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177 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Tunica intima
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innermost layer
simple squamous cells |
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tunica media
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concentric sheets of smooth muscles
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Tunica externa
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outermost
collagen and elastic fibers |
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shape of lumen artery
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appears smaller than veins
pleated retains shape |
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shape of lumen vein
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no pleats
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Elastic arteries
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large vessels
aorta, pulmonary, trunk, carotid |
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Muscular arteries
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conduct blood to organs and skeletal muscle
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arterioles
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service tissue
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aneurysm
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weakness of muscle resilience, due to decrease elasticity
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continueous capillaries
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located everywhere except cartilage and epithelial tissue
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Fenestrated capillaries
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choroid plexus, intestines, kidneys
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Sinusoidal caplillaries
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liver, spleen, bone marrow
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anastomeoses
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joining of 2 tubes
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angiogenesis
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formation of new bl vessels in heart
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vasomotion
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alternate bl flow to different areas of capillary bed
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autoregulation
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doesnt need NS innervation
regulated by chemical and materials |
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venules
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collect blood from capillaries
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hemorrhaging
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vasomotor of medulla oblongata
venoconstriction venous reserve mobilized- moved from liver, skin and lungs to brain and muscles |
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arterial pressure
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capillary network
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vessel length
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increase length
increase resistance by the amount it is lengthened |
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vessel diameter and resistance
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R=1/r4
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relationship between blood flow, blood pressure and resistance
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Flow is change of bp/ R
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Pulse Pressure
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difference between the systolic and diastolic pressure
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Mean arterial Pressure (MAP)
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Diastolic pressure+ Pulse pressure/3
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Blood Colloid Osmotic Pressure
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caused by osmosis H2O moves to increased solute concentration
Roughly 25mmHg |
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Net filtration
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CHP-BCOP
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Benefits of water out of capillaries and into lymphoid system
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ECT and plasma in constant communication
Distributes nutrients/hormones/gas assists in transport of insoluble lipids flushes bacteria |
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venous pressure
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16mmHg difference
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vasodialators
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co2, low o2, acid, potassium ions, hydrogen ions
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vasoconstrictors
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prostaglandins, thromboxanes, endothelins
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Neural vessel mechanisms
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medulla oblongata-sympathetic motor neurons
widespread vasoconstriction/dialation |
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widespread vasoconstriction
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wide spread release of norepinephrine
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widespread vasodialation
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Ach, endothelial cells release NO
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fully dialated resistance vs fully restricted
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80x more resistant
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aortic and carotid reflex and increased BP
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Vasomotor center-dilation
cardioinhibitory- stimulated cardioacceleratory-inhibited |
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aortic and carotid reflex and decreased BP
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constriction
cardioaccelaratory |
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Atrial reflex and increase BP (stretching of atrium)
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cardioacceleratory
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aortic and carotid reflex and Increased CO2
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constriction
cardioacceleratory |
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medulla oblongata and increase of CO2
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dialation of cerebral vessels
constriction of most other organs increase resp rate |
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Norepinephrine and epinephrine effects
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increase HR, vasoconstriction
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ADH effects
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decrease urine, increase BV, increase,BP,
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angiotension II affects
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stimulates ADH to conserve H2O
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Ace inhibitors
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prohibit angiotension II thus allowing release of H2O and dropping blood pressure
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secondary Hypertension
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increase of ADH, renin, aldosterone, and epinephrine
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causes of shock
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hemorrhage
heart damage external pressure on heart extensive peripheral dilation |
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coverings of heart from outside to inside
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parietal pericardium
paricardial cavity(sac) visceral pericardium Myocardium endocardium |
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cardiac tempanade
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accumulation of fluid int the pericardial cavity that restricts heart movement
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arteries
veins |
efferent
afferent |
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superior vena cava from....
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head, arms, kneck
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inferior vena cava from...
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lower extremities, midsection
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coronary sinus from...
