exam 1 Flashcards

Question 1

Q

Thoracic Wall : Surface Anatomy

1-clavicle

2-nipple

3-sternal angle

4-costal margin

Answer

A

1-attaches to manubrium of sternum—sternal notch is depression between r. & left sternoclavicular joints at level of T2 vertebra

2-male is superficial to 4th intercostal space

3-site of union between anubrium & sternal body at level of T4 vertebra & site of articulation of 2nd rib

4-formed by costal cartialges of rib 7-10 & xiphoid process

Question 2

Q

1-thoracic skeleton

2-ribs

3-bony rib structure

Answer

A

1-formed by vertebral column, ribs & sternum

2-bony rib & costal cartilage: 12 per side…1 rib w/ T1 vertebra 2nd w/ T2 and etc

3-head has 2 facets that articulate w/ vertebra…Rib 2 articulates w/ superior (T1) and same numbered (T2)

neck
costal tubercle—articulates w/ transverse process of like numbered vertebra 2 w/ T2
Body (shaft) w/ angle—curvature of rib—smooth superior border, inferior border has costal groove w/ nerves & BV
shaft attaches too costal cartilage (costochondral junction)

Question 3

Q

Rib Types

1-true

2-false

3-floating

—–4- sternum

5-superior thoracic aperture

6-inferior thoracic aperture

Answer

A

1-Ribs 1-7—attach directly to sternum via costal cartilage

2-Ribs 8-12—attach indirectly to sternum via costal cartilages of superior ribs

3-Ribs 11 & 12—no anterior attachment & terminate w/in musculature of ab wall

4-manubrium, body & xiphhoid process

5-upper boundary of thoracic cavity…by T1, 1st ribs & manubrium—superior lobes of lungs expand into space

6-formed by T12, ribs 11-12 & costal margin—attachhment site for thoracic diaphragm= forms floor of thoracic cavity & roof of ab cavity

Question 4

Q

1-articulations

2-costovertebral

3-costotransverse

4-sternocostal

5-interchondral

6-costochondral

Answer

A

1-joints of bony elements of thoracic wall for movememnts w/ respiration—SYNOVIAL except for **1st sternocostal & all costochondral **those are synchondroses

2-between head of rib, 2 adjacent veretbrae & Intervertebral disc===synovial

3-between rib tubercle & transverse process of like numbered rib (inferior)===synovial

4-between costal cartilage of ribs 1-7 & sternum = synovial EXCEPT for 1st= synchondrosis

5-between costal cartilages of ribs 6-10===synovial

6-between rib & costalcartilage &&& first costal cartilage & sternum===synchondrosis

Question 5

Q

Functions of thoracic wall

1-protection

2-respiration

3-quiet inspiration

4-quiet expiration

5-forced inspiration

6-forced expiration

Answer

A

1-protects underlying viscera—lungs, heart & neurovas

2-framework for respiration—expands during inspiration—superioinferior height increases while thoracic diaphragm descends

–rib elevation increases the transverse dimensions of thoracic wall (bucket handle)
–sternum elevation= inc anteroposterior dimension (pump)

3-done by thoracic diaphragm—intercostal muscles stiffen thoracic wall & assist w/ rib elevation

4-passive recoil of lungs & thoracic cavity, diaphragm relaxes & ascends

5- assisted by accessory muscles assist w/ elevation of wall

6-contraction of ab muscles= inc in intraab & intrathoracic pressure…depressing lower ribs

Question 6

Q

1-intercostal muscles

2-external intercostal muscle

3-inernal intercostal muscle

4-innermost intercostal muscle

Answer

A

1-in intercostal space between adjaent ribs—3 layers for respiration

2-superficial—run inferomedial (\/) from 1 rib to next…posteriorly near rib tubercle & extends anteriorly= less fibrous & more membranous near costochondral

3-deep to external…fibers go inferolaterally (/) from 1 rib to next—anteriorly at sternum and then membranous at angle of rib

4-deep to internal intercostal & fibers run in same direction…only in lateral portions of wall…doesnt go anteriorly towards sternum or posteriorly towards vertebrae

Question 7

Q

1-subcostal muscle

2-transversus thoracis muscle

3-serraturus posterior superior/inferior & levatores costarum

Answer

A

1-w/in thoracic cavity adjacent to vertebral colum…angle of rib to inner surface of rib. span 2-3 spaces—fibers in same diretion as internal intercostal )

2-deep to sternum—from body of sternum & xiphpid process and goes superiorly & laterally to instert onto costal cartilages of ribs 2-6
-internal thoracic artery is pinned to posterior side of breastplate by transversus thoracic

3-deep back—respiration

Question 8

Q

Nerves of Thoracic Wall

Answer

A

1-intercostal nerves are ventral rami T1-T11 w/in intercostal spaces
-intercostal nn go anteriorly between internal & innermost intercostal w/in groove on inferior surface of rib

2-2 branches off of intercostal n

–lateral cutaneous= lateral aspect of trunk
–anterior cutaneous= term branch that pierces overlying musculature lateral to sternum to supply anterior trunk wall

-intercostal nn T7-11 exit intercostal space when costal cartilages go superiorly—continue anteriorly to innervate ab mm. ventral ramus of T12 (subcostal n) courses and innervateds anterior ab wall

Question 9

Q

1-Blood supply of thoracic wall—intercostal arteries

2-veins

Answer

A

posterior & anterior intercostal aa that anastomose
posterior are branches of aorta & costocervical trunk and give rise to lateral cutaneous branches

internal thoracic a goes inferiorly on deep surface of rib near sternum—anterior are branches of internal thoracic and go lateral to sternum
–internal thoracic divides near 6th costal cartilage into the superior epigastirc & musculophrenic a.

2-w/ arteries and located superior to artery in intercostal space—from superior to inferior= VAN (veins, arteries, nerve)

drain into azygos venous system
if procedure= penetration of intercostal space happens near superior margin of lower rib to protect neurovasculature w/in costal groove along inferior margin of upper rib

Question 10

Q

1-Mammary Gland

2-in females

3-lobules

4-suspensory ligaments

5-lactiferous ducts

6-areola

Answer

A

1-breasts—modified sweatglands- composed of glandular tissue & fat
-w/in superficial fascia…separated from deep pectoral fascia by retromammary space—potential space occupied by loose CT & mobile against wall

2-has circular base & axillary tail (o spence) that goes to armpit

3-has 20 lobules of glandular tissue arranged radially like orange segments

4-lobules separated by fibrous CT that are firmly attached to deep surface of dermis

5-lonule drained by single lactiferous duct—into dilated lactiferous sinus—like spokes on wheel, converging on nipple—elevated papilla that has SM fibers that contract to comrpess ducts

6-pigmented region that surrounds nipple, contains numerous sebaceous glands whos secretions lubricate nipple during lactation

Question 11

Q

1-blood supply of mammary

2-lymph drainage of mammary

Answer

A

1-from arteries supplying pec & thoracic wall

medial mammary—branches perforating arteries from internal thoracic a
lateral mammary—branches of lateral cutaneous, lateral thoracic & pectoral branches from thoracoacromial
–venous drainage—through tributaries of axillary v, has some via tributaries of internal thoracic v

2-metastasis of cancer cells

lymph from lateral portion of breast drains to axillary lymph node via pectoral nodes (lateral thoracic v=75%)
lymph from medial & inferior drain into parasternal lymph nodes—drain to opposite breast or ab nodes
from axillary nodes, lymph is filtered through infra/supraclavicular nodes and then into subclavian lymph trunk and back into venous

Question 12

Q

1-Mammary Innervation

2-Breast Cancer

a-dimpling

b-depression/inversion of nipple

c-peau d’orange

d-fixation of breast

Answer

A

1-somatic & autonomic innervation of breast is via lateral & anterior cutaneous branches of 4-6th intercostal n

2-2nd leading cause of cacner deaths in women

2a- infiltration of cancer cells among suspensory ligaments= shorten & put traction on overlying skin

2b-result of cancer cells infiltrating among lactiferous ducts

2c-impeded lymph drainage may cause localized skin edema= thickened & puffy w/ prominent pores…like rind of orange

2d-tumors w/in retromamammary space & deep pectoral fascia, fixing breast to pectoral wall so breast elevate w/ contraction of pectoral muscles

Question 13

Q

1-Thoracic Diaphragm

2-boundaries

3-vertebral origin: r. crus

4-vertebral origin: l. crus

Answer

A

1-thin voluntary muscle that partitions the thoracic & ab cavities

dome structure, right side= higher than left bc of underlying liver
central tendon= aponeurosis where anterior & posterior muscle fibers insert—C shaped w/ anterior convexity

2-originates from inferior thoracic aperture

–sternal origin from xiphoid process
–costal origin from lower 6 costal cartilages & lower 2 bony ribs

3-from 1st 3 lumbar vertebral bodies & discs—larger & longer than left crus & surrounds esophageal hiatus

4-from 1st 2 lumbar vertebral bodies & discs—contributes to esophageal hiatus

Question 14

Q

Arcuate ligaments

1-median (unpaired)

2-medial (r & l)

3- lateral (r & l)

innervation of thoracic

4-phrenic nerve

5-T6-11 intercostal & subcostal T12

Answer

A

1-between crura & bounds aortic hiatus

2-between vertebral bodies & 1st lumbar transverse process—overlies psoas major m

3-between 1st lumbar transverse & 12th rib, overlies quadratus lumborum m

4-main suply= all motor supply & some sensory everywhere (except peripheral parts)

ventral rami of C3-C5—C3,4,5 keep diaphragm alive
descends on each side of pericardial sac anterior to root of lung, pierces diaphragm & branches along inferior surface

5-supplies periphery of diaphragm
-mostly sensory, but some motor fibers

Question 15

Q

Blood Supply

1-superior

2-inferior

Answer

A

1-faces thoracic cavity

superior phrenic aa- branches of aorta, supply posterior portion
pericardiacophrenic & musculophrenic= branches of internal thoracic, supply anterior & central portions
lower 6 posterior intercostal & subcostal arteries supplying lateral portions

2-faces ab cavity—inferior phrenic a from aorta supply inferior surface of diaphragm

Question 16

Q

Structures piercing diaphragm

Answer

A

1-inferior vena cava—through vena caval foramen in central tendon at T8 verebral level

2-esophagus via the esophageal hiatus at T10—accompanied by anterior & posterior vagal trunks CN10
lower esophage sphincter constricts when diaphragm contracts= prevents regurgitation

3-aorta via aortic hiatus under median arcuate ligament at T12—accompanied by thoracic duct & azygos vein

Question 17

Q

1-section of phrenic nerve

2-hiccups

Answer

A

1-complete paralysis & atrophy of half of diaphragm

accessory phrenic nerve from C5 joins phrenic nerve more inferiorly, preventing paralysis
during normal inspiration both sides of diaphragm descend(contracts) as lungs expand—if 1 side is paralzyed then it will ascend during inspiration bc of inc pressure from unaffected side

2-involuntary spasmodic contractions of diaphragm= sudden inhalations interrupted by closure of glottis
-bc of indigestation, diaphragm irritation, alcoholism, cerebral, thoracic, ab elsions…distrub phrenic nerve

Question 18

Q

1-referred pain

2-rupture of diaphragm

Answer

A

1-from diaphragm—pain from superior portion may be referred to other regions supplied by C3-5 (shoulders)
-from peripheral regions of diaphragm= localized & referred to nearby regions of thoracoab wall supplied by ventral rami of T6-T12

2-and herniation of viscera—inc in either intrathoracic or intra ab pressure= bc of trauma

ruptures are mor common on l. side bc the liver= barrier on right side and lumbocostal triangle, non muscular gap between lumbar & costal parts of diaphragm—-l. side is weaker
stomach, intesitins, mesentary & spleen may herniate into thorax

Question 19

Q

1-pleura

2-visceral pleura

3-parietal pleura

3a=costal pleura

b=diaphragmatic pleura

c=mediastinal pleura

d=cervical pleura

Answer

A

1-closed serous membrane enveloping lung & lining thoracic cavity—lung= invaginated into pleural sac

