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MS2 Unit 1 > Goljan's MSK > Flashcards

Goljan's MSK Flashcards

1
Q

What causes osteogenesis imperfecta?

A

Defect in synthesis of type I collagen (AD)

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2
Q

What is the mechanism of blue sclera in OI?

A

Reflection of the underlying choroidal veins through thin sclera

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3
Q

What causes achondroplasia?

A

AD mutation in the FGFR3 gene

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4
Q

How does achondroplasia present?

A

Normal head/axial skeleton, short arms/legs, impaired proliferation of cartilage at growth plate

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5
Q

What is the pathogenesis of osteopetrosis?

A

Deficiency of osteoclasts (AR); “too much bone”

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6
Q

What are the clinical findings in osteopetrosis?

A

Pathologic fractures, visual/hearing loss, anemia

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7
Q

How does osteomyelitis spread?

A

Usually spreads hematogenously to bone

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8
Q

What is the most common site of osteomyelitis?

A

Metaphysis

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9
Q

What is the most common pathogen causing osteomyelitis?

A

S. aureus

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10
Q

What is the most common pathogen causing osteomyelitis in sickle cell disease?

A

S. paratyphi

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11
Q

What is Pott disease?

A

Tuberculous osteomyelitis involving the vertebral column

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12
Q

What pathogen causes osteomyelitis following puncture of foot through rubber footwear?

A

P. aeruginosa

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13
Q

What is sequestra?

A

Devitalized bone

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14
Q

What is involucrum?

A

Reactive bone formation in periosteum

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15
Q

What is a late complication of draining sinus tracts?

A

Danger of SCC at sinus drainage orifice

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16
Q

What is the most common metabolic abnormality of bone?

A

Osteoporosis

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17
Q

What defines osteoporosis?

A

Loss of both mineralized bone and organic bone matrix (osteoid)

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18
Q

What is primary osteoporosis?

A

Idiopathic; most common in children and young adults

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19
Q

Who is prone to type I osteoporosis?

A

Postmenopausal women

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20
Q

What is type II osteoporosis?

A

Senile type; occurs in men and women

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21
Q

What are some causes of secondary osteoporosis?

A

↑ cortisol, heparin, hypogonadism, malnutrition, space travel

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22
Q

What is the role of estrogen in maintaining bone mass?

A

Estrogen normally inhibits production of osteoclasts and enhances the activity of osteoblasts

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23
Q

How does decreased estrogen affect bone mass?

A

↓EGN: ↑IL-1, IL-6, TNF → ↑osteoclastogenesis

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24
Q

What cytokines mediate osteoclastogenesis?

A

IL-1, IL-6, TNF

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25
Q

What are the effects of IL-1, IL-6, and TNF on bone?

A

↑ expression of RANK, RANKL genes, ↓ expression of osteoprotegerin (OPG)

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26
Q

What is the mechanism of bone loss in postmenopausal bone mass?

A

↓EGN: osteoclast activity > osteoblast activity

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27
Q

Which fractures occur most commonly in postmenopausal osteoporosis?

A

Vertebral compression fractures, Colles fracture

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28
Q

How is osteoporosis diagnosed?

A

Dual photon absorptiometry

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29
Q

How can osteoporosis be prevented?

A

Weight-bearing exercises, supplementation of calcium + vit D, smoking cessation

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30
Q

How is osteoporosis treated?

A

Bisphosphonates (first-line), Estrogen replacement in women

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31
Q

What is avascular necrosis?

A

Death of bone cells from blood supply interruption

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32
Q

What is the most common site of avascular necrosis?

A

Femoral head

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33
Q

What is the most common cause of avascular necrosis?

A

Long-term use of corticosteroids

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34
Q

What is the mechanism of avascular necrosis in the femoral head?

A

Subcapsular fracture disrupts blood supply (retinacular arteries from medial circumflex femoral artery)

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35
Q

Which wrist bone is most commonly fractured?

A

Scaphoid bone; susceptible to avascular necrosis

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36
Q

What is the most sensitive early test for avascular necrosis?

A

MRI

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37
Q

What is osteochondrosis?

A

Avascular necrosis of ossification centers in children

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38
Q

What is Legg-Calvè-Perthes disease?

A

Avascular necrosis of the femoral head ossification center; boys > girls

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39
Q

What is osteochondritis dissecans?

