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2012-02-27 22:11:38
PCM Exam II medical slides

Gout, Vasculitis, Autoimmune, bad back. (note: i also included Wegener's Granulomatosis just because it was in the reading for vasculitis last chapter and i might come back to haunt us)
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  1. A 40 y.o. m presents with painful swelling on his lft MTP x2 days. You note the lesion is a red erythematous nodule that is very sensitive to palpation. He also reports that it begain at the end of guys weekend, during which he proudly states that he and his friends mostly ate steaks and drank beer. what do you suspect?
  2. Purines are broken down by what enzyme into uric acid?
    xanthine oxidase
  3. What enzyme do humans lack that alows the buildup of uric acid in the system?
  4. Explain the pathophysiology of an acute gouty attack
    monosodium urate crystals are coated with IgG which triggers opsonization. when neutrophils phagocytize the crystals it stimulates release of inflammatory cytokines, but also sometimes bursts the neutrophil releaseing all intracelluar cytokines and creating disproprotionate localized inflammatory reaction, which leads to swelling and pain
  5. overproduction and underexcretion of uric acid creates this condition
  6. Name some medications that cause hyperuricemia?
    diuretics, low dose asprin, cyclosporine, niacin
  7. Name two myeloproliferative disorders that cause hyperuricemia
    multiple myeloma, hemoglobinopathies
  8. 70 y.o. F presents with hyper uricemia and a gouty attack on the MCP of the left hand, she is on coumadin for CVD, as well as hydrochlorothiazaide for BP, and low dose aspirin. She is very active and her favorite activity is go to to the pub to have a Guinness and listen to the band. She is fairly active and healthy other than the heart disease, her exam and labs are unremarkable except for hyperuricemia. What from her history could be causing her gouty attacks?
    • The Beer
    • hydrochlorothiazide
    • asprin
  9. T or F Chronic kidney disease, hyperparathyroidism, psoriasis, sarcoidosis, and lead poisoning can all lead to hyperuricemia
  10. T or F hyperuricemia invariably leads to gout
    False, in most cases of hyperuricemia the patient does not develope gout
  11. A swollen exquisitly tender nodule/nontender nodule (acute or chronic) with warm dusky red overlying skin and sometimes a white granulation tissue beneith is called a ___ and is caused by chronic gouty attacks
  12. Trophi on the ears is associated with what?
    a high uric acid level (usually around 10)
  13. Gout of the foot especially the big toe
  14. Why does gout typically precipitate on the first MTP?
    • not good circulation
    • stasis
    • cold temperatures
    • all these factors lead to stasis and chilling of the blood which allows dissolved substances to precipitate out into crystal form more easily
  15. You biopsy a nodule that you are unsure about, and the lab returns a report that states diffuse monosodium urate crystals found. your nodule is....
    A gouty trophus
  16. What is a possible urinary complication of hyperuricemia and gout?
    uric acid kidney stones
  17. What is a normal serum uric acid level? what is elevated?
    • 3.0-7.0 mg/dL
    • high = >7.5 mg/dL
  18. T or F during a gouty attack uric acid levels may be normal
  19. Gouty Crystals have a needle like appearance with a ___ colored perpendicular edge and a ___ colored parallel edge under polarized light
    • Yellow = parallel
    • Blue = perpendicular
  20. What pathopneumonic finding will you see on X-ray of a joint with chronic gout?
    "Rat Bite" erosion that has overhaning margins (overhaning rim of cortical bone with a punched out appearance)
  21. Which of the following would be most appropriate to treat an acute gouty attack?
    A. Probenicid
    B. Indomethacin
    C. Febuxistat
    D. HIGH dose Colchicine
    B. Indomethacin
    (this multiple choice question has been scrambled)
  22. What are some indications for treating with chronic gout medications?
    • multiple gouty attacks within one year (with trophi)
    • advanced gouty arthritis
    • renal stones
    • significant hyperuricemia
  23. What is the MOA of Colchicine?
    • blocks activation of proinflammatory cytokines in monocytes and inhibits microtubule function and adhesion molecules in neutrophils to prevent migration
    • (basically hog ties the monocytes and neutrophils and puts duct tape over their mouth so they can't eat any more crystals, colchicine you brute!)
