Pathology Chp 3 Immunity
|immune||is different than the inflammatory response in that it remembers and is quicker to respond|
|immune||type of response where the body reacts to Antigens or foreign substances|
|Antigens||these can be bacteria, virus, fungus, organ transplants, blood transfusions.|
|autoimmune||in these type of diseases the body can view their own tissue as an antigen; no invading organism but can fight inflammatory process w/ steroids|
|lymphocytes||Primary WBC in the Immune Response|
|Humoral (antibody response)||what is the B lymphocyte response|
|plasma cells||B lymphocytes turn into _______ ________ which produce antibodies and immunogloblins|
|memory||what cells B lymphocytes turn into-which remember the antigen and engulfs when it encounters the antigen again; like a macrophage w/ memory.|
|Memory, plasma||2 types of cells B lymphocytes turn into|
|Cell mediated||what is the T lymphocyte's response|
|helper, suppressor, killer||three types of T lymphocytes; *interlinked with B cells|
|Helper cells||t lymphocyte that increases function of B lymphocyte- (CD4); ***affected by the HIV virus "what is your T cell count"; if low don't have wbc's to fight infection--get opportunistic infections; as hygienists we introduce bacteria from scaling|
|Suppressor cells||t lymphocyte that turns off the functioning of the B lymphocytes; tell them when to quit working; think this is the cell that malfunctions in an autoimmune disease-- doesn't tell B lymphocyte when to quit working & they keep going...|
|Killer cells||t lymphocyte that is Cytotoxic or CD8; kills/engulfs invading organisms|
|IgE||Antibodies-Involved in Type I Hypersensitivity; involved in asthma, hayfever, anaphylactic shock; Common|
|IgG||what specific Antibody travels across the placenta (first *passive immunity for the newborn); immunity given to baby by mother|
|IgM||Antibodies-First to increase in the immune response.|
|IgA|| Type of antibodies:|
-Found in mucosal and gingival tissue (defense against antigens in body fluids)
|IgD|| Type of antibody|
Activates other B Lymphocytes
|passive natural and acquired active natural and acquired||4 types of Immunity|
|Passive natural||-short lasting immunity, acts fast; mother to fetus or baby|
|Passive Acquired (BQ**)||-short lasting immunity, acts fast; given **antibodies in a vaccine (outside source); does not cause your own body to create antibodies|
|Active Natural||-long lasting immunity, slow to act (1-2 weeks); *Being exposed to the disease; activate; activates production of your own antibodies|
|Active Acquired||-long lasting immunity, slow to act (1-2 weeks); *Given a vaccine of the dead or deactivated microorganism; activates production of your own antibodies; received from an Outside source|
|Anaphylactic (hayfever, asthma), cytotoxic (hemolytic), immune complex, cell mediated (T lymphocytes)||4 types of Hypersensitivity-Allergies|
|Anaphylactic, asthma, hayfever, IgE (BQ)|| Name types of reactions and antibody involved|
Type 1 Hypersensitivity
*caused by antibodies
|Cytotoxic (hemolytic), IgM, IgG|| Name the Type 2 Hypersensitivity and the immunoglobulins involved|
Ex: Blood incompatibility, Rh factor (factor on the blood cells)
*caused by antibodies
|Immune Complex, IgG|| Name Type 3 Hypersensitivity and the antibody|
Autoimmune diseases- Rheumatoid arthritis- antibodies attack tissues & cause lesions w/in the body ex. red welts; *caused by antibodies
|Cell mediated, T lymphocytes|| 2 names for Type 4 Hypersensitivity. |
Ex. dermatitis and PPD tuberculosis test
*NOT caused by antibodies-- caused by T lymphocyte reaction
Ex. poison Ivy, poison oak
|Type I (Typical Allergic Reaction)||Type of hypersensitivity reaction: |
1. Tissue contact with Antigen
2. Body produces Immunoglobulin against Antigen
3. IgE attaches to Mast Cell
4. Antigen comes into body again and attaches itself to IgE on Mast Cell.
5. Mast Cell breaks apart and releases Histamine, Bradykinin, Serotonin, Heparin, Leukotrines.
6. Vasodilation, increased permeability, itching, rash, possible bronchoconstriction. 1st exposure to the antigen, but caused an immunoglobulin to be produced (IgE--has memory for that specific antigen). 2nd exposure of antigen (pollen) IgE remembers & attacks antigen, causing Mast cell to split apart then mast cell releases histamine & buddies. Histamine causes vasodilation- bv enlarging blood vessels ex. in sinuses--hayfever: runny nose, itching, rash, maybe bronchial constriction--asthma; all through body anaphylactic shock
|Type 2 hypersensitivity, Erythroblastosis Fetalis (fetus)||2 names for this type of reaction:|
Rh factor: Rh- mother becomes sensitized by a Rh+ baby.
