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327 Cards in this Set
- Front
- Back
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Overview of the Cardiovascular System |
Cardiovascular system: - Heart and blood vessels Circulatory system: - Heart, blood vessels, and the blood - 2 major divisions: ==> Pulmonary Circuit ==> Systemic Circuit |
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Cardiovascular System Circuit Components |
-Heart: pumps blood -Arteries: O2 rich blood to tissues (systemic side) -Veins: O2 poor blood back to heart (systemic side) -Capillaries: small vessels (5-10nm) between arterioles and venules ==> Site of O2 and CO2 exchange ==> Nutrient discharge and waste uptake |
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Two Major Divisions of Circulatory System: Pulmonary Circuit |
-Right ventricle pumps blood to lungs ==> Carries blood to lungs for gas exchange and back to heart
-Right side of heart ==> Lesser oxygenated blood arrives from inferior and superior venae cave ==> Blood send to lungs via pulmonary trunk |
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Two Major Divisions of Circulatory System: Systemic Circuit |
- Left ventricle pumps blood to rest of the body ==> Supplies oxygenated blood to all tissues of the body and returns it to the heart -Left side of the heart ==> Fully oxygenated blood arrives from lungs via pulmonary veins ==> Blood sent to all organs of the body via aorta |
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Position, Size, and Shape of the Heart |
-Heart located in mediastinum, between lungs -Base: wide, superior portion of heart, blood vessels attach here -Apex: inferior end, tilts to the left, tapers to point -3.5in. wide at base, 5 in. from base to apex, and 2.5 in. anterior to posterior; weighs 10 ounces |
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Pericardium |
-Double-walled sac that encloses the heart (isolates heart from other organs) ==> Allows heart to beat without friction, provides room to expand, yet resists excessive expansion ==> Anchored to diaphragm inferiorly and sternum anteriorly |
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Pericardium layers |
Parietal pericardium (pericardial sac): out wall of sac - Superficial fibrous layer of dense irregular CT - Depp, thin serous layer Visceral pericardium (epicardium): heart covering - Serous lining of sac turns inward at base of heart to cover the heart surface Pericardial cavity: space inside of pericardial sac filled with 5 - 30mL of pericardial fluid |
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Pericarditis |
-Inflammation of pericardium -Causes: ==> Infection (viral/bacterial) ==> Heart attack ==> Trauma to chest ==> Swelling/inflammation of heart muscle ==> Radiation to chest -Painful -Treatment: ==> NSAIDS (ibuprofen to decrease swelling) ==> Antibiotics ==> Pericardiocentesis (stick need in heart to remove extra fluid, relives symptoms) |
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The Heart Wall: Epicardium |
Outermost layer (visceral pericardium) - Serous membrane covering heart - Mainly simple squamous epithelium overlying a thin layer of areolar (loose) CT - Thick layer of adipose tissue in some places - Coronary blood vessels travel through this layer |
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The Heart Wall: Endocardium |
Innermost layer - Smooth inner living of heart and blood vessels - Simple squamous epithelium overlying a thin layer of areolar (loose) CT - Covers the valve surfaces and is continuous with endothelium of blood vessels |
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The Heart Wall: Myocardium |
Middle layer - Cardiac muscle: Muscle spirals (wringing motion) - Fibrous skeleton (collagenous and elastic fibers) ==> Located mostly in wall between heart chambers, around valves ==> Structural support (cardiocytes, valves, and openings of vessels) ==> Electrical insulation between atria and ventricles; important in timing and coordination of contractile activity |
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Heart: Internal Anatomy |
Four chambers: - Right and left atria ==> Superior chambers ==> Blood returning to heart - Right and left ventricles ==> Two inferior chambers ==> Pump blood into arteries -Interatrial septum (dense CT): separates atria -Pectinate muscles: ridges in right atrium and auricles -Interventricular septum (dense CT): separates ventricles -Trabeculae carneae: ridges in both ventricles -Papillary muscles -Chordae tendinae: connect AV valves to papillary muscles |
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Anatomical Heart Defects |
-Patent ductus arteriosus ==> Duct fails to close between aorta and pulmonary trunk ==> Allows blood to go around baby's lungs before birth ==> Diagnosed by echocardiogram -Patent foramen ovale (PFO) ==> Incomplete closure between right atria and left atria ==> 1 in 4 adults have PFO -Septum abnormalities ==> Atrial or ventricular (Down's syndrome - ventricular septal defect) ==> Partial or complete Surgery required (around 6 months postnatal) |
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Valves: Atrioventricular (AV) |
Atrioventricular (AV) : flow into ventricles - Right is tricuspid valve - Left is mitral or bicuspid valve Function: - Blood into ventricles - Dense CT is stiff - "One way" flow - Attachment by chordae tendinae prevents regurgitation |
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Valves: Semilunar |
Semilunar valves : flow into arteries - Pulmonary semilunar valve: right ventricle to pulmonary trunk - Aortic semilunar valve: left ventricle to aorta Function: - Blood into great vessels - Pulmonary: right ventricle to pulmonary trunk - Aortic: left ventricle to aorta (coronary blood flow) - "One way" flow |
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Valve Disease or Insufficiency: Valvular stenosis |
- Valve scarring causes stiff cusps, restricts valve opening - Congenital or result of medical condition (Rheumatic fever - scarlet fever; strep throat) - Often detected as a heart murmur - Can lead to heart failure |
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Valve Disease or Insufficiency: Mitral Valve Prolapse (MVP) |
- Mitral valve bulges intro atrium during ventricular contraction - Blood leaks back to left atrium (mitral regurgitation) - Causes fatigue, shortness of breath, chest pain - May be genetic (Mainly thin women who may have minor chest wall deformities, scoliosis, or other disorders) |
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Blood Flow Through the Heart |
1. Blood enters right atrium from superior and inferior venae cavae 2. Bloodin right atrium flows through rightAVvalve into right ventricle 3. Contractionof right ventricle forcespulmonaryvalve open 4. Bloodflows through pulmonary valveintopulmonary trunk 5.Bloodis distributed by right and leftpulmonaryarteries to the lungs, where itunloadsCO2 and loads O2 6. Bloodreturns from lungs via pulmonaryveinsto left atrium 7. Bloodin left atrium flows through left AVvalveinto left ventricle 8. Contractionof left ventricle (simultaneous with step 3 ) forces aortic valve open 9. Bloodflows through aortic valve intoascendingaorta 10. Bloodin aorta is distributed to every organin the body, where it unloadsO2 and loads CO2 11. Bloodreturns to heart via venae cavae |
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Blood Flow Through Chambers: Relaxation |
Ventricular diastole - Pressure drops inside the ventricles - Semilunar valves close as blood attempts to back up into ventricles from the vessels - AV valves open - Blood flows from atria to ventricles |
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Blood Flow Through Chambers: Contraction |
Ventricular systole - AV valves close as blood attempts to back up into the atria - Pressure rises inside of the ventricles - Semilunar valves open and blood flows into great vessels |
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Arterial Supply: Left Coronary Artery (LCA) |
Anterior inter-ventricular branch(or LAD): - Supplies both ventricles and 2/3 of the interventricular septum Circumflex branch: - Left side of the heart in coronary sulcus - Gives off left marginal branch and then ends on the posterior side of the heart - Supplies left atria and posterior wall of left ventricle |
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Arterial Supply: Right Coronary Artery (RCA) |
Supplies right atrium, and SA node Right marginal branch: - Supplies lateral aspect of right atrium and ventricle Posterior interventricular branch: - Supplies posterior walls of ventricles |
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Myocardial Blood Supply |
-Blood flow to the heart muscle during ventricular contraction is slowed, unlike the rest of the body -Two reasons: ==> Contraction of the myocardium compresses the coronary arteries and obstructs blood flow ==> Opening of the aortic valve flap during ventricular systole covers the openings of the coronary arteries blocking blood flow into them -During ventricular diastole, blood in the aorta surges back toward the heart and into the opening of the coronary arteries ==> Blood flow to the myocardium increases during ventricular relaxation |
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Angina Pectoris |
- Partial obstruction of coronary blood flow - Causes some chest pain - Pain is due to ischemia, activity-dependent Treatment: - Statins (decrease cholesterol), cardiac rehab - Vasodilators (Nitroglycerin, beta blockers) - Possible surgery (angioplasty, stents) |
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Myocardial Infarction (MI) - "Heart Attack" |
- Interruption of blood supply to the heart from a blood clot or fatty deposit (atheroma) can cause death of cardiac cells within minutes - Severe chest pain that radiates to left arm - About 27% of all deaths in US - Some protection from MI is provided by arterial anastomoses which provides an alternative route of blood flow (collateral circulation) within the myocardium ==> Collateral circulation: Interconnections between arterial vessels, known as anastomosis, enables tissue perfusion by multiple routes (if one route is blocked, blood can still reach tissue by other route) Treatment: - Statins, cardiac rehab - Surgery (angioplasty, stents) - Vasodilators (Nitro, beta blockers) - Anticoagulants (heparin, clopidogrel, coumadin, aspirin) - Class IV cardiac drugs (Ca2+ channel blockers) - Adenosine related cmpds (dipyridamole) |
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Nitroglycerin |
- Dilate coronary arteries to increase blood flow, relieve chest pain, and reduce the workload on the heart ==> Partial obstruction of coronary blood flow causes ischemia (chest pain) - Mimics nitric oxide, an endogenous nitrate released by endothelial cells (vasodilation) - Administration: tab (SL), lotion or dermal patch, injection (critical/ER) |
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Structure of Cardiac Muscle |
Cardiocytes: - Striated, short, thick - Branched cells (Y shaped_ - Lots of mitochondria - Larger T tubules than skeletal muscle - Single nucleus Intercalated discs (3 sub-structures): - Interdigitating folds - Mechanical (tight) junctions - Electrical junctions (gap junctions) |
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Metabolism of Cardiac Muscle |
Aerobic respiration (ATP): - Rich in myoglobin and glycogen - Huge mitochondria: fill 25% of cell Adaptable to organic fuels: - At rest: ==> Fatty acids (60%) ==> Glucose (35%) ==> Ketones, lactic acid, and amino acids (5%) Fatigue resistant |
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CNS Control of Heart: Parasympathetic Division |
Preganglionic is vagus nerve (CN X) - Origin in medulla oblongata ==> Cardio-inhibitory center - Branches "wander" to targets ==> Heart, lung, intestine - Synapse at target - "Short" postganglionic relapse acetylcholine ==> Inhibitory Pharmacology: - Preganglionic (Ach), nicotinic receptors) - Postganglionic: usually near target; always Ach (muscarinic receptors) |
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CNS Control of Heart: Sympathetic Division |
Short preganglionic, long postganglionic fibers Synapse on postganglionic in cervical ganglia - "Long" path to heart - Release norepinephrine ==> Excitatory Pharmacology: - Preganglionic (Ach, nicotinic receptors) - Postganglionic: ==> Mostly norepinephrine (NE) (alpha, beta adrenoceptors) ==> Some Ach (muscarinic receptors) |
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Nerve Supply to Heart |
Origin: - Sympathetic: lower cervical to upper thoracic segments of spinal cord - Parasympathetic: Nuclei of Vagus nerves (medulla oblongata) Innervation: - Sympathetic: SA and AV nodes, atrial and ventricular myocardium, aorta, pulmonary trunk, and coronary arteries - Parasympathetic: R Vagus: SA node - L Vagus: AV node (Little or no myocardium innervation) Result: - Sympathetic: Increase HR, increase contraction strength, dilates coronary arteries (increase myocardial blood flow) - Parasympathetic: Decreases HR Speed of Response: - Sympathetic: slow - Parasympathetic: fast |
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'Fast' Receptors |
Fast (ionotropic): - Ligand-gated receptors (ion channel opens directly) - Excitatory (Increases Na+) or inhibitory (Increases Cl-) - Nerve signals open voltage-gated Ca2+ channels in - Ach receptors trigger opening of Na+ channels producing local potential (postsynaptic potential) - AP in postsynaptic neuron is triggered (parasympathetic) |
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'Slow' Receptors |
Slow (metabotropic): - G-protein coupled receptors (GPCRs) (2nd messenger system - extra step) - Binding of NE causes the G-protein to dissociate from receptor - G-protein binds: ==> Phospholipase: Increase Ca2+ via IP3 ==> Adenylate cyclase: ATP -> cAMP - cAMP induce several alternative effects in the cell |
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Adrenoceptor (NE) Pharmacology |
Norepinephrine (NE): - β1 (heart): Increase cAMP ==> Increases HR ==> Increases contraction force - β2 (lung): Increase cAMP ==> Bronchodilation (airways dilate in lung) - α1 (arterioles): Increase Ca2+ (IP3) ==> Vasoconstriction - α2 (diffuse): Decrease cAMP ==> Pancreas: Decrease insulin secretion ==> Platelets: Increases clotting |
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Cholinergic (Ach) Receptor Pharmacology |
Nicotinic Ach receptors: - Ionotropic ('fast') - Ligand-gated (increases Na+ conductance) - Excitatory Muscarinic Ach receptors (M2): - Metabotropic ('slow') - Increases K+ conductance (inhibitory at SA node) |
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CNS Control of Heart: Sympathetic Nerves |
- Innervate SA node ==> Increases HR (up to 230bpm) - Innervate ventricular myocardium ==> Increases contractile force - pumping action |
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CNS Control of Heart: Parasympathetic Nerves |
- Right vagus branch to SA node - Left vagus branch to AV node ==> Maintains vegal tone and HR at 70-8-bpm (slight inhibition) ==> Ach opens K+ channels causing hyper-polarization |
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Cardiac Electrophysiology: Conduction System |
