IM Flashcards

1
Q

Healthy immune system functions for: (3)

A
  1. Surveillance of the body
  2. Recognition of foreign material
  3. Destruction of entities deemed to be
    foreign
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2
Q

innate/Natural/Non-Specific Immunity:

A

Stimulated by structures common to groups of
related microbes; cannot distinguish between
fine differences of foreign substances.

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3
Q

Acquired Immunity:

A
Very specific response 
to a distinct macromolecule, also has the 
ability to “remember” macromolecule and 
respond more vigorously to the second 
exposure
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4
Q

The two systems influence

each other:

A

Innate
stimulates adaptive;
adaptive utilizes innate
mechanisms.

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5
Q

Agranulocytes: (2)

A
  1. Monocytes/Macrophages

2. Lymphocytes

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6
Q

Granulocytes (3)

A

1 Neutrophils
2 Eosinophils
3 Basophils

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7
Q

order of prevalence of leukocytes (5)

A
neutrophils
lymphocytes
monocytes
eosinophils
basophils
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8
Q

Leukocytes or White Blood Cells

All are — and are larger and less
numerous (6000–10,000/μL) than
erythrocytes.

A

nucleated

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9
Q

Leukocytes or White Blood Cells

The granulocytes are —.

A

polymorphonuclear

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10
Q

Acute inflammation is protective; it (3)

A

neutralizes harmful
agents, removes dead tissue and initiates the tissue repair
process.

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11
Q

Damaged cells release inflammatory mediators, which (3)

A

stimulate the inflammatory process but they can also injure

normal tissue. The mediators can act locally or systemically.

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12
Q

Cardinal Signs of Acute

Inflammation (5)

A
1. Rubor (Red 
Discoloration)
2. Calor (Heat)
3. Dolor (Pain)
4. Swelling
5. Loss of Function
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13
Q

Phagocytosis (2)

A
  • Non-self or damaged particles are engulfed by cells.

* Essential part of inflammation and acquired immunity.

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14
Q

Innate Immunity

Accomplished primarily by neutrophils & macrophages.

A

Macrophages can phagocytize far more & larger material than neutrophils.
Macrophages are already in the tissue.

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15
Q

Innate Immunity

How does a phagocyte recognize its “meal”? (4)

A
1. Phagocytes contain Toll-Like Receptors (TLRs) that are capable of 
recognizing generic Pathogen-Associated Molecular Patterns 
(PAMPs) and Damage-Associated Molecular Patterns (DAMPs)
2. Rough surface
3. Native substances should 
have protein coats that 
repel phagocytes
4. If a target has an 
immunoglobulin/antibody 
attached to it, then it is 
marked for phagocytosis 
(opsonization)
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16
Q

Interferons (INF)

• Virally-infected cell secrete —.

A

INF

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17
Q

Interferons (INF)

Secreted INF cause uninfected
cells to

A

produce enzymes that
inhibit viral replication, which
prevents spread of the virus to
neighboring cells.

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18
Q
Complement 
System• Consists of --- distinct 
components that are in plasma 
in an inactive form and must be 
cleaved to become active. 
Activated by
A

30
substances on the
surface of microbes.

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19
Q

Complement
System

Cascade of reactions leading to: (3)

A

(1) enhancement of inflammation,
(2) opsonization of pathogens,
(3) formation of a Membrane-Attack
Complex (MAC) that lyses
pathogens.

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20
Q

Complement
System

Also part of acquired immunity because

A

antibodies can activate the complement

system (Classical Pathway).

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21
Q

Acquired Immunity

A

very specific response to a distinct macromolecule (antigen), also has
the ability to “remember” macromolecule and respond more vigorously
to the second exposure. The process requires activation and
lymphocytes (B and T).

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22
Q

Antigens:

A

Each toxin or type of pathogen
contains one or more specific chemical
compounds in its make up that are different
(antigens). Antigens are molecules capable
of inducing an acquired immune response
by binding to B-cell and T-cell receptors and
the production of antibodies against them.
Antigens are usually surface peptides or
polysaccharides.

