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Year 2 > MSK: Part 2 > Flashcards

MSK: Part 2 Flashcards

1
Q

Define Osteoporosis

A
  1. A systemic skeletal disease characterised by low bone mass and a micro architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture
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2
Q

What parameters define osteoporosis

A

Defined as Bone mineral density MORE than 2.5 SDs below young adult mean value (T score < 2.5)

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3
Q

What is Osteopenia

A

Pre-cursor to osteoporosis characterised by lone bone density

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4
Q

What parameters define osteopenia

A

BMD between- 1 to -2.5 SDs below young adult mean value (-1

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5
Q

What is Osteomalacia

A

poor bone mineralisation leading to soft bone due to lack of Ca2+ (adults form of rickets)

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6
Q

How is T score calculated

A

SD score ascertained using DEXA scan

Compared to gender-matched young adult average (peak bone mass)

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7
Q

What is a normal T score

A

-1

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8
Q

In what gender is osteoporosis more common in and why

A

FEMALES

They lose trabculae over time

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9
Q

Risk factors for osteoporosis

A
  1. Old age
  2. Women
  3. Family history of osteoporosis or fracture
  4. Previous bone fracture
  5. Smoking/Alcohol
SHATTERED:
S - STEROID USE (PREDNISOLONE)
H - HYPERTHYROIDISM 
A- Alcohol and tobacco (bad for bones
T - Thin (BMI <22)
T - Testosterone
E- Early Menopause
R - Renal or liver failure
E - Erosive/inflammatory bone disease (Myeloma)
D - Dietary (calcium malabsorption)
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10
Q

What is the peak bone mass age

A

25

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11
Q

How does osteoporosis happen

A

Increased bone breakdown by osteoclasts and decreased bone formation by osteoblasts leading to loss of bone mass

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12
Q

What is the biggest influence on peak bone mass

A

genetic factors

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13
Q

What genes are responsible for peak bone mass

A

Collagen type 1A1
Vit D receptor
Oestrogen receptor genes

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14
Q

What determines bone strength

A

BMD - How much mineral in bone (determined by gained during growth and amount lost during ageing)
Bone size - Short and fat better than long and thin
Bone Quality - Bone turnover rate

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15
Q

What causes postmenopausal osteoporosis

A

Increased numbers of osteoclasts, premature arrest of osteoblastic synthetic activity
Perforation of trabecular with loss of resistance to fracture

High bone turnover (resorption greater than formation)

Predominantly cancellous bone loss

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16
Q

How does trabecular architecture change with ageing

A

Decrease in trabecular thickness - as we age the strain is felt on bones from head to tail, in response, we tend to preferentially preserve vertical trabecular and lose horizontal trabecular

Decrease in trabecular thickness in connections between horizontal trabecular resulting in decrease trabecular strength and increased susceptibility to fracture

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17
Q

Clinical presentation of osteoporosis

A
  1. Fractures!!

Vertebral crush fracture
Colles’ fracture of wrist following outstretched arm

Fractures on proximal femur usually occur in older individuals falling on their side or back

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18
Q

What is vertebral crush

A

Sudden onset of severe pain in the spine, radiating to the front

Thoracic vertebral fractures may lead to kyphosis (widows stoop)

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19
Q

How is osteoporosis diagnosed

A
  1. X-ray
  2. DEXA scan
  3. Bloods
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20
Q

What do x-rays show for osteoporosis

A

Demonstrate fractures but insensitive for osteopenia

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21
Q

What is DEXA

A
  1. Measures important fracture sites (lumbar spine and proximal femur)
  2. GOLD STANDARD - measures bone density and diagnosis
  3. Generates T scores
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22
Q

What T-score equals Osteoporosis

A

more than 2.5 SDs

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23
Q

Blood tests in osteoporosis

A
  1. Ca
  2. Phosphate
  3. Alkaline phosphate all normal
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24
Q

How is osteoporosis treated

A
  1. Quit smoking and alcohol
  2. Weight-bearing excersise (increases bone density)
    3/ Calcium and vit D rich diet
  3. Balance excercises to reduce falls
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25
Q

First line treatment for osteoporosis

A

Bisphosphanates

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26
Q

How do bisphosphonates work

A

Inhibit bone resorption through inhibition of enzyme (Farnesyl Pyrophosphate synthase - in cholesterol pathway) which reduces osteoclastic activity by removing their ruffled border

