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Renal Exam III > Darrow Osmolality CIS > Flashcards

Darrow Osmolality CIS Flashcards

1
Q

most common electrolyte order we will see

A

hyponatremia

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2
Q

normal serum sodium

A

normal 140 meq/L

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3
Q

normal serum K

A

n = 4.5 meq/L).

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4
Q

normal serum cl

A

meq/L (100)

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5
Q

normal serum bicarb

A

meq/L (25).

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6
Q

normal serum glucose

A

60 mg/dL(60 -100).

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7
Q

normal urine osmolality

A

(50-1200)

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8
Q

how to calculate serum osmolality

A

285 is normal

usually just double na

(Serum Osm= 2(Na) + BUN/2.8 + glucose/18)

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9
Q

The decreased vascular volume produces decreased baroreceptor stretch with resultant

A

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

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10
Q

The low BV activates

A

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.

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11
Q

Hyponatremia

(Na

A 
Artifactualpseudohyponatremia-
Extra fat and protein
Isotonic Hyponatremia
1. Hyperproteinemia(myeloma)
2. Hyperlipidemia (chylomicrons, tryaglycerides, rarely cholesterol)
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12
Q

Hyponatremia

(Na

A

Hypotonic Hyponatremia

Volume Status?

Focusing on hypotonic hyponatremiathe second step is to evaluate volume status

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13
Q

Hyponatremia

Na 295 mosm/kg

A 
Extra carbohydrate
Hypertonic Hyponatremia
1. Hyperglycemia
2. Mannitol, sorbitol, glycerol, maltose
3. Radiocontrastagents
4. Ethylene glycol, methanol
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14
Q

protein and fat dont have an effect on

A

osmolality

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15
Q

Hypovolemia(32%)

Una

A

ExtrarenalSalt Loss

  1. Dehydration
  2. Vomiting
  3. Diarrhea
  4. 3rdSpacing (burns, trauma)
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16
Q

Hypovolemia(32%)

Una> 20 meq/L

A

Renal Salt Loss

  1. Diuretics
  2. ACE Inhibitors
  3. Nephropathies
  4. Mineralocorticoid deficiency (Addison’s)
  5. Cerebral Sodium Wasting (BNP)
  6. Partial Obstruction
  7. Type IV RTA
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17
Q

Euvolemic(48%)

UNa+> 20mEq/L

A
  1. SIADH –35% (Uosm> 200 mOsm/L)
  2. Post-op hyponatremia
  3. Psychogenic polydipsia –4%(Uosm
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18
Q

Hypervolemic(20%)

Una

A

Edematous States

  1. Congestive heart failure
  2. Liver Disease
  3. Nephrotic syndrome (Renal Na retention)
  4. Advanced kidney disease (Una> 20 meq/L)
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19
Q

if there is hypokalemia think

A

alkalosis

20
Q

for every 2 sodiums you retain you get rid

A

1 hydrogen and 1 potassium

21
Q

An EKG is done on the patient and reveals flattened to inverted T waves with U waves. What abnormality does the
EKG reveal?

A

hypokalemia

22
Q

contraction alkalosis

A

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?

23
Q

Urea is passively reabsorbed in the proximal tubule. Thus, if volume is
low and BUN concentration high

A

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.

24
Q

Elevated BUN

in Dehydration

A

low flow so na is actively reabsorbed so bun becomes more concentrated in the tubule so it is passively reabsorbed

25
Q

What is meaning of the BUN/creatinineratio of 60/1.4?

A

•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.

26
Q

Causes of an elevated BUN/creatinine

A

High protein intake or breakdown:

Pre renal disease

Pre renal disease

27
Q

Causes of an elevated BUN/creatinine

High protein intake or breakdown

A

Catabolic state
Catabolic drugs, ietetracycline, steroids
GI bleed

28
Q

Causes of an elevated BUN/creatinine

Pre renal disease

A

Dehydration
CHF
Shock
Glomerulonephritis

29
Q

Causes of an elevated BUN/creatinine

Post renal disease

A

Prostatic obstruction

Ureteral obstruction

30
Q

BUN/creatinineof 10/1

A

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

31
Q

BUN/creatinineratio > 10/1

A

ie. BUN of 30 with creatinineof 1 =Prerenal(including glomerulo-nephritis), or postrenalazotemia, or catabolic state

32
Q

BUN/creatinine

A

non-renal), ielow BUN seen in liver failure, malnutrition, overhydration, pregnancy, SIADH

33
Q

hyaline or tamms horsfall cast

A

prerenalazotemia.

34
Q

Urine sediment with pigmented granular casts and renal tubular epithelial cells is pathognomonic for

A

ATN

35
Q

Causes of atn

A 
Ischemia:
post op
shock, sepsis
pancreatitis
hypophosphatemia
Toxins:
aminoglycosides
vancomycin
cyclosporine
radiographic contrast media
myoglobinuria
hemoglobin
hyperuricemia
BenceJones protein
36
Q

protein and fat do effect?

A

effective plasma volume

37
Q

An EKG is done on the patient and shows a prolonged PR

interval with peaked T waves, indicative of:?

A

Hyperkalemia

38
Q

what must one watch out for in phosphate replacement?

A

if you give phostphate be careful bc it can cause hypocalcemia

39
Q

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

A

slowly to avoid hypocalcemia.

40
Q

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

A

notwant to administer calcium as with improvement it will be released from the tissues.

41
Q

Urine sediment of pigmented granular castsand renal tubular epithelial cells is pathognomonic for

A

ATN

42
Q

ischemic causes of ATN

A

post op
shock, sepsis
pancreatitis
hypophosphatemia

43
Q

toxic causes of ATN

A 
aminoglycosides
vancomycin
cyclosporine
radiographic contrast media
myoglobinuria
hemoglobin
hyperuricemia
BenceJones protein
44
Q

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

A

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.

45
Q

GO THROUGH CASES

A

NOW

Renal Exam III (17 decks)

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