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Term 3 > Monoarthritis > Flashcards

Monoarthritis Flashcards

1
Q

What are the functions of the bone?

A
  • Haematopoiesis
  • Movement
  • Structure
  • Protection
  • Calcium reservoir
  • Energy store
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2
Q

What types of bone shape are there?

A
  • Long
  • Short
  • Irregular
  • Flat
  • Sesamoid
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3
Q

What hormones are involved in day to day bone homeostasis?

A
  • Vitamin D3

- Parathyroid hormone

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4
Q

Why is vitamin D3 a hormone?

A

Made in one place and acts in another

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5
Q

Which populations are mainly at risk of developing vitamin D deficiency?

A
  • Populations lacking sunlight

- Populations with a poor diet

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6
Q

Where is PTH synthesised?

A

Parathyroid glands

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7
Q

What is the purpose of calcium homeostasis?

A

Maintaining constant blood calcium concentration

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8
Q

Skeleton is divided into two organisation compartments?

A

Axial

Appendicular

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9
Q

What do embryonal bone development, longitudinal bone growth, and fracture healing all make use of?

A

Endochondral ossification

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10
Q

What types of cells are involved in bone metabolism?

A
  • Osteoclasts
  • Osteoblasts
  • Osteocytes
  • Blood vessels and nerves
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11
Q

What do tendons do?

A

Connect muscle to bone

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12
Q

What do ligaments do?

A

Connect bone to bone

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13
Q

What do aponeuroses do?

A

Connect muscle to muscle

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14
Q

How is muscular force transmitted to bone?

A

Initially via the musculotendinous junction

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15
Q

What are the two sites of muscular/tendinous attachment to bone?

A

Origin and insertion

  • Origin is stationary
  • Insertion moves
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16
Q

What are both tendons and muscles subdivided into?

A

Fascicles

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17
Q

What are two models of skeletal unloading?

A

Astronauts

Bed rest

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18
Q

How do you measure bone density?

A

DEXA scan
qCT: quantitative computerised tomography
Ultrasound

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19
Q

What is the gold standard for measuring outcomes of a trial for osteoporosis?

A

Fractures

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20
Q

What canals do osteocyte processes occupy?

A

Canaliculi

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21
Q

How to osteocytes respond to loading/mechanical stress?

A

In terms of bone metabolism

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22
Q

Where are osteocytes derived from?

A

They are derived from osteoblasts

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23
Q

Where do chondrocytes live?

A

In a hole called a lacuna

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24
Q

What are the major components of articular cartilage?

A
  • Water
  • Type II collagen
  • Proteoglycans
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25
Q

What are the main reasons cartilage heals poorly?

A
  • Avascular
  • Double diffusion systems
  • Loss of stem cell population in older people
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26
Q

What is the major proteoglycan

A

Aggrecan

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27
Q

What interventions can be used for small to medium sized defects in articular cartilage?

A
  • ACI
  • Debridement
  • Regeneration enhancement - includes microfracture
  • Osteochondral grafting
  • Cell based therapies
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28
Q

What are the functions of articular cartilage?

A
  • Distribute and transmit load of bone whilst moving
  • Minimise peak stresses on subchondral bone
  • Withstand low-friction repeated movement in everyday lifestyle
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29
Q

What do cartilage cells make?

A
  • Proteoglycan: aggrecan, decorim and biglycan

- Collagen

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30
Q

Why is aggrecan important?

A

It brings water into the cartilage which helps with compressive forces

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31
Q

What are the key radiological features of osteoarthritis?

A
  • Reduced joint space
  • Bone cysts (cracking in cartilage then fluid builds and cysts form)
  • Subchondral bone sclerosis
  • Osteophytes: bony spurs sticking up from the surface, an attempt to repair the bone
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32
Q

What are the histological features of osteoarthritis?

A
  • Cartilage degradation and proteoglycan loss
  • Surface fibrillation (breaking up)
  • Loss of metachromasia (staining)
  • Chondrocyte clustering (rather than being orderly organised in columns)
  • Chondrocyte apoptosis
  • Hyperplasia of synovium (thickened and inflamed and produces more fluid and thus swelling in the joints)
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33
Q

What are the features of cartilage focal lesions?

