Week 11 - connective tissue Flashcards

1
Q

Describe the basic epidemiology of polymyalgia rheumatica. (LO1)

A
  • Second most common autoimmune syndrome. 1-5 people in 10,000 affected.
  • Risk in women 2.4%, 1.7% in men.
  • Rarely affects <50 year olds.
  • Most patients >60. Mean age of onset is around 70.
  • 15-20% of PMR patients also have giant cell arteritis (GCA).
  • Mainly affects white patients. Uncommon in black, Hispanic, Asian and Native American individuals.
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2
Q

Describe the pathophysiology of polymyalgia rheumatica. (LO1)

A
  • Suggested genetic predisposition if white people are more affected.
  • Associated with HLA-DR4 gene.
  • PMR and GCA may start with the activation of dendritic cells at the adventitia-media border of large vessels, causing IL-1 and IL-6 production. This leads to the suppression of T-regulatory cells, leading to reduction in IFN-γ cytokine.
  • If there is no IFN-γ to stimulate macrophages, then GCA arterial inflammation does not stop.
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3
Q

Describe the presentation of polymyalgia rheumatica. (LO1)

A
  • Recent onset of significant stiffness in shoulder/hip girdle and pain in shoulder/hip muscles (proximal limbs) and neck muscles.
  • Symmetrical shoulder girdle aching for >2 weeks.
  • Morning stiffness >45 minutes.
  • Bilateral hip pain/limited range of motion.
  • Constitutional symptoms (33-50% patients): fever, anorexia, malaise, headache, myalgia.
  • Absence of objective weakness (don’t confuse with muscle guarding).
  • Difficulty rising from seat, prone position (lying flat on front).
  • Shoulder/hip bursitis.
  • Possible oligoarthritis (1-4 joints affected in first 6 months of disease).
  • Exclusion of other diagnosis (except GCA).
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4
Q

What do the letters in SECCRET stand for when regarding polymyalgia rheumatica? (LO1)

A
  • S = stiffness and pain.
  • E = elderly individuals.
  • CC = constitutional symptoms, caucasians.
  • R = rheumatism (arthralgias/arthritis).
  • E = elevated ESR.
  • T = temporal arteritis (GCA particularly at temples.
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5
Q

Describe the findings from a physical examination that would be indicative of polymyalgia rheumatica. (LO1)

A
  • Chronically ill.
  • Neck and shoulders tender.
  • Limited active range of motion.
  • Capsular contracture.
  • Muscle atrophy.
  • Increased pain on joint movement - felt at proximal extremities.
  • Synovitis often in knees, wrists, sternoclavicular joints.
  • Objective muscle strength testing should be normal unless atrophy.
  • GCA and PMR suggested to be different manifestations of the same disorder so check GCA for temporal/occipital headaches, scalp tenderness, jaw pain and visual disturbances.
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6
Q

Describe the investigations for polymyalgia rheumatica. (LO1)

A
  • CRP - elevated.
  • ESR - >40mm/hour (often over 100mm/hour).
  • Absence of RF and antibodies to citrullinated antigens (ACPAs).
  • Rule out neuromuscular dysfunction with neurological exam - no muscle weakness.

Lab abnormalities:

  • Anything showing systemic inflammation (normochromic normocytic anaemia, thrombocytosis, increased gamma globulins).
  • Abnormal liver enzymes (33% of cases) - increased alkaline phosphatase (ALP) level.

Synovial fluid:

  • Leukocyte 1000-20,000 cell/mm³.
  • Negative culture.
  • Negative crystal.
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7
Q

Describe the management of polymyalgia rheumatica. (LO1)

A
  • Initially: single daily dose of 12.5-25mg of prednisolone (or other glucocorticoid) OR intramuscular methylprednisolone 120mg every 3 weeks (if can’t take oral prednisolone).
  • Early: methotrexate 7.5-10mg/week, especially if it’s not possible to taper glucocorticoids.
  • Azathioprine: reduces long-term need for steroids (steroid-sparing agent). Given alongside fast-acting steroids so that when azathioprine has an effect (3-6 months later), the patient can stop taking steroids.
  • Tocilizumab is reported to be effective, inhibition of IL-6 in PMR.
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8
Q

Describe the tapering of glucocorticoids in polymyalgia rheumatica. (LO1)

A
  • Only once CRP and ESR are normalised - decrease by 2.5mg every 2-4 weeks until 10mg/day.
  • Further tapering by 1mg every 1-2 months while monitoring.
  • If CRP and ESR elevate again, don’t increase prednisolone straight away until the cause has been investigated.
  • If relapse (65% chance), small increase to dosage before relapse (often 5mg/day).
  • After 6-12 months have passed, taper again by 1mg/day every 2 months.
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9
Q

How long does treatment for polymyalgia rheumatica usually last? What could be a reason for treatment lasting a lot longer? (LO1)

A

Often lasts >2 years.

  • If prednisolone 20mg/day does not improve symptoms/normalise ESR and CRP within a month, suspect a giant cell arteritis (GCA).
  • If GCA suspected, do temporal artery biopsy/check other diagnosis (malignancy, infection).
  • Reassurance, education, regular monitoring, range of motion exercises, especially if muscle atrophying and contracture is present.
  • Treat glucocorticoid side effects with vitamin D and calcium supplements + regular dual x-ray absorptiometry screening, check glucose intolerance and hyperlipidaemia.
  • Strong no to tumour necrosis factor antagonists and Chinese herbal supplements.
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10
Q

List the differentials for polymyalgia rheumatica. (LO1)

A
  • Chronic pain syndrome, e.g. fibromyalgia.
  • Hyper/hypothyroidism.
  • Depression.
  • Polymyositis.
  • Malignancy (lymphoma, myeloma).
  • Inflammatory myopathy - including body myositis.
  • Lambert-Eaton syndrome.
  • Occult infection (TB, HIV, SBE).
  • Late onset spondyloarthropathy.
  • Late onset rheumatoid arthritis - distinguish with absence of RF and anti-CCP, lack of synovitis of hands and feet, no erosions on x-ray.
  • Psoriatic arthritis (enthesopathic).
  • Systemic vasculitis.
  • Frozen shoulder, rotator cuff, shoulder OA.
  • Multiple separate lesions.
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11
Q

Describe the prognosis for polymyalgia rheumatica. (LO1)

A
  • Patients should respond dramatically within a week of starting 20mg/day prednisolone.
  • 75% of patients can taper off prednisolone within 2 years.
  • 10-20% of patients likely to relapse within months to years.
  • 25-35% of patients require low dose glucocorticoids indefinitely due to relapse when tapered off.
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12
Q

Briefly describe systemic lupus erythematosus. (LO2)

A
  • Multi-system autoimmune disease with different presentations.
  • Treatments are tailored depending on different organ involvement.
  • Rheumatologist primary responsible for lupus patients.
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13
Q

Describe the epidemiology of SLE. (LO2)

A
  • 0.03% prevalence in Caucasians.
  • 0.2% prevalence in in Afro-Caribbeans.
  • 90% of affected patients are female.
  • 20-30 year olds mostly affected (can be seen in children).
  • Five fold increase in mortality compared to age-and-gender-matched controls (cardiovascular disease).
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14
Q

List the risk factors of SLE. (LO2)

A
  • Female sex - associated with the effects of oestrogen.
  • > 30 years of age.
  • African descent in Europe and US.
  • Alopecia, photosensitivity, oral ulcers, arthritis and malar rash may also be more common among female patients.
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15
Q

Describe the pathophysiology of SLE. (LO2)

A
  • No clear picture.

