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Oral Pathology > LO 4 > Flashcards

LO 4 Flashcards

1
Q

Describe the Acquired Immune Response

A
  1. Defends the body against injury
  2. Has memory capability
  3. Responds faster than inflammatory response
  4. Involves complex network of white blood cells (WBCs)
  5. May result in increased level of tissue damage and disease as it fights pathogens
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2
Q

List examples of the body seeing parts of itself as invading antigens

A
  1. Tumor cells
  2. Cells infected with viruses
  3. Organ transplant
  4. Tissue graft
  5. Incompatible blood transfusion
  6. Cells of own body: Autoimmune diseases
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3
Q

Recognition of the body’s own antigens as invaders is known as ___________

A

Autoimmune disease

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4
Q

The overreaction to antigens is known as _________

A

Hypersensitivity

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5
Q

List the cells involved in autoimmune response

A
  1. Cytokines
  2. Lymphocytes - B-cell lymphocytes, T-cell lymphocytes, Natural killer (NK) cells
  3. Macrophages
  4. Dendritic cells
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6
Q

Describe B-Cell Lymphocytes

A
  1. Develop from stem cells in bone marrow
  2. Mature and reside in lymphoid tissue - Lymph nodes, tonsils, and other body tissue
  3. B cells travel to the site of injury when stimulated by antigen
  4. Produce and release a protein (antibody) in response to presence of antigen
  5. Circulating antibodies: Immunoglobulins (Ig)
  6. Two main types:
    1. Plasma cell: Produces specific antibodies
    2. B-memory cell: Retains the memory of previously encountered antigen and will clone itself in the presence of antigen
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7
Q

List the 5 types of immunoglobulins

A
  1. IgA
  2. IgD
  3. IgE
  4. IgG
  5. IgM
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8
Q

Describe the development of T-cell lymphocytes

A
  1. Develop from bone marrow stem cells
  2. Travel to the thymus and mature
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9
Q

List the types of T-cell lymphocytes

A
  1. Memory cells
  2. T-helper cells: Increase functioning of B cells
  3. T-suppressor cells: Turn off functioning of B cells
  4. T-cytotoxic cells: Attack virally infected cells or tumor cells
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10
Q

Describe the function of T-cell lymphocytes

A
  1. Increase the function of B cells: Enhancing the antibody response
  2. Carry the CD8 marker
  3. Active in surveillance against virally infected cells
  4. Directly attack virally infected and neoplastic cells
  5. Start, regulate, and coordinate the overall immune response
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11
Q

Describe Natural Killer (NK) Cells

A
  1. Destroy foreign cells
  2. Located within the microcirculation
  3. Active against viruses and cancer cells
  4. Activity can be abnormal as in HIV infection= relation to secondary cancer mortality
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12
Q

Describe macrophages

A
  1. Accessory cells in immune response
  2. Located in connective tissue (CT) during inflammation
  3. Function - Phagocytosis/Assist B cells and T cells
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13
Q

Describe the functions of macrophages

A
  1. Phagocytosis: engulf invader antigens and destroy
  2. Messenger between inflammatory response and immune response
  3. Activating factor: Produce and secrete lysosomal enzymes
  4. Amplify the immune response but do not have memory of the encountered antigen
  5. Monocytes can transform into macrophages when required
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14
Q

Describe dendritic cells (DCs)

A
  1. Type of WBC found on skin, on mucosa, and in blood
  2. Antigen-presenting cells (APCs): Process antigenic material and present it to other immune system cells
  3. Messenger between innate immunity and acquired immunity
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15
Q

Describe cytokines in the immune response

A
  1. Immunomodulating agents: Alter the immune response
  2. Direct and control systemic immune response
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16
Q

Explain what the immune system has memory; the inflammatory system does not means

A
  1. Some lymphocytes retain memory of an antigen after an initial encounter
  2. This means the immune response will be faster and stronger the next time an antigen enters the body
  3. The retained memory is called immunity
  4. The inflammatory system does not have this
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17
Q

Describe passive immunity

A
  1. Using antibodies created by another person to prevent infectious disease
  2. Natural: female to fetus
  3. Acquired: Injection for centrifuged donor antibodies
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18
Q

Describe active immunity

A
  1. Antibodies created by the person
  2. Natural: Microorganism causes the disease and antibody production\
  3. Acquired: Immunization, vaccination, booster (Killed-type vaccine or Live-attenuated vaccine)
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19
Q

Describe herd immunity

A
  1. Type of indirect protection from an infectious disease that occurs when a large percentage of the population becomes immune to infection
  2. Can be achieved through vaccination or through exposure to and recovery from infection
  3. Approximately 70% to 90% of a population needs immunity to achieve
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20
Q

What are the 2 major divisions of the immune response?

