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77 Cards in this Set
- Front
- Back
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Front
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Back
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How are spinal cord injuries resulting in paralysis or paresthesia named?
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Injury named for the last level of function
i.e. Injury to spine with ability to flex elbow but not extend = C-6 quadraplegia spinal injury |
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Chronic inflamation that can involve the hips, SI Joint and vertebrae\nS/S\nGradual onset with bouts of back back that radiate down to thigh\nMid and low back\npain at rest\npersistent buttock pain\npainful SI\ndecreased ROM\n\nEventually:\nkyophosis and lordosis\n\nLabs\nElevated ESR, negative rheumatoid factor, + HLA-B27\n\nWithout xray, what is most likely DX?
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Ankylosing spondylitis\n\n(bamboo spine)
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Other areas the ankylosing spondylitis can affect?\n\nHow does it progress?\n\nDoes it have a genetic factor?
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Other articular areas:\nHips and SI Joint\n\nExtra-articular manifestations:\nOpthalmic-acute anterior uveitis\nCardiac-aortic regurg/insuff, pericarditis\nRenal-amyloidosis, IgA nephropathy\nPulmonary-fibrosis in upper lobes with cavitation and bronchioectasis (mimicks Tb)\n\nProgression:\nosteopenia-->erosions-->ossification\n\nGenetis Component\nHLA-B27 (90%)
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Treatment of Ankylosing Spondylitis
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Heat/Excercise to improve posture\n\nMeds\nNSAIDS are NOT effective in altering progress\nSteroids can limit progress\nTNF Inhiobitors\n\nSurgical\nHip replacement\nVertebral osteotomy
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71 yo male with low back pain and lower extremity dysfunction\nComplains of radicular pain down posterior leg. Pain is diminished with sitting.\nPain also improves with bending forward.\n\nYou suspect Lumbar Spinal Stenosis\n\nWhat is this and what are the most common causes of lumbar stenosis?\n\nWhich of the causes is most probable in the above presentation?
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Lumbar Stenosis\nNarrowing of the spinal canal/nerve root canal/intervert foramina resulting in compression of the spinal cord/neural elements at the Lumbar level\n\nCommon causes:\nanterior bulging of disk\ndisk degeneration\nbuckling of the ligamentum flavum posteriorly\nencroachment of the articular facets (spondylo pathology)\n\nThis presentation is most likely d/t ligamentum flavum buckling or articulat facet impingement because it get better with bending forward
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65 year old oil field trucker comes in complaining of pain/tingling shooting down back of right leg to level of calf. Pain worsens with spinal movement (bending) and sneezing/coughing.\nPE reveals pain with strait led raise, right leg/thigh loss of sensation, weakness, and decreased DTRs.\n\nWhat would be at the top of your differential based on the pt's work history?
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Describe the mechanism of Lumbar Disk Herniation? Most common level?\n\nName the chategories of herniation.
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Weakening of annulus fibrosis with resulting herniation of nucleus pulposis from center.\nMost commonly L4-5 (2nd is L5-S1)\n\nCategories
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35 year old Accountant comes it with localized pain in the lumbosacral area. No radiculopathy. PE - palpation of lumbar paraspinal muscles reveals spasms and limited motion, no pain with straight leg raise?\n\nWhat is Dx and Tx?
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Lumbar Strain\n\nTx:\npain usually self limiting with 50% recovery in 2 wks (90% in 6 weeks)\nmodification of posture/lifting technique\nmild analgesics and anti-inflams\nAVOID complete bed rest\n\nXray not usually necessary for first visit\nHOWEVER, get Xray if >50 with Hx of trauma, CA, wt loss, pain at rest, drug abuse, neuro deficit or elevated temp
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Term referring to degenerative osteoarthritis of the joints between the centra of the spinal vertebrae and/or neural foraminae.\n\nFacet joints are not involved.\n\nIf severe, it may cause pressure on nerve roots with subsequent sensory and/or motor disturbances, such as pain, paresthesia, or muscle weakness in the limbs.\n\nPt presentation may include increased pain with spinal extension
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Spondylosis
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15 yo female presents with persistent back pain. Pt is gymnist and pain began during the season. Pain worsens with extension of spine.\n\nMost likely Dx?\nDescribe mechanism
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Spondylolysis\nBasically a stress fx of pars interarticularis. The great majority of cases occur in the lowest of the lumbar vertebrae (L5), but spondylolysis may also occur in the other lumbar vertebrae, as well as in the thoracic vertebrae.\n"Scotty Dog" Fracture
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Treatment of Spondylolysis
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Sidelined for 4-6 weeks\nBrace during acute rehab phase\neventually PT\nMeds for pain
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18 yo football player walks into your office slightly bent forward. Pt is in obvious pain and says his back is ridiculously sore and stiff. He says it started after he landed landed with spine extended and was simultaneously hit in the back helmet first by member of the other team.\n\nHe is experiencing intermittent shocks of shooting pain beginning in the buttock traveling downward into the back of the thigh and/or lower leg. Sometimes symptoms include tingling and numbness. Sitting and trying to stand up is painful and difficult. Coughing and sneezing can intensify the pain. He says it almost feels like a "slipping sensation" when moving into an upright position.\n\nWhat is the most likely Dx?