Different factors:

  • Genetic factors.
  • Monozygotic twins.
  • Polymorphic variants at the the HLA locus.
  • Inherited mutations in complement components, C1q, C2 and C4, in the immunoglobulin receptor FcyRIIIb or in the DNA exonuclease TREX1.
  • Polymorphisms of genes that predispose to SLE, most of which are involved in regulating immune cell function.
  • Autoantibodies production usually directed against antigens present within the cell/nucleus.
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16
Q

Describe the systemic features of SLE. (LO2)

A
  • Fatigue.
  • Weight loss.
  • Fever.
  • Mild lymphadenopathy.
  • Arthralgia.
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17
Q

Describe the joint involvement in SLE. (LO2)

A
  • Arthralgia seen in 90% of patients with early morning stiffness.
  • Tenosynovitis may result in tendon damage.
  • Synovitis is rare.
  • Jaccoud’s arthropathy is rare - lupus related to joint damage to chronic tenosynovitis rather than to joint erosive disease specifically.
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18
Q

Describe the dermatological presentations of SLE. (LO2)

A
  • Malar (butterfly) rash.
  • Photosensitive rash.
  • Discoid rash.
  • Atrophic scarring.
  • Diffuse, non-scarring alopecia.
  • Urticaria.
  • Livedo reticularis.
  • Vasculitis.
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19
Q

What is meant by malar rash? (LO2)

A
  • Also known as butterfly rash.
  • Classic facial rash (in up to 20% of SLE patients).
  • Erythematous, raised and painful or itchy over the cheeks.
  • Sparing of the nasolabial folds.
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20
Q

What is meant by photosensitive rash? (LO2)

A
  • Occurs after sun exposure.
  • Can be painful and pruritic.
  • Usually lasts a few days, healing without scarring.
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21
Q

What is meant by discoid rash? (LO2)

A
  • Erythematous raised patches.
  • With adherent keratotic scaling (hyperkeratosis) and follicular plugging.
  • Can lead to alopecia if involving scalp.
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22
Q

Describe the renal involvement in SLE. (LO2)

A
  • Renal disease is a hallmark of severe SLE.
  • Do a regular urinalysis and BP check.
  • Proliferative glomerulonephritis.
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23
Q

Describe the presentations of proliferative glomerulonephritis as a result of SLE. (LO2)

A
  • Presents with heavy haematuria.
  • Proteinuria.
  • Casts on urine microscopy.
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24
Q

Describe the cardiovascular involvement in SLE. (LO2)

A
  • Heart: pericarditis, myocarditis, Libman-Sacks endocarditis (sterile vegetations; non-infection related, inflammation related).
  • Arteries: atherosclerosis greatly increased, causing a higher risk of stroke and myocardial infarction. Atherosclerosis occurs due to inflammatory disease on the endothelium.
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25
Q

What is meant by antiphospholipid syndrome? (LO2)

A
  • Antiphospholipid syndrome is where the antiphospholipid antibodies increase the risk of forming blood clots.
  • The most serious complication of this, is that women with this syndrome have a higher risk of miscarriage.
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26
Q

Describe lung involvement in SLE. (LO2)

A

Common:

  • Serositis (pleuritic pain) - inflamed lining of the chest wall and rubs against the lining of the lung.
  • Pleural effusion - local inflammation of the lining of the pleura.

Less common:

  • Pneumonitis.
  • Atelectasis.
  • Reduced lung volume.
  • Pulmonary fibrosis that leads to breathlessness.
  • Increased risk of thromboembolism (DVT, PE) is increased, especially if antiphospholiid antibodies are present.
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27
Q

Describe the neurological involvement in SLE. (LO2)

A

Common:
- Headache and poor concentration are common.

Less common:

  • Visual hallucinations.
  • Chorea.
  • Organic psychosis .
  • Transverse myelitis.
  • Lymphocytic meningitis.
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28
Q

Describe the gastrointestinal involvement in SLE. (LO2)

A

Common:
- Mouth ulcers.

Uncommon:

  • Peritoneal serositis - causes acute pain.
  • Mesenteric vasculitis is serious (abdominal pain, bowel infarction/perforation).

Rare:
- Hepatitis.

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29
Q

Describe the haematological involvement in SLE. (LO2)

A

Antibody-mediated destruction of peripheral blood cells may cause:

  • Neutropenia.
  • Lymphopenia.
  • Thrombocytopenia.
  • Haemolytic anaemia.
  • A degree of lymphopenia is an indicator of lupus activity.

Antiphospholipid syndrome (APLS):

  • Vascular thrombosis.
  • Pregnancy loss - early or late.
  • Lab criteria: on two occasions, 3 months apart:
    1. Lupus anticoagulant.
    2. Anticardiolipin antibodies.
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30
Q

Describe pregnancy outcomes in patients with SLE. (LO2)

A
  • Poor with or without APLS.
  • Pregnancy loss - 13.1% total.
  • Preterm birth.
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31
Q

How does neonatal lupus occur and how does it present? (LO2)

A
  • Maternal antibodies crossing the placenta causing lupus in the unborn baby.
  • Rash.
  • Pericardial effusion.
  • Conduction (heart beat) defects.
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32
Q

Describe the investigations for SLE. (LO2)

A

Autoantibody screen:

  • Anti-dsDNA antibodies.
  • Antinuclear antibodies (ANA).
  • Antiphospholipid antibodies.

If autoantibodies are present, U+Es to assess effect on kidneys (creatinine and eGFR) and use EULAR criteria (don’t need to know the specifics of this). If absent, do not classify as SLE.

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33
Q

Describe the education aspect of management for SLE. (LO2)

A
  • Control the symptoms and to prevent symptoms.
  • To prevent organ damage and maintain normal function.
  • Avoid sun exposure and use sun block (SPF 50).
  • Vitamin D supplementation due to avoidance of sunlight.
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34
Q

Describe the drug therapy aspect of management for SLE. (LO2)

A
  • Analgesics.
  • NSAIDs.
  • Hydroxychloroquine.
  • Prednisolone.
  • MMF (mycophenolate mofetil).
  • MTX.
  • Azathioprine.
  • Belimumab (monoclonal antibody targets the β-cell growth factor BLyS).
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35
Q

Describe the drug therapy required during end-organ disease of SLE. (LO2)

A
  • High dose glucocorticoids and immunosuppressants.
  • IV methylprednisolone (10mg/kg IV).
  • Renal: rituximab.
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36
Q

Describe the drug therapy required during end-organ disease of SLE. (LO2)

A
  • High dose glucocorticoids and immunosuppressants.
  • IV methylprednisolone (10mg/kg IV) + IV cyclophosphamide for 6 cycles. Side effects: infection, haemorrhagic cystitis, infertility.
  • Renal: rituximab.
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37
Q

What is vasculitis? (LO3)

A

Vasculitis is an umbrella term for a group of diseases involving the inflammation of blood vessels. They are classified according to the size of blood vessel affected. (This can predict how the vasculitis will respond to treatment.)

