AP3 - E1a
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Created by:
jennifernewwin on April 22, 2012
Description:
respiration
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149 terms
Terms | Definitions |
|---|---|
 conducting division | passages serve only for airflow; nose to bronchioles. Everything but alveoli |
| upper resp tract | organs in head and neck, nose through larynx |
| lower resp tract | organs of thorax, trachea through lungs |
| Respiratory division | any area with simple squamous epithelium like resp bronchiles, alveolar anything. |
| When you sneeze, what are you doing? | Clear upper resp system |
| When you are coughing, what are you doing? | Clear lower resp system. |
| Function of nose | warms, cleanses, humidifies, detects odor, resonating chamber for voice |
| What is the nose made out of generally? | bone superiorly, and hyalin catrilage and dense CT as you go down. |
| Rhinoplasty changes what? | shape of cartilage. |
| What kind of lining lines the nasal cavity? | roof = olfactory mucosa. Every where else = respiratory mucosa (ciliated pseudostratified epi) |
| Role of mucosa? | mucus from goblet cells trap inhaled particles and bacteria are destroyed by lysozyme |
| What is cilia of respiratory epi doing? | drives debris-laden mucus into pharynx to be swallowed. |
| Erectile tissue of inferior chocha | plexus will engorge, shut off air flow in one nasal fossa so air will go to the other side. Will switch from one side to the other to prevent drying out. **head colds when you don't switch and get drying out. |
| What is a nosebleed called? Where does it happen? | spontaneous epistaxis. Mostly in the inferior concha's plexus. |
| Function of upper respir? | warming, humidifying, and filtering. |
| nasopharyn location | interal/posterior nares down to back of soft palate/uvula. (pseudostr) |
| Oral pharynx | back of soft palate to top of trachea (stratified squammous); shared space. |
| Laryngopharyx | top of trachea and some going into esophogus and some into pharynx. Or hyoid bone to cricoid cartilage. (stratified squa) |
| uvula | blocks food from moving up thru nasal cavity |
| larynx | voice box. Epiglottis helps guard glottis by directing food to esophagus and NOT larynx. ***makes it so that adults cannot eat and breathe at same time however infants can because larynx is up higher. |
| walls of layrnx | contain vestibular folds (close glottis during swalloing; false folds) and vocal cords (produce sound) between thyroid to arytenoid cartilages. |
| What muscles allow you to change our voice? | intrinsic muscles rotate corniculate and arytenoid cartilages which either adducts (high pitch sounds due to tightening of vocal cords) or abducts vocal cords |
| extrinsic muscles of larynx do what? | elevate larynx during swallowing. |
| thyroid vs. cricoid cartilage | thryoid is partial ring (larger in males which allows voicebox to be bigger so voice deeper); partiality allows esophagous to expand into trachea. Cricoid only full ring. |
| open glottis | increases size of resonanc chamber to project sound farther and produce deeper sound. |
| closed glottis | whipsering. All sounds are changed by shape of mouth. |
| what is the adam's apple? | thyroid cartilage. |
| what is larynx and trachea lined with? | ciliated pseudostratified epi which functions as mucocilliary escalator; contains goblet cells. |
| How many tertiary bronchi in left and right lungs? | 10 in right, 8 in left. Left lung only has 2 lobes but right lung has 3 lobes. |
| What is a bronchopulmonary segment? | portion of lung supplied by each tertiary bronchi |
| bronchioles | no cartilage, have smooth muscle, each ventilate a pulmonary lobule |
| primary vs. secondary/tertiary bronchi | primary made up of cartilage rings; secndary/teritary made up of overllaping cartilage plates. |
| pathway once into bronchi? | bronchi --> bronchioles --> terminal bronchiles (have cilia) --> respi bronchioles --> alveolar ducts --> alveolar sacs. **alveoli in any respitory bronchioles, alvoelar ducts, or alveolar sacs. |
| Histology of bronchia tree | as you go further down into lungs: psuedostra ciliated columnar --> non ciliated simple cuboidal. Also, go from incomplete rings of cartilgae --> rings of smooth muscle --> CT |
| what causes you to dilate airway? | symp NS/adrenal gland release epine which relaxes smooth muscle and dilates airway |
