check your understanding 22, 23, 24, 25

Chronic bronchitis often leads to cor pulmonale because of a. increased pulmonary vascular resistance. b. left ventricular strain. c. ventricular hypoxia. d. hypervolemia.

a. increased pulmonary vascular resistance. Chronic bronchitis often leads to cor pulmonale as a result of increased pulmonary vascular resistance when right ventricular end-diastolic pressure increases. Ventricular hypoxia, left ventricular strain, and hypervolemia do not lead to cor pulmonale.

Cystic fibrosis is associated with a. chronic bronchitis. b. bronchiectasis. c. asthma. d. emphysema.

b. bronchiectasis. Fifty percent of cases of bronchiectasis are associated with cystic fibrosis. Cystic fibrosis is not associated with asthma, chronic bronchitis, or emphysema.

If an individual has a fully compensated metabolic acidosis, the blood pH is a. high. b. in the normal range. c. low. d. either high or low, depending on the type of compensation.

b. in the normal range. The blood pH is in the normal range if an individual has fully compensated for an acid-base imbalance. High blood pH indicates alkalosis. Low blood pH indicates uncompensated or partially compensated acidosis.

Respiratory acidosis is associated with a. increased pH. b. increased carbonic acid. c. hypokalemia. d. increased neuromuscular excitability.

b. increased carbonic acid. Respiratory acidosis causes an excess of carbonic acid that may be because of impaired gas exchange, inadequate neuromuscular function, and impairment of respiratory control of the brainstem. Hypokalemia is associated with alkalosis. Acidosis is associated with decreased neuromuscular excitability. Increased pH is associated with alkalosis; in acidosis the pH is low.

Effects of hypernatremia on the central nervous system typically include a. insomnia. b. hallucinations. c. confusion. d. excitation.

c. confusion. Hypernatremia causes osmotic shrinking of brain cells, which manifests as confusion or coma. Hypernatremia does not usually cause central nervous system excitation, insomnia, or hallucinations.

Which acid are the kidneys unable to excrete? a. Ammonia b. Metabolic c. Bicarbonate d. Carbonic

d. Carbonic The kidneys can excrete any acid except carbonic acid. The kidneys are able to excrete metabolic acids and ammonia. The kidneys are able to excrete bicarbonate, but bicarbonate is a base, not an acid.

Causes of hypomagnesemia include a. hyperphosphatemia. b. clinical dehydration. c. oliguric renal failure. d. chronic alcoholism.

d. chronic alcoholism. Hypomagnesemia is common with chronic alcoholism. Hyperphosphatemia causes hypocalcemia. Oliguric renal failure and clinical dehydration reduce magnesium excretion.

Respiratory acidosis may be caused by a. hyperventilation. b. tissue hypoxia. c. massive blood transfusion. d. hypoventilation.

d. hypoventilation. Hypoventilation causes carbonic acid retention and respiratory acidosis. Hyperventilation causes excretion of too much carbonic acid and respiratory alkalosis. The liver metabolizes the citrate in transfused blood into bicarbonate. Tissue hypoxia causes lactic acid production during anaerobic metabolism and metabolic acidosis.

A patient diagnosed with chronic compensated heart failure reports that, "My feet swell if I eat salt but I don't understand why" The nurse's best response is a. "Salt holds water in your blood and makes more pressure against your blood vessels, so fluid leaks out into your tissues and makes them swell." b. "Salt binds to the proteins in your blood and changes the osmotic pressure so more fluid can leak out and stay in the tissues, causing swelling." c. "Salt makes your blood vessels relax and the blood does not flow as fast, so some of it leaks into your tissues and makes swelling." d. "Gravity makes more pressure down by your feet than up at the top of your body, so more fluid leaks into your tissues at your feet and they swell."

a. "Salt holds water in your blood and makes more pressure against your blood vessels, so fluid leaks out into your tissues and makes them swell." Salt holds water in the ECV, thus increasing capillary hydrostatic pressure. Gravity leads to feet swelling, but it does not explain what the patient is asking. Salt does not cause vasodilation, nor does it bind to blood proteins and change osmotic pressure.

