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UTSW physio block 2
UT Southwestern School of Medicine physiology block 2, 2010
| Question | Answer |
|---|---|
| Normal alveolar ventilation | 4.5-5 L/min |
| Normal pulmonary blood flow | 5 L/min |
| alveolar dead space | ventilation but no perfusion (e.g. pulmonary embolism). blood diverted to other alveoli -> abnormal V/Q (<0.8) |
| normal alveolar V/Q | 0.8 = 4/5 |
| effects of alveolar dead space (physiological compensations) | 1) low [CO2] in dead space -> alkalosis in surrounding insterstitium -> bronchoconstriction. 2) decreased surfactant production in dead space -> decreased compliance -> decreased ventilation. |
| effects of airway obstruction (physiological) | V/Q = 0 for all lung. arteriolar O2 & CO2 reach levels similar to venous. . When airways only partially obstructed, anoxic alveoli = "PHYSIOLOGICAL SHUNT" of deoxy blood that mixes with normoxic blood in "VENOUS ADMIXTURE" |
| What mechanism compensates for venous admixtures? | average PaO2 is low b/c HbO2 equilibrium curve has sigmoidal shape. cannot compensate w/high V/Q elsewhere. NOTE: PaCO2 not much affected (linear Hb curve). hypoxemia with or without hypercapnia. |
| R-L pulmonary shunt | blood bypasses lungs, and so does not participate in gas exchange -> venous admixture. |
| normal pulmonary shunt | NORMAL 5% of blood = L-R shunt (bronchial circulation + thebesian vein in heart). Explains 1/3 of normal A-aDO2. |
| Pathological R-L shunt | 1) Tetrology of Fallot = 75% blood shunted past lungs. 2) Pulmonary Edema w/abnormal vasoregulation, 3) Chronic L-R shunt (e.g. patent ductus arteriosus)-> pulmonary hypertension -> increased pressure of pulmonary vessels -> R->L intracardiac shunt. |
| Alveolar Ventilation Equation | alveolar V = rate of CO2 production/alveolar PCO2 x K. K = 0.863. (NOTE: PACO2 = PaCO2) *USED TO COMPUTE WASTED VENTILATION TO OBTAIN INDEX OF EFFICIENCY OF VENTILATION. *HYPOVENTILATION ALWAYS -> HYPERCAPNIA. |
| normal MINUTE VENTILATION | 7500 ml/min @ rest |
| causes of hypoventilation | 1) damage to respiratory centers (barbiturates, heroin, stroke), 2) chest wall damage or respiratory muscle paralysis (e.g. ALS, SC injury, muscular dystrophy), 3) Airway obstruction (e.g. choking, COPD), 4) high altitude/burning building low PiO2 |
| Diffusion Impairment causes | 1) any change in components of Fick's Law of Diffusion, OR 2) large increase in rate of blood flow that decreases alveolar contact time. Not usually a cause of respiratory failure, but contributes to emphysema & ARDS. |
| Poiseuille's Law of flow | Q=(pi*r^4*deltaP)/8*viscosity*length (P=QR, do substitutions to find R equation) |
| systemic vascular bed (SVR) calculation | SVR = (P.aorta -P.right.atrium)/CO |
| blood & poiseuille's law | YES: incompressible fluid, v @ surface = 0, flow is (mostly) laminar. NO: tube is straight & rigid, viscosity is constant, flow is steady (not pulsatile) |
| Reynold's number | N=density*diameter*velocity/viscosity. above 2000 = not great. Above 4000 = turbulence. |
| viscosity of whole blood | decreases with increasing shear rate (not Newtonian). @ low shear rates (low velocities) viscosity increases due to RBC interaction w/fibrinogen. also higher viscosity @ higher % hematocrit. |
| mechanism for converting pulsatile bloodflow from heart into steady flow by arteries | arterial elasticity (pressure wave) |
| MAP equation & normal MAP | MAP= Pd+ 1/3(Ps-Pd) = CO x SVR . normal MAP = 93 mmHg |
| Korotkoff sounds | 1. tapping, 2. murmurs, 3. thumping, 4. muffling, 5. silence |
| BP for prehypertensive, stage I, & stage II hypertension | prehypertensive 120-139/80-89. stage I 140-159/90-99. stage II >160/>100. 5% = 2ndary hypertension due to disease process (e.g. renal artery stenosis or adrenal tumor) |
| fxn of blood vessels in closed circulatory system | PRIMARY: maintain pressure head. also: maintain selectively permeable barrier, distribute flow selectively, metabolize circulating materials, modulate hemostasis & inflammation, permit growth |
| site of the greatest pressure drop in circulation | systemic arterioles |
| pericytes | live on arterioles, capillaries, venules, create stability & secrete matrix proteins around microcirculation vessels |
| rate of material movement across a membrane | Rate of material movement = surface area * permeability * [ ] difference of material. add more capillaries = increase surface area. |
| Starling Equation | F =K*(Pc-Pi + Πi- +Πc). measures flow across a capillary wall. |
| endothelial permeability of different tissues | intestinal mucosa 15x > heart 8x > skin 25x > brain |
| substances that open EC junctions | histamine, bradykinin, lymphokines |
| leukocyte recruitment | 1. inflammatory signals = ECs display P-selectin & secrete PAF. 2. leukocytes bind P-selectin (rolling). 3. PAF binds R on leukocyte -> activates integrin on leukocyte. 4. Integrin adheres tightly to EC ICAM. 5. leukocyte extravasates |
| fxns of the lymphatics | 1. deliver fluid & protein from interstitium to circulation, 2. transport fat from si to circulation, 3. immunological defense via lymphocytes |
| lymph flow | 2-4 L/day. 100-200 g protein/day |
| structure of lymphatics | 1. no basement membrane (takes in large particles), 2. 1-way valves in vessels + smooth muscle, 3. filtration via lymph nodes before going to blood |
| causes of edema | 1. low plasma oncotic P, 2. elevated venous P, 3. increased capillary permeability, 4. lymphatic blockage, 5. LV failure/mitral stenosis |
| % blood in different blood vessels | systemic veins 60-68%. lungs 10-12%. heart 8-10%. arteries 10-12%. capillaries 4-5%. |
| factors increasing venous return | 1. cardiac suction, 2. respiratory pump, 3. muscle pump, 4. venomotor tone |
| % blood in different organs | liver 25% (incl. portal), kidney/intestine/skeletal muscle 20%, brain 15%, skin/other 8%, heart 4% |
| changes in blood flow x organ during exercise | brain 15 -> 4%. skeletal muscle 25 -> 75%. liver 25 ->4%. intestines/kidney 20 -> 3%. heart same. |
| intrinsic control of circulation | (serves organ needs) 1. autoregulation, 2. local metabolic regulation, 3. paracrine regulation |
| extrinsic control of circulation | (preserves MAP) 1. autonomic NS, 2. humoral factors |
| autoregulation of circulation | (intrinsic mech) 1. myogenic = response to stretch, impt't in kidneys , 2. metabolic = vasodilators wash out w/high flow e.g. H+ impt't in brain, 3. tissue pressure = high pressure from organ capsule constricts capillaries, kidney. |
| active hyperemia | (intrinsic mech: blood flow to organ =proportional to its metabolic ACTIVe-ity) 1. high CO2/lactate/H+ -> K channel opens -> vasodilation (+ Na/K ATPase), 2. low O2 lowers ATP -> adenosine released -> Gs R-> vasodilation |
| passive/reactive hyperemia | (intrinsic mech) vasodilators accumulate when no blood flow -> sudden increase in flow. longer ischemias -> larger response. |