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blood from heart
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regurgitation cause
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cut cordae tendinae or damaged papillary muscles
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moderator band
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connected with papillary muscle through conductor cells causing contraction before ventricles
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VHD valvular Heart Disease
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Valve stenosis creates cracks between cusps
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2 blood flow circuits
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systemic- organs and extremities
pulmonary- to and from lungs |
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anterior interventricular branch
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lies within ant interventricular sulcus
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circumflex branch
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meet and fuse with branches of right coronary artery
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Marginal arteries
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extend across right ventricle
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anastomoses
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PIA branches to meet AIA
an interconnection of vessels |
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drain straight into R atrium
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Great cardiac vein
small cardiac vein anterior cardiac veins |
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Drain into coronary sinus then right atrium
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Posterior cardiac vein
Middle cardiac vein |
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Coronary ischemia
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partial or complete blockage of coronary artery due to plaque or thrombus
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angina pectoris
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chest pain
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myocardial infarction
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coronary circulation block causes cardiac muscle cells to die (infarct)
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Treatments of MI
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drugs-vasodilators
surgical: catheter, balloon, stent, bypass surgery |
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conducting cells
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control and coordinate heart beat.
distribute electrical impulses |
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automaticity
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AP is initiated by autorhythmic cells, heart cells can contract without NS.
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sinoatrial node
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located in the wall of r atrium
80-100 AP/min |
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atrioventricular node
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impulse delays
40-60 AP/min |
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AV Bundle (bundle of His)
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only electrical connection between atria and ventricle
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Purkinje Fibers
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apex to base
20-40 AP/min |
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ectopic pacemaker
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abnormal cells generates an AP, can override SAor AV node. Can be a conducting or contractile cell
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pathway of heart stimulus
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sinoatrial node
atrioventricular node AV bundle R and L bundle branches Perkinje Fibers |
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R and L bundle branches
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moderator band
papillary muscles |
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arrhythmias
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abnormal patters of electrical activity
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Premature Ventricular Contractions
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purkinje fiber or ventricular myocardial cell depolorizes to threshold and causes a premature contractions
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A Fib
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atrium, survivable
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B Fib
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Ventricle
lethal |
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Fibrillation
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very fast, uncoordinated heart muscle contractions
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P Wave
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atrium AP
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QRS complex
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ventricle AP
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T wave
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repolarization of Ventricles
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large QRS
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enlarged heart, mainly left ventricle
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small T wave
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Ischemia
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large T wave
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heart attack
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resting potential
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-90mV
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threshold
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-75mV
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depolarization
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-75 to 30mv
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contraction occurs...and why?
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during plateau
incoming ca++ binds to troponin, which initiates contraction |
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Plateau
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30mv-0mv
prevents tetanus |
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effects of Hypercalcemia on heart
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contraction is strong and long
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effects of hypocalcemia on heart
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contraction is weak, may even stop
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Repolarization
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-90mv
K+ channels open and K+ exits cells |
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effects of hyperkalemia on heart
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repolarization is inhibited, muscle weakens, contractions slow and even stop
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effects of hypokalemia on heart
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myocardium is hyperpolarized, less responsive to stimulation and HR decreases
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Refractory Period
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membrane is not going to respond to another AP
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absolute refractory period
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no other AP, plateau extends without tetanus
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relative refractory period
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Na+ gates close
can if strong enough stimulus |
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intercalated discs
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interlocking of membranes of adjacent cells
connected mechanically, chemically,and electrically |
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systole
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chambers contract
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diastole
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chambers relax
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Pressure=
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1/Volume
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EDV End Diastolic Volume
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max amount of blood ventricle can hold in that cardiac cycle
130mL |
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ventricular ejection stroke volume (SV)
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70-80 mL
60% at end of EDV |
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ESV End Systolic Volume
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Volume left in the ventricle at the end of ventricular systole
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lubb (S1)
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blood smashing into AV valves
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Dubb (S2)
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SL valve closes
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S3
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blood flowing into ventricle
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S4
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atrial contraction
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Preload
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amount of stretch in ventricles
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ESV
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end systolic volume
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contractility
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ability of heart to contract
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positive inotropic agents
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increased contractility
Sympathetic NS epinephrine, glucoagons |
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Negative inotropic agents
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decreased contractility
parasympathetic NS |
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afterload
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amount of pressure needed to pen semilunar valve
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SV=
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EDV-ESV
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Ejection fraction
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% of EDV that leaves the heart
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cardiac output
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heart Rate x stroke volume
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caffeine affects
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increase depolarization of SA node
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nicotine affects
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stim activity of Sympathetic NS to increase HR
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affects of temperature on heart
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decrease temp slows depolarization
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ANS regulation adjust HR.
