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MSK final > Rheumo 2: OA, sclerosis, spondyloarthropathies > Flashcards

Rheumo 2: OA, sclerosis, spondyloarthropathies Flashcards

1
Q

Do all people with structural changes of OA have symptoms?

A

NO! many do not

do not treat if symptomatic

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2
Q

What are some characteristics of OA?

A

joint failure, NOT autoimmune

-hyaline cartilage loss and sclerosis of the bony end plate.

***osteophytes

  • mild swelling CAN be seen WITHOUT inflammation (WBC <2000)
  • mm weakness from not using joint
  • node formation (Bouchard and Heberdens nodes)
  • short morning stiffness
  • pain with use, better with rest
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3
Q

What can severing a nerve cause?

A

Charcot’s–> damage of the joint (secondary osteoarthritis)

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4
Q

What breaks down the hyaluronic acid and aggrecans in OA?

A

collagenases

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5
Q

A 78 year-old female, with pain at her thumb base, hips, and knees for the past 10 years, presents to clinic for relief of her pain. The pain is worse with standing for prolonged period of time and worse with walking. She has a strongly positive rheumatoid factor, and her knees have swelling but no warmth.
Which of the following would not be a typical location of arthritis for her diagnosis?
A. Shoulders
B. First carpometacarpal joint
C. Proximal interphalangeal joints
D. Cervical spine

A

A. shoulders

non-weight bearing

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6
Q

What 2 types of arthritis will affect the DIP and PIP?

A

OA and psoratic arthritis

RA will NOT

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7
Q

What will radiographic findings show in OA?

A
  • Joint space narrowing
  • Marginal osteophytes
  • Subchondral cysts
  • Bony sclerosis
  • Malalignment (normally only one compartment affected)
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8
Q

What labs should be ordered if you suspect OA?

A

NONE!!!!

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9
Q

What medications are used to treat OA? What are these used for?

A
  • NSAIDS -acetaminophen
  • tramadol (increase serotonin to decrease pain)

decrease pain to increase function

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10
Q

A 68 year-old African American female presents to your clinic with a three day history of right knee pain. The patient woke up with sudden knee pain at 4:00 in the morning. On examination, her right knee demonstrates erythema, heat, and a large amount of swelling.
What is the most critical condition to rule out?
A. Gout
B. Rheumatoid arthritis
C. Septic Arthritis
D. Fracture
E. Ruptured meniscus

A

C. Septic arthritis

**order arthrocentesis with culture

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11
Q

What does gout cause?

A

MSU (Monosodium urate) crystals in joints and connective tissue tophi and deposition on the kidney interstisium

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12
Q

What can a deficiency of HPRT (Hypoxanthineguanine phosphoribosyl transferase) or PRPP lead to? Why?

A

gout

hypoxanthine is not re-used and then turns more into urate–> causes gout

  • PRPP mutation==> increase urate
  • HPRT mutation–> hyperuricemia to Lesch Nyhan Syndrome (neurologic and behavioral dysfunction)
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13
Q

How does Urate lead to swelling?

A

Urate is phagocytized by neutrophils ==> release of lysozymes, leukotrienes, interleukins–> joint swelling

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14
Q

What is the only way to prove that a problem is gout?

A

needle–> check for crystals

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15
Q

What are some common risk factors for gout?

A
  • excessive beer intake
  • excessive meat intake
  • obesity
  • age
  • excessive soda intake
  • trauma
  • drugs that decrease uric acid secretion (thiazide diuretics)
  • increased cell turnover (psoriasis, cancer, tumor lysis)
  • ischemia: MI, sepsis, trauma
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16
Q

What will the synovial fluid in a gout pt look like?

A
  • WBC 5000-60000
  • cloudy
  • thick and chalky if excessive crystals
  • negative befringement crystals (blue with perpendicular light)
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17
Q

Can gout be diagnosed just off of an elevated uric acid level?

A

NO!

need a hot, swollen joint too

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18
Q

What is a tophi?

