Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
100 Cards in this Set
- Front
- Back
|
dvlp of lungs
|
outgrowth from ventral wall of foregut
|
|
|
bronchioles vs bronchi
|
bronchioles lack cartilage and submucosal glands within their walls
|
|
|
acinus
|
part of lung distal to terminal bronchiole (<2mm in diameter); roughly sperical with diamter ~7mm; composed of respiratory bronchioles, alveolar ducts, and alveolar sacs
|
|
|
lobule
|
cluster of 3 to 5 terminal bronchioles wach with its appended acinus; cluster of acini
|
|
|
microscopic structure of alveolar walss from blood to air
|
1) capillary endothelium 2) BM and surrounding interstitial tissue 3) alveolar epithelium 4) alveolar macrophages
|
|
|
pores of Kohn
|
holes within alveoli that permit passage of bacteria and exudate btwn adjacent alveoli
|
|
|
pulmonary hypoplasia
|
defective dvlp of both lungs resulting in decreased weight, V, and acini disproportional to body weight and gestational age
|
|
|
foregut cysts
|
arise from abnormal detachment of primitive foregut and most often located in hilium or middle mediastinum; classified as bronchogenic, esophageal, or enteric; surgical resection curative
|
|
|
pulmonary sequestration
|
presence of discrete mass of lung tissue without normal connection to airway system; blood supply from aorta or branches
|
|
|
atelectasis
|
incomplete expansion of lungs or collapse or previously inflated lung, producing areas of relatively airless pulmonary parenchyma
|
|
|
acquired atelectasis divisions
|
resorption (or obstruction), compression, and contraction
|
|
|
lung in resorption atelectasis
|
lung V diminished due to reabsortption of air within blocked lung-causes mediastinum to shift towards atelectatic lung
|
|
|
what causes resorption atelectasis
|
excessive secretions (mucus) or exudates within smaller bronchi; most often found in asthma, chronic bronchitis, bronchiectasis, postop states, aspiration of forgein bodies, and rarely neoplasms
|
|
|
compression atelectasis
|
pleural cavity is partially or completely filled by fluid exudate, tumor, blood, or air (pneumothorax); mediastinum shifts away from affected lung
|
|
|
contraction atelectasis
|
local/generalized fibrotic changes in lung or pleura prevent full expansion
|
|
|
lung injury in ARDS (acute respiratory distress syndrome)
|
imbalance of pro-inflammatory (NF-kB)and anti-inflammatory mediators; increased neutrophills
|
|
|
what does resolution of ARDS require
|
resorption of exudate, removal of dead cells, and their replacement by new endothelial and alveolar epithelial cells
|
|
|
majority of deaths due to ALI (acute lung injury)
|
sepsis or multi-organ failure
|
|
|
acute interstitial pneumonia
|
widespread ALI associated with rapidly progressive clinical course that is of unknown etiology
|
|
|
restrictive lung disorders occur
|
1) chest wall disorders 2) chronic interstitial and infiltrative diseases
|
|
|
what is included in the term COPD
|
emphysema (acinar level) and chronic bronchitis; overlao with asthma-except reverible portion in asthma
|
|
|
emphesema
|
irreversible enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis
|
|
|
four major types of emphesema
|
1) centriacinar 2) panacinar 3) paraseptal 4) irregular; 1 & 2 cause significant airway obstruction; 1 is 95% cases
|
|
|
centriacinar emphesema
|
central or proximal parts of acini formed by respiratory bronchioles are affected, distal alveoli spared; more common and severe in upper lobes
|
|
|
panacinar emphsema associations
|
more common in lung bases; a1-antitrypsin deficiency
|
|
|
distal acinar emphesema associations
|
more striking close to pleura, along lobular CT septa, and margins of the lobules; adjacent to fibrosis, scarring, or atelectasis; upper half lung more severe; cyst-like structure=may underlie spontaneous pneumothorax in young adults
|
|
|
irregular emphesema associations
|
scarring; most asymptomatic and clinically insignificant
|
|
|
a1-antitrypsin
|
normally in serum, tissue fluids, and macrophages; major inhibitor of proteases (especially elastase) secreted by neutrophils during inflammation
|
|
|
what do ppl with a1-antitrypsin deficiency dvlp
|
>80% symptomatic panacinar emphesema
|
|
|
emphesema clinical presentation
|
cough slight, overdistention severe, diffusion capacity low, blood gases relatively normal at rest
|
|
|
death in emphesema causes
|
1) respiratory acidosis and coma 2) R-sided heart failure 3) massive collapse of lings secondary to pneumothorax
|
|
|
compensatory hyperinflation
|
dilation of alveoli, but not destruction of septal walls in response to loss of lung substance elsewhere
|
|
|
interstitial emphysema
|
entrance of air into CT stroma of lung, mediastinum, or subQ tissue; alveolar tears or trauma
|
|
|
what can cause alveolar tears
|