A

Variant of osteochondrosis limited to articular epiphysis

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40
Q

What causes osteochondritis dissecans?

A

Trauma is primary insult; ischemia is secondary injury

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41
Q

What is the most common site of osteochondritis dissecans?

A

Lateral surface of medial femoral condyle

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42
Q

What occurs in osteochondritis dissecans of the knee?

A

Piece of cartilage along with a thin layer of bone detaches

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43
Q

What is a late complication of osteochondritis dissecans?

A

Osteoarthritis

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44
Q

What is Osgood-Schlatter disease?

A

Painful swelling of tibial tuberosity at patellar tendon insertion; affects physically active boys

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45
Q

What is a typical finding associated with Osgood-Schlatter disease?

A

Permanent knobby-appearing knees

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46
Q

What population is typically affected by Paget disease?

A

Primarily occurs in men >50 years of age

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47
Q

What is the etiology of Paget disease?

A

Unknown; possible paramyxovirus infection of osteoclasts

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48
Q

What bones are targeted in Paget disease?

A

Pelvis, skull, femur

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49
Q

What is the pathogenesis of Paget disease?

A

Osteoclastic phase followed by an osteoblastic phase

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50
Q

What are are the clinical findings in Paget disease?

A

↑ALP in osteoblastic phase, weak thick vascular bone

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51
Q

How does Paget disease typically present?

A

pain, ↑hat size

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52
Q

What are some complications of Paget disease?

A

Fractures, osteogenic sarcoma, high output heart failure

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53
Q

What causes fibrous dysplasia?

A

Defect in osteoblastic differentiation/maturation

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54
Q

What occurs in fibrous dysplasia?

A

Medullary bone replaced by fibrous tissue with cyst formation

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55
Q

What is the most common site of fibrous dysplasia?

A

Ribs

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56
Q

What are the features of [McCune]-Albright syndrome?

A

Polyostotic bone involvement, cafe au lait spots, precocious puberty

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57
Q

What are the complications of fibrous dysplasia?

A

Pathologic fracture, osteogenic sarcoma, fibrosarcoma

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58
Q

What is the most common bone malignancy?

A

Metastasis (breast cancer is most common source)

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59
Q

What is the most common benign bone tumor?

A

Osteochondroma

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60
Q

What are the characteristics of monosodium urate crystals?

A

Monoclinic (needle-shaped), Negative birefringence (yellow when parallel to slow ray)

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61
Q

What are the characteristics of calcium pyrophosphate crystals?

A

Monoclinic-like (needle-like) or triclinic (rhomboid), Positive birefringence (blue when parallel to slow ray)

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62
Q

What does a mucin clot test for?

A

Joint viscosity; hyaluronic acid is the key lubricant in synovial fluid

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63
Q

What joint disorders are classified as group I?

A

Noninflammatory: osteoarthritis, neuropathic joint

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64
Q

What joint disorders are classified as group II?

A

Inflammatory: rheumatoid arthritis, gout

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65
Q

What joint disorders are classified as group III?

A

Septic: lyme disease, dissemminated gonococcemia

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66
Q

What joint disorders are classified as group IV?

A

Hemorrhagic: trauma, hemophilia

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67
Q

Morning stiffness is a characteristic finding in which diseases?

A

Rheumatoid arthritis, SLE, polymyalgia rheumatica

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68
Q

What are some examples of joint effusion?

A

Blood, exudate

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69
Q

What is implied by a hot joint?

A

Acute inflammation; septic arthritis

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70
Q

What is joint crepitus?

A

Crackling feeling when joint moves; characteristic of osteoarthritis

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71
Q

What are some general signs and symptoms of joint disease?

A 
Arthralgia (joint pain), Arthritis (pain associated with joint swelling)
Morning stiffness
Abnormal joint mobility
Swelling of joint (effusion)
Redness and warmth of the joint
Joint crepitus with motion
72
Q

What is osteoarthritis?

A

Degeneration of articular cartilage; most common disabling joint disease

73
Q

What is alkaptonuria?

A

Homogentisic acid deposits in intervertebral disks causing osteoarthritis; characteristic black color

74
Q

What sites are commonly affected in osteoarthritis?

A

Femoral head, Knee
Cervical/lumbar vertebrae
Hands

75
Q

What are the components of normal articular cartilage?

