E. Tell her that everything is normal and discharge her from your clinic.
The important point to remember for this question is that an empty sella may be normal. This patient does not present any indication of pituitary dysfunction. The history of blood loss at the time of delivery may suggest Sheehan syndrome (hemorrhagic necrosis of the pituitary), but one of the most sensitive indicators of pituitary dysfunction is ovulation. This patient was able to get pregnant 6 more times; the hypothalamic-pituitary-ovarian axis must be working properly. She does not have Sheehan syndrome, but her obstetrical history offers another clue. Her 7 pregnancies have most likely caused her empty sella. With pregnancy, the pituitary enlarges and has a greater blood flow. This produces an upward pressure on the diaphragm covering the top of the sella, which stretches and expands the diaphragm. After pregnancy, the pituitary returns to a normal size with a normal blood flow, but the diaphragm is acellular and remains stretched. With each subsequent pregnancy, the diaphragm becomes progressively more stretched. This allows the diaphragm to bulge downward and into the sella under the pressure of the CSF fluid above it. In some cases, the diaphragm has become so loose that the CSF fluid displaces the majority of the pituitary to the periphery of the sella. A CT of the head will fail to identify pituitary tissue, and the term "empty sella" will be used. In actuality, the sella is not empty, but contains CSF fluid and normal pituitary tissue that has been pushed to the periphery. The pituitary tissue can work perfectly normally in this environment.
It is inappropriate to refer her to a neurosurgeon. Pituitary exploration may disrupt the normal functioning of her existing pituitary tissue and result in the development of hypopituitarism. While there is no evidence of pituitary dysfunction, the abdominal striae may trick some people to suspect Cushing syndrome, but there is no mention of hyperglycemia, hypokalemia, or the typical body habitus. Stretch marks are a common occurrence, especially following pregnancy. The typical stretch marks associated with Cushing syndrome are broad and appear purplish from the coloration of underlying tissue.
A 60-year-old woman is establishing care in your clinic. She has occasional numbness and tingling in her fingers and toes and has noted some numbness around her mouth, especially when she is stressed or anxious. She had thyroid surgery for Graves disease about 2 years ago and takes 100 µg of levothyroxine and 1 tablet of calcium daily. On exam, her blood pressure is 130/80, pulse 80, and she has cramping in her right forearm and fingers when the blood pressure cuff is attached.
Based on this history and exam, which of the following is most likely?
A) Calcium 8.5, PTH 65, PO4 4.5
B) Calcium 9.5, PTH 35, PO4 4.0
C) Calcium 6.0 (8.5-10.5), PTH 2 (10-65), PO4 6.0 (2.7-4.5)
D) Calcium 10.8, PTH 108, PO4 2.3
E) Calcium 8.0, PTH 98, PO4 2.1
D. Begin dexamethasone 4 mg IV and order an ACTH stimulation test.
There is a strong suspicion that this patient has adrenal insufficiency and is having an adrenal crisis. She is hypovolemic with a hyperkalemic metabolic acidosis. The hypotension responded well to saline fluids. The thin body habitus and loss of axillary and pubic hair imply a chronic adrenal insufficiency. The flight delay may have caused stress for some reason that she was not able to cope with because of the adrenal insufficiency. This may have been what tipped her over the edge. Whether she really has an adrenal crisis or not is not the issue. It is more important to begin treatment than it is to prove your suspicion. The treatment is to give her intravenous glucocorticoids as soon as possible. But which glucocorticoid should you give? Remember, you do not yet have proof of the adrenal insufficiency. You can start treatment based on a suspicion, but you must also pursue a diagnosis. The diagnostic workup begins with an ACTH stimulation test. To do this, order a baseline serum cortisol level, administer 1 ampule of ACTH, and repeat the cortisol level 30 minutes later. The important thing to remember is that the assay for cortisol will cross-react with most other glucocorticoids and also pick up prednisone, methylprednisolone, and especially hydrocortisone since it is cortisol under a different name. If any of these are administered, how will you know what her endogenous production of cortisol really is? The solution is to administer a glucocorticoid that does not interfere with the cortisol assay, such as dexamethasone. She needs a glucocorticoid to save her life; begin dexamethasone immediately. If her adrenal function proves to be okay, you can easily stop the steroid. To check her adrenal function, check for her response to ACTH. If the cortisol level is greater than 20 μg/dL, her adrenal reserve is intact and you can stop the dexamethasone. If the ACTH stimulation test shows adrenal insufficiency, stop the dexamethasone and switch her to hydrocortisone. This is the actual cortisol molecule, and it has an advantage over the other glucocorticoids. Hydrocortisone (cortisol) is primarily a glucocorticoid, but it also has some mineralocorticoid activity that will help with her electrolytes.
The other answers are incorrect because a glucocorticoid other than dexamethasone should not be used for the above reasons. Hypothyroidism is unlikely, so starting thyroxine is not indicated. Once her adrenal crisis has resolved, you can reevaluate her.
D. He has diabetes and must talk with a diabetes educator and dietitian to begin a diet, exercise program, and metformin.
He fulfills 2 diagnostic criteria for diabetes. The full set of criteria include: 1) random glucose ≥ 200 mg/dL with symptoms (polyuria, polydipsia, or unexplained weight loss); 2) fasting glucose ≥ 126 mg/dL; and 3) 2-hour 75 g oral glucose tolerance test (OGTT) ≥ 200 mg/dL. Now that you have diagnosed him, you must next determine whether he has Type 1 or Type 2 diabetes. He most likely has Type 2, because he is overweight, and there is no mention of metabolic decompensation. You must now determine whether to treat and, if so, how. There is no question about it―you must intervene immediately. There is nothing to benefit from waiting. However, in the absence of metabolic decompensation and severe hyperglycemia, it is most prudent to begin with lifestyle changes. He must be educated on the importance of an exercise program, and he must learn how to eat a healthful diet. Current recommendations now include beginning metformin in all patients with their initial diagnosis of Type 2 diabetes. This is because of the difficulty in achieving and sustaining glycemic control and achieving significant weight loss.
D. Surgical resection of her thyroid, followed by thyroxine replacement.
She is hyperthyroid due to Graves disease but also has a cold nodule. The best treatment option in someone with Graves disease complicated by a cold nodule is surgical resection, followed by appropriate thyroxine replacement. This will take care of both the Graves disease and the cold nodule. Even though most cold nodules are benign, any cancer that may be present is most likely to occur in a cold nodule. Radioactive iodine ablation is an excellent treatment option for Graves disease, but it will not have any effect on the cold nodule because cold nodules do not take up iodine, by definition. Thus, after ablation her nodule will still be present and will have to be biopsied, but now the architecture is altered, and the biopsy and any necessary nodule resection may be more difficult. Surgical resection will also give this patient a faster return to euthyroidism and probable return to regular menses and fertility. Granted, this is a difficult question with several possible treatment plans. However, this scenario is one of the reasons to refer a patient with Graves disease for surgical resection. The vast majority of cases are treated with radioactive iodine ablation.
