Exam 4-Inflammation, Immune System Flashcards

1
Q

What is the purpose of inflammation and immunity?

A

To protect through neutralizing, eliminating, or destroying organisms invading the internal environment.

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2
Q

Where are Human Leukocyte antigens found?

A

On the. surface of most body cells

  • specific too that personally
  • universal product code
  • capable of stimulating an immune response
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3
Q

What are other names for Human Leukocyte antigens?

A

Human transplantation antigens
Human histocompatibility antigens
Class I antigens

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4
Q

Functions of Human Leukocyte Antigens

A
  1. Determine tissue type

2. Key for recognition and self-tolerance

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5
Q

Self vs Non-Self

A
  • Self tolerance
  • Determination by the immune system of whether or not certain cells belong

“Hey you are not like the other cells! You can’t come in!”

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6
Q

Immune System Influences

A

Nervous system
Endocrine system
GI system

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7
Q

stem cells

A

-immature, undifferentiated cells

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8
Q

What are stem cells produced by?

A

bone marrow

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9
Q

Why are stem cells Pluripotent?

A

They can travel to any direction they choose to go (towards any RBC)

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10
Q

Leukocytes (WBCs)

A

protect body from effects of invasion by organisms

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11
Q

How do leukocytes provide protection?

A
  1. Recognition of self vs non-self
  2. Destruction of foreign invaders, cellular debris, & abnormal cells
  3. Production of ANTIBODIES against invaders
  4. Complement activation
  5. Production of CYTOKINES that stimulate increased formation of leukocytes in the bone marrow
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12
Q

Cytokine function

A

To initiate production of more leukocytes when the first round is used up

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13
Q

Full immunity requires what 3 processes…

A
  1. Inflammation
  2. Antibody-mediated immunity (AMI)
  3. Cell-mediated immunity (CMI)
    * ALL 3 MUST BE IN PLACE!
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14
Q

Innate Native Response

A
  • natural protective feature of a person
  • provides immediate protection
  • visible symptoms & can rid of harmful organisms

ex. inflammatory response activated through the skin, mucosa, antimicrobial chemicals on skin

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15
Q

What is a possible complication of excessive response of innate native immunity?

A

tissue damage

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16
Q

Infection

A
  • occurs in response to tissue injury, invasion of organisms
    ex. splinter in finger
  • usually accompanied by a inflammation, but can occur without infection
  • Body s trying to manage Neutrophils, Macrophages, Eosinophils, basophils
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17
Q

Does inflammation always mean infection?

A

NO!!!

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18
Q

Neutrophils (granulocytes)

A
  • 55%-70% of WBC
  • Mature called: SEGMENTED or polymorphonuclear (PMN)
  • Immature called: Bands
  • Stem cell to mature neutrophil takes 12-14 days
  • Lifespan once mature: 12-18 hrs
  • Function is phagocytosis
  • Absolute Neutrophil Count
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19
Q

Macrophages

A
  • from myeloid stem cells
  • phagocytocsis
  • repair
  • Antigen presenting/processing
  • secretion of cytokines
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20
Q

Basophils

A
  • cause the symptom of inflammation
  • blod to collect in capillaries & arterioles
  • increase capillary permeability
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21
Q

Eosinophils

A
  • active against parasitic larvae
  • limits inflammatory reactions
  • increases during an allergic response
22
Q

Phagocytosis process

A
  1. exposure/invasion
  2. Atraction
  3. Adherence
  4. Recogntion
  5. Cellular ingestion
  6. Phagosome formation
  7. Degradation
23
Q

5 Cardinal manifestations of inflammation

A
WARMTH
REDNESS
SWELLING
PAIN 
DECREASED FUNCTION
24
Q

STAGE I: Vascular

A

change in blood vessels

25
Q

STAGE I “Phase I”

A

constriction small veins (closes one door) & dilate arterioles (brings more people to the party) increasing delivery of nutrients to the area

26
Q

STAGE I “Phase II”

A

hyperemia & edema that can cause a capillary leak

27
Q

STAGE II: Cellular Exudate

A

Neurophils, pus forms a clear to yellow substance

28
Q

STAGE III: Tissue repair & replacement

A

WBCs trigger new blood vessels and growth (angiogenesis) & scar tissue formation

29
Q

Immunity

A

–adaptive internal protection resulting in long-term resistance to effects of invading microorganisms

