Exam 4 Flashcards

(64 cards)

1
Q

What kind of defense is skin and how does it protect against infection?

A

first line of innate defense

  1. physical barrier: cannot enter unless cut, collagen helps prevent jabs
  2. chemical factors: has low pH, salt, lysozyme - breaks down cell walls
  3. competition with normal bacteria/microbial antagonism
  4. epidermal dendritic cells - nonspecific phagocytosis - fingerlike projections that intercept invaders
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2
Q

What kind of defense do mucous membranes serve as and what are some examples?

A

first line or innate defense - contains tightly packed epithelial cells in thin layer

  • mucous traps pathogens
  • dilated cells clear mucus from respiratory system
  • lysozyme in nasal mucous
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3
Q

What are some other first line defenses against infection?

A

stomach - low pH in gastric juice prevents most microbial growth

lacrimal glands - tears remove pathogens and contain lysozyme

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4
Q

Define plasma and formed elements

A

plasma - liquid portion of blood that contains complement proteins and immunoglobulins - important for host defense

formed elements - cells and cell fragments
- includes RBC, leukocytes (WBC) and platelets

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5
Q

define hematopoiesis. What do lymphoid turn into? What to myeloids turn into?

A

development of stem cells in bone marrow to formed elements - RBC, platelets and leukocytes
- differentiation due to chemical signals called cytokines

lymphoid - lymphocyte - specific defense

Myeloid - turns into 4/5 leukocytes (besides lymphocyte) and platelets

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6
Q

What are the leukocytes?

A
  1. Neurtrophil - most common
  2. Monocyte - float in blood, can turn into macrophage
  3. Eosinophil - binds to eosin
  4. Lymphocyte - NK lymphocytes function in innate defense
  5. Basophil - associated with allergies/common cold
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7
Q

What are the steps of phagocytosis?

A
  1. chemotaxis - attraction of phagocytes to microorganism due to chemotactic factors that attract leukocyte
  2. adherence - attachment of phagocyte to microorganism - binding of complementary chemicals and opsonization increasing binding sites
  3. ingestion - engulfment of microorganisms by endocytosis - creates phagosome (food vesicle)
  4. digestion - breakdown pf microorganism in phagolysosome
  5. elimination - exocytosis of undigested remnants of microorganism
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8
Q

what is the complement cascade?

A

set of serum proteins that are important for directing a rapid host defense
three pathways - classical, alternative and lectin

outcomes - opsonization and phagocytosis

  • membrane attack complex and cell lysis of invading microbes
  • inflammation

all pathways meet at C3 protein and splits it into C3a and C3b

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9
Q

What is the classical pathway for the complement cascade

A

initiated by antibodies bound to the microbe

  • bind to antigen, produces complement 1,2,4 proteins
  • activated C3b for opsonization
  • activates C3a, C4a, and C5a for inflammation
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10
Q

what is the alternative pathway for complement cascade

A

initiated by microbial cell wall polysaccharides that interact with factors B, D, P

  • works with Cb3 on cell wall and splits more C3
  • C3b accumulates and works as an opsonin
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11
Q

what is the lectin pathway of the complement cascade

A

initiated by lectin binding to mannose on fungi, bacteria and viruses
- begins series of enzyme activities as in the classical pathway

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12
Q

what are the outcomes of a complement cascade?

A
  1. opsonization - microbes are covered by antibodies and C3b complement proteins that enhance phagocytosis
  2. inflammation - stimulates chemotaxis of leukocytes
    - stimulates basophils and mast cells to release histamine
    - involved C3a, C4a, C5a
  3. membrane attack complex (MAC) - cytolysis
    - complement proteins form a hole in microbe membrane
    - involved C5b, C6, C7, C8, C9: complement fixation
  4. inactivation of complement - occurs quickly, breakdown of activated complement
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13
Q

What is the role of interferon type 1?

A

alpha and beta interferon is produced by virus infected cells

  • stimulates other cells to make antiviral proteins (AVP) that destroy protein production in cell so that the virus cannot be replicated
  • when second cell is infected with virus, AVP is activated and stops protein synthesis
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14
Q

what is an interferon?

A

a protein molecule released by a host cell to nonspecifically inhibit the spread of viral infections

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15
Q

what is the role of interferon type 2?

