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Symptoms 2 > Joint Pain > Flashcards

Joint Pain Flashcards

1
Q

What is a useful mnemonic for creating a good arthritic/joint pain DDx?

What does each letter stand for?

A

VINDICATE

_V_ascular, _I_nflammatory, _N_eoplastic, _D_egenerative/ Deficiency, _I_diopathic/Intoxication, _C_ongenital, _A_utoimmune/ Allergic, _T_raumatic, _E_ndocrine

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2
Q

What are some exam findings with osteoarthritis?

A

Subchondral cysts, sclerosis, osteophytes, synovitis, Heberden nodes (DIP), Bouchard nodes (PIP), no MCP involvement

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3
Q

What are some classic presentations involved with osteoarthritis?

A
  • older patients
  • chronic joint pain and stiffness
  • pain is usually worse with activity and improves with rest
  • knees, hips, and hands are most commonly affected
  • on exam there is bony enlargement without significant effusions
  • mild tenderness may be present along the joint lines
  • limited ROM
  • no systemic symptoms
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4
Q

Describe gout pathophys with regards to source of the urate, its normal methods of excretion, and what leads to gout…

A
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5
Q
  1. When crystals from synovial fluid are needle-shaped and negatively birefingent under polarized light (and therefore are yellow when parallel to the light), what would be your dx?
  2. When the crystals instead are blue when parallel to the light, what would you think of?
A
  1. Gout! - yellow under parallel light (also think of allopurinol)
  2. Pseudogout - calcium pyrophosphate crystals
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6
Q

When looking at pseudogout, what are the crystals made of, and what will be seen on x-ray?

What joints are typically affected in pseudogout?

What are some diseases associated with pseudogout?

A

Crystals are calcium pyrophosphate and chondrocalcinosis will be seen on x-ray.

Usually affects the large joints like the knee.

Hemochromatosis and hyperparathryoidism can be associated with pseudogout.

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7
Q

What are classic presentations in gout?

A
  • An acute inflammatory monoarthritis (d/t precipitation of urate)
  • More common in males
  • Asymmetric joint distribution and the joints are swollen, red, and painful
  • Tophus formation is common on the external ear, olecranon bursa, and Achilles tendon
  • Looking at First Aid, a classic manifestation is a painful MTP joint of the big toe (AKA podagra)
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8
Q

What are the 2 main goals of gout treatment?

A

Reduce inflammation and reduce uric acid levels

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9
Q

If your patient with monoarticular joint pain had a synovial fluid that was filled with RBCs and WBCs, along what lines would you think?

A

Look for infectious causes! –> Do a gram stain

This could be a septic arthritis, which is a medical emergency

Joint needs to be drained and weeks of antibiotics are typically necessary

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10
Q

In septic arthritis, the etiology is typically from what kind of spread?

A

Hematogenous

This means that the pts are typically septic before the joint becomes seeded

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11
Q

You suspect your patient with monoarticular joint pain has an infectious etiology, but the cultures and gram stain are negative. What should you consider in your DDx?

A
  • Gonococcal arthritis
  • Lyme arthritis
  • Fungus (especially in the immunocompromised)
  • Mycobacteria
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12
Q

Gonococcal arthritis typically manifests in what population?

What is a finding you might have on skin exam?

A

Young women who like to bang bang

With skin exam might notice small pustules

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13
Q

During what clinical stages of Lyme dz can arthritis present?

What else should you consider in this dx?

A

During the second and third stages

You should consider the patient’s history if they were campnig or in areas with the ticks. Also there will be no crystals in the synovial fluid.

This is not a common manifestation in pts who contract Lyme dz

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14
Q

What if the synovial fluid looked like the one the second from the left?

A

This is still pretty clear. Think non-inflammatory. Think OA! (OA is characterized by non-inflammatory fluid)

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15
Q

Besides considering the useful mnemonic, what are 3 useful ways to frame a DDx when a pt presents with joint pain?

