anatomy and phys II final part 1

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anatomy and phys II final part 1
2010-05-05 18:00:35

hell test
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  1. Plasma
    • a) liquid portion of blood
    • b) H2O mostly about 91%
    • c) Plasma Proteins 9%

  2. Plasma Prteins
    • a) Albumin
    • b)Globulins
    • c)Fibrinogen
  3. Albumin
    • a) 58% of plasma proteins, most
    • b) regulates movement of H2O between the tissue spaces in blood vessels by contributing to the Plasma Colloid Osmotic Pressure(PCOP)
  4. Globulins
    • a) 38% of plasma proteins
    • b) 2 functions= some are antibodies
    • -protective proteins formed in response to antigens
    • -some are transport molecules and bind to other substances
  5. Fibrinogen
    • a) 24% of plasma proteins
    • b) contribute to the formation of blood cells
  6. Formed elements
    Red blood cells
  7. Red Blood Cells (Erythrocytes)
    • a) structure
    • b) function
    • c)Hemoglobin
    • d)Life history of RBC
    • e) breakdown of Hemoglobin from lysed RBC
  8. Struture of RBC
    • 1) Bioconcave discs with edges thicker than middle
    • -increses surface area(can do more with gases without gettin bigger)
    • - increases flexibility- allows to get through tight areas ( more efficient)
    • 2)At maturity RBC's have no nucleus or cellular organelles
    • 3) Main intracellular component is protein called Hemoglobin(Hb)
    • = lipids, ATP, Carbonic anhydrase
  9. Function of RBC's
    • transport O2 and CO2
    • - O2 from lungs to tissues
    • -CO2 from tissues to lungs
  10. Hemoglobin in RBC's
    • -protein made up of four polypeptide chains and four heme grps
    • - 4 polypeptide chains: 2 alpha and 2 beta subchains
    • -4 Heme grps: w/ in each grp is an Fe atom and the rest is pigment
    • -O2 binds to Fe portion of Heme ( Hb O2 = oxyhemoglobin )
    • -CO2 binds to globin portion (Hb CO2 = carboxyhemoglobin)
  11. Life history of RBC's
    • 1) RBC production is called erythropoiesis (stimulated by low plasma O2 levels)
    • 2)Erythropoiesis is regulated by the hormone erythropotein ( made in the kidneys)
    • 3) immature RBC's are called reticulocytes
    • 4) females = 4.3-5.2mil/mm cubed ; males = 5.1-5.8 mil/mm cubed
    • 5) lifespan of RBC in females= 110 days; males= 120 days
  12. Breakdown of Hemoglobin from lysed RBC
    • 1) remenants get trapped in two organs ( liver and spleen/rbc graveyard)
    • a) macrophages enzymatically seperate Heme from globin
    • - globin is broken down into amino acids ( then amino acids are used for protein synthesis)
    • - heme ( Fe portion is transported to bone marro and used to make more Hb)
    • ( pigment is converted to bilirubin and becomes part of bile secreted by the liver)
  13. Hemostasis
    • 3 steps
    • - vascular spasm
    • - platelet plug formation (has its own three steps)
    • - Coagulation
    • Fibronolysis occurs after 3 steps
  14. Vascular Spasm in Hemostasis
    • 1) Immediate but temporary closure of damage blood vessel
    • - due to reflexive retraction of smooth muscle within vessel wall
    • 2) Triggered by two different things
    • - endothelin from damages blood vessel endothelial cells
    • - nervous system due to stimulation of local pain receptors(nociceptors)
  15. Platelet Plug Formation of Hemostasis
    • 1) an accumulation of platelets at injury cite
    • 2) occurs in a series of steps
    • a) Platelet adhesion
    • b) Platelet release reaction
    • c) Platelet aggragation
  16. Platelet adhesion in PPF
    • 1) injured endothelial cells produce a protein called Von WillenBrand Factor
    • - allows platelets to bind to collagen that has been exposed due to injury
  17. Platelet release reaction of PPF
    • 1) Platelets bound to collagen and become activated , which causes platelets to release chemicals from their cytoplasmic granules
    • a) ADP
    • -Thromboxane A2 are released from granules ( recruits more platelets to injury cites)
  18. Platelet aggragation of PPF
    Plasma protein fibrinogen facilitates binding of platelets together PGI1 released from damaged endothelial cells (limits the aggragation to only damaged area)
  19. Coagulation of Hemostasis
    • - Prothrombin turns into Thrombin (by prothrombin activator from damaged endothelial cells) (prothrombin is made by liver and is not active)
    • - Fibrinogen turns into Fibrin ( by Thrombin) (Fibrinogen is mage by the liver and Fibrin is what holds the clot together)
  20. Fibronolysis (clot resolution) of Hemostasis
    -cells around clot release a protein called Tissue Plasminogen Activator (TPA)

