Brainscape's Knowledge GenomeTM

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


See full index

Pathology Term 4 > Week 5 - ARTHRITIS > Flashcards

Week 5 - ARTHRITIS Flashcards

Rheumatoid Arthritis, Osteoarthritis, Gout, Other

1
Q

What is ankylosis?

A
  • bone fusion
  • causes abnormal stiffening and immobility of a joint
  • result of RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is RA referred to as a multisystem disorder?

A

also affects skin, heart, BV, Lungs - similar to SLE

*mainly affects joints obviously

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

What is the genetic component of the etiology of RA?

A

HLA DRB1 in 75% pts.

-PTPN22 gene polymorphism

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

What infection in particular is related to etiology of RA?

A

? EBV

-environmental factor –> N.B. smoking is also an important environmental factor in the development of RA

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

What autoimmune factors are involved in etiology of RA?

A
  • IgM anti-IgG (Rheumatoid Factor - RF) –> IgM Abs that recognise the Fc portion of native IgG Abs
  • Anti-CCP Ab
  • T lymphocytes against collagen + cartilage glycoprotein 39
  • macrophages around RF –> type III (immune complex)
  • CCP –> cyclic citrullinated peptides (collagen, fibrinogen, vimentin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are CCP?

A
  • cyclic citrullinated peptides (collagen, fibrinogen, vimentin)
  • enxymatic modification (citrullination) of self-protein –> leads to production of anti-CCP antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the important cytokines/chemical mediators involved in RA pathogenesis?

A
  • IL-8
  • VEGF –> production of new BVs
  • TNF
  • IFN-gamma

**Th17/Th1 cells + Abs –> inflammatory response (cytokines) –> proliferation of synovium –> pannus formation (bone/cartilage destruction, fibrosis, ankylosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is pannus?

A
  • abnormal layer of fibrovascular/granulation tissue
  • comprised of lymphocytes, macrophages + plasma cells
  • results in destruction of bone, cartilage, fibrosis + ankylosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where are neutophils seen in RA: proliferative synovitis?

A
  • in the synovial fluid

- non-suppurative inflammation (no pus), sterile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are rice bodies?

A

-organising fibrin in joints of proliferative synovitis/RA

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

What occurs as a result of the extending inflammation in RA: proliferative synovitis?

A
  • juxta-articular osteopaenia, erosions, cysts, fibrosis (sclerosis) + ankylosis (fibrosis mainly, rarely bony)
  • loss of articular cartilage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the key difference in progression of disease between OA + RA?

A

RA:
-inflammation starts in synovium and extends/damages cartilage

OA:
-inflammation starts in cartilage and damage then extends to synovium

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

What is swan neck deformity and why does it occur?

A
  • flexion of DIP + extension of PIP
  • inflammation, scarring and contraction of muscles/tendons –> swan neck deformity
  • seen in RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why is morning stiffness typical of early stage RA?

A
  • synovial inflammation with excess fluid causes pain
  • movement/activity aids absorption of excess fluid which relieves pain Sx.
  • after nights sleep (morning) pt. has been immobile for a long period of time –> exacerbated stiffness due to inflammation/fluid accumulation (lack of absorption)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

True or False?

Arthritis in RA is usually asymmetrical

A

False

-usually symmetric arthritis (systemic) in 3 or more joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical features of RA?

A
  • start with malaise, fatigue, MSK pains (IL-1/TNF)
  • morning stiffness (synovial inflammaton/excess fluid)
  • arthritis in 3 or more joints
  • symmetric arthritis (systemic)
  • rheumatoid nodules on skin (i.e. elbow)
  • serum rheumatoid factor
  • radiographic changes –> swan neck, Z-deformity, boutonniere deformity (PIP flexion with DIP extension), ulnar deviation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is RA diagnosed?

A
  • characteristic radiographic findings
  • sterile, turbid synovial fluid (decreased viscosity/mucin clot formation + neutrophils with inclusions)
  • combination of RF + anti-CCP Ab (80% of pts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the most commonly affected joints in RA?

A
  • hands
  • foot
  • knees
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are examples of extra-articular RA?

