MSK, Reproduction and Psychiatry Summary Flashcards

1
Q

How do anti-psychotics work?

A

Antipsychotics act as dopamine D2 receptor antagonists, blocking dopaminergic transmission in the mesolimbic pathways

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2
Q

What are the extrapyramidal side effects caused by traditional anti-psychotics?

A

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)

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3
Q

What are the specific risks of antipsychotics in the elderly?

A

Increased risk of stroke

Increased risk of VTE

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4
Q

What are other side-effects of anti-psychotics?

A

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)

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5
Q

What mood stabilsing agent can cause hypothyroidism?

A

Lithium

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6
Q

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

A

Side-effects and toxicity in overdose

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7
Q

What are common side effects of tricyclic anti-depressants?

A

drowsiness

dry mouth

blurred vision

constipation

urinary retention

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8
Q

What is low does amitryptiline used for?

A

low-dose amitriptyline is commonly used in the management of neuropathic pain and the prophylaxis of headache (both tension and migraine)

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9
Q

What joints are affected in rheumatoid arthritis?

A

MCP

PIP

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10
Q

What are the joints affected in osteoarthritis?

A

Large weight-bearing joints (hip, knee)
Carpometacarpal joint
DIP, PIP joints

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11
Q

What are X-ray findings in osteoarthritis?

A

Loss of joint space
Subchondral sclerosis
Subchondral cysts
Osteophytes forming at joint margins

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12
Q

What are x-ray findings on rheumatoid arthritis?

A

Loss of joint space
Juxta-articular osteoporosis
Periarticular erosions
Subluxation

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13
Q

What are the risk factors for endometrial cancer?

A

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

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14
Q

What are the features of endometrial cancer?

A

post-menopausal bleeding is most common feature, abnormal vaginal bleeding (change in pre-menstrual bleeding)

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15
Q

What is the investigation for endometrial cancer?

A

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

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16
Q

What is FIGO staging?

A

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))

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17
Q

What is the management for endometrial cancer?

A

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

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18
Q

What are protective factors for endometrial cancer?

A

Combined oral contraceptive pill

Smoking

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19
Q

What cancers is the oral contraceptive protective for?

A

Ovarian cancer and endometrial cancer

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20
Q

What are the risk factors for breast cancer?

A

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)

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21
Q

What are the functions of oestrogen?

A
  • 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
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22
Q

What are the functions of progesterone?

A
  • Maintenance of endometrium and pregnancy
  • Thickens cervical mucous
  • Decreases myometrial excitability
  • Increases body temperature
  • Responsible for spiral artery development
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23
Q

What are the causative organisms for pelvic inflammatory disease?

A

Chlamydia trachomatis - the most common cause

Neisseria gonorrhoeae

Mycoplasma genitalium

Mycoplasma hominis

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24
Q

What are the features of Pelvic Inflammatory Disease?