| What does asthma/allergic reaction result in? | constriction of distal bronchiole smooth muscle. |
| Type 1 Alveolar cells | simple squamous cells where gas exchange occurs; NOT dominant cells. Increaes flux. |
| Types Ii alveolar cells (septal cells) | free surface has microvilli, secrete alveolar fluid containing surfactant. Most common. Surfactat decreaes surface tension of water and make it so alveoli stays open. |
| Alveolar dust cells | wandering macrophages remove debris ; can't digest elementary carbon. |
| What is the respiratory membrane made up of? | very thin. Used for exchange of gas from alveoli to blood. From alveoli to blood vessel must go thru 4 layers: alveolar epithelial wall of type I --> alveolar epithelial baesment membrane-->alveolar epithelial basement membrane --> capillary basement membrane --> endothelial cells of capillary. |
| What will pulmonary blood vessels do in response to low O2 levels? | constrict as to not pick up CO2 on their way to through the lungs |
| What is at the carina? | mechanoreceptors to stimulate coughing |
| how many primary bronchi for each lung | 2.1 |
| How many secondary bronchi for each lung? | 5.1 |
| terminal bronchiles | last ones to have cartilage in them; determine whether you are going to have air flow to all parts of lungs or not. |
| histology: terminal bronhioles vs. respirtaory bronchioles | termina = ciliated pseudostrat. Respit = simpled squamou epi |
| fick's law | flux = k(SA/dist) |
| What type of blood supply do lungs have? | double blood supply. Pumonary and systemic arteries because lungs need oxygen too. |
| Why are capp bed longer than needed sometimes? | because when doing activity, increase blood flow and more CO2 so it will take longer. |
| visceral, parietal layers and pleural cavity and fluid: Tell me about it | visceral layer = attached to lung. Parietal layer = on the outside/lines ribcage and covers upper surface of diaphragm. Between the two layers is the pleural cavity and contains serous lfuid to reduce friction. |
| Function of plurae and pleural fluid | reduce friction, create pressure gradient, compartmentalize |
| boyle's law | PV = nRT with constant T and n ---> what allows you to create negative pressure when thoracic cavity expands. ***pressure gradienti s between intrapulmonary pressure and atmospheric pressure |
| Charle's law | PV = nRT with constant P and n. Helps explain warming of air into lungs as lung expands. |
| Dalton's law | total pressure = sumof individual partila pressures |
| Henry's law | the more partial pressure of a gas in the air, the more soluble it will be in water. ***amount of gas that dissolves in water is determined by its solubility in water and its partial pressure in air. |
| flow of air into the nose | nostrils/external nares ---> guard hairs/vibrissae containing mucous membrane ---> vestibules (larger chamber so vel goes down) --> conchae (3 of them) ---> narrow meatueses (narrow) --> down 90 deg into tonsils in nasopharynx (tonsils also get rid of bad stuff). |
| muscle involved in inspiration | diaphragm, scalenes (fix first pair of ribs), external intercostals (elevate rib cage), pectoralis minor, sternocleidomastoid, and erector spinae muscles (for DEEP inhaling)**normal breathing, use only external inter. But when exercising, use external inter and diaphragm |
| pulmonary ventilation | moving air in and out. |
| inspiration | rib cage expands, intrapleural pressure decreases, visceral attachs to parietal pleura via cohesion/adhesion, intrapulmonary pressure decreases, lungs/alveoli expand, overall neg pressure in lungs so air flows in |
| transpulmonary pressure | intrapleural - intrapulmonary = not all pressure change in pleural cavity is transferred to lungs. |
| passive expiration | expiration achieved by elasticity of lungs and thoracic cage. Occurs when vol of thoracic cavity dec and intrapulmonary pressure increases. **after inspiration, phernic nerve continue to stimulate diaphragm to produce braking action to elastic recoil (?) |
| force expiration | interal intercostal muscles contract which deprsses ribs (reducing volume of rib cage) and contract abs (forces diaphragm upward) |
| pneumothorax | air in pleural cavity; can't create neg pressure and lungs collaspe. |
| atelectasis | collapse of lung or any part of lung |
| pleurosy | infection that damages serous membrane/visceral pleura leading to friction. |
| pressure of intrapleural vs. intrapulmonary space? | intrapleural always less than intrapulmonary |