2-inseparable from surface of lung and extending into fissures—innervated by visceral afferent fibers supplying lung & insensitive to pain

3-in contact w/ thoracic wal and diphragm

–subdivisions are named by what the structures contact
–supplied by somatic afferent fibers carried by intercostal & phrenic nerves & highly sensitive to pain

3a-contacts ribs and intercostal muscle

3b-contacts superior surface of diaphragm

3c-contacts structures of mediastinum

3d-dome of pleura that extends though superior thoracic aperture superior to 1st rib

Question 20

Q

1-pain in pleura

2-pleural cavity

3-inflammation of pleura

Answer

A

1-pain in costal pleura & peripheral portions of diaphragmatic plerua are referred to adjacent thoraco-ab wall…pain in mediastinal pleura & central portion of diaphragmatic pleura= referred to lower neck and shoulder

2-closed potential space between visceral & parietal pleurae

pleural cavity contains thin layer of of serous fluid that acts as lubcricant and facilitates free movememnt of lungs
lungs dont lie in pleural cavity

3-pleuritis or pleurisy—roughens surfaces= friction on respiration…audible through stethoscope as pleural fremitus (pleural rub)…inflam lead toa ccum of serous fluid in pleural cavity (pleural effusion) visible in radiographs

Question 21

Q

1-pleural reflections

2-sternal line

3-costal line

4-pericardiocentesis

Answer

A

1-regions of transitions between diff portions of parietal pleura—projected onto body wall= lines of pleura reflection and mark boudnaries of pleural sac

2-anterior reflection of costal pleura to mediastinal pleura= border of costomediastinal recess—parallel to lateral margins of sternum
-at level of 5th intercostal spcae and l. sternal line deviates to l. leaving the pericardial sac in contact w/ anterior thoracic wall

3-inferior reflection of costal pleura to diaphragmatic pleura= inferior border of costodiphragmatic recess

costal line slopes inferiorly & posteriorly
base of lung located 2 ribs superior to costal line

4-insertion of neddle into pericardial sac to draw off fluis…via l. 5th intercostal space—needle inserted to l. of l. sternal margin will pass through bare area f pericardium w/o encountering parietal pleura

Question 22

Q

1-pleura recesses

2-costodiaphragmatic recess

3-costomediastinal recess

4-pleurocentesis or pleural tap

Answer

A

1-regions of contact between diff portions of parietal pleura…potential spaces that accomodate expansion of lungs during deep inspiration

2-between costal & diaphragmatic pleurae—inferior region of pleural cavity & frequent site of fluid accum

3-between costal & mediastinal pleurae, adjacent & posterior to sternum

4-bc lungs dont fully occupy pleural sac, needle safely inserted into costodiaphragmatic recess to draw off lfuid…must be careful not to go too deep & hit liver

Question 23

Q

Lung
1-base

2-apex

3-costal surface

4-mediastinal surface

5-hilus

6-root

7-pleural sleeve

8-pulmonary ligament

Answer

A

1-rests on superior surface of thoracoab diaphragm

2-extends into root of neck superior to 1st rib

3-located posteriorly & laterally

4-located medially

5-indentation on mediastinal surface that transmits structures connecting lung to mediastinum

6-structures that connect lung to mediastinum= root of lung—primary bronchus, arteries/veins, nerves, & lymph

7-mediastinal pleura & visceral pleura continuous at hilus, making a sleeve that encloses structures of root

8-bilaminar fold of pleura extending inferiorly from pleural sleeve

Question 24

Q

1-R. Lung

2-L. Lung

Answer

A

1-shorter broader & heavier than l.
3 lobes= superior, middle, & inferior
2 fissures= horizontal & oblique

2-taller & narrower than r. lung
2 lobes= superior & inferior…separated by single oblique fissure
cardiac notch= accomodates heart
lingula=tongue like projection of superior lobe just inferior to cardiac notch…corresponds to middle lobe of r. lung

Question 25

Q

1-trachea

2-bronchi

3-bronchioles

4-cough reflex

Answer

A

1-membranous tube from larynx to level of sternal angle

patecy of tracheal airway is maintained by c shaped tracheal cartilage= deficient posteriorly to permit passage of food through adjacent esophagus
termiantes by bifrucating into r. & l. primary bronchi
carina= keel shaped projection of last tracheal cartialge, marks tracheal bifurcation internally

2-primary (r &l)= term branches of trachea—supply r & l lung—walls of primary bronchi have c shaped cartilage rings

r. primary= shorter, braoder & more vertically orietned
at hilus, primary bronchi divide into secondary lobar bronchi, supplies a single lobe
w/in lobe…2ndary bronchi divide into tertiary segmental bronchi

3-tertiary bronchi give rise to mult. generations of bronchioles, terminate in resp region of lung

4-tracheal & carina mucosae have sensory receptors for reflex in response to irritation or foreign objects. aspirated object that reach bronchi can be silent—differences in shape of bronchi direct aspirated objects towards r. lung

Question 26

Q

1-bronchopulmonary segment

2-clinical correlation

Answer

A

1-region of lung tissues supplied by single tertiary bronchus—8-10 named segments

bronchipulmonary segment is the smallest functionally self contained unit of lung tissueA
separted from adjacent segments by CT septa
supplied by tertiary branches of pulm arteries
each lobe has several adjacent segments—& functionally autonomous

-segmental structure of lung= surgical resection of 1 or more segments (segmentectomy) or entire lobe (lobectomy) w/ little impage on pulm tissue

Question 27

Q

1-BV & lymphatics

2-pulmonary embolis

Answer

A

1-pulm vesses carry deoxy blood to lung & return oxygenated blood to heart

pulm arteries (r. & l.) term branches of pulm trunk—located anterior & superior to primary bronchus at hilus
branches of pulm arteries off tree= secondary (lobar)& tertiary (segmental) pulm arteries
tertiary pulm arteries= intersegmental—tertiary branch supplies singl ebronchopulm segment and no arterial anastomosis between adjacent segments

2-interruption of perfusion of supplied region of lung tissue & acute respiratory distress…bc of blood clots, fat flobules or gas bubbles

Question 28

Q

1-pulm vein r & l

2-bronchial vessels

3-bronchial arteries

4-bronchial veins

Answer

A

1-2 per side…superior and inferior

located anterior & inferior to prim bronchus at hilus
w/in lungs, tributaries of pulm veins go independently of arteries
individual bronchopulm segments are drained by pulm vein tributes= intersegmental—venous communication

2-supply CT of lungs & conducting portions of bronchial tree

3-arise as direct branches of descending aorta, follow branching of bronchial tree

4-drain to azygos vein system
-much of blood distributed by bronchial arteries returns via pulm vein system…bronchial veins= smaller than bronchial arteries

Question 29

Q

1-lymphatics

2-inferior tracheobronchial lymph nodes

3-innervation

Answer

A

1-lymph drainage of lungs follows bronchial tree, pulm lumph nodes drain to bronchopulm nodes at hilus of lung
-bronchopulm nodes drain to tracheobronchial nodes, that are superior & inferior to bifurcation of trachea

2-sentinel nodes= enlargement of nodes bc of infection, lymphoma or tumor metastasis= deviation of carina seen via bronchoscopy…
enlarged tracheobronchial nodes interfere w/ swallowing or impinge on l. recurrent laryngeal nerve= hoarsness

3-via anterior & posterior pulm plexuses…surround bifurcation of trachea & extend laterally between layers of pulm ligaments

Question 30

Q

1-sympathetics

2-parasympathetics

3-visceral afferents

Answer

A

1-presynaptic symp arise in upper thoracic spinal and synapse on postsynaptic cell bodies in symp trunk

inhibits SM and glands of bronchial tree= bronchodilation & reduced secretion
stimulates SM in pulm vesses= vasoconstriction

2-presynaptic parasymp fibers are carried by vagus (10) post synp cell bodies in pulm plexuses and on bronchial tree

stimualtes SM & glands of bronchial tree= bronchoconstriction & inc secretion
inhibits SM in pulm vessels= vasodilation

3-from bronchial mucosa (cough reflex), bronchial tree (monitor bronchioconstriction) & pulm vessels (chemo & baro) are carried by vagus nerve CN X
-visceral afferent nerve fibers conveying other sensations from bornchial tree & visceral pleurae follow symp pathways

Question 31

Q

1-mechanisms of pulm ventilation

Answer

A

1-lung volume is maintained by physical forces that resist tendency of elastic lung tissue to recoil (collapse)

–serous fluid tension & neg pressure w/in pleural cavity (due to lymph drainage of serous fluid) causes lungs to expand and contract in response to changes in intrathoracic volume
–loss of neg pressure in pleural cavity= due to accum of air (pneumothorax), fluid (hydrothorax), or blood (hemothorax) causes lung collapse

Question 32

Q

1-thoracic volume

2-quiet inspiration

3-active/forced inspiration

4-quiet expiration

5-forced expiration

6-clinically

Answer

A

1-when inc, the lungs expand and intrapulm pressure dec—air passes in to equalize intrapulm & atmospheric pressure

descent of diaphragm= inc superoinferior diameter
elevation of ribs (bucket handle action) inc transverse diameter
elevation of sternum (pumphandle) inc AP diamter

2-normal breathing= diphragm
intercostal muscles stiffen thoracic wall & external intercostals actively elevate ribs

3-accessory muscles of respiration—sternocleidomastoid, serratus anterior, scalenes, pec minor…elevate sternum & ribs

4-via passive recoil of lungs as diaphragm relaxes & ascends

5-contraction of ab muscles= inc intraab pressure and forcefully depresses lower ribs

6-injuries w/ air into pleural cavity (pneumothorax) equalize pleural & atmospheric pressures=lung collapsed

open pneumothorax (sucking chest wound)= resp movememnts cause air to run in & out of thorac via open wound
tension pneumothorax= tissue flap admits air but prevents its escape
rapid accum of air in thorax displaces & compresses mediastinum & interferes w/ venous return to heart= jugular vein distention & tracheal shift towards uninjured side

Question 33

Q

1-respiration

2-ventilation

3-pulmonary diffiusion

4-bulk flow

5-tissue diffusion

6-cell respiration

Answer

A

1-process of moving O2 from atmosphere to cells & moving CO2 from cells to atmosphere

2-movement of air in/out of lungs

3-alveolocapillary—gas exchange—movement of O2 from alveoli to capillaries & of CO2 from capillaries to alveoli…diffusion is driven by each gases partial pressure gradient

4-blood gas transport—transport of O2 in blood from lungs to tissues & CO2 from tissues to lungs

5-capillary tissue—gas exchange—movement of O2 from capillaries to cells and CO2 in opposite direction…respective to partial pressure gradients

6-metabolic process used to convert biochemical energy into ATP

Question 34

Q

1-functions of resp system

secondary

2-phonation

3-air filter

4-blood filter

5-blood reservoir

6-endocrine

Answer

A

1-obtain O2 from environment, remove CO2 from body, in conjunction w/ kidney…regulates body acid/base balance

2-lungs & vocal cords produce sounds for comm.

