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Locomotor 2 > Things to know before exam > Flashcards

Things to know before exam Flashcards

1
Q

What are some of the main microscopical changes in cartilage structure seen in OA?

A
  • Chondrocyte necrosis (especially in superficial layers)
  • Focal clumps of isogenic chondrocytes (due to increased local proliferation)
  • Change to fibrocartilage from hyaline (type I collagen rather than type II) – reduces the thickness of articular cartilage; duplicated tidemark and thickening of calcified cartilage merging with subchondral bone
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2
Q

What gene loss is associated with OA and what is it responsible for?

A

HMGB2 (high mobility group protein 2) – epigenetic protection; uniquely expressed in superficial zone chondrocytes; supports their survival and regulates specific differentiation status; regulates protection of chondrocytes’ DNA; loss leads to superficial zone cell death, loss of progenitor cells and reduced synthesis of ECM contents

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3
Q

How does the inflammatory cytokines are released? What do they cause?

A

Damaged chondrocytes release stress cytokines (Il1, IL6 and TNF) into joint which cause reaction with synovial membrane resulting in a mild inflammatory process. Inflammatory cytokines influence disease progression, cause further damage to surrounding cartilage and bone, are main cause of pain, stimulate RANKL on osteoblasts and hence increase bone formation

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4
Q

What are the main characteristics of early OA and late OA?

A

Early OA: loss of superficial zone and changes to ECM; cell clusters
Late OA: continued loss of ECM and chondrocyte hypertrophy

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5
Q

What are some red flags for recognition of severe disease?

A

Fever or unexplained weight loss

  1. History of carcinoma
  2. Immune-suppression
  3. Ill health and presence of other medical illness
  4. Severe night pain/progressive pain
  5. Persistent mono-arthritis
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6
Q

What is enthesitis? What is its clinical feature

A

Inflammation of tendon to bone attachment; pain on resistant movement

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7
Q

What is De Quervain’s tenosynovitis? What are the clinical signs?

A

Inflammation of the first extensor tendon sheath containing APL and EPB; pain on resistant movement (on extension of the thumb against resistance), crepitus and positive Finkelstein’s test

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8
Q

What are the main causes of carpal tunnel syndrome?

A

60% idiopathic, pregnancy, hypothyroidism, RA

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9
Q

What might be the cause of articular and periarticular pain of the elbow?

A

Articular – trauma, OA

Periarticular – epicondylitis, bursitis

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10
Q

What is frozen shoulder? How can it be treated?

A

Adhesive capsulitis; shoulder capsule (CT) becomes inflamed and stiff greatly restricting motion and causing chronic pain; reassurance/education, analgesia, injection, physio

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11
Q

What movements are restricted in frozen shoulder?

A

External rotation the most but also internal rotation and abduction

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12
Q

What is the main sign of rotator cuff tendinitis? What is the treatment?

A

Painful arc on active and resisted abduction; physio, steroid injection and surgery

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13
Q

What is meralgia peresthetica?

A

Tingling, numbness and burning pain in the outer part of thigh due to compression of lateral cutaneous nerve.

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14
Q

What is Morton’s neuroma?

A

Benign neuroma most commonly between 2nd and 3rd metatarsal spaces

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15
Q

What is March fracture?

A

Fracture of the distal third of one of the metatarsals (2nd or 3rd) occurring because of recurrent stress.

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16
Q

What MHC molecule is strongly associated with Ankylosing spondylitis?

A

HLA B27

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17
Q

What MHC molecule is strongly associated with RA?

A

HLA-DR4

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18
Q

What is synovial fluid?

A

the ultra filtrate of blood with added hydraluronic acid

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19
Q

What two types of proteins are found in synovial fluid?

A

Albumin (60%) and globulin (40%)

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20
Q

What is the mucin clot test? What is the normal string length?

A

2-5% acetic acid added to synovial fluid – normal synovial fluid will form a clot surrounded by clear fluid; normal string is 4-6cm

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21
Q

What type of cells are found in subintima and in synovial fluid in RA?

