B4 CPR Pulmonology Flashcards

1
Q

respiratory epithelium contents

A

ciliated pseudostratified columnar epithelium
Goblet Cells

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2
Q

what structure is start of respiratory system

A

respiratory bronchiole

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3
Q

what part of nasal cavity lined with olfactory epithelium

A

superior conca

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4
Q

bronchus vs bronchiole

A

bronchus have cartilage

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5
Q

respiratory system 2 functioms

A

conducting
gas exchange

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6
Q

components of conduction portions of respiratory

A

seromucus & vascular network in lamina propria
vibrissae

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7
Q

fxn superficial vascular netwrok lamina propira

A

warm inspired air

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8
Q

fxn mucus & serous glands lamina propira

A

moisten inspired air

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9
Q

3 parts wall sx of respiratory

A

mucosa (epithelium & lamina propira)
submucosa (seromucous gland, smooth musc)
adventitia (outer layer)

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10
Q

5 cells respiratory epithelium

A

ciliated columnar
goblet
brush
basal
small granule

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11
Q

cytoskeletal structure for,s axoneme cilia

A

microtubules

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12
Q

Primary Cilia Dyskinesia/Kartagener’s syndrome

A

defective/absent dynein arms
prevent mucocilliary clearance
can be in all arms, outer or inner arms

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13
Q

Smoker respiratory epithelium changes

A

metaplasia to stratified squamous
decrease ciliated columnar cell
increase goblet cell

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14
Q

smoker melanosis

A

benign focal pigment of oral mucus from mutagentic chemical tobacco

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15
Q

Brush cells from what

A

microfilaments of akctin

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16
Q

brush cells receptor

A

chemosensory receptor
afferent nerve endings

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17
Q

basal cell fxn

A

undifferentiated stem cells

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18
Q

small granule cell names & fxn

A

Neuroendocrine, Kulchitsky
regulate bronchial & vascular muscle tone response to- hypoxia

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19
Q

what is only tissue type that increases in number as go down respiratory tract

A

elastic fibers (toward alveoli)

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20
Q

nasal cavities of lamina propira microorganisms

A

bind/inactivated by IgA in plasma cells

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21
Q

What does the nasal cavity mucosa contain to help warm, humidify, and clean inspired air

A

loop capillary
seromucus gland

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22
Q

what sx has lots of cartilage

A

larynx

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23
Q

Sx of trachea

A

C rings hyaline cartilage
relax in swallow
bifurcates to R & L primary bronchi

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24
Q

perichondrium

A

connective tissue layer lining both sides of the cartilage and contains its vascular supply and stem cell

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25
Q

major feature/fxn nasal cavity vestibules

A

Vibrissae
filter & humidify air

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26
Q

major feature/fxn nasal cavity

A

warm, humidify, clean air

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27
Q

major feature/fxn superior nasal cavity

A

solubize/detect odorants

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28
Q

major feature/fxn nasopharynx

A

conduct air to larynx, pharyngeal, palatine tonsils

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29
Q

major feature/fxn larynx

A

phonation

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30
Q

major feature/sx trachea

A

conduct air to primary bronchi of lung

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31
Q

R vs L primary bronchi

A

both have superior, secondary, tertiary bronchus
R bronchi has 3 lobes in R lung
L bronchi has 2 lobes in L lung

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32
Q

what is final part of conducting respiratory system

A

terminal bronchioles (from smaller generations of tertiary bronchi)

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33
Q

change in bronchi as they branch

A

progressiveky smaller

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34
Q

acute vs chronic bronchitits

A

acute = viral
chronic = smoking/pollutants, leave permanent change

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35
Q

subtype of non small cell lung cancer (85% all lung cancer)

A

Adenocarcinoma
Squamous cell carcinoma
large cell carcinoma

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36
Q

adeno carcinoma

A

non small cell, most common
from bronchiole glands & alveoli epithelial cells
well differentiated
from p53 mutate
rare metastasize, best prognosis

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37
Q

squamous cell carcinoma

A

non small cell
metaplasia of epithelium to stratified squaous epithelium (reversible)
can lead to dysplasia (irreversible)
makes keratin pearls
doesn’t spread normally

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38
Q

large cell carcinoma

A

non small cell
poorly differentiated
lack squamous/glandular morphology
grow faster/more than other nonsmall
clear in nucleus when stain
metastasize

