Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBBS - Y1 > Week 11 - connective tissue > Flashcards

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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the systemic features of SLE. (LO2)

A
  • Fatigue.
  • Weight loss.
  • Fever.
  • Mild lymphadenopathy.
  • Arthralgia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A
  • Presents with heavy haematuria.
  • Proteinuria.
  • Casts on urine microscopy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe pregnancy outcomes in patients with SLE. (LO2)

A
  • Poor with or without APLS.
  • Pregnancy loss - 13.1% total.
  • Preterm birth.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the epidemiology of vasculitis. (LO3)

A
  • Incidence of 40-60 cases/million/year.
  • Very rare.
  • Increases with age.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

List the the risk factors for vasculitis. (LO3)

A
  • Dust exposure.
  • Farming.
  • Infection.
  • Drugs.
  • Season.
  • Geography.
  • Ethnicity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

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

A
  • High inflammatory markers.

- Negative antibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

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

A
  • ANCA test is negative.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the investigation findings for Kawasaki disease. (LO3)

A
  • ANCA test is negative.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

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

A
  • Associated with proteinase 3 ANCA.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

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

A
  • No granulomata.
  • Predominantly kidney affected.
  • Skin involvement.
  • Peripheral nerves affected.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the investigation findings for microscopic polyangiitis. (LO3)

A
  • Myeloperoxidase ANCA.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

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

A
  • Can be associated with myeloperoxidase ANCA.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is jaw claudication? (LO3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

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

A
  • Blood test.
  • ANCA.
  • Urine - blood, protein, casts.
  • Tissue.
  • Imaging.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is meant by casts? (LO3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Describe the management for large vessel vasculitis. (LO3)

A
  • Glucocorticoids.

- Immunosuppressive agents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

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

A
  • Rituximab.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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

A
  • Comorbidities.

- Treatment side effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

List the prognostic factors for vasculitis. (LO3)

A
  • Age.
  • Target organ involvement.
  • Damage caused.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

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

A
  • Ehlers-Danlos syndrome.
  • Epidermolysis Bullosa.
  • Marfan syndrome.
  • Osteogenesis imperfecta.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

List some autoimmune inflammatory connective tissue diseases. (LO4)

A
  • Polymyositis.
  • Dermatomyositis.
  • Rheumatoid arthritis.
  • Scleroderma.
  • Sjogren’s syndrome.
  • Systemic lupus erythematosus (SLE).
  • Vasculitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

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

A
  • Fingers.
  • Toes.
  • Ears.
  • Nose.
  • Lips.
  • Nipples.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

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

A
  • Pain.
  • Numbness.
  • Pins and needles.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

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

A
  • Common symptoms and may predate other symptoms.

- Consider secondary Raynaud’s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

MBBS - Y1 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions