medications

  1. Why is screening for TPMT activity required prior to initiation of therapy of azathioprine?
    TPMT helps to inactivate the metabolites produced by the drugs alone with xanthine oxidase. Individuals with absent TPMT activity cannot effectively break down these metabolites, leading to their accumulation
  2. Azathioprine:
    broken down to 6 thioGMP and TIMP by TPMT 

    6thio: induces DNA strand breaks and base mispairs

    the other one inhibits formation of ribosyl 5 phosphate and prevents production of purines (guanine and adenine)
  3. Mycopehnolate Mofetil
    • converted to mycophenolic acid
    • inhibits IMPDH and thus purine synthesis
  4. TNF alpha causes new onset of
    • heart failure 
    • and can cause antibodies to form against this drug
  5. Biosimilars:
    a copy of the biologic medicine that is similar to BUT NOT IDENTICAL to the original medicine
  6. TNF alpha blocking drugs:
    • Certolizumab, golimumab, infliximab 
    • etanercept, adalimumab
  7. Anakira:
    IL1 receptor antagonist 

    can cause anaphylaxis
  8. Tocilizumab MOA:
    binds to IL6 receptor antagonist---causes neutropenia and thrombocytopenia
  9. Rituximab is less likely to:
    reactivate TB and cause lymphomas
  10. Rituximab:
    bind to CD 20 on B cells and activate NK cells and cytotoxic T cells---INFUSION RELATED RXN INCLUDING RASH
  11. Abatacep adverse effect:
    infusion related is the main COPD exacerbation 

    AVOID with TNF alpha blocking agents
  12. Abatacep:
    APC activates T cell through binding of costimulators CD80/86 as well--this drug prevents this from happening so T cells cannot proliferate
  13. Precautions that must be taken before taking biologics
    • --check for latent diseases like TB and hepatitis B 
    • --you can not have gotten a LIVE vaccine within 3 months of therapy/during 
    • --increase risk of cancer (except rituximab)
  14. Gold salts:
    mechanism is not known -- used to decrease inflammation but can cause nephrotoxicity
  15. Cyclophosphamide side effects:
    • hemorrhagic cystitis 
    • cardiotoxicity
  16. Cyclophosphamide MOA:
    • metabolized to phosphoramide mustard in the liver 
    • cross links DNA to prevent cell replication
  17. Cyclosporine side effects
    • Nephrotoxicity 
    • GINGIVAL hyperplasia 
    • hepatotoxicity
  18. Cyclosporine
    Calcineurin usually phosphorylates TF and the TF is able to produce IL2--> calcineurin is inhibited by this drug and so IL2 and T cell activation is not occurring
  19. Sulfasalazine
    • prodrug that is cleaved by bacteria in the colon into 
    • sulfapyridine (intended effect mediated by this) 
    • 5 ASA
  20. Chloroquine
    • Eye exams are required at baseline and yearly-- drug can cause a bull's eye retinopathy 
    • causes cardiomyopathy myopathy and anemia
  21. TOFACITINIB
    Jak stat inhibitor causes decreased proliferation and differentiation of NK B and T cells 

    also causes hepatotoxicity and GI perforation 
  22. Leflunomide MOA
    activated in the intestine to teriflunomide--> which inhibits DHODH and inhibit pyrimidine production

    causes hepatotoxicity
  23. Adverse effects of methotrexate:
    • Renal
    • hepatotoxicity 
    • teratogenesis 

    FOlate supplements are necessary
  24. Methotrexate unintended consequence:
    it also inhibits the dihydrofolate reductase-- preventing folic acid from being converted to the active form---DNA synthesis is altered, replication decreases apoptosis increases
  25. Imaging:
    CT: a lot of radiation, multiple XRs that are taken from many different views and combined into a single image 

    MRI: no radiation, magnetic view (if someone came in with a lot of nails in their brain--avoid using an MRI) 