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39
Q

small cell carcinoma

A

oat cell
smokers highly aggressive
metastasize far/wide very fast
neoplastic transformation of small granyle in bronchial respiratory epithelium
poor prognosis

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40
Q

bronchiole sx

A

no mucosal gland/cartilage
terminal bronchioles have ciiated simple columnar/simple cuboidal epithelium
start mucociliary appartays

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41
Q

significance mucociliary apparatus

A

trachea to bronchioles
inner lining of conducting airqay

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42
Q

parasympathetic response in terminal bronchioles

A

constrict

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43
Q

sympathetic response in terminal bronchioles

A

dilate

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44
Q

bronchiolitis

A

likely from RSV
very common babies/kids
old people with pre existing
inflammation of bronchial wall, epithelial necrosis

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45
Q

Which structures are lined by respiratory mucosa, with prominent spiraling bands of smooth
muscle and increasingly smaller pieces of hyaline cartilage?

A

bronchi

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46
Q

What are the last bronchiole branches that lack alveoli and are lined by simple cuboidal
epithelium consisting mainly of club cells with innate immune and surfactant secretory
functions

A

terminal bronchioles

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47
Q

terminal bronchiole division

A

respiratory bronchioles then branch into alveolar ducts that branch into alveolar sacs

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48
Q

atria sx

A

distal terminations of alveolar ducts
give rise to alveolar sacs

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49
Q

what are alveolar sacs

A

cluster of alveoli
very thin lamina propira

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50
Q

differemt anout lamina propira in alveoli

A

thin
elastic & reticular fibers
smooth muscle

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51
Q

3 components blood-air barrier

A

thin capillary endothelial cells
two attentuated thin cells line alveolus
fused basal laminae of thin cell with capillary endothelial cells

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52
Q

emphysema

A

destruction of interalveolar wall
reduce SA for gas exchange
common froim cigarettes

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53
Q

why does cigarette smoke cause emphysema?

A

inhibit a1AT (protect lung from elastase that marophages produce)
lungs are unable to recoil due to decrease elasticity

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54
Q

main components COPD

A

emphysema
chronic bronchitis

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55
Q

two cells of alveoli walls

A

type I (squamous) alveolar cells
type II (alveolar septal) alveolar cells

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56
Q

Ti alveolar cells

A

most of surface
minimal barrier that readily permeable to gas exchange

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57
Q

TII alveolar cells

A

cuboidal where septal walls converge
foamy appearance from lamellar bodies

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58
Q

lamellar bodies

A

organelles with phospholipid, glycosaminoglycabs, proteins

continuous secrete as pulmonary surfactant

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59
Q

function of lamellar bodies

A

post translational assemply/packing surfactant components
helps decrease surface tension in alveoli

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60
Q

incomplete differentation of TII alveolar cells & RDS

A

lead cause for infant respiratory distress
difficulty expanding alveoli
hyaline membrane disease as look glassy/protein rich when collapsed alveoli

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61
Q

alveolar macrophages/dust cell sx/fxn

A

darker from iron/erythrocytes
phagocytose erythrocyte from damaged capillaries/airboene particles
migrate to bronchioles to motor removal esophagus

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62
Q

dust cells = heart failure cells

A

in congestive heart failure
lungs congest with blood & phagocytozised
hemosiderin is chem rxn see occur

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63
Q

major fxn/sx bronchi

A

repeat branching
air deeper into lungs

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64
Q

major fxn/sx bronchioles

A

air conduction
help bronchoconstrict/bronchodikate

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65
Q

major fxn/sx terminal bronchioles

A

air to respiratory area lungs
exocrine club cells with protective/surfacant

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66
Q

major fxn/sx respiratory bronchioles

A

air deeper with gas exchange, protective/surfacant club cells

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67
Q

major fxn/sx alveolar sac/duct

A

conduct air
gas exchange

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68
Q

major fxn/sx alveoli

A

all gas exchange
surfacant TII dust celkl

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69
Q

path of sx from terminal bronchioles

A

to respiratory bronchioles
to alveoli ducts
to alveoli

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70
Q

what structure characterize TII alveolar with surfacant synthesis

A

lamellar bodies
mad of multivestibular bodies

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71
Q

what make regenerated epithelium

A

TII pneumocytes

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72
Q

blood circulation lungs consist of

A

pulmonary circulation (O2 poor)
bronchial circulation (O2 rich)