A
  1. Humoral immunity
  2. Cell-mediated immunity
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21
Q

Describe Humoral immunity

A
  1. Antibody-mediated immunity
  2. Production of antibodies
  3. Protection against bacteria and viruses
  4. B cells are the primary cells
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22
Q

Describe Cell-mediated immunity

A
  1. Cellular immunity
  2. T cells are the primary cells
  3. Regulates both major immune responses
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23
Q

Describe immunopathology

A
  1. The study of immune reactions involved in disease
  2. The study of diseases caused by the malfunctioning of the immune system
  3. E.g. Hypersensitivity, Autoimmune diseases, Immunodeficiency
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24
Q

List the 4 types of Hypersensitivity/Allergy

A
  1. Type I or anaphylactic type - Hay fever, Asthma, Anaphylaxis
  2. Type II or cytotoxic type - Autoimmune hemolytic anemia
  3. Type III or immune complex type - Autoimmune diseases
  4. Type IV or cell-mediated type - Granulomatous disease, Tuberculosis
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25
Q

Describe type 1 hypersensitivity - Immediate (anaphylactic type)

A
  1. The reaction occurs within minutes of exposure to an antigen
  2. Plasma cells produce IgE - IgE causes mast cells to release histamine, causing increased dilation and permeability of blood vessels and constricting smooth muscle in bronchioles of the lungs
  3. The reaction may range from hay fever to asthma and life-threatening anaphylaxis
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26
Q

Describe Anaphylaxis

A
  1. Occurs within minutes typically
  2. Widespread angioedema/urticaria which can restrict airway
  3. Administer epinephrine pen in emergent situations
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27
Q

Describe Type II Hypersensitivity (Cytotoxic type)

A
  1. Antibody combines with an antigen bound to the surface of tissue cells, usually a circulating red blood cell (RBC)
  2. Activated complement components and IgG and IgM antibodies in blood participate in this type of hypersensitivity reaction - This destroys the tissue that has the antigens on the surface of its cells (e.g., Rh incompatibility)
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28
Q

Describe Type III Hypersensitivity (Immune complex type (serum sickness))

A
  1. Immune complexes are formed between microorganisms and antibody in circulating blood - These complexes leave the blood and are deposited in body tissues, where they cause an acute inflammatory response
  2. Tissue destruction occurs after phagocytosis by neutrophils
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29
Q

Describe Type IV Hypersensitivity (Cell-mediated type (delayed))

A
  1. T cells that previously were introduced to an antigen cause damage to tissue cells or recruit other cells
  2. Responsible for the rejection of tissue grafts and transplanted organs
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30
Q

Describe drug hypersensitivity

A
  1. Drugs can act as antigens
  2. Topical administration may cause a greater number of reactions than oral or parenteral routes
  3. However, the parenteral route may cause a more widespread and severe reaction
31
Q

What is Immunologic tolerance?

A

The body learns to distinguish self from nonself

32
Q

What is an autoimmune disorder?

A

The immunologic tolerance recognition mechanism breaks down; some body cells are not tolerated and are treated as foreign antigens

33
Q

Describe immunodeficiency

A
  1. An immunopathologic condition
  2. A deficiency in number, function, or interrelationships of the involved WBCs and their products
  3. May be congenital or acquired
  4. Infections and tumors may occur as a result of the deficiency
34
Q

List the common Oral Immunologic Lesions and Diseases

A
  1. Aphthous ulcers
  2. Urticaria and angioedema
  3. Contact mucositis and contact dermatitis
  4. Fixed drug eruptions
  5. Erythema multiforme
  6. Lichen planus
  7. Reactive arthritis (Reiter syndrome)
  8. Langerhans cell disease
35
Q

Describe Aphthous Ulcers

A
  1. Painful oral ulcers with an unclear cause
  2. Reported incidence ranges from 5% to 56%
  3. Trauma is the most common precipitating factor - May be caused by emotional stress or certain foods
  4. May be associated with certain systemic diseases
  5. Thought to have an immunologic pathogenesis
  6. Occur in three forms - Minor, Major, Herpetiform
36
Q

What can cause Recurrent Aphthous Ulcers (Canker Sores, Aphthous Stomatitis)?

