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Pathophysiology II Exam 2 Renal > Renal Module III > Flashcards

Renal Module III Flashcards

1
Q

What does pH represent?

A

Concentration of plasma H+

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2
Q

Normal plasma pH?

A

7.4 (7.35-7.45)

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3
Q

Plasma pH in acidosis?

A

< 7.35

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4
Q

Plasma pH of alkalosis?

A

> 7.45

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5
Q

How much H+ is in the blood compared to other plasma ions (Na+, HCO3-, K+, etc.) in a healthy individual?

A

Small amount when compared to other ions (but critical to maintain plasma pH w/ narrow optimal range):
H+= 0.00004 mEq/L
Na+= 140 mEq/L
HCO3-= 24 mEq/L (22-26 mEq/L)
K+= 3.5-5 mEq/L

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6
Q

What happens to oxygen transport and delivery if plasma pH is not maintained within optimal range?

A

Impairment of O2 transport/delivery:
-Acidosis: R shift in oxyhemoglobin
-Alkalosis: L shift in oxyhemoglobin

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7
Q

What happens to cell function if plasma pH is not maintained within optimal range?

A

Disrupted cell function:
-acidosis/alkalosis disrupts structure of cell membrane proteins (ion channels, receptors, etc.) –> impairs cellular & enzyme function in all cells of the body

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8
Q

Death may occur within hours if pH reaches what levels?

A

Below 6.8 or above 8.0
*loss of cell function/O2 transport leads to system failure (cardio, CNS, pulmonary, renal, liver, etc.) and ultimately death

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9
Q

How is H+ produced from metabolism of proteins (amino acids)?

A

Body is constantly breaking down cellular/dietary proteins/amino acids to smaller byproducts
*catabolic rxns constantly producing H+ ions

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10
Q

What are protein/amino acid byproducts used for?

A

Biosynthesis of new proteins/amino acids needed for cell growth/fxn, NTs, NO, etc.
*these rxns recycle a majority of H+ ions preventing/buffers plasma from drastic decrease in pH

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11
Q

How are the remaining protein/amino acid byproducts excreted?

A

Through the ammonia/urea cycle that influences plasma/urine pH equilibrium

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12
Q

How is glutamine (protein/amino acid) broken down for H+ production?

A

Broken down into H+ and glutamate (an excitatory NT that plays a central role in regulation of amino acid pH buffering in liver/kidneys)

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13
Q

What happens in the liver during alkalosis?

A

Converts ammonia to urea which consumes bicarb and produces H+

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14
Q

What happens in the liver during acidosis?

A

Converts ammonia to glutamine which consumes H+ and produces bicarb

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15
Q

Where does converted glutamine circulate/travel?

A

Circulates to PCT pof kidney to feed ammoniagenesis-converts glutamine to ammontia and H+ that is secreted into urine

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16
Q

What happens during glycolysis/glucose metabolism?

A

if O2 not available, glucose is broken down into lactic acid to make ATP –> lactic acid dissociates into lactate and H+ & enter plasma –> lactate & H+ ions circulate to liver where they are recycled back into glucose (Cori cycle)

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17
Q

Does lactic acid contribute to plasma H+ accumulation?

A

No, except during pathology or extreme exertion

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18
Q

What happens during fat metabolism/ketogenesis?

A

Fatty acids broken down by liver to acetoacetate which dissociates into B-hydroxybutyrate and H+ / enters the plasma

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19
Q

Where do B-hydroxybutate and H+ circulate to? What happens to them?

A

Circulate to cells of the body where they will be oxidized/converted back to acetyl CoA & used for energy

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20
Q

Does ketogenesis occur continuously in a healthy individuals?

A

Yes

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21
Q

Dopes ketogenesis contribute to plasma H+?

A

No, except when excessive ketogenesis occurs (like in DKA)

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22
Q

How does aerobic metabolism of glucose and fats take place?

A

if O2 present, glucose and fats (FFA) are broken down/feed TCA/ETC to produce ATP and CO2
*CO2 diffuses into bloodstream, ATP used as energy

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23
Q

Is CO2 in the plasma hydrated?

A

Yes

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24
Q

What does hydrated CO2 in the plasma form?

A

Carbonic acid - can dissociate into H+ and bicarb

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25
Q

CO2’s ability to form H+ and HCO3- influences what?

A

Plasma pH equilibrium

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26
Q

Does aerobic metabolism continuously produce CO2 for dissociation into H+ and CO3-?

A

Yes

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27
Q

CO2 concentration influences what?

A

How easily carbonic acid dissociates into H+ and HCO3-

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28
Q

Increased CO2 will increase what?

A

H+ and HCO3- concentration

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29
Q

Decreased CO2 will decrease what?

A

H+ and HCO3- concentration

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30
Q

What organ system is responsible for regulating CO2 concentration?

A

The lungs

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31
Q

Hypoventilation will have what effect on CO2 concentration?

A

Increases

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32
Q

Hyperventilation will have what effect on CO2 concentration?

A

Decreases

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33
Q

What are the three mechanisms which regulate plasma pH?

A

Renal compensation, Respiratory compensation, Carbonic acid bicarbonate buffer system

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34
Q

How does renal compensation regulate plasma pH?

A

Kidneys regulate rate of H+ excretion and HCO3- reabsorption

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35
Q

Does renal compensation have a slow or fast response time?

A

Slow- kidneys take 1-2 hrs to start and take up to 24-72 hrs to to reach max effect

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36
Q

How does respiratory compensation regulate plasma pH?

A

Lungs regulate rate of CO2 excretion (CO@ conc. regulates how easily carbonic acid dissociates into H+ and HCO3-)

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37
Q

Does respiratory compensation have a fast or slow response time?

A

Fast- lungs take 1-2 min to start and take up to 12-24 hours to reach max effect

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38
Q

Does the carbonic acid bicarbonate buffer system have a fast or slow response time?

A

FAST, IMMEDIATE RESPONSE TIME

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39
Q

How does the carbonic acid bicarbonate buffer system regulate plasma pH?

A

H+, HCO3-, or CO2 cncentrations instantly regulate preference of carbonic acid to either form:
CO2 & H2O
or
H+ & HCO3-

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40
Q

How does the carbonic acid bicarbonate buffer system react to a left shift?

A

Carbonic acid is favored to form CO2 and H2O to buffer the excess H+

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41
Q

How does the carbonic acid bicarbonate buffer system react to a right shift?

A

Carbonic acid is favored to form H+ and HCO3- to buffer too little H+

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42
Q

The carbonic acid bicarbonate equation will maintain optimal H+ concentration if what remains at a constant ratio?

A

Ratio of HCO3- and CO2
Stable pH maintained at 7.35-7.45 if:
-normal CO2 and HCO3- values
-equally raised CO2 and HCO3- values
-equally lowered CO2 and HCO3- values

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43
Q

What is respiratory acidosis?

A

Too much CO2

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44
Q

What is respiratory alkalosis?

A

Too little CO2

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45
Q

What is high anion gap metabolic acidosis caused by?

A

Conditions that create too much H+

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46
Q

What is normal anion gap metabolic acidosis caused by?

A

Conditions that create too little HCO3-

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47
Q

What is metabolic alkalosis?

A

Too little H+ or too much HCO3-

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48
Q

What is mixed acid-base disorder?

A

Patient has two or more acid-base disorders

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49
Q

What kind of conditions cause too much CO2/respiratory acidosis?

A

Conditions that cause hypoventilation

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50
Q

Which medications depress the CNS or respiratory tract (increase CO2)?

A

Opioids, sedatives, tranquilizers, anticholinesterases, anesthetics

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51
Q

Which neuromuscular diseases/conditions depress the respiratory muscles (increase CO2)?

A

Stroke, spinal cord injury, ALS, GBS, myasthenia gravis, botulism, tetanus, muscular dystrophy, etc.

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52
Q

What conditions can cause airway obstruction (increase CO2)?

A

Obstructive sleep apnea (OSA)

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53
Q

What conditions can cause respiratory failure (increase CO2)?

A

Cardiac arrest, pneumonia, pulmonary edema, ARDS, restrictive lung disease, PE, pneumothorax, chest trauma, smoke inhalation

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54
Q

What other conditions can cause an increase in CO2 from hypoventilation?

A

COPD, extreme obesity

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55
Q

Hypoventilation increases CO2 and changes which ratio making the equation out of balance?

A

HCO3-/CO2 ratio

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56
Q

What is the carbonic acid bicarbonate (immediate) response to excess CO2?

A

Makes carbonic acid favor to form H+ and HCO3- (increases H+ concentration, creates an acidosis)

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57
Q

What is the renal compensation (slow, 1-2 hour to start) response to excess CO2?

A

Increase H+ excretion and increasing HCO3- reabsorption

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58
Q

After 24-72 hours, what is the result of renal compensation to excess CO2?

A

-Plasma H+ decreases (pH increases almost back to normal)
-Plasma HCO3- increases to match the high plasma CO2 (balances the equation to maintain the new pH)

59
Q

Does compensation return pH completely back to normal?

