Week 3 Flashcards

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1
Q

Hypersensitivity Reactions

A
  • immune system going wrong
  • sensitization of immune system by repeated exposure to allergen = immune reaction
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2
Q

Antigens = allergens

A
  • harmless allergens to most people
  • susceptible individuals, the immune system over-reacts
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3
Q

Most common hypersensitivity reaction

A

Type I

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4
Q

Type I hypersensitivity reaction + which antibody (2)

A

IgE mediated (most)
can by Th1 cell mediated (contact materials)

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5
Q

IgE mediated responses = which condition

A

Atopy

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6
Q

Atopic triad

A
  • atopic asthma
  • allergic rhinitis
  • atopic dermatitis
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7
Q

Atopic disease

A

IgE mediated hypersensitivity
have one of the triad = more likely to have another

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8
Q

First exposure to allergen - type I hypersensitivity

A

the first exposure = sensitization
- produces IgE Abs to the allergen

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9
Q

Re-exposure to allergen - Type I

A

allergen binds to IgE Abs = activates mast cell = histamine and cytokines = allergic reaction

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10
Q

Type I hypersensitivity - inhalation (location, symptoms, atopic condition)

A
  • repiratory tract (upper and lower)
  • overproduction of mucous, sneexing, congestion, bronchial smooth muscle constriction
  • rhinitis (hay fever) asthma
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11
Q

Type I hypersensitivity - injection (location, symptoms, atopic condition)

A
  • skin, bloodstream
  • local inflammation, systemic inflammation
  • urticaria (hives), anaphylaxis
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12
Q

Type I hypersensitivity - Ingestion (location, symptoms, atopic condition)

A
  • gastrointestinal tract
  • intestinal smooth muscle constriction
  • systemic inflammation - allergen enters blood
  • gastroenteritis (vomit, diarrhea), anaphylaxis
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13
Q

Anaphylaxis - what

A
  • medical emergency
  • anaphylaxis is a severe potentilaly life threatening allergic reaction
  • requires immediate attention’-
  • edema, dispnea, widespread shock
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14
Q

Anaphylactic shock

A
  • low blood pressure from dilation of blood vessels
  • temporarily controled by epi injection
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15
Q

anaphylaxis - CNS symptoms

A
  • lightheadedness
  • loss of consiousness
    confusion
    headache
  • anxiety
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16
Q

Anaphyllaxis - respiratory symptoms

A
  • SOB
  • wheezes
  • hoarsness
  • pain with swallowing
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17
Q

Anaphylaxis- GI

A
  • cramps abdominal pain
  • diarrhea
  • vomiting
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18
Q

Diagnosis of IgE hypersensitivity (3)

A

1) increased serum IgE levels
2) skin prick test or skin patch test
3) biopsy of GI tissue

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19
Q

Desensitization therapy

A
  • allergy shots
  • principle: divert immune response from IgE to IgG
  • mechanism is unclear but seems to have something to do with different route of entry for the allergen
  • side effects: redness, irritation at injection site, systemic reactions (less common more serious), throat swelling, wheezing, anaphylaxis, etc.
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20
Q

Hypersensitivity Type II - mediated by which antibody

A

IgG or IgM - cell surface antigens

21
Q

Hypersensitivity type II - destroys allergen HOW (3)

A
  • opsonization and phagocytosis
  • antibody dependent cellular cytotoxicity
  • complement activation
22
Q

Opsonization

A

when a cell is tagged to make it more likely to be destroyed by phagocytosis

23
Q

antibody dependent cellular cytotoxicity

A

IgG bonds to surface cells with antigen and attract killer T cells

24
Q

complement activation

A
  • complement system
  • causes lysis of the antigen by attacking its membrane complex/phagocytosis
  • recruitments of neutrophils and monocytes + enzymes = tissue damage
25
Q

Rh incompatibility - hypersensitivity type II

A
  • pregnancy if a woman has Rh - blood and her baby has Rh + blood
  • mom’s body will react to babies blood as a foreign substance, create antibodies against it = don’t cause problems during first pregnancy, but cause problems to second and later pregnancies = attack blood cells = hemolytic anemia in baby
  • prevent with immune globulin injections
26
Q

