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Medicine Specialities > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

what are the risk fx of OA?

A

obesity, age, occupation, trauma, being female and family history

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2
Q

what are the findings on x ray of OA?

A

L – Loss of joint space
O – Osteophytes
S – Subchondral sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone, aka geodes)

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3
Q

what are the sx of OA?

A

pain and stiffness
worsened by activity
deformity, instability, reduced function

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4
Q

what are the commonly affected joints of OA?

A

Hips
Knees
Sacro-iliac joints
Distal-interphalangeal joints in the hands (DIPs)
The CMC joint at the base of the thumb
Wrist
Cervical spine

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5
Q

what are the signs in the hands of OA?

A

Heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in the PIP joints) – BP
Squaring at the base of the thumb at the carpo-metacarpal joint
Weak grip
Reduced range of motion

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6
Q

what are the NICE guidlines for diagnosing OA?

A

diagnosis can be made without any investigations if the patient is over 45, has typical activity related pain and has no morning stiffness or stiffness lasting less than 30 minutes.

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7
Q

how is OA managed?

A

patient education
physio
weight loss
occupational therapy
analgesia - oral paracetamol, topical NSAIDS
can then add oral NSAIDS + PPI
then opiates such as codeiene or morphine
intra-articular steroid injections
joint replacements

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8
Q

define RA

A

an autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa. It is an inflammatory arthritis. Synovial inflammation is called synovitis. Rheumatoid arthritis tends to be symmetrical and affects multiple joints. Therefore it is a symmetrical polyarthritis. Inflammation of the tendons increases the risk of tendon rupture.

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9
Q

what are the risk fx for RA?

A

women (3x)
middle age
family hx
genetic - HLA DR4 (a gene often present in RF positive patients)
HLA DR1 (a gene occasionally present in RA patients)

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10
Q

how are antibodies involved in RA>

A

Rheumatoid factor is an autoantibody(USUALLY IgM) that targets the Fc portion of the IgG antibody
this causes activation of the immune system agaisnt the patient’s own IgG
Cyclic citrullinated peptide antibodies (anti-CCP antibodies) are autoantibodies - more sensitive and specific than RF so give early indication of development of RA

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11
Q

how does RA present?

A

symmetrical distal polyarthropathy -

Pain
Swelling
Stiffness
in small joints - wrist, ankle, MCP, PIP
systemic sx - fatigue, weight loss, flu like, muscle aches
pain improves after activity

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12
Q

define palindromic rheumatism

A
  • self limiting short episodes of inflammatory arthritis with joint pain, stiffness and swelling typically affecting only a few joints. The episodes only last 1-2 days and then completely resolve. Having positive antibodies (RF and anti-CCP) may indicate that it will progress to full rheumatoid arthritis.
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13
Q

what are the most commonly affected joints by RA?

A

Proximal Interphalangeal Joints (PIP) joints
Metacarpophalangeal (MCP) joints
Wrist and ankle
Metatarsophalangeal joints
Cervical spine
Large joints can also be affected such as the knee, hips and shoulders
NOT DIPJ

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14
Q

define atlantoaxial subluxation

A

cervical spine. The axis (C2) and the odontoid peg shift within the atlas (C1). This is caused by local synovitis and damage to the ligaments and bursa around the odontoid peg of the axis and the atlas. Subluxation can cause spinal cord compression and is an emergency. This is particularly important if the patient is having a general anaesthetic and requiring intubation. MRI scans can visualise changes in these areas as part of pre-operative assessment.

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15
Q

what are the signs in the hands for RA?

A

palption of the synovium - boggy feeling related to swelling
Z shaped deformity to the thumb
Swan neck deformity (hyperextended PIP with flexed DIP)
Boutonnieres deformity (hyperextended DIP with flexed PIP)
Ulnar deviation of the fingers at the knuckle (MCP joints)

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16
Q

define boutonnieres deformity

A

tear in the central slip of the extensor components of the fingers…when try to straighten finger, their lateral tendons that go around PIP pull on the distal phalynx causing DIP to extend and PIP to flex

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17
Q

what are the extra articular manifestations of RA?

A

Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
Bronchiolitis obliterans (inflammation causing small airway destruction)
Felty’s syndrome (RA, neutropenia and splenomegaly)
Secondary Sjogren’s Syndrome (AKA sicca syndrome)
Anaemia of chronic disease
Cardiovascular disease
Episcleritis and scleritis
Rheumatoid nodules
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis

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18
Q

which investigations are required for RA?

A
  • clinical diagnosis
  • check rheumatic factor
  • if RF neg check anti-CCP
  • inflammatory markers - CRP, ESR
  • x ray of hand and feet
  • USS of joints to confirm synovitis
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19
Q

what are the x ray changes of RA?

A

Joint destruction and deformity
Soft tissue swelling
Periarticular osteopenia
Boney erosions

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20
Q

what is the NICE recommendations for referral of RA?

A

any adult with persistent synovitis, even if they have negative rheumatoid factor, anti-CCP antibodies and inflammatory markers. The referral should be urgent if it involves the small joints of the hands or feet, multiple joints or symptoms have been present for more than 3 months.

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21
Q

how is the diagnosis of RA made?

A

criteria come from american college of rheuamtology
The joints that are involved (more and smaller joints score higher)
Serology (rheumatoid factor and anti-CCP)
Inflammatory markers (ESR and CRP)
Duration of symptoms (more or less than 6 weeks)
Scores are added up and a score greater than or equal to 6 indicates a diagnosis of rheumatoid arthritis.

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22
Q

how is RA monitored?

A

Disease activity score -
Swollen joints
Tender joints
ESR/CRP result

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23
Q

how is response to treatment measured?

A

Health Assessment Questionnaire - measures functional ability

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24
Q

what factors can negatively affect RA?

A

Younger onset
Male
More joints and organs affected
Presence of RF and anti-CCP
Erosions seen on xray

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25
Q

how is RA managed?

A

MDT team
short course of steroids at first presentation
NSAIDS/cox-2 inhibitors + PPI
CRP and DAS28 - monitor success of tx
aim is to reduce the minimal effective dose that can control the disease

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26
Q

what are the NICE guidlines for DMARDS?

A

First line is monotherapy with methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine can be considered in mild disease and is considered the “mildest” anti rheumatic drug.
Second line is 2 of these used in combination.
Third line is methotrexate plus a biological therapy, usually a TNF inhibitor.
Fourth line is methotrexate plus rituximab
in pregnancy - sx get better due to higher natural production of steroids - sulfasaline and hydroxychloroquine used

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27
Q

which biological therapies can be used for RA?

