exam 3 Flashcards
immune system
- 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
how do the two types of immunity differ
based on
- what cells are involved
- the specificity of cell response
- the mechanisms of eliminating harmful substances
- the amount of time for response
although innate and adaptive immunities are distinct,
they work together in body defense
innate immunity
immediate response to wide array of substances
adaptive immunity
delayed responses to specific antigens
innate immunity is subdivided into
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)
adaptive immunity subdivided
t-lymphocytes (cell mediated immunity)
B- lymphocytes (humoral immunity)
- plasma cells (synthesized and release antibodies)
characteristics of innate immunity
responds nonspecifically to a range of harmful substances
first line and second line of defense
first line of defense in innate immunity
skin and mucosal membrane
second line of defense in innate immunity
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
cells of innate immunity
neutrophils
macrophages
dendritic cells
basophils
mast cells
NK cells
eosinophils
interferons
neutrophils, macrophages, and dendritic cells are
phagocytic cells
basophils and mast cells
proinflammatory chemical secreting cells
NK cells
apoptosis initiating cells
eosinophils
parasite destroying cells
interferon
synthesizes enzymes that interfere with viral replication
complement system
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
complement activation following pathogen entry
- 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
opsonization
complement protein (opsonin) binds to pathogen
- enhances the likelihood of phagocytosis of pathogenic cell
inflammation is enhanced by
complement
- activates mast cells and basophils
- attracts neutrophils and macrophages
cytolysis
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)
elimination of immune complexes
- complement links antigen-antibody complexes to erythrocytes
- cells move to liver and spleen where complexes are stripped off
inflammation
immediate response to ward off unwanted substances
-local, nonspecific response of vascularized tissue to injury part of innate immunity
steps of inflammation
- release of inflammatory and chemotactic factors
- vascular changes include : vasodilation of arterioles, increase in capillary permeability, display of CAMs
- recruitment of immune cells
- delivery of plasma proteins
step 1: release of inflammatory and chemotactic factors
- 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
step 2: vascular changes include
- 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)
step 3: recruitment of immune cells
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
step 4: delivery of plasma proteins
increase of fluid accumulation in tissue carrying valuable proteins
- creates more hydrostatic pressure that helps drive fluid into lymphatic capillary lumens
cardinal signs of inflammation
- 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)
duration of acute inflammation
8-10 days
chronic inflammation
has detrimental effects
fever (pyrexia)
abnormal body temperature elevation
1°C or more from normal (37°C)
fever is the result of
release of pyrogens from immune cells or infectious agents
events of fever
- pyrogens circulate through blood and target hypothalamus
- in response, hypothalamus releases prostaglandin E2
- hypothalamus raises temperature set point leading to fever
benefits of fever
- 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
two branches of adaptive immunity
cell-mediated immunity
humoral immunity
cell-mediated immunity
involves t-lymphocytes
humoral immunity
involves B-lymphocytes, plasma cells, and antibodies
cell-mediated immunity is effective against
antigen within the cells; requires antigen presenting cells
what cells are formed after cell-mediated immunity is stimulated
cytotoxic T-lymphocytes and helper T-lymphocytes
effector response of cell-mediated immunity
apoptosis
humoral immunity is effective against
antigens outside cells; does not require antigen presenting cell
cells formed after humoral immunity is stimulated
plasma cells
effector response of humoral immunity
produce antibodies
cytotoxic t-lymphocytes
- directly kill abnormal cells
- destroys cells through apoptosis
- recognizes antigen on infected cells and releases chemicals to destroy infected cell
helper t-lymphocytes
release cytokines when recognizing own
promotes humoral immunity
antigens
substance that binds a t-lymphocyte or antibody
- usually a protein or large polysaccharide
pathogens are detected by lymphocytes because
they contain antigens
examples of antigens
protein capsid of viruses
cell wall of bacteria or fungi
bacterial toxins
abnormal proteins or tumor antigens
antigenic determinant
also known as EPITOPE
specific site on antigen recognized by immune system
each has different shape
pathogenic organisms can have multiple determinants
antigens can have more than one
antigenic determinants which stimulates adaptive immunity
immunogen
antigen that induces an immune response
immunogenecity
ability to trigger response
increases with antigen’s degree of foreignness, size, complexity, or quanity
haptens
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)
lymphocyte contact with antigen
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)
T-lymphocytes: cells of cell mediated immunity
