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Week 2 - Study Guide Flashcards

Immunity (69 cards)

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1
Q

Immune system has two intrinsic defense systems:

A
  1. Innate (nonspecific) (born with)
  2. Adaptive (Specific) (exposed to)
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2
Q

Innate Defense System

A
  1. Set of structures and Functions born with
  2. Nonspecific - born with
    Meaning - they do not help learn anything - they only do what their specialized functions are for our entire life.
  3. They do not change
  4. They do not get better
  5. Just keep doing what they do
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3
Q

Adaptive Immune System

A
  1. Exposed to
  2. About what we are exposed to during our life – we get sick, Fight, get better, remember it
  3. Some interconnection between innate functions and adaptive functions
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4
Q

Bacteria are the most common pathogens and typically cause illnesses by 2 names:

A
  1. Endotoxins
  2. Exotoxins
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5
Q

Endotoxins –

A

Components of bacterial cell wall

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6
Q

Bacteria are cellular - group -

A
  1. Prokaryotic cell
  2. simple and small
  3. No nucleus
  4. No organelles
  5. Have genetic material
  6. Makes ATP
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7
Q

Viruses are not cellular –

A
  1. Without a host cell, they cannot do anything
  2. Viruses enter the Host
  3. Take over the cell
  4. Commandeer the cell metabolism

– Use our structures to replicate their genetic material
– And create products of themselves over and over again.
– so much that they grab components (our cell membranes)
– then deplete our resources and damage our cell membranes. (toxin build-up)
– until our cells literally die

Death due to rupture
and
Release of viral particles

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8
Q

Innate Defenses are highly connected

(Born With)

A

Non-Specific - provide protection that is not selective

SURFACE BARRIERS -
Inhibit entry of most microorganisms
1. Skin
2. Mucus membranes, hair, & cilia
Mucus- pH balance
Catch irritants
3. and their secretions and contain antibacterial toxins
Oil, sweat, enzymes, acids
4. Keratin - resistant to weak acids and bases, bacterial enzymes, toxins
5. Tears - contain antimicrobial enzyme - Lysosome

Mucous membranes line our hollow tubes:
digestive, urinary, respiratory, reproductive

INTERNAL DEFENSES
1. Phagocytes
2. NK cells
3. Inflammation
4. Antimicrobial proteins
5. Fever

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9
Q

Adaptive Defenses are highly connected

(Exposed to)

A

Provides specific protection
and
generally requires a First-time exposure

Humoral Immunity
B cells

Cellular Immunity
T cells

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10
Q

Internal Defenses - Cells and Chemicals

Necessary of microorganisms invade deeper tissues:

A

NonSpecific

  1. Phagocytes
  2. NK - Natural Killers
  3. Fever
  4. Inflammatory Responses:
    Macrophages, mast cells, WBCs, inflammatory chemicals
  5. Antimicrobial Proteins (2)
    Complement proteins & Interferons
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11
Q

Phagocytes are WBCs and come in different forms - what is the most common

A

Macrophages

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12
Q

Macrophages

A
  1. Found in all organs
  2. Engulf particles by cellular eating - it pulls in what it is eating and creates a phagosome.
  3. Phagosome with the lysosome of the phagocyte - breaks down the nasty
  4. and release back into the interstitial fluid
  5. will be picked up
  6. and filtered out by the kidney
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13
Q

Phagosome

A

is a vesicle that fuses with the lysosome of the phagocyte

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14
Q

Macrophages recognition of pathogen:
Aided by

A

Recognition of Pathogen- Aided by:
1. Complement
OR
2. Antibody marking

Providing a binding site for Phagocyte

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15
Q

Antibodies are part of which immune process?

A

the Adaptive Immune Process.

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16
Q

We have better immune functions because of this interconnection:

A
  1. Possible interaction between:
    Phagocytes * Complement proteins - Both are Innate
  2. Antibodies are adaptive
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17
Q

Natural Killer cells (NK)

A

Innate cells (born woth)

  1. type of Lymphocyte
  2. Large
    –Target our damaged cells
  3. Target and induce the process of APOPTOSIS in cancer cells and virus infected cells

When - our cells our infected, potentially have damage

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18
Q

Apoptosis -

A

Programmed cell death`

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19
Q

Complement proteins

A

flag invaders

innate
assist adaptive immunity

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20
Q

Nonspecific

A

includes barriers - skin, mucous & more

Innate - born wot it

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21
Q

Specific

A

Adaptive - exposed to

  1. Complement proteins - flag invaders
  2. Generalist Phagocytes engulf invaders & commnuicate to specialist
  3. Specialist WBCs (T & B cells) learn to fight invaders and produce armies and munitions for future battles (memory cells)
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22
Q

