A 44-year-old Caucasian male complains of carpopedal spasms, peri-oral numbness, and paresthesias of the hands and feet. His wife also mentions that he had a seizure not too long ago. His past surgical history is significant for total thyroidectomy due to papillary thyroid carcinoma. They then realized all of the symptoms occurred after the surgery. Which of the following would be present in this patient?
Q2
A 41-year-old man presents to urgent care with a 1-week history of severe diarrhea. He says that he has been having watery stools every 2-3 hours. The stools do not contain blood and do not float. On presentation, he is observed to have significant facial flushing, and laboratory tests reveal the following:
Serum:
Na+: 137 mEq/L
K+: 2.7 mEq/L
Cl-: 113 mEq/L
HCO3-: 14 mEq/L
A computed tomography scan reveals a small intra-abdominal mass. Staining of this mass would most likely reveal production of which of the following?
Q3
A 67-year-old woman presents to the Emergency Department complaining of weakness and fatigue. She says she caught a “stomach bug” and has not been able to eat anything without vomiting for three days. Past medical history is significant for hyperlipidemia. She takes atorvastatin and a multivitamin daily, except for the last two days due to nausea. Today her heart rate is 106/min, respiratory rate is 16/min, temperature is 37.6°C (99.7°F) and blood pressure of 110/70 mm Hg. On physical examination, her oral mucosa is dry and she looks pale and uncomfortable. She is admitted for care and administered ondansetron. An intravenous infusion of normal saline is also initiated. An arterial blood gas is collected. Which of the following results is expected to be seen in this patient?
Q4
A 22-year-old woman presents to the physician due to lightheadedness. Earlier in the day, she had her first job interview since graduating from college 3 months ago. While waiting outside the interviewer’s office, she began to feel nervous and started breathing really fast. She then felt as if she was going to faint. She excused herself from the interview, and requested a friend to drive her to the clinic. Which of the following is responsible for her symptoms?
Q5
A 54-year-old man presents with 3 days of non-bloody and non-bilious emesis every time he eats or drinks. He has become progressively weaker and the emesis has not improved. He denies diarrhea, fever, or chills and thinks his symptoms may be related to a recent event that involved sampling many different foods. His temperature is 97.5°F (36.4°C), blood pressure is 133/82 mmHg, pulse is 105/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam is notable for a weak appearing man with dry mucous membranes. His abdomen is nontender. Which of the following laboratory changes would most likely be seen in this patient?
Q6
A 56-year-old woman with a longstanding history of gastroesophageal reflux presents for follow-up evaluation of endoscopically confirmed gastric and duodenal ulcers. Her symptoms have been unresponsive to proton pump inhibitors and histamine receptor antagonists in the past. Results for H. pylori infection are still pending. Which of the following changes is expected in the patient's duodenum, given her peptic ulcer disease?
Q7
A 72-year-old female is brought to the emergency department after being found unresponsive in her garage with an open bottle of unmarked fluid. She is confused and is unable to answer questions on arrival. Her medical history is significant for Alzheimer disease, but her family says she has no medical comorbidities. Serum analysis of this patient's blood shows a pH of 7.28 with a high anion gap. The electrolyte that is most likely significantly decreased in this patient follows which of the following concentration curves across the proximal tubule of the kidney?
Q8
A healthy 20-year-old male college student attempts to climb Mount Everest and travels to the Tibetan plateau by plane. Upon landing, he feels increasingly dizzy and fatigued. He notices that he is breathing faster than usual. What is the initial stimulus for the most likely acid-base disorder?
Q9
A 32-year-old man is brought to the emergency department after he was found unresponsive on the street. Upon admission, he is lethargic and cyanotic with small, symmetrical pinpoint pupils. The following vital signs were registered: blood pressure of 100/60 mm Hg, heart rate of 70/min, respiratory rate of 8/min, and a body temperature of 36.0°C (96.8°F). While being assessed and resuscitated, a sample for arterial blood gas (ABG) analysis was taken, in addition to the following biochemistry tests:
Laboratory test
Serum Na+ 138 mEq/L
Serum Cl- 101 mEq/L
Serum K+ 4.0 mEq/L
Serum creatinine (SCr) 0.58 mg/dL
Which of the following values would you most likely expect to see in this patient’s ABG results?
