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139 Cards in this Set
- Front
- Back
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Bone pathology
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What are the 3 major components of bone?
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1. Metaphysis (b/w diaphysis & epiphysis)
2. Diaphysis 3. Epiphysis |
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Why does healing of metaphysis occur faster than diaphysis?
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more vascularized
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Bone is made from what type of fiber?
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type 1 collagen
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Bone is also composed of?
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hydroxyappatite
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Mainly what 2 minerals makeup hydroxyappatitie?
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Ca2+ & phosphate
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Cortical vs cancellous bone?
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Cortical -- compact (outside gross bone)
Cancellous -- spongy (inside gross bone) |
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Lamellar vs woven bone?
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Lamellar -- disorganized collagen (present in growing bone or fractured)
Woven -- organized collagen |
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Woven bone is normally found where?
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growing children
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If woven bone found in adults, it is an indication of what?
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pathology
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What are the top 3 cancers that metastatsize to bone?
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PT Barnum
1. Prostate 2. Thyroid 3. Breast |
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How can tumors lead to ↑ bone resorption?
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↑ cytokine signals
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How do you tx disease w/ ↑ osteoclast activity (3)?
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1. Bisphosphonates → (-) osteoclast
2. Calcitonin → PTH antagonist 3. Antibodies for RANK-L |
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What Wolff’s law?
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form follows function; Force applied to bone determines remodeling
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Dysplasia (pathogenesis & major clinical findings)
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What are dysplasias?
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bone growth disorders
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Osteogenesis Imperfecta (type 1 vs Type 2)
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mt in COL1A1 or COL1A2 → defective synthesis of Collagen 1 → brittle bone
Type 1: Blue sclera, fractures throughout life Type 2: lethal |
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Achondroplasia
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mt Fibroblast Growth Factor Receptor (FGFr) → ↓ chondrocytes (cartilage) at growth plate → dwarfism
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Thanatophic dysplasia
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mt FGFr → telephone receiver femora (arms)
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Osteopetrosis (more common in men or women?)
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malfunction in osteoclasts → sclerosis of cortical bone → fractures
men |
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Osteoporosis (more common in men or women?)
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↓ osteoblast or ↑ osteoclast activity (in cancellous bone)→ ↓ bone mass → fractures
women |
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Paget Disease (osteitis Deformans)
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osteoclast dysfunction → skull enlarged
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Osteomalacia
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Ca2+/ Vit D deficiency → ↑ osteoclast activity (takes ca2+, phophate from bone, mineral bank) → ↓ bone mineralization (excess osteiod) → fractures
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How to differentiate osteiod from vs calcified bone?
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calcified bone is black
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Rickets
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osteomalacia for kids → bowing legs, ricket rosary
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What happens to growth plate of kids w/ rickets?
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↑ growth plate thickness
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What is the histopathological hallmark of hyperparathyroidism in bones?
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microfractures w/ ingrowth of macrophages & brown tumor (giant cells w/ hemorrhage)
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Aseptic (avascular) necrosis of bone
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corticosteroids → disrupt microcirculation, leading to ischemic necrosis of medullary bone!
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The most susceptible bone to avascular necrosis?
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scaphoid
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Osteomyelitis
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infection of bone → necrosis via inflammation (neutrophils enzymatically destroy) → forms sequestrum (dead bone)
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Osteomyelitis via hematogenous route is most common in what age?
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infants & young adults
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Why is osteomyelitis more common in infants & young children than adults?(3)
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1. slow blood flow to long bone
2. Metaphysis & epiphysis have connected blood supply 3. Adults develop growth plate that limits bacterial spread |
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How does the body respond to bone infection?
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↑ inflammatory signals → ↑ bone resorption
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Muscle Pathology
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What are the 2 types of muscles fibers? color? slow or fast twitch? mitochondria content? type of energy production? type of race it comes in handy?