A

gamma interferon - “macrophage activation factor” for phagocytosis

  • produced by activated T and NK lymphocytes
  • NK - natural killer - can kill some tumor, releases cytokines
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16
Q

what are the 4 symptoms of inflammation? what is the function of inflammation?

A

redness (rubber), edema (swelling), pain (dolor), localized heat (calor)

can confine and/or destroy harmful agent (microbe, physical/chemical agent)

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17
Q

What are the steps of inflammation?

A
  1. tissue injury - pressure due to inflammation
  2. vasodilation - increase blood vessel diameter
    - caused by histamine release from mast cells and basophils
    - prostaglandin and leukotrienes increase permeability of blood vessels - allows for phagocytes to move n and delivery of antimicrobial chemicals
    edema - accumulation of fluids around injury site
    - allows for host defense cells to reach infection site
    - causes pressure on nerve endings - pain
  3. phagocyte migration and phagocytosis
    - margination: attachment of leukocytes (neutrophils and monocytes) to blood vessel endothelium
    - diapedesis - leukocytes squeeze between cells of blood vessel and move toward injury site
  4. clotting factors accumulate to confine injury
  5. tissue repair
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18
Q

What are the advantages that fever gives the host?

A
  • increased body temperature is above optimum for pathogens and slows their growth
  • increased rate of chemical reactions in body to fight microbes
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19
Q

what are the chemical signals for a fever?

A
  • microbial products of exogenous pyrogens
  • phagocytes released endogenous pyrogens (IL1)
  • pyrogens cause hypothalamus to release prostaglandins
  • prostaglandin reset hypothalamus at higher temperature and results in fever
  • nerve impulse cause shivering, higher metabolic rate and inhibition os sweating and vasoconstriction
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20
Q

What is immunity and who can perform it?

A

the agility of an organism to resist specific foreign organisms or substances
- performed by vertebrates only

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21
Q

In specific immunity what are the two types?

A
  1. humoral - antibody mediated immunity
    - antibodies made by B cells circulate in the plasma and attack extracellular pathogens and toxins
  2. cell-mediated - carried out by t cells
    - involves cell-cell interactions that attack intracellular pathogens
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22
Q

What are the primary lymphoid organs?

A
bone marrow (B cell development)
- all cells in immune system are derived rom the stem cells in the bone marrow 

thymus (T cell development)

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23
Q

what are the secondary lymphoid organs?

A

tonsils, spleen, lymph nodes
- lymph nodes located at neck, groin axilla and abdomen and facilitates interaction between immune cells and body material (through medulla)

MALT - mucosal associated lymphoid tissue - contains most of the odds lymphocytes

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24
Q

what are antibodies

A

proteins found in blood serum - secreted immunoglobulin that is involved in specific immunity
- has high specificity to specific antigen

