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Gas exchange Bronchi: less extensive cartilage, allowing for motion, gone in bronchioles Smooth muscle from trachea to bronchioles, bronchioles almost entirely smooth muscle, obstructive diseases due to contraction of the smaller bronchi larger bronchioles. Muscles: external intercostals (most im...

Gas exchange Bronchi: less extensive cartilage, allowing for motion, gone in bronchioles Smooth muscle from trachea to bronchioles, bronchioles almost entirely smooth muscle, obstructive diseases due to contraction of the smaller bronchi larger bronchioles. Muscles: external intercostals (most import), sternocleidomastoid, anterior serrati, scaleni, up and P-A Expiration: external recti, internal intercostals Dorsal respiratory center: inspiration, mostly, rhythm of breathing. Dorsal medulla Ventral respiratory group: ventrolateral medulla, inactive during normal quiet respiration. DRG innervates VRG, but VRG not innervate DRG Pneumotach center: dorsal superior pons, rate and depth of breathing Apneustic center: caudal pons, prolong inspiration Hering-breuer inflation reflex: sensory stretch receptors in muscular walls of the bronchi and bronchioles, through vagus nerve to DRG, inhibit insipiratory, not activated till tidal volume 3x normal. Direct chemical control, center control Ventral medulla chemoreceptors, activated by CO2 and H+, excites respiratory center, most by H+, but H+ cant pass BBB, CO2+water crossing BBB, Acclimatization: respiratory center in brain less sensitive, so alveolar ventilation increases Adrenal gland stimulation: norepinephrine and epinephrine Parasym constriction: direct from vagua nerve, by ACH, also smoking etc Breathing=external respiration= air in and out of the respiratory system Internal respiration: exchange of gases between alveoli and blood Cellular respiration: use of oxygen by cells to generate ATP Conducting portion= anatomical dead space Respiratory portion= gas exchange=alveoli Physiological dead space= alveoli are damaged can not change gases Smooth muscle provide the major source of resistance to air flow Bronchiolar constrition by ACH in parasym, or histamine Bronchiolar dilation= by sympa release norepinephrine, adrenal stim releases E+NE Alveolar sacs: region of gas exchange, surrounded by capillaries, gas through single layer of alveolar epithelial cells Septal cells in alveolar produce surfactant, reduced surface tension of alveolar fliud, prevent collapse La place's law=smaller the alveoli has bigger surface tension and more likely to collapse Alveolar macrophages: phagocytize particle with PM smaller than 2.5 Pleura: parietal=inner surface of thoracic wall, visceral=outer surface of lung Intrapleural pressure, pressure on the fluid between the two pleura, help with expansion and compression and air movement Goblet cells and mucous produce sticky mucous, increase by exposure to contaminants in air Cilia in nasal cavity sweep the mucous down to the pharynx, musco-ciliart escalator=cilia in urt sweep mucous up to the pharynx Pulmonary ventilation= air in and out of lungs Internal intercostals are major muscles for forced inspiration and expiration Lungs remain inflated by intrapulmonary pressure bigger than intrapleural pressure about 4 mm HG Inhalation: atmospheric pressure bigger than alveolar pressure: -1mm Hg is adequate for quiet breathing, deep rapid inhalation requires -20 to --30 mm Hg difference Exhalation: alveolar pressure bigger than atmospheric pressure Skeletal muscle contraction increases the size of the thoracic cavity decreased alveolar pressure Eupnea=quiet breathing Hyperpnea=forced breathing Apnea=stop breathing Apneustic breathing=prolonged inspiration Cheyne stokes breathing=alternation of deep breaths and stoppage of breathing due to variations in blood CO2 Respiratory rate=number of breaths/minute Tidal volume=volume of air inhaled/breaths Respiratory minute volume=breaths/minute x tidal volume Alveolar ventilation=air available for gas exchange=breaths/min x(tidal volume-dead space) Increasing depth of breathing is more effective Factors affecting the volumes and capacities: Resistance to airflow: smooth muscle Compliance of the lungs: surfactant, when lungs expand, compliance decreases Pathological anatomical changes: elasticity of lungs-decreases in emphysema Strength of respiratory muscle: depends on use/health Body size, gender and altitude during childhood Dalton's law: partial pressures of gasses=sum of the partial pressures of individual gases Hery's law: diffusion between gas and liquid= amount of molecule dissolved in a liquid is proportional to the partial pressure of molecule in the gas CO2 is more soluble in water than O2 and N2 Atmospheric air is 16.9 O2, 78.6 N2, and 0M4 CO2 97% of O2 carried in blood is bound to hemoglobin At sea level large P1-P2 makes diffusion rapid, due to large surface area O2 and CO2 are lipid soluble, speeds diffusion through surfactant