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DMD 5246 > Bikman - Musculoskeletal Pathology > Flashcards

Bikman - Musculoskeletal Pathology Flashcards

1
Q

What are the functions of osteoblasts, osteocytes, and osteoclasts?

A

Osteoblasts: Produce osteoid (unmineralized bone)

Osteocytes: Osteoblasts within bone in a lacuna

Osteoclasts (macrophage): Multinucleated, resorbs bone

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2
Q

What regulates RANK-RANKL?

A

Osteoprotegerin (OPG)

OPG-RANKL then decreases osteoclast formation and bone-resorption

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3
Q

Congenital bone disorders

A

Osteogenesis imperfecta
Achondroplasia
Osteopetrosis
Fibrous dysplasia

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4
Q

Acquired bone disorders

A 
Osteoporosis
Paget disease
Rickets-Osteomalacia
Hyperparathyroidism
Scurvy
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5
Q

Osteogenesis imperfecta

A 
Congenital
"Brittle bone disease"
Mutations of collagen type I (alpha1 and 2)
Autosomal dominant
Multiple fractures
*Blue sclera*
Hearing loss
*Dentinogenesis imperfecta - dysplasia, lack of healthy dentin*
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6
Q

Achondroplasia

A 
Congenital
Most common form of dwarfism
*FGFR3 mutation*
- Inhibited chondrocyte proliferation
- Repressed growth of normal epiphyseal plates
- Autosomal dominant
- 80% are new mutations

Avg life span
Affects all bonds that develop via endochondral ossification

Thanatophoric dwarfism (lethal)

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7
Q

Osteopetrosis

A

Congenital
“Albers-Schonberg disease”; like stone

Reduced osteoclast-mediated bone resorption

  • Defective bone remodeling
  • Abnormally dense, yet unsound/brittle

Autosomal recessive and dominant

Can cause anemia and infections (due to decreased bone marrow); blindness, deafness, face paralysis (due to narrowing of cranial nerve foramina); delayed eruption of teeth

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8
Q

Fibrous Dysplasia

A

Congential
Replacement of bone with fibrous CT
Not a malignancy; reduction in healthy bone function

3 types:

(1) Monostotic - affects one bone (most common)
(2) Polyostotic - “Jaffe-Lichtenstein syndrome”; affects more than one bone, cafe au lait pigmentation on trunk and thighs
(3) McCune-Albright Syndrome - Polyostotic and precocious puberty

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9
Q

Osteoporosis

A

Acquired
An acquired condition characterized by reduced bone mass, not reduced quality.

  • Loss of bone: increased fragility, increased fracture risk
  • Existing bone has normal mineral content (just less of it)

Primary: You don’t know what’s causing it.
Secondary: You know what’s causing it.

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10
Q

Factors contributing to osteoporosis

A 
Menopause
- Decreased estrogen, increased osteoclast activity
Aging (senile osteoporosis)
- Decreased replicative activity of osteoprogenitor cells
- Decreased osteoblast activity
-Reduced physical activity
Nutrition
- Reduced Ca2+ and reduced vitamin D
Decreased physical activity
Endocrine
- Hyperparathyroidism
- Addison disease
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11
Q

Paget Disease

A

Acquired
“Osteitis deformans”
Random excess bone formation; net effect is bone mass gain; frenzied bone growth

(1) Repetitive episodes of frenzied, regional osteoclast activity, and resorption - Osteolytic stage
(2) Exuberant bone formation - Mixed osteoclastic-osteoblastic stage
(3) Exhaustion of cellular activity - Osteosclerotic stage

Can cause

  • Osteosarcoma
  • Heart disease
  • Deafness or blindness
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12
Q

Rickets-Osteomalacia

A

Acquired
“Soft bones”

Primary cause is vitamin D deficiency
Inadequate mineralization of bone
Rickets: Children - epiphyseal plates open
Osteomalacia: Adults - plates closed
Weak tooth enamel, increased caries
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13
Q

What is the role of parathyroid hormone?

A

Net effect: Increase in plasma Ca2+ concentration

  • Increase active transport of Ca2+ out of the proximal and distal tubule of kidney
  • Increase Ca2+ release from bone into the plasma (Ca2+ mobilization)
  • Stimulates the kidney to activate vitamin D, bringing in more Ca2+
  • Lowers plasma phosphate concentration by increasing renal excretion of phosphate (prevents precipitation of calcium phosphate from the blood into bone)
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14
Q

What inhibits PTH secretion?