-During pregnancy, red blood cells from the unborn baby can cross into the mother's bloodstream through the placenta.
-If the mother is Rh-, her immune system treats Rh+ fetal cells as if they were a foreign substance and makes antibodies against the fetal blood cells.
-These anti-Rh antibodies may cross back through the placenta into the developing baby and destroy the baby's circulating red blood cells.
-When red blood cells are broken down, they make bilirubin.
-This causes an infant to become yellow (jaundiced).
-The level of bilirubin in the infant's bloodstream may range from mild to dangerously high.
-*Because it takes time for the mother to develop antibodies, firstborn infants are often not affected unless the mother had past miscarriages or abortions that sensitized her immune system.
-However, *all children she has afterwards who are also Rh+ may be affected. Rh incompatibility develops only when the mother is Rh- and the infant is Rh+.
-Treat with vaccination called RhoGAM, which acts to counteract the effect of the mothers antibodies.
-Most common the second exposure from Symptoms to the baby:
Hemolytic anemia, jaundice, enlargement of spleen and liver, gross swelling of stomach, staining of infants teeth, brain damage and death.
-Marker Rh+, no marker Rh-
-Range of mild to severe symptoms
-2nd Rh+ baby has reaction
|Type 3 Immune Complex||Name the type of hypersensitivity reaction; Recognizes own tissue as an antigen; Thought to be caused by a malfunction in the suppressor T cells -when functions properly it shuts off the immune response when antigen is gone. Thought to be due to a failure to shut off the immune response?|
|Type 4, Dermatitis, Mucositis|| Name type of Hypersensitivity and 2 manifestations|
Due to an allergen contact Common in dentistry (intraoral and extraoral)
rash, burning, swelling, may have vesicles. T lymphocytes attacking the cells; not life threatening- not anaphylactic; skin reaction
|Immunodeficiency||AIDS-HIV a deficient response of Immune System;** don't confuse with autoimmune; immune system NOT working- decrease in function|
|Immunologic Pathogenesis||Oral Diseases; not caused by bacteria and/or viruses; *Your own body reacting because immune compromised|
|Apthous Ulcers, RAU (recurrent apthous ulcers)||two names|
Not caused by bacteria or viruses
Not contageous: Canker sores
Appears as an ulcerative lesion with a yellow or gray pseudomembane covering and encircled with a red halo;
Causative agent-none known.
Contributing factors-trauma, certain food, systemic diseases, stress, and systemic changes. (Bacteria can *accumulate in lesion.)
|Aphthous ulcers||-found on unattached mucosa. (movable mucosa-unattached; vestibule, under tongue, cheek, soft palate or *nonkeratinized mucosa) Cause-immunologic; Location-vestibule, under tongue, cheek, soft palate. know pg 132|
|Herpes Simplex||-found on attached mucosa or gingiva. (nonmovable mucosa or *keratinized mucosa: hard palate, attached gingiva). Cause-Viral; Location-attached gingiva, hard palate, lips. can spread on pt & to clinician; recurrent lesions; raised fluid filled bumps.. vesicles--can coalesce into an ulcer; also called vesicular|
|Minor Apthous||ulcers-usually one or a few, painful, ulcerative, can be *up to 1 cm. Treat with topical anesthetic or steroid (decrease immune response). can be caused by sodium lauryl sulfate in t-paste-- if constantly getting them|
|Herpes||multiple vesicles (can coalesce into an ulcer), painful, 1-2mm in size. Treat with antiviral agents like acyclovir or penciclovir.|
|Minor 3-5mm, major 5-10mm, herpetiform||3 Types of Aphthous Ulcers|
|Minor apthous||most common ulcer that is-3-5mm, circular, painful, *anterior region of oral cavity, no scarring, few in number. Lasts 7-10 days|
|Major apthous||ulcer that is 5-10mm, painful,* posterior region, scarring, few in number. Lasts a few weeks. usually found in other systemic diseases|
|Herpetiform||ulcer, not herpes, that is very small 1-2 mm, many lesions 1-100, anywhere on *unattached mucosa, no scarring. Differentiate from Herpes virus by location and *response to Tetracycline.|
|Urticaria||hives (swelling and itching); may not be direct cause; rash|
|Angioedema||diffuse swelling of tissue; may not have direct cause|
|urticaria, angioedema|| 2 conditions- hives & diffuse swelling of tissue|
Cause unknown-maybe infection, trauma, emotional stress, systemic diseases and allergic cause.
