Systems 5.txt

Home > Preview

The flashcards below were created by user emm64 on FreezingBlue Flashcards.


  1. How is histamine synth?
    Decarboxylation of histidine
  2. Which cells have Histamine and when is it released?
    • Mast and basophils exocytosis or degranulation, injury, IgE (allergy), drugs
    • Skin, bronchial & intestinal mucosa
  3. What are physiologic effects of histamine?
    • Relax vascular smooth muscle
    • Large vessel constriction, contract non vascular smooth muscle
    • Stimulate exocrine esp gastric
  4. What are the types of H receptors?
    • H1: vasodilation, bronchoconstriction, pain & itching (GCPR)
    • H2: stimulate gastric acid
    • H3: decrease neurotransmitter (NE, Ach, 5HT) rls
  5. What are alkylamines?
    • H antagonist, 1st gen, cold symptoms
    • Chlorpheniramine maleate
    • Bromopheniramin maleate
  6. What are ethanolamines?
    • Anti-cholinergic and sedation H antagonists
    • Benadryl, (diphenhydramine HCl)
    • Dimenhydrinate (Dramamine) anti-emetic
  7. Which H antagonist is a good anti emetic?
    Dimenhydrinate (Dramamine)
  8. Which H antagonist is used for allergic rhinitis, conjunctivitis?
    Phenothiazines: promethazine HCl
  9. What is the significance of piperidines?
    • 2nd gen antihist devoid of CNS effects
    • terfenadine (seldane)
    • fexofenadine HCl(allegra
    • Loratadine (Claritin)
  10. What is the action of antihistimines?
    • Inhibit GI/bronchial smooth muscle contraction
    • Inhibit capillary permeability
    • Antagonize salivary, lacrimal secretions
    • Relatively ineffective for bronchospasms (asthma & anaphalaxis)
  11. What are the side effects of antihistamines?
    • CNS depression (not H1 and anti-cholineric specific)
    • GI
    • Arrhythmia(rarely astemizol terfenadine)
  12. What antihistamine is dangerous with antibiotics?
    Astemizole and erythromycin
  13. How are antihistamines used in dentistry?
    • Adjuncts for angioedema
    • Hydroxyzine and diphenhydramine for sedation
  14. How do autoimmune diseases develop?
    • Problem w/negative selection in thymus
    • Infection (mimicry, super antigens)
    • Genetics(HLA)
    • T cell peripheral suppression
  15. What does every reactive Tcell express?
    FasL (eyes have Fas receptors-> Tcell death)
  16. What are the systemic autoimmune diseases(others organ-specific)?
    RA, SLE, primary sjogrens, scleroderma
  17. What is the only type I hypersensitivity that causes disease?
    Chronic urticaria: persistent itchy rash IgE
  18. What are the features of graves disease?
    • Type II stimulating thyroid antigen
    • 30’s, women, bug eyed
    • diffuse goiter and hyperthyroidism
    • HLA DR3 class II
    • ID: TSI(thy, stim Ig), TGSI(thy growth stim Ig), TBI (thy-binding inhibitory Ig)
  19. What is autoimmune hemolytic anemia?
    • Type II Rh Ag, I Ag, destroys RBC by FcR, phag -> anemia
    • IgM: kupffer (liver)
  20. What is thrombocytopenic purpura?
    Autoimmune, platelet integrin, abnormal bleeding
  21. What is goodpastures?
    • Non collagenous domain of BM col IV
    • Leads to glomerunephritis and pulmonary hemmrhage
  22. What is pemphigus vulgaris?
    • Epidermal cadherin autoantigen
    • Blisters
  23. What is acute rheumatic fever?
    • Strep cell wall antigens cross react w/ cardiac muscle
    • Arthritis, myocarditis
  24. What is cryoglobulinemia?
    • Type III Rheumatoid factor IgG complexes-> systemic vasculitis
    • Form when hypothermic
  25. What is SLE
    • Type III hypersensitivity