| AVP function | antidiuretic. released from post. pit. due to high osmolarity of blood (salt or dehydration) or low pressure receptors. aquaporins inserted in proximal collecting duct, increases plasma volume. vasoconstriction ONLY with hemorrhage. |
| AngII fx | increases plasma volume. vasoconstriction ONLY w/ intense decline in BP, or w/salt-free diet |
| ANP | diuretic, increases glomerular flow -> reduces plasma volume). vasodilation via membrane-bound guanylyl cyclase receptor. |
| VEGF | vascular endothelial growth factor. causes EC's to digest basement membrane, move & mitose. EC vacuoles combine to form a lumen -> new blood vessel. mechanism can be used by tumors. |
| carotid sinus receptor | 50-200 mmHg, sinus nerve -> glossopharyngeal -> medullary cardiovascular center. |
| aortic arch baroreceptor | 100-200+ mmHg, depressor/aortic nerve -> vagus nerve -> nucleus ambiguus & dorsal nucleus of vagus. requires hypothal. |
| baroreceptor firing rate | starts out signal-locked to systolic increase in arterial pressure, but @ ~200 mmHg, firing becomes tonic (saturation) |
| baroreceptor denervation | decreases specificity of MAP (broader and shorter curve) |
| hemostasis | >10% blood loss -> hypovolumic shock. >30% blood loss fatal (shock). 1 low BP & CO. 2 baroreceptor reflex -> sympathetics (tachycardia, vasoconstriction). 3 low kidney flow -> renin-ang-aldo. 4 atrial volume receptors decrease firing -> AVP release. |
| signs of hypovolumic shock | low BP, high pulse, cold skin, reduced urine |
| low pressure mechanoreceptors | venous side (atrial wall, RV, pulmonary arteries, liver). = volume receptors. |
| atrial mechanoreceptor reflexes | (promote diuresis & reduced blood vol.) 1. Bainbridge (increased HR via SA node), 2. inhibited sympathetics to kidney arterioles (increases flow), 3. inhibited AVP |
| V-P relationship in arteries & aging | given volume -> greater pressure w/age |
| relationship b/tw CO & circulating volume | directly related (volume control = essential for controlling MAP) |
| Aldosterone | renin ->Ang ->Aldo System (RAAS). renin released due to decreased MAP & increased sympathetics. inserts Na/K ch's in collecting duct (sodium resorption) |
| abdominal visceral receptors | stomach, small/large intestine, gallbladder, pancreas. mechano (distension) & chemoreceptors (capsaicin/bradykinin). reflex -> high HR & BP. |
| skeletal muscle receptors | isometric contraction of skeletal muscle -> high systemic BP (exercise pressor reflex). -> sympathetically induced increased peripheral resistance & CO. afferents via DRG's to SC & brain. |
| arterial chemoreceptors | carotid & aortic bodies. run w/ baroreceptor nerves. mainly low PO2 (also low pH, high CO2, & large change in BP). -> increased ventilation + sympathetic vasoconstriction-> increased arterial BP. not impt't in humans as much as in diving mammals. |
| treatment for hypertension | decrease blood volume |
| cardiovascular control from higher brain centers | increased HR & BP by strong emotions, anticipation of exercise. first hypothalamus, then medullary centers. hypothal regulates blood vessels in skin for body temp. |
| diving reflex | HR increases w/ventilation, but decreases when ventilation not possible (i.e. underwater) |
| CO equation | CO = HR x SV |
| % plasma that is protein | 7-9% |
| hemostasis mechanisms | 1 vascular spasm (myogenic, local nerves, 5HT, TXA2), 2 platelet plug (primary), 3 coagulation (2ndary, hematoma), 4 fibrous tissue deposition, 5 1st aid (pressure applied) |
| modulation of blood response to injury | 1 nonvascular cells-> TF-> extrinsic coagulation, 2 release fWF-> platelet adhesion, 3 release NO & PGI2-> inhibits platelet aggregation, 4 bind antithrombin III-> inactivates thrombin/Xa/IXa, 5 bind thrombin-> activates Protein C-> inactivates Va & VIIIa |
| platelet morphology | open cannaliculae, dense granules (ADP, serotonin), alpha granules (vWF, fibrinogen), Mt |
| # per mm^3 of blood of diff. elements | platelets 300k, |
| vWF | high affinity linking of platelet glycoprotein 1b (GPIb) to subendothelial collagen |
| substances promoting platelet activation | collagen, thrombin, ADP, TXA2, contact w/foreign surfaces. NOTE: TxA2 also released from platelets -> feed forward. |
| platelet intracellular activation pathway | binding -> increased PLA2 -> Arachidonic acid cleaved from P'lipids -> PGG2 -> PGH2 -> TXA2(thromboxane sythetase)-> Ca++ -> ADP+TxA2 (platelet aggregation) & 5HT (vasoconstriction) released |
| FX of aspirin on clotting | irreversibly blocks AA conversion to PGG2 (Cox) |
| platelet aggregation | platelets cross-link GPIIb & IIIa via fibrinogen & vWF. =clumping/agglutination. |
| procoagulation activity | plasma membrane PF3 (phosphatidylserine) moves to outer leaflet = docking site for Xa, Va, thrombin |
| platelet retraction | shrinkage of a clot by actomyosin |
| final common coagulation pathway | factor Xa-> converts prothrombin to thrombin -> converts fibrinogen to fibrin |
| activation of fibrin | thrombin cleaves fibrinogen alpha & beta chain n-terminals -> polymerization sites |
| Where are coagulation factors synthesized? | LIVER, except VIII is synthesized in ECs & megakaryocytes |
| Vitamin K is necessary for synthesis of which factors? | needed for Ca++ binding domain. Factors 2, 7, 9, 10 |
| Tissue Factor (TF) | integral membrane protein on non-vascular cells. increase fx of Factor7 1000x -> activates Factor10 |
| prothrombinase complex | = Factor10a, Factor5, Ca, PF3. increases thrombin activation 300K times over Factor10a alone. |
| interaction of extrinsic & intrinsic coagulation pathways | Factor3 + Ca + Factor7a can activate Factor9 |
| thrombin feed-forward effects | thrombin can activate factor5 to increase its production. can also activate Factor13a -> stabilizes fibrin polymers. |
| prevention of blood clotting | 1 antithrombin III (via heparin)-> inactivates thrombin + Xa + IXa. 2 thrombin binds thrombomodulin on EC -> Protein C activated -> inactivates Va & VIIIa. 3 NO & PGI2 released from EC -> inhibit platelet aggregation, 4 ECs physically block interstium |
| tissue factor pathway inhibitor | plasma protein. activated by Xa & Va. binds Factor7a & inhibits. Feedback inhibition. |
| antithrombin activity | 80-90% adheres to fibrin mesh -> prevents spread. antithrombinIII binds & inactivates thrombin (helped by Heparin) |
| thrombomodulin activity | thrombomodulin on EC binds thrombin -> Protein C activated (APC) -> binds protein X -> inactivates Factor5 & Factor8 |
| lysis of blood clots | 1 fibrin clot binds plasminogen (circulation). 2 tissue plasminogen activator (tPA) slowly released by EC's cleaves(activates) plasmin. 3 plasmin cleaves fibrin into soluble fragments. |
| inhibition of tPA | plasminogen activator inhibitor (PAI-1 & 2) from EC's (also inhibit plasmin formation) is released to prevent activation of tPA in general circulation. |
| disorders of excessive bleeding | 1. vitamin K deficiency (Factors 9,7,10), 2. hemophilia (B = Factor9; A = Factor8), 3. thrombocytopenia (PF-3 in intrinsic & common pathway) |
