Block F

Card Set Information

Author:
contacts4
ID:
267888
Filename:
Block F
Updated:
2014-04-10 19:06:49
Tags:
Block
Folders:

Description:
Block F
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user contacts4 on FreezingBlue Flashcards. What would you like to do?


  1. Describe the epithelium of the skin.
    Stratified squamous epithelium that is keratinized
  2. Skin and its integument comprises ___% of the total body weight.
    16%
  3. Describe the epithelium lining the oral cavity.
    It is lined by a stratified squamous epithelium that is non-keratinized.
  4. Name 5 functions of the skin and the type of cells responsible for each of them.
    • 1.protection - Keratinocytes
    • 2.Receives stimuli from the environment- Merkel cells
    • 3. Excretes variuos substances - Sebacous glands and sweat glands
    • 4.Thermorefulation and maintenance of water balance - secretion of keratinocytes
    • 5. Immunogenicity - Langerhans cells
  5. Where does Melanocyte come from?
    They arise from the neural crest cell.
  6. Briefly describe the stratum geminativum (basal layer).
    A single layer of cuboidal or columnar cells resting on the basement membrane. They are responsible for renewal of the skin by mitosis.

    * Desmosomes attach cells to each other and hemidesmosomes attach the cells to the BM.
  7. What are the desmosome for?
    They attach the cells together at the level of epidermis(mostly stratum germinativum and spinosum)
  8. Name the 5 layers of the epidermis
    • - stratum germinativum
    • - stratum spinosum
    • - stratum granulosum
    • - stratum lucidum (not always present)
    • - stratum corneum
  9. Where are the lamellated granules? What is their role?
    They are present in the cell of the stratum spinosum and they secrete glycolipid between the cell, so the skin becomes impermeable to water. They are also present in other layer, mostly stratum granulosum where they are more common where they collect at the cell periphery.
  10. Describe the desmosome attachment in the stratum spinosum.
    Tonofibril are cytosplasmic proteins which converges to the desmosomes. That are responsible for anchoring them to the cytoskeleton. Cadherins are the most important transmembrane proteins to have a role in cell adhesion. They are Ca dependant.
  11. Describe the Stratum Granulosum.
    • - 3 to 5 layers of flattened cells, with irregular, large keratohyalin granules (these are NOT secretory granules) that are responsible for keratinization.
    • - cystoskeletal can crosslink to form a tough adhernt and impenetrable barrier at the surface.
  12. How are the melanocyte anchored?
    They are not attached to the keratinoctyes by desmosomes, but they are attaches to the basal lamina by hemidesmosomes.
  13. What are Langerhans cell?
    They are a APC (antigen presenting cell) dentritic cells which participates in the immune respone and migrates from the skin to the lymph nodes.
  14. What are Merkel cells?
    They are responsible for sensory reception and they are associated with unmyelinated nerve fibers.
  15. Psoriasis is associated with activation of which cell?
    T-cell that may increase keratinocyte proliferation up to 7 folds.
  16. What are some functions of the dermis?
    • - Connects tissues together and provide a flexible support
    • - Nutritive and excretory role
    • - Role in the defence of the body against infection
  17. Name cells type that you can find in the dermis.
    • Mesenchyme(not in adult)
    • fibroblast(in young individual)
    • fibrocyte
    • macrophages(they can fuse and form the foreign body giant cells)
    • Mast cell (histamine + eosinophil chemotactic factor)
    • plasma cell
    • Adipocyte
  18. What is the difference between the brown fat and the yellow fat?
    • The BROWN fat is a multilocular adipocytes, meaning that there is numerous lipid droplets within 1 cell. It is used to produce heat. The nucleus is central to the cell.
    • The YELLOW fat, is unilocular, so only 1 drop of fat per cell, forming the signet ring cell.
  19. What are the proteins responsible for gathering information on the ECM(extracelllar matrix)?
    Integrins!
  20. Where are type I, II, III and IV collagen mostly seen?
    • I : ordinary connective tissue and bone
    • II : cartilage
    • III : reticular
    • IV : basal lamina
  21. Name the 4 major stages of normal wound healing
    • hemostasis
    • inflammation
    • Cell proliferation/matrix production
    • Remodeling
  22. Describe the important events in the hemostasis phase of wound healing.
    • - vascular constriction, platelet aggregation and degranulation and fibrin clot formation
    • - Release of pro-inflammatory cytokines and growth factor
  23. Describe the important events in the inflammation phase of wound healing.
    • infiltration of neutrophils, macrophage and lymphocytes
    • Release of cytokines and other factors(to stimulate keratinocyte, fibroblast and angiogenesis) by the macrophage
  24. Describe the important events in the cell proliferation phase of wound healing.
    • re-epithelialization
    • fibroblasts and endothelial cells become prominent, with associated ECM formationa nd angiogenesis (together forming the granulation tissue)
    • Migration of the keratinocyte is associated with disassembly of hemidesmosomal, retarction of tonofibril and dissolution of most of desmosomes.
    • ** The hair follicle represents a deep and protecetd repository of stem cells
  25. Describe the important events in the remodeling phase of wound healing.
    • ECM production
    • The wound also undergoes physical contraction throughout the entire wound-healing process in the stages above, mediated by contractile fibroblasts containing abundant actin called myofibroblasts that appear in the wound.
  26. What is TGF-beta?
    Transforming Growth Factor is a ligand for starting migration of epidermal keratinocytes during re-epithelialization. It is release by the platelets. It also promotes activation of the monocytes/macrophages.
  27. Why is oxygenation useful in a context of wound healing?
    It prevents Wound from infection, induces angiogenesis, increases keratinocyte differentiation and enhances fibroblast proliferation and collagen sythesis and promotes wound contraction.
  28. What are the difference between hypertrophic scarring and keloids?
    • Both : overabundance of dermal collagen
    • Hypertrophic scarring : generally stays within the confines of the initial wound and increase in size by pushing on the margins of the scar  Usually develop in wounds at anatomical location with high tension (shoulder, neck, kness, ankles). The collagen is primarily oriented parallel to the epidermal surface
    • keloids: invade the surrounding tissue. They persist and do not regress spontaneoulsy. They may ulcerate and have well-demarcated but irregular border. They tend to recur following excision. The collagen is running in all direction in a disorganized swirl fashion. Keloids fibroblasts show increased growth factor receptors.
  29. What is the Parkland formula?
    • It is a formula thta provides an estimate of fluid requirements following a burn. It states that you need 4cc/kg/%TBSA burned in the first 24 hours. 1/2 being given in first 8 hours that the other half in 16 hours.
    • * the formula only provides an estimate. Clinically you need to monitor urine output wth a foley cateheter to get to a urine output of 30cc/h in adults and 1cc/kg/h in children
  30. What is the TBSA cut-off where the patient may be given fluid orraly(not IV)?
    In general, it is <20% for adults and <10-15% for children
  31. What is the rule of nines?
    • Each arm = 9% of TBSA
    • Each leg = 18 % of TBSA
    • chest/back = 18%
    • head = 9%

