Pathophys > Pulmonary System > Flashcards

Pulmonary System Flashcards

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1
Q

Inhalation and Boyle’s Law

A

diaphragm moves down -> increasing lung volume -> decreasing pressure in lungs (expanding) -> allows air to flow in
lungs take up more space, pressure has to decrease bc more room (people in a huge atrium)

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2
Q

Exhalation and Boyle’s Law

A

diaphragm moves up -> decreasing lung volume (contracting)-> increasing pressure -> pushes air out
less room so increases pressure (people crowded in a small bathroom)

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3
Q

Function of the conducting airways (upper)?

A

responsible for filtering, humidifying, and warming inspired air before it reaches the lungs

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4
Q

Pharynx function

A

to guide food down to esophagus or air into the lungs

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5
Q

Larynx function

A

voice box, epiglottis for swallowing

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6
Q

Function of the lower airways?

A

conducts air to the lungs, facilitates gas exchange, protects lungs w mucociliary clearance

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7
Q

trachea function

A

windpipe, ensures smooth flow of air to the bronchi

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8
Q

bronchi function

A

carry air to the lungs

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9
Q

carina function

A

cough reflex trigger

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10
Q

bronchioles function

A

carry air to the alveoli

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11
Q

alveolus function

A

facilitate gas exchange

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12
Q

process of gas exchange

A

-swapping gases between the lungs and bloodstream
-diffused at respiratory membrane
-higher conc. of O2 in alveoli than blood - O2 moves to blood
-higher conc. of CO2 in blood than alveoli - CO2 moves to alveoli

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13
Q

forms walls of alveoli, allow gases out of lungs

A

type I alveolar cells

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14
Q

surfactant producing to reduce surface tension and keep alveoli from collapsing

A

type II alveolar cells

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15
Q

carry oxygen bound to hemoglobin

A

RBCs

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16
Q

form respiratory membrane barrier, control what passes between blood and lungs

A

endothelial cells of capillaries

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17
Q

describe pulmonary circulation

A

-starts in RV
-ends in LA
-oxygenates blood in lungs
-arteries carry deoxygenated blood
-veins carry oxygenated blood
-pick up route

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18
Q

describe systemic circulation

A

-starts in LV
-ends in RA
-delivers oxygen to the body
-arteries carry oxygenated blood
-veins carry deoxygenated blood
-delivery route

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19
Q

adhered to lung surface to protect and support lungs

A

visceral layer of pleura

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20
Q

lines the chest wall and produces and absorbs pleural fluid

A

parietal layer of pleura

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21
Q

pleural space

A

lies between the visceral and parietal layers, fluid filled cavity, pleural fluid acts as lubricant to allow layers to glide against each other, helps reduce friction & maintain negative pressure needed for lung inflation

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22
Q

anterior landmarks for lung auscultation

A

-above clavicles - apex of lungs
-2nd intercostal space - upper lobes
-4th IC space - right middle lobe & left upper lobe
-6th intercostal space - lower lobes

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23
Q

posterior landmarks for lung auscultation

A

-above scapula - apex
-between spine & scapula - upper lobes
-below scapula - lower lobes

