Pulm Flashcards
Majority of alveolar surface (95%) covered by what cells?
Squamous type I pneumocytes
Source of pulmonary surfactant
Cuboidal, clustered type II pneumocytes
Function of type II pneumocytes
Pulmonary surfactant (in lamellar bodies); precusors for type II and other type II’s; regenerate w/ lung damage
Histology of tracheobronchilal tree?
Pseudostratified columnar ciliated epithelium to the beginning of terminal bronchioles. Then changes to cuboidal. Airway smooth muscle extends to end of terminal bronchioles.
Club (Clara) Cells
Non-ciliated secretory cells found in TERMINAL portions of bronchioles; Regenerate ciliated cells of the bronchioles’ Degrade toxins; secrete component of surfactant. You’ve reached the END of the bronchi, and you will be Club’ed.
Function of goblet cells
Found in bronchi and larger bronchioles but NOT in alveoli; Produce Mucin. Goblet cells HOLD mucin.
Surfactant is made up of?
Lecithins (dipalmitoylphosphatidylcholine)
When is surfactant synthesized?
GA 26 wks; mature levels by GA 35 wks
Fetal lung maturity indicated via surfactant how?
lecithin:sphingomyelin ratio > 2.0 in amniotic fluid. Cortisol has greatest effect (zona glomerulosa)
Collapsing pressure =
2 x surface tension / radius. Smaller alveoli have higher collapsing pressure and EASIER to collapse.
Vagus nerve stimulation of lungs does?
Bronchoconstriction and increased mucus secretion (M3 receptor via Ach) -> inc. airway resistance and WOB.
Sarcoidosis
AA, constitutional, b/l hilar adenopathy, non-caseating granulomas. Elevated serum ACE levels. Liver involvement in up to 75% of cases.
At what point does the mucociliary elevator stop?
Terminal bronchioles. Distal, macrophages do the job.
Most common lung cancer in general population?
Adenocarcinoma (women and non-smokers). Peripheral, tumors cells forming glandular or papillary structures. Clubbing, hypertrophic osteoarthropathy.
Reid index?
Thickness of MUCOUS gland layer over thickness of bronchial wall from respiratory epithelium to cartilage. Sensitive measure of mucous gland enlargement, which is found in chronic bronchitis. Normally = 0.4
Honeycomb lung?
Subpleural cystic airspace enlargement characteristic of IPF
Don’t do surgery for this lung cancer?
Small cell carcinoma b/c it’s so invasive, they usu. have distant metastases even if it doesn’t appear so.
Where do the elastases in alveolar fluid come from?
Macrophages and neutrophils
Silicosis
Eggshell calcifications of hilar nodes and birefringent particles surrounded by fibrous tissue.
Asbestosis
Calcified PLEURAL PLAQUES and ferruginous bodies.
Clubbing
Associated w/ prolonged hypoxia. Large cell lung ca, TB, CF, bronchiectasis, pulm HTN, empyema, chronic lung diseases associated with hypoxia. Cyanotic congenital heart diseases, bacterial endocarditis. IBD, hyperthyroidism, and malabsorption.
Tracheal deviation in atelectasis vs. pleural effusion?
Towards atelectasis and away from pleural effusion
Cells involved in pathogenesis of emphysema?
Activated macrophages and neutrophils release proteases that degrade EXCM and generate O2 free radicals to inhibit alpha-1-antitrypsin and other PI’s. Imbalance between protease and anti protease -> acinar wall destruction. (Centriacinar emphysema)
Theophylline
Methylxanthine. Thought to inhibit phosphodiesterase. Narrow index and metabolized by cytochrome P450 while blocking adenosine. Tox = GI, arrhythmias, sz
PFT differences in COPD
Both have normal/low FVC, low FEV1, low FEV1/FVC. However emphysema as HIGH TLC, FRC, pulmonary compliance, and LOW DLCO.
Lung lobes
Left has TWO w/ lingual. Right has three (Superior, middle, inferior)
Lung hilus
RALS - Right Anterior; Left Superior. Pulmonary artery is anterior/superior to the bronchus.
Structures perforating the diaphragm?
T8 = IVC. T10 = esophagus and vagus. T12 = aorta, thoracic duct, and azygos vein. I 8 10 esopa-eggs AT 12.
Capacity vs. volume?