  24. What is the treatment for a patient who has gout secondary to diet or medications?
    change diet and discontinue or change medications... duh!
  25. You have a pt with history of gout who has recently also developed hypertension what two classes of drugs should you AVOID and what two class of drugs could you choose from instead?
    • AVOID! thiazide and loop diuretics
    • USE losartan or ARB
  26. Name a uricosuric drug (2 mentioned in class)
    probenicid, sulfinpyraone
  27. Name a Xanthine Oxidase inhibitor
    • Febuxostat (liver excretion use in pts with renal insuf.)
    • Allopurinol ( renal excret. with risk of hypersensativ. rxns)
    • Krystexxa, aka pegloticase (allergy is common give with benadryl, don't use in CHF and G6PD deficency)
  28. What gout med should you not use for a pt with CHF or G6PD deficiency?
    Krystexxa, pegloticase
  29. What age group usually gets calcium pyrophosphate dihydrate deposition disease?
    elderly 60 y.o. + with an average age of 72
  30. Males with Pseudogout tend to have more ___ while females with pseudogout tend to have more ____
    • Males= Acute attacks
    • Females = pseudo-ostoarthritis
  31. What is the eitiology of the majority of pseudogout?
  32. In this inherited disease the ankh gene for pyrophosphate transport is aberrant and pts are at higher risk of developing pseudogout
    Familial chondrocalcinosis
  33. What are some diseases that can change blood calcium levels and thus increase a persons susceptibility to CPPD?
    • Hemochromatosis
    • hyperparathyroidism
    • hypophosphatasia
    • hypomagnesemia
  34. syndrome characterized by the accumulation of homogentistic acid in the connetive tissues due to autosomal recessive trait or use of phenols on the skin, this syndrome is a risk factor for CPPD
    • Ochronosis
    • (I know it is an obscure question but it was in her slides and because there isn't alot for this exam she could pull weird facts)
  35. How fast do symptoms of pseudogout usually develop?
    quickly 24-48 hours often after surgery
  36. What joints are typically affected by CPPD?
    Knee and larger joints
  37. 64 y.o. M presents with pain and stiffness in his right knee following a surgery for colonic resection due to diffuse diverticulitis. You note a large swollen mildly erythematous knee that is not warm to the touch. His vitals reveal that he is running a fever (all others are normal) and labs show he has a mild leukocytosis and elevated ESR. The wound site is healed nicely with no sign of infection and he denies any other complaints. What do you dx? what is your next step
    Pseudogout, aspiration of the knee and visualize crystals under polarized light to confirm CPPD and rule out gout.
  38. What joints are commonly affected with pseudogout?
    • Knee
    • Hips
    • MCP
    • Shoulders
    • Elbows
    • Ankles
  39. What radiologic findings would you expect in a pt who has CPPD?
    • calcification of cartilaginous structures
    • degenerative joint disease signs
    • knee, symphysis pubis and wrist disease
  40. How would you test a joint which you suspect has CPPD
    • X-ray
    • Aspiration
    • Musculoskeletal ultrasound
  41. An aspiration sample you sent to the lab came back as postive for bifringent rhomboid shaped crystals with blue parallel edges and yellow perpendicular edges. You feel safe making the diagnosis of...
