Psoriasis is a a common chronic inflammatory skin condition, characterised by raised, red, itchy, scaly plaques on the skin. With treatment, it often follows a relapsing and remitting course, although in more severe cases it may never fully remit.

There is a strong genetic component to the inheritance of the disorder, and there are thought to be environmental triggers that bring on the condition in a genetically susceptible individual.

Pathologically, it is caused by a T-cell mediated abnormal immune response. The T cells release cytokines, resulting in keratinocyte proliferation.

Dermatologists may classify psoriasis into various subtypes, such as guttate psoriasis or palmar-pustular. 

In about 10-15% cases it is associated with psoriatic arthritis.

Epidemiology

• Affects 2-4% of the population
• Can start at any age, but has two peaks of incidence:
  • 15-25 years
  • 50-60 years
• 1/3 of patients have a relative with the condition
• More common in caucasians
• Usually life-long

Aetiology

Risk factors include:

• Genetic susceptibility
• Smoking
• Obesity
• Psychological stressors

Pathology

• Parakeratosis: retained nuclei
• Acanthosis: thick epidermis
• Absent granular layer
• Lengthened rete ridges
• Thin dermal papillae
• Dilated, tortuous capillaries
• Munro’s micro-abscesses
• T-cells in upper dermis

Clinical features

• Symmetrical
• Red scaly plaques
  • Scale is usually white or silvery coloured
• Often extensor surfaces – e.g. front of knees, backs of elbows
  • As opposed to eczema which is commonly the flexor surfaces
• Common locations:
  • Scalp (particularly behind ears)
    • Sometimes only the scalp is affected
  • Elbows
  • Knees
  • Can affect any part of the body
• Itchy (!)
  • Often accompanied by excoriation, or in longer term more severe cases – lichenification (thick leathery skin)
• Resolving patches of psoriasis often leave brown coloured marks that generally fade over a period of months

• Classical [or typical or chronic plaque psoriasis]
  • The most common type of psoriasis – approx 90% of cases
  • Plaques: Well-circumscribed erythematous plaques with silver scaling
    • Usually plaques >3cm diameter
  • Distribution: Esp. on extensor surfaces [elbow, knee], scalp/hairline, sacral
  • Features: Pain, itch [but less than eczema/dermatitis]
  • Nail changes – e.g. pits or ridges on nails
  • Auspitzs sign: Bleeding on scale removal
• Guttate psoriasis
  • Age: Young
  • Onset: often follows streptococcal tonsillitis (acute guttate psoriasis)
  • Plaques: Multiple discoid erythematous and scaly macules and plaques on trunk
    • Tend to be smaller than the plaques of typical psoriasis and not in the typical locations (trunk rather than flexor surfaces)
    • Plaques usually <3cm diameter
  • Good prognosis – cases of acute guttate psoriasis often resolve spontaneously after several months
  • In some instances it can become chronic, and chronic guttate psoriasis can often be much more resistant to treatment than classical psoriasis

• Palmoplanar pustular
  • Plaques: Yellow-brown pustules on palms and soles
• Flexoral
  • Plaques: Erythematous, but not scaly
  • Distribution: Submammary, axillary, anogenital, umbilical
  • Epidemiology: Esp. women; also the elderly and HIV +ve
  • Can be difficult to tell apart from eczema or difficult to tell that it is psoriasis due to its unusual distribution
• Erythrodermic [emergency!]
  • Features: Acute onset of erythroderma and pustular plaques
  • Management: Methotrexate
  • Others: only scales; only nails; and napkin

Nails

• Features: Pitting, onycholysis [nail lifting off the bed]; subungal hyperkeratosis; Beaus lines [horizontal, across the nail]
• Differential diagnosis: fungal infection, alopecia areata

Psoriatic arthropathy

• Patterns: [1] AnkSpond-like/spondylitis; [2] RA-like/symmetrical; [3] Asymmetrical, <3 joints;[4] DIP joints, hands; [5] Arthritis multilans

Differential diagnosis

• Dermatitis/eczema: discoid or seborrhoeic
• Lichen planus
• Pityriasis rosea [esp. guttate psoriasis]
• 2^o stage of syphilis
• Reiter’s syndrome [Esp. palmoplanar psoriasis]
• Discoid lupus
• Syphilis

Precipitating factors

• Trauma [known as Koebner’s phenomena]
• Infection
• Drugs: β-blockers, lithium, anti-malarials; NSAIDs and ACE-Is
• Emotional stress
• Sunlight
• Puberty
• Menopause
• Alcohol
• Obesity (insulin resistance)
• Smoking

Associated Disorders

• Psoriatic arthritis
  • Affects about 13% of psoriasis patients
  • Tends to have onset within the first 10 years of onset dermatological psoriasis
  • Also an associated with spondyloarthritis (e.g. ankylosing spondylitis)
• Inflammatory bowel disease
• Uveitis
• Coeliac disease
• Metabolic syndrome
  • T2DM
  • Hypertension
  • Hyperlipidaemia
  • Gout
  • Cardiovascular disease

Management

• Explain the diagnosis and advise about reducing the severity through management of lifestyle factors
• Smoking cessation
• Reduction of alcohol intake
• Weight loss
• Avoidance of sun exposure
• Management of stress / mental health

• Emollients
• Corticosteroids
  • The mainstay of treatment
  • In the past associated with “rebound psoriasis” on cessation of treatment – but this is thought to be rare. Higher risk when used alone and not in combination with vitamin D analogies – and as such are almost always prescribed with vitamin D analogues
  • Start with potent agent – e.g. betamethasone 0.1% (betnovate)
  • Dosing regimen recommends morning application of steroid and evening application of vitamin D analogue
  • Sometimes comes as a combined agent with a vitamin D analogue – such as daivobet or Enstillar Foam (betamethasone + Vit D) – which can greatly improve compliance!
  • If not responsding to steroids, or steroids + Vit D used separately, consider swapping to daivobet +/- adding coal tar preparations
  • Be aware of side effects of long term use of topical steroid agents – include stretch marks (striae) and skin atrophy / thinning of the skin
  • For the face, advise steroid only, not a combination – e.g. hydrocortisone 1%
• Vit. D analogues
  • Calcipotriol, tacalcitol and calcitriol
  • Mechanism: ↓ cell proliferation
  • Side-effects: Skin irritation, hypercalaemia if overuse
• Coal tar preparations
  • Mechanism: Inhibit DNA synthesis
  • Problems: Smelly, messy
  • Less concentrate version are less messy and just as effective (1-5% coal tar)
  • Scalp psoriasis is particualyl difficult to treat and is the most commonly used location for coal tar
• Dithranol
  • Anthralin
  • Mechanism: ↓ cell proliferation
  • Side-effects: Irritates neighbouring normal skin, stains clothes purple
• Keratolytics
  • Salicylic acid
• Retinoids
  • Tazarotene

Systemic

Usually only initiated in a secondary care setting

• Phototherapy
  • UVB for classic/plaque and especially for guttate psoriasis
    • Narrow band UVB therapy has a low risk of burning and ow risk of long-term sun damage. It is used before UVA
  • PUVA
    • Used in cases not responsive to UVA
    • Stands for “photochemotherapy UVA”
    • More likely to cause long-term skin damage and increases risk of skin cancer
    • Often used in combination with retinoids to reduce the dose of PUVA
• Retinoids
  • Acitretin
  • Note: Therapeutic effect after 4-6 weeks; used for <6 months
  • Side-effects
    • Teratogenic for up to 3 years
    • Dry mucous membranes: skin, eyes, lips [may cause epistaxis]
    • Others: hepatotoxicity; deranged lipid profile
•  Immunosuppressants
  • Methotrexate
  • Also ciclosporin, azathioprine, and hydroxyurea
  • Often used when all the above have failed
  • usually used in short-courses of 4-12 weeks and repeated in case of relapse
• Biological agents
  • Used when treatment to all else has failed or is contraindicated
  • Examples: etanercept, adalimumab, infliximab

Complicated regains of various topical agents lead to poor compliance and often then poor response to treatment.