t-cells have over 100,000 t-cell receptors as well as coreceptors that help successfuly link antigen to t-lymphocytes
helper t-lymphocytes contain
CD4 proteins
cytotoxic t-lymphocytes contain
CD8 proteins
b-lymphocytes have
b-cell receptors embedded in their membrane
specific class of antibodies that are proteins
helper t-lymphocytes assist in
cell-mediated immunity
humoral immunity
innate immunity
activate NK cells and macrophages
t-lymphocyte subtypes
cytotoxic t-lymphocytes
helper t-lymphocytes
memory t-cells
regulatory t-cells
antigen presentation
cells display antigen on plasma membrane so t-cells can recognize it
two categories of cells present antigens
- 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
antigen presentation requires
attachment of antigen to MHC
MHC
major histocompatibility complex
group of transmembrane proteins
CD4 interact specifically with
MHC class II molecules
CD8 interacts specifically with
MHC class I
three main events in life of lymphocyte
- formation and maturation of lymphocytes
- activation of lymphocytes
- effector response: action of lymphocytes to eliminate antigen
formation and maturation of lymphocytes
occurs in primary lymphatic structures (red marrow and thymus)
become able to recognize one specific foreign antigen
activation of lymphocytes
in secondary lymphatic structures they are exposed to antigen and become activated
replicate to form identical lymphocytes
effector response: action of lymphocytes to eliminate antigen
- 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
formation of lymphocytes
- 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)
activation of lymphocytes
lymph nodes, spleen, and tonsils are secondary lymphatic structures that house B-lymphocytes and T-lymphocytes
effector response of lymphocytes
interaction of T-lymphocytes and antibodies to eliminate foreign antigens at site of infection
activation of lymphocytes in helper T-lymphocyte
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
activation of lymphocytes : cytotoxic T-lymphocyte
- First Signal - CD8 binds with MHC class I molecule of infected cell; TCR interacts with antigen within MHC class I molecule
- 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
costimulation to activate B-lymphocyte for clonal selection
- First Signal - free antigen binds to BCR; B-lymphocyte engulfs and presents antigen to activated helper T-lymphocyte
- 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
effector response at infection site
mechanism used by lymphocytes to help eliminate antigen
each lymphocyte has its own
effector response
effector response for helper T-lymphocytes
releases IL-2, IL-4 and other cytokines
regulate cells of adaptive and innate immunity
effector response for cytotoxic T-lymphocytes
destroy unhealthy cells by apoptosis
effector response for plasma cells (differentiated B-lymphocytes)
produce antibodies
steps of effector response
- 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 - help activate B-lymphocytes
- activate cytotoxic T-lymphocytes w/ cytokines
- stimulate activity of innate immune system cells
effector response of cytotoxic T-lymphocytes
(cell mediated immunity)
release of cytotoxic chemicals induces apoptosis of abnormal cells by release of perforin and granzymes
effector response of B-lymphocytes
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
antibodies circulate through lymph and blood until
encountering antigen
antibody titer
circulating blood concentration of antibody against a specific antigen
- used as a measure of immune response
antibodies
immunoglobin proteins produced against a particular antigen
- antibodies “tag” pathogens for destruction by immune cells
- good defense against viruses, bacteria, toxins, yeast spores
soluble antigens are combatted by
humoral immunity
antibodies don’t require an APC, they can interact their receptors just in interstitial fluid
antibody structure
4 polypeptides bound together
2 light chains and 2 identical heavy chains
extension of Y shape referred to as Y region
disulfide bonds on antibody structure allows for
linkage between polypeptide
variable region of antibody
gives antibody a specificity on antigen binding site
unique to specific antibody
constant region
area among the bottom 75% of antibody structure that remains constant
Fc region
fragmented constant
binding of antigen-binding site of an antibody with antigen causes
- neutralization
- agglutination
- precipitation
neutralization
antibody covers biology active portion of microbe or toxin
neutralizes that organisms ability to be pathogenic
agglutination
antibody cross-links cells (e.g., bacteria) forming a clump
makes it easier for organism to be phagocytized
precipiation
antibody cross-links circulating particles (e.g., toxins), forming an insoluble antigen-antibody complex
precipitates them out of solution
exposed Fc portion following antigen binding by antibody promotes
complement fixation
opsonization
activation of NK cells
complement fixation
Fc region of antibody binds complement proteins; complement is activated
opsonization
Fc region of antibody binds to receptors of phagocytic cells, triggering phagocytosis
antibodies can tag organism for removal by phagocyte
activation of NK cells
Fc region of antibody binds to an NK cell, triggering release of cytotoxic chemicals (perforin/granzymes)
IgG
- major class
- 75-85%
- most versatile
- capable of all antibody reactions
IgM
- pentamer (5 monomers)
