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*med3* > Immunology - Clinical Immunology > Flashcards

Immunology - Clinical Immunology Flashcards

1
Q

what is hypersensitivity?

A

an exaggerated or inappropriate immune response that causes disease

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2
Q

what type of hypersensitivity are allergic reactions?

A

type I

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3
Q

describe the general mechanism that all hypersensitivity reactions follow

A

first contact with antigen “sensitizes” the pt to that Ag generating an immune response second contact with antigen causes hypersensitivity

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4
Q

What is a type I hypersensitivity and how does it cause a reaction?

A

aka “allergies”

immediate reaction to an antigen - minutes

pre-formed IgE Ab’s from 1º exposure bound to mast cells

Ag binds and cross links IgE Mast cell degranulates and release its contents (histamine)

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5
Q

in type I hypersensitivity individuals make _____Ab’s to Ag’s, whereas most people will make _____ Ab’s

A

IgE

IgG

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6
Q

How do you get IgE antibodies?

A

B cell class switching

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7
Q

What cell type triggers B cell class switching?

A

Th2 - humoral response

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8
Q

What is the key cytokine for IgE production?

A

IL-4

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9
Q

what does IL-4 do?

A

triggers B cell class switching to produce IgE

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10
Q

Why is complement not involved in a type I hypersensitivity rxn?

A

because IgE does not activate complement

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11
Q

Sx of Type I hypersensitivity of… skin resp. tract eye GI tract

A

Skin: Urticaria (hives)

Resp: Rhinitis, wheezing (asthma)

Eyes: conjunctivitis

GI: diarrhea

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12
Q

what is anaphylaxis?

A

systemic type I hypersensitivity reaction

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13
Q

what Sx does anaphylaxis cause?

A

itching, diffuse hives/erythema

resp. distress from bronchoconstriction

hoarseness - laryngeal swelling/edema

vomiting, cramps, diarrhea

can lead to shock and death

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14
Q

What is the treatment for anaphylaxis?

A

epinephrine

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15
Q

How does epinephrine treat anaphylaxis?

A

vasoconstrict to raise the BP

dilate bronchioles

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16
Q

What is Atopy? (Ah-toe-pee)

A

genetic predisposition to localized hypersensitivity

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17
Q

give examples of a type I hypersensitivity rx

A

asthma

penicillin drug allergy

seasonal allergies (allergic rhinitis)

allergic conjunctivitis

peanut allergy (children)

shellfish (food allergy)

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18
Q

what are the 2 “waves” of hypersensitivity seen in type I?

A

early Sx - within minutes

late Sx - 6 hrs later

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19
Q

what are the early Sx of type I HS?

A

edema

redness

swelling

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20
Q

Why do you get the Sx’s seen in early type I HS?

A

degranulation of mast cell causes release of pre-formed mediators (histamine) synthesis/release of leukotrienes and prostaglandins

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21
Q

What are the late Sx of type I HS?

A

induration

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22
Q

what causes the Sx seen in late type I HS?

A

synthesis/release of cytokines

influx of inflammatory cells (neutrophils, eosinophils)

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23
Q

what are the mediators of type I HS?

A

histamine

leukotrienes

PG’s

thromboxane

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24
Q

what effect does histamine have in a type I HS rxn?

A

vasodilation (warmth)

increased permeability of venules (swelling)

smooth muscle contraction (bronchospasm)

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25
Q

What type I mediators are derived from arachidonic acid?

A

leukotrienes

prostaglandins

thromboxanes

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26
Q

Of what class of signaling molecules are leukotrienes, prostaglandins, and thromboxanes?

A

Eicosanoids

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27
Q

what are eicosanoids derived from?

A

lipids in the cell membrane of cells by the enzyme phospholipase A2

PLA2 pulls lipids from the membrane to form arachadonic acid

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28
Q

what enzyme is used to convert arachadonic acid to leukotrienes?

A

lipoxygenase

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29
Q

what enzyme is used to convert arachadonic acid to prostaglandins and thromboxanes?

A

cycloxygenase

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30
Q

what does lipoxygenase synthesize?

A

leukotrienes

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31
Q

what does cycloxygenase synthesize?

A

prostaglandins

thromboxanes

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32
Q

what are the major eicosanoids seen in type I HS?

A

PGE2

PGD2

LTC4/LTD4

LTB4

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33
Q

what does PGE2 do?

A

vasodilation = redness increased vascular permeability = edema raise temp set point in hypothalamus = fever sensitizes nerves = pain

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34
Q

what does PGD2 do?

A

bronchoconstriction

eosinophil

infiltration

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35
Q

what does LTC4/LTD4 do?

A

vasoconstriction

bronchoconstriction

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36
Q

what does LTB4 do?