Capacity = sum of two volumes
RV vs. ERV vs. IRV
Residual volume = absolute air in lung after expiration. ERV = expiratory reserve volume = air that can be breathed out after normal expiration. IRV = inspiratory reserve volume = amount of air that can breathed after normal inspiration (after TV). FRC = ERV + RV
IC
Inspiratory capacity = IRV + TV
Functional reserve capacity
ERV + RV
VC
Vital capacity = IRV + TV + ERV
TLC
Total lung capacity = FRC + IC = RV + ERV + TV + IRV
Equation for physiological dead space?
= Tidal volume x (PaCO2 - PeCO2) / PaCO2; Where PeCo2 = expired air PCO2. We assume that all CO2 in expired air comes from ventilation, that there is no Co2 in inspired air, and that physiologic dead space neither exchanges nor contributes to CO2. (Also assume PaCO2 = PACO2). What percentage of your tidal volume is actually dead space?
Minute ventilation vs. alveolar ventilation?
Minute ventilation = total volume of gas entering lungs per minute. (TV x RR). Alveolar ventilation = volume of gas per unit time that reaches ALVEOLI = (TV - dead space) x RR
FRC
Where chest wall springiness outwards is balanced by lung collapsiness inwards is matched.
Two forms of Hgb?
T form = Taut. Low affinity for O2 = right-shifted. Taut in Tissues. R form = relaxed. High affinity for O2 w/ cooperativity and negative allostery. Relaxed in respiratory tract.
Fetal Hb
2 alpha, 2 gamma (instead of beta). Has LOWER affinity for 2,3 BPG —> higher affinity for O2 (less right-shifted)
Oxygen content of blood
= 1.3 * Hgb x O2Sat + PaO2; O2Sat = how well O2 can get onto Hgb (e.g. low in CO poisoning)
Major regulatory aspect of pulmonary blood flow
Alveolar O2. Hypoxic vasoconstriction to shunt blood away from poorly ventilated areas. Reduced P2 directly causes smooth muscles to vasoconstriction
Perfusion limited vs. diffusion limited
Perfusion limited means that gas equilibrates quickly along length of capillary, so you can only increase absorption via increased blood flow (O2, CO2, N2O). Diffusion-limited means that gas doesn’t equilibrate in-time (Pa<PA). CO and O2 in emphysema or fibrosis demonstrate.
Diffusion of gases in the alveoli is dependent mainly on what factors
Area (decreased in emphysema). Thickness (increased in pulmonary fibrosis). Difference in partial pressure
PVR =
Resistance = Change pressure / flow. PVR = (Ppa - Pla) / CO. Pla = pulmonary wedge pressure.
Alveolar gas equation
Explains how much O2 is in the alveoli. PAO2 = PIO2 - PaCO2/R = 150 - PaCO2/0.8. Basically, highly dependent on CO2 status.
A-a gradient
PAO2 - PaO2. Difference in alveolar O2 and arteriolar O2. Usu. 10-15 mmHg. Increased in hypoxemia (shunting, V/Q mismatch, fibrosis)
Etios of hypoxemia and hypoxia?
Hypoxia is decreased O2 delivery to tissue. Can be due to decreased hyperemia, dec. CO, anemia, CO poisoning. Hypoxemia is decreased PaO2. Could be due to high altitude, hypoventilation (normal A-a). Or V/Q mismatch, diffusion, right-to-left shunt (high A-a gradient)
Differences in V/Q in the three zones of the lung
Zone 1 (top) has worst V and Q. Not only that, but it’s V/Q is high (3 - wasted ventilation). PA>Pa>Pv. Zone 2 and 3 have V/Q < 1 (wasted perfusion). But Zone 2 is Pa > PA > Pv. While Zone 3 is Pa > Pv > PA (b/c gravity has inc. vessel pressures).
Haldane vs. Bohr effect
Haldane - Oxygenation of Hb leads to more CO2 release. (And deoxygenated Hb -> greater CO2 binding). Bohr - In tissue, increased H+ from metabolism right-shifts, leading to unloaded O2.
How is CO2 transported from tissue?
CO2 diffuses into RBC where it is acted on by CA -> bicarbonate + H+. H+ is buffered with deoxyhemoglobin while HCO3- enters blood stream via band 3 (HCO3-Cl anti-porter) and the majority of the CO2 is transported at HCO3.
Major pulmonary response to exercise?
Increased ventilation rate, more uniform V/Q ratio b/c of vasodilation of the apical capillaries. No change in PaO2 and PaCO2 but increased venous CO2 content and decreased venous O2 content.
Most common cause of rhinosinusitis?