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Spondylolysthesis\n\nBasically spondylolysis with migration of of vertebrae in ant/post direction (retrograde or antegrade)\n\nGrades 3-4 = surgery. Must decompress neural foramen
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What is the difference between:\n\nCervical Strain\n\nCervical Sprain\n\n**include presentation, Dx, and Tx
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Cervical SPRAIN\nStrain =Muscle/tendon injury. MC cervical injury in athletes\nPresents as painful neck motion, peaks after several hours/days\nTx: Anti-inflam, heat, rest\n\nCervical STRAIN\nInjury to ligaments and capsular structures connecting facet joints and vertebrae\nPain and limited ROM\nMay lead to instability and assoc neuro involvement\nTx: basically the same\n\n**very difficult to differentiate clinically
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Stiff neck associated with muscle spasm, classically causing lateral flexion contracture of the cervical spine musculature (a condition in which the head is tilted to one side). The muscles affected are principally those supplied by the spinal accessory nerve.\n\nWhat is this called?\nPossible causes?
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Torticollis\n(aka wryneck)\n\nIn newborns, caused by SCM injury during birth\nMay require surgery\n\nAcquired after newborn, usually develops overnight and will resolve spontaneously in 1-2 weeks
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The term used to describe pain radiating down the leg in a dermatomal distribution.\nMost common symptom of lumbar disc herniation.\n\nWhat is this called and where does it generally originate?
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Sciatica\n\nGenerally originates from the L4-5 or L5-S1 interspace\n\nL4 - pain/numbness to the medial lower leg and foot; weak quads,+/- inability to bring the foot upwards (heel walk). Pt may have reduced patella tendon reflex.\n\nL5 - weakness in extension of the big toe and potentially in the ankle (called foot drop). Pain/numbness at the top of the foot, particularly in the web between the great toe (big toe) and the second toe.\n\nS1 - pain/numbness to the lateral (outer) foot; weakness that results in difficulty raising the heel (can't walk on the tiptoes). Pt may have reduced ankle-jerk reflex.
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Pt presents acutely with following:\nback pain radiating to legs\nweakness in multiple root distribution\nreduced DTRs\nfecal incontence\nurinary retention\nsensory loss (multiple dermatomes)\nCan't "get it up" (sexual dysfuntion)\n\nWhat is likely Dx?\nCauses?\nTx?
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Cuada Equina Syndrome\n(EMERGENCY)\n\nDo a digital rectal exam to asses sphincter tone.\n* may have contralateral positive straight leg raise (let me know if you understand this?)\n\nCause:\nInjury to cauda equina nerves in canal or as they exit nerve foramen\nTumor, trauma (LP), inflamation, spinal stenosis\n\nTx:\nURGENT intervention and decompression <48 hrs to preserve bowel and bladder function
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Differentiate Kyphosis from Lordosis
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Kyphosis\n"hunchback"\nexagerated angulation of normal thoracic curve\nusually painful\noften involves compression fractures (elderly)\n\nLordosis\n"swayback"\nAbnormal anterior convexity of spine\nusually lumbar but can be cervical
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Lateral and rotary curvature of the spine. Becomes evident during adolescence.\nUsually consists of 2 curves (original abnl curve and compensatory curve)\n\nWhat is it?\n\nAngles associated?
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Scoliosis\n\n>12 degrees for Dx\n\nsurgery for >45 degrees\n(screws in pedicles)
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23 yo football player in the ER with severe neck pain in superior neck following head to head collision with linebacker.\n\nPt presents with no neuro deficits on any kind.\n\nWhat is likely Dx?\n\nWhat to watch out for?\n\nTx?