PTU will address the hyperthyroidism, but will not address the cold nodule. An ultrasound-guided biopsy is not a bad choice, but you must still address the hyperthyroidism after the nodule has been taken care of. If the nodule is benign, then you can proceed to the ablation. If the nodule is not benign, then you will have to refer her for surgical resection anyway. Again, radioactive iodine ablation will address the Graves disease, but will not address the cold nodule. Waiting 6 months to examine the nodule could cause unacceptable advancement of any malignancy that may be present. Starting oral contraceptives will not address any of her problems.
Remember: Any woman receiving a radioactive iodine ablation must avoid pregnancy for a minimum of 6 months. Also, since oral contraceptives are less effective in a woman who is hyperthyroid, she must use two forms of birth control or avoid sex altogether. The dose for a thyroid scan and uptake is considerably smaller, and no special precautions are required after the scan and uptake. Though the fetus is probably safe when exposed to the small dose used in scans, pregnant women should never receive radioactive iodine because of the potential threat to the fetus.
A 75-year-old man presents with visual loss. He has cold intolerance, fatigue, weight gain, and headaches. His exam shows BP 110/60, pale skin, ↓ beard growth, and breast enlargement. Lab shows prolactin 24, cortisol 2 (↓), testosterone 50 (↓), and free T4 0.4 (↓).
Replacement therapy is initiated, and he is scheduled for formal visual fields.
What is the next step?
A) Measure GH and IGF-1.
B) Neurosurgery consult.
C) Radiation therapy consult.
A 78-year-old woman was last seen for her annual Pap smear 1 year ago. At that time she was fatigued and had several yeast infections, which she treated with OTC preparations. She continues to be fatigued, has nocturia twice nightly, and has had several yeast infections. She takes no medications and occasionally takes calcium. Her mother died of an MI, her aunt of a stroke, and her uncle was on dialysis due to diabetes before his death due to myocardial infarction. You find BP 146/94; P 84, regular; Wt 187 lbs.; Ht 65.5". There is no retinopathy, no bruit; she has decreased sensation to fine touch.
FSBG (fasting serum blood glucose) 238 mg/dL, cholesterol 287 mg/dL, triglycerides 681 mg/dL
After receiving these numbers, you start her on diet, exercise, and an ACE inhibitor for her hypertension. She returns in 3 months with the following values:
FSBG is 189 mg/dL, cholesterol 224 mg/dL, triglycerides 187 mg/dL, weight 182 lbs, and BP 122/78. Her creatinine is 0.7 mg/dL.
At this point, which of the following is the next appropriate treatment?
C) NPH insulin
A new patient is seen in your clinic complaining of palpitations, tremors, heat intolerance, weight loss, hair loss, three bowel movements every day, and fatigue. He has a mild goiter that is nontender, smooth, symmetrical, and without nodules. There is no cervical lymphadenopathy. Feeling confident about diagnosing Graves disease, you prescribe a β-blocker for his symptoms and order TSH, FT4, and a thyroid scan and uptake. He returns in 2 weeks. His symptoms are much improved since taking the β-blocker, but he is still clinically hyperthyroid. The TSH is < 0.01 mU/L (0.5-5.0 mU/L) and FT4 is 2.5 ng/dL (0.7-1.5 ng/dL). The thyroid scan reveals a symmetrical goiter that is homogeneous. The thyroid uptake is 30% (10-35%).
What is most likely to explain his normal uptake?
A) Use of expired radioactive iodine by the nuclear medicine technician
B) Low dietary intake of iodine
C) Hashimoto thyroiditis
D) Presence of multiple hot nodules
E) High dietary intake of iodine
E. High dietary intake of iodine
This question requires you to know what factors influence a radioactive iodine uptake test. A high uptake (> 35%) signifies a greater than usual uptake of radioactive iodine by the thyroid. The most common cause of high uptake in this country is Graves disease. Other causes of a high uptake include iodine deficiency (common in other parts of the world), hot nodules (if hot enough), toxic multinodular goiter (sometimes), high levels of β-HCG (it resembles TSH and can activate TSH receptors when present in very high concentrations such as seen with molar pregnancy, choriocarcinoma, and some cases of germ-cell tumors), and a pituitary tumor secreting TSH.
A low uptake (< 5%) signifies a less-than-usual uptake of radioactive iodine by the thyroid. Causes of a low uptake include Hashimoto thyroiditis (most common), other causes of thyroiditis (e.g., subacute, postpartum, radiation, and amiodarone-induced), thyroid-suppressive drugs (e.g., propylthiouracil, methimazole, and lithium), iodine excess, ectopic thyroid tissue (struma ovarii), lack of a thyroid gland (radioablation or surgical removal), and expired radioactive iodine (extremely unlikely because of several quality assurance steps).
The patient in this question probably has Graves disease because of an elevated FT4 in the face of an undetectable TSH and a symmetrical goiter with homogeneous uptake. The uptake in Graves disease is normally greater than 35%. His thyroid is undoubtedly taking up iodine at a much higher rate than normal. However, the thyroid gland does not discriminate between radioactive iodine and non-radioactive iodine (cold iodine). Some patients take iodine supplements (e.g., kelp pills), and this excess cold iodine competes with the radioactive iodine. Thus, less radioactive iodine is taken up by the thyroid while greater amounts of cold iodine are being taken up. This results in a lower uptake than expected. High intake of iodine can be verified by checking a 24-hour urine for iodine.
The other choices are incorrect. Hyperthyroid Hashimoto thyroiditis (aka hashitoxicosis) can present with hyperthyroidism, symmetrical goiter, and suppressed TSH, but the uptake is low (< 5%). His uptake is too high for thyroiditis. Expired radioactive iodine is extremely unlikely. Low dietary intake of iodine would enhance the uptake, not suppress it. His scan is homogeneous, which argues against hot nodules.
C. Do a cosyntropin stimulation test.
This is a case of secondary hypothyroidism. The teaching point is to recognize that she likely also has secondary adrenal insufficiency and it is important to make the diagnosis and treat adrenal insufficiency before starting thyroid hormone. Starting IV levothyroxine is wrong because you would not give IV T4 to an elderly individual, especially one who might have adrenal insufficiency. Beginning hydrocortisone is wrong because you would not give hydrocortisone until it has been confirmed that the patient actually has adrenal insufficiency.
