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Respiratory 16
| Question | Answer |
|---|---|
| Type I alveolar | surface of the lung |
| Type II alveolar | secret the surfactant, ability to differentiate into Type I |
| Fibroblast | Collage & Elastin to create the scaffolding an attachment point |
| Immune Cells | Macrophage & White blood cells fight off antigen formed by a pathogens |
| Compliance | how easily it changes it shape |
| Elasticity | tendency to return to intial size after distension |
| Surface Tension (ST) | thin film of fluid on alveolar surface; fluid absorption osmosis driven by Na+ [phospholipid (phosphatidylcholine & phosphatidylglycerol secreted by Type II alveolar cells |
| Law of Laplace | alveolar pressure is directly proportional to ST; inversely to radius of alveoli (small sack more readily; bigger less prone) |
| RDS | respiratory distress syndrome |
| ARDS | acute respiratory distress syndrome |
| Partial pressure | pressure that a particular gas in a mixture exerts indep. |
| Dalton's Law | total pressure of a gas mix is the sum of partial pressures of each gas in mixture |
| Boyle's Law | implies changes in intrapulmonary pressure occur as a result of changes in lung volume - pressure of a gas is inversely proportional to volume; air moves from a higher to lower pressure GOOD AIR IN increase in lung vol decreases intra |
| Smooth surfaces | visceral pleura -> LUNG intraplural space/pressure -> parietal pleura CHEST |
| Transmural Pressure | difference b/t intrapulmonary and intraplural 756 mmHg Table 16.1 |
| Efforts to overcome during respiration | frictional resistance to gas flow & elastic resistance of the tissues themselves |
| Restrictive | pink puffers overcoming elastic recoil of chest wall, parenchymal tissue, and surface tension |
| Obstructive | blue blowers overcoming tissue resistance and airway resistance (asthma, bronchitis, emphysema) |
| Spirometer trace | watching air move in out of lungs; tidal volume (normal in and out volume); expiratory reserve volume (what you can take on top of your tidal volume); maximal expiration (max out without collapsing lungs); residual volume, with collapse; VC=IRV+ERV+TV |
| Inspiratory capcity | tidal volume plus inspiratory reserve volume |
| Functional residual capacity | expiratory reserve vol plue residual vol |
| Vital capacity | sum of IRV TV ERV |
| Ventilation and Perfusion Zones | air in and blood to the site; higher vent lower perf PA>Pa>Pv zone 1; Pa/PA/PV zone 2; Pa>PV>PA zone 3; higher perf lower vent |
| Pulmonary circulation=equates to flow in systemic circulation | |
| Ventilation-perfusion coupling=hypoxic vaso-constriction in the lung | |
| Physical Principles of Gas Exchange | membrane thickness of type 1 cells; diff coefficient of gas, surface area of membrane |
| Ventilation with Saturation | Partial pressure O, 40 & CO2, 46 -> O, 100 & CO2, 40 Left Atrium and Ventricle Systemic arteries |
| Partial pressure of oxygen | 50 mmHg getting oxygen onto hemoglobin of red blood cell; shift the curve to the right decrease affinity decrease in pH, increase in CO2, increase in temperature result in a decrease in the ability of hemoglobin to hold oxygen |
| Haldane Effect | |
| Bohr Effect | effect of hydrogen, acidic, shift affinity of hemoglobin to deliver oxygen and in the opposite carries away hydrogen |
| what happens at the level of the tissue pH lower CO2 higher Temperature higher, what happens at the level of the lung; pH higher, CO2 lower, Temperature lower drop-off CO2 drop-off | |
| Allosteric effects | |
| Carbon dioxide | .7 bicarbonate, .23 blood proteins, .07 soln with plasma |
| Carbaminohemoglobin | CO2 combined with hemoglobin CO2 + Hb-NH2 <——> H+ + Hb-NH-COO– |
| The chloride shift=antiport with chloride moves into RBC and bicarb out of the RBC; | |
| Reverse chloride shift=pulling chloride out and bicarb back into the RBC | |
| 7.35 less than acidosis [ normal pH levels ] 7.45 greater than alkalosis | |
