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Musculoskeletal System > 3 - Rheumatology > Flashcards

3 - Rheumatology Flashcards

1
Q

What types of arthritis are associated with the DIP joint?

A

Heberdens nodes - OA, Psoriatic, Reiters/Reactive

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2
Q

What types of arthritis are associated with teh PIP joint?

A

Buchards nodes - OA, SLE, RA, Psoriatic

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3
Q

What types of arthritis are associated with the MCP joint?

A

RA, Pseudogout, Hemochromatosis, SLE

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4
Q

What types of arthritis are associated with the 1st carpometacarpal joint?

A

OA

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5
Q

What types of arthritis are associated with the wrist?

A

RA, SLE, Pseudogout, Gonococcal, Juvenile

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6
Q

What types of joints are most commonly affected by OA?

A

Weight-bearing joints

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7
Q

Describe the pathology of OA.

A

Cytokines, mechanical trauma and altered genetics initiate degenerative cascade

DJD affects the entire joint structure

Irregularity, erosion & ulceration of the articular cartilage

Osteophyte formation in the joint margins and in the floor of cartilage lesions

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8
Q

What are the classifications of OA?

A

Idiopathic - common in hands, feet, knee, hip, spine. (uncommon in shoulder, TMJ, sacroiliac, ankle and wrists). *generalized idiopathic involves three or more joints.

Secondary - many different pathologic conditions can cause arthritis symptoms/pathology

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9
Q

What are some classic symptoms of osteoarthritis?

A

Night Pain, Morning Stiffness (short duration), Little or no swelling, Usually joint specific

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10
Q

Discuss the course of treatment for osteoarthritis.

A 
Psychological Intervention
Weight Loss
Temp Modalities (acute v chronic)
Exercise
Orthotics/Bracing
ADL modificatoin
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11
Q

Discuss the guidelines for can use in OA patients.

A

Place in hand of contralateral side to affected joint
Advanced with the affected limb while walking
20-degree flexion of the elbow during use
Height should be floor to greater trochanter

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12
Q

Discuss pharmacological interventions available for OA

A

Currently there is no treatment that prevents the progression of joint damage

Goal: Pain relief, Inflammation prevention

Non-narcotic: Acetominophen, NSAIDS, Celebrex (cox-2 inhib) in that order for choices of treatment

Narcotic: Tramadol, codeine, oxycodone (geriatric patients sensitive to narcotics** - increased falls/confusion/constipation)

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13
Q

What are some injections available for treatment of OA?

A

Glucocorticoids, Hyaluronate injection - useful when NSAIDs are contraindicated

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14
Q

Describe the topical agents and nutriceuticals available for treatment of OA?

A

Topical Agents: Capsaicin, NSAIDs (diclofenac), menthol based and salicylate based OTC

Nutriceuticals: Glucosamines, Chondroitin sulfate, Ginger extracts

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15
Q

What is the last resort treatment for OA??

A

Arthroscopy (debridement/lavage)
Osteotomies
Joint Replacements

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16
Q

What genes are associated with RA?

A

HLA-DR4 - human leukocytic antigen

More common in women

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17
Q

Describe the common environmental factors associated with increased RA?

A 
Tobacco
Infection
Stress
Trauma
Northern Hemisphere
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18
Q

What is the classical characteristic formation in the joint seen in RA?

A

Pannus Formation with loss of cartilage

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19
Q

What is the reasoning for Ca2+ supplementation in RA patients?

A

RA patients have synovitis associated symptoms, this pathology increases inflammatory mediators (IL-1, TNF, LTB4) which are known to induce osteopenia in these patients

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20
Q

Describe the laboratory findings in patients with RA

A

Rheumatoid Factor - Autoantibody that binds the Fc portion of IgG (forms immune complexes)

In pts. seronegative for RF, a definitive dx can be helped along with serum anti-ccp antibodies (CONFIRMATORY TEST). Nice because it is positive early in disease process.

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21
Q

Describe the classic clinical symptoms of RA

A 
Morning Stiffness (Longer Duration)
Polyarticular (hands often first affected), generally symmetrical, muscle atrophy, depression, anxiety, weightloss
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22
Q

Describe Palindromic Rheumatoid arthritis.

A

Minority of DX (waxing/waning course of disease)

Begins in one joint, worsens for hours-days, then sequence reverses and eventually resolves

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23
Q

Describe the nodules often associated with RA?

A

Almost always seen in RF+ patients (20-25% overall)

Hard rubbery mass attached to the periosteum, or can be amourphous and mobile too???

24
Q

Describe the hematologic abnormalities seen in RA patients?

A

Mild normocytic hypochromic anemia - anemia of chronic disease, correlates with ESR elevation and activity of disease

ESR correlated inversely with hemoglobin levels (inhibited erythropoeisis)

Eosinophilia and Thrombocytosis

25
Q

Describe the pulmonary complications seen in RA patients

A 
Effusion
Fibrosis
Nodules
Bronchiolitis
Arteritis, with pulm hypertension
Reactivation of TB by anti-TNF alpha biologic agents
26
Q

Describe the cardiac complications seen in RA patients,

A 
Effusion
Pericarditis (50%)
Myocarditis --- stressed this one
Endochonral Inflammation
Conduction Deficits --- stressed this one
27
Q

What types of cancers are increased in incidence in RA patients?

A

Lymphomas

28
Q

Describe the possible clinical courses for patients with RA.

A

3 Forms: Self-Limiting, Persistent Nonerosive, Persistent Erosive.

Typically whatever pathway is started, is the pathway the patient will continue to follow.

29
Q

What are the good predictors of RA outcomes?

