This week is the long awaited yearly cadaver lab! Please review your procedure logs prior to Thursday in order to know what to focus on. We’ll be going through LPs, cricothyroidotomies, lateral canthotomies and the Papa Wahl Thoracotomy. Below are some helpful videos to review prior to heading to cadaver lab.
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Question 1 of 10
1. Question
Which of the following actions is most appropriate in the treatment of an adult patient with diabetic ketoacidosis?
Correct
The management of diabetic ketoacidosis (DKA) involves administration of fluid, insulin, and potassium, in addition to searching for and treating any precipitant such as an infection. Initial hypokalemia is not common in DKA, and when present represents extreme total body potassium depletion. In this situation, potassium administration should be initiated before insulin. A reasonable guide is to delay insulin administration when the serum potassium level is below 3.3 mEq/L on presentation. Otherwise, as insulin and fluids are administered, hypokalemia worsens and predisposes patients to life-threatening respiratory paralysis and abnormal cardiac rhythms. Due to intracellular-to-extracellular shifting from acidosis and lack of insulin, most patients in DKA present with normal or slightly elevated serum potassium concentrations despite total body depletion of potassium. In the absence of renal failure, it is appropriate to initiate potassium administration in DKA when the potassium is 5.3 mEq/L or lower.
Sodium bicarbonate administration in DKA can delay a decrease in ketonemia and worsen hypokalemia. If administered, it is reserved for when the pH is less than 6.90 (not 7.15).
Insulin boluses are not required in the management of DKA and have not demonstrated benefit over beginning with an insulin infusion. If used, a bolus dose of 0.10 to 0.14 units/kg (not 0.01 units/kg) is appropriate.
During DKA treatment, administration of dextrose might be needed when the serum glucose falls but significant ketoacidosis remains. Guidelines recommend dextrose administration when the serum glucose is less than 200 mg/dL (not 350 mg/dL).
Incorrect
The management of diabetic ketoacidosis (DKA) involves administration of fluid, insulin, and potassium, in addition to searching for and treating any precipitant such as an infection. Initial hypokalemia is not common in DKA, and when present represents extreme total body potassium depletion. In this situation, potassium administration should be initiated before insulin. A reasonable guide is to delay insulin administration when the serum potassium level is below 3.3 mEq/L on presentation. Otherwise, as insulin and fluids are administered, hypokalemia worsens and predisposes patients to life-threatening respiratory paralysis and abnormal cardiac rhythms. Due to intracellular-to-extracellular shifting from acidosis and lack of insulin, most patients in DKA present with normal or slightly elevated serum potassium concentrations despite total body depletion of potassium. In the absence of renal failure, it is appropriate to initiate potassium administration in DKA when the potassium is 5.3 mEq/L or lower.
Sodium bicarbonate administration in DKA can delay a decrease in ketonemia and worsen hypokalemia. If administered, it is reserved for when the pH is less than 6.90 (not 7.15).
Insulin boluses are not required in the management of DKA and have not demonstrated benefit over beginning with an insulin infusion. If used, a bolus dose of 0.10 to 0.14 units/kg (not 0.01 units/kg) is appropriate.
During DKA treatment, administration of dextrose might be needed when the serum glucose falls but significant ketoacidosis remains. Guidelines recommend dextrose administration when the serum glucose is less than 200 mg/dL (not 350 mg/dL).
Question 2 of 10
2. Question
A 23-year old male with insulin dependent diabetes mellitus, presents with 3-days of diarrhea, fever, and malaise. He denies abdominal pain but states he is having intermittent abdominal bloating and cramping preceding nonbloody, watery and voluminous diarrhea. He has no recent travel, no drug or alcohol abuse, and no history of diarrhea. He states that he ate food from a street vendor an hour before his diarrhea started. Vital signs are: BP 123/72, P 121, RR 26, T 100.0F (37.8C). He is nontoxic and physical exam, including abdominal exam is grossly unremarkable. Blood tests are significant for arterial pH 7.27, serum bicarbonate 16 mEq/L, serum glucose 333 mg/dL, serum potassium of 2.9 mEq/L, and anion gap of 21. While IV normal saline and potassium is being administered, which of the following should be administered as well?
Correct
A. Magnesium sulfate IV
This patient is presenting with mild diabetic ketoacidosis likely secondary to acute infectious diarrhea from a contaminated food source. He is also hypokalemic, which is being repleted. Of the given answer choices, magnesium sulfate should be administered. Large volume diarrhea may cause total body potassium depletion, in addition to other electrolytes. Magnesium is an electrolyte that is often depleted in diarrhea as well, and repletion of hypomagnesemia is critical in the repletion of potassium, as hypokalemia often cannot be corrected until the magnesium deficit is reversed (PMID: 1728927).
B. Regular insulin IV
Potassium should be repleted first, until a repeat serum potassium level above 3.3 mEq/L (mmol/L) is documented, prior to administering insulin. Administering insulin in the setting of hypokalemia may worsen hypokalemia, risking the precipitation of cardiac arrhythmias.
C. Sodium bicarbonate IV
There is no indication for administering sodium bicarbonate in this patient.
D. Vancomycin IV
Although antibiotic administration may be indicated in this patient suffering from diabetic ketoacidosis likely secondary to acute infectious diarrhea (likely bacterial), vancomycin is a poor choice (primarily gram positive with little gram negative/anaerobic coverage).
Incorrect
A. Magnesium sulfate IV
This patient is presenting with mild diabetic ketoacidosis likely secondary to acute infectious diarrhea from a contaminated food source. He is also hypokalemic, which is being repleted. Of the given answer choices, magnesium sulfate should be administered. Large volume diarrhea may cause total body potassium depletion, in addition to other electrolytes. Magnesium is an electrolyte that is often depleted in diarrhea as well, and repletion of hypomagnesemia is critical in the repletion of potassium, as hypokalemia often cannot be corrected until the magnesium deficit is reversed (PMID: 1728927).
B. Regular insulin IV
Potassium should be repleted first, until a repeat serum potassium level above 3.3 mEq/L (mmol/L) is documented, prior to administering insulin. Administering insulin in the setting of hypokalemia may worsen hypokalemia, risking the precipitation of cardiac arrhythmias.
C. Sodium bicarbonate IV
There is no indication for administering sodium bicarbonate in this patient.
D. Vancomycin IV
Although antibiotic administration may be indicated in this patient suffering from diabetic ketoacidosis likely secondary to acute infectious diarrhea (likely bacterial), vancomycin is a poor choice (primarily gram positive with little gram negative/anaerobic coverage).
Question 3 of 10
3. Question
Which of the following statements regarding the treatment of thyroid storm is correct?
Correct
Thyroid storm is a life-threatening condition often precipitated by a significant physiologic stressor such as childbirth, an infection, surgery (particularly on the thyroid in a patient with thyrotoxicosis), and trauma. In addition to specific treatment of thyroid hormone excess, it is imperative to search for and treat the precipitating stressor. Since infections are a common precipitant and might not be clinically obvious, the clinician should have a low threshold for starting broad-spectrum antibiotics. Specific treatment to address the thyroid hormone excess includes administration of these four agents: thionamide (propylthiouracil [PTU] or methimazole); iodine (an hour after the thionamide); corticosteroids; and beta-blockers.
Corticosteroids (dexamethasone or hydrocortisone) decrease conversion of T4 to the more active T3 and also decrease thyroid hormone release. They should be administrated routinely to patients in thyroid storm and not reserved just for those with coincident adrenal insufficiency.
The administration of a thionamide should precede that of iodine. Thionamides (propylthiouracil [PTU] or methimazole) inhibit thyroid peroxidase and decrease production of thyroid hormone. Iodine administration decreases the release and production of thyroid hormone by a feedback mechanism but must be given an hour or two following the thionamide to prevent the iodine from being used to produce even more thyroid hormone.
Plasmapheresis, a method of removing circulating thyroid hormone, can be considered for patients who are worsening despite maximal standard therapy and in those with contraindications to thionamide use. It is not a part of standard therapy and is not used routinely.
Incorrect
Thyroid storm is a life-threatening condition often precipitated by a significant physiologic stressor such as childbirth, an infection, surgery (particularly on the thyroid in a patient with thyrotoxicosis), and trauma. In addition to specific treatment of thyroid hormone excess, it is imperative to search for and treat the precipitating stressor. Since infections are a common precipitant and might not be clinically obvious, the clinician should have a low threshold for starting broad-spectrum antibiotics. Specific treatment to address the thyroid hormone excess includes administration of these four agents: thionamide (propylthiouracil [PTU] or methimazole); iodine (an hour after the thionamide); corticosteroids; and beta-blockers.
Corticosteroids (dexamethasone or hydrocortisone) decrease conversion of T4 to the more active T3 and also decrease thyroid hormone release. They should be administrated routinely to patients in thyroid storm and not reserved just for those with coincident adrenal insufficiency.
The administration of a thionamide should precede that of iodine. Thionamides (propylthiouracil [PTU] or methimazole) inhibit thyroid peroxidase and decrease production of thyroid hormone. Iodine administration decreases the release and production of thyroid hormone by a feedback mechanism but must be given an hour or two following the thionamide to prevent the iodine from being used to produce even more thyroid hormone.
Plasmapheresis, a method of removing circulating thyroid hormone, can be considered for patients who are worsening despite maximal standard therapy and in those with contraindications to thionamide use. It is not a part of standard therapy and is not used routinely.
Question 4 of 10
4. Question
Which of the following statements regarding the clinical manifestations of hypoglycemia is correct?
Correct
The neurologic deficits associated with most toxic and metabolic causes of significant altered levels of consciousness (including hypoglycemia) are typically symmetrical (nonfocal). However, a small but not insignificant number of patients with hypoglycemia presents with focal neurologic deficits, including hemiplegia. The rapid identification and correction of hypoglycemia in all patients, including those with focal neurologic deficits, is critical to avoid severe complications of a rapidly reversible condition and to avoid unnecessary imaging (brain imaging) and potential interventions (thrombolytic therapy).
Although adrenergic symptoms such as diaphoresis and tachycardia are common manifestations of hypoglycemia, bradycardia is less common, and none of these symptoms should be relied on to determine if a patient is hypoglycemic.
Release of the counterregulatory hormone epinephrine in the setting of hypoglycemia can result in a variety of adrenergic symptoms (anxiety, diaphoresis, palpitations, tachycardia, tremors). Hypotension is not expected and is not common.
Syncope is a transient loss of consciousness associated with a loss of postural tone that spontaneously reverses without medical intervention. When a patient becomes comatose from hypoglycemia, the body has exhausted its ability to counteract the hypoglycemia. Spontaneous reversal is very unlikely to occur. Syncope is not a common manifestation of hypoglycemia.
Incorrect
The neurologic deficits associated with most toxic and metabolic causes of significant altered levels of consciousness (including hypoglycemia) are typically symmetrical (nonfocal). However, a small but not insignificant number of patients with hypoglycemia presents with focal neurologic deficits, including hemiplegia. The rapid identification and correction of hypoglycemia in all patients, including those with focal neurologic deficits, is critical to avoid severe complications of a rapidly reversible condition and to avoid unnecessary imaging (brain imaging) and potential interventions (thrombolytic therapy).
Although adrenergic symptoms such as diaphoresis and tachycardia are common manifestations of hypoglycemia, bradycardia is less common, and none of these symptoms should be relied on to determine if a patient is hypoglycemic.
Release of the counterregulatory hormone epinephrine in the setting of hypoglycemia can result in a variety of adrenergic symptoms (anxiety, diaphoresis, palpitations, tachycardia, tremors). Hypotension is not expected and is not common.
Syncope is a transient loss of consciousness associated with a loss of postural tone that spontaneously reverses without medical intervention. When a patient becomes comatose from hypoglycemia, the body has exhausted its ability to counteract the hypoglycemia. Spontaneous reversal is very unlikely to occur. Syncope is not a common manifestation of hypoglycemia.
Question 5 of 10
5. Question
Which of the following laboratory abnormalities is expected in primary adrenal insufficiency?
Correct
Destruction of the adrenal cortex in primary adrenal insufficiency (Addison disease) manifests with signs and symptoms of steroid deficiency (mineralocorticoids, glucocorticoids, gonadocorticoids) and increased adrenocorticotropic hormone (ACTH). The mineralocorticoid aldosterone stimulates the kidneys to reabsorb sodium and to excrete potassium. Aldosterone deficiency contributes to the presence of hyponatremia (seen 90% of the time), and hyperkalemia (seen 60% of the time). Deficiency in the glucocorticoid cortisol can lead to hypoglycemia, a common finding in children and infants. Signs and symptoms of gonadocorticoid deficiency are more common in women and include decreased axillary and pubic hair and decreased libido. Increased ACTH leads to skin hyperpigmentation. Causes of primary adrenal insufficiency include autoimmune disease (most common cause in Western countries), congenital conditions, drugs, hemorrhage, infections (tuberculosis is traditionally a common cause but is uncommon now in Western countries), infiltrative diseases (such as amyloidosis and sarcoidosis), and metastatic cancer.
Cortisol is involved with maintaining euglycemia. Cortisol deficiency in primary adrenal insufficiency leads to hypoglycemia, not hyperglycemia.
Hypercalcemia, not hypocalcemia, is seen in primary adrenal insufficiency. The hypercalcemia is thought to be a result of increased mobilization from bone and diminished renal excretion. It generally corrects quickly with hydration.
Aldosterone causes sodium resorption and potassium excretion. Aldosterone deficiency in primary adrenal insufficiency causes hyperkalemia, not hypokalemia.
Incorrect
Destruction of the adrenal cortex in primary adrenal insufficiency (Addison disease) manifests with signs and symptoms of steroid deficiency (mineralocorticoids, glucocorticoids, gonadocorticoids) and increased adrenocorticotropic hormone (ACTH). The mineralocorticoid aldosterone stimulates the kidneys to reabsorb sodium and to excrete potassium. Aldosterone deficiency contributes to the presence of hyponatremia (seen 90% of the time), and hyperkalemia (seen 60% of the time). Deficiency in the glucocorticoid cortisol can lead to hypoglycemia, a common finding in children and infants. Signs and symptoms of gonadocorticoid deficiency are more common in women and include decreased axillary and pubic hair and decreased libido. Increased ACTH leads to skin hyperpigmentation. Causes of primary adrenal insufficiency include autoimmune disease (most common cause in Western countries), congenital conditions, drugs, hemorrhage, infections (tuberculosis is traditionally a common cause but is uncommon now in Western countries), infiltrative diseases (such as amyloidosis and sarcoidosis), and metastatic cancer.
Cortisol is involved with maintaining euglycemia. Cortisol deficiency in primary adrenal insufficiency leads to hypoglycemia, not hyperglycemia.
Hypercalcemia, not hypocalcemia, is seen in primary adrenal insufficiency. The hypercalcemia is thought to be a result of increased mobilization from bone and diminished renal excretion. It generally corrects quickly with hydration.
Aldosterone causes sodium resorption and potassium excretion. Aldosterone deficiency in primary adrenal insufficiency causes hyperkalemia, not hypokalemia.
Question 6 of 10
6. Question
Which of the following most correctly pairs the mechanism of action with medications given as treatments in thyroid storm?
Correct
A. Glucocorticoids prevents peripheral conversion of T3 to T4
Glucocorticoids blocks the peripheral conversion of T4 to T3.
B. Iodine blocks the release of T3, but not T4, from the thyroid gland
Iodine blocks release of T4, not T3, from the thyroid. T4 is converted to T3 peripherally.
C. Methimazole blocks peripheral conversion of T3 to T4
Methimazole works by inhibiting thyroid hormone synthesis.
D. Thionamides block de novo synthesis of thyroid hormones
Both T3 and T4 are released from the thyroid gland with the stimulation of TSH, but in the peripheral organs, T4 is converted to T3, which is the active form. Glucocorticoids blocks the peripheral conversion of T4 to T3. Iodine blocks the release of both T3 and T4 from the thyroid gland. Thionamides, such as PTU or methimazole, block de novo thyroid hormone synthesis. In addition, PTU (but not methimazole) also blocks T4 to T3 conversion.
Incorrect
A. Glucocorticoids prevents peripheral conversion of T3 to T4
Glucocorticoids blocks the peripheral conversion of T4 to T3.
B. Iodine blocks the release of T3, but not T4, from the thyroid gland
Iodine blocks release of T4, not T3, from the thyroid. T4 is converted to T3 peripherally.
C. Methimazole blocks peripheral conversion of T3 to T4
Methimazole works by inhibiting thyroid hormone synthesis.
D. Thionamides block de novo synthesis of thyroid hormones
Both T3 and T4 are released from the thyroid gland with the stimulation of TSH, but in the peripheral organs, T4 is converted to T3, which is the active form. Glucocorticoids blocks the peripheral conversion of T4 to T3. Iodine blocks the release of both T3 and T4 from the thyroid gland. Thionamides, such as PTU or methimazole, block de novo thyroid hormone synthesis. In addition, PTU (but not methimazole) also blocks T4 to T3 conversion.
Question 7 of 10
7. Question
A 26 year old female with a history asthma presents to the ER with general malaise, loss of appetite, myalgias and arthralgias for 1 week. Vital signs are: BP 100/69, P 109, RR 14, T 98.4F (36.9C), 98%RA. Laboratory testing demonstrates Na 135 mEq/L, K 4.4 mEq/L, Cl 100 mEq/L, CO2 24 mEq/L, BUN 6 mg/dL, Creatinine 0.6 mg/dL, Hemoglobin 12.0 g/dL, Random serum cortisol level is below reference range. Which of the following findings is most likely?