Typical Regimen

Treating classic/typical psoriasis

• 1^st line: Vit. D analogues +/- topical steroids + tar or salicylic acid ± UVB
• 2^nd line: Retinoids, PUVA, UVB, immunosuppressants
• 3^rd line: Dithranol
• Goekerman regime = Tar + UVB
• Ingram regime = Goekerman + dithranol

Indications for referral

The majority of cases of psoriasis is managed in primary care. Possible indications for referral to dermatology include:

• >10% body surface area affected
• Psoriasis not responding to topical treatment
• Psoriasis in children
• Psoriasis having a major impact on psychological health

Complications

• Mental health disorders – e.g. depression or anxiety, secondary to their skin condition
• There is an associated with psoriasis and reduced rates of employment

Prognosis

• Course is very variable
• Often relapses
• Poor prognostic factors include strong family history and early age of onset
• Over-use of steroids can cause pustular flares – which can cause serious systemic infection

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Psoriasis – Dermnet NZ
• Psoriasis – Patient.info

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Definitions

• Psoriasis – umbrella term for the condition, but often used to describe the disease when only skin lesions are present. Affects 1-3% of the population
• Psoriatic arthritis – describes the joint involvement of the condition

Skin changes

• Inflammation and production of excess skin, causes characteristic erythematous lesions, with silvery ‘plaques’.
• Plaques are common at the knees and elbows, but can occur anywhere
  • Unlike eczema, they tend to occur on extensor surfaces, and around pressure points.

Nail changes

• Psoriatic nail dystrophy – particularly associated with psoriatic arthritis, and rarer in patients who suffer only skin changes.
• The nails will often be discoloured (a yellow/brown patchy colour)
• May also be onycholysis
• May be ‘pitting’ – small (needle sixed) little pits in the nail surface
• Subungal hyperkeratosis – where there is proliferation of the deeper keratine layers of the nail – causing the smooth nail surface to be raised, whilst a mesh of keratin grows underneath.
• ridging

Psoriatic Arthritis

Epidemiology and Aetiology

• Genetic component
  • Often a family history – which can aid the diagnosis
  • HLA-B27 – present in 50% of those with spinal signs
• Cause basically unknown
• Smoking and excessive alcohol intake may increase the risk of getting the condition
• Often associated with:
  • Rheumatoid Arthritis
  • Spondyloarthritides

Clinical features

• Can essentially present with any variation of arthritic symptoms!
  • Often indistinguishable from RA, but is seronegative, and in association with skin signs, should be considered a separate condition.
  • Usually an oligoarthritis (2-5 joints, usually asyymetrical), usually weight bearing joints.
• Check for psoriatic skin lesions, may not be obvious, and patients themselves may not even know they have them. Check specifically the
  • Natal Clef
  • Scalp
  • Umbilicus
• Check for nail changes
• In a minority of cases, the arthritis presents before skin and nail changes. In which case, you may be able to identify typical features of spondyloarthritides:
  • Dactylitis – literally – sausage shaped digit – results from inflammation of the whole finger
  • Enthesopathy – involvement of the enthesis. Can include enthesitis.
• Osteolysis – perhaps the most characteristic sign. As the bone in the fingers is lost, there may be telescoping of the fingers
• Spinal involvement – typically at the sacrum

Investigations

• Synovial biopsy – not routinely performed, but will show pathological differences from rheumatic conditions, even when the disease closely resembles RA.
• Radiographs – may show osteolysis, which appears as a ‘pencil-in-cup’

Treatment

• Essentially follows that of the condition of which features are most prominent…
• Treat as if RA – if RA signs are prominent
  • Methotrexate and leflunomide are the DMARD’s of choice. Hydrochlorequine is avoided as it exacerbates skin disease
  • Evidence for the efficacy of DMARD’s in PsA is not very conclusive
  • Anti-TNF-α treatments have not been used for very long, but look very promising!
• o   Treat as if AS – if AS signs are prominent

Prognosis

• PsA patients score slightly worse on QOL scores than the general population:
  • 1.0 is average value for general population
  • 0.9 is Psa
  • 0.8 in RA
• Slight increased mortality (1.6x normal risk)
  • Mainly due to increased risk of cardiovascular disease

References

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Aetiology

• Associated with STI – most commonly chlamydia – and typically affects men aged 20-40.
• Associated with GI infection:
  • Less common than STI involvement
  • Could be salmonella, shingella, Yersinia, or campylobacter

Presentation

• Acute, asymmetrical, polyarthritis
• The classic triad of:
  • Conjunctivitis – can’t see
  • Non specific urethritis – can’t pee
  • Acute arthritis – can’t bend the knee
• May be an oligoarthritis
• Tends to affect the large joints, particularly the ankle and knee. May sometimes involve the feet.
• May also involve:
  • Keratinous brown plaques on soles and palms
  • Mouth ulcers
  • Fever
  • Fatigue
  • Weight loss
  • Pustular vesicles (rare) – sometimes look like those seen in psoriasis
  • CNS involvement (rare)
  • Cardiovascular involvement (rare)
• Can vary from a very mild arthritis, to a serious multi-systemic condition.
• Presents 1-4 weeks after the initial infection

Pathology

Diagnosis

• High degree of clinical suspiscion:
  • STI / GI infection
  • Acute onset polyarthritis of lower limbs and feet
• Bloods:
  • ↑ESR
  • ↑CRP
• Consider:
  • Stool sample / culture
  • Test for chlamydia / other STI infection

Treatment

• Rest / splint affected joints
  • Up to 50% will resolve within 4 months
• Use NSAID’s and Steroid injections if necessary
  • These only provide symptomatic releif
  • Steroid injections are only rarely indicated in more severe cases of large joint involvement
• In some cases, may be chronic. This can result in deformity. In some patients, it may also relapse and remit. In these individuals, consider:
  • Sulfasalazine
  • Methotrexate

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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Features of inflammatory arthritis

• Pain and stiffness worse in the morning and after rest
  • Early morning pain and stiffness may last several hours (in OA, duration is much shorter)
• Inflammatory markers (ESR, CRP) usually raised
• Often accompanied by normochromic, normocytic anaemia

Rheumatoid Arthritis

Epidemiology and Aetiology

• affects 0.5-3% of the population worldwide
• can present at any age (from childhood to old age), but the peak incidence is between 30-50 years
• women affected more than men (M:F – 1:2)
  • before the menopause, risk is 3x higher for women
  • after the menopause it is equal
  • suggests sex hormones involved in some way
  • the contraceptive pill can delay the onset, but does not reduce the risk
• Genetic factors are involved. Certain HLA variants are implicated, especially in severe forms of the disease:
  • HLA-DR4 – occurs in 50-75% of patients, and is associated with a particularly poor prognosis
  • HLA-DR1 is another variant associated with RA, and poor prognosis
• Environmental factors:
  • Smoking
  • Stress
  • Infection

