Gout

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Gout

ETP Musculoskeletal System

ETP Musculoskeletal System

Introduction to the skeletal system
Introduction to the muscular system
Bones of the neck
Bones of the vertebral column
Joints of the vertebral column
Vessels and nerves of the vertebral column
Muscles of the back
Bones of the upper limb
Fascia, vessels and nerves of the upper limb
Anatomy of the brachial plexus
Brachial plexus
Anatomy of the pectoral and scapular regions
Anatomy of the arm
Muscles of the forearm
Vessels and nerves of the forearm
Muscles of the hand
Anatomy of the sternoclavicular and acromioclavicular joints
Anatomy of the glenohumeral joint
Anatomy of the elbow joint
Anatomy of the radioulnar joints
Joints of the wrist and hand
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Bones of the lower limb
Fascia, vessels and nerves of the lower limb
Anatomy of the anterior and medial thigh
Muscles of the gluteal region and posterior thigh
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Anatomy of the leg
Anatomy of the foot
Anatomy of the hip joint
Anatomy of the knee joint
Anatomy of the tibiofibular joints
Joints of the ankle and foot
Development of the axial skeleton
Development of the limbs
Development of the muscular system
Bone histology
Cartilage histology
Skeletal muscle histology
Skeletal system anatomy and physiology
Bone remodeling and repair
Cartilage structure and growth
Fibrous, cartilage, and synovial joints
Muscular system anatomy and physiology
Neuromuscular junction and motor unit
Sliding filament model of muscle contraction
Slow twitch and fast twitch muscle fibers
Muscle contraction
Radial head subluxation (Nursemaid elbow)
Developmental dysplasia of the hip
Legg-Calve-Perthes disease
Slipped capital femoral epiphysis
Transient synovitis
Osgood-Schlatter disease (traction apophysitis)
Rotator cuff tear
Dislocated shoulder
Winged scapula
Thoracic outlet syndrome
Carpal tunnel syndrome
Ulnar claw
Erb-Duchenne palsy
Klumpke paralysis
Iliotibial band syndrome
Unhappy triad
Anterior cruciate ligament injury
Patellar tendon rupture
Meniscus tear
Patellofemoral pain syndrome
Sprained ankle
Achilles tendon rupture
Spondylolysis
Spondylolisthesis
Back pain: Pathology review
Lower back pain: Clinical
Degenerative disc disease
Spinal disc herniation
Sciatica
Compartment syndrome
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Genu valgum
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Cleidocranial dysplasia
Lordosis, kyphosis, and scoliosis
Osteosclerosis
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Osteoporosis
Osteomalacia and rickets
Pediatric orthopedic conditions: Clinical
Juvenile idiopathic arthritis
Marfan syndrome
Achondroplasia
Osteomyelitis
Spondylosis
Spondylitis
Spinal stenosis
Bursitis
Baker cyst
Gout and pseudogout: Pathology review
Gout
Calcium pyrophosphate deposition disease (pseudogout)
Psoriatic arthritis
Reactive arthritis
Seronegative and septic arthritis: Pathology review
Seronegative arthritis: Clinical
Septic arthritis
Osteoarthritis
Rheumatoid arthritis and osteoarthritis: Pathology review
Rheumatoid arthritis
Rheumatoid arthritis: Clinical
Systemic lupus erythematosus (SLE): Pathology review
Systemic lupus erythematosus
Scleroderma: Pathology review
Scleroderma
Mixed connective tissue disease
Sjogren syndrome: Pathology review
Sjogren syndrome
Raynaud phenomenon
Ankylosing spondylitis
Antiphospholipid syndrome
Bone disorders: Pathology review
Paget disease of bone
Bone tumors: Pathology review
Bone tumors
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Myasthenia gravis
Inflammatory myopathies: Clinical
Muscle weakness: Clinical
Muscular dystrophy
Rhabdomyolysis
Polymyositis
Dermatomyositis
Inclusion body myopathy
Myalgias and myositis: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Polymyalgia rheumatica
Neuromuscular junction disorders: Pathology review
Fibromyalgia
Lambert-Eaton myasthenic syndrome
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Antigout medications
Osteoporosis medications

Flashcards

Gout

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Questions

USMLE® Step 1 style questions USMLE

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A 12-year-old boy is brought to the PA because of severe pain in his right big toe. He states the toe feels warm and looks swollen and red. He began chemotherapy last week for treatment of acute lymphoblastic leukemia. Temperature is 37.4°C (99.3°F), pulse is 77/min, respirations are 13/min, and blood pressure is 122/82 mm Hg. Physical examination reveals an erythematous and swollen right first metatarsophalangeal joint. It is tender to palpation with decreased active and passive range of motion. After further discussion with the physician, the patient begins prophylactic treatment with allopurinol to prevent additional flares. Which of the following best describes the mechanism of action of this medication?  

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Contributors

Gout is an inflammatory disease in which monosodium urate crystals deposit into a joint, making it red, hot, tender and swollen within hours.

When this happens, it’s called a gouty attack.

The underlying cause is hyperuricemia—too much uric acid in the blood, which results in the formation of sharp, needle-like crystals, in areas with slow blood flow like the joints and the kidney tubules.

Over time, repeated gouty attacks can cause destruction of the joint tissue which results in arthritis.

To understand where the uric acid comes from, let’s start with purines, which, together with pyrimidines, are nature’s most common nitrogen-containing heterocycles.

A heterocycle being any molecular ring or cycle with different types of atoms.

Purines, as well as pyrimidines, are key components of nucleic acids like DNA and RNA, and when cells, along with the nucleic acids in those cells, are broken down throughout the body, those purines are converted into uric acid—a molecule that can be filtered out of the blood and excreted in the urine.

Uric acid has limited solubility in body fluids, though. Hyperuricemia occurs when levels of uric acid exceed the rate of its solubility, which is about 6.8mg/dL.

At a physiologic pH of about 7.4, uric acid loses a proton and becomes a urate ion, which then binds sodium and forms monosodium urate crystals.

These crystals can form as a result of increased consumption of purines, like from consuming purine-rich foods like shellfish, anchovies, red meat or organ meat.

Also, though, they can result from increased production of purines, for example high-fructose corn syrup containing beverages could contribute to the formation of uric acid by increasing purine synthesis.

Another way crystals could form is from decreased clearance of uric acid, which can result from dehydration from not drinking enough water or from consumption of alcoholic beverages, both of allowing uric acid to precipitate out.

Regularly eating these kinds of foods can also lead to obesity and diabetes, both of which are risk-factors for gout.

Hyperuricemia can also develop as a result of chemotherapy or radiation treatment, since cells die at a faster-than-normal rate.

Also, some individuals have a genetic predisposition to overproduction of uric acid while others with chronic kidney disease may be unable to excrete the uric acid.

Finally, there are some medications like thiazide diuretics and aspirin which can also increase the levels of uric acid and therefore the risk of gout.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Gout" The Lancet (2016)
  6. "Update on gout: new therapeutic strategies and options" Nature Reviews Rheumatology (2010)
  7. "Diagnosis of Acute Gout: A Clinical Practice Guideline From the American College of Physicians" Annals of Internal Medicine (2016)