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23
Q

Antigen:

A

Peptides or
polysaccharide that are part
of a molecule on an
organism.

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24
Q

Epitope:

A

Molecular
group on the antigen
that is recognized by
the immune system.

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25
Antigen Presenting Cells (APCs) present Antigens on their surface via
Major Histocompatability Complex (MHC) Class II molecules.
26
APCs bind to and activate
T helper cells (CD4).
27
T helper (CD4) cells activate the two branches of Acquired Immunity:
1. Humoral | 2. Cell-Mediated
28
APCs: (3)
* Macrophages * Lymphocytes * Dendritic cells
29
• Macrophages
ingest the pathogen and induce an inflammatory response, if appropriate.
30
• Dendritic cells
ingest the antigen and | migrate to the nearest lymphoid organ
31
Cell-Mediated Immunity
Activated T cells (Natural Killer and Cytotoxic T, CD8) result in killing of infected cells and stimulation of phagocytosis of bacteria and fungi.
32
Humoral Immunity | aka Antibody-Mediated
``` Activated B cells develop into Plasma cells that secrete Immunoglobulins. The antibodies neutralize toxins and viruses and enhancing phagocytosis of bacteria (opsinization) ```
33
Activated T & B cells interact with | pathogens & initiate a response in
secondary lymphoid tissues (e.g. lymph nodes, spleen, nodules (tonsils, mucosa-associated lymphoid tissue, etc.)).
34
After activation, T and B Lymphocytes replicate a tremendous number of times (= clones) and are secreted into the lymphatic circulation. From there they
cycle through the blood, tissue, and back to the lymph, working as effector cells to eliminate the antigen for which they are activated.
35
Each B cell has ~--- antibodies in its membrane for a single antigen.
100,000
36
MHC Class II:
Found on Antigen Presenting Cells (macrophages, dendritic cells, etc.); involved in presenting antigens to T Helper cells for cell mediated immunity
37
MHC Class I:
code for markers that display unique characteristics of self and foreign antigens when the cell is infected
38
Antigen Presenting Cell Membrane (ex. Macrophage) Interaction causes (2)
activation of the T cell and creation of T cell clones.
39
Cell Membrane of All Nucleated Cells Interaction causes
destruction of an infected cell when it presents a foreign antigen
40
T Helper Lymphocytes/Cells (CD4 Cells) Activated by Antigen Presentation via MHC Class II (4)
``` 1. Growth and proliferation of Cytotoxic and Suppressor T lymphocytes 2. Growth and proliferation of B lymphocytes 3. Stimulates activation of more T Helper Cells 4. Activation of macrophage system ```
41
4. Activation of macrophage system (2)
``` a. Attract & slow/stop macrophage migration away from inflamed regions b. Stimulate more efficient phagocytosis ```
42
Cytotoxic T-Lymphocytes/Cells (CD8 Cells) Activated by Antigen Presentation via MHC Class I. All nucleated cells can present antigens to Cytotoxic T Cells because
``` all cells (except RBCs) have MHC I. ```
43
1. After binding antigens, Cytotoxic T cells: (2)
a. Secrete perforin molecules that punch holes in the membrane of the target. The targeted cell will swell and lyse. b. Release cytotoxic substances (granzymes) into the target through perforin channels that stimulate apoptosis
44
After secreting substances, Cytotoxic | Cells can
unbind and move on to another | cell
45
Suppressor T Cells (aka Regulatory T cells) (3)
1. Capable of suppressing functions of both cytotoxic and helper T cells 2. May be a separate type of cell, but they may not Many T cells may function as suppressors by secreting inhibitory cytokines 3. These cells are very important as they limit the immune system’s ability to attack one’s own tissues —they add to immune tolerance
46
B cells and the antibodies they secrete create humoral | immunity. (3)
