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PHASE 2A (Mine) > MSK > Flashcards

MSK Flashcards

1
Q

What causes osteoarthritis?

A

Combination of genetic factors, overuse and injury

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2
Q

What are the risk factors for osteroarthritis?

A

Obestiy, Age, occupation, trauma, female, family history

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3
Q

What are the 4 key X-ray changes in osteoarthritis?

A 
LOSS:
Loss of joint space
Osteophytes
Subchondral sclerosis 
Subchondral cysts
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4
Q

What is subchondral sclerosis?

A

Increased density of the bone along the joint line

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5
Q

What are subchondral cysts?

A

Fluid-filled holes in the bone.

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6
Q

What is the subchondral bone?

A

Layer of bone just below the cartilage in a joint (chondral= cartilage)

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7
Q

What are the two types of bone structure?

A

Macro and micro

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8
Q

What are the types of macro bone structure?

A

Cortical

Trabecular

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9
Q

What is the structure of cortical bone and where is it found?

A

Compact, dense. Only spaces are for cells and blood vessels.
Typically found in outer layer of long bones.
80% of bone mass

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10
Q

What is the structure of trabecular bone and where is it found?

A

Cancellous (spongy) with network of struts (trabeculae). Cells are in the trabeculae and blood vessels in holes.
Found in end of long bones.

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11
Q

What are the different micro bone structures?

A

Woven bone

Lamellar bone

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12
Q

What is woven bone and where is it found?

A

Made quickly, disorganised with no clear structure.

Found in places with rapid bone growth, replacement or high bone turnover.

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13
Q

What happens to woven bone after completion of growth?

A

It turns into lamellar bone

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14
Q

What is lamellar bone and how does it form?

A

Organised bone with a layered structure. Made slowly from the remodelling of immature woven bone.

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15
Q

What are the different types of bone?

A 
Long bones
Short bones
Flat bones
Irregular bones
Sesamoid bones
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16
Q

What are the main bone cells?

A

Osteoclast
Osteoblast
Osteocyte
Bone lining cell

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17
Q

What is the function of osteoblasts?

A

Form bone:

Produce type 1 collagen and mineralise the extracellular matrix

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18
Q

What is the function of osteoblasts?

A

Resorb bone:

Dissolve the mineralised matrix (acid) and breakdown collagen (enzymes)

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19
Q

How are bones made to be the right shape?

A

Modelling and remodelling: gross shape made, bone added and taken away then all bone is replaced.

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20
Q

What are osteocytes?

A

Mature bone cells involved in the maintenance of bone (osteoblast enclosed in the matrix)

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21
Q

What is the composition of bone?

A
  • 50-70% mineral (Hydroxyapatite)
  • 20-40% organic matrix: Type one collagen (90%), non-collagenous proteins (10%)
  • 5-10% water.
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22
Q

What is the purpose of mineral in bone and what is the purpose of the collagen?

A

Mineral provides stiffness

Collagen provides elasticity.

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23
Q

What is the function of joints?

A
  • Allow movement in 3 dimensions
  • Bear weight
  • Transfer load evenly
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24
Q

What are the different types of joint (with examples)?

A
  • Fibrous (teeth sockets)
  • Cartilaginous (Intervertebral discs)
  • Synovial (metacarpophalangeal and knee joint)
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25
Q

What is a synovial joint?

A

Articulating bones seperated by fluid filled cavity. Most joints are this.

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26
Q

What are osteophytes?

A

Bone lumps (bone spurs) that grow around the joints or spine.

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27
Q

What is the main presentation of osteoarthritis?

A

Joint pain and stiffness-usually worsened by activity.

Also leads to deformity, instability and reduced function.

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28
Q

What are the most commonly affected joints in osteoathritis?

A 
Hips
Knees 
Sacro-iliac joints
Distal-interphalangeal joints 
MCP (base of thumb) 
Wrist
Cervical spine
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29
Q

What are the signs of osteoarthritis in the hands?

A 
Heberden's nodes (DIP joints)
Bouchard's nodes (PIP joints)
Squaring at base of thumb 
Weak grip
Reduced range of motion
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30
Q

How is osteoarthritis managed?

A
  • Lifestyle changes: weight loss, physiotherapy to improve strength to support joint, occupational therapy, orthotics.
  • Stepwise analgesia:
    1. Paracetamol/ topical NSAIDS/ capsaicin
    2. Add oral NSAIDS (and protective PPI)
    3. Consider opiates (codeine/ morphine)
  • Intra-articular steroid injections
  • Joint replacement in severe cases.
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31
Q

What is rheumatoid arthritis?

A

Autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa

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32
Q

What is a bursa?

A

Small fluid-filled sac lined by synovial membrane with an inner capillary layer of viscous synovial fluid. Provides a cushion and reduces friction between the surfaces of bone and soft tissue.

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33
Q

What is a tendon sheath?

A

Thin layer of tissue surrounding each tendon in the body.

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34
Q

What type of arthritis is rheumuatoid?

A

Inflammatory symmetrical polyarthritis (affects multiple joints and is symmetrical)

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35
Q

In which gender is rheumatoid arthritis more common?

A

3X more common in women than men

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36
Q

What is Rheumatoid Factor (RF)?

A

An autoantibody present in around 70% of RA patients. Targets the Fc portion of the IgG antibody, activating the immune system.

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37
Q

What are cyclic citrullinated peptide antibodies (anti-CPP antibodies)?

A

Autoantibodies that are more sensitive and specific to RA than rheumatoid factor.

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38
Q

What are the key presentations of rheumatoid arthritis?

A

Symmetrical distal polyarthropathy (joint pain):

  • Pain
  • Swelling
  • Stiffness
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39
Q

Where does RA usually start and how quick is onset?

A

Usually complain of pain/stiffness in small joints of hands, feet, wrist, ankle, MCP/ PIP joints. Onset can be very rapid (overnight) or over months to years.

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40
Q

What are the systemic symptoms associated with RA?

A

Fatigue
Weight loss
Flu like illness
Muscle aches and weakness.

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41
Q

What is palindromic rheumatism?

A

Self limiting short episodes of inflammatory arthritis that typically last 1-2 and then resolve.