and cell membranes Increased blood flow to capillaries that serve the alveoli with the most O2 Gas transport in blood Hb-4 + 4O2 to Hb- 4 O2 Hb picks up O2 in lungs, and release O2 to Mb in tissues Bohr effect=falling pH=increased release of O2, shift of the hemoglobin curve to the right Rising temperature also cause shape change of Hb CO competes with O2 for the Fe2+ of Heme in the Hb subunits, CO has stronger binding affinity to Fe2+ of Hb due to shorter bond Fetal hemoglobin has a higher binding affinity for O2 than maternal Hb CO2 travels in blood as: 7% free CO2, 70% HCO3, 23% carbamino hemoglobin CO2 + H2O to H2CO to H+ HCO3- Reaction goes to the right in tissues as tissues produce CO2 Reaction goes to the left in the lungs, as CO2 is exhaled Haldane effect: In lungs, more O2 binds to Hb, binding affinity of Hb for CO2 decreases Erythropoiesis Erythropoietin production is increases in response to: local decrease in PO2 due to anemia or alkaline blood high pH, Decreased erythropoietin production due to kidney failure and estrogen (higher anemia rates in women) Erythropoietin is a hormone made by kidney and liver, acts on bone marrow to stimulate production of proerythroblasts and their development into RBCs Chloride shift: As HCO3 is produced, it leaves the RBCs and goes into the plasma and CL- moves into the RBCs. In the lungs CL- moves out of the RBS and HCO3 moves back into RBCs to form CO2+H2O Maximum expiratory flow: after inhaling inspiratory reserve volume, exhale as much as air as possible, recorded with a spirometer Constricted lungs: can not expand Obstructed lungs: easy to expand but hard to exhale, due to asthma, emphysema Forced vital capacity test; maximal inhalation and then exhale as forcefully and rapidly as possible Normal exhales more than 80% of VC in 1^st^ second Digestive functions of oral cavity include: Sensory, mechanical processing of the food, partial chemical processing of the food, protective function Swallowing act 3 phases: Oral phase: food is moistened by saliva, and moved to posterior oral part, in general voluntary phase Pharyngeal phase: bolus comes behind the palatinal arc, by 9 and 10 CN, move to esophagus. Unvoluntary Esophageal phase: propelling of bolus in esophagus, unvoluntary Beginning of swallowing is voluntary, later it becomes involuntary called deglutition reflex, occurs in pharyngeal and esophageal stages. Stimulate by afferent fibers at oropharyngeal region, via glossopharyngeal nerve to deglutition center. Saliva help reception of food, reception of food is possible only when food is moistened by saliva. Initial chemical processing of the food, formation of bolus, protection and trophic action 3 pair of salivary glands: Parotid glands, submandibular glands, and sublingual glands. Type of salivary glands: Serose glands= produce saliva with mucin, rich in enzymes, parotid glands Muscous glands= viscous saliva rich in mucous, subligual glands Mixed glands= combine the features of serose and mucous glands, submandibular glands Normally humans produce up to 2 L of saliva per day, pH of saliva is 5.8-7.3 Quantity of saliva produced depends on level of food dryness, level of food fragmentation, chemical composition of food. 99% is water, 1% is organic and non-organic waste Organic waste has protein and enzyme a-amylase, to breakdown carbohydrates. Also salivary lipase to breaks down fats, more in newborns Mucin moistens the food, lysozyme is protective enzyme kills bacteria. Non-organic waste includes electrolytes Salivatory reflex starts from stimulation in oral cavity, go via lingual, glossopharyngeal and vagus nerves to medulla oblongate. Sympathetic fibers inhibit secretion of saliva (small quantity of thick saliva), parasympathetic fibers stimulate high quantity of watery saliva. Vision, hearing and olfaction all can cause salivation Hemopoesis-gastric mucosa releases called intrinsic factor of castle, combines with vitamin B12 so it could be absorbed in intestines Chief cells: produce pepsinogen, inactive form of pepsin, mainly in fundus and body of stomach Parietal cells: produce HCL and intrinsic factor, mainly in fundus and body Accessory cells: produce gastric mucus, peotects gastric mucosa from HCL and enzymes, mostly in cardiac area and pyloric area G-cells: endocrine cells produce hormone, gastrin, stimulate acids influences motility and secretion of GI tract. It released into blood stream first and then returns back to GI tract, most pyloric area of stomach Enterochromaffin: like cell produce histamine stimulates acid D-cells: produce somatostatin, inhibits acid Gastric juice: secreted by the gastric glands, normal 1.5-2L produced perday, depends from time since intake of food, chemical composition of food. 99.5% water and 0.5% organic and non organic waste, most important part is HCl HCL active pepsinogen to pepsin, optimal pH for enzymes 1.5-2.5, denature proteins and killing microbes, stimulates prancreatic juice production, regulates