MSK, Reproduction and Psychiatry Summary Flashcards
How do anti-psychotics work?
Antipsychotics act as dopamine D2 receptor antagonists, blocking dopaminergic transmission in the mesolimbic pathways
What are the extrapyramidal side effects caused by traditional anti-psychotics?
Extrapyramidal side-effects
Parkinsonism
acute dystonia (e.g. torticollis, oculogyric crisis)
akathisia (severe restlessness)
tardive dyskinesia (late onset of choreoathetoid movements, abnormal, involuntary, may occur in 40% of patients, may be irreversible, most common is chewing and pouting of jaw)
What are the specific risks of antipsychotics in the elderly?
Increased risk of stroke
Increased risk of VTE
What are other side-effects of anti-psychotics?
antimuscarinic: dry mouth, blurred vision, urinary retention, constipation
sedation, weight gain
raised prolactin: galactorrhoea, impaired glucose tolerance
neuroleptic malignant syndrome: pyrexia, muscle stiffness
reduced seizure threshold (greater with atypicals)
sprolonged QT interval (particularly haloperidol)
What mood stabilsing agent can cause hypothyroidism?
Lithium
Why aren’t TCA’s commonly used for depression?
Side-effects and toxicity in overdose
What are common side effects of tricyclic anti-depressants?
drowsiness
dry mouth
blurred vision
constipation
urinary retention
What is low does amitryptiline used for?
low-dose amitriptyline is commonly used in the management of neuropathic pain and the prophylaxis of headache (both tension and migraine)
What joints are affected in rheumatoid arthritis?
MCP
PIP
What are the joints affected in osteoarthritis?
Large weight-bearing joints (hip, knee)
Carpometacarpal joint
DIP, PIP joints
What are X-ray findings in osteoarthritis?
Loss of joint space
Subchondral sclerosis
Subchondral cysts
Osteophytes forming at joint margins
What are x-ray findings on rheumatoid arthritis?
Loss of joint space
Juxta-articular osteoporosis
Periarticular erosions
Subluxation
What are the risk factors for endometrial cancer?
obesity
nulliparity
early menarche
late menopause
unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
diabetes mellitus
tamoxifen
polycystic ovarian syndrome
hereditary non-polyposis colorectal carcinoma
What are the features of endometrial cancer?
post-menopausal bleeding is most common feature, abnormal vaginal bleeding (change in pre-menstrual bleeding)
What is the investigation for endometrial cancer?
women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway
first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
hysteroscopy with endometrial biopsy
MRI pelvis
What is FIGO staging?
Endometrial cancer staging
(FIGO stage 1-4 according to depth of myometrial invasion, cervical involvement and lymph node involvement) and type (1 or 2)
stage 1 (carcinoma strictly confined to the uterus)
stage 2 (carcinoma extended to the endocervix (2A) or cervical stoma (2B))
stage 3 (spread to serosa of uterus, pelvic peritoneum or pelvic lymph nodes)
stage 4 (local metastasis to bladder/bowel (4A) or distant metastasis (4B))
What is the management for endometrial cancer?
localised disease is treated with total abdominal hysterectomy with bilateral salpingo-oophorectomy. Patients with high-risk disease may have post-operative radiotherapy
progestogen therapy is sometimes used in frail elderly women not consider suitable for surgery
What are protective factors for endometrial cancer?
Combined oral contraceptive pill
Smoking
What cancers is the oral contraceptive protective for?
Ovarian cancer and endometrial cancer
What are the risk factors for breast cancer?
BRCA1, BRCA2 genes - 40% lifetime risk of breast/ovarian cancer
1st degree relative premenopausal relative with breast cancer (e.g. mother)
nulliparity, 1st pregnancy > 30 yrs (twice risk of women having 1st child < 25 yrs)
early menarche, late menopause
combined hormone replacement therapy (relative risk increase * 1.023/year of use), combined oral contraceptive use
past breast cancer
not breastfeeding
ionising radiation
p53 gene mutations
obesity
previous surgery for benign disease (?more follow-up, scar hides lump)
What are the functions of oestrogen?
- Proliferation of endometrium
- Promotes development of genitalia
- Promotes growth of follicle
- Causes LH surge
- Responsible for female fat distribution
- Increases hepatic synthesis of transport proteins
- Upregulates oestrogen, progesterone and LH receptors
- Increases TBG levels
What are the functions of progesterone?
- Maintenance of endometrium and pregnancy
- Thickens cervical mucous
- Decreases myometrial excitability
- Increases body temperature
- Responsible for spiral artery development
What are the causative organisms for pelvic inflammatory disease?
Chlamydia trachomatis - the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis
What are the features of Pelvic Inflammatory Disease?
lower abdominal pain
fever
deep dyspareunia
dysuria and menstrual irregularities may occur
vaginal or cervical discharge
cervical excitation
perihepatitis (Fitz-Hugh Curtis Syndrome) occurs in around 10% of cases. It is characterised by right upper quadrant pain and may be confused with cholecystitis
What are the investigations for Pelvic Inflammatory Disease?
FBC, CRP, hCG (ensure negative), MSU, high vaginal swab, endocervical swabs, blood cultures if febrile, pelvic USS, screen for chlamydia and gonorrhoea (low vaginal swabs)
What is the treatment for Pelvic Inflammatory disease?
Low threshold for treatment
Oral oflaxacin and oral metronidaole
OR
Intramuscular ceftrioaxone and oral doxycycline and oral metronidazole
Surgical treatment may be indicated in the case of pelvic abscesses
What are complications of pelvic inflammatory disease?
Infertility
Chronic pelvic pain
Ectopic pregnancy
What are the features of dependant personality disorder?
Intense fear of separation and rejection
Clings to relationships, unfortunately this means that a lot of these people end up in abusive relationships. They hold on to someone who completely takes care of them. Lacks self confidence
Difficulty making simple decisions e.g what to eat.
How is the diagnosis of PCOS made?
2 of the three
- Polycystic ovaries on USS
- Oligo ovulation or anovulation
- Clinical hirsuitism, acne or biochemical signs of hyperandrogenism
What are complications of PCOS?
Type 2 diabetes
Sleep apnoea
Cardiovascular risk
Endometrial hyperplasia and carcinoma
What are the investigations for PCOS?
Pelvic USS
Testosterone and sex-hormone binding globulin
Glucose tolerance test
BP
FSH:LH
What is the management for PCOS?
get BMI within 18-30 range, if BMI is normal
then use ovulation induction agent (clomiphene, gonadotrophins, GnRH, according to the group),
oral contraceptive pill
antiandrogen (combined hormonal contraception, spironolactone, eflornithine cream)
endometrial protection (CHC, progestogens, mirena US (progestin IUD) (remember that endometrial hyperplasia is a complication.
fertility (clomiphene/metformin)
Cosmetic theapies for hirsuitism
What is the largest cause of mortality in pregnancy women?
VTE/PE
What are the signs and symptoms of maternal DVT/PE?
asymptomatic, SOB/chest pain, unilateral leg welling/pain, unexplained tachycardia, calf muscle tenderness,
What are the signs of maternal DVT/PE?
haemoptysis, pleural rub
What are the investigations / diagnosis for maternal DVT/PE?