Viral URI. May cause superimposed bacterial infection - Strep pneumo, H. flu, M. catarrhalis
Virchow triad
Stasis, hypercoagulability, endothelial damage
Homan sign
Dorsiflexion of foot -> calf pain. Think DVT.
How to distinguish between pre- and post-mortem thrombi?
Lines of Zahn - interdigitating areas of pink (PLT, fibrin) and red (RBC’s) only found in pre-mortem thrombi
Types of pulmonary emboli
Thrombus, Fat, Air, Bacteria, Amniotic fluid, Tumor
Obstructive lung disease parameters
Inc. RV, dec. FVC. Decreased FEV1/FVC (with FEV1 decreasing more than FVC)
Chronic bronchitis
Hyperplasia of mucus-secreting glands in bronchi (Reid index > 50%). Productive cough > 3 months for > 2 years.
Emphysema
Enlarged air spaces, decreased recoil and increased compliance, decreased DLCO b/c of alveolar wall destruction. Increased elastase. Pursed lips b/c it increases airway pressure and prevents airway collapse.
Centriacinar vs. panacinar
Smoking vs. alpha-antitrypsin deficiency
Asthma
Reversible bronchoonstriction. SMC hypertrophy. Curschmann spirals (shed epithelium -> mucus plugs) and Charcot-Leyden crystals (breakdown of eosinophils in sputum)
Bronchiectasis
Chronic necrotizing infection of bronchi that permanently dilates airways. Purulent sputum, recurrent infections, hemoptysis. Associated with bronchial obstruction, dc. ciliary motility (smoking), Kartagener syndrome, CF, allergic bronchopulmonary aspergillosis
Restrictive lung disease
Dec. FVC, TLC. But FEV1/FVC likely > 80%. Divide up by Normal A-a gradient (muscular, structural) vs. inc. A-a gradient (ARDS, hyaline, etc.)
Asbestosis
Ivory white pleural plaques. Increased incidence of bronchogenic carcinoma and mesothelioma. LOWER lobes. Golden-brown fusiform rods. Asbestosis from ROOF but affects BASE. Silica and coal from base but affect ROOF.
Coal workers’ pneumoconiosis
Coal dust exposure -> macrophages w/ carbon -> inflammation and fibrosis. Upper lobes. Anthracosis = asymptomatic condition found in urban dwellers
Silicosis
Macrophages respond to silica with fibrogenic factors -> FIBROSIS. Inc. risk of TB and bronchogenic carcinoma. Upper lobes. Eggshell calcification of hilar lymph nodes.
Neonatal respiratory distress syndrome
Surfactant deficiency (lecithin:sphingomyelin < 1.5). persistently low O2 tension -> risk of PDA. BUT therapeutic supplemental O2 can lead to retinopathy of prematurity and bronchopulmonary dysplasia (O2 radical problems). RF = prematurity, maternal diabetes, C-section (dec. fetal glucocorticoids). Tx = maternal steroids before birth; artificial surfactant for infant
ARDS
Etios include trauma, shock, aspiration, uremia, acute pancreatitis, amniotic fluid embolism. “Diffuse alveolar damage” (dmg to microvascular endothelium +/- alveolar epithelium) leads to inc. alveolar capillary PERMEABILITY. Intra-alveolar HYALINE membrane formation = protein-rich edema + necrotic tissue. Dmg from NEUTROPHILIC substances, coag cascade activation, O2 radicals. “White-out.” Exudative, proliferative, then fibrotic stage (honeycomb lung)
Pulmonary hypertension
> = 25 mmHg at rest (normal is 10-14). Primary = inactivating BMPR2 gene (inhibits vascular SMC proliferation. Poor prognosis). Secondary from COPD, MS, recurrent thromboemboli, autoimmune disease, L-R shunt (inc. shear), sleep apnea, hypoxic vasoconstriction (high altitude). Death from decompensated cor pulmonale.
Sleep apnea
Repeated cessation of sleep > 10 s. Comps include htn, arrhythmias (Afib/flutter), sudden death. Obesity hypoventilation syndrome = dec. PaO2 and increased PaCO2 during waking hours 2/2 hypoventilation.
Tracheal deviation
Toward atelectasis and away from TENSION.
Central lung cancers?
Squamous and small cell carcinomas are SENTRAL.
Squamous cell carcinoma
3 C’s. Cavitation, cigarettes, and hyperCalcemia 2/2 PTHrP. Path = keratin pearls and intracellular bridges. And Central..
