Endocrine and electrolyte board review
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Endocrine and electrolyte board review

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Endocrine and electrolyte board review Endocrine and electrolyte board review Presentation Transcript

  • Endocrine Emergencies and Electrolytes Board Review Dr. John Mathew
  • Question: 1
    • A 47 y/o female patient with a history of Graves disease presents with fever, mental status changes, severe diarrhea , and cough with productive sputum. The patient is emotionally labile, has pressured speech, and is profoundly diaphoretic. Vitals: T-100.4, P-180, RR-20, BP-160/80. Which of the following agents is most useful to block release additional stored thyroid hormone?
      • Methimazole
      • Propranolol
      • Propylthiourcil
      • Iodide
      • Charcoal Hemoperfusion
  • Question: 2
    • Which of the following statements regarding Hyperosmolar nonketotic coma is correct
      • Both disorder are characterized by elevations in serum glucose, usually below 400 mg/Dl
      • Both disorders have characteristic Kussmaul breathing
      • HONC is seen more commonly
      • HONC often occurs in patients who do not have a history of Diabetes
      • HONC usually develops over a shorter period of time
  • Question:3
    • A 62-year-old man has classic symptoms of hypothyroidism , m i ld hypothermia, bradycardia, hoarse voice, and bilateral carpal tunnel syndrome. You find no signs of infection. He has an extensive cardiac history, including an automatic internal defibrillator, and is on a waiting list for heart transplant. He takes many medications, but the one you suspect is probably causing his thyroid malfunction is: Choose one of the following
    • A. Amiodarone (Cordarone).
    • B. Bumetinide (Bumex).
    • C. Enalapril maleate/felodipine (Lexxel).
    • D. Lovastatin (Mevacor).
    • E. Sotalol (Betapace).
  • Question: 4
    • You are treating a patient in thyroid storm. You have given propranolol intravenously. An appropriate follow-up regimen would be:
    • A. Intravenous methimazole followed by rapid intravenous sodium iodide.
    • B. Intravenous propylthiouracil (PTU) followed by slow intravenous sodium iodide.
    • C. Oral propylthiouracil followed by slow intravenous sodium iodide.
    • D. Oral sodium iodide followed by intravenous methimazole.
    • E. Oral sodium iodide followed by intravenous propylthiouracil.
  • Question: 5
    • In a patient with diabetes insipidus, which of the following is correct
    • A. Fluid restriction is essential.
    • B. Hyponatremia is a common finding.
    • C. Intranasal vasopressin may be helpful
    • D.There is an osmolar gap.
        • E. Urine specific gravity is high.
  • Question: 6
    • In evaluating patients with alcoholic ketoacidosis (AKA) it is important to remember that:
    • A.Serum glucose is usually elevated, making differentiation from DKA difficult.
        • B. If serum and urine ketones are low and the anion gap is elevated in an alcoholic with a history of decreased food intake and vomiting, it is likely due to Lactic Acidosis.
        • C.Patients with DKA are likely to have a more of a metabolic acidosis than seen in patients with AKA.
        • D.Glycosuria is a common finding in both DKA and AKA.
        • E. Treatment of patients with AKA includes isotonic saline, glucose, and low-dose insulin therapy, and serial estimations of serum or urine ketones.
  • Question: 7
    • It is well known that vomiting leads to hypokalemia. The reason for this is:
    • A. Direct loss of potassium from stomach contents.
    • B. Hypovolemia from volume loss leads to increases in aldosterone secretion, causing the kidney to preserve sodium and bicarbonate in exchange for potassium, resulting in alkalosis, which causes potassium to shift into cells in exchange for hydrogen ions.
        • C.Vomiting causes hyperventilation, leading to respiratory alkalosis and compensatory extracellular to intracellular potassium shifts.
        • D.With the loss of hydrogen ions after a first episode of vomiting, the gastric parietal cells stop secreting potassium, so secretion cannot keep up with losses.
        • E. None of the above
  • Question 8.
    • Common laboratory findings in a patient with adrenal insufficiency include:
    • A. High sodium, high potassium, high glucose.
    • B. High sodium, low potassium, low glucose.
    • C. Low sodium, high potassium, low glucose.
    • D. Low sodium, low potassium, high glucose.
    • E. Low sodium, low potassium, low glucose.
  • Question. 9
    • Choose the true statement about hypoadrenal crisis:
    • A. The most common cause is the abrupt discontinuation of long-term corticosteroids.
    • B. Patients on short courses (less than a week) of high-dose corticosteroid therapy are at risk of developing the subacute adrenal crisis syndrome.
    • C. Hypervolemia is a common finding.
    • D. Rapid infusion of hypertonic saline can be a lifesaver.
    • E. Mineralocorticoids must be added to glucocorticoid therapy.