Increases bone mass at hip and spine

Reduce incidence of fracture and are cheap and effective

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27
Q

Name a bisphosphonate

A

ORAL ALDENRONATE

ORAL ZOLENDRONATE

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28
Q

When are oral bisphosphonates given

A

When fasting, with a large drink of water while standing or sitting upright

Associated with oesophagi’s

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29
Q

Name two anti-resorptive drugs other than bisphosphonates

A
  1. STRONTIUM RENELATE

2. DENOSUMAB

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30
Q

What is Strontium Renovate

A

Helps reduce fracture rates

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31
Q

When is Strontium renovate given

A

Alternative to those intolerant to bisphosphonates

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32
Q

How do DENOSUMABs work

A
  1. Osteoblasts produce RANK to activate osteoclasts and thus bone respiration
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33
Q

What is DENOSUMAB

A

Monoclonal antibody that inhibits RANK signals

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34
Q

2nd line treatment of osteoporosis

A

HRT (Hormone Replacement Therapy)

for menopausal women

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35
Q

Role of HRT

A

Reduces fracture risk and stops bone loss

Prevents hot flushes and other menopausal symptoms

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36
Q

Side-Effect of HRT

A

Breast cancer
Stroke
CVD

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37
Q

What is RALOXIFINE

A

Selective Oestrogen receptor modulator - activates oestrogen receptor on bone whilst having no stimulatory effect on endometrium

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38
Q

Side-effects of RALOXIFINE

A
  1. Increased risk of thrombus formation
  2. Cramps
  3. Strokes
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39
Q

What HRT is used for men in osteoporosis

A

Testosterone

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40
Q

What anabolic can be used for osteoporosis

A
  1. RECOMBINANT HUMAN PARATHYROID PEPTIDE
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41
Q

How does Recombinant human parathyroid peptide function

A
  1. Increases osteoblast activity and bone formation
  2. Reduce fracture risk
  3. Improves bone density, trabecular structures
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42
Q

Side-Effects of recombinant human parathyroid peptide

A

Increased risk of renal malignancy

Hypercalcaemia

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43
Q

Name a Recombinant human parathyroid peptide

A

TERIPARATIDE

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44
Q

Name some inflammatory markers

A

ESR

CRP

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45
Q

When does ESR raise

A

Inflammation and infection

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46
Q

Why does ESR raise in inflammation and infection

A

Increased fibrinogen makes RBCs ‘stick together’ and thus fall faster

47
Q

Rate at which ESR rises and fails

48
Q

Problem with ESR tests

A

False positives

49
Q

When is CRP released into the blood

A

Inflammation/infection

50
Q

Where is CRP produced

A

Liver in response to IL-6

51
Q

Define autoimmune disease

A

Pathological conditions caused by the immune response directed against an antigen within a host

52
Q

Name some auto-immunological disorders

A
  1. SLE
  2. SNTIPHOSPHOLIPID SYNDROME
  3. SJORGRENS
53
Q

What is SLE (SYSTEMIC LUPUS ERTHEMATOSUS)

A
  1. Multisystem autoimmune disorder with arthralgia and rashes

Cerebral and renal disease

54
Q

What gender does SLE effect

55
Q

Risk factors of SLE

A
  1. Family history
  2. Genetics
  3. Pre-menopausal women most affected
  4. Srugs: Hydrazine, isoniazid, procainamide and penicillamine
  5. UV light can trigger flares of SLE
56
Q

Pathophysiology of SLE

A
  1. When cells die by apoptosis, cellular remnants appear on the cell surface as small blebs that carry self-antigens
  2. In SLE, removal of blebs by phagocytes is inefficient so they are transferred to lymphoid tissues, where they can be taken yp by APCs
  3. Self-antigens from these blebs can be presented to T cells which stimulate B cells to produce AUTOANTIBODIES directed against the antigens
  4. Combination of self-antigens and failure of immune system to inactivate B and T cells that recognise these self-antigens as foreign leads to the following:
    AUTOANTIBODIES that either form circulating complexes or deposit by binding directly to tissues

ACTIVATION of complement and influx of neutrophils, causing inflammation to those tissues

ABNORMAL CYTOKINE PRODUCTION: Increased IL-10 and INF-alpha

57
Q

Name some antigens in SLE

A

Dna
Histones
Normally hidden from immunit system

58
Q

How is SLE of the skin and kidneys characterised

A

Deposition of compliment and IgG antibodies - influx of neutrophils and lymphocytes

59
Q

What would biopsy in SLE show

A

Vasculitis affecting capillaries, arterioles and venues

60
Q

Characteristics of joint synovium in SLE

A

Oedematous and contain immune complexes

61
Q

What can be seen in inflammatory infiltrates of SLE

A

Haematoxylin bodies from interaction of antinuclear antibodies and cell nuclei

62
Q

Clinical presentation of SLE in joints

A
  1. SYMMETRICAL SMALL JOINT ARTHRALGIA
  2. Joints are painful
  3. Soft tissue swelling
  4. Avascular necrosis of hip and knee rarely
63
Q