A

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

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25
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)
26
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
27
What are complications of pelvic inflammatory disease?
Infertility Chronic pelvic pain Ectopic pregnancy
28
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.
29
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
30
What are complications of PCOS?
Type 2 diabetes Sleep apnoea Cardiovascular risk Endometrial hyperplasia and carcinoma
31
What are the investigations for PCOS?
Pelvic USS Testosterone and sex-hormone binding globulin Glucose tolerance test BP FSH:LH
32
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
33
What is the largest cause of mortality in pregnancy women?
VTE/PE
34
What are the signs and symptoms of maternal DVT/PE?
asymptomatic, SOB/chest pain, unilateral leg welling/pain, unexplained tachycardia, calf muscle tenderness,
35
What are the signs of maternal DVT/PE?
haemoptysis, pleural rub
36
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
37
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
38
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)
39
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
40
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
41
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
42
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,
43
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
44
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
45
What is the managment for female infertility?
clomifene, gonadotrophins, laparoscopic ovarian drilling, GnRH, tubal surgery, oocyte donation
46
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
47
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
48
Why can hyperprolactinaemia cause infertility|?
Becasue prolactin inhibits GnRH
49
What are the different types of miscarriage?
Threatened Inevitable Incomplete Complete Septic Missed
50
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.
51
What is an inevitable miscarriage?
when there is dilation of the cervix
52
What is an incomplete miscarriage?
When there is only partial expulsion of the products of conception
53
What is a complete miscarriage?
Complete expulsion of the products of conception
54
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
55
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.
56
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
57
What is the presentation of a molar pregnancy?
Minor bleed, positive, pregnancy test, vomitting Enlarged uterus Feeling of pelvic pressure
58
What is the main finding in blood tests for molar pregnancy?
Increased beta HCG
59
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.
60
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.
61
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)
62
What are complications of molar pregnancy?
Malignancy Hyperthyroidism Hypermesis gravidarum (associated with large amounts of beta HCG) Preeclampsia
63
What are the investigations for molar pregnancy?
Transvaginal ultrasound Chest X-Ray to look for malignant spread
64
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
65
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)
66
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
67
What is the management of ectopic pregnancies?
- medical: methotrexate - surgical: laparoscopic salpingectomy/ salpinotomy for few indications conservative + USS in following pregnancies
68
What is the management for ectopic pregnancy?
- medical: methotrexate - surgical: laparoscopic salpingectomy/ salpinotomy for few indications conservative + USS in following pregnancies
69
What are risk factors for ectopic pregnancy?
Pelvic inflammatory disease Chlamydia Gonorrhoea Previous tubal surgery Previous ectopic Assisted conception
70
What are potential ectopic sites for ectopic pregnancy?
Fallopian tube is the most common (especially ampullary region) Cervical Abdominal Ovarian Uterine cesarean scar
71
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)
72
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)
73
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
74
What is the presentation of post partumhaemorrhage?
may present with tachycardia, tachypnoea, hypotension if severe bleeding
75
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
76
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)
77
What is placenta praevia?
PLacenta partially or completely covers the lower uterine segment
78
What are the symptoms of placenta praevia?
Asymptomatic or can present with painless PV bleeding which can range from light to torrential.
79
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
80
What is the management of placenta praevia?
Delivery by caesarean section
81
What is the potential complication assocaited with placenta praevia?
Post-partum haemorrhage
82
What is placental abruption?
Premature separation of the placenta from the uterine wall
83
What might increase the chances of placental abruption?
Trauma Higher risk in multiple pregnancy, polyhydramnios, pre-eclampsia, smokers
84
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
85
What is the management for placental abruption?
May have to do immediate C section in worst cases but vaginal delivery may be achieved
86
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’
87
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
88
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
89
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
90
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
91
What is the organism responsible for syphillis?
Spirochaete - treponema pallidum
92
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
93
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
94
What is the treatment of syphillis?
Penicillin
95
What is the outcome of congenital syphillis?
Spontaneous abortion, birth defects
96
What are the features of cardiovascular syphillis?
Aortic aneurysmn Aortic regurgitation
97
What are the features of neurosyphillis?
Tabes dorsalis Brain atrophy Argyll Robertson Pupil
98
What is the infective organism for Gonorrhoea?
Bacterial infection caused by Neisseria Gonorrhoeae
99
What is the presentation of gonorrhoea?
Purulent penile discharge Often asymptomatic in women
100
What is the investigation for gonorrhoea?
