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PHRM 825 > PHRM 825: Acid-Base Balance - Metabolic Disorders > Flashcards

PHRM 825: Acid-Base Balance - Metabolic Disorders Flashcards

1
Q

Metabolic acidosis is characterized by what 3 things?

A
  • Low pH (<7.35)
  • Low serum HCO3- (<24 mEq/L)
  • A compensatory decrease in PaCO2 from hyperventilation
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2
Q

2 classifications of metabolic acidosis

A
  • Non-anion gap metabolic acidosis

- Anion gap metabolic acidosis

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3
Q

Anion gap equation

A

Anion gap = Na+ - (Cl- + HCO3-)

Key cations - Key anions

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4
Q

Normal anion gap value

A

3-11 mEq/L

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5
Q

Why is there not a gap in non-anion gap acidosis?

A

The loss of plasma HCO3- is replaced by Cl-

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6
Q

Non-anion gap acidosis is also known as

A

Hyperchloremic acidosis (elevated Cl- prevents the gap)

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7
Q

Causes of non-anion gap acidosis

A
  • Gastrointestinal bicarbonate losses
  • Renal bicarbonate loss
  • Reduced renal H+ excretion
  • Acid and chloride administration
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8
Q

Gastrointestinal bicarbonate losses are caused by

A

Diarrhea and pancreatic fistulas/biliary drainage

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9
Q

Diarrhea is a common cause of what

A

Non-anion gap acidosis (hyperchloremic acidosis)

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10
Q

Diarrhea contains a large amount of what

A

HCO3-

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11
Q

Pancreatic fistulas and biliary drainage are rich in what

A

HCO3-

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12
Q

What does RTA stand for?

A

Renal tubular acisosis

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13
Q

Type II RTA occurs in which tubule?

A

Proximal

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14
Q

Which type of RTA causes renal bicarbonate loss?

A

Type II

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15
Q

What causes renal bicarbonate loss?

A

Various diseases or toxins (heavy metal toxicity, carbonic anhydrase inhibitor therapy, topiramate, etc.)

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16
Q

During renal bicarbonate loss, reabsorptive threshold for HCO3- is ____ in the proximal tubule

A

Reduced

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17
Q

What percentage of filtered bicarbonate is normally absorbed in the proximal tubule?

A

~85%

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18
Q

With enhanced bicarb loss, there will be increased ___ and ___ loss

A

Na+ and fluid

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19
Q

During bicarb loss, Na and water are also lost which activates the ____ system and leads to ____

A

renin-angiotension system; secondary hyperaldosteronism

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20
Q

Increased aldosterone augments ____ excretion, causing ___

A

K+; hypokalemia

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21
Q

Are patients still able to acidify their urine in response to an acid load during renal bicarb loss?

A

Yes

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22
Q

Type I RTA occurs in which tubule?

A

distal

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23
Q

Type IV RTA occurs in which tubule?

A

distal

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24
Q

Type I RTA is also know as what?

A

Hypokalemia RTA

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25
Q

Type IV RTA is also known as what?

A

Hypoaldosteronism or hyperkalemia RTA

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26
Q

What causes type I RTA?

A
  • Primary tubule defect
  • SLE (lupus)
  • Myeloma
  • Sickle cell
  • Li+
  • Ampho B
  • Toluene
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27
Q

During Type I RTA, what cannot be pumped into tubule lumen by cells of collecting duct?

A

H+

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28
Q

During type I RTA, what happens to urine?

A

It cannot be maximally acidified (pH>5.3)

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29
Q

During type IV RTA, there is less aldosterone, causing retention of what?

A

H+

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30
Q

During type IV RTA there are hyperkalemic conditions that lead to ____ retention, causing ___.

A

H+ retention; acidosis

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31
Q

During chronic renal failure, there is ____ H+ secretion and less ___ production

A

less; amonia

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32
Q

Excess administration of what can cause non-anion gap metabolic acidosis?

A
  • TPN

- HCl or Ammonium Cl

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33
Q

During anion gap metabolic acidosis, HCO3- losses are replaced with what?

A

Another anion besides Cl-

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34
Q

What is the delta gap?

A

Difference between the patient’s anion gap and the normal anion gap

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35
Q

Causes of anion gap metabolic acidosis

A
  • Lactic acidosis
  • Ketoacidosis
  • Drug intoxication
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36
Q

What is the most common cause of anion gap acidosis?

A

Lactic acidosis

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37
Q

Lactate is a normal product of ___ metabolism

A

anaerobic

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38
Q

Lactate formation is essential for tissues that need ____ to produce energy anaerobically

A

NAD+; anaerobically

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39
Q

Which tissues need NAD+ to generate energy anaerobically?

A
  • RBCs

- Exerciseing muscle

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40
Q

Lactate normally enters the circulation in ____ amounts and is promptly removed by the ___

A

small; liver

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41
Q

Increased blood levels of lactate almost always result from what?

