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nose
only external portion of respiratory system
moistens and warms entering air
filters and cleans inspired air
serves as resonating chamber for speech
houses olfactory receptors
rhinitis
inflammation of nasal mucosa
spreads from nose to throat to chest
also spread to tear ducts and paranasal sinuses, causing blockage of sinus passageways
respiratory zone
site of gas exchange
conducting zone
conduits that transport gas to/and from gas exchange sites
cleanses, warms, & humidifies air
larynx
voice box
provides patent airway
routes air and food into proper channels
houses vocal folds
epiglottis
prevents food & liquids from entering the trachea
laryngitits
inflammation of vocal folds that causes swelling, interfering with vibrations
results in changes to vocal tone or worst cases limited to a whisper
caused by viral infections but also be due to overuse of voice, dry air, bacterial infections, tumors, or irritating chemicals
mucosa
ciliated pseudostratified epithelium with goblet cells
submucosa
connective tissue with seromucous glands
supported by C-shaped cartilage rings (prevent collapse of trachea)
alveolar pores
connect adjacent alveoli
equalize air pressure throughout lung
provide alternate routes in case of blockages
alveolar macrophages
keep alveolar surfaces sterile
2 million dead macrophages/ hour carried by cilia to throat & swallowed
pleural cavity
between two pleurae
provides lubrication & surface tension that assists in expansion & recoil of lungs
inspiration
air flows INTO lungs down its pressure gradient
pressure in the lungs is less than atmospheric pressure
expiration
gases EXIT lungs
pressure in the lungs is GREATER than atmospheric pressure
atmospheric pressure “Patm”
pressure exerted by air surrounding the body
760 mm Hg at sea level= 1 atm
intrapulmonary pressure “Ppul”
pressure in ALVEOLI
eventually equalizes with Patm
intrapleural pressure “Pip”
pressure in PLEURAL CAVITY
always a negative pressure
fluid level must be kept at a minimum
excess pumped by lymphatic system
intrapleural pressure inward forces promoting lung collapse
lungs’ natural tendency to recoli
surface tension of alveolar fluid
atelectasis
lung collapse from
plugged bronchioles → collapse of alveoli
pneumothorax: air in pleural cavity
pulmonary ventilation “breathing”
inspiration & expiration
depends on volume changes in thoracic cavity
volume changes = pressure changes
pressure changes = flow of gases to equalize pressure
boyle’s law
relationship between pressure & volume of a gas
pressure varies inversely with volume
influence that ease air passage & amount of energy for ventilation
airway resistance
alveolar surface tension
lung compliance
airway resistance
friction (major nonelastic source of resistance to gas flow in airways)
resistance in respiratory tree is insignificant
diameters of airways in conducting zone are huge
branching of airways as they get smaller lead to increase in total cross-sectional area
usually occurs in medium-sized bronchi
disappears at terminal bronchioles (diffusion drives gas movement)
alveolar surface tension
attraction of liquid molecules to one another at a gas-liquid interface
H2O has very high surface tension, coats alveolar walls in a thin film
cause alveoli to shrink to smallest size
surfactant
detergent-like lipid and protein complex that helps reduce surface tension of alveolar fluid by reducing H-bonds between H2O-molecules
prevent alveolar collapse
infant respiratory distress syndrome
insufficient surfactant in premature infants
collapse of alveoli after each breath
lung compliance
measure of changes in lung volume that occurs with given change in transpulmonary pressure
measure of how much “stretch” the lung has
normally high
high = easier to expand lungs
diminishes lung compliance
nonelastic scar tissue replacing lung tissue (fibrosis)
reduced production of surfactant
decreased flexibility of thoracic cage
alveolar ventilation rate
flow of gases into and out of alveoli during a particular time
dalton’s law of partial pressure
total pressure exerted by mixture of gases is equal to sum of pressures exerted by each gas
pressure exerted by each gas in mixture
major gasses in the air we breathe in order of abundance
N- 78.6%
O- 20.9%
factors that influence external respiration
Partial pressure gradients and gas solubilities
Thickness and surface area of respiratory membrane
Ventilation-perfusion coupling
Partial pressure gradients and gas solubilities
venous blood PO2 = 40 mm Hg
alveolar PO2= 104 mm Hg
venous blood PCO2 = 45 mm Hg
alveolar PCO2= 40 mm Hg
Thickness and surface area of respiratory membrane
respiratory membranes are thin
Large total surface area of the alveoli is 40x the surface area of the skin
