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Clinical Pathology > Diseases of the Musculoskeletal System - Diseases (53 & 54) > Flashcards

Diseases of the Musculoskeletal System - Diseases (53 & 54) Flashcards

1
Q

How many bones?

A

206

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2
Q

What is arthritides?

A

Pain and stiffness of joint

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3
Q

Cause of arthritides

A

Inflammation of the joint, not a single disease

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4
Q

Acute arthritis

A

Pain, heat, redness and swelling

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5
Q

Chronic arthritis commonest types

A

Osteoarthritis and RA

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6
Q

Osteoarthritis

A

commonest type, degenerative, progressive erosion of articular cartilage

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7
Q

What to osteoarthritis result iin

A

Formation of bony spurs and cysts at margins of joints (subchondral cysts)

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8
Q

Secondary OA

A

Due to wear and tear, frequent use of a joint

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9
Q

Causes of OA

A

Aging, underling systemic disease (diabetes and obesity)

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10
Q

Commonest location of OA

A

Knees and hand in women and hip in men

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11
Q

OA pathogenesis

A

Deterioration and loss of cartilage (protective cushion),

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12
Q

Cellular basis of OA

A

Chondrocytes, produce IL-1 (matrix breakdown)

Prostaglandins derivatives > release of lytic enzymes (prevents matrix synthesis)

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13
Q

Primary OA

A

Abnormal stress in weight bearing joints

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14
Q

Where does primary OA affect?

A

Fingers (Herberden’s/Bouchard’s nodes), knees and cervical and lumbar spines

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15
Q

RA

A

Chronic systemic disorder, non-suppurative proliferative synovitis - destruction of articular cartilage and ankylosis of joints

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16
Q

RA affects..

A

Skin (rheumatoid nodules), muscles, heart, lung, spleen and blood vessels (Small joints of hands and feet > deformed joint)

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17
Q

RA is more common in men or women?

A

3-5 times more in women than men

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18
Q

Pannus (RA)

A

Inflammatory substances between two bones, sticky erodes into articular cartilage and penetrates subchondral bone and cyst formation > ankylosis of joint space

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19
Q

RA clinical features

A

Malaise, fatigue, generalised musculoskeletal pain, swollen, pain, warm and stiff joints

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20
Q

RA disease course

A

Slow/rapid course, fluctuates over 4-5 years

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21
Q

RA pathogenesis

A

Genetic (HLA-DR4 and DR1), EBV, Viruses, Borrelia, Autoimmune reaction with synovial membranes (CD4 positive T-cells), mediators of joint damage (cytokines), IL-1-6 and TNF-a/B

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22
Q

Criteria for diagnosis

A
  1. Morning stiffness
  2. Arthritis in 3 or more joint areas
  3. Arthritis of hand joints
  4. Symmetric arthritis
  5. Rheumatoid nodules
  6. Serum Rheumatoid factor
    (4 of above)
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23
Q

Rheumatoid factor

A

Present in most but not all

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24
Q

Analyse synovial fluid

A

Presence of neutrophils - inflammation

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25
Q

Sero-Negative arthritides

A

Lack RF

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26
Q

Examples of Sero-negative arthritis

A

Ankylosing spondylitis, Reiter’s syndrome, Psoriatic arthritis, Eneteropathic arthritis

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27
Q

Gout

A

Hyperuricemia (Uric acid end product of purine metabolism - deficiency of some enzymes involved)

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28
Q

Gout clinical features

A

Acute arthritis, chronic arthritis, tophi in various sites (uric acid crystals in joint spaces) > chronic gouty nephropathy and deposition of masses of rates in joints other sites (Tophi)

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29
Q

Pyogenic osteomyelitis clinical features

A

Systemic illness - fever, malaise, chills, marked pain over affected region

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30
Q

Pyogenic OM examinations

A

X-ray lytic focus of bone destruction surrounded by zone of sclerosis, Blood cultures positive (essential), biopsy (shows neutrophils not cause)

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31
Q

Pyogenic OM causes

A

Bacteria, haematogenous spread, extension from contiguous site, direct implantation

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32
Q

Infective arthritis

A

Acutely painful and swollen joints with restricted movements

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33
Q

Infective arthritis clinical presentation

A

Fever, leucocytosis and elevated ESR

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34
Q

Causes of infective arthritis

A

Bacterial (Staph, Strep, Gonococcus, Mycobacteria), Trauma, IVDU, debilitating illness

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35
Q

Osteoporosis

A

Increased porosity of skeleton, reduction in bone mass, locailised/entire skeleton, primary/secondary

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36
Q

Who does osteoporosis effect?

A

Primary-Age, post menopausal , physical activity, muscle strength, diet, hormonal status

37
Q

Osteoporosis clinical features

A

Vertebral fractures, kyphosis, scoliosis

38
Q

Secondary osteoporosis caused by

A

Endocrine disorders (Hyperparathyroidism, Type 1 diabetes), neoplasia (multiple myeloma), malnutrition

39
Q

Osteoclast dysfunction causes

A

Paget’s disease (collage of matrix madness), usually tidy up

  1. Osteolytic stage
  2. Predominant osteoblastic activity
  3. Burnt out ostesclerotic stage
  4. Net effect - gain in bone mass
  5. Newly formed bone is disordered and architecturally unsound
40
Q

What is osteoclast dysfunction caused by

A

Paramyxovirus infection

41
Q

Histological hallmark of osteoclast dysfunction

A

Mosaic pattern

42
Q

Paget’s disease affects who?