Coordinates the heartbeat - Internal pacemaker and conduction pathways Generates and conducts rhythmic electrical signals in the following order: - Sinoatrial (SA) node (pacemaker): modified cardiocytes - Signals spread throughout atria - Atrioventricular (AV) node ==> Electrical gateway to the ventricles ==> Fibrous skeleton - insulator - Atrioventricular (AV) bundle (bundle of His) ==> Bundle forks into right and left bundle branches - Purkinje fibers ==> Nerve-like processes spread throughout ventricular myocardium 1. SA node fires 2. Excitation spreads through atrial myocardium 3. AV node fires 4. Excitation spreads down AV bundle 5.Purkinje fibers distribute excitation through ventricular myocardium |
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Cardiac Rhythm: Sinus rhythm |
Control of resting heart rate (rhythmicity) - Sinus rhythm (SA node) ==> Intrinsic 'pacemaker' in SA node (60-100bmp) ==> Activity modulated by CNS --------: Parasympathetic NS (Ach) --------: Sympathetic NS (NE) |
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Cardiac Rhythm: Ectopic focus |
Another part of heart fires before the SA node - Caused by hypoxia, electrolyte imbalance, or caffeine, nicotine, and other drugs - Nodal rhythm: if SA node is damaged, heart rate is set by AV node (40-50bpm) (P wave is absent in ECG - no SA node activity) - Intrinsic ventricular rhythm: if both SA and AV nodes are not functioning (20-40bpm) |
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Arrhythmia |
Any abnormal cardiac rhythm - Failure of conduction system to transmit signals (heart block) ==> Bundle branch block ==> Total heart block (damage to AV node): Asynchronous ventricular contraction (Partial: some damage to AV node or bundle - irregular QRS internals) (atria and ventricles in different rhythms) |
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Cardiac Arrhythmia: Atrial flutter |
Ectopic focci in atria - Atria beat 200 to 400 times per minute - Atrial fibrillation (action potential keep circulating and causing heart to beat very fast) |
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Atrial Fibrillation |
Most common arrhythmia
- Atrial fibrillation: around 2.2 million Americans - "atrial flutter" hyperactive atrial ectopic foci (200-400bpm) aka supraventricular tachycardia (increased HR) (SVT) - Atrial fibrillation may lead to stroke (since atria ins't pushing blood right away, it can clot) - 'Noisy' or Sawtooth patter ECG Treatment: - Cadioversion (electrical procedure or medicine) - Drugs: variable; slow heart (digitalis, Flecanide, beta blockers, amiodarone) |
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Cardiac Arrhythmia: Premature ventricular contractions (PVC) |
- Ventricles depolarize before electrical signal comes from the SA node - Results in a wider QRS complex (wider, deeper pouch if formed in ECG) - Caused by stimulants, stress, lack of sleep, hypoxia, electrolyte imbalance |
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Cardiac Arrhythmia: Ventricular fibrillation |
- Serious arrhythmia caused by electrical signals reaching different regions at widely different times ==> Heart cannot pump blood (no coronary or brain perfusion) ==> ECG: QRS is absent ("bucket of worms") (twitching randomly - no blood flow/pushing out to rest of body) ==> Kills quickly if not stopped --------:> Defibrillation: strong electrical shock whose intent is to depolarize the entire myocardium, stop the fibrillation, and reset SA nodes to sinus rhythm |
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Electrical and Contractile Activity of the Heart |
Cycle of events in heart: - Systole: atrial or ventricular contraction - Diastole: atrial or ventricular relaxation |
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SA Node Excitability |
SA node cells have unstable resting membrane potential called 'pacemaker potential' Pacemaker potential - Slow Na+ influx - Slow depolarization (-60mV) Action potential - At threshold of -40mV - Depolarizes to 0 mV ==> Fast Ca2+ channels open and Ca2+ goes in - Repolarizing phase ==> K+ channels open - K+ leaves ==> K+ channels close at -60mV; pacemaker starts over Each cycle generates a heart beat - SA node at rest fires at 0.8 sec, about 75bpm |
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Cardiac Rhythm |
Sinus rhythm - Intrinsic rate set by SA node at 60 - 100 bpm - Vagal tone maintains at 70 -80 bpm in adults |
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Impulse Conduction to the Myocardium |
- SA node signal spreads at 1m/sec through atria - AV node slows signal to 0.05m/sec ==> Thin myocytes, few gap junctions ==> Delays signal by 100msec allowing ventricles to fill - AV bundle and Purkinje fibers ==> Signal at 4mm/sec to ventricles - Ventricular impulse begins at apex and progresses upwars ==> Spiral arrangement of myocytes twists ventricles slightly |
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Cardiocyte Action Potential |
1) Voltage-gated Na+ channels open 2) Rapid depolarization (Na+ in) 3) Voltage-gated Na+ channels inactivate ('close') 4) 'Slow' voltage-gated Ca2+ channels open (activate Ca2+ channels on SR) 5) Ca2+ channels close, voltage-gated K+ channels open causing repolarization and return to -90mV |
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Refractory Period |
-Period of resistance to stimulation -Absolute refractory period: ==> Na+ channels are open or inactivated ==> No stimulus will trigger AP -Relative refractory period: ==> K+ channels are still open ==> Strong stimuli trigger AP -Cardiomyocytes have long refractory periods ==> Allow synchrony during long ventricular contractions |
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Skeletal vs. Cardiocyte Action Potentials |
Skeletal muscle APs are very rapid (around 5ms) - Capable of incomplete and complete tetanus - Incomplete tetanus: 20-40 stimuli per second (each new stimulus arrives before previous twitch is over, new twitch "rides piggy-back" on previous generating higher tension) - Complete tetanus: 50+ stimuli per second, so much tension, line flattens Cardiac APs are prolonged (around 200 ms): - Long Ca2+ channels opening - Long K+ channel opening - Long refractory period |
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Electrocardiogram |
Sum of electrical activity in myocardium cells (sum of all action potentials of heart at a given time) - Recorded by surface electrodes on arms, legs and chest (only measure electrical activity in the heart, not mechanical) Key diagnostic for heart abnormalities |
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Electrocardiogram: P wave |
- SA node fires, atria depolarize and contract - Atrial systole begins 100 ms after SA signal (first small wave) |
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Electrocardiogram: QRS Complex |
- Ventricular depolarization - Complex shape of spike due to different thickness and shape of the two ventricles (high, acute peak) |
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Electrocardiogram: ST Segment |
ST segment - ventricular systole - Plateau in myocardial action potential (segment right after QRS complex) |
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Electrocardiogram: T wave |
- Ventricular repolarization and relaxation (Second small wave) |
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Electrocardiogram Process |
1) Atrial depolarization begins 2) Atrial depolarization complete (atria contracted) - P wave 3) Ventricles begins to depolarize at apex; atria repolarize (atria relaxed) 4) Ventricular depolarization complete (ventricles contracted) - QRS complex => ST segment 5) Ventricles begin to repolarize at apex 6) Ventricular repolarization complete (ventricles relaxed) - T wave |
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3-Lead and 12-Lead ECG |
Each lead represents a different view/angle of the heart (anterior, posterior, etc.) - The more leads, the better the diagnosis (if there's something wrong with a portion of the heart, one of the leads will be able to capture it) |
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Diagnostic Value of ECG |
- Conduction abnormalities & arrhythmias
==> Rx: anti-arrhythmic drugs - Myocardial infarction (MI): abnormal ST segments & T waves ==> Acute MI: segment elevation ==> Post-MI (chronic): enlarged Q waves, ST segment depression - Heart enlargement: enlarged QRD ==> Rx: Antihypertensives (ACE inhibitors, diuretics, vasodilators) - Electrolyte imbalance (Na+, K+, Ca2+) ==> supplements or antidiuretics ==> excess K+: large T waves is elevated - Hormone imbalance ==> Rx: Replacement therapy - Atrial scarring: Primary bundle block ==> Long PQ (PR) segment |
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Interpretation of ECG: Enlarged P wave |
- Atrial hypertrophy, often a result of mitral valve stenosis
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Interpretation of ECG: Missing or inverted P wave |
- SA node damage; AV node has taken over pacemaker role |
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Interpretation of ECG: Two or more P waves per cycle |
-Extrasystole; heart block |
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Interpretation of ECG: Extra, misshapen, sometimes inverted QRS not preceded by P wave |
Premature ventricular contraction (PVC) -Extrasystole |
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Interpretation of ECG: Enlarged Q wave |
- MI |
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Interpretation of ECG: Enlarged R wave |
Ventricular hypertrophy |
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Interpretation of ECG: Abnormal T waves |
Flattened in hypoxia; elevated in hyperkalemia (K+ excess) |
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Interpretation of ECG: Abnormally long PQ segment |
Scarring of atrial myocardium, forcing impulses to bypass normal conduction pathways and take slower alternative routes to AV node
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Interpretation of ECG: Abnormal ST segment |
-Elevated above baseline in MI -Depressed in myocardial hypoxia |
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Cardiac Cycle Overview |
The cardiac cycle: one complete cycle of contraction and relaxation in all 4 chambers of the heart - Simple scheme: ==> Systole (contraction) of chambers ==> Diastole (relaxation) of chambers Cardiac cycle dynamics are driven by pressure changes |
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Cardiac Cycle |
- Late diastole: both sets of chambers relaxes. Passive ventricular filling - Atrial systole: Atrial contraction foces a small amount of additional blood into ventricles - EDV = end-diastolic volume: The max amount of blood in ventricles acorns at the end of ventricular relaxation (EDV = 135mL) - Isovolumetric ventricular contraction: first phase of ventricular contraction pushes AV valves closed by does not create enough pressure to open semilunar valves - Ventricular ejection: as ventricular pressure rises and exceed pressure in the arteries, the semilunar valves open and blood is ejected - ESV = end-systolic volume, or minimum amount of blood in ventricles (ESV = 65mL) - Isovolumic ventricular relaxation: as ventricles relax, pressure in ventricles drops, blood flows back into cups of semilunar valves and snaps them closed - Late diastole again (cycle is continuous) |
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Principles of Pressure and Flow |
Two main variables govern fluid movement: - Pressure causes a fluid to flow: ==> Pressure gradient - pressure difference between two points - Resistance opposes fluid flow ==> Caused by contact (friction) between blood and vessel wall ==> Ventricular pressure must rise above the resistance for blood to flow into great vessels |
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Pressure Gradients and Flow |
Fluid flows only if there's a pressure gradient - Flow from high pressure to low pressure Events occurring on left side of heart ==> Ventricle relaxes and expands (decreases pressure) - Blood flows into left ventricle ==> Ventricle contracts (increases pressure) - AV valves close (1st heart sound), aortic valve opens Opening and closing of valves are governed by these pressure changes - AV valves loose when ventricles relaxed - Semilunar valves under pressure from blood in vessels when ventricles relaxed |
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Cardiac Cycle Phases |
Ventricular filling - 'quiescent period' - Rapid filling (blood enters very quickly) - Diastasis (slow filling of ventricle) (P wave occurs at the end of diastasis) - Atrial systole (Atria contract) (Passive filling during atrial and ventricular diastole) Atrial contraction Isovolumetric contraction 1st Heart sound: closing of AV valves Ventricular ejection (stroke volume) Isovolumetric relaxation 2nd Heart sound: closing of aortic valve |
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Isovolumetric Contraction |
- End-diastolic Volume (EDV): blood in each ventricle at end of ventricular filling (135mL) - Atria repolarize and relax - Ventricles depolarize, create QRS complex and begin to contract - AV valves close (1st Heart Sound, S1) - "Isovolumetric" because even though the ventricles contract, they do not eject blood ==> Because pressure in aorta (80mmHg) and in pulmonary trunk (10mmHg) is still greater than in ventricles - Cariocytes exert force, but with all four valves closed, the blood cannot go anywhere |
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Ventricular Ejection |
- Ventricular pressure > arterial pressure (semilunar valves open) - Rapid ejection - Stroke volume (SV) = blood ejected in each hear beat - End-diastolic volume (EDV) - the 135mL of blood in ventricle at end of diastole - End-systolic volume (ESV) - the 65mL of blood left behind ==> SV = End Diastolic Volume - End Systolic Volume ==> 135mL - 65mL = 70 mL (rest) ==> SV/EDV = Ejection fraction (around 54%) ==> As high as 90% in vigorous exercise |
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Isovolumetric Relaxation |
- Early ventricular diastole - When T wave ends and ventricles begin to expand - Semilunar valves close (2nd Heart Sound, S2) ==> Slight pressure rebound (dicrotic notch) - "Isovolumetric" because semilunar valves are closed and AV valves have not yet opened ==> Ventricles expand but do not fill (no change in volume) - When AV valves open, ventricular filling begins again |
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Ventricular Volume Changes |
End-systolic volume (ESV) ----------- 65mL Atrial diastole ----------------------------- +40mL Atrial systole ------------------------------ +30mL End-diastolic volume (EDV) ---------- 135mL Stroke volume (SV) ----------------------- -70mL End-systolic volume (ESV) ------------- 65mL *Both ventricles must eject same blood volume |
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Cardiac Pathologies: Congestive Heart Failure (CHF) |
- Failure of either ventricle to eject blood effectively (heart weakened by MI, hypertension, valvular insufficiency, etc.) ==> Left ventricular failure: blood backs up into the lungs causing pulmonary edema (Shortness of breath or sense of suffocation) 1. Right ventricular output exceeds left ventricular output 2. Pressure backs up 3. Fluid accumulates in pulmonary tissue ==> Right ventricular failure: blood backs up in the vena cava causing systemic or generalized edema (Enlargement of the liver, dissension of jugular veins, swelling of the fingers, ankles, and feet) 1. Left ventricular output exceeds right ventricular output 2. Pressure backs up 3. Fluid accumulates in systemic tissue - Eventually leads to total heart failure |
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Heart Sounds |
