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Renal Module > Acid-Base-Wall > Flashcards

Acid-Base-Wall Flashcards

1
Q

What is an Acid?

What is a Base?

A

Acid: a substance that can donate hydrogen ions
Base: a substance that can accept hydrogen ions

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2
Q

What are the two types of acids in the body?

A
  1. Carbonic/volatile

2. Non-carbonic/nonvolatile

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3
Q

What is an example of a carbonic/volatile acid? How much is produced each day? How is it eliminated from the body?

A

Carbon dioxide; 15,000mmol/day; eliminated by the lungs

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4
Q

What are some examples of non-carbonic/nonvolatile acids? How much are produced each day? How are they eliminated?

A

Phosphoric and Sulfuric acids (any acid that cant be converted to CO2 and eliminated by the lungs); 50-100 meq/day; they combine with buffers and are subsequently excreted by the kidney

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5
Q

What are the extremes of pH compatible with life?

A

ph between 7.80 and 6.80 (outside of this range patients die because enzymes are pH-dependent)

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6
Q

How do labs measure total CO2 concentration in venous samples?

A

Dissolved CO2 plus bicarbonate concentration, ~25-26 meq/L

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7
Q

What is normal dissolved CO2? Plasma Bicarbonate concentration?

A

CO2- 1 to 1.5 meq/L; HCO3- ~24 meq/L

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8
Q

What is acidemia?

What is alkalemia?

A 
Reduced pH (elevated H+ concentration);
Increased pH (reduced H+ concentration)
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9
Q

What is acidosis?

What is alkalosis?

A

Acidosis→process that lowers pH

Alkalosis→process that increases pH

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10
Q

What is the major extracellular buffer? It’s equation?

A

Bicarbonate Buffer System:

CO2+H2O←H2CO3→H+ +HCO3-

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11
Q

In a closed system, what is the pKa of the bicarbonate system? Why is this not the case in the body? Is this effective?

A

closed system pKa=6.1; But, we are an open system via the lungs excreting CO2, making this system a highly efficient buffer even though our normal pH is 7.40

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12
Q

What equation demonstrates the determinants of pH? (at normal pH what do H+ and HCO3- equal to?)

A

[H+]=24 x (pCO2/[HCO3-])
Therefore, at pH=7.4→[H+]=40nEq/L
(Normal [HCO3-]=24)

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13
Q

What is another way to estimate H+ concentration?

A

[H+]= 80 minus first two decimal digits of pH

i.e. at pH=7.40: [H+]=80-40= 40

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14
Q

What happens to pH when H+ concentration is doubled to 80? What about when it’s halfed to 20?

A

pH decreases by 0.3, so that pH=7.1;

pH increases to 7.7

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15
Q

What are the normal values of pH, pCO2, and [HCO3-]

A

pH=7.4
pCO2=40mmHg
HCO3-=24meq/L

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16
Q

What are metabolic disorders?

A

Processes that directly alter bicarbonate concentration

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17
Q

What happens in metabolic acidosis?

Metabolic alkalosis?

A

MetAcidosis: decreased bicarbonate
MetAlkalosis: increased bicarbonate

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18
Q

What are respiratory disorders?

A

Processes that directly alter CO2

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19
Q

What happens in respiratory acidosis?

Respiratory alkalosis?

A

RespAcidosis: increased CO2
RespAlkalosis: decreased CO2

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20
Q

What is the buffer effect with respiratory disorders?

A

Slightly increased HCO3 with respiratory acidosis; Slightly decreased HCO3 with respiratory alkalosis

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21
Q

What do buffers do?

A

They prevent wide changes in pH in response to the addition of acid or base.

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22
Q

What is the major extracellular buffer? How is intracellular pH maintained?

A

Bicarbonate; there are other intracellular buffers

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23
Q

How quickly does bicarbonate buffer respond to addition of acid or base?

A

immediate onset

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24
Q

What is the isohydric principle?

