Week 2 Diabetes and Endocrine Disorders Flashcards

1
Q

Pituitary gland releases what hormones

A

TSH
Adrenocorticotropic hormone (ACTH)
prolactin

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2
Q

thyroid gland releases what hormone

A

thyroid hormone

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3
Q

Adrenal gland releases what hormones

A

cortisol

catecholamines

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4
Q

parathyroid gland releases what hormones

A

parathyroid hormone

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5
Q

pancreas releases what hormones

A

glucagon

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6
Q

hypothalamus releases what hormones

A

thyrotropin- releasing hormone (TRH)

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7
Q

A 20-year-old female patient with tachycardia and weight loss but no optic symptoms presents with the following laboratory values: decreased TSH, increased T3, and increased T4 and free T4. A pregnancy test is negative. What is the initial treatment for this patient?

A. Beta blocker medications

B. Radioiodine therapy

C. Surgical resection of the thyroid gland

D. Thionamide therapy

A

A. Beta blocker medications

Beta blockers should be initiated for patients with Graves’ disease to alleviate the alpha-adrenergic symptoms of the hyperthyroidism. Radioiodine therapy is used for patients with Graves’ ophthalmopathy. Surgical resection is performed for pregnant women who cannot be managed with thioamides or for patients who refuse radioiodine therapy. Thioamide therapy is recommended for patients younger than 20 years old, pregnant women, those with a high likelihood of remission, and those with active Graves’ Orbitopathy

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8
Q

A female patient with hypothyroidism for the past 5 years presents for a positive home pregnancy test. She is taking levothyroxine 75 mcg daily and her TSH was 2.5 mIU/L six months ago at her routine physical. The nurse practitioner understands which of the following?

A. She will need to stop taking her medication and switch to a natural thyroid hormone replacement

B. She should continue taking her current dose of levothyroxine and have her TSH level checked at the end of the first trimester

C. Reduce her levothyroxine dose since thyroid requirements are lower in the first trimester of pregnancy

D. Thyroid requirements increase by 20-30% in pregnancy so she should have a TSH checked today

A

D. Thyroid requirements increase by 20-30% in pregnancy so she should have a TSH checked today

Thyroid requirements increase by 20-30% during pregnancy. The TSH should be less than 2.5 during the first trimester. Untreated hypothyroidism during pregnancy can have detrimental effects such as miscarriage and low birth weight. Levothyroxine is safe during pregnancy. TSH should be monitored at least once during each trimester, and is recommended every 4 weeks in the first and second.

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9
Q

A postpartum woman develops fatigue, weight gain, and constipation. Laboratory values reveal elevated TSH and decreased T3 and T4 levels. What will the nurse practitioner tell this patient?

A. A thyroidectomy will be necessary.

B. She should be referred to an endocrinologist.

C. She will need lifelong medication.

D. This condition may be transient.

A

D. This condition may be transient.

Postpartum hypothyroidism may be a transient condition and does not require surgical intervention, referral to a specialist, or lifelong medication unless it proves to be long-standing or refractory to treatment.

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10
Q

A patient has a thyroid nodule and the nurse practitioner suspects thyroid cancer. To evaluate thyroid nodules for potential malignancy, which test is performed?

A. Radionucleotide imaging

B. Serum calcitonin

C. Serum TSH level

D. Thyroid ultrasound

A

D. Thyroid ultrasound

Thyroid ultrasound evaluation should be performed for all patients with known thyroid nodules; high-resolution sonography can clearly distinguish between solid and cystic components. Radionucleotide imaging is not specific; many cold nodules are benign. The routine measurement of serum calcitonin levels is not useful or cost-effective. TSH levels are not specific to malignancy

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11
Q

Hypothyroidism labs

A

elevated TSH

low free T4

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12
Q

hyperthyroidism labs

A

low TSH

elevated free T4

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13
Q

Subclinical hypothyroidism labs

A

elevated TSH

normal free T4

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14
Q

Hypothyroidism d/t pituitary dysfunction labs

A

normal TSH

low free T4

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15
Q

euthyroid labs

A

normal TSH

normal free T4

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16
Q

A 40-year-old patient with primary hyperparathyroidism has increased serum calcium 0.5 mg/dL above normal without signs of nephrolithiasis. What is the recommended treatment for this patient?

A. Annual monitoring of calcium, creatinine, and bone density

B. Avoidance of weight-bearing exercises

C. Decreasing calcium and vitamin D intake until values normal

D. Parathyroidectomy

A

A. Annual monitoring of calcium, creatinine, and bone density

Medical management of primary hyperparathyroidism involves close monitoring of serum calcium and creatinine and bone density screenings. Weight-bearing exercises should be encouraged, and vitamin D and calcium intake should be adequate, not decreased. This patient does not meet criteria for parathyroidectomy because of age less than 50 years and serum calcium less than 1 mg/dL above the upper limit of normal.

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17
Q

Which of the following is true regarding Cushing disease?

A. Chronic use of systemic corticosteroids is the most common form of endogenous Cushing syndrome

B. The pathophysiology involves suppression of the adrenal gland leading to decreased production of cortisol

C. Levels of corticotropin releasing hormone are increased

D. Increased production of ACTH stimulates increased production of cortisol by the adrenal glands

A

D. Increased production of ACTH stimulates increased production of cortisol by the adrenal glands

Cushing disease is caused by the increased production of ACTH which then stimulates cortisol production from the adrenals. This leads to development of Cushing syndrome. Cushing disease accounts for 70% of Cushing syndrome. Corticosteroid use is a cause of exogenous Cushing syndrome which is due to suppression of the HPA axis.

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18
Q

Which of the following are symptoms of hyperparathyroidism? (Select all that apply.)

A. Chvostek’s sign

B. Cognitive impairment

C. Left ventricular hypertrophy

D. Perioral paresthesias

E. Renal calculi

A

B. Cognitive impairment

C. Left ventricular hypertrophy

E. Renal calculi

Cognitive impairment, left ventricular hypertrophy, and renal calculi all occur with hyperparathyroidism. Chvostek’s sign and perioral paresthesias occur with hypoparathyroidism.

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19
Q

Which laboratory values representing parathyroid hormone (PTH) and serum calcium are consistent with a diagnosis of primary hyperparathyroidism?

A. Appropriately high PTH along with hypocalcemia

B. Appropriately increased PTH and low or normal serum calcium

C. Inappropriate secretion of PTH along with hypercalcemia

D. Prolonged inappropriate secretion of PTH with subsequent hypercalcemia

A

C. Inappropriate secretion of PTH along with hypercalcemia

Primary hyperparathyroidism is characterized by the inappropriate secretion of PTH in the setting of hypercalcemia. Appropriately high PTH with hypocalcemia characterizes hypoparathyroidism. An appropriately increased secretion of PTH with low or normal serum calcium is characteristic of secondary hyperparathyroidism. Prolonged inappropriate secretion of PTH in which hypercalcemia develops is tertiary hyperparathyroidism.

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20
Q

A 25-year-old female patient presents with bilateral galactorrhea and irregular menses. She has a normal breast exam. In addition to checking a prolactin level, which of the following should be included in the initial work up?

A. Breast mammography

B. Human chorionic gonadotropin (HCG)

C. MRI of the pituitary gland

D. Estradiol level

A

B. Human chorionic gonadotropin (HCG)

Patients with symptoms of a prolactinoma should have a TSH, T4, HCG (woman of childbearing age), BUN, Creatinine, prolactin hormone, and liver transaminase. She does not require a mammogram since her breast exam is normal and symptoms are bilateral. Pituitary MRI may be needed, but it is not part of the initial work up. Estradiol is not included in the work up.

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21
Q

You meet with the patient and his husband to go over the test results and explain the diagnosis of diabetes. Given his age, body habitus, and lack of exercise, you feel certain that this patient has type 2 diabetes. You provide some basic education on the nature of diabetes, its natural history, and what can be done to manage it.

What is the most important next step for this patient?

