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ICM II > Rheumatology II > Flashcards

Rheumatology II Flashcards

1
Q

RA genetic loci?

A

DR4

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2
Q

RA inciting factors?

A

Maybe EBV, parvo, human herpesvirus 6, mycoplasma

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3
Q

Types of automimmune reaction in RA?

A

Type III

Type IV → CD4+ cells release inflammatory cytokines
• TNF is important cytokine from macrophages

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4
Q

What cells in RA probably produce RF?

A

Inflamed synovial cells express an antigen that triggers B cells to produce rheumatoid factor (RF).

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5
Q

Where do the immune complexes in RA come from?

A

RF and IgG join to form immunocomplexes

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6
Q

What likely causes inflammatory cells to enter the joint space in RA?

A

Once ICs deposit, they activate complement system.

C5a release acts as chemotactic agent for neutrophils and other leukocytes.

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7
Q

What is a pannus in RA?

A

Granulation tissue in the synovial tissue formed by fibroblasts and inflammatory cells.

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8
Q

Hand joints most commonly affected by RA?

A

Symmetric MCP, PIP joints

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9
Q

What is swan neck deformity?

A
  • Flexion of DIP

* Extension of PIP

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10
Q

What is Boutonniere deformity?

A
  • Extension of DIP

* Flexion of PIP

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11
Q

What non-hand joints are commonly affected by RA?

A
  • Knees
  • C-spine
  • Hips
  • Shoulders
  • Elbows
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12
Q

Lung manifestations of RA?

A
  • Chronic pleuritis with effusions

* Interstitial fibrosis

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13
Q

What are the hematological manifestations of RA?

A
  1. Chronic anemia
  2. Hemolytic anemia (autoimmune)
  3. Felty syndrome
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14
Q

What is Felty’s syndrome?

A

Autoimmune neutropenia and splenomegaly

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15
Q

What neuropathy is common in RA?

A

Carpal tunnel syndrome

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16
Q

What is common c-spine manifestation in RA?

A

Possible subluxation of atlantoaxial joint
• Possible cord compression → paralysis
• Possible vertebral artery occlusion → stroke

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17
Q

Where are rheumatoid nodules found?

A
  • Extensor surface of forearms

* Lungs

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18
Q

What are rheumatoid nodules typically correlated to?

A

High RF titers

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19
Q

What are common cardiac manifestations of RA?

A
  1. Fibrinous pericarditis
  2. Aortitis
  3. Immunocomplex small vessel vasculitis (usually around the ankles)
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20
Q

Popliteal cysts are common with what AI disorder?

A

RA

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21
Q

Serology of RA?

A
  • ANA (30%)
  • RF (70-90%)
  • Anti-CCP
  • Increased y-globulin
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22
Q

Initial RA treatment?

A
  • Exercise
  • NSAIDs
  • Disease modifying drugs
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23
Q

What is Sjogrens syndrome?

A

Autoimmune destruction of minor salivary and lacrimal glands

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24
Q

Which gender does Sjogrens typically affect?

A

Female

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25
Q

What are the main three clinical finds of Sjogrens?

A
  1. Rheumatoid arthritis
  2. Keratoconjunctivitis secca (sand in my eyes)
  3. Xerostomia
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26
Q

Serology of Sjogrens?

A
  1. ANA (almost always)
  2. RF (90%)
  3. SS-A, SS-B
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27
Q

How do you confirm Sjogrens?

A

Lip biopsy shows lymphoid destruction of minor salivary glands

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28
Q

How do you treat Sjogrens?

A
  1. Artificial tears
  2. Pilocarpine or cyclosporine eye drops
  3. Civemaline (cholinergic for dry mouth)
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29
Q

What is the definition of SLE?

A

Chronic multisystem autoimmune disease that primarily involves skin, joints, serosal membranes, blood cells, nervous system, and kidneys.

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30
Q

What genetic loci is associated with SLE?

A

DR3

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31
Q

How can complement affect how likely a PT is to get SLE?

A

Certain complement deficiencies (C2 for example) can increase risk

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32
Q

What are four environmental factors that might precipate SLE?

A
  1. Infection (EBV)
  2. Ultraviolet light
  3. Estrogen
  4. Medications
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33
Q

What types of autoimmunity is involved with SLE?

A 
Type III
• Skin
• Glomeruli/tubules
• Joints
• Small vessels
Type IV
• Blood components
34
Q

What is a very common arthritic finding with SLE?

A

Morning stiffness in the hands

35
Q

What are the common hemotalogic findings with SLE?

A
  • Hemolytic anemia
  • Thrombocytopenia
  • Leukopenia
36
Q

What joints are most often affected with SLE?

A
  • PIP, MCP

* Symmetric, nonerosive, not deforming

37
Q

Skin findings in SLE?

A
  • Malar rash on the face

* Rash worsened by UV light

38
Q

Renal findings in SLE?

A
  • Diffuse proliferative glomerulonephritis
  • Can present with nephrotic syndrome
  • CHRONIC RENAL FAILURE IS THE MOST COMMON CAUSE OF DEATH
39
Q

Cardiovascular findings with SLE?

A
  • Fibrinous pericarditis with or without effusions

* Libman-Sacks endocarditis (sterile vegetation on valve)

40
Q

Respiratory findings with SLE?

A
  • Pleuritic chest pain with or without effusions

* Interstitial fibrosis may occur leading to restrictive lung disease

41
Q

CNS findings with SLE?