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Jefferson Burst Fx\n(Atlas (C1) fracture)\n\nClassic is a 4 part atlas fracture: 2 part anterior ring and 2 part posterior ring\n(occipital condyles driven into atlas --> lateral masses moved outward)\n\n*actually 2 or 3 part more common\nposterior arch fracture with hyperextension\n\nWATCH OUT for vertebral artery involvement (may not present immediately)\n\nDifficult to see on lateral Xray\n(May show prevertebral soft tissue swelling anterior to C1. Pre-dentate space (distance between the anterior tubercle of C1 and the dens) may be widened to greater than 3 mm if there is damage to the transverse ligament)\nOpen-Mouth (odontoid) view is best\n(Classically there is bilateral, lateral offset of C1 on C2 )\nCT is diagnostic
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10 yo male presents with mild neck pain, numbness and tingling on the back of his head, and extreme vertigo if he leans his head a certain direction (also causes neck pain). No preceding trauma noted\nXray
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23 yo male\ndull pain just below knee all the time\nworse at night\nXray shows a round lucency, containing a dense sclerotic central nidus, surrounded by sclerotic bone\n\nWhat is it?\nTX?
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Osteoid Osteoma\n\nBENIGN\nusually 20s-30s\n<1.5 cm tumor surrounded by dense bone\nTibia and femur most often (vertebra)\nSeen well on CT and bone scan (radionuclide)\n\nTx: ASA or NSAID\nresolve spontaneously in approx 33 months
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20s and 30s; more in males\nMetaphysic of long bone – cartilage-capped bony spur “mushroom” on x-ray\nCan have multiple\nAsymptomatic\nBenign
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Osteochondroma
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20-30’s\nHalf occur in small tubular bones of hand and foot\nBenign cartilaginous growth in medullary cavity with central calcification
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Enchondroma
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Children and young adults\nLytic translucent area on metaphyseal side of growth plate\nBenign
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Cystic Bone Lesion\n(Solitary Unicameral Bone Cyst)
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Peaks in 30s\nPain, limited ROM\nDistal femur, proximal tibia, distal radius, sacrum\nLocal tenderness and swelling\nmaybe asymptomatic until pathological fracture\npresence of multinucleated giant cells\nBenign yet aggressive
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Giant Cell Tumors
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Lytic lesions > 2 cm & grow rapidly – painful (local swelling\nMost common in spine, sacrum, and long bones\nAggressive tumor forming osteoid\nBenign
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RF’s: 20s,Paget’s Disease\nMost common in distal femur\n(also upper tibia/humerous)\nAggressive Malignant\nX-ray: Codman’s triangle: characteristic periosteal elevation and spicule formation\nSolid "moth-eaten" or "sunburst" appearance on Xray
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Osteosarcoma
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Cancer of cartilage producing cells\nPelvis, femur, ribs, shoulder\nOften not painful\nMay present as a bump on bone felt through skin\nMay find d/t broken bone without significant trauma\nXRay-geographic, mildly expansile, lytic lesions, which may lead to mild cortical thinning.
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Chondrosarcoma\n\nPrimary: previous normal bone, pt over 40, expands into cortex to give pain\nSecondary: malignant degeneration of pre-existing cartilage tumor
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5-20 y/o\nMalignant\nIt can occur anywhere in the body, but most commonly in the pelvis and proximal long tubular bones, especially around the growth plates.\n“onion skinning” appearance on Xray
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Ewings Sarcoma
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Most common primary malignant tumor of bone in adults\n>40 y/o\nPresent with anorexia, anemia, renal failure\nPunched out lytic lesions on x-ray
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Multiple Myeloma
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5 yo male\nPain in knee following.\nPrevious Staph skin infection on same leg 1 week earlier\nChild is lethargic and has been observed with decreased activity\nPE: fever, tachycardic, swelling of distal femur (painful)\nLabs: Increased WBC, ESR, CRP\nRadiologic results showing a lytic center with a ring of sclerosis\n\nWhat is DX\nTx?
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Acute Osteomyelitis\n\nCulture of material taken from a bone biopsy is needed to identify the specific pathogen\n(Staph and Step A/B most common)\n\nTX:\nImmediate emperic Abx until culture ID\nSurgery for kids\n\nNOTE: Rarely crossed epiphyseal plate so rarely joint involvement (hip is exception)
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Result of Acute Osteomyelitis that was not adequately treated?\n\nProgression?\n\nTreatment Options?