A
  1. Acute vs Chronic?
  2. Inflammatory vs Mechanical?
  3. Polyarthritis vs oligoarthritis vs monoarthritis?
    • Because I wasn’t clear on this - oligoarthritis refers to 2-4 joints being involved…
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16
Q

What are other good questions to ask and signs of depression or chronic pain syndrome (like fibromyalgia)?

A
  • Good questions: recent stressors?
  • Signs: fatigue, weight loss, affect on every day life (like missing school), and diffuse pain
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17
Q

What are other good questions to ask and signs of hypothyroidism?

What tests could you run?

A
  • Questions and signs: fatigue, weight loss, diffuse pain
  • Tests: TSH
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18
Q

What are other good questions to ask and signs of EBV infection?

What tests could you run?

A
  • Questions: Sick contacts? Swollen LN? Sore throat?
  • Signs: fatigue, diffuse pain
  • Tests: monospot, EBV titers - would probably do the monospot first
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19
Q

What are other good questions to ask and signs of rhematoid arthritis?

What tests could you run?

A
  • Questions: persistent swelling/stiffness of joints?
  • Signs: multiple joint pain, fatigue
  • Tests: RF, CCP, hand x-rays
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20
Q

What are other good questions to ask and signs of psoriatic arthritis?

A
  • Questions: Persistent swelling/stiffness of joints? Rash? Nail abnormalities? FHx?
  • Signs: multiple joint pain
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21
Q

What are other good questions to ask and signs of IBD?

What tests could you run?

A
  • Questions: Abd pain? Diarrhea? Bloody stools?
  • Signs: multiple joint pain, mouth sores, weight loss, fatigue, hair loss
  • Tests: CBC, ESR, CRP, stool guiaic
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22
Q

What are other good questions to ask and signs of SLE?

What tests could you run?

A
  • Questions: Has facial rash been persistent? Photosensitive rashes? Leg swelling?
  • Signs: multiple joint pain, mouth sores, facial rash, fatigue, weight loss, hair loss, edema, neuro involvement
  • Tests: CBC, Cr, UA, ANA, anti-dsDNA, anti-Smith Ab
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23
Q

In class, SLE can be broken down into 3 aspects of its presentation. What are they?

A
  1. Mucocutaneous manifestations
    • oral ulcers (hard palate), malar rash (crosses the nasal bridge and spares the nasolabial fold), and the rashes are often photosensitive
  2. “-itis”
    1. CNS inflammation (cerebritis with seizures or psychosis, transverse myelitis)
    2. Nephritis (type III hypersensitivity)
    3. Arthritis (typically small joints of hands and wrists)
    4. Serositis (pericarditis, pleuritis)
  3. Lab abnormalities (see other slide)
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24
Q

What are typical lab findings in SLE?

A
  • Autoantibodies
    • ANA - sensitive but not specific
    • anti-dsDNA, anti-Smith - specific but not sensitive
    • Antiphospholipid Ab
    • Coombs
  • Cytopenia
  • Low complement - d/t immune complex formation

Another thing to consider if IF - IgG would stain the dermal-epidermal junction (and a C3 stain would show a similar pattern)

25
Q

Pt presents with with pain in fingers and wrists. On exam there is scaling on the extensor surfaces, nail pitting and the hands appear like the picture. What is the most likely dx?

A

Psoriatic arthritis

26
Q

What are the patterns of joint involvement in psoriatic arthritis? What are other PEx findings?

A
  • Patterns: DIP predominant arthritis, oligoarticular (typically large joints), polyarticular
    • Axial involvement is uncommon
  • Other findings
    • arthritis can precede onset of psoriasis
    • enthesitis (inflammation of where the tendons or ligaments insert into the bone)
    • dacytilitis = sausage fingers
27
Q
  • What are the seronegative spondyloarthropathies?
  • What does that even mean?
  • What is special about these genetically?
A
  • PAIR - Psoriatic arthritis, Ankylosing spondylitis, Inflammatory bowel disease, and Reactive arthritis

​

  • Arthritis without rheumatoid factor
  • Strong association with HLA-B27
28
Q

In psoriatic arthritis, what is the Auspitz sign and what is the Koebner pnenomenon?