| obstructive disorder to air flow | anything that reduces/affects air flow. i.e. astham due to constriction of bronchiole. Ephysema due to fibrosis making it less likely to do bronchiodilation. Tumors. Pneumonia due to mucous forming and decreaess size of bronchioles. |
| Restrictiv disorder to air flow | decrease SA. Arthritis due to ectopic calcification. Pneumonia. TB - scar tissue. |
| pulmonary compliance decreased by? | TB - scar tissue. Pulmonary edema - fluid in lungs and reduced surfactatn. Paraysis. |
| what causes bronchoconstri? | airborn irritants, cold air, parasympathetic stimul, histamine |
| what causes bronchodilation? | symp nerves, epinephrine |
| why is surfactatn important? | alveolus lined with thin film (need wet membrane for gas exchange) but it has surface tension which would cause alveoli to collapse. Surfactant breaks up surface tension. |
| dead air | air in conduction pathways. Also increases with respiratory illness, alergies etc. **every thing together = physiologic dead space |
| alevolar vent rate = ? | respiration rate * SA for gas exchange |
| eupnea | normal quiet breathing |
| apnea | temp cessation of breathing during sleep; often due to being overweight. Most common is obstructive apnea due to tongue getting in the way. During apnea, get decrease in oxygen to brain so more CO2 accomulation. Causes medulla to go thru ischemic reflex (symp respon)and BP spikes. BP spikes wil happen many times during the night and this is bad for body over the long run. **apnea normal in infants |
| dyspnea | difficult or labored breathing |
| tachypnea | rapid breathing **DOES NOT EQUAL HYPERVENTILATION. |
| diaphragmatic breathing | causes stmoach to bulge during inhalitng |
| costal breathing | just rib activity involved |
| Hiccuping | medulla is off and so casues problem with frenic nerve; get repetitive innervations. To fix, get a symp NS response. Hiccuping also due to muscle spasms in diaphragm due to ionic imbalances. |
| nonrespi air movement | speaking, yawning, sneezing, coughing, valsalva maneuver |
| difference in tidal volume b/w sexes | None but do have one with size. Smaller = same volume but higher respiratory rate due to larger SA to vol want to dissipate more heat so you can maintain body temp. |
| diff in inspiratory reserve volume? | Yes. Males have more due to testosterone. |
| vital capcity | TV + ERV + IRV; assess strength of thoracic muscles and pulmonary function. |
| expir capacity | TV + ERV |
| inspi capacity | TV + IRV |
| functional residual capacity | residivual + ERV; amount of air in lungs after a normal tidal expiration |
| forced expiratory volume 1 (FEV1) | should be 85% of vital capcity; means you hsould be able to get 85% out in a second. If you can't, you have a problem like asthma or emphysema or TB. |
| minute respiratory volume (MRV) | TV * respiratory rate |
| Neural control of ventilation | neurons in medulla and pons control unconscious breathing; voluntary control provided by motor cortex. Fibers run down spinal cord to lower motor neurons, fibers of phrenic nerve go to diaphragm and intercostal nerves go to inter muscles |
| when do inspiratory neurons and expiratory neurons fire? | inspiratory = during inspiartion. Expiratory = during FORCe expiration. |
| groups of neurons involved in respiration | medullary rhythmicity, pneumotaxic, and apneustic centers |
| Respiratory control centers in medulla | have inspiratory( dorsal respirttory gropu) and expiraotyr (ventral rspirtory) group. |
| The more frequently inspiratory center neurons fire, what happens? The longer they fire what happens? | more frequ = more ddeply you inhale. Longer duration = breath prolonged, slow rate. |
| When is the medullary expiratory center ever involved? | FORCED expiration |
| Pons includes what two rspiratory centers? | pneumotaxic (responsible for breathing when you are exercising by sending inhibitory impulses to inspiratory centerm aking breath shallow and fast) and apneustic (for deep sleep; prolongs inspiratory center to slow down breath and make it deeper). |
| Medullary rhythmicity area | controls basic rhythmof respiration ; inhale = 2 s. exhale = 3 sec |
| What outside/afferent things can affect breathing? | input from limbic system/hypothalamus (affects of pain and emotion), input from chemoreceptors (brainstem and arteries monitor pH, CO2, and O2), input from airways and lungs (response to inhaled irritatnts). |