| thrombus | =abnormal clot in blood vessel |
| Virchow Triad | 3 influences of thrombus formation: 1 endothelial injury (arteriosclerosis/infection/trauma). 2 stasis/turbulent blood (immobility). 3 blood hypercoagulability (insufficient anticoagulant factors) |
| thrombin-activatable fibrinolysis inhibitor (TAFI) | activated by thrombin, inhibits fibrinolysis. |
| heparin | anticoagulant, accelerates antithrombinIII inactivation of Xa & thrombin. |
| coumarin | e.g. warfarin, coumadin, dicumarol. interferes w/vitamin K-dpdt synthesis of procoagulants in liver. |
| TPA | dissolves clots via LOCAL administration |
| Ca chelators | removes Ca from blood to prevent clotting IN VITRO ONLY |
| normal venous O2 content | 15 ml/dl |
| hypoxemia definition & causes | =low PaO2 caused by: 1) hypoventilation, 2) impaired diffusion, 3) R->L shunt, 4) low V/Q, 5) low inhaled O2 |
| hypoxemia definition & cause | =inadequate tissue O2 caused by: 1) low PaO2, 2) inadequate tissue perfusion, 3) low O2 capacity of blood, 4) inability to use O2 effectively (e.g. histotoxic) |
| extreme causes of abnormal V/Q | pulmonary embolism. airway obstruction. |
| what are the compensatory reflexes for V/Q inequality? | 1) bronchoconstriction due to low PaCO2. 2) decreased surfactant production. 3) hyperventilation. |
| in what situation does pure O2 not increase PaO2 to high PAO2 values? | "absolute" shunt (very large intrapulmonary shunting in patients w/hypoxemia & elevated A-aDO2 |
| Alveolar Gas Equation | alveolarPO2 = (inhaled_PO2) -(arterial_PCO2/R). R = respiratory exchange ratio. (NOTE: PACO2 = PaCO2). used clinically to calculate PAO2 which is used to calculate AaDO2. |
| Normal alveolar ventilation | 4.5-5 L/min |
| Respiratory Exchange Ratio definition & normal value. | rate of generation of CO2/rate of O2 consumption. normal = 0.8. |
| FIO2 | fractional concentration of O2 in atmospheric air being inhaled. = 0.21 everywhere, when air is normal. |
| reduction of alveolar PO2 | 1) low O2 in inspired air (e.g. brning building), 2) decreased barometric pressure @ high altitude |
| PH2O value | ALWAYS 47 mm Hg |
| barometric pressure @ sea level vs. Mount Rainier | 760 mmHg sea level. 430 mm Hg Mount Rainier. |
| PIO2 | partial pressure of O2 that has been moistened in the trachea. PIO2 = (barometric pressure - PH2O)*FIO2 |
| physiological causes of hypercapnia | 1) hypoventilation, 2) severe V/Q mismatch (high physiologic dead space) |
| causes of hypoventilation | pump problem (respiratory muscle damage) or control problem (SC injury, stroke, drug overdose) |
| FVC | max. volume air exhaled rapidly after maximal inspiration. forced vital capacity. |
| FEV1 | volume of air expired in 1 second of forced expiration. < 25% predicted value associated w/increased PaCO2. "forced expiratory volume 1 sec". |
| FEV1/FVC definition & normal value | normal = 80%. airway obstruction =47%. severe airway obstruction (e.g. asthma) =20%. |
| spirometry & OBSTRUCTIVE disease | 1) volume of exhalation reduced (airway narrowing, loss of elasticity) -> low FVC. 2) slower exhalation (dynamic airway compression) ->VERY low FEV1. overall, FEV1/FVC = VERY LOW. decreased ERV, increased FRC, RV & TLC. |
| spirometry & RESTRICTIVE disease | 1) noncompliance of lungs -> low expiratory volume. 2) normal to high elastic recoil = FEV1 not very reduced. 3) FEV1/FVC = normal to HIGH. Decreased FRC, TLC. |
| Asthma | spastic bronchoconstriction caused by allergens/irritants. 1) mast cells activated -> histamine & cytokines -> local edema + mucus + spasm -> HIGH R. 2) dynamic airway compression. 3) LOW FEV1, FVC, FEV1/FVC. |
| COPD pathology | 1) chronic bronchitis: irritants -> cilia paralysis, HIGH mucus, inhibited macrophages, infection, edema -> stretched alveoli -> alveolar death (50-80%). 2) emphysema = enlarged lung airspace + alveolar wall destruction. |
| COPD causes | environment: smoking, pollution, dust, chemicals. genetics: alpha1-antitrypsin deficiency (1% cases). |
| COPD physiology | 1) LOW FEV1/FVC. 2) HIGH TLC & RV. 3) V/Q mismatch (shunts or dead space). 4) decreased diffusion (loss of alveolar walls). 5) fewer capillaries -> pulmonary hypertension -> right sided heart failure. 6) increased CO2 -> acidosis & mortality. |
| inspiratory ramp | 2 sec ramp-up (dorsal respiratory neurons) = inhalation + cutoff for 3 sec (pneumotaxic center) = exhalation |
| increasing ventilation to maintain tissue needs | HYPERPNEA |
| rapid but normal breathing | TACHYPNEA. Total ventilation HIGH. Alveolar ventilation depends on Vt & Vd/Vt |
| Vt definition & normal value | Tidal Volume = air entering body during single breath. ~400-500 ml @ rest. |
| FRC definition & normal value | Functional Residual Capacity = air in lung @ end of normal expiration (e.g. @ rest). ~2600-3400 ml. determined by compliance & elasticity. |
| VC definition & normal value | Vital Capacity = max. volume air exhaled after max. inhalation. ~3400-4500 ml. most common test. |
| RV definition & normal value | Residual Volume = air remaining in lung after max. expiration. ~1500-1900 ml. CANNOT BE MEASURED BY SPIROMETRY! |
| TLC definition & normal value | Total Lung Capacity = air in lung @ max. inspiration. ~6000 ml. determined by elasticity, stiffness of lung, inspiratory muscle strength. |
| awareness of difficulty in breathing (feels shot of breath) | DYSPNEA. |
| paused breathing | APNEA |
| dorsal respoiratory group, MEDULLA | responsible for INSPIRATION & general breathing rhythm. sensory afferents from vagus (lung chemo & stretch R's) & glossopharyngeal nerve (peripheral chemoR inputs). efferents -> phrenic nerve to diaphragm. |
| ventral respiratory group, MEDULLA | INACTIVE during passive breathing. ACTIVE during active respiration (e.g. exercise). |
| pneumotaxic center, UPPER PONS | cuts off inhalation ramp (regulates volume & rate). |
| apneustic center, LOWER PONS | prolongs inhalation, increases volume of inhalation. normally inhibited by pneumotaxic center of upper pons & vagus afferents. |
| Apneusis | deep & prolonged inspiration with periodic expiration |
| central chemoreceptors (ventilation) | sense H+ in CNS (only CO2 crosses BBB though). located near ventral resp. group (medulla). 75% of CO2-induced increase in ventilation. |
| peripheral chemoreceptors (ventilation) | sense PO2<60mmHg, high CO2, low pH. located in carotid/aortic bodies. detect hypoxemia & account for 25% of CO2 increase in ventilation. |
| adaptation to high PaCO2 | after 1-2 days of high CO2, kidneys reabsorb bicarbonate to equivocate blood pH. |
| hypercapnia ventilation response | BOTH peripheral & central chemoreceptors activated |
| hypoxic ventilation response | only begins when PaO2<60 mmHg (Hb saturation curve = steep). normally, low O2 enhances normal ventilatory response to CO2. |
