Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology II > Bones, Joints, and Tumors > Flashcards

Bones, Joints, and Tumors Flashcards

1
Q

Infectious arthritis joint seeding

A
  • Hematogenous spread
  • Contiguous sites
  • Direct extension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IA contiguous sites joint seeding (periarticular)

A
  • Osteomyelitis

- Soft tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

IA direct extension joint seeding

A
  • Penetrating trauma

- Arthrocentesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Suppurative infectious arthritis etiologies

A
  • Gonococcus
  • Staphylococcus (MRSA)
  • Streptococcus
  • Haemophilus influenzae
  • Pasteurella multocida
  • Eikenella corrodens
  • Fungi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Haemophilus ingluenzae

A
  • Gram-negative bacilli

- Pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology of IA

A
  • Synovial membrane contamination (1st)

- Synovial fluid contamination (2nd)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pathologic features of IA

A
  • Synovial membrane edema
  • Synovial membrane hypertrophy
  • Purulent exudate accumulation
  • Cartilage destruction
  • Fibrin deposition on cartilage
  • Joint destruction / Erosion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Predisposing conditions to acute bacterial arthritis (IA)

A
  • Immune deficiencies
  • Debilitating illness
  • Joint trauma
  • Chronic arthritis
  • Intravenous drug abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Definitive diagnosis of single/multi joint involvement acute bacterial arthritis

A
  • History
  • Aspiration of Synovial Fluid / culture
  • CBC
  • Rapid joint destruction (without treatment)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aspiration of acute bacterial arthritis synovial fluid

A
  • Non-inflammatory effusions (Leukocytes < 3k/uL)
  • Inflammatory effusions (Leukocytes 3k – 75k/uL)
  • Purulent (infectious) effusions (Leukocytes > 50k/uL)
  • Hemorrhagic Effusions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical presentation of infectious arthritis

A
  • Single joint involvement
  • Restricted ROM
  • Fever
  • Leukocytosis
  • Elevated ESR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Differential diagnosis of infectious arthritis

A
  • Cellulitis
  • Bursitis
  • Acute osteomyelitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Single joint infectious arthritis joints/symptoms

A
  • Knee, hip, shoulder, elbow
  • Acutely painful
  • Hot, swollen, erythema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Infections with variable clinical presentation

A
  • Disseminated Gonococcal Infection (DGI)
  • Symptoms are subacute
  • Single joint involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Gonococcal arhtritis

A
  • Bacteremic Infection (Stage): Migratory polyarthritis, tenosynovitis, dermatitis
  • Septic Arthritic: Joint localized (Stage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Manifestations of disseminated gonococcal infection

A
  • Myalgias
  • Fever
  • Chills
  • Rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Joint fluid in disseminated gonococcal infection

A
  • 20k + (> 50) leukocytes / ul
  • Synovial culture (-)
  • Blood cultures (+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Single joint/oligoarthritic pattern of disseminated gonococcal infection

A
  • Subacute
  • Knee
  • Ankle
  • Hip
  • Shoulder
  • Elbow
  • Wrist
  • Sternoclavicular joints
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Axial articulations affected in intravenous drug abuse

A
  • Spine
  • Sacroiliac
  • Sternoclavicular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tuberculous arthritis clinicopathological characteristics

A
  • Hematogenous dissemination (visceral, usually pulmonary, site of infection; adjoining osteomyelitis)
  • Chronic progressive
  • Monoarticular disease
  • Insidious in onset
  • Gradual progressive pain
  • Systemic symptoms vary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Tuberculous arthritis symptoms

A
  • Large weight baring joints
  • Monoarticular pain and swelling (variable time frame)
  • +90% synovial culture
  • Mycobacterium stain red (Fite stain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Tuberculous arthritis clinicopathological characteristics

A
  • Chronic progressive
  • Monoarticular disease
  • Systemic symptoms variable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tuberculous arthritis joint fluid

A
  • 20k / uL ~ 50% neutrophils
  • Acid fast staining
  • Synovial culture
  • PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Mycobacterial seeding of joints in tuberculous arthritis

