PA Days Presentation Brian K. Shrawder, PA-S LHU.

Slides:



Advertisements
Similar presentations
GOUT Disease caused by tissue deposition of Monosodium urate crystals as a result of supersatuaration of extra cellular fluid with MSU.
Advertisements

Little Rheumatology gems for GP Trainees HDR 7/12/10 Hayley Faries, ST1 Rheumatology.
Team Meeting Presentations
1. Describe the pathogenesis of hyperuricemia and gout Goup C1 Group C1.
FREEDOM FROM RHEUMATOLOGICAL DISORDERS
Purine degradation & Gout (Musculoskeletal Block) Purine degradation pathway Fate of uric acid in humans Gout and hyperuricemia: Biochemistry Types Treatment.
GOUT AND PSEUDOGOUT ANDRES QUICENO, MD Rheumatology Division
{ Gout and Bursitis Asfand Baig.   Inflammatory arthritis associated with hyperuricaemia* and intra-articular sodium urate crystals Gout.
Purine Degradation & Gout (Musculoskeletal Block)
Prepared by : Tamara Odeh Diana Jawhari Supervised by : Dr. Ola Ayesh.
Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Chapter 74 Drug Therapy of Gout.
Management of Rheumatoid arthritis, Osteoarthritis & Gout Dr. Eoin Casey MD FRCPI, FRCP.
Gout.
 Gout is characterized by elevated uric acid concentrations in blood and urine due to variety of metabolic abnormalities that include overproduction.
Gout & hyperuricemia.
Gout: Its not all crystal clear Robert L. Wortmann, M.D. Department of Internal Medicine The University of Oklahoma College of Medicine, Tulsa.
1 Uric acid and Gout James Witter MD, PhD Arthritis Advisory Meeting June 2, 2004.
Uric Acid Metabolism & Gout. Nucleic Acids Mononucleotide Base + Sugar + Phosphoric Acid Base: Purine or Pyrimidine Polynucleotide (DNA or RNA) Mononucleotides.
Gout Dr. Wael H.Mansy, MD Assistant Professor College of Pharmacy King Saud University.
Uric acid xiaoli.
Familial metabolic disease Characterized by : Acute arthritis Uric stones in the kidneys Hyperuricemia.
Uric Acid Metabolism & Gout. Nucleic Acids Mononucleotide Base + Sugar + Phosphoric Acid Base: Purine or Pyrimidine Polynucleotide (DNA or RNA) Mononucleotides.
Gout By Shravya & Helen. Gout is… An inflammatory arthritis associated with hyperuricaemia and intra-articular sodium urate crystals.
Uric Acid Metabolism & Gout
HYPERURICEMIA and GOUT PATHOGENESIS. HYPERURICEMIA Plasma/serum urate concentration >408 mol/L (6.8 mg/dL) Present in between 2.0 and 13.2% of ambulatory.
GOUT. By Prof. Azza El- Medany Dr. Osama Yousf OBJECTIVES At the end of lectures students should : Define gout Describe outlines of treatment Describe.
GOUT. Definition Heterogeneous group of diseases involving : An elevated serum urate concentration (hyperuricemia) Recurrent attacks of acute arthritis.
Diagnosis of gout.
Gout extra Q’s. After giving Marilyn analgesia you arrange an ultrasound and guided aspiration of Marilyn's first metatarsophalangeal joint. The initial.
Joints (arthritis) – Rheumatoid arthritis Inflammatory dz affecting synovial joints predominately Hyperplasia of synovial fibroblasts Severity is varied.
Definition of Gout Definition of Gout Pathological classification Pathological classification History of Gout History of Gout Gout Aetiology & Pathogenesis.