A
  1. rheumatoid nodules
  2. iridocyclitis, uveitis, SICCA syndrome
  3. vasculitis
  4. pleuritis, pericarditis
  5. tendonitis
  6. lung: fibrosing alveolitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are rheumatoid nodules?

A
  • degeneration of collagen tissue surrounded by macrophages (granuloma)
  • generally occurs at pressure points (i.e. elbows)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are novel biologic agents in RA therapy?

A
  • anti-TNFalpha –> etanercept, infliximab, golimumab, pegol
  • anti-B cell –> rituximab
  • T-cell costimulation blocker –> abatacept
  • anti-IL –> anakinra (IL-1 RA) and tocilizumab (anti-IL-6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are long term complications of RA therapy?

A
  • immunosuppressive therapy (steroids) –> increased infections
  • amyloidosis (5-10%pts.) from long term increased Abs in body (secondary amyloidosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

After how long in a patient with persistent joint swelling should referral be made?

A

-if persistent swelling beyond 6wks (even in RF +/or anti-CCP negative) –> refer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the differences between RA + OA?

A

RA:

  • young age, small joints
  • autoimmune/recurrent
  • synovial inflammation
  • synovium –> cartilage

OA:

  • old age, large joints
  • degenerative/progressive
  • cartilage degeneration
  • cartilage –> synovium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the common end result of OA/RA?

A
  • total destruction of joint
  • deformity
  • ankylosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the clinical differences between RA + OA?

A

RA:

  • sharp, severe pain relieved by activity
  • morning pain + stiffness
  • reduce with activity (early)
  • swan neck
  • boutonniere’s
  • ulnar deviation of MCP joints
  • z deformity

OA:

  • deep, mild pain exacerbated by activity
  • morning stiffness and crepitus
  • increases with activity
  • fusiform joint swelling
  • heberden’s/bouchards nodes (bony)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the etiology of osteoarthritis?

A
  • 95% primary/idiopathic –> ageing (>80% in >80yrs
  • 5% secondary in young –> trauma, obesity, deformity

*OA = “cartilage degeneration”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which joints are more commonly affected in OA?

A
  • weight bearing/most used joints –> limited ROM, deformity, instability
  • F –> knees + hands
  • M –> hips + spine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the classic presentation for OA?

A
  • stiffness, mild pain (morning*) –> lasts at least 1 hour

- increases with activity (c.f. RA - decreases with activity)

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

What is the pathogenesis of OA?

A

-progressive loss of chondrocyte (ageing, genetic, metabolic) –> erosion + fibrillation (breakdown) of articular cartilage –> forms Loose bodies

  • *3 stages:
    1. chondrocyte injury: genetics, wear & tear
  1. early OA: inflammation, proliferation of chondrocytes, releaase proteases –> softening of cartilage
  2. late OA: total loss of chondrocytes + matrix damage –> fissuring (breakdown of cartilage) –> entry of synovial fluid into cartilage/bone –>”eburnation”, subarticular cyst, sclerosis, osteophytes
31
Q

What is eburnation?

A
  • thickening + conversion of bone into a hard, ivory-like mass
  • occurs in late OA as a result of fissuring/cartilage degeneration leading to entry of synovial fluid into cartilage/bone
32
Q

What is the pathogenesis of subarticular cysts in OA?

A

-fissuring/degeneration of cartilage causes entry of synovial fluid + proteases into cartilage + bone –> dissolution of bone (subarticular/subchondral cysts)

33
Q

What are gross + microscopic features of OA?

A

Gross:

  • eburnation
  • subchondral/subarticular cysts
  • residual cartilage
  • sclerosis

Micro:

  • cartilage fissuring/flaking
  • loss of chondrocytes
  • Loose bodies (joint mice) - pieces of cartilage that remain in the joint
  • suabrticular cysts
  • eburnation/sclerosis (trabecular thickening)
34
Q

What is the pathogenesis of osteophyte formation in OA?

A
  • loss of cartilage causes exposure of bone

- grinding of bones causes surrounding reactive new bone formation (on edges) –> AKA bone spurs

35
Q

What are the radiological findings in OA?