    Pseudogout or CPPD
  42. What is the treatment for pseudogout?
    • rest the joint
    • splinting for joint protection
    • 1-2 joint aspiration or injection
    • NSAIDs
    • Colchicine (for more than 2 attacks per year)
    • Triamcinolone intraarticular injection
  43. What is the indication for using colchicine in pseudogout?
    more than 2 attacks per year
  44. Cryoglobulinemia can refer to two conditions what are they? (hint: one is asymptomatic and one is symptomatic)
    • - presense of asymptomatic cryoglobulins in the serum
    • - Cryoglobulinemic vasculitis: symptomatic and often associated with HepC, adenovirus, parvovirus, autoimmunes
  45. Which is more associated with APL livido reticularis, or livido racemosa?
  46. HSP is caused by Ig_?
  47. Which vasculitis is associated with Hep C, adenovirus, parvovirus, and other autoimmune conditions
    Cryoglobulinemic vasculitis
  48. What are the immunoglobulins/proteins that are involved with the pathology of Cryoglobulinmia
    Rheumatoid factor and IgG
  49. A 35 y.o. M presents with palpable purpura, and abdominal pain, with mild SOB. On PE you note that his toes have Reynauds phenomena and he has decreased vibratory sensation on the toes. He had a cold last week but is otherwise healthy with no other conditions. What do you think he has?
  50. Weird bruising, peripheral neuropathy, abdominal pain, SOB, acral cyanosis, gangrene of the periphery and reynauds phenomenon as well as palpable pupura and arthralgias
  51. How do you treat Cryoglobulinemia?
    • If it is associated with Hep C then treat with antivirals like interferon alpha or ribaviran
    • Otherwise:
    • corticosteroids
    • cyclophosphamide
    • plasmapheresis
    • Immunosuppressive therapy for pts without Hep C
    • Rituximab
  52. _____ is the most common systemic vasculitis in children
    Henoch-schonlein pupura (HSP)
  53. HSP is a leukocytoclastic vasculitis with ___ deposition
  54. Is HSP more common in males or females?
  55. 7y.o. M presents with abdominal pain and rash on the legs. Pt has a history of prior strep infection 2 wks prior... what vasculitis should be on your differential?
  56. What is the HSP Sx tetrad?
    • Arthralgia and/or arthritis
    • palpable purpura
    • Renal disease
    • Abdominal pain
  57. "tea colored urine"
  58. What joints are most commonly affected with arthralgias in HSP?
    Knees and ankles
  59. T or F pts concurrent coagulopathy leads to the purpuric lesions in HSP
  60. What causes the abdominal pain in HSP?
    colicky pain in the abdomen is secondary to vasculitis of the intestinal tract and can also be associated with GI bleed
  61. In HSP kids have worse ___ symptoms and adults have worse ___ symptoms
    • Children: abdominal pain
    • Adults: Kidney symptoms
  62. uveitis, scrotal pain and tenderness and pulmonary invovement are rare symptoms of this vasculitis...
  63. Scrotal pain/tenderness with palpable purpuric rash in a child
  64. What are the diagnostic criteria for HSP?
    • Must have at least 2 of the following
    • palpable purpura
    • age under 20 y.o.
    • intestinal angina (abnormal pain after meals, bowel ischemia with bloody diarrhea)
    • granulocytes in the walls of arterioles or venules on biopsy
  65. You feel unsure about a pt with palpable purpuric lesions on the legs. You biopsy and the pathology report is positive for granulocytes in the walls of arterioles and venules, what do they have?
  66. What is the treatment for HSP?
    • Corticosteroids
    • steroid sparing agents for long term: azanthioprine, mycophenolate
    • supportive care most resolve in a month
    • Urinalysis/BP checks
    • hydration,
    • bed rest
    • relief of joint and abdominal pain with NSAIDs
  67. Violaceous mottling or reticular pattern of the skin on the arms and legs that is benign and reversible
    Livido reticularis
  68. Skin mottling on the arms and legs that is in a closed circle of lacy pattern
    livideo reticularis
  69. livedo reticularis is usually not invoved with other immune processes however it can be associated with which syndrome?