- best at agglutination
IgA
- dimer
- areas exposed to environment (mucosal membranes; tonsils)
- best at neutralization (prevention of entry)
IgD
- B-cell receptors (id’s when B cells are ready for activation
IgE
- allergy and parasitism
- degranulation of basophils and mast cells
- chemotactic for eosinophils
adaptive immunity: effector response; cell-mediated immunity
- activated helper T-lymphocytes release cytokines to stimulate activity of B-lymphocytes and cytotoxic T-lymphocytes, and regulates cells of innate immunity
- activated cytotoxic T-lymphocytes release cytotoxic molecules (perforin and granzymes) causing apoptosis of foreign or abnormal cells
adaptive immunity: effector response; humoral immunity
- 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
- 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
immunologic memory
-memory results from formation of a long lived army of lymphocytes upon immune activation
adaptive immunity activation requires
contact between lymphocyte and antigen
- there is lag time between first exposure of the host a direct contact with lymphocyte
activation of adaptive immunity leads to
formation of many memory cells against a specific antigen
with subsequent antigen exposure…
- 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)
what is an effective way to develop memory
vaccines
don’t contain active viruses but help provoke initial response so if you are exposed, you will have ability to fight off infection
primary vs secondary response antibody titer
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
active immunity
production of memory cells due to contact w antigen
naturally acquired - direct exposure to antigen
artificially acquired - vaccine
passive immunity
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
acute hypersensitivity
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
autoimmune disorders
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
cross reactivity
a pathogen is so structurally similar, immune system can’t distinguish between self vs pathogen
rheumatic heart disease
altered self-antigen
something alters shape or makeup of antigen
random mutation or from infection causing cell to become foreign
type 1 diabetes
areas of immune privledge
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
acquired immunodeficiency syndrome
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
HIV and AIDS
- 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)
what are the 2 components of the structural organization of the respiratory system
upper and lower respiratory tracts
components of upper respiratory tract
nose
nasal cavity
pharynx
components of lower respiratory tract
larynx
trachea
bronchus
bronchiole
terminal bronchiole
lungs
respiratory bronchiole
alveolar duct
alveoli
what are the components of the functional organization of the respiratory system
conducting zone and respiratory zone
components of conducting zone
nose
nasal cavity
pharynx
larynx
trachea
bronchus
bronchiole
terminal bronchiole
components of respiratory zone
respiratory bronchiole
alveolar duct
alveoli
what is the function of the conducting zone
conduction of air
no gas exchange occurs
no oxygen and CO2 crossing
what occurs in respiratory zone
gas exchange
primarily in alveoli
microscopic
pharynx
- cavity posterior to nasal and oral cavity
- common passageway for air and food
- divided into 3 regions; nasopharynx, oropharynx, laryngopharynx
eustachian tube connects
middle ear to nasopharynx to equilibriate air pressure
larynx
- made of 9 pieces of cartilage bound together by various muscles and ligaments
- connected superiorly via ligaments and muscles to the hyoid bone
largest cartilage in larynx is
thyroid cartilage
laryngeal prominence
extends out, adam’s apple
vocal folds are found in
larynx
vocal folds
back of oral cavity through laryngoscope
vocal folds are bands of cartilage
sound is emitted as they vocal folds open, close, and move
trachea
- 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
angular ligament refers to
elastic cartilage between tracheal cartilage
carina is
inside trachea where it divides into left and right bronchi
- contains receptors stimulated by irritants (provokes cough reflec)
lining of trachea has
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
bronchial tree
vast network of airways that decrease in size as they continue to branch
trachea splits into
main bronchi
main bronchi divides into
right and left lungs into lobar bronchi
left lungs has how many lobes
2 lobes
right lung has how many lobes
3 lobes
segmental bronchi
each segmental bronchi delivers air to one bronchopulmonary segment
each lobe is further subdivided into segments that is portioned into multiple bronchopulmonary segments
flow of bronchial tree
trachea
main bronchi
lobar bronchi
segmental bronchi
smaller bronchi
bronchioles and alveoli
- 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)
alveoli
- 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
what is the most plentiful cell in respiratory system
alveolar type I cell
alveolar type I cell
makes up wall of alveola
contributes to respiratory membrane
respiratory membrane
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
alveolar type II cells
intermittent on alveoli
produce surfactant
surfactant
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
alveolar macrophages
immune cells that migrate around in lung tissue phagocytosing pathogens
