Gout_SpA+2024_student.pdf

1. Gout 2. Calcium Pyrophosphate Crystal Deposition Disease AKA: Pseudogout 3. Reactive arthritis 4. Ankylosing spondylitis Amber Herrick, MS, PA-C, DFAAPA Clinical Medicine I September 18, 2024 1 Lecture Objectives...

1. Gout 2. Calcium Pyrophosphate Crystal Deposition Disease AKA: Pseudogout 3. Reactive arthritis 4. Ankylosing spondylitis Amber Herrick, MS, PA-C, DFAAPA Clinical Medicine I September 18, 2024 1 Lecture Objectives For each of the disorders: -Compare and contrast the clinical presentation Gout: -Identify appropriate referrals and patient education Define gout and summarize the underlying stages/pathogenesis of gout Describe the clinical features of an acute gout flare Identify common etiologies that can cause an acute gout flare State the laboratory finding used to confirm the diagnosis of gout Describe the characteristic radiologic findings for gout Discuss management as it pertains to both acute flare treatment and long-term control with urate lowering therapy CPPD Disease (Pseudogout): Discuss risk/disease associations seen in CPPD disease Describe the clinical features of an acute flare Identify common etiologies that can cause an acute flare Describe the characteristic radiologic findings seen in CPPD disease State the laboratory finding used to confirm the diagnosis of gout Discuss treatment for an acute flare 2 Lecture Objectives, continued Reactive arthritis (ReA): Define ReA Describe the classic clinical features of ReA Discuss the extraarticular manifestations commonly seen in ReA Discuss the laboratory values used in the diagnostic evaluation of ReA State the first line treatment for ReA Ankylosing spondylitis (AS): Define and summarize the underlying pathophysiology of AS Describe the key components/clinical presentation of AS Discuss the characteristic radiologic findings seen in AS State the first line treatment for AS 3  Rheumatoid arthritis Osteoarthritis Rheumatology Mind Map “Joint Pain” Crystal-related arthropathies Spondyloarthropathies Gout Reactive arthritis Pseudogout Ankylosing spondylitis 4 https://rheumatologymindmap.com/download.html  Crystal-Induced Arthropathies Gout Outline of CPPD Disease Lecture Spondyloarthropathies Reactive arthritis Ankylosing spondylitis 5  Gout Monosodium Urate Crystal Deposition Disease 6 Case courtesy of Ian Bickle, Radiopaedia.org, rID: 50388. https://radiopaedia.org/articles/gout What Comes to Your Mind When I Say Gout? 7  What is Gout? Inflammatory arthritis Cardinal Feature: hyperuricemia Uric Acid precipitates into Deposits in and monosodium around joints, Pain and urate (MSU) bones, & soft inflammation crystals tissues 8 Uric Acid Breakdown product of Uric Acid purine metabolism Excreted by the kidney Defined as serum uric acid level exceeding 6.8 Hyperuricemia mg/dL Approximate limit of urate solubility 9  Hyperuricemia: Overproducers vs Underexcretors “Overproducers” “Underexcretors” (90%) Inherited enzyme defects Renal insufficiency High cell turnover Diuretics Psoriasis Volume depletion Myeloproliferative disease Lead nephropathy ↑ purine consumption (diet) 10 CURRENT: Rheumatology, 3e. Chapter 44. Gout. Table 44-1. Classification of Hyperuricemia. Urate overproduction & uric acid underexcretion, modified.  Gout: Prevalence: Affects ~ 4% of Unites States general population Prevalence Prevalence increases with age & Predominant age range: 30-60 Comorbid Conditions Men > Women Comorbid Conditions: HTN Obesity Chronic kidney disease (CKD) Type 2 Diabetes Hyperlipidemia 11  Gout: Risk Factors Non-Modifiable Modifiable Age Obesity, HTN, hyperlipidemia Sex Diabetes mellitus, CKD Ethnicity Dietary factors E.g., Pacific Rich in meat & seafood Islanders High fructose/sucrose content Genetic variants Alcohol Certain medications Organ transplant recipient status 12  Stages of Gouty Arthritis Asymptomatic hyperuricemia ~15% develop gout Acute gouty arthritis First acute flare (“attack”) Intercritical gout Asymptomatic interval between gout attacks Chronic gouty arthritis Involved joints can develop chronic swelling and tophi, if left untreated 13  White chalky material consisting of dense concentrations of MSU crystals