A. Initiation of insulin therapy

B. Initiation of an ACE inhibitor

C. Referral to an endocrinologist

D. Diabetic education classes

E. Initiation of glyburide or other sulfonylurea

A

D. Diabetic education classes

A general education program that includes information on diet, disease management, and the family’s role in successful diabetes care is the most important intervention listed. While specialist consultation may be useful in complex diabetic patients or in those who are not responding to treatment, primary care physicians provide care to the majority of patients with diabetes. Insulin therapy is not indicated at this point, and an ACE inhibitor may or may not be helpful depending on the patient’s blood pressure and urine protein. “E” is also incorrect

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22
Q

The pathologic factors involved in type 2 diabetes in adults include:

A. Pancreatic beta-cell destruction through a yet undetermined infectious process

B. The production of anti-insulin antibodies that cause precipitation of , insulin, /antibody complexes

C. Resistance to the effects of , insulin, at peripheral tissues and , a, relative , insulin, deficiency that is progressive over time

D. An autosomal-dominant process, with the diabetes gene located on the long arm of chromosome 18

E. Too much exercise and a complete lack of a “beer gut”

A

C. Resistance to the effects of , insulin, at peripheral tissues and , a, relative , insulin, deficiency that is progressive over time

DM2 is the result of the development of insulin resistance at the peripheral tissues (e.g., fat and muscle cells) and a relative lack of insulin compared to the increasing amount that the body requires. “A” is incorrect. Autoimmune destruction of beta-cells in the pancreas is responsible for causing DM1. “B” is incorrect, although there are anti-insulin antibodies found in DM1. “D” is incorrect as well, but there is a strong genetic component to DM2. The exact genetic factors that cause DM2 in adults have not been completely elucidated, but no single responsible gene is transmitted in an autosomal dominant fashion. “E” is incorrect because lack of exercise, weight gain, dietary factors, and truncal obesity (the “beer gut”) predispose persons to the development of DM2.

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23
Q

At the next visit, you review the patient’s medical record and try to assure that he is up to date on his preventive health care.

Which of the following is NOT true regarding preventive services in diabetics?

A. Patients diagnosed with type 2 diabetes should have a dilated eye examination at the time of diagnosis

B. Patients with type 1 diabetes should have a dilated eye examination at the time of diagnosis if they are over age 12

C. A urine microalbumin should be checked at least yearly in all type 2 diabetics

D. A foot examination using a 10-g nylon microfilament should be done annually for all diabetics

A

B. Patients with type 1 diabetes should have a dilated eye examination at the time of diagnosis if they are over age 12

Patients with diabetes type 1 should have an eye examination 3 to 5 years after the diagnosis and then yearly. Age at the time of diagnosis is not a factor in determining when an eye examination should be done. See Table 10-2 for components of recommended diabetes follow-up.

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24
Q

You are seeing a new patient in your office. He is a 47-year-old man with a presenting complaint of fatigue for several months. He denies fever, rigors, cough, nausea, or diarrhea. He has lost about 10 lb. Upon questioning him you discover that he is also having nocturia and is thirsty all the time. He has asthma, for which he uses an albuterol-metered dose inhaler occasionally. He has no other chronic medical problems and takes no other medications on a regular basis. He has a family history of diabetes, hypertension, and heart disease. He smokes about one pack per day, and he works as a teacher at the local high school. He is aware of no occupational exposure to toxins.

Physical examination reveals the following: T 37°C, BP 135/83 mm Hg, P 72 bpm, BMI 38 kg/m2. Aside from obesity, the remainder of the examination is normal.

Laboratory test results reveal the following: normal CBC, BUN/creatinine, and electrolytes. You ask him to return to the office the next day for fasting laboratory tests, which reveal a fasting glucose of 123 mg/dL and an HbA1c of 7.5%.

Does this patient have diabetes?

A. Yes; he has an elevated fasting glucose

B. Probably; he needs a second fasting glucose to confirm the diagnosis

C. Probably; he needs a second HbA1c to confirm the diagnosis

D. Yes; he has the classic symptoms of diabetes: fatigue, weight loss, and thirst, associated with an elevated glucose

E. Probably not; his HbA1c is not >8%

A

C. Probably; he needs a second HbA1c to confirm the diagnosis

If results of two different diagnostic tests for DM are discordant, the test that is diagnostic of diabetes should be repeated. “A” and “B” are incorrect because the fasting glucose is <126 mg/dL (the threshold for diabetes). “D” is incorrect because we do not have his random glucose value that is ≥200 mg/dL. “E” is incorrect because the A1c cutoff for diabetes diagnosis is ≥6.5%.

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25
Q

You are seeing a new patient in your office. He is a 47-year-old man with a presenting complaint of fatigue for several months. He denies fever, rigors, cough, nausea, or diarrhea. He has lost about 10 lb. Upon questioning him you discover that he is also having nocturia and is thirsty all the time. He has asthma, for which he uses an albuterol-metered dose inhaler occasionally. He has no other chronic medical problems and takes no other medications on a regular basis. He has a family history of diabetes, hypertension, and heart disease. He smokes about one pack per day, and he works as a teacher at the local high school. He is aware of no occupational exposure to toxins.

Physical examination reveals the following: T 37°C, BP 135/83 mm Hg, P 72 bpm, BMI 38 kg/m2. Aside from obesity, the remainder of the examination is normal.

What further study must be done to complete the diagnosis of diabetes and determine whether the patient has type 1 or type 2 diabetes?

A. C-peptide level

B. Anti-islet cell antibodies

C. Anti-insulin antibodies

D. None of the above

A

D. None of the above

This patient’s age, history, examination (BMI 38), and laboratory findings are consistent with the diagnosis of DM2. None of the other studies listed needs to be performed. However, if questions remain regarding the type of diabetes (which will then affect therapy, prognosis, follow-up, etc.), you may choose to perform further studies. In DM1, the C-peptide level (a marker of endogenous insulin production) is low. If it is equivocal, give a glucose load (e.g., large meal) and see if it goes up. If it goes up, the diagnosis is likely DM2. Anti-islet cell antibodies are present in 80% of type 1 diabetics and, if found in the patient with criteria for diabetes, are essentially diagnostic of type 1 diabetes. “C” is incorrect because anti-insulin antibodies have a low sensitivity for DM1 and may be elevated secondary to the use of exogenous insulin.

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26
Q

Which of the following is NOT a side effect of GLP-1 receptor agonists (exenatide, liraglutide, albigutide)?

A. weight gain

B. pancreatitis

C. Hypoglycemia

D. GI upset

E. Thyroid tumor

A

A. weight gain

GLP-1 agonists can cause weight loss of 1.5 to 2.5kg over 30 weeks. These drugs are associated with pancreatitis although rarely, and the association is tenuous. Due to an association with thyroid cancer, their use is contraindicated in patients with a personal or family hx of medullary thyroid carcinoma or MEN 2A or 2B. The risk of hypoglycemia is small - but not zero. Somewhere between 10%- 50% of patients may develop GI symptoms.

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27
Q

Which class of medications is the best choice for initial therapy of HTN in diabetics?

A. ACE inhibitors

B. Calcium-channel blockers

C. Loop diuretics

D. Vasodilators

E. Beta-blockers

A

A. ACE Inhibitors

ACE inhibitors have been shown to provide renal protection in patients with diabetes (types 1 & 2). Patients with albuminuria and HTN will certainly benefit from an ACE inhibitor. Loop diuretics (ex. furosemide) are not indicated for the PRIMARY tx of HTN in diabetics (or, really, anyone else). ARBs are a reasonable alternative in the hypertensive pt with albuminuria if an ACE inhibitor is not tolerated. Vasodilators and calcium-channel blockers (verapamil, diltiazem) are an option for renal protection in patients with worsening albuminuria especially in those who cannot tolerate an ACE inhibitor or ARB. Beta-blockers should not be used first line for treating HTN in patients without cardiac dx.