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42
Q

What are the most common joints affected in RA?

A 
Proximal interpharangeal joints (PIP)
Metacarpophalangeal (MCP) joints
Wrist and ankle
Metatarsophalangeal joints (in foot)
Cervical spine
Large joints (knee, hips, shoulders)
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43
Q

What is atlantoaxial subluxation?

A

Disorder of C1-C2 causing impairment in rotation of the neck. Caused by local synovitis and damage to the ligaments and bursa around the odontoid peg of the axis and atlas.
Can cause spinal cord compression and is an emergency.

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44
Q

What are common signs og RA in the hands?

A
  • ‘Boggy’ feeling when palpating synovium around joints.
  • Z-shaped deformity of thumb
  • Swan shaped neck deformity (of fingers)
  • Boutonnieres deformity (hyperextended DIP with flexed PIP)
  • Ulnar deviation of the fingers at the knuckle (MCP joints)
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45
Q

What other extra-articular (outside of a joint) manifestations may be present in RA?

A
  • Pulmonary fibrosis
  • Bronchiolitis obliterans
  • Felty’s syndrome
  • Secondary Sjogren’s syndrome
  • Anaemia of chronic disease
  • Cardiovascular disease-
  • Episcleritis/ scleritis
  • Rheumatoid nodules
  • Lymphadenopathy
  • Carpal tunnel
  • Amyloidosis
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46
Q

What investigations are done with suspected RA?

A

If there is Symmetrical polyarthropathy affecting small joints:

  • Check rheumatoid factor- if negative, check anto-CCP antibodies
  • Inflammatory markers (CRP/ ESR)
  • X-ray hands and geet
  • Ultrasound of joints can be used to confirm synovitis.
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47
Q

What X-ray changes would be seen in RA?

A
  • Joint destruction and deformity
  • Soft tissue swelling
  • Periarticular osteopenia
  • Bony erosions
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48
Q

How is RA diagnosed?

A 
Patients scored based on:
1. Joints involved
2. Serology (RF and anti-CCP)
3. Inflammatory markers (ESR and CRP)
4. Duration of symptoms (> or < 6 weeks) 
Scores added up and >6 = arthritis
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49
Q

What is the DAS28 score?

A

Disease activity score for RA: Assessment of 28 joints and points are given for swollen joints, tender joints and ESR/ CRP results.

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50
Q

What factors indicate a worse prognosis in RA?

A 
Younger onset
Male
More joints/ organs affected
Presence of RF and anti-CCP
Erosion seen on X-ray
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51
Q

What treatment is given at first presentation of RA and in subsequent flare ups?

A

Short course steroids to quickly settle disease.

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52
Q

Why are NSAIDS/COX-2 inhibitors often avoided in RA?

A

Risk GI bleed (can be co-prescribed with PPIs)

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53
Q

What are the guidelines for the prescription of disease modifying anti-rheumatic drugs (DMARDs)?

A

1st line: Monotherapy (methotrexate, leflnomide, sulfasalazine)
2nd line: Two of these in combination
3rd line: Methotrexate + biological therapy (TNF inhibitor)
4th line: Methotrexate + rituximab)

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54
Q

What are the different types of biological therapies to treat RA?

A 
Anti-TNF's (Adalimumab, infliximab, etanercept)
Anti-CD20 (Rituximab) 
Anti-IL6
Anti-IL6 receptor 
JAK inhibitors
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55
Q

What is the problem with biological therapies?

A

They all lead to immunosuppression so patients are prone to serious infections. Can also lead to reactivation of dormant infections (E.g. TB or Hep B)

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56
Q

How does Methotrexate work?

A

Interferes with the metabolism of folate and suppresses components of the immune system–> Reduces function of cells that cause inflammation of the joints (needs to be taken with folic acid)

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57
Q

What are the main side effects of methotrexae?

A 
Mouth ulcers
Liver toxicity
Pulmonary fibrosis
Bone marrow suppression and leukopenia
Teratogenic (harmful to pregnancy)
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58
Q

What is leflunomide and how does it work?

A

Immunosuppressant that works by interfering with the production of pyrimidine (component of RNA/ DNA)

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59
Q

What is Sulfasalzine and how does it work?

A

Immunosuppressive and anti-inflammatory with unclear mechanism.

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60
Q

What is Hydroxychloroquine and how does it work?

A

Immunosuppressive that inteferes with Toll-like receptors, disrupting antigen presentation and increasing pH in lysosomes of immune cells.

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61
Q

What are Anti-TNF drugs and how do they work?

A

Tumour necrosis factor= cytokine involved in stimulating inflammation. Therefore, blocking it reduces inflammation. (most are monoclonal antibodies to TNF)

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62
Q

What is Rituximab and how does it work?

A

Monoclonal antibody that targets CD20 protein on surface of B cells, causing their destruction. Used for immunosuppression.

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63
Q

What are Spondyloarthropathies ?

A

Forms of arthritis that form in the bones of the spine and nearby joints.

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64
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis.

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65
Q

What is arthritis mutilans?

A

Most severe form of psoriatic arthritis: condition where the joint is completely destroyed

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66
Q

What are the different patterns psoriatic arthritis can take on?

A

Symmetrical polyarthritis
Asymmetrical pauciarthritis
Spondylitic pattern

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67
Q

What is pauciarthritis?

A

When the arthritis only affects a few joints.

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68
Q

How does spondylitic pattern psoriatic arthritis usually present?

A

More common in men:
Back stiffness
Sacroilitis
Atlanto-axial joint involvement

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69
Q

What are the key signs of psoriatic arthritis?

A

Plaques of psoriases on skin
Pitting of nails
Onycholysis (seperation of nail from nail bed)
Dacytlitis (inflammation of full finger)
Enthesitis (Inflammation of points where tendons insert onto bone)

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70
Q

How is psoriatic arthritis screened for?

A

People with psoriases complete PEST (Psoriasis epidemiological screening tool) test.

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71
Q

What X-ray changes are seen with psoriatic arthritis?

A 
Periostitis (inflammation of periosteum) 
Ankylosis 
Osteolysis
Dactylitis
Pencil-in- cup appearance of digits
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72
Q

What is ankylosis?