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25
what is an antigen and what are some variables that affects its ability to cause a response
substance that causes an immune response shape, seize and complexity - bigger/more complex = more epitopes = better antigen - can be too small to be detected for immune response
26
what is an epitopes
the specific part of the antigen that is recognized by the immune system - makes antibodies that respond to it - can change over time - ex. why we need new flu vaccine
27
how do eosinophils kill pathogens without phagocytosis?
secrete antimicrobial chemicals against pathogens that are too large to inject like parasitic worms, also binds to LPS to form barrier that kills Gram -
28
how do NK lymphocytes kill pathogens without phagocytosis?
secretes toxins into surface of virally infected cells and neoplasms
29
how do neutrophils kill pathogens without phagocytosis?
enzyme in CM can make O2-, H2O2, hypochlorite enzyme makes NO and triggers inflammation extracellular traps (NET) - fibers from cell suicide traps Gram -/+
30
what is the structure of an antibody
variable region - antigen binding site - binds specifically to epitope Fc - heavy chains - determines what type of antigen - held together by disulfide bonds light chains also held to heavy chain by S-S
31
what are some ways that antibodies kill pathogens?
1. agglutination - clumping of pathogenic agent to hinder it from harming host and increasing chance of phagocytosis 2. neutralization - bind to critical point of toxin so that it can no longer function against the host 3. opsonization - antibodies bind to pathogenic agent by Fc receptor to stimulate phagocytosis 4. antibody-dependent cellular cytotoxicity - ADCC - Fc region binds to NK cells causing it to lyse cell target by releasing proteins into it - perforin: forms tubular structure in target CM - granzyme - enters cells and triggers apoptosis
32
describe IgG antibodies
most common best at getting into extracellular spaces can cross placenta from mother to fetus involved in complement activation, opsonization, neutralization, ADCC and inflammatory response
33
describe IgM antibiodies
1st antibody secreted by activated B lymphocyte in response to antigen pentameter structure - unable to cross placenta most efficient at complement activation and involved in agglutination and neutralization
34
describe IgA antibodies
found in mucous membranes and body secretions - tear ducts, mammary glands, mucous membranes, breast milk, saliva agglutinates and neutralizes J chain and secretory components keep IgA in mucous membranes
35
describe IgE antibodies
mostly a signaling molecule present in small amounts of blood serum involved in allergic response defense against parasitic worms
36
describe a B cell receptor
antigen receptor that contains two antigen binding sites identical to binding sites of secreted antibody - specific to each epitope, only one epitope per B cell - ability to respond to 10^9 antigens
37
what happens when an epitope binds to a BCR
1. B cell divides and secretes antibodies into blood and lymph 2. plasma cells and antibodies act against same original epitope 3. plasma cells no longer present BCR and secrete antibodies - affinity to antigen gets progressively better 4. also produces memory cells that can remain in suspended animation for months/years n lymph tissue
38
describe the differences between a primary and secondary specific immune response
primary - small amount of antibodies formed over days to weeks secondary - large amounts of antibodies due to clones, response much quicker than primary response - immune system ready - memory cells makes IgG and IgM faster and stronger
39
what is apoptosis?
programmed cell death - B and T cells unstimulated by antigen will go through - B ant T cell that are stimulated by self antigen will go through
40
what is tolerance?
surviving lymphocytes survive and respond only to foreign antibodies and is tolerant to self antigens - if they react to auto antigen it goes through apoptosis and clonal deletion - all daughter cells killed
41
describe the role of helper T cells
have CD4 protein assists B cell in antibody production and assists cytotoxic T cells - provides necessary signals (cytokines) growth factors needed for immune response
42
describe the role of cytotoxic T cells
have CD8 protein destroy target cells on contact - cells with infected virus or pathogen - abnormal cells
43
how do T cell recognize antigens?
can only recognize epitopes that are bound to MHC proteins - do not bind to native antigens antigen processing - modification of antigen for recognition by T cells APC = antigen presenting cells
44
what is the MHC
major histocompatibility complex (HLA in humans) - binds to antigen and carries it to cell surface - broad in binding: can bind to 1000s of epitopes MHC I: cytotoxic T cells MHC II: helper T cells
45
what are cytokines? describe the following: TNF, chemokines, interleukins, interferons, growth factors.
regulatory proteins that function as intracellular signals TNF: tumor necrosing factor - secreted by macrophages and T cells to kill tumors, regulate immune response and inflammation chemokines - chemotactic cytokines - signal to leukocytes to move to inflammation/infection interleukins - signal among leukocytes and other cells interferons - inhibit spread of vital infection - INF- gamma - potent phagocytic activation secreted by TH1 growth factors - stimulate leukocytes to divide
46
describe B cell activation by T helper cells
1. antigen presenting: APC present MHC II with epitopes - enduced Th with CD4 with complementary TCR to bind - releases IL1 to differentiate Th - Th2 2. Clonal selection - Th2 binds to B specific cell, releases IL4 that activated B cell and causes it to proliferate - creates clones of plasma cells - releases antibodies - also creates memory cells
47
describe the cytotoxic t cell response