| CO2 and Hydrogen | volatile acid can be converted to a gas |
| Nonvolatile acids | |
| Respiratory acidosis=caused by hypoventilation (CO2) rise in blood and thus carbonic acid | |
| Respiratory alkalosis=caused by hyperventilation (CO2) fall in blood | |
| Metabolic acidosis | keytone bodies in diabetes loss of bicarbs (for buffering) in diarrhea |
| Metabolic alkalosis | caused by too much bicarb or too little nonvolatile acids (from vomiting out stomach acid) |
| Henderson-Hasselbalch equation uses CO2 and HCO3 levels to calculate pH | 6.1 + log |
| Fibrosis | putting down too much collagen can be caused by toxicants; Type 1 necrosis, Type 2 cell proliferation, macrophage accumulation, fibroblast accumulation and smooth muscle cells, collagen increases, thickening of the air blood/ |
| Emphysema | loosing tissue, surface area and changing the compliance and elasticity (easy to get air in but difficult to get air out, less recoil) |
| Result in fewer, larger, alveoli | smoking stimulates release of inflammatory cytokines which attract macrophages and leukocytes that secrete enzymes that destroy tissue |
| Destruction of alveolar cell walls, Over-inflation and distention of alveoli, gas exchange is affected, toxicant-induced version is accompanied by inflammation | |
| Obstructive air out | Restrictive air in |
| FEV1 decreased | someone with emphysema Obstructive disorder |
| Dyspnea | a feeling of shortness of breath; asthma results from episodes of obstruction of air flow through bronchioles (chronic mucus generation, airway constriction, chronic mucus generation) |
| Trigger | allergens cold air |
| Graphics | normal, emphysema, fibrotic lung disease, pulmonary edema, asthma |
| Abestos | increase in collage in alveolar walls, presense of asbestos fibers Causes short fibers are engulfed by macrophages and leave the lung |
| Long fibers | |
| Coal | causes loss of tissue like an emphysema patient |
| Silica | macrophages recruit fibroblast to the scene fibrosis collagen silicotic nodule |
| Abestos | macrophages recruit fibroblast to scene fibrosis collagen |
| Oxidative burden | oxidative burst prolonged accumulation of inflammatory cells quick non-specific |
| 2nd hand smoke=more harmful temperature and unfiltered | |
| apneustic center | pons starts stimulates inspiration (inspiratories in medulla) |
| pneumotaxic center | stopping movement antagoizes apneustic center, inhibiting inspiration |
| smooth muscle recruitment | neuron levels and how they relate |
| chemoreceptors | central in medulla watch PCO2 and PO2 and pH and periphery, aortic bodies & carotid bodies,carotid sinus (neurons that are sensing) |
| CNS control of breathing | Cerebral Cortex, pons:apneu & pneu, med oblong:Chemoreceptors MO Aort and Cart, spinal cord (automatic breathing) |
| PCO2 | the most important or crucial matrix b/c of its effects on blood pH; low CO2 hyperventilation or hypocapnia; high CO2 hypoventilation or hypercapnia |
| Eff of Blood PCO2 and pH on Vent | periph responsive to hydrogen but it will not cross the blood brain barrier; so, in CSF CO2 will be converted to Hydrogen that is detected by central chemoreceptor |
| hypoxemia | low blood O2 has little effect on ventilation; partial pressure of oxgen in venous blood; hemoglobin has a high affinity for oxygen; |
| Hypoxic steps | low PO2, K channels close, cell depolarizes, Ca VG chan opens, Ca entry, exocytosis of neurotransmitters, AP signal to Medu to increase ventil |
| Perp | positive N respiratory pressure supplying air to lungs by supplying gas |
| Unmyelinated C fibers | are stimulated by noxious substances such as capsaicin; causes apnea followed by a rapid, shallow breathing |
| irritant receptors | rapidly adapting, respond to smoke, smog, and particulates (causes cough) |
| Hering-Breuer reflex | mediated by stretch receptors activated during inspiration (inhibits respiratory centers to prevent overinflation of lungs, forced exhalation) |
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