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Oral Pathology > Chapter 3 > Flashcards

Chapter 3 Flashcards

1
Q

what are some examples of tissues that can be antigens

A
  • foreign substances: mainly proteins, often microorganisms and their toxins
  • humans cells that have been transformed” may be tumor cells, or cells infected with viruses
  • human tissue: organ transplants, tissue grafts, incompatible blood types during a transfusion
  • autoimmune diseases: tissue from the person’s own body becomes and antigen
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2
Q

what are the 2 main types of b lymphocytes

A
  1. plasma cells: produce specific antibodies

2. b memory cell: retains the memory of previously encountered antigen and will clone itself in the presence of antigens

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3
Q

where do b lymphocytes mature and reside

A
  • develop in stem cells, reside in lymph nodes once mature, travel to injury site when stimulated by antigen
  • lymph nodes, tonsils and other body tissue
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4
Q

what do plasma cells do

A
  • produce antibodies that are categorized into 5 classes of immunoglobulins, which are carried in the blood serum
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5
Q

what are the 5 types of immunoglobulins that are specific to particular antigens and what do they do

A
  1. IgE – allergic response, anaphylaxis
  2. IgA – 2nd most common, saliva, secretions, defends against microorganisms
  3. IgD – activates B lymphocytes
  4. IgG – highest concentration, first passive immunity for newborn
  5. IgM – 1st Ab in response, complement system, early stages of B-cell activation
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6
Q

where do t lymphocytes travel to in order to mature

A
  • the thymus

- thymus is larger in infants and shrinks as the child matures

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7
Q

what are the 4 different types of t lymphocytes and what do they do

A
  1. t memory cells: retain memory of an antigen, antigen presents = t memory cells multiplies multiple times
  2. t helper cells: increase function of b lymphocytes
  3. t suppressor cells: turn off functioning of b lymphocytes
  4. t cytotoxic cells: attack virally infected cells or tumor cell
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8
Q

what are natural killer cells and what do they do

A
  • not a t lymphocyte
  • only within micocirculation
  • active against viruses/cancer cells
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9
Q

what do macrophages do

A
  • active in phagocytosis of foreign material
  • make monokines
  • help both t and b lymphocytes. after phagocytosis, they process and present antigen to lymphocytes – APC (antigen presenting cell) which stimulates lymphocytes to travel from the lymphoid tissue to the injury site
  • amplifies the immune response but do not remember the antigen like lymphocytes
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10
Q

what are monokines

A
  • cytokines
  • proteins made by cells to help the cells communicate with each other
  • made by macrophages
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11
Q

what are cytokines

A
  • proteins made by cells that are able to affect the behaviour of other cells
  • different cytokines have different functions – activate macrophages, enhance ability
  • produced by B cells and T cells (lymphokines)
  • produced by macrophages (monokines)
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12
Q

what are the 5 different types of cytokines and where do they comes from/what do they do

A
  1. lymphokines: from lymphocytes
  2. monokines: from macrophages
  3. interferons: antiviral properties
  4. chemokines: direct chemotaxis
  5. interleukins: stimulate WBC
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13
Q

what is the immune complex

A
  • when an antibody binds to an antigen
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14
Q

what is another name for antibodies

A
  • immunoblobulins
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15
Q

what are the 2 major divisions of the immune response

A
  1. humoral response

2. cell-mediated response

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16
Q

what is the humoral response

A
  • b lymphocytes are the primary cells

- involves production of antibodies

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17
Q

what is the cell-mediated response

A
  • t lymphocytes are the primary cells
  • lymphocytes may work alone or be assisted by macrophages
  • the cell mediated portion regulates both major responses
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18
Q

where do t cells and b cells come from before they mature

A
  • stem cells
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19
Q

stem cell -> b lymphocytes -> ______ -> ______

A
  • b lymphocytes -> plasma cell -> homoral response
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20
Q

does the immune system have memory

A
  • yes, the inflammatory does not
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21
Q

what are the 2 types of immunity

A
  1. passive immunity

2. active immunity

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22
Q

what is passive immunity

A
  • using antibodies created by another person to prevent infectious disease
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23
Q

what are the 2 types of passive immunity and what is an example of each

A
  1. natural passive immunity: when antibodies from the mother pass through the placenta to the developing fetus
  2. acquired passive immunity: when antibodies are acquired through injection. example: needle stick incident = hep B antibodies injected directly. short lived but fast acting
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24
Q

