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Musculoskeletal
FA complete review part 2 Pathology II
| Question | Answer |
|---|---|
| What is the pathogenesis of Osteoarthritis? | Mechanical- wear and tear destroys articular cartilage leading to inflammation with inadequate repair |
| What cell mediate the pathogenesis of Osteoarthritis? | Chondrocytes |
| What is the role of Chondrocytes in Osteoarthritis pathogenesis? | Mediate degradation an inadequate repair of the articular cartilage |
| Is the pathogenesis of Osteoarthritis, mechanical or autoimmune? | Mechanical |
| What are common predisposing factors of Osteoarthritis? | Age, female, obesity, and joint trauma |
| What is the clinical presentation of Osteoarthritis? | 1. Pain in weight-bearing joints after use, improving with rest 2. Asymmetric joint involvement 3. Knee cartilage loss beings mediall 4. NO SYSTEMIC symptoms |
| Which condition, rheumatoid arthritis or osteoarthritis, presents with "bowlegged" deformity? | Osteoarthritis |
| Joint involvement in osteoarthritis, is symmetric or asymmetric? | Asymmetric |
| True or False. Osteoarthritis present with systemic symptoms. | FALSE. Osteoarthritis has NO systemic symptoms |
| What are the joint finding of osteoarthritis? | 1. Osteophytes, 2. Joint space narrowing, 3. Subchondral sclerosis ans cysts 4. Synovial fluid noninflammatory 5. Involves DIP, PIP, and 1st CMC |
| Is the MCP involved in Osteoarthritis? | No |
| Which joint involvement in osteoarthritis produces the Heberden nodes? | DIP |
| The "nodes" of joint deformities are involved in Osteoarthritis or Rheumatoid arthritis? | Osteoarthritis |
| Which are joint deformities caused by DIP and PIP in osteoarthritis? | Heberden nodes (DIP) and Bouchard nodes (PIP) |
| Besides the PIP and DIP, which other joint is involved in Osteoarthritis? | 1st CMC |
| It the arthritic condition does NOT involve the MCP, it most likely is, osteoarthritis or RA? | Osteoarthritis |
| List of treatment options for Osteoarthritis: | Acetaminophen, NSAIDs, intra-articular glucocorticoids |
| What is the pathogenesis of Rheumatoid arthritis? | Autoimmune- inflammation induces formation of pannus which erodes articular cartilage and bone |
| What is Pannus? | Proliferative granulation tissue |
| What common articular condition is associated with pannus? | Rheumatoid arthritis |
| What are risk factors of Rheumatoid arthritis? | Female, HLA-DR4, smoking, (+) rheumatoid factor, anti-cyclic citrullinated peptide antibody |
| What is most specific antibody for Rheumatoid arthritis? | Anti-cyclic citrullinated peptide antibody |
| What is the clinical presentation of Rheumatoid arthritis? | Pain, swelling, and morning stiffness lasting > 1 hour, improving with use. Symmetric joint involvement and, Systemic symptoms such as fever, weight loss, and fatigue Extraarticular manifestations are common |
| Which RA or Osteoarthritis presents with symmetrical joint involvement? | Rheumatoid arthritis |
| Which, RA or osteoarthritis, is presented with systemic symptoms? | Rheumatoid arthritis |
| How is the pain in joint in RA in the morning? | Morning stiffness lasting > 1 hour, but improves with use |
| What are the extra-articular manifestation presented in RA? | 1. Rheumatoid nodules in subcutaneous tissue and lung 2. Interstitial lung disease 3. Pleuritis 4. Pericarditis 5. Anemia of chronic disease 6 .Neutropenia + splenomegaly 7. AA amyloidosis 8. Sjogren syndrome 9. Scleritis 10. Carpal tunnel syndrome |
| What are some joint findings in Rheumatoid arthritis? | Erosions, juxta-articular osteopenia, soft tissue swelling, subchondral cysts, joint space narrowing |
| What are the classical joint deformities in RA? | 1. Cervical subluxation 2. Ulnar finger deviation 3. Swan neck, 4 Boutonniere |
| Which joints are involved in Rheumatoid arthritis? | MCP, PIP, and wrist |
| Which joint is involved in RA but not in Osteoarthritis? | DIP or 1st CMC |
| Articular condition with synovial fluid inflammatory | Rheumatoid arthritis |
| What are the lung conditions associated with Rheumatoid arthritis? | Pneumoconiosis leading to Caplan syndrome |
