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MED-Y3 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is reactive arthritis ?

A

Occurs when synovitis occurs in the joints as a reaction to a recent infective trigger.

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2
Q

What are the common causes of reactive arthritis ?

A

Gastroenteritis

STI (Chlamydia is the most common cause)

Gonorrhea causes gonococcal septic arthritis

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3
Q

What are the seronegative spondyloarthropathies ?

A

Associated with AS

  • Ra
  • Psoriatic arthritis
  • IBD associated arthritis
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4
Q

What are some of the systemic associations with Reactive arthritis ?

A

Bilateral conjunctivitis

Anterior uveitis

Circinate balanitis (Derm of the head of the penis)

Can’t see, cant pee or climb a tree

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5
Q

How to manage reactive arthritis ?

A

Give antibiotics until aspiration in order to exclude septic arthritis.

NSAIDS

Steroid injections into the affected joints

Systemic steroids if multiple joints are affected

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6
Q

What are the symptoms of reactive arthritis ?

A

Acute monoarthritic

Often the knee

Warm and swollen

Painful

Infective trigger

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7
Q

What is rheumatoid arthritis ?

A

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

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8
Q

What are the antibody associations with Rheumatoid arthritis ?

A
  • RF (Autoantibody that presents in 70 percent of RA patients)
  • Anti CCP - More sensitive and specific than RF
  • HLA DR4 is present in RF positive patients
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9
Q

What are the symptoms of rheumatoid arthritis ?

A

Symmetrical distal Poly arthropathy

Pain

Swelling

Stiffness

Often in the small joints of the hands and feet. Typically the wrist, ankle, MCP and PIP joints - Does not affect the DIP

Fatigue

Weight loss

Flu like illness

Muscle aches and weakness.

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10
Q

In a patient with rheumatoid arthritis, will the pain be worse with rest or better ?

A

Worse with rest and better after activity. Mechanical activity.

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11
Q

What are Heberden’s nodes ?

A

Patients with enlarged painful DIP joints (found in OA)

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12
Q

What are some of the systemic manifestations of RA ?

A

Pulmonary fibrosis with pulmonary nodules

Feltys syndrome (RA, Neutropenia and splenomegaly)

CV disease

Anemia of chronic disease

Episcleritis/scleritis

Rheumatoid nodules

Lymphadenopathy

Amyloidosis

Carpel tunnel

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13
Q

What are some of the X-ray changes seen in patients with Rheumatoid arthritis ?

A

Joint destruction and deformity

Soft tissue swelling

Periarticular osteopenia

Boney erosions

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14
Q

How is rheumatoid arthritis managed (initial to final line) ?

A

At first presentation, NSAIDS/COX2 inhibitors are indicated but have the risk of GI bleeding hence prescribed with PPIs.

First line (Methotrexate, leflunomide (Both teterogenics or sulfalazine). Mildest

2nd line – Combination

3rd line – Methotrexate and biological therapy (TNF inhibitor)

4th line – Methotrexate and rituximab (Night sweats and thrombocytopenia)

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15
Q

What is important to consider when prescribing Anti TNF medications (MAB suffix)?

A

They cause immune suppression and can cause the reactivation of TB and Hep B.

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16
Q

What scoring system is used in order to monitor rheumatoid arthritis ?

A

DAS-28

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17
Q

What is first line treatment for Rheumatoid arthritis ?

A

Methotrexate

Prednisolone can be given in order to help with short term flare ups.

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18
Q

Main side effects of methotrexate ?

A

Nause and vomiting

Abdominal upset and diarrhoea (very well known to cause abdominal pains )

Mouth ulcers and sored

Headaches and fatigue

Feeling under the weather

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19
Q

Why is septic arthritis an emergency condition ?

A

It can cause joint destruction

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20
Q

In young adults, what is the most common cause of septic arthritis ?

A

Neisseria gonnohorea

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21
Q

Rheumatoid nodules found on the olecranon and the extensor surfaces of the fingers/wrists are found in what type of rheumatoid arthritis ?

A

Seropositive

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22
Q

What vitamin is given alongside methotrexate and why ?

A

Folic acid

Reduces side effects

Decreases mucosal and gastrointestinal side-effects of methotrexate and may prevent hepatotoxicity

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23
Q

What are some of the hand deformities seen in Rheumatoid arthritis ?

A

Z shaped deformity of the thumb

Swan neck deformity

Boutonnieres deformity

Ulnar deviation of the fingers at the knuckle

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24
Q

What is the RF for GCA ?