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73
Q

what structures accompany bronchial tree pulmonary circulation

A

pulmonary artery branches
respiratory bronchiole arterial branches give rise capillary networks in Intraalveolar septa
venules from capillary to small pulmonary veins

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74
Q

bronchial circulation blood path

A

from thoracic artery to bronchial arteries
branch in tree to anastamose with branch pulmonary artery
mix blood with cappilary netwroks

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75
Q

lymph drainage of lung

A

superficial near lung in visceral (parallel deep network)
deep lymph in CT (hilum nodes)

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76
Q

where are lymph vessels not foudn

A

past alveolar ducts

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77
Q

sympathetic NS lungs

A

from R & L sympathetic trunks
bronchodilation
vasoconstriction (increase ventilation-perfusion)
inhibit bronchial tree glands

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78
Q

parasympathetic NS lungs

A

R/L vagus nerves
bronchoconstriction
vasodilation

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79
Q

pleural fluid path

A

produce by parietal circulation
reabsord lymph system

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80
Q

inspiration

A

active
pressure in cavity decreases
contraction of muscle move cage up

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81
Q

expiration

A

passive
muscles relax
elastic tissue retract

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82
Q

blood path to lungs

A

sternal angle at 2nd rib trachea bifurcates
aortic arch
thoracic artery
bronchial artery

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83
Q

trachea location (spinal levels)

A

c6- T4/5
end at carina

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84
Q

what is carina

A

lowest cartilage ring of trachea
area of bifurcation

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85
Q

tracheal disorders & dyspnea

A

tracheal stenosis, tracheomalacia, foreign body aspiration

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86
Q

structural difference between R & L bronchi

A

R main bronchi is shorter, wider and vertical
L main bronchi is longer, narrower and horizontal

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87
Q

what bronchi most objects get stuck in

A

R bronchi almost always
lay Left recumbant as aspirate if on R

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88
Q

difference in lobes on Left side

A

cardiac notch for L side of heart
lingua

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89
Q

apex of lung location

A

2-3 cm above medial third of clavicle

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90
Q

anterior border lungs

A

behind sternum @ 2 costal cartilage then diverge @ 4 costal cartilage

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91
Q

lower border of lung location

A

6th rib midclavicular line
8th rib midaxillary line
10th rib paravertebra line
(chest tube 2 down from 10)

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92
Q

where does oblique fissure run

A

T4 posteriorly to 6th rib anteriorly

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93
Q

where does horizontal fissure run

A

around 4th intercostal

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94
Q

4 parts of parietal pleura

A

cervical
costal
diaphragmatic
mediastinal

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95
Q

innervation visceral pleura

A

vagus
insensitive pain

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96
Q

parietal pleura innervation

A

somatic nerevs
sensitive to pain

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97
Q

cupola

A

in pleural recess
@lung apex
vulnerable injury neck trauma

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98
Q

pancoast tumors

A

apical lung tumors in cupola

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99
Q

lay supine foreign body enters

A

the superior portion of right lower lobe
superior, posterior, medial

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100
Q

lay on R side foreign body enters

A

Right upper lobe
apical, posterior, anterior

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101
Q

upright, foreign body enters

A

lower portion of right lower lobe
medial basal, anterior basal, lateral basal, posterior basal

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102
Q

pulmonary vein clinical

A

need for afib treatment
diagnosing pulmonary veno-occlusive disease

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103
Q

bronchial circulation clinical

A

bronchial arteries enlarge in chronic lung disease
targets for embolism in sever hemoptysis

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104
Q

lymphatic drainage & lung cancer

A

carinal nodes enlargements
located in inferior tract of bronchiole, which makes this enlarged
when enlarged likely metastasized

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105
Q

pulmonary plexus

A

sympa & parasympa
@ root each lung

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106
Q

sympathetic lung nerve supply

A

upper thoracic sympa ganglia
T1-4
bronchodilator
vasoconstrictor

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107
Q

visceral afferent nerve lung

A

info about inflation & chemical irritation
send to central NS
doesn’t do pain

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108
Q

costal pleura innervation

A

supply by intercostal nerves

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109
Q

diapragmatic/mediastinal pleura innervation

A

phrenic nerve

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110
Q

auscultation upper lobes

A

anteriorly above 4th (R lung)
above 6th (L lung)