A

Subintima – lymphocytes

Synovial fluid – neutrophils

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22
Q

What is the function of each of these cells in RA:

a) Th17
b) Macrophages
c) B cells
d) Synovial fibroblasts

A

a) Orchestrate synovitis and damage, release inflammatory cytokines (IL-17)
b) Secretion of pro-inflam cytokines
c) Auto-Abs secretion (rheumatoid factor and anti-CC/ACPA); present antigen to T cels, stimulate synovial fibroblasts thru cytokines
d) Secretion of MMPs and cathepsins; expression of RANKL and stimulating differentiation of type A macrophages into osteoclasts

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23
Q

What is citrullination and when does it occur?

A

Changing of arginine to citrylline by deamination by peptifyl arginine deiminase which occur during apoptosis. When apoptosis is too high or clearance is defective, these proteins become extracellular. In some people anti-citrullinated antibodies are formed

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24
Q

What can the ACPAs induce?

A

They can stimulate osteoiclast differentiation and maturation by inducing RANKL expression and synergy with RANK on osteoclasts to enhance bone erosion

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25
Q

What is Dkk-1? How is it induced and what is its fun?

A

Dickkopf-related protein 1 expression stimulated by proinflam cytokines on synovial fibroblasts which directly inhibit osteoblast differentiation; it also acts indirectly by inducing expression of sclerostin in osteocytes

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26
Q

What is the downside of microfracture?

A

Creates fibrocartilage which is less durable and resilient

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27
Q

What is the material used in bone cement? What is the function of cement in THR?

A

Polymethyl methacrylate (PMMA) used to act as a filler between the bine and the implant

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28
Q

What are the 4 criteria sections for diagnosis of RA? What score must be achieved for the diagnosis of RA?

A

Joint involvement, serology, acute phase reactants, duration of symptoms; 6 or more/10 = diagnosis of RA

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29
Q

What is hydroxychloroquine? What is its mode of administration? What is its MOA?

A

Anti-malarial drug given orally with or after food; that blocks Toll-like receptor 9 which recognizes DNA containing immune complexes and hence leads to decreased DC activation and accumulates inb lysosomes increasing the pH and hence decreasing protein modifications

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30
Q

What is hydroxychloroquine? What is its mode of administration? What is its MOA?
What is a DMARD similar to methotrexate? What is its MOA?

A

Leflunomide; inhibits pyrimidine biosynthesis through inhibition of dihydroorotate dehydrogenase

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31
Q

What biologics inhibit IL-1?

A

Anakinra (SQ once a day)
Canakinumab
Rilonacept

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32
Q

What biologic is used to inhibit T cells? How?

A

Abatacept – prevents secondary stimulatory signal from being delivered to T cell; IV infusion once a month
Belatacept – anti-CD28, modulates T cell signaling

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33
Q

What are ADAs? What are their 2 types?

A

Anti-drug antibodies; neutralizing ADA directly interferes with biological drugs ability to work; non-neutralising ADA may form immune complexes around injection site, reducing drug concentration and pharmacokinetics (eg increased clearance)

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34
Q

Which joint is usually affected by OA?

A

Base of the thumb

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35
Q

What might be the cause of OA of premature onset?

A

Previous menisectomy and haemochromatosis

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36
Q

What might be the causes of secondary osteoporosis?

A

Thyrotoxicosis, Cushing’s syndrome, malabsorption, malignancy, hypogonadism and drugs

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37
Q

Which bisphosphonate is to be taken every day and which once a year?

A

Every day: etidronate

Once a year: zoledronate

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38
Q

What is the erosive OA?

A

Severe subset of nodal OA; it is a more inflammatory form of OA primarily characterized by erosions of cartilage in the DIP and PIP joints

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39
Q

What is swan neck deformity?

A

Hyperextension of PIP and flexion of the DIP

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40
Q

What might be the complications of systemic inflammation in RA?

A

Anaemia, thrombocytosis, fatigues, osteoporosis, acute-phase response

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41
Q

How does the NOF fracture present?

A

External rotation of the foot and shortening of the leg

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42
Q

What are the bony insertion points for:

a. Sartorius
b. Hamstrings
c. Rectus femoris
d. Calcaneous
e. Medial epicondyle

A

a. ASIS
b. Ischial tuberosity
c. AIIS
d. Achilles tendon – gastrocnemius an d soleus
e. Forearm flexors and ulnar nerve

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43
Q

What is fracture dislocation/sublaxation? What can be the complication of it and what is done to prevent it?