This question requires you to understand Schmidt syndrome. And this question tests your ability to consider the entire presentation and not to focus on the obvious. Of course she is clinically and biochemically hypothyroid, but don't miss the other possible issue. She has several clues that raise the possibility of adrenal insufficiency: thin body habitus, not gaining weight despite being hypothyroid, low blood pressure, and a hint of hyperkalemic metabolic acidosis. The blood pressure is not unusual for a woman, but hypothyroidism usually raises diastolic blood pressure. The blood pressure alone is not diagnostic of adrenal insufficiency, but it is highly suggestive when taken in context with her other findings. The glucose is also normal, but how many of your patients have a fasting glucose this normal?
The board examination is not likely to give you an obvious case of adrenal insufficiency, so be suspicious whenever you encounter a high-normal potassium with a somewhat low bicarbonate. It is imperative to recognize a possible case of Schmidt syndrome (combination of hypothyroidism and adrenal insufficiency) because the patients die soon after starting thyroid hormone replacement unless they begin glucocorticoid replacement. If you ever have any suspicion that a patient may have adrenal insufficiency, you must begin steroids and work up the patient. The standard test is an ACTH1-24 (cosyntropin) stimulation test. Because dexamethasone is the only available glucocorticoid that does not interfere with the cortisol assay, the patient must be started on dexamethasone until the results of the test are available.
If she truly has adrenal insufficiency, it should be treated with hydrocortisone because it also has some mineralocorticoid activity. Once she takes her first steroid pill, she can begin thyroxine.
B. He has Klinefelter syndrome and should start testosterone, 100 mg IM weekly.
This question tests your knowledge of Klinefelter syndrome and other causes of hypogonadism. He has Klinefelter syndrome, which is characterized by very small and fibrotic testes. The genotype is 47,XXY, and hence a Barr body (condensed chromatin seen in female cells due to an inactive X chromosome) can be seen in these men. They often have gynecomastia and poor social skills. They are not able to produce normal amounts of testosterone. The treatment is testosterone replacement, which is often done with weekly injections. One important point to remember is that the arm span is normal (arm span - height < 5 cm or 2½ inches).
He does not have Kallmann syndrome because such patients have an increased arm span (arm span - height > 5 cm or 2½ inches); testes that are larger than seen in Klinefelter syndrome, although they are still small; a normal genotype (46,XY) and no Barr bodies; usually no gynecomastia; have adequate social skills; and have an impaired sense of smell. Primary hypogonadism due to a postpubertal mumps infection would result in small soft testes, but they will be larger than seen in either Klinefelter or Kallmann syndrome. He clearly has primary hypogonadism and cannot have hypogonadotropic hypogonadism because the gonadotropic hormones LH and FSH are elevated, trying to compensate for the primary defect. He also does not have complete testicular feminization because these 46,XY individuals develop as phenotypical women but without a uterus or full introitus.
B. Begin thyroxine 50 µg per day and check lipids, TSH, FT4, and anti-thyroid antibodies in 2-3 months.
This patient may very well have subclinical hypothyroidism. By definition, the diagnosis is very difficult and easily missed: The FT4 is normal and the TSH may be normal or minimally elevated. This diagnosis is important because of the implications. Positive anti-thyroid antibodies contribute to the diagnosis of subclinical hypothyroidism and increase the risk of transforming into overt hypothyroidism in the future. Patients with subclinical hypothyroidism and a TSH>10 mU/L should be treated regardless of symptoms. For TSH between 5-10 mU/L, patients should be treated if they have symptoms of hypothyroidism. The Rotterdam study clearly showed that women ≥ 55 years of age with subclinical hypothyroidism have a significantly elevated risk of myocardial infarction and aortic atherosclerosis. Nevertheless, a clear benefit from treatment has not yet been published. However, hypothyroidism is well known to cause an elevated LDL, and her LDL is 175 mg/dL. Even though she is not symptomatic for hypothyroidism, her elevated TSH >10 mU/L in conjunction with her elevated LDL are both factors in your decision to treat with thyroxine supplementation.
It is premature to begin statin drug therapy, since treatment of hypothyroidism often reduces LDL levels. Starting a low-dose trial of thyroxine is very appropriate in this case. Since her anti-thyroid antibodies (anti-TPO) are positive, I would continue her thyroxine therapy even if the LDL does not improve. If the LDL remains elevated, you should consider statin therapy. A year-long revisit is too prolonged a follow-up to address both the lipid disorder and subclinical hypothyroidism. And finally, her likelihood of having an ovarian or uterine cancer in this post-menopausal patient without symptoms or an abnormal pelvic exam is very low. Therefore, the indication for a pelvic ultrasound is unnecessary.
E. Begin non-radioactive iodine (Lugol's solution) immediately.
The patient is clearly hyperthyroid based on clinical symptoms and biochemical testing. It is unclear if he has Graves' disease versus a toxic multinodular goiter as a radioactive uptake scan is not available at this time. Iodine preparations such as Lugol's solution and potassium iodide cause immediate inhibition of preformed thyroid hormone secretion. These iodine preparation are not indicated in this situation as should he have a toxic multinodular goiter, the iodine would provide addition substrate for new hormone synthesis, potentially worsening any hyperthyroidism. Should Lugol's solution be given, it is only recommended at least one hour AFTER thionamide (such as PTU) administration.
Elective surgery should ideally be postponed to correct hyperthyroidism in order to prevent the precipitation of thyroid storm. Though his surgery can be postponed for a short period of time to give the thyroid treatments a chance to start working, he needs the surgery soon. Sending him home with a suprapubic catheter until he is euthyroid is not a good option in this case. Therefore, your best strategy is to address his hyperthyroidism in anticipation of immediate surgery. PTU will decrease synthesis of new thyroid hormone, with the goal of decreasing hyperthyroidism in the post-operative period as it takes a few days to start working. A β-blocker will help control his symptoms of hyperthyroidism. A good choice would be a β-blocker that can be given IV and rapidly titrated during surgery, such as esmolol. Because he has A-fib, he must be suspected of having an atrial thrombus; therefore, he should be anticoagulated because he may revert to a normal rhythm once he becomes euthyroid. This can be done with a heparin product before surgery, which can be stopped preoperatively, and with warfarin after surgery.
A. Refer him for a thyroid fine-needle biopsy and aspiration (FNA).
This patient is euthyroid, but with a thyroid nodule. Perform a thyroid FNA yourself, or refer him to someone who can. If the biopsy is not conclusive, then most would repeat it. If the lesion is hot and the patient is euthyroid, they can either be followed or, if the patient is hyperthyroid, radioiodine therapy or surgery can be recommended. A near-total thyroidectomy would be needed only if cancer was present. Many physicians in the past have tried to shrink nodules with thyroxine, thinking that exogenous thyroxine will lower the TSH, which will reduce the growth stimulation to the nodule. Unfortunately, studies have shown this not to be the case; thyroxine should not be given in the hope of shrinking a nodule. Considering how easy and safe a thyroid biopsy is, it would be inappropriate to just follow him. Though the vast majority of nodules are benign, cancer cannot be excluded by simply watching the nodule.