Q10
A 67-year-old man presents to his primary care physician because of weak urine stream, and increasing difficulty in initiating and stopping urination. He also reports of mild generalized body aches and weakness during the day. The past medical history includes diabetes mellitus type 2 for 35 years and essential hypertension for 19 years. The medication list includes metformin, vildagliptin, and enalapril. The vital signs include: temperature 36.7°C (98.1°F), blood pressure 151/82 mm Hg, and pulse 88/min. The physical examination is remarkable for markedly enlarged, firm prostate without nodules. The laboratory test results are as follows:
Serum sodium 142 mEq/L
Serum potassium 5.7 mEq/L
Serum chloride 115 mEq/L
Serum bicarbonate 17 mEq/L
Serum creatinine 0.9 mg/dL
Arterial pH 7.31
Urine pH 5.3
Urine sodium 59 mEq/L
Urine potassium 6.2 mEq/L
Urine chloride 65 mEq/L
Which of the following most likely explains the patient’s findings?
Acid-base balance US Medical PG Practice Questions and MCQs
Question 1: A 44-year-old Caucasian male complains of carpopedal spasms, peri-oral numbness, and paresthesias of the hands and feet. His wife also mentions that he had a seizure not too long ago. His past surgical history is significant for total thyroidectomy due to papillary thyroid carcinoma. They then realized all of the symptoms occurred after the surgery. Which of the following would be present in this patient?
Explanation: ***Chvostek sign, QT prolongation, decreased PTH, decreased serum calcium, increased serum phosphate***
- The patient's symptoms of carpopedal spasms, peri-oral numbness, paresthesias, and seizures following a **total thyroidectomy** are classic signs of **hypocalcemia** due to **hypoparathyroidism**. This would lead to a **decreased PTH** level, which in turn causes **decreased serum calcium** and **increased serum phosphate** due to impaired renal phosphate excretion.
- **Hypocalcemia** characteristically causes **QT prolongation** on EKG and can manifest as the **Chvostek sign** (facial muscle twitching when tapping the facial nerve).
*Chvostek sign, QT prolongation, increased PTH, decreased serum calcium, decreased serum phosphate*
- This option incorrectly states **increased PTH**. The symptoms are due to iatrogenic hypoparathyroidism following thyroidectomy, which results in **decreased PTH** production.
- While **decreased serum calcium** and **Chvostek sign** are consistent, the PTH and phosphate levels described here are characteristic of **pseudohypoparathyroidism** or vitamin D deficiency, not post-surgical hypoparathyroidism.
*Chvostek sign, QT shortening, increased PTH, increased serum calcium, increased serum phosphate*
- **QT shortening** is typically associated with **hypercalcemia**, not hypocalcemia, and the patient's symptoms are indicative of hypocalcemia.
- **Increased serum calcium** and **increased PTH** would point towards primary hyperparathyroidism, which is the opposite of the clinical picture presented.
*Chvostek sign, QT shortening, decreased PTH, decreased serum calcium, increased serum phosphate*
- This option incorrectly states **QT shortening**. **Hypocalcemia** is known to cause **QT prolongation**, not shortening.
- While other findings like **decreased PTH**, **decreased serum calcium**, and **increased serum phosphate** are consistent with post-thyroidectomy hypoparathyroidism, the erroneous QT interval change makes this option incorrect.
*Chvostek sign, QT prolongation, decreased PTH, increased serum calcium, decreased serum phosphate*
- This option incorrectly states **increased serum calcium**. The symptoms of carpopedal spasms and paresthesias are classic manifestations of **hypocalcemia**.
- Additionally, **decreased serum phosphate** in the setting of decreased PTH would be unusual; **hypoparathyroidism** typically leads to **hyperphosphatemia** due to reduced renal phosphate excretion.