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28
Q

Which medication is the most appropriate first-line therapy for an obese patient with type-2 diabetes?

A. A thiazolidinedione (glitazone aka Actos)

B. A sulfonylurea (glipizide)

C. insulin

D. Metformin

E. DPP-4 or “gliptin” aka Januvia

A

D. Metformin

Metformin does not cause weight gain (unlike many other treatments for diabetes), has evidence for reducing the complications of diabetes, and is generally well-tolerated and inexpensive. Thus, it is the drug of choice in most DM2 patients. In addition, it carries very little risk of hypoglycemia. GI side effects are common, however (nausea, diarrhea). Some patients will lose weight from use os metformin. Thiazilidinediones known as “glitazones” are not 1st line for several reasons, chief among these being the possibility of increased CV events (rosiglitazone and pioglitazone can exacerbate CHF). The track record of rosiglitazone is somewhat spotty; it was removed from market due to an increase in CV events and then reintroduced even though there was not additional safety data. Sulfonylureas are also effective and well-tolerated but have a significant risk for hypoglycemia and are associated with weight gain. Studies comparing effects on end-organ dx show better outcomes with metformin than with sulfonylureas. All other oral drugs are best considered second-line agents. Dpp-4 inhibitors aka “gliptins” block the degradation of the body’s endogenous incretin, which helps to lower blood sugar. DPP-4 acts as a “glucagon-like peptide-1 (GLP-1)”. DPP-4 inhibitors (sitagliptin, saxagliptin, alogliptin) can be used as an “add-on” tx if traditional hypoglycemic agents are not effective and have the benefit of some weight loss. In a patient with very poor control (A1c > 9%) at diagnosis, insulin would be a potential first line agent, but not in this patient whose partially controlled.

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29
Q

Metformin should NOT be used in which class of patients?

A. pt w/ COPD

B. Pt w/ GFR < 30 mL/min

C. Leukemia or lymphomas

D. Post MI w/ normal systolic function

E. insufficient fat stores

A

B. GFR < 30 mL/min

Patients with renal dx are at a higher risk of lactic acidosis, the most severe complication of metformin therapy, although it is exceedingly rare. Current manufactor reccomendations state that metformin should be avoided if serum Cr >/= 1.5 mg/dL in M and >/= 1.4 mg/dL in F. However, metformin is safe to start as long as the GFR is > 45 mL/min and can be used until the GFR is 30 mL/min (max dose 1,000mg/day for those w/ GFR between 30 and 60 mL/min). Outcomes in patients with mild CHF and renal failure (GFR > 30mL/min) are actually better with metformin than without. Patients with pulmonary or neoplastic dx may take metformin unless they also have severe hepatic or renal failure. Metformin should be held for 48 hours after contrast studies.

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30
Q

Which of the following drugs (by itself - not in combination with other drugs) is the most likely to cause the patient’s edema, SOB, and possible HF?

A. Metformin

B. Glyburide

C. Pioglitazone

D. Lisinopril

E. Insulin

A

C. Pioglitazone

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

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31
Q

A patient with diabetes complains of parasthesias. Which of the following medications can cause sensory changes?

a. Glipizide
b. Sitagliptin (Januvia)
c. Metformin
d. Exenatide (Byetta)

A

c. Metformin

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32
Q

The major risk factor for development of thyroid cancer is

a. Inadequate iodine uptake
b. Presence of a goiter
c. Exposure to radiation
d. Smoking

A

c. Exposure to radiation

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33
Q

Your 62 yo patient has type 1 diabetes that has historically been well controlled by insulin. Recently, however, the patient has been experiencing marital difficulties that have caused the patient to have some emotional upset. What do you expect? The patient will:

a. Have an insulin reaction more readily than usual
b. Have an increased blood sugar level
c. Need less daily insulin
d. Need more carbohydrates

A

b. Have an increased blood sugar level

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34
Q

Which of the following steps will not slow or stop the progression of diabetic nephropathy?

a. Control of blood pressure
b. Use of ACE inhibitors
c. Restriction of protein intake
d. Use of calcium channel blockers

A

d. Use of calcium channel blockers

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35
Q

A patient with Type 2 diabetes mellitus is on the maximum dosage of three oral antidiabetic agents. The HgbA1C remains at 8.5% despite these interventions, and the patient is compliant with medication. Which of the following would be an appropriate basal insulin initiation order?

a. Insulin glargine (Lantus) 10 units nightly
b. Insulin detemir (Levemir) 10 units before each meal
c. Insulin aspart (NovoLog) 10 units before each meal
d. Regular insulin before each meal

A

a. Insulin glargine (Lantus) 10 units nightly

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36
Q

After achieving a euthyroid state after thyroidectomy, the provider should do a laboratory analysis of TSH level every

a. 3 months
b. 6 months
c. 1 year
d. 2 years

A

c. 1 year

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37
Q

DM dx criteria

A

fasting plasma glucose (FPG) >/= 126

OGTT 75-g w/ measured plasma glucose >/= 200 @ 2 hrs

A1c >/= 6.5 (National Glycohemoglobin Standardization Program)

random glucose >/= 200 AND classic symptoms of hyperglycemia (polyuria, polydipsia, or unexplained weight loss)

Per ADA, unless clear clinical dx, 2nd test required to confirm

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38
Q

DM screening tests

A

A1c
FPG
2-h OGTT

no one test preferred

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39
Q

What can make the A1c less accurate?

A

anemia or hemoglobinpathies (r/t rapid RBC turnover)
2nd/3rd trimester of pregnancy
recent blood loss, transfusion, erythropoietin therapy, hemolysis

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40
Q

DM screening asymptomatic adults

A

Test ALL adults beginning at age 45 regardless of weight

Recc for adults of any age that are overweight (BMI > 25 or >23 Asians) and additional RF:

  • member of high-risk ethnic group (AA, hispanic, American Indian, Alaskan, Asian, Pacific islander
  • 1st degree relative w/DM
  • hx gestational DM or giving birth to baby > 9 lbs
  • physical inactivity
  • HTN >/= 140/90 or tx
  • HDL-C < 35
  • fasting triglycerides > 250
  • PCOS
  • previously noted A1c >/= 5.7% (impaired glucose tolerance ot impaired fasting glucose)
  • other clinical conditions w/ insulin resistance (acanthosis nigricans, gestational age birth weight)
  • hx CVD
  • tx w/ atypical antipsychotics or glucocorticoids

if results are normal, reasonable to retest again at 3-y intervals, consider more frequent testing depending on initial results and risk status

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41
Q

DM screening asymptomatic children

A

ADA reccs screening for T2DM or prediabetes in children who meet following:

  • overweight (BMI > 85th percentile for age/sex)

AND:

  • maternal hx GDM during gestation
  • fma hx of T2DM in 1st or 2nd degree relatives
  • high risk ethnicity
  • signs on insulin resistance or conditions associated w/ insulin resistance (acanthosis nigricans, HTN, dyslipidemia, PCOS, small for gestational age birth weight)
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42
Q

T1DM

A

immune-mediated diabetes with evidence of autoimmune B-cell destruction, typically leading to absolute insulin deficiency

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43
Q

T2DM

A

multifactoral process, including relative insulin insufficiency, insulin resistance and often unregulated gluconeogensis in liver

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44
Q

gestational DM

A

dx during 2nd or 3rd trimester of pregnancy that was NOT clear prior to gestation

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45
Q

Dx tests for T1DM

A

C-peptide level

antibody tests:

  • islet cell autoantibodies (ICAs)
  • insulin autoantibodies (IAAs)
  • autoantibodies to glutamic acid decarbocylase 65
  • tyrosine phosphatase IA-2 transmembrane proteins
  • zinc transporter (ZnT8)
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46
Q

IAA (insulin autoantibodies) more likely to be seen in

A

IAA present in mostly all young patients with T1DM but may be absent in older patients w/ dx

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47
Q

anti-GAD antibodies more likely to be seen in

A

more likely present in young adults with T1DM than in children with dx

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48
Q

T1DM pt, screen for what other autoimmune dx?

