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NBDE Part 1 > Microbiology Immunology > Flashcards

Microbiology Immunology Flashcards

1
Q

Name and describe the three lines of defense

A

Lines of Defense

  • Skin and mucous membranes
  • Innate (natural) immunity
    • Functions immediately after microbial infiltration
    • Nonspecific targeting of antigens
    • No memory: Does NOT arise from previous infection or vaccination
      • Natural killer (NK) cells
      • Polymorphonuclear neutrophils (PMNs)
      • Macrophages
      • Complement system
      • Nonspecific enzymes (cytokines, lysozyme, etc)
  • Acquired (adaptive) immunity
    • Functions days after microbial infiltration
    • Specific targeting of antigens
    • Exhibits diversity: Responds to millions of unique antigens
    • Memory: improves on multiple exposure to microorganism
    • Two types of acquired immunity
      • Cell-mediated: T cells
      • Antibody-mediated (humoral): B cells, antibodies
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2
Q

Name and describe the two classifications of acquired immunity

A

Classification of Acquired Immunity

  1. Active
    • Mediators: Antibodies and T cells
    • Occurs after exposure to foreign antigens
    • Slow onset (days)
    • Lasts a long time (years)
    • Ex: Previous microbial infection, Vaccination with live attenuated or killed antigens
  2. Passive
    • Mediators: Antibodies
    • Occurs after exposure to preformed antibodies from another host
    • Immediate onset
    • Short duration (months)
    • Ex: Pregnancy (IgG), Breast feeding (IgA), Vaccination with antibodies
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3
Q

Name and describe what an antigen is and examples/characteristics listed below:

Immunogen

Hapten

Superantigen

Epitope

Adjuvant

A

Antigens

  • Most are proteins, but many are also polysaccharides, lipoproteins, and nucleoproteins
  • Immunogens: Molecules that react with antibodies to induce an immune response. All immunogens are antigens, but not all antigens are immunogens
  • Hapten: An antigen that cannot elicit an immune response on its own (Can’t activate Th cells); it must be bound to a carrier protein
    • Many drugs are haptens. ie. Penicillin
  • Superantigen: Activates a large number of Th cells at one time. (Eg. TSST)
  • Epitopes: The specific antibody-binding site on an antigen
  • Adjuvant: A molecule that enhances the immune response to an antigen
    • Added to a vaccine to decrease absorption and increase the effectiveness
    • Elicits stronger T and B cell response
    • Eliminates the need for repeated boosters
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4
Q

Explain the difference between cell-mediated and antibody-mediated immunity

A
  • Cell-Mediated Immunity
    • Host defense:
      • Viruses,
      • Bacteria (intracellular),
      • fungi
      • Protozoa
    • Mediators:
      • T cells
      • NK cells
      • Macrophages
    • Ex: Intracellular infections, Granulomatous infections, Tumor suppression, Organ transplant rejection, Graft vs. host reactions, Type IV (delayed) hypersensitivity
  • Antibody-mediated (humoral)
    • Hoste defense:
      • Bacteria
      • Some viruses
      • Helminths
    • Mediators:
      • B cells
      • Antibodies
    • Examples: Bacterial toxin-induced infections, Autoimmune reactions, Type I, II, III hypersensitivity
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5
Q

Explain Freund’s adjuvant

A

Freund’s adjuvant:

  • Inactivated M. tuberculosis suspended in lanolin and mineral oil
  • Functions as an immunopotentiator (booster)
  • Used for research as it is toxic in humans
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6
Q

State the cellular components of the immune system

A

T cells

B cells

Natural killer (NK) cells

Monocytes and Macrophages

Dendritic Cells

Polymorphonuclear Neutrophils (PMNs)

Eosinophils

Basophils and Mast Cells

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7
Q

Explain a T-cell and its differentiation pathway

A

T Cells

  • Differentiate in the thymus
  • Long lifespan, ranging from months to years
  • Have a CD3 associated T-cell receptor (TCR) , which recognizes a unique antigen only in conjunction with MHC proteins

T-cell differentiation:

  1. Made in bone marrow
  2. Thymus cortex = positive selection
    • CD4+ CD8+ T cell
  3. Thymus Medula = Negative selection
    • CD8+ T cell -> Cytotoxic T cell (lymph node)
    • CD4+ T cell -> Helper T cell (lymph node)
  4. Lymph node
    • CD8 T cell -> Cytotoxic T cell (lymph node)
      • Kills virus-infected, neoplastic, and donor graft cells
        • Endogenous MHC I
    • CD4 T cell -> Helper T cell (lymph node)
      • Th1 cell (cell-mediated response)
        • Makes IL-2, IFN-GAMMA, AND ACTIVATES MACROPHAGES AND CD8+ T cells
          • ​​Inhibited by IL-10
      • Th2 cells (humoral response)
        • Makes IL-4, IL-5, IL-10, and help B cells make antibody (IgE > IgG)
          • Inhibited by INF-gamma
      • Exogenous MHC II
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8
Q

Explain the following about the identified T Cell:

CD4 lymphocytes, helper T cells (Th Cells)

Th1 cells

Th 2 cells

  • Function
  • Characterization
A

CD4 lymphocytes, helper T cells (Th Cells)

  • Function: none listed
  • Characterization: Responds to antigen associated with Class II MHC proteins

Th1 cells

  • Function:
    • Signal CD8 cells to differentiate into cytotoxic T cells
    • Signal macrophages in Type IV (delayed) hypersensitivity reactions
  • Characterization:
    • Secrete:
      • IL-2 (CD8+ cells)
      • INF-gamma (macrophages)

Th2 cells

  • Function:
    • Signal B cells to differentiate into plasma cells, producing antibodies
  • Characterization:
    • Secrete:
      • IL-4
      • IL-5
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9
Q

Explain the following about the identified T Cell:

CD4 lymphocytes, cytotoxic T cells (Tc cells)

  • Function
  • Characterization
A

CD4 lymphocytes, cytotoxic T cells (Tc cells)

  • Function:
    • Kill virus-infected, tumor, and allograft cells
    • Two ways:
      • Release perforins (disrupt cell membranes)
      • Induce apoptosis (programmed cell death)
  • Characterization
    • Respond to antigen associated with Class I MHC proteins
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10
Q

Explain the following about the identified T Cell:

Memory T Cells

  • Function
  • Characterization
A

Memory T Cells

  • Function:
    • Activated in response to re-exposure to antigen
  • Characterization
    • Exist for years after initial exposure
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11
Q

Explain clonal selection

A

The process by which an antigen binds to a specific TCR (T cell) or Ig (B cell), activating that immune cell to clonally expand into cells of the same specificity is called clonal selection

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12
Q

Explain a B cell and state/describe its major types

Types (Plasma Cells, Mature B cells, Memory B cells)

  • Function
  • Characteristics
A

B cells

  • Differentiate in the bone marrow
  • Short life span, ranging from days to weeks

Major Types of B Cells:

Plasma Cells

  • Function:
    • Synthesize immunoglobulins (antibodies)
  • Characteristics:
    • Only monomeric IgM and IgD are expressed on their surface as antigen receptors

Mature B Cells

  • Function:
    • Antigen presentation
  • Characteristics:
    • Express class II MHC proteins
      • APC that presents to CD4 Th cells

Memory B Cells

  • Function:
    • Activated in response to re-exposure to antigen
  • Characteristics:
    • Exist for years after initial exposure

Recall:

  • Class I MHC surface proteins: on all nucleated cells. Recognition of self vs. non-self.
  • Class II MHC surface proteins: ONLY on ANTIGEN PRESENTING CELLS (APCs) Present antigen to Th cells
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13
Q

Explain Natural Killer (NK) Cells

A

Natural Killer (NK) Cells

  • Lack a CD3-associated TCR and surface IgM or IgD
    • IgG antibodies enhance NK cell effectiveness via antibody-dependent cellular cytotoxicity (ADCC)
  • Are NOT specific to any antigen and do not need to recognize MHC proteins
  • No memory : Do not require previous exposure to antigen
  • Activated by IL-12 and INF-Gamma
  • Functions:
    • Kill Virus-infected cells and tumor cells (induce apoptosis via perforins and granzymes)
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14
Q

Explain Monocytes and Macrophages

A

Monocytes and Macrophages

  • Agranular leukocytes
  • Derived from bone marrow histiocytes
  • Exist in plasma (monocytes) and in tissues (macrophages)
  • Activated by bacterial LPS, peptidoglycan, and DNA, as well as TH1 cell-mediated INF-Gamma
  • Functions:
    • Phagocytosis: Via Fc and C3b receptors
    • Antigen presentation: Express Class II MHC proteins
    • Cytokine Production: IL-1, IL-6, IL-8, INF and TNF

Monocytes and macrophages are major components of the reticuloendothelial system, which includes all phagocytic cells except for granulocytes (PMNs)

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15
Q

What are other phagocytes besides monocytes and macrophages?

