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MSS Weeks 3-5 > Gout, Pseudo gout, RA, and OA PART 1/2 > Flashcards

Gout, Pseudo gout, RA, and OA PART 1/2 Flashcards

1
Q

What are synovial joints? and what are they also known as?

A

Allow for gliding movement facilitated by lubricated cartilagenous surfaces.

Also known as diarthrodial joints.

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2
Q

What comprises a synovial joint?

A

Hyaline cartilage on articular surface

and

Synovial cavity

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3
Q

What are the functions and components of hyaline cartilage?

A

Functions:

  • Elastic shock absorber spreading weight across surface of joint
  • Friction-free surface (along with synovial fluid)

Components: AVASCULAR

  • Type 2 collagen (Tensile strength)
  • Water and Proteoglycans (elasticity and decrease friction)
  • Chondrocytes (Maintain cartilaginous matrix)
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4
Q

What are the components and function of the synovial cavity?

A

Synovial cells (1. Produce synovial fluid, 2. Remove debris (phagocytic fxn), 3. Regulate movement of solutes

Synovial fluid (Lubricant and provides nutrients to articular cartilage)

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5
Q

What are the categorizations or patterns of arthritis?

A

Inflammatory vs. non-inflammatory

Monoarthritis vs. polyarthritis

Acute vs Chronic

Large joint vs small joint involvement

Symmetry

Snyovial vs non-synovial

Axial vs. Peripheral Joints

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6
Q

What is the clinical assessment for inflammation?

A

History:

Morning stiffness > 1 hr

Improves as the day goes on

Physical exam:

  • Erythema and warmth
  • Synovitis - thickening of the synovium around joints; (tender and squishy w/ firm palpation)

Lab tests:

- Serologies: markers present in serum: eg Rh factor

  • Inflammatory markers (ESR and CRP, aka, Erythrocyte sedimentation rate and C reactive proteins, also anemia)
  • Peripheral blood leukocytosis (septic arthritis)
  • Joint fluid analysis

Radiographic changes:

-X ray, erosions of bone at joint margins, MRI, CT

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7
Q

What are the categories for NON-INFLAMMATORY/INFLAMMATORY/SEPTIC in synovial fluid analysis?

A

WBC: <2000, >2000, >50000

PMNS: <10%, 50-90%, >90%

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8
Q

What is gout?

A

A metabolic disorder resulting in elevation of uric acid (hyperuricemia) beyond the level of saturation.

Plus presence of inflammatory microcrystals in the joint

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9
Q

What percent of gout is due to overproduction vs. underexcretion?

A

10% overproduction

90% underexcretion

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10
Q

What is the male to female ratio for gout?

A

1.3 males : 0.5 females

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11
Q

What hormonal change can increase gout in females and why?

A

Increases in females after menopause because ESTROGEN PROMOTES URATE RENAL EXCRETION

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12
Q

What are specific causes for overproduction or underexcretion of urea (resulting in hyperuricemia)

A

Overproduction:

  • Enzymatic abnormalities
  • Increased cell turnover
  • Diet
  • Etoh

Underexcretion:

  • Metabolic syndrome
  • Renal disease
  • Drugs like diuretics or cyclosporine
  • Etoh
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13
Q

How do we produce uric acid and what are the proportions of the total?

A

1/3: Dietary nucleotides and nucleoproteins we eat

2/3: internal turnover of cellular nucleotides and nucleoproteins

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14
Q

Would the breakdown of RBCs result in increase of uric acid?

A

No, because they are NOT NUCLEATED (like WBC)

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15
Q

Where is uric acid excreted and what are the proportions?

A

1/3 Gut excretion (200mgms/day)

2/3 Renal excretion (600 mgms/day), so 10% of filtered load

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16
Q

What are the 3 Ls of polarizing microscopy w/red compensator

A

Parallell, Allopurinol, Yellow=gout

negatively birefringent crystal

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17
Q

What can precipitate a gout attack?

A

Elevation of uric acid

Reduction of uric acid

Release of crystals from pre-formed deposits

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18
Q

How does monosodium urate crystals MSU crystals cause inflammation

A
  1. Recognition by PAMPs
  2. Phagocytosis
  3. Inflammasome activation (capsase 1 activated)
  4. IL-1beta release
  5. Endothelium signal activation
  6. Pro-inflammatory mediators release
  7. Neutrophil recruitment
  8. More IL-1beta release
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19
Q

What is CPPD?