- Auscultation: listening to sounds made by body - First heart sounds (S1): louder and longer "lubb", occurs with closure of AV valves - Second heart sound (S2): softer and sharper "dump", occurs with closure of semilunar valves - S3: rarely heard in people < 30 ("rubs" and "murmurs") |
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Cardiac Output |
- Amount ejected by ventricle in 1 minute - Cadiac output = HR * SV ==> About 4 to 6 L/min at rest ==> A RBC leaving the left ventricle will arrive back at the left ventricle in about 1 minute ==> Vigorous exercise increases cardiac output to 21 L/min for a fit person and up to 35 L/min for a world-class athlete - Cardiac reserve: the difference between a person's maximum and resting cardiac output ==> Increase with fitness, decrease with disease |
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Heart Rate |
Pulse: surge of pressure in artery - Infants have HR of 120-150bpm - Young adult females average 72to 80bpm - HR rises again in the elderly (Why?) (Heart isn't able to pump as effective - stroke volume is lower) Tachycardia: resting adult HR > 100bpm - Stress, anxiety, drugs, heart disease, or fever Bradycardia: resting adult HR < 60bpm - In sleep, low body temp., and trained athletes Positive chronotropic agents: factors that increase HR Negative chronotropic agents: factors that decrease HR |
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Chronotropic Effects of the ANS Overview |
- Autonomic nervous system does not initiate the heartbeat, it modulates rhythm and force - Cardiac centers in medulla oblongata initiate autonomic output to the heart ==> Cardiostimulary effect: sympathetic pathways ==> Cadioinhibitory effect: parasympathetic signals via vagus nerve |
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Chronotropic Effects to ANS: Sympathetic System |
Sympathetic postganglionic fibers are adrenergic (SA and AV nodes, and myocardium) - They release norepinephrine - Bind to β1-adrenergic receptors in the heart - Activate cAMP 2nd-messenger system in cardiocytes and nodal cells ==> Lead to opening of Ca2+ channels in plasma membrane: Increases SA node depolarization, increases contraction strength in cardiocytes ==> Increase uptake of Ca2+ by SR: faster relaxation of cardiocytes - By accelerating both contract and relaxation, norepinephrine and cAMP increase the HR as high as 230bpm ==> Diastole becomes too brief for adequate filling ==> Both stroke volume and cardiac output are reduced |
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Chronotropic Effects to ANS: Parasympathetic System |
Cardioinhibitory center stimulates R vagus nerve (SA node), and L vagus nerve (AV node) - Acetylcholine (Ach) binds to muscarinic receptors - Open K+ gates in the nodal cells: hyperpolarized (Decreases HR) - Parasympathetics work on the heart faster than sympathetics (ligand-gated) ==> Parasympathetics do not need a 2nd-messenger system Vagal tone: hold down heart rate to 70 to 80bpm at rest - Lesion of vagus nerve increases HR (intrinsic rate around 100bpm) - Stimulate vagus nerve decreases HR to 20bpm |
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Inputs to Cardiac Center |
Higher brain centers - Cerebral cortex, limbic system, hypothalamus influence HR ==> Sensory input or emotional stimuli ("fight or flight") Proprioceptors - Muscle tension input to cardiac center increases HR Baroreceptors in aorta and internal carotids regulare HR - Pressure drop, signal rate drops, cardiac center increases HR - Pressure rise, signal rate rises, cardiac center decreases HR 1) Baroreceptors sense increase BP 2) Glossopharyngeal nerve transmits signals to medulla oblongata 3) Vagus nerve transmits inhibitory signals to cardiac pacemaker 4) Heart rate decreases |
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Input to Cardiac Center: Chemoreceptors |
- Senses blood pH, CO2, O2 - Located in aortic arch, carotid arteries and medulla - Primarily respiratory control, may influence HR ==> Increase CO2 (hypercapnia) causes increase in [H+] levels and acidosis (pH < 7.35) ==> Hypercapnia and acidosis stimulate center to increase HR -Carotid Body senses O2, CO2, pH -Aortic Body senses O2, CO2 -Medulla senses O2 -Carotid Body: chemoreceptor -Carotid Sinus: baroreceptor -Aortic Body: chemoreceptor -Aortic arch: baroreceptor |
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Chronotropic Effects on Chemicals: Drugs |
Chemicals affect HR as well as neurotransmitters from cardiac nerves - Blood-borne adrenal catecholamines (NE and epinephrine) are potent cardiac stimulants Drugs that stimulate heart: - Nicotine stimulates catecholamine secretion - Thyroid hormone increases number of adrenergic receptors on heart so more responsive to sympathetic stimulation - Caffeine inhibits cAMP breakdown prolonging adrenergic effect |
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Chronotropic Effects on Chemicals: K+ Electrolytes |
Potassium (K+) has greatest chronotropic effect - Hyperkalemia: excess K+ in cardiocytes ==> Inhibits cell repolarization ==> Myocardium less excitable, HR slows and becomes irregular - Hypokalemia: deficiency K+ in cardiocytes ==> Cells hyperpolarized, require increased stimulation so HR slows down |
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Chronotropic Effects on Chemicals: Ca2+ Electrolytes |
Hypercalcemia: excess of Ca2+ - Decreases HR (long refractory period) and increases contraction strength Hypocalcemia: deficiency of Ca2+ - Increases HR (short refractory period) and decreases contraction strength |
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Stroke Volume |
The other factor that determines cardiac output besides HR, is stroke volume (SV) - CO = HR * SV Three variables govern stroke volume: - Preload (Franklin-Starling Law) - Contractility (force of contraction at preload) - After-load ("back pressure" from aorta) Examples: - Increased preload or contractility increases stroke volume - Increased after-load decreases stroke volume |
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Preload |
The amount of tension in ventricular myocardium immediately before it begins to contract (ex. end diastolic volume) - Increased preload causes increased force of contraction - Exercise increases venous return and stretches myocardium - Cadiocytes generate more tension during contraction - Increased cardiac output matches increased venous return Frank-Starling Law of the heart: Stroke volume is directly proportional to end-diastolic volume - Stroke volume is proportional to the EDV - Ventricles eject as much blood as they receive - The more they are stretched, the harder they contract |
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Contractility |
Refers to how hard the myocardium contracts for a given preload |
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Contractility: Positive Inotropic Agents |
Increase contractility (stronger contraction) - Hypercalcemia can cause strong, prolonged contractions and even cardiac arrest in systole - Catecholamines (NE and epinephrine) increase Ca2+ levels - Glucagon stimulates cAMP production - Digitalis raises intracellular Ca2+ levels and contraction strength |
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Contractility: Negative Inotropic Agents |
Reduce contractility (weaker contraction) - Hypocalcemia can cause weak, irregular heartbeat and cardiac arrest in diastole - Hyperkalemia reduces strength of myocardial action potentials and the release of Ca2+ into the sarcoplasm - Vagus nerve have effects on atria but too few nerves to ventricles for a significant effect (parasympathetic - only innervates AV and SA node) |
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Afterload |
The blood pressure in the aorta and pulmonary trunk immediately distal to the semilunar valves - Opposed the opening of these valves - Limits stroke volume Hypertension increases after-load and opposes ventricular ejection (heart needs to worker harder to push blood out) Anything that impedes arterial circulation can also increase after-load - Lung diseases that restrict pulmonary circulation |
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Vasomotor Tone and After-load |
Rate of sympathetic nerve stimulation activates α1 adrenoceptors to regulate vessel radium: 1) Strong sympathetic tone 2) Smooth muscle contraction 3) Vasoconstriction Mean arterial pressure (MAP) is an estimate of the systemic pressure (after-load) 1) Weaker sympathetic tone 2) Smooth muscle relaxation 3) Blood pressure dilates vessels Vasomotor tone is the ability of arteries to contraction (constriction - increases after-load - back pressure is higher) or expand (dilates - decreases after-load) - depending on stimulus |
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Vasomotor Tone |
Beta blockers: - Decrease chronotropy and ionotropy (HR and contractility) - Decrease CNS sympathetic tone - Decrease renin release (kidney) Adverse side effects (labetalol and carvedilol): - α1 arterioles ==> dilation - β2 in lung ==> constriction |
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Dihydropyridines |
Ca2+ channel blockers: - Hypertension - Coronary artery disease Mechanism of action: Decreases Ca2+ influx, decreases smooth muscle tone Adverse effects: - Edema, fatigue, palpitations - Reduce heart contractility |
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Chronotropic Agents: Positive |
Influences HR - Sympathetic stimulation - Epinephrine and norepinephrine - Thyroid hormone - Hypocalcemia - Hypercapnia and acidosis - Digitalis |
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Chronotropic Agents: Negative |
Influences HR - Parasympathetic stimulation - Acetylcholine - Hyperkalemia and hypokalemia - Hypocalcemia - Hypoxia |
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Ionotropic Agents: Positive |
Influences contraction strength - Sympathetic stimulation - Epinephrine and norepinephrine - Hypercalcemia - Digitalis - Glucagon |
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Ionotropic Agents: Negative |
Influences contraction strength (Parasympathetic effect negligible) - Hyperkalemia - Hypocalcemia - Myocardial hypoxia - Myocardial hypercapnia |
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Exercise and Cardiac Output |
Exercise makes the heart work harder and increases cardiac output Proprioceptors signal cardiac center - At beginning of exercise, signals from joints and muscles reach the cardiac center of brain - Sympathetic output from cardiac center increases cardiac output Increased muscular activity increases venous return - Increases preload and ultimately cardiac output Increases in HR and SV cause an increase in cardiac output Exercise produces ventricular hypertrophy - Increased SV allows heart to beat more slowly at rest - Athletes with increased cardiac reserve can tolerate more exertion than a sedentary person |
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Coronary Artery Disease (CAD) |
A constriction of the coronary arteries - Usually the result of atherosclerosis: an accumulation of lipid deposits that degrade the arterial wall and obstruct the lumen - Starts when endothelium is damaged by hypertension, virus, diabetes, or other causes Monocytes penetrate walls of damaged vessels and transform into macrophages - Absorb cholesterol and fats to be called foam cells that form fatty streak on vessel wall Platelets adhere to damaged areas and secrete platelet-derived growth factor - Attracting immune cells and promoting mitosis of muscle of fibroblasts, and the deposition of collagen (forming atheroma- plaque) Bulging mass grows to obstruct arterial lumen Causes angina pectoris, intermittent chest pain, by obstructing 75% or more of the blood flow Immune cells of atheroma stimulate inflammation - May rupture, resulting in traveling clots or fatty emboli May cause coronary artery spasms due to lack of secretion of nitric oxide (vasodilator) Inflammation transforms atheroma into a hardened complicated plaque called atherosclerosis |
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Coronary Artery (CAD): Risks and Treatment |
Unavoidable risk factors: heredity, aging, gender (male) Preventable risk factors: obesity, smoking, lack of exercise, anxious personality, stress, aggression, and diet Treatment: - Coronary bypass surgery (Great saphenous vein) - Balloon angioplasty - Laser angioplasty |
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The Vessel Wall: Tunica interna (tunica intima) |
- Lines the blood vessel and is exposed to blood - Endothelium: selectively permeable barrier, secretes chemicals to dilate or constrict vessel - Thin basement membrane (loose CT) (inside portion, exposed to blood) |
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The Vessel Wall: Tunica media |
- Middle layer (thickest) - Consists of smooth muscle, collagen, and elastic tissue for vasomotion (dilate or constrict vessel) (thicker, middle - when endothelium cell secretes chemicals, it goes through smooth muscle in tunica media) |
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The Vessel Wall: Tunica externa (tunia adventitia) |
- Outermost layer with loose CT - Vasa vasorum: small vessels that supply blood to at least the outer half of the larger vessels ==> Blood from the lumen is thought to nourish the inner half of the vessel by diffusion |
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General Anatomy of the Blood Vessels |
- Arteries (composed of tunica interna, tunica media, and tunica externa) carry blood away from heart - Veins carry blood back to heart - Capillaries connect smallest arteries to veins |
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Arteries: Conducting Arteries |
- Largest size - Aorta, common carotid, subclavian, pulmonary trunk, and common iliac arteries - Large tunica media (thick layer of smooth muscle) - Expand during systole (contraction), recoil during diastole (relaxation) to decrease BP fluctuations |
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Arteries: Distributing Arteries |
- Medium size - Distributes blood to specific organs - Brachial (arm), femoral (leg), renal (kidney), and splenic arteries - Smooth muscle layers constitute 3/4 of wall thickness |
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Arteries: Resistance Arteries |
- Smallest size - Arterioles: Control amount of blood to various organs - Thicker tunica media in proportion to their lumen than large arteries and very little tune external (When blood isn't needed, it constricts and allows it to flow to other areas) (When blood in needed, it relaxes and allows blood to flow to organs) |
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Arteries: Metarterioles |
- Short vessels that link arterioles, capillary beds, and venues - Blood vessels regulated by muscle cells that form a precapillary sphincter capillary bed entrance ==> Constriction of these sphincters reduces or shuts off blood flow through their respective capillaries ==> Diverts blood to other tissues |
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Aneurysm |
Weak point in an artery or the heart wall - Thin-walled, bulging sac that pulsates with each heartbeat and may rupture at any time - Most common sites: abdominal aorta, renal arteries, and arterial circle at base of brain - Can rupture causing hemorrhage - Result from congenital weakness of the blood vessels or result of trauma or bacterial infections such as syphilis ==> Most common cause is atherosclerosis and hypertension (When vessel is damaged it gets more prone to having a bulging sac - even if it doesn't rupture, it can compress nerves and cause other problems) |
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Capillaries |
