podiatry test 1 2005 boards part 2

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  1. Pyoderma gangrenosum
    Pyoderma gangrenosum is thought to be an autoimmune disease and can be caused by many systemic diseases, although the exact etiology isunknown. It is associated with inflammatory bowel diseases such as ulcerative colitis and Crohn’sdisease.
  2. Sarcoidosis
    • Sarcoidosis-chronic, progressive, systemic granulomatous disease of unknown etiology, affecting any organ system, a common cause of pulmonary hilar adenopathy, histologically showing noncaseating epithel ioid cell tubercles (tuberculinnegative usually).
    • Sarcoidosis is a systemic granulomatous disease involving theskin, lungs, lymph nodes, and viscera. 10% of patients havebone involvement. Children are rarely affected.Radiographically dx is made with CXR; in the extremities themiddle and distal phalanges can show cyst-like punched outlesions in the cortex.
    • Sarcoidosis:a. Is a multisystem, multiorgan disorder of a autoimmune etiology and withassociated immunologic abnormalities, typified by the development ofnoncaseating granulomas in various organsb. Increased observance of HLA B8 antigenc. Sarcoid arthropathy occurs 3-15%, and presents as an acute polyarthritisd. This disease can affect the calcaneus with the symptom of heel pain.Radiographically there can be cortical defects or cyst formation
    • Erythema nodosum and subcutaneous noduleformation are common in the latter stages ofsarcoidosis. The presence of shortness of breath andnonproductive cough are also manifestations ofsarcoidosis.
    • GRAIN:GammaglobulinemiaRheumatoid arthritisACE increaseInterstitial fibrosisNoncaseating granulomas
  3. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
    • SYSTEMIC LUPUS ERYTHEMATOSUS(SLE)DEFINITIONA chronic, remitting, relapsing, inflammatory, and often febrile, multisystemicdisorder of connective tissue, acute or insidious in onset.Drug induced lupus may be caused by: Procainamide, Hydralazine,Chlorpromazine, Isoniazid, Penicillamine, GriseofulvinSIGNS/SYMPTOMS-age of onset 15-35 yrs-joint pain in 90% of patients(an early manifestation)-primarily small joints of the hands and feet-mainly in young women(10:1)-more common in blacks-fever(90% of patients)-abdominal pains-butterfly rash-skin lesions in sun exposed areas(photosensitivity)-fatigue, weight loss, and anorexia-Raynaud's phenomenon-alopecia-vision problems-proximal nail fold telangiectasis-renal, cardiac, splenic, and pulmonary problemsDIAGNOSIS-increased sed rate-(+)ANA(antinuclear antibody test)-antibodies to double-stranded DNA-decreased hemoglobin, WBC, and plateletsTREATMENT-symptomaticsteroidsantimalarials(chloroquine)immunosuppressantsavoid sunlight
    • I'M DAMN SHARP:1mmunoglo bulins(anti-dsDNA, auti-Sm,antiphospholipid)Malar rashDiscoid rashAntinuclear antibodyMucositis (oropharyngealulcers)Neurologic disordersSerositis (pleuritis,pericarditis)Hematologic disordersArthritisRenal disordersPhotosensitivity
    • Patients who take procainamide for prolongedperiods often develop anticardiolipin antibodies aswell as anti-DNA and anti-histone antibodies. Druginducedsystemic lupus erythematosus is rare andusually subsides once the medication is discontinued.
  4. PSORIATIC ARTHRITIS
    • PSORIATIC ARTHRITIS
    • DESCRIPTIONAn inflammatory arthritis seen in approximately 7% of patients with dermatologicalpsoriasis. Usually peripheral joints are involved, but theremay be associated back pain. The skin disease typically precedes thejoint disease, however arthritis can occasionally precede the psoriasisby months to years.SIGNS AND SYMPTOMS-asymmetrical arthritis of large and small(especially the DIPJs) joints,including the sacroiliac and the spine-male=female-peak age ~40yrs-associated psoriatic skin and nail lesions(pitting)DIAGNOSIS-(+)HLA-B27-radiographic- "Pencil in cup" deformity"whittling" of the distal tufts of the phalangesTREATMENT-NSAIDS
  5. Psoriasis
    Psoriasis-a common, chronic,inflammatory, dermatitis-affects 2% of thepopulation, whites > blacks-onset is usually between10-40 yrs-usually a positive familyhistory-typical course is chronicremission and recurrence-mostly a cosmetic problemunless associated with jointpain(psoriatic arthritis)-severity increases duringcold weatherLOCATION OF LESIONS-usually involves the scalp, extensor surfaces of the extremities(esp.knees and elbows), the back and the buttockPRESENTATION-lesions are well circumscribed, erythematous "salmon pink" papules orplaques covered with silvery shiny scales-lesions are not pruritic and heal without scaring-Auspitz phenomenon-removal of silvery scales results in pinpointbleeding-pitting of the finger and toenails seen in 25% ofpatientsTREATMENT-keratolytics-topical corticosteroids-exposure to sunlight generallyhelps heal lesions, howeveroccasionally sunburn canexacerbate the condition-Methotrexate is used to treatsevere resistant cases
  6. Which of the following ligaments is mostcommonly damaged in an inversion sprain of theankle?
    • Most inversion ankle sprain injuries occur when thefoot is plantarflexed and inverted at the ankle joint,which results in instability. The anterior talofibularligament is the first ligament of the lateral ankle areato be maximally stretched and torn with this type ofinjury.
    • STRESS INVERSION(TALAR TILT)-patient supine or sitting in chair, internally rotate foot 15° from 90°(tobring malleoli parallel to film. Stabilize leg with one hand and maximallyinvert foot with other hand)-examiner wears lead gloves-stabilize lower leg with onehand while forcefully invertingfoot with other hand-central ray at ankle joint-performed following ankleinversion sprains, may need toanesthetize foot(commonperoneal block) for pain reliefand to relax foot-assess lateral ligamentous injury-(+) test is a talar tilt greater than 4° ofinversion
    • Position of foot at time of injuryInversion sprain with foot dorsiflexed-calcaneofibular ligament is most likely damaged-rupture of this ligament may also tear the peroneal tendon sheathInversion sprain with foot plantarflexed-account for 95% of ankle sprains-talofibular ligament is most likely damaged
  7. Eversion sprains
    -Eversion sprains are very rareSchoolfied's ProcedureThe deltoid ligament is detached from the tibia, the foot ismaximally inverted and the ligament is reattached superiorly tothe dettachment site. The deltoid ligament is effectivelyadvanced.DuVries ProcedureA large cruciate form incision is made in the deltoid ligament andthen sutured back together. The theory behind the procedure isthat the resultant scar tissue will effectively reinforce andstabilize the medial ankle.Wittberger and Mallory's ProcedureThe tibialis posterior tendon is split longitudinally down to it'sinsertion. Half the tendon is dettached proximally and passedinferiorly to superiorly throught a drill hole in the distal tibia andsutured back on itself with the foot forcibly inverted.
  8. Freiberg's Infraction
    • Freiberg's Infraction
    • -osteochondrosis of the metatarsal head
    • -the second metatarsal head is most frequently involved followed by the 3rd, 4th, and then 5th
    • -more common in girls
    • -usually occurs between ages 10-18yrs, but can occur during adult life
    • -radiographic eval-sclerosis and fragmentation of the metatarsal head with flattening of the articular surface
    • Symptoms-pain on ROM of the affected MPJ- local tenderness and swelling-generalized thickening at the MPJ
    • Treatment-conservative-metatarsal pads, short leg casts, stiff post-op shoe
    • -surgical-aimed at removing any bony lipping from the perimeter of the metatarsal head, when DJD is severe an implant may be indicated
    • Freiberg's infraction-osteochondritis that usually affects the second metatarsal head,more common in females <13 years of age, resulting in flattening and widening of the metatarsal head, and attributed to traumatic disruption of the physeal blood supply.
    • Freiberg’s infraction is a true osteonecrosis of thesecond metatarsal head, with the inflammationcausing the initial joint space widening. The resultant osteoarthritis causes the subchondralsclerosis commonly seen.
    • > FreibergFreiberg AH: Infraction of the second metatarsal bone. Surg GynecoI19:191, 1914.Also known as osteochondrosis of the metatarsal head or avascular (aseptic) necrosis of thebone,' most commonly affects the r metatarsal.
    • Type I: no DJD; articular cartilage intact
    • Type II: periarticular spurs; articular cartilage intact
    • Type ill: severe DJD; loss of articular cartilage
    • Type IV: epiphyseal dysplasia: multiple head involvement
    • Etiology1. Trauma, or trauma followed by fracture2. Ischemia3. Prominent plantar metatarsal head with excessive loading, with compromise to thesubchondral bone circulation4. Often appears after age 13, affecting women 3x more frequently than menSigns and symptoms1. Pain in the MTPJ, usually dorsal; either sharp, dull, or aching in character2. Edema with increased activity3. Limitation of motion of the involved digit and MTPJ4. Palpable irregularities may be present dorsally5. Distal distraction of the toe will cause pain6. Adjacent MTPJ hyperkeratoses may be present as the involved metatarsal bears lessweightX-ray evaluation1. Initial findings include joint space widening 3-6 weeks after the onset of symptoms2. Then followed by increased density of subchondral bone3. As the disorder progresses, a zone of rarefaction develops surrounded by a sclerotic rim4. With time, the epiphyseal bone weakens and collapses with the formation of spicules andloose bodies .5. Flattening of metatarsal head with osteophytic lipping6. Joint narrowing7. Peripheral soft tissue swelling8. Sclerotic bone margins2.STreatment1. Conservative: directed toward preventing further damage and displacement of the MTPJ:casting and cortisone shots, followed by orthoses2. Surgical: later stagesa. Implant arthroplasty if symptoms are due to joint arthritisb. Metatarsal head remodeling: must preserve digital alignment - usepostoperative splint for 3 monthsc. Smillie advocates bone grafts to restore the contour of the metatarsal head byinserting a cancellous graft, good for stages I-ill3. Rotational osteotomies (Gauthier and Elbaz): rotate the lower aspect of the metatarsalhead dorsally after the section of damage cartilage has been excised. This allows theplantar cartilage to articulate with the proximal phalanx.
  9. Name the avascular necroses
    • Renandier Tibial sesamoid
    • Trevor Fibular sesamoid
    • Theiman Phalanges
    • Freiberg Metatarsal heads
    • Iselen 5th metatarsal base
    • Buschke Cuneiforms
    • Kohler Navicular
    • Lance Cuboid
    • Diaz Talus
    • Severe Calcaneus
    • Blount Proximal, medial tibial epiphysis
    • Osgood-Schlatter Tibial tuberosity
    • Legg-Calve-Perthes Femoral epiphysis
  10. MULTIPLE SCLEROSIS
    • MULTIPLE SCLEROSIS-a chronic inflammatory disease characterized by patchy demyelination of the CNS-the incident rises steadily from the teens to age 35, and declines gradually thereafter-the clinical course is highly variable and unpredictable, but generally follows one of relapsing and remitting-male to female ratio is 1:2
    • CAUSE-thought to be autoimmune
    • SIGNS AND SYMPTOMS-initially patients have discrete motor, sensory, cerebellar or visual attacks that come on over a 1-2 week period and resolve over a 4-8week period-there may be only partial recovery or no recovery from an attack-other symptoms include: ocular palsy, fatigability/weakness, clumsiness,bladder dysfunctions, spasticity-Charcot's triad-nystagmus, intention tremor, scanning speech(syllables are separated by pauses)-excess heat may accentuate symptoms(avoid hot baths and jacuzzis)
    • DIAGNOSIS-MRI-spinal tap-increased DTR's and (+) Babinski
    • TREATMENT-symptomatic(corticosteroid)
  11. charcot foot
    • charcot foot-a destructive arthropathy resulting from impaired pain perception and increased bone blood flow from reflex vasodilation-with increased bone blood flow the bone becomes washed out and weak, and with impaired deep pain sensation on proprioception small periarticular fractures go unnoticed until the entire joint is destroyed-diabetes is the leading cause of charcot foot-majority of charcot joint are the result of trauma and impaired sensation caused by neuropathy-male to female ratio is equal-B/L 30% of cases-painless swelling is the hallmark sign of charcot foot, however about half of the patients present with a chief complaint of pain-most feet with a charcot joint involve the midfoot
    • CAUSE diabetes, alcoholism, syphilis, Hansen's dz, syringomyelia, cerebral palsy, hereditary insensativity to pain, myelodysplasia, poliomyelitis,spina bifida, meningomyelocele, spinal or peripheral nerve injury
    • STAGES
    • Stage I (Fragmentation)-acute inflammatory process-foot is hyperemic, swollen, red, and hot-dissolution, fragmentation, and dislocation
    • Stage II (Coalescence)-beginning of the reparative process-edema, warmth and redness begins to disminish-radiographically there are signs of new bone formation
    • Stage III (Remodeling)-marked by bony consolidation and healing-residual bony deformity is common most notably collapse of the longitudinal arch resulting in the classic "rocker-bottom" foot-bony protuberences are clinically important because they may develop sites for future neuropathic pressure ulcers
    • TREATMENT-rest, elevation, and cast immobilization to prevent further bone destruction-once bony consolidation has begun and the foot has stabilized, a custom molded accommodative insert is indicated or a pair of custom molded shoes depending on the extent of the deformity-surgery on the charcot foot is aimed at either removing bony prominences or arthrodesis to realign and stabilize the architecture of the foot
  12. stress fracture
    • -bone scanning allows early diagnosis of a stress fracture(7 hours S/P)
    • fracture in a normal bone due to cyclic loading on a bone-95% occur in the lower extremity, most notably the neck of the 2nd metatarsal-may take 14-21 days to present radiographically after a bony callus has developed. If x-rays are inconclusive a three phase technetium bonescan may be positive as early as 2-8 days after onset of symptoms
    • Stress fractures of the metatarsals respond well to a gel-cast and surgical shoe, and digital fractures can be managed with gauze dressings and a surgical shoe.
    • Metatarsal stress fracture-this is also known as a march or fatigue fracture, and develops secondary to cumulative that surpasses the bone's ability to respond to repetitive load. This is frequently observed when a person initiates a new exercise program, undergoes basic training in the military (march fracture). suffers with a specific biomechanical abnormality wherein there is loss of adjacent metatarsal support (hypermobile first ray dumping force on the second ray, or following adjacent metatarsal fracture or osteotomy). The onset of pain is usually gradual, but exacerbated by recent increased activity. The pain is localized to the affected metatarsal, with associated edema and local heat. Stress fracture usually localizes to the metatarsal neck, and most commonly involves one of the intermediate rays. The differential diagnosis includes neuroma, MTPJ enthesitis, arthritis, and extensor tenosynovitis. Charcot fractures, pathological fracture, and osteoporosis should also be considered. Radiographic findings initially may reveal a small cortical break at site of maximum clinical tenderness. Periosteal reaction usually develops at the stress fracture site, and may become evident at about 10 days or longer from onset of pain. Repeat radiographs at 2-3 weeks after the onset of pain may be needed to confirm diagnosis. A bone scan or MRI should be obtained if standard films are equivocal.Treatment of metatarsal stress fracture entails a gel-cast and surgical shoe or a removable cast-boot for 3-5 weeks, and orthoses may be useful to address biomechanical abnormalities thereafter.
    • Also called: March fx, Hairline fx, Fatigue fx, Insufficiency fx, Deutschlander’s dz, Bone exhaustion,
    • What will a stress fracture show up as on MRI?T1 Linear zone of decreased signal intensity surrounded by a less defined area of signalintensityT2 Linear zone of decreased signal intensity surrounded by an increased signal intensity dueto edemaSTIR Increased signal intensity because fatty bone marrow is suppressed
  13. OSTEOID OSTEOMA
    OSTEOID OSTEOMA-benign bone forming tumor-occurs in the 1st and 2nd decade of life-M>F-occurs in the diaphysis of long bones(esp. tibia and femur) and may be located in the cortex, medullary canal, or parosteally. Occurs in the foot5-8% of the time and the talus and calcaneus are most commonly involved-symptoms are pain, worse at night, relieved by aspirin-radiographic appearance: oval or round radiolucent area, measuring <1cm in diameter surrounded by a zone of uniform bone sclerosis


