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Flashcards in LUNGS Deck (41):

Bronchi epithelium

pseudostratified ciliated columnar cells, goblet cells, basal cells, neuroendocrine cells


Terminal Bronchioles Epithelium

Ciliated columnar cells not pseudostratified, clara cells.


Bronchi contain the following to distinguish from bronchioles.

seromucinous glands and cartilage



Loss of lung volume secondary to alveolar collpase which leads to decreased oxygenation which leads to decreased ventilation perfusion.


Resorption atelectasis

consequence of COMPLETE airway obsctruction.(in bronchi, subsegmental bronci, or bronchioles.) prevents air from reaching alveoli. Resorption of air trapped in distal air spaces happens through the pores of Kohn, with the lack of air, the lung collpases.
Cause of obstruction- Mucus plug after surgery, Aspriation of foreign material, Bronchial asthma, bronchitis, bronchiectasis, Bronchial neoplasms
CLINICAL. Fever, dyspnea within 24-36 hours after surgery (commonest cause of post op surgery), Ipsilateral devation of trachea and diaphragmatic elevation. Absent breath sounds and tactile fremitus, lung doesn't expand. on inspiration.


Compression Atelectasis

Air or fluid accumulation in plueral cavity causes increased pressure and lung collpase, microscopically the alveoli don't have any spcae in between (slit like), Trache and mediastinum shift away from lung


Contraction atelectasis

fibrotic changes in lung or pleura prevent full expansion


neonatal atelectasis

Loss of surfactant. causes resipratory distress syndrome, this happens in premature babies, mothers with diabetes(fetal hyperglycemia stimulates insulin release, and children born cesarean section( labor and vaginal delivery causes increased stress and increased cortisol so increase of surfactant production.
MORPHOLOGY- collapsed alveoli are lined by hyaline membranes.
CLINICAL- RD within a few hours of birth, Hypoxemia and respiratory acidosis, Chest x-ray (Ground glass appearance)
COMPLICATIONS- Intraventricular hemorrhage, PDA, necrotizing enterocolitis, Hypoglycemia(excessive insulin release) O2 therapy can damage.


Lung surfactant

made of lipoprotein (phosphatidylcholine(lecithin), Phosphatidylglycerol, Surfactant proteins A and D for inate immunity and Surfactant protiens B and C which reduce surface tension at air liquid barrier in alveioli
--is synthesized in type 2 pneumocytes at 28th week and is stored in lamellar bodies.
- modulated by hormones, cortisol and thyroxin increase, insulin decrease.


Endothelial damage and epithelial damage cause

plasma leak into alveoli which produces fibrin and necrotic cells which gives you the hyaline membrane.


Acute Respiratory Distress Syndrome

CLINICAL- rapid onset, severe hypoxemia, BILATERAL pulmonary infiltrates, refractory to O2 therapy, econdary to both direct and indirect lung injury. (Alveolar epitheilum/capillary endothelium compromise) this increases vascular permeabliity , loss of diffuison and surfactant deficiency due to Type II cell damage. 40% mortality, (poor for older, bacteremia/spesp and organ fiaulre) compromise can continue after acute phase secondary to fibrois. normal function in 6-12 months.
ETIOLOGY- DIRECT Pneymonia, Aspiration, Emboli, Inhalation, drowning, O2 toxicity INDIRECT- Sepsis, trauma wiht shock, acute pancreatitis, Severe burns, Transfusion of blood products, Uremia, Drugs.-
MORPHOLOGY, HISTO- Acute- 0-7 days, heavy and firm lungs, interstial and intraalveolar edema/hemorrhage, necrosis and sloughing, hyaline membranes. -Organizing and proliferative phase 1-3 weeks- Proliferation of type II cells, fibrosis, septal thickening.


Acute Lung Injury

endothelial or epithelial injury can be non-heritable and heritable, mediators are cytokines, oxidants, growth factors (TNF, IL1,6 and, 10
MANIFESTS AS- pulmonary edema, diffuse alveolar damage (ARDS)


Obsctructive vs Restrictive

Obstructive: airway disorder, increased resistance to air flow and limited expiratory rates on forced experation, reduced FEV1/FCV ratio
RESTRICTIVE: Parenchymal disorder- Repspiratory bronchiole alveoli and alveolar ducts. decreased expansion with reduced total lung capacity, O@ diffusing copacity, Lung volumes and compliance. Increased FEV1/ FVC ratio.