Question 2: A 41-year-old man presents to urgent care with a 1-week history of severe diarrhea. He says that he has been having watery stools every 2-3 hours. The stools do not contain blood and do not float. On presentation, he is observed to have significant facial flushing, and laboratory tests reveal the following:
Serum:
Na+: 137 mEq/L
K+: 2.7 mEq/L
Cl-: 113 mEq/L
HCO3-: 14 mEq/L
A computed tomography scan reveals a small intra-abdominal mass. Staining of this mass would most likely reveal production of which of the following?
A. Insulin
B. Glucagon
C. Vasoactive intestinal peptide (Correct Answer)
D. Somatostatin
E. Gastrin
Explanation: ***Vasoactive intestinal peptide***
- The patient's presentation with **severe watery diarrhea**, **hypokalemia**, **metabolic acidosis** (low HCO3-), and **facial flushing** in the presence of an **intra-abdominal mass** is highly indicative of a **VIPoma**.
- VIPomas are neuroendocrine tumors that secrete large amounts of **vasoactive intestinal peptide (VIP)**, which stimulates intestinal fluid secretion and inhibits absorption, leading to characteristic symptoms.
*Insulin*
- **Insulinomas** typically cause symptoms related to **hypoglycemia** (e.g., sweating, palpitations, confusion), which are not described in this patient.
- While insulinomas can be associated with an intra-abdominal mass, the patient's symptoms are inconsistent with excessive insulin production.
*Glucagon*
- **Glucagonomas** classically present with a syndrome including **necrolytic migratory erythema**, **diabetes mellitus**, and weight loss, along with diarrhea in some cases.
- The distinct skin rash and hyperglycemia are absent in this patient's presentation.
*Somatostatin*
- **Somatostatinomas** are often associated with a triad of **diabetes mellitus**, **cholelithiasis**, and **steatorrhea**, and sometimes hypochlorhydria.
- The patient's symptoms of severe watery diarrhea and flushing are not typical of somatostatin overproduction.
*Gastrin*
- **Gastrinomas** (Zollinger-Ellison syndrome) cause severe **peptic ulcer disease** due to excessive gastric acid secretion, often leading to abdominal pain and chronic diarrhea.
- While diarrhea can occur, the prominent hypokalemia, metabolic acidosis, and flushing point away from a gastrinoma as the primary diagnosis.
Question 3: A 67-year-old woman presents to the Emergency Department complaining of weakness and fatigue. She says she caught a “stomach bug” and has not been able to eat anything without vomiting for three days. Past medical history is significant for hyperlipidemia. She takes atorvastatin and a multivitamin daily, except for the last two days due to nausea. Today her heart rate is 106/min, respiratory rate is 16/min, temperature is 37.6°C (99.7°F) and blood pressure of 110/70 mm Hg. On physical examination, her oral mucosa is dry and she looks pale and uncomfortable. She is admitted for care and administered ondansetron. An intravenous infusion of normal saline is also initiated. An arterial blood gas is collected. Which of the following results is expected to be seen in this patient?
A. pH: 7.48, pCO2: 44 mm Hg, HCO3-: 29 mEq/L (Correct Answer)
B. pH: 7.49, pCO2: 33 mm Hg, HCO3-: 18 mEq/L
C. pH: 7.31, pCO2: 62 mm Hg, HCO3-: 27 mEq/L
D. pH: 7.30, pCO2: 36 mm Hg, HCO3-: 17 mEq/L
E. pH: 7.36, pCO2: 42 mm Hg, HCO3-: 22 mEq/L
Explanation: ***pH: 7.48, pCO2: 44 mm Hg, HCO3-: 29 mEq/L***
- The patient's prolonged vomiting leads to a loss of **gastric acid (HCl)**, resulting in an increase in serum bicarbonate (**metabolic alkalosis**), which is reflected by the elevated pH (7.48) and HCO3- (29 mEq/L).
- The pCO2 (44 mm Hg) is slightly elevated above normal (40 mm Hg), indicating the expected **respiratory compensation** for metabolic alkalosis (hypoventilation to retain CO2 and normalize pH).
*pH: 7.49, pCO2: 33 mm Hg, HCO3-: 18 mEq/L*
- This option indicates a **respiratory alkalosis** with partial metabolic compensation, characterized by a high pH, low pCO2, and low HCO3-.