    • What are bone tumors typically located?
    • Epiphysis Chondroblastoma Giant cell tumor (forms in metaphysis)Metaphysis Enchondroma (also diaphyseal) Osteochondroma Nonossifying fibroma Unicameral bone cyst Aneurysmal bone cyst Giant cell tumor (extends into epiphysis) Medullary osteosarcoma Parosteal osteosarcoma Chondrosarcoma
    • Diaphysis Osteoid osteoma Osteoblastoma Enchondroma (also metaphyseal) Ewings sarcoma (also meta-diaphysis) Periosteal osteosarcoma
    • Centrally located Enchondroma Unicameral bone cystEccentrically located within medullary canal Giant cell tumor Chondrosarcoma OsteosarcomaCortical Osteoid osteoma Nonossifying fibroma
  14. OSTEOBLASTOMA
    OSTEOBLASTOMA ( giant osteoid osteoma, osteogenic fibroma)-rapidly growing benign bone forming tumor that can become malignant-occurs in the 2nd and 3rd decade of life-M>F-most commonly seen in the spine, skull and the diaphysis of long bones-mild pain worse at night not relieved by aspirin-radiographic appearance: well circumscribed, expansile, osteolytic lesion(> 1cm) with areas of calcifications and cortical thinning. Resembles and was once considered a large osteoid osteoma.