    Antiphospholipid syndrome
  70. Lacy skin mottling on the arms and legs that is not a closed circle
    livido racemosa
  71. Violaceous lacy mottling of the skin that is often associated with underlying autoimmune disease
    livido racemosa
  72. What autoimmune disease is livido racemose most closely associated with
    Antiphospholipid syndrome APL
  73. This pt has a palpable purpuric rash and what they describe as a bad sinus infection. On PE you note purulent nasal discharge that is also bloody. Before you reach for the antibiotics what vasculitis should you consider?
    Microscopic polyangitis (MPA)
  74. MPA most often affects what kind of blood vessels?
    small blood vessels, capillaries and arterioles
  75. What two major body systems are affected by MPA?
    • Pulmonary: causes pulmonary capillaritis, which can lead to pulmonary hemmorrhage and causes hempoptosis
    • Renal: causes segmental necrotizing glomerulonephritis which manifests as hematuria, protinuria, and red blood cell casts
  76. Your 42 y.o. patient has a palpable pupuric rash mainly on the extremities with brownish aged lesions as well as new red purpura. They also have splinter hemorrhages and vesicobullous lesions. What vasculitis is this?
    Microscopic polyangitis
  77. What are 3 diagnostic tests you should do for MPA?
    • Urinalysis: abnormal urinary sediment, microscopic hematuria with or without red cell casts, granulomatous inflammation on biopsy of an artery or perivascular area
    • CXR: abnormal chest X-ray with nodules, fixed infiltrates or cavities
    • ANCA testing
  78. Is MPA ANCA positive or ANCA negative?
    ANCA positive
  79. How do you treat microscopic polyangitis?
    • Prednisone
    • Cyclophosphamide
    • Rituximab
    • Azathioprine- but give pneumocystic Jerovici prophylaxis first. it is used as a sparing agent for cyclophosphamide
  80. What should you give to a patient with Azotihoprine to prevent complications from the drug?
    pneumocystic J. prophylaxis as azothioprine decreases the bodies ability to fight off this pathogen
  81. Is Wegener's granulomatosis ANCA positive or negative?
  82. An ANCA+ vasculitis of the small arteries, arterioles and capillaries causing necrotizing granulomatous lesions of both the upper and lower respiratory tract, glomerulonephritis, and other organ dysfunction.
    Wegener Granulomatosis
  83. How quick is the onset of Wegener's granulomatosis?
    it develops over 4-12 months (subacute)
  84. 47 y.o. M presents with a bad respiratory infection that he says has not gone away for 7 months. Sx include sinusitis, nasal congestion and a cough. He states he thought it could have been allergies but he decided to come in to get it checked because he is having trouble breathing and is coughing up blood. His ROS is positive for joint pain that is sometimes in the knee and sometimes in the elbows shoulders and hips. His PE reveals gum inflammation with an acute Otitis media and the possible beginnings of mastoiditis. He has several nasal and oral lesions. He also has stridor. What vasculitis do you think he has and what body system do you want to do lab tests for ?
    • Wegener's Granulomatosis
    • Renal:UA shows sediment containgin red cells with WBCs possibly but lots of red casts, renal biopsy shows segmental necrotizing glomerulonephritis with multiple crescents.
    • Pulmonary: pulmonary functioning tests, CXR/CT and bony sinus CT- shows infiltrates, nodules, masses and cavities with extensive sinusitis and bony sinus erosions
  85. ANCA has two subtypes, Against protinase-3 (or PR-3) and Myeloperoxidase subtype (MPO). These can help destinguish between Microscopic polyangitis and Wegener's granulomatosis. Which ANCA subtype goes with which disease?
    • PR-3: High specificity for Wegner granulomatosis (97% +) MPA may also be positive but not as often
    • Turn the 3 on its side it becomes a W

    • MPO: High specificity for microscopic polyangitis and Churg strauss
    • M= MPA
  86. Tissue biopsy from the lung of a pt with palpable purpura and sinus problems shows vasculitis, granulomatous inflammation, and geographic necrosis. A Renal biopsy from the same pt shows segmental necrotizing glomerulonepritis with multiple crescents. What does your patient have?
