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The KP for the reaction is 2.05 at 648 K. A sample of

Chemistry: Atoms First | 1st Edition | ISBN: 9780073511160 | Authors: Julia Burdge, Jason Overby ISBN: 9780073511160 60

Solution for problem 123AP Chapter 15

Chemistry: Atoms First | 1st Edition

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Chemistry: Atoms First | 1st Edition | ISBN: 9780073511160 | Authors: Julia Burdge, Jason Overby

Chemistry: Atoms First | 1st Edition

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Problem 123AP

The KP for the reaction is 2.05 at 648 K. A sample of SO2Cl2; is placed in a container and heated to 648 K. while the total pressure is kept constant at 9.00 atm. Calculate the partial pressures of the gases at equilibrium.

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Neurons, how they work How They’re Built 1. Fluid inside & out 2. Generating energy with ATP 3. Myelin coating made by glial cells a. Thicker coating= faster conduction of electrical signals 4. Chromosomes inside­­long strands of DNA Firing & Changing 1. Neurons can either change the polarity of other neurons by flooding them with ions until they fire or… 2. They send neurotransmitters into the synapses between the neurons. a. Neurotransmitters “switch on” genes in other neurons, causing them to produce proteins which essentially change them, conveying information to adjoining neurons 3. The changes can include generating new receptors, making more neurotransmitters, increasing enzymes, etc. 4. They fire when sodium enters the cells and raises the resting electrical charge past threshold until the neuron “fires” releasing neurotransmitters or passing its charge along to another neuron How Medicine for Mental Illnesses work 1. Psychopharmacology involves manipulating the levels of neurotransmitters in the brain – primarily seratonin, dopamine, and norepinephrine. These transmitters affect mood, thought and arousal (anxiety). 2. Psychiatric medication affects the ways that neurons produce and receive neurotransmitters. And so Prozac is a Selective Seratonin Re­Uptake Inhibitor – it increases the amount of seratonin in the synapses between neurons, thus raising the overall level of seratonin. Two Types of Receptors 1. Ionotropic (ion channels) 2. Metabotropic (G­proteins, second messengers, DNA changes) Neurotransmission 1. And so, the ionotropic and metabotropic neurons respond to imput from other neurons. One imput is simply responding to the firing of an adjacent neuron. 2. However, neurons also respond to chemicals created by endocrine glands, other neurons, or food (or chemicals) you bring into your body. 3. So, caffeine from cocoa beans, alcohol from fermented grains, opiates from poppy plants … these bring in neurochemicals which affect how your brain functions. 4. And, of course, experimenting with plants and their chemical properties gave rise to the invention of medicines. Amino Acid Transmitters ­ you can’t target where things like SSRIs go, they just go directly into your bloodstream ­ Women who have SSRIs are more likely to develop osteoporosis because serotonin is also involved in the development of bones/bone marrow 1. Glutamate made from a nonessential amino acid and is made when the body processes glucose 2. Build­up of glutamine in Glial cell→+ glutaminase→ Glu (glutamate) 3. Glu is “excitatory” neurotransmitter [excited neurons throughout the body, causes them to fire or to change metabolically] a. (amphetamines UP glutamate, which is why you shouldn’t take them before you go to sleep) 4. Glu is precursor to GABA (the main “inhibitory” transmitter)­­calms down the neurons to keep them from firing Acetylchoine­the classic neurotransmitter 1. The Ach neuron brings choline into the cell. ChAT transfers a molecule of acetate and voila you have Ach 2. Found throughout the body, 3. Involved in everything from joint flexibility to sleeping & dreaming 4. Serves different purposes depending on the kinds of neurons it affects throughout the nervous system Catecholamines: The crucial set of neurotransmitters 1. DA, NE, Epinephrine are built from tyrosine 2. Neurons build on the catechol nucleus, using the enzymes, to produce the three neurotransmitters 3. The enzyme Tyrosine hydroxylase sets the process in motion Graph in notes shows process by which tyrosine is turned into the 3 neurotransmitters (*for exam, just know that tyrosine turns into those 3*) Dopaminergic Neurons… 1. Vesicles​ @ terminal buttons → cell membrane → release into synapse 2. Autoreceptors ​ that receive DA that works like a thermostat 3. Transporters​ that vacuum up excess DA in synapse 4. All three work together to help neuron to maintain its function and the precise amount of DA in the synapse Balance of NE and DA ­ If disrupted, can be responsible for dramatic changes in functioning ­ [pic of bunnies pre and post reserpine, which blocks DA & NE, and causes supplies to run low. Bunnies are knocked out until the drug is out of their symptoms] Dopaminergic pathways in the brain 1. Starting in the midbrain, clusters of DA neurons project t​triatumin the forebrain. Th​ igrostriatal pathwis involved with gross motor movement, and