    • Autoantigen DNA, histones, ribosomes, snRNP, scRNP
    • Leads to glomerulonephritis, vasculitis, arthritis
    • Malar butterfly rash
  26. What is the dental presentation of SLE?
    Oral lesions on buccal mucosa and roof
  27. Which molecules do mycoplamic ones mimic?
    • RBC mb Ags (create rxn aginst host glycophorins
    • Autoimmune hemolytic anemia
  28. Explain type I diabetes.
    • Type IV hypersensitivity
    • TH1 (stim by IFN-gamma) attack Beta pancreatic cells
    • Glucogon and somatostatin still ok
  29. What gene puts you at risk for type I diabetes?
    HLA DR3/4
  30. What is rheumatoid arthritis?
    • Chronic type IV hypersensitivity w inflammatory polyarthritis of joints
    • Pannus: rheumatoid synovial mb
    • Erode joint and activate osteoclasts
    • Autoreactive CD4 T produce (TNF-a & IL-6) MMP and RANK by fibroblasts
  31. What do RA joints look like histologically?
    Hypercellular, not a lot of eosin (proteins, pink)
  32. What is MS?
    • Tcell activation against CNS (microglia or dendritic cells of brain)
    • Inflammatory reaction via mast cells degrades myelin
  33. Which dye to they use to diagnose MS?
    Gadolidium: binds myelin (show up as white plaques in CT)
  34. What is the pathophys of scleroderma?
    • Type IV (CD4+) Systemic sclerosis: excessive fibrosis (fibroblasts) CD4+ mainly in GI, muscles (diffuse or limited)
    • No elasticity
    • What is a suggested pathogensis of SLE?
    • Failure of T and B cell tolerace to defective clearance of nuclear antigens during apoptosis
  35. What is Sjogren’s syndrome?
    • Lymphocytic (CD4+ and B cells infiltration of exocrine glands
    • Ductal epithelial target
    • Xerostomia
  36. What is amyloidosis?
    • Secondary to autoimmune (never primary)
    • Proteinaceous materials in tissue interstitum (congo red)
  37. What are the 2 types of BMT?
    • Bone marrow transplant
    • Autologous: chemosensitive
    • Allogenic: leukemia
  38. What is a major hemostasis side effect of chemo?
    • Bone marrow suppression
    • Oral mucositis
  39. What are the main dental concerns for chemo?
    • Bone marrow: bleeding, infection, anemia
    • Mucositis: nutrition, hydration
  40. What is oral mucositis and the phases?
    • Mucosal inflammation ulceration (from chemo typically)
    • PHASES
    • 1: initiation (DNA injury)
    • 2: signaling (messengers)
    • 3: amplification (apoptosis)
    • 4: ulceration (pain)
    • 5: healing
    • Grades:
    • 0: no symptoms
    • 1: soreness
    • 2: ulcers, eat solids
    • 3: ulcers, liquids
    • 4: ulcers: alimentation not possible
  41. Which areas of oral cavity are keratinized?
    • Dorsum of tongue
    • Hard palate
    • Attached gingiva
  42. What are the early and late presentations of mucositis?
    • Early: Erythema, edema, sensitivity, soreness
    • Late: ulcerations, pain, infections, nutrition, bleeding
  43. What is the main goal of dental therapy for chemo?
    • Eliminate sources of infection
    • Treat between cycles
  44. What do PGs do?
    • Platelet aggregation, vasodilation, vasc permeability, pain sensitivity
    • PDX, PGI: vasodilation, antiaggregating
    • PGE2: erythema, edema, pain, fever
    • PGF2a: vasodilator, uterus contraction
  45. What do leukotrienes do?
    • Immediate hypersensitivity
    • LTC4, LTD4: broncioconstriction, mucosal edema
    • LTB4: chemotaxis
  46. Describe the secretions of lymphocytes.
    • IL: stimulate T and B cells
    • MCP-1: monocyte accumulation
