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Patho II > Bones and Joints > Flashcards

Bones and Joints Flashcards

1
Q

How many bones are there in the adult body?

A

206

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2
Q

What is the body weight of all the bones in the body?

A

12%

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3
Q

What are the functions of bones?

A 
Mechanical support
Transmission of forces
Protection of viscera
Mineral Homeostasis 
Production of blood cells
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4
Q

What are the constituents of bones?

A

1) ECM

2) Cellsq

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5
Q

What is the ECM of bones made up of?

A

Osteoids = 35% and Mineral = 65%

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6
Q

What are the cells of bones?

A

1) Osteoblasts/Osteocytes

2) Osteoclasts

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7
Q

What is osteoid?

A

Made up of Type 1 collagen and osteopontin

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8
Q

What is osteopontin?

A

Protein produced by osteoblasts that plays a role in calcium homeostasis

Measures osteoblastic activity

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9
Q

What is the mineral found in bone?

A

Hydroxyapatite

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10
Q

What is hydroxyapitite?

A

Stored Calcium and phosphorous

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11
Q

What are osteoblasts?

A

Bone forming cells

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12
Q

What are osteocytes?

A

Bone forming cells that have dendrites and perform mechanotransduction

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13
Q

What is mechanotransduction?

A

Translation of mechanical energy to biological activity

Bones bear body weight or they become weak

Osteocytes feel the pressure and turn this into biological function of building bone

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14
Q

What are osteoclasts?

A

Bone removing cells

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15
Q

Where is 99% of calcium stored in body?

A

In bones

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16
Q

What else plays a role in bone growth?

A

Growth, thyroid, and parathyroid hormones

Want-beta catenin

SOX9

FGF

BMP

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17
Q

What is the percentage of bone that we lose every year?

A

0.5% - 0.7%

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18
Q

What is the diaphysis?

A

Elongated hollow central portion of the bone located between the metaphyses

Made of compact tissue and encloses the medullary cavity

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19
Q

What is the epiphysis?

A

Enlarged terminal part of the bone

Made of spongy tissue and articulating with neighboring bones

Covered with articular cartilage that reduces friction and absorbs shock

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20
Q

What is the metaphysis?

A

Part of the bone between the epiphysis and the diaphysis

Contains the connecting cartilage enabling the bone to grow and disappears at adulthood

Contains growth plate

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21
Q

What is the Periosteum?

A

A dense layer of vascular connective tissue enveloping the bones except at the surfaces of the joints

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22
Q

What is compact bone?

A

Cortical bone

Dense bone in which the bony matrix is solidly filled with organic ground substance and inorganic salts

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23
Q

What is the endosteum?

A

Covers the inside of bones and surrounds the medullary cavity

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24
Q

What is the medullary cavity?

A

Central cavity of bones shafts where red bone marrow and/or yellow bone marrow is stored

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25
Q

What is the process of remodeling?

A

The adult skeleton is constantly turning itself over in this tightly regulated process

This process repairs microdamage or changes the shape of bones in response to structural and mechanical demands

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26
Q

What regulates events at the bone multicellular unit?

A

Cell-cell interactions and cytokines

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27
Q

What is the pathway in which osteoclasts are made which allows for remodeling to occur?

A

NF-kapa B pathway

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28
Q

How does the NF-kappa B pathway become activated?

A

1) RANK ligand on stromal/osteoblast cells binds to RANK receptors on osteoclast precursors cells
2) This binding also causes the binding of MAcrophage colony-stimulating factor (M-CSF) which causes the precursor cell to produce a functional osteoclast

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29
Q

How is the NF-kappa B pathway inactivated?

A

Stromal/osteoblast cells will produce a decoy receptor, osteoprotegerin (OPG), which prevents RANKL from binding to the RANK receptor on osteoclast precursor cells

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30
Q

What is the function of osteoprotegerin?

A

Prevents bone resorption by inhibiting osteoclast formation

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31
Q

What percentage of the skeleton is replaced annually?

A

10%

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32
Q

What are the most common developmental disorders?

A

Aplasia
Supernumerary digits
Syndactyly
Craniosynostosis

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33
Q

What is aplasia?

A

Complete absence of a bone or entire digit

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34
Q

What is achondroplasia?

