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Unit 3: Immune Related Diseases > Section 1: Hypersensitivity Reactions > Flashcards

Section 1: Hypersensitivity Reactions Flashcards

1
Q

Hypersensitivity

A

-effector mechanisms that the immune system uses to defend the host against a perceived threat are more damaging to the host than the threat itself
-are classified into four major major groups depending on the mechanisms responsible for that particular reaction (Gell and Coombs classification)

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2
Q

What is the classification of mechanisms for hypersensitivity?

A

Gell and Coombs’s classification
A.C.I.D
Type I
Type II
Type III
Type IV

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3
Q

What is Type I

A

anaphylaxis
-anaphylactic or immediate hypersensitivity reactions are mediated by IgE, mast cell degranulation
-results from the release of preformed or newly synthesized mediators from mast cells and basophils
-effects localized or systemic
- Ag stimulates an antibody-dependent immune response by activation of TH2-cells (helper T cells)
-TH2 cytokines cause class switching to IgE and activation of mast cells and basophils

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4
Q

What is Type II

A

Cell or surface-bound antibody
-is mediated by the complement-activating antibodies IgG and IgM predominately directed against cell-surface antigens (ABO, Drugs)
-mechanisms of cell destruction due to Ab-complement mediated;
* Lysis
* opsonization
* antibody- directed cellular cytotoxicity (ADCC)
-various cells and tissues affected; commonly blood cells, lungs, and kidneys
- clinical conditions: transfusion reactions, hemolytic anemia, hemolytic disease of the fetus and newborn (HDFN, erythroblastosis fetalis)

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5
Q

What is Type III

A

Immune complex method
-immune complexes formed when soluble antigens and IgG antibodies in the proper concentrations form large lattices that precipitate out of solution
-direct to an antigen in solution, not bound to the cell membrane
- the resultant immune complexes get stuck at various anatomical sites initiating an inflammatory response
-immune complexes also cause activation of complement and recruitment of inflammatory cells
-generally phagocytes clear these complexes without much problem… rarely they are of the proper size to cause serious problems in filtering tissues
ex: blood vessel walls, kidneys (glomerular basement membrane), lungs, and tissues in the joints
-the pathology response is determined by the sites of immune complex deposition

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6
Q

What is Type IV

A

Delayed type hypersensitivity
-occurs 1-3 days after exposure to antigen, are mediated not by Ab but effector T-cells
-the amount of Ag needed to trigger this reaction is 100-1000 times that required for Ab-mediated hypersensitivities
-classic examples are contact dermatitis and tuberculin test
-reaction mediated by Th1 and CD8 T-cells
-requires a sensitization phase
-second exposure or elicitation phase

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7
Q

Features, sample condition, and time to the onset of Type I

A
  • IgE-mediated, mast cell degranulation
  • asthma and hay fever
  • 2-30 minutes
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8
Q

Features, sample conditions, and time to the onset of Type II

A

-Ab-mediated cell surface reactions causing cytotoxicity, complement activation
-Hemolytic anemia, HDFN
- 5-8 hours

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9
Q

Features, sample conditions, and time to the onset of Type III

A
  • Immune complex-mediated, complement activation
    -Arthus reaction
  • 2- 8 hrs
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10
Q

Features, sample conditions, and time to the onset of Type IV

A

-cell-mediated, sensitized T cells, activated macrophages
- contact dermatitis
- 24- 72 hrs

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11
Q

Allergen

A

harmless antigens that stimulate an IgE response

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12
Q

Urticaria (Hives)

A

-skin rash associated with a Type I hypersensitivity

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13
Q

sensitization to an inhaled allergen

A
  1. first exposure to pollen
  2. Extraction of antigen
  3. activation of antigen-specific T cells
  4. Production of IgE and binding to mast cells
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14
Q

Type I hypersensitivity: clinical manifestations

A

-the effects of type 1 hypersensitivity are intended to combat potential parasitic pathogens
ex: clearing of the GI tract
: vomiting
: diarrhea
: contract or block airways
-upon first exposure to an allergen, no reaction occurs, and large amounts of IgE are produced
-usually, this immune response is limited to the local area of allergen exposure
-on occasion, the allergen can be introduced systemically (ex: bee sting) resulting in systemic anaphylaxis or anaphylactic shock
- 20% of human allergies in North America are thought to be caused by the dried feces of the house dust mite, dermatophagoides pteronyssimus