1. B Cells are activated by intact antigens but also by activated T helper cells. 2. When B cells are activated, they enlarge and look like lymphoblasts 3. Some B cells differentiate into plasmablasts which later become plasma cells
47
Some B cells differentiate into plasmablasts which | later become plasma cells (3)
``` a. One plasmablast will produce 500 plasma cells in 4 days b. A mature plasma cell can produce 2000 immunoglobulins/second c. Immunoglobulins are secreted into the lymph and carried into the blood for circulation. ```
48
Fc Region (Constant Portion) determines (3) The heavy chain also determines (1)
diffusivity through membranes & tissue, complement attachment, & other biological properties. Ig classification.
49
Phagocytes have Fc receptors, so antibody binding to an antigen can lead to
enhanced phagocytosis (OPSONIZATION).
50
Most abundant Ig in blood; crosses the placenta
IgG
51
IgG (7)
– Most abundant Ig in blood; crosses the placenta – Complement activation – Opsonizes bacteria – Neutralizes bacterial toxins and viruses – Antibody-dependent cell-mediated cytotoxicity mediated by NK cells & macrophages – Primary antibody in the secondary response – Mediates Type II (ex. blood transfusion reaction) and III (ex. Grave’s Disease, Myasthenia Gravis, Lupus) Hypersensitivity Reactions
52
IgE (3)
– Mediates immediate (type I) hypersensitivity reactions (asthma, hay fever, anaphalysix, food allergies, drug sensitivity, etc.) – Defends against parasitic infections – Activates basophils, mast cells, and eosinophils
53
IgA (3)
– Secretory Ig; synthesized by plasma cells in exocrine glands (saliva, tears, saliva, etc.) – Most abundant Ig in the body (mucosal sites) – Mucosal immunity and neonatal immunity (transfer via breast milk)
54
IgM (4)
– Most potent activator of complement – Largest of the immunoglobulins – The first type produced in response to an antigen – Membrane bound on B (monomer) but can also be secreted as a pentamer
55
Membrane bound on B (monomer) but can also be secreted as a pentamer B cells begin to express (2) when they reach maturity. Expression of (2) antibodies on their membrane surface allows the B cell to be able to
IgM and IgD IgM and IgD respond to antigens.
56
IgD (1)
– Membrane bound; Receptor on B lymphocytes surface and aids in antigen recognition by B lymphocytes
57
``` After activation by antigen, B cells undergo antibody class switching to produce (3) antibodies. This allows daughter cells from the same activated B cell to produce ```
IgG, IgA or IgE different types of antibodies
58
Mechanisms of Immunoglobulin Action (6)
1. Neutralization 2. Agglutination 3. Precipitation 4. Complement Fixation 5. Opsonization 6. Activation of NK Cells
59
TOLERANCE (immunologic unresponsiveness to self antigens) is vital for life and develops during preprocessing of T & B lymphocytes. (2)
1. Clonal deletion occurs within the fetal thymus & bone marrow (central tolerance). 2. Clonal anergy (peripheral tolerance) is when cells that are self-antigenic become non-functional.
60
If SELF tolerance fails =
autoimmune disease
61
--% of autoimmune diseases occur in women
90
62
skipped Theories for why immune tolerance fails... (5)
``` 1. Failure of regulation of self-reactive lymphocytes 2. Exposure of T lymphocytes to antigens previously sequestered from the immune system 3. Molecular mimicry by invading pathogens. 4. Modification of self antigens 5. Inappropriate expression of Class II MHC Molecules (antigen-presenting molecules) ```
63
skipped 3. Molecular mimicry by invading pathogens. (2)
``` a. Invading antigens have a similarity to self-antigens b. Occurs in Rheumatic Fever: Streptococcal M protein resembles a portion of cardiac myosin ```
64
skipped | Examples of Autoimmune Diseases (8)
``` • Rheumatic Fever • Myasthenia Gravis • Systemic Lupus Erythematosus • Rheumatoid Arthritis • Sjogren’s Syndrome • Multiple Sclerosis • Type I Diabetes • Graves’ Disease ```
65
Treatment includes (2)
