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BME 430 > Exam I (2.2) > Flashcards

Exam I (2.2) Flashcards

Host Reaction to Biomaterials and Their Evaluation

1
Q

Hematopoiesis

A

-White blood cells and leukocytes of the immune system
- They support homeostasis by removing foreign cells/pathogens

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2
Q

Hematopoietic stem cells

A
  • When in their niche, they stay undifferentiated
  • Upon removal, form into either red or white blood cells
  • Occur via the myeloid or lymphoid pathway
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3
Q

Myeloid pathway results

A
  • Platelets, mast cells, blood cells
  • Eventually (after more differentiation), neutrophils and macrophages
  • Polymorphonuclear leukocytes (PMNs), important for defense
  • Created in the bone marrow
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4
Q

Lymphoid pathway results

A
  • Natural killer cells, small lymphocytes (T/B cells), then eventually plasma cells
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5
Q

T/B Cells’ purpose

A
  • Body continually updates the immune system via these cells
  • Created in bone marrow, then mature in the spleen (B cells) or the thymus gland (T cells)
  • Transported in the lymph nodes
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6
Q

Lymphatic system

A
  • Responsible for constant pathogen surveillance
  • Allows for the rapid development of immune response
  • Receives excess water from veins (lymph)
  • Lymph nodes store B and T lymphocytes
  • Organs involved: thymus, spleen, tonsils, appendix
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7
Q

Regular repair steps

A

1) Blood clots
2) Neutrophils (PMNs) are first on the scene, alerting others
3) Macrophages/lymphocytes recruited
4) New blood vessels form
5) Fibroblasts deposit ECM

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8
Q

Biomaterials and Inflammation

A
  • Body is unable to get rid of the foreign material
  • A large fibrous capsule is formed at the site of implantation
  • If the material degrades, granulation tissue forms
  • Fibrosis always occurs
  • Frustrated phagocytosis can happen (persists for lifetime of implant)
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9
Q

Innate immune response

A
  • Primitive, evolutionary, non-specific response
  • Rapid, needed to mobilize adaptive response
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10
Q

Innate components

A
  • Physical barriers, opsonizing blood proteins (label unwanted bodies for clearance)
  • Lectins: mannose-binding lectin (MBL) binds to carbs on bacteria cell wall, setting off cleavage pathway so that WBC’s are recruited
  • leftover cleaved C proteins act as binding for defense cell receptors
  • Dendritic cells are resident defense cells
  • membrane attack complex
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11
Q

Membrane attack complex

A
  • When C5 is cleaved, a part of it forms a complex that begins poking holes in the bacteria
  • C9 further binds, and can enlarge these holes (lysis)
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12
Q

Crossover between immune and adaptive responses

A
  • When cytokines are released, adaptive response is initiated
  • Antigen-presenting cells take pieces of pathogen and present it to T cells
  • MHC is a label that marks a cell as one of yours
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13
Q

T-cells

A
  • Every T cell recognizes one antigen (via one receptor)
  • T-cells with new types of receptors are constantly generated, covering as much diversity as possible
  • Helper T (CD4+): orchestraters, can activate B cells, express cytokines, and activate macrophages/neutrophils
  • Cytotoxic T (CD8+): non-specific natural killer cells, can generate “memory” in the body for long term
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14
Q

Adaptive Immunity

A
  • Antibodies/immunoglobins, which are produced by B-Cells
  • Immunoglobins: IgG, IgA, IgM, IgE, IgD
  • both immediate and delayed mediators (to return things to normal after)
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15
Q

T-Cells vs. B-Cells

A
  • T-cells recognize antigen molecules only presented by antigen-presenting cells
  • B-cells recognize directly!
  • T-cells (cytotoxic) induce cell death for antigen-presenting, or have infected cells undergo apoptosis
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16
Q

Complement system

A
  • Part of the innate immune system
  • Complement activation initiates innate response, regulates the adaptive response
  • Proteins are constantly expressed in the blood, bind in high density to foreign bodies (opsonizing)
  • Stimulates phagocytosis, inflammation, membrane attack complex, etc
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17
Q

What are the pathways of activation?

A
  • Classical, lectin, and alternative
  • Converge on C5 activation
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18
Q

Classical pathway

A
  • Immune complexes (ICs), composed of antigen-antibody binding, are activators
  • Long enzyme cascade, hinging on cascade of various proteins
  • Upon cleavage of C5, defense cells are attracted, and membrane attack complex (MAC) can form
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19
Q

Lectin pathway

A
  • MBL plasma concentration increases with infection
  • Binds to complex carbs on the bacteria cell wall
  • Binds MBL-associated serine proteases, leads to cleaving of necessary proteins
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20
Q

Alternative pathway

A
  • Most biomaterials activate complement via AP!
  • C3 is constantly hydrolyzing its thioester group to form C3(H2O), binds to factor B
  • With factor D, C3 is cleaved multiple times
  • Eventually, following cascade, C5 convertase is formed, and MAC can occur
21
Q

How is complement controlled?