A

hazy area seen on an x-ray in a pt with gout

C-shaped erosion is also common

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19
Q

*What is the goal of treatment for gout pts?

A

keep uric acid < 6 mg/dL

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20
Q

Should Allopurinol be given to a pt during an attack of gout?

A

NO! –> give 1-2 weeks after attack

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21
Q

What is CPPD deposition disease?

A
  • common in elderly
  • an increased production of inorganic pyrophosphate (pts with ANKH mutation can have an increase in production of pyrophosphate
  • pyrophosphate combines with Ca2+ in collagen fibers–> decrease glucosamine in cartilage
  • associated with metabolic abnormalities
  • knees most commonly involved
  • x-ray: chondrocalcifications
  • POSITIVE befringement crystals (yellow w/perpendicular light)
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22
Q

What metabolic abnormalities can CPPD be associated with?

A
  • Primary hyperparathyroidism
  • Hemochromatosis
  • Hypophosphatasia
  • Hypomagnesemia
  • Chronic gout
  • Postmeniscectomy
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23
Q 
A 42 year old female with a 25 year history of renal stones, diffuse muscle pain and joint pain, presents to your office as a follow-up and a  knee x-ray report that states she has chondrocalcifications at the knees.  What should you order next?
A. Calcium, Parathyroid hormone
B. Magnesium
C. Phosphate, Creatinine
D. Uric acid
E. All of the above
A

E. all of the above

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24
Q

What are some characteristics of Calcium Apatite Deposition Disease occur?

A
  • Occurs in: Aging, Osteoarthritis hypercalcemic states (hyperparathyroidsm), areas of tissue damage
  • Most common sites of deposition include the joint capsule, bursa tendons, or articular surface and usually occurs in or around the knee, shoulders, hips, fingers.
  • synovial leukocytes <2000
  • Intra and or peri-articular with or without erosive, destructive changes hypertrophic
  • need crystals for definitive diagnosis
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25
Q

What are the 2 types of Calcium Oxalate Deposition Disease?

A
  1. Primary Oxalosis: a rare metabolic disorder
    - increase oxalic acid production–> hyperoxalemia and crystal deposit
  2. Secondary oxalosis (more common): is typically from end-stage disease on hemodialysis or peritoneal dialysis and many receive vitamin C (ascorbic acid supplementation)–> Ascorbic acid is metabolized to oxalate
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26
Q

What are seronegative spondyloarthropathies?

A
  • A group of disorders characterized by inflammation of the spine
  • Seronegative because they are rheumatoid factor negative
27
Q

What are the key symptoms of AS (ankylosing spondylitis)?

A
  • chronic inflammatory disease of the axial skeleton
  • back pain and progressive spine stiffness (including SI joint)
  • pain GREATLY improved with NSAIDS (not seen in OA)

**morning stiffness, better with exercise

28
Q

What is linked to AS? Does the presence of this in addition to back pain make the diagnosis of AS?

A
  • HLA B27–> tendency to misfold–> proinflammatory

- NO! –> nonspecific lab studies

29
Q

What pathologic findings will be seen in AS at the SI joint?

A
  • pannus formation
  • erosions
  • new cartilage formation
  • eroded joints will eventually be obliterated (ankylosed/fused)
30
Q

What is the age of onset of AS and who is most commonly affected?

A
  • 20-30

- M:F 2-3:1

31
Q

What joints are commonly affected by AS?

A

SI, shoulder, back

32
Q

What are some extra-articular involvements seen with AS?

A
  • uveitis
  • colitis
  • aortitis
  • pulmonary fibrosis
33
Q

What radiographic findings will be seen in AS?

A
  • Blurring of the cortical margins
  • Erosions
  • Sclerosis
  • Pseudo-widening of the joint space (due to erosions)
  • Fibrous and bony ankylosing
  • Symmetric changes of the SI joint**
  • loss of lordosis
  • bamboo spine*
  • squaring and syndesmophytes (ossification between the vertebrae)
34
Q

What are some characteristics of Reactive Arthritis (ReA)?

