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FA - Renal > Renal - Physiology (Electrolytes, Acid-Base, & Renal tubular acidosis) > Flashcards

Renal - Physiology (Electrolytes, Acid-Base, & Renal tubular acidosis) Flashcards

Pg. 532-534 in First Aid 2014 Pg. 487-488 in First Aid 2013 Sections include: -Potassium shifts -Electrolyte disturbances -Acid-base physiology -Acidosis/Alkalosis -Renal tubular acidosis (RTA)

1
Q

Name 2 substances that cause K+ to shift out of cells (causing hyperkalemia).

A

(1) Digitalis (2) Beta-adrengergic antagonist; Think: D & B in “Patient with hyperkalemia? DO Insulin LAB”

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2
Q

Name 4 conditions/processes that cause K+ to shift out of cells (causing hyperkalemia).

A

(1) HyperOsmolarity (2) Insulin deficiency (3) Lysis of cells (4) Acidosis; Think: O, Insulin, & LA in “Patient with hyperkalemia? DO Insulin LAB”

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3
Q

Name 6 factors (i.e., substances and conditions/processes) that cause K+ to shift out of cells (causing hyperkalemia).

A

(1) Digitalis (2) HyperOsmolarity (3) Insulin deficiency (4) Lysis of cells (5) Acidosis (6) Beta-adrenergic antagonists

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4
Q

Name 4 factors that cause K+ to shift into cells (causing hypokalemia).

A

(1) Hypoosmolarity (2) Insulin (increase Na+/K+ ATPase) (3) Alkalosis (4) Beta-adrenergic agonist (increase Na+/K+ ATPase)

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5
Q

What influence does insulin have on K+ equilibrium, and via what mechanism?

A

Increases Na+/K+ ATPase; Think: “INsulin shifts K+ INto cells”

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6
Q

What signs/symptoms are associated with a low versus high Na+ serum concentration?

A

LOW Na+ SERUM CONCENTRATION - Nausea and malaise, stupor, coma; HIGH Na+ SERUM CONCENTRATION - Irritability, stupor, coma

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7
Q

What signs/symptoms are associated with a low versus high K+ serum concentration?

A

LOW K+ SERUM CONCENTRATION - U waves on ECG, flattened T waves, arrythmias, muscle weakness; HIGH K+ SERUM CONCENTRATION - Wide QRS and peaked T waves on ECG, arrythmias, muscle weakness

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8
Q

What signs/symptoms are associated with a low versus high Ca2+ serum concentration?

A

LOW Ca2+ SERUM CONCENTRATION - Tetany, seizures, QT prolongation; HIGH Ca2+ SERUM CONCENTRATION - Stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria

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9
Q

What signs/symptoms are associated with a low versus high Mg2+ serum concentration?

A

LOW Mg2+ SERUM CONCENTRATION - Tetany, Torsades de pointes; HIGH Mg2+ SERUM CONCENTRATION - decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

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10
Q

What signs/symptoms are associated with a low versus high (PO4)3- serum concentration?

A

LOW (PO4)3- SERUM CONCENTRATION - bone loss, osteomalacia; HIGH (PO4)3- SERUM CONCENTRATION - Renal stones, metastatic calcifications, hypocalcemia

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11
Q

Give the pH, pCO2, and [HCO3-] changes associated with Metabolic acidosis. Which change is compensatory?

A

decreased pH, decreased pCO2 (compensatory), and decreased [HCO3-]

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12
Q

What is the compensatory response for metabolic acidosis? Is it immediate or delayed?

A

Hyperventilation; immediate

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13
Q

Give the pH, pCO2, and [HCO3-] changes associated with Metabolic alkalosis. Which change is compensatory?

A

increased pH, increased pCO2 (compensatory), increased [HCO3-]

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14
Q

What is the compensatory response for metabolic alkalosis? Is it immediate or delayed?

A

Hypoventilation; immediate

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15
Q

Give the pH, pCO2, and [HCO3-] changes associated with Respiratory acidosis. Which change is compensatory?

A

decreased pH, increased pCO2, increased [HCO3-] (compensatory)

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16
Q

What is the compensatory response for Respiratory acidosis? Is it immediate or delayed?

A

Increase renal [HCO3-] reabsorption; delayed

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17
Q

Give the pH, pCO2, and [HCO3-] changes associated with Respiratory alkalosis. Which change is compensatory?

A

increased pH, decreased pCO2, decrease [HCO3-] (compensatory)

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18
Q

What is the compensatory response for Respiratory alkalosis? Is it immediate or delayed?

A

Decrease renal [HCO3-] reabsorption; delayed

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19
Q

What is the Henderson-Hasselbach equation to use in acid-base physiology/disturbances?

A

pH = 6.1 + log ([HCO3-]/[0.03*pCO2])

20
Q

In what context is the Winter’s formula used? What is the formula?

A

The predicted respiratory compensation for a simple metabolic acidosis can be calculated using Winter’s formula; pCO2 = 1.5 (HCO3-) + 8 +/- 2

21
Q

What does it mean if pCO2 measured differs significantly from what’s predicted by Winter’s formula?

A

If the measured pCO2 differs significantly from the predicted pCO2, then a mixed acid-based disorder is likely present

22
Q

Aside from normal, what are the 2 possible findings from checking arterial pH? Give values and name.