| What does your body do if you have too much CO2 in your blood? | first will stimulate DRG (inspiratory center).If that doesn't work, stimulate pneumotaxic center (PRG). If that doesn't work, stimulate VRG (expiratory center) to do FORCED eshalation. If that doesn't work, you would probably die. |
| what kinds of chemoreceptors do you have and where? | located in carotid and aortic bodies. Have 3 sets each for protons, CO2, and oxygen. In CNS, respond mostly to protons. In Blood, respond mostly to CO2. oxygen receptors are wimps. |
| respiratory acidosis | pH is less than 7.35 due to failure of pulmonary ventilation. Diabetics tend to have elevated respiratory rates because they can't break down carbds so they break down lipid. To produce ketones which are acidic so need to breathe faster to get rid of proton. Respiration is fastest way to correct blood pH problems. Due to slow down breathing or decrease SA for gas exchange due to emphysema, TB. |
| what limits voluntary control of breathing? | blood CO2 and O2 limits |
| hypercapnia | slight increase in pCO2 is noticed |
| what is the MOST powerful respiratory stimulus? | pH of CSF. This is because CO2 can easily cross blood-brain border and react with water to release H. |
| What happens when you hyperventilate? | pushes CO2 + H20 equation to the left to get rid of acid. Helps to correct respiratory acidosis |
| Respiratory alkalosis | pH is less than 7.45 never really a problem because you are conscious of hyperventilation. HYPOventilation helps because it pushes equation to the right to counteract alkalinity by making more protons. |
| Direct effects of carbon dioxide? | stimulate peripheral chemoreceptors more than central chemoreceptors increasing ventilation more quickly that way. |
| whyi s oxygen such a poor receptor? | Solubility of CO2 is a lot greater than O2. Thus, when you increase Oxygen levels, only a tiny bit of that affects oxygen solubility that it isn't enough for receptors to pick it up. |
| What is the air mostly made out of ? | nitrogen, then oxygen, then water, then CO2. |
| Does alveolair air have more or less air than expired air? | has less O2 since absorbed by blood |
| Why does expired air have more O2 and less CO2 than alevolar air? | This is because therei s oxygen in your conducting airways so that when you exhale, you breathe out oxygen and it adds to what is in your conducting airway. |
| What is the partial pressure of nitrogen in alveolar air and expired air? | always 79% because it is inert and we don't usei t. |
| Effects of COPD | decrease pulmonary compliance and vital capcity, hypoexmia (can lead to polycythemia), hypercapnia, respiratory acidosis. Can also lead to cor pulmonale - hypertrophy and potential failure of right sideo f heart due to obstruction of pulmonary circulation. |
| COPD (chronic obstructive pulmonary disease) | usually asthma which triggers histamine release, intense bronchoconstriction. Also caused by chronic bronchitis where cilia immbolizized so all this excess mucus produced which gives ideal condition for bacterial growth and inflammation. Also caused by emphysema where alveolar walls bread down, less SA, lungs fibrotic and less elastic, air passages collapse and obstruct outflow of air and air gets trapped in lungs. |
| Anatomical dead space is how much of tidal volume? | 150 mL of 500 mL of tidal volume |
| Why doesn't oxygen come out of solution like nitrogen does when coming up from deep water? | Because oxygen binds to hemoglobin and we are using it. |
| hyperbaric oxygenation | clinical app of Henry's law. Basically, use pressure to force more O2 into blood. Used to treat anaerobic bacterial infections, heart disorders, CO poisoning, cerebral edema, bone infections, gas embolisms, and crush injuries |
| factors affecting fas exchange | conc. gradient, gas solubility, membrane thickness, membrane SA, ventilation-perfusion coupling (areas of good ventilation need good perfusion (vasodilation). |
| external respiration | b/w alveoli and blood |
| interal respiration | exchange of gas b/w tissue and blood; conversion of oxygenated blood into deoxygenated. |
| cellular respiration | use of oxygen by cells |
| why is CO2 so much more soluble than O2? | CO2 has polar bonds. |
| effects of pneumonia | decrease SA due to fluid build up wihtin alveoli. Areas underneath don't get gas exchange. Also build up mucous on membrane which thickens it and slows down gas exchange. |