Correct
A. ACTH serum level is increased
This is likely secondary adrenal insufficiency due to withdrawal of exogenous chronic steroid use, and is a result one would expect decreased ACTH levels
B. Aldosterone serum level is normal
This is likely secondary adrenal insufficiency due to withdrawal of exogenous chronic steroid use, and is a result of decreased ACTH levels with resulting low cortisol levels. Aldosterone levels are often unaffected in secondary adrenal insufficiency and will be normal in many cases, indicated by the lack of hyponatremia/hyperkalemia. Hypoglycemia, not hyperglycemia, is more commonly found in secondary adrenal insufficiency. Hyperpigmentation is found in primary, not secondary, adrenal insufficiency, due to increased prohormone production (the prohormone is cleaved into ACTH and melanocyte stimulating hormone).
C. Serum glucose is elevated
This is likely secondary adrenal insufficiency due to withdrawal of exogenous chronic steroid use. Glucose will likely be low
D. Hyperpigmentation of the skin is present
Hyperpigmentation is found in primary, not secondary, adrenal insufficiency, due to increased prohormone production (the prohormone is cleaved into ACTH and melanocyte stimulating hormone).
Incorrect
Question 8 of 10
8. Question
An 8-day old infant is brought in to the emergency department for lethargy, poor feeding, and vomiting. Vital signs on presentation are: heart rate 180, blood pressure 55/40, respiratory rate 60, and oxygen saturation of 98% on room air. He is afebrile. Laboratory analysis is as follows: Sodium 125 mmol/L, K 5.2 mmol/L, Chloride 106 mmol/L, bicarbonate 18 mmol/L, BUN 13 mg/dl, creatinine 0.74 mg/dl, and glucose of 60 mg/dl. Ammonia is 40 µmol/L (normal is less than 50 µmol/L). Physical exam reveals an ill appearing neonate with dry mucous membranes who is minimally reactive. Which of the following is the most likely etiology of this patient’s symptoms?
Correct
A. 11-beta-hydroxylase deficiency
11-beta-hydroxylase deficiency is a cause of congenital adrenal hyperplasia. However, 21 hydroxylase deficiency is the most common cause of CAH.
B. 21-hydroxylase deficiency
The correct answer is 21 hydroxylase deficiency. This patient’s presentation, particularly the hyponatremia and hyperkalemia, is consistent with congenital adrenal hyperplasia. 21 hydroxylase deficiency is the most common cause of CAH.
C. Carbamoyl phosphate synethetase I deficiency
Carbamoyl phosphate synethetase deficiency is a urea cycle disorder. It is a genetic deficiency that causes ammonia to build up in the blood.
D. Ornithine transcarbamylase deficiency
Ornithine transcarbamylase deficiency (OTC deficiency) is the most common urea cycle deficiency in humans. OTC deficiency results in high ammonia levels in the blood.
Incorrect
A. 11-beta-hydroxylase deficiency
11-beta-hydroxylase deficiency is a cause of congenital adrenal hyperplasia. However, 21 hydroxylase deficiency is the most common cause of CAH.
B. 21-hydroxylase deficiency
The correct answer is 21 hydroxylase deficiency. This patient’s presentation, particularly the hyponatremia and hyperkalemia, is consistent with congenital adrenal hyperplasia. 21 hydroxylase deficiency is the most common cause of CAH.
C. Carbamoyl phosphate synethetase I deficiency
Carbamoyl phosphate synethetase deficiency is a urea cycle disorder. It is a genetic deficiency that causes ammonia to build up in the blood.
D. Ornithine transcarbamylase deficiency
Ornithine transcarbamylase deficiency (OTC deficiency) is the most common urea cycle deficiency in humans. OTC deficiency results in high ammonia levels in the blood.
Question 9 of 10
9. Question
A 41-year-old man presents to the Emergency Department with left sided flank pain, diaphoresis and episodic headaches. He denies any drug or alcohol use. His vital signs are T 99.9ºF, HR 115 beats/minute, RR 12 breaths/minute, BP 168/110 mm Hg. He is diaphoretic and has left flank fullness on exam with no overlying dermatomal rash. Which of the following tests is most specific for this patient’s diagnosis?
Correct
Metanephrine is an intermediate metabolite between epinephrine and vanillylmandelic acid. It is considered the most sensitive and specific test for identifying the presence of pheochromocytoma. Pheochromocytomas are catecholamine-producing adrenal tumors that can lead to hypertensive crises that may be lethal. The average age at diagnosis is approximately 40 years. The classic “rule of 10s” for pheochromocytomas is that approximately 10% are bilateral, 10% are extra-adrenal, and 10% are malignant. These tumors may arise sporadically or as a feature of an inherited condition such as multiple endocrine neoplasia, neurofibromatosis type 1 or von Hippel-Lindau disease. Typical clinical presentations include paroxysms of headaches, palpitations and profuse sweating: the classic triad of pheochromocytomas. Paroxysms usually last less than one hour and are brought about by exercise, position changes, surgery, urination or certain medications (e.g., metoclopramide, tricyclic antidepressants). Patients may present in a hypertensive crisis with acute pulmonary edema, intracranial hemorrhages, heart failure or dysrhythmias. Other clinical features may include anxiety or panic attacks, nausea, flushing, abdominal or back pain, pallor or generalized weakness. The first step in diagnosis is measuring biochemical metabolites called metanephrines, the methylated products of catecholamine catabolism. Diagnostic imaging for tumor localization is a secondary diagnostic method. Treatment includes total or partial adrenalectomy. Preoperative blood pressure management with oral alpha-adrenergic antagonists (e.g., phenoxybenzamine or prazosin) or beta-blockers (e.g., propranolol) can be used to keep blood pressure consistently less than 160/90 mm Hg.
5-HIAA (A), or 5-hydroxyindoleacetic acid, is a serotonin metabolite used in the diagnosis of carcinoid tumors. Serotonin (C) levels are not utilized for diagnosing neuroendocrine tumors, whereas serotonin metabolites (e.g., 5-HIAA) are. Vanillylmandelic acid (D) is the least specific catecholamine metabolite in testing for pheochromocytoma. It has greater utility in the initial diagnosis and surveillance testing for neuroblastomas.
Incorrect
Metanephrine is an intermediate metabolite between epinephrine and vanillylmandelic acid. It is considered the most sensitive and specific test for identifying the presence of pheochromocytoma. Pheochromocytomas are catecholamine-producing adrenal tumors that can lead to hypertensive crises that may be lethal. The average age at diagnosis is approximately 40 years. The classic “rule of 10s” for pheochromocytomas is that approximately 10% are bilateral, 10% are extra-adrenal, and 10% are malignant. These tumors may arise sporadically or as a feature of an inherited condition such as multiple endocrine neoplasia, neurofibromatosis type 1 or von Hippel-Lindau disease. Typical clinical presentations include paroxysms of headaches, palpitations and profuse sweating: the classic triad of pheochromocytomas. Paroxysms usually last less than one hour and are brought about by exercise, position changes, surgery, urination or certain medications (e.g., metoclopramide, tricyclic antidepressants). Patients may present in a hypertensive crisis with acute pulmonary edema, intracranial hemorrhages, heart failure or dysrhythmias. Other clinical features may include anxiety or panic attacks, nausea, flushing, abdominal or back pain, pallor or generalized weakness. The first step in diagnosis is measuring biochemical metabolites called metanephrines, the methylated products of catecholamine catabolism. Diagnostic imaging for tumor localization is a secondary diagnostic method. Treatment includes total or partial adrenalectomy. Preoperative blood pressure management with oral alpha-adrenergic antagonists (e.g., phenoxybenzamine or prazosin) or beta-blockers (e.g., propranolol) can be used to keep blood pressure consistently less than 160/90 mm Hg.
5-HIAA (A), or 5-hydroxyindoleacetic acid, is a serotonin metabolite used in the diagnosis of carcinoid tumors. Serotonin (C) levels are not utilized for diagnosing neuroendocrine tumors, whereas serotonin metabolites (e.g., 5-HIAA) are. Vanillylmandelic acid (D) is the least specific catecholamine metabolite in testing for pheochromocytoma. It has greater utility in the initial diagnosis and surveillance testing for neuroblastomas.
Question 10 of 10
10. Question
A 45-year-old woman presents with paresthesias of her fingers and around her mouth that started today. She was discharged two days ago after having a thyroidectomy. Which of the following laboratory results are most likely in this patient?
Correct
Acquired hypoparathyroidism is most often the result of thyroid, parathyroid, or radical head and neck cancer surgery, or autoimmune damage of the parathyroid gland. This patient has symptoms consistent with hypocalcemia due to hypoparathyroidism. The parathyroid gland secretes parathyroid hormone which regulates calcium levels via effects on the bones, kidneys and gastrointestinal tract. Decreased levels of parathyroid hormone result in hypocalcemia and hyperphosphatemia. Classic symptoms consistent with hypocalcemia include neuromuscular irritability, such as perioral numbness, muscle cramping, paresthesias of the distal extremities, carpopedal spasm and seizures. Severe hypocalcemia can result in hypotension, dysrhythmias and cardiovascular collapse. A serum calcium level less than 8.5 mg/dL or an ionized calcium less than 2.0 mEq/L is considered diagnostic of hypocalcemia. Treatment depends on the current calcium level and presenting symptoms. Those with severe symptoms require intravenous calcium repletion with calcium gluconate. Patients with mild symptoms can be treated with oral calcium.
Laboratory findings of decreased calcium, decreased phosphorus, and increased parathyroid hormone (A) are consistent with hypocalcemia due to vitamin D deficiency. Hypoparathyroidism results in decreased calcium levels, not increased calcium levels (C). Increased calcium, decreased phosphorus, and increased parathyroid hormone (D) levels are consistent with primary hyperparathyroidism. Findings of hypercalcemia include lethargy, depression, constipation, ileus, kidney stones and abnormal bone remodeling.
Incorrect
Acquired hypoparathyroidism is most often the result of thyroid, parathyroid, or radical head and neck cancer surgery, or autoimmune damage of the parathyroid gland. This patient has symptoms consistent with hypocalcemia due to hypoparathyroidism. The parathyroid gland secretes parathyroid hormone which regulates calcium levels via effects on the bones, kidneys and gastrointestinal tract. Decreased levels of parathyroid hormone result in hypocalcemia and hyperphosphatemia. Classic symptoms consistent with hypocalcemia include neuromuscular irritability, such as perioral numbness, muscle cramping, paresthesias of the distal extremities, carpopedal spasm and seizures. Severe hypocalcemia can result in hypotension, dysrhythmias and cardiovascular collapse. A serum calcium level less than 8.5 mg/dL or an ionized calcium less than 2.0 mEq/L is considered diagnostic of hypocalcemia. Treatment depends on the current calcium level and presenting symptoms. Those with severe symptoms require intravenous calcium repletion with calcium gluconate. Patients with mild symptoms can be treated with oral calcium.
Laboratory findings of decreased calcium, decreased phosphorus, and increased parathyroid hormone (A) are consistent with hypocalcemia due to vitamin D deficiency. Hypoparathyroidism results in decreased calcium levels, not increased calcium levels (C). Increased calcium, decreased phosphorus, and increased parathyroid hormone (D) levels are consistent with primary hyperparathyroidism. Findings of hypercalcemia include lethargy, depression, constipation, ileus, kidney stones and abnormal bone remodeling.
Hey guys! Back again with more endocrine this week. We’ll be kicking off the day with a Flip led by Dr. Ratnam and facilitated by Dr. Welch covering thyroid disease, the parathyroid and pituitary. We’ve also got an endocrine foundations session with Drs. Saker and O’Neil. Following our main content, we’ve got some more senior Mock Oral Boards with Drs. Padgett and White. Capping off the day we have two faculty lectures – Hypothermia with Dr. Lagina and EM Coding and Billing with Dr. Janowicz. Rounding us off will be the CC/US duo of Drs. Marshall and Tausch.
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Question 1 of 10
1. Question
A pH of 7.1, HCO3 of 15 and PCO2 of 30 is best described by which of the following primary acid-base disorders?
Correct
Acidosis and alkalosis are processes that lead to acidemia (pH < 7.40) and alkalemia (pH > 7.40). Primary metabolic disorders result from a change in bicarbonate, while primary respiratory disorders result from a change in partial pressure of carbon dioxide. Compensation occurs when other system alterations bring the blood gas toward a normal pH of 7.35. A metabolic acidosis is present in any patient with a pH of < 7.35 and bicarbonate < 24. Causes of an increased anion gap acidosis [Na+ - (Cl- + HCO3-)] > 20 can be remembered by the MUDPILES mnemonic (Methanol, Metformin, Uremia, Diabetic (or alcoholic) ketoacidosis, Paraldehyde, Propylene glycol, Isoniazid, Iron, Lactic acidosis, Ethylene glycol, Salicylates). Normal anion gap acidosis is caused by: renal losses (tubular acidosis, acetazolamide), GI losses (diarrhea, malabsorption), and adrenal insufficiency. Compensation for an acid-base disorder never completely normalizes the pH. A pH of 7.45 in a patient with low bicarbonate indicates a second disorder (such as a primary respiratory alkalosis).
Metabolic alkalosis (B) is caused by an increase in bicarbonate leading to a pH > 7.35. This occurs secondary to gastric acid loss from vomiting or NG tube suctioning, diuretic use, and adrenocortical hormone excess. Respiratory acidosis (C) is caused by an increase in the partial pressure of carbon dioxide > 40 leading to a pH < 7.35. This is primarily a result of inadequate ventilation or increased dead space. Causes include head or chest trauma, oversedation, obtundation, neuromuscular disorders, Pickwickian syndrome (obesity-hypoventilation syndrome), and COPD. Respiratory alkalosis (D) is caused by a decrease in the partial pressure of carbon dioxide < 40 leading to a pH > 7.35. In this condition, carbon dioxide ventilation outpaces production.
Incorrect
Acidosis and alkalosis are processes that lead to acidemia (pH < 7.40) and alkalemia (pH > 7.40). Primary metabolic disorders result from a change in bicarbonate, while primary respiratory disorders result from a change in partial pressure of carbon dioxide. Compensation occurs when other system alterations bring the blood gas toward a normal pH of 7.35. A metabolic acidosis is present in any patient with a pH of < 7.35 and bicarbonate < 24. Causes of an increased anion gap acidosis [Na+ - (Cl- + HCO3-)] > 20 can be remembered by the MUDPILES mnemonic (Methanol, Metformin, Uremia, Diabetic (or alcoholic) ketoacidosis, Paraldehyde, Propylene glycol, Isoniazid, Iron, Lactic acidosis, Ethylene glycol, Salicylates). Normal anion gap acidosis is caused by: renal losses (tubular acidosis, acetazolamide), GI losses (diarrhea, malabsorption), and adrenal insufficiency. Compensation for an acid-base disorder never completely normalizes the pH. A pH of 7.45 in a patient with low bicarbonate indicates a second disorder (such as a primary respiratory alkalosis).
Metabolic alkalosis (B) is caused by an increase in bicarbonate leading to a pH > 7.35. This occurs secondary to gastric acid loss from vomiting or NG tube suctioning, diuretic use, and adrenocortical hormone excess. Respiratory acidosis (C) is caused by an increase in the partial pressure of carbon dioxide > 40 leading to a pH < 7.35. This is primarily a result of inadequate ventilation or increased dead space. Causes include head or chest trauma, oversedation, obtundation, neuromuscular disorders, Pickwickian syndrome (obesity-hypoventilation syndrome), and COPD. Respiratory alkalosis (D) is caused by a decrease in the partial pressure of carbon dioxide < 40 leading to a pH > 7.35. In this condition, carbon dioxide ventilation outpaces production.
Question 2 of 10
2. Question
A 55-year-old woman presents to the ED with crampy abdominal pain that has been progressing over the past three days. She notes non-bloody emesis, vomiting, and diarrhea alternating with constipation. She has previously undergone a hernia repair, cholecystectomy, and hysterectomy. On exam, her abdomen is soft and diffusely tender with quiet bowel sounds. A plain radiograph is obtained and reveals air-fluid levels and lack of air in the rectum. What is the most common electrolyte imbalance associated with this condition?
Correct
The patient has a small-bowel obstruction (SBO), most likely due to adhesions that have developed from her multiple abdominal surgeries. The common presentation of SBO includes crampy, poorly localized abdominal pain, vomiting, and abdominal distension. Bowel sounds can be hyperactive initially but become quiet or absent once complete obstruction occurs. Abdominal plain-film findings include air-fluid levels, dilated loops of small bowel above the point of obstruction, and lack of air in the rectum. Dehydration and associated hypokalemia are common. Treatment measures include IV hydration, potassium repletion, nasogastric tube placement, and surgical consultation.
Hypercalcemia (A) can occur with malignancy, hyperparathyroidism, drugs, immobilization, Paget’s disease, or excessive intake (vitamin D toxicity, milk-alkali syndrome). Major clinical findings can be remembered with the phrase “stones, bones, groans, and psychiatric overtones” (nephrolithiasis, weakness, abdominal pain/constipation, confusion/depression). Hypercalcemia shortens the QT interval. Hypocalcemia (B) can be seen in renal failure, hypoparathyroidism, pancreatitis, or chronic malabsorption syndromes. Neurologic symptoms include paraesthesias, carpopedal spasm, Chvostek’s or Trousseau’s sign, and hyperreflexia. Cardiovascular signs include hypotension, heart failure, dysrhythmias, and prolonged QT interval. Hyponatremia (D) can present in a variety of ways, depending on the etiology. The patient can appear dehydrated (hypovolemic hyponatremic) or edematous (hypervolemic hyponatremic), or the fluid status can be normal (syndrome of inappropriate ADH release, psychogenic water drinking, drugs, hypothyroidism).
