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Finals > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

OA : Joints affected and typical history

A
  • Large weight bearing joints - hip, knee
  • CMC
  • DIP, PIP
  • Joint pain and stiffness following use, improves with rest
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2
Q

Signs of OA in the hands

A
  • Heberden’s nodes (in the DIP joints)
  • Bouchard’s nodes (in the PIP joints)
  • Squaring at the base of the thumb (CMC joint)
  • Weak grip
  • Reduced range of motion
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3
Q

Signs of OA on X-ray

A
  • L : Loss of joint space
  • O : osteophyte formation
  • S : Subchondral cysts
  • S : Subarticular sclerosis
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4
Q

What are the non pharmacological management options for OA?

A
  • Therapeutic exercise to improve strength and function and reduce pain
  • Weight loss
  • Occupational therapy to support activities and function
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5
Q

Pharmacological management options of OA ?

A
  • 1st = Topical NSAIDs (Ibuprofen 5% gel, 3x a day).
  • 2nd = Oral NSAIDs with PPI cover (Ibuprofen 400mg 3x daily).
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6
Q

RA : presentation and typical joints affected

A
  • Symmetrical distal polyarthritis affecting the MCP, PIP, wrist and the MTP
  • Joint pain, swelling and stiffness -> better with use
  • Systemic Sx : fatigue, weight loss, flu-like illness, muscle aches and weakness
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7
Q

what antibodies are tested for in RA?

A
  • First line = rheumatoid factor (RF)
  • Anti-cyclic citrullinated peptide (anti-CCP)
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8
Q

what are hand signs seen in advanced RA disease ?

A
  • Z-shaped deformity to the thumb
  • Swan neck deformity (hyperextended PIP and flexed DIP)
  • Boutonniere deformity (hyperextended DIP and flexed PIP)
  • Ulnar deviation of the fingers at the MCP joints
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9
Q

What X-ray changes are seen in RA?

A
  • Early sign = Periarticular/Juxta-articular osteoporosis and loss of join space
  • Later : periarticular erosions, soft tissue swelling and subluxation
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10
Q

How is a flare or initial presentation of RA managed ?

A

Short term steroids (oral or IM)

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11
Q

what is the stepwise management of RA?

A
  1. Monotherapy with methotrexate, leflunomide or sulfasalazine
  2. Combination treatment with multiple cDMARDs
  3. Biologic therapies (usually alongside methotrexate)
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12
Q

what two cDMARDS are deemed safest for RA management in pregnancy ?

A
  • Hydroxychloroquine : only in mild disease or palindromic disease
  • Sulfasalazine (extra folic acid required)
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13
Q

when are biological therapies considered for RA management and give examples

A
  • Inadequate response to at least 2 DMARDS
  • TNF inhibitors (adalimumab, infliximab, etanercept)
  • Rituximab (anti-CD20 on B cells).
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14
Q

How often is methotrexate given and what is given alongside it on a different day ?

A
  • Once weekly
  • 5mg Folic acid
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15
Q

Give 4 SE of methotrexate

A
  • Mouth ulcers and mucositis
  • Liver toxicity
  • Bone marrow suppression and leukopenia (low white blood cells)
  • Teratogenic (harmful to pregnancy) and needs to be avoided before conception in both women and men
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16
Q

Give 4 SE of sulfasalazine

A
  • Orange urine
  • Oligospermia
  • Heinz body anaemia
  • ILD
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17
Q

Give a SE specific to leflunomide

A
  • Peripheral neuropathy
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18
Q

Give 3 SE of hydroxychloroquine

A
  • Retinal toxicity (reduced visual acuity)
  • Blue-grey skin pigmentation
  • Hair lightening (bleaching)
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19
Q

What is a unique SE of anti-TNF medication ?