    plasminogen -----> Plasmin (activated by TPA) (plasminogen is made by liver and Plasmin causes hydrolysis of fibrin holding clot together)
  21. Damaged Endothelial Cells Release 5 Things
    • - Edothelin
    • - Von WillenBrand Factor
    • - PGI2
    • - Prothrombin activator
    • - Tissue Plasminogen Activator
  22. Pericardial Sack
    • double layered closed sack surrounding the heart
    • a) fibrous pericardium
    • - tough fibrous CT
    • - prevents fro moverdistension of heart, anchors w/ in the mediastium
    • b) Serous pericardium ( simple squamous epithelium)
    • - 2 layers ( Parietal pericardium- thoracic cavity / Visceral pericardium- heart itself surrounds it)
  23. Heart Chambers
    • a) 2 atria and 2 ventricles
    • b) inter atria septum ( divides atria into left and right)
    • c) interventricular septum (divides ventricles into left and right)
  24. Atria
    • Auricles- structures on superior surface
    • Internal Posterior wall-smooth
    • Internal Poster wall- ridged w/ pectinate muscles
    • -smooth/ridged region is seperated by the crista terminalis

  25. Atria cont...
    • 1)On the right side of the interatrial septum is an oval depression called the fossa ovalis
    • -remnant of the foramen ovale, this was an opening between Right and Left atria in embryo/fetus
    • 2) Atria are recieving chambers
    • -right atria
    • -left atria
  26. Right Artia
    • Recieves deoxygenated blood from three veins
    • 1) Superior Vena Cava- from region above diaphragm
    • 2) Inferior Vena Cava- from region below diaphram
    • 3) Coronary sinus- from heart itself
  27. Left Atria
    • recieves oxygenated blood from lungs via four pulmonary veins
    • -2 from left and 2 from right lungs
  28. Ventricles
    • Known as "distributing chambers"
    • -Right ventricle
    • - Left ventricle
  29. Right Ventricle
    receives blood from the right atrium and pumps it to the pulmonary trunk to take to lungs
  30. Left Ventricle
    receives from left atrium and pumps blood to the aorta to be taken to blody tissue
  31. Atrioventricular vlalves
    • a) allow blood to flow from atria to ventricles( OPEN), but prevent blood from flowing backwards into the artia
    • -snapped closed when ventricles are contracted
    • b) The AV valve between the Right atrium and Right ventricle = Tricuspid valve
    • c) the AV valve between the Left atrium and the Left ventricle = Bicuspid valve
  32. Semilunar Valve
    • a) allows blood to flow out of ventricle into aorta/pulmonary trunk (open)
    • b) SL valve between right ventricel and pulmonary trunk = Pulmonary SL valve
    • c) SL valve between left ventricle and the aorta = Arota SL vlave
  33. Routes of Blood Flow
    Pulmonary Circuit

    Systemic Circuit
  34. Pulmonary Circuit
    • right side of the heart takes blood to lung picks up O2 and drops off CO2
    • Route: Deoxy Blood---superior/inferior vena cava ---right atrium
    • ---tricuspid valve---right ventricle---pulmonary SL valve---pulmonary trunk
  35. Systemic Circuit
    • Left side of ther heart brings oxy blood from lungs to tissues
    • Route: Oxy blood---pulmonary vein---left atrium---bicuspid valve
    • ---left ventricle---aortic SL valve---aorta---tissues
  36. Cardiace Muscle Phys.
    • 1) Cellular Components 6)Regulation of Heart
    • 2) Electrical Events
    • 3) Heart Sounds
    • 4)Abnormailities
    • 5)Cardiac Output
  37. Cellular Components of Cardiac Muscle Phys.
    • Contractile Cells
    • Conductile Cells
  38. Contractile cells
    muscle cells for actual heart pumping ( have actin and myosin )

