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2 Principles of Disease > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

Why should PTs care about the immune system?

A

immune system can be impacted by healthy exercise

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2
Q

Changes with adults & immune ssystem

A

increased susceptibility
more frequent reactivation of diseases
decreased vaccine efficacy
increased incidence of chronic/autoimmune/cancer

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3
Q

Immunosenescence

A

the decline in normal functioning of the immune system with aging

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4
Q

Inflammaging

A

chronic, mostly asymptomatic low grade inflammatory state that can eventually lead to chronic illnesses
examples include CVD, type 2 diabetes, some cancers, alzheimers

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5
Q

Can exercise cause changes in the immune system?

A

YES
intensity and direction of these changes depends on regularity, type, duration, and intensity

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6
Q

Antigens

A

any foreign molecules that do not have self-characteristic surface markers

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7
Q

Major histocompatability complexes (MHCs)

A

membrane surface proteins that mark each of our body’s cells
present antigenic peptides for recognition by T cells
have 2 classes; Class 1 and Class 2

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8
Q

Class 1 MHC

A

expressed on surface of almost all nucleated cells
we INHERIT these

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9
Q

Class 2 MHC

A

expressed on surface of antigen-presenting cells. Macrophages, dendritic cells, B-cells.
on cells that fight infections, not on infection themselves

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10
Q

Immune system

A

all the structures and processes that provide defense against potential pathogens
has innate and acquired

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11
Q

Innate immunity

A

nonspecific, we are born with it
inhereited defense mechanisms that are present at exposure to a threat. have external and internal defenses

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12
Q

Acquired immunity

A

specific and adaptive
based on prior exposure and provides long term memory, provides future protection against same invaders
includes active and passive acquired immunity
involve proliferation of antigen-specific B & T cells
2 types: humoral & cell-mediated

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13
Q

External defenses of innate immunity

A

Skin
Gi tract: stomach acidity, normal flora
respiratory tract: mucus, cilia, alveolar macrophages
genitourinary: pH, mucosal lining, urine flushing

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14
Q

Internal defenses of innate immunity

A

1st line of defense against pathogens that get past the external defenses

phagocytes
endogenous pyrogens
interferons
complement proteins

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15
Q

Phagocytes

A

ingest and destroy pathogens/cell debris
neutrophils, monocytes, macrophages, eosinophils, basophils, NK cells

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16
Q

Phagocytes and infection

A

decrease in number of phagocytes is primary cause of increased infection risk in individuals treated with radiation or chemotherapy

neutropenia is an example

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17
Q

Vascular changes in injury

A

Transient vasoconstriction
vasodilation
increased permeability

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18
Q

Cellular Events in infection

A

margination
diapedesis and movement toward pathogen by chemotaxis
recognition and adherence
phagocytosis

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19
Q

Phagocytosis

A

foreign particle becomes surrounded by pseudopods of phagocytes
phagocytes eventually engulf antigens, form vacuole, fuses with lysosomes

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20
Q

Infiltration of an Inflamed Site by Leukocytes

A

Neutrophils are first and most intense
Monocytes are second, least intense
T-lymphocytes are third

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21
Q

Endogenous pyrogens

A

generates a fever
cytokines released by host monocytes/macrophages in response to a pathogenic signal
common: interleukin-1 (IL-1)
results in increased activity of neutrophils, production of interferon, fever, sleepiness, decreased plasma iron

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22
Q

Interferons

A

think VIRUS
released by lymphoctyes, macrophages, virally infected cells
produce nonspecific and short acting resistance
inhibit viral replication and assembly of new viruses
act as messengers, protect nearby cells
used as drug interventions

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23
Q

Complement system

A

group of plasmas proteins in blood, interstitial fluid, and mucosal surfaces that are normally dormant until they are activated by microorganisms or antigen-antibody complexes

once activated complement proteins cause 4 events–vasodilation, attraction of EBCs, opsonization, MAC

