Exam 4 - Lecture 4 (Updated, non-shitty cards) Flashcards
1
Q
What is the role of buffers in the body?
A
They stabilize pH by binding or releasing protons. Bicarbonate, phosphate, and proteins are the main ones.
2
Q
What is a buffer?
A
A compound that reacts with free H⁺ to prevent drastic pH changes.
3
Q
What are the three main buffer systems in the body?
A
Bicarbonate, phosphate, and protein (especially hemoglobin intracellularly).
4
Q
What is the role of hemoglobin in buffering?
A
It’s a protein in red blood cells that binds H⁺ and CO₂, making it a strong intracellular buffer.
5
Q
What is the isohydric principle?
A
All buffers act on the same pool of protons simultaneously, enhancing buffering power.
6
Q
What happens when one buffer is removed?
A
All other buffers become less effective — they rely on each other.
7
Q
What happens to H⁺ when it binds a buffer?
A
It becomes inactive — only free H⁺ affects pH.
8
Q
Why are proteins excellent buffers?
A
Their side chains (like histidine) can accept or donate H⁺, and they are abundant intracellularly.
9
Q
What is the pK of a buffer?
A
It’s the pH at which it best resists changes — for bicarb, it’s 6.1.
10
Q
Why is bicarb still a good buffer at pH 7.4?
A
It works best at preventing acidosis, which is more common than alkalosis.
11
Q
What is phosphate’s role in buffering?
A
It’s important intracellularly and in renal tubules, helping excrete H⁺ as titratable acid.
12
Q
What is the dominant plasma protein buffer?
A
Albumin — though less potent than hemoglobin.
13
Q
What is the dominant intracellular protein buffer?
A
Hemoglobin — especially in RBCs.
14
Q
What happens when hemoglobin levels drop?
A
The buffer line on a nomogram flattens, indicating weaker buffering.
15
Q
What does a steep buffer slope indicate?
A
Strong buffering — greater ability to resist pH changes.
16
Q
What does a flat buffer slope indicate?
A
Weak buffering — less bicarbonate adjustment per pH unit.
17
Q
What are isobars on a nomogram?
A
Lines representing different PCO₂ levels.
18
Q
What shifts isobars on the buffer line?
A
Changes in CO₂ due to respiratory compensation.
19
Q
What causes respiratory acidosis?
A
Hypoventilation — CO₂ builds up and pH drops.
20
Q
What causes respiratory alkalosis?
A
Hyperventilation — CO₂ drops and pH rises.
21
Q
How fast can respiratory compensation occur?
A
Within minutes — much faster than renal compensation.
22
Q
What does acute respiratory acidosis look like?
A
High PCO₂, low pH, no renal bicarb compensation yet.
23
Q
What is chronic respiratory acidosis?
A
Sustained high CO₂ with increased bicarb from renal compensation.
24
Q
What does acute respiratory alkalosis look like?
A
Low CO₂, high pH, only small bicarb drop.
25
What happens in chronic respiratory alkalosis?
Kidneys reduce bicarb and retain H⁺ to normalize pH.
26
What causes metabolic acidosis?
Bicarb loss or acid accumulation — e.g., diarrhea, lactic acidosis, ketoacidosis.
27
What compensates for metabolic acidosis?
Hyperventilation — CO₂ is blown off.
28
What causes metabolic alkalosis?
Acid loss (vomiting) or bicarb gain (antacids, diuretics).
29
What compensates for metabolic alkalosis?
Hypoventilation — but it's limited by hypoxia risk.
30
Why is it hard to compensate for alkalosis?
Breathing can’t be reduced too much without endangering oxygen levels.
31
What is 'gain' in physiology?
A system’s ability to correct a deviation — high gain = strong correction.
32
What is the normal anion gap?
~12 mEq/L (Na⁺ - [Cl⁻ + HCO₃⁻]).
33
What causes a high anion gap?
Accumulation of unmeasured acids: lactate, ketones, toxins.
34
What causes a normal anion gap acidosis?
Loss of bicarb with compensatory Cl⁻ retention — e.g., diarrhea.
35
What happens if bicarb drops but Cl⁻ doesn’t rise?
The anion gap increases.
36
What happens in renal tubular acidosis?
Kidneys fail to reabsorb bicarb or secrete acid — normal gap acidosis.
37
Why are children more vulnerable to acidosis from diarrhea?
Their kidneys are immature and can’t compensate effectively.
38
Why is diluted formula dangerous in neonates?
Can cause volume overload — kidneys can’t excrete excess fluid well.
39
What does the Bohr effect describe?
Acidosis lowers hemoglobin's oxygen affinity — promotes oxygen unloading.
40
What is the effect of acidosis on protein structure?
Protonation changes charge and shape, altering protein function.
41
How does acidosis affect the Na⁺/K⁺ ATPase pump?
Excess H⁺ distorts the pump’s shape and slows it down — potentially leading to hyperkalemia.
42
What effect does acidosis have on mitochondrial function?
Impairs ATP synthesis by interfering with mitochondrial enzymes.
43
What is the danger of acidosis in cerebrospinal fluid (CSF)?
It can depress CNS activity and lead to coma.
44
What is a fixed (non-volatile) acid?
An acid not excreted via lungs — includes lactic acid, ketones, sulfuric acid.
45
What are examples of fixed acids produced by the body?
Lactic acid, acetoacetic acid, sulfuric acid, phosphoric acid.
46
What causes lactic acid buildup?
Hypoxia or poor perfusion — anaerobic metabolism.
47
What is acetoacetic acid associated with?
Ketosis — seen in starvation, diabetes, alcoholism.
48
What is butyric acid, and when is it seen?
A ketone body elevated in chronic illness and malnutrition.
49
What is the major buffer in toothpaste?
Sodium fluoride — a weak base that helps neutralize oral acids.
50
What strong base is found in drain cleaner?
Sodium hydroxide — highly caustic and dangerous.
51
Why are many drugs delivered as hydrochloride salts?
It increases solubility and helps absorption.
52
Why does pentobarbital burn during IV push?
It’s a very basic compound that irritates tissue when pushed quickly.
53
What does a buffer system do in the nephron?
Combines with H⁺ to allow excretion while keeping urine pH safe.
54
What is ammonia’s role in renal buffering?
Ammonia binds H⁺ to form NH₄⁺, helping acid excretion.
55
What’s the relationship between pH and [H⁺]?
pH = -log[H⁺] — a 10-fold change in [H⁺] per pH unit.
56
What is the [H⁺] at pH 7?
100 nmol/L (nanomoles per liter).
57
What is the [H⁺] at pH 6?
1,000 nmol/L (or 1 µmol/L).
58
What’s the normal pH range compatible with life?
6.9 to 7.8.
59
What is the main difference between respiratory and metabolic disorders?
Respiratory = CO₂ driven; Metabolic = HCO₃⁻ or acid-driven.
60
What are key signs of partial compensation on blood gases?
Abnormal pH with evidence of the other system adjusting (CO₂ or bicarb).
61
What are signs of full compensation on blood gases?
pH in normal range with abnormal CO₂ and/or HCO₃⁻.
62
How can aspirin toxicity affect acid-base status?
It can cause respiratory alkalosis and later metabolic acidosis.
63
What’s the primary acid eliminated by lungs?
CO₂ (volatile acid).
64
Why does vomiting cause alkalosis?
Loss of HCl from the stomach reduces acid, increasing pH.
65
Why does diarrhea cause acidosis?
Loss of bicarb-rich intestinal fluid.
66
How does the body maintain electrical neutrality?
By balancing cation and anion changes (e.g., Cl⁻ rises when HCO₃⁻ drops).
67
What is the role of albumin in the anion gap?
It’s the most abundant unmeasured anion — low albumin lowers the normal gap.
68
What are unmeasured cations?
Potassium, calcium, magnesium.
69
What are unmeasured anions?
Proteins (albumin), phosphates, sulfates, organic acids.
70
What is the impact of hypoalbuminemia on anion gap?
It lowers the baseline anion gap.
71
What do toxic alcohols like methanol or ethylene glycol do?
Increase the anion gap due to accumulation of acidic metabolites.
“Toxins add new acids the body wasn’t expecting — the bicarb tries to mop it up, and what’s left is a load of unmeasured crap sitting in the gap.”
72
Why do ketone bodies increase the anion gap?
They are unmeasured organic acids — like beta-hydroxybutyrate and acetoacetate.
73
What is the respiratory response to metabolic acidosis?
Increased respiratory rate and depth (Kussmaul breathing).
74
What is a key feature of chronic compensation?
Greater magnitude of change (renal or respiratory) with time.
75
How does compensation appear on a nomogram?
pH is nearer normal, but with abnormal CO₂ or HCO₃⁻.
76
What are examples of mixed acid-base disorders?
COPD with vomiting (respiratory acidosis + metabolic alkalosis); sepsis with diarrhea (metabolic acidosis + alkalosis).
77
What happens when H⁺ is added to a buffered solution?
The buffer binds the H⁺ and limits the drop in pH.
78
What happens when H⁺ is removed from a buffered solution?
The buffer releases H⁺ to stabilize the rise in pH.
79
What is the main determinant of respiratory rate in acid-base balance?
Central chemoreceptors sensing CO₂ levels.
80
What are central chemoreceptors most sensitive to?
CO₂ — they drive changes in ventilation to regulate pH.
“It’s protons that do the detecting — but CO₂ is what drives that change.”
Since CO2 crosses BBB then dissociates into H+ and HCO3-, the central receptors DETECT H+ and respond, but it's driven by CO2 entering CSF fluid to begin with.
81
What are peripheral chemoreceptors sensitive to?
O₂ levels — primarily located in the carotid and aortic bodies.
82
What happens to ventilation during metabolic alkalosis?
It may decrease slightly, but not much — due to risk of hypoxemia.
83
What is the most dangerous acid-base condition for a ventilated patient?
Combined metabolic and respiratory acidosis.
I believe what this means is that metabolic acidosis occurs and then if you're sedated and paralyzed on a vent, the body can't auto correct by increasing ventilation. So leads to severe acidosis.
84
Why is combined acidosis dangerous?
Both systems fail — little to no compensation available.
85
What does compensation aim to do in acid-base balance?
Bring pH closer to normal — never overcorrects or reverses the problem.
86
How is bicarbonate reabsorbed in the kidney?
Primarily in the proximal tubule via carbonic anhydrase activity.
87
What enzyme is critical for renal bicarbonate handling?
Carbonic anhydrase.
88
How does aldosterone affect acid-base status?
Promotes H⁺ secretion and K⁺ excretion — may contribute to metabolic alkalosis.
89
What is renal tubular acidosis (RTA)?
A disorder of bicarbonate reabsorption or H⁺ secretion, leading to metabolic acidosis.
90
What are the three types of RTA?
Type I (distal), Type II (proximal), and Type IV (aldosterone-related).
91
What type of RTA is associated with hyperkalemia?
Type IV — due to aldosterone deficiency or resistance.
92
What does the term 'titratable acid' refer to?
Acids like phosphate excreted in urine after binding H⁺.
93
What role does phosphate play in the nephron?
Acts as a titratable acid to help excrete H⁺.
94
What is the primary urinary buffer for H⁺?
Ammonia (NH₃), which binds H⁺ to form ammonium (NH₄⁺).
95
What limits how low urine pH can go?
Presence of buffers like phosphate and ammonia to bind free H⁺.
96
Why is urine pH not 1 despite high acid excretion?
Buffers prevent extreme acidity, protecting urinary tract tissues.
97
What are the symptoms of severe metabolic acidosis?
Kussmaul breathing, altered mental status, hyperkalemia.
98
What are the symptoms of severe metabolic alkalosis?
Muscle cramps, tetany, hypokalemia, mental status changes.
99
What is the Henderson-Hasselbalch equation?
pH = pK + log([HCO₃⁻]/[CO₂])
100
How can you use the Henderson-Hasselbalch equation clinically?
To understand how changes in CO₂ or HCO₃⁻ affect pH.
101
What causes lactic acidosis?
Tissue hypoxia, sepsis, shock, certain drugs/toxins.
102
What causes ketoacidosis?
Diabetes, alcoholism, starvation — ketone body accumulation.
103
What causes ingestion-related metabolic acidosis?
Methanol, ethylene glycol, or salicylate overdose.
104
What test can confirm elevated ketones in DKA?
Serum or urine ketone measurement — look for beta-hydroxybutyrate.
105
What is the osmol gap used for?
To detect unmeasured osmoles — elevated in toxic alcohol ingestion.
106
What’s the difference between compensation and correction?
Compensation adjusts pH toward normal; correction fixes the underlying cause.
107
Can respiratory and renal systems overcompensate?
No — they never fully normalize pH or overshoot it.
108
How does carbonic anhydrase inhibition affect acid-base?
It reduces HCO₃⁻ reabsorption, causing metabolic acidosis (e.g., with acetazolamide).
109
What effect do loop diuretics have on acid-base status?
Can cause metabolic alkalosis by increasing H⁺ and K⁺ loss.
110
What is contraction alkalosis?
Alkalosis from volume depletion — ECF contraction concentrates bicarbonate.
111
What is saline-responsive metabolic alkalosis?
Alkalosis that improves with volume repletion (NaCl and fluids).
112
What acid-base issue does vomiting cause?
Metabolic alkalosis due to HCl loss.
113
What acid-base issue does prolonged diarrhea cause?
Metabolic acidosis due to HCO₃⁻ loss.
114
Why do ventilated patients need close acid-base monitoring?
Ventilation directly alters CO₂ and affects pH — risk of iatrogenic imbalance.
115
What acid-base disorder can occur with COPD?
Chronic respiratory acidosis.
116
What is base excess/deficit?
A calculated value indicating non-respiratory contributions to acid-base status.
117
What does a negative base excess mean?
Base deficit — indicates metabolic acidosis.
118
What does a positive base excess mean?
Metabolic alkalosis — excess buffering base.
119
How do you differentiate respiratory from metabolic causes of abnormal pH?
Use PaCO₂ and HCO₃⁻ levels to determine the primary disturbance and compensation.
120
What does a widened anion gap indicate?
Accumulation of unmeasured anions, typically from added acid.
121
What does a normal anion gap in metabolic acidosis imply?
Bicarb was lost and replaced by chloride — no unmeasured acids.
122
What’s the mnemonic for high anion gap causes?
MUDPILES — Methanol, Uremia, DKA, Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.
123
What does Kussmaul respiration indicate?
Severe metabolic acidosis — body is trying to blow off CO₂.
124
How can you quickly estimate expected CO₂ in metabolic acidosis?
Use Winter’s formula: PCO₂ ≈ (1.5 × HCO₃⁻) + 8 ± 2.
125
What does it mean if actual CO₂ is higher than Winter’s formula?
There is a concurrent respiratory acidosis.
126
What if CO₂ is lower than expected from Winter’s formula?
There is a concurrent respiratory alkalosis.
127
What does delta gap analysis help detect?
Mixed acid-base disorders in high anion gap acidosis.
128
What is delta gap formula?
ΔAG = (measured AG – normal AG), compare to ΔHCO₃⁻ (24 – measured HCO₃⁻).
129
What does a large ΔAG but small ΔHCO₃⁻ suggest?
High anion gap acidosis with concurrent metabolic alkalosis.
130
What does a small ΔAG and large ΔHCO₃⁻ suggest?
Combined high and normal anion gap metabolic acidosis.
131
What’s the importance of a buffer line’s slope?
Reflects how much HCO₃⁻ can change per pH unit — steep = strong buffering.
132
What system is most responsible for short-term pH adjustment?
The respiratory system via CO₂ exhalation.
133
What system is most responsible for long-term pH adjustment?
The kidneys, through H⁺ excretion and HCO₃⁻ reabsorption.
134
What happens to CO₂ and HCO₃⁻ in chronic respiratory acidosis?
