Week 2 Diabetes and Endocrine Disorders

Question 1

Pituitary gland releases what hormones

Answer 1

TSH
Adrenocorticotropic hormone (ACTH)
prolactin

Question 2

thyroid gland releases what hormone

Answer 2

thyroid hormone

Question 3

Adrenal gland releases what hormones

Answer 3

cortisol

catecholamines

Question 4

parathyroid gland releases what hormones

Answer 4

parathyroid hormone

Question 5

pancreas releases what hormones

Answer 5

glucagon

Question 6

hypothalamus releases what hormones

Answer 6

thyrotropin- releasing hormone (TRH)

Question 7

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

Answer 7

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

Question 8

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

Answer 8

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.

Question 9

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.

Answer 9

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.

Question 10

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

Answer 10

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

Question 11

Hypothyroidism labs

Answer 11

elevated TSH

low free T4

Question 12

hyperthyroidism labs

Answer 12

low TSH

elevated free T4

Question 13

Subclinical hypothyroidism labs

Answer 13

elevated TSH

normal free T4

Question 14

Hypothyroidism d/t pituitary dysfunction labs

Answer 14

normal TSH

low free T4

Question 15

euthyroid labs

Answer 15

normal TSH

normal free T4

Question 16

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

Answer 16

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.

Question 17

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

Answer 17

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.

Question 18

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

Answer 18

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.

Question 19

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

Answer 19

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.

Question 20

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

Answer 20

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.

Question 21

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

Answer 21

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

Question 22

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”

Answer 22

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.

Question 23

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

Answer 23

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.

Question 24

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%

Answer 24

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%.

Question 25

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

Answer 25

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.

Question 26

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

Answer 26

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.

Question 27

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

Answer 27

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.

Question 28

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

Answer 28

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.

Question 29

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

Answer 29

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.

Question 30

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

Answer 30

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.

Question 31

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)

Answer 31

c. Metformin

Question 32

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

Answer 32

c. Exposure to radiation

Question 33

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

Answer 33

b. Have an increased blood sugar level

Question 34

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

Answer 34

d. Use of calcium channel blockers

Question 35

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

Answer 35

a. Insulin glargine (Lantus) 10 units nightly

Question 36

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

Answer 36

c. 1 year

Question 37

DM dx criteria

Answer 37

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

Question 38

DM screening tests

Answer 38

A1c FPG 2-h OGTT no one test preferred

Question 39

What can make the A1c less accurate?

Answer 39

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

Question 40

DM screening asymptomatic adults

Answer 40

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

Question 41

DM screening asymptomatic children

Answer 41

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)

Question 42

T1DM

Answer 42

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

Question 43

T2DM

Answer 43

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

Question 44

gestational DM

Answer 44

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

Question 45

Dx tests for T1DM

Answer 45

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)

Question 46

IAA (insulin autoantibodies) more likely to be seen in

Answer 46

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

Question 47

anti-GAD antibodies more likely to be seen in

Answer 47

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

Question 48

T1DM pt, screen for what other autoimmune dx?

Answer 48

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

Question 49

Metformin and renal function

Answer 49

considered safe whose eGFR >/= 30 mL/min

Question 50

nonpharm management DM/ prediabetes

Answer 50

- healthy eating - weight control - increased physical activity (1h/day)

Question 51

Impaired fasting glucose weight management

Answer 51

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

Question 52

DM preventative care

Answer 52

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

Question 53

How often do you check A1c in diabetic pt

Answer 53

every 6 months w/ stable glycemic control every 3 months if NOT at goal or tx changes

Question 54

recommended A1c nonpregnant adults after tx

Answer 54

< 7%

Question 55

recommended A1c for children on tx

Answer 55

< 7.5%, individualization encouraged

Question 56

ASA/antiplatelet agents DM

Answer 56

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

Question 57

BP screening in DM

Answer 57

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

Question 58

BP management in DM

Answer 58

lifestyle changes: DASH diet, weight loss, exercise Start meds if do not lower BP to target ACEI, ARBs, CCB, diuretics recc

Question 59

Cholesterol management in DM

Answer 59

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

Question 60

neuropathy screening

Answer 60

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

Question 61

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

Answer 61

every visit

Question 62

diabetic foot exam

Answer 62

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

Question 63

cardiovascular neuropathy

Answer 63

manifests as resting tachycardia and/or orthostatic hypotension

Question 64

GI neuropathy

Answer 64

gastroparesis screen if suspicious, gastric emptying study

Question 65

retiniopathy screening

Answer 65

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

Question 66

nephropathy screening

Answer 66

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

Question 67

albuminuria normal value

Answer 67

normal amount < 30mg/24 h persistent albuminuria marker for CVD

Question 68

DM & immunizations

Answer 68

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.