A

Reactivation of TB

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20
Q

Give 2 SE of rituximab

A
  • Night sweats
  • Thrombocytopenia
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21
Q

How is response to treatment monitored in RA

A
  • CRP and DAS28 score
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22
Q

what are the typically features of ankylosing spondylitits ?

A
  • Young man (20s), presenting with lower back pain and stiffness of insidious onset
  • Stiffness = worse in AM and improves with exercise
  • Pain at night which improves on getting up
  • Sacroiliac pain
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23
Q

Give 6 conditions associated with ank. spond

A
  • A – Anterior uveitis
  • A – Aortic regurgitation
  • A – Atrioventricular block (heart block)
  • A – Apical lung fibrosis (fibrosis of the upper lobes of the lungs)
  • A – Anaemia of chronic disease
  • A : Achilles tendonitis
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24
Q

what is seen on examination in ank. spond?

A
  • Reduced lateral flexion
  • Reduced forward flexion (<5cm increase on Schober’s test)
  • Reduced chest expansion
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25
Q

what is the most useful investigation for diagnosing ank. spond and what are the most common findings !

A
  • Plain X-ray
  • Sacroilitis : subchondral erosions, sclerosis
  • Squaring of lumbar vertebrae
  • Syndesmophytes
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26
Q

If X-ray is negative but suspicion of ank. spond is still high, what can be done ?

A
  • MRI
  • Shows bone marrow oedema
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27
Q

what is the stepwise management of ank. spond ?

A

REGULAR EXERCISE & physio

  1. NSAIDs
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28
Q

what are the most common triggers of reactive arthritis ?

A
  • STI = chlamydia
  • Gastroenteritis
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29
Q

How does reactive arthritis present ?

A
  • Develops 4 wks after infection
  • Arthritis (asymmetrical oligoarthritis).
  • Urethritis
  • Eye : conjunctivitis, anterior uveitis
  • Circinate balanitis
  • Dactylitis
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30
Q

How is reactive arthritis managed ?

A
  • Joint aspiration -> microscopy, culture and sensitivity and crystal examination (exclude septic arthritis)
  • Symptomatic : analgesia, NSAIDs, intra-articular steroids
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31
Q

What are the 5 patterns of arthritis associated with psoriasis ?

A
  • Symmetrical polyarthritis : (>4, similar to RA)
  • Asymetrical oligoarthritis : (1-4 joints).
  • Sacrolitis : (spine and sacroiliac joints)
  • DIP joint disease
  • Arthritis mutilans : (phalanges - osteolysis leads to telescoping digits).
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32
Q

what 5 other signs are seen in psoriatic arthritis ?

A
  • Plaques of psoriasis on the skin
  • Nail pitting
  • Onycholysis (separation of the nail from the nail bed)
  • Dactylitis
  • Enthesitis
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33
Q

what is seen on X-ray in psoriatic arthritis ?

A
  • Periostitis
  • ’ Pencil-in-cup’ appearance of digits
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34
Q

what is the stepwise management of psoriatic arthritis ?

A
  • NSAIDs
  • Steroids
  • DMARDs (e.g., methotrexate, leflunomide or sulfasalazine)
  • Anti-TNF medications (etanercept, infliximab or adalimumab)
  • Ustekinumab is a monoclonal antibody that targets interleukin 12 and 23
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35
Q

what is SLE ? What kind of hypersensitivty reaction is it ? and who is it more common in ?

A
  • Inflammatory autoimmune connective tissue disorder.
  • Type 3
  • Young to middle aged women
  • Asian, African, Caribbean and Hispanic ethnicity
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36
Q

what antibodies are associated with SLE

A
  • Anti-nuclear antibodies (Highly sensitive, low specificity).
  • anti-dsDNA (highly specific, less sensitive)
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37
Q

what bloods are used to monitor SLE ?

A
  • ESR
  • Low C3/C4
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38
Q

what lifestyle advice is given to people with SLE ?