A
  • Confluent granulomas
  • Central caseous necrosis
  • Pannus over the articular cartilage
  • Bone erosions along the joint margins
  • Fibrous ankylosis and obliteration of the joint space
  • Severe destruction
  • Weight-bearing joints
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pott’s Disease (associated wwith tuberculous arthritis)

A
  • Extrusion of disc after collapse of vertebra
  • Tuberculous pus and granuloma with lysis and collapse of bone
  • Anterior extrusion of pus to form psoas abscess
  • Posterior extrusion of pus into dura
  • Bamboo spine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Seronegative spondyloarthropathies: Ankylosing Spondylitis (AS)

A
  • Reactive Arthritis (ReA)
  • Psoriatic Arthritis (PsA)
  • Ulcerative colitis
  • Crohn disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ankylosing spondylitis primary sites of involvement

A
  • Vertebrae
  • Sacro – iIio – lumbar and areas (prominent region of tendon and ligament insertions)
  • Enthesis (point of tendon, ligament or muscle insertion into bone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Enthesitis

A
  • Inflammation at tendon/ligament/muscle insertion sites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Ankylosing spondylitis

A
  • Chronic inflammatory joint disease

- Sacroiliac infiltration (CD4 and CD8+ T cells, macrophages and high [TNF-α])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Ankylosing spondylitis symptoms

A
  • Usually 2nd and 3rd decades of life
  • Men 2-3x > frequently than woman
  • 80 - 90% of individuals are HLA-B27 positive
  • No specific lab test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

AS pathogenesis

A
  • Enthesopathy (inflammation)
  • Mononuclear cell infiltrate
  • PMN
  • Tumor Necrosis Factor (high levels)
  • CD4+ T cells
  • CD8+ T cells
  • Macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

AS pathology

A
  • Chronic synovitis
  • Destruction of articular cartilage
  • Bony ankylosis
  • Tendinoligamentous inflammation and ossification
  • Bony outgrowths (syndesmophytes) –> severe spinal immobility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Syndesmophytes

A
  • Osseous excrescence attached to a ligament
  • Bamboo Spine
  • Feature of AS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Ankylosing Spondylitis

clinicopathologic features

A
  • Chronic progressive
  • Low back pain
  • Peripheral joints (hips, knees, and shoulders)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Ankylosing spondylitis complications

A
  • Fracture of the spine
  • Uveitis
  • Aortitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Reactive arthritis (formerly Reiter Syndrome) associations

A
  • Genitourinary (Chlamydia)
  • Gastrointestinal tract infections (Shigella, Salmonella, Yersinia, Campylobacter)
  • Symptoms emerge 2-3 wks after infection
  • 80% + HLA-B27
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Reactive arthritis triad

A
  • Arthritis
  • Urethritis / Cervicitis
  • Conjunctivitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Reactive arthritis autoimmune reaction (prior infection)

A
  • Organisms associated with enteric Infections

- Immunologic responses against lipopolysaccharide components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Pathology of reactive arthritic autoimmune response

A
  • Enthesitis

- Macrophage infiltration of fibrocartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Reactive arthritis clinicopathological conditions

A
  • Arthritic symptoms (painful)
  • Develop within weeks of urethritis or diarrhea
  • Joint stiffness and low back pain
  • Asymmetrical (additiveknee/ankle)
  • Synovitis
  • Ossifications
  • Severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Reactive arthritis is indistinguishable from

A
  • Ankylosing spondylitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Extra-articular involvement of reactive arthritis

A
  • Circinate Balanitis
  • Keratoderma blenorrhagica
  • Plaques / erosions of tongue
  • Painful erosions on hands / fingers
  • Conjunctivitis
  • Cardiac conduction abnormalities
  • Aortic regurgitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Circinate balanitisis

A
  • Serpiginous ring-shaped dermatitis of the glans penis
  • One of the most common cutaneous manifestations of reactive arthritis
  • However,balanitiscircinata can also occur independently
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Keratinized skin, mucousy discharge (also called keratoderma blennorrhagica)

A
  • Skin lesions commonly found on the palms and soles in reactive arthritis
  • May spread to the scrotum, scalp and trunk
  • Lesions may resemble psoriasis
45
Q

