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Pathophysiology II Exam 2 Renal > MSK Module II > Flashcards

MSK Module II Flashcards

1
Q

Components of a synovial joint?

A

-Joint capsule (fibrous joint capsule: articular layer, synovial membrane: inner layer)
-Joint space (cavity)
-Synovial fluid
-Articular cartilage

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2
Q

What kind of cells are found in the synovial membrane?

A

Type A and Type B cells

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3
Q

Role of Type A cells in synovial membrane?

A

Immune function: secrete immunoglobulins, secrete lysosomal enzymes, contain macrophages that ingest debris

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4
Q

Role of Type B cells in synovial membrane?

A

Synovial fluid production:
Secretion of
-HA (hyaluronic acid)
-Glycoaminoglycan “gel” to improve viscosity of synovial fluid
-Lubricating glycoproteins (lubricin: reduces friction in joint)

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5
Q

What structure is enclosed by a capsule filled with synovial fluid?

A

Joint space (cavity)

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6
Q

What is synovial fluid?

A

Clear, viscous fluid that contains: hyaluronic acid and lubricin, proteinases, and collagenases

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7
Q

What is the function of synovial fluid?

A

Lubrication for joint surfaces to create “frictionless” surfaces between bones

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8
Q

What are the thixotropic properties of synovial fluid?

A

Viscosity varying inversely with velocity of movement:
-Rest: resists movement of joint
-Movement: provides less resistance

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9
Q

What is the thin covering on the ends of most bones?

A

Articular cartilage

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10
Q

Function of articular cartilage?

A

Reduces friction, absorbs/disperses compressive force

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11
Q

How much of the articular cartilage is made up of water?

A

60-80%

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12
Q

How much of the articular cartilage is made up of proteoglycans?

A

10-20%

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13
Q

How much of the articular cartilage is made up of collagen fibers?

A

10-20%

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14
Q

How much of the articular cartilage is made up of chondrocytes (chondroblasts)?

A

2%

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15
Q

Function of chondrocytes (chondroblasts) in articular cartilage?

A

Produce and maintain the extra-cellular matrix, secrete components needed to maintain matrix turnover (enzymes, collagen, PGs, etc.)

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16
Q

Function of collagen fibers in articular cartilage?

A

Role in regulating fluid flow in/out of cartilage, arranged to absorb mechanical stress

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17
Q

What kind of collagen fibers are found in articular cartilage?

A

Type 2 collagen

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18
Q

Function of proteoglycans in articular cartilage?

A

Regulate fluid flow in/out of cartilage

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19
Q

What do proteoglycans in articular cartilage consist of?

A

Hyaluronic acid & proteins that anchor glycosaminoglycans (chondroitin and keratin sulfate) to hyaluronic acid

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20
Q

What regulates water content in articular cartilage?

A

PGs, proteins, collagen

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21
Q

Zone of cartilage that has a smooth surface, reduces friction of the joint surface, and is without blood supply?

A

Zone 1 (superficial zone)

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22
Q

Zones of cartilage that are transitional, absorb compressive forces, and are without blood supply?

A

Zones 2 & 3 (middle and deep layers)

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23
Q

Zone of cartilage that is an interface between uncalcified and calcified layers?

A

Tidemark

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24
Q

Zone of cartilage that is calcified, anchors the cartilage to bone, and has blood supply?

A

Zone 4 (calcified cartilage layer)

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25
Q

Function of articular cartilage as a whole?

A

-Provides smooth/frictionless surface for joint movement
-Absorbs and disperses everyday compressive forces passing through joint to underlying bone

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26
Q

Articular health/function requires consistent matrix balance between what?

A

Anabolic and catabolic stimuli

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27
Q

What allows nutrients to pass in and out of articular cartilage/reach the chondrocytes?

A

Repetitive loading/unloading of compressive forces

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28
Q

What activity pushes fluid (water/synovial fluid) out of the cartilage?

A

Weight bearing: fluid flow slows/resistance becomes harder when cartilage is compressed

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29
Q

What activity pulls fluid back into the cartilage matrix (acts like a sponge)?

A

Non-weight bearing forces: proteoglycans, proteins & collagen can regulate fluid flow in/out of cartilage

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30
Q

What maintains articular cartilage matrix homeostasis/turnover?

A

Cytokine signaling/enzymes, hormones, mechanical stimuli

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31
Q

How does anabolic cytokine signaling/enzymes help maintain articular cartilage matrix homeostasis/turnover?

A

Chondrocytes will secrete enzymes and anti-inflammatory cytokines to promote in-matrix homeostasis (anabolic)

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32
Q

How does catabolic cytokine signaling/enzymes help maintain articular cartilage matrix homeostasis/turnover?