    Wegeners granulomatosis
  87. In Wegener's granulomatosis are granulomas more common on lung or renal biopsy?
  88. How do you treat Wegener's granulomatosis?
    • Prednisone, cyclophosphamide for initial remission
    • Azathioprine and/or methotrexate long term to spare the pt from having to take cyclophosphamide.
  89. This Autoimmune disorder primarily affects women in their childbearing years and men over 60, and presents initially with painless fluctuiating muscle weakness.
    Myathenia gravis
  90. What is Ocular myasthenia?
    • focal extraocular motion and difficulties and drooping of the eyes
    • MG that is limited to eyelides and extrocular muscles
  91. What is Generalized myasthenia?
    • weakness that involves more than just the ocular muscles
    • Proximal limb weakness with deep tendon reflexes preserved
  92. "proximal limb weakness with preserved deep tendon reflexes"
  93. What are the two types of Juvenile myasthenia?
    • transient neonatal MG
    • Congenital MG
  94. This drug can induce Myasthenia gravis
  95. Explain the pathophysiology of Myasthenia gravis
    • antibodies are formed to the acetylcholine receptors on the endplate of the posynaptic membrane/muscle surface
    • they destroy the acetylcholine receptors and result in weakness
    • In more detail... antibodies bind to the alpha subunit of Ach receptors and cuase damage to the postsynaptic membrane leading to decreased number and density of ach recptors on the motor end plate
  96. With drug induced myathenia gravis remission of symptoms typically occurs how long after discontinuation of the drug?
    4-6 mo but before 1 year
  97. Symptoms of Ocular myasthenia gravis can be exacerbated by...
    reading, television, driving any situation that requries continuous use of the eyes
  98. Pt with ptosis who complains of changes in voice after prolonged conversation, trouble chewing and swallowing, and new found trouble using a straw or whistling. what disease?
    Myasthenia gravis
  99. Thymic hyperplasia is associated with 3 prognostic changes in disease they are...
    • more severe generalized weakness
    • higher acetycholine receptor antibody titers
    • more severe findings on EMG
  100. What diagnostic studies do you do for MG?
    • AP and lateral chest X-ray for thymoma or MRI
    • EMG studies: decrease in msucle response
    • Ach antibodies: positive in 80-90% of cases
    • Tensilon Test: administer edrophonium watch for resolution of sx
    • EMG: decrementing muscle response is found
    • PFTs: to predict respiratory failure
  101. What is the tensilon test and what do you use it for?
    Myasthenia Gravis test

    • Confirmatory Testing

    • Edrophonium chloride (Tensilon test)

    • ·
    • + test = unequivocal resolution of weakness

    • ·
    • + test shows transient relief from all sx

    • ·
    • IV edrophonium briefly relieves weakness

    • Blocks the degredation of Ach to temporarily
    • increase the levels at the neuromuscular junction

    • Repetitive stimulation of a nerve during a nerve
    • condution study may demonstrate gradual decreases of the muscle action
    • potential due to impaired nerve to muscle transmission
  102. What is Seronegative MG?
    • ·
    • Seronegative myasthenia gravis= disease without
    • circulating antibodies to Ach receptors
  103. A baby born to a mother with MG has joint
    contractures with muscle weakness, symmetrical and involves all 4 extremities what is the name of this condition?
