Brainscape's Knowledge GenomeTM

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


See full index

Phase 2a > MSK > Flashcards

MSK Flashcards

1
Q

MSK symptoms?

A

Arthralgia

Arthritis

Mechanical problems

Periarticular pain

Enthesis (inflammation at the site of attachment of ligaments, tendons and joint capsules)

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

MSK investigations?

A

Bloods

Autoantibodies

X-ray

Bone scintigraphy - the severity of bone disease

Ultrasound - assessment of soft tissue

MRI - articular disease and spinal disorders

DXA - Duel energy x-ray absorptiometry

Arthroscopy - direct means of visualising into a joint

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

3 reasons for synovial fluid analysis?

A

Aspiration

Relieve pressure

Injection of inter-articular corticosteroid

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

Differences between mechanical and inflammatory back pian?

A

Mechanical - often sudden onset, worse in the evening with morning stiffness absent and aggravated by exercise

Inflammatory - Gradual onset, morning stiffness and exercise relieves pain

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

features of serious back pain?

A

Metastasis, multiple myeloma, osteomyelitis or spinal + root canal stenosis

  • 20 to 50
  • constant pain without relief
  • Bone tenderness
  • TB, HIV, Carcinoma and steroid use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Difference between the cause of acute and chronic disc disease?

A

Acute - prolapsed intervertebral disc which results in lumargo and sciatica

  • younger people

Chronic - Degenerative disease in the lower lumber discs of the facet joints - sciatic radiation to the butt and posterior thigh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical features of acute disc disease?

A

Sudden onset of severe back pain following strenuous activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Management of acute disc disease?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Management of chronic disc disease?

A

NSAIDS

Physio

Weight reduction

Surgery - if level or nerve root identified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between spondylothesis and spinal stenosis?

A

Spondylothelosis - condition where the lower vertebra slip forward onto the bone directly beneath associated with mechanical back pain

Spinal stenosis - compression of the cauda equina - back and butt pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Osteoarthritis?

A

Degenerative disease of synovial joints and the commonest form of arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathology of osteoarthritis?

A

Progressive destruction and loss of articular surface

Exposed subchondral Bone - sclerosis - increase vascularity - cyst formation

In an attempt to repair - cartilaginous growths calcify at the margin of the joints (OSTEOPHYTES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes the destruction in osteoarthritis?

A

Metalloproteinases - collagenases that degrade protein and proteoglycans

IL1 and TNF-alpha - stimulate metalloproteinases and inhibit collagen production

Deficiency of growth factors

Osteoprotegerin - Binds to RANKL and stimulates osteoclastogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clinical features of osteoarthritis?

A

Heberden Bouchard notes

Adducted thumb

Joint pain made worse by movement and better by rest

Gelling - stiffness at rest

Weigh bearing joining - knees, hips and vertebrae

Muscle wasting or surrounding muscle group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Key X-ray features of osteoarthritis?

A

Osteophytes

Subchondral sclerosis

cyst formation

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

Investigations to confirm osteoarthritis?

A
  • -ve rheumatoid factor
  • Normal FBS and ESR
  • X-ray
  • MRI - early cartilage changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Management of osteoarthritis?

A

Based on symptoms + disability

PHYSICAL CHANGES

MEDICATION

  • Paracetamol + weak opioid
  • Short course NSAIDS
  • Intra articular corticosteroid injections

SURGERY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

3 types of inflammatory arthritis?

A

Rheumatoid

Spondyloarthritis - axial spondyloarthropathies, Reactive, psoriatic

Crystal - Gout and pseudogout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Rheumatoid arthritis?

A

Chronic systemic autoimmune disorder causing symmetrical peripheral polyarthritis with prolonged morning stiffness associated with other autoimmune conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Aetiology of rheumatoid arthritis?

A

Gender - women before menopause

Family histology

Genetics - HLA DR4/ DRB1

Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathology of rheumatoid arthritis?

A

Synovial inflammation - activated by inflammatory T cells activating macrophages, mast cells and fibroblasts

Rheumatoid factor - autoantibodies against the FC portions of IgG produced by B cells - forms complexes and causes complement activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Synovitis?