A

Anti-TNF (adalimumab, infliximab, etanercept, golimumab and certolizumab pegol) - most important
Anti-CD20 (rituximab)
Anti-IL6 (sarilumab)
Anti-IL6 receptor (tocilizumab)
JAK inhibitors (tofacitinib and baricitinib)

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28
Q

what is the consequence of biological therapies for RA?

A

immunosuppression - prone to serious infections and lead to reactivation of dormant infection such as TB and hep B

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29
Q

what is the last resortof RA?

A

surgery

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30
Q

how does methotrexate work?

A

interferes with metabolism of folate and suppressing components of immune system
- injection or tablet
- folic acid 5mg is also prescribed once a week to be taken on a different day

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31
Q

what are the side effects of methotrexate?

A

Mouth ulcers and mucositis
Liver toxicity
Bone marrow suppression and leukopenia (low white blood cells)
It is teratogenic (harmful to pregnancy) and needs to be avoided prior to conception in mothers and fathers

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32
Q

how does leflunomide work?

A

an immunosuppressant medication that works by interfering with the production of pyrimidine. Pyrimidine is an important component of RNA and DNA.

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33
Q

what are the side effects of leflunomide?

A

Mouth ulcers and mucositis
Increased blood pressure
Rashes
Peripheral neuropathy
Liver toxicity
Bone marrow suppression and leukopenia (low white blood cells)
It is teratogenic (harmful to pregnancy) and needs to be avoided prior to conception in mothers and fathers

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34
Q

how does sulfasalazine work?

A

immunosupressive and anti inflamm
mechanism not known, poss related to folate metabolism

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35
Q

what are the side effects of sulfasalazine?

A

Temporary male infertility (reduced sperm count)
Bone marrow suppression

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36
Q

how does hydroxychloroquine work?

A

anti-malarial medication. It acts as an immunosuppressive medication by interfering with Toll-like receptors, disrupting antigen presentation and increasing the pH in the lysosomes of immune cells. It is thought to be safe in pregnancy.

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37
Q

what are the side effects of hydrochloroquine?

A

Nightmares
Reduced visual acuity (macular toxicity)
Liver toxicity
Skin pigmentation

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38
Q

how do anti TNF drugs work?

A

Tumour necrosis factor is a cytokine involved in stimulating inflammation. Blocking TNF reduces inflammation

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39
Q

what are the side effects of anti TNF?

A

Vulnerability to severe infections and sepsis
Reactivation of TB and hepatitis B

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40
Q

how does rituximab work?

A

monoclonal antibody that targets the CD20 protein on the surface of B cells. This causes destruction of B cells. It is used for immunosuppression for autoimmune conditions such as rheumatoid arthritis and cancers relating to B cells

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41
Q

what are the side effects of rituximab?

A

Vulnerability to severe infections and sepsis
Night sweats
Thrombocytopenia (low platelets)
Peripheral neuropathy
Liver and lung toxicity

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42
Q

what are the most notible side effects of the RA drugs - methotrexate, leflunomide, sulfasalazine, hydroxychloroquine, anti-TNF, rituximab?

A

Methotrexate: Bone marrow suppression and leukopenia and highly teratogenic
Leflunomide: Hypertension and peripheral neuropathy
Sulfasalazine: Male infertility (reduces sperm count)
Hydroxychloroquine: Nightmares and reduced visual acuity
Anti-TNF medications: Reactivation of TB or hepatitis B
Rituximab: Night sweats and thrombocytopenia

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43
Q

define psoriatic arthritis

A

inflammatory arthritis associated with psoriasis

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44
Q

what can occur from psoriatic arthritis?

A

mild stiffening and soreness in the joint or the joint can be completely destroyed in a condition called arthritis mutilans

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45
Q

how common is psoriatic arthritis?

A

occurs in 10-20% of patients with psoriasis within 10 yrs
occurs in middle age

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46
Q

what are the patterns affected by psoriatic arthritis?

A

Symmetrical polyarthritis - similarly to RA, more common in women. The hands, wrists, ankles and DIP joints are affected. The MCP joints are less commonly affected (unlike rheumatoid).

Asymmetrical pauciarthritis - mainly the digits (fingers and toes) and feet, describes when the arthritis only affects a few joints.

Spondylitic pattern is more common in men. It presents with - Back stiffness. Sacroiliitis, Atlanto-axial, joint involvement
Other areas can be affected:
Spine
Achilles tendon
Plantar fascia

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47
Q

what are the signs of psoriatic arthritis?

A

Plaques of psoriasis on the skin
Pitting of the nails
Onycholysis (separation of the nail from the nail bed)
Dactylitis (inflammation of the full finger)
Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)
other - eye disease, aortitis, amyloidosis

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48
Q

how does NICE recommend diagnosing psoriatic arthritis?

A

PEST tool to screen for psoriatic arthritis- asking about joint pain, swelling, a history of arthritis and nail pitting. A high score triggers a referral to a rheumatologist.

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49
Q

what are the x ray changes of psoriatic arthritis?

A

Periostitis is inflammation of the periosteum causing a thickened and irregular outline of the bone
Ankylosis is where bones joining together causing joint stiffening
Osteolysis is destruction of bone
Dactylitis is inflammation of the whole digit and appears on the xray as soft tissue swelling
Pencil-in-cup appearance - appear hollow and look like a cup due to central erosions

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50
Q

define arthritis mutilans

A

most severe form of psoriatic arthritis - occurs in phalanxes…osteolysis of bones causing progressive shortening of fingers, skin then folds as the digit shortens so looks like ‘telescopic finger;

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51
Q

how is psoriatic arthritis managed?

A

similar to RA
between derm and rheum
NSAIDs for pain
DMARDS (methotrexate, leflunomide or sulfasalazine)
Anti-TNF medications (etanercept, infliximab or adalimumab)
Ustekinumab is last line (after anti-TNF medications) and is a monoclonal antibody that targets interleukin 12 and 23

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52
Q

define reactive arthritis

A

synovitis occurs as a reaction to a recent infective trigger. AKA as Reiter Syndrome. usually monoarthritis, - single joint in the lower limb (most often the knee) presenting with a warm, swollen and painful joint.

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53
Q

what is the ddx for reactive arthritis?

