diabetic control, smoking, vascular supply, external pressure (splints/shoes/weight bearing), internal pressure (deformity), infection, nutrition


surgical: improve vascular supply, debride ulcers and get deep samples for microbiology, correct any deformity to offload area, amputation


What is the name of the foot deformity assocaited with diabetic foot?

Charco neuropathy


What is the managment for charcot foot?



immobilisation/non-weight bearing until acute fragmentation resolved


correct deformity (deformity leads to ulceration leads to infection leads to amputation)


What is the pathophyiology of charcot neuropathy?

2 theories:

neurotraumatic (lack of proprioception and protective pain sensation)


neurovascular (abnormal autonomic nervous system results in increased vascular supply and bone resorption


characterised by rapid bone destruction occuring in 3 stages (fragmentation, coalescence, remodelling)


What is management of RA?

effective suppression of inflammation will improve symptoms and prevent joint damage and disability






disease modifying anti-rheumatic drugs (DMARD): methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, penicillamine, gold



TNF alpha inhibitor (Anakinra), anti B cell therapies (CD20, Rituximab), anti T cell therapies (Abatacept), IL-6 inhibitors (Tocilizumab)


corticosteroids: (short term benefit vs long term toxicity) rarely appropriate as single drug therapy


patient education: encourage to alternate rest with exercise


What is presentation of RA?

Morning stiffness, improves with use
Bilateral symptoms
Systemic upset

Joint swelling (joints are swollen and warm, limitation of movement





Systemic - fatigue/lethargy, weight loss, anaemia

swollen, painful joints in hands and feet

stiffness worse in the morning

gradually gets worse with larger joints becoming involved

presentation usually insidiously develops over a few months

positive 'squeeze test' - discomfort on squeezing across the metacarpal or metatarsal joints

Swan neck and boutonnière deformities are late features of rheumatoid arthritis and unlikely to be present in a recently diagnosed patient.




What is the diagnostic criteria for RA?

diagnosis criteria: need 4 out of 7 (RF RISES)

Rheumatoid factor

Finger/hand joint involvement

Rheumatoid nodules

Involvement of 3 or more joints

Stiffness - early morning

Erosions/decalcification on XR

Symmetrical arthritis


What are the bloods seen on RA?

bloods: ESR + CRP (degree of synovial inflammation), anaemia of chronic disease, low albumin (correlates directly with disease severity), neutropenia (in Felty’s syndrome)


What are immunology findings in RA?


rheumatoid factor IgG, IgM

anti-cyclic citrullinated antibodies (anti CCP, ACPA)



What are the complications of RA?

A wide variety of extra-articular complications occur in patients with rheumatoid arthritis (RA):

respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy

ocular: keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy


ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus

increased risk of infections


Less common

Felty's syndrome (RA + splenomegaly + low white cell count)




What are normal hormonal changes for the start of labour?

Progesterone decreases whilst oxytocin and prostaglandins increase to allow for labour to initiate


What happens during stage 1 of labour?

Latent stage - intermittent, often irregular or painful contractions which bring about some cervical effacement and dilatation up to 4 cm.


Established stage - Contractions become regular and painful. Result in progressive effacement and cervical dilation from 4 cm



Complete when cervix is fully dilated (10 cm)


Primagravida = 8 hours (usually not longer than 18 hours)

Multigravida = 5 hours (unlikely to last more than 12 hours)


Anticipated progress 0.5-1.0 cm per hour


What is stage 2 of labour?

Full cervical dilation to the birth of the baby

Passive second stage of labour - Full dilation of the cervix with or without expulsive contractions

Active second stage - Presenting part is visible, expulsive contractions with full dilatation of the cervix, active maternal effort following confirmation of full dilatation of the cervix in the absence of expulsive contractions.


Primagravida = birth would be expected within two hours of active second stage commencing

Multigravida = 1 hour


What is the 3rd stage of labour?

Birth of the baby to the expulsion of the placenta and membranes


Active management management includes:

Routine use of uterotonic drugs

Deferred clamping and cutting of the cord

Controlled cord traction after signs of separation of the placenta.

Physiological management includes:

No routine use of uterotonic drugs

No clamping of the cord until pulsation has stopped

Delivery of the placenta by maternal effort.



Prolonged in:

Active management over 30 mins

Physiological management after 60 mins


How do we monitor pregnancy?

Monitoring of liquor (colour, smell and volume)

Auscultation of fetal heart (doppler, pinards or with CTG) - intermittent monitoring is undertaken every 15 minutes in the first stage of labour and every 5 minutes in the second stage. 

Palpation of uterine muscle contractions. 


What are different types of vertex presentation?


Sinciput (forehead)


Face Chin


What is the most common presentation of a baby?



Which bone in normal labour is the presenting part?

Anterior parietal 


What are the mechanisms of labour?



Internal rotation of the head

Crowning and extension of the head


Internal rotation of the shoulders

External rotation of the head

Lateral flexion


What are possible analgesias in pregnancy?

Analgesia in labour

Breathing, massage, TENS, paracetamol and dihydrocodeine

TENS = transcutaneous electrical nerve stimulation


Entonox (inhalational nitrous oxide and oxygen)

Opioids (morphine, diamorphine, pethidine)

Remifentanil patient controlled analgesia


Consider maternal position and mobility as means of reducing pain and facilitating progress in labour

Evidence demonstrates that continuous midwifery care reduces the need for analgesia and increased likelihood of SVD and maternal satisfaction with birth experience (RCM, 2012: Bohren et al 2017).