HPI A 52 yo male presents to his PCP on a Monday morning with exquisite right knee pain that started overnight. He spent Sunday tailgating with friends.
Purine degradation & Gout (Musculoskeletal Block) Purine degradation pathway Fate of uric acid in humans Gout and hyperuricemia: Biochemistry Types Treatment.
Gout Gouty Arthritis By Mike Parenteau.
Clinical Case #6 By Chen, chun-Yu (Kim) Chen, I -chun (Afra) Chen, I -chun (Afra)
Four Stages of Gout  Asymptomatic hyperuricemia Elevated levels of uric acid in the blood but no other symptoms Does not require treatment  Acute gout/Acute.
TAP PHARMACEUTICAL PRODUCTS INC. June 2, Arthritis Drugs Advisory Committee TAP Pharmaceutical Products Inc. June 2, 2004.
Gout Familial metabolic disease characterized by : Acute arthritis Uric acid stones in the kidneys Hyperuricemia.
GOUT. Demographics Affects middle-aged to elderly men postmenopausal and elderly women (usually have OA and HPN causing mild renal insufficiency, and.
Agents Used to Treat Hyperuricemia and Gout
GOUT A metabolic disease in which tissue deposition of crystals of monosodium urate occurs from supersaturated extracellular fluids and results in one.
GOUT: DIAGNOSIS AND MANAGEMENT. Gout Metabolic disorder due to excessive accumulation of uric acid in tissues leading to acute and chronic arthritis and.
Drug Therapy of Gout. Drug therapy of gout What Is Gout?
Gout Treatment Megan Chan, PGY-2 UHCMC Gout Acute gouty arthritis = monosodium urate crystals in synovial fluid leukocytes – Serum urate ≥ 6.8 =
Gout. The most common cause of inflammatory arthritis in US adults (3.9% of Americans; approx. 8.3 million people; ) Prevalence is greater in.
Metabolic Diseases of the Bone
Dr. Müge Bıçakçıgil Kalaycı
StagesClinical Features (1)Asymptomatic hyperuricemiahigh uric acid level is present but without symptoms (2) Acute Gouty Arthritishigh uric acid level.
Gout is a species-wide inborn error of purine metabolism D. Branch Moody, M.D. Professor of Medicine Immunology Laboratory, Smith Building
Colchicine: Colchicine: Effective & specific gout Rx, but less favored than NSAIDs because of slow onset of action & high incidence of side effects. Effective.
GERIATRICS Dr. Meg-angela Christi Amores. Musculoskeletal Disorders in the Elderly  Osteoarthritis  Rheumatoid Arthritis  Gout (Gouty arthritis) 
Purine Degradation & Gout (Musculoskeletal Block) Purine degradation pathway Fate of uric acid in humans Gout and hyperuricemia: Biochemistry Types Treatment.
GOUT Katie Margelot NURS 870. Definition Gout is an acute, sudden inflammatory disease of the joint, caused by high concentrations of uric acid in the.
Metabolism of purine nucleotides A- De Novo synthesis: of AMP and GMP Sources of the atoms in purine ring: N1: derived from NH2 group of aspartate C2 and.
Gout Ashley Guzman Primary Care I: Acute and Chronic Health Problems
GOUT GOUT.
Gout Disease of Kings Dr.Fakhir Yousif.
Crystalopathies Joanna Zalewska.
Gout Is recurrent inflammatory disorder characterized by
Gout.
History Salient Features Physical Exam
Drug Therapy of Gout 1.
  URIC ACID Muthana A. Al-Shemeri.
Lecture 9 Musculoskeletal Disorders Gout
Gout By: Patience Alley, Albert Watson, and Hunter Kimball.
Gout Scott Smith PGY-1 1/11/2018.
Presentation transcript:

