Clinical Skills/Critical care Flashcards

Question

Is the Fab fragment of a monoclonal antibody directed against the IIb/IIIa receptor A. Abciximab (ReoPro) B. Aspirin C. Clopidogrel (Plavix) D. Eptifilbatide (Integrilin) E. Ticlopidine (Ticlid)

Answer 1

**A. Abciximab (ReoPro)** B. Aspirin C. Clopidogrel (Plavix) D. Eptifilbatide (Integrilin) E. Ticlopidine (Ticlid) ## Footnote Aspirin (B) inactivates cyclooxygenase, the enzyme that produces the precursor of thromboxane A2. Ticlopidine (E) and clopidogrel (C) are thienopyridines that inhibit P2Y12, a G-protein-coupled receptor for adenosine diphosphate (ADP) on the platelet. They are both prodrugs requiring conversion to the active metabolite. Thrombocytopenia and leukopenia occur less commonly with clopidogrel than with ticlopidine. Abciximab (ReoPro [A]) and eptifilbatide (Integrilin [D]) are the inhibitors of glycoprotein IIb/IIIa receptor, but the former is the Fab fragment of a humanized monoclonal antibody against the receptor, and the latter is a cyclic peptide inhibitor of the arginineglycine-aspartate (RGD) binding site on the receptor.

Answer 2

A. Abciximab (ReoPro) B. Aspirin C. Clopidogrel (Plavix) **D. Eptifilbatide (Integrilin)** E. Ticlopidine (Ticlid) ## Footnote Aspirin (B) inactivates cyclooxygenase, the enzyme that produces the precursor of thromboxane A2. Ticlopidine (E) and clopidogrel (C) are thienopyridines that inhibit P2Y12, a G-protein-coupled receptor for adenosine diphosphate (ADP) on the platelet. They are both prodrugs requiring conversion to the active metabolite. Thrombocytopenia and leukopenia occur less commonly with clopidogrel than with ticlopidine. Abciximab (ReoPro [A]) and eptifilbatide (Integrilin [D]) are the inhibitors of glycoprotein IIb/IIIa receptor, but the former is the Fab fragment of a humanized monoclonal antibody against the receptor, and the latter is a cyclic peptide inhibitor of the arginineglycine-aspartate (RGD) binding site on the receptor.

Answer 3

A. Abciximab (ReoPro) **B. Aspirin** C. Clopidogrel (Plavix) D. Eptifilbatide (Integrilin) E. Ticlopidine (Ticlid) ## Footnote Aspirin (B) inactivates cyclooxygenase, the enzyme that produces the precursor of thromboxane A2. Ticlopidine (E) and clopidogrel (C) are thienopyridines that inhibit P2Y12, a G-protein-coupled receptor for adenosine diphosphate (ADP) on the platelet. They are both prodrugs requiring conversion to the active metabolite. Thrombocytopenia and leukopenia occur less commonly with clopidogrel than with ticlopidine. Abciximab (ReoPro [A]) and eptifilbatide (Integrilin [D]) are the inhibitors of glycoprotein IIb/IIIa receptor, but the former is the Fab fragment of a humanized monoclonal antibody against the receptor, and the latter is a cyclic peptide inhibitor of the arginineglycine-aspartate (RGD) binding site on the receptor.

Answer 4

**A. Decreased fibrinogen** B. Increased fibrin degradation products C. Increased prothrombin time (PT) D. Increased partial thromboplastin time (PTT) E. Increased thrombin time (TT) ## Footnote Disseminated intravascular coagulation (DIC) is a consumptive coagulopathy characterized by widespread microvascular thrombosis, thrombocytopenia, and depletion of circulating coagulation factors. Thrombocytopenia, reduced fibrinogen levels, and prolongation of the prothrombin time (C) are the result of depletion, while the elevated D-dimer (B) is due to increased thrombolysis. While all of these abnormalities can be observed in DIC, decreased fibrinogen (A) correlates most closely with bleeding

Answer 5

A. Amount of oxygen dissolved in plasma B. Fractional concentration of inspired oxygen C. Partial pressure of oxygen in the blood **D. Percentage of hemoglobin that is bound to oxygen** E. Ratio of unbound to bound hemoglobin ## Footnote The oxygen saturation refers to the percentage of hemoglobin (Hb) that is bound to oxygen. In other words: Oxygen saturation 5 (Hb bound to oxygen / Total Hb).

Answer 6

**A. Hypoglycemia** B. Increased rate of lipolysis C. Increased Na 1 reabsorption D. Increased water reabsorption E. Metabolic alkalosis ## Footnote Hyperglycemia, not hypoglycemia (A), is one of the metabolic responses to trauma

Answer 7

A. II B. V **C. VIII** D. X E. XII ## Footnote Deficiency of factors II (A), V (B), or X (D) causes prolonged PT and PTT. A deficiency of factor XII (E) causes a prolonged PTT but no clinical bleeding. Only a factor VIII deficiency (C, hemophilia A) would cause a prolonged PTT, normal PT, and a bleeding disorder

Answer 8

A. Factor II **B. Factor VII** C. Factor VIII D. Factor IX E. Factor X ## Footnote The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The activated partial thromboplastin time (aPTT) measures the integrity of the intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C], X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C). Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT. Factor VII (B) has the shortest half-life of the options listed

Answer 9

A. Factor II **B. Factor VII** C. Factor VIII D. Factor IX E. Factor X ## Footnote The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The activated partial thromboplastin time (aPTT) measures the integrity of the intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C], X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C). Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT. Factor VII (B) has the shortest half-life of the options listed

Answer 10

A. Factor II B. Factor VII **C. Factor VIII** D. Factor IX E. Factor X ## Footnote The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The activated partial thromboplastin time (aPTT) measures the integrity of the intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C], X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C). Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT. Factor VII (B) has the shortest half-life of the options listed

Answer 11

A. Factor II B. Factor VII C. Factor VIII **D. Factor IX** E. Factor X ## Footnote The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The activated partial thromboplastin time (aPTT) measures the integrity of the intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C], X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C). Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT. Factor VII (B) has the shortest half-life of the options listed

Answer 12

A. Factor II B. Factor VII **C. Factor VIII** D. Factor IX E. Factor X ## Footnote The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The activated partial thromboplastin time (aPTT) measures the integrity of the intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C], X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C). Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT. Factor VII (B) has the shortest half-life of the options listed

Answer 13

A. Factor II B. Factor VII C. Factor VIII D. Factor IX **E. Factor X** ## Footnote The prothrombin time (PT) measures the integrity of the extrinsic and common pathways (factors VII [B], X [E], V, prothrombin, and fibrinogen). The activated partial thromboplastin time (aPTT) measures the integrity of the intrinsic and common pathways of coagulation (factors XII, XI, IX [D], VIII [C], X [E], and V). Hemophilia A is caused by a deficiency in factor VIII (C). Hemophilia B (Christmas disease) is caused by a factor IX (D) deficiency. The vitam in K–dependent factors are factors II (A), VII (B), IX (D), and X (E). A deficiency of factor II (A), V, or X (E) would result in prolongation of PT and PTT. Factor VII (B) has the shortest half-life of the options listed

