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Human Anatomy and Phys Sp23 > exam 3 > Flashcards

exam 3 Flashcards

1
Q

immune system

A
  • protects us from infectious agents and harmful substances
  • composed of numerous cellular and molecular structures
  • function together to provide immunity
  • function dependent on specific type of infectious agent
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2
Q

how do the two types of immunity differ

A

based on
- what cells are involved
- the specificity of cell response
- the mechanisms of eliminating harmful substances
- the amount of time for response

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3
Q

although innate and adaptive immunities are distinct,

A

they work together in body defense

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4
Q

innate immunity

A

immediate response to wide array of substances

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5
Q

adaptive immunity

A

delayed responses to specific antigens

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6
Q

innate immunity is subdivided into

A

skin and mucosal membranes
non specific internal defenses
- cells (e.g., macrophages, NK cells)
- chemicals (e.g., interferon, complement)
- physiologic responses (e.g., inflammation, fever)

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7
Q

adaptive immunity subdivided

A

t-lymphocytes (cell mediated immunity)
B- lymphocytes (humoral immunity)
- plasma cells (synthesized and release antibodies)

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8
Q

characteristics of innate immunity

A

responds nonspecifically to a range of harmful substances
first line and second line of defense

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9
Q

first line of defense in innate immunity

A

skin and mucosal membrane

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10
Q

second line of defense in innate immunity

A

internal processes
- activities of neutrophils, macrophages, dendritic cells, eosinophils, basophils, mast cells, and NK cells
- chemicals such as interferon and complement
- physiological processes such as inflammation and fever

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11
Q

cells of innate immunity

A

neutrophils
macrophages
dendritic cells
basophils
mast cells
NK cells
eosinophils
interferons

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12
Q

neutrophils, macrophages, and dendritic cells are

A

phagocytic cells

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13
Q

basophils and mast cells

A

proinflammatory chemical secreting cells

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14
Q

NK cells

A

apoptosis initiating cells

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15
Q

eosinophils

A

parasite destroying cells

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16
Q

interferon

A

synthesizes enzymes that interfere with viral replication

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17
Q

complement system

A

group of over 30 plasma proteins
- work along with (“complement”) antibodies
- identified with letter C and number
- synthesized by liver, continuously released in inactive form (activation occurs by enzyme cascade)
- complement activation follows pathogen entry
- especially potent system against bacterial infections

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18
Q

complement activation following pathogen entry

A
  • classical pathway: antibody attaches to foreign substance and then complement binds to antibody
  • alternative pathway: complement binds to polysaccharides of bacterial or fungal cell wall
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19
Q

opsonization

A

complement protein (opsonin) binds to pathogen
- enhances the likelihood of phagocytosis of pathogenic cell

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20
Q

inflammation is enhanced by

A

complement
- activates mast cells and basophils
- attracts neutrophils and macrophages

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21
Q

cytolysis

A

complement triggers destruction of target cell
- complement proteins from membrane attack complex (MAC) that creates channel in target cell’s membrane (fluid enters causing lysis)

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22
Q

elimination of immune complexes

A
  • complement links antigen-antibody complexes to erythrocytes
  • cells move to liver and spleen where complexes are stripped off
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23
Q

inflammation

A

immediate response to ward off unwanted substances
-local, nonspecific response of vascularized tissue to injury part of innate immunity

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24
Q

steps of inflammation

A
  1. release of inflammatory and chemotactic factors
  2. vascular changes include : vasodilation of arterioles, increase in capillary permeability, display of CAMs
  3. recruitment of immune cells
  4. delivery of plasma proteins
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25
Q

step 1: release of inflammatory and chemotactic factors

A
  • mast cells and basophils help to provoke inflammation
  • mast cells contain histamines and kinines which help promote inflammation (foreign substances help mast cell degranulation)
  • basophils will release histamine and heparin when degranulation occurs
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26
Q

step 2: vascular changes include

A
  • vasodilation of arterioles (caused by histamine leading to increased blood flow, want to bring white blood cells and antibodies in to deliver to greater degree)
  • increase in capillary permeability (more substances can exit)
  • display of CAMs (on epithelial surface, cellular adhesion molecules embedded all the time under influence of histamine undergo conformational change and project slightly more)
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27
Q

step 3: recruitment of immune cells

A

margination - moves to wall of vessel where they can adhere to CAMS, also CAMs on surface of white blood cells
diapedesis - then able to diapedesis into permeable capillaries, allowing them to be outside blood vessel
chemotaxis - purposeful movement to stimulus of chemical problem, in this cause neutrophil will travel to injured tissues

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28
Q

step 4: delivery of plasma proteins

A

increase of fluid accumulation in tissue carrying valuable proteins
- creates more hydrostatic pressure that helps drive fluid into lymphatic capillary lumens

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29
Q

cardinal signs of inflammation

A
  • redness (from increased blood flow)
  • heat (from increased blood flow and metabolic activity within the area)
  • swelling (from increase in fluid loss from capillaries)
  • pain (from stimulation of pain receptors, due to compression (excess fluid) and chemical irritants (kinins, prostaglandins, microbial secretions)
  • loss of function (from pain and swelling severe cases)
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30
Q

duration of acute inflammation

A

8-10 days

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31
Q

chronic inflammation

A

has detrimental effects

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32
Q

fever (pyrexia)

