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36 Cards in this Set
- Front
- Back
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Describe the distribution of water in a 70 kg person
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Total Body water: 60%=42L
2/3 Intracellular 28L 1/3 Extracellular 14L 2/3 Interstitial 9L 1/3 Intravascular 5L |
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What determines a patients volume?
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Total salt content, not concentration
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What determines salt content?
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The input and output of salt
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What determines tonicity?
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The input and output of water
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What is the typical response to hypernatremia?
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Thirst
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Describe tonicity and serum [Na]
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-Cell membranes are freely permeable to water
-No osmotic gradients exist between fluid compartments (except the renal medulla which is a hypertonic environment) -The tonicity of the intravascular compartment reflects the tonicity of all fluid compartments |
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How do you calculate serum osmolality?
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([Na]*2)+([K]*2)+[gluc]/18+[BUN]/2.8
The major contributer is Na |
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Contrast osmolality and tonicity
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When we measure osmolality BUN is included in that. When we think of tonicity that is often restricted to the forces that can operate on cells. Urea can go through membranes so we don’t use that.
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Describe Free water
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-[Na] reflects balance of H2O relative to salt
-H2O input and output must be assessed but again relative to salt input and output -Free H2O is the amount of extra water over saline |
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Describe the determinants of tonicity
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-Free H2O intake vs Free H2O excretion + Free H2O losses
-Free H2O intake is through oral or IV -Free H2O losses are through respiratory and cutaneous -Free H2O excretion is through urine -Urine is regulated excretion that is a function of its volume and concentration |
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Describe what happens to fluid normally in the kidney
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-Blood enters the afferent arteriole and goes through the arcades
-The hydrostatic vs oncotic pressure gradient generates a protein free ultrafiltrate -This has the same concentration as body fluids -There is some proximal reabsorptopn based on the filtration fraction and the peritubular capillary oncotic pressure -You flux now into the concentrated medullary interstitium -Things are concentrated and then they become dilute. -They become maximally dilute. -The question then is due you put out dilute urine or do you equilibrate with the medullary interstitium and put out concentrated urine. |
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Describe the determinants of a large volume of dilute urine
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-Good GFR
-Low proximal reabsorption -Low permiability to water -These same mechanisms for diluting are engaged for concentrating |
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Describe the determinants of a concentrated urine
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-Pumping section has to work well because this active transport is where the gradient comes from
-Need appropriate permeability to water coming back in -These same mechanisms for diluting are engaged for concentrating |
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Describe what is important for free H2O excretion
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-Deliver
-High GFR (assessed by serum creatinine) -Low proximal reabsorption (assessed by BUN/creatinine ratio) -Diluting segment has to be working -Last bit of Na reabsorption generates a dilute urine -Collecting duct -Decreased H2O permeability |
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Describe what is important in Free H2O retention
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-Medullary gradient
-Thick ascending limb has to function well -Collecting duct -Increased H2O permeability |
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Describe vasopressin
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-Determines the concentration of urine
-Antidiuretic hormone -ADH binds V2 receptor in the collecting duct (cAMP mediated stimulation of aquaporins) -Vasopressin binds V1 receptors in vascular smooth muscle |
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Describe how vasopressin changes the concentration of urine
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-Urine starts as isosthenuric (urine concentration is the same as the tonicity of the body fluids)
-As we flux through the loop of Henle there is concentration and then dilution -As we cross over into the distal tubule we maximally dilute urine -At the level of the collecting duct/cortical medullary is where ADH is important -No ADH: we stay dilute -ADH: We reach the concentration of the medullary interstitium |
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Describe the release of vasopressin
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-Synthesized in the paraventricular and supraoptic nuclei
-Released from the pituitary neurohypophysis -Released in response to signals from an osmoreceptor but also there is a baroreflex mediated secretion |
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Describe how plasma vasopressin is related to plasma osmolality
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-Vasopressin is suppred when osmolality is low
-There is a set point above which osmolality is a potent stimulus for vasopressin release -Once you cross the set point a few % change is enough to get you levels of 5-7 pg/ml -Thirst is also stimulated -Osmolality drives intake as well as affects output |
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Describe the correlation between plasma vasopressin and urine osmolality
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-Urine is most dilute when vasopressin levels are low
-As vasopressin levels rise above 5-7 pg/ml we maximally concentrate urine -At maximal concentration the urinary has equilibrated with the medullary interstitum -Very low concentrations of the hormone are enough to give a very crist maximal effect |
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Describe situations where there is hyponatremia but a hyperosmolar state
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-Glucose is osmotically active so hyperglycemia can lead to hyponatremia but a hyperosmolar state
-Patient with a large amount of lipid in blood dont have room for water so when you measure Na in urine the Na isnt in the whole volume -Lipemia can give pseudo-hyponatremia -Paraprotein could show something similar |
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Describe hyponatremia/hypoosmolar states
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-Intake of free H2O > renal output+insensible losses
-failure to make a large volume of dilute urine -Failure to deliver (low GFR, high proximal reabsorption) -Failure to dilute -Failure to suppress ADH |
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Describe the response to arterial underfilling
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-AII restricts the efferent arteriole, raising the filtration fraction and increasing peritubular oncotic pressure
-Baroreceptor registers underfilling and vasopressin is released |
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Describe the relation between decrease in mean arterial pressure and plasma vasopressin levels
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-As mean arterial pressure goes down we can see logarithmic increase in levels of plasma vasopressin
-It only takes 5pg/ml to maximally concentrate urine |
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Describe the effect of % change of osmolality and volume on plasma vasopressin levels
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-A few % increase is osmolality and vasopressin shoots up
-A much larger % decrease in volume is needed to get a vasopressin increase -When volume changes cause vasopressin release things can get out of hand fast |
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How does volume change the plasma osmolality vs plasma vasopressin relationship?