Reactive arthritis prognosis

A
  • Self-limiting (resolution 3-12 months)

- Arthritis waxes and wanes (several weeks to months)

46
Q

50% of patients with reactive arthritis experience

A
  • Recurrent arthritis
  • Tendonitis
  • Fasciitis
  • Lumbosacral back pain
47
Q

Crystal-Induced Arthritis

A
  • Deposition of calcium pyrophosphate crystals within joint space
  • Occurs in patients > 50 years old; both sexes affected equally
  • Knee most commonly affected joint
48
Q

Crystal-induced arthritis diagnostic findings

A
  • Chondrocalcinosis (cartilage calcification) on x-ray

- Crystals are rhomboid and weakly ⊕ birefringent under polarized light (blue when parallel to light)

49
Q

Crystal-induced arthritis treatment and prophylaxis

A
  • Acute treatment: NSAIDs, colchicine, glucocorticoids

- Prophylaxis: colchicine

50
Q

Gout

A
  • Caused by precipitation of monosodium urate crystals in joints
51
Q

Risk factors for gout

A
  • Male sex
  • Hypertension
  • Obesity
  • Diabetes
  • Dyslipidemia
  • Hyperuricemia (strongest risk factor)
52
Q

Causes of gout

A
  • Underexcretion of uric acid (90% of patients)

- Overproduction of uric acid (10% of patients)

53
Q

Underexcretion of uric acid

A
  • Idiopathic
  • Potentiated by renal failure
  • Exacerbated by certain medications (eg, thiazide diuretics)
54
Q

Overproduction of uric acid

A
  • Lesch-Nyhan syndrome
  • Increased cell turnover (eg, tumor lysis syndrome)
  • von Gierke disease
55
Q

Uric acid crystals in gout

A
  • Needle shaped and ⊝ birefringent under polarized light

- Yellow under parallel light, blue under perpendicular light

56
Q

Osteoarthritis (DJD) characteristics

A
  • Degeneration of cartilage

- Structural and functional failure of synovial joints

57
Q

3 phases of chondrocyte changes in OA

A
  1. Chondrocyte injury
  2. Early OA
  3. Late OA
58
Q

Chondrocyte injury (phase 1 OA)

A
  • Genetic

- Biomechanical factors

59
Q

Early OA (phase 2)

A
  • Chondrocyte proliferation
  • Secrete inflammatory mediators
  • Remodeling of cartilaginous matrix
  • Initiation secondary inflammatory changes in the synovium and subchondral bone
60
Q

Late OA (phase 3)

A
  • Repetitive injury and chronic inflammation
  • Chondrocyte drop out
  • Marked loss of cartilage
  • Extensive subchondral bone changes
61
Q

OA morphology (1)

A
  • Fissures and clefts at the articular surface occur
  • Chondrocytes die
  • Full-thickness portions of the cartilage are sloughed
  • Dislodged pieces of cartilage and subchondral bone tumble into the joint, forming loose bodies (joint mice)
62
Q

OA morphology (2)

A
  • Exposed subchondral bone plate becomes the new articular surface
  • Bone eburnation
  • Fracture gaps force synovial fluid into the subchondral
  • Fibrous-walled cysts develop
  • Bony outgrowths develop at the margins
63
Q

OA clinical course

A
  • Insidious disease

- Asymptomatic until 50s

64
Q

Characteristic symptoms of OA

A
  • Deep, achy pain that worsens with use, morning stiffness , 20min
  • Crepitus, limitation ROM
  • Only one or a few joints are involved (asymmetrical)
65
Q

Joints commonly involved in OA

A
  • Hips, Knees, lower lumbar, cervical vertebrae
  • Proximal and distal interphalangeal joints of the fingers
  • First carpometacarpal joints, first tarsometatarsal joints
66
Q

Heberden nodes

A
  • Prominent osteophytes at the DIP joints (common in women)

- Feature of OA

67
Q

Impingement on spinal foramina by osteophytes (OA)

