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195 Cards in this Set
- Front
- Back
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what determines the speed of flow of blood throughout the circulatory system?
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total cross sectional area, the higher then increas in total cross sectional area, the slow the speed.
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what is laminar flow in blood vessels?
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blood adjacent to the vessel wall goes slower than blood in the middle due to friction.
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Where is most of the blood found in the body at any moment in time?
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veins (2/3 of total blood)
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where is the primary resistence of blood flow found?
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arterioles and capillary sphincters
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what allows blood vessels to strectch?
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elastin in the vessels
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what limits the amount of stretch in blood vessels
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collagen in the blood vessel
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what allows blood flow to continus during diastole?
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the stretched artery returns to it's smaller shaping, continuing to force the blood through the relaxed artery
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what is more distensible veins or arteries or arterioles or capillaries
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veins
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why is it more difficult to have an increase in arterial pressure in the pulmonary system than the systemic?
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b/c the pulmonary arteries are thinner to allow gas exchange, which allows more distention than the systemic arteries
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what is the difference between compliance and distensibility in blood vessels
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compliance means the distensibility of vessels multiplied by volume that they hold
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what is the problem with vericose veins
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increases expansion of vessel, which decreases velocity, increasing possibility of thrombus formation which can lead to a clot
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what mechanisms help in stopping blood from pooling in the legs
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valves in the veins and skeletal muscle pump
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what is the most potent vasodilator?
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adenosine
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what is the non-metabolic local regulatory mechanism ob flow rate in tissue?
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intrinsic property of smooth muscle, when it is stretched, it contracts.
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what determines the local flow of blood in tissues?
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the rate of local metabolism in the tisssues
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what happens if the increased pressure in prolonged in blood flow
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angiogenesis which leads to an increase in vascularity to lower the blood pressure
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what chemicals stimulate formation of blood vessels
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VEGF, FGF, Angiogenin
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what causes the blood vessel growth stimulating compounds to be released into the blood?
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increased metabolism of cells surrounding the local capillaries
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what compounds cause vasoconstriction in local tissues?
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epin and norepinephrine, angiotensin II, Vasopressin, and endothelin
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which vasoconstricting compound is released by damaged blood vessels to decrease local blood flow?
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endothelin
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what are the compounds can produce systemic vasodilation?
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bradykinin, histamine
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how does bradykinin work?
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injured cells release kallikrein, which activates plasma proteins Kallidin which cauaes bradykinin to be released and stimulates vasodilation
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how does histamine work
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mast cells in damaged tissues release histamine that causes tissue adema to cause better healing by increasing blood flow
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what effect does extracellular calcium have on vasculature
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increased calcium indicated higher amount of smooth muscle contraction, leads to vasoconstriction
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what effect do magnesium and potassium and low pH have on the vasculature
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vasodilate
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what parts of vasculature are effected by sympathetics
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effects all except capillaries, precapillary sphincters, and metarterioles
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what is vasovagal syncope?
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large parasympathetic outflow to the blood vessels that causes profound vasodilation that leads to a large drop in venous return due to a drop in arterial pressure which can cause you to faint. tied to strong emotions
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what happens when the baroreceptors sense a loss in blood pressure?
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arterioles and major veins vasoconstrict. arteriole constriction increases total peripheral resisance which increases blood pressure. vein constriction increases return, stroke volume and cardiac output, and the heart is directly stimulated to increase stroke volume
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does the vasodilator or vasoconstrictor center in the brain work faster?
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vasoconstrictor center reacts in about 10 seconds, vasodilator center takes about 40 seconds
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how does a change in pressure effect the stretch baroreceptors in the thoracic blood vessels?
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when stretched, it activates the vasodilation center and inhibits the vasoconstrictor center, and the opposite occurs when pressure drops
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what is orthostatic hypotension?
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a change in position that can cause a sudden drop in blood pressure. the baroreceptors in the thoracic blood vessels react to this quickly and work to bring your presure down
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what is the long term control of blood pressure?
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kidneys because the baroreceptors will reset to a new level if the blood pressure remains high for an extended period of time
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descibe the function of the stretch receptors in the atria and pulmonary arteries
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they are low pressure receptors. if a sudden increase in blood volume happens in those areas, it causes vasodilation to protect against edema formation in the lungs
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describe the atrial receptors as they act on the volume reflex
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volume reflex vasodilates afferent arterioles in the kidneys which leads to urine formation which leads to lower blood volume and less atrial stretch.