Site for exchange of nutrients, wastes, and hormones between blood and tissue fluid (composed of endothelium and basal lamina) - Continuous - Fenestrated - Sinusoids |
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Capillaries: Continuous |
Present in most tissues (ex. skeletal muscle) - Endothelial cells with tight junctions ==> Intercellular clefts (between endothelial cells) allow passage of solutes to tissue (glucose and small solutes, larger proteins held back) |
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Capillaries: Fenestrated |
Kidneys and small intestine - Organs specialized for rapid absorption or filtration ==> Filtration pores: thin glycoprotein layer over a pore allows passage of small molecules, but keep most proteins and larger particles in blood |
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Capillaries: Sinusoids |
Liver, bone marrow, spleen - Tissues specialized for filtration of macromolecules and cells ==> Usually blood enriched spaces ==> Large fenestration (pores) that allows movement of proteins and cells |
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Capillaries and Perfusion |
- Metarteriole: main channel through capillary bed to venule - Precapillary sphincters control perfusion ==> Around 1/4 of capillaries are open at rest (Sphincters are usually closed at rest) |
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Veins |
- Greater capacity for blood containment than arteries - Thinner walls, flaccid, less muscular and elastic tissue - Subjected to relatively low blood pressure - Collapse when empty, expand easily - Have steady blood flow - Merge to form larger veins (majority of blood is in veins - not arteries - at any given time) |
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Veins: Venules |
-Smallest Postcapillary venules: more porous ("leaky") than capillaries (exchange fluid with surrounding tissues) - Important for immune system and inflammation (ex. leukocytes out of bloodstream) Muscular venules: have tunica media (smooth muscle) and thin tunica externa |
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Veins: Medium Veins |
- Thinner walls, less muscular and elastic tissue than medium arteries - Radial and ulnar veins of the forearm - Expand easily (Increase vascular compliance) - Valves aid 'muscle pump' for venous return - Varicose veins result in part from the failure of these valves |
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Varicose Veins |
Blood pools in the lower legs - Cusps of the valves pull apart, blood back flows and further distends the vessels, their walls grow weak and develop into varicose veins Genetics, obesity, and pregnancy increase risk Hemorrhoids are varicose veins of the anal canal |
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Veins: Venous Sinuses |
- Veins with especially thin walls, large lumens, and no smooth muscle (can't constrict or dilate - so no capability of vasomotion) - Dural venous sinus and coronary sinus of the heart - Not capable of vasomotion |
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Veins: Large Veins |
- Some smooth muscle in all three tunics - Thin tunica media with moderate amount of smooth muscle - Tunica externa is thickest layer ==> Contains longitudinal bundles of smooth muscle - Venae cavae, pulmonary veins, internal jugular veins, and renal veins |
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Circulatory Routes: Simplest Pathway |
Simplest and most common route (single capillary bed) - Arteries => arterioles => capillaries => venules => veins |
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Circulatory Routes: Portal System |
2 consecutive capillary beds - Between hypothalamus and anterior pituitary - Kidneys - Between intestines and liver |
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Circulatory Routes: Arteriovenous Anastomosis |
Shunt - Fingers, palms, toes and ears |
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Circulatory Routes: Venous Anastomosis |
- Most common - One vein empties directly into another - Alternative routes to drain from an organ - Reason vein blockage is less serious than arterial blockage |
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Circulatory Routes: Arterial Anastomosis |
- Two arteries merge - Provides collateral (alternative) routes of blood supply to a tissue - Coronary circulation and around joints |
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Arterial Sense Organs |
Monitor blood pressure and chemistry Carotid sinus: - In walls of internal carotid artery - Monitors BP - signals brainstem ==> HR decreases and vessels dilate Carotid bodies: - Oval bodies near carotids - Monitor blood chemistry ==> Adjust respiratory rate to stabilize pH, CO2, and O2 Aortic bodies: - In walls of aorta - Same function as carotid bodies |
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Blood Flow and Perfusion |
Blood Flow: Amount of blood flowing through a tissue in a given time (mL/min) Perfusion: Rate of blood flow per given mass of tissue (mL/min/g) Important for delivery of nutrients and oxygen, and removal of metabolic wastes Hemodynamics - Physical principles of blood flow based on pressure and resistance ==> Flow is directly proportional to change in pressure per resistant (dP/R) |
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Blood Pressure: Systolic and Diastolic Pressure |
- Force blood exerts against vessel wall: Measured at brachial artery of arm)
- Systolic pressure: BP during ventricular systole (contraction) - Diastolic pressure: BP during ventricular diastole (relaxation) - Normal value for young adult: 120/75mmHg - Pulse pressure: systolic - diastolic ==> Important measure of stress exerted on small arteries - Mean arterial pressure (MAP): ==> Measurements taken at intervals of cardiac cycle, best estimate: diastolic pressure + (1/3 of pulse pressure) ==> Varies with gravity: standing; 62-head, 180-ankle |
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Pulse Pressure |
Pulse pressure = systolic BP - diastolic BP MAP = mean arterial pressure - MAP = diastolic pressure + 1/3pulse pressure - MAP = diastole + 1/3 (systolic BP-diastolic BP) |
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Blood Pressure: Arterial Elasticity |
Arterial elasticity: keeps blood flow steady during cardiac cycle (heart's ability to expand or recoil) - Smoothes pressure flux and decreases stress on small arteries (Fluctuation of pressure decreases due to elasticity (from aorta to capillaries - then it gives steady flow) Arteries less elastic with age: BP increases BP determined by cardiac output, blood volume and peripheral resistance |
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Abnormalities of BP: Hypertension |
- Chronic resting BP > 140/90 mmHg ==> Weakens blood vessels ==> Promotes atherosclerosis - Consequences: can weak small arteries and cause aneurysms - Treatment: ==> Diuretics (thiazides) ==> ACE inhibitors ==> Angiotensin II receptor blockers ==> β blockers ==> Ca2+ channel blockers - Around 50 million in USA (18.4%) - Prehypertension: 120/80 - 140/89 : Monitor lifestyle (exercise, weight, stress, tobacco, alcohol) - Hypertension: 140/90 - 160/100 |
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Abnormalities of BP: Hypotension |
- Chronic low resting BP - Caused by blood loss, dehydration, anemia - Increased vagal tone (athletes) |
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Determinants of Blood Pressure |
- Cardiac output - Blood volume (kidney) - Resistance ==> Blood viscosity ==> Vessel length ==> Vessel radius (The higher the resistance, the lower the blood flow (high pressure)) |
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Resistance: Blood Viscosity & Vessel Length |
Resistance: The opposition to flow that blood encounters in vessels - Blood viscosity: RBCs and albumin (makes blood very viscous normally - the thicker the blood, the higher the resistance) ==> Low viscosity with anemia, hypoproteinemia ==> High viscosity with polycythemia, dehydration - Vessel length: ==> Pressure and flow decrease with increased distance (Increased friction) |
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Resistance: Vessel Radius |
Vessel radius: key influence over flow - Finely regulated with rapid adjustment of resistance - Vasomotion: regulation of vessel radius by AND (vasoconstriction, vasodilation) - Laminar flow: blood flows in layers, faster in center - Blood flow (F) proportional to 4th power of radius (r^4) ==> Arterioles can constrict to 1/3 of fully relaxed radius ------------:> Given: r=1mm, F=1mL/sec ------------:> if r=3mm, F=81mL/sec ------------:> 3X increase in radius results in 81X increase in flow |
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Blood Velocity in the Body |
Aorta to capillaries velocity decreases - Greater distance, more friction - Smaller radii or arterioles and capillaries (High resistance) - Farther from heart, greater total cross sectional area Capillaries to vena cava, velocity decreases - Vessels radii large (Low resistance) - Never reaches velocity of large arteries (You want to slow velocity in capillaries to allow nutrient exchange and other processes to occur) |
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Regulation of Blood Pressure |
Vasomotion is a quick and powerful way of altering BP and flow 3 ways of controlling vasomotion: - Local control - Neural control ==> Vasomotor Center: -------:> Baroreflex -------:> Chemoreflex -------:> Medullary ischemic reflex ==> Higher CNS inputs: -------:> Hypothalamus -------:> Limbic system - Hormonal control |
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Local Control: Metabolic Autoregulation |
Tissues regulate their own blood supply - Decreased perfusion causes accumulation of waste (H+, CO2) => vasodilation |
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Local Control: Vasoactive Chemicals |
Substances secreted by platelets, endothelial cells, and perivascular tissue to stimulate vasomotion - Histamine, bradykinin, and prostaglandins stimulate vasodilation - Endothelial cells secrete prostacyclin and nitric oxide (vasodilators) and endothelins (vasoconstrictor) |
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Local Control: Reactive Hyperemia |
- If blood supply cut off then restored, flow increases above normal due to accumulation of metabolites during ischemia |
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Local Control: Angiogenesis |
Growth of new blood vessels (ex. in hypoxic tissue) - Controlled by growth factors (ex. VEGF) - Occurs in regrowth of uterine lining (after each menstrual period), around coronary artery obstructions, in exercised muscle, and malignant tumors (to provide nourishment of cancer cells) => targets for drug development (inhibitors) |
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Neural Control: Vasomotor Center |
Vasomotor center of medulla oblongata - Sympathetic control over most blood vessels throughout the body ==> Stimulates most vessels to constrict via α1 receptors ==> Dilates vessels in skeletal and cardiac muscle to meet demands of exercise via β receptors (Precapillary sphincters respond only to local and hormonal control due to lack of innervation) Integrates 3 autonomic reflexes: - Baroreflexes - Chemoreflexes - Medullary ischemic reflex |
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Neural Control: Baroreflex |
BP input from baroceptors near heart: - Aortic arch, aortic sinuses, carotid sinus, right atrium Autonomic negative feedback: - Constant signals from brainstem - Increased BP increases signal rate & inhibits vasomotor center ==> Decreases sympathetic tone, vasodilation causes BP to drop - Decreased BP signal rate & excites vasomotor center ==> Increases sympathetic tone, vasoconstriction and BP rises |
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Baroreflex and Syncope |
Orthostatic Hypotension: - Loss of baroceptor input ==> Sudden standing pools blood in limbs (gravity) ==> Short-term low venous return (blood going back to heart) - May cause fainting - Usually benign ==> Secondary to dehydration ==> Medications |
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Neural Control: Chemoreflex |
Chemoreceptors in aortic and carotid bodies respond to changes in blood chemistry (pH, O2 and CO2) - Aortic arch, subclavian arteries, external carotid arteries Primary role: adjust respiration Secondary role: vasomotion - Hypoxemia, hypercapnia, and acidosis stimulate chemoreceptors, acting through vasomotor center to cause vasoconstriction, high BP, high lung perfusion, and high gas exchange - Also stimulate breathing |
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Neural Control: Medullary Ischemic Reflex |
Automatic response to a drop in perfusion of the brain - Medulla oblongata monitors its own blood supply - Activates corrective reflexes when it senses ischemia (insufficient perfusion) - Cardiac and vasomotor centers send sympathetic signals to heart and blood vessels ==> Increases HR and contraction force ==> Causes widespread vasoconstriction ==> Raises BP and restores normal perfusion to the brain - Other brain centers (limbic/hypothalamus) can affect vasomotor center ==> Stress, anger, arousal can also increase BP |
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Hormonal Control |
Hormones influence blood pressure - Some through their vasoactive effects - Some by regulating water balance (blood volume) |
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Hormonal Control: Atrial Natriuretic Peptide |
Increases urinary Na+ excretion - Reduces blood volume and promotes vasodilation - Lowers BP |
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Hormonal Control: Angiotensin II |
Potent vasoconstrictor - Raises BP - Promotes Na+ and water retention by kidneys - Increases blood volume and BP |
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Hormonal Control: ACE |
Angiotensinogen - prohormone produced by liver -- | -- V -- Renin - enzyme released from kidney by low BP Angiotensin I -- | -- | -- ACE (angiotensin-converting enzyme) -- V -- ACE inhibitors block enzyme to drop BP Angiotensin II - potent vasoconstrictor (raises BP) |
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Hormonal Control: Aldosterone |
Increases Na+ and water retention kidneys - Increases blood volume and BP |
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Hormonal Control: Antidiuretic Hormone (ADH) |
Promotes water retention and raises BP - Pathologically high concentrations => vasoconstrictor |
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Hormonal Control: Epinephrine and Norepinephrine |
Effects: - Most blood vessels ==> Bind to a-adrenergic receptors - vasoconstriction - Skeletal and cardiac muscle blood vessels ==> Bind to β-adrenergic receptors - vasodilation |
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Two Purposes of Vasomotion |
Overall control of BP - Important in supporting cerebral perfusion during a hemorrhage or dehydration Rerouting blood where needed - Either centrally or locally controlled ==> Exercise -> Increased sympathetic outflow -> Decreases blood flow to kidneys and digestive tract and increases blood flow to skeletal muscles ==> Metabolite accumulation in a tissue affects local circulation without affecting circulation elsewhere in the body ==> Localized vasoconstriction enables routing blood to different organs as needed |
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Vasomotion Examples |
