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Block VII, Week VIa


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on average, what is the amount of our total body water?
on average, what is the amount of our extracellular fluid (ECV)?
on average, what is the amount of our intracellular fluid?
two compartments within the extracellular?
1. Interstitial fluid (11L)
2. Plasma (3L)
ratio of TBW: ICV: ECV
what would alter the percentage of our body weight that is water?
fat content (increase fat, decrease water)
which compartment do RBCs fall into?
which electrolyte is found in highest concentration in the intracellular compartment?
which electrolytes are found in highest concentration in the extracellular compartment? (3)
if you hydrate a patient with IV saline, in which compartment does the fluid distribute?
what are some clinical s/s that indicate an expanded ECF volume? (5)
1. HTN
2. elevated JVP
3. hepatic congestion
4. hepatojugular reflex
5. edema, rales
what are some clinical s/s that indicate a diminished ECF volume? (7)
1. orthostatic hypotension
2. decreased JVP
3. hypotension
4. shock
5. dry mouth and membranes
6. diminished skin turgor
7. diminished intraocular pressure
3 lab values that would indicate a diminished ECFV?
1. BUN/Cr > 20
2. FENA <1%
3. Urine osmolality >600mOSM/L
what is the formula for calculating FENA?
FENA = U[Na+] / P[Na+] x P[Cr] / U[Cr] x 100
treatment for an ECFV loss?
infuse isotonic saline (4:1)
what is the site of action of thiazide diuretics?
distal tubule
which ion do thiazides excrete in urine?
which type of diuretic is used to treat glaucoma?
carbonic anhydrase inhibitor
site of action of carbonic anhydrase inhibitors?
proximal tubule
ions excreted in urine when using a carbonic anhydrase inhibitor?
(great for use in volume overload or alkalotic patient - gets rid of bicarb)
where do K+ sparing diuretics work?
distal and cortical collecting tubule
name three K+ sparing diuretics
1. triamterene
2. amiloride
3. spironolactone
site of action of loop diuretics?
Loop of Henle - Duh!
MOA of loop diuretics?
inhibit Na/K/Cl pumps, therefore ions aren't pumped out of the lumen
what could make a loop diuretic not work?
they must be secreted into the proximal tubule, so if there is no secretion they won't work.
where in the nephron are Na+ channels found on the apical membrane?
in the DT and CD
where in the nephron is NaCl symport found?
on which side of the tubular epithelial cell is the Na/K/ATPase found?
basolateral membrane (interstitial side)
which hormone regulates Na+ transport in the distal tubule and collecting duct?
what effect does increased fluid flow in the tubular lumen have on K+ excretion?
increase flow -> increase K+ excretion
(diffusion only, remember?)
if you can't concentrate your urine, what three types of problems could you have?
1. Loop Problem
2. No ADH production or release
3. No receptors for ADH in CD
how does ADH regulate urine concentration?
adds water channels (aquaporins) to the collecting duct: water diffuses out as needed
if ADH regulates water retention, what does Aldosterone regulate?
Na+ retention
what are the two receptors for ADH?
V1 - vascular smooth muscle
V2 - distal tubule and collecting duct
which receptors can trigger ADH release?
1. osmoreceptors in hypothalamus (sense plasma osmolality and [Na+])
2. low volume receptors (atria)
3. arterial baroreceptors
which receptor is the most sensitive?
what happens to [Na+] during ECFV depletion?
at what plasma [Na+] do we start to have serious neurological concerns?
Plasma [Na+] <120 mMol/L
what is the formula to calculate plasma osmolarity?
Posm = 2 x [PNa+] + [glucose] / 18 + BUN/2.8
what [PNa+] counts as hyponatremia?
[PNa+] < 130 mEq/L
using the Posm formula: how would we know if we had pseudohyponatremia?
if the measured Posm >10 mOsm greater than calculated Posm. (This means there is an extra osmolyte producing hyponatremia via osmoreceptor stimulated ADH release)
what is the most common euvolemic cause of hyponatremia?
SIADH (syndrome of innapropriate ADH secretion)
what is the therapy for hypovolemic hyponatremia?
isotonic saline infusion
what is the therapy for euvolemic hyponatremia?
fluid restriction
therapy for hypervolemic hyponatremia?
fluid restriction
clinically, which is more dangerous: hypernatremia or hyponatremia?
what [PNa+] couts as hypernatremia?
[PNa+] > 145 mEq/L
in a hypernatremic state which fluid compartment is depleted?
intracellular fluid compartment
what are the three main classes of causes of hypernatremia?
1. pure water loss
2. more water loss than Na+ loss
3. Sodium gain in excess of water
examples of pure water loss resulting in hypernatremia?
1. respiratory
2. burns
3. DI (ADH deficiency)
4. nephrogenic DI (no AHD receptors)
two ways there could be more water loss than Na+ loss?
1. GI losses
2. Diuretics
therapy for hypernatremia?
add water
remove salt from diet
what are some ways to differentiate DI (nephrogenic or central)?