A

septic arthritis but no infection within the joint so isn’t

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54
Q

which infections trigger reactive arthritis?

A

gastroenteritis
STI - chlamydia or gonorhhoea
genetics - HLA B27 gene

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55
Q

what are the other associations for reactive arthritis?

A

can’t see, pee or climb a tree
bilateral conjunctivitis
anterior uveitis
circinate balantitis

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56
Q

how is reactive arthritis managed?

A

abx until septic arthritis is excluded
aspirate and send for gram staining, culture and sensitivity to exclude
aspirated fluid sent for crystal examination - gout and pseudogout
when defo not septic arthritis - NSAIDS, steroid injection, systemic steoirds, may need DMARDS and anti -TNF

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57
Q

what conditions are involved in seronegative spondyloarthropathy?

A

HLA B27 gene - Reactive arthritis, anklylosing spondylitis, psoriatic arthritis

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58
Q

which joints are usually affected in ankylosing spondylitis?

A

sacroiliac joints and joints of vertebral column

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59
Q

what are the sx of anklyosing spondylitis?

A

pain and stiffness - lower back and sacroiliac pain
young adult male
women and men in similar numbers
develop gradually over more than 3 months
pain is worse at night and in morning
takes at least 30 mins for stiffness to improve and gets better
can have flares

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60
Q

how can ankylosing spondylitis progress?

A

fusion of spine and sacroiliac joints…bamboo spine on x ray

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61
Q

what are the complications of AS?

A

vertebral fractures

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62
Q

what other systems can be affected in AS?

A

Systemic symptoms such as weight loss and fatigue
Chest pain related to costovertebral and costosternal joints
Enthesitis is inflammation of the entheses. This is where tendons or ligaments insert in to bone. This can cause problems such as plantar fasciitis and achilles tendonitis.
Dactylitis is inflammation in a finger or toe.
Anaemia
Anterior uveitis
Aortitis is inflammation of the aorta
Heart block can be caused by fibrosis of the heart’s conductive system
Restrictive lung disease can be caused by restricted chest wall movement
Pulmonary fibrosis at the upper lobes of the lungs occurs in around 1% of AS patients
Inflammatory bowel disease is a condition associated with AS

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63
Q

which test can be used to indicate AS?

A

Schober’s test - restriction in lumbar movement

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64
Q

which investigations are required for AS?

A

Inflammatory markers (CRP and ESR) may rise with disease activity
HLA B27 genetic test
Xray of the spine and sacrum
MRI of the spine can show bone marrow oedema early in the disease before there are any xray changes

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65
Q

which xray changes can be seen in AS?

A

Squaring of the vertebral bodies
Subchondral sclerosis and erosions
Syndesmophytes are areas of bone growth where the ligaments insert into the bone. They occur related to the ligaments supporting the intervertebral joints.
Ossification of the ligaments, discs and joints. This is where these structures turn to bone.
Fusion of the facet, sacroiliac and costovertebral joints

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66
Q

how is AS managed medically?

A

NSAIDS - if not adequate after 2-4 weeks of a maximum dose then consider switching to another NSAID.
Steroids - flares to control symptoms. This could oral, intramuscular slow release injections or joint injections.
Anti-TNF medications such as etanercept or infliximab, adalimumab or certolizumab pegol
Secukinumab is a monoclonal antibody against interleukin-17. It is recommended by NICE if the response to NSAIDS and TNF inhibitors is inadequate.

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67
Q

how else can AS be managed?

A

Physiotherapy
Exercise and mobilisation
Avoid smoking
Bisphosphonates to treat osteoporosis
Treatment of complications
Surgery is occasionally required for deformities to the spine or other joints

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68
Q

define SLE

A

inflammatory autoimmune connective tissue disease. It is “systemic” because it affects multiple organs and systems and “erythematosus” refers to the typical red malar rash that occurs across the face

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69
Q

which people is SLE most common in?

A

more common in women and Asians and usually presents in young to middle aged adults but can present later in life

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70
Q

what is the natural history of SLE?

A

relapsing-remitting course, with flares and periods where symptoms are improved - chronic inflammation means often have shortened life expectancy. Cardiovascular disease and infection are leading causes of death.

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71
Q

what is the pathophysiology behind SLE?

A

anti-nuclear antibodies - so the immune system targets the proteins within the person’s own cell nucleus…causing an inflammatory response which occurs chronically leading to sx of the condition

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72
Q

how does SLE present?

A

Fatigue
Weight loss
Arthralgia (joint pain) and non-erosive arthritis
Myalgia (muscle pain)
Fever
Photosensitive malar rash. This is a “butterfly” shaped rash across the nose and cheek bones that gets worse with sunlight.
Lymphadenopathy and splenomegaly
Shortness of breath
Pleuritic chest pain
Mouth ulcers
Hair loss
Raynaud’s phenomenon

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73
Q

how is SLE investigated?

A

Autoantibodies (see below)
Full blood count (normocytic anaemia of chronic disease)
C3 and C4 levels (decreased in active disease)
CRP and ESR (raised with active inflammation)
Immunoglobulins (raised due to activation of B cells with inflammation)
Urinalysis and urine protein:creatinine ratio for proteinuria in lupus nephritis
Renal biopsy can be used to investigate for lupus nephritis

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74
Q

which autoantibodies are associated with SLE?

A

Anti nuclear antibodies - ANA - 85% will be positive
Anti DS DNA - 70%
anti ENA antibodies - anti Smith - highly specific to SLE
Antiphospholipid antibodies and antiphospholipid syndrome can occur secondary to SLE. They can occur in up to 40% of patients with SLE and are associated with an increased risk of venous thromboembolism.

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75
Q

what are other types of anti-ENA antibodies that can confirm diseases?

A

Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)
Anti-Ro and Anti-La (most associated with Sjogren’s syndrome)
Anti-Scl-70 (most associated with systemic sclerosis)
Anti-Jo-1 (most associated with dermatomyositis)

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76
Q

how is SLE diagnosed?

A

SLICC Criteria or the ACR Criteria for establishing a diagnosis. This involves confirming the presence of antinuclear antibodies and establishing a certain number of clinical features suggestive of SLE.

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77
Q

what are the possible complications of SLE?