- Vigorous exercise dilates arteries in lungs, heart, and muscles ==> Vasoconstriction occurs in kidneys and digestive tract (During exercise: high perfusion of lungs, myocardium, and skeletal muscle - low perfusion of kidneys and digestive tract) ==> Total cardiac output: 17.5L/min - Dozing in armchair after big meal ==> Vasoconstriction in lower limbs raises BP avoid the limbs, redirecting blood to intestinal arteries ==> Total cardiac output: 5L/min Blood is never compromised in brain (consistent at rest and during exercise, around 700-750mL/min) |
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Vessel Radius and Blood Flow |
- Large radius = high flow rates - Small radius = low flow rates |
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Capillary Exchange |
Only through capillary walls are exchanges made between the blood and surrounding tissues Capillary exchange: two-way movement of fluid across capillary walls - Water, O2, glucose, amino acids, lipids, minerals, antibodies, hormones, wastes, CO2, ammonia 3 routes for exchange of chemicals through capillary wall: - Through endothelial cell cytoplasm - Intercellular clefts between endothelial cells - Filtration pores (fenestrations) of the fenestrated capillaries Mechanisms involves: diffusion, transcytosis, filtration, and reabsorption |
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Diffusion |
Most important form of capillary exchange - Glucose and O2: diffuse out of the blood - CO2 and other waste: diffuse into the blood Lipid-soluble substances - Steroid hormones, O2, and CO2 diffuse easily through plasma membranes Water-soluble substances - Glucose and electrolytes must pass through filtration pores and intercellular clefts Large particles such as proteins are held back |
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Transcytosis |
Endothelial cells pick up materialon one side of the plasma membrane by pinocytosis or receptor-mediatedendocytosis, transport vesicles across cell, and discharge material on otherside by exocytosis - Important for fatty acids, albumin, & somehormones (insulin) |
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Filtration and Reabsorption |
2 Opposing forces for fluidmovement: – Bloodhydrostatic pressure drives fluid out of capillary (andinto interstitial fluid) ==> Forceexerted against a surface by a liquid (i.e. BP) ==> Highon arterial end of capillary, low on venous end – Colloidosmotic pressure (COP) draws fluid into capillary (frominterstitial fluid) ==> Resultsfrom plasma proteins (albumin)—more in blood ==> Oncoticpressure – netCOP = blood COP − tissue COP Capillaries reabsorb about 85% ofthe fluid they filter Other 15% isabsorbed by the lymphaticsystem and returned to the blood |
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Capillary Filtration and Reabsorption |
-Arterial: Filtration (Net: 13 mmHg out) - fluid leaking out of capillary -Venous: Reabsorption (Net: 7 mmHg in) - fluid taken back into capillary Exceptions: - Kidney glomeruli: filtration - Alveolar capillary: absorption Activity or trauma can increase filtration rate (can lead to edema) |
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Edema |
Accumulation of excess fluid in a tissue (filtration > reabsorption) Three primary causes: - Increased capillary filtration (kidney failure, histamine release, old age, poor venous return) - Reduced capillary absorption (hypoproteinemia, liver disease, dietary protein deficiency) - Obstructed lymphatic drainage (surgical removal of lymph nodes) |
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Pathophysiology of Edema |
Tissue necrosis: O2 delivery and waste removal impaired Pulmonary edema: suffocation threat Cerebral edema: headaches, nausea, seizures, and coma Severe edema or circulatory shock: Excess fluid in tissue spaces causes low blood volume and low BP |
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Mechanisms of Venous Return |
Pressure gradient: - 7 to 13 mmHg venous pressure toward heart - Venules (12 to 18 mmHg) to central venous pressure (around 5 mmHg) (right atrium pressure) Gravity drains blood from head and neck Skeletal muscle pump in the limbs Thoracic (respiratory) pump: - Inhalation: thoracic cavity expands (drops thoracic pressure), abdominal pressure increases, forcing blood upward - Central venous pressure fluctuates ==> 2 mmHg: inhalation ==> 6 mmHg: exhalation ==> Blood flows faster with inhalation Cardiac suction of expanding atrial space (as it relaxes) |
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Venous Return and Physical Activity: Venous Return |
Exercise increases venous return in many ways: - Heart beats faster and harder, increases cardiac output and BP - Vessels of skeletal muscles, lungs, and heart dilate and increases flow - Increases respiratory rate and thoracic pump - Increases skeletal muscle pump |
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Venous Return and Physical Activity: Venous Pooling |
Venous pooling occurs with inactivity - Venous pressure not enough to force blood upward - With prolonged standing, cardiac output may be low enough to cause dizziness or syncope ==> Prevented by tensing leg muscles, activate skeletal muscle pump - Jet pilots wear pressure suits |
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Circulatory Shock: Cardiogenic and LVR Shock |
Any state in which cardiac output is insufficient to meet metabolic needs - Cardiogenic shock: inadequate pumping of heart (MI) - Low venous return (LVR) shock: cardiac output is low because too little blood is returning to the heart --- 1) Hypovolemic shock: most common ----------:> Loss of blood volume: trauma, burns, dehydration --- 2) Obstructed venous return shock: ---------:> Tumor or aneurysm compresses a vein --- 3) Venous pooling (vascular) shock: --------:> Long periods of standing, sitting, or widespread vasodilation |
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Circulatory Shock: Venous Pooling and Hypovolemic Shocks |
Venous pooling (vascular) shock: - Neurogenic shock: loss of vasomotor tone, vasodilation - Causes from emotional shock to brainstem injury Venous pooling and Hypovolemic shocks: - Septic shock: Bacterial toxins trigger vasodilation and increased capillary permeability (more fluid leaks out of circulation, drops blood volume) - Anaphylactic shock: Severe immune reaction to antigen, histamine release, generalized vasodilation, increased capillary permeability (vasodilation and loss of blood volume) |
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Responses to Circulatory Shock: Compensated Shock |
Several homeostatic mechanisms bring about spontaneous recovery - Example: if a person faints and falls to a horizontal position, gravity restores blood flow to the brain |
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Responses to Circulatory Shock: Decompensated Shock |
- Triggers when the compensated shock mechanism fails - Life-threatening positive feedback loops occur - "vicious cycles" - Low cardiac output => MI => low cardiac output - Condition gets worse causing damage to cardiac and brain tissue |
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Special Circulation - CNS |
Perfusion constant in CNS: - Lesion for seconds causes loss of consciousness - Lesion 4-5 minutes causes irreversible brain damage - Flow shifts rapidly from one region to another Sensitive to changes in BP and chemistry: - Cerebral arteries dilate as BP drops, constrict as BP rises - Main chemical stimulus: [H+] or pH ---:> CO2 + H2O => H2CO3 => H+ + (HCO3)- ---:> CO2increase (hypercapnia)pH decreases and vasodilation -------- Breathinginto a paper bag ---:> CO2decrease (hypocapnia)pHincreases andvasoconstriction -------- Hyperventilationand cause ischemia, dizziness and syncope |
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Transient Ischemic Attacks (TIA) |
– Episodiclack of blood to CNS (sec to hours) causing weakness, paralysis, aphasia,visual defects – Canbe caused by spasms of diseased cerebral arteries – Oftenan early warning for stroke |
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Cerebral Vascular Accident (CVA, Stroke) |
– Infarctionin CNS caused by ischemia ==> Atherosclerosis,thrombosis, ruptured aneurysm –Severityvariable including death ==> Blindness,paralysis, loss of sensation, loss of speech common –Recoverydepends on collateral circulation, rapid restoration of blood supply. |
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Skeletal Muscles |
- Highly variable flow depending on state of exertion - At rest: ==> Arteriolesconstrict, most capillary beds shut down ==> Totalflow about 1 L/min. - During exercise: ==> Arteriolesdilate in response to epinephrine and sympathetic nerves ==> Precapillarysphincters dilate due to muscle metabolites like lactic acid, CO2 ==> Bloodflow can increase 20-fold - Muscular contraction impedes flow ==> Isometriccontraction causes fatigue faster than intermittent isotonic contractions |
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Lungs |
- Low pulmonary blood pressure (25/10mm Hg) ==> Flowslower, more time for gas exchange ==> Engagedin capillary fluid absorption ---------:> Oncoticpressure overrides hydrostatic pressure ---------:> Preventsfluid accumulation in alveolar walls and lumens - Unique response to hypoxia ==> Pulmonaryarteries constrict in diseased area ==> Redirectsflow to better ventilated region |
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Cardiovascular System |
A circulatory transport system that consists of: - Fluid medium: blood - Pump: heart - Conducting system: blood vessels |
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Blood Functions |
- Transportation of O2, CO2, nutrients, hormones, heat and waste - Regulation of body acidity, temperature & water content - Protection against disease by WBCs and antibodies |
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Blood Composition |
- Plasma: 55% of whole blood - Buffy coat: leukocytes and platelets (< 1% of whole blood) - Erythrocytes: 45% of whole blood Buffy coat + erythrocytes = formed elements |
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Blood: Plasma Composition |
- Plasma proteins: 7% - Other solutes: 1% - Water: 92% ==> Transports organic and inorganic molecules, formed elements, and heat |
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Plasma Proteins: Albumin |
(~60%) - Controls blood viscosity, pressure, osmolarity, flow & fluid balance - Transports lipids, hormones and electrolytes |
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Plasma Proteins: Fibrinogen and Regulatory |
Fibrinogen (~4%) - Blood clotting precursor Regulatory proteins (~1%) - Proenzymes, enzymes & hormones |
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Plasma Proteins: Globulins |
(~36%) α: smallest size - Haptoglobin: transports hemoglobin - Ceruloplasmin: transports copper - Prothrombin: blood clotting enzyme β: intermediate size - Transferrin: transports iron - Complement proteins: immune function γ: largest size - Antibodies produced by plasma cells during an immune response |
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Other Solutes |
- Electrolytes - Nutrients - Enzymes - Hormones - Gases - Waste products |
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Hemopoiesis |
- Formation of all the blood cells - In red bow marrow and lymph tissue - Start from hemocytoblast stem cells that become lymphoid or myeloid stem cells - Lymphoid stem cells produce the WBCs called lymphocytes - Myeloid stem cells produce all the others (RBCs, platelets, and 4 WBCs) |
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RBCs: Erythrocytes |
Number: - Male ~ 4.6 - 6.2 million/nL - Female ~ 4.2 - 5.4 million/nL Lower values in women due to: -- 1) Androgens in men stimulate RBCs production -- 2) Loss of RBCs in women during menstruation -- 3) RBCs count and % of body fat are inversely proportional RBC's count and hemoglobin amount determine the blood oxygen carrying capacity -Hematocrit: -Men 42-52%, Women 37-48% -Hemoglobin: -Men 13-18, Women 12-15g/dL -One drop of blood ~ 250 million RBCs -Biconcave discs & no nucleus -Each cell contain ~250 million hemoglobin molecules, which contains 4 heme and 4 iron groups in each heme |
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RBC's Functions |
Hemoglobin: - Transports 97% of O2 - Transport 23% of CO2 - Releases nitric oxide which participates in the regulation of blood flow |
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Hemoglobin |
- Composed of four iron containing parts called heme an a protein part called globin - Each iron in the heme bind one oxygen molecule - Hemoglobin bind oxygen in the lungs and release it in tissues |
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RBCs Formation |
- Called erythropoiesis - Occur in the red bone marrow - 2.5 million RBC's made every second - Hemoglobin synthesis occur during cell development - Proceed through various cell stages and takes about 3-5 days |
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RBCs Formation Requirements |
- Iron, amino acids, vitamin B12, folic acid, vitamin C, copper - Supplied by diet and recycled from storage in the liver and spleen - Iron is lost in bleeding, urine & feces ==> Men: 0.9mg/day, women 1.7mg/day ==> Low absorption requires 5-20mg/day ==> Free iron is toxic & must be combined with proteins during absorption, transport or storage |
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Iron Metabolism |
1) Mixture of Fe2+ and Fe3+ is ingested 2) Stomach acid converts Fe3+ to Fe2+ 3) Fe2+ binds to gastroferritin 4) Gastroferritin transports Fe2+ to small intestine and releases it for absorption 5) In blood plasma, Fe2+ binds to transferrin 6) In liver, some transferrin releases Fe2+ for storage 7) Fe2+ binds to apoferritin to be stored as ferritin 8) Remaining transferrin is distributed to other organs where Fe2+ is used to make hemoglobin, myoglobin, etc. |
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Erythropoiesis |
Hemopoietic pluripotent stem cell --- | --- V Erythrocyte colony forming unit --- | --- V Erythroblast -- | -- V Reticulocytes -- | -- V Erythrocytes |
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Stimulation of Erythropoiesis |
1) Decreased RBCs number 2) Tissue hypoxemia (inadequate O2 trasport) 3) Kidneys & liver secrete erythropoietin hormone 4) Bone marrow stimulation 5) Erythroblasts (Accelerated erythropoiesis) 6) Erythrocytes (Increase RBC count - increase O2 transport) |
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Erythrocyte Cycle |
1) Small intestine 2) Nutrient absorption (amino acids, iron, folic acid, vitamin B12) 3) Erythropoiesis in red bone marrow 4) Erythrocytes circulate for 120 days 5) Expired erythrocytes break up in liver and spleen 6) Hemoglobin degraded + cell fragments phagocytized |
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Erythrocyte Break Down |
1) RBC death and phagocytosis (macrophages in spleen, liver, or red bone marrow) 2) RBCs broken down to heme and globin protein ==> Globin is further broken down to amino acids, which are reused for protein synthesis ==> Heme is further broken down to biliverdin, then bilirubin - bilirubin is taken to liver, then small intestine, it is converted to urobilinogen, and urobilin in kidney and is excreted as urine, or stercobilin in large intestine and is excreted as feces ==> Heme's iron is moved by transferrin to liver, which can be stored as ferritin or further moved to red bone marrow, where it can be reused for erythropoiesis |
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Erythrocyte Disorders: Polycythemia |