A

Calcium pyrophosphate dihydrate crystal deposition

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20
Q

What is the prevalence of CPPD?

What is the etiology of CPPD?

What are mixed crystals?

What (again) does CPPD stand for?

A

12% of elderly, 5% at age 60 rising to 30% by age 90

Etiology unknown, but in most cases related to overproduction of PPi

Multiple different presentations, CPPD crystals may be found with urate cyrstals (mixed crystals)

Calcium pyrophosphate dihydrate crystal deposition

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21
Q

How does Calcium pyrophosphate dihydrate crystal deposition work?

A
  1. Through ATP hydroysis to AMP, production of pyrophosphate PP
  2. Goes through ank channel (can have genetic deffects)
  3. PPi binds calcium easily and forms crystals
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22
Q

What are the colors of urate crystals and calcium pyrophosphate crystals when PARALLEL and PERPENDICULAR to the direction of the compensator?

A

Urate crystals: yellow parallel/blue perpendicular (Negatively birefringent, is gout)

Calcium crystals: blue parallel/white perpendicular (Positively birefringent, is CPPD)

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23
Q

What factors can evalulate CPPD for patients under 60?

A

Fe, TIBC- Hemochromatosis

Alk phos-Hypophosphatasia

Mg-Hypomagnesemia

Ca-Hyperparathryoidism

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24
Q

What is pseudogout?

How is pseudogout diagnosed?

A

Attacks of acute arthritis similar to gout, but usually in larger joints: knee, wrist, shoulder

Diagnosed by rhomboidal shaped, positively birefringent crystals in joint fluid.

Also, diagnosis may be suggested by chondrocalcinosis, but not seen in all cases.

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25
Q

What are the different presentations of CPPD arthritis?

A
  1. Asymptomatic- most common
  2. Pseudogout
  3. Osteoarthritis (OA), may be assoc. with widespread OA including OA in atypical joints
  4. RA-like (MCP joint enlargement)- may produce chronic low grade inflammation
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26
Q

What are the drugs used for Gout?

A

NSAID

Steroid

Colchicine

Allopurinol

Febuxostat

Pegloticase

Probenecid

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27
Q

What are the drugs used for Rheumatoid Arthritis?

A

Disease-modifying Rheumatic Agents (DMARDs)

Adalimumab

Etanercept

Infliximab

Abatacept

Rituximab

Tocilizumab

Tofacitinib

Anakinra

Azathioprine

Hydroxychloroquine

Leflunomide

NSAID

Steroid

Methotrexate

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28
Q

What are the therapeutic goals of Uric Acid Medications?

A
  1. Increase excretion of uric acid
  2. Inhibit inflammatory cells
  3. Inhibit uric acid biosynthesis
  4. Provide symptomatic relief (typically w/NSAIDS or steroids for short term)
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29
Q

What drugs provide symptomatic relief for gout?

A

NSAIDs and Steroids

NSAIDS (given within first 24 hours): Indomethacin and Naproxen

BUT NOT ASPIRIN

Steroids: most useful for patients with contraindict to NSAIDS, short term use only because adverse effects w/ extended use

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30
Q

For Colchicine, what is the MOA

A

Colchicine MOA:

  • Antimitotic, arresting cell division in G1 by interfering with microtubule and spindle formation, specifically in inflammatory cells=neutrophils, inhibiting their activation and migration. This lessens symptoms of the inflammation.
  • No effect on uric acid excretion
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31
Q

For Colchicine, what are the SE?

A

Colchicine SE:

  • Significant adverse effects w/ a narrow therapeutic-toxicity window.
  • GI, nausea/vomiting/diarrhea/abdominal pain
  • Usually has a latent period before symptoms
  • Effects the rapid proliferating cells of GI
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32
Q

For Colchicine, what are the important pharmacokinetics/contraindications?

A
  • Oral, Rapid variable absorp, deposits in tissue stores forming complex with tubulin (large vol of distribution)
    1. Hepatic or renal disease
    2. Elderly patients
    3. Taking CYP3A4 or P-gp inhibitors
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33
Q

What is the therapeutic use for Colchicine?