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describe the bainbridge reflex?
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an increase in atrial pressure causes the atrial receptors to increase heart rate which leads to an increase of cardiac output and leads to a decrease in the atrial pressure
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what normally happens if the kidney disfunctions?
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hypertension
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how does the kidney know to increase or decrease the urine production?
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juxtaglomerular apparatus in the kidney senses a change in blood pressure.
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describe what happens when you have a prolonged low pressure in vasculature
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juxtaglomerular apparatus produce Prorenin and it is converted to Renin and it circulates in the blood and causes angiotensinogen to change to angiotensin 1 (inactive). Angiotensin 1 convertes to 2. Angiotensin 2 vasoconstricts and also causes sodium retention and causes the adrenal gland to release aldosterone.
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excersise causes local regulation and sympathetic regulation of the veaculature, what is the dominant control?
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local regulation causes dilation and sympathetics cause constriction. The local regulation will dominate the systemic sympathetic control
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what are the causes of hypertension
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hypersecretion of renin, strong sympathetic outflow (acute neurogenic hypertension), and essential hypertension which is associaeds with excess weight and sedentary lifestyle
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how do you treat hypertension?
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decrease the blood volume by using diuretics. can also decrease blood volume in the arteries by lowering the cardiac output with B1 antagonists. Increase vascular volume by Ca blockers and ACE inhibitors
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what does the body do in response to a weakened heart
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compensates by a sympathetic response causing vasoconstriction in the arterioles
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what effect does compensated heart failure have on the kidneys?
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less blood flow to the kidneys, less urine, increasing blood volume, increasing angiotensin 2, causing more vasoconstriction, increasing venous return to an already weakened heart causing an increase of afterload that makes it harder for the heart to pump blood out of it because the arteries are constricted creating more resistence
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what are the characteristics of right ventricular failure
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bulging veins becuase of blood accumulation, low energy and edema in the ankles and legs
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what are the characteristcs of left ventricle failure
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low energy and edema in the lungs, which causes liquid to pool faster than the lymphatics can drain it.
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what can be used in the decompensated phase of heart failure
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can use digitalis which is + inotropic agent, increases calcium by inhibiting the calcium pumps
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what is shock?
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inadequate blood flow due to a decrease in cardiac output or and increase in vascular volume
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what problems can cause shock?
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heart problems and a decrease in venous return
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what is toxic shock?
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endotoxins from bacteria
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what is hypovolumic shock
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profound blood loss
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what is neurogenic shock
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venous dilation from deep anesthesia or brain damage
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what is anaphyactic shock?
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allergic response
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how do you treat shock
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increasing venous return by lifting legs upor using drugs to cause vasoconstriction (stmpathomimetic drugs) or you can administer O2 which also vasoconstricts
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stenosed valves cause what?
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causes the heart to pump harder and cause heart souns during diastole
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what is the normal inhilation and exhilation called?
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tidal volume
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What is it the exhalation called after your normal exhalation?
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expiratory reserve
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what is the air that can not be determined by spirometry and is the air that can nnot be exhaled?
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residual volume
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what is the functional residual capacity
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expiratory reserve + residual volume
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what is the air inhaled past a normal inhalation called?
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inspiratory reserve
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what is the inspiratory capacity?
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inspiratory reserve + tidal volume
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What is the vital capacity in breathing?
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Inspiratory reserve + tidal volume + expiratory reserve volume
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what is the total lung capacity
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inspiratory reserve volume + tidal volume + expiratory volume + residual volume
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what is the difference between anatomical dead space and physiological dead space?
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anatomical dead space is the air in the passage way that does not enter the alveoli. Physiological dead space is the air that does get to the alveoli but does not undetgo gas exchange due to compromised blood flow.
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what is the difference between minute repiratory volume and alveoli respiratory volume?
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minute is tidal volume X breathes per minute. alveoli is tidal volume - dead space X breathes per minute
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what are the different characteristics between normal and altered lungs in sounds?
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normal: breath sounds are predominantly vesicular, muffled "ee" is heard normal, whispered words are faint, spoken words are muffled, and tactile fremitus is normal. Airless lung, as seen with lobar pneumonia are typical bronchovesicular or bronchial sounds, not muffled, "ee" is heard as "ay", and tactile fremitus is increased
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What are the characteristics and causes of late inspiratory crackles?