A

neutrophil/eosinophil chemotaxis

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37
Q

what are other type I mediators?

A

ECF-A

serotonin

platelet activating factor

neutral proteases (chemise, tryptase)

heparin (anticoagulant)

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38
Q

What is ECF-A and how is it involved in type I HS?

A

eosinophil chemotactic factor of anaphylaxis

preformed in mast cells attracts eosinophils (various roles)

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39
Q

how is serotonin involved in type I HS?

A

preformed in mast cells causes vasodilation

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40
Q

how is platelet activating factor involved in type I HS?

A

bronchoconstriction

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41
Q

why would you test someone for IgE Abs to an allergen?

A

to see if someone is sensitized to a particular substance

42
Q

how do you test for IgE?

A

administer small amt of allergen by pinprick/puncture of skin or intradermal injection

43
Q

when you test for IgE what will you see if the person is sensitized to the substance?

A

wheal formation - raised, indurated, red area of skin where the allergen was injected

44
Q

How would you desensitize someone from an allergen?

A

gradual administration of increasing amounts of allergen causes the response to change from IgE to IgG

IgG Abs can block mediator release from mast cells

45
Q

why would you desensitize someone from an allergen?

A

if the response is dangerous/life threatening

if someone is allergic to a medication that they cannot live without – i.e. if a person is allergic to aspirin but they need to take it for a cardiac condition

46
Q

what is the modified Th2 response?

A

desensitization causes the change of IgE to IgG that can “block” mediator release from mast cells

47
Q

what are type II HS rxns?

A

autoimmune disorders where Abs (IgG/IgM) attack normal cells/tissue

IgG/IgM binds to normal structures

48
Q

what are the 3 mechanisms of tissue/cell damage in type II HS?

A

phagocytosis

complement-mediated lysis

ADCC (Ab dependent cytotoxicity)

49
Q

how does type II HS cause damage by phagocytosis?

A

macrophage or other phagocyte recognized the FcR on IgG or C3b from the complement pathway

50
Q

how does type II HS cause damage by complement?

A

IgM or IgG –> classical complement cascade formation of MAC –> cell death

51
Q

how does type II HS cause damage by ADCC?

A

NK cells bind Fc portion of IgG

52
Q

what are 6 main examples of a type II HS?

A

rheumatic fever

exposure to wrong blood type

autoimmune hemolytic anemia

pemphigus vulgaris

good pasture syndrome

myasthenia gravis

53
Q

what happens in rheumatic fever?

A

Abs to strep pyogenes cross-react with cardiac myocytes leading to myocardial damage and damage to the heart valves

54
Q

what happens if exposed to the wrong blood type?

A

RBC lysis by circulating IgG

erythroblastosis fetalis - when Rh- moms have Rh+ babies

55
Q

what happens in autoimmune hemolytic anemia?

A

Abs bind to and destroy RBCs

56
Q

What 2 drugs can cause autoimmune hemolytic anemia? how?

A

methyldopa and penicillin drugs bind to surface of RBCs and then Abs can bind to these targets and destroy the RBCs

57
Q

What bacteria can classically cause autoimmune hemolytic anemia? how?

A

mycoplasma pneumonia induces Abs against RBCs

58
Q

What happens in pemphigus vulgaris?

A

antibodies against desmosomes in epidermis

59
Q

What happens in Goodpasture syndrome?

A

pts develop Nephritic Syndrome and pulmonary hemorrhage caused by antibodies against type IV collagen

60
Q

what happens in myasthenia gravis?

A

antibodies against Ach R’s

61
Q

what is the common theme in type II HS?

A

antibodies directed against tissues or cells of our own bodies

62
Q

What is the general mechanism of type III HS?

A

Ag-Ab(IgG) complexes form and activate complement causing tissue and cell damage

63
Q

What is the difference between type II and type III HS?

A

in type II the Ab is directly attacking tissues/cells in type III Ab’s bind to small Ag and then they deposit in the tissues as a complex causing disease

64
Q

what are the 2 subtypes of type III HS?

A

generalized- serum sickness

localized- Arthus rxn

65
Q

What happens in serum sickness?

A

immune complexes in plasma causes systemic disease - usually IgG or IgM which can activate complement complexes deposit in various tissues causing an immune response w/ complement activation in addition to activating macrophages and neutrophils via their FcR’s

66
Q

what is the history behind serum sickness?

A

doctors used to take horse plasma/serum from horses that have been exposed to diphtheria and Scarlett fever and use it for passive immunization

67
Q

what was seen in the pts who were given horse serum?

