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357 Cards in this Set
- Front
- Back
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Question
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Answer
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Soccer player who was kicked in the leg suffered a damaged medial meniscus. What else is likely to have been damaged?
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Anterior cruciate ligament (remember the “unhappy triad”).
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Gymnast dislocates her shoulder anteriorly. What nerve is most likely to have been damaged?
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Axillary nerve (C5, C6).
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X-ray shows bilateral hilar ymphadenopathy.
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Sarcoidosis.
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Child exhibits weakness and enlarged calves.
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Duchenne’s muscular dystrophy; X-linked recessive.
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25-year-old woman presents with a low-grade fever, a rash across her nose that gets worse when she is out in the sun, and widespread edema.
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SLE.
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85-year-old man presents with acute knee pain and swelling. X-ray shows joint space without erosion. What is the diagnosis, and what would you find on aspiration?
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Pseudogout; rhomboid calcium pyrophosphate crystals.
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Epidermis layers From surface to base:
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Californians Like Girls in String Bikinis. Stratum corneum Stratum lucidum Stratum granulosum Stratum spinosum Stratum basalis
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Epithelial cell junctions surrounds perimeter just below zona occludens
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Zona adherens (intermediate junction)
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Epithelial cell junctions small, discrete sites of attachment
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Macula adherens (desmosome)
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Epithelial cell junctions connects cells to underlying extracellular matrix
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Hemidesmosome
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Epithelial cell junctions maintains integrity of basement membrane
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Integrin
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Epithelial cell junctions prevents diffusion across intracellular space
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Zona occludens (tight junction)
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Epithelial cell junctions type of protein that forms the Zona adherens (intermediate junction)
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Actin filaments and E-cadherin
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Epithelial cell junctions type of protein that forms the Macula adherens (desmosome)
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Keratin Desmoplakin
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Unhappy triad what
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damage to medial collateral ligament (MCL), medial meniscus, and anterior cruciate ligament (ACL).
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Unhappy triad when
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lateral hit to the knee
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Knee PCL = LCL =
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PCL = posterior cruciate ligament. LCL = lateral collateral ligament.
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“Anterior” and “posterior” in ACL and PCL refer to
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sites of tibial attachment.
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Knee Positive anterior drawer sign indicates
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tearing of the ACL.
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Knee Abnormal passive abduction indicates
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a torn MCL.
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Shoulder muscles that form the rotator cuff: just name them
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S I t S (small t is for teres minor). Supraspinatus Infraspinatus– Teres minor–– Subscapularis–
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Shoulder muscles that form the rotator cuff: names and functions
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Supraspinatus––helps deltoid abduct arm. Infraspinatus––laterally rotates arm. Teres minor––adducts and laterally rotates arm. Subscapularis––medially rotates and adducts arm.
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Skeletal muscle contraction role of ATP
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ATP binds to myosin head and releases actin filament, allowing cross-bridge cycling and shortening to occur.
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Skeletal muscle contraction role of Ca2+
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Ca2+ binds to troponin C, causing conformational change. This causes tropomyosin to move out of the way to allow actin/myosin cycling.
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Muscle conduction to contraction Ryanodine receptor
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Ryanodine receptors (RyRs) form a class of intracellular calcium channels (on SR) It is the major cellular mediator of calcium-induced calcium release (CICR) in animal cells.
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Muscle conduction to contraction Dihydropyridine receptor
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is a voltage-dependent calcium channel found in the transverse tubule of muscles. In skeletal muscle it associates with the ryanodine receptors of the sarcoplasmic reticulum to induce calcium release and thus muscle contraction.
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It is the major cellular mediator of calcium-induced calcium release (CICR) in animal cells.
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Ryanodine receptor
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Skeletal Muscle Action potential steps up to Ca2+ release
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1.depolarization opens voltage-gated Ca2+ channel 2.muscle cell depolarization in the motor end plate 3. impulse travels along muscle cell down the T tubule. 4. Ryanodine receptor and Dihydropyridine receptor cause Ca2+ release
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Skeletal Muscle Action potential steps after Ca2+ release
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5. Released Ca2+ binds to troponin C, causing a conformational change that moves tropomyosin out of the myosin-binding groove on actin filaments. 6. Myosin releases bound ADP and is displaced on the actin filament (power stroke).
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Skeletal Muscle what bands change and how
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Contraction results in H and I band shortening, but the A band remains the same length.
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Achondroplasia geneitcs
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Autosomal-dominant trait
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Achondroplasia mech and clinical features
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Failure of longitudinal bone growth → short limbs. Membranous ossification is not affected (skull, facial bones, and axial skeleton are normal). Impaired cartilage maturation in growth plate caused by fibroblast growth factor receptor mutation.
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Osteoarthritis mech
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Mechanical––wear and tear of joints leads to destruction of articular cartilage
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Osteoarthritis predisposing factors
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trauma, age, obesity, joint deformity.
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Osteoarthritis classic presentation
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pain in weight-bearing joints after use (e.g., at the end of the day),improving with rest. No systemic symptoms.
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Osteoarthritis different cysts and nodes
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subchondral cysts, sclerosis, osteophytes, eburnation, Heberden’s nodes (DIP), Bouchard’s nodes (PIP).