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persists breath to breath, may begin at first half of inspiration, persists through second half, begins at base and then spreads up. Is caused by interstitial lung disease and early congestive heart failure
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wgat are the characteristics and causes of early inspiratory crackles?
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appear soon after inspiration, don't continue later. Often coarse and few in number. Caused by chronic bronchitis and asthma. Can be associated with expiratory crackles
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when are midinspiratory and expiratory crackles heard?
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bronchiectasis, wheezes and rhonchi are sometimes associated
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Describe characteristics and causes of wheezes and rhonchi
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air flows rapidly through narrowed bronchi, causes include asthma, chronic bronchitis, COPD, congestive heart failure. Wheezes can be heard in expiration or in both with asthma.Rhonchi indicates fluid in the larger airways
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What is a wheeze that predominatly inspiratory called?
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Stridor - louder in neck, demands immediate attention
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describe what pleural rub is
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inflamed plueral surfaces rub against eachother causing friction. When surrounded by fluid, sound dissappears. Resembles crackles, but is localized to inflammed area.
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what is mediastinal crunch?
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crackles in synch with heart beat, not respiration. due to medialstinal emphysema
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what produces the first heart sound, S1?
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closure of the mitral valve at ventricular systole
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what produces the second heart sound, S2?
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closure of the aortic valve at ventricular diastole
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when may you hear the mitral valve opening?
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if the patient has mitral stenosis
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what produces a possible third heart sound, S3?
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blood flowing from the left atrium to the left ventrical.
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What produces a possible fourth heart sound, usually not heard in adults?
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atrial conraction
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when may you be able to hear both the left and the right semilunar valve closing?
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during inspiration
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Where is the best area to hear mitral valve defects
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around the cardiac apex
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intracellular pH?
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6.9-7.1
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extracellular pH?
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7.3-7.5
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primary extracellular buffer?
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HCO3-
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primary contributors to ECF regulation?
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weak acids(seconds), lungs(minutes), and kidneys(days)p
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pH of Carbanic acid?
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6.1 (good buffer)
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important buffer of urine?
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HPO4 -2
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important intracelluar buffer
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protiens (hemoglobin)
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if you have respiratory acidosis, how does the body compensate?
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metabolic alkalosis (acidic urine)
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respiratory alkalosis is compensated by what?
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metabolic acidosis (alkaline urine)
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metabolic acidosis os compensated by what?
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respiratory alkalosis (hyperventalate)
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metabolic alkalosis is compensated by what?
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repiratory acidosis (hold breath)
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kidneys are important for the regulation of what?
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water, ion, acid/base balance
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how much water does the body try to lose each day?
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same amount as is taken in
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what is the standard CHP?
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60 mm/hg (filtration)
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where does bulk reabsorption take place?
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proximal convuluted tubule
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where is the osmotic gradient produced?
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loop of henle (justaglomerular loops)
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where does fine tuning reabsorption take place?
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distal convuluted tubule
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where does fine tuning reabsorption of water take place?
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collecting tubule/duct
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what blood substances are not filtered, reabsorbed, or secreted?
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plasma protein
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what blood structure is filtered, but not reabsorbed or secreted?
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drugs
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what blood structure is filtered and reabsorbed, but not secreted?
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glucose, amino acids
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what blood structure is filtered and secreted, but not reabsorbed?
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PAH
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how many times a day is blood plasma filtered?
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60 times/day
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how much of the plasma that flows to the kidneys actually is filtered?
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20%
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what 3 components make up the glomerulr capsule?
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podocytes, basement membrane, capillary endothelium
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normal net filtration pressure?
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10 mmHg
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what factors decrease glomerular filtration rate?
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low Kf (hypertension, diabetes), high bowman's HP (stones) high Capillary Osmotic Pressure (dehydration)
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what increases glomerular filtration rate?
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high CHP(regulated by afferent and efferent arteriole resistence, and systemic pressure)
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what causes arterioles in kidneys to dialate and lower GFR?
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sympathetics (regulated by prostaglandins)
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what causes arterioles to constrict and increase GFR?
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angiotensin(efferent)used to maintain levels in times of hypotension
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what causes vasoconstriction and lower GFR?
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Norepinephrine, epinephrine, endothelin
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what causes vasodilation and increased GFR?
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nitric oxide
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what is the key to auto regulation in the kidneys of GFR?
