Pathophysiology and Clinical Aspects of OA/RA Flashcards

1
Q

What are the risk factors for osteoarthritis?

A

Increasing age
Female
Obese - especially wears on knee joints
Joint trauma

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2
Q

What joints are particularly affected in radiographically via OA, and which ones are most commonly symptomatically?

A

Radiographically - PIP and DIP joints most affected. But these are less likely to be symptomatic.

Symptomatically - hips and knees are most affected

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3
Q

What carpal or tarsal bone joints are most affected in primary OA?

A

1st MTP - like gout - OA

1st CMC - carpometacarpal. But NO MCP involvement!!

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4
Q

What are some unusual locations for primary OA which would make you suspect a secondary OA? Other factors which might suggest it?

A

Shoulder
Elbow
Wrist
MCP joints

Also likely if patient is young, there is a strong FHx, or accelerated course

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5
Q

What some common causes of secondary OA?

A

Hemochromatosis -> especially osteophytes forming at MCP joints.

Other endocrine / metabolic disorders

Postinflammatory (i.e. RA, post-septic)

Crystal deposition disorders

Connective tissue disease, dysplasias, Paget’s disease, posttraumatic

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6
Q

What is the gel phenomenon?

A

Phenomenon characterized in OA, sitting for long periods of time thickens the joint fluid (hyperviscous, like oil). Takes up to 30 minutes for joints to stop feeling stiff once you start moving.

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7
Q

What are the treatments for OA pharmacologically?

A

Acetaminophen, NSAIDs + PPIs to prevent bleeds, intra-articular glucocorticoids.

Hyaluronic acid supplementation may also be useful.

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8
Q

What are common systemic symptoms of rheumatoid arthritis? What organs are commonly affected via extraarticular manifestations?

A

Fever, fatigue, weight loss (chronic inflammation -> cachexia)

Commonly affected: skin, heart, lungs, and eyes.

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9
Q

What are the risk factors for RA other than genetics?

A

Female gender (autoimmune) -> infact if males get it, the prognosis is worse

Middle-age, and smoking

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10
Q

How is joint involvement of RA distinctively different from OA?

A

Affects MCP (not affected in OA unless hemochromatosis), wrist, shoulders, cervical spine (not affected unless secondary OA).

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11
Q

Why is there a reduction in finger flexion and grip strength in RA? What other nearby syndrome can this same process cause

A

Tenosynovitis of the flexor tendons from spreading of inflammation.

RA can also cause carpal tunnel syndrome

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12
Q

What can tendon and joint destruction in the hands and feet cause in RA other than Boutonniere deformity and swan neck?

A

Subluxation of the fingers and toes
-> i.e. metatarsophalangeal subluxation.

Can also cause hammertoes which is basically Boutonniere deformity of the 2nd toe, and hallux valgus which is lateral deviation of the first toe due to subluxation

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13
Q

What joints of the hand are characteristically spared in RA compared to OA?

A

RA - spares 1st CMC joint and DIP joints (commonly affected in OA)

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14
Q

How can RA affect the cervical spinal cord?

A

Instability can lead to cervical spinal subluxation -> especially between C1/C2.

This can lead to LMN spinal shock acutely and UMN symptoms chronically.

-> this is infact the only axial involvement seen in RA.

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15
Q

Why could RA lead to osteoporosis?

A

Systemic chronic inflammation in combination with immobilization and corticosteroid therapy -> generalized osteoporosis and bone wasting

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16
Q

What are the cardiovascular complications of rheumatoid arthritis?

A

Immune-mediated pericarditis
Accelerated atherosclerosis due to chronic inflammation
Small vessel leukocytoclastic vasculitis

17
Q

What are the eye and lung manifestations of rheumatoid arthritis?

A

Lungs - pleuritis, pulmonary nodules (identical to cutaneous rheumatoid nodules) which can lead to progressive fibrosis and honeycombing

Eyes - scleritis -> diffuse or nodular. The sclera is the layer which is continuous with the cornea in the fibrous tunic.

18
Q

Give three causes of anemia in RA.

A
  1. Anemia of chronic disease
  2. Hypochromic anemia -> due to GI blood loss associated with chronic NSAID use
  3. Aplastic anemia -> associated with DMARD therapy (i.e. methotrexate)
19
Q

What are the radiographic features of joint disease in RA?

A

Periarticular soft tissue swelling
Marginal erosions -> erosions worst at joint margins (due to inflammation starting at pannus)
Symmetrical involvement (i.e. MCP involvement of both hands, but does not need to be same digit)
Joint space narrowing (like OA)
Osteopenia

20
Q

How does a gout erosion differ from a RA erosion?

A

Gout erosion is more sharply demarcated with overhanging edges. RA erosion is more shallow generally and not as sharp.

21
Q

What is the general treatment scheme for RA?

A

NSAIDs and corticosteroids as rapid onset bridging therapy while the DMARDs and biologics come online.

DMARDs: MTX, sulfasalazine, hydroxychloroquine, leflunomide
Biologics: i.e. TNFalpha inhibitors, costimulation inhibitors, etc

22
Q

What will the patient complain of in fibromyalgia?

A

Widespread pain (over joints and non-joints), fatigue, decreased pain threshold / tolerance, and difficulty sleeping. Cognitive disturbance “fibro fog” is common.

23
Q

What will physical exam show in fibromyalgia? What about labs?

A

No objective signs of inflammation
No objective muscle weakness or neurologic abnormalities

Exquisite tenderness or “trigger points” may be noted.

Labs show normal ESR and CRP

24
Q

What endocrine conditions and drugs are associated with nonspecific arthralgias and myalgias?

A

Hypothyroidism, hyperparathyroidism, adrenal disease, diabetes, and acromegaly

Drugs: Statins, zidovudine, ethanol, colcichine

25
Q

What is the treatment goal of fibromyalgia and the non-pharmacologic therapy available?

A

Treatment goal is to keep the patient functional in spite of the pain

Non-pharmacologic: assure the patient of the non-destructive nature of the disease

Emphasize regular social interactions and engaging in a healthy exercise program: i.e. yoga

26
Q

What drugs are used in the treatment of fibromyalgia?

A

Neuropathic pain! Do not use corticosteroids or narcotics.

  1. Pregabalin and Gabapentin
  2. SNRIs - duloxetine and milnacipran
  3. Tricyclics - amitriptyline
27
Q

What is the clinical presentation of polymyalgia rheumatica? Who gets it?

A

Aching and stiffness in SHOULDERS, HIPS, and neck, often associated with morning stiffness. (proximal myalgias and stiffness) Can cause myalgias and RA-like soft tissue symptoms, but generally not as severe.

Occurs in elderly women >60 years.

28
Q

What are the lab findings of polymyalgia rheumatica? ESR / CRP / CK

A

Elevated inflammatory markers: ESR elevated, CRP elevated. CK will be normal cuz there is no true muscle disease going on.

Patient has increased inflammatory markers associated with constitutional symptoms (similar to rheumatoid arthritis).

Anemia is also common (anemia of chronic disease)

29
Q

Will a patient with polymyalgia rheumatic have hand / joint synovitis? How about a positive rheumatoid factor or CCP?

A

NO! synovitis is a RA only thing

Rheumatoid factor is nonspecific so its potentially positive, but not usually.

CCP more specific for RA, never positive.

30
Q

What is the treatment for polymyalgia rheumatica and what condition is it commonly associated with?

A

Low dose steroids which may need to be tapered after 1-2 years. The treatment is so effective that it is often diagnostic.

Highly associated with giant cell (temporal) arteritis -> monitor for this symptoms.