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33 Cards in this Set

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  • Back
Describe what characterizes disorders of pCO2.
*CO2 production is constant.

*Change in CO2 level is due to changes in excretion of CO2:  Only organ of CO2 excretion is the lung:  acid base disorders due to changes in CO2 are respiratory disorders!
*CO2 production is constant.

*Change in CO2 level is due to changes in excretion of CO2: Only organ of CO2 excretion is the lung: acid base disorders due to changes in CO2 are respiratory disorders!
What are the three main causes of respiratory acidosis?
1. Hypoventilation due to pulmonary disease.
2. Hypoventilation due to CNS disease.
3. Hypoventilation due to neuromuscular diseases.
List 5 causes of respiratory acidosis due to hypoventilation as a result of pulmonary disease:

What are the pCO2, H, and pH levels like?
-pneumonia
-pulmonary edema
-chronic obstructive lung disease
-respiratory failure
-pneumonia
-pulmonary edema
-chronic obstructive lung disease
-respiratory failure
List the causes of respiratory acidosis due to CNS disease:

What are the pCO2, H, and pH levels like?
*Drug overdose (narcotics, sedatives, hypnotics).
*Cerebrovascular accidents.
*CNS trauma, bleeding.
*Drug overdose (narcotics, sedatives, hypnotics).
*Cerebrovascular accidents.
*CNS trauma, bleeding.
List the causes of respiratory acidosis due to neuromuscular diseases:

What are the pCO2, H, and pH levels like?
*Muscular dystrophy
*Chest wall deformities
*Acute or chronic neuropathic processes: myasthenia gravis, Guillain Barre syndrome.
*Muscular dystrophy
*Chest wall deformities
*Acute or chronic neuropathic processes: myasthenia gravis, Guillain Barre syndrome.
List the causes of respiratory alkalosis:

What are the pCO2, H, and pH levels like?
*Hyperventilation:

1) Anxiety.
2) Pregnancy (high progesterone).
3) Pulmonary diseases:  asthma, pulmonary emboli, EARLY pneumonia.
5) Aspirin overdose.
*Hyperventilation:

1) Anxiety.
2) Pregnancy (high progesterone).
3) Pulmonary diseases: asthma, pulmonary emboli, EARLY pneumonia.
5) Aspirin overdose.
How do the kidneys compensate for respiratory acid-base disorders?
*pCO2 and H2CO3 are in equilibrium: as pCO2 increases (respiratory acidosis) , H+ secretion and HCO3- generation increases.  

*As pCO2 decreases (in respiratory alkalosis), H+ secretion and HCO3- generation decrease.
*pCO2 and H2CO3 are in equilibrium: as pCO2 increases (respiratory acidosis) , H+ secretion and HCO3- generation increases.

*As pCO2 decreases (in respiratory alkalosis), H+ secretion and HCO3- generation decrease.

*These compensations, by the Henderson equation, lead to normalization of the pH.
Metabolic acidosis and alkalosis are always due to changes in what?
*Serum bicarbonate!

*Decreased HCO3: Metabolic acidosis.
*Increased HCO3: Metabolic alkalosis.
What are the traits of metabolic acidosis?

What are the 3 big picture causes?
Discuss metabolic acidosis due to increased bicarb loss:
A. Gastrointestinal HCO3 loss:
*Diarrhea
*Infectious
*Inflammatory
*Secretory

B. Renal HCO3 loss: Proximal renal tubular acidosis (type II).
A. Gastrointestinal HCO3 loss:
*Diarrhea
*Infectious
*Inflammatory
*Secretory

B. Renal HCO3 loss: Proximal renal tubular acidosis (type II).
How does type II RTA causes metabolic acidosis?
*If the proximal tubule loses function, HCO3 cannot be reabsorbed into the circulation, leading to HCO3 loss.  This is termed proximal renal tubular acidosis (RTA).
*There is only carbonic anhydrase along the brush border of the proximal tubule! ...
*If the proximal tubule loses function, HCO3 cannot be reabsorbed into the circulation, leading to HCO3 loss. This is termed proximal renal tubular acidosis (RTA).
*There is only carbonic anhydrase along the brush border of the proximal tubule! If this goes down, you're screwed.
What would happen if you couldn't synthesize new bicarbonate? Where does this happen in the body?
*If there is a defect in H+ secretion and HCO3- generation in the intercalated cell in the cortical collecting duct, the HCO3- level does not increase, and metabolic acidosis will result.  