A

Chondrocytes may secrete/synovial fluid may contain enzymes & pro-inflammatory cytokines which inhibit in-matrix homeostasis (catbolic)

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33
Q

How do hormones help maintain articular cartilage matrix homeostasis/turnover?

A

Growth hormone and insulin-like growth factor (IGF-1) stimulate chondrocytes/play a role in regulating matrix turnover (anabolic signaling)

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34
Q

How does mechanical load help maintain articular cartilage matrix homeostasis/turnover?

A

Normal weight bearing of daily activity: required to maintain matrix homeostasis (anabolic signaling)

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35
Q

Does articular cartilage have direct blood supply?

A

No

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36
Q

What parts of the articular cartilage do have blood supply?

A

Subchondral bone below cartilage, tidemark, joint capsule

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37
Q

Is articular cartilage innervated by nerves?

38
Q

What parts of the articular cartilage are innervated by nerves?

A

Subchondral bone below cartilage, tidemark, joint capsule

39
Q

Does articular cartilage have good healing properties?

A

No, poor healing/ability to regenerate after injury due to poor blood supply

40
Q

Is articular cartilage pain sensitive?

A

No, pain insensitive
*pain associated w/ joint injuries/pathology does not originate from articular cartilage

41
Q

Where does pain from joint injuries/ pathology originate?

A

Damage to other structures of the joint that are pain sensitive (joint capsule, subchondral bone/periosteum)

42
Q

What is Osteoarthritis (aka degenerative joint disease)?

A

Non-inflammatory joint disease
Yet when acute trauma/physical stress occurs in a joint w/ OA, it signals pro-inflammatory cytokines contribute to further cartilage degeneration

43
Q

What is the most common joint disease?

A

Osteoarthritis (OA)

44
Q

How does normal cartilage appear?

A

Smooth/glossy surface

45
Q

How does cartilage appearance change in osteoarthritis?

A

Becomes a dull yellow/brown color w/ surface flaking fissures & fibrillations

46
Q

What is the primary defect of OA?

A

Cellular disruption of articular cartilage matrix (catabolic signaling exceeds anabolic signaling leading to matrix destruction)

47
Q

Etiologies of OA?

A
  • Genetics
  • Hx of cartilage trauma
  • Lifestyle (smoking, obesity, etc.) increase risk
48
Q

Catabolic enzymatic changes of OA?

A

Chondrocytes and synovium secrete catabolic enzymes that lead to matri breakdown

49
Q

Which catabolic enzyme disrupts proteoglycans by breaking down proteins that anchor glycosaminoglycans to HA?

A

Proteinases

50
Q

Which catabolic enzyme breaks down collagen fibrils and portions of the proteoglycans?

A

Collagenases

51
Q

Pro-inflammatory cytokine signaling in OA?

A

Chondrocytes and synovium secrete IL-1, TNF, other cytokines, nitric oxide that lead to matrix breakdown

52
Q

Role of IL-1 beta and TNF-alpha and others in OA?

A

promote inflammatory catabolic processes

**IL-1 inhibits normal cytokine secretion and stimulates nitric oxide secretion

53
Q

Role of nitric oxide in OA?

A

Not normally found in healthy synovial joint - when present, promotes chondrocyte apoptosis

54
Q

Role of hormone changes in OA?

A

Chondrocytes will become less sensitive to GH/IGF

55
Q

How do catabolic enzyme and cytokine changes lead to cartilage function loss?

A

Loss of proteoglycans, proteins, collagen –> disrupts fluid regulation
*water flows in/out too easily, cartilage loses ability to resist compressive weight bearing force

56
Q

How do catabolic enzyme and cytokine changes lead to cartilage loss?

A

Loss of collagen –> disrupts physical structure of cartilage
*flaking/thinning of cartilage

57
Q

What happens in weight bearing function in OA?

A

Cartilage unable to resist compressive force, water flows out too easily/rapidly

58
Q

What happens to non-weight bearing function in OA?

A

Cartilage will “pull back” too much water, can contain 90+% water

59
Q

What can result from OA promoting damage to surrounding structures?

A

Subchondral bone sclerosis and bone cysts, synovial thickening, osteophyte formation

60
Q

Subchondral bone sclerosis and bone cysts may be asymptomatic until when?

A

They become severe

61
Q

Subchondral bone sclerosis and bone cysts have the potential to communicate with what in the cartilage?

A

Fissures of cartilage (releasing content into synovial fluid of joint space)

62
Q

What can contribute to the loss of gross movement of a joint?

A

Synovial thickening and sometimes osteophyte formation

63
Q

What can occur due to osteophyte formation?

