Brainscape's Knowledge GenomeTM

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


See full index

NMSP Exam 2 (for the Gunners) > Chapter 26: Joints > Flashcards

Chapter 26: Joints Flashcards

1
Q

What are the 3 major components of hyaline cartilage?

A

70% H2O + 10% type II collagen + 8% proteoglycans

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

Which joints are most commonly affected in osteoarthritis in men vs. women?

A
  • Men = hips
  • Women = hands and knees
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 phases of changes to chondrocytes seen with the pathogenesis of osteoarthritis?

A
  • Chondrocyte injury, related to genetic and enviornmental factors
  • Early OA: proliferation for remodeling of cartilaginous matrix and secondary inflammatory changes
  • Late OA: repetitive injury and chronic inflammation lead to chondrocyte drop out, marked cartilage loss, and extensive subchondral bone changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which cytokines and diffusable factors have been implicated in the pathogenesis in osteoarthritis?

A
  • TGF-β –> which induces MMP’s
  • TNF
  • Prostaglandins
  • Nitric oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are 3 characteristic morphological findings of osteoarthritis?

A
  • Hunks of dead cartilage sloughed into the joint –> ‘joint mice’
  • Subchondrondal bone exposed and rubbed smooth = eburnation
  • Microfractures and cysts develop
  • Mushroom-shaped osteophytes (bony outgrowths)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Deep, achy pain that worsens with use, morning stiffness, crepitus, and limitation of ROM is characteristic of what?

A

Osteoarthritis

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

What are the prominent osteophytes which may form at the PIP and DIP joints of pt with osteoarthritis called?

A
  • PIP = Bouchard’s nodes
  • DIP = Heberden node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which joint disease may progress to deformity with time and which may progress to fusion?

A
  • OA may progress to joint deformity, not fusion
  • RA progresses to fusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

OA is a disease of what vs. RA?

A
  • OA = disease of cartilage
  • RA = disease of synovium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which inflammatory cells may initiate the autoimmune response in RA and how?

A

CD4+ T helper cell by reacting with an arthritogenic agent, perhaps microbial or a self-antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the most important cytokines isolated from the inflammed joint in person with RA; what is their role in the disease?

A
  • IFN-γ from TH1 cells activate macrophages and resident synovial cells
  • IL-17 from TH17 cells recruit neutrophils and monocytes
  • TNF and IL-1 from macrophages stimulate resident synovial cells to secrete proteases that destro__y hyaline cartilage
  • RANKL on activated T cells stimulate bone resportion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which cytokine has been most firmly implicated in the pathogenesis of RA?

A

TNF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Many of the autoantibodies produced in the lymphoid organs and in the synovium of pt with RA are specific for what?

A

Citrullinated peptides (CCPs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are 2 genetic factors associated with RA?

A

HLA-DRB1 alleles & PTPN22 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are 5 characteristic histologic features of RA?

A
  • Synovial cell hyperplasia and proliferation
  • Dense inflammatory infiltrates of CD4+ cells, B cells, plasma cells, dendritic cells, and macrophages
  • ↑ vascularity due to angiogenesis
  • Fibrinopurulent exudate on synovial and joint surfaces
  • Osteoclastic activity in underlying bone –> periarticular erosions ad subchondral cysts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which characteristic mass of edematous synovium, inflammatory cells, granulation tissue, and fibroblasts growing over articular cartilage is seen in joints affected by RA?

A

Pannus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

With time in RA, the pannus bridges apposing bones to form what?

A

Fibrous ankylosis, which eventually ossifies and results in fusion of the bones, called bony ankylosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which skin lesions are commonly seen in RA, what is their morphology?

A
  • Rheumatoid nodules: firm, non-tender, and round arising in subcutaneous tissue
  • Resemble necrotizing granulomas w/ central zone of fibrinoid necrosis + prominent rim of macrophages, lymphocytes and plasma cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are rheumatoid nodules most commonly seen?

A

Extensor surfaces at pressure points

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How may the blood vessels of patient with RA be affected and which vessels specifically?

A
  • Risk of acute necrotizing vasculitis of small and large arteries
  • May involve the pleura, pericardium or lung evolving into chronic fibrosing process
  • Obliterating endarteritis —> peripheral neuropathy, ulcers, and gangrene may occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Inflammation in the tendons, ligaments, and occassionally adjacent skeletal muscle accompanying RA produces what characteristic findings in the hands?

A
  • Radial deviation of the wRrist
  • UlNar deviation of the fiNgers
  • Boutonniere: deformity of finger –> hyperextension of DIP w/ flexion of PIP
  • Swan-neck: hyperextension of PIP, flexion of DIP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the radiographic hallmarks of RA?

A

Joint effusions and juxta-articular osteopenia w/ erosions and narrowing of the joint space + loss of articular cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diagnosis of RA, especially with presence of multisystem involvement, is supported by what 3 findings?