*This can occur as an isolated defect (classic distal ...
*If there is a defect in H+ secretion and HCO3- generation in the intercalated cell in the cortical collecting duct, the HCO3- level does not increase, and metabolic acidosis will result.

*This can occur as an isolated defect (classic distal renal tubular acidosis) or as a result of diffuse damage of the distal tubule (connective tissue diseases, multiple myeloma).

*New bicarb is ONLY made in the distal tubule and proximal CCD!
List the causes of metabolic acidosis as a result of decreased bicarb production:
1) Distal renal tubular acidosis (type I).

2) Hypoaldosteronism:
*Adrenal insufficiency (TB, AIDS, adrenal hemorrhage).

*Hyporeninemic hypoaldosteronism (type IV renal tubular acidosis).

*Pharmacologic effects (ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists). This is the most common of all the above.
Discuss metabolic acidosis as a result of addition of acid to the ECF:
HA + NaHCO3 --> NaA + H2CO3

*In this process, one molecule of the acid disappears and one HCO3- molecule is consumed.

*Normally, this occurs at a relatively low level, with the addition of about 50 to 150 mEq/day: 

H2SO4 + NaHCO3 --> NaHS...
HA + NaHCO3 --> NaA + H2CO3

*In this process, one molecule of the acid disappears and one HCO3 molecule is consumed.

*Normally, this occurs at a relatively low level, with the addition of about 50 to 150 mEq/day:

H2SO4 + NaHCO3 --> NaHSO4 + H2CO3
H3PO4 + NaHCO3 --> NaH2PO4 + H2CO3

*When large quantities of a low molecular weight acid is added to the ECF, large numbers of HCO3 are consumed; too many for the kidney to regenerate.
What are 4 clinical settings in which you'd get a metabolic acidosis as a result of adding too much acid to the ECF?
1) Addition of ketoacids to the ECF: acetacetic acid, beta hydroxybutyric acid in diabetics, alcoholic, or starvation states.

2) Addition of lactic acid to the ECF (tissue hypoxia, mitochondrial dysfunction).

3) Addition of low molecular weight acidic toxins (acetylsalicylic acid, methanol [which produces formic acid], and ethylene glycol [which produces oxalic acid]) to the ECF.

4) Failure to excrete ingested dietary acids (phosphoric acid, sulfuric acid) in acute or chronic renal failure.
How does lactic acidosis develop?
Lactic acidosis develops with anaerobic metabolism.
Lactic acidosis develops with anaerobic metabolism.
How does the anion gap work? What's a normal anion gap?
*This difference is normally about 8–12mEq/L, and is 
called the anion gap.  

*It’s defined as the ∆ between [Na] and [Cl + HCO3].
*This difference is normally about 8–12mEq/L, and is
called the anion gap.

*It’s defined as the ∆ between [Na] and [Cl + HCO3].
What happens to the anion gap when excess acid is added to the ECF?
*Whenever excess acid is added to the ECF and is buffered by bicarb (as in ketoacidosis, lactic acidosis, toxic acid ingestions, and renal failure), the [bicarb] decreases and a new anion is formed:
Ex:  lactic acid + NaHCO3 --> lactate + H2CO3
...
*Whenever excess acid is added to the ECF and is buffered by bicarb (as in ketoacidosis, lactic acidosis, toxic acid ingestions, and renal failure), the [bicarb] decreases and a new anion is formed:
Ex: lactic acid + NaHCO3 --> lactate + H2CO3

*So, the number of unmeasured anions (anions that are not Cl or HCO3) will increase, and the “anion gap” will increase. Patients who have a metabolic acidosis due to addition of acid to the ECF are said to have a “high anion gap” metabolic acidosis.
Compare/contrast high anion gap and normal gap metabolic acidoses?