    What are bone tumors typically located?Epiphysis Chondroblastoma Giant cell tumor (forms in metaphysis)Metaphysis Enchondroma (also diaphyseal) Osteochondroma Nonossifying fibroma Unicameral bone cyst Aneurysmal bone cyst Giant cell tumor (extends into epiphysis) Medullary osteosarcoma Parosteal osteosarcoma ChondrosarcomaDiaphysis Osteoid osteoma Osteoblastoma Enchondroma (also metaphyseal) Ewings sarcoma (also meta-diaphysis) Periosteal osteosarcomaCentrally located Enchondroma Unicameral bone cystEccentrically located within medullary canal Giant cell tumor Chondrosarcoma OsteosarcomaCortical Osteoid osteoma Nonossifying fibromaCROZER-KEYSTONE RESIDENCY MANUAL – SECOND EDITION 93Periosteal Osteochondroma Periosteal osteosarcoma
  15. CHONDROBLASTOMA
    • CHONDROBLASTOMA-benign cartilage forming tumor-occurs during the 2nd and 3rd decade of life-M>F-located in the epiphysis of long tubular bones (esp. femur, tibia, and humerus) when found in the foot it's usually in the talus or calcaneus-symptoms include pain, swelling, and tenderness-radiographic appearance: well defined round or oval osteolytic lesion,eccentrically or centrally located that may have a thin sclerotic border. Secondary changes such as hemorrhagic foci and cystic blood spaces may mimic an aneurysmal bone cyst.
    • Chondroblastoma - usually observed in 15 to 30 year-old age group, commonly localized to the calcaneus or epiphysis of a long bone, with a well-defined osteolytic appearance.
    • Name benign bone tumors of the foot(FOG MACHINES)F – fibrous dysplasiaO – osteochondromaG – giant cell tumorM – myelomaA – aneurysmal bone cystC – chondroblastoma, chondromyxoid fibroma, clear cellH – hemangiomaI – infectionN – non-ossifying fibromaE – eosinophillic granuloma, enchondroma, epidermal inclusion cystS – solitary bone cyst
  16. Name benign bone tumors of the foot
    Name benign bone tumors of the foot(FOG MACHINES)F – fibrous dysplasiaO – osteochondromaG – giant cell tumorM – myelomaA – aneurysmal bone cystC – chondroblastoma, chondromyxoid fibroma, clear cellH – hemangiomaI – infectionN – non-ossifying fibromaE – eosinophillic granuloma, enchondroma, epidermal inclusion cystS – solitary bone cyst
  17. CHONDROMYXOID FIBROMA
    • CHONDROMYXOID FIBROMA-benign cartilage forming tumor-occurs during the 2nd and 3rd decade of life-MSF-occurs in the metaphysis of long tubular bones(esp. tibia)-symptoms include slowly progressing pain, tenderness, and swelling-radiographic appearance: radiolucent lesions, some appearing lobulated or bubbly with well-developed sclerotic borders
    • chondromyxoid fibroma - coarse, and thick trabeculae
    • Chondromyxoid Fibroma (CF) is a very rare tumor that is metaphyseal, geographic, and multiloculated. It occurs in all ages and is seen in the LE. Pain is “vague.” It may extend all the way to the physis.

    Name benign bone tumors of the foot(FOG MACHINES)F – fibrous dysplasiaO – osteochondromaG – giant cell tumorM – myelomaA – aneurysmal bone cystC – chondroblastoma, chondromyxoid fibroma, clear cellH – hemangiomaI – infectionN – non-ossifying fibromaE – eosinophillic granuloma, enchondroma, epidermal inclusion cystS – solitary bone cyst
  18. Name the malignant bone tumors of the foot
    • Name the malignant bone tumors of the foot (FEM COP)
    • Fibrosarcoma
    • Ewings sarcoma
    • Multiple myeloma
    • Chondrosarcoma
    • Osteosarcoma
    • Periosteal sarcoma
  19. nsaids
    • What therapeutic effects are seen with most NSAIDs?Analgesic, anti-pyretic, and anti-inflammatory
    • What pathway do NSAIDs work on?Cyclooxygenase (COX)NSAIDs nonselectively inhibit both COX-1 and COX-2 pathways
    • What is the most common side effect of NSAIDs?GI disturbance (except with COX-2 inhibitors, because COX-1 protects the stomach lining)
    • What is the only FDA-approved COX-2 inhibitor?celecoxib (Celebrex)Others were withdrawn due to increased risk of heart attack and stroke
    • Which NSAIDs only have anti-inflammatory effects?indomethacin, tolmetin
    • Do NSAIDs decrease joint destruction?No, they only decrease inflammation
    • Do NSAIDs affect bone healing?NSAIDs and COX-2 inhibitors may inhibit bone healing via their anti-inflammatory effects
    • What NSAID causes irreversible inhibition of platelet aggregation?aspirin
    • What NSAID does not inhibit platelet aggregation?The COX-2 inhibitor, Celebrex
    • What is the only IV NSAID?ketorolac (Toradol)
    • Which NSAID is often given during surgery or immediately post-op to decrease pain and inflammation?Toradol 30 mg IV
    • What are the NSAIDs with the least nephrotoxicity?Celebrex, Relafen, Lodine
    • What is the effect of NSAIDs on asthma?Can increase symptoms of asthma
    • What are the safest NSAIDs for a patient with asthma?Diclofenac, ketoprofen
    • Which NSAIDs treat collagen vascular disease?Ibuprofen, sulindac, tolmetin
    • Which NSAIDs are not renally cleared?Indomethacin, sulindac
    • What are the cardiovascular effects of NSAIDs?Can cause vasoconstriction and increase blood pressure
    • Which NSAIDs have the least cardiovascular effects?Diclofenac, ketoprofen
    • Which NSAIDs are the most hepatotoxic?Ibuprofen, naproxen, diclofenac
    • What should be given for an indomethacin overdose?Benadryl – decreases serotonin and histamine release
    • What is Arthrotec?diclofenac/misoprostol – an NSAID with protection for the stomach
    • What is the anti-inflammatory dose of ibuprofen?1200-3200 mg/day in divided doses
    • What NSAIDS work on both the lipooxygenase and cyclooxygenase pathways?Ketoprofen and diclofenac
    • What is the difference between Cataflam and Voltaren?Cataflam is diclofenac potassium and has an immediate releaseVoltaren is diclofenac sodium and has a delayed release
    • What are the only pro-drugs for NSAIDs?nabumetone and sulindac
    • What is the only nonacidic NSAID?nabumetone
    • Which NSAIDs have fewer pulmonary problems?ketoprofen and diclofenac
    • What are some once a day NSAIDs?celecoxib (Celebrex), piroxicam (Feldene), oxaprozin (Daypro), nabumetone (Relafen), others
    • What drugs do NSAIDs interact with and what are the effects?Coumadin – increases action of CoumadinSulfonylureas – increases action of sulfonylureasCorticosteroids – increases GI riskAnti-epileptics – increases anti-epileptic toxicityAntihypertensives – antagonizes antihypertensive medsDigoxin – increases digoxin’s effectMethotrexate – decreases methotrexate’s clearanceLithium – decreases lithium’s clearanceProbenecid – increases concentration of NSAIDs

