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Patho 2 > 3 - Immune Physiology > Flashcards

3 - Immune Physiology Flashcards

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1
Q

What are the six types of leukocytes?

A
  1. Neutrophils (62%)
  2. Eosinophils
  3. Basophils
  4. Monocytes
  5. Lymphocytes (30%)
  6. Plasma Cells
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2
Q

Which leukocytes are granulocytes?

A

neutrophils

eosinophils

basophils

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3
Q

In progenitor cells, what are the two main lineages of WBCs?

A

myelocytic and lymphocytic

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4
Q

The myelocytic lineage begins with _____

The lymphocytic lineage begins with ______

A

Myeloblasts

Lymphoblasts

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5
Q

Which white blood cells are formed in the marrow?

A

Granulocytes and monocytes

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6
Q

Which leukocytes are not formed in bone marrow?

A

Lymphocytes and plasma cells

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7
Q

What happens to granulocytes and monocytes once they leave the bone marrow?

A

Circulate for a few hours, then move into tissues

when monocytes move into tissues they swell into tissue macrophages

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8
Q

How do WBCs enter tissue spaces?

How do they travel through tissue spaces?

A

Diapedesis

Amoeboid movement

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9
Q

What is chemotaxis?

A

The migration of a cell toward or away from a chemical gradient

When a tissue becomes inflamed, a dozen different products are formed that attract neutrophils and macrophages

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10
Q

What is a chemotactic substance?

A

A chemical beacon

In this case, something that attracts WBCs

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11
Q

Why is it noteworthy that chemotaxis is effective up to 100micrometers away?

A

Because most tissues are only 50 micrometers away from a capillary

makes it very easy for tissues to recruit macrophages etc from the capillaries into the inflamed area

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12
Q

The major function of neutrophils and macrophages is:

A

phagocytosis

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13
Q

How do antibodies and phagocytes cooperate to kill certain cells?

A

the immune system develops antibodies

those antibodies adhere to the infectious agent’s membrane, making it especially susceptible to phagocytosis

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14
Q

The process in which a pathogen is selected for phagocytosis and then destroyed is called:

A

opsonization

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15
Q

Describe a neutrophil’s phagocytic process

A

Neutrophil attaches itself to the particle

projects pseudopodia in all direction around the particle

pseudopodia meet up on the other side of the particle and fuse, creating a closed chamber

chamber invaginates and forms a phagocytic vesicle

Phagosome joins up with a lysosome and eats the particle

debris expelled via exocytosis

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16
Q

Macrophages are the end stage product of ______

A

monocytes that enter the tissues

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17
Q

Which is a more effective phagocyte: neutrophils or macrophages?

A

Macrophages! Can eat up to 100 bacteria, vs neutrophils’ 3-20

They can eat much larger particles, like RBCs and whole parasites

Macrophages survive much longer than neutrophils

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18
Q

What’s the difference between the reticuloendothelial system and the monocyte-macrophage system?

A

Same thing

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19
Q

In the lungs, macrophages phagocytize particles that become entrapped in the alveoli. What do they do with the digestive products?

A

Dump them into the lymphatic system

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20
Q

How are debris and old RBCs filtered in the spleen?

A

arterial blood to the spleen squeezes through trabeculae in the red pulp lined with macrophages

They phagocytize debris and old cells, then return the blood via splenic veins

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21
Q

What are the five basic characteristics of inflammation?

A
  1. vasodilation
  2. vascular permeability
  3. clotting of the interstitial fluid d/t large amounts of fibrinogen and proteins leaking from the capillaries
  4. migration of granulocytes and monocytes to the tissue
  5. swelling of the tissue cells
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22
Q

Why is it significant that the interstitial space and lymphatics are filled with fibrinogen clots during inflammation?

A

This is the walling off effect

prevents bacteria or toxin from spreading

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23
Q

Explain why staphylococcus is more likely than streptococcus to be isolated to a specific tissue, even though staph is much more destructive

A

staph releases extremely lethal cellular toxins that spark an inflammatory walling off that outpaces the ability of staph to multiply and spread

strep produces fewer toxins, and is able to reproduce and spread before inflammation walls it off

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24
Q

When a pathogen enters a tissue, what is the first line of defense?

