Chapter 16: Blood & Chapter 17: Respiratory System

Physiology (Ch 16/17) Finalexam will cover all chapters. (all 24 Chapters) Ch16 BL000 Approx. 51/blood blood composition (Proteins: will always end in "in" Albumin, Hemoglobin Ø all of them, but most of them 1/3 makes up your RBC'S 2/3 makes up plasma-you have more plasma. WBC, proteins protein albumin-contributes to plasma Colloid osmotic pressure Transfemn-helps to transport Iron in blood. Fats neutrophils-general fighters in Immunity Basophils-active in inflammation. Platelets-responsible for el elotting. red* Hematopoiesis-production of RBC (in bone manow) manow, erythropotein- released by Kidneys Butty coat- layer of WBC'S (Always making new RBC's) KBCS-120 day lifespan. mature Roe's loose their nudens can replicate. Steen-taken by spleen and recycled matenals come from here pleumopotin stem cells-differentiates to all kinds of cells. other all come from same ongin. -Platelets- thrombopreitini (protein needed for Platelet production) Bone is highly vascularized hame platelets is Size, shape color of Roic's matters-bic it can be indicator of overall well-being in patients. Ex Sickle-cell anemia. or anemia in general "crenated" ROE'S - "little spikes"-caused by "spherocytosis"-loose biconcare disk share infections/toxins (MORE KARE) Hap Zalpha globulin, 2 bela globulin (protein component) composition theme group can hold 4 02 in Heme me *Figure 14-6(c)* spend time on slide- Vilirubin 1st released from spleen (umonjigated)-does #get excreted sent back to liver-converted to direct excreted in bile GI tract** → If liver cannot convert conjugated bilinbin direct biluruban - JAUNDICE. > tired fatigue lack of BDC's > Can't fight off infections lack of WBC'S (common fiu) presentation in actual patients > be able to stop bleeding - lack of platelets (like when you get outs) When you have damage to blood vessel. CIUMP Hemostas-stop weeding through vasoconstinction) (platelels clog fogether) coagulation-formation agulation- of Actual clot there's 2 (coagulation cascade)-watch a video (exposure of damaged area will expose factors wich Inggers Hemostasis) ways will form fibrin clot that willallow vessel to heat, them once healed. You can break down the extrinsic Intrinsic clot (by plasmin) Sertonin-coagulation (complex) ADp-coagulation (von will brand) factor PAF-coagulation Platelet aggreganon Thromboxone A-cogulation VWF- allows platelets to attach to collagen. If you hare this patients tend to bleed out. I prolonged bleeding. trinsic extrungc) 2 pathways combine at factor X(ten) Intrinsic 12-factor 11 extrinsic 11-factor 9 factor 9-factor 8 8 will ALWAYS activate factor 10 factor To will convert prothromban→thrombin (most important protein blu fuit forms) fibrin (Plasminogen) Converts to fibrin (which makes actual Clot) Plasmin breaks down clot when you don't need it any mot activated by TPA-Hissue plasminogen actrator PE can also have hyperroagulation - Øget ble you can get DVT blockage. anticoagulation Heparin, antithrombin Il proton c (body makes these protein's) proteins -Factor 8/9 defiat Hemophelia Produces "weak" clot? different in struture. CHAPTER 17-Respiratory System Use respiratory system tor gas exchange, speech. point of control for homeostasis (in regard to pit) mecociliary escalator-epithelium has cilla (protective mechanism) that pushes things a way from respiratory tract/mngs respiration vs ventilation. #actual gas exchange ↳ morement of alr from outside to alveoli (inside) cellular respiration-actual exchange of gases. Pharynx-larynx-trachea-bronchioles - resp bronchioles-alreoli diaphgram-breathing at rect chest wall, diaphgram, external intercoastal/internal intercostal, abdominal muscles seratus antenor, (inhale) (exhale) neck muscles (Scalene) Sternocleidomastord -ALL used during exertion breathing -Lungs covered by pleura (thin membrane cant really see it) Functions @protect lungs from friction ②creates pressure difference betmen alreali and pleurd. (pleura will always have (-) pressure compared to alveoli) If it's - you end up tension pneumothorax (collapsed lung) Pleura (2 layers) directly visceral- attached to lung (translucent) in between you have pleural fluid (small amt) parietal-away from lung Rlung-3 lobes L lung-2 lobes aspirated objects likely to end up on Klung ble! Its more vertical Alreoli-Sacs Illed by flat cells + Pheuros cytes typel-hakes up malonty of calls in areoli (allon gas oxchange) → allows alreali to stay open type 2 phenmaytes-secrete substance called surtatant surface tension so that alveoli dous & collapse Figure 17.4 (Shows rentilation) respiration) as you go bronchiote tree-you 1 surface area. PV=nRT (IDEAL GAS Law) *pressure number of moles Ighore(R) its a constant_can be 8.315 or 0.826 *Iemperature PIV, PV, (start print) (end point) 2 ranables PP = T2. top bottom directly proportional Pressure-Volume Inversely related. pressure-temp-directly related 11 or 业 volume tem directly proportionat 11 or th P.VIP2V2 (Combined Gaslaw) T2 Spirometry tidal volume-500ml bair you breath in at rest /@exertion residual volume should herer loose more air than residual volume. Ils the volume that's sheft im lungsaber exhalation (LUNGS & ever filly collapse) Vilal capacity amt of air that can more in/out of lungs w/out comprimising resp system expirationd resere volume amount of air you can exhale -during-exertion. Mspiratory reserre volume additional amt of air you can inhale. total lung capauty amt of air lungs can bold. diaphgram main muscle for respiration (especially at rest) diaphgram contracts when you inhale DUH! When it contracts; It becomes flattened. relaxed -goes back to its dome shape.