Answer 14

A. Abnormal PT, PTT, and bleeding time B. Abnormal PT, normal PTT and bleeding time C. Normal PT, PTT, and bleeding time D. Normal PT, abnormal PTT and bleeding time **E. Hypercoagulable state** F. Normal PT, abnormal PTT, normal bleeding time ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 15

**A. Abnormal PT, PTT, and bleeding time** B. Abnormal PT, normal PTT and bleeding time C. Normal PT, PTT, and bleeding time D. Normal PT, abnormal PTT and bleeding time E. Hypercoagulable state F. Normal PT, abnormal PTT, normal bleeding time ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 16

A. Abnormal PT, PTT, and bleeding time B. Abnormal PT, normal PTT and bleeding time C. Normal PT, PTT, and bleeding time **D. Normal PT, abnormal PTT and bleeding time** E. Hypercoagulable state F. Normal PT, abnormal PTT, normal bleeding time ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 17

**A. Abnormal PT, PTT, and bleeding time** B. Abnormal PT, normal PTT and bleeding time C. Normal PT, PTT, and bleeding time D. Normal PT, abnormal PTT and bleeding time E. Hypercoagulable state F. Normal PT, abnormal PTT, normal bleeding time ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 18

A. Abnormal PT, PTT, and bleeding time **B. Abnormal PT, normal PTT and bleeding time** C. Normal PT, PTT, and bleeding time D. Normal PT, abnormal PTT and bleeding time E. Hypercoagulable state F. Normal PT, abnormal PTT, normal bleeding time ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 19

A. Abnormal PT, PTT, and bleeding time **B. Abnormal PT, normal PTT and bleeding time** C. Normal PT, PTT, and bleeding time D. Normal PT, abnormal PTT and bleeding time E. Hypercoagulable state F. Normal PT, abnormal PTT, normal bleeding time ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 20

A. Abnormal PT, PTT, and bleeding time B. Abnormal PT, normal PTT and bleeding time **C. Normal PT, PTT, and bleeding time** D. Normal PT, abnormal PTT and bleeding time E. Hypercoagulable state F. Normal PT, abnormal PTT, normal bleeding time ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 21

A. Abnormal PT, PTT, and bleeding time B. Abnormal PT, normal PTT and bleeding time C. Normal PT, PTT, and bleeding time D. Normal PT, abnormal PTT and bleeding time E. Hypercoagulable state **F. Normal PT, abnormal PTT, normal bleeding time** ## Footnote The two conditions listed that would cause prolongation of the PT, PTT, and bleeding time (A) are disseminated intravascular coagulation and dysfibrinogenemia. Factor VII deficiencies and nutritional factor deficiencies result in prolongation of the PT (vitam in K–dependent factors) without prolongation of the PTT or bleeding time (B). Factor XIII deficiency is not detected by routine laboratory screening and is characterized by normal PT, PTT, and bleeding times (C). von Willebrandʼs disease (vWD) is a disorder of platelet– vessel wall interaction, and the bleeding time is therefore prolonged. The PTT is also prolonged in vWD due to a concomitant factor XIII deficiency; the PT is normal (D). Antithrombin III is the major physiologic inhibitor of thrombin; its deficiency leads to unregulated thrombin formation, resulting in a hypercoagulable state (E). A factor VIII deficiency (hemophilia A) results in a normal PT, abnormal PTT, and normal bleeding time (F)

Answer 22

A. Increased anion gap metabolic acidosis B. Non-anion gap metabolic acidosis **C. Metabolic alkalosis** D. Respiratory acidosis E. Respiratory alkalosis ## Footnote An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion gap metabolic acidosis (B) and decreased extracellular uid volume due to decreased mineralocorticoid activity in the kidney. Conversely, in situations where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E) is the earliest abnormality and may be the only acid–base disorder in some patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Answer 23

A. Increased anion gap metabolic acidosis **B. Non-anion gap metabolic acidosis** C. Metabolic alkalosis D. Respiratory acidosis E. Respiratory alkalosis ## Footnote An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion gap metabolic acidosis (B) and decreased extracellular uid volume due to decreased mineralocorticoid activity in the kidney. Conversely, in situations where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E) is the earliest abnormality and may be the only acid–base disorder in some patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Answer 24

A. Increased anion gap metabolic acidosis B. Non-anion gap metabolic acidosis C. Metabolic alkalosis D. Respiratory acidosis **E. Respiratory alkalosis** ## Footnote An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion gap metabolic acidosis (B) and decreased extracellular uid volume due to decreased mineralocorticoid activity in the kidney. Conversely, in situations where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E) is the earliest abnormality and may be the only acid–base disorder in some patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Answer 25

A. Increased anion gap metabolic acidosis B. Non-anion gap metabolic acidosis C. Metabolic alkalosis **D. Respiratory acidosis** E. Respiratory alkalosis ## Footnote An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion gap metabolic acidosis (B) and decreased extracellular uid volume due to decreased mineralocorticoid activity in the kidney. Conversely, in situations where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E) is the earliest abnormality and may be the only acid–base disorder in some patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Answer 26

**A. Increased anion gap metabolic acidosis** B. Non-anion gap metabolic acidosis C. Metabolic alkalosis D. Respiratory acidosis E. Respiratory alkalosis ## Footnote An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion gap metabolic acidosis (B) and decreased extracellular uid volume due to decreased mineralocorticoid activity in the kidney. Conversely, in situations where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E) is the earliest abnormality and may be the only acid–base disorder in some patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Answer 27

A. Increased anion gap metabolic acidosis B. Non-anion gap metabolic acidosis **C. Metabolic alkalosis** D. Respiratory acidosis E. Respiratory alkalosis ## Footnote An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion gap metabolic acidosis (B) and decreased extracellular uid volume due to decreased mineralocorticoid activity in the kidney. Conversely, in situations where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E) is the earliest abnormality and may be the only acid–base disorder in some patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Answer 28

A. Increased anion gap metabolic acidosis B. Non-anion gap metabolic acidosis **C. Metabolic alkalosis** D. Respiratory acidosis E. Respiratory alkalosis ## Footnote An anion gap metabolic acidosis (A) is caused by fixed acids such as is seen in lactic acidosis, ketoacidosis, late salicylate toxicity, methanol poisoning, and ethylene glycol poisoning. A non-anion gap metabolic acidosis (B) is caused by decreased bicarbonate levels w ith a compensatory increase in chloride ions as is seen in diarrhea, early renal insufficiency, increased chloride load, and type II renal tubular acidosis. Addison’s disease is a form of primary adrenal insufficiency caused by the autoimmune-mediated destruction of the adrenal gland. Addison’s disease is associated with a hyperkalemic non-anion gap metabolic acidosis (B) and decreased extracellular uid volume due to decreased mineralocorticoid activity in the kidney. Conversely, in situations where there is increased mineralocorticoid activity, there is a tendency toward expansion of the extracellular fluid volume and hypokalemic metabolic alkalosis (C) as is seen in cases of Cushing’s disease and prim ary aldosteronism . Respiratory acidosis (D) is caused by hypoventilation and carbon dioxide retention as can be seen in myasthenia gravis. Respiratory alkalosis (E) is the earliest abnormality and may be the only acid–base disorder in some patients with salicylate overdose. Production of a mixture of endogenous acids, from a metabolic block, may later lead to metabolic acidosis.

