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Pathophysiology > Lungs > Flashcards

Lungs Flashcards

1
Q

COPD

A
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2
Q

Asthma

A
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3
Q

CAP- community acquired pneumonia

A
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4
Q

Acute Bronchitis

A
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5
Q

conducting airways

A

nasopharynx;
oropharynx
trachea
bronchi
bronchioles
air is inspired /expired out thru these

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6
Q

gas exchange

A

in alveoli and alveolar ducts
called the ACINUS

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7
Q

alveoli

A

primary gas exchange area of the lung

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8
Q

alveolocapillary membrane

A

membrane that surrounds each alveolus and contains the palm caps

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9
Q

pulmonary circulation

A

perfuses the gas exchange airways

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10
Q

bronchial circulation

A

perfuses the bronchi and other lung structures

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11
Q

Innervation of pulmonary system

A

ANS

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12
Q

vasodilation
vasoconstriction

A

controlled by local/humoral
arterial o2 and A/B balance.

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13
Q

parietal pleura

A

serous membrane lines the chest wall

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14
Q

visceral pleura

A

encases lungs

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15
Q

pleural space

A

where 2 pleura contact and slide over each other

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16
Q

diffusion

A

passsive
o2 into blood
Co2 out of the blood

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17
Q

ventilation

A

the process of air moving into and out of gas exchange airways

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18
Q

Chemoreceptors

A

in the circ system and brainstem sense effectiveness of ventilation
pH of CSF
02 of of arterial blood

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19
Q

surfactant

A

produced by type 2 alveolar cells
decreases surface tension
lets alveoli expand as air enters

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20
Q

elastic recoil

A

tendency of lungs and chest wall to return to resting state after inspiration

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21
Q

compliance

A

measure of lung and chest wall distensibility
volume change per unit of pressure change.

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22
Q

Gas Transport

A

depends on :
-ventilation of alveoli
-diffusion across th alveolocapillary membrane
-perfusion of pulm and systemic caps
-diffusion between caps and tissue cells

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23
Q

efficient gas exchange

A

Depends on :
even distribution of ventilation and perfusion
greatest at bases of lungs bc the alveoli are more compliant & perfusion is greatest at bases d/t gravity

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24
Q

02 transportation in cap blood

A

hemoglobin
rest dissolved in plasma

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25
Q

dyspnea

A

subjective difficulty breathing

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26
Q

cough

A

reflex initiated by stimulating irritant receptors in bronchi

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27
Q

Hemoptysis

A

bloody sputum
frank blood

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28
Q

kussmaul respirations

A

hyperpnea
inc vent rate
large tidal vol
no expiration pause

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29
Q

eupnea

A

normal breathing

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30
Q

large airway obstruct

A

inc vent
inc tidal vol
inc effort \stridor/wheeze
prolong I & E

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31
Q

Small AW obstruct

A

copd/asthma
dec vent rate
dec tV
inc effort
wheeze
prolonged Expiration

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32
Q

pulminary fibrosis

A

stiff lung wall /dec compliance
dec TV
tachypnea

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33
Q

tachypnea

A

increase in breathing rate

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34
Q

restricted breathing

A

tachypnea
small TV
decreased compliance

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35
Q

Cheyene-stokes breathing

A

cerebral hypoxia
shock
reduced blood flow two brainstem
irregular breathing - deep and shallow
apnea/ deep breaths

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36
Q

hypoxia

A

insufficient oxygen in brain and peripheral tissue

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37
Q

hypoventilation

A

inadequate alveolar ventilation
in relation to metabolic demands.
minute vol decreased ( TV X RR)
too much co2, removal doesn’t keep up with production
don’t notice until severe, confusion, tiredness.