Clinical features

• symmetrical swollen distal joints
• Often warm and tender joints
• sometimes presents as a sudden onset of widespread arthritis, but this is rare.
• Typically the joint of the hand (MCP, DIP and PIP’s)and the distal metatarsals of the foot.
• Sometimes it affects the wrists, elbows, shoulders, knees and ankles.
• Hips are very rarely affected
• Limitation of movement
• Muscle wasting
• Pain and stiffness – worse in the morning, may improve with activity. It is often described as an ache type pain.
• Disturbed sleep
• Nodules – in the early and mild stages of the disease, there are relatively few inflammatory cells in the joints. As the disease progresses, these increase in number and there may be nodular masses of inflammatory cells within the joint. Rheumatoid nodules occur when these inflammatory cells form similar inflammatory structures outside of the joint capsules. The nodules are usually pink/red and have a rubbery texture. They are painless. You should always check the elbows in a hand exam, looking for rheumatoid nodules!
• Osteoporosis – often occurs in the bones immediately around the affected joints, particularly in the fingers. This may be the first sign of RA.
• Secondary Osteoarthritis
• Deformity – as the joint capsule is destroyed, and the articular surface damaged, deformity occurs. Specific examples include
• Hands
  • Swan necking – the fingers become hyperextended at the PIP, and flexed at the DIP
  • Z-thumb
  • Subluxation of the MCP –not that this is not swelling!
  • Muscle wasting – “guttering” – ‘gutters’ seen between the extensor tendons on the back of the hand.
    • Why do the muscles waste so quickly in joint disease? – in a normal individual, if you don’t use a muscle, it will waste at a rate of about 1% of its mass/day. However, in joint disease, the rate of wasting in much greater. This is because in joint disease, there is inhibition of nerve afferents, for nerves that innervate the muscles around a joint. This alters the muscle tone/reflex feedback loop, leading to decreased innervation of the muscle, and as a result, wasting occurs very quickly.
  • Inflamed flexor tendon sheaths – these serious impair function.
  • Carpal tunnel syndrome is common
  • Ulnar deviation – the fingers point towards the ulnar side
  • Fixed flexion deformity – aka buttonhole or boutonniere deformity
• Shoulders – Shoulders are commonly affected, and at first it may mimic rotator cuff tendonitis. Later, the joint becomes stiffened. Rotator cuff tears can occur late on.
• Elbows – less commonly affected. Flexion may be lost, which makes eating very difficult
• Knees – massive synovitis and effusion. These respond well to steroid injection and aspiration. A persistent effusion may increase the risk of cyst formation, and these can rupture. Varus or valgus deformity can occur, and there may be joint space narrowing and secondary OA.
  • Knee replacement can restore much of the function, and relieve pain.
• Cervical spine – pain in the neck is more commonly muscular, but you can get joint disease itself in the cervical spine. There can be bone destruction, which poses a risk to the spinal cord.
  • Be wary loss of sphincter control, or unexplained weakness in late RA – could be due to cord compression!
• Feet – often the first signs of the disease may only be in the feet. The patient may describe an uncomfortable sensation that feels like walking on marbles. This is due to subluxation of the heads of the metatarsals in the feet.

Systemic Signs

• Subcutaneous rheumatoid nodules
  • Occur in about 1/3 of patients, usually in severe progressive cases. They most commonly occur on the extensor surfaces of the forearm, and sometimes on the dorsum of the foot. Sometimes also on the Achilles tendon.
  • They have a central area of necrotic collagen, surrounded by marcophages and fibroblasts. This resembles the synovitis – but there is no synovium!
  • Usually 2-4cm in diameter
  • Firm
  •  Occur over pressure points
  • Can be removed surgically, or injected with corticosteroids, and they will reduce over time if they are problematic, however, they will usually recur.
• Swollen bursae – particularly the olecranon.
• Anaemia – almost always occurs, and is usually normocytic, normochromic. Can sometimes be iron-deficiency related, due to NSAID’s.
• Lymphadenopathy – nd can
• Splenomegaly
• Sjogren’s syndrome
  • Salivary glands and tear ducts are destroyed, resulting in dry eyes and dry mouth
• Vasculitis – a very poor prognostic sign. Usually occurs in the fingers. It is the result of immune complex deposition in arterial walls. Smoking greatly increases the risk. Signs to look out for include:
  • Nail fold infarcts
  • Necrosis of the skin
  • Bowel infarction – due to arterial involvement in the bowels
• Septic arthritis – serious! – has a high mortality and morbidity. May present as a sudden onset effusion. Any sudden onset effusion needs to be aspirated! Staph. A. is the most common causatory organism. Treat with systemic AB’s and drainage.
• Amyloidosis
• Heart signs:
  • Pericarditis – rare, but in 30% of seropositive patients, there is some pericardial involvement
  • Endocarditis – even rarer
• Raynaud’s phenomenon
• Peripheral neuropathies – often in glove and stocking pattern. May also get mononeuritis multiplex (many nerves involved, but not in a distinct pattern). Usually sensory.
• Kidneys – nephrotic syndrome and renal failure
• Ruptured tendons
• Ruptured Baker’s cysts
• Depression – commonly occurs in RA patients

Eye Changes in Rheumatoid arthritis

• Dry eyes – can be managed with artificial tears.Also common in Sjogren’s syndrome – an autoimmune disorder associated with RA
• Episcleritis – inflammation of the covering of the sclera. Often causes mild discomfort and redness of the eye. Managed with steroid eye drops and anti-inflammatories. The blood vessels can look particularly prominent.
• Scleritis – inflammation of the sclera (White part of the eye). Causes constant severe eye pain. More serious than episcleritis, and often requires referral to ophthalmology. May be managed with steroid eye drops and anti-inflammatories.
  • in scleritis and episcleritis, the sclera can become thin. It may appear blue due to thinning, and sometimes the contents of the eye ball can bulge out,
• Cataracts – can be caused by inflammatory processes within the eye, but also can be caused by the steroid eye drops used to treat this inflammation. Usually causes cloudy, blurred and/or dim vision. The only effective treatment is surgery for lens replacement.
• Uveitis – inflammation of the interior of the eye. Acute visual loss and pain. May affect the iris, where the boarder of the iris becomes jagged. Treatment is with steroid eye-drops and anti-inflammatories
• Glaucoma – in the case of RA, usually caused by inflammatory processes within the eye. Very dangerous, as it can lead to visual loss. May present with eye pain, gradual visual loss, blurred vision. Can be treated with eye drops, but may require surgery.
• Hydrochlorequine – can cause ‘floaters’ and retinopathy. This is usually reversible and will disappear when the drug is stopped
• Steroids – can cause an eye muscle myopathy – eye movements may be reduced. They can also impair the immune system, making patients more prone to conjunctivitis.  

