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346 Cards in this Set

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hyperventilation
breathing in excess of metabolism resulting in decreased PaCO2
Avogadro's hypothesis
for all gases, an equal number of molecules in the same space and at the same time will exert the same pressure
Dalton's law
pressure exerted by each gas is independent of the pressures of other gases in the mixture
Boyle's Law
P1V1=P2V2
Charles law
if volume is kept constant, pressure is proportional to temperature
Henry's law
the concentration of dissolved gas is equal to the partial pressure of hte gas times the solubility coefficient
PO2 in alveolar vs arterial
alveolar is slightly higher because venous blood from myocardium and bronchial circulation mixes with freshly oxygenated blood as it goes to arteries
Alveolar PO2 and PCO2 differ from atmospheric because...
-effects of dead space,
-functional residual volume,
-continuous O2 utilization and CO2 production
arteral and mixed venous PCO2 values change less than PO2 values because...
differences btw O2 and CO2 dissociation curves
Gas gradients in anemic patient
-respiratory system moreso than Hg determine PO2 and PCO2 (arterial blood gases are normal, mixed venous will differ slightly because each unit carries less O2 and CO2 in bound form, so there are greater pressure changes)
gas gradients at high altitude
-reduction in PO2 at each step,
-non-uniform change of PO2 (mixed venous PO2 changes less bc unloading of O2 at tissues is on the steep part of O2 dissoc curve),
-PCO2 decreases d/t hyperventilation, not bc of reduced atmospheric CO2
gas gradients of patient with alveolar hypoventilation
-PaO2 and PAO2 are decreased by about the same amount PACO2 and PaCO2 are increased
gas gradients in alveolar-capillary gas exchange problem (Farmer's lyng)
-large increase in the difference btw alveolar and arterial PO2, hyperventilation
gas gradients in hypoventilation with abnormal alveolar-capillary exchange
-poor atmospheric to alveolar and alveolar to arterial gas exchange so PO2 and PCO2 is above normal
lung equilibrium position
total collapse (zero volume)
chest wall equilibrium position
60% total lung inflation
respiratory mechanics
relationships between pressure changes within the resp system and resulting changes in airflow and lung volume;
-three important pressures: alveolar, pleural, and transpulmonary
What causes air to flow btw the atmosphere and alveoli
-pressure difference btw alveolar and atmospheric press;
-alveolar press exceeds atmosph during expiration and is less than it during inspiration
what causes alveolar pressure to change during inspiration
alveolar pressure is negative relative to the atmospheric pressure because pleural pressure becomes more negative during inspiration
what causes pleural pressure to change during inspiration?
contraction of the diaphragm and external intercostal muscles--> increases pleural space volume --> reduces pressure
Why during inspiration and expiration does alveolar pressure change less than the change in pleural pressure?
because a portion of the pleural pressure (or energy) is required to overcome the lung elasticity
what causes alveolar and pleural pressures to change during expiration?
-result of lung recoiling toward its equilibrium position;
-when need increases, expiratory muscles contract and add to the positive alveolar pressure generated by the lung recoil
What is the sequence of events that accounts for airflow throughout the respiratory cycle?
inspiratory muscles contract--> expand pleural space--> reduced pleural pressure--> part of pressure chagnes overcomes lung elasticity to expand the alveoli --> reduces alveolar pressure to subatmospheric --> inspiration --> ends when inspiratory muscle activity ceases and lungs recoil (creates alv pressure higher than atmospheric)
What is the relationship btw pleural pressure and lung volume during inspiration?
lung vol increases and pleural pressure decreases
What is the relationship btw pleural pressure and lung volume during expiration?
lung vol decrease and pleural pressure increases
Lung elasticity (aka lung compliance)
-change in vol/change in TP press;
-when airflow is zero (at end of inspiration and expiration) becomes Ppl;
Airflow for any Pa
-determined by airway resistance;
-R=Pa/airflow
What is the relationship between Ptp and lung volume?
-lung volume increases as Ptp increases (as lung vol increases, the tendency to recoil also increases);
-Ptp is always positive reflecting the inward recoil of the lungs
Saline filled lung
-eliminates the effect of surface forces at air-liquid interface;
-allows subdivision of total pressure required to inflate lung into amounts necessary to overcome tissue forces and surface forces;
-takes less of a pressure change to fill lung;
-hysteresis (diff btw inflation and deflation limbs of curve) is virtually eliminated
Surfactant during expiration
surfactant molecules move closer together --> as lung vol decreases, concentration of surfactant molecules increases --> surface tension decreases
What does surfactant prevent during expiration
-surface tension decreases as lung vol decreases;
-prevents small alveoli from emptying into large alveoli which would occur as indicated by Laplace's law
Laplace's Law
P=2T/r
Elastic recoil pressure in emphysema
less than normal
Elastic recoil pressure in pulm fibrosis
greater than normal
What are the elastic characteristics of the chest wall?
-lung equil is 60% full;
-if chest wall is compressed--> attempts to expand;
-if chest wall if forced to TLC, it will attempt to collapse
At the end of normal expiration (FRC), why do the lungs remain partially filled?
-the chest wall is attempting to expand to 60% of VC while the lung is attempting to constrict to zero volume;
-balance results in equil point being at about 40% of VC
What factors determine airway resistance?
-length and diameter of airway plus density of inhaled gas;
-diameter is most important bc it is under phys control and most subject to disease
What is the importance of lung elastic tissue on airway diameter?
-airway resistance decreases dramatically as lung vol increases;
-bc of alveolar elastic tissue action on neighoring airways like a spring and causing them to dilate progressively as lung vol increases
Where is the greatest resistance in the airway?
-greatest in upper airways because TOTAL cross sectional area of airway is least
Structure of airway in order
Trachea--> Bronchi--> Bronchioles--> Resp bronchioles--> alveolar ducts--> alveolar sacs
What is the relationship btw max expiratory flow and lung vol?
-max expiratory flow is highest at TLC and decreases progressively as lung vol decreases;
-as lung vol decreases --> spring-like elastic tissue progressively decreases --> reduced airway diameter--> increased airway resistance--> reduced airflow
Why is flow rate at low lung volumes effort independent?
-contraction of expiratory muscles during forced expir increases intrapleural pressure above atmospheric, alv press is even higher;
-past equal pressure point--> airway compressed and effort doesn't matter
Lung reserve during exercise
-high capacity;
-respiratory reserve is preferred because due to airway compression at low lung volumes, it is costly or inefficient
Three types of work accomplished during inspiration
-compliance work (elastic work);
-tissue resistance work;
-airway resistance work
What changes about inspiration work when diameter of upper airway is reduced by 90%?
-airway resistance work increase; -elastic work of breathing doesn't change
What are 4 examples of inc airway resistance in humans?
