Loco Notes

Front 1

What type of Collagen is in Hyaline cartilage

Back 1

Type II

Front 2

What type of cells are responsible for maintenance and synthesis of the extracellular matrix of the hyalin cartilage?

Back 2

Chondrocytes

Front 3

What are the 5 layers of the articular cartilage?

Back 3

Tangential (superficial zone)

Transitional (middle zone)

radial (deep zone)

calcified

bone

Front 4

How does chondrocyte shape change according to position?

Back 4

Superficial zone - flatter smaller

intermediate - rounder and large

deep - stacked on top of one another.

Front 5

Where do chondrocytes sit?

Back 5

in lacuna in the cartilage

Front 6

How are deep chondrocytes adapted from more superficial chondrocytes?

Back 6

more prominent golgi apparatus and endoplasmic reticulum for protein synthesis

Front 7

Describe the collagen composition of the extracellular matrix from the superficial zone

Back 7

Superficial is mostly Type II, slowly changes to Type X as it gets deeper

Front 8

What gene is associated with OA?

Back 8

HMGB2 - High mobility group B2 protein.

Supports chondrocytes in superficial zone. Loss of HMGB2 increases likelihood of DNA damage and fewer progenitor cells and chondrocytes, reducing ECM.

Front 9

What type of cells form the Synovial Membrane?

Back 9

Synoviocytes:

Type A - macrophage like cells involved in the immune response

Type B - Fibroblast-like cells that produce hyluronic acid.

Front 10

How is Synovial Fluid produced?

Back 10

Ultrafiltrate of blood plasma.

Synovium is highly vascularised with fenestrated capillaries that leak plasma.

Synovium has no basement membrance between the synoviocytes and subintima making movement of plasma easier.

Type V synoviocytes add hyluronic acid to plasma

(Note: due to the above adaptations the synovium is easily damaged and has lower immune surveillance)

Front 11

What is the function of synovial fluid?

Back 11

Slippery weight bearing, to reduce friction

Nourish articular cartilage

forms a reserve volume

Front 12

What does antictrulinated protein do?

Back 12

stimulate osteoclast differentiation and proliferation in RA, leading to bone erosion

Front 13

define osteoporosis

Back 13

A skeletal disorder characterised by comprimised bone strength, increasing a persons risk of fracture

Front 14

What is a Z- score?

Back 14

A bone mineral density test that compares the bone density of the patient to someone of their own age.

The number is measured in standard deviations from the normal

Front 15

What is a T - Score

Back 15

A bone mineral density test that compares thebone density of the patient to that of an average 30-year old women.

Front 16

What are some causes of secondary Osteoporosis

Back 16

Cushing syndrome, malabsorption, thyrotoxicosis

Front 17

What are some pharmocological treatment for Osteoporosis

Back 17

Raloxifene (selective oestrogen receptor modulator)

Vit D and Calcium

Denosumab (inhibits RANKL, therefore inhibiting osteoclast activity);

Front 18

What is the crystal present in gout?

Back 18

monosodium urate

Front 19

What are risk factors for Gout?

Back 19

being male (higher uric acid levels than women)

Diet (more purines in diet = more uric acid, meat, seafood, alcohol)

Front 20

describe the pathophsyiology of gout

Back 20

high levels of uric acid caused by either: 1. insufficient protein to keep them inert 2. too much uric acid

increased uric acid causes urate crystals to precipitate

This attracts neutrophils. However the shape of the urate crystals causes them to burst, releasing inflammatory agents and lysosomes.

This lowers pH and causes more urate crystals to precipitate.

Front 21

What are Tophi?

Back 21

A symptom of gout where macrophages surround urate crystals which have been deposited in soft tissue such as ears or the elbow.

Front 22

What is uric acid?

Back 22

The end stage product or purine metabolism

Front 23

What is unique about the synovial fluid found in gout?

Back 23

It has many polymorphonuclear neutrophils

Front 24

What is are the pharmocological treatments for gout?

Back 24

NSAIDS for pain

Colchicine

Corticosteroids

Rilonacept

Allopurinol

Probenecid - increases uric acid excretion.

Front 25

What is the mechanism of action of allopurinol?

Back 25

Xanthase oxidase inhibitorXanthase oxidaseis responsible for the conversion of xanthase to uric acid

Front 26

how is gout different from pseudogout?

Back 26

Gout - primarily the first MCP joint, monosodium urate crystals (sharp, needle-like)

pseudo-gout - happens at soft tissue (shoulder, wrist), calcium pyrophosphate crystals (rhomboid), associated with osteoarthritis

Front 27

Where are the common sites of tendonitis?