A
  • Headache, psychosis, Seizures, stroke

* Vessel thrombosis causing stroke is most often associated with ANTI-PHOSPHOLIPID SYNDROME

42
Q

Pregnancy complications related to SLE?

A
  • Complete heart block can occur if IgG SS-A crosses

* Spontaneous abortion can occur (thrombosis from anti-phospholipid A)

43
Q

What two drugs are most often the cause of drug-induced SLE?

A

Procainamide and hydralazine

44
Q

Serology for SLE would show what?

A
  • ANA (100%) – for screening, 80% sensitive
  • Anti dsDNA – confirmation 99% specific
  • Anti-Smith – confirmation 100% specific
45
Q

Complement levels in SLE?

A

Usually decreased because of complement activation from ICs

46
Q

Immunofluorescent testing in SLE?

A

Band test – Shows ICs at dermal-epidermal border

47
Q

What structural component causes the symptoms of scleroderma?

A

Excessive collagen deposition in skin, GI tract, lungs, kidneys

48
Q

Who does scleroderma most often affect?

A

Women of child bearing age

49
Q

What is the pathogenesis of scleroderma?

A
  1. Small-vessel endothelial cell damage produces blood vessel fibrosis and ischemic injury
  2. T-cells release cytokines → excessive collagen synthesis
  3. Stimulatory autoantibodies against platelet-derived growth factor
50
Q

Hand findings in scleroderma?

A
  1. Raynaud’s phenomenon

2. Tapered fingers with digital infarcts

51
Q

Skin findings in scleroderma

A
  1. Skin atrophy and tightening that starts distally
  2. Parchment-like appearance
  3. Extensive dystrophic calcification in subQ
  4. Tightened facial features
52
Q

GI findings in scleroderma?

A
  1. Esophageal dysmotility
  2. Reflux due to loss of lower esophageal sphincter
  3. Loss of villi in small bowel
  4. Dysmotility and cramping
53
Q

Respiratory findings in scleroderma?

A
  1. Interstitial fibrosis

2. RESPIRATORY FAILURE IS MOST COMMON CAUSE OF DEATH

54
Q

Renal findings in scleroderma?

A
  1. Vasculitis involving arterioles

2. Infarcts → malignant HTN

55
Q

Common lab findings in scleroderma?

A
  • ANA (79-90%)

* Anti-topoisomerase (30%)

56
Q

What is CREST syndrome?

A 
C-calcification & centromere antibody
R-Raynaud's
E-Esophageal dysmotility
S-Sclerodactyly 
T-Telangiectasias
57
Q

What malignant neoplasm are DM and PM associated with

A

Lung cancer

58
Q

Mechanism of dermatomyositis damage

A

Antibody-mediated damage

59
Q

Mechanism of polymyositis damage

A

T cell-mediated damage

60
Q

Most common area for DM and PM pain

A

Shoulders

61
Q

Skin findings with dermatomyositis?

A
  1. Heliotrope rash around eyes

2. Purple pustules on knuckles GOTTRON’S PATCHES

62
Q

Laboratory findings with DM and PM

A
  • ANA (30%)
  • Increased creatine kinase
  • Muscle biopsy shows lymphocytic infiltrate
63
Q

Treatments for FM?

A
  • Have PT stay active
  • AVOID NARCOTICS
  • SSRI’s and TCAs might be beneficial
64
Q

Which gender does juvenille RA affect more?

A

Girls

65
Q

What occurs in 20% of JRA cases?

A

Still’s disease

66
Q

What is Still’s disease?

A
  • Commonly presents as an “infectious disease”
  • Fever, rash, polyarthritis
  • Generalized lymphadenopathy
  • Neutrophilic leukocytosis
67
Q

What is polyarticular JRA?

A
  • 40% of cases are this type

* Disabling arthritis of the joints dominates

68
Q

What is pauciarticular JRA?

A
  • 40% are this type
  • Arthritis is limited to a few joints
  • UVEITIS with potential for blindness can occur
69
Q

Seronegative SA involves which joints?

A

Axial joints

70
Q

Which genetic loci are associated with seronegative SA?

A

B27

71
Q

What is ankylosing spondylitis?

A

Targets SI joints in young men

72
Q

What disease causes bamboo spine?

A

Ankylosing spondylitis (causes forward curvature kyphosis)

73
Q

What result on a Schober’s test

A

Less than 5 cm

74
Q

What non-spine problems are associated with ankylosing spondylitis?

A
  • Prostatitis (80%)
  • Aortitis with regurgitation
  • Anterior uveitis
75
Q

What are treatment options for ankylosing spondylitis?

A
  1. NSAIDs
  2. Disease modifying drugs
  3. TNF-a inhibitors can slow down the progression of the disease drastically
76
Q

Hand findings in psoriatic arthritis?

A
  1. Sausage shaped DIP joints
  2. Pencil-in-cup deformity
  3. Extensive nail pitting
77
Q

What are late manifestations of Lyme disease?

A
  • Disabling arthritis
  • Bilateral Bell’s palsy
  • Myocarditis and pericarditis
78
Q

What might be seen on the penis of a patient with Reiter’s syndrome?

A

Circinate balanitis

79
Q

What type of damage might occur in osteoarthritis on a molecular level?

A

Particular cytokines which are released activate metalloproteinases and cause destruction of proteoglycans and collagen

80
Q

What is reactive bone formation of joint margins in osteoarthritis called?

A

Osteophyte

81
Q

What commonly protrudes into the bone in OA?

A

Subchondral cysts

82
Q

What are joint mice/

A

Fragments of articular cartilage that breaks free into a joint space from OA

ICM II (10 decks)

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