Week 3 Flashcards
1
Q
Type I Hypersensitivity
A
- IgE mediated
- Onset within 1 hour
- Ie) anaphylaxis
2
Q
Type II Hypersensitivity
A
- IgG/IgM or cytotoxic mediated
- Onset hours to days
- Ie) hemolytic anemia
3
Q
Type III Hypersensitivity
A
- Immune complex mediated
- 1-3 weeks
- Ie) serum sickness or SLE
4
Q
Type IV
A
- T cell mediated
- Onset days to weeks
- Ie) rash or SJS
5
Q
Th 1 Cell-Mediated Allergens
A
- Contacted materials
- Plant leaves
- Industrial products made from plants
- Synthetic chemicals in industrial products
- Metals
6
Q
IgE-Mediated Allergen
A
- Proteins
- Foods
- Plant pollens
- Drugs
- Insect products
- Mold spores
7
Q
Atopic
A
- Genetic tendency to develop allergic disease
- Associated with heightened immune response to common allergens
- Inhaled/food allergens
- 1 atopic condition = more likely to develop another
8
Q
Common Atopic Conditions
A
- Atopic asthma
- Allergic eczema
- Hay fever
9
Q
Allergy March
A
- Natural history of atopic manifestation
- IgE antibody responses clinical symptoms persist over years/decades
- Spontaneously omit with age
10
Q
First Exposure (Type I Reaction)
A
- Called sensitization
- Produce IgE Abs to the allergen
- Symptoms mild
11
Q
Re-Exposure (Type I Reaction)
A
- Allergen binds IgE
- Activates mast cell
- Releases histamine & cytokines
- Allergic reaction - more severe reaction
12
Q
First Exposure Process (Type I Reaction)
A
- Antigen presenting cell phagocytizes & processes antigen
- APC presents antigenic determinant to T cell
- IL-4 from T cell stimulates B cell
- B cell becomes plasma cell - secrete IgE
- IgE binds to mast cells, basophils, eosinophils
13
Q
Upper Resp Tract Allergies
A
- Overproduction of mucus, sneezing, nasal congestion
- Rhinitis (hay fever)
14
Q
Lower Resp Tract Allergies
A
- Bronchial smooth muscle contraction
- Asthma
15
Q
Skin Allergen
A
- Local inflammation
- Urticaria - hives
16
Q
Bloodstream Allergen
A
- Systemic inflammation
- Anaphylaxis
17
Q
GI Allergen Ingestion
A
- Intestinal smooth muscle contraction - gastroenteritis (V/D)
- Systemic inflammation - allergen enters blood if it is rapidly absorbed - anaphylaxis
18
Q
Anaphylaxis
A
- Medical emergency
- Life-threatening allergic reaction
- Injected directly into blood/rapid absorption
- Level of severity depends on level of previous sensitization
- Food allergies most common
19
Q
Anaphylactic Shock
A
- Fast/slow HR
- Low BP
20
Q
Epinephrine
A
- Temporary control of anaphylaxis
- Rapidly increased BP
- Causes vasoconstriction
21
Q
Anaphylaxis Diagnosis
A
- Increased serum IgE levels
- Biopsy - GI related intolerances
- Skin prick/patch test
- Allergens show local inflammation at injection site when person is allergic
22
Q
Desensitization Therapy
A
- Allergy shots - gradually increase dose
- Divert immune response from IgE tp IgG
- Different route of entry for allergen
- Long term treatment to decrease symptoms
23
Q
Desensitization Risk
A
- Reactions possible
- Mild (local) few hours of injection
- Systemic reactions - 30 mins of injection
24
Q
Type II Hypersensitivity Reaction
A
- Opsonization & phagocytosis
- Antibody dependent cellular cytotoxicity
- Complement activation
- Mediated by IgG or IgM antibodies
25
Cellular Cytotoxicity Process
IgG binds to surface antigen on infected cell NK then kill infected cell
26
Complement Activation Process
1. IgG binds to complement
2. Activating cell causing lysis
3. Recruitment of neutrophils & monocytes
4. Causing inflammation & tissue damage
27
Rh Factor
- Protein on red blood cells
- Inherited
- Most people Rh+
28
Rh Incompatibility
- Condition during pregnancy
- Rh+ father & Rh- mother
- Blood from baby (Rh+) crosses into blood stream from mom
- Mother creates Rh antibodies
- Antibodies don't usually cause issues during 1st pregnancy
- More likely to cause problems in later pregnancies
- Rh antibodies cross placenta & damage fetal RBCs
- Leads to hemolytic anemia in baby
29
RohGAM Injection
- Given to pregnant women Rh-
- Immunoglobulin to prevent antibody formation against baby's foreign antigen
30
Type III Hypersensitivity
- Immune complex mediated
- Mediated by formation insoluble antigen antibody complex
- Activate complement system
- Produce localized inflammation
- Produces damage when in contact in vessel lining/deposited in tissue
- Once deposited immune complexes illicit inflammatory response by activating complement
- Responsible for vasculitis, kidney damage
31
Type III Process
1. Immune complexes deposited in wall of blood vessel
2. Presence of immune complexes activates complement & attracts inflammatory cells (neutrophils)