| What are the treatment options for Rheumatoid arthritis? | NSAIDs, glucocorticoids, disease-modifying agents, and biologic agents. |
| What are common Disease-Modifying agents used in treatment of Rheumatoid arthritis? | Methotrexate, sulfasalazine, hydroxychloroquine, and Leflunomide. |
| What is Gout? | Acute inflammatory monoarthritis caused by precipitation of monosodium urate crystal in joints. |
| What risk factors associated with developing of Gout? | Male sex, hypertension, obesity, diabetes, and dyslipidemia |
| What is the strongest risk factor for Gout? | Hyperuricemia |
| Acute inflammatory monoarthritis caused by precipitation of monosodium urate crystals in joints. Dx? | Gout |
| What type of crystals are seen in joints of Gout patients? | Monosodium urate crystals |
| What are the two causes of hyperuricemia? | 1. Underexcretion of uric acid 2. Overproduction of uric acid |
| Which cause of hyperuricemia, underexcretion or overproduction of uric acid, is most common in causation? | Underexcretion of uric acid |
| What are some condition that lead to the underexcretion of uric acid leading to Gout? | Idiopathic but potentiated by renal failure |
| What type of diuretic are often associated with precipitating gout by underexcretion of uric acid? | Thiazide diuretics |
| What conditions cause the overproduction of uric acid leading to Gout? | Lesch-Nyhan syndrome, PRPP excess, increase cell turnover, and von Gierke disease |
| Description of Gout crystals | Needle shaped and (-) birefringence under polarized light |
| Crystal are needle-shaped and with a negative birefringent. Dx? | Gout |
| How are the crystals of Gout under polarized light? | Yellow under parallel light, and blue under perpendicular light |
| Needle-shaped crystal (-) birefringence under polarized light | Gout |
| How is the birefringent of Gout crystals? | Negative |
| What is the shape of crystal in gout? | Needle-shaped |
| What is a common condition that causes a elevated cell turnover? | Tumor lysis syndrome |
| What type or hyperuricemia is produced by Tumor lysis syndrome, that later develops into Gout? | Overproduction of uric acid |
| Is the joint affection in Gout, asymmetric or symmetric? | Asymmetric |
| Clinical description of affected joint in Gout? | Joint is swollen, red, and painful |
| What is the classical manifestation of Gout? | Painful MTP joint of big toe (podagra) |
| What is Tophus formation associated with? | Gout |
| Where in Gout is Tophus formation visible? | External ear, olecranon bursa, or Achilles tendon |
| What are events or actions that precipitate Gout? | 1. After large meal with foods rich in purines (red meat, seafood), 2. Trauma 3. Dehydration 4. Diuresis 5. Alcohol consumption |
| How does alcohol consumption precipitate acute Gout attacks? | Alcohol metabolites compete for same excretion sites in kidney as uric acid lead to decrease uric acid secretion and subsequent buildup in blood. |
| What are medications are used for acute flare of gout? | NSAIDs, glucocorticoids and colchicine |
| What are the chronic (preventive) medications of Gout? | Xanthine oxidase inhibitors |
| What are tow commonly used xanthine oxidase inhibitors used in gout? | Allopurinol and Febuxostat |
| MOA of Allopurinol and Febuxostat | Xanthine oxidase inhibitors |
| What was the old nomenclature for Calcium pyrophosphate deposition disease? | Pseudogout |
| What is the pathogenesis of Pseudogout? | Deposition of calcium pyrophosphate crystals within the joint space. |
| What are some associations causative of Calcium Pyrophosphate deposition disease (Pseudogout)? | Hemochromatosis, hyperparathyroidism, and joint trauma |
| What is the most commonly involved joint in Pseudogout? | Knee |
| Pain and swelling with acute inflammation and/or chronic degeneration (pseudo-osteoarthritis). | Clinical presentation of Pseudogout |
| What is the key feature of x-ray of Calcium Pyrophosphate deposition disease? | Chondrocalcinosis |
| What is chondrocalcinosis? | Cartilage calcification |
| How are the crystals in Calcium Pyrophosphate deposition disease? | Rhomboid and weakly (+) birefringent under polarized light |
| What is the treatment for Pseudogout? | NSAIDs, colchicine, and glucocorticoids |
