Lung 1 Flashcards
right lung bud develops into
3 branches of lobar bronchi
respiratory system is an outgrowth from
ventral wall of the foregut
left lung bud develops into
2 lobar branches
conducting airways
nasal, mouth, pharynx, larynx, trachea, bronchi, bronchioles
respiratory tissues
terminal respiratory bronchiole, alveolar ducts and sacs
lobar bronchi are lined by
columnar ciliated epithelium
distal to terminal bronchioles
pulmonary acinus (7mm)
A cluster of three to five terminal bronchioles with its
appended acinus is referred to as
pulmonary lobule
distinguished by lack of cartilage and submucosa glands
bronchioles
alveolar tissue total weight and surface
250g, 75 sqm
true vocal cords are lined by
stratified squamous epithelium
entire respiratory tree (larynx, trachea, bronchioles)
pseudostratified tall columnar ciliated epithelium
express high levels of the cystic fibrosis transmembrane conductance regulator (CFTR) and
appear to modulate the ion content and viscosity of bronchial secretions
ionocytes
bronchial mucosa contains neuroendocrine cells
serotonin, calcitonin, bombesin
are the ones also
producing mucus, it usually traps inhaled
foreign body like dust or inhaled microbes
and so they stick there, so it’s also a sort of
protection, preventing these smaller particles
from going directly to the pulmonary alveoli
goblet cells
an intertwining network of anastomosing capillaries lined with endothelial cells
alveolar walls
These pores allow gas exchange from one alveolus to another alveolus.
pore of Kahn
carbon particles in the lungs
anthracosis
amount of air inhaled and exhaled with each resting breath
tidal volume (70kg: 350-400ml)
amount of air remaining in the lungs at the end of a maximal exhalation
residual volume
total amount of air that can be exhaled following maximal inhalation
vital capacity
total lung capacity
vital capacity + residual volume
amount of gas in the lungs at the end of a resting tidal breath
functional residual capacity
lesser pleural pressure on the apex causes __________ expansion of the apical alveoli
greater
PaO2 falls below 60mmHg
respiratory failure
normal PaO2
80-100mmHg (10.7-13.3kPa)
normal PaCO2
35-45mmHg (4.7-6.0)
PaO2 is low but PaCO2 is within normal range
type 1
Type 2 resp failure
PaO2 is low but PaCO2 is raised
the only direct clinical sign of resp failure
central cyanosis (PaO2 is 50mmHg or lower)
less than 30mmHg PaO2
loss of consciousness
hypercapnia when severe causes
tremor bounding pulse vasodilation increased CO confusion leading to coma
2 main causes of chronic hypoxemia
pulmonary hypertension
polycythemia
Due
to
pulmonary
vasoconstriction. This occurs when the PaO2 falls below 60mmHg
Pulmonary hypertension
Due to stimulation of
erythropoietin release from the kidney when there is low oxygen
polycythemia
Provide anatomic assistance in reducing the
surface tension of alveoli
surfactant (type 2 pneumocytes)
phospholipids and proteins in a surfactant
Dipalmitoylphosphatidylcholine
Surfactant apoproteins
Calcium ions
what is the surface tension of water
72 dynes/cm
surface tension of alveolar fluid without surfactant
50 dynes/cm
surface tension of alveolar fluid with surfactant
5-30 dynes/cm
steroids which increase the prod of surfactant
thyroxin and cortisol
biochemical defenses
proteinase inh (alpha 1 protease inh) Antioxidants (transferrin, lactoferrin, glutathione)
main disease of the airways and the lungs
infection
inflammation
obstruction
incomplete expansion of the lungs
atelectasis (neonatal) (-) surfactant
collapse of previously inflated lungs
atelectasis (acquired)
3 main types of atelectasis
resorption
compression
contraction
complete obstruction of an airway
resorption atelectasis
Mediastinum shifted towards the atelectatic lung
resorption atelectasis
Significant amount of fluid (transudates,
exudate- infection: pneumonia, or blood),
tumor or air (pneumothorax) accumulate
within the pleural cavity
compression atelectasis
mediastinum is shifted away from the affected lung
compression atelectasis
type of atelectasis whch is more common in traumatic patients like stabbed wounds
compression atelectasis
Focal or generalized pulmonary or pleural
fibrosis prevents full lung expansion.
contraction atelectasis
presence of
fibrous tissue in between the alveolar
spaces, so in the alveolar septa, that will
prevent the lungs from expanding fully
interstitial fibrosis
also called non cardiogenic pulmonary edema
acute lung injury
Characterized by abrupt onset of significant hypoxemia and bilateral
pulmonary infiltrates in the absence of cardiac failure
Acute lung injury
histologic manifestation of ALI and ARDS
diffuse alveolar damage
made up of alveolar fluid rich in proteins that has precipitated.
Hyaline membrane
lining hyaline membrane surrounds the alveolar spaces which makes it difficult for gas exchange to happen
hyaline membrane disease
increase resistance to airflow due to partial or complete obstruction at any level from trachea and larger bronchi to the terminal and respiratory bronchioles
Obstructive diseases
reduced expansion of lung parenchyma and decreased total lung capacity
restrictive disease
Obstructive and Restrictive lung dse types
emphysema
Chronic bronchitis
asthma
bronchiectasis
irreversible enlargement of the airspaces distal to terminal bronchiole accompanied by destruction of their walls without obvious fibrosis
emphysema
Central or Proximal parts of the acini formed by
respiratory bronchioles are affected
CENTRIACINAR (CENTRILOBULAR) EMPHYSEMA
Both emphysematous and normal airspaces exist within the same acinus and lobule.
