Endocrinology Flashcards

0
Q

What is the typical strategy for thyroid hormone replacement and hypothyroidism?

A

“Two strategies may be used (1) start with 25 μg daily and titrate up every 1–2 months until the TSH is in the normal range or (2) start with full-dose therapy based on weight (1.6 μg/kg daily) and adjust based on TSH in 1–2 months. Either option is appropriate in young, otherwise healthy adults. But older patients (>65 years old) or those with multiple comorbidities should be started at a low dose (25 μg daily). If the patient is titrated up to 200 μg of levothyroxine and does not seem to be responding, the diagnosis needs to be reconsidered or the patient’s compliance needs to be carefully assessed. Iron and food will decrease the absorption of levothyroxine by as much as 40%. It usually takes 6–8 weeks for the body’s endocrine response and TSH to reach a steady state”

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1
Q

Name three symptoms of hypothyroidism.

A

“The history given is consistent with a hypothyroid state. Symptoms of hypothyroidism include thinning hair, dry skin, a hoarse, deep voice, bradycardia, and a prolonged relaxation in the reflexes.”

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2
Q

What is Graves’ disease?

A

“The family history, the symptoms and signs of hyperthyroidism (especially the diffusely enlarged goiter with a bruit), and the exophthalmos are all typical. Conjunctival injection is also frequently noted”

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3
Q

What is viral hyperthyroidism and how is it treated?

A

“Viral thyroiditis can cause hyperthyroidism and a goiter, but the thyroid gland is usually tender. Also, viral thyroiditis will likely not last 4 months, but is usually self-limited to <6 weeks”

“75% of patients with viral thyroiditis will progress from 2 weeks of self-limited hyperthyroidism to 3–6 months of hypothyroidism that is also self-limited. The hyperthyroid phase is best treated with NSAIDs, beta-blockers, and prednisone if needed.”

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4
Q

What should be the immediate management of hyperthyroidism?

A

“There is no need to wait before starting methimazole (Tapazole), which blocks production of thyroid hormone. PTU can also be used but methimazole is preferred because (1) it affords better control and (2) PTU is associated with more liver toxicity and bone marrow suppression (although these adverse effects can occur with both drugs). PTU is still preferred during pregnancy. Propranolol is helpful for controlling the symptoms of hyperthyroidism (tachycardia, tremor, etc) and prevents the conversion of T4 to active T3”

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5
Q

What is a thyroid storm?

A

“The syndrome of thyroid storm is characterized by fever, tachyarrhythmias, altered mental status, and high output cardiac failure. It is induced by a major stress (infection, surgery, myocardial infarction, etc.) in a patient with underlying hyperthyroidism (usually undiagnosed).”

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6
Q

Name three signs of thyroid storm.

A
A) Hyperthermia.
B) Right upper quadrant pain.
C) Diffuse muscle weakness.
D) Atrial fibrillation.
E) Hypomania, confusion, other central nervous system (CNS) signs and symptoms.

right upper quadrant pain, is from liver congestion secondary to high output congestive heart failure (CHF) and is a bad sign”

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7
Q

What is the appropriate treatment for thyroid storm?

A

“extremis (hypotensive and tachycardic) and needs fluid hydration, despite pulmonary edema. Cooling measures address hyperthermia, and beta-blockade (propranolol) will improve high output failure (and reduce the pulmonary edema). Corticosteroids help block release of thyroid hormone and decreases peripheral conversion of T4 to T3. Additionally, corticosteroids will treat any underlying adrenal insufficiency. Methimazole prevents thyroxine synthesis. This must be given before iodine. The iodine blocks any further release of thyroid hormone”

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8
Q

Where is the likely diagnosis for a patient that has all the signs and symptoms of hyperthyroidism but a low TSH and normal T4?

A

“Five percent of patients with hyperthyroidism have an isolated T3 hyperthyroidism. Thus, if you suspect hyperthyroidism and the patient has a low TSH but a normal free T4, check a T3-RIA”

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9
Q

Name a medication that can cause hyperthyroidism.

