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Phsyiology 210 > BLOOD 2 > Flashcards

BLOOD 2 Flashcards

(70 cards)

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1
Q

Defence

A

– “Self” vs “Non-self”

– protect from internal damage signals

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2
Q

Non-specific defenses (innate immunity)

A

– “Physico-chemical”

• Intact skin, enzymes in saliva, tear, mucus
• Acidic gastric secretion
• Role of WBCs (mainly granulocytes and
monocytes/macrophages )

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3
Q

Specific defenses (acquired immunity)

A

– Role of WBCs (mainly lymphocytes)

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4
Q

inate or natural defence

A
  • non-specific
  • no memory
  • fast
  • (neutrophils and macrophages)
  • complement system
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5
Q

Acquired or adapted defence

A
  • specific
  • has memory
  • slow

(Lymphocytes (B and T cells))

  • antibodies
  • cytotoxic molecules
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6
Q

Appropriate (“ Good”) role of immune systems

A

– defence against foreign invaders (eg. bacteria, viruses)
– Removal of own old reaction (attacking “self immune abnormal or mutant system”) cells
– Identify/destroy

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7
Q

Inappropriate (“Bad”) role of the immune systems

A

– Exaggerated response to “harmless” substances (allergies)

– Autoimmune reactions (attacking “self immune system”)

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8
Q

Inflammation

A

• Non-specific innate response to tissue injury initiates inflammation

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9
Q

• The inducers of

inflammation may include:

A 
– cut on skin surface 
– bullet wound 
– injuries due to sun burn 
– infected sutures during surgery 
– infection of tonsil by cold virus
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10
Q

Physical characteristics of inflammation

A
  • Redness (rubor)
  • Swelling (tumor)
  • Heat (calor)
  • Pain (dolor)
  • Loss of function
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11
Q

What is histamine the agent for

A
  • Redness (rubor)
  • Swelling (tumor)
  • Heat (calor)
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12
Q

What does increased blood flow the primary cause of?

A
  • Redness (rubor)
  • Swelling (tumor)
  • Heat (calor)
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13
Q

What is Bradykinin and prostaglandin (PGE2) the agent of

A

Pain ( Dolor)

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14
Q

What’s is pressure on the nerve endings the primary cause of ?

A

Pain (dolor)

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15
Q

Changes in vasculature (blood vessel wall)

A

Vascular (related to blood vessels) events:
• release of inflammatory mediators
• increased blood flow
• increased permeability of small blood vessels

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16
Q

VASCULAR EVENTS

A
  • release of histamine
  • local blood vessels dilate
  • blood vessels become leakier
  • accumulation of protein and fluid in the extracellular spaces
  • additional inflammatory mediators are released: eg., bradykinin, prostaglandins, complement proteins
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17
Q

CELLULAR EVENTS

A

• resident macrophages entrap and kill pathogens, release chemical signals
• increased movement of WBCs (neutrophils and monocytes) into infected area
• phagocytosis and destruction of foreign
“non-self” agent

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18
Q

Goal of cellular events associated with inflammation:

A

to accumulate leukocytes or WBCs in the inflamed tissue

and kill the “non-self” agent

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19
Q

Cellular events associated with inflammation

- How does this happen?

A
  1. Margination of WBCs
  2. Tethering and rolling of WBCs inside blood vessel
  3. Activation of WBCs and endothelial cells
  4. Arrest/firm attachment of WBCs to endothelial cells
  5. Emigration/diapedesis
  6. Chemotaxis of WBCs
  7. Recognition of “non-self” by WBCs
  8. Phagocytosis of “non-self” pathogen by WBC’s
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20
Q

What is chemotaxis?

A

The ability of WBCs to move against a concentration gradient (low to high) in response to chemical factors (chemotactic factors)

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21
Q

Chemotactic factors include:

A

– complement products (C5a)
– chemokines (IL-8)
– bacterial products
– damaged membrane products (arachidonic acid metabolites)

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22
Q

Sequence leading to phagocytosis:

A
  • recognition of foreign body (using PRRs)
  • attachment to the foreign body (opsonization)
  • internalization
  • destruction of the “non-self” pathogen
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23
Q