A
  • Focal lesions resulting from trauma mainly affect younger subjects, often during sports
  • Focal cartilage injury - either repetitive or traumatic impact
  • Pain, swelling and mechanical symptoms can be ongoing and lead to loss of function and joint degradation
34
Q

What are chondral lesions?

A

Lie entirely within the cartilage and do not penetrate subchondral bone

  • Don’t heal spontaneously
35
Q

What are osteochondral defects?

A

They penetrate through vascularised subchondral bone, some spontaneous repair occurs as chondroprogenitor cells invade the lesion

36
Q

What is the treatment for advanced osteoarthritis?

A

Total knee arthroplasty

  • Expensive
  • Tend to wear
37
Q

What are the possible first line intervention strategies for small defects?

A
  • Debridement

- Microfracture

38
Q

What are the second line treatments for small defects?

A
  • Osteochondral grafting
  • Cell based therapies
  • Osteotomy
39
Q

What does debridement do?

A

Aim to reduce friction and inflammation by shaving off frayed edges of a cartilage tear

40
Q

What does microfracture treatment do?

A
  • Perforation chondroplasty
  • Reparative procedure
  • Fibrocartilage repair
41
Q

What is an osteotomy?

A

Alters geometry of the knee to restore normal loading and relieve pain

42
Q

What is osteochondral grafting?

A

Regenerative procedure using either an autograft (from patient) or allograft (from donor) tissue to replace damaged area

43
Q

What is autologous chondrocyte implantation?

A

Cell based therapy, regenerative procedure that fills the defect

44
Q

What is matrix induced autologous chondrocyte implantation?

A

Modification of the ACI procedure but collagen in scaffold membrane

45
Q

What are stem cells?

A

Multipotent or pleuipotent cells capable of differentiating into a variety of mature cell types

46
Q

What is the meniscus?

A

Helps to distribute load over the joint and reduce wear and tear

47
Q

What can be done when the meniscus is damaged?

A 
Allograft
Cells (chondrocytes or stem cells) to develop an implant to restore joint function
48
Q

What are the functions of calcium?

A
  • Formation of calcified tissues
  • Normal activity of nerves and muscle
  • Neurotransmitter release, hormonal and glandular secretion
  • Excitation-contraction coupling (particularly in cardiac and smooth muscle)
  • Integrity and permeability of cell membranes
  • Cell adhesion
  • Blood clotting
49
Q

What is the primary purpose of calcium homeostasis?

A

Maintain constant blood calcium concentration

50
Q

How is blood calcium regulated?

A
  • Principle organ systems: gut, bone, kidneys
  • Hormones
  • Integrated physiology
51
Q

Which hormones are involved in blood calcium regulation?

A

Parathyroid hormone
Vitamin D3
(Calcitonin)

52
Q

What factors affect calcium flux into the blood?

A

Intestinal absorption

Bone reabsoprtion

53
Q

What factors affect calcium flux out of the blood?

A

Renal excretion

Bone formation

54
Q

What defines a hormone?

A

Made in one place (or sequentially in several places) and then acts in others

55
Q

What is vitamin D3?

A

A hormone

56
Q

How is vitamin D3 synthesised?

A

Skin

Digestion

57
Q

What is hypercalcaemia?

A

State of blood calcium concentration above the normal range

  • Too much calcium entering the blood
  • Too little calcium leaving the blood
58
Q

What are the symptoms of hypercalcaemia?

A

Stones, bones, groans, thrones and psychiatric overtones!

  • Blocks sodium channels so suppression of activity
  • CNS: altered mental state including lethargy, depression, decreased alertness, confusion, coma
  • GI: anorexia, constipation, nausea, vomiting
  • RENAL: diuresis, impaired concentrating ability, dehydration, hypercalciuria - risk for kidney stones
  • SKELETAL: associated with increased bone reabsorption so fracture risk
  • CV: cause/exacerbate hypertension, shortened QT interval
59
Q

What are the hormonal causes of hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Hypervitaminosis D
  • Paraneoplastic
60
Q

What are the non-hormonal causes of hypercalcaemia?