    • * patient's palm including finger is about 1%.
    • * It only counts for 2nd or 3rd degree burns
  32. Briefly distinguish between, first, superficial 2nd degree, deep 2nd degree, 3rd degree and 4th degree burn.
    • 1st : involves epidermis only. It looks red and dry.
    • superficial 2nd : involves epidermis and upper dermis. It looks pale pink with small blisters.
    • deep 2nd : involves epidermis and significant part of dermis. It looks blotchy red or pale deeper dermis where blisters have ruptured.
    • 3rd : Epidermis, dermis and cell adnexal structure are destroyed. It looks white waxy charred without blister or capillary refill. There is no more sensation.
    • 4Th : Extend trhough the subcutaneous soft tissue(muscle, tendon, bone). Associated with limb loss or the need for complex reconstruction.
  33. For how long does the damage to the skin continues after the initiail burn injury?
    For 24-48 hours
  34. What are the criterias for a burn center referral?
    • Pts <10y/o or >50y/o if >10% TBSA second and third degree burns
    • Second and third degree burns >20%
    • Second and third degree bruns with serious threat of functional or cosmetic impairments that involve the face, hands, feet, genitalia, perineum and major joints.
    • Third degree > 5%
    • Electrical burns, including lightning injury
    • Chemical burns with serious threat of functional or cosmetic impairment
    • inhalation injury with burn injury
    • Circumferential burns
    • Burn in patients with preexisting medical disorders that could complicate management, prolong recovery or affect mortality.
    • Any burn pts with cocomitant trauma in which the burn injury poses the greatest risk
    • hospitals without the qualified personnel or equipment for the care of chilfdren should tranfer burned children to a burn center with these capabilities.
  35. Name 5 types of white blood cells.
    • neutrophils
    • lymphocytes
    • monocytes
    • eosinophils
    • basophils
    • fixed leukocyte(eg: dentritic cell, mast cell)
  36. What is the difference between absolute and relative neutrophil count?
    The absolute count is the number of the neutrophil(useful for chemotherapy patients) but the relative count only indicate us the proportion of white blood cell that is neutrophil(used to assess infection and inflammation)
  37. Describe the neutrophils and their principal fonction.
    • Neutrophils normally account for the largest percentage of WBC. They have numerous pink granules and a dark nucleus, which have a different shape depending on its maturity. The segmented neutrophil, which is the mature neutrophil, have a nucleus that is separated into 2-5 segments or lobes.
    • They can do phagocytosis and activation of bactericidal mechanisms
  38. Describe the eosinophils and their principal function.
    • The nucleus is usually large and typically bilobate. They have pink granules. They kill parasites that are antibody-coated
    • Thyey fight off infectious agents/damage tissue throught release of toxic granule proteins (major basic protein, eosinophil-derived neurotoxin, eosinophil cationic protein, RNAses)
    • Important against parasites
    • ejects DNA of mitochondria producing a sticky network that captures bacteria and promote their extracellular killing
  39. Describe the basophils and their principal function.
    • Their nucleus is usually large, irregular and sometimes have 3 lobes. You can see dark-blue granule. They have a unknown function.
    • They have many similar characteristic than mast cells.
    • They are involved in allergic reponse, since they have FcεR
    • Plays a significatn trole in the anti-parasitic response
  40. Usually, eosinophils and basophils increase in number following a increased number of neutrophils, though not always(eg: age, pregnancy). Name some condition characterized by increase neutrophil, eosinophil and basophil.
    • bacterial infections
    • acute inflammatory diseases
    • cancer (particularly with marrow metastasis)
    • tissue necrosis
    • acute transplant rejection
    • surgical and orthopedic trauma
    • myeloproliferative diseases
    • steroid use
    • pregnancy (mainly 3rd trimester)
  41. Describe the monocytes and their principal function.
    • They are the largest WBC circulating in peripheral blood. Monocytes mature into macrophage when they enter a tissue. These macrophages have different name depending on where they are(eg: kupffer cells in the liver).
    • Macrophages arrive after injury and become the predominant leukocyte within 48 hours.
    • First cell to engulf and process the antigen and present it to the lymphocytes stimulating a specific immune response to that antigen
    • Macrophage can destroy the organism while keeping its cell surface markers to present to CD4 T cell (cytotoxic T lymphcyte)
  42. Where does the T lymphocytes mature? and the B cell?
    • T cells : in the Thymus
    • B cells : in the Bone marrow
  43. Which leukocyte is responsible for cell-mediated immunity? and for humoral immunity
    • T lymphocyte -> cell-mediated
    • B lymphocyte -> humoral, antibodies
  44. What triggers activation of NK(natural killer) cells?
    • changes in normal cell states
    • They are very effective against tumor cells and virally infected host cells.
  45. What are possible causes of neutrophilia(high neutrophil count)?
    • most common -> acute bacterial infection
    • myeloproliferative disorders including polycythemia Vera and chronic myelocytic leukemia
    • It is associated with obesity, smoking and stress of surgery
    • If SEVERELY neutrophilia : pathologic conditions causing the neutrophils to become hypermature and increased number of segments seen in liver disease, Down's syndrome and megaloblastic anemia
  46. What are possible causes of neutropenia?
    • sever prolonged infections
    • increased WBC destruction
    • drugs(antimicrobial, NSAID, antidepressant)
    • increased splenetic pooling known as hyperseplenism.
  47. What are different etiology for monocytosis(increased number of monocytes)?
    • absolute monocytosis : myeloproliferative disorder
    • relative monocytosis : seen during recovery from drug-induced neutropenia
    • Reactive absolute monocytosis : chronic infectious, inflammatory, granulomatour processes, metastatic cancer, lymphoma, radiation therapy and depression.
  48. What can lead to lymphocytosis?
    • if small normal appearing lymphocyte : viral etiology(mononucleosis, cytomegalovirus, measles)
    • B-cell leukemia
  49. What are the main etiologies for eosinophilia?
    • parasitic infections(eg toxoplasmosis, GI parasites)
    • bronchoallergic reactions(eg: asthma, allergic rhinitis and hay fever)
    • associated with skin rashes
    • * Hypereosinophilic syndrome
  50. What do we have to consider if there is monocytopenia?
    • is the patient on glucocorticoid therapy?
    • Does he have hairy-cell leukemia?
    • or aplastic anemia?
  51. Lymphopenia is a normal process of aging, but in children in may be a sign of...?
    immune deficiency
  52. What does CD stands for?(as in CD4, CD8...)
    Clister designation. It is used for cell surface markers/receptors
  53. What is a cytokine storm?
    It is a immune response that can be fatal during which there is a positive feedbackloop resulting in high level of different cytokines
  54. Name some function of immunity.
    • fight infection
    • prevent cancer
    • develop a memory response
    • maintain homeostasis
    • recognize self
    • repair damage
  55. What are the 4 signs of inflammation?
    • swelling
    • redness
    • heat
    • pain
  56. What are the mediators implied in the inflammation reaction?
    Prostglandins, leukotrienes and bradykinins. They will vasodilate, increase vascular permeability and recruit cells
  57. What are the function of the mast cells?
    release of granules containing histamine and active agents
  58. What does TLR-3 recognize? and TLR-5? TLR-7? TLR-8?
    • TLR-3 : double-stranded DNA, virus
    • TLR-5 : flagellin
    • TLR-7 : single standed DNA
    • TLR-8 : prokaryote
  59. what is the complement system?
    It is a series of proteins found in plasma, that are involved in recognition of paterns on the pathogen. They also activate innate cells and kill the pathogen and some inflammation product, thus preventing damages.
  60. Name and describe the 3 pathways responsible for C3 convertase activation in the complement pathway.
    • Classic : Triggered by an antigen-antibody complexe which is recognize by C1. Then C4, C2, C3.
    • Lectin pathway : mannose-binding lectin(MBL) wich looks like C1 directly binds to the pathogen ans the rest of the pathway is the same as the classical pathway.
    • alternative pathway : C3 convertase is always active but gets stabilize by the presence of pathogen
  61. What is the main role of TNF-a? of interferon-gamme? of IL-6)
    • TNF-α : promotes inflammation
    • interferon-γ : activate macrophages, promote inflammation and promote the adaptive response
    • IL6 : induce upregulation of acute phase proteins and induce fever.
  62. What is the cuticle?
    It is the skin that extends from the proximal nail fold and that fuses with the nail plate.
  63. How is called the part the create the new nail, under the proximal nail fold?
    The nail matrix
  64. What is the hyponychium?
    It is the cutaneous margin underlying the free nail.
  65. What is onychomadesis? What are possible etiologies?
    • Complete separation of the nail plate from the nail bed due to a arrest of growth of the nail matrix
    • trauma(including onychotillomania), demratologic diseases(Eczema, erythroderma), systemic conditions, high fever, viral illness
  66. What is trachyonychia? Name some etiologies.
    • Nail roughness and opacity due to excessive longitudinal ridging.
    • idiopathic, alopecia areata(hair loss), psoriasis, dermatitis, Lichen planus
  67. What can be associated with nail pitting?
    • psoriasis, eczema, alopecia aerata or trauma
    • * you give potent topical corticosteroid to help the healing process
  68. What is acute paronychia?
    • It is painful, erythematous indurated swelling of nailfolds with purulent draining developing over a few hours. 
    • Usually caused by staph aureus.
  69. How do you treat acute paronychia?
    • oral antibiotics with gram+ coverage against S. aureus.
    • If it progress to an abscess, it should be drained promptly.
  70. What is the most common cause of chronic paronychia?
    Candida(yeast) and irritation caused by saliva.
  71. What is an importnat difference between acute paronychia and herpetic Whitlow?
    Herpetic is recurrent
  72. What is melanonychia? What is the difference between this and racial melanonychia?
    • It is a browm or black line band along the length of the nail. 
    • It is caused by a nail matrix nevus or lentigo.
    • The difference is that racial involves several nails, but beware not to confuse with drug induced melanonychia(which can also involve many nails)
  73. What is onychomycosis?
    • It is a fungal infection of the nail.
    • You should look if there is tinea pedis(athlete's foot)
  74. How can we prevent recurrence of onychomycosis?
    • don't share shoes
    • no poorly fitted shoe
    • use antifungal sprays or powder in shoes and socks
    • avoid goig barefoot
    • discard old shoe
  75. Where is located the matrix cells responsible for hair growth?
    In the hair bulb
  76. What are the 3 phases of hair growth?
    • 1. anagen : matrix cell grow
    • 2. catagen : Hair start degenerating
    • 3. telogen : growth completely stops
  77. What is lakcing in a cicatricial alopecia?
    There is no follicular ostia9opening of the hair folicle)
  78. What is alopecia areata?
    recurrent nonscarring, non scaly hair loss. Hair look like exclamation points
  79. What is the ophiasis pattern of hair loss? Is this a good or a poor prognosis sign?
    It is hair loss localized to the sides and lower back of the scalp. It is a sign of poor prognosis.
  80. What is Tinea Capitis? What is the different types?
    • It is a fungal infection of the scalp that we mostly see in children.
    • Seborrheic type : scaling, often without notceable hair loss
    • black dot : made by the stubs of broken hairs
    • Kerion : hypersensitivity reaction to the fungus, looks like a inflmmaed mass surrounded by pustule
    • grey patch : circular scaling patch with broken hair close to the surface
  81. What does lamisil treat?
    Fungal infection. Eg: tinea capitis and onychomycosis
  82. What is the name associated with hair loss due to pulling on it?
    Trichotillomania
  83. As you get older, you tend to lose hair. How id this processed called? What is the typical pattern for men? and women?
    • Androgenetic alopecia
    • in men : starts on top and front.
    • in women : on top of the head
  84. What are the possible treatments for androgenetic alopecia? What is the main disadvantages of these?
    • minoxidil : mechanism poorly understood, but might increase the duration of the anagen phase or increase blood supply to the follicle
    • Finasteride: 5-alpha reductase type 2 inhibitor (block conversion of testosterone to DHT)
    • If you stop the treatment, you will restart loosing your hair
  85. Telogen effluvium is a loss of hair due to what?
    • It is a reaction pattern to mental and physical stressors.(surgery, medication, systemic illness, dietary insufficiency, postpartum, hypo/hyperthyroidism)
    • It is due to an increase % of hair follicle that are un a resting phase.
  86. How long does a typical urticaria lesion stays on the skin(foe each wheal)?
    It disappear in less then 24 hours, but as it disappears, some other appear, so it looks like the rash is oving around
  87. Describe what urticaria looks like?
    Well demarcated superficial erythematous or pale papules or plaques
  88. What is angioedema?
    It is non pitting edema, with swelling occuring deeper in the dermis and subcutaneous tissue. It mostly occur in loose connective tssue such as the face, lips, tongue and eyelids(hand and feet in children). It is not usually itchy, but can be associated with urticaria. It is rather painful and burning sensation.
  89. Explain why mediators and in particular histamine produce all the symptoms of urticaria.
    • it increases vascular permeability -> edema
    • it causes vasodilation -> Erythema
    • it causes nerve stimulation -> Itchiness
    • it also causes chemotaxis of inflamamtory cells.
  90. Name some etiology to urticaria.
    • IgE mediated : so allergen exposure in food, medication, contact allergen, allergen in the air(eg:pollen)
    • complement mediated : including viral infection(MOST common cause for child urticaria), bacterial infection, parasitic infections, systemic disease(auto-immune mostly)
    • non-immunologic mechanisms : direct degranulation of mast cell after exposure to certain food, drug or contact allergens
    • cold or sun exposure(could be due to porphyria or lupus)
    • idiopathic
    • auto-immune
  91. Name 3 things that can aggravate pre-existing urticaria.
    • NSAID
    • Food containing histamine (cheese, fish, tomatoes, pineapple, avocados)
    • Alcohol
  92. What is the difference between dermographism and delayed pressure urticaria?
    • Dermographism : It is whealing caused by stroking the skin. It can be asymptomatic or present with an itching sensation.
    • Delayed presure urticaria : you need to have sustained pressure for it to appear and it is usually associated with chronic urticaria. It is usually painful.
  93. What prokove cholinergic urticaria?
    It is sweating either from exercise, spicy food or emotional disturbance.
  94. How long does the urticaria reaction last?
    • It can stop after a few hours (eg: with food)
    • It can conitnue for days. And in 2/3 of patients it will resolve within 2 months.
    • The other 1/3 have chronic urticaria.
    • In children, the majority will resolve in 2 weeks.
  95. What do you do as a work up if you don't have any clue on what is causing the urticaria?
    • CBC
    • ESR (erythrocyte sedimentation rate)
    • Thyroid test
    • And some people suggest liver enzymes
  96. What can you do to treat urticaria?
    • You can only treat the symptoms
    • Block the effect of already released histamine : antihistamines (h1 or h2 if h1 doesn't work)
    • Block the release of histamine : ketotifen is mast cell stabilizer abd also a H1 antagonist
    • Block other mediator : Leukotrine antagonists
    • Modulate inflammatory, cellular and immunological component of urticaria : oral steroid, IV Ig...
  97. What is the main Ddx for urticaria?
    • Urticarial vasculitis which is painful rather than itchy and is associated with systemic symptoms like joint pain and fever. It resolves with residual purpura or pigmentation.
    • * Insect bite is another important Ddx
  98. What is the more medical name for a beauty spot?
    Benign aquired melanocytic nevi
  99. What are the 3 types of nevi?
    • Junctional : flat and dark
    • compound : slightly lighter and elevated
    • intradermal : raised and lighter still
  100. Physically, what is the difference between a benign acquired melanocytic nevus and a congenital melanocytic nevus?
    The congenital one is usually bigger and has bigger risk to developp into melanoma(proportional to size)
  101. What distinguish simple nevi (benign caquired) with dysplastic nevus syndrome?
    The hamartoma will be more numerous, have different size, shape and color.
  102. What are risk factors for developing melanoma?
    • Skin phototype I, II or even III
    • sun exposure/sunburns
    • Number of nevi (mostly the dysplastic ones)
    • Family history
    • Previous skin cancer, particularly melanoma
  103. What are some subtype of melanoma?
    • superficial spreading : horizontal growth
    • nodular : vertical growth
    • Acral lentiginous : on palms and soles
    • Lentigo maligna melanoma : evolves from in situ lentigo maligna
    • Amelanotic/hypomelanotic melanoma : look like pink bump
  104. What does the ABCDE rule stant for in respect to melanoma detection?
    • Asymmetry
    • border
    • colour
    • diameter
    • evidence of change
  105. What is the treatment for melanoma? And what is the follow-up?
    • treatment : biopsy, surgical excision with margins, SLNB(sentinel ymph node biopsy)
    • Follo-up : sun protection, monthly self-examination, total skin examination q3-6 months, check first degree relative each 12 months
  106. How do you treat lentigo maligna? Why is it importnant to treat?
    • Even if it is in situ, it will probably become invasive, thus a "true" melanoma.
    • It is hard th determine margins, but woods light helps.
    • You can do a surgicial excision, Mohs micrographic surgery(i.e. looking at the tissue removed during the procedure) and a topical chemotherapy.
  107. What is NMSC?
    • It stands for Non-melanoma skin cancer.
    • It includes BCC - Basal cell carcinoma (more common) and SCC - Squamous cell carcinoma (longer to dvp)
  108. What are risk factors for NMSC?
    • sun exposure (though not necessary)
    • previous skin cancer
    • immunosupression (mostly for SCC)
    • Other chronic inflammation
    • HPV
  109. How do we call chronic sun damage? What is the mechanism causing thick wrinkle?
    It is called dermatoheliosis and the wrinkles are due to the collagen becoming more elastic
  110. What are the subtypes of BCC (basal cell carcinoma)?
    • nodular : telangiectatic (spider vein pattern) and later ulcerated
    • pigmented : nodular + pigment, sometimes confuse with melanoma
    • superficial
    • Sclerosing or morpheaform : peraly luster, roleld borders, highest recurrence
  111. What are the treatment options for BCC?
    • ED&C (Currettage & Electrodessication)
    • Cryotherapy
    • Radiotherapy
    • Topical chemotherapy
    • SImple excision
    • Mohs surgery

