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Flashcards in Joints Deck (116):
1

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

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

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

2

what are the 2 types of synarthroses

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

3

what joints are syndesmosis, symphyses, synchondrosis

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

4

what are synovial joints AKA

cavitated joints

5

what are the diff types of synovial joints and give examples

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

6

what are the 2 types of synoviocytes

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)

7

what does expansion of type B fibroblast like synoviocytes indicate

hallmark of RA

8

what does the synovium control

-Diffusion in and out of the joint
-Ingestion of debris
-Secretion of hyaluronate, immunoglobulin and lysosomal enzymes
-Lubrication of the joints:

9

how does the synovium lubricate and nourish the joint

secret glycoproteins

10

what is the importance of the synovium lacking a basement membrane

allows quick exchange between blood and synovial fluid

11

what are characteristics of synovial fluid

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

12

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

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

13

what functions as the elastic shock absorber in synovial joints

hyaline cartilage

14

what is hyaline cartilage AKA

articular cartilage

15

what does hyaline carilage lack

Lacks blood supply
No lymphatic drainage
No nerve innervation

16

what is the pathophys of diseases that destroy the articular cartilage

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

17

what are the different hyaline cartilage zones

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

18

what is the Tidemark

separates radial from calcified zone

19

what are the 2 types of idiopathic (primary) OA

Localized OA: hands, feet, knee, hip, and spine common
Generalized OA: involvement of 3 or more joint sites

20

what causes secondary OA

Trauma
Congenital or developmental

21

what are typical OA locations with older compared to younger adults

older= wt bearing joints and fingers
younger= joints subject to trauma

22

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

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

23

is there a hereditary predisposition to OA

yes

24

what is the pathogenesis of primary OA

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

25

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

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

26

what are the 3 phases of chondrocyte activitye

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.

27

how are cytokines involved in OA

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

28

how is the WNT gene related to OA

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

29

what is COL2A1 gene

type 2 collagen gene related to OA

30

what is chondromalacia

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

31

what may X ray show with OA

Narrowing of joint space (from Loss of cartilage)

Increased thickness of subchondral bone

Subchondral bone cysts

Large peripheral growths of bone and cartilage (osteophytes)

32

what is eburnation

conversion of bone into hard ivory-like mass

33

what are joint mice

dislodged pieces of cartilage & subchondral bone into the joint

34

what are osteophytes

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

35

what are heberden nodes

osteophytes at distal interphalangeal joints

36

what can RA effect

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

37

what joints are more likely affected with RA

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

38

what is characteristic of synovial fluid from RA

Produces a NONSUPPURATIVE proliferative and inflammatory synovitis

39

what does RA progress to

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

40

what is the genetic component of RA

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

41

what is seroposative and seronegative RA? which is better prognosis

Seropositive RA (poor prognosis)
High frequency of arginine in the DR epitope

Seronegative RA (good prognosis)
High frequency of lysine in the DR epitope

42

what is the humoral(antibody) component of RA

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

43

what is the cellular immunity component of RA

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

44

what is the infectious agent component of RA

Antibodies against RANA: RA associated nuclear antigen
RANA is related to nuclear antigen encoded by EBV

45

how are the synovial cells affected by RA

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

46

how does RA cause osteoclastogenesis

up regulation of RANKL on T-cells and synoviocytes

47

what is pannus? what causes it?

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

what is produced by pannus? what is its effect

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

49

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

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

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

HANDS to WRIST to ELBOWS

51

what are rheumatoid nodules? what are they composed of

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

where are rheumatoid nodules found

found in areas of pressure (ie elbows)
may also be found in vessels causing necrotizing vasculitis

53

what are the s/sx of RA

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

54

what will Xray show with RA

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

55

how do you diagnose RA

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

what is abatacept

T cell modifier to tx RA

57

what is rituximab

blocks B cells to tx RA

58

what is anakinra

anti IL-1 to tx RA

59

what is tocilizumab

anti IL-6R to tx RA

60

what are etanercept, infliximab, and adalimumab

anti TNF alpha

61

what is the criteria for Juvenile idiopathic arthritis

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

62

what are the similarities between RA and JIA

Genetic: HLA
Environmental
Inflammatory synovitis and morphologic changes
Abnormal immunoregulation

