review slides for a&p ii lecture exam 1
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Review Slides for A&P II Lecture Exam 1. Please note : These slides highlight the MAJOR points you will need to know, but they do not contain everything you need to know for the exam! Your Study Guide for this exam is your reference for what you need to know for the exam. - PowerPoint PPT PresentationTRANSCRIPT
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Review Slides for A&P II
Lecture Exam 1
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Please note: These slides highlight the MAJOR points you will need to know, but they do not contain everything you need to know for the exam!
Your Study Guide for this exam is your reference for what you need to know for the exam.
DO NOT RELY ONLY ON THESE SLIDES FOR YOUR EXAM PREPARATION - USE YOUR STUDY GUIDE!
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Blood
• straw colored• liquid portion of blood• 55% of blood
45% of blood (hematocrit)
globulins globulins
γ globulins
Transport, Stability of interstitial fluid, distribute heat, hemostasis, prevent infection
Volume ≈ 5L
-cytosis = abnormal increase in cell number -penia = abnormal decrease in cell number
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Blood Cell Counts(1 mm3 = 1 microliter, µl)
Number of RBCs reflects blood’s oxygen carrying capacity
#RBCs - Average is about 5 x 106 RBCs / µl
Anemia – deficiency of RBCs or Hb in RBCs; reduces O2-carrying capacity of blood
#WBCs - 5,000 – 10,000 per mm3 (or μl) of blood• leukopenia (-penia = deficiency of cell number)
• low WBC count• typhoid fever, flu, measles, mumps, chicken pox, AIDS
• leukocytosis (-cytosis = increase in cell number) • high WBC count• acute infections, vigorous exercise, great loss of body fluids
#Platelets - 150,000 – 500,000 per mm3 of blood (average ≈ 350,000 per µl)
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Red Blood Cell Turnover
Figure From: Martini, Anatomy & Physiology, Prentice Hall, 2001
The average life span of an RBC is about 120 days
Iron is carried in the blood by transferrin to red bone marrow, liver
Porphyrin from worn out RBCs is converted into biliverdin an bilirubin
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Blood Viscosity and Osmolarity
• Viscosity (thickness)– Resistance to flow of blood– Whole blood is about 5x as viscous as water– Changes in viscosity can put strain on the heart– Erythrocytosis (polycythemia) viscosity
• Osmolarity– Due to NUMBER of particles dissolved, not the type– Na+, proteins, erythrocytes– Osmolarity determines fluid flow between blood and
tissues
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Blood Clots
• After forming, blood clot retracts (~60%) and pulls the edges of a broken vessel together
• Platelet-derived growth factor stimulates smooth muscle cells and fibroblasts to repair damaged blood vessels
• Thrombus – abnormal blood clot• Embolus – blood clot moving through blood
Serum is the fluid expressed from a clot, i.e., the plasma minus clotting factors
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White Blood Cells
• granulocytes• neutrophils• eosinophils• basophils
• agranulocytes• lymphocytes• monocytes
Two major classes of leukocytes (WBC)
Neutrophils first to arrive at infections, phagocytic, 55% - 65% of leukocytes, elevated in bacterial infections
Basophils release histamine and heparin in allergic reactions
Eosinophils participate in allergic reactions, defend against parasitic worm infestations
Monocytes Precursors of macrophages, elevated in viral infections, inflammation
Lymphocytes important in immunity, produce antibodies, 25% - 33% of leukocytes
WBCs leave the bloodstream and enter tissues by the process of diapedesis
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Plasma Proteins
Albumins• most numerous plasma proteins (~55%)• ‘transport’ proteins• originate in liver• help maintain osmotic pressure of blood
Fibrinogen• originates in liver• plays key role in blood coagulation
Alpha and Beta Globulins• originate in liver• transport lipids and fat-soluble vitamins
Gamma Globulins• originate in lymphatic tissues (plasma cells)• constitute the antibodies of immunity
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Hemostasis• cessation of bleeding
Blood Vessel Spasm• triggered by pain receptors, platelet/endothelial cell release of various substances
• smooth muscle in vessel contracts (vascular spasm)
Platelet Plug Formation
• triggered by exposure of platelets to collagen
• platelets adhere to rough surface to form a plug
Blood Coagulation• triggered by cellular damage and blood contact with foreign surfaces
• blood clot forms
1. Vascular phase 3. Coagulation phase2. Platelet phase
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Blood Coagulation
Three cascades:
1. Instrinsic
2. Extrinsic
3. Common
Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001
Coagulation is an example of positive feedback~ 15 sec. ~ 3-6 min.
