Exam 3. Lymphatic and Immune system Flashcards
A&P II chapter 22
1
Q
Functions of the lymphatic system
A
Fluid recovery: To maintain blood pressure
Immunity: Lymphatic cells in the lymph and nodes
Lipid absorption: Lacteals pick up that were not absorbed
2
Q
Components of the lymphatic system
A
Lymph Lymphatic vessels Lymphatic cells Lymphatic tissues Lymphatic organs
3
Q
Lymph
A
clear colorless similar to plasma. No formed elements
4
Q
Lymphatic vessels
A
Transport lymph back to the blood
5
Q
Lymphatic cells
A
B, T-lymphocyte, NK, Macrophage, dendritic cells the and reticular cells
6
Q
Dendritic and Reticular cells
A
Function like macrophages
Can also: Sound the alarm to alert other immune cells of a foreign substance, cancer cells, diseased cells
7
Q
Lymphatic tissue
A
Not a new tissue, a large aggregation of lymphatic cells
8
Q
Lymphatic organs
A
Several lymphatic cells
the structure will have a capsule that separates the lymphatic cell from everything else around them.
Bone marrow, Thymus, Lymph nodes, tonsils, spleen
9
Q
Lymphatic capillaries
A
Exchange of fluid
penetrate almost all tissue int he body
absent from CNS, cartilage, cornea and bone marrow
Blind-ended capillaries
Large gaps that allow continues to flow into it
10
Q
Lymphatic vessels
A
Very similar to veins
Tunica Interna, media and externa
11
Q
How do we move the lymph?
A
Skeleton muscle pump
Thoracic pump
One way valves
12
Q
Lymph flow
A
Lymphatic capillaries Collecting vessels Six lymphatic trunks Two collecting ducts Subclavian vein
13
Q
Six lymphatic trunks
A
Jugular- cephalic Subclavian- arms Bronchomedistinal- heart, bronchi, lungs Intercostal- ridge cage muscles Intestinal- abdominal organs Lumbar- legs
14
Q
2 Collecting ducts
A
End of line
RIght lymphatic duct: Right jugular, R. subclavian, R, bronchomediastenal, R intercostal.
Thoracic ducts: Everything else. Sarts below the diaphragm.
the starting point called cisterna chylii
15
Q
Redbone marrow function in the lymphatic system
A
Where the lymphatic cells are produced, NK B, T, macrophages
16
Q
Thymus in the lymphatic system
A
T-cell maturation
by secreting thymosin and thymopoietin
17
Q
Spleen
A
Red and White Pulp.
In red pulp: storage of erythrocytes
In white pulp: lymphatic tissue, cells. Where spleen monitors for anything foreign.
18
Q
Lymph Node
A
It monitors the lymph
Most numerous lymphatic organs
It cleanses the lymph
acts as a site of activation for T and B cell
The dendritic cells and macrophages will be the first to encounter foreign material here.
BMT cells will be activated here
19
Q
The tonsils
A
Protects against invaders via respiration or ingesting food
20
Q
1st line of defense against pathogens
A
External barriers
Skin, mucous membranes
Dermis, epidermis (stratifies squamous epithelium)
Sweating making it more acidic
21
Q
2nd line of defense against pathogens
A
- Innate, non-specific, built in mechanisms
- Leukocytes, antimicrobial proteins, immune surveillence (NK cells) inflammation and fever
22
Q
3rd line of defense against pathogens
A
- The immune system, most sophisticated
- Adaptive or specific immune response, meaning it can adapt to specific pathogens the boy is fighting.
- Once the pathogen is defeated, a memory will be produced so the body can respond it faster the second time.
23
Q
Phagocytes
A
Phagocytic cells that phagocytize foreign matter
24
Q
Five types of leukocytes
A
Neutrophils Eosinophils Basophils Monocytes Lymphocyte
25
Neutrophils
- 3-5 lobes
- most abundant
- defend against bacteria infection bu phagocytizing the bacteria, building NETS (neutrophil, extracellular traps) and they produce a cloud of chemicals through respiration burst
26
Respiration burst
Neutrophils dump their oxidizing chemicals into the environment.
