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Advanced Pathophysiology > Fluid, Electrolyte, and Acid-Base Balance > Flashcards

Fluid, Electrolyte, and Acid-Base Balance Flashcards

Exam I

1
Q

Renal control of sodium

A

Via aldosterone

  1. RAAS: Decreased renal perfusion is sensed by the juxtaglomerular cells in the kidney, resulting in increased renin secretion and the activation of the renin-angiotensin-aldosterone system
    -Angiotensin II causes vasoconstriction and stimulates the release of aldosterone by the adrenal cortex
    -Aldosterone promotes sodium retention in the distal nephron
  2. Volume receptors: Volume receptors in the great veins and atria are sensitive to small changes in venous and atrial filling
    -Increased atrial filling stimulates volume receptors and results in the release of atrial natriuretic factor/peptide (ANF/ANP) and brain natriuretic factor/peptide (BNF/BNP), which promote sodium excretion
  3. Baroreceptors: Pressure receptors in the aorta and carotid sinus are stimulated by volume depletion and subsequently active the sympathetic nervous system, leading to renal retention of sodium
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2
Q

Renal control of water

A

Via ADH

Two stimuli for ADH secretion:

  1. Osmotic stimulus: changes in plasma osmolality stimulate osmoreceptors in the hypothalamus
    - Osmoreceptor stimulation results in:
    1) an increase or decrease in thirst
    2) an increase or decrease in ADH secretion
  2. Volume/pressure stimulus: Changes in circulating blood volume/pressure are sensed by volume-sensitive receptors and baroreceptors:
    -Volume/baroreceptors stimulate an increase or decrease in ADH secretion

*If both the osmolality AND the volume/pressure decrease, the volume/pressure stimulus will be most significant

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3
Q

Osmolality

A

a value determined by the total solute concentration in a fluid compartment

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4
Q

Tonicity

A

The ability of the combined effect of all the solutes to generate an osmotic driving force that causes water movement from one compartment to another

Solutes capable of changing the tonicity (i.e., translocating water from one body fluid compartment to another) are effective osmoles

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5
Q

Examples of effective osmoles

A

sodium, glucose, mannitol, and sorbitol

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6
Q

Urea osmolality

A

Contributes to the osmolality, but easily crosses cell membranes and distributes evenly throughout total body fluids

An ineffective osmole

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7
Q

Serum osmolality calculation

A

2 X [sodium concentration] + [glucose concentration/18] + [BUN/2.8]

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8
Q

Normal body fluid osmolality

A

280-294 mOsm/Kg (milliosmoles per kilogram)

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9
Q

Isotonic alterations

A

volume depletion or volume excess with a normal osmolality

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10
Q

Hypertonic alterations

A

volume depletion or volume excess with an increased osmolality

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11
Q

Causes of hypertonic alterations

A

increase in sodium or loss of free water

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12
Q

Outcomes of hypertonic alterations

A

Intracellular dehydration, and if untreated, extracellular dehydration

This is often seen first in signs and symptoms of brain cell shrinkage

These patients are usually hypernatremic

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13
Q

Hypotonic alterations

A

normal volume, volume depletion, or volume excess with a decreased osmolality

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14
Q

Causes of hypotonic alterations

A

May be related to a decrease in sodium, but more commonly, by impaired renal water excretion or free water excess

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15
Q

Outcomes of hypotonic alterations

A

Intracellular swelling (fluid shifts into the cell where there are more solutes)

This is often seen first in signs and symptoms of brain cell or cerebral swelling and/or pulmonary edema

These patients are usually hyponatremic and hypotonic
○ The most common form of hyponatremia
○ Usually caused by impaired renal water excretion in the presence of continued water intake

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16
Q

Psuedohyponatremia

A

a rare condition in which serum sodium concentration is low, but serum osmolality and tonicity is normal or above normal

A low sodium concentration with normal osmolality may be an artifact due to the accumulation of other plasma constituents (triglycerides or proteins) in plasma

Severe hypertriglyceridemia, severe hyperproteinemia [multiple myeloma]