Microscopy of discharge reveals characteristic gram-negative diplococci
101
What is the treatment for gonorrhoea?
Cephalosporin, widespread antibiotic resistance
102
What are the complications of gonorrhoea?
Septic arthritis - most common cause of monoarthritis in sexually active adults
103
What is the presentation of chlamydia?
female: usually none, sometime cervicitis/cystitis, lower abdominal pain, intermenstrual bleeding male: often asymptomatic discharge, dysuria
104
What is the infective organism in chlamydia?
Chlamydia Trachomatis
105
What are the investigations for chlamydia?
enzyme immunoassays, nucleic acid amplification test, urine testing for Chlamydia
106
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.
107
What is a complication of chlamydia?
Peri-hepatitis (fitz hugh-curtis syndrome)
108
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
109
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
110
What is the investigation for vulvovaginal candidosis?
Gram stained preparation, culture
111
What is the treatment for vulvovaginal candidosis?
azole antifungals (clotrimazole (+ clotrimazole HC if vulvitis) and fluconazole)
112
What is the likely infective organism for vulvovaginal candidosis?
Candida albicans
113
What are the risk factors for vulvovaginal candidosis?
risk factors: diabetes, oral steroids, immune suppression including HIV, pregnancy, reproductive age group
114
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,
115
What are the investigations for bacterial vaginosis\>
Gram stained smear of vaginal discharge
116
What is the management of bacterial vaginosis?
Gram stained smear of vaginal discharge
117
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
118
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 ## Footnote 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)
119
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
120
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,
121
What is the presentation of gestational hypertension?
Normal signs of hypertension Headaches Dizziness Blurred vision Epistaxis Angina Syncope Signs of heart failure
122
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
123
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
124
What are the complications of pre-eclampsia on the fetus?
IUGR Intrauterine death Iatrogenic preterm delivery
125
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
126
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
127
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
128
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
129
What is the effect of gestational diabetes on a baby?
on fetus: increased risk of congenital anomalies, perinatal mortality, macrosomial, shoulder dystocia, polyhydramnios
130
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
131
What is the management of gestational diabetes?
on mother: diabetic nephropathy and retinopathy may deteriorate. Increased risk of miscarriage, pre-eclampsia and operative delivery
132
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
133
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)
134
What is the definition of primary amenorrhoea?
never had period, either \>14 and no secondary sexual characteristics or \>16 and sexual characteristics
135
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?
136
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
137
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.
138
What are casues of amenorrhoea?
Pregnancy PCOS Hypothalamic disorders Hyperprolactinaemia Ovarian failure / menopause Thyroid disease Anatomical disorders of outflow
139
What is the definition of secondary amenorrhoea?
absence of menstruation \> 6 months in a woman who has previously menstruated
140
What are signs of secondary amenorrhoea?
hirsutism and other androgen-linked features (enlarged clitoris, acne, deep voice)
141
What is management for secondary amenorrhoea?
control BMI, HRT if premature ovarian insufficiency, emotional support anatomical causes: surgery for imperforate hymen/transverse septum
142
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)
143
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
144
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)
145
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,
146
What causes female pelvico organ prolapse?
Caused by weakening of pelvic floor normally secondary to child birth
147
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
148
What are investigations for fibroids?
large fibroids are palpable abdominally, uterus may be enlarged on pelvic examination Transvaginal USS, Pelvic USS, hysteroscopy?
149
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
150
What are the complications of fibroids?
Pain Malpresentation/obstruction of labour
151
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)
152
What causes fibroids?
Benign tumour arising from the myometrium
153
What are the causes of menorrhoagia?
Uterine fibroids Dysfunctional uterine bleeding Coagulopathies Pelvic malignancies
154
What is the definition of menorrhagia?
Heavy menstrual bleeding (more than 80ml per cycle)
155
What are potential investigations for menorrhagia?
FBCs TFTs Pelvic USS hCG Hysteroscopy and endometrial biopsy if simple treatment fails or suspicous features
156
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
157
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
158
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
159
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
160
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
161
What are causes of dysmenorrhoea?
Endometriosis Pelvic adhesions Chronic PID Ovarian cysts Pelvic venous conegestion Uterine fibroids
162
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
163
What are the investigations for adenomyosis?
MRI, hysterectomy and histological diagnosis as diagnostic is often flawed
164
What is the managment for adenomyosis?
Hormonal contraception for heavy/painful periods (mirena US, progestogens, combined OCP)
165
What is the definition of adenomyosis?
Presence of endometrial tissue in the myometrium
166
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
167
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
168
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
169
What are genes associated with ovarian cancer?
