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Histology 2 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

Thorax vs thoracic cavity

A

thorax = boney; includes thoracic cavity & intra-thoracic part of abdominal cavity
thoracic cavity = separated from abdominal cavity by diaphragm

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2
Q

Nasal cavity is b/w what structures

A

external nares & choanae

has respiratory & olfactory functions

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3
Q

Extent of diaphragm

A

T7 to T13

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4
Q

Innervation of diaphragm

A

phrenic nerve

from C5 & C6 ventral primary branches

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5
Q

Fiber direction for external intercostal muscles

A

caudoventral to craniodorsal

inspiratory

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6
Q

Fiber direction for internal intercostal muscles

A

caudodorsal to cranioventral’

expiratory

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7
Q

Accessory muscles of inspiration

A

serratus ventralis & dorsalis cranialis
scalenus
rectus thoracis
abdominals (help support trunk)

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8
Q

Accessory muscles of expiration

A

transversus thoracis

abdominals

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9
Q

What is the pleura

A 
serous membrane
lines thoracic cavity & covers lungs
secretes fluid
capillary action
allows for smooth gliding of lungs against body wall
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10
Q

What is the pleural cavity

A

potential space b/w pleura

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11
Q

Costo-diaphragmatic recess

A

from pleura changing directions

lungs do not extend into this space

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12
Q

Line of pleural reflection

A

continous serous membrane makes an abrupt turn as it travels from he ribs (costal pleura) to the diaphragm (diaphragmatic pleura)

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13
Q

Auscultation triangle

A

diagonal line from tip of T5 to top of T11
ventral to epaxial muscles
caudal to thoracic limb
avoids heart & trapezius muscles (so that lungs can be heard)

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14
Q

Thoracentesis

A

needle into 7th to 10th intercostal spaces
must go cranial to ribs, not caudal (arteries & veins)
angle towards body wall to enter space

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15
Q

Clinical relevance of the line of pleural reflection for thoracocentesis

A

cranial to line = pleural cavity

caudal to line = peritoneal cavity

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16
Q

Type of epithelium for typical respiratory epithelium (TRE)

A

pseudostratified ciliated columnar epithelium w/ goblet cells

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17
Q

Cell junctions are affected by what

A

pathogens, autoimmune disease, & cancers

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18
Q

Tight junction

A

seal

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19
Q

Adherens

A

attachment (contact inhibition)

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20
Q

Desmosomes

A

lightly hold cells together

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21
Q

Hemidesmosome

A

holds cells lightly to basal lamina

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22
Q

Cell types in TRE

A

goblet, basal, ciliated, neuroendocrine, & brush

height & cell types of TRE change throughout dif regions

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23
Q

Goblet cells

A

no cilia
nuclei on basal surface
mucus produced & secreted towards apical surface

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24
Q

Basal cells

A

triangular/polyhedral shape
near basal lamina
contain desmosomes & hemidesmosomes
replace damaged cells

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25
Q

Ciliated cells

A

columnar
microvilli & vital organelles
escalator of mucus

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26
Q

Neuroendocrine cells

A

secrete pharmacologically active substances (calcitonin & hormones/chemicals)
diffuse endocrine system
granules face basal side to travel through blood
sense environment
involved in growth of respiratory sys cells

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27
Q

Brush cells

A

microvilli

sensory receptors for trigeminal nerve

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28
Q

Nasal vestibule is the transition from

A

skin to respiratory
external keratinized squamous epithelium (w/ or w/out hair) to non-keratinized & thin to cuboidal/ non-ciliated pseudostratified columnar epithelium

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29
Q

Glands, cartilage, & other present in nasal vestibule

A

serous & sweat glands
hyaline and/or elastic cartilage
nerves, blood vessels, & immune cells (propria submucosa)

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30
Q

Epithelium of caudal 2/3rd of nasal cavity proper (excluding olfactory region)

A

TRE

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31
Q

Function of nasal cavity

A

humidification & warming by thin walled veins & glands

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32
Q

Constriction of nasal cavity by

A

alpha-adrenergic stimulation via sympathetic nervous sys

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33
Q

Other features of nasal cavity

A

nerves
lymphatic nodules
P450 enzymes for detoxification

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34
Q

Olfactory region epithelium

A

high pseudostratified epithelium

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35
Q

Cells in olfactory region

A

olfactory, supporting, & basal

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36
Q

Olfactory cells

A 
bipolar neuron (axon & dendrite)
perikarya in basal zone
dendrites extend into lumen to sample odorant molecules
non-myelinated
lamina propria
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37
Q

Supporting (sustentacular) cells

A

protective
glial-like
occluding/ tight junctions
oval-shaped nucleus is closest towards the lumen
microvilli
wider on apical side & narrower on basal side
anchored to neighboring cells via tight junctions

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38
Q

Basal cell

A

tight junction

regenerate olfactory cells/ neurons & support/ sustentacular cells

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39
Q

Glands in olfactory region & function

A

olfactory/ Bowman’s glands
propria submucosa
secrete watery secretion that enhances the solubility of the odorant molecule & cleanse the cilia, allowing for the re-use of receptors for the next odorant molecule to be sampled

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40
Q

Pigmentation of olfactory region

A

lipofuscin

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41
Q

Location of olfactory region

A

dorso-caudal portion of nasal cavity

includes parts of ethmoidal conchae, dorsal nasal meatus, & nasal septum

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42
Q

How to olfactory cells allow for the sense of smell

A

club-like dendritic bulb has 10-30 non-motile cilia that contain olfactory receptors
when an odorant molecule arrives at the site, secretions from the olfactory gland solubilize the odorant molecule, leading to an action potential & odor sensation
axons from olfactory cells reach olfactory bulb of brain & leave as non-myelinated nerve fibers through the cribriform plate of the ethmoid bone

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43
Q

Location of vomeronasal organ

A

ventral portion on both sides of nasal septum

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44
Q

What is the vomeronasal organ

A

blind-ended tubes w/ internal epithelial ducts, propria submucosa, & J-shaped hyaline cartilage

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45
Q

Vomeronasal organ opens where

A

in most species (not horses), incisive duct opens caudal to the upper central incisors

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46
Q

Epithelium of vomeronasal organ

A

medial side = neurosensory cells, sustentacular/support cells, basal cells, & vomeronasal glands
lateral side = pseudostratified ciliated or non-ciliated epithelium

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47
Q

Function of vomeronasal organ

A

chemoreceptors of liquid born substances
sexual behavior
maternal instinct
fetal interaction w/ amniotic fluid

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48
Q

Function of muco-ciliary escalator

A

beat in one direction (towards pharynx) to clear the mucus into the exterior (via sneezing/spitting) or into the GI tract (via swallowing)

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49
Q

Describe stroke of cilia

A

forward (power) stroke followed by a backward (recovery) stroke
No contact w/ mucus on recovery stroke
Energy from mitochondria