Answer 29

A. (DBP 1 SBP)/2 B. DBP 1 (SBP 2 DBP)/2 C. DBP/2 1 SBP/3 **D. DBP 1 (SBP 2 DBP)/3** E. DBP/2 1 (SBP 2 DBP)/3 ## Footnote The mean arterial pressure can be estimated by adding the diastolic pressure to one-third of the pulse pressure. This formula assumes that diastole makes up one-third of the cardiac cycle.

Answer 30

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome) B. MEN type IIA (Sipple’s syndrome) **C. Both** D. Neither ## Footnote MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Answer 31

**A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)** B. MEN type IIA (Sipple’s syndrome) C. Both D. Neither ## Footnote MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Answer 32

**A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome)** B. MEN type IIA (Sipple’s syndrome) C. Both D. Neither ## Footnote MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Answer 33

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome) **B. MEN type IIA (Sipple’s syndrome)** C. Both D. Neither ## Footnote MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Answer 34

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome) **B. MEN type IIA (Sipple’s syndrome)** C. Both D. Neither ## Footnote MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Answer 35

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome) B. MEN type IIA (Sipple’s syndrome) C. Both **D. Neither** ## Footnote MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Answer 36

A. Multiple endocrine neoplasia (MEN) type I (Werner’s syndrome) B. MEN type IIA (Sipple’s syndrome) C. Both **D. Neither** ## Footnote MEN type I (Werner’s syndrome [A]) can be remembered as the “PPP” syndrome because it is characterized by parathyroid, pancreatic, and pituitary tumors. MEN type IIA (Sipple’s syndrom e [B]) is characterized by medullary thyroid carcinoma, pheochromocytoma, and tumors of the parathyroid glands. Rarely, pheochromocytomas may be seen in MEN type I (A). MEN type IIB (also know n as MEN type III) is associated w ith medullary thyroid carcinoma, pheochromocytoma, gastrointestinal and mucosal neuromas, and a marfanoid habitus

Answer 37

**A. Edema** B. Hypokalemia C. Increased diastolic blood pressure D. Metabolic alkalosis E. Suppression of plasma renin activity ## Footnote Hyperaldosteronism stimulates sodium reabsorption in the collecting ducts, causing renal potassium wasting and leading to a hypokalemic (B), hypochloremic metabolic alkalosis (D). Both primary and secondary hyperaldosteronism present with hypertension (C). Primary hyperaldosteronism , or Conn’s syndrome, is caused by autologous production of aldosterone either by an adrenal adenoma or adrenal hyperplasia and causes feedback inhibition of the renin-angiotensin system (E). Secondary hyperaldosteronism occurs as a result of increased tone in the renin-angiotensin system , usually caused by renal vascular disease. Secondary hyperaldosteronism usually responds to angiotensin-converting enzym e (ACE) inhibitors. In the absence of associated disorders, edema (A) is characteristically absent

Answer 38

A. FiO2 B. Oxygen saturation **C. PaCO2** D. Partial pressure of O2 in blood E. Tidal volume ## Footnote The partial pressure of arterial CO2 is directly related to the rate of CO2 production by the body and inversely related to the rate of alveolar ventilation. Of the choices listed, the adequacy of pulmonary ventilation is best assessed by PaCO2 (C).

Answer 39

A. Atrial brillation B. J-point elevation C. Peaked T wave **D. Prolonged QT interval** E. U wave ## Footnote Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Answer 40

A. Atrial brillation B. J-point elevation C. Peaked T wave D. Prolonged QT interval **E. U wave** ## Footnote Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Answer 41

A. Atrial brillation B. J-point elevation **C. Peaked T wave** D. Prolonged QT interval E. U wave ## Footnote Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Answer 42

A. Atrial brillation **B. J-point elevation** C. Peaked T wave D. Prolonged QT interval E. U wave ## Footnote Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with

Answer 43

**A. Atrial brillation** B. J-point elevation C. Peaked T wave D. Prolonged QT interval E. U wave ## Footnote Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Answer 44

A. Atrial brillation B. J-point elevation C. Peaked T wave **D. Prolonged QT interval** E. U wave ## Footnote Hyperthyroidism is associated with atrial fibrillation (A). Hypothermia is associated with pronounced waves at the QRS-ST interval known as J-waves (B) or Osborn waves. Hyperkalemia is associated with peaked T waves (C). A prolonged QT interval (D) can be seen with hypocalcemia and quinidine toxicity. Hypokalemia is associated with U waves (E)

Answer 45

A. Calcium is released from the muscle cell’s sarcoplasmic reticulum B. End-tidal pCO2 increases C. It is precipitated by the use of inhalational anesthetics. D. Treatment is with dantrolene. **E. Use of succinylcholine can help prevent it.** ## Footnote Malignant hyperthermia is an inherited disorder characterized by fever and rigidity that involves excessive release of calcium from the sarcoplasmic reticulum (A) of skeletal muscle precipitated by inhalational anesthetics (C) and depolarizing neuromuscular blocking agents such as succinylcholine (E is false). Diagnosis can be made by an early rise in endtidal CO2 (B) followed by muscle rigidity and fever that may progress to rhabdomyolysis and renal failure. The administration of dantrolene (D) is critical in the treatment of this disorder.

Answer 46

A. Clindamycin orally **B. Metronidazole (Flagyl) orally** C. Penicillin G orally D. Penicillin VK intravenously E. Vancomycin intravenously ## Footnote For the treatment of Clostridium difficile, a 10-day course of oral metronidazole (B) is the preferred treatment. Intravenous metronidazole can be used in patients who cannot receive oral medications. Oral vancomycin is also effective in the treatment of this infection, but it is a second-line agent in an effort to limit vancomycin use. Oral vancomycin is the treatment of choice in pregnant or lactating females. Intravenous vancomycin (E) is not effective in this setting

Answer 47

**A. Cardiac tamponade** B. Tension pneumothorax C. Both D. Neither ## Footnote Cardiac tamponade (A) occurs when pericardial flluid causes an increase in pericardial pressure and resultant decrease in ventricular filling. Physical exam in cardiac tamponade reveals jugular venous distention from increased atrial (venous) pressures, narrowing of the pulse pressure, and pulsus paradoxus (inspiratory drop in systolic pressure is . 15 m m Hg). In tension pneumothorax (B), intrathoracic pressure is elevated, w hich impairs ventricular filling, leading to increased atrial (venous) pressure.

Answer 48

A. Cardiac tamponade B. Tension pneumothorax **C. Both** D. Neither ## Footnote Cardiac tamponade (A) occurs when pericardial flluid causes an increase in pericardial pressure and resultant decrease in ventricular filling. Physical exam in cardiac tamponade reveals jugular venous distention from increased atrial (venous) pressures, narrowing of the pulse pressure, and pulsus paradoxus (inspiratory drop in systolic pressure is . 15 m m Hg). In tension pneumothorax (B), intrathoracic pressure is elevated, w hich impairs ventricular filling, leading to increased atrial (venous) pressure.

