anatomy test 3

processes involved in gas exchange

ventilation, external respiration, internal respiration, transport of gases

upper respiratory tract

nose, nasal cavity, throat

lower respiratory tract

lungs, trachea, bronchi, larynx

external nose

-nasal bones and cartilage
-covered with skin, lines with mucous membrane
-has 2 nostrils (external nares)
-has vibrissae (nasal hairs)

nasal cavity

-hollow cavity in skull, lined with ciliated mucous membrane (produces 1L of mucous daily)
-divided internally by internal nasal septum (perpendicular plate of ethmoid and vomer)
-floor of the nasal cavity is the palate
-opens into the nasopharynx at posterior nasal aperture (internal nares)

parts of the palate (floor of nasal cavity)

hard palate: bone covered with mucous membrane
-palatine bones and palatine process of maxilla
soft palate: skeletal muscle covered by mucous membrane
-has uvula: extension of soft palate
-soft palate elevates when swallowing to keep food/fluid out of nasopharynx and nasal cavity

function of nasal cavity

-warms, moistens, and cleans inhaled air
-has 3 pairs of nasal conchae to increase surface area to complete functions (superior and middle nasal conchae-ethmoid bones, and inferior nasal conchae is seperate bones)
-houses olfactory epithelium-superior aspect of nasal cavity
-has openings from sinuses and nasolacrimal ducts
-resonating chamber for speech

paranasal sinuses

-hollow cavity in skull bones (sphenoid, ethmoid, frontal, maxilla)
-makes skull lighter, resonating chamber for speech, produces extra mucus for nasal cavity

nasopharynx

-posterior to nasal cavity, opens into nasal cavity at posterior nasal aperture
-extends to tip of uvula
-designed as air passageway only: has ciliated mucous membrane
-has pharyngeal tonsils (adenoids) on posterior wall
-has opening to Eustachian (auditory, pharyngotympanic tube) goes from throat to middle ear
-function in ear is to equalize air pressure on 2 sides of tympanic membrane

outer ear (auricle/pinna)

-captures sound waves and funnel into external auditory meatus
-ends at the tympanic membrane (eardrum)

middle ear

-hollowed out chamber in temporal bone, lined with mucous membrane
-air filled
-has malleus, incus, and stapes

steps of hearing

1. sound waves enter ear canal
2. vibration of tympanic membrane
3. malleus vibrates, then incus, then stapes
4. stapes sits in oval window
5. vibration of stapes causes fluid in inner ear (cochlea) to vibrate

inner ear

-hollowed out cavity in temporal bone
-filled with membranous fluid filled sacs and tubes
-has semicircular canals: receptor for equilibrium, balance
-has cochlea: snail shaped, receptor for hearing
-has vestibule: between semicircular canals and cochlea, has utricle and saccule (balance receptors)

oropharynx

-opens into mouth via the fauces
-extends from tip of uvula to the tip of epiglottis
-has 2 pairs of tonsils: lingual tonsils at base of tongue and palatine tonsils on side of throat

laryngopharynx

extends from tip of uvula to opening of esophagus

larynx

-voice box
-helps to maintain an open airway
-directs food into esophagus, keeps food away from trachea

cartilage in larynx

-9 pieces, joined by CT and muscle
-3 unpaired (single cartilage) and 3 pairs

thyroid cartilage

-unpaired cartilage in larynx
-angle in front is called the thyroid angle (adam's apple, laryngeal prominence)
-adam's apple in men is 90 degrees and in women it is 120 degrees

circoid cartilage

-unpaired cartilage in larynx
-inferior to the thyroid cartilage
-at the base of the larynx
-broken in manual strangulation

epiglottis

-unpaired cartilage in larynx
-spoon shaped
-attaches to inner aspect of thyroid angle
-pointed upwards toward back of throat
-when you swallow, larynx rises, epiglottis tips over, covering opening of larynx and directs food into esophagus

arytenoid cartilage

-paired cartilage in larynx
-pyramid shaped
-sits on top of posterior aspect cricoid cartilage

corniculate cartilage

-paired cartilage in larynx
-hook shaped
-sits on top of arytenoid cartilage

cuneiform cartilage

-paired cartilage in larynx
-club shaped
-helps support fibroelastic CT

elastic ligaments and mucous membrane folds

-2 pairs of elastic ligaments stretched between arytenoid cartilage and inner aspect of thyroid angle
-covered by mucous membrane folds
-divided into superior pair and inferior pair

superior pair of elastic ligaments and mucous membrane folds

-called vestibular folds (false vocal cords)
-close when swallowing
-space between the folds is called the glottis

inferior pair of elastic ligaments and mucous membrane folds

-called the true vocal cords (folds)
-much thinner with less vessels
-vibrate when air from lungs are forced against them producing a humming sound (does not make words)