genes associated: BRAC1, BRAC2, HNPCC/Lynch type 2 familial cancer syndrome
170
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
171
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)
172
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
173
What is the presentation of endometrial cancer?
post-menopausal bleeding is most common feature, abnormal vaginal bleeding
174
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
175
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))
176
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)
177
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
178
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)
179
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
180
What are hormonal findings for menopause?
FSH and LH ar high Oestrogen is low
181
What are the relevant investigations for menopause?
DEXA scan for bone density LH FSH Oestrogen Progesterone
182
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)
183
What does HRT increase the risk of?
VTE Breast cancer Endometrial cancer Gall bladder disease Vascular disease
184
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
185
What is the risk of having a baby with Down's syndrome if the woman is aged 40?
around 1%
186
What are the symptoms of PID?
constant lower abdominal pain, purulent vaginal discharge, deep dyspareunia, pyrexia, irregular PV bleeding, adnexal tenderness dysuria, irregular periods
187
What is the cassical sign of PID?
Cervical excitation
188
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)
189
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
190
What are the differentials for lower abdominal pain in a young woman?
Ectopic pregnancy Appendicitis Endometriosis IBS Ovarian cyst accident / cyst rupture UTI
191
What are potential causative organisms for PID?
Causative organisms ## Footnote Chlamydia trachomatis - the most common cause Neisseria gonorrhoeae Mycoplasma genitalium Mycoplasma hominis
192
What are potential complications of PID?
infertility (10-20% after first episode), ectopic pregnancies, chronic pelvic pain, Fitz-Hugh-Curtis syndrome (in 10% cases)
193
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
194
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,
195
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,
196
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.
197
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
198
Where does breast cancer spread to?
Local skin Pectoral muscles Lymphatic axillary and internal mammary nodes Blood Bone Lungs Liver Brain
199
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
200
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)
201
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
202
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)
203
Who usually receives chemotherapy for breast cancer?
Node posistive Stage 3
204
Mastectomy vs wide local excision?
205
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
206
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.
207
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
208
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
209
What is the tool which calculates prognosis for breast cancer?
Nottingham prognosis index This accounts for tumour size, lymph node score and grade score
210
How many women are affected by breast cancer?
1 in 8
211
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
212
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
213
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.
214
What type of HPV virus is most assocaited with cervical cancer?
HPV 16 and 18 are highr risk subtypes
215
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
216
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
217
How is colposcopy carried out?
colposcopy involves inspection of ectocervix under magnification. Acetic acid and Lugol’s iodine is applied to identify abnormality.
218
How is histological diagnosis of CIN achieved?
Histological diagnosis is achieved with biopsies of abnormal area
219
CIN staging
CIN 1: low grade dysplasia–will regress CIN 2: moderate dysplasia – may regress CIN 3: severe dysplasia – unlikely to regress
220
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
221
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
222
What percentage of CIN 3 progresses to cervical carcinoma?
30-80%
223
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)
224
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
225
What are risk factors for cervical intraepithelial neoplasia?
HPV infection Smoking STDs Immunodeficiency Persistent infection
226
What are the investigations for cervical cancer?
Screening (prophylactic investigation) Cervical biopsy MRI of pelvis, CT of chest, abdomen, pelvis (to assess the spread)
227
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)
228
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
229
What are the most common types of cervical cancer?
80-90% = squamous cell 10-20% = adenocarcinoma Ectocervix = squamous cell Endocervix = columnar cell
230
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
231
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
232
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))
233
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)
234
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
235
What causes stress incontinence?
Defect in anterior vaginal wall and pubo-urethral ligament Suburethral hammock
236
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
237
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
238
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
239
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
240
What is the presentation of benign bone tumours?
Activity related pain Swelling Pathological fracture Deformity Neurovascular effects (limb weakness, numbness)
241
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
242
What is the characteristic X-ray finding for osteochondroma?
bony projection of bone which is capped with cartilage - exotosis
243
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
244
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
245
What are the characteristic features of Ewings sarcoma on x-ray?
Ewings sarcoma - forms lytic bone lesions that look like an onion ring appearance
246
What is the most common benign bone tumour?
Osteochondroma
247