hilum
blood vessels, lymphatic vessels
bronchi feed into hilum
pleural membrane of lungs
serous membrane in thoracic cavity
visceral layer lines the lung tissue
pariteal layer lines thoracic wall
pleural cavity contains serous fluid within pleural cavity
function of pleural membrane of lungs
allow breathing not be painful and provides fluid to ensure this
respiration
exchange of gases between atmosphere and body’s cells that involves:
- pulmonary ventilation
- alveolar gas exchange
- gas transport
- systemic gas exchange
pulmonary ventilation
movement of gases between atmosphere and alveoli
alveolar gas exchange
external respiration
exchange of gases between alveoli and blood
gas transport
transport of gases in blood between lungs and systemic cells
systemic gas exchange
internal respiration
exchange of respiratory gases between the blood and the systemic cells
steps of respiration
- Pulmonary ventilation
- air containing O2 - Alveolar Gas Exchange
- O2 moves into blood - Gas transport
- blood containing O2 travels - systemic gas exchange
- O2 moves into systemic cells - systemic gas exchange
- CO2 moves into blood - gas transport
- blood containing CO2 - Alveolar Gas Exchange
- CO2 moves into alveoli - pulmonary ventilation
- air containing CO2 goes into atmosphere
pulmonary ventilation (breathing)
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)
inspiration
brings air into the lungs (inhalation)
expiration
forces air out of the lungs (exhalation)
autonomic nuclei in brainstem regulate
breathing activity
muscles of quiet breathing
- 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
muscles of forced inspiration
pull upward and outward
located in superior part of thorax and neck
- sternocleidomastoid
- scalenes
- serratus posterior superior
- pectoralis minor
- erector spinae
muscles of forced expiration
pull downward and inward
lower back and posterior region of throax
- transversus thoracis
- serratus posterior inferior
- internal intercostal
- external oblique
- transversus abdominus
dimensional changes in throacic cavity : inspiration
- 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
dimensional changes of thoracic cavity : expiration
- 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
when inspiration is occurring the diaphragm
contracts; moves down
when expiration is occurring the diaphragm
relaxes; moves up
boyle’s gas law
relationship of volume and pressure
- at constant temperature, pressure (P) of a gas DECREASES if volume (V) of the container increases, and vice versa
P1 and V2 represent
initial conditions
P2 and V2 represent
changed conditions
what relationship does gas pressure and volume have
inverse relationship
as pressure increases volume decreases
as pressure decreases volume increases
formula for boyle’s gas law
P1V1 = P2V2
an air pressure gradient exists when force per unit area is
greater in one place than another
if the two places are interconnected…
air flows from high to low pressure until pressure is equal
during inhalation thoracic volume
increases so pressure decreases and air flows in
during exhalation thoracic volume
thoracic volume decreases and pressure increases so air flows out
where is the respiratory center
in the medullary part of brain stem
pons portion of brain stems sends
input to the main medullary respiratory center to modify and smooth out inhalation and exhalation
what is the minor respiratory center
pontine respiratory center
peripheral chemoreceptors
aortic bodies and carotid bodies detect:
- increased CO2
- increased H+ (blood pH)
- decreased O2
if something increases H+ ion concentration
it can lead to lowering of blood pH
baroreceptors
refer to changes in pressure
prevent overinflation of lungs
proprioceptors
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
motor output to accessory muscles
come from motor cortex
voluntary control
formula
CO2 + H2O <–> H2CO3 <–> HCO3- + H+
carbon dioxide + water <–> carbonic acid <–> bicarbonate + hydrogen ion
frontal lobe of cerebral cortex controls
voluntary changes in breathing patterns
bypasses respirator center stimulating lower motor neurons directly
hypothalamus
increases breathing rate if body is warm
works through respiratory center
limbic system
alters breathing rate in response to emotions
works through respiratory center
2 kinds of controls of breathing
reflexive controls
conscious controls
airflow
amount of air moving in and out of lungs with each breath
air flow depends on
- pressure gradient established between atmospheric pressure and intrapulmonary pressure
- the resistance that occurs due to conditions within the airways, lungs and chest wall
F =
deltaP/r
f=
flow
∆P
difference in pressure between atmosphere and intrapulmonary pressure
Patm - Palv
R
resistance
flow is directly related to
pressure gradient and inversely related to resistance
if pressure gradient increases, airflow to lungs
increase
if resistance increases ,airflow
decreases
pressure gradient can be changed by
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
resistance
greater difficulty moving air
may be altered by:
- change in elasticity of chest wall and lungs
- change in bronchiole diameter
- collapse of alveoli
compliance
ease with which lungs and chest wall expands
the easier the lung expands the greater the compliance
as we age compliance declines
pulmonary ventilation
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.