What are 4 causes for each?
Normal gap: The acidosis is due to loss of bicarb.
High gap: The acidosis is due to increased buffering of bicarb.
Normal gap: The acidosis is due to loss of bicarb.
High gap: The acidosis is due to increased buffering of bicarb.
A 27 year old woman shows up in your clinic for an initial visit. She has a generally negative medical history and complains of fatigue. Lab tests show an arterial pH of 7.28, a pCO2 of 31 mmHg, and a HCO3 of 15 mEq/L. The Na is 129 mEq/L, and the Cl is 88 mEq/L. Which of the following is the likely explanation for her acid base abnormality?

a) Chronic kidney disease
b) An aldosterone producing tumor
c) Pregnancy
d) Chronic diarrhea
a) Chronic kidney disease

*This is a high gap metabolic acidosis.
What is metabolic alkalosis?

What 3 scenarios cause it?
*Primary increase in the HCO3- level.

*This does not occur as a result of HCO3- ingestion;  HCO3- is freely filtered by the kidneys, and an increased ingestion would be met with increased renal excretion.
*Primary increase in the HCO3 level.

*This does not occur as a result of HCO3 ingestion; HCO3 is freely filtered by the kidneys, and an increased ingestion would be met with increased renal excretion.

*Metabolic alkalosis ONLY OCCURS with renal retention of HCO3; this occurs with three scenarios: 1) Decreased glomerular filtration of HCO3 (rare).
2) Increased renal synthesis of HCO3.
3) Increased renal tubular reabsorption of HCO3.
Wait. I learned that people with CKD get metabolic acidosis. How in the world would people with CKD get metabolic alkalosis?
*Decreased glomerular filtration of HCO3 occurs in acute or chronic kidney disease: practically speaking this doesn’t cause metabolic acidosis, because acid filtration and excretion is also impaired. 

*If patients with CKD are given large amo...
*Decreased glomerular filtration of HCO3 occurs in acute or chronic kidney disease: practically speaking this doesn’t cause metabolic acidosis, because acid filtration and excretion is also impaired.

*If patients with CKD are given large amounts of HCO3, however, metabolic alkalosis can occur.
What are 4 causes of xs aldosterone as a cause of metabolic alkalosis?

How does it happen?
1) Aldosterone producing tumors (primary).
2) Bilateral adrenal hyperplasia (primary).
3) Renal vascular disease, which increases renin and aldosterone (secondary).
4) Glucocorticoid excess.
1) Aldosterone producing tumors (primary).
2) Bilateral adrenal hyperplasia (primary).
3) Renal vascular disease, which increases renin and aldosterone (secondary to renal artery stenosis).
4) Glucocorticoid excess.
Aldosteronoma. A possible cause of metabolic alkalosis due to xs aldosterone.
Aldosteronoma. A possible cause of metabolic alkalosis due to xs aldosterone.
*Bilateral renal artery stenosis. A possible cause of metabolic alkalosis due to xs aldosterone.
*Bilateral renal artery stenosis. A possible cause of metabolic alkalosis due to xs aldosterone. Causes renin levels to skyrocket due to decreased renal perfusion--> JGA--> renin.
What happens with Na and Cl depletion?

When might this occur?
*When Na and Cl are both removed from the body, the decrease in total body Na will stimulate renal tubular reabsorption of Na. 

*Since Na+ must be reabsorbed with an anion, if Cl is depleted, HCO3 reabsorption occurs--> metabolic alkalosis!

...
*When Na and Cl are both removed from the body, the decrease in total body Na will stimulate renal tubular reabsorption of Na.

*Since Na+ must be reabsorbed with an anion, if Cl is depleted, HCO3 reabsorption occurs--> metabolic alkalosis!