Incorrect
The patient has a small-bowel obstruction (SBO), most likely due to adhesions that have developed from her multiple abdominal surgeries. The common presentation of SBO includes crampy, poorly localized abdominal pain, vomiting, and abdominal distension. Bowel sounds can be hyperactive initially but become quiet or absent once complete obstruction occurs. Abdominal plain-film findings include air-fluid levels, dilated loops of small bowel above the point of obstruction, and lack of air in the rectum. Dehydration and associated hypokalemia are common. Treatment measures include IV hydration, potassium repletion, nasogastric tube placement, and surgical consultation.
Hypercalcemia (A) can occur with malignancy, hyperparathyroidism, drugs, immobilization, Paget’s disease, or excessive intake (vitamin D toxicity, milk-alkali syndrome). Major clinical findings can be remembered with the phrase “stones, bones, groans, and psychiatric overtones” (nephrolithiasis, weakness, abdominal pain/constipation, confusion/depression). Hypercalcemia shortens the QT interval. Hypocalcemia (B) can be seen in renal failure, hypoparathyroidism, pancreatitis, or chronic malabsorption syndromes. Neurologic symptoms include paraesthesias, carpopedal spasm, Chvostek’s or Trousseau’s sign, and hyperreflexia. Cardiovascular signs include hypotension, heart failure, dysrhythmias, and prolonged QT interval. Hyponatremia (D) can present in a variety of ways, depending on the etiology. The patient can appear dehydrated (hypovolemic hyponatremic) or edematous (hypervolemic hyponatremic), or the fluid status can be normal (syndrome of inappropriate ADH release, psychogenic water drinking, drugs, hypothyroidism).
Question 3 of 10
3. Question
A patient is found to be hyponatremic. Laboratory evaluation reveals low serum osmolality, urine sodium concentration >20 mmol/L and a fractional excretion of sodium (FENa) >1%. He appears to be “fluid overloaded.” Which of the following is the most likely cause of this hyponatremia?
Correct
Hyponatremia is defined as sodium less than 135 mEq/L. Hyponatremia can occur in a hypovolemic, euvolemic, or hypervolemic state. Hypervolemic hypo-osmolar hyponatremia is is associated with fluid overload. The etiology is usually from a perceived low intravascular volume by the kidneys and active water reabsorbtion in excess to sodium retention. If urine sodium is low (<20) causes include liver failure, cirrhosis, hepatorenal syndrome, nephrotic syndrome, and CHF. If urine sodium is high (>20) causes include acute or chronic renal failure, such as that caused by hypertensive nephropathy. Treatment of hypervolemic hypo-osmolar hyponatremia is dialysis.
Cirrhosis (A) and congestive heart failure (B) is often the cause of hypervolemic hypo-osmolar hyponatremia when the urine sodium is low (<20). SIADH (D) results in euvolemic hyponatremia with urine osmolality greater than serum osmolality. The excess ADH causes total body water to increase thereby diluting total body sodium. Despite the increased total body water, these patients typically do not show evidence of edema or heart failure as the increased water is intracellular not intravascular.
Incorrect
Hyponatremia is defined as sodium less than 135 mEq/L. Hyponatremia can occur in a hypovolemic, euvolemic, or hypervolemic state. Hypervolemic hypo-osmolar hyponatremia is is associated with fluid overload. The etiology is usually from a perceived low intravascular volume by the kidneys and active water reabsorbtion in excess to sodium retention. If urine sodium is low (<20) causes include liver failure, cirrhosis, hepatorenal syndrome, nephrotic syndrome, and CHF. If urine sodium is high (>20) causes include acute or chronic renal failure, such as that caused by hypertensive nephropathy. Treatment of hypervolemic hypo-osmolar hyponatremia is dialysis.
Cirrhosis (A) and congestive heart failure (B) is often the cause of hypervolemic hypo-osmolar hyponatremia when the urine sodium is low (<20). SIADH (D) results in euvolemic hyponatremia with urine osmolality greater than serum osmolality. The excess ADH causes total body water to increase thereby diluting total body sodium. Despite the increased total body water, these patients typically do not show evidence of edema or heart failure as the increased water is intracellular not intravascular.
Question 4 of 10
4. Question
A 67-year-old man with hypertension and end-stage renal disease presents after an incomplete dialysis session secondary to shortness of breath. His vital signs are BP 110/95, HR 65, RR 22, T 37.3°C, and oxygen saturation 99% on 2L NC. You obtain the ECG above. Which of the following is the most appropriate next step in this patient’s management?
Correct
This ECG is indicative of hyperkalemia, one of the most lethal complications of chronic kidney disease encountered in the ED. A potassium level of 6 mEq/L should be considered potentially dangerous, even though many patients with ESRD chronically tolerate serum levels above this and do not manifest ECG changes. The most rapid treatment for hyperkalemia is intravenous calcium (gluconate with peripheral access, chloride with central access), which transiently reverses cardiac effects of hyperkalemia by antagonism of potassium at the cardiac membrane. Calcium is indicated in all patients with suspected hyperkalemia who have widening of the QRS, an unstable dysrhythmia, bradycardia, or hypotension.
Cardiology consultation (B) is not needed; the patient’s ECG findings are due to an underlying electrolyte abnormality, not a primary cardiac condition. Defibrillation (C) may be necessary if the rhythm deteriorates to ventricular fibrillation. However, should that occur, the definitive management remains removal of potassium from the serum. Transcutaneous pacing (D) can be used as a temporizing measure in patients with symptomatic bradycardia. Hyperkalemic bradycardia responds poorly to pacing. The primary treatment is cardiac membrane stabilization with calcium and subsequent lowering of the serum potassium.
Incorrect
This ECG is indicative of hyperkalemia, one of the most lethal complications of chronic kidney disease encountered in the ED. A potassium level of 6 mEq/L should be considered potentially dangerous, even though many patients with ESRD chronically tolerate serum levels above this and do not manifest ECG changes. The most rapid treatment for hyperkalemia is intravenous calcium (gluconate with peripheral access, chloride with central access), which transiently reverses cardiac effects of hyperkalemia by antagonism of potassium at the cardiac membrane. Calcium is indicated in all patients with suspected hyperkalemia who have widening of the QRS, an unstable dysrhythmia, bradycardia, or hypotension.
Cardiology consultation (B) is not needed; the patient’s ECG findings are due to an underlying electrolyte abnormality, not a primary cardiac condition. Defibrillation (C) may be necessary if the rhythm deteriorates to ventricular fibrillation. However, should that occur, the definitive management remains removal of potassium from the serum. Transcutaneous pacing (D) can be used as a temporizing measure in patients with symptomatic bradycardia. Hyperkalemic bradycardia responds poorly to pacing. The primary treatment is cardiac membrane stabilization with calcium and subsequent lowering of the serum potassium.
Question 5 of 10
5. Question
Which of the following conditions can result in refractory hypokalemia that is not correctable by the administration of potassium?
Correct
Hypokalemia frequently occurs concomitantly in patients with hypomagnesemia. Because magnesium is required for the normal functioning of the Na+/ K+ ATPase pump, hypomagnesemia can result in refractory hypokalemia that is not correctable by the administration of potassium alone. For potassium levels to increase, magnesium must also be administered.
Hypermagnesemia (A) enhances potassium retention. Hypernatremia (B) and hyponatremia (D) will not interfere with increasing the level of potassium in patients receiving potassium supplementation for hypokalemia.
Incorrect
Hypokalemia frequently occurs concomitantly in patients with hypomagnesemia. Because magnesium is required for the normal functioning of the Na+/ K+ ATPase pump, hypomagnesemia can result in refractory hypokalemia that is not correctable by the administration of potassium alone. For potassium levels to increase, magnesium must also be administered.
Hypermagnesemia (A) enhances potassium retention. Hypernatremia (B) and hyponatremia (D) will not interfere with increasing the level of potassium in patients receiving potassium supplementation for hypokalemia.
Question 6 of 10
6. Question
Hyperventalition in a healthy individual causes carpal spasm through which of the following processes?
Correct
D. Correct. Hyperventilation causes a respiratory alkalosis. This in turn increases serum pH and therefore enhances protein binding of calcium in serum. The end result is decreased free ionized calcium. This induced hypocalcemia causes muscle spasm and in severe cases may lead to a tetany like state
A. Incorrect. Decreased PaCO2 causes muscle fiber contraction
Decreased PaCO2 is not the cause of carpal spasm
B. Incorrect. Increased PaO2 causes neuronal activation
Increased PaO2 is not the cause of carpal spasm
C. Incorrect. Increased serum pH causes vasodilation of capillary beds
Hyperventilation would not increase serum pH and is not the cause of carpal spasm
Incorrect
D. Correct. Hyperventilation causes a respiratory alkalosis. This in turn increases serum pH and therefore enhances protein binding of calcium in serum. The end result is decreased free ionized calcium. This induced hypocalcemia causes muscle spasm and in severe cases may lead to a tetany like state
A. Incorrect. Decreased PaCO2 causes muscle fiber contraction
Decreased PaCO2 is not the cause of carpal spasm
B. Incorrect. Increased PaO2 causes neuronal activation
Increased PaO2 is not the cause of carpal spasm
C. Incorrect. Increased serum pH causes vasodilation of capillary beds
Hyperventilation would not increase serum pH and is not the cause of carpal spasm
Question 7 of 10
7. Question
Which of the following laboratory combinations is most expected in a 75-year-old woman with lung cancer and hyponatremia?
Correct
The syndrome of inappropriate secretion of ADH (SIADH) is defined by the secretion of ADH in the absence of an appropriate physiologic stimulus. Its hallmark is an inappropriately concentrated urine, despite the presence of a low serum osmolality and a normal circulating blood volume. Causes of SIADH include central nervous system disorders, pulmonary disease, drugs, stress, pain, and surgery. Therefore, the above patient, with a known history of lung cancer and hyponatremia, most likely has SIADH and exhibits the following lab findings: serum osmolarity low, urine osmolarity high, urine sodium high.
Psychogenic polydipsia (D) is a rare cause of euvolemic hyponatremia and is seen in psychiatric patients who consume large amounts of free water (in excess of 1 L/hr). This large consumption overwhelms the kidney’s ability to excrete free water. Patients will exhibit serum osmolarity low, urine osmolarity low, urine sodium low. Diabetes insipidus (B) results in the loss of large amounts of dilute urine from the loss of concentrating ability in the distal nephron. This may be due to a central cause—such as the lack of ADH secretion from the pituitary—or a nephrogenic cause—such as the lack of responsiveness to circulating ADH. Laboratory workup that invariably shows serum osmolarity high, urine osmolarity high, urine sodium low (A) rarely occurs.
Incorrect
The syndrome of inappropriate secretion of ADH (SIADH) is defined by the secretion of ADH in the absence of an appropriate physiologic stimulus. Its hallmark is an inappropriately concentrated urine, despite the presence of a low serum osmolality and a normal circulating blood volume. Causes of SIADH include central nervous system disorders, pulmonary disease, drugs, stress, pain, and surgery. Therefore, the above patient, with a known history of lung cancer and hyponatremia, most likely has SIADH and exhibits the following lab findings: serum osmolarity low, urine osmolarity high, urine sodium high.
Psychogenic polydipsia (D) is a rare cause of euvolemic hyponatremia and is seen in psychiatric patients who consume large amounts of free water (in excess of 1 L/hr). This large consumption overwhelms the kidney’s ability to excrete free water. Patients will exhibit serum osmolarity low, urine osmolarity low, urine sodium low. Diabetes insipidus (B) results in the loss of large amounts of dilute urine from the loss of concentrating ability in the distal nephron. This may be due to a central cause—such as the lack of ADH secretion from the pituitary—or a nephrogenic cause—such as the lack of responsiveness to circulating ADH. Laboratory workup that invariably shows serum osmolarity high, urine osmolarity high, urine sodium low (A) rarely occurs.
Question 8 of 10
8. Question
A 54-year old female with diabetes that takes metformin presents with altered mental status. Initial vital signs are: BP 95/55, HR 70, RR 24, O2 Sat 100%, temp 97.8 degrees F (36.56). Finger stick glucose is 215 mg/dL (11.95 mmol/L) and a urine dipstick shows no ketones. Basic labs are ordered and results with: pH 7.23, HCO3 8 mEq/L, PaCO2 22 mmHg, K 5.4 mEq/L, Na 134 mEq/L, Cl 100 mEq/L, lactate 7.5 mmol/l. This patient’s primary acid base disturbance is:
Correct
The patient is in an acute metabolic acidosis as is evident by the pH and low bicarbonate. A quick calculation shows that the anion gap is 26 and that the respiratory response with a drop in PaCO2 to 22mmHg follows the “rule of 15’s” with the HCO3 of 8, displaying a proper hyperventilatory response to an acute metabolic acidosis and no evident mixed acid/base disorder. Anion gap is calculated by Na -HCO3 – Cl. For the rule of 15’s, HCO3 + 15 should = the pCO2 and the last 2 digits of the pH. In this patient, 8+15 = 23. This is the correct CO2 indicating an appropriate response. It is also the last 2 digits of the pH (7.23). Thus this is not a mixed acid base disorder but rather an acidosis with appropriate compensation. There are no ketones in the patient’s urine, and the lactate is elevated, thus this patient is in an acute lactic acidosis secondary to metformin rather than DKA.
A. Incorrect. Acute anion gap diabetic ketoacidosis
There are no ketones in the patient’s urine to suggest diabetic ketoacidosis.
C. Incorrect. Acute non-anion gap metabolic acidosis
This patient has an anion gap of 26 which is elevated and consistent with an anion gap acidosis. Recall anion gap is calculated by Na -HCO3 – Cl.
D. Incorrect. Mixed acid/base disorder
This patient has an appropriate compensatory response. Recall the rule of 15’s – HCO3 + 15 should = the pCO2 and the last 2 digits of the pH. In this patient, 8+15 = 23. This is the correct CO2 indicating an appropriate response. It is also the last 2 digits of the pH (7.23). Thus this is not a mixed acid base disorder but rather an acidosis with appropriate compensation.
Incorrect
The patient is in an acute metabolic acidosis as is evident by the pH and low bicarbonate. A quick calculation shows that the anion gap is 26 and that the respiratory response with a drop in PaCO2 to 22mmHg follows the “rule of 15’s” with the HCO3 of 8, displaying a proper hyperventilatory response to an acute metabolic acidosis and no evident mixed acid/base disorder. Anion gap is calculated by Na -HCO3 – Cl. For the rule of 15’s, HCO3 + 15 should = the pCO2 and the last 2 digits of the pH. In this patient, 8+15 = 23. This is the correct CO2 indicating an appropriate response. It is also the last 2 digits of the pH (7.23). Thus this is not a mixed acid base disorder but rather an acidosis with appropriate compensation. There are no ketones in the patient’s urine, and the lactate is elevated, thus this patient is in an acute lactic acidosis secondary to metformin rather than DKA.
A. Incorrect. Acute anion gap diabetic ketoacidosis
There are no ketones in the patient’s urine to suggest diabetic ketoacidosis.
C. Incorrect. Acute non-anion gap metabolic acidosis
This patient has an anion gap of 26 which is elevated and consistent with an anion gap acidosis. Recall anion gap is calculated by Na -HCO3 – Cl.
D. Incorrect. Mixed acid/base disorder
This patient has an appropriate compensatory response. Recall the rule of 15’s – HCO3 + 15 should = the pCO2 and the last 2 digits of the pH. In this patient, 8+15 = 23. This is the correct CO2 indicating an appropriate response. It is also the last 2 digits of the pH (7.23). Thus this is not a mixed acid base disorder but rather an acidosis with appropriate compensation.
Question 9 of 10
9. Question
A mother brings in her 10-day-old son for evaluation of pallor and increased sleepiness. She says he has been a poor feeder since birth and that he has been vomiting and fussy for the past day. The child is somnolent through the examination and does not stir when the nurse draws blood. Vital signs include BP 58/36, P 180, R 72, T 37°C (98.6°F). Initial laboratory test results are sodium 128, potassium 6, and glucose 55.
What is the most likely diagnosis?
Correct
Congenital adrenal hyperplasia (CAH) is a disorder of steroid synthesis or function. Affected infants typically present between the second and fifth weeks of life; the presentation often is an acute crisis similar to the one described in the case, including hypovolemia and hyponatremia related to the salt wasting. The most common form of the disorder is 21-hydroxylase deficiency, accounting for 90% of cases; it is inherited in a recessive manner. Salt wasting with subsequent clinical manifestations is caused by the altered synthesis of the enzymes involved. Other characteristics due to excess androgen result in virilization that is more obvious in girls and that can lead to a missed diagnosis of a male child at or soon after birth. Although CAH is part of the normal neonatal screening, results might not be available for 3 to 4 weeks. Acute care consists of reversing the shock state as quickly as possible using hydration with isotonic fluids and providing mineralocorticoids using hydrocortisone 50 mg/m2 per day.
