Darrow Osmolality CIS Flashcards
most common electrolyte order we will see
hyponatremia
normal serum sodium
normal 140 meq/L
normal serum K
n = 4.5 meq/L).
normal serum cl
meq/L (100)
normal serum bicarb
meq/L (25).
normal serum glucose
60 mg/dL(60 -100).
normal urine osmolality
(50-1200)
how to calculate serum osmolality
285 is normal
usually just double na
(Serum Osm= 2(Na) + BUN/2.8 + glucose/18)
The decreased vascular volume produces decreased baroreceptor stretch with resultant
increased sympathetic tone to increase proximal tubular Na absorption and activate RAAS(increased Na absorption in the cortical collecting tubule). Decreased cardiac output in addition yields a decreased RBF and GFR. All these contribute to avid sodium retention and reabsorption with resultant low urinary sodium, ieUNa
The low BV activates
ADH secretionwith avid water retention which
outperforms the retention of Na to yield hyponatremia, especially if the patient has increased free water intake.Almost all cases of hyponatremia(except for PP, etc) involve a relative excess of ADH, which may be appropriate or inappropriate.
Hyponatremia
(Na
Artifactualpseudohyponatremia- Extra fat and protein Isotonic Hyponatremia 1. Hyperproteinemia(myeloma) 2. Hyperlipidemia (chylomicrons, tryaglycerides, rarely cholesterol)
Hyponatremia
(Na
Hypotonic Hyponatremia
Volume Status?
Focusing on hypotonic hyponatremiathe second step is to evaluate volume status
Hyponatremia
Na 295 mosm/kg
Extra carbohydrate Hypertonic Hyponatremia 1. Hyperglycemia 2. Mannitol, sorbitol, glycerol, maltose 3. Radiocontrastagents 4. Ethylene glycol, methanol
protein and fat dont have an effect on
osmolality
Hypovolemia(32%)
Una
ExtrarenalSalt Loss
- Dehydration
- Vomiting
- Diarrhea
- 3rdSpacing (burns, trauma)
Hypovolemia(32%)
Una> 20 meq/L
Renal Salt Loss
- Diuretics
- ACE Inhibitors
- Nephropathies
- Mineralocorticoid deficiency (Addison’s)
- Cerebral Sodium Wasting (BNP)
- Partial Obstruction
- Type IV RTA
Euvolemic(48%)
UNa+> 20mEq/L
- SIADH –35% (Uosm> 200 mOsm/L)
- Post-op hyponatremia
- Psychogenic polydipsia –4%(Uosm
Hypervolemic(20%)
Una
Edematous States
- Congestive heart failure
- Liver Disease
- Nephrotic syndrome (Renal Na retention)
- Advanced kidney disease (Una> 20 meq/L)
if there is hypokalemia think
alkalosis
for every 2 sodiums you retain you get rid
1 hydrogen and 1 potassium
An EKG is done on the patient and reveals flattened to inverted T waves with U waves. What abnormality does the
EKG reveal?
hypokalemia
contraction alkalosis
for every 2 sodiums you lose a hydrogenand potassium bc when you reabsorb k you reabsorb a bicarb with it and h takes a cl with it?
Urea is passively reabsorbed in the proximal tubule. Thus, if volume is
low and BUN concentration high
there will be increased reabsorption
according to the higher BUN gradient. Also, more urea is reabsorbed at
low tubular flow rates than at high tubular flow rates.
In addition, low effective plasma volume creates a resultant increased
ADH with the latter effecting more collecting tubule reabsorptionof
BUN in order to create the gradient for water reabsorption.
Elevated BUN
in Dehydration
low flow so na is actively reabsorbed so bun becomes more concentrated in the tubule so it is passively reabsorbed
What is meaning of the BUN/creatinineratio of 60/1.4?
•A high BUN/Cr ratio occurs in prerenalazotemiadue to the decreased GFR with avid Na and H2O and BUN (passive) reabsorptionin the proximal tubule. At the same time creatinineis actually secreted in the proximal tubule since the kidney is functioning normally. The result is a high BUN/creatinineratio.
Causes of an elevated BUN/creatinine
High protein intake or breakdown:
Pre renal disease
Pre renal disease
Causes of an elevated BUN/creatinine
High protein intake or breakdown
Catabolic state
Catabolic drugs, ietetracycline, steroids
GI bleed
Causes of an elevated BUN/creatinine
Pre renal disease
Dehydration
CHF
Shock
Glomerulonephritis
Causes of an elevated BUN/creatinine
Post renal disease
Prostatic obstruction
Ureteral obstruction
BUN/creatinineof 10/1
indicates either normal renal function (when creatinineis 1 or less) or intrinsic renal disease (when the creatinineis > 1), ie. BUN of 40 and creatinineof 4 = 40/4 = I0/1
BUN/creatinineratio > 10/1
ie. BUN of 30 with creatinineof 1 =Prerenal(including glomerulo-nephritis), or postrenalazotemia, or catabolic state
BUN/creatinine
non-renal), ielow BUN seen in liver failure, malnutrition, overhydration, pregnancy, SIADH
hyaline or tamms horsfall cast
prerenalazotemia.
Urine sediment with pigmented granular casts and renal tubular epithelial cells is pathognomonic for
ATN
Causes of atn
Ischemia: post op shock, sepsis pancreatitis hypophosphatemia Toxins: aminoglycosides vancomycin cyclosporine radiographic contrast media myoglobinuria hemoglobin hyperuricemia BenceJones protein
protein and fat do effect?
effective plasma volume
An EKG is done on the patient and shows a prolonged PR
interval with peaked T waves, indicative of:?
Hyperkalemia
what must one watch out for in phosphate replacement?
if you give phostphate be careful bc it can cause hypocalcemia
This patient has renal ATN due to rhabdomyolysisfrom starvation and alcohol related hypophosphatemia and subsequently decreased 2,3 DPG with oxygen starvation and tissue hypoxia. Phosphate replacement, should be done
slowly to avoid hypocalcemia.
Classic crush injury rhabdomyolysiswould cause massive release of phosphate, uric acid and potassium with decreased calcium due to Cax P precipitation in tissues. In that type of situation, one would
notwant to administer calcium as with improvement it will be released from the tissues.
Urine sediment of pigmented granular castsand renal tubular epithelial cells is pathognomonic for
ATN
ischemic causes of ATN
post op
shock, sepsis
pancreatitis
hypophosphatemia
toxic causes of ATN
aminoglycosides vancomycin cyclosporine radiographic contrast media myoglobinuria hemoglobin hyperuricemia BenceJones protein
As the renal tubular epithelium regenerates, as the double
nucleus (arrow) in this photomicrograph testifies to, the
kidney begins to produce large amounts of very dilute urine.
The reason for this is
that the complicated brush border
cells do not come back immediately, they are first replaced by
low cuboidalepithelium, which does little in the way of
resorptionof water. Thus large quantities of dilute urine
(polyuria) are produced by the patient. Eventually, the
epithelium differentiates into the more complex brush border
type, and normal urinary production is restored.
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