A

CV disease- hypertension, coronary artery disease
infection - immunosupressants
anaemia of chronic disease - chronic normocytic anaemia, leucopenia, neutropenia, thrombocytopenia
pericarditis
pleuritis
ILD
Lupus nephritis -> ESRF
Neuropsychiatric SLE - optic neuritis, transverse, myelitis, psychosis
recurrent miscarriage - intrauterine growth restriction, pre-eclampsia, pre term labour
VTE - antiphospholipid syndrome secondary to lupus

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78
Q

how is SLE treated?

A

anti inflamm meds and immunosupression
rheumatology specialist
First line treatments are:

NSAIDs
Steroids (prednisolone)
Hydroxychloroquine (first line for mild SLE)
Suncream and sun avoidance for the photosensitive malar rash

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79
Q

what other medications would be considered if lupus is severe/unresponding?

A

Methotrexate
Mycophenolate mofetil
Azathioprine
Tacrolimus
Leflunomide
Ciclosporin

Biological therapies-
Rituximab is a monoclonal antibody that targets the CD20 protein on the surface of B cells
Belimumab is a monoclonal antibody that targets B-cell activating factor

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80
Q

define discoid lupus erythematous

A

non-cancerous chronic skin condition. It is more common in women and usually presents in young adults between ages 20 to 40. It is more common in darker-skinned patients and smokers.

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81
Q

what can occur as a result of discoid lupus erythematous?

A

increased risk of SLE, and SCC

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82
Q

how does discoid lupus erythematous present?

A

occur in face, ears and scalp
photosensitive
scarring alopecia
hyper or hypopigmented scars
lesions are Inflamed, Dry, Erythematous, Patchy, Crusty and scaling

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83
Q

how is discoid lupus erythematous treated?

A

skin biopsy confirms diagnosis
sun protection, topical steroids, intralesional steroids, hydrochloroquine

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84
Q

define systemic sclerosis and scleroderma

A

most pt swith scleroderma ahve systemic sclerosis but when it just affects the skin - hardening of the skin is scleroderma
Systemic sclerosis is an autoimmune inflammatory and fibrotic connective tissue disease. The cause of the condition is unclear. It most notably affects the skin in all areas but it also affects the internal organs.

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85
Q

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

A

Limited cutaneous systemic sclerosis
Diffuse cutaneous systemic sclerosis

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86
Q

define limited cutaneous systemic sclerosis

A

more limited version of systemic sclerosis. It used to be called CREST syndrome

C – Calcinosis - calcium deposits under skin usually fingertips
R – Raynaud’s phenomenon - fingertips go white and then blue due to cold as vasoconstrict the vessels
E – oEsophageal dysmotility
S – Sclerodactyly - skin tightens around joints, restricts ROM, skin can break and ulcerate
T – Telangiectasia - small dilated blood vessels in skin, fine thready appearance

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87
Q

define diffuse cutaneous systemic sclerosis

A

includes the features of CREST syndrome plus many internal organs causing:

Cardiovascular problems, particularly hypertension and coronary artery disease.
Lung problems, particularly pulmonary hypertension and pulmonary fibrosis.
Kidney problems, particularly glomerulonephritis and a condition called scleroderma renal crisis(severe hypertension and renal failure)

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88
Q

which autoantibodies are involved in systemic sclerosis?

A

Antinuclear antibodies (ANA) are positive in most patients with systemic sclerosis. They are not specific to systemic sclerosis.

Anti-centromere antibodies are most associated with limited cutaneous systemic sclerosis.

Anti-Scl-70 antibodies are most associated with diffuse cutaneous systemic sclerosis. They are associated with more severe disease.

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89
Q

how is raynauds phenomenon investigated?

A

Nailfold capillaroscopy - This is a technique where the area where the skin meets the fingernails at the base of the fingernail (the nailfold) is magnified and examined. Abnormal capillaries, avascular areas and micro-haemorrhages indicate systemic sclerosis. Patients with primary Raynaud’s without systemic sclerosis will have normal nailfold capillaries

90
Q

how is the diagnosis of systemic sclerosis made?

A

classification criteria from the American College of Rheumatology (ACR) and European League Against Rheumatism (EULAR) . This involves meeting a number of criteria for clinical features, antibodies and nailfold capillaroscopy.

91
Q

how is systemic sclerosis managed?

A

specialist MDT
steroids and immunosuppressants
Avoid smoking
Gentle skin stretching to maintain the range of motion
Regular emollients
Avoiding cold triggers for Raynaud’s
Physiotherapy to maintain healthy joints
Occupational therapy for adaptations to daily living to cope with limitation
Nifedipine can be used to treat symptoms of Raynaud’s phenomenon
Anti acid medications (e.g. PPIs) and pro-motility medications (e.g. metoclopramide) for gastrointestinal symptoms
Analgesia for joint pain
Antibiotics for skin infections
Antihypertensives can be used to treat hypertension (usually ACE inhibitors)
Treatment of pulmonary artery hypertension
Supportive management of pulmonary fibrosis

92
Q

define polymyalgia rheumatica

A

an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck. There is a strong association to giant cell arteritis and the two conditions often occur together. Both conditions respond well to treatment with steroids.

93
Q

what are the risk fx for polymyalgia rheumatica?

A

above 50
women
caucasians

94
Q

what are the sx of polymyalgia rheumatica?

A

Bilateral shoulder pain that may radiate to the elbow
Bilateral pelvic girdle pain
Worse with movement
Interferes with sleep
Stiffness for at least 45 minutes in the morning
Systemic symptoms such as weight loss, fatigue, low grade fever and low mood
Upper arm tenderness
Carpel tunnel syndrome
Pitting oedema

95
Q

what are the ddx for polymyalgia rheumatica?

A

Osteoarthritis
Rheumatoid arhtirits
Systemic lupus erythematosus
Myositis (from conditions like polymyositis or medications like statins)
Cervical spondylosis
Adhesive capsulitis of both shoulders
Hyper or hypothyroidism
Osteomalacia
Fibromyalgia

96
Q

how is polymyalgia rheumatica diagnosed?

A

clinical presentation
response to steroids
ESR, CRP
Full blood count
Urea and electrolytes
Liver function tests
Calcium can be raised in hyperparathyroidism or cancer or low in osteomalacia
Serum protein electrophoresis for myeloma and other protein disorders
Thyroid stimulating hormone for thyroid function
Creatine kinase for myositis
Rheumatoid factor for rheumatoid arthritis
Urine dipstick
Additional investigations to consider:
Anti-nuclear antibodies (ANA) for systemic lupus erythematosus
Anti-cyclic citrullinated peptide (anti-CCP) for rheumatoid arthritis
Urine Bence Jones protein for myeloma
Chest xray for lung and mediastinal abnormalities

97
Q

how is polymyalgia rheumatica treated?