A

abnormal body temperature elevation
1°C or more from normal (37°C)

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33
Q

fever is the result of

A

release of pyrogens from immune cells or infectious agents

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34
Q

events of fever

A
  • pyrogens circulate through blood and target hypothalamus
  • in response, hypothalamus releases prostaglandin E2
  • hypothalamus raises temperature set point leading to fever
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35
Q

benefits of fever

A
  • inhibits reproduction of bacteria and viruses
  • promotes interferon activity
  • increases activity of adaptive immunity
  • accelerates tissue repair
  • increases CAMs on endothelium of capillaries in lymph nodes (additional immune cells migrating out of blood into lymphoid tissue)
  • recommended to leave a low fever untreated
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36
Q

two branches of adaptive immunity

A

cell-mediated immunity
humoral immunity

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37
Q

cell-mediated immunity

A

involves t-lymphocytes

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38
Q

humoral immunity

A

involves B-lymphocytes, plasma cells, and antibodies

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39
Q

cell-mediated immunity is effective against

A

antigen within the cells; requires antigen presenting cells

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40
Q

what cells are formed after cell-mediated immunity is stimulated

A

cytotoxic T-lymphocytes and helper T-lymphocytes

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41
Q

effector response of cell-mediated immunity

A

apoptosis

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42
Q

humoral immunity is effective against

A

antigens outside cells; does not require antigen presenting cell

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43
Q

cells formed after humoral immunity is stimulated

A

plasma cells

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44
Q

effector response of humoral immunity

A

produce antibodies

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45
Q

cytotoxic t-lymphocytes

A
  • directly kill abnormal cells
  • destroys cells through apoptosis
  • recognizes antigen on infected cells and releases chemicals to destroy infected cell
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46
Q

helper t-lymphocytes

A

release cytokines when recognizing own
promotes humoral immunity

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47
Q

antigens

A

substance that binds a t-lymphocyte or antibody
- usually a protein or large polysaccharide

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48
Q

pathogens are detected by lymphocytes because

A

they contain antigens

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49
Q

examples of antigens

A

protein capsid of viruses
cell wall of bacteria or fungi
bacterial toxins
abnormal proteins or tumor antigens

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50
Q

antigenic determinant

A

also known as EPITOPE
specific site on antigen recognized by immune system
each has different shape
pathogenic organisms can have multiple determinants

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51
Q

antigens can have more than one

A

antigenic determinants which stimulates adaptive immunity

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52
Q

immunogen

A

antigen that induces an immune response

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53
Q

immunogenecity

A

ability to trigger response
increases with antigen’s degree of foreignness, size, complexity, or quanity

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54
Q

haptens

A

small foreign molecules that induce immune response when attached to a carrier molecule in host
e.g., toxin in poison ivy
account for hypersensitivity reactions (penicillin, pollen)

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55
Q

lymphocyte contact with antigen

A

B-lymphocytes make direct contact with antigens
T-lymphocytes have antigen presented by some other cells (antigen is processed through another cell type, coreceptors (CD proteins) help with this interaction)

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56
Q

T-lymphocytes: cells of cell mediated immunity

A

t-cells have over 100,000 t-cell receptors as well as coreceptors that help successfuly link antigen to t-lymphocytes

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57
Q

helper t-lymphocytes contain

A

CD4 proteins

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58
Q

cytotoxic t-lymphocytes contain

A

CD8 proteins

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59
Q

b-lymphocytes have

A

b-cell receptors embedded in their membrane
specific class of antibodies that are proteins

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60
Q

helper t-lymphocytes assist in

A

cell-mediated immunity
humoral immunity
innate immunity
activate NK cells and macrophages

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61
Q

t-lymphocyte subtypes

A

cytotoxic t-lymphocytes
helper t-lymphocytes
memory t-cells
regulatory t-cells

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62
Q

antigen presentation

A

cells display antigen on plasma membrane so t-cells can recognize it

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63
Q

two categories of cells present antigens

A
  • all nucleated cells of the body
  • antigen-presenting cells (APCs) : immune cells that present both helper T-cells and cytotoxic T-cells, include dendritic cells, macrophages, and B-lymphocytes
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64
Q

antigen presentation requires

A

attachment of antigen to MHC

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65
Q

MHC

A

major histocompatibility complex
group of transmembrane proteins

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66
Q

CD4 interact specifically with

A

MHC class II molecules

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67
Q

CD8 interacts specifically with

A

MHC class I

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68
Q

three main events in life of lymphocyte

A
  1. formation and maturation of lymphocytes
  2. activation of lymphocytes
  3. effector response: action of lymphocytes to eliminate antigen
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69
Q

formation and maturation of lymphocytes

A

occurs in primary lymphatic structures (red marrow and thymus)
become able to recognize one specific foreign antigen

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70
Q

activation of lymphocytes

A

in secondary lymphatic structures they are exposed to antigen and become activated
replicate to form identical lymphocytes