    *rarely dvp metastasis
  112. What are the clinical features of SCC (squamous cell CA)?
    • keratoic, verrucous papule or nodule
    • May be crusted, ulcerated or tender(important, because not the case for BCC or melanoma)
  113. How do you treat actinic keratoses (precancerous SCC)?
    • sun protection
    • If you only have a few lesions : cryotherapy-liquid Nitrogen, excision/destruction
    • If you have many : cryotherapy, topical chemotherapy, photodynamic therapy, laser resurfacing/peel
  114. What is the treatment for SCC?
    • biopsy to confir Dx.
    • If small/low grade : ED&C, surgical excision
    • If large/high grade : Surgical excision+margins, Mohs surgery, Radiotherapy, metastatic investigation
  115. What are the key features to recognize psoriasis papulosquamous lesion?
    • symmetrical
    • thick scaly plaques (beefy red, silvery scale)
    • well defined
    • extensor
  116. What are the key features to Lichen Planus papulosquamous lesion?
    • pruritic
    • purple
    • planar
    • polygonal
    • papules
    • predilection for periphery
    • associated with oro-genital as well
  117. What are the key features to recognize atopic dermatitis/eczema papulosquamous lesion?
    • ill-defined borders
    • usually symmetrical (exception : contact)
    • morphology by phase :
    •         acute -> erythema sometimes with          bullae,
    •         subacute -> erythema, scaling, crust
    •         chronic -> dry, scalling, thickened with accentuation of skin lines sometimes with fissure
    • infants in the face
    • early childhood on the extensor
    • normal flexural but can be anywhere