What is the second?

A

The tissue macrophages

Neutrophil invasion

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25
How do tissue signal for neutrophils to come to their aid?
1. increased expression of adhesion molecules on the capillary endothelium literally sticks to circulating neutrophils and moves them into the tissue 2. endothelial cell junctions loosen to allow diapedesis/extravasation 3. chemotaxis
26
How is neutrophilia in response to a pathogen achieved?
Inflammatory mediators travel to the bone marrow, acting on stored neutrophils and mobilizing them into the circulation
27
When a pathogen enters a tissue, what is the third line of defense?
Monocytes Enter from the blood to the infected tissue and swell into macrophages This is a much slower response than that of neutrophils, but is much more effective and long lasting
28
When a pathogen enters a tissue, what is the fourth line of defense?
The production of more granulocytes and monocytes by the bone marrow Takes 3-4 days
29
What is pus?
necrotic tissue, dead neutrophils, dead macrophages, and tissue fluid
30
How do eosinophils compare to neutrophils?
They are very weak phagocytes but are not significant in protection against *the usual* types of infection
31
Eosinophils react to two types of inflammation/disease:
1. Parasites! 2. Allergic reactions
32
What is the most likely reason eosinophils are involved in allergic reactions?
Basophils and mast cells are the primary participants in reactions, and both of them release eosinophil chemotactic factor
33
What is the role of eosinophils in allergic reactions?
They help “buffer” some of the substances released by mast cells and basophils, controlling the amount of inflammatory mediators released
34
Why are eosinophils well designed for parasitic attack?
their granules release hydrolytic, highly reactive oxygen species, and a highly larvicidal polypeptide called major basic protein
35
Name two common parasitic infections that cause eosinophilia
schistosomiasis trichinosis
36
Both mast cells and basophils liberate ____ into the blood
heparin histamine bradykinin serotonin
37
Why are mast cells and basophils so heavily involved in allergic reactions?
because IgE has a special propensity for mast cells and basophils
38
There are two general kinds of leukemia:
lymphocytic and myelogenous
39
In myelogenous leukemia, the acuity of cancer is dependent on:
the level of differentiation in the abnormal WBCs The less differentiation, the worse the acuity
40
Why does leukemia cause bleeding, low platelets, and anemia?
displacement of normal bone marrow and lymphoid cells with nonfunctional leukemic cells
41
What is humoral immunity?
B cell Immunity the body develops circulating immunoglobulins, produced by B Cells
42
What is cell-mediated immunity?
T cell immunity formation of large numbers of activated T lymphocytes, specifically crafted in lymph nodes to destroy a foreign agent
43
Both cell mediated and humoral immunity are initiated by \_\_\_\_\_\_
presentation of antigens
44
What is antigen short for?
*Anti*body *Gen*erators
45
For a substance to be antigenic, it must be capable of \_\_\_\_\_
generating antibodies Usually has to be a relatively large molecule
46
Antigenicity relies on recurring molecular groups called:
epitopes
47
Why are proteins and large polysaccharides almost always antigenic?
They almost always have epitopes
48
T- Lymphocytes are responsible for:
forming activated lymphocytes to provide cell-mediated immunity
49
B-Lymphocytes are responsible for:
forming antibodies that provide humoral immunity
50
All lymphocytes originate from ______ in the embryo. Where are T cells *differentiated*? Where are B cells *differentiated*?
multipotent hematopoietic stem cells The Thymus gland (T is for thymus) Bone Marrow (B is for bursa, but pretend it's for bone)
51
Describe how T-cells are developed in the Thymus?
They divide rapidly and develop diversity against different antigens
52
What happens to T-cells once they leave the thymus?
They spread out through the blood to various lymph tissues to “stand guard”
53
Pretty much all large proteins are antigenic, including those native to the body. How do T cells know not to react with self-antigens?
Before T-cells are released, the thymus mixes incoming T-cells with a pool of all the self-antigens. If any of them react, they're phagocytized and aren't let out of the thymus
54
How are B cells different from T cells?
1. In T cells the entire cell is reacting. But B cells secrete antibodies that are the actual reactants. 2. B lymphocytes are way more diverse