| Acute FX of high altitude | decreased PAO2 -> hyperventilation (low O2) -> low CO2 -> central respiratory centers restore normal respiration. high pulmonary vascular resistance (vasoconstriction due to hypoxia). Hb saturation curve = right shift. |
| Chronic FX of high altitude (acclimatization) | chronic low O2 -> brain respiratory centers lose 80% sensitivity to H+ -> hypoxia @ peripheral R's is much more influential. |
| lung stretch R's | airway smooth muscles. respond to large inspiration. activate pneumotaxic center. protect lungs from overinflation. (Vt > 1500 ml) |
| Herring-Bruer response | lung stretch receptors signal pneumotaxic center to terminate inspiration |
| lung irritant R's | large airways. respond to gas, smoke, dust. initiate cough, bronchoconstriction, sneezing. protects alveoli. |
| J receptors | =juxtapulmonary capillary R's. in lung parenchyma, vessels, airways. respond to edema or too high blood flow. cause dyspnea, rapid shallow panting. |
| chest wall receptors | detect force by respiratory muscles. contribute to dyspnea. |
| PaO2 during moderate exercise | O2 usage can be 20x higher. CO2 increases as well. BUT ventilation adapts = arterial levels do not change dramatically. |
| anaerobic threshold | = threshold for metabolic acidosis in heavy exercise: pH decreases w/lactic acid generation. |
| damage to respiratory centers of brain caused by: | 1) brain edema. 2) drugs (anesthesia & narcotics) |
| Cheyne-Stokes breathing | deep breathing alternates w/ low/no breathing. depression of brain activity due to: slow blood delivery (congestive heart failure)/abnormal response by respiratory control centers (sleep @ high alt. or brain damage) |
| SIDS | likely due to CO2 ventilation response. infant on back = less risk of re-inhaling exhaled CO2 |
| sleep breathing | NonREM = eupneic, decreased CO2 sensitivity. REM = = irregular breathing, V. low CO2 response. barbiturates can stop ventilation in REM. |
| central sleep apnea | decreased central drive to breath |
| obstructive sleep apnea | def: >15 apneic incidents @ >10 sec each per hour sleep. decreased airway tone (collapse). decreased chemoreceptor/central drive, exacerbated by alcohol/depressants. |
| low rate of breathing or shallow breaths | HYPOPNEA |
| contributing factors to sleep apnea | supine position, nasal obstruction, large tonsils, age, obesity (e.g. fat deposits in pharynx & compression due to neck fat), pregnancy |
| pathophysiology of sleep apnea | 1) metabolic alkalosis when awake (CO2 builds up in apnea -> kidneys reabsorb HCO3-). 2) hypoxic pulmonary. 3) erythropoiesis -> polycthemia -> high ventricular load & afterload -> RV hypertrophy. |
| cor pulmonale | failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries and RV |
| normal AaDO2 | 5 mm Hg |
| normal Hb saturation of arterial blood | 97% (saturated @ 95 mmHg PaO2) (75% saturated in mixed venous blood) |
| CaO2 normal value | =oxygen content of arterial blood (CaO2 = HbO2 + O2 dissolved). ~ |
| O2 capacity of blood definition & normal value | = amt. O2 can be bound to Hb in 100 ml blood. ~20.1 mlO2/100ml blood. |
| %O2 saturation of Hb equation | %SO2 = [HbO2]/O2 capacity x 100 |
| normal amt. Hb in blood | normal ~ 15 g/100 ml blood |
| O2 bound to Hb (equation) | [Hb] g/dl x 1.34 ml O2/g Hb x % SHbO2 |
| normal oxygen consumption @ rest | ~250 ml O2/minute |
| AV shunts | increase blood flow to capillaries when contracted (thermoregulation & BP control). when open, connect arterioles directly to venules. |
| endothelin 1 | endothelial cell vasoconstrictor -- target of "red wine effect"? |
| prostacyclins & blood clotting | relased by tunica intima EC's -> anti-adhesion |
| VEGF | activates stem cells for endothelium for blood vessel growth & differentiation |
| Avastin | anti-VEGF = anti-angiogenic. treatment for metastatic colon cancer. |
| pericytes | contract to control blood flow @ capillaries & postcapillary venules. same stem cells as endothelium. die in diabetic retinopathy -> microaneurysms. serve as progenitors for fibroblasts in wound repair. |
| PDGF | induces stem cells to form into pericytes instead of endothelial cells |
| extrinsic innervation of GI tract | PARASYMP: (preganglionic fibers synapse on enteric interneurons) vagus nerve, pelvic nerve. celiac/sup. SYMP: postganglionic fibers synapse on smooth muscle/vessels/secretory cells) (mesenteric/inf. mesenteric & hypogastric plexi |
| vago-vagal reflex | local GI conditions -> afferents to vagus ->efferents to local circuit |
| GASTRIN | increases H+ secretion from parietal cells. released by G-cells in mucosa of stomach antrum (pyloric gland area), binds ECL cells in xyntic gland area -> histamine production -> parietal cell HCl release. MAY bind parietal cell directly. |
| CCK | released by I cells in duodenum/jejunm + neurons in ileum & colon. increases enzyme & fluid secretion by acinar cells, -> smooth muscle contraction in Ductal cells of pancreas/gallbladder. Decreases gastric emptying |
| SECRETIN | released by S cells of small intestine. -> Gs/PKA -> CFTR Ch. P'ated & opens in Ductule cells of pancreas to increase HCO3- & water secretion. |
| GIP (GASTRIC INHIBITORY PEPTIDE) | released by K cells of duodenum/jejunum. causes decreased fluid absorption, slows gastric emptying, inhibits acid production. |
| GUANYLIN | released x ileum & colon. targets small & large intestine to increase fluid absorption. |
| MOTILIN | released by endocrin cells in upper GI tract. targets stomach & duodenum to increase smooth muscle contraction. |
| PEPTIDE YY | endocrine cells in ileum & colon (maybe also enteric nerves) -> lowers acid secretion |
| SOMATOSTATIN | released by D CELLS in stomach & duodenum, due to pH < 4.5. Inhibits parietal, ECL, & G cells -> decrease acid secretion. |
| SUBSTANCE P | neurotransmitter between enteric neurons |
| VIP | released by enteric NS, causes smooth muscle cells to increase fluid secretions in small intestine. opens lower esophageal sphincter. inhibits BER. |
| Neurotensin | released by endocrine cells in GI tract. targets smooth muscle to release histamine. |
| BER (basic electrical rhythm) | periodic fluctuations in the V_rest of GI smooth muscles originating @ pacemaker(L-type Ca & Ca-activated K Chs). stretch/ACh -> higher Vrest + APs. NE/NO/VIP -> lower Vrest. |
| physiological ileus | inhibitory intrinsic neurons inhibit most of lumen smooth muscle. EXCEPTIONS: sphincters, parts of proximal stomach under chronic contraction. |
| contents of saliva | (hypotonic vs. plasma). alpha amylase, lingual lipase, lysozyme/RNase/DNase/peroxidase (antibiotic), mucus |
| generation of saliva | GENERATION: basal Na/K/2Cl, apical Cl, Na & H2O -> transcellular. CONCENTRATION: apical K/H, Na/H, anion exchanger, CFTR, ENaC (net K/HCO3 out). Basal K-leak, CFTR (net NaCl absorbed). |
| neural influence on saliva production | sympathetics: transient protein-rich, low vol. paraysmpathetics: long-lasting protein-poor, high vol. |