- emphysema (decreased tethering of airways by lung elastic tissue;
-bronchitis (reduced airway diameter due to increased mucous and airway inflamm);
-asthma (hyperreative airway smooth muscles causes xs contraction=airway narrowing);
-obstructive sleep apnea (closure/compression of pharyngeal airway due to xs adipose tissue or reduced airway dilator muscle activity
Maintaining a normal alveolar ventilation by using max TV and low freq
-lung vol changes over entire range including volumes of low compliance;
-thus, high elastic work and low flow resistive work
Maintaining a normal alveolar ventilation by using low vol and high flow rate
-repeated ventilation of dead space and high flow rate;
-airway resistive work is high
What is the time constant of an airway?
the rate of alveolar filling when a pressure change is applied
What determines the time constant of airway-alveolar units?
-increased resistance and decreased compliance will increase it, thereby slowing the rate of alveolar filling
What are the consequences of unequal time constants?
-uneven filling (minor when breathing freq is low);
-when breathing freq is high, pendelluft occurs because one is emptying while the other is still filling;
-reduces alveolar-capillary gas exchange
Asthma and measuring lung compliance
-time constants not uniform--> pendelluft;
-dynamic measurements become progressively reduced
Why are the lungs not completely filled during inspiration and completely emptied during expir?
-lungs are in elastic thoracic cavity with equil vol at about 60% of TLC;
-lung attempts to totally collapse, FRC is reached when there is no muscle activity at the end of a normal expiration;
-can only empty lungs to about 20% of TLC = RV
Throughout a resp cycle of inhalation and expiration, CO2 measured in the common chamber will reach a peak...
as expiration is ending (increase lags as dead space is cleared first)
The CO2 concentration in a bag containing all the air exhaled over several breaths will be dependent on:
the volume of the conducting airways
The PCO2 and PO2 measure in the common chamber near end of expiration approximate:
PACO2 and PAO2
Why does the amount of fresh atmospheric air that reaches the alveoli with each inspirate not equal the tidal vol?
Because of the vol of the airways, the first air that reaches the lungs will be the air that has just exited the lungs (dead space volume, VD)
Why do PACO2 (42) and PAO2 differ from atmosph PCO2 (0) and PO2?
-reflect combined effect of dead space, the FRC (don't completely empty lungs every breath), and the continuous alveolar-capillary gas exchange (continually add CO2 and remove O2 from the alveoli)
How do you calculate physiological dead space?
Using Bohr equation: VD= VT x (FACO2-FECO2)/FACO2
What is the diff btw anatomic and physiologic dead space?
-Anatomic= volume of the airways (measured using Bohr equation in healthy individuals);
-Physiological= alveolar plus anatomic dead space
Dog in warm environment increases breathing frequency, PACO2 remains same, what is happening
-NOT hyperventilating, increasing breathing for temp reg achieved only by increasing dead space ventilation; -alveolar ventilation and PACO2 are not changed
Why is pleural press more negative at the top of the chest than at the bottom during normal, upright breathing?
-pleural press gradient is an effect of gravity;
-weight of lungs pulls down and expands the upper lung regions creating a more neg pressure at top
Why is the lung relatively more filled at top of lung at FRC?
-pleural press is more neg at top --> TP press will be greater at top -->higher lung vol than bottom
When inspiring a tidal breath from FRC, more air will go to bottom of lung because?
-lung compliance is higher at bottom
When inspiring a tidal breath from RV, more air will go to top of lung because?
-lung compliance is less at bottom from RV
Closing volume
-low lung volume means most of air contributing is from the top of the lung where there is a lot more N2;
-increases with emphysema due to the greater collapse of airways
Wall thickness in pulmonary vs systemic veins
Less in pulmonary
Compliance in pulmonary vs systemic veins
Greater in pulmonary
Pressure in pulmonary vs systemic veins
Greater in systemic
Blood vol in pulmonary vasculature
About 10%
Affect of pulmonary compliance
High compliance means that when LA pressure increases, vasculature can absorb the difference without changing pressure much
What is the effect of alveolar pressure on blood flow in the lung?
-When alv presure is greater than arterial pressure, no flow
-when systolic arterial pressure rises above alv pressure (but diast is below), intermittent flow
-when arterial pressure remains greater than alv pressure at all times, continuous flow
How does pulmonary vascular resistance change as lung volume changes?
-increasing lung volume cases an enlargement of extraalveolar vessels (arterioles and venules) and a compression of alveolar vessels (capillaries)
In an upright position, how does blood flow change from bottom to top of lung?
-top of lung has a relatively lower perfusion pressure and flow than bottom
-slight downturn at very bottom of lung reflecting + pleural pressure compressing vessels
What explains regional differences in lung perfusion?
-gravity explains some-- why flow is higher at bottom of lung
-but, heterogeniety is seen within each isogravitational plane perhaps from sequential branching of pulmonary vessels
What is the effect of alveolar hypoxia on pulmonary vascular resistance?
-as inspired P02 is decreased, pvr increases
-effect is exaggerated as pH decreases
What occurs to maintain a long pulmonary transit time during conditions of increased flow?
Capillaries expand to increase lung volume; thus each unit of blood will remain in the lung for a longer period of time
What occurs to capillary flow if an alveolus is underventilated causing the PO2 in the alveoli to decrease?
-the blood supply to the capillary decreases diverting blood to a well ventilated alveoli
What factor accounts for difference in the rate at which various gases reach equilibrium between alveoli and capillaries?
-N2O is not bound in blood, so its partial pressure in blood rises rapidly to its partial pressure in alveoli
-CO is taken up by RBCs, so its partial pressure in blood only reaches a fraction of its partial pressure in the alveoli
-O2 is intermediate
What keeps the lungs dry?
-balance of hydrostatic and osmotic forces
-lymphatic pump removing fluid from pulmonary interstitial space
Why does pulmonary edema not occur until LA pressure has increased to about 25 mmHg?
-high compliance of pulm vasculature prevents pressure increases
-lymphatic pump is highly effective until this pressure
Four tubes are arranged at different heights in a water bath-- what is true about the diameter of the tubes?
-diameter depends on tube height
-diameter changes from beginning to end of each tube
Nonuniform time constants of pulmonary airways can lead to....
Frequency dependent lung compliance
Why is it ideal for all alveolar capillary units to receive the same proportion of alveolar ventilation and CO?
-don't want some units overventilated while others are underventilated
-air and blood must get together to exchange
What are PCO2 and PO2 in an alveolus which is ventilated but not perfused?
-no gas exchange is occuring
-will equal atmospheric values
What are PCO2 and PO2 of blood exiting a pulmonary capillary that was not ventilated?
-no gas exchange
-will be same as mixed venous blood-- volume is the venous admixture
How do V/Q ratios differ between alv-capillary units at top and bottom of lung?
-higher at top of lung than at bottom
-bottom (with greatest lung mass) has relatively constant V/Q necessary for ideal gas exchange
How does emphysema result in abnormal V/Q ratios in the lungs?
Loss of lung elasticity--> airways more readily collapse in some parts--> non uniform time constants--> abnormal V/Q
What is a normal physiological shunt
The passage of deoxygenated blood from the venous circulation to the arterial side without picking up any O2
Sources of physiological shunts?
