Week 2 Diabetes and Endocrine Disorders Flashcards
Pituitary gland releases what hormones
TSH
Adrenocorticotropic hormone (ACTH)
prolactin
thyroid gland releases what hormone
thyroid hormone
Adrenal gland releases what hormones
cortisol
catecholamines
parathyroid gland releases what hormones
parathyroid hormone
pancreas releases what hormones
glucagon
hypothalamus releases what hormones
thyrotropin- releasing hormone (TRH)
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. 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
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
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.
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.
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.
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
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
Hypothyroidism labs
elevated TSH
low free T4
hyperthyroidism labs
low TSH
elevated free T4
Subclinical hypothyroidism labs
elevated TSH
normal free T4
Hypothyroidism d/t pituitary dysfunction labs
normal TSH
low free T4
euthyroid labs
normal TSH
normal free T4
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. 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.
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
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.
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
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.
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
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.
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
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.
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
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
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”
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.
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
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.
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%
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%.
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
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.
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. 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.
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. 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.
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
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.
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
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.
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
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.
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)
c. Metformin
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
c. Exposure to radiation
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
b. Have an increased blood sugar level
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
d. Use of calcium channel blockers
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. Insulin glargine (Lantus) 10 units nightly
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
c. 1 year
DM dx criteria
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
DM screening tests
A1c
FPG
2-h OGTT
no one test preferred
What can make the A1c less accurate?
anemia or hemoglobinpathies (r/t rapid RBC turnover)
2nd/3rd trimester of pregnancy
recent blood loss, transfusion, erythropoietin therapy, hemolysis
DM screening asymptomatic adults
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
DM screening asymptomatic children
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)
T1DM
immune-mediated diabetes with evidence of autoimmune B-cell destruction, typically leading to absolute insulin deficiency
T2DM
multifactoral process, including relative insulin insufficiency, insulin resistance and often unregulated gluconeogensis in liver
gestational DM
dx during 2nd or 3rd trimester of pregnancy that was NOT clear prior to gestation
Dx tests for T1DM
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)
IAA (insulin autoantibodies) more likely to be seen in
IAA present in mostly all young patients with T1DM but may be absent in older patients w/ dx
anti-GAD antibodies more likely to be seen in
more likely present in young adults with T1DM than in children with dx
T1DM pt, screen for what other autoimmune dx?
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
Metformin and renal function
considered safe whose eGFR >/= 30 mL/min
nonpharm management DM/ prediabetes
- healthy eating
- weight control
- increased physical activity (1h/day)
Impaired fasting glucose weight management
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
DM preventative care
A1c < 7% (generally) ASA/antiplatelet agents BP management Cholesterol management screen neuropathy screen retinopathy screen nephropathy immunizations tobacco use assessment
How often do you check A1c in diabetic pt
every 6 months w/ stable glycemic control
every 3 months if NOT at goal or tx changes
recommended A1c nonpregnant adults after tx
< 7%
recommended A1c for children on tx
< 7.5%, individualization encouraged
ASA/antiplatelet agents DM
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
BP screening in DM
measure EVERY visit
goals:
Adults < 140/90 or <130/80 if younger and no burden
Children < 130/80 OR < 90th percentile
BP management in DM
lifestyle changes: DASH diet, weight loss, exercise
Start meds if do not lower BP to target
ACEI, ARBs, CCB, diuretics recc
Cholesterol management in DM
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
neuropathy screening
diabetic foot exam at least annually w/ T2DM and started within 5 years of dx w/ T1DM
How often do you examine feet if pt has deformities or ulcers?
every visit
diabetic foot exam
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
cardiovascular neuropathy
manifests as resting tachycardia and/or orthostatic hypotension
GI neuropathy
gastroparesis
screen if suspicious, gastric emptying study
retiniopathy screening
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
nephropathy screening
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
albuminuria normal value
normal amount < 30mg/24 h
persistent albuminuria marker for CVD
DM & immunizations
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.
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 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.