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Type 1-- Red, slow twitch, lots of mito, oxidative phos, long distance
Type 2-- white, fast twitch, little mito, glycolysis, short distance |
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What is normal makeup of the type of muscle fibers?
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mix of type 1 & 2
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What if you see only 1 type of muscle fiber?
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pathology!
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What is muscle atrophy?
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drastic ↓ muscle fiber size
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2 types of atrophy?
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1. neurodegenic
2. type 2 fiber atrophy |
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What causes type 2 fiber atrophy?
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1. corticosteroid use
2. disuse |
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How does neurodegenic atrophy occur?
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neuron dies → muscle dies
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What are the 2 major classes of muscle atrophy? Describe the nature of the disorder?
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1. Dystrophy -- develop after birth → progressive muscle weakness
2. congenital -- develop at birth → fixed muscle weakness |
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What is dystrophin?
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bridges membrane proteins together
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In what 2 disorders do you see messed up dystrophin? which has more severe defect in dystrophin?
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1. Duchenne muscular dystrophy -- severe
2. Becker muscular dystrophy |
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What is the inheritance of both? Therefore more common in?
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x-lined, more common in males
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What is the clinical hallmark of duchenne muscular dystrophy?
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1. Proximal muscle weakness → cower’s sign
2. Pseudohypertrophy of calves |
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What is meant by pseudohypertrophy of calves?
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calves don’t actually get larger, the fat around calves outgrow
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What diagnostic tests can be used to determine the type of dystrophy?
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1. Histochemical stain
2. Western assay |
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How does histochemical stain for dystrophin appear for the following conditions?
1. Normal 2. duchenne muscular dystrophy 3. Becker muscular dystrophy |
1. Normal -- dark dystrophin stain around muscle fiber
2. Duchenne muscular dystorphy -- no dystrophin stain around muscle fiber 3. Becker muscular dystrophy -- faint dystrophin stain around muscle fiber |
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How does western assay for dystrophin appear for the following conditions?
1. Normal 2. Duchenne Muscular dystrophy 3. Becker muscular dystrophy |
1.Normal --dark band
2. Duchenne -- no band 3 Becker -- light band |
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Whereas Duchenne muscular dystrophy affects proximal muscles, what dystrophy affects distal muscles?
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myotonic muscular dystrophy
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What are the 3 clinical hallmarks of myotonic muscular dystrophy?
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1. Myotonia (can’t relax muscles)
2. Hatchet like face 3. frontal blindness |
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What is the defective protein in myotonic muscular dystrophy?
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myosin protein kinase
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What type of muscle fiber is selectively affected?
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type 1 fibers
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How do you dx myotonic muscular dystrophy?
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must have histological TRIAD (all 3)
1. Large # central nuclei 2. Striated annulets 3. Selective atrophy of type 1 fibers |
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What are 5 types of congenital myopathy?
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1. Channelopathy
2. Glycogen storage myopathy 3. Lipid storage myopathy 4. Mitochondrial myopathy 5. Inflammatory myopathy (Polymyositis, dematomyositis) |
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What is clinical hallmark of a channelopathy?
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patient comes in → collapses suddenly → better suddenly
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Clinical hallmark of glycogen storage myopathy?
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red urine (myoglobinuria)
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When do you see sx in glycogen storage myopathy?
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After you eat (glycogen ↑)
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What is the histopathological hallmark of mitochondrial myopathies?
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ragged red fibers
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What muscle does it affect most? Why?
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eyes, lots of mitochondria there
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What are the 2 types of inflammatory myopathies?
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1. Polymyositis
2. Dermatomyositis |
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For polymyositits & dermatomyosistis, What type of inflammatory cells are involved? How does muscle dammage occur?
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Polymyositits -- CD8+ (CTL) → direct fiber damage
Dermatomyosistis -- B-cells & CD4 (helper) → antibody-mediated inflammation → ischemia of blood vessels that feed muscles → indirect damage |
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Histopathological hallmark in polymyositis? Dermatomyosistis?
