203,669views
00:00 / 00:00
Musculoskeletal system
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
Radial head subluxation (Nursemaid elbow)
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
Degenerative disc disease
Spinal disc herniation
Sciatica
Compartment syndrome
Rhabdomyolysis
Osteogenesis imperfecta
Craniosynostosis
Pectus excavatum
Arthrogryposis
Genu valgum
Genu varum
Pigeon toe
Flat feet
Club foot
Cleidocranial dysplasia
Achondroplasia
Osteomyelitis
Bone tumors
Osteochondroma
Chondrosarcoma
Osteoporosis
Osteomalacia and rickets
Osteopetrosis
Paget disease of bone
Osteosclerosis
Lordosis, kyphosis, and scoliosis
Osteoarthritis
Spondylosis
Spinal stenosis
Rheumatoid arthritis
Juvenile idiopathic arthritis
Gout
Calcium pyrophosphate deposition disease (pseudogout)
Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis
Spondylitis
Septic arthritis
Bursitis
Baker cyst
Muscular dystrophy
Polymyositis
Dermatomyositis
Inclusion body myopathy
Polymyalgia rheumatica
Fibromyalgia
Rhabdomyosarcoma
Myasthenia gravis
Lambert-Eaton myasthenic syndrome
Sjogren syndrome
Systemic lupus erythematosus
Mixed connective tissue disease
Antiphospholipid syndrome
Raynaud phenomenon
Scleroderma
Limited systemic sclerosis (CREST syndrome)
Back pain: Pathology review
Rheumatoid arthritis and osteoarthritis: Pathology review
Seronegative and septic arthritis: Pathology review
Gout and pseudogout: Pathology review
Systemic lupus erythematosus (SLE): Pathology review
Scleroderma: Pathology review
Sjogren syndrome: Pathology review
Bone disorders: Pathology review
Bone tumors: Pathology review
Myalgias and myositis: Pathology review
Neuromuscular junction disorders: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Sjogren syndrome: Pathology review
0 / 3 complete
of complete
Laboratory value | Result |
Hemoglobin | 10.2 g/dL |
Hematocrit | 31% |
Platelet count | 350,000/mm3 |
Leukocyte count | 3,000/mm3 |
Erythrocyte sedimentation rate | 52 mm/h |
Antinuclear antibodies | Positive |
Rheumatoid factor | Negative |
Anti-dsDNA | Negative |
Anti-Ro/La | Positive |
On your rounds, you see a 55-year-old female named Patricia who presents with fatigue, dry skin, and red eyes. She mentions that she's had a recurrent sensation of sand in her eyes and dry mouth every day for the past three months. She also mentioned that when it’s cold outside, the tips of her fingers turn white and hurt. On examination, there are signs of tooth decay and purpura on both lower extremities. Sialometry was performed, which detected salivary hypofunction.
Ok, so Patricia’s clinical picture is suggestive of Sjogren syndrome. Now, Sjogren syndrome is an autoimmune disorder that mostly affects middle-aged females. The high yield concept here is that the immune system attacks various exocrine glands, especially salivary and lacrimal glands. If Sjogren syndrome is primary or occurs alone, it’s called sicca syndrome. Alternatively, it can be secondary when it is accompanied by other autoimmune diseases like lupus, rheumatoid arthritis, and scleroderma. Now, the exact cause of Sjogren syndrome is unknown, but both genetic and environmental factors are involved.
In Sjogren syndrome, some helper T-cells perceive nuclear components that leak out of dead or damaged cells in the body as antigens. These T-cells become active and proliferate and then activate B-cells which start producing anti-nuclear antibodies, or ANAs, against the nuclear antigens. A high yield fact to remember is that the two types of ANA formed in Sjogren syndrome are anti-SSA/RO and anti-SSB/LA antibodies, which are formed against ribonucleoproteins SS-A and SS-B. Next, both T-cells and antibodies enter the circulation and reach the exocrine glands, where activated T-cells secrete cytokines to recruit even more immune cells. This results in a lymphocytic infiltration of the exocrine glands, which ends up damaging the exocrine gland tissue. Eventually, the secreted cytokines also activate fibroblasts, which produce fibrous tissue that replaces the damaged tissue. The end result is a loss of secretory cells in the glands.
Copyright © 2023 Elsevier, except certain content provided by third parties
Cookies are used by this site.
USMLE® is a joint program of the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME). COMLEX-USA® is a registered trademark of The National Board of Osteopathic Medical Examiners, Inc. NCLEX-RN® is a registered trademark of the National Council of State Boards of Nursing, Inc. Test names and other trademarks are the property of the respective trademark holders. None of the trademark holders are endorsed by nor affiliated with Osmosis or this website.