    * part of the atopic tris : asthma, hay fever, eczema
  118. What are the key features to recognize pityriasis rosea papulosquamous lesion?
    • Herald patch : larger, preceds others by average of 7 days
    • round-to-oval, peripheral scale
    • Trunk and proximal extremities
    • "fir tree" pattern
    • Lasts 3-4 months (worse, stable, involutes)
  119. What are the key features to recognize tinea versicolor papulosquamous lesion?
    • varying colors, but uniform in any one patient
    • confetti macules, becoming confluent
    • fine scale
    • upper torso
  120. What are possible etiologies for psoriasis?
    • autoimmune
    • genetic predisposition
    • triggered by lithium med
  121. What are possible etiologies for Lichen planus?
    • Mostly idiopathic
    • Rarely Hepatitis C
    • Drug-induced
  122. What are possible etiologies for atopic dermatitis?
    • genetic, immunological and environmental factors
    • Defective skin barrier allows exposure to aero and contact allergens
  123. What are possible etiologies for pityriasis rosea?
    • hypothesis of viral reactivation
    • sometimes drug-induced
    • More in spring or autumn
  124. What are possible etiologies for Tinea versicolor?
    lipophilic, dimorphic yeast (part of normal flora but clinical appearance related to genetics, warm moist environment, immunosuppression)
  125. What is the histopathology for psoriasis?
    • inflammatory/immune mediators
    • PMNs seen in epidermis
    • Hyperproliferation and rapid turnover of epidermal cells
    • elongation of dermal papillae without tortuous vessels
  126. What is the histopathology for lachen planus?
    • lymphocytic disorder
    • lymphs banlike infiltrate along DEJ, damage to DEJ, sawtooth pattern of rete ridges, pigmentary incontinence
    • patchy hypergranulosis
  127. What is the histopathology for atopic dermatitis?
    Initial Th2 activation produce hyper-IgE and eosinophilia, later shift to Th profile with secretion of pro-inflammatory cytokines, IL-2, IFN-gama and IL-12
  128. What is the histopathology for pityriasis rosea?
    • not higly specific, biopsy mor to exclude other Dx
    • Acanthosis(diffuse epidermal hyperplasia), focal parakeratosis, spongiosis, mild perivascular lymphocytes
    • Eosinophilia possible due to drug-induced
  129. What are the bio-psycho-social issues for psoriasis?
    • risk to pass on to children
    • not contagious
    • lifelong issue, can only be controlled
    • CV risk factor and compounds other CV metabolic risk factors
  130. What are the bio-psycho-social issues for Lichen planus?
    • Some subtypes are photosensitive
    • relationship with Hep C
    • highly pruritic
    • usually self-limited (9mo-2yr)
    • Risk of cancer in hypertrophic and ulcerative types
  131. What are the bio-psycho-social issues for atopic dermatitis?
    • it itches
    • associated conditions (triad with asthma and hay fever)
    • difficulty in treatment
    • you should eliminate exogenous factors (stress,wool,dry environment, dust mites, food)
  132. What are the bio-psycho-social issues for pityriasis rosea?
    • pruritus variable
    • self-limited, usualle 3-4 months
    • almost never get a 2nd time
    • almost never on face
    • Not contagious
  133. What are the bio-psycho-social issues for tinea versicolor?
    • generally recurs every summer
    • not contagious
  134. How can we estimate the photoaging effect on a particular patient?
    You can compare the sin that is rarely exposed to sun with the face.
  135. What are some signs of photoaging process?
    • fine wrinkles around the eyes and mouth/frown lines on the forehead
    • spider veins on the nose, cheeks, and neck
    • pigmented spots (freckles, lentigines)
    • uneven skin colour
    • loss of skin tone in sun exposed areas
    • lips with loss of colour and fullness
  136. Name 2 examples of systemic diseases associated with appearance of a rash.
    • Lupus : classic butterfly (purply red, thicken) 
    • Behçet's syndrome : orogenital occular triad
  137. What does TCR recognize? And BCR?
    • TCR : peptide/short sequences
    • BCR : 3D structure (so they can act as APC)
  138. Where are the naive T cells?
    In the Lymph node :)
  139. What cells have the MHCI? and MHCII?
    • MHCI : All the nucleated cells
    • MHCII : professional APCs (macrophage, B cells, dendritic)
  140. What is the innate immune receptor on the dendritic cell? What interleukin is released by dendritic cells in response to antigenic stimulation?
    • TLR-4
    • IL-12 ( for T cells to differentiate into Th1)
  141. How are MHC complex formed?
    • MCHI : pathogens are degraded in the protesome. They then get assembled with the complex which is then exported to the membrane
    • MCHII : The complex is already in the membrane and the pathogens are degraded in the vesicles used for the transport of the complex and then they bind together
  142. What is the biggest lymphoid organ in the body? and the second one?
    • 1st : the gut
    • 2nd : the spleen
  143. What does the T cell have to have to recognize an antigen?
    • a receptor that can recognize a specific peptide (TCR)
    • a signalign complex (CD3) -> tells the cell that it is connected
    • a CD4 or 8 molecule
  144. What happens when dendritic cells present a peptide to a T cells?
    • CD4 or CD8 of T cells interacts with MHC
    • CD28, a coreceptor on T cell, binds with CD80 or CD86 on dendritic
    • The T cell will than express IL-2(for T cell proliferation) and IFN-gama(activates macrophages)
    • The CD40L will be expressed(to later activate B cells)
  145. What are the roles of T-cells?
    • fight intracellular infections (CD8 cytotoxic T cells)
    • assist other cells by activating them and helping them multiple or differentiate (CD4 effector cells)
    • provide signals that inhibit or slow down inflammatory responses (T-reg -> CD4 and Foxp3)
  146. What are the specific function of Th1? Th2? Th17? Treg?
    • Th1 : intracelluar organisms (IFN-gama, IL-12, IL-2) -> activates monocytes
    • Th2 : Antibody production, parasite defense and allergy (Il-4, IL-5, IL-13)
    • Th17 : antobacterial, antifungal (IL-17, IL-22) -> activate phagocytes
    • Treg : Immune response regulation (IL-10, TGF-beta)
  147. When a T cell recognizes a peptide, its surface changes in what way?
    • cytokine receptors, eg -> IL2R
    • Adhesion molecules, eg -> CD28
    • Chemoine receptors, eg -> CCR3,4,5
  148. What are roles of CD8/T-cytotoxic cells?
    • recognition of infected cells
    • viral immunity
    • production of pro-apoptotic proteins, perforin and granzyme
    • can produce pro-inflammatory cytokines (eg. IFN-gama)
  149. What is T cell signal transduction?
    • a coordinated effort to sens signals from the TCR to the nucleus
    • it involves multiple enzymatic and phosphorylation steps
  150. What is SCID (Severe Combined Immune Deficiency)?
    It is a severe defect in T cell development leading to death from infection before 1 year unless transplanted. There are no T cells, no(or less) B cells and NK cells.
  151. What happens if T cells are not able to produce or recognize cytokines?
    • They can't grow or multiply
    • They can't defend agains specific pathogens
  152. Where does B cell complete their maturation?
    They undergo antigen dependent maturation in the lymph node or in the spleen
  153. What are the recptors present on the B cells?
    • CD19, CD20 : adhesion molecule
    • CD40 : to communicate with CD40L of CD4 T cells
    • BCR
    • MHCII
    • B7.1/CD80 to bind with CD28 of T cells
  154. What are the FDC(folicular dendritic cells)?
    They are cells that live in the lymph node and they trap the antigen to present it to the B cells
  155. What are the 2 parts of an antibody?
    • Fc fragment : constant region, binds to the phagocytic cells
    • F(ab')2 fragment : variable region
  156. Describe all types of antibody with their principal characteristics.
    • IgM : default setting, excellent at complement fixation
    • IgE : cross placenta, allergy, bound to mast cells and basophils, parasite
    • IgG : more common, excellent opsonization
    • IgA : 1st line defense at mucosal surface, excellent at neutralization
    • IgD : marker of B cell maturation, but no clear role
  157. What does the B cell require to elicit a strong antibody response?
    • antigen
    • T cells for direct contect(usually Th2)
    • Soluble cytokines
    • Certain adhesion molecules, mostly CD40
  158. What are the role of antibody?
    • opsonization
    • complement activation
    • neutralization
    • antibody dependent cellular cytotoxicity
  159. What causes fever?
    • release of IL-1, IL-6, TNF-alpha and interferon
    • initial response mediated by ceramide release in neurons of anterior hypothalamus
    • late response -> induction of COX-2 and microsomal PGE1 synhtase to form PGE2 (a prostaglandin)
    • PGE2 crosses BBB and act on thermosensitive neurons
    • this trigger hypothalamus to elevate body T°
  160. What are the main actions of NSAIDs?
    • analgesia
    • antipyretic (block PGE2 production)
    • anti-inflammatory (except acetaminophen)
    • Antiplatelet
  161. What are the adverse reactions of ASA?
    • GI(ulceration, obstruction)
    • bleeding
    • pregnancy
    • renal
    • sensitivity
  162. Which cells dies after the phagocytosis?
    Neutrophiles(in contrast with monocyte which don't)
  163. How does the NK cell participate in innate immune response?
    • Natural cytotoxicity receptors, NKp46 : release cytotoxic granules (perforin, granzyme = serine protease)
    • If mediated through Ab binding = ADCC(antibody-dependent cell-mediated cytotoxicity)
    • killer Ig-like receptors : KIR = specific for MHCI (when not enough MHCI is expressed by a defected cells Kir senses it and stop inhibiting the NK)
  164. Name the different types of PRR and give an example of each.
    • Secreted PRR : collectins including MBL(mannose binding lectin), Ficolins, surfactant proteins
    • Membranous PRR : TLR
    • Cytosolic PRR : NOD-like receptors
  165. From TLR1 to 9, say where they are and what they can recognize.
    • TLR1 : on plasma membrane -> Acyl-peptides 
    • TLR2 :  on plasma membrane -> lipomanan
    • TLR3 :  on vesicular membrane -> DS-RNA
    • TLR4 : on plasma membrane -> LPS
    • TLR5 : on plasma membrane -> Flagellin
    • TLR6 : on plasma membrane -> Acyl-peptides
    • TLR7 : on vesicular membrane -> SS-RNA
    • TLR8 : on vesicular membrane -> SS-RNA
    • TLR9 : on vesicular membrane -> unmethylated CgG DNA
  166. Where is NOD2 expressed?
    In paneth cells where it induces antibacterial substances -> alpha-defensin
  167. What are the 3 pathway for the complement system?
    • Classical : antibody/antigen complex recognize by C1
    • MBL : similar to the classical pathway, but with MBL directly activating C4
    • Alternative pathway : The pathogen stabilizes C3 convertase which is always there in the background
  168. What type of infection is associated with properdin?
    • Meningococcal bacteria
    • * properdin normally stabilizes C3 and C5 convertase
  169. What is the most common complement deficiency?
    C2
  170. Why would you have high neutrophil count in the blood if you have problems with secretin and/or integrin?
    Because the neutrophils can't cross  the endothelial wall of the blood vessel so they stay in the blood and the bone marrow keeps producing neutrophils because it receives signal of infections.
  171. What is LAD-1? LAD-2? LAD-3? LAD-4?
    • LAD = Leukocyte adhesion deficiency
    • LAD 1 : problems in sticking to the endothelial cells due to a problem with integrin, characterized by high WBC and test for CD18/CD11 integrin
    • LAD 2 : problems in rolling due to problem with glycolysation of selectin charcterized by recurrent infections and neurologic defect(retardation)
    • LAD 3 : problem in activation of integrin characterized by increase bleeding.
    • LAD 4 : Hyperadhesiveness of the cells characterized by failure of seperation of the umbilical cord.
