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Medicine II > immunology > Flashcards

immunology Flashcards

1
Q

type 1 hypersensitivity

A

IgE-mediated hypersensitivity

= immediate hypersensitivity

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2
Q

IgE crosslinking on a mast cell leads to

A

mediator release during type 1 hypersensitivity

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3
Q

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

A

IgE

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4
Q

allergies

A

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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5
Q

hay fever

A

allergic rhinitis

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6
Q

early phase mediators released by mast cells + basophils

A 
histamine
proteases
leukotrienes
prostaglandins
platelet activating factor (PAF)
chemotactic factors for neutrophils + eosiophils
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7
Q

platelet activating factor

A

causes platelet activating factor

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8
Q

eosinophils

A

parasites cause eosinophils to pour out of the blood

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9
Q

massive activation of PAF causes all vessels to

A

dilate

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10
Q

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

A
  • 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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11
Q

FEV1 measures

A

chest expansion

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12
Q

late phase of acute allergic reaction can be controlled by

A

corticosteroids that inhibit cytokine production

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13
Q

how many hours after acute phase will be late phase

A

5-6 hours

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14
Q

late phase (5-6 hours later)

A
  • he will feel tight chested

- takes longer to settle down

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15
Q

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

A

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

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16
Q

examples of IgE mediated allergic reactions

A
  • hay fever (allergic rhinitis)
  • depends on the season
  • rag weed season produces lots of pollen
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17
Q

allergic salute

A

nose is itchy + rubbing it gives relief

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18
Q

allergic rhinitis (hay fever)

A
  • IgE mediated
  • tree pollenss
  • grass pollens
  • ragweed pollen
  • cat hair
  • dog hair
  • house dust mites
  • moulds
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19
Q

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

A

dry feces of dust mites

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20
Q

cockroaches

A

-important cause of allergic reaction

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21
Q

what groups have higher rates of allergic reactions

A

lower socioeconomic group

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22
Q

examples of IgE mediated allergic reactions

A
  • allergic rhinitis (hay fever)
  • bronchial asthma
  • acute drug reactions
  • rubber gloves
  • food allergies
  • insect stings
  • acute urticaria (hives)
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23
Q

bronchial asthma

A
  • 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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24
Q

rubber allergies

A

pulling off the rubber glove releases aerosol of rubber

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25
Q

food allergies

A

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

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26
Q

insect stings that can cause allergies

A 
wasps
hornets
honey bees
yellow jackets
fire ants
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27
Q

acute urticaria (hives)

A
  • itchy, inflamed reaction

- corticosteroids will stop it

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28
Q

angioedema

A

swollen lips

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29
Q

wheals

A

circles from allergic reactions

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30
Q

diagnosis of acute allergic reactions

A
  • skin prick tests (intradermal skin tests)

- measure specific IgE antibodies to cat hair, pollens, house dust mites

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31
Q

skin prick tests (intradermal skin tests)

A

positive wheal and flare seen in 5-10 mins

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32
Q

treatment for type 1 allergic reactions

A
  • epinephrine (adrenaline)- treat acutes anayphylactic rxns
  • remove antigen
  • tx symptomatically w/ antihistamines, antileukotrienes, corticosteroids
  • omalizumab
  • hyposensitization therapy shots
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33
Q

what does epinephrine do

A

constricts

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34
Q

omalizumab

A

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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35
Q

hyposensitization therapy shots

A

weekly, increasing doses of antigen

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36
Q

hyposensitization (Desensitization) examples

A

bee venom, cat hair antigen, grass pollen antigen

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37
Q

hyposensitization (Desensitization)

A
  • 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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38
Q

type II hypersensitivities (cytotoxic reactions)

A

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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39
Q

examples of type II hypersenstivities

A
  • autoimmune hemolytic anemia
  • autoimmune thrombocytopenia
  • goodpasture’s syndrome
  • anti-receptor antibody diseases
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40
Q

autoimmune thrombocytopenia

A

platelets drop 300,000 to 20,000

  • antibody against paltelets
  • young women notice they have bruising
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41
Q

goodpasture’s syndrome

A

antibody against the basement membranes of alveoli in the lung

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42
Q

anti-receptor antibody diseases

A
  • myasthenia gravis

- grave’s disease

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43
Q

myasthenia gravis

A
  • due to abnormal antibodies to acetylcholine receptor on muscle cells
  • blocks receptor and causes muscular weakness
  • muscles don’t work and people become weak
44
Q

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

A
  • 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
45
Q

grave’s disease

A

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

46
Q

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

A

hormone synthesis

47
Q

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

A

TSH receptor

48
Q

graves disease

A

eyes swell up + huge thyroid swelling

49
Q

treat Graves

A
  • poison thyroid
  • provide drugs that will knock out 95% of the thyroid
  • exopthalmus
  • type II hypersensitvity
50
Q

exopthalmus

A

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

51
Q

type II hypersensitvity

A

block, killing, turning on antibody

52
Q

type III hypersensitivity

A

immune complex disease

53
Q

type III hypersensitivity

A
  • Ag-Ab complexes are trapped in small vessels of the body

- binding of complement triggers an inflamamtory reaction damaging the vessel walls (vasculitis)

54
Q

ag-ab complex is trapped in small vessels where?