Pathology: - Increased blood volume, viscosity and pressure - Cancer of the erythropoietic cell line in the red bone marrow - Treatment: Phlebotomy, radiation, interferon and immunosuppression Secondary/Relative Polycythemia: - Due to hypoxemic stimulation of erythropoietin secretion by high altitude, emphysema, smoking, air pollution, excessive exercise, etc - Treatment: treatment of hypoxemia causes and rehydration |
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Erythrocyte Disorders: Anemia (Hemorrhagic, Hemolytic, Aplastic) |
Hemorhagic Anemia: -Whole blood loss by bleeding Hemolytic Anemia: - Destruction of RBCs by diseases, drugs or toxins Aplastic/Hypoplastic Anemia: - Destruction of myeloid tissues by radiation, toxins or viruses |
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Erythrocyte Disorders: Anemia (Pernicious, Iron-deficiency, Erythropoietin) |
Pernicious/Megaloblastic Anemia: - Deficiency of intrinsic factor causes low vitamin B12 absorption producing megaloblastic RBCs Iron-Deficiency Anemia: - Causing low hemoglobin synthesis Erythropoietin Anemia: - Low erythropoietin due to kidney failure causing low erythropoiesis |
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Anemia: Pathology and Treatment |
Pathology anemia causes: - Tissue hypoxemia and necrosis - Shortness of breath and lethargy - Increased HR - Decreases BP and edema Treatment: - By treating the cause of the anemia |
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Erythrocyte Disorders: Sickle Cell Disease |
A hereditary defect in the hemoglobin β-globin chain producing (HbS) in Africans - Sickle Cell Trait: heterozygous for (HbS) and malaria resistant - Sickle Cell Disease: homozygous to (HbS) ==> Short life expectancy of 2 to 50 years ==> Hypoxemia elongates hemoglobin and forms sickle-shape RBCs ==> Elastic and sticky RBCs causes blood vessels and capillaries blockage ==> Intense pain, fatigue, paralysis, stroke, kidney or heart failure may occur |
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Erythrocyte Disorder: Thalassemia |
A hereditary defect causing absence of α or β hemoglobin chains in Mediterraneans - Results in chronic hemolytic anemias, anemias with RBCs counts less than 2 million/nL, fatigue, splenomegaly and heart enlargement |
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Erythrocyte Disorder: Malaria |
- 2 billion people (~ 40% of world population) at risk. ~400 million new cases each year causing more than 1 million deaths in children in Africa each year - Treatment: ==> Chloroquine (quinine) ==> Artemisia (artemisinin) |
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The Blood Types (A-B-AB-O) |
Determined by the presence or absence of the (A & B) antigens on the RBC surface - Type A RBCs has A antigen only - Type B RBCs has B antigen only - Type AB RBCs has both A and B antigens - Type O RBCs has no antigens |
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The Rh Blood Types |
- Rh (D) antigen in rhesus money (1940) - Determined by the presence or absence of the Rh antigens on the RBC's surface (D antigen) - Rh antigen present = Rh positive - Rh antigen absent = Rh negative - Rh+: A+, B+, AB+, O+ - Rh-: A-, B-, AB-, O- |
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Transfusion Reaction |
Donor: person giving blood Recipient: person getting blood - If do not and recipient blood type are not compatible, recipient plasma antibodies will attack antigens on donated RBCs - Blood agglutination (clumping) and RBC's hemolysis (degradation of RBCs) occur in recipient - Fatal circulatory shock |
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Hemolytic Disease of the Newborn (HDN) |
- Results from Rh incompatibility between Rh- mother and her Rh+ baby conceived from an Rh+ father - When Rh+ RBCs of first born child enter mother's circulation, mother will be sensitized, her plasma will carry anti-Rh antibodies and destroy the Rh+ RBCs of the second baby |
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White Blood Cells (Leukocytes) |
- General functions: Body protection by immune response or phagocytosis - Whole count: 5,000 - 10,000/nL - Differential: Determining the % of each type of WBCs (compared to total number of WBCs): ==> Neutrophils: 60 - 70% ==> Lymphocytes: 20 - 30% ==> Monocytes: 4 - 8% ==> Eosinophils: 2 - 4% ==> Basophils: <1% (Granulocytes: neutrophil, eosinophil, basophil cells contains granules in cytoplasm) (Agranulocytes: monocyte, lymphocyte cells contain no granules) |
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Formation of WBCs: Location |
Location: - Thymus for T-lymphocytes - Lymph tissue for lymphocytes - Red bone marrow for monocytes, neutrophils, basophils and eosinophils |
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WBCs Developmental Pathways |
Leukopoeisis: 1. Lymphoid stem cells 2. Lymphoblasts 3. Lymphocytes 1. Myeloid stem cells 2. Monoblasts 3. Monocytes 1. Myeloid stem cells 2. Myeloblasts 3. Neutrophils, Eosinophils, and Basophils |
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Function of WBC Types and Their Nuclei |
Neutrophils: - Function: bacterial infection & phagocytes - Segmented nucleus & pink granules Lymphocytes: - Function: immunity - Spherical nucleus & blue cytoplasm ring Monocytes: - Function: viral infection & tissue macrophages - Kidney-shaped nucleus & blue cytoplasm Eosinophils: - Function: parasites & anti-inflammatory - Bilobed nucleus & bright orange granules Basophils: - Function: allergies & inflammation - Bilobed nucleus & dark purple granules |
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Leukocytes Disorders |
Leukopenia: low WBCs (<5000/nL) - Treated with steroids and improved nutrition Leukocytosis: high WBCs (>10,000/nL) - Treated by infection management and with leukapheresis (taking WBC out, separating it from of plasma, putting plasma back in) (plasma dialysis) Leukemia: cancer of the hemopoietic tissues - Treated with targeted radiation and chemotherapy |
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Platelets (Thrombocytes( |
- Thrombopoietin: from the liver - Formation by Thrombopoiesis: Stimulated by thrombopoetin hormone secreted by liver - Development: Myeloid stem cell => megakaryoblast => megakaryocyte => platelets - Functions: Platelets plug formation in blood clotting - Number: 150,000-500,000/nL - Thrombocytopenia: low platelet count (<100,000/nL) |
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Hemostasis |
Responses that stop bleeding: - Vascular phase: contraction of the injured blood vessel smooth muscle fibers called vascular spasm (contraction of blood vessels - decreases blood loss by decreasing space where blood is escaping) to reduce the blood vessel diameter and decrease loss of blood (~1-2min) - Platelets phase: platelets plug formation (Release of chemicals - ADP, thromboxane A2, Ca2+, platelet factors - makes platelets stick to each other) (~10-20min) - Coagulation phase (clotting/coagulation): clot consists of fibrin fibers and trapped formed blood elements. Clot closes the broken blood vessel. Clot formation requires the presence and activation of clotting factors and calcium (~30min) |
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Coagulation Phase |
Occurs in three stages: - 1) Formation of Prothrombinase enzyme - 2) Formation of Thrombin enzyme - 3) Formation of Fibrin fibers |
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Prothrombinase Formation |
Extrinsic pathway: (outside factors influence) - Damaged tissue => tissue factor => activation of clotting factor VII Intrinsic pathway: (inside blood vessel factors influence) - Activation of platelets by collagen => platelets factors => activation of clotting factor X Common pathway: - Factor VII + Factor X = prothrombinase (extrinsic and intrinsic pathways come together) (clotting factors are proteins) |
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Blood Clotting |
Extrinsic Pathway (Involves tissue trauma & factor VII) + Intrinsic pathway (Involved blood trauma & facts X) + Ca2+ ==> Prothrombinase enzyme (common pathway) - Prothrombin + Prothrombinase =>Thrombin - Fibrinogen + Thrombin (+ Ca2+) => Fibrin fibers |
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Fibrinolysis |
Process of removal of clot (after tissue heals) Kallikrein (made by prekallikrein and factor XII) enzyme breaks plasmanogin to plasmin proteins - Plasmin breaks down fibrin (clot) into degradation products |
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Intravascular Clot |
- Intravascular clos is a clot within a closed vessel - Damaged vessel lining or slowing of blood flow - Platelets aggregate and release clotting factors - Resulting clot called a thrombus - Moving piece of the clot is an embolus - Clot moves downstream and blocks smaller vessel causing thromboembolism - May cut off blood supply to the heart causing a heart attack or to the brain causing a stroke Force of blood flow detaches clot (thrombus) and makes it flow (embolus) -Problem will arise if embolus tries to move to opening of a tiny blood vessel and block it (if it happens in capillaries of brain: stroke; if in capillaries of heart: heart attack) -For all capillaries, we have mechanisms embedded in our body to protect us against thromboembolism (anticoagulants) |
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Anticoagulants |
Chemicals that decrease or prevent blood clotting: - Heparin: blocks prothrombin activator formation and enhances anti-thrombin activity - Coumarins (warfarin): antagonism of vit. K. - Aspirin: inhibits Thromboxane A2 - Clopidogrel: inhibits fibrin formation - Hirudin: Thrombin inhibitor from leech saliva (used to restore circulation and enhance tissue survival after surgery) - EDTA (Ethylenendiaminetetraacetate) and CPD (citrate phosphate dextrose) calcium chelation |
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Hemophilia |
Caused by a genetic deficiency of a clotting factor in males - Hemophilia A: 83% males only - missing clotting factor VIII (8) - Hemophilia B: 15% males only - missing clotting factor IX (9) - Hemophilia C: males & females - missing clotting factor XI (11) |
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Lymphatic System Consists of: |
- Lymphatic fluid: similar to plasma with less proteins - Lymphatic vessels: similar to veins - Lymphatic tissues: mucosa associate lymph tissues (MALT) - Lymphatic organs: red bone marrow, tonsils, lymph nodes, thymus, spleen |
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Lymphatic System Functions |
- Draining excess interstitial fluid from tissue spaces - Draining plasma proteins from tissue spaces - Transport of one nutrient and some hormone - Immunity: specific defense against antigens by lymphocytes |
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Lymph Formation & Flow |
- Fluid and proteins filtered from blood capillaries are collected by lymphatic capillaries and returned to blood - Muscle contraction and breathing promote flow of lymphatic fluid - Lymphatic trunks empty into subclavian veins in the shoulders |
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Lymphatic Circulation: Lymphatic Capillaries |
– Capillariesstart as pocketswith a large diameter and thin walls – Endothelial cells overlap to form many one-way valves – Pickupfluid (lymph) from interstitial space between the tissues – Lacteals arespecial lymphatic capillaries inthe small intestine thattransport lipids (fats) |
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Lymphatic Circulation: Lymphatic Vessels |
– Lymphpasses from capillaries into lymphatic vessels – Resembleveins with thin walls & one-way valves – Afferentvessels carry lymph intolymph nodes – Efferentvessels carry lymph out oflymph nodes |
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Lymphatic Circulation: Lymphatic Trunks |
– Lymphpasses from lymphatic vessels into trunks – Bronchomediastinal(thoracicarea and lungs), jugular (headand neck region), subclavian(armsand shoulders), intestinal (intestinaland abdominal area) andlumbar lymphatic trunks (trunk– leg, back) |
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Lymphatic Circulation: Lymphatic Ducts |
Twoducts drain lymph from lymphatic trunks into the subclavianveins: – Right Lymphatic Duct:Smaller one that drains right side of head, right shoulder and right arm intothe right subclavianvein – Thoracic Duct: Larger one that drains rest ofbody lymph into the leftsubclavianvein |
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Lymphatic Circulation |
Interstitial fluid => lymph capillaries => afferent lymphatic vessels => lymph nodes => efferent lymphatic vessels => lymphatic trunks => lymphatic ducts => subclavian veins |
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Lymphatic Cells: Macrophages |
Antigen-presenting cells (APCs) that develop from monocyte as phagocytic cells in CT (APCs: cell capable of binding to antigen and flagging it out - macrophages developed from monocytes, stationary phagocytic cells) |
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Lymphatic Cells: Dendritic |
Mobile APCs (antigen presenting) found in the epidermis, mucous membranes and lymphatic organs |
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Lymphatic Cells: Reticular |
Stationary APCs in the stroma of lymphatic organs (antigen presenting cells that are stationary, found in lymphatic organs only) |
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Lymphatic Cells: T-lymphocytes |
Respond to intracellular antigens by dividing to produce: - Cytotoxic T-cells that kill antigen-bearing cells - Helper T-cells that help activate T-cells & B-cells - Memory T-cells |
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Lymphatic Cells: B-lymphocytes |
(bone marrow - bursa of chicken) - Respond to extracellular antigens by divind to produce: - Plasma cells: antibody secreting cells - Memory B-cells |
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Lymphatic Cells: Natural Killer Lymphocytes (NK) |
Can kill invading cells and tumor cells without the need to respond to antigens - nonspecific defense |
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Lymphatic Tissues |
Mucosa Associated Lymph Tissues (MALT): - They are aggregations of lymphocytes in mucous membranes within the digestive, urinary, reproductive and respiratory systems: ==> Appendix in the large intestine ==> Peyer's Patches in the small intestine ==> Lymphatic nodules in bronchi of the respiratory tract |
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Lymphatic Organs: Red Bone Marrow |
- A primary lymphatic organ - Produce B-lymphocytes and natural killer lymphocytes |
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Lymphatic Organs: Tonsils |
- Located in and around the throat for defense against inhaled or ingested microbes - Contain tonsilar crypts that trap microbes |
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Lymphatic Organs: Lymph Nodes |
Structure: capsule - Subcapsular sinus - Outer cortex (B cells) - Deep cortex (T cells) - Medulla (B cells) Function: filter lymph and trigger the immune response |
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Lymphatic Organs: Thymus |
- Located between the sternum and aortic arch in mediastinum - Right & left lobes with lobules - Lobule cortex: developing T-cells - Lobule medulla: mature T-cells - Secretes: thymopoietin, thymulin, thymosin, interleukin & interferon hormones |
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Lymphatic Organs: Spleen |
- Location: upper left quadrant - Red pulp: RBCs plus macrophages - White pulp: packed lymphocytes - Function: filters old blood cells and bacteria, stores platelets and iron |
