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FPP_MSS > Joint Diseases - Cochran, Pfister, Cronin > Flashcards

Joint Diseases - Cochran, Pfister, Cronin Flashcards

1
Q

Review the structure of synovial joints:

What type of cartilage is present? Is it vascular? How is it maintained?

What is the source of synovial fluid? Describe its composition.

A

(Synovial joints are encapsulated and fluid-filled to allow gliding movement)

Type 2 (car-two-lige), avascular. Maintained by chondrocytes.

Synovial cells lining the cavity produce the synovial fluid (in addition to serving phagocytic functions).

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2
Q

What physical exam findings are seen in inflammatory arthrites?

A

Morning stiffness > 1hr

Warmth, erythema (variable)

Synovitis (thickening, tenderness)

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3
Q

What lab findings are seen in inflammatory arthrites?

A

Elevated inflammatory markers (ESR/CRP), leukocytosis in blood.

Imaging reveals erosion of bone.

Synovial fluid has WBC count >2000 and >50% neutrophils.

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4
Q

What is gout?

What is its most common etiology?

A

Gout results from hyperuricemia causing MSU (monosodium urate) crystals to deposit in joints.

90% of cases are due to underexcretion in feces/urine.

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5
Q

What is the source of most of the filtered load of uric acid?

What percentage of that load is usually excreted?

A

Cellular byproducts (nucleotides, nucleoproteins).

10% of filtered load is excreted.

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6
Q

Which groups are most susceptible to gout?

Why is it becoming more common?

A

Males have a higher prevalence (estrogen promotes renal excretion), and incidence is higher in non-white races.

It correlates with BMI, which is increasing.

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7
Q

What is podagra?

When is it usually seen?

A

Podagra is pain of the great toe resulting from MSU deposition there.

During acute gout attacks (mobilization of urate).

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8
Q

Distinguish between the optical properties of crystals in gout and pseudogout.

A

Gout: MSU crystals are flat and negatively birefringent.

Pseudogout: Calcium pyrophosphate crystals are rhomboid and positively birefringent.

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9
Q

Why are the distral extremities most susceptible to MSU crystal deposition?

A

Decreased temperatures in the extremity reduces relative solubility, leading to deposition.

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10
Q

Chronic gout is associated with renal failure and tophi. What are tophi?

Where can they form?

A

Tophi are white, chalky urate aggregates.

They can deposit in nearly any tissue, but especially deposit in skin, joints, cartilage and bone.

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11
Q

How does gout precipitate an inflammatory response?

A

MSU crystals are phagocytsed by APCs, which trigger inflammasomal IL-1β production.

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12
Q

Describe the prevalence and etiology of CPPD deposition disease (pseudogout).

A

Pseudogout mostly affects the elderly, and results usually from pyrophosphate overproduction.

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13
Q

What joints does CPPD deposition usually affect?

What is its pathognomonic radiological finding?

A

Larger joints than gout: knee, wrist, shoulder.

Chondrocalcinosis (calcificaiton of articular cartilage.

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14
Q

How can gout be treated?

Describe the role of NSAIDs and steroids in the treatment of gout.

A

Reducing urate production, increasing its excretion, and reducing inflammation/symptoms.

NSAIDs can be used for short term relief (indomethacin or naproxen, but not aspirin!). Same is true of steroids.

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15
Q

Colchicine

Describe its mechanism of action.

What are its uses?

A

Colchicine

Interferes with tubulin dimers to prevent microtubule formation. This inhibits neutrophil expansion/activation, reducing inflammation.

Used for treatment of acute gout attacks, as well as prophylactically in chronic gout (side effects are limiting)

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16
Q

Colchicine

Describe its pharmacokinetics.

What are its side effects and contraindications?

A

Colchicine

Orally administered, rapidly absorbed with large Vd. CYP3A4 metabolized. P-gp substrate.

Major GI disturbances (limits proliferative cells). Not for the elderly, those with hepatic or renal disease, or with 3A4/P-gp inhibitors.

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17
Q

What are some indications for prophylactic gout therapy?

Name some non-pharmacological treatment measures.