| Cystic fibrosis | builds up mucus and decreases ability for oxygen to get to tissue. |
| NO's relationship with hemoglobin | NO is vasodilator. All endothelial cells make NO. NO is broken down fast by body's enzymes. As hemoglobin loads up with oxygen, hemoglobin's affinity for NO increases so it grabs ahold of NO. Hemoglobin acts as a chaperone for NO. Drop off oxygen in places where you have low oxygen. The places with the lowest oxygen you drop off more. When drop off Oxygen, affinity for NO decreases and NO is released. NO vasodilates that area which allows more blood flow to that tissue area. As hemoglobin leaving metabolically active tissue, Hb grabs CO2. As it gabs Co2, affinity for NO increases so it picks up new NO. Acts as chaperone. GO back to lungs. Drop off CO2 in areas where you have least amount of CO2. Drop off NO too leading to vasodilation. Increase vasodilation will have bring blood vessels to places with high Oxygen. |
| How does blood flow match airflow? I.E. how does perfusion adjust to ventilation | Increase air flow = elevated pO2 in blood vessels = vasodilation of pulmonary vessels = increase blood flow. Decreased air flow = decrease in pO2 = vasoconstriction of pulmonary vessles = less bloow flow. |
| How does airflow match blood flow? I.E. how does ventilation adjust to changes in perfusion? | increased blood flow = elevated pCO2 in alveoli = dilation of bronchioles = increased air flow. Decreased blood flow = reduced pCO2 in alveoli = constriction of bronchioles = decreased air flow. |
| What happens as H+ dissociate from Hb as Hb loads O2 and decreases its affinity for H+? | H+ binds to HCO3 and goes in that direction. |
| Chloride shift for alveolar gas exchange | Bicarb is brought into the RBC via antiport with CL. |
| What percentage of O2 is carried by Hb? What percent is dissolved in solution? | 98.5% carried by Hb. 1.5% dissolve din solution. |
| What portion of CO2 dissolves in plasma? What percent is carried as carboaminohemoglobin? How many transported as bicarb? | 7% dissolved in plasma, 23% carried as carboaminohemoglobin (HbCO2). 70% transported as bicarb in blood. |
| venous reserve? | the amount of O2 left on HB after O2 unloading in systemic gas exchange. |
| What will cause right shift/O2 unloading? | if ambient pO2 is low, increased temp, increased pCO2, decreased pH, Increased BPG |
| Bohr effect | increased CO2 leads to low pH/lots of protons. Protons bind to HbO2 causing Hb to release O2. |
| Haldane effect | CO2 decreases affinity of Hb for O2 so O2 is released. **low levels of HbO2 enables blood to tranport more CO2 because HbO2 does not bind CO2 as well as HHb and HHb binds more H+ than HbO2 shifting equation to the right making more H+ which causes right shift. |
| Effect of CO on Hb | CO binds a lot better to Hb so it can kick off O2 and take up O2 space on Hb so you can die. Get cherry red lipds and finger nail beds. |
| What is BPG? | intermediate in glycolysis for making ATP; so if you have a lot of BPG, means you are doing a lot of glycolysis. If you're doing a lot of glycolysis, you are trying to make ATP. If making ATP, want oxygen so you can do aerobic respiration. |
| Fetal hemooglobin | have 2 gamma instead of 2 beta. Has a higher affinity for oxygen due to lower partial pressure of oxygen. Causes left shift. |
| hypoxia | oxygen imbalances; primary effect is tissue necrosis, organs with high metabolic demands affected first. |
| hypoxemic hypoxia | due to inadequate pulmonary gas exchange due to high altitudes, drowning, aspiration, respiratory arrest, degenerative lung disease, CO poisoning. |
| Icshemic hypoxia | inadequate cirucatlion |
| anemic hypoxia | anemia |
| histotoxic hypoxia | metabolic poison (cyanide) |
| cyanosis | blueness of skin |
| when is oxygen toxic? | 2.5 atm or greater. Due to generating free radicles. |
| What does smoking do? | constricts terminal bronchioles, CO poisoning, irritatns in smoke causes excess mucous and inhibit cilia, destroys elastic fiber and leads to emphysema (trapping of air in alveoli and reduced SA) |
| squamous-cell carcinoma | most common; bronchiol epithelium turned into stratified squamous cause bleeding lesions in bronchil wall |
| small-cell carcinoma | leas common but most dangerous form of lung gancer. Originates in primary brochi; metastasizes quickly. |
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