A

Fragment involving joint; the surfaces may result in malalignment, so internal fixation is required

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44
Q

What is pathologic characteristic of the stress fracture? How can it be observed?

A

Periosteal reaction where osteoblasts proliferating more; well visualized ion bone scintography

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45
Q

What is the length of the healing process for lower and upper limb?

A

Lower 8wks

Upper 6 wks

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46
Q

What are the main characteristics of the fracture haematoma?

A

Hypoxic and acidic due to disruption of vessels

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47
Q

describe what happens in the fibrocartilage callus bone remodelling stage

A

New capillaries organize fracture haematoma into granulation tissue (procallus)  fibroblasts and osteogenic cells invade procallus  they make collagen fibres which connect ends together  chondroblasts begin to produce fibrocartilage

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48
Q

What is the name of a new lateral curve of the spine? What does it usually involve? Who is mostly affected by this?

A

Scoliosis, usually involved rotation of the vertebrae; girls around puberty mostly affected

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49
Q

What fracture can be observed in kyphosis?

A

Compression fracture

50
Q

what is schmorl’s node and what disease does it occur in

A

It is a protrusion of nucleus pulposus though endplate into vertebral body (looks like erosions on Xray); occurs in Sheuermann’s disease

51
Q

How does psoas dysfunction may cause lordosis?

A

Chronic psoas shortening and weakness, shortening of the thoraco-lumbar fascia and erector spinae muscles; stretching and weakness of abdo muscles, hams and gluteals tighten and often hypertonic

52
Q

What are the things to look for in age related diseases of vertebrae?

A

Osteophytes (syndesmophytes), loss of disk heigh, loss or increase in curves, spinal stenosis, ossification of vertebral ligaments

53
Q

what can osteophytes in the spinal cord lead to

A

vertebral- basilar artery insufficiency

54
Q

What is DISH?

A

Diffuse idiopathic skeletal hyperostosis; ossification of anterior longitudinal ligament with or without osteophytes; disc maintains the same height; does involve sacriiliad spine

55
Q

What are the zygapophysial joint?

A

Facet joints (planar synovial) between vertebrae

56
Q

Why a person suffering from RA would have thinned skin?

A

steroid use

57
Q

How can RA affect the knee, what are the signs?

A

Valgus deformity, Baker cyst (synovial fluid leaves the joint and inflamed fluid enters the calf)

58
Q

What muscles could be wasted in RA?

A

Hypothenar muscles (T1 lesion)

59
Q

What changes can be observed in the Xray of RA joint?

A 
Periarticular osteoporosis (can be speeded up by RA)
Bone erosion and soft tissue swelling
60
Q

Where is inflammation in ankylosing spondylitis?

A

Sacroiliac joint

61
Q

What is the ankylosing process in AS?

A

Syndesmophytes formed and bridge from one vertebrae to another = fusion of vertebra = stiffness

62
Q

How does MSU crystals activate immune system?

A

Interaction with intracell and surface receptors of local DC and macrophages

63
Q

How does the pH drops in gout and what I the significance of this?

A

Proteins released from neutrophils cause dec in pH and hence more MSU crystals can be formed (cycle starts again)

64
Q

Why gout usually affects small lower extremity joints?

A

Less blood supply and hence cooler and more acidic environment allow crystal deposition

65
Q

What is podagral?

A

Inflammation of the 1st MTP joint (big toe)

66
Q

What is characteristic in tophi histology?

A

Crystals surrounded by palisaded histocytes which in turn are surrounded by T cells

67
Q

Overconsumption of what foods may lead to hyperuricaemia?

A

High in purine foods: beef, pork lamb, seafood, beer, alcoholic beverages

68
Q

What is the appearance of gout crystals and how can they be visualized?

A

Visualized with polarizing light; urate crystals are needle like, very sharp and shiny

69
Q

What is characteristic of erosions in gout?

A

They have overhanging edges and look like a rat bite

70
Q

What imaging technique is able to detect uric acid crystals deposits?

A

Dual energy computed tomography (DECT)

71
Q

How can the tophaceous deposits lead to bone erosions?

A

MSU crystals surrounded by granulomatous tissue reaction and produce a lot of pro-inflamm cytokines which also stimulate osteoclasts via RANKL

72
Q

What is the most commonly affected joint in pseudogout?