B. Incorrect. Pavor nocturnus, otherwise known as night terrors, occurs in older children in the early stages of sleep (within the first 2 hours). Affected children are inconsolable but eventually go back to sleep and have no recollection of the event afterward. Pavor nocturnus can affect up to 20% of children, but incidents occur rarely and decrease with age, so treatment is often not required.
C. Incorrect. Pseudohyponatremia is present in patients with elevated glucose due to a displacement of fluid; it is not present with mild hypoglycemia as seen in this patient. It is often found in a patient in diabetic ketoacidosis. Actual serum sodium can be calculated with the following formula: Sodium + (glucose – 100/100) (for glucose >100 mg/dL).
D. Incorrect. Sepsis must always be considered, regardless of hyperthermia or hypothermia, in the evaluation of a neonate with an alteration from baseline. The abnormal laboratory values in this case are not consistent with this diagnosis, however, making CAH more likely.
Incorrect
Congenital adrenal hyperplasia (CAH) is a disorder of steroid synthesis or function. Affected infants typically present between the second and fifth weeks of life; the presentation often is an acute crisis similar to the one described in the case, including hypovolemia and hyponatremia related to the salt wasting. The most common form of the disorder is 21-hydroxylase deficiency, accounting for 90% of cases; it is inherited in a recessive manner. Salt wasting with subsequent clinical manifestations is caused by the altered synthesis of the enzymes involved. Other characteristics due to excess androgen result in virilization that is more obvious in girls and that can lead to a missed diagnosis of a male child at or soon after birth. Although CAH is part of the normal neonatal screening, results might not be available for 3 to 4 weeks. Acute care consists of reversing the shock state as quickly as possible using hydration with isotonic fluids and providing mineralocorticoids using hydrocortisone 50 mg/m2 per day.
B. Incorrect. Pavor nocturnus, otherwise known as night terrors, occurs in older children in the early stages of sleep (within the first 2 hours). Affected children are inconsolable but eventually go back to sleep and have no recollection of the event afterward. Pavor nocturnus can affect up to 20% of children, but incidents occur rarely and decrease with age, so treatment is often not required.
C. Incorrect. Pseudohyponatremia is present in patients with elevated glucose due to a displacement of fluid; it is not present with mild hypoglycemia as seen in this patient. It is often found in a patient in diabetic ketoacidosis. Actual serum sodium can be calculated with the following formula: Sodium + (glucose – 100/100) (for glucose >100 mg/dL).
D. Incorrect. Sepsis must always be considered, regardless of hyperthermia or hypothermia, in the evaluation of a neonate with an alteration from baseline. The abnormal laboratory values in this case are not consistent with this diagnosis, however, making CAH more likely.
Question 10 of 10
10. Question
Which of the following causes hypophosphatemia?
Correct
Diabetic ketoacidosis can result in severe hypophosphatemia due to metabolic acidosis, osmotic diuresis, and mobilization of intracellular phosphate stores leading to urinary loss. Severe hypophosphatemia leads to impairment of ATP production and inadequate energy metabolism. Clinical manifestations—including myocardial depression, hypotension, and respiratory insufficiency—may be present but typically occur only when serum phosphate levels are significantly diminished (< 1 mg/dL). Other causes of hypophosphatemia include malnutrition, chronic diuretic or antacid therapy, sepsis, and chronic alcoholism.
Hypophosphatemia can result from hyperparathyroidism (B), not hypo-parathyroidism. The high levels of parathyroid hormone that occur with hyperparathyroidism increase renal phosphate excretion. Renal failure (C) may be associated with hypophosphatemia, but renal insufficiency is associated with hyperphosphatemia. Rhabdomyolysis (D) can be induced by hypophosphatemia but does not independently cause it.
Incorrect
Diabetic ketoacidosis can result in severe hypophosphatemia due to metabolic acidosis, osmotic diuresis, and mobilization of intracellular phosphate stores leading to urinary loss. Severe hypophosphatemia leads to impairment of ATP production and inadequate energy metabolism. Clinical manifestations—including myocardial depression, hypotension, and respiratory insufficiency—may be present but typically occur only when serum phosphate levels are significantly diminished (< 1 mg/dL). Other causes of hypophosphatemia include malnutrition, chronic diuretic or antacid therapy, sepsis, and chronic alcoholism.
Hypophosphatemia can result from hyperparathyroidism (B), not hypo-parathyroidism. The high levels of parathyroid hormone that occur with hyperparathyroidism increase renal phosphate excretion. Renal failure (C) may be associated with hypophosphatemia, but renal insufficiency is associated with hyperphosphatemia. Rhabdomyolysis (D) can be induced by hypophosphatemia but does not independently cause it.
This week we will be focusing on Acid/Base and Fluid/Electrolyte Disorders. We will also be having a very special lecture on Glucose Metabolism by the one and only Dr. Robert P. Wahl. We know this stuff is complicated, but now that Inservice is over, let’s start preparing for next year’s exam with everyone’s favorite material: Endocrine!
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Question 1 of 10
1. Question
A 64-year-old man complains of pain and paresthesias in his right hand intermittently for several weeks. He works in a factory putting together electronics. On exam, he has decreased sensation of his right 1st through 4th digits and an atrophied thenar eminence. What test in the ED will help diagnose his condition?
Correct
This patient has median mononeuropathy, also known as carpal tunnel syndrome, a compression neuropathy of the median nerve as it traverses under the flexor retinaculum at the wrist. The median nerve provides sensation primarily to the palmar aspect of the 1st, 2nd, 3rd, and radial side of the 4th. When it is compressed, the patient experiences pain, paresthesias, and numbness in that distribution. The Tinel’s test is performed by lightly tapping the volar surface of the wrist over the median nerve. This should elicit a sensation of tingling or pins and needles in the distribution of the median nerve. Carpal tunnel syndrome is first treated with wrist splinting and initiation of a more ergonomic work environment. NSAIDs may also be helpful. If symptoms do not improve, the patient should be referred to a hand specialist who may elect to perform a carpal tunnel release procedure.
CT scan of the head (A) would be useful if there is suspicion that this patient’s symptoms are from a central process such as an acute stroke. However, his numbness is in a peripheral nerve distribution and not dermatomal. An EMG (B) is used most commonly by neurologists to confirm damage to peripheral nerves. It may be used for carpal tunnel syndrome if the symptoms do not resolve with conservative management. A variety of heavy metals are associated with a peripheral neuropathy (lead, mercury), but these require special serologic testing, not a urine drug screen (D). The patient is at risk for occupational exposures because he works in a factory; however, most heavy metal poisonings are associated with other symptoms.
Durkan’s test: reproduction of symptoms with carpal tunnel compression
Phalen’s sign: reproduction of symptoms with wrist hyperflexion
Tinel’s sign: reproduction of symptoms with percussion over carpal tunnel
Flick sign: patient reports shaking of the hand provides relief
NSAIDs, volar splint in neutral position
Incorrect
This patient has median mononeuropathy, also known as carpal tunnel syndrome, a compression neuropathy of the median nerve as it traverses under the flexor retinaculum at the wrist. The median nerve provides sensation primarily to the palmar aspect of the 1st, 2nd, 3rd, and radial side of the 4th. When it is compressed, the patient experiences pain, paresthesias, and numbness in that distribution. The Tinel’s test is performed by lightly tapping the volar surface of the wrist over the median nerve. This should elicit a sensation of tingling or pins and needles in the distribution of the median nerve. Carpal tunnel syndrome is first treated with wrist splinting and initiation of a more ergonomic work environment. NSAIDs may also be helpful. If symptoms do not improve, the patient should be referred to a hand specialist who may elect to perform a carpal tunnel release procedure.
CT scan of the head (A) would be useful if there is suspicion that this patient’s symptoms are from a central process such as an acute stroke. However, his numbness is in a peripheral nerve distribution and not dermatomal. An EMG (B) is used most commonly by neurologists to confirm damage to peripheral nerves. It may be used for carpal tunnel syndrome if the symptoms do not resolve with conservative management. A variety of heavy metals are associated with a peripheral neuropathy (lead, mercury), but these require special serologic testing, not a urine drug screen (D). The patient is at risk for occupational exposures because he works in a factory; however, most heavy metal poisonings are associated with other symptoms.
Durkan’s test: reproduction of symptoms with carpal tunnel compression
Phalen’s sign: reproduction of symptoms with wrist hyperflexion
Tinel’s sign: reproduction of symptoms with percussion over carpal tunnel
Flick sign: patient reports shaking of the hand provides relief
NSAIDs, volar splint in neutral position
Question 2 of 10
2. Question
A 20-year-old woman presents with weakness in her left wrist. She states that she fell asleep in a chair after a night of heavy drinking. On physical examination, she is unable to extend her wrist. What nerve is compromised?
Correct
This patient presents with a wrist drop caused by radial neuropathy also called “Saturday Night Palsy.” The radial nerve arises from the C5-T1 roots. It controls extension of the fingers, thumb, wrist and elbow. Symptoms of radial neuropathy depend on the location of compression. Compression in the axilla (typically from improper use of crutches) causes weakness of extension at the elbow, wrist and fingers. More typically, the nerve is compressed between the humeral shaft and another hard surface and results in weakness with extension at the wrist and fingers. This typically occurs from deep sleep (often secondary to inebriation). About 90% of radial nerve mononeuropathies that occur during sleep, coma or anesthesia recover within 6-8 weeks. Patients should be placed in a wrist splint with 60 degrees of dorsiflexion to prevent atrophy and contractures.
The axillary nerve (A) causes weakness of the shoulder (deltoid) and decreased sensation over the shoulder. Median nerve neuropathy (B) causes numbness in the 1st, 2nd and 3rd digits. Ulnar nerve (D) neuropathy symptoms depend on location but do not cause weakness with extension at the wrist.
The axillary nerve (A) causes weakness of the shoulder (deltoid) and decreased sensation over the shoulder. Median nerve neuropathy (B) causes numbness in the 1st, 2nd and 3rd digits. Ulnar nerve (D) neuropathy symptoms depend on location but do not cause weakness with extension at the wrist.
Incorrect
This patient presents with a wrist drop caused by radial neuropathy also called “Saturday Night Palsy.” The radial nerve arises from the C5-T1 roots. It controls extension of the fingers, thumb, wrist and elbow. Symptoms of radial neuropathy depend on the location of compression. Compression in the axilla (typically from improper use of crutches) causes weakness of extension at the elbow, wrist and fingers. More typically, the nerve is compressed between the humeral shaft and another hard surface and results in weakness with extension at the wrist and fingers. This typically occurs from deep sleep (often secondary to inebriation). About 90% of radial nerve mononeuropathies that occur during sleep, coma or anesthesia recover within 6-8 weeks. Patients should be placed in a wrist splint with 60 degrees of dorsiflexion to prevent atrophy and contractures.
The axillary nerve (A) causes weakness of the shoulder (deltoid) and decreased sensation over the shoulder. Median nerve neuropathy (B) causes numbness in the 1st, 2nd and 3rd digits. Ulnar nerve (D) neuropathy symptoms depend on location but do not cause weakness with extension at the wrist.
The axillary nerve (A) causes weakness of the shoulder (deltoid) and decreased sensation over the shoulder. Median nerve neuropathy (B) causes numbness in the 1st, 2nd and 3rd digits. Ulnar nerve (D) neuropathy symptoms depend on location but do not cause weakness with extension at the wrist.
Question 3 of 10
3. Question
A 19-year-old woman presents to the ED with pain and dyschromatopsia in her right eye. She also describes varying degrees of intermittent paresthesias over the previous month and occasional transient gait disturbance. An MRI shows white matter pathology. Which of the following lumbar puncture findings is associated with her condition?
Correct
This patient has multiple sclerosis, which is a neurologic disorder that causes variable motor, sensory, visual, and cerebellar dysfunction as a result of multiple focal areas of CNS demyelination. The patient’s orbital pain is likely due to optic neuritis. Dyschromatopsia is the change in color perception and may be more prominent than visual disturbance. Although MRI is the gold standard, lumbar puncture can aid in the diagnosis. The lumbar puncture in approximately 50% of the cases will show pleocytosis, which is an increased number of lymphocytes. In 85%–95% of cases, there will be oligoclonal bands of immunoglobulin G.
IgM and IgG antibodies to B. burgdorferi (A) is seen in the CSF in patients with secondary Lyme disease. A positive CSF VDRL (C) is seen in patients with tertiary syphilis. Xanthochromia (D) is a yellow discoloration of the CSF sometimes seen in patients with a subarachnoid hemorrhage.
Multiple Sclerosis
• Patient will be a caucasian female
• Complaining of pain with eye movement, monocular vision loss, sensory abnormalities
• PE will show spinal electric shock sensation with neck flexion (Lhermitte phenomenon)
• CSF will show ↑ IgG protein, WBC pleocytosis
• Diagnosis is made by T2-weighted MRI
• Most commonly caused by a demyelinating disorder
• Treatment is symptomatic, methylprednisolone
• Comments: Bilateral internuclear ophthalmoplegia (eyes can’t look at nose) is pathognomonic
Incorrect
This patient has multiple sclerosis, which is a neurologic disorder that causes variable motor, sensory, visual, and cerebellar dysfunction as a result of multiple focal areas of CNS demyelination. The patient’s orbital pain is likely due to optic neuritis. Dyschromatopsia is the change in color perception and may be more prominent than visual disturbance. Although MRI is the gold standard, lumbar puncture can aid in the diagnosis. The lumbar puncture in approximately 50% of the cases will show pleocytosis, which is an increased number of lymphocytes. In 85%–95% of cases, there will be oligoclonal bands of immunoglobulin G.
IgM and IgG antibodies to B. burgdorferi (A) is seen in the CSF in patients with secondary Lyme disease. A positive CSF VDRL (C) is seen in patients with tertiary syphilis. Xanthochromia (D) is a yellow discoloration of the CSF sometimes seen in patients with a subarachnoid hemorrhage.
Multiple Sclerosis
• Patient will be a caucasian female
• Complaining of pain with eye movement, monocular vision loss, sensory abnormalities
• PE will show spinal electric shock sensation with neck flexion (Lhermitte phenomenon)
• CSF will show ↑ IgG protein, WBC pleocytosis
• Diagnosis is made by T2-weighted MRI
• Most commonly caused by a demyelinating disorder
• Treatment is symptomatic, methylprednisolone
• Comments: Bilateral internuclear ophthalmoplegia (eyes can’t look at nose) is pathognomonic
Question 4 of 10
4. Question
A 55-year-old man presents to the ED with blurry vision and difficulty speaking and swallowing. His symptoms began gradually. He also complains of a dry mouth, painful tongue, and sore throat. Which of the following is the most likely diagnosis?
Correct
There are 7 types of botulinum toxin (A through G) produced by C. botulinum, but only types A, B, E, and F cause illness in humans. Clinically, patients first exhibit cranial nerve dysfunction, with diplopia, dysphonia, dysphagia, and dysarthria being most prominent. Vertigo is also a common symptom. Subsequently, a descending symmetrical weakness occurs, involving the upper and lower extremities and the muscles of respiration. Decreased salivation (due to blockade of cholinergic fibers) causes a dry mouth, which may be so severe that patients complain of a painful tongue and sore throat. This constellation of symptoms should prompt the emergency physician to inquire about the ingestion of home-canned foods.
Diphtheria (B) is associated with descending paralysis. It is distinguished by the prolonged interval between pharyngitis and neurologic symptoms. Eaton-Lambert syndrome (C) is a rare autoimmune disease associated with descending paralysis but usually does not involve bulbar muscles. More than half of patients with Eaton-Lambert syndrome have an underlying malignancy, most commonly small cell lung cancer; it is therefore regarded as a paraneoplastic syndrome. Myasthenia gravis (D) is an autoimmune disease associated with antibodies that block acetylcholine receptors at the postsynaptic junction. The hallmark of myasthenia gravis is fatigability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement, facial expressions, chewing, talking, and swallowing are especially susceptible. However, no autonomic symptoms are present.
Incorrect
There are 7 types of botulinum toxin (A through G) produced by C. botulinum, but only types A, B, E, and F cause illness in humans. Clinically, patients first exhibit cranial nerve dysfunction, with diplopia, dysphonia, dysphagia, and dysarthria being most prominent. Vertigo is also a common symptom. Subsequently, a descending symmetrical weakness occurs, involving the upper and lower extremities and the muscles of respiration. Decreased salivation (due to blockade of cholinergic fibers) causes a dry mouth, which may be so severe that patients complain of a painful tongue and sore throat. This constellation of symptoms should prompt the emergency physician to inquire about the ingestion of home-canned foods.
Diphtheria (B) is associated with descending paralysis. It is distinguished by the prolonged interval between pharyngitis and neurologic symptoms. Eaton-Lambert syndrome (C) is a rare autoimmune disease associated with descending paralysis but usually does not involve bulbar muscles. More than half of patients with Eaton-Lambert syndrome have an underlying malignancy, most commonly small cell lung cancer; it is therefore regarded as a paraneoplastic syndrome. Myasthenia gravis (D) is an autoimmune disease associated with antibodies that block acetylcholine receptors at the postsynaptic junction. The hallmark of myasthenia gravis is fatigability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement, facial expressions, chewing, talking, and swallowing are especially susceptible. However, no autonomic symptoms are present.
Question 5 of 10
5. Question
A 45-year-old woman presents complaining of one day of vision loss in her left eye associated with a left retro-orbital headache. She denies trauma or preceding illness. On exam, her vital signs are T 36.8ºC, BP 112/80 mm Hg, HR 74 bpm. Visual acuity is 20/20 in the right eye, 20/400 in the left eye, and 20/40 using both eyes. She has a left-sided afferent pupillary defect. Visual field testing reveals left-sided central vision loss. Which of the following is most accurate regarding her condition?