| alpha amylase | cleaves alpha-1,4 linkages, not alpha-1,6 linkages. mostly faced w/glucose-based amylose (alpha-1,4 only) & amylopectin (both), not as much glycogen (both). doesn't work @ low pH. |
| lingual lipase | cleaves FA's from triglycerides & cholesterol esters. functions well @ low pH but proteolytically degraded. |
| esophageal sphincters | UES (upper esophageal sphincter) = tonically contracted, but reflexively relaxes when food present. LES (lower) = opens when smooth muscle inhibited by VIP from vagus or by NO. |
| swallowing | PRIMARY (voluntary/pharyngeal reflex to food). SECONDARY if food doesn't reach stomach w/1st swallow (mechanoreceptors in esophagus initiate, can be local reflex or reinstation of full motor sequence by medulla) |
| Achalasia | LES doesn't open during swallow |
| normal pulmonary systolic & diastolic pressures & mean pressure | 25/8 mmHg (mean = 14 mmHg) |
| pulmonary : systemic vascular resistance | 1: 10 |
| equation for vascular resistance | R = (systolic P - diastolic P)/CO (P=QR). NOTE: pulmonary R drops as CO increases! |
| lung zones x pressure gradients | 1) A > a > v. 2) a > A > v. 3) a > v > A |
| controls of pulmonary blood flow | low PAO2 -> vasoconstriction. |
| Hypoxic Pulmonary Vasoconstriction | low PAO2 or blood pH -> decreased K+ current in smooth muscle of small arteries -> depolarization & Ca entry in L-type Ch's -> vasoconstriction |
| blood flow to the coronary arteries | Left coronary = blood flow only during diastole. Right coronary = blood flow during both systole & diastole. |
| is the LV or RV more susceptible to ischemia? | ? |
| tissue pressure in LV during systole | pressure is greater in subendocardium than subepicardium in the LV during systole (thus subendocardium has greater risk of ischemia during partial coronary artery occlusion) |
| cerebral blood flow | 750 ml/min. DOESN'T CHANGE. |
| neural pathway for swallowing | medulla to: 1) trigeminal/facial/hypoglossal nerves. 2) nucleus ambiguus -> esophageal striated muscle. 3) dorsal motor nucleus of the vagus -> enteric NS -> esophageal smooth muscle |
| gastric juice origin & composition | secreted from oxyntic glands of the gastric mucosa. HCl pepsinogen, mucus, Intrinsic Factor. |
| PEPSINOGEN | =protease. ACH -> stomach oxyntic gland CHIEF CELLS, pH <5 activates it-> pepsin. Cephalic & Gastric Phases. |
| acid secretion | PARIETAL CELLS. 1) Na/K ATPase brings K in basal (K leaks out). H+/K ATPase brings H+ out (K leaks in). net = H+ apical!!! 2) w/out H+, more HCO3 made. HCO3/Cl antiporter -> HCO3 out. Cl leaves apical. net = Cl apical & HCO3 basal!! sum = HCl apical, Na |
| regulation of acid secretion | H+/K+ ATPase pumps in vesicles moved to membrane during fed state, retrieved during non-fed state |
| molecular regulation of parietal cell acid secretion | histamine->Gs->cAMP->PKA->>>pumps in membrane OR (Gastrin?)/ACh ->Gq ->PLC->Ca++ & PKC ->>>pumps in membrane. POTENTIATION of diff. signaling pathways |
| histamine in the GI tract | paracrine-release from enterochromaffin-like (ECL) cells. binds H2 receptor on parietal cells |
| Zantac mech. of action | target H2 receptor on parietal cells to block histamine-related acid secretion |
| phases of acid secretion | CEPHALIC~30% response; vagus nerve ->ACh -> GRP (gastrin releasing peptide). GASTRIC~60%; distension-> ACh & GRP + vago-vagal reflex, peptides/aa's-> act on G cells. INTESTINAL~10%, aa's in s.i. -> parietal cell stim. OR enterooxyntin released. |
| GRP (gastrin releasing peptide) | released by intrinsic neurons of stomach, promotes gastrin release by G cells. stimulated by vagus nerve or mechanoreceptors of intrinsic neurons. |
| enterooxyntin | released by distension of duodenum or in response to aa's & peptides. stimulates parietal cell acid secretion (unknown mech) |
| attenuation of acid secretion | gastric pH, somatostatin, prostaglandins, CCK, secretin, VIP, GIP, peptide YY. |
| mucus in the stomach | 1) vagal ACh -> mucus neck cells produce SOLUBLE mucus (in response to irritating foods & alcohol). 2) |
| intrinsic factor | vitamin B12 absorption. secreted by parietal cells. |
| receptive relaxation of the tummy | tonically contracted smooth muscle -> relaxes in presence of bolus -> larger tummy space. initiated x mechanoreceptors, modified by vago-vagal reflex. |
| orad of stomach | in fundus toward cardia region. contractions = weak & infrequent. |
| mixing & grinding of tummy | contractions begin @ jxn of orad & caudad & propogate toward pylorus. w/time contractions initiate more and more rostral to "pinch off" portions of bolus in orad for processing. |
| ANTRAL SYSTOLE | BER occurs in pairs (bookending bolus). 1st wave -> closes pylorus even more. 2nd wave = bolus arrives @ closed sphincter & "slams" into pylorus = ANTRAL SYSTOLE |
| chyme | mixed-up digestive juice in tummy. |
| mechanisms that decrease gastric emptying | 1) duodenal chemoreceptors sense acid/fat/hypertonicity/peptides/aa's-> intrinsic NS. 2) intrinsic NS ->CNS -> increase symp decrease parasymp tone. 3) duodenal cells release SECRETIN, CCK, GIP, GASTRIN |
| renal blood flow | afferent arteriole = 50 mmHg pressure -> 20 mmHg @ efferent arteriole. blood flow = 25% systemic. increased colloid osmotic pressure due to fluid filtration almost stops filtration @ distal kidneys. |
| Cephalic Phase of pancreatic secretion | 1) vagus nerve (ACh) stimulates acinar cells. 2) Gastrin (neuro), VIP, GRP (enteric NS) potentiate FX. Gall bladder empties. |
| Intestinal Phase of pancreatic secretion | 1)H+-> SECRETIN-> ductule cell CFTR Ch's open-> HCO3 secreted. 2)vago-vagal reflex-> acinar&ductules increase secretion. 3)FA's & small peptides-> CCK-> acinar secretions increased + Gall bladder empties. |
| Gastric Phase of pancreatic secretion | tummy distenstion -> vago-vagal reflex = slight increase in acinar secretions |
| Bile composition | Bile acids/salts 70%, P-lipids 20%, Cholesterol 5%, Bilirubin 1%, "remainder" 4%. Isotonic to plasma (~290 mOsm). bile duct cells add HCO3 & H2O (secretin-stimulated). |
| Bile Acids | carboxylic acids. primary choleic acid -> 2ndary deoxycholic acid. primary chenodeoxycholic acid -> 2ndary lithocholic acid (via s.i. bacteria). 2ndary = VERY insoluble. |
| Conjugated Bile Acids | modified by the liver to increase solubility. covalent addition of glycine/taurine. low pKa, exist as Na+ salts. solubilize bilirubin in mixed micelles. [critical micelle] = dpdt on all components, not just bile acids. |
| Bilirubin export from liver | Bilirubin = from Hb in spleen (V. Hydrophobic, toxic) -> liver via Albumin chaperone in blood. Transporter into liver, conjugated w/Glucuronide to detoxify. APICAL: ATPase transporter. |
| control of bile secretion from liver | 1) bile acid-dpdt flow (bile secretion (electrolytes) promotes further secretion). 2) bile acid-indpdt flow (via. secretin -> fluid & HCO3) (3g bile acids secreted 4-12 x per day) amt. excreted == amt. synthesized. |
| Gallstones | excessive precipitation of cholesterol/bilirubin, etc. |
