PANCE Endo UW
Regular insulin drip with potassium-containing fluids Management of diabetic ketoacidosis IV fluids Infusion of 0.9% normal saline Add dextrose 5% when serum glucose is ≤200 mg/dL Insulin Start continuous IV insulin infusion; hold if K <3.3 mEq/L Switch to SQ (basal bolus) insulin for the following: able to eat, glucose <200 mg/dL, anion gap <12 mEq/L & serum HCO3− ≥15 mEq/L Overlap SQ & IV insulin by 1-2 hr Potassium Add IV K if serum K+ <5.3 mEq/L; hold if ≥5.3 mEq/L All patients K+ depleted, even with hyperkalemia Bicarbonate Consider for patients with pH ≤6.9 Patients require volume resuscitation with isotonic fluids (normal saline, lactated Ringer). Insulin is delayed until after the fluid bolus to minimize the risk of cerebral edema. Once the initial normal saline bolus is completed, patients are started on a regular intravenous insulin drip with isotonic fluids containing potassium.
13-year-old boy presents with vomiting and abdominal pain that began yesterday. For the last several weeks, he has had increased thirst, urination, and weight loss. Temperature is 36.7 C (98 F), blood pressure is 100/65 mm Hg, pulse is 124/min, and respirations are 28/min. Examination indicates dry mucous membranes and deep, rapid breathing. Initial serum chemistry shows a sodium of 133 mEq/L, potassium of 5 mEq/L, chloride of 96 mEq/L, and glucose of 382 mg/dL. Venous blood gas shows a pH of 7.2 and a bicarbonate level of 10 mEq/L. The boy receives a normal saline fluid bolus over 1 hour and repeat serum chemistry shows: Sodium 134 mEq/L Potassium 4.4 mEq/L Chloride 96 mEq/L Glucose 360 mg/dL Venous blood gas shows a pH of 7.2 and bicarbonate level of 12 mEq/L. Urinalysis continues to show large ketones. What is the best next step in management of this patient?
Reassure and observe Pubertal gynecomastia Etiology Imbalance of estrogens & androgens during midpuberty(Tanner stages 3-4) Clinical features Small (<4 cm) firm, unilateral or bilateral, subareolar mass No pathologic features (eg, nipple discharge, axillarylymphadenopathy, systemic illness) Management Reassurance & observation Resolution within a year
14-year-old boy is brought to the office due to a breast lump. For the last 2 months, he has felt a mass under his right nipple. The patient has no chronic medical conditions and takes no medications. He does not use tobacco, alcohol, or illicit drugs. His grandmother developed breast cancer at age 64. Height and weight are at the 60th and 40th percentiles, respectively. Physical examination reveals tender, glandular, right subareolar breast tissue that is 3 cm (1.2 in) in diameter. There is no overlying erythema or warmth, and no discharge can be expressed from the nipple. The left chest wall is flat without palpable breast tissue. He has Tanner 3 genitalia, including normal testicular volume. What is the best next step for this patient's condition?
Constitutional delay of growth and puberty Clinical features Family history of "late bloomers" Delayed puberty Short stature; normal growth velocity Delayed bone age Management Reassurance; watchful waiting ± Hormone therapy Prognosis Puberty onset correlates with family members Normal expected adult height This patient with short stature but normal growth velocity (4-6 cm/yr) most likely has constitutional delay of puberty. A family history of "late bloomers" would support this diagnosis; however, this history is not present in every case. In contrast to familial short stature, in which short stature and normal growth velocity are accompanied by a normal bone age, constitutional delay is associated with a delayed bone age on x-ray of the wrist, as seen in this patient
15-year-old boy is brought to the office by his parents due to concerns about his pubertal development. The patient's voice has not changed, and he has not developed any body hair. He has had no recent headaches, vomiting, or vision changes. His father is 178 cm (5 ft 10 in) and his mother is 160 cm (5 ft 3 in). Blood pressure is 116/70 mm Hg and pulse is 78/min. Weight and height are at the 15th and 3rd percentiles, respectively, unchanged from his last visit 12 months ago. The patient's height has increased 4.5 cm (1.8 in) since then. The thyroid is palpable and not enlarged. There is no gynecomastia. Cardiopulmonary examination is normal. The testes are soft and measure 2 mL (Tanner stage I). The phallus is normal in length. There is no axillary or pubic hair. Bone age x-ray is consistent with age 13.
Exogenous thyroid hormone intake This patient's symptoms (eg, weight loss, tachycardia, tremors, and hyperreflexia), elevated free thyroxine (T4), and suppressed TSH are indicative of thyrotoxicosis. However, her thyroid is small and serum thyroglobulin is undetectable, which suggests an exogenous source of thyroid hormone. Thyroglobulin is a glycoprotein produced by thyroid follicular cells that makes up a substantial component of follicular colloid and serves as the substrate for the formation of thyroid hormone. A small amount is released by the thyroid in normal function. Low levels, as in this patient, suggest noninflammatory suppression of thyroid activity. Excess T4 supplementation suppresses TSH, which decreases iodine organification and colloid formation resulting in atrophy of thyroid follicles.
16-year-old girl is brought to the office by her mother due to excessive weight loss. The patient has lost 4.5 kg (10 lb) over the past 2 months, but thinks she still appears overweight, and is worried about gaining weight. Her mother has hypothyroidism. Blood pressure is 130/70 mm Hg, and pulse is 105/min and regular. Examination shows a small, painless thyroid without palpable nodules. There is a fine tremor of outstretched hands. Deep tendon reflexes are 3+ diffusely. Laboratory results show decreased TSH, elevated free thyroxine (T4), and undetectable thyroglobulin levels. What is the most likely diagnosis for this patient?
Reduce dosage of basal and bolus insulins Repeated muscle contraction during exercise induces increased uptake of glucose by skeletal muscle cells. Patients taking exogenous insulin are vulnerable to exercise-induced hypoglycemia because insulin will continue to be released from the injection site. In addition, exercise may cause changes in skin perfusion that can lead to erratic insulin absorption. Because of the increased insulin sensitivity associated with exercise, a reduction in insulin dose is usually appropriate. For training sessions within 3 hours of a meal, the premeal bolus insulin dose preceding exercise should be reduced. For prolonged exercise (eg, distance running) the basal insulin will likely need reduction as well. Patients with diabetes who initiate a strenuous exercise regimen should also be counseled to increase carbohydrate intake, particularly if training sessions are >60 minutes in duration.
17-year-old boy comes to the office before participating in long-distance running. He has type 1 diabetes mellitus and takes insulin glargine at bedtime and insulin lispro before meals. His home blood glucose levels range from 90 to 130 mg/dL, and he has had no episodes of hypoglycemia. The patient wants to run a marathon and has begun training recently. Physical examination is normal. Hemoglobin A1c is 6.5%. What is the most appropriate recommendation to manage his diabetes mellitus during long-distance training?
Dexamethasone Acute adrenal insufficiency (adrenal crisis) Etiology Adrenal hemorrhage or infarction Illness/injury/surgery in patient with chronic AI Pituitary apoplexy Clinical features Hypotension & shock Nausea, vomiting, abdominal pain Fever, generalized weakness Treatment Hydrocortisone or dexamethasone Rapid intravenous volume repletion Adrenal crisis is characterized by severe hypotension and refractory shock. Associated symptoms include abdominal pain, vomiting, weakness, and fever. In addition to aggressive fluid resuscitation, treatment of adrenal crisis requires immediate glucocorticoid supplementation with hydrocortisone or dexamethasone. Treatment should begin immediately without waiting for results of diagnostic studies, and the response is usually rapid.
20-year-old woman is brought to the emergency department due to intractable vomiting and abdominal pain. She has had several weeks of anorexia and weight loss. Temperature is 37.6 C (99.7 F), blood pressure is 80/40 mm Hg, pulse is 120/min, and respirations are 18/min. The patient is mildly lethargic but oriented. Generalized hyperpigmentation is present and is most conspicuous over the face, neck, and dorsal surface of the hands. Urinalysis and chest x-ray are normal. Blood glucose level is 60 mg/dL. A 1-L bolus of normal saline is rapidly infused, and high-flow intravenous fluids are continued. This patient also requires immediate treatment with
Sheehan syndrome Pathogenesis Obstetric hemorrhage complicated by hypotension Postpartum pituitary infarction Clinical features Lactation failure (↓ prolactin) Amenorrhea, hot flashes, vaginal atrophy (↓ FSH, LH) Fatigue, bradycardia (↓ TSH) Anorexia, weight loss, hypotension (↓ ACTH) Decreased lean body mass (↓ growth hormone) due to pituitary hypoperfusion, causing anterior pituitary infarction classically due to postpartum hemorrhage. Progesterone levels normally drop significantly following delivery and no longer inhibit prolactin secretion. Prolactin levels also rise due to nipple stimulation during breastfeeding, which promotes lactation. However, women with Sheehan syndrome will have prolactin deficiency that leads to failure of postpartum lactation.
23-year-old woman comes to the office with 2 weeks of fatigue and excessive sleepiness. She delivered a healthy child 4 weeks ago, but the delivery was complicated by heavy bleeding. The patient has not lactated. She is otherwise healthy. Laboratory studies show hemoglobin of 9.8 g/dL, TSH of 0.2 µU/mL, and low total and free T4 levels.
