Module 4 - Adverse Reactions and Immune Defects Flashcards
(125 cards)
1
Q
What is immunodeficiency?
A
a disorder or condition where the IS has reduced function or is absent and can be traced to the failure of one or more parts of the immune system
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Q
2 types of immunodeficiencies
A
primary and secondary
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Q
Primary Immunodeficiency
A
Cogenital and derive from a genetic or developmental defect leading to abnormal maturation of the IS. May be associated with defects in innate or adaptive immunity
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Q
cogenital
A
present from birth
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Q
why are primary immunodeficiencies rare?
A
in most cases, the foetus will not survive
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Q
Secondary Immunodeficiency
A
acquired and a result from environemental factors affectong and compromising the IS
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Q
what is the most well studied secondary immunodeficiency?
A
AIDS, the causitave agent being HIV
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Q
causes of secondary immunodeficiency?
A
-undergoing chemo
-immunosuppressive medication
-chronic infection
-cancer
9
Q
Grouping primary immunodeficiecies
A
according to the faulty component of the immune system. Deficiencies:
-B-cell
-T-cell
-Complement
-Phagocytic
-Combined B and T cell
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Q
B-cell deficiencies
A
-characterized by dysfunctional B lymphocytes or a decrease in their prevalence
-deficiency in B-cell development results in an increased susceptability to infection, especially by encapsulated bacteria
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Q
encapsulated bacteria
A
encompass both Gram-positive and Gram-negative bacteria with the unifying feature being the production of capsule composed of polysaccharides
12
Q
T-cell deficiencies
A
-characterized by dysfunctional T-lymphocytes or a decrease in their prevalence
-a deficiency in T-cell development results in an increased susceptability to viruses, protozoans and fungi
13
Q
why do first symptoms of B-cell deficiencies usually appear around 7-9 months old?
A
during breastfeeding, the mother transfers IgG to the baby, around 7-9 months the antibody pool from the mother decreases. Because of B-cell deficiency, the infant is not able to synthesize normal levels of antibodies to compensate
14
Q
when do T-cell deficiencies occur?
A
-3-4 months after birth
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Q
Complement Deficiencies
A
-prone to frequent severe bacteria infections and complications arising from inability to clear immune complexes
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Q
C3 deficiencies
A
-display severest symptoms
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Q
Phagocytic Deficiencies
A
-deficiencies can appear at various stages
-bacterial and fungal infections are frequent and severe
- causing deep abscesses
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Q
Combined B and T cell deficiencies
A
-dysfunctional and/or low numbers of lymphocytes
-both hummoral and cell-mediated responses of ADAPTIVE IS are compromised
-characterized by little or no resistance to infection, thus pathogens that cause mild diseases in average human may be life threatening (chickenpox)
-suffer fatal infections in the first year of life
19
Q
what does AIDS stand for
A
Acquired Immunodeficiency Syndrome
20
Q
what does Acquired in AIDS stand for?
A
individuals do not inherit this type of disease, which is a major difference between AIDS and other primary immunodeficiencies
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Q
what does Immunodeficiency stand for in AIDS
A
the one disease characteristic AIDS has in common is the breakdown of their immune system
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Q
what does Syndrome stand for in AIDS
A
the plethora of rare but ravaging diseases that take advantage of the body’s collapsed defences
23
Q
Mode of transmission of HIV in north america
A
sexual intercourse is primary transmission of HIV
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Q
Mode of transission of HIV in eastern europe and central asia
A
non-sterile injecting drug paraphenalia is the parimary mode of transmisison
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Mode of transmission of HIV in Africa
heterosexual sex with a contaminant epidemic in children (mother to child)
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HIV outcomes without treatment
immunosuppression, neuropsychiatric abnormalities and death
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HIV: primary infection
-mount an effective immune response for first couple weeks
-over time this response will provide ineffective through the various stages of the disease, as the HIV virus compromises the individuals IS
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stages of HIV infection
1. Primary Infection
2. Acute Infection
3. Chronic Infction
4. AIDS
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CD4 T lmphoyte count at primary infection
HIGH
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HIV: acute infection
-HIV targets and infects cells with CD4 on their surface, including CD4+ helper T cells
-Viral infection causes a drastic decrease in the level of CD4+ helper T cells while the level of virus in the blood increases
-HIV in blood is HIGH increasing risk of transmission
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2-4 weeks after primary exposure to HIV
-some people experience flu-like symptoms including fever, headache and rash
-
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why do CD4+ cell levels stop crashing?