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Rheumatoid arthritis mech
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Autoimmune––inflammatory disorder 80% of RA patients have positive rheumatoid factor (anti-IgG antibody).
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Rheumatoid arthritis clinical findings
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pannus formation in joints (MCP, PIP), subcutaneous rheumatoid nodules, ulnar deviation, subluxation
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Rheumatoid arthritis what is RF
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rheumatoid factor (anti-IgG antibody).
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Rheumatoid arthritis who
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Females > males
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Rheumatoid arthritis Classic presentation
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Classic presentation: morning stiffness improving with use, symmetric joint involvement, and systemic symptoms (fever, fatigue, pleuritis, pericarditis).
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Osteoporosis definition
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Reduction of bone mass in spite of normal bone mineralization.
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Osteoporosis histo
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Sparse trabeculae.
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Osteoporosis WRT ethnicity
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whites > blacks > Asians.
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Osteoporosis Type I
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Postmenopausal; ↑ bone resorption due to ↓ estrogen levels. Estrogen replacement is controversial as prophylaxis (side effects).
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Osteoporosis Type II
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Senile osteoporosis––affects men and women > 70 years.
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Osteoporosis which type Postmenopausal
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Type I
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Osteoporosis which type affects men and women > 70 years.
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Type II
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Distal radius fractures aka
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Colles’
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Colles’ fractue aka
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Distal radius fractures
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Vertebral crush fracture clinical findings
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acute back pain, loss of height, kyphosis.
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acute back pain, loss of height, kyphosis.
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Vertebral crush fracture
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Osteopetrosis aka
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marble bone disease
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marble bone disease aka
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Osteopetrosis
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Osteopetrosis clinical and lab findings
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thickened, dense bones. Serum calcium, phosphate, and alkaline phosphatase are normal. Decreased marrow space leads to anemia, thrombocytopenia, infection.
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Osteopetrosis mech
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Bone defect is due to abnormal function of osteoclasts.
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Osteomalacia/rickets mech and lab findings
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Defective mineralization of osteoid → soft bones. Vitamin D deficiency in adults → ↓ calcium levels →↑ secretion of PTH, ↓ in serum phosphate.
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Osteomalacia/rickets Tx
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Reversible when vitamin D is replaced. Vitamin D deficiency in childhood causes rickets.
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Osteitis fibrosa cystica aka
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Von Recklinghausen's disease of bone
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Von Recklinghausen's disease of bone aka
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Osteitis fibrosa cystica
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Osteitis fibrosa cystica caused by
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Caused by hyperparathyroidism
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Osteitis fibrosa cystica characteristic finding and what are they
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Caused by hyperparathyroidism. Characterized by “brown tumors” (cystic spaces linedby osteoclasts, filled with fibrous stroma and sometimes blood).
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Osteitis fibrosa cystica lab findings
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High serum calcium, low serum phosphorus, and high alkaline phosphatase.
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Paget’s disease aka
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osteitis deformans
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osteitis deformans aka
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Paget’s disease
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Paget’s disease what is it
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Abnormal bone architecture caused by ↑ in both osteoblastic and osteoclastic activity.
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Paget’s disease lab values
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Serum calcium, phosphorus, and PTH levels are normal. Serum alkaline phosphatase is elevated.
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Paget’s disease clinical findings
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Long bone chalkstick (transverse to the long axis) fractures. Increased blood flow may cause high output CHF.
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Polyostotic fibrous dysplasia what is it
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Bone is replaced by fibroblasts, collagen, and irregular bony trabeculae.
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Albright’s syndrome
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a form of polyostotic fibrous dysplasia in which there are multiple unilateral bone lesions associated with endocrine abnormalities (precocious puberty) and unilateral pigmented skin lesions.
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multiple unilateral bone lesions associated with endocrine abnormalities (precocious puberty) and unilateral pigmented skin lesions.
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Albright’s syndrome (a form of polyostotic fibrous dysplasia)
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Polymyalgia rheumatica what is it
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Pain and stiffness in shoulders and hips, often with fever, malaise, and weight loss.Does not cause muscular weakness.
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Polymyalgia rheumatica wrt strength
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Does not cause muscular weakness.
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Pain and stiffness in shoulders and hips, often with fever, malaise, and weight loss.
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Polymyalgia rheumatica
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Polymyalgia rheumatica wrt labs
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↑ ESR
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Polymyalgia rheumatica who and associations
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Occurs in patients > 50 years of age; associatedwith temporal (giant cell) arteritis.
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Polymyalgia rheumatica Tx
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prednisone.
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Polymyositis describe
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progressive symmetric proximal muscle weakness caused by CD8 T-cell-induced injury to myofibers.
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Polymyositis Dx
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Muscle biopsy with evidence of inflammation is diagnostic.
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progressive symmetric proximal muscle weakness caused by CD8 T-cell-induced injury to myofibers.
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Polymyositis
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Dermatomyositis
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similar to polymyositis but also involves "shawl and face" (diffuse, flat, erythematous lesion over the chest and shoulders or in a "V" over the anterior neck and chest) skin rash and ↑ risk of malignancy.
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similar to polymyositis but also involves "shawl and face" skin rash and ↑ risk of malignancy.