A

“Amiodarone (see Helpful Tip) and Peginterferon Alfa-2a can cause hyperthyroidism.

Amiodarone is interesting because it can cause hyperthyroidism or hypothyroidism. It has multiple effects on the thyroid gland and on metabolism of T4 and T3, which can result in hypothyroidism. It carries a huge iodine load, which can result in hyperthyroidism. Somewhere between 2% and 30% of patients taking amiodarone will have thyroid dysfunction. Amiodarone is highly lipophilic and may have a half-life as long as 100 days, resulting in toxicity long after the drug is stopped”

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10
Q

How do you make a definitive diagnosis of a thyroid nodule?

A

“FNA can conclusively prove or disprove the presence of neoplasm and should be considered for all thyroid nodules and cysts”

“A “hot” nodule may cause hyperthyroidism, is usually nonmalignant (“hotis not”) and can be treated with I131. A cold nodule is either an adenoma or a malignancy and a biopsy is mandated”

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11
Q

What is the appropriate treatment for the thyroid adenoma as identified by a biopsy?

A

“Surgery for removal of the tumor is the most appropriate next step, but a CT scan is indicated to delineate the extent of the neoplasm.”

“Radiotherapy with I131 is used after surgery for metastatic disease, but external beam radiation is not used for thyroid cancers except for the palliative therapy of anaplastic carcinoma. Because these tumors are TSH responsive, suppression of TSH level following surgery for papillary carcinoma is achieved with thyroxine (usually 2.2–2.5 μg/kg—fairly high dose to completely suppress TSH production)”

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12
Q

The patient comes in a seemingly manic and a breast masses found physical examination. What kind of changes might be expected on EKG?

A

“This patient is likely to have hypercalcemia, probably from an undiagnosed metastatic breast cancer. The ECG in a patient with significant hypercalcemia will show a short QT interval; rarely there is diffuse ST elevation. Hypocalcemia is associated with a long QT interval, which can occasionally lead to arrhythmias due to an R on T phenomenon (an R-wave of a PVC fuses with the previous T-wave predisposing to torsades de pointes). Hypercalcemia produces symptoms in the CNS (confusion, psychosis, depression), GI system (abdominal pain, cramps, constipation), kidneys (nephrolithiasis, polyuria, renal insufficiency), and musculoskeletal system (weakness, myopathy, osteoporosis). To help you remember the symptoms of hypercalcemia, use the phrase “stones, bones, moans, groans, and psychiatric overtones”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

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13
Q

What is the emergent treatment for hypercalcemia?

A

Saline IV, adequate hydration and establishing urine output is critical to the treatment of hypercalcemia and should be the next step. A normal saline infusion will increase urinary calcium excretion by inhibiting proximal tubular sodium and calcium reab-sorption. Note that IV furosemide (and diuretics in general) are falling out of favor and should not be used. Hydration is the most important goal. An IV bisphosphonate infusion should then be started and will lower the calcium level over 2–4 days. Calcitonin has a limited duration of action and can be used in emergencies where saline is ineffective”

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14
Q

How can a chronically elevated hypercalcemia be treated when it’s from metastatic disease?

A

“Glucocorticoids decrease intestinal calcium absorption, but in and of themselves can lead to bone density loss and an increased risk for fractures. Oral phosphates can decrease intestinal calcium absorption and bone reabsorption of calcium. Bisphosphonates, as previously discussed, decrease the serum calcium and increase bone density”

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15
Q

Elevated parathyroid hormone in the presence of hypercalcemia is indicative of which disease?

A

“This patient has primary hyperparathyroidism. He has an elevated parathyroid hormone in the presence of hypercalcemia. This is usually caused by a functional parathyroid adenoma and is best treated in otherwise healthy patients with a parathyroidectomy. This can be done without significant loss of thyroid tissue. In elderly patients with mild hyperparathyroidism and asymptomatic hypercalcemia, medical management is an option. If the patient had a low or normal PTH level, occult cancer should be considered (check for PTH-like hormone in the serum), and a bone scan or body CT may be warranted”

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16
Q

A rare complication of removal of too much parathyroid gland may result in which disease that results in increased muscle spasms and fatigue?

