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Guyton & Hall Physiology > Ch 33-34: Body resistance to infection > Flashcards

Ch 33-34: Body resistance to infection Flashcards

1
Q

Summarize the genesis of myelocytes

A
  1. myeloblast
  2. Promyelocyte or monocyte development
    a. Promyelocyte becomes megakaryocyte or continues
  3. Neut/eosin/basophil

Neutrophil:
-myelocyte > metamyelocyte > band neut > mature/polymorphonuclear
Eosinophil: myelocyte > metamyelocyte >pmn eosin
Basophil: myelocyte to PMN basophil

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2
Q

How many wbc are in the bone marrow compared to the blood?

A

Triple the blood amount is in the bone marrow.

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3
Q

What is the lifespan of granulocytes vs lymphocytes?

A

granulocytes: 4-8 hours in blood, then 4-5 days in tissue

Monocytes: 10-20 hours in blood before tissue (months)

Lymphocytes: weeks-months

Platelets: replaced every 10 days

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4
Q

How far from a focus of inflammation can chemotaxis effectively recruit wbc’s?

A

up to 100 micrometers away

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5
Q

Briefly, what are the three main features/procedures that ‘encourage’ phagocytosis by Neut’s and macro’gs?

A
  1. Rough surfaces
  2. Loss of protein coating
  3. Antibody adherence leading to opsonization
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6
Q

How does the phagocytic activity and intracellular processing of the material differ between neutrophils and monocytes/macrophages? How are they alike?

A

Alike: both form pseudopodia and engulf their target as an intracellular phagosome, use proteolytic enzymes and bactericidal agents.

Different:
-Neuts only phagocytize 3-20 bacteria, then dies
-Macro’s can take 100 bacteria, parasites, and whole RBCs, extrude the ‘corpses’ and continue to function
-Macro’s lysosomes contain lipases to digest thick lipid membranes

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7
Q

What are the names or specific locations of the prominent tissue-specific macrophages of the reticuloendothelial system?

A

Skin/Subq: histiocytes
Lymph nodes: macrophages
Lungs: alveolar macrophages. Can form “giant cell” capsules around indigestible particles
Liver sinusoids: kupffer cells
Spleen and bone marrow: macrophages in trabeculae of splenic pulp

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8
Q

List the 5 basic changes that occur in tissue inflammation

A
  1. Local vasodilation and inc bloodflow
  2. Increased capillary permeability
  3. Clotting fluid in interstitial spaces (due to fibrinogen etc)
  4. Granulocyte and monocyte migration to tissue
  5. Swelling of tissue cells
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9
Q

What is the ‘walling-off’ effect?

A

Blocking tissue spaces and lymphatics with fibrinogen clots prevents spread of bacteria or toxins. More effective if inflammation develops rapidly

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10
Q

Briefly, what are the three main steps in neutrophil invasion of an area?

A

1.Margination: Rolling adhesion (selectins) and tight binding (ICAM)
cytokines cause increased production of adhesion molecules (selectins, ICAM-1) that react with integrin on neutrophils to make neut’s stick to the capillary walls of the inflamed area

  1. Diapedesis:
    intercellular attachments between endothelial cells of capillaries/venules losen and allow openings for neutrophils to enter
  2. Chemotaxis
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11
Q

Briefly, list the 4 lines of defense, in order

A
  1. Tissue macrophages
  2. Neutrophil invasion
  3. Second macrophage invasion
  4. Increased granulocyte & monocyte production by the bone marrow
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12
Q

How long after invading inflammed tissue does it take for tissue macrophages to be fully developed?

A

8 hours

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13
Q

How long does it take for the fourth line of defense to be able to leave the bone marrow?

A

3-4 days

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14
Q

Which five factors are most prominent in feedback control of macrophage and neutrophil responses?

A
  1. tumor necrosis factor
  2. IL-1
  3. granulocyte-monocyte colony stimulating factor (GM-CSF)
  4. granulocyte-colony-stimulating factor (G-CSF)
  5. monocyte colony stimulating factor (M-CSF)

**formed by activated macrophage cells in inflammed tissues and other inflammed cells

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15
Q

Which of the above factors causes increased production of granulocytes and monocytes?