63

what are the diff between RA and JIA

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

what is Pauci

2-4 joints effected

65

are spondyloarthropathies seroposative or seroneg

seroneg

66

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

fusion of joints caused by HLA-B27

AKA “rheumatoid” spondylitis, or Marie-Strumpell Disease

67

what are spondyloarthropathies

ankylosing spondylitis and reactive arthritis

68

what is the involvement of spondyloarthropathies

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

what is the T cell response with spondloarthropathies

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

70

what joints are typically affected with ankylosing spondylitis

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

who typically gets ankylosing spondylitis

almost exclusively in young men
90% have HLA-B27

72

what is reactive arthritis AKA

Reiter syndrome

73

what is the reiter syndrome triad

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

74

what is reiter syndrome associated with

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

75

what joints are most commonly effected from reiter syndrome

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

76

what is the pattern of symptoms from reiters

episodes come and go over weeks to 6 months

77

besides reiters, what is the other type of "reactive" arthritis

Enteritis-Associated Arthritis

78

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

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

2)Ulcerative colitis and crohn disease

79

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

Last approximate 1 year, then clears

80

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

only in UC, not in chrons

81

what joints are affected in Enteritis-Associated Arthritis

Knees and ankles most common
Can affect wrists, fingers, and toes

82

does enteritits associated arthritis cause ankylosing spondylitis

only rarely

83

what is HLA-B27 linked to

psoriatic SPONDYLITIS and inflammation of distal interphalangeal joints

84

what is HLA-DR4 associated with

rheumatoid pattern of involvement of Psoriatic arthritis

85

what joints are typically affected by psoriatic arthritis

Affects peripheral and axial joints
Can also have conjunctivitis and iritis

86

how does the severity of psoriatic arthritis compare to RA

Not as severe as RA but remissions more frequent

87

what is infectious arthritis from

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

88

what are the 4 cardinal signs of infectious arthritis

fever, leukocytosis,  ESR, pain

89

what joints are affected most in infectious arthritis

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

90

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

axial articulations (bones along the central axis)

91

how quickly does TB cause infectious arthritis

insidious onset since TB is a slow growing organism

92

what does infectious arthritis from TB form

Forms confluent granulomas with central caseousnecrosis

93

what is characteristic of joint involvement from LYME dz infectious arthritis

remitting and migratory
usually large joints: knee

94

why does LYME dz cause infectious arthritis

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

95

what might silver stains reveal with LYME dz infectious arthritis

a small number of organisms

96

what viral organisms can cause infectious arthritis

Parvovirus B19
Rubella
Hepatitis C

97

what is primary and secondary gout

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

98

does hyperuricemia always cause gout

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

99

what can cause increase in uric acid

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

how are thiazides related to gout

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

101

what is Probenecid

drug that inc uric acid excretion to tx gout

102

what is Apo-E coating

inhibit Ab response to gout crystals

103

how long after hyperuricemia will gout sx typically begin

Gout rarely appears before 20 to 30 years of hyperuricemia

104

what occurs with mutated HGPRT

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

105

besides age and genetics, what factors inc risk for gout

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

106

what are the manifestations of gout

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

107

what is the pathology of gout

-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

what is the spiral of gout

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

what are Xray findings with gout

Punched out juxta articular lytic lesions (Rat bite)
Minimal reactive new bone

110

what is the course of gout dz

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

what is podagra

painful redened big toe (metatarsophalageal) form gout

112

what are the renal manifestations of gout

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

what other diseases is gout associated with

1) Atherosclerosis
2) HTN

114

what is diff bt gout and pseudogout

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

115

what is pseudogout AKA

CHONDROCALCINOSIS, or CPPD (Calcium Phosphate Deposition Disease)

116

what does secondary pseudogout result from

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