immunosuppression and/or plasmapheresis.
66
mediator: Antibody (IgE) type: reaction:
I (immediate, anaphylactic) IgE antibody is induced by allergen, binds to mast cells and basophils. On succeeding exposures, the allergen cross-links bound IgE and induces degranulation of mast cells & basophils. Ex. Allergic and Anaphylactic reactions, Asthma
67
mediator: Antibody (IgG) type: reaction:
II (cytotoxic) Antigens on a cell surface combine with antibody; this leads to complement-mediated lysis. Ex. Blood transfusion reactions, Hemolytic disease of the newborn
68
mediator: Antibody (IgG) type: reaction:
III (immune complex) Antigen-antibody immune complexes are deposited in tissues, complement is activated, and polymorphonuclear cells are attracted to the site. They release lysosomal enzymes, causing tissue damage. Ex. Systemic Lupus Erythematous, Grave’s Disease, Myasthenia Gravis
69
mediator: cell type: reaction:
IV (delayed) Helper T lymphocytes sensitized by an antigen release lymphokines upon second contact with the same antigen. The lymphokines induce inflammation and activate macrophages, which, in turn, release various mediators. Ex. Contact dermatitis
70
Immediate Hypersensitivity Reactions, Type I (5)
a. One of the most powerful immune reactions b. Occurs when IgE stimulates mast cells and basophils c. Release of secretory products from mast cell granules (ex. Histamine) causes: d. Immediate Hypersensitivity begins within minutes of antigen introduction e. There is also a late phase reaction
71
b. Occurs when IgE stimulates mast cells and | basophils (2)
• There is an extremely strong attraction between the two (one mast cell/basophil can bind 500,000 IgEs) • Mast cells & basophils are most concentrated in the lung, skin, and GI tract
72
c. Release of secretory products from mast cell | granules (ex. Histamine) causes: (2)
• Increases vascular permeability, vasodilation, bronchial and visceral smooth muscle contraction, salivary and bronchial secretions, and inflammation • INCREASES respiratory resistance, DECREASES BP
73
Can be life threatening if severe due to | bronchoconstriction and vasodilation -
ANAPHALYXIS
74
d. Immediate Hypersensitivity begins within minutes of | antigen introduction
IgE-primed mast cells can remain in the tissues for years. A person retains the capacity to react immediately upon re-exposure. Next time allergen molecules contact the mast cells, they bind across adjacent receptors and stimulate degranulation
75
e. There is also a late phase reaction (2)
• Inflammatory infiltration of eosinophils, basophils, neutrophils, and lymphocytes 2-4 hours after degranulation of mast cells & basophils • This stage is capable of damaging tissue
76
``` Treatment and Prevention of Type I Allergic Response (3) ```
1. Avoid the allergen 2. Take drugs that block the action of lymphocytes, mast cells, or chemical mediators 3. Undergo desensitization therapy
77
3. Undergo desensitization therapy (3)
``` – Controlled injections of the antigen – Works by producing IgG antibodies rather than IgE – IgG considered to be “blocking antibodies” ```
78
If you are “allergic”, you produce --- antibodies in response to environmental allergens
IgE
79
If you are “allergic”, you produce IgE antibodies in response to environmental allergens (6)
``` • Hay Fever • Asthma • Drug hypersensitivity (penicillin) • Food allergies (most common: peanuts, fish, cow milk, eggs, shellfish, soybeans) • Urticaria (hives) • Anaphylaxis ```
80
Delayed –Type Hypersensitivity Reactions. Type IV | Hypersensitivity. Mediated by T cells (3)
``` a. The pathogen does not cause much damage to the tissue b. Instead, helper and cytotoxic T Cells are activated (increasingly so on repeat exposures) c. Produce a cell-mediated immune reaction, stimulating macrophage recruitment and inflammation d. Damage is delayed 1-2 days • Normally restricted to tissue area exposed to pathogen ```