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Prevention of Coagulation• The smooth lining (endothelium) of blood vessels discourages the accumulation of platelets
• As a clot forms, fibrin absorbs thrombin and prevents the reaction from spreading
• Antithrombin (in plasma) interferes with the action of excess thrombin
*
• Plasmin digests blood clots (generated from plasminogen via the action of a plasma enzyme, kallikrein)
• Prostacyclin released by endothelial cells (aspirin)
• Some cells secrete heparin (an anticoagulant)
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Pathway of Blood Through Heart
Know This! Figure from: Saladin, Anatomy & Physiology, McGraw Hill, 2007
veins
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Heart Valves
Tricuspid Valve• right A-V valve• between right atrium and right ventricle• Attached to chordae tendineae
Bicuspid (Mitral) Valve• left A-V valve• between left atrium and left ventricle• Attached to chordae tendineae
Pulmonary Valve• semilunar valve• between right ventricle and pulmonary trunk
Aortic Valve• semilunar valve• between left ventricle and aorta
Atrioventricular (AV) valves
Heart valves ensure one-way flow of blood through the heart
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Wall of Heart
Three layers• endocardium
• forms protective inner lining• membrane of epithelial and connective tissues
• myocardium• cardiac muscle• contracts to pump blood
• epicardium• serous membrane (visceral pericardium)• protective covering• contains capillaries and nerve fibers
Know all the layers depicted in the diagram, and know their correct order.
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Cardiac Conduction System
Specialized myocardial cells.
Instead of contracting, they initiate and distribute impulses throughout the heart.
S-A node = Pacemaker
Pacemaker firing rates:
SA Node – 80-100 bpm
AV Node – 40-60 bpm
Purkinje – 30-40 bpm
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Electrocardiogram• recording of electrical changes that occur in the myocardium during the cardiac cycle
• used to assess heart’s ability to conduct impulses, heart enlargement, and myocardial damage
P wave – atrial depolarizationQRS wave – ventricular depolarizationT wave – ventricular repolarization
Important points to remember:
- Depolarization precedes contraction- Repolarization precedes relaxation
Three waves per heartbeat
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Regulation of Cardiac Rate
Parasympathetic impulses reduce CO (rate); sympathetic impulses increase CO (rate/strength)
**ANS activity does not ‘make’ the heart beat, it only regulates its beat
Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2004
Tachycardia > 100 bpmBradycardia < 60 bpm
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Summary of Factors Influencing CO – Table Form
Effect on CO Affect HR, SV, or both? How?
