Acid-Base Disorders

Front 1

primary defect is decreased arterial pCO2 due to hyperventilation

Back 1

respiratory alkalosis

Front 2

2 phases of respiratory alkalosis

Back 2

1) Acute: buffering and mass action
2) Chronic: renal mechanisms after 2-3 days

Front 3

Causes of respiratory alkalosis

Back 3

Anxiety, Sepsis, Aspirin tox, pneumonia, asthma, pregnancy, cirrhosis

Front 4

Signs and symptoms of respiratory alkalosis

Back 4

Tachypnea; Dyspnea; Symptoms related to the alkalemia: circumoral paresthesias, light-headedness, cramps; Respiratory symptoms

Front 5

Tx of respiratory alkalosis

Back 5

Tx underlying cause.

For anxiety, breathe into paper bag to bring CO2 levels up!

Front 6

In respiratory alkalosis

__pH
__pCO2
__bicarb

Back 6

increased;
decreased;
decreased

Front 7

If bicarb (as calculated) is less than expected in respiratory alkalosis, what could have happened?

Back 7

Could ALSO have metabolic acidosis

Front 8

Disorder where primary defect is increased pCO2 due to hypoventilation

Back 8

Respiratory acidosis

Front 9

Renal mechs of compensation for Respiratory acidosis

Back 9

After 2-3 days.

Will have increasing ammoniagenesis and H secretion

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Causes of respiratory acidosis

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COPD, narcotic overdose

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Signs and symptoms of respiratory acidosis

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Non specific, like lethargy, confusion, fatigue, dyspnea.

Cyanosis (associated with hypoxemia).

...and of those, those specific to underlying disorder (like COPD)

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Tx of respiratory acidosis

Back 12

Tx underlying disorder.

Mechanical ventilation.

Front 13

For simple acid-base disorders, what should the direction of pCO2 and HCO3- be?

Back 13

Should always be in SAME direction

Front 14

If bicarb (as calculated) is higher than expected for compensation for respiratory acidosis, what could be the case?

Back 14

Mixed disorder - resp acidosis AND Metabolic alkalosis

Front 15

Disorder where primary defect is increase in arterial [H+]

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Metabolic acidosis

Front 16

Two causes of metabolic acidosis

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1) Addn of fixed acid to body (overproduction or ingestion)

2) Loss of bicarb from body

Front 17

Winter's formula

Back 17

pCO2 = (HCO3 * 1.5) * 8

Front 18

What is Winter's formula used for?

Back 18

Calculating expected pCO2 in Met Acidosis

Front 19

In what disorder might there be a normal or DECREASED anion gap? Why?

Back 19

Multiple myeloma. The Igs present in the blood in excess have + charges

Front 20

In normal anion gap metabolic acidosis, what is the bicarb that is being used up getting replaced by?

Back 20

Cl-

Front 21

Causes of normal anion gap metabolic acidosis

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1) Diarrhea (rich in bicarb)

2) Renal Tubular Acidoses (all)

Front 22

Causes of elevated anion gap metabolic acidosis

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Use mneumonic "MUDPILES"

M - methanol
U - uremia (aka kidney failure)
D - Diabetic ketoacidosis
P - Paraldehyde
I - Isoniazide
L - Lactic acidosis
E - Ethylene glycol or Ethanol
S - Salicylates

Front 23

Characterized by hyperglycemia, elevated anion gap metabolic acidosis, ketosis

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DKA

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Most common Causes of elevated anion gap metabolic acidosis

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DKA and lactic acidosis

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2 types of Lactic Acidosis

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Type A: tissue hypoxia or ischemia

Type B: no hypoperfusion

Front 26

How does uremia/kidney failure cause elevated anion gap metabolic acidosis?

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Accumulation of organic sulfates and phosphates and other unmeasured anions.

Associated with decreased ammonia synthesis and net acid secretion - so will have mixed acidosis of elevated and normal anion gap.

Front 27

difference between the measured osmolarity and the calculated osmolarity

Back 27

osmolal gap

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How is osmolal gap used clinically?

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Clinically we can use the osmolal gap to confirm suspected cases of toxin ingestions before the lab confirmation or to monitor therapy

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Signs and Sx of Metabolic Acidosis

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1) Those of underlying d/o
2) Decr cardiac contractility and activation of adrenergic receptors and inhibition of enzyme function
3) Kussmaul respirations

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When is acute metabolic acidosis tx?

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When pH < 7.2

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What occurs in chronic metabolic acidosis?