A

inflammation of synovium due infiltration by inflammatory cells - inflammation of joints, tendon sheaths and bursae

  • Cytokines cause angiogenesis and activation of adhesion molecules and endothelial cells - leukocyte infiltration

PANNUS - synovium proliferates and grows over the surface of cartilage - causes a tumour like mass that destroyed articular surfaces of bone causing bony erosions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical features of rheumatoid arthritis?

A

Symmetrical peripheral polyarthritis with early morning stiffness lasting more than 30 mins

Swollen MCP and PIP causing spindle shaped fingers

KEY:

ULNER DEVIATION

Z SHAPED THUMB

SWANN NECK DEFORMITY

BOUTONNIERE DEFORMITY - PIP flexion and DIP hyperextension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Non-articular manifestations of rheumatoid arthritis?

A

Muscle wasting

Rheumatoid nodules - elbow, finger, Achilles tendon - near joints affected by rheumatoid

Increased risk of infection

Pericardial effusion and pleural effusion

Episcleritis - inflammation of the white of the eyes

Ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Investigations to diagnose rheumatoid arthritis?

A

Bloods - normocytic normochromic anaemia (chronic disease and drug therapy) (normal size and normal concentration of Hb)

  • ESR and CRP increased

Serum autoantibodies - anti-citrullinated protein antibodies + rheumatoid factor

X-ray - soft tissue swelling, joint erosion and porosis of periarticular bone

Synovial aspiration - increased neutrophil count - if painful start thinking it might be septic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Management of rheumatoid arthritis?

A

No cure, just treat the symptoms and try to get back function of joint

  • NSAIDs + COXIBS (selective NSAIDS for COX2 not protective COX1) - relive joint pain but doesn’t slow down the progression of the disease
  • CORTICOSTEROIDS - decreases disease activity
  • DMARDs - inflammation of inflammatory cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

DMARDs drugs and which one is safe if pregnant?

A

Sulfasalazine - safe for preggo

Methotrexate - teratogenic

Leflunomide - longer-lasting and blocks T cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Gold standard Biological DMARD?

Infliximab - TNF-alpha inhibitor

Anakinra - IL1 receptor blocker

Rituximab - lysis of B cell

Tocilizumab - IL6 receptor antibody

Abatacept - Blocks T cell activation

A

Infliximab - TNF-alpha inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What joint needs to be involved for axial spondyloarthropathy to be ankylosing spondylitis?

A

Sacroiliac joint

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

Axial spondyloarthropathy?

A

Inflammation of the spine mainly found in you male adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical features of ankylosing spondylitis?

A

Compensatory hyperextension of the neck

Exaggerated thoracic kyphosis

Loss of lumbar lordosis

vertebra fused together

Fixed flexion of the hips

Compensatory flexion of the knees

  • Achilles tendonitis and plantar fasciitis - inflammation on heel and arch of foot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Investigations used to diagnose axial spondyloarthropathy?

A

Bloods - Increase ESR and normalish CRP

X-ray

  • bamboo spine
  • sclerosis/ erosions of sacroiliac joint

blurring of upper or lower vertebral arthritis at thoracolumbar junction

Syndesmophytes - new bony growths

Enthesitis

MRI - sacroilitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Management of axial spondyloarthropathy?

A

Early diagnosis

Morning exercise

slow release NSAIDS at night

Infliximab

Phosphodiesterase type 4 inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What percentage of patients with psoriasis develop psoriatic psoriasis?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Clinical features of psoriatic arthritis?

A

Dactilytis - sausage fingers

Arthritis mutilans - severe destruction of small bones in hands and feet due to severe inflammation

Sacroiliitis

mono- or oligoarthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is a pencil in cup deformity on a x ray indicative of?

A

Arthritis mutilans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Management of psoriatic arthritis?

A

Analgesics or NSAIDS

Local intraarticular corticosteroid injections

Methotrexate or TNF-alpha inhibitor

PDE4

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

Enteropathic arthritis?

A

Large joint mono or symmetrical oligoarthritis occurring in 10 to 15% of patients with IBD

The worse the IBD the worse the pain and visa versa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Reactive arthritis?

A

Arthritis mostly found in young patients within 4 weeks of infections such as GI infections or STIs

mostly lower limb joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

GI infections that can cause reactive arthritis?

A

Salmonella

shigella

Yesenia

campylobacter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Clinical features of reactive arthritis?