intensity of voice

determined by force of air directed against vocal cords

pitch of voice

-determined by the tension on vocal cords
-7 pairs of skeletal muscles in larynx that move adenoid cartilage and thyroid cartilage to change tension

laryngitis

inflammation of the larynx

trachea

-windpipe
-tube extends from larynx to sternal angle where it splits into 2 primary bronchi (right primary bronchi is more vertical, if you inhale an object it will likely go here)
-4-5" long, 1" diameter
-made up of 16-20 "c" shaped rings separated by fibroelastic CT
-no cartilage in posterior trachea
-has smooth muscle "trachealis muscle" that when it contracts, diameter of trachea decreases so air moves quicker and more forcefully
-lined with pseudostratified ciliated epithelium: lots of goblet cells that secrete mucus

effects of smoking on the trachea

-when exposed to smoke: cilia stop moving, gravity pulls mucus to lungs
-continuous smoking: increasing layers of stratified squamous epithelium, no cilia so mucus trapped in lungs
-can reverse effects if you stop smoking (3-9 months after quitting, epithelium starting to change back to ciliated kind)

lungs

-apex is the top of the lung, above clavicle
-base is at the bottom, at diaphragm

pleura

-serous membrane around the lungs
Parietal pleura: lines wall of thoracic cavity around lungs
Visceral pleura: covers outer surface of the lungs

pleural cavity

filled with pleural fluid produced by both layers of pleura
-decreases friction
-increased surface tension causes lungs to cling to inner wall of thorax, thoracic wall expands and so do lungs

pleurisy (pleuritis)

-inflammation due to infection, injury
-swelling of the pleura, may cause parietal and visceral pleura to rub against each other

lobes of the lungs

right lung: 3 lobes, divided by horizontal and oblique fissure
left lung; 2 lobes, divided by oblique fissure

hilum/hilus

-indented area on the medial aspect of each lung
-where bronchi, vessels, nerves, enter and exit lung (called the root of the lung, only physical connection to lung to rest of body)

bronchopulmonary segments

left lung: 9 segments
right lung: 10 segments
-each has own air supply (branches of bronchus), vessel supply, and all are separated by CT

lobules

-1/2 to 1 cm in size
-separated by CT

bronchial tree

trachea, primary bronchi (one to each lung), secondary (lobar) bronchi (one to each lobe), tertiary (segmental) bronchi (one to each bronchopulmonary segment), bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveoli

primary bronchi cartilage

incomplete cartilage (cartilage rings)
-pseudostratified ciliated columnar epithelium

secondary (lobar) bronchi cartilage

-cartilage plates
-pseudostratified ciliated columnar epithelium
-some circular smooth muscle

bronchioles

-1mm diameter
-no cartilage, more circular smooth muscle
-epithelium is ciliated simple columnar

terminal bronchioles

-1/3 diameter
-ciliated simple cuboidal epithelium

trends as you descend bronchial tree

-decreased cartilage, increased circular smooth muscle
-smooth muscle innervated by parasympathetic NS (contracts smooth muscle, decreased diameter) and sympathetic NS (relaxes smooth muscle, increased diameter)

respiratory bronchiole epithelium

non-ciliated simple cuboidal epithelium

asthma

-airways hypersensitive to small amounts of substances not usually harmful
-causes reflexive parasympathetic response- cx smooth muscle so diameter of airways decrease
-inflammation of airways
-increased mucus production
-use a sympathomimetic to dilate airways during asthma attack

alveoli

-thin elastic basement membrane and 1 layer of simple squamous epithelium
-has type 1 cells (pneumocytes)
-has macrophages to phagocytize debris
-has type 2 pneumocytes

respiratory membrane

where gas exchange occurs between the air on the alveolar side and the blood on the capillary side; the alveolar and capillary walls form the respiratory membrane
-capillary walls are simple squamous epithelium and a thin basement membrane

type 1 pneumocytes (alveolar cells)

extremely thin alveolar cells that are adapted to carry out gas exchange

type 2 pneumocytes (alveolar cells)