C. Vitamin A intoxication
This question requires you to know that hypercalcemia may be due to vitamin A intoxication. This patient has hypercalcemia and osteopenia, along with chronic ingestion of large doses of vitamins. The lack of an elevated level of 1,25(OH)2-vitamin D rules out an excess of this particular hormone, while an elevated level of 25(OH)-vitamin D indicates that he is ingesting an excess of this particular hormone. However, we are less interested in excess 25(OH)-vitamin D because it has limited activity and presents a problem only when at markedly high levels. His mild elevation of 25(OH)-vitamin D is too little to explain his hypercalcemia. The enzyme that converts 25(OH)-vitamin D into 1,25(OH)2-vitamin D (1α-hydroxylase) is regulated by PTH and will protect a person from developing high levels of 1,25(OH)2-vitamin D.
Another hormone with a well-recognized role in calcium homeostasis is PTH. This patient's PTH level is appropriate in the setting of hypercalcemia. A low PTH would indicate hypoparathyroidism only in the setting of low calcium. Primary hypoparathyroidism is not a cause of hypercalcemia. Because his PTH is low, renal excretion of phosphate is not being stimulated and the level of phosphate is elevated. There is no reason to suspect thiazide diuretics. His blood pressure and volume status are normal, and his potassium is high-normal. There is no reason to attribute his hypercalcemia to thiazide diuretic use. Increased dietary calcium intake rarely causes hypercalcemia and would not explain the patient's osteopenia. The only other choice is vitamin A excess.
Vitamin A excess is an uncommon cause of hypercalcemia, but it can be seen with chronically high ingestion of vitamin A, usually at levels 10-fold greater than the recommended daily allowance. For reasons unknown, high levels of vitamin A cause calcium resorption from bone. Vitamin A excess may also cause muscle and bone pain, hepatic dysfunction, dry skin, nausea, headache, fatigue, ataxia, alopecia, hyperlipidemia, and irritability.
A. IV hydrocortisone
Many patients with rheumatologic disease are treated with courses of steroid medication. This therapy, especially when extended over long periods of time, is a potent suppressant of the adrenal axis. During periods of stress, including infection, surgery or trauma, the adrenal gland is incapable of secreting sufficient quantities of cortisol, and the patient can experience an adrenal crisis. This is manifest with lethargy, nausea and vomiting, and circulatory collapse. If unrecognized and untreated, the patient is at significant risk of death. It is therefore extremely important that any patient who may demonstrate adrenal suppression should routinely be treated with IV corticosteroids during periods of significant stress. This should occur promptly and not be delayed pending results of other studies, such as a drug screen or a CT scan. Although this patient was diagnosed with a UTI, she had already received antibiotics; her WBC count is not elevated; she is afebrile, and the urine is unremarkable for active infection at the time of presentation. Antibiotics may be appropriate, but without steroid supplements, they would not reverse this patient's condition. The same is true for IV fluids. A drug screen may be appropriate in an individual with altered mental status, but by itself would not improve this patient's care. Without focal findings and without history of trauma, a CT scan would also delay the needed steroid supplementation.
A 70-year-old woman presents with complaints of constipation and leg and back pain. She had problems with rectal bleeding 6 months ago and was found to have a polyp on colonoscopy. This was removed, and the site cauterized. At the time of workup, she had a Hct of 27% with an MCV of 78. She was started on FeSO4.
Two months ago, she returned for her annual exam and was found to be in good shape except for complaints of constipation and pruritus. Her cholesterol was 300, and she was started on simvastatin. Today, she has even more problems with constipation than before. Her pruritus continues.
MEDICATIONS: Simvastatin 20 mg qd, FeSO4 325 mg tid, levothyroxine sodium 0.1 mg qd, ranitidine, psyllium 1 TBS qd, felodipine 10 mg qd.
On exam, VS: BP 120/70; P 55; Chest clear; Abd soft, tympanitic; Skin—xerosis present; Rectal—heme-negative; Ext—tenderness over the muscles on palpation.
Which of the following options would best explain her symptoms?
A) Colon cancer
B) Drug interaction between simvastatin and felodipine
C) Interaction between levothyroxine sodium and FeSO4
D) Interaction between ranitidine and simvastatin
E) Rhabdomyolysis due to HMG CoA reductase inhibitor
E. Hypoparathyroidism due to hypomagnesemia
This question requires you to know that the parathyroid cells require magnesium to secrete parathyroid hormone.
Calcium is generally required for exocytosis, so cellular secretion is impaired by low levels of calcium. However, the state of hypocalcemia is the very state when the parathyroid cells need to be most active in secreting parathyroid hormone. Fortunately, the parathyroid cells utilize another divalent cation, magnesium, for exocytosis. However, this causes PTH secretion to decrease with hypomagnesemia.
The normal albumin level eliminates pseudohypocalcemia. Barter syndrome is characterized by hypomagnesemia, hypokalemia, metabolic alkalosis, and hyperreninemic hyperaldosteronism. Pseudohypoparathyroidism refers to a syndrome caused by an abnormal PTH-receptor and presents with low calcium, high phosphorus, and high PTH levels. The patient in this vignette has a low PTH level. Familial hypocalciuric hypocalcemia does not exist. The syndrome being alluded to is familial hypocalciuric hypercalcemia.
A 62-year-old man presents with muscle aches and fatigue. Over the last 1 month he has been having more pain with movement, especially in his thighs and upper arms. He has difficulty getting out of a chair without using his arms. He has never had similar symptoms in the past, and he denies oral ulcers, hair loss, skin rash, swollen, or painful joints.
His past medical history is significant for coronary artery disease with 2 myocardial infarctions and multiple stents placed. He has a history of hypertension, diabetes, and hyperlipidemia His medications include atorvastatin, metoprolol, lisinopril, clopidogrel, metformin, aspirin, and gemfibrozil.
On physical exam, his blood pressure is 120/78; pulse is 65. His exam is significant for muscle tenderness of his thighs and upper arms. He has no rash, joint swelling, or joint pain.
Laboratory testing reveals a creatine kinase (CK) of 750 IU/L (normal is 60-400 IU/L) with a normal creatinine. You diagnose statin-induced myositis, and stop his atorvastatin. His CK normalizes; however, his LDL rises to 190.
What is the next step in management of his hyperlipidemia?
A) Restart atorvastatin, follow CK, and titrate dose.
B) Start a bile-acid sequestrant.
C) Begin ezetimibe.
D) Begin pravastatin, follow CK, and titrate dose.