Answer 49

A. Cardiac tamponade B. Tension pneumothorax C. Both **D. Neither** ## Footnote Cardiac tamponade (A) occurs when pericardial flluid causes an increase in pericardial pressure and resultant decrease in ventricular filling. Physical exam in cardiac tamponade reveals jugular venous distention from increased atrial (venous) pressures, narrowing of the pulse pressure, and pulsus paradoxus (inspiratory drop in systolic pressure is . 15 m m Hg). In tension pneumothorax (B), intrathoracic pressure is elevated, w hich impairs ventricular filling, leading to increased atrial (venous) pressure.

Answer 50

A. Haemophilus influenzae B. Neisseria meningitidis C. Staphylococcus aureus D. Staphylococcus epidermidis **E. Streptococcus pneumoniae** ## Footnote Streptococcus pneumoniae (E) is the m ost common cause of meningitis in the adult population

Answer 51

**A. Coagulase-negative staphylococci** B. H. influenzae C. Pseudomonas species D. S. aureus E. S. pneumoniae ## Footnote Coagulase-negative staphylococci (S. epider midis [A]) are the m ost common cause of postoperative shunt infections

Answer 52

**A. Atelectasis/postoperative inflammation** B. Deep vein thrombosis C. Pneumonia D. Urinary tract infection E. Wound infection ## Footnote Fever is present in 15–40% of patients in the rst postoperative day, is usually self-limited, and is attributed to atelectasis or postoperative inflammation (A). Atelectasis as a cause of fever is somewhat controversial; some authors argue that it is not atelectasis itself, but instead, postoperative inflammation that is the cause of early postoperative fever. Deep vein thrombosis (B), urinary tract infection (D), pneum onia (C), and wound infection (E) are less likely to cause fever on the first postoperative day

Answer 53

A. Dobutamine B. Dopamine **C. Both** D. Neither ## Footnote Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect. Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine is much less than that of dobutamine. At high doses, dopamine stimulates a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and dobutamine stimulate b2 receptors, w hich causes some degree of peripheral vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Answer 54

**A. Dobutamine** B. Dopamine C. Both D. Neither ## Footnote Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect. Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine is much less than that of dobutamine. At high doses, dopamine stimulates a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and dobutamine stimulate b2 receptors, w hich causes some degree of peripheral vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Answer 55

A. Dobutamine B. Dopamine C. Both **D. Neither** ## Footnote Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect. Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine is much less than that of dobutamine. At high doses, dopamine stimulates a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and dobutamine stimulate b2 receptors, w hich causes some degree of peripheral vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Answer 56

A. Dobutamine B. Dopamine C. Both **D. Neither** ## Footnote Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect. Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine is much less than that of dobutamine. At high doses, dopamine stimulates a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and dobutamine stimulate b2 receptors, w hich causes some degree of peripheral vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock.

Answer 57

A. Dobutamine **B. Dopamine** C. Both D. Neither ## Footnote Dobutamine (A) is a strong b1 receptor agonist and a weak b2 receptor agonist. b1 stimulation causes a positive chronotropic and ionotropic effect. Dobutamine (A) is typically used in patients with decompensated systolic heart failure who also have a normal blood pressure. Dopamine (B) has dosedependent effects and, at a low dose, causes changes in renal and splanchnic blood flow as well as increased sodium excretion by the kidneys. At intermediate doses, dopamine (B) has a positive ionotropic and chronotropic effect via agonism of b1 receptors, although the ionotropic effect of dopamine is much less than that of dobutamine. At high doses, dopamine stimulates a receptors, causing systemic vasoconstriction and increased cardiac afterload, counteracting the increase in cardiac output. Both (C) dopamine and dobutamine stimulate b2 receptors, w hich causes some degree of peripheral vasodilatation (only at low doses for dopam ine). Norepinephrine is the firstline pressor of choice in septic shock

Answer 58

A. H. influenzae B. Listeria species C. N. meningitidis D. Staphylococci **E. Group B streptococci** ## Footnote Gram -negative bacilli (Escherichia coli) and group B streptococci (E) are the most common causes of neonatal meningitis, followed by Listeria (B). Streptococcus pneumoniae is the most common pathogen in the 4- to 12-week age range. H. influenzae (A) is most common in the 3-m onth to 3-year range. N. meningitidis (C) is the most common pathogen in children and young adults.

Answer 59

A. Cyanide accumulation may lead to metabolic acidosis B. The cyanide is reduced to thiocyanate in the liver C. The half-life of thiocyanate is 3 to 4 days **D. Thiocyanate is excreted in the gastrointestinal (GI) tract** E. With prolonged administration, accumulation of thiocyanate may cause an acute toxic psychosis ## Footnote Nitroprusside is reduced by smooth muscle, and nitrous oxide and cyanide are released. Cyanide is reduced to thiocyanate in the liver (B) by the action of liver rhodanese, and the thiocyanate is then excreted in the urine (D is false). The half-life of thiocyanate is 3 days (C) in patients w ith normal renal function. Prolonged adm inistration of nitroprusside or infusions at high doses may lead to accumulation of cyanide (causing lactic acidosis [A]) or accumulation of thiocyanate (causing psychosis [E]).

Answer 60

A. Acts almost exclusively on a -receptors B. Decreases SBP C. Increases DBP D. Increases peripheral vascular resistance (PVR) **E. Relaxes smooth muscle** ## Footnote Isoproterenol is a nonselective b-receptor agonist, acting almost exclusively on b receptors (A is false). It increases (or leaves unchanged) systolic blood pressure (B is false) and decreases diastolic blood pressure (C is false), and mean arterial pressure typically falls. It also decreases peripheral vascular resistance (D is false) and relaxes smooth muscle (E)

Answer 61

**A. Corrects the anemia** B. Corrects the defects in red blood cells C. Has no effect on red blood cell survival D. Should not be preceded by vaccination E. Should be perform ed before age 3 ## Footnote Splenectomy for hereditary spherocytosis leads to normal or near normal red blood cell (RBC) survival (B is false), correcting the anemia (A). Splenectomy does not correct the underlying defect in red cell membrane structure (B is false) and should be performed after age 4–5, when the risk of severe infections is lower (E is false). Patients undergoing splenectomy should be given a polyvalent pneumococcal vaccine several weeks before surgery to reduce the risk of bacterial sepsis (D is false).

