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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=(pir^4deltaP)/8viscositylength (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=densitydiametervelocity/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 = -DAdeltaC/deltaX . in lung, V(dot)O2 = rate of O2 transfer = DA(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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UTSW physio block 2

UT Southwestern School of Medicine physiology block 2, 2010

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