A

Other Phagocytes:

  • Histocytes: CT
  • Microglia: CNS
  • Dust cells: Lungs
  • Kupffer cells: Liver
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16
Q

Explain Dendritic cells

What are Langerhans cells?

A

Dendritic cells

  • Agranular leukocytes
  • Located primarily in the skin and mucous membranes
  • Functions:
    • Antigen presentation express Class II MHC proteins

Langerhans cells: Are the major dendritic cells of the gingival epithelium

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17
Q

Explain Polymorphonuclear Neutrophils (PMNs)

What are the major contents of PMN cytoplasmic granules?

A

Polymorphonuclear Neutrophils (PMNs)

  • Granular leukocytes.
  • Cytoplasmic granules (lysosomes) contain several bacteriocidal enzymes
  • Functions:
    • Phagocytosis
    • Cytokine production

Major contents of PMN Cytoplasmic Granules

Granule Type/ Enzymes

Primary (azurophilic)

  • Hydrolase
  • Myeloperoxidase
  • Neuraminidase

Secondary

  • Collagenase
  • Lysozyme
  • Lactoferrin
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18
Q

Explain Eosinophils

A

Eosinophils

  • Granular leukocytes
  • Blind antigen-bound IgG or IgE, subsequently releasing cytoplasmic granules
  • Do not present antigen to T cells
  • Functions:
    • Defense against parasitic infections (especially nematodes)
    • Mediate hypersensitivity diseases: Release histaminase, leukotrienes, and peroxidase
    • Phagocytosis
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19
Q

Explain Basophils and Mast Cells

A

Basophils and Mast Cells

  • Granular leukocytes
  • Exist in plasma (basophils) and in tissues (mast cells)
  • Bind antigen-bound IgE, subsequently releasing cytoplasmic granules (histamine, heparin, peroxidase, and hydrolase) and inflammatory cytokines.
  • Functions:
    • Mediate immediate hypersensitivity reactions such as anaphylaxis
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20
Q

Explain what Opsonization is

What are the two major opsonins?

A

Opsonization

  • Enhances phagocytosis of encapsulated microorganisms
  • Antibody (IgG) or complement protein (C3b) coat the outer surface of microorganisms, allowing phagocytes to bind and engulf them more efficiently

THE TWO MAJOR OPSONINS ARE IgG AND C3b

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21
Q

What are Antigen presenting cells and what do they express?

A

Antigen-presenting cells (APCs) express class II MHC proteins and present antigen to CD4 T cells. The predominant APCs of the immune system are monocytes and macrophages, dendritic cells (langerhans cells) and B cells

22
Q

What are Chemokines (give examples)

A

Chemokines (IL-8, C5a, LT-B, FMLP) are chemotactic cytokines for PMNs and macrophages

23
Q

What is phagocytosis and what are the stages

Stage

event

characteristic

A

Phagocytosis

  • The process by which microorganisms, cell debris, dead or damaged host cells, and other insoluble particles are taken up and broken down by phagocytes

Stages of Phagocytosis

Adhesion

  • Plasma phagocytes (PMNs, monocytes) bind to vascular endothelium
  • Mediated by selectin and cellular adhesion molecules (CAMs)

Migration

  • Phagocytes migrate toward the microorganisms
  • Diapedesis is the movement of the phagocyte through the vascular endothelium
  • Mediated by chemokines (IL-8, C5a, LT-B4, FMLP)

Ingestion

  • The phagocyte cell membrane forms pseudopods, which surround and engulf the microorganisms
  • Phagosome formation occurs when the internalized endosome fuses with lysosomes
  • Mediated by opsonization (C3B, IgG)

Lysosomal degranulation

  • The lysosome empties its hydrolytic enzymes into the phagosome, killing the microorganism
  • Mediated by lysosomal enzymes
24
Q

State the lysosomal contents and what makes them up

A

Lysosomal Contents

  • Superoxide radicals (O2-)
  • Superoxide dismutase
    • Produces hydrogen peroxide (H2O2)
  • Myeloperoxidase
    • Produces hypochlorite ion, which damages cell walls
  • Lactoferrin
    • Chelates iron from bacteria
  • Lysozyme
    • Degrades bacterial cell wall peptidoglycan
  • Proteases
  • Nucleases
  • Lipases
25
Q

What are Lysosomes

A

Lysosomes

membrane-bound vesicles that contain hydrolytic enzymes necessary for intracellular digestion

26
Q

What are catalase and other peroxidases

A

Catalase and other peroxidases (enzymes that break down H2O2) are located in membrane-bound organelles called peroxisomes (microbodies).