Correct
The patient’s exam is consistent with optic neuritis, an acute monocular loss of vision caused by focal demyelination of the optic nerve. Most cases are retrobulbar and do not involve any visible changes on fundoscopy (especially during an acute episode). But, on occasion and with more protracted cases, optic disk pallor may be seen. An afferent pupillary defect, however, is always present. Approximately 30% of patients presenting with acute optic neuritis develop multiple sclerosis within 5 years. The classic clinical syndrome of MS consists of recurring episodes of neurologic symptoms that rapidly evolve over days and slowly resolve.
Controlling blood glucose levels (A) has not been shown to influence the course of optic neuritis or multiple sclerosis. Optic neuritis is not associated with (B) increased (i.e., > 20) intraocular pressure. Magnetic resonance venography (MRV) (C) does not have a role in the diagnosis of optic neuritis or MS. However, a T2-weighted MRI can aid in the diagnosis by demonstrating lesions in the periventricular white matter—a finding that differentiates simple optic neuritis (where white matter changes are absent) from MS. Such an approach is critical in restoring vision in cases of central retinal artery occlusion (E), not optic neuritis.
Incorrect
The patient’s exam is consistent with optic neuritis, an acute monocular loss of vision caused by focal demyelination of the optic nerve. Most cases are retrobulbar and do not involve any visible changes on fundoscopy (especially during an acute episode). But, on occasion and with more protracted cases, optic disk pallor may be seen. An afferent pupillary defect, however, is always present. Approximately 30% of patients presenting with acute optic neuritis develop multiple sclerosis within 5 years. The classic clinical syndrome of MS consists of recurring episodes of neurologic symptoms that rapidly evolve over days and slowly resolve.
Controlling blood glucose levels (A) has not been shown to influence the course of optic neuritis or multiple sclerosis. Optic neuritis is not associated with (B) increased (i.e., > 20) intraocular pressure. Magnetic resonance venography (MRV) (C) does not have a role in the diagnosis of optic neuritis or MS. However, a T2-weighted MRI can aid in the diagnosis by demonstrating lesions in the periventricular white matter—a finding that differentiates simple optic neuritis (where white matter changes are absent) from MS. Such an approach is critical in restoring vision in cases of central retinal artery occlusion (E), not optic neuritis.
Question 6 of 10
6. Question
A 34-year-old man presents with complaints of progressive lower extremity weakness over the past 2 days associated with 2 weeks of diarrhea that has since resolved. Vital signs are HR 89, BP 160/95, and RR 12. On exam, you note symmetric lower extremity weakness with intact sensation and absent ankle reflexes. Which of the following would help to support the most likely diagnosis?
Correct
The patient is most likely suffering from Guillain-Barré syndrome, a progressive, ascending demyelinating polyneuropathy that typically begins with lower extremity weakness. Classically, GBS presents with symmetric lower extremity weakness, decreased or absent deep tendon reflexes, and little or no sensory involvement (although variable). It follows a respiratory or gastrointestinal infection by weeks to days. Common organisms implicated include Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and Mycoplasma pneumoniae. Elevated proteinwith only a mild pleocytosis on cerebrospinal fluid analysis (termed albuminocytologic dissociation) is highly specific in the clinical setting of suspected GBS. Patients with probable GBS should receive a neurology consult and be admitted for either intravenous immunoglobulin (IVIG) therapy or plasma exchange. Both IVIG and plasma exchange have been demonstrated to be more effective than placebo has, but no advantage is incurred upon administration of both therapies. Neither therapy has been proven more effective than the other.
Selective enhancement of the anterior spinal nerve roots (D) on MRI is suggestive. Nearly 33% of patients diagnosed with GBS will require ventilator support. Factors associated with an increased need for ventilator support include a decreased forced vital capacity (FVC) (C) and a negative inspiratory force (NIF) less than 30 cm water. Other useful adjuncts include peak expiratory flow rate (PEFR) and arterial blood gas to evaluate for carbon dioxide retention. Corticosteroids alone (B) are no longer recommended, but IV steroids coadministered with IVIG may speed recovery. Regardless, steroids have no role in the diagnosis of GBS.
Incorrect
The patient is most likely suffering from Guillain-Barré syndrome, a progressive, ascending demyelinating polyneuropathy that typically begins with lower extremity weakness. Classically, GBS presents with symmetric lower extremity weakness, decreased or absent deep tendon reflexes, and little or no sensory involvement (although variable). It follows a respiratory or gastrointestinal infection by weeks to days. Common organisms implicated include Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and Mycoplasma pneumoniae. Elevated proteinwith only a mild pleocytosis on cerebrospinal fluid analysis (termed albuminocytologic dissociation) is highly specific in the clinical setting of suspected GBS. Patients with probable GBS should receive a neurology consult and be admitted for either intravenous immunoglobulin (IVIG) therapy or plasma exchange. Both IVIG and plasma exchange have been demonstrated to be more effective than placebo has, but no advantage is incurred upon administration of both therapies. Neither therapy has been proven more effective than the other.
Selective enhancement of the anterior spinal nerve roots (D) on MRI is suggestive. Nearly 33% of patients diagnosed with GBS will require ventilator support. Factors associated with an increased need for ventilator support include a decreased forced vital capacity (FVC) (C) and a negative inspiratory force (NIF) less than 30 cm water. Other useful adjuncts include peak expiratory flow rate (PEFR) and arterial blood gas to evaluate for carbon dioxide retention. Corticosteroids alone (B) are no longer recommended, but IV steroids coadministered with IVIG may speed recovery. Regardless, steroids have no role in the diagnosis of GBS.
Question 7 of 10
7. Question
A 45-year-old woman complains of two days of fluctuating diplopia and dysphagia. Her exam reveals a left cranial nerve VI palsy, ptosis, and proximal muscle weakness in her extremities. She notes significant exercise intolerance over the past two days as well. What is the pathophysiology of her disease?
Correct
This patient is having a myasthenic crisis, caused by antibodies to the acetylcholine receptor (AChR) at the neuromuscular junction. Failure to respond to acetylcholine stimulation leads to decreased muscle fiber activationand muscle weakness. The antibodies cause AChR degradation, dysfunction, and blockade. Ptosis and diplopia are most commonly the first symptoms. Patients may also experience dysphagia, proximal muscle weakness, and dyspnea. A full myasthenic crisis may lead to respiratory failure due to flaccid paralysis of the muscles of respiration.
Botulinum toxin inhibits acetylcholine release at the synapse (B). It is produced by Clostridium botulinum, an anaerobic spore-forming bacterium. C. botulinum occurs naturally in the soil and causes human disease when ingested. Botulism is associated with a descending symmetric paralysis. Amyotrophic lateral sclerosis (ALS) is caused by a mutation of superoxide dismutase (C) leading to an abnormal response to stress and cell death. Central and peripheral nerves are affected with sparing of sensory and cognitive function. Initial symptoms are muscle weakness, atrophy, fasciculations, dysarthria, and dysphagia. Parkinson’s disease is associated with depigmentation and dopaminergic neuron loss (D) in the midbrain, especially the substantia nigra. It is also characterized by Lewy bodies, which are cytoplasmic inclusions seen under the microscope. Parkinson’s disease is characterized by tremor, cogwheel rigidity, bradykinesia or akinesia, and postural and equilibrium impairment.
Incorrect
This patient is having a myasthenic crisis, caused by antibodies to the acetylcholine receptor (AChR) at the neuromuscular junction. Failure to respond to acetylcholine stimulation leads to decreased muscle fiber activationand muscle weakness. The antibodies cause AChR degradation, dysfunction, and blockade. Ptosis and diplopia are most commonly the first symptoms. Patients may also experience dysphagia, proximal muscle weakness, and dyspnea. A full myasthenic crisis may lead to respiratory failure due to flaccid paralysis of the muscles of respiration.
Botulinum toxin inhibits acetylcholine release at the synapse (B). It is produced by Clostridium botulinum, an anaerobic spore-forming bacterium. C. botulinum occurs naturally in the soil and causes human disease when ingested. Botulism is associated with a descending symmetric paralysis. Amyotrophic lateral sclerosis (ALS) is caused by a mutation of superoxide dismutase (C) leading to an abnormal response to stress and cell death. Central and peripheral nerves are affected with sparing of sensory and cognitive function. Initial symptoms are muscle weakness, atrophy, fasciculations, dysarthria, and dysphagia. Parkinson’s disease is associated with depigmentation and dopaminergic neuron loss (D) in the midbrain, especially the substantia nigra. It is also characterized by Lewy bodies, which are cytoplasmic inclusions seen under the microscope. Parkinson’s disease is characterized by tremor, cogwheel rigidity, bradykinesia or akinesia, and postural and equilibrium impairment.
Question 8 of 10
8. Question
A 75-year-old male presents to the ED with his son. The son reports a gradual loss of mental capacity and recent falls. His father now has to wear a diaper because of urinary incontinence. Exam is significant for a confused male with a wide-based gait. What is the expected Head CT finding?
Correct
Normal pressure hydrocephalus (NPH) is characterized by the following characteristics: wet, wacky, and wobbly. More specifically, it includes a triad of progressive dementia, ataxia and urinary frequency or incontinence. It is a reversible cause of dementia and results from defective uptake of CSF. Head CT will reveal ventricular enlargement. Atrophy may occur in chronic alcoholics or the elderly, but is neither sensitive nor specific for NPH. A brain mass can cause a variety of symptoms, but headache with a neurologic deficit would be a more common presentation
Incorrect
Normal pressure hydrocephalus (NPH) is characterized by the following characteristics: wet, wacky, and wobbly. More specifically, it includes a triad of progressive dementia, ataxia and urinary frequency or incontinence. It is a reversible cause of dementia and results from defective uptake of CSF. Head CT will reveal ventricular enlargement. Atrophy may occur in chronic alcoholics or the elderly, but is neither sensitive nor specific for NPH. A brain mass can cause a variety of symptoms, but headache with a neurologic deficit would be a more common presentation
Question 9 of 10
9. Question
Which of the following characteristics separates the clinical picture of alcoholic versus diabetic neuropathy?
Correct
The presence of myopathy and cerebellar degeneration helps distinguish alcoholic neuropathy. Otherwise, the clinical pictures are similar. Incontinence is not a typical feature of either.
Incorrect
The presence of myopathy and cerebellar degeneration helps distinguish alcoholic neuropathy. Otherwise, the clinical pictures are similar. Incontinence is not a typical feature of either.
Question 10 of 10
10. Question
You have intubated a patient in myasthenic crisis but do not have plasmapheresis immediately available in your hospital. Your next choice of therapy would be:
Correct
Though evidence supporting IV immune globulin is weak, it is an accepted alternative to plasmapheresis. Pyridostigmine and neostigmine are used orally for maintenance and not for acute crisis, and the IV dose might cause complications from the cholinergic excess such as increased secretions.
Incorrect
Though evidence supporting IV immune globulin is weak, it is an accepted alternative to plasmapheresis. Pyridostigmine and neostigmine are used orally for maintenance and not for acute crisis, and the IV dose might cause complications from the cholinergic excess such as increased secretions.
For our final week of Neuro, we will be doing a FLIP with Dr. Unold and Foundations with Dr. Praamsma. Special guests include Dr. Eden and Kelsey Neeley with Palliative Care.
CORE CONTENT Harwood and Nuss Chapter 160 Neuropathies & Disease of NMJ Transmission Harwood and Nuss Chapter 161 Demyelinating Disease Harwood and Nuss Chapter 162 Parkonsonism and Movement Disorders
Another week, more neuro! This week we’ll be starting off with a Follow Up Rounds with Dr. Shawn Sloan. Then we’ll kick off our Flips with Drs. Rousseau and Shane. We’ve got some attending led lectures this week as well – Dr. Dubey will be talking about CVAs and Dr. Wazim Mohamed from the neuro ICU will give us a deep dive into status epilepticus. We’ll wrap up the day with a journal club with Dr. McGlynn!
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Question 1 of 10
1. Question
A 66-year old male with a history of atrial fibrillation on coumadin presents to the Emergency Department with stroke-like symptoms for 30 minutes. Physical exam is significant for a right-sided facial droop, global aphasia, and right upper weakness. Bedside serum glucose is 99mg/dL (5.5mmol/L). ECG demonstrates atrial fibrillation with no ischemic changes, at a rate of 94. BP 191/100, HR 94, RR 14, T 99.0F (37.2C), O2Sat 100% room air. CT head image is shown. INR results 4.4. What is the most appropriate next step in management?
Correct
The correct answer is immediate reversal of the anticoagulation (whether with fresh frozen plasma, prothrombin complex concentrate, recombinant factor VIIa). High dose vitamin K intravenously should be administered, however its reversal mechanism takes approximately 12 to 24 hours, during which time the intracerebral hemorrhage may continue to enlarge. Plasma, prothrombin complex concentrate, or recombinant factor VIIa are more appropriate choices for immediate reversal of warfarin’s anticoagulant action. Protamine sulfate is the reversal agent for heparin, not coumadin. The 2010 AHA/ASA guidelines recommend against the use of prophylactic antiepileptic drugs. However, if a seizure occurs, then antiepileptic drugs would be appropriate to administer, in order to prevent recurrent seizures.
Incorrect
The correct answer is immediate reversal of the anticoagulation (whether with fresh frozen plasma, prothrombin complex concentrate, recombinant factor VIIa). High dose vitamin K intravenously should be administered, however its reversal mechanism takes approximately 12 to 24 hours, during which time the intracerebral hemorrhage may continue to enlarge. Plasma, prothrombin complex concentrate, or recombinant factor VIIa are more appropriate choices for immediate reversal of warfarin’s anticoagulant action. Protamine sulfate is the reversal agent for heparin, not coumadin. The 2010 AHA/ASA guidelines recommend against the use of prophylactic antiepileptic drugs. However, if a seizure occurs, then antiepileptic drugs would be appropriate to administer, in order to prevent recurrent seizures.
Question 2 of 10
2. Question
A 65-year-old male with a history of diabetes presents to the ED with 5 minutes of right arm paralysis. Symptoms resolved while at home, but the patient remains concerned. Past medical history is negative for hypertension and atrial fibrillation. Physical examination reveals blood pressure of 130/70 mmHg and a normal neurologic examination. Based on his ABCD2 score, what is the most appropriate disposition?
Correct
Transient ischemic attack is defined as a transient neurologic deficit that has complete resolution within 24 hours. The ABCD2 score can be used to predict likelihood of subsequent stroke within 2 days. Low risk patients (scores of 0-3) may be discharged home if they have reliable follow-up within two days, whereas moderate risk (4-5 points) and high risk (6-7 points) patients should be admitted for echocardiography, carotid dopplers, and likely carotid endarterectomy.
The scoring system is as follows:
Age of 60 years or greater = 1 point
Initial SBP of 140 or greater OR DBP of 90 or greater = 1 point
Clinical features (Unilateral weakness = 2 points; Speech disturbance without weakness = 1 point; Other symptoms = 0 points)
Duration of symptoms (<10 minutes = 0 points; 10-59 minutes = 1 point; 60 minutes or greater = 2 points)
History of diabetes = 1 point
This patient’s score = 4. He receives 1 point for age and 2 points for unilateral weakness as well as 1 point for history of diabetes.
Incorrect
Transient ischemic attack is defined as a transient neurologic deficit that has complete resolution within 24 hours. The ABCD2 score can be used to predict likelihood of subsequent stroke within 2 days. Low risk patients (scores of 0-3) may be discharged home if they have reliable follow-up within two days, whereas moderate risk (4-5 points) and high risk (6-7 points) patients should be admitted for echocardiography, carotid dopplers, and likely carotid endarterectomy.
The scoring system is as follows:
Age of 60 years or greater = 1 point
Initial SBP of 140 or greater OR DBP of 90 or greater = 1 point
Clinical features (Unilateral weakness = 2 points; Speech disturbance without weakness = 1 point; Other symptoms = 0 points)
Duration of symptoms (<10 minutes = 0 points; 10-59 minutes = 1 point; 60 minutes or greater = 2 points)
History of diabetes = 1 point
This patient’s score = 4. He receives 1 point for age and 2 points for unilateral weakness as well as 1 point for history of diabetes.
Question 3 of 10
3. Question
A 65-year old male is brought in by EMS to the Emergency Department for possible stroke. Physical exam is significant for right hemifacial, right arm and right leg weakness. The remainder of the motor and sensory exam is grossly normal. What is the most likely location of this patient’s stroke?
Correct
Incorrect
The correct answer is internal capsule (likely posterior limb) or thalamus. This patient has a pure motor lacunar stroke syndrome, manifested by: pure motor contralateral hemiparesis without any sensory deficits. Lateral frontoparietal, superior temporal is a complete middle cerebral artery distribution, which is manifested by: contralateral hemianesthesia, hemiparesis, hemianopia with gaze preference; If dominant hemisphere: aphasia and apraxia; if nondominant hemisphere: aprosodia, hemineglect. Lateral medulla also known as Wallenberg syndrome, this is a brainstem syndrome manifested by: ipsilateral facial sensory loss, Horner’s syndrome, palatal weakness, dysphagia and ataxia, contralateral body pain and temperature loss. Medial frontoparietal lobes is descriptive of anterior cerebral artery distribution stroke, which is manifested by: contralateral anesthesia, leg > arm hemiparesis, abulia. If dominant hemisphere: mutism; if nondominant hemi- sphere: acute confusional state.