3-resp system has surface area 30 x’s larger than surface area of skin…so defends against air born microbes—hair & mucous trap particles are larger than 10 um w/in nasal…smaller parties entering are trapped and elimated by mucociliary elevator. lymphoid tissues & adenoids= more defense

4-blood through pulm capillaries, small clots are trapped & dissovled before they reach the brain or other vital organs

5-pulm circulation= compliant…lungs= blood reservoir, especially when supine

6-endothelial cells line pulm capillaries can activate/inactivate blood borne chem messengers w/in lung…angiotensin I is converted to angiotensinIII by ACE
bradykinin and serotonin are either removed or inactivated as they pass through pulm circulation

Question 35

Q

Air Conduction

1-nose

2-paranasal sinuses

3-pharynx

Answer

A

1-warm, moisten, & filter inspired air and dehumidify expired air(lose 350 mL of water bc of it)

moistening of inspired= alveolar viability
nasal hair—vibrissae, filter large particles
small particles are trapped in moist mucous membranes that line nasal conchae & rest of cavity

2-frontal, sphenoidal, ethmoidal, & maxillary
-warm & moisten inspired air & reduce weight of skull
-sinusitis= inflammation of mucous membranes that line sinuses bc of colds, allergies, deviated septum (take decongestant to reduce flow to sinuses)
steroids for reduction in inflam, antibiotics for bacterials, and antihistamines for allergies

3-conducting pathway for resp & digestive systems
-respiratory only and gives connection w/ middle ear & eustachian tube…oropharynx= passage for inhaled air & foods. air can bypass nose when clogged

Question 36

Q

Air Conduction

1-larynx

2-trachea

3-bronchial tree

4-bronchi

5-bronchioles

6-terminal bronchioles

6-resp. bronchioles

Answer

A

1-maintains open airway to lungs & involved in production of sounds

mucosal surface of larynx= pseudostrat ciliated columnar epithelium
epiglottis= prevents swallowed food/water from entering airways

2-connects larynx to lungs—16-20 hyaling cartilage C rings for suppor…mucosal surface of trachea is lined w/ pseudostra cili columnar epitheloum

3-conducting airways w/in lung that lead to alveoli

4-primary bronchi divides into 2ndary bronchi and divide into tertiary bronchi…contain SM and irregular cartilage plates. SM in walls of bronchi can constrict/relax and will change the airway diameter of bronchi

5-airways that dont have cartilage anymore

6-end of conducting zone after first 16 divisions…no gas exchange occuring w/in first 16 divisions

7-contain alveoli & mark beginning of resp zone

Question 37

Q

1-Alveoli

2-acinus

3-wall of alveolus

4-surfactant

Answer

A

1-site of gaseous exchange—300 mil alveoli ine ach lung= spongy consitency of lung

alveoli supproted by parenchyma= mesh CT that has elastin & collagen
total surface area for gas exchange w/in lung= 60-80
large surface area of alveoli matched by dense vascular beds w/ 100 capillaries per alveolus

2-portion of lung supplied by resp bronchiole

each acinus has 100 alveolar ducts
duct terminates into 20 alveoli
alveoli w/in last 7 branches are are referred to as resp zone
resp zone= place w/n lungs where gas exchange w/ blood occurs

3-1 cell layer thick w/ simple squamous epithelium
type 1 alveolar= major part of alveolar walls & permit diffusion
scattered amongst type 1= type 2 alveolar cells that secrete lipoprotein (surfactant)

4-helps prevent alveolar collapse by decreasing surface tension of alveoli
—–wandering alveolar macrophages are w/in alveolar lumen

Question 38

Q

1-lungs

2-pleurae

Answer

A

1-r. lung has 3 lobes
l. lung is smaller w/ 2 lobes…has a cardiac impression where the heart is situated…
mediastinal surface is the mediasl aspect of lung where the pulm vessels pass
-costal surface of lung faces the ribs
-base of lung sits on top of diaphragm
-apec of lung above the clavicle

2-serous membranes that surround the lungs & line thoracic cavity—visceral pleura adheres to outer surface of lungs & parietal pleura lines thoracic walls & surface of diaphragm
-pleural cavity is located between the 2 and has fluid that allows movememnt of lung during inspiration/expiration= potential space bc there is no physical separation

Question 39

Q

1-airway epithelium

Answer

A

1-resp tract to level of bronchioles= larynx & trachea lined w/ pseudostrat ciliated colum epithlium

goblet cells w/in epi = sticky mucopolysacc mucous that traps small inhaled particles that contact walls
cilia move the mucous & any attached inspired particles upward & out of resp system…can be swallowed or coughed out of body
mucociliary elevator is imp defense against bacteria bc bacteria enter body attached to dust
airway branching continues w/in lung, the epi things to a simple cuboidal epithelium…losing cartilage & SM
w/in alveoli the simple squamous epi is flat & enlogated= optimal for gas exchange

Question 40

Q

Summary—description & function

1-nose

2-paranasal sinuses

3-pharynx

4-epiglottis

5-larynx

Answer

A

1-jutting external portion on face + nasal cavity
-warms moistens & filters inhaled air towards pharynx

2-air spaces= ethmoid, sphenoid, maxillary, & frontal
-warms & moistens inhaled air, produces mucous, resonance, lightens skull

3-connecting oral & nasal cavities to larynx
-passageway for air into larynx & for food into esophagus

4-flap of elastic cartilage attached to entrance of larynx
-prevents food & water from entering airways

5-voice box—short passageway that connects pharynx to trachea
-serves as passageway for air, produces sounds, prevents foreign from entering traching

Question 41

Q

Summary-description & function

1-trachea

2-bronchial tere

3-alveoli

4-lungs

5-pleurae

Answer

A

1-flexible tubular connection between larynx &bronchial tree
-passageway for air, pseudostrat ciliated colum, epithelium cleanses air

2-bronchi & branching bronchioles in lung, tubular connection between trachea & alveoli
-passageway for air, continued cleansing of air

3-microscopic membranous air sacs w/in lungs
-units of respiration, site of gaseous exchange between resp & circulatory systems

4-organs of respiration, in thoracic cavity
-bronchial trees, alveoli, & pulm vessels

5-serous membranes covering lungs & lining thoracic cavity
-compartmentalize, protext & lubricate lungs

Question 42

Q

1-lung volumes & capacities

2-tidal volume

3-Inspiratory Reserve Volume

4-Expiratory Reserve Volume

5-Residual Volume

Answer

A

1-can be measured w/ spirometers that measures volume of aire breathed in & out

has air filled drum floating in water-filled chamber
person breathes in/out…resultant rise & fall of drum are recored as a spirogram changes (V change)
RV residual volume, FRC functional residual capacity, & TLC total lung capacity & anatomic dead space cant be measured w/ simple spirometry.

2-V_T= volume of gas inspired/expired in single resp cycle…~500mL

3-IRV= max vol of gas that can be inspired starting at end of normal inspiration…~3000mL

4-ERV= max vol of gas that can be expired starting from end of normal expiration…~1100 mL

5-RV= vol of gas that remains in lungs after max expiration…~1200 mL

Question 43

Q

1-capacities

2-total lung capacity

3-vital capacity

4-inspiratory capacity

5-functional residual capacity

Answer

A

1-sum of 2 or more volumes

2-TLC= total amt of gas in lungs at end of max inspiration (sum of all 4 lung volumes…RV + ERV+ V_T +IRV)…~5800 mL

3-VC= max vol of gas that can be expired after max inspiration (ERV + V_T + IRV)…~4600 mL

4-IC= max amt of gas that can be inspired starting from FRC (VT + IRV)…~3500 mL

5-FRC= amt of gas in lungs at end of normal expiration (ERV + RV)…~2300 mL

Question 44

Q

1-ventilation

2-minute ventilation

Answer

A

1-air is moved in/out of lungs w/ each inspiration ~500mL of air enters body= V_t(tidal volume)…w/in gaseous exchange divison of resp system…O2 diffuses out of alveoli & into blood (VO2) while CO2 diffuses out of blood and into alveoli VCO2

2-V_E amt of air exhaled per minute…equal to product of V_T & resp rate (n)…V_E=V_T * n
-poor measure of fucntional ventilation…bc w/in each V_T there is a vol of gas that doesnt participate (dead space V_D)—dead space= nonfunctional air w/in diffusion
-w/in 1st to 16th generations of branching w/in lungs that dont participate in gas exchange= dead space, abt 20-25% tidal volume…parts of resp system that arent gas exchanging= nose, sinuses, pharynx, larynx, conducting
and alveoli that arent perfused.

Question 45

Q

1-anatomic dead space

2-alveolar dead space

3-physiologic dead space

4-Tidal Volume V_T

Answer

A

1-vol of air contained w/in nose, sinuses, pharynx, larynx & conducting pathway

2-vol of air contained w/in no perfused alveoli

3-functional measurement bc it is the sum of anatomic & alveolar dead space
-in patients w/ lung disease where ventilation doesnt match alveolar perfusion, alveolar dead space = higher so consider that expired CO2 comes from alveoli in which gas exchange occurs

4- V_T=V_{D +}V_A…dead space and alveolar volume

volume—
V_E= V_T * n
V_E= (V_D + V_A) * n

ventilation—
V_E= V_D + V_A
V_A=V_E-V_D

Question 46

Q

1-alveolar ventilation

2-turbulent flow in lungs

3-transitional flow in lungs

4-laminar flow in lungs

Answer

A

1-imp functional measurememnt bc it is the vol of air/unit time that participates in gas exchange

minute ventilation can be obtained by measuring exhaled air/time…dead space isnt easily measure and can vary depending on size/posture
rough estimate for dead space is approximated by assuming for every pound of body weight there is 1 mL of dead space
weighs 150 lbs has 150 mL dead space

2-disorganized flow w/ no smooth sheets of flow

greater driving pressure is required vs laminar flow
turblent flow may occur in trachea when flow velocities are high & result in wheezing sound

3-mixture of turbulent flow & laminar flow…transitional flow occurs throughout most of bronchial tree

4-parabolic profile and is smooth flow…rapidly branching system like lung has fully developed laminar flow, only in very small ariways

Question 47

Q

1-ohms law

2-poiseuilles equation

3- airflow laws

4-resistace expression

5-resistance to airflow laws

Answer

A

1-w/o difference in pressure between beginning & end of a tube there isnt flow
airflow mL/min in a tube is equal to driving pressure in tube mmHg dividied by resistance to airflow—driving pressure for airflow during respiration is generated by muscles of inspiration working in conjunction w/ recoil forces of lung… V= delta P/ R

2-relationship between pressure & flow V= (P*pi*r^4)/ (8*greek n * l) greek n=visocisity

3-airflow is: directly proportional to ^4 power of tubes radius
directly proportional to driving pressure
inversely proportional to viscosity
inversely proportional to length

4-substitute poiseuille into ohms—R= P/V= (8 * greek n * l)/ (pi * r^4)

5-resistance to airflow is directly proportional to viscosity
directly proportional to length
inversely proportional to ^4 power of tubes radius

Question 48

Q

1-airway resistance

Answer

A

1-conducting airway branch into lung they become more numerous & narrower
bc resistance to ariflow is inverse to radius side…the airway should get inc in resistance in the small airways but actually the pressure drops w/in the airways of the bronchial tree and that the resistance peaks w/in medium sized segmental bronchi
small bronchioles= little airway resistance bc total cross sectional area of the airways also increase very rapidly w/ branching
so the forward velocity of the gas during inspiration= small in region of resp bronchioles…so when TOTAL airway cross sectional area inc, airway resistance dec

Question 49

Q

1-lung volume on airways resistance

Answer

A

1-supproted by surrounded parenchymal lung tissue
-lung vol inc towards TLC, the surrounding lung tissue exerts radial traction forces on airways & stretches airways open
-large lung vol, airways widen & resistance to airflow dec
lower lung volumes, the airways are narrow & airflow resistance inc
very low lung volumes teh small airways might close completely, especially at th ebottom of the lung…patients who have inc airways resistances often breathe at higher lung volumes to help reduce airway resistance

Question 50

Q

1-obstructive lung disease

2-bronchitis

3-asthma

4-emphysema

5-chronic obstructive pulmonary disease

6-restritive lung disease

Answer

A

1-inc in airway resitance
-asthma, bronchitis, & emphysema

2prolonged exposure to bronchial irritants that leads to obstruction and may = hypersecretion of mucous w/in airways + hyeprtrophy of airway SM

3- inc responsiveness of airway SM to various stimuli= widespread narrowing of airways

4-destruction of lung parenchyma= reduction of radial traction w/in small airways & enlargement of alveoli= greater airway resistance during expiration bc of airway collapse

5-mixture of emphysema & chronic bronchitis

6-expansion of lung is rstricted bc of alterations in lung parenchyma or bc of disease of pleura, cheast wall or neuromuscular apparatus

characterized by reduced vital capacity & small resting lung volume, but airway resistance isnt inc.
–pulm fibrosis= thickening of interstitial spaces, like w/ scar tissue w/ inc of radial traction..making it hard to expand during inspiration.