A

Decreased clearance (not overproduction)

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42
Q

What is lactate converted to when it is eliminated?

A

Pyruvate

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43
Q

What will happen if there is persistent failure to oxidize lactic acid?

A

The buffering capacity will be exhaused

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44
Q

Possible causes of lactic acidosis include (8)

A
  • Shock
  • Drugs/toxins
  • Seizures
  • Leukemia
  • Hepatic/renal failure
  • Diabetes mellitus
  • Malnutrition
  • Rhabdomyolysis
45
Q

What drugs/toxins cause lactic acidosis?

A
  • Ethanol
  • Metformin
  • Nucleoside reverse transcriptase inhibitors (NRTIs)
  • Linezolid, isoniazid, propofol
  • Propylene glycol
46
Q

How does ethanol cause lactic acidosis?

A

Increases lactate and causes hypoglycemia impaired gluconeogenesis

47
Q

How does metformin cause lactic acidosis?

A

Mechanism is unclear

48
Q

How do NRTIs cause lactic acidosis?

A

Inhibit DNA polymerase, which is responsible for mitochondrial DNA synthesis

49
Q

How do linezolid, isoniazid, and propofol cause lactic acidosis?

A

Increase lactic acid

50
Q

How does propylene glycol cause lactic acidosis?

A

Propylene glycol is metabolized to lactic acid

51
Q

How do seizures cause lactic acidosis?

A

Seizures are self-limiting

52
Q

What causes lactic acidosis in leukemia survivors?

A

They have packed poorly perfused bone marrow cavities

53
Q

How does hepatic/renal failure cause lactic acidosis?

A

They cause impaired metabolism and excretion

54
Q

How does diabetes mellitus cause lactic acidosis?

A

DM can cause formation of ketones/lactate; use of metformin

55
Q

How does malnutrition cause lactic acidosis?

A

Deficiencies of vitamins and thiamine

56
Q

How does rhabdomyolysis cause lactic acidosis?

A

Sulfur-containing amino acids are released

57
Q

What causes ketoacidosis?

A

Increased acetoacetic acid and B-OH butyric acid

58
Q

How does salicylate toxicity cause respiratory alkalosis?

A

Stimulation of respiratory drive

59
Q

How does salicylate toxicity cause metabolic acidosis?

A

Accumulation of organic acids

60
Q

Symptoms of lactic acidosis (6)

A
  • Kussmaul respirations
  • Peripheral vasodilation causing flushing and tachycardia; as acidosis worsens, ventricular arrhythmias or reduced contractility may occur
  • Hyperkalemia
  • Lethargy/coma
  • Nausea/vomiting
  • Bone demineralization in chronic acidotic states
61
Q

Treatment of lactic acidosis

A
  • Treat the underlying cause
  • Acute bicarbonate therapy (for severe and acute bicarb losses)
  • Chronic bicarbonate therapy (for chronic metabolic acidosis)
  • Tromethamine (THAM)
  • Carbicarb/Dichloracetate
62
Q

When should acute bicarbonate therapy be considered for use?

A

when pH < 7.10 - 7.15

63
Q

What are good indications for acute bicarbonate therapy?

A
  • Hyperkalemia
  • pH < 7.10 with cardiac arrest after defibrillation
  • Ventilation
  • Other medications have been utilized
  • Overdoses
64
Q

What is the equation for dosing bicarb?

A

Dose (mEq) - [o.5 L/kg (IBW)] X (desired HCO3- - actual HCO3-)

Use 12mEq/L for the desired HCO3-

65
Q

How should you administer bicarb after an amount is calculated?

A

Give 1/3 to 1/2 the calculated dose and monitor the ABG

66
Q

What does ABG mean

A

Arterial blood gas

67
Q

During cardiac arrest, how much sodium bicarb can be given

A

~1 mEq/kg

68
Q

Bicarb can lower ___ blood levels

A

Potassium

69
Q

Hazards of bicarbonate therapy

A
  • Overalkanization
  • Hypernatremia/hyperosmolality
  • CSF acidosis
  • Electrolyte shift
70
Q

What can overalkanization caused by bicarb therapy result in?

A

Reduced cerebral flow and impaired oxygen release from Hgb to tissues

71
Q

How is CSF acidosis caused by bicarb therapy?

A

Occurs from the CO2 that is generated, which readily diffuses into the CSF

72
Q

When bicarbonate is administered, there is a decrease in _____ which decreases myocardial contractility

A

ionized calcium

73
Q

When should chronic bicarbonate therapy be considered for use?

A

When the patient has chronic metabolic acidosis

74
Q

What average dosing should be used for chronic bicarbonate therapy?

A

1-3 mEq/kg/day (may go up to 10+ mEq/kg/day)

75
Q

How does tromethamine (THAM) treat metabolic acidosis?