A

(1) pH < 7.4 (Acidemia) (2) pH > 7.4 (Alkalemia)

23
Q

What simple acid-base disturbance is most likely present if a patient has a pH < 7.4 and pCO2 > 40 mmHg?

A

Respiratory acidosis

24
Q

What type of breathing is associated respiratory acidosis? What are 5 other conditions associated with respiratory acidosis?

A

Hypoventilation; Airway obstruction, Acute lung disease, Chronic lung disease, Opioids/sedatives, Weakness of respiratory muscles

25
Q

What simple acid-base disturbance is most likely present if a patient has a pH < 7.4 and pCO2 < 40 mmHg?

A

Metabolic acidosis with compensation (hyperventilation)

26
Q

What further evaluation should be done if a patient is suspected to have a metabolic acidosis with compensation (hyperventilation)?

A

Check anion gap: Anion gap = Na+ - (Cl- + HCO3-)

27
Q

What are 8 conditions associated with metabolic acidosis with compensation (hyperventilation) and an increased anion gap?

A

(1) Methanol (formic acid) (2) Uremia (3) Diabetic ketoacidosis (4) Propylene glycol (5) Iron tablets or INH (6) Lactic acidosis (7) Ethylene glycol (oxalic acid) (8) Salicylates (late); Think: “MUDPILES”

28
Q

What are 7 conditions associated with metabolic acidosis with compensation (hyperventilation) and a normal anion gap?

A

(1) Hyperalimentation (2) Addison’s disease (3) Renal tubular acidosis (4) Diarrhea (5) Acetazolamide (6) Spironolactone (7) Saline infusion; Think: “HARD-ASS”

29
Q

What simple acid-base disturbance is most likely present if a patient has a pH > 7.4 and pCO2 < 40 mmHg?

A

Respiratory alkalosis

30
Q

What is the main condition associated with Respiratory alkalosis? What are 5 things that cause this?

A

Hyperventilation: (1) Hysteria (2) Hypoxemia (e.g., high altitude) (3) Salicylates (early) (4) Tumor (5) Pulmonary embolism

31
Q

What simple acid-base disturbance is most likely present if a patient has a pH > 7.4 and pCO2 > 40 mmHg?

A

Metabolic alkalosis with compensation (hypoventilation)

32
Q

What are 4 conditions/substances are associated with Metabolic alkalosis?

A

(1) Loop diuretics (2) Vomiting (3) Antacid use (4) Hyperaldosteronism

33
Q

What are the types of Rental tubular acidosis (RTA)? What is a “nickname” for each type?

A

Type 1 (“distal”), Type 2 (“proximal”), Type 4 (“hyperkalemic”)

34
Q

What is another name for type 1 RTA? What causes it?

A

(“distal”) RTA; Defect in ability of alpha intercalated cells to secrete H+

35
Q

Approximately what urine pH do untreated patients with type 1 RTA have? With what kind of electrolyte condition is type 1 RTA associated?

A

Untreated patients have urine pH > 5.5; Associated with hypokalemia.

36
Q

For what do type 1 RTA patients have an increased risk, and why?

A

Increased risk for calcium phosphate kidney stones (due to increased urine pH and bone turnover)

37
Q

What is another name for type 2 RTA? What causes it?

A

(“proximal”) RTA; Defect in proximal tubule HCO3- reabsorption.

38
Q

With what syndrome may Type 2 RTA be seen?

A

May be seen with Fanconi’s syndrome

39
Q

Approximately what urine pH do untreated patients with type 2 RTA have? With what kind of electrolyte condition is type 2 RTA associated? How do these two facts compare/contrast to Type 1 RTA?

A

Untreated patients typically have urine pH 5.5); Associated like hypokalemia (like type 1 RTA)

40
Q

For what condition do patients with type 2 RTA have an increased risk?

A

Increased risk for hypophosphatemic rickets.

41
Q

What is another name for type 3 RTA? What causes it?

A

(“hyperkalemic”) RTA; Hypoaldosteronism or lack of collecting tubule response to aldosterone.

42
Q

What is the underlying mechanism causing damage type 4 RTA? What are 2 major consequences of this?

A

The resulting hyperkalemia (from hypoaldosteronism, aldosterone resistance, or K+-sparing diuretics) impairs ammoniagenesis in the proximal tubule, leading to (1) decreased buffering capacity and (2) decreased urine pH

43
Q

What are 3 potential causes of Type 1 RTA?

A

Causes - (1) Amphotericin B toxicity (2) Analgesic nephropathy (3) Congenital anomalies (obstruction) of the urinary tract.

44
Q

What are 4 potential causes of Type 2 RTA?

A

Causes - (1) Fanconi syndrome (e.g., Wilson disease) (2) Chemicals toxic to proximal tubule (e.g., lead, aminoglycosides) (3) Multiple myeloma (light chains) and (4) Carbonic anhydrase inhibitors

45
Q

What urine pH range is associated with type 1, type 2, and type 4 RTA?

A

Type 1 (distal, pH > 5.5); Type 2 (proximal, pH < 5.5); Type 4 (hyperkalemic, pH < 5.5)

46
Q

What is RTA? In general, how is it defined?

A

Renal tubular acidosis; A disorder of the renal tubules which leads to non-anion gap hyperchloremic metabolic acidosis

FA - Renal (13 decks)

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