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64 Cards in this Set
- Front
- Back
for which of teh following do you care about anion gap and osmolar gap?
1. metabolic acidosis 2. metabolic alkalosis 3. respiratory acidosis 4. respiratory alkalosis |
metabolic acidosis
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formula to calculate anion gap
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anion gap = [Na] - ([Cl-] + [HCO3-])
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what is the normal value for anion gap?
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12 +/- 2 mEq/L
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elevated anion gap metabolic acidosis could be due to...
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collection of excess acids:
-lactic acid -ketoacids -toxic acids (e.g. methanol) -kidney failure (organic acids) "MUDPILES" Methanol Uremia (organic acids) Diabetic ketoacids Paraldehyde Isoniazid Lactic acd Ethylene glycol (antifreeze) Salicylates |
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normal anion gap metabolic acidosis could be due to...
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1. diarrhea (loss of HC03-)
2. loss of HCO3- from kidneys |
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how is is normal anion gap metabolic acidosis differ from hi anion gap metab. acidosis in terms of how HCO3- is lost?
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in hi anion gap M.A., the HCO3- is lost b/c it combines with xcess acid
in non-anion gap M.A. there is 'simple' loss of HCO3- via the gut (diarrhea) or via the kidneys (e.g. RTA) |
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how do you calculate osmolar gap?
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osmolar gap = measured - calculated
calculated = 2[Na] + [urea] + [glucose] + [EtOH] |
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what does an osmolar gap indicate?
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that there are significant uncharged osmoles present in the serum (usually toxic alcohols like methanol) that aren't accounted for in the formula
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H+ LOSS = HCO3- GAIN!!!
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just to push the point!
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2 major buffer systems in the body
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1. BBS
2. intracellular proteins |
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2 minor buffer systems in teh body
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1. inorganic intracellular phostphate
2. bone (chronically) |
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how is the body losing bicarb?
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via CO2 when we breathe
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where does most of the HCO3- reabsorption occur? what percentage occurs here?
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in the PCT. 85%
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where does non-PCT reabsorption of HCO3- occur?
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in the TAL (15%)
paracellular pathways (20%) |
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in order to get NEW HCO3-, what has to happen? MOA?
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H+ must get secreted AND trapped in the urine.
ways this can happen is if H+ attaches to a titratable acid (such as HPO4- or HSO4-) or ammonia (NH3) |
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where are the 2 places in the nephron where NH4 can be secreted into the lumen?
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the PCT and the DT
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list the 2 fates of glutamine once it is metabolized in kidney
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in kidney, glutamine is broken down into 2NH4+ and 2HCO3-. If the NH4s are put into the urine, you have a net loss of acid from the body. The 2HCO3- are taken up into the blood, and this is considered the 'generation of new bicarb.' However, if the NH4+ go to the liver instead to get converted into urea, this process releases 2H+ into the blood, which combine with the 2HCO3- that were originally generatede from the breakdown of glutamine. Thus, the charges balance out, and youi have no new generation of HCO3-
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what are the 4 modulators of DISTAL TUBULEAR acid/base?
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1. Na+
-aldosterone -lumen electric potential 2. K+ 3. ATP availability 4.pH |
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in RTA, would you have a normal A/G metabolic acidosis, or a wide A/G metabolic acidosis
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a normal A/G metabolic acidosis. Why? b/c HCO3- is "simply" being eliminated from the body (i.e. not being reabsorbed) - its not that its combining with any excess acids.
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does RTA cause chronic metabolic acidosis?
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yes - its a problem with reclaimin/regererating bicarbonate
it is a non-A/G metabolic acidosis |
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what would the effects of a carbonic anhydrase inhibitor be?
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decrease the formation of H+
lead to an alkaline urine; retain H+ (therefore could be a cause of RTA prevent Na+ from being reabsorbed via Na/H pump (b/c it retains H+). Thus acts as a weak diuretic (e.g. acetazolamide) |
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describe the SCr vs. GFR curve
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as GFR initially declines, this is accompanied by only a small elevation in serum creatinine. Thus, an elevation of Scr from 100 to 200 represents a greater decline in renal function than an increase in SCr from 300 to 400. SCr is also therefore a late indicator of declining renal f'n.
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how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: Una
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pre-renal Una < 10
instrinsic Una >20 (inability to reabsorb Na in intrinsic) |
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how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: FeNa
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pre-renal FeNa <1%
intrinsic FeNa >2% |
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how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: Uosm
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pre-renal: Uosm > 500
intrinsic: Uosm < 300 |
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how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: SpGr
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pre-renal: >1.018
intrinsic: <1.012 |
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how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: sediment (casts)
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prerenal: hyaline casts
intrinsic: granular cast, dysm. RBC, cellular cast, crystal/oxalate/Uric |
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where is ADH made (specifically)
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paraventricular and supraoptic nucleus in hypothalamus
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which of the following does ADH act on?
PCT, LOH, DCT, CCD, MCD |
DCT, CCD, MCD
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if you have a decreased effective circulating volume, are you necessarily hypovolemic?
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no - you could have normal/hi intravascular volume; the problem lies in the fact that it is poorly distributed, or that there is low CO
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low effective circ. volume is going to cause 3 things to happen. what are they?