Question 4 of 10
4. Question
A 70 year old female with diabetes and hypertension presents to the emergency department with a chief complaint of left arm and left face numbness and weakness, and difficulty speaking. The symptoms lasted for approximately 45 minutes and then resolved. Vitals are: BP 160/90 HR 92 RR 12 O2sat 99%. Neurologic exam is normal. Blood glucose is 285. EKG reveals atrial fibrillation. Upon admission, the patient has a carotid duplex which reveals right carotid stenosis of 65%. Which of the following interventions will most likely reduce this patient’s immediate mortality?
Correct
The patient had a transient ischemic attack. Two interventions that reduce mortality in patients with TIA are anticoagulation for patients with atrial fibrillation or LV thrombus, and carotid endarterectomy for carotid stenosis > 70%. The patient only has 65% stenosis, thus anticoagulation is the better answer choice. While long-term blood pressure control is important in decreasing morbidity and mortality for this patient, emergent blood pressure control has not been shown to decrease the immediate morbidity of this patient. Long-term blood glucose control is also important in decreasing morbidity and mortality for this patient, emergent blood glucose control has not been shown to decrease the immediate morbidity of this patient
Incorrect
The patient had a transient ischemic attack. Two interventions that reduce mortality in patients with TIA are anticoagulation for patients with atrial fibrillation or LV thrombus, and carotid endarterectomy for carotid stenosis > 70%. The patient only has 65% stenosis, thus anticoagulation is the better answer choice. While long-term blood pressure control is important in decreasing morbidity and mortality for this patient, emergent blood pressure control has not been shown to decrease the immediate morbidity of this patient. Long-term blood glucose control is also important in decreasing morbidity and mortality for this patient, emergent blood glucose control has not been shown to decrease the immediate morbidity of this patient
Question 5 of 10
5. Question
A 75 year old male presents with weakness and decreased sensation on the left side of his face, arm and leg. His home nurse reports onset of symptoms 2 hours ago. Strength is tested and found to be 1/5 in the face and arm, and 3/5 in the leg on the affected side. Gaze preference is towards the right. Head CT is shown. Which of the following is clearly an indication for thrombolysis?
Correct
The indications for tPA include age at least 18 years, clinical diagnosis of ischemic stroke (no finding on noncontrast Head CT), and time of symptoms onset <4.5 hours.
There are multiple contraindications to systemic thrombolysis (tPA) including: significant stroke/head trauma in prior 3months, prior intracranial hemorrhage, intracranial neoplasm/AVM/aneurysm, recent intracranial/intraspinal surgery, arterial puncture at noncompressible site in past 1 week, sustained SBP at least 185 or DBP at least 110 mmHg, serum glucose <50 mg/dL (<2.8 mmol/L), active internal bleeding or acute bleeding diatheses, current use of anticoagulants or INR > 1.7 and platelet count < 100,000/μL.
Incorrect
The indications for tPA include age at least 18 years, clinical diagnosis of ischemic stroke (no finding on noncontrast Head CT), and time of symptoms onset <4.5 hours.
There are multiple contraindications to systemic thrombolysis (tPA) including: significant stroke/head trauma in prior 3months, prior intracranial hemorrhage, intracranial neoplasm/AVM/aneurysm, recent intracranial/intraspinal surgery, arterial puncture at noncompressible site in past 1 week, sustained SBP at least 185 or DBP at least 110 mmHg, serum glucose <50 mg/dL (<2.8 mmol/L), active internal bleeding or acute bleeding diatheses, current use of anticoagulants or INR > 1.7 and platelet count < 100,000/μL.
Question 6 of 10
6. Question
A 36 year old female patient presents to the emergency department with a headache that started one hour prior to presentation. She describes it as acute onset, maximal at onset, and different from any previous headaches that she has had. Her CT scan was negative for any intracranial process. Her lumbar puncture results were the following: No organisms seen, WBC 1 per mm3, RBC 10,000 per mm3, protein 60 mg per dL, glucose 50 mg per dL. Which of the following blood vessels is most likely affected?
Correct
The patient has a subarachnoid hemorrhage, of which there are 3 major causes: ruptured aneurysm, leaking AVM, or a peri-mesencephalic bleed. Of ruptured aneurysms, the most common blood vessel affected is the anterior communicating artery in the circle of Willis.
Incorrect
The patient has a subarachnoid hemorrhage, of which there are 3 major causes: ruptured aneurysm, leaking AVM, or a peri-mesencephalic bleed. Of ruptured aneurysms, the most common blood vessel affected is the anterior communicating artery in the circle of Willis.
Question 7 of 10
7. Question
A 24-year-old man is brought to the emergency department by emergency medical services (EMS). The patient’s mother reports that she found her son seizing on the floor of her living room approximately 30 minutes before arrival at the hospital. Two months ago, the patient returned from Mexico, where he had been incarcerated for 6 months. The mother reports that during the past 2 months she has seen her son consistently take his seizure medicine and several other pills for a “bad lung infection” he got in Mexico. She cannot remember the names of any of the medications. Several doses of IV lorazepam have been administered with no effect on the patient’s seizure activity. Which of the following medications would be the most effective in aborting his seizure activity?
Correct
Several historical clues in this scenario point to tuberculosis being the “bad lung infection” in this patient. In patients with seizures that are refractory to benzodiazepines, isoniazid (a common medication for tuberculosis) overdose is a possibility and should be considered. Pyridoxine is the only fully effective pharmacologic treatment for toxic isoniazid seizures, although benzodiazepines have been shown to suppress seizure activity in some cases.
Incorrect
Several historical clues in this scenario point to tuberculosis being the “bad lung infection” in this patient. In patients with seizures that are refractory to benzodiazepines, isoniazid (a common medication for tuberculosis) overdose is a possibility and should be considered. Pyridoxine is the only fully effective pharmacologic treatment for toxic isoniazid seizures, although benzodiazepines have been shown to suppress seizure activity in some cases.
Question 8 of 10
8. Question
A mother arrives with her 10-year-old daughter (41 kg) who has been seizing for at least 10 minutes. The patient has a history of epilepsy, and a home dose of rectal diazepam has been ineffective. The mother states the child has been in her usual state of good health until the seizure began, and there has been no history of trauma. Which of the following is the most appropriate initial action?
Correct
Early, aggressive benzodiazepine administration is associated with decreased morbidity and mortality in status epilepticus. Intramuscular midazolam is superior to intravenous lorazepam; in addition, the dose of lorazepam is inadequate. Endotracheal intubation may ultimately be required, but is a secondary priority; use of a long-acting neuromuscular blockade agent, such as vecuronium, should be avoided. Cranial computed tomography may or may not be needed in this patient, depending on the response to benzodiazepine therapy. Bedside electroencephalograms are most useful in diagnosing nonconvulsive status epilepticus.
Incorrect
Early, aggressive benzodiazepine administration is associated with decreased morbidity and mortality in status epilepticus. Intramuscular midazolam is superior to intravenous lorazepam; in addition, the dose of lorazepam is inadequate. Endotracheal intubation may ultimately be required, but is a secondary priority; use of a long-acting neuromuscular blockade agent, such as vecuronium, should be avoided. Cranial computed tomography may or may not be needed in this patient, depending on the response to benzodiazepine therapy. Bedside electroencephalograms are most useful in diagnosing nonconvulsive status epilepticus.
Question 9 of 10
9. Question
A 28-year-old G3P3 woman who is 2-weeks postpartum after an uncomplicated vaginal delivery presents with acute onset of mild headache, lethargy, and double vision. Physical examination is remarkable for normal vital signs and a left eye lateral gaze palsy. The most appropriate intervention is likely to be which of the following?
Correct
Cerebral venous thrombosis may present with headache, lethargy, cranial nerve deficits, seizures, or even psychiatric complaints. CT scan and/or MRI/magnetic resonance angiography (MRA) are likely to reveal the diagnosis. Treatment includes heparin. Neurosurgical consultation is not useful. Subarachnoid hemorrhage would not be expected to cause a focal neurologic deficit. Eclampsia and meningitis would be expected to give characteristic findings on history and examination.
Incorrect
Cerebral venous thrombosis may present with headache, lethargy, cranial nerve deficits, seizures, or even psychiatric complaints. CT scan and/or MRI/magnetic resonance angiography (MRA) are likely to reveal the diagnosis. Treatment includes heparin. Neurosurgical consultation is not useful. Subarachnoid hemorrhage would not be expected to cause a focal neurologic deficit. Eclampsia and meningitis would be expected to give characteristic findings on history and examination.
Question 10 of 10
10. Question
A 33-year-old woman presents in status epilepticus. Her past history is remarkable for diabetes, hypertension, and chronic renal insufficiency. Her current medications are NPH insulin, enalapril, and furosemide. Urgent laboratory analysis reveals glucose 41 mg/dL, Na 124 mEq/L, K 5. 4 mEq/L, Cl– 91 mEq/L, HCO3– 17 mEq/L, BUN 48 mg/dL, calcium 7. 6 mg/dL, creatinine 4. 8 mg/dL, and albumin 2. 8 g/dL. What is the most likely explanation for her seizure activity?
Correct
Seizure activity may occur when the serum glucose concentration is less than 45 mg/dL. Although cation derangements may also cause seizures (hyponatremia, hypocalcemia, and hypomagnesemia), sodium levels less than 120 mEq/L are typically seen, with these levels having been achieved rapidly rather than slowly. This level of hypocalcemia is appropriate for the decreased albumin level, likely rendering ionized calcium levels normal. Hyperkalemia does not cause seizures. Uremia may cause status epilepticus, but only at higher levels in cases of a more rapid onset of untreated renal failure or during rapid fluid shifts such as during dialysis.
Incorrect
Seizure activity may occur when the serum glucose concentration is less than 45 mg/dL. Although cation derangements may also cause seizures (hyponatremia, hypocalcemia, and hypomagnesemia), sodium levels less than 120 mEq/L are typically seen, with these levels having been achieved rapidly rather than slowly. This level of hypocalcemia is appropriate for the decreased albumin level, likely rendering ionized calcium levels normal. Hyperkalemia does not cause seizures. Uremia may cause status epilepticus, but only at higher levels in cases of a more rapid onset of untreated renal failure or during rapid fluid shifts such as during dialysis.
Welcome to week one of our 3-part Neurology Series. Get ready for 2 great FLIPs and another awesome Foundations! This week is a lot of bread and butter of EM so make sure to review. See you there!
Hey friends! Another week, more bugs. This week we’re kicking off with another PGY-3 M&M with a DMC legacy, Dr. Saker. We’ll also have Dr. Berk joining us for another session of ECG rounds as well as a guest lecture from Dr. Ridelman on sepsis. Our flips this week will cover some environmental infectious with (our first intern Flip!!) Dr. Svinarich and fungal infectious with resident fun-guy, Dr. Pickos. We’ll wrap up the day with journal club with Krit-Kare-Keith Dr. Alangaden.
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Question 1 of 10
1. Question
A 24-year-old man presents to the ED after a syncopal episode. He is an avid hiker. He had a rash a few weeks prior that has since cleared. Vital signs are BP 100/74 mm Hg, HR 50 beats/minute, RR 18 breaths/minute, and T 99.1°F. What is the most likely finding on this patient’s electrocardiogram?
Correct
This patient is exhibiting signs and symptoms of Lyme disease. Lyme disease is the most common vector-borne disease in the United States. It is endemic to New England, the mid-Atlantic states, and the upper Midwest. It is caused by the spirochete Borrelia burgdorferi and transmitted by the Ixodes dammini tick, more commonly known as the deer tick. The tick must be attached for more than 48 hours for transmission to occur. There are three stages of clinical Lyme disease. Early Lyme disease is characterized by erythema migrans, an erythematous blanching patch that may have central clearing and classically has a “bull’s eye” appearance. Hematogenous spread leads to diffuse erythema migrans, which spares the palms and soles. Acute disseminated Lyme disease occurs approximately 4 weeks after initial infection and can include meningoencephalitis, Bell’s palsy (which may be bilateral), or carditis which often manifests with variable AV block. This AV blockade may be high-grade and require temporary transcutaneous or transvenous pacing; however, it nearly universally resolves gradually with IV antibiotics and has a favorable prognosis with no need for permanent pacemaker placement. Late Lyme disease develops greater than 1 year after initial infection and includes chronic arthritis with or without chronic subtle encephalopathy. Only 50% of patients remember a tick bite; thus, diagnosis may be difficult. Erythema migrans is diagnostic; however, not all patients present with this finding. Initial screening involves ELISA testing with Western Blot and PCR to confirm the diagnosis. If the diagnosis is suspected, empiric treatment should be administered. Treatment for early Lyme disease and mild acute disseminated Lyme disease is doxycycline for 3-4 weeks. In pregnant women or children under the age of 8 years, amoxicillin should be substituted. Patients with neurologic or cardiac manifestations should be admitted and treated with IV ceftriaxone.
Incorrect
This patient is exhibiting signs and symptoms of Lyme disease. Lyme disease is the most common vector-borne disease in the United States. It is endemic to New England, the mid-Atlantic states, and the upper Midwest. It is caused by the spirochete Borrelia burgdorferi and transmitted by the Ixodes dammini tick, more commonly known as the deer tick. The tick must be attached for more than 48 hours for transmission to occur. There are three stages of clinical Lyme disease. Early Lyme disease is characterized by erythema migrans, an erythematous blanching patch that may have central clearing and classically has a “bull’s eye” appearance. Hematogenous spread leads to diffuse erythema migrans, which spares the palms and soles. Acute disseminated Lyme disease occurs approximately 4 weeks after initial infection and can include meningoencephalitis, Bell’s palsy (which may be bilateral), or carditis which often manifests with variable AV block. This AV blockade may be high-grade and require temporary transcutaneous or transvenous pacing; however, it nearly universally resolves gradually with IV antibiotics and has a favorable prognosis with no need for permanent pacemaker placement. Late Lyme disease develops greater than 1 year after initial infection and includes chronic arthritis with or without chronic subtle encephalopathy. Only 50% of patients remember a tick bite; thus, diagnosis may be difficult. Erythema migrans is diagnostic; however, not all patients present with this finding. Initial screening involves ELISA testing with Western Blot and PCR to confirm the diagnosis. If the diagnosis is suspected, empiric treatment should be administered. Treatment for early Lyme disease and mild acute disseminated Lyme disease is doxycycline for 3-4 weeks. In pregnant women or children under the age of 8 years, amoxicillin should be substituted. Patients with neurologic or cardiac manifestations should be admitted and treated with IV ceftriaxone.
Question 2 of 10
2. Question
A 21-year-old man presents with a rash and fever. He was recently camping in North Carolina. He noted a rash that began on his ankles and wrists that is now present on his chest and back. Which of the following is the most likely diagnosis?
Correct
Rocky Mountain spotted fever (RMSF) is a tick-borne illness caused by Rickettsia rickettsii and transmitted to humans through the dog tick or Rocky Mountain wood tick. The disease is endemic in all 48 states, but most commonly occurs in thesoutheastern United States. After infection, the organism invades and replicates inside of vascular endothelial cells. The most common victims of RMSF are children. After a mean incubation period of 7 days, patients develop classic symptoms including fever, headache, myalgias, nausea and vomiting. Fever is usually the first symptom and may be the only symptom for up to one week. The rash is classically small red macules that are sometimes pruritic. The rash begins only on the ankles and feet and then spreads to the palms and soles. Thereafter, it moves centrally to the rest of the arms, legs and torso. After several days, the rash becomes papular and deeper red. In the early stage the rash blanches with direct palpation and enhances with warm compresses. In later stages, the rash becomes petechial and application of proximal pressure causes additional lesions to appear distally (Rumpel-Leede phenomenon). The cardiovascular system is affected with myocarditis and an impaired ejection fraction in some patients. Neurologically, the most common symptom is headache but may include seizures and an eosinophilic meningitis. Diagnosis is made through the identification of serum antibodies present 5 to 7 days after the infection begins. Treatment is with doxycycline
Babesiosis (A) is a tick-borne illnesses transmitted by the Ixodes tick in the northeastern part of the United States. The clinical symptoms are similar to malaria as the organism infects red blood cells causing fevers, myalgias headache and significant sweats. Approximately 20% of patients with babesiosis are co-infected with Lyme disease. Leptospirosis (B)is most commonly transmitted to humans through the urine of rodents. In most cases, patients have a flu-like illness with fever, myalgia and severe headache. Ten percent of patients develop severe leptospirosis with liver and renal failure.Lyme disease (C) is the most common vector-borne disease in the United States. The Ixodes ticks transmit the organism Borrelia burgdorferi. The initial manifestation of Lyme disease is the classic rash erythema migrans described as an erythematous macule with central clearing. With time patients develop fever, arthralgias, adenopathy and ultimately arthritis. Neurologically patients may develop unilateral or bilateral Bell’s palsy, aseptic meningitis and a neuritis causing similar pain symptoms to post-herpetic neuralgia.
