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140 Cards in this Set
- Front
- Back
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iron deficient enemia in males means
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CA of GI until proven otherwise
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prognostic indicator - colorectal CA
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extent of tumour at diagnosis
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detection, testing
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digital-rectal, fecal test, enema, CT, colonoscopy, biopsy
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4 chars bone disease
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lesion, cavity-lytic, unusual calcium deposition, zonal or sclerotic bone, neoplasms
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type I bone lesion
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geographic - central - slow growth
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Type II bone lesion
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‘moth eaten’ intermediate growth
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Type III bone lesion
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permeative pattern, rapid growth
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malignant bone lesions
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usually type III
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benign lesions
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usually type I
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bone structure (normal)
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calcium hydroxapatite in collagen scaffold with osteocalcin and osteonectin
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2 bone forming proteins
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osteocalcin, osteonectin
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% of bone types
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70 compact, 30 cancellous
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term - mature bone
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lamellar (has parallel strand orientation)
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main unit of bone
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osteon or haversian system
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cellular cycle of bone
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osteoblasts -osteocytes (imbedded in bone), - osteoclasts, absorb bone
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bone growth and shape change due to
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modelling (formation, resorption at independent sites
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bone growth type,new bone laid on existing periosteum
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appositional
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pattern of bone remodelling - cortical
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osteoclasts lead - cutting cone, osteoblasts follow - closing cone
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location of bone modelling - trabecular bone
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howships lacunae
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bone resp. for structure, protection
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cortical
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bone resp. for calcium homeostasis
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cancellous
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complications of fracture healing
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non-union, osteonecrosis
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causes of non-union
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other tissue trapped at site, periosteum lost
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most common occur of patho fracture
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lytic lesions, metastatic tumours
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bone healing - three phases
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inflammation (fracture callus), reparative(mineralization of callus), remodelling (endochondral bone forms, normal shape returns
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stress fracture
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partial break - pain (worse w/activity) caused by excessive imbal. bone remodelling
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bone destroying organisms within bone
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osteomyelitis
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osteomyelitis survives how
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relies on bone structure - cavity and blood supply
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osteomyelitis agents and transport mech
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S.aureus, H.Influenzae, Salmonella, via blood or joints
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area of dead bone and infection - osteomyelitis
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sequestrum
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area of fracture, reactive bone
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involucrum
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treatment osteomyelitis
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chronic antibiotics
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excessive remodelling of specific bones, in elderly, genetic disorder
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pagets disease
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3 phases pagets
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lytic (hot phase, bone resorption), mixed phase - bone formation, sclerotic (cold) phase
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diagnosis pagets
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abnormal lamellar bone - woven look, osteoclasts, lots of nuclei
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pagets complications
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brittle bone, nerve impingement
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bone cysts
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usually evident at metaphyseal plate, proximal humerus, femur, calcaneus
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bone cyst characteristics
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fluid filled cavity, with histiocytes, osteoclasts
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subperiosteal bone lesion with blood filled spaces
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aneurismal bone cyst, usually post-trauma. multiple levels of fluid within cyst.
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giant cell tumour
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benign with multinucleated giant cells, fibrous stroma
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location, population with giant cell tumour
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women, distal femur, prox. tibia, nr. growth plate
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unusual abt giant cell tumour
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invasive, bone necrosis, can metastasis
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giant cell reparative granuloma locations
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jaw, hands, feet
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giant cell rep.granuloma char
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giant cells and stroma, HIGHLY vascular, zonal pattern, reactive fibrosis
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failure of replacement joints
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septic or aseptic. histocytic reaction at interface membrane with mechanical wear. Cells react with breakdown of mech. replacement parts and materials
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most com. arthritis cause of disability
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osteoarth of knee
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osteoarthritis description
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chronic, noninflam. joint disease, loss of articular cart., synovial changes, subchondral bony formation, can heal
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contrib. factors - osteoarthritis
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age, weight(knee), genetic (esp. hands)
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obvious bone changes, OA
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disappearance of joint space, osteophytes at margins
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term for cartilage disappearing
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eburnation
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earliest stage osteo
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disruption in superficial cartilage layer
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2nd stage osteo
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fibrillation (cracks) in cartilage, followed by clumping of chondrocytes for repair
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chg to bone surface with osteo
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focal necrosis of osteocytes
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synovial leak into underlying bone
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subchondral bone cyst
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bone fragments in osteoarthritis
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necrosis and metaplasia of tips, become “loose bodies”
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define rheumatoid arthritis
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chronic inflammatory arthritis, primarily effecting synovial joints, autoimmune disease
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effected structures - rheum arth
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women 2-3x more than men, all joints, esp hands
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key feature of rheum arth
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pannus formation- granulation tissue, cytokines, necrosis, bone and cartilage destroyed
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gout - definition
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deposition of urate crystals in joints and tissues
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precipitates gout attack
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usually large meal or alcohol
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gout usually effects
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big toe MTP joint
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why gout
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hyperuricemia - purine metabolism error
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deposit of ureic acid crystals and fibrous conn. tiss.
