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Patho 2 > 3 - Immune Physiology > Flashcards

3 - Immune Physiology Flashcards

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
Q

How do tissue signal for neutrophils to come to their aid?

A
  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
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26
Q

How is neutrophilia in response to a pathogen achieved?

A

Inflammatory mediators travel to the bone marrow, acting on stored neutrophils and mobilizing them into the circulation

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27
Q

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

A

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

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28
Q

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

A

The production of more granulocytes and monocytes by the bone marrow

Takes 3-4 days

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29
Q

What is pus?

A

necrotic tissue, dead neutrophils, dead macrophages, and tissue fluid

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30
Q

How do eosinophils compare to neutrophils?

A

They are very weak phagocytes but are not significant in protection against the usual types of infection

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31
Q

Eosinophils react to two types of inflammation/disease:

A
  1. Parasites!
  2. Allergic reactions
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32
Q

What is the most likely reason eosinophils are involved in allergic reactions?

A

Basophils and mast cells are the primary participants in reactions, and both of them release eosinophil chemotactic factor

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33
Q

What is the role of eosinophils in allergic reactions?

A

They help “buffer” some of the substances released by mast cells and basophils, controlling the amount of inflammatory mediators released

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34
Q

Why are eosinophils well designed for parasitic attack?

A

their granules release hydrolytic, highly reactive oxygen species, and a highly larvicidal polypeptide called major basic protein

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35
Q

Name two common parasitic infections that cause eosinophilia

A

schistosomiasis

trichinosis

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36
Q

Both mast cells and basophils liberate ____ into the blood

A

heparin

histamine

bradykinin

serotonin

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37
Q

Why are mast cells and basophils so heavily involved in allergic reactions?

A

because IgE has a special propensity for mast cells and basophils

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38
Q

There are two general kinds of leukemia:

A

lymphocytic and myelogenous

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39
Q

In myelogenous leukemia, the acuity of cancer is dependent on:

A

the level of differentiation in the abnormal WBCs

The less differentiation, the worse the acuity

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40
Q

Why does leukemia cause bleeding, low platelets, and anemia?

A

displacement of normal bone marrow and lymphoid cells with nonfunctional leukemic cells

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41
Q

What is humoral immunity?

A

B cell Immunity

the body develops circulating immunoglobulins, produced by B Cells

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42
Q

What is cell-mediated immunity?

A

T cell immunity

formation of large numbers of activated T lymphocytes, specifically crafted in lymph nodes to destroy a foreign agent

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43
Q

Both cell mediated and humoral immunity are initiated by ______

A

presentation of antigens

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44
Q

What is antigen short for?

A

Antibody Generators

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45
Q

For a substance to be antigenic, it must be capable of _____

A

generating antibodies

Usually has to be a relatively large molecule

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46
Q

Antigenicity relies on recurring molecular groups called:

A

epitopes

47
Q

Why are proteins and large polysaccharides almost always antigenic?

A

They almost always have epitopes

48
Q

T- Lymphocytes are responsible for:

A

forming activated lymphocytes to provide cell-mediated immunity

49
Q

B-Lymphocytes are responsible for:

A

forming antibodies that provide humoral immunity

50
Q

All lymphocytes originate from ______ in the embryo.

Where are T cells differentiated?

Where are B cells differentiated?

A

multipotent hematopoietic stem cells

The Thymus gland (T is for thymus)

Bone Marrow (B is for bursa, but pretend it’s for bone)

51
Q

Describe how T-cells are developed in the Thymus?

A

They divide rapidly and develop diversity against different antigens

52
Q

What happens to T-cells once they leave the thymus?

A

They spread out through the blood to various lymph tissues to “stand guard”

53
Q

Pretty much all large proteins are antigenic, including those native to the body. How do T cells know not to react with self-antigens?

A

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
Q

How are B cells different from T cells?

A
  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
Q

What happens to B lymphocytes after they’re released from the bone marrow?

A

Also travel to lymph organs to stand guard and await invaders

56
Q

What happens when a T cell encounters an antigen?

A

T cell becomes activated and forms more activated T cells

57
Q

What happens when a B lymphocyte encounters an antigen?

A

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
Q

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?

A

Clone of lymphocytes

They are each a perfect clone of their progenitor

59
Q

How is it possible for a single type of stem cell to produce millions of distinct lymphocytes?

A

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
Q

When an invader hits lymph tissue, what is the first thing that happens?

A

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
Q

What do macrophages secrete that amps up lymphocyte production?

A

Interleukin-1

62
Q

How are T-cells involved in B-cell activation?

A

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
Q

How quickly can a plasma cell produces antibodies?

A

2000 molecules/second per plasma cell

64
Q

How are memory cells formed?

A

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
Q

Why does a second exposure produce a more rapid antibody response?

A

Memory cells are lying in wait

66
Q

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?

A

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
Q

All immunoglobulins are composed of:

A

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
Q

What is the main function of the complement system?

A

Enhance the actions of antibodies and phagocytes

69
Q

How is the classical pathway of the complement system activated?

A

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
Q

How does the complement system contribute to phagocytosis?

A

Opsonization:

activated phagocytosis of the bacteria to which the antigen-antibody complexes are attached

71
Q

How does the complement systems contribute to lysis?

