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Pathophys > Joints > Flashcards

Joints Flashcards

1
Q

what are the 2 types of joints and what is characteristic about them

A

1) synarthroses
- Provide structural integrity
- Allow minimal movement
- Lack joint space

2) synovial:
- freely movable
- Dense fibrous capsule reinforced by ligaments & muscles

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2
Q

what are the 2 types of synarthroses

A

1) fibrous synarthroses
- syndesmosis
2) Cartilaginous synarthroses
- symphyses(joined by fibrocartilaginous tissue and firm ligaments):
- Synchondrosis(articular cartilage without synovium)

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3
Q

what joints are syndesmosis, symphyses, synchondrosis

A

Syndesmosis(bones connected by fibrous tissue without cartilage): Cranial sutures, Tibiofibular syndesmosis
Symphyses (joined by fibrocartilaginous tissue and firm ligaments): vertebral bodies
Synchondrosis(articular cartilage without synovium):1st rib and sternum

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4
Q

what are synovial joints AKA

A

cavitated joints

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5
Q

what are the diff types of synovial joints and give examples

A

Uniaxial joint
Movement around only one axis= elbow hinge joint

Biaxial joint
Movement around 2 axes=wrist, thumb

Polyaxial joints
Movement in any axis= ball and socket

Plane joint: articular surfaces glide over one another =patella

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6
Q

what are the 2 types of synoviocytes

A

Type A: macrophage-like synoviocytes
-macrophages with lysosomal enzymes (ability to degrade cartilage)
Type B: FibroBlast-like synoviocytes
-Synthesize hyaluronic acid & proteins (allows for elasticity and fluid)

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7
Q

what does expansion of type B fibroblast like synoviocytes indicate

A

hallmark of RA

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8
Q

what does the synovium control

A
  • Diffusion in and out of the joint
  • Ingestion of debris
  • Secretion of hyaluronate, immunoglobulin and lysosomal enzymes
  • Lubrication of the joints:
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9
Q

how does the synovium lubricate and nourish the joint

A

secret glycoproteins

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10
Q

what is the importance of the synovium lacking a basement membrane

A

allows quick exchange between blood and synovial fluid

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11
Q

what are characteristics of synovial fluid

A

Clear
Viscous
Filtrate of plasma containing hyaluronic acid
Acts as a lubricant and nourishes chondrocytes of the articular cartilage

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12
Q

what is the importance of collagen, water, proteoglycans, and chondrocytes in hyaline cartilage

A 
Type 2 collagen:  tensile strength
Water:  		limits friction
Proteoglycans: 	elasticity
Chondrocytes:  synthesize matrix
-Secrete degradative enzymes in inactive form
-Enrich matrix with enzyme inhibitors
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13
Q

what functions as the elastic shock absorber in synovial joints

A

hyaline cartilage

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14
Q

what is hyaline cartilage AKA

A

articular cartilage

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15
Q

what does hyaline carilage lack

A

Lacks blood supply
No lymphatic drainage
No nerve innervation

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16
Q

what is the pathophys of diseases that destroy the articular cartilage

A

they activate the catabolic enzymes and decrease the production of inhibitor.

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17
Q

what are the different hyaline cartilage zones

A

1) Tangential or gliding zone: Closest to articular surface
- contains Chondrocytes and Type II collagen
2) Transitional zone
- contains Chondrocytes and Hyaline cartilage
3) Radial zone
- Contains Collagen fibers
4) Calcified zone: Calcified matrix
- Contains immature cells as Cartilage cells regenerated here and migrate upward

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18
Q

what is the Tidemark

A

separates radial from calcified zone

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19
Q

what are the 2 types of idiopathic (primary) OA

A

Localized OA: hands, feet, knee, hip, and spine common

Generalized OA: involvement of 3 or more joint sites

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20
Q

what causes secondary OA

A

Trauma

Congenital or developmental

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21
Q

what are typical OA locations with older compared to younger adults

A 
older= wt bearing joints and fingers
younger= joints subject to trauma
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22
Q

why is OA 55 years of age: more common in females

A

estrogen is protective of bone and joints (although more tears of ligaments occur when estrogen is high)