A

SURPRISE…duh…the colony stimulating factors

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16
Q

Describe the feedback system of Macpg and neut response

A

Activated macrophage stimulates release of TNF and IL-1, which stimulates the endothelial cells, fibroblasts, and lymphocytes to produce colony-stimulating factors.
Activated macrophages also release all 5 factors that stimulate the bone marrow, along with the cell products mentioned above, to stimulate further immune cell production

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17
Q

How do eosinophils attack and kill parasites?

A
  1. Releasing hydrolytic enzymes from granules (mod’d lysosomes)
  2. Releasing reactive oxygen species
  3. Releasing the larvacidal polypeptide Major Basic Protein
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18
Q

Why do eosinophils accumulate in the tissues where allergic reactions occur?

A

because mast cells and basophils release Eosinophil Chemotactic Factor to cause EOs migration

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19
Q

What are the functions of basophils and mast cells?

A

-heparin release
-histamine, bradykinin, slow-reacting sucbstance of ananphylaxis, lysosomal enzymes, and serotonin release
-They rupture on signal from reaction of IgE with antigen

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20
Q

What are the two main types of leukemia, and how are they different?

A
  1. Lymphocytic leukemia: neoplasia of lymphoid cells
  2. Myelogenous leukemia: neoplasia of young myelogenous cells in the bone marrow. The more “undifferentiated” the cell, the more acute and the worse px
21
Q

Where are T lymphs vs B lymphs pre-processed?

A

B-cells: fetal liver and bone marrow
T-cells: thymus

22
Q

What does a substance have to have, to be antigenic?

A

High molec. wt (> 8000)
Epitopes: regularly recurring molecular groups on the surface

23
Q

How does a common lymphoid progenitor cell develop into a T cell or B cell, respectively?

A
  1. CLP cell in bone marrow > b cell > B lymphocyte > reacts with antigen in peripheral lymphoid tissue > Plasma cell that produces antibodies
  2. CLP cell in bone marrow > Thymus for developing diverse reactivity against different specific antigens and ensure not self-reactive > T lymphocyte > reacts with antigen in peripheral lymphoid tissue > activated T lymphocyte
24
Q

In what two major ways do B cells differentiate from T cells?

A
  1. With T cells, the whole cell learns to be reactive. With B cells, they learn to secrete antibodies as the reactive portion
  2. B cells have even greater diversity than T lymphocytes by forming millions of antibodies
25
Q

What is a clone of lymphocytes?

A

Clone of lymphocytes = all the different lymphocytes capable of forming ONE specific antibody or T cell. All the cells in a clone are alike/trained for the same antigen/pathogen

26
Q

From where does the whole gene for forming each B/T cell originate?

A

The original stem cells only have gene segments. During preprocessing these are mixed together randomly to form whole genes

27
Q

Which protein (type of protein) lends specificity to T cells?

A

Surface receptor proteins (T-cell markers) on the surface, specific for one specified activating antigen

28
Q

How do macrophages participate in the activation of lymphocytes?

A
  1. Digest invaders and pass on the now-liberated antigens to the lymphocytic clones
  2. Produce IL-1 to promote further growth and reproduction of specific lymphocytes
29
Q

How do T cells participate in activating the B lymphocytes?

A

Helper T cells secrete lymphokines to activate B lymphocytes to a high degree

30
Q

What “upgrades” turn a b lymphocyte into a plasma cell?

A

Cytoplasm expands, rough endoplasmic reticulum proliferates, and they can produce gamma globulin antibodies

31
Q

What are memory B cells?

A

B lymphocytes that are similar to the original clone but remain dormant until a followup activation to create a more rapid and potent antibody response

32
Q

Describe the structure of an immunoglobulin. What is the functional purpose of each component?

A

Constant portion and a variable portion. Heavy and light polypeptide chains are bound by hinge regions.
The constant portion determines diffusivity in tissues, adherence to structures within tissues, attachement to the complement complex, how easily it can pass through memrbanes, and more.

The variable portion determines antibody specificity and attaches to an antigen. The amino acids have a different shape for each antigen, and the more specific an antibody is, the stronger it will bond

33
Q

What type of bonds bind antibody and antigen (such as in a very specific antibody)? How can you quantify bond tightness?