A
  • Results in cervical and lumbar nerve root compression
  • Radicular pain
  • Muscle spasms
  • Muscle atrophy
  • Neurologic deficits
68
Q

Rheumatoid Arthritis

A
  • Chronic inflammatory disorder of autoimmune origin
  • Affect many tissues and organs
  • Principally attacks the joints
69
Q

Rheumatoid arthritis produces

A
  • Non-suppurative proliferative and inflammatory synovitis
70
Q

Pathogenesis of rheumatoid arthritis

A
  • Mediated by antibodies against self-antigens
  • Cytokine-mediated inflammation (secreted by CD4+ T-cells)
  • Autoantibodies generated specific for citrullinated peptides (CCPs)
71
Q

Citrullination

A
  • Arginine residues are post-translationally converted to citrulline
  • Antigen-antibody complexes containing citrullinated fibrinogen, type II collagen, α-enolase and vimentin deposit in the joints
72
Q

Joint involvement in rheumatoid arthritis

A
  • Symmetric arthritis
  • Small joints of the hand and feet
  • Synovium
73
Q

Joint presentation of rheumatoid arthritis (bulbous villi)

A
  • Edematous
  • Thickened, hyperplastic
  • Dense inflammatory infiltrates
  • Lymphoid follicles
  • Increased vascularity
  • Fibrinopurulent exudate on the synovial and joint surfaces
74
Q

Rheumatoid arthritis effect on joints

A
  • Periarticular erosions and subchondral cysts
  • Pannus formation
  • Pannus bridges the apposing bones to form a fibrous ankylosis
  • Ossification and fusion of bone = bony ankylosis
75
Q

Rheumatoid subcutaneous nodules

A
  • Most common cutaneous lesions of RA

- Approximately 25% of individuals with severe disease

76
Q

Regions of the skin most affected by rheumatoid subcutaneous nodules

A
  • Ulnar aspect of the forearm
  • Elbows
  • Occiput
  • Lumbosacral area
77
Q

RA effects on blood vessels

A
  • Acute necrotizing vasculitis (small and large arteries)
  • Obliterating endarteritis (peripheral neuropathy, ulcers, gangrene)
  • Leukocytoclastic vasculitis (purpura, cutaneous ulcers, nail bed infection)
  • Ocular changes (such as uveitis and keratoconjunctivitis)
78
Q

Clinical presentation of RA

A
  • Symptoms usually develop in the hands (MCP, PIP)
  • Feet, followed by the wrists, ankles, elbows, and knees
  • Progressive joint enlargement
  • Decreased range of motion
  • Ankylosis
79
Q

Diagnosis of RA

A
  • Characteristic radiographic finding
  • Sterile, turbid synovial fluid
  • Combination of rheumatoid factor and anti-CCP antibody (80% of patients)
80
Q

Tumors and tumor-like lesions involving joints and tendons

A
  • Reactive (2° trauma or degenerative processes)
  • Neoplastic (cytogenetic studies reveal consistent chromosomal aberrations)
  • Benign neoplasms
81
Q

Giant cell tumor (benign)

A
  • 20–40 years old
  • Epiphysis of long bones (often in knee region)
  • Locally aggressive benign tumor
  • Significant bone destruction, local recurrence, and occasionally metastasis
82
Q

Giant cell tumor neoplastic mononuclear cells

A
  • Express high levels of RANKL

- Promotes proliferation of reactive multinucleated giant (osteoclast-like) cells

83
Q

Characteristics of giant cell tumor

A
  • Feedback between osteoblasts and osteoclasts is absent
  • “Osteoclastoma”
  • “Soap bubble” appearance on x-ray
84
Q

Morphology of giant cell tumor

A
  • Destroy the overlying cortex
  • Large, red-brown masses
  • Cystic degeneration
85
Q

Giant cell tumor make up

A
  • Sheets of uniform oval mononuclear cells
  • Numerous osteoclast-type giant cells
  • Necrosis and mitotic activity prominent
86
Q

Giant Cell Tumor of tendon Sheath (GCTTS)

A
  • Common localized form of GCTs
  • GCT of the tendon sheath
  • Often found in the hands and feet
87
Q