A

Any condition that changes the balance of one buffer (shifts the direction of its equation) will change/shift the balance of all the other buffers in the same direction

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25
Q

What is the purpose of acid-base balance?

A

Maintain normal pH by buffer systems

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26
Q

What are the major buffers and their 1) H+ acceptor and 2) H+ donor in:
a. ECF b. Urine (2) c. Intracellular?

A

a. ECF: Bicarbonate: 1. HCO3- 2. H2CO3
b. Urine: Phosphate:1.(H2PO4)2-;2.H2PO4; Ammonia: 1.NH3 2. NH4+
c. Proteins: 1. Protein 2. Protein

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27
Q

What is the purpose of phosphate and ammonia buffers in the urine?

A

To eliminate non-volatile acids

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28
Q

In addition to buffering mechanisms, what else happens in response to changes in pH?

A

Secondary (Compensatory) physiologic responses also occur in response to pH changes

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29
Q

What compensates for metabolic disorders? Organ? Speed of onset?

A

The respiratory system compensates by altering CO2 via the lungs; rapid onset, minutes

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30
Q

What compensates for respiratory disorders? Organ? Speed of onset?

A

Buffer compensation occurs by alterations in bicarbonate concentration via the kidney; slower onset, 1-2 days

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31
Q

Will the pH change be greater in acute or chronic respiratory disorders? Why?

A

pH changes will be greater in acute respiratory disorders because there is often not enough time for the buffer compensation to respond as well as it could to a slower-developing chronic disorder

32
Q

What are the mechanisms that buffer an acid load? (4) Where do they work? How long does it take them to respond?

A
  1. ECF buffer systems (primarily bicarb), immediate response
  2. Increased rate and depth of breathing to decrease CO2 in the lungs, minutes to hours
  3. ICF buffer systems (Phosphate, Bicarb, Protein), 2-4 hours
  4. In the kidney: H+ excretion, Bicarb reabsorption, and Bicarb generation; hours to days (much slower)
33
Q

What are the 4 cardinal acid-base disorders? How do they affect pH, HCO3-, and pCO2?

A

In metabolic disorders, all 3 markers go in same direction; in respiratory disorders, pH goes opposite direction from the other 2 markers

  1. MetAcidosis: decreased pH, HCO3-, & pCO2
  2. MetAlkalosis: increased pH, HCO3-, pCO2
  3. RespAcidosis: decreased pH, increased pCO2 (primary), increased HCO3- (compensatory)
  4. RespAlkalosis: increased pH, decreased pCO2 (primary), decreased HCO3- (compensatory)
34
Q

What are the three golden rules of simple acid-base disorders?

A
  1. pCO2 and HCO3 always go in same direction
  2. Secondary physiologic compensatory mechanisms must be present (always present)
  3. The compensatory mechanisms never fully correct the pH
35
Q

What is metabolic acidosis?

A

Process that reduces plasma bicarbonate concentration

36
Q

What are the 3 etiologies of metabolic acidosis?

A
  1. Decreased renal acid secretion
  2. Direct bicarbonate losses
  3. Increased acid generation (exogenous or endogenous)
37
Q

What are examples of increased acid generation? Which are endogenous? Exogenous?

A
  1. Lactic acidosis (endogenous, when we become anaerobic→shock)
  2. Ketoacidosis (endogenous, using fat as fuels during fasting)
  3. Ingestion of acids (exogenous: aspirin, ethylene glycol, methanol)
  4. Dietary protein intake (exogenous, animal source)
38
Q

What are the two places bicarbonate can be lost? Examples?

A
  1. GI tract→diarrhea, intestinal fistula

2. Renal (urine)→ Type 2 proximal renal tubular acidosis

39
Q

In what form is acid excreted in urine? What are causes of decreased acid excretion? (3)

A

Excreted as NH4+;
Causes: 1. Renal failure (reduced GFR→ reduced ammonium excretion)
2. Type 1 (distal) RTA
3. Type 4 RTA (hypoaldosteronism)

40
Q

What induces respiratory acidosis?