Clinical presentation of SLE in skin

A
  1. ERYTHEMA in a BUTTERFLY DISTRIBUTION
  2. Vasculitis lesions
  3. Alopecia
  4. Photosensitive rash
  5. Raynaud’s phenomenon
64
Q

Clinical presentation of SLE in lungs

A
  1. Recurrent pleural effusions and plueurisy, pneumonitis and atelectasis
  2. Pulmonary fibrosis (RARE)
65
Q

Clinical presentation of SLE in Heart

A

PERICARDITIS
ARRYTHMIAS
MYOCARDITIS
VENOUS THROMBOSIS

66
Q

Clinical presentation of SLE in the KIDNEYS (IMPORTANT)

A

GLOMERULONEPHRITIS with persistent proteinuria

67
Q

Clinical presentation of SLE in CNS

A
  1. SEIZURES

2. PSYCHOSIS

68
Q

Clinical presentation of SLE in eyes

A

Retinal vascultisis

Sjorgen’s

69
Q

Common clinical presentation of SLE in GI

A

Mouth ulcers

70
Q

Differential diagnosis of SLE

A

ACUTE PERICARDITIS
ANTIPHOSPHOLIPID SYNDROME
SJORGEN SYNDROME

71
Q

How is SLE diagnosed

A
  1. ESR raised but CRP NORMAL
  2. INFECTION if CRP is raised
  3. Blood tests
  4. Autoantibodies (ANA)
  5. Histology to see deposition of IgG and complement
  6. MRI and CT for lesions in brain
72
Q

Blood tests in SLE

A
  1. Raised ESR
  2. Normal CRP
  3. Leucopenia
  4. ANAEMIA of chronic disease
  5. UREA and creatinine only raised if renal disease is advanced
  6. seem C3/4 are reduced due to immune reaction
73
Q

What autoantibodies are seeing in SLE

A
  1. ANA (auto-nuclear antibodies)
  2. Raised anti-double stranded DNA antibody (Specific for SLE but not accurate - 60% of people with SLe are positive)
  3. 40% are rheumatoid factor positive
  4. anti-ro, anti-smith, anti-a
74
Q

How is SLE treated

A
  1. ACUTE SLE (IV CYCLOPHOSPHAMIDE + HIGH DOSE PREDNISOLONE)
  2. Reduce sunlight exposure
  3. Reduce CVD risk factors
  4. Prevent rashes with high-factor sunblock
  5. Treat blood pressure and give statins to control CVD risk
  6. NSAIDs for arthralgia, fever and arthritis (IBUPROFEN)
  7. ORAL corticosteroids for flares of arthritis and pericarditis
75
Q

Corticosteroid treatment for mild/moderated SLE

A

HYDROXYCHLOROQUINE or CHOLOQUINE help mild skin disease, fatigue, arthralgia

PREDNISOLONE (then reduce dose)

Immunosuppression - ORAL AZATHIOPRINE, ORAL METHOTREXATE

76
Q

Corticosteroid treatment for severe SLE

A
  1. ORAL AZATHIOPRINE, ORAL METHOTREXATE
  2. PREDNISOLONE AND ORAL CYCLOPHOSPHAMIDE (or MYCOPHENOLATE MOFETIL)
  3. Biological therapy - RITUXIMAB
77
Q

MYCOPHENOLATE MOFETIL vs ORAL CYCLOPHOSPHAMIDE

A

Fewer side-effects

78
Q

Define Antiphospholipid syndrome

A
  1. Syndrome characterised by thrombosis or recurrent miscarriages with positive blood tests for antiphospholipid antibodies
79
Q

What gender does APS effect

80
Q

Pathophysiology of APS

A

aPL antibodies bind to phospholipids on surface of cells causing thrombosis as functioning of endothelial cells stops or MISCARRIAGE

81
Q

Consequences of APS

A

CLOTs:

  1. Coagulation defects
  2. Lived reticularis (lace-like purplish discolouration of the skin)
  3. Obstetric issues (miscarriage)
  4. Thrombocytopenia (low platelets)
82
Q

Clinical presentation of APS

A
  1. Thrombosis
  2. Miscarriage
  3. Ischaemic stroke, TIA, MI - arteries
  4. Deep vein thrombosis, budd-chian syndrome - veins
  5. Thrombocytopenia
  6. Valvular heart disease, migraines, epilepsy
83
Q

How is APS diagnosed

A
  1. Anticardiolipin test
  2. Lupus anticoagulant test
  3. Anti-B2 glycoprotein I test

NOTE: YOU NEED POSITIVE ON AT LEAST TWO OCCASIONS more than 12 weeks apart in one or more tests to diagnose

84
Q

What is the anticardiolipin test

A

Detects IgG or IgM antibodies that bind to the negatively charged phospholipid - cardiolipin