A

ADA recommends screening for thyroid dx and celiac dx soon after T1DM dx

specific autoimmune dx have been reported in those w/ T1DM: Hashimoto thyroiditis, Graves dx, Addison dx, autoimmune hepatitis, dermatomyositis, myasthenia gravis, vitiligo, pernicious anemia

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49
Q

Metformin and renal function

A

considered safe whose eGFR >/= 30 mL/min

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50
Q

nonpharm management DM/ prediabetes

A
  • healthy eating
  • weight control
  • increased physical activity (1h/day)
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51
Q

Impaired fasting glucose weight management

A

refer to effective ongoing support program for a weight loss of > 5% body weight and to increase physical activity to 30 mins a day on most days

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52
Q

DM preventative care

A
A1c < 7% (generally) 
ASA/antiplatelet agents 
BP management 
Cholesterol management
screen neuropathy 
screen retinopathy 
screen nephropathy 
immunizations
tobacco use assessment
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53
Q

How often do you check A1c in diabetic pt

A

every 6 months w/ stable glycemic control

every 3 months if NOT at goal or tx changes

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54
Q

recommended A1c nonpregnant adults after tx

A

< 7%

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55
Q

recommended A1c for children on tx

A

< 7.5%, individualization encouraged

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56
Q

ASA/antiplatelet agents DM

A

ASA 75- 162mg/day
secondary prevention w/ hx of CVD

primary prevention in M&F >/= 50 y.o. w/ DM

NO benefit < 30 y.o.

Clopidogrel 75mg/day if allergy to ASA

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57
Q

BP screening in DM

A

measure EVERY visit
goals:
Adults < 140/90 or <130/80 if younger and no burden

Children < 130/80 OR < 90th percentile

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58
Q

BP management in DM

A

lifestyle changes: DASH diet, weight loss, exercise

Start meds if do not lower BP to target

ACEI, ARBs, CCB, diuretics recc

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59
Q

Cholesterol management in DM

A

Per ADA, obtain lipid profile at dx and at least every 5 years in pts < 60 y.o.

ASCVD risk of > 20% and age drives decision for statin tx

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60
Q

neuropathy screening

A

diabetic foot exam at least annually w/ T2DM and started within 5 years of dx w/ T1DM

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61
Q

How often do you examine feet if pt has deformities or ulcers?

A

every visit

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62
Q

diabetic foot exam

A

inspection, foot pulses, loss of protective sensation – light-touch perception w/ 10-g monofilament and at least one of the following: temperature, vibration, pinprick, ankle reflexes

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63
Q

cardiovascular neuropathy

A

manifests as resting tachycardia and/or orthostatic hypotension

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64
Q

GI neuropathy

A

gastroparesis

screen if suspicious, gastric emptying study

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65
Q

retiniopathy screening

A

dilated retinal exam @ dx w/ T2DM
> 10 y.o. w/ T1DM for >/= 5 y

if no retinopathy after serial annual exams, may screen every 2 years

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66
Q

nephropathy screening

A

leading cause of ESRD

serum Cr annually and calculate GFR

Urine albumin annually in ALL T2DM & T1DM for >/= 5 y
w/ spot urine to Cr ration annually

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67
Q

albuminuria normal value

A

normal amount < 30mg/24 h

persistent albuminuria marker for CVD

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68
Q

DM & immunizations

A

pneumococcal vaccine given ages 2- 64 w/ DM PPSV23, repeat after 65 y.o. w/ at least 5 years between doses

flu vaccine - annually > 6 months old

Hep B vaccine given to unvaccinated adults 19- 59 y.o., consider in adults > 60 y.o.

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69
Q

Which hypoglycemic agent should be avoided in patients with a glomerular filtration rate (GFR) less than 25 mL/min/1.73 m2?

A Metformin

B Glyburide

C Insulin

D Acarbose

A

A Metformin

In general, metformin should be avoided in patients with chronic kidney disease (CKD), although observational data suggests that it may be safe to use in patient with GFR less than 30 mL/min/1.73 m2. If it is used at lower GFRs, the dose should be decreased and patients should be counseled to stop metformin when they have a high likelihood of volume depletion, such as if they are vomiting or have diarrhea. Glyburide is a sulfonylurea and may be used in CKD, as can insulin. Acarbose is an alpha-glucosidase inhibitor and can be used in patients with CKD.

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70
Q

According to the American Diabetes Association (ADA), which of the following criteria can be used in the diagnosis of diabetes in nonpregnant adults?

A A1c greater than or equal to 7.0

B Fasting plasma glucose (FPG) of greater than or equal to 126

C Oral glucose tolerance test (OGTT) with 2-hour plasma glucose greater than or equal to 180

D Classic symptoms of hyperglycemia and random glucose of greater than or equal to 180

A

B Fasting plasma glucose (FPG) of greater than or equal to 126

According to the ADA guidelines, the diagnosis of diabetes in nonpregnant adults can be made by any of the following:
• A1c greater than or equal to 6.5%
• Fasting plasma glucose (FPG) greater than or equal to 126 mg/dL (7.0 mmol/L); fasting is defined as no caloric intake for at least 8 hours.
• Oral glucose tolerance test (OGTT, 75-gram anhydrous glucose) with measured plasma glucose greater than or equal to 200 mg/dL (11.1 mmol/L) at 2 hours (after the glucose load)
• Classic symptoms of hyperglycemia (polyuria, polydipsia, and unexplained weight loss) and random glucose greater than or equal to 200 mg/dL (11.1 mmol/L)

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71
Q

With what condition is prediabetes most commonly associated?

A. chronic pancreatitis

B. HLD

C. Obesity

D. Chronic steroid use

A

C. Obesity

• Prediabetes is diagnosed in patients with impaired glucose tolerance (blood glucose 140-199 mg/dL), impaired fasting glucose (blood sugar 100-125 mg/dL), or signs of insulin resistance (metabolic syndrome). This condition reflects worsening pancreatic beta cell function, and the most common cause of prediabetes is obesity. While patients with chronic pancreatitis and chronic steroid use may have impaired glucose metabolism, obesity is a more common cause. Hyperlipidemia is associated with the metabolic syndrome and obesity but does not cause prediabetes.

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72
Q

lifestyle modification and glycemic control

A

Lifestyle modifications which target weight loss and promote activity have been shown to improve glycemic control.
Even modest weight loss (as little as 4 kg) has been shown to improve glucose control.

Some of the most compelling data come from following patients with diabetes who undergo bariatric surgery. These procedures, which can result in sustained weight loss of greater than 20 kg may eliminate the need to take medications for diabetes. However, apart from surgery, the rate of observed eventual weight regain has blunted the impact for more modest lifestyle interventions.

