01a: Water/Na Balance Flashcards Preview

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Flashcards in 01a: Water/Na Balance Deck (76)
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1
Q

What’s being “measured” or sensed in osmoregulation? And in volume regulation?

A

Osmoregulation: plasma osmolality

V reg: effective circulating volume

2
Q

What are the sensors for osmoregulation? And for volume regulation?

A

Osmoregulation: hypothalamic osmoreceptors

V reg: Carotid sinus, JG cells (afferent arteriole), atria

3
Q

What are the effectors for osmoregulation? And for volume regulation?

A

Osmo: ADH

V reg: RAAS, SNS, ADH, natriuretic peptides

4
Q

In osmoregulation, (X) intake/excretion is affected. And in volume regulation?

A

X = water

V reg: Na

5
Q

Hypovolemia is loss of (X) from which compartments? Serum osmolality (increases/decreases/same).

A

X = Na and water
ECF

No change (reduced TBW and TBNa)

6
Q

Dehydration is loss of (X) from which compartments? Serum osmolality (increases/decreases/same).

A

X = water
ECF and ICF

Increases (reduction in TBW, so hypernatremia)

7
Q

Total body sodium content is proportional to (X) volume.

A

X = ECF (circulating volume)

8
Q

T/F: normally, nearly all Na excretion is in the urine.

A

True

9
Q

Excessive vomiting/diarrhea will result in (Na/H2O) loss.

A

Both, but moreso water (hypo-osmotic fluids lost)

10
Q

How many days of deficient Na intake will result in salt depletion?

A

Deficient intake alone won’t result in Na depletion! Urine Na excretion will drop

11
Q

Salt depletion occurs by one of which two mechanisms?

A
  1. Extra-renal (GI, sweat)

2. Renal/adrenal (tubular disease, adrenal insufficiency)

12
Q

Measuring (X) can help distinguish between renal and extra-renal Na depletion.

A

X = urine Na conc

Will be less than 10 mEq/L if extra-renal

13
Q

List some clinical findings that suggest Na depletion.

A
  1. Low turgor
  2. Postural hypotension
  3. Decreased BW
  4. Increased HCT
14
Q

T/F: In edematous state, all body volumes are high.

A

False - low effective circulating V

15
Q

Hyponatremia: (X) is decreased by definition. You should ask yourself “why doesn’t the patient (Y)?”

A

X = serum Na conc (imbalance with excess water relative to Na)

Y = secrete water normally

16
Q

List 5 causes for hyponatremia

A
  1. ECF depletion
  2. ECF excess
  3. Euvolemia
  4. Endocrine
  5. Drug
17
Q

Edema and low urine Na are clinical hallmarks of (hyper/hypo)-natremia, secondary to (X) syndrome/cause.

A

Hyponatremia;

X = ECF excess (CHF, cirrhosis)

18
Q

Measuring (X) will be valuable in determining if cause of (hyper/hypo)-natremia is due to Diabetes Insipidus. What do you expect (X) to be in DI?

A

X = urine Osm
Hypernatremia

Lower than serum Osm

19
Q

Decreased effective circulating volume (ECV) occurs in (hypo/hyper)-volemic states.

A

Both

20
Q

(X) is an indirect measure of ADH

A

X = urine Osm

21
Q

Key concepts: (X) reflects TBW and (Y) reflects TBNa

A
X = serum Na
Y = volume status
22
Q

Normal serum Osm

A

280-310 mOsm/kg

23
Q

Hyponatremia is serum (X) lower than which value?

A

X = Na conc
135 mM
(Note: under 120 mM is danger zone)

24
Q

How do you treat patient who is hyponatremic with isotonic serum Osm?

A

Do nothing - treat underlying cause

normal serum Osm means body likely producing molecule like Ig that is interfering with measurement

25
Q

Why might patient with uncontrolled diabetes mellitus present with hyponatremia?

A

Hypertonic hyponatremia (hyperglycemia may be causing water exit from cells, thereby diluting serum Na)

26
Q

Patient with mineralocorticoid deficiency will likely present with (hyper/hypo/eh)-volemic hyponatremia and should be treated with (X).

A

Hypovolemic

IV saline (isotonic)

27
Q

List some causes of hypovolemic hyponatremia.

A

Renal: diuretics, Na wasting nephropathy, mineralocorticoid deficiency
Extra-renal: GI/skin losses

28
Q

List two main classes of drugs that can cause SIADH and (hyper/hypo/eh)-volemic hyponatremia.