A

Srthritis within 4 weeks of an infection in young adults

Circinate balanitis - skin ulcers around the penile meatus - ring-shaped dermatitis around glans penis

Red plaques/ pustules on skin

Uveitis

Enthesis - Achilles tendonsiits, plantar fasciitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Reiter’s syndrome?

A

Uveitis, reactive arthritis and conjunctivitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Investigations used to diagnose reactive arthritis?

A

Bloods - increased ESR

Synovial aspirations - sterile with high neutrophil count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Management of reactive arthritis?

A

NSAIDs

Local corticosteroid injections

Antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are the crystals found under joint fluid microscopy in gout and pseudogout?

A

Gout - sodium urate

Pseudogout - calcium pyrophosphate dihydrate

Neutrophils ingest the crystals and initiate pro-inflammatory reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Gout

A

Inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals

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

Pathophysiology of gout?

A

Increased uric acid production and decreased excretion through kidneys and faeces

  • urate is derived from the breakdown of purines by xanthine oxidase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

clinical features of gout?

A

Acute sodium urate synovitis

Chronic interval / polyarticular / tophacus gout

Urate renal store formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the most common location for gout?

A

1st metatarsophalangeal joint of the big toe - middle aged, swollen and painful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What can put elderly women at risk of developing gout?

A

Long term diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Investigations used to confirm gout?

A

Joint fluid microscopy - needle-like crystals which are regularly birefringent under polarised light

Increased serum uric acid

Increased urea and creatinine if the kidneys are involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Management of gout?

A

NSAIDs and COXIB - diclofenac and lumiracoxib

Colchicine - inhibits activation and migration of neutrophils to sites of inflammation

DECREASE SERUM URIC ACID - decrease alcohol, weight, sugar, purine rich food,

ALLOPURINOL - Inhibits xanthine oxidase and decrease sodium urate rapidly

FEBUXOSTAT - non-purine analogue inhibitor of xanthine oxidase

ANAKINRA - IL1 beat blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what factors can cause impaired uric acid excretion?

A

CKD

Thiazide or aspirin

Hypertension

Primary hyperparathyroidism

Increased lactic acid production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Factors that can increase production of uric acid?

A

Increase turnover of purines

Myeloproliferative disorder - polycythemia

Leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Pseudogout?

A

Calcium pyrophosphate dihydrate crystals in articular cartilage and periarticular tissue that produces an image of chondrocalcinosis

Affects elderly women and affects the knees and wrist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Investigations used to confirm pseudogout?

A

X-ray - chondrocalcinosis

Joint fluid microscopy - small brick-shaped crystals which are positively birefringent under polarised light

Blood - raised which cell count

57
Q

Management of pseudogout?

A

Joint aspiration + colchicine

Local injection of corticosteroids

58
Q

Most common cause of septic arthritis?

A

Staphy Aureus

59
Q

What can cause septic arthritis?

A

Infection of the joint by direct injury or blood bourne infection

60
Q

Risk factors of septic arthritis?

A

Prosthetic joints, pre-existing joint disease or recent intra-articular corticosteroid injection

61
Q

Clinical features of septic arthritis?

A

Hot, painful, swollen joint + FEVER

20% involve more than 1 joint

Prosthetic joint - inflamed or visible discharge

62
Q

Investigations used to confirm septic arthritis?

A

JOINT ASPIRATION AND SYNOVIAL FLUID ANALYSIS OF APPEARANCE AND NEUTROPHIL COUNT

  • Opaque and 75000+ neutrophils

BLOODS - Increase ESR and CRP, bacterial culture and FBC

X-RAY

SWABS OF URETHRA, CERVIX OR ANORECTUM - looking for gonococcal infection

63
Q

Management of septic arthritis?

A

Flucloxacillin + oral fusidic acid (gentamicin is given to immunosuppressants)

Joint drainage

Immobilize the joint

NSAID

64
Q

Appearance and WCC when doing a synovial fluid analysis?

Normal

Inflammed

Septic

A

Normal - straw + <3000 wcc/mm^3

Inflammed - Cloudy + >3000 wcc/mm^3

Septic - opaque + 75000 wcc/mm^3

65
Q

Most common cause of septic arthritis in young people?

A

Gonococcal infection - genital, rectal or oral infection

66
Q

Meningococcal septic arthritis?