- The patient's condition of prolonged vomiting would not lead to an acidic (low HCO3-) or hyperventilatory (low pCO2) state.
*pH: 7.31, pCO2: 62 mm Hg, HCO3-: 27 mEq/L*
- This result suggests **respiratory acidosis** with partial metabolic compensation, indicated by a low pH, high pCO2, and slightly elevated HCO3-.
- Vomiting primarily causes metabolic alkalosis due to loss of acid, not respiratory acidosis.
*pH: 7.30, pCO2: 36 mm Hg, HCO3-: 17 mEq/L*
- This option points to **metabolic acidosis** with a low pH and low HCO3-, and a near-normal pCO2, indicating minimal respiratory compensation.
- While dehydration can occur, the primary acid-base disturbance from prolonged vomiting is a loss of acid, leading to alkalosis, not acidosis.
*pH: 7.36, pCO2: 42 mm Hg, HCO3-: 22 mEq/L*
- These values fall within the **normal range**, implying no significant acid-base disturbance.
- The patient's symptoms of prolonged vomiting and dehydration would inevitably lead to an acid-base imbalance.
Question 4: A 22-year-old woman presents to the physician due to lightheadedness. Earlier in the day, she had her first job interview since graduating from college 3 months ago. While waiting outside the interviewer’s office, she began to feel nervous and started breathing really fast. She then felt as if she was going to faint. She excused herself from the interview, and requested a friend to drive her to the clinic. Which of the following is responsible for her symptoms?
A. Increased arterial pO2
B. Decreased arterial pH
C. Decreased arterial pCO2 (Correct Answer)
D. Increased plasma lactic acid
E. Vagus nerve stimulation
Explanation: ***Decreased arterial pCO2***
- The patient's **lightheadedness** and sensation of fainting, coupled with **rapid breathing** during a stressful situation, are classic signs of **hyperventilation syndrome**.
- Rapid breathing leads to excessive elimination of carbon dioxide, causing **respiratory alkalosis** and a decrease in arterial pCO2.
- Low pCO2 causes **cerebral vasoconstriction**, reducing cerebral blood flow and leading to **lightheadedness and presyncope**.
*Increased arterial pO2*
- While hyperventilation can slightly increase arterial pO2, this increase generally has **minimal physiological impact** and does not cause lightheadedness or syncope.
- The primary physiological consequence in this scenario is due to the **alteration of CO2 levels**, not O2.
*Decreased arterial pH*
- This symptom describes **acidosis**, which would typically result from conditions like hypoventilation (leading to CO2 retention) or metabolic disturbances.
- The patient's rapid breathing indicates **respiratory alkalosis**, which involves an **increased arterial pH**, not decreased.
*Increased plasma lactic acid*
- While stress can induce some **anaerobic metabolism**, leading to lactic acid production, the primary and most immediate cause of symptoms in acute hyperventilation is not lactic acidosis.
- **Lactic acidosis** is associated with more severe metabolic disturbances or sustained intense physical exertion, not acute anxiety-related hyperventilation.
*Vagus nerve stimulation*
- **Vagal stimulation** can lead to symptoms like lightheadedness and fainting by causing **bradycardia** and **vasodilation** (vasovagal syncope).
- However, this is typically associated with specific triggers and leads to a direct cardiovascular response rather than the **rapid breathing** pattern seen in this patient, which points to a respiratory cause.
Question 5: A 54-year-old man presents with 3 days of non-bloody and non-bilious emesis every time he eats or drinks. He has become progressively weaker and the emesis has not improved. He denies diarrhea, fever, or chills and thinks his symptoms may be related to a recent event that involved sampling many different foods. His temperature is 97.5°F (36.4°C), blood pressure is 133/82 mmHg, pulse is 105/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam is notable for a weak appearing man with dry mucous membranes. His abdomen is nontender. Which of the following laboratory changes would most likely be seen in this patient?
