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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
Q

Secondary lymphoid

A

lymph nodes
spleen
peyer’s patches
tonsils
appendix

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26
Q

Maturity of T lymphocytes

A

stem cells in bone marrow
travel to thymus gland to complete development

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27
Q

Antibodies

A

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

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28
Q

types of B-cells

A

memory cells and plasma cells

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29
Q

What do B-cells do?

A

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)

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30
Q

B-lymphocytes

A

effective against bacterial infections
mature in bone marrow
high concentration in spleen, low concentration in blood

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31
Q

Plasma B-cells

A

antibody factories that secrete antigen specific antibodies

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32
Q

Memory B cells

A

identical clone of original b cell, type of acquired immunity that yields permanent resistance. important in active immunity

33
Q

Opsonization

A

process by which targets are identified for immunologic attack

34
Q

Why don’t we have a immune response with stints/grafts/joint replacements?

A

they don’t have epitopes, so they aren’t recognized as being foreign by the antibody

35
Q

IgG

A

main type in circulation, production increased after immunization, secreted during secondary response, crosses placenta

36
Q

5 main classes of antibodies

A

IgG
IgA
IgE
IgM
IgD

37
Q

IgA

A

main type in external secretions (saliva, breastmilk) and mucous membrane surfaces

38
Q

IgE

A

Responsible for allergic symptoms in immediate hypersensitivity reactions

39
Q

Complement system

A

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
Q

Complement and antibodies work as a team

A

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
Q

Membrane attack complex

A

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
Q

Activated complement proteins go on to….

A

direct destruction by membrane attack complex
vasodilation
increased capillary permeability
chemotaxis
opsonization

43
Q

Cell mediated immunity w/T-cells

A

able to recognize these hidden intracellular organisms, search them out, and destroy them on cell-by-cell basis

44
Q

What do T-cells attack?

A

host cells infected with viruses and fungi
transplanted human cells
cancer cells

45
Q

T-lymphocytes growth

A

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
Q

Thymus gland

A

primary lymphoid organ that begins to shrink around puberty

47
Q

types of t-cells

A

Cytotoxic killer T cells
Helper T cells (majority of T cells)
Suppressor T cells

48
Q

Killer T-Cells/CD8

A

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
Q

Steps of cell-mediated immunity

A

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
Q

Helper/Suppressor T-cells

A

participate in acquired immune response by regulating responses of the B-cells and Killer T cells

51
Q

Helper T-cells

A

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
Q

Suppressor T-cells

A

inhibit T cell and B cell activities
purpose is to moderate immune response

53
Q

Steps of Helper T cells

A

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
Q

Tumor immunology

A

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
Q

Natural killer cells

A

large granular non T or B cells
do not require thymus for development
back up CD8 T-cells
kill host cells & tumor cells

56
Q

Active acquired immunity

A

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
Q

Natural active acquired immunity

A

created after exposure

58
Q

Artificial active acquired immunity

A

via active vaccination, provokes your immune system to make antibodies

59
Q

Primary response active acquired immunity

A

1st exposure to pathogen
immune response is insufficient to combat disease
5-10 day latency of antibody production

60
Q

Secondary response active acquired immunity

A

subsequent exposure to same antigen
antibody production is more rapid
max antibody concentration within 2 hours
usually prevents the disease

61
Q

Passive acquired immunity

A

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
Q

Natural passive acquired immunity

A

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
Q

Artificial passive acquired immunity

A

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
Q

Factors affecting immunity

A

aging
nutrition/malnutrition
burns
sleep deprivation
surgery/anesthesia
present of concurrent disease
Medications
Iatrogenic factors that increase exposure
Stress

65
Q

Aging and immuntiy

A

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
Q

Burns and immunity

A

increased susceptibility to severe bacterial infections due to loss of largest external barrier

67
Q

Sleep deprivation and immunity

A

decreased neutrophils, NK, T4, T8, B cells
increased monocytes
7 hours a night

68
Q

Surgery/anesthesia and immunity

A

suppresses T cell and B cell function for up to 1 month post op

69
Q

Presence of concurrent disease and immunity

A

illness/disease, malignancy, diabetes, chronic renal failure, HIV infection

70
Q

Metastasis

A

movement of cancerous cells via blood or lymph to a new distant site

71
Q

Grading

A

histologic differentiation of cancer tissue
refers to degree of resemblance of cancerous tissue to tissue of origin

72
Q

Staging

A

refers to degree of spread or metastasis
classification systems vary by type of cancer

73
Q

Medication and immunity

A

immunosuppressive drugs (like glucocorticoids)

74
Q

Iatrogenic factors that increase exposure to pathogens

A

urinary catheters, external fixation devices, chest tubes, etc
infections that result from actions of HCP

75
Q

Exercise immunology

A

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
Q

What does exercise help increase

A

plasma concentration
activity of neutrophils
phagocytic action of macrophages
number and activity of NK cells
number of circulating WBCs

77
Q

What does exercise help decrease

A

circulating levels of pro-inflammatory markers

78
Q

Extreme exercise

A

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
Q

Neck Check extra credit

A

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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