Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Step 1 12.1.12
Muscle II
| Question | Answer |
|---|---|
| What binds to troponin C in SM? What does its binding do? | Ca++ bind it, moving tropomysin out of the way allowing actinb/myosin cycleing |
| How does rigor mortis happen? | ATP is required to bind to myosin head allowing for cross bridge cycling, lack of it and cross bridges cant dissassociate, |
| How does smooth muscle contract? | AP-->membrane depolarization-->intracellular Ca++ incr--> ca++ binds callmodulin-->activates MLCK-->phosphrylation of mysoin |
| What is the mechanism of action of nitric oxide on SMM? | NO-->gunalyate cyclase-->cGMP--->inhibits MLCK |
| What is the process of endochondral ossifications and when do bones use it? | for longitudinal bone growth. cartilagenous model of bone is made by chondrocytes. osteoblasts and osteoclasts later replace it with woven bone and remodel to lamellar bone |
| What is the stem cell source for periosteum? | mesenchymal Stem cells |
| What is the process of membranous ossification and when is it used in bones? | flat bone growth (skull, facial bones, axial skeleton). woven bone fromed directly without cartilage. later remodeled into lamella bone |
| What is the mechanism of disease as it relates to physical features in achondroplasia? | failure of longitudinal bone growth (endochondral ossification)= short limbs. membranous ossification is not affected so there is a large head |
| What is the genetic defect in achondroplasia and how is it inherited? | constituative activation of FGFR3 which inhibits chondrocyte proliferation. >85% are sporadic and are associated with advance paternal age. but autoD inheritance |
| Do people with FGFR3 mutation have normal life span and fertility? | yes |
| What is the mechanism of osteoporosis? | trabecular spongy bone loss and interconnection despite normal bone mineralization and lab values |
| What are some common PE findings in osteoporosis? | vertebral crush fractures, acute back pain, loss of height, kyphosis |
| What is themech of osteoporosis type I? | postmenopausal. incr bone resorbtion due to decr estrogen levels |
| What are some common PE findings in type I osteoporosis? | femoral neck fracture, distal radius (Colles) fracture |
| What is the mech of Type II osteoporosis? | senile osteoporosis-affects men and women >70 y/o |
| What is a useful prophylaxis for type II osteoporosis? | exercise and calcium before age 30 |
| How do you treat osteoporosis? What is contraIndicated? | estrogen (SERMs) calcitonin, biphosphates, pulsatile PT. Glucocorticoids are CONTRAI |
| What is the mechanism of marble bone disease (osteopetrosis? | failure of normal bone resorbtion-->thickened, dense bones that are prone to fracture. due to abnormal function of osteoclasts |
| What lab values might you see in marble bone disease ( osteopetrosis)? | serum calcium, phosphate, alkaline phosphatase is NORMAL |
| what are some associated problems of marble bone disease ( osteopetrosis)? | primary spongiossa fills the medullary cavity causing decr space for marrow and get anemia, thrombocytopenia, infection, incr extamedullary hematopoesis. Also see CN nerve impingement due to narrow foramina |
| What is the genetic derangement in marble bone disease ( osteopetrosis)? | deficiency of carbonic anhydrase II |
| What is seen on XR in marble bone disease ( osteopetrosis)? | "Erlenmeyer flask" bones that flare out |
| What is the mechanism of osteomalacia/ricketts? | defective mineralization/calcification of osteoid= soft bones. vitamine deficiency in adults-->low ca++ lev els-->incr PTH secretion, decr serum PO4 |
| How can you reverse osteomalacia/rickets? | supplemental vitamin D |
| What is the pathophys of Paget's disease (ostetitis deformans)? | abnormal bone archuitecture caused by incr in both osteoblastic and osteoclastic activity. possibly viral in origin |
| What labs might you expect in Paget's disease (ostetitis deformans)? | normal serum Ca++, phosphorus, PTH. incr ALP (alkaline phosphatase) |
| What is seen in the bones in Paget's disease (ostetitis deformans)? | mosaic bone pattern, long bone chlak stick fractures |
