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63 Cards in this Set
- Front
- Back
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true or false? any time you have edema, the total body sodium is increased.
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true
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sodium salts constitute __ of the total solute in extracellular fluid
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90%
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retention of sodium is usually accompanied by retention of a ___ volume of ___.
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retention of sodium is usually accompanied by retention of an ISOSMOTIC volume of WATER.
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the volume/size of the extracellular fluid compartment is a function of the total amount of ___, which is in turn determined by ___.
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the volume or size of the extracellular fluid compartment is a function of the total amount of SODIUM and accompanying anions. the total amt of sodium in the ECF compartment is determined by EXCRETION of this ion by the kidney. **RENAL SODIUM EXCRETION DETERMINES SODIUM BALANCE.
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true or false: the relative amt of sodium (compared to water) determines ECF volume.
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false. the TOTAL amount of sodium is what determines ECF volume (and therefore edema).
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the intake of sodium will lead to increased sodium content in ECF compartment, increased plasma sodium concentration and increased osmolality. what are 3 physiologic changes that follow this?
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1. thirst 2. movement of water from cells 3. osmotic release of ADH
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compare water excretion by the kidneys to sodium excretion by the kidneys. which happens faster? which ones will result in a return to the set point?
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in a healthy patient, water excretion happens faster than sodium excretion. both will eventually return to the set point, however.
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salt intake --> water moves into ECF --> drink water --> ___ --> osmotic release of ADH --> excrete salt + water --> return to set point
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extracellular fluid volume expansion
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osmoregulation v. volume regulation. what is the factor being regulated?
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osmo: plasma osmolality. volume: effective circulating volume
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osmoregulation v. volume regulation. what is the afferent limb?
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osmo: hypothalamic osmoreceptors. volume: carotid sinus, afferent arteriole in glomerulus, atria.
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osmoregulation v. volume regulation. what is the efferent limb?
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osmo: ADH. volume: MULTIPLE --> sympathetic nervous system, renin-aII-aldosterone, natriuretic peptide, pressure natriuresis, ADH
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osmoregulation v. volume regulation. what is the factor that is effected?
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osmo: water excretion and water intake (thirst). volume: sodium excretion
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true or false: in order to excrete both water and sodium, there are multiple neurohormones affected.
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false. sodium excretion requires a lot of coordination between the SNS, RAAS, natriuretic peptide, and ADH, but water excretion only changes ADH levels.
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define positive sodium balance
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consuming more sodium than you are excreting. this occurs when you rapidly increase amount of sodium intake. this is accompanied by weight gain (due to increased ECF volume). eventually, you will reach a new steady state (sodium balance).
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what determines sodium excretion/retention?
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the effective arteriole blood volume (EABV).
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EABV. is it on the arterial or venous side? where is the receptor located?
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arterial (15% of total body plasma, so can sense small changes). located in the chest we think (b/c thoracic organs are less well perfused in many conditions of decrease EABV).
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name 2 conditions when EABV and exctracellular fluid volume are no longer closely related.
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congestive heart failure, cirrhosis.
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explain volume homeostasis (signal --> sensors --> effectors --> renal response)
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change in EABV --> high pressure baroreceptors + low pressure baroreceptors + afferent arteriole sense change --> RAAS + symp nervous system + ADH release/suppression + other hormones/physical factors respond --> salt + water excretion/retention
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how do you calculate the filtered load of sodium?
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plasma sodium x GFR
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where is sodium absorbed along the nephron? include percentages.
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67% in proximal tubule, 25% in thick ascending limb, 5% in distal convoluted tubule, 3% in cortical and medullary collecting duct. (recall that fine regulation occurs mostly in distal convoluted tubule)
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about what % of the filtered load of sodium is excreted?
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0.6%. this should equal sodium intake!
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what are 3 mechanisms by which the kidney adjusts to spontaneous (primary) changes in GFR?
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1. glomerular tubular balance 2. tubuloglomerular feedback 3. autoregulation of renal blood flow (and GFR)
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where is tubuloglomerular feedback controlled?
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in the macula densa
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how does the kidney adjust to changes in sodium intake?