ventilation-perfusion coupling
P: blood flow reaching alveoli
V: amount of gas reaching alveoli
rates must be matched for optimal, efficient gas exchange
controlled by local autoregulatory mechanisms
PO2 in alveoli
change cause changes in diameters of arterioles
HIGH = arterioles dilate
LOW = arterioles constrict
PCO2 in alveoli
change cause changes in diameter of bronchioles
HIGH= bronchioles dilate
LOW= bronchioles constrict
allows elimination of CO2 more rapidly
Tissue PO2
always lower than in arterial blood PO2 (40 vs. 100 mm Hg)
oxygen moves from blood to tissues
Tissue PCO2
always higher than arterial blood PCO2 (45 vs. 40 mm Hg)
CO2 moves from tissues into blood
molecular O2 transportation
dissolved in plasma (1.5%)
loosely bound to each Fe of hemoglobin (Hb) in RBC (98.5%)
carry 4 O molecules
Oxyhemoglobin (HbO2 )
hemoglobin-O2 combination
O2 is bound to hemoglobin
Reduced hemoglobin (deoxyhemoglobin) (HHb):
hemoglobin that has released O2
change in shape of Hb
facilitates loading & unloading of O2
O2 BINDS= affinity for O2 increases
O2 RELEASED= affinity for O2 decreases
factors that influence hemoglobin saturation
PO2
Temperature
Blood pH
PCO2
Concentration of BPG
arterial blood
PO2 is 100mm Hg
20 ml of O2/ 100 ml blood
Hb is 98% saturated
venous blood
PO2 is 40 mm Hg
contains 15 volume % oxygen
Hb is 75% saturated at rest
BPG
produced by RBC during glycolysis
levels rise when oxygen levels are low
modify structure of hemoglobin
Increases in temperature, H+ , PCO2 , and BPG\
Results in a decrease for Hb’s affinity for O2
Occurs in systemic capillaries
Enhances O2 unloading (curve to right)
glucose metabolism using O2 cause
increases in PCO2 & H+ in capillary blood
declining blood pH (acidosis) & increasing PCO2 cause HB-O2 bond to weaken (Bohr effect)
hypoxia
inadequate O2 delivery to tissues; can result in cyanosis
ischemic hypoxia
impaired or blocked circulation
histotoxic hypoxia
cells unable to use O2, as in metabolic poisons
hypoxemic hypoxia
abnormal ventilation; pulmonary disease
CO2 transportation in blood
7-10% is dissolved in plasma as Pco2
20% is bound to the globin in hemoglobin (carbaminohemoglobin)
70% is transported as bicarbonate ions (HCO3) in plasma
HCO-3 in systemic capillaries
after created it diffuses from RBCs into plasma
Outrush from RBC is balanced as Cl moves into RBCs from plasma
Chloride shift
HCO3- in pulmonary capillaries
moves into RBCs while Cl moves out of RBCs back into plasma -
binds with H+ to form H2CO3
H2CO3 is split by carbonic anhydrase into CO2 and H2O
CO2 diffuses into alveoli
Haldane effect
Increased blood O2 decreases ability to carry CO2
CO2 release in lungs
Decreased blood O2 increases ability to carry CO2
CO2 pick up in tissues
bohr effect
Increased blood CO2 decreases ability to carry oxygen
↑blood CO2 = ↓ blood pH
decreased affinity of hemoglobin for O2
O2 release in tissues
Decreased blood CO2 increases ability to carry oxygen
↓ blood CO2 = ↑ blood pH
increased affinity of hemoglobin for O2
O2 pick up in lungs
Carbonic acid–bicarbonate buffer system
helps blood resist changes in pH
If H+ concentration in blood rises
excess is removed by combining with HCO3 to form H2CO3 which dissociates into CO2 and H2O
If H+ concentration drops
H2CO3 dissociates, releasing H+
HCO3 – is the alkaline reserve
Slow shallow breathing
causes an increase in CO2 in blood, resulting in a drop in pH
Rapid deep breathing
causes a decrease in CO2 in blood, resulting in a rise in pH
affect respiratory centers
Chemical factors
Influence of higher brain centers
Pulmonary irritant reflexes
Inflation reflex
chemical factors influence respiratory rate
changing levels of PCO2, PO2, pH
Pco2 & pH are most potent and closely controlled
levels are sensed by central & peripheral chemoreceptors
rising CO2 levels
most powerful respiratory stimulant
influence of PCO2
if blood levels decrease, respiration becomes slow and shallow
Declining PO2 normally has only slight effect on ventilation because of huge O2 reservoir bound to Hb
Requires substantial drop in arterial PO2 (below 60 mm Hg) to stimulate increased ventilation
Apnea
breathing cessation that may occur when PCO2 levels drop abnormally low
Hyperventilation
increased depth and rate of breathing that exceeds body’s need to remove CO2
Leads to decreased blood CO2 levels (hypocapnia)
influence of arterial pH
can modify respiratory rate and rhythm even if CO2 and O2 levels are normal
Mediated by peripheral chemoreceptors
Decrease may reflect CO2 retention, accumulation of lactic acid, or excess ketone bodies
Respiratory system controls attempt to raise pH by increasing respiratory rate and depth
arterial PO2
if falls below 60 mm Hg, it becomes major stimulus for respiration (via peripheral chemoreceptors