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
248
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)
249
Where do secondary bone cancers often come from?
Be prepared for the laughing kid Breast Prostate Thyroid Lungs Kidneys
250
What are malignant primary tumours of the bone?
Chondrosarcoma Osteosarcoma Fibrosarcoma - fibrous tissue Multiple myeloma - this is from plasma cells
251
What is the most common malignant bone tumour?
Osteosarcoma?
252
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
253
Where does primary bone cancer often spread to?
primary bone cancer spreads to breast, bronchus, prostate, kidney, thyroid
254
Which is more common, primary or secondary bone tumour?
secondary bone tumour 25x commoner than primary
255
What is the gene assocaited with Ewings sarcoma?
associated with t(11;22) translocation which results in an EWS-FLI1 gene product
256
What is the most common soft tissue tumour?
Lipoma
257
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
258
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
259
What are the radiological features of OA?
Loss of joint space Osteophytes Subchondral sclerosis Subchondral cyst
260
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)
261
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.
262
OA and RA comparison
263
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
264
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
265
What is the most common type of IJA?
Pauciarticular (this is 55%) THEN Polyarticular (25%) Systemic onset (20%)
266
What type of autoantibody may be present in JIA?
ANA
267
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
268
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.
269
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
270
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.
271
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)
272
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
273
What are risk factors for osteomyelitis?
diabetes mellitus sickle cell anaemia intravenous drug user immunosuppression due to either medication or HIV alcohol excess
274
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
275
What are potential outcomes of osteomyelitis?
septicaemia death metastatic infection pathological fracture septic arthritis altered bone growth
276
Where does osteomyelitis often start?
Starts at the metaphysis of long bones
277
What is the mean age of osteomyelitis?
6 years old
278
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
279
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)
280
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
281
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
282
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
283
What are potential outcomes from septic arthritis?
Complete recovery OR partial loss of the articular cartilage OR Fibrous bony ankylosis Joint destruction
284
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
285
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
286
What are differentials for septic arthritis?
acute osteomyelitis, trauma, irratable joint, haemophilia, rheumatic fever, gout, Gaucher’s disease
287
What is the presentation of fracture?
pain nerve, blood vessel, skin damage visceral damage (pneumotheorax in rib fracture) disruption to overlying soft tissue
288
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
289
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)
290
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
291
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
292
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)
293
What is the aetiology of dupytrens disease?
Autosomal dominant but onset may be sex linked, white people disease
294
Which fingers are most commonly affected by dupuytrens diusease?
Ring finger follwed by little and middle fingers
295
What causes dupuytrens disease?
Formation of abnormal connective tissue within the palmar fascia
296
What are risk factors fordupuytrens disease?
Male Old age Alcohol Diabetes Tobacco HIV Epilepsey
297
How does dupuytrens disease progress?
Starts in the palms causing puckering of the skin. Metacarpophalangeal (MCP) joints affected before the proximal interphalangeal (PIP) joints.
298
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
299
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.
300
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.
301
Who is more likely to be affected by trigger finger?
Women Over 40 People who have had dupuytrens disease Diabetes RA
302
What muscles are contained in the sheath which is inflamed in de quervain's tenosynovitis?
extensor pollicis brevis and abductor pollicis longus tendons
303
Who does de quervain's tenosynovitis usually affect?
Usually affects women who are aged 30-50 years old
304
What is the test for de quervains tenosynovitis?
Finklestein's
305
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
306
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
307
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
308
What is the management of ganglia?
Non - operative = aspiration Operative = excision (including the root)
309
Where do ganglia arise from ?
Joint capsule, tendon sheath or ligament
310
What is the presentation of base of thumb OA?
pain (opening jars, pinching), stiffness, swelling, deformity, loss of function
311
What is the management of base of thumb OA?
non op: NSAIDs, splint, steroid injection op: trapeziectomy (gold standard), fusion, replacement
312
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.
313
What can cause median nerve palsy?
Wrist lacerations Carpal tunnel syndrome
314
Which nerve is likely to be affected in fracture of humeral condyles?
Ulnar nerve
315
What is the presenation of ulnar nerve palsy?
•motor deficit - claw hand, hypothenar & 1st dorsal interosseous wasting Sendory deficit is in little finger
316
What is the presentation of radial nerve palsy?
Motor wasting (wrist drop - extensors) Sensory deficit - 1st web space dorsally
317
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)
318
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
319
What causes klumpkes palsy?
breech delivery, T1 damage (upward traction): occurs with shoulder disclocation or cervical rib
320
What causes erbs palsy?
birth injury or fall on side of neck (downward traction): forced contralateral neck adbuction Shoulder dystocia