INCREASE
Atrial reflex HR HR
Sympathetic stimulation HR and SV HR, SV
Epinephrine, thyroxin HR and SV HR, SV
Preload (Frank-Starling Mechanism)
SV EDV, ESV
Contractility SV ESV
Venous return, CVP HR and SV Preload, atrial reflex
Ca2+ (hypercalcemia) SV Contractility, ESV
Temperature HR HR
DECREASE
Parasympathetic stimulation (vagus nerves)
HR HR
Afterload SV ESV
Ca2+ (hypocalcemia) SV Contractility, ESV
K+ (hyperkalemia) HR, SV Arrhythmia, cardiac arrest
K+ (hypokalemia) HR, SV Arrhythmia, cardiac arrest
Temperature HR HR
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Coronary Circulation
Coronary vessels fill mainly during diastole
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Systole and Diastole
Atrial Systole/Ventricular Diastole Atrial Diastole/Ventricular Systole
Systole = contraction; Diastole = relaxation
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Review of Events of the Cardiac CycleFigure from: Martini, Anatomy & Physiology, Prentice Hall, 2004
1. Atrial contraction begins
2. Atria eject blood into ventricles
3. Atrial systole ends; AV valves close (S1)
4. Isovolumetric ventricular contraction
5. Ventricular ejection occurs
6. Semilunar valves close (S2)
7. Isovolumetric relaxation occurs
8. AV valves open; passive atrial filling
S1
S2
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Factors Affecting Cardiac Output
Contractility
Afterload
CVP
CO
HR
SV
ESV
EDV
ANSParasympathetic Sympathetic
CO – Cardiac Output (~5L/min). Dependent upon Stroke Volume (SV; ~70 ml) and Heart Rate (HR)
CVP – Central Venous Pressure; Pressure in vena cava near the right atrium (affects preload; Starling mechanism)
Contractility – Increase in force of muscle contraction without a change in starting length of sarcomeres
Afterload – Load against which the heart must pump, i.e., pressure in pulmonary artery or aorta
ESV – End Systolic Volume; Volume of blood left in heart after it has ejected blood (~50 ml)
EDV – End Diastolic Volume; Volume of blood in the ventricle before contraction (~120-140 ml)
= EDV - ESV
= HR x SV
Figure adapted from: Aaronson & Ward, The Cardiovascular System at a Glance, Blackwell Publishing, 2007
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Regulation of Cardiac OutputRecall: SV = EDV - ESV
Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001
Be sure to review, and be able to use, this summary chart
CO = heart rate (HR) x stroke volume (SV)
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The Frank-Starling Mechanism
• Amount of blood pumped by the heart each minute (CO) is almost entirely determined by the venous return
• Frank-Starling mechanism – Intrinsic ability of the heart to adapt to
increasing volumes of inflowing blood– Cardiac muscle reacts to increased stretching
(venous filling) by contracting more forcefully– Increased stretch of cardiac muscle causes
optimum overlap of cardiac muscle (length-tension relationship)
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Comparison of Skeletal and Cardiac Muscle
Cardiac and skeletal muscle differ in:
1. Nature of action potential
2. Source of Ca2+
3. Duration of contraction
Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001
Ca2+ ions enter from
1. Extracellular fluid (20%)
2. Sarcoplasmic reticulum (80%)
So, Cardiac muscle is very sensitive to Ca2+ changes in extracellular fluid
Recall that tetanic contractions usually cannot occur in a normal cardiac muscle cell
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Overview of the Cardiovascular System (CVS)
CVS = Heart + Blood Vessels
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Overview of Blood Vessels
Figure from: Saladin, Anatomy & Physiology, McGraw Hill, 2007
Large/med sized arteries regulate blood flow to organ systems; high press.
Arterioles regulate blood flow to capillary beds
Capillaries are site of fluid exchange
Arteries and veins are constructed of three layers: 1) tunica intima 2) tunica media 3) tunical externa
Veins return blood to heart, hold most of body’s blood and have valves; low press.