A
  1. Trauma
  2. Perceived food associations
  3. Menstruation
  4. Systemic diseases
  5. Tobacco cessation
  6. Stress
37
Q

Describe Minor Aphthous Ulcers

A
  1. Discrete, round or oval ulcers
  2. Occur on movable mucosa
  3. Up to 1 cm in diameter
  4. Erythematous halo surrounding a yellowish-white fibrin surface
  5. May have single or multiple lesions
  6. May have a prodrome of 1 to 2 days
38
Q

Describe Major Aphthous Ulcers (Sutton Disease, Periadenitis Mucosa Necrotica Recurrens)

A
  1. Larger than minor aphthous ulcers (>1 cm)
  2. Deeper and longer lasting than minor aphthous ulcers
  3. Very painful
  4. Occur in the posterior of the mouth more often than do minor aphthous ulcers
  5. May require several weeks to heal leaving a scar
  6. May require a biopsy
39
Q

Describe Herpetiform Aphthous Ulcers

A
  1. Tiny (1 to 2 mm)
  2. Resemble herpes simplex ulcers
  3. Painful, generally occur in groups
40
Q

What systemic disease are Aphthous Ulcers associated with?

A
  1. Chronic gastrointestinal symptoms
  2. Crohn disease
  3. Gluten-sensitive enteropathy/celiac disease
  4. Inflammatory bowel syndrome
  5. Intestinal lymphoma
  6. Ulcerative colitis
  7. Arthritis
  8. Skin lesions (Behçet syndrome)
  9. Childhood periodic fevers
41
Q

List the treatments for aphthous ulcers

A
  1. Topical corticosteroids
  2. Topical nonsteroidal anti-inflammatory drugs (NSAIDs)
  3. Pain relief: Lidocaine, benzocaine
  4. Systemic steroids
  5. Nicotine replacement therapy
42
Q

Describe urticaria (hives)

A
  1. Appear as multiple areas of well-demarcated swelling of skin
  2. May include itching (pruritus)
  3. Lesions are caused by localized areas of vascular permeability in superficial connective tissue
43
Q

Describe angiodema

A
  1. Lesions caused by diffuse swelling as a result of increased permeability of deeper blood vessels
  2. The skin covering the swelling appears normal
  3. Usually do not itch
44
Q

List the causes and treatments of Urticaria and Angioedema

A

Causes:
1. Idiopathic
2. Infection
3. Trauma
4. Emotional stress
5. Systemic diseases
6. Ingested allergens

Treatment:
1. Antihistaminic drugs
2. Epinephrine

45
Q

Describe Allergic Contact Mucositis and Dermatitis

A
  1. Lesions result from contact of an allergen with skin or mucosa
  2. Involves T cells in a cell-mediated immune response
  3. Type IV hypersensitivity
46
Q

List the causes and treatments for Allergic Contact Mucositis and Dermatitis

A

Causes:
1. Preservatives in local anesthetics
2. Topical medications
3. Acrylics
4. Metal-based alloys
5. Epoxy resins
6. Flavoring agents
7. Gloves

Treatment
1. Topical corticosteroids
2. Systemic corticosteroids

47
Q

Describe fixed drug eruptions

A
  1. Lesions that appear in the same site each time a drug is introduced
  2. Generally appear suddenly after a latent period and subside when the drug is discontinued
  3. May be single or multiple, slightly raised, reddish patches or clusters of macules on the skin, or sometimes the mucous membranes
  4. Occurrence may include pain or pruritus
48
Q

What type of allergic reaction are fixed drug eruptions

A
  1. Immune complexes are deposited along the endothelial walls of blood vessels
  2. Inflammation causes vasculitis with damage to the vessel wall
  3. This creates erythema and edema in superficial layers of the skin or mucosa
  4. Treatment - The drug causing the reaction should be identified and discontinued
49
Q

Describe Erythema Multiforme

A
  1. Acute, self-limited disease that affects skin and mucous membranes
  2. Cause: Not clear; may be a hypersensitivity reaction
  3. Target or bull’s-eye lesion - Concentric erythematous rings alternating with normal skin color
  4. Diagnosis - Based on clinical features and by exclusion of other diseases; Eye lesions may lead to blindness
  5. Treatment - Remove cause, if possible; Topical or systemic corticosteroids; Systemic antiviral medications
50
Q

Describe Stevens-Johnson Syndrome

A
  1. Used to be considered a very severe form of erythema multiforme; now classified as a variant of toxic epidermal necrolysis (TEN)
  2. Extensive and painful oral lesions
  3. Genital mucosa and mucosa of eyes may be involved
  4. Lips generally are encrusted and bloody
51
Q

Describe lichen planus

A
  1. A benign, chronic disease affecting the skin and oral mucosa
  2. Unknown cause, relation to immune response
  3. Lesions have characteristic Wickham striae (lacelike/spiderweb)
  4. Most commonly on buccal mucosa - Lesions may be on the tongue, lips, floor of mouth, and gingiva
  5. Present in about 2% of the U.S. population - Most common in middle age; Slightly more common in women
52
Q

What are the types of lichen planus?