Adrenal Insufficiency Clinical features of primary adrenal insufficiency Etiology Autoimmune Infections (eg, tuberculosis, HIV, disseminated fungal) Hemorrhagic infarction Metastatic Clinical presentation Fatigue, weakness, anorexia/weight loss, salt craving Gastrointestinal symptoms Postural hypotension Hyperpigmentation or vitiligo Hyponatremia, hyperkalemia May lead to acute adrenal crisis (abdominal pain, shock, fever, altered mental status) Diagnosis ACTH, serum cortisol & high-dose (250 µg) ACTH stimulation test Primary adrenal insufficiency: low cortisol, high ACTH Secondary/tertiary adrenal insufficiency: low cortisol, low ACTH
24-year-old woman with type 1 diabetes mellitus has 6 months of increasing fatigue and occasional lightheadedness. The patient takes 2 or 3 naps during the day due to feeling exhausted. Blood pressure is 92/60 mm Hg and pulse is 95/min. BMI is 18 kg/m2. Physical examination shows hyperpigmentation around her lips and in the palmar creases. Serum creatinine and liver function tests are normal.
Propanolol This patient has signs and symptoms of thyrotoxicosis, including tremor, dysphoria, sweating, and tachycardia with palpitations. Hyperthyroidism is associated with upregulation of beta-adrenergic receptors and increased adrenergic tone, which is responsible for many of the associated clinical features. Beta-adrenergic antagonists (eg, propranolol) are indicated to alleviate the adrenergic symptoms of thyrotoxicosis and are usually prescribed early, while completing the diagnostic evaluation and initiating definitive management.
25-year-old woman comes to the office because of jitteriness, frequent mood swings, and palpitations for the past 2 months. At times, her symptoms make her worry that she may be having a heart attack. The patient has no prior medical conditions. Temperature is 37 C (98.6 F), blood pressure is 120/82 mm Hg, pulse is 102/min, and respirations are 12/min. Examination shows warm, moist skin and a fine tremor of the fingers. What would most likely provide the fastest relief of this patient's symptoms?
Maternal hepatotoxicity Hyperthyroidism treatment in pregnancy Monitoring Thyroid function tests every 4 weeks Goal Maintain mild hyperthyroid state TSH 0.1-0.3 µU/mL Free T4 just above trimester-specific range Total T3/T4 1.5 times nonpregnant range Treatment Propylthiouracil (1st trimester) Methimazole (2nd & 3rd trimesters) Beta blockers (metoprolol) Thyroidectomy Methimazole is preferred for most patients due the hepatotoxicity of PTU; PTU often causes transient elevations in hepatic transaminases and occasionally can cause severe idiosyncratic liver injury with acute liver failure. However, methimazole has potential teratogenic effects (eg, aplasia cutis [Choice B], esophageal atresia, facial anomalies [Choice A]), so PTU is preferred in the first trimester of pregnancy. Thereafter, the patient should be returned to methimazole therapy.
26-year-old woman at 16 weeks gestation comes to the office for prenatal follow-up. The patient has a 2-year history of mild hyperthyroidism due to Graves disease and started taking propylthiouracil when she decided to attempt pregnancy. The patient has had no tremulousness, palpitations, diarrhea, or heat intolerance. Temperature is 36.7 C (98 F), blood pressure is 110/60 mm Hg, and pulse is 88/min. Physical examination reveals no lid lag, exophthalmos, or hand tremors. The thyroid gland is normal to palpation. Fetal heart rate is normal. Thyroid hormone levels are at goal. During this visit, her thyroid treatment is changed from propylthiouracil to methimazole. Switching the patient's therapy at this time is aimed at decreasing what complications?
Fine-needle aspiration biopsy Risk factors for malignant thyroid nodules Patient characteristics Exposure to ionizing radiation (especially in childhood) Family history of thyroid cancer or thyroid cancer syndrome (eg, MEN2, familial polyposis coli, Cowden syndrome) Age <30 or >60 Iodine deficiency Elevated TSH Nodule characteristics Rapid growth, hard/fixed nodule Associated cervical lymphadenopathy Obstructive symptoms (eg, hoarseness, dysphagia) Ultrasound: size >1 cm, microcalcifications, hypoechoic, increased vascularity, infiltrative margins, length > width
27-year-old woman is evaluated for a thyroid nodule. The patient has no heat or cold intolerance and no skin changes. Vital signs are normal. Physical examination shows a 1.5-cm nodule in her right thyroid gland. Serum TSH is normal. Thyroid ultrasound reveals a 1.5-cm hypoechoic nodule in her right thyroid lobe with irregular margins, internal microcalcifications, and internal vascularity. What is the best next step in management of this patient?
Performance-enhancing substance use Growth hormone Joint pain, myalgia, fluid retention, carpal tunnel syndrome, hyperglycemia Androgens Gynecomastia, baldness, infertility, impotence, severe acne, aggression Creatine Gastrointestinal discomfort, fluid retention, renal/liver damage, unknown long-term effects Diuretics Dehydration, hypotension, electrolyte disturbances Stimulants(eg, amphetamines,caffeine) Insomnia, arrhythmias, hypertension, weight loss, stroke, addiction, tolerance This patient has carpal tunnel syndrome, which is common in body builders. However, this patient also has hypertension and hyperglycemia, which are unexpected in a healthy athlete. These findings raise suspicion for use of performance-enhancing substance, specifically a growth hormone.
28-year-old man comes to the office due to pain and numbness in the right hand. For the past month, the pain has awakened him at night. The patient has also had pain occasionally in other joints but no swelling or stiffness. He is a professional body builder and is training for an upcoming championship. The patient is sexually active with multiple partners. Blood pressure is 150/92 mm Hg. BMI is 35 kg/m2. The patient is muscular and has normal body hair distribution. Tapping the volar surface of the right wrist elicits tingling of the right thumb and index finger. Mild, bilateral pedal edema is present. Fasting laboratory results are as follows: Hemoglobin 14.4 g/dL Platelets 320,000/mm3 Leukocytes 8,200/mm3 Glucose 142 mg/dL Aspartate aminotransferase (SGOT) 38 U/L What is the most likely underlying cause of this patient's current condition?
Serum anion gap A primary derangement in DKA is anion gap metabolic acidosis generated by the unmeasured ketoacid anions acetoacetate and beta-hydroxybutyrate. Beta-hydroxybutyrate is derived from the reduction of acetoacetic acid and can become the predominant ketoacid in severe DKA. With volume resuscitation and correction of hyperosmolality and hyperglycemia, these ketoacids disappear and the anion gap normalizes, pointing to resolution of ketosis. Posttreatment hyperchloremic acidosis may occur due to the infusion of normal saline; however, the anion gap will be normal.
28-year-old man with type 1 diabetes mellitus comes to the emergency department due to abdominal pain, nausea, and vomiting for the past 2 days. The patient has not used insulin for the past 5 days. Temperature is 36.7 C (98.1 F), blood pressure is 96/62 mm Hg, pulse is 112/min, and respirations are 26/min. Examination shows dry mucous membranes. Basic metabolic panel reveals an anion gap of 25 mEq/L and glucose of 400 mg/dL. Arterial blood gas includes a pH of 7.19, PaO2 of 85 mm Hg, and PaCO2 of 25 mm Hg. Serum and urine are positive for ketones. What is the best index for monitoring the response to treatment of this patient's condition?
Measure 24-hour fractionated urinary metanephrines Indications for diagnostic testing for pheochromocytoma Signs & symptoms Episodic headaches, diaphoresis & tachycardia Hyperadrenergic spells (eg, nonexertional palpitations, pallor) Resistant hypertension or onset of hypertension at young age Family history Pheochromocytoma Predisposing familial syndrome (eg, MEN2, NF1, VHL) Other Adrenal incidentaloma on imaging Pressor response during surgery/anesthesia Idiopathic dilated cardiomyopathy
29-year-old man comes to the emergency department (ED) due to palpitations, sweating, and a severe headache. His symptoms resolve spontaneously by the time he is evaluated. The patient has had at least 2 similar episodes during the past 2 months. He does not use tobacco, alcohol, or illicit drugs. Physical examination shows a thin man who appears anxious and diaphoretic. The thyroid is normal to palpation without any obvious nodules. Vital signs are within normal limits. During the patient's prior ED visit for an identical episode, his blood pressure was 150/100 mm Hg and pulse was 120/min. Laboratory results at that time showed normal thyroid function tests. What is the best next step in management of this patient?