A
  • Negatively regulated pathways, ensure inflammation is localized to the site of injury
  • Decay or dissociation of convertase complexes
  • Proteolytic degradation of active components
  • Control proteins for various components
  • Cell membrane-bound regulators protect bystander cells
22
Q

Complement receptors

A
  • Blood and immune cells express receptors for complement proteins
  • Neutrophils, monocytes, B/T cells, RBC’s, antigen-presenting cells, platelets, etc
23
Q

Additional pathways

A
  • C3a, C4a, C5a leads to histamine release and smooth muscle contraction (allergic reaction)
24
Q

Heparin

A
  • Powerful anticoagulant
25
Q

System toxicity

A
  • Failures of implants due to this are rare
  • Standards involve how quickly the substance becomes toxic
  • Limited (less than 24 hours), prolonged (24 hours - 30 days), permanent (more than 30 days)
  • Toxic substances released can be adsorbed into tissue or distributed by the blood/lymph system (or, upon phagocytosis, tiny matter distributes easily)
  • Possible effects can occur in unrelated organs, and can take years to develop
26
Q

Hypersensitivity

A
  • Immune system overreacts to a small amount of foreign bodies
  • Condition resulting in overreaction upon contact with foreign substances
  • Requires previous exposure
27
Q

Intolerance

A
  • Inherited reaction that does NOT depend on previous sensitization
28
Q

Haptens

A
  • Lead to allergic reactions after combining with proteins in the body (like metal ions)
29
Q

Metal/metal alloy toxicity

A
  • Implants can be made with essential or nonessential metals
  • Essential: normally in body, critical for function (cobalt, iron, copper), become toxic in excess or when oxidized
  • Nonessential: might mimic or displace essential metals, can lead to delayed hypersensitivity (gold, nickel, etc)
  • Chronic inflammation can cause release of metal ions
30
Q

Delayed hypersensitivity

A
  • Types I-IV, reaction mechanisms differentiate
  • I-III are associated with humoral antibodies, B-lymphocytes
  • IV are T-cell mediated, delayed, brought on by “memory”
31
Q

Hemostasis

A
  • Blood coagulation and formation of clots
  • Interconnected/plays a role in inflammation, wound healing, and the innate/adaptive immune responses too
32
Q

Coagulation

A
  • Formation of a thrombus
  • Activated through intrinsic or extrinsic pathways
  • Involves platelets
  • Anticoagulants and fibrinolysis (which degrades thrombus) are involved in negative regulation
33
Q

Platelet structure

A
  • Lack a nucleus, disc shaped
  • Made up of fragments of mature blood cells
  • Have a phospholipid bilayer membrane with essential membrane-bound receptors
  • Membrane also contains a connected network of internal tubes to better release granules
34
Q

Glycoproteins in platelets

A
  • GP Ib can bind connective tissue such as collagen
  • GP IIb / GP IIIa binds to adhesive plasma proteins like fibrinogen
35
Q

What are the kinds of granules secreted by platelets?

A
  • Dense: Contain ADP, calcium ions, and serotonin (stimulates other platelets to activate, serotonin can widen veins and activate inflammation)
  • Alpha: Platelet factor 4 and beta thromboglobin, as well as plasma proteins (neutralizes heparin and attracts fibroblasts for wound healing)
  • Lysosomal: contain enzymes for acid hydrolysis (released last)
36
Q

Heparin

A

Capable of deactivating coagulation

37
Q

Platelet activation process

A
  • Platelets become sticky, adopt an irregular shape with spiny pseudopods
  • Adhere to injury or biomaterial via binding GP proteins, and secrete granules
  • Many processes are undergone to continue activation of other platelets
  • Thrombin is secreted to turn fibrinogen into fibrin, stabilizing thrombosis
38
Q

How are platelets activated by adsorbed proteins?

A

Unclear part of the mechanism

39
Q

Coagulation cascade: intrinsic pathway

A
  • Triggered by biomaterials/external factors
  • Factor XII absorbs to changed surfaces
    (DO MORE WORK…)
  • Factor VIII acts to localize reaction
40
Q

Coagulation cascade: extrinsic pathway

A
  • Triggered by tissue-derived factors
  • Dependent on calcium
  • Results in thrombin, converting to fibrin and helping to stabilize the clot
41
Q

Anti-coagulation measures

A
  • Anti coagulation includes dilution by blood flow, localization of critical reactions to platelet surface, and inhibitors like antithrombin III
  • Coagulation cofactors can also be degraded
42
Q

Fibrinolysis

A
  • Also aides in preventing over-coagulation
  • Removes unnecessary fibrin, improves blood flow and facilitates
  • Plasminogen (also) circulates and adheres to fibrin clots to degrade
43
Q

Crosstalk

A
  • Reb Blood Cells, White Blood Cells, and neutrophils assist in the process too
44
Q

Sepsis

A
  • Possible consequence where pathogenic organisms with toxins are overly present in blood/tissue
45
Q

Biofilm

A
  • A community of bacteria that attaches to, and further grows upon, surfaces of both abiotic materials and host tissue
  • Sugar molecules are released that act as support
  • Can produce enzymes that degrade the material surface
  • Develops diversity, with dormant bacteria within that resist antibiotics
  • Additionally, new strains of tolerant bacteria can form when antibiotic treatment is attempted
46
Q

Attachment of the biofilm

A
  • Planktonic (free floating) bacteria attach via protein adsorption, glycocalyx involvement, or physical trapping due to topography
  • Can colonize a variety of surfaces with different conditions
  • Protein gene expression can change up to 70% after attachment
47
Q

EPS (slime)

A
  • Similar to the ECM, acts as support and can provide tensile strain
  • 10% cells, 90% EPS matrix in biofilm, can hold onto water and make a hydrophilic barrier
  • NOT structurally stable, so constantly fragmenting and leaking into blood stream
48
Q

“Race to the Surface”

A
  • Bacteria, host cells, and proteins all interact and compete for adhesion
49
Q

Strategies for avoiding biofilm

A

1) Killing (ex: covering surface with anti-microbial peptides)
2) Antifouling (superhydrophobic or hydrophilic surfaces, steric hindrance repulsion)
3) Affecting biofilm formation (enzyme modified surfaces)

BME 430 (17 decks)

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