    make up 99% of cardiac cells
  39. Conductile Cells
    • -Make heart auto rythymic
    • a) self excitable cells that generate theis own action potentials
    • b) the action potentials then initiate action potentials in contractile cells
  41. Electrical events of Cardiac Muscle
    AP in contractile cell

    AP in conductile cell
  42. AP in contractile cell
    • 1) electrical stimulation cause Na channels to open; Na influx ; intracellular positivity
    • 2)at threshold, more Na channels open; causing the steep uprise
  43. AP contractile cell cont...
    • 3) Plateau Phase:
    • a) "slow" Ca channels open; Ca influx; they stay open
    • for several tenths of a second; keeping inside of cell positive and
    • inhibits repolarization
    • b) membrane pereability to K decreases by 5times, further inhibiting repolarization
    • 4) Repolarization:
    • a) Ca channels close
    • b) membrane permeability increase for K allows for K eflux (intracellular negativity)
  44. AP conductile cells
    • 1) conducting system
    • 2) AP trace
  45. Conduction in AP conductile cell
    • a) Sino atrial(SA) node- heart "pacemaker" because it depolarizes the fastest and begins sequence of citation
    • b) Internodal Pathway- electrical connection between SA and AV nodes
    • c)Atrioventricular(AV) node- depolarization is delayed here ( AV nodal Delay) to give atria time to fully contract
    • and empty blood into ventricles before ventricles are stimulated to contract
    • d) Bundle of His- divided left and right bundle brnaches within intraventricular septum / AP progated to apex
    • e) Purkinge Fibers- penetrate heart apex, then the wind superiorly toward base of the heart
    • cause ventricles to contract upward
  47. AP trace of Conducting cells
    • have no resting potentials ( electrical signals runnging)
    • a) membrane gradually depolarizes to threshold due to:
    • i. Decreased permeability to K, decrease K eflux
    • ii. Constant Na influx through "Leaky channels"
    • iii. "transient" Ca channels open; Ca eflux
  48. AP trace of Conducting cells cont
    • b) Fast uprise/ spike at threshold due to Ca influx through "longer lasting" Ca channels
    • c) Repolarization- increased K permeability: K eflux
    • d) K channels or gates begin to close; decrease K eflux
  50. Electrocardiogram ( EKG)(ECG)
    • Uses electrodes placed on body surface to detect a summation of all AP's being transmitted
    • through heart at a given time