CD4+ helper T cell levels increase after the initial decrease, as some antibodies are formed against the virus allowing the immune system to recover some of the lost cell population
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HIV: Chronic Infection
-clinical latency
-HIV continues to multiply in the body at a steady state
-do not experience any HIV-related symptoms, transmission is still possible
-Anti-HIV antibodies are detectable
-HIV can begin to evade the immune response that is present by changing antigens through high mutation rates
-8-10 years
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HIV: AIDS
-CD4 helper t cells get exhausted
-diagnosed with AIDS if CD4 level less than 200 cells/mm3
-viral load drastically increases as the virus continues to acquire mutations that allow it to further avoid immune defenses
-as the IS is weakened, patients become susceptible to infections
-survive for about 3 years
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Antiretroviral therapy
-firs twas approved in 1987
-do not sure or kill HIV but prevent it from replicating
-led to declines in AIDS
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which immune cell does HIV preferably replicate in?
Helper T cells
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Autoimmunity
when the IS initiates a reaction in response to its own cells (overactivated and attacks healthy cells)
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Autoimmune Disease
-failure of an organism to distiguish self from non-self and any disease that results from this is an autoimmune disease
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how much of the human population do autoimmune diseases affect
5-7%
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Gender Rates wthin autoimmune disease population
78% of people with autoimmune disease are female
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What is the main cause of an autoimmune disease
-genetics (mainly)
-infection by bacteria/virus
-chemical exposure
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two classifications of autoimmune diseases
organ-specific and systemic
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Autoantibody
produced by the immune system that is directed against a self antigen
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Organ-specific Autoimmune diseases
-immune response directed to an antigen that is unique to a single organ or gland
-disease manifestations are limited to specific organ
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Most common target organs of auntoimmune diseases
-thyroid
-stomach
-adrenal glands
-pancreas
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Thyroid organ specific autoimmune disease
Graves, overactivty of thyroid gland, known as hyperthyroidism
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Graves Disease
Thyroid-stimulating hormone (TSH) is produced by pituitary gland to regulate hormone production. Graves patients produce autoantibodies that engage TSH receptors resulting in an overproduction of thyroid hormones
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Goiter
enlarged thyroid due to overstimulation of thyroid cells. Other symptoms include weightloss, rapid heartbeat, irritability, poor regulation of body temp etc
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Systemic Autoimmune Diseases
-immune response is directed towards a broad range of antigens that are characteristic of a number of organs and tissues
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Rheumatoid arthritis
-systemic autoimmune disorder that presents as chronic inflammation of joints, other organ systems can be affected
-common women age 40-60
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How does Rheumatoid arthritis ocurr?
-produce autoantibodies most commonly IgM to portion of the Fc receptor of IgG (rheumatoid factors)
-factors bind to ciculating IgG forming immune complexes that become deposited in joints
-deposits activate cascade leading to prolonged inflammation and joint tissue damage
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cure for autoimmune diseases
none
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treatment for autoimmune disease
immunosuppression; reducing strength of bodys immune response
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in additon to autoimmune drugs, when would immunosuppressants be used
organ transplant, during this time paitents may not be able to fight infection as their immune system is inhibited
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Understanding rejection: 3 signals of inflammation
T-cell activation signal:
1. Antigen Presentation
2. Co-stimulation
3. Proliferation
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4 main classes of immunosupressive drugs
1. Corticosteriods
2. Cytotoxic drugs
3. Immunophils
4. Lymphocyte-depleting Therapies
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Corticosteriods
Anti-imflammatory; kills T-cells
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Cytotoxic Drugs
Blocks cell division nonspecifically
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Immunophilin
blocks T cell response
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Lymphocyte-depleting Therapies
Kills T-cells non-specifically, kills activated T-cells
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Side effects of immunophilin
Drug: Cylosporine
Effects: nephrotocicity, hypertension, hirsutism, hypertrichosis, gingival hyperplasia
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Side effects of Cytotoxic drugs
Drug: Methotrexate
effects: nausea, vomitting, hair loss, tired, dizzy, chills, headache, sores, skin infection, sun sensitivity, rash, stuffy, low blood cell levels...