Which electrolyte imbalances cause increased neuromuscular excitability? a. Hypocalcemia and hypomagnesemia b. Hyperkalemia and hypophosphatemia c. Hypercalcemia and hypermagnesemia d. Hypokalemia and hyperphosphatemia

a. Hypocalcemia and hypomagnesemia Hypocalcemia and hypomagnesemia both cause increased neuromuscular excitability. Hypokalemia, hyperkalemia, hypophosphatemia, hypercalcemia, and hypermagnesemia do not cause increased neuromuscular excitability.

When exposed to inhaled allergens, a patient with asthma produces large quantities of a. IgE. b. IgG. c. IgM. d. IgA.

a. IgE. During an allergic response, plasma cells produce large quantities of IgE. IgG, IgA, and IgM are not part of the pathophysiology of asthma.

What age group has a larger volume of extracellular fluid than intracellular fluid? a. Infants b. Young adults c. Older adults d. Adolescents

a. Infants Infants have a larger volume of extracellular fluid than intracellular fluid. Adolescents, young adults, and older adults have a larger volume of intracellular fluid than extracellular fluid.

Viral pneumonia is characterized by a. a dry cough. b. exudative consolidation. c. a productive cough. d. significant ventilation-perfusion imbalance.

a. a dry cough. No exudative fluids are produced. Viral pneumonia does not produce exudates, so the cough is non-productive. Ventilation-perfusion imbalance does not usually occur in viral pneumonia.

Lack of α-antitrypsin in emphysema causes a. destruction of alveolar tissue. b. chronic mucous secretion and airway fibrosis. c. bronchoconstriction and airway edema. d. pulmonary edema and increased alveolar compliance.

a. destruction of alveolar tissue. Lack of α1-antitrypsin in emphysema causes destruction of alveolar tissue, as it is a protective enzyme that prohibits proteolytic breakdown of alveolar tissue. Lack of alpha1-antitrypsin does not cause chronic mucous secretion and airway fibrosis, pulmonary edema and increased alveolar compliance, or bronchoconstriction and airway edema.

Renal compensation for respiratory acidosis is evidenced by a. elevated bicarbonate ion concentration. b. elevated carbon dioxide. c. decreased bicarbonate ion concentration. d. decreased carbon dioxide.

a. elevated bicarbonate ion concentration. Elevated bicarbonate ion concentration is evidence of compensation for a respiratory acidosis. The lungs manage the carbon dioxide concentration. Elevated carbon dioxide is evidence of respiratory acidosis, not of compensation for it. Decreased bicarbonate ion concentration would make acidosis worse.

Asthma is categorized as a(n) a. obstructive pulmonary disorder. b. type of acute tracheobronchial obstruction. c. restrictive pulmonary disorder. d. infective pulmonary disorder.

a. obstructive pulmonary disorder. Asthma is an obstructive pulmonary disorder. Asthma is not a restrictive pulmonary disorder or a type of tracheobronchial obstruction. Although asthma can be associated with infection, it is not an infective pulmonary disorder.

Fully compensated respiratory acidosis is demonstrated by a. pH 7.36, PaCO2 55, HCO3- 36. b. pH 7.40, PaCO2 40, HCO3- 24. c. pH 7.45, PaCO2 40, HCO3- 28. d. pH 7.26, PaCO2 60, HCO3- 26.

a. pH 7.36, PaCO2 55, HCO3- 36. Compensation for respiratory acidosis involves conservation of HCO 3 - in the body; an HCO 3 - of 36 is a key finding; the normal pH (7.36) indicates compensation. Low HCO 3 - is not indicative of compensated respiratory acidosis. Low pH indicates no compensation or only partial compensation. Values of pH 7.40, PaCO 2 40, and HCO 3 - 24 are all normal.