shortages of DA lead to tremors and parkinsonian symptoms 2. Starting in a nearby area, the ventral tegmental area, clusters of the DA neurons project to tlimbic system​ affecting amond others thhippocampus a​nd amygdala​ . This is the importan​esolimbic DA pathway ​affecting emotion & memory 3. Also starting in the VTA, clusters of DA neurons project to t​erebral cortex­­arriving in th​refrontal are..and they form the crucia​esocortical DA pathway i. Yes these dopamine neurons are affected by LSD, marijuana, etc (mess with neocortex) ii. To treat scizophrenia, you need to lower DA in brain. BUT doing that could affect the nigrostriatal pathways­­leaving some patients with parkinson’s that they can never get rid of Noradrenergic Pathways ­ Mother­of­all pathways ­ Starts in brainstem locus coeruleus)​ ­ NE neurons project to almost every part of the forebrain [cortex, limbic system, thalamus, hypothalamus] ­ Plays an essential role in hunger, sexual behavior, arousal, sleep, fear, pain, anxiety Serotonin 1. Functions throughout the nervous system 2. Tryptophan (amino acid)­­> +tryptophan hydroxylase & aromatic l­amino acid decarboxylase → Serotonin (5­HT) 3. Rapid tryotophan depletion leads to symptom relapse in recovered depressed patients Seratonergic Neurons 1. Neurons create vesicles at terminal buttons → cell membrane → 5­HT released from synapse 2. Autoreceptors​ which receive 5­HT work like thermostat 3. Transporters​ vacuum up excess 5­HT in synapse 4. All three work together to help neuron to maintain its function and the precise amount of 5­HT in the synapse 5­HT Receptors ­ Contribute to motor movement, arousal, and various other functions ­ **Receptor 5­HT 1A contributes to mood & anxiety ­ Genetic deletion leads to depression Seratonergic Pathway ­ Begins along the midline of the brainstem (r ​aphe nuclei) ­ Seratonergic neurons project into virtually every part of the brain (neocortex, thalamus, hypothalamus, limbic system) *** Increase Seratonin in the brain: a) by adding seratonin agonists that power up the receptors b) by blocking re­uptake by transporters c) by forcing release of 5­HT from nerve terminals and you sometimes decrease anxiety and depression ***** The Brain­basic anatomy & functions The Brain 1. What we can tell from the observed behavior: AR Luria and f​unctioning systems a. eg the difference between your first time driving and when you’re finally comfortable driving b. Basically the theory: when you’re learning something, you’re using different parts of the brain than when you’ve mastered it i. Called this learning system (that codes a macro system) “functioning systems” 2. We a​re the environment (our perceptions) 3. What we share with lower mammals Species Specific Behavior Tasks of the brain for all animals: ­ Eating & Drinking ­ Fighting ­ Courting ­ Mating ­ Caring for Offspring ­ ...perceiving & responding to environment How the Brain is Organized . The hind brain takes information, fed to the spinal column from the nervous system and sensory organs … and gives it to the mid­brain • Where the information is processed, refined (affecting physical & psychological experience) and shared with the cortex … • Through clusters of neurons which project from the midbrain into the lobes of the brain, bringing information experienced as thought, anxiety, and mood. (No surprise that these pathways of neurons respond to dopamine, seratonin, & norepinephrine.) Brain Stem 1. Medulla: basic essential function (heart rate, blood pressure, rate of respiration) 2. Pons: switch for sleep & wakefulness 3. Midbrain: body movement (in fighting, sex) and lowers pain when doing both, carries out orders from cortex (in lower mammals, it calls the shots) 4. Cerebellum: communicates with frontal lobe to produce precise and nuances in movement (fighting, sex, everything else), takes sensory information from the nervous system a. When damaged by a stroke, motions become jerky and “gross” 5. Basal Ganglia: higher level of motor control (controls slow movements and large muscles) involved with specific learning action Thalamus & Hypothalamus 1. Thalamus: 2 parts, one for each hemisphere, evolved to process more deeply and with more detailed sensory information before sending it on to the frontal lobes 2. Hypothalamus: “Little Thalamus”, takes information from sensory organs, regulate pituitary gland (powerful influences on the body through the release of hormones), involved with eating, drinking and sexual behavior Limbic System 1. Emotional system 2. Fight or flight reactions (amygdala) 3. treatment resistant depression 4. Hippocampus: episodic memory (storage and retrieval), spatial memories 5. Amygdala: instinctive aggression (increased activation in PTSD Patients ­ On the border of the cerebral hemispheres and the brain stem ­ Brings in info from the cerebellum, ­ Routes to centers of the brain generating conscious thought ­ Contributes to awareness, emotion, aggression, and memory Exterior Cerebral Cortex This is what separates us from most other animals (esp the prefrontal association cortex) ­ Two hemispheres connected by the corpus collosum ­ Each hemisphere has four “lobes” 1. Occipital Lobe: Visuals a. Visual