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127 Cards in this Set
- Front
- Back
- 3rd side (hint)
changes in body fluid levls and osmolarity with cholera
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"isotonic contraction:" decreased ECV, no change in osmolality
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DPC vs DCC
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oncogenes on 18q: DCC causes ColonCancer, DPC causes PancreaticCancer
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tumor suppressors / oncogenes on c17
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17q: NF1, BRCA-1; 17p: p53
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pigmented macules on buccal mucosa, lips, palms, soles, skin not exposed to skin
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peutz-jeghers! (colonic JAMMertomas + Peutz all over (her) face, hands, genitals)
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treatment of hypernatremia
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water replacement, but slowly (2mEq/L/hr) -- avoid cerebral edema
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measurement of interstitial fluid vol
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plasma volume via albumin, ECF volume using inulin, subtract
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measuring fluid volmes: inulin, albumin, heavy water
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inulin: ECF; albumin: plasma volume; heavy water: total body volume
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pyknosis
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nuclear shrinking and basophilia from DNA condensation ("pykno ~ pico = small nuc and DNA")
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karyolysis
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loss of nuclear basophilia -- "lyse the karyo (nucleus) and the color leaks out"
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type of necrosis seen in an abscess
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liquefactive (same as brain?)
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karyorrhexis
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"RHECKING" the nucleus (fragmentation)
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type of amyloidosis in cardiac tissue
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usu primary amyloidosis (AL or ATTR); manifests as restrictive cardiomyopathy
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amylin
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islet amyloid polypeptide (type 2 DM)
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port wine stain
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vascular lesions a/w Sturge-Weber disease (which also includes leptomeningeal angiomatosis -- similar lesions of meninges)
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sturge-weber disease
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"sturge-chuck-weber:" port-wine stains (capillary hemangiomas), meningeal hemangiomas; eye involvement: glaucoma, retinal detachment; cns: MR, convulsions
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MCC aortic stenosis in a 25 yo
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congenitally malformed valve (mono- or bicuspid)
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vasculitis of the aortic arch
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takayasu arteritis (chronic inflam changes --> stenosis --> upper body ischemia, aka pulseless disease)
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widened pulse pressure
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AR (decreased diastolic pressure) or arteriosclerosis (increased systolic pressure)
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alkphos in kids vs adults
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kids have much higher alk phos (needed for growth), usu up to 5x greater
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Legg-Calve-Perthes disease
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idiopathic aseptic necrosis of femoral head; boys > girls, 3-10yo; can lead to osteoarthritis
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posterior wall of heart formed by
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LA (can compress esophagus)
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left border of heart formed by
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LV
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osteoid
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protein mixture (type I collagen) secreted by osteoblasts; can mineralize to become bone
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failure of osteoid mineralization
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osteomalacia / rickets
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sparse trabeculae
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osteoporosis (bony trabeculae are in normal abundance in osteomalacia, just not mineralized)
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harsh systolic murmur
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VSD
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VSD vs PDA
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VSD murmur is harsh, systolic; PDA is continuous and machinery like; VSD causes increased O2sat of RV, PDA can eventually cause R-->L shunt (once pulm vasc resistance increases), so no change in RV O2sat
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diastolic pressure gradiant between atrium and ventricle
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AV stenosis (mitral, tricuspid)
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GI diseases a/w arthropathy
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MCC: IBD (UC and Crohn's); others: bypass surgery, Whipple disease, celiac disease
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cardiac myxoma
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most frequent primary cardiac tumor: benign, 90% in atria (LA), "ball-valve" obstructions --> MS
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Prinzmetal's angina
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coronary artery spasm at rest, usu with fixed obstruction near site of spasm; tend to be younger than pts with unstable angina (due to atherosclerosis)
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artery frequently injured in knee dislocation
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popliteal (extension of superficial femoral artery, ends below the knee in a 'trifurcation:' ant tib, post tib, and peroneal)
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subendocardial vs transmural infarct
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subendocardial usu in setting of shock, affects most EKG leads; transmural is more common, ST elev in a few leads (due to coronary artery occlusion)
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thenar vs hypothenar innervation
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thenar: median n; hypothenar: ulnar n;
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congenital defect a/w osteium primum ASD (often accompanied by tricupsid/mitral valve malformations)
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down syndrome
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firing rate of IX and X nerves with respect to blood pressure
