Immuno Final Flashcards
(78 cards)
1
Q
What is hypersensitivity?
A
Exagerrated or an inappropriate immune response caused by inflammatory rxn and tissue damage. It is uncertain why it happens
2
Q
What are the two classifications of hypersensitivity based off of symptoms?
A
- Immediate - symptoms occure directly following exposure to an allergen (2-8hr)
- Delayed - symptoms delayed 3-4 days following allergen exposure. Prostaglandin response
3
Q
What are the classifications of hypersensitivity based off of immunoglobulins? What are examples of these rxn.
A
- Type 1 - IgE, IgG4 (more rare than IgE) - ie hay fever, anaphylaxis
- Type 2 - IgM, IgG, complement - Ab mediated (blood incompatibilities)
- Type 3 - Immune complexes secondary to macrophages, IgG, complement (RA, serum sickness)
- Type 4 - Ab independent rxn. T cells - ie TB skin test
Type 1-3 are immediate rxn, type 4 are delayed rxn
4
Q
What are the two severities of type one hypersensitivity?
A
- Atopic - chronic localized allergic reaxtion (asthma, hay fever)
- Anaphylaxis - systemic allergic rxn - airway obstruction, circulatory collapse, potentially lethal
5
Q
What are Type 1 Hypersensitivity risk factors?
A
- Hereditary - genes which favor an over productoin of IgE/ mast cells
- Age/ Infection - molecular mimcry, cellular abnormality and age can cause new allergies to arise
- Geography - environment can contribute to allergens (ie exposure to mold/ pollen/ pollutants)
6
Q
Do elderly have decreased allergies?
A
Incidence and severity tend to decrease with age, but elderly tend to suffer from pre-existing allergies. Chronic allergy can result in irreversible airway damage. However, in the elderly this can be dt damage
7
Q
What are Type 2 Hypersensitivity rxns?
A
IgM, IgG and Complement
- Includes drug rxns(penecillin) - penecillin (hapten) binds to RBC surface proteins. Abs bind to the RBC antigen with CF. Results in hemolysis
- Molecular mimicry - Abs against streptococcus target RBCs. Abs target cardiac proteins which lead to rheumatic fever
- Idiopathic thrombocytompenia - 60% of platless are bound by IgG
8
Q
What are type 3 hypersensitivies?
A
Involves Abs (IgG), but there is more Ag than Ab (ie in the log phase of infection)
Abs form chains of Ab-Ag complexes which accumulate in the tissues (kidney and liver most frequent). Clogs up the tissue
9
Q
What can cause excess amounts of Ag in the blood?
A
- Serum sickness: large amount of foreign Abs in blod stream
- Systemic lupus erythmatous - Ab + Ag complexes form. Instead of clearing, they are deposited around the body (systemic)
- Rheumatoid arthritis - Ab-Ag complexes deposited between joints
10
Q
What are Type 4 hypersensitivies?
A
T cell specific immuno response following the Tc/ MH1 pathway. Delayed hypersensitivity (24-72 hrs)
11
Q
What are examples of Type 4 hypersensitivities?
A
- IDDM - T cells target the beta cells of the pancreatic islet (may also have partial B response)
- MS - T cells target specific proteins of myelinated oligodendrocytes, leading to death of these cells
- RA - T cells target the synovial membrane of the joint
12
Q
What are allergens?
A
Antigens which elicit an exaggerated immune response
13
Q
What are characteristics of immunogens?
A
- Not haptens
- Not self
- Static, not repeating structures
14
Q
Can babies have allergic rxns?
A
No, they do not have IgE. Can have food intolerances
15
Q
Are the organs affected by allergies the same as the portal of entry?
A
Not necessarily
16
Q
What are the four types of allergens?
A
- Inhalant - found in the air. May be animal hair / dander, feathers, saliva, dust mite feces and exoskeleton
- Injestant - consumed food or drug
- Injectant - vacinnes, serum, venom, drugs, bee stings (Bees = natural source)
- Contactant - latex, detergent, cosmetics
17
Q
What causes hay fever, asthma and eczema? What are S&S?
A
- Hay fever - Caused by pollen/ mold. Causes milkd bronchioconstriction, nasal congestion, sneezing, coughing, mucous, itchy, red and teary eyes
- Asthma - caused by inhaled allergen/food/infection. Cuases laboured breathing, coughing, wheezing. If mucous plugs form in resp tract, could cause long term damage
- Eczema - Caused by ingestion, inhal, contact. Causes skin lesions and irritation
18
Q
What are common non allergic reactions which are mistaken for allergic reactions?