A. Metabolic alkalosis and hyperkalemia
B. Non-anion gap metabolic acidosis and hypokalemia
C. Respiratory acidosis and hyperkalemia
D. Metabolic alkalosis and hypokalemia (Correct Answer)
E. Anion gap metabolic acidosis and hypokalemia
Explanation: ***Metabolic alkalosis and hypokalemia***
- Persistent **vomiting** leads to the loss of **gastric acid** (HCl) and **potassium**, resulting in **metabolic alkalosis** and **hypokalemia**. The loss of HCl directly removes acid from the body, and the subsequent renal compensation to conserve volume often exacerbates potassium loss.
- The patient's presentation with **dry mucous membranes**, increased heart rate (pulse 105/min), and persistent non-bloody, non-bilious emesis suggests significant volume depletion and electrolyte imbalances consistent with prolonged vomiting.
*Metabolic alkalosis and hyperkalemia*
- While metabolic alkalosis is expected due to gastric acid loss from vomiting, **hyperkalemia** is unlikely. Vomiting typically causes **hypokalemia** due to direct potassium loss and renal compensation mechanisms.
- The body attempts to compensate for volume depletion, leading to increased activity of the **renin-angiotensin-aldosterone system**, which promotes potassium excretion in the urine.
*Non-anion gap metabolic acidosis and hypokalemia*
- **Metabolic acidosis** is characterized by a decrease in blood pH and bicarbonate; however, profuse vomiting of gastric contents primarily leads to **alkalosis** due to the loss of hydrogen ions.
- **Non-anion gap metabolic acidosis** is usually seen in conditions involving bicarbonate loss from the kidneys or gut (e.g., diarrhea, renal tubular acidosis), not vomiting.
*Respiratory acidosis and hyperkalemia*
- **Respiratory acidosis** results from hypoventilation, leading to an increase in blood CO2, which is not suggested by the patient's normal respiratory rate and oxygen saturation.
- Profuse vomiting causes a loss of gastric acid and can lead to compensatory **hypoventilation** to retain CO2 (acid), but this is a secondary response to metabolic alkalosis, and primary respiratory acidosis is not the underlying issue.
*Anion gap metabolic acidosis and hypokalemia*
- **Anion gap metabolic acidosis** typically occurs with the accumulation of unmeasured acids (e.g., lactic acidosis, ketoacidosis, renal failure, poisoning), which is not indicated by the patient's symptoms.
- While **hypokalemia** is consistent with vomiting, the primary acid-base disturbance from prolonged emesis is metabolic alkalosis, not acidosis.
Question 6: A 56-year-old woman with a longstanding history of gastroesophageal reflux presents for follow-up evaluation of endoscopically confirmed gastric and duodenal ulcers. Her symptoms have been unresponsive to proton pump inhibitors and histamine receptor antagonists in the past. Results for H. pylori infection are still pending. Which of the following changes is expected in the patient's duodenum, given her peptic ulcer disease?
A. Proliferation of secretin-releasing S cells
B. Increased secretions from crypts of Lieberkühn
C. Increased glucose-dependent insulinotropic peptide (GIP) release from K cells
D. Expansion of gastrointestinal lymphoid tissue
E. Hyperplasia of submucosal bicarbonate-secreting glands (Correct Answer)
Explanation: ***Hyperplasia of submucosal bicarbonate-secreting glands***
- The duodenum attempts to protect itself from excessive acid due to gastric and duodenal ulcers by increasing **bicarbonate secretion**.
- **Bicarbonate-secreting glands (Brunner's glands)** in the duodenum undergo hyperplasia to neutralize the acidic chyme entering from the stomach, especially when peptic ulcers are present.
*Proliferation of secretin-releasing S cells*
- While secretin is released in response to acid in the duodenum and stimulates bicarbonate secretion, **S cell proliferation** itself is not a primary expected histological change in peptic ulcer disease.
- The main adaptation is the increased functional capacity of bicarbonate-secreting glands, rather than an increase in the number of secretin-producing cells.
*Increased secretions from crypts of Lieberkühn*
- The **crypts of Lieberkühn** are involved in fluid and electrolyte secretion, as well as cell turnover in the small intestine.