A

Migratory polyarthritis due to meningococcal septicaemia so there is a deposition of immune complexes containing m. antigens

67
Q

Osteomyseltiits?

A

Infection of bone by bloodstream, open fracture or surgery

Staphy - Haemophilus influenza or salmonella

CLINICAL FEATURES: Fever, local pain, erythema and sinus formation

INVESTIGATIONS: CT, MRI, BONE SCAN, BLOOD CULTURE AND BONE DENSITY

MANAGEMENT: Flucloxicilin and fusidic acid

68
Q

5 types of autoimmune rheumatic disease?

A

SLE

Antiphospholipid syndrome

Systemic sclerosis (scleroderma)

Polymyositis + dermatomyositis

Sjogren’s syndrome

69
Q

SLE?

A

An inflammatory multisystem disease characterised by the presence of serum autoantibodies against nuclear components

70
Q

Pathophysiology of SLE?

A

Environmental trigger causes apoptosis - increase nuclear antigens and apoptotic bodies

Genetic susceptibility - not able to clear the apoptotic bodies and recognising the nuclear antigens as foreign

Autoantibodies (antinuclear antibodies and Anti ds-DNA) - form antigen-antibody complexes and they deposit in tissue and blood vessel walls causing inflammation

complement system causes pores to form and cells to burst

71
Q

Aetiology of SLE?

A

Ultraviolet light

Genetics - HLA B8, DR3, A1

Oestrogen

Drugs - Procainamide (antiarrhythmic), isoniazid (TB antibiotic), hydralazine (heart failure)

EBV

72
Q

Clinical features of SLE?

A

Fever, joint pain and rash

Organ specific symptoms

ULCERS - Malar rash, discoid rash and photosensitivity

SEROSA - pericarditis (can affect other layers of the heart), pleuritis

JOINTS - Arthritis in 2 or more joints

KIDNEY - abnormal urine protein

BRAIN - neurological disorders - seizure and psychosis

BLOOD - haematological disorders (anaemia, leukopenia, thrombocytopenia)

ANTIBODIES - Anti-nuclear antibodies, Anti-smith (ribonucleoproteins), Anti-dsDNA, Anti-phospholipids syndrome (targets proteins bound to phospholipids)

73
Q

3 types and antiphospholipid autoantibodies?

A

Anticardiolipin

Lupus anticoagulant

Anti-Beta 2 Glycoprotein 1

74
Q

Discoid lupus?

A

lupus where only skin is involved - facial rash with erythematous plaques

Coin shaped lesions

SCALP, EARS, BUTTERFLY AND LOWER LIP

75
Q

Investigations to diagnose SLE?

A

BLOODS - normochromic normocytic anaemia, haemopoietic deficiencies, Increased ESR but noremal CRP, urea and creatinine/ low serum albumin if renal impairment

SERUM AUTOANTIBODIES - Antinuclear antibodies, anti-smith, anti-dsDNA and anti-phospholipids

SERUM COMLEMENNT 3 AND 4

HISTOLOGY OF RENAL OR SKIN BIOPSY - Deposition of IgG and complement

76
Q

Management of SLE?

A

Dependant on severity and symptoms of the disease

AVOID SUNLIGHT AND DECREASE CARDIOVASCULAR RISK

NSAIDs

CHLOROQUINE OR HYDROXYCHLOROQUINE - anti-malarials and anti-inflammatory (mild and cutaneous)

CORTICOSTEROIDS - prednisolone - moderate to severe

IMMUNOSUPPRESANTS - severe with cerebral and renal impairment

TOPICAL STEROIDS

77
Q

What are SLE patients at risk of developing?

A

Osteonecrosis of femoral head + mitral valve regurgitation

78
Q

What is associated with anti-phospholipid syndrome?

A

Recurrent miscarriage

Recurrent thrombosis

Anti-phospholipid autoantibodies

hypercoagulable states and more likely to have clots

79
Q

Clinical features of anti-phospholipid syndrome?

A

Arteries - stroke, TIA, MI

Veins - DVT and Budd-Chiari syndrome

Recurrent miscarriage

80
Q

Management of antiphospholipid syndrome?

A

Long term warfarin

Pregnant - aspirin and heparin

Prophylaxis - aspirin and clopidogrel

81
Q

Systemic sclerosis (scleroderma)?