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71
Q

effector response: action of lymphocytes to eliminate antigen

A
  • T-lymphocytes migrate to site of infection
  • B-lymphocytes stay in secondary lymphatic structures (as plasma cells): synthesize and release large quantities of antibodies, antibodies are transported to infection site through blood and lymph
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72
Q

formation of lymphocytes

A
  • primary lymphatic structures aka red bone marrow produce lymphocytes
  • pre-T lymphocyte go to the thymus for maturation
  • overall produce of immunocompetent B-lymphocytes and T-lymphocytes (cytotoxic and helper)
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73
Q

activation of lymphocytes

A

lymph nodes, spleen, and tonsils are secondary lymphatic structures that house B-lymphocytes and T-lymphocytes

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74
Q

effector response of lymphocytes

A

interaction of T-lymphocytes and antibodies to eliminate foreign antigens at site of infection

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75
Q

activation of lymphocytes in helper T-lymphocyte

A

First Signal -
1. CD4 binds with MHC class II molecule of antigen presenting cell
2. T-cell receptors interact with antigen within MHC class II molecule
Second Signal -
1. other receptors interact and the helper T-lymphocyte releases IL-2 which binds with helper T-lymphocytes
activated helper T-lymphocyte proliferates and differentiates to form a clone of activated and memory helper T-lymphocytes

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76
Q

activation of lymphocytes : cytotoxic T-lymphocyte

A
  1. First Signal - CD8 binds with MHC class I molecule of infected cell; TCR interacts with antigen within MHC class I molecule
  2. Second Signal - IL-2 released from activated helper T-lymphocyte activates the cytotoxic T-lymphocyte
    activated cytotoxic T-lymphocyte proliferates and differentiates to from a clone of activated and memory cytotoxic T-lymphocyte
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77
Q

costimulation to activate B-lymphocyte for clonal selection

A
  1. First Signal - free antigen binds to BCR; B-lymphocyte engulfs and presents antigen to activated helper T-lymphocyte
  2. Second Signal - IL-4 released from activated helper T-lymphocyte stimulates B-lymphocyte
    activated B-lymphocyte proliferates and differentiates to form a clone of plasma cells and memory B-lymphocytes
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78
Q

effector response at infection site

A

mechanism used by lymphocytes to help eliminate antigen

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79
Q

each lymphocyte has its own

A

effector response

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80
Q

effector response for helper T-lymphocytes

A

releases IL-2, IL-4 and other cytokines
regulate cells of adaptive and innate immunity

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81
Q

effector response for cytotoxic T-lymphocytes

A

destroy unhealthy cells by apoptosis

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82
Q

effector response for plasma cells (differentiated B-lymphocytes)

A

produce antibodies

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83
Q

steps of effector response

A
  1. after exposure to antigen (in secondary lymphatic structures) activated and memory helper T-cells migrate to infection site
    - continually release cytokines to regulate other immune cells
  2. help activate B-lymphocytes
  3. activate cytotoxic T-lymphocytes w/ cytokines
  4. stimulate activity of innate immune system cells
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84
Q

effector response of cytotoxic T-lymphocytes

A

(cell mediated immunity)
release of cytotoxic chemicals induces apoptosis of abnormal cells by release of perforin and granzymes

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85
Q

effector response of B-lymphocytes

A

most activated B-lymphocytes become plasma cells
plasma cells synthesize and release antibodies
- the cells remain in the lymph nodes
- they produce millions of antibodies during 5-day life span

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86
Q

antibodies circulate through lymph and blood until

A

encountering antigen

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87
Q

antibody titer

A

circulating blood concentration of antibody against a specific antigen
- used as a measure of immune response

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88
Q

antibodies

A

immunoglobin proteins produced against a particular antigen
- antibodies “tag” pathogens for destruction by immune cells
- good defense against viruses, bacteria, toxins, yeast spores

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89
Q

soluble antigens are combatted by

A

humoral immunity
antibodies don’t require an APC, they can interact their receptors just in interstitial fluid

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90
Q

antibody structure

A

4 polypeptides bound together
2 light chains and 2 identical heavy chains
extension of Y shape referred to as Y region

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91
Q

disulfide bonds on antibody structure allows for

A

linkage between polypeptide

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92
Q

variable region of antibody

A

gives antibody a specificity on antigen binding site
unique to specific antibody

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93
Q

constant region

A

area among the bottom 75% of antibody structure that remains constant

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94
Q

Fc region

A

fragmented constant

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95
Q

binding of antigen-binding site of an antibody with antigen causes

A
  • neutralization
  • agglutination
  • precipitation
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96
Q

neutralization

A

antibody covers biology active portion of microbe or toxin
neutralizes that organisms ability to be pathogenic

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97
Q

agglutination

A

antibody cross-links cells (e.g., bacteria) forming a clump
makes it easier for organism to be phagocytized

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98
Q

precipiation

A

antibody cross-links circulating particles (e.g., toxins), forming an insoluble antigen-antibody complex
precipitates them out of solution