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Dermatomyositis
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polymyositis/dermatomyositis wrt labs
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↑ CK, ↑ aldolase, and positive ANA, anti-Jo-1.
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↑ CK, ↑ aldolase, and positive ANA, anti-Jo-1.
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polymyositis/dermatomyositis
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Mixed connective tissue disease clinical findings
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Raynaud’s phenomenon, arthralgias, myalgias, fatigue, and esophageal hypomotility.
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Mixed connective tissue disease what type of antibodies
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Antibodies to U1RNP.
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Mixed connective tissue disease Tx
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Responds to steroids.
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Antibodies to U1RNP
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Mixed connective tissue disease
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Raynaud’s phenomenon, arthralgias, myalgias, fatigue, and esophageal hypomotility.
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Mixed connective tissue disease
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similar to polymyositis but also involves "shawl and face" skin rash and ↑ risk of malignancy.
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dermatomyositis
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Sjögren’s syndrome clinical findings
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-xerophthalmia -xerostomia -arthritis. -dental caries -Parotid enlargment
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Sjögren’s syndrome wrt cancer
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↑ risk of B-cell lymphoma
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Sjögren’s syndrome antibodies
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Autoantibodies to ribonucleoprotein antigens, SS-A (Ro), SS-B (La).
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Autoantibodies to ribonucleoprotein antigens, SS-A (Ro), SS-B (La).
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Sjögren’s syndrome
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Sjögren’s syndrome who
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Predominantly affects females between 40 and 60 years of age.
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Sjögren’s syndrome associated conditions
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rheumatoid arthritis.
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Sicca syndrome
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dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis.
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dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis.
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Sicca syndrome
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SLE who
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90% are female and between ages 14 and 45. Most common and severe in black females.
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SLE cause of death
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death from renal failure and infections.
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SLE False positives
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False positives on syphilis tests (RPR/VDRL) due to antiphospholipid antibodies.
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SLE Lab tests Antinuclear antibodies (ANA)
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sensitive, but not specific for SLE
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SLE Lab tests Antibodies to double-stranded DNA
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very specific, poor prognosis
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SLE Lab tests Anti-Smith antibodies (anti-Sm)
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very specific, but not prognostic
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SLE Lab tests Antihistone antibodies
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drug-induced lupus
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SLE Lab tests sensitive, but not specific
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Antinuclear antibodies (ANA)
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SLE Lab tests very specific, poor prognosis
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Antibodies to double-stranded DNA
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SLE Lab tests drug-induced lupus
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Antihistone antibodies
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SLE mnemonic
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I’M DAMN SHARP: Immunoglobulins (anti-dsDNA, anti-Sm, antiphospholipid)- Malar rash - Discoid rash - Antinuclear antibody - Mucositis (oropharyngeal ulcers) - Neurologic disorders - Serositis (pleuritis, pericarditis) - Hematologic disorders - Arthritis - Renal disorders - Photosensitivity
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Gout what is it
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Precipitation of monosodium urate crystals into joints due to hyperuricemia,
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Gout causes
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caused by Lesch-Nyhan syndrome, PRPP excess, ↓ excretion of uric acid, or glucose-6-phosphatase deficiency. Also associated with the use of thiazide diuretics, which competitively inhibit the secretion of uric acid.
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Gout joint pattern and presentation
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Asymmetric joint distribution. Classic manifestation is painful MTP joint in the big toe (podagra). Tophus formation (often on external ear or Achilles tendon).
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Gout lab
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Crystals are needle shaped and negatively birefringent.
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Gout who and when
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birefringent. More common in men. Acute attack tends to occur after alcohol consumption or a large meal
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Gout Tx
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allopurinol, probenecid, colchicine, and NSAIDs.
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Pseudogout cause
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Caused by deposition of calcium pyrophosphate crystals within the joint space.
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Pseudogout labs
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Caused by deposition of calcium pyrophosphate crystals within the joint space. Forms basophilic, rhomboid crystals that are weakly positively birefringent
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Pseudogout joints
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Usually affects large joints (classically the knee).
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Pseudogout who
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> 50 years old; both sexes affected equally.
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Pseudogout Tx
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No treatment.
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Sarcoidosis histo and lab
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Characterized by immune-mediated, widespread noncaseating granulomas and elevated serum ACE levels.
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Sarcoidosis who
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Common in black females.
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Sarcoidosis associated with
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Associated with restrictive lung disease, bilateral hilar lymphadenopathy, erythema nodosum, Bell’s palsy, epithelial granulomas containing microscopic Schaumann and asteroid bodies, uveoparotitis, and hypercalcemia (due to
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Associated with restrictive lung disease, erythema nodosum, Bell’s palsy, epithelial granulomas containing microscopic Schaumann and asteroid bodies, uveoparotitis, and hypercalcemia
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Sarcoidosis
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Sarcoidosis mech of hypercalcemia
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elevated conversion of vitamin D to its active form in epithelioid macrophages
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Sarcoidosis mnemonic
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GRAIN: Gammaglobulinemia Rheumatoid arthritis ACE increase Interstitial fibrosis Noncaseating granulomas
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Seronegative spondyloarthropathies name them
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Ankylosing spondylitis Reiter’s syndrome
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Seronegative spondyloarthropathies lab findings
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Arthritis without rheumatoid factor (no anti-IgG antibody). Strong association with HLA- B27
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Seronegative spondyloarthropathies who
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more often in males.