| Gall Bladder secretion of bile | vagal ACh -> gall bladder smooth muscle contraction (cephalic & intestinal phases). CCK increases gall bladder contraction & inhibits Sphincter of Oddi. |
| bile acid reabsorbtion in s.i. | APICAL: Apical sodium-dependent bile acid transporter (ASBT)(Na 2ndary active transport coporter)(recovers>95% bile acids). BASAL: OST (Organic Solute Transporter) transports bile acids into blood stream |
| bile acid recycling in liver & "Bile Acid-Dpdt Component of Bile Secretion" | BASAL: Na-dpdt 2ndary active transport. APICAL: ATPase (primary active transport). Bile Acid movement drives movement of H2O, ions!!! |
| pancreatic amylase | lumenal enzyme: degrades alpha 1-4 linkage of starch -> di/trimers. [NOTE: alpha 1-6 linkages degraded by membrane bound enzymes]. -> glucose/galactose/fructose |
| sugar absorption | monosaccharides only can be absorbed. APICAL: SGLT1 = Na coporter for glucose or galactose. GLUT 5 = fructose passive absorption. BASAL: GLUT2 transports all sugars to bloodsream. |
| protein digestion: lumenal | ENDOPROTEASES: Trypsin, Chymotrypsin, Elastase. EXOPROTEASES: Carboxypeptidases A & B. Trypsinogen activated by trypsin/enterokinase |
| Enterokinase | = PROTEASE that cleaves & activates trypsinogen |
| protein absorption | aa's, di/tripeptides transported. 2ndary active transport (Na-based) or facilitated diffusion. further degraded to aa's in EC cytoplasm, then basal transporters. |
| pancreatic lipid digestive enzymes | 1) pancreatic lipase, 2) cholesterolesterase, 3) phospholipase. watersoluble enzymes work @ lipid interface. |
| fat emulsification | 1) mixing in stomach. 2) duodenal bile salts retard separation of water & fat. NOTE: emulsions are not truly in solution |
| colipase | binds lipase, displaces molecule of bile salt from fat droplet. prevents displacement of lipase by bile acids. |
| mixed micelles | formed by bile acids + emulsion. contain CONTAIN LIPID BREAKDOWN PRODUCTS. digestion IN EMULSION, absorption IN SOLUTION (mixed micelle). |
| fat absorption | glycerols: water soluble, diffuse in. micelles: pass through unstirred water layer = lipids transported into cell & bind carrier proteins |
| fat processing in absorptive cells | FAs & monoglycerides + binding protein -> DAGs & TAGs -> chylomicrons. Cholesterol adds straight to chylomicron. |
| NPC1L1 | transports unesterified cholesterol & plant sterols into absorptive epithelial cells. Ezetemibe Drug blocks this cholesterol carrier!!! (statins block cholesterol synthesis) |
| ABC5/8 | trasports plant sterols & cholesterol back to lumen from intestinal absorptive cells (in bilirubin family) |
| fat soluble vitamin absorption | A, D, E, K into mixed micelles or protein-mediated, likely transported into epithelial cells |
| water soluble vitamin absorption: e.g. FOLATE | B, C, Folate, Biotin. protein-mediated absorption. Folate glutamates are cleaved until Pteroyl-Glu(1). antiported against OH- -> converted in cell to biologically active BH2 & BH4 |
| iron absorption in s.i. | Heme imported directly (endocytosis) -> Heme Oxygenase extracts iron + bilirubin -> liver w/transferrin. Iron converted to Fe2, coported w/H+ (apical), transported to transferring (basal) in circulation. |
| migrating motor complex (MMC) | begin in duodenum/stomach. point of initiation moves more distal until @ 6 hours reaches ileum. intrinsic enteric NS activity. hormone motilin = initiates. food ingestion ends it. |
| motilin | initiates migrating motor complex. |
| vomiting reflex | vomiting center (4th ventricle chemoreceptor trigger zone)/emotional brain/mechanoreceptors in throat/chemoreceptors in GI tract. |
| retching | proceeds vomiting. reverse peristalsis in s.i. = pyloric sphincter & tummy relax, then sphincter closes again. air inhaled into esophagus. LES opens for gastric contents but UES stays closed. When UES opens = vomiting. |
| modulation of body temperature via skin blood vessels | apical skin: cold = sympathetics -> vasoconstriction = decreased heat loss. nonapical skin: no anastomoses, vasoconstriction when warm. vasodilation with continued warming (sympathetic withdrawal). sweat stimulation = bradykinin causes more vasodilation. |
| apical vs. nonapical skin | apical = nose, lips, ears, hands, feet w/anastomoses/shunts/glomus bodies. nonapical = trunk & limbs. |
| splanchnic circulation | 25% of CO. sympathetic control. decreased flow during quiet standing, exercise, hemorrhage.veins = large blood reservoir. |
| ascites cause | cirrhosis of the liver |
| fetal circulation | before birth, 2 left-right shunts. @ birth, umbilical cord tied off -> hypoxia & increased peripheral resistance -> gasp & lungs inflate |
| patent ductus arteriosus treatment | COX inhibitors or surgical closure |
| measuring coronary blood flow | Nitrous Oxide method or radioactive washout technique |
| coronary vein drainage | LEFT: coronary sinus (& ant. cardiac veins). RIGHT: anterior cardiac veins (also direct communication via arteriosinusoidal, arterioluminal & thebesian vessels). |
| neuromodulation of coronary vessels | sympathetics -> increased HR & contractility -> vasodilation (2ndary fx). alpha adrenergic blockers can decrease sympathetic tone. ACh -> vasodilation but also decreased HR -> vasoconstriction |
| myocardial oxygen usage | maximal @ rest. must increase blood flow to increase O2 delivery. cardiac muscle extracts ~70% O2 & skeletal muscle extracts ~15%. |
| hypoxic vasodilators of the coronary circulation | K, prostaglandins, NO, adenosine |
| myocardial O2 consumption | electrical activation = .05% total usage. Myocardial O2 use correlates w/wall tension (not external work). 1) HR, 2) Wall Tension, 3) Contractility. |
| Double Product | Systolic Blood Pressure x HR. used most frequently to measure myocardial O2 usage. heart disease = reduced blood flow + pain + ischemic ECG @ given double product. |
| Triple Product | Systolic Blood Pressure x HR x Ejection Time |
| ischemic threshold | myocardial O2 demand exceeds O2 supply. measured w/double product. |
| Restoring coronary artery supply-demand balance | 1) Ca Ch blockers increase blood supply. 2) beta blockers decrease cardiac O2 demand. |
| conducting zone of airways | trachea, bronchi, bronchioles |
| respiratory zone of airways | 17th airway branches to alveolar sacs. gas exhange @ terminal respiratory unit (bronchioles, alveolar ducts, alveoli) |
| examples of obstructive lung diseases | asthma, COPD (e.g. emphysema). HIGH resistance, LOW airway diameter -> air trapped in lungs. |
| examples of restrictive lung diseases | Fibrosis, Silicosis, Asbestosis, Scoliosis. Cannot expand lungs. |
| Helium Dilution Method | determines RV (cannot be measured w/spirometry). known amt Helium inhaled & exhaled until equilibrium. [He]0 x volume of tank = [He]final x (volume of tank + lungs). volume of lungs ==FRC |
| Anatomic Dead Space estimation (V_subD) | dead space in ml ~= body weight in lb |