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38
Q

Describe the epidemiology of vasculitis. (LO3)

A
  • Incidence of 40-60 cases/million/year.
  • Very rare.
  • Increases with age.
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39
Q

List the the risk factors for vasculitis. (LO3)

A
  • Dust exposure.
  • Farming.
  • Infection.
  • Drugs.
  • Season.
  • Geography.
  • Ethnicity.
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40
Q

Describe the pathophysiology of vasculitis. (LO3)

A
  • Can be primary or secondary.
  • Thought to be immune-mediated.
  • Primary - no known cause.
  • Secondary - could be a result of drugs, infection or rheumatological conditions such as rheumatoid arthritis or SLE.
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41
Q

List the vasculitidities included under the term vasculitis. (LO3)

A
  • Giant cell arteritis.
  • Takayasu arteritis.
  • Polyarteritis Nodosa.
  • Kawasaki disease.
  • Wegener’s granulomatosis (WG).
  • Microscopic polyangiitis (MPA).
  • Churg-Strauss syndrome (CSS).
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42
Q

List the vasculitidities included under the term vasculitis. (LO3)

A
  • Giant cell arteritis.
  • Takayasu arteritis.
  • Polyarteritis Nodosa (PAN).
  • Kawasaki disease.
  • Granulomatosis with polyangiitis (GPA), aka, Wegener’s granulomatosis (WG).
  • Microscopic polyangiitis (MPA).
  • Eosinophilic granulomatosis with polyangiitis (EGPA), aka, Churg-Strauss syndrome (CSS).
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43
Q

Describe the presentation of giant cell arteritis. (LO3)

A
  • New headache.
  • Temporal artery abnormality - biopsy might be diagnostic.
  • Jaw claudication.
  • Polymyalgic symptoms - pain and shoulder/pelvic girdle morning stiffness.
  • Visual symptoms - medical emergency.
  • > 50 years of age.
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44
Q

Describe the investigation findings for giant cell arteritis. (LO3)

A
  • High inflammatory markers.

- Negative antibodies.

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45
Q

Describe the presentation of Takayasu arteritis. (LO3).

A
  • <40 years of age.
  • Generally unwell, fever.
  • Weight loss.
  • Myalgia, arthralgia.
  • Claudication.
  • Feeble or unequal pulse.
  • Possible aortic murmur.
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46
Q

Describe the presentation of polyarteritis Nodosa (PAN). (LO3)

A
  • Elderly.
  • Weight loss.
  • Neuropathy - peripheral nerve involvement.
  • Gastrointestinal involvement - bowel ischaemia/infarction, pancreatitis.
  • Testicular involvement.
  • Skin involvement - leg ulcers/livedo reticularis.
  • Renal involvement - hypertension.
  • Rare, medium-sized vasculitis is associated with a Hep B infection.
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47
Q

Describe the investigation findings for polyarteritis Nodosa (PAN). (LO3)

A
  • ANCA test is negative.
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48
Q

Describe the presentation Kawasaki disease. (LO3)

A
  • Small, medium-sized vessels.
  • Seen in childhood.
  • 50% of cases are seen in children <2 years.
  • Fever.
  • Bilateral conjunctival congestion.
  • Mucosal involvement - reddening of lips, lining of the mouth and/or strawberry
  • Small, medium-sized vessels.
  • Fever.
  • Skin rash on the the trunk.
  • Red palms and soles.
  • Oedema of the hands and feet.
  • Cervical lymphadenopathy.
  • Seen in childhood.
  • 50% of cases are seen in children <2 years.
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49
Q

Describe the investigation findings for Kawasaki disease. (LO3)

A
  • ANCA test is negative.
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50
Q

Describe the presentation of granulomatosis with polyangiitis (GPA). (LO3)

A
  • Also known as Wegener’s granulomatosis (WG) - changed cos he was evil (Nazi).
  • Granulomata and vasculitis.
  • ENT involvement - nasal, collapsed nose (saddle nose).
  • Pulmonary-renal syndrome - histologically seen granuloma formation.
  • Generalised form is fatal if untreated.
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51
Q

Describe the investigation findings for granulomatosis with polyangiitis (GPA). (LO3)

A
  • Associated with proteinase 3 ANCA.
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52
Q

Describe the presentation of microscopic polyangiitis (MPA). (LO3)

A
  • No granulomata.
  • Predominantly kidney affected.
  • Skin involvement.
  • Peripheral nerves affected.
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53
Q

Describe the investigation findings for microscopic polyangiitis. (LO3)

A
  • Myeloperoxidase ANCA.
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54
Q

Describe the presentation of eosinophilic granulomatosis with polyangiitis (EGPA). (LO3)

A
  • Also known as Churg-Strauss syndrome (CSS) - changed cos he was also an evil Nazi.
  • Resistant asthma.
  • Neuropathy.
  • Cardiac involvement.
  • Other features of renal disease.
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55
Q

Describe the investigation findings for eosinophilic granulomatosis with polyangiitis (EGPA). (LO3)

A
  • Can be associated with myeloperoxidase ANCA.
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56
Q

What is jaw claudication? (LO3)

A

Fatigue of the jaw muscles from chewing. Predictive of temporal arteritis.

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57
Q

List the differential diagnoses for vasculitis. (LO3)

A
  • Bacterial endocarditis.
  • Cancer (paraneoplastic).
  • Systemic lupus erythematosus (SLE).
  • Atrial myxoma (tumour originating in the heart).
  • Cholesterol emboli.
  • Calciphylaxis (calcium accumulation in the small blood vessels of fat and skin tissues).
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58
Q

List the different categories of investigations for vasculitis. (LO3)

A
  • Blood test.
  • ANCA.
  • Urine - blood, protein, casts.
  • Tissue.
  • Imaging.
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59
Q

List the aspects of a blood test used for vasculitis investigations. (LO3)

A
  1. Haematology:
    - FBC - neutrophilia, eosinophilia (EGPA).
    - ESR - raised.
  2. Biochemistry:
    - Assesses organ involvement and the severity.
    - CRP - raised.
  3. Immunology.
  4. Complement levels.
  5. Rheumatoid factor.
  6. Protein electrophoresis.
  7. Serum immunoglobulins.
  8. Cryoglobulins.
  9. ANCA.
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60
Q

What is the ANCA test? (LO3)

A

There are two techniques.

  1. Indirect immunofluorescence technique:
    - Cytoplasmic (C-ANCA) pattern found or,
    - Perinuclear (P-ANCA) pattern found.
  2. ELISA technique:
    - Proteinase 3 (PR3) antibody or,
    - Myeloperoxidase (MPO) antibody - associated with granulomatosis polyangiitis.
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61
Q

What is meant by casts? (LO3)

A

Casts are cells that can be detected in the urine in renal disease.

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62
Q

What is the definitive test for diagnosing vasculitidies? (LO3)

A
  • Biopsy is highly recommended, although the yield is variable.
  • Renal biopsy is best and almost always positive.
  • Biopsy can be taken from any tissue.
  • Arteries can be biopsied but only small vessels are easily biopsied.
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63
Q

List the different types of imaging used for investigation vasculitis. (LO3)

A

Artery-specific imaging for large and medium vessel disease:

  • Angiography - dye is injected into an artery.
  • Magnetic resonance imaging (MRI).
  • Positron emission tomography (PET).
  • Ultrasound.

Tissue-specific imaging for small vessel vasculitis.

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64
Q

Describe the management for large vessel vasculitis. (LO3)

A
  • Glucocorticoids.

- Immunosuppressive agents.

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65
Q

Describe the management for polyarteritis Nodosa (PAN), microscopic polyangiitis (MPA), granulomatosis with polyangiitis (GPA) and eosinophilic granulomatosis with polyangiitis (EGPA). (LO3)

A

Localised:

  • Methotrexate.
  • Steroids.

Generalised:

  • Cyclophosphamide.
  • Steroids.
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66
Q

Describe the management for resistant vasculitis (ANCA positive). (LO3)

A
  • Rituximab.
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67
Q

List the reasons for needing to monitor vasculitis patients closely. (LO3)

A
  • Comorbidities.

- Treatment side effects.