A
  1. Reticular lichen planus - Most common form; Classic Wickham Striae
  2. Erosive and bullous lichen planus - Epithelium separates from connective tissue
53
Q

__________ (Bright red gingiva) can be associated with lichen planus

A

Desquamative gingivitis

Papules (2 to 4 mm) most commonly in lumbar region, flexor surfaces of the wrist, anterior ankle

54
Q

Describe diagnosis of Lichen Planus

A
  1. Epithelium is generally parakeratotic
  2. Either hyperplastic or atrophic
  3. Degeneration of basal cell layer of epithelium
  4. Broad band of lymphocytes in CT
  5. Separation of epithelium from CT = erosive areas
  6. May be premalignant
55
Q

Describe the Treatment and Prognosis
for Lichen Planus

A
  1. Treated when symptomatic
  2. Topical corticosteroid medications
  3. Meticulous oral hygiene
  4. Discontinuation of drugs causing condition
  5. Regular oral examination
  6. Biopsy of suspicious lesions is necessary because these patients may be at increased risk of development of squamous cell carcinoma
56
Q

Describe reactive arthritis (Reiter Syndrome)

A
  1. Classic syndrome includes arthritis, urethritis, and conjunctivitis
  2. An antigenic marker called HLA-B27 is present in most patients, meaning there may be a genetic influence
  3. Predicted to be an abnormal immune response to a microbial antigen
  4. May see aphthous ulcers, erythematous lesions, and geographic tongue–like lesions
  5. Diagnosis is made on basis of clinical signs and symptoms, along with identification of HLA-B27 antigenic marker
57
Q

List the common Autoimmune Diseases
with Oral Manifestations

A
  1. Sjögren syndrome
  2. Systemic lupus erythematosus
  3. Pemphigus vulgaris
  4. Mucous membrane pemphigoid
  5. Bullous pemphigoid
  6. Behçet syndrome
58
Q

Describe Sjögren Syndrome

A
  1. Affects the salivary and lacrimal glands
  2. Results in a decrease in saliva and tears, causing a dry mouth (xerostomia) and dry eyes (xerophthalmia)
  3. Keratoconjunctivitis sicca: Damage to eyes
  4. May be associated with other autoimmune disorders - Primary Sjögren syndrome: When it occurs alone; Secondary Sjögren syndrome: When it occurs with other autoimmune disorders
  5. Affects both major and minor salivary glands - Parotid gland enlargement occurs in about 50% of patients
59
Q

Describe the symptoms of Sjögren Syndrome

A
  1. Oral discomfort caused by dry mouth
  2. Lips: Cracked and dry
  3. May see loss of filiform and fungiform papillae on the dorsum of the tongue
  4. High risk for caries, periodontal disease, and oral candidiasis
60
Q

Describe biopsy of Sjögren Syndrome

A
  1. Biopsy reveals a characteristic appearance
  2. Major salivary glands - Replacement with lymphocytes and the presence of islands of epithelium called epimyoepithelial islands
  3. Minor salivary glands - Aggregates of lymphocytes surrounding salivary gland ducts
61
Q

Describe the diagnosis and management of Sjögren Syndrome

A

Diagnosis:
1. Diagnosis is made when two of three components are present:
2. Xerostomia - Measurement of salivary flow and biopsy can help
3. Keratoconjunctivitis sicca - Confirmed by eye examination
4. Rheumatoid arthritis

Treatment (treated by the symptom):
1. For most patients, the course of the disease is chronic and benign, but these patients are at risk for the development of other, more serious diseases
2. Nonsteroidal antiinflammatory agents for arthritis - May need corticosteroids and immunosuppressive drugs for severe cases
3. Saliva substitutes for xerostomia - Humidifier, sugarless gum, or lozenges; Pilocarpine
4. Glasses and/or artificial tears to protect eyes
5. Good oral hygiene
6. Fluoride
7. Frequent re-care appointments

62
Q

Describe Systemic Lupus Erythematosus (SLE)