Question 51

Q

1-pulm function testing

Answer

A

1-measuring lung volumes & flow rate of air
Forced Vital Capacity—FVC is accomplished under max muscular effort to ensure max flow rates at all lung volumes
-flow rate is determined at various times during FVC maneuver…something useful= forced expiratory volume at one second FEV1—expressed as percentage of FVC= FEV1/FVC
-FEV1/FVC ratio= 0.8…in obstructive diseases such as asthma, FEV1 is reduced more than FVC= low ratio, if less than 0.6= obstructive lung disease
-in pulm fibrosis FEV1 & FVC are reduced sooo ratio may be normal or inc in restrictive disease

Question 52

Q

1-forced vital capacity

2-forced expiratory volume

3-forced expiratory flow rate

Answer

A

1-FVC= amt of gas expelled from lungs by expiring as forcible as possible after max inspiration…<4600

2-FEV₁=max amt of gas that can be expired in 1st second of FVC, following max inspiration…3800

3-FEF—measured over middle half of FVC maneuver which is between 25-75% of vital capacity. w/in obstructive lung disease such as asthma, FEF is dec & dec is proportional to severity of obstruction
FEV1 & FEF are impaired & time required to expel the vital capacity is prolonged

Question 53

Q

1-flow volume loops

Answer

A

1-max expiratory flow volume curve is constructed by plotting airflow vs lung volume
-go in clockwise direction starting at TLC
-airflow is at peak near beginning of forced expiration…as lung vol decreases the rate of airflow dec throughout remainder of forced expiration
=max inspiration generated during rapid forceful inspiration from RV to TLC…changes in airflow w/ changes in lung volume differ during max
-max inspiratory maneuver…flow reaches high level while lung volume is still low, but inspiratory flow remains constance until TLC is approached

obstructive disease the flow rate is low and lung volumes (TLC & RV) are inc -scooped out appearnce seena fter point of max flow
restrictive disease= the flow and lung volumes are reduced…arched curve may be seen after max flow

Question 54

Q

1-parasymp stimulation

2-symp stimulation

Answer

A

1-releases acetylcholine that causes contraction of SM that line the airways. produces bronchoconstriction, a reduction in bronchiolar caliber… that will inc airway resistance
in humans the parasymp nervous system has greatest influence on airway SM tone

2-bronchiolar SM relaxation=bronchodilation and dec airway resistance

catecholamines epinephrine & norepinephrine react w/ B2 adrenergic receptors in airway SM
inhaled isoproterenol, nonselevtive B adrenergic receptor agonis has low affinity for A adrenergic receptors= bronchodilation, used for asthma attacks when SM tone is inc
to avoid cardiac effects of B1 adrenergic, selective B2 adrenergic agonists (albuterol or metaproterenol) are used

Question 55

Q

1-histamine & leukotrienes

2-physical irritants & airway pollutants

Answer

A

1-mast cells in CT underlying airway SM

constriction of airway SM producing bronchoconstriction
histamine constrict SM by binding to H1 receptors, histamine & leukotrienes also inc production of prostaglandins
produce bronchoconstriction (prostaglandin F-2a) while others produces bronchodilation (prostaglandin E)

2-smoke, dust, and sulfar dioxide can incite coughing & airway constriction

reactions are initiated through stimulation of irritant receptors w/in airway submucosa
produces releases of acetylcholine from efferent parasymp nerve fibers= bronchoconstriction
inc in airway resistance promotes trapping of physical irritants & expulsion via mucociliar elevator & coughing

Question 56

Q

1-autonomic nervous system

2-chemical

3-physical

Answer

A

1-Contraction= parasym= cholinergic, acetylcholine, muscarinic receptor subtype
Relaxation= symp= adrenergic, circulating epinephring/norepinephring, B3 receptor subtype

2-Contraction= histamine (mast cells), leukotrienes, prostaglandin
Relaxation= prostaglandin E & nitric oxide

3-smoke, dust, SO2

Question 57

Q

Obstructive
1-Bronchitis

2-Emphysema

restrictive

3-pulm fibrosis

Answer

A

1-TLC= inc
FRC= inc
RV=inc
FVC= dec
FEV1= dec
FEV1/FVC= dec
lung compliance= normal
airway resistance= inc

2-TLC= inc
FRC= inc
RV=inc
FVC= dec
FEV1= dec
FEV1/FVC= dec
lung compliance= inc
airway resistance= inc

3-TLC= dec
FRC= dec
RV=dec
FVC= dec
FEV1= dec
FEV1/FVC= inc
lung compliance= dec
airway resistance= dec

Question 58

Q

1-conducting portion

2-respiratory portion

Answer

A

1-nasal cavities, pharynx, larynx, trachea, bronchi & bronchioles—provides passageway for air to travel to and from lungs, and to moisten & cleanse incoming air

rigid walls to keep airway open
extrapulmonary & intrapulmonary

2-respiratory brochioles, alveolar ducts & sacs & alveoli
-gas exchange (O2 & CO2) between blood & air occurs in respiratory portion

Question 59

Q

Extrapulmomary
1-nasal cavity

Answer

A

1-lined with strat squamous in beginning and then rest w/ pseudostrat ciliated colum w/ goblet cells

mucus produced by goblet cells move towards pharynx via cilia
roof of nasal cavity is lined w/ specialized epithelium called olfactory epithelium—olfactory epithelium= reception of odors, sensory cell is a bipolar neuron
–supporting cells (sustentacular cells)= present
mucosa of nasal cavity modifies incoming air===serous secretions moistens air, mucous secretions trap incoming particles & venous sinuses warm air
paranasal sinuses are lined by mucosa but is thinner & fewer goblet cells & lamina propria is thin

Question 60

Q

extrapulmonary

1-pharynx/larynx

2-trachea/primary bronchi

Answer

A

1-lined wi/ ciliated pseudostrat colum except in areas of abrasion (oropharynx, laryngopharynx & epiglottis)
-scattered lymph tissue = present and aggregates in a larger mass, forming a tonsil

2-consist of mucosa (epithelium & lamina propria), cartilage/SM & adventitia

mucosa—cililated pseudostrat columnar w/ goblet cells “resp epithelium” (no gas excahnge)
thick basement membrane
epithelium ontop of loose CT= lamina propria—has mucous & serous glands & thin wenous sinuses
lamina propia fuses w/ perichondrium of cavity= muchopericondrium
external to lamina propria= C shaped rings of hyaline= 16-20 rings, open posteriorly & connected via fibroelastic ligament and trachealis muscle(SM)
–hyaline cartilage surrounded by perichondrium & gaps between adjacent rings are filled w/ fibroelastic CT
external to cartilage/SM= CT adventitia

Question 61

Q

epithelium of trachea/primary bronchi (5)

Answer

A

1-ciliated columnar cells= most abundant—300 cilia on surface

2-mucus secreting goblet cells

3-brush cells= columnar w/ microvilli on surface…have afferent ending on basal surface= sensory receptors

4-basal cells= cuboidal lie next to basal lamina, are stem cells that generate columnar & goblet

5-small granule cells= like enteroendocrine of gut & have smallg ranules of catecholamines, serotonin, calcitonin, & other hormones

–part of digguse neuroendocrine system DNES
–act as effectors in integration of mucous & serous processes

Question 62

Q

Intrapulmonary parts

1-secondary/successive bronchi

Answer

A

1-mucosa///SM & cartilage///adventitia
-additional SM between epithelium & cartilage—divides the CT into a lamina propria that lies closer to epithelium & into a submucosa that lies closer to the cartilage layer —SM is a part of the lamina propria

layer=
1-mucosa= pseudostrat ciliated colum w/ goblet on thick basement membrane
—lamina propria= diffuse lymph tissue & SM, SM spirals around bronchus in R/L handed direction
2-submucosa= 2nd CT layer external to SM, mucous and mucoserous glands are present in layer
3-layer of hyaline cartilage—irregular rings or sheets, at first completely surrounds but then gets scattered w/ smaller bronchi
4-adventitia= CT

-as bronchi undergo sucessive branchings= smaller in size & layers of wall get thinner…smallest branches have isolated cartilage plates, when diameter = less than 1, the cartilage disappears and = bronchiole

Question 63

Q

Intrapulmonary parts

1-bronchioles

Answer

A

layers
1-epithelium=(bigger to smaller) epitheliums goes from pseudostrat ciliated columnar w/ goblet to simple colum or cuboidal w/ cilia and no goblet
-goblet cells end before the cilia do so mucous doesnt become trapped in small resp passages
-epithelium of smallest bronchioles have cell called clara cell that will secrete glycosaminoglycans to protect bronchiole epithelium

2-lamina propria has SM & elastic fibers—SM is controlled by autonomic nervous system

3-cartilage & glands arent present in wall of bronchiole

Question 64

Q

1-resp bronchioles

2- alveolar ducts

3-alveolar sacs

4-macrophages

Answer

A

1-transitional structures between conducting & resp portions of resp tract
-each term bronchiole divides into 2 resp bronchioles
layers=
1-epi of resp bronchiole goes from simple cuboidal w/ ciliated to low simple cuboidal w/o cilia
2-underlying lamina propria has collagenous CT w/ interlacing bundles of SM & elastic fibers
3-wall of resp bronchiole= interrupted by alveoli that bud off wall

-resp bronchioles divide into alveolar ducts

2-lined by numerous alveoli or clusters of alveoli opening onto its surface
-lamina propria surorunding rim of alveoli, there is a knob of SM cells, SM is covered by simple cuboidal cells

3-alveolar ducts terminate in irregular spaces surrounded by alveoli===alveolar sacs

4-in interstitum of alveolar septum & alveolar lumen

derived from blood monocytes
alveolar macrophages= dust cells bc has inhaled dust
eliminated via conducting system and appear in sputum

Answer 65

A

1-terminal component of resp system—small sacs which open on 1 side to allow air to enter cavity

O2 & CO2 are exchange between air & blood in alveolus
alveolus is lined by epithelial cells, lining has 2 cell types that are joined by desmosomes & occluding junctions

2-attenuated squamous alveolar. 97% of alveolar surface. provides barrier of minimal thickness that is permeable to gases

3-great alveolar septal cells, interspreced w/ type 1. cuboidal & have lamellar bodies in cytoplasm… lamellar have mixture of phospholipid, neutral lipids & protein that after secretion= pulmonary surfactant
-surfactant dec surface tension on alveolar surface so less inspiratory force is needed to inflate alveoli
-surfactant prevents alveolar collapse during expiration
fetus= no surfactant until last weeks, so if premature the infant= resp distress bc no surfactant…usually renewed w/in alveolus

Answer 66

A

has central region that has type 1 capillary network surrounded by fibroblasts, SM, mast cells, elastic, & collagen fibers—central region= interstitium
interstitium surrounded on either side by epithelial lining of adjacent alveoli—epithelium has Type 1 & type 2 pneumocytes
air in alveolus is separted from bloom in capillary by alveolar septum…the barrier=blood air barrier(.5-1.5um)
–has attenuated cytoplasm of type 1 pneumocytes, fused basal laminae of type 1 pneumocyte & capillary endothelial cell, & cytoplasm of endothelial cell
small openings in alveolar septum= alveolar pores= communication/eqaulization of air pressure between adjacent alveoli

Answer 67

A

1-primary muscle of respiration during quiet breathing

dome shaped sheet of skeletal muscle between thoracic cavity & ab cavity
when diaphragm contracts, vertical dimension of thoracic cavity= inc and lower rib margins are lifted & moved out w/ inc transverse diameter of thorax
normal= 1 cm, forced = 10cm
phrenic nerve innervates sides—also C3-C5, if damaged may need help

2-inspiratory actions of diaphragm—connect adjacent ribs, contract the lower ribs are pulled up & forward= inc in thoracic dimensions (secondary to diaphragm)

3-inc thoracic volume, raising sternum and/or upper ribs

–scalene & sternocleidomastoid
some may reduce resistance to airlfow= flaring of nostrils, laryngeal opening.
mainly during exercise/ forced inspiration…not quiet breathing