Stimulation of pituitay dopamine receptors Prolactinoma Clinical features Premenopausal women: oligomenorrhea/amenorrhea, infertility, galactorrhea, hot flashes, decreased bone density Postmenopausal women: mass-effect symptoms (headache, visual field defects) Men: infertility, decreased libido, impotence, gynecomastia Laboratory/imaging Serum prolactin (often >200 ng/mL) Tests to rule out renal insufficiency (creatinine) & hypothyroidism (TSH, thyroxine) MRI of the head/pituitary Treatment Dopamine agonist (cabergoline) Transsphenoidal surgery
29-year-old nulligravid woman comes to the office due to a 2-month history of worsening bilateral nipple discharge that stains her bra. The patient has felt no breast mass and has had no breast pain, headaches, or vision changes. Her last menstrual period was 3 months ago, and home pregnancy tests have been negative. Previously, she had regular monthly menses. The patient has no other medical conditions and takes no medications. Vital signs are normal. Visual fields are intact by confrontation. A whitish fluid is expressed bilaterally on nipple compression. There are no breast masses or lymphadenopathy. Pelvic examination is normal. Pregnancy test is negative. Serum prolactin level is 220 ng/mL. Brain imaging shows a 0.6-cm pituitary mass. Pharmacotherapeutic treatment is begun, and on a follow-up visit the patient reports that her symptoms are improving. What is the mechanism of action of this medication?
Thyroid Adenoma This patient has a thyroid nodule with symptoms (sweating, heat intolerance, decreased exercise tolerance) and laboratory findings (low TSH, high T3 and T4) of thyrotoxicosis. Patients with a thyroid nodule and a low TSH undergo a radioiodine scan, or thyroid scintigraphy, to determine how the thyroid nodule is functioning based on iodine uptake. The scan measures the amount of uptake (ie, amount of thyroid hormone production) in the nodule compared to surrounding normal thyroid tissue. This patient's scan shows a hyperactive or "hot" nodule, indicating an increased thyroid hormone synthesis and therefore increased uptake of radioactive iodine compared to the rest of the thyroid. This pattern is consistent with a toxic thyroid adenoma, a benign tumor that produces thyroid hormones autonomously (ie, regardless of changes in serum TSH).
30-year-old woman comes to the office for evaluation of excessive sweating. She often feels hot when others are not and frequently sweats, even at rest, and feels her exercise tolerance is decreased. Temperature is 37 C (98.6 F), blood pressure is 140/78 mm Hg, and pulse is 98/min. Physical examination shows a nontender, firm, 1.5-cm nodule in the right thyroid lobe. Serum TSH is low, and T3 and T4 are elevated. A radioiodine scan is performed and shows a small nodule in the right upper lobe with increased uptake of radioactive iodine.
low Na, high K, high Cl Primary adrenal insufficiency Etiology Autoimmune adrenalitis (most common) Infection (eg, tuberculosis) Hemorrhagic infarction Clinical features Fatigue, weakness, anorexia/weight loss Nausea/vomiting/abdominal pain Postural hypotension Hyperpigmentation Acute adrenal crisis: confusion, shock Laboratory findings Hyponatremia, hyperkalemia Low morning cortisol, high ACTH Eosinophilia As a result, patients with primary adrenal insufficiency present with hyponatremia, hyperkalemia, hyperchloremia, and nonanion gap metabolic acidosis.
30-year-old woman is evaluated for 3 months of progressive fatigue, decreased appetite, and 10-lb (4.5-kg) weight loss. The patient has type 1 diabetes mellitus and has noticed decreased insulin requirements over this time. She has no other medical conditions. Physical examination shows a generalized increase in pigmentation of the skin, especially involving the palmar creases. Measurement of serum cortisol before and after administration of exogenous adrenocorticotropic hormone (ACTH) shows no difference in the levels. What changes in serum laboratory values is most likely present in this patient?
Postpartum Thyroiditis Thyroiditis Types Chronic autoimmune(Hashimoto) Predominant hypothyroid features Diffuse goiter Positive TPO antibody Variable radioiodine uptake Painless(silent) Variant of chronic autoimmune thyroiditis Mild, brief hyperthyroid phase Small, nontender goiter Spontaneous recovery Positive TPO antibody Low radioiodine uptake Subacute(de Quervain) Likely postviral inflammatory process Prominent fever & hyperthyroid symptoms Painful/tender goiter Elevated ESR & CRP Low radioiodine uptake
31-year-old woman, gravida 1 para 1, comes to the office 5 weeks after an uncomplicated vaginal delivery. The patient has fatigue, sweating, heat intolerance, and has also lost a significant amount of weight. The patient is not breastfeeding, and menses have not resumed. Blood pressure is 122/68 mm Hg and pulse is 109/min. Examination shows an enlarged, nontender thyroid gland with no nodules. Ocular examination shows mild lid lag without proptosis. Laboratory results are as follows: TSH <0.01 μU/mL Total thyroxine (T4) 18 μg/dL (normal: 4.6-11.2) Anti-thyroid peroxidase antibody 23 IU/mL (normal: <9) Serum thyroglobulin 57 ng/mL (normal: <33) The radioactive iodine uptake in the thyroid gland is 1.5% (normal: 8%-25%).
ACTH stimulation test Although this patient's fatigue, anorexia, memory impairment, lack of motivation, and loss of libido can be attributed to major depressive disorder (MDD), salt craving and reduced body hair are suggestive of primary adrenal insufficiency (PAI), also known as Addison disease. PAI usually presents with: Mineralocorticoid deficiency: salt craving Glucocorticoid deficiency: fatigue, anorexia, and psychiatric manifestations of adrenal insufficiency (irritability, depressed mood) Androgen deficiency: suppression of secondary sexual characteristics (reduced pubic hair) In patients with suspected AI, salt craving and hyperpigmentation are specific for PAI and help differentiate it from secondary AI. The diagnosis of PAI is made by stimulation testing with cosyntropin, a synthetic form of ACTH. Low production of cortisol following cosyntropin administration is diagnostic of PAI.
32-year-old woman comes in for evaluation of persistent fatigue, lack of motivation, memory impairment, and loss of libido. The patient has also had nausea and anorexia but reports an unusual craving for salty foods. Blood pressure is 110/62 mm Hg and pulse is 88/min. BMI is 19.8 kg/m2 with a 9-kg (19.8-lb) weight loss since her last visit. Cardiopulmonary and abdominal examinations are normal. The patient's skin appears tanned, and there is decreased axillary and pubic hair. Mental status examination reveals a restricted affect. What is most likely to establish the diagnosis in this patient?
High 24-hr urinary cortisol, high ACTH, high DHEAS Categorization of Cushing syndrome ACTH dependent Cushing disease (ACTH-secreting pituitary adenoma) Ectopic ACTH secretion Hyperpigmentation Hyperandrogenism (eg, hirsutism, oligomenorrhea/amenorrhea) ↑ ACTH ACTH independent Adrenal mass (adenoma or carcinoma) Exogenous glucocorticoids ↓ ACTH
34-year-old, previously healthy woman comes to the office due to irregular menstruation and a 4.5 kg (10-lb) weight gain over the past 6 months. The patient also reports muscle weakness causing difficulty climbing stairs or lifting her child. Blood pressure is 152/86 mm Hg and pulse is 72/min. BMI is 31 kg/m2. Physical examination shows excessive fat accumulation in the abdomen and supraclavicular area. Sun-exposed areas and skin creases are hyperpigmented and there are wide striae over the abdomen. Coarse hair is present on the face, chest, and abdomen. What sets of laboratory findings are most likely to be seen in this patient?
Bone loss Hyperthyroidism Clinical features Behavior disturbances Weight loss Goiter Proptosis Tachycardia, wide pulse pressure Tremor, hyperreflexia Warm, sweaty skin Diagnosis ↑ T3/T4, ↓ TSH TSI (Graves disease) Treatment Methimazole Radioactive iodine Complications Arrhythmia, cardiomyopathy Osteoporosis This patient with hyperthyroid symptoms, a suppressed TSH, and a "hot" thyroid nodule has a toxic adenoma, a common cause of hyperthyroidism due to activating mutations in the TSH receptor. Initial treatment includes a beta blocker to alleviate the symptoms of hyperthyroidism and a thionamide (eg, methimazole, propylthiouracil). Options for definitive management include surgery and radioiodine ablation. If left untreated, hyperthyroidism can develop into rapid bone loss, leading to osteoporosis and increased risk of fracture. Hypercalcemia and hypercalciuria can also develop due to increased bone turnover.
36-year-old woman comes to the office due to weight loss. Over the last 3 months, she has lost 5 kg (11 lb) and has had palpitations, heat intolerance, persistent tremors, and excessive sweating. Blood pressure is 140/70 mm Hg and pulse is 104/min and regular. A 2 × 2 cm nodule is present in the left thyroid lobe. The rest of the thyroid gland is normal, and there is no cervical lymphadenopathy. The patient has a fine tremor in both upper extremities. Thyroid function test results are as follows: Serum TSH <0.03 µU/mL Total T 3330 ng/dL Free T4 14 µg/dL Radioactive iodine scan shows uptake only in the nodule. If left untreated, this patient is at greatest risk for developing what complication?
Tx w/ cabergoline Patients with macroprolactinomas or symptomatic tumors of any size (as in this patient) are treated with dopaminergic agonists (eg, cabergoline, bromocriptine), which can normalize prolactin levels and reduce tumor size. Patients who fail to respond or who have very large tumors (>3 cm) should be referred for transsphenoidal resection
37-year-old woman comes to the office with a 7-month history of galactorrhea and amenorrhea. She has also had worsening vaginal dryness, but no headaches or visual symptoms. The patient's medical history is unremarkable. Temperature is 36.7 C (98 F), blood pressure is 120/80 mm Hg, pulse is 72/min, and respirations are 14/min. Visual field testing is normal. Pregnancy test is negative, serum prolactin level is 150 ng/mL (154 ng/mL on repeat measurement), and TSH and serum creatinine are normal. MRI of the pituitary gland reveals a 6-mm hypointense lesion, consistent with a pituitary microadenoma. What is the best next step in management of this patient?