They deploy their NETs to trap bacteria nearby
Since they use their own chromosomes to make the NETs the neutrophil will also die
27
Eosinophils
2 lobe, red granules
- Defend against parasitic infection
- Migrate to the area to bombard the parasite with enzymes
- Regulate cells that promote the inflammatory response
- Phagocytise antigen-antibody complex
- Promote basophils during allergic reactions
28
Basophils
Rare, dark and grany
| - Initiates inflammatory response (leukotrienes, histamine, and heparin)
29
Leukotrienes
Signal chemical by basophils.
| It attracts leukocytes to the area, neutrophils, and eosinophils
30
Histamine
Vasodilator
| this speeds leukocytes tot he area of injury
31
Heparin
Prevent coagulation,
| prevents the formation of clots to allow leukocytes to get to the area
32
Mast cells
Also, secrete same substances as basophils
| they come from connective tissue
33
Monocytes
Large, kidney bean
- can leave blood vessel and go into the tissue
- Once they leave blood vessel they become macrophages
- Macrophages are cells that will phagocytize anything that is foreign, dead, damaged or diseased
34
Wandering macrophages
Macrophages that move from blood to tissue, to back into the blood
35
Fixed macrophages
Macrophages that cant leave an area or organ
Microglia: CNS
Alveolar: Lungs
Hepatic: Liver
36
Antimicrobial Proteins
Proteins that inhibit microbial reproduction and provide short term, non-specific resistance to pathogenic bacteria and viruses.
37
The two families of antimicrobial proteins
Interferons
| Complement system
38
Interferons
Work against viral infection when they infect a lymphocyte.
Lymphocyte realizes they are infected and are dying
The lymphocyte will secrete interferons to alert cells of what is coming.
This prevents the virus from binding to other cells
39
Complement system
Part of antimicrobial proteins
It consists of about 30 proteins that complement the specific immunity and non-specific resistance
-It is activated by 3 different pathways
- Once it is activated it can start 4 methods of destructions
3 pathways, once they are activated they end up at complement protein C3. They become activated C3a or C3b. After, those go on to activate the 4 methods of destruction
40
3 pathways of the complement system
- Classical
- Alternative
- Lectin
41
Classical Pathway
- Activation depends on antibody
- Part of specific immunity
- The antibodies bind to the antigen-antibody complex, changing its shape which reveals a complement protein binding site.
- C1 binds to that site and causing other complement proteins (like C3b) to attach to the antibody. This cascade reaction is called complement fixation
- basically binding of C1 to antigen-antibody complex activates the classical pathway
42
Alternative pathway
- Spontaneous sampling
- non-specific
- does not require antibody
- Once a foreign material is identified, C3 breaks down to C3a and C3b
43
Lectin
Relies on lectins
- Some pathogens have lectins as their markers
- After identifying the lectins the complement proteins react
- The proteins become active and initiate the methods of destruction
44
4 methods od destruction
Inflammation
Immune clearance
Phagocytosis
Cytolysis
45
C3a
- Inflammatory response
- It influences basophils and mast cells to produce an inflammatory response
- Basophils and mast cells degranulate and secrete their chemicals (leukotrienes, histamine, heparin)
46
C3b
- Immune clearance
- phagocytosis
- Cytolysis
47
Immune clearance and C3b
- C3b binds antigen-antibody complexes to erythrocytes
- The erythrocyte will transport the chain to the liver and spleen.
- Lymphocytes and macrophages will destroy the complex, clearing it from the system.
48
Phagocytosis and C3b
- A signal on the surface of a foreign cell tells macrophages to eat it that cell.
- C3b binds to the pathogen and it functions as a signal this is called "opsonization"
49
Opsonization
Coating a pathogen with C3b to mark it for destruction
50
Cytolysis and C3b
- The cell bursts
- Several C proteins work to put a hole in the pathogen's cell membrane.
- C3b activates C5b activates C5-C9.