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68
Q

List the relevant comorbidities to be aware of when monitoring vasculitis patients. (LO3)

A
  • Elderly - they may have other comorbidities that may be exacerbated by vasculitis.
  • Cardiac comorbidity - vasculitis would exacerbate cardiac symptoms.
  • Risk of relapse - vasculitis could become chronic.
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69
Q

Describe the treatment side effects to be aware of when monitoring vasculitis patients. (LO3)

A
  • Steroids - bone health, prescribe bisphosphonates and dosage of steroids should be reduced where possible.
  • Immunosuppressive agents, especially cyclophosphamide can cause bladder complications.
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70
Q

Describe the prognosis of vasculitis. (LO3)

A
  • If left untreated, survival chances are low.

- With treatment, 60-75% of patients survive 10 years post-vasculitis.

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71
Q

List the prognostic factors for vasculitis. (LO3)

A
  • Age.
  • Target organ involvement.
  • Damage caused.
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72
Q

List the secondary causes of death from vasculitis. (LO3)

A
  • Infection.
  • Target organ damage.
  • Cancer.

Obviously, death could be directly due to the vasculitis itself.

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73
Q

What is meant by connective tissue disease? (LO4)

A

This describes conditions where the connective tissues of the body are targeted. Generally, these are multi-system inflammatory disorders associated with immunological abnormalities. They share many clinical features.

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74
Q

List some single-gene defect connective tissue diseases. (LO4)

A
  • Ehlers-Danlos syndrome.
  • Epidermolysis Bullosa.
  • Marfan syndrome.
  • Osteogenesis imperfecta.
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75
Q

List some autoimmune inflammatory connective tissue diseases. (LO4)

A
  • Polymyositis.
  • Dermatomyositis.
  • Rheumatoid arthritis.
  • Scleroderma.
  • Sjogren’s syndrome.
  • Systemic lupus erythematosus (SLE).
  • Vasculitis.
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76
Q

What is Raynaud’s phenomenon? (LO4)

A
  • Temporary spasm of blood vessels which block the flow of blood.
  • Triphasic colour change: white, blue, red.
  • Fingers, toes, ears, nose, lips or nipples affected.
  • Usually triggered by cold temperatures, anxiety or stress.
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77
Q

Describe the triphasic colour change in Raynaud’s phenomenon. (LO4)

A
  1. White: immediate lack of blood.
  2. Blue: lasting lack of blood.
  3. Red: when blood flow is restored (rushes back in).
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78
Q

List the areas that can potentially be affected by Raynaud’s phenomenon. (LO4)

A
  • Fingers.
  • Toes.
  • Ears.
  • Nose.
  • Lips.
  • Nipples.
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79
Q

List the symptoms of Raynaud’s phenomenon. (LO4)

A
  • Pain.
  • Numbness.
  • Pins and needles.
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80
Q

Describe the management of Raynaud’s phenomenon. (LO4)

A
  • Keep warm.
  • Stop smoking.
  • Calcium-channel blockers.
  • Iloprost.
  • Sildenafil (usually used in erectile dysfunction).
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81
Q

Describe Raynaud’s phenomenon as part of SLE. (LO4)

A
  • Common symptoms and may predate other symptoms.

- Consider secondary Raynaud’s.

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82
Q

Describe the signs of Raynaud’s phenomenon. (LO4)

A
  • Capillary nail-fold loops (and vegatable oil placed on skin) can show loss of normal loop pattern.
  • Chronic ischaemia may lead to colour change.
  • Digital ulcers in severe diseases.
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83
Q

Describe the maintenance therapy for SLE. (LO4)

A
  • Taper prednisolone, long-term, low-dose.
  • Immunosuppressants: azathioprine. methotrexate, MMF.
  • Assess cardiovascular risk factors (hypertension and hyperlipidaemia).
  • Patients should be advised to stop smoking.
  • Anticoagulation with warfarin if thrombosis and antiphospholipid syndrome.
  • Assess risk of osteoporosis and hypovitaminosis D.
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84
Q

What is systemic sclerosis (SS)? (LO4)

A
  • Causes fibrosis affecting: skin, internal organs and vasculature.
  • Categorised by Raynaud’s phenomenon, sclerodactyly and cardiac, lung, gastrointestinal and renal disease.
  • Subdivides into:
    1. Diffuse cutaneous systemic sclerosis.
    2. Limited cutaneous systemic sclerosis.
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85
Q

Describe the epidemiology of systemic sclerosis. (LO4)

A
  • Onset in 40-50s.
  • 10-20 cases per 100,000.
  • More likely in women, 4:1.
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86
Q

List the main clinical features of systemic sclerosis. (LO4)

A
  • Dermatological involvement.
  • Raynaud’s phenomenon.
  • Musculoskeletal features.
  • Gastrointestinal involvement.
  • Pulmonary involvement.
  • Renal involvement.
  • Hypertensive renal crisis - rapid increasing hypertension and renal failure.
87
Q

Describe the dermatological clinical features of systemic sclerosis. (LO4)

A
  • Non-pitting oedema of fingers and flexor tendon sheaths.
  • Becomes shiny and taut.
  • Capillary loss.
  • Limited sclerosis: face and neck are often involved with thinning of lips and radial furrowing.
  • Diffuse sclerosis: involvement proximal to the knee and elbow and on trunk.
88
Q

Describe Raynaud’s phenomenon as a clinical feature of systemic sclerosis. (LO4)

A
  • May precede other features by many years when severe and progressive.
  • Critical tissue ischaemia with distal skin infarction and necrosis.
89
Q

Describe the musculoskeletal features of systemic sclerosis. (LO4)

A
  • Arthralgia and flexor tenosynovitis are common.
  • Restricted hand function due to skin rather than joint disease.
  • Muscle weakness and wasting can result from myositis.
90
Q

Describe the gastrointestinal involvement in systemic sclerosis. (LO4)

A
  • Erosive oesophagitis.
  • Dysphagia.
  • Malabsorption due to bacterial overgrowth.
  • Dilation of the bowel.
91
Q

Describe the pulmonary involvement in systemic sclerosis. (LO4)

A
  • Pulmonary hypertension more prevalent in limited SS than diffusion SS.
  • Shortness of breath on exertion.
  • Interstitial lung disease is common.
92
Q

Describe the investigations for systemic sclerosis. (LO4)

A

Multiple organ involvement so:

  • Blood test.
  • Urinalysis.
  • Lung function tests - spirometry.
  • Imaging.
93
Q

List the aspects of a blood test needed for investigation of systemic sclerosis. (LO4)

A
  • FBC.
  • U+Es.
  • LFTs.
  • Bone group.
  • ANA positive - in about 70% of patients.
  • Scl70 positive - in about 30% of patients with dcSScl.
  • Autocentromere antibodies - in 60% of patients with lateral sclerosis syndrome.
94
Q

List the types of imaging required for investigation of systemic sclerosis. (LO4)

A
  • Chest x-ray.
  • Chest CT.
  • Barium swallow - assesses oesophageal involvement.
95
Q

Describe the management for systemic sclerosis. (LO4)

A
  • Nothing can stop or reverse fibrosis.

- Try to slow the effect of the disease on target organs.

96
Q

Describe the management of Raynaud’s phenomenon (and digital ulcers) due to systemic sclerosis. (LO4)

A
  • Avoid cold.
  • Thermal gloves/socks.
  • High core temperature (calcium channel blockers).
  • Losartan.
  • Fluoxetine.
  • Sildenafil.
  • Intravenous prostacycline.
  • Bosentan.
97
Q

How do we manage gastrointestinal complications in systemic sclerosis? (LO4)

A

Proton pump inhibitors.