D-dimer is unreliable, use ECG, leg Doppler, CXR, CTPA, V/Q scans to assess mismatch
What is the management of maternal DVT/PE?
low molecular weight heparin, (WARFARIN IS TERATOGENIC)
thromboprophylaxis (stockings, increase mobility) should be considered in those with risk factors or following C section, for 6w post-partum
Why is there an increase risk of maternal PE/DVT?
pregnancy is hypercoagulable state: increase in fibrogen, factor VIII, VW factor, platelets, decrease in natural anticoagulants (antithrombin III), increse in fibrinolysis)
What are risk factors for DVT/PE?
older mothers, increasing parity, increased BMI, smokers, IV drug users, PET, dehydration (due to hyperemesis), decreased mobility, infections, operative delivery, prolonged labour, haemorrhage, blood loss >2L, previous VTE, FH of VTE, sickle cell disease
What is the definition of primary infertility?
primary infertility: unprotected sexual intercourse for over 1 year and no history of pregnancy
secondary infertility: unprotected sexual intercourse for over 1 year with a previous history of pregnancy
What might be in a males history for pirmary infertility?
change in shaving frequency (testosterone), mumps infection, STI (chlamydia/gonorrhoea), history of varicoceal repair, vasectomy, Klinfelter’s
What is the investigation for male infertility?
semen analysis, repeat semen analysis if required
CF screening if azoospermia,
fat and hair distribution,
STDs (chlamydia, gonorrhoea, NSTD),
caryotype (Klinefelter syndrome),
congenital absence of vas deferens,
What are the investigations for female infertility?
rubella immunity,
chlamydia,
TSH,
mid luteal progesterone if periods are regular, day 1-5 FSH, LH, PRL, testosterone if periods irregular, pelvic US, tubal patency test
What is managment for male infertility?
surgical sperm retrieval,
reversal of vasectomy,
donor insemination,
intra-uterine insemination,
IVF/ICSI (intracytoplasmic sperm injection,
injection of mature egg with single sperm,
overnight incubation), DI (?)
sperm donation
What is the managment for female infertility?
clomifene, gonadotrophins, laparoscopic ovarian drilling, GnRH, tubal surgery, oocyte donation
What are the casues of male infertility?
CF, testicular maldescent, testicular problem, pre-testicular (hypothalamus) or post-testicular. Previously mentioned that there can also be absence of vas deferens
failure of production (35%)
Klinfelter’s syndrome
previous mumps or TB
failure of transport
sterilisation
CF
impotence
What are the causes of female infertility?
ovulatory disfunction (25%)
PCOS
premature menopause
Turner’s
surgical removal
hyperprolactinaemia
weight loss/stress
Sheehan’s syndrome
tubal dysfunction (25%)
previous PID
endometriosis
sterilisation
uterine abnormality
Why can hyperprolactinaemia cause infertility|?
Becasue prolactin inhibits GnRH
What are the different types of miscarriage?
Threatened
Inevitable
Incomplete
Complete
Septic
Missed
What is a threatened miscarriage?
This is when there is bleeding from the gravid uterus before 24 weeks gestation, when there is a viable fetus and no evidence of cervical dilation. The uterus may remain viable and the pregnancy continues without any further problems. The cervix is closed in speculum examination.
What is an inevitable miscarriage?
when there is dilation of the cervix
What is an incomplete miscarriage?
When there is only partial expulsion of the products of conception
What is a complete miscarriage?
Complete expulsion of the products of conception
What is a septic miscarriage?
Following incomplete abortion there is always a risk of ascending infection into the uterus which can spread through the pelvis and is known as septic abortion
What is the definition of a missed miscarriage?
When the fetus has died but the uterus has made no attempt to expel the products of conception. No symptoms or could have bleeding vaginally. Gestational sac seen on scan. No clear fetus or fetal pole with no fetal heart seen in the gestational sac.
What is the aetiology of spontaneous miscarriage?
Abnormal conceptus
chromosomal, genetic, structural - It is estimated that 50% of spontaneous miscarriages may be due to abnormal chromosomes.
Uterine abnormality
congenital, fibroids - Congenital uterine abnormalities result from a failure of normal fusion of the mullerian ducts - incidence of spontaneous miscarriage in this group is estimated to be double that of the normal population. Submucosal fibroids are especially associated with spontaneous miscarriage due to distortion of the uterine cavity.
Cervical incompetence
Primary, secondary - The cervix opens prematurely with absent or minimal uterine activity and the pregnancy is expelled. Trauma to the cervix can be an important aetiological factor such as cone biopsy treatment?
Maternal
increasing age, diabetes - Hormonal imbalances are also said to be a cause of spontaneous miscarriage. The corpus luteum is essential for ensuring the survival of the pregnancy during the first 8 weeks of term. If the corpus luteum is to be removed surgically then abortion will usually occur within 7 days. In threatened miscarriage, those that continue to have inevitable miscarriages will have lower levels of progesterone than those that continue pregnancies to term.
Maternal causes of spontaneous miscarriage can include SLE, thyroid disease, acute maternal infection such as appendicitis, pyelitis. Maternal infection causes general toxic illness with high temperature that can stimulate uterine activity and loss of pregnancy.
Unknown
What is the presentation of a molar pregnancy?
Minor bleed, positive, pregnancy test, vomitting
Enlarged uterus
Feeling of pelvic pressure
What is the main finding in blood tests for molar pregnancy?
Increased beta HCG
What is a molar pregnancy?
Molar pregnancy is an abnormal form of pregnancy in which a non-viable fertilized egg implants in the uterus and will fail to come to term.
A molar pregnancy is a gestational trophoblastic disease which grows into a mass in the uterus that has swollen chorionic villi. These villi grow in clusters that resemble grapes. A molar pregnancy can develop when fertilized egg had not contained an original maternal nucleus. The products of conception may or may not contain fetal tissue. It is characterized by the presence of a hydatidiform mole. Molar pregnancies are categorized as partial moles or complete moles, with the word mole, being used to denote simply a clump of growing tissue, or a growth.
What is the difference between a complete and an incomplete hydatiform mole?
Complete = single sperm fertalises enucleate egg, this means that the moile only contains paternal DNA. There are no fetal cells and there is a risk of GTN (gestational trophoblastic neoplasia) - this includes invasive mole, choriocarcinoma and placental site trophoblastic tumour.
Partial = One normal egg cell fertilised by two normal sperm cells, usually triploid. Some fetal cells are evident such as amnion and RBC,s there isn’t really an association with choriocarcinoma.
What are risk factors for molar pregnancy?
Spontaneous abortion
Previous molar pregnancy
Infertility
Maternal age of extremes (less than or equal to 15 or older than 35)
Low dietary carotene (this is a precursor for vitamin A)
What are complications of molar pregnancy?
Malignancy
Hyperthyroidism
Hypermesis gravidarum (associated with large amounts of beta HCG)
Preeclampsia
What are the investigations for molar pregnancy?