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99
Q

exposed Fc portion following antigen binding by antibody promotes

A

complement fixation
opsonization
activation of NK cells

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100
Q

complement fixation

A

Fc region of antibody binds complement proteins; complement is activated

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101
Q

opsonization

A

Fc region of antibody binds to receptors of phagocytic cells, triggering phagocytosis
antibodies can tag organism for removal by phagocyte

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102
Q

activation of NK cells

A

Fc region of antibody binds to an NK cell, triggering release of cytotoxic chemicals (perforin/granzymes)

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103
Q

IgG

A
  • major class
  • 75-85%
  • most versatile
  • capable of all antibody reactions
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104
Q

IgM

A
  • pentamer (5 monomers)
  • best at agglutination
105
Q

IgA

A
  • dimer
  • areas exposed to environment (mucosal membranes; tonsils)
  • best at neutralization (prevention of entry)
106
Q

IgD

A
  • B-cell receptors (id’s when B cells are ready for activation
107
Q

IgE

A
  • allergy and parasitism
  • degranulation of basophils and mast cells
  • chemotactic for eosinophils
108
Q

adaptive immunity: effector response; cell-mediated immunity

A
  1. activated helper T-lymphocytes release cytokines to stimulate activity of B-lymphocytes and cytotoxic T-lymphocytes, and regulates cells of innate immunity
  2. activated cytotoxic T-lymphocytes release cytotoxic molecules (perforin and granzymes) causing apoptosis of foreign or abnormal cells
109
Q

adaptive immunity: effector response; humoral immunity

A
  1. fab region of antibody binds to antigen to cause several consequences including neutralization of microbial cells and particles; agglutination of cells; and precipitation of particles
  2. Fc region serves as point of interaction with several structures including complement to cause complement activation, binding of phagocytic cells to cause phagocytosis of an unwanted substance or cell, and binding of NK cells to induce apoptosis of unwanted cell
110
Q

immunologic memory

A

-memory results from formation of a long lived army of lymphocytes upon immune activation

111
Q

adaptive immunity activation requires

A

contact between lymphocyte and antigen
- there is lag time between first exposure of the host a direct contact with lymphocyte

112
Q

activation of adaptive immunity leads to

A

formation of many memory cells against a specific antigen

113
Q

with subsequent antigen exposure…

A
  • many memory cells make contact with antigen more rapidly
  • produce more powerful secondary response (pathogen is typically eliminated before symptoms start, virus eliminated by memory T and B lymphocytes, antibodies before causing harm)
114
Q

what is an effective way to develop memory

A

vaccines
don’t contain active viruses but help provoke initial response so if you are exposed, you will have ability to fight off infection

115
Q

primary vs secondary response antibody titer

A

primary response:
- rise in IgM and IgG
- IgM and IgG decrease after sickness but memory cells are produced

secondary response:
- briefer lag time
- isn’t any activation due to memory cells
- magnitude of IgG is far greater than primary response

116
Q

active immunity

A

production of memory cells due to contact w antigen
naturally acquired - direct exposure to antigen
artificially acquired - vaccine

117
Q

passive immunity

A

no production of memory cells; antibodies from another person or animal
naturally acquired - transfer is mother to child through placenta or breast milk
artificially acquired - transfer of serum containing antibody from person or animal

118
Q

acute hypersensitivity

A

allergy
overreaction of immune system to a noninfectious substance - allergen (pollen, latex, peanuts)
- runny nose
- watery eyes
- hives
- labored breathing
- vasodilation and inflammation
- anaphylactic shock

119
Q

autoimmune disorders

A

immune system lacking tolerance for specific antigen
- initiates immune response as if cells were foreign
- due to cross reactivity, altered self-antigens, or entering areas of immune privilege

ex. rheumatic heart disease, type 1 diabetes, multiple sclerosis

120
Q

cross reactivity

A

a pathogen is so structurally similar, immune system can’t distinguish between self vs pathogen
rheumatic heart disease

121
Q

altered self-antigen

A

something alters shape or makeup of antigen
random mutation or from infection causing cell to become foreign
type 1 diabetes

122
Q

areas of immune privledge

A

evolution has provided areas in the body that are uniquely important so they are sequestered away from immune response
ovaries and testes, antigens are tolerated

123
Q

acquired immunodeficiency syndrome

A

life threatening condition as a result of HIV
- infects and destroys helper T-lymphocytes
- resides in body fluids of infected individuals
- can be transmitted by intercourse, needle sharing, breastfeeding, or placental transmission

prevention through safe sex

124
Q

HIV and AIDS

A
  • HIV tests look for HIV antibodies in the blood
  • becomes AIDS when helper T-lymphocytes drop below a certain level (opportunistic infections, CNS complications)
  • no cure for HIV (treatments alleviate symptoms and prevent spread)
125
Q

what are the 2 components of the structural organization of the respiratory system

A

upper and lower respiratory tracts

126
Q

components of upper respiratory tract

A

nose
nasal cavity
pharynx

127
Q

components of lower respiratory tract

A

larynx
trachea
bronchus
bronchiole
terminal bronchiole
lungs
respiratory bronchiole
alveolar duct
alveoli