98
Q

How do we manage hypertension in systemic sclerosis? (LO4)

A

ACE inhibitors.

99
Q

How do we manage joint complications in systemic sclerosis? (LO4)

A

NSAIDs, analgesia.

100
Q

How do we manage progressive pulmonary hypertension in systemic sclerosis? (LO4)

A

Bosentan or heart/lung transplant.

101
Q

How do we manage interstitial lung disease in systemic sclerosis? (LO4)

A

Glucocorticoids and (pulse intravenous) cyclophosphamide.

102
Q

What is Sjogren’s syndrome? (LO4)

A

Lymphocytic infiltration and fibrosis of salivary and lacrimal glands.

103
Q

Describe the epidemiology of Sjogren’s syndrome. (LO4)

A
  • Typical age of onset between 40-90 years.
  • More common in men, 9:1.
  • May occur with other autoimmune diseases (secondary).
104
Q

Describe the clinical features of Sjogren’s syndrome. (LO4)

A
  • Mouth - dry with dental caries (tooth decay).
  • Fatigue.
  • Small joint pain.
  • Interstitial lung diseases (rare).
  • Interstitial nephritis (rare).
  • Eye - dry/gritty eyes with conjunctivitis and blepharitis and damage to the cornea.
  • 40-fold increased lifetime risk of lymphoma.
105
Q

Describe the investigations for Sjogren’s syndrome. (LO4)

A
  • FBC.
  • U+Es.
  • Rheumatoid factor.
  • Antinuclear antibody (ANA).
  • Schirmer’s test - 6mm after 5 mins.
106
Q

What is Schirmer’s test (dry eye test)? (LO4)

A
  • Place a paper strip at the bottom eyelid.
  • In a normal person, tears will wet the paper beyond the line.
  • In Sjogren’s, there’s no tear production so the paper remains relatively dry.
107
Q

Describe the management of Sjogren’s syndrome. (LO4)

A

Only if symptomatic:

  • Eyedrops
  • Artificial saliva sprays, saliva stimulating tablets and oral gels.
  • Chewing gum.
  • Oral hygiene.
  • Lubricants for vaginal dryness.
  • Pilocarpine - in early disease.
  • Hydroxychloroquine.
  • Immunosuppressions.
  • Lymphadenopathy.
108
Q

What are the main functions and properties of tendons? (LO5)

A
  • They bind bone and muscle.
  • Give stability.
  • Have elastic properties which allow them to store energy and release it to muscle with no additional work leading to smooth movement.
109
Q

How do the elastic properties of tendons allow for smooth movement? (LO5)

A
  • Reorientation of collagen type I fibres.
  • Straightening of the wavy fibrils.
  • Sliding between adjacent collagen fibrils and fibres.
110
Q

Describe tendon formation. (LO5)

A
  • During postnatal development, tendons enlarge by interstitial growth, particularly at myotendinous junctions where there is a high concentration of fibroblasts.
  • Growth decreases along a tendon as you get closer to the bone attachment than the muscle attachment.
111
Q

Describe how tendon strength and thickness develop. (LO5)

A
  • Thickness attained by a tendon depends on the size and strength of the associated muscle.
  • Also influenced by the degree of pennation* of the muscle.
  • Can adapt their strength and stiffness to match prevailing mechanical demands (but this process is slow and incomplete).

*Muscle fibers may run parallel or obliquely to the axis of pull, the latter resulting in fibers inserting into the tendon at an angle (usually between 0° and 30°); this is called the “angle of pennation”.

112
Q

Describe the biomechanics of tendons. (LO5)

A
  • Strong in tension only.
  • Can sustain 5-10% tensile strength before failure.
  • Have a viscoelastic structure.
113
Q

What is meant by a viscoelastic structure? (LO5)

A
  • Deform slowly when exposed to external forces.
  • Once the deforming process has been removed, it returns to its original shape.
  • If you pull fast - it snaps.
  • If you pull slow - it stretches.
114
Q

Where do tendons insert into bone? (LO5)

A

The point at which a tendon and bone meet is called an enthesis or osteotendinous junction. These entheses can either be fibrocartilaginous or fibrous.

115
Q

What are the two categories of entheses. (LO5)

A
  • Fibrocartilaginous enthesis.

- Fibrous enthesis.

116
Q

Describe the structure of fibrocartilaginous entheses. (LO5)

A
  1. Pure dense fibrous connective tissue - continuous with and indistinguishable from the tendon.
  2. Fibrocartilage.
  3. Calcified fibrocartilage.
  4. Bone - continuous with and indistinguishable from the rest of the bone.
  • There are no sharp boundaries between zones.
  • Proportions of each component vary between entheses.
  • Usually found where a tendon approached the bone at a high angle, e.g. triceps brachii.
117
Q

Describe the structure of fibrous entheses. (LO5)

A
  • Characteristic of the shafts of long bones.
  • Tendon approached the bone at an acute angle and merges with the periosteum before attaching to bone by dense fibrous connective tissues, e.g. pronator teres.
  • Generally, they attach to a greater area of bone compared to fibrocartilaginous entheses and this can reduce stress.
118
Q

List the pathologies of tendons. (LO5)

A
  • Tendinositis.
  • Tendinosis.
  • Tendinopathy.
  • Tenosynovitis.
  • Rupture.
119
Q

What is meant by tendinositis? (LO5)

A
  • Inflammation of a tendon.

- The term tendinositis is usually used for tendon injuries that involve acute injuries accompanied by inflammation.

120
Q

What is meant by tendinosis? (LO5)

A
  • Means chronic degeneration of a tendon without inflammation.
  • The main problem is failed healing of repeated minor injuries rather than inflammation.
121
Q

What is meant by tendinopathy? (LO5)

A
  • More general term than tendinositis and tendinosis.

- Just means tendon injury, without specificying the type of injury.

122
Q

What is meant by tenosynovitis? (LO5)

A
  • Means inflammation of the sheath that surrounds a tendon - the synovium.
123
Q

Describe the pathology of tendinopathy. (LO5)

A
  • Sometimes occurs as part of a systemic inflammatory condition.
  • Sometimes due to injury/overuse.
  • Mostly idiopathic.
124
Q

List the clinical features of tendinopathy. (LO5)

A
  • Pain - worse on active movement and further increased when active movement is performed against resistance.
  • Tenderness.
  • Soft tissue swelling (not always present).
125
Q

List some examples of tendinopathy. (LO5)

A
  • Rotator cuff injury.
  • Tennis elbow.
  • Golfer’s elbow.
  • Jumper’s knee.
  • Achilles tendon injury.
  • Sprained ankle.
126
Q

Describe the clinical presentation of tennis elbow. (LO5)

A
  • At common extensor origin, at the lateral epicondyle.
  • Tender.
  • Pain exacerbated by resisted wrist extension.
127
Q

Describe the clinical presentation of golfer’s elbow. (LO5)

A
  • At common flexor origin, at the medial epicondyle.
  • Tender.
  • Pain exacerbated by resisted wrist flexion.
128
Q

Describe the clinical presentation of jumper’s knee. (LO5)

A
  • Overuse syndrome.
  • Pain at inferior pole of patella.
  • Can also occur at insertion of quads.
129
Q

Describe the clinical presentation of rotator cuff injury. (LO5)

A
  • In the subacromial space.
  • When subacromial space becomes narrowed.
  • Supraspinatus irritation.
  • Painful arc.
130
Q

Describe the management of tendinopathy. (LO5)

A
  • Better to treat early.
  • Rest and avoid the cause.
  • NSAIDs.
  • Physiotherapy.
  • Local corticosteroid injection.
  • Surgery.
131
Q

Describe the management of tendinopathy involving steroid injections. (LO5)

A
  • Local anaesthetic inserted with orange needle into skin.
  • Steroid mixed with local anaesthetic.
  • Insert needle into the bone.
  • Inject in fan distribution.
  • Warn of increasing pain for 48 hours, followed by improvement.
  • May need second injection in 6 weeks.
132
Q

Describe the management of tendinopathy involving surgery (with the example of tennis elbow). (LO5)

A
  • Day case.
  • Skin incised.
  • Extensor tendon origin exposed.
  • Extensor tendon detached.
  • Bone debrided and damaged tissue removed.
  • Extensor tendon slides about 1cm.
133
Q

What are the two main causes of tenosynovitis? (LO5)

A
  • Inflammatory arthritis.