tidal volume
amount of air per breath
respiration rate
number of breaths per minute
pulmonary ventilation formula
tidal volume x respiratory rate = pulmonary ventilation
500 mL x 12 breaths/min = 6,000 mL/min = 6 L/min
typical amount
anatomic dead space
conducting zone space
no exchange of respiratory gases here
about 150 mL of air
alveolar ventilation
amount of air reaching alveoli per minute
(tidal volume - anatomic dead space) x respiration rate = alveolar ventilation
alveolar ventilation formula
(tidal volume - anatomic dead space) x respiration rate = alveolar ventilation
(500 mL - 150 mL) x 12 breaths/min = 4.2 L/min
deep breathing maximizes
alveolar ventilation
spirometer
measure respiratory volume
can be used to assess respiratory health (standard values are available (e.g., different ages)
spirometer measures
- tidal volume: amount of air inhaled or exhaled per breathing during quiet breathing
- inspiratory reserve volume (IRV): amount of air that can be forcibly inhaled beyond the tidal volume (measure of compliance)
- expiratory reserve volume (ERV): amount that can be forcibly exhaled beyond tidal volume (elasticity of lungs and chest wall)
- residual volume: amount of air left int he lungs after most forceful expiration
four capacities calculated from respiratory volumes
- inspiratory capacity
- functional capacity
- vital capacity
- total lung capacity
inspiratory capacity (IC)
tidal volume + inspiratory reserve volume
functional residual capacity (FRC)
expiratory reserve volume + residual volume
volume left in lungs after quiet expiration
vital capacity
tidal volume + inspiratory and expiratory reserve volumes
total amount of air a person can exchange through forced breathing
total lung capacity (TLC)
sum of all volumes, including residual volume
maximum volume of air that lungs can hold
partial pressure
pressure exerted by each gas within a mixture of gases, measured in mmHg
each gas moves independently down its partial pressure gradient
atmospheric pressure
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
dalton’s law
the total pressure in a mixture of gases is equal to the sum of the individual partial pressure
partial pressure of gas formula
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
partial pressures added together equal
total atmospheric pressure
partial pressure gradients
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
alveolar gas exchange depends on
gradients between blood in pulmonary capillaries and alveoli
systemic gas exchange depends on
gradients between blood in systemic capillaries and systemic cells
henry’s law
at a given temperature, the solubility of a gas in liquid is dependent upon the
- partial pressure
- solubility coefficient
partial pressure is the driving force…
moving gas into liquid
determined by total pressure and percentage of gas in mixture
CO2 is forced into soft drinks under hgih pressure
solubility coefficient
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
alveolar gas exchange (external respiration) : oxygen
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
alveolar gas exchange (external respiration) : carbon dioxide
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
systemic gas exchange (internal respiration): oxygen
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
systemic gas exchange (internal respiration): carbon dioxide
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
blood’s ability to transport oxygen depends on
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
means of transport for CO2
- CO2 dissolved in plasma (7%)
- CO2 attached to amine group of globin portion of hemoglobin (23%)
- HbCO2 is carbaminohemoglobin - 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
conversion of CO2 to HCO3- at systemic capillaries
- CO2 diffuses into an erythrocytes
- 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+ - 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
conversion of HCO3- to CO2 at pulmonary capillaries
- HCO3- moves into the erythrocytes as Cl- moves out
- HCO3- recombines with H+ to form H2CO3, which dissociates into CO2 and H2O
- CO2 diffuses out of the erythrocyte into the plasma CO2 then diffuses into alveolus
oxygen-hemoglobin saturation curve
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)
cooperative binding effect
each O2 that binds causes a conformational change in hemoglobin making it easier for next O2 to bind
other variables that influence oxygen release from hemoglobin during systemic exchange
- temperature
- H+ binding to hemoglobin (Bohr effect)
- CO2 binding to hemoglobin
- prescence of 2,3 BPG
PO2 levels within blood and systemic cells
40 mm Hg
75% saturated (O2 reserve)
temperature increase
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)
H+ increase (Bohr effect)
- 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
2,3 BPG binding
- 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
CO2 binding
increase oxygen release and causes right shift (increase in release of oxygen)
right shift
increase in release of O2
left shift
decrease in release of oxygen
while exercising breathing shows
hyperapnea to meet increased tissue needs
breathing depth increases while rate remains the same
Blood PO2 and Blood CO2 remain relatively constant
- 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
