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type I alveolar cells
flat squamous epithelial cells across which gas exchange takes place
type II alveolar cells
produce surfactant, a lipoprotein substance that decreases surface tension in alveoli and allows for greater ease of lung inflation
during inspiration…
contraction of diaphragm and expansion of chest cavity →
increase thoracic cavity volume →
decrease intrapleural P →
increase transpulmonary P and lungs expand →
alveolar P < atm P →
air moves into lungs
lung compliance
ability of lungs to stretch (expand)
low compliance (more stiff) due to:
reduce elasticity of lungs
block bronchi or smaller airways
increase surface tension in alveoli
impair flexibility of thoracic cage
ventilation (V)
because of weight of lung and gravity when standing, intrapleural pressure is more negative at apex than at base
at rest, alveoli at apex are more fully expanded than those at base
during inspiration, alveoli at base expand more
perfusion (Q)
in upright position, distance of upper apices above heart level exceed perfusion capabilities of pulmonary arterial P
blood flow in upper part of lungs < in base of lungs
V/Q mismatch
with shunt (oirway obstruction), there is perfusion w/o ventilation = low V/Q = 0
occurs in atelectasis, foreign body aspiration
with dead air space (blood flow obstruction), there is ventilation w/o perfusion, resulting in a high V/Q = infinity
occurs in pulmonary embolism
influenza
clinical manifestations:
abrupt onset of fever and chills, rigors, malaise, muscle aching, headache, profuse watery nasal discharge, nonproductive cough and sore throat
1 distinguishing feature of influenza viral infection is rapid onset (1 to 2 min) of profound malaise
pneumonia
inflammation of lung parenchyma in LRT, lung consolidation w/ alveoli filled w/ exudate
classification according to type of agent:
typical— infection by bacteria that cause inflammation and exudation of fluid into air-filled spaces of alveoli
atypical— caused by viral and mycoplasma infections that involve alveolar septum and interstitium of lung
typical pneumonia
inflammation and exudation of fluid into air-filled spaces of alveoli
atypical pneumonia
lack lung consolidation, production of moderate amounts of sputum, moderate elevation of WBC count and lack of alveolar exudate
pneumococcal pneumonia
sxs:
sudden onset of malaise, severe, shaking chills and fever
during congestive stage, productive cough (mucopurulent sputum) and limited breath sounds w/ fine crackles
as disease progresses, character of sputum changes → blood tinged or rust colored to purulent
pleuritic pain: sharp pain that is more severe w/ respiratory movements
tuberculosis (TB)
transmission:
airborne infections spread by droplet nuclei
minute, invisible particles of organisms suspended in air
pathogenesis:
cell mediated immune response
confers resistance to organism
development of tissue hypersensitivity to tubercular antigens
cell mediated immune response initiated that contains infection
infected macrophages degrade mycobacteria and present antigens to T lymphocytes
sensitized T lymphocytes stimulate macrophages to increase lytic enzymes
also damages lung tissue
results in gray-white, circumscribed granulomatous lesion = Ghon focus
contains tubercle bacilli, macrophages and T cells
T cell hypersensitivity rxn produces tissue necrosis → central portion of Ghon focus undergoes soft, caseous necrosis
lung cancer
primary risk factor: cigarette smoking
other risks:
cigars, pipes, passive exposure
environmental and occupational carcinogens
asbestos
genetic susceptibility
benign chronic lung disorders
diet
gender
paraneoplastic syndromes
produced in lung cancer
ectopic hormones secreted by tumor cells or from autoantibodies released in response to tumor that cross-reacts w/ other tissues
symptoms occur at sites distant from tumor or its metastasis
clinical manifestations of lung cancer
chronic cough, SOB, whezzing
compression of nerves or veins, erosion of blood vessels, GI obstruction
hemoptysis, retrosternal pain, hoarseness, dysphagia, dyspnea w/ pleural effusion
nonmetastatic paraneoplastic manifestations involving endocrine, neurologic, and connective tissue function
nonspecific sxs: cachexia, anorexia, and weight loss
disorder of pleura
pleural effusion: abnormal collection of fluid in pleural cavity
hemothorax: type of pleural effusion in which there is blood in pleural cavity
pneumothorax:
presence of air in pleural space
causes partial or complete collapse of affected lung
spontaneous pneumothorax
occurs when air-filled blisters on lung surface ruptures
allows atmospheric air from airways to enter pleural cavity
air flows from alveoli into pleural space, causing involved portion of lung to collapse as a result of its own recoil
tension pneumothorax
occurs when injury to chest or respiratory structures permits air to enter but not leave pleural space
results in a rapid increase in pressure w/in chest →
compression atelectasis of unaffected lung
shift in mediastinum to opposite side of chest
emphysema
loss of lung elasticity
abnormal enlargement of airspaces distal to terminal bronchioles
hyperinflation of lungs and increase in total lung capacity (TLC)
destruction of alveolar walls and capillary beds
pathogenesis of emphysema
antiprotease production and secretion may be inadequate to neutralize excess protease production resulting in breakdown of elastin
clinical manifestations of emphysema
“pink puffers”
lack of cyanosis, use of accessory muscles and pursed-lip (“puffer”) breathing
enhance airflow and prevents airway collapse
barrel chest
loss of lung elasticity and hyperinflation of lungs → airways collapse during expiration
air becomes trapped in alveoli and lungs, producing an increase in anteroposterior dimensions of chest
decrease breath sounds
chronic obstructive bronchitis
airway obstruction of major and small airways
pathogenesis:
hypersecretion of mucus in large airways, associated with hypertrophy of submucosal glands in trachea and bronchi
clinical manifestations of chronic obstructive bronchitis
“blue bloaters”
cyanosis
fluid retention associated w/ right-sided heart failure
sputum overproduction, an early manifestation
hemoptysis
gastrin
produced by G cells in antrum of stomach
stimulates secretion of gastric acid and pepsinogen
cholecystokinin (CCK)
produced by I cells in intestinal mucosa
stimulates contraction of gall bladder
stimulates secretion of pancreatic enzymes
secretin
produced by S cells in mucosa of duodenum and jejunum
released in response to acidic chyme in duodenum
inhibits gastric acid secretion by inhibiting gastrin
parietal cells secrete…
HCl (gastric acid)
chemically breaks down and disinfects ingested food
intrinsic factor (IF)
necessary for absorption of vitamin B12
chief cells secrete…
pepsinogen
converted to pepsin when exposed to low pH of gastric juices
enzyme that initiates proteolysis