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Chronic Osteomyelitis (too obvious?)\n\nInfection walled off by involcrum or fibrous tissue\nEach cavity contains piece of dead bone (sequestrium), bacteria, and granulation tissue\nCan remain quite for up to years or drain to outside tissue\nIncreased risk of cancer\n\nTx options:\nOpen Drainage\nSequestrectomy\nAmputation\nHyperbaric Oxygen (gas gangrene)
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5 yo with strep throat one month prior to visit\nrefuses to walk and hold hip in slightly flexed position\nPE: pain even with passive movement, red/hot/swollen hip area\nLabs: Inc WBC, ESR\n\nLikely Dx?\nTx?
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Septic Arthritis\n\nJoint aspiration for bacteria ID\n(aspirate will be pure pus)\nemperic abx until ID\nI&D if no improvement in 24-48 hrs
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23 yo female presents to the Family Med Clinic\nafter admitting elicit drug use she tells you she has gone into prostitution for $\nS/S - bad wrist pain / swelling, feverish, chills, body aches\nLabs: indicative of infn\nAspirate: Positive for G- bacteria\n\nLikely Dx?\nTx?
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Gonococcal Arthritis\n(most common septic arthritis in US)\n\nTx: admit for IV abx, treat other infxns
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48 yo female\nknee pain\nstiff in the morning but better while walking\nslightly limited ROM\n\nXray shows slight joint space narrowing, osteophytes on medial femur near condyle\n\nDx?\nTx?
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Osteoarthritis\n(most common form)\nwt bearing joints\ndestruction of articular cartilage\novergrowth of bone\n\nTx\nNSAIDS, wt loss, PT, Joint injections
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Age related decrease in bone mass caused by a reduction and disarray of the bone's microarcitecture organic callagenous matrix leading to increased bone fragility.\n\nWhat is this?\n\nHow is it diagnosed and what are the 3 major threshold levels?\n\nTypes and causes?
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Osteoporosis\n\nDx with a DEXA scan - measure BMD\nT-Score:\n> -1.0 = normal\n-1 to -2.5 = osteopenia "low bone mass"\n< -2.5 = osteoporosis\n\nType I - caused by postmenopause decline in estrogen\nHigh turnover (Inc bone resorption; nl formation) affects trabecular bone\n\nType II - caused by increasing age\nLow turnover (Inc bone resorption; decreased bone formation) both trabecular and cortical
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Osteoporosis Major Risk Factors
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Age >65 years\n\n\nVertebral compression fracture\nFragility fracture after age 40\nLow peak bone mass\nFamily history of osteoporotic fracture (especially maternal hip fracture)\nCaucasian or Asian female\nSystemic glucocorticoid therapy of >3 months duration (2nd most common cause of osteoporosis – causes increased resorption and decreased formation)\nMalabsorption syndrome\nPrimary hyperparathyroidism\nPropensity to fall\nOsteopenia apparent on x-ray\nHypogonadism\nEstrogen-related bone loss\nEarly menopause (before age 45), Oophorectomy, Amenorrhea
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Osteoporosis Minor Risk Factors
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Secondary medical disease - Rheumatoid arthritis or hyperthyroidism\nChronic anticonvulsant therapy\nLow dietary calcium intake\nSmoking\nExcessive alcohol or caffeine intake\nMinimal weight-bearing physical activity\nWeight <57kg\nWeight loss >10% of weight at age 25\nChronic heparin therapy
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Osteoporosis screening recommended for the following...
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Patients >65 years of age or\nPrevious fragility fracture or\nWeight <60kg or\nOne major or two minor risk factors\nPatients not meeting criteria should be reassessed every 1-2 years
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Collapse fracture of vertebral bodies in mid-dorsal region often indicative of Osteoporosis
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Dowager's Hump
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Chronic, widespread pain with characteristic multiple tender points and without objective signs of inflammation\n\nWhat is it?\n\nPopulation most commonly found?\n\nCharacteristics for Dx?\n\nTx?