Answer 62

**A. 12 hours** B. 5 days C. 17 days D. 42 days E. 2 years ## Footnote This question refers to the time line for wound healing associated with a surgical incision w ith approximated edges (healing by primary intention). In the first 12 hours of wound healing (A), epithelial cells migrate to the wound edge laying down basement membrane as they travel, fusing in the midline. Within 5 days (B) visible collagen synthesis has begun, the wound begins to gain tensile strength, and wound contraction begins. Within 6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Answer 63

A. 12 hours B. 5 days C. 17 days D. 42 days **E. 2 years** ## Footnote This question refers to the time line for wound healing associated with a surgical incision w ith approximated edges (healing by primary intention). In the first 12 hours of wound healing (A), epithelial cells migrate to the wound edge laying down basement membrane as they travel, fusing in the midline. Within 5 days (B) visible collagen synthesis has begun, the wound begins to gain tensile strength, and wound contraction begins. Within 6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Answer 64

A. 12 hours **B. 5 days** C. 17 days D. 42 days E. 2 years ## Footnote This question refers to the time line for wound healing associated with a surgical incision w ith approximated edges (healing by primary intention). In the first 12 hours of wound healing (A), epithelial cells migrate to the wound edge laying down basement membrane as they travel, fusing in the midline. Within 5 days (B) visible collagen synthesis has begun, the wound begins to gain tensile strength, and wound contraction begins. Within 6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Answer 65

A. 12 hours B. 5 days C. 17 days **D. 42 days** E. 2 years ## Footnote This question refers to the time line for wound healing associated with a surgical incision w ith approximated edges (healing by primary intention). In the first 12 hours of wound healing (A), epithelial cells migrate to the wound edge laying down basement membrane as they travel, fusing in the midline. Within 5 days (B) visible collagen synthesis has begun, the wound begins to gain tensile strength, and wound contraction begins. Within 6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Answer 66

A. 12 hours **B. 5 days** C. 17 days D. 42 days E. 2 years ## Footnote This question refers to the time line for wound healing associated with a surgical incision w ith approximated edges (healing by primary intention). In the first 12 hours of wound healing (A), epithelial cells migrate to the wound edge laying down basement membrane as they travel, fusing in the midline. Within 5 days (B) visible collagen synthesis has begun, the wound begins to gain tensile strength, and wound contraction begins. Within 6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Answer 67

A. 12 hours **B. 5 days** C. 17 days D. 42 days E. 2 years ## Footnote This question refers to the time line for wound healing associated with a surgical incision w ith approximated edges (healing by primary intention). In the first 12 hours of wound healing (A), epithelial cells migrate to the wound edge laying down basement membrane as they travel, fusing in the midline. Within 5 days (B) visible collagen synthesis has begun, the wound begins to gain tensile strength, and wound contraction begins. Within 6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Answer 68

A. 12 hours B. 5 days C. 17 days **D. 42 days** E. 2 years ## Footnote This question refers to the time line for wound healing associated with a surgical incision w ith approximated edges (healing by primary intention). In the first 12 hours of wound healing (A), epithelial cells migrate to the wound edge laying down basement membrane as they travel, fusing in the midline. Within 5 days (B) visible collagen synthesis has begun, the wound begins to gain tensile strength, and wound contraction begins. Within 6 weeks (42 days [D]), the wound reaches its maximum amount of total collagen and collagen synthesis slows considerably. The wound may not reach its greatest tensile strength for a full 2 years (E).

Answer 69

**A. Decrease in serum gastrin with secretin injection** B. Duodenal ulcer C. Duodenal wall gastrinoma D. Pancreatic gastrinoma E. Increased serum gastrin level ## Footnote Gastrinomas of the pancreas (D) or duodenal wall (C) cause an increase in the serum gastrin level (E). Peptic ulcer disease of the duodenum (B) caused by gastric acid production associated w ith a gastrinoma is known as the Zollinger-Ellison syndrome. Intravenous secretin increases serum gastrin in patients w ith a gastrinoma (A is false)

Answer 70

A. Type I (distal) renal tubular acidosis (RTA) B. Type II (proximal) RTA **C. Both** D. Neither ## Footnote Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A). Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA type I and t ype II result in non-anion gap metabolic acidosis.

Answer 71

A. Type I (distal) renal tubular acidosis (RTA) B. Type II (proximal) RTA C. Both **D. Neither** ## Footnote Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A). Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA type I and t ype II result in non-anion gap metabolic acidosis.

Answer 72

**A. Type I (distal) renal tubular acidosis (RTA)** B. Type II (proximal) RTA C. Both D. Neither ## Footnote Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A). Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA type I and t ype II result in non-anion gap metabolic acidosis.

Answer 73

**A. Type I (distal) renal tubular acidosis (RTA)** B. Type II (proximal) RTA C. Both D. Neither ## Footnote Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A). Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA type I and t ype II result in non-anion gap metabolic acidosis.

Answer 74

A. Type I (distal) renal tubular acidosis (RTA) **B. Type II (proximal) RTA** C. Both D. Neither ## Footnote Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A). Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA type I and t ype II result in non-anion gap metabolic acidosis.

Answer 75

A. Type I (distal) renal tubular acidosis (RTA) B. Type II (proximal) RTA **C. Both** D. Neither ## Footnote Type I (classic, or distal) renal tubular acidosis (RTA; A) is a hypokalemic, hyperchloremic metabolic acidosis caused by a selective defect in distal acidification (inability to lower urinary pH sufficiently in the distal nephron). The urinary pH is therefore inappropriately high in type I RTA (A) w ith a urine pH . 5.5. Nephrocalcinosis and nephrolithiasis are common in type I RTA (A). Type II (proximal) RTA (B) is a hyperchlorem ic, hypokalemic metabolic acidosis that is caused by a selective defect in proximal acidification—urine pH is usually acidic in periods of acidosis. Proximal RTA (B) is rare and usually found in patients with Fanconiʼs syndrome. The loss of 15% or more of filltered bicarbonate at a normal serum bicarbonate level is pathognomonic of RTA type II (B). Hyperkalemia is found in RTA type IV. Nephrocalcinosis is rare in RTA type II (B), and the urine pH is less than 5.5 in this type. Both (C) RTA type I and t ype II result in non-anion gap metabolic acidosis.

Answer 76

A. 5% B. 15% **C. 20%** D. 40% E. 60% ## Footnote For the average adult male, total body water (TBW) makes up approximately 60% (E) of body weight. Intracellular fluid makes up 60% (E) of the TBW and extracellular fluid makes up 40% (D) of the TBW. Extracellular fluid is com prised of interstitial fluid (75%), transcellular fluid (5%), and blood plasma (20% [C]).

Answer 77

A. Decrease in cardiac output **B. Increase in end-tidal pCO2** C. Increase in pulmonary artery pressure D. Increase in pulmonary vascular resistance E. Ventilation-perfusion mismatch ## Footnote Small air bubbles in the circulation can obstruct vascular flow. Venous air embolism can travel to the pulmonary circulation obstructing small vessels, causing pulmonary vasoconstriction, increased pulmonary vascular resistance (D), and, therefore, increased pulmonary artery pressure (C). Decreased pulmonary perfusion in areas of preserved ventilation results in a ventilation–perfusion m ism atch (E) leading to decreased end-tidal pCO2 (B is false). Air in the right atrium may lead to im paired cardiac filling, and therefore a reduction in cardiac output (A)

Answer 78

A. Auscultation of the chest w th a stethoscope B. End-tidal pCO2 C. End-tidal pN2 **D. Precordial Doppler** E. Pulm onary artery catheterization ## Footnote The most sensitive test for venous air embolism is transesophageal echocardiography. The most sensitive noninvasive monitor is the precordial Doppler (D).

Answer 79

A. Hyperacute T wave B. Q wave **C. ST depression** D. ST elevation E. T wave inversion ## Footnote Subendocardial ischemia is associated w ith ST depression (C) in the anterior leads. Transmural ischemia may lead to ST elevation (D) in the electrocardiogram (EKG).