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23
Q

is there a hereditary predisposition to OA

A

yes

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24
Q

what is the pathogenesis of primary OA

A

either 1)damage to normal articular cartilage by physical force or 2)defective cartilage (genetic) fails under normal joint loading =friction is sensed by osteocytes= inc osteoblast function= subchondral bone thickening= nonfunctioning painful joint

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25
Q

how does cracks in articular cartilage cause death of chondrocytes and formation of osteophytes

A

1-Crack in articular cartilage allows influx of synovial fluid
2-Further loss and degeneration of cartilage
3-Cartilage gradually worn away
4-Below tidemark, new vessels grow in from epiphysis & fibrocartilage deposited
5-Fibrocartilage plug is not mechanically sufficient & can be worn away
6-Exposes subchondral bone plate which becomes thickened
7-If there is a crack, synovial fluid leaks into marrow space producing subchondral bone cyst
8-Focal regrowth of articular surface leads to formation of osteophytes

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26
Q

what are the 3 phases of chondrocyte activitye

A

1) Chondrocyte injury: related to age, genetic and biochemical factors
2) Early OA: chondrocytes proliferate and secrete inflammatory mediators, collagens, proteoglycans, and proteases=Act to remodel cartilaginous matrix and initiate secondary inflammatory changes
3) Late OA: repetitive injury and chronic inflammation lead to chrondrocyte drop out, marked loss of cartilage and extensive subchondral bone changes.

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27
Q

how are cytokines involved in OA

A

cytokines (IL-1B, TNF) activate chondrocytes that produce substances (MMP, ADAMTS-4) that destroy cartilage

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28
Q

how is the WNT gene related to OA

A

WNT= inc B-catenin= inc osteoblast activity= inc bone growth

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29
Q

what is COL2A1 gene

A

type 2 collagen gene related to OA

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30
Q

what is chondromalacia

A

Subcategory of osteoarthritis
Patellar surface of femoral condyles
Pain and stiffness of knee

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31
Q

what may X ray show with OA

A

Narrowing of joint space (from Loss of cartilage)

Increased thickness of subchondral bone

Subchondral bone cysts

Large peripheral growths of bone and cartilage (osteophytes)

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32
Q

what is eburnation

A

conversion of bone into hard ivory-like mass

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33
Q

what are joint mice

A

dislodged pieces of cartilage & subchondral bone into the joint

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34
Q

what are osteophytes

A

bony outgrowths develop at margins of articular surface. Capped by fibrocartilage and hyaline cartilage that ossify

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35
Q

what are heberden nodes

A

osteophytes at distal interphalangeal joints

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36
Q

what can RA effect

A

Affect many tissues and organs—mainly joints but also skin, blood vessels, heart, lungs, and muscles

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37
Q

what joints are more likely affected with RA

A

usually bilaterally in Proximal interphalangeal and metacarpophalangeal joints, elbows, knees, ankles and spine

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38
Q

what is characteristic of synovial fluid from RA

A

Produces a NONSUPPURATIVE proliferative and inflammatory synovitis

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39
Q

what does RA progress to

A

Often progresses to destruction of the articular cartilage and ANKYLOSIS of the joints(consolidation of bone).

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40
Q

what is the genetic component of RA

A

HLA proteins and PTPN22 (Tyrosine phosphatase=activates inflammatory cells(B and T cells))

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41
Q

what is seroposative and seronegative RA? which is better prognosis

A 
Seropositive RA (poor prognosis)
High frequency of arginine in the DR epitope
Seronegative RA (good prognosis)
High frequency of lysine in the DR epitope
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42
Q

what is the humoral(antibody) component of RA

A

1)Seroposative-RA has antibodies(IgM RF and either IgG RF or IgA RF), made to HLA-DR4 that bind to the Fc region of other antibodies(IgG) = large structures(IgG RF+IgGFc) that get deposited in joints

2) Seronegative-Abs to citrulline modified peptides (CCP)
- Antibodies to filaggrin with cross reactivity to keratin and perinuclear factor