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Fibromyalgia\n\nMore common in Female in 20s\nstrong association with psychiatric illness\n\nDx of exclusion\n(check thyroid)\n\nWidespread pain for at least 3 months in 4 quadrants of the body\nReproducible pain in 11 or 18 tender points\nOften chronic aching, sleep disturbance, HA, IBS, emotional stress\n\nTx:\nEducation, Exercise\nMeds - low does tricyclic antidepressants, NSAIDS\nNEVER opioids or steroids
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47 yo male\ncomes in with sore ankle\nsays he has been trying a new diet that has him fasting 2 days a week\nafter one day of fasting he had a booze bender and got real drunk\nwoke up with this sore ankle, getting worse\nworsening pain at night\n\nPE: erythematous, hot and swollen lateral ankle\nlimited ROM neuromuscular test all good\n\nBased on the Hx, what might be a possible cause of this wore ankle?\n\nOther RF's for this disorder
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Gout\n\nRFs:\nInjury\nSurgery\nFasting\nExcessive food/alcohol
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Form of acute arthritis caused by excessive uric acid in blood (overproduction or underexcretion)\n\nWhat is it?\n\nHow does the above casue joint pain?\nCommon joints?\n\nTx?
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Gout\n\nDeposits urates of sodium (crystals) in and around joints: Base of big toe\nDorsum of feet\nankles\nknees\nelbows\n\nSporadic attacks with pain-free intervals lasting mo-yrs\n\nTx:\nNSAIDS are mainstay (high dose w/tapering\nColchicine\nAllopurinol (prophylactic)\nAvoid foods that precipitate: anchoves, sardines, liver, food high in purines
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If a pt presents with all the symptoms of gout but blood comes back negative for high uric acid, what might you suspect is the cause?\n\nWhat is the mechanism of this?
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Pseudogout\n\nCrystals found in synovial fluid are Calcium Pyrophosphate Dihydrate - same inflam mechanism as urate crystals
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10 yo male comes in with mother\nMother says he has not been eating, has been lethargic and has developed a limp.\nBoy appears ill (flu-like symptoms)\nPE reveals painful knee, ankle and wrist joints with passive and active ROM\nFurther questions reveals that this is worse in the morning.\nRest of exam nl except for eye pain\n\nXrays are normal\nLabs: WBC, ESR, platelets, and rheumatoid factor all normal\n\nWhat is a possible cause of this patients pain?\nCause?\nOutlook?
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Juvenile Rheumatoid Arthritis\n(aka Juvenile Idiopathic Arthritis)\n(<16 yo)\n\nAutoimmune chronic disorder but rarely presents with a positive rheumatoid factor. Body produces cells that attack self possibly d/t viral induced or defective gene.\n\n3 Classifications:\nSystemic JRA involves joint swelling or pain, fevers, and rash. It is the least common category.\nPolyarticular JRA involves many joints. This form of JRA may turn into rheumatoid arthritis. It may involve large and small joints of the legs and arms, as well as the TMJ and cervical spine.\nPauciarticular JRA involves only a few joints, usually the hips, knees, or ankles.
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55 yo female\nComes in complaining of progressive morning stiffness for the past 6 months.\nPain/stiffness changes but is always symmetrical\nFatigue usually accompanies the stiffness and occasionally it feels like she is running a fever.\nPrevious doctor thought she just had some osteoarthritis but lately she thinks some "bumps" have appeared on her hands and her toes seem to be spreading out.\n\nWhat is at the top of your differential for this women.\n\nAssociated Symptoms
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Rheumatoid arthritis\n\nChronic systemic inflam disease characterized by inflammatory changes in the joints and related structures that result in crippling deformities.\nInhibited bone formation\nIncreased bone resorption\nEnzymes produced that destroy cartilage\nEventually destruction of articular cartilage and ankylosing of joints\n\nCan also effect:\nSkin - nodules\nLungs - fibrosis\nKidneys - amyloiditis\nHeart - Inc risk for atherosclerosis\nMany other organs
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Rheumatoid arthritis XRAY EXAMPLES ONLY
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Treatment of Rheumatoid Arthritis
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High Dose Salicylates/NSAIDs\nGluccocorticoids, Methotrexate, Gold\nPT, rest, exercise, heat\nSurgical removal of the synovium
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50 yo male complains of recent wt loss, malaise and fever. Thought it was a cold but no head symptoms and not getting better. Also has pain joints, testicles, and muscles of legs (worst in calf). Describes symptoms indicative of neuropathy. ROS also reveals N/V and abd pain with eating and Hepatitis B positive (dx 4 months ago)\n\nPE reveals some skin ulcers\n\nWhat is likely Dx?\n\nTx?