A

15mg of prednisolone
after 1 week if not work - stop
after 3-4 weeks - 70% improvement
if good response - reducing regime

98
Q

how is polymyalgia rheumatica treated?

A

15mg of prednisolone
after 1 week if not work - stop
after 3-4 weeks - 70% improvement
if good response - reducing regime

99
Q

what is important to recognise when prescribing steroids to patients?

A

DON’T – Make them aware that they will become steroid dependent after 3 weeks of treatment and should not stop taking the steroids due to the risk of adrenal crisis if steroids are abruptly withdrawn
S – Sick Day Rules: Discuss increasing the steroid dose if they become unwell (“sick day rules”)
T – Treatment Card: Provide a steroid treatment card to alert others that they are steroid dependent in case they become unresponsive
O – Osteoporosis prevention: Consider osteoporosis prophylaxis whilst on steroids with bisphosphonates and calcium and vitamin D supplements
P – Proton pump inhibitor: Consider gastric protection with a proton pump inhibitor (e.g. omeprazole)

100
Q

define giant cell arteritis

A

systemic vasculitis of the medium and large arteries. It typically presents with symptoms affecting the temporal arteries

101
Q

what are the risk fx for giant cell arteritis?

A

polymyalgia rheuamtica
females over 50

102
Q

what is the key complication of giant cell arteritis?

A

vision loss - usually irreversible

103
Q

what are the main sx of giant cell arteritis?

A

Severe unilateral headache typically around temple and forehead
Scalp tenderness my be noticed when brushing hair
Jaw claudication
Blurred or double vision
Irreversible painless complete sight loss can occur rapidly
Fever
Muscle aches
Fatigue
Weight loss
Loss of appetite
Peripheral oedema

104
Q

how is a diagnosis of temporal arteritis made?

A

Clinical presentation
Raised ESR: usually 50 mm/hour or more
Temporal artery biopsy findings - showing multinucleated giant cells

105
Q

what other investigations can be used for temporal arteritis?

A

Full blood count may show a normocytic anaemia and thrombocytosis (raised platelets)
Liver function tests can show a raised alkaline phosphatase
C reactive protein is usually raised
Duplex ultrasound of the temporal artery shows the hypoechoic halo sign

106
Q

how is temporal arteritis managed?

A

start steroids immediately
aspirin and PPI can also be used
refer - vascular surgeons, rheumatology and opthalmology

107
Q

what are the early and late complications of giant cell arteritis?

A

Early neuro-ophthalmic complications:
Vision loss
Cerebrovascular accident (stroke)

Late:
Relapses
Steroid related side effects and complications
Cerebrovascular accident (stroke)
Aortitis leading to aortic aneurysm and aortic dissection

108
Q

define polymyositis

A

condition of chronic inflammation of muscles

109
Q

define dermatomyositis

A

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

110
Q

how is myositis diagnosed?

A

elevate creatine kinase >1000
other causes - rhabdomyolysis, AKI, MI, statins, strenuous activity

111
Q

what could be an underlying cause for polymyositis or dermatomyositis?

A

cancer - paraneoplastic syndromes
- lung, breast, ovarian, gastric

111
Q

what could be an underlying cause for polymyositis or dermatomyositis?

A

cancer - paraneoplastic syndromes
- lung, breast, ovarian, gastric

112
Q

what are the symptoms of polymyositis?

A

Muscle pain, fatigue and weakness
Occurs bilaterally and typically affects the proximal muscles
Mostly affects the shoulder and pelvic girdle
Develops over weeks

113
Q

what are the symptoms of dermatomyositis?

A

Gottron lesions (scaly erythematous patches) on the knuckles, elbows and knees
Photosensitive erythematous rash on the back, shoulders and neck
Purple rash on the face and eyelids
Periorbital oedema (swelling around the eyes)
Subcutaneous calcinosis (calcium deposits in the subcutaneous tissue)

114
Q

which autoantibodies are involved in polymyositis?

A

Anti-Jo-1 antibodie

115
Q

which autoantibodies is involved in dermatomyositis?

A

Anti-Mi-2 antibodies: dermatomyositis.
Anti-nuclear antibodies: dermatomyositis.

116
Q

how is the diagnosis of polymyositis made?

A

Clinical presentation
Elevated creatine kinase
Autoantibodies
Electromyography (EMG)
Muscle biopsy can be used to establish a definitive diagnosis.

117
Q

how is polymyositis managed?

A

by rheumatologist
new casws checked for underylying cancer
physio and OT for muscle strength
corticosteroids
immunosupressants, IV immunoglobulins and biological therapies can be used too

118
Q

define antiphospholipid syndrome

A

disorder associated with antiphospholipid antibodies where the blood becomes prone to clotting. The patient is in a hyper-coagulable state. The main associations are with thrombosis and complications in pregnancy, particularly recurrent miscarriage.

119
Q

what are the causes of antiphospholipid syndrome?

A

can occur by its own
or secondary to SLE

120
Q

which antibodies are involved in antiphospholipid syndrome?

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

121
Q

which conditions are associated with antiphospholipid syndrome?

A

DVT, PE - venous
stroke, MI, renal thrombosis - arterial
recurrent miscarriage, stillbirth, preeclampsia
livedo reticularis - purple rash, mottled appearance
libmann-sacks endocarditis -non bacterial endocarditis, usually mitral valve
thrombocytopenia

122
Q

how is antiphopsholipid syndrome diagnosed?

A

history of thrombosis or pregnancy complications plus antibodies

123
Q

how is antiphospolipid syndrome managed?

A

rheumatology, haematology, obstetrics
long term warfarin with INR between 2-3 to prevent thrombosis
LMWH if pregnant plus aspirin

124
Q

define sjogren’s syndrome

A

autoimmune condition that affects the exocrine glands. It leads to the symptoms of dry mucous membranes, such as dry mouth, dry eyes and dry vagina.

125
Q

what is sjogrens syndrome caused by?

A

primary - no cause
secondary - from SLE or RA

126
Q

which antibodies are involved in sjogrens syndrome?

A

anti-Ro, anti-La

127
Q

how is sjogrens syndrome confirmed?

A

schirmer test - folded piece of paper under lower eyelid with strip hanging over eyelid…left for 5 mins..ditsnace along strip that becomes moist is measured. healthy - 15mm, <10mm - bad

128
Q

how is sjogrens syndrome managed?