| Alveolar Ventilation | = minute ventilation - minute dead space. same overall minute ventilation w/more breaths/min & lower tidal volume -> lower alveolar ventilation. |
| Alveolar Dead Space | due to alveoli that don't receive adequate blood flow |
| Physiological Dead Space | = Anatomical + Alveolar Dead Space |
| water vapor pressure during inhalation | PO2(inhaled) = (P_barometric -PH2O) x Fractional%O2 in air. Thus, water vapor added in airways decreases the partial pressure of O2. when overall barometric pressure is low (e.g. high altitude), PH2O is the same, & so less O2 is inhaled. |
| Hypoventilation def. | inadequate alveolar ventilation for a given amount of CO2 production. |
| minute ventilation | v(dot)E or v(dot)T. = vol. gas entering or leaving breathing passageways in 1 minute |
| Transpulmonary Pressure | P(sub)TP. = transmural pressure across alveolar wall. measure of elasticity working to collapse lungs @ end inhalation. = alveolarP - pleuralP |
| lung compliance | measure of lung distensibility. inversely related to elasticity. C(sub)L = change in lung volume/transpulmonaryP . = slope of lung volume-pressure curve. |
| collapsing pressure of the alveoli | P = 2*surface tension/radius . surfactant reduces surface tension in small more than in large alveoli. decreased surface tension minimizes transudation (leaking) of plasma from capillaries into alveoli. |
| atelectasis | alveolar collapse due to increased surface tension |
| factors influencing FX of surfactant | 1) surface density of surfactant (works better @ higher density). 2) whether alveolus is expanding/contracting |
| hysteresis in lung V-P curve | due to fx of surfactant (size-dpdt variable surface tension & prevention of small alveoli collapse during exhalation) |
| lung surfactant physiology | secreted by Type II alveolar cells. Consists of Dipalmitoyl Phosphatidylcholine (DPPC). Rapidly metabolized, so must be constantly remade. pulmonary embolism stops production (->increased work of breathing + atelectasis). |
| alveolar pressure (P(sub)A) | determined by elasticity of alveolar wall. = force that drives out air during exhalation. |
| turbulent air flow | most likely when diameter of tube is large & velocity is high. w/breathing 80% of resistance to airflow b/tw nose & medium sized airways (diam>2mm). COPD increases airway resistance in smaller airways <2mm. |
| what are symptoms and indications related to turbulent flow in a patient's central airways? | "wheezing" indicative of bronchospasm generating turbulent flow. |
| airway cross-sectional area dpdt on: | 1) lung volume (i.e. radial traction opens airways during inspiration). 2) elasticity (airways collapse when decreased elasticity holding them open). 3) Bronchiol smooth muscle contraction (i.e. asthma narrows airways) |
| flow in large vs. small diameter airways | in large cross-sectional area (e.g. peripheral) there is more pressure exerted against the walls of the airway. In small cross-sectional areas (trachea) velocity increass -> decreased pressure against walls -> more likely for airway to collapse |
| factors affecting expiratory flow rate | beginning of exhalation = high lung volumes -> effort-dependent flow. end of exhalation = low lung volumes = effort-independent flow. |
| Equal Pressure Point | where airway pressure = pleural pressure (transpulmonary pressure = 0). -> dynamic airway compression. @ low lung volumes, EPP moves down to airways unprotected by cartilage (transpulmonary pressure of alveoli decreases b/c less elastic recoil) |
| EPP & emphysema | less elastic recoil due to missing lung tissues -> dynamic compression of airways @ higher lung volumes (maybe entire exhalation). 1) exhale slowly through pursed lips (lower velocity = less drop in P). 2)deeper breaths (more radial traction) |
| control of bronchoconstriction | 1) ACh, 2) irritants, 3) histamine |
| control of bronchodilation | 1) Norepi (weak) & Epi (strong) @ beta2R. 2) beta2 agonists ALBUTEROL |
| factors affecting diffusion constant of a gas | Diffusion Constant varies directly w/Solubility. Indirectly w/sqrt of Molecular Weight |
| factors affecting rate of diffusion of a gas | Directly Variable: 1) Diffusion Constant, 2) surface area, 3) [O2] difference b/tw alveoli & venous blood. Indirectly Variable: distance traveled for diffusion |
| Diffusion Capacity of the Lung (D_sub_L) | = amt O2 diffusing across barrier membrane in 1 minute under a pressure difference of 1 mm Hg. Increased during exercise, decreased in some diseases (fibrosis, edema, emphysema/bronchial obstruction, low compliance in silicosis) |
| O2 capacity | max. amt O2 that can combine with Hb. dpdt on: 1)amt Hb, 2) ability of Hb to bind O2. |
| normal amt. Hb/100 ml blood | 15 g |
| normal O2 capacity of blood Hb | 20.1 ml O2/100 ml blood |
| O2 content | = total amt. O2 in blood (in Hb & in solution). O2 content = (O2 binding capacity x % Hb saturation) + dissolved O2 |
| O2 saturation (SO2) | =% total O2 binding sites in Hb not bound to O2. NOT dpdt on amount of Hb. %SO2 = O2 content - O2 dissolved in blood/O2 capacity x 100 |
| normal PO2 & SO2 of blood leaving lungs | 95 mm Hg, SO2 = 97% |
| normal PO2 & SO2 of venous blood entering lungs | 40 mm Hg, SO2 = 75% |
| PO2 for near complete saturation of Hb | PO2 < 70 mmHg |
| Normal amt. O2 dissolved in blood | 0.3 ml |
| P50 | PO2 @ which 50% Hb saturated. high P50 = low O2 binding affinity |
| normal P50 of human blood | 26.5 mm Hg |
| right shift of Hb saturation curve | low pH, high 2-3-DPG & Temp |
| left shift of Hb saturation curve | high pH, low 2-3-DPG & Temp |
| CO2 % in different forms in blood | 7% dissolved, 70% bicarbonate, 23% carbaminohemoglobin |
| CO2 content: pressure curve | pretty much linear |
| Haldane Effect | venous blood can transport more CO2 than arterial @ any PCO2 |
| Bohr Shift | CO2 binds to Hb decreases Hb's affinity for O2 |
| fraction of pulmonary capillaries open @ rest | 1/3 |
| increase in blood flow through lungs during exercise | 4-7x higher |
| passive control of pulmonary vascular resistance | distension & recruitment of capillaries. 1) minimizes load on right heart. 2) prevents edema (lower vascular resistance). 3) ensure adequate O2 exchange (increased perfusion & capillary surface area) |
| hypoxic pulmonary vasoconstriction (HPV) | pulmonary capillaries constrict @ low PO2. pathological systemic HPV during COPD & @ high altitude |
| hypoxemia definition | Arteriolar PO2 < 85 mm Hg. extreme cases = arteriolar CO2 > 45 mm Hg. |
| ARDS | adult respiratory distress syndrome. caused by decreased surfactant production -> pulmonary edema |
| effects of gravity on lung physiology | pleural pressure is less negative @ base than apex -> alveoli more distended @ apex than base of lung. (think suspended slinky). |
| V/Q ratio @ top vs. bottom of lungs | 3.6 @ top. 0.6 @ bottom. |
| Normal A-aDO2 | 10-15 mmHg |