A

Auspitz sign = bleeding with peeling of scale

Koebner phenomenon = rash at sites of trauma

29
Q

You patient instead is presenting with a migratory polyarthritis, urticarial rash, murmur that radiates to the axilla, and has a h/o a sore throat. What is the leading DDx?

A

Acute rheumatic fever

30
Q

Your patient decides this time she is presenting with an additive polyarthritis (more joints keep becoming involved) that is very painful and erythematous, along with a fever, pustular rash, and a h/o sore throat. Later on in the interviewing you also find out she is sexually active. Now what is your leading DDx?

A

Gonococcal arthritis

31
Q

Another young female presents to your office with a h/o acute polyarthritis. She has a lacy rash in stocking/glove distribution, a h/o febrile illness, and her little brother was also sick with a fever and red sheeks. What is your leading DDx?

A

Parvovirus

Little brother with Fifth’s disease

32
Q

Be able to know where the main gout medications work:

which blocks formation of uric acid?

which breaks down uric acid?

which increases excretion of uric acid in urine?

which reduces the degree of inflammation

A
33
Q

What is the risk factor when using NSAID therapy for acute gout in this patient?

Elderly male pt with renal disease

A
  • Pt is dependent on vasodilatory PGs to maintain renal blood flow
    • Renal review: PGs act act the afferent arteriole causing vasodilation to increase RBF and keep GFR normal
      • NSAIDs inhibit PG synthesis
34
Q

What is the risk factor when using NSAID therapy for acute gout in this patient?

55 y/o woman with peptic ulcer

A
  • NSAIDs block cytoprotective PGs in the GI tract
    • Review: COX-1 is constitutively expressed and leads to PGs that protect the gastric mucosa
35
Q

What is the risk factor when using NSAID therapy for acute gout in this patient?

68 y/o male with previous MI and FMHx of heart dz

A
  • NSAIDs (not ASA) may increase risk or not prevent an MI
    • ASA inhibits COX-1 whereas NSAIDs inhibit both COX-1 and COX-2
36
Q

What is the risk factor when using NSAID therapy for acute gout in this patient?

Female pt with nasal polyps and a previous reaction to ASA

A
  • Hypersensitivity reaction - d/t leukotrienes
37
Q

What is the risk factor when using NSAID therapy for acute gout in this patient?

45 y/o male taking warfarin for DVT prophylaxis

A
  • Increase risk of bleeding
38
Q

Why is ASA contraindicated in the treatment of gout?

A

ASA has a dose-dependent effect on uric acid excretion:

Low doses lead to decreased excretion (bad)

Large doses increase excretion

Review: urate reabsorption occurs in the 1st and 3rd segments of the proximal tubule and secretion in the 2nd segment

39
Q

What are some potential options for pts with acute gout symptoms who cannot take NSAIDs for relief?

A
  • Wait until sx subside (usually within a few days)
  • Take low dose colchicine
  • Intraarticular glucocorticoid injections
  • Take celecoxib
  • Low dose oral steroids
40
Q

What does DMARD stand for?

A

Disease Modifying Anti-Rheumatic Drugs

There are both biological and non

They are drugs that slow or halt the progression of disease

41
Q

What are biologic DMARDs and what are some examples of them?

A

They are a class of drugs including monoclonal Abs, receptor analogues, and chimeric small molecules designed to bind to or mimic their molecular target

Ex: etanercept, infliximab, adalimumab, rituximab, anakinra, abatacept, tocilizumab, belimumab, apremilast, tofacitinib…

42
Q

Be able to recognize where different DMARDs act

A
43
Q

Which of the following drugs are human monoclonal antibodies?