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111
Q

auscultation middle lobe/lingua

A

anterior between 4-6ribs

112
Q

auscultation lower lobes

A

posterior below scapular spine

113
Q

percussion thorax sounds

A

should be resonant, cardiac/liver dullness
hyperresonace is overinflation (emphysema/pneumothorax)
dullness (consolidation, pleural effusion, tumor)

114
Q

types pneumothorax

A

primary - spontaneous in healthy people
secondary - occur in people with underlying lung disease

115
Q

presentation of pneumothorax

A

chest pain, decreased sound, hyperresonance of percussion

116
Q

what can pneumothorax lead to

A

lung collapse

117
Q

COPD level of diagnosis

A

see 7th rib on xray

118
Q

active expiration muscles

A

contract abdomen to reduce vertical dimension
contract internal intercostal to decrease transver & anteroposterior dimension

119
Q

intrapleural pressure

A

made of parietal & visceral pleura pressures
should always be negative
only forced expiration makes positive pressure

120
Q

transpulmonary pressure

A

difference alveolar & intrapleural pressure
elastic nature
great pressure this is, larger lungs

121
Q

relationship of resistance, diameter, lymph, volume, pressure lungs

A

Resistance is proportional to lymph
Resistance & lymph inversely proportional to diameter
as diameter increases, velocity decreases
volume decreases, pressure increases + resistance increases

122
Q

decrease in lung volume causes

A

increase in resistance
increase in pressure

123
Q

resistance change of lungs to asthmatics

A

increase resistance due to increase muscle spasm this decreases volume

124
Q

ressitance change of lungs to bronchitis

A

increase resistance due to increase of mucus
air can’t move in or out

125
Q

intrapleural pressure change in exercise

A

heavy breathing out and faster
intrapleural pressure elevated
intraalveolar pressure elevated
resistance low

126
Q

pressure change in forced expiration

A

airway collapse, from constipation strain
both intraalveolar & intrapleural pressures increased
blocks air from expiring

127
Q

COPD airway collapse forced expiration

A

pressure drop magnified as increase resistance
intrapleural pressure higher due to emphysema as recoil decreased

128
Q

pursed lip breathing creates

A

high resistance @ mouth
raise airway pressure

129
Q

FEV1

A

forced expiratory volume in 1 second

130
Q

FVC

A

forced vital cpacity

131
Q

tidal volume

A

volume air in inhalation or exhalation

132
Q

functional residual capacity

A

expiratory reverse volume + residual volume

133
Q

residual volume

A

volume air in lung after forceful expiration

134
Q

total lung capacity

A

maximum volume lungs can expand with greatest effort
vital capacity + residual volume

135
Q

what would happen if puncture parietal pleura and cause pneumothorax

A

interpleural pressure no longer 0
collapsed lung as no P hold to chest wall
present with chest pain, SOB, tachycardia, cyanosis
puncture acts as a valve where air can only come in, nowhere for air to escape

136
Q

dead space

A

no gas exchange occurs here, about 150mls of air

137
Q

alveolar ventilation & dead space

A

when inhale always 150mL of dead air first
then come in fresh air
exhale out the old 150 first and new 150 stays stuck in dead space

138
Q

breathing pattern in exercise

A

deep, fast breaths
increased amplitude of breath
increased frequency of breath
don’t keep reserve air

139
Q

surface tension & pressure

A

increase pressure leads to increase of surface tension, decrease radius
smaller alveoli have greater surface tension (surfactant)

140
Q

law of laplace

A

collapsing pressure is directly proportional to surface tension & inversely proportional to radius of alveolus

141
Q

what phase of breathing are lungs more compliant

A

exhalation
decreasing the amount ofpressure change needed to move volume
lung wants to recoil and is getting to

142
Q

what phase of breathing are lungs less compliant

A

inhalation
need more pressure to move volume
lung wnats to recoil but forcing to expand

143
Q

excess H2O in lung causes

A

collapsed lung
if person has decreases in surfactant, this will occur as surface tension remains high (premie)

