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Block 4: Musculoskeletal > Rheumatology (Week 2--Weinreb) > Flashcards

Rheumatology (Week 2--Weinreb) Flashcards

1
Q

Autoimmunity

A

Tolerance (normal mechanisms that prevent immune activity against self-antigens) is lost

Abnormal response by immune system against individuals own tissues resulting in tissue damage

Due to genetic, environmental and immune/cellular factors

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2
Q

Innate immune system produces which key inflammatory cytokines?

A

TNF

IFN (interferon)

IL-1beta

Does this by neutrophils and APCs recognizing PAMPs

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3
Q

Pathologic complement activation

A

Mechanism for autoimmunity

Antigen-antibody (immune) complexes deposited on tissues then bound to complement and Fc receptors –> immune dysregulation and complement activation

Results in localized tissue injury

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4
Q

Antigen presenting cells (APCs)

A

Process foreign antigens for presentation to immune cells as part of adaptive immune system

Present self-antigens during development to generate immune tolerance

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5
Q

MHC/HLA

A

HLA antigens expressed on cell surface (MHC I on all cells and MHC II on immune cells) and function to present antigens to immune system as peptides that were processed intracellularly

T and B cell receptors recognize these and activate an immune response

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6
Q

HLA genes

A

Highly polymorphic (many alleles for each gene encoding different HLA chain)

Lots of genetic diversity in HLA at the population level

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7
Q

Peptide, MHC, type of T cell

A

CD4 helper T cell = MHC II = intracellular organisms and cellular proteins

CD8 cytotoxic T cell = MHC I = extracellular organisms and antigens

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8
Q

T helper cells

A

Activate specific B cells through specific T cell receptor and MHC II/peptide antigen binding

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9
Q

B cells

A

Produce antibody

Contribute to T cell activation via specific MHC II/peptide antigen and T cell receptor interaction

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10
Q

Cytokines

A

Dysregulation of cytokines can contribute to autoimmunity

TNF-alpha

IL-1alpha

IL-1beta

IL-17A

IL-17F

Remember these because we have drugs to interfere with them!

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11
Q

Tolerance

A

To prevent a response to self antigens (prevent autoimmunity)

Double signaling/costimulation, regulatory T cells, regulatory B cells, clearance of self-antigens (apoptosis)

Also, see “mechanisms of tolerance”

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12
Q

Two signal immune cell activation

A

Two signals required for B cell and T cell activation to ensure only activation when threat by foreign antigen

Foreign antigen activates innate immune system to produce cytokines which cause increased costimulatory B7 family (CD80/86) ligand expression and likelihood of second signal (costimulatory) binding

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13
Q

Regulatory T cells

A

5-10% of CD4 T cells

Downregulate effector T cells with similar specificity

Downregulate autoreactive lymphocytes

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14
Q

Regulatory B cells

A

Population of B cells found in mice, suggested in humans

Suppresses intestinal inflammation, may be defective in lupus

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15
Q

Apoptosis

A

Controlled, regulated cell death

Cell and nuclear condensation, membrane bleb, DNA fragmentation, activated capsase, nuclear condensation, crescents, fragmentation

No inflammatory cytokines produced, anti-inflammatory

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16
Q

Mechanisms of tolerance

A

1) Clonal deletion
2) Anergy (if no second signal)
3) Inhibition/suppression

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17
Q

Factors contributing to tolerance failure

A

1) Genetic susceptibility genes (innate and adaptive immune systems) can cause: altered cytokine production/response, immune cell function/interactions, apoptosis (leading to secondary necrosis with autoantigen exposure/inflammation)
2) Environmental triggers that affect immune responses: toxins, UV light, infection, alterations in microbiome (dysbiosis)

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18
Q

How does necrosis cause autoimmunity?