A

5-10 days later “classic triad” appears

fever rash arthralgias

68
Q

explain the “classic triad” of Sx’s seen in serum sickness and other type III HS

A

pts mounted and immune response agains horse serum Ag and immune complexes of horse Ag-Ab were depositing in the skin and joints to cause the classic triad of fever, rash, & arthralgias

69
Q

What Sx can be seen in someone with a generalized type III serum sickness rxn?

A

urticaria or palpable purpura

low serum complement levels

elevated ESR

diffuse LAD

acute glomerulonephritis

70
Q

what would cause classic serum sickness?

A

administration of rabies or tetanus anti-toxin

penicillin monoclonal antibodies

71
Q

how does administration to rabies or tetanus anti-toxin cause serum sickness?

A

anti toxins are pooled plasma from humans and sometimes horses designed to passively immunize people against rabies or tetanus and sometimes a serum sickness like illness can develop

72
Q

how does penicillin cause serum sickness?

A

drug can act as a hapten

73
Q

what is a hapten?

A

a small molecule that illicits an immune response and Ab’s can be formed and bind to penicillin, deposit in the tissue and cause serum sickness

74
Q

what monoclonal antibody therapies are known to cause serum sickness?

A

rituximab - Ab against B cells

infliximab - TNF-alpha Ab

75
Q

what are other type III diseases?

A

post-streptococcal glomerulonephritis

SLE (anti-DNA Ab’s)

polyarteritis nodosa

76
Q

what happens in polyarteritis nodosa?

A

when it’s associated w/ Hep B can have an immune complex mediated mechanism where complexes bind to Hep B Ag and deposit in the tissues to cause the Sx of this vasculitis

77
Q

what happens in post-streptococcal glomerulonephritis?

A

Ab’s bound to strep Ag that can deposit in the glomeruli

78
Q

An immune complex mediated disorder w/ Ab’s against DNA that deposit in tissue and cause disease

A

SLE

79
Q

what is a localized type III HS called?

A

arthus reaction

80
Q

What is the difference between serum sickness and arthus reaction?

A

serum sickness - immune complexes circulate in plasma and deposit in tissues

arthus reaction - immune complexes form in the tissue where they cause disease

81
Q

is serum sickness localized or systemic?

A

systemic

82
Q

describe the arthus reaction

A

inject Ag –> preformed Ab’s in plasma/tissue will bind Ag —> localized immune complexes –> complement activation, edema, necrosis

83
Q

how long does it take to see Sx of the arthus rxn?

A

4-10 hrs

84
Q

how can you identify arthus rxns?

A

immunofluorescent staining - you will see antibodies and complement in the vessel wall to know they are being deposited in the tissue causing the rxn

85
Q

what are some clinical example of the arthus reaction?

A

skin injections (boosters/insulin)

hypersensitivity

pneumonitis

86
Q

how does an arthus reaction happen with skin injections?

A

administering a tetanus/diphtheria/hep B booster, is putting Ag’s under the skin of someone who has been previously exposed and they may have circulating Ab’s that can deposit and bind to the Ag at the site of injection causing swelling and redness a few hours after the injection

87
Q

What is “Farmer’s lung”?

A

hypersensitivity pneumonitis is a hypersensitivity rxn to environmental Ag - some pts have circulating Ab’s and when certain Ag’s are inhaled the Ab’s bind forming immune complexes in the lung

88
Q

what is type IV HS?

A

delayed-type HS, cell-mediated rxn

89
Q

How is type IV HS different from the rest?

A

no antibodies, entirely cell-mediated

90
Q

what initiates the immune response seen in type IV HS?

A

memory T cells

91
Q

what is the classic type IV HS rxn?

A

PPD test

92
Q

How does the PPD test work?

A

–> tuberculin protein injected into skin

–> previously exposed person has memory T cells that recognize the tuberculin Ag which will be presented by APC’s and placed in the context of MHC II where memory CD4 T cells can recognize it and respond

–> there will be a Th1 response which is cell-mediated

–> IFN-gamma is secreted activating macrophages that secrete IL-12 to stimulate Th1

93
Q

what would you see on a positive PPD test?

A

redness and induration 24-72 hrs later

94
Q

What are examples of type IV HS?

A

immune response to many pathogens (mycobacteria, fungi)

contact dermatitis

MS

95
Q

what type of HS is triggered by mycobacteria and fungi?

A

type IV

96
Q

how do you get contact dermatitis?

A

chemicals (oils) attach to skin cells and CD8 T cells recognize the oils and attack skin cells causing erythema and itching

97
Q

how long after exposure will you see Sx of contact dermatitis?

A

12-48 hrs

98
Q

what type of HS is poison ivy?

A

a type of contact dermatitis - type IV HS

99
Q

a type IV HS rxn to myelin basic protein is one of the mechanisms causing _____ ______ by demyelination

A

multiple sclerosis

100
Q
A

*med3* (21 decks)

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