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50
Q

Damage to muco-ciliary escalator due to toxins or other defects results in

A

cilia unable to remove bacteria, allergens, & dust trapped in the mucus bilayer (gel & soluble layers)

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51
Q

Structure of muco-ciliary escalator

A

9 peripheral & 2 central microtubules
peripheral tubules held by nexin protein to prevent sliding & ensure unity
inner & outer dynein protein arms of the peripheral generate a sliding motion using ATP

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52
Q

Cause of primary ciliary dyskinesia

A

immotile ciliary syndrome or Kartagner syndrome

autosomal recessive genetic disorder -> defect in coding of the dynein protein

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53
Q

Result of primary ciliary dyskinesia

A

excessive mucus build up -> chronic respiratory & middle ear infections
sitrus inversus totalis
sitrus ambiguous or heterotaxy syndrome
reproductive failures
inner, outer, or both dynein arms affected

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54
Q

Diagnosis & treatment of primary ciliary dyskinesia

A

electron microscopy of nasal/ bronchial epithelium

no treatment, but remove from breeding

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55
Q

Horses are obligate nasal breathers w/ a long soft palate. What diseases commonly affect them

A

dorsal displacement of the soft palate, laryngeal hemiplegia, & pharyngeal collapse

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56
Q

Epithelium of nasopharynx & larynx

A

TRE excluding epiglottis & vocal folds

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57
Q

Lamina propria of nasopharynx & larynx has what

A

loose CT & seromucous glands

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58
Q

Epithelium of epiglottis

A

oral side & tip = stratified squamous epithelium (non-keratinized)
tracheal side = TRE

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59
Q

Glands & cartilage of epiglottis

A

no glands

elastic cartilage

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60
Q

Epithelium of vocal folds

A

stratified squamous epithelium (non-keratinized)

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61
Q

Glands & cartilage of epiglottis

A

none

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62
Q

Club cells/ bronchiolar exocrine cells

A

no cilia
secrete glycosaminoglycan
stem cell
metabolize xenobiotics
club cell secretory protein is a biomarker
contain tryptase & activate hemagglutinin of influenza A

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63
Q

Trachea epithelium

A

lumen lined w/ TRE & supported by c-shaped hyaline cartilaginous rings

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64
Q

Structure of trachea allows for what

A

semi-flexible & semi-collapsible tube

permits bending/ rotating of neck w/out affecting ventilation

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65
Q

Glands & cartilage of trachea

A

sero-mucous/ sub-mucosal glands

hyaline cartilage

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66
Q

Trachealis muscle & function w/ swallowing

A

smooth muscles
faces esophagus on dorsal side, allows for shape change of trachea when food passes through the esophagus
trachea can flatten & expel air when coughing
cartilage provides rigidity to prevent collapse

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67
Q

Tunica adventitia of trachea has

A

loose CT & longitudinal elastic fibers

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68
Q

Hyaline cartilage of trachea has

A

chondrocytes, matrix, & type II collagen fibers

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69
Q

Tracheal collapse

A

“goose honk” coughing
common in toy breeds
sound occurs primarily in expiration
50% collapse = 16x increase in airway resistance

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70
Q

Treatment of tracheal collapse

A

medical management is a temporary fix

surgical treatment w/ a stent is necessary

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71
Q

Epithelium of bronchi

A

TRE w/ goblet cells

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72
Q

Cartilage of bronchi

A

in pieces/ plates

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73
Q

Intra-pulmonary bronchi changes how

A

height decreases & glands become sparse

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74
Q

Bronchi & trachea smooth muscle comparison

A

bronchi has more

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75
Q

Bronchioles epithelium

A

simple columnar/ cuboidal epithelium (ciliated or non-ciliated)
+/- goblet cells

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76
Q

Smooth muscle of bronchioles

A

circular & oblique fascicles

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77
Q

Glands & cartilage of bronchioles

A

none

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78
Q

Functional blood

A

pulmonary trunk & left/right pulmonary veins

gas exchange

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79
Q

Nutritional blood

A

bronchial artery branches supply pulmonary lymph nodes, bronchi, & bronchioles w/ oxygenated blood

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80
Q

Smaller airways do not need nutritional blood b/c

A

do fine on just functional blood

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81
Q

Deoxygenated blood from the nutritional blood goes where

A

into pulmonary vein, mixing w/ oxygenated blood

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82
Q

Pulmonary art

A

thin
deoxygenated blood
low pressure
both internal & external elastic laminae

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83
Q

Bronchial art

A

thick
oxygenated blood
high pressure
only internal elastic laminae

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84
Q

Pulmonary vein

A

thin

only external elastic laminae

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85
Q

Pulmonary lymphatics

A

thin
valves
no erythrocytes

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86
Q

Pulmonary hypertension

A

may affect veins or arteries
results from inflammatory lung disease (asthma or COPD) that leads to thickening of the pulmonary artery branches
could occur from a left atrioventricular valve defect that backs blood into pulmonary veins

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87
Q

Terminal bronchiole is considered what portion

A

conducting portion

no alveoli or gas exchange

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88
Q

Epithelium of terminal bronchiole

A

simple cuboidal epithelium (ciliated or non-ciliated)

no goblet cells

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89
Q

Glands & cartilage of terminal bronchiole

A

none

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90
Q

Smooth muscle in terminal bronchioles

A

greatly reduced

directly below the lining epithelium

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91
Q

Respiratory bronchiole is considered what portion

A

respiratory portion or transitional zone

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92
Q

Epithelium of respiratory bronchiole

A

simple cuboidal epithelium (few ciliated)
no goblet cells
some alveoli

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93
Q

Type I alveolar epithelial cells

A 
squamous cells
only nuclei well seen
cover 95% of alveolar area
very thin blood-gas barrier
tight junctions
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94
Q

Type II alveolar epithelial cells

A 
large round cells/ cuboidal
granular
cover 5% of alveolar area
mostly in corners of alveoli
produce surfactant
act as stem cells for Type I AEC
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95
Q

Pathological conditions like chronic inflammation may result in thickening of the respiratory membrane, leading to

A

decreased efficiency of gas diffusion

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96
Q

Alveolar macrophages are found where

A

in air spaces w/in alveoli

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97
Q

Function of alveolar macrophages

A

guard against invading pathogens & their products

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98
Q

Appearance of macrophages when they ingest foreign bodies (dust particles or bacterial products) or dead cells

A

foamy cytoplasm

may be due to the processing of internalized materials w/ the help of enzymes present in lysosomes

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99
Q

Are there other immune cells in the lungs except for alveolar macrophages

A

no, unless there is a danger signal (bacteria) -> neutrophils

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100
Q

Surfactant

A

contained is osmiophilic lamellar bodies
reduce surface tension
allow alveoli to stay open