A patient exhibiting respiratory distress as well as a tracheal shift should be evaluated for a. pneumothorax. b. pneumonia. c. pulmonary edema. d. pulmonary embolus.

a. pneumothorax. Pneumothorax leads to a tracheal shift to the side opposite the pneumothorax. Pneumonia, pulmonary edema, and pulmonary embolus do not lead to tracheal shift.

The person at highest risk for developing hypernatremia is a person who a. receives tube feedings because he or she is comatose after a stroke. b. has ectopic production of ADH from small cell carcinoma of the lung. c. is receiving IV 0.9% NaCl at a fast rate. d. self-administers a daily tap water enema to manage a partial bowel obstruction.

a. receives tube feedings because he or she is comatose after a stroke. Tube feedings are associated with hypernatremia as a result of intake of highly concentrated solution that causes the kidneys to excrete extra water to remove the solute load. Absorption of excessive water from daily tap water enemas would cause hyponatremia. Uncontrolled secretion of ADH causes renal retention of water that leads to hyponatremia. An IV solution of 0.9% NaCl (normal saline) is isotonic.

Emphysema results from destruction of alveolar walls and capillaries, which is because of a. release of proteolytic enzymes from immune cells. b. autoantibodies against pulmonary basement membrane. c. air trapping with resultant excessive alveolar pressure. d. excessive α1-antitrypsin.

a. release of proteolytic enzymes from immune cells. The pathologic changes leading to alveolar destruction are associated with the release of proteolytic enzymes from inflammatory cells such as neutrophils and macrophages. While air trapping occurs in emphysema, the destruction of alveolar walls and capillaries is because of release of proteolytic enzymes. Lack of α1-antitrypsin can result in emphysema. Autoantibodies are not involved in destruction of alveolar walls and capillaries in emphysema.

The fraction of total body water (TBW) volume contained in the intracellular space in adults is a. two thirds. b. one half. c. three fourths. d. one third.

a. two thirds. Approximately two thirds of TBW is contained inside the cells. Two thirds, not three fourths, of TBW is contained inside the cells. Two thirds, not one-half, of TBW is contained inside the cells. One-third of the TBW is extracellular in adults.

Emesis causes a. respiratory acidosis. b. metabolic alkalosis. c. respiratory alkalosis. d. metabolic acidosis.

b. metabolic alkalosis. Emesis causes metabolic alkalosis as the stomach is a major reservoir for acids. Emesis causes a metabolic acid-base imbalance as it is not related to the respiratory system. Emesis involves loss of gastric acid and fluid and causes an alkalotic disruption.

Which clinical manifestation is not likely the result of a tuberculosis infection? a. Night sweats b. Productive cough c. Cyanosis d. Low-grade fever

c. Cyanosis Cyanosis is not a typical manifestation of tuberculosis infection. A productive cough, low-grade fever, and night sweats are the typical manifestations of tuberculosis infection.

A 3-year-old is diagnosed with starvation ketoacidosis. What signs and symptoms should you anticipate in your assessment? a. Rapid, deep breathing, tremors, elevated blood pressure b. Slow, shallow breathing, belligerence, hyperexcitability c. Rapid, deep breathing, lethargy, abdominal pain d. Slow, shallow breathing, numbness and tingling around his mouth

c. Rapid, deep breathing, lethargy, abdominal pain Rapid, deep breathing, lethargy, and abdominal pain are clinical manifestations of metabolic acidosis and its respiratory compensation. The other answer options are not clinical manifestations of metabolic acidosis and its respiratory compensation.

Croup is characterized by a. an inability to cough. b. drooling, sore throat, and difficulty swallowing. c. a barking cough. d. a productive cough.

c. a barking cough. Croup is characterized by a barking cough with stridor. A productive cough is not characteristic of croup. Croup is associated with coughing. Drooling, sore throat, and difficulty swallowing are not characteristics of croup.