A
  • non-uniform joint space loss (narrow joint space)
  • loose bodies (remaining cartilage)
  • deformity, osteophyte (bone spurs on edges)
  • subchondral cysts + sclerosis (due to synovial fluid entering cartialge/bone)
36
Q

True or False?

Bow leg/varus deformity of the knee can be seen in OA

A

True

-as a result of collapse of the joint space with destruction of medial cartilage and the subchondral space

37
Q

What occurs as a result of excess osteophyte formation in the fingers in OA?

A
  • fusiform bony owergrowth at the interphalangeal joints
  • Distal –> Heberden nodes
  • Proximal –> Bouchard’s nodes
  • projection of bone on either side of the joint
38
Q

What endogenous crystals are responsible for gout + pseudo gout?

A

Gout –> monosodium urate

Pseudo gout –> calcium pyrophosphate

39
Q

What are the exogenous causes of crystal induced arthritis?

A
  • corticosteroids
  • silicone
  • polyethylene

*anything injected into the joint

40
Q

What is gout due to?

A
  • increased uric acid (hyperuricemia) –> increased production = common/decreased excretion = rare
  • released from purine metabolism via enzyme uricase
  • deposition of monsodium urate crystals in the joints
41
Q

Which 2 organs are prone to monosodium urate crystal deposition?

A
  1. Joints *** first

2. Kidneys

42
Q

What is secondary gout due to?

A
  • 10% (rare)
  • cell breakdown* (cancers)
  • renal disease (decreased excretion)
  • high protein diet
  • alcohol abuse
  • obesity
  • thiazide diuretics
  • lead toxicity
43
Q

What is the usual progression of gout?

A

acute attacks –> remission + repeated attacks –> chronic

44
Q

What occurs in chronic gout?

A

-large deposits of uric acid –> tophus formation (tophaceous)

45
Q

What occurs as a result of uric acid crystal precipitation in joints?

A
  • activation of inflammation –> release of cytokines –> extensive cartilage + joint damage
  • acute activation = neutrophils
  • chronic activation = macrophages (granuloma + giant cells)
46
Q

What are the 4 clinical stages of gout?

A
  1. asymptomatic hyperuricemia
  2. acute arthritis
  3. asymptomatic resolution (+repeated acute attacks)
  4. chronic tophaceous gout
47
Q

What are the renal complications of gout?

A
  • gout nephropathy*
  • lithiasis* (stone formation)
  • renal colic
  • pyelonephritis
  • renal failure
48
Q

What is the microscopy of gouty tophi (chronic) and acute gout?

A

Chronic-:
central monosodium urate crystals/tophus
-surrounding granulomatous inflammation (chronic inflammation) with giant cells
-fibrosis

Acute:
-neutrophils + intracytoplasmic crystals (instead of central core tophus in chronic)

49
Q

What is pseudo gout AKA?

A

-chondrocalcinosis
OR
-Calcium Pyro-Phosphate Disease (CPPD)

50
Q

What is seen in pseudo gout?

A

-calcium deposits within the cartilage/menisci/vertebral discs etc –> opacities within joint spaces on X-ray –> crystals can cause inflammation and pain (acute/subacute/chronic arthritis) but commonly asymptomatic

51
Q

What are the primary and secondary causes of pseudo gout?

A

primary:
-idiopathic* (commonest), genetic

secondary:
-trauma, hemochromatosis, hyperparathyroidism, etc

52
Q

What is typically diagnostic for CPPD?

A
  1. medial/lateral knee compartment opacifications

2. triangular fibrocartilage of the wrist

53
Q

Compare appearance of monosodium urate crystals vs calcium pyrophosphate crystals

A

monosodium urate –> fine, needle like

calcium pyrophosphate –> thick, rhomboid

54
Q

Where are monosodium urate crystals seen in acute gout?

A

-within neutrophils (intracytoplasmic)

55
Q

What is juvenile idiopathic arthritis?

A
  • AKA juvenile RA
  • before age 16yrs, arthritis > 6wks with unknown cause
  • predominantly systemic involvement unlike adult RA –> feverm uveitis, splenomegaly - N.B. NO RA nodules
56
Q

True or False?