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increases with increasing blood pressure, causes increased sympathetic outflow; IX = carotid sinus baroreceptors, X = aortic arch baroreceptors
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bullous pemphigoid vs pemphigus vulgaris
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PV: anti-desmosomal Abs (intrapeidermal bullae), BP: anti-BM Abs (subepidermal bullae); PV: 1st lesion in oral mucosa --> skin --> denuded surface --> infection --> death, BP: blistering, pruritic, but spares oral mucosa and less serious than PV
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intramembranous vs. endochondral bone growth
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intramembranous: spontaneous bone formaton w/o pre-existing cartilage; endochondral: ossification of cartilaginous molds (eg long bones)
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unhappy triad
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ACL, medial collateral ligament (MCL), medial meniscus
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which side of leg is fibula on
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lateral
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anterior and posterior in ACL / PCL refer to
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sites of TIBIAL attachment (=> ACL tear allows tibia to move forward -- anterior drawer sign)
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sign of MCL tear
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abnormal massive aBduction (no ligament to restrain motion)
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None
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rotator cuff muscles
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SItS (Supraspinatus, Infraspinatus, Teres minor, Subscapularis)
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Role of Supraspinatus
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helps deltoid aBduct arm
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role of teres minor
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laterally rotates and aDducts arm (along w/ subscapularis)
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role of subscapularis
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medially rotates and aDducts arm (along w/ teres minor)
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role of infraspinatus
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laterally rotates arm
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name the muscular dsytrophies and their inheritence
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all involve progressive muscle degeneration, increased CPK (unlike congenital myopathies): duchennes/beckers (XR); fascioscapulohumeral (AD); limb-girdle (AR); myotonic (AD, CTG repeat)
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myotonic dystrophy
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AD, CTG repeats (anticipation), wasting of muscles + cataracts and heart conduciton defects
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myasthenia gravis vs lambert eaton syndrome
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MG: improves with rest, 1' affects head/neck, Abs against nAChR, a/w thymomas; LE improves with USE, does NOT 1' affect face, Abs against presynaptic CALCIUM channels, a/w paraneoplastic tumors (eg small cell of lung);
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changes in 'bands' during muscle contraction
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HIZ shrinks: H band, I band, Z-band
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calcium channels in t-tubules
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dihydropyradine receptors (opened by depolarization of postsynaptic -muscle- cell)
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conduction to contraction of skeletal muscle
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presynaptic NT release --> small depol of postsynaptic (muscle) cell --> depol travels down to t-tubules --> opens voltage-gated Ca++ channels (dihydropyradine receptors) --> small Ca++ influx --> opens calcium-gated ryanodine receptor/channels on SR --> big increase in intracytoplasmic Ca++ --> bind Troponin C --> move tropomyosin (via Troponin I) out of the way, allow myosin-actin binding
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conduction to contraction of smooth muscle
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requires increased intracell Ca; 2 methods: 1) AP --> voltage-gated Ca++ channels open, or 2) alpha1/M3 stim --> Gq --> IP3 --> inc Ca++; once calcium increases, get unified pathway: Ca++ binds calmodulin --> activates myosin light chain kinase --> phosphorylates (activates) myosin --> cross-bridge formation and contraction
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hormonal regulators of smooth muscle contraction
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alpha1 (vasculature) and M3 (sweat glands) both cause contraction via Gq --> IP3 --> Ca++; beta2 (vasodilation) causes relaxation via Gi --| cAMP --> myosin light chain kinase activation (ie beta2 prevents activation of MLCK)
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skeletal vs smooth muscle
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skeletal has Z-lines, uses Ca++ - TropnoninC complexes to facilitate bindin, striated, multinucleated, and AP upstroke is driven by SODIUM; smooth has no Z-lines, is single nucleated, not striated, AP upstroke is driven by CALCIUM and Ca++ binds calmodulin to activate myosin light chain kinase
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pannus formation
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RA: tissue flap (inflammatory?), causes cartilage and bone destruction
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jointspace in RA vs OA
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increased in RA (inflammation), decreased in OA (wear-and-tear destruction of cartilage brings bones closer together)
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systemic sx in RA / OA
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none in OA (it’s a mechanical wear and tear process); fever, fatigue, pleuritis and pericarditis in RA
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joints affected in RA / OA
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RA: synoval joints, MCP/PIP (boutenierres, swan neck, z-thumb); OA: weight-bearing joints (hip), PIP/DIP (Bouchard's and Heberden's nodes)
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age of onset of RA/OA
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RA in middleage women (F 20-50) -- same as most AI diseases; OA: old people (disease of wear and tear)
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change with rest in RA/OA
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OA improves with rest (worse at end of the day); RA improves with movement (characterized by morning stiffness)
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infectious causes of arthritis (septic arthritis)
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MCC: S.Aureus; in sexually active young people: gonococcus--monoarticular; others: lyme disease: a/w ECM, polyarticular. See **IgM**
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Seronegative arthrititides
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a/w HLA-B27 (unlike RA: HLA-DR4): 1) ANKYLOSING SPONDYLITIS (spine and sacroiliac, uveitis); 2) REITER SYNDROME (urethritis, conjuncitivitis, arthritis); 3) PSORIATIC ARTHRITIS (10% of psoriasis patients); 4) IBD