    NSAIDs-action: anti-inflammatory, antipyretic, analgesia-blocks production of prostaglandins by inhibiting cyclo-oxygenase-ASA-irreversibly inhibits cyclo-oxygenase all other NSAID's reversibly inhibit cyclo-oxygenase-major side affect is increased bleeding tendency, contraindicated inpatients with stomach ulcers-may be taken with food to reduce Gl irritation-may precipitate asthmatic attack by diverting the arachidonic acid pathway to produce bronchoconstrictor mediators(leukotrienes)
  20. ANTICOAGULANTS
    • ANTICOAGULANTS
    • Heparin
    • Full dose(treatment for DVT)
    • IV ADMINISTRATION-get baseline PTT-5,000-10,000u IV bolus, then 750-1,500u/hr IV-monitor PTT q8h(maintain PTT at V/z-2 above control)
    • SubQ ADMINISTRATION-get baseline PTT-5,000u IV bolus and 10,000-20,OOOu subQ, then 8,000-10,OOOusubQ q8h or 15,000-20,OOOu subQ BID-monitor PTT q8h(maintain PTT at VA-2 above control)
    • Mini dose(prophylaxis for DVT)-5,OOOu subQ bid-surgical patients-give 1 hour pre-op followed by bid dose until ambulatory
    • Warfarin(Coumadin, Panwarfin)loading dose 10mg PO qd x2-4 days maintenance dose 2-7.5mg PO qd maintain PT about 2-2.5 times normal treat 1st DVT episode for 3 months-Coumadin requires 16-48hrs to cause a measurable change in the PT,therefore begin Tx 2 days before discontinuing Heparin
  21. INSULIN
    • INSULIN
    • Rapid-Regular(Humulin R) 10-30min 15-30min 30-60min IV0.5-1hr 2-4hrs 6-8hrs SC-
    • Semilente 0.5-2hr 2-8hrs 10-15hrs SC
    • Intermediate-NPH(Humulin N) 1-4hrs 6-12hrs 18-24hrs SC-Lente(Humulin L) 1-4hrs 6-12hrs 18-24hrs SC
    • Long Acting-Protamine zinc(PZI) 4-8hrs 14-24hrs 36+ SC-Ultralente(Humulin U) 4-8hrs 18-24hrs 36+ SC

    • INSULIN SHOCK-hypoglycemia(plasma glucose of <50mg/dL)
    • Causes-overdose of insulin-skipped meal in an insulin dependent diabetic-strenuous exercise in an insulin dependent diabetic
    • Symptoms-Tachycardia-hunger-increased irritability(nervousness)-sweating and clammy(fainting)-mental confusion and bizarre behavior-seizures-mild hypothermia-coma
    • Treatment If conscious-give fruit juice(orange juice)If unconscious-IV 50% dextrose(50ml at 10ml/min)-most patients regain consciousness in 5-10 minutes

    • Islet of Langerhans
    • A type of tissue found scattered throughout the pancreas involved in glucose metabolism. The Islet of Langerhans contain alpha, beta, and delta cells. The beta cells compose about 60% of all the cells and secrete Insulin.

    • Somogyi effect
    • A rebound phenomenon occuring in diabetics who take too much insulinin the evening resulting in hyperglycemia in the AM. When a patient is given too much insulin at night the body responds by releasing epinephrine,ACTH, glucagon, and growth hormones which stimulate lipolysis, gluconeogenesis, and glycogenolysis which, in turn, result in a rebound hyperglycemia when the patient wakes up in the morning.
  22. DIABETES
    • DIABETES-6% of Americans(12 million people) have diabetes-glucose levels >200mg/dl-when treating a diabetic with Insulin one should always error on the side of hyperglycemia; hypoglycemia results in permanent neuron destruction
    • SYMPTOMS
    • HYPERGLYCEMIA-polyuria-polydipsia-polyphagia-weight loss-fatigue-blurred vision
    • HYPOGLYCEMIA-diaphoresis/syncope-tachycardia/palpitations-hunger-anxiety/irritability-tremors-weakness-mental confusion-seizures-headache
    • TYPE I vs. TYPE II
    • TYPE I-IDDM-juvenile onset-prone to ketosis-onset less than 30yrs. of age-accounts for 10% of diabetics-due to the pancreas not making sufficient quantities of insulin-abrupt onset-must take insulin
    • TYPE II-NIDDM-adult onset-ketosis resistant-onset usually over 40 yrs. of age-accounts for 90% of diabetics-caused by patient's body not responding properly to it's insulin-slow onset and progression-controlled with oral hypoglycemics,diet, and/or insulin-patients tend to be overweight
    • DIABETIC-given early morning surgical preference-hyperglycemia(>200mg/dL) impairs wound healing but hypoglycemia causes organic brain damage and death. Therefore, hypoglycemia is amore hazardous condition than hyperglycemia "better sweet than sour"-there is no standarized protocol for diabetic glucose control during the day of surgery while the patient is NPO but a few general guide lines are:
    • GLUCOSE CONTROL THE DAY OF SURGERY WHILE PATIENT IS NPO1. plasma glucose levels should be maintained between 150-250mg/dL2. if surgery is delayed or patient expected to be NPO for many hours start IV D5W to avoid hypoglycemia and check glucose q2-3h3. for NIDDM patients they should not take their diabetic medication the day of surgery if they are NPO4. have IDDM patients check their sugar the morning of surgery before they arive at the hospital and if it is very high(>300mg/dL) have them take half their normal morning dose and check again once they reach the hospital5. once the patient has reached the hospital elevated glucose level scan be controlled with a sliding scale6. exact values for insulin sliding scales vary depending on the doctoror hospital
    • INSULIN SLIDING SCALE<150 0 units151-200 2 units201-250 4 units251-300 6 units301-350 8 units351-400 10 units>400 12 units

