BIOC34 Final Exam Notes.docx

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Department
Biological Sciences
Course
BIOC34H3
Professor
Stephen Reid
Semester
Winter

Description
Final Exam Notes Lecture 13: In sickle cell anemia there is not a decrease in the absolute # of red blood cells just in the # of normal red blood cells Humans are the animal that have RBCs that are not nucleated p50 value, Left shift, Hb-O bi2ding affinity p50 value, Right shift, Hb-O b2nding affinity Temperature Effect: main effect is high temp reduce affinity, low temp enhance affinity 1) You usually breathe cool air relative to the temp in your body, then the lungs are cold, reduced temperature lowers p50 value, p50 value, Left shift, Hb-O b2nding affinity 2) Metabolically active tissues have hot air, so elevated temperature raises p50 value, p50 value, Right shift, Hb-O b2nding affinity, which will facilitate oxygen delivery to tissues pH (Bohr effect): main effect is high pH enhances affinity, low pH reduces affinity 1) Metabolically active tissues have a decrease in pH which causes an increase in p50 value, p50 value, Right shift, Hb-O b2nding affinity, which enhances the unloading of O2 2) In the lungs Co2 is excreted causing pH levels to rise, decreasing p50 value, p50 value, Left shift, Hb-O b2nding affinity Effect of CO2: 1) CO2 and pH intimately related, if CO2 is enhances then it will hydrate and form + - hydrogen ions (H 0 2 CO2  H + HCO3 ) lowering the pH, which cases an increase in p50 value, p50 value, Right shift, Hb-O bi2ding affinity, which enhances the unloading of O2 2) There’s also the direct binging of CO2 to Hb and that’s called the Carbamino Effect, which causes a reduced affinity for Hb-O2 binding since it blocks the binding sites, and that causes a p50 value, Right shift In the lungs: + - 1) Co2 is produced to be excreted so H+ are being used up (H + HCO3 H 2 + CO2) and the pH increases, decreasing p50 value, p50 value, Left shift, Hb-O bi2ding affinity 2) Lower temp (cooler air relative to body) and so , p50 value, Left shift, Hb-O 2 binding affinity • Effect in lungs is not that extreme In the tissues: 1) Higher temp in tissues (metabolically active) so elevated temperature raises p50 value, p50 value, Right shift, Hb-O b2nding affinity, which will facilitate oxygen delivery to tissues 2) Tissues also use up CO2 enhancing # of H+ ions so pH decreases, causes an increase in p50 value, p50 value, Right shift, Hb-O b2nding affinity, which enhances the unloading of O2 • Effect in tissues more extreme 2,3- DPG effect: effect of this is a trade-off between oxygen loading at the lungs and oxygen unloading at the tissues Blood-oxygen levels high, enzyme that produces 2,3-DPG inhibited, no 2,3-DPG produced Blood oxygen levels low, 2,3-DPG produced, causes p50 value, Right shift, Hb-O 2 binding affinity, promotes unloading of oxygen. But this may be detrimental because lower p50 values also causes less oxygen to be loaded at the lungs, but actually loading at the lungs will not really be affected, its more important to get the Co2 off the tissues *The effects of these 4 things are the same in both anaemia and a normal person but the absolute content of O2 is less in an anemic person *CO is very bad because it has a higher affinity that O2 and also once it binds it takes a long time for it to come off ( a few days, if you’re even lucky enough to live that long after breathing a lot of CO) unlike O2 which comes off really quickly. Since it has muchhhhh higher affinity, once it binds it blocks O2 and stays there for a long time, so you’re tissues doesn’t receive O2 Haldane effect: deoxygenated blood carries more CO2 then oxygenated blood (which carries less CO2) Because in the lungs where there is a lot of oxygen (oxygenated blood) were losing CO2 Lecture 14: Phrenic nerve is the nerve that innervates the diaphragm During normal breathing the phrenic nerve fires slowly, and the graph is a slow increase During gasping there is an abrupt increase in the graph Dorsal respiratory group is equivalent to the nucleus solitary tract, it is a very important relay center, it’s the site of first synapse for many things, including the baroreceptors (those from both the carotid arch and the carotid labyrinth), the carotid chemoreceptors, and the stretch receptors of the lungs Ventral respiratory group is like an integrative center, consists of both inspiratory and expiratory neurons. It consists of 3 nuclei. The expiratory neurons only fire though when breathing becomes an active process (ex. During exercise). Pre-Botzinger complex is not the same as the Botzinger complex. It’s slightly superior (rostral) and a little ventral to the ventral respiratory group in the medulla. Substance P is a neurotransmitter that is found in high abundance in the Pre-Botzinger complex Glomus cells (type 1 cells) are O2 sensors and they send signal through the sinus nerve, saying that since blood oxygen levels are low increase breathing. The glomus cells releases mainly acetylcholine to the carotid sinus nerve. They also release dopamine which feedbacks and inhibits their own function. The signal goes along the carotid sinus nerve and then it reports to the dorsal respiratory group (nucleus tractus solitarius) which then sends signals to our ventral respiratory group and then motor output is conveyed to the diaphragm as well as other respiratory muscles. If Co2 in the blood decreases (say from 40 to 30) then we can’t breathe. It doesn’t matter how much oxygen is in our blood. If the PC02 in our blood isn’t at least 30mmHg then were not going to breathe. Big question was how did the glomus cells sense low oxygen? 