A

Plasma Ca2+ concentration

Active vitamin D

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15
Q

Hyperparathyrodism

A

Acquired.
Too much PTH

Primary: Almost always growth/tumor related
- Excess secretion of PTH from one or more parathyroid glands
Secondary: Some other problem causing too much PTH
- Increase in PTH from a chronic disease that causes hypocalcemia (i.e. renal failure)

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16
Q

What effect might hyperparathyroidism have on teeth?

A

Loss of lamina dura, ground glass appearance, and mandibular cortical width reduction

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17
Q

Scurvy

A

Acquired
Too little vitamin C
Leads to impaired osteoid matrix formation

Manifestations:

  • Bleeding gums
  • Subperiosteal hemorrhage
  • Osteoporosis
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18
Q

Langerhans’ cell histiocytosis

A

Acquired
“Histiocytosis X”; “Langerhans’ cell granuloma”
A group of disorders that exhibit histiocyte-like Langerhans cells that cause bone lesions (and others)
Langerhans cells contain Birbeck granules and eosinophils

3 types:

(1) Letterer-Siwe disease: Acute, disseminated, fatal in infants
(2) Hand-Schuller-Christian disease: Chronic (because you can live longer with it)
- Bone lesions - skull, mandible, vertebrae, ribs
- Exophthalmos (bulging eyes)
- Diabetes insipidus (polyuria with no particular taste)
(3) Eosinophilic Granuloma of bone: Localized, least severe; May overcome without tx; more common in young adults

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19
Q

Fractures

A

Repair process:

(1) Fracture ruptures BVs
(2) WBC activated
- Clot formation
- Bone progenitor cells recruited
- New matrix synthesis
(3) New matrix synthesis

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20
Q

Osteonecrosis

A

Bone death.
Ischemia causes loss of bone - no infection

May be result of:

  • Trauma
  • Bone infarction (emboli)
  • Corticosteroids
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21
Q

Bisphosphate-associated osteonecrosis (BON)

A

Occurs in patients with history of bisphosphonate use.

  • Drugs aimed at neutralizing osteoclasts - Actonel, Boniva, Fosamax
  • Effects are highest among bones with active remodeling (jaw)

Develops after manipulation of bone, extraction, implant, perio or endo surgery

Caution and informed consent for patients >3yr on drug

Phossy jaw

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22
Q

Osteomyelitis

A

Inflammation of bone and bone marrow.
Can be secondary to systemic infection but more frequently occurs as a primary isolated focus

2 types:
Pyogenic
Tuberculous

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23
Q

Pyogenic Osteomyelitis

A

Most causes of acute osteomyelitis are caused by bacteria.

Bacteria reaches bone:

(1) Hematogenous (blood borne) dissemination
(2) Contiguous (touching/spreading) infection spread
(3) Traumatic implantation (via fracture or procedure)

Most common causative organism is Staph. aureus

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24
Q

Tuberculous Osteomyelitis

A

Mycobacterial infection of the bone - gets there via hematogenous dissemination

Bone infections accompany 1-3% of pulmonary TB
Long bones and vertebrae are favored sites.
Pott Disease: Vertebral deformity, collapse, posterior displacement

