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Hypersensitivity Flashcards

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1
Q

what is a hypersensitivity reaction?

A

a condition in which the normally protective immune system has a harmful effect on the body by excessive or inappropriate immune response

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2
Q

Allergy

A

abnormal immunological response to otherwise harmless environmental stimulus
e.g. food, pollen, animal and dander

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3
Q

Autoimmune disease

A

abnormal immunological response directed against an antigen within the body

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4
Q

what are the stages of a hypersensitivity reaction?

A

sensitisation

effect

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5
Q

what is sensitisation?

A

initial asymptomatic contact with an antigen

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6
Q

what is effect?

A

harmful immune response following sensitisation and subsequent antigen contact

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7
Q

what are the types of hypersensitivity reaction?

A

1-4
1-3 = antibody mediated
4 = cell mediated

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8
Q

type 1 hypersensitivity

A

allergic or immediate
onset within minutes
develop IgE antibodies in response to harmless antigens
can be localised - allergic rhinitis and asthma
can be systemic - anaphylaxis
exposure by ingestion, inhalation, injection or direct contact

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9
Q

pathogenesis of type 1 hypersensitivity

A

contact with antigen
IgE formed as a result
coats mast cells and basophils - next time your body encounters the allergen it results in an IgE-mediated reaction by preformed IgE antibodies
Free allergen binds to 2 adjacent IgE antibodes - crosslinking
causes degranulation of cells which causes release of histamine and other mediators - prostaglandins, platelet-activating factor, leukotrienes
has varying effects on all these to cause the symptoms associated with allergy/ atopy

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10
Q

what do vasoactive amines effect?

A 
smooth muscle
blood vessel
mucous gland
platelets
sensory nerve endings
eosinophils
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11
Q

what do vasoactive amines do to smooth muscle?

A

bronchospasm, abdominal cramping, rhinitis, hypovolemia and hypoxia

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12
Q

what do vasoactive amines do to blood vessels?

A

cause vasodilation and leaky capillaries
extravasation of capillary blood - causing erythema
fluid shift into the interstitial space - oedema and pulmonary oedema

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13
Q

what do vasoactive amines due to eosinophils?

A

eosinophilia -

eosinophil and neutrophil chemotaxis induced by basophil and mast cell mediators

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14
Q

what are some common allergies?

A 
drugs 
foods 
Insect venom
Inhaled or environmental allergens
blood transfusion products
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15
Q

examples of type 1 hypersensitivity

A

anaphylaxis

allergies

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16
Q

is anaphylaxis humoral or cell mediated?

A

humoral

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17
Q

how to treat anaphylaxis?

A 
adrenaline intramuscularly to lateral thigh 
airway
resuscitate
anaesthetics 
cardiac arrest call 
antihistamines slow to work
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18
Q

type 2 hypersensitivity reaction

A

cytotoxic
onset within minutes or few hours
involves IgG and IgM antibodies
5 mechanisms by which these antibodies can cause disease

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19
Q

mechanism 1 for type 2 hypersensitivity

A

Antigen-antibody complex on host tissue
activates complement cascade which creates a membrane attack complex. Inserts itself into the membrane of the cell it attacks. Allows fluid to rush into cell - swells and bursts cell - cell lysis

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20
Q

mechanism 2 for type 2 hypersensitivity

A

complement activate complement binds to Fc portion of the antibody. Some of the cascade become cleaved and chemotaxic - attracts neutrophils. Neutrophils undergo degranulation and release enzymes which generate oxygen radicals which cause cytotoxic damage to cell

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21
Q

mechanism 3 for type 2 hypersensitivity

A

activation of complement cascade causing opsonisation and phagocytosis. The phagocytes engulf cells in the spleen

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22
Q

mechanism 4 for type 2 hypersensitivity

A

antigen-antibody complex recognised by NKs, they bind to the antibody. NKs release perforins forming pores in the cells. Granzymes and granulysin enter the cell and cause apoptosis

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23
Q

mechanism 5 for type 2 hypersensitivity

A

antibody mediated cellular dysfunction, antigen-antibody complex blocks normal receptor activator from getting to receptor e.g. myasthenia or simulates a signalling molecule and over activate a receptor e.g. graves disease