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Body Defenses |
Nonspecific Defense: - Innate Immunity: genetically specified and present from birth Specific Defense: - Acquired immunity: produced by exposure to antigens or by transfer of antibodies ==> Active acquired immunity: develops by induced or natural exposure to antigens ==> Passive acquired immunity: develops by induced or natural transfer of antibodies |
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Nonspecific Defense: Innate Immunity - First Line of Defense |
First line of defense: External barriers - Skin: dry & poor in nutrients ==> Keratin: tough surface protein ==> Lactic acid mantle & dermicidin from sweat ==> Hyaluronic acid layer of areolar tissue ==> Defensins & cathelicidins by keratinocytes - Mucous membranes: stickiness traps the microbes and lysozymes dissolve them - Saliva: lysozymes & antimicrobial proteins - Tears: lysozymes dissolve bacterial cell walls - Stomach acid: dissolve bacterial cell walls |
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Nonspecific Defense: Innate Immunity - Second Line of Defense |
- Immune Surveillance: Natural killer cells patrol kills bacteria, viruses and cancer cells with Perforins and Granzymes - Antimicrobial proteins: Interferons and the complement system proteins - Leukocytes and macrophages: neutrophils, eosinophils, basophils, monocytes and natural killer lymphocytes - Inflammation and Fever |
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Leukocytes: Neutrophils |
- Phagocytosis and digestion of bacteria - Formation of a killing zone with hydrogen peroxide (H2O2), superoxide and hypochlorite to kill the surrounding bacteria |
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Leukocytes: Eosinophils |
- Phagocytizeantigen-antibodycomplexes - Antiparasitic effectsfor tapeworms & roundworms - Promotetheactions ofbasophils and mastcells - Secreteenzymes that block excessinflammationand limit the actions ofhistamine allergicresponses (Granules create toxins that fight parasites and destroy antigen-antibody complexes) |
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Leukocytes: Basophils |
Secretes: - Histamin (vasodilator): increases blood flow to infected tissue to deliver leukocytes to the urea - Heparin (anticoagulant): prevents immobilization of phagocytes (Histamineopens way in, so fighting leukocytes can come in and fight infections - Heparinneeded here to prevent coagulation and immobilization so leukocytes can fightinfections) |
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Leukocytes: Monocytes |
- Are circulating precursors that form macrophages - Specialized macrophages found in specific locations: ==> Dendritic cells in mucosa ==> Microglia in the CNS ==> Alveolar macrophages in lungs alveoli ==> Hepatic macrophages in liver |
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Leukocytes: Natural killer lymphocytes |
- Secrete Perforin and Granzymes - Require cell-to-cell contact to kill bacteria, virus-infected cells and tumor cells (Very capable of dissolving, perforating, making holes through cell walls of bacteria/virus cell) |
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Inflammation |
A local defensive response to tissue injury that: - Limits the spread of pathogens - Remove damaged tissues - Initiate tissue repair Cardinal signs: - Redness, swelling, heat and pain |
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Inflammation Processes: Mobilization of Defenses |
- Hyperemia by leukotrines and histamine vasodilation - Recruitment of leukocytes by endothelial cells selectins - Margination and diapedesis of leukocytes in the tissue fluid (Hyperemia: increased blood flow to a specific area) (Mobilization of defenses: bring in the fighters) |
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Inflammation Processes: Containment & Destruction of Pathogens |
- Chemotaxis of leukocytes by inflammatory chemicals - Margination, diapedesis and phagocytosis by neutrophils - Activation of macrophages, antibodies and T-lymphocytes (Containment:surround and destroy pathogens) (Chemotaxis: movement of chemicals that causesleukocytes to go to exact spot where inflammation is occurring) |
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Inflammation Processes: Tissue Cleanup and Repair |
- Macrophages engulf dead bacteria and damaged cells - Edema promotes lymphatic drainage of dead bacteria and tissue debris - Platelet-derived-growth-factor promotes tissue repair (Edema: accumulation of fluid in interstitial space) |
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Fever (Pyrexia) |
An abnormal elevation of body temperature as an adaptive defense mechanism that: - Promotes interferon activity - Accelerates tissue repair by elevating the metabolic rate - Inhibit reproduction of pathogens (Makes environment very unfavorable for pathogens to survive and reproduce) |
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Fever Stages |
1) Exogenous pyrogens secreted by pathogens plus the endogenous pyrogens secreted by neutrophils and macrophages 2) Hypothalamic thermostat is reset to a higher body temperature 3) Onset of fever: body temperature rises to a net set point 4) Stadium: body temperature oscillates (elevates) at the new set point 5) As infection ends, hypothalamic set point returns to normal 6) Defervescence: return of body temperature to normal |
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Immunity Overview |
Immunity: responds to threat on individualized basis - Innate Immunity: genetically determined - no prior exposure or antibody production involved - Acquired Immunity: produced by prior exposure or antibody production ==> Active Immunity: produced by antibodies that develop in response to antigens --------:> Induced active: develops after administration of antigen to prevent disease (vaccination) --------:> Naturally acquired active: develops after exposure to antigens in environment ==> Passive immunity: produced by transfer of antibodies from another person --------:> Naturally acquired passive: conferred by transfer of maternal antibodies across placenta or in breast milk --------:> Induced passive: conferred by administration of antibodies to combat infection (AIDS) |
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Immunity Molecules |
- Antigens: any molecule that triggers an immune response such as a toxin, bacteria or virus - Epitopes: certain regions of an antigen molecule that trigger an immune response - Haptens: small molecules that need to bind to a macromolecule to trigger an immune response |
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Specific Immunity: Acquired Immune Responses |
Immunity is provided by the coordinated activity of T and B lymphocytes in response to the presence of specific antigens Two types of immune responses: - Cellular (Cell-mediated) Immunity: T-lymphocytes respond to intracellular antigens such as virus infected cells and tumor cells (T-cells develop from thymus) - Humoral (Antibody-mediated) Immunity: B-lymphocytes respond to extracellular antigens such as bacteria (B-cells develop from red bone marrow) |
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Cellular Immunity: T-cells Involved |
- Cytotoxic T-cells (CD8): attack foreign antigens - Helper T-cells (CD4): activate cytotoxic T cells - Regulatory T-cells (TR): limit the immune response - Memory T-cells (TM) |
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Cellular Immunity Stages (intracellular) |
1) Recognition: APCs presentation of antigens activates helper & cytotoxic T-cells 2) Reaction (attack): Cytotoxic T-cells deliver a lethal hit of chemicals that destroy antigens 3) Remembering (memory): Immune memory by memory T-cells |
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Humoral Immunity Stages (extracellular) |
1) Recognition: ==> Binding the antigens and their intake by receptor-mediated-endocytosis ==> Helper T-cells activate B-cells differentiation into plasma cells ==> Plasma cells secrete antibodies called immunoglobulins 2) Reaction (attack): ==> IgA, IgD, IgE, IgG, & IgM destroy antigens by four mechanisms: -------:> neutralization (neutralizes toxins), complement fixation (proteins that eat/kill antigens), agglutination (clump antigens so they can't spread), precipitation (makes antigens leave) 3) Remembering (memory): immune memory by memory B-cells |
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Specific Acquired Immunity: Primary Response |
First time to an antigen causes a slow rise in antibodies production, first as the small immunoglobulin M (IgM) then IgG - slower |
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Specified Acquired Immunity: Secondary Response |
Subsequent exposures to same antigen and the presence of memory cells causes faster antibodies production and mainly immunoglobulin G (IgG) - faster |
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Hypersensitivity |
Excessive harmful immune reactions (overactivity) to antigers that include: - Autoimmunity: reactions to one's own tissues - Alloimmunity: reactions to tissues transplanted from another person - Allergies: reactions to allergens from environmental antigens |
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Hypersensitivity: Type I |
- Acute - An IgE-mediated reaction that begins in seconds and subsides in 30 minutes such as asthma, good or drug allergies - Basophils and mast cells secrete histamine causing hives, runny nose, watery eyes or cramps - Anaphylactic shock is a severe Type I hypersensitivity reaction |
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Hypersensitivity: Type II |
- Antibody-Dependent Cytotoxic - Occurs when IgG or IgM attacks antigens on cell surfaces causing cell destruction (transfusion reactions), interferes with cell functions (Myasthenia Gravis) or overstimulates the cell functions (toxic goiter) (Attacks surface of own body cells and destroys cells) (Tranfusion: attacks unknown antigens from other person's blood) (Myasthenia graves: attacks Ach receptors of neuromuscular junctions) (Toxic goiter: produces too much thyroid hormone) |
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Hypersensitivity: Type III |
- Immune Complex Hypersensitivity - Occurs when IgG or IgM forms antigen-antibody complexes that precipitate in tissues or beneath the blood vessels endothelium - Trigger severe inflammation and tissue destruction - Acute glomerulonephritis (in kidneys, glomeruli becomes inflamed) and systemic lupus erythematosis (autoimmune inflammation reaction) |
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Hypersensitivity: Type IV |
- Delayed - A mixture of specific & nonspecific immune responses to antigens by helper & cytotoxic T-cells - Signs appeal 12 -72 hours after exposure to antigens - Allergies to cosmetics, poison ivy, TB test, and type I diabetes mellitus |
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Autoimmune Diseases |
Failure of the immune system to distinguish self-antigens from foreign antigens - Autoantibodies attach the body's own tissues - This failure of self-tolerance may occur due to 3 reasons: ==> Cross-reactivity: antibodies against foreign antigens react against similar self-antigens ==> Abnormal exposure: of some self-antigens to the blood due to a break in a blood barrier ==> Structural changes: in some of the self-antigens structure |
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Immunodeficiency |
Severe-Combined-Immunodeficiency-Disease (SCID): - Caused by recessive alleles that result in a scarcity or absence of both T & B lymphocytes Acquired-Immunodeficiency-Syndrome (AIDS): - Human immunodeficiency virus (HIV) infection severely depresses the immune system responses |
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Digestive System Anatomy |
30 ft long muscular tube extending from mouth to anus - Mouth, teeth, & tongue - Pharynx - Esophagus - Stomach - Small and large intestine - Salivary glands - Liver - Pancreas |
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Functions of the GI tract |
- Ingestion - Mechanical digestion - Chemical digestion - Secretion - Absorption - Excretion |
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Layers of the GI tract |
- Serosa: outer tough CT membrane for protection - Muscularis Externa: longitudinal and circular muscle layers for contraction - Submucosa: loose CT, blood vessels and glands for secretion - Mucosa: made of 3 layers (inner) ==> Muscularis Mucosa (interna) ==> Lamina propria made of loose CT ==> Epithelium lining: (innermost) function for digestion and absorption of nutrients |
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Enteric Nervous System |
The GI tract "Little Brain" which is able to function independent of the CNS Composed of two nerve networks: - Myenteric plexus (Auerbach): ==> Neurons net between circular & longitudinal muscle layers ==> Controls contractions of muscularis externa ==> Controls peristalsis, segmentation, haustration, mass movement - Submucosal Plexus (Meissner): ==> Scattered neurons in the submucosal layer ==> Controls contractions of only muscularis mucosa (interna) ==> Controls glandular secretion of mucosa |
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The Oral Cavity
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- Cheeks and lips: ==> Keep food between teeth for chewing; essential for speech and suckling in infants ==> Vestibule: space between teeth and cheeks - Tongue: sensitive, muscular manipulator of food ==> Papillae and taste buds on dorsal surface ==> Lingual glands secrete saliva, tonsils in root - Hard and soft palate: ==> Allow breathing and chewing at same time ==> Palatoglossal and palatopharyngeal arches |
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Tooth Structure
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- 20 baby or 32 adult teeth - Periodontal ligament is a modified periosteum that anchors into the alveolus - Cementum and dentin are living tissues - Enamel is non-cellular secretion formed during teeth development - Root canal leads into pulp cavity which contain nerves and blood vessels - Gingiva or gums cover |
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Mastication |
- Breaksfood intosmaller pieces to be swallowed - Increasessurfacearea exposedtodigestive enzymes - Contactof food with sensory receptors triggers the chewing reflex ==> Tongue, buccinator and orbicularis oris manipulatefood ==> Masseter and temporalis elevatethe teeth to crush food ==> Medial and lateral pterygoids swingteeth in side-to-side grinding action of molars |
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Salivary Glands |
- Help with mastication: sublingual, parotid, and submandibular glands (they produce saliva) - Histology: each gland is made of acini ==> Mucous acinus: mucous cells ==> Serous acinus: serous cells ==> Mixed acinus: both serous & mucous cells |
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Saliva |
Hypotonic solution of 99.5% water and solutes - Salivary amylase begins starch digestion - Lingual lipase digests fat, activated by stomach acid - Mucus aids in swallowing by lubrication - Lysozyme enzymes kills bacteria - Immunoglobulin A inhibits bacterial growth - Electrolytes: Na+, K+, Cl-, phosphate and bicarbonate Functions: - Moisten - Begin starch and fat digestion - Cleans teeth - Inhibit bacteria - Bind food together into a bolus |
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Salivation |