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1. activation of thirst sensation
2. ADH secretion 3. SNS activation - RAS - NaCl reabsorption |
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hyponatremia, or low serum [Na] has two requirements:
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1. source of free water
2. ADH is acting |
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hypernatremia, or hi serum [Na] has two requirements:
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1. no source of free water (otherwise it would be absorbed in other places besides the DCT/CD
2. ADH not acting (centra/nephrogenic DI) |
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how is polyuria usually defined in terms of volume excreted?
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3 L/day in an adult
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how is urine volume calcuclated?
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urine volume = (# osmoles)/Uosm
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2 things that could cuase an increase in urine volume
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1. osmotic diuresis (hi osmoles)
2. water diuresis (urine osmolality is too low b/c the kidney can't concentrate urine) |
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not all osmoles can lead to osmotic diuresis. Only effective osmoles can. 4 examples are
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"GUMS"
1. glucose (Diab. mellitus) 2. urea (hi protein, GI bleed - only place in body where urea is an effective osmole!) 3. mannitol (iatrogenic) 4. salts (Na, BHB, NaCl) |
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2 ways of determining whether polyuria is due to (i) water diuresis or (ii) osmolar diuresis
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a) could measure Uosm.
-if Uosm > 250 mosmol/l, then its osmolar diuresis -if Uosm <250 mosmol/l, then its water diuresis 2. assuming that you know Uosm, measure the 24 hour urine output. using these two values, calculate the # of osmoles excreted. Knowing that an avg # of excreted osmoles is <900 in a 75 kg male, you can figure out whether the polyuria is due to greater excretion of osmoles |
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once you know that polyuria is due to osmotic diuresis, what calculation do you perform next? why?
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calculate the osmolar gap. b/c you want to determine what osmoles are responsible for the polyuria. Are they "measured" (Na, urea, glu) or "non-measured" (ketoacids, mannitol)
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name one occasion in which water diuresis is deemed appropriate
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psychogenic DI - body NEEDS to get rid of excess water consumed
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if the osmolar gap is greater than what value can you conclude that osmolar diuresis is due to unmeasured osmoles
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if Uosm gap is >100
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definition of hyperkalemia?
definition of hypokalemia? |
plasma [K]> 5 mEq/L
plasma [K] < 3.5 mEq/L |
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describe the external and internal means of K balance
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external: GI absorp - (urine + stool) excretion
internal: 98% ICF, 2% ECF (any compartment shift will change the K balance) |
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would a K shift from ICF to ECF be described as catabolic or anabolic?
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catabolic
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what 2 things could increase the K+ movement INTO ICF?
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insulin
B-agonists |
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ROM-K is characteristic of what part of the renal tubule?
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LOH
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aldosterone secretion is triggered either by _____ or ______
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AII
hi serum [K] |
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3 actions of aldosteron on teh principle cell
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1. activates existing ENaC
2. produces new ENaC 3. upregulates Na/K pump on basolateral membrane, thus driving the gradient |
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a negative/positive lumen will favor K secretion
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negative lumen
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how does flow influence the secretion of K in the CCD?
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the greater the flow, the greater the secretion of K
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3 ways you could get hypokalemia
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1. renal K wasting
2. reduced dietary intake 3. compartmental shift into ICF |
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what is the major concern with hypokalemia?
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cardiac arrhythmia
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which of the following drugs could cause K wasting?
NSAIDS purgatives diuretics anti-emetics laxatives |
purgatives
diuretics laxatives |
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when treating hypokalemia, would you first increase body content of K? or first increase the serum concentration of K?
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first increase serum concentration of K. This is because body content of K is only loosely related to the plasma [k]
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what does pseudo-hiK refer to?
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a dx of hyperkalemia that is false b/c the measured hi K is due to a technical error (e.g. tight tourniqet, or hemolysis) i.e. its the doctor's fault THE PATIENT DOESNT ACTAULLY HAVE HYPERKALEMIA
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what types of things could elevate your K intake?
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salt substitutes (KCl)
transfusion of old blood IV K+ drugs containing K blackstrap molasses geographia = clay eaters!! |
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what might cause a redistribution of K from the ICF to the ECF (causing hyperkalemia)
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lack of insulin
b-antagonists cell damage medications fasting (catabolic state) physical exertion hyperchloremic acidemia |
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would hypercloremic acidemia cause hyper or hypokalemia?
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hyperkalemia
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would reduced flow throught eh CCD result in hyper or hypokalemia?
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hyperkalemia (recall that luminary flow is a determinant of K secretion)
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would digitalis result in hyperkalemia or hypokalemia (think about its MOA)
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hyperkalemia (Na/K ATPase will keep Na inside the cell, and K outside)
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if you have an INAPPROPRIATELY low TTKG, what could this be due to? Name 2 things
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1. defective aldosterone responses (hyporeninemia, drugs...)
2. increased Cl- reabsorption |
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what salts can you administer to antagonsize the cardiac effectws of HiK
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Calcium salts
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what is the preferred method for shifting K into the ICF from teh ECF? waht other methods are there to shift K into ICF
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insulin + glucose infusion
B-agonists |
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what are 3 ways you could remove K from teh body?
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1. increase renal excretion (loop diuretic, mineralocorticoid, CA inhibitor)
2. increasing GI excretion (K adsobing resin, kayexalate 3. dialysis (HD more effcient that PD) |