55
What happens to B lymphocytes after they're released from the bone marrow?
Also travel to lymph organs to stand guard and await invaders
56
What happens when a T cell encounters an antigen?
T cell becomes activated and forms more activated T cells
57
What happens when a B lymphocyte encounters an antigen?
The B lymphocyte enlarges and forms lymphoblasts these differentiate into plasmablasts the plasmablasts divide into plasma cells (about 500 plasma cells per plasmablast) Plasma cells produce gamma globulin antibodies
58
When activated, B cells produce high numbers of antibodies, and T cells produce high numbers of activated T cells. What are both of these products called?
Clone of lymphocytes They are each a perfect clone of their progenitor
59
How is it possible for a single type of stem cell to produce millions of distinct lymphocytes?
Prior to processing, all of the cells produced by hematopoietic stem cells do not have whole genes. They just have hundreds of gene segments During processing, these segments are mixed in random combinations, forming unique whole genes
60
When an invader hits lymph tissue, what is the first thing that happens?
A macrophages lining the sinusoids of the lymph tissue eats it, then passes the antigens by cell-to-cell contact directly to the lymphocytes, who get to work developing activated T cell and antibodies
61
What do macrophages secrete that amps up lymphocyte production?
Interleukin-1
62
How are T-cells involved in B-cell activation?
Most antigens activate B cells and T cells, but some of the T cells that are then formed are T-helper cells These secrete lymphokines, which activate B lymphocytes B lymphocytes are very dependent on T helper cells!
63
How quickly can a plasma cell produces antibodies?
2000 molecules/second per plasma cell
64
How are memory cells formed?
When B cells are activated and start transitioning to lymphoblasts, some of those lymphoblasts don't go on to form plasma cells Instead, they form new B lymphocytes that are identically sensitive to the same antigen These are called memory cells. They circulate and increase sensitivity to a particular invader
65
Why does a second exposure produce a more rapid antibody response?
Memory cells are lying in wait
66
If plasma cells only stick around for a few days or weeks, How is it possible that a 90-year-old can still be immune to a disease they had as a 4-year-old?
When B cells are activated, they form large numbers of short-lived plasma cells that are highly productive, but they also form long-lived plasma cells The long-lived plasma cells hang around in lymph tissues and are slow-and-steady responders
67
All immunoglobulins are composed of:
light polypeptide chains and heavy polypeptide chains The number of chains varies, but they always exist in heavy-light pairs If there are ten heavy, there will be ten light etc.
68
What is the main function of the complement system?
Enhance the actions of antibodies and phagocytes
69
How is the classical pathway of the complement system activated?
When an antibody binds with an antigen, a reactive binding site on the constant portion of the antibody becomes uncovered The uncovered site binds to C1, which sets the rest of the chain into motion
70
How does the complement system contribute to phagocytosis?
Opsonization: activated phagocytosis of the bacteria to which the antigen-antibody complexes are attached
71
How does the complement systems contribute to lysis?
Membrane attack complex: composed to multiple complement factors bound together inserts itself into the lipid bilayer, causing osmotic rupture
72
What are the seven effects of activating the complement cascade?
1. Opsonization 2. Lysis 3. Agglutination 4. Virus Neutralization 5. Chemotaxis 6. Mast cell/basophil activation 7. Inflammation
73
B cells are able to recognize any intact antigen, but T cells respond only to antigens:
that are bound to Major Histocompatibility Complex (HMC) proteins
74
Where are MHC proteins found?
on the surfaces on antigen-presenting cells
75
What are the three types of antigen-presenting cells?
Macrophages B Lymphocytes Dendritic cells
76
What are the three groups of T cells?
T-helper Cells Cytotoxic T Cells Regulatory (suppressor) T Cells
77
75% of T cells are _____ cells
T-helper
78
How do T-helper cells regulate immune function?
Form a series of protein mediators called *lymphokines* lymphokines act on other immune cells and the bone marrow cells
79
Why does HIV cause immunodeficiency?
Destroys T-helper cells, leaving the body almost totally unprotected against infectious disease