  104. What is Myasthenic crisis?
    life threatening severe weakness that requires intubation
  105. What drugs can increase MG weakness?
  106. Drugs increase weakness in MG- antibiotics
    • (aminoglycosides, erythromycin, and azithromycin) cardiac drugs (beta-blockers,
    • procainamide, and quinidine) magnesium
  107. How can you treat Myasthenia Gravis?
    • Thymectomy
    • Cholinesterase inhibitors
    • immunosuppressives
    • corticosteroids
    • IVIG
    • Plasmapheresis
  108. acute immune mediated polyradiculopathy that typically follows an infection and results in paralysis
    Guillian Barre Syndrome
  109. "albuminocytologic dissociations"
  110. GQ1B antibody is found in 80-90% of pts with...
    Miller Fisher syndrome
  111. This disease typically starts in the legs and arms and facial muscles and ascends over a period of about 2 wks following a viral infection
  112. What are some non-musculoskeletal Sx of GBS
    • dysautonomia
    • tachycardia/bradycardia
    • dysrhythmias
    • urinary retention
    • respiratory- paradoxical breathing
    • hypertension
  113. This is a variant of GBS that also includes opthalmoplegia, ataxia and areflexia
    Miller Fisher Syndrome
  114. This disease has inexcitable nerves on early nerve studies
  115. What is the diagnostic criteria for GBS
    • progressive weakness in more than one limb
    • minimal leg weakness to paralysis of all four limbs
    • includes bulbar and facial mucles
    • external opthalmoplegia
    • progression of sx over 4 days to 4 weeks
    • relative symmetry
    • mild sensory sx
    • cranial nerve involvement
    • recovery begins at 2-4 wks
    • autonomic dysfrunction
    • no fever
    • elevated CSF protein more than 10mm3
  116. How do you treat GBS?
    • Supportive (monitor vitals and pain treatment with gabapentin or carbamazipine)
    • plasma exchange, IVIG
    • Rehab- PT
  117. When can a pt who had a GBS follwoing an immunization by 6 wks get that immunization again?
  118. If GBS follows an immunization how long should they not recieve any other immunizations
    not until 1 yr. post GBS resolution unless the GBS followed the immunization by less than 6 wks in which case never!
  119. ____ is caused by a sympathetic response that is usually activated with inury or insult. Healing never occurs and there are abnormal impulses to stimulate the inflammatory response from teh sympathetic nervous system.
  120. What are the two types of CRPS
    • Type 1- no identifiable lesion in the area with uknown eitiology
    • Type 2- identifiable nerve lesion present in the affected area
  121. Stage II CRPS is characterized by...
    • progressive soft tissue edema
    • thickening of the skin and articular soft tissues
    • brawny dark skin coloration plus all of the changes in stage I
  122. Stage I CRPS is characterized by
    • pain in the limb following an event or with no apparent cause
    • burning/throbbing pain diffuse aching, sensitivity to touch or cold, and localized edema
    • distribution of pain is not just along a single peripheral nerve trunk or root lesion but instead diffuse pain
    • vasomotor disturbances occur with variable intensity producing altered colro and temperature
    • radiograph may show patchy demineralization
  123. Stage III CRPS is characterized by
    • limited ROM
    • shoulder and hand syndome (capsular retraction producing frozen shoulder, digital contractures, waxy atrophic skin changes with brittle ridges and nails
    • bony radiograph with severe demineralization
  124. "catchers mitt hand"
    Complex regional pain syndrome
  125. Capsular retraction producing frozen shoulder paired with digital contractures, waxy atrophic skin changes and patchy bone demineralization is called.
    Shoulder and hand syndrome
  126. Sudeck atrophy
    • associated with CRPS, atrophy of the bone and demineralization due to chronic inflammation
    • post-traumatic variant of CRPS that shows characteristic and generalized osteopenia of the area
  127. What are the 4 categories of symptoms in the diagnostic criteria for CRPS?
    • sensory
    • Vasomotor
    • Sudomotor/Edema
    • Motor/trophic
  128. Sensory symptoms of CRPS include
    hyperesthesia and/or allodynia
  129. Vasomotor symptoms of CRPS include
    temperature asymetry, skin color changes and/or skin color asymetry
  130. Sudomotor/edema sx of CRPS include
    reports of edema andor sweating changes and/or sweating asymetry
  131. Motor/trophic sx of CRPS include
    reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes in the hair skin or nails
  132. What is the treatment for CRPS?
    • there is no cure
    • refer to chronic pain managment
    • PT is key
    • antidepressants
    • nerve blocks
    • smoking cessations
    • bisphosphonates
    • oral glucocorticoids
    • nasal calcitonin
    • sympathectomy
  133. a positve HLA-B27 has a high association with what disease?