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tx for osteoporosis
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bisphophonates --| bone resoprtion (also used for paget's disease, bone mets, multiple myeloma)
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2 types of osteoporosis
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1: post-menopause --> dec estrogen; 2: senile, M/F > 70yo
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osteopetrosis
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failure of bone marrow resorption (osteoclastic failure); can cause: 1) anemia, 2) cranial nerve dysfunction (impingment of neural foramina), 3) blindness, 4) deafness
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increased thickness of epiphyseal plates
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rickets (osteomalacia of kids): dec Vit D --> dec Ca++ --> dec mineralization of osteoid --> "Soft bones"
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brown tumor
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cystic space lined with osteoclasts and filled with fibrous stroma / blood (seen in osteitis fibrosa cystica = Von Recklinghausen's Dz of bone)
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osteitis fibrosa cystica
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primary increase in PTH --> inc Vit D, inc Ca++, dec Phosphorus; --> inc osteoclast activity, inc alk phos
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paget's disease
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inc osteoclast and blast activity --> elevated alk phos (rest normal); mosaic pattern of bone (disorganized), "cap won't fit" b/c of increased bone density, but poor structural integrity --> increased fractures; common in elderly, and can lead to osteosarcoma (rarely, but the only time you see osteosarcoma in elderly)
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osteosarcoma in elderly
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2' to paget's disease
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McCune Albright syndrome
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polyostotic fibrous displasia in little girls: café au lait spots, short stature, precocious puberty
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consequences of paget's disease
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1) bone pain from fractures (poor structural integrilty); 2) high output heart failure (shunts in highly vascular bone); 3) hearing loss; 4) osteosarcoma (rare, but only cause of osteosarcoma in elderly)
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osteomyeleitis in: 1) neonates; 2) kids; 3) adults; 4) sickle cell; 5) IVDU
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1) neonates: e.coli/grp B strep --> heme spread; 2) kids: s.aureus --> heme spread; 3) adults: surgery/fracture complication; 4) sickle cell: salmonella; 5) IVDU: pseudomonas
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histiocytosis x
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clonal proliferation of langerhans cells; see birbeck granules in cells (tennis-racket shaped cytoplasmic structures)
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types of histiocytosis x
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from worse to better: 1) Letterer-Siwe (multiorgan, multifocal); 2) Hans-Schuller-Christian (unisystem, multifocal): skull, DI, exophthalmus; 3) Eosinophilic Granuloma (unifocal, usu bone), best prognosis
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polymyalgia rheumatica
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muscle pain, stiffness, NO WEAKNESS; a/w temporal arteritis (elev ESR); usu >50yo, tx w/ prednisone
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polymyositis vs dermatomyositis
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both a/w anti-Jo-11 1, elev CK and aldolase, progressive proximal muscle weakness caused by CD8+ T-cell injury; dermatomyositis adds rash (in pattern of woman's shawl)
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anti-RNP Abs
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mixed connective tissue disease
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bone tumors around knee
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epiphysis: giant cell tumor (benign); metaphysis: osteochondroma (aka exostosis; benign), osteosarcoma (osteogenic carcinoma; malignant)
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giant cell tumor of bone
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FEMALES 20-40 yo (only bone tumor more common in females); occurs in epiphyseal end (knee), locally aggressive but benign; "soap bubble" on xray, spindle shaped cells with multinucleated giant cells histologically
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osteochondroma (exostosis)
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males < 25yo; most common benign bone tumor
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enchondroma
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benign cartilaginous tumor found in intrameddulary bone, distal extremities (hands and feet)
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3 main types of malignant bone tumors and locations
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osteosarcoma (metaphysis around knee, M 10-20y); Ewing's sarcoma (intramedullary, M < 15yo); Chondrosarcoma (intramedullary, M 30-60)
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osteosarcoma
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most common malignancy of bone, found in metaphysis near knee; M 10-20yo; Rad findings: Codman triangle, sunburst pattern; early heme spread; PREDISPOSING factors: Paget's dz (elderly), Rb gene mutation;
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chondrosarcoma
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malig intramedullary cartilaginous tumor; M 30-60yo; can be 1' or from osteochondroma
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ewing sarcoma
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intramedullary tumor; boys < 15yo; t(11;22); *extremely malignant*, early mets; histo: small blue cells, onion skin on xray; "Patrick Ewing dribbling a small blue onion; he's a little kid, but still so tall that the tumor cant get to the end of his bone (intramedullary)"
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rhabdomyosarcoma
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malig tumor of skeletal muscle, most common soft tissue sarcoma of kids; tx with dactinomycin
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anti-histone antibodies
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drug-induced lupus
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what precipitates gouty attack
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alcohol, large meal
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linear staining on immunofluorescence
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goodpasture's (anti-BM IgG)
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non-caseating granulomas
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sarcoidosis -- cause increased ACE, increased Vit D --> inc Ca++, bilateral hilar adenopathy, erythema nodosum, Bell's palsy
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psoriasis vs eczema
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psoriasis is on EXTENSOR surfaces and NON-pruritic; eczema on FLEXOR surfaces and PRURITIC
