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DMD 5244 (Immunity) > Hypersensitivities (complete) > Flashcards

Hypersensitivities (complete) Flashcards

1
Q

What are hypersensitivities

A

when harmless antigens elicit an immune response. Ranging from uncomfortable to fatal

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2
Q

what are the 4 types of hypersensitivities

A

1, 2, 3, and 4,

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3
Q

what is another name for a hypersensitivity

A

allergy

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4
Q

what is anaphlaxis

A

allergic reactions that cause rapid, multiorgan inflammation, can result in death

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5
Q

What is type 1 hypersensitivity

A

Allergy and atopy

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6
Q

what is the immune mediator for type 1 hypersensitivity

A

IgE

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7
Q

what is the mechanism of a type 1 allergy

A

IgE crosslinking induced by the antigen causes the release of vasoactive mediators by basophils and mast cells

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8
Q

what are the manifestations of a type 1 hypersensitivity

A 
systemic and local anaphylaxis
hay fever
athsma
hives
food allergies
eczema
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9
Q

what is type 2 hypersensitivity

A

antibody-mediated hypersensitivity

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10
Q

what is the immune medaitor for type 2 hypersensitivities

A

IgG or IgM

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11
Q

what is the mechanism of type 2 hypersensitivities

A

Ab on cell surface mediates cell destruction via complement of ADCC

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12
Q

what are the typical manifestations of type 2 hypersensitivity

A

blood transfusion reactions
erythroblastosis fetalis
autoimmune hemolytic anemia

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13
Q

What is type 3 hypersensitivity

A

immune-complex mediated hypersensitivity

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14
Q

what is the immune mediator for type 3 hypersensitivity

A

immune-complexes

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15
Q

What is the mechanism of type 3 hyper sensitivity

A

Ag-Ab complexes deposited in various tissues cause activation of complement and ensuing inflammatory response, causing high levels of neutrophils coming

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16
Q

what are the typical manifestations of type 3 hypersensitivities

A 
localized arthus reactions
serum sickness
necrotizing vasculitis
SLE
rheumatoid arthritis
glomerulonephritis
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17
Q

what is type 4 hypersensitivity

A

delayed type hypersensitivity

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18
Q

what is the immune mediator for type 1 hypersensitivity

A

T-cells

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19
Q

what is the mechanism of type 4 hypersensitivities

A

specialized T-cells release cytokines, that activate macrophages and Cytotoxic t-cells

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20
Q

what are the typical manifestations of type 4 hypersensitivities

A 
dermatitis
tubercular lesions
graft rejection
poison ivy reaction 
tuberculin skin test
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21
Q

what type of T-cell is active is type 1 hypersensitivities

A

TH2 (via IgE)

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22
Q

do you see hypersensitivities on the first encounter with the allergen

A

nope, because they are antibody, or effector T-cell driven

first exposure is call sensitization

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23
Q

What are haptens

A

small organic molecules that can become covalently bound to proteins and can cause TH1 or TFH cells to become activated

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24
Q

what do you call a protein with a hapten bound to it

A

haptenated protein

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25
Q

how do haptens cause immune responses

A

they bind to proteins, and when those proteins are processed by APCs, they are presented to, and can activate Th1 and TFH cells.

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26
Q

what do the TH1 cells that have been activated by haptenated proteins go on and do

A

activate macrophages

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27
Q

whad to the TFH cells that have been activated by haptenated proteins go on and doo

A

activate B-cells to produce antibody

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28
Q

what does sensitization cause to happen, in immediate type (type 1 ) hypersensitivity

A

IgE is produced and bound to mast cells

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29
Q

what is the receptor on mast cells and basophils that binds the IgE

A

FceRI

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30
Q

what things are found in the granules of mast cells, and are thus released in type 1 hypersensitivity reactions

A

histamine
proteoglycans
proteases
TNF

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31
Q

what does histamine cause

A

vasodilation and increased vascular permeability

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32
Q

what are the two proteoglycans found in the granules of mast cells

A

heparin, chondroitin sulfate

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33
Q

what are the proteases found in the granules of mast cells

A

tryptase and chymase

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34
Q

how does the allergen skin test work

A

you inject a potential allergen into the skin, and if you are allergic the histamine will result in edema (swelling) and erythemia (redness) in the area where the allergen was placed