A

Normal tissue is replaced with thick fibrous connective tissue - excessive collagen production

multisystem condition that has skin involvement and raynaud’s phenomenon occurring early

82
Q

Aetiology of scleroderma?

A

Increased vascular permeability so there is infiltration and activation of inflammatory cells and adhesion molecules - migrate to the extracellular matrix - fibroblasts are stimulated to produce more collagen

UNCONTROLLED IRREVERSIBLE PROLIFERATION OF CONNECTIVE TISSUE AND THICK VASCULAR WALLS

83
Q

Limited cutaneous scleroderma?

A

70%

Calcinosis (hands)

Raynaud’s phenomenon

Oesophageal Involvement

Sclerodactyly - thick and dough-like then hard a claw-shaped

Telangiectasia - wide blood vessels that cause thread-like patterns

MICROSTOMIA

84
Q

Diffuse cutaneous scleroderma?

A

30%

Skin changes more rapidly and more widespread involvement

GI - GORD, dysphagia and malabsorption

Renal - AKD or CKD

Lung - lung fibrosis and pulmonary vascular disease

Heart - myocardial fibrosis and conduction disturbances

85
Q

Investigations used to diagnose scleroderma?

A

Blood - normocytic normochromic anaemia, increase U and C, serum auto-antibodies

X-ray - calcium deposits around fingers

Barium swallow - showing oesophageal dysmotility

86
Q

Autoantibodies associated with scleroderma?

A

Antinuclear antibodies

DCS - anti-topiosomerase 1 (SL70) and anti-polymerase 1 and 3

LCS - Anti-centromere

87
Q

Management of scleroderma?

A

Vasodilators, warfarin and O2 - P. hypertension

ACEi - hypertension and KD

Cyclophosphamide, azathioprine or low dose prednisolone - Pulmonary fibrosis

88
Q

polymyositis?

A

Inflammation and necrosis of skeletal muscle fibres due to molecular mimicry of proteins found on their surface ‘

  • Perofrins form holes and granulozymes enter = apoptosis
  • FAS ligands - signals a cascade of reactions leading to apoptosis

REPEATED ATTACKS LEADS TO NECROSIS

89
Q

Dermatomyositis?

A

Complement mediated and autoantibodies against blood vessels - tissue ischaemia

Immune complexes using proteins of damaged cells travel to the BM of skin - cell damage

90
Q

Clinical features of polymyositis?

A

Bilateral proximal muscle weakness of shoulders and hips

Difficulty - swallowing, going upstairs, raising arms and rising from a chair

Involvement of pharynx and oesophagus - dysphagia, dysphonia and respiratory failure

91
Q

Clinical features of dermatomyositis?

A

Heliotrope rash - rash on upper eyelids

Gottrons plaque - red scaly rash on the back of fingers and knees that are photosensitive

associated with malignancy :(

92
Q

Investigations used to diagnose poymyositis/ Dermatomyositis?

A

MUSCLE BIOPSY - inflammatory cell infiltration and necrosis of muscle cells

ELEVATED SERUM MUSCLE ENZYMES - creatine kinase, aldolase and aminotransferase

SERUM ANTIBODIES - Anti-tRNA synthetase (anti -jo), Anti-mi2, ANA

ELECTROMYOGRAPHY - Detect regions of dead muscle

MRI - muscle inflammation

ESR not raised

93
Q

Management of polymyositis/ dermatomyositis?

A

Corticosteroids

Immunosuppressants

Anti-malarial medication

Exercise therapy

Avoid sun and wear protective clothing

94
Q

Sjogren’s syndrome?

A

Immunologically mediated destruction of epithelial exocrine glands in particular lacrimal and salivary glands

95
Q

Clinical features of Sjogren’s syndrome?

A

Keratoconjunctivitis sicca - dry eyes

Xerostoma - dry mouth

Difficulty eating dry biscuits and absence of pool of saliva when the lifting tongue

Associated of other autoimmune diseases

Arthritis

96
Q

Investigations used to confirm Sjorgren’s syndrome?

A

SERUM AUTOANTIBODIES - ANA, Anti-Ro

LABIAL GLAND BIOPSY -lymphocyte infiltration and destruction of acinar tissue

+VE SCHIRMER TEST - standard stip of filter paper placed on lower lid and if positive it will wet less than 10cm in 5mins

97
Q

Management of Sjorgren’s syndrome?