A

Membrane attack complex:

composed to multiple complement factors bound together

inserts itself into the lipid bilayer, causing osmotic rupture

72
Q

What are the seven effects of activating the complement cascade?

A
  1. Opsonization
  2. Lysis
  3. Agglutination
  4. Virus Neutralization
  5. Chemotaxis
  6. Mast cell/basophil activation
  7. Inflammation
73
Q

B cells are able to recognize any intact antigen, but T cells respond only to antigens:

A

that are bound to Major Histocompatibility Complex (HMC) proteins

74
Q

Where are MHC proteins found?

A

on the surfaces on antigen-presenting cells

75
Q

What are the three types of antigen-presenting cells?

A

Macrophages

B Lymphocytes

Dendritic cells

76
Q

What are the three groups of T cells?

A

T-helper Cells

Cytotoxic T Cells

Regulatory (suppressor) T Cells

77
Q

75% of T cells are _____ cells

A

T-helper

78
Q

How do T-helper cells regulate immune function?

A

Form a series of protein mediators called lymphokines

lymphokines act on other immune cells and the bone marrow cells

79
Q

Why does HIV cause immunodeficiency?

A

Destroys T-helper cells, leaving the body almost totally unprotected against infectious disease

80
Q

What are the (4) major actions of lymphokines?

A
  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
Q

Cytotoxic T cells are ______ cells

A

Killer

82
Q

What causes the autoimmune destruction that follows rheumatic fever?

A

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
Q

How can you achieve passive immunity?

A

Transfusion of antibodies, activated T cells, or both obtained from the blood of someone who’s immune

Lasts 2-3 weeks

84
Q

Any delayed reaction allergy is caused by:

A

activated T-cells, NOT antibodies

85
Q

Poison ivy is the result of:

A

T cell reaction

86
Q

What is an allergen?

A

an antigen that reacts specifically with a specific type of IgE reagin antibody

87
Q

IgE antibodies have a strong propensity to attach to:

A

mast cells and basophils

88
Q

Name four diseases caused by IgE activation

A
  1. Anaphylaxis
  2. Urticaria
  3. Hay Fever
  4. Asthma
89
Q

What causes the circulatory collapse of anaphylaxis?

What causes the respiratory collapse?

A

Massive vasodilation and increased permeability cause circulatory collapse

Slow-reacting substance causes respiratory collapse

90
Q

What is slow-reacting substance?

A

mixtures of leukotrienes released from activated basophils and mast cells

91
Q

Is inflammation specific or non-specific?

A

Non-specific

It follows the same course regardless of cause of damage

92
Q

What are the three pathways of complement activation?

A
  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
Q

All of the complement activation pathways converge at:

A

C3

94
Q

What are the three plasma protein systems?

A

Complement

Clotting

Kinin

95
Q

What does the kinin system do?

What is its primary product?

A

augments inflammation

Bradykinin

96
Q

What does bradykinin do?

A
  1. vasodilation
  2. stimulates nerve endings to cause pain
  3. causes smooth mm contraction
  4. increases vascular permeability
  5. increases leukocyte chemotaxis
97
Q

What are cytokines?

A

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
Q

What are the two major types of cytokines?

A

Interleukins

Interferons

99
Q

Interleukins are produced by ______

A

macrophages and lymphocytes

100
Q

What are the effects of interleukins?

A
  1. Molecular adhesion
  2. Chemotaxis
  3. Proliferation/maturation of leukocytes in marrow
  4. Enhance/Suppress inflammation
  5. Mediate development of acquired immune response
101
Q

Which interleukin is pyrogenic?

A

Interleukin 1

102
Q

Which substance is probably responsible for fatalities from shock caused by gram-negative bacterial infections?

A

Tumor Necrosis Factor (TNF) Alpha

103
Q

Which cytokines primarily protect against viral infections?

A

Interferons

104
Q

Prostaglandins are produced from ____ by _____

A

arachidonic acid

cyclooxygenase

105
Q

Which COX is associated with inflammation?

A

COX 2

106
Q

Generally, activating a platelet does three things:

A
  1. relocates plasma membrane phosphatidylserine to cell surface, allowing adhesion
  2. degranulates to release mediators
  3. synthesis of thromboxane A2 from prostaglandin H2
107
Q

The two most important phagocytes are ____ and _____

A

neutrophils

macrophages

108
Q

The three primary systemic changes associated with acute inflammation are:

A

Fever

Leukocytosis

Increased levels of plasma proteins (acute phase reactants)

109
Q

Only three types of cells are capable of complete mitotic regeneration:

A

epithelial

hepatic

bone marrow

110
Q

Why does ongoing bleeding delay healing?

A

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
Q

Adhesions can form in which cavities?

A

Pleural

Pericardial

Pertioneal

112
Q

Why do steroids prevent wound healing?

A

prevent macrophages from migrating to site and releasing collagenase and plasminogen activator

inhibit fibroblast migration into the wound, delaying epithelialization

113
Q

What the difference between a hypertrophic scar and a keloid?

A

A hypertrophic scar stays within the original boundaries of the wound

A keloid does not

Patho 2 (24 decks)

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