D. The patient probably does not have any thyroid problems.
This patient is critically sick. In severe illness, the pituitary secretes less TSH, which results in a low or low-normal FT4. However, T4 is not the active hormone; T3 is active. In severe illness, T3 levels are greatly suppressed. With the T4 being lower, there is less T4 available to be converted into T3. However, there is still considerable T4 present. In order to protect the body from the active T3 hormone, the T4 is converted into an inactive hormone called reverse T3 (rT3). Levels of rT3 are rarely measured, but if it was measured in this patient, it would be greatly elevated.
This patient is most likely euthyroid, but also very sick. He does not have hypothyroidism or hyperthyroidism, either primary or secondary. There is no need to act on his abnormal thyroid tests; instead treat his underlying illness.
A. Check serum IGF-1 and 24-hour urine cortisol.
Whenever a pituitary incidentaloma is discovered, two main questions must be answered. One, is the mass inhibiting secretion of any pituitary tumors? Two, is the tumor secreting something? Let's review the inhibiting scenario first. Many pituitary tumors do not appear to secrete anything and are called null cell tumors. With the advent of sensitive assays, it has been learned that some of these null-cell tumors actually do secrete. They may be secreting α-chains or gonadotrophins (LH or FSH), which rarely cause symptoms. After all, what man is going to complain about larger testes or a higher sperm count? However, some of these tumors get large enough that they inhibit secretion of pituitary hormones because of a mass effect. In this patient, the tumor is a microadenoma (< 10 mm) and is too small to inhibit secretion.
The other scenario is one of excess secretion. Does the pituitary tumor secrete any hormones? Remember the main 6 anterior pituitary hormones: ACTH, LH, FSH, GH, TSH, and PRL. A fishing expedition to test all hormones is not recommended. Instead, evaluate the patient for signs or symptoms that may point toward a particular excess such as galactorrhea or loss of libido (PRL); amenorrhea (LH, FSH); weight loss, hyperdefecation, tachyarrhythmia, or heat intolerance (TSH); hypertension, hypokalemia, or alkalosis (ACTH). These findings can be very subtle or even absent in the case of a new tumor or a very small one. If your evaluation does not point toward a particular hormone, then check the adrenal and thyroid axes. A screening test for the adrenal axis is a 24-hour urine for cortisol; a value < 70 μg is normal. The thyroid axis can be checked by a TSH and T4 drawn at any time of the day.
You are cautioned to check one more hormone. A small tumor may be secreting GH. The effects of over-secretion of GH take many years to become evident, and many more years usually transpire before it is recognized. These patients develop acromegaly and its many serious complications. Though GH is pulsatile, its effect on IGF-1 is not. Measure a random IGF-1 in any patient with a pituitary incidentaloma. In this patient, the central obesity and hypertension may indicate hypercortisolism (Cushing syndrome). Order a 24-hour urine for cortisol and don't forget to check the IGF-1 level.
"Refer him to a neurosurgeon for transsphenoidal resection of the pituitary mass" is incorrect because there are no reasons to refer this patient for surgery at this time.
"Return to your clinic in a few weeks to recheck blood pressure" is incorrect because the pituitary tumor must be evaluated and his blood pressure management must be followed.
"Discharge him from your clinic on a drug to treat hypertension and encourage him to stop riding motorcycles" is incorrect because, once again, the pituitary tumor must be evaluated.
"Check an ACTH stimulation test, TSH, and a total testosterone" is incorrect because hyposecretion of ACTH, secondary hypothyroidism, and secondary hypogonadism are not suspected.
A. Reduce her evening NPH insulin and follow closely.
Her symptoms of vivid nightmares and waking in a cold sweat are compatible with nocturnal hypoglycemia. The most likely explanation for the early morning hyperglycemia is that the nocturnal hypoglycemia is causing the contra-insular hormones (glucagon, cortisol, growth hormone, and epinephrine) to be secreted. Many Type 1 diabetics lose the ability to secrete glucagon in response to hypoglycemia, but the remaining hormones are unaffected. These hormones will raise the glucose level. However, insulin-deficient persons such as this patient do not have the ability to make their own insulin to control the hyperglycemic effect of the contra-insular hormones, and her morning fasting glucose levels are elevated. Every patient taking insulin needs to perform self-monitoring of their blood glucose levels. They should check their glucose before and 2 hours after every meal, at bedtime, and in the middle of the night around 3 a.m. Of course it's impractical to constantly check glucose levels this often on a daily basis. One alternative is to have patients check their glucose level twice every day, choosing different times each day so that the log book will have some numbers at each time point. The 3 a.m. glucose level should be checked at least once each month, but doesn't need to be checked much more frequently—unless the patient is having evidence of nocturnal hypoglycemia or has changed the insulin regimen. Once this patient no longer has hypoglycemia, the insulin can always be carefully and slowly increased.
It is inappropriate to begin an anxiolytic rather than decreasing the insulin. Hypoglycemia can be life-threatening. Increasing her evening insulin further could be fatal. There is no evidence that she has insulin resistance in addition to her insulin deficiency, and adding an insulin sensitizer is inappropriate. Switching her to a 70/30 premix is also inappropriate. The goal of treating a Type 1 diabetic is to replace the insulin in a physiologic way. Her insulin regimen is already physiologic by offering basal coverage with NPH twice daily and bolus coverage with a rapid-acting insulin analog with each meal.
B. Start cabergoline and repeat the CT/MRI in a few days.
This patient has a large prolactinoma, and the primary physician wants it to be removed. However, in the absence of visual field defects, seizures, severe headaches, and other findings, the surgery is not emergent and can probably wait a few days. In the meantime, start the patient on cabergoline. This drug may shrink the tumor enough to avoid surgery. Though it usually takes much more than a few days to show an appreciable reduction in size, the prolactinoma may nevertheless begin to shrink within a short period of time. Beginning the preoperative evaluation is justified, but it is more important to begin cabergoline. High-dose glucocorticoids might be justified if the patient presented with neurologic symptoms, but they are not needed in this case.
A. Dexamethasone + fludrocortisone and order an ACTH stimulation test.
The problem list:
Hypotension in a tanned male with sparse hair
Hyponatremia and hyperkalemia
Anion gap = 10
This case is straightforward primary adrenal insufficiency (Addison's), but the question asks you indirectly about methods of diagnosis. The patient is tan because of an elevated ACTH level in response to inadequate cortisol production by the adrenal. The adrenal cortex is abnormal (because of tumor or vascular damage), and aldosterone is also deficient, causing the hyponatremia and hyperkalemia. (In cases where the defect is in the pituitary and ACTH is not formed [secondary adrenal insufficiency], patients are not tanned, and they do not have the sodium and potassium derangements because the adrenal secretes aldosterone perfectly fine.)