Answer 80

**A. Decreased thyroid-stimulating hormone (TSH) and decreased free thyroxine (T4)** B. Decreased TSH and increased free T4 C. Decreased TSH and normal free T4 D. Increased TSH and decreased free T4 E. Increased TSH and increased free T4 ## Footnote Under normal conditions, thyrotropin-releasing hormone (TRH) is secreted by the hypothalamus, driving TSH production by the anterior pituitary and T4 production by the thyroid gland. Primary hypothyroidism is caused by dysfunction of the thyroid gland itself, and would result in increased levels of TSH and TRH w ith low T4 levels (D). In cases of secondary or tertiary hypothyroidism (pituitary or hypothalam ic dysfunction, respectively), there is a reduction in T4 levels as well as a reduction in TSH levels (A). To distinguish between secondary and tertiary hypothyroidism , a TRH challenge must be administered, and the TSH response measured (as TRH is diffcult to measure in vivo). In cases of tertiary hypothyroidism (hypothalam ic dysfunction), the pituitary gland will appropriately produce TSH in response to a TRH challenge. In secondary hypothyroidism (pituitary dysfunction), the pituitary gland will not produce TSH in response to a TRH challenge test. Choices B and E are hyperthyroid states (increased free T4). Choice C is a euthyroid state (norm al free T4). Note: Occasionally, in patients w ith hypothyroidism of pituitary or hypothalamic origin, serum TSH concentrations may be slightly increased rather than decreased if the form of TSH secreted is immunoactive but not bioactive

Answer 81

A. **Calcium** B. Cation-exchange resins C. Hemodialysis D. Insulin E. Sodium bicarbonate ## Footnote Calcium gluconate (A) infusion is useful for cardiotoxicity (antagonizes the membrane effects of potassium ), but it does not reduce serum potassium concentrations. Cation-exchange resins (B) such as Kayexalate enhance potassium clearance across the intestinal mucosa reducing serum potassium . Hemodialysis (C) is effective for reducing the serum potassium concentration in patients with renal failure. The administration of insulin (D) and dextrose causes a transient decrease in serum potassium levels by driving potassium into muscle cells. The administration of sodium bicarbonate (E) also causes a transient reduction in serum potassium levels via cellular shifts.

Answer 82

A. Respiratory acidosis B. Respiratory acidosis and metabolic acidosis C. Metabolic acidosis D. Metabolic acidosis and compensatory respiratory alkalosis **E. Respiratory alkalosis** F. Respiratory alkalosis and compensatory metabolic acidosis G. Uninterpretable ## Footnote The first step in the diagnosis of acid–base disorders is determining whether the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is normal, the direction change in PaCO2 identifies the nature of the respiratory disorder, and if the PaCO2 is normal, the change in pH identifies the nature of the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis, the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an expected pH value. If the pH is lower than expected, a metabolic acidosis is also present. If the pH is higher than expected, a metabolic alkalosis is also present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Answer 83

**A. Respiratory acidosis** B. Respiratory acidosis and metabolic acidosis C. Metabolic acidosis D. Metabolic acidosis and compensatory respiratory alkalosis E. Respiratory alkalosis F. Respiratory alkalosis and compensatory metabolic acidosis G. Uninterpretable ## Footnote The first step in the diagnosis of acid–base disorders is determining whether the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is normal, the direction change in PaCO2 identifies the nature of the respiratory disorder, and if the PaCO2 is normal, the change in pH identifies the nature of the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis, the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an expected pH value. If the pH is lower than expected, a metabolic acidosis is also present. If the pH is higher than expected, a metabolic alkalosis is also present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Answer 84

A. Respiratory acidosis B. Respiratory acidosis and metabolic acidosis C. Metabolic acidosis **D. Metabolic acidosis and compensatory respiratory alkalosis** E. Respiratory alkalosis F. Respiratory alkalosis and compensatory metabolic acidosis G. Uninterpretable ## Footnote The first step in the diagnosis of acid–base disorders is determining whether the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is normal, the direction change in PaCO2 identifies the nature of the respiratory disorder, and if the PaCO2 is normal, the change in pH identifies the nature of the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis, the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an expected pH value. If the pH is lower than expected, a metabolic acidosis is also present. If the pH is higher than expected, a metabolic alkalosis is also present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Answer 85

A. Respiratory acidosis B. Respiratory acidosis and metabolic acidosis C. Metabolic acidosis D. Metabolic acidosis and compensatory respiratory alkalosis E. Respiratory alkalosis **F. Respiratory alkalosis and compensatory metabolic acidosis** G. Uninterpretable ## Footnote The first step in the diagnosis of acid–base disorders is determining whether the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is normal, the direction change in PaCO2 identifies the nature of the respiratory disorder, and if the PaCO2 is normal, the change in pH identifies the nature of the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis, the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an expected pH value. If the pH is lower than expected, a metabolic acidosis is also present. If the pH is higher than expected, a metabolic alkalosis is also present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Answer 86

A. Respiratory acidosis **B. Respiratory acidosis and metabolic acidosis** C. Metabolic acidosis D. Metabolic acidosis and compensatory respiratory alkalosis E. Respiratory alkalosis F. Respiratory alkalosis and compensatory metabolic acidosis G. Uninterpretable ## Footnote The first step in the diagnosis of acid–base disorders is determining whether the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is normal, the direction change in PaCO2 identifies the nature of the respiratory disorder, and if the PaCO2 is normal, the change in pH identifies the nature of the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis, the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an expected pH value. If the pH is lower than expected, a metabolic acidosis is also present. If the pH is higher than expected, a metabolic alkalosis is also present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Answer 87

A. Respiratory acidosis B. Respiratory acidosis and metabolic acidosis **C. Metabolic acidosis** D. Metabolic acidosis and compensatory respiratory alkalosis E. Respiratory alkalosis F. Respiratory alkalosis and compensatory metabolic acidosis G. Uninterpretable ## Footnote The first step in the diagnosis of acid–base disorders is determining whether the primary abnormality is an acidosis or an alkalosis, which can be determined by the pH. If the pH and pCO2 are both abnormal, a change in the same direction indicates a primary metabolic disorder; a change in opposite directions indicates a primary respiratory disorder. If either the pH or pCO2 is normal, there must be a mixed m etabolic and respiratory disorder; if the pH is normal, the direction change in PaCO2 identifies the nature of the respiratory disorder, and if the PaCO2 is normal, the change in pH identifies the nature of the metabolic disorder. If there is a prim ary metabolic alkalosis or acidosis, the measured serum bicarbonate should be used to calculate the expected pCO2. If the measured pCO2 is higher than predicted by the formula, a respiratory acidosis is also present. If the measured pCO2 is lower than predicted by the formula, a respiratory alkalosis is present. If a primary respiratory acidosis or alkalosis is present, the measured PaCO2 should be used to calculate an expected pH value. If the pH is lower than expected, a metabolic acidosis is also present. If the pH is higher than expected, a metabolic alkalosis is also present. Formulas helpful in the calculation of simple acid–base disturbances are listed here

Answer 88

A. Cc/(Cc 2 Cv) B. (Ca 2 Cv)/Cv C. (Cv 2 Ca)/Cc **D. (Cc 2 Ca)/(Cc 2 Cv)** E. (Ca 1 Cv)/(Ca 1 Cc 1 Cv) ## Footnote The shunt fraction is the portion of the cardiac output that represents the intrapulmonary shunt (Qs/Qt). The shunt fraction can be estimated from measurements of the oxygen content of arterial blood, mixed venous blood, and pulmonary capillary blood. The shunt fraction is expressed as (Qs/Qt) 5 [(Cc 2 Ca )/(Cc 2 Cv)] (D). Since pulmonary capillary oxygen tension cannot be directly measured, it is estimated with the patient on 100% O2.