321
What is the diagnosis if there is tenderness in the anotomical snuff box?
Scaphoid fracture
322
What are the complications of scaphoid fracture?
avascular necrosis in proximal part of scaphoid (AVN) (because blood supply is distal to proximal), non-union
323
Who is more predipsposed to DDH?
More common in girls More common in the left hip Common in the eastern euroean demographic
324
What increases your chances of getting DDH?
First born Oligohydramnios Breech presentation Family history Lower limb deformities
325
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
326
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
327
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.
328
What are the symptoms of perthes disease?
hip pain: develops progressively over a few weeks limp stiffness and reduced range of hip movement
329
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
330
How is diagnosis of perthes disease achieved?
plain x-ray technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms persist
331
What are complications of perthes disease?
Premature fusion of growth plates OA Phases = Avascular necrosis Fragmentation - revascularisation (pain) Reossification - bony healing Residual deformity
332
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
333
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
334
What are the classifications of SCFE?
Acute v chronic (3 weeks) Syable vs unstable
335
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
336
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
337
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
338
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
339
What is the radiographical sign of SCFE?
Trethowan
340
What is the commonest cause of hip pain in children?
Transient synovitis
341
What is the common history for transient synovitis?
Typical age group = 2-10 years Acute hip pain associated with viral infection
342
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)
343
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
344
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)
345
What are immunology results for RA?
rheumatoid factor IgG, IgM anti-cyclic citrullinated antibodies (anti CCP, ACPA) ANA(?)
346
What are findings on X-ray of RA?
Loss of joint space Peri-articular erosions Juxta articular osteoporosis Subluxation
347
What are the features of synovial fluid on RA?
Incerased WBC Increased protein
348
What is the presentation for shoulder dyslocation?
Pain Decreased movement Loss of deltoid coutour Arm held internally rotated and adducted
349
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
350
When are posterior disocations more likely to happen?
Secondary to epileptic seizures
351
What is the most common type od seizure?
Antero-inferiorly
352
Who is affected by frozen shoulder?
It is most common in middle-aged females. The aetiology of frozen shoulder is not fully understood. Associations ## Footnote diabetes mellitus: up to 20% of diabetics may have an episode of frozen shoulder
353
What are the features of adhezive capsulitis?
Features typically develop over days ## Footnote 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
354
What is the management of rozen shoulder?
Management ## Footnote no single intervention has been shown to improve outcome in the long-term treatment options include NSAIDs, physiotherapy, oral corticosteroids and intra-articular corticosteroids
355
What is the difference between golfers elbow and tennis elbow?
356
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
357
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
358
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
359
Where is a cervical prolapse most likely to happen?
Most commonly C5/6
360
Where is a thoracic prolapse most likely to happen?
T11/T12
361
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
362
What are investigations for cauda equina syndrome?
MRI PR exam Lumbar CT myelogram if MRI is contraindicated
363
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)
364
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
365
Which condition is better walking up hill vs worse walking downhill?
Spinal claudication
366
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
367
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
368
What is the presentation of central cord syndrome?
Weakness of arms moreso than legs, perianal sensation and lower extremity power is preserved
369
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
370
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
371
What are investigations for Traumatic subarachnoid haemorrhae?
CT Cerebral angiogram
372
What is the cause of paget's disease of the bone?
Excessive bone resorption follwoed by disorganised compensatory bone formation
373
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
374
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
375
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)
376
What are bloods in paget's disease?
Normal Ca2+ but raised alkaline phosphatase
377
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
378
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)
379
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
380
What is osteomalacia?
normal bony tissue but decreased mineral content rickets if when growing osteomalacia if after epiphysis fusion
381
What is the presentation of osteomalacia?
rickets: knock-knee, bow leg, features of hypocalcaemia osteomalacia: bone pain, fractures, muscle tenderness, proximal myopathy
382
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
383
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)
384
What is the management of osteomalacia?
calcium with vitamin D tablets
385
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
386
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
387
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
388
What are the two ways of assessing osteoporosis fracture risk?
FRAX Qfracture
389
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)
390
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) ## Footnote 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).
391
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
392
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
393
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
394