Drug: Cyclophosphamide
Effects: nausea, vomitting, loss appetite, stomach ache, diarrhea, darkening of skin/nails
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Side effects of corticosteriods
Drug: Prednisone
Effects: osteoperosis, hirsutism, hypertrichosis, diabetogenic
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types of infections immunosupressive drugs can have on the host due to weakend immune system
Latent or Opportunistic infections
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Latent Infections
-infections that are inactive, hidden or dormant
Most common: TB, HSV1/2, CMV, EBV and VZV
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Opportunistic Infections
-commonly occur when there is reactivation of pathogen that is already present in the host
-also result when pathogen is picked up but the blunted immune response of host is unable to combat pathogen
-can arise from bacteria, viruses, parasites or fungi
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FUNGAL opportunistic infections
-Pneumocystis
-Cryptococcosis
-Candidiasis
-Aspergillosis
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Pneumocystis Jiroveci
common name: PCP
Infects: pneumonia of lungs
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Cryptococcosis
common name: Crytptococcal Disease
Infects: Lungs, may spread to brain
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Candidiasiss
Common name: thrush
Infects: mouth, throat & vagina
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Aspergillosis
Infects: Lungs
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BACTERIAL opportunistic Infections
-tuberculosis
-Mycobacterium Avium COmplex
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Tuberculosis
common name: consumption
Infects: Lungs
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Mycobacterium Avium Complex
common name: MAC
Infects: lungs, lymph nodes, or entire body depending on site of infection
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PARASITIC opporitunistic infections
Toxoplasmosis
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Toxoplasmosis infects:
skeletal muscle, myocardium, brain and eyes
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VIRAL opporitunistic infections
-Cytomegalovirus
-Herpes simplex virus
-Varicella Zoster Virus
-Mononucleosis
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Cytomegalovirus
common name: CMV
infects: eyes, brain, other internal organs
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Herpes Simplex Virus (HSV)
common name: herpes
infects: mouth, skin, lips, eyes & genitals
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Varicella Zoster Virus
common name: chickenpox
Infects: skin or internal organs
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Mononucleosis
Common name: Epstein Barr virus or kissing disease
infects: lymph nodes, throat, salivary glands, liver, spleen & blood
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Hypersensitivity
excessive reactions produced by the normal immune system. Clinical conditions cary based on the mechanisms involved and time taken for rxn to develop
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Hypersensitivity Type I
Immediate/Anaphylaxis
ex. allergies
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Hypersensitivity Type II
Cytotoxic
ex. blood diseases like transfusion reactions OR Hemolytic disease of the newborn
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Hypersensitivity Type III
Immune complex-mediated
ex. Comtribute to development of autoimmune diseases: systemic lypus OR rheumatoid arthritis
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Hypersensitivity Type IV
Delayed Type
ex. Skin reactions: contact dermatitis
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Mediators for type I hypersensitivity
Allergens: normally a harmless substance, but in this case produces an abnormal immune response called allergic reaction
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8 major food allergens
-milk
-eggs
-wheat
fish
-crustacean shellfish
-tree nuts
-peanuts
-soya
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what cells do allergens affect
IgE, Basophils and mast cells
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Mechanisms of reactions to allergens
primary and secondary
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primary exposure to an allergen
the allergen induces hummoral response where plasma cells secrete an excessive amount of IgE antibodies whiich bind to mast cells and basophils
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secondary exposure to same allergen
membrane-bound IgE cross-links with the allergen which initiates degranulation of basophils and mast cells, releasing vasoactive mediators causing vasodilation and smooth muscle contraction
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degranulation
release of granules
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Reaction time of Type I hypersensitivty reactions
can be immediate (minutes for anaphylatic) and can lead to death in as little as 15 mins. Rarely type 1 reactions take longer (after 24 hrs) but most occur soon after exposure
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Clinical manifestations of Type I hyper sensitivity
-Allergic rhinitis
-Atopic dermititis (eczema)
-Asthma
-Hives (urticaria)
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Mediators of type II hypersensitivity
-IgG
-IgM
-NK cells
-the complement system
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Mechanism of reaction for type II hypersensitivity