Bacteria that contain catalase (staphylococci) are able to resist* *cidal* *effects of H2O2

27
Q

What are immunoglobulins and what are the types

Type

  • Location of action
  • Function
  • Characteristics
A

Immunoglobulins (antibodies)

  • Y-shaped glycoproteins secreted by plasma cells
  • Contain two identical light polypeptide chains and two identical heavy polypeptide chains linked by disulfide bonds

IgA

  • Location of action
    • Blood plasma (monomer)
    • Exocrine secretion (dimer)
  • Function: prevents microbial attachment to mucous membranes
  • 2nd most abundant antibody

IgD

  • Location of action:
    • B cells
  • Function: Uncertain
  • Least abundant antibody

IgE

  • Location of action:
    • Mast cells
    • Basophils
    • Eosinophils
  • Function: Mediates type I hypersensitivity rxn. (anaphylaxis)
  • Main host defense against parasites (especially helminths)

IgM

  • Location of Action
    • B cells (monomer)
    • Plasma (pentamer
  • Function: Main antimicrobial defense of primary response , Activates complement, opsonizes B cell
  • Largest antibody, Most potent activator of complement, Has highest avidity of all antibodies

IgG

  • Location of Action: Plasma
  • Function: Maintain antimicrobial defense of secondary response , Opsonized bacteria, Activates complement, Neutralizes bacterial toxins and viruses
  • Most abundant antibody, Crosses the placenta, Has four subclasses
28
Q

Explain the Immunoglubulin structure

A
  • The constant regions of the two heavy chains form the Fc site, which binds to APCs or C3b. They define the immunoglobulin class (isotype)
  • The two variable regions of the heavy and light chains form the Fab sites, which are specific for binding antigen and determine the idiotype
  • Can be bound to plasma membrane of B cells, or free in extracellular fluid
  • Functions:
    • Neutralize bacterial toxins and viruses
    • Opsonization (enhances phagocytosis)
    • Activates complement via the classical pathway
    • Inhibit microbial attachment to mucosal surfaces
29
Q

Explain the specialness of IgA and IgM

A

IgA and IgM are the only antibodies that can exist as polymers, as a dimer, and a pentamer, respectively. Only the polymeric forms contain a J chain, which initiates the polymerization process

30
Q

Explain the difference between secretory IgA (sIgA) and serum IgA

A

Secretory IgA (sIgA) differs from serum IgA in that it is more resistant to proteolytic degradation. It always exists as a dimer

31
Q

What are the only two antibodies that can activate complement?

A

IgM and IgG are the only two antibodies that can activate complement

32
Q

What is complement and what are the pathways of complement activation

A

Complement:

  • Consists of about 20 plasma proteins
  • Mostly synthesized in the liver
  • Augment the humoral immune system (B cell) and inflammation
  • All modes of activation lead to the production of C3

Pathways of Complement Activation

Pathway/Characteristics

Classic:

  • Primarily activated by antigen-antibody complexes with IgG (1,2,3) or IgM

Alternate:

  • Primarily activated by bacterial LPS (endotoxin)

Lectin

  • Primarily activated by microorganisms containing cell-surface mannan (a polymer of mannose)
33
Q

State the Major functions of complement and its mediators

A

Complement

Viral neutralization

  • Mediator: C1, C2, C3, C4

Opsonization

  • C3b

Chemotaxis

  • C5a

Anaphylaxis

  • C3a, C5a (most potent)

Cell lysis (cytolysis)

  • Membrane attack complex (MAC) disrupts cell membrane permeability (composed of C5b and C6-9)
34
Q

Explain the types of Grafts

A

Types of Grafts

  • Autograft: Transplantation of tissue from one site to another within the same individual
  • Isograft: Transplant of tissue between two genetically identical individuals in the same species
  • Allograft: Transplant of tissue between two genetically different individuals in the same species
  • Xenograft: Transplant of tissue between two different species
35
Q

Explain Graft Rejection Process

A

Graft Rejection

  • T-cell-mediated (mostly CD8 Tc cells) immune response against donor alloantigens
  • The severity and rapidity of graft rejection is determined by the degree of differences between donor and recipient class I and II MHC proteins
  • If a second graft from the same donor is given to a sensitized recipient, an accelerated rejection response occurs due to the presence of presensitized Tc cells
  • Allografts are the most common grafts used for organ transplantation, blood transfusions, and other tissue grafts
  • Graft rejection can occur at different time intervals
36
Q