A

most common form of dwarfism

Autosomal dominant

Retarded growth of cartilage

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35
Q

What are the clinical features of Achondroplasia?

A

Shortened Proximal extremities
Trunk of relatively normal length
Enlarged head with bulging forehead
Conspicuous depression of the root of the nose

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36
Q

What is achrondroplasia caused by?

A

A mutation in FGF3 gene which remains always active and causes excessive suppression of bone growth

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37
Q

What is osteogenesis imperfecta?

A

Deficiency in synthesis of type 1 collagen

Brittle bone disease

Most common inherited disorder of connective tissue

Principally affects bone, but also joints, eyes, skin, ears, and teeth

Autosomal dominant

Helical structure of collagen isn’t formed correctly

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38
Q

What is the fundamental abnormality in Osteogenesis Imperfecta?

A

Too little bone, resulting in extreme skeletal fragility

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39
Q

What is type 1 osteogenesis imperfecta?

A

Normal life span but experience childhood fractures

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40
Q

What is type 2 osteogenesis imperfecta?

A

Fatal in utero

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41
Q

What is osteopenia?

A

Decreased bone mass < 1-2.5 SD

Reversible

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42
Q

What is Osteoporosis?

A

Severe osteopenia; bone mass < 2.5 SD

Not reversible

Normal mineral content isn’t effected

Can be generalized or local

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43
Q

What are the types of primary generalized osteoporosis?

A

Idiopathic
Postmenopausal
Senile

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44
Q

What are the types of secondary generalized osteoporosis?

A

Endocrine disorders - Diabetes Type 1, Hyperparathyroidism, Hyper/hypothyroidism
Neoplasia
Drugs

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45
Q

Who is most common types of osteoporosis?

A

Senile and postmeopausal

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46
Q

What is Rickets and Osteomalacia?

A

Vit. D deficiency causing impairment of mineralization which leads to accumulation of unmineralized matrix

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47
Q

What are the causes of osteoporosis?

A 
Age related changes
Reduced Physical activity
Genetic factors
Calcium nutritional state
Hormonal influences
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48
Q

What is senile osteoporosis?

A

Low turnover and age related

Decreased osteoclasts

49
Q

What is postmenopausal osteoporosis?

A

HIgh turnover and hormonally influenced

Increased osteoclasts

50
Q

What is the clinical course of osteoporosis?

A

Vertebral fractures = painful

Complications of fractures of femoral neck, pelvis, or spine such as pulmonary embolism and pneumonia

51
Q

What can prevent and treat osteoporosis?

A

Exercise
Vitamin D and calcium intake = osteopenia
Pharmalogical agents - bisphosphates for osteoporosis

52
Q

What is pagets disease (osteitis deformans)?

A

Disorder of increased, but disordered and structurally unsound bone mass

Usually begins in late adulthood ~ 70

53
Q

What are the three stages of Pagets?

A

1) Initial Osteolytic stage = Overfunctioning of osteoclasts
2) Mixed Osteoclastic-osteoblastic stage = both are functioning
3) Final Osteosclerotic stage = Silent stage when bone becomes really dense

54
Q

What is the cause of pagets?

A

Uncertain but genetics and environmental factors play a role

Two possible causes are mutations in SQSTM1 gene which increases NF-kappa B pathway or RNA virus infection which makes osteoclasts more sensitive by effecting Vit. D and IL6

55
Q

What are the symptoms of Pagets?

A

Usually asymptomatic

Pain localized to effected bone

56
Q

What bones are mostly effected in Pagets?

A

Axial skeleton or proximal femur

57
Q

What are the common clinical features of Pagets?

A

Enlargement of craniofacial skeleton = leontiasis ossea

Invagination of skull base = platybasia

Compression of posterior fossa

58
Q

What are the complications of Pagets?

A

Weight bearing - anterior bowing of femurs and tibiae which distorts the femoral heads causing secondary osteoarthritis

Chalk-stick fractures in long bones of lower limb

Compression fractures of spine causing kyphosis

Osteosarcoma or fibrosarcoma

59
Q

What is renal osteodystrophy?

A

Skeletal changes that occur in chronic renal disease

60
Q

What are the manifestations of Renal osteodystrophy?

A

Osteopenia/Osteomalacia
Secondary Hyperparathyroidism
Growth Retardation

61
Q

What are the histological changes seen in renal osteodystrophy?