Fasting blood glucose Screening criteria for diabetes & prediabetes in asymptomatic adults 1. Adults with a BMI ≥25 kg/m2 (overweight or obesity) with ≥1 of the following risk factors: First-degree relative with diabetes High-risk race/ethnicity (eg, African American, Latino, Native American, Pacific Islander) CVD history Hypertension (stage 2 or on therapy for hypertension) HDL level <35 mg/dL &/or triglyceride level >250 mg/dL Polycystic ovary syndrome Physical inactivity Other clinical conditions associated with insulin resistance (eg, obesity, acanthosis nigricans) 2. Yearly in patients with existing prediabetes 3. At least every 3 years in women with a history of GDM 4. All other patients should begin testing at age 35 5. Repeat testing at least every 3 years with normal initial results; more frequently depending on initial result & individual risk status 6. Patients with HIV
38-year-old man comes in for a routine health maintenance examination. The patient has no health concerns and no prior medical history. Family history is significant for diabetes mellitus type 2 in his father, who was diagnosed at age 48. He is an active smoker with a 15-pack-year smoking history and does not drink alcohol. BMI is 28 kg/m2. Vital signs are normal. Examination shows no abnormalities. What is the best next step in management?
Measure urinary free cortisol Features of Cushing syndrome Clinical manifestations Central obesity Skin atrophy & wide, purplish striae Proximal muscle weakness Hypertension Glucose intolerance Skin hyperpigmentation (if due to ACTH excess) Depression, anxiety Diagnosis 24-hr urinary cortisol excretion Late-night salivary cortisol assay Low-dose dexamethasone suppression test Neuropsychiatric symptoms in Cushing syndrome are common and include depressed or labile mood, anxiety or panic attacks, irritability, insomnia, memory deficits, and fatigue. Initial diagnostic tests for Cushing syndrome include 24-hour urinary cortisol excretion, late-night salivary cortisol assay, and overnight low-dose dexamethasone suppression test.
38-year-old man comes to the office due to disturbed sleep and depressed mood for several months. The patient has had difficulty falling and staying asleep and constantly feels exhausted at work. He has also felt depressed and irritable, which he attributes to his weight. Blood pressure is 148/90 mm Hg and pulse is 86/min. BMI is 34 kg/m2. The patient has a flat affect and a ruddy appearance with central obesity. The thyroid is normal. Proximal limb muscles are mildly weak with no associated pain or tenderness. The patient has no suicidal ideation. Laboratory results are as follows: Sodium 140 mEq/L Potassium 3.4 mEq/L Creatinine 1.0 mg/dL Glucose 140 mg/dL TSH 2.9 µU/mL What is the best next step in management of this patient?
Autoimmune adrenalitis Clinical features of primary adrenal insufficiency Etiology Autoimmune Infections (eg, tuberculosis, HIV, disseminated fungal) Hemorrhagic infarction Metastatic Clinical presentation Fatigue, weakness, anorexia/weight loss, salt craving Gastrointestinal symptoms Postural hypotension Hyperpigmentation or vitiligo Hyponatremia, hyperkalemia May lead to acute adrenal crisis (abdominal pain, shock, fever, altered mental status) Diagnosis ACTH, serum cortisol & high-dose (250 µg) ACTH stimulation test Primary adrenal insufficiency: low cortisol, high ACTH Secondary/tertiary adrenal insufficiency: low cortisol, low ACTH
38-year-old woman comes to the office with a 3-week history of fatigue, weight loss, nausea, abdominal pain, and postural dizziness. The patient has hypothyroidism treated with levothyroxine. She has no recent travel. Blood pressure is 90/60 mm Hg and pulse is 96/min. Skin examination shows increased pigmentation at the palmar creases and mucous membranes as well as a few patches of vitiligo. Initial laboratory testing shows mild hyponatremia and hyperkalemia with normal renal function. Follow-up testing confirms a low 8 AM serum cortisol. What is the most likely cause of this patient's adrenal insufficiency?
Cushing Syndrome Features of Cushing syndrome Clinical manifestations Central obesity Skin atrophy & wide, purplish striae Proximal muscle weakness Hypertension Glucose intolerance Skin hyperpigmentation (if due to ACTH excess) Depression, anxiety Diagnosis 24-hr urinary cortisol excretion Late-night salivary cortisol assay Low-dose dexamethasone suppression test Hypercortisolism can be characterized as ACTH-dependent and ACTH-independent: High levels of ACTH (eg, ACTH-secreting pituitary adenoma/Cushing disease, ectopic ACTH production) cause hyperpigmentation. ACTH also increases androgen production from the adrenal cortex, leading to androgenic symptoms (irregular menses, acne), as seen in this patient. ACTH-independent hypercortisolism (eg, exogenous glucocorticoid administration, adrenal adenoma) is not associated with hyperpigmentation or androgen excess.
39-year-old woman comes to the office due to a 4-month history of progressive muscle weakness. The patient has had difficulty combing her hair because her arms feel weak when she holds them above her head. In addition, she has had a 9-kg (20-lb) weight gain as well as irregular menses. Medical history is significant for hypertension and hyperlipidemia. Blood pressure is 150/100 mm Hg and pulse is 90/min. BMI is 37 kg/m2. Physical examination shows oily facial skin with scattered bruises on her arms and lower legs. The abdomen is obese, soft, and has purple striae. Deep tendon reflexes are normal. Laboratory results are as follows: Serum chemistry Sodium 142 mEq/L Potassium 3.6 mEq/L Chloride 104 mEq/L Bicarbonate 29 mEq/L Glucose 166 mg/dL Creatine kinase, serum 68 U/L Which of the following is the most likely cause of this patient's symptoms?
Obtain thyroid function studies Clinical features of hypothyroidism Generalized slowing of metabolic processes Weakness & fatigue Weight gain Bradycardia Delayed deep tendon reflexes Constipation Cognitive slowing Cold intolerance Matrix glycosaminoglycan accumulation Coarse, dry skin Hoarseness Nonpitting edema (myxedema) Macroglossia Other mechanisms Depression Myalgia & arthralgia Hypercholesterolemia
40-year-old man comes to the office for a medical evaluation. The patient has no prior medical conditions but says that lately he has been feeling fatigued and has had occasional muscle aches. He has also gained 4.5 kg (9.9 lb) over the past year. Family history is not significant. Blood pressure is 130/92 mm Hg and pulse is 60/min. BMI is 26 kg/m2. Physical examination shows no abnormalities. Fasting serum lipid results are as follows: Total cholesterol 280 mg/dL HDL 40 mg/dL LDL 180 mg/dL Triglycerides 300 mg/dL What is the best next step in management of this patient's dyslipidemia?
Lithium Diabetes insipidus (DI) is a leading cause of euvolemic hypernatremia. It typically presents with severe polyuria and mild hypernatremia. It can be divided into 2 types based on etiology or urine osmolality. Based on etiology, DI may be central or nephrogenic: Central DI is due to decreased production of antidiuretic hormone (ADH) by the pituitary. Common causes include trauma, hemorrhage, infection, and tumors. Nephrogenic DI results from renal ADH resistance. The sodium level may be in the high-normal range (intact thirst mechanism). Common causes of nephrogenic DI include hypercalcemia, severe hypokalemia, tubulointerstitial renal disease, and medications. The most commonly implicated medications are lithium, demeclocycline, and amphotericin. DI most likely caused by lithium, which is one of the first-line drugs for bipolar disorder.
43-year-old woman comes to the emergency department due to confusion. She has also had increased thirst and has needed to "use the bathroom more frequently." She has not had any fever, chills, headache, chest pain, shortness of breath, or cough. Her medical history is significant for bipolar disorder that is well-controlled by medication. She does not use tobacco, alcohol, or illicit drugs. Vital signs and physical examination are unremarkable. Laboratory results are as follows: Sodium 151 mEq/L Urine osmolality 250 mOsm/kg (normal 300-900 mOsm/kg) Serum osmolality 326 mOsm/kg (normal 275-295 mOsm/hg) What is the most likely cause of this patient's symptoms and laboratory findings?
Initiate alpha-adrenergic blockade An adrenal mass, in combination with elevated plasma metanephrines, is diagnostic of pheochromocytoma. All pheochromocytomas should undergo surgical resection due to the risk for complications caused by catecholamine surges and the potential for malignancy. Surgical removal of a pheochromocytoma is a high-risk procedure To help prevent these complications, adrenergic blockade is needed prior to surgery The order of administration of adrenergic blockade is critical. Beta-blocker therapy without prior alpha-adrenergic blockade can lead to lethal hypertensive crisis due to unopposed alpha-1 stimulation. Therefore, alpha-adrenergic blockade is administered first, usually 7-14 days prior to surgery. Once adequate alpha-adrenergic blockade is established, then beta-adrenergic blockade (eg, propranolol) can be safely initiated, usually 2-3 days prior to surgery
45-year-old woman comes to the office for preoperative evaluation. The patient had been having intermittent headaches and sweating for several months. During that time, plasma metanephrines were found to be markedly elevated, and she underwent an CT scan of the abdomen that showed a 4.9-cm left adrenal mass. Blood pressure is 136/84 mm Hg and pulse is 92/min. Surgical resection of the mass is scheduled in 2 weeks. What is the best next step in preparation for surgery?