what is active immunity

A
  • antibodies created by the person themselves
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25
Q

what are the 2 types of active immunity and what is an example of each

A
  1. natural active: protection conferred following survival from an infectious disease
  2. acquired active: injection or ingestion of either altered pathogenic microorganisms or products of those microorganisms – immunization with a vaccine
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26
Q

what is hypersensitivty

A
  • an allergic reaction
  • an exaggerated response
  • tissue destruction occurs as a result of the immune response
  • 4 main types
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27
Q

what are the 4 main types of hypersensitivity

A
  1. type I
  2. type II
  3. type III
  4. type IV
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28
Q

what is type I hypersensitivity

A
  • immediate (anaphylactic type)
  • the reaction occurs within minutes after exposure to an antigen
  • 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
  • the reaction may range from hay fever to asthma and life threatening anaphylaxis
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29
Q

what is anaphylaxis

A
  • a systemic reaction
  • causes severe vasodilation
  • smooth muscle constriction
  • bronchiole constriction
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30
Q

what is type II hypersensitivity

A
  • cytotoxic type
  • antibody combines with an antigen bound to the surface of tissue cells, usually a circulating red blood cell
  • activated complement components, 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 – blood transfusion and Rh incompatibility
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31
Q

what is type III hypersensitivity

A
  • immune complex type (serum sickness)
  • 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
  • tissue destruction occurs following phagocytosis by neutrophils
  • arthritis, lupus
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32
Q

what is type IV hypersensitivity

A
  • cell-mediated type (delayed)
  • t lymphocytes that previously have been introduced to an antigen cause damage to tissue cells or recruit other cells
  • delayed
  • responsible for the rejection of tissue grafts and transplanted organs
  • ex. TB testing
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33
Q

what is a hypersensitivity reaction to drugs

A
  • drugs can act as antigens
  • topical administration may cause a greater number of reactions than oral or parenteral routes
  • but the parenteral route may cause a more widespread and severe reaction
34
Q

what are autoimmune diseases

A
  • self attacks self
  • self now recognized as foreign
  • diabetes – pancreas
  • thyroid diseases: hashimoto’s (hypo), graces (hyper, no neg feedback), multiple sclerosis
35
Q

what is immunodeficiency

A
  • an immunopathologic condition
  • a deficiency in number, function, or interrelationships of the involved WBCs and their products
  • may be congenital or acquired
  • infections and tumors may occur as a result of the deficiency
36
Q

what are aphthous ulcers

A
  • painful oral ulcers with an unclear cause
  • occur in about 20% of the population
  • trauma is the most common precipitating factor
  • may be caused by emotional stress or certain food
  • may be associated with certain systemic diseases
  • thought to have an immunologic pathogenesis
  • occur in 3 forms
  • found on non-keratinized, moveable mucosa: vestibule, buccal mucosa, labial mucosa, floor of mouth, tongue
37
Q

what are the 3 forms of aphthous ulcers

A
  1. minor
  2. major
  3. herpetiform
38
Q

what systemic diseases put people more at risk for aphthous ulcers

A
  • crohn’s disease
  • behcet syndrome
  • cyclic neutropenia
  • ulcerative colitis (autoimmune)
39
Q

what are minor aphthous ulcers

A
  • common
  • small, oval
  • 3-5 mm
  • yellow necrotic centre
  • red halo (anterior areas, 1-2 days pain, 7-10 days healing)
40
Q

how can we diagnose minor aphthous ulcers

A
  • clinical appearance
  • location: aphthous = moveable vs herpetic = mucosa fixed to bone
  • clinical history: aphthous ulcers do not produce systemic signs of symptoms as do herpetic lesions
41
Q

what are major aphthous ulcers

A
  • larger, 5-10 mm
  • posterior area
  • deeper and more painful
  • may take several weeks to heal
  • differential diagnosis (biopsy, other disease, HIV)
42
Q

what are herpetiform aphthous ulcers

A
  • tiny (1-2 mm)
  • resemble herpes simplex ulcers
  • painful, generally occur in groups
  • differential from primary herpes, difficult to tell
  • lack of systemic effects in herpetiform aphthous ulcers
43
Q

how can we treat aphthous ulcers

A
  • several OTC medications such as orabase and zilactin
  • topical or systemic steroids may help
  • topical anesthetic may help
  • topcial steroids – antiinflammatory
  • systemic steroids for major
  • liquid tetracycline for herpetiform
  • if viral – herpes simplex (steroids contraindicated)
44
Q