Answer 68

A

1-quiet breathing, expiration= passive process bc of recoil of lungs= no muscle contraction

expiration can be active during exercise/forced/hyperventilation…during active expiration the ab muscles contract (obliques, abs) , itraab pressure= inc and diaphragm pushed up
active during coughing, vomiting, defecation, singing, valsalva maneuver
active expiration= internal intercostal muscles may contract so that will pull ribs down & in (opposite to external intercostal) = dec thoracic volume

Answer 69

A

1-descend downward inc vertical dimension of thoracic cavity…during active inspiration + primary muscle

2-elevate lower ribs up & out, enlarging thorax ffront to back & side to side…during active & secondary to diaphragm

3-raise sternum, elevate top 2 ribs, enlarge upper thoracic cavity…during forced inspiration, accessory inspiratory

4-patency of conducting upper airways to reduce airflow resistance…during forced inspiration= accessory inspiratory muscles

Answer 70

A

1-inc intra-ab pressure, exerts an upward force on diaphragm to dec vertical dimension of thoracic cavity
—only during active (forced) expiration

2-flatten thorax by pulling ribs down & in, decreasing front to back & side to side dimensions of thoracic cavity
—only during active (forced) expiration

3-lungs expand & contract during inspiration/expiration…slide back & forth w/in cavity
to facilitate there is a thin layer of seroud fluid between visceral & parietal pleura. the lymph system pumps excess serous fluid from pleural cavity and by doing it= neg pressure in pleural cavity
-neg intrapleural pressure keeps the lungs pulled tightly against parietal pleura of chest cavity

Answer 71

A

1-flow of air in/out of lungs is a function of pressure, gradients= flow

changing volume of thoracic cavity= pressure changes
volume of enclosed space increases, the pressure w/in space dec…vol decreases, pressure increases
change in intrathoracic volumes during resp cycle are produced by action of resp muscles

2-At the end of expiration the muscles are relaxed—inward elastic recoil of lung is balanced by outward elastic recoil of chest wall
-intrapleural= -5 cm alveolar = 0c= cm transpulmonary= 0 cm - (-5cm) = 5c…so alveolar= atmospheric= no airflow

during inspiration, contraction of muscles of inspiration= intrapleural pressure to be more negative…so the transpulm pressure gradient will increase & the alveoli distend…
decrease in alveolar pressure below atmospheric pressure= air to flow into alveoli

Answer 72

A

1-contraction of muscles for inspiration inc intrathoracic vol

thorcic cavity inc= intrapleural pressure dec
during quiet breathing intrapleural dec from -4.5 cm to -8 cm
lungs are pulled out & into larger thoracic volume…the intrapulm dec
air flows into lungs down the pressure gradient
pressure gradient dissipiates as air flows into lungs & intrapulm pressure goes to 0 (atmospheric pressure)
strong inspiratory effor= reduce intrapleural pressure to -40 cm= stronger lung inflation
normal expiration, inspiratory muscles relax & intrapleural pressures inc (become less neg)
intrapulm pressure inc & creates pressure gradient for air to flow out of lungs…pressure gradient dissipates, air flow ceases & intrapulm pressure returns to atmospheric pressure

Answer 73

A

1-pressure exerted by weight of air in atmosphere above earths surface, 760 mm Hg

2-same as barometric pressure..atmospheric pressure is a 0 preessure pt of ref.

3-pressure w/in pleural cavity exerted outside lungs w/in thoracic cavity…less than atmospheric pressure

4-pressure w/in alveoli…bc communciate w/ atmosphere through conducting airways, air quickly flows down pressure gradient any time intrapulm pressure differs from atmospheric pressure

5-diff in pressure between inside & outside of alveoli, equal to intrapulm pressure minus intrapleural pressure

Answer 74

A

1-depend upon physical characteristics of lung tissues & surface tension of film lining alveolar walls

2-elasticity from elastin & collagen fibers in lung parenchyma, surrounding bronchioles & pulm capillaries

elastin can be streteched to double resting length
collagen resist stretch & act to limit further expansion of lungs, especially at large lung volumes
lungs expand during inspiration via unfolding & rearrangement of fibers w/in parenchyma
elasticity=elastic recoil, opposing compliance. if high elastic recoil= low complaince & inflates w/ difficulty…low recoil=high compliance= inflates easily
inc age=change in physical & chemical properties of elastin & collagen fibers in lungs= dec recoil= inc compliance
emphysema= degradation of elastin & collagen of lung—release of trypsin from alveolar macrophages bc of smoking= dec recoil= inc compliance = airway collapse during expiration

Answer 75

A

1-inc fibrous material w/in lung interstitium…lungs to stiffen which dec lung complaince. recoil= inc, smaller changes in lung volume…compliance= dec w/ edema or pulm venous pressure is inc…inhibit proper inflation of alveoli

2-recoil & radial traction are caused by effects of elastin on lung tissue…elastin surrounds single airways produces raadial traction that keeps airway open. overall elastin in lung produces inward recoil

3-lung has air, innersurface has liquid film=airliquid interface…at interface the attractive force between molecules= surface tension…attractive force= bubble that can collapse & resist expansion of alveoli during inspiration

spherical thin walled structures. smaller spheres have higher pressures
2 alveoli of unequal sizes have same surface tension T are joined by same airwar (pores of kohn) the alveolus w/ the smaller radius will have a higher pressure P) and will empty air into larger alveolus—laplaces law

Answer 76

A

1-lipid protein complext by type 2 granular pneumocytes w/in alveolar wall

surfactant has both hydrophilic/phobic regions that are incorporated into air liquid interface.
interferes w/ attractive forces between H20 molecules & reduces surface tension…surfactant inc compliance of lung (reduces work for inhalation) by reducing surface tension
minimizes fluid accum in alveoli by reducing alveolar surface tension that would draw fluid to alveolar surface

Answer 77

A

1-air water interface is there and surface tension= very high…bc high surface tension the lung would be hard to inflate and have low complaince

2-filled w/ saline, removing air-water interface—-surface tension forces would be gone, complaince is greater than air filled lung…portion of lung elastic recoil is bc of surface tension by alveolar air liquid interface

3-surfactant is added and long compliance is midway between 2 extremes

Answer 78

A

1-surface area of surfactant film inc the surface tension inc…the surface area of surfactant film dec the tension dec

behavior is critical in maintaining stability of diff sized alveoli and preventing collapse—smaller alveoli have smaller surface area and lower tension, collapsing pressures of smaller & larger alveoli are similar
presence fo pulm surfactant, smalla lveolus doesnt collapse & empty into a larger alveolus…surfactant helps prevent alveolar collapse (atelectasis) by reducing surface tension in small vs large

2-type 2 granular pneumocytes begin at 28-32 wk of gestation. if delayed or born premature= resp distress syndrome= less compliant lung & smaller sized alveoli= atelectasis

3-reduces surface tension in smaller vs larger–counters laplaces law, promotes stability & prevents atelectasis

reduces surface tension which increases lung compliance (reduces work requried to expand lung)
reduces surface tension which minimizes fluid accum in alveoli (otherwise it would draw fluid to surface)

Answer 79

A

1-elastic properties of lungs…intrapleural pressure is reduced (engative) the lung expands

at each lung volume, transpulm pressure is determined from diff between intrapulm & intrapleural pressure.
transpulm pressure constant for a little & measure lung volume w/ spirometer = PV curve
difference between inflated & deflated curves= hysteresis= changes in surface tension at alveolar air liquid interface
at 0 pressure, lung still has volume…as intrapleural pressure surrounding lung becomes less negative or positive, small airways collapse, trapping air inside alveoli = residual volume

2-compliance of lung C is change in volume of lung per change in pressure…slope of PV curve. measure of distensibility…steep curve= high compliance
at lung volumes near FRC (functional residual capacity ~40%) of TLC and very compliant lung…but as get closer to TLC lung = less compliant…so at high lung volumes a greater change in pressure is required to get a chnage in volume
C= delta V/ delta P

Answer 80

A

1-contributes to stability of alveoli in lung

surrounded by other alveoli in a honeycomb arrangement & supported by them too
1 alveolus reduces or increases its volume is opposed by adjacent alveoli…if alveoli start to collapse the physical forced by others will prevent the collapse
1 alveolus tries to overinflate the others will prevent it

2-when chest wall at functional residual capacity the elastic recoil of chest wall is directed outward
-assist inspiration, if chest wall was unoppsed by tendency of lungs to recoil inwards, the chest wall would spring out to 705 TLC…equilibrium/resting volume of chest wall

Answer 81

A

-lung and chest in dyanmic equilibrium
passive inward recoil of lung Pl and passive outward recoil of chest Pcw can give you recoil pressure of system Prs…. Prs= Pl + PCW
-FRC functional residual capacity is where Pl and PCW are equal but opposite…all resp muscles are reaxed and lung and chest wall systems are at equilibirum at FRC
-chest wall is pulled inward by lungs and lungs are pulled out by chest wall
-the pleural cavity w/ subatmospheric intrapleural pressure -5, glues lungs to chest wall so lung and chest move in and out together
-at volumes above FRC, net recoil pressure of resp system decreases in lung volume…volumes above FRC can only be maintained by actions of muscles of inspiration
-at lung volumes below FRC, net recoil pressure of resp system favors inc in lung volume
-lung volume below FRC can be mainted by expiration muscles

intrapleural pressure raised to atmospehric pressure (puncture pneumothorax), unopposed lung will recoid in, while unopposed chest will spring out…results inc ollapsed lung
–pneumothorax= intrapleural pressure becomes the same as atmospheric pressure…as a result the lung collapses in and the chest wall springs out

Answer 82

A

1-gas exchange at the pulm capillaries & tissue capillaries involve simply diffusion of O2 and CO2 down their pressure gradients…there are no active transport mechanisms

2-atmospheric air= N, O2 w/ CO2, H2…combined= barometric pressure= 750 mm.
barometric= sum of individual pressures that each gas contributes

3-is directly proportional to the percentage of that gas in the total air mixture…
daltons law= partial pressure of specific gas in mixture, is the pressure it would exert if it ocupied the total V in absence of others…P_x= P_B* F_x
Px= partial pressure of gas x, Pb= barometric dry gas pressure and Fx= fractional component of gas X…barometric changes w/ altitude but everything else is the same

Answer 83

A

1-as soon as dry atmospheric air is inspired it is warmed/mositened by conducting passages of upepr resp

water vapor exerts a partial pressure—at body temp it is 47 mmHg
humidifcation of inspired aire dilutes the partial pressure of other gases by 47 mmHg
–sum of all individual gas partial pressures must equal total barometric pressure and thennn subtract 47 to get the humidified air in lungs

2-gases dissolved in a liquid=partial pressure

amt of gas that will dissolve in fluid depends on solubility of gas in fluid & on partial pressure of gas
Henrys law===conc of gases dissolved in liquid C is equal to solubility in liquid (a) x’s partial pressure of gas Px: C= a * Px

—-solubility of O2 and Co2 in blood remains constant so the amt of O2 & CO2 dissolved in pulm capillaries= directly proportional to PAO2 & PACO2

Answer 84

A

1-gas always diffuses from High to low partial pressure
O2 diffuses from alveoli and dissolves in pulm capillary blood until PO2 becomes equal to partial pressure of O2 in alveolar gas (PAO2)
CO2 diffuses from pulm capillary blood and evolves as CO2 gas in alveoli PACO2, until alveolar PCO2 is equal to PCO2

2-before inspiration, alveoli and airways are filled w/ old air (FRC)—inspiration= fresh air enters lung & occupies dead space & alveoli. 13% of alveolar air is replaced by fresh atmospheric air w/ each breath

only air in alveoli can exchange O2 & CO2 w/ blood
vol of air expire V_Eis sum of volumes coming from dead space & alveoli V_D & V_A
expired air is similar to inspired air in the beginning bc it comes from dead space…but later dead space & alveolar air are expired bc not all alveoli empty at the same time so they mix, so towards the end of expiration the air being expired= alveolar air

