click below
click below
Normal Size Small Size show me how
physiology-respirato
Stack #186542
Question | Answer |
---|---|
internal respiration refers to | cellular respiration (ie. ETC) |
what is the respiratory quotient (RQ)? | ratio of CO2 produced to O2 consumed |
what is the respiratory quotient of carbohydrate | 1 (6 O2 consumed, 6 CO2 produced therefore 1:1) |
in respiratory system what direction do cilia beat | towards pharynx (unidirectional beatings) |
affect of breathing in dry air on mucus in respiratory tract? | mucus covering the airway get too dense. |
which cells in airway produce H2O to hydrate mucus? | all epithelial cells in airway |
affect of dense mucus on cilia | dense mucus - cilia don't beat at all |
affect of dilute mucus on cilia | cilia beat too fast |
role of cilia in airway | remove dust particles out of the airway |
major glands in respiratory system + their function | goblet cell - secrete viscous mucous serous cell - secrete serin which dilutes mucus |
when sick body produces excess mucous because | increased number of goblet cell |
which nerves signal (indirectly) mucus glands (goblet, serous, etc) to secrete mucus | cholinergic afferent nerve in intercellular space sends signal to brain which receives the information and stimulates secretions via cholinergic efferent nerve. |
contraction of __ causes an ejection of mucus in ducts | myoepithelial cells |
symptom of cystic fibrosis | thick, dehydrated mucous, due to defected Cl- channels. |
cystic fibrosis transmembrane conductance regulator (CFTR) pumps __ in which directions? | Cl- to apical surface, Na+ to inside of epithelial cell. |
airway epithelial cells held together by | tight junctions |
in airway epithelial cells __ surface is more negative than ___ surface. this is called | apical, basal. depolarized |
how is apical airway epithelial surface hydrated/dehydrated? | hydrated by opening up Cl- channels dehydrated by opening up Na+ channels |
how is Cl- in airway epithelial cell pumped out passively? | 1.NA/K pump creates high [Na+] in basal surface 2.pumped Na+ from basal surface diffuse into the cell, the energy is harnessed to pump K+ and Cl- into the cell. |
body's response to compensate for breathing in humid air | close Cl- channel and open Na+ channel |
thick mucus in airway a symptom of | cystic fibrosis |
defensin, function | antimicrobial peptide, kill bacteria by forming channels in membrane. |
two characteristics of defensin | 1.amphiphilic(one side more hydrophilic), cationic(+v charged) 2.stored, delivered on stimulation (eg. presence of bacteria) |
results from infecting healthy and cystic fibrotic cell with bacteria. | Normal cell:bacteria killed(defensin was active) CF cell:bacteria survives(Defensin was inactive) |
function of alveolar 1 cells | form continuous alveolar walls |
function of alveolar 2 cells | produce surfactant, replace damaged type 1 cells |
function of alveolar macrophage | ingest pathogens |
surfactant increase or decrease lung compliance | increase |
surfactant level increase when | taking deep breaths |
surfactant level decreases when | taking small breaths |
in Laplace equation P represents | pressure directed inward towards alveola |
high P in Laplace equation represents | low lung compliance |
alveoloar surface tension caused by | attractive forces between water molecules lining alveoli |
laplace formula | P= 2gamma/radius |
surfactant affects which variable in laplace equation | lowers gamma(surface tension) |
how do small alveoli collapse into large alveoli | small alveoli has higher P (because of smaller radius) hence air will flow to bigger alveoli because it has a higher lung compliance |
how should distribution of surfactant be in alveoli of different sizes? | smaller alveoli -> more surfactant larger alveoli -> less surfactant so that you don't get alveoli collapsing |
2 functions of surfactin | 1.lower surface tention 2.alter surface tension depending on radii of alveoli |
respiratory distress syndrome (RDS) | immature type 2 alveolar cells in infants |