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38
Q

hypercapnia

A

too much PCO2 in arterial blood
resp acidosis

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39
Q

hyperventilation

A

alveolar vent exceeding metabolic demands
co2 removed too fast
resp alkadosis
anxiety
head injury pain
in response to hypoxia
hypocapnia

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40
Q

hypocapnia

A

dec PaCO2
resp alkadosis

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41
Q

cyanosis

A

blue skin and MM
desaturated hemoglobin
peripheral vasoconstriction , blood not circulating .
peripheral- finger nails
central -lips/mm
only present in serve hypoxemia

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42
Q

clubbing

A

selective bulbous enlargement of end of finger
chronic dec pulm circ and hypoxia
painless
cystic fibrosis
heart disease
permanent
megakaryctes plug up fingers

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43
Q

pain

A

Plura
airways and chest wall

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44
Q

pleurodynia

A

pain from pulm dx
pleura stretching during inhalation
plural rub
common with pulm infarction /PE

45
Q

hypercapnia

A

increased p CO2

hypovent alveoli
inc CO2 in arterial blood
co2 easy diffuses from blood to alveolar space
resp acidocis that may lead to heart arrhythmias
high co2 leads to cerebral oedema
leads to decreased tissue o2

46
Q

Hypercapnia causes

A

D/T decreased drive to breath or can’t respond to vent stimuli
medications depress resp center
disease of MEDULLA
spinal cord injury
dis of neuromuscular junction - MG or MD
thoracic cage changes
large AW obstruction - tumours /apnea
emphysema - increased work of breathing

47
Q

hypoxemia

A

reduced oxygenation of arterial blood caused by resp changes

48
Q

hypoxia/ischemia

A

reduced oxygen in cells of tissues

49
Q

hypoxemia causes :

A

prob with oxygenation
to alveoli
o2 from alveoli to blood
V/Q mismatch
perfusion of pulmonary caps

50
Q

PaO2

A

amount of 02 in alveoli
-need enough o2 in air 21%
-minute volume( Tv x RR) , hypo vent dec it
compensate by changing rate and depth of breathing

51
Q

diffusion from alveoli to blood
factor 1

A

v/q
v=amount ofd air that enters alveoli
q=amount of blood perfusing capillaries.
V/Q probs most common cause of hypoxemia
0.8
most common cause of high VQ is PE

52
Q

shunting

A

areas with no ventilation are vasoconstrictor. and left to right shunt occurs , decreased o2 in body

53
Q

alveolar dead space

A

ventilated but not perfused.

54
Q

diffusion from alveoli to blood
factor 2

A

alveolocapillary membrane
dec 02 diff is thick or surface area I decreased.
edema/fibrosis
destruct of alveoli -emphasyma

55
Q

hypercapnia

A

not impacted by impaired diff because CO2 diffuses easily av to caps

56
Q

hypoxemia

A

heart problems shunting blood away from lungs
hyper vent
increased ph

57
Q

acute respiratory failure

A

inadequate gas exchange
Pa02 >= 60mm hg
PaCO2>= 50 mmhm
ph<=7.25

58
Q

acute respiratory failure

A

if from hypercapnia usu inadequate alveolar vent
need to assist with ventilation

59
Q

acute respiratory failure

A

from hypoxemia
inadequate O2 xc between alveoli and caps
give oxygen
sometimes a combo of both

60
Q

Chest wall restriction

A

deformations increase work of breathing
decreased tidal volume
at risk for infection and failure
neuromuscular- muscular dystrophy , hypovent hypoxia

61
Q

flail chest

A

fracture of sternum and ribs
paradoxial mmt , impairs gas movement in/out of lungs
decrease in Tidal vol , inc resp rate to compensate

62
Q

pneumothorax

A

air or gasin pleural space d/t rupture in visceral pleura ( around lungs ) priatatl pleura or chest wall
can’t recoil properly and collapses around hilus

63
Q

primary pneumothorax

A

spontaneous
men 20-40
rupture of blebs on visercal pleura
genetic

64
Q

secondary pneumothorax

A

injury
etc

65
Q

pneumothorax

A

open( air in/out with breathing ) or tension ( more dangerous) air only comes in on inspiration , builds up , compression injury atelectasis
and moves heart etc
severe hypoemia
aspirate it