  • Question. 10
    • Choose the correct statement about thyroid disease:
    • A. The most common cause of hypothyroidism is chemical or surgical ablation for Graves disease.
    • B. With treatment, the mortality of myxedema coma is less than 20%.
    • C. Most hypothyroid patients present with myxedema coma during the summer heat waves.
    • D. Approximately half of the patients ultimately diagnosed with myxedema coma first present for treatment in a stuporous or comatose condition.
    • E. Hypernatremia, bradycardia, and diarrhea are common presenting signs in patients with significant hypothyroidism.
  • Question: 1
    • A 47 y/o female patient with a history of Graves disease presents with fever, mental status changes, severe diarrhea , and cough with productive sputum. The patient is emotionally labile, has pressured speech, and is profoundly diaphoretic. Vitals: T-100.4, P-180, RR-20, BP-160/80. Which of the following agents is most useful to block release additional stored thyroid hormone?
      • Methimazole
      • Propranolol
      • Propylthiourcil
      • Iodide *
      • Charcoal Hemoperfusion
  • Answer to Question # 1
    • Thyroid storm is a rare life threatening complications of hyperthyroidism despite treatment mortality rates are 20% to 50% typical features include fever , tachycardia out of proportion to fever wide pulse pressure diet for recess and mental status changes and central nervous system abnormalities are common and include emotional lability restlessness irritability agitation manic behavior psychosis and coma gastrointestinal manifestations include abdominal pain and nausea vomiting and diarrhea hyper defecation thyroid storm can progress to congested heart failure pulmonary edema as circulatory collapse the treatment of thyroid storm must be based on clinical impression And should not be delayed pending confirmatory laboratory data , management includes five components supportive care , blockade of peripheral effects , inhibition of thyroid hormone synthesis , slowing of thyroid hormone released , and treatment of precipitating calls support of care includes airway protection's, oxygen, intravenous fluids treatment of fever, and, if necessary, antidysrhymic agents. Furosemide is occasionally required for the treatment of pulmonary edema. Blockade of the peripheral effects of thyroid hormone is crucial in the treatment of thyroid storm. (Propranolol 2 mg IV q5min)Is the recommended agent. If the contraindication to propranolol exist (asthma congested heart failure, COPD) a selective the Beta-1 blocker are alternative agents may be substituted. reserpine and guanethidine are alternative agents to provide effective autonomic blockade. In addition of thyroid hormone synthesis is achieved with PTU or methimazole The onset of action is within one hour but the full effect do not occur for several weeks. PTU and methimazole block the synthesis of new thyroid hormone but do not prevent the release of stored thyroid hormone. Iodine is necessary to block the release of stored thyroid hormone. Iodine should be administered one hour after PTU to ensure that the exogenous iodide is not taken up and used to make more thyroid hormone. Lithium and can be used in place of iodine in patients with a history of iodine allergies. Blocking the peripheral effects of thyroid hormone is crucial in the treatment of thyroid storm. Precipitates of thyroid storm include infection, myocardial infarction, surgery, DKA, trauma, and idiopathic causes. Causes should be sought and treated accordingly. In patients on clinical deterioration occurs despite appropriate therapy, removal of thyroid hormone may be attempted to exchange transfusions, plasmapheresis, or charcoal hemoperfusion
  • Question: 2
    • Which of the following statements regarding Hyperosmolar nonketotic coma is correct
      • Both disorder are characterized by elevations in serum glucose, usually below 400 mg/Dl
      • Both disorders have characteristic Kussmaul breathing
      • HONC is seen more commonly
      • HONC often occurs in patients who do not have a history of Diabetes *
      • HONC usually develops over a shorter period of time
  • Answer to Question # 2
    • DKA and HONC have many similar features and probably represent two extremes on the clinical spectrum of disease. DKA usually affects insulin dependent diabetics and occurs more commonly then HONC. Blood glucose level is elevated in DKA, but it is usually below 600 mg/dL. Ketoacidosis is present in these patients, resulting in Kussmaul breathing. Most patients presenting with a HONC have not been previously diagnosed with diabetes mellitus. The fluid and electrolyte disturbances seen with HONC developed over a longer period of time and then with DKA usually days to weeks. The blood glucose level is elevated to a higher degree in HONC, usually about 800 mg/dL. As its name reflects HONC usually is characterized by a lack of ketosis and acidosis, in contrast to DKA. Thus, patients with HONC do not exhibit Kassmaul breathing unless they have a metabolic acidosis of another etiology (lactic acidosis).
  • Question:3
    • A 62-year-old man has classic symptoms of hypothyroidism , m i ld hypothermia, bradycardia, hoarse voice, and bilateral carpal tunnel syndrome. You find no signs of infection. He has an extensive cardiac history, including an automatic internal defibrillator, and is on a waiting list for heart transplant. He takes many medications, but the one you suspect is probably causing his thyroid malfunction is:
    • A. Amiodarone (Cordarone) *.