A
  • Suncream and sun avoidance !! For photosensitive malar rash
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39
Q

what are the 3 first line treatment options for SLE?

A
  • Hydroxychloroquine
  • NSAIDs
  • Steroids (e.g., prednisolone)
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40
Q

what is discoid lupus erythematosus and 3 RF ?

A
  • Autoimmune chronic skin condition
  • Women, darker skin and smoking
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41
Q

What are the features of DLE

A
  • Photosensitive erythematous, raised rash
  • Common on face, neck, ears and scalp
  • Can lead to scarring alopecia
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42
Q

How is DLE managed ?

A
  • Skin biopsy to confirm
  • Sun protection
  • Topical steroids
  • Hydroxychloroquine if necessary
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43
Q

what is systemic sclerosis ?

A
  • Autoimmune connective tissue disease involving inflammation and fibrosis of the connective tissues, skin and internal organs
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44
Q

what are the features of limited cutaneous systemic sclerosis ?

A
  • C : Calcinosis
  • R : Raynaud’s
  • E : oEsophageal dysmotility
  • S : Sclerodactyly
  • T : Telangiectasia
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45
Q

what extra features are associated with diffuse cutaneous systemic sclerosis ?

A
  • Cardiovascular problems (e.g., HTN and coronary artery disease)
  • Lung problems (e.g., pulmonary hypertension and pulmonary fibrosis)
  • Kidney problems (e.g., glomerulonephritis and scleroderma renal crisis)
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46
Q

what is used to manage Raynaud’s and what can make it worse ?

A
  • Keeping hands warm and CCB (nifedipine)
  • BB can worsen the symptoms
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47
Q

What antibodies are seen in systemic sclerosis ?

A

-> ANA
-> Anti-centromere = limited
-> Anti-Scl-70 = diffuse

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48
Q

what is the common presentation of polymyalgia rheumatica (PMR)

A
  • > 60yrs
  • Rapid onset (<1mnth)
  • Pain and stiffness of shoulders, pelvic girdle and neck.
  • Worse : in morning, after rest, interferes with sleep.
  • Raised ESR
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49
Q

What is the management of PMR?

A
  • 15mg prednisolone daily
  • If no respone = consider alt. diagnosis. Usually respond rapidly and v well to steroids
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50
Q

what are the additional management points for patients on long term steroids ?

A

Don’t STOP

  • Don’t abruptly stop
  • S : Sick day = increase in unwell
  • T : Treatment card
  • O : Osteoporosis prevention with bisphosphonates, calcium & vit D
  • P : PPI
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51
Q

what is GCA, who does it more commonly affect and what is it strongly linked too ?

A
  • Systemic vasculitis affecting medium and larger arteries
  • Older white pts
  • Linked to PMR
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52
Q

How does GCA typically present ?

A
  • Unilateral headache
  • Jaw claudication
  • Tender and thickened temporal artery
  • Blurred / double vision
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53
Q

what investigations are done in GCA ?

A
  • ESR (Raised)
  • Temporal artery biopsy = multinucleated giant cells
  • Duplex USS = hypoechoic “halo” sign and stenosis of temporal artery
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54
Q

how is GCA managed ?

A
  • No vision loss = high-dose pred (40-60mg)
  • Evolving vision loss = IV methylpred (500-1000mg)
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55
Q

what other medications are considered in GCA ?

A
  • Aspirin 75mg daily decreases vision loss and strokes
  • PPI while on steroids
  • Bisphosphonates and calcium and vitamin D for bone protection while on steroids
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56
Q
  • Severe pain in the first MTP joint
  • Swelling
  • Erythema
A

Gout

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57
Q

what is seen on aspiration of joint fluid in gout ?

A
  • Needle shaped negatively birefringement crystals of monosodium urate
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58
Q

what can be seen in x ray in gout ?

A
  • Maintained joint
  • Lytic lesions in the bone
  • Punched out erosions
  • Erosions can have sclerotic borders with overhanding edges
59
Q

what is the acute management of gout ?