128
Q

what are the components of the functional organization of the respiratory system

A

conducting zone and respiratory zone

129
Q

components of conducting zone

A

nose
nasal cavity
pharynx
larynx
trachea
bronchus
bronchiole
terminal bronchiole

130
Q

components of respiratory zone

A

respiratory bronchiole
alveolar duct
alveoli

131
Q

what is the function of the conducting zone

A

conduction of air
no gas exchange occurs
no oxygen and CO2 crossing

132
Q

what occurs in respiratory zone

A

gas exchange
primarily in alveoli
microscopic

133
Q

pharynx

A
  • cavity posterior to nasal and oral cavity
  • common passageway for air and food
  • divided into 3 regions; nasopharynx, oropharynx, laryngopharynx
134
Q

eustachian tube connects

A

middle ear to nasopharynx to equilibriate air pressure

135
Q

larynx

A
  • made of 9 pieces of cartilage bound together by various muscles and ligaments
  • connected superiorly via ligaments and muscles to the hyoid bone
136
Q

largest cartilage in larynx is

A

thyroid cartilage

137
Q

laryngeal prominence

A

extends out, adam’s apple

138
Q

vocal folds are found in

A

larynx

139
Q

vocal folds

A

back of oral cavity through laryngoscope
vocal folds are bands of cartilage
sound is emitted as they vocal folds open, close, and move

140
Q

trachea

A
  • major windpipe that brings air to lungs
  • composed of cartilaginous rings that help maintain structure (met by trachealis muscle)
  • needs to bend so we can move our necks back and forth
141
Q

angular ligament refers to

A

elastic cartilage between tracheal cartilage

142
Q

carina is

A

inside trachea where it divides into left and right bronchi
- contains receptors stimulated by irritants (provokes cough reflec)

143
Q

lining of trachea has

A

mucous membrane so it can entrap thigs that are brought in so cilia can help elevate pathogens and evoke a cough to get pathogen out of trachea

144
Q

bronchial tree

A

vast network of airways that decrease in size as they continue to branch

145
Q

trachea splits into

A

main bronchi

146
Q

main bronchi divides into

A

right and left lungs into lobar bronchi

147
Q

left lungs has how many lobes

A

2 lobes

148
Q

right lung has how many lobes

A

3 lobes

149
Q

segmental bronchi

A

each segmental bronchi delivers air to one bronchopulmonary segment
each lobe is further subdivided into segments that is portioned into multiple bronchopulmonary segments

150
Q

flow of bronchial tree

A

trachea
main bronchi
lobar bronchi
segmental bronchi
smaller bronchi

151
Q

bronchioles and alveoli

A
  • smaller bronchi divides and become bronchioles and then terminal bronchioles which turn into respiratory bronchioles because there is gas exchange
  • respiratory bronchioles lead to alveolar duct which leads to alveoli (microscopic)
152
Q

alveoli

A
  • rounded thin-walled sac like structures surrounded by meshwork of capillaries perfectly designed for gas exchange
  • majority of gas exchange occurs here
  • 300-400 million
  • separated by the interalveolar septum that wall between alveoli
  • each alveolus has alveolar pores which allow for lateral transmission of air meaning one alveoli can get air moving to another
153
Q

what is the most plentiful cell in respiratory system

A

alveolar type I cell

154
Q

alveolar type I cell

A

makes up wall of alveola
contributes to respiratory membrane

155
Q

respiratory membrane

A

composed of:
- alveolar lumen
- lumen of capillary
- type I alveolar cell

structure that oxygen and CO2 need to diffuse across
extremely thin
2 cell layers thick so diffusion can occur

156
Q

alveolar type II cells

A

intermittent on alveoli
produce surfactant

157
Q

surfactant

A

oily thin film made up of proteins and lipids that prevents collapse of alveoli
helps alveoli stay open and not stick
made by alveolar type II cells

158
Q

alveolar macrophages

A

immune cells that migrate around in lung tissue phagocytosing pathogens

159
Q

hilum

A

blood vessels, lymphatic vessels
bronchi feed into hilum

160
Q

pleural membrane of lungs

A

serous membrane in thoracic cavity
visceral layer lines the lung tissue
pariteal layer lines thoracic wall
pleural cavity contains serous fluid within pleural cavity

161
Q

function of pleural membrane of lungs

A

allow breathing not be painful and provides fluid to ensure this

162
Q

respiration

A

exchange of gases between atmosphere and body’s cells that involves:
- pulmonary ventilation
- alveolar gas exchange
- gas transport
- systemic gas exchange

163
Q

pulmonary ventilation

A

movement of gases between atmosphere and alveoli

164
Q

alveolar gas exchange

A

external respiration
exchange of gases between alveoli and blood

165
Q

gas transport

A

transport of gases in blood between lungs and systemic cells

166
Q

systemic gas exchange

A

internal respiration
exchange of respiratory gases between the blood and the systemic cells

