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Flashcards in immunology Deck (106):
1

type 1 hypersensitivity

IgE-mediated hypersensitivity
= immediate hypersensitivity

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IgE crosslinking on a mast cell leads to

mediator release during type 1 hypersensitivity

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IL-4 + IL13 released from TH2 cells cause B cells to release

IgE

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allergies

1 first exposure to pollen
2 IL4 drives B cells to produce IgE in response to pollen antigens
3 Pollen-specific IgE binds to mast cell
second exposure to pollen
4 second exposure to pollen
5 acute release of mast cell contents causes allergic rhinitis (hay fever)

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hay fever

allergic rhinitis

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early phase mediators released by mast cells + basophils

histamine
proteases
leukotrienes
prostaglandins
platelet activating factor (PAF)
chemotactic factors for neutrophils + eosiophils

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platelet activating factor

causes platelet activating factor

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eosinophils

parasites cause eosinophils to pour out of the blood

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massive activation of PAF causes all vessels to

dilate

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late phase mediators released in late phase of the acute allergic reaction (5-6 days after phase begins)

-cytokines from mast cells, TH2 cells, macrophages, eosinophils
-numerous inflammatory mediators present in eosinophils + neutrophils that have been brought to the site of chemokines

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FEV1 measures

chest expansion

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late phase of acute allergic reaction can be controlled by

corticosteroids that inhibit cytokine production

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how many hours after acute phase will be late phase

5-6 hours

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late phase (5-6 hours later)

-he will feel tight chested
-takes longer to settle down

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at night, ppl inhale dust, mites, and then 5-6 hours later, they are tight again (late phase)

many people with sprays for allergic things are in the late phase

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examples of IgE mediated allergic reactions

-hay fever (allergic rhinitis)
-depends on the season
-rag weed season produces lots of pollen

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allergic salute

nose is itchy + rubbing it gives relief

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allergic rhinitis (hay fever)

-IgE mediated
-tree pollenss
-grass pollens
-ragweed pollen
-cat hair
-dog hair
-house dust mites
-moulds

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house dust mites eat skin scales and defecate. What do allergic people inhale

dry feces of dust mites

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cockroaches

-important cause of allergic reaction

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what groups have higher rates of allergic reactions

lower socioeconomic group

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examples of IgE mediated allergic reactions

-allergic rhinitis (hay fever)
-bronchial asthma
-acute drug reactions
-rubber gloves
-food allergies
-insect stings
-acute urticaria (hives)

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bronchial asthma

-bronchus of patient with astma supposed to be smooth but it's not
-they can take air in, but they wheeze when they let air out

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rubber allergies

pulling off the rubber glove releases aerosol of rubber

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food allergies

shrimp, peanuts, pollen, let babies eat peanuts early and then later they have a decrease incidence of peanut allergies

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insect stings that can cause allergies

wasps
hornets
honey bees
yellow jackets
fire ants

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acute urticaria (hives)

-itchy, inflamed reaction
-corticosteroids will stop it

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angioedema

swollen lips

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wheals

circles from allergic reactions

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diagnosis of acute allergic reactions

-skin prick tests (intradermal skin tests)
-measure specific IgE antibodies to cat hair, pollens, house dust mites

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skin prick tests (intradermal skin tests)

positive wheal and flare seen in 5-10 mins

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treatment for type 1 allergic reactions

-epinephrine (adrenaline)- treat acutes anayphylactic rxns
-remove antigen
-tx symptomatically w/ antihistamines, antileukotrienes, corticosteroids
-omalizumab
-hyposensitization therapy shots

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what does epinephrine do

constricts

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omalizumab

a monoclonal antibody that inhibits IgE binding to mast cells
-blocks binding site so it can't attach to mast cells

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hyposensitization therapy shots

weekly, increasing doses of antigen

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hyposensitization (Desensitization) examples

bee venom, cat hair antigen, grass pollen antigen

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hyposensitization (Desensitization)

-consists of multiple exposures to increasing concentrations of the antigen
- this results in an increase of IgG antibodies
-venom will be neutralized by the IgG when he gets stung again

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type II hypersensitivities (cytotoxic reactions)

abnormal antibody directed against a target organ causes destruction of the target cell
-antibody punches holes in rbcs= anemia due to destruction of rbcs