Answer 85

A

1-during inspiration, inspired air loses O2 to blood & gains CO2. if amt of O2 removed= amt of CO2 gained (CO2 production= O2 consumption) then…
PIO2- PAO2 = PACO2 - PICO2
if PICO2= 0 then: PAO2= PIO2-PACO2

basis for alveolar gas equation= alveolar O2 pressureu can be determinded by inspired O2 pressure & alveolar PCO2—
ratio of O2 consumed to CO2 produced= resp quotient…RQ
individuals who have total carb diet have equal CO2 production & O2 consumption= 1.0
individuals w/ mixed diet= 0.8, less CO2, more O2
total fats= 0.7

so you have to factor diet into the PACO bc the O2 consumption is underestimated…
PAO2= PIO2 - PACO2/RQ

2-0.21

Answer 86

A

1-rate of CO2 production, the alveolar CO2 conc (PACO2) is determined by rate of alveolar ventilation VA
-inverse relationship between PACO2 & alveolar ventilation—ventialtion doubles then PACO2 reduced by 1/2

2-bc of humidifcation & small turnover of alveolar air w/ new inspired tiday volume, avarge PAO2= 100mmHg and atomospehric PO2=160 mmHg
-O2 w/in alveoli moves down partial pressure gradient into the blood, so the new O2 arriving in lungs w/ each breath replaces that which has been diffused into capillaries…bc pulmonary blood PO2 equilibrates w/ alveolar PO2, the PO2 w/in arterial blood= 100mmHg

-similarly, for CO2, body tissues try to continuously produce CO2…and is added to the blood in the systemic capillary beds & then transported to the lungs…once in the lungs, CO2 diffuses down its partial pressure gradient from blood into alveoli.
CO2 is removed from lungs during expiration…
because CO2 arriving from body tissues is constantly removed from the lungs, the PACO2= constant at 40 mmHg

Answer 87

A

1-diffusion= principal process that accounts for transfer of O2 & CO2
factors affecting= partial pressure gradients for O2, CO2
-size of surface area of alveolar membrane
-solubility of O2 & CO2
-thickness of alveolar membrane
-anything that significantly increases the thickness of the alveolar membrane can interfere w/ normal resp exchange of gases—pulm edema, fibrosis, pneumonia

2-excess accum of interstitial fluid between alveoli & pulm capillaries bc of pulm inflammation or left sided congestive heart failure

3-replacement of delicate lung tissue w/ thick fibrous tissue in response to chronic irritants

4-inflammatory fluid accum w/in or around alveoli

Answer 88

A

1-rate of transfer inc as partial pressure gradient inc—major determinant of rate of transfer

2-rate of transfer inc as surface area inc—suface area is constant under resting…surface area inc during exercise….surface area dec w/ pathological like emphysema & atelectasis

3-rate of transfer dec as thickness inc—thickness usually constant…thickness inc w/ pulm edema, pulm fibrosis, pneumonia, any pathological

Answer 89

A

1-w/in blood is 2 forms—dissolved O2 & chemically bound to hemoglobin. O2 is poorly soluble in fluids

amt of dissolved O2 in blood is proportional to PO2 of blood
PaO2 of 100 mmHg—only 3 ml of O2 is dissolved in 1 L of blood…resting cardiac output of 5 L/min = 15 mL/min of O2 carried in blood
resting O2 consumption of body is 250 ml of O2 per min so needs hemoglobin

Answer 90

A

iron bearing protein w/in RBC…has a globin & heme group
globin= 4 highly folded polypep chain—2 identical alpha and 2 identical beta
each globin has a heme—heme is an iron containing, non protein nitrogen group & can bond w/ O2 (4 molecules of it)
98% of it is transported w/ hemoglobin…so O2 content is blood is w/ hemoglobin
crucial role in permitting tansfer of large quant of O2 from alveoli to tissues
–hypothetical situation is presented w/ no hemoglobin in blood—alveolar PO2 and blood PO2 would equilibrate…hemoglobin added then O2 wil bind to it keeping PO2 low(storage depot for O2) O2 will move into blood until equilibrium between alveolar PO2 and blood PO2

Answer 91

A

normal alveolar PO2 =100mm Hg and PvO2=40mmHg and sets the alveolar to blood PO2 at 60. = large initial O2 flux, O2 moves into capillary blood then binds to hemoflobin and equilibriates w/ PAO2
reduces partial pressure gradient for O2 and slows down O2 flux—PO2 in blood equilibrates w/ PAO2
high rate of O2 diffusing capacity= bc of large surface area and short diffusion distance in lung
transit time in pulm capillaries= .75 s—additional time allows for adequate O2 diffusion during exercise when time is shortened
in some athelets the output can reduce transit time in lungs= arterial hypoxemia

CO2 has greater solubility, comparable volume of CO2 can be transferred so it has a smaller gradient than O2

Answer 92

A

1-O2 saturation of hemoglobin is ratio between actual O2 combined w/ Hb in unit vol of blood and total amt of O2—can be combined w/ Hb in same vol of blood.
S_O2= amt of O2 combined w/ Hb / O2 capacity
-imp factor that determines O2 saturation is PO2 of blood= conc of O2 physically dissolved in blood
-PO2 inc, O2 will dissolve into blood, bind to hemoglobin & then blood PO2 will equilibrate w/ alveolar PAO₂
-PO2 dec, partial pressure gradient favors O2 unloading and O2 diffuses into tissues, disassociates w/ Hb and then blood PO2 equilibrate w/ tissue PO2…
-as blood PO2 changes, O2 saturation changes in non-linear fasion

2-blood PO2 against O2-Hb saturation (SO2) figure= S shaped, sigmoidal curve

Answer 93

A

1-high range of PO2 (60-100 mmHg) w/in pulm capillaries, a small inc in PO2 gives only small inc in SO2—bc plateau portion of ODC at high PO2 values—PO2 at 100= Hb 99% saturated…so blood leaving lungs=saturated.

PO2=60 the HB =90%saturated
plateau= safety net in loading O2 onto HB in pulm capillaries

2-ODC steepens at PO2 between 40-60 mmHg…venous PO2 of 40=75% Hb saturated w/ O2
blood in systemic at 99% saturation means that 24% of O2 bound to Hb has dissociated & diffused into tissue down the partial pressure gradient
-change in PO2 of 59 leads to 24% O2 release

3-ODC= very steep at low PO2 from 10-40

at exercise—if tissue PO2 were to fall w/in this range there would be small changes in PO2 that would lead to large changes in Hb O2 saturation= O2 unloading at the tissues
systemic capillary PO2= reduced, even larger amts of O2 are available to meet O2 demand

Answer 94

A

1-PCO2, pH, temp, conc of 2,3 DPG (BPG)

P50 =O2 pressure that is required for 50% Hb saturation
if Hb O2 affinity= dec then a greater pressure is required to get to 50% Hb saturation—P50=inc and ODC is shifted right
greater HbO2 affinity will shift the ODC to the left & P50 will dec
–high affinity= greater uptake in lungs but less release into the tissues…low affinity=less uptake in lungs but graeter release into tissues

Answer 95

A

1-rise in PCO2 or fall in pH will shift ODC to right (inc in P50)—reduces Hb-O2 affinity and matches w/ metabolically active tissue, producing more CO2 and becoming more acidic bc of production of carbonic acid or lactic acid—–facilitate in unloading of O2 to tissue
—dec in O2 affinity of Hb when pH blood falls= BOHR effect, utility of Bohr effect is w/ shifting ODC…greater amt of O2 can be release at tissues an greater amt of O2 can be taken up at lungs

2-Dec in PCO2 or rise in pH will shift ODC to left (dec p50)—lower PO2 is needed to bind given amt of O2 to Hb= inc in O2 affinity. (acid forming CO2 removed= inc in pH) so Hb has higher affinity for O2 in pulm capillaries= inc loading of O2 onto Hb

3-changes in temp alter thermodynamics of Hb-O2 binding—higher temp= dec HbO2 affinity & facilitate O2 unloading—lower temp= inc HbO2 affinity & facilitate O2 loading into blood

4-made w/in RBC during anaerobic metabolism—highly charged anion that binds deoxy Hb but not oxyhemoglobin—causes inc in 23 BPG conc = shift ODC to right= higher PO2 required to bind same amt of O2 to Hb
-2,3, BPG production in RBC is inc when total Hb conc is low (anemia) or when PO2 is low (high altitude)

Answer 96

A

1-effect of blood PO2 on amt of O2 in blood= blood oxygen content—amt of O2 per unit volume

dissolved O2= 2%—Henrys law: C_x= alpha * P_{x<br></br>C=conc of gas dissolved…Px=partial pressure alpha= solubity}
O2 solubility= 0.003/100mL
at arterial PO2 of 100= 0.3 O2/100 mL
at venous PO2 of 40= 0.1 O2/100 mL
when Hb is 100% saturated as in arterial blood, 1 gram of Hb will hold 1.34 mL of O2—conc of Hb in blood= 15 g Hb/100mL—-can be reduced w/ anemia or inc w/ blood doping or erythropoietin
– O2 content= (1.34 * Hb conc * SO2) + (0.003 * PO2)
–O2 capacity=(1.34 * Hb conc * 100) + (0.003 * PO2) —capacity is at MAX amt of O2 carried in blood

Answer 97

A

1-PO2 graphed aginst Blood O2 content—since most of O2 in blood is bound to Hb there are a couple of differences—O2 content will keep increasing after 100% Hb saturation bc O2 will continue to dissolve at rate of .0003 as PO2 inc
& position of curve depends upon Hb conc…PO2 & saturation, the O2 content of blood is directly proportional to Hb conc

Answer 98

A

1-low O2 levels in body

2-blood as low PO2 and Hb is poorly saturated—hypoventilation when gas exchange in lung is disrupted (edema or pneumonia) —right-left shunt, ventilation/perfusion mismatch and when PIO2 is low (high altitude)

3-PO2 normal, but the Hb conc is low= reduced O2 carrying capacity & O2 content
Carbon Monoxide (CO) posioning---formation of carboxyhemoglobin= anemic hypoxia
CO poisoning O2 carrying capacity is norm but O2 content is reduced

4-circulatory, ischemic, stagnant—reduction in tissue blood flow
-decrease in cardiac output during shock/congestive heart failure—obstruction to blood flow in vascular bed

5-toxic substance like cyanide intereferes w/ tissues utilization of O2—O2 conc of venous blood is high, O2 consumption by tissues is low

Answer 99

A

1- 3 forms: 1-physically dissolved, 2-carbamino compound, 3-as bicarbonate
-as blood goes through systemic capillaries—picks up 5 mL of CO2…additional CO2 is transported to lungs where it is exhaled

2-blood through systemic capillaries—CO2 diffuses down partial pressure gradient from tissues into blood
-dissolved CO2 in blood doesnt remain in dissolved form but CO2 transported in blood in 3 forms…

3-amt of CO2 physically dissolved in blood depends upon blood PCO2–CO2 is more soluble than O2 so a greater proportion is in dissolved form

Answer 100

A

1-CO2 binds w/ globin of Hb=carbamino Hb—reduced Hb (no O2) has higher affinity for CO2…so unloading of O2 from Hb in systemic capillaries= loading of CO2 by Hb—5% venous blood totals CO2

2-90% venous blood total CO2—chemical reaction takes place w/in RBC…CO2 combines w/ H20 to make carbonic acid—reaction occurs slowly in plasma
-buuut w/in RBC—carbonic anhydrase accelerates reaction making bicarbonate, causing bicarb and H to accum w/in RBC—RBC membrane has a transported that facilitates movememnt of bicarb & Cl. but membrane is impermeable to H—so bicarb not H diffused down conc gradient out of RBC & into blood

Answer 101

A

1-bicarb are more soluble in blood than CO2—diffuse out of RBC and replaced by CL ions to maintain neutrality w/in RBC= chloride shift

H ions remainign w/in RBC after dissociation of H2CO3 bind w/ reduced Hb that just released its O2 molecule w/in systemic capillary
reduced Hb has a greater affinity for H than oxyhemoglobin—removal of O2 from hb inc ability of hb to bind w/ CO2 —deoxy of Hb inc ability to carry CO2=haldane effect
uptake of CO2 into RBC inc conc of HCO3 and H w/in RBC…inc osmotic pressure of RBC which draws H20 into cells—RBC vol increaseas as RBCS go through systemic capillaries