A fib Cardiovascular effects of hyperthyroidism Increased rate Tachycardia/palpitations Atrial fibrillation Increased contractility ↑ Ejection fraction & cardiac output ↑ Myocardial oxygen demand & angina ↑ Pulmonary artery pressure Peripheral vasodilation ↓ Systemic vascular resistance Additional effects ↓ Diastolic pressure ↑ Systolic pressure ↑ Pulse pressure High-output heart failure This patient is on thyroid replacement therapy for hypothyroidism and has a suppressed TSH (normal range: 0.5 to 5.0 µU/mL), indicating that her current dose is too high. Excess thyroid hormone, whether due to endogenous hyperthyroidism or iatrogenic over-replacement with levothyroxine, causes increased beta-adrenergic receptor expression. The resulting hyperadrenergic state can lead to significant cardiovascular complications.
48-year-old woman comes to the office for follow-up of primary hypothyroidism due to chronic autoimmune (Hashimoto) thyroiditis. She feels well and has no palpitations, heat/cold intolerance, diarrhea/constipation, or changes in weight. The patient takes levothyroxine daily on an empty stomach. Blood pressure is 120/70 mm Hg and pulse is 72/min. BMI is 27 kg/m2. On physical examination, the thyroid is normal to palpation. There is no peripheral edema. Serum TSH level is <0.01 µU/mL. Maintaining the current dose of levothyroxine would put this patient at the greatest risk for what complication?
Insulin-like growth factor 1 levels This patient's presentation (eg, coarse facial features, arthralgia, uncontrolled hypertension, enlargement of the digits, carpal tunnel syndrome) is consistent with acromegaly. This condition is caused by excessive growth hormone (GH) secretion, usually due to a pituitary somatotroph adenoma. Other common features include jaw malocclusion, hyperhidrosis, cardiomyopathy, macroglossia, and pituitary mass effect symptoms (eg, headache, visual field defects). GH stimulates hepatic insulin-like growth factor 1 (IGF-1) secretion, which mediates most of the clinical manifestations of acromegaly. IGF-1 levels in patients with acromegaly are consistently elevated throughout the day and are useful as an initial test.
49-year-old man comes to the office due to a 3-month history of fatigue. He also reports diffuse joint pain, finger swelling, and difficulty gripping objects with his right hand. The patient has poorly controlled hypertension despite compliance with medications, a low-salt diet, and regular exercise. Temperature is 36.7 C (98 F), blood pressure is 146/98 mm Hg, pulse is 90/min, and respirations are 14/min. On examination, facial features appear coarse and differ significantly from those on his driver's license photograph taken 3 years ago. The palms are sweaty and have a doughy feel. The skin is oily. Multiple skin tags are noted, particularly on the neck. Tapping the ventral aspect of the right wrist produces shooting pain on the lateral side of the right hand. What is the best next step in evaluation of this patient?
Left ventricular hypertrophy This patient has bony overgrowth (ie, frontal bossing; enlarged jaw, hands, and feet) consistent with acromegaly. Acromegaly is caused by excessive production of growth hormone (GH) and is most often due to a pituitary adenoma. Excess GH both directly and indirectly (via release of insulin-like growth factor 1 from the liver) leads to overgrowth of many tissues, including bone, cartilage, and visceral organs. In the heart, chronic GH elevation stimulates cardiac growth, causing left ventricular hypertrophy, diastolic dysfunction, and possible heart failure.
5-year-old man comes to the office due to slowly progressive joint pain. His knee and ankle joints are stiff and painful when he walks. Over the past year, the patient has also experienced excessive sweating, and his ring and shoe sizes have increased. He has no prior medical issues and takes no medications. Physical examination shows coarse facial features with a prominent forehead, protruding jaw, and widely separated maxillary teeth. There is mild swelling and crepitus of the knees and ankles bilaterally. What heart abnormality is most likely to be associated with this patient's condition
Parathyroid gland injury Hypoparathyroidism Etiology Postsurgical: thyroidectomy, parathyroidectomy Genetic disorder (eg, DiGeorge syndrome) Radiation Autoimmune disease Symptoms Asymptomatic Perioral or peripheral numbness/tingling, muscle cramps Carpal spasm (Trousseau sign) & facial twitch (Chvostek sign) Prolonged QT interval, tetany, seizure Diagnostic findings Hypocalcemia, hyperphosphatemia Low or inappropriately normal parathyroid hormone level Elevated 24-hr urinary calcium excretion Management Mild hypocalcemia (corrected calcium >7.5 mg/dL):Oral calcium & calcitriol Severe hypocalcemia (corrected calcium ≤7.5 mg/dL):Intravenous calcium gluconate
50-year-old hospitalized woman is seen for follow-up after thyroid surgery. Yesterday, she underwent total thyroidectomy under general anesthesia. The patient has no significant neck pain or difficulty breathing but has had cramps in her calves since this morning. Her fingers also feel like they are asleep, and she has a tingling sensation on the lips and tip of the tongue. Medical history is significant for rheumatoid arthritis and panic disorder. Temperature is 37 C (98.6 F), blood pressure is 130/70 mm Hg, and pulse is 96/min. Cardiopulmonary examination is normal. Pulses are strong in all extremities. What is the most likely underlying cause of this patient's symptoms?
Subacute thyroiditis Etiology Likely postviral inflammatory process Destruction of thyroid gland with release of thyroid hormone Clinical features Fever Painful/tender goiter Hyperthyroid symptoms Diagnosis Elevated free thyroxine (T4), suppressed TSH Elevated C-reactive protein & erythrocyte sedimentation rate Low radioiodine uptake Management Nonsteroidal anti-inflammatory drugs Beta blockers Condition is self-limited, with transient hypothyroidism & return to euthyroid state
50-year-old man comes to the office with a 2-day history of malaise, fever, fatigue, and pain in the front of his neck. He recovered from an upper respiratory illness a week prior to the onset of his current symptoms, but he previously had felt well. Temperature is 38.5 C (101.3 F), blood pressure is 150/70 mm Hg, and pulse is 110/min. The thyroid gland is diffusely enlarged and tender. Laboratory results are as follows: Complete blood count Hematocrit 44% Platelets 200,000/mm3 Leukocytes 10,500/mm3 TSH <0.001 µU/mL Free T4 4.6 ng/dL (0.9-2.4 ng/dL) Erythrocyte sedimentation rate 100 mm/hr
Papillary thyroid carcinoma Risk factors for thyroid cancer Patient & environmental factors Age <30 (papillary cancer) or >60 (anaplastic cancer) Female gender Radiation exposure (papillary & follicular cancer) Iodine deficiency Inherited disorders MEN2, RET mutations (medullary thyroid cancer) Familial polyposis coli, Cowden syndrome (papillary cancer)
51-year-old man comes to the office for a preventive care visit. The patient feels well. Thirty years ago, he had mediastinal Hodgkin lymphoma that was treated with external beam radiation therapy, and he has had no relapses. The patient had a normal colonoscopy a year ago. He does not use tobacco, alcohol, or illicit drugs. Vital signs and physical examination are normal. Compared to the general population, this patient is at highest risk of developing what malignancy?
Subacute thyroiditis
52-year-old woman comes to the office due to 3 days of pain that is in the anterior lower neck and radiates to the jaw. The pain is exacerbated when she turns her head. The patient has also had palpitations and a feeling of being "hot." She had an upper respiratory infection 4 weeks ago; otherwise, her medical history is unremarkable. Temperature is 37.5 C (99.5 F), blood pressure is 144/80 mm Hg, and pulse is 125/min and regular. Because of neck pain, the patient does not allow neck palpation. The oropharynx is not erythematous. Erythrocyte sedimentation rate is 100 mm/hr. TSH is 0.005 µU/mL and free T4 is 2.7 µg/dL (normal: 0.9-2.4).
Canagliflozin Glucagon-like peptide-1 (GLP-1) agonists (eg, semaglutide, liraglutide) Sodium-glucose cotransporter 2 (SGLT2) inhibitors (eg, canagliflozin, empagliflozin)
54-year-old man presents for a diabetes follow-up visit. The patient has a 5-year history of type 2 diabetes mellitus, which is treated with metformin. He also has hypertension and had coronary stenting for a myocardial infarction a month ago. Blood pressure is 130/74 mm Hg and pulse is 68/min. BMI is 30 kg/m2. Hemoglobin A1c is 7.8%. What medications has an added protective effect on this patient's cardiac and weight-related comorbidities
Serum Cr Metformin Metabolic effects ↓ Hepatic glucose production ↓ Intestinal glucose absorption ↑ Peripheral glucose uptake/use ↓ Lipogenesis Adverse effects Diarrhea Lactic acidosis Vitamin B12 deficiency Precautions/contraindications Renal insufficiency (check serum creatinine) Hepatic insufficiency Congestive heart failure Although rare, the risk is increased for those with significant renal dysfunction or other disorders causing decreased lactate clearance (eg, hepatic impairment, congestive heart failure). Therefore, the glomerular filtration rate should be estimated using serum creatinine measurement prior to the initiation of metformin therapy.