describe pattern |
sensory reception-->hypothalamus-->medulla oblongata (cardioacceleratory (sympathetic) cardioinhibitory (parasympathetic))-->cardiac plexus (innervation of SNS and PNS at SA node)
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Cardiac reserve
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difference between rest and maximum cardiac output
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describe heart beat action
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-90mv-->-75mv-->Na+ enters cell, depolarizes-->30mv Na+ closes-->Na+exits, slow Ca++ enters (plateau/contraction)--> 0mv slow Ca++ closes K+ channels open (repolarization)--> -90mv
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blood characteristics
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100.4 degrees, 5x more viscous, 4-6 Liters, 7% of body weight
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plasma
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92% H2O, electrolytes, connective tissue, matrix of blood, Proteins
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Albumins
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lg proteins, maintain BCOP
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Globulins
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involved in immune function
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Fibrinogen
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clotting
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serum
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blood with clotting factors removed
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Hematocrit
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% of formed elements in blood
include platelets, RBC, and WBC 99.9% RBC |
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RBC shape
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biconcave
rouleaux-stacking of RBC |
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RBC contents
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95% hemoblobin
lacks organells |
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oxyhemoblin
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O2 bound hemoglobin
4 O2 molecules/hemoglobin |
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deoxyhemoglobin
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no oxygen, dark red
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carbaminohemoglobin
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bound to CO2 but not on heme
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anemia
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decrease hematocrit and decreased or defective hemoglobin
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iron deficiency anemia
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low hemoglobin
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pernicious anemia
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B12 deficiency, needed for RBC production
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Form and function of Golgi Complex or Golgi apparatus:
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Modifies, stores, sorts and ships cell's chemical products.
This structure is stacked to increase surface area. |
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requirements of erythropoiesis
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AA
iron B12 intrinsic factor B6 |
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hormonal controls of erythropoiesis
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throxine-thyroid, metabolism
EPO- kidneys release Growth Hormone |
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recycle RBC
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liver/spleen/bone marrow
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recycling flow chart of RBC
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Heme-->iron and Biliverdin (green)-->Bilirubin-->kidneys (urine) and Urobilins/stercobilins (feces)
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parts of RBC that are recycled into new RBC
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A.A. and Fe2 (iron)
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why does blocked bile ducts result in jaundice
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diffuses into peripheral tissues becaus it is normally eliminated in bile
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hemoglobinuria
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Red/brown urine due to hemolysis in circulatory system
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hematuria
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intact RBC in Urine
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antibodies of A antigen
blood donors compatible |
B
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A, O
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antibodies of B antigen
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A
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B,O
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antiobodies of AB antigens
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none
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accept A,B,O
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antibodies of O antigen
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A,B
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O
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+Rh antigen
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no Rh antibodies
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-Rh antigen
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may have anti-Rh antibodies
-only if exposed to Rh anigen |
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Hemolytic disease of newborn
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Rh- mother with an Rh+ newborn
during delivery |
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Rhogam
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prevents Rh antibodies from forming
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Diapedesis
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movement of WBC thru the walls of blood vessels by migration between adjacent endothelial cells
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Ameboid motion
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a gliding motion accomplished by the flow of cytoplasm into slender cellular processes extended in front of the cell
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positive chemotaxis
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guides WBC's to invading pathogen, damaged tissue, and other active WBC
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Phagocytosis
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the engulfing of EC materials or pathogens
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Leukopenia
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Low WBC's
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Leukocytosis
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excessive numbers of WBCs
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Leukemia
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Excessive numbers of dysfunctional WBC
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Megakaryocyte
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breaks into little packets called platelets
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thrombocytopenia
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too few platelets
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thrombocytosis
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too many platelets
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essential for blood coagulation
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Calcium and vitamin K
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vascular phase of hemostasis
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vascular spasm so that basal lamina can be exposed
endothelial cells release factors and hormones, andbecome sticky |
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platelet phase of hemostasis
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platelets stick to sticky endothelial cells
release compounds to attract more platlets platelet aggregation becomes plug |
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coagulation phase
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fibrinogen-fibrin traps platelets and blood cells froming blood clot
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thrombus
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blood clot attached to blood vessel
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embolism
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drifting mass that is capable of inhibiting the flow at a different site
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cascades
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extrinsic, intrinsic, and common pathway
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extrinsic pathway
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shorter/first
reaction to tissue damage |
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intrinsic pathway
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activated by proenzymes
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hemophilia
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lack factor 8
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abnormal clot prevention
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coumadin, aspirin
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