A

High-turnover osteodystrophy
Low-turnover or aplastic
Mixed

62
Q

What is the pathogenesis of renal osteodystrophy?

A

1) Tubular dysfunction causing renal tubular acidosis which decreased pH and dissolves hydroxyappatite –> Osteomalacia
2) Renal failure causes decreased phosphate excretion which leads to chronic hyperphosphatemia and hypocalcemia –> Secondary hyperparathyroidism
3) Decreased secreted factors like Vitamin D and proteins BMP-7 and Klotho

63
Q

What is a fracture?

A

Break in the rigid structure of the bone

most common traumatic musculoskeletal disorders

64
Q

What are the causes of fractures?

A

Falls
Motor vehicle accidents
Sports-related injuries
Conditions that weaken the bone like osteoporosis, Pagets and bone cancer

65
Q

What is a simple fracture?

A

A single break with bone ends maintaining their alignment and position

66
Q

What are the types of simple fractures?

A

Transverse fracture
Oblique fracture
Spiral fracure

67
Q

What is a transverse fracture?

A

Break straight across the bone shaft

68
Q

What is an oblique fracture?

A

At an angle to the bone shaft

69
Q

What is a spiral fracture?

A

Twists around the bone shaft

70
Q

What is a comminuted fracture?

A

Multiple fracture lines and bone pieces

71
Q

What is a greenstick fracture?

A

An incomplete break in which the bone is bent and only the outer curve of the bend is broken

72
Q

What is a compression fracture?

A

Bone is crushed or collapses into small pieces

73
Q

What is a pathologic fracture?

A

Involving bone weakened by an underlying disease process such as tumor

74
Q

What are the steps of healing of a fracture?

A

1) Hematoma formation
2) Necrosis of the broken bone ends
3) Fibroblasts invade the clot within a few days
4) Fibrblasts secrete collagen fibers which form a mass of cells and fibers called a callus
5) Callus bridges the broken bone ends together inside and outside over 2 - 6 weeks
6) Osteoblasts invade the callus and slowly converts it to bone over 3 weeks to several months

75
Q

How long does it take for a fracture to completely heal?

A

12-15 weeks

76
Q

What is osteomyelitis?

A

Inflammation of bone and marrow secondary to infection

77
Q

What is the most common organism that causes pyogenic osteomyelitis?

A

Staph aureus

78
Q

How do the organisms reach the bone?

A

1) Hematogenous spread
2) extension from a contiguous site
3) direct implantation

79
Q

What are the symptoms of osteomyelitis?

A 
Malaise
Fever
Chills
Leukocytosis 
Throbbing pain over the affected region
80
Q

How do you diagnose osteomyelitis?

A

X-ray lytic focus of bone destruction surrounded by a zone of sclerosis which can only be seen if 60% of bone is lysed

81
Q

What are the complications of osteomyelitis?

A 
Chronic osteomyelitis
Pathologic fracture
Secondary amyloidosis
Endocarditis 
Sepsis
Carcinoma
82
Q

What causes non-pyogenic osteomyelitis?

A

M. Tuberculosis

83
Q

What does M. tuberculosis cause?

A

Pott disease

84
Q

What is Potts disease?

A

Destruction of discs and vertebrae which causes scoliosis or kyphosis and neurologic deficits

85
Q

What is the dead bone called?

A

sequestrum

86
Q

What is the newly deposited bone that forms a shell of living tissue around the segment of devitalized infected bone called?

A

involucrum

87
Q

What are osteoid osteoma and osteoblastoma?

A

Benign bone-producing tumors that have identical histologic features but differ in size, sites of origin, and symptoms

Malignant transformation is rare

88
Q

What is osteoid osteomas?

A

< 2 cm in diameter
Teens and 20s
Appendicular skeleton

89
Q

What is osteoblastoma?

A

> 2 cm in diameter

Involves posterior spine

90
Q

What is osteosarcoma?

A

Most common primary malignant tumor of bone

cancerous cells produce osteoid matrix or mineralized bone

Bimodal age distribution

91
Q

What are the predisposing factors of osteosarcoma?

A

Paget disease
Bone infarcts
Prior radiation

92
Q

What are the symptoms of osteosarcoma?

A

Painful, Progressively enlarging masses

Pathological fracture

93
Q

What causes osteosarcoma?

