R2 LOCO3 Flashcards

1
Q

Which region of the muscle tissue connects the muscle fibre to the tendon?

A

Endomysium is around each muscle fibre & blends into tendon

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2
Q

Whats the difference between tendinitis and tendinosis? [2]

A

Tendinitis: acute inflammation of tendon, does not have microscopic tendon damage

Tendinosis: chronic inflammation of tendon; characterised by disorganised fibres and a hard, thickened, scared and rubbery appearance

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3
Q

What is difference in structure between normal tendon and tendon with tendinosis? [2] Why is this clinically significant [1]

A

Normal structure: tendon allows contraction of muscle to cause movement of skeletal system

Tendinosis: disorganiesd collagen means that stresses are not transmitted efficiently: can lead to full thickness tear

Note the disorganise collagen

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4
Q

Achilles tendinitis

Which physiological process may occur during the healing process? [1]

A

Form heterotopic calcified regions (formation of extraskeletal bone in muscle and soft tissues)

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5
Q

Where in the tendon does tendonitis usually occur? [1]

A

Tendonitis usually occur in the middle of the tendon as this is the weakest spot [1]

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6
Q

Explain the pathophysiology of heterotopic bone [3]

A

Fibroblasts, osteoblasts and chondroblasts come from same precursors

Tendon fibroblast differentiate into chondrocytes / hypertrophic chondrocyte and osteoblasts via COX-2

Pro-inflammtory cytokines like prostaglandin E2 induces osteoblasts to differentiate

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7
Q

Describe how healing compares when undergo unloading by temporary paralysis versus overloading by active mobility or exercise for:

  • tendon-bone healing
  • flexor tendon healing
A

Complete unloading by temporary paralysis:
* Beneficial for tendon-bone healing
* Detrimental for flexor-tendon healing

Overloading by active mobility or exercise:
* Detrimental for tendon-bone healing
* Beneficial for flexor-tendon healing

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8
Q

State which is more beneficial for shorter [1] or longer [1] tendons

Unloading by temporary paralysis

Overloading by active mobility or exercise

A

Short: Unloading by temporary paralysis / cast immobilisation

Long:loading by active mobility or exercise

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9
Q

Describe the different types of enthesis in body [2]

A

Fibrous
* tendon extends all way up to bone: collagen bundles extend all the way to periosteum & become calcified
* Both are made from type 1 collagen

Fibrocartilaginous: when want to dissapate the stress
* Small section of fibrocartilage at attachment site
* Fibrocartilage calcififies at insertion
* Helps stiffen the tendon / ligament and creates a gradual change in mechanical properties

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10
Q

Name two locations of fibrous enthesis ligaments [2]

Name three locations of fibrocartilage enthesis ligaments [2]

A

Fibrous enthesis
* spring ligament
* periodontal ligament

Fibrocartilage enthesis
* rotator cuff muscles
* achilles tendon
* plantar fascia

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11
Q

What type of enthesis is depicted? [1]

A

Fibrous enthesis

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12
Q

Define sharpey fibres [1]

A

Sharpey’s fibres: are a matrix of connective tissue consisting of bundles of strong predominantly type I collagen fibres connecting periosteum to bone.

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13
Q

Label A

A

sharpey fibres

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14
Q

State the 4 zones of the fibrocartilage enthesis [4]

A
  1. Tendon proper
  2. Fibrocartilage
  3. Mineralised fibrocartilage
  4. Bone
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15
Q

What is name for inflammed enthesis? [1]

A

Enthesitis

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16
Q

Describe enthesitis pathogenesis:

Normal enthesitis insertion occurs at a location with lots of which structure? [1]

How does this influence enthesitis pathogenesis? [3]

A

Normal enthesis inserts into porous bone at a location with lots of small transcortical vessels (TCV)

Mechanical trauma; TCVs become inflammed:
* Vasodilation
* Efflux of immune cells (neutrophils)
* Osteoblasts form bone at enthesis - causes bone to be formed

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17
Q

Enthesitis is associated with which three conditions? [3]

A

Ankylosing spondylitis
Psoriatic arthritis
IBD

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18
Q

How do you differentiate between enthesophytes and osteophytes? [2]