144
Q

saline filled vs air filled lung compliance

A

air filed lungs have larger increase of surface tension, which decreases compliance and need more pressure to fill

145
Q

lung compliance & emphysema

A

increased compliance
loss of elasticity means it is easier to stretch the lung and it doesn’t want to recoil

146
Q

lung compliance & fibrotic disease

A

reduce compliance
fibers want to stay close together & recoil which requires more pressure ot overcome and fill lungs

147
Q

components of compliance

A

lung compliance (alveolar-intrepleural pressure),, positive
chest wall compliance (intrapleural-atmospheric pressure),, negative

these pressures when balanced lead to good compliance as large volume changes will occur with small pressure changes

148
Q

passive resting point

A

balanced point of recoil and expansion forces

149
Q

FEV1 and normal parameters

A

forced expiratory volume in 1 second
80% of vital capacity

150
Q

obstructive lung diseases measure/character

A

partial/complete obstruct
normal TLC (tot lung capacity)
normal FVC (forced vital capacity)
Decrease FEV1 (forced expiratory volume 1 sec)

151
Q

restrictive lung diseases measure/character

A

decreased TLC (total lung capacity)
reduced FVC (forced vital capacity)
reduced/normal FEV1

152
Q

when to measure peak expiratory flow

A

maximally forceful & rapid exhalation that immediately follows maximal inhalation

153
Q

where in flow volume loop would you see if there’s an obstruction

A

at the peak wxpiration flow rate
should be rapid rise then linear fall in flow

154
Q

obstructive pattern flow-volume loop

A

scoop out of expiration
increased lung volumes (take longeras increased resistance)

155
Q

restrictive pattern

A

witches hat
refduced flow rate
reduced lung volume

156
Q

humid air effect partial pressures

A

decrease partial pressures

157
Q

3 reasons alveolar gas pressures differ from atmospheric pressures

A

alveoli air saturatted with water vapor (decrease partial pressure)
mix of fresh air with high CO2/low O2 air from dead space
continual exchange of gases continually between alveolar air and capillary blood

158
Q

Why is hypoxia likely to occur faster than blood alkalosis

A

CO2 twenty times more soluble in blood than O2
likely to have higher partial pressure of CO2 as higher concentration

159
Q

henry law

A

concentration of gas in liquid is proportional to partial pressure

160
Q

Determinants of Diffusion/Fick’s Law

A

pressure gradient
surface area
distance
fixed solubility

161
Q

why does blood CO2 levels reach equilibrium faster than O2

A

20x more soluble
dfiffusion only occures until reach equilibrium

162
Q

PIO2

A

pressure of Inspired Oxygen

163
Q

3 factors affect gas exchangne

A

partial pressure gradients/gas solubility
alveolar ventilation/pulmonary blood perfusion match
presentation of pathological changes respiratory membrane

164
Q

what pathological changes can affect gas exchange

A

fibrosis (decrease in surface area, restrict from exchanging gas)
emphysema (decrease in surface area, volume incerase)
Diffuse alveolar hemorrhage/ goodpasture synfrome (decrease surface area in basement membrane)

165
Q

high altitude affect gas exchange

A

decreased partial pressure of O2
low pulmonary alveolar pressure of O2
decrease gradient
decrease diffusion
decrease gas exchange

166
Q

what is carbon monoxide diffusing capacity clinically useful for

A

test TLC, RV, FRC which can’t be tested by spirometry
help distinguisb between emphysema & asthma

167
Q

A-a gradient

A

from Alveolar to arterial difference of O2
5 mmHg normal

168
Q

PAO2

A

alveoli end of capillary blood

169
Q

PaO2

A

arterial end of capillary blood

170
Q

FiO2

A

fraction of inspired oxygen
% of oxygen in the inspired air

171
Q

D-O

A

oxygen diffusing capacity

172
Q

when is there reduced oxygen diffusing capcity in lung

A

pulmonary edema
pneumonia
fibrosis pulmonary fibers
less O2 in the alveoli than in blood as less time to equilibriate with capillaries

173
Q

common pathologies fro R to L shunt

A

patent foramen ovale
atrial nseptal defect
ventricular septal defect
PE
congenital heart disease
pericardial tamponade