A

Knee

73
Q

What is the hallmark of pseudogout seen on Xrays?

A

Chondrocalcification – calcification of soft tissue

74
Q

What cells present in the muscle provide infinite potential for repair?

A

Satellite cells

75
Q

What is a floppy baby syndrome? What can be the cause of it?

A

Infantile hypotonia; myopathic cause – congenital fibres disproportion: most of fibres small and round with a few massively hypertrophic fibres

76
Q

What is the difference between type 1 and type 2 muscle fibres?

A

Type 1: slow type; large and pale, aerobic only

Type 2: fast type; small and dark, aerobic and anaerobic

77
Q

What type of diseases are dermato- and polymyositis? What are they associated with?

A

Autoimmune (ANAs); associated with microbial/viral infections

78
Q

What are the main EMG findings in these conditions?

A

Fibrillation potentials and positive waves at rest; reduced duration and amplitude of motor unit potentials; irritability of 90% - muscle constantly active

79
Q

What ANAs are present in polymyositis and dermatomyositis? What do they target?

A

Anti-Jo1 antibody present; cause subcutaneous calcification in muscle and skin

80
Q

What can be observed in the biopsy of the muscle with IBM?

A

Inclusion bodies containing amyloid material and empty holes (vacuoles)

81
Q

What are the two most common muscular dystrophies and what is their inheritance pattern?

A

Duchenne and Becker muscular dystrophies; X-linked

82
Q

What is the level of creatine kinase in Duchenne and why?

A

Elevated bc there is a constant tearing of muscle fibres

83
Q

What is fibromyalgia?

A

Widespread muscle pain with associated fatigue and sleep disturbance

84
Q

What is present in 50% of patients with fibromyalgia?

A

Antipolymer antibodies

85
Q

What are 6 indications for joint replacement in adults?

A
  1. Degenerative disease (OA)
  2. Inflammatory disease (RA)
  3. Trauma (NOF of NOH fracture)
  4. Tumour
  5. AVS
  6. Revision of previously failed/worn out joint replacement
86
Q

What is oxinium?

A

Zirconium alloy metal substitute that transitions into ceramic zirconium oxide outer surface (blad)c

87
Q

What are two sources of tendon for an ACL reconstruction? Which one is better?

A

Patella ligament tibia – incorporated to bone quicker
Semitendinosus and/or gracillis tendons
No difference in performance!

88
Q

What is distraction osteogenesis?

A

Bone lengthening procedures that allow progressive correction with use of an external fixator (Ilizarov technique)

89
Q

How can the vasospasms develop?

A

Crush injury cause the damage to tissues and ischaemia, smooth muscle in vascular wall go into spasm which creates a turbulent flow (vasospasm)

90
Q

What can be used as an intramedullary nail in kids?

A

K wires

91
Q

What are the absolute indications for operative treatment of fractures?

A
  • Displaced intra-articular fractures
  • Open fractures
  • Fractures with vascular injury or compartment syndrome
  • Pathological fractures
  • Non-unions
92
Q

What are the relative indications for operative treatment of fractures?

A

 Loss of position with closed method
 Poor functional result with non-anatomical reduction
 Displaced fractures with poor blood supply
 Economic and medical indications

93
Q

What is the difference between fracture union and consolidation?

A

Union – when bone becomes one

Consolidation – new laid down bone has been remodeled (woven bone removed and replaced by a compact bone)

94
Q

What is the source of fat embolism?

A

Fatty bone marrow displaced when the intramedullary node is placed during e.g. THR

95
Q

What are the 6 P’s of compartment syndrome which one is the last?

A

Pain, pallor, polar, paralysis, paresthesia, pulseless (pulses are the last to go)

96
Q

What are the main layers of epidermis?

A 
Britney Spears grows like cancer (from the bottom)
Stratum basale
Stratum spinosum
Stratum granulosum
Stratum lucidum
Stratum conreum
97
Q

What is characteristic about stratum spinosum?

A

Numerous desmosomes give cells spiny appearance

98
Q

What is the function of adherens junctions and what receptor is found within it?

What is the function of desmosomes and what receptor is found within it?

A

Cadherin receptor linked to actin cytoskeleton; cell to cell connection

Cadherin receptor linked to keratin cytoskeleton; cell to cell connection

99
Q

What are the components of pilosebaseous unit?