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43
Q

what is the cellular immunity component of RA

A

T cell activation with production of TNF and IL-1=Increased vascular permeability and activate macrophages= activates B and T cells even more

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44
Q

what is the infectious agent component of RA

A

Antibodies against RANA: RA associated nuclear antigen

RANA is related to nuclear antigen encoded by EBV

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45
Q

how are the synovial cells affected by RA

A

1-Decreased response to glucocorticoids
2-Increased production of hyaluronate
3-Release connective tissue activating peptide which causes increase in prostaglandins (PGE2)

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46
Q

how does RA cause osteoclastogenesis

A

up regulation of RANKL on T-cells and synoviocytes

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47
Q

what is pannus? what causes it?

A

a collection of diff cells that accumulate on the joint surface forming a “cloak” formed by Synovia hyperplasia with mast cells=Contains cells which cause cartilage destruction and erosion of subchondral bone(synoviocytes, osteoclasts and inflammatory cells.)

48
Q

what is produced by pannus? what is its effect

A

collagenase, PGE2, and IL-1 which stimulate osteoclasts =erodes the articular cartilage and adjacent bone

49
Q

where does bone loss occur with RA? what does it lead to?

A

juxta-articular (immediately adjacent to both sides of the joint)

  • Pannus penetrates subchondral bone involving tendons and ligaments
  • Leads to deformities and instabilities
  • Joint undergoes fibrous fusion: ankylosis
  • Long standing cases develop bony bridging: bony ankylosis
50
Q

RA typically starts in the fingers. Where does it progress to?

A

HANDS to WRIST to ELBOWS

51
Q

what are rheumatoid nodules? what are they composed of

A

Movable firm, rubbery and occasionally tender nodles composed of Central core of fibrinoid necrosis and a Rim of macrophages surrounded by lymphocytes, plasma cells

52
Q

where are rheumatoid nodules found

A

found in areas of pressure (ie elbows)

may also be found in vessels causing necrotizing vasculitis

53
Q

what are the s/sx of RA

A 
Symmetrical 
Small joints affected before larger one
Swollen, warm, painful
Stiff on arising or following inactivity
Limitation of motion
Malaise
Fatigue
54
Q

what will Xray show with RA

A

Joint effusions
Juxta-articular osteopenia
Erosions and narrowing of joint space
Loss of articular cartilage

55
Q

how do you diagnose RA

A

4 of the following

MORNING STIFFNESS, MEAN AGE 45 YRS
ARTHRITIS in MORE THAN 3 JOINT AREAS
“TYPICAL” hand findings, MP ULNAR deviation
SYMMETRIC ARTHRITIS
SERUM RHEUMATOID FACTOR
“TYPICAL” X-RAY findings
Rheumatoid nodules
56
Q

what is abatacept

A

T cell modifier to tx RA

57
Q

what is rituximab

A

blocks B cells to tx RA

58
Q

what is anakinra

A

anti IL-1 to tx RA

59
Q

what is tocilizumab

A

anti IL-6R to tx RA

60
Q

what are etanercept, infliximab, and adalimumab

A

anti TNF alpha

61
Q

what is the criteria for Juvenile idiopathic arthritis

A

1-All forms of arthritis that develop before 16 years of age &
2-Persist for a minimum of 6 weeks

62
Q

what are the similarities between RA and JIA

A

Genetic: HLA
Environmental
Inflammatory synovitis and morphologic changes
Abnormal immunoregulation

63
Q

what are the diff between RA and JIA

A

In JIA

  • oligoarthritis(4 or more joints) is more common
  • Systemic disease is more frequent
  • Large joints greater than small joints
  • Rh nodule and Rh factor are usually absent
  • ANA seopositivity is common
64
Q

what is Pauci

A

2-4 joints effected

65
Q

are spondyloarthropathies seroposative or seroneg

A

seroneg

66
Q

what is ankylosing spondylitis? what causes it? what is it AKA

A

fusion of joints caused by HLA-B27

AKA “rheumatoid” spondylitis, or Marie-Strumpell Disease

67
Q

what are spondyloarthropathies

A

ankylosing spondylitis and reactive arthritis

68
Q

what is the involvement of spondyloarthropathies

A

joints: Asymmetric involvement of only a few peripheral joints
Tendency to inflammation of periarticualr tendons and fascia
Systemic involvement of other organs: uveitis, carditis, and aortitis