A

Age (Over 50)

Female

PMR

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25
Q

What are some of the clinical features of GCA ?

A

Subacute onset unilateral headache in the temporal region.

Tonge and jaw claudication

Scalp tenderness (REDFLAG)

Painless complete or partial loss of vision

Diplopia

PHX – PMR (Bilateral shoulder stiffness and pelvic girdle pain worse in the mornings)

Systemic features – Fatigue, fever, weight loss and depression.

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26
Q

What is a red flag headache symptom for GCA ?

A

Scalp tenderness

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27
Q

What would be identified on a clinical examination for GCA ?

A

Scalp tenderness

Reduced or absent temporal pulse

Pallor (Oedema of optic disc)

Axillary/brachial and carotid bruits)

Asymmetric bp

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28
Q

What would be abnormal when investigating GCA ?

A

FBC - (Normocytic anemia and increased platelets)

Increased CRP

ESR raised

LFT – May show increased ALP/AST

Temporal artery USS (Thickening of the wall-Halo sign)

TA biopsy – Granulations multinucleated giant cells, granulomatous inflammation.

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29
Q

How is GCA managed ?

A

Rheumatology referral

Oral prednisolone (60mg - 100mg one off dose)

Visual symptoms (40-60 MG prednisolone)

Visual loss – 500mg-1g IV methylprednisolone for 3 days (opd) followed by steroid regime.

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30
Q

What is first line treatment for GCA without visual changes ?

A

Oral prednisolone (60mg - 100mg one off dose)

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31
Q

What is the first line of treatment for GCA with visual symptoms ?

A

Visual symptoms (40-60 MG prednisolone)

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32
Q

What is the first line treatment for GCA with visual loss ?

A

Visual loss – 500mg-1g IV methylprednisolone for 3 days (opd) followed by steroid regime.

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33
Q

How is GCA managed long term ?

A

Slow reduction of steroid over 1 to 2 years.

Regular monitoring

Before starting prednisolone, asses for hypertension and hyperglycemia.

SE – PPI in GI bleeding and risk of OA.

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34
Q

What are some of the complications of GCA ?

A

Irreversible vision loss

AAA, A dissection

CV events like stroke and mi

Steroid treatment – Bruising, diabetes, hypertension and osteoporosis (Maybe give with supplements or bisphosphonates)

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35
Q

RF for PMR ?

A

Over 50

PMHx of GCA

Female

FHX

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36
Q

how will a patient with PMR present ?

A

Presents sub-acute over days to weeks.

Symptoms worst in the morning (stiffness) lasting over an hour.

Pain, stiffness and weakness in the muscles of the neck, shoulders, buttocks and hips

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37
Q

What are some of the symptoms of PMR ?

A

Shoulders – Reduced range of motion and difficulty with reaching overhead

Hips – Difficulty getting up from chair or climbing stairs without support

Low grade fevers, weight loss, night sweats, malaise, fatigue and anorexia.

MAKE SURE TO INVESTIGATE FOR MORE SINSISTER PATHOLOGIES

Patients with PMR should be screened for GCA.

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38
Q

Present on clinical examination of PMR ?

A

Bilat proximal muscles may be tender to touch.

Active and passive motion limited by pain.

Muscle strength is normal or limited by pain

Scalp may be tender as a result of GCA

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39
Q

What investigations will be abnormal in PMR ?

A

Normocytic anemia or thrombocytosis may be see in ongoing inflammation

ESR and CRP is almost always elevated

Tests to rule out other causes

USS – Joint effusion, synovitis or bursitis.

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40
Q

Diagnostic criteria for PMR ?

A

Age over 50 years

The classical presentation of symptoms with proximal muscle stiffness and pain that is worse in the mornings

A blood test showing elevated inflammatory markers (ESR and CRP)

Improvement of symptoms with the initiation of steroid therapy

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41
Q

First line treatment for PMR ?

A

Prednisolone

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42
Q

Side effects of steroids ?

A

Diabetes (cause hyperglycemia and may cause HSS in patients with diabetes)

GORD – ADD PPI

Osteoporosis – Denosumab.

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43
Q

Describe the rash commonly seen in SLE

A

Red malar rash with a butterfly distribution. Photosensitive and found on the face

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44
Q

Common presentation of SLE ?

A

Presents with nonspecific symptoms

Fatigue and weight loss

Arthralgia and myalgia

Fever

Photosensitive malar rash – Butterfly shaped rash that gets worse with sunlight.