A
  • First : NSAIDs (naproxen) with PPI
  • 2nd : Colchicine
  • 3rd : Oral prednisolone (15mg/day)

If the pt is already on allopurinol it should be continued

60
Q

When is colchicine given for the acute management of gout over NSAIDs?

A
  • In those with renal impairment or significant heart disease
  • SE : diarrhoea
61
Q

What is given for gout prophylaxis ?

A
  • Xanthine oxidase inhibitors
  • Allopurinol -> 100mg of, titrated up to aim for uric acid <300umol/L
  • Colchicine cover when starting allopurinol
62
Q

What is a typical presentation of pseudogout ?

A
  • Pt >65 y/o with a rapid onset hot, swollen, stiff joint
  • Usually : knee, shoulder, hip or wrist
63
Q

what is seen on joint aspiration in pseudogout ?

A
  • Rhomboid shaped weakly positively birefringent crystals of calcium pyrophosphate
64
Q

what is commonly seen on X-ray in pseudogout ?

A
  • Chondrocalcinosis
65
Q

what are 4 underlying RF for pseudogout which can cause it to develop at a younger age

A
  • Haemochromatosis
  • Hyperparathyroidism
  • Low magnesium, low phosphate
  • Acromgely, wilson’s disease
66
Q

Define osteoporosis

A
  • Significant reduction in bone density = weaker and more fracture prone
  • Osteopenia = less severe decrease in bone density
67
Q

Define the T / Z score

A
  • DEXA scan = measures bone mineral density
  • T score = no. of standard deviations pt is from an average healthy young adult
  • Z score = no. of standard deviations pt is from the average for their age, sex and ethnicity
68
Q

Explain the diagnosis based on T score at femoral neck

A
  • Normal : > -1
  • Osteopenia : -1 to -2.5
  • Osteoporosis : <-2.5
  • Severe osteoporosis : <-2.5 + fracture
69
Q

What are the RF for osteoporosis ?

A
  • Advancing age
  • Female sex
  • Histort of glucocorticoid use
  • RA
  • Alcohol excess
  • Hx of parental hip fracture
  • Low BMI
  • Current smoking
  • Post menopausal
70
Q

when should somebody be assessed for a 10 yr risk of major osteoporotic fracture and hip fracture ?

A
  • Anyone on long-term oral corticosteroids or with a previous fragility fracture
  • Anyone 50 and over with risk factors
  • All women 65 and over
  • All men 75 and over
71
Q

What 2 tools are used to osteoporotic fracture risk

A
  • QFracture tool
  • FRAX tool
72
Q

Based on the QFracture tool, what pts are considered for a DEXA scan ?

A

Pts >10%

73
Q

what are the 3 steps to managing osteoporosis

A
  1. Address reversible RF : increase exercise, healthy weight, stop smoking, reduce alcohol
  2. Calcium (1000mg) and vitamin D (400-800 IU)
  3. Treatment : bisphosphonates
74
Q

Give 4 SE of bisphosphonates

A
  • Reflux and oesophageal erosions
  • Atypical fractures (e.g., atypical femoral fractures)
  • Osteonecrosis of the jaw (regular dental checkups are recommended before and during treatment)
  • Osteonecrosis of the external auditory canal
75
Q

How should bisphosphonates be taken ?

A
  • Alendronate (70mg once weekly)
  • Empty stomach with a full glass of water
  • Remain upright for 30 mins afterwards)
76
Q

How are patients >=75 yrs following a fragility fracture managed ?

A
  • Presumed to having underlying osteoporosis
  • Begin alendronate without need for DEXA scan
77
Q

How is a patient <75 yrs following fragility fracture managed ?

A
  • Arrange DEXA
78
Q

what is osteomalacia ?

A
  • Softening of bones secondary to low vitamin D levels = decreased bone mineral content
79
Q

How can osteomalacia present ?