  172. What is CGD?
    • chronic granulomatous disease
    • Absence or malfunction of NADPH oxidase subunits which normally genreate microbicidal oxygen radicles and liberation of proteases
    • Defective respiratory burst
  173. What are the 10 signs pointing to immuno-deficiency?
    • 8 or more new ear infections within 1 year
    • 2 or mor serious sinus infections within 1 year
    • 2 or more months on antibiotics with little effect
    • two or more pneumonias within 1 year
    • failure of an infant to gain weight or grow normally
    • Recurrent, deep skin or organ abscesses
    • persistent thrush in mouth or elsewhere on skin, after age of 1
    • Need for IV antibiotics to clear infections
    • 2 or more deep-seated infections
    • Family history of primary immunodeficiency
  174. What is the initial screening tests for immundeficiency?
    • Blood count
    • quantitative immunoglobulin
    • Ab response to previous vaccines
    • Total hemolytic complement
    • infecion evaluation
  175. What does the CH50 test tests?
    • It tests the function of the classical pathway. It tells us the dilutaion you need to have 50% activity.(Meaning: if you can dilute a lot before loing function = well working)
    • *AH50 is for alternate-pathway
  176. What are the 4 types of hypersensitivity?
    • Type I : immediate hypersensitivity (IgE)
    • Type II : Antibody-dependent cell dependent cytotoxicity (ADCC, IgG, IgM)
    • Type III : Immune complex mediated (IgM, IgG)
    • Type IV : Delayed type (T cell mediated -> Th1 mostly but also CD4 and CD8)
  177. Explain Type II hypersensitivity.
    • Intrinsic Ag (normal self antigens) : failure in immune tolerance, cross reactivity foreign antigen with self molecule on the surface of host cells
    • Extrinsic Ag (absorbed on host's cell surfaces) : eg. penicillin at the surface of RBC
  178. What is in excess in type III hypersensitivity?
    Immune complex formed of antibody/antigen complexex, but with antigen in excess
  179. What is serum sickness?
    Deposition of immune comples causing chills, fever, rash, arthritis, sometimes glomerulonephritis
  180. What are the cells expressing FCεRI? What is it for?
    It is for anchoring IgE on mast cells, basohpils and eosinophils.
  181. What is the hygiene hypothesis?
    Infections that evoke Th1 response early in life might reduce the likeliood of TH2 response (allergy) later in life and vice-versa
  182. What is the modified hygiene hypothesis?
    • It was created because ther eis also an increase of Th1 mediated auto-immune diseases
    • It states that infections might protect against dvp atopy by driving the production of Treg
  183. What are the effects of epinephrine?
    • stimulation of α1 adrenergic receptor : vasoconstriction thus improving angioedema and coronary perfusion
    • β1 : increased inotropic and chronotropic effect
    • β2 : bronchodilation, decrease release of inflammatory mediators from mast cells and basophils
  184. What is the difference between hyperpyrexia and hyperthermia?
    • Hyperpyrexia is an extreme of fever (>41.5) which is an increase in core temperature due to a change of the hypothalamic set points, though it rarely goes over 41.1
    • Hyperthermia is due to an overriding of the set point, temperature can be >41.5
  185. What does fever increases?
    • O2 requirement
    • CO2 production
    • water loss
    • Cerebral injury
    • discomfort
    • Seizure activity
  186. What is the normal range of temperature?
    • From 35.6-38.5
    • Lowest at 6 an and highest at 4-6pm
    • Rectal temperature average .6 higher
    • Axillary temperatures inconsistently lower
    • Tympanic temperature ->core, but not always relaible
    • Remote scans are unreliable
    • Ovulating women -> 0.6 degrees higher after ovulation
  187. What are some causes of fever?
    • Viral, bacterial and fungal infections
    • rheumatic disease (autoimmune, autoinflammatory)
    • tissue damage
    • Malignancies
    • Endocrine
    • Immune reactions
  188. What does the NFκβ do?
    • stimulate secretion of IL-1, TNF-α and possibly IFNα and IFN-g
    • Which in turn stimulates production of IL-6
  189. What are the effects produced by IL1, IL6 and TNF-α?
    • fever and malaise
    • acute phase proteins : CRP, MBL (improve complement activation)
    • Pulmonary surfactant proteins SP-A and SP-D
    • Protein and energy mobilization
    • Migration of dendritic cells to lymph node
  190. How is the heat conserved in fever?
    • Blood is shunted away from extremities
    • This leads to a sensation of cold, thus changing our behaviour
    • Shivering
    • Non-shivering thermogenesis within brown fat.
  191. How is the heat loss in fever?
    • increased blood flow to the skin
    • increased water loss through the skin and lungs
    • behavioral changes
  192. What is the prevalence of food allergy?
    • adult : 2.5%
    • Children less than 3 years old : 6-8%
  193. What is SPT?
    Skin prick test to see reaction to diverse substances
  194. Why would you want to have a food challenge even if the SPT is positive?
    Because there is 50% false positive
  195. What is the most common food allergy?
    • CMA -> cow milk allergy
    • 35% of those with CMA develop allergic to other food
    • CMA is an early indicator of atopy (asthma, hay fever, or dermatitis to inhalant allergens later in life)
  196. What kind of milk can you use if you are allergic to cow milk?
    Hydrolyzed formulas
  197. What is the major allergen in cow milk? in egg? in fish? in shellfish?
    • milk : caseins
    • egg : ovomucoid
    • fish : parvalbumin
    • Shellfish (shrimps) : tropomyosin
  198. Histamine receptors are part of what type of receptors?
    GPCR, G-protein coupled receptor
  199. Where are H1 receptor and what are its functions? What about H2, H3 and H4?
    • H1 : smooth muscle, endothelium, CNS --> bronchoconstriction, vasodilation, separation of endothelial cells, pain and itching, allergic rhinitis, motion sickness
    • H2 : parietal cells, vascular smooth muscle, basophils --> Regulate HCl secretion, vasodilation, inhibition of IgE-dependent degranulation
    • H3 : CNS and som PNS --> feedback inhibition of histmaines synthesis and release
    • H4 : bone marrow and WBC --> mediate mast cell chemotaxis
  200. What are the effects of histamine?
    • Primary stimulant for gastric acid and pepsin secretion
    • Neurotransmitter
  201. What are side effects of first generation anti-histamine(eg:benadryl)?
    • sedation
    • dizziness
    • fatigue
    • tachydysrhythmias in overdose
    • peripheral antimuscarinic effects(dry mouth, blured vision, constipation, urinary retention)
    • potentiate CNS depressants(opioids, sedatives, analgesics, alcohol)
  202. Name some mast cell stabilizer.
    • Cromolyn Na
    • Nedocromil
    • albuterol
    • ketotifen
  203. Name some H2 antagonists.
    • Ranitidine
    • cimetidine
  204. How common is allergies to asthmatic patients?
    • 70% of childhood asthmatics
    • 50% of adult asthmatics
  205. What are the 3 phase in response to inhaled antigens?
    • immediate phase : mast cells + epithelium
    • Subacute phase : cell recruitment, chemokines, cytokine, innate immune cells
    • Chronic phase : cellular invasion(innate + adaptive)
  206. What is omalizumab?
    It is a monoclonal anti-IgE antibody. It binds to the Fcε region, so the IgE can't bind to mast cells. It will thus form small complexes that will be cleared
  207. What is the difference between Type A and Type B ADR(adverse drug reaction)?
    • Type A is predictable and it is dose dependent related to pharmalogical action. It occurs in normal individuals.
    • Type B is a unpredictable reaction occuring in susceptible individuals in a dose independent fashion. It is unrelates to pharmalogical action.
  208. Name some predictable ADR.
    • over-dosage
    • side effect
    • secondary effect
    • drug-drug interactions
  209. Name some unpredictable ADR.
    • intolerance
    • idiosyncratic
    • hypersensitivity
    • pseudoallergic(anaphylactoid)
  210. To what does hapten bind?
    • protein : soluble or cell bound
    • MHC molecule
    • MHC peptide
  211. What are the confirmatory tests for drug hypersensitivity?
    • in vivo : SPK(for IgE), patch test(for T cell mediated), gradual challenge tests(for either)
    • In vitro : Serum IgE(specific to drug), lymphocyte transformation test
  212. Whom should we NOT skin test?
    • severe unpredictabl hypersensitivity drug reactions
    • Stevens-Johnson syndrome
    • toxic epidermal necrolysis
    • serum sickness
    • drug reaction with eosinophilia and systemic symptoms
    • acute generalized exanthematous pustulosis
    • agranulocytosis
  213. What is desensitization?
    • It is a process where the patient is giving increasing dose of the allergens until it can tolerate it, but the patient will lose this tolerance if he is not exposed every day.
    • It is useful if there are no alternate antiobiotics.
  214. Hoe do we develop autoimmunity?
    • failure of central tolerance : negative selection
    • Failure of peripheral tolerance : failure of regulatory cells, cross-reactive foreign antigens, failure of normal apoptosis mechanisms
  215. What are the 3 outcomes possible  if a B cell react to self? and for T cells?
    • B cell : deletion, receptor editing, anergy
    • T cell : deletion, anergy
  216. What are the 3 signals for B cell activation?
    • Receptor MHCII with a TCR
    • co-receptor CD40 with CD40L and CD80/86 with CD28
    • Cytokines milieu
  217. Where does the immune system doesn't normally go?
    • brain
    • eyes
    • testis
    • uterus in pregnancy
  218. What is the transcription factor characterizing Treg?
    • FOXP3 dor development of CD4+ CD25+ Treg
    • They also have CTLA-4 which bind to CD80/86 and downregulate the activity of APC(B cell)
  219. What is AIRE?
    • Autoimmune Regulator
    • It is a transcriptionf actor responsible for initiating transcription of proteins that we don't usually find in the thymus to provide the stimuli needed for the negative selection process to occur.
  220. What is IPEX?
    • immune dysregulation polyendocrinopathy enteropathy X-linked
    • Fatal autoimmune disease caused by a FOXP3 deficiency or mutation
    • Sx : massive lymphoproliferation, diabetes, exfoliative  dermatitis, thyroiditis and enteropathy
  221. Explain how infection can lead to autoimmunity.
  222. How does necrosis lead to autoimmunity?
    Certains molecules that are normally intracellular would be extracellular thus causing immune reaction. Then the APC could express self antigen on MHCII, but also have a co-stimulatory signal thus be activated against self.
  223. What autoantibodies are a hallmark for lupus?
    • antinuclear antibodies
    • anti-DNA
    • anti-ribonucleoprotein complex
    • Anti-phospholipid antibodies (promote thrombosis)
  224. How do you treat a autoimmune disease?
    • corticosteroids : supression of T cell proliferation
    • cyclophosphamide : cross-linking of DNA interfers with growth of rapidly proliferating cells
    • hydroxychloroquine : possible effect on antigen-presentation
    • Methotrexate : inhibit new DNA synthesis
    • * Will supress immune system, thus carry a higher risk for infection and malignancy
  225. What are some tumour markers?
    • out of place : paraneoplastic syndromes (eg : ACTH, ADH), chromosomal translocations (eg: BCR-ABL)
    • Out of normal range : over production (eg : PSA)
    • Out of time : oncofetal antigen (eg : CEA, AFP)
  226. How did we learned the basis of tumour immunology?
    With TSTA (tumour-specific transplantation antigens) into mice
  227. What are the applications of tumour markers clinically?
    • detection
    • diagnosis
    • monitoring
    • classification
    • prognosis
    • staging
    • pathology
    • localization
    • therapy
  228. What is the role of the CEA(Carcinogenic Embryonic Antigen) molecule?
    • adhesion
    • cell differentiation