A

Proteoglycans (provide elasticity), Type II collagen (provides tensile strength)

76
Q

What is the pathogenesis of osteoarthritis?

A

Cytokines activate metalloproteinases → degrade proteoglycans/collagen

77
Q

What are the joint findings in osteoarthritis?

A

Osteophytes at joint margins, Clefts, subchondral cysts

No joint fusion

78
Q

What is the most common clinical complaint in osteoarthritis?

A

Pain aggravated by movement

79
Q

When does joint stiffness present in osteoarthritis?

A

After inactivity

80
Q

How does osteoarthritis affect the hands?

A

Heberden nodes: DIP joint enlargement/pain, Bouchard nodes: PIP joint enlargement/pain

81
Q

What are the vertebral findings in osteoarthritis?

A

Degenerative disk disease, compressive neuropathies , Typically in cervical/lumbar region

82
Q

What occurs in neuropathic arthropathy (Charcot joint)?

A

Loss of proprioception and deep pain sensation, leading to recurrent trauma

83
Q

What are some common causes of neuropathic arthropathy?

A

Diabetes mellitus, Syringomyelia

Tabes dorsalis

84
Q

What population is typically affected by rheumatoid arthritis?

A

Women > men, HLA-DR4

85
Q

What is the role of T cells in the pathogenesis of rheumatoid arthritis?

A

Activated CD4+ T-cells release proinflammatory agents

86
Q

What is the role of B cells in the pathogenesis of rheumatoid arthritis?

A

B cells produce rheumatoid factor (IgM antibody against Fc portion of IgG)

87
Q

What is a pannus?

A

Granulation tissue formed within the synovial tissue by fibroblasts and inflammatory cells

88
Q

What role does pannus play in the pathogenesis of rheumatoid arthritis?

A

Pannus (granulation tissue): releases cytokines that destroy articular cartilage

89
Q

How does ankylosis occur in rheumatoid arthritis?

A

Repair of damaged cartilage causes fusion of the joint

90
Q

How does rheumatoid arthritis affect the hands?

A

MCP and PIP joints, Bilateral ulnar deviation
Swan neck deformity
Boutonnière deformity

91
Q

What is a swan neck deformity?

A

DIP flexed, PIP extended

92
Q

What is a boutonnière deformity?

A

DIP extended, PIP flexed

93
Q

What are the pulmonary complications of rheumatoid arthritis?

A

Interstitial fibrosis, effusions

94
Q

What are the hematologic complications of rheumatoid arthritis?

A 
Anemia of chronic disease, Autoimmune hemolytic anemia
Felty syndrome (autoimmune neutropenia, splenomegaly)
95
Q

How does rheumatoid arthritis affect the cervical spine?

A

Subluxation of atlantoaxial joint, cord/vertebral artery compression

96
Q

What common neurologic syndrome can affect the hand in rheumatoid arthritis?

A

Carpal tunnel syndrome; median nerve entrapment

97
Q

Where do rheumatoid nodules typically occur?

A

Extensor surface of forearms; lungs

98
Q

What are the cardiovascular complications of rheumatoid arthritis?

A

Pericarditis, Aortitis

Vasculitis

99
Q

What is a Baker cyst?

A

Outpouching of semimembranous bursa into posterior joint space

100
Q

What are the characteristic lab findings in rheumatoid arthritis?

A

Positive serum rheumatoid factor (RF), Positive antinuclear antibody (ANA)
Polyclonal gammopathy

101
Q

What is Sjögren’s syndrome?

A

Destruction of minor salivary glands and lacrimal glands; female dominant

102
Q

What are the characteristic findings of Sjögren’s syndrome?

A

Rheumatoid arthritis, Dry eyes

Dry mouth

103
Q

What are the characteristic lab findings in Sjögren’s syndrome?

A

Positive serum ANA, RF, anti-SS-A/anti-SS-B, Lip biopsy confirms diagnosis

104
Q

What lab finding differentiates juvenile rheumatoid arthritis from the adult form?

A

RF usually negative

105
Q

What is Still disease?

A

Form of juvenile rheumatoid arthritis that presents with fever, rash, polyarthritis

106
Q

What is the main finding of polyarticular juvenile rheumatoid arthritis?