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101
Q

Epithelium of pleura

A

simple squamous epithelium (mesothelium) w/ underlying CT & vessels

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102
Q

Pleuritis

A

may result in pain & affected individuals could sense gliding of their lungs against the body wall in the affected area

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103
Q

Respiration processes involve

A

ventilation (movement of air)
diffusion
transportation
tissue delivery & return

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104
Q

At higher elevations, how does amount of air & % composition change

A

amount of total air decreases

% composition stays the same

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105
Q

Air composition at a higher altitude may accentuate certain pathological conditions or physiological performances like

A

patient w/ lung disease moved to a higher elevation may not be able to perform strenuous activities & experience breathing difficulties
healthy human/animal may have sub-optimal performances when moved to a higher elevation w/ less O2

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106
Q

Upper respiratory tract includes

A

nares, nasal conchae, pharynx, larynx, trachea, & principle bronchi

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107
Q

Species w/ most & least pliable nostrils

A

horse - most

pig - least

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108
Q

Function of upper respiratory tract

A

conditions air
warms it to body temp
entraps inhaled substances in mucus

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109
Q

Nasal conchae (turbinate bones) function

A 
create laminar (slow) slow
help trap dust
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110
Q

Other accessory structures of upper respiratory tract

A

auditory tube, guttural pouches, vomeronasal organ, nasolacrimal duct, & paranasal sinuses

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111
Q

As airways branch, what happens

A

total cross-section area increases & resistance to flow decreases

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112
Q

Ventilation definition

A

process of inhaling & exhaling air to acquire O2 & expel CO2

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113
Q

Ventilation is dependent on

A

pressure differences b/w atmosphere & inside of thoracic cavity

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114
Q

Neg pressure ventilation

A

created by respiratory muscles

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115
Q

Expiration is usually passive, but can be affected by

A

pathological conditions like heaves or physiological conditions like strenuous exercise
requires aid of abdominal muscles

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116
Q

Pos pressure ventilation

A

created by O2 devices used when anesthetizing an animal

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117
Q

VE = VT * f

A 
VE = total amount of air breathed per min
VT = volume of each breath during normal breathing
f = respiratory frequency; # of respiratory cycles per min
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118
Q

Dead space

A

no gas exchange
conducting portion
respiration wasted

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119
Q

Anatomic dead space

A

nostril, mouth, trachea, auditory tube, guttural pouches, & paranasal sinuses

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120
Q

Equipment dead space

A

endotracheal tube

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121
Q

Alveolar dead space

A

poor or no perfusion of alveoli

caused by hydrostatic pressure failure, embolus, emphysema, or pre-capillary constriction

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122
Q

Function of dead space

A

eliminates heat (panting in dogs)

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123
Q

Drawback of dead space

A

shallow & higher frequency breathing is not desired due to the increase in the amount of total ventilation wasted in the dead space
could lower the amount of effective gas reaching the alveoli

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124
Q

VEdot = VAdot + VDdot

A 
VEdot = tidal volume per min
VAdot = alveolar ventilation per min
VDdot = dead space ventilation per min
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125
Q

Primary symbols

A

physical quantities to be measured

uppercase

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126
Q

Name these primary symbols:

P, V, S, F, Q, R, & D

A 
P = pressure
V = volume
S = saturation w/ O2
F = fractional conc of gas
Q = blood volume
R = resistance
D = diffusing capacity
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127
Q

Secondary symbols

A

indicated location of gas

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128
Q

Name these secondary symbols:

a, V, & A

A 
a = arterial
V = venous
A = alveolar
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129
Q

Final symbol

A

refers to the gas being measured

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130
Q

Describe these symbol modifications:
dot above
bar secondary symbol
prime sign after secondary symbol

A

dot = quantity measured w/ respect to time
bar = mean or mixed sample
prime sign = end of a structure/ end of expiration or inspiration

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131
Q

Respiratory cycle

A

one inspiration & one expiration

except horses have two of each

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132
Q

Respiratory pattern waveform

A

smooth & symmetrical

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133
Q

Complementary breathing cycle (sigh)

A

deep rapid inspiration & expiration
not seen in horses
created using a breathing bag

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134
Q

Types of breathing

A 
abdominal = most common (except during peritonitis)
costal = rib movement (not during pleuritis)
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135
Q

Eupne

A

normal, quiet breathing

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136
Q

Dyspnea

A

difficulty breathing

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137
Q

Hyperpnea

A

increased depth & rate

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138
Q

Polypnea

A

rapid & shallow (panting)

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139
Q

Apnea

A

temporary cessation in breathing

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140
Q

Tachypnea

A

excessive rapidity of breathing

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141
Q

Bradypnea

A

abnormal slowness of breath

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142
Q

Respiratory frequency

A 
# of respiratory cycles/min
indicates health status of animal
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143
Q

What increases respiratory frequency

A

pregnancy, digestive tract fullness, lying down, & diseases

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144
Q

What decreases respiratory frequency

A

low temp & sleeping

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145
Q

Normal sound of lungs is due to

A

air movement through tracheobronchial tree (turbulent air flow)

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146
Q

Adventitious lung sounds are

A

extrinsic to normal breath sounds

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147
Q

Crackles

A

edema & exudates

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148
Q

Wheezes

A

airway narrowing

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149
Q

Lung volume

A

air w/in lung or breath

all are measured except residual volume (only assessed)

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150
Q

Tidal volume (VT)

A

volume of each breath

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151
Q

Inspiratory reserve volume (IRV)

A

extra volume that can still be inhaled after a normal breath (VT)

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152
Q

Expiratory reserve volume (ERV)

A

extra volume that can still be expired after a normal breath (VT)

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153
Q

Residual volume (RV)

A

amount of air remaining in lungs after most forceful expiration

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154
Q

Lung capacity

A

combination of volumes

all are inferred

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155
Q

Inspiratory capacity (IC)

A

VT + IRV

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156
Q

Functional residual capacity (FRC)

A

ERV + RV

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157
Q

Vital capacity (VC)

A

IRV + VT + ERV

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158
Q

Total lung capacity (TLC)

A

IRV + VT + ERV + RV
VC + RV
IRV + VT + FRC

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159
Q

FRC is affected by

A

position, sex, diseases, & body condition

only source of O2 during apnea

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160
Q

Ex of restrictive lung diseases & what they are characterized by

A

fibrosis, muscular diseases, sarcoidosis, & chest wall deformities
fibrotic processes in lung parenchyma -> restrictive inspiration

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161
Q

Volumes & capacities indicating restrictive lung disease

A

decreased VC, TLC, RV, & FRC

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162
Q

Ex of obstructive lung diseases & what they are characterized by

A

emphysema, chronic bronchitis, & asthma

inflammation of bronchioles & bronchiolar smooth muscle that contracts upon expiration -> restrictive expiration