State and explain the three types of Graft Rejections

  • time after transplant
  • common reason for rejection
A

Types of Graft Rejection

  • Hyperacute
    • Minutes after transplant
      • Preformed antibody-mediated immune response to graft antigens
  • Acute
    • Weeks after transplant
      • T=cell=mediated immune response to foreign class I and II MHC proteins
  • Chronic
    • Months to years
      • Antibody-mediated necrosis of graft vasculature

NOTE: The most common type of hyperacute rejection are ABO blood mismatches

37
Q

What are Graft-Versus-Host (GVH) Reaction

A
  • Immunocompetent T cells from the graft recognize the recipient’s cells as foreign, eliciting their destruction
  • Host cells are targeted because the recipient generally undergoes radiation therapy, inducing severe immunocompromise
  • Occurs most commonly after bone marrow transplants and can be fatal
38
Q

What is a Hypersensitivity?

Name and describe each type

A

Hypersensitivity

  • Hypersensitivity reactions elicit exaggerated immune responses, which are damaging and destructive to the host

Remember ACID

Type I : immediate (anaphylactic)

  • Mediator: IgE
  • RxN: Antigen-bound IgE activates the release histamine and other mediators from mast cells and basophils
  • Ex: Atopic allergy, Angioedema, Anaphylaxis

Type II: Cytotoxic (Binds with Ab)

  • Mediators: IgM and IgG
  • RxN: IgM or IgG bind to host cell surface antigens, activating complement and producing MAC-mediated cell destruction
    • (antigen on cell membrane -> antibody + complement = cell death)
  • Ex: Hemolytic anemia

Type III: Immune-complex (Binds soluble Ag)

  • Mediator: Antigen-antibody complexes
  • RxN: Antigen-antibody complexes (IgG, IgM, and IgA) are deposited in various tissues, activating complement and eliciting PMN/macrophage-mediated tissue destruction
    • (antigen+antibody complex in blood -> deposited on vessel walls, complement activated -> cell death)
  • Ex: Arthritis reaction, Glomerulonephritis, Serum sickness

Type IV: Delayed (cell-mediated)

  • Mediator: T cell
  • RxN: Macrophage present antigen (MHC Class II), activating T cells and producing lymphokine-mediated tissue destruction
    • (macrophage produces IL-1, IL-12 -> Th and Helper T cell produces INF-Gamma -> macrophage)
    • Starts hours - days after contact with antigen
  • Ex: Contact dermatitis, Tuberculin (PPD) tests, Tuberculosis, Sarcoidosis, Leprosy
39
Q

What are Atopic allergies

A

Common type I hypersensitivity reactions that have a strong genetic predisposition for excessive IgE production. Clinical manifestations include asthma, edema, and erythema (“wheal and fire”) and urticaria (hives).

Common allergens include pollen, animal danders, food (shellfish and peanuts) drugs (penicillin), bee venom, and latex

40
Q

What is Angioedema

A

Angioedema = a more generalized version of type I hypersensitivity.

It involves larger areas and deeper tissues beneath the skin and underlying tissues, causing a more diffuse swelling. May involve the hands, feet, lips, eyelids, genital, oral mucosa, and airway

Rapid(immediate) onset

41
Q

What is anaphylaxis?

A

Anaphylaxis

The most severe form of type I hypersensitivity, leading to bronchoconstriction and hypotension (shock); can be life-threatening without treatment.

Its treatment is epinephrine IV. Once vital signs are stabilized, antihistamines or corticosteroids can be administered

42
Q

Name the 5 common antigen-antibody laboratory tests

  • Function
  • Common use
A

Common Antigen-Antibody Laboratory Tests

Agglutination

  • Antibody cross-links with a particulate antigen, creating visible clumping is positive
    • Common use: ABO blood typing

Precipitation

  • Antibody cross-links with a soluble antigen, creating visible precipitates if positive
    • Common use: Detection of serum antigen or antibody

Radioimmunoassay (RIA)

  • Radio-labeled antibodies cross-link with unlabeled (unknown)antigen, creating measurable radioactive complexes is positive
    • Common use: Detection of serum antigen or hapten

Enzyme-linked immunosorbent assay (ELISA)

  • Enzyme-labeled antibody binding to serum antibody-antigen complexes. A substrate is then added, activating the enzyme and eliciting a color reaction (determined by spectrophotometry) is positive
    • Common use: Detection of antigen or antibody in patient specimens

Immunofluorescence:

  • Fluorescent-labeled antibodies bind to unlabeled (unknown) antigen, creating visible fluorescence in UV light if positive
    • Common use: Detection of antigen in histologic sections or tissue specimens
43
Q

What is the universal donor for blood?