    • Displays electrical events that are responsible for mechanical events of contraction (systole)
    • and relaxtion(diastole)
  51. EKG cont...
    • P-wave -atrial depolarization about .1 sec after artia contract(systole)
    • QRS complex- ventricle depolarization after ventricles contract ( hides atrial diastole)
    • T-wave- ventricles repolarize .225 sec later ventricles relax
  52. EKG PIC
  53. Heart Sounds
    • use a Stethoscope to listen
    • 1st is "Lubb"- AV valves closing (beginning of ventricular systole)
    • 2nd is "Dubb"- SL valves closinf and begining of ventricular diastole
  54. Abnormalities of Heart
    • 1)Tachycardia
    • 2) Bradycardia
    • 3) Arythmias
  55. Tachycardia
    abnormal high rate- 100bpm
  56. Bradycardia
    abnormal low rate- less than 60bpm
  57. Arythmias
    • are abnormal series of excitement
    • 1) SA nodal Block (missing P-wave and HR decreases)
    • 2) AV nodal Block - ventricles dont recieve all implulses from atria
    • 3types: 1st(interval between P and QRS > .2 sec)
    • 2nd (some P waves trigger QRS and some dont)
    • 3rd ( complete heart block / atrial bpm 100 and ventricle bpm lower than 40)
    • V-fib- ventricles never fully fill or empty( drecrease blood supply to tissues)
  58. Cardiac Output (CO)
    • 1) amount of blood pumped through heart per minute
    • - HR times SV
    • - SV is amount of blood the heart beats per beat
  59. Regulation of Heart
    • 1)Intrinsic- the more the ventricle muscle is stretched the more
    • forceful the next contraction would be
    • - occurs when venous return increase (amount of blood entering the right atrium from superior vena cava)
    • -if you increase venous return you increase SV and therfore CO
  60. Blood Vessel Walls have 3 Layers
    • Tunica Intima
    • Tunica Media
    • Tunica Adventitia
  61. Tunica Intima of BV
    • contacts blood
    • endothelial cells and basement membrane cells
  62. Tunica Media of BV
    smooth muslce and is innervated from sypmathetic nervous system which causes vasoconstriction and lack mean vasodialation
  63. Tunica Adventitia of BV
    • outermost layer
    • has collagen fibers tha anchor BV to the surrounding structure
  64. Capillaries
    • Continuous Capillaries
    • Fenestrated Capillareis
    • Sinusoidal Capillaries
  65. Contiuous Capillaries
    • skin, muscle, and blood brain barrier
    • most common
    • least permeable
    • intercellular clefts- unjoined membrane
  66. Fenestrated Capillaries
    • large pores (fenestrations)
    • SI, Kidneys, Endocrine organs
  67. Sinusoidal Capillaries
    • leaky capillaries
    • most permeable
    • liver, bone marrow. adrenal medulla, spleen
    • Hepatic macrophages ( kuppfer cells)
  68. Veins
    • have much thinner tunica media and have larger lumens
    • cna hold up to 65% of blood volume at one time
    • are blood reservoirs
    • venus valves- prevents blood from pooling to ensure one way flow to heart
  69. Regulation of BP
    Neural regulation

    Chemical regulation
  70. Neural regulation of BP

    receptors involved
    • Baroreceptors- sense pressure in Arch of Aorta and bifurcation of carotids
    • monitors minute to minute fluctuations
    • affaerent signals are sent from aorta to the vagus (X) adn from the carotids to the glosspharyngeal (IX)
    • efferent signals are then sent to cardioregulatory systems and medulla oblongata
  71. Neural regulation of BP

    Centers involved
    • 1) vasomotor center
    • 2) Vagal Center
    • 3) Processes invovled
  72. Vasomotor Center
    • is sympathetic and recieve afferent signals from baroreceptors
    • if BP decreases it will efferently stimulate nerves in the thoracic region( T1-T2)
    • the release of norepinepherine or epinephrine one the Beta recpetors on the heart( increase CO and BP) and the alpha receptors on the blood vessels ( vasoconstriction to increase TPR)
  73. Vagal Center
    • in under parasympathetic control and it recieves afferent signals from the baroreceptors
    • -stimulated by an increase in BP
    • -sends effernent signals via the vagus which causes the release of Ach on the M2 receptors on the heart
    • -Decreases HR and CO
    • - lack of stimulation from barorecptors causes vasodialation and decrease in TPR
    • -this yeilds a decrese in BP
  74. Process of Regulation of BP
    • -an increase in BP will excite the Vagal center and inhibit the vasomotor center( cause decrese in BP)
    • - a decrese in BP will excite the Vasomotor center and inhibit the Vagal center ( cause increase in BP)
  75. Chemical Regulation (hormones) of BP
    • 1) ADH( anti-diuretic hormone)
    • 2) Renin
  76. ADH
    • vasopressin
    • 1) made by hypothalamus
    • 2) stored in Posterior pituitary
    • 3) release of ADH is triggered by a decrese in BP
    • 4) ADH targets the kidney tubule system ( cause more water reabsorbtion)
    • 5) increse BC, venous return, SV, CO, and therefor BP
  77. Renin
    • 1) made by kidneys
    • 2) triggered by decrese in BP
    • 3) once in the blood it cuases and enzyme to catalyze production of Angiotensin 2
    • - A2 targets adrenal gland and cause the adrenal cortex to release Aldosterone
    • - aldosterone cause incres in NaCl reabsorbtion in circulatory system ( water follow osmatically)
    • 4) increase H2O, BV, and therefor BP