    XR: radiation but more localized to where you want it done
  26. For arthritis:
    it is good to get a weight-bearing XR-- gravity will be accounted for and you can see narrowing of the joint space
  27. Mets and tumor response--the modality of choice is:
    scintingraphy--PET scan
  28. Stress fractures, infections, primary tumors
    MRI--with or without--this is the modality of choice but clinically and with insurances-- the initial imaging ordered should be XR.
  29. Acute fractures--primary modality
    XR-- may require them to come back for a repeat incase you missed it the first time/or it didn't show as obviously on the initial xr.
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  31. Explain this MRI image: Image Upload 6
    the white is not continuous--suggesting a patellar tendon tear causing a patella alta pathology
  32. Image Upload 8
    • Normal patellar location should be in between the two condyles 
    • Image Upload 10in abnormal it sits above the condyles
  33. Image Upload 12
    black line--patellar tendon

    the triangles: Anterior horn (near the patellar tendon) of the menisci and posterior horn
  34. On MRI
    soft tissue is black--the PCL is usually thicker than the ACL
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  37. Femoral stress fractures can be...either *** or ***
    compression side: occur on the concave side (inferior medial)

    tension side: occur on the convex side (superior lateral)-- restricts weightbearing because there is a greater chance that the fracture can break off
  38. On a T2 MRI--
    any sort of fluid--edema, inflammation-- is going to light up 

    in t1 the bone will light up instead of the soft tissue
  39. Image Upload 22
    the contour is not nice and smooth implying a step off/fracture
  40. Image Upload 24
    Acetabular fracture
  41. Evaluating the hip
    • order XR of the AP pelvis
    • AP Hip 
    • frog leg (take heel of the foot and rest it on the opposite knee
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    Image Upload 28
  43. With imaging you always want to:
    confirm with at least 2 different views (AP and lateral are the most common--but the main diagnosis is coming from the history using the image as a confirmatory)

    1 VIEW IS NOT DIAGNOSTIC
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    Image Upload 32
  45. Pes anserine bursitis
    Located on the medial tibia-- gracilis, semitendinosus, and sartouris all attach here--- people with osteoarthritis get greater articulation at the medial aspect causing bowing at the lateral side 

    more pressure at the articulation end and causes bursitis
  46. Symptoms of a strangulated femoral hernia include
    • sudden groin pain abdominal pain nausea and vomiting 
    • --strangulated hernia is when there is no blood flow to the hernia and it can become necrotic
  47. Loss of hamstring muscles would cause
    profound loss of knee flexion and some weakness with hip extension
  48. Medial thigh's blood supply:
    obturator artery and perforating branches
  49. Quadricep contusion:
    treated by immobilizing the knee in 120 degree of knee flexion for 24 hours to avoid hematoma formation-- and then PT

    complication: myositis ossificans
  50. Sartorius loss will 
    cause no active deficit
  51. iliopsoas:
    main hip flexor--loss will cause profound deficit
  52. the iliotibial tract runs from
    the iliac tubercle to gerdy's tubercle
  53. What is the best treatment for Thromboangitis obliterans:
    smoking cessation 

    Angiograph will show collateral blood vessels made to combat the decreased blood flow
  54. Thromboangitis obliterans:
    • associated with smokers and caused by reduced blood flow 
    • -gangrene
    • -raynauds phenomena
  55. How is Polyarteritis nodosa different from all the other large and medium vasculitis
    it has a granulomatous biopsy but also with necrotizing fibers
  56. Polyarteritis nodosa:
    Associated with hepatitis B--and does have cutaneous involvement
  57. Kawasaki syndrome
    medium vessel-- asian children will present with rashes (hands and feet) that can desquamate-- they also present with strawberry tongue, and fever, joint pain 

    NOT accompanied or preceded by a sore throat or sandpaper rash 

    --> Tx: aspirin and Immunoglobulin
  58. takayasu arteritis
    • affects the aorta and its branching arteries-- causes limb claudification, and pulse differences in the extremities 
    • bruits 
    • stroke
  59. What is temporal arteritis associated with?
    • polymalgia rheumatica-- symmetrical pain 
    • and on biopsy is associated with giant cells and granulomatous appearance
  60. Pseudogout radiographic imaging:
    there is a faint white line going across the joint (chondrocalcinosis)
  61. How can you tell CPDD from gout:
    requires synovial fluid sampling-- gout is needle like and has a negative infringence--- so when the crystals are parallel to the red compensator it appears yellow and blue when perpendicular--opposite with CPDD (positive and rhomboid)
  62. Role of genetics in CPDD
    8q and 5p-- 5p has a greater effect and linked with ANKH transmembrane protein that releases ATP, PPi into the extracellular matrix... ATP is the greatest contributor (ENPP breaks it into PPi) 

    binds with calcium to form calcified deposits
  63. What are the risk factors associated with CPDD
    • hypmagnesium 
    • hypophospate 
    • hyperparathyroidism 
    • hemochromatosis
  64. Pegloticase
    uricase--which is not found in humans--its a recombinant protein which is given to break down the uric acid
  65. Probenecid
    Lesinurad
    both inhibit tubular reabsorption of uric acid
  66. What is a classical radiographic finding in gout:
    hole punched/mickey mouse ears
  67. What are tophi?
    they are granulomas surrounding the deposits of MSU crystals and are also seen in chronic forms of CPP disease 

    they can result in destructive arthopathy
  68. What medications can cause gout:
    • salicylates 
    • diuretics
    • cyclosporine 
    • pyrazinamide
  69. Myositis ossificans is associated with:
    blunt trauma
  70. What are the antibodies associated with cutaneous dermatomyositis
    Mi: against DNA helix--benign 