Both are elevated — compensation brings pH closer to normal.
135
What acid-base disorder do loop diuretics commonly cause?
Metabolic alkalosis.
136
What acid-base disorder can occur with prolonged NG suctioning?
Metabolic alkalosis due to HCl loss.
137
What is one way body responds to acidosis besides breathing?
Shifting H⁺ into cells in exchange for K⁺ — causes hyperkalemia.
138
What is one effect of alkalosis on electrolytes?
H⁺ leaves cells, K⁺ shifts in — may cause hypokalemia.
139
What does a low HCO₃⁻ and normal CO₂ indicate?
Uncompensated metabolic acidosis.
140
What does a high HCO₃⁻ and high CO₂ with normal pH suggest?
Compensated respiratory acidosis.
141
What happens to anion gap in renal failure?
It increases due to retention of unmeasured acids (sulfate, phosphate, urate).
142
How does hypoalbuminemia affect anion gap interpretation?
Lowers expected normal range — true gap may be underestimated.
143
What adjustment is made for low albumin and anion gap?
Add ~2.5 mEq/L to normal AG for every 1 g/dL albumin below normal.
144
What acid-base pattern is typical in salicylate poisoning?
Early respiratory alkalosis, followed by metabolic acidosis.
145
Why can asthma attacks paradoxically lead to alkalosis?
Anxiety-driven hyperventilation, even with impaired airflow.
146
What is the danger of mixed alkalosis and acidosis?
pH may appear near-normal, masking a serious dual disturbance.
147
What is the first sign of metabolic acidosis compensation?
Increased respiratory rate and depth.
148
What are expected ABG findings in DKA?
Low pH, low HCO₃⁻, low PCO₂ (compensated metabolic acidosis).
149
What is a “respiratory buffer”?
The ability of lungs to regulate CO₂ and thus pH.
150
What kind of buffer is phosphate?
A non-volatile, titratable buffer — active in kidney and intracellular fluid.
151
What determines if urine pH is 4.5 or higher?
Presence of urinary buffers (ammonia, phosphate).
152
What does a urine pH of 6.5 with acidosis suggest?
Impaired renal acid excretion — possible renal tubular acidosis.
153
What is the most abundant urinary acid buffer?
Ammonium (NH₄⁺).
154
How does glutamine metabolism contribute to acid-base balance?
Produces ammonia (NH₃) in proximal tubule — buffers secreted H⁺.
155
What is the normal bicarbonate range?
22–26 mEq/L.
156
What is the normal PCO₂ range?
35–45 mmHg.
157
What is the normal pH range in arterial blood?
7.35–7.45.
158
What is the expected renal response to chronic respiratory alkalosis?
Increased HCO₃⁻ excretion, H⁺ retention.
159
What is the expected renal response to chronic respiratory acidosis?
Increased H⁺ excretion and HCO₃⁻ reabsorption.
160
What acid-base change occurs in sepsis?
Lactic acidosis — high anion gap metabolic acidosis.
161
What causes ethylene glycol acidosis?
Metabolized to oxalic acid — increases anion gap and osmolar gap.
162
What acid-base disorder occurs in uremia?
High anion gap metabolic acidosis — retention of acids.
163
What electrolyte abnormality often accompanies alkalosis?
Hypokalemia — due to cellular shifts and renal loss.
164
How do carbonic anhydrase inhibitors affect acid-base?
Cause a mild metabolic acidosis — loss of HCO₃⁻.
165
What condition can cause both respiratory and metabolic acidosis?
Cardiac arrest — CO₂ retention + lactic acid buildup.
166
What condition causes respiratory alkalosis and high anion gap acidosis?
Salicylate toxicity.
167
What is one test clue for ethylene glycol poisoning?
Calcium oxalate crystals in urine.
168
What are clinical signs of metabolic alkalosis?
Mental status change, muscle cramps, arrhythmias from electrolyte shifts.
169
What are the key clues for a mixed disorder on ABG?
pH doesn’t fit the compensation pattern; CO₂ and HCO₃⁻ are both abnormal in inconsistent ways.