A
  1. An acute and chronic inflammatory autoimmune disease - No known cause, genetic link suspected
  2. Affects women eight times more frequently than men, predominantly during childbearing years - Three times more frequent in African American women than in Caucasian women
  3. A syndrome with a wide range of disease activity - Usually chronic and progressive; Periods of remission and exacerbation
63
Q

Describe the clinical features of Clinical Features: Systemic
Lupus Erythematosus (SLE)

A
  1. Skin lesions occur in 85% of individuals - “Butterfly” rash on bridge of nose; There may be erythematous lesions on fingertips; Arthritis and arthralgia are common
  2. Oral lesions accompany skin lesions in about 25% of patients with discoid lupus erythematosus - Erythematous plaques or erosions; May have white striae; resemble lichen planus but are less symmetric
  3. Medical consultation may be needed before dental treatment
64
Q

Describe the diagnosis the treatment of Systemic Lupus Erythematosus (SLE)

A

Diagnosis:
1. Based on multiorgan involvement and presence of antinuclear antibodies in serum
2. Inflammatory infiltrate is around blood vessels in connective tissue

Treatment:
1. Aspirin and antiinflammatory drugs
2. Hydroxychloroquine and corticosteroids along with immunosuppressive agents

65
Q

Describe Pemphigus Vulgaris

A
  1. A severe, progressive autoimmune disease affecting the skin and mucous membranes
  2. Characterized by intraepithelial blister formation resulting from acantholysis, a breakdown of cellular adhesion between epithelial cells
  3. The first signs of disease occur in the oral cavity in more than 50% of cases
  4. There may be shallow ulcers, to fragile vesicles, to bullae
  5. Nikolsky sign - Rubbing with a finger can produce a bulla which can burst can create ulcerated tissue; Secondary infections are a concern
66
Q

Describe treatment and prognosis for Pemphigus Vulgaris

A
  1. High doses of corticosteroids
  2. May include immunosuppressive drugs
  3. Mortality rate of 8% to 10% in 5 years is related to complications of corticosteroid treatment
67
Q

Describe Mucous Membrane Pemphigoid (Benign Mucous Membrane Pemphigoid; Cicatricial Pemphigoid)

A
  1. A chronic autoimmune disease
  2. Affects oral mucosa, conjunctiva, genital mucosa, and skin
  3. Not as severe as pemphigus vulgaris
  4. Will see positive Nikolsky sign
  5. Gingival lesions have been called desquamative gingivitis, but this condition may be seen with lichen planus and pemphigus as well
68
Q

Describe diagnosis of Mucous
Membrane Pemphigoid

A
  1. Made by biopsy and histologic examination
  2. No degeneration of epithelium occurs
  3. An inflammatory infiltrate, usually with predominant plasma cells and eosinophils, is seen in connective tissue
69
Q

Describe the treatment/prognosis for Mucous Membrane Pemphigoid

A
  1. A chronic disease with a benign course
  2. Topical corticosteroid for mild cases
  3. Systemic corticosteroids may be required for more severe cases
  4. Eye lesions can lead to eye damage
70
Q

Describe Bullous Pemphigoid

A
  1. Some investigators believe bullous and mucous membrane pemphigoid are variants of a single disease
  2. Most patients are older than 70
  3. Oral lesions are less common than in cicatricial pemphigoid
  4. Treatment - Systemic corticosteroids and NSAIDs
71
Q

Describe Behçet Syndrome

A
  1. A chronic, recurrent autoimmune disease - Primarily oral ulcers, genital ulcers, ocular inflammation; No sex predilection; Autoantibodies to human mucosa may be found
  2. Oral ulcers are similar in appearance to aphthous ulcers
  3. Diagnosis requires that two of three types of lesions (oral, genital, and ocular) be present
  4. A pustular lesion after needle puncture suggests Behçet syndrome
  5. Treatment - Systemic and topical corticosteroids; Chlorambucil is used for ocular lesions
72
Q

Describe Sarcoidosis

A
  1. Multisystem granulomatous disease of unclear etiology
  2. Women aged 20 to 50 are most frequently seen involving the lungs and the lymph nodes
  3. Erythema nodosum: Type of skin inflammation seen in the lower extremities
  4. Most common sites for oral sarcoidosis: Jawbones, buccal mucosa, gingiva, floor of mouth, tongue, and palate
73
Q

Describe the diagnosis and treatment of Sarcoidosis

A

Diagnosis:
1. Made based on correlation of the patient’s clinical presentation with the biopsy findings

Treatment and prognosis:
1. Chronic condition with no cure
2. Most cases produce only mild symptoms that will resolve on their own after several months without treatment

Oral Pathology (6 decks)

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