Answer 102

A

1-reactions at tissue level are reversed once blood is in lungs—Co2 diffuses down partial pressure gradient & removed from body during expiration—draws HCO3 from plasma into RBC= dissolved CO2 & H20—CO2 molecules diffuse out of RBC into plasma and then into alveoli

2-relates CO2 of blood to blood PCO2 w/ all 3 forms

haldane effect= lower PO2 there will be a higher CO2 for any given PCO2
reduced Hb has greater ability to bind H ions produced when carbonic acid dissociates and bc reduced Hb is more likely to form a carbamino compound—
tissue capillaries the haldane effect= inc pickup of Co2 bc of O2 removal from Hb
in lungs haldane effect= inc release of CO2 bc of O2 pickup by Hb

Answer 103

A

MAXIMIZE O2 & CO2 TRANSPORT

haldan effect & bohr effect work together to maximize O2 & CO2 transport w/in blood
bohr= when pH of blood dec there is a dec in affinity of hemoglobin for O2= hemoglobin release an O2 molecule
haldane effect—release O2 from heme portion of hemoglobin molecule inc affinity of globin portion of hemoglobin molecule for Co2
–bc tissue are acidic both of these happen in systemic capillaries–work together to maximize O2 relase and binding of Co2 molecules to hemoglobin

-in pulm cappillaties the pH becomes less acidic= bohr & haldane to work oppositely—pH inc= inc affinity of hemoglobin for O2 = hemoglobin bing to O2
so binding of O2 to heme portion of hemoglobin decreases affinity of glbin portion of hemoglobin for CO2…so hemoglobin releases CO2—so w/in pulmonary bohr and haldane work together to maximize binding of O2 molecules + release of CO2 w/ hemoglobin

Answer 104

A

begins at main pulmonary artery—receives mixed venous blood pumped by r. ventricle
artery branches successively—close to the branching of the airways to the level of terminal bronchioles
pulmonary arteries break up to supply pulmonary capillary bed which lies in wall of the alveoli
pulm capillaries form dense ,thin sheet in alveolar wall—covering 85-95% of alveolar surface area= efficient gas exchange
oxygenated blood is collected from capillary bed by small pulm veins—merge to form large veins that drain into l. atrium

Answer 105

A

1-systemic circulation—broncial arteries come from descending aorta and return to lungs

arteries have fully oxygenated blood that supply O2 and nutrients to intra pulm structures like tracheobronchial tree, pulm nerve & ganglia and SM & CT.
blood from bronchial circulation returns to r. atrium via zygos & intercostal veins

2-interconnected—join together in short circut= anastomosis

bronchial capillary bed (deoxy blood) can anastomose w/ pulm capillary bed—mixed blood becomes oxygenated in pulm capillaries & then leaves lungs via pulm vein
bronchial capillary bed (deoxy) can also drain into pulm vein —here the deoxy bvenous blood to the oxy blood is called a right to left shunt—why blood leaving lungs isnt always 100% oxygenated

Answer 106

A

1-BP w/in pulm circulation= low compared w/ systemic circulation

pulm artery has pressures of 25/8 w/ mean pressure of 15
aorta has pressures of 120/80, mean of 100
left atrium, mean = 5-8 so pulmonary arteriovenous=10
pulmoanary capillary mean= 10 mm
bc the mean pulm pressure is lower than mean aortic pressure the walls of pulm artery are thinner w/ less SM & elastin than the aorta—pulm veins= thin too
systemic arterioles= thick w/ circular SM
pulm arterioles cant vasoconstrict like systemic arteriole

2-pulm circulation is in series w/ systemic circulation gets entire cardiac output—Q
P= Q*R

Bc Q is high and P (pulm circulation pressure) is low, this means Resistance is low…the pulm vascular resistance= 1/10 of systemic vascular resistance

pulm circulation is low resistance system bc of low SM tone in pulm arterioles and large cross sectional area of pulm capillaries
pulm circulation= low resistance, circulation = low resistance even when pulm pressures inc
when pulm arterial or venous inc, pulm vascular resistance dec bc of the recruitment of new pulm beds that open up & distension of already opened vessels.
distension= inc the caliber of capillary segments & predom mechanism for fall in pulm vascular resistance as pulm arterial pressure inc

3-15 & 5

4- 100 & 2

Answer 107

A

1-can be measured using radioactive xenon that is dissolved in saline and injected into peripheral vein

xenon reaches pulm vapillaries it is evolved into alveoli bc of low solubility
evolved xenon is counted by radiation detectors placed over chest—measured amt of radiation from eveolved xenon is proportional to pulm blood flow
results= all parts of lungs dont receive same pulm blood flow—base of lung gets more blood flow per volume than the apex of the lung—happens bc of gravity, bc of hydrostatic pressures w/in vessels & effect of starling resistors

2-pump is pumping h20 around rigid tubes—pressure in tube higher than pump will be less than pressure at level of pump
-pressure in tube that is lower than pump will be greater than pressure at level of the pump—like the lungs…the pulm arterial/venous BP are lower at the lung apex and higher at the base of the lungs

Answer 108

A

1-pulm capillaries are surrounded by alveoli & get little support from lung parenchym—so they are liable to collapse or distend depending on pressure in/around them

blood flow through systemic capillary depends on difference between arterial & venous pressure
in lungs, alveolar pressure has to be considered
starling resistor stimulates situation in pulm capillaries, where there is arterial pressure (Pa), alveolar pressure PA, and venous pressure Pv…if PA is greater than Pa the capillar will be squeezed shut and therell be no flow

2-exposed to surrounding alveolar pressure—flow through these is determined by relationship between alveolar pressure & pressure w/in them.

3-all arteries & veins that run through lung parenchyma

pulled open by radial traction of surrounding tissue
caliber of extra alveolar vessels is greatly affected by lung volume bc this determines the pull of the parenchyma

Answer 109

A

1-passive factors dominate pulm vascular resistance & distribution of flow w/in pulm circulation
-pulm BV are innervated by symp & parasymp nervous system—but is doubtful that autnomic nervous system has function in normal control of pulm Blood flow

2-distribution of pulm blood flow is dec when PO2 of small airway is reduced

hypoxic region of lung, SM w/in arteriole will contract—directs blood flow away from hypoxic region of lung…hypercapnia, acidosis & hypertrophy of vascular SM accentuate it
benefit===diverts mixed venous blood away from poor ventilated areas of lung that have low PAO2, by increasing vascular resistance—so mixed venous blood is sent to better ventilated areas of lung
–in states like pneumonia, hypoxic pulm vasoconstrction is limited to diseased lung
high altitude= HPV constricts pulm arteriloles throughout entire pulm circulation= inc in pulm vascular resistance
local effect, intrinsic to lungs, and = no autonomic nervous system innervation

—–systemic= hypoxia causes vasodilation

Answer 110

A

1-dec O2= vasodilation inc O2= vasoconstriction

2-decreased O2=vasoconstricton inc O2= vasodilation

3-regional diff measured by radioactive xenon…when gas inahled, its radiation is detected by counters outside chest…base of lung= greater ventilation than does the apex of the lungs
-regional effects is bc of gravity
-weight of tissue above it there is distortion of lung tissue at bottom of lung—tissue at base of lung= compressed by weight of tissue above it,
while apex of lung is expanded, so alveoli at base of lung are compressed and alveoli at apex are stretched open
-weight of lungs compress the intrapleural space at base of lungs= vertical distribution of intrapleural pressure…intrapleural pressure= greater at base of lungs compared to apex.
-gradient of intrapleural pressure and transpulm pressure from base of lungs to apex

Answer 111

A

1-at end of normal expiration the lung is at runctional residual capacity FRC—so the alveolus at the base of the lung has a low resting volume bc it is compressed by weight of tissue above it and there is a reduced expanding pressure bc the intrapleural pressure is less negative
-at FR the alveolus at base of lung is on steep part of compliance curve…so any change in intrapleural pressure= large increase in volume of that alveolus
-although an alveolus at the base of the lung has a small resting volume, it has greater expansion during inspiration
-at FRC an alveolus at apex has higher resting volume than at base bc there is less lung tissue above it and there is large expanding pressure bc the intrapleural pressure is more neg, apex is also on less steep part of complaince curve,= smaller inc in the volume of that alveolus for change in intrapleural pressure
===why base is better ventilated, has more room to expand while apex is already almost fully expanded

Answer 112

A

1-gas exchange is maximally efficient when both ventillation V & perfusion Q are appropriately matched in all areas of the lungs…amt of O2 extracted & CO2 delivered is proportion to the blood flow

2-perfusion of alveolus inc, venilation is unchanged, more CO2 in blood will be delviered to alveolus and more O2 will be moved from alveolus into blood in that alveolus, PACO2 will inc, and PAO2 will dec.
-if ventilation stays same but perfusion dec, less CO2 brough to alveolus in blood and less O2 move from alveolus into blood—alveolus PACO2 dec and PAO2 inc

3-upright posture, ventilation/perfusion is greater at base of lungs than at apex…
-ventilation to perfusion ratio (V/Q) is high at apex and low at base
-V/Q=1 then ventilation is same as perfusion
-V/Q >1 there is more ventilation than perfusion
-V/Q <1 more perfusion than ventilation
V/Q ratio at apex of lungs= 3.3 while at base V/Q is .63—so apex of lungs is over ventilated while base is over perfused

4-can range from 0 to infinity…alveolus well perfused w/ no ventilation V/Q= 0

alveolus ventialted w/ no perfusion V/Q= infinity
normal lung the range of ventilation/perfusion= narrow and overall the ventilation to perfusionr atio of alveolar ventilation to pulm blood flow= 0.8

Answer 113

A

1-partial pressures of O2 & CO2 w/in pulm capillary will come into equilibrium w/ gas tensions in alveoli

alveolus that is well perfused & well ventilated the PO2 & PCO2 of blood entering pulm capillary will be 40 & 46
after gas exchange & equilbration the blood leaving pulm capillaries will have equilibrated w/ alveolar PO2 & PCO2
end capillary blood= 100 & 40
some alveoli may have reduced ventilation bc of airway obstruction—no ventilation VQ=0, the PO2 & PCO2 of blood leaving pulm cap= same as blood entering 40 & 46—no difusion gradient or gas exchange
some alveoli may get reduced pulm blood flow bc of BV occlusion, when no perfusion VQ=infinity, therell be no blood flow through pulm cap…and no gas exchange…so alveolar PO2 & PCO2 will be same as inspired air 150 & 0

Answer 114

A

for gas excahnge between alveoli & pulm cap blood there must be ventilation & perfusion
apex of lung has a high VQ ratio, but bc of relative low perfusion there is reduced gas exchange at apex
limited amt of O2 goes from alveoli into pulm cap blood and limited amt of CO2 move from pulm cap into alveoli sooo alveoli at apex of lung, PAO2 will be high and PACO2 will be low..but blood that does pass through pulm cap beds at apex of lung will become well oxygenated bc of high PAO2

-base of lung has low VQ ratio…alveoli at base get more ventilation & more perfusion so large O2 will go from alveoli into pulm capillary blood & large CO2 will go from pulm cap into alveoli…so base of lung the PAO2 will be low and PACO2 will be high—so bc of greater perfusion= more O2 uptake and more CO2 output ill occur

Answer 115

A

-VQ ratio is high at apex & low at base of normal upright lung
VQ inewuality affects gas exchange of lung & overall amt of O2 that can be transferred from lung into blood
-PO2 at apex of lung= 40 higher than at base but major share of blood leavinglung comes from base where PO2 is low
-depressing Po2 of blood in pulm vein below that of mixed alveolar PO2
-mixed alveolar PO2 can be determined by using alveolar gas equation or PO2
-2 alveoli w/ low & high VQ ratio…each alveolus receives systemic venous blood that contains 14.6 bc of their differing V/Q ratios, the O2 content of blood leaving pulm caps will be different
-blood leaving alveoli w/ low VQ ratio= less O2 content 19, but higher blood flow this alveoli will contribute more O2 to blood leaving lung
-blood leaving alveoli w/ high VQ ratio the O2 content will be 20, but bc of low blood flow there will be less O2 to blood leaving lungs
—80% of blood goes through alveoli w/ low ratio and 20% through high —between the 2= 19.2