    SAE- against TF-- systemic systems (weight loss and fevers)

    NXP- against nuclear matrix protein, calcinosis and edema

    TIF--transcription factor, psoraisis and hyperkerototic lesions

    MDP--against RNA helicase-- causes lung disease, severe skin path, and amyopathic
  71. What has to be highly monitored when on a statin?
    CK levels and other enzymes-- because correlated with muscle damage--
  72. Myositis specific antibodies?
    Anti synthease: anti jo-- associated with Raynauds, Arthritis, and mechanic fingers, LUNG disease 

    Anti-SRP: severe--necrotizing myopathy with minimal inflammation 

    HMCRP: against reductase--associated with statin use and causes necrotizing myopathy
  73. Myositis associated antibodies?
    • SSA SSB SCL 
    • U1 U2 U3
    • ANA
  74. What cytokine is associated with dermatomyositis vs polymyositis
    Dermatomyositis has IFN and CD4+ atrophy/perimysial inflammation 

    Polymyositis is associated with CD 8
  75. Diagnostic criteria for systemic JIA:
    quotidian fever for at least 2 weeks (has to occur around the same time) 

    atleast 2 of the following: serositis, rash (salmon pink), hepato/splenomegaly, lymphadenopathy
  76. What can systemic JIA lead to:
    Macrophage Activation syndrome-- thrombocytopenia, low fibrinogen, elevated ferritin, AST, activated macrophages
  77. what are the different types of JIA
    • systemic (not associated with uveitis)
    • oligo (less that 4 joints) --associated with uveitis (esp if ANA +)
    • poly (more than 5 joints)--associated with uveitis greater risk if ANA and RF positive (Rf is worse prognosis)
  78. What are the causes of reactive arthritis?
    • chlamydia, campylobacter
    • e. coli 
    • yersina 
    • salmonella, shigella
  79. Reactive arthritis
    • can't see (conjunctivitis) 
    • can't pee (urinary complaints)
    • can't climb a tree (arthritis)
  80. What is the treatment for Rheumatic fever
    antibiotics and aspirin 

    • steroids if heart is involved 
    • -all family members who test positive should be treated with antibiotics even if asymptomatic
  81. Diagnostic criteria for rheumatic fever:
    throat culture for strep=+ or antibodies are present (ASO. DNAase B)

    and 2 major or 2 minor, 1 major 

    Major: joint pain (migratory, inflammatory), carditis, nodules, erythema margin, synder chorea

    Minor: fever, arthralgia, acute phase reactants, PR interval prolonged
  82. Hands feet and mouth is a
    self resolving disease
  83. what is the first line treatment for staphylococcal scalded skin syndrome—
    accompanied by honey gold crusting—treated with mupirocin (impetigo)

    IV  cephalosporin for scalded skin syndrome

    furuncles first-line treatment is cephalosporin, folliculitis it is mupriocin
  84. Genital warts:
    imiquimod, 5FU liquid nitrogen

    • low risk: HPV 6 and 11
    • high risk: 16 and 18
  85. Molluscum is caused by
    poxvirus… if adults get it it is usually sexually transmitted or HIV—cantharone imiquimod cryotherapy
  86. Oral hairy leukoplakia is caused by
    EBV-- and cannot be scraped off like thrush can be 

    treat it via HAART
  87. Herpes:
    orolabial herpes are commonly acquired during dental procedures

    dentists are likely to acquire cold sores on their fingers-- because they come into close contact with individuals and their cold sores
  88. Phantom factor:
    is a pore forming molecule 

    and MECA gene causes a mutation in the penicillin binding protein that acts as the trasnpeptidase to make the cell wall
  89. Methotrexate intended MOA
    - Aicar transaminase so Aicar increases inhibiting AMP deaminase- AMP increases causing decreased function of WBC
Author
pooja.march
ID
365131
Card Set
medications
Description
Updated