A
  • Fatigue
  • Bone pain
  • Muscle weakness
  • Muscle aches
  • Pathological or abnormal fractures (especially femoral neck)
80
Q

What is seen on bloods in osteomalacia ?

A
  • Low vit D (serum 25-hydroxyvitamin D of <25 nmol/L = deficiency)
  • Raised ALP
  • Low calcium, phosphate
81
Q

What can be seen on x-ray in osteomalacia

A
  • Translucent bands (looser zones or pseudofractures)
82
Q

How is osteomalacia treated ?

A
  • Colecalciferol (vitamin D supplements)
  • 50,000 IU once weekly for 6 weeks
  • 4000 IU daily for 10 weeks
83
Q

Following the loading regime (if needed) what is the maintenance dose of vitamin D in osteomalacia treatment ?

A

800-2000 IU per day

84
Q

What is Paget’s disease of bone ?

A
  • Increased, uncontrolled bone turnover
85
Q

where is most commonly affected in Paget’s disease ?

A
  • Skull
  • Spine / pelvis
  • Long bones of lower extremeties
86
Q

What is seen on bloods in paget’s disease of the bone ?

A
  • Isolated raised ALP
87
Q

what are common X-ray findings in paget’s ?

A
  • Bone enlargement and deformity
  • Osteoporosis circumscripta
  • Cotton wool appearance of the skull (poorly defined patchy areas of increased and decreased density)
  • V-shaped osteolytic defects in the long bones
88
Q

How is paget’s managed and monitored?

A
  • Bisphosphonates (either oral risedronate or IV zoledronate)
  • Checking serum ALP
89
Q

What are 4 key complicatons of paget’s ?

A
  • Hearing loss
  • Heart failure
  • Osteosarcoma
  • Spinal stenosis and spinal cord compression
90
Q

what is antiphospholipid syndrome ?

A
  • Autoimmune disorder where antiphospholipid antibodies bind the cell surface and cause inflammation and increased thrombosis risk
  • Can occur in isolation or secondary to conditions like SLE
91
Q

what are the key complications of antiphospholipid syndrome ?

A
  • VTE (DVT/PE)
  • Arterial thrombosis (stroke, MI)
  • Pregnancy related (recurrent moscarriage)
92
Q

what investigations are done in antiphospholipid syndrome ?

A
  • Antibodies : Lupus anticoagulant, Anticardiolipin antibodies, Anti-beta-2 glycoprotein I antibodies
  • FBC : thrombocytopenia
  • Clotting : prolonged APTT
93
Q

How is antiphospholipid syndrome managed ?

A
  • No previous thrombosis = low dose aspirin
  • Previous venous / arterial blood clot = Long term warfarin with INR target of 2-3
94
Q

what rash is associated with antiphospholipid syndrome ?

A

Livedo reticularis (netlike reddish-blue skin discoloration)

95
Q

What heart condition is associated with anti-phospholipid syndrome ?

A
  • Libmann-Sacks endocarditis
  • Non bacterial endocarditis
  • Vegetations on the heart valves
96
Q

what is Sjogren’s syndrome ?

A
  • Autoimmune disorder affecting exocrine glands = dry mucosa
  • Can be primary or secondary to RA / other connective tissue disorders
97
Q

what are the features of sjogren’s

A
  • Dry eyes
  • Dry mouth
  • Vaginal dryness
  • Arthralgia
  • Raynaud’s
  • More common in women, presents in middle age
98
Q

what malignancy does Sjogren’s increase the risk of ?

A

lymphoid

99
Q

what antibodies are seen in Sjogren’s

A
  • Anti-SS-A = anti-Ro
  • Anti-SS-B = anti-La
  • RF
  • ANA
100
Q

what test can be done for Sjogren’s ?