A

Hair follicle and sebaceous gland

100
Q

Secretion of sweat gland is odourless so why our sweat smells?

A

Sweat is broken down on the skin by bacteria which release volatile fatty acids

101
Q

What skin changes can be observe if CHD is suspected?

A

Double crease (asymmetric gluteal folds), leg turned into externa rotation

102
Q

What structures in NOF undergo necrosis? in perthes disease and why is this not serious

A

Chondrocytes and bone marrow – NOF compression
Self-limiting, NOF will grow back again once the fibrovascular tissue is reestablished; 85% no long-lasting problems or deformations

103
Q

What is the Klein’s line and how is it used to diagnose SUFE?

A

Line along superior border of femoral neck – should cross at least a portion of femoral head; in SUFE, NOF below the line

104
Q

What is the Blount’s disease?

A

Growth problem of distal tibia resulting in increased weight on the medial condyle leading to compression of growth plate and tibia varus; cause unknows

105
Q

What is the mechanism of Osgood-Schlatters?

A

Repeated traction from the patellar ligament (overdeveloped quads) on the tibial tuberosity or avulsion fractures to parts of the tibial tuberosity

106
Q

Which cells are mostly activated in

  1. Extracellular bacterial or viral infections
  2. intracellular bacterial and fungi infections
  3. Helminths
A
  1. Th17
  2. Th1
  3. Th2
107
Q

What is the MOA of Der P1 allergen?

A

Cleaves occluding in tight junctions which helps it to cross mucosa

108
Q

What is acantholysis?

A

Loss of cohesion between epidermal keratinocytes due to breakdown of desmosomes by autoantibodies

109
Q

What is Ruxolitinib?

A

JAK 1/2 inhibitor – target T cell – very effective for alopecia

110
Q

What is the difference bt acute and chronic SA?

A

Acute – pyogenic, chronic – non-pyogenic

111
Q

What can be seen on X-ray of SA cause by mycobacterial infection?

A

Joint space narrowing, effusion, erosions, cyst formation

112
Q

What are the predisposing factors for OM?

A

Immune inefficiency – elderly, young, malnutrition; impairment of local vascular supply – diabetes, venous stasis, radiation fibrosis, sickle cells disease (capillaries become blocked during sickle cell crisis)

113
Q

What is the presentation of OM?

A

Decreased limb movement, adjacent joint effusion, local non-specific pain, mild fever, cold insidious onset with vague Sx

114
Q

What are the risk factors for prosthetic bone/joint infection?

A

Priori surgery at site of infection, RA, corticosteroid therapy, diabetes mellitus, obesity, malnutrition, old age

115
Q

What is the target of immune complexes in SLE? What type of hypersensitive is it?

A

Immune complexes damage blood vessels and connective tissue (any tissue with rich blood supply affected); type III hypersensitivity with some type II involvement

116
Q

What is the MOA of Belimumab?

A

Inhibits BAFF (BLyS) – B cell activating factor is inhibited so prevents production of antibodies

117
Q

what does chronic pain represent

A

CHRONIC PAIN STATE NO LONGER REPRESENTS A PHYSIOLOGICAL STATE BUT MALADAPTION WITHIN THE CNS TO A PREVIOUS PAIN STATE.

118
Q

What psychological management of pain should be incorporated?

A

Acceptance and Commitment therapy (ACT), placebo effect, mindfulness, reassurance (explain pain, diagnosis, prognosis)

119
Q

Which NSAIDs are usually used for:

a. Inflammation
b. Inflammation and pain
c. Mainly pain
d. Eye drops
e. Cardiovascular dis

A

a. Aceclofenac, etoricoxib, fenbufen, tiaprofenic acid
b. Acematcin, celecoxib, diclofenac, ibuprofen, indomethacin, naproxen, piroxicam
c. Paracoxib
d. Ketorolac
e. Aspirin

120
Q

Which prostaglandin is found in uterus?

A

Prostaglandin F

121
Q

What is the normal function of PGs in the stomach?

A

Gastric protection by increased mucus secretion, increased bicarbonate levels and increased mucosal blood flow

122
Q

What are the treatments for alopecia arata and vitiligo

A

JAK inhibitors - inhibits chemokine production

Ruxolitinib

Locomotor 2 (30 decks)

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