A

If attacks are frequent, disabling, or are associated with urate stones, nephropathy, or tophi (chronic).

Dietary adjustment (no alcohol, rich foods). Discontinue meds that block urate secretion (OAT).

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18
Q

Allopurinol

Describe its mechanism of action.

What are its indications?

A

Allopurinol

Metabolized to oxypurinol > blocks xanthine oxidase > reduces urate production.

For prevention of primary hyperuricemia.

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19
Q

Allopurinol

Describe its pharmacokinetics.

What are its side effects and contraindications?

A

Allopurinol

Prodrug activated by aldehyde oxidoreductase. 1-2hr half-life, but metabolite lasts 18-30hrs.

Can cause hypersensitivity reaction and may provoke acute gout attacks.

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20
Q

Febuxostat

Describe its mechanism of action.

Contrast it with Allopurinol.

A

Febuxostat

Inhibitor of XDH/XO.

Binds both oxidized and reduced form of XO. More potent, better for patients with renal failure, but with higher side effects (eg cardiovascular).

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21
Q

Pegloticase

Describe its mechanism of action.

What are its indications?

A

Pegloticase

Recombinant & PEGylated uricase; converts urate to allantoin.

For treatment of chronic refractory gout.

22
Q

Pegloticase

Describe its pharmacokinetics.

What are its adverse effects?

A

Pegloticase

IV administration (big molecule!), biweekly. Long lasting.

Infusion site reactions and immune response to PEG portion. May provoke gout flares.

23
Q

Probenecid

Describe its mechanism of action.

What are its indications?

A

Probenecid

Uricosuric: Competes with OAT/URAT1 to increase urate excretion.

For treatment of chronic gout, except in overproducers & those with kidney disease.

24
Q

Describe the etiology of rheumatoid arthritis.

What are some of its risk factors?

A

Type IV hypersensitivity (T-cell, with some B involvement) directed against synovial joints.

Smoking, HLA-DR4, being female. (infections, stress?)

25
Q

Describe the pathology of rheumatoid arthritis.

(talk about open-ended…)

A

Chronic inflammation of the synovium along with papillary synovial cell hyperplasia causes formation of a pannus, cartilage destruction, and joint ankylosis.

26
Q

What are rheumatoid nodules?

A

A clinical finding in rheumatoid arthritis resulting from fibrinoid vascular necrosis. They are firm, round, and develop usually on skin subjected to pressure.

NOTE: Histology reveals palisaded inflammation.

27
Q

How does the patient history in rheumatoid arthritis differ from that of osteoarthritis?

A

Rheumatoid arthritis is symmetrical, involves morning stiffness lasting >1hr, and lasts for weeks.

28
Q

What is rheumatoid factor (RF)?

What are some other blood factors seen in rheumatoid arthritis?

A

RF is an IgM directed against the Fc portion of IgG.

CCP is seen in some cases of RF- rheumatoid arthritis.

29
Q

Summarize some diagnostic criteria for RA diagnosis.

A

Morning stiff >1hr

Symmetrical arthritis

At least 3 swollen joints

Wrist, MCP, PIP involvement

Rheumatoid nodules

RH+

Confirming X-ray

30
Q

Summarize the effects of RA on the cardiovascular system.

Summarize the effects of RA on the pulmonary system.

A

Patients with RA are at an increased risk of cardiovascular events, presumably due to inflammation-mediated atherosclerosis.

RA is associated with interstitial fibrosis, nodules, Caplan’s syndrome (pneumoconiosis), and pleuritis with “low-glucose exudate”.

31
Q

What are the goals of treatment of RA?

What role do NSAIDs play?

A

Relieve inflammation, slow/stop joint damage, reduce pain and improve function.

NSAIDs are a good first-line treatment to reduce inflammation and pain, but the large doses and long course results in side effects.

32
Q

Etanercept

What is its mechanism of action?

What are its indications?

A

Etanercept

It is a soluble TNFa receptor, bound to IgG Fc. It therefore inihibits TNFa to reduce inflammation.

Used in many stages of RA: Moderate, severe, juvenile, early…? In addition to many other inflammatory conditions.

33
Q

Etanercept

Describe its pharmacokinetics.

