Week 3 Flashcards

1
Q

Hypersensitivity Reactions

A
  • immune system going wrong
  • sensitization of immune system by repeated exposure to allergen = immune reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Antigens = allergens

A
  • harmless allergens to most people
  • susceptible individuals, the immune system over-reacts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common hypersensitivity reaction

A

Type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type I hypersensitivity reaction + which antibody (2)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

IgE mediated responses = which condition

A

Atopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Atopic triad

A
  • atopic asthma
  • allergic rhinitis
  • atopic dermatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Atopic disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

First exposure to allergen - type I hypersensitivity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Re-exposure to allergen - Type I

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A
  • skin, bloodstream
  • local inflammation, systemic inflammation
  • urticaria (hives), anaphylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anaphylaxis - what

A
  • medical emergency
  • anaphylaxis is a severe potentilaly life threatening allergic reaction
  • requires immediate attention’-
  • edema, dispnea, widespread shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anaphylactic shock

A
  • low blood pressure from dilation of blood vessels
  • temporarily controled by epi injection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

anaphylaxis - CNS symptoms

A
  • lightheadedness
  • loss of consiousness
    confusion
    headache
  • anxiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Anaphyllaxis - respiratory symptoms

A
  • SOB
  • wheezes
  • hoarsness
  • pain with swallowing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Anaphylaxis- GI

A
  • cramps abdominal pain
  • diarrhea
  • vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Rh incompatibility - hypersensitivity type II
- 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
Hypersensitivity III reactions - antibody
- 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
Hypersensitivity III reacitons - consequences
- vasculitis (seen in autoimmune disorders) - kidney damage (acute glomerular nephritis)
28
Post streptococcal glomerulonephritis (6)
- 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
Type IV reactions - antibody?
cell mediated
30
Type IV hypersensitivity reactions
- 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
Type IV hypersensitivity reaction - examples (2)
- Tuberculin skin test - Poison Ivy
32
Self antigen
antigen expressed on your own cells
33
auto-reactive cells
- T or B cells that bind to a self antigen
34
Autoantibody
antibody that binds to a self-antigen
35
Immune tolerence
- self tolerence - delete self-reactive immune cells
36
Central tolerance
deletion of self-reactive T cells in the Thymus and B cells in the bond marrow are eliminated
37
Peripheral tolerance
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
Autoimmune - defined
when the body loses self tolerance = attacks own cells
39
Factors that influence autoimmunity (3)
- genes - environment (trigger) - gender (mostly women)
40
environmental factors for autoimmunity (4)
- infection - toxins - stress - food
41
infection and autoimmunity - strep EX
- antibodies for certain strep antigens can resemble self-antigens on heart + kidney = innflamation of heart and kidney
42
classification of autoimmunity (2)
- organ specific autoimmune diseases - systemic autoimmune diseases classifications can overlap
43
Organ specific autoimmune diseases + example
- target antigen present in a specific organ - EX Grave's disease, hasimotos, type I diabetes, Multiple sclerosis
44
Systemic autoimmune diseases + examples
- target an antigen present on many organs- - EX: systemic lupus erethomatosis, rheumatoid arthritis
45
Grave's disease - hyperthyroidism
- 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
Type I diabetes mellitus - autoimmune
- 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
Multiple sclerosis
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
Treatment for autoimmune disease (6)
- 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)