    Ankylosing spondilitis
  134. What age group gets ankylosing spondylitis?
    Young adult (males) 20-30 y.o.
  135. _____ is a chronic inflammatory disease that is characterized by progressive spine stiffness moving up from the hips and lumbar spine
    Ankylosing spondylitis
  136. enthesis is
    the point at which the tendon or ligament inserts into the bone
  137. Explain the pathophysiology of Ankylosing spondylitis
    The immune system attacks the entheses on the axial skeleton. This attack is caused by T-cell invation of the enthesis releasing inflamatory agents especially TNF alpha which leads to inflammation. This chronic inflammation leasds to granulation tissue formation calcification and ossification
  138. What are the primary sites affected by ankylosing spondylitis?
    • intervertebral disc margins, apophyseal joint capsule insertion on bone and ligamentous insertions on the spine
    • sacroilliac joints are the primary site of disease
  139. a 32 y.o. M presents to you with a dull aching in in his back that he reports has been going on for a year. He reportes that it becan in his hips and lower back and seems to be slowly getting worse. He says that is is worse in the morning and gets better after he goes to the gym before work. He is presenting to you today because for the past few weeks the back pain has been disrupting his sleep. your next course of action is..
    A. Give him muscle relaxer
    B. Give him a muscle relaxer and a sleep aid perscription
    C. Perform a Shober's Test
    D. CT
    C. Perform a Shober's Test, your patient is showing classic signs of ankylosing spondylitis and should be tested and possibly sent for an X-ray
    (this multiple choice question has been scrambled)
  140. If a pt with ankylosing spondylitis has acute anterior uveitis you should...
    A. Treat the ankylosing spondylitis with oral prednisone the uveitis is related and should go away with treatment of the AS
    B. topical medication for glaucoma
    C. rever to optometry for an apointment sometime that week, preferably the next day
    D. Immediate referal for urgen slit lamp examination
    D. immediate referral
    (this multiple choice question has been scrambled)
  141. What are some non-axial symptoms of ankylosing spondylitis?
    • synovitis of large lower extremity joints
    • supraspinatus and/or achilles tendonitis or enthesopathy
    • temporomandibular joint involvment
    • sternocostal joint
    • costosternal joint and costovertebal joints
    • Cardiac: aortic root dilitation, aortic regurgitation, mitral regurgitation, conduction abnormalities, 3rd degree heart block.
    • Pulmonary: Restrictive lung disease, pulmonary fibrosis of the upper lungs
  142. What diagnostic studies do you do for a pt with ankylosing spondylitis?
    • Shober's Test
    • Palpation of joints: spinal paraspinal regions, ishial tuberosities, illac crests, costovertebral/costochondral, achilles tendon/plantar fascia
    • X-ray
  143. What are some changes on X-ray that you will see with ankylosing spondylitis?
    • symmetric sacroilitis
    • sclerosis of the si joint
    • errosive changes
    • squaring of the vertebral bodies
    • syndesmocyte formation
    • bamboo spine
  144. "shiny corner"
    ankylosing spondylitis
  145. "bamboo spine"
    Ankylosing spondylitis
  146. Is a grade 4 sacroiliitis good or bad?
  147. What is the treatment for ankylosing spondylitis?
    • NSAIDs: first line, usually affective
    • Peripheral Sx refractory to NSAIDS: sulfasalazine, methotrexate
    • Axial Sx refrac. to NSAIDs: etanercept, infiximab, adilmumab, golimumab
    • Steroid intraarticular injections
    • surgery is last resort
  148. ___ is the narrowing of the spinal canal compressing nerver roots. It primarily affects the lumbar region but can occur at any point in the spine.