66
Q

pneumothorax S&S

A

pleural pain
tachypnea
dyspnea

67
Q

pleural effusion

A

fluid in pleural space
from blood vessels or lymph or abscess
transdudative- watery
exudative ( WBC , plasma proteins ) pus blood chyle ( milk lymph & fat )
similar s& S to pneumothorax
plural friction rub

68
Q

empyema

A

infected pleural effusion
pus
pulm lymphatics get blocked
from pneuma , surgery ,tumour staph a , e-coli , pleb pneumo
fever, cyanosis , tachycardia, cough and pleural pain

69
Q

restrictive lung diseases

A

aspiration
atelectasis
bronchiectasis
bronchiolitis
pulmonary fibrosis
inhalation disorders
pulmonary edema
acute lung injury/ARDS
asthma
copd
chronic bronchitis
emphysema

70
Q

restrictive lung diseases

A

dec compliance of lung tissues
more work in inspiration
more work to breath

dyspnea
inc rate
dec TV

dec in FVC
V/Q mismatch
impact alveolocap membrane- decrease diffusion of 02 from alv to blood

hypoxemia

71
Q

Aspiration

A

fluid/solids into lung
poor cough /swallow reflex

Right lung more susceptible d/t gravity and straightness of bronchus
cause airway collapse
pneumonia
hemmmorage in lung
hypo vent may lead hypotension

72
Q

Aspiration

A

S& S
chocking/cough
fever
dyspnea
wheezing
no symptoms just get recurrent infections, cough etc
treat with o2
vent
corticosteroids
fluid restriction to dec edema

73
Q

atelectasis

A

collapse of lung tissue
3 types :
compression
absorption
surfactant impairment

often with surgery

74
Q

atelectasis compression

A

external pressure - fluid , tumour air in pleural; space , abd distension

75
Q

atelectasis absorption

A

remove air from obstructed alveoli
or inhaled o2 or anaesthetic agents

76
Q

atelectasis surfactant impairment

A

decreased prod of surfactant
(prevents lung collapse during EXPIRATION)

77
Q

Bronchiectasis

A

dilation of bronchi
caused by lots
primary see chronic productive cough
LRTI, tons of gross sputum
cough blood , clubbing
cor pulmonaire

78
Q

bronchiolitis

A

diffuse , inflammatory obstruct or small airways or bronchioles.
kids
adults - viral
lung transplantation .
leads to
BRONCHIOLITIS OBLITERANS - fibrosis, scarring

79
Q

pulmonary fibrosis

A

excessive fibrotic or connective tissue
scar tissue from infection
autoimmune
coal dust /asbestos
LOSS OF LUNG COMPLIANCE
hypoxemia
o2 can’t diffuse across A/V membrane
leads to dec TV and hypocapnia

80
Q

pulmonary fibrosis

A

no known cause
chronic inflam
old people , men
S&S dyspnea, inspir crackles

81
Q

Inhalation disorders

A

toxic gas
damage epithelium -mucus
edema , Hillary damage etc
ARDS/pneumo
oxygen given steroids etc

82
Q

Pneumoconiosis

A

dust
fibrosis
slice, asbestos, coal
no treatment

83
Q

hypersensitivity pneumonitis

A

allergic /inflam
organic particles or fumes
lymphocytes/inflam cells into lung tissues
acute , subacute chronic - fibrosis

84
Q

pulmonary Edema

A

excess fluid in lungs
lung normally dry
heart disease
toxic gases
ARDS
LEFT Sided Heart failure
dyspnea, hypoxemia, work
diuretics, vasodilators
oxygen

85
Q

lung usually dry

A

balance of
capillary hydrostatic pressure
capillary oncostic pressure
cap permeability
surfactant repels water on alveoli