A

Where bones joining together causes joint stiffness

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73
Q

How is psoriatic arthritis managed>

A 
Same as rheumatoid:
NSAIDS for pain
DMARDS (methotrexate, leflunomide, sulfasalazine)
Anti-TNFS
Usterkinumab (last line)
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74
Q

What is reactive arthritis?

A

(REITER SYNDROME) Where synovitis occurs in the joints as a reaction to a recent infective trigger.

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75
Q

What does reactive arthritis cause/ present with?

A

Acute monoarthritis- inflammation of single joint (usually the knee), presenting with warm, swollen and painful joint.

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76
Q

What are the most common infections to trigger reactive arthritis?

A

Gastroenteritis, STI’s (chlamydia, gonorrhoea)

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77
Q

What other problems can reactive arthritis cause?

A

-Bilateral conjunctivitis
-Anterior uveitis (inflammation of middle layer of eye)
-Circinate balanitis (dermatitis of penis head)
(CAN’T SEE, PEE OR CLIMB A TREE)

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78
Q

How is reactive arthritis managed?

A

Antibiotics given until septic arthritis excluded.
Aspirate joint and send sample to exclude septic arthritis.
NSAIDS
Steroid injection to joint

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79
Q

What is ankylosing spondylitis?

A

Inflammatory condition mainly affecting the spine that causes progressive stiffness and pain.

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80
Q

What gene do the seronegative spondyloarthropathy conditions relate to?

A

HLA B27 gene.

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81
Q

What key joints are affected in ankylosing spondylitis?

A

Sacroiliac joints, joints of vertebral column.

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82
Q

What are the main presenting features of ankylosing spondylitis?

A

Lower back pain and stiffness
Sacroiliac pain in buttock region.
(Worse with rest and improves with movement, is worse at night and in the morning- takes at least 30 mins for stiffness to improve)

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83
Q

What are key complications of ankylosing spondylitis?

A

Verterbal fractures

Fusin of the spine or sacroiliac joints (bamboo spine on X-ray)

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84
Q

What is the usual onset of ankylosing spondylitis?

A

Gradual development of symptoms over > 3 months

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85
Q

What other organ systems can ankylosing spondylitis affect and what does it cause?

A 
Systemic symptoms: Weight loss, fatigue
Chest pain (costovertebral/ sternal joints)
Enthesitis 
Dactylitis
Anaemia
Anterior Uveitis
Aortitis
Heart block
Restrictive lung disease
Pulmonary fibrosis
IBS
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86
Q

What is Schober’s test?

A

Assessment of mobility of spine:
Patient stands straight, L5 found and marks placed 10cm above and 5cm below. Patient bends forward and distance between points measured.
If < 20cm, indicates restriction in lumbar movement.

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87
Q

What investigation can be done to diagnose ankylosing spondylitis?

A 
Schobers test
Inflammatory markers (CRP, ESR)
HLA B27 Genetic testing
Xray of spine and sacrum 
MRI of spine (bone marrow oedema)
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88
Q

What X-ray changes may be seen in ankylosing spondylitis?

A 
Bamboo spine (vertebrae fusion) 
Squaring of vertbral bodies
Subchondral sclerosis/ erosions
Syndesmophytes
Ossification
Fusion of joints
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89
Q

How is ankylosing spondylitis managed?

A 
NSAIDS
Steroids
Anti-TNFs
Secukinumab
Lifestyle changes: physio, exercise, avoid smoking
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90
Q

What is SLE?

A

Systemic lupus erythematosus (lupus): Inflammatory autoimmune connective tissue disease.

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91
Q

What is the pathophysiology of lupus?

A

Anti-nuclear antibodies (antibodies to proteins in the patients nucleus) cause an immune response that targets these proteins, initiating systemic inflammatory response.

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92
Q

What is erythematosus?

A

Red molar rash that occurs across the face in lupus

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93
Q

What are the symptoms of SLE?

A

Usually relapse-remitting course with flare ups:

  • Fatigue
  • Weight loss
  • Arthralgia (joint pain)/ arthritis
  • Myalgia (muscle pain)
  • Fever
  • Photosensitive malar rash (nose and cheeks)
  • Lymphadenopathy/ splenomegaly
  • Shortness of breath
  • Pleuritic chest pain
  • Mouth ulcers
  • Hair loss
  • Raynauds phenomenon
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94
Q

What is Raynaud’s phenomenon?

A

When the fingers and toes change colour due to cold, anxiety or stress

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95
Q

What investigations are done in SLE?

A

Autoantibodies
Full blood count (normocytic anamia of chronic disease)
C3/4 levels
CRP and ESR
Immunoglobulins
Urinalysis and urine protein:creatinine ratio
Renal biopsy

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96
Q

What is the initial investigation when someone presents with SLE symptoms?

A

ANA (anti-nuclear antibody) blood test (present in 80% of cases)

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97
Q

What autoantibodies are indicative of SLE?

A

Anti-nuclear antibodies (80%)
Anti-double stradned DNA (Anti-dsDNA) (70%- specific to SLE)
Anti-extractable nuclear antigen antibodies (anti-ENA antibodies)

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98
Q

What are the main complications of SLE?

A 
Cardiovascular disease
Infection
Anaemia of chronic disease
Pericarditis
Pleuritis
Interstitial lung disease
Lupus nephritis
Neuropsychiatric SLE
Recurrent miscarriage
Venous thromboembolism
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99
Q

How does SLE cause cardiovascular disease?

A

Chronic inflammation in blood vessels leads t hypertension and coronary artery disease

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100
Q

How is SLE treated?

A 
Anti-inflammatories and immunosuppression: 
NSAIDS
Steroids
Hydroxychloroquine
Methotrexate e.t.x.
Biological therapies (Rituximab)
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101
Q

What is discoid lupus erythematosus?

A

Chronic skin condition, causing photosensitive lesions on face, ears and scalp.

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102
Q

What is osteoporosis?

A

Condition that causes reduction of bone density

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103
Q

What is osteopenia?

A

Reduced bone mineral density that is not as severe as osteoporosis

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104
Q

What does reduced bone density make bones more at risk of?

A

Fractures

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105
Q

What are the risk factors for osteoporosis?