A

Initial xray score, and RF+ titers are the best predictors of expected outcome.

30
Q

What is the overall RA dx Criteria (2010 ACR)

A

Number of Joints Involved
Serological Abnormality - RF, anti-ccp, symptom duration greater than 6wks

Points assigned to each presenting criteria (minimum of 6 needed to qualify as RA)
REVIEW SLIDE FOR POINT ASSIGNMENTS FOR CERTAIN CRITERIA

31
Q

Describe Felty’s Syndrome

A

A triad of RA symptoms: 1. Chronic RA, 2. Splenomegaly, 3. Granulocytopenia

Known to progress faster

32
Q

What is the preferred treatment for Felty’s syndrome?

Describe mechanism, Type of drug, and Side Effects

A

Methotrexate

33
Q

Describe Sjogrens syndrome

A

Primary: Dry everything due to autoimmune dysfunction of exocrine glands

Secondary: Usually in the presence of RA

34
Q

What lab studies are specific to Sjogren syndrome?

A

Antibody to SS-A
Antibody to SS-B
2/3 ANA+ and RF+

35
Q

Describe treatments for Sjogren syndrome

A

External Moisture Replacement

Pilocarpine, Cevemiline - stimulate excretions

36
Q

What are the 3 major clinical features (stages) of gout?

A

Acute gouty arthritis
Intercritical (interval) gout
Chronic Tophaceous

37
Q

Describe Stage 1 gout.

A

90% of first attacks happen at big toe
Knee second most common
Can be polyarticular at first onset in patients with multiple contributing factors
Sudden onset - resolves in a few days/wks

38
Q

What is the critical criteria for acute gout?

A

Point System involves: gender, previous arthritis, onset timing, joint involved, HTN, Serum Uric acid level.
(5.88 score required for dx)
>8 points = high probability of gout

39
Q

Describe Stage 2 gout

A

Multiple gouty attacks with intermittent periods
2nd attack generally appears within 2 yrs.
Must address the reversible causative factors and try to eliminate
Initiate prophylactic/antiuremic treatment

40
Q

Describe Stage 3 gout.

A

Major factor is the presence of tophi (increase in number with duration of hyperuricemia)

Can have tense shiny skin over the joints with tophi that could ulcerate and extrude white pasty urate crystals

Erosions with sclerotic margins and thin overlying calcified edges seen on radiograph (can use US, MRI, and CT can

41
Q

Describe the renal complications seen in gout patients.

A

Nephrolithiasis - kidney stones
Elevated serum creatinine
Urinary sediment
Hyperuricemia duh

42
Q

What is Podagra, with regard to gout?

A

The commonly seen pathology of gout experienced in the 1st MTP joint

43
Q

Describe the treatment course for gout patients depending on their 24hr urine uric acid levels.

A

Normal: 600mg/d - goal of treatment is to increase urinary uric acid excretion (use probenecid)

High: >600mg/d - goal is to decrease production of uric acid (use allopurinol)

44
Q

Describe treatment pathways for acute and chronic gout patients.

A

Acute: NSAIDs, Colchicine (inhibit leukocyte entry into joints), Glucocorticoids

Chronic: Uricosurics (probenecid - increase excretion), Inhibit uric acid synthesis (allopurinol)

45
Q

What is the first line of treatment of acute gout?

A

NSAIDS (indomethacin) - look out for GI toxicity

46
Q

What is the second line of treatment of acute gout?

A

Colchicine - MOA that decreases lactic acid release, maintain higher pH and allow greater uric acid solubility

Look out for GI problems also because this drug inhibits epithelial regeneration by impeding mitosis due to its effects on the microtubules needed for the splitting phase

47
Q

Describe the first line of treatment for prophylaxis in interval stage gout patients?

A

Probenicid - uricosurics - increase excretion
Hydrate to avoid stones
Biggest side-effects are headache and rash

Allopurinol - decrease formation

48
Q

How will you try to stop the formation of a urate stone in gout patients/

A

Alkalinize the urine (calcium citrate or sodium bicarb)

49
Q

Describe the recommended dietary modifications for gout patients/

A

Decrese red meat, seafood, hard alcohol

50
Q

Describe Calcium Pyrophosphate Dihydrate (CPPD)

A

PSEUDOGOUT/Chondrocalcinosis
Crystals deposited in articular and fibrocartilage
Most commonly seen in knee
DX/ Weakly birefringement, rhomboid, rod-shaped
Radiograph - heavy punctuate and linear calcification in chondral regions

51
Q

Describe (BCP) Basic Calcium Phosphate Crystals

A

Crystals deposited in periarticular structures
Common in rotator cuff and subacromial bursa (old lady can’t raise her arm)
DX/ Negative birefringement

52
Q

What is milwaukee shoulder/

A

Bilateral shoulder pain associated with BCP calcifications

53
Q

What is the most common cause of urinary stones?

A

Calcium Oxalate - may cause arthritic changes, multifactorial etiology

54
Q

FOR GOUT

A

REVIEW TABLE AT END OF PWRPT

55
Q

Describe the clinical features/symptoms of Fibromyalgia

A 
Pain 
Fatigue
Crawling Skin Sensation
Sleep Problems
Depression/Anxiety
56
Q

Describe the common treatment options for patients with fibromyalgia.

A 
Go kill yourself
Stress reduction 
Meditation
Exercise
Acupuncture
OMT
57
Q

Describe the medications that may be indicated for fibromyalgia.

A 
Tricyclic Antidepressants
SSRIs
Dual  reuptake inhibitors (norepi/serotonin)
Anticonvulsants (CNS pathway)
Analgesics

Musculoskeletal System (21 decks)

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