- Total of 1 - 1.5 liters of saliva per day - Cells filter water from blood and add electrolytes, amylase, lipase, mucin and lysozymes to it - Food stimulates receptors that signal salivatory nuclei in medulla and pons ==> Parasympathetic stimulation: salivary glads produce thin saliva, rich in enzymes ==> Sympathetic stimulation: produce less abundant, thicker saliva, with more mucus - High brain centers stimulate salivatory nuclei so sight, smell and thought of food causes salivation |
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Digestion in Mouth |
Salivary amylase, secreted by salivary glands digests starch into smaller molecules, the smallest being disaccharides (it will further need to be broken down to monosaccharides later for digestion) |
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Swallowing |
- Buccal phase (voluntary): tongue pushes bolus of food from oral cavity into oropharynx - Pharyngeal phase (involuntary): soft palate closes nasopharynx and epiglottis closes larynx (glottis); food bolus pass from oropharynx into laryngopharynx; choking can occur if food bolus is in laryngopharynx - Esophageal phase (involuntary): upper esophageal sphincter opens; peristalsis (squeezing contraction) propels bolus down esophagus toward stomach; cardiac (lower esophageal) sphincter opens and bolus enters stomach |
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Stomach Functions |
- Storage: can eat lots of food at one sitting - Mechanical Digestion: ==> Reduce food to liquid acid chyme by mixing waves ==> Force small amount of chyme from stomach into small intestine - Chemical Digestion: ==> Protein digestion begins by pepsin ==> Fat digestion by activated lingual lipase - Limited Absorption: ==> Aspirin, alcohol, electrolytes, water & drugs |
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Stomach Anatomy |
Not tubular like esophagus and intestines, but more like a pouch, so it can function as storage (gastric rugae can expand and shrink without rupturing mucosa) - Rugae (foldings) that are on surface of gastric pit and gastric glands - Made of: fundic region, cardiac region and body - 2 sphincters: ==> Lower esophageal (cardiac) sphincter: controls what enters the stomach ==> Pyloric sphincter: controls how much liquid comes out of stomach at a time - 3 muscle layers: longitudinal, circular, oblique - Lesser omentum connects stomach to liver |
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Gastric Glands |
- Mucous neck cells secrete protective surface mucus - Parietal cells secrete HCl and intrinsic factor - Chief cells secrete pespsinogen, gastric lipase and chymocin - Entroendrocrine cells secrete gastric hormones - Regenerative cells produce new cells |
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HCl Secretion |
Done by parietal cells - Cl- from blood into lumen of gastric gland - Bicarb buffer system produces H+ and HCO3- ==> HCO3- is taken to buffer blood ==> H+ is taken in gastric gland, which combines with Cl- and produces HCl |
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HCl Functions |
- Activates pepsin and lingual lipase - Breaks CT and plant cell walls - Liquifies food to form chyme - Coverts ingested Fe3+ (ferric) to Fe2+ (ferrous) ions for absorption and use in Hb synthesis - Destroys ingested bacteria and pathogens |
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Gastric Enzymes: Intrinsic Factor |
- Essential for vitamin B12 absorption by small intestine which is necessary for RBCs production and maturation - Deficiency causes Pernicious anemia |
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Gastric Enzymes: Gastric Lipase and Chymosin |
- Lipase digest butterfat of milk in infants - Chymosin curdles milk by coagulating proteins |
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Gastric Enzymes: Pepsin |
Protein for digestion - Secreted as inactive pepsinogen zymogens (by chief cells) - HCl (by parietal cells) converts it to active pepsin |
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Regulation of Gastric Secretions |
1) Cephalic phase: Vagus nerve stimulates gastric secretion even before food is swallowed (10% of total gastric secretions) 2) Gastric phase: food stretches the stomach and activates myenteric and vasovagal reflexes. These reflexes stimulate gastric secretion. Histamine and gastrin also stimulate acid and enzyme secretion (70% of total gastric secretions) 3) Intestinal phase: Intestinal gastrin briefly stimulates the stomach, but then secretin, GIP, CCK, and the enterogastric reflex inhibit gastric secretion and motility while the duodenum processes the chyme already in it. Sympathetic nerve fibers suppress gastric activity, while vagal (parasympathetic) stimulation of the stomach is now inhibited (20% of total gastric secretions) |
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Small intestine anatomy |
Made of 3 major parts: duodenum (connects to stomach and to jejunum), jejunum (middle), and ileum (connects to cecum of large intestine) - All parts held together by mesentery membrane (carries blood vessels with nutrients) - Long tube, so food can come in contact with mucosa in order for absorption and digestion to occur |
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Small intestine histology |
Lined with about 4.5 million villi - Small finger like extensions - Each villus is covered with a simple columnar mucous membrane (increases surface area for absorption and digestion) - Blood capillaries inside for absorbing most substances - Single lymph capillary called a lacteal for absorbing most fat - Villi are simple columnar cells containing: ==> Absorptive cell (most abundant, responsible for absorption) ==> Goblet cell (produce mucus, makes acid chyme slide easily) ==> Endocrine cell (produces intestinal hormones) ==> Paneth cell of intestinal crypt (macrophages - capable of eating bacteria) |
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Small intestine functions |
Mechanical digestion: - Peristalsis propels chyme along intestine - Segmentation move chyme back and forth to mix it thoroughly Chemical digestion: - Enzymes from pancreas and small intestine complete digestion of protein, starch, disaccharide sugars and fat - Gallbladder empties bile into small intestine to aid in fat digestion Absorption of most substances |
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Pancreas anatomy |
- Head, neck, body and tail - Head into duodenum - Tail to spleen - Pancreatic duct joins bile duct and connect to duodenum |
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Histology of Pancreas |
- Acini are exocrine cells that secrete digestive enzymes into the ducts - Duct cells secrete a bicarbonates solution that buffer the acidic chyme from stomach and raise its pH from 2-3 to 7-8 |
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Hormonal Control of Pancreatic Secretion: Cholecystokinin |
Released from duodenum in response to arrival of acid and fat - Causes contraction of gallbladder, secretion of pancreatic enzymes, relaxation of hepatopancreatic sphincter |
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Hormonal Control of Pancreatic Secretion: Secretin |
Released from duodenum in response to acidic chyme - Stimulates all ducts to secrete more bicarbonate |
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Hormonal Control of Pancreatic Secretion: Gastrin
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Gastrin from stomach and duodenum weakly stimulates gallbladder contraction and pancreatic enzyme secretion |
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Digestion by Pancreatic Enzymes: Protein |
- Enzymes are secreted as inactive zymogens - Trypsinogen activated to trypsin by entrokinase enzyme from duodenum epithelium cells - Chemotrypsinogen activated to chymotrypsin by the trypsin enzyme - Procarboxypeptidase activated by the trypsin enzyme to carxopeptidase - The activated enzymes digest proteins into small peptides |
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Digestion by Pancreatic Enzymes: Starch |
- Remaining starch is digested in intestine by pancreatic amylase - Digestion same as in the mouth |
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Digestion by Pancreatic Enzymes: Fats |
- Triglycerides digested in small intestine by pancreatic lipase - Digestion of each triglyceride yields a monoglyceride molecule and two fatty acid molecules |
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Role of Bile |
- Bile from the gallbladder is required for lipase to digest fat more efficiently - Bile flows from gallbladder down the bile duct into duodenum to mix with and emulsify the fat - Emulsification is breaking fat drops into very small droplets ==> Fat globule is broken up and coated by lecithin and bile acids (amphipathic molecule) |
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Liver anatomy |
- Right and left lobe |
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Liver Histology |
- Lobescontain microscopic lobules - Lobulesconsist of rows (plates) of liver cells (hepatocytes) and rich blood supply - Bloodsupplied by branches of the hepatic artery and portal vein at the six cornersof each lobule - Bloodflows toward the center of each lobule through liver capillaries (sinusoids) - Rowsof liver cells surround the capillaries - Bloodflows from the capillaries into the central vein in the center of the lobule - Livermacrophages called Kupffercells are found in the capillaries for phagocytosis |
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The Biliary System |
- Hepatocytessecretes bile - Bileflows from the liver through hepatic ducts into the gallbladder - Gallbladderstores and concentrates bile - Commonhepatic duct and cystic duct from GB unite to form common bile duct - Commonbile duct unites with pancreatic duct - Bileand pancreatic juices enter the duodenum |
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Functions of the Liver |
- Carbohydrate, lipid and proteinmetabolism - Removal of waste products &detoxification - Storage of glycogen, vitamins and iron - Phagocytosis by Kupffer cells - Activation of vitamin D - Bile synthesis and secretion - Plasma proteins synthesis |
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Digestion by Intestinal Enzymes |
Intestinal enzymes called brush-border enzymes - Located on microvilli of intestinal absorptive cells (cells that digest & absorb nutrients) - Peptidases digest peptides to amino acids - Intestinal lipase digest fats to glycerol and fatty acids - Oligosaccharides digested to monosaccharides |
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Protein Digestion by Intestinal Enzymes |
Actions of pancreatic enzymes - Trypsin and chymotrypsin hydrolyze other peptide bonds, breaking polypeptides down into smaller oligo peptides - Carboxypeptidase removes one amino acid at a time from the carboxyl end of an oligopeptide |
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Protein Absorption by Small Intestine |
Actions of brush border enzymes (contact digestion) - Carboxypeptidase of the brush border continues to remove amino acids from the carboxyl end - Aminopeptidase of the brush border removes one amino acid at a time from he amino (-NH3) end - Dipeptidase splits dipeptides into separate amino acids |
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Fats Digestion by Small Intestine |
Fat hydrolysis - Emulsification droplets are acted upon by pancreatic lipase, which hydrolyzes the first and third fatty acids from triglycerides, usually leaving the middle fatty acid Lipid uptake my micelles: - Micelles in the bile pass to the small intestine and pick up several types of dietary and semi-digested lipids |
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Fats Absorption by Small Intestine |
Chylomicron formation - Intestinal cells absorb lipids from micelles, resynthesizes triglycerides, and package triglycerides, cholesterol, and phospholipids into protein-coated chylomicrons |
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Carbohydrate Digestion by Small Intestine |
Disaccharidases digest disaccharides to monosaccharides - Sucrose + sucrase => Glucose + Fructose - Maltose + maltase => Glucose + Glucose - Lactose + lactase => Glucose + Galactose |
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Carbohydrate Absorption by Small Intestine |
Tight junction H2O, glucose |
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Absorption in Small Intestine |
- DNA and RNA hydrolyzed by nucleases to nucleotides ==> Nucleosidases and phosphatases of brush bordersplit them into phosphate ions, ribose or deoxyribosesugar and nitrogenous bases then absorbed - Vitamins areabsorbed unchanged ==> A, D, E and K with other lipids --B complex and C by simple diffusion and B12 ifbound to intrinsic factor - Minerals areabsorbed all along small intestine ==> Na+co-transported with sugars and amino acids ==> Cl-exchanged for bicarbonate ==> Iron and calcium absorbed as needed |
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Large Intestine Anatomy |
anal canal |
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Large Intestine Histology |
- Simplecolumnar mucosa - Deepcrypts with intestinal glands - Glandssecrete lots of mucus - Nocircular folds or villi |
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Functions of Large Intestine |
- Feces formation - Limited digestion of undigested food by bacteria - Formation of vitamin K and some B vitamins by bacteria - Absorption of some water, electrolytes, vitamins and bile acids |
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Motility and Absorption of Large Intestine |
- Transittime is 12 to 24 hours during which water and electrolytes are absorbed. - Fecesconsist of water, bacteria, undigested fiber, mucus, fat and sloughedepithelial cells - Haustralcontractions occur every 30 minutes when stimulated by distention - Massmovement occur 1 to 3 times a day triggered by gastrocolic and duodenocolicreflexes from stomach and duodenum filling. - Massmovement push feces into the rectum. |
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Anal Canal Anatomy |
Rectal valve |
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Neural Control of Defecation |
1.An intrinsic reflexactivate mass movement that fill the rectum and stimulate rectal stretchreceptors 2.A spinal cord reflex cause contraction of the rectum and relaxation of the internal anal sphincter 3.A pudendalnerve reflexcause conscious voluntary relaxation of the external sphincter & defecation |
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Water Balance |
- Digestivetract receives about 9 L of water/day ==> 0.7 L in food, 1.6 L in drink, 6.7L in secretions ==> 8 L is absorbed by small intestineand 0.8 L by large intestine - Wateris absorbed by osmosis following the absorption of salts and organic nutrients - Diarrheaoccurs when too little water is absorbed ==> feces pass through too quickly ifGI is irritated ==> feces contains high concentrationsof an unabsorbed solute such as lactoseor chloride |
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Digestive System Disorders |
- Gingivitis: Inflammation of the gums - Periodontal disease: Inflammations of the teeth, ligamentsand alveolar bones - Stomatitis: Inflammation of the mouth mucusmembranes - Esophagitis: Inflammation of esophagus - Dysphagia: Difficulty of swallowing - Gastritis: Inflammation of the stomach - Enteritis: Inflammation of small intestine - Diverticulitis: Inflammation of the colon - Hepatitis: Inflammation of the liver - Pancreatitis: Inflammation of the pancreas - Hemorrhoids: Permanently distended veins |