Answer 116

A

1-matchign ventilation & blood flow w/in regions of lungs= gas ecahnge

inequality= mismatch of ventilation & perfusion= defective gas excahnge in diseases—cant transfer as much O2 or CO2 as lung that is ventilated/perfused
any situation with VQ inequality= dec in arterial PO2 Hypoxemia
VQ inequality can lead to CO2 retention

Answer 117

A

1-collapse of airways—emphysema

bronchoconstriction—asthma
dec lumen diameter bc of inflammation—bronchitis
obstruction by mucous—astham/bronchitis
compression of airways—edema or tumor

2-fibrosis

regional variations in surfactant production
pulm vascular congestion or edema
emphysema
diffuse or regional atelectasis
pneumothorax
compression by tumors or cysts

3-pulm emboli/thrombosis

compression of pulm vessesl (high alveolar pressure, tumors, edema, or pneumothorax)
destruction of pulm vessels
pulmonary vascular hypotension
collapse/overexpansion of alveoli

Answer 118

A

1-continuous cyclical pattern
inspiratory muscles rhythmically contract & relax, changing volume of thoracic cavity
-fills & empties lungs
-resp muscles are skeletal muscles —require nervous stimulation for contraction

2-within the brainstem, responsible for generating basic pattern of breathing

aggregations of inspiratory & expiratory neurons w/in resp centers inc neuronal firing date during inspiration/expiration
respiration is under direct neural control from brain
control of respiration doesnt reside in lungs or resp muscles
organized into sausage shaped columns w/ long axis
dorsal resp group DRG= inspiratory, descending fibers synapse on motor that supply inspiration muscl
ventral resp group VRG= inspiratory & expiratory, only active during forced inspiration/expiration
–pre-botzinger complex= rostral end of VRG, resp rhythm

Answer 119

A

1-pons: apneustic & pneumotaxic centers influence output from medullary—fine-tuning

apneustic= prolongs inspiratory effort by givign excitatory input to inspiratory neurons w/in prebotzinger
penumotaxic= impulses to apneustic & prebotzinger that switch off inspiratory effort
pneumotaxic & apneustic have antagonistic but = smooth transitions between inspiration & expiration

2-rhythmic resp activity= automatic process

cortex can modify activity of brainstem neurons bc breathing can be modified voluntarily
speaking & yaning & coughing—interrupt rhythmic breathing
hyperventilation & breath holding can alter blood gases

3-limbic system & hypothalamus= emotional ersponses, alter pattern for breathing (fear/stress)

nucleus tractus solitarus NTS- autonomic center w/in brainstem…DRG neurons located in ventrolateral portion—lots of cardioresp afferents
–lots of chemoreceptors, pulm stretch receptors (lateral), arterial baroreceptors (dorsolateral)

Answer 120

A

1-diaphragm & external intercostal innervated by phrenic & intercostal nerves

cell bodies are located in spinal cord
neural impulses from inspiratory neurons in medullary centers synapse on cell bodies of resp motor neurons
inspiratory neurons w/in brainstem are activated= motor neurons connected to inspiratory muscles to activate===contraction of diaphragm & external intercostal muscles= inspiratory effort
when inspiratory neurons in brainstem stop firing—diaphragm & external intercostal relax= passive expiration

-expiratory neurons w/in brainstem to expiration muscles (internal intercostal & ab muscles)—forced expiration &hyperventilation, motor neurons connected to expiratory muscles become activated after they are activated by brainstem expiratory neurons

Answer 121

A

1-responds to a change in chemical comp of blood or fluid

2-peripheral arterial chemoreceptors are in the carotid bodies at the bifurcation of the common carotid & in aortic bodies above and below aortic arch

respond to changes in chemical composition of blood, especially PaO2 and send afferent impulses to lateral NTS w/in medulla
carotid body chemo affterents travel via glosso
aortic body chem afferents travel via vagus
when PaO2 falls below 60, resp centers are stimulated by signaling periph chemorec to inc ventilation—so periph chemoreceptors dont play a role in min by min control of resp only when really low
arterial chemoreceptors respond to inc in PaCO2 and dec in pHa= inc in ventilation

Answer 122

A

1-carotid body chemo contain glomus cells

–type 1= large vesicles w/ doapmine—close to carotid sinus nerve (glosso)
–type 2=no dapamine
PaO2 dec = inc in firing rate along carotid sinus nerve—partial pressure of O2 is the stimulus for inc discharge rate, so anemia doesnt stimulate ventilation bc O3 ontent is depressied but PO2 is normal

2-peripheral chemo= stimulates when PAO2 falls below 60
-central chemo= no direct effect, severe hypoxia depresses neuronal activity of brain (resp centers too)

3-periph chemo= weakly stimulates
central chemo= strongly stimulates, primary resp signal

4-periph chemo= stimulates, acid base balance
central chemo= no affect, cant penetrate blood brain barrier

Answer 123

A

most important bc it is min by min control of ventilation
along ventrolateral surface of medulla—near VRG
applying H/dissolved CO2 to brain ECFbathes central chemoreceptors= breathing
inc in arterial PCO2= rise in PCO2 of CSF that surrounds brain
blood brain barrier is impermeable to HCO2 & H but permeable to CO2
when blood PCO2 rises, CO2 diffuses into brain CSF and CO2 then dissociates & causes inc in H conc (dec pH) in CSF
H ions diffuse from CSF into ECF, dec ECF pH stimulates central chemoreceptors which will stimulate medullary resp centers to inc ventilation
hyperventilation blows off excess Co2 & arterial PCO2 so pH will go back to normal

-inc in local ECF pH (dec PCO2) will inhibit ventilation…hyperventilation will temporarily reduce the urge to breathe

Answer 124

A

1-afferent fibers of these receptors travel to brainstem in vagus nerve to lateral NTS

2-W/in SM layer of lung airways & streating of lungs during inspiration activates the receptors

towards end of inspiration, action potentials from pulm stretch receptors travel to medullary resp center to inhibit inspiratory neurons
*Breuer Hering Reflex**- neg. feedback—cut inspiration short before lung becomes overinflated—imp when tidal volume is over 1000 (large) aka during exercise

3-lie between airway epithelial cells—noxious gas, cig smoke, inhaled dust, cold air stimulate these ones and they will bronchoconstrict & have rapid shallow breathing

this breathing w/ bronchonstriction may limit penetration of agents into gas excahnge surfaces of lungs
may play role ina sthma attacks, producing bronchoconstriction in response to released histamine
cough/sneeze

4-in lung interstitium near alveolar capillaries…J Receptors…excited by interstitial edema in lung

stimulation of pulm c activates j reflex= laryngeal closure and apnea, w/ rapid & shallow breathing
may be responsible for rapid breathing in patients w/ pulm embolus/edema or pneumonia
pulm C = dyspnea during pulm vascular congestion bc of L. ventricular failure or exercise in healthy people

Answer 125

A

1-mechanical or chemical stimulation of nose= explosive expiratory event===sneeze…stimulation can produce apnea & diving response

2-trachea & upper resp tract have irritant receptors…cause coughing, bronchoconstriction, apnea. laryngeal spasm can occur when larynx is stimulateed mechanically & endotracheal intubation

3-receptors in chest walls signal to brainstem resp neurons about forces exerted by resp muscles & movements of chest wall
-impoulses from moving limbs are though to stimulate ventilation during early stages of exercise

Answer 126

A

1-ventrolateral surface of medulla, near CN 9&10 roots

-stimulus= dec pH of brain ECF…inc ventilation

2-carotid bodies in bifurcation of carotid artery
afferent= CN 9—stimulus= dec PO2: inc ventilation

3-aortic bodies over aorta & thoracic arteries
afferent= CN 10—stimulus=dec PO2: inc ventilation

4-SM of bronchi/bronchioles
afferent= CN 10—stimulus= stretch of lungs during inflation: inhibition of further inflation

5-Among airway epithelial cells
afferent= CN 10—stimulus= allergens, lung inflam, histamine: bronchoconstriction & rapid shallow breathing

Answer 127

A

1-in lung interstitum—afferent= CN 10
stimulus= interstitial pulm edema—apnea, rapid shallow breathing

2-w/in mucosa of nosa—afferent= CN 5
stimulus= mechanical/chemical irritants—sneeze or apnea

3-w/in laryngeal mucosa—afferent= CN 10
stimulus= mechanical/chemical irritants—cough, bronchoconstriction & hypoventilation/apnea

4-w/in pharyngeal mucosa—afferent= 9
stimulus= mechanical/chemical irritants—sniff, aspiration or swallowing movements

5-skeletal joints & muscles—afferent= spinal nerves
stimulus= limb movement: inc ventilation during exercise

Answer 128

A

1-most imp factor in control of ventilation= PCO2 of arterial blood

arterial PCO2 is tightly controlled varying w/ 3 mm
inc in PaCO2= inc in ventilation
at any PO2…raising PCO2 will inc ventilation—body is more sensitive to dec in PO2 when it is hypercapnic
dec PO2 while PaCO2 is constant = inc ventilation
at normal PCO2 of 40 the PO2 can reduce to about 60 before any inc in ventilation occurs
Po2 can be below norm level of 100 mm w/o invoking response…hypoxia min by min is small
at ane level of PaCO2 with dec PO2 = inc ventilation
w/ normal PO2 100, ventilation will increase for each 1 mm rise in PCO2
lowering PO2 below 100= greater ventilation for any PCO2 & lower Po2= inc ventilation for ever 1 mm inc in PCo2
body is sensitive to inc in PCO2 when it is hypoxic

Answer 129

A

1-inc in pulm ventilation that excees the bodys need for removal of CO2…CO2 is blown off to atmosphere and PaCO2 & PaCO2 will dec

2-below normal value for PCO2—alveolar PO2 will inc as more fresh O2 is delivered to alveoli but because hemoglobin is almost fully saturated at normal arterial Po2, little O2 is added to the blood
-only small amt of extra dissolved O2 will be added to O2 content of blood during hyperventilation

3-inc ventilation that matches an inc i metabolic demand like during exercise
-steady state exercise, PaO2 & PaCo2 remain constance w/ inc in gas exchange keeping pace w/ inc in O2 consumption & CO2 production—hyperventilation isnt synonmous w/ inc ventilation

4-pulm ventilation less that what is needed to meet bodys metabolic requirements for O2 delivery & CO2 removal—results in accum of CO2 in bood= hypercapnia

5-accum of Co2 in blood—alveolar Po2 will dec…during hypoventilation, CO2 accum occurs concurrently w/ O2 deficit bc both O2 & Co2 excahnge at lungs are equally affected

Answer 130

A

1-alveolar PO2= dec
alveolar PCO2=no change

2-alveolar PO2= inc
Alveolar PCO2=dec

3-alveolar PO2= dec
alveolar PCO2=inc

4-alveolar PO2=dec
Alveolar PCO2=inc

5-Alveolar PO2=no change
alveolar PCO2= no change

Answer 131

A

blood entering pulm capillaries= systemic venous w/ PO2= 40 & PCO2= 46
flows through…PAO2= 100 PACO2= 40
O2 goes down partial pressure gradient from alveolar air into blood
O2 equilibrates—so blood leaving pulm capillary has PO2 of 100
CO2 goes down partial pressure gradient from blood into alveolar air—blood leaving cap. has PCO2 of 40

Arterial PO2= 100 PCO2= 40
Cellular PO2= 40 PCO2= 46

PAO2= 100 PaO2= 100 Tissue=40 PvO2=40—
Presure gradient= 60
PACO2=40 PaCO2=40 Tissue= 46 PvO2=46
Pressure Gradient= 6

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exam 1 Flashcards

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