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
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)
With what condition is prediabetes most commonly associated?
A. chronic pancreatitis
B. HLD
C. Obesity
D. Chronic steroid use
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.
lifestyle modification and glycemic control
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.
DM medications that are weight neutral or cause weight loss
biguanides - metformin
GLP-1 receptor agonists - “tide”
Amylin agonist - pramlintide
DPP-4 inhibitors -“gliptin”
SGLT2 inhibitors - “gliflozin”
monotherapy tx
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
monotherapy tx for DM with high risk for ASCVD or CKD 3 or HF
long-acting GLP-1 receptor agonist
SGLT-2 inhibitor
Metformin contraindications
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
Tx options w/ Metformin
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
When to start dual tx for DM
initial A1c >/= 7.5%
if not at goal in 3 months, intensify tx
DM tx A1c > 9%
start with insulin with or w/o other agents
especially if symptoms of diabetes present
Biguanides
Metformin
reduces A1c 1- 1.5%
MOA: 70% of effect in liver to reduce gluconeogensis
30% in skeletal muscles to decrease insulin resistance
GLP-1 receptor agonists
“-tide”
reduces A1C 1- 1.5%
MOA: potentiates glucose-stimulated insulin secretion
MAY stimulate production of new beta-cells & prevent beta- cell apotosis
Sulfonylureas
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
Thiazolidinediones
Pioglitazone
reduces A1c 1- 1.5%
MOA: Increases insulin sensitivity of skeletal muscle, adipose tissue, and liver
SGLT2 inhibitors
“-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
Non-sulfonylurea secretagogues
“-glinides”
reduce A1c 0.5- 1%
MOA: enhance insulin secretion from pancreas by interacting with ATP-sensitive potassium channels in the beta cell membranes
alpha-glucosidase inhibitors
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
DPP-4 inhibitors
“-gliptin”
reduces A1c 0.5- 1%
MOA: slows degradation of GLP-1 and glucose dependent insulinotropic peptides (GIPs) which is done by DPP-4
Amylin agonists
pramlintide
reduces A1c 0.5%
MOA: Inhibits glucagon production in glucose dependent fashion, mostly decreases postprandial glucose excursions
Biguanides (metformin) SE
metallic taste, nausea, diarrhea, abdominal pain, lactic acidosis (rare – but potentially fatal); B12 deficiency
- GLP-1 agonists SE
Albiglutide, dulaglutide , exenatide, liraglutide, lixisenatide, and samaglutide
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
Sulfonylureas SE
eg, glimepiride, glipizide, glyburide
hypoglycemia (particularly in the elderly or in patients with renal impairment); weight gain; possible aggravation of myocardial ischemia
Thiazolidinedinone (TZDs) SE
pioglitazone
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
SGLT2 inhibitors SE (canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin)
genital mycotic infections; Fournier’s gangrene; volume depletion; decreased eGFR; acute kidney injury; hypotension; fractures; hyperkalemia; hypermagnesemia, hyperphosphatemia; euglycemic diabetic ketoacidosis
Non-Sulfonylurea Secretagogues SE (repaglinide and nateglinide)
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)
Alpha-Glucosidase Inhibitors SE (acarbose and miglitol)
abdominal pain, diarrhea, and flatulence–due to osmotic effects and bacterial fermentation; transaminase elevations; fatal hepatic failure; contraindicated in pts with chronic intestinal diseases
DPP-4 inhibitors SE (alogliptin, linagliptin, saxagliptin, and sitagliptin)
pancreatitis, hypersensitivity reactions, hypoglycemia if used in conjunction with sulfonylureas; fatal hepatic failure; possible worsening of heart failure; possible and severe joint pain
Amylin agonists SE (Pramlintide)
nausea, vomiting, anorexia; headache; severe hypoglycemia (when given with insulin
Bile acid sequestrants SE (colesevelam)
constipation, nausea, and dyspepsia; increased triglycerides; interference with absorption of oral drugs
Bromocriptine SE
nausea; vomiting; fatigue; headache; dizziness; somnolence; syncope
long-acting (basal) insulin
insulin glargine (lantus) - 24h insulin detemir (Levemir) - 12h insulin degludec (Tresiba) - 48h `
insulin initiation recommendations
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
Which of the following hypoglycemic agents have been associated with weight loss?
A Metformin
B Insulin
C Glyburide
D Pioglitazone
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.
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
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.
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 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
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
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.
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
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.
Rapid Acting Insulin
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
Short acting insulin
Onset 30 to 60 minutes, Peak 2 to 3 hours, Duration 8 to 10 hours
o Regular insulin (Humulin R, Novolin R)
Intermediate acting insulin
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)
long acting insulin
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
premixed insulin
Onset 30 to 60 minutes, Dual Peak, Duration 10 to 16 hours
o 70% NPH / 30% regular insulin (Humulin 70/30)
screening recommendations for complications of T1DM
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
congenital hypothyroidism S/S
lethargy hypotonia hoarse cry feeding issues constipation macroglossia open posterior fontanelle umbilical hernia dry skin hypothermia prolonged jaundice
Newborn screen hypothyroidism
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
Tx congenital hypothyroidism
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
Hashimoto thyroiditis
most common cause of acquired hypothyroidism
autoimmune condition
Hashimoto thyroiditis S/S
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
hypothyroidism labs
TSH elevated T4 normal (subclinical) or decreased thyroid antibodies (thyroid peroxidase antibody and thyroglobulin antibody)
Hashimoto thyroiditis tx
Levothyroxine
based on lab values, age, & weight of child
monitor free T4 & TSH 3- 6 months
The most common physical finding in a child with congenital hypothyroidism is:
A Open posterior fontanelle
B Macroglossia
C Hypotonia
D Normal physical exam
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.
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 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.
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
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.
most common cause of hyperthyroidism
Graves dx: autoimmune condition
Graves dx S/S
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
Graves dx labs
TSH - depressed or undetectable T4- elevated T3 - elevated TRAbs present in 95% thyroid peroxidase and antithyroglobulin antibodies +
24-h radioiodine uptake
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).
24-h radioiodine scan
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.
Pertechnetate thyroid scan
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.
other individualized tests in hyperthyroidism
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
Graves dx tx
antithyroid med: methimazole & propylthiouracil (PTU)
radioiodine therapy
thyroidectomy - fail med tx, drug reactions, large goiters, severe ophthalmopathy
permanent hypothyroidism is goal of tx
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
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.
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
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.
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 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.
Cushing syndrome
overproduction of cortisol, ACTH levels also increased
Cushing syndrome causes
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
Cushing syndrome S/S
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
Cushing syndrome PE
central obesity, moon face, buffalo hump, increased supraclavicular fat pads, HTN, muscle weakness & wasting, hisutism, red-purple striae > 1cm, acne, emotional liability or depression
Cushing syndrom dx
measurement of > 100 mcg coritsol in urine in 24- hr
single midnight (nadir) serum cortisol value > 7.5 mcg/dL
Cushing syndrome management
depends on source of hypercorisolism
pituitary tumor resection - 1st choice w/ chemo/radiation
bone density measurements obtained r/t chronic glucocorticoid levels and osteoprosis
prediabetes
HbA1c 5.7% - 6.4% FPG 100- 125 OGTT 140- 199 impaired fasting glucose test yearly
insulin requirements decrease with
weight loss
added exercise
insulin requirements increase with
illness, infection, surgery, stress, growth spurts
ketoacidosis
DM follow up monitor Q3 months
BP
HbA1c
lipids
renal status
weight, eye, foot exams, review blood glucose log
DM follow up labs/ frequency
every 3 months: lpids, renal status, HbA1c