- While they contribute to the intestinal environment, their primary role is not to counteract the high acid load seen in peptic ulcer disease, and their secretions are not predominantly bicarbonate-rich.
*Increased glucose-dependent insulinotropic peptide (GIP) release from K cells*
- **GIP** is released from K cells in response to glucose and fat in the duodenum, stimulating insulin secretion.
- Its release is primarily linked to nutrient absorption and glucose homeostasis, not a direct compensatory mechanism for acid-induced peptic ulcer disease.
*Expansion of gastrointestinal lymphoid tissue*
- **Gastrointestinal lymphoid tissue (GALT)**, such as Peyer's patches, is involved in immune surveillance in the intestine.
- While chronic inflammation can lead to lymphoid hyperplasia, it is not a direct or primary protective mechanism against acid per se in peptic ulcer disease; rather, it indicates an immune response, which might occur with H. pylori infection but isn't the duodenum's main anti-acid adaptation.
Question 7: A 72-year-old female is brought to the emergency department after being found unresponsive in her garage with an open bottle of unmarked fluid. She is confused and is unable to answer questions on arrival. Her medical history is significant for Alzheimer disease, but her family says she has no medical comorbidities. Serum analysis of this patient's blood shows a pH of 7.28 with a high anion gap. The electrolyte that is most likely significantly decreased in this patient follows which of the following concentration curves across the proximal tubule of the kidney?
A. Curve C
B. Curve E
C. Curve B
D. Curve A
E. Curve D (Correct Answer)
Explanation: ***Curve D***
- The patient presents with **high anion gap metabolic acidosis**, which, in the context of an unknown fluid ingestion, is highly suggestive of **methanol** or **ethylene glycol poisoning**. These toxins are metabolized into toxic acids (**formic acid** from methanol; **glycolic acid, oxalic acid** from ethylene glycol).
- These toxic acid anions displace **bicarbonate** (HCO3-) in the blood to maintain electroneutrality, leading to a **decreased bicarbonate level**. Curve D represents bicarbonate, which is largely reabsorbed in the proximal tubule but significantly reduced in this scenario.
*Curve C*
- This curve likely represents a substance like **phosphate** or **urea**, which is partially reabsorbed and partially excreted.
- While phosphate levels can be affected in various metabolic derangements, it's not the primary electrolyte significantly decreased in **high anion gap metabolic acidosis** from toxic alcohol ingestion.
*Curve E*
- This curve typically represents a substance that is **filtered and then minimally reabsorbed** or even secreted, such as **creatinine** or **potassium** when excess is being excreted.
- **Potassium** levels can be variable in acidosis but are not typically the most significantly decreased electrolyte in this poisoning scenario.
*Curve B*
- This curve would normally represent an electrolyte that is **highly reabsorbed** in the proximal tubule, with very little remaining.
- This might represent substances like **glucose** (under normal conditions) or **amino acids**, which are not the primary electrolyte affected in this case.
*Curve A*
- This curve represents a substance that is **freely filtered** and then **neither reabsorbed nor secreted** significantly in the proximal tubule, such as **inulin**.
- This pattern does not correspond to an electrolyte whose level would be significantly decreased due to high anion gap metabolic acidosis.
Question 8: A healthy 20-year-old male college student attempts to climb Mount Everest and travels to the Tibetan plateau by plane. Upon landing, he feels increasingly dizzy and fatigued. He notices that he is breathing faster than usual. What is the initial stimulus for the most likely acid-base disorder?
A. Decreased partial pressure of alveolar oxygen (Correct Answer)
B. Undiagnosed atrial septal defect
C. Increasing arterial partial pressure of carbon dioxide
D. Worsened diffusion limitation of oxygen
E. Hypoxic pulmonary vasoconstriction
Explanation: ***Decreased partial pressure of alveolar oxygen***
- Upon rapid ascent to high altitude (like the Tibetan plateau), the ambient atmospheric pressure decreases, leading to a significant drop in the **partial pressure of inspired oxygen (PiO2)**.