GCTTS characteristics

A
  • Discrete nodule on a tendon sheath (wrist, fingers)
  • Arise in the 20s – 40s
  • Affect the sexes equally
88
Q

GCTTS clinical presentation

A
  • Solitary
  • Slow-growing
  • Painless mass
  • Cortical erosion
  • Often recurs locally
  • Surgery
89
Q

Morphology of GCTTS

A
  • Localized

- Well circumscribed (walnut shaped)

90
Q

Microscopic presentation of GCTTS

A
  • Polyhedral
  • Histiocytes
  • Multinucleated Giant Cells
  • Resemble synoviocytes
91
Q

Peripheral nerve sheath tumors

A
  • Tumors that show evidence of Schwann cell differentiation
  • Schwannomas (Neurilemmoma)
  • Neurofibromas
  • Malignant Peripheral Nerve Sheath Tumors
  • Neurofibromatosis Type 1 Type 2
92
Q

Schwannomas

A
  • Arise directly from peripheral nerves
  • Benign
  • Encapsulated
93
Q

2 most common benign peripheral nerve sheath tumors

A
  • Schwannomas

- Neurofibromas

94
Q

Ewing sarcoma

A
  • Most common in boys (< 15 years old)
  • Anaplastic small blue cells (neuroectodermal origin)
  • “Onion skin” periosteal reaction in bone
  • Aggressive with early metastases
  • Responsive to chemotherapy
95
Q

Ewing sarcoma location

A
  • Diaphysis of long bones (especially femur)

- Pelvic flat bones

96
Q

Anaplastic small blue cells of Ewing sarcoma differentiate from

A
  • Conditions with similar morphology

- Lymphoma, chronic osteomyelitis

97
Q

Testing for Ewing sarcoma

A
  • T (11;22) (fusion protein EWS-FLI1)
98
Q

Osteosarcoma pathogenesis (molecular mutations)

A
  • 70% have acquired genetic abnormalities
  • RB
  • TP53
  • INK4a
  • MDM2 and CDK4
99
Q

Presentation of osteosarcoma

A
  • Painful (particularly pain with activity)
  • Progressively enlarging masses
  • Sudden fracture of the bone is the first symptom
100
Q

Osteosarcoma radiographs usually show

A
  • Mixed lytic and blastic mass with infiltrative margins
  • Tumor breaks through the cortex and lifts the periosteum
  • Codman triangle
101
Q

Codman triangle (feature of osteosarcoma radiograph)

A
  • Shadow between the cortex and raised ends of periosteum
102
Q

Osteosarcoma (osteogenic sarcoma) occurence

A
  • All age groups
  • Bimodal age distribution
  • 75% in persons younger than 20
  • Second peak occurs in older adults (Paget disease, bone infarcts, prior radiation)
  • Men affected more than women (1.6 : 1)
103
Q

Osteosarcoma (osteogenic sarcoma) often found in

A
  • Metaphysis of long bones (often in knee region)

- Pleomorphic osteoid-producing cells (malignant osteoblasts)

104
Q

Morphology of osteosarcoma

A
  • Arises in the metaphysis of long bones
  • Destroy the surrounding cortices and produce soft tissue masses
  • Spread extensively in the medullary canal, infiltrating and replacing hematopoietic marrow
105
Q

Osteosarcoma description

A
  • Bulky tumors that are gritty, gray-white
  • Often contain areas of hemorrhage and cystic degeneration
  • Tumor cells vary in size and shape and frequently have large hyperchromatic nuclei
  • Bizarre tumor giant cells are common, as are abnormal mitoses
  • Vascular invasion is usually con­spicuous
106
Q

Formation of bone by the tumor cells is diagnostic for

A
  • Osteosarcoma
107
Q

Diagnosis of osteosarcoma

A
  • X-ray

- Biopsy

108
Q

Osteosarcoma prognosis

A
  • Spread hematogenously to the lungs
  • Approximately 10% to 20% have pulmonary metastases at diagnosis
  • Outcome for patients with metastases, recurrent disease or secondary osteosarcoma is poor (<20% 5-year survival rate)

Pathology II (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions