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Medical Physiology > Test 5 Lecture 1 > Flashcards

Test 5 Lecture 1 Flashcards

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USMLE® Step 1 flashcards
1
Q

What does the acid-base balance help to maintain in the body?

A

Normal hydrogen ion concentration in the body fluids

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2
Q

How is the balance of hydrogen ions achieved?

A
  • utilization of buffers in extracellular fluid and intracellular fluid (mins to hours)
  • Respiratory mechanisms that excrete CO2 (mins to hours)
  • Renal mechanisms that reabsorb bicarbonate and secrete hydrogen ions (hours to days)
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3
Q

What type of relationship exists between H+ concentration and pH?

A

logarithmic, equal changes in pH do not reflect equal changes in H concentration

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4
Q

What is the normal range of arterial pH?

A

7.37 - 7.42

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5
Q

What is considered acidemia? Alkalemia?

A 
Acidema = < 7.37
Alkalemia = > 7.42
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6
Q

Is the hydrogen concentration relatively high or low?

A

Low, 6 times lower than the sodium concentration

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7
Q

As H concentration increase, pH _______.

A

Decreases

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8
Q

Arterial pH is slightly _____ despite production of large amounts of acid on a daily basis.

A

alkaline (7.4)

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9
Q

What are the 2 forms of acid production?

A 
Volatile acid (CO2)
Nonvolatile/fixed acid
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10
Q

What acid can CO2 be converted into? What does it need to react with?

A

H2CO3

Reacts with H20

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11
Q

What enzyme catalyzes the reaction between H20 and CO2? Is it a reversible reaction?

A

Carbonic anhydrase

Yes

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12
Q

How much fixed acid is produced per day?

A

50 mmol/day

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13
Q

What produces fixed acid?

A

Catabolism of proteins and phospholipids

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14
Q

What type of acid is formed from proteins containing amino acids?

A

Sulfuric

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15
Q

What type of acid is formed from phospholipids?

A

Phosphoric acid

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16
Q

What do fixed acids need to do in order to be removed from the body?

A

First must be buffered in body fluids until can be excreted by the kidneys

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17
Q

When are beta hydroxybutyric acid and acetoacetic acid formed?

A

Ketoacids formed in untreated diabetes mellitus

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18
Q

When is lactic acid formed?

A

During strenuous exercise or when tissues are hypoxic

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19
Q

What are some examples of ingested fixed acids?

A 
Salicylic acid (aspirin overdose)
Formic acid (methanol)
Glycolic and oxalic (ethylene glycol)
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20
Q

What occurs with an overproduction or ingestion of fixed acids?

A

metabolic acidosis

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21
Q

What is a buffer?

A

Weak acid + conjugate base

Weak base + conjugate acid

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22
Q

Weak Acid

A 
Acid = HA, H+ donor
Base = A-, H+ acceptor
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23
Q

Weak Base

A 
Base = BH, H+ donor
Acid = B, H+ acceptor
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24
Q

What occurs when H+ is added or removed from a buffered solution?

A

minimal change in pH

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25
Q

Do weak acids have high or low pKs?

A

High, less dissociated and have lower equilibrium constants

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26
Q

What shape is the titration curve?

A

sigmoid

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27
Q

Where is the linear portion of the titration curve?

A

1 pH unit above and below the pK, most effective buffering occurs here (only small changes in pH occur when H is added or removed)

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28
Q

What are the major buffers of the ECF?

A

bicarbonate and phosphate

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29
Q

What are the A and HA forms of bicarbonate?

A 
A = HCO3
HA = CO2
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30
Q

What are the A and HA forms of phosphate?

A 
A = HPO4
HA = H2PO4
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31
Q

Which buffer is most important in the ECF?

A

HCO3/CO2 buffer, utilized as the first line of defense when H is gained or lost from the body

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32
Q

What characteristics of HCO3/CO2 cause it to be so important?

A

1) concentration of A form is high (24 mEq/L)
2) pK is 6.1, fairly close to pH of ECF
3) CO2 is volatile and can be expired by the lungs

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33
Q

Explain the HCO3/CO2 buffer’s role when HCl is added to the body

A

H combines HCO3 to form H2CO3 (strong acid converted to weak) further dissociates into CO2 and H2O (expired by lungs)

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34
Q

What is the pH for the 2 ECF buffers?

