Block 9: RA, SLE Flashcards
RA diagnostic criteria
- Two or more swollen joints
- Morning stiffness
- Rheumatoid Factor
Investigations in RA
- Blood Tests: FBC (neutropenia, normocytic anaemia), ESR, CRP, Rheumatoid Factor (not specific), Anti-CCP, ANA
- Plain X-ray
RA synovium joint
Immune mediated destruction, causes thickening of synovium and joint diffusion. Destruction of articular cartilage and erosion of the subchondral bone resulting in cysts. Starts to affect the ligaments causing joint instability.
RA: x-ray
- Narrowing joint space
- Marginal erosions: due to destruction of subchondral bone
- Periarticular osteopenia: due to disease and side effect of steroids
- Irregular joint surface
- Deformity / subluxation (patrial disarticulation of joint) / dislocation
- Soft tissue swelling
- Secondary Osteoarthritis: can affect hips and knees
- LESS
RA: surgery
- Early and intensive pharmacological treatment in the critical first few months of disease - ‘window of opportunity’
- Overall reduced rates of surgical intervention on patients with RA
- Main indications for surgery - pain relief / improvement in function
- Correcting deformities; stabilising joints; decreasing disability
- Types of surgery: Arthroscopy and synovectomy; tendon transfer; resection arthroplasty; arthrodesis; total joint replacement
Nerve conduction study/Electromyography
- NCS: test function of peripheral nerves by the speed of electric current conduction
- EMG: tests electrical activity produced by skeletal muscles
- Helps diagnose peripheral neuropathy like in carpal and cubital tunnel syndrome
Types of surgery for RA
- Tendon transfer: when there is tendon rupture, move a tendon from a functional unit to a compromised one. Tend to be in hand
- Arthrodesis: fusion of joint, causes reduction of pain but loss of function as the joint can no longer move. Ankylosis is when the disease causes fusion of the joint- causes pain.
- Excision arthroplasty: the metatarsal heads are excised allowing freer movement at the joints. Metal wires are then inserted to stabilise the joint, removed a few weeks after the surgery. Helps with pain relief can cause instability
- Arthroscopic synovectomy: removal of inflamed synovium
Indications for total joint replacement
- Painful synovitis / swelling
- Reduction in range of movement (lack of full extension)
- Ulnar nerve neuropathy (compression by inflamed synovium): cubital tunnel syndrome
- Laxity of soft tissues (ligaments) > instability
- Destruction of articular surfaces (joint erosion / cyst formation / bone loss)
RA steroid injections
Relieve symptoms and reduce need for joint replacement. Aseptic technique, given every 4 months, repeated injections can weaken ligaments. Don’t do injection within 6 months of joint replacement
SLE
- Peak incidence 20-35
- Strong genetic component: HLA-DRB1
- Common in afro-caribbeans
- Potential triggers: EBV, family history
- Drug induced lupus: Hydralazine, Isoniazid, Chlorpromazine, Minocycline, TNF inhibitor
- Photosensitive rash: often in butterfly distribution but not always, avoids eyelids
- Fatigue
- Arthritis: symmetrical polyarthropathy similar to RA though non deforming i.e. can still make fist and no x-ray changes
Other SLE symptoms
- Alopoecia: patches of baldness
- Headaches
- Sicca symptoms: dryness of eyes and mouth
- Mouth ulcers: large, painful
- Pleuritic chest pain
- Raynaud’s phenomenon: colour change in the cold- white → blue/purple, when rewarming go red
- Recurrent miscarriages
- Can affect other systems: renal, Neurological/psychiatric (personality change, psychosis), haematological, can mimic other conditions
SLE investigations
- FBC: normochromic, normocytic anaemia with leukopenia and thrombocytopenia
- renal function (urinalysis, urineprotein:creatinine ration, renal biopsy), ESR, CRP, others depending on symptoms/signs
- ANA positive in 95%
- Anti-smith antibodies: most specific but present in less than half of cases. Antibodies are diagnostic
- dsDNA, complement C3 and C4 – useful as disease activity markers. With disease activity dsDNA rises and complement falls
- Lupus anticoagulant (causes clotting), antiphospholipid antibodies
- BP and urinalysis
SLE organ specific symptoms
- Renal disease: often asymptomatic till late stage, lupus nephritis
- Pregnancy loss, obstetric complications: lupus tends to get worse during pregnancy
- Respiratory: pleuritis, pneumonitis, pulmonary emboli
- Thrombotic risk
- Cardiovascular: Pericarditis, Raynaud’s, endocarditis, Atherosclerosis
- Neuropsychiatric: Headache or migraine, seizures, psychosis
- Complications of treatment
SLE treatment
- Education and advice
- NSAIDs
- Sun block: for the rash but also sun increases disease activity generally
- Nutrition: healthy diet
- Smoking cessation
- Steroids for flares of arthritis
- DMARDs: Hydroxychloroquine (first line)
- Moderate to severe: Methotrexate, Azathioprine, Mycophenolate, Cyclophosphamide (fertility risk if male or female). DMARD’s
- Biologic drugs: Rituximab, Belimumab for more severe SLE
- Psychological support: CBT, support groups
Skin manifestations of SLE
- photosensitive ‘butterfly’ rash
- discoid lupus: discoid raised patches with scaling and follicular plugging
- alopecia
- livedo reticularis: net-like rash. Mottled skin rash with purple discolouration
Lupus criteria
- Uses 11 criteria of which 4 or more are required for diagnosis
- Malar rash.2 clinical and 2 laboratory
- Discoid lupus
- Photosensitivity
- Non-erosive arthritis involving 2+ peripheral joints
- Oral or nasopharyngeal ulcers
- Pleuritis or pericarditis
- Renal involvement
- Seizures or psychosis
- Haematological disorder: Haemolytic anaemia, Leukopenia, Lymphopenia, Thrombocytopenia.