-produce alveolar fluid: keeps alveolar surface moist, has antimicrobial chemicals, and has surfactant to decrease surface tension of alveolar fluid

production of surfactant

production begins the 7th month of pregnancy and continues throughout life

function of surfactant

Thin layer of fluid that covers the alveoli.
Reduces surface tension of the fluid layer lining the alveoli, preventing the alveoli from collapsing

respiratory distress syndrome (RDS) in newborn

-preterm babies may have decreased surfactant
-alveoli collapse because they don't have enough surfactant

hyaline membrane in infant RDS

-develops inside alveoli and interferes with gas exchange
-fluid, proteins, dead cells, WBC's
-#1 cause of death in infants in 1st month of life in US

risks for infant RDS

-preterm babies
-being born via C-Section
-male babies
-multiple birth babies
-mom has gestational diabetes

infant RDS treatment

-stop preterm labor is mom and baby are healthy
-cortisone to mom: crosses placenta and causes type 2 cells in baby to mature and increase surfactant production
-genetically engineered surfactant at birth: place tube where trachea divides and spray in surfactant, decreases death rate of RDS by 1/2
-ventilator support

intrapulmonary (alveolar) pressure

changes with ventilation but always equalizes to atmospheric pressure
-760 mmHg

intrapleural pressure

-changes with ventilation
-4mm less than pressure in lungs= 756 mmHg
-negative intrapleural pressure so lungs stay inflated, created by opposing forces (surface tension of alveolar fluid and elastic recoil of the lungs pulling lungs inward and surface tension of pleural fluid pulling lungs outward)

pneumothorax

air in pleural cavity, breaks suction in pleural cavity so lung collapses: "Atelectasis"
-when tear occurs because of Bleb rupturing, air enters pleural cavity causing pneumothorax and atelectasis
-tall, thin men susceptible to bleb

hemothorax

blood in pleural cavity

pneumohemothorax

air and blood in the pleural cavity

treatment of pneumothorax, hemothorax, and pneumohemothorax

-chest tube into pleural cavity
-allows air/fluid to drain out and not re-enter

ventilation

-breathing
-occurs due to pressure changes in the lungs
-air moves in and out of lungs from high to low pressure
-change pressure in lungs by changing lung volume (high volume= low pressure)

inhalation

-diaphragm contracts and moves downward
-external intercostals contract and lift thorax up and out
-diaphragm and external intercostals both increase volume of thoracic cavity (pressure decreases)
-lungs follow (lungs cling to inner wall of thorax because of surface tension of pleural fluid)
-air enters lungs until pressure in lungs equals atm pressure

exhalation

-diaphragm and external intercostal muscles relax, and elastic recoil of lungs pulls lungs and thorax back to original location
-lung volume decreases, increasing pressure
-air flows out of lungs until pressure in lungs is equal to atm pressure

compliance

-ease of expansion of lungs
-increased compliance=easier to expand

factors that affect compliance

-surface tension: increased surface tension (decreased surfactant)= decreased compliance
-elasticity of lungs= scar tissue makes it harder to expand lungs (decreased compliance)
-condition of thoracic wall: rib fracture, damage to thoracic wall makes it harder to expand (decreased compliance)

airway resistance

-how easy it is to move air through airways
-low resistance= easy to move air through

factors that affect airway resistance

-diameter of airways (decreased diameter= increased air resistance)
-decreased diameter can come from contraction of circular smooth muscle, swelling of airways, increased mucus)

gas exchange

air moved into blood from lungs and from blood to tissues by diffusion (high concentration to low concentration)

partial pressure of gases

-how we measure concentration
-pressure that an individual gas exerts when in a mixture of gases
-each gas diffuses independently of any other gas from high to low concentration

factors affecting rate of diffusion fo gases

-steepness of concentration gradient: difference in partial pressure of specific gas in 2 different areas
-increased difference= steeper concentration gradient
-oxygen has steeper concentration gradient than CO2- O2 diffuses faster

-solubility of the gases in H2O (from air to blood)
-the more soluble in H2O: faster diffusion
-CO2 more soluble in H2O than O2- CO2 diffuses faster

external respiration

-gases will diffuse between lungs and deoxygenated blood arriving at lungs, until pO2 and pCo2 in blood= pO2 and pCO2 in lungs
-Oxygen from lungs to blood (pO2 in lungs is 105mm, deoxy blood has 40mm. O2 diffuses into blood until oxy blood= pO2 of 105)
-CO2 goes from blood to lungs (pCO2 in deoxy blood is 45mm, pCO2 in lungs are 40mm. CO2 diffuses into blood until oxy blood= pCO2 of 40)

internal respiration

-gases will diffuse between tissues and oxygenated blood arriving at tissues until pO2 and pCo2 in blood= pO2 and pCO2 in tissues
-O2 goes from blood to tissues
-CO2 goes from tissues to blood

transport of oxygen

-enters blood at lungs
-1.5% dissolved in plasma
-98.5% enters RBC & transported by hemoglobin

At lungs: Hb+ O2= HbO2
At tissues: HbO2= Hb+O2

hemoglobin saturation (Oxygen Sats/ O2 sats)

