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Bloc F - Defense > Mar27 M1-Hypersensitivity disease > Flashcards

Mar27 M1-Hypersensitivity disease Flashcards

1
Q

Coombs and Gell classification of hypersensitivity

A

type 1 = immediate (IgE): allergies, asthma, dermatitis
type 2 = ADCC (Ab dependent cell mediated cytotoxicity) (IgM, IgG)
type 3 = immune complex mediated (IgM, IgG)
type 4 = delayed type (T cell mediated)

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2
Q

can you have allergic response upon first exposure to an allergen

A

no. never happens. not possible. always circulating IgE first that binds mast cells, ready for 2nd response

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3
Q

IgE is on surface of what cells

A

tissue mast cells and circulating IgE

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4
Q

substances released by mast cells when activated (pro inflam substances)

A

immediate = histamine, TNF-a, proteases, heparin (in the granules)
in minutes = PGs, LTs
over hours = IL4, IL13
lead to local AND systemic effects

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5
Q

different routes for type 1 rx to occur

A
  • skin contact
  • injection
  • ingestion
  • inhalation
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6
Q

in ADCC (type 2), what are the IgG or IgM made against

A
  1. intrinsic Ag (normal self Ag) = failure of immune tolerance OR cross reactivity of self ag with foreign one and we recognize both
  2. extrinsinc Ag (penicillin at surface of RBCs)
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7
Q

ADCC what happens after Ab binds self cell surface

A
  • opsonization
  • complement (classical MAC)
  • NK cell activation
  • activation or blockage of important Rs
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8
Q

effect of ADCC when penicillin rx

A
  • complement or opsonization (MAC)

- get hemolytic anemia

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9
Q

ADCC: how NK cells kill self cells

A
  • recognize Fc portion of the IgG Ab

- release perforin (makes pore) and granzyme (enters cell, causes apoptosis)

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10
Q

examples of ADCC mediated pathologies

A
  • autoimmune diseases like ITP, myasthenia gravis, Grave’s (thyroid), Goodpasture’s
  • AB and Rh blood group incompatibilities (transfusion reactions)
  • some drug rxs
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11
Q

type III HS rx: immune complex mediated: what happens

A
  • Ag excess compared to amount of Ab
  • Ag-Ab complexes form and large amounts in circulation
  • deposit in end capillaries of certain organs (skin, joints, kidneys, etc.)
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12
Q

effect of deposited immune complexes in type III HS rx

A
  • encourage neutrophil influx = lead to immune response
  • MACs (complement) happen
  • aggregation of platelets
  • inflammation and vasculitis results
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13
Q

immune complex mediated (type III HS) pathologies: give 3

A
  • serum sickness
  • immune complex GN
  • extrinsic allergic alveolitis (Farmer’s lung)
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14
Q

serum sickness def

A
  • happens upon 2nd injection of horse serum in the pre-Abx era
  • prod of Abs against horse Ags recognized as foreign
  • complexes form bc Ags&raquo_space; Abs
  • get chills, fever, rash, arthritis, GN sometimes
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15
Q

kid given Ceclor (Abx) for otitis media and comes 7 days later with rash and refuses to walk: what type of HS is that

A
  • type III immune complex mediated.
  • Abx known to produce serum sickness like rxs
  • stop the Abx
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16
Q

good example of type IV HS rx (delayed)

A
  • PPD test (for M, TB). helps determine previous exposure

- intradermal injection

17
Q

pathophysiology in type IV delayed T cell HS rx

A
  • APCs see Ag, present through MHC 2 to CD4+
  • pro inflam cytokines (chemokines IFN-g, TNF-a, TNF-b, IL-3) released and recruit macrophages, plasma cells etc.
  • swelling, redness after hours
18
Q

type IV HS pathologies

A

-contact dermatitis (with poison ivy for ex)

19
Q

how IgE produced by plasma cells (1st exposure is TH2 mediated) binds mast cells

A

through FceRI receptor expressed on tissue mast cells and circulating baso and eosi

20
Q

name of a protease released by mast cell + clinical use

A
  • tryptase

- if above 11.5 ng per mL = anaphylaxis or allergic or sensitivty rx

21
Q

atopy charact

A
  • tendency in certain individuals to mount an increased IgE response to Ags
  • genetics involved a lot
22
Q

2 things explaining increased prevalence of allergic diseases in developed countries

A
  • genetic susceptibility
  • hygienic environment
  • hygiene hypothesis*
23
Q

cytokines of Th1 cells

A

IFN gamma and IL-2

-for pathogens, infectiosn, defense

24
Q

cytokines of th2 cells

A

IL-4,5,13. for allergic diseases

stim production of IgE and recruit eosinophils

25
Q

why hygiene hypothesis turned out to be wrong

A
  • drop in infections lately

- increased asthma and autoimmune diseases (latter is th1 mediated)

26
Q

real reason why see more allergic diseases and autoimmune diseases in developed countries (modified hygiene hypothesis)

A
  • when get more infections, T reg cells downregulate Th1 and Th2
  • developed countries = not a lot of infections = th1 and th2 mediated diseases NOT downregulated
27
Q

importance of beginning of life in tolerance

A
  • have a critical window in beginning of life with a better tolerogenic response to Ags by T reg cells
  • T reg cells downregulate th1 and th2 much better between 3 and 12 months of age
28
Q

other possibilities for higher allergic diseases number in developed countries

A
  • climate (pollution and vit D deficiency bc not much sun)
  • obesity
  • western diet
  • housing
  • all these may drive th2 response in predisposed individual*
29
Q

(important) what not to do in the ER when see an allergic reaction (anaphylaxis**)

A

DO NOT GIVE ANTIHISTAMINES (all they do is oppose histamine alone)

30
Q

effects of epinephrine given in anaphylaxis

A
  1. alpha 1 R agonist: higher PVR (higher BP), vasoconstriction, reduces angioedema, better coronary perfusion
  2. beta 1 R agonist. increased inotropic and chronotropic effect
  3. beta 2 R agonist. bronchodilation, decreased release of inflam mediators from mast cells and basophils (they express beta2 adr. R too)
31
Q

(important) treatment of anaphylaxis

A

EPINEPHRINE IM. (not subcu) (not antihistamines)

32
Q

fundamental role of mast cells in immunity (their real role)

A
  • parasite defense
  • express many pattern recognition receptors (PRRs)
  • their major growth factor is stem cell factor (SCF), acting on the mast cell R c-Kit
33
Q

(important) mastocytosis def and cause

A
  • excessive proliferation of mast cells and they infiltrate diff organs and cause damage to them
  • cause = hypermorphic (gain of fct) mutation of c kit (R for SCF)
34
Q

basophils fct

A
  • role as important as mast cells in allergy but basophils circulate
  • express IgE Rs.
  • important in anti-parasitic response
35
Q

eosinophils fct

A
  • fight infectious agents and damage tissues by releasing toxic granule proteins like major basic protein, eosinophil derived neurotoxin, eosinophil cationic protein
  • parasites defense
  • viral defense (RNAses in their granules)
  • can measure these in pt with eosinophil rx (like eosinophilic infiltration of GIT)
36
Q

how eosinophils fight bacteria

A
  • eject DNA of mitochondrial origin to make DNA webs traps

- capture bacteria and promote their killing

37
Q

summary of 5 functions of eosinophils

A
  1. allergic rx
  2. Ag presentation
  3. parasite removal
  4. RNA viral removal
  5. tissue remodeling

Bloc F - Defense (57 decks)

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