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73
Q

DM medications that are weight neutral or cause weight loss

A

biguanides - metformin

GLP-1 receptor agonists - “tide”

Amylin agonist - pramlintide

DPP-4 inhibitors -“gliptin”

SGLT2 inhibitors - “gliflozin”

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74
Q

monotherapy tx

A

T2DM w/ initial A1c < 7.5%

Metformin
GLP-1 agonists (injection)
SGLT-2 inhibitors
(strongest evidence for monotherapy)

DPP-4 inhibitors
TZDs
alpha glucosidase inhibitors 
Sulfonylurieas 
(use w/ caution) 

A1c goal not met in 3 months = dual tx

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75
Q

monotherapy tx for DM with high risk for ASCVD or CKD 3 or HF

A

long-acting GLP-1 receptor agonist

SGLT-2 inhibitor

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76
Q

Metformin contraindications

A
lactic acidosis - fatal 
decompensated CHF 
severely impaired renal function (eGFR < 30)
liver failure
heavy alcohol use 
patients undergoing major surgery 

Stop w/ iodine contrast and restart in 48 hrs

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77
Q

Tx options w/ Metformin

A

GLP-1 receptor agonists

SGLT2 inhibitors (jardiance)

DPP-4 inhibitors (Januvia)

TZDs

colesevelam (bile acid sequestrant lowers LDL and improves glycemic control)

bromocriptine-QR (cycloset)

alpha-glucosidase inhibitors

sulfonylureas

non-sulfonylureas secretagogues (“glinides”

amylinomimetic agents

insulin

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78
Q

When to start dual tx for DM

A

initial A1c >/= 7.5%

if not at goal in 3 months, intensify tx

79
Q

DM tx A1c > 9%

A

start with insulin with or w/o other agents

especially if symptoms of diabetes present

80
Q

Biguanides

A

Metformin

reduces A1c 1- 1.5%

MOA: 70% of effect in liver to reduce gluconeogensis
30% in skeletal muscles to decrease insulin resistance

81
Q

GLP-1 receptor agonists

A

“-tide”

reduces A1C 1- 1.5%

MOA: potentiates glucose-stimulated insulin secretion
MAY stimulate production of new beta-cells & prevent beta- cell apotosis

82
Q

Sulfonylureas

A

1st gen: Chlorpropamide, tolazamide, tolbutamide

2nd gen: glyburide, glipizide, glimepriride

reduce A1c 1- 1.5%

MOA: enhance insulin secretion from pancreas by interacting with sensitive potassium channels in beta cell membranes

83
Q

Thiazolidinediones

A

Pioglitazone

reduces A1c 1- 1.5%

MOA: Increases insulin sensitivity of skeletal muscle, adipose tissue, and liver

84
Q

SGLT2 inhibitors

A

“-gliglozin”

reduces A1c 0.5 -1%

MOA: Inhibits SGLT2 membrane protein in proximal tubule, which results in decreased renal glucose reabsorption and increased urinary glucose excretion

85
Q

Non-sulfonylurea secretagogues

A

“-glinides”

reduce A1c 0.5- 1%

MOA: enhance insulin secretion from pancreas by interacting with ATP-sensitive potassium channels in the beta cell membranes

86
Q

alpha-glucosidase inhibitors

A

acarbose & miglitol

reduce A1c 0.5 - 1%

MOA: inhibits alpha-glucosidase enzymes in small intestinal brush border, which interferes with carb digestion and slows absorption of glucose and other monosaccharides

87
Q

DPP-4 inhibitors

A

“-gliptin”

reduces A1c 0.5- 1%

MOA: slows degradation of GLP-1 and glucose dependent insulinotropic peptides (GIPs) which is done by DPP-4

88
Q

Amylin agonists

A

pramlintide

reduces A1c 0.5%

MOA: Inhibits glucagon production in glucose dependent fashion, mostly decreases postprandial glucose excursions

89
Q

Biguanides (metformin) SE

A

metallic taste, nausea, diarrhea, abdominal pain, lactic acidosis (rare – but potentially fatal); B12 deficiency

90
Q
  1. GLP-1 agonists SE

Albiglutide, dulaglutide , exenatide, liraglutide, lixisenatide, and samaglutide

A

nausea, vomiting, diarrhea; renal impairment acute renal failure associated with dehydration caused by GI toxicity; injection-site reactions; risk of acute pancreatitis; thyroid C-cell hyperplasia; possible risk of thyroid C-cell carcinoma

91
Q

Sulfonylureas SE

eg, glimepiride, glipizide, glyburide

A

hypoglycemia (particularly in the elderly or in patients with renal impairment); weight gain; possible aggravation of myocardial ischemia

92
Q

Thiazolidinedinone (TZDs) SE

pioglitazone

A

increased risk of CHF (and possibly coronary artery disease); peripheral edema; macular edema; weight gain; possible decrease in bone mineral density/increased incidence of fractures in women; hepatic failure; possible bladder cancer risk

93
Q

SGLT2 inhibitors SE (canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin)

A

genital mycotic infections; Fournier’s gangrene; volume depletion; decreased eGFR; acute kidney injury; hypotension; fractures; hyperkalemia; hypermagnesemia, hyperphosphatemia; euglycemic diabetic ketoacidosis

94
Q

Non-Sulfonylurea Secretagogues SE (repaglinide and nateglinide)

A

hypoglycemia; weight gain; partly metabolized by CYP3A4 (therefore levels are increased by macrolides which inhibit the enzyme and decreased by rifampin, which induces the enzyme)

95
Q

Alpha-Glucosidase Inhibitors SE (acarbose and miglitol)

A

abdominal pain, diarrhea, and flatulence–due to osmotic effects and bacterial fermentation; transaminase elevations; fatal hepatic failure; contraindicated in pts with chronic intestinal diseases

96
Q

DPP-4 inhibitors SE (alogliptin, linagliptin, saxagliptin, and sitagliptin)

A

pancreatitis, hypersensitivity reactions, hypoglycemia if used in conjunction with sulfonylureas; fatal hepatic failure; possible worsening of heart failure; possible and severe joint pain

97
Q

Amylin agonists SE (Pramlintide)

A

nausea, vomiting, anorexia; headache; severe hypoglycemia (when given with insulin

98
Q

Bile acid sequestrants SE (colesevelam)

A

constipation, nausea, and dyspepsia; increased triglycerides; interference with absorption of oral drugs

99
Q

Bromocriptine SE

A

nausea; vomiting; fatigue; headache; dizziness; somnolence; syncope

100
Q

long-acting (basal) insulin

A
insulin glargine (lantus) - 24h 
insulin detemir (Levemir) - 12h 
insulin degludec (Tresiba) - 48h `
101
Q

insulin initiation recommendations

A

start with basal insulin

A1c < 8% TDD 0.1- 0.2 U/kg

A1c > 8% TDD 0.2- 0.3 U/kg

STOP or reduce sulfonylurea when basal insulin started

102
Q

Which of the following hypoglycemic agents have been associated with weight loss?

A Metformin

B Insulin

C Glyburide

D Pioglitazone

A

A Metformin

Metformin is a biguanide and is associated with weight loss. Insulin therapy is associated with weight gain of approximately 1 to 3 kg. Glyburide is a sulfonylurea and is associated with weight gain. Pioglitazone is a thiazolidinedione and is associated with weight gain.

103
Q

What is the onset of action of short-acting insulin such as lispro and aspart?

A 2 to 3 minutes

B 5 to 15 minutes

C 30 to 60 minutes

D 90 to 120 minutes

A

B 5 to 15 minutes

The onset of action of short-acting insulin (lispro, aspart, glulisine) is 5 to 15 minutes, the peak onset is 30 to 90 minutes, and the duration of action is 4 to 6 hours.

104
Q

Diabetes mellitus can be diagnosed in a patient with which of the following lab abnormalities?

A Hemoglobin A1c (HbA1c) greater than 6.5%

B Anti-insulin autoantibodies

C Fasting plasma glucose of 120

D Anti–glutamic acid decarboxylase (GAD) antibodies

A

A Hemoglobin A1c (HbA1c) greater than 6.5%

The diagnosis of diabetes mellitus types 1 and 2 is made in one of the following clinical situations: (1) HbA1c greater than or equal to 6.5% or (2) fasting plasma glucose level greater than or equal to 126 mg/dL or (3) 2-hour glucose tolerance test greater than or equal to 200 mg/dL or (4) random plasma glucose level greater than or equal to 200 mg/dL in a patient with signs and symptoms of hyperglycemia (polydipsia, polyuria, polyphagia, and weight loss). Although autoantibodies such as anti-insulin, anti–glutamic acid decarboxylase (GAD), or anti–tyrosine phosphatase can be detected in most patients for years before clinical signs and symptoms develop, these may also be present in patients who will never go on to develop diabetes mellitus type 1 and are not part of the diagnostic criteria

105
Q

When is the timing of the peak onset of action of insulin glargine?

A 30 to 90 minutes

B 2 to 4 hours

C 20 to 24 hours

D Glargine does not have a peak onset

A

D Glargine does not have a peak onset

Insulin glargine is a long-acting insulin with an onset of 2 to 4 hours and a duration of 20 to 24 hours. Glargine does not have a peak onset of action.