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Ankylosing spondylitis Lab findings
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RF negative HLA-B27 positive
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Reiter’s syndrome Lab findings
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RF negative HLA-B27 positive
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Ankylosing spondylitis clinical findings
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Chronic inflammatory disease of spine and sacroiliac joints → ankylosis (stiff spine), uveitis, and aortic regurgitation. Bamboo spine.
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Reiter’s syndrome clinical findings
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Classic triad: 1. Urethritis 2. Conjunctivitis and anterior uveitis 3. Arthritis
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Reiter’s syndrome who
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Post-GI or chlamydia infections.
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Scleroderma aka
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progressive systemic sclerosis
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progressive systemic sclerosis aka
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Scleroderma
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Scleroderma mech
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Excessive fibrosis and collagen deposition throughout the body
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Scleroderma 2 main types
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1. Diffuse scleroderma 2. CREST syndrome
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Scleroderma who
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75% female
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Diffuse scleroderma describe
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widespread skin involvement, rapid progression, early visceral involvement. Associated with anti-Scl-70 antibody.
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Associated with anti-Scl-70 antibody
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Diffuse scleroderma
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CREST syndrome describe
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Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. Limited skin involvement, often confined to fingers and face. More benign clinical course. Associated with anticentromere antibody
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Associated with anticentromere antibody
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CREST syndrome
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describe the skin disorder Impetigo
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Superficial skin infection. Honey crusting. Highly contagious.
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describe the skin disorder Dermatitis
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A group of inflammatory pruritic skin disorders. Etiology: allergy (usually type IV hypersensitivity), chemical injury, or infection.
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describe the skin disorder Atopic dermatitis
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Pruritic eruption, commonly on flexor surfaces. Often associated with other atopic diseases (asthma, allergic rhinitis).
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describe the skin disorder Psoriasis
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Epidermal hyperplasia (acanthosis) with parakeratotic scaling (nuclei still in stratum corneum) especially on knees and elbows.
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describe the skin disorder Allergic contact dermatitis
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Type IV hypersensitivity reaction that follows exposure to allergen (poison ivy, poison oak, nickel, rubber, chemicals). Lesions occur at site of contact.
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describe the skin disorder Dermatitis herpetiformis
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Pruritic papules and vesicles. Deposits of IgA at the tips of dermal papillae. Associated with celiac disease.
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describe the skin disorder Lichen planus
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Pruritic, purple, polygonal papules; infiltrate of lymphocytes at dermoepidermal junction.
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describe the skin disorder Erythema multiforme
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multiple types of lesions, including macules, papules, vesicles, and target lesions (red papules with a pale central area).
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describe the skin disorder Seborrheic keratosis
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Flat, pigmented squamous epithelial proliferation with keratin-filled cysts (horn cysts). Benign.
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describe the skin disorder Actinic keratosis
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Caused by sun exposure. Small, rough erythematous or brownish papules. Premalignant lesion. Risk of carcinoma is proportional to epithelial dysplasia.
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describe the skin disorder Keloid
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Tumor of connective tissue elements of dermis that causes raised, thickened scars. Follows trauma to skin,
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describe the skin disorder Bullous pemphigoid
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Autoimmune disorder with IgG antibody against epidermal basement membrane hemidesmosomes (linear immunofluorescence). Similar to but less severe than pemphigus vulgaris––affects skin but spares oral mucosa
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describe the skin disorder Pemphigus vulgaris
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Potentially fatal autoimmune skin disorder. Intraepidermal bullae involving the oral mucosa and skin. Findings: acantholysis (breakdown of epithelial cell-to-cell junctions), IgG antibody against epidermal cell surface desmosomes
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describe the skin disorder Verrucae
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Soft, tan-colored, cauliflowerlike lesions. Epidermal hyperplasia, hyperkeratosis, koilocytosis.
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Atopic dermatitis aka
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eczema
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eczema aka
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Atopic dermatitis
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Verrucae aka
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warts
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warts aka
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Verrucae
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Psoriasis wrt different skin layers
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↑ stratum spinosum, ↓ stratum granulosum
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parakeratotic scaling what is it and when do you see it
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nuclei still in stratum corneum Psoriasis
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nuclei still in stratum corneum aka
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parakeratotic scaling
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Atopic dermatitis aka
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eczema
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eczema aka
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Atopic dermatitis
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Verrucae aka
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warts
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warts aka
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Verrucae
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Psoriasis wrt different skin layers
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↑ stratum spinosum, ↓ stratum granulosum
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parakeratotic scaling what is it and when do you see it
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nuclei still in stratum corneum Psoriasis
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nuclei still in stratum corneum aka
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parakeratotic scaling
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Superficial skin infection. Honey crusting. Highly contagious.
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Impetigo
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A group of inflammatory pruritic skin disorders. Etiology: allergy (usually type IV hypersensitivity), chemical injury, or infection.
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Dermatitis
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Pruritic eruption, commonly on flexor surfaces. Often associated with other atopic diseases (asthma, allergic rhinitis).
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Atopic dermatitis (eczema)
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Type IV hypersensitivity reaction that follows exposure to allergen (poison ivy, poison oak, nickel, rubber, chemicals). Lesions occur at site of contact.
