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Boards: Immunology/Hemolymphatic > Immunology Physiology > Flashcards

Immunology Physiology Flashcards

1
Q

What are 2 main lineages of WBCs?

A

myelocytic lineage
lymphocytic lineage

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2
Q

What is the normal proportion of WBCs stored in bone marrow compared to circulation? How many days supply does to circulation provide?

A

6 days supply

3 times as many WBC in bone marrow

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3
Q

After being released from the bone marrow what is the granulocytes’ life span in the blood versus in the tissues?

A

hours (4-8 hours)

several days in tissues

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4
Q

What is the monocytes life span in the blood stream versus in tissues?

A

hours (10-20)
months

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5
Q

What is the life span of lymphocytes? How much time do they spend in the circulation at once?

A

weeks to months
just few hours

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6
Q

What is the life span of platelets?

A

10 days

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7
Q

What are the steps of neutrophil and monocyte extravasation?

A

margination
increased endothelial permeability
diapedesis
chemotaxis

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8
Q

Name examples of substances creating the Chemotaxis source

A
  • DAMPs
  • PAMPs
  • complement cascade products
  • clotting products
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9
Q

Chemotaxis is effective up to XXXXX micrometer.

A

100

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10
Q

List 3 mechanisms by which the phagocytic cells differentiate physiologic from pathophysiologic structures

A
  • smooth surface of healthy tissues –> the rougher surface the more likely phagocytized
  • healthy tissues are covered by protective protein coat - repell phagocytes
  • pathologic structures identified by antibodies and complement (C3) - opsonization
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11
Q

What are the 2 major phagocytic cells?

A

macrophages
neutrophils

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12
Q

Describe the steps of phagocytosis by neutrophils or macrophages

A

identifies particle/bacteria etc –> attaches itself –> psuedopodia formed “hugging” the particle and engulfing it –> chamber formed –> breaks away from the cell surface and swims in the cytoplasm “phagocytic vesicle” –> lysosomes added to vesicle to digest particle –> released by exocytosis

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13
Q

List the digestive and bactericidal agents in phagocytic lysosomes

A
  • proteases
  • lipases (macrophages only)
  • oxidizing agents (suproxide, hydrogen peroxide, hydroxyl ions)
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14
Q

List the components of the reticuloendothelial system

A
  • monocytes/macrophages
  • specialized cells in the endothelium, bone marrow, spleen, lymph nodes
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15
Q

Inflammation is characterized by the following 5:

A
  1. vasodilation –> increased blood flow
  2. increased capillary permeability –> fluid extravasation
  3. coagulation/ clotting of fluid in the interstitial space
  4. leukocyte accumulation (granulocytes and monocytes)
  5. tissue cell swelling
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16
Q

How is inflammation walled off? Describe how this differs between Staph and Strep bacteria

A

fibrinogen clots block of the lymphatics and tissue spaces

the more invasive/destructive the pathogen the quicker the wall-off response
* staph infection is causing severe damage but is walled off faster
* strep infection is more subtle initially and the walling off is slower –> strep more commonly causes hematogenous spread and death

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17
Q

Describe the steps of neutrophil extravasation

A
  • adhesion molecules on endothelial surface (e.g., selectins, ICAM-1)
  • neutrophils have integrins on surface making it stick to the endothelium
  • loseing of capillary and small venule walls
  • neutrophil squeezes through gaps - diapedesis
  • chemotaxis attracts neutrophils
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18
Q

List th 5 most important factors in controlling the response of macrophages to inflammation

A
  • TNF-alpha
  • IL-1
  • granulocyte-monocyte colony-stimulating factor
  • GCSF
  • MCSF
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19
Q

List 7 components of the innate immunity

A
  1. phagocytic cells
  2. stomach acid secretion
  3. skin barrier
  4. lysozymes in blood - attacks and dissolutes bacteria
  5. polypeptides in blood inactivating bacteria
  6. complement complex
  7. natural killer lymphocytes
20
Q

Explain the difference between cellular and humoral immunity

A

both part of the adaptive/acquired immunity

cellular: T-killer cells
humoral: antibodies produced by B-lymphocytes

21
Q

How do macrophages interplay with lymphocytes?

A

present antigens - digests pathogens and then presents parts of it as antigens - stimulate lymphocyte clone activation
macrophages can produce IL-1 –> promotes growth and reproduction of lymphocytes

22
Q

What is the function of T-helper cells?