174
Q

what do R to L shunts cause

A

hypoxia
skip capillary so not exchange of gasses

175
Q

infinite V/Q

A

dead space
no gas exchange occurs here (PE)
Ventilation occurs
blood perfusion not occurring
hypoxia

176
Q

0 V/Q

A

R-L shunt
only perfusion (blood)
no ventilation
hypoxemia (low PaO2)

177
Q

PCO2 and PO2 in R-L shunting

A

high PCO2
low PO2

178
Q

PCO2 and PO2 in dead space

A

high PO2
low PCO2

179
Q

what does PACO2 come from

A

tissue metabolism
ventilation match metabolism, PA CO2 is constant

180
Q

in nornmal person what is alveolar PO2 equal to

A

pulmonary arterial PO2

181
Q

in normal person what is alveolar PCO2 equal to

A

pulmonary arterial PCO2
systemic arterial PCO2

182
Q

hyperventilation PACO2

A

PACO2 < 40

183
Q

hypoventilation PACO2

A

PACO2 > 40

184
Q

relationship alveolar PO2 & PCO2

A

inversely related

185
Q

Very low pressures in pulmonary circulation due to

A

low resistance
increased surface area

186
Q

hypoxic vasoconstriction

A

not to perfuse non-ventilated alveolus
body need oxygen, won’t perfuse an area that has no oxygen

187
Q

zone 1 blood flow & driving pressure

A

lowest blood flow
alveolar (PA) > arterial (Pa) > venous (PV)
capillaries collapse

188
Q

zone 2 blood flow & driving pressure

A

medium blood flow
arterial (Pa) > alveolar (PA) > venous (PV)
in systole capillaries are open
in diastole capillaries are closed

189
Q

zone 3 blood flow & driving pressure

A

highest blood flow
partially due to gravity
arterial (Pa) > venous (PV) > alveolar (PA)
diastolic pressure greater than alveolar so continuous flow

190
Q

ventilation/perfusion ratio

A

gravity make intrapleural pressure less negative @ base
greater complinace
more ventilation so smaller ratio
less oxygenated blood

191
Q

local controls of CO2 & O2

A

CO2 is bronchiolar smooth muscle regulator
O2 is arteriolar smooth muscle regulator

192
Q

blood flow & exercise

A

increase blood flow all areas
bottom lung more perfusion still

193
Q

CaO2

A

arterial oxygen content

194
Q

how long does it take for oxygen to equilibriate across capillary

A

0.75s

195
Q

what is tissue PO2 determined by

A

rate of O2 transport to tissues in blood
rate of O2 use by tissues

196
Q

what happens to flow if hemoglobin present

A

the Oxygen binds to heme first and then will go into the alveolar flow

197
Q

change of tissue PO2 with normla metabolism, increase flow

A

higher PO2 at eqilbm

198
Q

change of tissue PO2 with increased metabolism, normal flow

A

decreased PO2
consume oxygen faster

199
Q

change in metabolism affect carbon dioxide diffusion

A

increase metabolism increase CO2
decrease metabolism decrease CO2

200
Q

what type of gas causes partial pressure

A

free, dissolved gas

201
Q

what does CaO2 represent

A

absolute quantity of blood
content of arterial with both the free disolved oxygen & molecular

202
Q

oxygen cooperativity

A

more O2 binds, O2 affinity increases
more O2 releases, O2 affinity decrease

203
Q

hemoglobin & pulmonary capillaries

A

Hb almost fully saturated
O2 binds to Hb before dissolve in fluid

204
Q

hemoglobin & systemic capillaries

A

Hb has increased unloading
small decline of blood PO2

205
Q

how does CaO2 change with increase RBC

A

increases
increase in hemoglobin causes increase O2
(polycythemia)

206
Q

Bohr Effect

A

how CO2 and pH affect O2 affinity
oxygen dissociation curve right to unload oxygen into tissue
decrease pH/increase CO2 causes more offload