A
  • A nonpurulent arthritis complicating an infection elsewhere in the body
  • ->Classically: Uveitis, urethritis, and arthritis
  • *symptoms 1-4 weeks after infection (pts might not know of infection)
  • acute onset arthritis normally in LEs (knees, ankles and feet)
  • asymmetrical (unilateral) and 1-3 joints involved and Additive**
  • thicker syndesmophytes than in AS, and asymmetrical

-common constitutional features (e.g.: fever, malaise, weight loss)

35
Q

How will the SI joint changes be different in AS and ReA?

A

AS=symmetrical

ReA=unilateral

36
Q

What are some features of Psoriatic arthritis? (PsA)

A

-Inflammatory arthritis associated with psoriasis

  • morning stiffness > 30 min–> alleviated with physical activity
  • less tender than RA
  • DIP and spine likely affected
  • seronegative
  • There is a greater tendency for joints to ankylose in PsA
  • Sacroiliitis is asymmetric
  • ochynosis (nail come up from bed) is seen in 90%
  • dactylitis or sausage fingers
37
Q

Does a pt have PsA if they have psoriasis and joint pain?

A

not necessarily

Patients with psoriasis may have coexistent rheumatoid arthritis, osteoarthritis, arthritis of inflammatory bowel disease, and gout

38
Q

In what two types of arthritis would asymmetrical sacroilitis be seen?

A

ReA and PsA

39
Q

What radiologic changes will be seen in PsA?

A
  • erosive changees and new bone formation in the distal joints
  • lysis of terminal phalanges
  • “pencil in cup” image
  • no osteoporosis
40
Q

What are some characteristics of Inflammatory Bowel Disease Associated arthritis?

A
  • asymptomatic normally
  • oligoarthritis
  • migratory
  • can subside with IBD tx (except for SI and spondylitis seen independent of IBD)
41
Q

44 year-old female with IBD associated spondyloarthritis and ulcerative colitis presents presents to your office with low back pain. Her ulcerative colitis has been controlled for years.
Her back pain may be from IBD associated SpA and progressing.
A. True
B. False

A

TRUE!!!

42
Q

What is systemic sclerosis or scleroderma? What are the classifications?

A

An autoimmune disease characterized by varying degrees of organ fibrosis

Diffuse Scleroderma (dcSSc): skin thickening is present on the trunk, face, proximal and distal extremities. 10 yr survival=50%

Limited scleroderma (lcSSc) which includes CREST. Skin thickening is restricted to sites distal to the elbows and knees, but also involving the face and neck

43
Q

What lab test is positive in over 95% of scleroderma patients?

A

ANA

-if not +, it is likely another diagnosis

44
Q

What disease and organ problems are associated with Scl-10 autoantibodies? RNA I, II, III? U1RNP? Centromere?

A

Scl-10: dcSSc, interstitial lung fibrosis

RNA I, II, III: dcSSc, renal

U1RNP: overlap diseases, muscle

Centromere: IcSSc, pulmonary hypertension

45
Q

A thirty-two year-old female has skin tightness at the distal extremities only.
Which antibody is most commonly associated with her disease?
A. Anti-SCL-70
B. Anti-RNA III
C. Anti-Centromere
D. Anti_U1 RNP

A

C. anti-centromere

46
Q

scleroderma of which organ has a poor prognosis?

A

heart

47
Q

what body part is affected in 90% of pts w/ scleroderma? what does this lead to?

A
  • esophagus–> Reduction or absent peristaltic waves in the lower 2/3 of the esophagus, and lower esophageal sphincter tone
  • Reflux esophagitis, diffuse esophageal spasms & hypertonic esophageal sphincter, strictures. Leads to eosphageal dysmotility/dysphagia,
48
Q

What is the pathology behind the injury seen in scleroderma?

A

endothelial cell injury—> endothelial cell dysfunction decreased NO and PG, increased ET-1) –> vascular wall remodeling–> luminal narrowing (increase shear stress)

–> leads to both more remodeling of the vascular wall and slow blood flow and hyper coagulable state

–>allows vessels to spasm

49
Q

What induces fibrosis of vascular smooth muscles?