A 
Older age
Female
Reduced mobility/activity
Low BMI (<18.5)
Rheumatoid arthritis
Alcohol/ smoking
Long term corticosteroids
Other medications (SSRIs, PPIs, Anti-epileptics)
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106
Q

What group of people are most at risk of osteoporosis and why?

A

Post-menopausal women and oestrogen is protective against it.

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107
Q

What is the FRAX tool?

A

Gives a prediction of the risk of a fragility fracture in the next 10 years.
Involves inputting information such as age, BMI, co-morbidities, risk factors e.t.c. and gives % 1- year probability of major osteoporotic or hip fracture

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108
Q

What does a DEXA scan measure and what does DEXA stand for?

A

Bone mineral density

Dual-energy xray absorptiometry

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109
Q

How do DEXA scans work?

A

Use brief X-ray scans that measure how much radiation is absorbed by the bones, indicating how dense they are.

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110
Q

Where is the most common location for performing a DEXA scan?

A

T-score at Hip.

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111
Q

How is bone density represented?

A

Z score/ T score:
Z score–> Number of standard deviations the patients bone density falls below mean for their age
T-score–> No. S.D’s below the mean for a healthy young adult they are.

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112
Q

What T-score at the hip indicates:

  1. Osteopenia
  2. Osteoporosis
  3. Severe osteoporosis?
A
  1. -1 to -2.5

2.

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113
Q

What are the steps in assessing for osteoporosis?

A
  1. FRAX assessment on patients at risk.
  2. If indicates intermediate risk: DEXA scan
  3. If high risk: offer treatment
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114
Q

What lifestyle changes are recommended in osteoporosis?

A

Lifestyle changes:

  • Increase activity/ exercise
  • Maintain healthy weight
  • Adequate calcium intake
  • Adequate vit. D
  • Avoid falls
  • Stop smoking
  • Reduce alcohol consumption.
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115
Q

How is osteoporosis managed?

A

Lifestyle changes
Bisphosphonates

(Denosumab, Stonritum ranelate, Raloxifene, Hormone replacement therapy)

116
Q

How do bisphosphonates work to treat osteoporosis?

A

Interfere with osteoclasts to reduce their activity, preventing the reabsorption of bone.

117
Q

What side effects do bisphosphonates cause?

A

Reflux/ oesophageal erosions.
Atypical fractures
Osteonecrosis of jaw and external auditory canal

118
Q

What are the main inflammatory markers?

A

ESR: Erythrocyte sedimentation rate
CRP: C-reactive protiein

119
Q

What is ESR and what does it indicate? How quick is its onset?

A

Erythrocyte sedimentation rate- increases with inflammation/ infection.
Increased fibrinogen makes RBCs stick together and therefore fall faster. Therefore if ESR is higher, the rate of RBC destruction is faster. Rises and falls SLOWLY (days to weeks)

120
Q

What is CRP and what does it indicate? How quick is its onset?

A

C-reactive protein:
Acute phase protein released in inflammation. Produced by the liver in response to IL-6 (pro-inflammatory cytokine). Rises and falls rapidly (6-48 hours)

121
Q

What is antiphospholipid syndrome?

A

Disorder associated with antiphospholipid antibodies where the blood becomes prone to clotting.

122
Q

What are the main problems caused by antiphospholipid syndrome?

A
  • Thrombosis (DVT, pulmonary embolism, stroke, MI, renal thrombosis)
  • Pregnancy complications (e.g. recurrent miscarriage, stillbirth, preeclampsia)
123
Q

What do antiphospholipid antibodies do and give some examples?

A

Interfere with coagulation and create a hyper-coagulable state where the blood is more prone to clotting. e.g. Lupus anticoagulant, Anticardiolipin antibodies

124
Q

What less common symptoms can antiphospholipid syndrome cause?

A

Livedo reticularis–> Purple rash
Libmann-Sacks endocarditis–> Non-bacertial endocarditis
Thrombocytopenia–> Low platelets

125
Q

How is antiphospholipid syndrome diagnosed?

A

History of thrombosis/ pregnancy complication + persistent antibodies.

126
Q

How is antiphospholipid syndrome managed?

A

Long term warfarin to prevent thrombosis

Low molecular weight heparin and aspirin given to pregnant women

127
Q

What is Sjorgens syndrome?

A

Autoimmune condition that affects the exocrine glands.

128
Q

What is:
Primary Sjogren’s
Secondary Sjogren’s?

A

Primary–> Where the condition occurs in isolation

Secondary–> When it occurs related to SLE or rheumatoid arthritis.

129
Q

What are the main symptoms of Sjogren’s?

A

Dry mucous membranes:
Dry mouth
Dry eyes
Dry vagina

130
Q

How is Sjogren’s tested for?

A

Schirmer test- placing filter paper under lower eyelid with a strip hanging out, leaving for 5 minutes and measuring how far the tears travel.

131
Q

How is Sjogren’s managed?

A

Artificial tears
Artificial saliva
Vaginal lubricants
Hydroxycholoroquine to halt progression of disease

132
Q

What are the main complications of Sjogren’s?

A

Eye infections
Oral problems
Vaginal problems/ infection.

133
Q

What is systemic sclerosis/ scleroderma?

A

Autoimmune inflammatory disease that attacks the connective tissue under the skin and around organs and blood vessels.

134
Q

What are the two main patterns of disease in systemic sclerosis?

A

Limited cutaneous systemic sclerosis

Diffuse cutaneous systemic sclerosis

135
Q

What is Limited cutaneous systemic sclerosis and what are its features?

A 
(CREST sydnrome) More limitied version of the disease:
Calcinosis
Raynaud's phenomenon
Eosophagueal dysmotility
Sclerodactyly
Telangiectasia
136
Q

What is Sclerodactyly?

A

Hardening of the skin of the hand that causes the fingers to curl inwards (claw-like shape)

137
Q

What is telangiectasia?

A

Spider web like venules appear on skin.

138
Q

What is diffuse cutaneous systemic sclerosis and what are its features?

A 
All features of CREST syndrome + effects internal organs.
Cardiovascular problems (hypertension/ coronary artery disease)
Lung problems (Pulmonary hypertension/ fibrosis)
Kidney problems (Glomerulonephritis, scleroderma renal crisis)
139
Q

What are the main features of systemic sclerosis?