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163
Q

Volumes & capacities indicating restrictive lung disease

A

decreased VC

increased TLC, RV, & FRC

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164
Q

Atmospheric pressure

A

760 mmHg at sea level

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165
Q

At higher elevations, why does atmospheric pressure decrease

A

less air

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166
Q

Gauge pressure

A

pressure measured against atmospheric pressure at a particular location

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167
Q

Absolute pressure

A

atmospheric pressure + gauge pressure

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168
Q

Dalton’s law

A

total pressure = sum of individual gases in a mixture

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169
Q

Boyle’s law

A

pressure & volume are inversely proportional

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170
Q

Charle’s law

A

w/ constant pressure, volume & temp are directly proportional

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171
Q

Moles law

A

at constant temp & pressure, volume of a sample of gas is directly proportional to the number of moles of gas in the sample

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172
Q

Ideal gas law

A

pressure is directly proportional to moles & temp of gas

pressure is inversely proportional to volume of gas

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173
Q

When PAW < PB, what happens

PAW = pressure w/in airways; PB = atmospheric pressure

A

air flows in until PAW = PB

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174
Q

When PAW > PB, what happens

PAW = pressure w/in airways; PB = atmospheric pressure

A

air flows out until PAW = PB

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175
Q

Breathing creates what pressure

A

neg pressure

176
Q

A ventilator creates what pressure

A

pos pressure

177
Q

Transpulmonary pressure gradient (PAW - Ppl) is important for what
(PAW = pressure w/in airways; Ppl = pressure in pleural cavity)

A

inspiration & expiration

if Ppl increases (ex: pneumonothorax), then lungs do not expand

178
Q

Function of thin film of fluid in pleural cavity

A

allows pulmonary/visceral pleura & parietal pleurato have a vacuum-like seal but still be able to slide

179
Q

How is neg pressure created in the pleural cavity

A

chest wall & alveoli try to recoil

180
Q

What happens to intrapleural pressure & alveolar transmural pressure during inspiration

A

intrapleural: becomes more neg

alveolar transmural: increases

181
Q

During inspiration, what do the alveoli do

A

expand so pressure w/in them decreases

air flows in until pressure w/in alveoli = atmospheric pressure

182
Q

What happens to intrapleural pressure & alveolar transmural pressure during expiration

A

intrapleural: becomes less neg

alveolar transmural pressure: decreases

183
Q

During expiration, what do the alveoli do

A

alveoli return to normal size by elastic recoil

air flows out until pressure w/in alveoli = atmospheric pressure

184
Q

What aides in lung recoil

A

elastic & collagen fibers

surface tension of alveolar fluid lining/ air-fluid interface

185
Q

When water molecules at the air-liquid interface pull towards each other to try to collapse the alveoli, what counteracts this

A

surfactant molecules cut the H bonds of water to nullify this effect due to surface tension

186
Q

Law of LaPlace states that what feature of alveoli should be true if they have a smaller diamter

A

have high pressure & thus be likely to empty or burst into a larger alveoli

187
Q

What keeps small alveoli from popping

A

surfactant molecules in a higher density compared to large alveoli, which helps to equalize the pressure

188
Q

Describe alveolar interdependence

A

recoil effect of surrounding alveoli can pull the collapsing alveoli back to stabilize it

189
Q

Alveolar interdependence is altered by what

A

emphysema since many alveoli are destroyed

190
Q

Compliance

A

opposite of elasticity

191
Q

What diseases affect compliance

A

emphysema: increases
fibrosis: decreases

192
Q

Poiseulle’s law

A

resistance is directly proportional to viscosity of gas & length of airway
resistance is inversely proportional to pi*r^4

193
Q

Compare pressure b/w pulmonary & systemic circulation

A

pulmonary < systemic

194
Q

Why is it advantageous that the pulmonary system has a lower pressure

A

less work for the heart
thin blood-gas membrane/ alveolar respiratory membrane can be protected
lower chance of edema

195
Q

Compare density of capillaries b/w pulmonary & systemic

A

pulmonary has a dense capillary network around alveoli

196
Q

Describe pulmonary vessels

A

neg pressure
sm amount of smooth muscle & vasomotor n’s
great distensibility & compliance

197
Q

Compare hypoxia in pulmonary vs systemic

A 
pulmonary = vasoconstriction (to redirect blood flow towards other alveoli that are well ventilated)
systemic = vasodilation
198
Q

Describe recruitment & distension

A

meets demand of increased blood through the lungs w/out an increase in arterial pressure
results in a decrease of pulmonary vascular resistance

199
Q

Why is the equation for pulmonary vascular resistance an estimation

A

blood is not a Newtonian fluid

pulmonary blood flow is pulsatile

200
Q

Alveolar vessels are found where

A

w/in wall of alveoli

201
Q

What happens to alveolar vessels as the alveoli expand

A

capillaries are crushed & pinched

202
Q

Alveolar vessels on pulmonary vascular resistance graph

A

high PVR from FRC -> TLC

203
Q

Extra-alveolar vessels are found where

A

in the corner of alveoli

204
Q

What happens to extra-alveolar vessels as the alveoli expand

A

get pulled open

205
Q

Extra-alveolar vessels on pulmonary vascular resistance graph

A

high PVR from RV -> FRC

206
Q

When is pulmonary vascular resistance the lowest

A

during FRC

207
Q

Hypoxic conditions affect pulmonary vascular resistance according to what relationship

A

directly proportional to the amount of smooth muscle present in the wall of the pulmonary art & branches

208
Q

Which species are more susceptible to hypoxic vasoconstriction

A

cattle & pigs

209
Q

Where is hypoxic vasoconstriction more likely to occur

A

high elevations

210
Q

Brisket edema is the word for hypoxic vasoconstriction in cattle due to high elevations; what are the clinical signs

A

right ventricular hypertrophy, dilation, & failure
distension of system veins & edema of brisket region
low exercise intolerance, tachycardia, jugular pulse, & pulmonic 2nd heart sound

211
Q

Brisket edema treatment

A

return to low elevation

O2 therapy

212
Q

Exercise induced pulmonary hemorrhage occurs when

A

horses exercise at a high intensity, which increases blood flow/ pressure & leads to RBCs entering the alveoli

213
Q

Treatment of exercise induced pulmonary hemorrhage

A

nasal strips - hold tissue around nasoincisive notch open so horse can breathe better, which decreases the pressure
furosemide - diuretic drug that decreases total body fluid & pressure exerted by flood flow

214
Q

Zone 1 where PA > Pa > Pv

A

no blood flow
seen w/ blood loss & +ve pressure ventilation
absent in healthy lungs