80
What are the (4) major actions of lymphokines?
1. Stimulation and growth of cytotoxic T cells and regulatory T cells 2. Stimulation of B cell growth and differentiation 3. Activation of macrophage system 4. Feedback stimulation of T-Helper Cells
81
Cytotoxic T cells are ______ cells
Killer
82
What causes the autoimmune destruction that follows rheumatic fever?
the body becomes immunized against tissues in the joints and heart (especially heart valves) after exposure to a specific type of strep toxin that has an epitope very similar to some self-antigens
83
How can you achieve passive immunity?
Transfusion of antibodies, activated T cells, or both obtained from the blood of someone who's immune Lasts 2-3 weeks
84
Any delayed reaction allergy is caused by:
activated T-cells, NOT antibodies
85
Poison ivy is the result of:
T cell reaction
86
What is an allergen?
an antigen that reacts specifically with a specific type of IgE reagin antibody
87
IgE antibodies have a strong propensity to attach to:
mast cells and basophils
88
Name four diseases caused by IgE activation
1. Anaphylaxis 2. Urticaria 3. Hay Fever 4. Asthma
89
What causes the circulatory collapse of anaphylaxis? What causes the respiratory collapse?
Massive vasodilation and increased permeability cause circulatory collapse Slow-reacting substance causes respiratory collapse
90
What is slow-reacting substance?
mixtures of leukotrienes released from activated basophils and mast cells
91
Is inflammation specific or non-specific?
Non-specific It follows the same course regardless of cause of damage
92
What are the three pathways of complement activation?
1. Classical (activated by antibodies binding to antigens) 2. Lectin (activated by mannose-containing bacteria) 3. Alternative (activated by gram negative bacterial and fungal cell wall proteins)
93
All of the complement activation pathways converge at:
C3
94
What are the three plasma protein systems?
Complement Clotting Kinin
95
What does the kinin system do? What is its primary product?
augments inflammation Bradykinin
96
What does bradykinin do?
1. vasodilation 2. stimulates nerve endings to cause pain 3. causes smooth mm contraction 4. increases vascular permeability 5. increases leukocyte chemotaxis
97
What are cytokines?
intercellular-signaling molecules that are secreted, bind to specific cell membrane receptors, and REGULATE innate or adaptive immunity can be either pro-inflammatory or anti-inflammatory
98
What are the two major types of cytokines?
Interleukins Interferons
99
Interleukins are produced by \_\_\_\_\_\_
macrophages and lymphocytes
100
What are the effects of interleukins?
1. Molecular adhesion 2. Chemotaxis 3. Proliferation/maturation of leukocytes in marrow 4. Enhance/Suppress inflammation 5. Mediate development of acquired immune response
101
Which interleukin is pyrogenic?
Interleukin 1
102
Which substance is probably responsible for fatalities from shock caused by gram-negative bacterial infections?
Tumor Necrosis Factor (TNF) Alpha
103
Which cytokines primarily protect against viral infections?
Interferons
104
Prostaglandins are produced from ____ by \_\_\_\_\_
arachidonic acid cyclooxygenase
105
Which COX is associated with inflammation?
COX 2
106
Generally, activating a platelet does three things:
1. relocates plasma membrane phosphatidylserine to cell surface, allowing adhesion 2. degranulates to release mediators 3. synthesis of thromboxane A2 from prostaglandin H2
107
The two most important phagocytes are ____ and \_\_\_\_\_
neutrophils macrophages
108
The three primary systemic changes associated with acute inflammation are:
Fever Leukocytosis Increased levels of plasma proteins (acute phase reactants)
109
Only three types of cells are capable of complete mitotic regeneration:
epithelial hepatic bone marrow
110
Why does ongoing bleeding delay healing?
excess blood cells at the site must be cleared Formation of a clot increases the amount of space that granulation tissues has to cover Hypovolemia hinders inflammation (less factors circulating)
111
Adhesions can form in which cavities?
Pleural Pericardial Pertioneal
112
Why do steroids prevent wound healing?
prevent macrophages from migrating to site and releasing collagenase and plasminogen activator inhibit fibroblast migration into the wound, delaying epithelialization
113
What the difference between a hypertrophic scar and a keloid?
A hypertrophic scar stays within the original boundaries of the wound A keloid does not

Patho 2 (24 decks)

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