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BIO 233 > Week 2 - Study Guide > Flashcards

Week 2 - Study Guide Flashcards

Immunity

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
Q

Effectors =

A

Plasma cells & fight right away
Take action

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26
Q

Memory =

A

Fights future battles with the same foe

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27
Q

Walk thru the steps in Antibody-Mediated Immunity
AKA - Humoral
Targeting stuff not inside the cell - plasma, interstitial fluid

A

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

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28
Q

APCs. -

A

Antigen Presenting Cells

Presenting piece of the antigen
to communicate to
Naive cells

29
Q

Walk Thru steps in Cell-Mediated Immunity

Targets things inside the cell

Example HIV

A
  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
Q

HIV example - cell-mediated immunity

A

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
Q

Primary Response to 1st exposure - lag time

A

Lag 3-6 days

Max - [plasma antibosy] ~10 days and declines from there

32
Q

Secondary response - timing
(Booster shot or natural exposure)

A

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
Q

Acquired Immunity

A

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
Q

Exotoxins

A

Proteins secreted by bacteria

35
Q

Macrophages

A

found in all organs -
engulf particulates with pseudopods

36
Q

Pseudopds

A

fake arms to engulf

37
Q

Phagosome

A

produces vesicle – fuse with lysosomes to break down the nasties

38
Q

Recognition of pathogen aided by

A

complement protein OR antibody marking

Flag antigens - pathogens for destruction

Coordinates activity with WBCs

39
Q

Natural Killers

A

Target & Induce apoptosis - -program cell death - in cancer and virus-infected cells

40
Q

Inflammation

Solution to Pollution is dilution

A
  1. mobilizes resources
  2. Immobilize, dilute toxins
  3. Activate clotting proteins
  4. Repair
41
Q

Inflammation

Histamines

A

Vasodilation & capillary Permeability

42
Q

Inflammation

Prostaglandins

A
  1. Vasodilation & capillary Permeability
  2. Induces Pain
  3. Chemotaxis - release chemical to attract WBCs to come and fight injury
43
Q

Inflammation

Complement proteins

A
  1. Mark invaders (for destruction)
  2. Enhance inflammation
44
Q

Inflammation

Lymphokines

A

Chemotaxis - release chemical to attract WBCs to come and fight injury

45
Q

Cardinal signs of inflammation

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain
46
Q

Cardinal signs of inflammation

Redness

A

Send more blood to area - appears red

Vasodilation
Increased metabolic rate of cells

47
Q

Cardinal signs of inflammation

Heat

A

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
Q

Cardinal signs of inflammation

Swelling

A

Swelling - edema

Leakes protein-rich fluid in tissue spaces (interstitial fluid) & Water follows

Possible temporary limitation of joint movement

49
Q

Cardinal signs of inflammation

Pain

A

Swelling pinches nerve endings and induces pain

Possible temporary limitation of joint movement

50
Q

Inflammation:

Some specific Inflammatory Mediators

A
  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
Q

Inflammation:

Benefits of Edema (4)

A
  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
Q

Two pathways to prolong inflammation

A
  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
Q

Interferons. (IFNS)

Activate during viral infection

A

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
Q

Difference between Complement Proteins and Interferons

A

Complement proteins go after cellular things - bacteria

Interferons - interfere with the viral replication process

55
Q

Fever

Benefits - metabolism costs - denaturation risk

A

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
Q

Adaptive defenses -

A

Specific & has a memory

  1. Antibodies
  2. Lymphocytes
  3. Aided by complements & phagocytes
  4. Must recognize self-antigens
  5. Amplifies inflammatory response
  6. Targets infectious agents & abnormal body cells
  7. Works with complement proteins
  8. Works best with prior exposure
57
Q

Cells of the Immune system

A

Adaptive
1. B Lymphocytes- antibody producers, aids in humoral immunity - antibody-mediated. (things in the body fluids not cells)

  1. 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
Q

Immunocompetence

A
  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
59
Q

Antigens - 2 types

A

Complete Antigens

Incomplete Antigens

60
Q

Complete Antigens

A
  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

61
Q

Incomplete Antigens

A

(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

62
Q

Immunity =

A

Specificity

63
Q

Antibodies

A

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

64
Q

Antigenic Determinant

A

Part of the antigen-stimulating immune response

Lock and Key

65
Q

3 ways antibodies work

A
  1. Direct - Antigen binding
  2. Indirect - Stimulating phagocytosis of antibody-antigen complex
    – we called for backup
  3. Indirect - Enhances inflammatory response & activates complements
66
Q

Transplant Issues =

A

MHC antigens are unique

  1. Donor-recipient matching
  2. Immune suppressing drugs
  3. Artificial parts benefits…
67
Q

Allergy =

A

Reaction not dangerous

  1. Hypersensitivity to non-pathogenic antigen

But can become dangerous if anaphylactic shock - huge amounts os histamines - dangerous

68
Q

Autoimmune disease =

A

Attack self

Genes, infection, antigen & self similarity

Exposed earlier in life

69
Q

Cytokins

A

facilitate mitosis

BIO 233 (62 decks)

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