- Trauma - result of repetitive or unaccustomed movement.

134
Q

What are the common sites of tenosynovitis? (LO5)

A
  • Abductor pollicis longus.
  • Extensor pollicis brevis tendon (de Quervain’s tenosynovitis - pain on the radial aspect of the wrist).
  • Finger flexors.
135
Q

Describe the clinical features of tenosynovitis. (LO5)

A
  • Pain.
  • Tendon is swollen and tender O/E.
  • Crepitus may be felt on palpation.
  • May result in trigger finger or thumb (tenosynovitis of the flexor tendons).
136
Q

How does trigger finger occur in tenosynovitis? (LO5)

A
  • Nodule develops on the tendon in response to constriction of the tendon sheath.
  • Nodule catches as it enters or leaves the flexor tendon pulleys.
  • Flexors are stronger than extensors, so the finger gets stuck in flexion.
137
Q

Describe the management of tenosynovitis. (LO5)

A
  • Rest.
  • Splinting.
  • Local corticosteroid injections.
  • Surgical decompression of the tendon sheath.
138
Q

Describe the pathophysiology of tendon rupture. (LO5)

A
  • May result from chronic inflammation.
  • May result from degeneration.
  • May result from trauma.
  • E.g. rupture of the extensor tendons of the finger are commonly seen in rheumatoid arthritis.
139
Q

Describe the clinical features of tendon rupture. (LO5)

A
  • Loss of movement at the joint to which the tendon provides power.
  • Deformity.
  • Swelling.
  • E.g. Popeye sign after rupture of the long head of biceps.
  • E.g. Achilles tendon rupture.
140
Q

Describe the management of tendon rupture. (LO5)

A
  • Sometimes, no intervention required, e.g. long head of biceps rupture. This is because function is preserved with other muscles (short head of biceps, brachialis, supinator).
  • Splinting, e.g. mallet splint.
  • Surgey is often required to restore function - may require direct repair of the tendon/tendon transfer.
141
Q

What can be said about the cellularity and metabolic rate of a tendon? (LO5)

A

The cellularity and metabolic rate of a large adult tendon is low, but increases during infection or injury.

142
Q

How are tendons repaired? (LO5)

A
  • Initial proliferation of fibroblasts.
  • Interstitial deposition of new collagen fibres.
  • Complete remodelling of the tissue, e.g. in the bone - this doesn’t happen in adult tendons so healing tendons never recover to their original strength.
143
Q

Describe the structure of tendons. (LO5)

A
  • Soft collagenous tissues.
  • Many components make up the matrix.
  • Made of parallel rows of fibroblasts, organised into microfibrils and wavy fibrils = non-linear strength.
  • These parallel rows (to the long axis) are organised into fascicles which can glide across each other within a sheath, independently.
  • Fascicles are interwoven to some extent.
  • Long tendons may be ridged longitudinally by coarse fasciculi, e.g. obturator internus.
  • Loose connective tissue between the fascicles act as a conduit for small vessels and nerves.
144
Q

List the components of the matrix of tendons. (LO5)

A
  • Mostly collagen type I.
  • Collagen type II.
  • Collagen type V.
  • Elastin.
  • Glycoproteins.
  • Proteoglycans.
145
Q

Describe the loose connective tissues between the fascicles in tendons. (LO5)

A
  • Condenses on the surface as a sheath or epitendineum.
  • May contain elastin and irregularly arranged collagen fibres.
  • Loose attachments between the sheath and the surrounding tissues allows for little resistance to the movements of the tendon.
  • Synovial sheath separates the tendon from the surroudings in situations where the tendon needs extra freedom of movement.
146
Q

Describe the vacular supply to tendons. (LO5)

A
  • Sparse - longitudinal plexus.
  • Small arterioles from adjacent muscle tissue enter longitudinally between the fascicles - branching freely.
  • The arterioles are accompanied by venae comitantes and lymphatic vessels.
  • Augmented by small vessels from adjacent loos connective tissue or synovial sheaths.
  • Vessels rarely pass between bone and tendon at osseus attachments.
  • Junctional surfaces are usually devoid of foramina, except the Achilles’ tendon which received blood supply across the osteotendinous junction.
147
Q

Describe the nerve supply to the tendons. (LO5)

A
  • Largely sensory.
  • No evidence of any capacity for vasomotor control.
  • Golgi tendon organs.
148
Q

What is meant by golgi tendon organs when referring to nerve supply to tendons? (LO5)

A
  • Specialised endings that are sensitive to force.
  • Are found near myotendinous junctions.
  • Their large myelinated afferent axons run within branches of muscular nerves or in the small rami of adjacent peripheral nerves.
  • Play an important role in tendon reflexes - protect MSK from injury.
149
Q

List the functions of connective tissue. (LO6)

A
  • Makes up most of the tissue in our body.
  • It provides mechanical support.
  • Allows movement.
  • Acts as an arena for fighting infection.
  • Regulates cell behaviour.
150
Q

List the components of connective tissue. (LO6)

A
  • Main two molecules are collagen and elastic fibres.
  • There are three types of fibres:
    1. Collagen fibres.
    2. Retinacular fibres.
    3. Elastic fibres.
151
Q

Describe the elastic fibres in connective tissue. (LO6)

A
  • 10-12nm microfibrils.

Made up of:

  • Elastin.
  • Fibrillin’s.
  • Fibulins.
  • Matrix associated with glycoproteins.
152
Q

Describe the collagen fibres in connective tissue. (LO6)

A
  • 30% of our dry body weight is collagen.
  • Consists of 3 alpha chains arranged in a triple helix.
  • Glycine is essential to form the triple helix.
  • Each alpha chain is a single gene product.
  • Either 3 identical alpha chains.
  • Helix is stabilised by hydrogen bonds.
  • Proline and OH proline provide rigidity and stability.
  • Unique amino acid sequence.
153
Q

What are proteoglycans (connective tissue)? (LO6)

A

The connective tissues contain ‘ground substance’ and these are the proteoglycans (everything other than collagen). They are variable in size - 40kDa to over 100kDa. They have glycosaminoglycan (GAG) side chains.

  • Aggrecan.
  • Decorin.
  • Versican.
  • Biglycan.
  • Fibromodulin.
154
Q

List the functions of proteoglycans in connective tissue. (LO6)

A
  • Can hold water in tissues.
  • Confer viscoelastic properties.
  • Interact with other cells, cytokines and collage.
155
Q

Describe the structure and function of aggrecan. (LO6)

A
  • Forms huge multimeric aggregates in cartilage.
  • Link protein.
  • Stabilises binding to hydrogen.
  • It is highly hydrophilic and and allows high turgor pressure to help resist compression.
  • Damage to this ability to suck in water means it cannot resist compression. Example: osteoarthritis.
156
Q

List the cells involved in connective tissue. (LO6)

A
  • Fibroblasts.
  • Chondrocytes.
  • Osteocytes.
  • Myofibroblasts.
157
Q

Describe the function of fibroblasts in connective tissue. (LO6)

A
  • Cells that make up skin, tendons and ligaments.
  • Produced in the mesenchymal stem cells in the mesoderm.
  • Allow synthesis of the extracellular matrix.
158
Q

Describe the function of chondrocytes in connective tissue. (LO6)

A
  • Cells that make up cartilage.