Answer 89

A. Blurred vision B. Decreased intestinal peristalsis C. Dry mouth D. Increased pulse **E. Increased sweating** ## Footnote High doses of atropine ( 10 mg) may cause a rapid, thready pulse (D); blurry vision (A); skin dryness and flushing; ataxia, hallucinations; dry mouth (C); delirium ; urinary retention; decreased intestinal peristalsis (B); dilated pupils; and com a. Decreased sweating is a manifestation of atropine toxicity (E is false).

Answer 90

A. Free fatty acid concentration is lower than in ketoacidosis B. Glucose concentration is higher than in ketoacidosis **C. It is more common in type 1 diabetes mellitus than in type 2 diabetes mellitus** D. Mortality is more than 50% E. Volume depletion is usually severe ## Footnote Hyperosmolar, nonketotic diabetic coma is usually a complication of type 2 diabetes mellitus (C is false). The other responses regarding hyperosmolar nonketotic coma are true. The free fatty acid and glucose concentrations tend to be higher than in ketoacidosis (A and B). Volume depletion is usually m ore severe (E) than in ketoacidosis, and mortality is greater than 50% (D).

Answer 91

A. Clonidine **B. Isoproterenol** C. Phenoxybenzamine D. Phentolamine E. Prazosin ## Footnote Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1 and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Answer 92

A. Clonidine B. Isoproterenol C. Phenoxybenzamine D. Phentolamine **E. Prazosin** ## Footnote Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1 and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Answer 93

A. Clonidine B. Isoproterenol **C. Phenoxybenzamine** D. Phentolamine E. Prazosin ## Footnote Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1 and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Answer 94

A. Clonidine B. Isoproterenol C. Phenoxybenzamine **D. Phentolamine** E. Prazosin ## Footnote Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1 and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Answer 95

**A. Clonidine** B. Isoproterenol C. Phenoxybenzamine D. Phentolamine E. Prazosin ## Footnote Clonidine (A) is a centrally acting a 2 receptor agonist that is used in the treatment of hypertension. Isoproterenol (B) is a nonselective b agonist. Phenoxybenzamine (C) is an irreversible a agonist that is somewhat selective for a 1 receptors. Phentolamine (D) is a competitive nonselective antagonist at a 1 and a 2 receptors. Prazosin (E) is a highly selective a 1 agonist

Answer 96

A. Acetylcholine **B. Bethanechol** C. Carbachol D. Choline E. Methacholine ## Footnote Bethanechol (B) and carbachol (C) selectively stim ulate the urinary and gastrointestinal (GI) tract. Carbachol (C) is less desirable for urinary retention, however, because it has greater nicotinic action at autonom ic ganglia.

Answer 97

A. Budd-Chiari syndrome is common. B. Hyperuricemia can complicate the disorder. C. It is the most common of the myeloproliferative disorders. **D. Massive splenomegaly is usually the presenting sign.** E. The use of alkylating agents should be avoided. ## Footnote Polycythemia vera is a chronic myeloproliferative disorder that results in increased red cell mass. It is the most common of the myeloproliferative disorders (C). More than 20% of patients present w ith thrombosis; there is a 10% incidence of abdominal major vessel thrombosis such as the Budd-Chiari syndrome (A). The diagnosis is generally made by increased hemoglobin and hematocrit on routine CBC (D is false). Hyperuricemia may complicate the disorder (B), and alkylating agents are generally avoided (E). Although massive splenomegaly can be the presenting sign, the disorder is usually first recognized by a high hematocrit (D is false).

Answer 98

A. 276 **B. 285** C. 296 D. 304 E. 310 ## Footnote Serum osmolarity can be calculated from the formula Serum osmolarity = 2(Na 1 K) 1 Glucose/18 1 BUN/2.8 = 2(130 1 4) 1 126/18 1 28/2.8 = 2(134) 1 7 1 10 5 285, where BUN = blood urea nitrogen

Answer 99

A. Decreased cerebral perfusion pressure **B. Decreased physiologic dead space** C. Decreased work of breathing D. Improved lung compliance E. Predisposition to barotraumas ## Footnote Positive end-expiratory pressure (PEEP) increases physiologic dead space (B is false) by raising intra-alveolar pressure and lung perfusion, thereby impairing CO2 elimination

Answer 100

A. I, II, III **B. I, III** C. II, IV D. IV E. All of the above ## Footnote The oxyhemoglobin dissociation curve is shifted to the right by acidosis (I), fever (III), increased 2,3-diphosphoglyceric acid (DPG [II is false]), and hypoxemia, and to the left by alkalosis, hypothermia, banked blood (IV), and decreased 2,3-DPG (II).

Answer 101

**A. Appendix** B. Colon C. Ileum D. Rectum E. Stom ach ## Footnote Forty-six percent of carcinoid tumors of the GI tract are located in the appendix (A), the most common site for GI carcinoids. The ileum (28% [C]) and the rectum (17% [D]) are less frequently involved

Answer 102

**A. I, II, III** B. I, III C. II, IV D. IV E. All of the above ## Footnote The excretion of weak acids is facilitated by alkalinization of the urine and serum . Compounds such as phenobarbital (III), salicylates (I), chlorpropamide, tricyclic antidepressants (II), 2,4-dichlorophenoxyacetic acid, diflunisal, fluoride, and methotrexate are weak acids. Amphetamines (IV) are weak bases, the excretion of which is enhanced by acidification of the urine

Answer 103

**A. Cryoprecipitate** B. Fresh frozen plasm a C. Both D. Neither ## Footnote von Willebrandʼs disease is an autosomal dominant condition of altered hemostasis resulting from a deficiency of von Willebrand factor (vWF). vWF, under normal conditions, aids in platelet–platelet and platelet–subendothelial interactions and stabilizes factor VIII. Treatment goals include replacing vWF and factor VIII, w hich is best accom plished with the administration of cryoprecipitate (A). Hemophilia B is caused by a deficiency of factor IX that causes inadequate generation of thrombin by the coagulation cascade. Historically, fresh frozen plasm a (FFP [B]) was the treatm ent of choice for factor replacement in hemophilia. The use of FFP, however, has been supplanted by the use of recombinant factor IX, with a reduced risk of bloodborne diseases and transfusion reactions

Answer 104

A. Cryoprecipitate B. Fresh frozen plasm a C. Both **D. Neither** ## Footnote von Willebrandʼs disease is an autosomal dominant condition of altered hemostasis resulting from a deficiency of von Willebrand factor (vWF). vWF, under normal conditions, aids in platelet–platelet and platelet–subendothelial interactions and stabilizes factor VIII. Treatment goals include replacing vWF and factor VIII, w hich is best accom plished with the administration of cryoprecipitate (A). Hemophilia B is caused by a deficiency of factor IX that causes inadequate generation of thrombin by the coagulation cascade. Historically, fresh frozen plasm a (FFP [B]) was the treatm ent of choice for factor replacement in hemophilia. The use of FFP, however, has been supplanted by the use of recombinant factor IX, with a reduced risk of bloodborne diseases and transfusion reactions