A

Extracellular exposure of autoantigens and a release of DAMPs (danger associated molecular patterns) that can promote an inflammatory response

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19
Q

Working hypothesis for loss of tolerance to self-antigens

A

Autoimmune predisposing alleles and environmental factors (cross-reactive infectious antigens or exposure of hidden self-antigens) contribute to abnormal apoptosis and altered immune function; this leads to exposure of self intracellular antigens and release of inflammatory cytokines that generate pathologic cellular and autoantibody responses

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20
Q

Subchondral bone

A

Bone right beneath cartilage and there may be changes there that will help you diagnose different conditions

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21
Q

Pannus

A

Proliferative synovium which may cause erosions to bone

(inflamed synovium, hypertrophy, kind of like aggressive benign tumor)

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22
Q

Joint space narrowing

A

Decrease in distance between articulating bones due to loss of cartilage

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23
Q

Erosions

A

Areas of bone loss within or around a joint

(can be caused by crystals)

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24
Q

Subluxation

A

Partial dislocation of a joint

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25
Q

Arthritis vs. arthralgia

A

Arthritis: symptoms due to abnormalities in structure and/or inflammation directly involving the structures within the joint capsule

Arthralgia: pain involving a joint not associated with any obvious joint abnormality

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26
Q

Periarthritis

A

Symptoms due to abnormalities in structure and/or function of the structures around a joint (tendons, bursae, nerves)

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27
Q

Synovitis

A

Inflammation and proliferation of the tissue layer lining the inside of a joint (consists of synovial lining cells and underlying connective tissue)

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28
Q

Tenosynovitis

A

Inflammation and proliferation of the tissue layer lining the inside of a tendon sheath

(joints won’t be painful but around tendon will be)

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29
Q

Enthesitis

A

Inflammation of the sites of tendon or ligament insertion (entheses) into bone

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30
Q

Arthroscopy

A

Imaging used to look in a joint

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31
Q

What can you see on an X-ray regarding arthritis?

A

Periarticular osteopenia (bone loss around joint)

Subluxation

Joint space narrowing

Erosion

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32
Q

Additive sequence of involvement

A

Involvement of a joint or joints followed by an increasing number of affected joints

More typical of chronic polyarticular types of arthritis (rheumatoid arthritis)

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33
Q

Migratory sequence of involvement

A

Involvement of one joint, followed by resolution then shortly after get involvement of another joint (arthritis “jumps” from joint to joint over hours or a few days)

Less common presentation

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34
Q

Intermittent sequence of involvement

A

Involvement of a joint or joints, followed by resolution then recurrence in same or different joint usually time between is weeks to months

Typical of crystal arthropathies

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35
Q

Extraarticular involvement in arthritis

A

Eye symptoms: pain, redness, dryness

Mucocutaneous: oral ulcers, rashes, photosensitivity, skin ulcers, skin thickening

Respiratory: cough, shortness of breath, dyspnea on exertion, hemoptysis, pleuritic chest pain

Gastrointestinal: dysphagia, GERD, post-prandial pain, GI bleeding

Lab abnormalities suggesting organ involvement: hematuria, proteinuria, renal failure, hematologic abnormalities, liver function abnormalities, etc

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36
Q

Exam findings suggesting inflammatory articular source of symptoms

A

Joint swelling

Increased warmth and/or erythema

Joint tenderness to palpation

Joint effusion

Pain on passive range of motion

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37
Q

Monoarticular arthritis

A

Septic arthritis

Crystal arthropathy

Other monoarthritis

38
Q

2 classes of polyarticular arthritis

A

Inflammatory (symmetric/small joint or asymmetric/large joint)

Noninflammatory (degenerative/osteoarthritis)

39
Q

Inflammatory symmetric/small joint arthritis

A

Rheumatoid arthritis

SLE

Systemic sclerosis/scleroderma

Sjogren’s syndrome

Other collagen-vascular diseases

40
Q

Inflammatory asymmetric/large joint arthritis

A

Seronegative spondyloarthropathy (oligoarticular, 2-4 joints)

Ankylosing spondylitis

Reactive arthritis/Reiter’s syndrome

Psoriasis

Inflammatory bowel disease

41
Q

Indications for arthrocentesis (joint aspiration)

A

To rule out a septic joint

To evaluate for crystal arthropathy

To determine whether an effusion is inflammatory or noninflammatory

Therapeutic drainage (to remove joint damaging enzymes; pain relief)

42
Q

Tests for synovial fluid analysis

A

Appearance: clear (noninflammatory) vs. cloudy (inflammatory or hemorrhagic)

Cell count and differential: WBC, neutrophil %, RBC

Gram stain: gram positive vs. gram negative organism

Culture and sensitivities: aerobic organisms, special cultures and/or testing for fungi or mycobacteria when suspected

Polarizing microscopy for crystals: negatively vs. positively birefringent crystals

43
Q

Types of joint effusions

A

Normal: clear, colorless, viscous; <200 WBC

Noninflammatory: clear, yellow, viscous; 200-2000 WBC, <25% PMNs

Inflammatory: cloudy, yellow, decreased viscosity; 2,000-100,000 WBC, <50% PMNs

Pyarthrosis (subset of inflammatory): purulent, markedly decreased viscosity; usually >50,000 WBC, >95% PMNs

Hemarthrosis: grossly bloody (trauma vs. coagulopathy); similar to CBC (?)

