Physio Reinforcing Concepts Pt1 PDF

Obstructive vs restrictive lung disease Obstructive: hard to get air out due to increased airway resistance. Can happen from inflammation, mucus plugging, bronchospasm, bronchial smooth muscle hypertrophy and hyperplasia. Increased resistance will lead to air trapping. Examples are Chronic Bronchiti...

Obstructive vs restrictive lung disease Obstructive: hard to get air out due to increased airway resistance. Can happen from inflammation, mucus plugging, bronchospasm, bronchial smooth muscle hypertrophy and hyperplasia. Increased resistance will lead to air trapping. Examples are Chronic Bronchitis, Emphysema, Asthma ● Obstructive disease will cause slow and deep breathing to maintain alveolar ventilation. There is a larger nonelastic work, so to minimize energy spent, the respiratory rate is decreased. To maintain alveolar ventilation tidal volume increases Restrictive: inability to get air in due to decreased compliance. If there is fibrosis, parenchymal edema/hemorrhage, decreased nerve stimulation, or increased abdominal pressure there will be a decreased ability for the lung to expand. Examples are PAINT: pleural effusion or fibrosis, alveolar edema/hemorrhage, interstitial lung disease or fibrosis, ALS, obesity, ascites ● Restrictive lung diseases will breath rapid and shallow to maintain alveolar ventilation. There is a large elastic work, to overcome that the tidal volume is decreased. To maintain alveolar ventilation respiratory rate is increased. Arterial-alveolar gas exchange As we inhale, our airway warms and humidifies the air we breathe as a protective mechanism for our bronchioles and alveoli. Adding water vapor to the air mixture reduces the partial pressure of O2 our trachea sees, and that PO2 decreases even more as we reach the alveoli when PCO2 increases. Air going from environment into the airway, down to alveoli, into arteries, then veins loses PO2 at every step 160->150->102->95->40 Arterial blood has less PO2 than alveolar blood because of natural shunting of deoxygenated blood into the pulmonary vein. Bronchial arteries, pleural arteries, alveoli that get no ventilation are examples of natural shunts. PCO2 increases once we reach capillary beds that participate in gas exchange(in lungs and peripheral tissues) 0->0->40->40->46 The PCO2 of the alveoli matches the PCO2 of the arteries, normally 40mmHg. PCO2 in the pulmonary artery is 46mmHg. CO2 diffuses from the capillaries into the alveoli, O2 diffuses from alveoli into capillaries. CO2 and O2 are in a steady state The terms hypo and hyperventilation refer to arterial PCO2, too much CO2 shows we are hypoventilating, too little CO2 shows we are hyperventilating Alveoli have uneven ventilation due to multiple factors, gravity, resistance, and compliance This is the alveolar gas equation where R is respiratory quotient, the ratio of CO2 produced to O2 consumed which is 0.8 at sea level. Fatty diets decrease this, Carb heavy diets increase this quotient Alveoli Anatomical dead space: regions like the trachea that hold air but do not participate in gas exchange Alveolar dead space: some alveoli do not receive the blood flow needed to perform gas exchange, in this situation these alveoli are dead space too. They are ventilated but not perfused Physiologic dead space: anatomical + alveolar, this is the total amount of each tidal volume that does not participate in gas exchange Peripheral gas exchange PO2 in the capillary drops from 95->40 as it reaches the peripheral tissues. Equilibrium is reached in the first ⅓ of the capillary length. CO2 leaves the peripheral tissues, and is mainly turned into bicarbonate in RBCs, some CO2 binds Hb creating a carbamino compound, some CO2 directly dissolves in plasma to carbonic acid Respiratory acidosis: too much CO2, hypoventilation would cause respiratory acidosis, kidneys compensate by increasing bicarbonate reabsorption, excreting H+ Respiratory alkalosis: too little CO2, hyperventilation would cause respiratory alkalosis, kidneys compensate by increasing bicarb secretion, reabsorbing H+ Metabolic acidosis: too little bicarb creates acidic environment sensed by peripheral and central chemoreceptors, respiratory compensation by increasing ventilation to blow off CO2 Metabolic alkalosis: too much bicarb creates a basic environment sensed by central chemoreceptors to decrease ventilation rate, however respiratory compensation is limited because peripheral chemoreceptors will sense low O2 environment and increase ventilations Ventilation-perfusion matching Arterial blood gas stability is determined by the ventilation:perfusion ratio. The optimal ratio is 0.84 ● Decreasing this ratio shows the perfusion to the alveoli exceeds the ventilation, too much blood is flowing to the alveoli it is unable to pick up oxygen. The system will be hypoxemic, hypercapnic, respiratory acidosis ● Increasing this ratio shows ventilation outweighs blood flow, too much CO2 leaves the system, too much O2 enters the system, it will become hyperoxemic, hypocapnic, respiratory alkalosis Shunts: Mixing deoxygenated/lower oxygenated blood with oxygenated blood drops arterial PO2. The diluting blood can come from: ● alveoli with low V/Q ● bronchial veins ● pleural veins ● thebesian veins ● patent foramen ovale Anoxia= no O2 Hypoxemia= low arterial blood PO2, hypoxic hypoxia Hypoxia: inadequate O2 available for tissue needs, 3 types ● Hematologic hypoxia: low Hb carrying ability, examples are anemia or carbon monoxide poisoning ● Ischemic