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35
Q

what does the activation of mast cells cause on other cells

A

TNF recruits other cells
eosinophils - perform ADCC release granules toxic for worms and TGF alpha and beta (wound healing)
basophils - make luekotrienes (attract neutrophils) and IL-4 and IL-13
TH2 cells

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36
Q

where do you see allergic responses

A

where epithelial surfaces meet the environment

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37
Q

how are allergies best treated

A

by avoiding the allergen
immunotherapy (shots)
steroids (dampen immune response)
Anti- IgE prevents IgE from binding FceRI on mast cells

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38
Q

are some people more genetically predisposed to allergies

A

yes

39
Q

what besides genetic predisposition can increase the likelyhood of allergies

A

the timing in life of sensitization

40
Q

what can cause systemic anaphylaxis

A

it is an allergic reaction usually caused by injected or gut absorbed allergens. (bee sting venom, penicillin, seafood, nuts)

41
Q

what are the symptoms of systemic anaphylaxis

A

labored breathing
drop in blood pressure
contraction of smooth muscle, leading to defecation, urination, and brachial constriction

42
Q

what is the treatment for systemic anaphylaxis

A

epinephrine injections (epi pen)

43
Q

what are some common examples of haptens

A

penicillin
substances in latex gloves
venoms
radiocontrast media

44
Q

what are the different types of Type 1 hypersensitivities

A

systemic anaphylaxis

localized hypersensitivity

45
Q

what is localized hypersensitivity

A

pathology is limited to a specific tissue or organ

46
Q

What are examples of localized hypersensitivity

A

allergic rhinitis (hay fever)
asthma
atopic dermatitis (eczema)
food allergies

47
Q

what type of hypersensitivity is urticaria (hives)

A

behaves like type 1

48
Q

asthma is associated with common allergies, but what is its root cause

A

dysregulated Th2 response

allergens that get into the lower airways, along with TH2 cells and Eosinophils

49
Q

when can asthma begin to cause serious problems

A

when you have repeated episodes, and the inflammation in the lungs can’t be controlled. They can even be fatal (die from hypoxia)

50
Q

what is stage one of asthma

A

immediate mast cell degranulation

resolved after one hour

51
Q

what is stage two of asthma

A

4-6 hours later

newly infiltrating eosinophils, basophils, and TH2 cells

52
Q

what is stage three of asthma

A 
AIRWAY REMODELING (caused by repeated episodes)
loss of epithelial cells 
goblet cell hyperplasia
submucosal collagen build up
thickening of airway walls
mast cell accumulation
increases in smooth muscle
53
Q

What is the hygene hypothesis concerning asthma diseases

A

it states that children in developed countries are more likely to suffer from asthma

54
Q

What do allergy injections do to help combat allergies

A

they increase IgG and IgG4

and decrease IgE and lymphocyte response

55
Q

we know that mast cells have activating receptors (FceR1), but do they have inhibiting receptors

A

yes, FcyRIIB

56
Q

what binds to the FceR1 receptors on mast cells

A

IgE (activates mast cells)

57
Q

what binds to the FcyRIIB receptors on mast cells

A

IgG (inhibits mast cell activation)

58
Q

if both bind, which wins out IgE binding to the FceR receptor, or IgG binding to FcyRIIB

A

IgG binding to FcyRIIB inhibits the activation of the mast cells and overrides the IgE binding to the FceR

59
Q

what is the mechanisms that many drugs (not allergy shots) use to prevent hypersensitivity

A

maintaining high levels of cAMP (this prevents mast cell degranulation)

60
Q

Are type 2 hypersensitivities cytotoxic

A

yep

61
Q

What are examples of type 2 hypersensitivities

A

Transfusion reactions
hemolytic disease of the newborn
Drug-induced anemia

62
Q

what is the problem in transfusion reactions, and what are the two ways that transfusion reactions can manifest

A

widespread destruction of RBCs

it can be IgM mediated or IgG mediated

63
Q

what are the symptoms if transfusion reactions are IgM mediated

A

fever, chills, nausea, back pain, free hemoglobin and bilirubin in the blood, kidney and brain damage.