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25
How do bone tumors typically arise?
Primary bone tumors are uncommon. Usually the tumor has metastasized to the bone. - Bone forming - Cartilage forming - Misc.
26
Benign bone-forming bone tumors
Osteoma - Face, skull - 40-50yrs - Similar to normal bone Osteoid osteoma - Metaphysis femur, tibia - 10-20yrs - Woven bone Osteoblastoma - Vertebral column - 10-20yrs - Similar to osteoid ostoma
27
Malignant bone-forming bone tumors
Primary Osteosarcoma - Metaphysis of distal femur - 10-20yrs - Sun burst pattern on rads Secondary Osteosarcoma - Femur, humerus, pelvis Jaw osteosarcoma occurs about a decade after long bones are affected. Typically includes elevated plasma alkaline phosphatase. Codman Triangle is a feature.
28
Benign cartilage-forming bone tumors
Osteochondroma - Metaphysis of long bones - 10-30yrs Enchondroma - Small bones of hands and feet - 30-50yrs - Medullary cavity
29
Malignant cartilage-forming bone tumors
Chondrosarcoma - Femur, humerus, pelvis - 40-60yrs - Within medullary cavity; malignant cells form cartilage (abnormal)
30
Miscellaneous bone tumors
Giant Cell Tumor of Bone - Epiphysis of long bones - 20-40yrs - Cortical lesions Ewing Sarcoma - Small, undifferentiated round cells - 10-15yrs - Genetic component (whites more affected) - Diaphysis of long bones
31
How do most bone cancers arise?
Most bone cancers arise from metastatic tumors. | 75% arise from prostate, breast, kidney, lung
32
Osteoarthritis
Degenerative joint disease *Most common joint disorders* Common in 65+ yrs Fundamental feature: degeneration of the articular cartilage Primary: - Appears insidiously with age - No apparent cause Secondary: - Common form in youth - Caused by trauma, deformity, diseases, etc
33
What is the progression of osteoarthritis?
1. Bone 2. Cartilage 3. Thinning of cartilage 4. Cartilage remnants 5. Destruction of cartilage
34
Rheumatoid Arthritis
Systemic, chronic inflammatory autoimmune diseases. Destruction of articular cartilage and underlying bone. Rare - more common in women Bilateral Likely a combination of genetics (HLA and PTPN22) and the environment. Type IV sensitivity. CD4+ THCs RHEUMATOID FACTOR
35
Stages of rheumatoid arthritis
(1) Healthy (2) Synovitis (3) Pannus Formation (4) Fibrous Ankylosis (5) Bony Ankylosis
36
Atlanto-axial dislocation
Occurs in rheumatoid arthritis. - Instability at joint between C1-C2 due to laxity of ligaments and cartilage destruction with RA - Causes neck pain, difficulty swallowing and talking
37
Seronegative Spondyloarthropathies
Pathologic changes that originate in the ligamentous attachment (not the synovium) NO RF! But does look like RA HLA associated
38
Gout
Uric acid accrual in tissues Monosodium urate crystals precipitate from supersaturated body fluids - Induce inflammation - Gouty tophi 2 ways of occurring: via neutrophils/complement or monocytes Primary and Secondary
39
Hyperuricemia via neutrophils
(1) Precipitation of urate crystals in joints (2) Complement activation (3) Phagocytosis of cystals (4) Lysis and activation of neutrophils (4. 5) Release of crystals (5) Release of lysosomal enzymes
40
Hyperuricemia via monocytes
(1) Precipitation of urate crystals in joints (2) Phagocytosis by monocytes (3) Release of cytokines
41
Primary Gout
Hyperuricemia in the absence of other disease - Enzyme defects Altered (high or low) uric acid renal secretion
42
Secondary Gout
Cause of hyperuricemia is known. - Leukemia - Renal disease - Metaolic defects Consequences: Joint pain, renal failure, urate stones
43
Pseudogout
Chondrocalcinosis "Calcium pyrophosphate crystal deposition" 50+yrs Crystal deposits in joints trigger inflammation (similar to gout)
44
Suppurative Arthritis
Infectious Arthritis Microorganisms can lodge in joints during hematogenous dissemination - Haemophilus influenzae in kids - S. aureus and N. gonorrhea in adults - Those with deficient complement are suspectible - Joint aspiration typically yields purulent fluid
45
Lyme Arthritis
Infectious Arthritis Microorganisms can lodge in joints during hematogenous dissemination Caused by infection with spirochete: Borrelia burgadorferi Advances in stages: (1) Tick passes spirochetes (2) Spirochetes spread (3) 2-3yrs after infection, symptoms appear as arthritis
46
Tumor types
Ganglion | Synovial cysts
47
Ganglion Tumors
A small tendon cyst (fluid filled) Often near wrist "Bible therapy"
48
Synovial Cyst Tumors
Herniation of synovium through a joint capsule
49
Tenosynovial giant cell tumor
Catchall term for several benign neoplasms of synovium
50
Lipoma
Adipose Tumor Benign tumors of fat Most common soft tissue tumor