    info : CEA is normally present in the fetus but has also been observed in patients with tumour and other non-malignant disease
  229. Why is the fever periodic in the caswe of malaria infection?
    Malaria infects mostly the RBC and since they are not nucleated, they can't present an zntigen on MHCI and NK isn't activated, so there is no immune response. But once in a while, the parasite comes out of RBC to infect more cells and at this moment they are extracellular and can be recognized and fought, thus the fever appears. And then the parasite would hide again and so on...
  230. What does CRP do?
    they bind to phophocoline on bacterial surfaces, acting as an opsonin and also activate complement
  231. What does MBL do?
    Binds to mannose residues on bacterial surfaces, acting as an opsonin, and activates complement
  232. How do vaccines work?
    • stimulate immunity
    • stimulate memory
    • herd immunity
    • goal is to prevent morbidity and mortality, not always infection
    • risk from vaccinatioun must be less than risks of natural infection
  233. Un peu de traduction! Can you translate these in french: pertussis, measles, mumps and chicken pox
    • Pertussis : coqueluche
    • Measles : rougeole
    • Mumps : oreillons
    • Chicken pox : Varicelle
  234. What does polio cause?
    risk of paralysis and death
  235. What ares some complications of measles?
    • diarrhea
    • pneumonia
    • encephalitis
    • corneal ulceration
    • Complications are more sever amongst adult who catch the virus
  236. Who should we vaccinate?
    • those at risk (children under 1 y/o and elerdly are particularly vulnerable, chemotherapy, transplant, immunodeficiency, travelers)
    • family contact
    • health professionals
  237. What is herd immunity?
    In areas of good vaccine coverage, herd immunity reduces the frequency and severity of outbreaks and minimizes the risk to young children and those who are immunocompromised
  238. What are some common side effects of vaccination?
    • fever
    • irritability
    • rash
    • pain/myalgias
    • headache
    • other (Guillain Barre with influenza vaccin or disseminated BCG-osis, varicella in patients who are immunocompromised)
  239. What is different in a bone marrow transplant versus a solid organ transplant?
    The solid organ have cell presenting MHCI that has to match with the patient. But bone marrow also have APC, so MHCII also needs to be a match
  240. What are the characteristic of tha HLA?
    • polymorphic : class I and class II shape
    • polygenic : more than 1 gene expressed : alpha and beta chain
    • linkage disequilibrium : some type are more common associated with other
    • Co-dominantly expressed : meaning you have 1 from your mother and 1 from your father
  241. What are the 3 types of MHC class I protein?
    • HLA-A(≃400 subtypes)
    • HLA-B(≃700 subtypes)
    • HLA-C(≃200 sutypes)
  242. What are 3 technics used for tissue typing?
    • serology : using antibodiesthat recognize specific component of some HLA class
    • Genetic : better precision of HLA mathc based on gene sequencing
    • mixed lymphocyte reaction : Put lymphocytes of the patients with inactivated cells from the donor and assess the activity (if high = rejection more likely)
  243. Why does the blood type (AB, RH) changes with bone marrow transplant?
    Because the bone marrow is responsible for production of RBC.
  244. What transplant doesn't require matching and why?
    RBC transfusion and corneal transplants because these are NOT nucleated.
  245. Is it always better to have a perfect match for transplantation?
    • No, since I asked the question :P
    • In leukemia and other malignancy, you have a better outcome if there is some degree of difference.
  246. Name some CV disease modulated by the immune system.
    • atherosclerosis
    • ACS(acute coronary sydromes -> unstable angina, NSTEMI, STEMI)
    • CHF (congestive heart failure)
    • Metabolic syndrome
  247. What are the impacts of HIV therapy on CV disease?
    • hyperlipidemia
    • hypertriglycemia
    • metabolic syndrome
    • lipodystrophy syndrome
    • accelerates atherosclerosis
  248. Where are TLR (toll-like receptors) found?
    • immune cells : macrophage, dendritic cells, B cells, granulocytes, NK cells and T cells
    • Non-immune cells : fibroblasts and epithelial cells, platelets, adipocytes
  249. What cytokine could be associated with type II diabetes?
    IL-1 might cause beta-cell functional impairment or apoptosis
  250. What is atheromata?
    asymmetric focal thickening of intima layer of arteris consisting of inflammatory cells, endothelial cells, smooth muscle cells, lipids and cell debris
  251. Where are the scavenger receptors? What are they for?
    • They are on macrophages
    • They can stimulate endocytosis of LDL, detect diaglycerides, malaria, TB and they can bind and internalize apoptotic cells
    • Once the macrophage uptake LDL, they become foam cells
  252. What is OxLDL?
    • oxidatiely modified low density lipoprotein which is a self antigen
    • atheroscleoric lesions contain oxLDL specific T cells and IgG antibodies
  253. What is B2-glycoprotein I?
    it is a phospholipid binding protein found in atheromatous plaques
  254. What is the role of Th1 in plaque rupture of atherosclerosis?
    • IFN-g induces CD4L : boosting the production of proteases that degrade collagen, weakening the fibrous cap
    • IFN-g inhibit proliferation f smooth muscle cells affecting collagen synthesis
    • CD40-CD40L : elicit tissue factor triggering the coagulation cascade and thrombus formation
  255. What cells have a protective role concerning atherosclerosis?
    • B cells : specific antibodies against plaque antigens
    • Spleen B cells : recognize phosphorylcholine present in oxidized LDL, apoptotic cell membranes and cell wall of Streptococcus pneumoniae
    • Treg : by supressing the activity of other T cells
    • * Leptin has a role in promoting atherosclerosis
  256. What is replicative senescence?
    It is when a cell reach its innate proliferative limit due to a shortening (or even consumption) of telomere.
  257. How do statins interact with the immune system?
    • inhibit MHCII presentation
    • inhibit T cell proliferation
    • impair Th1 differentiation
    • inhibit expression of adhesion molecules on endothelial cells
    • affect leukocyte mobility
    • Decrease leukocyte  activation
    • induce Fox P3 expression on naive CD4 T cells
  258. What is the difference between primary and secondary immunodeficiency?
    • primary : heritabl defect, congenital
    • secondary : acquired defect due to another disease process or treatment (eg:HIV, chemotherapy)
  259. What is the incidence of immunodeficiency in the population?
    • 1/10 000
    • but the most common, IgA deficiency is 1/500
  260. Name some primary B cell deficiencies.
    • agammaglobulinemia
    • hyper IgM immunodeficiency (HIGMS)
    • common variable immunodeficiency (CVID)
    • selective IgA deficiency
    • anti-polysaccharide antibody deficiency
    • transient hypogammaglobulinemia of infancy (THI)
  261. What is agammaglobulinemia?
    • It is a autoimmune deficiency characterized by arrest of B cell development at pre-B cell stage. So all major classes of immunoglobulin are affected
    • Sino-oto-pulmonary infections starting at the age of 4-6 months when maternal immunity wanes
  262. What is Hyper-IgM syndrome?
    • It is a immune deficiency caused by a defect in T cells. There is no CD40L, so B cells can't switch antibody type production.
    • The most common initial infection is PCP (pneumocystic pneumonia)
    • Need IV IG for life
  263. What is CVID(common variable immune deficiency)?
    • It occurs in a heterogenous group of patients that develop hypogammaglobulinemia usually in 2nd or 3rd decade of life. But they have normal T and B cells numbers. 
    • Increased risk of autoimmunity and risk of malignancy
  264. What is anti-polysaccharide antibody deficiency?
    • Also known as SADNI (selective antibody deficiency with normal immunoglobulins).
    • Everything is working well except antibody for a specific pathogen or familiy of pathogens.
  265. Name some primary T cell deficiencies.
    • Severe combined immunodeficiency (SCID)
    • DiGeorge syndrome
    • Wiskott-Aldrich syndrome
    • Ataxia-telangiectasia
    • Miscellanous CID
  266. What is DiGeorge syndrome?
    • It is a immune deficiency that presents with a triad -> thymic hypoplasia, parathyroid hypoplasia, cardiac anomalies.
    • It is due to a hemizygous deletion of chromosome 22q1.2
    • It overlap with velocardiofacial syndrome
    • Low T cells at birth, but it increases with age
  267. What is Wiskott-Aldrich syndrome?
    • It is a triad (eczema, recurrent respiratory infections, bleeding diathesis(predisposition)) due to a defectip WASP. 
    • WASP normally regulates actin physiology.
    • It affects T and B cell function and platelet production
  268. What is Ataxia-Telangiectasia?
    • It is caused by an abnormal gene which impair DNA repair mechanisms. 
    • It presents clinically with a triad (progressive neurologic deterioration, oculocutaneous telangiectasias(spider veins), immune deficiency-> T and B) along with insulin resistance.
  269. Recurrent infections with encapsulated bacteria suggest what type of immunodeficiency?
    antibody deficiency
  270. What is the estimate of birth prevalence of SCID?
    1/75 000
  271. What cell types are the most often problematic in immunodeficient patients?
    B cells
  272. The age of onset can give an idea about wich lymphocyte is causing an imunodeficiency. Are the B cell problem occuring earlier than for T cell related problem?
    • 4-5 months : Combined T/B cell deficiency
    • 7-9 months : B cell deficiency
  273. What should you ordered to test for immunodeficiency?
    • Number and fonction for :
    • B cell
    • T cell
    • Phagocytic cell
    • complement proteins
  274. How can you differenciate between each type of lymphocytes?
    By using flow cytometry and fluorescence activated cell sorter, so you know which cell have which CD.
  275. How do you assess B cell function?
    • You can count antibodies of each type
    • Serology testing
    • in most case of B-lymphocyte deficiency : lack of a defined germinal center, deficient in plasma cells
    • DNA sequencing
  276. How do you assess T cell function?
    • Using Mitogens(stimulatory substance) to see if T cells are activable and if they replicate
    • look at thymus size
    • intracellular cytokine detection (by flow cytometry)
    • thymic biopsy **controversial**
    • DNA sequencing
    • Enzymatic measurment
  277. How do you assess phagocytic cell function?
    • You give dihydrorhodamine (DHR) to the phagocytic cells. If they are working, they will reduce it to produce rhodamine, a stonlgy fluorescent compound. Then you look a fluorescence using flow cytometry.
    • DNA sequencing
  278. What does it mean if AH50 level is low?
    It suggests a deficiency in factor B, D or properdin
  279. Except having a immunodeficiency in the complement system, what can cause a low CH50?
    Inappropriate handling, since complement components lose activity very rapidly at room temperature
  280. How do you assess the complement system function?
    • CH50/AH50
    • immunochemical methods used to demonstrate specific antigen deficiencies
    • functional assays are requires for further evaluation, if normal levels
    • Serum MBL assay, MBL gene sequencing
  281. What are the 3 different sites of the oral mucosal immune system?
    • oral mucosa
    • salivary glands
    • gingival crevice