    • DIABETES MELLITUS
    • Diabetes mellitus (DM) affects about 10 million people in the US. It is a leading cause of blindness, renal disease, PVD, peripheral neuropathy, lower extremity ulceration and amputation, and death. In DM, the ability to oxidize carbohydrates is diminished or lost.usually due to pancreatic dysfunction, particularly of the islets of Langerhans, with resultant disruption of insulin function. Classification includes insulin-dependent diabetes mellitus(IODM, Type 1, juvenile-onset [although it can develop in adulthood]), and non-insulin dependent diabetes mellitus (NIDDM, Type 2, adult-onset). 100M is caused by autoimmune destruction of pancreatic beta cells, and must be treated with insulin replacement NIDDM can be divided into obese and non-obese groups, the obese group displaying the possibility of returning to euglycemia associated with weight loss and dietary control. Gestational OM is observed during pregnancy, and usually subsides postpartum. Findings include hyperglycemia,polyuria, polydipsia, polyphagia, emaciation, weakness, acidosis due to dysfunctional fat metabolism, dyspnea, ketonuria, and coma. Immunopathy accompanies long-standing hyperglycemia. Diabetic ketoacidosis or nonketotic hyperosmolar coma may result from prolonged or severe hyperglycemia. Diabetic retinopathy and nephropathy are the result of small vessel diseases associated with long-standing hyperglycemia. Diabetic peripheral neuropathy produces pain and paresthesia, pedal insensitivity, anhidrosis, vasodialation,brittle hyperkeratosis, mal perforans ulceration, and Charcot neuroarthropathy. All patients suspected of having OM, or previously diagnosed with the disease, should undergo pedal monofilament esthesiometer testing to determine whether protective sensation is present.Diabetic dermopathy creates thin, atrophic, and friable skin in the pretibial region, wounding of which results in post-inflammatory hyperpigmentation. Necrobiosis lipoidica diabeticorum also affects the pretibial area as an atrophic plaque with telangiectasia, and microscopically displays palisading granuloma formation. The laboratory diagnosis of OM hinges on an abnormal glucose tolerance test, and/or repetitively high fasting blood glucose measurements. C-peptide assay can be used to distinguish endogenous insulin, and Type 2OM, from exogenous insulin (administered for therapy), since exogenous insulin doe not contain C-peptide. The GAD 65 antibody assay can also be used to distinguish Type 1 from Type2 OM. Therapy includes efforts to identify the cause, after which dietary controls and exercise are instituted (as indicated). Patient education is a crucial part of the managementof OM. Oral hypoglycemic agents may be used in conjunction with dietary control, and include sulfonylureas (chlorpropamide, tolbutamide, tolazamide, and acetohexamide), as well as metformin. Insulin preparations are indicated when the blood glucose level is not adequately controlled with diet and oral medication, and in cases of Type 10M. Adjusting the administration of insulin requires close communication between the internist and the patient,and often entails lifestyle alteration. In the peri-operative period, a sliding scale of insulin,based on the blood glucose value, can be useful until a regular regimen is resumed. The goal of therapy in the perioperative phase is to maintain plasma glucose between 150-250 mg%.Pancreas and islet cell transplantation can also be used in an effort to cure OM.

    • For diabetic patients, who gets diabetic ketoacidosis and who gets diabetic coma?
    • Type I (IDDM) – DKA Type II (NIDDM) – coma
    • What are signs of hypoglycemia?Nervousness, tachycardia, diaphoresis, nausea, headache, confusion, tremor, seizures, coma
    • What are signs of hyperglycemia?Polyuria, polydipsia, weight loss
  23. DIABETIC KETOACIDOSIS
    • DIABETIC KETOACIDOSIS-complication of diabetes melitus resulting from extreme hyperglycemia-plasma glucose in the range of 350-900mg/dL
    • Causes-failure to take adequate amounts of insulin-1st manifestation of an undiagnosed diabetic-conditions that increase the patients requirements for insulin(infection, trauma)
    • Symptoms-orthostatic hypotension with tachycardia and poor skin turgor(due to dehydration)-abnormal mentation or unconscious-Kussmaul breathing-deep, rapid respiratory pattern(due to acidosis)-fruity breath odor(due to acetone)-UA is strongly positive for both glucose and ketones
    • Treatment-Insulin-IV fluids-in severe cases give bicarbonate to correct pH
  24. staphlococcus
    Coagulase-positive Staphylococcus aureus has consistently been the most common infecting organism in postoperative infections. This also applies to foot and ankle surgery. Closely following this is the less but increasingly virulent organism coagulase-negative Staphylococcus epidermidis.