Incorrect
Rocky Mountain spotted fever (RMSF) is a tick-borne illness caused by Rickettsia rickettsii and transmitted to humans through the dog tick or Rocky Mountain wood tick. The disease is endemic in all 48 states, but most commonly occurs in thesoutheastern United States. After infection, the organism invades and replicates inside of vascular endothelial cells. The most common victims of RMSF are children. After a mean incubation period of 7 days, patients develop classic symptoms including fever, headache, myalgias, nausea and vomiting. Fever is usually the first symptom and may be the only symptom for up to one week. The rash is classically small red macules that are sometimes pruritic. The rash begins only on the ankles and feet and then spreads to the palms and soles. Thereafter, it moves centrally to the rest of the arms, legs and torso. After several days, the rash becomes papular and deeper red. In the early stage the rash blanches with direct palpation and enhances with warm compresses. In later stages, the rash becomes petechial and application of proximal pressure causes additional lesions to appear distally (Rumpel-Leede phenomenon). The cardiovascular system is affected with myocarditis and an impaired ejection fraction in some patients. Neurologically, the most common symptom is headache but may include seizures and an eosinophilic meningitis. Diagnosis is made through the identification of serum antibodies present 5 to 7 days after the infection begins. Treatment is with doxycycline
Babesiosis (A) is a tick-borne illnesses transmitted by the Ixodes tick in the northeastern part of the United States. The clinical symptoms are similar to malaria as the organism infects red blood cells causing fevers, myalgias headache and significant sweats. Approximately 20% of patients with babesiosis are co-infected with Lyme disease. Leptospirosis (B)is most commonly transmitted to humans through the urine of rodents. In most cases, patients have a flu-like illness with fever, myalgia and severe headache. Ten percent of patients develop severe leptospirosis with liver and renal failure.Lyme disease (C) is the most common vector-borne disease in the United States. The Ixodes ticks transmit the organism Borrelia burgdorferi. The initial manifestation of Lyme disease is the classic rash erythema migrans described as an erythematous macule with central clearing. With time patients develop fever, arthralgias, adenopathy and ultimately arthritis. Neurologically patients may develop unilateral or bilateral Bell’s palsy, aseptic meningitis and a neuritis causing similar pain symptoms to post-herpetic neuralgia.
Question 3 of 10
3. Question
Which of the following statements regarding AIDS and parasitic infections is TRUE?
Correct
Isospora and coccidial organisms may cause an almost cholera-like diarrheal illness. Eradication is very difficult.
Malaria and invasive amebiasis are not considered opportunistic infections.
AIDS patients have much more severe allergic manifestations to the antiparasitics.
Schistosomiasis enhances HIV pathogenesis.
Incorrect
Isospora and coccidial organisms may cause an almost cholera-like diarrheal illness. Eradication is very difficult.
Malaria and invasive amebiasis are not considered opportunistic infections.
AIDS patients have much more severe allergic manifestations to the antiparasitics.
Schistosomiasis enhances HIV pathogenesis.
Question 4 of 10
4. Question
A macrocytic anemia would suggest infection from which parasite?
Correct
The fish tapeworm is associated with pernicious anemia. Hookworm and whipworm are associated with gastrointestinal iron loss and microcytic anemia. Malaria causes hemolytic anemia.
Incorrect
The fish tapeworm is associated with pernicious anemia. Hookworm and whipworm are associated with gastrointestinal iron loss and microcytic anemia. Malaria causes hemolytic anemia.
Question 5 of 10
5. Question
Parasite-induced loss of vision would be suggested by which of the following?
Correct
Onchocerciasis is a major cause of blindness worldwide. Ninety-five percent of cases occur in Africa. The biting flies are found near rivers, and humans are the only host for the parasite. It occupies the skin, resulting in pruritus, edema, and later atrophy with redundant skin folds. The following are other causes of parasite-induced visual loss: Toxoplasma can cause retinal hemorrhages, Toxocara can cause inflammatory retinal granulomas, and Acanthamoeba may cause a keratitis in contact lens wearers.
Incorrect
Onchocerciasis is a major cause of blindness worldwide. Ninety-five percent of cases occur in Africa. The biting flies are found near rivers, and humans are the only host for the parasite. It occupies the skin, resulting in pruritus, edema, and later atrophy with redundant skin folds. The following are other causes of parasite-induced visual loss: Toxoplasma can cause retinal hemorrhages, Toxocara can cause inflammatory retinal granulomas, and Acanthamoeba may cause a keratitis in contact lens wearers.
Question 6 of 10
6. Question
A 45-year-old man with HIV-AIDS and a CD4 count of 150 cells/mm3 presents with several days of fever and dry cough. His oxygen saturation is 85% on room air. Lung auscultation is notable for decreased breath sounds bilaterally and crackles at the bases. A chest X-ray reveals bilateral interstitial infiltrates. Which of the following medication regimens is most appropriate?
Correct
This patient has clinical and radiographic evidence for pneumonia. Community-acquired pneumonia caused by Streptococcus pneumoniae is the most common cause of pneumonia in HIV-infected patients. Therefore, he should receive ceftriaxone and azithromycin. Additionally, his low CD4 count puts him at risk of opportunistic infections, such as Pneumocystis jiroveci pneumonia (PJP), formerly known as Pneumocystis carinii pneumonia (PCP). PJP is the most common opportunistic infection among AIDS patients. Signs and symptoms of PJP pneumonia include fatigue, fever, cough, and hypoxia. Chest radiographs typically show diffuse interstitial infiltrates, though negative radiographs are not unusual in PJP. Serum lactate dehydrogenase levels are often elevated. Initial therapy for PJP includes trimethoprim/sulfamethoxazole. In severe cases, corticosteroids are also given. The indications for corticosteroid use include an arterial oxygen partial pressure of < 70 mm Hg (equivalent to an oxygen saturation of <~93%) and an alveolar-arterial gradient > 35 mm Hg. Prophylaxis with oral trimethoprim-sulfamethoxazole is recommended for all HIV-positive patients with CD4 counts less than 200 cells/mm3 to prevent PJP pneumonia.
Amphotericin B (A) is used in the treatment of disseminated fungal infections, such as Aspergillus fumigatus and Cryptococcus neoformans. These infections are typically seen at a higher degree of immunosuppression. Azithromycin and ceftriaxone (B) treat most community-acquired pathogens, but do not cover opportunistic infections like PJP. Trimethoprim/sulfamethoxazole and prednisone (D) is incorrect because the patient should also receive treatment for community-acquired pneumonia.
Incorrect
This patient has clinical and radiographic evidence for pneumonia. Community-acquired pneumonia caused by Streptococcus pneumoniae is the most common cause of pneumonia in HIV-infected patients. Therefore, he should receive ceftriaxone and azithromycin. Additionally, his low CD4 count puts him at risk of opportunistic infections, such as Pneumocystis jiroveci pneumonia (PJP), formerly known as Pneumocystis carinii pneumonia (PCP). PJP is the most common opportunistic infection among AIDS patients. Signs and symptoms of PJP pneumonia include fatigue, fever, cough, and hypoxia. Chest radiographs typically show diffuse interstitial infiltrates, though negative radiographs are not unusual in PJP. Serum lactate dehydrogenase levels are often elevated. Initial therapy for PJP includes trimethoprim/sulfamethoxazole. In severe cases, corticosteroids are also given. The indications for corticosteroid use include an arterial oxygen partial pressure of < 70 mm Hg (equivalent to an oxygen saturation of <~93%) and an alveolar-arterial gradient > 35 mm Hg. Prophylaxis with oral trimethoprim-sulfamethoxazole is recommended for all HIV-positive patients with CD4 counts less than 200 cells/mm3 to prevent PJP pneumonia.
Amphotericin B (A) is used in the treatment of disseminated fungal infections, such as Aspergillus fumigatus and Cryptococcus neoformans. These infections are typically seen at a higher degree of immunosuppression. Azithromycin and ceftriaxone (B) treat most community-acquired pathogens, but do not cover opportunistic infections like PJP. Trimethoprim/sulfamethoxazole and prednisone (D) is incorrect because the patient should also receive treatment for community-acquired pneumonia.
Question 7 of 10
7. Question
Which of the following best describes the most common symptoms of acute human immunodeficiency virus infection?
Correct
In the United States, an estimated 1.2 million individuals are HIV positive, with approximately 50,000 people newly diagnosed each year. The clinical presentation of acute HIV infection, also known as acute retroviral syndrome, is variable both in type and severity of symptoms. The classic presentation is abrupt onset of a viral-like illness, which develops 10–14 days following exposure to the virus. Symptoms may include fever, malaise, sore throat, headache, arthralgias, anorexia, nausea, vomiting, and rash. Physical examination findings vary and may include generalized lymphadenopathy, nonexudative pharyngitis, mild hepatosplenomegaly, mucocutaneous ulcers, and oral thrush. A maculopapular rash on the thorax, face, and limbs may also be present. Due to the nonspecific and self-limited nature of symptoms, many affected individuals do not seek care and thus the true incidence of acute HIV is unknown. However, experts estimate that 60–90% of individuals who contract HIV develop an acute illness. Identification of acute HIV has tremendous public health implications, as acute infection represents the peak infectivity of the disease, characterized by high levels of viral shedding. Routine HIV tests used in most emergency departments measure anti-HIV antibodies, which are often falsely negative during acute infection. Therefore, when acute HIV is suspected, nucleic acid amplification tests, which directly measure viral RNA in the patient’s blood, should be utilized.
Incorrect
In the United States, an estimated 1.2 million individuals are HIV positive, with approximately 50,000 people newly diagnosed each year. The clinical presentation of acute HIV infection, also known as acute retroviral syndrome, is variable both in type and severity of symptoms. The classic presentation is abrupt onset of a viral-like illness, which develops 10–14 days following exposure to the virus. Symptoms may include fever, malaise, sore throat, headache, arthralgias, anorexia, nausea, vomiting, and rash. Physical examination findings vary and may include generalized lymphadenopathy, nonexudative pharyngitis, mild hepatosplenomegaly, mucocutaneous ulcers, and oral thrush. A maculopapular rash on the thorax, face, and limbs may also be present. Due to the nonspecific and self-limited nature of symptoms, many affected individuals do not seek care and thus the true incidence of acute HIV is unknown. However, experts estimate that 60–90% of individuals who contract HIV develop an acute illness. Identification of acute HIV has tremendous public health implications, as acute infection represents the peak infectivity of the disease, characterized by high levels of viral shedding. Routine HIV tests used in most emergency departments measure anti-HIV antibodies, which are often falsely negative during acute infection. Therefore, when acute HIV is suspected, nucleic acid amplification tests, which directly measure viral RNA in the patient’s blood, should be utilized.
Question 8 of 10
8. Question
A 39-year-old man presents to the ED with the findings seen in the above image. The lesions cannot be scraped off the surface of his tongue. Which of the following statements best describes this patient’s diagnosis?
Correct
The tongue lesions seen in the image are characteristic for oral hairy leukoplakia(OHL). This is a disease of the lingual squamous epithelium and is thought to be caused by the Epstein-Barr virus (EBV). It is highly specific for concomitant HIV infection and rarely seen in other immunocompromised states. OHL is often confused with oral candidiasis (thrush). However, unlike the lesions of thrush, OHL cannot be scraped off the tongue.
OHL most commonly develops on the lateral portions of the tongue, not the posterior oropharynx (A). The disease is caused by the Epstein-Barr virus, unlike oral thrush, which is caused by the yeast (C)Candida albicans. The plaques are painless (D), and most patients are asymptomatic.
Incorrect
The tongue lesions seen in the image are characteristic for oral hairy leukoplakia(OHL). This is a disease of the lingual squamous epithelium and is thought to be caused by the Epstein-Barr virus (EBV). It is highly specific for concomitant HIV infection and rarely seen in other immunocompromised states. OHL is often confused with oral candidiasis (thrush). However, unlike the lesions of thrush, OHL cannot be scraped off the tongue.
OHL most commonly develops on the lateral portions of the tongue, not the posterior oropharynx (A). The disease is caused by the Epstein-Barr virus, unlike oral thrush, which is caused by the yeast (C)Candida albicans. The plaques are painless (D), and most patients are asymptomatic.
Question 9 of 10
9. Question
12 year old presents to the emergency department with sudden fatigue and shortness of breath. He has a history of sickle cell disease. HR 125, BP 110/86, RR 18, temp. 38.6. Physical exam is significant for finding shown in picture below. IV access is obtained and labs are sent. What is the cause of the patients condition?
Correct
Aplastic crisis is defined as having a reticulocyte count of less than 1%. Patients with sickle cell disease who are infected with Parvovirus B19 are at risk for developing an aplastic crisis. Parvovirus B19 is the causative agent of Fifth disease and can lead to an aplastic crisis by causing a temporary arrest of red blood cell production. This is characterized by a sudden decrease in hemoglobin production by bone marrow resulting in severe anemia. Patients may present with pallor, lethargy, and shock. Treatment includes hemodynamic support and blood transfusion.
Labs that should be sent include type and cross, CBC, and reticulocyte count. This is usually self-limited disease and resolves once the viral syndrome resolves. Blood transfusions to support the patient through the anemia is the treatment along with other supportive measures.
Incorrect
Aplastic crisis is defined as having a reticulocyte count of less than 1%. Patients with sickle cell disease who are infected with Parvovirus B19 are at risk for developing an aplastic crisis. Parvovirus B19 is the causative agent of Fifth disease and can lead to an aplastic crisis by causing a temporary arrest of red blood cell production. This is characterized by a sudden decrease in hemoglobin production by bone marrow resulting in severe anemia. Patients may present with pallor, lethargy, and shock. Treatment includes hemodynamic support and blood transfusion.
Labs that should be sent include type and cross, CBC, and reticulocyte count. This is usually self-limited disease and resolves once the viral syndrome resolves. Blood transfusions to support the patient through the anemia is the treatment along with other supportive measures.
Question 10 of 10
10. Question
23 year old presents to the emergency department with a rash. They state that they were diagnosed with strep throat 5 days ago. They recently started on antibiotics which they do not know the name of. Yesterday they started to breakout in a rash which is shown below. What is the cause of the rash?
Correct
Infectious mononucleosis is caused by the Epstein-Barr virus. While young children with the disease typically have minimal, if any, symptoms related to the infection, adolescents and young adults usually have a more pronounced course. It is uncommonly seen in adults as most are immune due to a previous exposure. Patients may have a prodrome of low-grade fever, headache, and malaise. There is pharyngeal erythema and tonsillar exudates that may appear white, gray-green, or necrotic. Palatal petechiae can also be seen, but may be present in streptococcal pharyngitis as well. Severe fatigue is common and often the symptom that persists the longest. The lymphadenopathy is usually mildly tender, symmetric and involves the posterior cervical chain. Hepatosplenomegaly can be noted on examination. A generalized maculopapular rash almost always occurs following administration of amoxicillin or ampicillin although the mechanism of this is unclear. Diagnosis is made based on history and physical and can be confirmed with a positive heterophile antibody test (monospot test). Treatment is supportive. Symptoms generally resolve in 1-3 weeks although the fatigue may persist for months. Patients should refrain from contact sports for four weeks post-infection.
Incorrect
Infectious mononucleosis is caused by the Epstein-Barr virus. While young children with the disease typically have minimal, if any, symptoms related to the infection, adolescents and young adults usually have a more pronounced course. It is uncommonly seen in adults as most are immune due to a previous exposure. Patients may have a prodrome of low-grade fever, headache, and malaise. There is pharyngeal erythema and tonsillar exudates that may appear white, gray-green, or necrotic. Palatal petechiae can also be seen, but may be present in streptococcal pharyngitis as well. Severe fatigue is common and often the symptom that persists the longest. The lymphadenopathy is usually mildly tender, symmetric and involves the posterior cervical chain. Hepatosplenomegaly can be noted on examination. A generalized maculopapular rash almost always occurs following administration of amoxicillin or ampicillin although the mechanism of this is unclear. Diagnosis is made based on history and physical and can be confirmed with a positive heterophile antibody test (monospot test). Treatment is supportive. Symptoms generally resolve in 1-3 weeks although the fatigue may persist for months. Patients should refrain from contact sports for four weeks post-infection.
Welcome to week one of our Infectious Disease Block. This week, we will be delving deep into HIV, STDs and Pediatric Infections! It’s a wide variety of stuff but great review for the boards and the ultimate bread and butter. Get excited for another fun Foundations session as well!
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Question 1 of 10
1. Question
28 year old woman reports to emergency room for sudden vision loss in her right eye that occurred while she was getting ready for her mother’s funeral. In the preceding months she was present for her mother’s arduous struggle against an aggressive cancer. On exam the patient has a normal pupillary reflex and a normal fundoscopic examination. The remainder of the physical exam is normal. B-scan ocular ultrasound, CT scan, and labs are unremarkable. An emergent evaluation by the ophthalmologist also is unremarkable. What is the most likely cause of this patient’s vision loss?
Correct
Conversion disorder is typically characterized by the sudden, and often dramatic, onset of a single nonpainful neurologic disorder. The symptom cannot be explained by any known organic etiology. Conversion disorder will often be associated with recent severe stressor or conflict. The most common presentations include pseudoseizures, paralysis, numbness, aphonia, coordination disturbance, blindness and tunnel vision. This disorder has a female predominance and typically appears in adolescence and early adulthood. Patients with conversion disorder have a nondeliberate symptom and will have a flatter affect than expected under the circumstances, termed la belle indifference. This is a diagnosis of exclusion and all organic etiologies must be ruled out. The treatment involves identifying the stressor and addressing the underlying issue.