    ** Part of the MALT (mucosal associated lymphoid tissue)
  282. What cell is responsible for sampling the environment in the oral mucosa?
    intraepithelial dendritic cells
  283. What antibody is the most present in the mouth?
    IgA
  284. What does the saliva contain regarding the immune system?
    • IgA (to inhibit attachment of bacteria and viruses to the oral epithelium)
    • Lactoferrin
    • lysozyme
    • complement
    • leukocytes
    • other antimicrobial elements
  285. What is responsible for the immunity into the gingival crevice?
    • Neutrophils continously traffic from gingival capillaries into the sulcus
    • leukocytes accumulate in response to plaque
    • neutrophils in the gingiva are activated by local cytokine production and co-receptors and are able to phagocytose and kill microorganisms
  286. Where are Peyer's patches found? what do they do?
    • small intestine, appendix and lymphoid follicles o large intestine
    • they contain specialized epithelial cells -> M cells which interact directly with molecules and particles of the gut lumen.
  287. How is the gut protected from infection?
    • Specialized T cells can preferentially kill infection cells
    • Intraepithelial lymphocytes play roles in minimizing gut inflammation and facilitating repair
    • IgA neutralizes toxins and prevents adherence of viruses and bacteria to epithelial cells
  288. How can antibiotics cause super-infection?
    If the commensal flora is disturbed in the gut, opportunistic organisms such as c. difficile can penetrate the gut epithelial layer through M cells.
  289. What causes Crohn's disease?
    It is a failure to maintain tolerance to normal antigen present in the gut.
  290. Why is gut immunity so important?
    • Because it is the first barrier encountered by many pathogens.
    • Because it can prepare yourself for later if you see an antigen elsewhere in your body
  291. Where is a bone marrow usually done?
    In the bone marrow of the pelvis
  292. Where can you find bone maroow in adults?
    • skull
    • ribs
    • sternum
    • vertebrae
    • pelvis
    • proximal femur in epiphysis
  293. Describe the origin of immune cells starting at the hematopoitic stem cell in the bone marrow.
    An hematopoietic cell can differenciate into a myeloid or a lymphoid precursor.The lymphoid can then differentiate into NK, T cells or B cells.The myeloid can become either a RBC, a mast cell, a megakaryocyte(to form platelet) or a myeloblast.The myeloblast can diffenrentiare further into a basophil, eosinophil, neutrophil or monocytes.
  294. When the bone marrow is severly compromised by disease, which organ can take over and do extramedullary hematopoiesis?
    Organs that used to do it during the prenatal phase -> spleen and liver
  295. What are the 2 types of bone marrow?
    • red marrow : active hematopoeisis
    • yellow : inactive with adipocytes.
  296. What is the approximate proportion of T and B cell overall?
    2/3 T cells (except 100% in the thymus)
  297. What cell marker does B lymphoblasts have?
    • CD19
    • TdT
    • CD34
    • CD10
  298. Describe the cells in the cortex of the thymus.
    • Large cortical epithelial cells with desmosomes form the cortico-medullary barrier, function as APCs and secerte cytokine
    • Macrophages
    • T-lymphoblasts = thymocytes = precursor T-cells : RdR+, initially double negative and then double positive for CD4 and CD8
  299. Decrbie the cells in th medulla of the thymus.
    • Mature naïve T cells : TdT-, CD3, CD4 or CD8
    • epithelial cels are smaller, spindle-shaped and they form hassall's corpuscles
    • Dendritic cells
    • small population of mature B cells, CD20+ and CD23+ : closely associated with epithelial cells and may play a role in T-cell differentiation
  300. Where is the negative selction done for T cells? And the positive selection?
    • Positive : Cortex of the thymus
    • Negative : Medulla of the thymus
  301. How many lymph node do we usually have?
    • Between 400 and 450
    • With a maximum diameter of 1 cm
  302. Describe the cortex of the lymph node.
    • Mostly contain B cell
    • Quiescent node(no antigenic stimulation) : B cells wait in the follicle
    • AG stimulation : formation of germinal centers
    • Germinal center : B-lymphocyte in various stage of activation, CD4 T cells, follicular dendritic cells(CD23+), macrophages
  303. Describe the paracortex of the lymph node.
    • Mostly contain T cells
    • With ag stimulation, t enlarges but no follicles or germinal center formation
    • T cells in variable stage of activation, dendritic cells, scattered B cells
    • HEV - site of high endothelial venules : specialized entry points for blood lymphocytes coming from bone marrow and thymus
  304. Describe the medulla of the lymph node.
    • medullary cords : B and T lymphocytes, plasma cells
    • Medullary sinuses : lined by dicontinuous endothelial cells allowing free trade and final filtering of lymph, and containing numerous macrophages
  305. In what context is there proliferation of B-blasts?
    • During an early primary immune response
    • It occurs outside the germinal center, in the paracortex
    • It is a T cell-INDEPENDENT activation of Na¨ve B cells
    • B blasts are in fact short-lived IgM plasma cells(no memory cells), but Ab have a lower affinity to Ag
    • Some of the B-blasts will migrate to primary B follicle to initiate the secondary response.
  306. Describe the activty of B cells during a secondary immune response
    • T-cell dependent activation of naïve B cells to proliferate into B centroblasts -> immunoblasts -> IgG secreting long-lived plasma cells and memory cells
    • occurs inside the germinal center
    • In normal or reactive germinal center, the anti-apoptotic bcl2 is downregulated
  307. What are the 4 key steps in germinal center?
    • proliferation : mostly of B cells
    • somatic hypermutation : increase affinity of Ab for Ag
    • selection : class switch, centrocytes with low affinity with the Ag undergo apoptosis
    • differentiation : into memory cells or plasma cells
  308. Each plasma cell can secrete only 1 type light chain and 1 heavy chain. What are the tyoes possible for the light chain?
    • kappa
    • lambda
  309. Where does APC presents antigen to T cells?
    In the paracortex of the lymph node
  310. What are the functions of the spleen?
    • filter blood
    • destroy old erythrocytes
    • produces Abs and effector T cells
  311. The spleen parenchyma has 2 types of "pulp". Can you describe them?
    • White pulp : 20% of the spleen composed of lymphoid nodules and periarteriolar lymphoid sheaths(PALS)
    • Red pulp : 80% of the spleen composed of sinusoids and filled with blood, made of splenic cords(of Billroth)
  312. What is the Waldeyer ring?
    It describes the lymphoid tissue in the pharynx and the tonsils
  313. What is the cause of infectious mononucleosis?
    EBV -> Epstein-Barr virus
  314. What is dermatopathic lymphadenopathy?
    Enlarged lymph nodes draining areas of skin disease
  315. Name the most common etiologies for reactive lymphadenopathy.
    • Infections : bacteria, viruses, protozoa, fungi
    • immune or CT disorder : rheumatoid arthritis, SLE
    • Iatrogenic causes : drugs
    • Idiopathic : progressive tranformation of germinal centers
  316. What is the difference between lymphoma and leukemia?
    • Lymphoma is a solid tissue masses
    • Leukemia involve the bone marrow and the blood
  317. What are the most common origin of lymphomas?
    From B-cell, especially in the germinal center
  318. Briefly describe the classification of lymphomas.
    • Hodgkin lymphomas : nodular or classical
    • Non-Hodkin lymphomas : Precursor vs Mature and B-cell vs T-cell
  319. What are the 4 most prevalent type of mature B-cell lymphomas?
    • Diffuse large B cell : aggressive B-cell lymphoma with diffuse large cell
    • Follicular : follicle center B-cells, centrocytes and centroblasts, >50y/o, most diffuse adenopathy, few extra-nodal, inhibition of apoptosis
    • MALT marginal B cell : can be either nodal, extra-nodal or splenic
    • Small lymphocytic : naïve B cells(poorer prognosis) or post-germinal center B-cell(better prognosis)
  320. Which type of hodkin lymphoma have a lot of similarity with B cell lymphoma?
    Nodular
  321. What is the most common type of T cell lymphoma?
    Peripheral T cell lymphoma
  322. What is the classical clinical presentation of lymphoblastic lyphoma(LBL)?
    • symptomatic mediastinal mass
    • pleural or pericardial effusion
    • supradiaphragmatic lymphadenopathy