    • GM-CSF: granulocyte/macrophace colony
    • INF-a: antiviral, macrophage
  47. What is the difference between COX 1 & 2?
    • COX1: constitutive regulate renal, mucosa integrity
    • COX2: inducible (inflammation)
  48. What is prostaglandin role in GI?
    Mucosa protective
  49. What is a hapten?
    Protein-free that can combine and elicit immune response
  50. What does a dentist need to ID in allergy?
    • Severity, speed of onset, extent(local/general)
    • Know HX: specifics, timing, treatment
  51. What are manifestations of allergy?
    • Skin: Erythema, urticarial, wheals, rash pruritus
    • Resp: bronchospasm, laryngeal edema
    • GI: nausea, pain
    • CV: angioedema, hypotension, lightheadedness, tachycardia, syncope
  52. What is allergenic in LA?
    Sodium bisulfite (antioxidant)
  53. What is allergenic in dental office?
    LA(Na bisulfite antioxidant), Antibiotics, latex, pain meds
  54. Which allergic reaction is faster IV or PO?
    IV
  55. What should you prescribe for suspected generalized allergy?
    • Diphenhydramine (Benadryl) 25-50mg PO TID 3x
    • (can be given IV/IM should be escored home)
  56. What if respiratory or CV allergy?
    • Stop, 911, upright if breathing problems, supine/trendelenberg if hypotensive
    • Oxygen, bronchodilator
    • EPI: .3-.5mg SC/IM (every 5 minutes)
  57. What is the common factors of CT?
    • Cells (fibroblasts, chondrocytes
    • ECM(collagens, proteoglycans
    • CD44, integrins
    • Enzymes
  58. What is ANCA?
    • Anti-neutrophil cytoplasmic antibody
    • Seen in systemic vasculitis
  59. Which autoantibodies found in Sjogrens?
    RNA-assosciated (Ro & La)
  60. Which autoantibodies seen in scleroderma?
    Anticentromere, antitopoisomerase
  61. What is a bursa?
    Synovial lined sac separate bone and muscle/skin
  62. What is enthesis?
    Attachement of muscle tendon and ligaments
  63. What is the characteristic feature of RA?
    • Persistent inflammatory synovitis (slows down with advanced AIDS and pregnancy)
    • What is a rheumatoid pannus?
    • Early formation of granulation tissue w proliferating fibroblasts and some inflammatory cells
  64. What are early signs of RA?
    • Morning stiffness > 1 hour
    • Swelling of 3 or more joints
    • Leads to swan neck deformities
  65. What are x-ray differences of OA and RA?
    • Osteo: no cartilage, bone spurs
    • RA: synovial inflammation w bone erosion
  66. What is a complication of RA in dental setting?
    Subluxation of C1 and C2 cant’ move head, may need to be ligated
  67. What is felty’s syndrome?
    RA, splenomegaly and neutropenia
  68. How is RA dignosed?
    • No specific, RF in 80%
    • ESR and eanemia
    • Variable
  69. How is RA treated?
    • Drugs: NSAIDS, corticosteroids (disease modifying antirheumatic drugs (DMARDs)
    • Surgery
    • Immunologic: entanercept or infliximab (TNF-a inhibitors)
  70. How is SLE diagnosed?
    • ANA (antinuclear Ab)
    • Anti-dsDNA & anti-Sm MORE specific, LESS sensitive
    • Lupus band test: Ig & complement in dermal epidermal junction
  71. What is the lupus band test?
    Looks for Ig and & complement in dermal-epidermal junction
  72. Describe the various lesions of scleroderma.
    • Plaques(morphea)
    • Streaks(linear) (en coup de sabre)
    • Nodules(nodular)
  73. What is CREST syndrome?
    • Type of systemic slceroderma
    • Cutaneous calcinosis
    • Raynaud’s
    • Esophageal dysfunction
    • Sclerodactyly
    • Telangiectasias (dilated suface vessels)
