acid base disorders Flashcards

1
Q

Equation for acidity as it relates to bicarb and CO2

A

Acidity = [bicarb]/ [CO2]

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2
Q

Describe compensation in metabolic and respiratory acid base disorders

A

Metabolic: CO2 changes in same direction as the change in bicarb (ie. In metabolic acidosis, bicarb is decreased so CO2 decreases to compensate). Respiratory: bicarb changes in same direction as the change in CO2 (ie. In respiratory alkalosis, CO2 is low, so bicarb decreases to compensate)

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3
Q

How does CO2 change for metabolic acidosis/alkalosis

A

acidosis: ∆PCO2 = 1 to 1.5 x ∆ HCO3. Alkalosis: ∆PCO2= 0.25 to 1.) x ∆HCO3

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4
Q

How does HCO3 change for respiratory acidosis/alkalosis

A

Acidosis: ∆ HCO3- = increased 1:10 PCO2 (acute) ∆ HCO3- = increased 4:10 PCO2 (chronic). Alkalosis: ∆ HCO3- = ↓2:10 PCO2 (acute) ∆ HCO3- = ↓4:10 PCO2 (chronic after 3-5 days)

Acidosis: ∆ HCO3- = increased 1:10 PCO2 (acute) ∆ HCO3- = increased 4:10 PCO2 (chronic). Alkalosis: ∆ HCO3- = ↓2:10 PCO2 (acute) ∆ HCO3- = ↓4:10 PCO2 (chronic after 3-5 days)

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5
Q

Causes of respiratory alkalosis

A

Breathing too much (hyperventilation): anxiety, lung disease, liver disease, sepsis, pregnancy

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6
Q

Causes of respiratory acidosis

A

Breathing too little: brain stem injury, drugs, hypothyroidism, primary alveolar hypoventilation, muscle fatigue

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7
Q

Causes of generation of metabolic alkalosis

A

inability to excrete bicarb, loss of H ions (vomiting, severe hypokalemia) contraction alkalosis, excess consumption (in packed RBCs, parenteral nutrition), increased H excretion (cuases bicarb resorption, seen in diureics and mineralocorticoid excess) and hypokalemia

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8
Q

What is contraction alkalosis

A

Loss of Cl rich and bicarb poor fluid (such as from vomiting, NG suctioning, diuretics) results in a loss of fluid, so bicarb concentration goes up

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9
Q

How does renal H excretion cause alkalosis

A

H excretion causes bicarb resorption. H excretion is increased with mineralocorticoids and diuretics

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10
Q

Causes of mineralocorticoid excess

A

Primary hyperaldosteronism, Cushings syndrome, congenital adrenal hyperplasia, hyperreninism, renal artery stenosis

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11
Q

How do diuretics cause metabolic alkalosis

A

Loop and thiazide diuretics increase the amount of Na in the tubule at the distal segments, so more Na is reabsorbed in these distal segments than normal. This increases the negative charge in the lumen, which enhances secretion of H and consequently the reabsorption of bicarb

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12
Q

Causes of an inability to excrete bicarb

A

hypovolemia and excess mineralocorticoid acitivity

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13
Q

What causes maintenance of metabolic alkalosis

A

ALWAYS due to the inability of the kidney to excrete excess bicarb. Chloride depletion, K depletion, increased mineralocorticoid activity, hypovolemia

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14
Q

Chloride responsive vs resistant metabolic alkalosis

A

Responsive: urine Cl is low (<20mEq) and chloride depletion with hypovolemia is the cause of the metabolic alkalosis. Seen in contraction, addition of bicarb, GI loss, renal H loss. Responds to saline. Resistant: chloride depletion with hypovolemia is NOT the cause of alkalosis. Seen in excess mineralocorticoid activity, intracellular H loss or rare conditions.