What is the universal recipient of blood?

A

Universal donor: Type O blood

(no A or B antigens)

Universal Recipient: Type AB blood

(Neither anti-A or anti-B antibody)

44
Q

What is an autoimmune disease and what are examples

A

Autoimmune Diseases

  • Caused by immune reactions versus self (host tissue)
  • Usually involves auto-antibodies
  • HLA antigen association
  • Mechanism:
    • Hypersensitivity reactions
    • Disordered immunoregulation
      • Increased Th cell function
      • Decreased Ts cell function
      • Nonspecific B-cell activation
  • Examples:
    • Graves’ disease
    • Hashimoto’s thyroiditis
    • Pernicious anemia
    • Sjogren’s syndrome
    • Systemic lupus erythematosus
    • Scleroderma
    • Polyarteritis nodosa
    • Rheumatoid arthritis
    • Reiter’s syndrome
    • Ankylosing spondylitis
    • Myastheria gravis
    • Multiple sclerosis
45
Q

What is the Thymus gland important for?

A

Thymus gland

  • Important for development of the immune system, beginning prenatally
  • Involved in T cell development and differentiation
  • Located behind the sternum
  • Functions in childhood then gradually atrophies with age
46
Q

Name the 4 autoimmune diseases affecting oral mucosa

A
  1. Lichen planus
  2. Mucous membrane pemphigoid
  3. Pemphigus vulgaris
  4. Erythema multiforme
47
Q

Explain Lichen planus

  • Autoantibody
  • Histopathology
  • IF
  • Clinical signs
A

Lichen planus

  • Autoantibody: Unknown
  • Histopathology:
    • Epithelial acanthosis with “sawtooth” rete pegs
    • Dense accumulation of T cells in underlying CT and into epithelium
  • IF: Fibrinogen in a “shaggy” linear pattern along BM
  • Clinical signs:
    • Oral lesion on buccal mucosa, tongue, and gingiva
    • Types: Reticular (with Wickham’s striae), erosive, plaque
    • Certain medications can cause lichenoid reaction
    • Skin lesions appear as clusters of pruritic purplish papules with a white keratotic “cap”
48
Q

Explain Mucous membrane pemphigoid

  • Autoantibody
  • Histopathology
  • IF
  • Clinical signs
A

Mucous membrane pemphigoid

  • Autoantibody: Anti-BP-1 (of hemidesmosomes)
  • Histopathology:
    • Separation of epithelial basal cells from BM
  • IF:
    • IgG and C3 in linear pattern along BM
  • Clinical signs:
    • Erythematous and erosive lesions on gingiva precede other oral areas: buccal mucosa, palate, FOM
    • Can extend to other mucosa: nasopharynx, esophagus, vaginal, eye conjunctiva (symblepharon formation) and skin
49
Q

Explain Pemphigus vulgaris

  • Autoantibody
  • Histopathology
  • IF
  • Clinical signs
A

Pemphigus vulgaris

  • Autoantibody: Anti-desmoglein (of desmosomes)
  • Histopathology:
    • Suprabasilar acantholysis with Tzanck cells
  • IF:
    • IgG antibody in “fishnet” pattern within spinous layer
  • Clinical signs:
    • Oral lesions often precede skin lesions
    • Erosive lesions on soft palate, buccal mucosa, gingiva, lateral tongue
    • High mortality rate
50
Q

Explain Erythema Multiforme

  • Autoantibody
  • Histopathology
  • IF
  • Clinical signs
A

Erythema Multiforme

  • Autoantibody: Immune complexes
  • Histopathology:
    • Intraepithelial pooling of eosinophilic amorphous coagulum
    • Perivascular infiltration of mononuclear cells with lamina propria
  • IF:
    • IgM and C3 in perivascular pattern with lamina propria
  • Clinical signs:
    • Causative agents include infections (HSV), medications, GI diseases (Crohn’s, UC)
    • Bullous “Target” lesions on skin and oral mucosa (25% prevalence), which may collapse and crust over (stevens-johnson syndrome)
    • Severe form is toxic epidermal necrolysis (TEN)
51
Q
A

NBDE Part 1 (7 decks)

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