LUNGS Flashcards
(41 cards)
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
Atelectasis
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.
EMPHYSEMA
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.
Asthma
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.