nitrogen narcosis | high ambient pressure under water causing more N2 to be dissolved in the tissue. (high pN2) => reduce excitability of neurons |
what happens during rapid ascend in water? | ambient pressure decreases fast causing N2 dissolved in blood and tissue to leave and thereby forming bubbles |
the diffusion coefficient of CO2 is __ than O2 and the result is | higher, rapid diffusion for a given pressure gradient |
diffusion of gases depends on what variables? | area through which the diffusion occurs(A), diffusion coefficient(D), pressure difference(P1-P2), distance through which the gas must travel(L) |
affect of fibrosis | fibrotic tissue accumulates in alveoli and thickens it ie. increases the L in Fick's equation |
affect of pulmonary adema | fluid accumulation in alveoli causing thickened membrane ie. increase the L Fick's equation |
J in fick's law is | diffusion rate |
muscles involved in inspiration | scalenes, externernal intercostals, diaphragm |
muscles involved in forced expiration | abdominal muscles, internal intercostal |
for lung mechanics purposes, all pressures compared to ___ pressure which is equal to | Patm = 0 |
Palv is negative or positive during inspiration | negative |
Palv negative means | it is small than Patm |
Ppl is | pressure in pleural cavity |
Ptr is | pressure difference between the inside and the outside of the lungs |
static recoil pressure of lung called | Ptr |
Palv is negative or positive during expiration | positive |
which pressure holds the lung expanded | Ptr |
during inspiration | 1.volume of pleural cavity inc. which decreases Ppl 2.dec. Ppl inc. Ptr 3.inc.Ptr expands lung 4.volume of alv inc. which dec. Palv. 5.air rushes in |
Palv when all muscles relaxed | 0 (= 760 mmHg) |
Pneumothrorax | punch hole thorugh parietal pleura |
when happens if you punch a hole through parietal pleura | Ppl = 0, Palv = 0 => Ptr = 0. lung collapse |
Ppl is usually | lower than Patm. ie Ppl<0 |
pulmonary fibrosis is | proliferation of connective tissue making the lungs less compliant |
relation between compliance and stiffness | inc. compliance => dec. stiffness |
a condition in which the lungs become stiff is called | pulmonary fibrosis |
in patients with pulmonary fibrosis you would expect the total lung capacity to be (at a specific Ptr) smaller or bigger | smaller, because lungs cannot fully expand |
in patients with emphysema you would expect the total lung capacity to be (at a specific Ptr) smaller or bigger | bigger |
lung compliance depends on | lung volume wrt Ptr |
pulmonary ventilation(PV) | amount of air moved out of the lungs each minute |
pulmonary ventilation(PV) calculated by | freq*depth of breathing |
amount of air moved out of the lungs each minute called | pulmonary ventilation (PV) |
anatomical dead space is | space where no air exchange occurs (ie. conducting portion of respiratory system) |
alveolar ventilation (AV) | volume of air EXCHANGED (ie not at anatomical dead space) between the atmosphere and alveoli per minute |
volume of air exchanged between the atmosphere and alveoli called | alveolar ventilation (AV) |
AV is calculated by | PV-DSV (deadspace ventilation) |
space where no air exchange occurs (ie. conducting portion of respiratory system) called | anatomical dead space |
alveolar dead space is | alveoli with no blood supply for gas exchange |
physiological dead space is | sum of all dead spaces (anatomical + alveolar) |
alveoli with no blood supply for gas exchange is | alaveolar dead space |
dead space ventilation(DSV) is calculated | dead space volume * freq |
hypoventilation means | low alveolar ventilation |
high __ ventilation means hyperventilation | alveolar ventilation |
tidal volume is | air exchange when resting |
residual volume is | volume in lung that cannot be removed. ie. volume of air remaining after force exhalation |
expiratory reserve is | air that can be exhaled forcefully |
inspiratory reserve is | air that can be inhaled forcefully |
volume of air that can be exhaled forcefully is | expiratory reserve |
volume of air that can be inhaled forcefully is | inspiratory reserve |