Chronic obstructive lung disease COPD

4th leading cause of deaths, in US and 3rd worldwide by 2020. Men and women afected equally with smokers hte most affected. Obstruction is secondary to limitation of airflow.
ETIOLOGY- Reverible- astham, Irreversible, Chronic Bronchitis, Emphysema, Bronchoectasis.
INVESTIGATIONS- TLC Increased, FVC normal or slight decrease, FEV1 decreased ratio is reduced.



airspace inlargement, destruction of airspace walls, WITHOUT fibrosis.
PATHGENESIS- Imbalance of proteases, inhalation of toxic agents leads to inflammatory response which leads to elastase cytokines an oxidant stress, leads to epithelial injury and proteolysis of ECM due to failure of antioxidants and antiproteases. which leads to destruction of alveolar parenchyma
ETIOLOGY- Alpha-1 antitrypsin deficiency( point mutation causes retention in hepatocyte1% of emphysema) Pi gene on chromosome 14 PIMM is normal PiZZmost abnormal, causes protein to accumulate in liver and therefore chornic liver disease. -- polymorphisms in the TFGB gene/Matrix metalloproteinases.- TGFB inadequate repair of elastin injury, MMP (some have increased MMP9 and 12)
MORPHOLOGY Gross- hyperinflated lungs with bulla formation, parenchyma has moth eaten appearance. Destruction of alveolar septa without fibrosis, destruction of elastin in small airways.
CLINICAL- Pink puffers. Barrel chest, dyspmnea, prolonged expiration. sitting forward to try to squeeze air out. X ray flat domes of diaphragm. weak and skinny. weight loss becasue of excess puffing and punting. Glodd gases normal until ate with onset of hypoxia, hypercapnia and respiartory acidosis


centrilobular (centriacinar) emphysema

smoking, upper lung zones, respiratory bronciole is affected.


Panlobluar (panacinar) emphysema

Alpha 1-antitrypsin deficiency, lower lung zones, acinus distal to RB is involved chromosomal.


Septal (distal acinar) emphysema

rare, next to atelectasis, along septa, margins of loves, subpleural, more comon in upper lobes, may form bullae. can lead to pneumothorax.


Irregular pneumothorax

surrounding a scar, asymptomatic.


Chronic Bronchitits

CLINICAL DIAGNOSIS! - occurs longer than 3 months in 2 or more consectutive years. Cough is productive.
-Blue bloaters, hypoxia, hypercapnea, cyanosis --> insensitivity to pCO2 in respiratory centers, and respiratory drive is driven by low pO2, this is a problem when you treat with O2, need to give low flow.
-pulmonary hypertension/cor pulmonale.

ETIOLOGY- Common among smokers and urban dwellers(SO2 and NO2). Can occur in conjunction with Emphysema

PATHOGENESIS- -Hypertrophy of seromuinous glands, - increased goblet cells, Infitrate of CD8+, macros, PMNs, NO EOSINOPHILS
- airflow obstruction in CB is peripheral and results from goblet cell metaplasia in bronchioles,
-Coexisting emphysema increases impairment
-coexisting infection can complicate and exaxerbate

DISTINCT FEATURE- hypersecretion of mucus.

GROSS- hyperemia, swelling and edema of mucous membranes, muinous and mucupurulent secretions.
-large airways

HISTO- hypertrophy, hyperplasia of seromucinous glands, increased Reid index, inflammatory cells
-small aireways, goblet cell metaplasia, mucus plugging, inflammation and FIBROSIS


Reid Index

ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and cartilage.



ETIOLOGY- chronic inflammatory disease, hyperactive airways. Recurrent wheezing, breathlessness, chest tightness and cough, episodic, reverible bronchoconstriction.

GROSS- occusion of airways by thick mucus, hyperinflation of lungs, Edema, patchy necrosis, mucus plugs with Curschmann spirals, Charcot leyden crystals and eosinophils.
HISTO- Eosinophils deposit on the subbasement membrane . basement membrane thickening, hypertrophy of the smooth muscle.
goblet cells hyperplasia

CLINICAL- Episodic, nights and early morning, porgrssive hyperinflation of lungs with air trapped ind distal to mucus packed bronchi. attacks last a couple of hours. obstruction during expiration, FEV1 less than 30 % hyperventilation hypoxia hypercapnia, respiratory acidosis, Status asthmatics have severe prolonged asthma and are unresponsive to therapy.


Atopic Asthma

PATHOGENESIS- allergic sensitization, Type I IGE mediated hypersensitivity reaction, TH2 cytokines- IL-4 stimulates IGE production, IL- activates eosinophils, IL-13 stimulates mucus and promotes IGE production of B cells. IgE coats mast cells which degranulate with antigen exposure.
Early phase-bronchoconstriction, increased mucus, vasodilation
Late Phase-4-24 hours, activation of eosinophils, PMNs and T cells, epithelial cells are activated and recruit more Th2 cells and eosinophilsl

CLINICAL- Patients have allergic rhinits or eczema


Non Atopic Asthma

PATHGENESIS- no IgE, secondary to viral infections of upper respiratory tract or inhaled SO2, NO2 and O3, virus induces mucosal damage--> lowers threshold of subepithelial vagal receptors to irritants. Ultimate inflammatory mediators are the same as atopic astham so treatment is similar.


Drug Induced Asthma

PATHOGENESIS- Drug like aspirincauses recurrent rhinitis, nasal polyps, urticaria, and bronchospasm, inhibits cox pathway of AA without affecting lipooxygenase route--> bronchoconstriction mediated by leukotrienes


Occupational asthma

PATHOGENESIS- astham stimulated by fumes, organic dusts, chemical dusts and gases, Epoxy resins, plastics, wood, cotton, platinum, toluene, Asthma attacks following repeated exposure.