A

Enthesophytes: originate from insertion of the joint capsule, ligament or tendons: no articular border involvement

Osteophytes: orginate from border of articular cartilage

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19
Q

How do you treat enthesitis:

  • If mechanical? [2]
  • If Inflammatory [5]
A

Mechanical:
* RICE
* NDSAIDs

Inflammatory:
* Sulfasalazine
* Methotrexate
* Anti-TNF therapy (restricted use for severe autoimmune enthetitis)
* Local radiotherapy
* Corticosteroid injection
* Hyperosmolar dextrose (initiates proliferation of intrinsic fibroblasts - race to repair damage c.f. osteoblasts)

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20
Q

Which drug class is used for ankylosing spondylitis enthesitis? [1]

A

Anti-TNF treatment

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21
Q

What are the names for arteries that supply tendons (of the hands)? [1]

A

Vincular arteries

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22
Q

Name two tenosynovitis conditions [2]

A

De Quervain’s tenosynovitis

Trigger finger

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23
Q

Explain pathophysiology of De Quervien tenosynovitis [3]

A

Fibrosis and narrowing of tendon sheath: extensor retinaculum

Around anatomical snuffbox

Causes tendons and sheath rubbing over radial styloid process

Thickening and narrowing of tendon sheath

Lymphocyte inflammation

24
Q

State and describe the name for test of De Querviens tensynovitis [1]

A

Finkelstein test:

  • Patient resting their forearm on a surface in a neutral position with the wrist hanging off and unsupported
  • The examiner holds the patient’s thumb and passively flexes the thumb into the palm, causing the wrist to adduct (ulnar deviation), putting **strain on the APL and EPB tendons. **
  • If this causes pain at the radial aspect of the wrist, the test is positive, indicating De Quervain’s tenosynovitis.
25
Q

Describe pathophysiology of trigger finger

A

Enlargement of tendon within sheath

26
Q

Treatment for tenosynovitis?
Treatments [4]
Surgery - for trigger finger [1] and De Quervains [1]

A

Treatment:
* RICE
* Splinting
* Anti-inflam
* Corticosteroids

Surgery:
* TF: cut annular ligament
* DQ: shave styloid processs or cut sheath

27
Q

Describe pathophysioloy of SLE [1]

A

Antibodies agaisnt a wide range of self antigens:
* Anti-nuclear antibodies (ANA): intranuclear and cytoplasmic proteins (95% are positive)
* Anti-Histone
* Anti-Ro
* Anti-La
* (loads of antibodies due to B cell hyperactivity)

28
Q

Describe lesions seen in SLE [1]

A

Discoid lesions

29
Q

Describe the arthritis seen in SLE patients [1]

A

Jaccoud arthropathy: due to tendinitis

Can move back into the correct position.

30
Q

DMARD treatments for SLE? [4]

A

Cylcophosphamide
Mycophenolate mofetil
Methotrexate
Tacrolimus

31
Q

Describe two biological DMARDs for SLE? [2]

A

Belimubab: inhibits BAFF (B cell activating factor)
Rituximab: CD20 blocker

32
Q

Describe the role of Langerhan cells [3]

A

Dendritic cell - spine-like projections

Efficient at presenting antigen to CD4+ helper T-cell

Pick up antigens that enter the skin and transport them to the lymph node

Staining dendritic cells n epidermis in a patient with skin infection.

33
Q

Describe pathway of mast cell degranulation after exposure to an antigen [3]

A

APC picks up the antigen and presents to the T cell.

Th2 produces IL4 & IL5, which activates the B cells to make IgE, which then activate the mast cell and degranulation occurs

IgE producition- produced after a second exposure.

34
Q

What do mast cells release into systemic circulation? [4]

A

histamine, leukotrienes, prostaglandins,
platelet aggregating factor

35
Q

Histamine is important as it causes which symptoms seen in an allergic reaction? [6[

A

Smooth muscle contraction
Vessel leak and oedema
Bronchospasm
Arteriole dilatation causing headache and hypotension
Modulation of immune response via H2 receptors

36
Q

Name an allergen produced by dust mice [3]

How does it cause damage to airway epithelium? [1]

A

Der P1 is an enzyme allergen
from the faecal pellets
of the dust mite.