44
Q

Polarizing microscopy for detection of birefringent crystals

A

Put crystal between two filters that are perpendicular to each other

Plane of polarized light is rotated by a birefringent crystal

Orientation of second filter is the plane of polarized light and is used to orient long axis of crystals

45
Q

Gout crystals on polarizing microscopy

A

Yellow parallel and blue perpendicular crystals = negatively birefringent = urate crystals (gout)

Intracellular crystals are highly indicative of an acute gouty flare (usually not seen between attacks)

46
Q

Calcium pyrophosphate (pseudogout) crystals on polarizing microscopy

A

Blue parallel and yellow perpendicular crystals = positively birefringent = calcium pyrophosphate (pseudogout) crystals

47
Q

Noninflammatory effusion could mean which diseases?

A

Osteoarthritis

Internal derangements (tendon/ligament/meniscal injuries)

48
Q

Inflammatory effusion could mean which diseases

A

Infection

Crystal disease

Rheymatoid arthritis

Seronegative spondyloarthropathy

SLE

49
Q

Pyarthrosis effusion could mean which dieseases?

A

Infection

Intense inflammation: crystal disease, psoriatic arthritis

50
Q

Hemarthrosis effusion could mean which diseases?

A

Trauma (intraarticular fracture)

Coagulopathy (hemophilia, anticoagulant related)

51
Q

Acute phase response

A

Increase in liver-synthesized proteins and immunoglobulins that occurs in response to trauma/tissue injury or a variety of inflammatory/immunologic stimuli

Acute phase proteins: fibrinogen (major contributor), C-reactive protein, haptoglobin, ceruloplasmin, alpha-1-antitrypsin, complement C3 and C4, serum amyloid A protein, immunoglobulins

52
Q

Testing for systemic inflammation

A

Use ESR and CRP

Sensitive for inflammation, but not specific enough to be used to make diagnosis of specific disease

53
Q

Erythrocyte sedimentation rate (ESR)

A

Measures distance in mm that RBCs fall over 1h

Normal range: 0-20mm/h

Age adjustment (>50yrs) for upper limit of normal: Males = age/2; females = age+10/2

Indirect measure of acute phase proteins because acute phase proteins are anionic (fibrinogen) so allow RBCs to pack together more closely, decrease surface area and sediment more rapidly

High sensitivity for many inflammatory conditions

Not very specific: many diseases and non-disease states can result in increased ESR

Slow decay time (weeks) so can’t follow changes over short periods of time

54
Q

C-reactive protein (CRP)

A

Increased specificity because is a directly measured protein level so less affected by non-disease factors than the ESR

Increases within 24h of inflammatory stimulus, peaks within 24-48h and rapidly normalizes with resolution of stimulus

More useful measure for changes over shorter periods of time (days) than ESR

55
Q

Why shouldn’t you measure ESR every day?

A

ESR won’t change every day because is affected by anionic acute phase proteins, which stick around for weeks!

Ex: fibrinogen stays around for 2 weeks after initial inflammatory stimulus

56
Q

Points about using ESR and CRP

A

Nonspecific: these tests should NOT be used as general screening test for any disease; limited role in diagnosis and prognosis; most useful for monitoring disease activity and response to therapy

False-positives: most are of short duration and spontaneously normalize

False-negatives: ESR and CRP can be normal with many conditions, so a normal result alone cannot rule out a specific disease

57
Q

Rheumatoid factor

A

Rheumatoid factor (RF) is an IgM, IgG, or IgA antibody which binds to Fc portion of an IgG immunoglobulin

IgM RFs are clinically measured

Not specific for any given condition: reflects a state of chronic immune activation

Increased RF occurs normally in older individuals with chronic infections and other autoimmune diseases

Helps to make diagnosis of RA, but is NOT diagnostic of RA (could mean many other things)