215
Q

Zone 2 where Pa > PA > Pv

A

optimal hydrostatic pressure w/ intermittent flow

216
Q

Zone 3 where Pa > Pv > PA

A

due to gravity, has continuous flow w/ distended capillaries

217
Q

When does pulmonary fluid clearance increase

A

exercise (increased lymph flow) or left sided heart ailure

218
Q

Steps leading to clinical edema

A

lymphatic capacity exhausted
proteoglycan bridges break
fluid enters alveoli & bronchioles

219
Q

Why is pulmonary edema fluid foamy

A

mix of air, edema fluid, & surfactant molecules

220
Q

Causes of pulmonary edema

A

decreased plasma oncotic pressure (hypoproteinemia/ inflammatory lung disease)
increased vascular permeability
inflammation
lymphatic obstruction

221
Q

Lung edema impedes what

A

ventilation & oxygenation

222
Q

Where is pleural fluid reabsorbed

A

through stromata (holes) on parietal pleura

223
Q

Hypoxia

A

specific region or whole body is deprived of O2 at the tissue level

224
Q

Hypoxemia

A

abnormally low level of O2 in the blood

225
Q

Hypoxemia results from

A 
hypoventilation
diffusion impairment
low P1O2/F1O2
R -> L shunt
VQ mismatches
226
Q

What happens in hypoventilation

A

alveolar ventilation rate decreases to an abnormally low rate, then PAO2 decreases & PACO2 increases

227
Q

Causes of hypoventilation

A

respiratory center depression (inflammation & morphine/barbiturates)
peripheral nerve injury (chest wall injury & dislocation of vertebrae)
neuromuscular disease
lungs resisting inflation (airway resistance, mucus, large endotracheal tube, dense gas, & deep diving)

228
Q

Hypoventilation A-a gradient & 100% O2 therapy

A

normal A-a gradient

responds to O2 therapy

229
Q

What happens in diffusion impairment

A

decreased diffusion leads to decreased oxygenation

230
Q

Causes of impaired diffusion

A

exercise
low P1O2 or low F1O2 (at high altitude)
abnormal lung (due to a pathogen) w/ a thickened alveolar gas-exchange area

231
Q

Diffusion impairment A-a gradient & 100% O2 therapy

A

increased A-a gradient

responds to O2 therapy

232
Q

Normal physiologic shunts

A

bronchial circulation

thebesian veins

233
Q

Pathological shunts

A 
arterial-venous anastamoses
absolute intra-pulmonary shunts
patent ductus arteriosus
foramen ovale
interventricular septal defects
234
Q

R -> L shunt A-a gradient & 100% O2 therapy

A

increased A-a gradient

does not respond to 100% O2 therapy

235
Q

Why do R -> L shunts not respond to O2 therapy

A

limit to amount of O2 that can be carried by Hb

236
Q

Normal lungs have an average V/Q ratio of .8 to 1.2, but certain parts of the lungs differ b/c why

A

gravity results in units w/ poor perfusion

low compliance of alveoli results in units w/ poor ventilation

237
Q

V/Q = 0

A

complete occlusion of an airway

shunt

238
Q

V/Q < .8

A

lungs are affected

239
Q

V/Q > 1.2

A

pulmonary vessels are affected

240
Q

V/Q = infinity

A

total occlusion of pulmonary circulation

dead space

241
Q

When are V/Q mismatches accentuated

A

under pathological conditions

242
Q

V/Q mismatch A-a gradient & 100% O2 therapy

A

increased A-a gradient

responds to O2 therapy

243
Q

Physiological response to V/Q mismatches

A 
hypoxic vasoconstriction
brisket disease
right side heart failure
pulmonary embolism
COPD
asthma
pneumonia
244
Q

Clinical intervention for V/Q mismatches

A

anesthesia

O2

245
Q

External respiration

A

exchange of O2 & CO2 at the alveolar respiratory membrane or blood-gas exchange area

246
Q

Internal respiration

A

individual cells of tissues that receive O2 & eliminate CO2

247
Q

Kinetic motion allows for what

A

diffusion of O2 & CO2

248
Q

What happens to gas at 0 K or -273 degrees C

A

no kinetic motion

gas volume = 0

249
Q

Composition of gas in the air

A 
N2 = 78%
O2 = 21 %
Ar = .93 %
CO2 = .3 %
250
Q

Air breathed in has what partial pressure once you take into account that the air is humidified

A

713 mmHg

partial pressure of H20 = 47 mmHg

251
Q

Partial pressure is dependent on

A

conc of dissolved gas

solubility coefficient

252
Q

Is CO2 or O2 more soluble

A

CO2

253
Q

Since O2 is less soluble, what is required for diffusion across the membrane

A

higher pressure gradient

254
Q

Under high pressure when scuba diving, N2 gets dissolved in the blood; if a diver comes up too quickly, what happens

A

N2 forms bubbles in various body tissues -> decompression sickness or bends

255
Q

When helium is mixed w/ O2, the air is lighter so there is less what

A

airway resistance

256
Q

Fick’s law of diffusion

A

diffusion coefficient is directly proportional to solubility & inversely proportional to molecular weight of the gas

257
Q

Area of diffusion is increased in what pathologic conditions

A

emphysema

258
Q

Thickness of diffusion barrier is increased in what pathologic conditions

A

sepsis, lung edema, & lung inflammation

259
Q

What effect does providing an increased % of O2 have on gas diffusion

A

increase P1; overcomes thickness of membrane

260
Q

RBCs spend .75 sec in the capillaries to get oxygenated, so any increase in thickness does what

A

increases the distance & tine of diffusion -> reduces oxygenation

261
Q

Hyperbaric O2 therapy involves what

A

O2 administered under high pressure (3-4 atms)

262
Q

Hyperbaric O2 therapy is useful for treating what conditions

A 
anaerobic bacterial infections
wound healing
stroke
heart conditions
CO poisoning
cerebral edema
gas embolism
bone infections
COPD
263
Q

Hyperbaric O2 therapy increases the dissolved fraction of O2 in the blood, which is important b/c

A

overcomes limitation of O2 carrying capacity of Hb by raising the O2 portion carried in the plasma

264
Q

Humidification is essential for what

A

getting inspired air ready for effective gas exchange

for upkeep of mucociliary function

265
Q

As body temp increases, what happens to vapor pressure & PO2

A

vapor pressure increases

PO2 decreases

266
Q

Why does water boil at decreased temps when there is increased elevation

A

decreased atmospheric pressure, so heat is able to counteract the atmospheric pressure faster

267
Q

Percent of O2 bound to Hb

A

98.5%

268
Q

Percent of O2 dissolved in plasma

A

1.5%

269
Q

Hemoglobin is the main component of RBC’s & has what components

A

1 globin

4 heme

270
Q

Globin in adult vs fetal

A

adult: 2 alpha & 2 beta chains
fetal: 2 alpha & 2 gamma -> greater affinity for O2