    • B. Bumetinide (Bumex).
    • C. Enalapril maleate/felodipine (Lexxel).
    • D. Lovastatin (Mevacor).
    • E. Sotalol (Betapace).
  • Answer to question # 3
    • The many complex effects of iodine-rich amiodarone on thyroid physiology may lead to asymptomatic abnormalities of thyroid hormone levels, including an elevated TSH, as well as clinically relevant hypofunction of the thyroid gland. Hypothyroidism has been estimated to occur in 1–32% of patients taking amiodarone, which is 37% iodine by molecular weight
  • Question: 4
    • You are treating a patient in thyroid storm. You have given propranolol intravenously. An appropriate follow-up regimen would be:
    • A. Intravenous methimazole followed by rapid intravenous sodium iodide.
    • B. Intravenous propylthiouracil (PTU) followed by slow intravenous sodium iodide.
    • C. Oral propylthiouracil followed by slow intravenous sodium iodide.*
    • D. Oral sodium iodide followed by intravenous methimazole.
    • E. Oral sodium iodide followed by intravenous propylthiouracil.
  • Answer to Question # 4
    • Thioamides, including propylthiouracil (PTU) and methimazole, inhibit thyroidal peroxidase, thereby preventing hormone synthesis. PTU is generally preferred over methimazole because it has the additional minor effect of inhibiting peripheral conversion of T4 to T3. PTU is given by mouth (PO) or by nasogastric (NG) tube every 4–6 hours. Further organification of iodine will be blocked within 1 hour of PTU administration, but the drug should be continued for several weeks while the hyperthyroidism is brought under control. Because preformed T4 and T3 are stored in the thyroid colloid, release of hormone can occur for weeks despite synthesis inhibition. Thus prevention of colloid hormone release is the second goal of therapy. Both iodine and lithium can inhibit thyroid hormone release. Lithium is not generally used because it can be difficult to titrate the dose, and toxic effects are common. Thioamides should be given at least 1 hour before iodine therapy to prevent organification of the iodine. Lugol’s iodine solution, PO or by NG tube; potassium iodide (SSKI), PO or by NG tube; or sodium iodide, intravenous (IV) drip is acceptable.
  • Question: 5
    • In a patient with diabetes insipidus, which of the following is correct
    • A. Fluid restriction is essential.
    • B. Hyponatremia is a common finding.
    • C. Intranasal vasopressin may be helpful*
    • D.There is an osmolar gap.
        • E. Urine specific gravity is high.
  • Answer to Question #5
    • Diabetes insipidus (DI) results in loss of large amounts of dilute urine because of the loss of concentrating ability in the distal nephrons. DI can be central (lack of ADH secretion from the pituitary) or nephrogenic (lack of responsiveness to circulating ADH). Patients are usually able to maintain near-normal serum levels as long as access to water is maintained. Patients will have a low urine-specific gravity (<1.005) and low urine osmolality. Patients with central DI require administration of parenteral or intranasal vasopressin.
  • Question: 6
    • In evaluating patients with alcoholic ketoacidosis (AKA) it is important to remember that:
    • A.Serum glucose is usually elevated, making differentiation from DKA difficult.
        • B. If serum and urine ketones are low and the anion gap is elevated in an alcoholic with a history of decreased food intake and vomiting, it is likely due to Lactic Acidosis.
        • C.Patients with DKA are likely to have a more of a metabolic acidosis than seen in patients with AKA.*
        • D.Glycosuria is a common finding in both DKA and AKA.
        • E. Treatment of patients with AKA includes isotonic saline, glucose, and low-dose insulin therapy, and serial estimations of serum or urine ketones.
  • Answers to Question # 6
    • Alcoholic ketoacidosis develops in patients with heavy alcohol intake, decreased food intake, and vomiting. As a result of the vomiting, hypochloremic alkalosis is superimposed on a metabolic acidosis. Beta-hydroxybutyrate is preferentially produced, and the serum or urine ketone test may be falsely low or negative. Unlike the case in diabetic ketoacidosis, serum glucose in alcoholic ketoacidosis is near normal. Treatment of alcoholic ketoacidosis includes IV thiamine (to prevent precipitating Wernicke’s encephalopathy) followed by isotonic saline and glucose.
  • Question: 7
    • It is well known that vomiting leads to hypokalemia. The reason for this is:
    • A. Direct loss of potassium from stomach contents.
    • B. Hypovolemia from volume loss leads to increases in aldosterone secretion, causing the kidney to preserve sodium and bicarbonate in exchange for potassium, resulting in alkalosis, which causes potassium to shift into cells in exchange for hydrogen ions.*
        • C.Vomiting causes hyperventilation, leading to respiratory alkalosis and compensatory extracellular to intracellular potassium shifts.