A

Schirmer’s test
<10mm = significant

101
Q

how is Sjogren’s managed

A
  • Artifical tears
  • Pilocarpine = stimulates muscarinic receptors = promoting salivary and lacrimal gland secretion
102
Q

what is Behcet’s syndrome and its associations ?

A
  • Complex inflammatory condition
  • HLA B51
  • More common in men, young adults and eastern mediterranean pts
103
Q

What are the classical symptoms of Behcet’s ?

A
  1. Oral ulcers (3x a year).
  2. Genital ulcers
  3. Anterior uveitis

AND

  • Thrombophlebitis and DVT
  • Arthritis
  • Erythema nodosum
  • GI : abdo pain, diarrhoea, colitis
104
Q

what investigation can support the diagnosis of bechet’s

A
  • Pathergy test
  • Erythema and enduration 24-48 hrs after skin pricking
105
Q

what is polymyositis and what can 2 conditions can it be associated with

A
  • Inflammatory disorder causing symmetrical, proximal muscle weakness
  • Connective tissue disorders
  • Malignancy
106
Q

How does polymyositis present ?

A
  • Gradual onset symmetrical proximal muscle weakens +/- tenderness
  • Raynaud’s
  • Resp muscle weakness
  • Dysphagia, dysphonia
107
Q

what is elevated in polymyositis and dermatomyositis

A
  • Creatinine kinase
108
Q

what antibody is associated with polymyositis ?

A
  • Anti-Jo-1
  • More common in a pattern of disease that also involves the lungs, raynaud’s and fever
109
Q

What is the first line treatment for polymyositis and dermatomyositis ?

A

Corticosteroids

110
Q

Along with proximal muscle weakness, what else is seen in dermatomyositis ?

A

CHARACTERISTIC SKIN LESIONS

  • Gottron papules on hands (roughened red papules over extensor surfaces of fingers)
  • Heliotrope rash on eyelids
  • Periorbital oedema
  • Photosensitive erythematous rash on the back, shoulders and neck
111
Q

Name 3 small-vessel vasculitis

A
  • Microscopic polyangitis
  • Granulomatosis with polyangitis (Wegener’s granulomatosis)
  • Eosinophilic granulomatosis with polyangitis (Churg-Strauss)
112
Q

What are the main features of microscopic polyangitis and what is its associated antibodies ?

A
  • p-ANCA
  • Glomerulonephritis = renal failure
  • Diffuse alveolar haemorrhage = haemoptysis
113
Q

What are the main features of granulomatosis with polyangitis and what is its associated antibody ?

A
  • URT: epistaxis, sinusitis, saddle shaped nose, nasal crusting
  • LRT : cough, wheeze, haemoptysis
  • Kidneys : glomerulonephritis
  • c-ANCA
114
Q

what are the common findings of eosinophilic granulomatosis with polangitis and what antibody is associated

A
  • Lungs, skin and kidneys
  • Severe asthma in middle age
  • Sinusitis and allergic rhinitis
  • Raised eosinophils
  • p-ANCA
115
Q

Name 2 medium vessel vasculitis

A
  • Polyarteritis nodosa
  • Kawasaki disease
116
Q

what are the typical features of polyarteritis nodosa

A
  • Renal impairment
  • Hypertension
  • Tender, erythematous skin nodules (similar to erythema nodosum)
  • Myocardial infarction
  • Stroke
  • Mesenteric arteritis causing intestinal symptoms
117
Q

Name 2 large vessel vasculitis

A
  • GCA
  • Takayasu’s arteritis
118
Q

Where does takayasu’s arteritis affecrt and how does it present ?

A
  • Aorta + branches
  • Pulmonary arteries
  • <40 yrs
  • Claudication symptoms
  • Non specific : fever, malaise, muscle aches
119
Q

what is the approach to diagnosing vasculitis ?