3. Enzymes release from neutrophils cause damage to endothelial cells from basement membrane
32
Post Streptococcal Glomerulonephritis
- Following streptococcal infection - group A (neptorgentic)
- Impacts nephriti and small vessels of kidneys
- Children 1-2 weeks after sore/strep throat, skin infection by strep impetigo
- Causes infiltration of leukocytes & proliferation of other cells in glomerulus
- Impairs capillary perfusion & glomerular filtration rate
33
Post Streptococcal Glomerulonephritis Complications
- Renal failure
- Acid/base imbalance
- Electrolyte Abnormalities
- Fluid volume overload
- Edema
- Hypertension
34
Post Streptococcal Glomerulonephritis Symptom Triad
- Hematuria (tea coloured)
- Edema
- Hypertension
35
Type IV Hypersensitivity
- Cell-mediated
- Delayed type hypersensitivity
- T-cells activated by antigens
- Occurs over 24-72hrs
- Previous exposure to antigen to mount immune response to 2nd exposure
36
Type IV Process
1. Antigen introduced into subcutaneous tissue & processed by local antigen presenting cells
2. Th1 effector cell recognizes antigen & release cytokines which act on vascular endothelium
3. Recruitment of T cells, phagocytes, fluid, protein to site of antigen injection causes visible lesion
37
TB Skin Test
- Inactivated TB injected under the skin
- Previous exposure - develop local redness in 8-12 hrs
- Perivascular accumulation of CD4+ T cells, macrophages
- Local secretion of cytokines = increased vascular permeability
- Causing local redness & swelling
- Measure reaction of induration not surrounding redness
38
Normal Immune Response
1. Invader (virus) enters body
2. Lymphocytes create antibodies to fight invader
39
Autoimmune Disease
- Immune system creates antibodies that attack own cells
- Breakdown in immune system to differentiate between self & non-self
- Results in destruction of own cells/organs
- 5-10% of population
- Chronic with relapses & remissions
- Damage is progressive
40
Causes of Autoimmune Disease
- Foreign substance resembles bodily substance
- Normal body cells become altered
- Lymphocytes malfunction & make abnormal antibodies
41
Self Antigen or Autoantigen
Antigen expressed on your own cells
42
Autoreactive Cells
- T/B cells that bind to a self antigen
- BAD
43
Autoantibody
- Antibody that binds to a self antigen
- BAD
44
Self Tolerance
Ability of the immune system to recognize self-produced antigens as a non-threat while appropriately mounting a response to foreign substances
45
Central Tolerance
- Eliminating any developing T/B lymphocytes that are autoreactive
Thymus - T cells
Bone marrow - B cells
46
Peripheral Tolerance
Immunological tolerance developed after autoreactive T&B cells mature and enter periphery
47
Autoimmunity
- Result of loss of self-tolerance
- Inheritance of susceptibility genes
- Gender - women 5:1
- Trigger event: alter immune state
48
Trigger Event
Microbe shares immunological epitope with host
49
Environmental Factors
Promote activation of self-reactive lymphocytes
50
Autoimmunity Classification
Area of overlap of organ specific & systemic characteristics
51
Organ Specific
- Response targets antigen present in specific organ
- Graves disease
- Hashimoto's thyroiditis
- T1D
- MS
52
Systemic Characteristics
- Antigen present at many different sites - involve multiple organs
- Rheumatoid arthritis
- Systemic scleroderma
- Systemic lupus erythematosus (SLE)
53
Graves Disease - Hyperthyroidism
- Immune system attacks thyroid - too much thyroid hormone produced
- Produce TSH receptor antibodies (TSI)
- Abs bind to TSH receptor
- Constant over secretion of T3, T4
54
Healthy Thyroid
- TSH secreted by pituitary
- TSH binds to TSH receptor on thyroid cells
- Stimulates release of thyroid hormones (T3, T4)
- Inhibit TSH production
55
Insulin-Dependent Diabetes Mellitus - Type I Diabetes
- Chronic autoimmune destruction of insulin producing beta cells in pancreas
- Autoreactive CTLs kill insulin-producing B-cells in pancreas
- Results in reduced insulin production, hyperglycemia
- Unknown what triggers inflammation in the pancreas
- Clusters in spring & fall
56
Multiple Sclerosis - MS
- Myelin sheath of nerve fibers in brain & spinal cord destroyed by autoreactive T cells
- Disrupts electrical signals & causes paralysis
- Unclear what triggers myelin damage & CNS inflammation
- Inflammatory process
57
Autoimmune Disease Treatments
- Treatment focus on mechanism
- Immunosuppression
- Plasmapheresis
- Block MHC with similar peptide
- Use antibodies that block B cells/T cells
- Disease specific treatments
58
Immunosuppression
- NSAIDS
- Prednisone
- Cyclosporin A
59
Plasmapheresis
- Remove antibodies
- Temporary fix