A

“This patient likely has hypocalcemia due to excessive removal of parathyroid gland tissue. This is a rare, but unfortunate, complication of parathyroid gland removal and is usually detected in the immediate postoperative course. The patient’s physical exam demonstrates Chvostek sign (tapping over the facial nerve elicits a twitch) and Trousseau signs (carpopedal spasm after placement of a blood pressure cuff). Vitamin D deficiency, although a cause of hypocalcemia, is unlikely to develop so quickly”

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17
Q

Do you have to correct for hypoalbuminemia when determining serum calcium level?

A

Yes. “To correct for albumin, add 0.8 mg/dL to the serum calcium level for each 1 g/dL the albumin is <4g/dL. In other words, corrected serum calcium = [(4-albumin) × 0.8] + measured serum calcium, or in this case the equation is [(4–3) × 0.8] + 5.1 = 5.9 mg/dL”

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18
Q

When a patient is given exogenous steroids during the dexamethasone suppression test in there is little to no effect, what does this indicate?

A

“When the patient was given exogenous steroids during the test, there was a partial suppression of cortisol production (mild decrease in 24-hour urinary free cortisol). But more importantly, the serum ACTH level remained normal despite the high steroid load. It should have been low in the presence of dexamethasone, or any exogenous steroid, which would act to shut off ACTH production in the normal patient.
Normal mechanisms provide negative feedback on the pituitary gland (the source of ACTH) when cortisol levels are high. If ACTH is still being produced despite a high steroid load, then there must be an ACTH-producing neoplasm somewhere in the body (either ectopic production from a lung, renal, or pancreatic cancer, or an ACTH-producing pituitary tumor that has escaped normal regulatory feedback mechanisms”

19
Q

Name 3 characteristic signs or symptoms of adrenal insufficiency.

A

“First, the hyperpigmentation found at stress/crease points on the peripheral skin suggests the diagnosis of adrenal insufficiency. The low blood pressure and orthostasis is also more likely to be seen in adrenal insufficiency” fatigue.

20
Q

How does one verify the cause of adrenal insufficiency as a mineralocorticoid deficiency?

A

“The laboratory chemistry results (hyperkalemia, hyponatremia, and hypoglycemia), combined with the history and physical exam, strongly suggest a mineralocorticoid deficiency. A cosyntropin stimulation test uses synthetic ACTH to try to induce a burst of cortisol secretion. No increase in the serum cortisol in response to the cosyntropin suggests that the adrenal glands are unable to respond to the body’s mineralocorticoid and glucocorticoid needs. A positive cosyntropin test makes the diagnosis of adrenal insufficiency. A random serum cortisol is definitely second best, as cortisol levels normally fluctuate widely throughout the diurnal cycle”

21
Q

Why would hyper pigmentation of skin creases indicate primary adrenal insufficiency?

A

“Hyperpigmentation at skin creases occurs in primary adrenal insufficiency (but not secondary adrenal insufficiency). This is because in primary adrenal insufficiency, the pituitary is intact. As a result, the ACTH level is high, as is the level of melanocyte-stimulating hormone. It is this melanocyte-stimulating hormone that causes hyperpigmentation”

22
Q

How does all Doster own figure in distinguishing between primary and secondary adrenal insufficiency?

A

“Patients with primary adrenal insufficiency may present with low serum sodium and high serum potassium (although many will have normal electrolytes). This is primarily because of loss of the aldosterone system. Patients with secondary adrenal insufficiency (e.g., pituitary cause) have intact adrenal glands and therefore intact aldosterone. Thus, they will generally have normal electrolytes and less dehydration, hypotension, etc.”

23
Q

How do you treat primary adrenal insufficiency?

A

“Corticosteroids (prednisone 5 mg or hydrocortisone 15 mg) daily plus mineralocorticoid (fludrocortisone 0.1 mg) daily indefinitely”

“chronic corticosteroid supplementation, and mineralocorticoid supplementation”

24
Q

What is addisonian crisis and how is it treated?