Pulmonary changes in RA

• Diffuse pulmonary fibrosis – will shows as a restrictive pattern on spirometry. SOB in RA patients can be particularly serious. Often RA patients have very poor mobility, and so when they get SOB,you know it must be sever, because they are hardly doing anything to increase the O2 requirements!
• How to remember the causes of lung fiobrosis:
  • All connective tissue diseases cause lower lobe fibrosis – except AS, which causes upper lobe fibrosis
  • All occupational diseases cause upper lobe fibrosis, except asbestosis, which causes lower lobe fibrosis
  • Remember, the ‘A’ are the exception!
• Lung nodules – these are specific to RA, and are basically the same as the subcutaneous nodules, but they form in the lungs. They are generally asymptomatic, but they can cavitate.
• Pleural effusion – often recurrent

Presentations

• Palindromic – monoarticular attacks, last 24-48 hours. 50% of cases will progress to other types of RA
• Transient – lasts <12 months, then permanently remits. Usually seronegative. No lasting damage
• Remitting – may be active for several years at a time, before remitting. Lasting damage is minimal
• Chronic, persistent – the most common form. May be seronegative or seropositive. Follows a relapsing remitting course over many years. Seropositive patients have worse joint disease and higher risk of long-term disability.
• Rapidly progressive – rapid progression occurs over several years. Severe joint damage, disability and high rate of complications

Pathology

• Various rheumatoid factors are produced in normal individuals, and physyiologically, they are used to remove old IgG from the blood. But in RA, something goes wrong
• About 70% of cases of RA have RF’s in the blood
  • Patients who have seronegative disease tend to have a baetter prognosis, and disease that is just limited to synovial manifestations
•  RF’s are themselves generally IgM, but they can be IgG or IgA.

• Chronic inflammatory synovitis
• Progressive erosion of articular cartilage, which exposes the underlying bone.
• Pannus- this is essentially the inflamed synovium. It damages the cartilage by restricting its normal nutrient flow, and by released inflammatory factors.

Systemic pathology

Cytokines cause:

• fatigue
• atherosclerosis
• increased bone turnover rate

Investigations

• Morning stiffness >1 hour
• > 3 joints involved
• Hands and wrist involvement
• Symmetrical
• Nodules
• Positive RF
• Radiological changes
• Symptoms present for > 6 weeks

Normal initial investigations

• Blood count:
  • Anaemia
  • ESR/CRP raised due to inflammation. Monitoring levels of these can be used to assess treatment
•  Serology – check for rheumatoid factor – only present in 70% of cases.
  • ANA’s – anti-nuclear antibodies – these are also regularly tested for, and show up in 30% of cases
  • Anti-CCP – testing for this is becoming more common.
• X-ray – useful to get a baseline reading at the start of the disease. Normally only soft tissue swellings initially. Later there may be:
  • Boney erosions
  • Osteopenia (lower than normal bone density)
• Joint aspiration – in the presence of effusion. Aspirate will appear cloudy due to the presence of white cells. If the joint is suddenly painful, always aspirate to check for septic arthritis, as this can rapidly destroy joints.
• MRI – very rarely used, but can show early bone erosions. Also used in widespread disease to assess the extent of the joint damage.

Differentials

Management

Symptomatic relief

• In all patients over 65, and those with previous history of GI problems, you should use gastric protection (e.g. omeprazole).

Steroids

• The exact dose and length of regimen that is most beneficial is still not widely accepted
• Remember to look for signs of long-term steroid use when examining for rehaumatological and arthritis conditions! – if there are any, then these patients will nearly always be RA.
• Steroids are also used in acute flare ups of the disease (typically an IM preparation 80-120mg).

DMARD’s – Disease modifying anti-rheumatic drugs

• Methotrexate –an antifolate drug, often used to treat cancer, but also effective in autoimmune disease. Probably the most widely used drug in RA. It generally targets cells with a high turnover rate (folic acid is needed to synthesize DNA)this is generally the first line treatment and is often given weekly (25mg dose) or daily (3mg).
  • Side effects – can cause mouth ulcers, GI upset, (due to the high cell turnover rates in these areas) and possibly liver and haematological disturbances. GI Side effects can be reduced by giving folic acid supplement – folic acid should be taken once per week, and blood test for folate levels taken every two weeks.
    • Liver problems
    • Teratogenic
    • Myelosuppression
    • Rashes
    • Shouldn’t take with alcohol
  • Less effective than anti-TNFs, but also, much cheaper, so NICE recommends try this first, before anti-TNF’s.
• Sulfasalazine – initially used in IBD, also effective in RA. Not quite as well tolerated as methotrexate.
  • Mechanism – not really understood. Thought that it inhibits inflammatory mediators, but does not directly cause immunosuppression.
  • Side effects –myelosuppression, nausea, rash, oral ulcers, decreased sperm count
• Leflonamide – often used as an alternative to sulfasalazine. Similar side effects. Contra-indicated in pregnancy.
• Hydrochlorequine – this is the least toxic of these agents, but probably also the least effective. Causes rashes and retinopathy – vision should be checked at least every 12 months.
• Gold – given IM. More toxic than sulfasalazine or methotrexate. Causes myelosuppression, renal toxicity, mouth ulcers, and photosensitivity
• Cyclosporin
• Azathiaprine

• Myelosuppression – (bone marrow suppression) – can be caused by pretty much all of the DMARD’s. leads to a pancytopenia, and can be dangerous is it greatly increase susceptibility to infection. Can cause death if there is severe sepsis.

• Side effects – can allow the reactivation of latent infections, such as TB – as TNF-α is involved in the maintenance of these latencies. However, these agents are actually usually well tolerated compared to other DMARDs.
  • Long-term safety is not known. Some concerns about increased cancer risk, but unproven.
• Contra-indications – pregnancy / breast feeding, ongoing infection, heart failure

Managing other risk factors

• Cardiovascular disease risk is increased – due to atherosclerotic effects of RA
• Smoking –increases the risk of RA. Stopping smoking may be beneficial

As always, the best care is patient centred, and provided by a multidisciplinary team! – if you are asked about treatment in the OSCE, remember to say these two things!

General Prognosis

Modern treatments have greatly reduced the degree of deformity, and improved function for many patients. However, it many cases it is still very disabling. Many patients are able to cope remarkably well despite reduced function. Functional aids help (e.g. modified cutlery, kitchen tools, and modifications on taps (for turning) and stairways etc.).

There is also an increased mortality risk (About 1.5x that of the general population), due mainly to cardiovascular involvement of the disease. The risk of mortality is increased most in those with extra-articular manifestations, and in the most aggressive disease types.

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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The shoulder is a ball and socket joint with a wide range of movement. The joint is somewhat unusual, in that the “socket” (glenoid) is very shallow, and as-such, much of the stability of the shoulder joint is provided by the rotator cuff muscles and surrounding ligaments and soft tissues, rather than the bony structures. This is what gives the shoulder its unique wide range of movement.

Along with the knee, the shoulder is one of the most commonly presenting joint pathologies. Common shoulder pathologies include rotator cuff injury (usually Supraspinatus – typically associated with a shoulder impingement), AC (acromioclavicular) joint injury, osteoarthritis and shoulder dislocation.

Like all examinations you should have a systematic approach. The most commonly used approach is the Look, feel move approach:

• Look
• Feel
• Move
• Special tests

Explain the examination to the patient, and once you have their consent, wash your hands and ask the patient to expose the shoulders and clavicles bilaterally.

Starting off the examination

Start with the basics:

• Wash hands
• Introduce yourself
• Greet the patient
• Explain the nature of the examination
• Gain consent – which usually involves asking the patient to remove the clothes from the upper half of the body

Inspection (Look)

• Wasting at the side – likely to be deltoid. This could cause the shoulder to become flattened. Often secondary to nerve lesion.
• Wasting at the back – likely to be trapezius

Deformity

• Deformity over the middle of the clavicle – suggests previous fracture
• Deformity over the distal part of the clavicle – may suggest AC joint pathology or subluxation
• Generalised swelling – most likely caused by effusion
• Flex the arm at the elbow – look for ruptured biceps tendon. You will see a large mass of muscle, that can either be near the elbow joint, or anywhere further up the humerus. The “popeye sign”.
• ‘Winged scapula’ – asking the patient to push against a wall can exaggerate this. It is where the scapula is abnormally laterally rotated. It is the result of a lesion of the long thoracic nerve, or of the muscle this nerve supplies – serratus anterior.

