Cell Bio 3 Flashcards
2 essential fxns of lungs. hypo vs hyperpnea
breathing, circ. distensibility; shallow or slow breathing vs inc breathing to meet demand (like exer or needing O2); sign of refractory sepsis
hb O2 sat vs hypoxemia vs hypoxia. causes of hypoxia?
%age of hb bound to O2 vs low O2 in arterial blood, <60mmHg & dec O2 sat; low PaO2 vs low O2 in tissue. hypoxemia, anemia, CO, cyanide, blood flow/cardiac output
components of upper vs lower resp tract. where do cough receptors reside?
columnar, ciliated cells, goblet cells; conduction zone -> trachea + bronchi/oles, humidify air, particle deposits, mucociliary clear (cilia terminate in condxn zone) vs special resp epith; resp zone -> resp bronchioles + alveoli, lg surface area for gas exchange. post wall of trachea & pharynx
resp passages = coated in what? for what?
mucus, periciliary fluid, surfactant. keep surface moist, trap small particles, dec surface tension
what kind of cells = found in mucociliary clearance system?
goblet cells secreting mucus, club/clara cells in bronchioles secreting GAG to protect bronchiole lining, pseudostratified ciliated columnar epith secreting periciliary fluid
type I vs II vs III vs macs vs mast cells of alveolar cells (pneumocytes from embryo)
elong, gas exchange; more susceptible to toxins vs cuboidal, surfactant by lamellar bodies, progenitor of type I to restore dmged barrier, prolif at 24wks vs brush cells throughout airway, assoc w/ nn vs kill bacteria, make cytok & ROS -> toxic to type II vs hist, sero for immunity
how do lungs get blood/O2 (which vessels)? where does blood get oxygenated?
bronchial a for nourishment, pulm a/v for blood. pulm capillaries
is inspiration vs expiration active or passive w/ what mechanism? mm for forced inspiration vs expiration?
active by impulses from resp center in brainstem to diaphragm & ext intercostal mm (T1-11) vs passive by passive relax diaphragm, lung recoil via mechanoreceptors in lung & chest wall and chemoreceptors in carotids. SCM, scalenes vs int intercostals & abd mm like in emphysema d/t loss recoil
relationship b/w lung & chest wall. fxns of surfactant
lung wants to close, chest wall wants to open; find equil to maximize gas exchange. dec surface tension & capillary filtration forces, prevent atelectasis -> prevent alveolar edema; inc alveolar opening & pulm compliance
factors affecting gas exchange vs compliance
too much dead space = not good, compliance/elastance, dec area of diffusion/fick’s law, fluid in lungs/PNA, perfusion (blood clot), not enough diff in pressure/vol vs tissue itself (elastin, collagen, A1AT), surface tension & lining of alveoli (collapsing pressure/Law of LaPlace = 2T/r)
pathogenesis vs major probs of ARDs. what hormone produces surfactant? tx?
premies have no surfactant -> pink fibrin rich hyaline mem -> unopened alveoli d/t inc surface tension -> dec compliance -> harder recoil, atelectasis, pulm edema vs thick mem -> gas exchange harder, hyaline mem = sticky -> inc alveolar collapse after ea breath -> hard to reopen to breathe -> need PEEP. stress, no insulin -> cortisol -> surfactant. exogenous surfactant, corticoids, pos pressure
emphysema vs fib w/ causes?
too floppy, can’t ctx -> high compliance; smoking, A1AT, pollution vs too stiff, can’t stretch -> high elastance; occupation, sarcoid, drugs, rads, RA & sclerosis, genetics
causes of pulm edema
inc hydrostat pressure (MI, mitral sten), dec colloid osmotic pressure (hypoalbumin), inc capillary permeability (rads, ARDs, NO), dec interstitial pressure (hyperinflation, pneumothorax), lymphatic insufficiency (blocked lymph drain)
4 major + 1 sites for ctrlling respiration
- dorsal/ventral resp centers in the medulla; apneustic & pneumotaxic centers in pons
- central chemoreceptors in CSF
- periph chemoreceptors in the carotids, aortic bodies, blood
- mechanoreceptors in lungs & joints
- cerebral cortex (like breathing during swallowing, hypo/hypventilate)
Hering Breuer reflex
lung stretch receptors sense distended lungs/airway -> prolong expiratory time -> dec breathing rate
dorsal/insp center vs ventral/expi center
ctrl basic rhythm & freq, CN9/10/phrenic, ctrlled by apneustic/taxic centers vs for exer since nml expiration = passive
apneustic vs pneumotaxic centers
lower pons; turn on inspiration by prolong AP -> ctx diaphragm vs upper pons; turn off inspriation by limiting AP, tidal vol, RR; still nml breathing
central vs periph chemoreceptors. what about COPD pts?
pH: CO2 diffuse into BBB -> become H+ -> diffuse out of CSF & bind to central chemoreceptors -> inc breathing vs C/O2, pH; <60mmHg O2 -> inc PCO2 & H+ -> CN9/10 relay to DRG -> medullary insp center regulates minute ventilation. dec sensitivity to PCO2 b/c chronic CO2 rtn -> hypoxemia -> resp drive
resp drive or response to PCO2 change can dec if you’re what? (3)
hyperventilating, drugs/anesthesia, inc work of breathing/COPD
biggest problem w/ anesthesia?
resp depression, alter gas exchange dec FRC -> dec elastic recoil -> atelectasis. preO2 w/ 80% O2 when inducing anesthesia, raise FRC enough not to cause atelectasis, PEEP or CPAP to keep alveoli open
OSA vs central sleep apnea. conseq of sleep apnea?
closure upper airway during insp, resp effort; transient hypoxemia/hypercapnia vs cess of resp drive to resp mm, no resp effort. hypoxic vasoconstrict, sympathetic stim -> pulm HTN, R heart fail
biots vs Cheyne Stokes vs Kussmaul
quick shallow insp -> silent -> rpt, etc; poor prog b/c dmged pons d/t stroke, trauma, pressure, opioids vs deeper faster breathing -> silent/apnea w/ cres-diminuendo pattern vs deep labored breathing, hyperventilation; common for ketoacidosis & renal fail to get rid of H+
changes of breathing in exer
no change in arterial PC/O2 or pH, V/Q = 1; Hb-O2 to the right. O2 consumption, ventilation rate, venous PCO2, cardiac output inc. physiologic dead space dec
anatomic vs physiological shunts. what would V/Q be? O2 in fib or stren exer = ___-limited
venous blood shunted to arterial blood w/o gas exchange -> buildup CO2 -> central chemoreceptors -> inc ventilation; PaO2 improve if given 100% O2 vs no ventilation -> hypoxic vasconstriction; PaO2 doesn’t improve if 100% O2 given. V/Q = 0. diffusion limited
