1
Q
Types of Alterations in Immune Function (2)
A
- Excessive - autoimmunity, hypersensitivity
2. Deficient - immunodeficiency
2
Q
Autoimmunity
A
Recognizes self antigens as foreign:
- tolerance of self-antigens in bone marrow and thymus
- passes multiple check points if non-tolerant cells escape
3
Q
Types of Autoimmunity that Occur (3)
A
- Antigen mimicry (cross-reactive antigens)
- Release of sequestered antigens
- Lymphocyte defects (T/B cells)
4
Q
Autoimmunity Genetic Factors
A
- Affects women more than men (7-10x more in some cases)
- MHC Associated - MHC antigen DR4 (causes 63% of rheumatoid arthritis and 73% of systemic lupus cases)
- Genetics is important for autoimmunity, but so is environment
5
Q
Antigen Mimicry
A
- Similarity between pathogen and self antigens
- Several examples of this autoimmunity
6
Q
Guillain-Barre Syndrome
A
- Campylobacter jejuni bacterial infection
- Only occurs in certain strains reacting with certain individuals
- Makes antibodies against myelin sheath of nerve which attacks nerves and affects communications
- Affects myelin sheaths of PNS and causes ascending paralysis (starts at feet and moves upwards)
- Signs appear 1-8 weeks after etiological event
- Peaks at 10-14 days and then descends gradually and causes long-term disabilities
7
Q
Rheumatoid Fever
A
- Group A Streptococci
- Example of sequaelae after Group A infection
- Mimicry between M protein and myosin of heart
- Damages heart valves, subsequent attacks lead to further damage
8
Q
Celiac Disease
A
- Cross-reactivity between gluten proteins and small intestine proteins
- Attacks damage villi and microvilli
- Decreases absorption, weight loss, anemia, diarrhea, and pain are all symptoms of Celiac Disease
9
Q
Sequestered Antigen Release
A
- Antigens hidden during lymphocyte maturation: cornea, testicles, and brain
- Antigens are exposed and released after infections, injuries, or surgeries
- Leads to cases like corneal metling
10
Q
Lymophocyte Defects
A
- Thymus gland defects - site of maturation for T-Cell, its breakdown of tolerance leads to autoimmunity and can cause things like lupus and diabetes
- B-Cell defects also leads to breakdown of tolerances
11
Q
Multiple Sclerosis
A
- Autoimmune attacks myelin sheaths and oligodendrocytes that make the myelin for CNS neurons
- Etiology is complicated and can be T/B cell related or antibody related
- Impacts nerve transmission - decreased or blocked
12
Q
Multiple Sclerosis + Genetics
A
- more common in females
- Northern European ancestry
- MHC antigen association (higher rates in identical twins than fraternal)
13
Q
Multiple Sclerosis + Environment
A
- More common above the 37th parallel
- Viral infections may trigger it
- Environmental toxins or community clusters could also be an explanation but the clusters are too small to analyze
14
Q
Hypersensitivity
A
- Damaging reactions of normal immune response
- Antibody-mediated: Types I, II, and II
- T-cell Mediated: Type IV
15
Q
Type I Hypersensitivity
A
- Immediate hypersensitivity (minutes
- IgE-mediated response to allergens
- IgE prime mast cells (500,000 coat the cell)
- Mast cells and basophils release mediators
- Connected to seasonal allergies, asthma, hives, and anaphylaxis
16
Q
Type I Hypersensitivity + Genetics
A
- T-cell must recognize allergens and mount IgE response
- Children born to allergic parents and more likely to be allergic
17
Q
Type I Hypersensitivity Therapeutic Strategies
A
- Antihistamines primarily
- Immuno-therapy
18
Q
Type II Hypersensitivity
A
- Antibodies target tissue-specific antigens
- Many diseases fall under this category
- Cell damage and lysis by complement and cellular (NK cells, macrophages, dendritic cells, etc) components occurs
19
Q
Acute Transfusion Reaction
A
- Type II
- IgM antibodies react to environmental antigens in early life
- ABO mismatch
- Includes fever, chills, nausea/vomiting, hypotension, hematuria, anaphylaxis, and death
20
Q
Delayed, Acquired Reactions
A
- Type II
- Antigen other than ABO
- Anamnestic - multiple transfusions, most common
- Primary - first transfusion (delay in antibody production)
21
Q
Myasthenia Gravis
A
- Type II
- Autoimmunity at neuromuscular junction
- Antibodies bind to ACh receptors and block ACh binding
- Complement activation destroys membrane
- Symptoms: severe muscle weakness, double vision, drooping eyelids
22
Q
Graves Disease
A
- Type II
- Antigens target thyroid stimulating hormone receptors
- Overproduction of thyroid hormones
- Hyperthyroidism symptoms - enlarged thyroid, hyperactive and tremors, tachycardia, weight loss with normal eating, heat sensitivity, bulging eyes
23
Q
Acute Graft Rejection
A
-Type II
Host v.s Graft
-Introduction of foreign tissue antigens
-Recipient immune response against foreign tissue antigens
-Antibodies, complements, effector cells attack
-Attack transplant tissue or organ
-Inflammation and hemorrhaging (rejection)
24
Q
Graft v.s. Host
A
NOT TYPE II
- Stem cell/bone marrow transplants
- Donor immune cells recognize recipient antigens as foreign
- “Autoimmunity” reaction against recipient tissues/organs
- Severe and wide-spread complications
25
Type III Hypersensitivity
- Immune complex disease
- Antibodies don't directly attack our cells
- Antigen-antibody complexes deposit in tissues
- Complement activation leads to inflammation and the inflammation causes the damage
- Tends to occur more in areas where the agglutination gets lodged, ex: blood vessels, heart, skin, joints, kidneys
- Also targets sites of high blood pressure, turbulence, and cellular junctions so it can stick to things
26
Post-Streptocoocal
- Type III
- Glomerulonephritis
- Another sequelae - Group A Steptococcus Pyogenes
- Usually starts 10-14 days after infection
- Hypertension, hematuria, proteinuria, flank pain, and possible joint pain can occur
27
Systemic Lupus Erythematosus
- Type III
- Aka SLE
- Auto-antibody reaction against DNA, RNA, and nuclear proteins (unusual since nucleic acids aren't usually antigenic
- Immune complexes deposit in tissues
- Glomeruli and dermal-epidermal junctions are most common place to deposit
- Cell damage releases more nucleic acids and more damage occurs from more complexes forming
28
Type IV Hypersensitivity
- Delayed hypersensitivity (24+ hours)
| - T cells and macrophages respond - NO ANTIBODIES
29
Contact Hypersensitivity Examples
- Poison Ivy
- Poison Oak
- Metals
- Latex
- Cosmetics
- Dyes
30
Tuberculin Hypersensitivity
- Previous expose to Mycobacterium tuberculosis allows for tuberculin test
- Inject under skin and in 48-72 hours a type IV reaction develops
- Reaction is usually short lived due to small dose but some reactions are severe
- May not occur in HIV patients
31
Granulomatous Hypersensitivity
- Type IV
- Primary defense against intracellular pathogens
- Failure of macrophages to kill
- Many cell types called in to wall off infection and create a granuloma, macrophage is main cell utilized
32
Deficient Immune Response
- Decrease in 1+ components of immune system
- 2 categories: Primary (inherited) and Secondary (acquired)
- Detection - unusual, recurrent, or unmanageable infections
33
B-Cell/T-Cell Combined Deficiency
- Severe Combined Immunodeficient Disorder (SCID)
- Failure of ALL WBCs to develop appropriately
- Absence or dysfunction of T-Cells: impacts cellular and humoral response, B-Cell may be present or absent but they don't function
- Mechanism primarily focused on defective lymphocyte receptors
* *Boy in the Bubble**
34
Wiskott-Aldrich Syndrome
- Genetic mutation in WASP gene
- lack of WASP (protein) that is produced by hematopoietic cells and is essential for maturation
- Impacts T cells and the production of IgM
- Infants can't fight bacterial infections
- Passive antibody and transplants utilized to treat
35
T-Cell Disorders (2)
1. DiGeorge Syndrome
| 2. Chronic Mucotaneous Candidiasis
36
DiGeorge Syndrome
- Genetic disease impacting migration and development of multiple tissues in fetus
- Thymus hypoplasia with partial or complete loss of function
- Many defects of body
- Claims that B-Cells function normally
37
Chronic Mucotaneous Candidiasis
- Defective IL-17 receptors and production
- TH17 cells specifically involved
- Manifests in severe infections with candida species and infection with staphylococcus species
38
B-Cell Disorders (2)
1. Selective IgA Deficiency
| 2. Bruton's X-linked Agammaglobulinemia
39
Selective IgA Deficiency
- Most common
- IgA producing B-cells don't mature into plasma cells
- No secretory IgA for respiratory, gastrointestinal, or genitourinary infections
40
Bruton's X-linked Agammaglobulinemia
- Lack of B-cell differentiation or maturation
- No antibodies in serum
- Extracellular pathogens have less immune response like Strep, Staph, and haemophilus
41
Secondary Immunodeficiency
- Decreased immunity due to outside factors: infections, hospitalization, pharmaceuticals, cancer chemo, nutrition
- Decreased immunity due to internal factors: neuro-endocrine-immune system interactions and pregnancy
- Age related lack of immunity (infants and geriatrics)
805
flashcards
Decks in class (18)
# Cards
-
Lecture 1 (Quiz 1)32
-
Lecture 2 (Quiz 2)50
-
Lecture 349
-
Lecture 4 (Cut off for Exam 1)47
-
Lecture 4 - Sleep Apnea8
-
Lecture 551
-
Lecture 6 (Quiz 3)48
-
Lecture 6 - Inflammation + Fever9
-
Lecture 7 (Cut off for Exam 2)75
-
Lecture 841
-
Lecture 940
-
Lecture 1020
-
Lecture 1136
-
Lecture 12 (Cut off for Exam 3)24
-
Lecture 1336
-
Lecture 1444
-
Lecture 1533
-
Lecture 16 (Cut off for Exam 4)49