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15
Q

sensitization phase

A

1st exposure primes mast cells and basophils large numbers of IgE and high affinity Fc receptor complexes (FceRI)

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16
Q

Activation phase

A

2nd exposure, antigens bind to IgE effectively cross-linking the FCERI receptors and initiating signal cascades

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17
Q

Type I hypersensitivity: sensitization to an inhaled allergen

A
  • first exposure to pollen
    -extraction of antigens
    -activation of antigen-specific T cells
  • production of IgE and binding to mast cells
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18
Q

effector phase

A

-the biological effects of mediators released by mast cells and basophils in response to activation
-mediators are released at different times (performed vs synthesized) meaning there are early and late phases of these effects
-allergen is crossing linking or bringing the two IgE’s together, so the intracellular portion of the Fc get closer and cause dephosphorylation and kinases cascade and send granuales to cell and nucleus , which make proteins

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19
Q

early response in effector phase

A

-peaks in 10-20 minutes
-contraction of smooth muscle
-leakage of blood vessels
-secretion of mucus

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20
Q

late phase in the effector phase

A

-peaks in 2-6 hours
-recruitment and infiltration of neutrophils and eosinophils
-production of cytokines
-later infiltration of macrophages and fibroblast

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21
Q

Histamine: action

A
  • increased permeability of capillaries, smooth muscle contraction
    -an early pre-formed mediator
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22
Q

Serotonin: action

A

-increased permeability of capillaries, smooth muscle contraction
-an early pre-formed mediator

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23
Q

HMW-NCF: action
(High Molecular Weight Neutrophil Chemotactic Factor )

A

-neutrophil recruitment
- an early pre-formed mediator

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24
Q

Proteases (Tryptase): action

A

-cleave of complement proteins, membrane degradation
-an early pre-formed mediator

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25
Q

Leukotrienes (C, D, and E): Action

A

-increased permeability of capillaries, smooth muscle contraction
- a newly synthesized (late) mediator

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26
Q

Platelet-activating factor (PAF)

A

-platelet aggregation, smooth muscle contraction
-a newly synthesized (late) mediator

27
Q

prostaglandin (D2)

A

-constriction of bronchial smooth muscle
-a newly synthesized (late) mediator

28
Q

IL-4, IL-5, IL-6

A

-various actions
-a newly synthesized (late) mediator

29
Q

Type I hypersensitivity: Etiology

A

-people with allergies are prone to an over-activated Th2 response and tend to have higher levels of circulating IgE
-there is a genetic basis for why some people are allergic and others are not
-particular combinations of MHC haplotypes that favor a strong Th2 response
-mutations that promote or favor cytokines that enhance the IgE/Th2 response ( i.e. IL-4, IL-3, IL-5, IL-9, IL-13, GM-CSF)
-variants of FceRI
-MHC II (DRB1-1501) (specific to) allergy to plant pollen
* note in regions where parasitic infections are common, allergic reactions are rare! presumably because IgE specific to parasitic antigens are saturating the mast and basophilic cells

30
Q

Type I Hypersensitivity: Clinical testing

A

-two approaches: testing for components of the immune response
* IgE, allergen-specific IgE
-Testing the physiological reaction to an allergen
* skin testing
-modern forms of these tests are the same in principle but radioactive labels have been replaced with chemiluminescent enzyme markers

31
Q

Radioimmunoabsorbent test (RIST)

A

-total serum IgE levels
1. solid phase anti-human IgE in plate
2. Add human IgE (capture IgE in patient serum)
3. Detect capture IgE with radiolabeled anti-IgE

32
Q

Radioallergosorbent test (RAST)

A

-allergen-specific IgE activity
1. Disk coated with test antigen
2. Incubate with test serum (specific IgE bound
3. Radiolabeled anti-human IgE
3.

