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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
formula to calculate anion gap: anion gap = [Na] - ([Cl-] + [HCO3-])
what is the normal value for anion gap?: 12 +/- 2 mEq/L
elevated anion gap metabolic acidosis could be due to...: 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
normal anion gap metabolic acidosis could be due to...: 1. diarrhea (loss of HC03-)
2. loss of HCO3- from kidneys
how is is normal anion gap metabolic acidosis differ from hi anion gap metab. acidosis in terms of how HCO3- is lost?: 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)
how do you calculate osmolar gap?: osmolar gap = measured - calculated

calculated = 2[Na] + [urea] + [glucose] + [EtOH]
what does an osmolar gap indicate?: that there are significant uncharged osmoles present in the serum (usually toxic alcohols like methanol) that aren't accounted for in the formula
H+ LOSS = HCO3- GAIN!!!: just to push the point!
2 major buffer systems in the body: 1. BBS
2. intracellular proteins
2 minor buffer systems in teh body: 1. inorganic intracellular phostphate
2. bone (chronically)
how is the body losing bicarb?: via CO2 when we breathe
where does most of the HCO3- reabsorption occur? what percentage occurs here?: in the PCT. 85%
where does non-PCT reabsorption of HCO3- occur?: in the TAL (15%)

paracellular pathways (20%)
in order to get NEW HCO3-, what has to happen? MOA?: 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)
where are the 2 places in the nephron where NH4 can be secreted into the lumen?: the PCT and the DT
list the 2 fates of glutamine once it is metabolized in kidney: 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-
what are the 4 modulators of DISTAL TUBULEAR acid/base?: 1. Na+
-aldosterone
-lumen electric potential
2. K+
3. ATP availability
4.pH
in RTA, would you have a normal A/G metabolic acidosis, or a wide A/G metabolic acidosis: 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.
does RTA cause chronic metabolic acidosis?: yes - its a problem with reclaimin/regererating bicarbonate

it is a non-A/G metabolic acidosis
what would the effects of a carbonic anhydrase inhibitor be?: 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)
describe the SCr vs. GFR curve: 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.
how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: Una: pre-renal Una < 10
instrinsic Una >20

(inability to reabsorb Na in intrinsic)
how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: FeNa: pre-renal FeNa <1%
intrinsic FeNa >2%
how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: Uosm: pre-renal: Uosm > 500
intrinsic: Uosm < 300
how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: SpGr: pre-renal: >1.018
intrinsic: <1.012
how can you distinguish b/w a pre-renal vs. intrinsic cause of RTA in terms of: sediment (casts): prerenal: hyaline casts
intrinsic: granular cast, dysm. RBC, cellular cast, crystal/oxalate/Uric
where is ADH made (specifically): paraventricular and supraoptic nucleus in hypothalamus
which of the following does ADH act on? PCT, LOH, DCT, CCD, MCD: DCT, CCD, MCD
if you have a decreased effective circulating volume, are you necessarily hypovolemic?: 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
low effective circ. volume is going to cause 3 things to happen. what are they?: 1. activation of thirst sensation
2. ADH secretion
3. SNS activation - RAS - NaCl reabsorption
hyponatremia, or low serum [Na] has two requirements:: 1. source of free water
2. ADH is acting
hypernatremia, or hi serum [Na] has two requirements:: 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)
how is polyuria usually defined in terms of volume excreted?: 3 L/day in an adult
how is urine volume calcuclated?: urine volume = (# osmoles)/Uosm
2 things that could cuase an increase in urine volume: 1. osmotic diuresis (hi osmoles)
2. water diuresis (urine osmolality is too low b/c the kidney can't concentrate urine)
not all osmoles can lead to osmotic diuresis. Only effective osmoles can. 4 examples are: "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)
2 ways of determining whether polyuria is due to (i) water diuresis or (ii) osmolar diuresis: 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
once you know that polyuria is due to osmotic diuresis, what calculation do you perform next? why?: 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)
name one occasion in which water diuresis is deemed appropriate: psychogenic DI - body NEEDS to get rid of excess water consumed
if the osmolar gap is greater than what value can you conclude that osmolar diuresis is due to unmeasured osmoles: if Uosm gap is >100
definition of hyperkalemia? definition of hypokalemia?: plasma [K]> 5 mEq/L
plasma [K] < 3.5 mEq/L
describe the external and internal means of K balance: external: GI absorp - (urine + stool) excretion

internal: 98% ICF, 2% ECF (any compartment shift will change the K balance)
would a K shift from ICF to ECF be described as catabolic or anabolic?: catabolic
what 2 things could increase the K+ movement INTO ICF?: insulin

B-agonists
ROM-K is characteristic of what part of the renal tubule?: LOH
aldosterone secretion is triggered either by _____ or ______: AII
hi serum [K]
3 actions of aldosteron on teh principle cell: 1. activates existing ENaC
2. produces new ENaC
3. upregulates Na/K pump on basolateral membrane, thus driving the gradient
a negative/positive lumen will favor K secretion: negative lumen
how does flow influence the secretion of K in the CCD?: the greater the flow, the greater the secretion of K
3 ways you could get hypokalemia: 1. renal K wasting
2. reduced dietary intake
3. compartmental shift into ICF
what is the major concern with hypokalemia?: cardiac arrhythmia
which of the following drugs could cause K wasting? NSAIDS purgatives diuretics anti-emetics laxatives: purgatives
diuretics
laxatives
when treating hypokalemia, would you first increase body content of K? or first increase the serum concentration of K?: first increase serum concentration of K. This is because body content of K is only loosely related to the plasma [k]
what does pseudo-hiK refer to?: 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
what types of things could elevate your K intake?: salt substitutes (KCl)
transfusion of old blood
IV K+
drugs containing K
blackstrap molasses
geographia = clay eaters!!
what might cause a redistribution of K from the ICF to the ECF (causing hyperkalemia): lack of insulin
b-antagonists
cell damage
medications
fasting (catabolic state)
physical exertion
hyperchloremic acidemia
would hypercloremic acidemia cause hyper or hypokalemia?: hyperkalemia
would reduced flow throught eh CCD result in hyper or hypokalemia?: hyperkalemia (recall that luminary flow is a determinant of K secretion)
would digitalis result in hyperkalemia or hypokalemia (think about its MOA): hyperkalemia (Na/K ATPase will keep Na inside the cell, and K outside)
if you have an INAPPROPRIATELY low TTKG, what could this be due to? Name 2 things: 1. defective aldosterone responses (hyporeninemia, drugs...)
2. increased Cl- reabsorption
what salts can you administer to antagonsize the cardiac effectws of HiK: Calcium salts
what is the preferred method for shifting K into the ICF from teh ECF? waht other methods are there to shift K into ICF: insulin + glucose infusion

B-agonists
what are 3 ways you could remove K from teh body?: 1. increase renal excretion (loop diuretic, mineralocorticoid, CA inhibitor)
2. increasing GI excretion (K adsobing resin, kayexalate
3. dialysis (HD more effcient that PD)

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