Clearly, the option to address only the thyroid gland is wrong. The answer with hydrocortisone instead of dexamethasone and fludrocortisone asks you to 1) differentiate between methods of diagnosis; and 2) include treatment for the comorbid mineralocorticoid deficiency. This question is included specifically to teach you about ACTH-stimulation tests and query whether you understand that primary adrenal disease includes both aldosterone and glucocorticoid deficiencies. Empiric therapy should include dexamethasone if you plan to try to diagnose Addison's with an ACTH-stimulation test, because every steroid except dexamethasone cross-reacts with the assay. The fludrocortisone replaces the missing mineralocorticoids.
Patients who are clearly hypothyroid should never receive thyroid replacement if they are also adrenally insufficient (Schmidt syndrome) until after cortisol has been replaced. If you give thyroid replacement first, patients can die quickly due to an inability to respond to the increased metabolic demand. The clinical scenario in this question, however, gives no indication that the patient has comorbid hypothyroidism.
B. Begin antithyroid medication now and postpone the surgery until he is euthyroid or nearly so.
This question requires you to understand the dangers of hyperthyroidism in a patient going into surgery. This patient has signs of hyperthyroidism, which is verified by laboratory tests. In a patient with hyperthyroidism, any kind of surgery can trigger a severe uncompensated hyperthyroidism (thyroid storm), which can be fatal. Treatment of the hyperthyroidism should be initiated before the surgery takes place. The question of whether to postpone the operation is a little more problematic and depends on whether the surgery is emergent, urgent, or routine. Obviously, if the surgery is an emergency and cannot be postponed, ask the anesthesiologist to administer iodine to inhibit thyroid hormone synthesis (this can be administered as intravenous radiocontrast agents), β-blockers to block the adrenergic effects of hyperthyroidism, and glucocorticoids to protect from the stress of hyperthyroidism and to inhibit the conversion of T4 to T3. If the surgery is routine and can be delayed, as in this case, the patient should be started on antithyroid medications, and the operation should be postponed until the patient is rendered euthyroid or nearly euthyroid. An operation that is urgent, but not emergent, can be postponed for a limited amount of time. During this interval, begin antithyroid medications (PTU or methimazole), iodide, and β-blockers. Though the patient will probably not be euthyroid before surgery, his hyperthyroidism will at least be lessened in severity and may protect him from developing thyroid storm.
A 47-year-old woman comes to your clinic complaining of night sweats and marked mood swings. She says that she is experiencing the same unbearable symptoms of menopause that her mother experienced and she wants relief. She routinely exercises, and she has already tried the diet changes recommended in the lay press. She had a hysterectomy 20 years ago due to a complication of childbirth. There is no family history of breast cancer or thromboembolic disease. You agree with her that she is most likely experiencing marked symptoms of menopause. She asks about hormone replacement therapy because her mother got relief from it. You review the recent evidence against it and discuss other options with her, but she insists on trying hormones. You give her some literature, refer her for a mammogram, ask the lab to measure FSH, and schedule a follow-up appointment. The mammogram is negative, and the FSH confirms menopause. She still wants to try hormone therapy, so you start her on low-dose estrogen.
She comes back in three months and reports feeling much better and thanks you for the estrogen. You remind her that hormone therapy can increase her risk of death, but she still wants the hormone therapy. It has been almost five years since you last checked her lipids, so you ask her to return in 3-4 months for fasting lipids. The HDL and non-HDL cholesterol are acceptable, but the triglycerides have markedly increased from 107 mg/dL to 820 mg/dL.
Which of the following should be done at this time?
A) Stop treating her symptoms despite her preferences.
B) Hold the estrogen and resume once the triglycerides are normal again.
C) Continue the estrogen and recheck lipids in 6-12 months.
D) Switch from oral estrogen to a transdermal patch.
E) Switch from estrogen to black cohosh from her local health food store
A 16-year-old high school student is referred for evaluation of amenorrhea. She is an "A" student and has been active in school activities. She denies any other health problems.
Vital signs: BP 140/80, P 60, RR 18, Temp 98.7° F
Height: 4' 4"; weight 130 lbs
HEENT: Wears glasses; otherwise normal
Neck: Possible short neck
Heart: RRR with II-III/VI systolic murmur
Breast: Tanner Stage I-II; widely spaced nipples
Abdomen: +BS, soft, no hepatosplenomegaly
Extremities: Short legs noted
GU: Normal pubic hair distribution
Based on your findings, what do you expect her LH, FSH levels to be?
A) Her LH will be low, FSH high.
B) It depends on what time of day you draw the levels.
C) Her LH will be high, FSH low.
D) Her LH will be high, FSH high.
E) Her LH will be low, FSH low.
D. Her LH will be high, FSH high.
She has Turner syndrome: short stature, broad chest with widely spaced nipples, short neck (I didn't use the keyword "webbed," but that would have made it really easy), short legs, little breast development, and normal pubic hair. The gonadotropins, LH and FSH, are usually elevated continuously. Her murmur is likely aortic stenosis, and the hypertension she has is common.
B. Fasting plasma glucose
There have been numerous recommendations published on screening for diabetes. There are currently 3 validated tests: hemoglobin A1c, fasting plasma glucose, and an oral glucose tolerance test. Hemoglobin A1c testing is now widely used in screening for diabetes. However, hemoglobin A1c testing is not valid in patients with abnormal red cell turnover, such as those with hemolytic anemia, pregnancy, blood loss/transfusions, or use of erythropoietin. Since this patient is on erythropoietin, recommended screening would use either a fasting plasma glucose or an oral glucose tolerance test. This patient underwent screening by her nephrologist with equivocal results. The current recommendation for screening and diagnosis of diabetes would be to repeat the test that indicates a diagnosis of diabetes. Since her 2-hour oral glucose tolerance test was negative, it would not be recommended to repeat this time to screen for diabetes.
For this patient, the fasting plasma glucose was > 126 mg/dL, indicating possible diabetes. If the FPG remains > 126 mg/dL on repeat testing, the diagnosis of diabetes would be confirmed. Serum fructosamine has been used as a test to monitor long-term glycemic control in patients in whom an A1c measurement would be invalid, but is not validated as a screening method to diagnose diabetes
B. Vitamin D deficiency
This lady has probably had hypocalcemia for quite some time and came to medical attention only because she experienced an osteoporotic hip fracture. An extremely common cause of hypocalcemia is vitamin D deficiency, and she exhibits a classic presentation. Her 25-OH-vitamin D level is low, reflecting both her poor diet and her low exposure to sunlight due to her reluctance to leave the house. Hypocalcemia normally gives rise to an elevated parathyroid hormone level (secondary hyperparathyroidism) and this in turn stimulates the conversion of 25-OH-vitamin D to 1,25-(OH)2-vitamin D. Unfortunately, her levels of 25-OH-vitamin D are already low, and her conversion to 1,25-(OH)2-vitamin D is thus impaired. The phosphate level is low because of the hyperparathyroidism, which stimulates renal excretion of phosphates.