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1. secondary changes in GFR 2. altered sodium reabsorption --> RAAS, sympathetic tone + catecholamines, oncotic and hydrostatic pressure, atrial natriuretic peptide, other hormones/factors
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describe the integrated response to an increase in effective arterial blood volume. what happens at the level of the JGA? aortic arch and carotid sinus? cardiac atria? increased hydrostatic pressure?
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JGA decreases renin, angiotensin, and aldosterone. AORTIC ARCH and carotid sinus decreases catecholamines and sympathetic outflow. CARDIAC ATRIA increases atrial natriuretic factor. increased HYDROSTATIC PRESSURE increases glomerular filtration rate and increases the pressure around the peritubular capillaries.
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in a healthy patient, after an increase in EABV: renin levels __. sympathetic tone __. ANP __. glomerular filtration ___.
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renin decreases. sympathetic tone decreases. ANP increases. glomerular filtration increases. (the point is to excrete salt and water).
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where is renin secreted? what is its function?
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juxtaglomerular apparatus. geared to maintain blood volume, sodium, blood pressure, potassium balance.
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explain the RAAS pathway
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renin is secreted by the JGA. renin cleaves angiotensinogen to angiotensin I. angiotensin I is converted by ACE into angiotensin II. this is then converted to aldosterone. this acts on the tubules to change Na retention and excretion.
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what are the components of the JGA?
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afferent and efferent arteriole. macula densa cells, juxtaglomerular cells, sympathetic nerves.
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what do juxtaglomerular cells look like?
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granular. they are storing lots of renin!
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what are 3 things that stimulate renin secretion in the JGA?
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1. afferent arteriole acts as a baroreceptor (if BP falls, will stimulate renin release). 2. macula densa cells sense NaCl through chemoreceptor mechanism. 3. sympathetic nerves stimulate renin secretion when activated.
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an increase in angiotensin II will lead to a ___ in secretion of renin.
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decrease. this is a feedback system! (recall that the normalization of blood volume will also lead to a decrease in the secretion of renin.
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renin release is meant to __ blood volume.
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increase
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the activity of the SNS is regulated by ___ interactions with inputs from ___ nerves activated by changes in ___ and ___.
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the activity of the SNS is regulated by REFLEX interactions w/inputs from BARORECEPTOR nerves activated by changes in ECF volume and BLOOD PRESSURE.
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how does the SNS decrease GFR?
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changes renal vascular resistance and renal blood flow
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stimulation of the SNS results in the release of ___ from ___ granular cells of the ___ arteriole.
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stimulation of the SNS results in the release of RENIN from JUXTAGLOMERULAR granular cells of the AFFERENT arteriole
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true or false: the sympathetic nervous system directly increases salt reabsorption from proximal and distal nephron segments.
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true!
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define edema
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an increase of the interstitial fluid volume manifested as palpable swelling of subcutaneous tissues.
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generalized edema does not become apparent until the ___ has increased by at least ___ at the expense of the ___.
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generalized edema does not become apparent until the INTERSTITIAL VOLUME has increased by at least 2.5-3 Liters at the expense of the PLASMA VOLUME.
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what is the normal plasma volume? what is the implication of this for edema?
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3-3.5 liters. because edema requires a 2.5-3L increase in interstitial volume, this means that the kidneys have to retain dietary salt and water. (this is a key concept!)
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what are the 2 basic steps of edema formation?
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1. alteration in capillary hydrostatic and/or oncotic pressures. 2. retention of dietary sodium and water by the kidneys
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what are the 3 major salt retaining states?
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congestive heart failure, liver disease, nephrotic syndrome.
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salt-retaining states may be induced by primary alterations of starling forces in peripheral capillaries, causing a decrease in effective arterial blood volume. alternatively it may be that primary sodium retention by the kidneys leads to a secondary change in starling forces in peripheral capillaries. which one is probably more important?
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probably the second one. primary sodium retention by the kidneys with a resultant increase in pressure from the venular side, leading to edema.
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explain the hemodynamic factors controlling fluid movement across the capillary wall.
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starling's forces! hydrostatic pressure pushes fluid out of capillary into interstitium. oncotic pressure pulls fluid into capillary from the interstitium.