A

Irritation of synovium, may contribute to loss of gross movement

64
Q

What are Herberden’s nodes (OA)?

A

Bony enlargement of the DIP joints from cartilage destruction/osteophytes
“hip-dip”

65
Q

What are Bouchard’s nodes (OA)?

A

Bony enlargement of PIP joints from cartilage destruction/osteophytes

66
Q

Does exercise (running, walking) have any risk for development of OA?

A

Very low or no risk
*high impact sports may increase risk due to traumatic forces/injuries –> twisting high impact movements increase stress

67
Q

Risk factors for the development of OA?

A

-Previous trauma and genetics are MC**
-Age 40/50 and up
-Obesity
-Females > Males
-Others: joint/ligament laxity, inflammatory conditions, neurological disorders

68
Q

How can neurological disorders contribute to development of OA?

A

Loss of normal sensory pathways can result in abnormal movement/damage joint

69
Q

What are the provoking pain patterns of OA?

A

-Morning pain
-Prolonged postural positions
-Increased pain with extreme/intense activity

70
Q

Relieving pain patterns of OA?

A

Feels better w/ easy low impact activity, heat and sometimes cold, OTC NSAIDs

71
Q

Referred pain from OA?

A

-OA of the spine (potential nerve root entrapment)
-OA of LE joints (hip may refer to knee, hip to ankle, knee to hip)

72
Q

How is the joint deformed in OA?

A

Joint capsule thickening

73
Q

What loss of function/mobility is present in OA?

A

-Limited ROM (decreased joint congruency, osteophytes, pain)
-OA of lower extremity: gradual loss of wt bearing activity

74
Q

Treatment strategies for OA?

A

-Lifestyle changes (conservative)
-Pharmaceutical (targeted @ sx relief)
-PT
-Injections (steroids or viscosupplementation)
-Surgery

75
Q

Which surgery options are available for treatment of OA?

A

Arthroscopic lavage/debridement (limited evidence to support use), and joint replacement (arthroplasty) as a last resort if all other tx fails

76
Q

Which injection for OA contains gel-like substances (hyaluronates) thought to improve viscous properties of synovial fluid? How many injections are given over several weeks?

A

Hyaluronic acid injection (viscosupplementation),
1-5 given over several wks

77
Q

Which injection for OA contains growth factors such as fibroblast GF, epidermal GF, vascular endothelial GF, transforming GF-B, and platelet derived GF?

A

Platelet rich plasma (PRP) injection

78
Q

Which injection for OA has better pain relief?

A

PRP injection (yet results not conclusive)

79
Q

Are injections for OA high or low risk procedures?

80
Q

Which procedure has limited evidence effectiveness for routine use for OA according to the American Academy for Orthopedic Surgeons?

A

Arthroscopic lavage and debridement - used as temporary relief for sx, does not repair cartilage

81
Q

Criteria for joint replacement for OA is determined by what?

A

Pain and QOL

82
Q

Does joint replacement for OA have positive outcome rates?

83
Q

Cost of joint replacement in U.S. as of 2020?

84
Q

What are treatment options for cartilage injury?

A

Marrow stimulating techniques (microfracture)
Osteochondral transplants (OATS)
Autologous chondrocyte implantation (ACI)

85
Q

What are marrow stimulating techniques for cartilage injury?

A

Microfracture with growth factor/cytokine augmentation:

Use of a bone pick to penetrate subchondral bone (below tidemark exposing BV and promotes bleeding),
bone marrow bleeding allows fibrocartilage to fill defect

86
Q

Are the long term outcomes of marrow stimulating techniques good or bad?

A

Poor w/ microfracture alone
*current approaches include GF and cytokines!

87
Q

What are osteochondral autograft transplants for cartilage inury?

A

Autografts (from patients own body):
-Osteochondral plugs are taken from non-wt. bearing area of the knee and inserted into pre-drilled holes in the chondral defect

*plugs comprised of hyaline cartilage, but small space around plugs fill w/ fibrocartilage

88
Q

What are osteochondral allograft transplants for cartilage injury?

A

Grafts that come from another person/cadaver:
same as OATS procedure just from cadaver

89
Q

What is an advantage of allografts?

A

Allows for more osteochondral tissue to be taken, larger areas of defect can be repaired

90
Q

What are the phases of autologous chondrocyte implantation (ACI) for cartilage injury?

A

Phase 1: harvest chondrocytes from non-wt bearing area of joint, culture/grow more chondrocytes in lab for 3-6 weeks
Phase 2: Prepare chondral defect/implant new chondrocytes from lab

Pathophysiology II Exam 2 Renal (5 decks)

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