Incorrect
Conversion disorder is typically characterized by the sudden, and often dramatic, onset of a single nonpainful neurologic disorder. The symptom cannot be explained by any known organic etiology. Conversion disorder will often be associated with recent severe stressor or conflict. The most common presentations include pseudoseizures, paralysis, numbness, aphonia, coordination disturbance, blindness and tunnel vision. This disorder has a female predominance and typically appears in adolescence and early adulthood. Patients with conversion disorder have a nondeliberate symptom and will have a flatter affect than expected under the circumstances, termed la belle indifference. This is a diagnosis of exclusion and all organic etiologies must be ruled out. The treatment involves identifying the stressor and addressing the underlying issue.
Question 2 of 10
2. Question
A 48-year old male presents to the Emergency Department for chronic abdominal pain. He has a history of multiple presentations for the same, with no underlying diagnosis found despite an extensive workup. He demands hydromorphone IV for his pain, stating that his last doctor was “the best doctor he’s ever had” and immediately treated his pain. He also requests a new nurse, stating, “My current nurse is terrible, where’s the last one I had? She was the best!” Which of the following is the most likely diagnosis in this patient?
Correct
This patient likely has borderline personality disorder, characterized by unstable relationships, self image issues, labile affect, poor impulse control, and polarizing interactions with others. Antisocial personality disorder is characterized by pervasive disregard for the rights of others and failure to conform to social/legal norms, often highlighted by a history of crime/legal problems/aggressive behavior. Histrionic personality disorder is characterized by a pattern of excessive emotions and attention-seeking behavior, characterized by inappropriately seductive behavior and excessive need for approval (e.g. dramatic, flirtatious, overly enthusiastic). Narcissistic personality disorder is characterized by an excessive preoccupation with personal adequacy, power, prestige and vanity.
Incorrect
This patient likely has borderline personality disorder, characterized by unstable relationships, self image issues, labile affect, poor impulse control, and polarizing interactions with others. Antisocial personality disorder is characterized by pervasive disregard for the rights of others and failure to conform to social/legal norms, often highlighted by a history of crime/legal problems/aggressive behavior. Histrionic personality disorder is characterized by a pattern of excessive emotions and attention-seeking behavior, characterized by inappropriately seductive behavior and excessive need for approval (e.g. dramatic, flirtatious, overly enthusiastic). Narcissistic personality disorder is characterized by an excessive preoccupation with personal adequacy, power, prestige and vanity.
Question 3 of 10
3. Question
A 45-year-old female presents with sudden onset of fear and intense apprehension. She says the symptoms started 30 minutes prior when she was doing her taxes. Her only other symptoms include tingling around her mouth and in both hands. She has never had symptoms like this before. Basic laboratory studies and electrocardiogram are within normal limits. Given the most likely diagnosis, what pharmacologic therapy would be most effective in the acute setting?
Correct
Panic attacks are defined as a discrete period of sudden onset of intense apprehension and fear. Panic disorder is defined as recurrent, unexpected panic attacks and at least one month of worry surrounding the attacks. Panic attacks may be treated with short-acting benzodiazepines, whereas panic disorder may be treated with SSRIs, short-acting benzos, beta blockers and/or CBT. Long-acting benzodiazepines are generally indicated for generalized anxiety disorder.
Incorrect
Panic attacks are defined as a discrete period of sudden onset of intense apprehension and fear. Panic disorder is defined as recurrent, unexpected panic attacks and at least one month of worry surrounding the attacks. Panic attacks may be treated with short-acting benzodiazepines, whereas panic disorder may be treated with SSRIs, short-acting benzos, beta blockers and/or CBT. Long-acting benzodiazepines are generally indicated for generalized anxiety disorder.
Question 4 of 10
4. Question
A 23-year old male is brought in to the Emergency Department by his family for “odd behavior.” They deny any acute change, however they state that the patient refuses to go outside or interact with people, preferring to stay in his room. They also state that the patient believes he can see the future and read minds. The patient has no past medical history and works as a computer programmer from home. Physical exam reveals a strangely dressed young man in bright clothes. He is alert, oriented, and denies any history of auditory or visual hallucinations. His affect is slightly blunted. What is the most likely diagnosis in this patient?
Correct
The correct answer is schizotypal personality disorder, characterized by social and relationship discomforts, decrease in close relationships, and magical thinking (eccentric). Paranoid schizophrenia is unlikely in the absence of hallucinations. Also this patient, while withdrawn from society, holds a job and is highly functional.
Incorrect
The correct answer is schizotypal personality disorder, characterized by social and relationship discomforts, decrease in close relationships, and magical thinking (eccentric). Paranoid schizophrenia is unlikely in the absence of hallucinations. Also this patient, while withdrawn from society, holds a job and is highly functional.
Question 5 of 10
5. Question
A 22-year-old female is brought to the ED by her roommate for evaluation. Per the roommate, the patient has stayed-up all night for two weeks shopping online. She has missed her classes saying that she is “too smart for college-level courses.” Her roommate reports also that last month the patient did not get out of bed for a week, and was continually crying and over-eating. On physical examination the patient has pressured speech and is having difficulty keeping still for the exam. She reports she is wokring on “grand projects to save the world.” Based on these features, what type of mood disorder is exhibited by this patient?
Correct
Bipolar disorder, depression and dysthmic disorder are all mood disorders. The patient in this question presents with Bipolar Type I. Type I is indicated by one or more manic episodes cycling with depressive episodes. Type II is characterized by one or more major depressive episodes with at least one hypomanic episode. Hypomania presents with similar symptoms as mania, but lacks psychotic features and impairment of function. Dysthmic disorder is chronic and fluctuating low-grade depression for at least two years. Major depression is diagnosed by specific symptoms that are present almost every day for at least 2 weeks that impair daily function. In diagnosing and differentiating mood disorders it is important to understand the time-frame associated with each disease.
Incorrect
Bipolar disorder, depression and dysthmic disorder are all mood disorders. The patient in this question presents with Bipolar Type I. Type I is indicated by one or more manic episodes cycling with depressive episodes. Type II is characterized by one or more major depressive episodes with at least one hypomanic episode. Hypomania presents with similar symptoms as mania, but lacks psychotic features and impairment of function. Dysthmic disorder is chronic and fluctuating low-grade depression for at least two years. Major depression is diagnosed by specific symptoms that are present almost every day for at least 2 weeks that impair daily function. In diagnosing and differentiating mood disorders it is important to understand the time-frame associated with each disease.
Question 6 of 10
6. Question
A 16-year old female presents to the Emergency Department with epigastric pain for several days. The pain is worse with foods. Vital signs are: BP 110/72, P 100, RR 18, O2Sat 100% room air. Physical exam is unremarkable, except you note discolored teeth, slightly dry oral mucous membranes and the image shown. Which of the following is the most likely associated diagnosis?
Correct
This image depicts scarring/callus on the dorsal metacarpophalangeal joints known as Russell’s sign, which in the appropriate clinical context, suggests self-induced purging behavior. Russell’s sign is due to pressure of the teeth against the skin while inducing a gag reflex to cause vomiting. Binge eating episodes is classically associated with bulimia nervosa, followed with inappropriate compensatory mechanisms such as self-purging via vomiting/laxatives/diuretics, excessive exercise, diets, etc. Other dermatologic manifestations of bulimia nervosa include xerosis, poor dentition (due to gastric acid eroding enamel), poor skin turgor, telogen effluvium, and acne.
Incorrect
This image depicts scarring/callus on the dorsal metacarpophalangeal joints known as Russell’s sign, which in the appropriate clinical context, suggests self-induced purging behavior. Russell’s sign is due to pressure of the teeth against the skin while inducing a gag reflex to cause vomiting. Binge eating episodes is classically associated with bulimia nervosa, followed with inappropriate compensatory mechanisms such as self-purging via vomiting/laxatives/diuretics, excessive exercise, diets, etc. Other dermatologic manifestations of bulimia nervosa include xerosis, poor dentition (due to gastric acid eroding enamel), poor skin turgor, telogen effluvium, and acne.
Question 7 of 10
7. Question
A 16-year-old girl presents to the ED via ambulance for general pain. She is a refugee from a conflict area who is known to have frequent nighttime visits to the ED over the past year for the same chief complaint. She’s undergone multiple medical workups that have all been negative. In the ED she appears angry, irritable, and demonstrates hypervigilance. After a brief conversation with the patient her pain resolves and she feels much better. Which of the following is the most likely diagnosis?
Correct
Posttraumatic stress disorder (PTSD) is a long-lasting anxiety response following a traumatic or catastrophic event. Although most people encounter trauma over a lifetime, about 20-30% develop PTSD but over half of these people will recover without treatment. Prediction models have consistently found that childhood trauma, chronic adversity, and familial stressors increase risk for PTSD. Other risk factors include military experiences, war-zone exposure, domestic violence, and foster care. PTSD often leads to patients having difficulty falling or staying asleep, problems with concentration, hypervigilance, irritability, angry outbursts, and increased startle response. The patient in the above clinical scenario is a refugee from a conflict region and exhibits symptoms consistent with PTSD (anger, irritability, and hypervigilance). An important management principle when caring for a patient with PTSD is to ensure his or her safety and to validate his or her symptoms. Detailed questioning should be avoided as it may trigger severe symptoms.
Borderline personality disorder (B) is characterized by unstable personal relationships, unstable self-image, and inappropriate behaviors. Patients with BPD usually present to the ED after deliberate self-injury or suicidal attempts. Malingering (C) is fabricating or exaggerating the symptoms of mental or physical disorders for secondary gain. This may include financial compensation, avoiding school, work or military service, obtaining drugs, getting lighter criminal sentences or to attract attention or sympathy. An adjustment disorder (A) occurs when an individual is unable to adjust to or cope with a particular stressor, like a major life event. The condition is different from anxiety disorder, which lacks the presence of a stressor, or posttraumatic stress disorder that is associated with a more intense stressor.
Incorrect
Posttraumatic stress disorder (PTSD) is a long-lasting anxiety response following a traumatic or catastrophic event. Although most people encounter trauma over a lifetime, about 20-30% develop PTSD but over half of these people will recover without treatment. Prediction models have consistently found that childhood trauma, chronic adversity, and familial stressors increase risk for PTSD. Other risk factors include military experiences, war-zone exposure, domestic violence, and foster care. PTSD often leads to patients having difficulty falling or staying asleep, problems with concentration, hypervigilance, irritability, angry outbursts, and increased startle response. The patient in the above clinical scenario is a refugee from a conflict region and exhibits symptoms consistent with PTSD (anger, irritability, and hypervigilance). An important management principle when caring for a patient with PTSD is to ensure his or her safety and to validate his or her symptoms. Detailed questioning should be avoided as it may trigger severe symptoms.
Borderline personality disorder (B) is characterized by unstable personal relationships, unstable self-image, and inappropriate behaviors. Patients with BPD usually present to the ED after deliberate self-injury or suicidal attempts. Malingering (C) is fabricating or exaggerating the symptoms of mental or physical disorders for secondary gain. This may include financial compensation, avoiding school, work or military service, obtaining drugs, getting lighter criminal sentences or to attract attention or sympathy. An adjustment disorder (A) occurs when an individual is unable to adjust to or cope with a particular stressor, like a major life event. The condition is different from anxiety disorder, which lacks the presence of a stressor, or posttraumatic stress disorder that is associated with a more intense stressor.
Question 8 of 10
8. Question
Which of the following disorders best describes a patient with a wide variety of complaints, a long and complicated medical history with no apparent medical cause, and multiple ED visits?
Correct
Somatization disorder is most common in young to middle-aged women who have particular complaints or symptoms for which no medical explanation can be identified. These symptoms cause the patient significant distress or impairment in social, occupational, or other areas of functioning. Some patients have a wide variety of complaints and long, complicated histories of medical problems that have no apparent cause. This disorder often leads to many unnecessary diagnostic and surgical interventions.
Compulsive disorder (A) is a mental disorder in which someone engages in compulsive behavior or rituals such as excessive washing, repetitive checking, or counting. When these behaviors occupy a great deal of time, the patient may become significantly disabled and seek psychiatric attention. Hypochondriasis (B) is defined by preoccupation with fears of serious illness that persists despite appropriate medical evaluation and reassurance. Malingering (C) is the intentional invention or exaggeration of physical or psychological symptoms for external gain. The external gain may be to avoid work or to obtain drugs.
Incorrect
Somatization disorder is most common in young to middle-aged women who have particular complaints or symptoms for which no medical explanation can be identified. These symptoms cause the patient significant distress or impairment in social, occupational, or other areas of functioning. Some patients have a wide variety of complaints and long, complicated histories of medical problems that have no apparent cause. This disorder often leads to many unnecessary diagnostic and surgical interventions.
Compulsive disorder (A) is a mental disorder in which someone engages in compulsive behavior or rituals such as excessive washing, repetitive checking, or counting. When these behaviors occupy a great deal of time, the patient may become significantly disabled and seek psychiatric attention. Hypochondriasis (B) is defined by preoccupation with fears of serious illness that persists despite appropriate medical evaluation and reassurance. Malingering (C) is the intentional invention or exaggeration of physical or psychological symptoms for external gain. The external gain may be to avoid work or to obtain drugs.
Question 9 of 10
9. Question
Which of the following best defines delusions?
Correct
Delusions are erroneous beliefs that usually involve a misinterpretation of perceptions or experiences. Their content may include a variety of themes (persecutory, referential, somatic, religious, or grandiose). In persecutory delusions the person believes he or she is being tormented, followed, tricked, spied on, or ridiculed. In referential delusions the person believes that certain gestures, comments, passages from books, newspapers, song lyrics, or other environmental cues are specifically directed at him or her.
Psychosis (B) is restricted to delusions or prominent hallucinations, with the hallucinations occurring in the absence of insight into their pathological nature. Hallucinations (D) are sensory perceptions without external stimulation. Hallucinations may occur in any sensory modality (auditory, visual, olfactory, gustatory, and tactile). Auditory hallucinations are the most common. Delirium (C) is characterized by marked disorientation, confusion, and fluctuating consciousness.
Incorrect
Delusions are erroneous beliefs that usually involve a misinterpretation of perceptions or experiences. Their content may include a variety of themes (persecutory, referential, somatic, religious, or grandiose). In persecutory delusions the person believes he or she is being tormented, followed, tricked, spied on, or ridiculed. In referential delusions the person believes that certain gestures, comments, passages from books, newspapers, song lyrics, or other environmental cues are specifically directed at him or her.
Psychosis (B) is restricted to delusions or prominent hallucinations, with the hallucinations occurring in the absence of insight into their pathological nature. Hallucinations (D) are sensory perceptions without external stimulation. Hallucinations may occur in any sensory modality (auditory, visual, olfactory, gustatory, and tactile). Auditory hallucinations are the most common. Delirium (C) is characterized by marked disorientation, confusion, and fluctuating consciousness.
Question 10 of 10
10. Question
Which of the following predicts a higher risk of suicide completion?
Correct
Suicidal ideation is very common with up to one-third of the population experiencing it in their lifetime. Suicide rates vary with multiple factors including age, gender, race, and marital status. Females attempt suicide three to four times more often than men, but men are more successful in suicide completion. Up to one-quarter of suicides by men are successful as opposed to 5% in women because men tend to use more violent methods. Patients with active substance abuse, including alcohol, are among the highest risk for suicide completion. Other very high risk groups include those with underlying psychiatric disorders, adolescents, elders, and patients with some chronic illnesses. A history of prior suicide attempt raises the risk significantly although 60-70% of successful suicides occur in individuals without any previous attempt. Additionally, the presence of a firearm in the household is an independent risk factor.
Unemployment (D) appears to be a risk factor for suicide in 18 to 24 year old men as the highest risk. It does slightly increase the risk in other age groups. Females (A) attempt suicide more often than men but are less successful in completing the attempt. Pregnant women and mothers are at lower risk than others. Being married (B) is protective against suicide. Those at highest risk are single persons or those who are separated, widowed or divorced.
Incorrect
Suicidal ideation is very common with up to one-third of the population experiencing it in their lifetime. Suicide rates vary with multiple factors including age, gender, race, and marital status. Females attempt suicide three to four times more often than men, but men are more successful in suicide completion. Up to one-quarter of suicides by men are successful as opposed to 5% in women because men tend to use more violent methods. Patients with active substance abuse, including alcohol, are among the highest risk for suicide completion. Other very high risk groups include those with underlying psychiatric disorders, adolescents, elders, and patients with some chronic illnesses. A history of prior suicide attempt raises the risk significantly although 60-70% of successful suicides occur in individuals without any previous attempt. Additionally, the presence of a firearm in the household is an independent risk factor.
Unemployment (D) appears to be a risk factor for suicide in 18 to 24 year old men as the highest risk. It does slightly increase the risk in other age groups. Females (A) attempt suicide more often than men but are less successful in completing the attempt. Pregnant women and mothers are at lower risk than others. Being married (B) is protective against suicide. Those at highest risk are single persons or those who are separated, widowed or divorced.
This week concludes our discussion on Psychiatric Emergencies! We will be focusing on diagnosis and treatment of common psychiatric conditions and discuss some of the Pharmacology of Psych meds and sedation meds. See you there!
Hey team! This week starts our two week block into our psychiatry/psychology block. We’ll start off with an M&M from US Extraordinaire, Dr. Simon Yousif. Then we’ll get into some substance use disorders with Dr. Marshall and how to recognize patterns of abuse in vulnerable populations with Dr. Gyory. Everyone’s favorite nocturnal toxicologist will also be joining us (in the daylight!) for a focused talk on managing alcohol withdrawal. We’ll finish off the day with our first oral boards with Drs. Darr & Saker.