Tx can be antihistamine- histamine is released from the mast cell.
Can have together or separate.
|Dermatitis, Mucositis||Due to an allergen contact-Type 4 hypersensitivity. Common in dentistry -rash, burning, swelling, may have vesicles occurring.|
|Erythema Multiforme||Possible type III hypersensitivity reaction -intraoral/extraoral (because of immune complex lesions--don't always know cause) |
1. Skin lesions: *BQ
A.*Target lesion (circle w/in a circle), iris or bulls eye
B. *Bullae lesions on hands, feet, arms and legs.
2. Oral lesions:
Large ulcers mainly, erythematous can occur. Lips crusty and bleeding and edematous. Tongue can be effected.
-Skin and Oral lesions can be seen separately
-Treatment is remove cause and steroids--decrease inflammation
**No bacteria--Immune reaction
|Stevens-Johnson Syndrome|| More severe form of *Erythema Mutliforme; -Found in children and young adults |
-Skin lesions throughout body.
-Mucosa lesions throughout mouth, eyes and genitals.
-Can cause blindness and rare occasions death.
|Lichen Planus||Cause unknown-stress and medications maybe the cause? Chronic, Benign disease with oral and skin manifestations.|
1. Oral symptoms are most commonly in the *buccal mucosa--lace-like pattern, or spider web.; can be on tongue & other places in mouth
2. Skin lesions (*2-4mm crusty papules-raised lesion, found only on wrists and ankles--may or may not be present.)
3. Gingiva can be affected with desquamative gingivitis--ulcers, epithelium sluffs off (not generally everywhere, follows margin) (an erosive breakdown of the gingival margin and papilla.)
Somewhat common-- not severe, more of an annoyance; can occur in different diseases
|reticular, erosive, plaque like, atrophic||Four types of Lichen Planus; Treatment is to eliminate cause and possible use steroids. **with all can have skin lesions and desquamative gingivitis; refer for biopsy|
|Reticular (BQ)||type of lichen planus-(most common type) thin white lines (lace-like, or spider web) called Wickam's Striae - usually in buccal mucosa, but can be on tongue, lips, floor of the mouth and gingiva. can also have skin lesions & desquamative gingivitis|
|Erosive||type of lichen planus; in buccal mucosa epithelium separates from the connective tissue causes ulcers or erosions.|
|Plaque like||type of lichen planus; plaque like appearance. may have to biopsy to differentiate from cancer, etc.|
|Atrophic||type of lichen planus; Loss of whole top layer of epithelium causing a smooth, red, shiny area.|
|Reiter Syndrome|| Condition that has:|
Oral lesions-aphthous like ulcers, erythematous lesions, geographic tongue. Also has Arthritis, Urethritis, Conjunctivitis; Treatment - Aspirin and NSAIDs
|Sjogren Syndrome||Autoimmune disease; effects the salivary glands and lacrimal glands. |
1. Classic symptom: (Very) Dry mouth-xerostomia-causes dry cracked lips, increased caries, perio disease, candidiasis. Loss of filliform and fungiform papillae on dorsum of tongue.
2. Dry eyes- xerophthalmia
3. Rheumatoid arthritis can occur.
4. Enlargement of Parotid gland can occur
5. Raynaud Disease (vasoconstriction in extremities-hands & feet can turn white/blue from lack of circulation) **in 20% of patients. Treatment is NSAID for arthritis. Corticosteroids; Saliva substitutes-Pilocarpine; Artificial tears; Maintain good oral health -fluoride, brush, frequent recalls. Common.
Don't necessarily have all symptoms
|Systemic( SLE), discoid (DLE)||two types of Lupus Erythematous; Autoimmune|
|SLE||type of Lupus Erythematous; (involves the whole body-both extraorally-skin and internallly)|
|Discoid||type of Lupus Erythematous (only involves the skin and oral lesions) not organ involvement|
|SLE (Systemic Lupus Erythematosus)||Autoimmune Disease|
1.Skin lesions-(occur in **85% of patients) erythematous classic symptom *butterfly rash on bridge of nose and erythematous lesions on fingers and face.
2. Systemic symptoms- arthritis and painful joints, *Raynaud disease, loss of vision, psychoses and depression due to CNS involvement, involvement heart and kidney and the pleura of lung.
3. Oral lesions:
A. Erythematous plaques or erosions
B. White Wickham striae similar to lichen planus, but not as symmetrical. Oral lesions not always present, only **25% to 35% of patients.