Lymphadenopathy and splenomegaly

SOB, Pleuritic chest pain

Mouth ulcers

Hair loss

Raynauds

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45
Q

What would commonly be abnormal when investigating SLE ?

A

Normocytic anemia of chronic disease

Decreased C3 and C4

Raised CRP and ESR

Raised immunoglobulins

Lupus nephritis (proteinuria)

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46
Q

What autoantibodies are commonly used in SLE diagnosis but why are they not relied on alone to diagnose a patient ?

A

ANA antibodies. Although they are found in a high number of patients, they are not credible enough alone to diagnose as they can be positive in patients without SLE and hence should be used in clinical context.

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47
Q

What criteria are used in the diagnosis of SLE ?

A

SLICC or ACR criteria

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48
Q

What syndrome can occur secondary to SLE?

A

Antiphospholipid syndrome, hence patients aee at a higher risk of developing a VTE

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49
Q

Complications of SLE ?

A

CV disease (CAD and hypertension)

Infection

Anemia of chronic disease.

Pericarditis

Pleuritis

ILD and pul fibrosis

Lupus nephritis due to inflammation in the kidney

Recurrent miscarriage.

VTE

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50
Q

First line treatment for SLE ?

A

NSAIDS

Steroids (prednisolone)

Hydroxychloroquine

Sun avoidance for rash

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51
Q

Treatment for resistant SLE or severe ?

A

Rituximab

BIOLOGICs

52
Q

What crystals are found in gout ?

A

Monosodium urate crystals

53
Q

What joints are most commonly affected in gout.

A

DIP
Base of the big toe
Wrists
Base of the thumb
Can affect the knee and ankle.

54
Q

Common presentation of gout

A

Red hot and swollen and painful joint

55
Q

How is gout diagnosed ?

A

Clinical
Aspiration (Neg biofringent-needle shaped)
X ray - Lytic lesions of the bone, punched out erosions and sclerotic borders with overhanging edges.

56
Q

First line for an acute flair of gout and when are they not indicated ?

A

NSAIDS - GORD, CV DISEASE AND RENAL IMPAIRMENT

57
Q

Second- and third-line treatment for Gout (given 1st line is NSAIDS) ?

In an acute flair, NOT prophylactic

A

Colchicine (Diarrhoea SE)

Steroids

58
Q

What is used for the prophylaxis of gout ?

A

Allopurinol (don’t use until the acute flair subsides) and lifestyle changes

59
Q

Myasthenia gravis and what tumor have a link ?

60
Q

What is the characteristic feature of patients with myasthenia gravis?

A

Fatigue worse with activity and improved with rest.

61
Q

Symptoms of myasthenia gravis (remember facial symptoms)?

A

Charachteristic feature – Weakness that gets worse with muscle use and improves with rest

Minimal in morning and worst at the end of the day.

Symptoms effect the proximal muscles and the small muscles of the head and neck.

Diplopia and ptosis

Weakness in facial movement

Fatigue in jaw when chewing.

Difficulty with swallowing

Slurred speech

Progressive weakness with repetitive movements.

62
Q

What would be found OE in MG ?

A

Repeated blinking=Ptosis

Prolonged upward gazing = Diplopia on further eye movement testing

Repeated abduction of the arm will result in increased fatigue in that arm compared to the other.

Look for thymectomy scar (As thyroid tumor is linked to myasthenia gravis)

63
Q

What antibodies are found in most patients with MG ?

A

AcH-R antibodies

64
Q

What is the edrophonium test (used to test for mynsthenia gravis.

A

Used when there is a doubt about the diagnosis.

Patients given an IV dose of neostigmine.

Results in an increase in the amount of ACH and temporary relief of weakness.

65
Q

First line treatments for MG ?

A

Reversible ach inhibitors (Pyridostigmine/neostigmine)

Immunosuppression like prednisolone

Thymectomy

66
Q

Second line treatment for MG ?

A

Rituximab and eculizumab (Monoclonal antibodies) - Used if normal immunosuppression is ineffective.

67
Q

What is myasthenic crisis ?

A

Causes the acute worsening of symptoms often triggered by illness. This can lead to resp failure due to weakness of the muscles of respiration

Patients need BiPAP or intubation and ventilation.

IV immunoglobulins and plasma exchange.

68
Q

Typical MCQ question for sarcoidosis ?

A

The typical MCQ exam patient is a 20-40 year old black woman presenting with a dry cough and shortness of breath. They may have nodules on their shins suggesting erythema nodosum. It can effect almost any organ in the body but most commonly effects the lungs.