cortex: Generates visuals from info sent up through brain stem b. Visual Association Cortex: visual memories, categories, and focus 2. Temporal Lobe: primary auditory cortex & its association area 3. Parietal Lobe: including primary somato­sensory cortex & association area 4. Frontal Lobe: language, thought, judgements, controls fine movement. rewires during adolescence to produce abstract thinking & higher analysis and creativity Mood Disorders­ symptoms, causes Range of Mood ­ At the extremes of the spectrum: psychotic thoughts­thoughts that don’t really make sense ­ Depression: think their sadness/toxicity affects everyone else ­ Manic Episode: think they’re a savior ­ Depression is more common than mania ­ Serious depression looks like a disease Kind of Depression ● Dysthymia (mild depression) ○ Display 2­3 symptoms for most days (consistently) over 2 yrs+ ● Unipolar depression (depression only) ○ Some depression episodes ● Bipolar Depression I (depression/mania) ○ Cycles of depression & mania ● Bipolar Depression II (depression/hypomania) ○ Cycles of depression & hypomania ○ Different from BD1 because of the lack of psychotic thoughts in hypomania ● Cyclothymia (dysthymia/hypomania) ○ Cycles of mild depression & hypomania Depression (Facts) 5 ­11% lifetime prevalence 10­15 million people a year 50% recurrence after a single episode Rule of 7’s: 1/7 with recurrent depressive illness commits suicide 70% of suicides have depressive illness 70% of suicides see their primary physician within 6 weeks of suicide Suicide is the 7​h leading cause of death Ways to Explain Depression 1. Anger turned toward the self 2. Defense: Sadness blocks Anger (and Guilt about feeling angry) ­ Sometimes originates from family culture towards expressing these emotions 3. Attributional Style: Global, Permanent, Internal ­ Internal: “I’m not good enough” ­ Permanent: “I’ll never be good enough” ­ Global: “I’m just a sucky person in general” ­ ***THIS IS THE FOCUS OF CBT*** 4. Problems with Attachment: depression=mourning 5. Biological Disorder Cognitive Model of the Emotions Multi­Hit Model Explains why identical twins don’t identically come down with depression RF4→ could be the result of attachment formations in childhood RF5→ influenced by the environment in which you grew up Three Kinds of People 1. Those who don’t suffer from depression or dysthymia, who have bad days, will grieve a loss, but don’t spiral down into a major depressive episode. 2. Those who usually don’t suffer from depression but, when stressed beyond a certain point, develop depressive symptoms and benefit from a short­term use of medication and therapy to come out of it. When the stress or crisis resolves, they often taper off their meds without a relapse. 3. Those who are chronically depressed without medication. Psychotherapy may be helpful in that it provides insight and ways to minimize stress, but these people only experience substantial relief with medication. Brain & Depression Depression, Stress and the HPA­Axis [Threat stimulus]​­­> CRH from Hypothalamus→ ACTH→ body→ A (cortisol)→ CRH shut off Brain Structure 1. Prefrontal Cortex – decreased volume and increased activity linked to depression 2. Hippocampus also seems smaller in chronically depressed patients 3. But the amgydala (really part of the hippocampus) is larger – perhaps because it processes emotional experience 4. Anterior Cingulate Cortex: It is activated by extreme sadness. 5. Nucleus Accumbens: linked to adaptability and response to behavior. It is less active in depressed patients. Anti­Depressant Medications­how they work 1. The first discovery was as drug which inhibits the monoamine oxidase (MAO), an enzyme which breaks down excess 5H­T and NE in the neuron. By blocking MAO, the neuron increases the amount of neurotransmitter it releases into the synapse. Note that the long term effect is the “down regulation” of receptors on the post­synaptic neuron. Serious side effects – due in part to excess NE in the body – included liver damage, sleep disturbance, and elevated blood pressure. Also affected diet – certain kinds of meat and cheese would boost tyramine levels in the body causing headaches & possibly strokes. 2. Tricyclics were the first reuptake inhibitors – that is, they block the transporters in the presynaptic neuron which vacuum up excess neurotransmitters. Block the transporters, i.e. the reuptake, and there is more neurotransmitter in the synapse. The problem with tricyclics lies with their molecular structure – they block reuptake of 5H­T and NE all right, but they also block other receptors, causing a variety of side effects. 3. The selective serotonin reuptake inhibitors (SSRIs) depend on molecules that target receptors more carefully, leaving out the histamine receptors among others, so that side effects are reduced. Unfortunately, there are still side effects, including loss of sexual drive and some interference with sexual function.

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Textbook: Chemistry: Atoms First
Edition: 1
Author: Julia Burdge, Jason Overby
ISBN: 9780073511160

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The KP for the reaction is 2.05 at 648 K. A sample of