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Polymyosistis --lymphocytes invade intact fiber
Dermatomyosistis --Perifascicular atrophy |
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Knee
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What are the 3 major structures that stabilize the knee?
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1. Ligaments
2. Meniscus 3. Articular cartilage |
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Ligaments
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What is the function of the ligament (2)?
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1. guide motion
2. Stabilize (lax at low tension, stiff at high tension) |
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What is the major structural protein of the ligament?
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collagen type 1
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Describe ligament structure hierarchy?
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collagen → fibril → fasciles
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What protein holds fasicles together?
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endotenon
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What provides the strength to resist strain in ligaments? (2)
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1. fibrils
2. crimp (waviness of fibrils -- allows it to be more elastic) |
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What is strain?
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stretching force on the ligament that can cause damage
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What is stress?
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ability of ligament to resist strain
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What are the 3 phases of the stress-strain curve w/ increasing strain?
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1. Toe -- no stress (stretch out crimp)
2. Linear -- as strain ↑ , stress ↑ 3. Yield & failure -- strain ↑, no more stress b/c irreversible tissue damage |
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When there is overloading strain on ligaments what precedes structural damage?
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cell death
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What does it mean that ligaments are strain-rate dependent?
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rate the load is applied ~ how fast ligament tenses up to resist
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What does it mean that ligaments are history dependent?
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the more cycles of strain & stress → > ability of ligaments to resist
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What additional feature allows ligaments to resist strain?
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viscoelasticity
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What about the ligament allows it to be viscoelastic?
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ligament is biphasic -- both solids & liquids
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How does viscoelasticity protect ligament?
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force is absorbed in liquids and distributed to the rest of the body
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What are the 2 most vunerable knee ligaments?
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ACL & MCL
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What do knee ligaments prevent? (2)
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1. subluxation (partial disengagement)
2. dislocation (complete disengagement) |
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Damage to a knee ligament is called?
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sprain
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How are ligament sprains graded?
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Grade 1-3
Grade 1 -- overstretch, no damage to ligament Grade 2 --overstretch, damage ligament Grade 3 -- overstretch, torn ligament |
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Which ligament (ACL or MCL) is less likely to heal? Why?
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ACL b/c < vascular
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What are the 2 potential complications due to ACL tears?
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1. Meniscus tear
2. Articular cartilage worn out → osteoarthritic |
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Meniscus
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Where is the meniscus located? Function?
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overlay articular cartilage
Protect articular cartilage |
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What are the 2 types of meniscus?
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Medial & lateral
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Which is more likely to tear?
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medial (more firmly attached)
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Tx goal of meniscus tear?
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preserve functional meniscus and remove damaged meniscus via partial menisectomy
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Articular cartilage
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What type of cartilage makes up articular cartilage?
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hyaline
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What is required for metabolic activity of cartilage?
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movement!
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What happens when no movement at knee joint?
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cartilage can degenerate
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What happens when articular cartilage is damaged?
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osteoarthritis
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Common orthopedic Injuries
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Musculoskeletal Emergencies
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What is the primary survey protocol after a musculoskeletal injury?
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A-- Airway
B-- Breathing C-- Circulation D-- Disability (brain injury) E-- Exposure (look for trauma site) |
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What are the top 4 musculoskeletal Emergencies?
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1. Compartment syndrome
2. Necrotizing fascitis 3. Bite wound 4. Occult fractures |
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What is a musculoskeletal compartment?
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group of muscles wrapped up by fascia
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What is a compartment syndrome? Pathogenesis?
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↑ pressure → ↓ O2 (perfusion) → necrosis
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What is a major complication due to dead muscle tissue?
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kidney damage ( ↑ CPK)
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Clinical hallmark of compartment syndrome? What are the late signs?
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pain out of proportion at passive muscle movement → numbness
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What are the external factors that can lead to compartment syndrome? Internal factors?