A known cause of hypokalemia is a. pancreatitis. b. oliguric renal failure. c. insulin overdose. d. hyperparathyroidism.

c. insulin overdose. Insulin overdose causes hypokalemia by shifting potassium into cells. Oliguric renal failure decreases electrolyte excretion. Pancreatitis causes fat malabsorption, which binds calcium and magnesium, but not potassium, in the gastrointestinal tract. Hyperparathyroidism regulates calcium, not potassium.

Vomiting of stomach contents or continuous nasogastric suctioning may predispose to development of a. metabolic acidosis. b. carbonic acid excess. c. metabolic acid deficit. d. carbonic acid deficit.

c. metabolic acid deficit. Gastric contents are rich in hydrochloric acid; loss of this through suctioning or vomiting leads to a metabolic acid deficit and alkalosis. Carbonic acid is related to the respiratory system. Vomiting produces metabolic alkalosis as a result of loss of acid-rich gastric contents, it does not increase carbonic acid.

What is the most likely explanation for a diagnosis of hypernatremia in an elderly patient receiving tube feeding? a. Kidney failure b. Excess of feedings c. Too much sodium in the feedings d. Inadequate water intake

d. Inadequate water intake Failure to provide adequate water when a patient is receiving tube feedings could result in hypernatremia. The feedings may have too much sodium, or the patient may be receiving too much feeding solution, but most likely the patient is not receiving enough water. Kidney failure is most likely not the cause of hypernatremia in this patient.

In individuals who have asthma, exposure to an allergen to which they are sensitized leads to which pathophysiologic event? a. Pulmonary edema and decreased alveolar compliance b. Mast cell degranulation that causes decreased surfactant c. Loss of alveolar elastin and premature closure of airways d. Inflammation, mucosal edema, and bronchoconstriction

d. Inflammation, mucosal edema, and bronchoconstriction In asthma, exposure to an allergen causes mast cell degranulation and release of inflammatory mediators that trigger airway inflammation, mucosal edema, and bronchoconstriction. In asthma, exposure to an allergen does not cause loss of alveolar elastin, pulmonary edema and decreased alveolar compliance, or decreased surfactant.

Obstructive sleep apnea would most likely be found in a patient diagnosed with a. poliomyelitis. b. myasthenia gravis. c. pneumonia. d. Pickwickian syndrome.

d. Pickwickian syndrome. Pickwickian syndrome is hypoventilation caused by obesity. Sleep apnea is often a problem in obese individuals. Obstructive sleep apnea is not likely to be found in a patient with myasthenia gravis, poliomyelitis, or pneumonia.

Widespread atelectasis, non-cardiogenic pulmonary edema, and diffuse, fluffy alveolar infiltrates on chest radiograph are characteristic of a. asthma. b. chronic obstructive pulmonary disease. c. cor pulmonale. d. acute respiratory distress syndrome.

d. acute respiratory distress syndrome. Acute respiratory distress syndrome is characterized by widespread atelectasis, non-cardiogenic pulmonary edema, and diffuse, fluffy alveolar infiltrates. These findings are not characteristics of chronic obstructive pulmonary disease, asthma, or cor pulmonale.

COPD leads to a barrel chest, because it causes a. muscle atrophy. b. prolonged inspiration. c. pulmonary edema. d. air trapping.

d. air trapping. Destruction of alveolar walls reduces lung elastic recoil, which allows airway collapse during exhalation. Air enters the alveoli during inhalation, but has difficulty escaping during exhalation. When air is trapped in the alveoli, residual volume increases, causing a barrel chest. Destruction of alveolar walls does not cause pulmonary edema, muscle atrophy, or prolonged inspiration.