A

Mutations in:

RB
TP53
Inactivated INK4
MDM2 and CDK4

94
Q

What is the radiological finding for osteosarcoma?

A

Sun ray appearance

95
Q

What is the function of joints?

A

Allow movement while providing mechanical stability

96
Q

What are solid, non-synovial joints?

A

Provide structural integrity and allow only minimal movement

They lack a joint space

Ex. cranial sutures

97
Q

What are synovial joints?

A

Elbow, knee, shoulder

Have a joint space that allows for a wide range of motion

98
Q

What is osteoarthritis?

A

Most common type of joint disease

Degeneration of cartilage causing structural/functional failure of joints

99
Q

What is most commonly affected area of osteoarthritis in women?

A

Knees and hands

100
Q

What is most commonly affected are of osteoarthritis in men?

A

hip

101
Q

What is the pathogenesis of osteoarthritis?

A

Chondrocytes response to biochemical and mechanical stresses resulting in breakdown of matrix

Breakdown occurs because tissue macrophages are activated and they secrete TNF-alpha, IL6, and IL1

These cytokines cause proteases to be secreted and they destroy the bone even more

102
Q

What are the primary causes of osteoarthritis?

A

Aging

103
Q

What are the secondary causes of osteoarthritis?

A

Obesity

Diabetes

104
Q

When do symptoms of osteoarthritis start to appear?

A

age 50

105
Q

What are the symptoms of osteoarthritis?

A 
Deep, achy pain that worsens with use
Morning stiffness
Crepitus
Limitation of ROM
Nerve root compression and radicular pain
Muscle spasms
Muscle atrophy
Neurologic deficits
106
Q

Where does osteoarthritis typically occur?

A 
Hips
Knees
Lower lumbar and cervical vertebrae
Proximal and distal IP joints of the fingers
First CMC joints
First TMT joints
107
Q

What occurs over time with osteoarthritis?

A

Joint deformity but NOT fusion

108
Q

What is Rheumatoid arthritis?

A

Chronic inflammatory disorder of autoimmune origin principally affecting the joints, producing a non-suppurative, proliferative and inflammatory synovitis

109
Q

What does RA involve?

A

Extra-articular

Skin (nodules)
Hear (MI)
Blood vessels (atherogenesis)
Lungs

110
Q

What is caused by RA?

A 
Inflammation
Articular cartilage destruction
Bone erosion
Angiogenesis
Ankylosis
111
Q

What is the pathogenesis of RA?

A

1) CD4+ T helper cells initiate the autoimmune response by reacting with arthitogenic agent
2) T cells produce cytokines that stimulate other inflammatory cells to effect tissue injury = IFN-gamma, IL-17, TNF, and IL-1
3) These cytokines recruit and activate other immune cells causing cartilage damage
4) RANKL is expressed on activated T cells and this stimulates bone resorption
5) Serum IgM and IgA autoantibodies are formed and bind to Fc portions of the patients own IgG - RA factor

112
Q

What are the symptoms of RA?

A

Malaise
Fatigue
Generalized musculoskeletal pain, likely mediated by IL-1 and TNF-alpha
Symmetrical joint involvement - small joints first
Swollen, warm, painful joints that are stiff in morning or not used
Progressive joint enlargement
Decreased ROM

113
Q

What are the clinical features of RA?

A

Radial deviation of wrist = Swan-neck deformity

Ulnar deviation of the fingers and flexion hyperextension of the fingers = Boutonniere deformity

114
Q

How is RA diagnosed?

A

1) Radiographic findings
2) Sterile, turbid synovial fluid with decreased viscosity, poor mucin clot formation, and inclusion-bearing neutrophils
3) RA factor and anti-CCP antibodies

115
Q

What is Gout?

A

Transient attacks of acute arthritis initiated by crystallization of monosodium urate within and around the joint

116
Q

What is gout caused by?

A

hyperuricemia = plasma urate > 6.8 mg/dL

117
Q

What are the risk factors for Gout?

A 
Age
Genetic predisposition
Heavy alcohol consumption
Obesity
Drugs
Lead toxicity
118
Q

What are the morphologic changes of gout?

A

Acute arthritis
Chronic tophaceous arthritis
Tophi in various sites
Gouty nephropathy

Patho II (16 decks)

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