| What is a major complication of Paget's disease (ostetitis deformans)? | incr blood flow from AV shunts can cause high output heart failure. also can cause osteogenic sarcoma. hat size is incr, hearing loss common due to auditory foramen narrowing |
| What serum Ca++, phosphate, ALP and PTH are seen in osteoporosis? | all normal |
| What serum Ca++, phosphate, ALP and PTH are seen in osteopetrosis? | all normal |
| What serum Ca++, phosphate, ALP and PTH are seen in osteomalacia/rickets? | decr Serum Ca++, decr phosphate, normal ALP, incr PTH |
| What serum Ca++, phosphate, ALP and PTH are seen in ostetitis fibrosa cystica? | incr Ca++, decr phosphate, incr ALP, incr PTH |
| What serum Ca++, phosphate, ALP and PTH are seen in Paget's disease? | all normal except ALP which is elevated |
| What happens in polyostotic fibrous dysplasia? | bone is replaced by fibroblasts, collagen, irregular bony trabeculae |
| What is McCune-Albright syndrome?> | form of polyostotic fibrous dysplasia characterized by multiple unilateral bone lesions associated with endocrine abnormalities (precocoius puberty) and cafe-au-lait spots |
| What is the epidemiology/location of giant cell tumor (osteoclastoma)? | 20-40 y/o, epiphyseal end of long bones |
| What are the aggression characterisitcs of giant cell tumor (osteoclastoma)? | aggressive benign tumor often around the distal femur, proximal tibial region (knee) |
| What is seen on XR and histology of giant cell tumor (osteoclastoma)? | see "double bubble" or soap bubble appearance on XR. spindle shaped cells with multinucleated giant cells |
| What is the epidemioloy of osteochondroma (exostosis)? | most common benign tumor, men <25 y/o |
| What are the major characteristics of osteochondroma (exostosis)? | mature bone with cartilagenous cap. commonly originates from long metaphysis. malignant tranformation is rare |
| What are the epidemiological and location features of osteosarcoma (osteogenic sarcoma)? | malignant. men 10-20 y/o. metaphysis of long bones often around distal femur, proximal tibia |
| What are some major predisposing factors to osteosarcoma (osteogenic sarcoma)? | Paget's disease, bone infarcts, radiation, familial retinoblastoma |
| What is seen on XR and what is the prognosis in osteosarcoma (osteogenic sarcoma)? | Codman's triangle or sunburst pattern (from elevation of periosteum on CXR). poor prognosis |
| What is the epidemiology and location of Ewing's sarcoma? | boys <15 y/o. commonly in diaphysis of long bones, pelvis, scapula and ribs |
| What is the aggresion characteristics of Ewing's sarcoma? | anaplastic small blue cell malignant tumor. extremely aggressive with early metastases, but responds to chemo |
| What is the genetic mutation in Ewing's sarcoma and what is seen in the bone? | "onion skin" appearance in bone. 11;22 translocation |
| What is epidemiology and location of Chondrosarcoma? | Men 30-60 y/o. usually located in pelvis, spine, scapula, humerus, tibia, femur |
| What is the aggression characteristcs of Chondrosarcoma? What does it look like? | malignant cartilagenous tumor. expansile glistening mass withing the medullary cavity |
| What is a benign bone cancer seen in the epiphysis? | Giant cell tumor |
| What are 1 benign and 1 malignant tumors seen in the bone metaphysis? | osteosarcome = malignant, osteochrondroma=benign |
| What are 2 malignant tumors found in the bone diaphysis? | Ewing's sarcoma, Chondrosarcoma |
| What is the mechanical process of osteoarthritis and what can be seen? | wear and tear of joints leads to destruction of articular cartilage, subchondral cysts, sclerosis, osteophytes (bone spurs), eburnation (ivory appearance of bone), Heberden's nodes (DIP), Bouchard's nodes (PIP) |
| What are 3 predisposing factors to osteoarthritis? | age, obesity, joint deformity |
| What is the classical presentation of osteoarthritis? | pain in weight bearing joints after use, improves with rest. in the knees, loss begins medially (bowlegged). non inflammatory with no systemic sx |
| What is the mech and location of rheumatoid arthritis? | inflammatory disorder affecting synovial joints, with pannus in MCP, PIP, subcutaneous rheumatoid nodules (fibrinoid necrosis surrounded by palidsading histicytes), ulnar deviation, subluxation. Baker's cysts behind the knee |