106
Q

For a child diagnosed with type 1 diabetes mellitus (T1DM) at age 7, when should screening for diabetic retinopathy begin?

A 8 years old

B 10 years old

C 15 years old

D 18 years old

A

B 10 years old

According to the American Diabetes Association’s “Standards of Medical Care in Diabetes” (2016), children with T1DM should be screened for diabetic retinopathy with dilated eye exam annually started after a child is 10 and has had T1DM for 3 to 5 years, then annually thereafter.

107
Q

Rapid Acting Insulin

A
Onset 5 to 15 minutes, Peak 30 to 90 minutes, Duration 4 to 6 hours
o	Lispro (Humalog)
o	Aspart (Novolog, Fiasp)
o	Glulisine (Apidra
108
Q

Short acting insulin

A

Onset 30 to 60 minutes, Peak 2 to 3 hours, Duration 8 to 10 hours
o Regular insulin (Humulin R, Novolin R)

109
Q

Intermediate acting insulin

A

Onset 2 to 4 hours, Peak 4 to 10 hours, Duration 12 to 18 hours
o Isophane insulin (neutral protamine Hagedorn [NPH], Humulin N, Novolin N)

110
Q

long acting insulin

A
o	Glargine (Lantus, Basaglar, Toujeo) -- Onset 2 to 4 hours, no peak, Duration 20 to 24 hours
o	Detemir (Levemir) -- Onset 2 to 4 hours, Peak 3 to 9 hours, Duration 6 to 24 hours
o	Degludec (Tresiba) – Onset 1 hour, Peak 9 hours, Duration greater than 42 hours
111
Q

premixed insulin

A

Onset 30 to 60 minutes, Dual Peak, Duration 10 to 16 hours

o 70% NPH / 30% regular insulin (Humulin 70/30)

112
Q

screening recommendations for complications of T1DM

A

Nephropathy: annual for albuminuira w/ random spot urine sample for albumin/cr ratio after child 10 y.o. or older and has had DM for at least 5 years

Retinopathy: annual dilated eye exam after age 10 and dx for 3- 5 years

Neuropathy: annual foot exam starting at age 10 or after puberty has started (whichever is earlier) after dx for 5 years

HTN: BP measurement at every visit, elevated BP confirmed on 3 diff says

Dyslipidemia: fasting lipid panel at age 10. If LDL < 100, repeat every 3- 5 years. If abnormal, yearly

Thyroid dx: TSH soon after dx and improvement in glucose control. if normal test every 1- 2 years or sooner if symptoms of hypothyroidism

Celiac dx: screen with tissue tissue transglutaminase or deamidated gliadin antibodies, along with serum IgA level soon after dx

113
Q

congenital hypothyroidism S/S

A
lethargy
hypotonia
hoarse cry 
feeding issues 
constipation
macroglossia
open posterior fontanelle
umbilical hernia 
dry skin 
hypothermia
prolonged jaundice
114
Q

Newborn screen hypothyroidism

A

TH needed for growth and neuro development

TSH testing followed by T4 testing if TSH levels are elevated
some states repeat screening at 2 weeks to identify delayed onset

115
Q

Tx congenital hypothyroidism

A

levothyroxine - start ASAP

10- 15mcg/kg/day
tabs preferred, dosing more reliable, crush and give in breastmilk, formula

Do NOT give w/ Ca or iron

116
Q

Hashimoto thyroiditis

A

most common cause of acquired hypothyroidism

autoimmune condition

117
Q

Hashimoto thyroiditis S/S

A
decline in linear growth 
weight gain 
fatigue
constipation 
cold intolerance 
poor school performance 
bradycardia 
dry skin 
proximal muscle weakness
delayed relaxation phase of DTR 
irregular menstrual periods 
delayed puberty 

enlarged thyroid gland, firm w/ pebbly texture

118
Q

hypothyroidism labs

A
TSH elevated 
T4 normal (subclinical) or decreased 
thyroid antibodies (thyroid peroxidase antibody and thyroglobulin antibody)
119
Q

Hashimoto thyroiditis tx

A

Levothyroxine
based on lab values, age, & weight of child

monitor free T4 & TSH 3- 6 months

120
Q

The most common physical finding in a child with congenital hypothyroidism is:

A Open posterior fontanelle

B Macroglossia

C Hypotonia

D Normal physical exam

A

D Normal physical exam

Most children with congenital hypothyroidism do not have clinical manifestations of hypothyroidism due to the presence of maternal thyroid hormones or a small amount of thyroid tissue in the infant. If present, signs and symptoms of congenital hypothyroidism may include lethargy, hypotonia, hoarse cry, feeding problems, constipation, macroglossia, open posterior fontanelle, umbilical hernia, dry skin, hypothermia, and prolonged jaundice.

121
Q

The most common cause of congenital hypothyroidism is:

A Abnormal development of the thyroid gland

B Decreased thyroid-stimulating hormone (TSH) levels

C Hashimoto thyroiditis

D Inborn error in thyroxine synthesis

A

A Abnormal development of the thyroid gland

Approximately 85% of cases of congenital hypothyroidism are due to thyroid dysgenesis, which includes agenesis, hypoplasia, and ectopy. Approximately 10% to 15% of cases of congenital hypothyroidism are due to inborn errors of thyroxine synthesis which are inherited in autosomal recessive pattern. Hashimoto thyroiditis is the most common cause of acquired hypothyroidism. Central hypothyroidism is due to disruption in the hypothalamus or pituitary leading to decreased TSH levels, and is a rare cause of congenital hypothyroidism.

122
Q

Which of the following lab abnormalities is associated with subclinical hypothyroidism?

A Low TSH and normal free T4

B Low TSH and high free T4

C Elevated TSH and normal free T4

D Elevated TSH and low free T4

A

C Elevated TSH and normal free T4

Subclinical hypothyroidism is characterized by elevated TSH and normal free T4. Overt hypothyroidism is characterized by elevated TSH and low free T4. Low TSH and normal free T4 is characteristic of subclinical hyperthyroidism. Low TSH and high free T4 is characteristic of overt hyperthyroidism.

123
Q

most common cause of hyperthyroidism

A

Graves dx: autoimmune condition

124
Q

Graves dx S/S

A
weight loss
heat intolerance 
difficulty sleeping 
tremor
increased frequency of defecation 
irritability 
menstrual irregularity 
behavioral disturbances: decreased attention span, difficulty concentrating, emotional lability, hyperactivity (child) 

thyroid gland diffusely enlarged w/ soft texture, well-delineated border
tachycardia, palpitations, widened pulse pressure, afib (> 50 y.o.)
tremors, shortened relaxation phase in DTRs, fatigue, proximal muscle weakness
ophthalmopathy - proptosis and periorbital edema

125
Q

Graves dx labs

A
TSH - depressed or undetectable 
T4- elevated 
T3 - elevated 
TRAbs present in 95% 
thyroid peroxidase and antithyroglobulin antibodies +
126
Q

24-h radioiodine uptake

A

This test provides measures of iodine uptake at 4 and 24 hours, and results are given in percentages. The percentage will be high in conditions with de novo synthesis of thyroid hormone (including Graves disease and toxic nodular goiter) and low in conditions with inflammation and destruction of thyroid gland (thyroiditis), thyroid hormone ingestion, or exposure to iodine (such as iodinated contrast and amiodarone).

127
Q

24-h radioiodine scan

A

This test is often done at the same time as the 24-hour radioiodine uptake and provides images of the thyroid. This test can help distinguish among Graves disease, toxic adenoma, and toxic multinodular goiter. In Graves disease, radioiodine uptake distribution is generally diffuse and homogenous, whereas it is focal in a toxic adenoma and heterogeneous with multiple areas of focal increased and suppressed uptake in toxic multinodular goiter.