Small cell carcinoma
Undifferentiated tumor that is very aggressive. ACTH, ADH, Ab’ against presynaptic Ca2+ (Lambert-Eaton), Amplification of myc genes. NO surgery. Path - NEUROENDOCRINE Kulchitsky cells (small dark blue cells)
Adenocarcinoma
Most common lung cancer in NON-smokers and overall. Peripheral. Activating mutations includek-ras, EGFR, ALK. Bronchioalveolar subtype grows on ALVEOLAR septa = “thickening” of alveolar walls. MALIGNANT. Bronchorrea.
Large cell carcinoma
Highly anapestic undifferentiated, poor prognostic, peripheral tumor. Surgery > Chemo. Path shows pleomorphic giant cells.
Bronchial carcinoid tumor
Good prognosis. Symptoms from mass effect +/- carcinoid syndrome (flushing, diarrhea, wheezing). Path - nests of neuroendocrine cells with + chromogranin A.
Mesothelioma
A malignancy of pleural -> hemorrhagic effusions and thickening. Psammoma. Associated with asbestosis.
Pancoast
Apex - Horner, SVC syndrome, sensorimotor, hoarsness
Anatomical differences between lobar PNA, bronchopneumonia, and interstitial/atypical pneumonia
Lobar PNA is INTRAalveolar. Bronchopneumonia is patchy involving >=1 lobe. Atypicals are also >=1 lobe.
Organisms between lobar PNA, bronchoPNA, atypical PNA
Lobar - Strep, legionella, klebs. BronchoPNA - Strep, staph, H flu, klebs. Atypical - Viral, Mycoplasma, Legionella, Chlamydia
Mechanistic causes of lung abscess?
Aspiration (e.g. alcoholic or epileptic - Peptostrep, Prevotella, Bacteroides, Fusobacterium tx = clinda). Complication of pneumonia. Hematogeneous spread. Bronchial obstruction.
Transudate vs. exudate in pleural effusion
Transudate more likely due to CHF, nephrotic syndrome, cirrhosis. Exudate more likely malignancy, PNA, collagen vascular disease, trauma. Exudate should be drained b/c of infection risk.
Chylothorax
Lymphatic pleural effusion 2/2 thoracic duct injury from trauma or malignancy. Notable for INC TGs.
Difference between spontaneous pneumothorax and tension pneumothorax?
In a tension pneumo, air can enter but CANNOT exit 2/2 trauma or infection. In spontaneous, accumulation of space 2/2 rupture of apical bleb.
Expectorants
Guaifenesin - thins secretions but doesn’t suppress cough reflex. N-acetylcysteine loosens mucous plugs in CF patients (antidote for tylenol overdose)
Antitussive?
Dextromethorphan. Antagonizes NMDA glutamate receptors. Synthetic codeine analog. Mild abuse potential
Nasal decongestant
Sympathomimetic ALPHA-agonists (Pseudoephedrine, phenylephrine). Reduce hyperemia, edema, nasal congestion, open eustachian tubes. Tox = HTN.
Ipratropium
Muscarinic antagonist to prevent bronchoconstriction. Tiotropium is LA.
Antileukotrienes
Zileuton, Montelukas, Zafirlukast
Zileuton
5-lipoxygenase pathway inhibitor that blocks arachidonic acid -> leukotrienes.
Montelukast, zafirlukast
Blocks leukotriene receptors. Good for ASA-induced asthma
Bosentan
Treats pulmonary arterial HTN by competitively antagonizes endothelin-1 receptors to decrease vascular resistance
High altitude ABG?
Respiratory alkalosis. However, after 10-14 days, EPO production will be sufficient to restore arterial O2 content to near sea level values.
Pathogenesis of ASA-sensitive aspirin?
Shunt arachidonic acid metabolism down lipooxygenase pathway to make leukotrienes –> increase bronchial tone
PE leads to what acid-base?
Respiratory ALKalosis. B/c hyperventilating to compensate for V/Q mismatch.
Where is the most airway resistance during breathing?
1/2 from upper respiratory tract. In lower respiratory tract, first 10 generations contribute most (2nd-5th most) b/c of turbulent airflow
Pulmonary stretch receptors?
Myelinated and unmyelinated C fibers in lungs and airways that protect against overinflation
Pulmonary embolism ABG?
Hypoxemia leads to respiratory hyperventilation = respiratory alkalosis with hypoxemia and a HIGH A-a gradient.