A

“This patient has adrenal insufficiency and requires additional “stress doses” of steroids in times of severe physical stress (e.g., infection, trauma, and chest pain). The steroids he regularly takes for his disease may not be sufficient during these periods, precipitating Addisonian crisis. Without this additional treatment, the patient may experience intractable hypotension and possibly death.
If you suspect adrenal insufficiency crisis, start steroids immediately even if you do not have laboratory confirmation. Dexamethasone is an option for treatment, and it will not interfere with the cortisol assay when doing a cosyntropin stimulation test”

25
Q

What is adult onset type one diabetes?

A

“adult onset type 1 diabetes do not have insulin resistance. Adult onset type 1 diabetes (also known as latent autoimmune diabetes in adults or slowly progressing type 1) is a relatively new concept. Patients with adult onset type 1 diabetes develop diabetes as an adult, which is similar to those with DM2. However, they are generally thin, not hypertensive and do not have the rest of the constellation of disease in DM2 (low HDL, high triglycerides). Generally, they need insulin relatively early in the course of their treatment, although they will initially respond to oral hypoglycemic agents”

26
Q

What is the definition of prediabetes?

A

“The American Diabetes Association (ADA) suggests that a blood sugar of 100 mg/dL is now “prediabetes” and represents “impaired fasting glucose.” The authors think calling a normal blood sugar prediabetes is absurd. So does the European Diabetes Epidemiology Group that advocates using the original 110 mg/dL as impaired fasting glucose”

27
Q

What is the treatment for diabetic ketoacidosis with greater than 10% volume depletion?

A

“0.9% (normal) saline with 20 mEq potassium/L to run at 1000 cc/hr.”
“Initial volume replacement should be with isotonic saline infused at a rapid rate (in the absence of cardiac disease) until the volume deficit is replaced. In general, potassium should be added to the second liter of fluid unless the patient is already hypokalemic on the first blood gas (getting a potassium, glucose, and sodium on the first blood gas is good policy). Potassium replacement is essential even in the hyperkalemic patient, as correction of the ketoacidosis leads to a rapid shift of potassium into the intracellular compartment. Remember that an acidosis artificially increases the serum potassium by shifting potassium extracellularly. The potassium increases by approximately 1 mEq/L for every pH point of 0.1 below 7.4 (so, a pH of 7.3 will increase the potassium from 4 to 5 mEq/L).”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

Check out this book on the iBooks Store: https://itun.es/us/vRMUI.l

28
Q

What is the insulin regimen in a patient with diabetic keto acidosis?

A

“A bolus of IV regular insulin, followed by a constant infusion, adjusted to reduce the blood glucose level by 50–75 mg/dL/hr, is the appropriate therapy. This may frequently require <0.1 U/kg/hr, but 0.05–0.1 U/kg/hr is a good place to start. Intramuscular insulin administration is an alternative, but absorption is unreliable, especially in hypotensive patients. Long-acting insulins and subcutaneous insulin administration have no place in the initial management of DKA”

29
Q

How do you treat a patient in Medford diabetic ketoacidosis who’s sugar has normalized after treatment but they have continued acidosis?

A

“This patient is still acidotic and will need continued insulin to reverse his catabolic state. Thus, the appropriate treatment is to increase the amount of sugar he is getting. Remember, DKA is not primarily a result of too much sugar but rather of too little insulin.
Bicarbonate plays no role in the treatment of DKA no matter what the pH. In fact, the administration of bicarbonate actually prolongs acidosis and ketosis and produces a paradoxical CNS acidosis. Additionally, it shifts the oxygen disassociation curve to reduce oxygen delivery to the tissue. Finally, the only predictor of cerebral edema in children treated for DKA is the administration of bicarbonate”

30
Q

Dietary indiscretion usually causes diabetic ketoacidosis. True or false?