| What specific joint is not inviolved in rheumatoid arthritis? | DIP |
| Who gets RA? What type of hypersensitivty is it? | Females>males. Type II hypersensitivity |
| What labs are seen and which HLA is commonly associated with RA? | 80% of pt have + rheumatoid factor ( anti-IgG Ab), anti-CCP is less sensitive but more specific. Strong association with HLA-DR4 |
| What is the classic presentation of RA? | morning stiffness lasting >30 min and improves with use. symmetric joint involvement, systemic sx like fever faitgue, pleuritis, pericarditis |
| How do you tx RA? | NSAIDs, COx-2 inhibitors, glucocorticoids, disease modifying drugs (MTX, sulfasalazine, hydroxychloroquine) |
| Boutonniere deformity, swan-neck deformity, Z-thumb deformity are all associated with which disease? | RA |
| What is the classic triad of Sjogren's syndrome? | 1. Xeropthalmia (dry eyes, conjunctivitis, "sand in my eyes") 2. xerostomia (dry mouth, dysphagia)3. arthritis |
| What are some common associated Sx of Sjogren's syndrome? | parotid enlargement, incr risk of B cell lymphoma and dental carries. |
| What auto Ab are seen in Sjogren's syndrome? | auto Ab to ribonuclear proteins, SS-A (Ro), SS-B (La) |
| Who mainly gets Sjogren's syndrome? | women 40-60 y/o |
| What other disease is Sjogren's often associated? | RA |
| What is Sicca Syndrome? | dry eyes, dry mouth, nasal and vaginal drynesz, chronic bronchitis, reflux esophagitis, no arthritis |
| What is gout? | precipitation of moonosodium urate crystals into joints due to hyperuricemia |
| What are some causes of gout? | Lesch-Nyhan syndrome, PRPP excess, decr excretion of uric acid (thiazide diuretics), incr cell turnover, von Gierke's disease |
| What do the crystals in gout look like? Who is more likely to get gout? | needle shaped and negatively birefringent = yellow crystals under parallel light. more common in men |
| What are the usual Sx of gout? | asymmetric joint distrobtuin with swollen red and painful joints. classic manifestations: painful MTP joint of big toe (podagra) Tophus formation (external ear, olecranon bursa, achilles tendon). |
| When do acute attacks of gout happen? Why? | after big meals or EtOh consumption ( EtOH metabolites compete for same excretion sites in the kidney causing decr uric acid secretion and buildup) |
| What is used to treat an acute gout attack? | NSAIDs (indomethacin), colchicine |
| What is used to tx chronic gout? | allopurinol, febuxostat, uricosurics (ex. probenecid) |
| What is pseudogout? | deposition of Calcium pyrophosphate crystals within the joint space. forms basophilic rhomboid chystals that are weakly birefringent |
| What joints are affected in pseudogout and who gets it? | affects large joints (classically the knee), >50 y/o both sexes |
| How do you treat pseudogout? | NSAIds, steroids, colchi9cine |
| What is the difference between gout and pseudogout crystals using light? | gout: yellow when parallel, blue when perpindicular pseudogout: crystals are yellow when perpindicular and blue wehn parallel to the light |
| What are 3 common pathogenis of septic arthritis? | S. aureus, Streptococcus, N. gonorrhoeae |
| What is seen in gonoccacal arthritis? | STD which presents as migratory arthritis with an asymmetrical pattern. affected joint is swollen, red, painful. See STD= synovitis (knee), tenosynovitis ( hand), dermatitis (pustules) |
| What are 2 pathogens which can cause a chronic infectious arthritis? | TB, lyme disease |
| What is seen in osteonecrosis (avascular necrosis)? What causes it? | infarction of bone and marrow. pain with activity, caused by trauma, high dose corticosteroids, alcoholism, SCA |
| what are 4 seronegative spondyloarthropathies? | psoriatic arthrtis, ankylosing spondylitis, inflammatory bowel disease, reactive arthrtis (Reiter's syndrome) |
| What is a seronegative spondyloarthropathy? What HLA are they associated with? | arthritis without rheumatoid facotr. strong association with HLA-B27 (codes for MHC I). more often seen in males |