167
Q

steps of respiration

A
  1. Pulmonary ventilation
    - air containing O2
  2. Alveolar Gas Exchange
    - O2 moves into blood
  3. Gas transport
    - blood containing O2 travels
  4. systemic gas exchange
    - O2 moves into systemic cells
  5. systemic gas exchange
    - CO2 moves into blood
  6. gas transport
    - blood containing CO2
  7. Alveolar Gas Exchange
    - CO2 moves into alveoli
  8. pulmonary ventilation
    - air containing CO2 goes into atmosphere
168
Q

pulmonary ventilation (breathing)

A

air movement
- consists of inspiration and expiration
- quiet, rhythmic breathing occurs at rest
- forced, vigarous breathing accompanies exercise
- skeletal muscles contract and relax changing thorax volume
- volume changes result in changes in pressure gradient between lungs and atmosphere
- air moves down pressure gradient (enter during inspiration; exits during expiration)

169
Q

inspiration

A

brings air into the lungs (inhalation)

170
Q

expiration

A

forces air out of the lungs (exhalation)

171
Q

autonomic nuclei in brainstem regulate

A

breathing activity

172
Q

muscles of quiet breathing

A
  • diaphragm
  • external intercostal

when these muscles contract, it serves to increase dimensions of thoracic cavity
diaphragm flattens out and lowers the floor of thoracic cavity therefore increasing in size

173
Q

muscles of forced inspiration

A

pull upward and outward
located in superior part of thorax and neck
- sternocleidomastoid
- scalenes
- serratus posterior superior
- pectoralis minor
- erector spinae

174
Q

muscles of forced expiration

A

pull downward and inward
lower back and posterior region of throax
- transversus thoracis
- serratus posterior inferior
- internal intercostal
- external oblique
- transversus abdominus

175
Q

dimensional changes in throacic cavity : inspiration

A
  • increase in height width and depth of thoracic cavity
  • diaphragm contracts; vertical dimensions of thoracic cavity increase
  • ribs are elevated and thoracic cavity widens
  • inferior portion of sternum moves anteriorly and thoracic cavity expands
176
Q

dimensional changes of thoracic cavity : expiration

A
  • thoracic cavity decreases in height, width, and depth
  • diaphragm relaxes; vertical dimensions of thoracic cavity narrow
  • ribs are depressed and thoracic cavity narrows
  • inferior portion of sternum moves posteriorly and thoracic cavity compresses
177
Q

when inspiration is occurring the diaphragm

A

contracts; moves down

178
Q

when expiration is occurring the diaphragm

A

relaxes; moves up

179
Q

boyle’s gas law

A

relationship of volume and pressure
- at constant temperature, pressure (P) of a gas DECREASES if volume (V) of the container increases, and vice versa

180
Q

P1 and V2 represent

A

initial conditions

181
Q

P2 and V2 represent

A

changed conditions

182
Q

what relationship does gas pressure and volume have

A

inverse relationship
as pressure increases volume decreases
as pressure decreases volume increases

183
Q

formula for boyle’s gas law

A

P1V1 = P2V2

184
Q

an air pressure gradient exists when force per unit area is

A

greater in one place than another

185
Q

if the two places are interconnected…

A

air flows from high to low pressure until pressure is equal

186
Q

during inhalation thoracic volume

A

increases so pressure decreases and air flows in

187
Q

during exhalation thoracic volume

A

thoracic volume decreases and pressure increases so air flows out

188
Q

where is the respiratory center

A

in the medullary part of brain stem

189
Q

pons portion of brain stems sends

A

input to the main medullary respiratory center to modify and smooth out inhalation and exhalation

190
Q

what is the minor respiratory center

A

pontine respiratory center

191
Q

peripheral chemoreceptors

A

aortic bodies and carotid bodies detect:
- increased CO2
- increased H+ (blood pH)
- decreased O2

192
Q

if something increases H+ ion concentration

A

it can lead to lowering of blood pH

193
Q

baroreceptors

A

refer to changes in pressure
prevent overinflation of lungs

194
Q

proprioceptors

A

in muscles joints and tendons
stimulated when muscles contract
when these structures become more active they increase the demand for oxygen causing increase in respiratory rate and depth

195
Q

motor output to accessory muscles

A

come from motor cortex
voluntary control

196
Q

formula

A

CO2 + H2O <–> H2CO3 <–> HCO3- + H+
carbon dioxide + water <–> carbonic acid <–> bicarbonate + hydrogen ion

197
Q

frontal lobe of cerebral cortex controls

A

voluntary changes in breathing patterns
bypasses respirator center stimulating lower motor neurons directly

198
Q

hypothalamus

A

increases breathing rate if body is warm
works through respiratory center

199
Q

limbic system

A

alters breathing rate in response to emotions
works through respiratory center

200
Q

2 kinds of controls of breathing

A

reflexive controls
conscious controls

201
Q

airflow

A

amount of air moving in and out of lungs with each breath

202
Q

air flow depends on

A
  1. pressure gradient established between atmospheric pressure and intrapulmonary pressure
  2. the resistance that occurs due to conditions within the airways, lungs and chest wall
203
Q

F =

A

deltaP/r

204
Q

f=

A

flow

205
Q

∆P

A

difference in pressure between atmosphere and intrapulmonary pressure
Patm - Palv