271
Q

Site for O2 binding on the heme

A

Fe2+

272
Q

Nitrate poisoning makes Hb unable to transport O2 by

A

converting Fe2+ -> Fe3+

273
Q

Carbon monoxide poisoning occurs b/c

A

CO occupies the same site as O2 & has 200 times greater affinity

274
Q

Treatment for CO poisoning

A

100% O2, CO2, & fluids

275
Q

O2-Hb binding is reversible & follows what law

A

law of mass action

276
Q

As O2 partial pressure increases, does O2 binding to Hb increase or decrease

A

increase

277
Q

Describe allosteric conformational change properties of Hb

A

once the 1st O2 binds, then it is easier for the rest of the O2 to bind

278
Q

O2-Hb saturation curve starts flattening at what saturation

A

90% saturation

279
Q

At normal PaO2 of 100 mmHg, Hb has what saturation

A

97.5% saturation

280
Q

PaO2 < 60 mmHg is considered hypoxemic b/c

A

this is 90% saturation

any decrease beyond this leads to a significant reduction in O2

281
Q

PaO2 = 25 mmHg has what saturation

A

50% saturation

282
Q

PvO2 = 40 mmHg has what saturation & occurs when

A

72-75% saturation; occurs in tissues under extreme exercise/ hypoxia conditions

283
Q

Each gram of Hb combines w/ how many mLs of O2

A

1.34 - 1.39 mL

284
Q

Why is a range given for the mLs of O2 that a fully saturated Hb holds

A

presence of impurities may result in lower O2 binding

285
Q

If patient becomes anemic due to a reduction in Hb conc, what happens to the O2-Hb curve

A

shape almost stays the same, but total O2 content will be reduced

286
Q

Right shift O2-Hb curve means

A

Hb affinity for O2 decreases

delivery of O2 is facilitated

287
Q

Left shift O2-Hb curve means

A

Hb affinity for O2 increases

delivery of O2 is difficult

288
Q

Bohr effect

A

increased PCO2 or decreased blood pH reduces the affinity of Hb to O2
right shift

289
Q

Why are pH & PCO2 related

A

CO2 can combine w/ H2O to produce H2CO3 & H

rxn is favored in RBCs b/c they have carbonic anhydrase

290
Q

2,3 DPG is a product of glycolysis w/in RBC’s that has what effect on the O2-Hb curve

A

right shift

291
Q

When does production of 2,3 DPG increase

A

in anemia & at high altitudes

292
Q

Effect of 2,3 DPG is reduced when blood is

A

stored

293
Q

Why must a CO-oximeter be used to diagnose CO poisoning

A

regular pulse oximetry does not distinguish b/w HbO2 & HbCO

294
Q

PaO2 levels may look normal w/ CO poisoning, but tissues still experience what

A

hypoxia

left shift

295
Q

O2 therapy can help treat CO poisoning b/c

A

O2 knocks CO off from Hb

296
Q

Why are fluids & 5% CO2 also necessary when treating CO poisoning

A

stimulate peripheral chemoreceptors to increase drive for ventilation
ensures that CO will be expired

297
Q

CO2 is produced where

A

in metabolizing tissues

298
Q

CO2 is removed b/c

A

high levels -> confusion, coma, death, & acidosis

low levels -> alkalosis

299
Q

Why is hydration rxn favored in RBCs

A

have carbonic anhydrase

300
Q

Acetazolamide, a carbonic anhydrase inhibitor, is used to treat

A

glaucoma & metabolic acidosis

301
Q

Why does Cl- move into RBCs after the hydration rxn occurs

A

to maintain electrical neutrality as HCO3- leaves

302
Q

H+ formed are buffered by

A

oxyhemoglobin

303
Q

CO2 is eliminated in the alveoli b/c of

A

partial pressure gradient

hydration rxn in reverse

304
Q

Modes of CO2 elimination

A

dissolved in plasma
transported as HCO3-
bound to hemoglobin
at lung alveoli

305
Q

Describe haldane effect

A

reverse of Bohr effect
for a given PCO2, the content of CO2 increases as PO2 levels decrease (loading of CO2)
as PO2 levels increase, CO2 delivery increases

306
Q

CO2 dissociation curve

A

steep
no cooperativity/ allosteric effect
lacks a plateau

307
Q

Acid

A

donate [H+] to soln

308
Q

Base

A

accept [H+] from soln

309
Q

Buffer

A

mix of weak acid & its conj base

310
Q

Strong acid/ base

A

dissociate completely in a soln

311
Q

Weak acid/ base

A

do not dissociate

312
Q

Relationship b/q pH & [H+]

A

inverse & exponential

313
Q

Acids/ bases made by the body

A

food, digestion, & cellular metabolism (CO2)

314
Q

Normal blood pH

A

7.35-7.45

315
Q

Acidemia

A

blood pH < 7.35

316
Q

Alkalemia

A

blood pH > 7.45

317
Q

Define acidosis/ alkalosis

A

physical processes & chemical rxns that progress into acidemia or alkalemia

318
Q

Normal PCO2

A

40 mmHg

319
Q

High PCO2

A

acidosis

320
Q

Low PCO2

A

alkalosis

321
Q

ATOT

A

total weak non-volatile acids

322
Q

High ATOT

A

acidosis

323
Q

Low ATOT

A

alkalosis

324
Q

High SID

A

alkalosis

325
Q

Low SID

A

acidosis

326
Q

Function of buffers

A

exchange strong acid or base for a weak one

help prevent deleterious effects of increased or decreased [H+]

327
Q

For Henderson-Hassalbalch eq, what do the kidneys/ lungs manage

A

kidney - base [HCO3-]

lung - acid PCO2

328
Q

Addition of a strong acid into a buffer yields

A

weak acid & salt

329
Q

Addition of a strong base into a buffer yields

A

weak base & water

330
Q

Bicarbonate buffer system (pK = 6.1)

A

NaHCO2 & H2CO3

independently regulated by lungs & kidneys

331
Q

Phosphate buffer system (pK = 6.8)

A

NaH2PO4 & Na2HPO4
major intracellular buffer
tubular fluid in kidneys

332
Q

Protein buffer sys (pK = 6.6 if ox & 8.2 if deox)

A

carboxyls give up H+ & amino groups accept H+

Hb has imidazole groups

333
Q

Anderson-Devenport nonogram

A

normal PCO2 line plotted w/ intersections at pH = 7.4 & HCO3- = 24 mEq/L

334
Q

Top left corner on Anderson-Devenport

A

respiratory acidosis w/ increased renal H+ excretion & retention of HCO3-

335
Q

Bottom left corner on Anderson-Devenport

A

metabolic acidosis w/ decreased PCO2 & H+

336
Q

Top right corner on Anderson-Devenport

A

metabolic alkalosis w/ increased PCO2 & H+

337
Q

Bottom right corner on Anderson-Devenport

A

respiratory alkalosis w/ decreased renal H+ excretion & retention of HCO3-

338
Q

Describe the central controller DRG

A

in dorsal medulla
inspiratory activity
basic rhythm of breathing

339
Q

Input & output for DRG

A

input: vagus & glossopharyngeal n
ouptut: phrenic n to diaphragm

340
Q

Describe the central controller VRG

A

in ventral medulla
expiratory & some inspiratory
inactive during normal, quiet breathing
active during exercise/ heaves