what is uticaria

A
  • hives
  • appears as multiple areas of well demarcated swelling of the skin
  • may have itching (pruritus)
45
Q

what causes lesions with uticaria

A
  • localized areas of vascular permeability in superficial connective tissue
46
Q

what is angioedema

A
  • lesions caused by diffuse swelling due to increased permeability of deeper blood vessels
  • the skin covering the swelling appears normal
  • usually do not have itching
47
Q

what causes uticaria and angioedema

A
  • often unknown cause
  • may be due to infection, trauma, emotional stress and certain systemic diseases
  • may be due to ingested allergens
48
Q

what is contact mucositis and dermatitis

A
  • lesions resulting from contact of an allergen with skin or mucosa
  • involved CMI (cell-meditated immunity) – mucosa initially becomes erythematous and edematous. often there is burning and pruritus. later, the area becomes white and scaly
49
Q

how can we treat contact mucositis and dermatitis

A
  • topical and/or systemic corticosteroids
50
Q

what can cause contact mucositis and dermatitis in the dental office

A
  • topical (antibiotics and anesthetics)
  • dental materials
  • gloves, powder
  • gums, toothpaste
51
Q

how can we treat contact mucositis and dermatitis

A
  • mostly topical steroids
52
Q

what is erythema multiforme

A
  • cause is not clear; may be a hypersensitivity reaction
  • can be drug induced
  • blood vessels are destroyed and then skin supplied by them falls apart
  • most commonly occurs in young adults, affects men more commonly than women
53
Q

what are the lesions of erythema multiforme like

A
  • causes a ‘target lesion’; characteristic skin lesion with concentric erythematous rings alternating with normal skin colour
  • skin lesions can range from macules to papules to bullae
  • oral lesions are usually ulcers
  • frequently form on lateral borders of the tongue
  • crusted and bleeding lips are frequently seen
  • gingival involvement is rare
  • may be chronic or may have recurrent acute episodes
54
Q

how can we diagnose erythema multiforme

A
  • based on clinical deatures and by exclusion of other diseases
55
Q

how do we treat erythema multiforme

A
  • topical or systemic corticosteroids

- eye lesions may lead to blindness

56
Q

what is lichen planus

A
  • a benign, chronic disease affecting skin and oral mucosa
  • unknown cause
  • lesions have characteristic wickham striae (spider web-y look)
  • present in about 1% of the US population
  • most common in middle age
  • slightly more common in women
57
Q

where do we find lichen planus

A
  • most commonly on the buccal mucosa

- lesions may be on the tongue, lips, floor of the mouth, and gingiva

58
Q

what are the 3 types of lichen planus

A
  1. reticular lichen planus (most common)
  2. erosive lichen planus
  3. bullous lichen planus
59
Q

how can we diagnose lichen planus

A
  • based on clinical appearance and possibly biopsy
  • epithelial atypia and dysplasia may occur in lesions that clinically appear to be lichen planus
  • these lesions may be premalignant
60
Q

how can we treat lichen planus

A
  • treated when symptomatic
  • topical corticosteroid
  • regular oral exam (every 6 months) and biopsy of suspicious lesions (eg reticular that becomes erosive – higher risk of cancer) are necessary as these patients may be at increased risk of development of squamous cell carcinoma
61
Q

what is sjogren syndrome

A
  • an autoimmune disease
  • unknown cause, humoral and CMI. 50% associated with autoimmune disease. primary syndrome – only sjogren. secondary syndrome – other diseases
62
Q

what are symptoms of sjogren syndrome

A
  • sicca: dry moth and eyes. affects salivary and lacrimal glands. affects some organs
  • causes severe xerostomia. erythematous mucosa. dry, cracked lips. oral discomfort. depapillation
  • rheumatoid factor: positive in sjorgen. auto antibody – arthritis
  • patient may complain of burning and itching of eyes and photophobia. severe eye involvement may lead to ulceration and opacification of the eyes
63
Q

how can we diagnose sjogren symptoms

A
  • 2 of 3 present:
    1. xerostomia
    2. keratoconjunctivitis
    3. arthritis or other autoimmune
64
Q

how can we treat sjogren syndrome

A
  • treat the symptoms
  • anti inflammatory for arthritis
  • saliva substitutes
  • artificial tears, good OHI
  • fluoride rinses – high caries risk plus low dexterity
  • modifications for RA
65
Q