69
Q

what is the T cell response with spondloarthropathies

A

initiated against unidentified antigen(infectious agent) that cross reacts with native molecules of M/S system

70
Q

what joints are typically affected with ankylosing spondylitis

A

Chronic inflammatory arthropathy that starts at sacroiliac joints joints and works its way up the vertebral column.=spine fuses
May accompany asymmetric peripheral arthritis and systemic manifestations

71
Q

who typically gets ankylosing spondylitis

A

almost exclusively in young men

90% have HLA-B27

72
Q

what is reactive arthritis AKA

A

Reiter syndrome

73
Q

what is the reiter syndrome triad

A

Seronegative polyarthritis
Conjunctivitis/uveitis
Nonspecific urethritis(nongonococcal) or cervicitis

74
Q

what is reiter syndrome associated with

A

follows venereal exposure or episode of bacillary dysentery= common in HIV+

75
Q

what joints are most commonly effected from reiter syndrome

A

ankles, knees, and feet most common but severe chronic dz affects the spine resembling ankylosing spondylitis

76
Q

what is the pattern of symptoms from reiters

A

episodes come and go over weeks to 6 months

77
Q

besides reiters, what is the other type of “reactive” arthritis

A

Enteritis-Associated Arthritis

78
Q

what are the two types of causes of Enteritis-Associated Arthritis

A

1)GI infection:salmonella, shigella, campylobactor
Contain lipopolysaccharides as a major component

2)Ulcerative colitis and crohn disease

79
Q

what is the pattern of symptoms of GI inf causing Enteritis-Associated Arthritis

A

Last approximate 1 year, then clears

80
Q

does resection of the affected bowel in UC and crohns relieve the arthritis in Enteritis-Associated Arthritis

A

only in UC, not in chrons

81
Q

what joints are affected in Enteritis-Associated Arthritis

A

Knees and ankles most common

Can affect wrists, fingers, and toes

82
Q

does enteritits associated arthritis cause ankylosing spondylitis

A

only rarely

83
Q

what is HLA-B27 linked to

A

psoriatic SPONDYLITIS and inflammation of distal interphalangeal joints

84
Q

what is HLA-DR4 associated with

A

rheumatoid pattern of involvement of Psoriatic arthritis

85
Q

what joints are typically affected by psoriatic arthritis

A

Affects peripheral and axial joints

Can also have conjunctivitis and iritis

86
Q

how does the severity of psoriatic arthritis compare to RA

A

Not as severe as RA but remissions more frequent

87
Q

what is infectious arthritis from

A

osteomyelitis (USUALLY SUPPURATIVE

GC, staph, strep, H. flu, E. coli, (Salmonella in sicklers))

88
Q

what are the 4 cardinal signs of infectious arthritis

A

fever, leukocytosis,  ESR, pain

89
Q

what joints are affected most in infectious arthritis

A

knee, hip, shoulder, elbow, wrist then sternoclavicular joints

90
Q

what joints are more commonly affected from infectious arthritis in drug addicts

A

axial articulations (bones along the central axis)

91
Q

how quickly does TB cause infectious arthritis

A

insidious onset since TB is a slow growing organism

92
Q

what does infectious arthritis from TB form

A

Forms confluent granulomas with central caseousnecrosis

93
Q

what is characteristic of joint involvement from LYME dz infectious arthritis

A

remitting and migratory

usually large joints: knee

94
Q

why does LYME dz cause infectious arthritis

A

HLA-DR molecules bind an epitope of the borrelia which initiates a T-cell reaction