1. measure AHD blood levels
(increased in nephrogenic DI, decreased in central DI)
2. water deprivation test
(complete DI will respond to exogenous ADH, NDI will not)
what is the MC outpatient cause of acute renal failure?
clinical recognition of drug-induced renal disease?
1. increased BUN, SCr
2. decreased urine output
what symptoms are associated with uremia?
clinically, how can you tell if the proximal tubule vs. the distal tubule is damaged?
proximal tubule: glycosuria, hypophosphatemia, hypouricemia
distal tubule: polyuria, hyperkalemia
which drug classes are MC associated with drug-induced renal disease? (6)
1. aminoglycosides
2. amphotericin B
4. ACEIs and ARBs
5. Radiocontrast dyes
6. chemotherapeutic agents (cisplatin)
what is pseudo-renal failure?
a rise in BUN and/or SCr despite a normal GFR
what could cause pseudo-renal failure? (3)
1. steroids
2. tetracyclines
3. patients of TPN (due to high aa content)
what is the pathogenesis behind renal damage caused by ACEIs and ARBs?
decreased glomerular capillary hydrostatic pressure
(pressure at glomerulus is reduced, therefore GFR is reduced)
which 2 vasoactive substances act on the afferent arteriole?
1. PGE2
2. angiotensin II
which vasoactive substance acts on the efferent arteriole?
angiotensin II
what are two risk factors for renal disease caused by ACEIs/ARBs?
1. Renal Artery Stenosis
2. decresed effective arterial renal blood flow for any reason
how can renal disease caused by ACEIs/ARBs be prevented?
when starting the medication:
use a short acting med (captopril), start with low doses, and titrate slowly. if all is well convert to long term med.
*monitor renal function and K+ during initiation of therapy*
how can we manage acute hyperkalemia if it is seen with renal disease caused by ACEIs/ARBs?
sodium polystyrene sulfate (kaexalate - K+ binding agent).
which NSAID has been associated with ARF after just one dose?
(parenteral NSAID)
pathogenesis of ARF caused by NSAIDs?
* COX inhibitor decreases prostaglandin synthesis
* no more vasodilatory prostaglandins to dilate afferent arteriole. get unopposed vasoconstriction -> reduced blood flow -> decreased GFR
other analgesics that have less prostaglandin inhibition (therefore we would recommend them for anyone at risk for ARF)? (3)
nonacetylated salicylates
what is unique about the clinical presentation of ARF caused by aminoglycosides?
decreased urine volume is uncommon.
(ARF caused by other drugs typically presents with decreased urine output).
pathogenesis of aminoglycoside induced nephrotoxicity? (big picture)
* proximal tubul epithelial cell damage leads to obstruction of tubular lumen and backleak of glomerular filtrate across damaged epithelium.
how does nephrotoxicity vary among different aminoglycosides?
nephrotoxicity is related to the # of cationic charges the drug has (facilitates binding to epithelial cell)
* neomycin has highest nephrotoxicity (most + groups)
* gentamycin - intermediate
* amikacin - least
what happens once the aminoglycosides are bound to the epithelial cell?
they are taken up into the cells and concentrated in the lysosomes
*cellular dysfunction and death is due to release of lysosomal enzymes
risk factors (related to dosing)that lead to aminoglycoside nephrotoxicity? (4)
1. large total accumulated dose
2. prolonged therapy
3. high trough concentrations
4. recent previous aminoglycoside therapy
four drugs that synergistically can be nephrotoxic alongside aminoglycosides?
1. cyclosporine
2. amphotericin B
3. vancomycin
4. diuretics
prevention of aminoglycoside toxicity?
* adequate hydration
* avoid concomitant nephrotoxic drugs
* higher doses less frequently (once daily)
what is an alternative antibiotic that is "kidney friendly" if a switch from aminoglycosides is desired?
when a patient is on aminoglycosides - how often should SCr be monitored?
every 2-4 days
what is the pathogenesis of radiographic contrast media induced nephrotoxicity?
direct tubular toxicity and renal ischemia
-ischemia is due to dehydration (contrast dye is a very osmolar compound, acts as a diuretic)
#1 prevention tactic for radiographic contrast media nephrotoxicity?
(isotonic saline IV)
what is mucormyst (n-acetylcysteine)?
antioxidant, free radical scavenger - thought to lower chances of radiographic contrast media induced nephrotoxicity?
what is the pathogenesis of cisplatin induced nephrotoxicity?
proximal, distal and collecting duct tubular necrosis
4 risk factors for cisplatin induced nephrotoxicity?
1. increased age
2. dehydration
3. renal irradiation
4. ETOH abuse
what can be administered if a patient has cisplatin induced nephrotoxicity?
(Chelates cisplatin)
pathogenesis of Amphotericin B induced nephrotoxicity?
proximal and distal tubule damage
(direct toxicity with increased tubular permeability and necrosis)
- results in arterial vasoconstriction
Cockraft-Gault formula for estimating creatinine clearance (CrCl)?
CrCl = (140-age)LBW / 72(SCr)
what is the CrCl "cutoff" for renal dosing?
when CrCl is below 30 - dose adjustment required

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