A

Rarely

60
Q

What is the expected renal compensation for acute respiratory acidosis?

A

HCO3- should increase by 1 for every 10 mmHg increase in pCO2

61
Q

What is the expected renal compensation for chronic respiratory acidosis?

A

HCO3- should increase by 4 for every 10 mmHg increase in pCO2

62
Q

If HCO3- does not equal the expected value, what does is suggest?

A

Second acid-base disorder is present

63
Q

Normal values for pCO2 and HCO3-?

A

HCO3- = 24 mEq/L (22-26)
pCO2 = 40 mmHg

64
Q

Which conditions cause hyperventilation and too little CO2/respiratory alkalosis?

A

Fear/anxiety
Early shock
Pregnancy
Salicylate toxicity
Altitude and anemia
Pulmonary disease
Sepsis
Hyperthyroidism
Stroke/TBI

65
Q

What is the earliest acid-base disorder of hypovolemic shock (early shock)?

A

Respiratory alkalosis

66
Q

How does pregnancy cause hyperventilation (too little CO2)?

A

Progesterone stimulation of brainstem respiratory centers causes hyperventilation

67
Q

What does salicylate toxicity stimulate to cause hyperventilation?

A

Brainstem respiratory centers

68
Q

How do altitude and anemia cause hyperventilation (too little CO2)

A

Hypoxia/Hypoxemia stimulate hyperventilation

69
Q

Which pulmonary diseases can cause hyperventilation?

A

CHF, asthma, pneumonia, PE

70
Q

Carbonic acid bicarbonate (immediate) response to too little CO2?

A

Carbonic acid favors turning into CO2 and H2O (decreases H+ concentration, creates an alkalosis)

71
Q

Renal compensation (slow 1-2 hr start) response to too little CO2?

A

Decrease H+ excretion and increase HCO3- reabsporption

72
Q

After 24-72 hours, what is the result of renal compensation to too little CO2?

A

-Plasma H+ increases, pH decreases almost back to normal
-Plasma HCO3- decreases to match the low plasma CO2/balance the equation & maintain new pH

73
Q

Expected renal compensation in acute respiratory alkalosis?

A

HCO3- should decrease by 2 for every 10 mmHg decrease in pCO2

74
Q

Expected renal compensation in chronic respiratory distress?

A

HCO3- should decrease by 5 for every 10 mmHg decrease in pCO2

75
Q

Metabolic acidosis can be caused by what two mechanisms?

A

too much H+ & too little HCO3-

76
Q

If metabolic acidosis is caused by conditions that cause too much H+, what is this known as?

A

High anion gap metabolic acidosis (HAGMA)

77
Q

If metabolic acidosis is caused by conditions that cause too little HCO3-, what is this known as?

A

Normal anion gap metabolic acidosis (NAGMA)

78
Q

What happens in excess in HAGMA?

A

Lactic acid synthesis, ketogenesis, acid metabolites/inability to excrete acid

79
Q

Conditions that cause H+ accumulation (HAGMA)?

A

“GOLDMARK”
Glycols
Oxoproline
L-Lactate
D-Lactate
Methanol
Aspirin (salicylic acid)
Renal failure (uremic acidosis)
Ketogenesis

80
Q

How do glycols cause H+ accumulation (HAGMA)?

A

Ethylene glycol & propylene glycol produce acids when metabolized in the liver

81
Q

How does oxoproline cause H+ accumulation (HAGMA)?

A

Pyroglutamic acid: acid metabolite of excessive acetaminophen or paracetamol

82
Q

How does L-Lactate cause H+ accumulation (HAGMA)?

A

Lactic acid is produced in anaerobic metabolism caused by hypoxia (shock, CHF, anemia, CO, poisoning) or from drug metabolism (cyanide, ibuprofen, INH, iron)

83
Q

How does D-Lactate cause H+ accumulation (HAGMA)?

A

Lactic acid produced by gut bacteria

84
Q

How does Aspirin cause H+ accumulation (HAGMA)?

A

Produce acidic metabolites in liver

85
Q

How does renal failure cause H+ accumulation (HAGMA)?

A

unable to excrete H+ (uremic acidosis)

86
Q

What kinds of ketogenesis cause H+ accumulation (HAGMA)?

A

Diabetic, alcoholic, starvation ketosis

87
Q

Carbonic acid bicarbonate (immediate) response to too much H+?

A

Carbonic acid favors turning into CO2 and H2O, increases CO2 and decreases HCO3- concentration and equation is now out of balance

88
Q

What is the respiratory compensation (fast, 1-2 minute to start) response to excess H+?

A

Lungs hyperventilate to solve pH problem, increase CO2 excretion to balance equation

89
Q

After 12-24 hours, what will the result of respiratory compensation to excess H+ be?

A

-Plasma H+ decreases, pH increases almost back to normal
-Plasma CO2 decreases to match the low plasma HCO3-, balances equation to maintain new pH

90
Q

Expected respiratory compensation for metabolic acidosis?

A

PaCO2 = [1.5 x (serum HCO3-)] + 8 (+/- 2)

91
Q

If pCO2 does not equal the expected value, what is suggested?

A

Second acid-base disorder

92
Q

If patients pCO2 is higher than expected, what secondary acid-base disorder is present?

A

Respiratory acidosis

93
Q

If patients pCO2 is lower than expected, what secondary acid-base disorder is present?

A

Respiratory alkalosis

94
Q

Patients can’t typically hyperventilate beyond a pCO2 of what value in response to metabolic acidosis?

A

12-14 mmHg

95
Q

Metabolic alkalosis can be caused by what two mechanisms?

A

too little H+ & too much HCO3-

96
Q

Are there high or normal anion gaps for metabolic alkalosis?

A

No

97
Q

What conditions cause too little H+ (metabolic alkalosis)?

A

GI loss of H+
Renal loss of H+
Hypokalemia

98
Q

How does the GI tract lose excess acid?

A

vomiting, NG suctioning

99
Q

How do the kidneys lose excess H+?

A

-Thiazide diuretics (inhibit NaCl in early DCT but promote K+ excretion (hypokalemia) and H+ excretion downstream in DCT/CD
-Hyperaldosteronism (Conn’s syndrome-adrenal tumor) promotes K+ and H+ excretion in DCT/CD

100
Q

How does Hypokalemia cause excess loss of H+?

A

Shifts K+ out of cells and H+ into cells (moves H+ from blood)

101
Q

Carbonic acid bicarbonate (immediate) response to too little H+?

A

Carbonic acid favors turning into H+ and HCO3-, decreasing CO2 and increasing HCO3- making equation out of balance

102
Q

Respiratory comensation (fast, 1-2 minute start) response to too little H+?

A

Lungs hypoventilate to solve pH problem by decreasing CO2 excretion

103
Q

Expected result of respiratory compensation to decreased H+ after 12-24 hours?

A

-Plasma H+ increases, pH decreases almost back to normal
-Plasma CO2 increases to match increased plasma HCO3- to maintain new pH

104
Q

Conditions that cause excess HCO3- accumulation (metabolic alkalosis)?

A

GI ingestion of bicarb (sodium bicarb, sodium citrate, antacids) & Cystic fibrosis (alters chloride/bicarb balance)

105
Q

Carbonic acid bicarbonate (immediate) response to excess HCO3-?

A

Instantly buffers with H+ and creates alkalosis, equation is out of balance
Carbonic acid now favors turning into H+ and HCO3-, decreasing CO2

106
Q

Respiratory comensation (fast, 1-2 min start) response to excess HCO3-?

A

Lungs hypoventilate to solve pH problem by decreasing CO2 excretion

107
Q

Expected result of respiratory compensation in response to excess HCO3-?

A

-Plasma H+ increases, pH decreases almost back to normal
-Plasma CO2 increases to match high plasma HCO3- to maintain new pH

108
Q

Expected respiratory compensation for metabolic alkalosis?

A

The increase of PaCO2 should = (0.6 x increase of HCO3-) (+/- 2)

109
Q

A patient with metabolic alkalosis typically can’t hypoventilate past what pCO2 value without potential respiratory arrest?

A

pCO2 value of 55-60 mmHg

110
Q

What does the anion gap compare?

A

Cations and anions, electroneutrality of the plasma

111
Q

Anion gap (AG) measurement only includes what three major electrolytes?

A

Na+, HCO3-, Cl-
Values reported in labs (BMP, chem7, chem panel, etc.)

112
Q

Equation to assess anion gap?

A

Anion gap = Na+ - (HCO3- + Cl-)

113
Q

Normal anion gap value?

A

8-12

114
Q

What is the clinical goal of measuring the anion gap?

A

Determine if AG gap is normal or high (NAGMA or HAGMA)

115
Q

Normal values for sodium ions?

A

140 mEq/L

116
Q

Normal value for chloride ions?

A

104 mEq/L

117
Q

Normal value for HCO3- ions?

A

24 mEq/L (“CO2”)

118
Q

The higher the anion gap, the more likely the patient has what?

A

High anion gap metabolic acidosis

119
Q

Anion gap is used to determine what?

A

Cause of metabolic acidosis
High AG: conditions that create too much H+
Normal AG: conditions that create too little HCO3-

120
Q

Anion gap can also detect if what condition is also present in patients that have another type of acid-base disorder?

A

HAGMA
Ex. if patient has respiratory alkalosis and a high AG, also have a high anion gap metabolic acidosis

121
Q

Important to always check what value regardless of acid-base disorder?

A

AG

122
Q

The loss of HCO3- in NAGMA will be replaced with what anion to maintain the “normal” gap of 8-10?

A

Cl-

123
Q

What is NAGMA sometimes referred to as?

A

Hyperchloremic metabolic acidosis

124
Q

HAGMA anion gap value?

A

AG >12

125
Q

What is the lost HCO3- in HAGMA replaced with to cause the gap to increase >12?

A

lactates, B-hydroxybutyrate, etc.
Ex. lactic acid dissociates into H+ and lactate C3H5O3-, lactate replaces decreased plasma HCO3- to maintain electroneutrality

126
Q

Short-cut approaches (like acid-base tic tac toe) to assess acid-base diosorders are often limited to which disorders?

A

More complex acid-base disorders

127
Q

HCO3- is sometimes referred to CO2 in some lab panels, what is this NOT the same as?

A

NOT the same as PaCO2 measures in ABG
*It measures plasma HCO3- and is used as an estimate of plasma CO2

128
Q

Normal arterial blood gas (ABG) values?

A

pH= 7.4
PaCO2= 40 mmHg
PaO2= 100 mmHg
HCO3- = 24 mEq/L

Acid-base is estimated (calculated) in the BG report based on PaCO2 and PaO2
*can be used if needed, but better to use chem screen

129
Q

What is an important tip for acid-base assessment?

A

Try to recognize patterns, de-emphasize memorization of equations and tables

130
Q

Step 1 of acid-base assessment?

A

Determine pH status (acidemia or alkalemia)

131
Q

Step 2 of acid-base assessment?

A

Determine the primary disturbance (respiratory acidosis/alkalosis or metabolic acidosis/alkalosis?)

How:
-Figure out if HCO3- or CO2 is consistent with the pH

132
Q

Low CO2 or high HCO3- are consistent with what?

A

alkalosis

133
Q

High CO2 or low HCO3- are consistent with what?

A

acidosis

134
Q

Low PCO2 (<40 mmHg) and high pH (>7.4) is consistent with what?

A

Respiratory alkalosis

135
Q

High PCO2 (>40 mmHg) and low pH (<7.4) is consistent with what?

A

Respiratory alkalosis

136
Q

Low HCO3- (<24 nm) and low pH (<7.4) is consistent with what?

A

Metabolic acidosis

137
Q

High HCO3- (>24 nm) and high pH (>7.4) is consistent with what?

A

Metabolic alkalosis

138
Q

Step 3 of acid-base assessment?

A

Determine type of compensation
If respiratory = renal compensation
If metabolic = respiratory compensation
AND
If expected compensation has occurred (use equations) to determine if single or mixed acid-base disorder

139
Q

What is the Step 3 acid-base clinical short cut “1,2,3,4,5” rule for assessing renal compensation in patients with respiratory acidosis and alkalosis?

A

Simple table to calculate metabolic compensation:

-Resp. acidosis: increased PaCO2, for every 10mmHg rise should have INCREASE in HCO3- by 1 (acute) or 4 (chronic) for compensation

-Resp. alkalosis: decreased PaCO2, for every 10mmHg rise should have DECREASE in HCO3- by 2 (acute) or 5 (chronic) for compensation

140
Q

What is “Winter’s formula” for assessing respiratory compensation in patients with metabolic acidosis?

A

PaCO2= [1.5 x (serum HCO3-)] + 8 (+/- 2)

141
Q

If the patients PaCO2 is lower than expected PaCO2, the patient also has what disorder?

A

Respiratory alkalosis

142
Q

Clinical shortcut to bypass Winter’s formula?

A

The expected PaCO2 is approximately equal to the last two digits of the pH -/+ 2

143
Q

Step 4 of acid-base assessment?

A

Determine if the anion gap is normal or high
High AG: pathology that produces excess acid or ingests acid
Low AG: Pathology that causes loss of HCO3-
Determine with AG= Na+ - (Cl- + HCO3-)

144
Q

Step 5 of acid-base assessment?

A

Calculate the “delta-delta”
helps detect previously undetected metabolic disorder not discovered on previous 4 steps
Delta ratio = change in anion gap (AG-12) / change in HCO3- (24-HCO3-)

Pathophysiology II Exam 2 Renal (5 decks)

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