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15
Q

How does K depletion maintain metabolic alkalosis

A

increased aldosterone release

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16
Q

How does increased mineralocorticoid activity maintain metabolic alkalosis

A

Mineralocorticoids act on the H+-ATPase pump of the intercalated cell in the distal tubule. Stimulation of the H+-ATPase pump leads to secretion of H+ into the tubule lumen which is accompanied by bicarbonate resorption and thus maintains the metabolic alkalosis

17
Q

How does hypovolemia cause metabolic alkalosis

A

Hypovolemia causes Na resorption which then causes bicarb and Cl resorption to maintain electroneutrality

18
Q

Treatment of chloride responseive and resistant metabolic alkalosis

A

responsive: infusions of NaCl and/or KCl. Chloride resistant: block mineralocorticoid effect with spironolactone

19
Q

How much acid is produced daily

A

60mEq. So it consumes 60mEq of bicarb

20
Q

What parts of the nephron are involved in handling the daily acid load

A

proximal tubule (reabsorbs bicarb) and distal tubul/collecting duct (secretes H, makes bicarb, acidifies urine, excretes daily acid load)

21
Q

Cortical vs medullary collecting ducts.

A

Corticle collecting duct is influenced by the resorption of sodium. Whereas the medullary collecting duct lumen is negative and the H atpase is more under the influence of aldosterone.

22
Q

Types of cells in distal tubule and functions

A

Principle cell has apical Na channel and basolateral Na/K pump for Na resorption. Alpha intercalated cell has H ATPase on apical side for H excretion. Beta intercalated cell is responsible for bicarb resorption and has a bicarb/Cl co transporter on the basolateral side

23
Q

Causes of metabolic acidosis

A

loss of bicarb( proximal tubule fails to reabsorb) or addition of acid ( distal tubule fails to secrete H)

24
Q

Calculate serum and urine anion gap

A

serum: Na-Cl-bicarb (nl is 6-12). Urine: NH4 + Na + K - Cl

25
Q

What causes positive urine anion gap

A

Renal loss of bicarbonate (renal tubular acidosis) causes positive urine anion gap . GI loss of bicarb causes negative urine anion gap

26
Q

Causes of non-anion gap metabolic acidosis

A

Loss of bicarb from GI tract (diarrhea) or kidney ( renal tubular acidosis)

27
Q

Types of renal tubular acidosis

A

Proximal: proximal tubule is damaged so that bicarb resorption can not occur. Distal: Distal tubule is damaged so that H excretion (and bicarb generation) does not occur. urine anion gap is positive. Hyperkalemic: ammonia production is inhibited by hyperkalemia, and ammonia usually binds to H and aids in H excretion. urine anion gap is positive number

28
Q

Discuss urine pH in metabolic acidosis

A

Normally, urine pH should be low during metabolic acidosis as the kidneys try to remove H ions. So, in a non-anion gap metabolic acidosis, if the pH is acidic, the kidneys are functioning normally and a GI loss of bicarb is present. If urine is not acidic (ie. >5.3), renal tubular acidosis is occuring

29
Q

What does urine anion gap tell us?

A

In metabolic acidosis, urine NH4 should increase (if kidneys are functioning normally), but NH4 is hard to measure, so it is inferred from urine anion gap. If NH4 is increased, urine Cl should also be increased to maintain electroneutrality and as Cl increases, urine anion gap becomes negative. A negative anion gap suggests that kidney function is normal and thus GI loss of bicarb must be occuring.

30
Q

Causes of anion gap metabolic acidosis

A

MUDPILES: methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acid, ethylene glycol, salicylates

31
Q

Treatment of metabolic acidosis

A

Chronic: sodium bicarb therapy. Acute: sodium bicarb therapy is controversial b/c it may cause cardiovascular compromise

32
Q

Mixed acid base disturbance

A

Two or more primary acid baste disorders. Compensation will be less than or greater than expected. If CO2 and bicarb differ from normal in opposite direction, a mixed disorder is always present.