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Bone acts as large pool of buffer for H+, can inhibit bone growth and cause osteopenia.

Muscle breaks down protein to make more glutamine available to generate ammonia as a buffer.

ESPECIALLY a problem in kids - see growth retardation and muscle wasting.

Front 32

group of disorders in which the kidney is unable to maintain acid-base balance despite normal or near normal GFR

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Renal Tubular Acidoses

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Defect is in deficient bicarb reabsorption from the filtrate

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Type 2 RTA(proximal)

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Causes of type 2/Proximal RTA

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Isolated defects in bicarb reabsorption (deficient carbonic anhydrase either from drugs or genetics); or generalized defects in proximal tubule transport

Front 35

What does type 2 RTA look like in steady state?

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Because there has been so much loss of bicarb from blood, the filtered load is very low, and they're able to absorb almost all of it. The patient will have an acidemia AND the urine will be acidic (ph < 5.5)

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What happens if you treat type 2 RTA in the steady state?

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They won't be able to reabsorb the bicarb so urine will be basic (>5.5). It takes a lot of bicarb to keep them in acid-base balance.

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Why are Type 2 RTA patients hypokalemic?

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Due to increased urine flow - bicarb in tubular lumen means less water is reabsorbed proximally. Kidney also attempt to reclaim sodium in distal nephron resulting in K secretion in exchange for the Na.

Front 38

Defect is in hydrogen ion secretion or inability to acidify the urine

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Distal/Type I RTA

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Causes of Type I / Distal RTA

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Defective H+ ATPase, or bicarb/Cl- exchanger. Certain drugs.

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Defect is primarily ammonia excretion

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Type IV RTA

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In what patients is Type IV RTA seen?

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hyporenin hypoaldosteronism states which frequently accompany diabetics with early diabetic nephropathy (still have preserved GFR)

Front 42

What is the primary problem in Type IV RTA?

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Hyperkalemia - turns off ammonia synthesis.

Decreased ammonia limits the amount of H+ that can be secreted because there's no buffer in the urine.

Front 43

increase in serum bicarb

Back 43

metabolic alkalosis

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Compensation for metabolic alkalosis

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inhibition of respiratory centers - increased pCO2

Front 45

What are the two phases for development of metabolic alkalosis?

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Generation phase and maintenance phase.

Vomiting causes loss of H+ ions, which wuld normally be compensated for. However, if the vomiting causes volume depletion - there is increased reabsorption of bicarb and thus contraction alkalosis.

Front 46

T/F Volume depletion is a significant component to disorders that cause alkalosis

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T

Front 47

What is saline responsive alkalosis?

Back 47

Caused/exacerbated by volume contraction such that giving saline corrects the volume depletion and the excess bicarb is excreted.

Front 48

What is a saline unresponsive metabolic alkalosis?

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Group of disorders where volume status is normal or even increased

Front 49

How to tx metabolic alkalosis caused by loss of H+?

Back 49

PPIs

Front 50

Giving citrate or acetate in patients with decreased GFR can result in what?

Back 50

They are bicarb precursors, can cause metabolic acidosis due to gain of bicarb.

Front 51

What can happen when treating a respiratory acidosis?

Back 51

It takes a few days for the kidney to start excreting all the bicarb it has been accumulating when treating a respiratory acidosis, so a metabolic alkalosis can occur.

Front 52

Renal A. Stenosis; Renin secreting tumor; and Estrogen replacement are associated with what?

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High renin

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Disorders associated with low renin

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Adrenal adenoma; Adrenal hyperplasia

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How is urine chloride used to help determine cause of metabolic acidosis?

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1) If Urine Cl- is &lt;15> 15, there is a saline resistant disorder aka problem with aldosterone secretion or action.
What's happened is a point is reached where kidney "escapes" from action of aldo because of pressure "pressure natriuresis". Keeps patient from continuing to accumulate sodium and water until they explode.

Front 55

Steps to evaluate acid-base disorder

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1) Look at pH, pCO2, and HCO3-. If abnormal, there is at least one disorder.

2) From pH, determine if they're alkalotic or acidotic. Then look at pCO2. If it can explain the pH, it's respiratory. If not, look at HCO3 - can it explain the pH? If yes, then disorder is metabolic.

3) Calculate compensation. If it's adequate, then it's a simple disorder. If not, then it's a mixed disorder.

4) Calculate anion gap.

5) Using history and other available data, determine the metabolic disorder.

Front 56

Vomiting and DM can result in what mixed disorder?

Back 56

Metabolic alkalosis and Metabolic acidosis (DKA)