A

artifical tears, artificial saliva, vaginal lubricants, hydrochloroquine

129
Q

what are the complications of sjogrens syndrome?

A

eye infections - conjuncitivtis, corneal ulcers
oral - dental cavitites, candida
vaginal - candida, sexual dysfunction
rare - Pneumonia and bronciectasis
Non-Hodgkins lymphoma
Peripheral neuropathy
Vasculitis
Renal impairment

130
Q

define vasculitis

A

inflammation of the blood vessels

131
Q

what are the types of vasculitis affected small vessels?

A

Henoch-Schonlein purpura
Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)
Microscopic polyangiitis
Granulomatosis with polyangiitis

132
Q

what are the types of vasculitis affected medium vessels?

A

Polyarteritis nodosa
Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)
Kawasaki Disease

133
Q

what are the types of vasculitis affected large vessels?

A

Giant cell arteritis
Takayasu’s arteritis

134
Q

how does vasculitis present?

A

Purpura. These are purple-coloured non-blanching spots caused by blood leaking from the vessels under the skin.
Joint and muscle pain
Peripheral neuropathy
Renal impairment
Gastrointestinal disturbance (diarrhoea, abdominal pain and bleeding)
Anterior uveitis and scleritis
Hypertension
Fatigue
Fever
Weight loss
Anorexia (loss of appetite)
Anaemia

135
Q

which test are used to diagnose vasculitis?

A

CRP, ESR
ANCA!!! -
p-ANCA (AKA anti MPO) - Microscopic polyangiitis and Churg-Strauss syndrome
c-ANCA (AKA anti-PR3) - Granulomatosis with polyangiitis

136
Q

how is vasculitis managed?

A

rheumatologist
STEROIDS - Oral (i.e. prednisolone)
Intravenous (i.e. hydrocortisone)
Nasal sprays for nasal symptoms
Inhaled for lung involves (e.g. Churg-Strauss syndrome)
IMMUNOSUPRESSANTS - Cyclophosphamide
Methotrexate
Azathioprine
Rituximab and other monoclonal antibodies

137
Q

define henoch-schonlein purpura

A

igA vasculitis - purpuric rash in lower limbs and buttocks in children, due to igA deposits in blood vessels. usually triggered by gastroenteritis or airway infection, the inflammation causes leaking of blood vessels. also joint pain, abdo pain and renal involvement
supportive management - analgesia, rest and hydration
usually recurrence within 6 months

138
Q

define eosinophilic granulomatosis with polyangiitis

A

AKA churg-strauss syndrome
- lung and skin problems, and kidneys
severe asthma in teenage years
elevated eosinophils

139
Q

define microscopic polyangiitis

A

small vessel vasculitis
renal failure
SOB and haemopytsis

140
Q

define granulomatosis with polyangiitis

A

small vessel vasculitis - wegener’s granulomatosis
resp tract and kidneys
nose bleeds
crusty nasal secretions
hearing loss
sinusitis
saddle shaped nose as perforated septum
cough, wheeze, haemopytsis
consolidation on chest x ray
glomerulonephritis

141
Q

define polyarteritis nodosa

A

medium vessel vasculitis
hep B, C, HIV
skin, GI tract, kidneys, heart
renal impairment, stroke, MI
livedo reticularis - rash

142
Q

define kawasaki disease

A

medium vessel vasculitis
<5 yrs
persistent high fever > 5 days
rash
bilateral conjuncitivits
erythema and desquamation of palms and soles
strawberry tongue
coronary artery aneurysm - treated with aspirin and IV immunoglobulins

143
Q

define takayasu’s arteritis

A

large vessel vasculitis
mainly aorta and its branches - pulmonary arteries
pulseless disease
<40 with fever, malaise and muscles aches
diagnosed with CT, MRI angiography, doppler USS of carotids

144
Q

define behcet’s disease

A

complex inflammatory condition. It characteristically presents with recurrent oral and genital ulcers. It can also cause inflammation in a number of other areas such as the skin, gastrointestinal tract, lungs, blood vessels, musculoskeletal system and central nervous system. The presentation can vary a lot between patients, with some patients mildly affected and others affected dramatically.

145
Q

which gene is associated with behcet’s disease?

A

HLAB51 gene

146
Q

what are the ddx of behcet’s disease?

A

differentials of mouth ulcers ->
Simple aphthous ulcers are very common
Inflammatory bowel disease (particularly Crohn’s disease)
Coeliac disease
Vitamin deficiency (B12, folate or iron)
Herpes simplex ulcers
Hand, foot and mouth disease (coxsackie A virus)
Squamous cell carcinoma

147
Q

what are the sx of behcet’s disease?

A

3 episodes of oral ulcers per year - painful,sharply circumscribed wirh red halo
genital ulcers
erythema nodosum, papules and pustules, vascultiis type rashes
uveitis, retinal vasculitis, retinal haemorrhage
morning stiffness, arthralgia, oligoarthritis
ulceration - ileum, caecum, ascending colon
Memory impairment
Headaches and migraines
Aseptic meningitis
Meningoencephalitis
Budd Chiari syndrome
Deep vein thrombosis
Thrombus in pulmonary veins
Cerebral venous sinus thrombosis
pulmonary artery aneurysms

148
Q

how is behcets disease investigated?

A

clinical diagnosis
pathergy test - sterile needle to create a subcutaneous abrasion on the forearm. This is then reviewed 24 – 48 hours later to look for a weal 5mm or more in size. It tests for non-specific hypersensitive in the skin. It is positive in Behçet’s disease, Sweet’s syndrome and pyoderma gangrenosum.

149
Q

how is behcets disease managed?

A

Topical steroids to mouth ulcers (e.g. soluble betamethasone tablets)
Systemic steroids (i.e. oral prednisolone)
Colchicine is usually effective as an anti-inflammatory to treat symptoms
Topical anaesthetics for genital ulcers (e.g. lidocaine ointment)
Immunosuppressants such as azathioprine
Biologic therapy such as infliximab

150
Q

what is the prognosis of behcet’s disease?

A

relapsing remitting
normal life expectancy
increased mortality with haemopytsis, enurological involvement and other

151
Q

define gout

A

crystal arthropathy associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint causing it to become hot, swollen and painful.

152
Q

define gouty tophi

A

subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears. The DIP joints are most affected in the hands.