Question 69

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

Answer 69

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.

Question 70

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

Answer 70

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)

Question 71

With what condition is prediabetes most commonly associated? A. chronic pancreatitis B. HLD C. Obesity D. Chronic steroid use

Answer 71

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.

Question 72

lifestyle modification and glycemic control

Answer 72

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.

Question 73

DM medications that are weight neutral or cause weight loss

Answer 73

biguanides - metformin GLP-1 receptor agonists - "tide" Amylin agonist - pramlintide DPP-4 inhibitors -"gliptin" SGLT2 inhibitors - "gliflozin"

Question 74

monotherapy tx

Answer 74

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

Question 75

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

Answer 75

long-acting GLP-1 receptor agonist | SGLT-2 inhibitor

Question 76

Metformin contraindications

Answer 76

``` 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

Question 77

Tx options w/ Metformin

Answer 77

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

Question 78

When to start dual tx for DM

Answer 78

initial A1c >/= 7.5% if not at goal in 3 months, intensify tx

Question 79

DM tx A1c > 9%

Answer 79

start with insulin with or w/o other agents | especially if symptoms of diabetes present

Question 80

Biguanides

Answer 80

Metformin reduces A1c 1- 1.5% MOA: 70% of effect in liver to reduce gluconeogensis 30% in skeletal muscles to decrease insulin resistance

Question 81

GLP-1 receptor agonists

Answer 81

"-tide" reduces A1C 1- 1.5% MOA: potentiates glucose-stimulated insulin secretion MAY stimulate production of new beta-cells & prevent beta- cell apotosis

Question 82

Sulfonylureas

Answer 82

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

Question 83

Thiazolidinediones

Answer 83

Pioglitazone reduces A1c 1- 1.5% MOA: Increases insulin sensitivity of skeletal muscle, adipose tissue, and liver

Question 84

SGLT2 inhibitors

Answer 84

"-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

Question 85

Non-sulfonylurea secretagogues

Answer 85

"-glinides" reduce A1c 0.5- 1% MOA: enhance insulin secretion from pancreas by interacting with ATP-sensitive potassium channels in the beta cell membranes

Question 86

alpha-glucosidase inhibitors

Answer 86

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

Question 87

DPP-4 inhibitors

Answer 87

"-gliptin" reduces A1c 0.5- 1% MOA: slows degradation of GLP-1 and glucose dependent insulinotropic peptides (GIPs) which is done by DPP-4

Question 88

Amylin agonists

Answer 88

pramlintide reduces A1c 0.5% MOA: Inhibits glucagon production in glucose dependent fashion, mostly decreases postprandial glucose excursions

Question 89

Biguanides (metformin) SE

Answer 89

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

Question 90

2. GLP-1 agonists SE | Albiglutide, dulaglutide , exenatide, liraglutide, lixisenatide, and samaglutide

Answer 90

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

Question 91

Sulfonylureas SE | eg, glimepiride, glipizide, glyburide

Answer 91

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

Question 92

Thiazolidinedinone (TZDs) SE | pioglitazone

Answer 92

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

Question 93

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

Answer 93

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

Question 94

Non-Sulfonylurea Secretagogues SE (repaglinide and nateglinide)

Answer 94

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)

Question 95

Alpha-Glucosidase Inhibitors SE (acarbose and miglitol)

Answer 95

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

Question 96

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

Answer 96

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

Question 97

Amylin agonists SE (Pramlintide)

Answer 97

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

Question 98

Bile acid sequestrants SE (colesevelam)

Answer 98

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

Question 99

Bromocriptine SE

Answer 99

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

Question 100

long-acting (basal) insulin

Answer 100

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

Question 101

insulin initiation recommendations

Answer 101

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

Question 102

Which of the following hypoglycemic agents have been associated with weight loss? A Metformin B Insulin C Glyburide D Pioglitazone

Answer 102

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.

Question 103

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

Answer 103

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.

Question 104

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

Answer 104

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

Question 105

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

Answer 105

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.

Question 106

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

Answer 106

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.

Question 107

Rapid Acting Insulin

Answer 107