A 
HCO3/CO2 = 6.1 (5.1-7.1)
HPO42/H2PO4 = 6.8
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35
Q

Why isn’t PPO42/H2PO4 as effective as a buffer?

A

1) low concentration (1-2 mmol/L vs 24 mmol/L0

2) Is nonvolatile

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36
Q

What are 2 main types of ICF buffers?

A

Organic phosphates and proteins

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37
Q

What are 3 mechanisms that H must use to cross the cell membrane?

A

1) CO2 can cross membranes
2) with an organic anion (ex, lactate)
3) H exchanges with K

38
Q

H and Ca2 can bind to…

A

negatively charged groups on plasma proteins

39
Q

What changes in Ca2 free concentration occur with acidemia? Alkalemia?

A 
Acidemia = more free, H is bound to plasma proteins
Alkalemia = less free Ca, hypocalcemia
40
Q

What are the symptoms of hypocalcemia?

A

Occurs in respiratory alkalosis, includes tingling, numbness, tetany

41
Q

What are the organic phosphates in the ICF?

A

ATP, ADP, AMP, gluocse-1-phosphate, and 2,3_DPG

42
Q

What is the pK values for the organic phosphates?

A

6 to 7.5

43
Q

Why do intracellular proteins serve as buffers?

A

they contain a large number of acidic or basic groups

44
Q

Which dissociable groups on proteins have a pK within the physiologic range?

A

Imidazole group of histadine (6.4-7)

Alpha amino groups (7.4-7.9)

45
Q

What ist the most significant intracellular buffer?

A

hemoglobin, has 36 histidine residues

46
Q

Which form of hemoglobin is the most effective buffer?

A

Deoxyhemoglobin (pK 7.9)

Oxyhemoglobin has a lower pK (6.7) not as effective

47
Q

What are the major roles of the kidneys in maintaining the normal acid-base balance?

A

1) reabsorption of HCO3

2) excretion of H (produced from protein and phospholipid catabolism)

48
Q

What are the 2 mechanisms for excreting H?

A

1) as a titratable acid buffered by urinary phosphate
2) as NH4

**both mechanisms are accompanied by synthesis and reabsorption of new HCO3

49
Q

How much of HCO3 is reabsorbed?

A

99.9%

50
Q

Where does most reabsorption of HCO3 occur?

A

proximal tubule

51
Q

What are the steps for reabsorption of HCO3?

A

1) conversion of HCO3 to CO2 in the lumen
2) diffusion of CO2 into the cell
3) conversion back to HCO3 in the cell
4) reabsorption of HCO3 into the blood

52
Q

What type of transport mechanism is the NaH exchanger?

A

Na dependent secondary active transport

53
Q

What occurs with the NaH exchanger?

A

Na moves from lumen down its gradient, H moves into lumen against its gradient

54
Q

What occurs when H is secreted into lumen?

A

combines with HCO3 to form H2CO3, decomposes into CO2 and H20, crosses back into the cell

55
Q

What enzyme catalyzes H2CO3 into CO2 and H2O?

A

brush border carbonic anhydrase

56
Q

What happens when CO2 and H2O enter the cell?

A

recombine into H2CO3, converted back into H and HCO3, H is secreted by NaH exchanger, HCO3 transported into the blood

57
Q

What enzyme catalyzes CO2 and H2O into H2CO3?

A

intracellular carbonic anhydrase

58
Q

What 2 mechanisms allow HCO3 to enter the blood?

A

1) NaHCO3 contransport

2) ClHCO3 exchange

59
Q

What are the special features of the mechanism for reabsorption of HCO3?

A
  • results in net reabsorption of Na and HCO3 (portion is directly linked)
  • no net secretion of H
  • produces little change in tubular fluid pH
60
Q

When HCO3 concentration is greater than _____ some must be excreted.

A

40 mEq/L

61
Q

What effects does ECF volume expansion have on HCO3 reabsorption? ECF volume contraction?

A 
Expansion = inhibits isosmotic reabsorption in proximal tubule, inhibits HCO3 reabsorption
Contraction = stimulates it
62
Q

What effects does Angiotensin II have on HCO3 reabsorption?

A

stimulates NaH exchange in proximal tubule, thus stimulating HCO3 reabsorption and blood HCO3 concentration

63
Q

What is contraction alkalosis?

A

Metabolic alkalosis that occurs secondary to ECF volume contraction

64
Q

When does contraction alkalosis occur?