Transvaginal ultrasound
Chest X-Ray to look for malignant spread
What is the management of molar pregnancy?
remove tissue by curretage, if beta hCG returns to normal then no further treatment, if beta hCG stays high (persistent disease) then cure by methotrexate
What is the presentation for a molar pregnancy?
period amenorrhoea +/- positive pregnancy test, +/- vaginal bleeding, +/- pain in the abdomen +/-GI or urinary symptoms,
syncope, lower abdominal pain, bleeding (normally light)
What is the investigation / diagnosis for ectopic pregnancy?
US scan (no intrauterine gestational sac, may see adnexal masses, fluid in pouch of Douglas), serum Beta HCG levels, serum progesterone levels, FBC, diagnostic laparoscopy
What is the management of ectopic pregnancies?
- medical: methotrexate
- surgical: laparoscopic salpingectomy/ salpinotomy for few indications
conservative
+ USS in following pregnancies
What is the management for ectopic pregnancy?
- medical: methotrexate
- surgical: laparoscopic salpingectomy/ salpinotomy for few indications
conservative
+ USS in following pregnancies
What are risk factors for ectopic pregnancy?
Pelvic inflammatory disease
Chlamydia
Gonorrhoea
Previous tubal surgery
Previous ectopic
Assisted conception
What are potential ectopic sites for ectopic pregnancy?
Fallopian tube is the most common (especially ampullary region)
Cervical
Abdominal
Ovarian
Uterine cesarean scar
What are the sypmtoms of ectopic pregnancy rupture?
Severe abdominal pain (may refer to shoulder with phrenic nerve irritation)
Rebound tenderness
Guarding indicates peritoneal irritation
Haemodynamic instability (feeling faint, syncope, tachycardia, hypotension, diaphoresis)
What are the causes of antepartum haemorrhage?
Placenta praevia
Placental abruption
APH of unknown origin
Local lesions of the genital tract
Vasa praevia (very rare)
What is the definition of primary and secondary postpartum haemorrhage?
primary PPH :>500 mL blood loss within first 24h delivery
secondary PPH: >500 mL blood loss after 24h of delivery
What is the presentation of post partumhaemorrhage?
may present with tachycardia, tachypnoea, hypotension if severe bleeding
What is the management of PPH?
obstetric emergency, resuscitation and treat cause (fluids, uterine massage, drugs to stimulate contractility (oxytocin, ergometrine)
if still bleeding then insertion of intrauterine balloon, uterine artery embolisation, uterine artery ligation, hysterectomy
What are the casues of PPH?
pathology: 4 Ts
tone (uterine atony) (commonest)
trauma (cervical, vagina and perineal tears)
tissue (retained placenta or membranes)
thrombin (coagulation disorder)
What is placenta praevia?
PLacenta partially or completely covers the lower uterine segment
What are the symptoms of placenta praevia?
Asymptomatic or can present with painless PV bleeding which can range from light to torrential.
What is the investigation for placenta praevia?
Low-lying placenta identified at 20 week anomaly ultrasound
Needs confirmation in third trimester as may migrate away from lower segment
What is the management of placenta praevia?
Delivery by caesarean section
What is the potential complication assocaited with placenta praevia?
Post-partum haemorrhage
What is placental abruption?
Premature separation of the placenta from the uterine wall
What might increase the chances of placental abruption?
Trauma
Higher risk in multiple pregnancy, polyhydramnios, pre-eclampsia, smokers
What is the presentation of placental abruption?
Pain
Vaginal bleeding
May be concealed and present with abdominal pain
Woody hard uterus is a classic sign
What is the management for placental abruption?
May have to do immediate C section in worst cases but vaginal delivery may be achieved
What are the complications of placental abruption?
complications include maternal shock, collapse, fetal death, maternal DIC (disseminated intravascular coagulation), renal failure, postpartum haemorrhage, ‘couvelaire uterus’
What is the definition of pre-term labour?
onset of labour before 37 completed gestational weeks. sign is contraction with evidence of cervical change on vaginal examination
What are risk factors for preterm labour?
Acute illness
Low BMI
Multiple pregnancy
Polyhydramnios
Pre-term rupture of membranes
Previous cervical surgery
Previous preterm deliver
Smoking
Uterine abnormalities
What is the managment of preterm labour?
The mother should deliver the baby in a unit where adequate facilities to care for the neonate are available
Medical = corticosteroids associated with significant reduction in neonatal death, respiratory distress syndrome and intraventricular haemorrhage in the newborn
Tocolytics = atosiban, nifedipine
Surgical = cervical cerclage for those at risk or identified as having a short cervix
What is the presentatino of syphillis?
primary: chancre lesion, raised painless papule with ulcerated centre, usually found at the site of inoculation; lymphadenopathy
secondary: widepsread mucocutaneous lesions, fever, malaise, headache, lymphadenopathy, sore throat
tertiary: characteised by gumma, usually found in liver, bone and testes
What is the organism responsible for syphillis?
Spirochaete - treponema pallidum
What is the presentation of syphillis?
primary: chancre lesion, raised painless papule with ulcerated centre, usually found at the site of inoculation; lymphadenopathy
secondary: widepsread mucocutaneous lesions, fever, malaise, headache, lymphadenopathy, sore throat
tertiary: characteised by gumma, usually found in liver, bone and testes
What are the investigations for syphillis?
microscopy of fluid from mucocutaneous lesions, veneral diseases research lab (VDLR), treponema pallidum haemagglutination assay (TPHA),
CXR, CT/MRI, lumbar puncture looking for complications
What is the treatment of syphillis?
Penicillin
What is the outcome of congenital syphillis?
Spontaneous abortion, birth defects
What are the features of cardiovascular syphillis?
Aortic aneurysmn
Aortic regurgitation
What are the features of neurosyphillis?
Tabes dorsalis
Brain atrophy
Argyll Robertson Pupil
What is the infective organism for Gonorrhoea?
Bacterial infection caused by Neisseria Gonorrhoeae
What is the presentation of gonorrhoea?
Purulent penile discharge
Often asymptomatic in women
What is the investigation for gonorrhoea?
Microscopy of discharge reveals characteristic gram-negative diplococci
What is the treatment for gonorrhoea?
Cephalosporin, widespread antibiotic resistance
What are the complications of gonorrhoea?
Septic arthritis - most common cause of monoarthritis in sexually active adults
What is the presentation of chlamydia?
female: usually none, sometime cervicitis/cystitis, lower abdominal pain, intermenstrual bleeding
male: often asymptomatic discharge, dysuria
What is the infective organism in chlamydia?
Chlamydia Trachomatis
What are the investigations for chlamydia?
enzyme immunoassays, nucleic acid amplification test, urine testing for Chlamydia
What is the treatment for chlamydia?
The two most commonly prescribed antibiotics for chlamydia are:
azithromycin – given as 2 or 4 tablets at once
doxycycline – given as 2 capsules a day for a week
Your doctor may give you different antibiotics, such as amoxicillin or erythromycin, if you have an allergy or are pregnant or breastfeeding. A longer course of antibiotics may be used if your doctor is concerned about complications of chlamydia.