| changes in pulmonary physiology w/age | 1) less gas exchange (fewer working alveoli, more physiologic deadspace). 2) less alveolar ventilation (lower compliance, decreased muscle strength). 3) increased V/Q mismatch. 4) increased residual volume & residual capacity (less elastic recoil) |
| gross structure of the large intestines | longitudinal layer is v. thin w/3 thicker teniae coli. haustra = pouch-like structures in series. external anal sphincter = voluntary skeletal muscle. vagus innervates ascending & transverse colon, pelvic sacral nerves innervate descending colon & anus. |
| colon motility | 1) localized movement of muscularis mucosa rubs chyme on absorptive cells. 2) Haustral movement for mixing/segmentation. 3) mass movement 3x/day (peristalsis) |
| defecation | 1) stretch reflex relaxes internal & contracts external anal sphincter (dpdt on intact SC) -> feeling of need to poo. 2) conscious relaxation of external sphincter. 3) reflex = peristalsis in rectum, relaxation of puborectalis (normally kinks anal canal). |
| valsalva maneuver | contract abdominal muscles to aid in pooing |
| BP during defecation | high abdominal pressures -> pressure on large thoracic veins -> LOW venous return & LOW arterial pressure (decreased CO). can -> stroke. |
| digestion in the large intestine | bacteria break down remaining nutrients into small fatty acids that are absorbed ty epithelium. can contribute significantly to nutrition |
| ileogastric reflex | distended ileum inhibits gastric motility |
| gastroileal reflex | gastric motility increases ileal motility |
| colonocolonic reflex | distension of one part of colon decreases tension & motility in other parts of the colon |
| gastrocolic reflex | distension & motility in the tummy increases motility in the colon, promotes defecation |
| water secretion & absorption in GI tract | 10 L/day enter GI tract (2 from intake, 8 from secretion). Crypt Cells in small intestine secrete water & NaCl. 8.5L absorbed by s.i. & 1/2 L absorbed by colon. 100 ml excreted. |
| water secretion by crypt cells | Na/K/2Cl pump basolateral, Cl Ch. apical (opened by phosphorylation by PKA or PKC). Na & H2O follow intercellularly. cholera toxin activates Gs -> PKA -> CFTR opens (treat w/H2O+NaCl+glucose. |
| signaling involved in water secretion by crypt cells | enteric NS: ACh, VIP, 5-HT. Vagus: ACh increases secretion. Hormones: CCK, Gastrin, NO. Motility & GI smooth muscle contraction -> more water secretion (via neurons that stimulate smooth muscle) |
| Immodium | anti-diarrheal medication. decreases GI smooth muscle contractions, therefore lower water secretion & increased absorption |
| Na absorption in GI tract | 1) Na/sugar or Na/aa coporter (s.i.). 2) Na/H exchanger (duodenum/jejunum). 3) Na/H exchanger + Cl/HCO3 exchanger (ileum & colon). 4) ENaC channel (colon). all apical |
| Cl absorption in GI tract | 1. passive (electrical gradient in whole GI tract; transcellular & paracellular), 2. Cl/HCO3 exchanger (ileum/colon/rectum), 3. Na/H + Cl/HCO3 exchangers (ileum/colon/rectum) |
| K absorption & secretion in GI tract | 1. passive paracellular (absorption in tummy & ileum; secretion in colon & rectum), 2. active secretion K Ch (colon), 3. active absorption K/H pump (rectum) |
| GALT | 1) Peyer's Patches: mucosa/submucosa in ileum, B-lymphocytes. 2) lamina propria lymphocytes (B-cells) -> IgA. 3) Intraepithelial lymphocytes(basolateral lumenal epithelium) |
| Microfold Cells | = M Cells. endocytose proteins & antigens, give them to dendritic cells & macrophages -> present them to T cells in GALT to produce IgA |
| Pulse Pressure | = systolic-diastolic pressure. normal ~40 mmHg |
| Fick's Law of Diffusion | Flux = -D*A*deltaC/deltaX . in lung, V(dot)O2 = rate of O2 transfer = D*A*(alveolar-venousPO2)/deltaX |
| Why does transmural pressure decrease from smaller to larer airways during expiration? | 1) energy loss to overcome friction. 2) transition from laminar to turbulent flow. 3) decreased radial tethering. 4) lower intra-airway pressure (faster velocity) |
| Determinant of alveolar PO2 & PCO2 | V/Q ratio! |
| COPD | low-grade inflammation (asthma = high). small airways 60% degraded, low IRC, FEV1<1L -> diff. breathing. 20% smokers = susceptible. cough/sputum/dyspnea/infection/wheezing. >10 pack-years. FEV1<80%, FEV1/FVC<70%, cor pulmonale, holes in lung on CT |
| airway resistance | from medium-sized to 7th generation airways (small airways have laminar flow). small airways <25% resistance (in parallel) |
| "pink puffer" | COPD: V/Q ratio still matched b/c capillaries destroyed @ same rate as alveoli |
| "blue bloater" | Chronic Bronchitis. mucous plugging in large airways --> V/Q mismatch. barrel-chest (can't get air out) + flat diaphragm (doesn't work as well) |
| bronchodilator challenge | COPD patients don't improve long-term with bronchodilators, but show short-term symptom relief (due to hyperconstricted bronhchi). helps most during exercise. |
| Pulmonary Function Testing | D(subL) of CO = diffusion capacity to CO. CO taken-up proportional to lost surface area. Deep breath of 0.3% CO, hold in, measure [CO breathed out]. low values = COPD/obstruction/fluid buildup/loss of capillaries/fibrosis/anemia/chronic CO (smoking) |
| Ulcerative Colitis | colon. starts @ rectum, extends up. neutrophils collected in crypt (microabscess), macroulceration, bloody diarrhea. inflammation in mucosa ONLY. |
| Crohn's Disease | can occur in colon/ileum/combination. ulcers through entire wall. Granulomas (instead of neutrophil microabscesses). FISTULAS (holes in GI tract fuse), scarring -> obstruction. eye & arthritis problems, bloody diarrhea. |
| Indeterminate colitis | cannot be distinguished b/tw Ulcerative Cholitis & Crohn's |
| ileum in irritable bowel diseases | impaired intrinsic factor & B12 absorbtion. impaired bile salts & fat-soluble vitamins absorption (D, A, K). no fat absorption b/c no bile -> diarrhea & gall stones. Ca (bound by free FAs) not absorbed. Kidney stones. |
| IBD (irritable bowel disease) susceptibility | Genes: IRGM, ATG1601, immune & LRR domain for bacterial recognition, Nod2 protein, Tol-like R. environment: smoking risk for Crohn's (protective for ulcerative colitis), appendectomy protective for u.c., G.I. flora autophagy & antigen presentation. |
| osmotic vs. secretory diarrhea | Osmotic = e.g. lactase deficiency. Secretory = when intestinal crypt cells move H2O w/Na & Cl. |
| cell turnover in GI crypts | 3-5 days |
| PepT1 | oligopeptides absorbed w/H+ coport. (Na/H pump also in apical membrane). works best w/tripeptides. ~2ndary active Na transport (others use Na coport directly). Chopped up -> single aa's in cell ->basolateral transport. |
| Hartnup Disease | protein deficient, mutation in B-transport system -> tryptophan deficiency import (only as single aa). Cystinuria = kidney stones, no cysteine through s.i. |
| lipase | TAG -> 2-monoglyceride + 2 free FA's |
| phospholipid break down | Lecithin -> Lysolecithin + free FA (PLA2) |
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