A
  1. Acute gout attacks (w/in hours)
  2. Prophylactically in patients with chronic gout

*however not drug of choice due to adverse effects

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34
Q

What are indications for prophylactic gout therapy?

A
  1. Frequent attacks
  2. Disabling attacks
  3. Urate nephrolithiasis
  4. Urate nephropathy
  5. Tophaceous gout
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35
Q

What are non-pharmacological measures for gout?

A
  1. Abstaining from alcohol
  2. Weight loss
  3. Discontinue medications impairing uric acid excretion (ASPIRIN AND THIAZIDE DIURETICS)
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36
Q

What are potential drug therapies to prevent gout flare and destructive effects on joints and kidneys?

A

Allopurinol

Febuxostat

Probenecid

Pegloticase

37
Q

What is the MOA for Allopurinol?

A

Inhibits terminal steps in uric acid biosynthesis by blocking xanthine oxidase

RESULTING in plasma uric acid concentration decreases and uric acid crystals dissolve

38
Q

What are the important pharmokinetics of Allopurinol?

A

Allopurinol (structural analog of hypoxanthine) is converted to the active compound oxypurinol by aldehyde oxidoreductase

39
Q

What are the SE of Allopurinol?

A
  1. Hypersensitivity:
    - not always immediate
    - increases if taken with ACE inhibitors, thiazide diuretics, amoxicillin
    - serious
  2. Acute gout attack
    - mobilizes tissue stores of uric acid
    - Give the drug with colchicine or NSAID
40
Q

What are the therapeutic uses of Allopurinol?

A
  • Prevents primary hyperuricemia of chronic gout (for severe forsm of gouty nephropathy, tophaceous deposits, renal urate stones)
  • Prophylactic treatment in secondary forms of hyperuricemia due to hematological disorders or anti-neoplastic therapy
41
Q

What is Febuxostat?

A

A non-purine xanthine oxidase inhibitor that forms a stable complex w both the reduced and oxidized enzyme and inhibits catalytic fxn in both states.

42
Q

What are the advantages of Febuxostat vs. Allopurinol?

A
  1. Febuxostat is more potent than allopurinol
  2. Febuxostat was more effective than allopurinol in the subset of patients with impaired renal fxn
  3. Incidence of adverse effects dizziness/diarrhea/headache/nausea was similiar between the two
  4. CV side-effects (Antiplatelet trialists collaboration events) was higher w/ febuxostat
43
Q

What is the MOA for Pegloticase?

What are the pharmokinetics?

Adverse effects?

Therapeutic uses?

A

Recombinant form of Uricase (uric oxidase enzyme), normally absent in humans, converts uric acid to allantoin an inactive and water soluble metabolite of uric acid. PEGylated (polyethylene glycol covalently linked to molecule

Pharmoacokinetics: IV administration but at least with has long half life (every 2 weeks) .

SE:

  1. Infusion site reactions
  2. Gout flare (need to provide prophylaxis for acute gout flares)
  3. Immune response directed at the PEG portion of the molecule

Therapeutic Uses:

Used for refractory chronic gout

44
Q

What is Probenacid?

MOA?

Pharmacokinetics?

SE?

A

A drug that increases the rate of excretion of uric acid.

MOA:

Increase uric acid excretion by competing with the renal tubular acid transporter so less urate is reabsorbed (OAT=organic acid transporter also called URAT1)

Pharmacokinetics:

-Oral, dose-dependent half life, plasma protein binding

SE:

Some GI SE/Ineffective in pt. with renal insufficiency/CI in pt. with uric acid kidney stones

45
Q

What is the therapeutic use for Probenacid?

A

Used for chronic gout but rarely in pts. with any kidney disease or overproducers of uric acid. More likely to produce uric acid stones in kidney

46
Q

What is Rheumatoid Arthritis? What percent of the population does it affect?

What type of cells are associated?

Is there a genetic predisposition? What is an example?

What gender has it more?

A

An inflammatory polyarthritis, affecting 1% of the population

An immunological (T cell) disease, but with significant B cell contribution

There is a genetic predisposition (eg HLA-DR shared epitope)

Hormonal contribution (F>M)

47
Q

What is the pathology of Rheumatoid arthritis?