86
Q

acute lung injury/
ARDs

A

spectrum of inflammation and diffuse alveocapillary injury
-inflitrates bilat on xray
-low ratio of PaO2 vs inhaled O2
-no edema cause
tons die , 50% die

from acute injury to A/C membrane.

covid

87
Q

Pulmonary edema

A
88
Q

acute lung injury/
ARDs

A

The clinical manifestations of ARDS are progressive, as follows:1. Dyspnea and hypoxemia with poor response to O2 supplementation
2. Hyperventilation and respiratory alkalosis
3. Decreased tissue perfusion, metabolic acidosis, and organ dysfunction
4. Increased work of breathing, decreased tidal volume, and hypoventilation
5. Hypercapnia, respiratory acidosis, and worsening hypoxemia
6. Respiratory failure, decreased cardiac output, hypotension, and death

89
Q

vaping

A

dx of exclusion

90
Q

asthma

A

-chronic inflammatory disorder
-bronchial hyper-responsiveness
-constriction of airways
-variable airflow obstruction -reversible.
most common cd in kids

91
Q

asthma pathophysiology

A

epithelial exposure antigens - irate and adaptive immune responses
inflame of bronchial mucous & hyper responsiveness of airways.
dendritic cells
IGE

vasodilation
cap perm
mucosal edema
bronchial smooth muscle contraction
mucus from goblet. cells
narrowing and obstruct of airways
eosinophils cause injury and hyper bronchial response
chronic leads to fibrosis-irreversible.

92
Q

asthma

A

impaired EXPIRATION
air trapping
decreased perfusion of alveoli
hyperventilation
hypoxemia no Co2 retention
resp ALKALOSIS

93
Q

status asthmatics

A

acute severe bronchospasm

94
Q

COPD

A

common
preventable
-persistent airflow limitation
assoc inflam response airways and the lung from toxins

95
Q

COPD

A

most common lung disease

96
Q

chronic bronchitis

A

hypersectretion of mucous & chronic productive cough of at least 3 months of the year. for at least 2 consecutive years.
usually in large bronchi
FEV/FCV ratio <0.7

97
Q

emphysema

A

abnormal permanet enlargement of gas-exchange airways ( acini) with destruction of alveolar walls without obvious fibrosis.

destruction of alveoli - larger spaces- no gas exchange , V/P mismatch , lypoxemia

primary cause of airflow limit is loss of elastic recoil. can’t EXPIRE. AIR Trapping
Farrell chest

98
Q

primary emphysema

A

1-3%
genetic
antitrypsin enzyme deficiency

99
Q

secondary emphysema

A

smoking
pollution

100
Q

Respiratory Tract Infections

A

acute bronchitis
Pneumonia
Tuberculosis
Access

101
Q

Pulmonary Vascular Disease

A

Pulmonary embolism
Pulmonary Artery Hypertension
Cor Pulmonale

102
Q

Malignancies of RT

A

Laryngeal cancer
Lung cancer

103
Q

Clinical Manifestations of Pulmonary Alterations

A

Clinical Manifestations of Pulmonary Alterations1. Dyspnea is the feeling of breathlessness and increased respiratory effort.2. Coughing is a protective reflex that expels secretions and irritants from the lower airways.3. Changes in the sputum volume, consistency, or colour may indicate underlying pulmonarydisease.4. Hemoptysis is expectoration of bloody mucus.5. Abnormal breathing patterns are adjustments made by the body to minimize the work ofrespiratory muscles. They include Kussmaul, obstructed, restricted, gasping, and Cheyne-Stokesrespirations as well as sighing.6. Hypoventilation is decreased alveolar ventilation caused by airway obstruction, chest wallrestriction, or altered neurological control of breathing and results in increased partial pressure ofcarbon dioxide in arterial blood (PaCO2), or hypercapnia.7. Hyperventilation is increased alveolar ventilation produced by anxiety, head injury, or severehypoxemia and causes decreased PaCO2 (hypocapnia).8. Cyanosis is a bluish discoloration of the skin caused by desaturation of hemoglobin, polycythemia,or peripheral vasoconstriction.9. Clubbing of the fingertips is associated with diseases that interfere with oxygenation of the tissues.10. Chest pain can result from inflamed pleurae, trachea, bronchi, ribs, or respiratory muscles.11. Hypoxemia is a reduced PaO2 caused by (a) decreased O2 content of inspired gas, (b)hypoventilation, (c) O2 diffusion abnormality, (d) ventilation–perfusion mismatch, or (e) shunting.