128
Q

Pertechnetate thyroid scan

A

Provides an image of the thyroid and can distinguish between Graves disease, toxic adenoma, and toxic multinodular goiter. The advantage of this test is that it takes only about 20 minutes to perform; however it does not provide a numerical measurement of uptake and cannot be used to dose radioiodine therapy.

129
Q

other individualized tests in hyperthyroidism

A

irregualr HR - ECG to determine if afib present

postmenopausal women - bone-density test obtained

large goiters associated with airway or esophageal obstruction - CT or MRI of neck

130
Q

Graves dx tx

A

antithyroid med: methimazole & propylthiouracil (PTU)

radioiodine therapy

thyroidectomy - fail med tx, drug reactions, large goiters, severe ophthalmopathy

permanent hypothyroidism is goal of tx

131
Q

Which of the following lab abnormalities is associated with subclinical hyperthyroidism?

A Elevated thyroid-stimulating hormone (TSH) and normal free T4

B Elevated TSH and low free T4

C Low TSH and normal free T4

D Low TSH and high free T4

A

C Low TSH and normal free T4

Low TSH and normal free T4 is characteristic of subclinical hyperthyroidism. Low TSH and high free T4 is characteristic of overt hyperthyroidism. Subclinical hypothyroidism is characterized by elevated TSH and normal free T4. Overt hypothyroidism is characterized by elevated TSH and low free T4.

132
Q

What is the mechanism of hyperthyroidism in Graves disease?

A Hyperfunctioning thyroid nodule

B Antibodies bind and stimulate the TSH receptor

C Release of thyroid hormone from an inflamed thyroid gland

D Ingestion of exogenous thyroid hormone

A

B Antibodies bind and stimulate the TSH receptor

Graves disease is an autoimmune condition in which antibodies bind and activate the TSH receptor causing increased thyroid hormone release. Other causes of hyperthyroidism include hyperfunctioning thyroid nodules, thyrotoxic phase of autoimmune Hashimoto thyroiditis caused by release of preformed thyroid hormone from the inflamed thyroid gland, and factitious hyperthyroidism from exogenous thyroid hormone.

133
Q

In hyperthyroidism due to Graves disease, what are the expected findings on 24-hour radioiodine uptake and thyroid scan?

A Increased uptake with diffuse homogenous appearance on scan

B Decreased uptake with heterogeneous findings on scan

C Increased uptake in multiple focal areas of the thyroid

D Increased uptake in focal area of the thyroid

A

A Increased uptake with diffuse homogenous appearance on scan

Radioiodine uptake provides measures of iodine uptake of the thyroid at 4 and 24 hours. In Graves disease, uptake is elevated with diffuse homogenous image on the scan. The radioiodine scan in patients with thyroiditis shows decreased uptake and heterogenous distribution throughout the thyroid. Radioiodine is concentrated in one spot of the thyroid in patients with toxic adenoma and concentrated in multiple areas in patients with toxic multinodular goiter.

134
Q

Cushing syndrome

A

overproduction of cortisol, ACTH levels also increased

135
Q

Cushing syndrome causes

A

excess ACTH from pituitary tumors or adrenal gland hyper production
mostly from suppression of ACTH production when steroids given in high doses for long periods

secondary - ACTH- secreting tumors of pituitary and small cell lung CA

136
Q

Cushing syndrome S/S

A

rapid weight gain, loss of menses, decreased libido, weakness, bruising
HTN, glucose intolerance, insomnia
memory and mental health disturbance
pedi - depressed linear growth & excess weight gain

137
Q

Cushing syndrome PE

A

central obesity, moon face, buffalo hump, increased supraclavicular fat pads, HTN, muscle weakness & wasting, hisutism, red-purple striae > 1cm, acne, emotional liability or depression

138
Q

Cushing syndrom dx

A

measurement of > 100 mcg coritsol in urine in 24- hr

single midnight (nadir) serum cortisol value > 7.5 mcg/dL

139
Q

Cushing syndrome management

A

depends on source of hypercorisolism

pituitary tumor resection - 1st choice w/ chemo/radiation

bone density measurements obtained r/t chronic glucocorticoid levels and osteoprosis

140
Q

prediabetes

A
HbA1c 5.7% - 6.4%
FPG 100- 125
OGTT 140- 199
impaired fasting glucose
test yearly
141
Q

insulin requirements decrease with

A

weight loss

added exercise

142
Q

insulin requirements increase with

A

illness, infection, surgery, stress, growth spurts

ketoacidosis

143
Q

DM follow up monitor Q3 months

A

BP
HbA1c
lipids
renal status

weight, eye, foot exams, review blood glucose log

144
Q

DM follow up labs/ frequency

A

every 3 months: lpids, renal status, HbA1c

Yearly: LFTs

145
Q

DM yearly screening

A

urinary microalbumin & UA
ophthalmological exam
refer for CV if needed

146
Q

Consult endocrinologist

A

new dx of T1DM
poorly controlled T2DM despite 2 or more meds
discovery of diabetic complication
after hospitalization
initiation of insulin pump or other intensive insulin tx
contemplated or confirmed pregnancy
patient request

147
Q

DKA lab values

A

BG > 250
arterial pH < 7.3
serum bicarb < 15
WITH ketonuria or ketonemia

148
Q

HHS

A

impaired mental status, dehydration, serum osmolarity > 320, plasma glucose > 600

149
Q

hypoglycemia with neuroglycopenia

A

BG < 50 that does NOT respond to tx

coma, seizures, altered behavior, persistent hypoglycemia from sulfonylurea

150
Q

DM refer to nephrologist

A

when microalbumninuria present to prevent further renal dx

151
Q

Insulin dose changes

A

adjust dose every 2- 3 days based on fasting BG levels

increase by 2- 5 units in obese or insulin-resistant pt

1- 2 units in insulin-sensitive pt w/ thin body frame & frequent hypoglycemia

152
Q

DM in pregnancy

insulin requirements

A

1st trimester: insulin doses may be LOWER than prepregnancy r/t hypoglycemia

2nd trimester until 3rd: insulin requirements INCREASED

plateau around 36 weeks

153
Q

A1c < 7.5 management

A

start with metformin

not at goal in 3 months = dual tx

154
Q

A1c > 7.5 management

A

dual tx: metformin or other 1st line AND
GLP-1 RA, SGLT2i, DPP4i, TZD, basal insulin, colesevelam, Bromocriptine QR, AGi, SU/GLN

NOT at goal in 3 months = triple tx

155
Q

A1c > 9%

A

+ symptoms = insulin and other agents

- symptoms = dual or triple tx

156
Q

GDM screening

A

screen with OGTT after overnight fast 24- 28 weeks gestation

157
Q

Sick day management DM

A

monitor BG at least every 4 hr
BG > 250 in T1 assess for ketones

w/ increased BG levels, supplemental rapid-acting insulin can be given every2-4 hr

maintain adequate hydration

take diabetic meds even if not eating

158
Q

URGENT referral to ophthalmologist

A

New report of a sensation of “floaters” or “cobwebs” in eye

Sudden, painless loss of vision

159
Q

Earliest indication of renal damage from DM

A

microalbuminuria

160
Q

Microalbuminuria analysis

A

albumin/creatinine ratio, random spot urine, or a timed (4 hr or overnight) collection

Dx at more than 30mg/24h excretion

Two of three positive collections in 3- to 6- month period are necessary to confirm

161
Q

Consult w/ nephrologist when:

A

Microalbuminuria 30- 300mg/24 h

Albuminuria > 2 mg/dL

Decreased GFR < 50 mL/min

162
Q

Tx when microalbuminuria confirmed

A

ACE-I or ARB initiated
control of BP = most important to prevent/delay renal dx

target 130/80 w/ ASCVD risk of 15%

diet, exercise, weight loss, smoking cessation

163
Q

hyperparathyroidism

A

over secretion of PTH

164
Q

primary hyperparathyroidism

A

Inappropriate secretion of PTH in setting of hypercalcemia

RF: AA, increasing age after 6th decade, ionizing radiation

Causes:
Single parathyroid adenoma
Hyperplasia of all 4 glands, associated w/ multiple endocrine neoplasia (MEN) type I or II
Multiple adenomas