IgM mediated transfusion reactions are due to ABO antigens

64
Q

what are the symptoms if the transfusion reactions are IgG mediated

A

delayed
Jaundice and anemia\

IgG mediated transfusion reactions are due to Rh, and other antigens

65
Q

why are transfusion reaction problems delayed when mediated by IgG

A

because the RBCs are destroyed at extravascular sites by phagocytosis

66
Q

What is hemolytic disease of the newborn

A

when an RH- mother has had a RH+ baby, her body made antibodies against the RH antigen. so the next time she has an RH+ baby, her antibodies attack the RH antigen of the baby and destroys the RBCs

67
Q

how is hemolytic disease of the newborn treated

A

transfusion of the fetus, plasmaresis of mother

68
Q

how do you prevent hemolytic disease of the newborn

A

Rhogam

69
Q

what is drug induced anemia

A

chemicals get absorbed onto RBCs, and those stimulate complement-mediated destruction

70
Q

what is another name for hemolytic disease of the newborn

A

erythroblastosis fetalis

71
Q

what type of hypersensitivity is mediated by immune complexes

A

type 3

72
Q

how do immune complexes cause a hypersensitivity

A

ones that aren’t cleared get deposited in tissues, and those can trigger the release of inflammatory mediators, and vasoactive mediators (they can also activate platelets to form clots)

73
Q

What are symptoms of type 3 hypersensitivity (immune complex mediated)

A

fever, rash, joint pain, lymph node enlargement, and protein in the urine

74
Q

what are examples of type 3 sensitivity

A

vasculitis (if the complex deposited in the blood vessel)
glomerulonephritis (if the complex is in the kidney)
Arthritis (if the complex is in the joints)

75
Q

what happens to immune complex mediated hypersensitivities over time

A

they can eventually resolve over time as the complexes are cleared as long as the Ag goes away.

76
Q

what can cause type 3 hypersensitivities to not resolve with time

A

autoantigens

77
Q

What type of hypersensitivity is SLE

A

type 3

78
Q

What type of type 3 hypersensitivity (localized or generalized) is an arthus reaction

A

localized type 3 hypersensitivity

79
Q

what are the characteristics of type 4 hypersensitivity

A
  1. Purely cell related, not antibody mediated
  2. Initiated by T-cells
  3. Delayed reaction
  4. macrophage recruitment to the inflammation site
80
Q

what is the most common example of a type 4 hypersensitivity

A

Poison Ivy contact dermatitis

81
Q

What is another name for type 4 hypersensitivity

A

delayed type hypersensitivity (the first exposure just causes sensitization)

82
Q

what type of T-cell is created during the sensitization of type 4 hypersensitivity

A

CD4+ TH1 cells

83
Q

what happens when there is a second exposure to the antigen in type 4 hypersensitivity

A

with the second exposure the TH1 cell produces cytokines that activate macrophages, and the destruction of substances begins

84
Q

what type of hypersensitivity gives rise to tuberculin response, allergic contact dermatitis, celiac disease, and graft rejection

A

type 4 hypersensitivity

85
Q

what kind of MHC class, and thus T-cell, is usually generated by lipid soluble antigens

A 
MHC class 1, and CD8+ cytotoxic t-cells
this is because the lipid soluble antigens can cross the plasma membrane and are now endo- (come from within the cell)
86
Q

celiac disease is a type of which type of hypersensitivity

A

type 4

87
Q

what causes celiac disease

A

the binding of glutamic acids to HLA-DQ2 or HLA-DQ8 (found in the mucosal surface of the small intestine) this initiates a TH1 response against and the destruction of the mucosal surface of the small intestine

88
Q

What are the two types of inflammatory bowel disease, and what is the difference between them

A 
Crohn's disease (located in the terminal ileum and ascending colon)
Ulcerative Colitis (located in the colon and rectum)
89
Q

What is the cause of inflammatory bowel disease

A

an aberrant immune reactivity to normal intestinal flora

90
Q

what disease (hypersensitivity type 4) is associated with crypt abscesses, the rectum and colon, and a dysregulated Th2 response

A

ulcerative colitis

91
Q

What things can cause chronic inflammation

A
  1. continual microbial invasion
  2. ineffectively cleared microbes
  3. DAMPS (noninfectious)
  4. Obesity
92
Q

how does obesity lead to chronic inflammation

A

visceral adipocytes are secretors of proinflammatory cytokines TNF-alpha and IL-6

93
Q

how does obesity lead to insulin resistance

A

TNF-alpha and IL-6 released by visceral adipose inhibit the ability of insulin receptors to function

94
Q

can chronic inflammation lead to increased tumor growth? how?

A

yes, because inflammation increases the ability of blood vessels to be produced.

DMD 5244 (Immunity) (16 decks)

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