A
- Food intolerance - ie lactase deficiency
- Idiopathic food bourne illness - (MSG - IBS, migraine), (Sulfites - asthma)
- Anaphalactoid reactions - appear to be an anaphylactic reactions but no IgE - scromboid fish
19
Q
How can scromboid fish induce an anaphylactoid reaction?
A
Scromboid fish have histadine on them. When scomboid fish spoil (>16 C), bacteria converts histadine to histamine
(tuna fish)
20
Q
How does blood typing work? What antigens are on which cells?
A
Blood typing refers to recognizing the surface antigens on RBCs.
May be antigen A or B. (O is the absence of any antigens)
A+ RBCS have A antigens, B+ RBCs have B antigens, AB+ RBCs have AB antigens
21
Q
How do blood type agglutination tests work?
A
- Pt RBCs are isolated
- Using monoclonal anti-A and anti-B Abs, mix cells and Abs
- If the cells clump, then antigen is present
(If anti A is used on an A+ RBC, they will clump together b/c antigen is present)
22
Q
What are the following blood typing results?
A
- A
- O
- B
- AB
23
Q
What are type 2 hypersensitivities? How do they work?
A
Naturally occuring Abs
24
Q
what is Rh factor? Who has it?
A
Antigen on RBCs, but not sensitive enough to mount an IgM response (first response)
Requires IgG response to cause damage (secondary exposure.
85% caucasians and 99% asians are Rh +
25
## Footnote
If mom is Rh- and dad is Rh+, is there a chance the the fetus to be Rh+ ? why does this matter?
## Footnote
If baby has Rh+, if the placenta breaks, mom can be exposed to baby blood. blood is recognized as foreign and mom has a response (IgM - cannot cross placental barrier). Mom creates immunological memory (ani-Rh IgG) However, on baby 2, IgG responds, which can cross the placenta barrier and results in hemolytic anemia/ death of the fetus dt Ag-Ab-CF
26
## Footnote
What is RhoGAM?
Anti-RhD IgG immunoglobulin which gives passisve immunity to mom
27
## Footnote
when is RhoGAM given? How does it work?
## Footnote
it is given at 28 weeks and 72 hours delivery
Rhogam circulates maternal blood and searches for fetal RBCs and neutalizes them
28
## Footnote
Is there a risk of RhoGAM with the fetus?
## Footnote
Rhogam may cross the placenta and may cause fetus to react. However, it is given in such low dose that it does not cause significant fetal hemolysis
29
How does streptococcus cause kidney damage? What type of hypersensitivity is this?
Excess Ab-Ag complexes circulate in the blood and get fltered by the kidneys. They get lodged in the glomeruli and attract cytokines, neutrophils and other inflammatory factors. The following inflammation causes damage to the kidneys
30
How do type III hypersensitivities work?
1. Ab binds to exess Ag
2. Circulating Ab/Ag complexes lodge in the basement membrane
3. Complement activation causes inflammation
4. Attracts neutrophils, enzymes, cytokines which causes tissue damage
31
What are the types of hypersensitivities with drug and vaccine allergies?
1. Type 1 HS - Drug illicts an abnormal IgE reaction
2. Type 3 - Serum sickness and an arthus reaction in pre-sensitized individuals
32
What is serum sickness?
Often a result after delivering plasma from polyclonal Abs. Body recognizes proteins in the plasma as foreign and produces Abs against proteins.
Forms ab-ag complexes which are deposited in the lymph nodes and joints. Results in swelling, rash, fever. May result in chronic renal failure
33
What is an arthus reaction?
Type 3 hs
acute response (pain/ inflammation) at the site of injection. Localized ab/ag deposit at site which can lead to necrosis of the tissue
34
What are type 4 reactions? Why are they special?
Involves Tc cells which recognize self antigens as foreign. Delayed (72 hrs after exposure- time for Tc cells with specific epitopes to divide) still requires prior sensitization
35
How does the tb test take advantage of type 4 hs?
* people exposed to TB become allergic to the tubercullin protein
* TB protein induces inflammation at the site of injection if previous exposure
36
What are other diseases which can be tested for using type 4 hs?
Leprosy, syphilis, yeast infection
37
How does the TB test?
1. TB is injected
2. Immune system is recruited to the injection site
3. Tuberculin is absorbed by MHC1 or phagocytized and presented by MHC2
4. If person is pre-sensitized - T cell response, INF & TNF cause chemotaxis and inflammation
38
What is poisen ivy? What does cause? How is it treated?
Poisen ivy produces urishol oil which is higly immunogenic
Normally, people are sensitized in childhood. Presented by MHC1 which ilicits a th1 response
Results in a rash and blisters
Tx with IL2s (cyclosporin)
39
What is autoimmunity?
When an individual's immune system reacts against self antigens. May be dt Type 1 &2 hs (formation of autoantibodies)
May be dt Type 4 HS (autoreactive Tc)
Can be systemic or organ specific, depending on the expression of the antigen
40
What is Cehiak-Higashi Syndrome?
Autosomal recessive disease which decrease the ability of phagocytes (basophils, eosinophils and neutriophils) to phagocytize dt inability to form phagolysosomes (granules leak into cells)
Results in albinoism, peripheral neuropathy, and increased infections.
Life threatening during outh
41
What are the differences between primary and secondary infections?
**Primary:** Congenital - present at birth. dt genetic/ development error
**Secondary**: Acquired- after birth. Dt disease/ age
42
What happens if you can't produce hematopoetic stem cells?
You will not be able to produce any blood cells (RBCS, WBC, lymphocytes)
43
What are diseas which combine B & T cell defects? What cell do they target?
SCID (severe immunocompromised disease)
Wiskott-alderitch syndrome
ataxia- telangiectasis
These diseases target Myeloid stem cells
44
What is hypogammaglobulinemia? hypoalphaglobilinemia?
Hypogammaglobulinemia - deficiencty of IgG
Hypoalphaglobenimia - deficiency of IgA (most common)
45
What are the similarities of DiGeorge syndeome and congenital agammagolbulinema?
Failure of the lymphocytes to mature
46
What are the results of B cell defects? Who are most often affected
Affect anti-body expression. In some cases, single Ig classes are diminished.
Many cases, these B cell deficiencies are x linked recessive (men get them)
47
What are IgG deficincies? How is it treated?
Absent: agammaglobulinemia. Deficiency: hypogammaglobulinemia
Evident after 6 mos of birth (when mom's IgG are diminished). At risk for recurrent bacterial, protoazoan and viral infections outside of the cell.
Intravenous immunoglobulin treatment (IVIG) q3-4weeks for rest of life, pooled from thousands of blood donor.
48
What are IgA deficiencies? What is the result? How are they treated?
Most common Ab defect
Results in recurrent resp and GI infections
IgA is not found in high levels in blood b/c it is secreted. Therefor IVIG is not an effective tx
49
What is an example of T cell defects? What are risks? treatments?
ie DiGeorges syndrome - inability to combat intracelluar diseases dt abormal thymus (no place for T cells to mature)
ie chickenpox, mealsels and mumps - may be fatal. Attentuated vaccines may also be harmful.
There is decreased risk of transplant rejection
Tx = thymus tissue transplant
50
What is SCIDS?
Severe combined immunodeficiencies
Complete absence of lymphocytes and lymphocyte stem cells
Extremely rare. Extremely fatal - usually dies from opportunistic infections within days of birth
51
What are the different subtypes of SCIDs?
* ADA-SCIDs (adenosine deaminiase deficiency). Toxins build up within and kill lymphocytes
* Bare lymphocyte syndrome
* Type 1: Lack MHC 1
* Type 2: Lack MHC 2
52
What are the purpose of SCIDs mice?
Help understand lymphocyte maturation and how to combat SCIDs
53
What is HIV? What cells does it affect?
Virus which binds to the CD4 complex. Virus targets dendrites then spreads to organs where they bind to T helper cells
Monoctyes, dendrites, macrophages and Th cells express Cd4
HIV affects both the innate and adaptive sysrem
54
What is the relationship between HIV, Tb, leprosy and malaria?
All result in secondary (acquired) immunodeficiency
55
How does TB result in immunodeficiency?
Infects alveolar macrophages and overcomes them. T cells circle disease to capture TB (granuloma) but TB can excape
56
How does leprosy result in ID?
Infects macrophages, like TB; reduces T cell recognition of host cell
57
How does malaria result in immuno D?
Evades the immune system by interfering with the interactions between APC and T cells
58
What are examples of organic diseases which result in immunoD? How??
1. Leukemia - overproduction of immature leukocytes impaires the proper function of the legitamate immune cells
2. Malnutrition - Thinning of physical barriers. Body lacks specific micronutrients which are involved in specific immunological responses (Vit A & D, Zinc)
59
What micronutrients help maintain the immmune system?