A

Disabling arthritis predominates

107
Q

What is the main finding of pauciarticular juvenile rheumatoid arthritis?

A

Limited arthritis

108
Q

What is gout?

A

Deposition of monosodium urate in tissue; due to prolonged hyperuricemia

109
Q

In which gender does gout predominate?

A

Males

110
Q

What is the most common mechanism of gout?

A

Underexcretion of uric acid

111
Q

What clinical conditions are commonly associated with gout?

A

Urate nephropathy, Renal stones
Hypertension
Coronary artery disease
Lead poisoning

112
Q

What causes an episode of acute gout?

A

Free uric acid crystals in joint are responsible for initiating the attack

113
Q

How is acute gout diagnosed?

A

Must confirm with joint aspiration; hyperuricemia does not define gout

114
Q

What is a tophus?

A

Monosodium urate deposits in soft tissue around the joint

115
Q

What are the effects of tophi?

A

Erosive arthritis; bone distintegrates, leaving overhanging edges

116
Q

What is the nonpharmalogical treatment of gout?

A

Eliminate high-purine diet, Moderate alcohol intake

117
Q

What is the pharmacologic treatment of acute gout?

A

NSAIDS or colchicine

118
Q

What drugs can be used to prevent gout?

A

1) Uricosuric agents for underexcretors, 2) Allopurinol for overproduces

119
Q

What is calcium pyrophosphate dihydrate deposition disease?

A

Calcium pyrophosphate deposited in tissues

120
Q

Incidence of CPPD increases in the presence of which diseases?

A

Hemochromatosis, Hemosiderosis

Primary hyperparathyroidism

121
Q

What is the most common variant of CPPD?

A

Osteoarthritis variant; most commonly affects knee; chondrocalcinosis present

122
Q

What is chondrocalcinosis?

A

Linear deposits of calcium pyrophosphate in articular cartilage

123
Q

What is the meaning of “seronegative” in seronegative spondyloarthropathies?

A

RF negative arthritis

124
Q

What are the key characteristics of seronegative spondyloarthropathies?

A

Negative RF, Positive HLA-B27
Male
Sacroiliitis

125
Q

What are the four main types of seronegative spondyloarthropathies?

A

Ankylosing spondylitis, Reactive arthritis
Psoriatic arthritis
Enteropathic arthritis

126
Q

What is the typical progression of ankylosing spondylitis?

A

Begins with bilateral sacroiliitis; over time, vertebrae fuse (bamboo spine)

127
Q

What extra-articular signs are associated with ankylosing spondylitis?

A

Aortitis, Uveitis with potential for blindness

128
Q

What is Reiter syndrome?

A

C. trachomatis urethritis, arthritis, conjunctivitis, circinate balanitis

129
Q

What is the diagnostic sign of Reiter syndrome?

A

Achilles tendon periostitis

130
Q

What are the characteristic findings of psoriatic arthritis?

A

Sausage-shaped DIP joints, Pencil-in-cup deformity

131
Q

What is the most common cause of nongonococcal septic arthritis?

A

S. aureus

132
Q

What is the most common cause of septic arthritis in urban populations?

A

N. gonorrhoeae

133
Q

What are the signs of disseminated gonococcemia?

A

Septic arthritis, Tenosynovitis, and Dermatitis (STD), Associated with C6-C9 deficiency

134
Q

What causes Lyme disease?

A

B. burgdorferi (gram-negative spirochete) via Ixodes tick bite

135
Q

What are the animal reservoirs for B. burgdorferi?

A

White-footed mouse (nymphs; most common cause), White-tailed deer (adult ticks)

136
Q

What is the geographic distribution of B. burdorferi?

A

Northeast, Upper Midwest US

137
Q

Where does Lyme disease tend to localize?

A

Skin, CNS, joints, heart, eyes

138
Q

What is the mechanism of Lyme disease?

A

Organism causes inflammation; cross-reactivity leads to type II/III hypersensitivity

139
Q

What is the pathognomonic sign of early localized infection with B. burgdorferi?

A

Erythema migrans

140
Q

What are the treatment implications of erythema migrans?

A

When erythema migrans is observed (sign of early localized infection), empiric treatment can be given without laboratory confirmation

141
Q

What characterizes the early disseminated phase of Lyme disease?