206
Q

R

A

resistance

207
Q

flow is directly related to

A

pressure gradient and inversely related to resistance

208
Q

if pressure gradient increases, airflow to lungs

A

increase

209
Q

if resistance increases ,airflow

A

decreases

210
Q

pressure gradient can be changed by

A

altering volume of thoracic cavity
- small volume changes of quiet respiration allow 500 mL of air to enter
- if accessory muscles of inspiration are used, volume increases more
- airflow increases due to greater pressure gradient

211
Q

resistance

A

greater difficulty moving air
may be altered by:
- change in elasticity of chest wall and lungs
- change in bronchiole diameter
- collapse of alveoli

212
Q

compliance

A

ease with which lungs and chest wall expands
the easier the lung expands the greater the compliance
as we age compliance declines

213
Q

pulmonary ventilation

A

process of moving air into and out of the lungs
amount of air moved between atmosphere and alveoli in 1 minute
tidal volume x respiratory rate = pulmonary v.

214
Q

tidal volume

A

amount of air per breath

215
Q

respiration rate

A

number of breaths per minute

216
Q

pulmonary ventilation formula

A

tidal volume x respiratory rate = pulmonary ventilation
500 mL x 12 breaths/min = 6,000 mL/min = 6 L/min
typical amount

217
Q

anatomic dead space

A

conducting zone space
no exchange of respiratory gases here
about 150 mL of air

218
Q

alveolar ventilation

A

amount of air reaching alveoli per minute
(tidal volume - anatomic dead space) x respiration rate = alveolar ventilation

219
Q

alveolar ventilation formula

A

(tidal volume - anatomic dead space) x respiration rate = alveolar ventilation

(500 mL - 150 mL) x 12 breaths/min = 4.2 L/min

220
Q

deep breathing maximizes

A

alveolar ventilation

221
Q

spirometer

A

measure respiratory volume
can be used to assess respiratory health (standard values are available (e.g., different ages)

222
Q

spirometer measures

A
  1. tidal volume: amount of air inhaled or exhaled per breathing during quiet breathing
  2. inspiratory reserve volume (IRV): amount of air that can be forcibly inhaled beyond the tidal volume (measure of compliance)
  3. expiratory reserve volume (ERV): amount that can be forcibly exhaled beyond tidal volume (elasticity of lungs and chest wall)
  4. residual volume: amount of air left int he lungs after most forceful expiration
223
Q

four capacities calculated from respiratory volumes

A
  1. inspiratory capacity
  2. functional capacity
  3. vital capacity
  4. total lung capacity
224
Q

inspiratory capacity (IC)

A

tidal volume + inspiratory reserve volume

225
Q

functional residual capacity (FRC)

A

expiratory reserve volume + residual volume
volume left in lungs after quiet expiration

226
Q

vital capacity

A

tidal volume + inspiratory and expiratory reserve volumes
total amount of air a person can exchange through forced breathing

227
Q

total lung capacity (TLC)

A

sum of all volumes, including residual volume
maximum volume of air that lungs can hold

228
Q

partial pressure

A

pressure exerted by each gas within a mixture of gases, measured in mmHg
each gas moves independently down its partial pressure gradient

229
Q

atmospheric pressure

A

760 mm Hg at sea level
total pressure of all gases collectively exert in the environment
includes: N2, O2, CO2, H2O, and other minor gases

230
Q

dalton’s law

A

the total pressure in a mixture of gases is equal to the sum of the individual partial pressure

231
Q

partial pressure of gas formula

A

total pressure x % of gas = partial pressure
nitrogen is 78.6% of the gas in air
760 mm Hg x .786 = 587 mm Hg = partial pressure of nitrogen

232
Q

partial pressures added together equal

A

total atmospheric pressure

233
Q

partial pressure gradients

A

gradient exists when partial pressure for a gas is higher in one region of the respiratory system than another

gas moves from region of higher partial pressure to region of lower partial pressure until pressure is equal

234
Q

alveolar gas exchange depends on

A

gradients between blood in pulmonary capillaries and alveoli

235
Q

systemic gas exchange depends on

A

gradients between blood in systemic capillaries and systemic cells

236
Q

henry’s law

A

at a given temperature, the solubility of a gas in liquid is dependent upon the
- partial pressure
- solubility coefficient

237
Q

partial pressure is the driving force…

A

moving gas into liquid
determined by total pressure and percentage of gas in mixture

CO2 is forced into soft drinks under hgih pressure

238
Q

solubility coefficient

A

volume of gas that dissolves in a specified volume of liquid at a given temperature and pressure

a constant that depends upon interactions between molecules of the gas and liquid

239
Q

alveolar gas exchange (external respiration) : oxygen

A

PO2 in alveoli is 104 mm Hg (760 mmHg x 13.7%)
PO2 of blood entering pulmonary capillaries is 40 mm Hg

oxygen diffuses across respiratory membrane from alveoli into the capillaries
continues until blood PO2 is equal to that of alveoli
levels in alveoli remain constant as fresh air continuously enters

240
Q

alveolar gas exchange (external respiration) : carbon dioxide

A

PCO2 in alveoli is 40 mm Hg (760 x 5.2%)
PCO2 in blood of pulmonary capillaries if 45 mm Hg