While hypomagnesemia can cause hypocalcemia due to impaired secretion of parathyroid hormone, her hypermagnesemia is not contributing. Hyperphosphatemia may cause hypocalcemia because of local precipitation of calcium-phosphate salts. Her hypophosphatemia is not the cause of the hypocalcemia. Thiazide diuretics are associated with hypercalcemia, not hypocalcemia. Primary hyperparathyroidism causes hypercalcemia, not hypocalcemia.
You are asked to see a 68-year-old woman who became dizzy and fell last week. She reports becoming shaky, sweaty, and slumping to the floor while shopping at about 11:30 a.m. She recovered after lying on the floor for several minutes and eating candy. She takes calcium and multivitamins. Past medical history includes a Billroth II for ulcers in 1962, C-section, and penicillin allergy. She had met a friend for breakfast at a donut shop that morning. Her usual breakfast consists of a boiled egg, brown toast and butter, and fruit. She generally eats a late-morning snack, and a meat-containing salad and hard roll for lunch at 1 p.m. She occasionally has similar, milder episodes, but in the past 10 years has had very few such episodes. She runs 3 miles three times weekly, does yoga daily, and works out with free weights twice weekly. She has no cardiac history, and her parents are still alive in their late 80s, as are their siblings. Physical exam reveals BP 116/78 and P 68. Musculature in upper arms and calves is well developed and delineated. Other than well-healed surgical scars on the abdomen, the exam is physiologic.
The above is a prelude to asking you to identify "Whipple's triad."
Which of the following comprise Whipple's triad?
A) Symptoms of hypoglycemia, pancreatic lesion, and low serum glucose
B) High serum glucose, symptom relief with insulin, and symptoms of hyperglycemia
C) Symptoms of hypoglycemia, pancreatic lesion, and high serum glucose
D) Symptoms of hypoglycemia, low serum glucose, and symptom relief with glucose
E) Low serum glucose, abdominal pathology, and symptom relief with glucose
A 49-year-old man presents for a follow-up exam. He was diagnosed with Type 2 diabetes 10 years ago. Current therapy includes metformin 500 mg bid and glyburide 5 mg bid. He is also treated for hypertension with hydrochlorothiazide 25 mg/day. He does not test blood glucose at home. He feels well. BMI = 44; BP is 145/90; he has no edema. Funduscopic exam is unremarkable.
Serum creatinine 0.8 mg/dL (0.5-1.4 mg/dL)
Hemoglobin A1c 8.8% (4-6%)
Fasting plasma triglycerides 1,077 (< 150 mg/dL)
Urine microalbumin-creatinine ratio 131 (0-30 mcg/mg)
Which of the following is the best set of adjustments for his therapeutic regimen?
A) Begin enalapril, begin fenofibrate, and begin insulin glargine.
B) Increase glyburide to 10 mg bid, begin lisinopril, and begin pravastatin.
C) Begin 70/30 insulin bid, stop metformin, and increase HCTZ to 50 mg/day.
D) Stop glyburide, begin 70/30 insulin bid, begin amlodipine 5 mg/day.
E) Increase metformin to 1,000 mg bid, increase glyburide to 10 mg bid, and begin gemfibrozil.
A. Begin enalapril, begin fenofibrate, and begin insulin glargine.
Key points: The patient requires better control of hyperglycemia, initiation of an ACE inhibitor for control of hypertension associated with microalbuminuria, and initiation of therapy for severe hypertriglyceridemia. The latter poses a danger of causing acute pancreatitis. Increasing metformin to 100 mg bid is appropriate but will not make a major impact on HbA1c. The maximal effective dose of glyburide is 10 mg per day. Either gemfibrozil, fenofibrate, or niacin would be appropriate therapy for hypertriglyceridemia. Until the triglycerides are lowered to < 400 mg/dL, LDL cannot be calculated, and thus, the need for a statin is unclear. Although a third oral agent, such as a TZD or a GLP-1 agent, could be added to metformin and glyburide, the addition of nightly basal insulin, such as detemir, glargine, or NPH, is more likely to lower HbA1c to < 7.5%.
E. Thyroid scan and uptake
You need to know thyroid function, not just its anatomy. The absence of symptoms due to mass effect from the thyroid—e.g., no recurrent laryngeal nerve impingement (i.e., no voice change, weakness, or "gravelly" sound), and no dysphagia or dyspnea—excludes the need for anatomic studies: MRI, CT, ultrasound, and scan. By obtaining a thyroid scan and uptake (which reveal the gland's functional ability to concentrate 131I), you will find diminished uptake except in the left lower pole of the thyroid where there is a "hot" nodule.
A 62-year-old woman comes to clinic with diarrhea for 3 weeks. The patient began having nonbloody diarrhea three weeks ago. She has 4-5 soft bowel movements per day. She has no abdominal pain, nausea, or vomiting. Over the same time, she has developed fatigue and has become anxious about work and her family. On review of systems, she complains of palpitations.
She has a past medical history of hypertension and hyperlipidemia and coronary artery disease. Medications include aspirin, simvastatin, hydrochlorothiazide, and lisinopril.
On physical exam her heart rate is 110; blood pressure is 148/89, and she is anxious appearing. Her heart exam shows tachycardia, and no murmurs, rubs, or gallops. Her lung and abdominal exam is unremarkable. She has a resting tremor, and her reflexes are brisk.
Blood testing shows an undetectably low TSH and elevated T 4 and T 3 .
What is the next step in the management of this patient?
A) Order a radioactive iodine uptake scan.
B) Order a thyroid-stimulating antibody panel.
C) Refer to endocrinology.
D) Begin propranolol.
A 47-year-old febrile, diabetic man presents to the emergency department after being found down by his wife. Initial evaluation reveals a left lower lobe pneumonia.
Admission labs: Na 128, K 3.2, Cl 98, HCO3 7, Glu 700
He is given 2 L of 0.9% NaCl, a bolus of insulin, and started on a continuous insulin infusion.
Repeat labs: Na 136, K 3.0, Cl 105, HCO3 19, Glu 375
Which of the following is the most appropriate next step with regard to insulin and IVFs?
A) Change to 5% dextrose with 0.45% NaCl and continue the insulin infusion at the current rate.
B) Continue the current IVF and double the insulin infusion rate.
C) Continue the current management.
D) Give 10 U regular insulin, stop the IVF and the insulin infusion, and allow the patient to eat.
E) Give 10 U regular insulin, stop the IVF, continue the insulin infusion for 2 hours at the current rate, then stop.
C. Continue the current management.
The initial laboratories reveal hyperosmolar hyponatremia with an elevated anion gap. The sodium corrects into normal range when considering the hyperglycemia.
To correct sodium for hyperglycemia, increase the sodium by 1.6 for each 100 increment in glucose over 100:
Measured glucose - Normal glucose = 700 - 100 = 600, or 6 increments over 100.