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examples of type II hypersenstivities

-autoimmune hemolytic anemia
-autoimmune thrombocytopenia
-goodpasture's syndrome
-anti-receptor antibody diseases

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autoimmune thrombocytopenia

platelets drop 300,000 to 20,000
-antibody against paltelets
-young women notice they have bruising

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goodpasture's syndrome

antibody against the basement membranes of alveoli in the lung

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anti-receptor antibody diseases

-myasthenia gravis
-grave's disease

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myasthenia gravis

-due to abnormal antibodies to acetylcholine receptor on muscle cells
-blocks receptor and causes muscular weakness
-muscles don't work and people become weak

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myasthenia gravis= in the morning, acetylcholine receptors are back on cells looking normal, as they start working

-antibody attaches to them so that during the day the body gets weaker and weaker
-women are able to taket heir kids to school but by the afternoon, they are using masking tape to hgold their eyelids up bc they are becoming weaker

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grave's disease

makes abnormal antibody that continously turns on the receptor, making excessive thyroid hormone
-autoimmune bc you are making antibodies against the receptor

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pituitary makes TSH which goes to the TSH receptors and typically stimulates

hormone synthesis

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in grave disease, and autoantibody instead of the TSH binds to the

TSH receptor

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graves disease

eyes swell up + huge thyroid swelling

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treat Graves

-poison thyroid
-provide drugs that will knock out 95% of the thyroid
-exopthalmus
-type II hypersensitvity

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exopthalmus

TSH works on every tissue behind the eye, causing hypertrophy of the fat behind the eye

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type II hypersensitvity

block, killing, turning on antibody

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type III hypersensitivity

immune complex disease

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type III hypersensitivity

-Ag-Ab complexes are trapped in small vessels of the body
-binding of complement triggers an inflamamtory reaction damaging the vessel walls (vasculitis)

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ag-ab complex is trapped in small vessels where?

skin, joints, and kidneys

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vasculitis in small vessels

type III hypersenstivities

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Ag-Ab bind ocmplement

-complement makes chemotactic factors C3a + C5a that attract neutrophils
-degranulate in the vessel wall= those granules are there to destroy bacteria, not vessel walls; but they cause vasculitis= inflammation

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neutrophil chemotaxis during type III hypersensitivities

complement makes chemotactic factors C3a + C5a that attract neutrophils
-neutrophils degranulate in vessel wall, releasing lysosomal enzymes
-lysosomal enzymes cause vessel wall damage (vasculitis)

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inflammation=vasculitis

lymphocytes, chemicals, blocking vessels

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type III hypersensitivity (immune complex disease) review

-Ag-Ab complexes become trapped in small vessels, especially in joints, skin, + kidneys
-they bind complement which results in complement levels falling as the complement is consumed
-C3a + C5a attract neutrophils that migrate into the vessel wall where they die releasing lysosomal granules. These damage the vessel wall leading to vasculitis

60

in type III, complement levels become

-consumed and used up
-people with lupus (measure complement levels)

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examples of systemic immune complex disease

1 systemic lupus erythromatosus (SLE)
2 post streptococcal glomerulonephritis
3 serum sickness
4 drjug reactions (penicillin)

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systemic lupus erythromatosus (SLE)

-antigen is DNA + other nuclear components
-antibody is anti-DNA + other anti nuclear antibodies (ANA)
-complexes are trapped in small vessels, skin, kidney, and joints
-there is no antibody against DNA in our blood, but in lupus there are

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lupus

small vessels on face, when they are sunexposed, the butterfly rash is more dominant

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post streptococcal glomerulonephritis

circulating anti-streptococcal antibodies combine with streptococcal antigen complexes are trapped in the glomeruli

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serum sickness

-if a person is bitten by a snake, inject him with horse serum that made antibodies to snake
-person bitten by snake= take venom and insert it into a horse and make antibodies; then give that serum to person who is bitten

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person was bitten by snake and given horse serum; then he had serum sickness

a yr later he was bitten again and dialyzed
-then he was bitten again, they made serum in goats and he didn't ahve any antibodies to goats so he was fine
-if he got goat serum again though, he would get serum sickness