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Polyarteritis nodosa\n(vasculitis (arteritis) of medium sized vessels)\n\nInflam response within small-medium muscular arteries. Usually affects skin, periph nerves, mesenteric vessels, heart, and brain\n(can cause thrombosis/aneurysm)\n\nDX must have (at least 4 of...):\nWeight loss\nMyalgias, weakness, or leg tenderness\nMottled skin\nNeuropathy\nTesticular pain or tenderness\nElevated diastolic blood pressure\nElevated creatine or BUN\nHepatitis B virus\nBiopsy of artery showing presence of granulocytes in artery wall or\nBiopsy of symptomatic site (skin, nerve or muscle)\n\nTx: Prednisone (HD), Immunosuppressor (cyclophophamide)
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Name the two Idiopathic Inflammatory Myopathies.\n\nWhat do they have in common?\n\nWhat distinguishes them?\n\nTx?
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Polymyositis and Dermatomyositis\n\nBoth have (need 3-4 of these):\n(1) symmetric proximal muscle weakness; (2) elevated serum levels of muscle enzymes; (3) myopathic changes on electromyography; (4) characteristic muscle biopsy findings (necrosis, atrophy, perivascular inflam)\nUsually 5th and 6th decade (women 2x as much)\n\nPolymyositis\nCD8 cell-mediated necrosis\n**difficult lifting head off pillow or rising from chair\n\n\nDermatomyositis\nB-cell and CD4 immune complex mediated perifasicular vasculitis\nOtherwise, basically PM manifestations plus a cutaneous rash\nGrotton's papules/sign = patches/mottling of dorsal IP joints\nHeliotrope rash = rash over eyelids (+/- edema)\nShawl sign = erythematous rash over neck, upper chest, shoulders\nHigher incidence of malignancy\n\nTx: high dose steroids (long-term), methotrexate
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50 yo female\nhaving trouble combing hair, putting on a coat, and rising from a chair\ncomplains of profound pain/stiffness in proximal extrimities and neck for two months. Mostly in the morning, symmetrical muscle groups.\nAlso experiencing fever, wt loss, and malaise\n\nPE: tender muscles of proximal arms and legs but no neuropathy or weakness\n\nLabs: Inc ESR, and anemic\n\nWhat is likely Dx?\n\nTx?
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Polymyalgia Rheumatica\n(inflam, not autoimmune like polymyositis)\nclosely related to giant cell arteritis\n\nTx:\nrapid and lasting response to corticosteroids\n(15-20 mg/day)\nimprovement in 72 hours, taper over 1-2 years after 2-4 weeks
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After a trip to a cheap brothel in Cuba, Dan was treated for a series of STDs and GI infections (Chalmydia, Dysentery, Shigella, Salmonella, Yersinia, Campylobacter) two week ago.\nThe pus flow has diminished but now he is experiencing peripheral arthritis in his knees, ankles, and hips not to mention a second round of diarrhea and bloody stool\n\nPE: erythematous conjunctiva, hyperkaratotic skin lesions on palms and soles, oral sores, and last but not least small, painless ulcers (Balanitis circinata) on the glans and urethral meatus of his love muscle.\n\nHe has read through Current's and Epocrates but this one stumps even his vast knowledge of Clinical Medicine.\nWhat does he have and how do you tell him to treat it?
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Reactive Arthritis\n(Reiter's Syndrome)\n\nClinical Triad: Urethritis, Conjunctivitis, Arthritis, Mucocutaneous lesions.\n\nAlso HLA-B27\n\nTx:\nLocal - PT, intra-articular injections (steroids)\nSystemic - NSAIDs, corticosteroids, Abx for STDs\n\nOuch Dan...ouch
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Chronic inflammatory, autoimmune, multisystem disease characterized by production of autoantibodies to certain parts of the body causing multi-organ inflammation.\nMostly affects women (85%) in reproductive years (MC in blacks and asians)\n\nSome highlights:\nHLA-B8\nMalar (butterfly) rash\nArthritis\nNeuro (seizures, psychosis)\nRenal - Proteinurea, cellular casts (RBC, tubular, granular mix)\nHematologic - anemia, leukopenia, lymphopenia\n\nBottom Line - This is a BIG ONE...Going to have to study it on your own!!!