Hering-Breuer reflex (inflation reflex)
Stretch receptors in pleurae and airways are stimulated by lung inflation
Send inhibitory signals to medullary respiratory centers to end inhalation and allow expiration
can be a protective response
hypernea
increased ventilation in response to metabolic needs
Pco2, Po2, & pH remain constant
alimentary canal “GI tract”
Muscular tube that runs from the mouth to anus
Digests food
Absorbs fragments through lining into blood
Organs: mouth, pharynx, esophagus, stomach, small intestine, large intestine, anus
accessory digestive organs
organs: Teeth, Tongue, Gallbladder, Digestive glands
produce secretions that help break down food
Salivary glands, Liver, Pancreas
Processing of food
ingestion
Propulsion
Mechanical breakdown
Digestion
Absorption
Defecation
mechanical breakdown- digestion
chewing, mixing food with saliva, churning food, & segmentation
segmentation: alimentary canal organs contract and relax to mix and mechanically break down food
chemical digestion
catabolic steps that involves enzymes
propulsion
movement of food through the alimentary canal
swallowing
peristalsis: alimentary canal organs alternately contract and relax to move food along the tract
peritoneum
serous membranes of abdominal cavity
visceral & parietal
mesentery
double layer of peritoneum; layers fuse back to back
provides routes for blood vessels, lymphatics, & nerves
holds organs in place & stores fat
digestive organs layes “tunics”
mucosa
submucosa
muscularis externa
serosa
mucosa
lines lumen
function: secretes, absorbs, & protects
secretes mucus, digestive enzymes, & hormones
absorbs end products of digestion
protects against infectious disease
made up of epithelium, lamina propria, & muscularis mucosae
epithelium
secretes mucus
protects digestive organs from enzymes
eases food passages
may secrete enzymes & hormones
lamina propria
rich supply of capillaries for nourishment & absorption
lymphoid follicles that help defend against microorganisms
Muscularis mucosae
Smooth muscle that produces local movements of mucosa
submucosa
consists of areolar connective tissue
contains blood & lymphatic vessels, lymphoid follicles, & submucosal nerve plexus which supply surrounding GI tract tissues
has abundant elastic tissue that helps organs to regain shape
muscularis externa
muscle layer responsible for segmentation & peristalsis
contains inner circular muscle layer & outer longitudinal layers
enteric nervous system
intrinsic nerve supply to the alimentary canal
contains more neurons than spinal cord
their neurons communicate extensively with each other
participates in short & long reflex arcs
submucosal nerve plexus
regulates glands and smooth muscle in mucosa
made up by enteric neurons
myenteric nerve plexus
controls GI tract motility
made up by enteric neurons
long reflexes
respond to stimuli arising inside/outside of gut
parasympathetic system ENANCES digestion
sympathetic system INHIBITS digestion
tongue
Form bolus (mixture of food and saliva)
Intrinsic muscles change shape of tongue
Extrinsic muscles alter tongue’s position
filiform papaillae
gives tongue roughness to provide friction
only one that does not contain taste buds
ankyloglossia “tongue-tied” "fused tongue”
congenital condition in which children are born with an extremely short lingual frenulum
restricted movement distorts speech
saliva
compacts into bolus
begins breakdown of starch with enzyme amylase
produced by major (extrinsic) glands located outside oral cavity
mostly water
slightly acidic
mumps
inflammation of parotid glands caused by myxovirus
common children’s disease
salivation
1500 ml/day can be produced
Intrinsic glands keep mouth moist
Extrinsic salivary glands are activated by parasympathetic nervous system
Strong sympathetic stimulation inhibits it and results in dry mouth (xerostomia)
teeth
Crown: exposed part above gingiva (gum)
Covered by enamel, the hardest substance in body
Heavily mineralized with calcium salts and hydroxyapatite crystals
Enamel-producing cells degenerate when tooth erupts
Root: portion embedded in jawbone; connected to crown by neck
gastroesophageal sphincter
junction of the esophagus and the stomach
Prevents heartburn
gingivitis
Plaque calcifies to form calculus (tartar)
Calculus disrupts seal between gingivae and teeth
Anaerobic bacteria infect gums
Infection is reversible if calculus removed
periodontitis (periodontal disease)
Neglected gingivitis can escalate to disease
Immune cells attack bacterial intruders & body tissues
May increase heart disease and stroke
esophagus
Flat muscular tube that runs from laryngopharynx to stomach
joins stomach at cardial orifice
alimentary canal that transitions from skeletal muscle to smooth muscle
From stratified squamous to simple columnar epithelium?