A

“False. Dietary indiscretion does not generally precipitate DKA. DKA is actually a state caused by a lack of insulin rather than by increased intake of carbohydrates. Certainly dietary indiscretion will complicate glucose control, but it will not precipitate DKA. All of the other options can cause DKA”

31
Q

What is the Somogyi effect?

A

“Consensus is that the Somogyi phenomenon does not exist regardless of what we were taught (N Engl J Med 1987;317(25):1552). If you see it on the test though, it was thought to occur when a patient becomes hypoglycemic (often in the middle of the night) and there is a reactive hyperglycemia from adrenergic outpouring”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

Check out this book on the iBooks Store: https://itun.es/us/vRMUI.l

32
Q

Poorly controlled diabetic patient has postprandial fullness and occasional vomiting. A study shows delayed emptying. What is the diagnosis and treatment?

A

Diagnosis is diabetic gastroparesis. “Both metoclopramide and erythromycin will speed gastric emptying. A third drug, cisapride, is available on compassionate use protocol. It was removed from the general market secondary to prolonged QT and subsequent torsades de pointes. It is clear that diabetic gastropathy is at least somewhat reversible with good glucose control. The higher the sugar, the worse the stomach empties”

33
Q

Why should Met Forman not be given with renal disease patients?

A

“Patients with renal disease are at a higher risk of lactic acidosis, the most severe complication of metformin therapy, although it is exceedingly rare (0 patients of 75,000 in one study). Patients with pulmonary or neoplastic diseases may take metformin unless they also have severe hepatic or renal failure. Postmyocardial infarction patients may use metformin as long as they do not have CHF, but metformin should be held for 48 hours after contrast studies”

34
Q

Name 2 risk factors for amputation with a patient with diabetes.

A

“The risk of ulcers or amputations is increased in patients who have had diabetes for 10 years or more, are male, have a history of poor glucose control, or have evidence of microvascular complications of diabetes. Bony deformities, loss of protective sensation, and severely dystrophic toe-nails are also risk factors for amputation. An elevated CRP in and of itself is not a known risk factor for amputation, but CRP may be elevated if there is lower extremity infection present”

35
Q

Which drug use to manage diabetes type two is contraindicated with congestive heart failure?

A

“The “glitazones” (thiazolidinediones) tend to cause edema as one of their major side effects. Thus, they are contraindicated in patients with a history of heart failure. Some drug combinations can cause edema, including the “combination of glimepiride and metformin”

36
Q

Which type of diabetes patient should be admitted for observation after a bout of hypoglycemia, type one or type two?

A

Type 2 Patients on an oral “agent should be admitted for observation. This is because of the somewhat erratic absorption of oral hypoglycemic agents and their prolonged effect. The patient may have an additional episode of hypoglycemia for up to 36–48 hours after the initial episode. This is not true of patients on NPH insulin who are using a drug that is relatively short acting. Finally, one of the benefits of metformin is that it rarely (if ever) causes hypoglycemia. Its main action is to reduce gluconeogenesis and release of glucose from the liver (although it also improves skeletal muscle use of glucose).”

37
Q

Do patients on beta blockers not notice the signs and symptoms of hypoglycemia?

A

“Beta-blockers do not significantly interfere with patients’ ability to recognize hypoglycemia. The main thing that contributes to unawareness of hypoglycemia in diabetics is the rate of glucose drop (a slow drop is less likely to be noticed) and autonomic insufficiency (patients cannot respond with tachycardia, sweating, etc. to the out-pouring of adrenergics). ACE inhibitors, like beta-blockers, are actually associated with hypoglycemia in diabetics”

38
Q

What would be the best regimen for Starting insulin therapy in the patient with type two diabetes and trying to minimize injections?

A

Insulting glargine. “Because of its slow release, insulin glargine provides a steady-state insulin level throughout 24 hours and is less likely to cause nocturnal hypoglycemia. Other options include insulin detemir and ultralente insulin (off the market in the United States), both of which have prolonged action. A single injection of 70/30 insulin is a reasonable alternative, but should be given at dinnertime, not at bedtime. Multiple daily insulin injections may be necessary for type 1 diabetics, but rarely are so for type 2 patients”

39
Q

Tight glycemic control is recommended for the hospitalized patient with diabetes. T or F?