MHC

A
  1. genes that allows us to have our own specific antigens
    AND
  2. Recognize the difference between our cell markers, the antigens, and Foreign cell markers.
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23
Q

Humoral Body Fluids -

A

Plasma
Interstitial Fluid
Not specifically inside the cell

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24
Q

Lymphocytes

A

T & B cells

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25
Effectors =
Plasma cells & fight right away Take action
26
Memory =
Fights future battles with the same foe
27
Walk thru the steps in Antibody-Mediated Immunity AKA - Humoral Targeting stuff not inside the cell - plasma, interstitial fluid
All about B cells and Antibody-Mediated Immunity T cells hanging out in the background 1. Bacteria enters 2. APCs (Antigen Presenting dendritic cell) phagocytize 3. Non-infected agent is presented 4. Helper Ts activated 5. Helper Ts selected 6. Helper Ts bind with B cell 7. Activated B cell stimulated by helper T cell 8. Selected B cell forms clones - mitosis 9. B cell makes plasma and memory cells 10. Plasma cells produce antibodies 11. Bacteria disabled by antibody causing more phagocytosis
28
APCs. -
Antigen Presenting Cells Presenting piece of the antigen to communicate to Naive cells
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Walk Thru steps in Cell-Mediated Immunity Targets things inside the cell Example HIV
1. Virus enters 2. APCs (Antigen Presenting dendritic cell) phagocytize 3. Non-infected agent is presented 4. Helper Ts activated & cloned (mitosis) 5. Cytotoxic T activated but waits for go signal 6. Effector Helper Ts send cytokines 7. Activated cytotoxic T cell clones (mitosis) 8. Activated Cytotoxic T cell produces Memory and effector T cells 9. Effector cytotoxic T performs apoptosis like a Natural Killer cell - (program cell death) 10. Cell self destructs
30
HIV example - cell-mediated immunity
What kills an AIDS patient? - weakened immunity - secondary issues What type of WBC do they monitor in HIV patient? -- T cells What issue with the T cells? no communication W/O T cells? You never get the cytokine - the communication is affected - will not be able to create effectors or memory cells. Cannot do teh final step
31
Primary Response to 1st exposure - lag time
Lag 3-6 days Max - [plasma antibosy] ~10 days and declines from there
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Secondary response - timing (Booster shot or natural exposure)
Sensitized memory cells responds in hours - much faster Much higher [antibody] peaks 2-3 days Greater antibody affinity to antigen (better - learn for next time) [antibody] can remain high for much longer
33
Acquired Immunity
*Active* - antigen-induced (you did the work). - Natural or Artificial Vaccines -- Killed, weakened, inactive toxins (not a cellular component), antigens only (extracted) Long Term - body did the work (from our won memory cells, antibodies - learned to fight) *Passive* - antibodies only (did not do the work) Did not learn how to fight those pathogens gained from some other source Nonhuman source or mother Immediate protection SHortterm - body did NOT do the work Occurs during development Antibodies - placenta breast feeding
34
Exotoxins
Proteins secreted by bacteria
35
Macrophages
found in all organs - engulf particulates with pseudopods
36
Pseudopds
fake arms to engulf
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Phagosome
produces vesicle -- fuse with lysosomes to break down the nasties
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Recognition of pathogen aided by
complement protein OR antibody marking Flag antigens - pathogens for destruction Coordinates activity with WBCs
39
Natural Killers
Target & Induce apoptosis - -program cell death - in cancer and virus-infected cells
40
Inflammation Solution to Pollution is dilution
1. mobilizes resources 2. Immobilize, dilute toxins 3. Activate clotting proteins 4. Repair
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Inflammation Histamines
Vasodilation & capillary Permeability
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Inflammation Prostaglandins
1. Vasodilation & capillary Permeability 2. Induces Pain 3. Chemotaxis - release chemical to attract WBCs to come and fight injury
43
Inflammation Complement proteins
1. Mark invaders (for destruction) 2. Enhance inflammation
44
Inflammation Lymphokines
Chemotaxis - release chemical to attract WBCs to come and fight injury
45
Cardinal signs of inflammation
1. Redness 2. Heat 3. Swelling 4. Pain
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Cardinal signs of inflammation Redness
Send more blood to area - appears red Vasodilation Increased metabolic rate of cells
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Cardinal signs of inflammation Heat
Send more blood to area not only appears more red but also heats up due to blood being warm Blood holds heat Vasodilation Increased metabolic rate of cells
48
Cardinal signs of inflammation Swelling
Swelling - edema Leakes protein-rich fluid in tissue spaces (interstitial fluid) & Water follows Possible temporary limitation of joint movement
49
Cardinal signs of inflammation Pain
Swelling pinches nerve endings and induces pain Possible temporary limitation of joint movement