PA Days Presentation Brian K. Shrawder, PA-S LHU

Patient of the Day 51 y/o Caucasian male, swollen, red, painful MTP joint. Started last night; Pain – sharp/stabbing; exacerbated with anything touching; No relief Hx: MI ~ 2 months ago; medications – thiazide diuretics for B/P; ~30 12oz beers / weekend; father had this condition. Denies recent trauma, infections, penetrations or constitutional symptoms.

Patient of the Day What’s in your differential? 1.Gout*** 2.Calcium Pyrophaosphate “Pseduo-gout” 3.Calcium Apatite 4.Septic Joint

Gout: Background “Disease of Kings” Found exclusively in Humans, Birds & Dalmatian canines Heterogeneous disease including: –Elevated serum urate concentration (hyperuricemia) –Reoccurring attacks of monosodium urate monohydrate crystals –Deposits of monosodium urate crystals (TOPHI) –Renal disease of glomerular, tubular, interstitial tissues & blood vessels –Uric acid nephrolithiasis

Gout: Background Occurs with HYPERURICEMIA – elevations above 7 mg/dl (men) or 6 mg/dl (women). Deposits in superstaturations joints or kidneys

Gout: Epidemiology Rates: 2.3 -> 41.3% of ‘normal’ population Factors: higher serum BUN, Creatinine, body wt, ht, age, B/P, & ETOH “Body Bulk” -> estimated bw, surface area, or BMI most important predictors of hyperuricemia

Gout: Epidemiology At puberty, serum urate concentrations increase ~ 1-2 mg/dl & sustained Females, lower changes until menopause (estrogen) Urate levels > 9 mg/dl – incidences highest rates

Gout: Clinical Features 4 stages : –Asymptomatic Hyperuricemia –Acute gouty arthritis –Intercritical gout –Chronic tophaceous

Gout: Clinical Features 1. Asymptomatic Hyperuricema –Serum urate elevated, but no manifestations –Tendency increases with elevated levels –This phase ends with first attack (stone or arthritis) –First attack, occurs after AT LEAST 20 years of sustained

Gout: Clinical Features 2. Acute Gouty Arthritis: –40 -> 60 years (men) & > 60 (females) –Onset BEFORE 25 -> enzymatic defect due to overproduction purine, renal disorder or cyclosporine use –1 st MCP site = #1 –‘works way up to foot’ –Explosive onset after falling asleep ‘well’ –Joint: Hot, red, dusky, swelling, extremely painful

Gout: Clinical Features 2. Acute Gouty Arthritis (continued) –Precipitating factors: anti-hyperuricemic therapy, diuretics, IV heparin & cyclosprine –Also: trauma, infection, ‘foreign protein’ therapy, hemorrhage, radiographic contrast

Gout: Clinical Features Diagnosis: –Aspiration of joint –Inspections of fluid Needle shaped, negative birefringence (CUB) –Clinical features of GOUT: Max inflammation w/in 1 day, one joint, red, swelling, painful, hyperuricemia, asymmetical

Gout: Clinical Features 3. Intercritical Gout: –“interval gout” – periods between attacks –Some may never have 2 nd attack –62% within first yr, 11% 2 – 5 yrs, 4% 5-10yrs –Later attacks, less explosive onset, polyarticular, more severe, last longer, abate more gradually

Gout: Clinical Features 4. Chronic Tophaceous Gout: –Polararticular gout with no pain free intervals –Correlations with degree and duration of hyperuricemia –Irregular, asymmetrical nodules –Destructions of joints, grotesque deformities, progressive to crippling –Skin overlying may ulcerate: extrude a white, chalky or pasty material composed of urate crystals

Gout: Abortive Treatment 1) Colchicine:.5 mg/hr until Joint symptoms ease N/V/D Maximum 10 doses –Preferred for unconfirmed dx –NSAIDs preferred with secure dx

Gout: Abortive Treatment 2) NSAIDs (Indomethacin – DOC) 50 – 75 mg every 4 – 8 hours until 200 mg total 3)Glucocorticoids – Intra-articular injections; useful in limited joint treatment 4)*Prophylaxis – (colchicine) anti-inflammatory 2 weeks use prior anti-hyperuricemia therapy

Gout: Preventative Treatment Hyperuricemia – control uric acid levels < 6 mg/dl (a) Xanthine oxidase inhibitors (allopurinal) – ‘over producers’ *block production of uric acid *pass > 700 mg/day (b) Uricosuric agents (Probenecid) – ‘under excretory’ *enhance renal excretion of uric acid

Thanks Any Questions? References: Cush, John, Kavanaugh, Arthur, Stein, Michael. (2005) Rheumatology: Diagnosis & Therapuetics. Lippincott, Williams & Willkins Hang-Korng, Ea MD. (2006) Gout: Update on Some Pathogenic and Clinical Aspects. Rheumatic Diseases Clinics of North America. 32, (2) 295 – 311 Harris, Edward D., et al. (2005) Kelley’s Textbook of Rheumatology. Philadelphia: Elsevier Science. Nuki, George MB. (2006) Treatment of Crystal Arthropathy – History and Advances. Rheumatic Diseases Clinics of North America. 32 (2), Rakel, Robert MD, Bope, Edward MD (2007) Conn’s Current Therapy. Philadelphia: Saunders Elsevier.