54-year-old woman comes to the office due to elevated blood glucose. The patient was recently seen at an urgent care center, where she was found to have a nonfasting blood glucose level of 190 mg/dL. Medical history is insignificant, and she has not seen a health care provider for several years. BMI is 31.5 kg/m2. Physical examination shows no abnormalities. Hemoglobin A1c is 8.5% and fasting plasma glucose level is 146 mg/dL. Recommendations for dietary modification and exercise are provided, and pharmacotherapy with metformin is planned. What laboratory tests should be obtained prior to administering this medication?
Amiodarone Amiodarone adverse effects Cardiac Bradycardia QT interval prolongation* Pulmonary Interstitial pneumonitis Organizing pneumonia, lung nodules Endocrine Hyperthyroidism or hypothyroidism Hepatic Hepatitis Ophthalmic Corneal microdeposits Optic neuritis Dermatologic Blue-gray skin discoloration Neurologic Peripheral neuropathy Amiodarone is indicated for patients with serious ventricular arrhythmias and for rhythm control in those with atrial fibrillation and left ventricular systolic dysfunction. However, it can cause thyroid dysfunction (hyper-or hypothyroidism) due to its high iodine content and intrinsic effects on thyroid metabolism.
56-year-old man comes to the office due to progressively worsening fatigue, difficulty concentrating, and increasing forgetfulness over the past several weeks. In addition, the patient has had vague abdominal pain and constipation and has gained 2.7 kg (6 lb) unintentionally over the last 3 months. Medical history is significant for hypertension, nonischemic cardiomyopathy with left ventricular systolic dysfunction, and atrial fibrillation. Blood pressure is 140/90 mm Hg and pulse is 75/min. Patient's skin appears dry but physical examination is otherwise normal. What medication is most likely responsible for this patient's current symptoms?
Start ACE inhibitor In addition to ACEIs/ARBs, sodium-glucose cotransporter-2 inhibitors appear to prevent the progression of kidney disease; they can be considered in patients with severely increased albuminuria (albumin/creatinine ratio >300 mg/g).
56-year-old man comes to the office for evaluation. The patient was diagnosed with type 2 diabetes mellitus 4 years ago and was prescribed metformin. However, he has not followed up since and has stopped taking his medication. The patient says he feels well but wants to check up on his diabetes. Blood pressure is 142/86 mm Hg and pulse is 72/min. BMI is 30 kg/m2. Laboratory results are as follows: Serum chemistry Sodium 136 mEq/L Potassium 4.2 mEq/L Blood urea nitrogen 14 mg/dL Creatinine 0.8 mg/dL Glucose 220 mg/dL Hemoglobin A1c 7.8% Urinalysis no protein, cells, or casts Urine albumin/creatinine ratio 250 mg/g In addition to recommending lifestyle modification and the resumption of metformin and to obtaining a comprehensive ophthalmologic evaluation, what is most appropriate in this patient?
Hydrochlorothiazide Adverse effects of SGLT-2 inhibitors Genitourinary infections Vulvovaginal candidiasis Urinary tract infection Fournier gangrene (rare) Osmotic diuresis Volume depletion, symptomatic hypotension Acute kidney injury Metabolic disturbance Euglycemic diabetic ketoacidosis Orthopedic complications Low-trauma fracture Foot ulcers that may increase amputation risk SGLT2 inhibitors can induce an osmotic diuresis, which can lead to hypotension and decreased renal perfusion. Elderly patients and those taking diuretics or drugs which affect the renin-angiotensin-aldosterone system (eg, ACE inhibitors, angiotensin receptor blockers) are at greatest risk. This patient is on a diuretic and is already hypotensive and should have her hydrochlorothiazide dose decreased or discontinued prior to initiating canagliflozin
56-year-old woman comes for follow-up of her type 2 diabetes mellitus. Despite optimal lifestyle and compliance with medications, her A1c remains elevated at 8.2%. The patient also has hypertension; her current medications include metformin, sitagliptin, amlodipine, hydrochlorothiazide, and aspirin. Blood pressure is 102/70 mmHg. If canagliflozin is added to this patient's diabetes management, which of her medications will most likely need dose adjustment
Weight gain and edema Noninsulin antidiabetic agents for type 2 diabetes mellitus Insulin secretagogues Sulfonylureas Meglitinides ↑ Insulin secretion by inhibiting β-cell KATP channels Hypoglycemia Weight gain Biguanides Metformin Stimulate AMPK & inhibit mitochondrial gluconeogenesis, ↓ hepatic glucose production & ↑ peripheral glucose uptake Diarrhea Lactic acidosis Thiazolidinediones Pioglitazone Activate transcription regulator PPAR-γ, ↓ insulin resistance Fluid retention/heart failure Weight gain GLP-1 agonists Exenatide Liraglutide ↑ Glucose-dependent insulin secretion, ↓ glucagon secretion, delayed gastric emptying Pancreatitis Weight loss DPP4 inhibitors Sitagliptin Saxagliptin ↑ Endogenous GLP-1 & GIP levels Nasopharyngitis SGLT-2 inhibitors Canagliflozin Dapagliflozin ↑ Renal glucose excretion Urinary tract infections Hypotension
56-year-old woman comes in for follow-up for type 2 diabetes mellitus. She manages her condition with lifestyle modifications and takes the maximum tolerated dose of metformin. However, the patient's diabetes mellitus has been inadequately controlled for the past 6 months, with an average fasting glucose level of 170 mg/dL and a hemoglobin A1c of 8.0%. Pioglitazone is added to her current regimen. Before starting this medication, this patient should be educated about what adverse drug effects?
Serum calcitonin This patient has medullary thyroid cancer (MTC), a neuroendocrine malignancy arising from the calcitonin-secreting parafollicular C cells. Most cases are sporadic; approximately 25% are due to multiple endocrine neoplasia type 2 (MEN2), which is characterized by MTC, pheochromocytoma, and either parathyroid hyperplasia (type 2A) or marfanoid habitus and mucosal neuromas (type 2B). Unless there is concomitant hyperparathyroidism, serum calcium is usually normal. The diagnosis of MTC is confirmed with fine-needle aspiration. Primary treatment is total thyroidectomy; therefore, postoperative thyroid replacement therapy is necessary. Serum calcitonin levels correlate with the risk of metastasis and are measured at the time of diagnosis; they also correlate with risk of recurrence and are therefore measured serially following surgery.
57-year-old man comes to the office for follow-up after recent thyroid surgery. A month ago, the patient was found to have a solitary thyroid nodule, and a fine-needle aspiration biopsy of the mass revealed medullary thyroid cancer. He underwent an uncomplicated total thyroidectomy and removal of surrounding lymph nodes. The patient feels well and is taking levothyroxine as prescribed. Vital signs are normal. On examination, there is a well-healing incision on his lower anterior neck with no surrounding erythema or edema. What should be monitored to evaluate for recurrent medullary thyroid cancer in this patient?
Increased waist circumference
58-year-old man is hospitalized due to sudden onset of chest pain. Blood pressure is 160/110 mm Hg and pulse is 90/min. BMI is 26.9 kg/m2. A baseline ECG shows nonspecific ST-segment and T-wave abnormalities, and serial troponin measurements are normal. The patient's fasting plasma glucose level is 160 mg/dL, although he has not been diagnosed previously with diabetes mellitus. Serum triglyceride level is elevated, and the HDL level is low. What additional findings would be most suggestive of increased insulin resistance in this patient?
Continue lisinopril and repeat testing in 2-3 weeks This patient has diabetic nephropathy (ie, albuminuria of >300 mg/day or >300 mg/g creatinine on random urine sample), a complication of long-standing and/or poorly controlled diabetes mellitus. In addition to glycemic (Hgb A1c <7%) and blood pressure (<130/80 mm Hg) control, inhibition of the renin-angiotensin-aldosterone system reduces the progression of diabetic neuropathy. Angiotensin-converting-enzyme (ACE) inhibitor and angiotensin II receptor blocker (ARB) therapy can cause an initial decrease in glomerular filtration rate (GFR) and rise in serum potassium (from reduced levels of aldosterone). These side effects should be monitored closely, especially at the outset of therapy or during dose titration. A rise in serum creatinine of up to 30%-35% from baseline is acceptable and should not cause discontinuation of therapy.
58-year-old man with type 2 diabetes mellitus comes to the office for a follow-up appointment. The patient also has chronic kidney disease with a baseline creatinine of 1.5 mg/dL and urine protein excretion of 1100 mg/day. He has failed to lose weight despite diet adjustments and aerobic exercise. The patient takes insulin daily. His blood pressure is 140/89 mm Hg and his pulse is 83/min. BMI is 30 kg/m2. He is started on lisinopril 5 mg daily. The patient returns for a follow-up appointment 2 weeks later and reports feeling well. His blood pressure is 133/85 mm Hg. Repeat testing shows creatinine of 1.8 mg/dL and potassium of 4.8 mEq/L. What is the best next step in management of this patient?