1) When excess vomiting and nasogastric suction occur, HCl and NaCl are both excreted into the upper GI tract lumen, causing a depletion of both Na and Cl, and Cl is lost to a greater extent than Na.

2) Diuretics can cause it, too, especially loops and thiazides.
How do diuretics cause metabolic alkalosis? What types of diuretics cause this? What genetic syndromes mimic this?
1) Loop diuretics increase Na, Cl, and K loss in the urine.  
*Bartter syndrome is a congenital or acquired defect in renal tubular function that mimics loop diuretic use.

2) Thiazides increase Na, Cl and K loss in the urine.  
*Gitelman synd...
1) Loop diuretics increase Na, Cl, and K loss in the urine.
*Bartter syndrome is a congenital or acquired defect in renal tubular function that mimics loop diuretic use.

2) Thiazides increase Na, Cl and K loss in the urine.
*Gitelman syndrome is a congenital or acquired defect in renal tubular function that mimics thiazide diuretic use.

*In total body Na and Cl depletion, there is excess
HCO3 reabsorption in the proximal tubule.
The anion gap is a helpful clue to the etiology of metabolic acidosis. What's an analogous clue that will help determine the etiology of metabolic alkalosis?
*Just as the anion gap is helpful in differentiation between causes of metabolic acidosis, the urine [Cl] is helpful in differentiation between causes of metabolic alkalosis:

1) Patients with hyperaldosteronism are volume expanded, and urine [Cl] is high (> 30 mEq/L).

2) Patients with Na and Cl loss are volume contracted, and urine [Cl] is low (< 30 mEq/L).
A 79 year old woman has CHF and HTN and is on digoxin and furosemide and metolazone. You see her in follow up, and you obtain labs which show: BUN 11 mg/dL, creatinine 0.9 mg/dL, arterial pH 7.58, pCO2 44 mmHg, HCO3 40 mEq/L. Of the following, which is the main factor that explain the primary acid base abnormality?

a) Hypoventilation
b) Increased urinary loss of chloride
c) Decreased serum levels of aldosterone
e) Decreased renal filtration of bicarbonate
f) Increased ingestion of bicarbonate
b) Increased urinary loss of chloride

*She IS actually hypoventilating, but the pCO2 is not low, so that's not the problem. The problem is high bicarb, so this is a metabolic alkalosis. That, combined with the med list and PMH, makes the correct answer B.
A 14 year old boy is referred to you for headaches and anxiety. He takes no meds, and his FH is negative. His BP is 140/90, and the exam is negative.

The Na+ is 137 mEq/L, K+ is 3.1 mEq/L, Cl- is 90 mEq/L, HCO3- is 35 mEq/L, and the arterial pH is 7.50. The pCO2 is 47 mmHg. His urine Cl is 45 mEq/L. What do you think could be the cause of his problems?

a) Chronic kidney disease
b) Surreptitious use of sedatives/narcotics
c) Vomiting
d) An aldosterone producing tumor
e) Proximal (type II) renal tubular acidosis
d) An aldosterone producing tumor

*pCO2 is high, bicarb is high; this is a metabolic alkalosis. Only feasible choice is d.

-CKD is associated with metabolic acidosis much more than alkalosis.
-Sedatives/narcotics cause a respiratory acidosis.
-Vomiting is a possibility, but you'd also see low BP and low urinary [Cl].
-Type II RTA would have a metabolic acidosis.
Discuss respiratory compensation for metabolic acidosis and alkalosis:
*Hyperventilation drops the pCO2. Compensates for acidosis.
*Hypoventilation raises the pCO2. Compensates for alkalosis.
*Hyperventilation drops the pCO2. Compensates for acidosis.
*Hypoventilation raises the pCO2. Compensates for alkalosis.
Discuss metabolic compensation for respiratory acidosis and alkalosis:
So, do respiratory and metabolic compensation for pH disorders work?
*Respiratory compensation for metabolic disorders, and metabolic compensation for respiratory disorders, NEVER correct the H+ concentration and the pH to normal values.

*But, it's a critical diagnostic clue.