CENTRIACINAR (CENTRILOBULAR) EMPHYSEMA
more common and severe (CENTRIACINAR (CENTRILOBULAR) EMPHYSEMA)
upper lobes
Acini are uniformly enlarged from the level of the
respiratory bronchiole to the terminal blind
alveoli
Panacinar emphysema
Panacinar emphysema tend to occur more in the _______________
lower zones
Panacinar emphysema is associated with ______________ deficiency
alpha 1 antitrypsin
Proximal portion of the acinus is normal and the
distal part is predominantly involved
Paraseptal/ DIstal acinar emphysema
Distal Emphysema is more striking adjacent to the pleura,
more on the
upper half of the lung
can sometimes form cyst-like structures
Usually in small foci and is clinically significant
irregular emphysema
most common cause of emphysema
Inhaled cigarette smoke
Factors (emphysema)
o Inflammatory mediators and leukocytes
– released from resident epithelial cells
and macrophages.
o Protease-antiproteases imbalance
o Oxidative stress
o Infection
Symptoms of emphysema do not appear until atleast __
1/3 of the functioning lung parenchyma is damaged.
Manifestations of emphysema
Dyspnea, cough and expectoration, wheezing, weight loss
Generally, in patients with smoking-related
disease, the _________ are
more severely affected
upper 2/3 of the lungs
apical blebs or bullae are characteristics of
irregular emphysema
Persistent cough with sputum production for at
least 3 months in at least 2 consecutive
years
chronic bronchitis
most important risk factor of chronic bronchitis
cigarette smoking
Dominant pathology features of chronic bronchitis
mucous hypersecretion
persistent inflammation
– ratio of thickness of the mucous
gland layer to the thickness of the wall between the epithelium and the cartilage
reid index
normal measure in reid index
not more than 0.4
reid index: chronic bronchitis
> 0.4
Is a heterogeneous disease, usually
characterized by chronic airway inflammation
and variable expiratory airflow obstruction that
produces symptoms such as wheezing,
shortness of breath, chest tightness, and cough,
which vary over time and in intensity
asthma
Episodic bronchoconstriction due to increased
airway sensitivity to a variety of stimuli.
asthma
2 types of asthma
atopic and non atopic
Evidence of allergen
sensitization and immune activation
atopic (more common)
No evidence of allergen
sensitization
non- atopic
▪ IgE – mediated (type 1 hypersensitivity reaction)
▪ Usually begins in childhood and is triggered by
environmental allergens (dust, pollen, cockroach
or animal dander and food)
atopic asthma
▪ Usual triggers are respiratory infections (viral),
air pollutants (smoking, sulfur dioxide, ozone,
exposure to cold and exercise).
non-atopic asthma
▪ Inhibits cyclooxygenase pathway of arachidonic acid metabolism leading to a rapid decrease in Prostaglandin E2 (aspirin)
Drug-induced asthma
▪ Fumes in workplace (epoxy resins, plastics)
▪ Organic and chemical dusts (wood, cotton,
platinum)
▪ Gases (Toluene)
▪ Others: formaldehyde, penicillin products
occupational asthma
Bronchoconstriction is triggered by direct
stimulation of
subepithelial vagal
(parasympathetic) receptors
asthma-pharmacologic mediators
leukotrienes c4, d4, e4
acetylcholine
asthma suspects
ILF3/IL4
IL13
One susceptibility locus for asthma is
located on
chromosome 5q
are linked to
production of IgE antibodies
Particular class II HLA
may be linked to increased
proliferation of bronchial smooth muscle and
fibroblasts
Polymorphisms in the gene encoding
ADAM33
IL-4 receptor gene variants are associated
with
atopy, elevated serum IgE, and asthma
morphology of asthma
lungs are distended
Occlusion of bronchi and bronchioles by thick, tenacious mucus plugs
Charcot-Leyden crystals
asthma-airway remodelling
▪ Thickening of airway wall ▪ Sub Basement membrane fibrosis ▪ Increased in the size of submucosal glands and number of airway goblet cells ▪ Hypertrophy and/or hyperplasia of the branchial wall muscle
severe form of asthma
status asthmaticus
▪ Destruction of smooth muscle and elastic tissue
by chronic necrotizing infections
▪ Permanent dilation of bronchi and bronchioles
bronchiectasis
bronchiectasis is associated with
o Congenital or inherited conditions, e.g cystic fibrosis o Infections- necrotizing pneumonia o Bronchial obstruction- tumor, foreign bodies o Others: rheumatoid arthritis, SLE ,inflammatory bowel disease, COPD and post transplantation
smaller bronchioles are
progressively obliterated as a result of fibrosis
bronchiolitis obliterans
is an autosomal
recessive disease. The disease causing
mutations result in ciliary dysfunction due to
defects in ciliary motor proteins
Primary ciliary dyskinesia
Approximately half of patients with primary ciliary
dyskinesia have
Kartagener syndrome
occurs
in patients with asthma or cystic fibrosis and
frequently leads to the development of
bronchiectasis. It is a hyperimmune response to
the fungus Aspergillus fumigatus.
Allergic bronchopulmonary aspergillosis