104
Q

Disorders of chest wall and Plura

A

. Chest wall compliance is diminished by obesity and kyphoscoliosis (which compress the lungs),and by neuromuscular diseases that impair chest wall muscle function.2. Flail chest results from rib or sternal fractures that disrupt the mechanics of breathing.3. Pneumothorax is the accumulation of air in the pleural space. It can be caused by spontaneousrupture of weakened areas of the pleura or can be secondary to pleural damage caused by disease,trauma, or mechanical ventilation.4. Tension pneumothorax is a life-threatening condition caused by trapping of air in the pleuralspace, producing displacement of the great vessels and heart.5. Pleural effusion is the accumulation of fluid in the pleural space resulting from disorders thatpromote transudation or exudation from capillaries underlying the pleura or from blockage orinjury to lymphatic vessels that drain into the pleural space.6. Empyema is the presence of pus in the pleural space (infected pleural effusion); it usually occursbecause of lymphatic drainage from sites of bacterial pneumonia.

105
Q

Pulmonary Disorders

A
106
Q

Pulmonary embolism (PE)

A

Pulmonary embolism (PE) is occlusion of a portion of the pulmonary vascular bed by an embolus. PEmost commonly results from embolization of a clot from deep venous thrombosis involving the lower leg(see Chapter 24). Other less common emboli include tissue fragments, lipids (fats), a foreign body, an airbubble, or amniotic fluid. Risk factors for PE include conditions and disorders that promote bloodclotting as a result of venous stasis (immobilization, heart failure), hypercoagulability (inheritedcoagulation disorders, malignancy, hormone replacement therapy, oral contraceptives), and injuries tothe endothelial cells that line the vessels (trauma, infection, caustic intravenous infusions). Genetic risksinclude factor V Leiden, antithrombin II, protein S, protein C, and prothrombin gene mutations. Nomatter its source, a blood clot becomes an embolus when all or part of it detaches from the site offormation and begins to travel in the bloodstream.

107
Q

Pulmonary embolism (PE)

A
108
Q

Cor pulmonale

A

Cor pulmonale is defined as right ventricular enlargement (hypertrophy, dilation, or both) caused byPAH (see Figure 27-17).97PathophysiologyCor pulmonale develops as PAH exerts chronic pressure overload in the right ventricle. Pressureoverload increases the work of the right ventricle and causes hypertrophy of the normally thin-walledheart muscle. This pressure overload eventually progresses to dilation and failure of the ventricle.Clinical manifestationsThe clinical manifestations of cor pulmonale may be obscured by underlying respiratory or cardiacdisease and appear only during exercise testing. The heart may appear normal at rest, but with exercise,cardiac output falls. The electrocardiogram may show right ventricular hypertrophy. The pulmonarycomponent of the second heart sound, which represents closure of the pulmonic valve, may beaccentuated, and a pulmonic valve murmur also may be present. Tricuspid valve murmur mayaccompany the development of right ventricular failure. Increased pressures in the systemic venouscirculation cause jugular venous distension, hepatosplenomegaly, and peripher

109
Q

lung cancer

A

Lung CancerThe term lung cancer refers to tumours that arise from the epithelium of the respiratory tract(bronchogenic carcinomas). Other pulmonary tumours, such as mesotheliomas (associated with asbestosexposure), occur less commonly (Table 27-3).TABLE 27-3

Pathophysiology (17 decks)

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