- Immunological disorder: Anti-DNA antibody, Anti-Sm, Antiphospholipid antibodies.
- Positiveanti-nuclear antibody
SLE complications
- Infection: made worse by treatment
- Lupus nephritis: more closely associated with positive anti-dsDNA SLE. Typical nephritic picture of peripheral oedema and haematuria
- Atherosclerosis: particularly bad if antiphospholipid syndrome as well
- Osteoporosis: often due to early menopause, reduced sun exposure and glucocorticoids
- Malignancy: particularly haematological, cervical or lung
Diffuse pleural thickening (DPT)
- Asbestos related lung disease
- Diffuse pleural thickening in a similar pattern to empyema or haemothorax, occurs after BAPE in 40% of cases.
- Can be uni or bilateral and involves both the visceral and parietal pleura.
- On X-ray it appears as a smooth, conglomerate opacity along the pleura. On CT the pleura must be > 3mm thick.
- Causes pain and breathlessness from lung restriction.
- VC and TLCO will be low
Gonadotropin adenoma
Women:
- If hypogonadism: Hot flushes, vaginal dryness
- If hypergonadism: Irregular menstruation, ovarian hyperstimulation syndrome
Male:
- If hypogonadism: Mood swings, decreased libido
- If hypergonadism: Enlarged testicles, deeper voice, balding on temples
Somatotroph adenomas
Secrete growth hormone
- Cause acromegaly
- Enlarged hands, feet, head size, rounded face, macroglossia, frontal bossing
- O/E: Hypertension, T2DM, hypertrophic heart, carpal tunnel syndrome
Pituitary apoplexia i.e. Sheehans syndrome
Sudden onset vision loss, headache, hydrocephalus, neck stiffness, visual field defect, extra-ocular nerve palsies
Management: Urgent steroid replacement, Careful fluid balance
What are the different types of thyroid nodules
Solitary nodules
Multiple nodules
Hyperplastic nodules
Thyroid follicular adenomas (most common)
Thyroid cyst
Thyroid cancer
Risk factors for thyroid nodules
Increasing age, female, pregnancy, low iodine consumption, radiation exposure, smoking, FHx
- Uncommon in children and adolescents but risk of them being malignant in age group higher
How thyroid cancer presents
As a thyroid nodule
- Tend to be hard/firm nodules that are non-tender on palpation
- Firm cervical masses can suggest lymph node infiltration
When are you concerned for thyroid cancer if there is a thyroid nodule
Nodules >4cm
Firmness to palpation
Fixation of node to adjacent tissue
Cervical lymphadenopathy
Vocal fold immobility
Investigations for thyroid nodules
Bloods: TFT
Imaging: Thyroid USS
Special tests: Thyroid fine needle biopsy
Criteria for referal to endocrinology in thyroid nodules
Same day referral: associated stridor
2WW:
- Unexplained hoarseness/voice changes
- associated with goitre
- Thyroid nodule in child
- Palpable cervical lymphadenopathy
- Rapidly enlarging painless thyroid mass over weeks
Non-urgent
- Abnormal TFTs and thyroid nodule
- Sudden onset of pain in thyroid lump
Management of thyroid nodules
Most benign nodules don’t need any intervention unless compressive symptoms
Malignant/suspicious thyroid nodules require removal and analysis of aspirate
Thyroid cancer - removal of thyroid gland and levothyroxine treatment. Surgery can cause recurrent laryngeal nerve palsy
Papillary thyroid cancer
Most common
Often in young females
Local METS common but distant uncommon
Excellent prognosis
Management: Total thyroidectomy + radioiodine
Follicular thyroid cancer
10% thyroid cancers
Typically aged 40-60 years
More aggressive but good prognosis
Distant METS common - lung, neck, brain
Management: Total thyroidectomy and radioiodine
Medullary thyroid cancer
Not associated with radiation
lower cure rate
Local METS and distant METS common
What can cause secondary Hyperthyroidism
Pituitary hypoplexy
Lesion compressing pituitary
Drugs: Lithium, amiodarone
Causes of Thyrotoxicosis
Grave’s disease
Toxic multinodular goitre
Iodine excess
Iatrogenic - drugs (Amiodarone, Lithium)
Viral infection: subacute de Guervain’s thyroiditis
Post-partum thyroiditis
Medical treatment for thyrotoxicosis