Palpation (Feel)

• Acromio-clavicular joint – common site of arthritis. To find this part of the joint, move laterally along the clavicle. It is also commonly damaged in injuries that result from a blow to the shoulder – e.g. falling from a bicycle, rugby injuries to other contact sports or falls
• Greater tuberosity – the insertion point of the rotator cuff muscles
• General Palpation – feel (and sometimes you can also hear it!) for any creptius. This is a crunching, grating feeling inside the joint, indicative of degeneration.
• The subacrominal space – specific tenderness hear can help localise an impingement pathology
• Swelling – feel for any generalised swelling. This can be caused by:
  • Effusion
  • Bursitis
  • Dislocation
  • Previous fractures
• Palpation of the dorsal spine and interscapular area – this area is sometimes called a trigger point for fibromyalgia. Palpating this area in individuals with this condition can elicit pain.

Movement

• Abduction and Adduction – 180 degrees is normal
  • Supraspinatus and deltoid. Deltoid assists from 15 to 90 degrees of abduction, but Supraspinatus does the first 15 degrees all by itself.
  • Suprapsinatus is a common cause of restricted abduction
• Flexion – 180 degrees is normal
• Extension – 180 degrees is normal
• Internal rotation – Ask patient to put the their thumb as high up their back as they can reach. You can measure this in relation to the scapula (should be able to reach inferior border) or the level of thoracic vertebra.
• External rotation – Ask the patient to keep their elbows tucked into their abdomen and external rotate their shoulders. External rotation is particularly badly affected in frozen shoulder (adhesive capsulitis), although this condition limits all movements, and is also affected in glena-humeral joint arthritis. Another test of external rotation is to ask the patient to put their hand behind their head.

Assessing individual muscles

Movements against resistance (isometric contractions)

• Supraspinatus (abduction) – Arms flexed and abducted to 30’, with palms pointing laterally, and thumbs pointing downwards. Patient tries to flex arms further against resistant.
• Infraspinatus / teres minor (external rotation) – Elbow tucked into chest well, flexed at 90’. Patient tries to move palms apart (external rotation) against resistance
• Subscapularis (internal rotation) – Elbow tucked into chest well, flexed at 90’. Patient tries to move palms together (internal rotation) against resistance OR
  • The lift off test – patient has hand behind back (“lifts off” their hand form their back) and pushes backwards against resistance

Special Tests

Hawkins-Kennedy Test

Also tests for for shoulder impingement – which is essentially inflammation of the tendons of the rotator cuff – specifically the supraspinatus tendon. Ask the patient to flex their arm to 90’. Then flex the elbow to 90’ so that this forearm is parallel to the floor. Now, press down on the patient’s wrist and at the same time try to forcibly inwardly rotate the shoulder joint. This is a passive movement, so the patient should be relaxed. This basically presses the tendons of the shoulder cuff against the coraco-humeral ligament. you may also want to repeat the test with external rotation to check the tendon of subscapularis.

• Positive test – pain is elicited. Particularly if the pain is greater, the greater the degree of internal rotation
• Negative test – no pain

The test is not specific enough to give an exact diagnosis – but may help to confirm the diagnosis when there is a strong degree of clinical suspicion.

Scarf Test aka cross-arm test

Apprehension Test

Ask the patient to externally rotate and abduct the shoulder, whilst also flexing the elbow:

• You can double-check your findings. If you repeat the test, but instead, push the patient’s arm backwards, this should releive/not elicit any pain. This is known as the relocation manouvre.
• This tests for shoulder instability / anterior dislocation of the shoulder

The post Shoulder Examination appeared first on almostadoctor.

• Inflammation
• Fibrosis / scarring
• Vasospasm (including Raynaud’s Syndrome)
• Vascular Thrombosis

Epidemiology

• Prevalence is roughly 1 in 4000
• About 10x more common in women!
• 2-3x more common in Indian Asians than Caucasians
• 5x more common in black Africans than in Caucasians
• Can present at any age
  • Peak incidence is between 25-35
  • Second peak of incidence is between 50-60

Aetiology

• Strong genetic disposition
  • Family members 50x more likely to have the disease than members of the general population
• UV light exposure thought to increase the risk
• Drugs
  • Chlorpromazine, hydralazine, isoniazid

Clinical features

Photosensitive rash – can occur anywhere on the body, but typically seen on the face – as this area is most likely to be exposed to the sun!
Nonspecific symptoms

• General malaise
• Fatigue
• Low-grade fever
• Weight loss
• Alopecia
• Mucosal ulceration – particularly in the mouth

Vascular Changes

• Nail edge infarcts
• Splinter haemorrhages

Arthritis – Usually:

• Symmetrical
• Small joints
• Polyarthritis
• The arthritis is non-erosive, and thus the joint is permanently damadged, but there may be ligament damage, which can cause deformities similar to rheumatoid arthritis. However, unlike in RA, the deformities are reducible, and they should not affect joint function – e.g. the patient should be able to make a fist.

Systemic involvement

• Nephrosis – anti DNA antibodies are toxic to the kidney
  • You should always do a urine dipstick on any patient you suspect with SLE! If there is nephro damage it will show up as excess protein on dipstick! – there will also possibly excess blood.

Nervous system involvement

Diagnosis

According to the American College of Rheumatology (ACR), for a patient to be diagnosed with SLE, they must fulfil 4 of the following 11 criteria:
Malar Rash
Oral ulceration
Discoid Rash – a round or oval rash seen on areas of skin exposed to sunlight
Arthritis
Photosensitivity
Serositis
Neurological disorders

• Seizures
• Psychosis

Renal disorder

• Proteinuria (>0.5g/day)
• Red cell casts in urine

Haematological disorder

• Leucopenia
• Lymphopenia
• Haemolyitc anaemia
• Thrombocytopaenia

Immunological disorder

• Antibodies to double stranded DNA
• Anti-Sm antibodies

ANA positive

Investigations

• Urine dipstick – increased protein, red cell casts
• Blood – anaemia, thrombocytopenia, leukopenia, lymphpaenia, raised ESR and CRP.
• ANA testing – positive in 90% of patients. Concentration of antibodies does not reflect the severity of the disease.
• Antibodies to doublestranded DNA (dsDNA)– highly specific for SLE – but only present in 60% of cases. In some patients, the concentration of the antibodies may reflect the severity of the underlying disease

Complications

• Increased incidence of atherosclerotic disease
• Increased risk of thrombosis
• Increased risk of infection
  • Usually due to immunosuppressive treatment of the disorder

Management

• Mild disease – No specific therapies may be needed. The patient may be able to use topical NSAID therapy on the affected areas, and make lifestyle changes (E.g. avoiding the sun), and may otherwise need no further therapy
• Mild to moderate disease – Treatment is essentially similar to RA. Patients may use disease modifying drugs (e.g. methotrexate, leflunomide, azathiaprin, hydroxychlorequine), and use steroid injections for specific flare ups.
• Organ involvement – Treat the organ complications as separate entities with specific treatments
• Neurological disorders – Also treated with specific therapies, e.g. anticonvulsants

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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• However, it is important to remember that 5-10% of the population have this variant of HLA, and most do NOT have spondyloarthritis!