- This reduction in PiO2 directly causes a decrease in the **partial pressure of alveolar oxygen (PAO2)**, which is the primary stimulus for activation of peripheral chemoreceptors, leading to hyperventilation and a respiratory alkalosis.
*Undiagnosed atrial septal defect*
- An atrial septal defect (ASD) would cause a **left-to-right shunt** in a healthy young adult, not typically presenting with acute dizziness and fatigue immediately upon high-altitude exposure.
- While an ASD can lead to cyanosis and dyspnea with exertion, it would not be the initial stimulus for the observed hyperventilation response to high altitude.
*Increasing arterial partial pressure of carbon dioxide*
- An increasing **arterial partial pressure of carbon dioxide (PaCO2)** would stimulate central chemoreceptors and increase ventilation, but it is not the initial trigger in this scenario.
- In response to **hypoxia** at high altitude, the body *hyperventilates*, which would lead to a *decrease* in PaCO2, not an increase.
*Worsened diffusion limitation of oxygen*
- **Diffusion limitation** of oxygen refers to impaired gas exchange across the alveolar-capillary membrane, usually due to conditions like fibrosis or edema.
- While gas exchange can be affected at extreme altitudes, it is not the primary initial physiological trigger for the body's acute response (hyperventilation) in a healthy individual.
*Hypoxic pulmonary vasodilation*
- **Hypoxic pulmonary vasoconstriction** (not vasodilation) is a physiological response in the lungs where pulmonary arterioles constrict in areas of low oxygen, redirecting blood flow to better-ventilated areas.
- This mechanism aims to optimize V/Q matching and is a *response* to hypoxia, not the initial stimulus for the systemic acid-base derangement leading to symptoms like dizziness and increased breathing rate.
Question 9: A 32-year-old man is brought to the emergency department after he was found unresponsive on the street. Upon admission, he is lethargic and cyanotic with small, symmetrical pinpoint pupils. The following vital signs were registered: blood pressure of 100/60 mm Hg, heart rate of 70/min, respiratory rate of 8/min, and a body temperature of 36.0°C (96.8°F). While being assessed and resuscitated, a sample for arterial blood gas (ABG) analysis was taken, in addition to the following biochemistry tests:
Laboratory test
Serum Na+ 138 mEq/L
Serum Cl- 101 mEq/L
Serum K+ 4.0 mEq/L
Serum creatinine (SCr) 0.58 mg/dL
Which of the following values would you most likely expect to see in this patient’s ABG results?
A. pH: decreased, HCO3- : increased, Pco2: increased (Correct Answer)
B. pH: increased, HCO3- : decreased, Pco2: decreased
C. pH: decreased, HCO3- : decreased, Pco2: decreased
D. pH: increased, HCO3- : increased, Pco2: increased
E. pH: normal, HCO3- : increased, Pco2: increased
Explanation: ***pH: decreased, HCO3- : increased, Pco2: increased***
- The patient's **depressed respiratory rate** (8/min) indicates severe hypoventilation, leading to **CO2 retention** and subsequent **respiratory acidosis** (decreased pH, increased PaCO2).
- In **acute respiratory acidosis**, the body initiates immediate buffering, causing a **mild increase in HCO3-** (approximately 1 mEq/L per 10 mmHg rise in PaCO2). Over 3-5 days, renal compensation leads to more significant HCO3- retention, but in this acute presentation, some HCO3- elevation is expected from acute buffering mechanisms.
- The **decreased pH** indicates that compensation is incomplete, which is typical in the acute setting.
*pH: increased, HCO3- : decreased, Pco2: decreased*
- This pattern is characteristic of **respiratory alkalosis** (increased pH, decreased PaCO2) with metabolic compensation (decreased HCO3-), which would occur in hyperventilation, opposite to the patient's presentation.
- The patient's **slow respiratory rate** of 8/min directly contradicts the finding of decreased PaCO2.
*pH: decreased, HCO3- : decreased, Pco2: decreased*
- This suggests a **metabolic acidosis** (decreased pH, decreased HCO3-) with respiratory compensation (decreased PaCO2), typically seen in conditions like DKA or lactic acidosis.