1. **Vit A & D** - Assists in lymphocyte proliferation and differentiation
2. **Zinc** - required for the maitenence of B & T cells
60
What factors influence auto-immunity?
1. Genetics
2. Environmental factors (infectious agents / drugs & chemicals)
3. Aging
61
How do genetics influence autoimmunity?
Cases of specific autoimmune diseases tend to cluster in families. May be dt specific MHC/ HLA types
62
Why would evolution permit the formation of autoantibodies?
1. **Custodial lymphocytes** - low levels of autoreactive Abs/ T cells eliminate old cells and cell debris
2. **Sequestered antigen theory** - some tissues are immunologically privilidged (ie blood-brain barrier) and are not attacked. If these tissues are exposed during aging / trauma - they are recognized as foreign
3. **Forbidden clones** - failulre to actively perform clonal deletion could allow for autoreactive lymphocytes to develop
63
How do environmental factors cause auto-immunity?
Infectious agents with similar antigens to self can influence the immune system to attack self antigens
ie Streptococcus . antigens are similar to myocytes which can result in rhematic fever
64
What are some diseases that result in autoab cross reactivity?
* Chlamydia - arthritis
* Shigella/ samonella/ campylobacter
65
What are examples of chemicals/ drugs which cause autoimmunity?
1. Hydralazine - anti-HTN. Caused lupus like symptoms by binding and modifying nuclear proteins and DNA. When these cells ages, these molecults are autoreactive and progressively stimulate auto AB production
2. Hormones - mechanism unknown. Autoimmunity more common in females (10:1). More susceptible during child bearing
66
How can aging affect autoimmunity?
Increase with age. May be dt senesence (aging) of the immune regulatory function of break down of anatomical battiers.
Older cells may have increased CF on the surgace
67
What is sympathetic opthalmia?
1. Traume from eye results in the release of sequestered intraoccular antigens
2. intraoccular Ags are carried to lympho nodes and activate T cells
3. Tc cells return to the eyes and attack both eyes
68
What is SLE?
Systemic lupus erythamatous - one of the most severe chronic autoimmune diseases
Characterized by a butterfly rash across the face
Abs are produced against several tissues in the body
69
What is the pathophysiology of SLE? What type of hypersensitvity is this?
Anti-nuclear antigen (ANA) Abs enter the cell and localize the nuclie. (normally these Abs do not enter the cell)
This can be a type 2 rxn (abs do damage to a wide array of tissues)
Type 3 - Ab/ag complexes accumulate in the basal membrane. Results in kidney failure, joint pain and inflammation
Sunlight stimulates SLE (sunlight may boost the immune system)
70
What is Graves disease?
Endocrine autoimmunity
Auto Abs bind to secretory receptors in the thyroid. Results in overproduction and secretion of thyroxin. Results in hyperthyroidism.
tx with radioactve iodine (accumulates in thyroid and kills thyroid cells)
71
What are S&S of hyperthroidism?
Goiter, heat intolerance, hand tremor, irritability, nervousness, warm, moist skin, weight loss, tachycardia, opthalmopathy, extremity and facial edema
72
What is hasimoto's diease?
AutoAbs and t cells destroy thyroid cells. Causes hypothyroidism
73
What causes IDDM?
Autoimmune response which targets pancreatic beta cells which produce insuline. Most common in individuals under 30.
Some genetic predisposition
74
What is MS?
Multiple sclerosis
Normal: electrical impulses are transmitted rapidly along axons because they are insulated by myelin
MS - autoimmune response which targets the myelin sheath. Results in muscular weakness and tremors
75
What is autoimmune RA?
Chronic, recurrent and systemic inflam disease primarily involving the joints
Abs can (themselves) can be Ags
Synovial B cells produce IgG which is recognized as foreign which stimulates the production of anti-igG abs (aka rhematoid factor)
IgG-Rh complexes form + CF = classical complement pathways
results in inflammation, cell lysis in the joint
76
What is Rheumatoid factor?
An autoreactive IgM. Results in an influx of leukoctes into the synovial space.
Frustrated phagocytosis occurs - damage caused by protease and collagenase
77
How are autoimmune diseases tx?
Organ specific AD - metabolic control (insulin, anti-thyroid drugs)
Systemic AD
* Antiinflammatories (NSAIDS/ steroids)
* Immunosupression -
* t cell - IL2 ihibitors (cyclosporin)
* B cell Rituximab (destroys CD20+ cells)
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