-thesbian circulation perfusing LV
-bronchial circulation emptying into pulm veins
-atelectatic or collapsed alveoli
-congenital defects (septal defects)
A shunt exceeding 50% of CO...
-increasing inspired air can no longer make up the PaO2 whereas without a shunt, increasing inspired O2 quickly raises PaO2
What determines movement of gas btw gas and liquid phases?
Pressure gradients (difference) irrespective of whether it is in gas or liquid phase
What is the partial pressure of O2, CO2, and N2 in a beaker of water at sea level?
-O2=159
-CO2=0.23
-N2=597 mmHg
What gas has the highest solubility in water?
-CO2 has highest, O2 has lowest
What is the pathway of gas diffusion in the lung?
-pulm capillaries are embedded in the space btw adjacent alveoli
O2: water and surfactant in alveoli--> alveolar epith--> epith basement membrane--> interstitial fluid space--> capillary BM → capillary endothelium--> plasma--> RBC membrane
What determines diffusion of gases in the lung?
-the diffusion process (pressure gradient, surface area, gas solubility, diffusion distance, gas MW)
-time required for O2 to react with the Hb
Diffusion process equation
D=(P*A*S)/(D*sqrtMW)
How is diffusing capacity of the lung determined in pulmonary function labs?
-total amount of gas exchange/mean capillary gradient of the gas
-use CO bc high reaciton rate of CO with Hb keep the capillary PCO near zero
-so, DCO= VCO/PACO
Do diffusion limitations affect both PaO2 and PaCO2?
-yes, but PaO2 is affected relatively more because limitations are due primarily to the diffusion process
How does exercise affect lung-diffusing capacity?
-capillary transit time for blood is reduced
-capillaries totally/partially closed at rest are now expanded to increase SA for exchange
-diffusing capacity increases
How does hypoxia affect lung-diffusing capacity?
-the driving pressure for O2 is reduced
-equil btw the alveoli and capillaries requires more than the normal 0.25 sec
How does emphysema affect lung-diffusing capacity?
-coalescence of alveoli → reduced surface area → reduced diffusing capacity
How does pulmonary fibrosis affect lung-diffusing capacity?
Thickened alveolar-capillary membrane → reduced diffusing capacity
-may not be evident at rest, but is evident during exercise when diffusing demand is increased
How does high altitude residence affect lung-diffusing capacity?
-stimulated lung growth in childhood → increased alveolar-capillary SA → increased lung diffusing capacity
How does O2 move from systemic capillaries to the tissues?
-diffuses to cells where it is used by mitoch
-CO2 diffuses in opposite direction
-gases move only in dissolved state (O2 won't go into tissue bound with Hb)
How is O2 carried in blood?
-0.3ml/100ml is dissolved
-19.7ml/100ml is bound to Hb
What is the difference btw blood gas partial pressure and blood gas contents?
-Pressure reflects KE of the dissolved gas and it is the component of the gas that is freely diffusable
-Content reflects total amount of gas in the blood
Factors that decrease Hb's affinity for O2
-inc PCO2, H+, temp, 2,3DPG
What is the effect of anemia and CO poisoning on O2 delivery
-total blood O2 is reduced → PO2 in capillary blood must decrease more than normal to deliver the same amount of O2
-result of less O2 and less of a gradient for diffusion
CO affects O2 delivery to tissue how?
-CO attaches to O2 binding site, meaning decreased total O2 in blood
-CO binding to Hb causes the oxygen to be bound more tightly
What are the major factors that affect the decrease in PO2 as blood transverses the systemic capillaries?
-metabolic rate of the tissue
-arterial O2 content
-Hb affinity for O2
-rate of capillary blood flow
How is CO2 carried in the blood?
-~70% in HCO3- form
-25% bound to Hb
-5% dissolved form
What is the Haldane effect?
-opposite of Bohr effect
-Hb can carry more CO2 during hypoxia
What is the importance of erythrocyte carbonic anhydrase to CO2 transport?
-increases rate of hydration of CO2
-without it, less CO2 is carried from tissue to lung in HCO3- form, thus venous PCO2 and dissolved CO2 will increase more than normal
What is the chloride shift in blood?
-the movement of HCO3- out of RBCs in exchange for Cl- from the plasma
-keeps HCO3- in RBCs relatively low so that carbonic anhydrase rxn can continue to occur
Why does the arterial-mixed venous O2 content difference exceed the CO2 content difference?
-if only carbs were used for energy, there would be no difference in arterial-mixed venous CO2 and O2
-when only fat is used, less CO2 is liberated than O2 is utilized
Why does arterial-mixed venous PO2 difference approximate 60mmHg while PCO2 difference approximates only 5mmHg?
-the difference in the characteristic of the O2 and CO2 dissociation curve in physiological range
How can one increase O2 delivery to cells in a normal individual?
-increasing blood flow and Hb concentration are the most efficient ways
Patient with COPD, why does PaO2 decrease nearly 40% but O2 content decrease only 12%?
-oxygen's relatively flat dissociation curve means that you can tolerate lung disease without a large decrease in tissue oxygen
Patient with headache, disorientation, normal PaO2, PaCO2, arterial pH, and Hb, but very low arterial O2 content, what is his diagnosis?
Carbon monoxide poisoning
Patient with fatigue, low work tolerance, normal PaO2, low O2 content, low Hb
-anemic
-giving inspired O2 won't help bc PaO2 is normal, will only add to dissolved O2 which is not major
When can a hyperventilated lung compensate for a hypoventilated lung?
-CAN to maintain a normal PaCO2
-CANNOT to maintain a normal PaO2
What areas of the brain are involved in the control of breathing?
-mainly pons and medulla
-cerebellar, hypothalamic and other supra-pontine structures have a role
Lesion rostral to pons
normal breathing
Lesion through rostral pons
-breathing slowed
Lesion at pontomedullary junction
erractic breathing
lesion at medulla/spinal cord
stopped breathing
Minimal substrate needed for breathing:
Medulla (but also need pons to have regular breathing)
Respiratory neurons
-any neuron active in some phase of respiration cycle
-each fires in one of 3 phases: inspiration, late inspiration, expiration
Pre Botz C
-site critical for respiratory rhythm generation
ventral resp group (VRG)
-includes nucleus ambiguous and retroambiguous
-sites of pump muscles and airway muscle premotor neurons
Respiratory pattern generation areas
-PB (parabracheal) nucleus
-KF (Kolliker-Fuse) nucleus
Nucleus Tractus Solitarius (NTS)
-first order chemoreceptor and proprioceptor sensory neurons
RTN
chemoreceptor and integration site
What is the difference between resp rhythm generation and resp pattern generation?
-rhythm generator activates pattern generator which activates appropriate order of breathing muscles sequentially
Where is the site of resp rhytmogenesis?