-IgGs/IgMs bond to antigens on the surface of cells such as erythrocytes
-once antibodies attached through antigen-binding regions, the Fc region is free and can activate 2 processes: CLASSICAL COMPLEMENT ACTIVATION (leading to MAC or opsonization) & ANTIBODY DEPENDENT CELL MEDIATED TOXICITY
-these mediate destruction of cells, leading to excessive inflammatory response
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Membrane Attack complex
creates holes in cell membrane leading to cell lysis
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Opsonization
leads to phagocytosis by phagocytes such as macrophages
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Type II hypersensitivity reaction time
minutes to hours
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clinical manifestation type II hypersensitivity
-Drug induced hemolytic anemia
-Transfusion rxns
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Transfusion rxns
Depending on blood type, you will only be able to safely recieve ceratin blood types during a blood transfusion. This is due to expression of specific antigen on your RBCs, meaning if you dont express antigens, you have the antibodies against them
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Drug Induced Hemolytic anemia
-Some antibiotics can bind nonspecifically to proteins on RBC membranes and form complex which sometimes induced complement-mediated cell lysis
-As RBCs rupture, the # of RBCs decrease resulting in anemia
-anemia disappears when drug removed
*pennicillin
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universal donor
O negative
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Universal reciepnt
AB
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Type III hypersensitivity mediators
-Immune complexes (antigen-antibody complexes)
-Neutrophils
-Complement proteins
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Mechanism of reaction type III hypersensitivity
-the reaction of antibodies with antigens generates immune complexes. When immune complexes are not cleared, they can accumulate and deposit in tissue
-the immune complexes will activate the complement which will induce inflammatory reactions through neutrophil attraction to the site of deposition
-Neutrophils release lytic enzymes as they attempt to phagocytose the immune complexes, which weakens surrounding cell membranes causing tissue damage
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Type III hypersensitivity reaction time
3 to 10 hours after exposure to an antigen (sometimes days to weeks)
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Clinical manifestation Type III hypersensitivity
Serum sickness
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Serum sickness
-rxns are observed after administration of antitoxins containing foreign serum
-recipent of antiserums develop specific antibodies for this protein & form immune complexes
-after days -week symptoms occur
-complexes accumulate in tissues where filtration of plasma occur and can contribute to pathogenesis
-clinical efects subside when antigen broken down
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whats an antitoxin
and antibody that counteracts a toxin
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Type IV hypersensitivity mediators
-CD8+ cytotoxic T cells
-CD4+ Helper T cells
-Macrophages
***only type of hypersensitivity NOT mediated by antibodies
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Type IV Hypersensitivtiy mechanism of Reaction
-after exposure to antigen, T cells become activated and initiate an immune response
-sensitized helper T cells will release cytokines that activate macrophages or cytotoxic T cells which mediate direct cellular damage
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Type IV Hypersensitivtiy Reaction time
two - three days
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Type IV hypersensitivity clinical manifestation
-Inflammatory Bowel Disease
-Contact Dermatitis
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Inflammatory Bowel Disease
group of conditions characterized by chronic inflammation of all or parts of digestive tract
2 most common: chrons & collitis
-falls into class of autoimmune disease
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Contact Dermatitis
-type of DTH response causing red itchy rash on skin that has been in contact with small, reactive molecules which create complexes with skin proteins
-poison ive, formaldehyde, nickel ...
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Erythrocyte sedimentation rate (ESR)
rate at which RBC sediment in one hour
*non-specific measure of inflammation
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Microcytic anemia
presence of small RBC
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what type of hypersensitivity does not involve antibodies and is only cell-mediated
type IV
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Albuterol
used to relax muscles found in the airways to increase airflow to the lungs
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Asthma
-abnormal inflammatory response to a specific or nonspecific stimuli in the bronchial lining, resulting inn obstruction of small and large airways
-muscles contract and become inflammed
-increase in mucous secretion
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which immunoglobin is responsible for asthma
IgE
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what type of hypersensitivity is asthma
Type I
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