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17
Q

Hyponatremia with hyperosmolality

A

Usually due to severe hyperglycemia

Increase in glucose in the extracellular fluid moves water from the cells to extracellular compartment and dilutes the sodium concentration

The sodium concentration falls about 1.6 mEq/L for every increase of 100 mg/dl in glucose concentration over normal (100 mg/dl)

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18
Q

Water deficit calculation

A

Current TBW = weight in kg x (0.4 for women/0.5 for men/0.6 for infants)

Ideal TBW = (Na (current) X TBW)/140 (ideal sodium concentration)

Water deficit = (Na (current) X TBW)/140) - TBW

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19
Q

Water excess calculation

A

Current TBW = weight in kg x (0.5 for women/0.6 for men/0.7 for infants)

Water excess = TBW x (1 – (Na/125))

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20
Q

TBW composition in fluid compartments

A

2/3 of TBW is intracellular (28 L) and 1/3 of TBW is extracellular [(3/4 interstitial (11 L) and 1/4 intravascular (3 L)]

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21
Q

Causes of edema

A

1) Increased capillary venous hydrostatic pressure
2) decreased capillary oncotic pressure
3) lymphatic obstruction/dysfunction
4) increased capillary permeability
5) sodium and water retention

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22
Q

Pitting edema

A

If the fluid contains few proteins, it will be pitting

Caused by increased capillary venous hydrostatic pressure or decreased capillary oncotic pressure

23
Q

Non-pitting edema

A

If the fluid contains a lot of protein, it will be non-pitting

Caused by increased capillary permeability or lymphatic obstruction

24
Q

Spurious hypokalemia

A

The serum potassium is not really low, but appears so due to insulin administration

A dose of insulin right before blood drawing can cause temporary movement of potassium into cells in the blood tube and a falsely lower serum potassium

Decrease of about 0.3 mEq/L

25
Q

Pseudohyperkalemia

A

The serum potassium is not really high, but appears so due to:
· 1) Hemolysis during blood draw
· 2) Platelets > 1,000,000
· 3) WBC > 200,000
· 4) Mononucleosis
· 5) Familial pseudohyperkalemia

26
Q

Serum K+ response in alkalosis

A

Serum potassium falls about 0.3 mEq/L for each 0.1 increase in pH (alkalosis)

27
Q

Serum K+ response in respiratory acidosis

A

Serum potassium rises about 0.3 mEq/L for each 0.1 decrease in pH in respiratory acidosis

28
Q

Serum K+ response in metabolic acidosis

A

Serum potassium rises about 0.7 mEq/L for each 0.1 decrease in pH in metabolic acidosis

29
Q

Serum ical response in alkalosis

A

Decrease

In metabolic alkalosis, bound hydrogen ions dissociate from albumin, which increases the amount of albumin available to bind ionized calcium

30
Q

Serum ical response in acidosis

A

Increase

31
Q

Causes of metabolic acidosis

A
  1. A primary loss of bicarbonate from the body (usually GI or renal)
  2. An increase in the production or addition of metabolic, nonvolatile acids (in other words, NOT carbonic acid [carbon dioxide])
  3. A decrease in acid excretion

The last 2 mechanisms lead to “using up” bicarbonate stores (as opposed to “losing” bicarbonate from the body)

32
Q

Anion gap calculation (without K)

A

Anion gap = Na - (Cl + HCO3)

33
Q

Normal anion gap (without K+)

A

12 ± 2

(10-14)

34
Q

Causes of normal anion gap metabolic acidosis

A

Loss of bicarbonate (usually from the GI tract or kidneys)

GI: diarrhea or diarrheal equivalents
Renal: renal tubular acidosis

35
Q

Type 1 RTA

A

Distal RTA

Involves a decrease in the ability of the distal nephron to produce new bicarbonate (or secrete hydrogen ions into the tubular fluid)

Can be caused by a defect in any step in the production of bicarbonate

Classic distal RTA can result in hypokalemia

36
Q

Type 2 RTA

A

Proximal RTA

Involves a decrease in the ability of the proximal tubule to reabsorb filtered bicarbonate