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tophi
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locations tophi
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ear, achilles tendon
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also effected by urea crystal deposit
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kidneys
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most comm. cause of arthritis
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pseudogout
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define pseudogout
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chondrocalcinosis - inflamm react. in cartilage caused by CPPD deposition
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CPPD
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calcium pyrophosphate dihydrate
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pseudogout usually effects
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knee, hip, discs
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PVNS
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pigmented villonodular tenosynovitis
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PVNS def
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synovial proliferative disorder - kids especially - neoplasia in knees
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osteomyelitis usually caused by
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pyogenic organisms
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organisms causing osteomyelitis - in what groups
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staphlococcus aureus (adults), haemophilus influenze (kids), salmonella - sickle cell patients
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osteosarcoma produces and percentage
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osteoid matrix 20percent of tumours,
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conventional osteosarcoma effects
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mainly men, around knee. Have TP53 and or Rb gene mutation
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pathology osteosarcoma
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metaphysis of long bone, areas of hemorrhage, necrosis: destroys cortex.
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mechanism osteosarcoma
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osteoblasts form osteoid - bone matrix
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osteosarcoma behaviour
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aggressive, hematogenous spread, usually already metastasis at diagnosis
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main joint type
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diarthroidal - articular cartilage, synovium, capsule, stabilized by ligaments
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main cartilage type in joints
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hyaline - type II collagen
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articular cartilage nutrition
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no vessels, no nerves, can’t perceive injury, nutrition is via synovial fluid, during movement
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2 types of osteoarthritis
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primary - no obvious predisposing factors, secondary - dmgd joint
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imbalance causing osteoarthritis
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decreased tensile strength, degenerative chgs overwhelm reparative
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nodes on fingers in osteoarthritis
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heberdens nodes
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biochemical changes - osteoarth
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more water, less proteoglycans (nutrients), less collagen synthesis - collagen breakdown incr, apoptosis, reduction in functional chondrocytes.
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4 endocrine functions
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homeostasis, survival, emotion, metabolism
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2 thyroid hormones
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T3 and T4
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what are T3 and T4
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tri-iodothyronine, tetra-iodothyronine
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prod. of thyroid hormones requires
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dietary source of iodine
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thyroid purpose
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metabolic pacemaker - controls rate of food conversion to energy
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define goiter
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enlargement of thyroid
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hypothyroidism - cause
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TSH reduced, iodine deficiency, T3/T4 synth. impaired
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hashimotos thyroidosis
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AUTOIMMUNE, mostly effects women, HYPOthyroid
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cause of hashimotos
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autoagressive lymphocytes attack thyroid
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4 causes hyperthyroidism
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adenoma, toxic goiter, thyroiditis, graves disease
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graves disease
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autoimmune, thyrotoxicosis
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underlying mechs - graves disease
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IgG antibody, is not TSH but stimulates thyroid
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signs of hyperthyroidism
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nervousness, restlessness, palpitations, fatigue, weakness, diarrhea, weight loss, heat intolerance
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graves disease treatment
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radioactivity - destroy gland, give HRT
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parathyroid purpose
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regulate circulating blood calcium
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cause of hyperparathyroid
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adenomas
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mechanisms hyperparathyroid
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CA from bone, blood CA levels rise, phosphate levels decr
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symptoms hyperparathyroidism
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painful urination, hematuria, GI sounds, kidney and urine stones
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dental implications - hyperparathyroid
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lamina dura around teeth disappear
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diabetes def
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chronic persistent elevation of blood sugar
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diabetes effects
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chronic disorder of carb, fat, and protein metabolism
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diabetes feature
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impaired glucose use, hyperglycemia
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mechanism of diabetes
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destruction of insulin producing cells
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poss.mech. for type I diabetes
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CMV (cytomegalovirus), mumps?
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insulin mechanism
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promotes glucose transport across cell memb of musc, fat, fibroblasts
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type I diabetes
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childhood onset autoimmune
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Bloor of type I diabetes shows
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serum IgG antibody to beta cells
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main reason decrease insulin in type II
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fewer insulin receptors
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Main reason typeI diabetes
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pancreas can’t produce insulin
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signs diabetes
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polyuria, polydipsia, polyphagia
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polyuria mechanism, type II
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high glucose (diuretic) levels in urine, results in forced fluid loss
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mech. tissue reactions, typeII
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musc. weakness, weight loss, fatigue, glucose depleted, not replaced
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iron overload
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hemochromatosis
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iron overload consequence
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can cause diabetes
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why musc. weakness in diabetes
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glycogen used up, no energy
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diabetic chgs in musc
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musc. protein breakdown, amino acids to liver
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musc. amino acids in liver undergo
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gluconeogenesis
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fat degradation yields
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keytones
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3 ways acids disposed of
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utilization by skin, musc. filtration through kidney (loss of electrolytes), expiration via lung buffer system
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diabetic vessel problems
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atherosclerosis, peripheral circ. probls, increased risk MI
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diabetic kidney probs
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sclerosis, glomerulosclerosis, renal failure
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diabetic eye problems
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retinopathy, cataracts(blindness)
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cause of diabetic eye problems
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retinal exudates, edema, hemorrhage
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treatments of diabetes
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cyclosporine, pancreas transplant, blood sug. monitor, insulin pump, DIET.
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erythropoeisis where
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marrow
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what cytokines req. for erythropoeisis
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TNF, IL-1, B1FN, 2IFN
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RBC production influences
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hemoglobin level, O2 content and affinity of RBS
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RBC lifespan
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120days
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# RBCs per ml per kilo
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2000 per ml, 300 x 10 to the 9 per Kilo
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percent RBCs destroyed daily
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about 1 percent
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Required for RBC production
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erythropoetin, marrow stroma, iron, VitB12, Folate
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where are iron, B12, folate producted
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renal peritubular interstitium
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finction of iron folate and B12 on RBCs
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proliferation and maturation
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anemia deficiency
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decreased hemoglobin
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2 types anemia (functional)
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kinetic or nutritional
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