-Pre Botz C
-also a generator rostral to pre-Botz in parafacial area
Network model of resp rhythmogenesis
-via reciprocal inhibition, a network of neurons may underlie resp rhythmogenesis
Pacemaker model of resp rhythmogenesis
-pacemaker neurons in preBotzC spontaneously depolarize to initiate the cycle
Result of vagotomy on breathing
-prolonged inspiration
Creation of eupneic breathing pattern
-vagus, pons, parafacial and preBotz network interact
Medullary neurons role
-contribute to multiple physiological behaviors
-ie breathing and vomiting
Resp chemoreceptors
-alter breathing
-discharge rate is altered by changes in PO2 or PCO2 in their environment
Carotid Body
-major site of O2 and CO2 chemoreceptors
-innervated by sensory fibers from petrosal gang and sup cervical gang
-chemoreceptor cells with synaptic vesicles and sustentacular cells
Carotid body sensitivity
-as PaO2 increases, impulse freq decresases
-as PaCO2 increases, impulse freq increases
-greater relative sensitivity to hypoxia
Roles in control of breathing of the carotid body
-major site of O2 chemoreceptors
-site of CO2 chmoreception
-stabilize breathing to minimize breath-breath variations in PCO2 and PO2
-tonic excitatory input to medullary neurons
-high altitude ventilatory acclimization
Relationship between medullary ECF H+ and respiration
-as H+ increases, firing of phrenic nerve increases
3 major excitatory inputs into resp control neurons
-carotid chemoreceptors
-wakefulness
-ventrolateral medullary neurons (CO2/H+ chemoreceptors)
Attenuation of all 3 main excitatory inputs into resp control neurons
-rhythm generator is non functional
-sustained apnea
Why do PETCO2 and PETO2 increase when breathing a CO2 enriched mixture
-PETCO2 increased because inspired CO2 increased
PETO2 increased because breathing increased
Why does breathing rate increase during CO2 breathing?
-activation of carotid and intracranial chemoreceptors stimulate increased breathing
How would you characterize the subjects H+ status during CO2 breathing?
Acute resp acidosis (will decrease .01 for each mmHg PCO2 goes up)
What are the similarities between COPD and CO2 breathing?
Only hypercapnia
What are the effects on breathing and plasma H+ of chronic alveolar hyPOventilation?
-kidneys would generate increased HCO3- to restore plasma H+ near normal in spite of hypercapnia
-CO2-H+ chemoreceptors become less sensitive to the hypercapnia and any residual acidosis
Why did PETCO2 and PETO2 decrease when breathing a hypoxic gas mixture?
-PETO2 decreased bc inspired O2 was reduced
-PETCO2 decreased bc of increased breathing--> hyperventilation
How would you characterize the subject's H+ status during hypoxia?
acute respiratory alkalosis
Four phases to the changes in breathing during prolonged hypoxia
-initial hypernea causes activation of carotid O2 chemoreceptors
-return of breathing near normal bc attenuated CO2-H+ stimulation and by hypoxic brain depression
-second increase in breathing bc inc sensitivity to hypoxia of carotid
-return to normal breathing by attenuation of carotid chemoreceptor sensitivity
What is hypoxic brain depression?
-direct depressant effect of hypoxia on the excitability of neurons
-use less O2= survive longer
SIDS postulated causes
-low CO2-H+ chemoreceptor sensitivity
-low carotid O2 sensitivity
-hypoxic brain depression
-failure of sleep arousal mech's
-airway obstruction
-airway receptor inhibition of breathing
-reduced density of excitatory serotonin receptors in medullary resp neurons
Congenital Central Alveolar Hypoventilation (CCAH)
-absent CO2-H+ chemoreceptor sensitivity
-absent carotid hypoxic chemoreceptor sensitivity
-central sleep apnea
-normal exercise hyperpnea
-normal airway reflexes and resp mech's
-treated by diaphragm pacing or mechanical ventilation during sleep
During inhalation of 7% CO2, what is the primary stimulus for hypernea?
-intracranial chemoreceptors
Chronic hypercapnia...
-characteristic of emphysema pts
-partially compensated respiratory acidosis
-results in attenuation of ventilatory sensitivity to CO2
-can be caused by a chronic increase in airway resistance
Sleep-wake cycle in humans
-90 min period
-4 stages of NREM, REM, arousal
How does breathing change during REM sleep?
-irregular in timing and amplitude of ventilatory movements
-can has paradoxical respiration (rib cage moves in while abdomen moves out)
Overall ventilation during sleep
-greatest during awake state
-lowest during NREM stage 4
-in btw during REM
What is central apnea?
-cessation of airflow and all respiratory muscle activity
-probably from a failure of resp rhythm generating mechanisms
What is obstructive sleep apnea?
-cessation of airflow in spite of sustained activity of resp pump muscles
-airway must be obstructed
Where is airway obstruction in obstructive apnea
-retropataltal and at base of tongue (retroglossal)
Why does airway obstruction occur in obstructive apnea?
-loss of rhythmic and tonic genioglossus muscle activity
-near abolition of tidal vol during phasic eye movements of REM
What occurs during OSA?
-upper airways collapse during sleep d/t anatomical and neural mechanisms including unstable sleep states and loss of airway protective reflexes
What does OSA result in?
-fractionated sleep, hypoxemia, increased symp nerve activity, acute and chronic arterial HTN, daytime somnolence, psychiatric disorders
How is OSA treated?
-positive pressure breathing
-oral mechanical devices
-surgery to remove portion of tongue/oral pharynx
-tracheotomy
What causes of Cheyne-Stokes respiration?
-increased gain of carotid chemoreceptors resulting in overcorrection of small fluctuations
What is Cheyne-Stokes respiration?
-periods of hyperpnea alternate with periods of apnea
-waxes and wanes smoothly
-hyperpnea phase is usually longer
Filtration defenses
-filtering in the vaso-oropharynx and conducting airways
-sneezing
-coughing
-mucociliary clearance
Host-defense functions in the alveoli
-surfactant
-other opsonins like IGs
-innate immune cells (mac's and neutrophils)
Surfactant
-complex of lipids and proteins (10%)
-SP-B and C reduce surface tension
-SP-A and D immune function
SP-A and D
-surfact proteins with immune function
-aggregate bact, alter mac function and enhance bact clearance
-bind to bact and virus
-don't cause inflamm repsonse that could damage the thin, delicate gas exchange epith
Epipharyngeal aspiration reflex
-sniffing to dislodge substance lodged in throat
-brief, strong inspiratory efforts
Laryngeal apnea reflex
-response to injection of water into larynx
-apnea is a prolonged expiratory period
What is a mech that contributes to terminating inspiration?
-slow adapting receptors that respond to increases in tracheal pressure (lung inflation)
-rapid adapting receptors are for coughing
Hering-Beuer deflation reflex
-expiratory duration is markedly shortened by lung deflation
Why does the signal for hyperpnea during exercise have to have both a fast and slow component?
