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Ch 9 Txt Notes.docx

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Department
Psychology
Course
PSY100H1
Professor
Michael Inzlicht
Semester
Fall

Description
CHAPTER 9: Temp Reg, Thirst, and Hunger Body Temp • If too cold, ice crystals form within cells damaging the cell membrane • If too hot, proteins necessary for carrying out cell fxns become unstable • Higher S.A. : Volume ratio = must work harder to maintain core temp o Ex. Rat has to work harder • Endoterhms: mammals + birds, maintain body temp through internal metabolic activity • Ectotherms: reptiles + fish + amphibeans, rely on external factors like basking in sun • Despite common terms, it’s not really warm-blooded and cold-blooded. All animals fall within a few degrees of one another • Human temp set point = 98.6F or 37C • In response to cold  shivering, and if cold still persists: o Throid gland increases release of thyroid hormones  greater overall metabolic activity o Deficits in thyroid activity are often found in people who commonly are cold • In human infants + small animals, sympathetic NS stimulates greater metabolic activity in brown fat cells = mainly located in torso near vital organs o Appear brown bc lots of mitochondiria • Warm  we have 2.5 mill sweat glands and lose roughly 1 liter to sweat each day Deviations in Core Temp: • Fevers above 41 C can cause brain damage • Fevers result when pyrogens = chem. by products of bacteria/viruses enter the brain and gradually increase the body’s set point. They target the POA in the hypothalamus bc the blood-brain barrier is relatively weak theire. o Once in the POA, pyrogins stimulate release of prostaglandin E2 o This in turn inhibits firing of warm-sensitive neurons • Hyperthermia = different from a fever = heat stroke = not a carefully monitored increase in body temp set point = when body’s normal internal mechs cannot keep core temp within lim’s o Above 40 C and person may become confrontational, faint, confused o Sweating stops, making it even worse o Also interacts with immune sys fxn o More likely if already an existing infection • Hypothermia = below 35 C = uncontrolled, intense shivering, slurred speech, pain, discomfort o Below 31  pupils dilate, appear drunk , consciousness is gradually lost o Deliberately producing mild hypothermia has become a common way to reduce brain damage following cardiac arrest or open heart surgery o Cooling counteracts typical negative rxns to an interruption in blood supply of brain (such as excess free radicals, excitatory neurotrans, and Ca) Brain Mechs for Temp Reg: • Temp reg results from a structural hierarchy staring with spinal cord  brainstem  hypothalamus • For SC, temp has to change by 2-3 degs away from set point • Hypothalamus initiates compensation with as little as 0.01 deg deviation • Preoptic area (POA) = part of hypothalamus that, along with anterior hypothalamus + septum, coordinates incoming info from thermoreceptors to trigger responses to warmer core temps o POA contains 3 types of neurons:  Warm-sensitive (increase firing as temp increases + inhibit cold-sensitive)  Cold-sensitive  Temp-insensitive = retain a fairly steady rate under all temps  Set points are possibly from a comparison of temp-sensitive to the temp- insensitive standard • Posterior hypothalamus is responsible for initiating responses to cooler core temps • Temp sensors in hypothal can override input from skin sensors Temp Reg in Infancy: • Newborns are relatively helpless bc of age-related metabolism, high surface to volume ratio, immature shivering ability, and low body fat stores o Premature infants have an especially difficult time maintaining temp Thirst • Electrolyte = dissolved ions • Body has 3 major compartments for storing water: o 2/3 = intracellular o 1/3 = extracellular  Blood = 7% of body’s water total  Interstitial fluid = 26% of body’s water total  Cerebrospinal fluid = a very small percentage • Though Extra = mainly Na and Cl and Intra = mainly K, the relative concentration of total solutes is the same in both o Isotonic, in other words  Like IV fluids o So identity of solutes can be diff while overall concn is the same Osmosis: • Isotonic solutions means there won’t e much movement of fluid due to ~ • ~ = force that causes water to move from an area of low solute concn to high solute concn o In diffusion, it was the solutes that would move from high to low o But in ~ it’s the water that moves from low to high • Hypotonic = solution that is low in concn of solutes o if freshwater near-drowning, extra will be hypotonic and water will move into cell, possibly rupturing cell membrane • Hypertonic = solutions that are high in concn of solutes o In saltwater near-drowning, extra will be hypertonic and water will move out of cell causing cells to dehydrate, shrivel Kidneys: • ~ = excretes any excess sodium or water • Blood enters ~ where it is filtered by nephrons which remove impurities + excesses and sends them to the bladder o Filtered blood then returns to circulation • Water is also