3 types:
- continuous (muscle)
- fenestrated (endocrine glands, kidney, small intestine)
- sinusoids (liver, spleen, bone marrow)
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Capillaries• smallest diameter blood vessels (fit 1 RBC at a time)• extensions of inner lining of arterioles• walls consist of endothelium and basement membrane only – NO smooth muscle• semipermeable (plasma fluid can escape, but not proteins)
3 types:
- continuous (muscle)
- fenestrated (endocrine glands, kidney, small intestine)
- sinusoids (liver, spleen, bone marrow)
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Exchange in the Capillaries• major mechanism involved in exchange of solutes is diffusion• substances move in and out along the length of the capillaries according to their respective concentration gradients• Fluid movement in systemic capillaries is determined by two major factors 1. hydrostatic pressure; varies along portions of capillary 2. osmotic pressure; remains about the same along the length of the capillary
Excess tissue fluid is drained via lymphatics
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Arterial Blood Pressure
Blood Pressure – force the blood exerts against the inner walls of the blood vessels
Arterial Blood Pressure• rises when ventricles contract• falls when ventricles relax• systolic pressure – maximum pressure• diastolic pressure – minimum pressure
Pulse pressure – difference between systolic and diastolic pressures (systolic : diastolic : pulse pressure ~ 3:2:1)
- Pulse pressures usually rise with age because of an increase in blood vessel resistance (arteriosclerosis)
Recall: Blood Flow (CO) Pressure / Resistance
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Mean Arterial Pressure
Mean Arterial Pressure (MAP) – Average effective pressure driving blood flow through the systemic organs
MAP = CO x Total Peripheral Resistance (TPR)
**Thus ALL changes in MAP result from changes in either cardiac output or peripheral resistance
If CO increases, MAP ? If TPR decreases, MAP ?
If TPR decreases, what must be done to keep MAP the same?
If blood volume decreases, what must be done to keep MAP the same?
MAP can be estimated by the equation:
diastolic bp + (pulse pressure / 3) (Roughly 1/3 of the way between systolic and diastolic pressures)
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Factors Affecting Blood Pressure (MAP)
Contractility
Afterload
CVP
CO
HR
SV
ESV
EDV
ANSParasympathetic Sympathetic
MAP – Mean Arterial Pressure = Average effective pressure driving blood flow through the systemic organs
**The MAP is dependent upon CO and TPR, i.e., MAP = CO x TPR
TPR – Total Peripheral Resistance; depends upon *blood vessel radius, vessel length, blood viscosity, and turbulence
MAP (BP) TPR1/radius4; Vessel length; Viscosity; Turbulence
Figure adapted from: Aaronson & Ward, The Cardiovascular System at a Glance, Blackwell Publishing, 2007
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Factors Affecting Blood Pressure (MAP)
MAP = X TPR 1 / radius4
Vessel length
Viscosity Turbulence
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Autoregulation of Blood Flow/Pressure
• Local vasodilators increase blood flow– Decreased O2 (except pulmonary circulation) or
increased CO2
– Increase in lactic acid production
– Release of nitric oxide (NO)
– Increased K+ or H+
– Mediators of inflammation (histamine, NO)
– Elevated local temperature
• Local vasoconstrictors decrease blood flow– Prostaglandins, thromboxanes (released by activated
platelets and WBCs)
– Endothelins released by damaged endothelial cells
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Central Venous Pressure• Central Venous Pressure = pressure in the vena cava near the right atrium (~ 2-4 mm Hg)
• determines the filling pressure of the right ventricle- determines the EDV of the right ventricle which- **determines ventricular stroke volume (Frank-Starling)
• affects pressure within the peripheral veins
• weakly beating heart causes an increase in central venous pressure (backup of blood)
• increase in central venous pressure causes blood to back up into peripheral veins
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Hepatic Portal VeinHepatic portal vein drains one set of capillaries and leads to another set of capillaries before it becomes a vein
Note that veins in the abdominal cavity drain into the hepatic portal vein
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Aorta and Its Principal Branches
**Need to know this table; if I give you an artery, you need to know which branch of the aorta it arises from
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Major Veins - Upper Limb and Shoulder
*
*
*
*
***
Median cubital vein is often used to draw blood (venipuncture)*
**
(deep)
(superficial)
(superficial)
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Arteries to Neck, Head, and Brain
*
*
*
*
* *
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Major Veins of the Brain, Head, and Neck
*
*
*
*
*
External jugular v. drains blood from face, scalp, and superficial neck regions
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Arteries to Shoulder and Upper Limb
*
**
*
**
= pulse points
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Cerebral Arterial Circle• Also called the Circle of Willis• Formed by anterior and posterior cerebral arteries, which join the internal carotid and basilar arteries
Know the names of the vessels that make up the cerebral arterial circle