Beware of spondyloarthritis being misdiagnosed as the much more common mechanical back pain.

Epidemiology & Aetiology

• Aetiology is essentially unknown
• Associated with HLA-B27
• Sometimes associated with other disorders – such as Crohn’s disease, UC, chlamydial urethritis, psoriasis.
  • There is often a lot of overlap of symptoms with psoriasis

• 15-20% risk of the condition if there is a known first degree relative with the disorder
• The prevalence of AS varies between races. HLA-B27 is particularly common in caucasians, but uncommon in black Africans, and Japanese populations.
• Prevalence of 0.1 – 2%
• Peka age of onset is 20-30
• M:F is 3:1
  • But men tend to present earlier – at age 16, the M:F is 6:1
  • The disease is also often milder in women

Definitions

• Spondylitis – inflammation of the spine
• Spondylosis – degenerative osteoarthritis changes
• Ankylosis – stiffness in a joint

Pathology

Clinical features

• Episodic Pain – usually in the buttocks and/or lower back in the late teenage years or early 20’s in the first sign. The pain is:
  • Worse in the morning
  • Relieved by exercise
  • May wake the patient during the night – particularly in the second half of the night – after about 2am.
  • May be felt in the buttocks – especially if the sacroiliac joints are affected
• Spinal stiffness – can be measured with Schoeber’s test:
  • Measure 10cm above the dimples of Venus with the patient standing upright. Place a dot here. As the patient to flex forward (touch their toes). Then re-measure the gap with the patient in this position. Normally, the gap should increase to >15cm. In AS, the gap increases less than this
  • Stiffness is typically worse in the mornings
• Fever and weight loss may occur during episodes of pain
• Diagnosis often missed due to lack of symptoms between episodes
• Retention of lumbar lordosis in spinal flexion
• Paraspinal muscle wasting (occurs later)
• You may get costo-vertebral joint involvement – which can cause reduced chest expansion and anterior chest pain.
• No radiological abnormalities in early stages
• Late stages
  • Increased thoracic kyphosis – “question mark posture”
• May also have peripheral joint symptoms

• Peripheral osteoarthritis – 30% of patients. Pathologically the same as osteoarthritis, but has an unusual distribution. Usually the hands are spared, but the lower limbs and shoulder joints are particularly badly affected.
  • Asymmetrical
• Uveitis – inflammation of the inner parts of the eye. Usually in this case, anterior parts of the eye, including the iris and ciliary body
  • Acutely painful red eye with photophobia
  • 20-30% of patients
  • Of all patients who present with anterior uveitis – up to 50% will go on to develop AS
• Cutaneous lesions – that are identical to pustular psoriasis
• Aortic incompetence (in 1-2% of cases of AS) and other cardiovascular complications
  • Typically those with long-standing severe disease
  • AS increases the risk of cardiovascular disease
• Respiratroy complications
  • Restrictive lung disease
  • Pulmonary fibrosis
• Inflammatory bowel disease (Crohn’s, UC)
• Peripheral enthesitis
  • Achilles tendinopathy
  • Plantar fasciitis
• Neurological complications
  • Typically direct physical effects of a deformed spine
  • Can rarely cause cauda equina syndrome
• Increase risk fo osteoporosis
  • DEXA scans often underestimate the risk in AS

Examining for AS

• In the early stages of the disease, you may be able to elicit pain by pressing on the lower portion of the sacrum, whilst the patient is laid flat, face down.
• Schoeber’s Test – as described above
• Examiner peripheries for enthesitis
• Check eyes for uveitis
• Assess lumbar forward flexion
• Assessment of chest expansion

Diagnosis

Diagnosis is often delayed and difficult, due to the insidious and often fairly mild features of at symptom onset, and the broad range of differentials.

Consider AS particularly in patients with chronic back pain and:

• Aged under 30
• Morning stiffness >30 minutes
• Pain that improves with exercise but not with rest
• Buttock pain
• Previous anterior uveitis

Diagnosis can be made using the modified New York criteria. 

Diagnosis requires any of:

• x1 clinical criteria + radiological criteria met
• x3 clinical criteria present
• Radiological criteria present

Diagnosis does not require radiological evidence

Criteria include:

• Clinical criteria
  • Low back pain >3 months, improves with exercise, not relieved by rest
  • Limited chest expansion relative to normal values for age and sex
  • Limited lumbar spine motion in both the fontal and sagittal planes
• Radiological criteria – sacroiliitis on x-ray

Differential diagnosis

Differentials are broad and I highly recommend reading the lower back pain article for an overview of assessing lower back pain.

Differentials include:

• Mechanical back pain
• Sciatica – caused by disc prolapse
• Inflammatory arthritis – including ankylosing spondylitis and psoriatic arthritis
• Osteoarthritis of the spine
• Myeloma
• Bony metastases
• Osteoporotic crush fractures

Investigations

There is no specific diagnostic investigations. Tests can help to rule out other causes, and x-rays can be used as part of the modified New York criteria to assist in making a diagnosis (see above).

• Bloods – ESR and CRP may be raised, but are often normal
• HLA testing – not really much use due to high incidence of HLA-B27 in normal population
• X-Ray – usually normal in early disease. Later signs may include:
  • Sacroiliac joint margins lose definition – as they have become eroded and sclerotic.
  • Blurring of upper and lower rims of vertebrae – particularly in thoracolumbar junction. This is best seen on a Lateral X-ray
  • Syndesmophytes – these are boney lesions in the enthesis, as a result of enthesitis. They tend to be vertically orientated, and not beak-shaped, unlike osteophytes (seen in spondylosis), and also the disc is preserved (again, unlike spondylosis)
  • Joint fusion – may be seen in late disease. Sacroiliac, and costovertebral (reducing chest expansion), and intervertebral.
  • Together, these changes are sometimes referred to as “bamboo spine”

MRI is good at detecting very early changes of sacroiliitis, and being increasingly used in AS for this purpose.

CT scan can better detect some of the bony changes seen in late disease on x-ray.

Treatment

• AS is a chronic, life-long condition. Treatment aims to reduce symptoms and maximise function.
• All patients with newly diagnoses Ankylosing spondylitis should be referred to a rheumatologist.
• The basic treatment is exercise – this reduces long-term disability and other problems.
• Early diagnosis is important – this allows the regimen of exercises to be implemented early. Spinal exercises should be performed in the morning.
• Without exercise, patients are more likely to develop wasted paraspinal muscles, and irreversible kyphosis.
• Physiotherapy referral should be made early to guide this process
• Sleeping on a firm mattress with a thin pillow reduced the risk of kyphosis
• Hypotherapy and swimming may also be useful to maintain mobility

• Peripheral arthritis is managed with NSAID’s or local steroid injections.
• NSAIDs have been shown to effectively reduced symptoms and maintain function
• DMARDs – such as sulfasalazine or methotrexate – as used in other inflammatory arthritis conditions have, unfortunately, not been shown to be of benefit in ankylosing spondylitis
• TNF-α therapy is useful in severe disease, and can reduce inflammation. But the inflammation will return as soon as treatment is stopped.
  • e.g. etanercept and adlimumab
  • Should only be used under the supervision of a rheumatologist
  • Can increase the risk of serious infections

Surgery

• Rarely used, but can be used to correct spinal deformities

Preventative actions

• Monitor for the risk of cardiovascular disease
  • Increased risk with AS
  • Treat any other risk factors, such as hyperlipidaemia and hypertension
• Assess the risk of osteoporosis

Prognosis

• Long-term prognosis can be predicted by the level of disability at 10 years after diagnosis – those with only mild disease at 10 years, have a 75% of never progressing to severe disease
• Poor prognostic indicators:
  • Peripheral joint involvement
  • Young age of onset
  • Elevated ESR
  • Poor response to NSAIDs
• Mortality is increased compared to the general population
  • Increased risk of MI and stroke
  • Increased risk of malignancy
  • Increased risk of poor psychological health as a result of pain and disability

References

• Ankylosing spondylitis – AS – patient.info
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

The post Spondyloarthritides (ankylosing spondylitis) appeared first on almostadoctor.