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Allergic contact dermatitis
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Epidermal hyperplasia (acanthosis) with parakeratotic scaling (nuclei still in stratum corneum) especially on knees and elbows. ↑ stratum spinosum, ↓ stratum granulosum (see Color Image 65). Auspitz sign.
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Psoriasis
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Pruritic papules and vesicles. Deposits of IgA at the tips of dermal papillae. Associated with celiac disease.
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Dermatitis herpetiformis
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Pruritic, purple, polygonal papules; infiltrate of lymphocytes at dermoepidermal junction.
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Lichen planus
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Flat, pigmented squamous epithelial proliferation with keratin-filled cysts (horn cysts). Benign.
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Seborrheic keratosis
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Caused by sun exposure. Small, rough erythematous or brownish papules. Premalignant lesion. Risk of carcinoma is proportional to epithelial dysplasia.
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Actinic keratosis
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Tumor of connective tissue elements of dermis that causes raised, thickened scars. Follows trauma to skin, especially in African-Americans.
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Keloid
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Autoimmune disorder with IgG antibody against epidermal basement membrane
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Bullous pemphigoid
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Potentially fatal autoimmune skin disorder. Intraepidermal bullae involving mucosa and skin. Findings: acantholysis (breakdown of epithelial cell-to-c junctions), IgG antibody against epidermal cell surface desmosomes
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Pemphigus vulgaris
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Soft, tan-colored, cauliflowerlike lesions. Epidermal hyperplasia, hyperkeratosis, koilocytosis.
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Verrucae (warts)
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Auspitz sign.
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appearance of punctate bleeding spots when psoriasis scales are scraped off
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appearance of punctate bleeding spots when psoriasis scales are scraped off
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Auspitz sign.
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target lesions
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Erythema multiforme
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Actinic keratosis wrt cancer
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Risk of carcinoma is proportional to epithelial dysplasia.
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Keloid who
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African-Americans.
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Autoimmune disorder with IgG antibody against epidermal basement membrane hemidesmosomes (linear immunofluorescence).
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Bullous pemphigoid
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acantholysis
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breakdown of epithelial cell-to-cell junction
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breakdown of epithelial cell-to-cell junction
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acantholysis
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warts on hands versus on genitals
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Verruca vulgaris on hands, condyloma acuminatum on genitals.
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Skin cancer Squamous cell carcinoma associations
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excessive exposure to sunlight and arsenic exposure.
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Skin cancer Squamous cell carcinoma where and spread
|
Commonly appear on hands and face. Locally invasive, but rarely metastasizes.
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Skin cancer Squamous cell carcinoma histo
|
keratin “pearls”
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Skin cancer Basal cell carcinoma where and spread
|
Most common in sun-exposed areas of body. Locally invasive, but almost never metastasizes.
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Skin cancer Basal cell carcinoma histo
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“palisading” nuclei.
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Skin cancer Basal cell carcinoma gross
|
pearly papules- characteristic "pearly white" translucent quality on the periphery
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Skin cancer melanoma where and spread
|
Common tumor with significant risk of metastasis
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Skin cancer melanoma who
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Associated with sunlight exposure; fair-skinned persons are at ↑ risk.
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Skin cancer melanoma prognosis factors
|
Depth of tumor correlates with risk of metastasis
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Skin cancer melanoma precursor
|
Dysplastic nevus is a precursor to melanoma.
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Dysplastic nevus is a precursor to
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melanoma.
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name the benign Primary bone tumors
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-Osteoid osteoma -Osteoblastoma -Giant cell tumor -Osteochondroma (exostosis) -Enchondroma
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name the Malignant Primary bone tumors
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-Osteosarcoma (osteogenic carcinoma) -Ewing’s sarcoma -Chondrosarcoma
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Describe Osteoid osteoma
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Interlacing trabeculae of woven bone surrounded by osteoblasts. < 2 cm and found in proximal tibia and femur.
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Describe Osteoblastoma
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Same morphologically as osteoid osteoma, but larger and found in vertebral column.
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Describe Giant cell tumor
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old. Locally aggressive benign tumor often around the distal femur, proximal tibia region. Characteristic “double bubble” or “soap bubble” appearance on x-ray.
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Describe Osteochondroma
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Mature bone with cartilaginous Commonly originates from long metaphysis.
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Describe Enchondroma
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Benign cartilaginous neoplasm found in intramedullary bone. Usually distal extremities
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Describe Osteosarcoma
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Commonly found in the metaphysis of long bones. Codman’s triangle (from elevation of periosteum) on x-ray.
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Describe Ewing’s sarcoma
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Anaplastic small blue cell malignant tumor
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Describe Chondrosarcoma
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Malignant cartilaginous tumor. Usually located pelvis, spine, scapula, humerus, tibia, or femur. Expansile glistening mass within the medullary cavity.
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Interlacing trabeculae of woven bone surrounded by osteoblasts. < 2 cm and found in proximal tibia and femur.
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Osteoid osteoma
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Same morphologically as osteoid osteoma, but larger and found in vertebral column.
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Osteoblastoma
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Characteristic “double bubble” or “soap bubble” appearance on x-ray. Spindle-shaped cells with multinucleated giant cells.