| What medication is often used as prophylaxis for Pseudogout? | Colchicine |
| Rhomboid calcium crystal in the knee joint. Dx? | Pseudogout |
| Birefringent of crystal in Pseudogout | Weakly (+) birefringent |
| What is Systemic juvenile idiopathic arthritis? | Childhood arthritis seen in < 12 year olds. |
| What is the clinical presentation Systemic Juvenile Idiopathic arthritis? | 1. Daily spiking fevers 2. Salmon-pink macular rash 3. Uveítis 4. Arthritis (2+ joints) |
| What are accompanying lab results in Systemic Juvenile idiopathic arthritis? | Leukocytosis, Thrombocytosis, Anemia Increased ESR, Increased CRP |
| What are the treatment options of Juvenile arthritis? | NSAIDs, steroids, methotrexate, TNF inhibitors |
| What is the key cutaneous (skin) feature of Juvenile Arthritis? | Salmon-pink macular rash |
| A 9 year old complains of joint pain, and PE is (+) for a salmon-pink macular rash. Dx? | Systemic Juvenile Idiopathic Arthritis |
| What is Sjogren syndrome? | Autoimmune disorder characterized by destruction of exocrine glands by lymphocytic infiltrates. |
| Which exocrine glands are commonly destroyed n Sjogren's syndrome? | Lacrimal and salivary glands |
| Autoimmune disorder that is featured by the destruction of lacrimal and salivary glands by lymphocytic infiltrates, most commonly in women. Dx? | Sjogren syndrome |
| What is the epidemiology of Sjogren's syndrome? | Women of 40-60 years old |
| What are the findings in Sjogren syndrome? | 1. Inflammatory joint pain 2. Keratoconjunctivitis sicca 3. Xerostomia 4. Presence of several antibodies |
| What is Keratoconjunctivitis sicca? | Decreased tear production and subsequent corneal damage |
| What is Xerostomía? | Decreased saliva production |
| What autoimmune disorder is associated with Xerostomia? | Sjogren syndrome |
| What occular (eye) condition is associated with Sjogren syndrome? | Keratoconjunctivitis sicca |
| What are the antibodies associated with Sjogren syndrome? | - Antinuclear antibodies - Rheumatoid factor - Anti-ribonucleoprotein antibodies - Bilateral parotid enlargement |
| What are the anti-ribonucleoprotein antibodies associated with Sjogren syndrome? | SS-A (anti-Ro) and/or SS-B (anti-La) |
| Other than Sjogren syndrome, which other condition has (+) anti-SSA and anti-SSB? | SLE |
| What is the risk of (+) anti-SSA in pregnant women with SLE? | Congenital heart block in the newborn |
| What is a common primary or secondary syndrome assocaited with other automimmune disorders such as RA, SLE, and systemic sclerosis? | Sjogren syndrome |
| What are common complications of Sjogren syndrome? | Dental caries, mucosoa-associated lumphoid tissue (MALT) lymphoma, . |
| What is the key finding of Sjogren syndrome in a biopsy? | Focal lymphocytic sialadenitis on labial salivary gland |
| Focal lymphocytic sialadenitis on labial salivary gland biopsy. Dx? | Sjogren syndrome |
| What are the common pathogens that cause Septic arthritis? | S. aureus, Streptococcus, and Neisseria gonorrhoeae. |
| How is the synovial fluid in Septic arthritis? | Purulent with WBC > 50, 000/mm3 |
| What is the common triad of Gonococcal arthritis? | Polyarthralgia, tenosynovitis (hand), and dermatitis. |
| STI that presents as either purulent arthritis (knee) with a triad of polyarthritis, tenosynovitis, and dermatitis. Dx? | Gonococcal arthritis |
| Which part is Gonococcal arthritis tenosynovitis present? | Hand |
| What type of arthritic conditions are without rheumatoid factor? | Seronegative Spondyloarthtirtis |
| What is the MHC class serotype is associated Seronegative spondyloarthritis? | MHC class I |
| List of Seronegative Spondyloarthritis: | 1. Psoriatic arthritis 2. Ankylosing spondylitis 3. Inflammatory bowel disease 4. Reactive arthritis |
| What are general clinical signs of Seronegative spondyloarthritis? | 1. Inflammatory back pain 2. Peripheral arthritis 3. Enthesitis 4. Dactylitis 5. Uveitis |
| What is Enthesitis? | Inflamed insertion sites of tendons |
| What is a common way to refer to Dactylitis? | "sausage fingers" |
| What is the HLA association with all Seronegative spondyloarthritis? | HLA-B27 |
| Description of inflammatory back pain associated with HLA-B27 arthritic conditions | Morning stiffness, that improves with exercise |