A

Artificial tears or saliva replacement solutions

98
Q

Vasculitis?

A

Inflammation of blood vessels walls associated with other haematological conditions such as SLE, RA and allergic reactions

99
Q

Systemic vasculitits?

A

Group of multisystem disorders in which:

vasculitis is the principle features

classification is based on the size of the vessel affected

Anti-Neutrophilic cytoplasmic autoantibodies

100
Q

Polymyalgia and giant cell arteritis?

A

Abrupt stiffness and instance pain of muscles in shoulder, neck, hips and lumber

Giant cell arteritis is when inflammation occurs in the arteries of the head and neck - specifically the superficial temporal artery - headache and tender heads

GCA - can cause stroke or sudden loss of vision

101
Q

Investigations used to confirm Polymyalgia and giant cell arteritis?

A

Increased ESR and CRP

Normochromic Normocytic anaemia

Temporal artery biopsy

102
Q

Management of Polymyalgia and giant cell arteritis?

A

Corticosteroids - prednisolone

103
Q

Takayasu arteritis?

A

Vasculitis of major vessels such as the aortic arch and other major vessels mostly affecting Japanese people

  • linked to hypertension, absent peripheral pulse, stroke, cardiac failure
  • Corticosteroids treatment
104
Q

Polyarteritis Nodosa?

A

Vasculitis secondary to immune complex deposition after Hep B antigenaemia

Necrotising arteries resulting in microaneurysms, thrombosis and infarction

  • fever, malaise, myalgia and weight loss
105
Q

Moneuritis multiplex?

A

Painful asymmetrical asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve endings

simultaneous malfunction of 2 or more peripheral nerves in different areas of the body

e.g. abdo pain due to visceral infarction, MI/HF due to affecting cardiac ateries and even renal failure

106
Q

Investigation and management of polyarteritis nodosa?

A

Angiography for microaneurysms

Biopsy of affected organs

Corticosteroids and immunosuppressants

107
Q

What organs are affected by microscopic polyarteritis?

A

Lungs and kidneys - Haemoptosis, haematuria, proteinuria and renal failure

  • arthralgia and purpuric rashes
108
Q

Investigations used to confirm microscopic polyarteritis?

A

Renal biopsy and serum ANCA

109
Q

Eosinophilic granulomatosis with polyangiitis?

A

Asthma, eosinophilia and a systemic vasculitis affecting peripheral nerves and skin

110
Q

Henoch-Scholein purpura?

A

Purpuric rash mainly on legs and butt of children

Vascular depositions of IgA dominant immune complexes and it comes before acute respiratory tract infection

Abdo pain, arthritis, haematuria and nephritis

111
Q

Cryoglobulinaemic vasculitis?

A

Cryoglobulin - Ig and complement components protein that precipitates in cold and causes obstruction of finger and toes

purpura, glomerulonephritis and polyneuropathy

112
Q

Behcet’s disease?

A

Inflammation of blood vessels and tissue associated with recurrent oral ulceration, eye lesions -uveitis, genital lesions, GI ulcers and arthritis

Immunosuppressants or even thalamide - inhibits IL6

113
Q

Osteoporosis?

A

Reduction in bone mass and micro-articular destruction of bone tissue - bone fragility and increased risk of fracture

bone mass density Is greater than 2.5 below the young adult mean value

114
Q

Aetiology of osteoporosis?

A

Inadequate peak bone mass and ongoing bone loss

115
Q

What would be seen on an x-ray of a patient with osteoporosis?

A

Fractures at:

Kyphosis and loss of heigh in thoracic and lumber vertebrae

Proximal femur

Distal radius (colles)

116
Q

Investigations used to confirm osteoporoiss?

A

DXA - Dual-energy x-ray absorptiometry

X-ray - fractures

Normal serum biochem

Look at secondary causes of osteoporosis

117
Q

FRAX?

A

10 year probability of hip fracture and major osteoporotic fracture combined for an untreated patient between 40 and 90 years old

118
Q

Biphosphonates MOA?

A

Alendronate, Risedronate and Zolendronate

Inhibit osteoclasts and bone resorption

increase bone mass at hip and spine and decrease the risk of fracture

119
Q

Denosumab MOA?