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tubuloglomerular feedback by monitoring Na and Cl at macula densa (contricting efferent and dilating afferent)
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what substances are coompletely reabsorbed in the PCT?
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glucose, bicarbonate, sodium, calcium
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what is partially reabsorbed in the PCT?
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potassium, urea
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what is not reabsorbed at all in the PCT?
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creatine
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what are reabsorbed across tight junctions in the PCT?
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water and ions
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what things are absorbed by primary transcellular active transport?
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Na
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what is absorbed by sencondary transcellular active transport?
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glucose, AA,
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what sybstance does not have a Tmax because it also has passive reabsorption?
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Na
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what is secreted in the PCT
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bile salts, uric acid, PAH
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what is secreted in the DCT and collecting tubule?
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H+
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what is the purpose of the juxtaglomerular apparatus in the DCT
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monitoring filtrate leaving the loop, regulate the GFR
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what does the diluting segment of the DCT do specifically
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reabsorbs Na, Cl, and K, but not H20
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how does ADH work?
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binds to V2 receptors in late DCT and collecting tubule and increases H20 absorption
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why is urea hard to get rid of?
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b/c it is highly concentrated in the medulla, and makes an important part of the osmotic gradient
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what increaes [k] lost in urine
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high [K] in plasma, aldosterone, increased tubuar flow,
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what causes a decrease in [K]loss in urine?
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acidosis
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why is H+ secreted in the kidneys?
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to reabsorb the HCO3
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what happens if [HCO3] is low?
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H+ is lost in the urine
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what is lost in urine during acidosis?
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HCO3 and HPO4
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what substances are used to trap the H+?
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HPO4 and ammonia (ammonia is secreted)
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what are the regulators of the kidneys?
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aldosterone and antidiuretic hormone
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how and when are sypmathetics used to regulate the kidneys?
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used to constrict the arterioles, lowering GFR, increasing tubular reabsorption, holds on to as much water as possible to maintain blood volume. Used in sever hemmorhage
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how does angiotensin work?
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decreased BP causes renin secretion, causes Angiotensin release, causing vasoconstriction, lowering GFR and increasing BP, and Na absorption
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what does ADH do?
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causes water retention in DCT and collecting tubule
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what does atrial natriuretic peptide do
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lowers plasma volume by increasing urine volume
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what is a normal intrapleural pressure?
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-5cm H2O
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what is the first change to be recorded in the inhalation cycle?
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a drop in the pleural pressure, from -5 to -7.5
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what happens prior to air entering the the lungs?
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alveolar pressure drops
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what is the difference between the pleural pressure and the alveolar pressure called?
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transpulmonary pressure,
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what forces cause the lungs to collapse?
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transpulmonary presseure(1/3), and surface tension (2/3)(water wanting to be with other water)
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what secretes surfactant?
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type II alveolar epithelial cells
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how much energy is normally taken by breathing, how much when excersizing?
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3-5%, up to 50%
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What is functional residual capacity?
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amount of air left in the lungs after a normal exhale (ERV + RV)
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what is residual volume?
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air left in the lungs after you have exhaled as much as you can.
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what is tidal volume?
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air inhaled and exhaled in a normal breath (500 ml)
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what is inspiratory reserve volume
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air inhaled after a normal inhalation (3liters)
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what is Inspiratory capacity?
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IRV + TV
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what is vital capacity?
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as much as you can breath in an out (ERV + TV + IRV)
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what volume of the lungs can't be measured with a spirometer?
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residual volume
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what is the difference between physiological and anatomical dead space?
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anatomical- dead space, physiological - alvioli that can't perform gas exchange (totals about 150 ml)
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where is the greatest resistence to blood flow found in the lungs?
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larger bronchi (smaller brochi in diseases)
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what do epinephrine and norepinephrine do to the lungs?
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bronchodilation by adrenergic B2 receptors
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how does the vagal nerve effect the lungs?
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releases acetylcholine and causes bronchoconstriction
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what is the normal mucous motile rate?
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1cm/min
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what causes the discrepency between alveolar oxygen partial pressure and plasma oxygen partial pressure?
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systemic supply to lungs drains back into the pulmonary veins
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what occurs becuase of alveolar hypoxia?
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vasoconstriction of neighboring vessels, causing less blood to flow to that area
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what happens to the partial pressures of oxygen and nitrogen when we inhale?
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they decrease because the air has been humidified?
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how much of the gas is replaced with each breath in the lungs?