RA nodules are present in JIA

A

False

57
Q

Which joints are more commonly affected in JIA?

A
  • oligoarthritis
  • large joints > small joints
  • i.e. knees, ankles, etc
58
Q

True or False?

JIA is ANA (anti nuclear Ab) positive but RF/anti-CCP negative

A

True

  • seronegative
  • it is still autoimmune but not exactly same as RA
  • HLA, PTPN22, inflammation –> same as RA
59
Q

What is Still’s disease?

A
  • one of the 3 subtypes of JIA
  • massive systemic manifestations (i.e. splenomegaly) with little arthritis
  • N.B. other 2 subtypes = oligoarthirits + polyarthritis
60
Q

What are important DDx. for JIA in arthritis in children?

A
  • septic arthritis
  • osteomyelitis
  • trauma
  • tumours
  • ARF
  • IBD
  • Henoch Schonlein Purpura (HPS)
  • SLE
  • Leukemia/Lymphoma (fever/splenomegaly)
61
Q

What is the commonest seronegative arthritis?

A

Ankylosing Spondylitis:

  • HLA B27 + in 90%
  • youth
  • sacroiliac joint with bony ankylosis (fused vertebrae)
  • hips + knees in 30% cases
62
Q

What is the triad of Reiter Syndrome/Reactive Arthritis (ReA)?

A
  1. arthritis
  2. non-gonococcal urethritis
  3. conjunctivitis

(+skin rash, genital rash, fever)

63
Q

What is reiter syndrome initiated by?

A
  • chlamydia bacteria

- still an autoimmune disorder (HLA B27)

64
Q

What is enteropathic arthritis caused by?

A
  • salmonella/shigella bowel infections
  • autoimmune –> HLA B27+
  • development of arthritis after the bowel infection is cleared
65
Q

What % of psoriatic patients develop arthritis and which joints are commonly affected?

A
  • 5% –> psoriatic arthritis
  • HLA B27
  • starts in DIP joints
  • v similar to RA
66
Q

What are the features of gonococcal arthritis?

A
  • gram neg. diplococci –> present in synovial fluid (intracytoplasmic - neutrophils)
  • arthritis dermatitis syndrome
  • septic polyarthritis, tenosynovitis –> with pus formation
  • sexually active adults, incr. in F
  • swollen, painful joints, skin lesions, fever
  • rarely joint destruction (unlike staph.)
67
Q

Which organisms are responsible for infective arthritis in adults?

A
  • staph aureus
  • e. coli
  • pseudomonas
68
Q

What is the causative pathogen in Lyme arthritis? and how is it Tx.?

A
  • Borrelia burgdoferi
  • spirochete bacteria transmitted by ticks
  • oral antibiotics –> doxycycline
69
Q

What are the 3 stages of lyme arthritis?

A
  1. site reaction (circular erythematous rash), fever, lymphadenopathy - transient
  2. migratory joint pains, cardiac arrhythmias, meningitis
  3. years later –> chronic debilitating arthritis, encephalitis
70
Q

What is the cause of ganglion cyst and where are they commonly located?

A
  • idiopathic (?trauma, repeated use), incr. in middle age Females
  • cystic degeneration of tendon or herniation of synovial sheath

*wrist, fingers, foot

71
Q

What is the Tx. for ganglion cyst?

A
  • regresses on its own
  • aspiration
  • steroid injection
  • excision
72
Q

What is degenerative disc disease?

A

-herniation of nucleus pulposus due to ageing/trauma which causes compression of nerve roots resulting in lower back pain/deformity, and can result in complications such as nerve damage (radiating pain, tingling, numbness)

73
Q

Which direction does OA and RA spread with regards to interphalangeal joints?

A

OA:
-typically begins in DIP joints and spreads proximally

RA:
-typically begins soft/tender in MCP joints/PIP joints and spreads distally

74
Q

What is the microscopy of RA?

A
  1. papillary proliferation (of a normally flat synovium)
  2. lymphocytes
  3. plasma cells
  4. lymphoid follicles

Pathology Term 4 (6 decks)

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