A

Human monoclonal antibody for RANKL which usually stimulates and activates osteoclasts

120
Q

Selective oestrogen receptor modulator?

A

Activates oestrogen receptors on the bone while having no stimulatory effect on the endometrium - decrease the bone mass lost

cramps, flushing, strokes and increase risk of thromboembolism

121
Q

Recombinant human parathyroid peptide 1 - 34 MOA?

A

Stimulates bone formation in severe osteoporosis

Hypercalcaemia

122
Q

Other forms of management for osteoporosis?

A

Oestrogen therapy for post-menopause women

Testosterone for men with hypergonadism

Strontium Ranelate - post-menopausal

123
Q

Osteonecrosis?

A

Death of bone and bone marrow due to reduced blood flow

Drugs - glucocorticoids, bisphosphonates (maxillofacial skull)

Alcohol

Sickle cell

Radiation

HIV

124
Q

Paget’s disease?

A

Increased osteoclast activity and get replaced with new weaker bone associated with latent infection in osteoclasts or being genetically susceptible

Increased local bone blood flow and fibrous tissue

125
Q

Clinical features of paget’s?

A

Pelvis, femur, lumber spine, skull or tibia

Pain in bone or nearby joint

Deformities - enlarged skull and bowing of the tibia

126
Q

Investigations used to confirm paget’s disease?

A

Increased serum alkaline phosphatase

Increased urine hydroxyproline excretion

X-ray - enlargement, distortion or osteolytic changes

Radionuclide bone scan

127
Q

Management of paget’s disease?

A

Biphosphonates - Zolendronide

Constant monitor of serum alkaline phosphatase and urine hydroxyproline excretion

128
Q

Complications of paget’s?

A

Nerve compression

Pathological fracture

High output cardiac failure

Osteogenic sarcoma

129
Q

Osteomalacia/ Rickets?

A

Osteomalacia - adults - weak, soft and risk of fracture

Rickets- children - softening, impaired growth and malformation

Bone softening due to faulty bone mineralization - deficiency or impaired metabolism of it D, Calcium or phosphate

130
Q

What can cause vit D deficiency?

A

Decreased intestinal absorption - Crohns or coeliac

Chronic kidney or liver disease

Decreased UV light exposure

Long term phenytoin or anticonvulsants because they use up the hydrolase enzymes

131
Q

Clinical features of osteomalacia and rickets?

A

Diffuse bone and joint pain

Proximal muscle weakness

Bone fragility

Increased risk of low trauma fractures

Muscle spasms and numbness

132
Q

Rickets specific symptoms?

A

Craniotabey - thin and soft cranial bones

Delayed closure of fontanelles

Genu varum

Prominent frontal bone

Protruding abdomen

Rachitic rosary - bumps on chest due to coastal widening between ribs and cartilage

133
Q

Investigations used to confirm osteomalacia?

A

Decreased serum 2,5-dihydroxyvitamin D

Decreased calcium - increased PTH - decreased phosphate

Increase alkaline phosphatase

X-ray - looser zones (pseudofractures), Rickets - metaphyseal clubbing and fraying or genu varum

134
Q

Fibromyalgia?

A

Chronic widespread muscle pain mostly in women alongside tenderness and sleep disturbances

135
Q

Pathology of fibromyalgia?

A

Nociceptor detects pain (skin, joints and walls of organs) - from dorsal root ganglion they release substance P to second or the inhibitory centre releases serotonin or norepinephrine to cancel the stimulatory effect of substance P

If substance P strong enough then it goes to the brain

At the site - Epithelial cells and mast cells release nerve growth factor

136
Q

function of nerve growth factor?

A

They affect nociceptors

  • increase growth

increase sensitivity to pain

increase amount of substance P produced

137
Q

Diagnosis of Fibromyalgia?

A
  1. Pain in >7 or >5 areas of the body
  2. Sensitivity score - >5/12 or >9/12
  3. > 3 months

Pain can’t be due to other conditions

pain can also be associated with emotion

138
Q

Management of fibromyalgia?

A

Exercise

Relaxation techniques and sleep hygiene

Medication - Amitriptyline, Serotonin-norepinephrine reuptake inhibitors, Anticonvulsants - pregabalin or gabapentin which slow down nerve impulses

Phase 2a (7 decks)

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