A

skin, joints, and kidneys

55
Q

vasculitis in small vessels

A

type III hypersenstivities

56
Q

Ag-Ab bind ocmplement

A
  • 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
57
Q

neutrophil chemotaxis during type III hypersensitivities

A

complement makes chemotactic factors C3a + C5a that attract neutrophils

  • neutrophils degranulate in vessel wall, releasing lysosomal enzymes
  • lysosomal enzymes cause vessel wall damage (vasculitis)
58
Q

inflammation=vasculitis

A

lymphocytes, chemicals, blocking vessels

59
Q

type III hypersensitivity (immune complex disease) review

A
  • 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
Q

in type III, complement levels become

A
  • consumed and used up

- people with lupus (measure complement levels)

61
Q

examples of systemic immune complex disease

A

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

62
Q

systemic lupus erythromatosus (SLE)

A
  • 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
63
Q

lupus

A

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

64
Q

post streptococcal glomerulonephritis

A

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

65
Q

serum sickness

A
  • 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
66
Q

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

A

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
67
Q

drug reactions

A

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

68
Q

delayed hypersensitivity mechanisms are the same as those for

A

cell mediated immunity

69
Q

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

A

delayed hypersensitvity is tissue damage

70
Q

reaction of delayed hypersenstivitiy is delayed for how long

A

24-48 hours

71
Q

CD8 cell can damage tissue with which MHC

A

MHC I

72
Q

CD28 of T cellscells attach to

A

B7 of APC

73
Q

cell mediated immunity

A
  • T cell response goes up
  • make clones of T cells
  • they get rid of antigen and then you have memory cells
74
Q

examples of delayed hypersenstivity

A
  • contact dermititis
  • poison ivy
  • cosmetics
  • foreign chemicals
  • latex - rubber
  • metals
75
Q

contact dermatitis

A

put things on your skin that call CD4 cells and cytokines

76
Q

examples of metals that lead to delayed hypersensitivities

A

nickel, zinc reacting with skin proteins

  • watch strap syndrome- metal watch straps- nickel rubbing on the skin sensitizes and there’s a reaction
  • earrings
77
Q

poison ivy

A

-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

78
Q

what causes poison ivy damage?

A

CD4 +CD8 cells = wet blistering

79
Q

cosmeticsdelayed hypersensitvity

A

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
Q

foreign chemicals delayed hypersensitivities

A
  • any foreign chemicals can develop hypersensitivity

- cement workers or people who make varnish typically get hypersensitivity to these chemicals

81
Q

deodorant hypersensitvities

A

buy one with a different chemical

82
Q

rubber glove reaction is similar to

A

poison ivy reaction

83
Q

gold earrings are hardened with

A

nickel

84
Q

patch tests

A
  • 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
85
Q

positive reaction of patch test is after

A

48 hours

86
Q

acute reactions (immediate reactions) test results are seen in

A

5-10 mins

87
Q

other forms of delayed hypersensitvity

A

tuberculin skin test

88
Q

tuberculin skin test

A 
inject PPD (Purified Protein deritavtive of M. tuberculosis) into th eskin
-read after 48 hours
89
Q

PPD

A

purified protein derivative

90
Q

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

A

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

91
Q

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

A

2-5 days

92
Q

tb skin test

A
  • 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
Q

problem with tuberculin testing

A

BCS vaccine in other countries

-they have memory T cells that can produce a positive tb skin test

94
Q

individuals born in other countries may have received

A

BCG, a vaccine a gainst tb

95
Q

BCG

A
  • 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

96
Q

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

A

20 years

97
Q

other forms of delayed hypersensitivty

A
  • tb skin test

- chronic infections

98
Q

chronic infections- delayed hypersensitivity

A
  • T cells play a major role in causing tissue damage
99
Q

examples of chronic infections with delayed hypersensitivity

A
  • viral hepatitis
  • chronic bacterial diseases e.g. tuberculosis, syphilis, leprosy
  • chronic fungal infections like candidiasis
  • parasitic diseases like Leishmaniasis
100
Q

delayed hypersensitivity may cause a number of important autoimmune diseases

A
  • insulin dependent -diabetes mellitus (IDDM)
  • rheumatoid arthritis
  • multiple sclerosis
  • crohn’s disease
  • psoriasis
  • celiac disease
101
Q

treatment of autoimmune diseases relating to delayed hypersensitivity

A

suppress T cells

102
Q

most important and serious autoimmune diseases that are caused by

A

T cells, NOT ANTIBODIES

103
Q

What causes type I diabetes

A

T cells

104
Q

What rejects islets of langerhans

A

T cells

105
Q

What rejects myelin in Multiple sclerosis

A

T cells

106
Q

What rejects keratinocyes in psoriasis?

A

T cells

Medicine II (8 decks)

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