immunology Flashcards
1
Q
type 1 hypersensitivity
A
IgE-mediated hypersensitivity
= immediate hypersensitivity
2
Q
IgE crosslinking on a mast cell leads to
A
mediator release during type 1 hypersensitivity
3
Q
IL-4 + IL13 released from TH2 cells cause B cells to release
A
IgE
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)
5
Q
hay fever
A
allergic rhinitis
6
Q
early phase mediators released by mast cells + basophils
A
histamine proteases leukotrienes prostaglandins platelet activating factor (PAF) chemotactic factors for neutrophils + eosiophils
7
Q
platelet activating factor
A
causes platelet activating factor
8
Q
eosinophils
A
parasites cause eosinophils to pour out of the blood
9
Q
massive activation of PAF causes all vessels to
A
dilate
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
11
Q
FEV1 measures
A
chest expansion
12
Q
late phase of acute allergic reaction can be controlled by
A
corticosteroids that inhibit cytokine production
13
Q
how many hours after acute phase will be late phase
A
5-6 hours
14
Q
late phase (5-6 hours later)
A
- he will feel tight chested
- takes longer to settle down
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
16
Q
examples of IgE mediated allergic reactions
A
- hay fever (allergic rhinitis)
- depends on the season
- rag weed season produces lots of pollen
17
Q
allergic salute
A
nose is itchy + rubbing it gives relief
18
Q
allergic rhinitis (hay fever)
A
- IgE mediated
- tree pollenss
- grass pollens
- ragweed pollen
- cat hair
- dog hair
- house dust mites
- moulds
19
Q
house dust mites eat skin scales and defecate. What do allergic people inhale
A
dry feces of dust mites
20
Q
cockroaches
A
-important cause of allergic reaction
21
Q
what groups have higher rates of allergic reactions
A
lower socioeconomic group
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)
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
24
Q
rubber allergies
A
pulling off the rubber glove releases aerosol of rubber
25
food allergies
shrimp, peanuts, pollen, let babies eat peanuts early and then later they have a decrease incidence of peanut allergies
26
insect stings that can cause allergies
```
wasps
hornets
honey bees
yellow jackets
fire ants
```
27
acute urticaria (hives)
- itchy, inflamed reaction
| - corticosteroids will stop it
28
angioedema
swollen lips
29
wheals
circles from allergic reactions
30
diagnosis of acute allergic reactions
- skin prick tests (intradermal skin tests)
| - measure specific IgE antibodies to cat hair, pollens, house dust mites
31
skin prick tests (intradermal skin tests)
positive wheal and flare seen in 5-10 mins
32
treatment for type 1 allergic reactions
- epinephrine (adrenaline)- treat acutes anayphylactic rxns
- remove antigen
- tx symptomatically w/ antihistamines, antileukotrienes, corticosteroids
- omalizumab
- hyposensitization therapy shots
33
what does epinephrine do
constricts
34
omalizumab
a monoclonal antibody that inhibits IgE binding to mast cells
-blocks binding site so it can't attach to mast cells
35
hyposensitization therapy shots
weekly, increasing doses of antigen
36
hyposensitization (Desensitization) examples
bee venom, cat hair antigen, grass pollen antigen
37
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
38
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
39
examples of type II hypersenstivities
- autoimmune hemolytic anemia
- autoimmune thrombocytopenia
- goodpasture's syndrome
- anti-receptor antibody diseases
40
autoimmune thrombocytopenia
platelets drop 300,000 to 20,000
- antibody against paltelets
- young women notice they have bruising
41
goodpasture's syndrome
antibody against the basement membranes of alveoli in the lung
42
anti-receptor antibody diseases
- myasthenia gravis
| - grave's disease
43
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
44
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
45
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
46
pituitary makes TSH which goes to the TSH receptors and typically stimulates
hormone synthesis
47
in grave disease, and autoantibody instead of the TSH binds to the
TSH receptor
48
graves disease
eyes swell up + huge thyroid swelling
49
treat Graves
- poison thyroid
- provide drugs that will knock out 95% of the thyroid
- exopthalmus
- type II hypersensitvity
50
exopthalmus
TSH works on every tissue behind the eye, causing hypertrophy of the fat behind the eye
51
type II hypersensitvity
block, killing, turning on antibody
52
type III hypersensitivity
immune complex disease
53
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)
54
ag-ab complex is trapped in small vessels where?
skin, joints, and kidneys
55
vasculitis in small vessels
type III hypersenstivities
56
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
57
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)
58
inflammation=vasculitis
lymphocytes, chemicals, blocking vessels
59
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)
61
examples of systemic immune complex disease
1 systemic lupus erythromatosus (SLE)
2 post streptococcal glomerulonephritis
3 serum sickness
4 drjug reactions (penicillin)
62
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
63
lupus
small vessels on face, when they are sunexposed, the butterfly rash is more dominant
64
post streptococcal glomerulonephritis
circulating anti-streptococcal antibodies combine with streptococcal antigen complexes are trapped in the glomeruli
65
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
66
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
67
drug reactions
penicillin + other drugs can cause type I, II, III + IV hypersensitivity reactions
68
delayed hypersensitivity mechanisms are the same as those for
cell mediated immunity
69
the diff between delayed hypersensitivity + cell-mediated immunity is that
delayed hypersensitvity is tissue damage
70
reaction of delayed hypersenstivitiy is delayed for how long
24-48 hours
71
CD8 cell can damage tissue with which MHC
MHC I
72
CD28 of T cellscells attach to
B7 of APC
73
cell mediated immunity
- T cell response goes up
- make clones of T cells
- they get rid of antigen and then you have memory cells
74
examples of delayed hypersenstivity
- contact dermititis
- poison ivy
- cosmetics
- foreign chemicals
- latex - rubber
- metals
75
contact dermatitis
put things on your skin that call CD4 cells and cytokines
76
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
77
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
78
what causes poison ivy damage?
CD4 +CD8 cells = wet blistering
79
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
81
deodorant hypersensitvities
buy one with a different chemical
82
rubber glove reaction is similar to
poison ivy reaction
83
gold earrings are hardened with
nickel
84
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
85
positive reaction of patch test is after
48 hours
86
acute reactions (immediate reactions) test results are seen in
5-10 mins
87
other forms of delayed hypersensitvity
tuberculin skin test
88
tuberculin skin test
```
inject PPD (Purified Protein deritavtive of M. tuberculosis) into th eskin
-read after 48 hours
```
89
PPD
purified protein derivative
90
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
91
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
96
those who are pos from BCG vaccine become neg after how many years
20 years
97
other forms of delayed hypersensitivty
- tb skin test
| - chronic infections
98
chronic infections- delayed hypersensitivity
- T cells play a major role in causing tissue damage
99
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
100
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
101
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
103
What causes type I diabetes
T cells
104
What rejects islets of langerhans
T cells
105
What rejects myelin in Multiple sclerosis
T cells
106
What rejects keratinocyes in psoriasis?
T cells