37
Q

Type 4 RTA

A

Hyperkalemic RTA

Involves a lack of aldosterone activity at the distal nephron

A hallmark of type 4 RTA is hyperkalemia

38
Q

Causes of elevated anion gap metabolic acidosis

A

Retention or addition of acid

Retention: renal failure (GFR <25% normal)

Addition: via derangements in metabolism or exogenous ingestions

39
Q

You’re doing great sweetie

A
40
Q

Derangements in metabolism causing elevated anion gap metabolic acidosis

A

Ketoacids and lactic acidosis

Ketone bodies: 2 organic acids (acetoacetic acid and beta-hydroxybutyric acid) and acetone (ketone) produced by the liver from triglycerides

Lactic acid: a byproduct of anaerobic metabolism

41
Q

Type A lactic acidosis

A

Results from tissue hypoxia, leading to increased anaerobic metabolism (e.g., all types of shock, respiratory failure, severe anemia, carbon monoxide poisoning)

42
Q

Type B lactic acidosis

A

Results from a mitochondrial defect in oxygen utilization (e.g., cyanide toxicity, malignancies [leukemia, lymphoma, sarcoma], medications [isoniazid, phenformin, salicylates, AZT])

43
Q

Causes of ketoacidosis

A

DKA

Starvation

Alcoholism

44
Q

Exogenous ingestions causing elevated anion gap metabolic acidosis

A

Their metabolism produces toxic acids and other products that can cause severe acidosis

PLUMSEEDS:
Paraldehyde
Lactic acidosis
Uremia
Methanol
Salicylates
Ethanol
Ethylene glycol
DKA
Starvation

45
Q

K+ and Ca2+ levels in metabolic acidosis

A

hyperkalemia and hypercalcemia

Acidosis is associated with an increase in the ionized calcium and hypercalcemic effects

46
Q

Causes of metabolic alkalosis

A

Addition of bicarbonate to the body, loss of hydrogen ions, or contraction alkalosis

47
Q

Contraction alkalosis

A

Involves the loss of fluids from the body that are low in bicarbonate (and usually high in chloride)

The fluid losses “contract” the vascular/blood volume

There is decreased water content, but because the loss of bicarbonate is slight, the bicarbonate concentration increases

Vomiting, GI suction, and the administration of thiazide or loop diuretics can result in contraction alkalosi

48
Q

H+ loss causing metabolic alkalosis

A

For every hydrogen ion lost, one bicarbonate ion is added

Extrarenal or renal

Extrarenal hydrogen ion loss: Usually results from GI losses (vomiting, GI suction) or a shift of hydrogen ions from the extracellular to the intracellular compartment

Renal loss of hydrogen ions: Usually occurs due to increased mineralocorticoid (aldosterone) activity (primary hyperaldosteronism, Cushing’s, congenital adrenal hyperplasia, renal artery stenosis

49
Q

K+ and Ca2+ levels in metabolic alkalosis

A

hypokalemia and hypocalcemia

50
Q

Causes of inability to excrete bicarb

A
  1. Excessive mineralocorticoid activity
    - Increased hydrogen ion excretion and increased bicarbonate retention
  2. Hypovolemia
    -Stimulates aldosterone secretion –> increased hydrogen ion excretion and increased bicarbonate retention
  3. Hypokalemia and hypochloremia:
    -Both stimulate renal secretion of hydrogen ions and retention of bicarbonate ions (These two abnormalities, because they tend to maintain a state of metabolic alkalosis, must be corrected before acid base imbalances from any cause can be successfully treated)
51
Q

Saline-responsive metabolic alkalosis

A

Associated with hypovolemia and is corrected when the ECF is expanded with a solution of sodium chloride and potassium (as above the chloride and potassium levels must be corrected)

52
Q

Saline-resistant metabolic alkalosis

A

Associated with excessive mineralocorticoids (aldosterone)

53
Q

Corrected sodium in hyperglycemia

A

The sodium concentration falls about 1.6 mEq/L for every increase of 100 mg/dl in glucose concentration over normal (100 mg/dl)

Corrected sodium = Na+ + ( [BGL-100]/100 x 1.6)

54
Q

Normal serum calcium

A

8.5-10.5 mg/dL

Advanced Pathophysiology (3 decks)

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