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Giant cell tumor
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|
Most common benign bone tumor
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Osteochondroma (exostosis)
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Benign cartilaginous neoplasm found in intramedullary bone. Usually distal extremities
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Enchondroma
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Most common 1° malignant tumor of bone.
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Osteosarcoma (osteogenic carcinoma)
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Osteosarcoma who
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Peak incidence in men 10–20 years old.
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Osteosarcoma where
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Commonly found in the metaphysis of long bones
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Osteosarcoma Gene involved
|
familial retinoblastoma. Rb
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Rb and bone cancer
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Osteosarcoma (osteogenic carcinoma)
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Osteosarcoma and predisposing factors
|
Paget’s disease of bone, bone infarcts, radiation, and familial retinoblastoma.
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Ewing’s sarcoma who
|
Most common in boys < 15
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Ewing’s sarcoma prognosis
|
Extremely aggressive with early mets, but responsive to chemotherapy.
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Ewing’s sarcoma mnemonic
|
“onion-skin” appearance in bone 11:22 (“going out for Ewings and onion rings at 11:22”)
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Expansile glistening mass within the medullary cavity.
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Chondrosarcoma
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|
|
May be of 1° origin or from osteochondroma.
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Chondrosarcoma
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Chondrosarcoma who
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Most common in men aged 30–60
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Buerger’s disease aka
|
thromboangiitis obliterans
|
|
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thromboangiitis obliterans aka
|
Buerger’s disease
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Buerger’s disease Findings
|
Intermittent claudication, superficial nodular phlebitis, cold sensitivity (Raynaud’s phenomenon), severe pain in affected part; may lead to gangrene.
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Buerger’s disease Treatment
|
Quit smoking.
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Buerger’s disease mech and who
|
idiopathic, segmental, thrombosing vasculitis of intermediate and small peripheral arteries and veins. Seen in heavy smokers.
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Takayasu’s arteritis aka
|
“pulseless disease”
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“pulseless disease” aka
|
Takayasu’s arteritis
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Takayasu’s arteritis clinical findings
|
FAN MY SKIN On Wednesday. Fever, Arthritis, Night sweats, MYalgia, SKIN nodules, Ocular disturbances, Weak pulses in upper extremities.
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Takayasu’s arteritis mech
|
granulomatous thickening of aortic arch and/or proximal great vessels.
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Takayasu’s arteritis labs
|
Associated with an elevated ESR.
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Temporal arteritis aka
|
giant cell arteritis
|
|
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giant cell arteritis aka
|
Temporal arteritis
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|
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Most common vasculitis that affects medium and small arteries
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Temporal arteritis
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Temporal arteritis which arteries
|
branches of carotid artery.
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Temporal arteritis lab values
|
ESR is markedly elevated
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Temporal arteritis who
|
elderly females.
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Temporal arteritis findings
|
unilateral headache, jaw claudication, impaired vision (occlusion of ophthalmic artery, which can lead to blindness). Half of patients have systemic involvement and polymyalgia rheumatica
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Temporal arteritis mech
|
Focal, granulomatous
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Temporal arteritis Tx
|
steroids.
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Polyarteritis nodosa Characterized by
|
necrotizing immune complex inflammation of medium-sized muscular arteries typically involving renal and visceral vessels.
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Polyarteritis nodosa Symptoms
|
Fever, weight loss, malaise, abdominal pain, melena, headache, myalgia, hypertension, neurologic dysfunction, cutaneous eruptions.
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|
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Polyarteritis nodosa Findings
|
Hepatitis B seropositivity in 30% of patients. Multiple aneurysms and constrictions on arteriogram. Typically not associated with ANCA.
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Polyarteritis nodosa Treatment
|
Corticosteroids, cyclophosphamide.
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Wegener’s granulomatosis mech
|
Characterized by triad of focal necrotizing vasculitis, necrotizing granulomas in the lung and upper airway, and necrotizing glomerulonephritis.
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|
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Wegener’s granulomatosis Symptoms
|
hemoptysis, hematuria, and upper respiratory symps
|
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Wegener’s granulomatosis Findings
|
C-ANCA chest x-ray may reveal large nodular densities; hematuria and red cell casts.
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Wegener’s granulomatosis Treatment
|
Cyclophosphamide and corticosteroids.
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|
ANCA-positive vasculitides
|
Wegener’s C-ANCA Microscopic polyangiitis P-ANCA. 1° pauciimmune crescentic glomerulonephritis p-ANCA Churg-Strauss syndrome P-anca
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p-ANCA target
|
neutrophil (myeloperoxidase )
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c-ANCA target
|
proteinase 3
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|
describe Churg-Strauss syndrome
|
p-ANCA Granulomatous vasculitis with eosinophilia. Involves lung, heart, skin, kidneys, nerves. Often seen in atopic patients.
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Kawasaki disease what/who/mech
|
Acute, self-limiting disease of infants/kids. Acute necrotizing vasculitis of small/medium-sized vessels.
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Kawasaki disease clinical findings
|
Fever, congested conjunctiva, changes in lips/oral mucosa, lymphadenitis. can develop coronary aneurysms.
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Fever, congested conjunctiva, changes in lips/oral mucosa, lymphadenitis. can develop coronary aneurysms.