Serum chemistry profile and urinalysis Hyperosmolar hyperglycemic state
59-year-old woman is brought in by her husband due to increasing fatigue and drowsiness for the past week. The patient has also been urinating frequently with several episodes of incontinence. Medical history is significant for type 2 diabetes mellitus, primary hypothyroidism, and bipolar disorder. Four weeks ago, the patient was prescribed olanzapine for refractory depression. Temperature is 36.7 C (98.1 F), blood pressure is 110/65 mm Hg, pulse is 100/min, and respirations are 12/min. Physical examination shows dry mucous membranes and decreased skin turgor. The patient is confused and disoriented but moves all extremities on command. There is no nuchal rigidity. The rest of the examination is unremarkable. What is most likely to reveal the underlying cause of this patient's symptoms?
Insulin aspart This patient has normal fasting glucose levels, suggesting that his long-acting basal insulin therapy is appropriate. However, his postprandial glucose readings are elevated. Adding a rapid-acting insulin analog (eg, aspart, lispro, glulisine) with meals would reduce postprandial glucose and improve overall glycemic control.
60-year-old man comes to the office for follow-up of type 2 diabetes mellitus. His current treatment regimen includes metformin and a once-daily injection of a long-acting subcutaneous insulin. Review of his home glucose measurements shows that his postprandial glucose levels are frequently elevated; however, fasting levels are normal. Today, his hemoglobin A1c is 8.3%. Additional insulin therapy 3 times a day before each meal is planned to improve glycemic control. What is the most appropriate additional therapy?
Gabapentin Drugs for neuropathic pain Tricyclic antidepressants(eg, amitriptyline, nortriptyline) SNRIs (eg, duloxetine) ↓ Reuptake of serotonin & norepinephrine Inhibition of pain signals Anticonvulsants(eg, gabapentin, pregabalin) Decreased depolarization of neurons in the CNS Opioids Activation of central opioid receptors Capsaicin (topical) Loss of membrane potential in nociceptive fibers Lidocaine (topical) Decreased depolarization of neurons in peripheral nerves
60-year-old man is seen for follow-up. The patient has a 10-year history of type 2 diabetes mellitus. Over the past 2 years, he has had burning pain and pins-and-needles sensations in his feet, which are worse at night. The patient takes the maximal dose of nortriptyline but states that the symptoms have not improved. What medication would provide additional benefit without increasing the risk for serotonin syndrome
Postprandial hyperglycemia Hemoglobin A1c reflects average glucose levels over the lifespan of hemoglobin (about 3 months). A1c is influenced by both fasting and postprandial glucose concentrations and is useful for estimating overall glycemic control in patients with diabetes mellitus. The target A1c is <7% in most patients. Very high A1c levels (>10%) suggest significant hyperglycemia throughout the day, whereas lesser abnormalities are often due to elevations in only postprandial glucose levels. This patient's hemoglobin A1c is elevated despite an acceptable morning (fasting) glucose (usual target range: 80-130 mg/dL). In association with her markedly elevated random glucose levels, this suggests the patient is experiencing frequent postprandial hyperglycemia leading to impaired overall glycemic control.
62-year-old woman comes to the office for follow-up of diabetes treatment. She has had type 2 diabetes mellitus for 10 years, which is managed with oral metformin twice daily and insulin glargine at bedtime. The patient has no chest pain, dizziness, sweating, polyuria, or palpitations. Her fasting blood glucose levels have been 75-132 mg/dL, and her random blood glucose levels, usually several hours after the patient's last meal, have been between 220-298 mg/dL. Today's hemoglobin A1c is 8.1%. What best explains the suboptimal glycemic control in this patient?
CT of the abdomen Pancreatic adenocarcinoma Risk factors Age≥65 Smoking Chronic pancreatitis Genetic predisposition (Hereditary pancreatitis; Peutz-Jeghers syndrome; MEN syndromes; Hereditary nonpolyposis colon cancer) Clinical presentation Weight loss, anorexia Abdominal/back pain or painless obstructive jaundice Migratory thrombophlebitis Hepatomegaly & ascites (with metastasis) This patient's older age, weight loss, constant epigastric pain, smoking history, and recent diagnosis of diabetes mellitus (DM) raise suspicion for pancreatic cancer. Major risk factors include cigarette smoking, chronic pancreatitis, and disorders of glucose metabolism such as insulin resistance and DM.
65-year-old man comes to the office due to 4 weeks of persistent epigastric pain and nausea. The pain is constant and has not changed with diet. The patient lost 4.5 kg (9.9 lb) over this period. He was diagnosed with type 2 diabetes mellitus 6 months ago, which is controlled with a low-carbohydrate diet. He has a 45-pack-year history of smoking. Vital signs are normal. BMI is 21 kg/m2. The abdomen is soft with mild epigastric tenderness to deep palpation. No hepatosplenomegaly or shifting dullness is present. Complete blood count, serum chemistry, and liver function studies is all normal except a fasting blood sugar of 130 mg/dL. What is the best next step in management of this patient?
IV hypertonic saline Syndrome of inappropriate antidiuretic hormone Etiologies CNS disturbance (eg, stroke, hemorrhage, trauma) Medications (eg, carbamazepine, SSRIs, NSAIDs) Lung disease (eg, pneumonia) Ectopic ADH secretion (eg, small cell lung cancer) Pain &/or nausea Clinical features Mild/moderate hyponatremia: nausea, forgetfulness Severe hyponatremia: seizures, coma Euvolemia (eg, moist mucous membranes, no edema, no JVD) Laboratory findings Hyponatremia Serum osmolality <275 mOsm/kg H2O (hypotonic) Urine osmolality >100 mOsm/kg H2O Urine sodium >40 mEq/L Management Fluid restriction ± salt tablets Hypertonic (3%) saline for severe hyponatremia
66-year-old hospitalized man is evaluated after an episode of generalized tonic-clonic seizure. The patient has no previous history of seizure. He underwent right hemicolectomy for cecal adenocarcinoma the previous day. Postoperatively, he has been receiving intravenous infusion of 5% dextrose with 0.45% saline. He is also receiving morphine via a patient-controlled device. On physical examination, he is postictal. Vital signs are normal. Laboratory results are as follows: Sodium 114 mEq/L Potassium 4.2 mEq/L Chloride 90 mEq/L Bicarbonate 22 mEq/L Glucose 120 mg/dL What is the best next step in management of this patient?
Symptomatic hypoglycemia Sulfonylureas are second-line agents that are frequently used as add-on therapy or as a replacement for metformin. Sulfonylureas inhibit the potassium channel on the pancreatic beta cell membrane, which stimulates beta cell insulin release independent of blood glucose concentrations. Meglitinides (eg, repaglinide, nateglinide) are short-acting drugs that are functionally similar to sulfonylureas. Sulfonylureas continue to stimulate insulin secretion, even when blood glucose levels are normal and can therefore cause hypoglycemia. Hypoglycemia due to sulfonylureas can be induced by exercise, missed meals, acute illness, or initiation of additional antidiabetic medications. Symptomatic presentation includes altered mental status, tremor, and diaphoresis.
67-year-old woman comes to the office for follow-up of type 2 diabetes mellitus diagnosed 6 months ago. Lifestyle modification was initially advised, with no significant glycemic improvement. One month ago, the patient was started on metformin, to which she has been adherent; however, she has been experiencing abdominal discomfort and diarrhea attributed to the therapy. After further discussion, metformin is discontinued and glyburide is prescribed. This new therapy is most likely to increase the risk of what SE?
Volume resuscitation Hyperosmolar hyperglycemic state In patients with HHS, serum bicarbonate is generally near the lower limits of normal (rather than an anion gap acidosis). Dehydration (eg, dry mucous membranes, tachycardia) occurs from osmotic diuresis caused by hyperglycemia. Neurologic symptoms occur because of markedly increased serum osmolality. Patients are frequently hyperkalemic due to relative insulin insufficiency and hyperosmolality; this is despite an overall body potassium deficit caused by increased urinary excretion. These patients frequently have had large-volume fluid loss; therefore, the first step in management is aggressive fluid resuscitation, typically with isotonic saline.