  1. Adalimumab
  2. Belimumab
  3. Tocilizumab
  4. Rituximab
  5. Infliximab
A

Adalimumab
Belimumab
Tocilizumab

Human = -umab; humanized = -zumab

Murine = -momab; Chimeric = -ximab

44
Q

What are some examples of non-biological DMARDs?

A

Methotrexate, Sulfasalazine, Hydroxychloroquine, Azathioprine, N-penicillamine, Mycophenolate mofetil, and Leflunomide

(Review the MOA in the ppt for the day…)

45
Q

Looking at the pharmacokinetics, which route of administration will have the highest % bioavailability?

  1. SubQ
  2. IM
  3. IV
A
  1. IV = 100%
    • SubQ and IM range from 24-95%
46
Q

Do therapeutic antibodies from a human source have a longer or shorter half-life than those from a mouse source?

A

Longer: 20-21 days opposed to 12-48 hrs in murine Abs

47
Q

What is the general mechanism for the longer half life of human MABs vs mouse MABs?

A

Concept of neonatal FcR for IgG - the FcRn functions to protect IgG from degradation, but the mouse IgG does not bind it

48
Q

Which of the following drugs inhibits TNF-alpha?

  1. Infliximab
  2. Adalimumab
  3. Etanercept
  4. Only infliximab and adalimumab
  5. All of the above
A

All of the above

Review: TNF-alpha can be both membrane-bound and secreted. Infliximab and adalimumab can bind both types. Etanercept can only bind the soluble secreted version.

49
Q

What is the MOA of belimumab?

A

It inhibits the activity of the B lymphocyte stimulator (BLSP or BLyS) which is the costimulator for B-cell survival and function –> decreases B cell survival thereby decreasing production of auto-antibodies

50
Q

What is the MOA of tocilizumab?

A

it is a humanized IL-6 receptor antibody - which competes with binding the IL-6 receptor - which interferes with this cytokine’s effects

51
Q

Is rituximab’s MOA related to complement-dependent cytotoxicity (CDC) or antibody-dependent cellular cytotoxicity (ADCC)?

A

Both!

CDC activates the complement system resulting in cell lysis

ADCC leads to lysis or phagocytosis by immune cells

52
Q

What is immunogenicity?

A

It is the generation of endogenous antibodies against the therapeutic antibodies –> this could result in neutralization of the therapeutic antibody’s effect, and a potential hypersensitivity reaction

53
Q

For each pair of drugs, which has the greater potential for immunogenicity?

  • Infliximab vs Adalimumab
  • Rituximab vs Belimumab
  • Tocilizumab vs Infliximab
  • Ibritumomab vs Tocilizumab
A
  • Infliximab vs Adalimumab
  • Rituximab vs Belimumab
  • Tocilizumab vs Infliximab
  • Ibritumomab vs Tocilizumab
54
Q

What are some biologic DMARDs that are not biologic?

A

Abatacept

Anakinra

Tofacitinib

Apremilast

55
Q

Which non-biologic DMARD is a fusion protein that binds the CD80/86 thereby preventing the second signal which also then prevents activation of T cells?

A

Abatacept

(used in pts with RA who have had an inadequate response to other drugs)

56
Q

Which non-biologic DMARD is a recombinant protein that is a competitive antagonist of IL-1?

A

Anakinra

(Used in pts with RA who have failed at least one other DMARD)

57
Q

Which non-biologic DMARD is orally administered, inhibits JAK and thereby prevents cytokine or growth factor mediated gene expression and intracellular activity of immune cells?

A

Tofacitinib

Of note: this drug undergoes metabolism by CYP3A4 and 2C19

Used in combo with MTX or in pts who have not responded to MTX

58
Q

Which non-biologic DMARD is an orally available small molecule inhibitor of PDE-4 that is also known for having some neuropsychiatric effects and causing weight loss?

A

Apremilast

Neuropsych effects include depression, suicidal ideation, and mood changes

This one also undergoes CYP3A4 metabolism

59
Q

What is a common risk associated with essentially all of the DMARDs?

A

Increased risk of infections

Symptoms 2 (11 decks)

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