A

Euvolemic

Antidepressants and antipsychotics

29
Q

SIADH: Urine Osm (higher/lower/same) compared to serum Osm.

A

Higher (over 300) - water can’t get out of body!

30
Q

Tea and toast diet leads to (hyper/hypo/eu)-volemic hyponatremia because there is too (much/little) (X) in diet.

A

Euvolemic hyponatremia
Too little
X = solute

31
Q

How would you treat patient with hyponatremia secondary to SIADH?

A

Euvolemic hyponatremia; restrict water and liberalize dietary Na

Consider hypertonic saline

32
Q

T/F: Hypernatremia is always a hyperosmolar state (high serum Osm).

A

True

33
Q

Rate of Na correction in hyponatremic state: under (X) over first 24 hours and under (Y) over first 48 hours.

A
X = 6-10 mEq/L
Y = 18 mEq/L
34
Q

List the three mechanisms the kidneys use to handle an acid load.

A
  1. Recycle H+ to reabsorb bicarb
  2. Titratable acid secretion (to bind H+)
  3. Excrete NH4+
35
Q

List the locations along the nephron that NH4+ is secreted

A

Proximal tubule, ALOH, and collecting ducts

36
Q

You would expect VBG to have higher (pH/pCO2/HCO3/O2) relative to ABG. Which value(s) should not be estimated from VBG (difference is too big).

A

pCO2 and HCO3

Don’t estimate O2 from VBG

37
Q

Anion gap must be corrected for if patient has too (high/low) (X) in blood. Why and how is this accounted for?

A

Low
X = albumin

It’s a major unmeasured anion that constitutes the Gap, so must be accounted for if low levels

Every 1g/dL drop in albumin decreases anion gap by 2.5

38
Q

List differential for metabolic acidosis with anion gap

A

MUDPILES

  1. Methanol
  2. Uremia
  3. DKA
  4. Pyroglutamic acidosis, propylene glycol
  5. INH overdose
  6. Lactic acidosis
  7. Ethanol, ethylene glycol
  8. Salicylates, starvation ketoacidosis
39
Q

Anion gap over 20 is red flag to calculate (X). What’s the formula?

A

X = Osm gap

Expected serum Osm - measured serum Osm

40
Q

Normal Osm gap is:

A

10-15

41
Q

Serum Osm calculated with which equation?

A

2(Na) + (Glucose/18) + (BUN/2.8) + (EtOH/4.6)

42
Q

Anion gap is 25 so you calculate (X) and it’s also 25. You have high suspicion for (Y) as the cause for metabolic acidosis.

A
X = Osm gap
Y = intoxication by ethylene glycol, methanol, or propylene glycol
43
Q

Patient with metabolic acidosis has anion gap of 18. How do you figure out if another metabolic disorder is present?

A

Delta gap calculation:

= 24 means just AGMA
Under 24 means AGMA + non-gap acidosis
Over 24 means AGMA + metabolic alkalosis

44
Q

Patient with metabolic acidosis has anion gap of 18. How do you figure out if there is additional respiratory disorder present?

A

Winter’s formula:

Expected pCO2 = (1.5)(HCO3) + 8

Range is plus/minus value calculated

45
Q

Differential for non-gap metabolic acidosis

A

RUN-DIC

  1. RTA
  2. Uremia
  3. NaCl (large V of isotonic saline)
  4. Diarrhea
  5. Intestinal-bladder fistula
  6. Carbonic Anhydrase Inhibitors
46
Q

What’s the problem in proximal RTA (Renal Tubular Acidosis) Type 2?

A

Decreased ability for proximal tubule to reabsorb HCO3

47
Q

What’s the problem in distal RTA (Renal Tubular Acidosis) Type 1?

A

Unable to acidify urine

Unknown but likely decrease in H+ secretion or diffusion back into cell

48
Q

What’s the problem in distal RTA (Renal Tubular Acidosis) Type 4?

A

Hyporeninemia, hypoaldosteronemia, OR aldosterone insensitivity

49
Q

DKA: patients are volume (overloaded/depleted) as a result of (X). Despite their (low/high) total body K, their serum K concentration is (low/high).