68-year-old man is brought to the emergency department due to confusion and lethargy. The patient lives alone and has type 2 diabetes mellitus and hypertension. Temperature is 36.1 C (97 F), blood pressure is 99/59 mm Hg, pulse is 132/min, and respirations are 22/min. The patient is drowsy and has dry mucous membranes. Neurologic examination shows disorientation to time and place. Laboratory results are as follows: Serum chemistry Sodium 151 mEq/L Potassium 6.1 mEq/L Chloride 121 mEq/L Bicarbonate 18 mEq/L Blood urea nitrogen 42 mg/dL Glucose 810 mg/dL Serum ketones negative ECG shows atrial fibrillation with a rapid ventricular response. What is the best next step in management of this patient?
block sympathetic hyperactivity Cardiovascular effects of thyrotoxicosis Rhythm Sinus tachycardia Premature atrial & ventricular complexes Atrial fibrillation/flutter Hemodynamic effects Systolic hypertension & ↑ pulse pressure ↑ Contractility & cardiac output ↓ Systemic vascular resistance ↑ Myocardial oxygen demand Heart failure High-output failure Exacerbation of preexisting low-output failure Angina symptoms Coronary vasospasm Preexisting coronary atherosclerosis Thyroid hormones increase sympathetic activity due to increased responsiveness to catecholamines, which is responsible for many symptoms of hyperthyroidism (eg, palpitations, tachycardia, anxiety, tremors). Beta blockers (eg, propranolol, atenolol) are initiated as soon as hyperthyroidism is recognized because they ameliorate hyperadrenergic symptoms and control heart rate.
68-year-old woman comes to the emergency department due to increasing palpitations. The patient has had no associated chest pain or shortness of breath but has had fatigability and a 4-kg (8.8-lb) weight loss. Blood pressure is 151/68 mm Hg, pulse is 122/min, and respirations are 16/min. The thyroid gland is diffusely enlarged and nontender. Lid lag is noted on eye examination. The heart has an irregularly irregular tachycardia with a variable intensity of S1. Serum glucose is 122 mg/dL, TSH is <0.01 μU/mL, and free T4 is 4.7 ng/dL (normal: 0.9-2.4). What is the best next step in management of this patient?
The risk of testosterone replacement likely outweigh the benefits Testosterone replacement therapy Indications Symptomatic hypogonadism (fatigue, decreased libido, loss of bodyhair, reduced erections, gynecomastia) Low testosterone level confirmed on repeat testing (8-10 AM/fasting) Contraindications Prostate or breast cancer Severe lower urinary tract symptoms* Hematocrit >50%* Severe sleep apnea* PSA >4.0 µg/L (>3.0 µg/L with other prostate cancer risk factors) Heart failure* Contraindications to TRT include polycythemia, unstable heart failure, and untreated obstructive sleep apnea (OSA). This patient has an elevated hematocrit, hypertension, obesity, and a large neck circumference, which together suggest possible OSA. The patient also has multiple risk factors for cardiovascular disease. As a result, the risks likely outweigh the benefits of TRT in this patient
70-year-old man seeks advice regarding testosterone replacement therapy. He has diminished sexual desire and moderate erectile dysfunction that responds to sildenafil. The patient's ability to perform endurance exercise at a high level is significantly lower than it was 10 years ago. His other medical conditions include hypertension, type 2 diabetes mellitus, benign prostatic hyperplasia, and hyperlipidemia. BMI is 30 kg/m2. Neck circumference is enlarged at 20 in (51 cm). The testes appear normal for age. Digital rectal examination shows a symmetrical prostate that is enlarged. Hematocrit is 54%, serum testosterone level is 280 ng/dL (normal: 300-1,000), and prostate-specific antigen is 3.5 ng/mL. Which statement regarding testosterone replacement is appropriate for this patient's condition?
Hyperosmolar hyperglycemic state Patientcharacteristics Type 2 diabetes mellitus Older age Inciting factors Acute illness, trauma, infection Insulin nonadherence Medications: glucocorticoids, diuretics, atypical antipsychotics Clinical features Subacute or acute onset of: Altered mentation Hyperglycemic symptoms (eg, polyuria) Volume depletion Laboratory studies Glucose >600 mg/dL (33.3 mmol/L) Bicarbonate >18 mEq/L (18 mmol/L) Normal anion gap Negative or small serum ketones Serum osmolality >320 mOsm/kg (320 mmol/kg)
75-year-old man is brought to the emergency department due to 2 days of progressive lethargy and confusion. He has had fatigue and blurred vision over the last several days. The patient was recently diagnosed with polymyalgia rheumatica and is taking prednisone. He also has diet-controlled type 2 diabetes mellitus. Temperature is 37.9 C (100.2 F), blood pressure is 90/60 mm Hg, pulse is 112/min, and respirations are 18/min. Oral mucous membranes are dry. The patient is somnolent but arousable and moves all extremities equally on command. Laboratory results are as follows: Sodium 129 mEq/L Potassium 3.5 mEq/L Chloride 94 mEq/L Bicarbonate 24 mEq/L Blood urea nitrogen 36 mg/dL Glucose 1,170 mg/dL Urinalysis shows trace ketones.
Graves Disease Thyroid autoantibodies Thyrotropin (TSH)receptor antibody Graves disease Functional bioassay (thyroid-stimulating immunoglobulin) is also available Thyroid peroxidaseantibody Chronic lymphocytic (Hashimoto) thyroiditis Silent thyroiditis Postpartum thyroiditis Some patients with Graves disease Thyroglobulin antibody Nonspecific, but more common in hypothyroidism than hyperthyroidism
A 32-year-old woman comes to the office due to a persistent sensation of warmth. For the past 6 months, she has felt unusually warm compared to others in the same room. The patient has no medical conditions and takes no medications or supplements. Temperature is 36.7 C (98.1 F), blood pressure is 130/60 mm Hg, and pulse is 104/min. BMI is 20 kg/m2. On physical examination, there is exophthalmos, lid lag, and a diffusely enlarged thyroid with an audible thyroid bruit. The patient has a fine tremor on outstretched arms, and the skin is warm and moist. Laboratory results are as follows: TSH <0.01 μU/mL T4 3.4 ng/dL (normal: 0.8-1.9) T3 196 ng/dL Thyrotropin receptor antibody positive Thyroid peroxidase antibody negative
Prescribe insulin therapy Gestational diabetes mellitus Target blood glucose levels Fasting ≤95 mg/dL (5.3 mmol/L) 1-hour postprandial ≤140 mg/dL (7.8 mmol/L) 2-hour postprandial ≤120 mg/dL (6.7 mmol/L) Treatment 1st-line: Dietary modifications 2nd-line: Insulin, metformin
A 32-year-old woman comes to the office for a follow-up appointment at 32 weeks gestation. She was diagnosed with gestational diabetes mellitus at 28 weeks gestation. The patient has since been eating 3 small, healthy meals and 2 snacks daily. Blood pressure is 126/80 mm Hg and pulse is 76/min. BMI is 24 kg/m2. Blood glucose levels over the last week are recorded below: What is the best next step in management of this patient?
Serum TSH Thyroid nodules once found, cancer risk factors (family history, radiation exposure) should be assessed Physical examination should evaluate the size, mobility, and firmness of the thyroid nodule and whether enlarged cervical lymph nodes are present. Serum TSH levels should be obtained, and a thyroid ultrasound to determine nodule size and sonographic features. Certain sonographic features carry a much higher risk of malignancy than others. Thyroid nodules >1 cm with these high-risk sonographic features and all noncystic thyroid nodules >2 cm should undergo fine-needle aspiration (FNA) biopsy. If the TSH is low eval with radionuclide thyroid scan A hyperfunctioning ("hot") nodule (increased isotope uptake) is ass with low cancer risk; a hypofunctioning ("cold") nodule (decreased isotope uptake) is ass with higher risk of cancer.
A 36-year-old woman is found to have a thyroid nodule during a routine physical examination. She has had no heat or cold intolerance, skin changes, or fatigue. Her appetite and stooling habits have not changed, and her weight is stable. Menstrual cycles are regular with no excessive bleeding. She has had no prior radiation exposure. Family history is negative for thyroid disorders. Vital signs are normal. Physical examination shows no abnormalities with the exception of a 1-cm, discrete, nontender, and firm nodule in the left thyroid lobe. What is best next step in management of this patient?
Glucagon-like peptide-1 agonist Type 2 diabetes and comorbid cardiovascular disease Lifestyle Smoking cessation, regular exercise Reduced saturated fat, refined sugar intake Cardioprotective antidiabetic agents GLP-1 receptor agonists (eg, liraglutide) SGLT-2 inhibitors (eg, empagliflozin) Lipid/antiplatelet therapy Statins Low-dose aspirin Blood pressure control Goal BP <130-140/80-90 mm Hg ACE inhibitor/ARB preferred This patient has a history of myocardial infarction and mild obesity. Recommended options for add-on therapy in patients with established cardiovascular disease include the following: Glucagon-like peptide-1 (GLP-1) agonists (eg, exenatide, liraglutide) Sodium-glucose cotransporter 2 (SGLT2) inhibitors (eg, canagliflozin, empagliflozin)
A 55-year-old man comes for a follow-up visit. The patient has type 2 diabetes mellitus and hypertension and had an acute myocardial infarction 2 years ago. He reports no symptoms but has been unable to lose weight despite diet and exercise. The patient takes metformin and has noticed frequently elevated blood glucose readings at home. Blood pressure is 126/70 mm Hg and pulse is 74/min. BMI is 32 kg/m2. Physical examination is otherwise unremarkable. Laboratory results are as follows: Blood urea nitrogen14 mg/dLSerum creatinine1.0 mg/dLFasting blood glucose156 mg/dLHemoglobin A1c8.0% Lifestyle modifications are reinforced, and an additional medication is prescribed to improve glycemic control and assist with weight loss. What medication was most likely prescribed?