A

Migratory polyarticular to monoarticular arthritis (Knee is most common site), Neuroborreliosis (bilateral facial nerve palsy)
Meningeal irritation

142
Q

What are the signs of chronic Lyme disease?

A

Disabling arthritis (knee)

143
Q

What is Babesiosis?

A

Tick-transmitted hemolytic anemia; may accompany Lyme disease

144
Q

What causes septic arthritis and tendinitis due to a cat/dog bite?

A

Pasteurella multocida

145
Q

What are type I muscle fibers?

A 
Slow twitch (red), Rich in mitochondria and oxidative enzymes        
Poor in ATPase enzymes
146
Q

What are type II muscle fibers?

A 
Fast twitch (white), Poor in mitochondria and oxidative enzymes
Rich in ATPase enzymes
147
Q

What is the pathogenesis of muscle weakness?

A

Abnormality of motor neuron, Abnormality of neuromuscular synapse
Muscle dysfunction

148
Q

What occurs in neurogenic atrophy?

A

Motor neuron or axon degenerates

149
Q

What causes Trichinosis?

A

Trichinella spiralis (nematode); from eating encysted larvae in pig muscle

150
Q

What findings are associated with Trichinosis?

A

Calcified larvae visible on x-ray

151
Q

What is the presentation of Trichinosis?

A

Muscle pain, Periorbital edema

Splinter hemorrhages

152
Q

What invasive infections are caused by group A streptococcus?

A

Necrotizing fasciitis, myositis

153
Q

What is the pathogenesis of invasive group A streptococcus?

A

Exotoxin A (superantigen), Exotoxin B (protease)

154
Q

What is the morphology of C. tetani?

A

Gram-positive anaerobic rod

155
Q

How is tetanus transmitted?

A

Spores enter via closed wounds, skin-popping IVDA, umbilical cord/circumcision site

156
Q

What promotes germination of tetanus spores?

A

Enhanced with necrosis, poor blood supply

157
Q

What is the mechanism of tetanospasmin?

A

Inhibits release of glycine/GABA by binding to ganglioside receptors on spinal afferent fibers

158
Q

What are the presenting features of tetanus?

A

Lockjaw, Risus sardonicus

Opisthotonus

159
Q

What is the role of vaccination in tetanus?

A

No permanent immunity; require tetanus toxoid vaccine every 10 years

160
Q

What are the morphologic features of C. perfringens?

A

Gram-positive anaerobic rod

161
Q

What infections are caused by C. perfringens?

A 
Myonecrosis (gas gangrene), Food poisoning
Sepsis
Peritonitis
PID
Septic endometritis
162
Q

What causes Duchenne muscular dystrophy?

A

X-linked recessive absence of dystrophin

163
Q

What is one of the characteristic physical findings in Duchenne muscular dystrophy?

A

Pseudohypertrophy of calf muscles

164
Q

What is one of the characteristic clinical findings in Duchenne muscular dystrophy?

A

Waddling gait due to weakness of pelvic muscles

165
Q

What lab findings are associated with Duchenne muscular dystrophy?

A

↑↑↑serum CK at birth; ↓as muscles degenerate

166
Q

What causes myotonic dystrophy?

A

CTG trinucleotide repeat; autosomal dominant, most common adult muscular dystrophy

167
Q

What is myotonia?

A

Inability to relax muscles

168
Q

What are the clinical findings in myotonic dystrophy?

A

Sagging face, Frontal balding
Cataracts
Testicular atrophy
Cardiac involvement

169
Q

What is myasthenia gravis?

A

Autonomic disorder of postsynaptic neuromuscular transmission

170
Q

What is the mechanism of myasthenia gravis?

A

Antibodies block and/or destroy ACh receptors

171
Q

What is the most common initial finding of myasthenia gravis?

A

Ptosis; diplopia common

172
Q

What are some other clinical findings in myasthenia gravis?

A

Oropharyngela dysphagia for solids/liquids

173
Q

What is the mechanism of Tensilon?

A

Inhibits acetylcholinesterase

174
Q

What is a Dupuytren contracture?

A

Fibromatosis of palmar fascia

175
Q

What is a Desmoid tumor?

A

Fibromatosis of anterior abdominal wall; associated with polyposis syndromes

176
Q

What is the most common adult sarcoma?

A

Liposarcoma

MS2 Unit 1 (11 decks)

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