Yearly: LFTs
DM yearly screening
urinary microalbumin & UA
ophthalmological exam
refer for CV if needed
Consult endocrinologist
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
DKA lab values
BG > 250
arterial pH < 7.3
serum bicarb < 15
WITH ketonuria or ketonemia
HHS
impaired mental status, dehydration, serum osmolarity > 320, plasma glucose > 600
hypoglycemia with neuroglycopenia
BG < 50 that does NOT respond to tx
coma, seizures, altered behavior, persistent hypoglycemia from sulfonylurea
DM refer to nephrologist
when microalbumninuria present to prevent further renal dx
Insulin dose changes
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
DM in pregnancy
insulin requirements
1st trimester: insulin doses may be LOWER than prepregnancy r/t hypoglycemia
2nd trimester until 3rd: insulin requirements INCREASED
plateau around 36 weeks
A1c < 7.5 management
start with metformin
not at goal in 3 months = dual tx
A1c > 7.5 management
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
A1c > 9%
+ symptoms = insulin and other agents
- symptoms = dual or triple tx
GDM screening
screen with OGTT after overnight fast 24- 28 weeks gestation
Sick day management DM
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
URGENT referral to ophthalmologist
New report of a sensation of “floaters” or “cobwebs” in eye
Sudden, painless loss of vision
Earliest indication of renal damage from DM
microalbuminuria
Microalbuminuria analysis
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
Consult w/ nephrologist when:
Microalbuminuria 30- 300mg/24 h
Albuminuria > 2 mg/dL
Decreased GFR < 50 mL/min
Tx when microalbuminuria confirmed
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
hyperparathyroidism
over secretion of PTH
primary hyperparathyroidism
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
Primary hyperparathyroidism S/S
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
Primary hyperparathyroidism dx
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
primary hyperparathyroidism management
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
Criteria for parathyroidectomy
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
Secondary hyperparathyroidism
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)
secondary hyperparathyroidism dx
PTH, serum Ca, albumin, fasting phosphorus
Serum 25-hydroxyvitamin D if < 20
24-h urine for Ca and Cr
KDIGO guidelines for CKD- metabolic bone dx screening
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
secondary hyperparathyroidism tx
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
TSH measurements
hyperthyroid TSH < 0.3
Hypothyroid TSH > 4
Euthyroid TSH 0.3 - 4
thyroid nodules
Nodules larger than 0.5 cm to 1 cm are palpable
Only 3- 5% are malignant
thyroid nodules S/S
Asymptomatic
Anaplastic tumor → enlarging, painful mass
Hoarseness, dysphonia, dysphagia, dyspnea
Pathologic fx of spine or hip
Toxic nodules → S/S of hyperthyroidism
thyroid nodule PE
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
Pemberton maneuver
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
thyroid nodule dx
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
thyroid US findings higher likelihood of malignancy
Hypoechoic nodules Irregular margins Absent halo Microcalcifications Shape taller than width in transverse dimension
thyroid US findings predictive of benign nodules
Spongiform nodules and simple cysts
hot nodules
autonomously functioning nodules
rarely CA, FNA not required
cold nodules
nonfunctioning nodules
FNA biopsy
hyperthyroidism extra labs
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
thyroid storm
life-threatening temp 102- 105F profuse sweating pulse > 120-140 bpm a. fib restlessness confusion agitation coma severe vomiting, diarrhea, hepatomegaly w/ jaundice
myxedema coma
hypothermic stuporous state by respiratory depression and death from untreated hypothyroidism
triggers: cold, trauma, infection, meds that depress CNS
dietary iodine requirements pregnancy
increased
oral supplement containing 150 mcg of potassium iodine
pregnancy and hyperthyroidism
HCG can cause hyperthyroidism in pregnancy
management Hyperthyroidism in pregnancy
PTU - 1st trimester
methimazole after 1st trimester r/t hepatotoxicity with PTU
pregnancy and hypothryoirisim
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
pituitary prolactinoma S/S
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
prolactinoma exam
thyroid exam
neuro exam
ophthalmic exam - visual filed defect
children: pubertal changes, hypogonadism
Prolactinoma dx
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
prolcatinoma mangement
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