A

hypercapnia (decreased alveolar ventilation); this raises pCO2

41
Q

How do mechanisms respond to resp acidosis and how fast and to what extent?

A

they raise plasma HCO3- concentration (rapid but limited response, ~1-2meq/L)

42
Q

How do kidneys minimize change in extracellular pH? How fast?

A

Kidney minimizes change in ECF pH by increasing acid excretion (NH4+) generating new bicarbonate ions; delayed response, 2-3 days

43
Q

What are causes of respiratory acidosis?

A

Things that slow or stop breathing
Acute: anasthesia, sedative overdose cardiac arrest, etc (not superimportant
Chronic: COPD (know this one), primary hypoventilation, etc.

44
Q

What happens in respiratory alkalosis? Due to what?

A

Reduced CO2 due to increased alveolar ventilation→breathing too much

45
Q

How do buffering processes respond to resp alkalosis? Speed and extent of response?

A

They lower plasma bicarb concentration; rapid but limited response, ~1-2meq/L

46
Q

How do the kidneys respond/compensate in resp alkalosis? How fast?

A

They reduce net acid excretion by eliminating bicarbonate into urine or decreasing ammonium excretion; delayed response, 1-2 days

47
Q

Causes of resp alkalosis?

A

a. Anxiety, hysteria, panic
b. Fever
c. CNS diseases
d. CHF, Pneumonia, pulmonary emboli→ these make us hypoxic so we breath faster

48
Q

Why do acute resp disorders have greater pH change than chronic resp disorders?

A

Kidneys have less time to compensate

49
Q

How does plasma Cl- concentrate relate plasma HCO3- concentration in resp disorders?

A

Plasma Cl- changes equally and inversely with plasma HCO3-

50
Q

What does not change with resp disorders? Is plasma sodium directly altered by acid-base disorders?

A

Plasma anion gap; NO

51
Q

What is the range of HCO3 in plasma the kidney can produce in response to resp disrders? Acute? Chronic?

A

16(low end)-24(normal)-32 (high end)
Acute: 24+/- 1 or 2
Chronic: close to the extremes (bc more time)

52
Q

What is metabolic alkalosis? Etiologies?

A

Processes that raise plasma bicarbonate concentration
Etiologies: 1. Loss of H+ from GI tract (vomiting removes gastric secretions) or into urine (diuretic therapy)
2. Excessive urinary net acid excretion (i.e. primary hyperaldosteronism)
Rare causes:3. Movement into cells in severe hypokalemia→very rare
4. Administration of bicarb or organic acid like citrate that can be metabolized to bicarb

53
Q

What are two important parameters to measure to diagnose and characterize a patient’s metabolic acidosis?

A
  1. ECFV 2. Urine Cl- concentration
54
Q

How do the urine Cl concentrations differ in Cl-responsive met alkalosis and Cl-resistant met alkalosis?

A

Cl-responsive: Urine Cl< 20 meq/L (usually< 10 meq/L)

Cl-resistant: Urine Cl> 20 meq/l (usually> 50 meq/L)

55
Q

What are the expected pH changes for respiratory disorders?

A

A. Acute Resp Acidosis: HCO3 increases 1mEq for each 10mm increase in pCO2

b. CRAcidosis: HCO3- increases 4mEq for each 10mm increase in pCO2
c. ARAlkalosis: HCO3- decreases 2mEq for each 10 mm decrease in pCO2
d. CRAlkalosis: HCO3- decreases 5mEq for each 10mm decrease in pCO2

56
Q

Where is HCO3 reabsorbed? How much ends up in the urine?

A

90% of filtered HCO3- is reabsorbed in PT, the rest is reabsorbed in DT; usually none is in urine

57
Q

In what cells of the nephron does most H+ secretion occur? How?

A

Intercalated alpha cells in the CCD; H2O+CO2→H2CO3, which CA breaks down into HCO3- (gets reabsorbed in exchange for Cl- into cell) and H+ (gets secreted via H+ATPase pump)

58
Q

In what cells in the CCD is HCO3- secreted?