What is a complication of chlamydia?
Peri-hepatitis (fitz hugh-curtis syndrome)
What is managment of HIV to prevent vertical transmission?
mother is given antiviral therapy anyway (highly active anti-retroviral therapy, HAART), C-section and no breastfeeding if high load of anti-viral (zidovudine) prior to delivery and given to infant, maybe vaginal delivery if low viral load
What is the presentation of vulkvovaginal candidosis?
usually asymptomatic, symptomatic trush (itching, discharge, classically thick, ‘cotton cheese’, but often just increased amount)
Itch and discharge
fissuring, erythema with satellite lesions, characteristic discharge
What is the investigation for vulvovaginal candidosis?
Gram stained preparation, culture
What is the treatment for vulvovaginal candidosis?
azole antifungals (clotrimazole (+ clotrimazole HC if vulvitis) and fluconazole)
What is the likely infective organism for vulvovaginal candidosis?
Candida albicans
What are the risk factors for vulvovaginal candidosis?
risk factors: diabetes, oral steroids, immune suppression including HIV, pregnancy, reproductive age group
What is the presentation of bacterial vaginosis?
usually asymptomatic, watery grey/yellow ‘fishy’ discharge, may be worse after period/sex, sometimes sore/itch from dampness,
What are the investigations for bacterial vaginosis>
Gram stained smear of vaginal discharge
What is the management of bacterial vaginosis?
Gram stained smear of vaginal discharge
What is the treatment for bacterial vaginosis?
oral metronidazole for 5-7 days
70-80% initial cure rate
relapse rate > 50% within 3 months
the BNF suggests topical metronidazole or topical clindamycin as alternatives
What is Amsel’s diagnostic criteria for diagnosing bacterial vaginosis?
Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present
thin, white homogenous discharge
clue cells on microscopy: stippled vaginal epithelial cells
vaginal pH > 4.5
positive whiff test (addition of potassium hydroxide results in fishy odour)
What is the bacterial change assocaited with bacterial vaginosis?
increased gardnerella, ureaplasma, mycoplasma, anaerobes, reduced lactobacilli
Bacterial vaginosis (BV) describes an overgrowth of predominately anaerobic organisms such as Gardnerella vaginalis. This leads to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH
What are typical antihypertensive agents used in chronic hypertension in pregnancy?
lifestyle changes
change in medication as ACE inhibitors like ramipril and enalopril cause birth defects and impaired growth), use angiotensin receptor blockers (losartan, candesartan), anti diuretics and lower dietary sodium. Aim to keep BP < 150/100 (labetolol (Beta blocker), nifedipine (ARB), methyldopa (alpha2 receptor adrenergic agonist), monitor for superimposed pre-eclampsia, if on beta-blockers for hypertension then monitor fetal growth,
What is the presentation of gestational hypertension?
Normal signs of hypertension
Headaches
Dizziness
Blurred vision
Epistaxis
Angina
Syncope
Signs of heart failure
What is the presentation of pre-eclampsia?
asymtomatic or headache, blurry vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands, face and legs, clonus, brisk reflexes, papilloedema, reduced urine output, convulsions, epigastric pain, right upper quadrant pain, visual disturbance, leg swelling
Eclampsia is characterised by tonic clonic seizures
Can also cause pulmonary oedema, cerebral haemorrhage, HELLP syndrome, placental abruption
HELLP syndrome is haemolysis, elevated liver enzymes and low platelets
What changes would you see in the blood in pre-eclampsia?
High Bp
Raised liver enzymes
Bilirubin
Raised urea and creatinine
Raised urate
Low platelets
Low haemoglobin
Signs of haemolysis
Features of DIC
What are the complications of pre-eclampsia on the fetus?
IUGR
Intrauterine death
Iatrogenic preterm delivery
What is the diagnostic criteria for pre-eclampsia?
creatinine ratio >30mg/mmol,
24h urine protein collection >300mg/day,
mild HT on two occasions or more, more than 4 hours apart or moderate to severe HT
What are the investigations for pre-eclampsia?
Serial blood pressure
Urinalysis
Urine protein/creatinine ratio
FBC
U and E
LFT
Coagualtion
Group and save if delivery thought to be likely
CTG to assess fetal well-being
What is the management of pre-eclampsia?
oral labetalol is now first-line following the 2010 NICE guidelines. Nifedipine and hydralazine may also be used
delivery of the baby is the most important and definitive management step - caesarean section
Magnesium sulphate is used to prevent seizures
Methyldopa can also be used for lowering blood pressure.
Steroids are given for fetal lung maturity
Induction of labour (avoid ergometrine - this precipitates
What are the complications of pre-eclampsia in the mother?
mother: eclampsia, severe HT, cerebral haemorrhage, stroke, hemolysis, elevated liver enzymes, low platelets, liver and renal failure, disseminated intravascular coagulation, renal failure, pulmonary oedema, cardiac failure,
impaired placenta perfusion,, growth, HELLP syndrome, pappiloedema, pulmonary oedema, placental abruption, disseminated intravascular coagulation
What is the effect of gestational diabetes on a baby?
on fetus: increased risk of congenital anomalies, perinatal mortality, macrosomial, shoulder dystocia, polyhydramnios
What are the effects of gestational diabetes on the mother?
on mother: diabetic nephropathy and retinopathy may deteriorate. Increased risk of miscarriage, pre-eclampsia and operative delivery
What is the management of gestational diabetes?
on mother: diabetic nephropathy and retinopathy may deteriorate. Increased risk of miscarriage, pre-eclampsia and operative delivery
Here is management of diabetes in pregnanct women
Important to note that there is increase in insulin requirement, early induction of labour and early feeding of baby to reduce neonatal hypoglycaemia
before pregnancy, to prevent malformations: make sure blood sugars are 4-7mmol/L pre-conception and HbA1c <6,5% (<48mmol/L), folic acid 5mg, dietary advice, retinal and renal assessement
during pregnancy, to prevent metabolic complications: increase insulin, can continue oral anti-diabetic agents, should be aware of hypos risk, watch for ketonuria/infections, repeat retinal assessement 28 and 34w, watch fetal growth, observe mother for PET, oral hypoglyacemics are usually avoided (according to book page 259)
giving birth: induction of labout at 38-39 weeks is the norm, consider C-section if significant fetal macrosomia, maintain blood glucose in labour with insulin-dextrose insulin infusion, continuous CTG fetal monitoring in labour, early feeding of baby to reduce neonatal hypoglycaemia, switch back to pre-pregnancy regimen for insulin post delivery
What are the complications of pre-exiswting diabetes in pregnancy?
increased risk of congenital fetal abnormalities (especially if blood sugars high peri-conception), miscarriage, pre-eclampsia, fetal macrosomia, polyhydramnios, operative delivery, shoulder dystocia, worsening of maternal nephropathy, retinopathy, hypoglycaemia, reduced awareness of hypoglycaemia, infections, stillbirth, increased perinatal mortality, neonatal death (impaired lung activity, neonatal hypoglycaemia, jaundice, obstruction of labour)
What is the definition of primary amenorrhoea?
never had period, either >14 and no secondary sexual characteristics or >16 and sexual characteristics
What are the investigations for primary amenorrhoea?