341
Q

Input & output for VRG

A

input & output: vagus n

innervates intercostal & abdominal m

342
Q

Function of pontine respiratory centers & their names

A

modify output of medullary centers

apneustic & pneumonotaxic center

343
Q

Location of pontine respiratory centers

A

pons & medulla

344
Q

Pontine respiratory centers input & output

A

input: chemoreceptors, lungs, cortex, & other receptors
output: diaphragm & respiratory m
Vagus n has neg feedback signals

345
Q

Apneustic center does what

A

stimulates inspiratory neurons of DRG & VRG

over-stimulation -> apneusis

346
Q

Pneumotaxic center does what

A

stimulates inhibitory signals to DRG & VRG
fine tunes inspiration & expiration
increased signals increases the respiration rate

347
Q

Central chemoreceptors are found where

A

ventral surface of the meddula

348
Q

Central chemoreceptors respond to what by doing what

A

pH of ECF or CSF
if decreased pH, then inspiratory neurons are stimulated
leads to increased tidal volume & frequency of breathing

349
Q

Peripheral chemoreceptors are found where

A

in carotid bodies at the bifurcation of common carotid art & aortic bodies near the aortic arch

350
Q

Carotid bodies are innervated by

A

glossopharyngeal n

351
Q

Carotid bodies are fast adapting receptors that respond to

A

decrease in PO2 & pH; increase in PaCO2

352
Q

Aortic bodies are baroreceptors that sense changes in

A

partial pressures of O2 & CO2

353
Q

Cell types in aortic bodies

A

Type I: contain dopamine

Type II: sustentacular/supporting

354
Q

Pulmonary stretch receptors are slow adapting & respond to what

A

increase in lung volume beyond a certain limit & inhibit inspiration (Hering-Breuer reflex)

355
Q

Irritant receptors in the airway epithelium are rapidly adapting pulmonary stretch receptors that respond to

A

gases, dust, & cold air

356
Q

Impulses from irritant receptors travel where

A

in vagus n to cause bronchoconstriction & hyperpnea

357
Q

J receptors are endings of non-myelinated c fibers in the wall of the alveoli that respond to

A

injected materials in pulmonary circulation

358
Q

Impulses from J receptors travel via what nerve, sense what, & result in what

A

vagus n
lung edema
rapid, shallow breathing & dyspnea

359
Q

Bronchial C fibers are similar to J receptors & are supplied by

A

bronchial circulation

360
Q

Bronchial C fibers lead to

A

rapid, shallow breathing, bronchoconstriction, & mucus

361
Q

Nose & upper airway receptors are found where

A

nose, nasopharynx, larynx, & trachea

362
Q

Nose & upper airway receptors respond to

A

mechanical & chemical stimuli w/ sneezing, coughing, & bronchoconstriction

363
Q

Joints & muscle receptors stimulate

A

ventilation

364
Q

Gamma system is found where & sense what

A

diaphragm & intercostals - sense elongation of muscle spindles

365
Q

How does the gamma system respond to elongation of muscle spindles

A

controlling the strength of contraction

important in sensing airway obstruction & efforts to overcome the resistance

366
Q

Increased arterial blood pressure leads to what responds in arterial baroreceptors

A

hypoventilation or apnea through stimulation of aortic & carotid sinus baroreceptors

367
Q

Decreased arterial blood pressure leads to what response in arterial baroreceptors

A

hyperventilation

368
Q

Pain leads to

A

apnea -> hyperventilation

369
Q

Heat leads to

A

hyperventilation

370
Q

Compare fetal to adult circulation

A

Fetal: parallel, mixing of arterial & venous blood, placenta for gas exchange, anatomic shunts, & increased Hb O2 affinity
Adult: in series, no mixing of arterial & venous blood, lungs for gas exchange, shunts are abnormal, & decreased Hb O2 affinity

371
Q

Describe gas exchange in the fetus

A

simple diffusion of simple molecules in the placenta

transfer of O2 depends on uterine arterial PO2 levels

372
Q

Placenta has passive & active transport

A

passive - glucose transport

active - AAs & ions

373
Q

Fetal Hb has a higher affinity for O2 than adult Hb; some species also have what in relation to Hb

A

higher Hb conc in fetal blood (human, sheep, & cows)

374
Q

Relative to body mass, fetuses have a higher cardiac output than adults, which helps to

A

deal w/ hypoxia

375
Q

Ruminant fetal Hb

A

increased O2 affinity is an intrinsic property

376
Q

Pigs & horses fetal Hb

A

do not have it

377
Q

Primates fetal Hb have the inability to do what

A

bind 2,3 DPG

378
Q

In fetal circulation, is blood flow increased in the placenta or the lung

A

placenta

379
Q

Pulmonary vascular resistance & Pa are higher in fetus or adult

A

fetus

380
Q

Fetal lung is in a psuedo-glandular stage at birth w/ what type of cartilage

A

eosinophilc hyaline cartilage (does not have proteoglycans like adult lungs)

381
Q

Important signals that a fetus experiences after birth

A

hypoxia & hypercapnia
fetus cools & fetal fluids evaporate
sensory input from mother

382
Q

Describe the first breath

A

great inspiratory effort
not all alveoli open at first
surfactant is important

383
Q

Carotid bodies in a newly birthed animal start to function & sense what

A

decrease in O2 & increase in PCO2

384
Q

As lungs expand in a newly birthed animal, pulmonary vascular resistance

A

decreases

385
Q

What vessels rupture upon birth

A

umbilical vessels

386
Q

When to fetal shunts close

A

aortic pressure > Pa & LA pressure > RA pressure

387
Q

Avian embryo is wrapped in

A

fetal membranes & chorioallantosis (CAM)

in contact w/ egg shell

388
Q

Egg shell internal & external sides

A

external: hard layer of CaCO3 coated by a thin cuticle
internal: two soft membranes

389
Q

What connects the environment w/ the CAM & what does it allow for

A

10,000 pores

diffusion

390
Q

As the embryo in the egg grows, what happens

A

increase in CAM
increase in O2 affinity for Hb
increase in cardiac output & hematocrit values
increase in diffusion gradient

391
Q

Heat stress in an egg leads to

A

hyperventilation & decrease in PCO2 -> decrease in HCO3- levels -> affects normal amount of CaCO3 -> poor eggshell quality -> dehydration of developing chick embryo

