Renal Module 3 Flashcards
(74 cards)
1
Q
How is acid-base balance related to ECF?
A
Closely related!
- H concentration in ECF represents body’s pH
- ECF volume changes will influence pH due to Na/H exchange in kidney
2
Q
A change of pH by 1 unit is equal to ____ concentration of H in the ECF
A
10-fold
3
Q
How are acids classified?
A
- Respiratory (aka volatile)
- Metabolic (aka non-volatile or fixed)
4
Q
Describe respiratory acids
A
- Carbonic acid is technically true respiratory acid
- However, CO2 is commonly thought of as respiratory acid
- High PCO2 is “same as” respiratory acidosis
5
Q
Describe metabolic acids
A
- Nonvolatile or “fixed”
- Represents acids produced by body
- Examples: lactic acid, ketoacids
6
Q
Mechanisms to maintain acid-base homeostasis
A
- Buffering acid (immediate response)
- Resp compensation (few mins to hours)
- Renal compensation (few days)
- Bone plays a role? (long term adaptation)
7
Q
What is the first line of defense against acid-base variations?
A
Buffers
8
Q
Describe buffers
A
Maintains pH when acids accumulate in the blood
9
Q
What is the major intracellular buffer?
A
Hemoglobin in RBCs
10
Q
How does hemoglobin act as an intracellular buffer?
A
- As CO2 enters RBC, it combines with H2O to form carbonic acid
- Carbonic acid dissociates into H and HCO3 (bicarb)
- H binds to the hemoglobin
11
Q
Hemoglobin in the ICF are responsible for buffering which types of acids?
A
Respiratory acids
12
Q
What is the major extracellular buffer?
A
HCO3 (bicarb)
13
Q
Bicarb in the ECF is the major mechanism for buffering which acids?
A
Metabolic acids
14
Q
What is ventilation’s role in acid-base balance?
A
- Lungs eliminate CO2 from body (may take few mins to hours)
- Carbonic acid buffering (Henderson-Hasselbach)
15
Q
Describe carbonic buffering by ventilation
A
- CO2 and H2O form carbonic acid (respiratory acid)
- Carbonic acid easily gives up H
- If too much CO2 then H will accumulate
16
Q
Hyperventilation will ____ pH
A
Increase (more alkaline)
17
Q
What is the clinical result of hyperventilation (creation, correction, compensation)?
A
- Reduced H concentration
- Creation Respiratory alkalosis
- Correction of respiratory acidosis
- Compensation for metabolic acidosis
18
Q
What is the clinical result of hypoventilation (creation, correction, compensation)?
A
- Increased H concentration
- Creation of resp acidosis
- Correction of resp alkalosis
- Compensation for metabolic alkalosis
19
Q
Hypoventilation will ____ pH
A
Decrease (more acidic)
20
Q
How do kidneys regulate acid-base balance in arterial blood?
A
- Excrete fixed (metabolic) acids
- Alter bicarb absorption/excretion
21
Q
How do the kidneys regulate acidic arterial blood?
A
- Increase reabsorption of HCO3
- Increase excretion of H (to decrease acid in arterial blood)
22
Q
How do the kidneys regulate alkaline arterial blood?
A
- Decrease reabsorption of HCO3
- Decrease excretion of H (to increase acid in arterial blood)
23
Q
How does the PCT regulate acid-base balance?
A
- Production of ammonium
2. Reabsorption of bicarb
24
Q
What is reabsorbed with bicarb in the PCT and what is excreted?
A
- One Na+
- NO excretion of H ions
25
Factors that will increase HCO3 reabsorption in the PCT?
- Increased GFR
- Increased PCO2 (acidemia) of arterial blood
- ECF contraction
- Angiotensin II (stimulates H/Na exchange)
26
If the ECF expands, will reabsorption of bicarb in the PCT increase or decrease?
DECREASE - H concentration is diluted so kidneys excrete more HCO3
27
How does the late DCT/collecting duct regulate acid-base balance?
1. Reabsorption of bicarb
| 2. Excretion of H via phosphate and ammonium buffering
28
What is reabsorbed with bicarb in the late DCT/collecting duct and what is excreted?
- One Na+
| - Excretion of one H+
29
What is the end result of phosphate and ammonium buffering in the late DCT/collecting duct?
Renal excretion of H+
30
Describe the mechanism of titratable acid (phosphate buffering) in late DCT/collecting duct
- H combines w/dibasic phosphate to form monobasic phosphate
- Amt of H excreted depends on pH in tubular fluid
- Once tubular fluid reaches pH 4.5 or less, this mechanism cannot continue
31
What ranges of pH does phosphate buffering stop working?
4.5 or less
32
pH of human urine ranges from:
4.5 to 8
33
Which mechanism of the late DCT/collecting duct is most effective at excreting H in normal circumstances?
Phosphate buffering
34
Describe ammonia buffering of the late DCT/collecting duct
- H combines w/NH3 to form ammonium (NH4+)
| - Once tubular fluid pH reaches 4.5 or less, ammonium buffering INCREASES so excretion of H increases
35
When is the ammonium buffer mechanism most effective at excreting H?
Acidic conditions (4.5 pH and lower)
36
Which mechanism of the late DCT/collecting duct is most effective at excreting H in acidic circumstances?
Ammonium buffering
37
When is the phosphate buffer mechanism most effective at excreting H?
Normal circumstances (4.5 pH and higher)
38
Factors that increase excretion of H from DCT/collecting duct
1. Hypokalemia (stimulates ammonia synthesis which increases H excretion)
2. Elevated PCO2 (resp acidosis)
3. Aldosterone (stimulates Na reabsorption along w/H and K secretion)
39
Bone density loss is a/w what condition?
Chronic metabolic acidosis
40
How is bone density loss a/w chronic metabolic acidosis?
- Ca Carbonate released from bone
- It buffers metabolic acids
- Chronic release results in osteoporosis
41
Simple acid-base disorders:
1. Resp acidosis (high PCO2)
2. Resp alkalosis
3. Metabolic acidosis (too much H or not enough HCO3)
4. Metabolic alkalosis
42
Mixed acid-base disorders:
- One disorder may mask the ABGs of 2nd disorder
| - Example: resp alkalosis w/metabolic acidosis
43
How do respiratory acid-base disorders affect potassium levels?
They do NOT affect K levels as much as metabolic disorders
44
How do metabolic acid-base disorders affect potassium levels?
K levels are affected MORE compared to resp disorders
45
Metabolic acidosis is a/w what levels of potassium?
Hyperkalemia
46
Metabolic alkalosis is a/w what levels of potassium?
Hypokalemia
47
How to determine simple vs. mixed acid-base disorder?
Calculated compensation
- If equal to expected response then ONE disorder
- If NOT equal to expected response, then more than one disorder present
48
Respiratory acidosis: cause, primary disturbance, initial A/B disruption, compensation
- Limited ventilation
- Increased PCO2 in arterial blood
- Increased H and NORMAL HCO3
- Increased PCO2, increased HCO3, decreased pH w/trend to normalizing pH
49
Clinical causes of respiratory acidosis
(Aka limited ventilation)
- Meds like opiates, sedatives, anesthetics
- Neuro conditions like GBS, MS, ALS, polio
- Pulmonary pathology
50
Respiratory alkalosis: cause, primary disturbance, initial A/B disruption, compensation
- Increased ventilation
- Decreased PCO2 in blood
- Decreased H and normal HCO3
- Decreased PCO2, decreased HCO3, increased pH w/trend toward normalizing pH
51
Clinical causes of respiratory alkalosis
(Aka increased ventilation)
- PE
- High altitude
- Panic/anxiety
- Anemia
- Pregnancy
52
Metabolic acidosis: cause, primary disturbance, initial A/B disruption, compensation
- Excessive fixed acid formation or ingestion, or loss of base
- Decreased HCO3
- Increased H due to inadequate HCO3
- Lungs hyperventilate to reduce PCO2 which in turn will reduce H
53
Major categories of anion gap formation
- Renal failure
- Ketoacidosis
- Toxins
- Lactic acidosis
* All create increased fixed acid
54
Causes of metabolic acidosis w/increased anion gap formation
- Ketoacidosis
- Lactic acidosis
- Aspirin intoxication
- Analgesics
- CO
- Chronic renal failure
55
Causes of metabolic acidosis w/normal anion gap formation
- Diarrhea
- Renal tubular acidosis
- Diuretics (carbonic anhydrase inhibitors, K+ sparing)
* All create loss of base (HCO3)
56
Metabolic alkalosis: cause, primary disturbance, initial A/B disruption, compensation
- Loss of fixed acid formation or gain of base
- Increased HCO3
- Decreased H
- Lungs hypoventilate to retain PCO2 which in turn will increase H+
57
Clinical causes of metabolic alkalosis
- Vomiting
- Loop or thiazide diuretics
- Volume contraction
- Hypokalemia
58
Describe serum anion gap
Anion gap is a comparison of cations and anions in blood
59
Which cations and anions are measured in anion gap?
Cations: Na
Anions: Cl, bicarb
60
Which cations and anions are NOT measured in serum anion gap?
Cations: Ca, Mg, K
Anions: Proteins, phosphate, sulfate, etc.
61
How is anion gap calculated?
Na - (Cl + HCO3)
62
What is the normal anion gap range?
6 - 16 (approx. 12)
63
In the healthy individual, what is the anion gap a result of?
Unmeasured anions in blood (primarily due to plasma proteins like albumin)
64
Relationship of anion gap and metabolic acidosis
- The anion, HCO3, decreases as it buffers increased H
| - Another anion must replace this to maintain electroneutrality
65
Define normal anion gap in metabolic acidosis
Concentration of Cl is increased (replaced HCO3) to maintain normal gap
66
Define increased anion gap in metabolic acidosis
Non measured anions are increased to maintain normal gap, but they are not measured so clinically this shows a "gap"
67
What is the purpose of identifying the anion gap?
To identify possibility of co-existing metabolic acidosis in other A/B disorders
68
What does the anion gap represent?
Presence of metabolic acidosis and what is causing it
| *If gap is present in some other A/B disorder, then it suggests a mixed disorder
69
The larger the anion gap:
The much better diagnostic tool
70
Steps in analyzing acid-base
1. Determine acidemia or alkalemia
2. Determine primary disturbance (respiratory vs. metabolic)
3. Is the compensation appropriate?
4. Normal or increased anion gap?
5. If metabolic acidosis, then determine if additional disorder occurring concurrently.
71
Normal ABG levels (pH, PCO2, HCO3, anion gap)
pH = 7.4
PCO2 = 40 mm Hg
HCO3 = 24 mEq/L
Anion gap = 12
72
How to tell respiratory vs. metabolic acidosis?
- Respiratory is HIGH PCO2 and HCO3
| - Metabolic is LOW PCO2 and HCO3
73
How to tell respiratory vs. metabolic alkalosis?
- Resp is LOW PCO2 and HCO3
| - Metabolic is HIGH PCO2 and HCO3
74
How is acute vs. chronic respiratory disorder determined?
Acute is less than 72 hours
| Chronic is more than 72 hours