motor function of pylorus Gastric juice contains: proteolytic enzyme, break down proteins: pepsin, gastriksin, parapepsin, chymosin (baby) amylolytic enzyme digest carbo to oligosaccharides lipolytic: enzyme digests lipids: gastric lipase (most important in lipid digestion of infants, tri to di), gastric phospholipase digestions actions of stomach make chyme gastric mucus lubricates stomach, can protect stomach, neutralize HCL absorb B12 and other active enzymes 3 phases of gastric secretion cephalic 30%, gastric 60%, intestinal 10% cephalic phase starts before food enter, trigger by look smell taste of food, and when it processed in the oral cavity, from cerebral cortex, by vagus nerve gastric phase: starts when food at stomach, triggers by distension (stretch of stomach), chemical composition of food. Stretch wall active mechanoreceptors leads to ACH release, it could increase the secretion of gastric juice by direct stimulation of gastric muscosal glands or stimulate G cells to release gastrin peptides and amino acids have direct effect of stimulation of G-cells to produce gastrin, it inhibited when pH of gastric juice decreases intestinal phase: starts when chyme enters to duodenum, trigger is small amount of gastrin released by duodenal mucosa. Secretin is a hormone released by duodenal mucosa and can suppression of gastric acid secretion parasympathetic nervous system vagus nerve secretory influence of gastric secretion sympathetic nervous system inhibits gastric secretion layers from outer surface inward in intestinal wall serosa, longitudinal muscle layer, inner circular muscle layer, the submucosa, the mucosa the motor functions of the gut by smooth muscle, muscle fibers are electrically connected through large numbers of gap junctions, allow low resistance movement of ions to move, each muscle layer functions as a syncytium an action potential solicited anywhere within muscle, smooth muscle of GI is excited by continual slow, intrinsic electrical activity, slow waves and spikes most GI contractions occur rhythmically, determined by frequency called slow waves of smooth muscle membrane potential, not action potentials, intensity usually between 5-15 mvs the rhythm of contraction: body of stomach 3 per min, duodenum 12 per min, ileum 8-9 per min interstitial cells of cajal is electrical pacemakers for smooth muscle cells, they are interposed between the smmoth muscle layers, synaptic contacts to muscle cells the cajal undergo cyclic changes in membrane potential due to its unique ion channels that periodically open and produce currents generate slow wave activity slow waves only cause muscle contraction in the stomach, they mainly excite the appearance of intermittent spike potentials, spike potentials excite muscle contraction spike potentials is true action potentials, occur automatically when RMP of GIT smooth muscle more positive than -40, normal RMP is around -50 -60 the higher the slow wave potential rise, the greater frequency of the spike potential, can be 1-10 spikes per second spike potentials last 10 to 40 times in GIT muscle, 10 to 20 ms large number of Ca and small numbers of Na enter it called CaNa channels, slower to open and close, long duration of the action potential, baseline voltage level of smooth muscle RMP can change factors could depolarize the membrane: stretch of muscle, stimulate by ACH, by parasympathetic nerve, by GI hormones hyperpolarize the membrane: norepinephrine and epinephrine, stimulation of sympathetic nerves slow waves don't cause calcium to enter the muscle fiber, only sodium, no muscle contraction, spike potentials caused Ca enter the fivers and construction tonic contraction is continuous, serval min or even hours, is continuous repetitive spike potentials, greater the frequency, greater the degree of contraction hormones could bring continuous partial depolarization with causing action potentials enteric nervous system lies win wall of gut from esophagus to anus, controlling GI movement and secretion outer plexus lying between the longitudinal and circular muscle layers, called myenteric or Auerbach's plexus, mainly control the GI movements inner plexus called submuscosal or meissners plexus, lies in the submuscosa, mainly controil GI secretion and local blood flow extrinsic sympathetic and parasympathetic fibers connect both the myenteric and submucosal plexuses enteric nervous system can function on its own, idependently of these extrinsic nerves sensory nerve endings originate in gastrointestinal epithelium or gut wall myenteric plexus consists of a linear chain of many interconnecting neurons, it increased tonic contraction, increased intensity of rhythmical contractions, slightly increased rate of rhythmical contraction, increased velocity of conduction of excitatory waves along the gut wall, causing more rapid movement of the gut peristaltic waves inhibitory transmitter, vasoactive intestinal polypeptide- pyloric sphincter, sphincter