-initial rapid increase in VA at onset of exercise within seconds
-slower increase to a steady state
Exercise and homeostasis of blood gases
-homeostasis occurs until about 60% of max exercise
-thus, signal for hyperpnea cannot be from increased stim of carotid and intracranial chemoreceptors
Is hyperpnea critically dependent on central command?
-NO
-ventilatory response does not differ btw voluntary and electrically-induced exercise
Is hyperpnea critically dependent on spinal afferents?
-NO
-ventilatory response to electrically-induced exercise is the same in normal and paraplegic subjects
Humoral elements of exercise hyperpnea
-Carotid chemoreceptors (oscillations in blood gases, transient hypercapnia, hyperkalemia)
-pulmonary (CO2 sensor, blood flow)
-cardiodynamic
Neural elements of exercise hyperpnea
-Brain (central command, short-term potentiation, memory)
-Spinal Afferents (muscle spinds and golgi tendon organs, muscle chemoreceptors, group III and IV afferents)
Why is it essential to maintain H+ within a narrow range in living organisms?
-H+ affects protein and enzyme function
-ie deficit in H+ can incrases excitability of neurons and cause seizures
What is meant by physical-chemical H+ buffering?
-the capability of compounds in a solution to minimize the change in H+ when strong acid or base is added
What are the primary H+ buffers in the difference fluid compartments of the body?
-ECF: HCO3, H2PO4, proteins
-ICF: minimal HCO3, other 2 prevalent
How can you distinguish a respiratory from a metabolic acidosis?
-Metabolic: low HCO3, resp conpensation causes low PCO2

-Respiratory: high PCO2, renal compensation causes high HCO3-
What is the isohydric principle?
-alter level of all buffer pairs when H+ is altered
What are the determinants of the H+ buffering capacity of a buffer pair within a solution?
-concentration or amt of bufffer pair
-the pK of the buffer pair relative to the pH of the solution (want them close)
How is plasma H+ regulated by transmembrane exchange?
-ICF has a high conc of physical-chemical buffers
-ie during resp acidosis, you can move H+ into cells in exchange for Na+ or K+
How is plasma H+ regulated by pulmonary ventilation?
-quick way to compensate for acidosis, but limited by amount of bicarb available
-can convert acid --> H2CO3 --> CO2 which can be blown off
What is the role of the BBB in regulation of brain H+?
-restricts the movement of charged paricles like H+ into brain
-during systemic acidosis and alkalosis, CSF changes only 10% of the change in the blood
What are the roles of NH3 and lactic acid production in the brain for regulating H+?
-BBB can't buffer resp acidosis and alkalosis
-glial cells in brain increase production of NH3 and lactic acid
Acid infusion: what happens over time?
-initial 30 min: over 40% acid is buffered by HCO3 in plasma and interst fluid with resp system
-few hours: over 50% acid is buffered by exchange of H+ in ICF
-renal mechanisms slowly correct respiratory and transmembrane exchange over several days
Anion gap
-Normal: 12 mM/L
-metabolic acidosis: increased anion gap (bc decreased HCO3- and inc lactate to maintain neutrality)
Principles of GI motility
-functions as a syncytium
-smooth muscle arranged longitudinally
-electrically connected via gap junctions to allow ionic flow
Membrane potentials in smooth muscle are stimulated by...
-stretch
-Ach
-parasympathetics
What generates the BER of the gut?
-interstitial calles of Cajal
Slow waves of GI smooth muscle
-generated by interstitial cells of Cajal in muscularis externa, connected via gap jx
-not APs, don't cause contraction but do control rate of gen of spike potentials
-rate differs, fastest in duod slowest in stomach
Spike potentials of GI smooth muscle
-occur automatically on top of slow waves at RMP >-40 mV
-due to influx of Ca2+ (some Na+) means slower depolar
-influx of Ca2+ impacts contractile force
Factors controlling RMP
-depolarizing stimuli (stretch, Ach, PNS, gastrin, motilin)
-hyperpolarizing stimuli (NE, Epi, SNS, secretin, CCK)
Enteric NS
-Meissner's submucosal and Auerbach's myenteric plexuses
-integrate motor/secretory activities
-can continue wo/ SNS-PNS input
Auerbach's myenteric plexus
-controls motor activity in gut
-lies btw muscle layers
-increases tonic contractions, intensity and rate of rhythmic contractions, conduction velocity
-some inhibitory neurons inhibit sphincter tone
Meissner's submucosal plexus
-receives sensory signals from epith
-integrated to control LOCAL secretion, absorption, contraction
GI smooth muscle relaxation via inhibitory substances:
-VIP increases cAMP
-NO inreases cGMP
-symp stim causes hyperpolarization
Cranial division of PSN innerv of GI
-vagus nerves
-to esophagus, stomach, pancreas
-less to small and large intest
Sacral division of PSN innerve of GI
-2nd, 3rd, 4th sacral segments of cord
-through pelvic nerves to distal large intest
-to sigmoidal, rectal, anal regions (defecation reflexes)
Postganglionic neurons in PNS innerv of GI
-myenteric and submucosal plexuses
-increases activity of entire ENS
-increases activit of most GI functions
Sympathetic innerv of GI
-originates btw T5-L2
-pregang fibers enter symp chain to postpang neurons in celiac, mesenteric ganglia
-fiber term on ENS neurons
-inhibit smooth muscle
Afferent sensory nerve fibers entirely within ENS
-stimulated by mucosal irritation, gut distention, chemical presences
-cause be inhibitory or excitatory
Afferent sensory nerve fibers exiting ENS
-cell bodies in ENS, axons termintate in prevertebral symp ganglia (celiac, mesenteric, hypogastric)
-cell bodies in dorsal root ganglia of cord or CN nuclei
-transmit signals to cord or medulla, send impulses back via vagus
GI reflexes within ENS
-secretion, peristalsis, mixing contractions, local inhibition
GI reflexes from gut to prevertebral symp ganglia and back to GI tract
-gastrocolic reflex (empty colon when stomach fills)
-enterogastric (stomach motility inhibited when intest fill)
-colonileal (inhibit ileal motility when colon fills)
GI reflexes from gut to cord/brainstem and back to GI tract
-from stomach/duod to brain and back (vagus) to control gastric motility/secretion
-pain reflexes
-defecation reflexes
Vagovagal intest reflex
-stretch info --> brainstem --> vagal efferents to (ie) parietal and G cells in stomach
CCK and gastric motility
-secreted by I cells in mucosa of duod/jejunum in presence of fat
-increase GB motility to release bile
-inhibit stomach motility so bile can work
Secretin and gastric motility
-secreted by S cells of duod mucosa with acidic gastric contents entering via pylorrus
-general mild inhibitor of GI motility
GIP and gastric motility
-secreted by mucosa of upper SI in response to fatty acids, AAs, CHO