  74. What does schrirmer’s test measure?
    Tera production (confirm sjogrens w/biopsy of salivary glands of lower lip
  75. Drugs with negative log ratio are selective for?
    COX2
  76. What is Burton’s x-linked agammaglobulinemia?
    • Males w/o Ig’s
    • No mature B cells, germinal centers, plasma
    • Tx: Ig replacement
    • Defective bTK stops development from pre-B to immature B
    • Dx: NO CD19+ cells
  77. What are the 3 ways Ig work?
    • 1. neutralized
    • 2. Opsonized
    • 3. Complement activation
  78. What is isolated IgA def?
    • Intrinsic B cell defect (TH dystfunction, suppressor T cells) may have anti-IgA Abs
    • Asymptomatic, may have some sickness
    • Other Ig levels are normal
  79. What is often associated w/ IgG subclass deficiency?
    • Ataxia-telangiectasia
    • Tx: IV IgG
  80. What is Hyper IgM def?
    • X linked mutation in CD40L-> high IgM low other Ig
    • Pyogenic bacteria infections
    • Dx: hypercellular node w/ no distinguishable germinal center
  81. What is DiGeorge syndrome?
    • 3rd and 4th branchial arch, no thymus, no mature T Cells -> no active B cells
    • ears/eyes lower, eyes spaced apart
  82. What happens in the thymus?
    T cells mature: cortex=education
  83. What is CVID?
    • Umbrealla for impared B cells
    • High infection, autoimmune
  84. What is SCID?
    • Severe combined immunodeficiency
    • Variable forms most commonly x-linked (IL-2 receptor)
    • Defective T and B cell function
    • Tx: antimicrobial & BMT
  85. What does a mutated IL-2 receptor cause?
    No activation of T cells (gamma chain)
  86. What does a SCID thymus look like?
    No germinal centers, no clonal expansion, different architecture
  87. What is Wiskott-Aldrich?
    • X linked: eczema, bacterial infections thrombo-cytopenia (WASp)
    • Decreased T cell, defective NK-cells, increased autoimmune/cancers
    • WASp expressed in lymphocytes and megakaryocytes
  88. What is CGD?
    • Defect in monocyte and neutrophil respiratory burst (H2O2, O2, NO, myeloperoxidase)
    • Cannot kill CATALASE+ bacteria
  89. What is the respiratory burst?
    NADPH + 2 O2 -> NADP+ 2O- -> SOD-> H2O2
  90. What does myeloperoxidase do?
    Creates chloramines (bleach)
  91. What is hereditary angioneurotic Edema?
    • HAE C1 defect (lacks inhibition)
    • Prevented immune complex formation
    • Alternative pathway: C3
    • Classical pathway: C1qrs, C4 C2
    • Terminal Complement: C5-9
  92. Chemo regimen of induction, consolidation and maintenance/conditioning.
    • Induction: 1st cycle, decrease the number of malignant cells.
    • Consolidation – once the cells are no longer detectable another cycle is given to further reduce the ones that are not seen. (once the numbers get below 5% of the cells seen on a smear/biopsy, then it is considered undetectable)
    • Maintenance – done to keep the cells undetectable
  93. What is non-myeloablative?
    Chemo then TBI(radation) on day of transplant-> mild pancytopenia, delays GVHD
  94. What is critical to prevent infections for oral mucositis?
    Depressed immune, open sores, different oral flora
  95. How are Fl trays used?
    Daily, 1-3 drops, 4-10 minutes at night when less salivary flow
  96. What does GVHD increase risk for?
    Cancer (graft v host)

Card Set Information

Author:
 emm64
ID:
 167908
Filename:
 Systems 5.txt
Updated:
2012-08-29 01:54:40
Tags:
S5final
Folders:

Description:
S5Final
Show Answers:

What would you like to do?

Home > Flashcards > Print Preview