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 ( rheumatic: rheumatoid arthritis, ankylosing spondylitis, polymyalgia rheumatica, osteomalacia GI: inflammatory- UC and Crohns liver- PBC, CAH, alcoholic cirrhosis, viral cirrhosis (hepC) malabsorption- CF, chronic pancreatitis, coeliac disease, Whipple’s disease, short gut syndromes, ischaemic bowel medication, chronic renal failure medications, steroids, PPI, enzyme inducting antiepileptic medications, aromatase inhibitors, GnRH inhibitors, warfarin
395
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
396
What medications might predispose you to osteoporosis?
Steroids PPI Enzyme inducting antiepileptic mediations Aromatase inhibitors GnRH inhibitors Warfarin
397
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)
398
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
399
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)
400
What are the blood results for SLE?
bloods: Coomb’s +ve haemolytic anaemia, neutropenia, lymphocytopenia, thrombocytopenia, increased ESR, normal CRP, renal profile
401
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
402
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.
403
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
404
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
405
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)
406
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
407
Are antinulear antibodies and RF present in scleroderma?
ANA positive in 90% RF positive in 30%
408
What is the treatment for scleroderma?
409
What is the cause of sjogren's syndrome?
Chronic autoimmuned infalmmatory disease Lymphocytic infiltration Destruction of exocrine glandsof eyes and mouth
410
What are the causes of sjogrens?
Primary = sicca syndrome Secondary (to other autoimmune diseases, RA is the most common)
411
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)
412
What are blood results for sjogren's?
Leukopenia Thrombocytopenia Anaemia Increased ESR
413
What are the findings in the urine for sjogren's?
Proteinuria/haematuria reflecting glomerulonephritis
414
What would you find in a salivary gland biopsy in sjogren's?
Focal lymphocyte foci (collections of tightly aggregated lymphocytes)
415
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
416
What test can measure tear production in Sjogren's?
Schirmer's test: filter paper near conjunctival sac to measure tear formation
417
What is the treatment for Sjogren's?
artificial saliva and tears pilocarpine may stimulate saliva production Moderate to severe SS = immunosuppressive treatment
418
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).
419
Who is more likely to be affected by Sjogren's?
Sjogren's syndrome is much more common in females (ratio 9:1).
420
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)
421
What is the triad of granulomatosis with polyangitis?
Focal necrotising vasculitis Necrotizing granulomas in the upper airway, lungs Necrotizing glomerulonephritis (renal vasculitis)
422
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
423
What is the blood marker for granulomatosis with polyangitis?
c-ANCA
424
What are the features of polymyositis and dermatomyositis?
Polymyositis = proximal muscle weakness Dermatomyositis = proximal muscle weakness + gottron's papules and heliotrope rash
425
What is the specific antibody for polymyositis?
Jo-1 (this is a specific ANA profile)
426
What disease affects large vessles?
Giant cell arteritis Takayasu arteritis
427
What type of vasculitis affects medium sized vessels?
Kawasaki's disease Polyarteritis nodosa
428
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
429
How do we diagnose giant cell arteritis?
Extremely elevated ESR (over 100mm/hr) Temporal artery biopsy
430
What is the general treatment for multi-system autoimmune diseases?
431
What is the treatment for GCA?
Corticosteroids
432
What is the treatment for Wegners?
Corticosteroids Cyclophosphamide / rituximab
433
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)
434
What type of hypersensitivity is present in Sjogren's syndrome? (in reference to the destruction of lacrimal and salivary glands)
Type 4
435
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)
436
What are the investigations for ankylosing spondylitis?
X-ray of lungs (remember they have apical fibrosis and restrictive lung disease) MRI Bloods
437
What are the findings of bloods on ankylosing spondylitis?
Chronic anaemia RhF negative Increased ESR
438
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
439
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
440
What clinical test could be used to show reduced forward flexion in ankylosing spondylitis?
Schober's test
441
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
442
What are the nail changes associated with psoriatic arthritis?
Oncholysis Transverse nail ridging Nail pitting
443
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
444
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
445
What are blood findings in psoriatic arthritis?
Raised ESR RhF negative ANA negative
446
What are imaging findings in psoriatic arthritis?
imaging: XR (para-marginal erosions, fluffy periosteal bone formation, **bony ankylosis, asymmetrical sacroiliitis**
447
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
448
What infections might cause reactive arthritis?
Infections include- Salmonella, Shigella, Yersinia, Campylobacter, Chlamydia trachomatis or pneumoniae, Borrelia, Neisseria and streptococci Infections- throat, urogenital & GI
449
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)
450
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)
451
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
452
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
453
What is the crystal in both gout and pseudogout?
Gout = monosodium urate Pseudogout = Calcium pyrophosphate
454
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**
455
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
456
What is the difference in crystal histology for gout and pseudogout?
Gout = needle shaped, negatively birefringent Pseudogout = Rhomboid, positively birefringent
457
What are the complications of gout?
Stone passage causing renal colic Renal failure - death in 20% of individuals with chronic gout
458
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
459
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