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24
Q

Primary Lymphoid organs

A

bone marrow
thymus

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25
Secondary lymphoid
lymph nodes spleen peyer's patches tonsils appendix
26
Maturity of T lymphocytes
stem cells in bone marrow travel to thymus gland to complete development
27
Antibodies
produced by B lymphoctyes only bind to specific antigens, at the epitope. elicit immune response help to recruit other cells to attack antigen once binded to it
28
types of B-cells
memory cells and plasma cells
29
What do B-cells do?
have surface receptors that can recognize a single specific antigen when it binds to B-cell (and gets signal from T cell), change into protein synthesizing cells (plasma and memory cells)
30
B-lymphocytes
effective against bacterial infections mature in bone marrow high concentration in spleen, low concentration in blood
31
Plasma B-cells
antibody factories that secrete antigen specific antibodies
32
Memory B cells
identical clone of original b cell, type of acquired immunity that yields permanent resistance. important in active immunity
33
Opsonization
process by which targets are identified for immunologic attack
34
Why don't we have a immune response with stints/grafts/joint replacements?
they don't have epitopes, so they aren't recognized as being foreign by the antibody
35
IgG
main type in circulation, production increased after immunization, secreted during secondary response, crosses placenta
36
5 main classes of antibodies
IgG IgA IgE IgM IgD
37
IgA
main type in external secretions (saliva, breastmilk) and mucous membrane surfaces
38
IgE
Responsible for allergic symptoms in immediate hypersensitivity reactions
39
Complement system
helps to directly kills antigen although part of innate immune response, complement works with antibodies to destroy pathogens present in plasma in inactive state until activated by antibodies
40
Complement and antibodies work as a team
IgG and IgM attach to antigens on invading cell membrane and activate C1 activated C1 splits into C4b which binds to invader's cell membrane (fixation) this triggers activation of other complement proteins until finally the membrane attack complex is inserted into the invader's cell membrane
41
Membrane attack complex
C5 to C9 create large holes in membrane, causes H2O to influx into cell, causes cell death complement proteins kill the invaders that were labeled by antibodies
42
Activated complement proteins go on to....
direct destruction by membrane attack complex vasodilation increased capillary permeability chemotaxis opsonization
43
Cell mediated immunity w/T-cells
able to recognize these hidden intracellular organisms, search them out, and destroy them on cell-by-cell basis
44
What do T-cells attack?
host cells infected with viruses and fungi transplanted human cells cancer cells
45
T-lymphocytes growth
originate in bone marrow, complete development in thymus gland after thymus, enter blood and populate lymph nodes/secondary lumphoid organs repopulation of T-cells in adulthood occurs slowly unstimulated T cells live for months/years
46
Thymus gland
primary lymphoid organ that begins to shrink around puberty
47
types of t-cells
Cytotoxic killer T cells Helper T cells (majority of T cells) Suppressor T cells
48
Killer T-Cells/CD8
cause cell-mediated destruction can only destroy infected host cells that present antigens in association with class-1 mhc molecules secrete perforins that form cylindrical channels through the membrane, helps to cause osmotic cell death defend against viral, fungal, transplants
49
Steps of cell-mediated immunity
virus enter the cell abnormal peptides replicate Class 1 MHC proteins incorporate abnormal peptides Class 1 MHC proteins transported to cell membrane Abnormal peptides are displayed by Class 1 MHC proteins on cell membrane CD8 recognizes abnormal peptides bound to MHC1 CD8 secretes perfornins to kill cell
50
Helper/Suppressor T-cells
participate in acquired immune response by regulating responses of the B-cells and Killer T cells
51
Helper T-cells
must activate B cells before they differentiate into memory and plasma cells cannot bind directly to a free antigen antigens are presented to helper T cells by antigen presenting cells (macrophages/dendritic cells) can only be activated by class-2 MGC presenting antigens
52
Suppressor T-cells
inhibit T cell and B cell activities purpose is to moderate immune response
53
Steps of Helper T cells