how is volume of air breathed in and out of lungs measured? | using spirometer |
what is spirometer | measures volume of air breathed in and out of lungs |
Inspiratory capacity is | inspiratory reserve volume + tidal volume |
inspiratory reserve volume + tidal volume | inspiratory capacity |
functional residual capacity is | expiratory reserve volume + residual volume |
vital capacity is | inspiratory reserve volume + tidal volume + expiratory reserve volume |
expiratory reserve volume + residual volume | functional residual capacity |
inspiratory reserve volume + tidal volume + expiratory reserve volume | vital capacity |
term capacity when describing lung volume is used when | a volume can be broken down into smaller volumes |
a person takes a maximal inspiration. maximum amount of air that this person can expire is | vital capacity = inspiratory reserve + tidal + expiratory reserve |
changing from standing to supine position changes | decreases functional residual capacity |
total lung volume is calculated (using what formula) | C1V1 = (V1+Vlung)C2 |
forced expiratory volume(FEV1) is | maximum volume of air expired in the first second of expiration (after max inspiration) |
if airway is obstructed how would it affect the forced expiratory volume? | decrease FEV1 to vital capacity ratio |
agonists for muscarinic receptors | ACh |
ACh binds to what receptor | muscarinic |
muscarinic receptor results in __ in airway | brochoconstriction |
NE binds to what receptor | alpha-adrenoceptor |
E binds to what receptor | beta-adrenoceptor |
agonists for alpha and beta adrenoceptor | NE and E |
alpha adrenoceptor results in __ in airway | bronchoconstriction |
beta adrenoceptor results in __ in airway | bronchodilation |
___ receptor results in bronchoconstriction | muscarinic, alpha adrenoceptor |
___ receptor result sin bronchodilation | beta adrenoceptor |
therapy for asthma | 1.anti-inflammatory drugs(glucocorticoid) 2.bronchodilator drug(binds to beta-ad. receptor) - short term treatment |
Chronic Obstructive Pulmonary Disease (COPD) | narrowing airway due to excess mucous secretion |
two types of COPD (Chronic obstructive Pulmonary Disease) | 1.Chronic bronchitis, 2.Emphysema |
Chronic bronchitis symptom | excessive mucus production. mucus get trapped |
Emphysema symptom | collapsing smaller airways, breakdown of alveoli. |
Emphysema caused by | overexpression of digestive enzyme (trypsin) and / or inability to produce enough alpha1-antitrypsin |
overexpression of digestive enzyme (trypsin) and / or inability to produce enough alpha1-antitrypsin results in | Emphysema, or destruction of lung tissue |
cure for emphysema | alpha-antitrypsin to remove excess trypsin |
pulmonary resistance higher or lower than systemic resistance | much lower |
pO2 and pCO2 in systemic arteries | pO2 = 100, pCO2 = 40 |
how does CO2 diffuse across membrane when the pressure difference between capillary and cell is only ~6 | CO2 has a very high diffusion coefficient thus 6 is enough for diffusion from tissue to blood |
CO2 at lung moves which direction? | out of blood into alveoli |
there is no blood flow in ___ region of lung due to | upper, Alveolar pressure higher than pulmonary artery pressure. (results in negative Ptr) |
driving pressure for blood in middle region of lung | Pa-Palv |
driving pressure for blood in lowest region of lung | Pa-Pv |
PO2 in pulmonary vein is about 5mmHg less than PO2 in alveoli. Why is this the case | the uppermost lung has Palv = Pa therefore no gas exchange occurs there (dead space) |
Ventilation-perfusion balance for | diverting blood away from the poorly ventilated alveoli to achieve maximum efficiency of gas exchange |
ion channels involved in ventilation perfusion balance | O2 sensing K+ channel, Volt dependent Ca2+ channel |
How is blood diverted away from area of no gas ventilation? (what channels are involved) | 1.O2 sensing K+ channel close causes depolarization 2.Volt dependent Ca2+ channel open, Ca2+ rush into cell 3.cause smooth muscle contraction |