Eosinophilic Granuloma

pulmonary disease in the adult almost exclusively involved smokers, treatment centers on cessation, results in dyspnea, cough, interstitial nodular and fibrocystic disease and obstructive and restrictive changes in spirometry, Culprit cell in the LAngerhans cell, not the eosinophil, contain Birbeck Granules on EM.



Permanent dilation of Bronchi, Bronchioles secondary to destrucitno of supporting tissue,

ETIOLOGY- obstructino and chronic infection- tumor, foreign body
-congenital hereditary condistions- CF, immunodeficiency states, Kartagener syndrome
-Necrotizing/supperative pneumonia- virulent organisms.

PATHOGENESIS- Obstruction hampers clearances-->secondary infectino--> damaged bronchial walls-->bronchiectasis. -->persistent necrotizing infection-->obstructive secretions and damage-->peribronchial/peribronchiolar fibrosis--> traction, ectasia-->Bronchiectasis.

GROSS- Dilated airways out to pleural sacs. appear as cysts filled with mucupurulent secretions.

HISTO- Intense acute and chronic inflammatory exudate in bronchial walls, necrotizing ulceration.
-Squamos metaplasia of bronchial epithelium,
-lung abscesses may be present, fibrosis of bronchial walls leading to bronchiolitis obliteranse,
-cultures are usually positive.


restrictive lung disease

parenchymal disorders, involves interstitum of alveolar walls, bilateral patchy chronic lung involvement.
intra alveolar space also might be involved,

AKA infiltrative lung disease or Diffuse parenchymal lung disease.

PATHOGENESIS- Alveolitis, damage to pneumocytes and endothelial cells. leads to cytokines which mediate and stimulate interstitial fibrosis, which decreases lung compliance, elasticity, expansion

chronicity of exposure, effectiveness of lung defenses, extent of injury, intactness of BM, Individual susceptibility.

GENERAL FEATURES: fibrosis, decreased lunc compliance V-P mismatch, hypoxia, progression to repsiratory failure with pulmonary hypert. Reduced FEV Reduced FEV1 so /Normal ratio and normal PEFR.



UIP, NSIP, COP, CVD, Pneumoconiosis


Granulomatous RLD

Sarcoid, HP


Eosinophilic RLD

Leoffler syndrome, drug allergy related, chornic eosinopihilic pneuonia


smmoking releated RLD



IPF/Usual interstitial Pneumonia

males more than females, over 60, bilateral fibrosing with severe hypoxia and cyanosis, relentless progression with mean survival less than 3 years. need lung transplant

Is the radiographic pathologic correlate to IPF Radiology and/or pathology required for diagnosis.

must exclude asbestosis and collagen).
GROSS- cobblestoned pleural surface, firm fibortic parenchyma with lower lobe and subpleural accentuation. (differential for emphysema.)
Have honey comb cystic spaces lined by type II pneumocytes.

HISTO- Temproal and geographic heterogeneity meaning it can have both mature fibrosis and young fibroblast foci, with areas of spared normal lung,

CLINICAL- gradual fry cough, dyspnea, crackles, relentless progression with cyanosis, cor pulmonale and peripheral edema in late stages.



better prognosis than UIP, younger demographic can treat with steroids and immunomodulatory therapies.
HISTO- uniform fibrosing process (CHICKENWIRE) you can have cellular variant with lymphocytes or fibrosing variant lacks honeycomb change and fibroblast foci.


Cryptogenic organizing pneumonia

cough dyspnea, patchy peribronchial or subpleuaral consolidation.

POLYPOID plugs of loos organizing tissue, in alveolar ducts, MASSON bodies, alveolar struture no destroyed, can recover spontaneously, can also be seen in pneumonia, Collagen VD, transpalnt(thereore not cryptogenic)


Collagen vascular disease

Lupus, Rheumatoid arthritis, systemic sclerosis, dermatomyositis, polymyospitis

pathlogical patterns seen with these include UIP, NSIP, organizing pneumonia, bronchiolitis fibrosis, LIP,

Pleural involvement can occur, pleuritis, pelural nodules, pleuarl effusion.


Acute Interstitial pneumonia

Hamman Rich Syndrome, is an affressive ILD presents with alveolar damage and haline membranes


Lympohid interstital pneumonia

expansion of intersittium by groups and sheets of lymphoid cells, occurs in assocaition with connective tisue diseases, auto immundesases or HIV infection. can undergo transforamtion to lymphoma.


Respiratory Bronchiolitis interstiial lung disease

smokers, accumulation of smokers' macrophages, peribronchiolar fibrosis. STOP smoking.


Desquamative interstitial pneymonia

also occurs in smokers, prominent filing of alveolar spaces by smoker's macrophages, with minimal fibrosis. not just in respiratory bronchioles.