Can be very painful & cause death. If heart involvement may need premed.
|DLE (Discoid Lupus Erythematosus)||Autoimmune disease|
1. Skin lesions-classic butterfly on bridge of nose & erythematous lesions
2. Oral lesions in only **25% of patients-symptoms same as systemic form
3. *No systemic involvement-milder form of disease. Treatment-corticosteroids, aspirin and NSAIDs. Benign version-- no organ involvement
|Scleroderma|| Autoimmune disease of the connective tissue|
Means "Hard skin"
Symptoms: Overproduction of collagen leading to formation of scar tissue in the skin and organs
4 times more common in women.
|Localized, Systemic||two types of scleroderma (hard skin)|
|Localized Scleroderma||Autoimmune disease of mainly CT|
Increase production of **collagen (4x), nonpliable, nonmovable
Only involves the skin and sometimes the muscle, never the organs.
*First sign is reddish patches of skin that thicken into firm oval shaped areas.
Usually fades out in 3-5 years, but left with darkened skin patches. not too debilitating
|Systemic Scleroderma|| Autoimmune disease|
Symptoms-calcium deposits in skin, increased collagen in skin, *Raynaud's syndrome, impaired function of esophagus- difficult swallowing, and telangiectasia (swelling of blood vessels in skin) and organ involvement causing damage to lungs, heart and kidneys
Hard for organs to function w/ increase w/ collagen
|Pemphigus Vulgaris (BQ) (think Nikolsy sign, oral lesions come 1st)||Autoimmune Disease|
-Cause is unknown
-Mainifests multiple bullae (blisters) in mouth and on the skin.
-Breakdown of the epithelial cell to epithelial cell adhesions-called acantholysis (separation).
-*Separation is within the epithelium.
-Initial sign is most commonly seen in mouth.
-Oral lesions are ulcerative and bulla formation- starts as bullae then ulcers once broken open.
-Adhesion is malfunctioning
-With gentle pressure cleavage occurs when the epithelial cells separate forming a bulla
-clinical lesion is called a *Nikolsky sign
*** Main manifestation bullae & ulcers (only in mouth) & skin lesions (on skin)
**The basal layer to the connective tissue is intact.
-The breakdown is* intraepithelial (epi cell to epi cell)
-Breakdown between *desmosomes
-Basement membrane intact.
-The epithelial cells that detach are rounded and are called acantholytic cells or Tzanck cells.
Most common symptom is:
1. Nicolsky's sign and oral lesions (bullae)
2. Intraorally desquamative gingivitis can occur, but are secondary to Nicolsky's sign. Treat with steroids.
Can be fatal, due to involvement into organs or overuse of steroids.
|Mucous membrane (cicatricial, benign), bullous||two types of Pemphigoid; whole epithelium will sluff off; basically variants of the same disease- think of them as the same disease|
|Pemphigoid (think desquamative gingivitis, skin lesions come 1st)||Autoimmune-cause unknown; |
Manifests Bullae formation
Lesions occur in the *eyes, genital mucosa and skin
***Intraorally the cleavage (adhesion malfunction) occurs between the epithelial layer and the connective tissue layer.
At the basement membrane to basal layer--the *hemi-desmosomes connection.
Whole epithelium will sluff off.
#1. *Desquamative gingivitis (ging margin & papilla epithelium sluffs off) is the most common sign.
2. Nicolsky's sign can occur, but not severe Lesions don't rupture as easily.
***Skin lesions come first before the oral lesions.
Treatment is corticosteroids.
Blisters DO lead to scarring.
|Behcet Syndrome|| Autoimmune- Unknown cause.|
Large Aphthous ulcers present.
Triad 1. Oral 2. Genital 3. Ocular
*Need two of three to be diagnosed
|Fixed Drug|| Type of reaction|
Type 3 Hypersensitivity due to reaction to a drug; auto immune; slow progressing--delayed reaction. Examples of drugs: Antibiotics like Sulfonamides and Barbituates like Phenobarbital. Appears as red patches sometimes called Erythema Multiforme like lesion.
|mother Rh-, baby Rh+||only scenario where there is an Rh reaction; happens in second Rh+ baby-- not necessarily 2nd baby!!!!|
|syndrome||group of signs & symptoms that occur together|
|sjorgen's (20%), lupus, scleroderma||3 diseases that have Raynaud's as a manifestation|
|acantholysis (separation), desmosomes|| -Breakdown of the epithelial cell to epithelial cell adhesions|
-what is the connection called
|acantholytic, Tzanck||2 Names for the epithelial cells in Pemphigus Vulgaris that detach from each other, and are rounded|
|Wickam's Striae|| found in lichen planus|
-thin white lines (lace-like, or spider web)