-decreases stomach motility, slows emptying into SI
Peristalsis
-forward movement of contractile ring
-stim is distension of wall via ENS
-intact, active myenteric plexus is required
Mixing movements of GI tract
-heterogenous within GI tract
-can be peristaltic movements against a closed sphincter
-local, intermittent constrictive contractions
Splanchnic circulation
-flow through gut, spleen, pancreas, liver
-drains to portal vien--> sinusoids--> hepatic vein --> IVC
Vasoconstrictors of splanchnic circulation
-angII, endothelin, NE (alpha-2 agonists), PGF2a, vasopressin
vasodilators of splanchnic circulation
-Ach, adenosine, bradykinin, CGRP, histamine, NO, VIP, beta2 agonists
Postprandial hyperemia
-blood flow increases in response to a meal
-release of dilators during digestion (CCK, VIP, gastrin, secretin)
-GI glands secrete kinins
-decreased O2 means increased adenosine
Pharyngeal stage of food ingestion
-entrance of bolus= epith swallowing reflex --> impulse to brainstem --> soft palate raises to close post nares, palatopharyngeal tonsils pulled medially to make slit, epiglottis covers larynx, UES relaxes, pharynx contracts
-respiration interrupted
Esophageal peristalsis
-skel muscle upper 1/3 (CN XII)
-intest smooth m lower 2/3
-primary= continue wave started in pharynx
-secondary= if nec; via myenteric plexus
Receptive relaxation of stomach
-relaxes before receiving food
-via myenteric inhib neurons preceding peristaltic wave
gastroesophageal (LE) sphincter
-normally tonically constricted
-receptively relaxed by peristaltic wave font
-prevents reflux of stomach contents
Achalasia
-stenosis of LES
-dilation of body of esophagus
Hiatal hernia
-LES protrudes into thoracic cavity
-LES tends to be patent due to negative pressure in thoracic cavity
Vagovagal reflex in stomach
Food enters --> reflex from stomach to brainstem and back --> reduce wall tone in fundus and body --> bulging outward --> keeps pressure in stomach low
Emptying of stomach
-promoted by intense peris waves in antrum initiated by stretch via myenteric plexus and vagovagal reflexes
-most are weak, just to mix
Pyloric sphincter
-much thicker than stomach antrum
-tonically constricted
-allows fluid to move with relative ease (food must be chyme or retropulsion will occur)
Factors promoting stomach emptying
-food volume (not pressure)
-stretching--> myenteric reflex increases pyloric pump, inhibit sphincter
-gastrin secretion
-increased acid secretion
Factors inhibiting stomach emptying
-DENR prevents overfilling
-extrinsic nerves to prevert symp nerves to stomach
-vagal nerves to brainstem to inhibit vagal tone to stomach, inhibit pyloric pump, increase sphincter tone
Factors activating DENR-enterogastic reflexes
-duodenal distension, irritation of duod mucosa, duod chyme acidity, duod chyme osmolarity
-presence of breakdown products from proteins/fats
Hormonal factors inhibiting emptying of stomach
-hormonal feedback from duod
-fats--> CCK release from duod/jej
-acid--> secretin release
-hypertonicity--> enterogastrone

travel via blood stream to stomach to inhibit pyloric pump and increase sphincter tone
Propulsive contractions of SI
-chyme propelled by weak peristaltic waves
-net chyme movement= 1cm/min (~4 hours pylorus to ileocecal)
Neural/hormonal increase in SI motility
-gastrin, CCK, insulin, serotinin (OPPOSITE OF STOMACH)
Neural.hormonal inhibition of SI motility
-secretin, glucagon, GIP, VIP
Cecum reflexes
-distension: increases tone, inhibits ileal peristalsis
-irritation= appendicitis
-mediated by myenteric plexus and ANS (via prevert symp gang)
-opens after a meal via gastroileal reflex
Mixing movements in colon
-haustrations
-constrictive rings, obstructs lumen, followed by contraction of long muscle (tenaie coli)
-rolls and digs into feces for better absorption
Defecation
-rectum usually empty
-internal anal sphincter= circular smooth muscle, autonomic control
-external= striated vol muscle, conscious control via pudendal nerve
Single cell mucous glands (goblet cells)
-respond to mechanical stimulation
-extrudes mucous onto the epith surface to act as a lubricant
Crypts of Liberkuhn
-pits in the surface of GI tract
-invaginations of epithelium
-specialized secretory cells fluid secretion
Tubular glands
-stomach/ upper duod
ie oxyntic glands
Complex glands
-salivary, pancreatic, hepatic
-outside walls of GI tract
-digestion/emulsification of food
Secretory mech by glandular cells
-delivery of substrate for formation of secretion
-formation of ATP from mitoch
-secretory materials transferred ER to golgi vesicles
-materials modified in golgi discharged into vesicles
-stored until neural/hormonal stimuli causes extrusion (inc Ca2+)
Sympathetic stim of GI glands
-increase secretion from some local glands but also vasoconstricts = dual effect
Secretion of saliva
-large quantities of K+ and HCO3-
-acini: primarily secrete NaCl
-Ducts: Na+ reab> K+secretion causes electroneg, Cl-reabsorption; HCO3- ion secreted
Regulation of saliva secretion
-nervous: mostly PNS--> dilator --> release of kallikrien --> splits blood proteins to form bradykinin
Esophageal secretion
-body is lined with simple mucous glands
-each end also has complex mucus glands
-lubrication and protection
gastric secretion
-mucus secreting cells in entire lining
-tubular glands= oxyntic/gastric glands (prox 80%, HCl, pepsinogen, IF, mucus) and pyloric glands (distal 20%, mucus, some pepsinogen and gastrin)
Pepsinogen secretion from oxyntic glands occurs in response to:
-stim of peptic cells by Ach from vagus or gastric ENS
-stim in response to stomach stretch
Three cell types secreted by oxyntic glands
-Mucus neck cells= mucus and pepsinogen
-peptic (Chief) cells= secrete pepsinogen
-parietal (oxyntic) cells= secrete HCl and IF; contain large branching canaliculi where HCl forms
Secretion/activation of Pepsinogen
-Peptic/chief cells
-not active until contact with HCl or esp pepsin+HCl
-Pepsin active pH 1.8-3.5, breaks up collagen
Intrinsic factor
-from parietal cells in oxyntic glands
-vital for vit b12 absorption in ileum to prevent pernicious anemia (failure of maturation of RBCs)
Surface mucus cells
-entire surface of stomach, secrete large quantities of highly viscous, insoluble mucus for protecting stomach lining
-very alkaline
Pyloric glands
-mostly mucus cells
-secrete a little pepsinogen and gastrin
Histamine and gastrin and gastric secretion
-activate acid secretion by parietal glands
ACh and gastric secretion
-activates all types of secretions in gastric glands
-pepsinogen (peptic cells), HCl (parietal cells), Mucus (mucus cells)
Stim of parietal cells
-enterochromaffin cells--> secrete histamine--> increase HCl secretion
-gastrin from antrum of stomach mucosa in response to meat