GnRH, hCG, TFT, LH, FSH, prolactin, chromosomal karyotype, pelvic USS, oestrogen, TSH, progesterone challenge test (oral progesterone for 5 days, if there is endogenous oestrogen and normal anatomy, withdrawal bleeding will occur), pregnancy test, testosterone?
What is management of primary amenorrhoea?
Gradual build up with estrogen
Effect on breast development
Add progesterone
Once maximum height potential is reached
At least 20 mg of estrogen dose
How can you interpret the progesterone withdrawal test?
So if there is anovulation then - progesterone given and then removed, bleeding 2-7 days later. This is dependant on sufficient estradiol concentration in the serum.
If no bleeding = Low serum estradiol, hypothalamic pituitary axis dysfunction, non-reactive endometrium, outflow tract abnormality such as cervical stenosis.
If it is not an outflow tract obstruction then it is likely to be due to low oestrogen. Withdrawal bleeding occurs after removal of oestrogen / progesterone therapy.
What are casues of amenorrhoea?
Pregnancy
PCOS
Hypothalamic disorders
Hyperprolactinaemia
Ovarian failure / menopause
Thyroid disease
Anatomical disorders of outflow
What is the definition of secondary amenorrhoea?
absence of menstruation > 6 months in a woman who has previously menstruated
What are signs of secondary amenorrhoea?
hirsutism and other androgen-linked features (enlarged clitoris, acne, deep voice)
What is management for secondary amenorrhoea?
control BMI, HRT if premature ovarian insufficiency, emotional support
anatomical causes: surgery for imperforate hymen/transverse septum
What are causes of secondary amenorrhoea?
causes: pregnancy, breast feeding, contraception, polycystic ovaries, early menopause, thyroid disease, cushing’s, raised prolactin (medication related or prolactinoma), hypothalamic, androgen secreting tumour (high testosterone), Sheehans syndrome (pituitary failure), Asherman’s syndrome (intrauterine adhesions)
What are is the presentation for female pelvic organ prolapse?
“mass down below”, “dragging sensation”
vaginal: feeling/seeing a bulge, sensation of bulge, difficulty in inserting tampons, dyspareunia
urinary: hesitancy, incomplete emptying, poor stream, prolonged stream, urinary incontinence, frequency/urgency, manual reduction of prolapse to start or complete void
bowel: incontinence of void/flatus, feeling of incomplete emptying, straining, urgency, digital evacuation to complete defecation, splinting or pushing on or around the vagina or perineum to start or complete defecation
What are investigations for POP?
POP quantification (POPQ score) stage 0-6, measure of cm, USS/MRI (thickness of levator ani), urodynamics (exclude concurrent UTI), IVU (view ureters, bladder and kidneys with contrast), renal USS (if suspicion of obstruction)
What is the managment of female pelvico organ prolapse?
prevention: avoid constipation, manage chronic chest pathology (COPD, asthma), smaller family size, muscle training (PFMT)? (cannot treat fascial cases)
conservative: pelvic floor exercises, ring and shelf pessaries (except if inability to hold it for 2 weeks)
surgical: vaginal hysterectomy, anterior and posterior vaginal wall repair
+ perineometer, biofeedback, vaginal cones, electrical stimulation,
What causes female pelvico organ prolapse?
Caused by weakening of pelvic floor normally secondary to child birth
What is the presentation of fibroids?
usually asymptomatic or dysmenorrhoea (painful periods), menorrhagia (excessive bleeding), pelvic pain, pressure symptoms on bladder, intermenstrual bleeding (for submucous or intramural types), bloating
What are investigations for fibroids?
large fibroids are palpable abdominally, uterus may be enlarged on pelvic examination
Transvaginal USS, Pelvic USS, hysteroscopy?
What is the management of fibroids?
same as menorrhagia
medical treatment is less efficient if fibroids are large and distort the cavity
only if symptomatic myomectomy, hysteroctomy, transcervical resection (submucous), GnRH analogues or ulipristal acetate to temperarily shrink the fibroids (pre-op)
progestin IUD, tranexamic acid, OCP,
surgery
interventional radiology: uterine artery embolisation and MRI- guided ablation of fibroids may be possible in specialist centres
What are the complications of fibroids?
Pain
Malpresentation/obstruction of labour
What are the different types of fibroids?
smooth muscle growth, can be:
submucosa (protrude into uterine cavity)
intramural (within uterine wall)
subserosal (project out of uterus into peritoneal cavity)
What causes fibroids?
Benign tumour arising from the myometrium
What are the causes of menorrhoagia?
Uterine fibroids
Dysfunctional uterine bleeding
Coagulopathies
Pelvic malignancies
What is the definition of menorrhagia?
Heavy menstrual bleeding (more than 80ml per cycle)
What are potential investigations for menorrhagia?
FBCs
TFTs
Pelvic USS
hCG
Hysteroscopy and endometrial biopsy if simple treatment fails or suspicous features
What is the treatment of menorrhagia?
medical: progesterone only pill, tranexamic acid, mefenamic acid, combined oral contraceptive, mirena, GnRH analogues,
surgery:
trans-cervical resection of submucous fibroids, endometrial ablation, myomectomy, hysterectomy
What is the presentation of endometriosis?
dysmenorrhoea, deep dyspareunia, chronic pelvic pain, ovulation pain, infertility, dyschezia (pain of defecation), tenderness or palpable nodules on bimanual examination, frozen pelvis
Passmedicine:
chronic pelvic pain
dysmenorrhoea - pain often starts days before bleeding
deep dyspareunia
subfertility
non-gynaecological: urinary symptoms e.g. dysuria, urgency, haematuria. Dyschezia (painful bowel movements)
on pelvic examination reduced organ mobility, tender nodularity in the posterior vaginal fornix and visible vaginal endometriotic lesions may be seen
What would you find on examination of endometriosis?
adnexal masses or tenderness
nodules or tenderness in posterior vaginal fornix or uterosacral ligaments,
fixed (because of fibrous scar tissue) retroverted uterus,
rectovaginal nodules
What are the investigations for endometriosis?
laparoscopy (gold standard) look for clear, red, bluish lack or with lesions,
pelvic MRI for deep endometriosis, if severe disease is suspected and surgical planning necessary
pelvic USS can diagnose endometrioma (chocolat cyst) or large nodules
What is managment of endometriosis?
medical:
NSAIDs, COCP, danazol/gestrinone, mirena IUS, GnRH agonist (leuprorelin), progesterone, levonorgestrel (LNG), GnRH analogues
surgical:
remove endometriosis, goes from laparoscopic ablation of lesions to hysterectomy and bilateral salpingo-oophorectomy
pain management
What are causes of dysmenorrhoea?
Endometriosis
Pelvic adhesions
Chronic PID
Ovarian cysts
Pelvic venous conegestion
Uterine fibroids
What is the presentation of adenomyosis?
dysmenorrhoea, dysparenunia, menorrhagia, bulky tender uterus
Endometriosis doesn’t have menorrhagia by the looks of it so this would be the key difference between the two
What are the investigations for adenomyosis?