Back 27

lateral epicondlitis (Tennis elbow)

Achilles tendonitis

Suprasinatus Tendonitis

Front 28

What are the common causes of tendonitis?

Back 28

Overuse of tendon

Collagen Type I disorders (Vit C deficiency, Osteogenesis imperfecta)

Renal Dialysis - Causes dissarangement of collagen production and excretion (unclear what this means)

Front 29

What is RICE?

Back 29

Rest

Ice

Compression

Elevation

Front 30

What is a common complication of achilles tendonitis?

Back 30

heterotopic ossification

calcification of the tendon

Front 31

What are the two types of Entheses?

Back 31

Fibrous

Fibrocartilage

Front 32

What conditions are assoiated with enthesitis

Back 32

Inflammatory Bowel Disease

Ankolysing spondylitis (targets anterior longitudinal ligament)

Psoriatic Arthritis

Front 33

What is the difference between an enthesophyte and an osteophyte?

Back 33

Enthesophytes originate from the insertion point of the tendon/ligament. No articular border involvement

Osteophytes originate from the border of the articular cartilage

Both are bony spurs

Front 34

What is the treatment for enthesitis?

Back 34

RICE

NSAIDS

DMARDS - Methotrexate, Sulfasalazine

Anti-TNF alpha - Infliximab

Front 35

What is the purpose of the tendon sheath?

Back 35

Cushions tendon

Guides Tendon

Nourishes Tendon: Synovial fluid produced by it + vincula blood supply

Front 36

What is the pathophsyiology of systemic lupus erythematosus?

Back 36

Antibodies against a wide number of self antigens (e.g. intranuclear proteins, DNA, ribonucleic acids) are produced by b-cells

The autoantobody immune complexes can cause clots in smaller blood vessels such as thoe in the renal system, causing renal failure.

Front 37

What is Malar rash a sign of ?

Back 37

Also known as "butterfly sign" it is caused by SLE (systemic lupus erythematous

Front 38

Why does SLE lead to tendonitis/tendosynovitis?

Back 38

Autoantibody immune complexes clump together in smaller blood vessels such as those present in the tendon and tendon sheath.

This damage to these blood vessels and can lead to tendon and tendon sheath damage that can cause deformities that resemble arthropies.

Front 39

What is the treatment for NSAIDS?

Back 39

DMARDS - methotrexate

NSAIDS

Abatabacept - prevents APC from signalling T-cells. Preventing T-Cell activation

Infliximab - TNF alpha monoclonal antibody

Front 40

Describe Heterotopic Ossification

Back 40

COX-2 acts on mesenchymal stem cells to chondrocyte, then it acts again with prostaglandins to cause chondrocyte hypertrophy.

Then a variety of factors such as RANKL act on hypertrophic chondrocytes to cause ossifcation.

Front 41

Describe Polymyositis and Dermatomyositis

Back 41

CD8+ Tcells invade muscle fibres primarily around the fascicles of the muscles and cause inflammation and damage. Macrophages then absorb the necrotic fibres

They are very hard to differentiate without very specialised antibody tests.

Front 42

What is the most noticable difference between dermatomemyositis and polymyositis?

Back 42

Dermatomemyositis sometimes has a rash that appears on the back, eyes and cheeks.

Front 43

What is a common complication of dermatomyositis?

Back 43

subcutaneous calcification

calcification at junction between dermis and epidermis (skin).

Front 44

What is subcutaneous calcification

Back 44

An autoimmune connective tissue disease.

Caused by anti-nuclear antibodies. (anti-jo1 found in 20%-40% of cases.

Calcification in skin and muscle

Front 45

What is the treatment for subcutaneous calcification?

Back 45

High dose Prednisolone - maintained 2 weeks after symptoms stop, as if it is stopped early there is a more significant rebound flare

Methotrexate

Azathioprine

Front 46

What is inclusion body myositis

Back 46

Muscle disease of the elderly

More likely to effect certain muscle (e.g. knee extensors, muscles of swallowing)

vacuoles where they shouldn't, or amyloid like material appear in muscle fibres.

Front 47

What is the inheritance pattern of duchenne and becker muscular dystropy

Back 47

x-linked recessive

Front 48

What is the pathophysiology of duchenne and becker muscular dystrophy

Back 48

Loss of dystrophin means that the muscle is damaged everytime it is contracted. This leads to a slow decline by 7-12 years old.

Front 49

What muscles are affected by duchenne becker muscular dystrophies

Back 49

shoulders, elbow flexors and extensors

Hips, foot dorsiflexors, knee extenders