69
Q

Typical pulmonary findings in sarcoidosis ?

A

Lymphandenopathy
Pulmonary fibrosis
Pulmonary nodules

70
Q

Systemic features of sarcoidosis ?

A

Fever

Fatigue

Weight loss

71
Q

Hepatic features of sarcoidosis ?

A

Liver nodules
Cirrhosis
Cholestasis

72
Q

Ophthalmologic features of sarcoidosis?

A

Uveitis

Optic neuritis

Conjunctivitis

73
Q

Common skin changes in sarcoidosis

A

Erythema nodusum (tender red nodules on shins caused by inflammation of subcut fat)

Lupus pernio (raised purple lesions commonly on cheeks and nose)

Granulomas develop in scar tissue.

74
Q

What is lorgens syndrome ?

A

Specific presentation of sarcoidosis and is characterized by a triad of erythema nodosum, bilateral hilar lymphadenopathy and polyarthralgia.

75
Q

What would be present on Imaging in sarcoidosis ?

A

Hiliar lymphadenopathy on CXR

Hiliar lymphadenopathy and pul nodules on MRI

76
Q

What would be found on histology in sarcoidosis ?

A

non caseating granulomas and epithelioid cells.

Done via a bronchoscopy.

77
Q

What would be found on investigation in sarcoidosis ?

A

Raised serum ACE and hypercalcemia.

Raised CRP and serum soluble IL-2 receptor.

Raised immunoglobulins.

78
Q

What is first line treatment for moderate sarcoidosis ?

A

Oral steroids like prednisone and bisphosphonates to protect against Osteoporosis

79
Q

Second line treatment for sarcoidosis ?

A

Methotrexate or azathioprine in severe cases

80
Q

If sarcoidosis does not self-resolve, what are some of the possible side effects.

A

In others it can progress with pulmonary fibrosis and pul hypertension and sometimes can require a heart transplant.

81
Q

What are the two most common places to develop bursitis ?

A

olecranon and greater trochanter.

82
Q

Common causes of bursitis ?

A

Friction from repetitive movements or leaning on the elbow.

Trauma

Inflammatory conditions

Infection (Septic bursitis)

83
Q

How will bursitis from an infective cause present ?

A

Hot to touch

More tender

Erythematous

Fever will be present

Features of sepsis like tachycardia, hypotension and confusion.

To differentiate from septic arthritis, consider if there is swelling in the joint rather than the bursae.

84
Q

In bursitis when is aspiration indicated ?

A

When infection is indicated (PUS) AND WILL BE SENT FOR CULTURES

85
Q

Management of non-infective bursitis.

A

Rest, ice and compression

Analgesia

Protecting the joint from pressure or trauma

Aspiration of the fluid to relive pressure

Steroid injections in problematic cases

86
Q

First line treatment for infective bursitis ?

A

First line flucloxacillin and clarithromycin as a penicillin alternate

87
Q

A patient presents to the GP with what they describe as pain all over there body for the last 6 months. It is affecting their ability to conduct everyday tasks and their sleep. They have a PMH of IBS and on investigation there are no abnormal results. What is the likely diagnosis?

A

Fibromyalgia

88
Q

Apart from education, CBT and exercise, what pharmaceutical intervention can be given in fibromyalgia ?

A

TCAs like amitriptyline to reduce pain and help with sleep.

89
Q

A patient presents with an acutely swollen knee. On General inspection, it is hot, erythematous and very painful. No other sign PMHx. What is the most likely diagnosis?

A

Septic arthritis

90
Q

What is the most common causative organism of septic arthritis ?

A

Staphylococcus aureus

91
Q

If a patient presents with septic arthritis at a young sexually active stage, what is the most likely causative organism?

A

Neisseria gonorrhea

92
Q

After aspiration, what is the first line treatment of septic arthritis

A

Flucloxacillin (vancomycin in penicillin allergy) and rifampicin

93
Q

Psoriatic arthritis is a seronegative spondyloarthropathy. Would RF and ANTI CCP be positive ?

A

No, they would be negative. If positive, it would be more indicative of rheumatoid arthritis

94
Q

A patient with a FHX or arthritis presents with joint pain. They have a PMH or psoriasis and depression. Joints appear swollen and painful. They describe pain being worst in the morning, but it does get better in the day. What is the most likely diagnosis?

A

Psoriatic arthritis.

95
Q

What are some extraarticular manifestations of spondyloarthropathies?

A

Mitral valve prolapse

Aortic rood dilation

Aortic regurgitation

Uveitis

Urethritis

96
Q

IS ESR and CRP commonly raised in Psoratic arthritis ?