MRI, hysterectomy and histological diagnosis as diagnostic is often flawed
What is the managment for adenomyosis?
Hormonal contraception for heavy/painful periods (mirena US, progestogens, combined OCP)
What is the definition of adenomyosis?
Presence of endometrial tissue in the myometrium
What is the presentation of ovarian cancer?
non-speciifc bowel symptoms (indigestion, early satiety, loss of appetite, altered bowel habit/pain, bloating, discomfort, weight loss)
overlap with IBS symptoms
pelvic mass (asymptomatic or pressure symptoms), adnexal mass on pelvic examination,
late-stage disease may present as a large pelvic mass, ascites, palpable lymph nodes and pleural effusion
How is the diagnosis of ovarian cancer made?
diagnosis: Ca125 (carcinoma antigen), pelvic USS,
staging: pelvic MRI/CT chest/abdomen/pelvis, colonoscopy/OGD may be indicated is there is a possibility of primary GI malignancy, US guided biopsy of omentum, staging (1-4)
stage 1 (tumour limited to ovaries)
stage 2 (tumour involves one or both ovaries with pelvic extension
stage 3 (tumour with peritoneal implants outside the pelvis or retroperitoneal and or inguinal nodes)
stage 4 (tumour with distant metastasis)
Diagnosis is difficult and often relies on diagnostic laparotomy
What is the managment of ovarian cancer?
protective: OCP, prophylactic oophorectomy, having many children
Platinum based chemotherapy
stage 1:
total abdominal hysterectomy and bilateral salpingoophorectomy and omentectomy +/- chemotherapy
stage 2:
stage 1 + /- lymphadenectomy with surgical effort to remove all disease
stage 3:
stage 2 +/- neoadjuvant chemotherapy to reduce tumour mass before surgery
stage 4:
stage 3 + pallative chemotherapy
What are genes associated with ovarian cancer?
genes associated: BRAC1, BRAC2, HNPCC/Lynch type 2 familial cancer syndrome
What is the most common type of ovarian cancer?
around 90% of ovarian cancers are epithelial in origin, with 70-80% of cases being due to serous carcinomas
What are risk factors for ovarian cancer?
FH, >30 y/o, FH (2 or more relatives), cancer gene mutation carriers)
for risk (combines menopausal status, ultrasound score and CA 125) use RMI I score (if 250 or greater then referral to specialist team)
What are potential causes for raised CA125?
CA 125 (glyco-protein antigen) can indicate malignancies (ovary, colon/pancreas and breast) and benign conditions such as menstruation, PID, endometriosis, liver disease, recent surgery, effusions
What is the presentation of endometrial cancer?
post-menopausal bleeding is most common feature, abnormal vaginal bleeding
What is the investigation for endometrial cancer?
women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway
first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
hysteroscopy with endometrial biopsy
MRI pelvis/CT chest, abdomen, pelvis for staging
What is the staging of endometrial cancer?
(FIGO stage 1-4 according to depth of myometrial invasion, cervical involvement and lymph node involvement) and type (1 or 2)
stage 1 (carcinoma strictly confined to the uterus)
stage 2 (carcinoma extended to the endocervix (2A) or cervical stoma (2B))
stage 3 (spread to serosa of uterus, pelvic peritoneum or pelvic lymph nodes)
stage 4 (local metastasis to bladder/bowel (4A) or distant metastasis (4B))
What is the management of endometrial cancer?
surgery:
stage 1: total abdominal hysterectomy and bilateral salpingoophorectomy
stage 2: radical total abdominal hysterectomy (TAH) + bilateral salpingoophorectomy (BSO) + radiotherapy +/- lymphadenactomy
stage 3: surgery + radiotherapy or radiotherapy alone
stage 4: palliative radiotherapy (with progesterone if advanced stage)
other:
peritoneal washings (all laparoscopically), chemo if high risk histology, radiotherapy (external beam or caesium insertion)
What are the two common types of endometrial cancer?
type 1 (commonest): endometrioid adenocarcinoma, linked to excess oestrogen, hyperplasia with atypia precursor
type 2: uterine serous & clear cell carcinoma, high grade, more aggressive, worse prognosis, generally older ladies, serous intraepithelial carcinoma precursor
95% is adenocarcinoma
What are risk factors for endometrial cancer?
Obesity
Tamoxifen therapy (although antagonistic with respects to breast tissue tamoxifen may serve as an agonist at other sites. Therefore risk of endometrial cancer is increased cancer)
Early menarche / late menopause
Oestrogen secreting tumours
HRT
Endometrial hyperplasia with atypia
Genetic predisposition (lynch syndrome)
What is the presentation of menopause?
lack of menstruation for >1 year
hot flushes and night sweats (vasomotor symptoms)
vaginal dryness/soreness (vasomotor symptoms)
dyspareunia (vasomotor symptoms)
atrophy and thinning of vaginal epithelium
overactive bladder symptoms (urgency, frequency)
mood changes,
loss of libido
osteoporosis
increase in cardiovascular risk
What are hormonal findings for menopause?
FSH and LH ar high
Oestrogen is low
What are the relevant investigations for menopause?
DEXA scan for bone density
LH
FSH
Oestrogen
Progesterone
What are the different forms of hormone replacement therapy?
Combined (oestrogen and progestogen) for a women with a uterus
Oestrogen alone for those with hysterectomy
Can be given sequentially (monthly withdrawal bleeding) or can be given continuously (period free)
What does HRT increase the risk of?
VTE
Breast cancer
Endometrial cancer
Gall bladder disease
Vascular disease
What are investigations for downs syndrome in utero?
first trimerster screening: combined test
nuchal translucency, hCG and PAPP-A (pregnancy associated plasma protein A), AFP (alpha fetoprotein)
first and second trimester: intergrated test
combined test and ALP (alpha fetoprotein), oestriol, inhibin A
second trimester: quadruple test
hCG, estriol, AFP, inhibin A
second trimester: anomaly USS
if risk is <1 in 250 then are offered chorionic villus sampling or amniocentesis
What is the risk of having a baby with Down’s syndrome if the woman is aged 40?
around 1%
What are the symptoms of PID?
constant lower abdominal pain, purulent vaginal discharge, deep dyspareunia, pyrexia, irregular PV bleeding, adnexal tenderness
dysuria, irregular periods
What is the cassical sign of PID?
Cervical excitation
What are investigations for pelvic inflammatory disease?
FBC, CRP, hCG (ensure negative), MSSU, high vaginal swab, endocervical swabs, blood cultures if febrile, pelvic USS, screen for chlamydia and gonorrhoea (low vaginal swabs)
What is the management of PID?
medical:
- mild: oral ofloxacin + metronidazole for 14 days
- moderate: intramuscular ceftriaxone + oral doxycycline + metronidazole for 14 days
severe: inpatient IV therapy if clinically unwell and severe
surgical:
may be indicated in severe cases with evidence of pelvic abscess
prevention: contact tracing for sexual partners
What are the differentials for lower abdominal pain in a young woman?