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15%
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what happens to the gas partial pressures of oxygen and CO2 when the demand increases?
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stays the same
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what causes an increase in the space between the alveolar capillaries and gas to increase?
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edema, fibrosis, emphysema (by increasing alvioli diameter
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how many mls of oxygen can diffuce into blood at normal rates?
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231 ml/min
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what happens to CO2 in the blood?
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7% remains in plasma, rest enters red blood cells (23% binds to hemoglobin, 70%converted to carbanic acid)
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what happens to the carbanic acid produced in redblood cells
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dissociates to form bicarbonate and is released back into plasma
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what provides the safety margin of oxygen diffusion during times of strenous activity?
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increase oxygen diffusing capacity (open previously closed alveoli), improved ventilation - perfusion matching, and distance of capillariy that gas echange happens
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where is the highest partial pressure of carbon dioxide found in the body?
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mitochondrial matrix
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How much oxygen is found in plasma, and how much is found bound to hemoglobin?
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3% in solution, 97% in hemoglobin
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what causes a shift to the right in the disassociation curve?
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increased blood acidity, carbon dioxide, 2,3-diphosphoglycerate, and body temperature
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What is the Bohr effect?
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shift in the disassociation curve to the left in the lungs, shift to the right in the capillaries
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what causes a shift to the left of the disassociation curve?
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low blood acidity, carbon dioxide, fetal hemoglobin
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how much CO2 must be excreted in 100 ml of blood?
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7-10 % (4ml)
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What is the Haldene affect?
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an increase of binding of oxygen leads to a decrease in affinity for hemoglobin to carbon dioxide
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why is the Haldene effect important?
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it doubles the amount of carbon dioxide that can be transported in th e blood at any given time.
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what part of the brain regulates inhalation?
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dorsal respiratory group located in the dorsal medulla, the vagal and glossopharyngeal nerves also end here, providing parasympathetics.
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what is the role of the ventral respiratory group of neurons in the medulla?
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are activated when dorsal group is working hard, and helps to contract the muscles that aid in forced exhalation
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What is the role of the pneumotaxic center in the upper pons?
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regulates amount of air brought in and the rate of respiration (dog panting)
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What does the Apneustic center do?
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becomes active when the vagal nerve is cut. produces deep breaths, and panting exhales
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What does the Hering-Breuer reflex do?
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prevents over-inflation via receptors in the bronchi
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why are the cetral chemoreceptors particularly sensitive to CO2 and not to pH?
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becuase of the blood/brain barrier, which blocks a lot of H+ diffusion, but is permeable to CO2.
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describe the effect of the central chemoreceptors
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strong acute respnse, but weak chronic response
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What are the peripheral chemoreceptors primarily responsive to?
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oxygen, although the peripheral respond quicker to CO2 than the central.
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what causes an increase in respiration during excersize?
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joint movement causes afferent signals, hypoxia in contracting muscles, motor cortex activity increase, NOT CHEMORECEPTORS.
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What leads to COPD?
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chronic infection, accululation of mucous and edema, resistence to exhalation (increasing anatomical dead space)
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What causes Pneumonia?
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alveoli fill with fluid and RBC's. Pneumococci
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What is Atelectasis?
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collapsed alveoli due to either airway obstruction or lack of surfactant.
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what is asthma?
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spastic contraction of smooth muscles in bronchioles?
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what is tuberculosis?
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tubercule bacilli are attacked by macrophages, and the lungs heal themselves with fibroius tissue
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Hypercapnia?
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high carbon dioxide levels in the blood. happens b/c of hypoventilation or circulatory deficiency.
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Dyspnea?
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fell that not breathing enough
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Cheyne-Stokes breathing?
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hyperventilation followed by hypoventilation, can be seen in chronic heart failure and brain damage
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How does the body grow acustomed to high altitudes?
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increases RBC synthesis, increases diffusion capacity of lungs, increased cardiac output, mitochondrial adaptation
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What long term changes are seen i n people that live at highg altitudes?
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barrel chest, small body size, hemoglobin disassociation curve shifted to the left
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Nitrogen Narcosis?
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At increased pressure Nitrogen can become toxic and permeate into our system and have the same affects as anesthetics
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Hyperbaric Oxygen Toxicity?
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high pressure oxygen can cause convolsions and disorientation, and eventual brain damage
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Decompression syndrome
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bends, resurfacing after being under large pressure causes nitrogen bubbles that can block arteries
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