1) Mitochondrial theory: ultimately calcium is released from the mitochondria into the cytosol and elevation of calcium triggers the release of neurotransmitter by exocytosis. 2) The primary model of oxygen sensing though is probably the heme model: it is believed that there is an oxygen sensitive molecule on the plasma membrane of the glomus cell that is made up of a heme based protein. Low PO2 sensed by the protein because there’s oxygen is no longer bound to it, so heme protein is activated it then causes the closure of the potassium channel, causes a buildup of K+ and since they’re positive it causes the plasma membrane to depolarize and this triggers the opening of voltage gated calcium channel which causes Ca to enter into the cell which triggers the release of neurotransmitter by exocytosis. The experimental evidence for this theory came from experiments where they made a cell culture of glomus cells in a petri dish, then you suck up a little of the membrane is a glass pipette. Then you record current movement and membrane potential. They did an experiment where they sent a current to open potassium channels and then looked at the graph, under normal conditions more potassium channels opened so you get more current, but under hypoxic conditions less potassium channels opened because they’re oxygen sensitive and need oxygen to open so you get less of a current. Predominate site of CO2 sensing is in the brain. There are CO2 sensitive chemoreceptors located in the ventral surface of the medulla oblongata. H+ ions activate the chemoreceptors and they send signals to say the ventral respiratory group that CO2 levels are high so we need to increase our breathing Lung (pulmonary) stretch receptors – mechanoreceptors in the lungs and as the lung inflates, they stretch and stimulate the stretch receptors and sends signal to the brain that the lungs are inflating time to stop breathing. This phenomenon is called the Hering-Breuer Inspiratory Off- Switch Ventricular acclimatization: for humans it takes 9-10 days to get acclimatized to high altitude situations Lecture 15: Alpha waves – associated with relaxation Beta waves – associated with intense concentration and anxiety Theta waves occur when we’re starting to get into deeper stages of slow wave sleep, associated with daydreaming and severe emotional stress Delta waves – slow waves, mixed amplitudes, occur during very deep sleep ECG is useful to determine what type of sleep stage the person is in Hypothalamus has a region that is responsible for slow wave sleep The raphe nucleus in the pons is responsible for REM Slow wave sleep we cycle rapidly through stages 1-4, and then we enter REM sleep, and then go back to slow wave sleep stages 1-4. But as the night progresses we spend less time is stage 1 of slow wave sleep, and we don’t come back up to stage 1 because it’s close to wakefulness, and we also don’t go back down to stage 4 because that’s more of the early stages of sleep In slow wave sleep there is an overall decrease in muscle tone, in REM sleep all the postural muscles are paralyzed We start off in sleep with beta waves, then we go to alpha waves, then we reach the stages of sleep, in stage 2 it’s a mix of theta waves and alpha waves (they call the alpha waves sleep spindles). Stage 3 sleep has a mix of the two lower frequencies: theta and delta. In stage 4, the deepest stage of slow wave sleep, you get all delta waves. When you leave slow wave sleep and enter REM sleep the pattern of ECG activity reverts to beta waves (which is alert, concentrated pattern of activity that you see during wakefulness) Case 1: In obstructive apnea the trachea collapses because of the fat pushing down on it. During obstruction the abdomen and the chest go in opposite directions (ex. Like closing your nose and trying to breathe). Normally the abdomen and the chest go in the same direction. As blood O2 decreases there is an increase in breathing efforts, and this tells us that O2 and CO2 sensing are probably normal, so there is normal chemoreception, so automatic control of breathing appears to be fine. The person then gets aroused and more wakeful, there is an increase
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