A
  • Renal failure

- Milk-alkali syndrome

61
Q

What drugs can cause hypercalcaemia?

A
  • Thiazides

- Lithium

62
Q

What is hypocalcaemia?

A

Blood calcium below normal range

63
Q

How is hypocalcaemia assessed?

A

Ionised calcium levels

64
Q

What are the symptoms of hypocalcaemia?

A
  • Causes stimulation of activity as it lowers threshold for depolarisation
  • Pins and needles
  • Tetany
  • Facial spasm
  • Hyperactive tendon reflexes
  • Larygospasm
  • Cardiac arrhythmias
  • Diarrhoea
65
Q

What are the causes of hypocalcaemia?

A

Hypoparathyroidism

  • Post surgical
  • Autoimmune
  • Pseudohypoparathyroidism (PTH resistance)
  • Idiopathic

Hypovitaminosis D

  • Dietary deficiency
  • Rickets, osteomalacia

Organ disfunction

  • GI malabsorption
  • Renal loss

Endocrine response to non-hypoparathyroid hypocalcaemia
- Secondary hyperparathyroidism

66
Q

What should any investigations aim to rule out?

A

INFECTION

67
Q

What is septic arthritis?

A

Acute inflammation of a joint caused by direct infection

68
Q

What are possible bacterial causes of septic arthritis?

A 
Staph. aureus (mainly)
Gonococcus (young adults)
Streptococcus
E. coli
Salmonella
Proteus
69
Q

What are the other causes of septic arthritis?

A
  • Bacterial
  • Mycobacterial
  • Rarely fungal/viral
70
Q

What are typical features of septic arthritis?

A
  • Sudden/subacute onset
  • Pain
  • Difficulty weight bearing
  • Difficulty moving
  • Swelling
  • Erythema
  • Hot
  • Tender
71
Q

What are the predisposing factors to septic arthritis?

A
  • Prosthetic joint
  • Immunosuppression
  • Elderly
  • Diabetic
  • Rheumatoid arthritis
  • Existing joint damage
  • IV drug abuse
  • Source of infection
72
Q

What is the outcome of septic arthritis if left untreated?

A
  • Rapid joint destruction
  • Sinus/abscess formation
  • Septicaemia
  • Multi-organ failure
73
Q

What happens in septic arthritis?

A
  • Narrowing of the joint space and irregularity of subchondral bone
  • Subchondral erosions and sclerosis of head
  • Osteonecrosis and complete collapse
74
Q

What investigations should occur in suspected septic arthritis?

A
  • Bloods
  • X-ray
  • Joint fluid
75
Q

What is gout?

A

Clinical syndrome caused by an inflammatory response to monosodium urate monohydrate crystals which may form in people with hyperuricaemia

Can be acute or chronic

76
Q

What happens in gout?

A

Overproduction of urate

  • Purine rich diet
  • Increased synthesis of purines

Underexcretion of urate

  • 90% of cases due to decreased urate clearance
  • Can be due to renal impairment
77
Q

What happens in purine metabolism?

A

Adenosine -> inosine -> hypoxanthine -> O2 and xanthine -> O2 and uric acid -> excretion - ⅔ renal, ⅓ gastrointestinal

78
Q

What are the risk factors for gout?

A
  • Age
  • Male
  • Genetics
  • Impaired renal function
  • Hyperuricaemia
  • High purine diet
  • Alcohol consumption
  • Obesity
  • Diuretics
79
Q

Which drugs modify the renal excretion of urate?

A
  • Aspirin (high dose)
  • Phenyl butazone
  • Probenecide
  • Sulphinpyrazone
  • Others
80
Q

What are the features of acute gout?

A
  • Pain
  • Swelling and erythema
  • Many attacks occur on first MTP joint (big toe) - most have osteoarthritis in and are colder so more prone to crystallisation
  • Almost any joint affected though lower more than upper
  • Mild attacks resolve in a few days
  • Tophi are signs of gout on hands and ears

Term 3 (6 decks)

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