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microbiology > unit 10 > Flashcards

unit 10 Flashcards

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1
Q

Antigen

A
  • immunogen/ allergen/ AG
  • usually proteins or large polysaccharides
  • any substance that causes antibody formation
    -can be a microbe
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2
Q

Antibody

A

-immunoglobulin, Ab, Ig
- protein made in response to an antigen
- binds to Antigen

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3
Q

Anitgen-antibody reaction

A
  • antibody will attach to an antigen at a specific site
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4
Q

Valence

A

of Ag’s that will attach to an Ab

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5
Q

Types of accquired immunity

A

passive and active

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6
Q

active accquired immunity

A
  • natural active and artificial active
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7
Q

natural active immunity

A
  • come across antigen naturally
  • ex= cold viruses
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8
Q

artificial active immunity

A
  • antigen artificially introduced (vaccine)
  • Hib MMR Dtap
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9
Q

Natural passive immunity

A

-Ab goes from mother -> infant
-placental or colostrum

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10
Q

Colostrum

A

first breast milk when baby is born

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11
Q

Artificial passive immunity

A
  • Ab recieved via injection
    -ex= antitoxins or rhogam ( anti-RH antisera)
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12
Q

Serum immunoglobulins

A

IgA
IgD
IgE
IgG
IgM

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13
Q

IgA

A
  • secretory Ab
  • 70,000 or 400,000 Daltons
    -found in mucous, saliva , tears, colostrum, blood
  • 1st / 3rd line of defense
    -monomer in blood, dimer in secretions
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14
Q

IgD

A

-180,000 daltons
- internal marker on B cells
-monomer
- sticks to lymphatic b cells

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15
Q

IgE

A
  • 200,00 daltons
    -allergic Ab
  • involved in allergic reactions/ hypersensitivity
  • monomer
    -least abundant Ab
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16
Q

IgG

A
  • circulatory Ab
  • 160,000 daltons
  • protects against microbes
    -triggers complements
  • increases phagocytosis
  • crosses fetal- placental membrane
  • monomer
    -most abundant Ab
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17
Q

What special about IgG

A

first antibody to increase at first antigenic response

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18
Q

IgM

A

-circulatory Ab
- 900,000 Ab
- 1st Ab to arrive in response to initial exposure to Ag
-short lived
- does not cross fetal-placental membrane
-Pentamer

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19
Q

anamnestic response (antibody memory)

A

initial = 4->7 days (IgM) 10 -> 17 days (IgG)
Secondary = 2 -> 7 days (IgG) with greater magnitude

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20
Q

Does an antibody destroy an antigen

A

no

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21
Q

Antibody structure of a monomer

A
  • 4 polypeptide chains (2 heavy 2 light)
  • joined by disulfide bonds to form a Y shape
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22
Q

Arms of Y (Fab region -fragment of antigen binding)

A
  • region where Ag binds
    -has variable amino acid sequence
  • specific for Ag
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23
Q

Stem of Y (FC region - fragment of cell binding)

A

-has constant amino acid sequence
- binds to cells , proteins, complements

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24
Q

Which Ab are monomers?