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Systemis Lupus Erythematosus\n(SLE)\nTOO MUCH FOR SLIDES...Study this one!!\n\nantigen-antibody complex trapped in capillaries of visceral structures\nautoantibody-mediated destruction of host cells\nHLA-B8\nEstrogen related (prepubertal and postmenopause women same incidence as men)\nAssociated with many drugs
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45 yo female\nComplains of arthralgia/arthritis and a new palpable purpura rash. She has seen several NPs and they have done some tests but she doesn't think they know what they are doing. They did discover diffuse interstitial lung disease on a Chest Xray and indicator of renal disease.\nLately she has noticed that she can't drink enough and her eyes and mouth are always dry. She can't even wear her contacts. Also says things taste funny.\n\nPE: Blepharitis, Dental decay, oral candidiasis, angular cheilitis, parotid gland enlargement.\n\nWhat is likely cause and what would you do for a difinitive Dx?
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Scleroderma Sjogren's Syndrome\nAutoimmune condition causing chronic dysfunction of the exocrine glands in many areas of the body.\n\nCharacterized by dry eyes (keratoconjunctivitis) and dry mouth (xerostomia)\n- lymphocytic infiltration of salivary glands\n\nCan be secondary (assoc w/ RA, SLE, DMY, HIV)\n\nSystemic manifestations:\nArthralgias/arthritis\nSubclinical diffuse interstitial lung disease\nRenal disease\nPalpable purpura\nSystemic vasculitis\nLymphoma – common w/severe exocrine dysfxn\n\nDifinitive Dx (SSASSS)\nSchirmer test (assess tear flow)\nSlit lamp exam\nAutoantibodies\nSalivary flow measurements\nSialography\nSalivary gland biopsy: gold standard
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Scleroderma Sjogren's Syndrome\nTreatment?
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Good dental hygiene\nartificial tears or punctal occlusion\nadequate hydration\nNystatin/clotrimazole for oral candidiasis
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50 yo male\nDeep pain of the pelvis and femur\nHe also says he knows it's weird but thinks his hat size has increased lately and has had a dull headache for 2-3 days\n\nPE: Kyphosis, leg and thigh are very warm to the touch, bowing of the tibia observed\n\nLabs: Elevated serum Alk Phos and urinary hydroxyproline\n\nXray
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Paget's Disease\n\n(Unknown Cause)Metabolic skeletal disease with excessive bone destruction and repair leading to chronic inflammation of bones resulting in thickening and softening of bones and bowing of long bones\n- increased osteoclastic activity --> increased bone resorption\n- osteoblastic activity increased to compensate but new bone is structurally abnormal\n\nImaging Dx:\nBone scan - useful to dx and to determine extent\nInitial lesion may be destructive and radioluscent\nInvolved bones are expanded with cortical thickening and denser than normal\nMultiple fissure fractures in long bones
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Paget's Disease Treatment?
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Kind of like osteoporosis\n\nSymptomatic\nCalcitonin\nBisphosphonates\nAdequate Ca and Vit D to prevent hyperparathyroidism
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Gait described when kid spends less time on painful limb (puts foot down and it hurts so much that he lifts it back up)
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Antalgic Gait
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Gait seen with stroke cerebral palsy, muscular dystrophy, and stroke.\nPt not able to lift toes so they compensate by swinging their whole leg out as they walk.
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Circumduction Gait
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"Toe to Heel"\n(instead of heel to toe)\nGait seen with neurosyphilis
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Equinas Gait
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Gait caused by weak abductors (gluts) and unstable pelvis.\nCan be d/t cerebral palsy, congenital hip dysplasia just to name a few.
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Abductor Lurch\n(Trendelenberg Gait)
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At what age does toe walking become abnormal
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Toe walking that persists past two years old needs to be looked at
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Most common cause of hip pain in toddlers.\nusually preceded by URI\nLow grade temp but not septic\nAntalgic Gait (worse in AM)\nPE reveals pain in anteromedial aspect of hip and thigh\nNormal Xray\nESR may be slightly elevated\n\nWhat is this and what if the phrase that helps you remember it?
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Transient Synovitis\n"Runny Hip"\n\nTx with bedrest, self-limiting, NSAIDs
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Fracture that cannot be detected by radiographic standard exam until several weeks later\n\nWhere do they most often occur?\n\nHow to find acutely?
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Occult Fracture\n\nRibs, Tibia, Metatarsals, Hip, and Navicular\n(pain after trauma and possibly soft tissue edema)\n\nCan use MRI or bone scan to confirm suspected occult fracture
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Febrile sick kid (16 months old) comes in with acute onset of pain and limp. His hip is held in flexion, abduction, and external rotated (frog-leg) when he is not moving.\nHip joint is swollen and warm\n\nLabs: elevated WBC with left shift, elevated ESR,\nAspiration of hip reveals cloudy joint fluid\n\nXray - possible slight bone resorption at hip joint\n\nWhat is this?\n\nWhat is the common cause?\n\nTX?