33
Q

clinical testing: skin testing

A

-test the individual’s in vivo response to a test allergen
-simple
-sensitive
-specific
-in vivo

34
Q

prick test

A

-In most common skin tests, a small amount of sample allergen is injected into the skin and observed for a local reaction

35
Q

intradermal testing

A

-100 to 1000 times less antigen is injected between the different layers of the skin
Controls
-both tests use similar controls
- positive: histamine
- negative: saline
Results
-the size of the wheel and flare is measured in response to the allergen and compared to the control responses

36
Q

transfusion reactions

A

-hemolytic responses that occur when large amounts of blood are transfused between individuals with incompatible ABO blood groups
-people posse naturally occurring antibodies that develop after exposure to cross-reactive antigens, such as bacteria
-no antibodies developed to self-antigen blood groups because of immunological tolerance
-reactions occur rapidly, minutes to hours
-mediated predominately by IgM, which initiates complement activation and results in:
* hemolysis of donor RBCs
* capillary permeability
* dilation of arterioles
* hypotension
* disseminated intravascular coagulation
* renal failure

37
Q

hemolytic anemia

A

-deposition of antibodies on the surface of RBCs results in hemolytic anemia
-IgG and IgM mediated
-exposure to medication and chemicals primary cause
-penicillin and sulfonamides can bind to the surface of RBCs and elicit AB formation
-long term exposure to formaldehyde can alter RBC surface antigens resulting in them being recognized as foreign

38
Q

hemolytic disease of the fetus and newborn (HDFN)

A

-occurs when a pregnant woman makes Abs against the RBCs of the her fetus
-These Abs can cross the placenta
-most common antigens to elicit this response are the D antigens (RH blood group)- Rh-positive baby and Rh-negative mother
-first pregnancy results in the sensitization of the mother to the Rh blood group, stimulating a B-cell response and producing memory B cells to the Rh antigen
-usually doesn’t affect the first child, but is very serious for subsequent pregnancies with an Rh-positive fetus
-IgG crosses the placenta attacking the fetus’s RBCs: anemia, jaundice, and fetal death

39
Q

indirect antiglobulin test (IAT)

A

-tests the mother’s serum for Ab to the Rh antigen

40
Q

direct antiglobulin test (DAT)

A

-tests if the baby’s RBCs are coated with anti-Rh antibodies

41
Q

Type II hypersensitivity: Treatment

A

-it is now common to give Rh-negative mothers anti-RhD antiglobulin (Rhogam)
-this destroys any leaked fetal RBCs that are in the mothers’ circulation thus preventing an antibody response to these antigens

42
Q

Arthus reactions

A

-the 1900s Maurice Arthus observed this reaction in immunized animals who developed high titers of Abs to antigens
-sensitized individuals are injected intradermally resulting in a localized reaction (inflammation, severe cases, necrosis, and ulceration)
-IgG infiltrates the tissues and forms complexes with injected antigen
-deposition of complexes in anatomical sites induce an unspecified inflammatory response that damages the tissue associated with those sites

43
Q

serum sickness

A

during the late 19th and early 20th century bacterial infections such as diphtheria, scarlet fever, and tetanus, were treated by injecting serum from horses that had been immunized with the particular bacterial toxin
-the horse antibodies helped clear the toxin but also could produce a systemic type III hypersensitivity
-7-10 days after the administration of the serum
-caused by the production of Ab to horse serum proteins and the deposition of small immune complex in tissue

44
Q

elicitation phase

A

-memory Th1 cells need to come into contact with the antigen, clonally expand, and initiate an immune response
- fluid backup
-macrophage recruitment
-localized tissue damage

45
Q

tuberculin test (mantoux test)

A

-a diagnostic test used to determine if a person has been infected with mycobacterium tuberculosis. Takes advantage of the Type IV hypersensitivity response
-a small amount of protein extracted from M. tuberculosis is injected intradermally
-individuals who have been infected or vaccinated (BCG strain- only UK) develop an inflammatory response in 1-3 days

46
Q

contact dermatitis

A

-contact of certain substances with skin can elicit a type of IV response (poison ivy)
-pentadecacatechol (poison ivy) is a hapten that penetrates the skin and indiscriminately forms covalent bonds with
-extracellular proteins (extracellular matrix)
-skin cell surface proteins
-intracellular proteins (freely crosses the plasma membrane and alters proteins that can be presented by MHC I- CD8)

47
Q

celiac disease

A

-an inflammatory autoimmune disease of the gut mucosa
- caused by an immune response to gluten proteins in wheat or the related proteins in barley or rye
-CD4 cells respond to gluten-derived peptides in the GALT producing an inflammatory response in the small intestine
-with a persistent intake of gluten the inflammation becomes chronic causing: atrophy of intestinal villi, malabsorption of nutrients, diarrhea, increased GI cancer risk
-strong genetic predisposition: 80% have the allotype HLA-DQ2, most the remaining 20% have HLA-DQ8 allotype (common in caucasian)
-hard to detect unless take a chunk of your small intestine to really know