A 
Scleroderma
Sclerodactyly
Telangiectasia
Calcinosis
Raynaud's phenomenon
Oesophageal dysmotility 
Systemic/ pulmonary hypertension
Pulmonary fibrosis
Scleroderma renal crisis
140
Q

What is scleroderma

A

Hardening of the skin (most notable on hands and face)

141
Q

What is calcinosis?

A

Where calcium deposits build up under the skin, most commonly in fingertips.

142
Q

What is Raynaud’s phenomenon?

A

Where the fingertips go completely white and then blue in response to cold, due to vasoconstriction of the vessels supplying the fingers.

143
Q

What key autoantibodies are involved in systemic sclerosis?

A

Antinuclear antibodies (ANA)
Anti-centromere antibodies (limited)
Anti-Scl-70 antibodies (diffuse)

144
Q

What test is used to investigate systemic sclerosis?

A

Nailfold capillaroscopy: Where the base of the fingernail is magnified and examined to understand the health of the peripheral capillaries.

145
Q

What features would be seen in a nailfold capillaroscopy in systemic sclerosis?

A

Abnormal capillaries, avascular areas and micro-haemorrhages.

146
Q

How is systemic sclerosis managed?

A

Steroids and immunosuppressants.

147
Q

What is vasculitis?

A

Inflammation of the blood vessels caused by autoimmune disease

148
Q

What types of vasculitis affect the small vessels?

A
  • Henoch-Schonlein purpura
  • Eosinophilic granulomatousis with polyangitis
  • Microscopic polyangitis
  • Granulomatosis with polyangitis
149
Q

What types of vasculitis affect the medium sized vessels?

A
  • Polyarteritis nodosa
  • Eosinophilic granulomatosis with Polyangitis
  • Kawasaki diseae
150
Q

What types of vasculitis affect the large vessels?

A

Giant cell arteritis

Takayasu’s arteritis

151
Q

What are the generic features of vasculitis?

A

Purpura
Joint and muscle pain
Peripheral neuropathy
Renal impairment
GI disturbance (diarrhoea/ abdominal pain/ bleeding)
Anterior uveitis and scleritis (eye inflammation)
Hypertension

152
Q

What is purpura?

A

Purple-coloured non blanching spots on the skin caused by leaking blood.

153
Q

What are the systemic symptoms of vasculitis?

A 
Fatigue
Fever
Weight loss
Anorexia
Anaemia
154
Q

What tests can be done to diagnose vasculitis?

A

Anti neutrophil cytoplasmic antibodies (ANCA):
-p-ANCA
-c-ANCA
Inflammatory markers (CRP/ ESR raised)

155
Q

What is the other name for P-ANCA antibodies and what forms of vasculitis are they associated with?

A

Anti-MPO antibodies: Microscopic polyangilitis and Churg-Strauss syndrome

156
Q

What is the other name for C-ANCA antibodies and what forms of vasculitis are they associated with?

A

anti-PR3 antibodies: Wegener’s granulomatosis

157
Q

How is vasculitis managed?

A

Steroids to affected area
Immunosuppressants
(management depends on type)

158
Q

How is Henoch-Schonlein purpura (vasculitis) managed?

A

Typically supportive (analgesia, rest, hydration)

159
Q

What is Henoch-Schonlein purpura?

A

IgA vasculitis that commonly presents with a purpuric rash affecting the lower limbs of buttocks in children.

160
Q

What are the 4 key features of Henoch-Schonlein purpura?

A 
Purpura
Joint pain
Abdominal pain
Renal involvement (IgA nephritis)
161
Q

What is Churg-Strauss syndrome?

A

Eosinophilic granulomatosis with Polyangitis: Small/ medium vessel vasculitis associated with lung and skin problems. (asthma common symptom)

162
Q

What is microscopic polyangitis?

A

Small vessel vasculitis that causes renal failure

163
Q

What is Wegener’s granulomatosis?

A

Granulomatosis with polyangitis: Small vessel vasculitis that affects the resp. tract and kidneys.

164
Q

What are the common symptoms of Wegener’s granulomatosis?

A 
Nose bleeds/crusty nasal secretions
Hearing loss
Sinusitis
Saddle shaped nose (due to perforated nasal septum) 
Cough
Wheeze
Haemoptysis
Glomerulonephritis
165
Q

What is polyarteritis nodosa?

A

Medium vessel vasculitis associated with hep B.

166
Q

What is Kawasaki disease?

A

Medium vessel vasculitis commonly affecting children under 5.

167
Q

What are the main clinical features of Kawasaki disease?

A 
>5 day high fever
Erythematous rash
Bilateral conjunctivitis
Erythema and desquamatio (skin peeling) of palms and soles
Strawberry tongue
168
Q

What is Takayasu’s arteritis?

A

Form of large vessel vasculitis, mainly affecting aorta and its branches

169
Q

What is giant cell arteritis?

A

Systemic vasculitis of the medium and large arteries, typically affecting the temporal arteries.

170
Q

What disease is giant cell arteritis linked to?

A

Polymyalgia rheumatica

171
Q

What is the key complication of giant cell arteritis?

A

Vision loss

172
Q

What are the main presenting features of giant cell arteritis?

A 
Severe unilateral headache around temple and forehead
Scalp tenderness
Jaw claudication
Blurred/ double vision
Irreversible sight loss
173
Q

What systemic symptoms may be present in giant cell arteritis?

A 
Fever
Muscle aches
Fatigue 
Weight loss
Anorexia
Peripheral oedema
174
Q

How is giant cell arteritis diagnosed?

A

Clinical presentation
Raised ESR
Temporal artery biopsy (Shows multinucleated giant cells)

175
Q

What is the initial management of giant cell arteritis?

A

Steroids (started before diagnosis to prevent permenant sight loss)
Aspirin
PPI

176
Q

How is giant cell arteritis managed once diagnosis is confirmed?