A

Chronic Papillary synovitis

  • Chronic inflammation of the synovium: CD4+ T cells/Plasma cells/Macrophages/Giant cells (Frequently forming lymphoid follicles)
  • Accompanied by synovial cell hyperplasia (Resulting in papillary [FINGERLIKE PROJECTIONS]pattern on the surface of the synovium)
  • Neutrophils and fibrin on joint surfaces in acute phase
  • Hyperplastic inflammed synovium extends over the articular surface forming a pannus which fills the joint space.

*Over time, articular cartilage destroyed

*Increased osteoclast activity in underlying bone causing it to be eroded

*End result may be joint fusion[ANKYLOSIS]due to fibrosis and ossification

*Osteophytes and new bone formation are not prominent [unlike osteoarthritis]_

48
Q

Where do Rheumatoid nodules form,

what are they like,

and why do they develop?

A

Develop most commonly on skin in areas exposed to pressure

Grossly: non-tender, firm, round/oval

Microscopically: Central zone of fibrinoid necrosis surrounded by rim of epithelioid histiocytes, and then lymphocytes and plasma cels

Cause: Necrosis secondary to vascular damage possibly secondary to vasculitis (inflammation of the vessel walls) associated with RA

49
Q

What feature is not consistent with a history of Rheumatoid Arthritis?

morning stiffness lasting 2 hrs

pains worse towards the end of the day

joint swelling in the hands and the feet

pains starting 6 months ago

A

PAINS WORSE TOWARDS THE END OF THE DAY IS NOT CONSISTENT WITH A HISTORY OF RHEUMATOID ARTHRITIS

50
Q

Describe Rheumatoid nodules:

  • Location:
  • Gross Appearance:
  • Microscopic Appearance:
A
  • Location:
    • ​Develop most commonly on skin (subcutaneous) in areas exposed to pressure (extensor surfaces of forearm & elbow)
  • Gross Appearance:
    • non-tender, firm, round/oval
  • Microscopic Appearance:
    • ​central zone of fibrinoid necrosis surrounded by rim of epithelioid histiocytes, and then lymphocytes and plasma cells
51
Q

What causes rheumatoid nodules?

A

necrosis secondary to vascular damage

possibly secondary to vasculitis associated with RA

52
Q

What are the major risk factors associated with RA?

A
  • Genetics: specific HLA genes increase risk of developing RA (HLA-DR4 and HLA-DR1)
    • First degree relatives of an RA patient at 1.5 fold higher risk of developing the disease
  • Ethnic prevalence (0.1% in rural Africans to 5% in Pima or Chippewa Indians)
  • Gender (females 2.5 times more than males)
    • Estrogen decreases apoptosis of B cells, potentially permitting selection of autoreactive clones
    • 75% of pregnant women with RA experience spontaneous remission
  • Infections
  • Cigarette smoking
  • Stress
53
Q

What is the significance of anti-cyclic citrullinated peptide (“CCP”)

A
  • May be seen in early RA (RF-)
  • Positive in some cases of RF negative RA
  • Same sensitivity as RF but more specific (25% false + RF w/Hep C)
  • Correlates with overall disease activity
54
Q

1987 CRITERIA FOR CLASSIFICATION OF RA:

A
  1. AM stiffness > 1 h
  2. Symmetrical arthritis
  3. At least 3 swollen joints
  4. Wrist, MCP, PIP involvement
  5. Rheumatoid nodules
  6. Positive rheumatoid factor
  7. X-ray change typical of RA in hand/wrist

Dx: 4/7 > 6 wks

55
Q

How are in the Social hx and Family hx important in RA?

A
  • Social hx:
    • uncommon, but some families have multiple affected members
  • Family hx:
    • more often smokers
    • risk for disability
56
Q

RA: Pulmonary Involvement

A
  • Rheumatoid pleuritis with effusion
    • Exudate, low glucose
  • Interstitial fibrosis
  • Nodules
  • Caplan’s syndrome – rheumatoid pneumoconiosis
  • Medication related:
    • MTX
    • leflunomide
    • anti-TNF (unusual chronic infections)
57
Q

Cardiovascular Disease in RA

A
  • CV events (age 25-65)
    • RA pts – 3.43/100 pt yrs
    • Controls – 0.59/100 pt yrs
  • RR – 3.96 (95% CI 1.86-8.43)
  • After adjustment for other CV risk factors, RR – 3.17 (CI 1.33-6.36)
  • “inflammation-mediated atherosclerosis”
  • RA – a CV risk factor as significant as DM
58
Q

What are the therapeutic goals for treating RA?