48
Q

Genes associated with susceptibility to asthma

A
  1. MHC class II genes
  2. T-cell receptor a locus
  3. TIM gene family
  4. IL-4
  5. IL4 receptor a chain
  6. High affinity IgE receptor B chain
  7. 5 lipoxygenase
  8. B2- Adrenergic receptor
  9. ADAM33
49
Q

Type II Hypersensitivity graph

A

1.complement coated penicillin-modified erythrocytes cells are phagocytosed by macrophages using their complement receptor
2. macrophages present peptides from the penicilline-protein conjugate and actviate specific CD4T cells to become Th2 cells
3. B cells are acivated by antigen and by help from activated Th2 cells
4. Plasma cells secrete penicillin-specific IgG which bind to modified erythrocytes
5. Penicillin specific IgG binds to pencillin-modified protein on erythrocyes
6. activation of complement components C1-C9 and formation of MAC causes lysis of erythrocytes
7.Activation of complement components C1-C3 leads to covalent bonding of C3B and phagocytosis of antibody- and complement coated erythrocytes

50
Q

Arthus reaction: In the body

A

-1-2 hours
-locally injected antigen in immune individual with IgG antibody
- local immune complex formation activates complement. C5a binds to a C5a a receptor on the mast cell
-binding of immune complex to FcyRIII on mast cell induced degranulation
-local inflammation, increased fluid and protein release, phagocytosis, and blood vessel occlusion

51
Q

Type III: Intravenous (high dose)

A
  1. vasculitis (blood vessel walls
  2. Nephritis (renal glomeruli)
  3. Arthritis (joint spaces)
52
Q

Type III: Subcutaneous

A

-arthrus reaction: perivascular area

53
Q

Type III: Inhaled

A

-farmers lung: alveolar/capillary interface

54
Q

Delayed-type hypersensitivity: Antigen

A

-proteins
-insect venom
- mycobacterial proteins (tuberculin, lepromin)

55
Q

Delayed-type hypersensitivity: consequences

A

-local skin swelling
-erythema
-induration
-cellular infiltration
-dermatitis

56
Q

Contact hypersensitivity: antigen

A

-haptens
-pentadecacatechol (poison ivy)
- DNFB
- small metal ions
-nickel
-chromate

57
Q

contact hypersensitivity: consequence

A

-local epidermal reaction:
-erythema
-cellular infiltrate
-vesicles
-intraepidermal abscesses

58
Q

contact: gluten-sensitive enteropathy (celiac disease): antigen

A

-gliadin

59
Q

contact: gluten-sensitive enteropathy (celiac disease): consequence

A

-villous atrophy in small bowel
-malabsorption

60
Q

Type IV hypersensitivity: Graph

A
  1. antigen is introduced into subcutaneous tissue and processed by local antigen-presenting cells
  2. A Th1 effector cell recognizes antigens and releases cytokines which act on intravascular endothelium
  3. recruitment of T-cells phagocytes. fluid and protein to the site of antigen injection causes visible lesions
    -takes 24-72 hours
61
Q

QuantiFERON-TB Gold Plus (QFT-PLUS)

A

-fourth generation of testing the cell-mediated reponses to MTB throught the production of IFN-Y
-pheripheral blood is collected in specific tubes containing recombinant M. tuberculosis anitgens, then incubate for up to 24 hours. CD4 and CD8 T cells than can recognize MTB antigens will produce IFN-y
-After incubation blood is centrifuged and plsma is tested for the amount of IFN-Y produced using traditional ELISA
-more sensitive and specific than the TST and produces results quicker but is still an indirect test that should be accompanied by additional clinical exams (chest ray) before diagnosis

62
Q

celiac disease: graph

A
  1. gluten is degraded in the gut lumen to give a resistant fragment
  2. gluten fragment enters gut tissue and is deminated by transglutaminase
  3. naive CD4 T cell responds to deaminated peptides presented by HLA-DQ
  4. Inflammatory effector T cells cause villous atrophy
63
Q

antigen is processed by tissue macrophages and stimulates TH1 cells

A

chemokines: macrophage recruitment to site of antigen
IFN-Y: activate macrophages, increasing release of inflammatory mediators
TNF-a and LT: local tissue destruction, increased expression of adhesion molecules on local blood vessels
IL-3/GM-CSF: monocyte production by bone marrow stem cells

Unit 3: Immune Related Diseases (4 decks)

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