A

High dose steroids until symptoms resolved (may take several years)

177
Q

What are the rules for patients on long term steroids? (Don’t STOP)

A 
Don't stop taking them abruptly
Sick day rules
Treatment card
Osteoporosis prevention with bisphosphonate and calcium/ Vit D supplementation
Proton pump inhibitors
178
Q

What is polymylagia rheumatica?

A

Autoimmune condition that causes inflammation of connective tissues, causing pain and stiffness in the muscles around the shoulders, neck and hips.

179
Q

What are the main symptoms of polymyalgia rheumatica?

A

Pain/ stiffness in the shoulders, pelvic girdle and neck.

180
Q

Who typically presents with polymyalgia rheumatica?

A

Caucasian females >50

181
Q

What features do NICE guidelines use to diagnose PMR?

A

-Bilateral shoulder pain that may radiate to the elbow
-Bilateral pelvic girdle pain
-Worse with movement/ interferes with sleep
-Stiffness for at leat 45 mins in the morning
> 2 weeks

182
Q

How is PMR diagnosed?

A

Based on clinical presentation + response to steroids + ruling out other conditions.

183
Q

How is PMR treated?

A

Steroids:
15mg prednisolone per day.
Assess after 1 week and 3-4 weeks.

184
Q

What other symptoms might PMR cause?

A 
Weight loss
Fatigue
Fever
Low mood
Upper arm tenderness
Carpal tunnel 
Pitting oedema
185
Q

What are crystal arthopathies?

A

Group of joint disorders caused by deposits of crystals in the joints and soft tissues.

186
Q

What are the most common crystal arthropathies?

A

Gout

Calcium pyrophosphate deposition

187
Q

What are the two main types of crystal that account for the majority of crystal induced arthritis?

A

Monosodium urate crystals

Calcium pyrophosphate crystals

188
Q

What is gout?

A

A type of arthritis (crystal arthropathy) associated with chronically high blood uric acid levels.

189
Q

What are the main symptom sof gout and what causes it?

A

Painful, hot, swollen joints caused by urate crystal deposition.

190
Q

What are gouty tophi?

A

Subcutaneous deposits of uric acid that typically affect the small joints and connective tissues of the hands, elbows and ears.

191
Q

What is the main/ most important differential diagnosis for gout?

A

Septic arthritis

192
Q

What are the risk factors for gout?

A 
Male
Obesity
High purine diet
Alcohol
Diuretics
Cardiovascular/ kidney disease
Family history
193
Q

What are the most commonly affected joints by gout?

A 
Metatarsophalangeal joint (Base of big toe)
Wrists
Carpometacarpal joint (Base of thumb)
194
Q

How is gout diagnosed?

A

Clinically
Aspiration of fluid from the joint
Joint X-ray

195
Q

What will aspirated fluid from gout show?

A

Needle shaped crystals
Negatively birefringent of polarised light
Monosodium urate crystals
(No bacterial growth)

196
Q

What will a joint X-ray show in gout?

A

Joint space maintained
Lytic lesions
Punched out erosions (may have sclerotic borders with overhanging edges)

197
Q

How is gout managed?

A 
During acute flare:
-NSAIDs
-(Colchicine, steroids)
Prophylaxis:
-Allopurinol (reduces uric acid level)
-Lifestyle changes (losing weight, stay hydrated, reduce consumption of alcohol/ purine-based food)
198
Q

What is pseudogout?

A

Crystal arthropathy caused by calcium pyrophosphate crystals depositing in joints. (also called chondrocalcinosis)

199
Q

What is the typical presentation of pseudogout?

A

Older adult with hot, swollen, stiff, painful knee (/shoulder/wrists/hip)

200
Q

How is pseudogout diagnosed?

A

Aspiration of synovial fluid from joint

X-ray

201
Q

What will aspiration of pseudogout show?

A
  • Calcium pyrophosphate crystals
  • Rhomboid shaped crystals
  • Positive birefringent of polarised light
202
Q

What is the main X-ray change in pseudogout?

A

Chondrocalcinosis–> Thin white line in the middle of the joint space caused by calcium deposition.

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts 
(similar to osteoarthritis)
203
Q

How is pseudogout managed?

A 
Action not always required
NSAIDS
Colchicine
Joint aspiration
Steroid injections
Oral steroids
204
Q

What is Paget’s disease?

A

Disorder of excessive bone turnover

205
Q

What happens in Paget’s disease?

A

There is excessive activity of both osteoblasts and osteoclasts, causing excessive formation and reabsorption, leading to patchy areas of high and low density.

206
Q

What does Paget’s disease result in?

A

Enlarged and misshapen bones with structural problems that increase the risk of fracture.

207
Q

What are the key presentations of Paget’s disease?

A

Bone pain
Bone deformity
Fractures
Hearing loss

208
Q

What are the key investigations into Paget’s disease?

A

X-ray

Biochemistry- raised alkaline phosphatase, normal calcium and phosphate

209
Q

What would be found on an X-ray in Paget’s diseae?

A 
Bone enlargement and deformity
Osteoporsis circumscripta (well defined osteolytic lesions) 
Cotton wool appearance of skull
V-shaped defects in long bones
210
Q

How is Paget’s disease managed?

A

Bisphosphonates (intefere with osteoclast activity)
NSAIDs for pain,
Calcium + Vit D supplementation

211
Q

What are the key complications in Paget’s?

A

Osteogenic sarcoma

Spinal stenosis/ spinal cord compression

212
Q

What is osteosarcoma?

A

Type of bone cancer

213
Q

What is osteomalacia?

A

Condition where defective bone mineralisation causes ‘soft’ bones.

214
Q

What causes osteomalacia?

A

Insufficient vitamin D

215
Q

What are the main presentations of osteomalacia?

A

Weak bones, bone pain, muscle weakness, fractures/

Rickets in children

216
Q

What can cause vitamin D deficiency?

A

Insufficient amounts in diet
Lack of sun exposure
Malabsorption disorders (IBD)
Chronic kidney disease

217
Q

How is vitamin D created and altered to be used by the body?

A
  1. Cholesterol in the skin is converted to vitamin D3 in the presence of UV radiation.
  2. In the liver, D3 is converted to 25-Hydroxyvitamin D.
  3. In the kidney, 25-Hydroxyvitamin D is converted into 1,250dihydrocyvitamin D (CALCITROL)–> The metabolically active form.
218
Q

What is the metabolically active form of vitamin D called?