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drug reactions

penicillin + other drugs can cause type I, II, III + IV hypersensitivity reactions

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delayed hypersensitivity mechanisms are the same as those for

cell mediated immunity

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the diff between delayed hypersensitivity + cell-mediated immunity is that

delayed hypersensitvity is tissue damage

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reaction of delayed hypersenstivitiy is delayed for how long

24-48 hours

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CD8 cell can damage tissue with which MHC

MHC I

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CD28 of T cellscells attach to

B7 of APC

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cell mediated immunity

-T cell response goes up
-make clones of T cells
-they get rid of antigen and then you have memory cells

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examples of delayed hypersenstivity

-contact dermititis
- poison ivy
-cosmetics
-foreign chemicals
-latex - rubber
-metals

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contact dermatitis

put things on your skin that call CD4 cells and cytokines

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examples of metals that lead to delayed hypersensitivities

nickel, zinc reacting with skin proteins
-watch strap syndrome- metal watch straps- nickel rubbing on the skin sensitizes and there's a reaction
-earrings

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poison ivy

-leaves have tiny hairs
-when you rub against them, the hair breaks and releases an oil onto your skin
-that sensitizes CD4 + CD8 cells
= > blistering rash that is poison ivy rash

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what causes poison ivy damage?

CD4 +CD8 cells = wet blistering

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cosmeticsdelayed hypersensitvity

people who have been using a particular eye makeup for 20 yrs and then they have swollen eyes= rubbing the stuff on the skin has attched it to proteins under the skin which turns on CD4 and CD8 cells and reject the skin on the eyes

80

foreign chemicals delayed hypersensitivities

-any foreign chemicals can develop hypersensitivity
- cement workers or people who make varnish typically get hypersensitivity to these chemicals

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deodorant hypersensitvities

buy one with a different chemical

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rubber glove reaction is similar to

poison ivy reaction

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gold earrings are hardened with

nickel

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patch tests

-each with a diff chemical
-used for industrious people who have industrious reactions at work
-read after 48 hours
-2 to 5 days to do this (Delayed reactions)
-acute reactions (5-10 minues

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positive reaction of patch test is after

48 hours

86

acute reactions (immediate reactions) test results are seen in

5-10 mins

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other forms of delayed hypersensitvity

tuberculin skin test

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tuberculin skin test

inject PPD (Purified Protein deritavtive of M. tuberculosis) into th eskin
-read after 48 hours

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PPD

purified protein derivative

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what are we looking for during a positive tuberculin skin test?

wheal; bump
- this person has T cells that have been sensitized to tb either from a prior infection, an infection now, or form past vaccines

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how many days does it take to read a tb skin test

2-5 days

92

tb skin test

-trying to detect sensitized T cells and we all want to be neg
-why would the med student be treated if he didn't show signs? = we want the skin test to be negative

93

problem with tuberculin testing

BCS vaccine in other countries
-they have memory T cells that can produce a positive tb skin test

94

individuals born in other countries may have received

BCG, a vaccine a gainst tb

95

BCG

-vaccine against TB but does not work very well
-people who have received bCG are skin test positivie, but we dont' use this so we would be neg

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those who are pos from BCG vaccine become neg after how many years

20 years

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other forms of delayed hypersensitivty

-tb skin test
-chronic infections

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chronic infections- delayed hypersensitivity

- T cells play a major role in causing tissue damage

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examples of chronic infections with delayed hypersensitivity

-viral hepatitis
-chronic bacterial diseases e.g. tuberculosis, syphilis, leprosy
- chronic fungal infections like candidiasis
-parasitic diseases like Leishmaniasis

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delayed hypersensitivity may cause a number of important autoimmune diseases

-insulin dependent -diabetes mellitus (IDDM)
-rheumatoid arthritis
-multiple sclerosis
-crohn's disease
-psoriasis
-celiac disease

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treatment of autoimmune diseases relating to delayed hypersensitivity

suppress T cells

102

most important and serious autoimmune diseases that are caused by

T cells, NOT ANTIBODIES

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What causes type I diabetes

T cells

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What rejects islets of langerhans

T cells

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What rejects myelin in Multiple sclerosis

T cells

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What rejects keratinocyes in psoriasis?

T cells