- Also responsible for synthesis and organisation of the extracellular matrix.

159
Q

Describe the function of osteocytes in connective tissue. (LO6)

A
  • Osteocytes make up bone.
  • Osteoblasts build bone.
  • Osteoclasts resorb bone.
160
Q

Describe the function of myofibroblasts in connective tissue. (LO6)

A
  • Myofibroblasts are modified fibroblasts.

- Assist with wound contraction and are therefore abundant in areas undergoing wound healing.

161
Q

List the types of connective tissue. (LO6)

A
  • Skin.
  • Tendon/ligament.
  • Bone.
  • Cartilage.
162
Q

List the components of skin as a connective tissue and state how they are arranged. (LO6)

A
  • 60% type I collagen.
  • 30% type III collagen.
  • Meshwork of fibres.
163
Q

List the components of tendons/ligaments as a connective tissue and state how they are arranged. (LO6)

A
  • > 90% type I collagen - this is what gives tendons and ligaments tensile strength.
  • 5% type III collagen.
  • Fibres are parallel which also increases tensile strength.
164
Q

List the components of bone as a connective tissue and state how they are arranged. (LO6)

A
  • 90% type I collagen.
  • 3% type V collagen.
  • The type I collagen forms sheets known as lamellar.
165
Q

List the components of cartilage as a connective tissue and state how they are arranged. (LO6)

A
  • 95% type II collagen.

- Meshwork of fibres that contain a mixture of collagen and aggrecan.

166
Q

What is the general function of the anterior compartment of the upper arm? Which nerve innervates this compartment? (LO7)

A
  • Function: flexion of the elbow.

- Innervation: MUSCULOCUTANEOUS nerve.

167
Q

List the muscles of the anterior compartment of the upper arm. (LO7)

A
  • Biceps brachii.
  • Coracobrachialis.
  • Brachialis.
168
Q

Describe the attachments of the biceps brachii and state its function. Which nerve innervates it? (LO7)

A
  • 2 heads.
  • One attaches to the coracoid process.
  • One attaches to the supraglenoid tubercle of the scapula.
  • Both heads attach distally at the radial tuberosity.
  • Function: supination, but also play a major role in flexion of the elbow.
  • Innervation: MUSCULOCUTANEOUS nerve.
169
Q

Describe the attachments of the coracobrachialis and state its function. Which nerve innervates it? (LO7)

A
  • From the coracoid process to the humeral shaft.
  • Function: flexion of the elbow.
  • Innervation: MUSCULOCUTANEOUS nerve.
170
Q

Describe the attachments of the brachialis and state its function. Which nerve innervates it? (LO7)

A
  • From the humeral shaft to the ulnar tuberosity.
  • Function: flexion of the elbow.
  • Innervation: MUSCULOCUTANEOUS nerve.
171
Q

What is the general function of the anterior compartment of the upper arm? Which nerve innervates this compartment? (LO7)

A
  • Function: extension of the elbow.

- Innervation: RADIAL nerve.

172
Q

Which muscle makes up the posterior compartment of the upper arm? (LO7)

A

Triceps brachii.

173
Q

How many heads does the triceps brachii have and where do they attach? State the function and innervation of this muscle. (LO7)

A
  • 3 heads.
  • Long head attaches at the infraglenoid shaft.
  • Medial head attaches at the humeral shaft.
  • Lateral head attaches at the humeral shaft.
  • All three heads converge and join at the olecranon.
  • Function: extension of the elbow.
  • Innervation: RADIAL nerve.
174
Q

What is the general function of the anterior forearm? Which nerve innervates this compartment? (LO7)

A
  • Function: flexion of the forearm, wrist and fingers.
  • Innervation: MEDIAN nerve (except for flexor carpi ulnaris and medial half of flexor digitorum profundus which are innervated by the ulnar nerve).
175
Q

How are the muscles of the anterior forearm categorised? (LO7)

A
  • Superficial.
  • Intermediate.
  • Deep.
176
Q

How many muscles reside in the superficial layer of the anterior forearm? Name them. (LO7)

A

4 muscles:

  • Flexor carpi ulnaris.
  • Palmaris longus.
  • Flexor carpi radialis.
  • Pronator teres.
177
Q

How many muscles reside in the intermediate layer of the anterior forearm? Name them. (LO7)

A

1 muscle:

- Flexor digitorum superficialis.

178
Q

How many muscles reside in the deep layer of the anterior forearm? Name them. (LO7)

A

3 muscles:

  • Flexor pollicis longus.
  • Flexor digitorum profundus.
  • Pronator quadratus.
179
Q

Describe the attachments of the superficial muscles of the anterior forearm and state their function. Which nerve innervates these muscles? (LO7)

A
  • Originate from the medial epicondyle and insert into various places.
  • Function: flexion of the wrist, pronation of hand, ulnar and radial deviation of the hand.
  • Innervation: MEDIAN nerve, except flexor carpi ulnaris (ulnar nerve).
180
Q

Describe the attachments of the flexor digitorum superficialis (intermediate anterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Lies between the superficial and deep muscles.
  • From medial epicondyle to the MCP and PIP joints of all fingers (except thumb).
  • The muscle splits into the tendons in the carpal tunnel.
  • Function: flexion of the MCP and PIP in fingers, flexion of the wrist.
  • Innervation: MEDIAN nerve.
181
Q

Describe the attachments of the flexor digitorum profundus (deep anterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Ulnar interosseous membrane into the carpal tunnel, where it divides into 4 tendons attaching to the DIP of 4 fingers (excluding thumb).
  • Function: flexion of the DIPs (only muscle in the arm that does this).
  • Innervation: medial half supplied by ULNAR nerve, lateral half supplied by MEDIAL nerve.
182
Q

Describe the attachments of the flexor pollicis longus (deep anterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Anterior surface of the radius to the base of the MCP and PIP of the thumb.
  • Function: flexion of the interphalangeal joints and MCP of the thumb.
  • Innervation: MEDIAN nerve.
183
Q

Describe the attachments of the pronator quadratus (deep anterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Square-shaped muscle lying under the flexor pollicis longus (FPL) and flexor digitorum profundus (FDP).
  • Function: pronation of the arm.
  • Innervation: MEDIAN nerve.
184
Q

What is the general function of the superficial posterior forearm muscles? Which nerve innervates this compartment? (LO7)

A
  • All of these muscles generally originate at the LATERAL epicondyle.
  • Function: extension of the wrist.
  • Innervation: RADIAL nerve.
185
Q

How are the muscles of the posterior forearm categorised? (LO7)

A
  • Superfial.

- Deep.