51
Liposarcoma
Adipose Tumor Malignant neoplasms with adipocyte differentiation 50-60yrs Prognosis depends on differentiation
52
Nodular Fasciitis
Fibrous Tumor/Tumor-like Lesions Self-limited fibroblastic proliferation Forearm, chest, back Rarely recurs after excision
53
Fibromatosis
``` Fibrous Tumor/Tumor-like Lesions Benign lesion Does not metastasize Superficial (superficial fascia) Deep (abdominal wall and muscles) ```
54
Fibrosarcoma
Fibrous Tumor/Tumor-like Lesions Highly malignant neoplasms of fibroblasts Deep tissue of thigh, knee, and retroperitoneal area Often recur after excision "Herringbone pattern"
55
Fibrohistiocytic Tumors
A mix of neoplastic fibroblasts and myofibroblasts
56
Benign Fibrous Histiocytoma
Fibrohistiocytic Tumors "Dermatofibroma" Common benign mobile nodules in the dermis or subcutaneous tissue Tx'd by excision
57
Pleomorphic Fibroblastic Sarcoma
Fibrohistiocytic Tumor Usually large, gray-white mass Often in the extremities Exhibit a swirling pattern - hard to tell cell of origin
58
Rhabdomyoma
Skeletal muscle tumor | Commonly in the tongue or heart
59
Rhabdomyosarcoma
Skeletal muscle tumor Most common soft tissue sarcoma Aggressive neoplasm Before 20yrs Usually appears at head and neck or genitourinary tract (little skeletal muscle) Large skeletal muscle fibers with prominent nuclei
60
Leiomyoma
SM Tumor Well-circumscribed neoplasms arising from SM Most common in uterus
61
Leiomyosarcoma
SM Tumor 10-20% of soft tissue tumors More common in females Most common in skin and deep soft tissues
62
Synovial Tumors
Synoviocyte neoplasm <10% are intra-articular 10% of all soft tissue tumors Most common in 20-40yrs Biphasic and Monophasic
63
Biphasic Synovial Tumor
Epithelial type cells Spindle cells Glandlike histology
64
Monophasic Synovial Tumors
Spindle cells only
65
Inherited SM disorders
Dystrophies: Progressive, early-onset diseases Myopathies: Perinatal or early childhood diseases with static deficits
66
Dystrophies
Inherited SM disorder X-linked Loss of function/mutation in the dystrophin gene
67
Duchenne Muscular Dystrophy
Inherited SM disorder X-linked Loss of function/mutation in the dystrophin gene Wheelchair bound by teens Lethal by early adulthood
68
Becker Muscular Dystrophy
Inherited SM disorder X-linked Loss of function/mutation in the dystrophin gene Slower progression Partial dystrophin function Nearly normal lifespan
69
Myotonic Dystrophy
Inherited SM disorder X-linked mutationss in the gene encoding dystrophia myotinica protein kinase (DMPK) Manifests in late childhood - Gait abnormalities - Sustained involuntary contractions - Atrophy of facial muscles, ptosis
70
Myopathies
Inherited SM disorder Perinatal or early childhood diseases with static deficits Defect in: - Ion channels: Channelopathy - Metabolism: Metabolic Myopathy - Mitochondria: Mitochondrial Myopathy
71
Channelopathy
Myopathy - Myotonia - excessive contraction - Hypotonia - NO contraction - Or both
72
Mitochondrial Myopathy
Myopathy - Maternal inheritance - Manifestation - proximal muscle weakness, ocular impairment
73
Acquired SM Disorders
A diverse group of disorders that manifest with muscle weakness, muscle cramping, or muscle pain Inflammatory myopathies Toxic myopathies
74
Inflammatory Myopathies
Acquired SM disorder (1) Polymyositis (2) Dermatomyositis (3) Inclusion Body Myositis
75
Polymyositis
Acquired SM disorder > Inflammatory Myopathy - Autoimmune disorder - CD8 CTCs - Myofiber necrosis and regeneration - Tx'd with corticosteroids
76
Dermatomyositis
Acquired SM disorder > Inflammatory Myopathy - Most common in children - Autoimmune - Rash and muscle weakness
77
Inclusion Body Myositis
Acquired SM disorder > Inflammatory Myopathy - Most common in adults >60yrs - "Alzheimer" of the muscle - protein aggregates in the muscle
78
Intrinsic Toxic Myopathy
Acquired SM disorder > Toxic Myopathy Thyrotoxic Myopathy - Muscle weakness from hyperthyroidism
79
Extrinsic Toxic Myopathy
Acquired SM disorder > Toxic Myopathy Ethanol Myopathy - Rhabdomyolysis from excess alcohol consumption - Renal failure form myoglobinurea Drug Myopathy - Rhabdomyolysis from drugs - Statins
80
Myasthenia Gravis
Autoimmune disease in which Ab's are produced against AchR localized to the NMJ - This decreases the number of functional AchR's Dx: - Electromyography - Cholinesterase inhibitor test (edrophonium) Clinical manifestations: - Muscle weakness - Fatigue - In a myasthenic crisis, the muscle weakness can become so severe that muscle movement can be completely inhibited and the patient dies from respiratory failure

DMD 5246 (3 decks)

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