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24
Q

lateral landmarks for lung auscultation

A

-mid-axillary line for middle and lower lobes

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25
Primary pneumothorax
-occurs w/o underlying disease -healthy ppl 20-40 yo -spontaneous rupture of bleb on visceral pleura -could be genetic, random
26
secondary pneumothorax
results from underlying disorders (COPD, cystic fibrosis, trauma)
27
open pneumothorax
-external wound -air enters and exits pleural space thru opening -lung collapses -pressure does not build
28
tension pneumothorax
-one way valve -air enters during inspiration (cannot escape) -pressure builds -mediastinum shifts (displaces heart & trachea) -compromises venous return -life-threatening emergency
29
how does a pleural effusion develop?
-hydrostatic pressure (heart failure) -oncotic pressure (hypoalbuminemia) -capillary permeability (inflammation or infection) -lymphatic drainage (malignancy)
30
types of pleural effusions
CHEET chyle hemothorax empyema exudate transudate
31
clear, watery fluid, low protein, leaking out of capillaries under lining in lungs
transudate
32
thicker fluid with immune cells and protein leaks from inflamed blood vessels
exudate
33
collection of pus in pleural space - infected exudate
empyema
34
bleeding into space around lungs
hemothorax
35
milky fluid with fat and lymph leaking into pleural space
chyle
36
pathophys of transudate
↑ hydrostatic pressure ↓ oncotic pressure Fluid seeps out into pleural space
37
pathophys of exudate
↑ capillary permeability or pleural inflammation causes protein to accumulate
38
pathophys of empyema
Infection leads to massive neutrophilic infiltration -> thick, purulent fluid
39
pathophys of hemothorax
Bleeding in pleural space increases pressure and can compress lungs
40
pathophys of chyle
Disruption of thoracic duct causes chyle to leak into pleura
41
cause of transudate
↑ hydrostatic pressure: Congestive heart failure ↓ oncotic pressure: Cirrhosis (liver failure – can't make more albumin) & Nephrotic syndrome (kidneys lose protein in urine)
42
cause of exudate
Infection (pneumonia or tuberculosis), pulmonary embolism, malignancy
43
cause of empyema
Post lung infections (pneumonia), abscesses, infected wounds
44
cause of hemothorax
Trauma, surgery, cancers that damage blood vessels
45
cause of chyle
Trauma to thoracic duct or surgical involvement of thoracic duct, lymphoma, congenital lymphatic anomalies in children, chylothorax: ↑ triglycerides in pleural fluid
46
transudate exam
clear
47
exudate exam
cloudy
48
empyema exam
purulent
49
hemothorax exam
bloody
50
chyle exam
milky
51
virchow's triad
-predispose to thrombus formation, how and why clots form, drivers of thrombosis 1. endothelial injury (pro-thrombotic) 2. stasis of blood flow (stasis or turbulence) 3. hypercoagulability (inherited or acquired)
52
where is the most common site for clot development?
deep veins of lower extremities
53
pulmonary embolism
-clot lodges in pulmonary vasculature -thrombus forms in DVT -> travels to lungs -> lodges in pulmonary artery -> obstructs blood flow -> impaired gas exchange and increased pulmonary pressure result: obstructs blood flow & reduces oxygenation symptoms: sudden dyspnea, chest pain, tachycardia, tachypnea
54
cor pulmonale
right sided heart failure due to problem w lungs (pulmonary hypertension)
55
how does pulmonary hypertension lead to cor pulmonale
chronic high pressure in pulmonary arteries results in harder for RV to pump blood -> RV hypertrophies -> O2 demand exceeds O2 supply -> right sided heart failure (cor pulmonale)
56
difficulty w exhalation, prolonged expiration, wheezing, barrel chest
obstructive lung disease
57
difficulty w inhalation, shallow rapid breathing, wheezing rare, reduced chest expansion
restrictive lung disease
58
pores of kohn
openings between adjacent alveoli, allow collateral ventilation, important in preventing atelectasis -provide a backup system to keep alveoli inflated even when some airways are partially blocked, help lungs stay open and maintain ventilation -reduces risk of alveolar collapse like seen in obstructive lung diseases
59
bronchiectasis
-permanent dilation and damage of bronchi -large & medium bronchi affected -infections, cystic fibrosis, immune disorders -common in adults w chronic lung disease -chronic inflammation -> permanent dilation and damage -> impaired mucus clearance
60
bronchiolitis
-inflammation of small airways -small bronchioles affected -viral infections, inhalation injury -common in infants & young children -inflammation & narrowing of bronchioles leading to obstruction
61
ARDS
acutre respiratory disress syndrome lungs become inflamed and filled w fluid, eventually leads to tissue remodeling (lasting damage) -alveoli become filled w fluid & inflammatory cells -blocks gas exchange
62
day 1-7 alveolar filling SOB, hypoxemia, lung inflammation/stiffness
exudative phase of ARDS
63
day 7-21 lung repair attempts w fibroblast activity (healing)
proliferative phase of ARDS
64
after day 21 lungs become thickened and stiff (fibrosis) long term disability
fibrotic phase of ARDS
65
Role of inflammatory & immune process in asthma
-mast cells: bronchoconstriction & increased vascular permeability -eosinophils: damage airway lining, causing inflammation -Th2 lymphocytes: allergic response, promote IgE production -Goblet cells: contribute to airway obstruction, mucus plugging -smooth muscle cells: contract stronger & faster, increase bronchoconstriction
66
early phase of asthmatic response
in minutes bronchoconstriction & bronchospasm coughing, wheezing, SOB driven by mast cells
67
late phase of asthmatic response
4-12 hours later inflammation mucous production more severe and prolonged symptoms involves immune cells: eosinophils & T cells
68
COPD
chronic obstructive pulmonary disease -group of progressive lung diseases causing airflow limitation -chronic inflammation -> narrowing of airways, ↑mucous production, destruction of alveolar walls -> airflow obstruction
69
main types of COPD
-chronic bronchitis -emphysema
70
chronic bronchitis
-hyper-secretion of mucus and chronic productive cough continuing for at least 3 months/year for at least 2 consecutive years -airway inflammation -> bronchial edema -> smooth muscle hypertrophy and hyperplasia -> accumulation of mucus & air trapping
71
emphysema
-damage to alveoli -alveoli walls break down & lose elasticity from enzymes -> alveolar surface area is reduced & air gets trapped -> less gas exchange -> harder to breathe out
72
-skin cancer in squamous cells in central lung tissue -smoking related -moderate growth time
squamous cell carcinoma
73
-cancer in glandular cells that produce mucous in peripheral lung tissue -mostly occurs in non smokers -slow to moderate growth time
adenocarcinoma
74
-most common neuroendocrine tumor in neurosecretory granules in cells in central lung tissue -very strong association w smoking -very rapid, highly aggressive
small cell carcinoma
75
-tumors that come from hormone-producing cells in body in neuroendocrine cells of bronchial mucosa both central or peripheral -smoking relation is variable -growth time is variable
neuroendocrine tumors
76
Describe the role of surfactant in neonate and premature infants
surfactant: lipoprotein made by cells in the lungs to reduce surface tension in alveoli and keep lungs from collapsing -neonates produce it around 20-24 weeks, enough by 35-37 weeks -premature: before 34 weeks = insufficient surfactant -respiratory distress syndrome, atelectasis, respiratory failure
77
caused by parainfluenza virus -> inflammation & swelling of larynx, trachea, sometimes bronchi -> narrowed airway
croup
78
croup manifestations
barking cough like a seal, may have stridor
79
Hib bacterial virus -> rapid swelling of epiglottis
epiglottitis
80
epiglottitis manifestations
can cause sudden airway obstruction, high fever, drooling, trouble swallowing, tripod position, muffled voice
81
pathophysiology of cystic fibrosis
-genetic disease from mutation in CFTR gene -affects exocrine glands in lungs, pancreas, GI -defective CFTR protein -> chronic inflammation -> lung damage -> respiratory failure
82
risk factors for SIDS
-sleeping on stomach or side-lying -soft bedding or objects in crib -overheating during sleep -prematurity of low birth weight -parental smoking -co-sleeping most common: 2-4 months old, rare after 6 months
Pathophys
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