207
Q

temperature & O2 affinity

A

increase temperature increases pH. forcing offload

208
Q

shift oxygen dissociation curve lung vs tissue

A

are opposites
right shift @ tissue = left shift @ lung

209
Q

hypoventilation changes PACO2, A-aO2, FIO2 response

A

PACO2 increase
A-aO2 gradient normal
FIO2 response increases

210
Q

decrease barometric pressure changes PACO2, A-aO2, FIO2 response

A

PACO2 decreases
A-aO2 gradient normal
FIO2 response increases

211
Q

R-L shunt changes PACO2, A-aO2, FIO2 response

A

PACO2 normal
A-aO2 gradient increases
FIO2 decreases

212
Q

V/Q mismatch changes PACO2, A-aO2, FIO2 response

A

PACO2 normal
A-aO2 gradient increases
FIO2 increases

213
Q

diffusion limitation changes PACO2, A-aO2, FIO2 response

A

PACO2 normal
A-aO2 gradient increases
FIO2 increases

214
Q

high altitude affect alveolar PO2

A

decrease

215
Q

high altitude affect ventilation

A

causes hyperventilation
decrease PaCO2

216
Q

high altitude affect arterial blood

A

increase pH causing respiratory alkalosis
decrease PaCO2

217
Q

high altitude affect pulmonary blood flow

A

increase pulmonary resistance (low PO2 leads to constriction)
increase pulmonary artery pressure

218
Q

high altitude affect O2 hemoglobin curve

A

shift curve to R as increase RBC
decrease affinity for O2

219
Q

high altitude affect erythropoietin

A

a kidney hormone in hypoxemia
decrease PaO2
hypoxia

220
Q

CO poisoning change dissociation curve

A

CO bind to hemoglobin and causes a lack of oxygen in the tissue
this increases oxygen affinity for hemoglobin further limiting O2 tissue

221
Q

Haldane effect

A

removing O2 from Hb increases Hb able pick up CO2

222
Q

Bohr effect

A

influence of CO2and H+ on release O2

223
Q

diffusion limited gas exchange

A

total amount of gas transported limited by the partial pressure gradient
CO don’t equilibriate at end of capillary

224
Q

perfusion limited gas exchange

A

partial pressure not maintained
regulated by blood flow
not much perfusion occur

225
Q

what type of limit on N2O

A

perfusion limited
partial pressure equilibriate with alveolar pressure

226
Q

what type of limit CO2 and O2

A

perfusion limited
low PO2 gradient

227
Q

what type of limit CO

A

diffusion limited
PCO don’t equilibriate with alveolar pressure

228
Q

type of limit on O2 in fibrosis

A

alveolar wall thickens
increase diffusion distance so diffusion limited

229
Q

type of limit of O2 in strenuous exercise

A

diffusion limited as less O2 going to pulmonary more in tissues

230
Q

type of limit of O2 in high altitude

A

diffusion limited
reduced partial pressure gradient for O2 mean equilibriate slower

231
Q

What is unilateral renal agenesis?

A

Failure of the Ureteric Bud and Metanephric Blastema to produce a kidney on one side. The intact kidney typically undergoes hypertrophy as a compensatory mechanism.

232
Q

What is bilateral renal agenesis?

A

Generally not seen congenitally as it is lethal in utero.

233
Q

What is renal dysplasia?

A

The kidney develops but there is malformation of the nephrons due to genetic mutations disrupting molecular signaling mechanisms.

234
Q

What are Congenital Polycystic Kidney Diseases?

A

Genetic mutations, either autosomal dominant or recessive, disrupt nephron structural development or cellular functions (e.g. ion channels, cilia in epithelial cells).

235
Q

What are Wilm’s tumors?

A

A spectrum of nephroblastoma tumor types that appear by age 4, involving defects in nephron development and mutations in tumor suppressor genes.

236
Q

What are renal tumors?

A

Various types can originate from different cell types.

237
Q

What is a double-ureter?

A

A condition where either complete or partial duplications of ureters are possible.

238
Q

What is the primary functional problem associated with double-ureter?

A

One of the ureters can have an ectopic distal drainage point, leading to improper waste drainage.

239
Q

What are potential fistula sites in double-ureter?

A

Fistula sites can be the urethra, vagina, or vestibule (also in females).