    -Aerobic Gram Positive CocciStaph aureus 1-Ceph Vanco, Clinda, AzithromycinMRSA Vanco Bactrim, Cubicin, Zyvox, ClindaStaph epi 2-PCN 4-PCN, 1,2-Ceph, VancoMRSE Vanco Zyvox, Cubicin, SynercidEnterococcus 3-PCN Vanco, Tetracyclines, QuinolonesVRE Linezolid Macrobid, Cubicin, ChloramphenicolStrept pyogenes (Group A) 3-PCN 4-PCN, 1,2-Ceph, Vanco, ClindaStrept agalactiae (Group B) 3-PCN 4-PCN, 1,2-Ceph, Vanco, ClindaStrept bovis (Group D) 3-PCN 4-PCN, 1,2-Ceph, Vanco, ClindaStrept Viridans 3-PCN 4-PCN, 1,2-Ceph, Vanco, Clinda
  25. streptococcus
    gram +, catalase -

    Pharyngitis, soft tissueinfection, pneumonia,abscesses

    Penicillin G Cephalosporin, (1 st generation), cefuroxime,cefotaxime, ceftriaxone, clindamycin,vancomycin, erythromycin, clarithromycin,azithromycin

    What organisms may form gas in soft tissue?Gram positive – Clostridium perfringens, Staphylococcus, Streptococcus, PeptostreptococcusGram negative – Bacteroides, E. coli, Klebsiella, Serratia
  26. cavernous hemangioma
    Pain and the rapid increase in size without trauma make cavernous hemangioma the most likely diagnosis.

    An aggressive lesion is best treated with surgicalcurettage and packing.

    Cavernous Hemangioma-an edematous vascular lesion characterized by soft compressible tissue-may be associated with surface varicosities or nevus flammeus-like changes-lesions are not apparent at birth but become visible during childhood-Maffucci's syndrome-a variant of cavernous hemangioma associated with dyschondroplasia and hard nodules on the fingers or toes-lesions are asymptomatic except from cosmesis
  27. compensation for a long limb
    • Compensation for a structurally long limb produces excessive pronation of the foot on the involved side.The wear pattern of the shoe on the involved foot would, therefore, be greatest on the medial side.
    • Unequal limb length - may be structural within the thigh, leg or both femoral and tibial/fibular segments; or functional secondary to scoliosis induced pelvic tilt with lower side of pelvis effecting functionally longer limb, unilateral supination or pronation of the foot.Compensation for limb inequity involves pedal pronation on the longer side, along with ipsilateral inferior pelvic tilt (tilts downward) due to hyperpronating hindfoot, ipsilateral shoulder tilt downward, scoliosis, ipsilateral head tilt toward longer limb, increased stance phase on the longer side. On the short side, the hindfoot supinates, pelvis rises, shoulder rises, and there is less stance phase weight bearing.
    • Deep Posterior leg Compartment
    • The deep posterior leg compartment contains tibialis posterior (TP), flexor digitorum longus(FDl), and flexor hallucis longus (FHL). The muscles are innervated by the tibial nerve, and supplied by the posterior tibial artery. The tendons of these muscles traverse deep to the flexor retinaculum (laciniate ligament) to enter the plantar vault.
    • Tibialis Posterior (TP)
    • origin-from the posteromedial aspect of the fibula, the posterior aspect of the tibia dista lto the popliteal line and lateral to the vertical line, the IO membrane, and adjacent intermuscular septae; FHL and FDL both overlap the belly of TP; and TP passes through the first(medial) canal of the tarsal tunnel.
    • insertion-primarily into the tuberosity of the navicular, with additional slips inserting into the plantar aspect of the intermediate 3 metatarsal bases and every tarsal except the talus.
    • Flexor Digitorum Longus (FDL)
    • origin-from the posterior aspect of the tibia distal to the soleal line, and from fascia of TP;the tendon traverses the second canal of the tarsal tunnel to enter the foot where it first crosses superficial to FHL, and then over TP, where it shares a vinculus (master knot of Henry) with FDL; thereafter, FDL splits into 4 slips.
    • insertion-into the plantar aspect of the distal phalanx of the lesser 4 toes.
    • Flexor Hallucis Longus (FHL)
    • origin-from the distal 2/3 of the posterior surface of the fibula, the posterior aspect of the peroneal septum, the anterior surface of the deep transverse intermuscular septum (separating the superficial and deep posterior groups), and the fascia about TP. The tendon courses through the fourth canal of the tarsal tunnel.
    • insertion-into the plantar aspect of the base of the distal phalanx of the hallux·
    • FLEXOR DIGITORUM LONGUS
    • Origin: the posteromedial aspect of the middle third of the tibial shaft
    • Insertion: plantar surface of the base of phalanges 2-5
    • Action: flexes the DIPJ, PIPJ, MPJ of digits 2-5, and plantarflexes the ankle
    • Innervation: tibial nerve(S2, S3)
    • Arterial Supply: posterior tibial artery
    • TIBIALIS POSTERIOR MUSCLE
    • Origin: posterior two thirds of the interosseous membrane and the adjacent tibia and fibula
    • Insertion: plantarly on the navicular(major insertion site), medial and intermediate cuneiform, and base of the second, third, and fourth metatarsal
    • Action: invert the foot, adduct foot, plantarflex ankle
    • Innervation: tibial nerve(L4, L5)
    • Arterial Supply: sural, peroneal, and posterior tibial arteries
    • FLEXOR HALLUCIS LONGUS
    • Origin: Most of the inferior two-thirds of the posterior surface of the fibular and the lower part of the interosseous membrane
    • Insertion: plantar surface of the base of the distal phalanx of the hallux
    • Action: flexes the IPJ, 1st MPJ, plantarflex ankle
    • Innervation: tibial nerve(S2, S3)
    • Arterial Supply: peroneal, and posterior tibial arteries
  28. Which of the following is a life-threatening dysrhythmia most likely to experience during the first hour following a myocardial infarction?
    • Ventricular fibrillation is a life-threatening dysrhythmia that occurs in the early phases of a myocardial infarction.
    • -rapid, irregular, disorganized ventricular rhythm-results in lack of cardiac output, no pulse, no BP