186
Q

How many muscles reside in the superficial layer of the posterior forearm? Name them. (LO7)

A

7 muscles:

  • Brachioradialis.
  • Extensor carpi radialis longus and brevis.
  • Extensor digitorum.
  • Extensor digiti minimi.
  • Extensor carpi ulnaris.
  • Anconeus.
187
Q

Describe the attachments of the brachioradialis (superficial posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Odd one out among the posterior muscles.
  • Originates from lateral epicondyle and attaches to distal end of radius.
  • Function: flexion of the elbow.
  • Innervation: RADIAL nerve.
188
Q

Describe the attachments of the extensor carpi radialis longus and brevis (superficial posterior forearm) and state their function. Which nerve innervates these muscles? (LO7)

A
  • Lateral epicondyle to MCP of 2nd and 3rd fingers.
  • Function: extension of the wrist and abduction.
  • Innervation: RADIAL nerve.
189
Q

Describe the attachments of the extensor digitorum (superficial posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Lateral epicondyle, splits into 4 tendons, inserting to the distal hood of 4 fingers (excluding the thumb).
  • Function: major extensor of the wrist (especially while the wrist is pronated).
  • Innervation: RADIAL nerve.
190
Q

Describe the attachments of the extensor digiti minimi (superficial posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Lateral epicondyle and follows the same path as the extensor digitorum, attaching to the distal hood of the pinky finger.
  • Function: extension of the pinky finger and some contribution to extension of the wrist.
  • Innervation: RADIAL nerve.
191
Q

Describe the attachments of the extensor carpi ulnaris (superficial posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Lateral epicondyle to the base of the 5th metacarpal.
  • Function: wrist extension and adduction.
  • Innervation: RADIAL nerve.
192
Q

Describe the attachments of the anconeus (superficial posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Lateral epicondyle to posterior part of the olecranon.
  • Function: extension and stabilisation of the elbow, abduction of the ulna during pronation.
  • Innervation: RADIAL nerve.
193
Q

What is the general function of the deep posterior forearm muscles? Which nerve innervates this compartment? (LO7)

A
  • Generally from radial/ulnar interosseus membranes.
  • Function: extension of fingers.
  • Innervation: RADIAL nerve.
194
Q

How many muscles reside in the deep layer of the posterior forearm? Name them. (LO7)

A

6 muscles:

  • Supinator.
  • Abductor pollicis longus.
  • Extensor pollicis brevis.
  • Extensor pollicis longus.
  • Extensor indicis.
195
Q

Describe the attachments of the supinator (deep posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • First head - attaches to the lateral epicondyle.
  • Second head - attaches to the posterior surface of the ulnar.
  • Both lead to and attach to the posterior surface of the radius.
  • Function: supination of the forearm.
  • Innervation: RADIAL nerve.
196
Q

Describe the attachments of the abductor pollicis longus (deep posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Interosseous membrane to the base of the 1st metacarpal (thumb).
  • Function: abduction of the thumb.
  • Innervation: RADIAL nerve.
197
Q

Describe the attachments of the extensor pollicis brevis (deep posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Posterior surface of the radius and interosseous membrane to the proximal phalanx of the thumb.
  • Function: extension of the MCP and carpometacarpal joint of the thumb.
  • Innervation: RADIAL nerve.
198
Q

Describe the attachments of the extensor pollicis longus (deep posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Posterior surface of the ulna to distal phalanx of the thumb.
  • Function: extension of all the joints of the thumb (carpometacarpal, MCP, interphalangeal).
  • Innervation: RADIAL nerve.
199
Q

Describe the attachments of the extensor indicis (deep posterior forearm) and state its function. Which nerve innervates it? (LO7)

A
  • Posterior surface of the ulna to the extensor hood of the index finger.
  • Function: extension of the index finger.
  • Innervation: RADIAL nerve.
200
Q

What are the two main characteristics of muscles in the hand? (LO7)

A
  • Extrinsic: crude movements and forceful grip.

- Intrinsic: fine motor control.

201
Q

How are the muscles of the hand categorised? (LO7)

A
  • Thenar muscles.
  • Hypothenar muscles.
  • Lumbricals.
  • Interossei.
202
Q

How many thenar muscles reside in the hand? Name them. (LO7)

A

3 muscles:

  • Opponens pollicis.
  • Abductor pollicis brevis.
  • Flexor pollicis brevis.

Reside in the thenar eminence. Generally innervated by MEDIAN nerve.

203
Q

Describe the attachments of the opponens pollicis (thenar muscles of the hand) and state its function. Which nerve innervates it? (LO7)

A
  • Trapezium bone and flexor retinaculum to the lateral margin of the 1st metacarpal.
  • Function: opposition of the thumb (medial rotation and flexion).
  • Innervation: MEDIAN nerve.
204
Q

Describe the attachments of the abductor pollicis brevis (thenar muscles of the hand) and state its function. Which nerve innervates it? (LO7)

A
  • Scaphoid and trapezium to the proximal phalanx of the thumb.
  • Function: abduction of the thumb.
  • Innervation: MEDIAN nerve.
205
Q

Describe the attachments of the flexor pollicis brevis (thenar muscles of the hand) and state its function. Which nerve innervates it? (LO7)

A
  • Trapezium and flexor retinaculum to the base of the proximal phalanx.
  • Function: flexion of the MCP of the thumb.
  • Innervation: MEDIAN nerve and some innervation from the ULNAR nerve.
206
Q

How many hypothenar muscles reside in the hand? Name them. (LO7)

A

3 muscles:

  • Opponens digiti minimi.
  • Abductor digiti minimi.
  • Flexor digiti minimi.

Reside in the hypothenar eminence. Generally innervated by ULNAR nerve.

207
Q

Describe the attachments of the opponens pollicis (thenar muscles of the hand) and state its function. Which nerve innervates it? (LO7)

A
  • Hook of the hamate to the 5th metacarpal.
  • Function: opposition of the little finger (rotation of pinky into the palm).
  • Innervation: ULNAR nerve.
208
Q

Describe the attachments of the abductor pollicis brevis (thenar muscles of the hand) and state its function. Which nerve innervates it? (LO7)

A
  • Pisiform bone to the base of the proximal phalanx of the pinky.
  • Function: abduction of the little finger.
  • Innervation: ULNAR nerve.
209
Q

Describe the attachments of the flexor pollicis brevis (thenar muscles of the hand) and state its function. Which nerve innervates it? (LO7)

A
  • Hook of the hamate to the base of the proximal phalanx.
  • Function: flexion of the MCP of the little finger.
  • Innervation: ULNAR nerve.
210
Q

How many lumbrical muscles reside in the hand? Name them. (LO7)

A

4 muscles:

  • Lateral: I + II (unipennate).
  • Medial: III + IV (bipennate).

Found on the dorsal aspect of the hand.

211
Q

Describe the attachments of the lumbricals (hand) and state their function. Which nerve innervates these muscles? (LO7)

A
  • Originate from the flexor digitorum profundus tendon, inserting on the extensor hood.
  • Function: flexion of the MCP joints, extension of the interphalangeal joints of each digit.
  • Innervation: Lateral I + II by the MEDIAN nerve. Medial III + IV by the ULNAR nerve.

Denervation of the 2 medial lumbricals causes the ulnar claw.

212
Q

How many interossei muscles reside in the hand? (LO7)

A

Dorsal interossei:
- 4 muscles.

Palmar interossei:
- 3 muscles.

213
Q

Describe the attachments of the dorsal interossei muscles and state their function. Which nerve innervates these muscles? (LO7)

A
  • Lateral and medial surface of the metacarpals, attaching to the proximal phalanx and the extensor hood of each finger.
  • Function: abduction of the MCP joints.
  • Innervation: ULNAR nerve.
214
Q

Describe the attachments of the palmar interossei muscles and state their function. Which nerve innervates these muscles? (LO7)

A
  • Medial/lateral surface of the metacarpal to the extensor hood and proximal phalanx of the same finger.
  • Function: adduction of the MCP joints.
  • Innervation: ULNAR nerve.