In normoxia what channel remains open/closed? | K+ open, Ca2+ closed => no smooth muscle contraction |
most of CO2 in body is carried as | bicarbonate (HCO3-) |
What molec in Hb does O2 bind to | Fe2+ |
affect of CO on sigmoidal Hb curve | shifts the curve to left |
affect of H+ on sigmoidal Hb curve | shifts the curve to right |
affect of 23DPG on sigmoidal Hb curve | shifts the curve to right |
affect of pCO2 on sigmoidal Hb curve | shifts the curve to right |
how is CO2 converted to bicarbonate? where does this occur | CO2 + H2O ->(carbonic anhydrase) H2CO3 -> HCO3- + H+, occurs in rbc |
H+ produced by converting CO2 to bicarbonate is neutralized by | H+ + Hb -> HbH |
anion exchanger move what ions | move HCO3- and Cl- in opposite directions |
different hypoxia | hypoxic hypoxia, circulatory hypoxia, anemic hypoxia, histotoxic hypoxia |
hypoxis hypoxia | inadequate Hb saturation with O2. causes:high altitude, low ventilation |
circulatory hypoxia | too little blood delivered to tissue causes:cardiac arrest, Emboli(blod blood flow to specific areas) |
anemic hypoxia | reduced O2 carrying capacity of blood causes:low Hb conct, CO poisioning |
Histotoxic hypoxia | cells cannot utilize O2 (eg. CN- poisioning) |
condition where cell cannot utilize O2 for cellular respiration called | Histotoxic hypoxia |
condition in which blood has a reduced O2 carrying capacity called | Anemic Hypoxia |
condition in which too little blood is delivered to tissues called | circulatory hypoxia |
condition in which blood has a low arterial pO2 is called | hypoxic hypoxia |
different CO2 disorders | hypercapnia, hypocapnia |
hypercapnia is | excess cO2 in arterial blood cause:hypoventilation |
hypocapnia is | below normal arterial pCO2 (affect pH) cause:hyperventilation |
H-H eqn for pH can be simplified to | pH = [HCO3-]/pCO2 |
respiratory acidosis | increased H+ due to CO2 retention (hypoventilation) |
opposite of acidosis | alkalosis |
metabolic acidosis cause and compensation | cause:loss of bicarbonate(results in accumulation of acid in blood) comp:remove CO2, excrete H+ in kidney |
loss of bicarbonate results in | metabolic acidosis |
respiratory acidosis cause and compensation | cause:hypoventilation(increased pCO2) comp:kidney makes more bicarbonate |
hypoventilation results in | respiratory acidosis |
metabolic alkalosis cause and compensation | cause:accumulation of bicarbonate(loss of acid) comp:less CO2 blown off, kidney excrete excess bicarbonate |
accumulation of bicarbonate results in | metabolic alkalosis |
respiratory alkalosis cause and compensation | cause:hyperventilation comp:kidney excretes more bicarbonate |
what part of brain contains respiratory center | medulla |
the diaphragm receives respiratory signal from medulla via __ nerve | phrenic |
dorsal respiratory group (DRG) | controls autonomic inspiratory nerve |
ventral respiratory group (VRG) | controls autonomic expiratory nerve |
what part of medulla controls autonomic inspiratory nerve | dorsal respiratory group |
what part of medulla controls autonomic expiratory nerve | ventral respiratory group |
different chemoreceptors | central, peripheral |
central chemoreceptor | medulla, respond to [H+] |
effect of PO2 on central chemoreceptor | no effect |
how does H+ cross the blood brain barrier to activate central chemoreceptor ? | CO2 crosses the barrier, and is converted to bicarbonate and H+ in brain |
effect of CO2 on central chemoreceptor | too much CO2 will inhibit respiratory neuron, indirect activation via conversion to bicarb + h+ |
peripheral chemoreceptor | in aorta, carotid artery |
effect of O2 on peripheral chemoreceptor | decrease in O2 activates peripheral chemoreceptor |
effect of CO2 on peripheral chemoreceptor | indirect activation via conversion to bicarbonate and H+ |
effect of H+ on peripheral chemoreceptor | activate peripheral chemoreceptor |
obstructive lung disease, example and symptom | emphysema, small expiratory reserve volume, big reserve volume. |
restrictive lung disease, example and symptom | pulmonary fibrosis, small inspiratory reserve voluume, because of stiff alveoli |