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Kawasaki disease
|
|
|
Most common form of childhood systemic vasculitis
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Henoch-Schönlein purpura
|
|
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Henoch-Schönlein purpura clinical findings
|
Skin rash (palpable purpura), arthralgia, intestinal hemorrhage, abdominal pain, and melena.
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Lesion age in Polyarteritis nodosa
|
Lesions are of different ages.
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Lesion age in Henoch-Schönlein purpura
|
Multiple lesions of the same age.
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Telangiectasia what and look
|
Arteriovenous malformation in small vessels. Looks like dilated capillary.
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Hereditary hemorrhagic telangiectasia genetics
|
autosomal dominant inheritance.
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|
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Hereditary hemorrhagic telangiectasia presentation
|
nosebleeds and skin discolorations.
|
|
|
autosomal dominant inheritance. Presents with nosebleeds and skin discolorations.
|
Hereditary hemorrhagic telangiectasia
|
|
|
Opioid Mechanism
|
Act as agonists at opioid receptors to modulate synaptic transmission.
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Opioid Clinical use
|
Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for addicts (methadone).
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|
|
Opioid Toxicity
|
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs.
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|
|
Opioid names
|
Morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan.
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|
|
Opioid Tolerance does not develop to
|
miosis and constipation.
|
|
|
Opioid Toxicity treated with
|
naloxone or naltrexone (opioid receptor antagonist)
|
|
|
Opioid what contraindicated if morphine overdose
|
Oxygen (might contribute to respiratory failure)
|
|
|
Opioid specific receptors
|
(mu = morphine, delta = enkephalin, kappa = dynorphin)
|
|
|
Arachidonic acid products Lipoxygenase pathway yields
|
L for Lipoxygenase and Leukotriene. Leukotrienes.
|
|
|
Arachidonic acid products LTB4 function
|
neutrophil chemotactic agent.
|
|
|
Arachidonic acid products LTC4 , D4 , and E4 function
|
bronchoconstriction, vasoconstriction, contraction of smooth muscle, and ↑ vascular permeability.
|
|
|
Arachidonic acid products which mediate bronchoconstriction, vasoconstriction, contraction of smooth muscle, and ↑ vascular permeability.
|
LTC4 , D4 , and E4
|
|
|
Arachidonic acid products neutrophil chemotactic agent
|
LTB4
|
|
|
Arachidonic acid products PGI2 function
|
"Platelet-Gathering Inhibitor." inhibits platelet aggregation and promotes vasodilation.
|
|
|
Arachidonic acid products inhibits platelet aggregation and promotes vasodilation.
|
"Platelet-Gathering Inhibitor." PGI2
|
|
|
non specific NSAIDs names
|
asa, Ibuprofen, naproxen, indomethacin, ketorolac.
|
|
|
non specific NSAIDs Mechanism
|
Reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block prostaglandin synthesis.
|
|
|
non specific NSAIDs Clinical use
|
Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.
|
|
|
non specific NSAIDs Toxicity
|
Renal damage, aplastic anemia, GI distress, ulcers.
|
|
|
COX-2 inhibitors Names
|
celecoxib, valdecoxib
|
|
|
COX-2 inhibitors Mechanism
|
Reversibly inhibit specifically the cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and mediates inflammation and pain; spares COX-1
|
|
|
COX-2 inhibitors Clinical use
|
Rheumatoid and osteoarthritis.
|
|
|
COX-2 inhibitors Toxicity
|
Increased risk of thrombosis. Less toxicity to GI mucosa (lower incidence of ulcers, bleeding).
|
|
|
Acetaminophen Mechanism
|
Reversibly inhibits cyclooxygenase 3, mostly in CNS. Inactivated peripherally.
|
|
|
Acetaminophen Clinical use
|
Antipyretic, analgesic,
|
|
|
Acetaminophen Toxicity
|
hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in liver.
|
|
|
Acetaminophen Toxicity Tx
|
N-acetylcysteine is antidote––regenerates glutathione.
|
|
|
Gout drugs names
|
Colchicine and indomethacin Probenecid Allopurinol
|
|
|
Colchicine mechanism
|
Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.
|
|
|
Colchicine clinical use
|
Acute gout.
|
|
|
Colchicine Toxicity
|
GI side effects, especially if given orally. (Note: indomethacin is less toxic, more commonly used.)
|
|
|
more commonly used for acute gout
|
indomethacin is less toxic, more commonly used than colchicine
|
|
|
Probenecid mechanism
|
Chronic gout. Inhibits reabsorption of uric acid (also inhibits secretion of penicillin).
|
|
|
Probenecid clinical use
|
Chronic gout due to under excretion
|
|
|
Allopurinol mech
|
↓ conversion of xanthine to uric acid.
|
|
|
Allopurinol Clinical use
|
Chronic gout due to overproduction Also used in lymphoma and leukemia to prevent tumor lysis –associated urate nephropathy.
|
|
|
Etanercept Mechanism
|
Recombinant form of human TNF receptor that binds TNF-α.
|
|
|
Etanercept Clinical use
|
Rheumatoid arthritis, psoriasis, ankylosing spondylitis.
|
|
|
Infliximab Mechanism
|
TNF-α antibody.