153
Q

what is the main ddx of gout?

A

septic arthritis

154
Q

what are the risk factors for gout?

A

Male
Obesity
High purine diet (e.g. meat and seafood)
Alcohol
Diuretics
Existing cardiovascular or kidney disease
Family history

155
Q

which joints are typically affected in gout?

A

Base of the big toe (metatarsophalangeal joint)
Wrists
Base of thumb (carpometacarpal joints)

156
Q

how is gout diagnosed?

A

clinically
aspiration of fluid - Needle shaped crystals
Negatively birefringent of polarised light
Monosodium urate crystals

157
Q

what is found on x ray of gout?

A

Typically the space between the joint is maintained
Lytic lesions in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanging edges

158
Q

how is gout managed?

A

NSAIDs (e.g. ibuprofen) are first-line
Colchicine second-line (causes GI upset)
Steroids can be considered third-line
prophylaxis after acute attack is settled - Allopurinol is a xanthine oxidase inhibitor used for the prophylaxis of gout. It reduces the uric acid level. and losing weight, staying hydrated and minimising alcohol and purine-based food (such as meat and seafood).

159
Q

define pseudogout

A

crystal arthropathy caused by calcium pyrophosphate crystals. Calcium pyrophosphate crystals are deposited in the joint causing joint problems. It is also known as chondrocalcinosis.

160
Q

how does pseudogout present?

A

older adult
hot, swollen, stiff, painful knee, other joints - shoulders, wrists, hips
chronic
can be asx

161
Q

how is pseudogout diagnosed?

A

septic arthritis must be excluded - aspiration:
No bacterial growth
Calcium pyrophosphate crystals
Rhomboid shaped crystals
Positive birefringent of polarised light

162
Q

how does pseudogout appear on x ray?

A

chondrocalcinosis - calcium deposition
similar to OA(LOSS)

163
Q

how is pseudogout managed?

A

if asx - nothing
sx - NSAIDs
Colchicine
Joint aspiration
Steroid injections
Oral steroids
arhtocentesis

164
Q

what is the difference between osteoporosis and osteopenia?

A

Osteoporosis is a condition where there is a reduction in the density of the bones. Osteopenia refers to a less severe reduction in bone density than osteoporosis. Reduced bone density makes bone less strong and more prone to fractures.

165
Q

what are the risk factors for osteoporosis?

A

Older age
Female
Reduced mobility and activity
Low BMI (<18.5 kg/m2)
Rheumatoid arthritis
Alcohol and smoking
Long term corticosteroids. NICE suggest the risk increases significantly with the equivalent of more than 7.5mg of prednisolone per day for more than 3 months)
Other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogens
POST MENOPAUSAL WOMEN (as oestrogen is protective against osteoporosis, unless on HRT)

166
Q

how is osteoporosis quantified?

A

FRAX tool gives a prediction of the risk of a fragility fracture over the next 10 years. This is usually the first step in assessing someone’s risk of osteoporosis.

It involves inputting information such as their age, BMI, co-morbidities, smoking, alcohol and family history. You can enter a result for bone mineral density (from a DEXA scan) for a more accurate result but it can also be performed without the bone mineral density.

It gives results as a percentage 10-year probability of a:

Major osteoporotic fracture
Hip fracture

167
Q

how is bone mineral density measured?

A

DEXA scan - how much radiation is abosrbed by bones..how dense the bone is
Z score or T score. Z scores represent the number of standard deviations the patients bone density falls below the mean for their age. T scores represent the number of standard deviations below the mean for a healthy young adult their bone density is.

The most clinically important outcome is the T score at the persons hip

168
Q

define WHO classification for the hip

A

T Score at the Hip

Bone Mineral Density

More than -1

Normal

-1 to -2.5

Osteopenia

Less than -2.5

Osteoporosis

Less than -2.5 plus a fracture

Severe Osteoporosis

169
Q

how is osteoporosis assessed?

A

The first step is to perform a FRAX assessment on patients at risk of osteoporosis:

Women aged > 65
Men > 75
Younger patients with risk factors such as a previous fragility fracture, history of falls, low BMI, long term steroids, endocrine disorders and rheumatoid arthritis.

The NOGG Guidelines from 2017 suggest the next step in management based on the probability of a major osteoporotic fracture from the FRAX score:

FRAX outcome without a BMD result will suggest one of three outcomes:

Low risk – reassure
Intermediate risk – offer DEXA scan and recalculate the risk with the results
High risk – offer treatment

FRAX outcome with a BMD result will suggest one of two outcomes:

Treat
Lifestyle advice and reassure

170
Q

how is osteoporosis managed?

A

Activity and exercise
Maintain a healthy weight
Adequate calcium intake
Adequate vitamin D
Avoiding falls
Stop smoking
Reduce alcohol consumption
calcium supplements with vit D - calcichew-D3
bisphosphonates - Alendronate 70mg once weekly (oral), Risedronate 35 mg once weekly (oral), Zoledronic acid 5 mg once yearly (intravenous)

171
Q

what are the side effects of bisphosphonates?

A

Reflux and oesophageal erosions. Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this.
Atypical fractures (e.g. atypical femoral fractures)
Osteonecrosis of the jaw
Osteonecrosis of the external auditory canal

172
Q

what other medical options are available if bisphosphonates are contraindicated?

A

Denosumab is a monoclonal antibody that works by blocking the activity of osteoclasts.
Strontium ranelate is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction.
Raloxifene is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus.
Hormone replacement therapy should be considered in women that go through menopause early.

173
Q

how is osteoporosis followed up?

A

Patients on bisphosphonates should have a repeat FRAX and DEXA scan after 3-5 years and a treatment holiday should be considered if their BMD has improved and they have not suffered any fragility fractures. This involves a break from treatment of 18 months to 3 years before repeating the assessment

174
Q

define osteomalacia

A

defective bone mineralisation…sofr bones
due to insufficient vit D
weak bones, bone pain, muscle weakness and fractures
if in children prior to growth plates closing - rickets

175
Q

whcih onciditons are vit d deficiency common in?

A

IBD - malabsorption
CKD

176
Q

how does low vit d cause osteomalacia?

A

Inadequate vitamin D leads to a lack of calcium and phosphate in the blood. Since calcium and phosphate are required for the construction of bone, low levels result in defective bone mineralisation. Low calcium causes a secondary hyperparathyroidism as the parathyroid gland tries to raise the calcium level by secreting parathyroid hormone. Parathyroid hormone stimulates increased reabsorption from the bones. This causes further problems with bone mineralisation.