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-Hypovolumia lowers the set point and makes the curve steeper
-That is, lower volume results in a larger change in plasma vasopressin for the same change in plasma osmolality |
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Describe non-osmotic stimuli to ADH
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-Hypovolumic states from frank extracellular volume depletion or arterial underfilling of CHF, advanced cirrhosis, patients with nephrosis
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Describe the hyponatremia in CHF
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-Free water intake has exceeded free water output
Why the kidney failre to make a large volume of dilute urine -Patients who are arterially underfilled and have high levels of AII will be thirsty -With AII and increased proximal reabsorption, distal delivery may be down -Very severe CHF can have loss of GFR -This could be pre-renal renal failure and will decrease the propensity to excrete volume -In the diluting segment we could see if the patient is on diuretics or hypokalemic -A volume stimulus to ADH, the failure to stimulate ADH despite a hyperosmolar state, is the most critical |
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Since you do not measure vasopressin clinically, how do you assess vasopressin levels?
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-You use other clinical findings
-You can see urine manifestations such as having concentrated urine despite the fact the patient has hyponatremia -When renin is high, serum sodium tends to be low. These correlate with vasopressin. |
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Describe what occurs after a cardiac insult and a down shift in the Starling curve
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-There is arterial underfilling and Na retention mechanisms are activated
-Salt intake exceeds salt excretion -There is expansion of volume and some of that volume is intravascular so you move to a better position on the starling curve. -It is possible for a big insult or a second insult to occur that shifts the starling curve so low that it is not possible to get a volume capable of suppressing the neurohumeral axis/Na retention mechanism/vasopressin -The level of compensation is very important |
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Describe the importance of serum Na levels in patients with untreated heart failure
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-Serum sodium is a good indicator of survival
-Patients with high serum sodium/compensation live longer than those without |
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Describe situations of hyponatremia with increased ADH
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-Volume stimulus is overwhelmingly the major cause
-ECF volume depletion or one of the edematous states with arterial underfilling -Syndrome of inappropriate ADH -Certain drugs, endocrinopathies |
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Describe the results of the model for inappropriate secretion of ADH
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-When you give ADH water reabsorption occurs
-Urine volume plummets and urinary concentration instantly rises -If free water intake has remained constant we have gone from a large amount of dilute urine to a small amount of concentrated urine -We not longer have free water balance and this is reflected in a change in the serum sodium concentration -For any given amount of salt, if you add water then the volume has increased a little bit -The little increase in volume will further suppress sympathetics, renin, aldosterone -In that suppression you may see an increase in urine salt excretion -Patients with SIADH are not edematous, they are euvolumic on physical exam -They are primed to excrete salt because they are slightly volume expanded |
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What are the different etiologies of SIADH
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-Ectopic ADH production from tumors
-Pulmonary disease associated with SIADH -SIADH in CNS disease |
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Describe the approach taken with hyponatremia
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-Assess for renal failure. If the patient has profound renal failure you dont need to get involved with the whole mechanism in the kidney
-If the kidney is fine then you have to assess the reasons that ADH is high despite low serum Na -There can be a loss in fluid and salt volume -ECF and intravascular compartments depleted (diarrhea) -ECF expanded but intravascular compartment arterially underfilled (CHF) -Assess BUN/Cr -It is possible to have derangement in ADH disconnected from the volume stimulus -Assess for drugs and endocrinopathies -If SIADH, use history to distinguish between: -Tumors -Pulmonary -CNS |
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Describe vasopressin as a pressor agent
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-100x more potent than NE
-If you give vasopressin to normal subjects there is no change in BP -Normotensive patients are insensitive to vasopressin as a pressor -Exogenous vasopressin is a potent pressor in shock (when pressure is threatened) -Sensitivity of blood vessels are regulated by baroreflex so they are sensitive at low volumes |