        • D.With the loss of hydrogen ions after a first episode of vomiting, the gastric parietal cells stop secreting potassium, so secretion cannot keep up with losses.
        • E. None of the above
  • Answer to Question #7
    • The hypokalemia associated with vomiting has very little to do with the actual potassium lost in the vomitus and much more to do with the metabolic alkalosis that follows. The hypovolemia from volume loss leads to increases in aldosterone secretion, which acts on the kidney to preserve Na+ and bicarbonate in exchange for K+. The resultant alkalosis also causes K+ to shift into cells in exchange for H+.
  • Question 8.
    • Common laboratory findings in a patient with adrenal insufficiency include:
    • A. High sodium, high potassium, high glucose.
    • B. High sodium, low potassium, low glucose.
    • C. Low sodium, high potassium, low glucose*.
    • D. Low sodium, low potassium, high glucose.
    • E. Low sodium, low potassium, low glucose.
  • Answer to Question# 8
    • The usual laboratory findings in patients with primary adrenal insufficiency include hyponatremia, hyperkalemia, hypoglycemia, and azotemia. Hyponatremia is present in 88% of cases and is usually mild to moderate; severe hyponatremia (<120 mEq/L) is rare. Hyperkalemia is present in 64% of cases, usually mild; the potassium level rarely exceeds 7 mEq/L. Two-thirds of patients with adrenal failure have hypoglycemia and the glucose levels less than 45 mg/dL; the pathophysiology is decreased gluconeogenesis and increased peripheral glucose use secondary to lipolysis.
  • Question. 9
    • Choose the true statement about hypoadrenal crisis:
    • A. The most common cause is the abrupt discontinuation of long-term corticosteroids.*
    • B. Patients on short courses (less than a week) of high- dose corticosteroid therapy are at risk of developing the subacute adrenal crisis syndrome.
    • C. Hypervolemia is a common finding.
    • D. Rapid infusion of hypertonic saline can be a lifesaver.
    • E. Mineralocorticoids must be added to glucocorticoid therapy.
  • Answer to Question # 9
    • . Chronic treatment with corticosteroids is necessary for the development of adrenal crisis from acute corticosteroid withdrawal. There is no such syndrome as subacute adrenal crisis. Other less frequent causes of adrenal crisis include bilateral gland hemorrhage and necrosis from meningococcal or other fulminant infections, or stress of a person with a low adrenal reserve, as in those patients with metastatic involvement of the adrenal from cancer. Patients who present with persistent hypotension unresponsive to the usual measures may have occult adrenal insufficiency. Patients with adrenal insufficiency have chronic volume depletion with a total body deficit that may reach 20%. Treatment of adrenal crisis includes volume resuscitation and intravenous administration of corticosteroids. Hydrocortisone or other steroids provide sufficient mineralocorticoid activity. Unresponsive hypotension can be treated with dopamine. Other important metabolic abnormalities include hyperkalemia and hypoglycemia. The major causes of death are hyperkalemia-induced cardiac arrhythmias and cardiovascular collapse.
  • Question. 10
    • Choose the correct statement about thyroid disease:
    • A. The most common cause of hypothyroidism is chemical or surgical ablation for Graves disease* .
    • B. With treatment, the mortality of myxedema coma is less than 20%.
    • C. Most hypothyroid patients present with myxedema coma during the summer heat waves.
    • D. Approximately half of the patients ultimately diagnosed with myxedema coma first present for treatment in a stuporous or comatose condition.
    • E. Hypernatremia, bradycardia, and diarrhea are common presenting signs in patients with significant hypothyroidism.
  • Answer to Question# 10
    • Primary thyroid failure, usually in patients treated for Graves disease, is the most common reason for hypothyroidism; autoimmune hypothyroidism is the second most common cause. Women are more commonly affected than men. Mild hypothyroidism is accompanied by fatigue, cold intolerance, and skin changes. Hypothyroidism should be considered in patients with chronic constipation, bradycardia, or cardiomegaly. Myxedema coma is a rare but lethal stage of severe hypothyroidism most commonly occurring in patients older than 55 years. Cold exposure is a common precipitating event for the development of hypothyroidism. Although only a small percentage of hypothermic patients have hypothyroidism, 80% of patients with myxedema coma are hypothermic. Physical signs include respiratory failure, abdominal distention, seizures, psychosis, and sinus bradycardia. Laboratory findings include hypercholesterolemia, hypoglycemia, and elevated CSF protein, as well as low serum T3 and T4 levels. Treatment includes intravenous administration of thyroxine and corticosteroids because many of these patients may have adrenal insufficiency. Even with aggressive therapy, the mortality rate is close to 50%.