A
  • Relieve pain
  • Reduce inflammation
  • Slow down or stop joint damage
  • Improve a person’s sense of well being and ability to function
59
Q

How are NSAIDs effective in treating RA?

A
  • Large doses, long duration of treatment
  • No effect on progression of disease
  • Relieve symptom of pain
60
Q

What are DMARDs? Which ones are used to treat RA?

A

Disease-Modifying Anti-Rheumatic Drugs

  1. Etanercept
  2. Infliximab
  3. Tocilizumab
  4. Tofacitinib
61
Q

What is the mechanism of action for etanercept?

A
  • inhibits the ability of TNF-a to bind to its receptor
  • recombinant fusion protein
    • two soluble TNF p75 receptor moities linked to the Fc portion of human IgG
62
Q

Etanercept:

Pharmacokinetics

A
  • IV or Subcutaneous adminstration
  • Onset of action: 1-2 weeks
  • Elimination half-life > 3 days
63
Q

Etanercept:

Adverse Effects

A
  • injection site reactions
  • increased risk of infections
  • lymphomas in children/adolescent patients
64
Q

What are the therapeutic indications for etanercept?

A
  • moderate to severe RA
  • juvenile RA
  • early stage RA
65
Q

What is the mechanism of action for adalimumab?

A
  • IgG monoclonal antibody
    • All human
  • Binds to soluble and transmembrane forms of TNF-a
  • Prevents TNF-a binding to its receptor
66
Q

Adalimumab

  • Pharmacokinetics
  • Adverse effects
A
  • Pharmacokinetics
    • ​Subq
    • Every other week
  • Adverse Effects
    • ​injection site reactions
    • increased risk of infections
    • lymphomas in children/adolescent patients
67
Q

Adalimumab

Therapeutic Indications

A
  • active rheumatoid arthritis
    • moderate-to-severe
  • active juvenile idiopathic arthritis
    • moderate-to-severe
68
Q

Tocilizumab:

Mechanism of Action

A
  • humanized antibody, binds to soluble and membrane-bound IL-6 receptors
  • Inhibits IL-6-mediated signaling via these receptors
69
Q

Tocilizumab:

  • Pharmacokinetics
  • Adverse events
A
  • Pharmacokinetics:
    • I.V. administration
    • SubQ
  • Adverse events:
    • ​Injection site reactions
    • Increased risk of infections
    • Alterations in lipid profile
      • ​increases in total cholesterol, triglycerides, LDL , and/or HDL
70
Q

What are the therapeutic indications for tocilizumab?

A
  • indicated for adult patients with moderately to severely active RA
    • have had an inadequate response to one or more TNF antagonists
71
Q

What is the mechanism of action for tofacitinib?

A

Janus kinase (JAK) inhibitor

72
Q

Tofacitinib:

  • Pharmacokinetics
  • Adverse events
A
  • Pharmacokinetics
    • administered orally
    • metabolism mediated by CYP3A4
      • minor contribution from CYP2C19
  • Adverse Events
    • Increase risk of infections
    • Increase in cholesterol
73
Q

How is tofacitinib used therapeutically?

A
  • treatment of moderately to severely active RA in patients who have had an inadequate response to or intolerance to methotrexate
  • It may be used as monotherapy or in combination with methotrexate or other nonbiologic disease-modifying antirheumatic drugs (DMARDs)
74
Q

Describe the pathogenesis of RA:

A
  1. Dendritic (antigen-presenting) cells phagocytose antigens and present them to T cells
  2. Activated T cells stimulate the production of B and T cells
  3. B cells produce plasma cells that form rheumatoid antibodies
  4. Helper T cells activate macrophages and cytotoxic T cells
  5. Together, T cells, macrophages, and cytotoxic T cells produce cytotoxic cytokines (tumor necrosis factor [TNF] α, interleukin (IL)-1, IL-6, and others) and prostaglandins that cause joint inflammation, synovial proliferation, and bone and cartilage destruction
75
Q

Sites of action of RA drugs:

A
  1. Abatacept blocks the co-stimulation of T cells
  2. Methotrexate and leflunomide inhibit the proliferation and activity of T cells and B cells
  3. Etanercept, infliximab, adalimumab, golimumab, and certolizumab inactivate TNF - α
  4. Anakinra blocks the action of IL-1
  5. Tocilizumab inactivates IL-6
  6. Glucocorticoids that inhibit T-cell activation and IL-2 production by regulation of gene transcription
  7. Glucocorticoids and nonsteroidal antiinflammatory drugs (NSAIDs) also inhibit the formation of prostaglandins
76
Q

Define osteoarthritis:

A
  • Progressive disorder of the joints caused by gradual loss of cartilage
  • Results in the development of bony spurs and cysts at the margins of the joints
77
Q

Name the risk factors associated with OA:

A
  1. Female gender (particularly knee and hand)
  2. Increasing age
  3. Race or ethnicity (variable)
  4. Genetic predisposition
  5. Obesity (more marked for the knee)
  6. Trauma
78
Q

What are the early changes in the pathophysiology of OA?

A
  • Superficial layers of cartilage are destroyed
    • Fibrillation and cracking of the cartilage matrix
  • Limited chondrocyte proliferation and new matrix formation
79
Q

What is eburnation?

What is a subchondral sclerosis?

What is a subchondral cyst?

A
  1. eburnation:
    • Absence of articular cartilage
    • polished appearance of exposed bone
  2. subchondral sclerosis:
    • more dense bone develops underneath areas where cartilage is gone
  3. subchondral cyst:
    • ​​formed by break in cartilage
    • allows synovial fluid to be forced into subchondral space, forming a fibrous walled cyst
80
Q

What is osteophyte formation?

What is a hip joint?

Where are Heberden nodes found?

Where are Bouchard nodes found?

A
  1. Osteophyte formation: bony outgrowths develop at margins of articular surface in characteristic locations for specific joints
    • result in increased joint size
  2. Hip joint: occur all around entire joint margin, but typically large flat osteophyte on medial surface extending to fovea
  3. Distal interphalangeal joints: Heberden nodes
  4. Proximal interphalangeal joints: Bouchard nodes
81
Q

Describe the pathogenesis of OA:

  • Imbalance in:
  • Resulting in:
A
  • Imbalance in:
    • cytokine
    • growth factor activity
  • Resulting in:
    • matrix loss
    • degradation
82
Q

What are the risk factors associated with OA?

A
  1. female
  2. age
  3. trauma
  4. obesity
  5. genetic factors
  6. race
83
Q

What are some secondary causes of osteoarthritis?

A
  1. Post-traumatic
  2. Other joint/bone disease
  3. Calcium deposition diseases
  4. Gout
  5. Congenital/developmental diseases
  6. Metabolic
  7. Neuropathic arthropathy
84
Q

What joints are typically affected in osteoarthritis?

A

Osteoarthritis most commonly affects:

  1. big toes
  2. hands
  3. hips
  4. knees
  5. spine
85
Q

What is crepitus?

A

palpable creaking on movement

86
Q

What are the main physical exam presentations for a patient with OA?

A
  • Mild-to-moderate firm swelling around the joint line
    • due to formation of chondrophytes or osteophytes at the joint margin
  • Crepitus
  • Restricted range of motion limited by pain
  • Weakness and wasting of muscles acting on the joint
87
Q

What are secondary characteristics of OA on physical exam?

A
  • Periarticular tenderness
  • Deformities, instability of the joint
  • Heberden’s and Bouchard’s nodes
  • Squaring of the 1st CMC
  • Hallux valgus (bunion)
  • Genu varus (bow legs)
  • Genus valgus (knock knees)
88
Q

What would you use to diagnose osteoarthritis?

A
  • Blood tests
    • typically not helpful to the diagnosis of OA
    • may be helpful in determining what treatments could be used
  • Imaging
  • Synovial fluid aspiration
    • typically viscous and translucent
    • non-inflammatory white blood cell count (<2000/mm^3)
89
Q

What would you expect to find on a radiography of a patient with OA?

A
  1. _Narrowing of the joint space _
    • _​_due to loss of articular cartilage
  2. Osteophytes
  3. Changes in subchondral bone
    • cysts, sclerosis, shape changes, loss of bone volume
  • Patients with moderate OA, particularly in the spine, may have no symptoms
  • Early on, minimal x-ray changes can be associated with severe symptoms

MSS Weeks 3-5 (22 decks)

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