| What is seen in psoriatic arthritis? on XR? | joint pain and stiffness associated with psoriasis. asymmetric and patchy involvement. "pencil in cup" deformity on XR |
| What is ankylosing spondylitis and what is it associated with? | chronic inflammatory disease of spine and and sacroiliac joints. see uvetitis, ankylosis, aortic regurgitation. bamboo spine |
| What is inflammatory bowel disease associated with? | Crohn's ulcerative colitis |
| What is the classic triad of Reactive arthrtis (Reiter's syndrome)? | 1. conjunctivitis with anterior uveitis 2. urethritis 3. arthritis (cant see, cant pee, cant climb a tree) |
| What is a common setting for Reactive arthrtis (Reiter's syndrome)? | post GI or chlamydia infections |
| What is the major deomographic for SLE? | 90% female b/w 14-15. most sever in black females |
| What are the sx of SLE? | fever, fatigue, weight loss, Libman-Sacks endocarditis (verrucous, wart like, sterile vegetation on both sides of valve), hilar adenopathy, Raynaud's pneonomenon |
| What is seen in the kidney in SLE? | wire loop lesions with immune complex deposition (nephritic), death from renal failure |
| What test could SLe give a false positive for? | syphilis (RPR/VDRL |
| What is a userful mnmonic for the possible presentations of SLE? | I'M DAMN SHARP: Immunoglobulins (anti-dsDNA, anti-SM, antiphospholipid) 2. malar rash 3. discoid rash 4. antinuclear an 5. mucositis (oraopharyngeal ulcers) 6. neruo7.serositis (pleuritis, pericarditis) 8. hemo 9. arthritis 10. renal 11. photosensitivity |
| What do labs in SLE detect? | 1. ANA 2. anti-ds DNA (poo prognosis) 3. Anti-amith (SM) ab = specific 4. anti-histone ab= drug induced liupus |
| What are the key characterisitcs of sarcoidosis? Who gets it? | immune mediated widespread noncaseating graulomas most common in black females |
| What are some common associations of sarcoidosis? | restrictive lung disease, bilateral hilar lymphadenopathy, erythema nodosum, Bell's palsy, granulomas contains Schaumann and asteroid bodies, uveoparotitis, hyperclacemia |
| Why is there hypercalcemia in sarcoidosis? | elevated apha hydroxylase mediated vitamin D activation in macrophages |
| How do you treat sarcoidosis? | steroids |
| What are the Sx of polymyalgia rheumatica? | pain and stiffness in shoulders and hips often with fever, malaise and weight loss. does not cause muscular weakness. |
| Who gets polymyalgia rheumatica? | pt > 50 y/o, associated with giant cell arteritis |
| What are the key findings in polymyalgia rheumatica? | incr ESR, normal CK |
| What is the tx for polymyalgia rheumatica? | predisone |
| Who gets fibromyalgia? What is required for the dx? | women 30-50 y/o. widespread musculoskeltal pain associated with stiffness, parasthesia, poor sleep, fatigue. need >11 of 18 tender points |
| What is polymyositis, what cuases it, and where does it most common occur? | progressive symmetric proximal muscle weakness cause by CD* T cells injuring myofibers. most often involved shoulders |
| What is seen in dermatomyositis? | muscle weakness but has a malar rash, Gottron's papules, heliotrope rash, "shawl and face" rash, "mechanics hands". incr risk of cancer. |
| What on muscle biopsy is diagnostic for dermatomyositis? | perifasicular atrophy |
| What are the key findings in polymyositis and dermatomyositis? | incr CK, incr aldolase, positive ANA, anti-Jo-1 |
| How do you treat dermatomyositis and polymyositis? | steroids |
| What is the mech of myasthenia gravis? | ab to post synaptic ACHR causes ptosis, diplopia, general weakness. sx worsen with use (dx with nerve stim/compound muscle AP test). |
| What neoplasm is myasthenia gravis associated with? | thymoma |
| What helps reverse myasthenia gravis and what agent helps distinguish under and overdosing? | reverses with ACHE inhibitors, edrophonium is used to distinguish dosage |
| What is the mech of Lambert-Eaton syndrome? | auto ab to preseynaptic Ca++ channel results in decr ACH release leading to proximal muscle weakness |
| What is a STRONG association of Lambert-Eaton Syndrome? | paraneoplatic ( small cell lung cancer). |
| How do Sx improve in Lambert Eaton syndrome? | use, not with ACHE Inhbitors alone |
Created by:
tjs2123
Popular USMLE sets