coughing plus some bronchiolar obstruction; whooping cough and bronchitits, artificial ventilation, irritant gas inhalation
|
|
|
chronic bronchitis
|
persistant cough with sputum production for >3 months in at least 2 consecutive years (with absence of any other identifying cause)
|
|
|
earliest feature of chronic bronchitis
|
hypersecretion of mucus in airways (hypertrophy of submucosal glands in trachea and bronchi)
|
|
|
Reid index
|
ratio of thickness of mucous gland layer to thickness of wall btwn epithelium and cartilage; normally 0.4; increased in chronic bronchitis
|
|
|
bronchiolitis obliterans
|
bronchiole lumens obliterated due to fibrosis
|
|
|
atopic asthma
|
most common type; type I IgE-mediated hypersensitivity rxn
|
|
|
what does the cytokine IL-4 stimulate the production of
|
IgE
|
|
|
what does the cytokine IL-5 stimulate the production of
|
activates locally recruited eosinophils
|
|
|
what does the cytokine IL-13 stimulate the production of
|
mucus secretion from bronchial submucosal glands and promotes IgE by B cells
|
|
|
early vs late phase rxn
|
early=bronchoconstriction, increased mucus, variable vasodilation eith increased vascular permeability; late=inflammation with leukocyte recruitment (eosinophils, neutrophils, and more T cells)
|
|
|
eotaxin
|
produced by airway epithelial cells-potent chemoattractant of eosinophils
|
|
|
histamine in lungs
|
potent bronchoconstrictor
|
|
|
prostaglandin D2 in lungs
|
bronchoconstrition and vasodilation
|
|
|
platelet-activating factor in lungs
|
aggregation of platelets and release of histamine and serotonin from their granules
|
|
|
airway remodeling in asthma
|
1) overall thickening of airway wall 2) sub-BM fibrosis 3) increased vascularity 4) increase size of submucosal glands and mucous metaplasia of airway epithelial cells 5) hypertrophy/hyperplasia of bronchial wall muscle
|
|
|
bronchiectasis
|
permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic tissue, resulting from or associated with chronic necrotizing infections; common in CF
|
|
|
primary ciliary dyskinesia
|
autosomal recessive; absence/shortening of hyein arms responsible for coordinated bending of cilia; half have Kartagener syndrome
|
|
|
clinical bronchiectasis
|
severe, persistent cough; expectoration of foul-smelling, sometimes bloody sputum; dyspnea and orthopnea in severe cases; occasional life-threatening hemoptysis
|
|
|
chronic interstitial diseases (restrictive)
|
inflammation and fibrosis of pulmonary CT, principally the most peripheral and delicate interstitium in the alveolar walls
|
|
|
idiopathic pulmonary fibrosis
|
histo pattern of usual interstitial pneumonia (UIP); caused by repeated cycles of epithelial activation/injury by unidentified agent; TGF-B1 driver of process
|
|
|
TGF-B1
|
known to be fibrogenic and is released from injured type 1 alveolar epithelial cells
|
|
|
caveolae
|
flask-shaped invaginations of the plasma membrane present in many terminally differentiated cells
|
|
|
clinical course of idiopathic pulmonary fibrosis
|
gradual with increaing dyspnea on exerction and dry cough; 40-70 yrs at presentation; mean survival <3 yrs
|
|
|
Nonspecific Interstitial Pneumonia (NSIP)
|
cellular and fibrosing patterns
|
|
|
cellular NSIP
|
mild/moderate chronic interstitial inflammation containing lymphocytes and few plasma cells in a uniform or patchy distribution
|
|
|
fibrosing NSIP
|
diffuse/pathcy interstitial fibrosis without temporal heterogeneity characteristic of UIP; fibroblastic foci and honeycombing absent
|
|
|
clinical course of NSIP
|
dyspnea and cough several months duration; 46-55 yrs; cellular better outcome, generally younger
|
|
|
cryptogenic organizing pneumonia aka bronchiolitis obliterans organizing pneumonia
|
cough and dyspnea and have subpleural or peribronchial patchy areas of airspace consolidation radiographically; histo polyploid plugs of loose organizing CT (Masson bodies) within alveolar ducts, alveoli, and often bronchioles
|
|
|
rheumatoic arthritis and lung involvement
|
30-40% patients; 1) chronic pleuritis with/without effusion 2) diffuse interstitial pneumonitis and fibrosis 3) intrapulmonary rheumatoid nodules 4) pulmonary hypertension
|
|
|
systemic sclerosis and lung involvement
|
aka scleroderma; diffuse interstitial fibrosis (NSIP>UIP)
|
|
|
lupus erythematosus and lung involvement
|
pathcy, transient parenchymal infiltrates; occasionally severe lupus pneumonitis
|
|
|
pneumoconioses
|
non-neoplastic lung rxn to inhalation of mineral dusts, inorganic particulates, and chemical vapors/fumes
|
|
|
small vs large particles
|
small more likely to cause acute lung injury (appear in pulmonary fluids and reach toxic levels rapidly); large resist dissolution and persist for years=fibrosing collagenous pneumoconioses (eg silicosis)
|
|
|
anthracosis
|