A

Depleted
X = hyperglycemia (glucose in urine acts as diuretic)
Super low TBK, but high extracellular conc (acidemia pulls K out of cells in exchange for H)

50
Q

Treatment of DKA

A

Insulin and saline (replace K, Na, and water)

Note: if pH super low, bicarbonate admin too

51
Q

What’s your differential for patient presenting with DKA symptoms but normal blood glucose?

A

Starvation or alcoholic ketoacidosis

52
Q

Patient with (gap/nongap) metabolic acidosis has oxylate crystals in urine, so you know the cause is:

A

Gap

Ethylene glycol ingestion

53
Q

Distal RTAs (Type 1 and 4) can be distinguished by serum measurement of (X).

A

X = K

Type 1 (hypokalemic)
Type 4 (hyperkalemic - aldosterone issues)
54
Q

T/F: Proximal RTA (Type 2) has normal serum K.

A

True (or on the low side)

55
Q

A serum bicarbonate under 10 would make you suspect which RTA?

A

Type 1 (distal, hypokalemic)

56
Q

A serum bicarbonate over 15 would make you suspect which RTA?

A

Could be Type 2 (proximal) or Type 4 (distal hyperkalemic)

57
Q

A serum bicarbonate over 20 would make you suspect which RTA?

A

Type 4 (distal hyperkalemic)

58
Q

List some causes for acquired Type 1 (distal hypokalemic) RTA

A
  1. Sjogren’s
  2. Hyperparathyroidism
  3. Amphotericin B
59
Q

List some causes for acquired Type 2 (proximal) RTA

A
  1. Multiple myeloma
  2. Acetazolamide
  3. Heavy metals
60
Q

Urine anion gap equation:

A

(Na+K) - (Cl)

61
Q

Patient has non-gap MA and you decide to calculate (X) to figure out if RTA is the cause.

A

X = urine anion gap

If positive, tubules not working (too little NH4Cl around)

62
Q

List examples of Cl-sensitive metabolic alkalosis etiologies

A
  1. Vomit/Gastric drainage
  2. Diuretics
  3. Relief of chronic hypercapnia
63
Q

List examples of Cl-insensitive metabolic alkalosis etiologies

A
  1. Cushing
  2. Conn’s (1o aldosteronism)
  3. Bartter’s
64
Q

In order to “maintain” metabolic alkalosis, (X) becomes a key player in stimulating kidney to detrimentally continue bicarbonate reabsorption.

A

X = aldosterone

V depletion stimulates RAAS and aldosterone stimulates Na reabsorption (along with anions such as bicarb)

65
Q

Chronic metabolic alkalosis will present with (hyper/hypo)-kalemia.

A

Hypokalemia (remember aldosterone key player in maintaining this alkalosis)

66
Q

Chronic metabolic alkalosis: urine pH (low/high), and what about Na, K, Cl values?

A

Low (paradoxically);

K is high; Na and Cl at minimum values

67
Q

How do diuretics cause Cl-sensitive metabolic alkalosis?

A

Similar to vomiting, secreting of H+ in excess amounts in urine Leads to volume depletion and aldosterone secretion

68
Q

T/F: in Cl insensitive metabolic alkalosis, patients are V overloaded.

A

True (may be hypertensive)

69
Q

Key corrective maneuvers that should be taken to correct acute metabolic alkalosis

A
  1. Restore IV volume
  2. Replete K (to upper limit of normal)

Also monitor pCO2 and pO2 carefully

70
Q

T/F: Urine is hypotonic to your blood.

A

True

71
Q

Post-obstructive renal failure patients produce liters of urine once catheter is in. What are the main driving forces for all this urine production?

A
  1. Lots of urine build up from obstruction

2. Urea (build up in blood) acts as diuretic

72
Q

Carpal spasm occurs in the setting of (X) acid-base disorder. What’s the mechanism behind this?

A

X = respiratory alkalosis

Increase pH decreases ionized Ca and induces muscle spasm

73
Q

T/F: Serum Ca falls during respiratory alkalosis, leading to carpal spasm.

A

False - serum levels unchanged

74
Q

Management of acute respiratory alkalosis.

A

Breathe into closed system and manage underlying disorder (if any)

75
Q

Your patient with stage 4 CKD likely has (gap/non-gap) metabolic acidosis.

A

High anion Gap (retention of phosphates, sulfates, and organic acids that make up anion gap)

76
Q

Your patient with stage 3 CKD likely has (gap/non-gap) metabolic acidosis.

A

Non-gap (reduced ability to generate ammonia)