A
  • Characteristic radiohgraphic findings
  • Sterile, turbid synovial fluid w/ ↓ viscosity, poor mucin clot formation, and inclusion-bearing neutrophils
  • Combo of rheumatoid factor and anti-CCP antibody
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do the joints being affected differ between OA and RA?

A
  • OA: usually large, weight bearing joints
  • RA: symmetrical pattern w/ small joints affected first
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does activity affect the pain in OA vs. RA?

A
  • OA = worse with activity
  • RA = improves with activty, worse with rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What may develop in the knee as increased intra-articular pressure causes herniation of synovium in some pt’s with RA?

A

Baker cyst of the posterior knee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which ocular changes due to blood vessel involvement may be seen with RA?

A

Uveitis and Keratoconjunctivitis

28
Q

Which heterogenous group of disorders present with arthritis before age 16 and persist for at least 16 weeks?

A

Juvenile idiopathic arthritis (JIA)

29
Q

In what 5 ways is Juvenile idiopathic arthritis (JIA) different than RA?

A
  • Oligoarthritis = more common
  • Systemic dz is more frequent
  • Large joints affected more often
  • Rheumatoid nodules and rheumatoid factor typically absent
  • Antinuclear antibody (ANA) is common
30
Q

What are the 4 features unifying the seronegative spondyloarthropathies?

A
  • Changes in ligamentous attachments rather than synovium
  • Involvment of the SI joint +/- others
  • Absence of RF
  • Association of HLA-B27
31
Q

What joints involved in ankylosing spondylitis and typical presentation?

A
  • Destruction of articular cartilage and bony ankylosis, typically of sacroiliac and apophyseal joints
  • Involvement of SI joint & vertebrae becomes symptomatic in 2nd - 3rd decade of life as LBP and spinal immobility
32
Q

Who is most affected by reactive arthritis and at what age?

A
  • Men in their 20s or 30s
  • Also affects pt’s with HIV
33
Q

Reactive arthritis most often follows what?

A
  • GU infection –> Chlamydia
  • GI infection –> Shigella, Salmonella, Yersinia, or Campylobacter
34
Q

What are the common early sx’s of reactive arthritis and which joints are most often affected?

A
  • Early sx’s = joint stiffness + LBP
  • Ankles, knees, and feet are affected most often; frequently asymmetric
35
Q

What are the extra-articular manifestations that may be seen with reactive arthritis?

A
  • Inflammatory balanitis
  • Conjunctivitis
  • Cardiac conduction abnormalities
  • Aortic regurgitation
36
Q

Involvement of the digital tendon sheath in reactive arthritis produces what?

A

Sausage fingers or toes

37
Q

What is the typical presenation of enteric associated arthritis, joints involved, and how does it differ in course from reactive arthritis?

A
  • Appears abruptly tends to involve knees and ankles; sometimes the wrists, fingers,andtoes
  • Lasts for about a year vs. reactive arthritis which wax and wanes for about 6 weeks
38
Q

Sx’s of psoriatic arthritis typically manifest when and predominantly consist of what?

A
  • Between ages 30-50 y/o
  • Predominantly a peripheral arthritis of hands and feet
  • DIP joints affected 1st, asymmmetric distribution –> “pencil in cup” deformity
39
Q

Gonococcal arthritis has a predilection for which sex; how does the presenation differ from other casuses of suppurative arthritis?

A
  • Mainly sexually active women
  • Presents in a more subacute fashion
40
Q

What is the classic presentation of suppurative arthritis and what are the systemic findings?

A
  • Sudden development of acutely painful and swollen joint w/ restricted ROM
  • Fever + leukocytosis + ↑ ESR
41
Q

90% of nongonococcal cases of suppurative arthritis involve how many joints and which joints are most frequently affected?

A

Single joint, most commonly the knee > hip > shoulder > elbow > wrist > SC joint

42
Q

Pt’s with deficiency of complement MAC (C5, C6, C7) are at greater risk for suppurative arthritis from which organism?

A

Gonoccocal infections

43
Q

How is suppurative arthritis diagnosed?

A

Joint aspiration yielding purulent fluid in which causal agent is identified

44
Q

Which joints are most often affected in Lyme Arthritis and what is course of the disease?

A
  • Primarily large joints –> knee > shoulder > elbow and ankles
  • 1-2 joints at a time, attacks last few weeks to months, migration to new sites
45
Q

How may lyme arthritis be diagnosed?

A
  • Spirochetes identified in joints w/ arthritis in about 25% of cases
  • Serologic testing for anti-Borrelia antibodies
46
Q

Hyperuricemia is a plasma urate level of what?

A

>6.8 mg/dL

47
Q

Which syndrome is due to a complete absence of HGPRT interrupting the purine salvage pathway resulting in hyperuricemia?