| What are common associations of Psoriatic arthritis? | Skin psoriasis and nail lesions |
| What are clinical signs of Psoriatic arthritis? | - Asymmetric and patchy involvement. - Dactylitis and "pencil-in-cup" deformity of DIP on x-ray |
| What is a classic finding of DIP x-ray in Psoriatic arthritis? | "pencil-in-cup" deformity of DIP |
| "Pencil-in-cup" deformity of DIP on x-ray. Dx? | Psoriatic arthrtitis |
| Which arthritic condition is characterized by symmetric involvement of spine and sacroiliac joints? | Ankylosing spondylitis |
| What are the results of the joint inflammation in Ankylosing spondylitis? | Ankylosis (joint fusion), uveitis, and aortic regurgitation |
| Which heart condition is associated with Ankylosing spondylitis? | Aortic regurgitation |
| Bamboo spine. Dx? | Ankylosing spondylitis |
| What is a possible respiratory complication in Ankylosing spondylitis? | Costovertebral and costosternal ankylosis may cause restrictive lung disease |
| What is the cause of a respiratory lung disease in Ankylosing spondylitis? | Costovertebral and costosternal ankylosis |
| Which inflammatory bowel diseases are associated with Spondyloarthritis? | Crohn disease and Ulcerative colitis |
| What was the former name of Reactive arthritis? | Reiter syndrome |
| What is the classic triad of Reactive arthritis? | 1. Conjunctivitis 2. Urethritis 3. Arthritis |
| A person complains of conjunctivitis, inability to urinate, and peripheral arthritis. Dx? | Reactive arthritis |
| What are the pathogens associated with causing Reactive arthritis? | Shigella, Yersinia, Chlamydia, Campylobacter, and Salmonella |
| Systemic Lupus Erythematosus (SLE) is a : | Systemic, remitting, and relapsing autoimmune disease |
| What causes organ damage in SLE? | Primarily due to a type III hypersensitivity reaction and, to a lesser degree, a type II hypersensitivity reaction. |
| What is the cause of a decrease in clearance of immune complexes in SLE? | Deficiency of early complement proteins (C1q, C4, and C2) |
| What is the classic clinical presentation of SLE? | Rash, joint pain, and fever in a female of reproductive age |
| Which ethnicities are more common to develop SLE? | African-American and Hispanic descent |
| Which are the early complement proteins associated with the pathogenesis of SLE? | C1q, C4 and, C2 |
| What is Libman-Sacks Endocarditis? | Nonbacterial, verrucous thrombi usually on mitral or aortic valve and can be present on either surface of the valve |
| What subtype of endocarditis is associated with SLE? | Libman-Sacks Endocarditis |
| SLE endocarditis (name) | Libman-Sacks Endocarditis |
| Glomerular deposition of DNA-anti-DNA immune complexes. | Lupus nephritis |
| What is Lupus nephritis cause? | Glomerular deposition of DNA-anti-DNA immune complexes |
| What is the common and severe type of Lupus nephritis? | Diffuse proliferative |
| What are the common causes of death in SLE? | 1. Renal disease 2. Infections 3. Cardiovascular disease |
| What is the MCC of death in SLE? | Renal disease |
| In a anti-SSA (+) pregnant woman ---> | Increased risk of newborn developing neonatal lupus |
| What are the clinical features of Neonatal lupus? | Congenital heart block, Periorbital/diffuse rash, Transaminitis and, Cytopenias |
| What is the common mnemonic used to summarize SLE? | RASH OR PAIN |
| RASH OR PAIN: | Rash (malar or discoid) Arthritis (nonerosive) Serositis Hematologic disorders Oral/nasopharyngeal ulcers Renal disease Photosensitivity Antinuclear antibodies Immunologic disorder Neurological disorders |
| What is the type of rash seen in SLE? | Malar or discoid rash |
| How is the arthritis in SLE described as? | Nonerosive |
| What are the anti-antibodies associated with SLE immunologic disorders? | anti-dsDNA, anti-Sm, and antiphospholipid |
| Mixed connective tissue disease has features of: | SLE, Systemic sclerosis, and/or polymyositis |
| What is the associated antibody of Mixed CT disease? | anti-U1 RNP antibodies |
| (+) anti-U1 RNP antibodies. Dx? | Mixed connective tissue disease |
| Antiphospholipid syndrome is: | A primary or secondary disorder, most commonly in SLE |