A

produce lymphokines - activate B lymphocytes

23
Q

Describe the process of B cells producing antibodies

A

B lymphocytes are activated by macrophages –> start forming plasma cells –> produce large amounts of antibodies

24
Q

What are memory cells?

A

B-lymphocytes that reproduce after initial insult and antibody production - at subsequent exposures a large amount of antibodies can be rapidly produced

25
Q

Fill the gaps

A
26
Q

What is the antibody-antigen coupling held together by? (4)

A
  • hydrophobic bonding
  • hydrogen bonding
  • ionic attraction
  • van der Waals forces
27
Q

What is the affinity constant?

A

concentration of bound antigen-antibody complexes / antibody cc times the antigen concentration

28
Q

What percentage of all antibodies do IgG constitute?

A

75%

29
Q

When are IgM primarily produced and why are they so effective despite their small numbers?

A

during initial insult
have many antigen binding sites (10 compared to the 2 in IgG)

30
Q

List the 4 ways by which antibodies can directly inactivate invading agents

A
  • aggregation
  • precipitation
  • covering toxic site on surface - neutralization
  • lysis
31
Q

What are the 11 most important proteins of the complement system?

A
  • C1 - C9, B and D
32
Q

Draw the complement cascade (classical pathway)

A
33
Q

List the 7 effects of the classical pathway of the complement system

A
  • Opsonization, i.e., activates phagocytic cells - C3b
  • lysis - membrane attach complex
  • agglutination
  • neutralization
  • chemotaxis C5a
  • mast cells and basophil activation - C3a, C4a, C5a
  • inflammation
34
Q

What is part of the membrane attack complex?

A

C5b6789

35
Q

What has to be present on the antigen presenting cells in order for T lymphocytes to respond to them? What are its 2 types?

A

Major histocompatibility complex proteins (MCH)

MCH I - presents antigens to cytotoxic T cells/natural killer cells
MCH II - present antigens to T helper cells

36
Q

What are the 3 main antigen-presenting cells?

A

macrophages
dentritic cells
b-cells

37
Q

What are the 3 types of T cells?

A

T helper cells
Cytotoxic T cells
Suppressor T cells

38
Q

What do T-helper cells produce?

A

lymphokines

39
Q

How do cytotoxic T cells kill cells and what is another name for them?

A
  • secrete perforins - hole forming proteins - “punch holes” in the membrane of the attacked cells
  • fluid flows through holes into the cell - cell death
    natural killer cells
40
Q

Describe how IgE causes allergic rections

A

activates basophils and mast cells - cause rupture of these cells –> histamines, proteases, leukotrines, etc.

41
Q

During an allergic reaction when basophils and mast cells rupture, what do they release?

A
  • Histamines
  • Eosinophil chemotactic susbtance
  • Heparin
  • Leukotrines
  • Proteases
  • Neutrophil chemotactic substance
  • Platelet-activating factors
42
Q

Describe type I hypersensitivity reactions

A

antigen exposure –> via skin, GI tract, respirtory tract –> activates antigen specific T helper cell subset –> stimulates B lymphocytes –> become plasma cells –> make a lot of IgE –> IgE binds to mast cells

reexposure –> antigen binds to IgE on mast cells, causes cross linking between two IgE –> triggers degranulation of mast cells

43
Q

Explain type II hypersensitivity reactions

A

mediated by antibody-antigen binding
IgG or IgM against self-antigens on cell surfaces (e.g., RBCs, PLTs)

binding of Ag-Ab initiates complement cascade
* inflammation
* membrane attack complex
* opsonization of phagocytic cells
* natural T killer cells attracted

–> cell destruction

e.g., IMHA, ITP, myasthenia gravis

44
Q

Explain type III hypersensitivity reactions

A

IgG formed against exposed antigen - IgG binds to antigen and forms AbAg complex - immune complexes then deposit in tissues and activate complement proteins - causing local inflammation

if not localized to a tissue but spreading through circulation (if antigen excess) –> can reposit in vascular beds of the kidneys, joints, eyes, skin

examples: FIP, glomerulonephritis, systemic lupus erythematosus, rheumatoid arthritis

45
Q

Explain type IV hypersensitivity reactions

A

Antigens directly stimulate T helper cells - no antibody mediation

cell-mediated so takes longer (24-72 hours)
APC present antigent to T-helper cells –> produce cytokines attracting phagocytic cells –> tissue inflammation

examples: leishmaniasis, contact hypersensitivity, polymyositis, immune-mediated thyroiditis

Boards: Immunology/Hemolymphatic (12 decks)

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