A

beta-intercalated cells (aka Type B) via the same mechanism as alpha-intercalated cells but ions go opposite directions because transporters are in opposite membranes)

59
Q

What is the result of Na+ reabsorption by principal cells in CCD?

A

Makes the lumen of CCD very electronegative

60
Q

How is the Plasma Anion Gap (PAG) determined?

A

PAG=Na-(Cl+HCO3)

61
Q

Strong acids (HA) fully dissociate at pH 7.4, what happens to the resulting H+? What happens to resulting conjugate base and how does that affect PAG and Cl levels?

A

a) H+ is buffered by HCO3-, decreasing HCO3 levels
b) 1. A- is either excreted into urine (normal PAG, increased plasma Cl- concentration)
or 2. A- is reabsorbed by kidney and retained in plasma (i.e. a ketoacid anion of lactic acid that we dont want to lose), as an unmeasured anion (Increased PAG, minimal change in plasma Cl concentration)

62
Q

What is the normal PAG? Why?

A

10; due to unmeasured albumin under normal conditions

63
Q

How is metabolic acidosis usually classified?

A

based on the PAG:

  1. Normal PAG acidosis (w/ hyperchloremia equal to decrease in HCO3)
  2. High PAG acidosis (normal chloride level with 10 or more meq of some unmeasured anion)
64
Q

Quick trigger: If high PAG, patient has what?

A

Metabolic acidosis

65
Q

What are major causes of MetAcidosis with increased PAG?

A
  1. Renal Failure (PO4, SO4, urate, hippurate)
  2. Lactic acidosis (lactate(
  3. Ketoacidosis (Beta-hydroxybutarate)
  4. Ingestions
66
Q

Major causes of metAcidosis with normal PAG or hyperchloremia? Then look at the 2 tables on p 13 of ppt

A
  1. Renal tubular acidosis
  2. Diarrhea
  3. Some cases of chronic renal failure
67
Q

If you have normal AG metabolic acidosis, how can you determine if the cause is RTA or diarrhea/external losses?

A

Look at the Urine AG (UAG):
Positive UAG→RTA
Neg UAG→Diarrhea, etc.

68
Q

In Renal acid excretion, what happens to bicarbonate that enters filtrate and where?

A

All filtered HCO3 must be reabsorbed (mostly in PT and L of H)

69
Q

In renal acid excretion, what happens in CD?

A

Primary site where final excretion of daily acid load is excreted (~50-100 meq/day)

70
Q

What is an effective buffer at low urinary pH? How much H+ excretion does it account for each day? Can this amount be increased?

A

Monobasic phosphate accounts for 10-40 meq H+ excretion per day; cant be increased beyond this point due to fixed amount of phosphate in urine (just enough to maintain phosphate homeostasis in the body)

71
Q

What accounts for the major adaptive response to an elevated acid load in urine? How much H+ does it excrete each day? can this be increased?

A

Ammonium; normally 30-40 meq/d up to a max of ~300 in response to physiologic needs

72
Q

Why is NH4+ trapped in urinary lumen?

A

it’s lipid insoluble

73
Q

How is UAG determined? What is it measuring indirectly?

A

UAG = (Na+K) - Cl

It is an indirect estimate of urinary NH4+ excretion.

74
Q

What is a normal UAG? What caused UAG to decrease?

A

Normal UAG= +10;

UAG becomes less positive or negative with increased urinary NH4+ excretion bc Cl- must accompany it.

75
Q

Is Na altered by acid-base disorders? What about Cl?

A

Na concentration is not altered by acid-base disorders.

Plasma Cl is altered in all acid-base disorders except increased PAG metAcidosis

76
Q

Under normal conditions how are Na and Cl levels related?

A

Law of electroneutrality

77
Q

If you have a normal constant Na concentration, but your Cl concentration has changed, what do you have?

A

An acid-base disorder is present

Renal Module (13 decks)

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