A

Males > females

43
Q

What age does Paget’s disease effect?

A

5th decade

44
Q

What’s mainly involved in Paget’s disease?

A

Axial skeleton and proximal skeleton

45
Q

What’s most common symptom of Paget’s disease?

A

Pain

46
Q

Complications of Paget’s disease

A
  • Chalk stick type fractures

- Tumours (Benign - giant cell, malignant - osteosarcoma, chondrosarcoma, malignant fibrous histiocytoma)

47
Q

Osteomalacia

A

Defects in matrix mineralisation, lack of Vit d, decreased bone density (osteopenia), skeletal deformities not seen

48
Q

Hyperparathyroidism increases

A
  • Bone resorption and calcium metabolism from skeleton

- Renal tubular reabsorption and retention of calcium

49
Q

Hyperpararthyoridism complications

A

Hypercalecemia, osteitis fibrosa cystica (loss of bone mineral with osteoporosis)

50
Q

Real osteodystrophy

A

Skeletal changes of CKD

  • Increased osteoclastic bone resorption
  • Delayed matrix mineralisation
  • Osteosclerosis
  • Growth retardation
  • Osteoporosis
51
Q

Soft tissue

A

Non-epithelial extraskeletal structures exclusive of supportive tissue of organs and lymphoid/hematopoietic tissue

52
Q

Embryological origin of soft tissue

A

Mesodermal

53
Q

Are benign soft tissue tumours common or rare?

A

Common

54
Q

Sarcomas

A

Malignant soft tissue tumours, rare and lymph node involvement is uncommon

55
Q

Neurofibromatosis Type 1

A

Neurofibroma

56
Q

Gardner syndrome

A

Fibromatosis

57
Q

Carney syndrome

A

Myxoma, melanotic schwannoma

58
Q

Turner syndrome

A

Cystic hygroma

59
Q

Diagnosis of soft tissue tumour

A
  • Ultrasound guided core biopsy
  • Cytogenetics (fresh tissue and karyotype)
  • Molecular genetics (FISH, PCR and RT-PCR)
60
Q

Benign bone tumours

A

Osteomas, Osteoblastomas

61
Q

Benign cartilage tumours

A

Chondromas

62
Q

Mixed benign tumours

A

Osteochondromas

63
Q

Malignant bone tumours

A

Osteosarcoma

64
Q

What age group does malignant bone tumours effect?

A

Young

65
Q

Where is commonest site for malignant bone tumours?

A

Knee (60%)

66
Q

Other bone tumours

A

Chrondosarcomas, Ewing’s sarcoma, Giant cell tumours

67
Q

Metastatic bone tumours

A

Thyroid, prostate, kidney, breast, GI tract

68
Q

SLE

A

Complex multi-system disease, predominantly cutaneous

69
Q

Is SLE more common in males or females?

A

Females

70
Q

Clinical presentation of SLE

A

Butterfly rash, cardiomegaly, endocarditis, CNS (convulsions, hemiplegia), 45% patients nephron syndrome and glomerulonephritis

71
Q

Pathogenesis of systemic sclerosis

A

Vessel damage, inflammatory response, cytokines, diffuse - widespread cutaneous lesions

72
Q

Which systems does systemic sclerosis effect?

A

Renal, Cardiorespiratory, GIT, osteoarticular involvement (arthralgia, arthritis)

73
Q

What is prognosis for systemic sclerosis?

A

Poor

74
Q

Localised variant of systemic sclerosis

A

Limited cutaneous and oesophageal involvement, SI malabsorption, CREST syndrome

75
Q

CREST syndrome

A

Calcinosis, Raynaud’s phenomenon, Oesophageal dysfunction, Sclerodactyly, Telangiectasia

76
Q

Symptoms of Polymyalgia Rheumatica

A

Stiffness, weakness, aching and pain in muscles of neck, limb girdles and upper limbs

77
Q

Polymylagia Rheumatica associated with

A

Giant cell arteritis

78
Q

Giant cell arteritis affects what

A

Occipital or facial arteries

79
Q

Giant cell arteritis symptoms

A

Pyrexia, headache and severe scalp pain

80
Q

Myopathy

A

Muscle disease unrelated to any disorder of innervation/neuromuscular junction

81
Q

Myositis

A

Muscle fibres and overlying skin are inflamed and damaged resulting in muscle weakness

82
Q

Muscular dystrophy

A

Heterogenous group, inherited, progressively severe muscle weakness and wasting

83
Q

When’d does muscular dystrophy start

A

Childhood

84
Q

Malignant hyperthermia

A

(Inherited) Fast rise in body temperature and severe muscle contraction

85
Q

When does malignant hyperthermia occur?

A

When affected person gets general anaesthesia

86
Q

Rhabdomyolysis

A

Destruction of skeletal muscle, release of muscle fibre content into blood, myoglobin is released into blood, filtered through kidneys > myoglobinuria (brown urine)

87
Q

Causes of rhabdomyolsis

A

Trauma, crush injuries, drugs (cocaine, amphetamine), extreme temp, severe exertion, lengthy surgery, severe dehydration, complication (acute renal failure)

88
Q

Metabolic myopathies

A

Glycogen synthesis and degradation, disorders of mitochondrial metabolism

89
Q

Symptoms of malignant hyperthermia

A

Bleeding, dark brown urine, muscle rigidity, quick rise in body temp 40 degrees and higher

Clinical Pathology (60 decks)

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