    • Other dysrhythmia:
    • CARDIAC RHYTHMS
    • 1) First degree heart block-delay in transmission of the electrical impulse from the atria to the ventricles-prolonged P-R interval beyond .20 seconds but constant in duration
    • 2) Second degree heart block-
    • Type l (Wenckebach's) not all atrial impulses reach the ventricles P-R interval progressively lengthens until a QRS complex is dropped,then the cycle repeats
    • Type II Mobitz: not all atrial impulses reach the ventricles no delay or prolongation of P-R interval
    • 3) Third degree heart block-none of the atrial impulses reach the ventricles-atrium and ventricles beat independently at their own regular rates(atrial rate 60-100bpm, ventricular rate 40bpm)-no correlation between P's and QRST's
    • 4) Sinus Arrhythmia-NSR with varying rate depending on respiration-rate increases with inspiration, rate decreases with expirationm
    • 5) Asystole(sinus arrest, flatline)-failure of the sinus to produce an impulse resulting in a prolonged pause
    • 6) Sinus Bradycardia-less than 60 beats a minute
    • 7) Sinus tachycardia-more than 100 beats a minute
    • 8) Premature atrial contraction(PAC)-a focus in the atrium(other than the SA node) depolarizes prematurely-P wave appears early and abnormally shaped or it may be lost in the previous T wave-causes: stimulants-coffee, tobacco, EtOH, heart disease, CHF, meds, hypoxia, low K+ levels
    • 9) Paroxysmal atrial tachycardia(PAT) or Paroxysmal supraventricular tachycardia(PSVT)-a focus in the atrium(other than the SA node) depolarizes, giving rise to a series of rapid beats at a regular rate between 150-250/minute-begins and ends suddenly(paroxysmal)
    • 10) Atrial flutter-rapid firing of an ectopic atrial focus"sawtooth" pattern-only some beats pass to the AV node
    • 11) Atrial fibrillation-multiple atrial foci depolarizing in a chaotic manner-a small number pass through the AV node
    • 12) Premature ventricular contraction(PVC)-ectopic depolarization in any portion of the ventricular myocardium-PVC's are of little concern if they arise from the same foci or if thereare less than 5/minute-If they arise from more than one foci or there are greater than5/minute, can lead to V-fib
    • 13) Ventricular tachycardia-ectopic depolarization of ventricles usually at a rate of 150-250/minute-can degenerate to V-fib
    • 14) Ventricular fibrillation-rapid, irregular, disorganized ventricular rhythm-results in lack of cardiac output, no pulse, no BP
    • 16) Wolff-Parkinson-White Syndrome(WPW)-an electrical bridge exists between the atrium and ventricles causing a conduction bypass of the AV node-rapid impulse transmission occurs between atrium and ventricles resulting in PR interval < .12sec
    • 17) Junctional Rhythm-heart beat originating in the AV junctional tissue as a safety mechanism when the higher pacemaker site(SA node) is not functioning or if the impulses are not getting through-inverted P wave -the AV junctional tissue beats at 40-60bpm
  29. neuromuscular causes of cavus foot
    • cerebral palsy
    • myelomeningocele
    • Charcot-Marie-Tooth disease

    • CEREBRAL PALSY
    • DESCRIPTION-A broad term used to describe several static nonprogressive neuromuscular disorders resulting from brain damage before, during, or immediately after birth
    • -Types of CP include Spastic CP(most common, 70%) Athetoid CP(20%) Ataxic CP(10%) Rigidity CP, Tremor CP, Atonic CP
    • SIGNS AND SYMPTOMS
    • -"Scissors gait" due to adductor spasticity-Speech defects, retardation, seisures, visual defects-Ankle equinus
    • TREATMENT-PT, OT, splinting, bracing

    • CHARCOT-MARIE-TOOTH DISEASE (CMT,PERONEAL MUSCULAR ATROPHY)
    • -named for the 3 physicians who first recognized the disease-a hereditary, demyelinating, hypertrophic neuropathy of the peripheral nervous system-characterized by slow progressive distal muscle atrophy(esp. peroneals)resulting in foot drop-there may or may not be sensory changes, but these are less severe than muscle atrophy-when autosomal-recessive, the disease manifests at around age 8years of age, when dominant, the disease manifests at around age 30years old-the earlier the onset, the poorer the prognosis
    • CAUSE-hereditary
    • SIGNS/SYMPTOMS-weakness in the peroneal muscles-pes cavus-"stork leg"-skinny legs due to peroneal atrophy-inverted Champagne bottle legs-foot drop(slapping gait)-unsteady gait/tending to trip easily-stocking-glove sensory loss-decrease ankle DTR's-later in the disease the hallux becomes fixed and rigidly plantarflexed and the hands may become involved TREATMENT-symptomatic-AFO for foot drop

    • CAVUS FOOT TYPE
    • PES CAVUS)DESCRIPTION-
    • High arched foot-Elevated longitudinal arch-Primarily a sagittal plane deformity-Painful calluses under metatarsal heads-Chronic inversion ankle sprains-Heel, knee or hip pain may develop secondary to lack of shock absorption from the abnormal architecture of the foot
    • RADIOLOGICAL EVALUATION-Take WB and NWB to determine if deformity is reducible-"Bullet hole" sinus tarsi
    • SIGNS CAVUS FOOT
    • CIA >30°
    • Angle of Meary >6°
    • Angle of Hibbs >150°
    • CLASSIFICATION(LOCATE APEX OF DEFORMITY)-
    • Metatarsal cavus Lisfranc's joint
    • Lesser tarsus cavus Lesser tarsal bones
    • Forefoot cavus Chopart's joint
    • Combination Apex generalized over lesser tarsals
    • CAUSES
    • Cavus foot is often the first manifestation of many neuromuscular disorders including: spina bifida, Charcot-Marie Tooth disease, Friedreichs ataxia, poliomyelitis, spinal cord tumors, myelomeningocele, CP,infection, syphilis, trauma, spinal cord lesion
    • CONSERVATIVE-Shoe modification and orthotics can alleviate symptoms by increasing the weight bearing surface of the foot and relieving painful callus under the ball of the foot-In young patients passive stretching, manipulation and casting may be beneficial-Extra depth shoes combined with a metatarsal bar
    • SURGICAL
    • Soft tissue for flexible deformities
  30. muscular dystrophy
    In muscular dystrophy, contractures of the gastrocnemius muscles appear early and result in tightening of the heel cords, which causes the patient to have an equinus deformity and walk on the toes.

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