- They create the "membrane attack complex"
- Water can now come in until it lysis the cell
- Macrophages will eat the remainings
51
Membrane attack complex
Complement proteins form a ring in the plasma membrane of the target cell causing it to lysis.
52
Immune surveillance
- NK continually patrol the body looking for pathogens and diseased host cells
- They will attack and destroy
53
NK
- Natural Killer cells
- Lymphocyte
- Immune Surveillance
- bacteria, cells of transplanted organs, cells infected with viruses and cancer cells
- Use proteins: Perforins, Granzymes
54
Perforins
Nk's protein
| They perforate the membrane of the target cell
55
Granzymes
NK's protein
- Once the cell has a perforated hole from the perforins
- The NK will also dump in lytic enzymes into the cell
- The enzymes destroy the machinery inside the cell
56
Inflammation
Local response to tissue injury
- itis suffix means inflammation of that organ
- Initiated by basophils which release their leukotrienes especially cytokines
57
Purposes of inflammation
- Limits spread of pathogens, then destroys them
- removes debris from damaged tissue
- initiate tissue repair
58
Cytokines
- Chemicals during inflammation that bring other cells to the area by chemotaxis
- Neutrophils and Eosinophils, and macrophages
- Basophils and mast cells will come in and secrete histamine and heparin
59
Hyperemia
- The increase of blood flow to the area during the inflammation process
- Responsible for redness, swelling, heat
60
Four cardinal signs of inflammation
Redness
Swelling
Heat
Pain
61
Fever
- Elevated blood temp to increase metabolic rate and get immune cells working
- Regulated by hypothalamus
- Molecules that are known as pyrogens
- The pyrogens stimulate the hypothalamus to reset the body temperature
- 3 stages
62
Stages of fever
Onset: Temperature is reset and it starts to go up. (shivers)
Stadium: Temperature oscillates as long as a pathogen is present (Up/down)
Defervescence: Temperature returs to normal. (sweating, warm, flushed skin)
63
Exogenous pyrogens
Fever producing agents from outside the body.
| Sometimes found on the surface of bacteria or viruses
64
Endogenous pyrogens
Stimulate neurons in the hypothalamus to raise the set point of body temperature
65
Specific immunity and its two characteristics
-The adaptive immune response
Specificity:
-Specific to what we are attacking
- Will adapt to attack a pathogen and it will be very specific to only that pathogen
Memory:
- Produces a memory of what that pathogen was
- When re-exposed the body reacts so quickly we don't notice the illness
66
Two types of immunity
Cellular
| Humoral
67
Cellular immunity
- Cells physically defend against pathogens
- T-cell, lymphocyte
- Directly destroy the pathogens
68
Humoral immunity
- Antibody-mediated
- Fluids of the body lymph and blood
- More indirect
- B-cells that differentiate into another cell that secrete other antibodies
- The antibodies go into lymph and blood circulating in those fluids until they find their target
69
4 forms of immunity
Natural active immunity
Artificial active immunity
Natural passive immunity
Artificial passive immunity
70
Natural active immunity
Active production of our own antibodies or T-cells as a result of infection or natural exposure to antigen.
- memory made
71
Artificial active immunity
Actively production of our own antibody or T-cells as a result of vaccination against the disease.
- memory made
72
Natural passive immunity
Temporary immunity that results from antibodies produced by another person.
- fetuses acquire antibodies from the placenta
- no memory
73
Artificial passive immunity
Temporary immunity that results from the injection of immune serum (antibodies) from another person to animal
- snakebite treatment. Antivenom
- no memory
74
Antigen
Antibiotic generator
Any molecule that triggers an immune response
Large molecule
75
Epitopes
- part of the antigen molecule, smaller part
| - the part that we respond to
76
Haptens
- Smaller molecules are too small to be recognized by themselves.
- Once they bind to macromolecules will elicit a response.