Beta blockers (propranolol) can be used to provide symptomatic relief
Block and replace: Carbimazole + levothyroxine
Definitive: Radio-iodide
Surgery: Thyroidectomy- considered if causes compression/malignancy. Patients will need long term replacement with Levothyroxine
What thyroid drugs are used in pregnancy
First trimester: Propylthiouracil
Second trimester +: Carbimazole
Complications of thyrotoxicosis
Thyroid storm
Cardiac: AF, HF, angina
Osteoporosis
Causes, management and presentation of thyroid storm
Causes: Thyroid surgery, Trauma, Infection, Acute iodine overload i.e. contrast media
Presentation: Palpitations, fever, Tachycardia, Confusion/agitation, seizures, reduced level of consciousness, N+V
Management: anti-thyroid drug, IV propanolol, IV dexamethasone
Imaging and Management in thyroid eye disease
CT orbit - detect optic nerve involvement
USS - can detect extra-ocular muscle enlargement
MDT with opthalmology and endocrine
Smoking cessation
Hyperthyroidism: Block and replace with carbimazole and levothyroxine
Surgical: Orbital decompression and lid surgery
In compressive optic neuropathy: give urgent IV methylprednisolone
Hepatitis A
- Type of virus: RNA
- Transmission: Faecal-oral route
- Vaccine
- Supportive treatment
Hepatitis B
- Type of virus: DNA
- Transmission: blood/bodily fluids
- Vaccine: yes
- Treatment: supportive/anti-virals
Hepatitis C
- RNA
- Transmission: blood
- No vaccine
- Treatment: direct acting antivirals
Hepatitis D
- RNA
- Always with hepatitis B. Transmitted through blood or bodily fluids
- No vaccine
- Treatment: pegylated interferon alpha over at least 48 weeks. Not very effective has significant side effects
- Hepatitis D increeases the complications and severity of hepatitis B
Hepatitis E
- Type of virus: RNA
- Transmission: faecal oral
- No vaccine
- Supportive treatment
- Very rare in the UK and produces only a mild illness with no treatment required. Rarely it can progress to chronic hepatitis and liver failure but typically in immunocompromised
Hepatitis A presentation
- Usually in contaminated food or water
- Can cause cholestasis (slowing of bile flow through biliary system) with pruritus, significant jaundice, dark urine and pale stools
- Diagnosis is based on IgM antibodies to hepatitis A.
- It usually resolves without treatment.
- Rarely it can lead to acute liver failure (fulminant hepatitis).
- Management is supportive, with basic analgesia.
Hepatitis B treatment
- Most people fully recover within 1-3 months. However 5-15% become chronic hepatitis B carriers
- Screen for other viral infections (e.g., HIV, hepatitis A, C and D)
- Referral to gastroenterology, hepatology or infectious diseases for specialist management
- Avoid alcohol
- Education about reducing transmission
- Contact tracing and informing potential at-risk contacts
- Testing for complications (e.g., FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma)
- Antiviral medication can be used to slow the progression of the disease and reduce infectivity
- Liver transplantation for liver failure (fulminant hepatitis)
Hepatitis B viral markers
Surface antigen (HBsAg) – active infection
E antigen (HBeAg) – a marker of viral replication and implies high infectivity
Core antibodies (HBcAb) – implies past or current infection
Surface antibody (HBsAb) – implies vaccination or past or current infection
Hepatitis B virus DNA (HBV DNA) – a direct count of the viral load
Hepatitis C presentation and treatment
- Curable with direct acting anti-virals i.e. sofosbuvir
- Without treatment 1/4 make a full recovery and the rest develop chronic hepatitis C
- Complications of hepatitis C: liver cirrhosis and Hepatocellular carcinoma
- Hepatitis C antibody is the screening test. Hepatitis C RNA testing confirms the diagnosis and is used to calculate the viral load and identify the genotype
Grave’s antibodies
AChR, MuSK
What NIV
Type 1 respiratory failure: CPAP
Type 2: BiPAP
CNS Lesion presentation
Increased tone and brisk reflexes. Bladder involvement and sensory level