58
Q

Antinuclear antibody (ANA)

A

ANA test detects antibodies directed against different nuclear antigens

Antinuclear antibody in plasma caused LE cells (PMN) to phagocytose nuclei, which happened a lot in people with SLE (not specific for SLE though)

ANA titer is highest dilution giving positive signal (immunofluorescence); abnormal result is titer >1:40

59
Q

Approach to diagnosing arthritis

A

1) Determine if complaints due to true arthritis or periarticular
2) Monoarticular or polyarticular arthritis?
3) Inflammatory or non-inflammatory?
4) Symmetric of asymmetric?
5) Is there axial joint involvement?

Now in the right diagnostic “neighborhood”

6) Modify hypotheses based on mode of onset, duration, sequence of involvement, presence of extraarticular findings
7) Rule out or confirm diagnoses with appropriate lab, radiologic and other testing

60
Q

Monoarticular arthritis

A

Most common types are acute septic arthritis and crystal arthritis…and they present identically!

61
Q

Septic arthritis

A

Inflammatory arthritis caused by an infectious process involving the synovium and joint space

Most commonly a single joint, but polyarticular presentation 10-20% of the time

Infections can be acute or chronic

Considered a medical emergency because: (1) marker for underlying systemic infection with increased morbidity and mortality, and (2) can result in irreversible damage to the joint in just a few days resulting in impaired joint function and/or chronic pain

Two most common causes of septic joint are nongonococcal bacterial arthritis and gonococcal bacterial arthritis (disseminated gonococcal infection)

62
Q

Mechanisms of entry of nongonococcal bacterial arthritis into the joint

A

1) Hematogenous spread: most common; bacteremia (bacteria in the blood) results in seeding of joint
2) Direct innoculation: following procedures or penetrating trauma
3) Direct spread from an adjacent tissue infection: cellulitis (skin infection), bursitis, or osteomyelitis (bone infection)

63
Q

Progression and pathology of nongonococcal bacterial arthritis

A

Bacterial seeding results in acute inflammation with migration of neutrophils into synovium, synovial hyperplasia, and development of joint effusion

Over next 5-7 days, release of various inflammatory cytokines, host proteolytic enzymes and bacterial toxins contribute to cartilage and bone degradation (bones look mushed together on x-ray: irregular bony margins, joint space narrowing, osteopenia)

64
Q

What is the most common cause of nongonococcal bacterial arthritis?

A

Staphylococcus aureus (gram positive coccus)

Gram negative bacterial joint infections are much less common and associated with older age, GI infections, GU infections, and IV drug use

65
Q

Clinical presentation of nongonococcal bacterial arthritis

A

Acute onset of inflamed joint

Typically monoarthritis (polyarticular 10-20% and usually with immunosupression or marked bacteremia)

Most commonly large (shoulder, hip, knee (50%, most common)) or intermediate (wrist, ankle) joints; small or fibrous joints (sacroiliac, sternoclavicular) much less common

Constitutional symptoms: fever, chills, rigors (bacteremia)

Signs of infection in other organ systems

Physical exam: erythema and warmth, tenderness to palpation, pain on passive range of motion, swelling and effusion

66
Q

Risk factors for nongonococcal bacterial arthritis

A

Anything contributing to increased risk of bacteremia, joint seeding, or decreased ability to clear infection from joint

Local factors: prior joint damage, surgery/arthrocentesis, prosthetic joint

Systemic factors: younger/older age, immunosuppression, comorbid disease

Social factors: IV drug abuse, homelessness, animal exposures

67
Q

Gonococcal bacterial arthritis

A

Neisseria gonorrhea (gram negative) enters into joint via hematogenous spread from its mucosal site of infection (urethra, cervix, rectum, pharynx)

Develops in only 1-3% of people infected with Neisseria gonorrhea

Most common form of septic arthritis in youg sexually active adults in the US but can occur in older adults too

3x more common in women and more common in homo/bisexual men

68
Q

Two types of clinical presentation of gonococcal bacterial arthritis

A

1) Purulent arthritis: mono or oligoarticular arthritis (wrist, knee, and/or ankles); purulent joint effusion present from which organism can be cultured; may not be associated with other signs of gonococcal infection
2) Triad: macular or vesicopustular skin lesions; tenosynovitis involving tendon sheaths of wrists, fingers, ankles, toes (important distinguishing feature); blood and mucosal cultures usually positive but synovial fluid cultures negative

69
Q

Risk factors for gonococcal bacterial arthritis

A

Local factors: female, previous gonococcal infection (increased risk of asymptomatic infection)

Systemic factors: bacterial factors, complement deficiencies that impair the formation of the attack complex (C5-8)

Social factors: unprotected sexual activity, IV drug abuse, lower educational status, urban residence

70
Q

Diagnosis of septic arthritis

A

Clinical: monoarthritis is considered a septic joint until proven otherwise!