what is the raynaud phenomenon

A
  • 20% of patients with sjogren syndrome will have this disorder affecting the fingers and toes
  • initial pallor and subsequent cyanosis of skin due to cold or stress
  • hyperemia when blood vessels are warmed
66
Q

what is systemic lupus erythematosus

A
  • an acute and chronic inflammatory autoimmune disease, no known cause
  • affects women 8 times more frequently than men, predominantly during child bearing years and more common in black women than white
  • syndrome with a wide range of disease activity, usually chronic and progressive. periods of remission and exacerbation
  • autoantibodies to DNA are present in serum
  • may have a genetic component
67
Q

what are some clinical features of systemic lupus erythematosus

A
  • skin lesions occur in 85% of individuals
  • ‘butterfly’ rash on bridge of nose
  • may be erythematous lesions on fingertips
  • arthritis and arthralgia are common
  • depression, psychoses
  • endocarditis, kidneys
  • lungs
  • important to know extent of disease
  • remission or active
68
Q

what is discoid LE

A
  • lupus erythematosus that affects the skin
  • oral lesions accompany skin lesions in about 25% of patients with discoid LE – erythematous plaques or erosions. may have white straie; resemble lichen planus but are less symmetric
69
Q

how can we diagnose systemic lupus erythematosus

A
  • multi-organ involvement

- auto antibodies (antinuclear antibodies/ANA test – against your DNA)

70
Q

how do we treat systemic lupus erythematosus

A
  • depends on extent of disease
  • aspirin
  • corticosteroids
  • immunosuppressive
71
Q

what is the prognosis of systemic lupus erythematosus

A
  • can be fatal
  • can be very complex or simple, must investigate. kidney failure, nervous system involvement, thrombocytopenia
  • possible endocarditis risks in later stages of disease
72
Q

what is pemphigus vulgaris

A
  • progressive autoimmune
  • skin and mucosa
  • separates epithelial attachment – autoantibodies
  • acantholysis – loss of cellular connections
  • positive nikolsky sign
  • rare condition – genetic and ethnic, more common in ages 50+
73
Q

how do we get a positive nikolsky sign

A
  • pinch healthy skin around blistered unhealthy skin and move it
  • cleavage will form and another blister will appear too
74
Q

where do the first signs of pemphigus vulgaris appear 50% of the time

A
  • oral cavity

- bullae/vesicles to ulcers

75
Q

how do we diagnose pemphigus vulgaris

A
  • biopsy and histological

- auto antibody titre correlates with disease activity

76
Q

how do we treat pemphigus vulgaris

A
  • topical steroids
  • systemic if condition worsens
  • 60-90% mortality rate if untreated, vs 5% if treated
77
Q

what is mucous membrane pemphigoid (BMMP)

A
  • aka cicatricial pemphigoid
  • a chronic autoimmune disease, affects oral mucosa, conjunctive, genital mucosa, and skin
  • not as severe as pemphigus vulgaris but scarring may result
  • gingival lesions have been called desquamative gingivitis, but this may be seen with lichen planus and pemphigus as well
  • will see positive mikolsky sign but NO acantholysis (loss of coherence between epidermal cells)
78
Q

how can we diagnose mucous membrane pemphigoid

A
  • made by biopsy and histologic examination
  • no degeneration of epithelium occurs
  • an inflammatory infiltrate, usually with prominent plasma cells and eosinophils, is seen in connective tissue
79
Q

how can we treat mucous membrane pemphigoid

A
  • a chronic disease with a benign course
  • topical corticosteroid for mild cases
  • systemic corticosteroids may be required for more severe cases
  • eye lesions can lead to eye damage
80
Q

what is bullous pemphigoid

A
  • differences to BMMP
  • usually ages 70+
  • oral lesions less common
  • treated systemically
  • more lesions on skin
  • autoab not correlated with lesions
  • no nikolsky sign present
  • similar to BMMP, gingival lesions similar when present, histologically, remission and exacerbation
81
Q

what causes bullous pemphigoid

A
  • some investigators believe bullous and mucous membrane pemphigoid are variants of a single disease, but 80% of these patients are older than 60
  • oral lesions are less common than in cicatricial pemphigoid
82
Q

how can we treat bullous pemphigoid

A
  • systemic corticosteroids and nonsteroidal antiinflammator drugs
  • periods of remission

Oral Pathology (9 decks)

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