165
Q

Primary hyperparathyroidism S/S

A

Asymptomatic hypercalcemia
Fasting hypophosphatemia
Nonspecific neurocognitive symptoms:
Weakness, easy fatigability, depression, intellectual weariness, cognitive impairment, loss of initiation, anxiety, irritability, insomnia
CV: HTN, CAD, left ventricular hypertrophy, cardiac or valvular calcifications
Kidney stones
Band keratopathy - white cloudiness at nasal and temporal borders of cornea
Bone tenderness - sternum and tibia
Palpable neck mass

166
Q

Primary hyperparathyroidism dx

A

PTH, serum Ca, albumin, 25-hydroxyvitamin D, fasting phosphorus
Bone mineral density assessment of cortical bone site (radius) w/ lumbar spine & hip → assesses risk for osteoporosis
Renal imaging (US) → nephrolithiasis
24-h urine collection for Ca and Cr
< 400mg/day consider kidney stone risk

167
Q

primary hyperparathyroidism management

A
Surgery → ONLY cure 
Refer 
Medical management:
Monitor serum Ca and Cr → annually 
Monitor bone dentist every 1-2 years 
Adequate calcium & Vit D intake
Maintain weight-bearing activity and adequate fluid intake
Medication
Cinacalcet → calcimimetic agent
168
Q

Criteria for parathyroidectomy

A

Age < 50
Serum Ca 1mg/dL above upper limit of normal
Vertebral fx
24-h urine for Ca > 400mg/d and increased stone risk
Presence of nephrolithiasis or nephrocalcinosis
GFR < 60
In perimenopausal or postmenopausal women & men > 50 y.o.
T-score of -2.5 at lumbar spine, femoral neck, total hip, or distal radius
Premenopausal women and men < 50 y.o.
Z-score of -2.5 or lower at same sites

169
Q

Secondary hyperparathyroidism

A

Appropriately increased secretion of PTH in setting of low or normal serum calcium concentration and can be caused by vitamin D deficiency or renal failure
Common in:
CKD, often when GFR < 50
Vit D deficiency/insufficiency < 20 ng/mL and 30 ng/mL
RF: minimum sun exposure, inadequate Vit D intake, obesity, malabsorption, prior gastric surgery, meds ( rifampin, ketoconazole, anticonvulsants)

170
Q

secondary hyperparathyroidism dx

A

PTH, serum Ca, albumin, fasting phosphorus
Serum 25-hydroxyvitamin D if < 20
24-h urine for Ca and Cr

171
Q

KDIGO guidelines for CKD- metabolic bone dx screening

A

Serum Ca, phophorus, and PTH be measured in adult CKD 3 & children CKD 2
Frequency depends on severity of CKD & metabolic bone dx
Ranges from 1- 3 months to every 6- 12 months

172
Q

secondary hyperparathyroidism tx

A

glucocorticoids or PPIs → decrease Ca absorption
Depends on cause:
Renal fx: renal transplantation
CKD 4- 5: calcimimetics, calcitriol or Vit D analogs
CKD 3-5 NOT responding to this: parathyroidectomy indicated

173
Q

TSH measurements

A

hyperthyroid TSH < 0.3

Hypothyroid TSH > 4

Euthyroid TSH 0.3 - 4

174
Q

thyroid nodules

A

Nodules larger than 0.5 cm to 1 cm are palpable

Only 3- 5% are malignant

175
Q

thyroid nodules S/S

A

Asymptomatic
Anaplastic tumor → enlarging, painful mass
Hoarseness, dysphonia, dysphagia, dyspnea
Pathologic fx of spine or hip
Toxic nodules → S/S of hyperthyroidism

176
Q

thyroid nodule PE

A

Swallowing enhances visualization & palpation of thyroid
Nodule size, consistency, mobility, presence and consistency of associated lymphadenopathy
Examine supraclavicular, anterior cervical, and submandibular lymph nodes
Thyroid cancers
Most feel firm or hard
Some can feel soft and fluctuant
Pemberton maneuver

177
Q

Pemberton maneuver

A

Used to examine when substernal extension of nodule/goiter suspected
Elevate both arms until they touch sides of head
Flushing of face, cyanosis, and respiratory distress may occur as result of impingement of structures within thoracic inlet (Pemberton sign)
Distension of neck veins may be apparent

178
Q

thyroid nodule dx

A

TSH
Exclude hyper/hypothyroidism
If TSH suppressed w/ nodules > 1cm → thyroid scan to r/o hyperfunctioning nodule
Most hot nodules benign
Elevated TSH associated w/ increased risk of malignancy
Thyroid US
FNA biopsy

179
Q

thyroid US findings higher likelihood of malignancy

A
Hypoechoic nodules 
Irregular margins 
Absent halo 
Microcalcifications 
Shape taller than width in transverse dimension
180
Q

thyroid US findings predictive of benign nodules

A

Spongiform nodules and simple cysts

181
Q

hot nodules

A

autonomously functioning nodules

rarely CA, FNA not required

182
Q

cold nodules

A

nonfunctioning nodules

FNA biopsy

183
Q

hyperthyroidism extra labs

A
Baseline CBC & LFTS 
Check before initiation of tx w/ thioamides 
Abnormal LFTs common (elevated) 
ESR 
Radioiodine uptake 
Distinguish Graves from thyroiditis
Iodine scan 
Identifies toxic multinodular goiter or solitary nodular goiter
184
Q

thyroid storm

A
life-threatening
temp 102- 105F
profuse sweating
pulse > 120-140 bpm
a. fib 
restlessness
confusion
agitation
coma
severe vomiting, diarrhea, hepatomegaly w/ jaundice
185
Q

myxedema coma

A

hypothermic stuporous state by respiratory depression and death from untreated hypothyroidism
triggers: cold, trauma, infection, meds that depress CNS

186
Q

dietary iodine requirements pregnancy

A

increased

oral supplement containing 150 mcg of potassium iodine

187
Q

pregnancy and hyperthyroidism

A

HCG can cause hyperthyroidism in pregnancy

188
Q

management Hyperthyroidism in pregnancy

A

PTU - 1st trimester

methimazole after 1st trimester r/t hepatotoxicity with PTU

189
Q

pregnancy and hypothryoirisim

A

TH dose increased by 30%

pre pregnancy levothyroxine dose 100 mcg daily, 1 tab taken Monday- Friday and 2 tabs taken Saturday and Sunday (increase from 7 tabs per week to 9 tabs per week

monitor TSH & T4 every month in 1st half of pregnancy then once every trimester

190
Q

pituitary prolactinoma S/S

A

Females:

  • oligomenorrhea or amenorrhea
  • galactorrhea
  • vaginal dryness
  • hirsutism

Males:

  • ED
  • decreased hair
  • gynecomastia

Both:

  • infertility
  • loss of interest in sex
  • low bone density
  • HA
  • visual disturbances
  • delayed puberty
191
Q

prolactinoma exam

A

thyroid exam
neuro exam
ophthalmic exam - visual filed defect

children: pubertal changes, hypogonadism

192
Q

Prolactinoma dx

A

prolactin hormone increased

  • asymptomatic repeat in AM
  • levels correlate with size

BUN/cr - r/o CKD

HCG- r/o pregnancy

TSH/free T4 - t/o hypothyroidism

ALT/AST - r/o liver dx/hepatitis

R/o other causes = MRI pituitary gland

193
Q

prolcatinoma mangement

A

refer endocrine
refer ophthalmology

microadenoma & asymptomatic - NO tx needed

macroadenoma OR symptomatic - dopamine agonists
- cabergoline, symptoms typically resolve quickly

monitor prolactin level
repeat MRI - ensure decreasing

Patient can come off meds after a few years if prolactin levels & MRI normal