Function of the duration and severity of hyperuricemia May occur at any site: joints, bone, cartilage, and skin http://images.medicinenet.com/images/slideshow/gout_big_toe_s5.jpg 14 Tophi (or Tophus) Medicinenet.com, Medscape. com  Hyperuricemia Pathogenesis Deposition of crystals in/around joint for Gout Inflammatory cascade Without treatment, (painful joint) deposition of crystals continue, forming tophi Chronic gouty arthritis → joint destruction (eroding bone and cartilage) 15 Clinical Manifestations of Gout Acute inflammatory arthritis “acute gout flare” Chronic gouty arthritis Palpable tophi, joint limitation, persistent inflammation, and joint deformity Renal complications Uric acid nephrolithiasis Urate nephropathy 16 Acute Gout Flare (“attack”) 17  Acute Gout Flare: Clinical Features Monoarticular (85-90%) and intensely inflammatory Can be polyarticular ( 3 months More sudden onset Morning stiffness > 60 min < 30 min Nocturnal pain Frequent, improvement upon rising Absent Effect of exercise/activity Improvement Exacerbation Rest No improvement Improvement Inflammatory Back Pain vs. Mechanical Back Pain 51 Duba et al., 2018; Poddubnyy et al., 2015 Peripheral Arthritis: Also referred to as Asymmetric Oligoarthritis Predominantly involves the lower extremities; Frequently asymmetrical; Often affects only 1-3 joints (oligoarthritis) Generally swollen and painful 52  Enthesitis: Inflammation around the Enthesis Enthesis: site of insertion of ligaments, tendons, joint capsule, or fascia to bone Kaeley and Kaler, 2020 53  “Heel Pain” Example of Enthesitis Insertion of the achilles tendon or the UpToDate plantar fascia ligament into the calcaneus Patients may present with plantar fasciitis and have difficulty walking on the heels when barefoot May appreciate swelling and local tenderness on exam 54  Reactive Arthritis Formerly “Reiter’s Syndrome”  Reactive Arthritis (ReA) An arthritis that arises following an infection Usually occurring 1-4 weeks following a GI (diarrheal illness) or GU infection (urethritis) GI: Shigella, Salmonella, Yersinia, Campylobacter, C. difficile, E. coli GU: Chlamydia trachomatis Relatively rare; typically, in young adults; affecting both men and women Genetic predisposition/association with HLA-B27 56 FYI: The spectrum of pathogens known to cause reactive arthritis is broadening to include Mycobacterium, Staphylococcus, and SARS-CoV-2  Reactive Arthritis (ReA): Clinical Features Manifests as an asymmetric sterile oligoarthritis (peripheral arthritis) Typically, of the lower extremities (knee and ankle) Can’t Climb a Tree Frequently associated with enthesitis (remember: “heel pain”) May also have inflammatory back pain (i.e., sacroiliitis) Extraarticular manifestations: common Conjunctivitis Can’t See Urethritis Keratoderma blennorrhagica Can’t Pee Circinate balanitis Oral ulcers 57 Reactive Arthritis: Keratoderma blennorrhagica Conjunctivitis/Uveitis Circinate Balanitis Oral ulcers 58 Differential Diagnosis for ReA Ankylosing spondylitis Bacterial infection Septic arthritis & Lyme disease Rheumatoid arthritis Psoriatic arthritis Gonococcal arthritis Behçet disease Crystal arthritis Gout, pseudogout 59  Evidence of antecedent or concomitant infection Inability to identify causative pathogen does not exclude the diagnosis Elevated ESR or CRP may be seen ReA: Positive HLA-B27 Antigen in 50-80 % of patients Diagnostic Evaluation Synovial fluid analysis Often inflammatory, negative for crystals or infection Imaging May see abnormalities consistent with enthesitis or inflammatory arthritis (joint swelling) 60  Treatment of infection, as indicated Treatment of the arthritis Initial therapy: NSAIDs Other: DMARDs Management Referral to Ophthalmology (for uveitis) of ReA Referral to Rheumatology Majority of patients have a self-limited course, however; The arthritis may persist for several months/become chronic 61 Take Home Points for ReA Usually follows diarrheal illness or STI Can’t See Peripheral arthritis Can’t Pee Conjunctivitis Urethritis Can’t climb a Tree Positive HLA B27 62 Ankylosing Spondylitis (AS) Ankylosis = stiffening of a joint Spondylo = vertebra  Ankylosing Spondylitis (AS) Chronic inflammatory arthritis of the axial skeleton (spine and SI joints) Manifested clinically by pain and progressive fusion of the spine Males > females Age at onset: late teens, early 20s Whites > nonwhite ethnic groups Prevalence in the United States, ~ 1-1.5% of the adult population A 6th-century skeleton showing fused vertebrae, a sign of severe ankylosing spondylitis (Current, 2023) Ankylosing Etiology unknown Spondylitis Combination of genetic/environmental factors Altered gut microbiome Strong hereditary component Associated with HLA-B27 (>85% of patients) Complications Low bone mass, fractures, neurologic compromise due to changes in spine 65  AS: Pathophysiology Enthesitis with chronic inflammation Initial presentation generally relates to the SI joints Moves proximal New bone formation (ossification) and formation of syndesmophytes Condition can progress to the characteristic “bamboo spine” appearance 66 AS: Pathophysiology 67 AS: Progression of Disease 68 UpToDate: 5-year progression  Ankylosing Spondylitis vs. Normal Spine X-ray 69  AS: Key Features Chronic (inflammatory) back pain before age 45 Pain and stiffness (SI joints) Intermittent, often alternating buttocks Symptoms worse in the morning or with inactivity Improvement of symptoms with exercise Extraspinal*: enthesitis, peripheral arthritis, uveitis Fatigue, poor sleep Good response to NSAIDs 70 http://www.mayfieldclinic.com/Images/PE-Sacroiliac_fig1.jpg  Spine: Physical Examination Findings in AS Limited spinal mobility Postural abnormalities Hyperkyphosis Loss of normal lumbar lordosis Limited chest expansion 71  Mechanical Lumbar strain/sprain Spondylolisthesis Herniated disc Spinal stenosis AS: Congenital disease Differential Infection Diagnosis Osteomyelitis Epidural abscess SI joint infection Malignancy Primary or metastatic malignancy Multiple myeloma Leukemia/lymphoma Inflammatory Reactive arthritis Psoriatic arthritis 72 *Not an all-inclusive list IBD-associated arthritis  AS: Labs and Imaging Laboratory Studies Elevated ESR and/or CRP Often a positive HLA-B27 Negative RF and anti-CCP CBC: may have mild anemia of chronic disease Imaging: X-ray and MRI Sacroiliitis (hallmark of disease) May take 5-10 years to develop on x-ray Bamboo spine Signature abnormality in late AS 73  Axial Manifestations: Peripheral Manifestations: Predominant Manifestation back pain and stiffness arthritis, enthesitis, dactylitis NSAIDs (Indomethacin, Naproxen, etc.)—FIRST LINE! First-line therapy Non-pharmacological treatment: education, exercise, physical therapy, rehabilitation, self-help groups, smoking cessation Local Steroids DMARDs Second-line therapy TNF-alpha blocker, IL-17A blocker, Jak Inhibitors Additional therapy in special clinical Analgesics situations Surgery AS: Management, Referral to Rheumatology 74  Inflammatory back pain/stiffness Extraspinal manifestations Positive HLA B27 Bamboo spine Tx: NSAIDs first line! AS: Take Home Points 75 Questions? 76 Resources and References 77 Gout is caused by uric acid. Everyone has uric acid in their blood, but some people have too much of it, and some of those people get gout. In those who get gout, the uric acid accumulates around the joints and acts like matches. When you get a gout attack, one of the matches strikes and catches the joint on fire. When that happens, you should take your indomethacin (or “Gout is nonsteroidal anti-inflammatory drug of choice). It is important to take it right away. If not, more matches will catch fire and the attack will worsen. Like Taking indomethacin does not cure the gout because it only puts out the fire. The matches are still there and can light again. Matches” A urate-lowering drug will remove the matches. If there are no matches, you cannot get gout. But until the urate-lowering drug has time to work, you can still get gout. Therefore, you should take colchicine, one pill twice a day. Colchicine is very good at preventing gout attacks. You can think of colchicine as something that makes the matches damp and harder to strike. 78 CURRENT: Rheumatology, 3e. Chapter 44. Gout. Data from Wortmann RL. Effective management of gout: an analogy. Am J Med. 1998;105:513.  