460
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)
461
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.
462
Gout vs Pseudogout comparison
463
What are the causes of pseudogout?
Sporadic Hereditary component Secondary to previous joint damage, hyperparathyroidism, haemachromatosis, hypothyroidism, ochronosis, diabetes
464
What are risk factors for pseudogout?
Usually affects individuals over 50 years Decreased magnesium levels
465
What is treatment of pseudogout?
Acute flares: NSAIDs Colchicine Glucocorticoids Management and prevention: Colchicine
466
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
467
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
468
What are causes of polymyalgia rheumatica?
Genetic defects (assocaited with HLA DR4) Exposure to adenovirus / human parovirus B19
469
What is the treatment for polymyalgia rheumatica?
Low dise corticosteroids The condition can regress after 1 or 2 years (or it can remain chronic)
470
What condition is polymyalgia rheumatic closely related to?
Giant cell arteritis
471
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
472
What are potential complications of fractures?
Compartment syndrome Refracture Non-union Superficial radial nerve injury Posterior interosseous nerve injury
473
What is a galeazzi fracture?
fracture of radial shaft with dislocation of the distal radio-ulna joint
474
What is a monteggia fracture?
Fracture of proximal ulna with dislocation of radial head
475
What is the most common type of fracture in a child?
Forearm fracture - 80% of which occur in the distal third
476
What is the presentation for hallux valgus (forefoot problems)
**bunions**, pressure symptoms from shoe wear, pain from crossing over of toes, **metatarsalgia**
477
What are the investigations for hallux valgus?
clinical, XR (determine severity of underlying bony deformity, exclude associated degenerate change)
478
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
479
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
480
What is the aetiology of hallux valgus?
Genetic foot wear
481
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
482
What is the presentation of hallux rigidus?
Stiff big toe Asymptomatic Pain (often at extreme of dorsiflexion) Limited ROM
483
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
484
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?
485
What is hammer toe?
hammer toe is flexion between proximal and intermediate phalanx of any lesser toe
486
What is claw toe?
Flexion between proximal and intermediate phalynx AND between intermediate and distal phalynx of any lesser toe
487
What is mallet toe?
mallet toe is flexion between intermediate and distal phalanx of any lesser toe
488
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)
489
What is operative treatment of lesser toe deformities?
flexor to extensor transfer **fusion** of interphalageal joint release of metatarsophalangeal joint shortening **osteotomy** of metatarsal
490
What is the cause of lesser toe deformities?
Imbalance between flexors/extensors Shoe wear Neurological Rheumatoid arthritis Idiopathic
491
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
492
What is midfoot arthritis management?
Activity/shoewear/orthotics XR guided injections Fusion
493
What is the pathophysiology of midfoot arthritis?
Post-traumaic arthritis Osteoarthritis Rheumatoid arthritis
494
What are the signs and symptoms for plantar fibromatosis?
asymptomatic unless very large or on weightbearing area
495
What is the cause of plantar fibromatosis?
Progressive connsctive tissue build up
496
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)
497
What are the tests for achilles tendon rupture?
Simmonds - squeeze test Matles test - angle of dangle
498
What are investigations for achilles tendonopathy?
USS MRI
499
What is the management for achilles tendonopathy?
Non-operative: ## Footnote 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
500
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)
501
What are the investigations for plantar fasciitis/fasciosis?
diagnosis is clinical mainly, XR, USS and MRI
502
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
503
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?)
504
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
505
What tendon dysfunction might cause medial or lateral pain and cause medial heel to move inwards and downwards?
Tibialis posterior tendon dysfunction
506
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)
507
What are the investigations for tibialis posterior tendon dysfunction?
Clinical MRI to assess tendon
508
What is the management of tibialis posterior tendon dysfunction?
orthoses or surgery (reconstruction of tendon (tendon transfer), triple fusion (subtalar, talonavicular and calcaneocuboid)
509
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
510
What is the name of the foot deformity assocaited with diabetic foot?
Charco neuropathy
511
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)
512
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)
513
What is management of RA?
effective suppression of inflammation will improve symptoms and prevent joint damage and disability ## Footnote 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
514
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.
515
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
516
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)
517
What are immunology findings in RA?
immunology: rheumatoid factor IgG, IgM anti-cyclic citrullinated antibodies (anti CCP, ACPA) ANA(?)
518
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
519
520
What are normal hormonal changes for the start of labour?
Progesterone decreases whilst oxytocin and prostaglandins increase to allow for labour to initiate
521
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
522
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
523
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
524
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.
525
What are different types of vertex presentation?
Vertex Sinciput (forehead) Brow Face Chin
526
What is the most common presentation of a baby?
LOA
527
Which bone in normal labour is the presenting part?
Anterior parietal
528
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
529
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).