| What is the criteria for diagnosis of Antiphospholipid syndrome? | 1. Hx of thrombosis 2. Hx of Spontaneous abortion 3. (+) antibodies: lupus anticoagulant, anticardiolipin, and anti-B2 glycoprotein I antibodies |
| What is the treatment for antiphospholipid syndrome? | Systemic anticoagulation |
| Anticardiolipin antibodies can cause: | False-positive VDRL/RPR |
| What can produce false-positive VDRL/RPR? | Anticardiolipin antibodies |
| What is a adverse effect of Lupus anticoagulant? | Prolonged PTT that cannot be corrected by the addition of normal platelet-free plasma. |
| What condition is closely associated with Polymyalgia rheumatica? | Giant cell (temporal) arteritis |
| What are the symptoms of Polymyalgia rheumatica? | Pain and stiffness in proximal muscles, often with fever, malaise, and weight loss. |
| What is the population most commonly affected by Polymyalgia rheumatica? | Women > 50 years old |
| A person with Giant cell (temporal) arteritis, is often also found with what muscle condition? | Polymyalgia rheumatica |
| What are the lab findings of Polymyalgia rheumatica? | Elevated ESR and CRP, and normal CK |
| Lab findings: - Increased ESR - Increased CRP - Normal CK Dx? | Polymyalgia rheumatica |
| The treatment of Polymyalgia rheumatica has a -----> | Rapid response to low-dose corticosteroids |
| What is Fibromyalgia? | Chronic, widespread musculoskeletal pain associated with "tender points," stiffness, paraesthesias, poor sleep, fatigue, cognitive disturbance. |
| What is the etiology of Fibromyalgia? | Women 20-50 years old |
| What is the treatment for Fibromyalgia? | Regular exercise, antidepressants, and neuropathic pain agents |
| What neuropathic pain agent is often use in Fibromyalgia treatment? | Gabapentin |
| What type of antidepressants are used in the treatment of Fibromyalgia? | TCAs and SNRIs |
| What are the non-specific lab findings of Polymyositis/Dermatomyositis? | (+) ANA and elevated CK |
| What are the SPECIFIC lab findings of Polymyositis/ Dermatomyositis? | 1. (+) anti-Jo-1 (histidyl-tRNA synthetase) 2. (+) anti-SRP (signal recognition particle), 3. (+) anti-Mi-2 (helicase) |
| Anti-Jo-1 antibody = | Histidyl-tRNA synthetase |
| What is Polymyositis? | Progressive symmetric proximal muscle weakness, characterized by endomysial inflammation with CD8+ T cells |
| Endomysial or Perimysial inflammation is seen with Polymyositis? | Endomysial inflammation |
| Endomysial or Perimysial inflammation is seen with Dermatomyositis? | Perimysial inflammation |
| What are the distinguishing features of dermatomyositis, that separate it from Polymyositis? | Gottron papules, photo disturbed facial erythema, "shawl and face" rash, darkening and thickening of fingertips and sides resulting in irregular, "dirty"-appearing marks |
| Polymyositis + cutaneous involvement. Dx? | Dermatomyositis |
| Perimysial inflammation and atrophy with CD4+ T cells. | Dermatomyositis |
| What CD + T cells are involved in Dermatomyositis? | CD4+ T cells |
| Which CD+ T cells are involved in Polymyositis? | CD8+ T cells |
| What is the facial rash/erythema seen with Dermatomyositis? | Heliotrope (violaceus) edema of the eyelids |
| What part of the body is most often involved in Polymyositis? | Shoulders |
| Helicase antibody = | anti-Mi-2 antibody |
| What are the two most common Neuromuscular junction diseases? | Myasthenia gravis and Lambert-Eaton myasthenic syndrome |
| What is the most common NMJ disorder? | Myasthenia gravis |
| What is the pathophysiology of Myasthenia gravis? | Autoantibodies to postsynaptic ACh receptor |
| What condition is due to autoantibodies to postsynaptic ACh receptor? | Myasthenia gravis |
| What are the clinical fatigable muscle weakness features of Myasthenia gravis? | Ptosis; Diplopia; Proximal weakness; Respiratory muscle involvement --> dyspnea Bulbar muscle involvement --> dysphagia, difficulty chewing |
| What is the result of bulbar muscle involvement in Myasthenia gravis? | Dysphagia and difficulty chewing |
| Myasthenia gravis or Lambert-Eaton myasthenic gravis syndrome, worsens with muscle use? | Myasthenia gravis |
| Myasthenia gravis or Lambert-Eaton myasthenic gravis syndrome, improves with muscle use? | Lambert-Eaton myasthenic syndrome |
