Chapter 3 Flashcards
(82 cards)
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
2
Q
what are the 2 main types of b lymphocytes
A
- 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
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
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
5
Q
what are the 5 types of immunoglobulins that are specific to particular antigens and what do they do
A
- IgE – allergic response, anaphylaxis
- IgA – 2nd most common, saliva, secretions, defends against microorganisms
- IgD – activates B lymphocytes
- IgG – highest concentration, first passive immunity for newborn
- IgM – 1st Ab in response, complement system, early stages of B-cell activation
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
7
Q
what are the 4 different types of t lymphocytes and what do they do
A
- t memory cells: retain memory of an antigen, antigen presents = t memory cells multiplies multiple times
- t helper cells: increase function of b lymphocytes
- t suppressor cells: turn off functioning of b lymphocytes
- t cytotoxic cells: attack virally infected cells or tumor cell
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
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
10
Q
what are monokines
A
- cytokines
- proteins made by cells to help the cells communicate with each other
- made by macrophages
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)
12
Q
what are the 5 different types of cytokines and where do they comes from/what do they do
A
- lymphokines: from lymphocytes
- monokines: from macrophages
- interferons: antiviral properties
- chemokines: direct chemotaxis
- interleukins: stimulate WBC
13
Q
what is the immune complex
A
- when an antibody binds to an antigen
14
Q
what is another name for antibodies
A
- immunoblobulins
15
Q
what are the 2 major divisions of the immune response
A
- humoral response
2. cell-mediated response
16
Q
what is the humoral response
A
- b lymphocytes are the primary cells
- involves production of antibodies
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
18
Q
where do t cells and b cells come from before they mature
A
- stem cells
19
Q
stem cell -> b lymphocytes -> ______ -> ______
A
- b lymphocytes -> plasma cell -> homoral response
20
Q
does the immune system have memory
A
- yes, the inflammatory does not
21
Q
what are the 2 types of immunity
A
- passive immunity
2. active immunity
22
Q
what is passive immunity
A
- using antibodies created by another person to prevent infectious disease
23
Q
what are the 2 types of passive immunity and what is an example of each
A
- natural passive immunity: when antibodies from the mother pass through the placenta to the developing fetus
- acquired passive immunity: when antibodies are acquired through injection. example: needle stick incident = hep B antibodies injected directly. short lived but fast acting
24
Q
what is active immunity
A
- antibodies created by the person themselves
25
what are the 2 types of active immunity and what is an example of each
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
26
what is hypersensitivty
- an allergic reaction
- an exaggerated response
- tissue destruction occurs as a result of the immune response
- 4 main types
27
what are the 4 main types of hypersensitivity
1. type I
2. type II
3. type III
4. type IV
28
what is type I hypersensitivity
- 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
29
what is anaphylaxis
- a systemic reaction
- causes severe vasodilation
- smooth muscle constriction
- bronchiole constriction
30
what is type II hypersensitivity
- 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
31
what is type III hypersensitivity
- 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
32
what is type IV hypersensitivity
- 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
33
what is a hypersensitivity reaction to drugs
- 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
what are autoimmune diseases
- self attacks self
- self now recognized as foreign
- diabetes -- pancreas
- thyroid diseases: hashimoto's (hypo), graces (hyper, no neg feedback), multiple sclerosis
35
what is immunodeficiency
- 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
what are aphthous ulcers
- 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
what are the 3 forms of aphthous ulcers
1. minor
2. major
3. herpetiform
38
what systemic diseases put people more at risk for aphthous ulcers
- crohn's disease
- behcet syndrome
- cyclic neutropenia
- ulcerative colitis (autoimmune)
39
what are minor aphthous ulcers
- common
- small, oval
- 3-5 mm
- yellow necrotic centre
- red halo (anterior areas, 1-2 days pain, 7-10 days healing)
40
how can we diagnose minor aphthous ulcers
- 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
what are major aphthous ulcers
- larger, 5-10 mm
- posterior area
- deeper and more painful
- may take several weeks to heal
- differential diagnosis (biopsy, other disease, HIV)
42
what are herpetiform aphthous ulcers
- 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
how can we treat aphthous ulcers
- 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
what is uticaria
- hives
- appears as multiple areas of well demarcated swelling of the skin
- may have itching (pruritus)
45
what causes lesions with uticaria
- localized areas of vascular permeability in superficial connective tissue
46
what is angioedema
- 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
what causes uticaria and angioedema
- often unknown cause
- may be due to infection, trauma, emotional stress and certain systemic diseases
- may be due to ingested allergens
48
what is contact mucositis and dermatitis
- 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
how can we treat contact mucositis and dermatitis
- topical and/or systemic corticosteroids
50
what can cause contact mucositis and dermatitis in the dental office
- topical (antibiotics and anesthetics)
- dental materials
- gloves, powder
- gums, toothpaste
51
how can we treat contact mucositis and dermatitis
- mostly topical steroids
52
what is erythema multiforme
- 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
what are the lesions of erythema multiforme like
- 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
how can we diagnose erythema multiforme
- based on clinical deatures and by exclusion of other diseases
55
how do we treat erythema multiforme
- topical or systemic corticosteroids
| - eye lesions may lead to blindness
56
what is lichen planus
- 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
where do we find lichen planus
- most commonly on the buccal mucosa
| - lesions may be on the tongue, lips, floor of the mouth, and gingiva
58
what are the 3 types of lichen planus
1. reticular lichen planus (most common)
2. erosive lichen planus
3. bullous lichen planus
59
how can we diagnose lichen planus
- 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
how can we treat lichen planus
- 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
what is sjogren syndrome
- an autoimmune disease
- unknown cause, humoral and CMI. 50% associated with autoimmune disease. primary syndrome -- only sjogren. secondary syndrome -- other diseases
62
what are symptoms of sjogren syndrome
- 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
how can we diagnose sjogren symptoms
- 2 of 3 present:
1. xerostomia
2. keratoconjunctivitis
3. arthritis or other autoimmune
64
how can we treat sjogren syndrome
- 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
what is the raynaud phenomenon
- 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
what is systemic lupus erythematosus
- 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
what are some clinical features of systemic lupus erythematosus
- 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
what is discoid LE
- 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
how can we diagnose systemic lupus erythematosus
- multi-organ involvement
| - auto antibodies (antinuclear antibodies/ANA test -- against your DNA)
70
how do we treat systemic lupus erythematosus
- depends on extent of disease
- aspirin
- corticosteroids
- immunosuppressive
71
what is the prognosis of systemic lupus erythematosus
- 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
what is pemphigus vulgaris
- 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
how do we get a positive nikolsky sign
- pinch healthy skin around blistered unhealthy skin and move it
- cleavage will form and another blister will appear too
74
where do the first signs of pemphigus vulgaris appear 50% of the time
- oral cavity
| - bullae/vesicles to ulcers
75
how do we diagnose pemphigus vulgaris
- biopsy and histological
| - auto antibody titre correlates with disease activity
76
how do we treat pemphigus vulgaris
- topical steroids
- systemic if condition worsens
- 60-90% mortality rate if untreated, vs 5% if treated
77
what is mucous membrane pemphigoid (BMMP)
- 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
how can we diagnose mucous membrane pemphigoid
- 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
how can we treat mucous membrane pemphigoid
- 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
what is bullous pemphigoid
- 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
what causes bullous pemphigoid
- 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
how can we treat bullous pemphigoid
- systemic corticosteroids and nonsteroidal antiinflammator drugs
- periods of remission