6 x 1.6 = 9.6. To correct the sodium, add 9.6 to the measured sodium (128) = 137.6 = Normal.
Anion gap = 128 - 98 - 7 = 23. (Although controversial, consensus is to use the measured serum sodium concentration when calculating the anion gap.)
The repeat labs show correction of the anion gap, but the patient remains hyperglycemic. New anion gap = 136 - 105 - 19 = 12. Therefore, the acidosis has resolved, but hyperglycemia is still present.
The question next queries if you know when to change the IVF to a dextrose-containing fluid. The patient's blood glucose is 375, and recommendations state that the fluids should be supplemented with dextrose when the serum glucose concentration is < 200 mg/dL. Therefore, none of the answers that suggest changing the fluids or stopping the fluids is correct. Because the patient's high anion gap has resolved and the glucose has lowered by > 70 mg/dL, the rate of insulin infusion is adequate, and increasing the insulin rate is unnecessary. Current management should be continued until the blood glucose is < 200 mg/dL, at which time dextrose-containing fluids should be substituted, and the insulin infusion should be titrated to a blood glucose of 100-200 mg/dL. Once the glucose is 100-200 mg/dL, and the anion gap remains in the normal range, the IV insulin is continued until the patient is able to eat. At that time, give a subcutaneous injection of regular insulin, continue the infusion for 1-2 hours after the injection, and allow the patient to eat. Titrate the regular insulin to the blood sugar and initiate long-acting insulin when the insulin infusion is discontinued.
A 37-year-old man is referred to you for cholesterol of 256 mg/dL. He states he has decreased intake of meat, fried foods, and dairy other than low- or no-fat products, and has trouble jogging due to leg cramps. Despite diet change, his weight increased 5 pounds in the past 3 months. Pulse is 66 and BP is 146/88. His thyroid is difficult to feel in his large neck. His hair is not shiny, his skin is dry, and there are no bruits, xanthomas, or xanthelasma.
He returns in 2 weeks, training for a half triathlon, with his LDL 196 and triglycerides 123; total cholesterol is 252 and HDL 21.
Which of the following pharmacologic treatments is best to begin at this time?
A) Nothing; wait longer for diet to take effect
D) Bile acid resins
D. Check TSH.
This patient has signs and symptoms of hypothyroidism. The next test that should be ordered is a TSH level, which is expected to be markedly increased. The obvious evidence for hypothyroidism includes feeling tired, moving slowly, talking slowly, and dry skin. But don't overlook the galactorrhea, pituitary mass, and mildly elevated prolactin level. At first glance, this can be mistaken for a prolactinoma, but a prolactinoma of this size (macroadenoma) should be associated with prolactin levels > 200 ng/mL. A prolactin level < 100 ng/mL should always prompt you to look elsewhere―in this case, the thyroid. Some other causes of a mildly elevated prolactin that have been ruled out include pregnancy and excessive nipple stimulation. The pituitary mass in this patient is most likely not a tumor. It is a pseudotumor composed of TSH-secreting cells (thyrotrophs), which have hypertrophied in response to TRH stimulation. TRH also stimulates the secretion of prolactin; hence the elevated levels.
"Start bromocriptine" and "refer her to a neurosurgeon" are incorrect because it is important to rule out a thyrotroph pseudotumor first prior to any therapeutic intervention. It would be inappropriate to treat with bromocriptine or surgery. "Look for an unknown non-pituitary cancer" is incorrect because the described clinical scenario does not suggest any reason to look for a non-pituitary cancer. "Recheck the prolactin in 6-12 months" is incorrect because, although rechecking the prolactin level would be appropriate at some time in the future, her hypothyroidism must be addressed first.
E. Add an ACE inhibitor or an angiotensin-receptor blocker (ARB).
The random urine screen indicates microalbuminuria. Normal albumin excretion is < 30 mg/day, microalbuminuria is 30-300 mg/day, and macroalbuminuria is > 300 mg/day. Collecting an accurate 24-hour urine is difficult and problematic. Fortunately, creatinine excretion is somewhat consistent when adjusted for standard body surface area. This has led to use of the albumin:creatinine ratio in a random spot urine as a surrogate marker. A normal ratio is < 30 μg/mg, microalbuminuria is 30-300 μg/mg, and macroalbuminuria is > 300 μg/mg. If the ratio is only slightly above normal, it is best to repeat the random urine or to ask for a 24-hour urine to better quantitate the albumin excretion. In addition, any urinary tract infection must be completely resolved before checking for albuminuria. His ratio is well within the range of microalbuminuria, and there is no suspicion of a urinary tract infection. Once a diabetic has microalbuminuria, the patient must be treated. The goal of treatment is to slow the progression of the nephropathy in an attempt to prevent end-stage renal disease. Several studies have shown that an ACE inhibitor is an excellent drug for this purpose, and some recent studies have shown that ARBs may be just as beneficial. The best course of action for this patient is to begin one of these drugs.
The patient is certainly doing a good job by watching his diet, consistently walking, and losing weight. He should be praised for this, but he also needs treatment for the nephropathy. There is no reason to increase his statin, since the LDL is less than 100 mg/dL (goal). A calcium-channel blocker may be useful for hypertension, but is not the initial drug of choice in diabetics with nephropathy. Likewise, a diuretic can be useful for blood pressure control, but is not the i nitial drug of choice in a diabetic with nephropathy
A. Switch him to cabergoline.
The question states that the patient has a prolactinoma and is being treated with bromocriptine. Unfortunately, he is experiencing considerable nausea and vomiting, which are common side effects of bromocriptine; many patients are unable to tolerate it. An alternative drug, cabergoline, is available. This drug is just as effective at reducing prolactin levels and is much less likely to cause nausea and vomiting. Unfortunately, cabergoline is expensive. In some centers, bromocriptine is the initial drug of choice because it is cost-effective. However, cabergoline has become the drug of choice in many centers because it has fewer side effects and is much better tolerated.
It would be inappropriate to just stop the bromocriptine without starting the cabergoline, because without a brief period of overlap, the patient would most likely experience a flare-up in his symptoms. Resection of a prolactinoma should be done only when the mass effect of a large tumor warrants it, such as seizures or an impaired field of vision. Adding prochlorperazine for nausea is not appropriate, because he hasn't tried a course of cabergoline. Finally, the addition of cabergoline to bromocriptine should not be done. These two drugs work by the same mechanism, and using them together would not lessen the severity of the nausea and vomiting and would increase any potential side effects.
7th EditionGary A. Thibodeau, Kevin T. Patton
7th EditionJulie S Snyder, Mariann M Harding
7th EditionJulie S Snyder, Linda Lilley, Shelly Collins
2nd EditionMcGraw-Hill Education