    Spinal stenosis
  149. "Neurogenic claudication"
    spinal stenosis
  150. What are the 3 types of spinal stenosis?
    • Aquired: most common, degenerative disease, trauma, post spine surgery, endocrine, metabolic, pagets
    • Congenital: achondroplasia or idiopathic
    • Mixed: congenital and aquired a little
  151. What is the pathology of spinal stenosis?
    narrowing of the spinal canal/intervertebral foramen caused by bone and/or ligametn hypertrophy ex. thickening of the ligamentum flavum
  152. When does congenital spinal stenosis present?
    30-40 y.o.
  153. "spagettie legs"
    spinal stenosis
  154. "walking like a drunken soldier"
    spinal stenosis
  155. Back pain with relief sitting or lying or bending forward
    spinal stenosis
  156. Aching pain originating in the lower back that radiates to the buttocks and upper legs and worsens with walking or standing especially prolonged standing
    Spinal stenosis
  157. What will you find on PE with a pt who has spinal stenosis?
    • Focal weakness and/or sensory loss in the distribution of one or more spinal nerves
    • may have absent achilles and/or patellar DTR
    • wide based gait
    • Postive romberg sign
  158. What imaging study should you get for a pt with possible spinal stenosis?
  159. What are some non-surgical treatments for spinal stenosis?
    • PT: increased stabilization leads to relieved impingment
    • Wt loss
    • Pharmacotherapy: NSAIDs, opiates
    • Epidural injections
  160. What surgical proceedure to pts with spinal stenosis get?
    Laminectomy or laminotomy
  161. What are the most common locations for compression fracture?
    T8-T12 L1 and L4
  162. What are the two types of spinal compression fracture?
    Burst and wedge
  163. Burst compression fractures occur in the __ spine only
  164. A person with a compression fracture will have increased pain with what movements? and decreased pain with what movements?
    • standing or walking
    • supine possition
  165. What is the conservative treatment for a vertebral compression fracture?
    • Analgesic Tx
    • bed rest but only a few days max
    • early mobilization
    • bracing
    • PT, back stretching, lumbar strengthening
  166. What are some indications to do surgical repair on a compression fracture?
    • chronic pain refractory to conservative tx
    • pain for more than 10 wks
    • neck pain b/c of compensation
  167. What are some types of surigal repair that can be done for compression fracture?
    • Vertebroplasty
    • kyphoplasty
  168. Injection of cement into the broken fragments of the vertebral body with little height correction is a surgical repair called ____
  169. Injection and filling of a balloon inside a fractured veterbral body to create a void then inject cement into it with repair of height of the vertebrae is called
  170. ___ is caused by degeneration of the outter layers of the intervertebral disc, leading to weakening of the annulus fibrosus and tearing or fissure of the formation of the annular layers
    Herniated disc disease
  171. 40 y.o. pt presents with sudden onset of sharp burning stabbing pain which radiates down posterior or lateral aspect of the leg to below the knee with knumbess and tingling after spending the day moving stones to refinish the path to his pool. He states that the pain worsens with sitting or bending and is relieved by standing or laying down.
    Herniated disc disease
  172. leaning to the opposite side of an impinged nerve root is called a ___ list
  173. difficulty heal walking indicates...
    herniated disk disease
  174. What is the gold standard imaging for herniated disk disease?
  175. What is the treatment for herniated disc disease?
    • Bed rest for 2-7 days
    • Exercise- abdominal strenghtening back extensor then back flexors
    • Surgery if symptoms are refractory for more than 6 wks of conservative therapy
    • Diskectomy
  176. Non-specific back pain, urine or stool incontinence, and saddle paresthesia are all symptoms of
    cauda equina syndrome
  177. What reflex will be absent in pts with cauda equina syndrome?
    anal wink
  178. What is the treatment for cauda equina syndrome?
    • Emergency surgical removal of the impinging lesion
    • permanent nerve damage can ensue if not corrected surgically