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in normal conditions, starling forces have a slight preference for capillary fluid to move into the interstitium. how come we don't constantly swell up?
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lymphatics return this to the circulation
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at the level of the capillaries, explain 3 ways that edema can occur. (hint: talk about starling's forces)
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increase in hydrostatic pressure (primary sodium retention). decrease in oncotic pressure as a result of low protein (malnutrition, protein losing enteropathy, nephrotic syndrome). leakiness of the capillaries (due to interleukins, cytokines, etc.)
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which plays a bigger role in causing the edema associated with nephrotic syndrome: low oncotic pressure or primary salt and water retention?
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primary salt and water retention. you need a very very low oncotic pressure in order for that to have an effect.
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how can lymphedema cause general edema?
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if lymph nodes get swollen enough (e.g., with cancer), they can't drain the interstitium.
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in the ICU setting, patients get really really swollen because of the release of cytokines. should you give a diuretic? why or why not?
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no! the problem is that the vessels are leaking. the kidney is doing everything it can to restore the blood presssure! if you diurese the patient, they'll just lose more fluid. you need to solve the medical problem.
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what are some compensatory mechanisms that allows you to reach a steady state with edema?
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1. increase in hydrostatic pressure in the interstitium (fluid is building up there). 2. decrease in oncotic pressure in interstitium because of dilution. 3. compensatory increase in lymphatic flow.
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true or false: in both high and low output cardiac failure, the patients have a low EABV accompanied by edema.
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true.
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explain how DIMINISHED RENAL HEMODYNAMICS contributes to edema in CHF
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CHF can cause constriction of the efferent arteriole --> decrease in renal blood flow is greater than the decrease in GFR --> increase in filtration fraction --> increased oncotic pressure in peritubular capillaries favors sodium reabsorption. also, hydrostatic pressure is low in these capillaries, so this further favors sodium and water reabsorption.
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how come there is such a large increase in ECFV and yet such a big decrease in EABV in CHF?
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because it's a vicious cycle! heart, brain, SNS, and kidneys are all involved and they keep triggering more release of aldosterone etc., and that just makes everything worse.
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describe the underfill mechanism in liver disease
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liver disease --> hypoalbuminemia, peripheral vasodilation, splanchnic pooling --> ascites --> decreased EABV --> activates RAAS, non-osmotic realse of ADH, SNS --> diminished renal hemodynamics and diminished renal sodium and H2O excretion --> ascites, edema
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liver disease --> (3 things) --> ascites
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hypoalbuminemia + peripheral vasodilation + splanchnic pooling
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what is the difference between the underfill and overfill mechanism for explaining liver disease edema?
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underfill: problem is that there is low oncotic pressure, which causes ascites, which then causes kidneys to retain salt and water. overfill: liver disease causes increased sinusoidal pressure, which in turn causes a reflex that tells the kidneys to retain salt and water.
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describe the overfill mechanism in liver disease
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liver disease --> increased sinusoidal pressure --> mysterious hepatorenal reflex --> renal sodium and H2O retention --> increased plasma volume --> ascites + peripheral edema
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what are 2 diseases that the underfill and overfill mechanisms apply to?
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liver disease, nephrotic syndrome
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nephrotic syndrome is characterized by ___.
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urinary protein excretion of more than 3.5gm per 24 hr.s
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5 cardinal features of nephrotic syndrome
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urinary protein excretion, hypoalbuminemia, peripheral edema, lipiduria, dyslipidemia
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what is the basic underfill hypothesis for nephrotic syndrome?
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heavy proteinuria --> hypoalbuminemia and decreased colloid osmotic pressure --> change in capillary starling forces --> increased interstitial fluid and arterial underfilling --> stimulates salt retention w/SNS, RAAS, ADH, and changing kidney blood flow and GFR --> edema
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what is the overfill hypothesis for nephrotic syndrome?
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primary increase in renal sodium and water retention b/c of the glomerular disease (unknown mechanism) --> expansion of ECF volume --> change in capillary starling forces --> edema
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what's more likely in nephrotic syndrome: the overfill hypothesis or the underfill hypothesis?
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the overfill hypothesis. kids on coricosteroids lost edema before they corrected their protein deficiencies.
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