-body must learn to generate specific immune responses when injected by or exposed to specific organisms

30
Q

ANTIBODY-MEDIATED IMMUNITY

A

Humoral immunity

-antibodies produced by B-lymphocytes(B-cells)

31
Q

B-cells

A
  • start from as stem cells
  • released from bone marrow into blood
  • migrate to secondary lymphoid tissues : spleen, parts of lymph nodes, tonsils, mucosa of intestinal tract (AMI process occurs in all)
32
Q

ANTIBODY-MEDIATED IMMUNITY: Steps to produce specific antigen

A
  1. Exposure
  2. Antigen recognition
  3. Sensitization
    - plasma celll
    - memory cell
  4. Antibody production & release
    - circulating antibodies can be transferred to another person
  5. Antibody-antogen binding
  6. Antigen-binding actions
    - agglutination, lysis, complement fixation, precipitation, inactivation
33
Q

Components of AMI

A
  • Antibodies: Immunoglobulins or gamma globulins
  • Antibody classification: IgA, IgD, IgE, IgM
  • 1st exposure the B-cell produces the IgM antibody type against the antigen
  • Re-exposure, then produces large amounts of IgG type of antibody
34
Q

What type of immunity is ANTIBODY-MEDIATED IMMUNITY?

A

Adaptive

35
Q

Active Immunity

A

Body takes an active role in producing antibodies

36
Q

Natural active immunity

A

antigens enters body without assistance

ex. having chicken pox & developing immunity to it

37
Q

Artificial active immunity

A

protection developed by vaccination or immunization

38
Q

Passive immunity

A

short term effect transferred from another person

39
Q

Natural passive immunity

A

mother to baby when breast fed

40
Q

Artificial passive immunity

A
  • injecting antibodies from another person
  • short-term

ex. injected an individual with antibodies from a person who had Eboli and is now immune from it

41
Q

CELL-MEDIATED IMMUNITY (Cellular Immunity)

A
  • involves many WBC actions & interactions

- for total immunocompetence, CMI must function optimally

42
Q

Is CELL-MEDIATED IMMUNITY adaptive?

A

YES!!!!

43
Q

CMI: T-lymphocytes (helper/inducer cells)

A

T-4 or CD4 cells, secrete lymphokines, increase bone marrow production when needed

44
Q

CMI: T-lymphocytes (suppressor cells)

A

T-8 cells, prevent hypersensitivity, secrete lymphokines, inhibit growth & activation of immune system (keeps things in check)

-Cytotoxic/cytolytic T-cells (Tc) : destroys cells containing processed antigens HLA, effective against parasites, protozoa

45
Q

Natural Killer cells (NK)

A
  • CD16, can destroy without previous sensitization

- Destroys abnormal or unhealthy cells

46
Q

CMI: Cytokines

A

small protein hormones

  • act as messengers that tell specific cells how to respond
  • control many inflammatory & immune responses

Monokines: when produced by marcrophages, neutrophils, eosinophils or monocytes

Lymphokines: when produced by T-cells

ex. interleukins, interferons, colony stimulating factors, tumor necrosis factor

47
Q

CMI Protection

A
  • helps protect body through ability to differentiate self from non-self
  • prevents development of cancer and metastasis after exposure to carcinogens
48
Q

Transplant Rejection: HYPERACUTE

A
  • immediate
  • antibody-mediated response
  • antibody-antigen complexes activate complement
  • blood clotting cascade is activated
  • massive clotting-ischemia-destruction of organ
49
Q

Transplant Rejection: ACUTE

A
  • 1 wk to 3 months

- Antibody mediated or cellular

50
Q

Transplant Rejection: CHRONIC

A

fibrotic scar tissue with reduced function

51
Q

Transplant Rejection: Maintenance therapy

A
  • continuous drug therapy
  • specific immunosuppressants (ex. Cyclosporine)
  • Less specific immunosuppressants (ex.Azathioprine)
  • Corticosteroid (ex. Prednisone)

*Many side effects of drugs

52
Q

Transplant Rejection: Rescue therapy

A
  • increased dosages of maintenance drugs
  • antilymphocyte globulin (ALG)
  • Muromonab-CD3 antibody