95
Q

what might silver stains reveal with LYME dz infectious arthritis

A

a small number of organisms

96
Q

what viral organisms can cause infectious arthritis

A

Parvovirus B19
Rubella
Hepatitis C

97
Q

what is primary and secondary gout

A

primary: hyperuricemia present w/o other dz
secondary: other dz present(often in fast growing malignancies)

98
Q

does hyperuricemia always cause gout

A

no, 10% of population has hyperuricemia (>7 mg/dl), but only 1/20 of these has gout

99
Q

what can cause increase in uric acid

A 
Overproduction
Increased catabolism of nucleic acids
Greater cell turnover
Decreased salvage of free purine bases
Decreased urinary uric acid excretion (most cases of primary gout)
100
Q

how are thiazides related to gout

A

Thiazides reduce excretion of urate (switch to a diff diuretic if gout s/sx begin)

101
Q

what is Probenecid

A

drug that inc uric acid excretion to tx gout

102
Q

what is Apo-E coating

A

inhibit Ab response to gout crystals

103
Q

how long after hyperuricemia will gout sx typically begin

A

Gout rarely appears before 20 to 30 years of hyperuricemia

104
Q

what occurs with mutated HGPRT

A

hypoxanthine transferase involved in the salvage pathway of free purine bases. A mutation inc risk for gout

105
Q

besides age and genetics, what factors inc risk for gout

A

ETOH abuse, Lead toxicity, obesity,drugs (thiazides)

106
Q

what are the manifestations of gout

A

TOPHACEOUS ARTHRITIS
-Tophi: large aggregates of urate crystals
GOUTY NEPHROPATHY
-Urate nephropathy

107
Q

what is the pathology of gout

A
  • Sodium urate crystals precipitate from supersaturated body fluids
  • Precipitated crystals absorb fibronectin, complement and other proteins on their surfaces.
  • Neutrophils that have ingested urate crystals release activated oxygen species and lysosomal enzymes: mediate tissue injury and promote an inflammatory response
  • Cells die releasing crystals stimulating further inflammatory reaction
  • Extracelular soft tissue deposit of urate crystals surrounded by foreign body giant cells(macrophages): TROPHUS
108
Q

what is the spiral of gout

A

attack starts= crystals form= WBC attack= crystals “pop” the cell= cell releases proteins= proteins call in more WBC and cause inflamm/pain and proteins lower pH making it possible for more crystals to form

109
Q

what are Xray findings with gout

A

Punched out juxta articular lytic lesions (Rat bite)

Minimal reactive new bone

110
Q

what is the course of gout dz

A

1)Asymptomatic hyperuricemia: precedes clinical manifestations
-Can last years
2)Acute gouty arthritis: Painful
Involves one joint: later in course of disease is polyarticular
>50% have podagra: painful redened big toe (metatarsophalageal)
Fever
3)Intercritical period
Asymptomatic interval between initial acute attack and subsequent episodes: Can last 10 years
4)Tophaceous gout
Appearance in cartilage, synovial membranes, tendons, and soft tissues.

111
Q

what is podagra

A

painful redened big toe (metatarsophalageal) form gout

112
Q

what are the renal manifestations of gout

A

1)Renal failure
Responsible for 10% of deaths in persons with gout
2)1/3rd have mild albuminuria, reduced GFR & decreased renal concentrating ability
3)Urate Stones
10% of all renal calculi in US are urate stones
Urate stones correlates with serum concentatriton of uric acid
Also have increased freuqency of calcium containing stones (uric acid may serve as a nidus)

113
Q

what other diseases is gout associated with

A

1) Atherosclerosis

2) HTN

114
Q

what is diff bt gout and pseudogout

A

Gout: Monosodium Urate
-younger
Pseudo-GOUT: Calcium Pyrophosphate
-“condition of old age”

115
Q

what is pseudogout AKA

A

CHONDROCALCINOSIS, or CPPD (Calcium Phosphate Deposition Disease)

116
Q

what does secondary pseudogout result from

A

joint damage, hyperparathyroidism, hemochromatosis, hypomagnesemia, hypothyroidism, ochronosis, and diabetes

Pathophys (15 decks)

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