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805 > Lecture 8 > Flashcards

Lecture 8 Flashcards

Alterations in Immune Function

1
Q

Types of Alterations in Immune Function (2)

A
  1. Excessive - autoimmunity, hypersensitivity

2. Deficient - immunodeficiency

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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
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3
Q

Types of Autoimmunity that Occur (3)

A
  1. Antigen mimicry (cross-reactive antigens)
  2. Release of sequestered antigens
  3. Lymphocyte defects (T/B cells)
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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
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5
Q

Antigen Mimicry

A
  • Similarity between pathogen and self antigens

- Several examples of this autoimmunity

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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
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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
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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
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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
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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
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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
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12
Q

Multiple Sclerosis + Genetics

A
  • more common in females
  • Northern European ancestry
  • MHC antigen association (higher rates in identical twins than fraternal)
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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
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14
Q

Hypersensitivity

A
  • Damaging reactions of normal immune response
  • Antibody-mediated: Types I, II, and II
  • T-cell Mediated: Type IV
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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
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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

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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
Q

Type III Hypersensitivity

A
  • 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
Q

Post-Streptocoocal

A
  • 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
Q

Systemic Lupus Erythematosus

A
  • 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
Q

Type IV Hypersensitivity

A
  • Delayed hypersensitivity (24+ hours)

- T cells and macrophages respond - NO ANTIBODIES

29
Q

Contact Hypersensitivity Examples

A
  • Poison Ivy
  • Poison Oak
  • Metals
  • Latex
  • Cosmetics
  • Dyes
30
Q

Tuberculin Hypersensitivity

A
  • 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
Q

Granulomatous Hypersensitivity

A
  • 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
Q

Deficient Immune Response

A
  • Decrease in 1+ components of immune system
  • 2 categories: Primary (inherited) and Secondary (acquired)
  • Detection - unusual, recurrent, or unmanageable infections
33
Q

B-Cell/T-Cell Combined Deficiency

A
  • 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
Q

Wiskott-Aldrich Syndrome

A
  • 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
Q

T-Cell Disorders (2)

A
  1. DiGeorge Syndrome

2. Chronic Mucotaneous Candidiasis

36
Q

DiGeorge Syndrome

A
  • 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
Q

Chronic Mucotaneous Candidiasis

A
  • Defective IL-17 receptors and production
  • TH17 cells specifically involved
  • Manifests in severe infections with candida species and infection with staphylococcus species
38
Q

B-Cell Disorders (2)

A
  1. Selective IgA Deficiency

2. Bruton’s X-linked Agammaglobulinemia

39
Q

Selective IgA Deficiency

A
  • Most common
  • IgA producing B-cells don’t mature into plasma cells
  • No secretory IgA for respiratory, gastrointestinal, or genitourinary infections
40
Q

Bruton’s X-linked Agammaglobulinemia

A
  • Lack of B-cell differentiation or maturation
  • No antibodies in serum
  • Extracellular pathogens have less immune response like Strep, Staph, and haemophilus
41
Q

Secondary Immunodeficiency

A
  • 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 (18 decks)

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