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psoriasis: epidermal changes
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epidermal hyperplasia (acanthosis); increased stratum spinosum, DECREASED stratum granulosam (psoriasis gets you more STRINGs, less GIRLS)
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auspitz sign
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a/w psoriasis: bleeding punctate spots when lesoin scraped off
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dermatitis herpetiformis
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a/w celiac disease; group (herpetiformis) of pruritic papules and vesicles
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lichen planus
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Pruritic Planar Purple Polygonal Papules; lymphocytes
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erythema multiforme
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target lesions (multiple types of lesions: macules, papules, vesicles); stevens-johnson is a very serious type
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stevens-johnson syndrome
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major form of erythema multiforme, high mortalitiy rate (necrosis and ulceration of skin)
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albinism vs vitiligo
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vitiligo is acquired, autoimmune (a/w graves, addisons), and patchy; albinism is usu result of tyrosinase deficiency (impaired tyrosine --> L-DOPA --> melanin)
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spitz nevus
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juvenile melanoma (but MISNOMER -- benign!); spindle shaped cells
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basal cell vs squamos cell carcinomas
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BASAL cell: upper face, pearly papule w/ overlying telangiectasia, pallisading nuclei; SQUAMOUS cell: lower face, sheets of cells with KERATIN PEARLS, a/w arsenic and actinic keratosis
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congenital hypothyroidism
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lethargic, poor feeding, prolonged jaundice, muscle hypotonia, macroglossia, MR (T4 needed for brain dev); inc risk of ASD/VSD
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sporothrix infection
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dimorphic fungus, xmit by thorbrick --> subq mycosis, nodules along lymphatics
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apocrine vs eccrine glands
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both used for sweat; apocrine glands "rip off piece of membrane" --> fatty, smelly (sweat); eccrine glands secrete NaCl ('sweat') directly to skin via exocytosis
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apocrine vs eccrine glands
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RANK
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essential for formation/differntiation of osteoclasts (they have RANK-receptors); hypoestrogen --> overexpression --> osteoporosis
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"gluteus medius gait"
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hip drops downoward when ipsilateral foot lifted -- caused by injury to superior gluteal nerve or gluteus medius muscle
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GVHD
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acute: within 1wk of procedure, mediated by CD4 and CD8 T cells (B Cells don't really play any role)
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2 most imp factors for osteoclast differentiation
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M-CSF and RANK-L (osteoclasts, mature and precursors, possess receptors for both)
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roles of FGF
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nevascularization, wound healing, and bone matrix formation (FGF-R mutation --> achondroplasia)
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parvovirus in kids and adults
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kids: erythema infectiousum (5th disease); adults: arthritis
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antibodies against neutrophil myeloperoxidase
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p-ANCA (PAN, Churg-Strauss)
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atherogenesis
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endothelial injury --> endothelial dysfunction / collagen exposure --> platelet adhesion/aggregation/release of {PDGF, TGF-beta} --> migration of SMC from media to intima, SMC proliferation
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hemangiosarcoma (angiosarcoma) a/w what toxins
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thorotrast, PVC, arsenic
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pulseless disease
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takayasu arteritis: granulomatous thickening of aortic arch, elevated ESR, azn females < 40yo
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which organ is rarely involved in PAN
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lung
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fatty streaks
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earliest lesion of athersclerosis, present after age 10; lipid-laden foam cells in intima
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vasculitis a/w HBV
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PAN
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malignant HTN vs diabetic hyaline arteriolosclerosis
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malignant HTN causes hyperplastic arteriolosclerosis (homogenous, onion-like, concentric thickening of arterial walls); diabetic hyaline arteriolosclerosis causes intimal thickening with homogeneous hyaline deposition in intima
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temporal arteritis is morphologically most similar to?
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takayasu arteritis (pulseless disease)
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most specific sx of giant cell (temporal) arteritis
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jaw claudication
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takayasu vs giant cell (temporal) arteritis
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usu distinction is size and location (takayasu: aorta, proximal aortic branches; temporal: distal carotids); however, both can present similarly so distinction often made based on AGE (takayasu: < 40; temporal: elderly)
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temporal arteritis vs PAN
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temporal (and takayasu) are GIANT CELL arterititides --> involve giant cells and mononuclear infiltrates; PAN is characterized by immune complexes, complement, and plasma proteins --> fibrinoid necrosis
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main mechanisms for dev of varicose veins
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incompetent venous valves
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vascular effects of tertiary syphilis
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vaso vasorum endarteritis / obliteration --> weakened adventitia --> aortic aneurysm --> AR
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