pathogen phagocytized by antigen presenting cell (macrophage) lysosome action produces antigenic fragments Class 2 MHC proteins are produced antigenic fragments are bound to MHC 2 antigenic fragments are displayed on cell brane helper T cells bind to MHC molecule go on to activate B cell
54
Tumor immunology
tumors are clones of single cells division is not effectively controlled by normal mechanisms tumor cells often de-differeniate, become similar to other cells
55
Natural killer cells
large granular non T or B cells do not require thymus for development back up CD8 T-cells kill host cells & tumor cells
56
Active acquired immunity
person produces his own antibodies in response to the foreign organism resistance is usually permanent can be natural or artificial has a primary and secondary response
57
Natural active acquired immunity
created after exposure
58
Artificial active acquired immunity
via active vaccination, provokes your immune system to make antibodies
59
Primary response active acquired immunity
1st exposure to pathogen immune response is insufficient to combat disease 5-10 day latency of antibody production
60
Secondary response active acquired immunity
subsequent exposure to same antigen antibody production is more rapid max antibody concentration within 2 hours usually prevents the disease
61
Passive acquired immunity
produced by transfer of antibodies from donor to recipient donor has been actively immunized, the recipient is passively immunized resistance is temporary can be natural or artificial
62
Natural passive acquired immunity
mother to fetus during pregnancy via placenta mother to infant during nursing via breastfeeding disappears when infant is 1 month old, infant starts to develop immunocompetence
63
Artificial passive acquired immunity
passive immunization = injection of anti-serum rabies vaccine, snake anti venom. for infections that you don't have time to make antibodies before becomes fatal
64
Factors affecting immunity
aging nutrition/malnutrition burns sleep deprivation surgery/anesthesia present of concurrent disease Medications Iatrogenic factors that increase exposure Stress
65
Aging and immuntiy
innate = external defenses break down, phagocytes function decreases acquired = antigen specific antibody response decrease, self antigen responses increase, # circulating T cells decrease, T cells not as responsive
66
Burns and immunity
increased susceptibility to severe bacterial infections due to loss of largest external barrier
67
Sleep deprivation and immunity
decreased neutrophils, NK, T4, T8, B cells increased monocytes 7 hours a night
68
Surgery/anesthesia and immunity
suppresses T cell and B cell function for up to 1 month post op
69
Presence of concurrent disease and immunity
illness/disease, malignancy, diabetes, chronic renal failure, HIV infection
70
Metastasis
movement of cancerous cells via blood or lymph to a new distant site
71
Grading
histologic differentiation of cancer tissue refers to degree of resemblance of cancerous tissue to tissue of origin
72
Staging
refers to degree of spread or metastasis classification systems vary by type of cancer
73
Medication and immunity
immunosuppressive drugs (like glucocorticoids)
74
Iatrogenic factors that increase exposure to pathogens
urinary catheters, external fixation devices, chest tubes, etc infections that result from actions of HCP
75
Exercise immunology
depending on intensity, frequency, type of exercise, immune system can be enhanced or suppressed acute bouts of exercise tend to promote release cytokines, chronic exercise reduces chronic inflammation can lessen detrimental effects of stress on immune system
76
What does exercise help increase
plasma concentration activity of neutrophils phagocytic action of macrophages number and activity of NK cells number of circulating WBCs
77
What does exercise help decrease
circulating levels of pro-inflammatory markers
78
Extreme exercise
suppresses lymphocyte concentration suppresses NK cell concentration and activity increases susceptibility to viral infections increases circulating pro-inflammatory cytokines deleterious oxidation of cellular macromolecules
79
Neck Check *extra credit*
when completing an intense exercise while sick with bacterial or viral infection, you should do the following: if symptoms are above the neck, begin workout at 1/2 speed, check in 10 min. If improved, can continue. If worse, stop and get rest if symptoms are below the neck, exercise should not be started

2 Principles of Disease (7 decks)

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