``` 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 ```

Question 108

Short acting insulin

Answer 108

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

Question 109

Intermediate acting insulin

Answer 109

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)

Question 110

long acting insulin

Answer 110

``` 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 ```

Question 111

premixed insulin

Answer 111

Onset 30 to 60 minutes, Dual Peak, Duration 10 to 16 hours | o 70% NPH / 30% regular insulin (Humulin 70/30)

Question 112

screening recommendations for complications of T1DM

Answer 112

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

Question 113

congenital hypothyroidism S/S

Answer 113

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

Question 114

Newborn screen hypothyroidism

Answer 114

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

Question 115

Tx congenital hypothyroidism

Answer 115

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

Question 116

Hashimoto thyroiditis

Answer 116

most common cause of acquired hypothyroidism | autoimmune condition

Question 117

Hashimoto thyroiditis S/S

Answer 117

``` 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

Question 118

hypothyroidism labs

Answer 118

``` TSH elevated T4 normal (subclinical) or decreased thyroid antibodies (thyroid peroxidase antibody and thyroglobulin antibody) ```

Question 119

Hashimoto thyroiditis tx

Answer 119

Levothyroxine based on lab values, age, & weight of child monitor free T4 & TSH 3- 6 months

Question 120

The most common physical finding in a child with congenital hypothyroidism is: A Open posterior fontanelle B Macroglossia C Hypotonia D Normal physical exam

Answer 120

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.

Question 121

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

Answer 121

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.

Question 122

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

Answer 122

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.

Question 123

most common cause of hyperthyroidism

Answer 123

Graves dx: autoimmune condition

Question 124

Graves dx S/S

Answer 124

``` 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

Question 125

Graves dx labs

Answer 125

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

Question 126

24-h radioiodine uptake

Answer 126

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).

Question 127

24-h radioiodine scan

Answer 127

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.

Question 128

Pertechnetate thyroid scan

Answer 128

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.

Question 129

other individualized tests in hyperthyroidism

Answer 129

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

Question 130

Graves dx tx

Answer 130

antithyroid med: methimazole & propylthiouracil (PTU) radioiodine therapy thyroidectomy - fail med tx, drug reactions, large goiters, severe ophthalmopathy permanent hypothyroidism is goal of tx

Question 131

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

Answer 131

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.

Question 132

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

Answer 132

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.

Question 133

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

Answer 133

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.

Question 134

Cushing syndrome

Answer 134

overproduction of cortisol, ACTH levels also increased

Question 135

Cushing syndrome causes

Answer 135

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

Question 136

Cushing syndrome S/S

Answer 136

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

Question 137

Cushing syndrome PE

Answer 137

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

Question 138

Cushing syndrom dx

Answer 138

measurement of > 100 mcg coritsol in urine in 24- hr single midnight (nadir) serum cortisol value > 7.5 mcg/dL

Question 139

Cushing syndrome management

Answer 139

depends on source of hypercorisolism pituitary tumor resection - 1st choice w/ chemo/radiation bone density measurements obtained r/t chronic glucocorticoid levels and osteoprosis

Question 140

prediabetes

Answer 140

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

Question 141

insulin requirements decrease with

Answer 141

weight loss | added exercise

Question 142

insulin requirements increase with

Answer 142

illness, infection, surgery, stress, growth spurts | ketoacidosis

Question 143

DM follow up monitor Q3 months

Answer 143

BP HbA1c lipids renal status weight, eye, foot exams, review blood glucose log

Question 144

DM follow up labs/ frequency

Answer 144

every 3 months: lpids, renal status, HbA1c Yearly: LFTs

Question 145

DM yearly screening

Answer 145

urinary microalbumin & UA ophthalmological exam refer for CV if needed

Question 146

Consult endocrinologist

Answer 146

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

Question 147

DKA lab values

Answer 147

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

Question 148

HHS

Answer 148

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

Question 149

hypoglycemia with neuroglycopenia

Answer 149

BG < 50 that does NOT respond to tx | coma, seizures, altered behavior, persistent hypoglycemia from sulfonylurea