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Septic Arthritis\n\nStaph Aureus, Group B Strep (<4mo), Kingella kingae, MRSA\n\nTx: IV Abx (nafcillin, oxacillin, 3G ceph)\nSurgery if not immediate improvement
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2 yo male\nRefuses to walk but NO limp.\nCannot not tell you specifically where it hurts\nOnly abnormality on PE is limited passive hyperextension of spine when prone, splinting of paraspinous muscles and pain when palpated.\n\nLabs: ESR nl, no radiologic findings on XRAY, Bone scan however did show some extra absorption in area of spinal tenderness.\n\nWhat is this?\n\nTx?
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Discitis (Infectious Spondylitis)\nage 2-6\nlow grade inflam process usually lumbar intervert disk\nMC culture is S. Aureus\n\nTx:\nmany times self-limited with spontaneous improvement\nelevated ESR should prob be aspirated and cultured\nBest just to treat all with empiric anti-Staph abx PO
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INFO SLIDE
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What is wrong with this Xray?
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2 yo male\nPainless limp\nLate walking\nFirst child\n\nHx reveals born in Japan, breech presentation at birth, and oligohydramnios during term.\n\nPE: asymmetrical gluteal folds, and difference in limb length\n\nWhat do you suspect?\n\nWhat would you expect to see on an Xray?\n\nTx?
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Developmental Hip Dysplasia\n\n\ndislocation of acetabulum\ndegeneration or lack of formation of head of acetabulum if severe\n(can also Dx with US)\n\nMay be able to treat with bracing. May require surgery if severe\n(WANT TO CATCH EARLY)
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Some physical tests used to test for hip dysplasia
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Galeazzi Test - child supine, knees bent with feet flat on table. Compare knee height to assess limb length\n\nPassive hip abduction - listen, feel\n\nBarlow Test - hip adducted and gently posteriorly and laterally. Feel for "pistoning" - femoral head subluxing over posterior rim of acetabulum\n\nOrtolani - hip is abducted and femur lifted. Feel for sensation of hip slipping back into acetabulum
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6 yo male\nwas walking fine and sudenly won't walk (antalgic gait)\nlimited internal rotation and extension of hip\nESR slightly elevated\n\nDisorder characterized by idiopathic avascular osteonecrosis of the capital femoral epiphysis of the femoral head leading to an interruption of the blood supply of the head of the femur close to the hip joint. Males > Females (age 2-12)\n\nWhat is this?\n\nWhat two views do you need?
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Legg-Calve Perthes\n\nNeed AP and frog leg view\n\nCrescent sign (early)\n\nFragmentation (Late)
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INFO - Legg-Calve Perthes\n\n\nTreatment\nnonsurgical or surgical containment of femoral head
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Name 4 Overuse Syndromes and where they occur
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1. Stress Fractures - tibia, metatarsals common\n2. Apophysitis - stress/inflam at insertion of large tendon or muscle\n- Osgood-Schlatter - patella\n- Sever's Disease - Calcaneal apohysitis\n3. Patellafemoral Plain Syndrome\n4. Patella Tendonitis (Jumper's Knee)
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4 yo chubby black boy comes in with his chubby mom complaining of pain in his groin and leg.\nPresents with antalgic gait\nSays pain is achy and getting worse\nHurts most when he runs but hurts all the time\n\nWhat do you expect?\nDiagnostics you need?\nComplications?
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Slipped Capital Femoral Epiphysis\n\nDisplacement of the femoral head from femoral neck. (always a posterior slip)\n\nNeed an AP and Frog Leg Xray\n(Graded I-III)\n\nComplications:\nAvascular Necrosis\nDegenerative Arthritis\nChondrolysis
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Types of slipped capital femoral epiphysis based on how it happened?\n\nRisk factors?
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Chronic (60%) - ache in hip, to knee, antalgic gait but still walking\nAcute (10-15%) - Usually trauma related, severe pain and limping (often immobile)\n\n**20% bilateral slip\n\n\nRFs: overweight kids, steroids, ETOH, post trauma, idiopathic, chemo and radiation are common causes.
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Categories of Slipped Capital Femoral Epyphisis based on amount of slip
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Type I is less than 33% displacement\nType II is 33-50% displacement\nType III is greater than 50% displacement.
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