Der P1 breaks down components of tight junctions which helps it to cross mucosa.

Binds to mast cells and causes degranulation

37
Q

Describe anaphylaxis occurs [2]

A

Generalised: antigen released into blood stream, binds to IgE on basophils: massive release of inflammatory mediators- bronchospasm and circulatory collapse

38
Q

How can you treat resistant urticaria and asthma?

A

Omalizumab: binds free IgE in the serum, forming trimers and hexamers

39
Q

What is Pemphigus Vulgaris? [2]

A

autoimmune disease caused by antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule

Antibody and complement binds to desmoglein 3: causes acantholysis (loss of coherence between epidermal cells due to the breakdown of intercellular bridges)

40
Q

Treatment of Pemphigus Vulgaris? [3]

A

Oral steroids

Immunosuppresion: mycophenolate mofetil or azathioprine

Rituximab (targeting CD20 on B cells)

41
Q

Describe the features of Immune Complex Mediated Vasculitis [4]

A

Antigen and antibody form an immune complex

This causes production of proteins and aggregation of platelets into micro thrombi

This results in:
* Deposition of fibrin
* Leaky vessel and extravasation of blood and oedema.
* The proteases degrade vessel BMZ
* Necrosis of the vessel wall

42
Q

How does Cutaneous Manifestations of Vasculitis differ if its:

Early, Established or Severe?[3]

A

Early - erythema and oedema
Established - palpable purpura
Severe - ulceration and necrosis

43
Q

Name this disease [1]

A

Leukocytoclastic Vasculitis: Blood induced- there are black and necrotic areas on the legs.

44
Q

Allergic Contact Dermatitis pathogenesis? [3]

A

Promotion of Th1 response:

  • Secretion of IL2, IL3, GM-CSF, IFNg and TNF
  • This promotes a macrophage rich response
  • Causes inflammation to the skin around 48 hours to 72 hours after the challenge
45
Q

Describe formation of granulomas

A

Clonal T-cell expansion

Secretion of
Th1 cytokines:
IL-2, IFN-g, TNF causes the creation of macrophages

46
Q

New drug class treatments for AA and Vitiligo? [1]

Name an example drug [1]

A

JAK Inhibitors

E.g Ruxolitinib

47
Q

Two potential AEs of JAK inhibitors? [2]

A

Thromboembolic events
Cancer related events

48
Q

Omalizumab works by reducing which molecule? [1]

A

IgE

49
Q

Pemphigus Vulgaris occurs due to autoantibodies directed at a cadherin-type epithelial cell adhesion molecule called what? [1]§

A

Desmoglein 3

50
Q

Oral steroids; mycophenolate mofetil or azathioprine and / or Rituximab would be used to treat which skin condition? [1]

A

Pemphis vulgaris

51
Q

Allergic contact dermatitis is caused by an Th1 response causing an increase in:

neutrophils
lymphocytes
macrophages
killer cells

A

macrophages

52
Q

Allergic contact dermatitis is caused by which type of response

Th1
Th2
Th17
Th5

A

Allergic contact dermatitis is caused by which type of response

Th1

53
Q

Granuloma formation is a which type of hypersensitivity reaction?

Type 1
Type 2
Type 3
Type 4

A

Type 4

54
Q

This person with a tattoo has an adverse reaction. This occurs due to

Mast cell-mediated inflammation
Antibody-mediated inflammation
Immune complex mediated inflammation
Delayed hypersensitivity
Automimmunity

A

Immune complex mediated inflammation

55
Q

Ruxolitinib is a JAK inhibitor used to treat [2]

Vitiligo
Phemphis vulgaris
Leukocytoclastic vulgaris
Urticaria

A

Ruxolitinib is a JAK inhibitor used to treat

Vitiligo
Phemphis vulgaris
Leukocytoclastic vulgaris
Urticaria

56
Q

Omalizumab is used to treat

Vitiligo
Phemphis vulgaris
Leukocytoclastic vulgaris
Urticaria

A

Urticaria

57
Q

Granuloma formation is caused by which type of response

Th1
Th2
Th17
Th5

A

Th1