What are its adverse effects?

A

Etanercept

IV/SubQ (big molecule…). 1-2wk onset from subQ, >3d half-life.

Injection reactions, infection susceptibility, and occasionally lymphomas. (same as adalimumab)

34
Q

Adalimumab

Describe its mechanism of action.

What are its therapeutic indications?

A

Adalimumab

Monoclonal IgG against TNFa.

For active RA (and other inflammatory conditions)

35
Q

Adalimumab

Describe its pharmacokinetics.

What are its adverse effects?

A

Adalimumab

SubQ, given every other week.

Injection reactions, infection susceptibility, and occasionally lymphomas. (same as etanercept)

36
Q

Tocilizumab

Describe its mechanism of action.

What are its therapeutic indications?

A

Tocilizumab

Monoclonal antibody; binds to IL-6 receptors (membrane-bound or soluble!)

For adult patients with severe RA. (wiki says: juvenile too)

37
Q

Tocilizumab

Describe its pharmacokinetics.

What are its adverse effects?

A

Tocilizumab

IV admin (4 weeks) or SubQ (2 weeks). This makes no sense.

Injection site reactions, infection susceptibility, and increases in lipid profiles.

38
Q

Tofacitinib

Describe its mechanism of action.

What are its indications?

A

Tofacitinib

It is a JAK inhibitor; blocks expansion of immune cells.

For methotrexate-intolerant RA patients, and other inflammatory conditions.

39
Q

Tofacitinib

Describe its pharmacokinetics.

What are its adverse effects?

A

Tofacitinib

Oral administration. Metabolized by 3A4 > 2C19.

Infection susceptibility, cholesterol increase.

40
Q

Define osteoarthritis.

A

A progressive joint disorder caused by (mostly) non-inflammatory cartilage loss. “Wear and tear”. Characterized by bony spurs and subchondral cysts.

41
Q

Summarize the typical osteoarthritis patient history.

A

Morning stiffness <30min. Stiffness after inactivity, pain with use. Crepitus and joint locking. No fever/warmth/erythema.

42
Q

Describe the course of injury to the joints in early and late stage osteoarthritis.

A

Early stages: The superficial layers are destroyed leading to fibrillation and cracking of the matrix. This is somewhat offset by chondrocyte action.

Late stages: Fuller cartilage loss, eburnation of underlying bone, subchondral sclerosing and cyst formation. Osteophytes.

43
Q

Where do osteophytes generally develop?

What is the name given to osteoarthritis of the IP joints?

A

At the margins of articular surfaces of worn joints.

DIP: Heberden nodes. PIP: Bouchard nodes.

44
Q

What are some secondary causes of osteoarthritis?

A

Trauma, deposition diseases, and a boatload of other developmental and metabolic diseases.

45
Q

Why is osteoarthritis accompanied by mild-to-moderate swelling around a joint?

Distinguish between hallux valgus, genu varus, and genu valgus.

A

Osteophyte formation can cause mild inflammation.

Hallux valgus is a bunion (lateral deviation of great toe). Genu varus is bowlegging, genu valgus is knocking knees.

46
Q

Describe synovial fluid findings in osteoarthritis.

Describe radiographic findings in osteoarthritis.

A

Translucent and non inflammatory. Viscous?

Joint space narrows, osteophytes form. Subchondral bone changes eg cysts, sclerosis.

47
Q

What is the mechanism of action of Anakinra?

A

BRM: blocks IL-1R

48
Q

What is the mechanism of action of abatacept?

A

BRM: inhibits T-cell activation

49
Q

What is the mechanism of rituximab?

A

BRM: antibody directed against CD20 antigen (anti B-cell)

50
Q

What is azathioprine?

A

A nucleotide analog that disrupts DNA synthesis; an immunosuppressant used in rheumatoid arthritis.

51
Q

What is Leflunomide?

A

A DMARD which inhibits Dihydroorotate dehydrogenase >> immunosuppression.

52
Q

Hydroxychloroquine, mother fucker! What is it!

A

An antimalarial which can apparently also be used for lupus and RA.

FPP_MSS (30 decks)

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