A

Lesch-Nyhan syndrome –> Mental retardation + Self-mutilation + 2’ gout

48
Q

Describe the inflammatory response following the precipitation of MSU crystals into joints and contribution to gout.

A
  • Inflammasome recognizes crystals –> activates caspase-1 —> prod. of IL-1β —> accumulation of neutrophils + MΦ’s in joint
  • Urate crystals may also activate complement –> chemotactic complement byproducts
49
Q

Describe how the solubility of MSU in a joint is modulated by both temperature and the chemical composition of the fluid?

A
  • Synovial fluid is inherently a poorer solvent for MSU than plasma
  • Lower temp. of peripheral joints also favors precipitation
50
Q

How long does it take a patient with hyperuricemia to typically develop gout?

A

20-30 years

51
Q

What are the 4 distinct morphological changes in gout?

A

1) Acute arthritis
2) Chronic tophaceous arthritis
3) Tophi in various sites
4) Gouty nephropathy

52
Q

What is the pathognomonic hallmark of gout; where are they seen?

A
  • Tophi = large aggregations of urate crystals surrounded by intense inflammatory rx of foreign body giant cells
  • Articular cartilage, ligaments, tendons, and bursae; sometimes soft tissues (earlobes, fingertips) or kidneys
53
Q

Which drug may reduce the excretion of urate and contribute to the development of gout?

A

Thiazide diuretics

54
Q

Which heavy metal toxicity may contribute to gout?

A

Lead toxicity –> saturnine gout

55
Q

Where do MSU crystals deposit in kidney and what are some of the complication which arise with gouty nephropathy?

A
  • Deposit in the renal medullary interstitium or tubules
  • Complications = uric acid nephrolithiasis + pyelonephritis, particularly when urates induce urinary obstruction
  • 20% of chronic gout –> death due to renal failure
56
Q

In the final stage of gout progression, chronic tophaceous gout, what will characteristically be seen on radiographs?

A

Juxta-articular bone erosion due to osteoclastic bone resorption and loss of joint space

57
Q

When does gout vs. pseudo-gout typically develop and in whom?

A
  • Gout = more common in men and after age 30
  • Pseudo-gout = both sexes equally affected and occurs in pt’s >50 y/o becoming more common w/ ↑ age
58
Q

An autosomal dominant variant of pseudo-gout leading to the development earlier in life is due to germline mutations in what?

A

Pyrophosphate transport channel

59
Q

Secondary form of pseudo-gout is associated with what underlying conditions?

A
  • Previous joint damage
  • Hyperparathyroidism
  • Hemochromatosis
  • Hypomagnesemia
  • Ochronosis
  • Diabetes
60
Q

What do the crystals of pseudo-gout form and how are they seen histologically?

A
  • Form chalky, white, friable deposits
  • Seen histologically as oval blue-purple aggregates
  • Individual crystals are rhomboid and positively birefringent
61
Q

Where is a common location for ganglion cyst’s to arise, how to they appear, and arise as a result of what?

A
  • Around joints of wrist
  • Firm, fluctuant, pea-sized translucent nodule
  • Arise as result of cystic or myxoid degeneration of CT; hence the cyst wall lacks a cell lining
62
Q

What is a synovial cyst and what is a common example of one?

A
  • Herniation of the synovium thru a joint capsule or massive enlargement of a bursa
  • Baker cyst seen in popliteal space in setting of RA
63
Q

What are common locations to find the diffuse vs. localized type of tenosynovial giant cell tumor; occur in which age group?

A
  • Diffuse = tends to involve large joints; commonly knee (80%)
  • Localzied = usually occurs as discrete nodule attached to tendon sheath, commonly in hand
  • Both occur in pt’s 20-40 y/o; both sexes equally
64
Q

Which reciprocal translocation is seen with tenosynovial giant cell tumors and what does this mutation cause?

A
  • t(1;2) —> fusion of type VI collagen α-3 promoter upstream of the coding sequence of M-CSF
  • Leads to overexpression of M-CSF –> stimulates macrophage proliferation
65
Q

What is the behavior of the localized type of tenosynovial giant cell tumors; how common are they?

A
  • Manifests as solitary, slow-growing, painless mass that frequently involves tendon sheaths along wrists and fingers
  • Most common mesenchymal neoplasm of hand
66
Q

What is characteristic morphology of the diffuse type of tenosynovial giant cell tumor?

A

Joint synovium converted into tangled mat by red-brown folds + finger-like projections and nodules

67
Q

How does the diffuse type of tenosynovial giant cell tumor commonly present?

A
  • Commonly knee > hip > ankle > calcaneocuboid joints, pt’s typically complain of pain + locking + recurrent swelling
  • As tumor grows joint becomes stiff –> ↓ ROM
  • Sometimes a palpable mass can be appreciated
  • Aggressive tumors erode into adjacent bones and ST’s

NMSP Exam 2 (for the Gunners) (19 decks)

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