A

IgA (monomer in blood , dimer in secretions)
IgD
IgE
IgG

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25
T cells and cellular immunity
- produced by stem cells in red bone marrow - matures in thymus - makes up 65% of lymphocytes - responds to ags - secrete cytokines
26
what are cytokines
chemical messengers
27
Types of T cells
T helper cells Regulatory T cells Cytotoxic cells
28
T helper cells
- cd4 cells - activates B cells to make Abs/ macrophages - secretes cytokines
29
Regulatory T cells
= suppressor = cd8 cells - suppresses other T cells -protects fetus from rejecting body cells
30
Cytotoxic Cells
- cd8 cells - recognize/ kill target cells - non self or hijakced cells - programmed cell death (apoptosis) - not capable of attaching to helper cells
31
Cytokines
- chemical messengers of immune cells -also known as interleukins / interferon - more than 200 types - attracts macrophages/ protects against viral infections - toxic to tumor cells -increases Ab production - sends info -> host cell about foreign material
32
B cells and humoral immunity
-produced by stem cells -matures in bone marrow - makes up 35% of lymphocytes - primarily found in blood/ lymphoid organs
33
function of B cells
- carry old immunoglobbulins (IgD or Igm) on surface - when they recognize an Ag, the B cell is activated with the assistance of T cells to produce memory cells/ plasma cells
34
Memory cells ( B cell)
- stores info based on specific amino acid sequence
35
plasma cells (b cell)
produce new Ab's
36
Results of antigen-antibody binding
1) when Ab encounters specific Ag / it forms an Ag-AB complex form 2) Ab molecule is not damaging to Ag but it triggers mechanisms that are 3) types of mechanisms - aggulutination - Opsonization - Neutrilization - Complement activation
37
Aggulination
reduces number of microbes
38
Opsonization
enhances phagocytosis
39
Neutralization
blocks viral attachment/ neutrilizes toxins
40
Complement activation
serum protein that causes inflammation/ cell lysis
41
Congenital immunodeficiencies
SCID Bruton's disease DiGeorge syndrome
42
SCID - severe combined immunodefiency (congenital immunodefiency)
- deficiency in both T/ B cells - no Ab's - treatment = gene therapy/ restriction enzymes - rare
43
Bruton's disease
- decrease # of B cells - less Ab's - more prone to infections
44
DiGeorge Syndrome
-Defective thymus (Less T cells) - more prone to infections
45
Autoimmune disease
- Ab against itself - rheumatoid arthritis (anti gammaglobulin Ab's) - Systemic Lupus Erythematosus (anti-dna Ab's)
46
AID's acquired immunodefiency syndrome
- HIV attaches to cd4 receptors on T helper cells -decreased # of T helper cells - normal levels of B cells - B cells not turned on because of lack of T helper cells (decreased # of Ab's)
47
Graft
transfer of tissue from one part of the body to another or from one person to another
48
Autograft
tissue graft from oneself
49
Isograft
tissue graft from an identical twin
50
Allograft (homograft)
transfer of graft from one person to another person of the same species
51
Xenograft
tissue graft from different species
52
Immediate or Antibody Mediated
1) Type I : Anaphylactic reaction 2) Type II: Cytotoxic reaction 3) Type III: Immune complex reaction
53
Delayed or cell mediated
Type IV: delayed type reaction (T helper cell usually delayed)
54
Type I: Anaphylactic reaction
- ex = insect stings / drug or food allergies / hay fever/ allergic asthma - 2-> 30 minutes - 1st exposure to allergen
55
Sensitizing dose: 1st exposure of Type I
produces IgE: Fab recognizes allergen and Fc attaches to basophils or mast cells
56
Shocking dose: 2nd exposure of Type I
- basophils/ mast cells increase result in histamines increasing - gastric, lacrimal, and nasal secretions - vascular permeability increase - BP decreases resulting anaphylactic shock - localized hives/ itching/ reddening
57
Treatment for Anaphylactic reaction
Anti-histamine or epinephrine (constrict blood vessels/ increases BP)
58
Lab tests for Anaphylactic reaction
skin test Eosinophilia IgE (Rast)
59
Type II: Cytotoxic reaction
- examples = transfusion blood reactions, hemolytic disease of newborn - 5 -> 12 hrs - body exposed to Ag/ attaches to target cells (rbc, wbc, platelets) - complement activated / cytolysis occurs
60
Type III: Immune complex reaction
-Examples = post-streptococcal / Glmerulonephritis / Rheumatic fever - sequelae infection : secondary consquence - 3 -> 8 hrs - Body exposed to Ag , makes IgG or IgM Ab - Ab binds with Ag and forms Ab-Ag immune complex IC's
61
what are IC's
- deposits on blood vessel walls - penetrates walls to cause inflammation
62
Type IV: Delayed type hypersensitivity reaction
-Examples = TB Tine skin test / some drug allergies / poison ivy - 2 -> 3 days ( due to time for T cells/ macrophages -> Ag) - No Ab involvement; caused by T cells
63
Purpose of Type IV: delayed type hypersensitivity reaction
- Ag -> body and attaches to target tissue (skin) - T cells react with Ag to destroy Ag but it also destroys target tissue (dermatitis)

microbiology (15 decks)

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