A

Endothelin 1

50
Q

What is the role of TGF beta in scleroderma?

A
  • Secreted by macrophages, lymphocytes, fibroblasts, epithelial cells, endothelial cells
  • Enhanced secretion in patients with scleroderma
  • Increases expression of collagen, fibronectin, and proteoglycans
  • Activates fibroblasts and is a chemoattractant
51
Q

What oropharyngeal changes are seen with scleroderma? GI? vascular?

A
  • aspiration, nasal regurgitation, coughing
  • GI: wide-mouthed diverticuli
  • vascular: raynaud’s, renal, pulmonary HTN
52
Q

What are the 3 phases of skin changes in scleroderma?

A
  • inflammatory edematous
  • indurative/fibrotic (thickened skin with reduced sweet and oil)
  • atrophic: atrophy of fat mm ad fibrosis of fascia–> contractors
    (acrosclerosis: bone resorption of the terminal tufts of fingers)
53
Q

What are the differences seen in primary vs. secondary Raynaud’s?

A

Primary Raynaud’s is not associated with any disease digital pitting, ulcerations or antibodies.

secondary: due to scleroderma or something else–> pitting of finger pads

54
Q

How will a pt with a scleroderma renal crisis present? What are some risk factors for getting renal involvement?

A

HA, CHF, altered vision, seizures with BP>150/90

labe: high creatinine, proteinuria, hematuria (small), microangiopathic hemolytic anemia, thrombocytopenia

*only 10%  will get this 
Risk: diffuse > limited
-anemia
-high dose steroids
-cyclosporin
55
Q

What is a common cause of death in scleroderma pts?

A

pulmonary involvement

seen in 70% of scleroderma pts

56
Q

What are the 2 types of pulmonary involvement of scleroderma? How is this monitored?

A
  1. interstitial lung disease
  2. pulmonary vascular disease
    - Chest Xray, high resolution CT, DLCO to measure pulmonary function, right sided heart catheterization**( GOLD STANDARD for pulmonary function but dangerous)
57
Q

What features of scleroderma are more commonly seen in limited than diffuse?

A

limited=more telangectasia, pulmonary HTN, calcinosis

Diffuse: more tendon friction, interstitial lung dx

58
Q

How is renal involvement of scleroderma treated?

A

ACE inhibitors

59
Q

What is Sjogren’s Syndrome?

A

Chronic inflammatory disorder characterized by lymphocytic infiltrate of the lacrimal and salivary glands resulting in dryness of the mouth and eyes.

SS may be either primary or secondary in association with RA, SLE, or progressive Systemic Sclerosis

60
Q

A 64 year-old female presents with a history of Sjogren’s syndrome visits your office with a two month history enlarging non-movable cervical lymph node.
The most appropriate management decision would be to:
A. Obtain a lymph node biopsy
B. Order an anti-SSA and Anti-SSB antibody
C. Observe and reassure the patient
D. Prescribe amoxicillin

A

A. Obtain a lymph node biopsy

lymphoma is commonly associated with sjogrens

61
Q

What are some common symptoms of Sjogrens?

A 
Xeropthalmia	(dry eyes)			47%
Xerostomia (dry mouth)				42%
Arthralgia/Arthritis		28%
Parotid Enlargement (bilateral)
24%
Raynaud’s					21%
Fever/fatigue				10%
Dyspareunia				5%
-can get teeth issues--> refer to dentist
62
Q

What cancer is a pt with Sjogrens at a 40% higher risk of getting?

A

lymphomas

salivary glands and cervical lymph nodes

63
Q

What are some tests for Sjogrens?

A
  • Schirmer test –> stick paper in eye and < 5 mm in 5 min of tear production =diagnosis
  • rose bangal stain: increaes uptake of the stain in the eye–> turns really pink in Sjogrens
64
Q

What antibodies are associated with Sjogrens?

A

anti-SSA and anti-SSB

seen in primary Sjogrens

MSK final (21 decks)

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