A

False. “Chasing the insulin for tight control in the hospital is counterproductive and does not improve outcomes! Even though patients with hyperglycemia may do worse, it is clear that the elevated glucose is a marker for metabolic stress and thus for sicker patients. Shoot for a blood sugar of between 120 and 180 mg/dL. This has been found to be superior to intensive glycemic control.”

40
Q

How often should a patient and oral hypoglycemics measure blood sugar?

A

“Daily measurements of finger stick sugars in patients on oral hypoglycemic agents do nothing to improve glycemic control (BMJ 2012 Feb 27; 344:e486). In these patients, we are not reacting to daily fluctuations in glucose control but rather making changes in response to the HbA1c. Occasional random sugars are not unreasonable to get a general idea about glycemic control. Type 2 diabetics on insulin (and all type 1 diabetics) should measure their blood glucose at least daily, and ideally twice a day, regardless of the presence or absence of symptoms.”

41
Q

What is the medical management of a microadenoma that is resulting in a prolactinoma?

A

“A pituitary tumor <1 cm in size is considered a microadenoma, and tumors 1 cm or greater in size are considered macroadenomas. The treatment implications are slightly different. In both cases, medical therapy with a dopamine agonist (e.g., bromocriptine and cabergoline) is indicated. Successful shrinkage of even macroadenomas is possible with this therapy. Remember that the secretion of prolactin is under a negative feedback loop. As CNS dopamine levels go up, prolactin levels go down. When dopamine levels go down, prolactin levels go up”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

Check out this book on the iBooks Store: https://itun.es/us/vRMUI.l

42
Q

What is bromocriptine? what is it used for and what are the common side effects?

A

It is a dopamine agonist used to treat pituitary adenomas. The most common side effects of dopamine agonists are nausea, postural hypotension, and difficulty concentrating. These symptoms tend to be lessened when lower doses are used and the dose is increased very slowly. Cabergoline tends to be better tolerated than bromocriptine” “Dopamine agonists can be stopped at menopause”

43
Q

What is the treatment for a pituitary microadenoma in a patient with acromegaly?

A

“Acromegaly is caused by a GH-secreting pituitary tumor. Surgery is the treatment of choice for patients with a microadenoma (1 cm or less in diameter) or for patients with a macroadenoma that appears to be fully resectable. Somatostatin analogs and pegvisomant (Somavert®) may be useful adjuncts to surgery, and are an option for patients who are not surgical candidates. Bromocriptine is not very effective, and only about 10% of acromegaly patients will achieve normal IGF-I levels with bromocriptine; however, cabergoline seems to work in about half of patients. Cabergoline has an advantage over somatostatin analogs in that it can be taken orally. Radiation is also an option for therapy, especially for those patients who are not surgical candidates and do not tolerate or do not respond to medical therapy”

44
Q

What is Pramlintide and is it indicated in type One or two diabetes?

A

“Pramlintide, indicated in both type 1 & 2 DM, is a synthetic analogue of amylin, which is secreted by the body along with insulin. This drug (1) prolongs gastric emptying leading to lower spike in serum glucose, (2) suppresses postprandial glucagon secretion (again lowering blood sugars) and (3) suppresses hunger leading to lower calorie intake. It should only be used in patients who are already on insulin but can be used for both type 1 and type 2 diabetes. Nateglinide (Starlix) is a meglitinide that releases glucose from the pancreas similar to sulfonylureas. Precose (Acarbose) is an alpha-glucosidase inhibitor that prevents the conversion of starches to simple sugars in the GI tract and thus slows absorption of glucose from the GI tract. Finally, glimepiride (Amaryl) is a sulfonylurea”

Excerpt From: Mark Graber & Jason Wilbur. “Family Practice Examination and Board Review, Third Edition.” McGraw-Hill Medical, 2013. iBooks.
This material may be protected by copyright.

Check out this book on the iBooks Store: https://itun.es/us/vRMUI.l