% O2 tht Hb is carrying compared to total amount of O2 that Hb can carry
ex. 25 Hb molecules can carry 100 O2
-hemoglobin saturation is 100% if they are actually carrying 100Hb
-25% if they are carrying 1 O2 each

oxyhemoglobin dissociation curve

O2 blood leaving lungs- pO2=105mmHg
-Hb saturation is 98%

Deoxy. blood arriving at lungs- pO2=40mmHg
-Hb saturation is 75%

oxygen released to tissues: 98-75=23% (Hb released 23% of O2 it was carrying to tissues)

oxygen release to active tissues

actively contracting muscles uses more O2 to make ATP so has decreased pO2 due to using so much O2
-way that tissues that need more O2 gets O2

oxyhemoglobin dissociation curve- actively cx muscles

O2 blood leaving lungs- pO2=105mmHg
-Hb saturation is 98%

Deoxy. blood arriving at lungs- pO2=15mmHg
-Hb saturation is 25%

oxygen released to tissues: 98-25=73% (Hb released 73% of O2 it was carrying to tissues)

shifting curve to the right

Increased CO2
decreased pH
increased temperature
increased lactic acid

-all will increase release of O2 from Hb
-lower Hb saturation, more O2 released to tissues

shifting curve to the left

decreased CO2
increased pH
decreased temperature

-all will decrease release of O2 to tissues

hypoxia

low O2 in tissues/low O2 use in tissues

anemic hypoxia

decreased O2 in blood because anemia (decreased Hb, decreased RBCs, or abnormal Hb)

ischemic hypoxia

circulation is blocked/impaired- O2 blood cannot get to tissues
ex. thrombus, congestive heart failure

histotoxic hypoxia

tissues are unable to use O2 (because of poison, toxin)
-ex. cyanide (prevents O2 from being final electron acceptor)

hypoxemic hypoxia

low levels of O2 in blood unrelated to anemia
ex. high altitude, respiratory problems

carbon monoxide poisoning

hypoxia due to carbon monoxide (CO) competing with oxygen for binding sites on hemoglobin
-brighter red appearance

carbon dioxide transport

-CO2 enters blood at tissues
-8% dissolves in plasma (some CO2 joins with water (CO2+H2O=H2CO3=H+ +HCO3-))
-92% enters RBC (20% binds to globin (CO2+Hb=HbCO2), 72% joins with H2O (CO2+H2O=H2CO3=H+ +HCO3-))
-all reactions reverse at lungs- CO2 diffuses into lungs and is exhaled

medullary respiratory center

-in medulla
-monitors the basic rhythm of breathing
-has inspiratory and expiratory neurons

inspiratory neurons-medullary respiratory center

phrenic nerve: send impulses to diaphragm
intercostal nerves: send impulses to external intercostal muscles
-happens around every 5 seconds

expiratory neurons-medullary respiratory center

-after 2 seconds of inhaling, expiratory neurons inhibit inspiratory neurons, 0 impulses to diaphragm and external intercostal muscles, muscles relax, elastic lungs recoil to original position, decreased lung volume, air leaves lungs
-lasts 3 seconds

pontine respiratory center

-in pons
-smooth transition between inhaling and exhaling

modifying respiratory rate and depth

-chemicals in blood and CSF
-cerebral cortex
-emotions (fear, crying)
-stretch receptors in lungs
-respiratory irritants (coughing, sneezing)
-proprioceptor stimulants

modifying respiratory rate and depth-CO2

-primary factor affecting ventilation is level is CO2 in blood and CSF
-an increase of 5mm CO2 in arterial blood doubles ventilation (increased ventilation causes the exhalation of more CO2 than is produced)
-central chemoreceptors in medulla indirectly monitor CO2 (increased CO2, increased acid in CSF, decreased pH)
-if CO2 in blood is high, more CO2 diffuses into CSF, more carbonic acid in CSF, detected by central chemoreceptors, increased ventilation
-increased ventilation, exhale more CO2 than produced, blood CO2 will decrease, as blood CO2 decreases, more CO2 diffuses out of CSF and into blood, decreased CO2 in CSF, decreased acid in CSF, decreased stimulus to breathe

modifying respiratory rate and depth-oxygen

-detected by peripheral chemoreceptors
-changing oxygen levels in arterial blood have little effect on ventilation
-oxygen levels have to drop to almost 1/2 of normal (55-60 mmHg) to stimulate breathing

modifying respiratory rate and depth-pH in arterial blood

-detected by peripheral chemoreceptors
-decreased pH (increased acid) in arterial blood causes increased ventilation
-does not matter what causes the decrease in pH

cerebral cortex

-voluntarily alter breathing within limits
-when CO2 levels are too high, will begin to breathe

stretch receptors in lungs

-monitor degree of stretch in lungs
-if lungs are stretched too much, stretch receptors send info to medullary resp. center to stop inhalation

proprioceptor stimulants

-position receptors in muscles and joints
-when you exercise, increased input from proprioceptors, increase ventilation even before CO2 levels begin to change