Answer 105

A. 2 L B. 4 L **C. 6 L** D. 7 L E. 8 L ## Footnote Free water deficit can be calculated from the formula: Free water deficit (L) = [(Na 2 140)/140] 3 body weight (kg) 3 0.6 = [(160 2 140)/140] 3 70 3 0.6 - 20 2 3 0.6 5 6 L

Answer 106

A. Amrinone B. Dopamine C. Epinephrine **D. Neo-Synephrine** E. Norepinephrine ## Footnote Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent the degradation of cAMP, resulting in positive cardiac inotropy and vascular smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral vasoconstriction occurs, w hich m ay cause undesirable increases in afterload in patients with a tenuous cardiac status. Epinephrine (C) stimulates both a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure a 1 receptor agonist. Norepinephrine (E) has similar activity as compared with epinephrine at a and b1 receptors, but has relatively little action at b2 receptors

Answer 107

**A. Amrinone** B. Dopamine C. Epinephrine D. Neo-Synephrine E. Norepinephrine ## Footnote Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent the degradation of cAMP, resulting in positive cardiac inotropy and vascular smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral vasoconstriction occurs, w hich m ay cause undesirable increases in afterload in patients with a tenuous cardiac status. Epinephrine (C) stimulates both a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure a 1 receptor agonist. Norepinephrine (E) has similar activity as compared with epinephrine at a and b1 receptors, but has relatively little action at b2 receptors

Answer 108

A. Amrinone **B. Dopamine** C. Epinephrine D. Neo-Synephrine E. Norepinephrine ## Footnote Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent the degradation of cAMP, resulting in positive cardiac inotropy and vascular smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral vasoconstriction occurs, w hich m ay cause undesirable increases in afterload in patients with a tenuous cardiac status. Epinephrine (C) stimulates both a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure a 1 receptor agonist. Norepinephrine (E) has similar activity as compared with epinephrine at a and b1 receptors, but has relatively little action at b2 receptors

Answer 109

A. Amrinone B. Dopamine C. Epinephrine D. Neo-Synephrine **E. Norepinephrine** ## Footnote Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent the degradation of cAMP, resulting in positive cardiac inotropy and vascular smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral vasoconstriction occurs, w hich m ay cause undesirable increases in afterload in patients with a tenuous cardiac status. Epinephrine (C) stimulates both a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure a 1 receptor agonist. Norepinephrine (E) has similar activity as compared with epinephrine at a and b1 receptors, but has relatively little action at b2 receptors

Answer 110

A. Amrinone B. Dopamine **C. Epinephrine** D. Neo-Synephrine E. Norepinephrine ## Footnote Amrinone (A) and milrinone are phosphodiesterase inhibitors that prevent the degradation of cAMP, resulting in positive cardiac inotropy and vascular smooth muscle contraction. Dopamine (B) has dose-dependent pharmacologic and hemodynamic effects. At intermediate doses, dopamine increases cardiac output via stimulation of cardiac b receptors; at higher doses, peripheral vasoconstriction occurs, w hich m ay cause undesirable increases in afterload in patients with a tenuous cardiac status. Epinephrine (C) stimulates both a and b adrenergic receptors. Neo-Synephrine (phenylephrine [D]) is a pure a 1 receptor agonist. Norepinephrine (E) has similar activity as compared with epinephrine at a and b1 receptors, but has relatively little action at b2 receptors

Answer 111

A. Cardiac dysfunction B. GI disturbance **C. Hirsutism** D. Lower extremity joint pain E. Peripheral neuropathy ## Footnote Thallium intoxication is characterized by cardiac dysfunction (A), gastrointestinal disturbance (B), alopecia (C is false), lower limb joint pain (D), and peripheral neuropathy (E). Thallium poisoning causes alopecia, not hirsutism (C)

Answer 112

A. Abdominal pain **B. Hypotension** C. Polyneuropathy D. Psychosis E. Tachycardia ## Footnote Acute intermittent porphyria is characterized by colicky abdominal pain (A), psychosis (D), (a predominantly motor) polyneuropathy (C), and tachycardia (E). Hypertension, not hypotension (B), typically occurs during an attack

Answer 113

A. Acquire cardiology consultation **B. Discontinue the offending agent** C. Initiate broad-spectrum antibiotics D. Insulin administration E. Renal dialysis ## Footnote The triad of bradycardia, hyperlipidemia, and rhabdomyolysis is consistent with a propofol infusion syndrome in this ventilated neuro intensive care patient. This disorder involves the abrupt onset of heart failure, bradycardia, lactic acidosis, hyperlipidem ia, and rhabdomyolysis. It typically occurs in the setting of high-dose, prolonged propofol infusions. The most appropriate next step after making the diagnosis is to discontinue the offending agent (B). A cardiology consult (A) m ay be necessary if external pacing is needed, but the propofol needs to be discontinued. Renal dialysis (E) may become necessary depending on the severity of the rhabdomyolysis but is not the next best step. Antibiotic therapy (C) would be appropriate for sepsis, but not for the propofol infusion syndrom e. Insulin adm inistration (D) is unlikely to be helpful.

Answer 114

A. Breathing is irregularly interrupted, and each breath varies in rate and depth B. Few rapid deep breaths alternate w ith apneic cycles (2–3 second pause in full inspiration) in short cycles C. Increase in rate and depth of respiration leading to respiratory alkalosis **D. Waxing and waning hyperpnea regularly alternates with shorter apneic periods** E. None of the above ## Footnote Cheyne-Stokes respiration is characterized by waxing and waning hyperpnea regularly alternating w ith shorter apneic periods (D) and is thought to be related to isolation of the brainstem respiratory centers from the cerebrum rendering them more sensitive to carbon dioxide. Central neurogenic hyperventilation is an increase in rate and depth of respiration leading to respiratory alkalosis (C) associated w ith lesions of the lower midbrain and upper pontine tegmentum . Apneustic breathing is caused by either basilar artery occlusion or low pontine lesions and is characterized by a few rapid deep breaths alternating w ith apneic cycles (2–3 second pause in full inspiration [B]). With Biot breathing, or ataxic breathing, breathing is irregularly interrupted and each breath varies in rate and depth (A); Biot breathing is associated with lesions of the dorsomedial medulla

Answer 115

A. Increased heart rate in response to increased intracranial pressure **B. Increased systolic arterial pressure in response to increased intracranial pressure** C. Parasympathetic outflow in response to increased intracranial pressure D. All of the above E. None of the above ## Footnote Cushing was the first neurosurgeon to recognize that increases in intracranial pressure (ICP) com prom ise cerebral blood ow. Cushing’s reflex refers to the rise in systemic arterial pressure (B) due to increased sym pathetic activity (C is false) in response to rises in ICP. As the system ic arterial pressure rises, bradycardia may also occur (A is false). The triad of hypertension, bradycardia, and abnormal breathing is known as Cushing’s triad.