A
  • Combines with H+ from H2CO3 to form HCO3-

- Acts as an osmotic diuretic to increase urine flow, urine pH, and excretion of fixed acids

76
Q

Highly alkaline patients can experience ___ and ___

A

inflammation and extravasation

77
Q

It is important to administer THAM ___ while monitoring ____

A

slowly; pH to avoid alkalosis

78
Q

Adverse effects of THAM

A
  • Hyperkalemia
  • Hypoglycemia
  • Hypocalcemia
  • Impaired coagulation
79
Q

What is carbicarb?

A

Mixture of sodium carbonate (Na2CO3) and sodium bicarbonate (NaHCO3)

80
Q

How does carbicarb help treat metabolic acidosis?

A

Preferentially buffers hydrogen ions resulting in the formation of bicarb rather than CO2

81
Q

How does dichloroacetate (DCA) help treat metabolic acidosis?

A

It facilitates lactate metabolism

82
Q

Metabolic alkalosis is characterized by what 3 things?

A
  • pH > 7.45
  • Increased HCO3-
  • Compensatory hypoventilation resulting in increased PaCO2
83
Q

What causes a rise in plasma HCO3-?

A
  • Loss of acid from GI tract or urine
  • Administration of HCO3- or a bicarb precursor
  • Contraction of alkalosis (loss of Cl- rich, HCO3- poor fluid)
84
Q

Impairment of renal ___ excretion can result in the maintenance of metabolic alkalosis

A

HCO3-

85
Q

How do volume and chloride depletion contribute to metabolic alkalosis?

A
  • Decrease in arterial blood volume
  • Decrease in ability of kidney to excrete HCO3-
  • With volume depletion, capacity of the proximal tubule to reabsorb HCO3- increases
86
Q

What is the most common cause of saline responsive alkalosis?

A

Diuretic therapy

87
Q

In saline responsive alkalosis, urinary chloride is ____ mEq/L

A

< 10-20

88
Q

What are causes of saline responsive alkalosis?

A
  • Diuretic therapy
  • Vomiting & NG suction
  • Exogenous HCO3- administration or blood transfusions
  • Maintenance of the alkalosis
89
Q

What are some examples of diuretic therapy?

A

Furosemide, torsemide, HCTZ, bumetanide

90
Q

Diuretic therapy enhances excretion of ___ and ___, resulting in extracellular volume contraction

A

Sodium chloride and water

91
Q

Volume contraction stimulates ____ release

A

aldosterone

92
Q

Aldosterone increases distal tubular ____ reabsorption adn induces ___ and ____ secretion

A

Na+, K+ and H+

93
Q

H+ secretion is associated with ____ reabsorption

A

HCO3-

94
Q

Normally Cl- is absorbed with ____

A

Na+

95
Q

Without Cl- (hypochloremia), Na- is reabsorbed with ___

A

HCO3-

96
Q

What is the second most common cause of alkalosis?

A

Vomiting and NG suction

97
Q

How much fluid can be lost per day with vomiting?

A

1 L/day

98
Q

What is used to preserve blood products and what does it do in the body?

A

Citrate –> Breaks down to HCO3-

99
Q

What 3 things can result in maintenance of alkalosis?

A
  • Reduced GFR
  • Enhanced proximal tubular HCO3- reabsorption
  • Effects of hypokalemia
100
Q

What happens during reduced GFR that leads to alkalosis?

A

Na+ reabsorption is increased in distal and proximal tubules, leading to H+ secretion and HCO3- reabsorption in those respective areas

101
Q

What causes enhanced proximal tubular HCO3- reabsorption that leads to alkalosis?

A

With hypochloremia, Na+ is reabsorbed with HCO3-

102
Q

How does hypokalemia cause alkalosis?

A
  • With less K+, H+ is secreted while Na+ is reabsorbed

- H+ secretion is associated with HCO3- reabsorption and ammoniagenesis

103
Q

In saline resistant alkalosis, urinary chloride is ____ mEq/L

A

> 20

104
Q

During saline resistant alkalosis, there is enhanced___ excretion and ___ reabsorption

A

H+; HCO3-

105
Q

What is the key difference between saline responsive and saline resistant alkalosis?

A

In saline resistant alkalosis there is no chloride depletion or there is an inability to reabsorb chloride

106
Q

What causes saline resistant alkalosis?

A
  • Increased mineralcorticoid activity
  • Hypokalemia
  • Renal tubular chloride wasting
107
Q

What are symptoms of saline resistant alkalosis?

A
  • Muscle cramps; weakness; paresthesias
  • Postural dizziness
  • Cellular hypoxia; mental confusion, coma; seizures
  • Direct myocardial suppression; CV collapse; arrhythmias
108
Q

What are possible treatment options for saline resistant alkalosis

A
  • Correct underlying cause

- Rapid correction not necessary but treatment is still needed

PHRM 825 (36 decks)

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