of the ileocecal valve submucosal plexus is mainly concerned with controlling function within the inner wall, local inteisnal secretion, absorption, and local contraction of the submucosal muscle neurotransmitters: ACH, NE autonomic control parasympathetic cranial parasympathetic: mouth, pharyngeal regions, esophagus, stomach, pancres and fiest half of the large intestine sacral parasympathetic , distal half of large intestine and all the way to the anus sigmoidal, rectal and anal regions supplied better with parasympathetic fibers than other intestinal areas, defecation reflexes sympathetic innervation spinal cord between T5-L2 innervate all of GI tract, for inhibitory direct effect of secreted NE to inhibit intestinal tract smooth muscle, to major extent by and inhibitory effect of NE on the neurons of the entire enteric nervous system sensory nerves can be stimulated by irritation of the gut mucosa, excessive distention of the gut, presence of specific chemical substances in the gut reflexes that are integrated entirely in gut wall nervous system: secretion, peristalsis, mixing contractions and local inhibitory effects reflexe from gut to the prevertebral sympathetic ganglis and then back to the GIT: gastrocolic reflex: from stomach to cause evacuation of the colon enterogastric reflexes: from colon and small intestine to inhibit stomach motility and secretion colonoileal reflex: from colon to inhibit emptying of ileal contents into the colon reflexes from the gut to the spinal cord or brain stem and them back to the GIT pain reflexes, defecation reflexes gastrin secreted by G cells and response to stimuli like distention of stomach, products of proteins, gastrin releasing peptide (released by the mucosa during vagal stimulation). Stimulation of gastric acid secretion Secretin by S cells in duodenum mucosa, in response to acidic gastric juice emptying into the duodenum from pylorus. Has mild effect on motility of GIT and promote pancreatic secretion of bicarbonate which helps to neutralize the acid in the small intestine. CKK sercreted by I cells in the mucosa of the duodenum and jejunum, mainly response to fat, this hormone strongly contracts the gallbladder to help release the bile, also inhibit stomach contraction moderately Gastric inhibitory peptide secreted by upper small intestine mucosa, mainly response to fatty acids and amino acids and a lesser extent to carbohydrate. Mild effect in decreasing motor activity of the stomach and therefore slows emptying of gastric contents into the duodenum when small intestine is overloaded Motilin secreted by upper duodenum during fasting, for increase GI motility, its released cyclically and stimulates waves of GI motility called interdigestive myoelectric complexs, move through stomach and small I very 90 min in as fasted person Peristalsis is basic propulsive movement of the GIT, it moves forward by contractile ring, stimulation at any point in the gut can cause a contractile ring to appear in circular muscle Also occurs in the bile ducts, glandular ducts ureters and other smooth muscle tubes Most common stimulus is distention Chemical physical irritation of lining of gut and strong parasympathetic nervous signals Medications that stimulate the sympathetic nervous system slows peristalsis It normally dies out rapidly in the oral direction but continuing for a considerable distance toward the anus Law of the gut-receptive relaxation, myenteric reflex or the peristaltic reflex segmentation Mixing movements differ in different parts of the alimentary tract, peristaltic contractions cause most of the mixing When blocked by a spincter, peristaltic wave can only churn the contents cant move them forward Local intermittent constrictive contraction occur every few centimeters in the gut wall, usually last 5 to 30 s, it chopping and shearing the contents Splanchnic circulation All the blood that course through the gut, spleen, and pancreas, portal vein, liver, hepatic veins, vena caba This allows reticuleonduothelial cells line the liver sinusoids to remove bacteria might enter the blood from GIT Nonfat water soluble nutrients absorbed from the gut transpoeted in portal venous blood, fats into intestinal lymphatics than bypassing the liver and goes to thoracic duct Blood supply from celiac, s and inf mesenteric arteries During active absorption, blood flow increase eight fold, it could increases motor activity in the gut Sympathetic stimulation has direct effects cause intense vasoconstriction and decreased blood flow, after a few minutes the flow often returns almost to normall called autoregulatory escape Local metabolic vasodilator mechanisms by ischemia more prepotent over symphatetic vasoconstraction. Sympathetic stimulation also causes strong vasoconstriction in interstinal and mesenteric veins, could displacing large amounts of blood into circulation In hemorrhagic shock, this mechanism can provide 200-400 ml more blodd in the general circulation