50
Inflammation: Some specific Inflammatory Mediators
1. *Histamines & Kinins* - Vasodilation - capillary permeability 2. *Prostaglandins* - Vasodilation - capillary permeability - Chemotaxis (calling other WBCs to the site - backup taxis) - Induces Pain 3. *Complementary Proteins* - Tag invaders - lyses - increase inflammation response - increase immune response 4, *Lymphokines* - chemical that aids in chemotaxis - initiates it - calls for WBCs to come and help
51
Inflammation: Benefits of Edema (4)
1. *Immobility* - immobilize the damaged region 2. *Dilute Toxins* - Get rid of nasty and filter at kidneys 3. *Activates clotting proteins* & - more resources, more chemicals in the area to initiate blood clotting 4. *Distribute Resources* - water everywhere - moves things easily
52
Two pathways to prolong inflammation
1. *Classical Pathway* - flagging a cell Antibodies & complements bind to bacteria & flag it for phagocytosis 2. *Alternate Pathway* - form a pore Form a pore and insert into cell wall & cause lysis *Both pathways 1. "CASCADE" - 2. Destroy pathogens 3. Prolong inflammatory response
53
Interferons. (IFNS) Activate during viral infection
ALL ABOUT VIRUSES 1. Infected cells produce & secrete IFNS and send to neighbors - healthy cell - gives them the code to fight the infection - preventing viral reproduction 2. Activates macrophages & NK cells to target infected cells & possibly malignant cells
54
Difference between Complement Proteins and Interferons
Complement proteins go after cellular things - bacteria Interferons - interfere with the viral replication process
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Fever Benefits - metabolism costs - denaturation risk
Increases body temperature - speeds up metabolism 1. Inhibits bacterial reproduction 2. Improves lymphocyte activity 3. Prostaglandins produce endogenous pyrogens - (go to brain and say turn up the heat Aspirin interferes with prostaglandin production - fights off the formation of them. Is a negative feedback loop
56
Adaptive defenses -
Specific & has a memory 1. Antibodies 2. Lymphocytes 3. Aided by complements & phagocytes 1. Must recognize self-antigens 2. Amplifies inflammatory response 3. Targets infectious agents & abnormal body cells 4. Works with complement proteins 5. Works best with prior exposure
57
Cells of the Immune system
*Adaptive* 1. *B Lymphocytes*- antibody producers, aids in humoral immunity - antibody-mediated. (things in the body fluids not cells) 2. *T Lymphocytes* - cell-mediated immunity *Innate* 1. Antigen-presenting cells (APCs) - do not respond to specific antigens - they are innate. - Play an essential auxiliary roles in immunity, - Assisting - help the process - not the ones causing the memory, creating the long term protection
58
Immunocompetence
1. *During maturation -* - Any cells that fail to differentiate between our antigens (self-antigens) and foreign antigens will be destroyed. - Allows T & B cells to interact with our antigens and should not bind with our antigens. 2. *Upon Release - * - Cell family = 1 receptor + 1 antigen - Receptors are genetically determined - Able to recognize & bind to specific antigen 3. *Naive (unexposed) B & T cells reside* - - Lymph nodes, spleen, & lymphoid organs
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Antigens - 2 types
Complete Antigens Incomplete Antigens
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Complete Antigens
1. Hangs out on its own 2. Does not need to bind Proteins, polysaccharides, lipids, & nucleic acids *Stimulates immune cells & Reacts to products of immune response*
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Incomplete Antigens
(Haptens) 1. Chemicals from environment that bind to our proteins and acts like a complete protein EXAMPLE - poison ivy, animal dander, detergents, & cosmetics Chemicals on own ok - On our protein they become a complete protein - attach to our structures - problem *React but do not activate a response directly, but can if attached to body protein*
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Immunity =
Specificity
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Antibodies
Proteins that combine with specific antigens Constant & variable regions Y - antibody. - the fork part is the variable and attaches to foreign substance - stem is the constant
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Antigenic Determinant
Part of the antigen-stimulating immune response Lock and Key
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3 ways antibodies work
1. Direct - Antigen binding 2. Indirect - Stimulating phagocytosis of antibody-antigen complex -- we called for backup 3. Indirect - Enhances inflammatory response & activates complements
66
Transplant Issues =
MHC antigens are unique 1. Donor-recipient matching 2. Immune suppressing drugs 3. Artificial parts benefits...
67
Allergy =
Reaction not dangerous 1. Hypersensitivity to non-pathogenic antigen But can become dangerous if anaphylactic shock - huge amounts os histamines - dangerous
68
Autoimmune disease =
Attack self Genes, infection, antigen & self similarity Exposed earlier in life
69
Cytokins
facilitate mitosis
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