- many times an allervic response
- pollen, cosmetics, detergents, poison
77
Major cells of immune system
Major cells of the immune system
- lymphocytes
- macrophages
- dendritic cells
78
Dendritic cells
- Sound the alarm that something is there
79
3 categories of lymphocytes
NK- not involved with specific immune, they are immune surveillance
T-Lymphocyte
B-lymphocyte
80
Life cycle of T and B cells
- Born in bone marrow
- B-cells stay there
- T-cells migrate to the thymus where they mature
81
T-cells maturation
- They maturate in the thymus.
- The thymus secretes hormones that will influence the T-cells to produce receptors on their surface
- Those receptors allow them to function in their roles
- While developing they are isolated and tested
- If the cell doesn't react to our own body antigen they pass the test and are deployed to lymphatic tissue and organs.
82
What happens when T-cells fail the test
- The ones that fail the test either get destroyed and all cells that come from that line (clonal deletion)
. They also go through anergy,
receptors are removed so they can't do anything.
83
APCs
Antigen-presenting cell
- They present foreign antigens
- macrophages, dendritic cells and B-cells
- All cells have self-markers
- The APC won't recognize the self-marker of foreign cell, it phagocytizes the cell and takes its self-marker.
it then comes over to a T-cell and shows it the foreign marker. That activates specific immune response to that marker.
- The t-cell transforms into other t-cells including memory cells and cytotoxic-t-cell
84
Cytotoxic T-cell
- Programmed to destroy a cell based on the marker shown to the T-cell by the APCs.
- Effectors of cellular immunity
- Recognizes MHCI
- Delivers lethal chemicals like NK cells do
85
Helper T-cells
- The most important immune cell in the body
- The T-cell that starts the cellular immune response, that the cell the marker is shown to
- Also activates humoral immunity by recognizing that the B-cell acting as an APC has a foreign marker.
- Involved in non-specific defense mechanisms
86
TM memory
Responsible for memory in cellular immunity
descend from T-cells
Circulate in blood and lymph
87
MHCI
Self-marker
Major histocompatibility complex
T-cytotoxic cells only recognize MHCI
88
MHCII
Major histocompatibility complex
Only found on APCs
The site where APC can display foreign MCHI complex
T helper cell only recognizes MHCII
89
Humoral immunity
Indirect
relies on antibodies
neutrolizing
B-cell main cell by initiating a response
The B-cells don't make the antibodies, they have to be activated and made into the plasma cell or effector cell
90
Stages of humoral immunity
Recognition
attack
memory
91
Recognition stage of humoral immunity
- The B-cells have unique antibodies, once they bind to the corresponding antigen the B-cell will use it to function as an APC
- That B-cell goes over to T-helper, they bind and the Th cell recognizes the foreign cell and it activates that B-cell
- Activated B-cell differentiates into memory cells and plasma cells
- The plasma cells will become an antibody factory and release the antibodies that will bind to that specific antigen
92
Attack stage of humoral immunity
-antibodies bind to antigen, it renders it harmless and tags it for destruction
93
Memory stage of humoral immunity
- Some B-cells differentiate into memory cells that circulate for a long time
94
Antibody parts
```
A protein with amino acid chains
The light chains are pure amino acids
The heavy chains
both chains are bound together by disulfide bonds
Complement binding sites
The constant region
The variable region
Antigen binding site
```
95
Humoral antibodies
IgM
| IgG
96
IgM
pentameter in plasma and lymph
| secreted in primary immune response, agglutination and complement fixation
97
IgG
Monometer
80% of circulating antibodies
crosses the placenta to fetus
secreted in secondary immune response, complement fixation
98
5 classes of antibodies
```
IgA
IgD
IgE
IgG
IgM
```
99
IgA
Monometer in plasma
dimer in mucus, saliva, tear, milk, intestinal secretions
prevents pathogen adherence to epithelia
provides passive immunity to newborns
100
IgD
Monometer
B-cell transmembrane antigen receptor
thought to function in B cell activation by antigens
101
IgE
monometer
transmembrane protein on basophils and mast cells
stimulates the release of histamine and other inflammatory chemicals
attracts eosinophils to parasitic infection
produces immediate hypersensitivity reactions