A

Loop or thiazide diuretics, caused by vomiting. Treated by infusing isotonic NaCl

65
Q

What effects do an increase in PCO2 have on HCO3 reabsorption?

A

increase it

66
Q

What occurs, in terms of PCO2, in respiratory acidosis?

A

PCO2 increases, more is available to renal cells to generate H for secretion, more HCO3 can be reabsorbed (increases pH as compensation)

67
Q

What is the amount of H produced and excreted by a normal person eating a relatively high protein diet?

A

Produced = 50 (100%) excreted
Excreted as titratable acid = 20 (40%)
Excreted as NH4 = 30 (60%)

68
Q

What is the amount of H produced and excreted by a person with diabetic ketoacidosis?

A

Produced = 500 (10 fold that of normal value)
Titratable acid = 100
NH4 = 400

69
Q

What is the amount of H produced and excreted by a person with chronic renal failure?

A

Produced = 50
Titratable acid = 10
NH4 = 5

70
Q

What 2 reasons cause the renal mechanisms for excreting acid to become impaired in chronic renal failure?

A

1) Titratable acid excretion is reduced because GFR is reduced, which reduces filtered load of phosphate, thus amount of phosphate that serve as a buffer
2) NH4 is reduced because synthesis of NH3 is impaired in diseased nephrons

71
Q

What causes metabolic acidosis?

A

decrease in HCO3 concentration, leads to decrease in pH

72
Q

What causes respiratory acidosis?

A

hypoventilation, CO2 retention, increased PCO2, decreased pH

73
Q

What are the defense mechanisms to keep the pH in the normal range?

A

1) ECF and ICF buffering

2) Respiratory and Renal compensation

74
Q

What are the 2 rules of thumb for respiratory and renal compensation?

A

1) If acid-base disturbance is metabolic, compensatory response is respiratory
2) In metabolic acidosis, disturbance decreases HCO3, respiratory compensation also decreases PCO2 (same direction)

75
Q

What are cations and anions that are usually measured in the anion gap?

A 
Cation = Na
Anions = HCO3 and Cl
76
Q

What does plasma use to fill the gap?

A

Unmeasured anions including proteins, phosphate, citrate and sulfate

77
Q

What is the equation for the plasma anion gap?

A

Na - (HCO3 + Cl)

78
Q

What is the normal range for the gap?

A

8 to 16 mEq/L

79
Q

What is the anion gap useful for?

A

Differential diagnosis of metabolic acidosis

80
Q

When might there be an increase in the anion gap during metabolic acidosis?

A

Diabetic ketoacidosis, lactic acidosis, salicylate poisoning, methanol poisoing, ethylene glycol poisoning, chronic renal failure

81
Q

What occurs additionally with methanol and ethylene poisoning?

A

Osmolar gap, gap between measured and estimated plasma osmolarity

82
Q

When does the anion gap remain normal during metabolic acidosis?

A

diarrhea, renal tubular acidosis

83
Q

How does the body offset for the decrease in HCO3 if the anion gap doesn’t increase?

A

Increase Cl concentration, called hypercholermic metabolic acidosis with a normal anion gap

84
Q

What is the arterial blood profile during metabolic acidosis?

A

decrease pH
decrease HCO3
decrease PCO2

85
Q

What does the body do in order to correct excessive production/ingestion of H?

A

increase anion gap (also increase osmolar gap with ethylene and methanol poisoning)

86
Q

What does the body do in order to correct for a loss of HCO3 from diarrhea and Type 2 RTA?

A

normal anion gap, hypercholeremia

87
Q

What does the body do when it is unable to excrete H due to renal failure and Type 1,4 RTA?

A

CRF = increase anion gap
Type 1 = normal gap
Type 4 = normal gap

88
Q

What are the steps involved in metabolic acidosis?

A

1) Gain H in body through some sort of mechanism
2) Excess H is buffered, produces decrease HCO3 concentration, hyperkalemia occurs
3) Hyperventilation, decreased PCO2
4) Days later, renal correction, H excreted

89
Q

What is the arterial blood profile for metabolic alkalosis?

A

increased pH
increased HCO3
increased PCO2

90
Q

What does the body do to compensate for a loss of H due to vomiting or hyperaldosternism?

A

vomit = volume contraction

hypokalemia

91
Q

What does the body due to compensate for a gain of HCO3 from NaHCO3 ingestion?

A

renal failure

Medical Physiology (4 decks)

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