Ectopic pregnancy
Appendicitis
Endometriosis
IBS
Ovarian cyst accident / cyst rupture
UTI
What are potential causative organisms for PID?
Causative organisms
Chlamydia trachomatis - the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis
What are potential complications of PID?
infertility (10-20% after first episode), ectopic pregnancies, chronic pelvic pain, Fitz-Hugh-Curtis syndrome (in 10% cases)
What is the presentation of breast cancer?
hard lump, fixed mass, tethering to skin, dimpling of skin, often painless lump or thickening in breast, discharge or bleeding, change in size or contours of breast, change in colour of areola, redness or pitting of skin over the breast like the skin of an orange
What are the investigations for breast cancer?
triple assessement of any breast lump (clinical examination, radiological investigation (mammography/US) and biopsy)
FNA cytology, core biopsy, mammography, US, sentinel lymph node biopsy (assess lymphatic spread), nipple scrape (Paget’s disease) or use discharge for analysis if present,
What are staging investigations for breast cancer?
staging investigations: Hb FBC, U&Es, LFTs, CXR, CT thorax and abdomen, isotope bone scan if lymph node spread,
What is the screening programme for breast cancer in Scotland?
he Scottish Breast Screening Programme invites women aged between 50 and 70 years old for screening every three years. Women over 70 years old are able to attend through self-referral.
What are the subtypes of breats cancer?
Non-invasive = Ductal carcinoma in situ, lobular carcinoma in situ
Invasive = Invasive ductal carcinoma (most common)
Invasive lobular carcinoma and its variants
Where does breast cancer spread to?
Local skin
Pectoral muscles
Lymphatic axillary and internal mammary nodes
Blood
Bone
Lungs
Liver
Brain
What is the purpose of histological assessment of breast cancer?
Histological assessment should be carried out to assess tumour type and to deter- mine oestrogen and progesterone receptor (ER/PR) status and HER2 status
What is management of breast cancer?
wide local excision or mastectomy, removal of sentinel lymph node;
hormonal markers predict response to hormonal treatment (trastuzumab herceptin)
antihormonal therapy is tamoxifen or chemotherapy
tumours <4cm usually are eligible for breast conservation therapy
if sentinal node biopsy contains tumour then radiotherapy on all of the axillary lymph nodes or remove all (clearance)
micrometastases are treated with hormonal therapy or chemo
trastazumab to patients with over expression of Her2 (monoclonal Ab)
+follow up (yearly mammograms for 10 years)
What is the hormone therapy for breast cancer?
What Type of Hormone Therapy do we Usually Give?
If premenopausal – tamoxifen for 5 years
If postmenopausal – tamoxifen for 5 years if excellent prognosis.
BUT others get an aromatase inhibitor, eg ANASTROZOLE for 5-10 years
What type of breast cancers responds well to hormonal therapy?
About 70% of breast cancers are ER positive. They respond well to treatment with hormonal therapies.
Most commonly used hormone therapy drugs used to treat breast cancer are:
tamoxifen
aromatase inhibitors (anastrozole, exemestane and letrozole)
goserelin (Zoladex)
fulvestrant (Faslodex)
Who usually receives chemotherapy for breast cancer?
Node posistive
Stage 3
Mastectomy vs wide local excision?
What genes can result in breast cancer?
Both genetic and hormonal factors play a role; about 5–10% of breast cancers are hereditary and occur in patients with mutations of BRCA1, BRCA2, AT or TP53 genes
What drug can be used to treat HER 2 positive breast cancer?
Some breast cancers have high numbers of receptors for the protein HER2 (human epidermal growth factor 2). They are called HER2 positive breast cancers. About 1 in 7 women (15%) with early breast cancer have HER2 positive cancer. A drug called trastuzumab (Herceptin®) is an effective treatment for this type of breast cancer.
What are triple negative breast cancers?
If the cancer does not have receptors for either HER2 or the hormones oestrogen and progesterone, it is called triple negative breast cancer. It affects up to 1 in 5 women (15–20%) with breast cancer and is more common in younger women
What is the TNM staging of breast cancer?
Tumour (T)
T1 – 0-2cm
T2 - 2-5cm
T3 - >5cm
T4 – fixed to skin or muscle
Nodes (N)
N0- none
N1 – nodes in axilla
N2 – large or fixed nodes in the axilla
Metastases (M)
M0 – none
M1 - metastases
What is the tool which calculates prognosis for breast cancer?
Nottingham prognosis index
This accounts for tumour size, lymph node score and grade score
How many women are affected by breast cancer?
1 in 8
What are risk factors for breast cancer?
Female sex
Age
Family history (BRCA1 and BRCA2)
Early menarche late menopause
Nullparity, higher age at first pregnancy
Higher socioeconomic group
HRT
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?
30-80%
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
Smoking
STDs
Immunodeficiency
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:
smoking
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),
medical:
duloxetine
surgery:
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?
Age
Parity
Menopause
Smoking
Medical problems
Increased intra abdominal pressure
Pelvic floor trauma
Denervation
Connective tissue disease
Surgery
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,
medical:
anticholinergics (oral or transdermal antimuscarinic), tri-cyclic antidepressants,
surgical:
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
Swelling
Pathological fracture
Deformity
Neurovascular effects (limb weakness, numbness)
What are invesitagtions for bone tumours?
- MRI
- XR (lesion is inactive or aggressive),
- CT (ossification and calcification)
- isotope bone scans (bone mets for staging)
- angiography
- PET
- biopsy
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?
Osteochondroma
What is the presentation for malignant bone tumour?
Pain
NOT- activity related
Deep-deated boring nature
Night pain
Difficulty weight bearing
Analgesics are usually ineffective
Swelling
Warmth
Pathological fractures
Osteoporosis
Joint effusion
Deformtity
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
Breast
Prostate
Thyroid
Lungs
Kidneys
What are malignant primary tumours of the bone?
Chondrosarcoma
Osteosarcoma
Fibrosarcoma - fibrous tissue
Multiple myeloma - this is from plasma cells
What is the most common malignant bone tumour?
Osteosarcoma?
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?
Lipoma
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
Osteophytes
Subchondral sclerosis
Subchondral cyst
What is the management of osteoarthritis?
non-operative:
analgesia (NSAIDs, codeins, topical capsaicin)
lifestyle changes (social, quality of sleep, especially weight loss)
physiotherapy
occupational therapy
walking aids
intra-articular steroid injection
thermotherapy, electrotherapy, aids and devices)
operative:
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
tenderness
warmth
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%)
THEN
Polyarticular (25%)
Systemic onset (20%)
What type of autoantibody may be present in JIA?
ANA
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
Polyarticular
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.
Hepatosplenomegaly
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?
MRI
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?
septicaemia
death
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?
bloods:
FBC, WCC, ESR, CRP, blood cultures, XR, US, uric acid (exclude gout), Ab (exclude RA),
synovial fluid:
aspiration, culture (cloudy?), increased leucocytes
urine:
MC&S (microscopy, culture, sensitivity)
microbiology:
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
Passmedicine:
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?