A

Calcitriol.

219
Q

What is the action of vitamin D in the body?

A
  • Essential for the absorption of calcium and phosphate in the intestines and kidneys
  • Regulates bone turnover and promotes bone reabsorption to boost serum calcium levels.
220
Q

What does lack of vitamin D cause a lack of in the blood?

A

Calcium and phosphate

221
Q

What happens when there are low levels of serum calcium and phosphate?

A
  • Both are required for the construction of bone, so low levels result in defective bone mineralisation.
  • Low calcium causes secondary hyperparathyroidism
222
Q

What are the key presentations of vitamin D deficiency?

A 
Osteomalacia: 
Fatigue
Bone pain
Muscle weakness
Muschle aches
Pathological/ abnormal fractures
223
Q

What are the risk factors for vitamin D deficiency?

A

Dark skin
Low exposure to sunlight
Colder climates
Spend majority of time inside

224
Q

What investigation diagnoses Vitamin D deficiency?

A

Serum 25-hydroxyvitamin D

225
Q

What results would be seen with vitamin D deficiency, insufficiency and optimal vitamin D levels?

A

Vitamin D deficiency: <25 nmol/L
Insufficiency: 25-50 nmol/L
Optimal: 75nmol/L

226
Q

What other investigations results might be found in osteomalacia?

A 
Low serum 25-hydroxyvitamin D
Low serum calcium and phosphate
High serum alkaline phosphatase
High PTH
X-rays show osteopenia
DEXA scan shows low bone mineral density
227
Q

How is osteomalacia treated?

A

Supplementary vitamin D–> High initially and then maintenance supplementary dose of 800 IU or more per day

228
Q

What are polymyositis and dermatomyositis?

A

Autoimmune disorders that cause inflammation of the muscles (myositis)

229
Q

What is polymyositis?

A

Condition of chronic inflammation of muscles

230
Q

What is dermatomyositis?

A

Connective tissue disorder where there is chronic inflammation of the skin and muscles

231
Q

What is the key investigation for diagnosing myositis?

A

Creatine kinase blood test

232
Q

What is creatine kinase and what do high levels indicate?

A

An enzyme found inside muscle cells that is released when the cells are inflamed.

233
Q

What are the normal levels of creatine kinase and what would the results be in myositis?

A

Normal <200 U/L

Myositis >1000 U/L

234
Q

What can cause poly/dermamyositis?

A

Infection
Injury
Autoimmune
Malignancy (paraneoplastic syndrome)

235
Q

How do poly/dermamyositis usually present?

A 
Muscle pain
Fatigue
Weakness
Affects proximal muscles bilaterally
Mostly affects shoulder and pelvis girdle
Develops over weeks
(only dermatomyositis involves the skin)
236
Q

What are the skin features of dermatomyositis?

A

Gottron lesions (scaly red patches on knuckles, elbows and knees)
Photosensitive erythematous rash on back, shoulders, neck
Purple rash on face and eyelids
Periorbital oedema
Subcutaneous calcinosis

237
Q

What autoantibodies are associated with poly/dermatomyositis?

A

Anti-Jo-1 antibodies
Anti-Mi-2 antibodies
Anti-nuclear antibodies

238
Q

How is myositis diagnosed?

A 
Clinical presentation
Elevated creatine kinase
Autoantibodies
Electromyography 
Muscle biopsy
239
Q

How is myositis managed?

A 
By rheumatologist
Check for underlying cancer
Physio/ occupational therapy 
Corticosteroids
(Immunosuppressants, IV immunoglobulins, biological therapy_
240
Q

What is Behcet’s disease?

A

Complex inflammatory condition that causes recurrent oral and genital ulcers and inflammation of other areas

241
Q

What gene is associated with Behcet’s disease?

A

HLA B51 gene

242
Q

What are the main presenting features of Behcet’s disease?

A

Mouth ulcers (at least 3 episodes per year)
Genital ulcers
Inflamed skin
Inflamed eyes -> Uveitis, retinal vasculitis, retinal haemorrhage
Inflamed MSK system-> Morning stiffness, arthralgia, oligoarthritis
GI inflammation/ ulceration
CNS inflammation -> memory impairment, headaches, asceptic meningitis, eningoencephalitis
Vasculitis -> vein thrombosis
Lung inflammation -> pulmonary artery aneurysms

243
Q

What investigations can be done into Behcet’s disease?

A

Diagosed based on clinical features
Pathergy test-> Neefle creates subcutaneous abrasion on forawm which is reviewed 24 hours later to look for a weal. (tests for hypersensitive skin)

244
Q

How is Behcet’s managed?

A 
Topical steroids to ulvers
Systemic steroids
Colchicine (anti-inflammatory)
Topical anaestetics
Immunosuppresants
Biologicala therapy
245
Q

What is septic arthritis?

A

When an infection occurs within a joint

246
Q

What is the mortality of septic arthritis and why?

A

10%- medical emergency as the infection can quickly begin to destroy the joint and cause systemic illness.

247
Q

What is the most common cause of septic arthritis?

A

Joint replacement

248
Q

How does septic arthritis present?

A 
Hot, red, swollen, painful joint
Stiffness and reduced range of motion
Systemic symptoms (fever, lethargy, sepsis)
249
Q

What are the most common organisms to cause septic arthritis?

A 
Staph. aureus most common
Gonorrhoea (gonococcus)
Streptococcus
Influenza
E.coli
250
Q

How is septic arthritis managed?

A

(Have low threshold for treatment until it is excluded by joint aspiration. )
Empirical IV antibiotics followed by specific sensitivity antibiotic for 3-6 weeks.

251
Q

How is septic arthritis diagnosed?

A

Aspirate joint and send sample for gram staining, crystal microscopy, culture and antibiotic sensitivities.

252
Q

What is Marfan syndrome?

A

A genetic disorder of the connective tissue

253
Q

What causes Marfan’s?

A

Autosominal dominant genetic mutation affecting gene responsible for fibrillin (part of connective tissue) creation.

254
Q

What are the key features of Marfan’s?