240
Q

Relationships right and left kidneys

A

right more inferior than left
Move rhythmically with breathing

241
Q

Posterior position kidney significance

A

Allow for posterior surgical access
Hard to approach anterior due to fat

242
Q

3 most likely locations for constriction/lodge kidney stones

A

Renal pelvis
Cross iliac arteries
Piece wall bladder

243
Q

Blood flow through nephron

A

Filtered at glomerulus into glomerular capsule
Fluid move from capsule into proximal convuluted tubule, defend limb, ascend limb, distal convuluted tubule, collecting duct, papillary duct, minor calyx, major calyx, renal pelvis, ureter

244
Q

Blood flow through kidney

A

Start I. Afferent arteriole
Goes to capillaries in glomerular
Flows out of efferent arteriole

245
Q

Blood supply for adrenal areteries

A

Superior and middle suprarenal arteries from aorta
Inferior renal artery from renal artery

246
Q

Sympathetic innervation kidney arteries

A

Mostly lesser sphlancnic nerve from T10-12

247
Q

Parasympathetic innervation kidney artery

A

None from vagus
All indirect

248
Q

Dermatome pain kidney

A

L1-2 and T11-12
Low back pain

249
Q

Adrenal medulla cells

A

Act as post ganglionic sympathetic neurons
Release NE/E
Innervated by pre-ganglionic via greater splanchnic nerve

250
Q

Adrenalblood vessel innervation

A

Sympathetic via greater sphlancnic to celiac ganglion
Post ganglionic neurons from celiac to blood vessels (in smooth muscle)

251
Q

What is antibody-mediated glomerulonephritis?

A

It is an autoimmune attack against an antigen in the basement membrane.

252
Q

What happens if antibodies cross-react with antigens in the alveolar basement membrane?

A

It leads to Goodpasture Syndrome.

253
Q

What is the consequence of inflammatory damage to the glomerulus?

A

It impairs filtration.

254
Q

What is Diabetic Nephropathy?

A

Thickening of basement membrane and arteriosclerosis, progressive failure of renal function.

255
Q

What causes Sickle Cell Nephropathy?

A

Due to reduced oxygen in vasa recta of renal medulla, normal erythrocytes convert to sickle shape, occlude blood flow, induces ischemic damage.

256
Q

What is Pyelonephritis?

A

Inflammation and neutrophil accumulation in collecting ducts.

Secondary to bacterial infection via urinary tract.

257
Q

What is Cystitis?

A

Inflammation of bladder mucosa due to infection.

258
Q

What is Bladder cancer?

A

Proliferation or instability of urothelium.

259
Q

What is Urethritis?

A

Inflammation due to infection, typically Chlamydia.

260
Q

Where does each collecting duct of kidney drain into

A

Papillary duct, minor calyx, major calyx, renal pelvis, ureter

261
Q

Contents of renal corpuscle

A

Glomerulus (capillary)
Capsular space (bow,an space where form urine)

262
Q

Contents of glomerular capsule

A

Bowman capsule & epithelial celss

263
Q

Contents of glomerular capsule

A

Bowman capsule & epithelial cells

264
Q

Blood filtration through glomerulus

A

Lumen of capillary to Bowman space to proximal convoluted tube through me[horn to urine

265
Q

Structural elements of blood filtration

A

Fenestrated glomerular capillary, basement membrane, podocytes

266
Q

Structural elements of blood filtration

A

Fenestrated glomerular capillary, basement membrane, podocytes

267
Q

Filtration step nephron

A

Basal laminate traps substances, prevent into capsular space
Podocytes (become pedicles) surround capillary to further fikter

268
Q

Normal urine content

A

Low protein concentration, no cells
If high protein shows problem with filtration

269
Q

What is first structure affected by low BP in kidneys

A

Afferent arterioles

270
Q

Justaglomerular cells

A

Sensory cells that detect arterial blood pressure

271
Q

Response to deceased BP in kidney

A

JG cells detect change
Secrete renin which activates forming angiotensin
Angiotensin is vasoconstrictor to increase BP

272
Q

Macula Densa job

A

In distal convoluted tubule (near afferent arteriole)
Monitors Na and regulate it through transporters

273
Q

Macula Densa in reduced BP

A

Detects lack of Na
Releases chemical signals to JG
Activate renin release to increase BP

274
Q

Mesangial cells locations and function

A

Inside glomerulus
Phagocytosis and endocytic between extraglomerular arteriole and intreaglomerukar
Helps increase pressure by contraction and structure repair in capillary

275
Q

Functions of intraglomerular mesangial cell

A

Surround capillary
Phagocytose
Repair
Constriction