• You should always consider connective tissue diseases in ill patients with multisystem involvement, when there is no infection present.
• Also remember that, even though the common presentations are discussed below, connective tissue disorders can present with strange symptoms, that can be just about anything!

• C – Calcinosis – calcium deposits, usually seen in the fingers
• R – Raynaud’s phenomenon
• E – Esophogeal Dysmotility
• S – Sclerodactyly – thickening of the skin
• T – Telangiectasia – red spots on the skin

Limited cutaneous scleroderma – aka scleroderma – in this variation, the signs are mostly confined to the hands, arms and face – i.e. mostly to the skin. In 80% there is also pulmonary hypertension.

• 5 year survival is >90%
• 10 year survival is >75%
• Generally only those with pulmonary involvement with have life threatening illness
• Usually skin changes on the upper limb are distal to the elbow.

Diffuse cutaneous scleroderma – aka systemic sclerosis – tends to be more rapidly progressing and severe. Affects larger areas of the skin, and there is multi-systemic involvement. Can be life-threatening, e.g. if the heart/lungs/liver/kidneys become involved.

• 5 year survival is 70%
• 10 year survival is 55%
• Skin changes can occur anywhere, and in advanced cases, may cover the whole body!
• Patches typically appear on the trunk

Epidemiology / Aetiology

• 4x as common in women
• Prevalence is about 1 per 1000
• Peak incidence is between 30-50
• Children sometimes affected in localised skin patches – sometimes called linear scleroderma or morphea

Pathology

• The disease is the result of vascular damage within the skin and organs.
• Organ damage is usually the result of fibrosis.
• Renal and pulmonary complications are the most life-threatening
• In normal disease progression, there can be some element of disease regression. This might include periods, perhaps a few weeks long, where the patient says their symptoms feel much less severe – although they are usually still apparent.

Clinical features

Sclerodactyly – thickening of the skin
Skin pigmentation changes – commonly a loss of pigment around the affected areas, but there may also be patches of hyperpigmentation.
Calcinosis of the fingertips – calcium deposits at the fingertips. You may see these at little pits near the finger tips (digital pitting), and they are often visible as white dots around the distal phalanges on radiograph.
Raynaud’s phenomenon – the result of vascular spasms that reduce the blood supply to the fingers, usually when the hands get cold. The phenomenon may also be triggered by emotional stress. There is a classic pattern of colour change – the fingers will go white, then blue, then as they warm up, or the episode passes, they will become red. The red part of the cycle is the result of hyperaemia that occurs after a period of reduced blood flow. The episodes are often painful.

• Sometimes also occurs in the tongue, toes, nose and ears.
• Occurs in 4-30% of all women. Rarer in men
• Can be divided into primary and secondary disease. In primary disease, it is often symmetrical, and will usually not result in any complications (e.g. ulceration, tissue necrosis, gangrene).

Secondary disease is what we see when it is related to connective tissue disease. This is often asymmetrical, and extremely painful. There may be associated ulceration, tissue necrosis, and gangrene.

• Smoking is a big risk factor!

It is important to remember when asking about this in the history that everybody’s fingers will turn white/blue if they are cold for long enough! You need to find out if they think these changes are abnormal, and often there may be a clear horizontal line across the fingers where the colour changes appear.
It commonly occurs in association with connective tissue disorders, but it can be idiopathic, and occur in isolation, or in association with other disorders, or as the result of medications (e.g. β-blockers). It also occurs in pregnancy.

Treatment

• Avoid sudden changes in temperature / low temperature. This might involve wearing gloves in moderate weather
• Stop smoking
• Try medications – Calcium channel blockers, Angiotensin-II agonsits, SSRI’s may also be useful

• Oesophageal Complications
• Telangactasia
• Pulmonary complications
• Reduced movements of the fingers/wrists – due to the swelling and skin thickening involved in the disease

General features of connective tissue disease

• Mouth ulcers
• Dry eyes
• Dry mouth
• Hair loss – mostly associated with SLE – but remember there is a lot of overlap! If symptoms of more than one connective tissue disorder are present, we would probably call it mixed connective tissue disease.
• Hand, foot and leg ulcers – particularly when Raynaud’s phenomenon is present.

Investigations

• Anti-centromere antibodies – associated with limited cutaneous scleroderma. Foud in 70% of cases.
• Anti-Scl-antibodies – associated with Diffuse cutaneous scleroderma. Found in 40% of cases.

Treatment

Specific organ treatments

• Renal crisis – ACE inhibitors often used
• Oesophageal involvement – PPI’s widely used
• Pulmonary Hypertension – usually treated with calcium channel blockers. However, in many patients this is not sufficient. Other drugs can be used IV, e.g. prostacyclin.
  • In very severe cases, patients may be considered for lung transplant.
• Interstitial lung disease – occurs in many patients, and restrictive lung disease will occur in about 20% of patients, and many of these will die as a result. This may be treated with low dose long term corticosteroid therapy (e.g. 7mg daily of prednisolone), and can also be treated with cyclophosphamide. However, it is often resistant to treatment.

• ECG
• Spirometry

Immunosu​ppressive therapy

Mixed Connective Tissue Disease

• Systemic sclerosis
• SLE
• Polymyositis

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

The post Systemic Sclerosis (Scleroderma) appeared first on almostadoctor.

Knee examination is an important clinical skill, and knee problems are a common presenting complaint to general practice and emergency departments. Knee examination is also a common OSCE station.

The knee is a hinge joint, but it depends on external structures for its stability, including the cruciate and collateral ligaments, and the menisci.

Inspection (look)

• Valgus deformity – ><
• Varus deformity – <>
• Recurvatum deformity – hyperextendibility of the knee beyond the normal 10’
• Limp and gait

• Leg length – compare to opposite side
• Position – values and various, patella position
• Gross deformity, growths

Palpate (feel)

• Feel the temperature with the back of your hand. If it is warm, state there is a local rise in temperature. 
  • Increase in temperature suggests inflammation. Common causes of a red inflamed joint include septic arthritis and gout.
• Feel for the joint line – if you feel distal to the patellar, on both the medial and lateral aspects of the joint you can feel two soft triangular hollows. Pressing into the superior aspect of these hollows, you will be able to feel the joint line. Check for tenderness at the joint line.
• Patella Tap – tests for larger effusions.
  • Similar to the bulge test, try to empty the suprapatellar bursa. Make sure you maintain constant downwards pressure on the thigh.
  • Now put two fingers on the patella and press firmly and briskly downwards. If fluid is present you will feel the patella move downwards (it might feel ‘squishy’) before hitting the underlying bone. In a normal patient, there will be little movement of the patella, and you should not feel it hit the underlying bone.
  • Also check the patella position and freedom of lateral movement

• Bulge test – can be sensitive for a small effusion.