A
  1. hydrophobic bonding
  2. hydrogen bonding
  3. ionic attractions
  4. van der Waals forces

Ka = affinity constant. A measure of bond tightness

34
Q

In what 2 ways do antibodies protect from invaders?

A
  1. Direct attack:
    a. Agglutination: clumping together of multiple particles with surface antigens
    b. Precipitation: antigen-antibody complex makes the antigen insoluble
    c. Neutralization: toxic sites covered by antibodies
    d. Lysis: antibodies rupture the agent’s membrane
  2. Activating the complement system:
    -System of 20 complement proteins, starting with the proenzyme C1 (explained further later)
35
Q

What are the most important effects of the complement cascade? Which complement is most associated with each?

A
  1. Opsonization and phagocytosis: C3b. Activates Neuts and Macro’pg to make them engulf the “tagged” bacteria
  2. Lysis: C5b6789. Ruptures cell membranes of invaders.
  3. Agglutination: change invader surfaces to make them stick together
  4. Neutralization of viruses: attack virus structures and make them non virulent
  5. Chemotaxis: C5a initiates macrophage/neut chemotaxis
  6. Activation of mas cells and basophils: C3a, C4a, C5a. Activation causes increased blood flow, fluid/protein leakage, and local reactions to immobilize the invader
  7. Inflammatory effects: perfusion, permeability of capillaries, protein coagulation
36
Q

What follows when a clone of T cells is presented with the proper antigen?

A
  1. The clone proliferates and whole activated T cells release into lymph.
    Can circulate the body for years
  2. Some new cells stay in the lymphoid tissue to become T-lymphocyte memory cells
37
Q

What is needed for a T cell to be activated?

A

Antigen must be bound to an MHC protein on an antigen presenting cell (dendritic cells are the pro’s, but also B lymphs and macrophages).

Cell adhesion proteins must interact for T cells to bind long enough to activate

38
Q

What are MHC proteins?

A

Major histocompatibililty complex genes encode them.
1. MHC 1 present antigens to cytotoxic T cells
2. MHC II present antigens to T helper cells

39
Q

What is the functional purpose of Helper T cells?

A

-most numerous
-form lymphokines: IL2 - 6, Interferon gamma, GM-colony stimulating factor

40
Q

What are the functions of lymphokines?

A
  1. IL-2 (and some others) stimulates growth and proliferation of cytotoxic and suppressor T cells
  2. IL4, 5, and 6 are B cell stimulating/growth factors, and stimulate antibody secretion
  3. All lymphokines activate the macrophage system by slow/stopping cell migration to targets and stimulate more efficient phagocytosis
  4. IL-2 (and more) have direct positive feedback in stimulating helper T cells to amplify response
41
Q

What is the functional purpose of cytotoxic T cells?

A

“killer cells”
-secrete perforins to perforate invader membranes
-release cytotoxic substance into cells
-destroy cancer cells, heart transplant cells, etc

42
Q

What are the functions of suppressor T cells?

A

can suppress the cytotoxic and helper T cells. “regulatory” T cells

43
Q

What occurs in delayed-reaction allergy?

A

-Activated T cells, after repeated exposure to an antigen, elicit cell-mediated immunity that leads to macrophage tissue invasion and release of toxic substances into tissues.
-Usually a local response

44
Q

What causes an atopic allergy? How is IgE involved?

A

-Heritable
-large quantities of IgE in the blood (reagins or sensitizing antibodies) react when an allergen enters the body
-IgE has a strong propensity to attach to mast cells and basophils. Result is immediate changes in the cell membrane and rupture, releasing histamine, protease, toxic leukotrienes, eos/neut chemotaxic substance, heparin, platelet activating factors

45
Q

What occurs in anaphylaxis?

A

Widespread allergic reaction:
-body-wide vasodilation and increased capillary permeability with marked loss of plasma from circulation
-can cause circulatory shock
-Bronchiolar spasm may follow due to slow-reacting substance of anaphylaxis

46
Q

What causes urticaria?

A

Local histamine release causes vasodilation in red flare, increased local permeability and local areas of swelling. “hives”

47
Q

What causes asthma?

A

Slow-reacting substance of anaphylaxis is key here: bronchiolar smooth muscle spasm and difficulty breathing. Antihistamines are NOT useful

48
Q
A

Guyton & Hall Physiology (26 decks)

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