392
Q

Describe the trachea of birds

A

size & shape varies across species
full circular cartilage
hyaline cartilaginous rings appear as double rings (telescoping)
wider & longer than mammals, but resistance is about the same

393
Q

Large tracheal dead space is compensated by what in birds

A

1/3rd respiratory frequency
VT 1.7x larger
lg expansible volume
greater compliance of respiratory system (decreased work & energy of breathing)

394
Q

Birds lack an epiglottis & use what to produce sound

A

syrinx (instead of larynx)

395
Q

Describe the bronchial tree of birds

A

primary: extra pulmonary & intra pulmonary
secondary: 4 groups
tertiary: parabronchi

396
Q

Basic unit of gas exchange in the bird

A

parabronchi

397
Q

Air sacs are connected to what & function as

A

lungs & long (pneumatic) bones
bellows -> move air
do not exchange gas

398
Q

Lungs of birds are

A

fixed in dorsal part of the body & cannot expand

399
Q

Name the air sacs in birds

A 
2 cervical
1 clavicular
2 cranial thoracic
2 caudal thoracic
2 abdominal
400
Q

Describe neopulmonic parabronchi

A

in some species
accounts for 10-12 % of total lung volume if present
meshwork

401
Q

Describe paleopulmonic parabronchi

A

present in all birds
unidirectional air flow
always in contact w/ fresh air

402
Q

Each volume of air in birds w/ paleopulmonic parabronchi is

A

eliminated via 2 cycles of respiration

403
Q

Arrangement of capillaries in paleopulmonic parabronchi

A

air capillaries are surrounding by blood capillaries

404
Q

Paleopulmonic gas exchange is

A

cross-current & highly efficient as it allows for an increase in percent of O2 capture & elimination of CO2

405
Q

A thin blood-gas exchange area in paleopulmonic parabronchi is advantageous according to

A

Fick’s law

406
Q

Type IVc collagen in the basement membrane of paleopulmonic parabronchi provides what

A

strength needed to keep the thin gas exchange area stable

407
Q

Yaks live where O2 content is 33-66%, so they have what advantages

A

larger heart & lungs
persistence of fetal Hb
other genes for hypoxia & metabolism under low O2

408
Q

Yaks do not do well in

A

temps above 59 degrees C or elevations below 1000 ft

409
Q

How do fish breathe

A

using gills
extract dissolved O2 in water
countercurrent flow

410
Q

Mammalian diving reflex

A

bradycardia -> from 125 bpm to 10 bpm

peripheral vasoconstriction -> more blood can be used by heart & brain

411
Q

Diving adaptations of seals to manage the pressure changes

A

compliant chest
ability to collapse alveoli followed by terminal bronchioles
cavernous sinuses to prevent rupture of middle ear
presence of cartilage in bronchioles & sometimes alveoli to help in collapse/re-inflation of alveoli
specialized surfactants to make re-inflation easier

412
Q

Seals deal w/ N2 narcosis how

A

collapse lungs & hold air in dead space
switch to anaerobic metabolism
elastic aorta keeps blood pressure constant

413
Q

Other adaptations of seals

A 
aortic bulb & slender abdominal aorta
lg heart w/ glycogen store
increased muscle myoglobin
increase O2 in lungs, muscles, & blood
increased hematocrit values
lg spleen
lungs have great rigidity & elasticity
deep divers have small RV
414
Q

Name the 3 forces that affect the settling of particles

A

sedimentation
inertial force
Brownian motion

415
Q

Sedimentation

A

deposition due to gravity & mass of particles

go to nasal cavity & tracheobronchial tree

416
Q

Inertial force

A

due to velocity

go to nasal cavity, pharynx, & tracheobronchial tree

417
Q

Brownian motion

A

property of small particles

go to small airways & alveoli

418
Q

Respirable particles

A

less than 10 micrometers

could end up in blood-gas exchange area

419
Q

Non-respirable particles

A

more than 10 micrometers

retained in dead space & processed through the mucociliary escalator

420
Q

Upper respiratory tract clearance

A

for regions cranial to alveolar duct

mucociliary escalator pushes particles to the pharynx, which are then sent to the GI system & deposited in the feces

421
Q

Low respiratory tract clearance

A

for particles w/in alveoli
absorptive sites near alveolar ducts where particles accumulate & are cleared through lymphatics
fluid flow towards bronchiolar epithelium & cleared by mucocilary escalator
insoluble & microbial particles are phagocytized by alveolar macrophages
alveolar epithelial cells engulf particles & clear them through desquamation & mucociliary escalator
cleared to lymph nodes to be phagocytized

422
Q

Panting is a response to increased core body temp that does what

A

increases dead space ventilation to cool off

increases glandular secretions or vascular transudate

423
Q

Inhalation & exhalation through nose

A

least cooling
resting dogs
running at slow speed in cold temps

424
Q

Inhalation through the nose & exhalation through the nose & mouth

A

most cooling
exercise
resting at > 30 degrees C

425
Q

Inhalation & exhalation through the nose & mouth

A

greatest alveolar ventilation
exercise
resting at > 30 degrees C

426
Q

Purring results from

A

highly regular, alternating action of the diaphragm & intrinsic laryngeal m
frequency is 25x/sec
oscillating mechanism w/in CNS

427
Q

Phases of purring

A

glottal closing
initiation of glottal opening & sound production
complete glottal opening (decreases resistance & increases air flow)

428
Q

Purring may provide better ventilation during

A

shallow breathing

429
Q

Sneeze reflex

A

foreign objects/irritation of nose mucosa
strong inspiration & vigorous expiration through the nose
defensive

430
Q

Aspiration/sneeze reflex

A

foreign object/irritation of pharynx

series of inspiratory efforts (reverse sneezing)

431
Q

Swallowing reflex

A

food/drink pushes down on the soft palate
epiglottis bends to close the larynx
respiration continues once the bolus is in the esophagus

432
Q

Filtration of lungs

A

particulate matter & blood clots can be handled in the lungs

433
Q

Pulmonary intravascular macrophages

A

present in horses, cats, cattle, & pigs

increases susceptibility to pulmonary inflammation

434
Q

Lungs are a major source of arichiodonic acid metabolites, which are a site for

A

synthesis, metabolism, uptake, & release

435
Q

Angiotensin-converting enzyme is produced where

A

pulmonary epithelium
converts Angiotensin I -> Angiotensin II
maintains blood pressure

436
Q

Nonspecific lung defense mechanisms

A 
surfactant proteins A & D
host defense particles
mucociliary escalator
cough/sneezing
alveolar macrophages
TLRs
437
Q

Specific lung defense mechanisms

A

surface IGs
pulmonary dendritic & T cells
intranasal vaccines

Histology 2 (1 decks)

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