85
Q

What is the Lupus anticoagulant test

A

Detects changes in the ability of the blood to clot

86
Q

What is the Anti-B2-glycoprotein I test

A

Detects antibodies that bind B2-glycoprotein I, a molecule that interacts closely with phospholipids

87
Q

Treatment of APS

A
  1. LONGTERM WARFARIN
  2. Pregnant women:
    Oral aspirin, SC heparin

Reduces chance of miscarriage but pre-eclampsia is common

  1. Prophylaxis (ASPIRIN or CLOPIDOGREL)
88
Q

What is Sjorgren’s syndrome

A

Chronic inflammatory autoimmune disorder:

Immunologically destruction of epithelial exocrine glands, lacrimal and salivary glands particularly

89
Q

What is Primary Sjorgren syndrome

A
  1. Dry eyes (keratoconjunctivitis sick) in the absence of RA or any autoimmune disease
90
Q

What antigens is primary sjogren syndrome associated with

A

HLA-B8/DR3

91
Q

What is secondary sjogren syndrome

A

Associated connective tissue disease

92
Q

Pathophysiology of sjorgren syndrome

A
  1. Lymphocytic infiltration and fibrosis of exocrine glands
93
Q

Clinical presentation of sjorgren syndrome

A
  1. Dry Eyes (KERATOCONJUNCTIVITIS SICCA) - due to decreased tear production
  2. Dry mouth due to decreased saliva production (xerostomoia)
  3. Salivary and parotid gland enlargement
  4. Dryness of skin and vagina
94
Q

What are systemic symptoms of Sjogren’s syndrome

A
  1. Arthralgia + non-progressive polyarthritis
  2. Raynauds
  3. Dysphagia and abnormal oesophageal motility as seen in systemic sclerosis
  4. Organ specific autoimmune diseases (THYROID, MYASTHENIA GRAVIS etc)
  5. Renal tubular defects (RARE)
  6. Pulmonary diffusion defects and fibrosis
  7. Polyneuropathy (FITS and DEPRESSION)
  8. Vasculitis
  9. Increased incidence of non-Hodgkin’s B-cell lymphoma
95
Q

How is Sjorgren’s syndrome diagnosed

A
  1. Schirmer tear test
  2. Rose Bengal staining
  3. Laboratory tests
  4. Salivary gland biopsy
  5. Person asked to spit into a cup
  6. Contrast agent injected into parotid duct which should show lymphocytic infiltration
96
Q

What is the Schemer tear test

A
  1. Strip of filter paper places on inside of lower eyelid: wetting of <10mm in 5 mins indicates defective tear production and thus sjogren
97
Q

What is Rose Bengal stating

A

Staining of the eyes shows punctate or filamentary keratitis

98
Q

Lab tests for Sjogren’s syndrome

A
  1. Raised IgG levels
  2. Rheumatoid factor is positive
  3. ANA found
  4. Anti-RO antibodies
99
Q

What does salivary gand biopsy show

A

Lymphocytic infiltration

100
Q

How is Sjorgren’s syndrome treated

A
  1. Artificial tears and saliva replacement solutions
  2. NSAIDs and HYDROXYCHLOROQUINE to help with arthralgia
  3. Corticosteroids RARELY needed
101
Q

If corticosteroids are rarely needed for Sjorgren’s then when are they used

A

Treat persistent salivary gland swelling and neuropathy

102
Q

When can APS lead to death

A

Thrombosis can cause organ failure = Catastrophic antiphophospholipid syndrome)

103
Q

Why does APS result in miscarriages

A

PLACENTAL INFARCTIONS

104
Q

How does APL effect a newborn

A

Causes development retardation due to APL induced inhibition of trophoblast differentiation

105
Q

Difference between aPL syndrome in SLE and as a stand-alone condition s

A

SLE miscarriages occur in later trimesters

106
Q

Genetic risk factor for APS

107
Q

How does APL effect the adrenal glands

A

Causes bleeds leading to Wateehouse-Friderichsen syndrome

108
Q

What is Waterhouse-Friderichsen syndrome

A

Adrenal gland failure due to bleeding: Caused by neisseria Meningitidis

109
Q

Role of Lupus anticoagulant

A

Binds to prothrombin to increase cleavage to thrombin

110
Q

what does anti-cardiolipin inhibit

A

Protein C which regulates coagulation pathway (degrades factor V)

111
Q

Role of Annexin A5

A

SHIELD around phospholipid molecules reducing availability for coagulation

112
Q

What diseases can cause Sjogren’s syndrome

A

Rheumatoid Arthritis

SLE

113
Q

What condition does Sjogren’s syndrome lead to

A

NHL: Diffuse large B-cell lymphoma or marginal zone lymphoma

114
Q

Complications of Sjogren’s syndrome in babies

A

Can result in SLE for the baby and congenital heart block

Year 2 (155 decks)

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