• • Place your hand about 15cm proximal to the knee joint on the anterior part of the thigh. Then slide your hand down towards the knee. This empties the suprapatellar bursa of fluid
  • keeping the first hand in place, using your other hand, press on the medial side of the knee joint to empty the medial compartment. Now all of the bursal fluid should be in the lateral compartment
  • Take your hand off the medial compartment, and press on the lateral compartment – you may see a bulge in the medial compartment as it fills with fluid. This shows a small effusion

• Soft tissues – check for tenderness
  • Patellar tendon
  • Quadriceps tendon
  • Iliotibial band (ITB)
  • Collateral ligaments
  • Popliteal fossa
    • Painful if ruptures bakers cyst or ligament rupture
    • Ruptured Baker’s cyst – is an important differential for DVT. Both produce calf swelling, pitting oedema, pain and redness.
    • The baker’s cyst is located in the popliteal fossa. If it rupture it causes sudden calf pain. Can only really be differentiated for DVT with ultrasound (checks veins in legs, and can also look for swelling of knee joint, and remnants of a baker’s cyst).
• Neruovascular examination
  • Not often indicated
  • Motor
    • Knee flexion – Sciatic nerve
    • Knee extension – femoral nerve
    • Foot plantarflexion – tibial nerve
    • Foot dorsiflexion – deep perineal nerve
  • Sensory
    • Medial thigh – Obturator nerve
    • Anterior thigh – Femoral nerve
    • Dorsal foot – Peroneal nerve
    • Plantar foot – Tibial nerve
  • Pulses
    • Knee – popliteal
    • Ankle – (medial) poster tibialis
    • Foot – dorsals pedis
  • Reflexes
    • Patellar – L4

Move

• Extension – check both legs. Ask the patient to extend their knee as far as possible. Normal range – 0 – 10 degrees
• Flexion – ask the patient to bring their foot to their bottom. About 125-135 degrees is normal.
• Rotation – 10-15 degrees of tibial rotation is normal (whilst holding the femur fixed with your other hand)
• Compare both sides!

Examining knee stability

• Lateral ligament – apply valgus force – “valgus stress test”
• Medial ligament – apply varus force – “varus stress test”
• Feel for laxity of the knee joint
• As you are doing this, you might want to try to feel the joint line with the hand that is holding the thigh (usually left hand) – to see if you are abnormally opening up the joint on the stressed side. Any weakness or tear of a collateral ligament will result in a joint line that separates abnormally. 

Cruciate ligaments

• Anterior cruciate ligament – runs from the posterior aspect of the femur to the anterioraspect of the tibia. Prevents the tibia slipping forward
  • Abnormal movement anteriorly of the tibia in relation to the femur in Lachman’s or drawer tests suggests ACL injury.
• Posterior cruciate ligament –  runs from a more anterior aspect of the femur to the anterior posterior of the tibia. Prevents the tibia slipping backwards
  • Abnormal movement posteriorly of the tibia in relation to the femur in drawer test suggests ACL injury.

Lachman’s Test – assesses the anterior cruciate ligament

• Flex the leg to 30 degrees
• Hold the femur securely by holding the thigh securely
• Try to move the tibia forward on the femur. Normally little movement is possible. Movement >5mm is suggests an ACL injury

• Flex the leg to 90’
• Put your fingers of both hands into the popliteal fossa, and the thumbs of both hands on the front of the tibia.
• Try to pull the tibia forward relative to the femur – Some doctors suggest you sit on the foot as you do this to anchor the foot and ankle
• Normally, there will be little movement, movement suggests pathology
• Any rotation at the hip joint prevents this test from properly assessing the cruciate, and thus many people say this test is inferior to Lackman’s

• Same as the anterior draw test, except that you push instead of pulling on the tibia.

Meniscus tests

• Joint line tenderness is the most sensitive test for meniscal tear

McMurray’s Test

Apley’s compression test

Further special tests

• Assesses an fixed flexion deformity. As the patient to lie with their legs flat. If the knee does not fully extend, then there is fixed flexion deformity. Often occurs due to tight hamstrings in sportsmen and women. The calf will often not touch the couch. As you try to passively extend the leg, the resistance will come on gradually.
• Locked knee – as you try to passively extend the leg, resistance will occur suddenly. Often due to debris in the knee joint (e.g. meniscal tear) – requires urgent orthopaedic attention.

Quadriceps weakness

• Ask the patient to flex knee, and then life the heel off the couch. If the quadriceps is weak, there will be a delay before the heel lifts. This is called quadriceps lag. Compare both legs

References

• Knee Physical Exam – Adult – Orthobullets

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Look

From front – are the shoulders level?
From side – look for kyphosis and lordosis.Are these normal? Exaggerated?

• Loss of lordosis – degenerative disc disease
• Exaggerated Lordosis :
• Spondylolisthesis – where one vertebra has moved anteriorly relative to the one below it. Most commonly occurs in the lumbar spine.
• Fixed flexion deformity in the hips
• Pregnancy
• Obesity

From Back – any scoliosis, check shoulder level again. Look for any scars, and any wasting of the paraspinal muscles.

Feel

Move

Lateral flexion – ask the patient to stand up straight with their hands down by their sides. Then ask them to lean to their left sliding the left arm towards their knee. Do the same on the right.
Forward flexion – ask the patient to touch their toes, or reach as far as they can.

• Shober’s test – this is a quantitative assessment of flexion of the lumbar spine. There are several variations. Essentially, with the patient stood upright, you should find the dimples of venus near the base of the lumbar spine. Imagine a line between these, and put a dot along this line. Then measure 10cm above this line, and mark another dot. Then ask the patient to touch their toes (or as far as they can). Whilst in this position, re-measure this distance between your two dots. It should be >15cm – ie. The distance should have increased by 5cm or more.
• In another variation, you should measure 5cm below the dimples of venus, and mark a dot 15cm above this point. Then check that the distance increases to >20cm on flexion.
• In a positive test, the distance is increases by <5cm. This is commonly caused by ankylosing spondylitis.

Extension – Make sure you are able to support the patient if necessary. Ask them to lean backwards, whilst keeping their hips in place. -/span>
Rotation – Easiest if you stand behind the patient and put your hands on their hips. Then ask them to look over their shoulder

Special tests

Sciatic nerve stretch test – aka – straight leg raiseask the patient to lie on their back on the couch. The couch should be flat. Raise the leg of the bed (flexion of the hip). This should not elicit any pain whilst the leg raise is within normal limits. If it does elicit pain, note the site at which pain is elicited, then, lower the leg, until it is back below the site of pain. One the leg is in this position, then dorsiflex the foot – if the pain is the result of sciatica – this will elicit pain again

• The straight leg raise in itself can result in pain from many causes (bursitis, hamstring damage). Dorsiflexing the foot helps isolate the sciatic nerve as the test. Applying pressure to the popliteal fossa also helps to anchor the sciatic nerve and may increase the sensitivity of the test where there is only mild sciatic nerve involvement.
• Result of herniation of the L4/L5 or L5/S1 discs
• Patients will have symptoms of lower leg, and buttocks

Femoral nerve stretch test herniation at L3-4– ask the patient to lie prone (on their front). The extend the hip, and flex the knee to 90’. Pain felt at the back of the thigh indicates femoral nerve involvement.

• Result of herniation of discs higher up the lumbar spine
• Patients will have symptoms of anterior thigh (inc weakness and pain)

References

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