lost through breathing +perspiration + evap from skin = roughly 1 L for those three and defecation = 0.2 L apart from urination = 1.5L o To a total of about 2.5L = roughly 8 glasses lost and 2.5 consumed bc input and output should always be roughly the same o We take in about half the fluids we need through food Mechs of Osmotic Thirst: • Responds to cellular dehydration from drops in intracellular fluid volume • This is the more common mechanism • Most common cause of ~ = salty foods • More salt makes blood hypertonic relative to intra • Osmotic pressure will move water out of cells and receptors will sense (osmoreceptors = specialized neurons that alter firing rate when intracellular fluid lvls change) less water in cells and we’ll feel thirsty • Polydipsia = overdrinking o Is typical of untreated diabetes mellitus = unable to move sugars out of blood supply, making blood hypertonic o Cells attempt to compensate by releasing water and then feel very thirsty o The polydipsia will be accompanied by frequent urination • OVLT = area around 3 ventricle that detects cellular dehydration o Blood-brain barrier is also weak here Mechs of Hypvolemic Thirst: • Responds to drops in volume of interstitial fluid or blood or both • Most obvious case is the loss of blood to internal bleeding or severe injury • This is more of an emergency backup mechanism • Baroreceptors: in heart and kidneys and sense decreases in blood pressure which occur with decreases in blood volume • Thirst is initiated and kidneys act to conserve remaining fluids Hormones, Sodium, and Thirst: • In either form of thirst, stimulates the posterior pituitary gland to release ADH = antidiuretic hormone = vasopressin o Promotes water retention o Signals kidneys to reduce urine prod o Also stimulates kidney to release hormone renin into the blood supply  Renin triggers conversion of angiotensinogen  angiotensin II • Angiotensin II= constricts blood vessels to help maintain blood pressure and it also triggers release of hormone aldosterone (= promotes sodium retention) from the adrenal glands • low blood volume can also stimulate sodium hunger o formalin can induce hypovolemia experimentally and this produces excessive thirst + salt cravings • if excretion of sodium by kidneys is inadequate, high b.p  stroke may occur • chronically high sodium lvls in blood promote release of water from cells by osmosis o higher blood volume then increases blood pressure • most high bp meds are diuretics o bc promoting urination is an effective way to reduce blood volume • Lower than normal sodium is also bad. o Vomiting + diarrhea can reduce sodium: decreases blood volume and decreases bp Initiation of Drinking: • Angiotensin II stimulates drinking through acting on subfornical organ (SFO) o Located near junction of two lateral ventricles, below the fornix o Also in a place where blood-brain barrier is weak o SFO increases firing rates when angiotensin II is present o Electrical stim produces drinking behv o Has connections with median preoptic nucleus  unlike OVLT and SFO, NOT located where blood-brain barrier is weak  Does contain angiotensin II receptors, it cannot respond to it  Possibly angiotensin is a neurotrans between SFO and MPN  MPN also receivs input from NST = nucleus of the solitary tract = located in medulla = and the NST receives input from baroreceptors in circulatory sys and osmoreceptors in digestive tract  MPN also communicates with LH = lateral hypothalamus = LH projects to zona incerta of the midbrain = ZI sends info to motor region including basal ganglia, red nucleus, and ventral horn of spinal cord • ZI stim produces drinking behv Cessation of Drinking: • We typically stop drinking before lvls return to normal • Fluid recpetors in mouth, throat, digestive sys • Lesions of septal area can produce overdrinking o So septal area = for cessation of drinking • Overdrinking can lead to hyponatremia = a condition where extracellular sodium lvls drop by 10% or more below normal o If untreated  vomiting, nausea, cramps, disorientation  seizures, coma (bc brain swells )  death o Many med problems can result in this: congestive heart failure, kidney failure, tumors o Become more common lately due to increased popularity of extreme endurance events • MDMA = ecstasy = can increase ADH secretion which inhibits urination + stimulates drinking o May overdrink  too much water in brain  coma  death • Alcohol = diuretic BUT, it’s also a general anesthetic  dulls message from bladder o Binge drinkers may rupture bladder by overfilling o Can be mistakenly diagnosed as UTI • Under normal circumstances: etracellular fluid lvls are negatively correlated with sodium concns = HYPONATREMIA o But, during extreme endurance, low fluid and low sodium o Conflicting messages and release of ADH cannot simultaneously resond o Protecting blood volume si more important so ADH still released o Water retained, urination inhibited BUT sodium concns still decrease o Extracellular fluid becomes increasingly hypotonic o Stro
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