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MSK: Part 2 Flashcards

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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
First line treatment for osteoporosis
Bisphosphanates
26
How do bisphosphonates work
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
27
Name a bisphosphonate
ORAL ALDENRONATE ORAL ZOLENDRONATE
28
When are oral bisphosphonates given
When fasting, with a large drink of water while standing or sitting upright Associated with oesophagi's
29
Name two anti-resorptive drugs other than bisphosphonates
1. STRONTIUM RENELATE | 2. DENOSUMAB
30
What is Strontium Renovate
Helps reduce fracture rates
31
When is Strontium renovate given
Alternative to those intolerant to bisphosphonates
32
How do DENOSUMABs work
1. Osteoblasts produce RANK to activate osteoclasts and thus bone respiration
33
What is DENOSUMAB
Monoclonal antibody that inhibits RANK signals
34
2nd line treatment of osteoporosis
HRT (Hormone Replacement Therapy) for menopausal women
35
Role of HRT
Reduces fracture risk and stops bone loss Prevents hot flushes and other menopausal symptoms
36
Side-Effect of HRT
Breast cancer Stroke CVD
37
What is RALOXIFINE
Selective Oestrogen receptor modulator - activates oestrogen receptor on bone whilst having no stimulatory effect on endometrium
38
Side-effects of RALOXIFINE
1. Increased risk of thrombus formation 2. Cramps 3. Strokes
39
What HRT is used for men in osteoporosis
Testosterone
40
What anabolic can be used for osteoporosis
1. RECOMBINANT HUMAN PARATHYROID PEPTIDE
41
How does Recombinant human parathyroid peptide function
1. Increases osteoblast activity and bone formation 2. Reduce fracture risk 3. Improves bone density, trabecular structures
42
Side-Effects of recombinant human parathyroid peptide
Increased risk of renal malignancy | Hypercalcaemia
43
Name a Recombinant human parathyroid peptide
TERIPARATIDE
44
Name some inflammatory markers
ESR | CRP
45
When does ESR raise
Inflammation and infection
46
Why does ESR raise in inflammation and infection
Increased fibrinogen makes RBCs 'stick together' and thus fall faster
47
Rate at which ESR rises and fails
SLOWLY
48
Problem with ESR tests
False positives
49
When is CRP released into the blood
Inflammation/infection
50
Where is CRP produced
Liver in response to IL-6
51
Define autoimmune disease
Pathological conditions caused by the immune response directed against an antigen within a host
52
Name some auto-immunological disorders
1. SLE 2. SNTIPHOSPHOLIPID SYNDROME 3. SJORGRENS
53
What is SLE (SYSTEMIC LUPUS ERTHEMATOSUS)
1. Multisystem autoimmune disorder with arthralgia and rashes Cerebral and renal disease
54
What gender does SLE effect
Females
55
Risk factors of SLE
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
Pathophysiology of SLE
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
Name some antigens in SLE
Dna Histones Normally hidden from immunit system
58
How is SLE of the skin and kidneys characterised
Deposition of compliment and IgG antibodies - influx of neutrophils and lymphocytes
59
What would biopsy in SLE show
Vasculitis affecting capillaries, arterioles and venues
60
Characteristics of joint synovium in SLE
Oedematous and contain immune complexes
61
What can be seen in inflammatory infiltrates of SLE
Haematoxylin bodies from interaction of antinuclear antibodies and cell nuclei
62
Clinical presentation of SLE in joints
1. SYMMETRICAL SMALL JOINT ARTHRALGIA 2. Joints are painful 3. Soft tissue swelling 4. Avascular necrosis of hip and knee rarely
63
Clinical presentation of SLE in skin
1. ERYTHEMA in a BUTTERFLY DISTRIBUTION 2. Vasculitis lesions 3. Alopecia 4. Photosensitive rash 4. Raynaud's phenomenon
64
Clinical presentation of SLE in lungs
1. Recurrent pleural effusions and plueurisy, pneumonitis and atelectasis 2. Pulmonary fibrosis (RARE)
65
Clinical presentation of SLE in Heart
PERICARDITIS ARRYTHMIAS MYOCARDITIS VENOUS THROMBOSIS
66
Clinical presentation of SLE in the KIDNEYS (IMPORTANT)
GLOMERULONEPHRITIS with persistent proteinuria
67
Clinical presentation of SLE in CNS
1. SEIZURES | 2. PSYCHOSIS
68
Clinical presentation of SLE in eyes
Retinal vascultisis | Sjorgen's
69
Common clinical presentation of SLE in GI
Mouth ulcers
70
Differential diagnosis of SLE
ACUTE PERICARDITIS ANTIPHOSPHOLIPID SYNDROME SJORGEN SYNDROME
71
How is SLE diagnosed
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
Blood tests in SLE
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
What autoantibodies are seeing in SLE
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
How is SLE treated