Blood
Eruption of bone abscess
Direct invasion (penetrating wound, intra-articular injury, arthroscopy)
Dissemination from osteomyelitis
What are potential outcomes from septic arthritis?
Complete recovery
OR
partial loss of the articular cartilage
OR
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?
pain
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:
reduce
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
operative:
internal fixation Kirschner wire (screws and plates)
external fixation uniplanar or ring (ie. Ilizarov frame)
rehabilitate
physiotherapy
occupational therapy
What are complications of bone fracture?
minutes to hours complications (immediate):
fat embolism
hours to days complications (early):
compartement syndrome
immobility
wound infection
DVT and PE
neurovacular damage
weeks to months complications (late):
stiffness
Sudek’s atrophy
malunion
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?
Male
Old age
Alcohol
Diabetes
Tobacco
HIV
Epilepsey
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?
Women
Over 40
People who have had dupuytrens disease
Diabetes
RA
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?
Finklestein’s
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?
analgesia
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
ganglia
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
Oligohydramnios
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
limp
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
OA
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?
Detection:
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:
Limping
Walking may be painful
Pain worse on excersize
Stiffness
Leg on affected side may be shorter
Muscle wasting on affected side
What are investigations for SCFE?
Physical examination
X-Ray
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
Chondrolysis
Deformity
Early osteoarthritis
What is the radiographical sign of SCFE?
Trethowan
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)
ANA(?)
What are findings on X-ray of RA?
Loss of joint space
Peri-articular erosions
Juxta articular osteoporosis
Subluxation
What are the features of synovial fluid on RA?
Incerased WBC
Increased protein
What is the presentation for shoulder dyslocation?
Pain
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
Physiotherapy
Surgery
When are posterior disocations more likely to happen?
Secondary to epileptic seizures
What is the most common type od seizure?
Antero-inferiorly
Who is affected by frozen shoulder?
It is most common in middle-aged females. The aetiology of frozen shoulder is not fully understood.
Associations
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?
Management
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?
T11/T12
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?
MRI
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:
tetraplegia/quadriplegia
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
Photophobia
What are investigations for Traumatic subarachnoid haemorrhae?
CT
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?
Osteoarthritis
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?
FRAX
Qfracture
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
Smoking
Premature menopause
Low body weight
Caucasians and Asians
What is the management of osteoporosis?
Family history
Female sex
Increasing age
Deficient diet
Sedentary lifestyle
Smoking
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 -
Oesophagitis
Iritis/uveitis
Not safe when eGFR<30 mls/min
ONJ
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
ONJ?
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 (<up></up>
<p>rheumatic:</p>
<p>rheumatoid arthritis, ankylosing spondylitis, polymyalgia rheumatica, osteomalacia</p>
<p>GI: </p>
<p>inflammatory- UC and Crohns </p>
<p>liver- PBC, CAH, alcoholic cirrhosis, viral cirrhosis (hepC)</p>
<p>malabsorption- CF, chronic pancreatitis, coeliac disease, Whipple’s disease, short gut syndromes, ischaemic bowel</p>
<p>medication, chronic renal failure</p>
<p>medications, steroids, PPI, enzyme inducting antiepileptic medications, aromatase inhibitors, GnRH inhibitors, warfarin</p>
</up>
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?
Steroids
PPI
Enzyme inducting antiepileptic mediations
Aromatase inhibitors
GnRH inhibitors
Warfarin
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,
stroke)
What are the blood results for SLE?
bloods:
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
antibodies
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
fibrosis
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?
DIAGNOSTIC IMAGING
Upper endoscopy
Esophageal fibrosis/reflux esophagitis
LAB RESULTS
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
OTHER DIAGNOSTICS
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?
Leukopenia
Thrombocytopenia
Anaemia
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)
Myalgia
Arthralgia
Episcleritis
What is the blood marker for granulomatosis with polyangitis?
c-ANCA
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?
Corticosteroids
What is the treatment for Wegners?
Corticosteroids
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
uveitis
cardiac-aortic incompentence, heart block
pulmonary-restrictive disease, apical fibrosis
GI-IBD
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)
MRI
Bloods
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
Passmedicine:
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?
Physiotherapy
Occupational therapy
NSAIDs
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?
Oncholysis
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
Enthesitis
Dactylitis
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
NSAIDs, DMARD
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
Male
Alcohol
Obesity
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?
acute:
monoarthritis, severe pain lasting 7-10 days, most commonly first metatarsophalangeal joint (podogra)
chronic:
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?
Sporadic
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:
NSAIDs
Colchicine
Glucocorticoids
Management and prevention:
Colchicine
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?
Buckle
Green stick
Complete
Buckle = 3/4 weeks
Greenstick = 4-6 weeks
Complete = 6 weeks
What are potential complications of fractures?
Compartment syndrome
Refracture
Non-union
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?
non-operative:
shoe wear modification (wide +/- high toe box)
orthotics to offload pressure/correct deformity
activity modification
analgesia
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
Asymptomatic
Pain (often at extreme of dorsiflexion)
Limited ROM
What is the managment of hallux rigidus?
Non-operative:
- Activity modification, shoe wear with rigid sole, analgesia
Operative:
cheilectomy (remove dorsal bone impingement)
arthrodesis = 1st MTPJ fusion (gold standard, permanent)
arthroplasty
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
Neurological
Rheumatoid arthritis
Idiopathic
What are the rheumatoid forefoot management options?
Shoewear/orthotics/activity
Operative:
- 1st MTPJ arthrodesis (this is also a treatment in hallux rigidus)
2-5th toe excision arthroplasty
What is midfoot arthritis management?
Activity/shoewear/orthotics
XR guided injections
Fusion
What is the pathophysiology of midfoot arthritis?
Post-traumaic arthritis
Osteoarthritis
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
operative:
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?
USS
MRI
What is the management for achilles tendonopathy?
Non-operative:
activity modification, weight loss, shoe wear modification (slight heel), physiotherapy (eccentric stretching), extra-corporeal shockwave treatment, immobolisation (in below knee cast)
Operative:
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?
Clinical
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?
prevention
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?
prevention
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
analgesics
NSAIDs:
disease modifying anti-rheumatic drugs (DMARD): methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, penicillamine, gold
biologics:
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
Lymphadenopathy
Splenomegaly
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?
immunology:
rheumatoid factor IgG, IgM
anti-cyclic citrullinated antibodies (anti CCP, ACPA)
ANA(?)
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
osteoporosis
ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus
increased risk of infections
depression
Less common
Felty’s syndrome (RA + splenomegaly + low white cell count)
amyloidosis
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?
Vertex
Sinciput (forehead)
Brow
Face Chin
What is the most common presentation of a baby?
LOA
Which bone in normal labour is the presenting part?
Anterior parietal
What are the mechanisms of labour?
Descent
Flexion
Internal rotation of the head
Crowning and extension of the head
Restitution
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
Water
Entonox (inhalational nitrous oxide and oxygen)
Opioids (morphine, diamorphine, pethidine)
Remifentanil patient controlled analgesia
Epidural
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).