CO2 diffuses from blood to alveoli
continues until blood levels equal alveoli levels
levels in alveoli remain constant

241
Q

systemic gas exchange (internal respiration): oxygen

A

oxygen diffuses out of systemic capillaries to enter systemic cells
- partial pressure gradient drives the process
PO2 in systemic cells 40 mm Hg
PO2 in systemic capillaries is 95 mm Hg
continues until blood PO2 is 40 mm Hg
systemic cell PO2 stays fairly constant
- oxygen delivered at same rate it is used until engaging in strenuous activity

242
Q

systemic gas exchange (internal respiration): carbon dioxide

A

diffuses from systemic cells to blood
partial pressure gradient driving process
- PCO2 in systemic cells = 45 mmHg
- PCO2 in systemic capillaries = 40 mm Hg
diffusion continuing until blood PCO2 is 45 mmHg

243
Q

blood’s ability to transport oxygen depends on

A

solubility coefficient of oxygen
- very low, so little oxygen dissolves in plasma
presence of hemoglobin
- iron of hemoglobin attaches to oxygen
- 98% of O2 in blood is bound to hemoglobin

244
Q

means of transport for CO2

A
  1. CO2 dissolved in plasma (7%)
  2. CO2 attached to amine group of globin portion of hemoglobin (23%)
    - HbCO2 is carbaminohemoglobin
  3. bicarbonate dissolved in plasma (70%)
    - CO2 diffuses into erythrocytes and combines with water to form bicarbonate and hydrogen ions
    - bicarbonate diffuses into plasma
    - CO2 is regenerated when blood moves through pulmonary capillaries and the process is reversed
245
Q

conversion of CO2 to HCO3- at systemic capillaries

A
  1. CO2 diffuses into an erythrocytes
  2. once inside RBC, CO2 is joined to H2O to form H2CO3 by carbonic anhydrase. carbonic acid (H2CO3) splits into bicarbonate and hydrogen ion (H+)
    - CO2 + H2O –> H2CO3 –> HCO3- + H+
  3. HCO3- (- charge), exits erythrocyte. a same time, chloride ion goes into erythrocyte to equalize charges to prevent development of negative charge on outside. the movement of HCO3- out of the erythrocyte as Cl- moves into the erythrocyte is called chloride shift
246
Q

conversion of HCO3- to CO2 at pulmonary capillaries

A
  1. HCO3- moves into the erythrocytes as Cl- moves out
  2. HCO3- recombines with H+ to form H2CO3, which dissociates into CO2 and H2O
  3. CO2 diffuses out of the erythrocyte into the plasma CO2 then diffuses into alveolus
247
Q

oxygen-hemoglobin saturation curve

A

oxyhemoglobin dissociation curve
- each hemoglobin can bind up to 4 O2 molecules (one on each iron atom of hemoglobin)
- percent O2 saturation of hemoglobin is crucial (amount of oxygen bound to available hemoglobin)
- saturation increases as PO2 increases
- graphed (s-shaped, nonliner realationship)

248
Q

cooperative binding effect

A

each O2 that binds causes a conformational change in hemoglobin making it easier for next O2 to bind

249
Q

other variables that influence oxygen release from hemoglobin during systemic exchange

A
  1. temperature
  2. H+ binding to hemoglobin (Bohr effect)
  3. CO2 binding to hemoglobin
  4. prescence of 2,3 BPG
250
Q

PO2 levels within blood and systemic cells

A

40 mm Hg
75% saturated (O2 reserve)

251
Q

temperature increase

A

if body temp increases, hemoglobin is going to give off oxygen to greater degree
less saturated hemoglobin because hemoglobin is releasing oxygen at greater degree
cooling body temperature shows hemoglobin carries on to that oxygen so pressure of oxygen is going to increase (95% saturation)

252
Q

H+ increase (Bohr effect)

A
  • hydrogen ions binding to Hb will cause release of oxygen
  • at 7.4 pH
  • lower pH means higher amount of hydrogen ions and Hb releases more oxygen
  • higher pH means lower amount of hydrogen ions and Hb releases less oxygen
253
Q

2,3 BPG binding

A
  • increase in 2,3 BPG causes increase oxygen release
  • higher BPG causes O2 to be more readily released causing a right shift because there will be more unsaturated hemoglobin
254
Q

CO2 binding

A

increase oxygen release and causes right shift (increase in release of oxygen)

255
Q

right shift

A

increase in release of O2

256
Q

left shift

A

decrease in release of oxygen

257
Q

while exercising breathing shows

A

hyperapnea to meet increased tissue needs
breathing depth increases while rate remains the same

258
Q

Blood PO2 and Blood CO2 remain relatively constant

A
  • increased cellular respiration compensated for by deeper breathing, increased cardiac output, and greater blood flow
  • the respiratory center is stimulated from one or more causes
    1. proprioceptive sensory signals in response to movement
    2. corollary motor output from cerebral cortex relayed to respiratory center
    3. conscious anticipation of exercise

Human Anatomy and Phys Sp23 (5 decks)

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