177
Q

what are the sx of vit d and osteomalacia?

A

Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological or abnormal fractures
looser zones - fragility fractures that go partially throguh bone

178
Q

what are the risk factors for osteomalacia meaninf they have low vit D?

A

darker skin
low sunlight exposure
colder climates
spend time indoors

179
Q

which investigations are required for osteomalacia?

A

serum 25-hydroxyvitamin D:
<25 nmol/L – vitamin D deficiency
25 – 50 nmol/L – vitamin D insufficiency
75 nmol/L or above is optimal
Serum calcium is low
Serum phosphate is low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high (secondary hyperparathyroidism)
Xrays may show osteopenia (more radiolucent bones)
DEXA scan shows low bone mineral density

180
Q

how is osteomalacia treated?

A

vit D - colecalciferol
50,000 IU once weekly for 6 weeks
20,000 IU twice weekly for 7 weeks
4000 IU daily for 10 weeks

181
Q

define paget’s disease

A

disorder of bone turnover. There is excessive bone turnover (formation and reabsorption) due to excessive activity of both osteoblasts and osteoclasts. This excessive turnover is not coordinated, leading to patchy areas of high density (sclerosis) and low density (lysis). This results in enlarged and misshapen bones with structural problems that increase the risk of pathological fractures. It particularly affects the axial skeleton (the bones of the head and spine).

182
Q

how does paget’s disease present?

A

Bone pain
Bone deformity
Fractures
Hearing loss can occur if it affects the bones of the ear

183
Q

what are the x ray findings of paget’s disease?

A

Bone enlargement and deformity
“Osteoporosis circumscripta” describes well defined osteolytic lesions that appear less dense compared with normal bone
“Cotton wool appearance” of the skull describes poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)
“V-shaped defects” in the long bones are V shaped osteolytic bone lesions within the healthy bone

184
Q

what are the biocehmistry results for paget’s disease?

A

raised alkaline phosphatase (and other LFTs are normal)
Normal calcium
Normal phosphate

185
Q

how is paget’s disease managed?

A

bisphosphonates
NSAIDS for bone pain
calcium and vit D
surgery for fractures, sevre deformity and arthritis
monitor seum ALP

186
Q

what are the complications of paget’s disease?

A

Osteogenic sarcoma (osteosarcoma)
Spinal stenosis and spinal cord compression

187
Q

What are the most common rheumatological conditions?

A

Gout
Fibromyalgia
RA
Lupus
GCA
PMR
Sjögren’s syndrome
Phospholipid syndrome

188
Q

What are some key features of polymyalgia rheumatica?

A

Affects peri articular joints - bursitis
Stiffness!!
Response to steroids - 1-2 yrs
ESR/CRP
if elderly, and not respond to steroids - likely to be secondary cause - multiple myeloma, paraneoplastic syndrome

189
Q

What are some key features of Sjögren’s syndrome?

A

Symptomatic relief
Complications - B cell lymphoma, arthritis, Vasculitis - ask about weight loss
Can use hydroflouroquinine
Can cause respiratory sx (ILD)

190
Q

shober’s test <5cm

A

ankylosing spondylitis

191
Q

upus

A

nifedipine

192
Q

dermatomyositis antibodies

A

Dermatomyositis is associated with the anti-Jo-1 antibody

193
Q

side effect of steroids

A

skin thinning
small risk of addisons
withdrawal reactions

194
Q

dermatomyositis

A

CT chest/abdomen/pelvis as it is quick to obtain and has a high specificity for picking up any underlying malignancy.

195
Q

septic arthritis

A

synovial fluid analysis
young people - neisseria gonorrhoea most commmon

196
Q

osteomalacia

A

Bone pain, tenderness and proximal myopathy (→ waddling gait) → ?osteomalacia

197
Q

giant cell artertitis biopsy normal

A

continue steroids as skip lesions

198
Q

hyperparathyroidism risk factor

A

pseudogout

199
Q

pseudogout crystals

A

weakly positively birefringent rhomboid-shaped crystals.

200
Q

hypocalcaemia

A

pancreatitis severity

201
Q

osteomalacia electrolytes

A

Low serum calcium, low serum phosphate, raised ALP and raised PTH - osteomalacia

202
Q

paget’s disease

A

aget’s disease - old man, bone pain, raised ALP

203
Q

type of reaction ITP

A

Type II hypersensitivity reaction - ITP

204
Q

polmyositis

A

Proximal muscle weakness + raised CK + no rash → ?polymyositis

205
Q

gottron’s papules

A

over knuckles
dermatomyositis

206
Q

recurrrent miscarriage

A

Arterial/venous thrombosis, miscarriage, livedo reticularis → anticardiolipin antibody +ve

207
Q

ankylosing spondylitis

A

x ray - sacroillitis, syndesmophytes

208
Q

methotrexate toxicity tx

A

Folinic acid is the treatment of choice for methotrexate toxicity

209
Q

Gout Tx

A

Acute attack - NSAIDs, colchine
Maintenance - allopurinol,

210
Q

Marker of severity ra

A

Anti-ccp

211
Q

Reactive arthritis

A

Dactylitis

212
Q

Ankylosing spondylitis first line

A

Exercise regimes and NSAIDs are the 1st line management for ankylosing spondylitis

213
Q

Antiphospholipid syndorme

A

Lifelong warfarin

214
Q

Polymyalgia rheumatic a

A

Normal ck

215
Q

X ray psoriatic

A

Periarticular erosions

Inflammatory arthritis involving DIP swelling and dactylitis points to a diagnosis of psoriatic arthritis

216
Q

T score due a scan

A

T score
> -1.0 = normal
-1.0 to -2.5 = osteopaenia
< -2.5 = osteoporosis

217
Q

Sickle cell pt with osteomyelitis

A

Sickle cell patients are prone to Salmonella osteomyelitis

218
Q

Limited cutaneous systemic sclerosis

A

Limited to below elbows

219
Q

Enteropathic arthritis

A

Enteropathic arthritis is a seronegative spondyloarthropathy associated with HLA-B27

220
Q

Gout urate levels

A

In suspected gout, serum urate should be checked once the inflammation has settled down as it may be high, normal or low during the acute attack

221
Q

Drug induced lupus

A

Antihistone antibodies are associated with drug-induced lupus

Medicine Specialities (11 decks)

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