Lab: WBC possibly elevated but normal 40% of the time; positive blood cultures indicate bacteremia; culture mucosal sites if suspect disseminated gonococcal infection

Joint aspiration: inflammatory fluid (WBCs > 2,000mm3, increased neutrophils); gram stain of fluid may be positive (but sensitivity only 20-45%); synovial fluid culture to confirm infection is gold standard (allow culture to grow for 72 hours)

71
Q

Management of septic arthritis

A

If you suspect septic joint, start IV antibiotics right after joint aspiration/sent for culture/blood culture taken

Evaluate other organ systems for infection

Joint should be serially drained to remove damaging inflammatory and toxic mediators and to monitor cell count and if cell count > 50,000mm3, call orthopedics to perform washout of joint (using big tube to wash w/saline)

After clinical improvement, low level rehab starte

Treatment delay increases the risk of chronic joint damage

72
Q

Crystal arthropathy (gout)

A

Purines metabolized to uric acid but uric acid exists in ionic urate form in plasma, which is excreted by the kidney

Physiologic saturation of plasma causes monosodium urate crystals (gout crystals) to form in tissues

Inflammatory response to urate crystals via innate immune system (same as rsponse to septic joint, which is why they present identically!)

73
Q

Causes of hyperuricemia

A

Increased production: increased cell turnover (some tumors/chemotherapy, psoriasis), increased intake of purine rich food (shellfish, organ meat, beer), increased alcohol intake (binging causes increased breakdown of ATP/ADP), genetic predisposition (mutations in purine metabolizing genes)

Decreased excretion: acute/chronic renal failure, drugs that interfere w/excretion (thiazide diuretics), diabetes (increased insulin interferes with excretion), genetic predisposition (polymorphisms in renal urate transporters)

74
Q

Pathophysiology of gout

A

Not completely known

Not just urate crystal deposition, because extracellular crystals found in non-inflamed joints

Changes in serum uric acid concentrations (increases AND decreases) associated with flare ups

75
Q

3 phases of gout

A

1) Acute arthritis: acute monoarthritis
2) Intercritical gout: asymptomatic period between attacks, but extracellular MSUM crystals may still be present in synovial fluid
3) Chronic tophaceous gout: increasing frequency and severity of attacks with formation of tophic and erosive polyarticular arthritis

Can cycle through phases 1 and 2 or 2 and 3

76
Q

Clinical presentation of gout

A

History of hyperuricemia or condition associated with hyperuricemia

Sudden onset of monoarthritis

Inflammation 3-10 days, spontaneous resolution 3-7 days

Most common at 1st metarsalphalangeal, ankle, knee, wrist

Tenosynovitis and bursitis bc urate crystals in synovium of tendon sheaths and bursae

With longstanding hyperuricemia, chronic gout can develop

Low grade fever, inflamed joint, tophi in soft tissues (skin, bursae, tenosynovium)

77
Q

Chronic gout

A

Develop with longstanding hyperuricemia

Flares can become more frequent, more prolonged, polyarticular

Associated with nodular collections of monosodium urate crystals (tophi)

Chronic low to moderate joint inflammation that doesn’t spontaneously resolve and is poorly responsive to treatment

Tophi formation can cause bony erosions

Can cause renal precipitation of urate crystals and thus kidney damage

78
Q

Diagnosis of gout

A

Should be suspected in acute monoarthritis or tenosynovitis, especially if there are risk factors

Since identical to septic joint on appearance, synovial fluid must be obtained for cell count, gram stain, culture, crystal analysis

Definitive diagnosis of gouty arthritis made by finding negatively birefringent (yellow parallel) needle-shaped crystals (and intracellular crystals mean acute gouty flare)

Can sometimes have septic joint at same time

79
Q

Management of gout

A

First treat inflammation (colchicine, steroids, NSAIDs, intraarticular steroid injection)

Avoid anything that would change serum uric acid concentration (don’t give allopurinol bc that would decrease uric acid concentration and don’t want it to change at all!)