FYI Nice Example: Approach to Clinical Decision Making  FYI Copyrights apply  Assessment of SpondyloArthritis International Society (ASAS) criteria for peripheral spondyloarthritis In patients with peripheral manifestations ONLY Arthritis* or enthesitis or dactylitis plus Sensitivity = 77.8% Specificity = 82.2% ≥ 1 SpA Feature ≥ 2 SpA Features Uveitis Preceding infection Arthritis Psoriasis HLA-B27 Or Enthesitis Crohn’s/ UC Sacroilitis on imaging Dactylitis Inflammatory back pain (ever) FHx for SpA 81 *Peripheral arthritis: usually predominantly lower limb and/or asymmetric arthritis Braun et al.,2012; Rudwaleti et al.,2011 Assessment of SpondyloArthritis International Society (ASAS) criteria for axial Spondyloarthritis In patients with ≥ 3 months back pain and age at onset < 45 years Sacroiliitis on imaging HLA-B27 plus plus Or ≥ 1 SpA feature ≥ 2 SpA features SpA Features Inflammatory back pain Dactylitis FHx of SpA Arthritis Psoriasis HLA-B27 Enthesitis (heel) Crohn’s/ UC Good response to Elevated CRP NSAIDs Uveitis Sensitivity = 82.9% 82 Specificity = 84.4% Sieper, 2017 References Sivera F, Andres M, Dalbeth N. A glance into the future of gout. Ther Adv Musculoskelet Dis. 2022; 14: 1-18. Kakkak M and Lanney H. Management of Gout: Update form the American College of Rheumatology. Am Fam Physician. 2021; 104(2): 209-210. CURRENT Medical Diagnosis & Treatment, 2022 UpToDate Medscape Young People, Bad Backs: Understanding Inflammatory Back Disease. Benjamin J Smith, PA-C, DFAAPA. 2018 AAPA Conference. Rheumatology 101: Understanding the Basics of Degen/Autoimmune Syndromes: OA, RA, Ankylosing Spondylitis (AS), SLE. Antonio Giannelli MsA, PA-C, DFAAPA. 2018 AAPA Conference. Gout and its Cousins: Crystal Arthritis 2018. Benjamin J Smith, PA-C, DFAAPA. 2018 AAPA Conference. Frellick M. Mortality risk doubles for gout when uric acid not optimal. Medscape. October 24, 2018. https://www.medscape.com/viewarticle/903929?nlid=125711_4503&src=wnl_dne_181025_mscpedit &uac=163995EG&impID=1780200&faf=1. Seronegative Spondyloarthropathies: The Great Deceiver. Antonio Giannelli MsA, PA-C, DFAAPA. 2017 AAPA Conference. 83 References Perez-Ruiz F, Castillo E, Chinchilla S, Herrero-Bites AM. Clinical manifestations and diagnosis of gout. Rheum Dis Clin N Am. 2014; 40: 193-206. McQueen FM, Doyle A, Dalbeth N. Imaging in the crystal arthropathies. Rheum Dis Clin N Am. 2014; 40: 231-249. Chaichian Y, Chohan S, Becker MA. Long-term management of gout: Nonpharmacologic and pharmacologic therapies. Rheum Dis Clin N Am. 2014; 40: 357-374. Ea H and Liote F. Diagnosis and clinical manifestations of calcium pyrophosphate and basic calcium phosphate crystal deposition disease. Rheum Dis Clin Am. 2014: 40: 207-229. Rosen T and Furman J. Acute calcium pyrophosphate deposition arthropathy. JAAPA. 2016; 29(6): 1-3. Ellis JM. Acute monoarthritis. JAAPA. 2019; 32(3): 25-31. Higgins P. Gout and pseudogout. JAAPA. 2016; 29(3): 50-52. Edmiston J. A middle-aged man with a painful toe. JAAPA. 2014; 27(40): 50-51. Pennisi M, Perdue J, Roulston T, Nicholas J, Schmidt E, Rolfs J. An overview of reactive arthritis. JAAPA. 2019; 32(7): 25-28. 84 References Duba AS and Mathew SD. The seronegative spondyloarthropathies. Prim Car Clin Office Pract. 2018; 45: 271-287. Sieper J and Poddubnyy D. Axial spondyloarthritis. Lancet. 2017; 390: 73-84. Braun J and Sieper J. Classification, diagnosis, and referral of patients with axial spondyloarthritis. Rheu Dis Clin N Am. 2012; 38: 477-485. Rudwaleit M et al. The assessment of spondyloarthritis international society classification criteria for peripheral spondyloarthritis and for spondyloarthritis in general. Ann Rheum Dis. 2011; 70: 25-31. Poddubnyy D and Landewe R. Development of an ASAS-endorsed recommendation for the early referral of patients with a suspicion of axial spondyloarthritis. Ann rheum Dis. 2015; 74: 1483-187. Assessment of Spondyloarthritis International Society (ASAS). ASAS Slide Library. https://www.asas- group.org/. Rosenthal AK, Ryan LM. Nonpharmacologic and pharmacologic management of CPP crystal arthritis and BCP arthropathy and periarticular syndromes. Rheum Dis Clin N Am. 2014; 40: 343-356. 85