Question 150

DM refer to nephrologist

Answer 150

when microalbumninuria present to prevent further renal dx

Question 151

Insulin dose changes

Answer 151

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

Question 152

DM in pregnancy | insulin requirements

Answer 152

1st trimester: insulin doses may be LOWER than prepregnancy r/t hypoglycemia 2nd trimester until 3rd: insulin requirements INCREASED plateau around 36 weeks

Question 153

A1c < 7.5 management

Answer 153

start with metformin | not at goal in 3 months = dual tx

Question 154

A1c > 7.5 management

Answer 154

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

Question 155

A1c > 9%

Answer 155

+ symptoms = insulin and other agents | - symptoms = dual or triple tx

Question 156

GDM screening

Answer 156

screen with OGTT after overnight fast 24- 28 weeks gestation

Question 157

Sick day management DM

Answer 157

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

Question 158

URGENT referral to ophthalmologist

Answer 158

New report of a sensation of “floaters” or “cobwebs” in eye Sudden, painless loss of vision

Question 159

Earliest indication of renal damage from DM

Answer 159

microalbuminuria

Question 160

Microalbuminuria analysis

Answer 160

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

Question 161

Consult w/ nephrologist when:

Answer 161

Microalbuminuria 30- 300mg/24 h Albuminuria > 2 mg/dL Decreased GFR < 50 mL/min

Question 162

Tx when microalbuminuria confirmed

Answer 162

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

Question 163

hyperparathyroidism

Answer 163

over secretion of PTH

Question 164

primary hyperparathyroidism

Answer 164

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

Question 165

Primary hyperparathyroidism S/S

Answer 165

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

Question 166

Primary hyperparathyroidism dx

Answer 166

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

Question 167

primary hyperparathyroidism management

Answer 167

``` 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 ```

Question 168

Criteria for parathyroidectomy

Answer 168

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

Question 169

Secondary hyperparathyroidism

Answer 169

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)

Question 170

secondary hyperparathyroidism dx

Answer 170

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

Question 171

KDIGO guidelines for CKD- metabolic bone dx screening

Answer 171

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

Question 172

secondary hyperparathyroidism tx

Answer 172

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

Question 173

TSH measurements

Answer 173

hyperthyroid TSH < 0.3 Hypothyroid TSH > 4 Euthyroid TSH 0.3 - 4

Question 174

thyroid nodules

Answer 174

Nodules larger than 0.5 cm to 1 cm are palpable | Only 3- 5% are malignant

Question 175

thyroid nodules S/S

Answer 175

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

Question 176

thyroid nodule PE

Answer 176

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

Question 177

Pemberton maneuver

Answer 177

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

Question 178

thyroid nodule dx

Answer 178

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

Question 179

thyroid US findings higher likelihood of malignancy

Answer 179

``` Hypoechoic nodules Irregular margins Absent halo Microcalcifications Shape taller than width in transverse dimension ```

Question 180

thyroid US findings predictive of benign nodules

Answer 180

Spongiform nodules and simple cysts

Question 181

hot nodules

Answer 181

autonomously functioning nodules | rarely CA, FNA not required

Question 182

cold nodules

Answer 182

nonfunctioning nodules | FNA biopsy

Question 183

hyperthyroidism extra labs

Answer 183

``` 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 ```

Question 184

thyroid storm

Answer 184

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

Question 185

myxedema coma

Answer 185

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

Question 186

dietary iodine requirements pregnancy

Answer 186

increased oral supplement containing 150 mcg of potassium iodine

Question 187

pregnancy and hyperthyroidism

Answer 187

HCG can cause hyperthyroidism in pregnancy

Question 188

management Hyperthyroidism in pregnancy

Answer 188

PTU - 1st trimester | methimazole after 1st trimester r/t hepatotoxicity with PTU

Question 189

pregnancy and hypothryoirisim

Answer 189

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

Question 190

pituitary prolactinoma S/S

Answer 190

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

Question 191

prolactinoma exam

Answer 191

thyroid exam neuro exam ophthalmic exam - visual filed defect children: pubertal changes, hypogonadism

Question 192

Prolactinoma dx

Answer 192

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

Question 193

prolcatinoma mangement

Answer 193

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