PRR

A

Pattern recognition recpetors

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24
Q

Opsonins speed up the process of

A

phagocytosis

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25
Two types of opsonins
1) antibodies | 2) complement proteins
26
Opsonization:
- process of “opsonin” addition on bacteria to enhance attachment and engulfment of the injurious agent (eg., bacteria) • bacteria are coated with host factors (factors made by “self” or own body) called opsonins
27
Steps of phagocytosis
1) engulfment | 2) killing by neutrophils
28
Engulfment
– injurious agent surrounded by pseudopods and internalized in a membrane bound phagocytic vacuole
29
Killing by neutrophils
* Oxygen dependent killing * Oxygen-independent enzymatic killing * Suicidal killing
30
Oxygen dependent killing:
corrosive free radicals are produced to destroy a foreign body
31
Oxygen-independent enzymatic killing using:
– lysozymes – lactoferrin – Defensins
32
Oxygen dependent killing (inside neutrophils)
- production of oxygen free-radicals: * superoxide anion O2- * hydrogen peroxide H2O2 * myeloperoxidase produces HOCl. - OXIDATIVE BURST
33
Oxygen-independent killing
bactericidal proteins and enzymes: – lysozyme (action inside the cell) – Lactoferrin (act in the extracellular space) – Defensins (act outside the cell)
34
suicidal killing outside the neutrophils:
- NETs (Neutrophil extracellular traps; 2004)
35
Is to much killing by neutrophils good? Why or why not
NO. Because neutrophil is killing is : - destructive - indiscriminately
36
products produced during | phagocytosis also released extracellularly
– lysosomal enzymes | – oxygen-derived active metabolites
37
Is inflammation beneficial?
– Yes (short term) | – No (long term)
38
MAC
Membrane attack complex
39
What are complement proteins?
– inactive proteins in plasma (about 30 proteins) – cascade of activation reaction amplifies signal – involved in innate defense
40
OIL
– Opsonization – Inflammatory mediators – Lysis
41
Killing by MAC formation (lysis)
Once complemented proteins are deposited on surface of bacteria, they form a pour, and fluid form body floods into the bacteria and kills it.
42
Cellular event (innate immunity)
1) large reserves of neutrophils stored in BM and are released to fight infection 2) neutrophils travel to and enter the effect tissue, engulfed bacteria. Neutrophils then die in the tissue and are engulfed and degraded by macrophages
43
Vascular events (innate immunity)
1) bacteria trigger macrophage to release cytokines and chemokines 2) vasodilation and increased vascular permeability cause, redness, heat, and swelling 3) Inflammatory cells migrate into tissue, releasing inflammatory mediators that cause pain.
44
Primary lymphoid organs
where B and T lymphocytes develop (either bone marrow or thymus)
45
Secondary lymphoid organs
organs that T and B lymphocytes where they first encounter a forgiven antigen and that is what activates them. Before they do this they aren’t activated.
46
``` All lymphocytes (B and T cells) must be able to do the following ```
– Recognize antigens (foreign agents) in a specific manner – Respond to antigens (bringing about their destruction) – Remember the first encounter with an antigen, so they can better respond if exposed to the same antigen again
47
Antigen
A toxin/foreign substance that triggers and immune response which causes antibodies to bind to it
48
Antibody
Y shaped protein binds to antigen to prevent illness
49
Antigen structure contains :
- light chain - heavy chain - Disulphides bridges holding them together
50
Acquired immunity :Role of B cells
Colonial selection, in which the only B cell contains the antigen (red dots) will be selected to further go on to go through mitosis. As it goes through mitosis (colonal expansion) some develop to be plasma cells and others develop to be plasma cells , plasma make antibody molecules that are released into the plasma. Memory cells remember the antigens (red dots) and will go through this process again.
51
Plasma cells are _____ lived
Short
52
Memory cells are ____ lived
Long
53
When B cells go through colonal expansion, what are the two types of cells that form
Plasma cells and memory cells
54
Free, circulating antibodies provide
humoral immunity
55
Anitbodies bound to B cells, act as B cell receptor to
recognize antigen
56
Humoral immunity (major defence against bacteria
Free floating Antibodies bind to the antigens to protect the recpetors on the surface of cells and destroy them by the lysosome
57
Cellular immunity:
• major defense against viruses, cancer, transplants
58
major cells involved:
``` T cells (helper T cells, cytotoxic T cells, and memory T cells) ``` • T cells also do the three “R”…s
59
T cells require
“antigen presentation”
60
Processing and presentation of external foreign antigen
The entire process of having a macrophage (antigen presenting cell) breakdown the antigen and place. It into a MHC so that it is given to the T cells or any other defence cells is known as antigen presenting
61
Interaction between antigen presenting cell (APC) and T cells require three signals for triggering an immune response
1. APC presents antigen on MHC 2. expression of co- stimulatory molecules on APC 3. cytokine secretion by APC
62
Two types of MHC proteins
MHC l and MHC ll
63
MHC I present on virtually all
nucleated cells
64
MHC II is present on
specialized antigen-presenting cells (eg., Macrophages, Dendritic cells)
65
Helper T cells produce cytokines that go to both
B cells and cytotoxic T cells
66
The cytokines form the helper T cells cause cytotoxic T cells to
Directly attacks antigen bearing cells
67
The antibodies produce by the plasma form the B cells
Guide phagocytes, NK cells to attack antigen-bearing cells or to neutralize free antigen
68
Immunological memory
First injection causes minimum all production of memory cells and activated cells, second injection causes a much larger production of these cells
69
Passive Immunity
- acquired by Ingestion of Ab across placenta or through mother’s milk - Pre-formed - Immediate effect - lasts a Few weeks - To combat existing infection
70
Active Immunity
- squired by exposure to disease or injection of altered antigen (vaccine) - Self-generated - takes Weeks (primary) Days (secondary) to acquire - lasts Months to years - to combat future infection

Phsyiology 210 (18 decks)

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