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
Corticosteroid treatment for mild/moderated SLE
HYDROXYCHLOROQUINE or CHOLOQUINE help mild skin disease, fatigue, arthralgia PREDNISOLONE (then reduce dose) Immunosuppression - ORAL AZATHIOPRINE, ORAL METHOTREXATE
76
Corticosteroid treatment for severe SLE
1. ORAL AZATHIOPRINE, ORAL METHOTREXATE 2. PREDNISOLONE AND ORAL CYCLOPHOSPHAMIDE (or MYCOPHENOLATE MOFETIL) 3. Biological therapy - RITUXIMAB
77
MYCOPHENOLATE MOFETIL vs ORAL CYCLOPHOSPHAMIDE
Fewer side-effects
78
Define Antiphospholipid syndrome
1. Syndrome characterised by thrombosis or recurrent miscarriages with positive blood tests for antiphospholipid antibodies
79
What gender does APS effect
Females
80
Pathophysiology of APS
aPL antibodies bind to phospholipids on surface of cells causing thrombosis as functioning of endothelial cells stops or MISCARRIAGE
81
Consequences of APS
CLOTs: 1. Coagulation defects 2. Lived reticularis (lace-like purplish discolouration of the skin) 3. Obstetric issues (miscarriage) 4. Thrombocytopenia (low platelets)
82
Clinical presentation of APS
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
How is APS diagnosed
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
What is the anticardiolipin test
Detects IgG or IgM antibodies that bind to the negatively charged phospholipid - cardiolipin
85
What is the Lupus anticoagulant test
Detects changes in the ability of the blood to clot
86
What is the Anti-B2-glycoprotein I test
Detects antibodies that bind B2-glycoprotein I, a molecule that interacts closely with phospholipids
87
Treatment of APS
1. LONGTERM WARFARIN 2. Pregnant women: Oral aspirin, SC heparin Reduces chance of miscarriage but pre-eclampsia is common 3. Prophylaxis (ASPIRIN or CLOPIDOGREL)
88
What is Sjorgren's syndrome
Chronic inflammatory autoimmune disorder: Immunologically destruction of epithelial exocrine glands, lacrimal and salivary glands particularly
89
What is Primary Sjorgren syndrome
1. Dry eyes (keratoconjunctivitis sick) in the absence of RA or any autoimmune disease
90
What antigens is primary sjogren syndrome associated with
HLA-B8/DR3
91
What is secondary sjogren syndrome
Associated connective tissue disease
92
Pathophysiology of sjorgren syndrome
1. Lymphocytic infiltration and fibrosis of exocrine glands
93
Clinical presentation of sjorgren syndrome
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
What are systemic symptoms of Sjogren's syndrome
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
How is Sjorgren's syndrome diagnosed
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
What is the Schemer tear test
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
What is Rose Bengal stating
Staining of the eyes shows punctate or filamentary keratitis
98
Lab tests for Sjogren's syndrome
1. Raised IgG levels 2. Rheumatoid factor is positive 3. ANA found 4. Anti-RO antibodies
99
What does salivary gand biopsy show
Lymphocytic infiltration
100
How is Sjorgren's syndrome treated
1. Artificial tears and saliva replacement solutions 2. NSAIDs and HYDROXYCHLOROQUINE to help with arthralgia 3. Corticosteroids RARELY needed
101
If corticosteroids are rarely needed for Sjorgren's then when are they used
Treat persistent salivary gland swelling and neuropathy
102
When can APS lead to death
Thrombosis can cause organ failure = Catastrophic antiphophospholipid syndrome)
103
Why does APS result in miscarriages
PLACENTAL INFARCTIONS
104
How does APL effect a newborn
Causes development retardation due to APL induced inhibition of trophoblast differentiation
105
Difference between aPL syndrome in SLE and as a stand-alone condition s
SLE miscarriages occur in later trimesters
106
Genetic risk factor for APS
DR7
107
How does APL effect the adrenal glands
Causes bleeds leading to Wateehouse-Friderichsen syndrome
108
What is Waterhouse-Friderichsen syndrome
Adrenal gland failure due to bleeding: Caused by neisseria Meningitidis
109
Role of Lupus anticoagulant
Binds to prothrombin to increase cleavage to thrombin
110
what does anti-cardiolipin inhibit
Protein C which regulates coagulation pathway (degrades factor V)
111
Role of Annexin A5
SHIELD around phospholipid molecules reducing availability for coagulation
112
What diseases can cause Sjogren's syndrome
Rheumatoid Arthritis | SLE
113
What condition does Sjogren's syndrome lead to
NHL: Diffuse large B-cell lymphoma or marginal zone lymphoma
114
Complications of Sjogren's syndrome in babies
Can result in SLE for the baby and congenital heart block

Year 2 (155 decks)

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