-Ach from vagus nerve endings
stim of HCl secretion by gastrin
-gastrin produced by G cells in pyloric glands of distal stomach (G-34 and G-17 forms)
-PNS stim: GRP, inhib: ACh
-gastrin contacts chromaffin cells in stomach body --> release histamine directly into deep gastric glands--> HCl secretion
Increased acidity and gastrin secretion
-inc acidity blocks secretion from gastrin cells secondary to release of somatostatin from D cells
-causes inhib nervous reflexes that inhibit gastric secretion through inhibition of GRP release
Paradox of gastric secretion
-intest chyme stimulates gastric secretion= intest phase of secretion
-intest chyme inhibits gastric secretion= gastric phase of secretion (inhibit stomach secretion and prevent overload)
3 phases of gastric secretion
1) Cephalic phase via vagus (30%)
2) Gastric phase via local nervous secretory reflexes, vagal reflexes, gastrin stim (60%)
3) Intestinal phase via nervous and hormonal mech's (10%)
pancreatic secretion
-large, compound gland
-enzymes secreted by acini
-NaHCO3 secreted by ducts
-pancreas-->pancreatic duct-->hepatic duct-->papilla of Vater (sphincter of Oddi)-->duodenum
-in response to chyme in duod
Pancreatic secretion of HCO3-
-CO2 diffuses to cell from blood-->carbonic acid-->HCO3- --> transported with Na+ into duct lumen, causes influx of water
-neutralizes HCl
Pancreatic amylase
-CHO digestive
-hydrolyzes starch, glycogen, etc to form di and tri saccharides
Lipid digestion
-pancreatic lipase (neutral fats--> FAs and MGs)
-cholesterol esterase (hydrolyzes cholest)
-phospholipase (splits FAs from phosphlipids)
Proteolytic enzymes
-trypsin/chymotrypsin (cleave proteins to smaller)
-carboxypolypeptidase (cleave polypeptides into AAs)
-secreted as zymogens
Activation of proteolytic enzymes
-Intestinal mucosa secrete enterokinase when chyme is present --> activates trypsin --> activates all others
-delay protects pancreas from autodigestion
-acini cells also secrete trypsin inhibitor to further protect pancreas
Stimuli of pancreatic secretion
-ACh (stim acini, not ducts, enzyme production)
-CCK (from duod/jej mucosa in response to fats/proteins, stim acini, enzyme prod)
-Secretin (from duod/jej mucosa in response to highly acidic food, stim DUCTS, bicard fluid production, no enzymes)
CCK and pancreatic secretion
-released by I cells (duod/jej mucosa) in response to poteases and peptones and FAs, some HCl
-moves in blood to pancreas--> causes secretion of digestive enzymes from acinar cells
-strong response, 75% of total panc enzyme secretion
Regulation of cephalic phase of pancreatic secretion
-same signals as stomach
-cause ACh release by vagus
-causes moderate amounts of enzymes to be secreted by acini into ducts
-no fluid
Gastric phase of pancreatic secretion
-continuance of cephalic phase
-still little flow
Intestinal phase of pancreatic secretion
-chyme enter duod--> secretin and CCK release
-copious release of pancreatic secretions
Bile flow
hepatocytes --> bile canaliculi --> interlobular septa --> terminal bile ducts --> hepatic duct --> common bile duct --> duod or cystic duct/GB
Storage/concentration of bile
-stores ~50ml in GB until needed by duod
-Na+ primary active transport through GB mucosa--> water follows --> very concentrated
Composition of bile
-50% bile acids (chenodeoxcholic, deoxycholic, lithocholic)
-phospholipids (lecithin) solubilized by bile salts
-cholesteral
-bile pigments (bilirubin glucuronide)
Bile acids
-product of cholesterol + 7a-hydroxylase
-form micelles
-conjugated to taurine or glycine, pK goes down and allows them to be soluble in the intestine
Emptying of GB
-digestion of food in upper GI and presence of fatty food causing release of CCK begins emptying
-CCK=potent stimulus for contractions/relaxation of sphincter of oddi
-ACh=less potent stim
Function of bile salts
-detergent action on fats (emulsification)
-absorption of FAs, MGs, cholest, other lipids
Enterohepatic circulation
-bile salts reabsorbed into blood from SI
-enter portal circulation and return to liver where salts are recycled
-6% lost in feces
role of secretin in bile secretion
-strong stim of bile secr after a meal
-causes mostly a secretion of the weak NaHCO3
-aid in acid neutralization and optimal functioning of pancreatic enzymes
Formation of gall stones
-cholesterol precipitates
-chronic high fat diet
-inflamm of GB epithelium
Secretion of SI
-mucus via Brunner's glands in duod
-mostly btw pylorus and papilla of vater
-large amount of alkaline mucus when irritated, vagal stim, GI tract hormone esp secretin
-protect duod
-strongly inhibited by symp stim (makes duod vulnerable to ulcers)
Crypts of Lieberkuhn in SI
-small pits btw intestinal villi
-epith of goblet cells producing mucus and enterocytes secreting water and electrolytes
-secretions rapidly reabsorbed by villi- circulation assists absorption from substances in chyme
Enzyme secretion of SI
-most in brush border of mucosal enterocytes
-peptidase, sucrase/maltase/lactase, intestinal lipase
Mucus secretion in LI
-many crypts of Lieberkuhn
-no enzyme presence in epith cells
-no villi
-many goblet cells
-mucus with moderate HCO3-
Diarrhea
-LI irritated as in fection of mucosa
-secrete lots of water and electrolytes
Basic process of digestion
-HYDROLYSIS
Digestion of carbs in mouth/stomach
-chewing= mixed with alpha-amylase form parotid glands
digestion of carbs in SI
-pancreatic amylase much more powerful than salivary
-lactase, sucrase, maltase, a-dextrinase from enterocytes lining microvilli of SI (brush border)
Digestion of proteins in stomach
-Pepsin active in acidic environ via parietal cell HCl secretion, can digest collagen
-pepsin initiate digestion to produce proteoses, peptones, polypeptides
digestion of proteins by pancreatic secretions
-trypsin and chymotrypsin to smaller polypeptides
-carboxypolypeptidase to AAs
-elastase digests elastin fibers holding meat together
digestion of proteins by peptidases
-by enterocytes of duod/jej villi (brush border)
-split proteins to make them easily transported to enterocyte interior
digestion of fats
-pancreatic lipase
-Si contains enteric lipase
-a little from lingual lipase
-TG split into FFA and 2-MGs
digestion of cholesteral esters
(cholest and FA)
hydrolyzed by cholesterol ester hydrolase
digestion of phospholipids
hydrolyzed by phospholipase A2
GI absorption in SI
-total surface area= tennis court
-central lacteal for lymph absorption
-pinocytic vesicles
-continual movement by actin filaments
-absorption via active transport, diffusion, solvent drag
normal daily absorption in SI
-300g CHO
-100g fat
-75g AAs
-75g ion
-8L water
Active transport of sodium in SI
-20-30g secreted each day, must absorb at least 25g to prevent net loss in feces