| What associated conditions with Myasthenia gravis? | Thymoma and Thymic hyperplasia |
| AChE inhibitor administration in Myasthenia gravis? | Reverses symptoms |
| What is a common medication used in Myasthenia gravis to reverse symptoms? | Pyridostigmine |
| Pyridostigmine is used to reverse ________________________ symptoms. | Myasthenia gravis |
| What is the pathophysiology of Lambert-Eaton myasthenic syndrome? | Antibodies to presynaptic Ca2+ channel leading to a decrease in ACh release |
| Myasthenia gravis involves pre- or postsynaptic receptors in NMJ? | Postsynaptic ACh receptors |
| Lambert-Eaton myasthenic syndrome, involves pre- or postsynaptic receptors? | Presynaptic Ca2+ channels |
| The antibodies in LEMS that attach the presynaptic Ca2+ channels cause ---> | Decrease in ACh release |
| What are clinical characteristics of LEMS? | Proximal muscle weakness, autonomic symptoms (dry mouth, constipation, and impotence) Hyporeflexia Improves with muscle use |
| What condition is associated with Lambert-Eaton myasthenic syndrome (LEMS)? | Small cell lung cancer |
| Which NMJ condition is often associated with Small cell lung cancer? | Lambert-Eaton myasthenic syndrome |
| Which NMJ condition is associated with minimal effect when treated with AChE inhibitors? | Lambert-Eaton myasthenic syndrome |
| What is the color change seen in Raynaud phenomenon? | From white to blue to red |
| What does the color white in Raynaud phenomenon represent? | Ischemia |
| What causes the change in color into blue form white in Raynaud phenomenon? | Hypoxia |
| What does the change from blue to red in Raynaud phenomenon? | Reperfusion |
| What is the cause of Raynaud phenomenon? | Decrease blood flow to skin due to arteriolar (small vessel) vasospasm in response to cold or stress |
| What areas of the body are most often seen with Raynaud phenomenon? | Fingers and toes |
| When is Raynaud phenomenon called Raynaud disease? | Only when it is idiopathic |
| When does Raynaud syndrome occur? | Secondary to a disease process such as mixed connective tissue disease, SLE, or CREST syndrome. |
| Digital ulceration is seen in Raynaud phenomenon, disease, or syndrome? | In secondary Raynaud's syndrome |
| What is a key feature of Raynaud syndrome? | Digital ulceration |
| What is the common treatment of Raynaud phenomenon? | Ca2+ channel blockers |
| What is another form to refer to Scleroderma? | Systemic sclerosis |
| What is the triad that defines Scleroderma? | 1. Autoimmunity 2. Non-inflammatory vasculopathy 3. Collagen deposition with fibrosis |
| What common features of Systemic sclerosis? | Sclerosis of skin manifested as puffy, taut skin without wrinkles, fingertip pitting. |
| Which other organ systems, besides skin, are often associated or involved in Scleroderma? | Renal, pulmonary, gastrointestinal, and cardiovascular systems. |
| What is the feature of renal involvement in Scleroderma? | Renal crisis treated with ACE inhibitors |
| What are pulmonary conditions seen with Scleroderma? | Interstitial fibrosis and Pulmonary HTN |
| What GI conditions are associated with Scleroderma? | Esophageal dysmotility and reflux |
| What are the 2 major types of Scleroderma? | 1. Diffuse scleroderma 2. Limited scleroderma |
| What is Diffuse scleroderma? | Widespread skin involvement, rapid progression, ealy visceral involvement. |
| What is the antibody associated with Diffuse Scleroderma? | anti-Scl-70 antibody |
| What is another name for anti-Scl-70 antibody? | anti-DNA topoisomerase I antibody |
| (+) anti-DNA topoisomerase I antibody. Dx? | Diffuse scleroderma |
| The extend of Limited Scleroderma involves which areas? | LImited skin involvement confined to fingers and face |
| What syndrome is associated with Limited Scleroderma? | CREST syndrome |
| What are the characteristics of CREST syndrome? | Calcinosis cutis anti-Centromere antibody Raynaud phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia |
| What is the antibody seen with CREST syndrome? | anti-Centromere antibody |
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rakomi
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