hypoxia: low blood flow causing low tissue O2, arterial PO2 is normal ● Histotoxic hypoxia: normal O2 supplied but can’t be utilized, example is cyanide poisoning(cyanide arrests the ETC yielding O2 ineffective) Reflexes and control of breathing DRG=dorsal respiratory group, mediates inspiration by stimulating phrenic nerve to contract diaphragm(contraction of diaphragm flattens it, enlarging the chest cavity and decreasing intrathoracic pressure) Nucleus tractus soltarius(NTS) is in the DRG, it is the site of input by glossopharyngeal and vagus VRG=ventral respiratory group, mediates forced expiration (normal respiration is passive, mediated by relaxation of inspiratory muscles) by recruiting the inner intercostals and the abdominal muscles, VRG helps with inspiration as well by flaring nostrils and dilating larynx Pontine Respiratory group: pneumotaxic center: turns off inspiration by inhibiting apneustic center, damage to the pneumotaxic center removes limitations on apneustic center, inspiration will be prolonged and expiration shortened Basic respiratory rhythm is generated in the medulla by the central pattern generator(CPG). Nerve impulses to inspiratory muscles increase in frequency during inspiration, the impulses are absent in expiration. This ramping up rhythm can be modulated by changing inspiration time, afferent input from mechano/chemoreceptors, actions of pneumotaxic center. The lungs inflate throughout the time the nerve impulse ramps up(the lungs fill when we inspire), more nerve impulses will increase tidal volume Hering-Breuer Inflation: reflex against overinflation 1. 2. 3. 4. 5. Too much lung expansion Smooth muscle is stretched, SARs depolarize SARs transmit signal through vagus to the DRG DRG sends less signal to inspiratory muscles Decreased TV, decreased inspiration duration Hering Breuer Deflation: reflex against rapid deflation 1. 2. 3. Rapid lung deflation causes lack of stretch on RARs RARs signal to DRG via the vagus Inspiration is promoted increasing tidal volume(hyperpnea) and respiratory rate(tachypnea) GI Secretions Saliva: Hypotonic solution with high bicarb concentration, amylase(starch breakdown), lingual lipase Saliva is secreted by parasympathetic stimulation, when we see/smell/ think about food, when we have food in our mouth we secreted more saliva Sleep, fatigue and fear inhibit saliva secretion Stomach Secretions: Parietal Cells secrete HCl to kill bacteria and activate pepsin, and Intrinsic factor to help with vitamin B12 absorption. Destruction of parietal cells or intrinsic factor causes pernicious anemia, a type of macrocytic anemia. Chief cells release pepsinogen, when it activates in the acidic stomach it begins digesting proteins. Chief cells also secrete gastric lipase for fat digestion G cells respond to the presence of food in the stomach and secrete gastrin, which acts on the parietal cells to secrete HCl ● ● ● Somatostatin decreases H+ secretion directly by acting on Gi proteins of the parietal cell, or indirectly by inhibiting histamine and gastrin secretion Cephalic phase: sight, thought, smell, taste of food stimulates the stomach to begin secreting acid, priming the system Gastric phase: G sense sense presence of food, secrete gastrin, enhancing acid. Pepsinogen is activated and protein breakdown begins Peptic ulcers: hostile factors outbalance protective factors. Can be caused by H. Pylori(use urea breath test) NSAIDs(give misoprostol for NSAID ulcers EXCEPT if pregnant) excess acid production-proton pump inhibitor, H2 antagonist Duodenal ulcers: pain is alleviated while eating, patient will gain weight Gastric ulcers: pain is aggravated by eating, patient will lose weight H Pylori: leading cause of peptic ulcer disease, flagellated bacteria burrow into the mucosal lining of the stomach, and create a neutral environment for themselves using urease(produces ammonia and carbon dioxide which is sensed on urea breath test). Infiltration of the mucosal layer disrupts its protective ability causing peptic ulcers. Intestines+pancreas Small intestines: Site where most digestion and absorption occurs. There is a combination of secreting neutralizing compounds to counteract the HCl in chyme, and enzyme secretion to break molecules down to absorbable parts ● Passive diffusion, co transport, and exchange of Na and Cl creates a osmotic gradient for water to follow into the body. Absorption of water is dependent on osmosis ● Glucose is absorbed by SGLT1, once in the body it enters cells via GLUT transporters ● Peptides are cotransported with Na into enterocytes(these peptides are di- and tri- peptides) larger peptides need endocytosis ● Micelle formation aids in the absorption of triglycerides and fat soluble vitamins ● Iron: absorbed in duodenum ● B12: absorbed in ileum Need bile and bile salts to emulsify and absorb fats, secretin is released by S cells in the duodenum to stimulate bile secretion Pancreas: Exocrine function: Secretion of neutralizing compounds (bicarb is secreted by duct cells) and digestive enzymes (trypsin, chymotrypsin, lipase, amylase are secreted by acinar cells) ● ● Most of the pancreatic enzymes are inactive until they reach the intestinal lumen, inactive enzymes are zymogens and have the ending -ogen Trypsinogen is activated by enterokinase at the brush border, turning it into trypsin, which goes onto activate the other pancreatic enzymes CCK(cholecystokinin) and Ach stimulate pancreatic secretion. CCK is released by I-cells in the duodenum in response to fat. Ach is from vagus