1. antigen presentation: MHC I presents epitope for Tc (CD8) 2. helper t differentiation: MHC II of the Th (CD4) also binds to epitope of dendritic cell - dendritic cell release IL12 - stimulates TH- TH1 - TH1 secretes IL2 3. Clonal expansion: signal from dendrite and IL2 from TH1 signal Tc cells to release IL2 - triggers Tc division into memory T cells and Tc 4. self stimulation: Tc daughter cells produce IL2 receptors and their own IL2 - no longer need APC or Th - leaves lymph and attacks infected cells
48
What is acquired immunity
the protection developed against specific microbes or foreign substances
49
describe natural active vs passive immunity
active - body mounts an immune response against ex. flu passive - newborns get IgG antibodies that cross placenta, IgA from breast milk - baby is not actively producing these antibodies
50
describe artificial active vs passive immunity
active - vaccines that introduce antigens mounts immune response passive - inject antibodies - typical for toxins or pathogens that act to quickly for immune response
51
what is a vaccine
organisms or fractions of organisms that is used to induce active immunity - acquire immunity without disease symptoms or severity
52
describe attenuated vs inactivated vaccines
attenuated - live vaccine with weakened microbes - can be more risky inactivated: safer, requires booster - whole agent - contains killed microbes - subunit - contains components of organism
53
describe toxoid vs recombinant vaccines
toxoid - contains inactivated toxins, require multiple childhood doses and reinoculation every 10 years recombinant - express antigen in genes - isolate antigen protein in vaccine - virulence is deletes from pathogen
54
describe passive immunization. what does it \entail?
administration of antibodies to pt immediately without waiting for an immune response - vaccine contains antisera: serum and gamma antibioses - can be administered intravenously rabes, tetanus not long lasting, no memory B cell production
55
what are hybridomas and what is its role with monoclonal antibodies
hybridoma - cell lines created by fusing and antibody producing plasma cell and myeloma cell so that it reproduces continuously - produces many of the desired antibody - monoclonal antibody
56
what is the ELISA test
ELISA : enzyme linked immunoabsorbent assay - anti-antibodies that are chemically linked to color changing enzymes help to identify particular molecules - color change only occurs if the anti-antibody is bound to antigen
57
what are some immunological disorders?
hypersensitivity - immune response occurs in an exaggerated of inappropriate fashion that causes harm to the host autoimmune disorders - host immune system attacks itself immunodeficiency - absence of normal immune response
58
describe hypersensitivity type I
immediately response after exposure to allergen localized anaphylaxis upper respiratory system- allergic rhinitis - hay fever lower respiratory system - asthma GI tract - food allergy acute anaphylaxis - rapid suffocation by contraction of bronchial smooth muscle exceeds body's ability to adjust - tx with epi prevention of anaphylaxis by desensitization: injection of dilute amounts of allergen
59
describe the mechanism of how hypersensitivity type I develops
1st exposure - cytokine stimulate B cells - become plasma cells and produce IgE = IgE sensitize basophils, eosinophils and mast cells that will make the resent to future exposures to allergen 2nd exposure - allergen binds to IgE molecule on sensitized cells and causes degranulation degranulation - mast cells release histamine: - dilates blood vessels - local redness and swelling - simulation of muscle secretion - leads to congestion of airways - constriction of bronchial airways - leads to wheezing - stimulation of nerve endings - leads to itching and pain
60
describe cytotoxic ii hypersensitivity
cytotoxic Rxn - antibodies bind to cell surface of antigens in host cells - results in phagocytosis and complement activation ex. transfusion reaction - agglutination of foreign RBC - activation of complement system - hemolysis - lysis of RBC releases hemoglobin into the bloodstream and can cause kidney damage ex. Rh antigens in newborns 1st pregnancy - Rh - mom and Rh + baby: mom makes anti-Rh antibodies bc of baby - IgM molecules only 2nd pregnancy - Rh - mom has another Rh + baby - produces IgG anti Rh - can cross placenta and destroy baby's RBC's - enlarged liver and spleen Rhocam injection given to mother after first birth to prevent - destroys fetal RBC before mom can produce anitbodies
61
describe immune complex type III hypersensitivity
``` antibody antigen complexes form in circulation and get deposited in organs and cause inflammatory damage - complement and neutrophils activated - damage from inflammation examples - hypersensitivity pneumonitis glomerulonephritis - affected kidneys ```
62
describe cell mediated or delated type IV hypersensitivity
T lymphocytes activated by antigen memory cells produced subsequent exposure to antigen, memory T cells release cytokines macrophages accumulate at site of hypersensitive reaction inflammation and tissue damage occurs contact dermatitis tuberculin hypersensitivity - TB test Graft rejection due to MHC incompatibility - rejected by immune system - prevented by tissue typing and immunosuppressive drugs
63
what is an autoimmune disease
immune system is hypersensitive to self antigens how it happens - loss of self tolerance - cross reaction: antibodies against foreign antigen recognize a self antigen that looks similar
64
what are some examples of autoimmune disorders
RA - immune completes of IgM, IgG and complement is deposited in joints - inflammation and restriction of cartilage in joints SLE - lupus - autoanitbodies made against many self components including DNA - antibody-antigen completes cause inflammation ex. glomerulonephritis