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24
Q

type 2 hypersensitivities examples

A 
autoimmune haemolytic anemia
good pasture syndrome
drug-induced neutropenia
immune thrombocytopenia
graves disease
myasthenia gravis
bullous pemphigoid
pemphigus vulgaris
rheumatic fever
acite hemolytic transfusion reaction 
hemolytic disease of the fetus and newborn
hyperacute transplant rejection
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25
distribution of type 2 hypersensitivity diseases
limited to a particular tissue type
26
diagnosis of type 2 hypersensitivity
autoantibody testing and coombs test
27
coombs test
used to detect antibodies that act against the surface of cells
28
hemolytic anemia
form of anemia due to hemolysis, the abnormal breakdown of red blood cells in the blood vessels or spleen opsonisation and phagocytosis of erythrocytes
29
Good pasture syndrome
rare, autoimmune disease which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs and kidney failure Complement and Fc receptor mediated inflammation Nephritis and lung hemorrhage
30
Autoimmune thrombocytopenic purpura
opsonisation and phagocytosis of platelets causing bleeding
31
Pemphigus vulgaris
antibody-mediated activation of proteases, disruption of intracellular adhesions . Skin blisters
32
Vasculitis
Neutrophil degranulation and inflammation. Vasculitis
33
Acute rheumatic fever
inflammation and macrophage activation. Myocarditis and arthritis
34
Myasthenia gravis
antibody inhibits acetylcholine binding and down modulates receptors muscle weakness and paralysis
35
Graves disease
Antibody mediated stimulation of TSH receptors causing hyperthyroidism
36
Pernicious anemia
neutralisation of intrinsic factor and decreased absorption of vitamin B12. Abnormal erythropoiesis, anemia, neurologic symptoms
37
is graves disease local or systemic?
local as it only effects thyroid tissue but shows systemic effects because of role of thyroid
38
type 3 hypersensitivity
immune complex hypersensitivity onset between 2 and 6 hours can be local or systemic antigens causing it can be exogenous or endogenous
39
pathogenesis of type 3 hypersensitivity
formation of antigen antibody immune complexes with slight antigen excess complement is activated by the immune complexes via the classical pathway . This causes basophils to degranulate, releasing mediators that increase vascular permeability. complexes circulate and are trapped in the basement membrane of small blood vessels activated complement attracts neutrophils and causes them to degranulate neutrophils release enzymes responsible for much of the tissue damage
40
what is an immune complex?
antigen-antibody complex formed when the antigen is found in the blood stream, so is soluble .
41
clinical examples of type 3 hypersensitivities
``` systemic lupus erythematosus drug-induced hypersensitivity vasculitis poststreptococcal glomerulonephritis polyarteritis nodosa wegeners granulomatosis arthus reaction hypersensitivity pneumonitis - Farmer's/ pigeon fanciers lung serum sickness serum sickness-like reaction ```
42
wegners granulomatosis
rare condition in which blood vessels become inflamed, affecting the ears, nose, sinuses, kidneys and lungs
43
arthus reaction
post tetanus vaccination
44
hypersensitivity pneumonitis
triggered by exposure to proteins present in bird droppings . The lungs become inflamed with granuloma formation - farmers lung
45
serum sickness
a reaction to medications or often serums - such as antivenom
46
systemic lupus erythrmatosus
nephritis arthritis vasculitis
47
polyarteritis nodosa
vasculitis
48
poststrptococcal glomerulonephritis
nephritis
49
type 4 hypersensitivity
delayed hypersensitivity reaction, inflammation by 2-6hours and peaks at 24-48hrs result from interaction of T cell-initiated inflammation and doesnt involve antibodies the inflammatory responses result from the manner in which the T cells encounter and respond to the antigen can be transferred by sensitised T cells but not serum
50
Pathogenesis of type 4 hypersensitivity reactions
foreign antigen enters the body uptake by langerhans cell migration to lymph nodes and formation of sensitised T lymphocytes secretion of lymphokines and cytokines - IFN gamma and TNF alpha by sensitised T lymphocytes macrophage attaches to antigen macrophage presents antigen to T lymphocytes forms a cytotoxic T cell autoimmune reaction - cytotoxic T cell attaches to similar antigen in healthy tissue killer T cells release perforin and granzymes tissue destruction
51
examples of type 4 hypersensitivities
``` contact dermatitis drug reactions - stevens-johnson syndrome Graft-versus-host disease Mantoux tuberculin skin test for latent TB rheumatoid arthritis IBD MS Guillain-Barre syndrome Hashimoto's thyroiditis type 1 diabetes mellitus ```
52
rheumatoid arthritis
inflammation mediated by TH1 and TH17 cytokines
53
MS
inflammation mediated by TH1 and TH17 cytokines | myelin destruction by macrophages
54
Type 1 diabetes
T cell mediated inflammation and destruction of islet cells | killer T cells
55
IBD
inflammation mediated by TH1 and TH17 cytokines
56
Psoriasis
inflammation mediated by T cell derived cytokines
57
Stevens Johnson drug reaction
affects skin and mucus membranes | flu-like symptoms, rash and blistering . the skin eventually dies
58
common drug allergies
penicilin and muscle relaxants
59
common food allergies
nuts, shellfish, eggs, soy and wheat
60
common insect venom allergies
Insect venom - bee and wasp
61
common environmental allergies
Inhaled or environmental allergens - dust mites, animal dander, pollen, latex

Physiology (46 decks)

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