-rapidly absorbed through intestinal mucosa, vital for sugar and AA absorption
Effects of aldosterone on Na+ absorption
-dehydration--> aldo secreted from adrenal gland
-increases all transport of Na+ by intest epith
-secondary increase in Cl- and H2O absorption
-especially powerful in large intest
Absorption of Ci- in duod/jej
-very rapid
-diffusion as a result of electronegativity in chyme/ electropositivity in paracellular space from Na+ reabsorption
Absorption of bicard ions in duod/jej
-must be reabsorbed d/t large secretions from pancrease and bile
-absorbed indirectly
-with Na+ reab, some H+ secretion, combines with HCO3- to form carbonic acid--> H2O and CO2--> blown off by lungs
Secretion of HCO3-/absorption of Cl- in ileum and LI
-epith cells here secrete HCO3- in exchange for Cl- absorption
-provides alkaline for neutralization of acids produced by LI bacteria
Ca2+ absorption
-actively absorbed in duod, tightly regulated by need
-PTH via activation of vit D --> enhances absorption
Fe2+ and monovalent ion absorption
-actively absorbed
-in proportion to body's need
general absorption of carbs
-actively absorbed mostly as monosacc's (80% glucose), some disacc's
-remaining 20% as galactose (milk), fructose (cane sugar)
Glucose absorption
-co-transport with Na+ (needs Na+ to be absorbed)
-AT of Na+ through basolateral membrane into paracellular space, depleting intracell. Na+ --> glu cotransported with Na+ into cell via facilitated diffusion --> diffuses out of cell into interstitium and capillaries
absorption of monosacc's
-galactose transported like glucose
-fructose transported by facilitated diffusion across epith INDEP. of Na+ (slower, eventually converted to glucose)
Absorption of proteins
-through luminal membrane of intestinal epith as di- tri-peptides and free AAs
-energy via Na+ cotransport (like glucose)
-some AAs use special membrane transport proteins like fructose
absorption of fats
fats--> MGs and FFAs--> micelles --> soluble in chyme --> go to surface of brush border --> diffuse into cell interior --> taken up by smooth ER --> form new TGs --> transported in lymph chylomicrons to thoracic duct to enter circ duct
Direct absorption of fatty acid into portal blood
-some short/med FAs can be absorbed directly into portal blood
-bc of increased water solubility
absorption in LI
-formation of feces
-90% of water and electrolytes in chyme are reabsorbed in colon
-mostly proximal
-distal=storage
Absorption/secretion of electrolytes and water in LI
-AT of Na, causes Cl absorption
-tight jx prevent back diffusion
-mucus secretes HCO3- while absorbing Cl- for acid neutralization
-osmotic gradient created for absorption of H2O
Bacterial action in colon
-colon bacilli are constantly present
-can digest small amts of cellulose
-form vit K, B12, thiamin, riboflavin, some gases
-vit K necessary for vitK-dep coagulation factors
Composition of feces
-75% water, 25% solid (dead bact, fat, organic matter, protein, undigested roughage, etc)
-stercboilin and urobilin cause color
-odor: indole, skatole, mercaptans, hydrogen sulfide
disorders of swallowing reflexes
-damage to CN 5, 9, 10
-stroke, polio, encephalitis, MD, myast gravis, botulism, deep anesthesia, heavy drinking
-can't swallow, glottis doesn't close, soft palate doesn't clsoe nares, vomit enters airway
Achalasia and megaesophagus
-damage to myenteric plexus of lower esoph--> loss of receptive relaxation
-irritation: hypertrophy and infection
GIRD
-caused by inc intragastric pressure, pregnancy, overweight, loss of LES tone, hiatal hernia
-treated with antacids, H2 receptor blockers, H+-ATPase inhibitors
Peptic ulcer
-imbalance btw secretions of enzymes and mucus in stomach and alkaline secretion by Brunner's glands in duod/ HCO3- secretions by pancreas and bile duct
Helicobacter pylori infection
-main cause of gastritis, gastric atrophy, pernicious anemai, peptic ulcers
-treat with antibiotics, H2 receptor blockers, antacids, H+-ATPase inhibitors
Gastric and duod ulcers from H. pylori
-weakened mucus barrier, inc acid, dec bicarb
-drinking, smoking, and NSAIDS can contribute
-gastric carcinomas secrete gastrin- xs acid
-treat with triple therapy (2 antibiotics, 1 antacid/bismuth) or vagotomy
dumping syndrome
-uncontrolled gastric emptying due to lack of feedback inhibition by duod
-undigested food makes it to the colon
-barely makes it to the bathroom
pyloric stenosis
-projectile vomiting
-peds: FTT, wall's sign of projectile vomiting after breast feeding, from atresia/improper formation of duod
Cholestasis
-absence of bile flow
-from failure to secrete bile acids and salts or obstruction of biliary tree
-signs: jaundice from bilirubin backup in plasma (indirect=unconj, direct=conj)
Lack of pancreatic secretions
-loss of trypsin, chymotrypsin, carboxypeptidase, amylase, pancreatic lipas
-can't reabsorb 60% of the fat, 1/3-1/2 proteins and carbs
-wasting, large amts of fatty feces
Pancreatitis
-inflammation
-xs alcohol, blockage of duct with gall stone
-enzymes in pancreas too long, digest pancreas and cause lack of pancreatic secretions in SI
Sprue
-malabsorption by mucosa
-damage to intestinal enterocytes or microvilli
-gluten intolerance
Steatorrhea
-loss of fat reabsorption
-impaired absoprtion of proteins, carbs, vitamins
Whipple procedure
-for pancreatic cancer
-remove head of pancreas, gb, duoud
-no duod= loss of enterogastric reflexes (no feedback inhibition)
-loss of panc enzyme and fluid secretion, no GB
-poor digestion, fat absorption, bloating, high gas production
Diarrhea causes
-enteritis
-mucus becomes irritated
-dec AT and increased secretion
cholera
-cholera toxin stim cAMP to stim secretions from crypts of Lieberkuhn in ileum
ulcerative colitis
-immune disorder
consequences of GI obstructions
-at pylorus= acidic vomit
-below duod= neutral or basic vomit
-high obstruction= extreme vomiting
-low obstruction= extreme constipation with less vomiting
Vomiting
-vagal and symp afferents to vomit center
-motor impulses via 5, 7, 9, 10, 12
-antiperistalsis
-deep breath--> gag reflex to open LES --> closing of glottis --> lifting soft palate --> strong contract of ab wall
-controlled by chemoreceptors in brain/medulla
short bowel syndrome consequences
-diarrhea, steatorrhea
-dehydration
-weight loss
-vit and mineral deficiencies
jejunal resection
-adequate absorption unless >75% resected
-preserved absorption of B12 and bile salts
-good ileal adaptation
-normal transit
ileal resection
-adequate calorie and fluid absorption
-malabsorption of bile salts and vit B12
-poor jej adaptation
-rapid intestinal transit
extensive bowel resection
-large fluid losses
-nutrient malabsorption
-poor jej adaptation
-acid hypersecretion
-rapid gastric emptying
-rapid intest transit