|
|
|
Infliximab Clinical use
|
Crohn’s disease, rheumatoid arthritis, ankylosing spondylitis.
|
|
|
Infliximab Toxicity
|
Predisposes to infections (reactivation of latent TB).
|
|
|
Recombinant form of human TNF receptor that binds TNF-α.
|
Etanercept
|
|
|
TNF-α antibody.
|
Infliximab
|
|
|
which Immunosuppressive agents act at the proliferation stage
|
this is stage 2 All except Rh3(D) immune globulin
|
|
|
which Immunosuppressive agents act at the Antigen recognition (B and T cells) stage
|
This is stage 1 Only -Antilymphocytic globulin -monoclonal anti- T-cell antibodies -Rh3(D) immune globulin
|
|
|
which Immunosuppressive agents act at the Differentiation synthesis stage
|
This is stage 3 -Cyclosporine -Dactinomycin -Antilymphocytic globulin and monoclonal anti-T-cell antibodies -Tacrolimus
|
|
|
which Immunosuppressive agents act at the Cytokine secretion stage
|
This is stage 4 only Tacrolimus
|
|
|
which Immunosuppressive agents act at the Tissue injury stage
|
This is stage 5 only Prednisone
|
|
|
Cyclosporine Mechanism
|
Binds to cyclophilins. Complex blocks the differentiation and activation of T cellsby inhibiting calcineurin, thus preventing the production of IL-2 and its receptor.
|
|
|
Cyclosporine Clinical use
|
Suppresses organ rejection after transplantation; selected autoimmune disorders.
|
|
|
Cyclosporine Toxicity
|
Predisposes patients to viral infections and lymphoma; nephrotoxic (preventable with mannitol diuresis).
|
|
|
Cyclosporine Toxicity Tx
|
nephrotoxic (preventable with mannitol diuresis).
|
|
|
Tacrolimus aka
|
FK506
|
|
|
FK506 aka
|
Tacrolimus
|
|
|
Tacrolimus Mechanism
|
Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.
|
|
|
Tacrolimus Clinical use
|
Potent immunosuppressive used in organ transplant recipients.
|
|
|
Tacrolimus Toxicity
|
Significant––nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia.
|
|
|
Azathioprine Mechanism
|
Antimetabolite derivative of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes.
|
|
|
Azathioprine Clinical use
|
Kidney transplantation, autoimmune disorders (including glomerulonephritis and hemolytic anemia).
|
|
|
Azathioprine Toxicity
|
Bone marrow suppression. Active metabolite mercaptopurine is metabolized by xanthine oxidase; thus, toxic effects may be ↑ by allopurinol.
|
|
|
Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.
|
Tacrolimus (FK506)
|
|
|
Binds to cyclophilins. Complex blocks the differentiation and activation of T cells by inhibiting calcineurin, thus preventing the production of IL-2 and its receptor.
|
Cyclosporine
|
|
|
Antimetabolite derivative of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes.
|
Azathioprine
|
|
|
Recombinant cytokines Clinical use for Aldesleukin (interleukin-2)
|
Renal cell carcinoma, metastatic melanoma
|
|
|
Recombinant cytokines Clinical use for epoetin
|
Anemias (especially in renal failure)
|
|
|
Recombinant cytokines Clinical use for Filgrastim
|
Recovery of bone marrow
|
|
|
Recombinant cytokines Clinical use for Sargramostim
|
Recovery of bone marrow
|
|
|
Recombinant cytokines Clinical use for α-interferon
|
Hepatitis B and C, Kaposi’s sarcoma, leukemias, malignant melanoma
|
|
|
Recombinant cytokines Clinical use for β-interferon
|
Multiple sclerosis
|
|
|
Recombinant cytokines Clinical use for gamma-interferon
|
Chronic granulomatous disease
|
|
|
Recombinant cytokines Clinical use for Oprelvekin
|
Thrombocytopenia
|
|
|
Recombinant cytokines Clinical use for Thrombopoietin
|
Thrombocytopenia
|
|
|
Which Recombinant cytokine is used for Renal cell carcinoma
|
Aldesleukin (interleukin-2
|
|
|
Which Recombinant cytokine is used for metastatic melanoma
|
Aldesleukin (interleukin-2)
|
|
|
Which Recombinant cytokine is used for Anemias (especially in renal failure)
|
Erythropoietin (epoetin)
|
|
|
Which Recombinant cytokine is used for Recovery of bone marrow
|
Filgrastim (granulocyte colony-stimulating factor) Sargramostim (granulocyte- macrophage colony- stimulating factor)
|
|
|
Which Recombinant cytokine is used for Hepatitis B and C
|
α-interferon
|
|
|
Which Recombinant cytokine is used for Kaposi's sarcoma
|
α-interferon
|
|
|
Which Recombinant cytokine is used for leukemias
|
α-interferon
|
|
|
Which Recombinant cytokine is used for malignant melanoma without mets
|
α-interferon
|
|
|
Which Recombinant cytokine is used for Multiple sclerosis
|
β-interferon
|
|
|
Which Recombinant cytokine is used for Chronic granulomatous disease
|
gamma-interferon
|
|
|
Which Recombinant cytokine is used for Thrombocytopenia
|
Oprelvekin (interleukin-11) Thrombopoietin
|