If more than 2 flares per year then lower serum uric acid concentration (hypouricemic therapy): decrease purine intake, decrease meds that would cause hyperuricemia, take hypouricemic meds

80
Q

Calcium pyrophosphate deposition disease (CPPD), or pseudogout

A

CPPD crystals can form in cartilage and intraarticular fibrous structures and shedding of crystals can cause inflammatory response that occurs through same innate immune pathway as gout

Clinical presentation of joint inflammation, tenosynovitis, bursitis identical to gout except NO tophi

81
Q

Clinical presentations of CPPD

A

Acute arthritis (pseudogout causes inflammation, monoarticular)

CPPD arthropathy (degenerative changes similar to osteoarthritis)

Tenosynovitis alone or with inflam arthritis

Radiologically as chondrocalcinosis (calcification of cartilage/fibrocartilage)

Common with older age but sometimes associated with metabolic disease (parathyroid, thyroid, hemachromatosis)

82
Q

Diagnosis of CPPD

A

Positively birefringent (parallel blue) rhomboid-shaped crystals on polarizing microscopy

83
Q

Treatment of CPPD

A

Inflammation treated same way as gout (colchicine, steroids, NSAIDs, intraarticular steroid injection)

No hypouricemic therapy (uric acid isn’t a problem!)

Consider metabolic workup

84
Q

Osteoarthritis

A

Complex group of non-autoimmune mechanically-induced conditions due to altered joint loading that results in failure and loss of intraarticular cartilage and dysfunction of other articular components (synovium, ligaments, neural components, bone) resulting in chronic joint pain and loss of joint function

Most prevalent type of arthritis

85
Q

Primary vs. Secondary osteoarthritis

A

Primary osteoarthritis: not associated with trauma or other medical condition; joint involved usually DIP, PIP, 1st CMC, wrists, acromioclavicular, cervical/lumbar spine, hips, knees, MTPs

Secondary osteoarthritis: associated with trauma or other metabolic conditions (such as CPPD); joint involved usually NOT the ones listed above

86
Q

Pathology of osteoarthritis

A

In the cartilage, get fibrillations and fissures

Thinning and loss of cartilage in response to altered forces which cause osteophytes

87
Q

Clinical presentation of osteoarthritis

A

Mechanical joint pain exacerbated by weight bearing and/or relieved by rest (can contribute to inactivity)

Stiffness less than 30 min in the morning or after not moving for a while

Decreased range of joint motion secondary to pain or severe joint damage

Muscle weakness/atrophy secondary to pain and inactivity, can result in altered gait and increased risk for fall

Non-inflammatory swelling

Characteristic presentation: bilateral DIP joint space narrowing with osteophytes

Trauma, CPPD and other metabolic conditions suggest secondary osteoarthritis

88
Q

Physical exam findings of osteoarthritis

A

Tenderness to palpation without joint swelling

Decreased ROM with crepitus (crackling due to loss of cartilage)

Pain on passive range of motion (if disease is in advanced stage)

Osteophytes, joint malalignment

Altered gait

Bursitis and/or tendonitis due to altered gait and joint deformities

89
Q

Diagnosis of osteoarthritis

A

History and associated joint exam findings in absence of inflammation

Secondary osteoarthritis diagnosed if joints other than those usually seen in primary, if trauma or underlying associated condition

Only do lab testing for underlying condition for secondary osteoarthritis

X-rays helpful to confirm diagnosis

90
Q

X-rays in diagnosis of osteoarthritis

A

Only take x-ray to confirm the diagnosis

Asymmetric joint space narrowing

Osteophytes

Subchondral bony sclerosis (hardening from inflammation)

Subchondral bony cysts (looks darker)

Note: radiologic severity does not always correlate with given patient’s pain or level of joint function

91
Q

Management of osteoarthritis

A

No therapy can restore lost cartilage

Goal of treatment is to control pain (meds, PT, weight loss), restore function (pain control, PT), prevent/minimize progression (PT, weight loss)

If pain/loss of function severe, consider joint replacement surgery

Block 4: Musculoskeletal (37 decks)

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