    Progresses rapidly to involve blood, bone maroow, CNS and gonad
  323. What is Mycosis Fungoides?
    An epidermotropic primary cutaneous T-cell lymphoma characterized by infiltrates of small/medium T lyphocytes with cerebriform nuclei
  324. What are some key characteristics of Hodkin lymphoma?
    • orderly spread by contiuity
    • often a single group of lymph nodes(mostly cervical)
    • mesenteric nodes and Waldeyer ring rarely involved
    • Extra-nodal involvement very uncommon
    • Leukemia phase extremely rare
    • Prognosis is very good
  325. What characterized hodgkin lymphoma?
    Hodgkin's lymphoma is characterised by the orderly spread of disease from one lymph node group to another and by the development of systemic symptoms with advanced disease. When Hodgkins cells are examined microscopically, multinucleated Reed–Sternberg cells (RS cells) are the characteristic histopathologic finding.

    • From Wikipedia... :)
    • For more info : http://www.raschfoundation.org/reports/hodgkins/5/
    • or
    • http://www.diffen.com/difference/Hodgkin's_Lymphoma_vs_Non-Hodgkin's_Lymphoma
  326. What is the name of a lesion which is flat and < 0.5cm?
    macule
  327. What is the name of a lesion which is flat and >0.5cm?
    patch
  328. What is the name of a lesion which is raised and < 0.5cm?
    papule
  329. What is the name of a lesion which is raised and >0.5cm?
    plaque
  330. What is the name of a lesion which is raised-with depth and < 0.5cm?
    nodule
  331. What is the name of a lesion which is raised-with depth and > 0.5cm?
    tumour
  332. What is the name of a lesion which is raised-with clear fluid and < 0.5cm?
    vesicle
  333. What is the name of a lesion which is raised-with clear fluid and > 0.5cm?
    bulla
  334. What is the name of a lesion which is raised and lined by true epithelium?
    cyst
  335. What is erosion?
    • Lack of substance
    • moist circumscribed depression
    • due to loss of all or part of epidermis
  336. What is crust?
    • surface change
    • hardened deposit of serum, blood or pus
  337. What is scale?
    • surface change
    • desquamation (skin peeling)
    • Flake arisinf from stratum corneum
  338. What is atrophy?
    • lack of substance
    • a wastinf of tissue
    • characterized by striae
  339. What is an ulcer?
    • Lack of substance
    • circumscribed depression due to loss of epidermis and all or art of the dermis
  340. What cells are important in the process taking place in rheumatoid arthritis?
    • Macrophages
    • TNF-α and IL-1 : proliferation of T cells, activation of B cells. initates proinflammatory/joint damaging process
    • Th1
    • B cells
    • Osteoclasts : bone erosion, juxta-articular and systemic osteoporosis
  341. What is the rheumatoid factor?
    • an IgM antibody against IgG
    • present in most rheumatoid patients
    • produced by B-cells in synovial fluid
    • It triggers complement and thus tissue damage
  342. What is a pannus?
    • Scar-like tissue containing PMN)polymorphonuclear neutrophil), macrophages, fibroblasts that accumulates in the joint.
    • Il-1 anf TNF-α produced by pannus will stimulate bone resorption by osteoclasts
  343. What is different in therapy for athritis between before and the newer guidlines?
    • Before : start conservatively, only give DMARDs and GC to the most severly affected patients
    • Now : Use of early DMARD, combination of conventional DMARDs and newer agents
  344. What are DMARDs?
    • Disease Modified Anti-Rheumatoid Drugs
    • control the inflammation
    • modify the course of the disease : reduce joint damage and deformity, reduce radiographic progression, reduce long-term disability
  345. What's the mechanism for 2nd generation DMARD?
    • Cytotoxic B/T cell inhibitors
    • block synthesis of pyrimidines (used to make DNA)
    • Prevent B and T cell proliferation -> Rheumatoid factor not produced
    • Eg : Methotrexate, leflunomide
  346. What are some common side effects of Methotrexate?
    • Malaise, nausea
    • rise in liver enzymes
    • oral ulcers
    • alopecia
    • liver and bonne marrow toxicity
  347. What is hydroxycloroquine?
    • Anti-malarial medication found useful for the treatment of inflammatory arthritis
    • Interferes with cell's abiity to degrade and process proteins
    • Can also be used for auto-immune disease
  348. What is Sulfasalazine?
    • Salicylic acid (anti-inflammatory)
    • Sulfapyridine (antibiotic)

    *take 6-8 weeks to work
  349. What is Leflunomide?
    • Newer DMARD
    • inhibit de novo synthesis of pyrimidines
  350. What are 3 types of biologics?
    • substances that are very similar to the body's own key signalling proteins
    • monoclonal antibodies
    • Receptor constructs, usually based on a naturally-occurring receptor linked to the immunoglobulin frame
  351. What does the current biologics act upon?
    • TNF inhibitors (infliximab, adalimumab)
    • IL-1 inhibitors (kineret)
    • T-cell Co-stimulatory blockade (abatacept)
    • B-cell depletion (rituximab)
  352. What is the most widely accepted hypothesis on the immune response present in RA (rheumatoid arthritis)?
    • APC present the antigen to a CD4.
    • In a genetically predisposed individual, this start a immune reaction.
    • Immune system is confsed and targets healthy tissue

What would you like to do?

Home > Flashcards > Print Preview