Clinical manifestations of severe symptomatic hypophosphatemia are caused by a. excess proteins. b. hypocalcemia. c. renal damage. d. deficiency of ATP.

d. deficiency of ATP. Clinical manifestations of severe symptomatic hypophosphatemia are caused by a deficiency of ATP. Phosphate is an important component of ATP, which is the major source of energy for many cellular substances. Severe symptomatic hypophosphatemia does not cause excess protein accumulation, damage the kidneys, or cause hypocalcemia.

The patient who requires the most careful monitoring for development of metabolic acidosis is a patient who a. is in the diuretic phase of acute renal failure. b. has newly diagnosed Cushing syndrome. c. has had hypokalemia for over a week. d. has had diarrhea for over a week.

d. has had diarrhea for over a week. Diarrhea causes increased excretion of the base bicarbonate, which can lead to metabolic acidosis. Although the oliguric phase of acute renal failure causes metabolic acidosis, the diuretic phase does not, because the kidneys can still excrete metabolic acids. Hypokalemia is associated with metabolic alkalosis. Cushing syndrome is cortisol excess, which can cause metabolic alkalosis from increased renal excretion of hydrogen ions.

The body compensates for metabolic alkalosis by a. increasing bicarbonate ion excretion. b. decreasing arterial carbon dioxide. c. hyperventilation. d. hypoventilation.

d. hypoventilation. In metabolic alkalosis, the lungs compensate by hypoventilation to conserve CO 2 in the body. Decreasing arterial carbon dioxide would worsen metabolic alkalosis. The respiratory system compensates for metabolic acid and base disturbances; the lungs do not increase bicarbonate ion excretion. Hyperventilation would blow off CO 2 and cause respiratory alkalosis.

The finding of ketones in the blood suggests that a person may have a. respiratory alkalosis. b. respiratory acidosis. c. metabolic alkalosis. d. metabolic acidosis.

d. metabolic acidosis. Ketones are produced from breakdown of fat in the body as a result of starvation or lack of ability to utilize glucose in diabetes mellitus. Ketoacids in the blood indicate a very high ketone level in the body, which leads to metabolic acidosis. Ketonuria from high ketones in the blood would not indicate metabolic alkalosis. The respiratory system does not influence ketone level.

Two primary acid-base disorders that are present independently are referred to as a. metabolic acidosis. b. metabolic alkalosis. c. respiratory alkalosis. d. mixed acid-base imbalance.

d. mixed acid-base imbalance. Mixed acid-base disorders occur when two primary acid-base disorders are present independently. They may arise from simultaneous dysfunction of the respiratory system and kidneys. Metabolic acidosis is an acid disorder. Metabolic alkalosis and respiratory alkalosis are base disorders.

The process responsible for distribution of fluid between the interstitial and intracellular compartments is a. active transport. b. filtration. c. diffusion. d. osmosis.

d. osmosis. Distribution of fluid between the interstitial and intracellular compartments occurs by the process of osmosis. Filtration is responsible for the distribution of fluid between the vascular and interstitial compartments. Active transport moves ions across membranes, but does not move water. Diffusion involves movement of particles, not movement of water.

Accumulation of fluid in the pleural space is called a. an abscess. b. flail chest. c. pleurisy. d. pleural effusion.

d. pleural effusion. Pleural effusion is accumulation of fluid in the pleural space. A lung abscess is a circumscribed area of suppuration and lung tissue destruction. Pleurisy is inflammation of the pleura that often manifests with pain on inspiration, fever, and chills. Flail chest is the fracture of several consecutive ribs.

The hypersecretion of mucus resulting for chronic bronchitis is the result of a. reduced inflammation. b. destruction of alveolar septa. c. barrel chest. d. recurrent infection.

d. recurrent infection. Mucus provides a hospitable environment for bacterial colonization and recurrent infection. Destruction of alveolar septa and reduced inflammation are not complications of chronic bronchitis. Hypersecretion of mucus does not contribute to barrel chest.