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↑ pressure from outside (i.e cast) or ↑ volume from inside (i.e: internal bleeding)
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How do you tx compartment syndrome?
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fasciotomy → cut fascia, let muscles spill out → ↓ pressure
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What type of tissue is affected in necrotizing fascitis?
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subcutaneous & skin, not muscle!
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Do all cases of necrotizing fascitis have prior trauma?
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No!
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what causes necrotizing fascitis?
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bacterial infection
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What are the 3 types of infections? Most common?
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Type 1 -- mix; most common
Type 2 -- staph Aureus Type 3 --vibrio |
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What are the first 3 things you do when someone comes in with a bite wound?
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1. IV antibiotics
2. tetatnus 3. X-ray for dislodged teeth |
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What are occult fractures?
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fractures that are difficult to detect on x-ray
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What is the danger of occult fractures?
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lead to avascular necrosis (AVN)
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Most common occult fracture?
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scaphoid
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Which occult fracture is a major orthopedic ER?
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femoral head from hip fracture
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What is the blood supply to the femoral head and neck?
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medial circumflex femoral artery
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How do you fix hip fracture? (2 methods) What method is used depends on?
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1. Internal fixation -- good intact blood supply
2. Arthroplasty -- blood supply is disrupted |
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Who is at most risk for hip fractures?
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females & elderly
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Other Common Orthopedic Injuries
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What are compression neuropathies?
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compress peripheral nerve → loss sensation to myotome
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What are the 2 most common compression neuropathies?
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1. Carpal tunnel syndrome
2. Ulnar nerve syndrome |
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What nerve is damage in carpal tunnel syndrome? Myotome affected?
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median nerve → thumb, 2 fingers, ½ of ring
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What nerve is damaged in ulnar nerve syndrome? Myotome affected?
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ulnar nerve → pinky, ½ ring
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What is the common name to lateral epicondylitis? Clinical hallmark?
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tennis elbow → lateral epicondyle bone pain
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How do you differentiate radial tunnel syndrome w/ lateral epicondylitis?
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radial tunnel -- tissue pain
lateral epicondylitis -- bone pain |
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What is sprengle’s deformity?
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shoulder fails to descend!
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Common ddx for sprengle’s? Why is it clearly not this ddx?
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scolosis, b/c it is a problem w/ shoulder not spine
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What are the 2 causes of winged scapula?
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1. Serratus anterior palsy
2. Long thoracic nerve palsy |
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Poland’s syndrome is a syndrome of what muscle, presenting at birth? There are an associated problem where? Why?
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pectoralis
Hands b/c develops at same time as pectoralis during gestation |
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Pediatric Orthopedics
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What bone disorders are common in children? (4)
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1. Achondroplasia (congenital)
2. Osteomyelitis (hematogenous infection) 3. Rickets (Vitaman D or Ca2+ deficiency) 4. osteogenesis imperfecta (congenital) |
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WHat is mucopolysacchardiosis?
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congenital absence of enzyme that digest GAG → GAG accumulates in tissue → progressive disorder
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Ex of a mucopolysacchardosis leading to orthopedic problems in kids?
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Morquio syndrome
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Pathogenesis & CP of Moquio syndrome?
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defect in N-actylgalactosamine or B-galactosidase → genu valgum (knocking knees) & thoracolumbar kyphosis
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Pathogenesis & CP of Marfan’s syndrome?
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mt in Fibrillin 1 → tall & thin, arachnodactylyl (long fingers), ligamentous laxity, cardiovascular problems
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What is fibrillin important for?
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elastin in aortic media & suspensory ligaments
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What is hip dysplasia?
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hip problems due to a structural predisposition (Not a problem w/ enzymes, etc)
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Pathogenesis & CP of Hip dysplasia?
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Thickened cartilage ridge (labrum) or ligamental laxity → subluxation or dislocation of hip joint
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