Hypersensitivity III reactions - antibody

A
  • immune complex mediated
  • localized inflammation (complement system)
  • produce damage when come into contact with vessel lining/deposited into tissues = inflammatory response, recruitment of neutrophils/inflammatory cells = injury to tissue
27
Q

Hypersensitivity III reacitons - consequences

A
  • vasculitis (seen in autoimmune disorders)
  • kidney damage (acute glomerular nephritis)
28
Q

Post streptococcal glomerulonephritis (6)

A
  • body responds to nephrogenic streptococcus by forming these immune complexes with a human antibody
  • immune complexes deposited into nephrons glomeruli/ in situ formation of antigen/antibody formation
  • rapid deterioration of kidney function following glomerulonephritis
  • children 1-2 weeks after sore throat/skin infection
  • infiltration of neutrophils and other recruited cells = renal failure, acid base imbalance, HTN, electrolyte imbalance
  • hematuria (tea coloured urine), edema, HTN
29
Q

Type IV reactions - antibody?

A

cell mediated

30
Q

Type IV hypersensitivity reactions

A
  • cell mediated
  • delayed (24 hours later)
  • T cells are activated by antigens
  • must be a previous exposure to amount a reaction to second exposure (ex poison Ivy)
  • release cytokines that act on vascular endothelium = visible lesion on skin
31
Q

Type IV hypersensitivity reaction - examples (2)

A
  • Tuberculin skin test
  • Poison Ivy
32
Q

Self antigen

A

antigen expressed on your own cells

33
Q

auto-reactive cells

A
  • T or B cells that bind to a self antigen
34
Q

Autoantibody

A

antibody that binds to a self-antigen

35
Q

Immune tolerence

A
  • self tolerence - delete self-reactive immune cells
36
Q

Central tolerance

A

deletion of self-reactive T cells in the Thymus and B cells in the bond marrow are eliminated

37
Q

Peripheral tolerance

A

maintenance of tolerance in secondary tissue (spleen and lymph nodes) = deletion of self-reactive cells via apoptosis, suppression of T cells that escape central tolerance

38
Q

Autoimmune - defined

A

when the body loses self tolerance = attacks own cells

39
Q

Factors that influence autoimmunity (3)

A
  • genes
  • environment (trigger)
  • gender (mostly women)
40
Q

environmental factors for autoimmunity (4)

A
  • infection
  • toxins
  • stress
  • food
41
Q

infection and autoimmunity - strep EX

A
  • antibodies for certain strep antigens can resemble self-antigens on heart + kidney = innflamation of heart and kidney
42
Q

classification of autoimmunity (2)

A
  • organ specific autoimmune diseases
  • systemic autoimmune diseases

classifications can overlap

43
Q

Organ specific autoimmune diseases + example

A
  • target antigen present in a specific organ
  • EX Grave’s disease, hasimotos, type I diabetes, Multiple sclerosis
44
Q

Systemic autoimmune diseases + examples

A
  • target an antigen present on many organs-
  • EX: systemic lupus erethomatosis, rheumatoid arthritis
45
Q

Grave’s disease - hyperthyroidism

A
  • overactive thyroid
  • immune system attacks thyroid = causes it to make more thyroid hormone than the body needs
  • antibody = thyroid stimulating immunoglobbin = tells thyroid to make more hormone
46
Q

Type I diabetes mellitus - autoimmune

A
  • chronic autoimmune destruction of insulin producing beta cells
  • islets of langerhans
  • reduced insulin production = hyperglycemia
  • not known what triggers this immune response (ex a trigger event, previous viral illness, clusters in different times of year)
47
Q

Multiple sclerosis

A

myelin sheath of nerve fibres in brain and spinal cord destroyed by autoreactive T cells
- disease causes permanent damage and destruction to nerves
- inflammatory T cells trigger injury of axons and myelin sheath (autoimmune process)

48
Q

Treatment for autoimmune disease (6)

A
  • dependent on type of tissue involved, effect or mechanism involved, magnitude of disease process
  • immunosuppression (NSAIDS, prednisone)
  • plasmapheresis (remove antibodies) = temp fix
  • block MhC with similar peptide (mimic)
  • use antibodies that block B cells and/or T cells
  • disease-specific treatments (insulin for T1D, joint replacements for rheumatoid arthritis)