97
Q

Is psoriatic arthritis a clinical diagnosis?

98
Q

First line treatment for peripheral psoriatic arthritis?

A

NSAIDS

DMARDS like methotrexate

99
Q

Treatment for psoriatic arthritis with axial involvement

A

TNF-a inhibitors like infunimab. Make sure to screen for underlying infections

100
Q

In patients with peptic ulcer disease/ hypertension of DM. What treatment should be initiated in gout rather than NSAIDS?

A

Colchicine

101
Q

Second line treatment for RA

A

-Methotrexate

Then methotrexate and biologic (TNF)

Then methotrexate and rituximab.

102
Q

When starting biologics - what is it important to inform patients of ?

A

That it is an immunosuppressant and can cause reactivation of latent infection like TB.

103
Q

A patient with known history of SLE presents after suffering a VTE. What is most likely to be the cause of the VTE?

A

Antiphospholipid syndrome.

104
Q

What is APS normally associated with ?

A

Thrombosis
Complications in pregnancy

105
Q

What is the common clinical presentation of APS ?

A

C - Clots
L - Livedo reticularis (Rash mottled)
O - Obstetric Loss
T - Thombocytopenia

106
Q

What medication is CI in APS ?

A

HRT or oestrogen containing contraceptives

107
Q

What antibodies will be present (More than 1 occasion over 12 weeks) in APS ?

A
  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti beta 2 glycoprotein antibodies
108
Q

How is APS managed in non-pregnant patients?

A

Long term warfarin (INR 2-3 whilst on warfarin, this should increase to 3-4). CI in pregnancy

Lifestyle advice for CV Rf

109
Q

How is APS managed in pregnant patients ?

A

Pregnant women = LMWH (Enoxaparin) and aspirin 75mg

Lifestyle advice – Removal of modifiable RF for VTE/ATE. - Smoking cessation, avoid HRT and control of BP cholesterol ect

110
Q

A 25-year-old patient presents with developing lower back pain over the last 2 months. He also describes a pain in his buttocks. He says it is worst in the morning but gets better with exercise. What is the most likley diagnosis based on hist symptoms ?

111
Q

What is Schober’s test?

A

Find the L5 vertebrae with the patient standing straight.

Mark 10cm and 5CM below this point

Ask the patient to bend forward as far as they can and measure the distance between the points.

Less than 20 cm distance between the points = Restriction of lumbar spine

AS diagnosis confirmation

112
Q

What is enthesis and what seronegative spondyloarthropathy is it associated with ?

A

Swelling of the ligaments and tendons that attach tendons to bone.

113
Q

What are the range of treatments available for AS ?

A

Physiotherapy and exercise/mobilization

NSAIDS

Steroids in flares

Anti TNF

Seckinumab if NSAIDS and ANTI TNF are ineffective

114
Q

What antibody is used in monitoring SLE disease progression and why ?

A

Anti ds DNA. More specific to SLE and is less likley to be found in patients without SLE

115
Q

What immunosuppressant can be used apart from hydroxychloroquine in resistant or more severe sle ?

A

Methotrexate

116
Q

What are the characteristic antibodies of SLE ?

117
Q

What is SLE ?

A

inflammatory autoimmune connective tissue disease that is systemic

118
Q

What is one of the definitive characteristics of SLE ?

A

Red photosensitive malar rash

119
Q

What is the first line treatment for acute gout flair ?

A

Nsaids and colchicine if the patient is unfit for NSAIDS like in renal impairment.

120
Q

What is used in gout prophylaxis ?

A

allopurinol

121
Q

A patient with long term steroid use develops a rash in a deratomal distribution on the face. What is the most likely cause ?

A

Re-activation of HZ (shingles) due to prolonged steroid use

122
Q

_______________ Combination with methotrexate can cause hematological toxicity ?

A

Trimethoprim

123
Q

Most common causative organism of septic arthritis in young patients ?

A

Neisseria gonorrhoea

124
Q

Most common causative organism of septic arthritis ?

A

Staph aureus

125
Q

What are the symptoms of Churg strauss syndrome (eosinophilic granulomatosis with polyangiitis )?

A

Late onset asthma, eosinophilia and rapidly progressive glomerulonephritis with palpable rash and GIT bleeding

126
Q

What vaccination advice should be given to patients on DMARDS ?

A

Influenza vaccine every 1 year and pneumococcal every 5 years.

MED-Y3 (24 decks)

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