A
  • Urinalysis for haematuria and proteinuria
  • Bloods:
    urea and creatinine for renal impairment,
    full blood count: normocytic anaemia and thrombocytosis may be seen
  • CRP: raised
  • ANCA testing
  • Chest x-ray: nodular, fibrotic or infiltrative lesions may be seen
120
Q

what antibodies are seen in those with drug induceded lupus

A

Anti-histone antibodies

121
Q

what is seen on arthrocentesis in RA ?

A
  • High WBC count
  • Predominantly polymorphonuclear neutrophil predominance
  • Appearance is yellow and cloudy
122
Q

Exam questiin presentation of osteomalacia

A

Bone pain, tenderness and proximal myopathy (-> waddling gait).

123
Q

what should NEVER be prescribed alongside methotrexate

A
  • Trimethoprim : can cause fatal pancytopenia
  • Co-trimoxazole also contains trimethoprim !
124
Q

what is antisynthetase syndrome, what causes it and how does it present

A
  • Subtype of dermatomyositis caused by anti-Jo-1 antibodies
  1. Myositis
  2. Interstitial lung disease
  3. Thickened and cracked skin of the hands (mechanic’s hands)
  4. Raynaud’s phenomenon
125
Q
  • Red, hot swollen joint
  • Aspiration = gram +ve cocci in clusters that are coagulase positive
  • Likely organism
A

Staphylococcus aureus

126
Q
  • Red, hot swollen joint
  • Aspiration = gram +ve cocci in clusters that are coagulase positive
  • Flucloxacillin resistant
  • Likely organism
A

MRSA (methicillin-resistant S.aureus)

127
Q

Management of septic arthritis caused by MRSA

A

Vancomycin

teicoplanin and linezolid could also be used

128
Q

What antibodies are seen in antiphospholipid syndrome

A

Anti-cardiolipin

129
Q

IV antibiotic for septic arthritis

A

Flucloxacillin
Clindamycin if pen allergic
4-6 wks (switched to oral after 2)

130
Q

what blood results are seen in osteoporosis ?

A

all normal !

131
Q

Presentation of SLE

A
  • Young female
  • Fatigue, fever, mouth ulcers
  • Skin : malar rash
  • MSK : arthralgia
  • CVD : pericarditis, myocarditis
  • Resp : pleurisy
  • Renal : proteinuria
  • Neuro : anxiety, depression, psychosis
132
Q

Presentation of primary Raynaud’s disease

A

Young women
Bilateral symptoms

133
Q

6 secondary causes of Raynaud’s phenomenon

A
  • Connective tissue
  • Leukaemia
  • Type 1 cryoglobulinaemia
  • Use of vibrating tools
  • Drug : COCP
  • Cervical rib
134
Q

2 common causes of drug induced lupus

A

Procainamide
Hydralazine

135
Q

Inheritance of EDS and what is affected

A
  • AD
  • Connective tissue disorder affecting type III collagen
136
Q

6 features / complications of EDS

A
  • Elastic, fragile skin
  • Joint hypermobility: recurrent joint dislocation
  • Easy bruising
  • Aortic regurgitation, mitral valve prolapse and aortic dissection
  • Subarachnoid haemorrhage
  • Angioid retinal streaks
137
Q

How many points does a pt need to be tender in for a diagnosis of fibromyalgia

A

11 out of 18

138
Q

Inheritance and effect of Marfan’s

A

AD : chromosome 15
Defect in protein filbrillin-1
Connective tissue disorder

139
Q

6 general features of marfan’s

A

Tall statue with wide arm span
Arachnodactyly
Pes planus
Pectus excavatum
Scoliosis
High arched palate

140
Q

Effect of marfans on heart

A
  • Mitral valve prolapse
  • Dilation of aortic sinus : AAA, dissection, aortic regurg
141
Q

Effect of marfan’s on lungs

A

Repeated pneumothoraces

142
Q

Effect of marfan’s on eyes

A

Upward lens dislocation

143
Q
A

Finals (92 decks)

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