- Although the pH is decreased, the patient's severe bradypnea (RR 8/min) indicates increased CO2 retention, not decreased CO2.
*pH: increased, HCO3- : increased, Pco2: increased*
- This combination of findings is indicative of **metabolic alkalosis** (increased pH, increased HCO3-) with respiratory compensation (increased PaCO2).
- This is inconsistent with the patient's pinpoint pupils, cyanosis, and **severe bradypnea**, which are classic signs of opioid overdose causing respiratory depression and acidosis, not alkalosis.
*pH: normal, HCO3- : increased, Pco2: increased*
- A normal pH despite increased HCO3- and PaCO2 indicates **fully compensated respiratory acidosis**, which requires days of renal compensation to develop.
- In this **acute, severe drug overdose** with profound respiratory depression, the body would not have sufficient time to achieve full compensation, thus the pH would remain low.
Question 10: A 67-year-old man presents to his primary care physician because of weak urine stream, and increasing difficulty in initiating and stopping urination. He also reports of mild generalized body aches and weakness during the day. The past medical history includes diabetes mellitus type 2 for 35 years and essential hypertension for 19 years. The medication list includes metformin, vildagliptin, and enalapril. The vital signs include: temperature 36.7°C (98.1°F), blood pressure 151/82 mm Hg, and pulse 88/min. The physical examination is remarkable for markedly enlarged, firm prostate without nodules. The laboratory test results are as follows:
Serum sodium 142 mEq/L
Serum potassium 5.7 mEq/L
Serum chloride 115 mEq/L
Serum bicarbonate 17 mEq/L
Serum creatinine 0.9 mg/dL
Arterial pH 7.31
Urine pH 5.3
Urine sodium 59 mEq/L
Urine potassium 6.2 mEq/L
Urine chloride 65 mEq/L
Which of the following most likely explains the patient’s findings?
A. Fanconi syndrome
B. Type 1 renal tubular acidosis
C. Type 2 renal tubular acidosis
D. Type 4 renal tubular acidosis (Correct Answer)
E. End-stage renal disease
Explanation: ***Type 4 renal tubular acidosis***
- The patient presents with **hyperkalemia** (serum potassium 5.7 mEq/L) and **non-anion gap metabolic acidosis** (serum bicarbonate 17 mEq/L, pH 7.31) with a relatively low urine pH (5.3). This combination is characteristic of **Type 4 RTA**, which often results from **hypoaldosteronism** or renal **aldosterone resistance**.
- His long-standing **diabetes mellitus** can cause damage to the **juxtaglomerular apparatus** or autonomic neuropathy, impairing renin and ultimately aldosterone secretion. Additionally, **enalapril** (an ACE inhibitor) contributes to reduced aldosterone levels, further exacerbating the condition.
*Fanconi syndrome*
- This syndrome is characterized by a generalized defect in the **proximal tubule**, leading to the loss of **glucose**, **amino acids**, **phosphate**, and **bicarbonate** in the urine.
- While it causes RTA, it typically presents with **hypokalemia** due to increased potassium excretion, which is contrary to this patient's **hyperkalemia**.
*Type 1 renal tubular acidosis*
- This type involves a defect in **distal tubule** hydrogen ion secretion, resulting in **metabolic acidosis** with a **high urine pH** (>5.5) despite systemic acidosis.
- Patients with Type 1 RTA typically present with **hypokalemia** due to increased potassium excretion, unlike the hyperkalemia seen in this patient.
*Type 2 renal tubular acidosis*
- This condition involves impaired **bicarbonate reabsorption** in the **proximal tubule**. Initially, it leads to metabolic acidosis with a high urine pH.
- However, once the filtered bicarbonate load falls below the compromised reabsorptive capacity, the urine pH can become acidic. Like Type 1 RTA, it is typically associated with **hypokalemia**.
*End-stage renal disease*
- While ESRD can cause metabolic acidosis and hyperkalemia due to severe reduction in GFR, the patient's **creatinine** (0.9 mg/dL) is within the normal range, indicating preserved renal function.
- Also, ESRD typically involves much broader complications of uremia beyond just electrolyte imbalances, which are not described here.