coal-induced pulmonary lesion (some in urban dwellers and smokers); inhaled carbon engulfed by alveolar/interstitial macrophages and accumulate in CTs along lymphatics or lymphoid tissue
|
|
|
silicosis
|
most prevalent occupational chronic disease in world; decades of exposure, slowly progressing, nodular, fibrosing pneumoconiosis
|
|
|
silicosis is associated with increased susceptibility to
|
TB; possible depression of cell-mediated immunity and ability of pulmonary macrophages to kill TB
|
|
|
distinct geometric forms of asbestos
|
serpentine (crysotiles, most used in industry) and amphibole (more pathogenic)
|
|
|
mesothelioma is associated with what asbestos form
|
amphibole
|
|
|
asbestos bodies
|
golden brown, fusiform or beaded rods with transluscent center and consist of asbestos fibers coated with an iron-containing proteinaceous material
|
|
|
pattern of asbestos fibrosis
|
similar to UIP except with asbestos bodies; begins in lower lobes and subpleurally; honeycomb appearance eventually
|
|
|
pleural plaques
|
most common manifestation of asbestos exposure; well-circumscribed plaques of dense collagen, often containing calcium
|
|
|
drugs that cause pulmonary damage
|
bleomycin-fibrosis; amiodarone-pneumonitis
|
|
|
acute radiation pneumonitis
|
lymphocytic alveolitis or hypersensitivity pneumonitis; fever, dyspnea, pleural effusion, radiologic infiltrates; 10-20% patients receiving fractionated irradiation
|
|
|
sarcoidosis
|
systemic disease of unknown cause; noncaseating granulomas in many tissues and organs; bilateral hilar lymphadenopathy in 90%, eye and skin lesions
|
|
|
other diseases that cause noncaseating (hard) granulomas
|
mycobacterial and fungal infections and berylliosis; sarcoidosis diagnosis made on exclusion
|
|
|
factors contributing to sarcoidosis
|
immunologic, genetic, environmental
|
|
|
marker of sarcoidosis activity
|
TNF concentration in bronchoalveolar fluid
|
|
|
lymph nodes involvement in sarcoidosis
|
hilar and mediastinal frequently involved; enlarged, discrete, and sometimes calcified; tonsils in 1/3 cases
|
|
|
bone marrow in sarcoidosis
|
involved in 1/5 cases; phalangeal bones of hands and feet-small circumscribed areas of bone resorption within marrow cavity
|
|
|
ocular involvement of sarcoidosis
|
iritis or iridocyclitis bi or unilaterally
|
|
|
Farmer's lung
|
exposure to dust from humid, warm hay that permits rapid proliferation of actinomycete spores
|
|
|
histologic changes in hypersensitivity pneumonitis
|
1) interstitial pneumonitis 2) noncaseating granulomas in 2/3 3) interstitial fibrosis, honeycombing, and obliterative bronchiolitis (in late stages)
|
|
|
desquamative interstitial pneumonia clinical presentation
|
insidious onset dyspnea and dry cough over weeks to months; mild restrictive abnormality with moderate reduction of diffusing capacity of CO2; ~100% respond to steroids and smoking cessation
|
|
|
respiratory bronchiolitis
|
common histologic lesion in cigarette smokers; pigmented intraluminal macrophages within 1st and 2nd order respiratory bronchioles
|
|
|
pulmonary alveolar proteinosis (PAP)
|
rare; bilateral patchy aymmetric pulmonary opacifications; accumulation of acellular surfactant in intra-alveolar and bronchiolar spaces; aquired, seondary, or congenital
|
|
|
what is throught to be responsible for PAP
|
anti-GM-CSF antibody; autoimmune disorder
|
|
|
presentation of PAP
|
nonspecific respiratory difficulty of insidious onset, cough, abundant sputum that contains chunks of gelatinous meterial
|
|
|
2 consequences of pulmonary emboli
|
respiratory and hemodynamic compromise
|
|
|
electromechanical dissociation
|
ECG has rhythm, but no pulses palpated; occurs in large pulmonary embolus because no blood is eneting pulmonary circulation
|
|
|
diagnosis of PE
|
spiral computed tomographic angiography
|
|
|
unresolved, multiple small emboli over time may lead to
|
pulmonary hypertension, pulmonary vascular sclerosis, and chronic cor pulmonale
|
|
|
when does pulmonary hypertension occur
|
when mean pulmonary P reaches 1/4 systemic levels (normally 1/8)
|
|
|
pulmonary hypertension familial form cause
|
mutation in bone morphogenetic protein receptor type 2 (BMPR2) signaling pathway
|
|
|
common pathologic features of all forms of pulmonary hypertension
|
medial hypertrophy of muscular and elastic arteries, atheromas of pulmonary artery and its major branches, right ventricular hypertrophy
|
|
|
pulmonary hemorrhage syndromes
|
1) Goodpasture 2) idiopathic pulmonary hemosiderosis 3) vasculitis-associated (hypersensitivity vasculitis, Wegener granulomatosis, lupus)
|
|
|
Goodpasture syndrome
|
kidney and lung injury caused by circulating autoantibodies against noncollagenous domain of a3 chain of collagen 4
|
|
|
Goodpasture syndrome manifestation
|
proliferative, rapidly progressive glomerulonephritis and necrotizing hemorrhagic interstitial pneumonitis
|