A 
Tall stature
Long neck 
Long limbs
Long fingers (arachnodactyly)
High arch palate
Hypermobility
Pectus carinatum/ excavatum (abnormal chest) 
Downward sloping fissures (eyes)
255
Q

What is arachnodactyly and how is it tested for?

A

Long fingers:
Cross thumb across palm and see if it the tip goes past the opposite edge of the hand.
Wrap thumb and fingers of one hand around other wrist and see if they overlap.

256
Q

What other conditions are associated with Marfan’s?

A 
Scoliosis
Lens dislocation
Hypermobility/ joint dislocation
Pneumothorac
GORD
Mitral/ aortic valve prolapse/ regurgitation
Aortic aneurysm
257
Q

How is Marfan’s managed?

A

Surgically correct cardiovascular complications.
Minimise heart rate and blood pressure–> avoid intense exercise, caffiene, stimulants. Beta blockers
Physiotherapy to strengthen joints
Genetic counselling if considering children
Monitor for complications (yearly echos and ophthalmologist review)

258
Q

What is Ehlers-Danlos Syndrome?

A

Group of genetic conditions that cause defects in collagen, resulting in hypermobility of joints and abnormal connective tissue.

259
Q

What are the main types of Ehlers-Danlos syndrome?

A

Hypermobile E-D syndrome
Classical
Vascular
Kyphoscoliotic

260
Q

What is the most common Ehlers-Danlos syndrome?

A

Hypermobile Ehlers-Danlos syndrome (least severe)

261
Q

What is the key feature of hypermobile Ehlers-Danlos syndrome?

A

Joint hypermobility and pain

Soft/ stretchy skin

262
Q

What are the key features of classical Ehlers-Danlos syndrome?

A

Very stretchy skin that feels smooth and velvety
Severe joint hypermobility and pain
Abnormal wound healing
May develop lumps over pressure points
Prone to hernia, prolapse, mitral regurgitation and aortic root dilation

263
Q

What is vascular Ehlers-Danlos syndrome?

A

The most dangerous form of EDS where the blood vessels are particularly fragile as a result of defective collagen.

264
Q

What are the key features of vascular Ehlers-Danlos syndrome?

A

Thin, transulacent skin

Skin, organs and arteries prone to rupture

265
Q

What are the key features of Kyphoscoliotic Ehlers-Danlos syndrome?

A 
Poor tone (hypotonia) 
Kyphoscoliosis (outward and lateral curvature of the spine) 
Joint hypermobility
266
Q

What is used to assess the extent of hypermobility?

A

Beighton score–> One point scored for each side of the body:

  • Palms flat on floor with straight legs
  • Elbows hyperextend
  • Knees hyperextend
  • Thumbs bend to touch forearm
  • Little finger extends past 90 degrees
267
Q

How is EDS managed?

A

No cure- maintain healthy joints, monitor complications and minimise symptoms
(Physio/ occupational therapy, maintain good posture, moderate intensity activity)

268
Q

What is postural orthostatic tachycardia syndrome?

A

Complication of hypermobile EDS that is a result of autonomic dysfunction. Causes inappropriate tachycardia resulting in presyncope, syncope, headaches, disorientation, nausea and tremor.

269
Q

What are seronegative spondyloarthropathies?

A

Group of joint disorders that cause arthritis in the bones of the spine and nearby joints but test negative for RH.

270
Q

What conditions are seronegative spondyloarthropathies?

A

Ankylosing spondylitis, (axial spondylarthritis), psoriatic arthritis, reactive arthritis, enteropathic arthritis and undifferentiated SpA.

271
Q

What are the key features of seronegative spondyloarthropathies? SPINEACHE

A 
Sausage-like digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAID response
Enthesitis 
Arthritis
Crohns/ colitis/ CRP high
HLA-B27
Eye (uveitis
272
Q

What genetic marker is associated with spondylarthropathy?

A

HLA B27

273
Q

What are the clinical features of SpA (spondylarthropathy)?

A 
Inflamattory arthritis of axial skeleton
Peripheral arthritis
Acute anterior uveitis
Enthesitis
Psoriasis
IBD
274
Q

What is enthesitis?

A

Inflammation of the junction between ligament/ tendon and bone

275
Q

When should you be suspicious of spondylarthritis?

A 
Inflammatory back pain
Asymmetrical arthritis
Skin psoriases
IBD 
Inflammatory eye disease/
276
Q

What are the two main types of joint pain?

A

Inflammatory and non-inflammatory

277
Q

What are the two types of non-inflammatory joint pain?

A

Degenerative and non-degenerative

278
Q

What are the 3 main causes of inflammatory joint pain?

A

Autoimmune
Crystal arthropathies
Infection

279
Q

What are the 3 main causes of autoimmune joint pain?

A

RA
Spondylarthropathies
Connective tissue disease.

280
Q

What is the difference between osteopenia, osteomalacia and osteoporosis

A 
Osteopenia= reduced mineral content of bones
Osteomalacia= softening of bones caused by severe vit. D deficiency
Osteoporosis= weak bones
281
Q

Does inflammatory pain or degenerative pain get better with movement?

A

Inflammatory pain

282
Q

Is inflammatory pain or degenerative pain worse in the mornings?

A

Inflammatory pain.

283
Q

What is the presentation od multiple myeloma?

A 
OLD CRAB:
Old age
Calcium elevated (bones, stones, groans, moans)
Renal impairment
Anaemia
Bone lytic lesions.
284
Q

What is seen in the blood film of mulitple myeloma?

A

Rouleax formation

285
Q

What are the key X-ray findings in:

  1. psoriatic arthritis
  2. Ankylosing spondylitis
  3. Paget’s disease
  4. Multiple myeloma
A
  1. Pencil in a cup deformity
  2. Bamboo spine
  3. Cotton wool appearance
  4. Rain drop skull.
286
Q

What is the mechanism of bisphosphonates?

A

Reduce bone turnover by inhibiting osteoclasts and promoting apoptosis.

287
Q

Give examples of bisphosphonates and what disaese are they the first line treatment in?

A

Alendronate, Zolendronate

Osteoporosis. (also used in Paget’s disease and myeloma)

PHASE 2A (Mine) (15 decks)

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